ORL, H&N Surgery

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Part One Otology and Neurotology

Examination of the ear 1
Physology of hearing 9
Functional examination of hearing 16
Vestibular function tests 27
Congenital malformation of the ear 31
Ear trauma 33
Barotraumas 40
Otitis media 43
Chronic otitis media in children 67
Mastoid surgery 77
Reconstructive middle ear surgery 90
Otosclerosis 97
Facial nerve paralysis 112
Labyrinthitis 127
Menier’s disease 131
Ototoxicity 139
Hearing loss 142
Deafness in children 153
Hearing aids 171
Cochlear implants 178
Tinnitus 184
Vertigo 192
Nystagmus 198
Vestibular disorders in children 203
Tumors of the ear 216
Vestibular Schwannoma 221
Glomus tumor 226
Part Two Nose and Paranasal sinuses
Examination of the nose 235
Nasoendoscopy 237
Congenital anomalies 242
ORL , Head & Neck surgery 2

Lectures series in Basra teaching centre of ORL , Head & neck surgery … Dr. Aws A. Alhussona
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Fracture of the facial skeleton 248

Fracture of the nasal bones 253
Epistaxis 260
Rhinitis 268
Sinusitis 276
Nasal obstruction and rhinorrhea in children 301
Nasal polyps 307
Nasal septum 317
Rhinoplasty 326
Snoring and sleep apneoa 336
Non-healing granulomas 343
CSF rhinorrhea 347
Trans-sphenoidal hypophysectomy 356
The orbit 363
Olfaction and disorders 373
Oro-antral fistula 384
Tumors of the nose and sinuses 386
Facial pain and headache 395
Part Three Oral cavity and salivary glands
Examination of the throat 402
Oral cavity conditions 405
Salivary glands 420
Drooling 443
Cysts , granuloma and tumors of the jaw 448
Part Four Pharynx
Pharyngitis 452
Pharyngeal pouch 460
Nasopharyngeal carcinoma 465
Tumors of the oropharynx 471
Tumors of the hypopharynx 479
Angiofibroma 487
Tonsillectomy and adenoidectomy 491
Tumors of the ITF and PPS 497
Part Five Larynx and trachea
Congenital disorders of the larynx & trachea 504
Acute laryngeal infections in children 509
Recurrent respiratory papillomatosis 517
Trauma and stenosis of the larynx and trachea 519
Foreign body in the larynx and trachea 527
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Stenosis of the larynx 531

Stertor and stridor 534
Voice disorders 537
Vocal cord paralysis 542
Tumors of the larynx 551
Carcinoma of the larynx 556
Carcinoma of the larynx , treatment options 564
Voice rehabilitation after toatal laryngectomy 585
Endoscopic management of laryngeal lesion 588
Tracheostomy 601
Part Six Thyroid gland and parathyroids
Anatomy and physiology 612
Thyroid nodules and cysts 614
Goiter 617
Thyroid neoplasia 619
Hyperparathyroidism and hypercalcaemia 622
Part Seven General otorhinolaryngology
Radiography of the head and neck 626
Mass in the neck 627
Metastatic neck diseases 640
Laser in the head and neck surgery 651
AIDS in otorhinolaryngology 659
Chemotherapy in the head and neck cancers 666
Radiotherapy in the head and neck cancers 670
Paediatric endoscopy 675
ENT manifestations of systemic diseases 681
Appendix
A . Commonly asked questions at the oral exam 685
B. Branchial apparatus 719
C. Cranial nerves 720

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Examination of the ear

I. History , which include ;
a. Otalgia , the ear supply from 5th , 7th , 9th & 10 th cranial nerves , pain may be local or
referred otalgia , local like herpes zooster , dermatitis …etc .
b. Aural discharge (otorrhea) , which is either ;
(1) Itch , watery discharge odourless ; otitis externa .
(2) Clear fluid discharge , from the ear after trauma ; CSF leak .
(3) Discharge containing mucous is arise from the glands in the middle ear .
(4) A thick brown discharge of liquefied wax , healthy ear or acute otitis media .
(5) Foul smell & discharge means chronic suppurative otitis media (CSOM).
(6) Bloody discharge ; CSOM with neoplastic changes .
(7) Bleeding from the ear without trauma ; glomus , vascular anomalies in the
external ear .
c. Abnormalities of the auditory perception ;
- Conversation : 40 dB hearing level .
- Doorbell : 60 dB hearing level .
- Telephone 40-70 dB hearing level , frequency 200-1200 Hz .
(1) Hearing loss ;
- Paracusis Willisi , hear better in the noisy environment , i.e. otosclerosis .
- SNHL , loss of discrimination particularly in background noise .
- Recruitment of loudness , charcteristic of choclear hearing loss , slightly
increased in intensity of the auditory stimuli can cause frank discomfort , i.e.
poor discrimination without recruitment (auditory nerve lesion) .
- Diplacusis , one ear different in hearing (tonal) from other ear in
endolymphatic hydrops .
- Autophony , abnormal perception of once own breath & viscus sounds ,
patulous Eustachian tube .
- Fluctuant hearing loss , either CHL or SNHL .
- Onset of hearing loss , sudden in vascular , unknown , viral , acoustic neuroma ,
malaria , perilymphatic fistula …etc .
- Previous otological procedures .
- Family history .
- Occupational history .
- Past medical history .
- Drug history , loop diuretics , aminoglycosides , cytotoxic , salicylate , quinine .
- In children , history of poor speech development .
(2) Tinnitus ;
- Nature , charcter of Tinnitus , beating , bounding ; vascular .
- Dull continuous in CHL .
- Noise of life insect in patent Eustachian tube .
- Character ; rushing , hissing , or ringing i.e. choclea , neuropathy …etc .
II. Physical examination , this include examination of the :
a. Pinna ; shape , size , symmetry , signs of inflammation & ulcers ..etc .
b. External auditory meatus ; patency (atresia , stenosis) , swelling (inflammatory ,
neopastic) , discharge (wax , mucoid , purulent , haemorrhagic , watery) , tragal
tenderness , sagging of the postero-superior meatal wall .

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c. Tympanic membrane ; using naked eye , otoscope & otomicroscope , look for the
position , color (heamorrhage , dullness , blue , bullae) , ossicles , perforations
(marginal , central , size , number) , mobility (retraction) by using pneumatic
otoscope or Siegle’s speculum .
d. Middle ear ; can be examined through a perforation , look at the color of the mucosa
, oedema , discharge , polyps , promontory …etc .
e. Eustachian tube function
Qualitative methods are ;
(1) Valsalva maneuver ; this is used to demonstrate the tubal patency without any
external aids .
After taking a deep breath , the patient pinch his nose & closes his mouth in an
attempt to blow air in his ears , otoscopy shows movement of the drum &
auscultation reveal crackling .
Failure of this maneuver doesn’t prove pathological occlusion of the tube , also
in case of nasal & nasopharyngeal infection it carries the risk of transmitting
infection to the ears .
(2) Toynbee’s test ; it is safer & confirm normal tubal function .
The nose is closed & the patient swallows , there is drawing of the tympanic
membrane confirmed by otoscopy & on ausculatation when the noise is heard .
(3) Politzer’s test ; when the soft palate is elevated , the pressure in the
nasopharynx is increased which opens the tube .
Occlude one of the patient’s nostrils with olive of rubber balloon & pinch the
other nostril tightly , the patient elevates the palate by swallowing or saying
KAY KAY , at the same time air pressure in the closed nasal cavity is increased
by pressing the Politzer’s bag . The doctor hear the rush of air into the middle
ear by auscultation using a tube (optical assessment can be used also) .
(4) Tubal catheterization ; it is to artificially blow air through the tubal opening , a
silver catheter with an angulated tip is passed through the nose to engage the
tubal opening , air is forced into the ear by connecting the catheter to a balloon
Complications like ; tubal OM , rupture of an atrophic drum , nasal bleeding ,
damage to the tubal ostium .
Quantitative methods : (1) Manometry (2) Sonomanometry (3) Acoustic impedence &
(4) Tympanometry .
f. Tests of hearing (mention in separate topic) .
g. Tests of balance (mention in separate topic) .
h. Eyes .
i. Cranial nerves .
j. Post-aural area & lymph nodes ; for tenderness , masses , redness ..etc .
III. Radiology
A. Conventional radiology
1. Lateral oblique view (Stockholm B) ;
- Mastoid antrum & air cell system .
- LAevel of the middle cranial fossa .
- Position of the lateral sinus .
2. Posteroanterior oblique vies (Stevers)
- Internal auditory meatus .

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- Cochlea & semicircular canals .

-Petrous apex .
- Mastoid process
3. 25-35 fronto-occipital view (Townes)
- Internal auditory meatus .
- Cochlea & semicircular canals .
-Middle ear & bony external auditory meatus .
4. Submentovertical view
- Skull base .
- Petrous apex .
- Cochlea & SCC .
- Mastoid air cell system
B. Tomography
- Fractures .
- Bony destruction .
- Specific structures ; IAM , Middle ear & ossicles, inner ear & Jugular fossa .
C. CT scan ; Tumors .
D.Carotid arteriography ; Glomus tympanicum/Jugulare .

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Physiology of hearing
For physiological purposes , the ear is divided into two parts :
A. Conducting apparatus , consisting of :
1. External ear .
2. Tympanic membrane.
3. Chain of ossicles .
4. Eustachian tube .
5. Labyrinthine fluids .
B. Perceiving ( sensorineural )apparatus consisting of:
1. Endorgan (organ of Corti ) .
2. Auditory division of VIIIth cranial nerve .
3. Central connections
Outer ear
The outer ear have two influences on the coming sounds ;
(1) Increase the pressure at the tympanic membrane in frequency sensitive way .
(2) It increases the pressure at the tympanic membrane in a way that depends on the
direction of the sound source & this aid in sound localization .
The gain in the sound pressure at the tympanic membrane ;
o The pinna-concha system itself acts like ear trumpet concentrating & increasing the
sound energy on the tympanic membrane .
o The resonance in the external canal changes the sound pressure at the tympanic
membrane in a frequency selective way , if the tube is one quarter the wave length
long with one end open & the other end closed in which there is higher pressure &
this described in the external meatus .
o The total effect of reflection from the pinna & head and various external ear
resonance is to add 15-20 dB to the sound pressure in frequency range 2-7 KHz .
The sound localization
o The most powerful cues for sound localization are provided by binaural interactions
, however the outer ear provide important cues which are useful in monaural
localization
o If the sound source is moved around the head starting in front & moving around to
the side , the main change produced is on attention of us to 10 dB in frequency range
2-7 KHz , by interference between the more transmitted directly & the wave settled
off pinna
o The dip in the transfer function around 10 KHz give information as the elevation of
the sound source above the horizontal plane .
o The direction from which a sound is presented by correlation within the CNS of the
difference , between the sound pattern on the 2 sides of the head , the clues are ;
(1) Loudness difference in high frequencies .
(2) Difference in time of reception in the two ears .
(3) Phase difference in low frequencies .
Middle ear
As the alternating compressions and rarefactions of the oncoming sound waves strike the
tympanic membrane , it moves in and out. The malleus, attached to the fibrous layer of the
drumhead, moves in and out (together with the movement of incus) are transmitted, in
turn, to the stapes.

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o Conduct sounds energy to the inner ear .

o Physiological protection of the cochlea .
o Match the impedance of the air to the higher impedance of the labyrinthine fluid .
o Apply sound preferentially to the only one window of the cochlea .
The mode of vibration of the middle ear structures ;
o The calculation of the transfer action required a detailed knowledge of the way that
the middle ear structures move in response to sound .
o It suggest that the movement of the malleus is somewhat less than the mean
movement of the tympanic membrane , Khonna & Toundont (1972) , show that for
frequencies below 6 KHz , the displacement of the malleus is some 0.5 times the
mean displacement of the tympanic membrane , while for frequencies > 6 KHz the
pattern become much more complex , the vibration broken to many zones with a
reduction in the efficacy of the transfer of vibration to the malleus .
o The axis of rotation of the ossicles & the axis of the suspension by their ligaments
merely coincide with their centre of rotational inertia .
o At low frequencies , the coincidence of the centre of inertia of the ossicles with their
center of rotation will help reduce the perception of bone conducted sound .
o Experiments on human cadavers suggest that the stapes rocked in the oval window
as well as move in & out , this was described by asymmetry in the annular ligaments
which fits more tightly on its posterior edge .
The impedance transformer action of the middle ear ;
o The impedance of the middle ear considered to the impedance of the cochlea .
o The impedance of the cochlea determined by factors , such as ;
(1) Mass of cochlear fluid .
(2) Stiffness of the cochlear membranes .
(3) The pattern of movement of the cochlear fluids .
o By effective impedance transformer of the middle ear will change low pressure high
displacement vibration of the air into high pressure low displacement vibration
suitable for driving the cochlear fluid .
o Three components have been identified in the mechanism by which this happens ;
(1) The sound waves collected by the relatively large surface area of the
tympanic membrane are carried by the chain of ossicles to the much smaller
surface area of the oval window so the vibrations are delivered with greater
force to the inner ear. The effective areal ratio of the tympanic membrane to
the oval window is about 14 : 1 .
(2) The ossicles constitute a lever mechanism, acting through the rotational axis
of the malleus and incus, which has a further mechanical advantage of 1.3 to
1.
The product of these areal and lever ratios is about 18 to 1. which represents
the transformer ratio of the hole mechanism. Amplifying the sound increases
the energy, which is necessary for the vibrations to travel through the fluid of
the inner ear. Fluid offers more resistance than air, so requires a greater
force to push through .
(3) The tympanic membrane buckle as it moves to & fro , it also increase the
force & decrease displacement of the stapes .

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So by all these transformer action of the middle ear (with outer ear) , 50% of
increment energy transmitted to the cochlea (instead of 1%) .
Transfer as a function of frequency
o For properly describing the action of the middle ear , it is necessary to consider
transfer over the whole available frequency range & not only at used frequency
(1KHz) .
o In transmission at low frequencies , is probably due to elastic stiffness of the various
components of the middle ear .
o In high frequencies is affected by many factors , the one important is the pattern of
vibration of the tympanic membrane which above 6 KHz break up into many
independent zones reducing the coupling to the malleus .
o If a sound is too loud, muscles in the middle ear (intratympanic musclesstpedius and
tensor tympani) constrict to reduce the effects of the sound as an attempt to protect
the inner ear. This is known as acoustic reflex . Influence of the middle ear muscles
(1) Reflex provide protection from noise .
(2) May provide selective attention to the low frequency status components .
(3) May have beneficial effect in reducing the influence of some of the resonance
of the middle ear .
Conduction of sound
Sound can be transmitted to the inner ear in one of thee ways :
1. By way of the ossicular chain, from the vibrating tympanic membrane to the oval
window . This the most important route.
2. By bone conduction, sound energy is taken up and transmitted to the inner ear
through the bones of the skull. Bone conduction is the normal route for hearing some
of our own voice . Mechanism of bone conduction ;
o Inner ear factors , by differential distortion of the bony wall of the cochlea &
the wall of the labyrinthine spaces closely contributes to it will produce
movement of the cochlear fluids .
o Middle ear factors ; the centre of inertia of the middle ear bones does not
coincide exactly with their point of attachment , translational vibration of the
skull will therefore produce a rotational vibration of bones which can be
coupled to the inner ear .
o Outer ear factors ; vibration of the bones is coupled to the walls of the ear
canal is open , when the ear occluded , the sound pressure changes in the
canal are increased & transmitted to the inner ear by normal ear route .
The inner ear
There are 2 fluid spaces in the cochlea ; the perilymphatic & endolymphatic space .
The endolymph formed in the stria vascularis across which most of the energy consuming
pumping of the stria vascularis take place .
The stria vascularis has high concentration of Na/K ATPase , adenyl cyclase & carbonic
anhydrase which are enzymes , with active pumping of ions & traping of fluid into
endolymph .
The cells also has level of a-iditine enzyme for metabolism of glucose as fuel for vigorous
active transport system .
The composition & electric potential of the cochlear fluids ;
oThe endolymph ;

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- Is unique ICF , has high K contents & low Na contents resembling ICF (K:144-188
& Na: 0.2-2 mM) .
- It has strong charge (+50 - +120 mV) with respect to the plasma , higher values
being found in the basal turn & the potential are also higher near the stria vascularis
.
- The positive endocochlear potential is directly dependant on energy coming Na-K
ATPase in the marginal cells of the stria vascularis.
oThe perilymph ;
- The values are in the range of normal ECF concentration , although the K contents
of the scala vestibule are somewhat higher than in the scala tympani .
- The electrical potential of the scala tympani (+7 mV) , scala vestibule (+5mV) in
refer to the blood plasma .
The organ of Corti & subtectorial space ;
oThe true border of the perilymphatic space in the organ of Corti is not basilar
membrane , but likely to make apically for instance at the reticular lamina .
oThe fluid in the liner spiral sulcus & in the subtectorial space (between the tectorial
membrane & the reticular lamina) has generally been thought to be continuous with
the endolymph & so would have a high positive charge .
oThe chemical & electrical border between the endolymph & the perilymph would then
be the reticular lamina & would include the transducing surface of the hair cells .
The cochlear mechanics
oThe inward movement of the footplate of the stapes allows the sound waves to travel
along the upper gallery of perilymph fluid ( scala vestibule).
oThis fluid movement is transmitted to the endolymph fluid (in the scala media) and so
to the lower perilymph gallery (scala tympani ).
oWithin the cochlea the vibrations of the cochlear fluids are processed and analysed in
such a way that data representing frequency, intensity and phase relationships, In
order that the necessary hydrodynamic, electrical and metabolic processes may occur
special biological conditions are present in the cochlea before the sound being passed
to the higher centers in the brain for storage and interpretation.
oThe effect of the fluid movements in the cochlea is to cause the basilar membrane
(together with the organ of Corti ) to vibrate up and down, and at this point the sound
conduction ends and sound sensation begins
oIf the actual vibration of the basilar membrane are observed, a traveling wave (
Bekesy) is seen to start from the base of the cochlea and progress towards the
helicotrema with increasing amplitude to a sharply defined region of maximum
displacement , the position of which depends upon the frequency . Beyond this the
wave is rapidly dissipated and disappears
oFor high frequencies maximum displacement of basilar membrane is confined to the
basal turn. Low frequencies cause a longer traveling wave with maximum amplitude
near the apex of the cochlea .
oThe fact that the basilar membrane tuning become less selective at high stimulus
intensities is a reflection of the non-linearity of its response , the non-linearity makes
the tuning less selective at high intensities because the response in the sharply tuned
tie of the tuning curve are influenced most by the non-linearity .

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oThe basilar membrane contain an active mechanical amplifier which uses biological
energy to booster the mechanical vibrations of the basilar membrane .
oMechanical Excitation of Hair Cells
Each cochlear nerve fiber makes contact with several hair cell..
The inner hair cells receive more fibers than the outer hair cells.
oStimulation of the auditory nerve
The conversion of acoustical energy into nervefibre activity , is not understood .
Possibly CM stimulates the nerve endings ,a chemical mediation may play a part.
The transduction by hair cells ;
oThe individual sterocilia on the apical surface of the hair cells are mechanically rigid
& braced together with cross links , so that they move as a stiff bundle .
oThere are fine links running upwards from the tips of the shorter sterocilia on the the
hair cells which joins the adjacent taller sterocilia of the next row . It is significant that
when the sterocilia are deflected in the direction of the tallest sterocilia , the links are
stretched opening the ion channels , in the cell membrane , when the sterocilia are
defelected in the opposite direction , the tension is take off the links & the channel
close , this hypothesis is consistent with all present electrophysiological evident on
transduction in hair cells .
oThe tip links responsible for coupling the stimulus movement to the transducer
channels . The stimulus is coupled to the sterocilia by means of shear or relative
motion between the tectorial membrane & reticular lamina . The hairs of the hair cells
are thus displaced relative to their cell bodies this motion produces the cochlear
microphonic (CM) and this final mechanical event preceding neuronal stimulation .
oAs basilar membrane & organ of Corti are driven upwards & downwards by the sound
stimulus , the sterocilia are moved away from & towards the modiolus .
oBoth inner & outer hair cells , the tip links are organized in such away that they run in
a direction most suited for picking up radial shear .
oWhen the channels on the sterocilia are open , ions will enter or leave the cell
depending on the electrical & chemical gradients across the apical cell surface .
The electrical response of the cochlear hair cells
o The inner hair cells
- 95% of all afferent nerve fibers (auditory nerve) makes contact with the IHC & each
IHC has terminals from about 20 afferent fibers & the IHC detect the movement of
the basilar membrane & transmit it to the auditory nerve .
- If the electrical potential of the IHC is measured during a low frequency acoustic
stimulus , approximately sinusoidal oscillations of the membrane potential are
obtained as a transducer channel are open & close .
- Consideration of the IHC responses is not complete without including the mode of
coupling of the movement to the sterocilia & it is shown that IHC respond to the
velocity rather than just the displacement of the basilar membrane .
oThe outer hair cells
- Only few afferent auditory nerve fibers makes contact with the OHC , so it is not
seem so important step in transforming information about the basilar membrane
vibration to the CNS .
- Rather the OHC are probably involved in generating the cative mechanical
amplification of the basilar membrane movement which give rise to the relatively

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large amplitude & sharply tuned mechanical traveling wave . They also generate the
cochlear microphonics & this may be essential step in the mechanical amplification .
- The motile response of the OHC thought to be part of the mechanism by which the
OHC amplifying the traveling wave to increase the cochlear sensitivity & frequency
selectivity.
- The most recent idea is that the OHC membrane is tightly packed with geometrically
& electrically an isotopic proteins particles , so a voltage across the membrane will
reorientate the particles changing the surface area of the cell membrane .
The gross electrical response of the cochlea ; can be divided in to three components ;
(1) Cochlear microphonics (CM) , which is an action response that follows the wave
form of the stimulus . The CM drived almost entirely from the OHC . CM1 (oxygen
dependant) & CM2 (present a while after cells death) .
(2) Summating potential (SP) can appears as either a positive or a negative shift
depending on the stimulus condition , probably arise from IHC & it occur with very
high intensity stimulus .
(3) Action potential (AP) , the neural potential arise from the mass of the action
potentials in the auditory nerve which are produced at the onset of a stimulus .
Fibers responding to the higher frequencies are arranged around the outside of the
nerve trunk , consisting with their origin from the basal turn of the cochlea .
The responses of the auditory nerve fibers
Neurotransmitter is released in the synapses at the base of the IHC & this give rise to action
potentials in the auditory nerve fibers .
The sound stimulus is transmitted up in the auditory nerve fibers in 2 ways ;
(1) Phase locking ; in which the transmitter release & action potential generation occur
in synchrony with identical cycles of the stimulus .
(2) Frequency selectivity ; by which it incode information , when the IHC detect the
movement of the basilar membrane at one point along the cochlear duct , also called
place coding .
The intensity responses of the auditory nerve fibers ; as the stimulus intensity is increased ,
the amplitude of the basilar membrane vibration grows , the activation of the IHC grows
similarly & also does the firing of the auditory nerve fibers .
Non-linear interactions in the cochlea & auditory nerve ; single auditory stimulus are
always excitatory , one stimulus can change the responsiveness of the auditory nerve fibers
to other stimulus where the application of one stimulus can reduce the response to a second
stimulus , the reduction in activity is called "two-tone suppression" . The most favorable
mechanism is that the suppression drives the OHC to the upper limits of their amplitude
range of sensitivity . This reduce the extent to which hair cells can increase their response
to a second super-imposed stimulus .
The Centrifugal innervations of the cochlea ; the cochlea receives a centrifugal efferent
nerve supply arising in the superior olivatory complex of the brainstem (oliviocochlear
bundle"OCB") The functional importance of the OCB is suggested that by affecting the
state of the OHC , the OCB can modify the active mechanical amplification of the traveling
wave in the cochlea .
Cochlear echos ; the cochlea can emits sounds , it appear that the vibration arise from the
hair cells themselves or at least that hair cells are an essential components of the process
producing the sound . It suggesting that as a traveling wave progressed up the cochlea , it

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might meet impedance discontinuities perhaps formed by irregularities in the active system
feeding energy back in to the traveling wave . The discontinuities would reflect a newer
pressure wave which would emerge through the middle ear & be recovered in the canal .
Theories of hearing
Attempt to explain the conversion of all the dimensions of sound in to a representative
pattern of auditory nerve fiber activity .
The possible variation in the nerve action pattern depends upon ;
(1) Which particular nerve fiber activated .
(2) The total nuber of the fibers activated .
(3) The rate of firing in the individual fibers (<1000Hz) .
(4) The temporal relationships of the neural discharge between the individual fibers & a
group of fibers .
A. Place theories of cochlear action (e.g. that of Helmholtz)
Postulate that perception of pith relies upon the selective vibratory action of the
basilar membrane . The hair cells and the particular nerve fibres activated by them
correspond to the point of maximum displacement of the membrane by the traveling
wave .
B. Rutherford's telephone theory
Suggest that pith perception is based upon the rate firing in individual nerve fibers
C. Wever's volly theory
Combines both place and telephone principles. Postulating that:
o High frequencies are perceived by place alone(in the basal turn).
o Low frequencies (below 1000 Hz) stimulate nerve action potentials at a rate
equal to stimulus frequency.
o Intermediate frequencies are represented in the auditory nerve by
asynchronous discharges in groups of neurones, whose combined activity
represents the frequency of the stimulus.

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FUNCTIONAL EXAMINATION OF HEARING

Hearing defined as , a perceptive process which means the ability to detect sounds & then
to associate those sounds with a specific memory within the brain , so they become
meaningful .
This process requires intact ears , auditory nerve & brainstem .
Sound defined as energy waves of particle displacement within an elastic medium causing
sensation of hearing , both compression & rarefaction waves .
Amplitude of sound , the extent of vibratory movement from rest to farthest point of rest in
compression & rarefaction phases of energy .
Intensity of sound , the amount of sound energy through the area per time , refers in
psychoacoustics as loudness .
Decibel (dB) , unit used to express the intensity (Log 2 intensities = 1/10 Bell) , it is
expressed by sound pressure level (SPL) , hearing level (HL) & sensation level (SL) .
Sound pressure , sound force over a surface per unit of time .
Frequency , number of cycles of the vibrating medium per unit of time .
Hertz (Hz) , unit to express the frequency (cycle/second) , human ear capable of hearing
from 20 – 20 000 Hz .
Pure tone sounds , single frequency sound , rarely occur in nature .
Complex sound , sound with more than one frequency .
Noise , periodic complex sound , of many types ;
- White noise ; contain all frequencies in the audible spectrum at average equal
amplitude
- Narrow band noise , white noise + frequencies above & below a current frequency
filtered out .
- Speech noise , white noise + frequencies >3000 & < 300 Hz reduced by filter .
Resonant frequency , a frequency at which the mass vibrate with the same amount of the
external force , determined by the elasticity of the mass , the mass & the frictional
characteristics of the medium .
Live voice & whisper test
The simplest test , using either single phrase or sentence , but it is of limited value &
impossible to standardized .
Tuning fork tests
The more commonly used are 512 & 256 Hz forks at C tone .
1. Rinne test ;
- Tuning fork placed closely to the meatus (AC) & then put the base of the fork on the
mastoid (BC) , then ask the patient which is loud heard .
- Normal subject AC better than BC (Rinne +ve) .
- CHL , BC better than AC (Rinne –ve) .
- SNHL , AC better than BC (often BC not heard , Rinne +ve) .
- False Rinne –ve in unilateral SNHL (BC better than AC) .
2. Weber test ;
- Bone conduction test .
- Put the base of the tuning fork on the forehead .
- Useful in cases of unilateral deafness or when there is marked difference appear
between the two ears .
- Normally the sound heard in the midline .

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- CHL , the sound heard towards the deafened ear .

- SNHL , the sound heard toward the better ear .
3. Absolute bone conduction test (ABC) ;
- Press the tragus inward & occlude the external auditory meatus & compare with
the examiner ear assuming the examiner has normal hearing .
- CHL , normal ABC (the same of the examiner) .
- SNHL , decreased ABC (less than the examiner) .
4. Stenger test ;
- Test for non-organic HL .
- Two identical forks presented each one to one ear from different distances normally
, normally person can perceive the nearer one .
- One fork placed 25 cm from the good ear , the patient says he heard sound .
- Other fork placed 8 cm from the ear under test , the patient with true deafness will
still hear a fork placed 25 cm .
- The patient with non-organic deafness deny that he heard any sound at all .
5. Chimani – Moose test;
- It is a modification of the Weber test , to detect non organic hearing loss .
- A fork is placed on the forehead , malingerer hear the sound in the good ear , the
same for SNHL .
- If the meatus of good ear occluded , truly deaf still hear sound in the occluded ear ,
but in malingerer may deny that he heard the tuning fork at all .
Audiometry
Audiometry either ;
- Subjective , only can show that the entire system functioning .
 PTA .
 Bekesy self recording audiometry .
 Speech audiometry .
- Objective , can identify responses to the sound stimuli at lower neurological &
peripheral levels .
 Impedance audiometry ; tympanometry & intraaural reflexes (non acoustic reflex
& stapedial reflex) .
 Evoked response audiometry ; electrocochleography , brainstem response ,
cortical ERA , postauricular magnetic response .
Pure tone audiometry (PTA)
It is the most useful technique which determine the subjective hearing threshold for pure
tone , so it can measure the sensitivity , the pure tone delivered to the ear either through
earphone (AC) or by vibrator applied to the mastoid (BC) .
All adults can be tested & children > 4 years old .
The aim ;
1. Degree of hearing loss .
2. Site of the lesion .
3. Need for further testing .
The results , either
1. Normal ; all air conduction (-10 – 20 dB) .
2. Conductive hearing loss , HL by air conduction with normal bone conduction .
3. SNHL , HL by air & bone conduction of similar degree .
Lecture notes in
4. Mixed , HL by air conduction & bone conduction with air conduction worse .
Configurational PTA either flat , rising , sloping , falling , notched or saucer-shaped .
Scales are ;
HL (dB) Degree of impairment
-10 – 20 Normal
20 -35 Mild HL
35 – 50 Moderate HL
50 – 65 Moderately severe HL
65 – 90 Severe HL
> 90 Profound HL
Procedure ;
1. The patient sitting in a sound proofed room , visible & understood the procedure ,
start with the normal ear first .
2. The duration of signal should be 1-3 seconds .
3. AT 1 st , 1000 Hz tested , at 50 dB , if can't be seen , then increase the intensity in 10
dB stages until become audible .
4. The intensity decreased then in 10 dB until lack of response , then increased in 5 dB
steps until heard again .
5. If there is difference in the air conduction threshold exceeding 40 dB at any
frequency , then need masking .
6. The bone conduction threshold tested between 0.5 – 4 KHz .
7. The BC assessment is essential in all cases where CHL suspected clinically .
8. The difference between the threshold to AC & BC is called air-bone gap .
Masking
Mask 2 or 3 frequencies , the sound stimulus to the tested ear may be heard by the non-
tested ear , so the patient unable to decide which ear hear the sound , this called crossover
phenomena , occur in AC as low as 45 dB & in BC as low as 0 dB .
The reduction in sound energy from one side of the skull to the other is called interaural
attenuation , for AC about 40-65 dB & for 0-10 dB . \
The masking indicated in ;
1. When the AC level to the test ear exceeds the BC level of the non-tested ear by 40 dB or
more .
2. In bone conduction , when there is air-bone gap greater than 10 dB in the tested ear
(i.e. air-bone gap , AC : 40 dB & BC : 10 dB).
Factors influence the PTA validity
1. Test location . 2. Equipment calibration .
3. Personnel . 4. Clear instruments .
5. Patient comfort . 6. Placement of the headphone & bone
oscillator correctly .
Symbols of the PTA
Right ear Left ear
Air conduction (unmasked) O X
Air conduction (masked)  
Bone conduction (unmasked) < >
Bone conduction (masked) [ ]
Threshold beyond output  
Lecture notes in
Bekesy audiometry
Sweep frequency test , signal frequency is swept from low to high , the traverse requiring
about 10 minutes .
The intensity is switched , so as to increase or decrease by the patient himself , he is
instructed to decrease the volume as soon as he can hear the tone & to be increased the
volume whenever the tone becomes inaudible , interrupted (pulsed) or continuous tone are
used .
The intensity as determined by the patient is automatically plotted or graft against
frequency , the resulting curve indicate the pure tone threshold , small amplitude indicates
recruitment .
- Type I ; the continuous & pulsed tracing overlap through out the recording , means
normal ears & CHL .
- Type II ; they overlap t low frequency , but between 500-1000 Hz , the continuous
tracing drops at 10-20 dB below the pulsed one & then runs parallel to it , usually
decreased with greater sensitivity to difference limen ("DL" the amplitude intensity
variation) .
- Type III ;dropping off continuous trace below the interrupted from 125 Hz with
separation increase across the range 50 dB , means retrocochlear pathology (8th
nerve) .
- Type IV ; the continuous drops below the interrupted , beginning in low frequency by
about 30 dB , but parallel , means 8 th nerve disease .
- Type V ; the continuous above the interrupted tracing , means non-organic HL
(malingerer) .
Speech audiometry
It is the simplest clinical tool , used to analyze graphically the percentage of words heard
correctly by the subject .
Method ; the patient sit in a sound proof room , need cassette player or microphone with
volume control producing various intensities , need masking to the tested ear (because it is
suprathreshold testing) .
The patient asked to repeat the words as accurately as possible , then calculate the
percentage of correctly repeated words , this plotted on a graph .
Speech discrimination , is the percentage of the phonetically balanced monosyllabic words
heard correctly when present at different intensities .
The speech audiogram is normally a sigmoid like curve with maximum speech
discrimination (100%) at the 40 dB & 50% speech discrimination score (half peak level
"HPL") at 25 dB .
The sensitivity of speech audiogram is usually measured at 50% point on the intensity curve
, speech reception threshold , alternatively it may measured at point corresponding to a
score which is half of the maximum obtained for that ear (HPL) .
In CHL , the curve shifted to the right with 100% discrimination at higher relative speech
level (higher dB) , this mean there is increase of speech reception threshold without
concomitant reduction in optimal discrimination score .
In SNHL , due to retrocochlear pathology , the 100% discrimination in not attained & in
higher level of dB , the discrimination decreased due to synchronization at neural level &
the HLP elevated with decrease in optimal discrimination score , while in cochlear
pathology the HLP is normal , the speech reception threshold .

Lecture notes in
Speech reception threshold , is the lowest level in dB at which a patient can repeated
spondaic words in 50% of the presentation , the spondee is two syllable word (side walk ,
ear drum) .
The interpretation ;
90-100 % Normal
76 – 88 % Slight difficulty
60 – 74 % Moderately difficulty
40 – 58 % Poor
40 % correct Very poor
Tone decay
Phenomenon where a pure tone of constant intensity is perceived to grow faint (temporary
threshold drift "TTD") , in physiological term it is expressed as abnormal auditory
adaptation or fatigue “ adapatation means decrease with time in sensitivity or
responsiveness of a asystem during prolonged stimulation” , decay of pure tone remains
easy & useful audiological assessment of retrocochlear pathology .
Or , A phenomenon in which there is progressive elevation of the auditory threshold for a
continuous pure tone .
It is found in retrocochlear deafness , e.g. acoustic neuroma , & when central auditory
connections are impaired while small amount of tone decay especially at higher frequencies
is very common in sensory disorders , the more useful test frequency appear to be between 1
KHz & 4 KHz ( above 8 KHz there are more false +ve results) .
It is done by ;
1. Tuning forks , one testing BC at a point when the tone is no longer heard , the fork is
removed & then re-placed (without re-striking it) , if it is heard , then these is
significant tone decay .
2. Cahart's test , tone presented continuously at 5 dB above the subject threshold for 60
seconds , if the subject cease to hear the tone , then the intensity increased 5 dB , this
procedure is continue until the level is found where the subject is able to perceive the
tone for full 30 seconds or until maximum of 3 minutes have elapsed from the start .
The difference in dB between the subject initial threshold & the final intensity of the
tested tone at the termination of the procedure is recorded as his tone decay for that
frequency .
A decay of 0 -15 dB Normal & CHL
A decay of 0-20 dB Sensory HL
A decay of over 30 dB Neural deafness
Tests of recruitment
Recruitment is an aspect of certain forms of deafness , it is an abnormal growth of loudness
, where the growth of loudness of sound of increasing intensity is greater than in normal
ears (an inappropriate increase in perception of loudness with increased sound intensity) .
Abnormally rapid loudness growth, which causes distortion and discomfort and the patient,
asks us not to shout.
It is present only in cases of sensory deafness (cochlear defects), due to affection of the
organ of Corti (end organ deafness) .
It is absent or incomplete in neural deafness due to affection of the nerve & never occurs in
conductive deafness .

Lecture notes in
Mechanisms:
- The sensation of loudness is determined partly by the number of cochlear nerve fibers
that are activated by a stimulating sound.
- Recruitment is depend on the fact that each cochlear nerve fiber makes contact not only
with one hair cell, but with several.
- The inner hair cells receive more fibers than the outer hair cells.
- If a sound of weak intensity is applied to the deafened ear, the stimulation of the
remaining outer hair cells is only sufficient to activate a few of the nerve fibers which
innervate them, so the sensation of loudness experienced by the deafened ear is less than
normal.
- If a sound of strong intensity is applied, the stimulation of the inner hair cells is able to
saturate a large number of nerve fibers, so the sensation of loudness experienced by the
deafened ear equal that of the normal ear.
- At very high intensities, the deafened ear may hear the sound louder than the normal
ear.
- A neural feedback circuit exists by the outer hair cell inhibits the output of the inner hair
cells .
- Loss of the outer hair cells damages this mechanism and result in the output of the inner
hair cells being unchecked.
Complete recruitment occur when the sensation of loudness in deafened ear grows towards
but doesn't equal that the other ear .
Incomplete recruitment occur when sensation of loudness in the deafened ear grows
towards but doesn't equal to that in the other ear .
Over recruitment occur when the sensation of loudness in the deafened ear become greater
than that in the other ear .
Absence of recruitment is noted when the sensation of loudness in the deafened ear grows
equal (in parallel) with other ear , mean conductive or neural (retrocochlear) HL.
Loudness reversal occur when the sensation of loudness in the deafened ear grows more
slowly than that in the other ear which is pathognomic of neural deafness .
Many tests for evaluating it ;
1. Fowler' test (Alternate binaural loudness balance "ABLB")
This compare the stimulus intensities which give equal loudness in normal &
deafened ear in patient with unilateral deafness (one ear normal /near normal & the
other at least 25 dB worse) .
Frequency of 1 KHz is the commonest used & the loudness is compared at threshold
& then at 10 dB steps (the intensity of the tone is fixed to the good ear while varied to
the worse one until the patient judges the tones to be of equal loudness) .
2. Reger's test (Monoaural loudness balance test)
Compare two sensation of loudness as in Fowler's test but uses sounds of different
frequencies in the same ear , only applied for the smart patients .
3. Difference limen (DL) test
Measures the changes in the intensity of sounds just sufficient to produce perceptible
alteration of loudness , if DL remains unchanged or increased with increased
intensity this means that the recruitment is absent , if DL decreased with increased
intensity this means presence of recruitment .
Applied to cases of unilateral and bilateral deafness.

Lecture notes in
4. Short increment sensitivity test (SISI)

It has the ability to detect small changes in intensity .
Continuous pure tone of given frequency , 20 dB above the patient threshold is
presented & increase in intensity by 1 dB for 0.3 seconds every 5 seconds , this cycle
occur 20 times & the tester records score of 5% for each correct recognition .
Any audiometric frequency may be used , but SISI tests are usually performed on one
high & one low frequency (500Hz & 4 KHz) .
Score under 20% means normal , CHL or neural HL , while scores over 60% is
typical of severe cochlear deafness (e.g. MD) .
Tympanometry (By Terkildsen & Thomson 1959)
It is an objective test which measures the mobility of the tympanic membrane (compliance)
as a function of the applied air pressure in the external auditory canal .
Acoustic definitions
- Impedance ; the difficulty that acoustic energy (sound) encounters when it is
transmitted through the auditory conducting system .
- Admittance ; the ease of acoustic energy flow through the auditory conducting
system .
- Immittance ; impedance = admittance .
- Stiffness ; is the characteristic of ear that maintains its shape & brings about a
return to the original position after a force has been applied (springiness of the
auditory conducting system) .
- Compliance ; represents the mobility of the middle ear system & it is the reciprocal
of stiffness .
The types of tympanogram are ;
1. Type A ; normal , 0.25 – 1.0 mm H2o .
2. Type As (shallow) , < 0.25 mm H2o , occur in otosclerosis , scarred tympanic
membrane & fixation of the malleus .
3. Type Ad (deep) , loose , occur in flaccid tympanic membrane (perforation heald by
secondary tympanic membrane) & discontinuity of ossicular chain .
4. Type B , flat , occur in fluid in the middle ear & perforated tympanic membrane or
ventilation tube .
5. Type C , negative middle ear pressure , occur in Eustachian tube dysfunction with
retracted tympanic membrane
Other conditions ;
- Eustachian tube dysfunction , positive middle ear pressure , autoinflation of the
middle ear (sticky Eustachian tube) .
If with perforation & patent tube no graph can be obtained , if obstructed then we
have flat with high compliance & large ear canal volume .
If without perforation & functioning tube then the curve will be normal , but if
obstructed then we have flat curve & -ve pressure , while if patulous it will be
pulsatile with respiration .
- Glomus tumor , pulsatile with heard beat .
- Palatal myoclonus , irregular marked twitching in admittance recording .
- Osteogenesis imperfecta , normal or high peaked curve .
- F.B. or wax , round , normal middle ear pressure .
- SNHL , normal .

Lecture notes in
The acoustic reflex

An objective measure of the lowest stimulus that elicit the stapedial reflex called acoustic
reflex test , the reflex contraction of the stapedial muscle in response to the sound stimulus .
A reflex contraction of the stapedius muscle in response to loud sound . When contracted,
the muscle can attenuate the passage of sound through the middle ear by up to 30dB .
It is suggested that the middle ear muscle reflex may protect the ear against some of the
harmful effects of noise.
The complex crossed reflex demands an intact afferent arm, brain stem and 7th cranial
nerve.
When the muscle contract pulls in perpendicular to the main axis of the ossicles , stiffen the
chain decreasing the tympanic membrane admittance .
The reflex is consensual , it occur in normal ear for tones above 85 dB & the strength of the
contraction increased with increasing the stimulus , the resultant admittance changes
recorded on the ipsi- & contra-lateral sides with equal sensitivities .
The stapedial reflex pathway , this pathway determined by the stimulation- recording
arrangement:
- Ipsilateral recording
 Acoustic nerve
 Ipsilateral ventral cochlear nucleus
 Trapezoid body
 Ipsilateral facial nerve
 Ipsilateral stapedius muscle
OR
 Trapezoid body
 Ipsilateral facial motor nucleus
 Ipsilateral facial nerve
 Ipsilateral stapedius muscle
- Contralateral recording
 Acoustic nerve
 Contralateral medial superior olive
 Contralateral facial motor nucleus
Procedure ; The reflexes are measured at the ear canal pressure producing maximum
compliance, which corresponds to middle ear pressure.
- For ipsilateral recording , the acoustic reflex elicited by admittance meter probe , the
artifacts can be detected as the instrument indicator (goes the wrong way) .
- For the contralateral recording , the artifact occur at 0.5 -1 KHz at intensity above
105 dB hearing level .
Acoustic reflex threshold ; It is the minimum intensity required to evoke the reflex
In recruiting deafness, the ART is less than 70 dB above subjective threshold .
In non recruiting deafness (usually neural),the ART is greater than 70 dB above the
subjective threshold .
The effects on the acoustic reflex of the pathology of the probe ear

Lecture notes in
Reduced mobility of the middle ear structures, as caused by many types of conductive
hearing loss, prevent the stapedius muscle contraction
Uses ;
The acoustic reflex provides diagnostic information with regard to the site of a neurological
lesion based on the pattern of response to ipsilateral and contralateral testing.
1. Assess the integrity of the facial nerve up to the branch to stapedius tendon.
2. Assess recruitment and stapedial reflex decay .
Stapedial reflex decay (Adaptation) ; Determined by producing a persistent tone in
the test ear and measuring the reflex in the contralateral ear.
Normal adaptation occurs only after 10 second, decay being no more than 50%.
Its an accurate pointer in distinguishing a cochlear (recruiting) from a retrocochlear
(abnormal decay) lesion.
3. Assess the presence of a conductive hearing loss.
4. Assess brainstem function.
5. Detect malingerers .
6. Cochlear & retrocochlear lesions .
7. PTT .
The afferent part of the arc , the conductive apparatus & the cochlea & the 8th nerve , while
the efferent ; brainstem & the facial nerve .
The effect of pathology of the probe ear on acoustic reflex ;
1. Conductive deafness (commonest disorder) , reduce the mobility of the middle ear
structures , prevent the stapedius muscle contraction , decreasing compliance .
As conductive impairment increase , the acoustic reflex decreased , e.g. patients with
air-bone gap ; 20 dB lead to 50% abnormal reflex , while 35 dB lead to abnormal
acoustic reflex .
Sometime even with air-bone gap there is normal acoustic reflex .
2. In early otosclerosis , biphasic pattern of acoustic reflex .
3. Bell's palsy , abolish the acoustic reflex .
4. Mysthania gravis , also abolish acoustic reflex .
The effect of pathology of the stimulated ear on the acoustic reflex (the main indicator is
stapedial reflex threshold (SRT) ;
1. Conductive impairment of the stimulated ear , increase of the SRT is than magnitude
of the air-bone gap (conductive recruitment) there is increase in the SRT with single
attenuation of the stimulus .
2. Cochlear impairment of the stimulated ear ; SRT increased < auditory threshold
increased in a manner similar to loudness recruitment .
3. Peripheral neural type loss of the stimulated ear , SRT relatively more elevated & the
reflex may be unobtainable .
Reflex decay ; response to prolonged stimulus , the mechanism similar in that of tone decay;
1. Normal , no loss at 0.5-1 KHz .
2. Neural loss , 50% adaptation in <5 seconds (3 seconds) at 0.5 – 1 KHz (also in
mysthania gravis & thyroid disease) .
The presence of ipsilateral reflex with absence of the contralateral reflex means intra-axial
brainstem lesion .
The absence of the contralateral & ipsilateral reflex occur in facial nerve lesions , if present
means incomplete palsy & good prognostic sign for recovery .

Lecture notes in
The diagnostic importance of acoustic reflex measurement should be considered in tow

separate ways:
1. Ability to record reflex contractions of the stapdius muscle in the probe ear which is
a function of the efferent branch of the reflex arc governed mainly by the status of the
middle ear on the probe side and by the efferent innervation.
2. The effect of an impairment of the afferent portion of the reflex arc , the conductive
apparatus, cochlea and auditory nerve on the stimulus ear. Rarely central effect due
to brain stem abnormality.
Auditory brainstem response
It is an objective non invasive test to record the electrical activity (impulses) occurring in
the area of the brainstem & midbrain in response to sound stimuli & their detection by
surface electrodes placed on the mastoid , forehead & vertex .
The stimulation technique ;
1. Wide band clicks , not accurate estimation of the threshold , especially in sloping
type of curves .
2. Tone bursts , tone pips .
3. Filtered clicks , 2& 3 are more frequency specific & can estimate the threshold .
Recording techniques ; electrodes on the vertex (+ve) , mastoid ,tested ear (-ve) & mastoid
, contralateral ear (ground) .
The electrical activity filtered with pass band from 100 Hz to 3 KHz , then amplified more
than 100000 times .
Sedation ;
1. In adults & small infants , no need for sedation , as they may sleep during the
procedure
2. In incooperative children , 25 mg meperidin i.m. , promethazin 6.25 mg i.m. ,
chlorperazin 6.24 mg i.m. , or chloralhydrate 500 mg / 5ml (1-2 ml orally) .
Subject variables
 Age ; at birth , incomplete ABR (only I , III & V) , or longer latencies especially V
due to external & middke ear factors or immaturity .
 While in elderly (>55 years) there is prolongation of the wave V (0.1-0.2 mseconds) .
 Gender ; in female shorter latency (0.2 msec.) , larger amplitudes & shorter
interwave latency .
 Temperature ; below 36o& above 38 othere is increased latencies .
 Drugs ; not affected by sedation , barbiyurates , anesthesia & relaxants , but
affected by phyntoin , lidocaine , diazepam & alcohol .
Clinical applications of ABR ;
1. Threshold testing in infants , young children & malingerer .
2. Diagnosis of acoustic neuroma , increased latency due to stretching of the nerve by
the tumor .
3. Diagnosis of the brainstem lesions & neuropathies .
4. Screening of nursery ICU infants at risk for hearing loss .
5. Intraoperative monitoring of the surgical procedures such as vestibular nerve
vascular decompression & vestibular nerve transection when auditory nerve at risk .
A scheme for ABR use in neuro-otological evaluation ;
1. x-ray & ABR , if enlarged IAM & abnormal ABR .
2. MRI , if not available .

Lecture notes in
3. CT with i.v. contrast , if normal .

4. air contrast CT , if not Dx , small dose pentopaque study .
In brainstem lesions , it is diagnostic & can localize the lesion , in multiple sclerosis ,
absence of ABR will be an early identifiable feature , while in other CPA tumors we can
identify it by ABR when there is pressure on the auditory nerve .
Tests to diagnose non –organic hearing loss
Many social and psychological conditions can lead to non-organic hearing loss, so the
clinician must always be aware of the possibility.
1. Stenger test
- Audiometric procedures assume that patient responds genuinely to presented stimuli.
- Excellent test for unilateral or asymmetrical
- hearing losses in which the difference between ears is at least 25 dB.
- Based on the Stenger effect: when two tones of the same frequency are presented
simultaneously to both ears, only the ear in which tone is louder will perceive the tone.
- To perform the Stenger test, simultaneously present a tone 5 dB above threshold to the
good ear and an identical tone 5 dB below the voluntary threshold to the poor ear.
- If the patient responds, the test is negative because the patient heard the tone in the
good ear. If the patient does not respond, the test is positive: The patient should
respond, because the tone presented to the good ear is 5 dB above its threshold.
- If the patient not respond, it because the tone was perceive in the poor ear and the
patient chooses not to respond.
- A speech Stenger can performed in the same manner using spondee (SRT) words in
place of pure tones.
2. Lombard test
- Based on phenomenon that one increases the volume of ones voice in the presence of
loud background noise, because the noise interferes with self-monitoring.
- To perform the test, the patient is seated a sound –treated booth and wears headphone.
Masking noise is introduced through the headphones as the patient reads aloud. The
tester monitors the volume of the patient s voice through talkback of the audiometer.
- With a true hearing loss there is no change in the volume of the patient s voice.
- If the loss is nonorganic –since the patient not hear the masking noise –the volume of
the patient s voice will increase.
3. Delayed auditory feedback
- Based on the principle that individuals monitor the loudness and rate of their speech
by an auditory mechanism.
- Applicable to monaural and binaural losses
- Has good sensitivity and can provide an estimate of SRT.
4. Doerfler-Stewart test
- Based on the principle that normal individuals and individuals with hearing loss can
repeat wards in the presence of masking noise as loud as the speech signal, individual
with non organic hearing loss may stop responding at lower masking noise level.
- Time consuming-fair accuracy.
5. Bekesy audiometery.
6. Acoustic reflex testing.
7. Otoacoustic emission.
8. Auditory brainstem response.

Lecture notes in
VESTIBULAR FUNCTION TESTS

The objective of vestibular investigations is to ;
1. Identify the presence & site of the vestibular pathology .
2. Gather information which may lead to aetiological diagnosis .
3. Formulate a method of management .
A full general medical examination with special attention to the CVS , CNS , ears , eyes &
locomotor system is essential before preceding to vestibular investigations .
The aim of vestibular examination is to discover the presence of an underlying vestibular
imbalance at the level of ;
1. Vestibular end organ , vestibular ganglia & nerve within the IAM (peripheral) .
2. CPA , brainstem , cerebellum & vestibular projections to the cerebral cortex
(central) .
The vestibular tests either ;
A. Vestibulo-ocular reflex test .
B. Vestibulo- spinal reflex test .
C. Miscellaneous tests .
A. Vestibulo-ocular reflex test
Eyes movement depends on the visuo-ocular pathway & vestibule-ocular pathway .
Before performing the vestibule-ocular tests , the integrity of the visuo-ocular pathway
must be ascertained by testing the visual acuity , field & eye movement .
Ocular stabilizing systems are ;
- Saccades ; rapid eye movements which corrects errors in the direction of the gaze &
brings the desired object of fixation to the fovea in the shortest possible time .
Clinically , ask the patient to look back & forth between 2 targets infront of him 30 oto
the right & left of the midline & 30oabove & below the eye level .
In vestibular disease the eye may overshoot .
Abnormal saccadic movement means , central pathology or ocular myopathy , while
peripheral vestibular disease doesn't cause abnormal saccadic eye movement .
- Smooth pursuit system ; maintaining gaze on a moving object , the object stabilized on
the fovea (while in saccades there is no target) .
Clinically ask the patient to follow the finger of the examiner in pendular swinging
from side to side & up & down .
Bilateral impairment , non-specific & occur in elderly , alcohlol , psychotropic
medications , anticonvulsants , fatigue & sedation .
Unilateral impairment occur in acute peripheral vestibular disease & central
pathology .
This test is of great value & clinical importance because it is related with mechanism
by which the vestibule-ocular reflex is suppressed by optic fixation which is important
in differentiation between peripheral & & central pathology .
- Nystagmus (Mention in separate topic in details) .
- Oscillopsia ; term used to describe the illusion of motion of the environment caused by
inadequacy of the vestibule-ocular reflex , this reflex hold the movement of images
steadily during head & body movement .
It occur in patient with reduced peripheral vestibular function & acquired nystagmus
(this with congenital nystagmus seldom have this problem) , it caused also by uni- &
bi-lateral vestibular hypofunction .

Lecture notes in
It diagnosed by testing the patient for visual acuity with Snellen chart , & no Rx
available for it.
Specific tests based on the vestibule-ocular reflex ;
1. Rotational test
The nystagmus induced by the acceleration & deceleration in a rotating chair ,
the test has the disadvantage of stimulating both labyrinths simultaneously .
2. Caloric test
Its one of tests used to investigate vestibular function and was first described by
Robert Barany in 1906 who postulated that altering the temperature of the
endolymph induced convection currents and the fluid movement leads to
stimulation of the stereocilia and consequent nystagmus and vertigo.
In 1942 Fitzgerald and Hallpike they described a standardized bithermal caloric
test which remains an essential vestibular investigation.
The advantages of it are ;
a. Each horizontal SCC function tested independently .
b. Simple & widely used .
c. No need for sophisticated equipments .
The disadvantages are ;
a. Inter-subjects variability .
b. Use of imprecise stimuli .
c. Need intact tympanic membrane (in water caloric) .
The principle of the test ; direct thermal stimulation of the vestibular sensory
epithelium & the ampulary nerve ending (warm increase nerve discharge) .
Before doing the test need otoscopic examination to see if there is tympanic
membrane perforation , any wax or infection .
Method ; 30o & 44o for 40 seconds , flow rate of 350-500 ml/min. , rest period of 5
minutes (at least) between irrigations to avoid cumulative effects , direct
observation of the eyes to detect nystagmus & the end point of nystagmus .
The measure of the response is the number of seconds between the
commencement of the stimulation and the cessation of nystagmus .Results are ;
a. Normal with fixation 90-140 seconds from the irrigation onset & returns
fro further 30-60 seconds following the removal of the optic fixation .
b. Canal paresis ; loss of labyrinthine function in one ear (complete or
partial) , if complete , then the test repeated with cold water of 20o for 60
seconds , it is due to ipsilateral lesion of the labyrinth , vestibular nerve or
vestibular nucleus .
c. Directional preponderance , excess of nystagmus to one direction , due to
imbalance of tone arriving at the occulomotor nerve from an imbalance of
the vestibular tone between the 2 half of the vestibular system , so the
lesion in the labyrinth , vestibular nerve , vestibular nucleus , cerebellum
or cortico-fugal in the temporal lobe .
d. Mixed directional preponderance & canal paresis .
Air caloric test ; 17.5 & 45.5ofor 100 seconds & the irrigations rate is 13 l/min. ,
advantages are ; not wetting the patient & can be used in perforated tympanic
membrane .

Lecture notes in
Problems ;
a. High cost of the equipments .
b. The thickness of the bone over the lateral SCC varies .
c. The temperature of the air in the EAM must be accurately known as air
cools rapidly .
d. Difficulty in heating the air , need greater temperature gradient than
needed in water .
Hot caloric test ; it is a screening test with optic fixation index .
3. Electronystagmography
It is based upon the +ve potential which exist between the cornea & retina ,
electrodes are attached to the skin at each outer canthus close to the eyes & a
ground electrode applied to the sternum .
Two types of amplifiers are ;
- AC ; the pen recorder return to its original position after tracing .
- DC ; the pen recoreder remains constant in its position until the eye moves
again.
The corneo-retinal potential is having dependant upon the amount of light falling
on the retina , so alteration in lighting needs recalibration .
Eye deflection to the ; left cause downward deflection of the pen & right cause
upward deflection of the pen .
Signal & noise cause blink & muscular activity leading to atypical ENG .
The electrodes can detect the horizontal movement , difficult to detect vertical
because of blinking .
Calibration , ask the patient to look straight forwards , then 10 mm pen
deflection/10o
Velocity of slow components (VSC) = 9/SD .
Benefits ;
a. Evaluate the nystagmus .
b. Differentiate peripheral from central nystagmus .
c. Diagnose nystagmus which are difficult to detected on clinical examination
(like gaze periodic nystagmus & periodic alternating nystagmus) .
ENG recording of eye movement , less sensitive than direct observation of the eye
& it is of little value if the response has signal electrode in vertical plane .
B. Vestibulo-spinal reflex test
These tests commonly neglected in the evaluation of the patient with balance dysfunction
1. Romberg test
Used to assess the patient ability to stand , feet together , arm by the side with eyes
open & then closed .
Positive test when the patient fall towards the side of a recent paralyzed vestibular
lesion
Significance ;
Vestibular lesion , fall to the same side .
Cerebellar lesion , fall to the same side with little enhancement with eye closure .
Central lesion , different sides .
Extrapyramidal , forward or backward .
Non-organic , falling straight backward .
Lecture notes in
2. Unterburger's test
Stepping test , the patient clasp his hands together & stretch arms out infront of him ,
step up & down on the same spot for 30 seconds with closed eyes .
Abnormal test when the body rotate more than 30o or forward or backward
displacement of more than one meter .
3. Gait testing
The gait is assessed by watching the patient walk straightly quickly between two
points 3-4 m with eye open then closed .
In bilateral vestibular failure , can walk with open eyes normally , but when close his
eyes the patient tend to fall .
Normal patient can do 10 accurate steps in 3 trials .
Abnormal gait like ; hemiplegic gait , cerebellar ataxia , Parkinsonism , shuffling
gait , high stepping gait & hysterical gait .
4. Posturography
Is the recording of postural sway by force platforms technique (static or moving) .
C. Miscellaneous tests
1. Vestibular evoked response
Research technique , has some difficulties like ;
Long time constant of mechanics of vestibular system .
The response may be countered by corneoretinal potential .
The stimulus should be refired to the vestibular end organ & not involving the
properioception , visual & somatosensory reflex .
2. Galvanic testing
- Saline pad attached on tragus to the cathode electrode .
- Patient in dark , stimulus applied 1 mA .
- Body sway to the opposite side & vertigo toward the cathode .
- When the stimulus is stopped , the reverse will occur .
- Results assessed by posturography or ENG .
- It can differentiate between labyrinthine & retro-labyrinthine diseases as it
depends on the integrity of the scarpas ganglia .
- Threshold increased in vestibular neuronitis & long standing MD .
3. Jono-ocular test
Localize pathology to the vestibular end organ , the test is based on Tullio
phenomena .
Clinically , Tullio phenomena occurs when there is more than one mobile window in
the vestibular side of the vestibular membrane & it is caused by ;
a. Fenestration operations .
b. Others ; congenital , direct vestibular trauma , MD & after stapedectomy .
Method ; loud sound introduced to the ear in 2 pulses ;
- 110 dB HL at 500-4000 Hz .
- 120 dB HL at 250 Hz .
The resultant nystagmus is measured by ENG or posturography .

Lecture notes in
Congenital malformation of the ear

Anatomical classification
1. Abnormalities of the external ear
a. Abnormalities of the auricle
(1) Minor variation in shape .
(2) True deformities like fissures (horizontal or longitudinal) , microtia , macrotia ,
anotia , accessory auricle .
(3) Congenital fistulae .
(4) Congenital tumors .
b. Abnormalities of the EAM
(1) Atresia .
(2) Atresia with microtia .
(3) Atresia with microtia & middle ear abnormalities .
(4) Atresia with inner ear abnormalities .
c. Abnormalities of the tympanic membrane .
2. Abnormalities of the middle ear
a. Abnormalities of the ossicles & associated structures
(1) Stapes .
(2) Malleus & incus .
(3) Facial nerve .
(4) Fallopian canal .
(5) Round & oval windows .
b. Abnormalities of the tympanic cavity
(1) Vascular abnormalities ; jugular vein anomalies , persistent stapedial artery ,
internal carotid artery anomalies .
(2) Congenital tumors .
(3) Congenital anomalies leading to OME .
c. Abnormalities of the Eustachian tube
3. Abnormalities of the inner ear
a. Aplasia
(1) Michel’s deformity .
(2) Mondini deformity .
(3) Bing-Siebenmann deformity .
(4) Sciebe deformity .
(5) Alexander deformity .
b. Heredodegenerative abiotrophies
(1) Alone ; infantile or adult .
(2) Associated with other deformities
- Mesodermal (Marfan syndrome) .
- Ectodermal (Waardenberg’s syndrome) .
- Neuroectoderma (Cerebellar degeneration) .
c. Chromosomal aberration ; trisomy 18 & 21 .
Aetiological classification
1. Heriditory
a. Non-syndromic (70%)
(1) Autosomal recessive (80%) .

Lecture notes in
(2) Autosomal dominant (20%) .

(3) Sex linked .
(4) Mitochondrial .
b. Syndromic (30%)
(1) Multifactorial .
(2) Monogenic .
(3) Chromosomal .
2. Prenatal infections , like Rubella , CMV , Influenza , Syphilis .
3. Perinatal ; prematurity , low birth weight , jaundice , obstructed labour , anoxia &
hypoxia .
Classification according to the type of hearing loss
1. Sensorinueral
a. Hereditory
(1) At birth .
(2) Appear in childhood .
b. Secondary
(1) Intrauterine conditions .
(2) Infections .
(3) Ototoxic drugs .
(4) Metabolic disease .
(5) Perinatal disorders .
2. Conductive
a. Hereditory abnormalities of the external & middle ear
(1) At birth ; Crouzon’s syndrome .
(2) Appear in childhood ; otosclerosis ..etc .
b. Congenital disorders leading to OME .
c. Miscellaneous conditions like cholesteatoma ..etc.
3. Mixed
Syndrome with abnormalities of the ear
1. Otocraniofacial (Ear , Face , Skull) ; Goldenhar’s syndrome , Treacher Collin’s
syndrome , ..etc .
2. Otocervical (Ear , Face , Shoulder) ; Klippel-Fiel syndrome .
3. Otoskleletal (bony dysplasia) oseteogenesis imperfecta .
4. Chromosomal abnormalities
a. Autosomal trisomies (13, 15 , 18 ,21) .
b. Sex trisomies (Turnner’s , Klienfilter’s , ..etc) .
5. Miscellaneous
a. With endocrine ; Pendred’s syndrome .
b. With drugs ; thalidomide .
c. With neurocutaneous skeletal disorders ; neurofibromatosis .

Lecture notes in
EAR TRAUMA
External ear
- Laceration
It may be due to accidental auricular injury ; e.g. boxing , child abuse , sport injury , RTA
…etc . It varies from simple laceration to amputation of the auricle .
Treatment , by restore the normal contour of the pinna by suturing the laceration under
aseptic technique .
Prevent the infection of the skin wound or the exposed cartilage which may lead to
chondritis.
This achieved by good cleansing of the wound , good debridemnet of the necrotic &
proper antibiotics (local & systemic) .
Perichondritis if occur lead to damage to the cartilage with loss of the cartilage &
disfigurement .
The treatment with local antibiotics with removal of the pus & necrotic tissue .
- Heamatoma
It may result from closed trauma , e.g. sport injury or boxing , there is extravasations of
the blood between the perichondrium & the cartilage lead to soft doughy swelling , then
the blood is organized causing thickened cartilage lead to cauliflower ear deformity .
Treatment ; early cases by aspiration using wide bore needle & with pressure bandaging.
In long standing cases , incision & evacuation of the clot , with firm dressing or sheets of
silastic applied on both surfaces of the pinna .
The incision should be placed along the margin of the helix .
In recurrent haematoma , further aspiration , but if get infection , abscess developed
which need drainage & antibiotics .
Middle ear & tympanic membrane
- Traumatic perforation of the tympanic membrane
It may be due to changes in the air pressure , fluid or solid objects .
Pathogenesis
Air pressure
- Gradual air pressure may cause tympanic membrane rupture .
- Sudden increase in air pressure more often cause tympanic membrane rupture .
- Sudden forceful blow in the EAM , may increase in the air pressure causing rupture
of the tympanic membrane .
- Blast injury & barotrauma.
- Eustachian tube inflation by valsalva maneuver or by the use of catheter can lead to
rupture of weakened tympanic membrane by previous disease .
- Pressure changes in the middle ear because of nitrous oxide anaesthesia or by
hyperbaric oxygen .
Perforation occur due to air pressure changes in the EAM , mostly in the anterolateral
quadrant usually at the atrophic segments .
Fluid
- Syringing of the ear ; should ensure that the fluid is at the body temperature & the
force of the jet should be directed to the posterior meatal wall & not the tympanic
membrane .
- Caloric test ,
- Diving .

Lecture notes in
Solid objects
- Foreign bodies & their removal .
- Match sticks or hair clips when inserted through the ear .
- Sometimes , the ventilation tube after extrusion , the tympanic membrane fail to heal .
Management
- Traumatic perforation usually occur in healthy tympanic membrane & so the
prognosis is excellent .
- Failure of the tympanic membrane to heal is due either to secondary infection or loss
of the tissue .
- Small perforation are more likely to heal spontaneously .
- Nothing to do & keep the ear dry .
- The ear should not be cleaned unless contaminated material is found , antibiotics
given only if there is infection .
- Some surgeons advocate examination under microscope & do eversion of the edges
of perforation because inverted edges are undesirable .
- Immediate grafting is not indicated , surgical closure done only when failure to close
spontaneously after 3-6 months (by grafting) .
Complications
1. Secondary infections .
2. Sequamous epithelial cyst due to implantation or inversion .
3. Other associated injury , e.g. ossicular dislocations , conductive deafness , SNHL ,
inner ear damage , facial nerve injury .
- Blast injury
The explosive material changes suddenly from solid to gaseous form causing massive
increase in the volume & pressure lead to blast wave spreading outwards , so there is
short lived +ve pressure phase for few milliseconds & a longer less marked –ve pressure
phase .
The external factors affecting such damage ;
1. rising time .
2. site of explosion .
3. intensity of the pressure .
4. duration of the +ve pressure phase .
5. presence of the objects .
The patient related factors are ;
1. position of the head .
2. shape of the EAM .
3. state of the tympanic membrane .
Exposure to the blast injury may cause hyperaemia or subepithelial bleeding in the
tympanic membrane & perforation caused by the +ve pressure phase, most of perforation
heal spontaneously with conservative treatment .
- Radiation injury
Radiotherapy to the ear or to the nasopharynx may affect the ear causing middle ear
effusion , carcinoma or osteoradionecrosis .
- Surgical injuries
Chorda tympani

Lecture notes in
Theoretically , there is disorder of taste & salivary secretion which may follow
surgical injury to the chorda tympani .
Practically ; dysguesia is uncommon after chorda tympani is cut , it may be divided or
bruising may occur which lead to abnormal taste which is metallic in character .
Jugular bulb
It may be dehiscent in the posteroinferior quadrant of the mesotympanum .
It is at risk when separating fibrous annulus from the sulcus tympanicus during
stapedectomy or transcanal tympanoplasty .
Brisk venous bleeding may occur & can controlled by replacing the tympanic
membrane & applying a small pack , then if bleeding stop when complete the pressure
.
Facial nerve
In middle ear surgery , the middle ear may be completely filled with granulation tissue
or cholesteatoma , then the best landmark which is resistant to the disease is the
Eustachian tube .
From there we can dissect posteriorly to the promontory & then superiorly to the base
of the cochleoformis process which marks the junction of the labyrinthine & tympanic
segment . When the cochlear process is destroyed , then the alternative guide or
landmark is the belly of the tensor tympani muscle .
The digastric ridge or chorda tympani nerve can be used as a guide for the facial
nerve .
In the mastoid segment the following are landmarks ; lateral SCC , fossa incudis or
digastric ridge .
The safety of the facial nerve depend on ;
1. Knowledge of the important landmarks & anatomy .
2. awareness of the risk .
3. knowledge of the possible abnormalities of the facial nerve like ; facial nerve
overlying the footplate , Korner’s septum which may give rise to confusion ,
bifid facial nerve below the genu .
4. surgical skills .
Treatment
1. direct anastamosis not necessarily give best results .
2. grafting with piece of the greater auricular nerve should be delayed for 3 weeks .
3. axonplasmal regeneration is optimal when the tension is avoided .
4. excessive connective tissue proliferation can be decreased by removal of few
5. foreign body reaction can be decreased by avoiding the suture material .
Temporal bone & inner ear
- Fractures of the temporal bone
It can be longitudinal , transverse or mixed .
A. Longitudinal fracture
80% of the temporal bone fractures are longitudinal , it result from blow to the
parietal or temporal .
It begins in the sequamous part of the temporal bone extending along the roof of the
EAM tearing the meatal skin & tympanic membrane , crossing the roof of the middle
ear & pass to the petrous temporal bone involving the labyrinthine capsule & the
carotid canal & end near the foramen spinosum or foramen lacerum .

Lecture notes in
Damage to the meatal skin or tympanic membrane cause bleeding from the ear .
Battle sign (discoloration of the skin over the mastoid process) , in absence of any
other obvious cause , bleeding from the ear following head injury indicate fracture of
the base of the skull usually longitudinal despite –ve x-ray .
Rarely labyrinthine capsule is involved causing high frequency SNHL , also
displacement of the fractured bone is rare .
B. Transverse fracture
It accounts for 20% of the temporal bone fractures , it results from frontal or
occipital blow , it extend transversely across the petrous pyramid passing through
the vestibule of the inner ear .
50% of the cases can be demonstrated audiologically .
There is haemotympanum , but no bleeding because the tympanic membrane is
intact , tinnitus & severe SNHL on the affected side , usually permanent , also severe
rotatory vertigo with nausea & vomiting due to severe vestibular damage with
nystagmus to the affected side .
The patient unsteady & unable to walk without support , central compensation
during the subsequent weeks .
There is more severe meural injury than those with longitudinal fracture , facial
nerve injury in 50% of cases , usually immediate , sometimes there is delayed
C. Mixed fracture
It is combination of both .
Management of temporal bone fractures ;
- With CSF leak
Most CSF leaks stops spontaneously within 7-10 days , the policy is not to prescribe
antibiotics prophylactically , also leave any clot in the EAC & avoid introduction of
infection , sometimes use spinal drains .
If the CSF leak is profuse & fail to stop spontaneously (close properly) , the surgerical
exploration & closure is indicated .
The approach is usually from the middle cranial fossa through which is explored &
exposure of the tear is done , the defect is covered with graft of fascia lata or temporalis
fascia .
Some surgeon prefer mastoid approach which is possible , less major & shorter , but the
access to the site is impaired & the positioning of the graft is less secure .
There is possibility of meningitis if there is middle ear infection
- Meatal damage
Tears in the meatal skin may occur & heal with fibrous band formation which lead to
pockets which collect epithelial debris , so the fibrous band should be removed
surgically , sometimes there is cholesteatoma which due to invasion of the sequamous
epithelium to the middle ear through the fracture line , however this cholesteatoma can
be differentiated from pre-existing one by the degree of pnuematization of the temporal
bone .
- Deafness
Conductive deafness , commonly seen in longitudinal fracture & it is due to ; tears of
the tympanic membrane , blood in the middle ear , ossicular dislocation or fractures
&/or adhesions .

Lecture notes in
The most common affected ossicle is incus because both malleus & stapes are relatively
more stable , the defect is commonly seen is dislocation of incudostapeadial joint .
Conductive deafness with air-bone gap about 40 dB need exploration of the middle ear
& ossiculoplasty which have better results than CSOM .
SNHL , it occur following head injury with labyrinthine damage & concussion , it is
commonly seen after longitudinal fractures , usually untreatable but some with
spontaneous recovery , in transverse fracture unlikely to recover .
If the head injury sufficiently severe to cause loss of consciousness , it usually lead to
immediate SNHL .
- Vertigo
It is common after head injury & can be due to ;
Postconcussional syndrome , which is the most common cause & can occur even
without skull fractures , it settle within 6-12 months .
Following transverse fracture which may involve the vestibular apparatus , it lasts 1-
3 weeks & can be relieved by labyrinthine sedatives & central compensation &
improvement may occur but it is gradual & slow .
BPPV , due to damage of the utricle & otolithic memebrane , it is short lived &
transient & fatiqueable & precipitated by head movement , it is usually self limiting
but takes about 2 years .
Delayed endolymphatic hydrops , occur due to cochlear duct & vestibular aqueduct
involvement which lead to vertigo similar to that of Mineir’s disease .
Perilymph fistula .
- Facial paralysis
It may follow transverse fracture of the temporal bone (50%) .
Immediate paralysis may be due to tearing of the fibers of the facial nerve or entrapment
in the fracture line (need exploration) .
Delayed facial paralysis , the nerve is anatomically intact , but there is oedema within
the bony canal , treatment similar to that of idiopathic facial palsy .
- Penetrating injury of the temporal bone
Like bullets , missile , explosion , ..etc , gun shots has remained in the temporal bone for
many years without any complications
If there is gunshot in the middle ear cleft , there is possibility of brain herniated through
the damaged tegmen tympani or there is infection of the middle ear cleft , this need
surgical exploration & removal is indicated .
If there is no infection or not causing symptoms , then no need for treatment .
- Whiplash
It implies an acceleration –extension injuries of the neck & some authorities include
deceleration –flexion movement of the neck , it is seen in rear-end collision in RTA .
Always there is history of RTA for passengers in a car involved in rear-end collision after
which the patient have pain & ache in the neck which increase to severe pain &
associated with dizziness , deafness , tinnitus & dysphagia .
Dizziness & rotatory vertigo & increasing unsteadiness may be occur few days after
injury & it associate with positional nystagmus .
The deafness is not due to direct effect of whiplash on the ear but due to associated head
injury . Tinnitus is frequent complaint & it is not due to direct effect of whiplash injury on
the ear but due to brain concussion .
Lecture notes in
Theories which explain these symptoms ;

1. Neuromuscular effect ; with abnormal properioceptive impulses causing dizziness .
2. Neurovascular effect with abnormal cervical symptoms & nervous system .
3. Mechanical vascular problems with kinking of the vertebral artery .
4. Brain damage .
Typical history , of whiplash injury followed by short period of symptoms free , then
development of pain in the neck during the next week , there is dizziness which may persist
for months to years .
Treatment ;
Acute phase by ;
a. Splinting of the neck (by collar) .
b. Bed rest to relive the neck of head weight .
c. Heat & massage .
Chronic phase by ;
a. prolonged immobilization or heat application of benefit .
b. neck traction & muscle exercise of some benefit .
c. tranquilizers & labyrinthine sedatives .
d. discussion with the patient about the possible disordered function .
Precautions
a. Extending the back of the seat .
b. Supporting the head with head movement (with strain) .
- Perilymph fistula
It is a perilymph leak from the inner ear to the middle ear .
Caused by ;
1. Rupture of the stapediovestibular joint .
2. Fracture of the footplate .
3. Tear of the round window membrane , more often seen with oval window .
Clinical feature
 History of head injury or stapes or middle ear surgery or cases with increased
intracranial , with associated with coughing or straining or exertion with lead to
sudden increase in middle ear pressure , these are the predisposing factors .
 The most common symptoms is unsteadiness , usually positional , this dizziness
persist until the fistula is closed spontaneously or by surgery .
 SNHL & tinnitus .
 High index of suspicion is necessary .
On examination
 Fluid level in the middle ear not expected to be seen because the amount of the
perilymph fluid is small .
 Fistula test is usually but not always –ve
 +ve Romberg test ; the following characteristic can differentiate positional
nystagmus from nystagmus of BPPV ;
1. Short or no latency period .
2. Nystagmus is not so violent .
3. Duration is longer .
4. Fatigability is slowly or not at all .
5. Rarely reverse direction when the patient is brought to a sitting position .
Lecture notes in
6. Not necessary beat toward the involved ear .

7. Only occasionally rotatory .
 PTA , reveal SNHL , speech reception threshold & speech discrimination score is
decreased .
Diagnosis by ;
 Injection of Fluorescein or radioactive substance into the CSF before surgical
exploration , +ve detection at surgery or in nasopharynx .
 Definitive Dx with certainty is by surgical exploration .
Treatment ;
 Medical treatment ;
1. Bed rest with the head of the bed elevated 30-40 degree for 5 days .
2. Sedation & fecal softener .
3. Avoid any exertion .
4. Limit his activity for further 10 days .
 Surgical treatment
Indicated in ;
1. Failure of medical treatment .
2. Symptoms persist for over 1 month .
Procedure ; tympanomeatal flap is elevated with inspection of the middle ear carefully , if
the procedure done under LA , then valsalva maneuver may help to identify the leak .
Care should be taken during probing the stapes & not to create fistula at this stage (from
the round window) , after identification of the fistula , the area around it should be denude
of the mucosa , then a graft of fascia or perichondrium should be applied to the denuded
area & packed with gel foam .
Dramatic response of vertigo , but rarely improve SNHL .
- Blast injury
It is said that the tympanic membrane rupture secondary to the blast injury have
protective effect on the inner ear .
Blast injury may lead to SNHL which is the most marked after explosion with tendency for
spontaneous resolution for up to 6 months .
Treated usually by vasodilator drugs , steroids , anticoagulants , Co2 inhalation or low
molecular weight dextran (i.v.) .
Blast injury may also improve spontaneously or stay permanently .
- Surgical trauma
The causes of loss of cochlear function during tympanoplasty ;
1. Removal of the cholesteatoma matrix & granulation tissue from the labyrinthine
fistula commonly involving the lateral SCC .
2. Removal of the cholesteatoma or tympanosclerosis from the area around the oval
window with fracture of the stapes footplate or rupture of its annular ligaments .
3. Excessive movement of the stapes footplate .
4. Contact between the burr & any part of the intact ossicular chain , most commonly
the body of incus , which may cause extensive hair cell damage .

Lecture notes in
BAROTRAUMA
It is defined as non-infective inflammatory reaction in the middle ear cleft lining , when
there is negative intratympanic pressure , the condition is caused by rapid rise in the
extracorporal pressure that the body unable to adapt .
Pathophysiology
The cartilaginous Eustachian tube is normally closed , it opens only when there is positive
pressure in the nasopharynx (like in yawing) , or during swallowing , primarly due to the
contraction of the levator veli , tensor veli & salpengopharyngeous muscles .
Developmental narrowing , inflammation or oedema of the tubal mucosa compromise its
patency & predispose to inadequate middle ear pressure equilibrium usually during descent
in flying & diving .
The development of barotrauma is dependent upon the rate of descent or the rate of ambient
pressure in contrast to the rate of increase of middle ear pressure , which is affected by the
patency of the Eustachian tube .
At the depth of 2.6 feet , a pressure differential of 60 mm Hg cause mucosal congestion ,
oedema & microscopic haemorrhages lead to narrowing of the Eustachian tube lumen
decreasing the ability to open & ventilate the middle ear by increasing the nasopharyngeal
pressure .
The tympanic membrane & round window bulge into the middle ear with inward
displacement of the stapes footplate , the diver may notice pain & pressure in his ears with
CHL & s.t. vertigo
At 3.9 feet & a 90 mm Hg pressure differential , it is usually impossible to open the
Eustachian tube by increasing the nasopharyngeal pressure , this due to a valve effect from
pressure on the tubal cartilage , together with further mucosal haemorrhage (locked tubed)
At 4.3 – 17.5 feet & pressure differential of 100-400 mm Hg , there will be rupture of the
tympanic membrane .
Significant middle ear & Eustachian tube mucosal oedema with microscopic haemorrhage
develop with negative pressure of 30-35 mm Hg .
Maneuvers to equilibrate the middle ear pressure during diving & flying
1. Modified valsalva maneuver , controlled expiration with the lips closed & nose
obstructed by digital compression .
2. Frenzel maneuver , closing the glottis , mouth & nose while simultaneously
contracting the muscles of the floor of the mouth & the superior constructor muscles
3. Toynbee maneuver , swallowing with a closed nose .
4. Modified yawn or swallow , the simplest , thrusting the lower jaw anteriorly &
slightly opening the jaw , while maintaining the mouth closed & the nasal passages
open .
Clinical features of middle ear barotrauma
- Symptoms
1. Initial symptoms , sensation of fullness or blockage (early during descent) , with
further descent there will be ear pain .
2. Conductive hearing loss is always present .
3. Tinnitus & Vertigo & SNHL (severe) means inner ear barotrauma .
Alternate baric vertigo lead to mild tinnitus with vertigo , when , there is difference in
pressure between the right & left middle ear .

Lecture notes in
The suggestion of inadequate Eustachian tube function occur in ; (1) nasal dysfunction
like congestion & discharge (2) Otitis media (3) mastoid inflammatory disease (4)
previous mastoid &/or middle ear surgery .
Divers should equilibrate middle ear pressure every 1-2 feet .
- Signs ;otoscopy reveal oedema & haemorrhage in the middle ear mucosa , we have 6
grades (but not dependant for the management) :
1. Grade O : symptoms with no otoscopic signs .
2. Garde I : diffuse redness & tympanic membrane retraction .
3. Grade II : I + slight haemorrhage within the tympanic membrane .
4. Grade III : I + gross haemorrhage within the tympanic membrane .
5. Grade IV : dark , slightly bulging tympanic membrane due to free blood in the middle
ear , fluid level might be present .
6. Grade V : free haemorrhage with tympanic membrane perforation .
Scarred tympanic membrane from previous disease or surgery can obscure these signs .
Prevention
1. Adequate pre flying or diving ENT examination which emphasis nasal & Eustachian
tube function .
2. Avoidance of diving with significant nasal obstruction & discharge .
3. Refraining from diving in rough seas with swells in excess of 2 feet .
4. Discontinuing descend without adequate middle ear pressure equilibration every 1-2
feet .
5. Predive or preflight use of topical long acting nose drops "0.05% oxymetazoline" .
6. Systemic decongestant &/or antihistamines .
N.B.: Tympanic membrane perforation & Grommet acts as preventive for the disease .
Management
The 1st step is exclude inner ear trauma by examination (loud dizziness , SNHL , vertigo) ,
by auditory & vestibular tests .
The management depends upon the degree of the injury & the presence or absence of
tympanic membrane perforation (management according to the type)
- Type I middle ear barotrauma ; include symptoms immediately after the diving or flying
with minimal otoscopic signs (Grade I & II) , the management lines are ;
1. Avoid further diving & flying until pre-existing nasal & ear symptoms have cleared
& the individual can easily auto-inflate both ears at the surface (24-48 hours) .
2. Systemic or /& long acting topical nasal decongestant .
- Type II middle ear barotrauma ; symptoms with obvious otoscopic signs , diffuse
haemorrhage , serious middle ear effusion &/or haemotympanum (Grade III & IV) ;
1. Rest & avoid further diving until complete resolution & the ear can be easily auto-
inflated (7-21 days) .
2. Systemic & long acting topical nasal decongestant with short acting steroids .
3. Prophylactic systemic antibiotics , if purulent nasal discharge &/or cough with
sputum , indicate systemic antibiotics .
4. In intact tympanic membrane , use topical ear drops (pain reliever) like auralgan® .

Lecture notes in
- Type III middle ear barotrauma ; symptoms with perforation (Grade V) , management
are;
1. Avoid further dive until resolution & tympanic membrane repair , either
spontaneously or surgically .
2. Solution containing alcohol or acids with antibiotics should be avoided , do C&S
under microscopy .
3. Systemic & topical nasal decongestant & antibiotics .
4. Surgical repair of the tympanic membrane (if fail to heal) .

Lecture notes in
OTITIS MEDIA
Acute suppurative otitis media (ASOM)
It is an episode of inflammation of the middlw ear associated with pain , fever , hearing loss
& s.t. discharge .
Aetiology
- Spread of infection
1. Eustachian tube ; usually in URTI in children (Eustachian tube is competent) .
2. Pre-existing perforation due to trauma , infection , ventilation tube ...etc .
3. Blood borne infection ; viral or bacterial .
- The peak age incidence at 5-7 years (95% of children in the preschool age , <7) .
- Socioeconomic factors , the disease highly present in low hygein population (overcrowded
& malnurished) .
- Speciefic abnormalities like immune suppression , cleft palat , Down's syndrome .
- Adenoids ; infection will impair the mucocilliary flow leading to stagnation predisposing
to infection which ascend through the eustachian tube to the middle ear causing mucosal
odema preventing drainage .
Bacteriology
The commonest pathogens are ; St. Pneumonia (19%) , H. influenza (9%) , half of the
patients have Beta-lactmase M.O.
Some consider H. influenza as 50% especially for those with OME (20%) , s.t. Pseud.
aerogenosa & Staph. aureus commonly found in the discharging ear .
Clinical features
- The presenting Symptoms are ; pain (abscent in young children) , irritability , baby head
on the normal side , while some are very quite , baby refuse food & not sllep well .
It usually associated with recent URTI or tonsilitis .
- Signs ; fever , incooperative , listless , O/E bulging red tympanic memberane , hearing
loss , ear discharge , or it might be only red or congestion around the handle of malleus .
- Investigations ; (1) Ear swab for C&S (2) Mastoid x-ray .
Treatment
a. conservative Medical Rx
a. Bed rest .
b. Analgesia (Paracetemol) .
c. Antibiotics ; Amoxil or Augmentin for 10 days , while those bacteria producing
lactmase use Claforan .
Lines of antibiotics Rx are ; 1 st by Amoxil , Septren or Erythromycine , the 2nd
Augmentin or Claforan .
The management failure depend on ; (1) Age , high in the 1 st year of life (2) non-
compliance (3) viral illness superimposed (4) Hx of recurrent SOM (5) Antibiotics given
To avoid failure , repeat the course of 1st line antibiotics for 10 days , change to the 2nd
line (especially in areas which are prevaence with Beta-lactmase M.O.) & myringotomy
The management of the recurrent ASOM is by ; long term low dose antibiotics will
reduce the number of episodes (& minimize the side effects) , adenoidectomy & insertion
of ventilation tube .
d. Topical antibiotics , if there is TM perforation , Aminoglycoside drops is the
most effective with less risk of ototoxicity so less risk of SNHL .

Lecture notes in
b. Surgical Rx
a. Myringotomy , in severe pain this will relieve pain & allow drainage .
b. Ventilation tube , usually stop recurrent OM (>6 attacks /year) .
c. Adenoidectomy , alone may be preferable (avoided in cleft palat , even with
sunmucosal cleft because it will cause worsening of the postnasal discharge) .
d. Tonsillectomy , has no difference than adenoidectomy alone , so no indication .
Adenoidectomy & ventilation tune are accepted as a day case surgical procedure .
Complications
1. Acute mastoiditis ; pain , fevr , swelling over the mastoid process (behind the ear) ,
tender MacEwen triangle , saging of the posterosuperior wall of the deep ear canal
(subperiosteal abscess , this dangerous condition should be differentiated from otitis
externa by saging , this abscess formed due to perforation of the outer cortex of
mastoid bone) .
It is managed by ; (1) 48 hrs i.v. antibiotics against Staph. & Pneumococci (2) cortical
mastoidectomy , subperiosteal abscess & CNS complications (Bezold's abscess due to
spread to the sternomastoid m. & to the chin through the digastric m.)
2. Latent or masked mastoiditis ; mastoiditis with less dramatic clinical picture ,
develope despite oral antibiotics .
3. Sigmoid sinus thrombosis & intracranial sepsis ; irritability , swinging fever , Dx by
CT scan & MRI , it is managed by ligation of the internal jugular vein in the neck (to
prevent spread of clot) & cortical mastoidectomy to clear & evacuate the infected
clots .
4. Meningitis ; 63% after ASOM , recurrent meningitis predisposed by Mandini
deformity of the middle & apical turn of the cochlea (dilated apical 7 middle turn &
fused together) , any CSF otorrhea may lead to meningitis .
5. SNHL ; high frequency hearing loss (because it destroy the hair cells in the basal
turn of the cochlea) , pus through the oval & round windows will lead to otitis
interna .
6. Facial palsy ; especially in dehescent facial canal or in AIDS , it must be urgently
drainded surgically (myringotomy or cortical mastoidectomy) with antibiotics &
biopsy taken for C&S from the mastoid mucosa .
Mastoid surgery
- Indications ;
a. Subperiosteal abscess .
b. No response after 24-48 hrs of conservative Rx .
c. Any complication .
- Procedure ;
a. Simple mastoidectomy in 90% .
b. Simple drainage by incision & drainage of abscess , in small number .
c. Extensive mastoidectomy in few patients .
Cortical mastoidectomy
- an operation for acute mastoiditis aimed to wide exenteration of the entire cell system of
mastoid ( Schwartze' mastoidectomy) .
- Preoperative investigations ;
a. Mastoid x-ray to assess the status of the mastoid .
b. Routine lab. Tests ; CBP , B. Urea , RBS ...etc for assess fittness for anasthesia .
Lecture notes in
c. CT scan to see whether there is pus collection .

d. Facial nerve integrity by assessing facial movement .
e. Consultation to neurosurgery .
- Preparation ;
a. Shave 1 cm of hair behind the ear ( the incision is close to the hair line) .
b. Intraoperative VII nerve monitoring by needles that record the action potential from
muscles of the face .
- The operation ;
a. the Incision ; child at birth has no mastoid process & so the facial nerve vulnerable
(superficial) & higher than expected , postauricular incision will damage the nerve , so
in very small infants the incision above the ear & extends posteriorly & inferiorly but
not lower than the level of the meatus .
Typically the incision start at the point at which the auricle leave the skull to the level of the
mastoid tip (1 cm behind the postauricular sulcus) to avoid sinus postoperatively .
b. Any subperiosteal pus aspirated with needle & the pus sended for C&S .
c. Once the cortex is uncovered , the bone is removed (cortex) with drill (exposing the
antrum) & the mastoid aircell system entered & so do cortical mastoidectomy
All cells should be entered ; (1) Tip (2) Perisinus (3) Sinodural angle –petrosal- (4)
Perilabyrinthine (5) Dural (6) Perifacial & (7) Zygomatic .
d. sure when doing the operation that the antrum has a good communication with the
middle ear & block not present (membranes , adhesions or granulation) , this can be
assessed by passing the seeker into the aditus , if the communication small or closed we
do fine bone curette or fine drilling to enlarge the aditus .
e. If the operation become techniquecally difficult (due to bleeding or granulation) , close
the wound with drainage & re-explore the ear a week or later with help if necessary (by
more experience surgeon) & so management with antibiotics (surgical enviroment
within the ear with complete resolution of infection) .
- Extension to the petrous apex ; rare , Allam's classification of pneumatized space in
temporal bone ;
a. Middle ear region ; mesotympanic area , epitympanic area , hypotympanic area ,
posterior & anterior tympanic area .
b. Mastoid region ; mastoid antrum , peripheral mastoid area which include tegmental ,
sinal , sinodural , facial & tip .
c. Perilabyrinthine region ; supra & infra-labyrinthine area .
d. Petrous apex region ; peritubal & apical area .
e. Accessory region ; zygomatic area , squamous area , occipital area & styloid area .
Aircells withis these areas connect with each others to form tract along with infection occur
The route of infection to the petrous apex is either through superior route (Eagleton's ,
Thornvsldt's & Freckner's) or inferior route (Hypotympanum , Almoor's , Ramadier's) .
Approaches to the petrous apex are through ;
1. Eaglton's operation ; superior approach to the petrous apex involving the removal of
the tegmen to the base of the zygoma with removal of part of sequama , then elivate
dura of the middle fossa to expose the petrous apex .
2. Thornvaldt's operation ; superior approach along the supra labyrinthine , dissection
then preceed as above operation .

Lecture notes in
3. Almoor's operation ; inferior approach to the petrous apex through space bounded
by cochlea , carotid artery & tegmen tympani .
4. Lemport-Ramadier's operation ; anterior to thw Almoor's operation that purses the
peritubal cells to the petrous apex between the cochlea & crotid artery .
Otitis media with effusion (OME)
It is the commonest cause of hearing loss , it has a variety of synonyms ; catarrheal OM ,
exudative OM , serous OM , seromucinous OM , secretory OM & non-suppuritive OM .
It is charcterized by the presence of effusion with the middle ear cleft which may be serous ,
mucoid , but not frankly purulent .
In every case of ASOM followed by effusion , 90% have resolved within 3 months (OME ,
50% resolved within 3 months , only 5% persist >1 year) .
Many risk factors are present ; cleft palate , adenoid , obstruction of the nasal passages &
mucocilliary system pathology .
The management depends on the duration , severity & on the age & general condition of the
patient .
Incidence , about 42% of 3 years old children have it , the mean hearing loss about 20 dB .
Although it has difficulty in assessing the precise natural history of the disease due to its
fluctuating course & tendency to spout-resolution .
Pathoplogy
It is due ; (1) exess amount of glycoprotien material secreted by goblet cells , together with
(2) Deficient middle ear drainage & ventialtion .
Once the middle ear fluid is established , middle ear mucosa replaced by ;
1. thickened pseudostratified mucous secreting epithilium with goblet cells & mucous
glands
2. also the cilliary lining will be less efficient in removing the secretions .
3. the sunbmucosa will be odematous with dialted blood vessels & macrophages ,
plasma cells & lymphocytes (& even bacteria) .
The fluid is a mixture of secretions of the epithelial cells , goblet cells , mucous glands & the
inflammatory exudate .
The biochemical composition ; is high total protien concentration with enzyme & antibodies
(glycoprotien) , carbohydrates (oligosaccharide) .
The maority of children with OME resolve & return to normal (50%) , some patients may
have retraction pockets , tympanosclerosis ...etc .
Classification
1. Acute OME ; sudden onset of accumulation of nonpurulent fluid in the middle ear
commonly seen in adults , this due to (1) Eustachian tube dysfunction (2) URTI (3) Allergy
(4) Idiopathic .
It is charcterized by mucosal swelling with gland hypertrophy leading to effusion .
There are deafness of sudden onset (cardinal symptom) , diplacusis (hearing different
voices in both ears) , earache , fullness , tinnitus or vertigo .
O/E , there is TM retraction , bubbles , bluish TM , altered TM mobility , conductive
hearing loss , type B tympanometry , PTA , x-ray of the mastoid .
Managed ; medically by ; valsava manouver & catheterization leading to inflation of the
middle ear , vasoconstructor nasal drops & antihistamine (Actifed) in allergy .
When failure of medical Rx for 2 weeks , then myringotomy .

Lecture notes in
2. Chronic OME ; gradual onset of accumulation of non purulent fluid within the middle
ear , usually in children due to (1) Eustachian tube dysfunction (2) Bacterial infection (3)
Allergy .
It charcterized by deafness , viscid fluid (glue) , pale grey or yellow tympanic membrane .
Managed medically by decongestant & antihistamine , & when failure occur by
myringotomy .
Risk factors
1. Race ; high in American indian more than white population , low in blacks .
2. Syndrome of skull base & nasopharyngeal anatomical abnormalities , like
Down's syndrome , Hurler's syndrome & Fragile x syndrome .
3. Sex ; M>F , the male has less pneumotized aircell system .
4. Cleft palate , usually associated with tube dysfunction due to impaired tensor
palati muscle (child with bifid uvula has no extra risk for developing OME) .
5. Breast feeding < Bottle feeding .
6. Family size & passive smoking ( contraversial) .
7. Mouth breathing habit (posture) account for 20% of OME .
Aetiology (Infection & Eustachian tube dysfunction are the main cause)
I.Eustachian tube dysfunction
A. due to Palatal abnormalities ; (1) cleft palate (2) sunmucous cleft palate
normally the Eustachian tube alter to adult configuration at about 7 years old .
B. due to Altered mucocilliary system ;
(1) Infection ; +ve bacterial culture in up to 50% of OME (simillar to these of ASOM) ,
surface endotoxins of H. influenza may be responsible for the induction of OME , also
respiratory syncytial virus increase the rate of OME .
(2) Allergy ; it increase the susceptibility to respiratory infection , it cause odema
closing the eustachian tube .
(3) Immunological factors ; IgA found in the middle ear effusion & IgA plasma cells
found in the inflamed mucosa of the middle ear cleft , Ig & immune complexes may be
the key factor in generation of secondary immune related response in the middle ear
leading to OME , also rheumatoid factor present in 85% of OME .
(4) Surfactant deficiency , bacteria will secret proteolytic enzymes whcih decrease the
surfactant in the tube .
(5) Cillial abnormalities , tubacco smoking , immotile cillia synd. & Kartegner's
syndrome .
(6) Hormonal factors , hormonal dysfunction with high oestrogen level &
hypothyroidism leading to tubal dysfunction & then to OME .
II. Middle ear gas composition ; increase loss of middle ear gas by increase diffusion into
the blood which enhanced as a result of the increased vascularity of inflammation causing –
ve middle ear pressure & atelectasis .
III. Nasopharyngeal disproportion ;
(1) Craniofacial abnormalities ; like Down's syndrome , Hunter's syndrome & Hurler's
syndrome , these will increase the basal angle of the skull in relation to the cranial
cavity causing Eustachian tube dysfunction .
(2) Adenoid & nasopharynx , growth of the adenoids outstrips that of the nasopharynx in
children aged 3-5 years with resultant reduction in the nasopharyngeal airway (80% of
ENTist advice for adenoidectomy for OME) .

Lecture notes in
In adults ; (1) Idiopathic (2) Nasopharyngeal Ca. (unilateral OME) (3) Barotrauma (4)
AIDS , increased the incidence of URTI , lymphoid & adenoid hypertrophy & increasing
incidence of nasopharyngeal tumors (5) Radiotherapy , fibrosis around the Eust. Tube .
Clinical presentation
1. Covert or overt hearing loss , fluctuating in relation to seasonal changes , it leads to
impaired speech & decrease in language developement , behavioral & scholastic difficulties
2. Otalgia due to secondary bacterial or viral infection of the fluid in the middle ear cleft ,
it also coexist with URTI , sinusitis & allergic rhinitis , also it often resultant from bacteria
found in the nasopharynx & ascend to the Eustachian tube .
3. the Diagnosis have 5 aspects ;
a. History ; of the hearing loss optained from parent in 19% of patient with glue ear .
b. Otoscopy ; by the use of pneumatic otoscopy or opearting microscope , it has 75-
95% sensitivity & specificity .
(1) Colour , pale gray-amber to black , blue drum , thickened & dull or thin & reflective
(2) Increased red vascularization of the radial vessels & increase in malleular
vasculature .
(3) Fluid level & air bubble .
(4) Retraction of pars tensa & in severe cases retraction of pars flaccida .
(5) Reduces mobility of the TM (by Seigle's otoscope) .
c. Tympanometry ; rapid & reliable even in infants , it has 4 types , type A (Ad & As) ,
type B (flat) , type C (-ve pressure) subdivided into C1 & C2 .
Type B 93% sensitive in detecting OME & 75% specific .
New micrtympanometer & automatic impedence tympanoscopy
d. PTA , of limited value for children less than 4 years , shows dry ear (17dB loss) ,
minimal OME (23dB loss) , moderate OME (29dB loss) & impacted middle ear
(34dB loss) , also voice test fail to detect 20% of children with hearing loss of < 20
dB . Tunning fork may be helpfull in children below 4 years (Rinne test –ve if
loss>15-20 dB)
e. Myringotomy & aspiration of the fluid (the golden standard for OME diagnosis) , it
has been sugested that N2o 2 displace the middle ear fluid at operation .
Management
1. Medical management ; 50% of the OME resolve within 3 months spontaneously , only
5% persist > 1 year , No medical Rx for OME can effect a long term cure , the medical trial
are;
a. 0.5% ephidren HCl nasal drops (antihistamine) , no improvement assessed .
b. Mucolytic agents . short term effect (Bromohexin HCl) .
c. Gaseos ventilation of middle ear with sulphurhexafluride .
d. Autoinflation of the Eustachian tube , short term effect .
e. Treating the associated nasal conditions & nasal allergy , improving the condition .
f. Antibiotic & steroids or antiinflammatory drugs (2 weeks course) , Amoxil or
Augmentin with Prednisolon or Brufen for 2 weeks .
g. Immunization (oral or intranasal) against respiratory syncytial virus & H. influenza
B.
2. Hearing aid ; for chronic OME (till now no study prove it) .
3. Surgical management ; it is recommended for persistant disease with significant
hearing loss causing symptomatic morbidity , the condition should observed otoscopically

Lecture notes in
& monitor with tympanometry & hearing tests for at least 3 months prior to surgery &
reassessment shpuld be made at preadmission to confirm the persistance of the disease , the
opeations are ;
a. Myringotomy with short stay ventilation tube ; mayringotomy with fluid aspiration
done at the anteroinferior or superoanterior quaderants of the TM (to avoid damage to
the middle ear structures) & avoid the excessive damage to the fibrous layer of the TM
(preventing subsequent tympanosclerosis) , usually Shah or Shepard ventilation tube ,
producing short term hearing gain about 20 dB .
b. Long stay ventilation tube ; Paparella & Goode ventilation T-tube , it could cause
increased otorrhea & persistant perforation , used for long periods (>1 year) in more
severe atelectatic tympanic membrane .
c. Adenoidectomy ; it relieves Eustachian tube , tonsillectomy have no role in the Rx of
OME , the tube more effective than adenoidectomy alone at 6 months & at 2 years there
is no difference between the tube alone , adenoidectomy or both in combination .
Sequelae
1. Scarring , attic retraction & pars tensa atelectasis leading to
myringoincudostapedopexy in 5% of children .
2. Tympanosclerosis ; 50% of ear Rx by ventilation tube develope some degree of
tympanosclerosis , haemorrhage at tha time of tube insertion is partly responsible for
sclerosis .
3. Otorrhea ; mucoid or purulent one (short term complication) & respond tp aural toilet
& ear drop of antibiotics & steroid (Methadin-N drop) , removal of the tube stopping
discharge in 79% of cases within one month .
4. Perforation ; following long stay tube .
5. Cholesteatoma ; 11-18 years after the ventilation tube insertion , attic cholesteatoma
develope in 1.7% of cases .
6. Inner ear , disequilibrium in 22% of cases .
7. effects on speech , language , learning & behavior ;
a. Poor language & learning in early years .
b. Poor shool performance .
c. Changes in language developement was no longer persist at school age (Schilder
1993) .
8. Effects on asymmetrical hearing loss ; small difference in bimaural making level
difference in children with OME , difficulties for children in perception of signal in noisy
enviroment .
Chronic suppurative otitis media (CSOM)
It is chronically discharging ear with perforation with or without hearing loss .
ASOM (less than 3 weeks) . subacute OM (3 weeks – 3 months) , CSOM (> 3 months) .
Incidence
Depends on race & socio-economic factors , more common in Eskimo , American Indian &
black south Afericans , also increase in those with overcrowding , poor hygiene &
malnurished.
Classifications

Lecture notes in
1. Tubotympanic disease ; charcterized by a perforation of pars tensa (safe) or central

perforation , it is the residue of an ASOM , infection usually acquired in infancy or early
childhood , usually associated with acute infectious disease .
2. Atticoantral disease ; most commonly involve the pars flaccida & charcterized by the
formation of retraction pocket in which keratin accumulates to produce cholesteatoma .
Pathology (It is either one of the following)
1. Inactive (mucosal) COM ; perforation of the TM at pars tensa without inflammation .
2. Active (mucosal) COM ; perforation , odematous mucosa & ear discharge .
3. Inactive sequamous epithelium COM ; retraction pockets at the pars flaccida .
4. Active sequamous epithelium COM (cholesteatoma) ; active mucosal with depris &
sequamous retraction .
Clinical assessment
1. History
a. Ear discharge
(1) in tubotympanic disease it is profused , mucoid , inttermittent , percipitated by water
through the perforation .
(2) in atticoantral disease it is scanty , foul smelling & more chronic .
(3) bloody discharge in cases of polyps or granulation tissue .
b. Hearing loss (may be the only symptom) , usually conductive & may decreased by
bridging by cholesteatoma , or severe mixed or even dead ear .
Hearing loss here usually conductive & due to ; (1) TM perforation (2) loss of the round
window baffle (occur with posterior perforation exposing the round window niche
lossing the protection which is normally afforded by the TM) (3) ossicle distruction
(severe loss) (4) tympanosclerosis (5) presence of cholesteatoma (6) shallow middle ear
space with distructive or fibrosed ossicles (decrease the impedance transformer) & (7)
presence of actiev mucosal disease .
Sometimes there is sensorineural hearing loss due to diffusion of the toxic products of
the inflammation through the scala tympani via the round window memberane .
c. Otalgia ; uncommon , but occasionally occur in cholesteatoma .
d. Others ; headache , vertigo & facial palsy (due to complications) .
2. Examination
a. Inspection ; the pinna should be inspected for both sides to exclude the presence of
scar from previous ear surgeries .
b. Palpation ; over the mastoid area to elicit any tenderness , also examine for pre- &
postauricular lymph nodes .
c. Otoscopy ; for discharge , depris , polyps , narrowing , colour of the skin & if there
is meatoplasty , the TM to see the site , size & shape of the perforation , retraction
pockets or flecks of cholesteatoma , also can assess the mucosa of the middle ear
through the perforation (odematous or polypodal or flecks of cholesteatoma) .
d. Operative microscope (microear) ; assessment under the operating microscope
allows the discharge & attic crusts to be removed (the child examined under GA) .
e. Tunning fork tests .
f. Other ENT examination to the nose , throat , neck & cranial nerves .
3. Investigations
a. Labrotary ; swab taken for C&S to see what type of bacteria (usually Proteus ,
Pseudomonas & Staph aureus & E. Coli or Bacteroids "anaerobes") .

Lecture notes in
b. Audilogical assessment ;
(1) PTA ; to assess the degree of hearing loss , determine the air-bone gap & as a
baseline for comparision with that taken postop. .
(2) Speech audiogram ; valueable in attempting to improve the diagnosis .
c. Radiological assessment ;
(1) x-ray for mastoids ; to see the pathology (cavity) , any variation of temporal bone
anatomy & see the pneumotization of the temporal bone .
(2) CT scan ; see the anatomy of the temporal bone , eroded ossicles & intracranial
complications .
(3) MRI ; see the cholesteatoma , granulation tissue & polyps .
d. Haematological tests ; CBP , biochemistry ...etc , for fittness for surgey & GA .
DDx of a cavity over the EAM (by radiology) ; (1) cholesteatoma (2) big antrum (3) big
aircells (4) granulomatous disease like Wegner's granuloma (5) iatrogenic like trans
labyrinthine approach for vestibular Shwannoma (6) neoplastic distruction of the
temporal bone .
Cholesteatoma
It is a three dimensional epidermal structure exhibiting independent growth , replacing the
middle ear mucosa , resorbing the underlying bone & tend to recur after removal .
OR defined as a bad skin in the middle ear cleft or benign keratinizing sequamous cell cyst
"keratoma" .
The term cholesteatoma 1st used by the German physiologist Johannes Muller at 1838
Classification
(1) Congenital Cholesteatoma .
(2) Acquired Cholesteatoma ;
i. Primary Acquired cholesteatoma .
ii. Secondary acquired cholesteatoma .
iii. Tertiary acquired cholesteatoma .
Congenital Cholesteatoma
Shown by Michaels to be the result of the persistence of small nidus of epidermal ectoderm
that occurs in the 1st trimester in the normal fetus & is normally resorbed , it has 4 features
1. Developed behind an intact tympanic membrane .
2. No previous history of OM .
3. An origin from embryonal inclusion of sequamous epithelium
4. No iatrogenic cause (Grommet) .
In childhood it present as CHL when invade the ossicles , while in adulthood it may press
on the facial nerve or the brain stem .
The average age at presentation is 2.5 – 5 years & F:M about 3:1 .
It is found either in the middle ear or in the apex of the temporal bone , its expansion may
lead to secondary infection , also it may developed in association with congenital atresia of
the ear .
Acquired Cholesteatoma
1. Primary which associated with a defect in pars flaccida , at the attic , no previous
history of infection , associated with retraction pockets , containing keratin debris . .
2. Secondary which associated with defect in the pars tensa , associted with marginal
perforation with history of previous infection & foul smelling discharge .

Lecture notes in
3. Tertiary which exist behind normal intact TM as of implantation or previous middle

ear infection .
Theories of pathogenesis
Congenital cholesteatoma
Though to be a true inclusion epidermoid , there is an area of keratinizing epithelium within
the middle ear cleft , usually seen after an intact tympanic membrane , mostly present at the
cerebellopontine angle & petrous apex .
There are four stages (By Potsic) :
 Stage I : Limited to one quadrant .
 Stage II : Involving multiple quadrants without ossicular involvement .
 Stage III : Ossicular involvement without mastoid extension
 Stage IV : mastoid involvement .
Acquired cholesteatoma
A. Invagination theory .
Collapse of the pars flaccida or atenuated part of the pars tensa due to negative
middle ear pressure & repeated infections lead to retraction pockets in which the
desquamated keratin accumulate , at 1st can be self cleansed , but as it gradually
expanded & extended backwards into the aditus & inbetween the ossicles , the
isthmus of the sac become narrow & keratin retained in the sac exerting a pressure
effect & infection expands the sac more & more (with excretion of the inflammatory
products & lytic enzymes) causing underling ostetitis & bone erosion .
B. Invasion theory .
The epithelial cells (Prickle cells) in the basal layer of the skin of the outer layer of
the tympanic membrane could invade the subepithelial layer of the middle ear
mucosa by the means of proliferating columns of epithelial cells , then proliferating
causing basal cells hyperplasia leading to the formation of the microcholesteatomas
which then expands .
C. Migration theory .
Keratinizing sequamous epithelium in the outer layer of the tympanic membrane may
migrate through the marginal perforation in the tympanic membrane invading the
middle ear cleft mucosa forming cholesteatoma .
D. Metaplasia theory .
The simple cuboidal epithelium of the middle ear cleft undergoes metaplasia due to
chronic irritation forming keratinizing sequamous epithelium in the middle ear
Retraction pockets
Pars tensa retraction pocket ; classified into 4 grades , in grade III the TM is not
adherent & can be seen to move on pneumatic otoscopy , while in grade IV it is adherent
to the promontory
Attic retraction pocket ; 4 grades ;
 grade I : the pars flaccida is not in contact with malleus neck .
 grade II : pars flaccida is in contact with malleus neck .
 grade III : limite outer attic wall erosion
 gradeIV:severe outer attic wall erosion
PATHOLOGY
Macroscopically ; There is a round pearly white mass of variable size , often surrounded
by friable granulations from infected bone or polyp formation from infected mucosa .

Lecture notes in
Microscopically ; Cholesteatoma is benign keratinizing sequamous cell cyst , in the

centre are fully differentiated keratin sequamous surrounded by an epithelial several
cell layers , thick , in turn surrounded by a matrix of inflamed subepithelial connective
tissue .
The epithelial matrix of the acquired cholesteatoma has approximately 15 layers , while
that of congenital cholesteatoma has only about 5 layers .
Electron microscope shows normal epithelial cells plus Langerhan's cells & Merkel cells
Cholesteatoma contain all the layers of the skin with the basal layer at the outer side (in
contact with the middle ear structures) & the keratin debris at the core of the cyst .
Cholesteatoma invariably enlarges , but little is known as how this growth is controlled ,
infection with bacteria cause an increase in clinical progression .
Initially the cyst of skin grows into the area of least resistance , usually into the mastoid
antrum & then into the aircells , the epithelium being naturally migratory , probably
acounts for some of the growth but other changes in the surrounding peri-matrix
probably bought on by infection leading to desruction of the bone , locally these changes
include the activation of osteoclasts & the production of lysozymes .
Clinical assessment
The symptoms depend on the activity of the disease arise either from the disease itself or
from the complications , the disease usually produce ;
1) Discharge ; scanty or just a flaky waxy deposit , often foul & creamy
2) Deafness may occur , either conductive secondary to ossicular erosion or SNHL
due to toxins through the round window .
3) Dizziness may indicate a labyrinthine fistula .
The signs are ; (1) attic crust (2) marginal perforation or pocket of involving keratin
debris (3) marginal granulations (4) polyps protruding from the middle ear cleft indicate
ostetitis & mucosal hyperplasia , respectively , & (5) a +ve fistula sign indicate
labyrinthine erosion.
Investigations
1) Micro-ear ; examination of the TM under higher magnification (microscope) &
removal of the attic crusts & polyps allowing the Dx to be made .
2) PTA with masking , either CHL or SNHL .
3) Radiology ;
i.Plain mastoid x-ray may indicate the height of the middle fossa dura & site of
sigmoid sinus , but usually give little information on the disease extent .
ii.CT scan reveal a non-enhancing mass of eroding bone including ossicles with
sharply defined smooth margin , isodense with CSF .
iii.MRI shows a mass with low intensity T1 weight signal & a high T2 signal .
In practice it is difficult on imaging to distinguish between cholesteatoma & pure
mucosal disease .
Treatment
The main stay in treating cholesteatoma is the surgical excision , cholesteatoma can not
be eradicated completely from the temporal bone without surgery , the purpose of
surgery ;
1) Eradication of the disease
2) Management of the complications
3) Reconstruction of the middle ear & any surgical defect .

Lecture notes in
The judgment of surgery depends on ;

1) Nature & extent of the disease .
2) Existence of complications .
3) Mastoid pneumatization .
4) Eustachian tube function .
5) Degree of hearing impairment in both ears .
6) Patient factors ; age , reliability , general condition …etc .
7) Experience of the surgeon
Surgical approaches are ;
1) Atticotomy .
2) Simple mastoidectomy .
3) Canal wall up procedures with/without facial recess approach
4) Canal wall down procedures .
In children , the disease is more aggressive , usually we do canal intact surgery .
Risk of residual disease (about 13-30%) , need manditory re-exploration of ear underwent
intact canal surgery one year after the origional operation , at this stage ossiculoplasty do
appropriate & if any residual disease is present , modified radical conversion .
Conservative treatment may control the early disease (or it is the management of unfit
patients or elderly) , it include ;
1) Suction clearance to remove the entrapped keratin .
2) Direct or saline irrigation .
3) Irrigation with 1:1 distilled white vinegar & 70% isopropyl alcohol
Complications
May occur in acute exacerbation of the disease & either within the temporal bone or
intracranially ,they are (in order of frequency) ;
1) Semicircular canal erosion , fistula & dizziness
2) Extraduarl or perisinus abscess
3) Serous or suppurative labyrinthitis
4) Facial nerve paralysis
5) Meningitis secondary to tegmen erosion
6) Epidural , subdural or parachymal brain abscess
7) Sigmoid sinus thrombosis & thrombophelibitis
8) Subperiosteal abscess , Bezold's abscess due to erosion of mastoid cortex .
9) Recurrence of cholesteatoma
Management
1. Medical management
a. avoid the contamination with water .
b. Aural toilet ; by dry mopping or suction , removal of the small polyps can be
achieved at the same time & granulation tissue can be cauterized with silver nitrate .
c. Topical antibiotics ; antibiotics &/or steroids ear drops (Methadin-N) , powder like
boric acid with/without iodine , nystatin ointment .
2. Surgical management
a. Tympanic memeberane perforation ; by myringoplasty .
There is no need to treat the perforation unless aiming for ; (1) preventing of recurrent
discharge (2) Hearing impairment & (3) Swim witout the fear of discharge .

Lecture notes in
The factors that affect the outcome of the operation ; (1) size of perforation , large less
favourable outcome (2) site of perforation , anterior less favourable outcome (3) age of
the patient , fail in children under 12 years , operated in bilateral cases with significant
hearing loss waiting untill age of 12 in cases of unilateral perforation with adequate
hearing for better posop. care & (3) infection , ideal result in dry ear, but infection not
affect the success
Procedure of the operation ;
(1) Incision carried out permeatal or endaural or postaural .
(2) The graft introduced either medially (underlay) in which the middle ear space
entered to allow the inspection of the mucosa & ossicles , or lterally (onlay) not required
opening through the middle ear space , but it has disadvantages like ; intratympanic
keratin pearls formation due to the inadequate removal of sequamous epithelium from
the outer layer of the TM & blunting at angle between the anterior portion of the TM &
canal wall which impair the drum movement .
The types of graft are ;
(1) Autologus , temporalis fascia , most common , because it has good results & redialy
available , when endaural or postaural incision done .
(2) Autologus perichondrium & vein .
(3) Homograft (dura) , abandaned recently due to viral infection (Creutz-Feldt-Jacob
diease) .
b. Cholesteatoma
There are small groups of elderly & medically unfit patients who are best managed by
regular suction clearance of keratin in the out patient department .
Surgey is the main management of choice in the maority of cases , either ;
(1) Radical mastoidectomy ; which is an operation performed to eradicate all the middle
ear & mastoid disease in which the mastoid antrum & aircells system (if present) ,
aditus ad antrum , attic & middle ear are converted into a common cavity , exteiorized
to the external audiotry meatus , leaving the stapedial footplate or superstructures .
It is associated with poor healing , high incidence of chronic or intermittent discharge .
(2) Modified radical mastoidectomy ; here the remenant of the TM & ossicles remenants
(usually the handle of malleus & stapes) retained (to overcome the disadvantages of (1))
Its synonym atticoantrostomy , if the operation done by an anterior to posterior
technique , i.e. the operation exposing the attic 1 st (atticotomy) & then preceeding
backwards into the aditus ad antrum & mastoid antrum .
(3) Intact canal wall mastoidectomy ; combined approach tympanoplasty with
mastoidectomy , it is performed to remove the disease from the middle ear & mastoid
process by way of mastoid , posterior tympanoplasty , trans canal route , followed by
reconstruction of the middle ear transformer mechanism .
The aim is to ; avoid an open cavity with its problems of retenion of wax & recurrent
discharge , facilitate functional reconstruction of the middle ear & improve the chances
of being able to fit a hearing aid in a dry ear with a suitable external audiotry meatus .
The disadvantages are ; residual cholesteatoma (reperesent failure to eradicate the
original disease, occur in 13-36% of cases) , recurrent cholesteatoma which arise as a
result of postop. drum retraction (occur in 5-13%) , therefore mandatory re-explore the
ear underwent intact canal surgery one year after the original operation , at this stage ,

Lecture notes in
ossiculoplasty do appropiate & if residual disease is present then modified radical

mastoidectomy .
Cholesteatoma occuring in children is often more aggressive than in adult , but lower
incidence of lateral semicircular canal fistula , also children have higher incidence of
residual disease in the canal intact surgery & good hearing obtained by modified radical
mastoidectomy & ossiculoplasty .
Cholesteatoma matrix removed completely except if it adherent to ; (1) the dura (2)
semisircular canal (3) facial nerve & (4) mesotympanum covering the stapes footplate .
Disadvantages of open mastoid cavity surgery in children are ;
1) Large cavity avoided by not follow the aircells down to mastoid tip , so limit cavity
size .
2) Hearing result , postop. disappointing , but not worse than the preoperative one .
3) Variation in anatomy of the temporal bone ; anteriorly placed lat. venous sinus , low
middle cranial fossa dura , prominent Korner's septum , when breached by the drill , the
operator may think that the mastoid antrum has entered rather than the antral group of
mastoid aircells & densely sclerotic mastoid process make the approach to the antrum
more difficult because there are fewer landmarks to follow .
c. Atticotomy in the management of limited attic disease (open canal) , which is an
operation performed to remove all or part of the outer attic wall (scutum) & adjacent
deep posterior medial wall to expose the attic & when necessary the aditus ad antrum in
order to gain access to these sites & thier contents &/or remove disease to these sites .
d. Ossicular chain pathology ; ossicular damage occur in all types of CSOM but more
extensive in cholesteatoma cases , the choice of reconstructive surgery depends on
chances of success , so ;
(1) In patients with serviceable hearing in other ear (bone conduction at 1000 Hz should
be 30 dB or better) .
(2) In bilateral hearing loss , improvement in hearing threshold .
e. Retraction pocket
(1) if shallow self cleansing pocket , then no need for any management .
(2) Attic pocket, need observation to confirm that it is stable .
(3) Pars tensa pocket , the pocket can be everted & the drum reinforced with temporalis
fascia or tragal cartilage & cortical mastoidectomy to provide a larger air reservior
or insertion of grommet , also the thin TM segment can be excised leading to
perforation which can be heal .
Recurrent are common after management .
f. Cortical mastoidectomy ; an operation done to remove the disease from the mastoid
antrum & aircell system (if present) , & the aditus ad antrum with preservation of an
intact posterior bony external audiotory canal wall without disturbing the midlle ear
content .
The indication of surgery in the tubotympanic disease are ; (1) presence of complications
(2) presence of polyps or granulation tissue & (3) unresolved by medical Rx .
Mastoidectomy classified into ;
A. Open or canal wall down procedures ; (1) atticotomy (2) radical mastoidectomy (3)
modified radical mastoidectomy .
B. Closed or canal wall uo procedures ; (1) cortical mastoidectomy (2) combined
approach tympanoplasty with mastoidectomy .

Lecture notes in
Mastoid revision surgery

20% of the mastoid cavities remain unhealed 6 months after surgery & of the remainder ,
some begin to discharge again subsequently (30-60%) .
Cavities are more likely to be dry if they are ; (1) not excessively large (2) have a low facial
ridge (3) adequate meatal opening (4) closed middle ear space (no TM perforation) .
Surgical procedures (approaches0 to discharging cavity are ;
(1) cavity revision alone , dry ear in 57% of cases .
(2) combination of the above approach with meatoplasty , increase the success rate
(83%) .
(3) meatoplasty alone , good result .
(4) obliteration of the mastoid cavities by ; pedicle muscle flap , musculoperiosteal flap
or mixture of bone dust & water (bone paste) to fill in the mastoid bowl , dry ear in
63-94%
(5) tympanomastoid reaeration technique .
(6) myringoplasty , in case of discharging from perforation of the TM reminant .
Unusual presentation of CSOM
1. Tuberculous CSOM ;rare , 3-5% (at past) , typically presented as ;
a. painless otorrhea which fail to responds to topical Rx with evidence anywhere .
b. pale granulation with hearing loss greater than expected .
c. complications like facial palsy , mastoiditis , SNHL & labyrinthitis .
d. multiple tympanic membrane perforations .
e. atypical presentation like otalgia & otorrhea with no evidence of TB anywhere .
T.B. CSOM should be suspected in case of CSOM not respond to conventional Rx , so
culture for the discharge will reveal T.B. bacilli , Rx with antitunerculus drugs with multiple
agents .
2. Wegner's granuloma ; charcterized by developement of granulomatous lesions in the
kidenys , lungs , nose & sinuses & infrequently the middle ear , which may be presented as
subacute OM or OME or CSOM , there also mixed hearing loss of sudden onset .
3. Immune deficiency ; may be idiopathic or secondary to the use of drugs which depress
the immune response , the difficeiency of IgG & IgA which increased the incidence of URTI
& OM , s.t. need surgery which should be associated with good cover with Ig fraction .
4. Histiocytosis X ; langerhan's cell histiocytosis , granulomatous disease charcterized by
idiopathic proliferation of lLangerhan's cells or their bonemarrow precuresors , OM may
be the presenting feature & lesion in the temporal bone & increase in ESR .
Managed with chemotherapy , radiotherapy & steroids .
Complications of CSOM
They are ;
1. Intracranial complications
a. Extradural , subdural , brain abscesses .
b. Meningitis .
c. Sigmoid sinus thrombophelibitis .
d. Otitic hydrocephalus .
2. Extracranial complications
a. Facial n. paralysis .
b. Serous or purulent labyrinthitis .
c. Petrosistis & Gradenigo's syndrome .

Lecture notes in
d. Sequamous cell Ca. of the middle ear .

e. Ossicular discontinuity from ossicular erosion .
f. Tympanosclerosis causing ossicular chain fixation .
g. Chronic otitis externa & meatal stenosis .
3. Other rare complications
a. Subclavian vein thrombosis .
b. Internal carotid artery aneurysm .
The Routes of spread are ;
1. Extension through the bone , which is either demineralized during the acute infection
or resorbed by cholesteatoma or osteitis in chronic disease .
2. Spreading of infected clot within the small veins through bone & dura to venous
sinuses & so intracranial structures .
3. Normal anatomical pathways , oval & round windows into the internal meatus ,
cochlea & vestibular aqueducts & dehescince .
4. Through non-anatomical bony defects caused by trauma or bu neoplastic erosion .
5. Through other surgical defects like fenestration of the LSSC for stapedectomy .
6. Along the periarteriolar spaces of the Virchow's Robin leading to intracranial
extension
The propensity for spread of infection & the developement of complications depend on ;
1. Patient factors ; age , immunity , current chronic disease like DM .
2. Bacterial factors ; virulence , susceptibility for drugs .
3. Efficacy of treatment of the underlying middle ear disease .
The symptoms of the inracranial infection are those of infection & those of brain tissue
compression ; headache , malaise , fever, drowsiness & otalgia . do need Investigations ;
1. CT scan ; is the one of choice .
2. Previously ; plain x-ray , EEG & arteriography .
3. MRI ; recognize the early infection (espicially early brain abscess) , used especially
with contrast (Gadolinium enhancement can recognize the changes in the dura &
arachenoid in meningitis) .
4. LP for the Dx of meningitis .
The principle of the management to all intracranial complications include ;
1. Systemic antibiotics therapy ; many regiems ;
a. Gentamycine (4.5 mg/kg/d then 1.5mg/kg/d) , Ampicillin (100mg/kg/d) & Flagyl
(400-600mg/8hr) , for brain abscess , lat. sinus thrombophelipitis & subdural
abscess .
b. others ; Claforan (1gm/8hr) & Chloramphenicol (instead of garamycine ,
100mg/kg/d) .
2. Local neurological attension .
3. Management of ear infection .
In ASOM , the above antibiotics +/- myringotomy & s.t. do cortical mastoidectomy (with
removal of the bony covering of the sigmoid sinus & dura) .
In CSOM , radical or modoified radical mastoidectomy whic done after controlling the
intracranial complications .

Lecture notes in
Extradural abscess
The commonest intracranial complication , the bone loss (due to demineralization in ASOM
& erosion by cholesteatoma in CSOM) lead to dura involvement (pachymeningitis) leading
to pus formation between the tough dura & the bone (extradural abscess) .
If found in the middle cranial fossa it will strip the dura leading to mass formation causing
focal neurological signs & papillodema , usually through the tegmen tympany .
It s.t. subperosteal abscess leading to Pott's puffy tumor (frontal sinusitis) .
Rarely the abscess may develope medially to the arcuate eminence over the petrous apex
involving the Gasserian ganglion of the V & VI cranial nerves causing Gradingo's
syndrome (facial pain , diplopia & aural discharge) .
The posterior extension to the sigmoid sinus causing perisinus abscess leading to sigmoid
sinus thrombophelibitis (also transverse sinus) , s.t. it extend through the jugular foramen to
the neck.
The clinical presentation depend on the site , size , duration & the rate of its developement
, it is either asymptomatic , discovered incidently at the mastoidectomy or as CSOM with
epsilateral headache with malaise , if the abscess comunicate with the middle ear , there
will be intermittent pain releified after aural discharge .
The diagnosis mainly by CT sacn & th eoperative finding .
It is managed by surgical exploration with pus evacuation without disturbing the
granulation tissue attached to the dura , followed by i.v. antibiotics (espicially if it follow an
ASOM) .
Subdural abscess
When the infection spread through the dura exposing the subdural space , it manifested as
leptomeningitis or subdural effusion or abscess .
The infection under the dura lead to granulation tissue on its inner surface (which obliterate
the adjacent space) causing fibrous tissue , then necrosis of the dura leading to infection of
the subdural space which at 1st as serop[urulent effusion collection & then become frankly
purulent & extend over the surface of the cerebral hemisphere (which limited by the
granulation tissue) , then it may extend widely as space occupying lesion .
Also cortical vein thrombophelibitis leading to small multiple abscesses within the brain .
It is clinically presented as ;
1. Severe headache , fever & drowsiness followed by focal neurological signs (fit &
paralytic) , the mortality is 100% (now 8-25% with the use of modern antibiotics) .
2. Drowsiness , then coma .
3. Hemiplegia , hemianopia & hemianaesthesia .
4. Jacksonian epileptic fits (affect one side of the body) .
5. Uncommon , papilloedema & cranial nerves palsies .
The diagnosis by ; (1) clinical picture , charcteristic neurological signs (2) CT , MRI , LP ,
angiography (3) explorative burr hole needed to establish the diagnosis .
The management by cooperation with the neurosurgeon ;
1. Massive dose of i.v. antibiotics ; Pencillin , Chloramphenicol with Gentamycine .
2. Removal of the subdural fluid by burr hole or craniotomy .
3. Treating the ear disease , ASOM by myringotomy & cortical mastoidectomy , CSOM
by modified radical or radical mastoidectomy .
4. The patient may need antiepileptic drugs for many months after controlling the
disease .

Lecture notes in
Lateral sinus thrombophelibitis (sigmoid & transverse sinuses)

Usually the sinus filled with suppurative blood clot preceeded by extradural perisinus
abscess , the extradural perisinus abscess lead to mural thrombus occluding the sinus , then
the clot become partially organized & may be partly breakdown & softened by suppuration
releasing the infected M.O. & infected materials into the systemic venos circulation causing
bacteraemia , septicaemia & septic embolization , this spread ;
1. Upward to the sinus confluence & superior sagittal sinus , then cavernous sinus
leading to brain abscess .
2. Downward to the internal jugular vein , then to the subclavian vein .
The mortality 100% (now 50%) .
The bacteriology shows mixed flora (Proteus , Str. Pneumonia , Bacteroid oralis , E. coli &
Staphylococci) .
The clinical presentation ;
1. Before the antibiotic modification , infection by virulent M.O.
ASOM ; several weeks later , severe pyrexial wasting illness , high swinging fever
following a picket fence pattern , rigor , profuse sweating (shaking the bed) , also
headache & neck pain with emaciation & progressive anorexia .
Other symptoms depend on the propagation of the thrombus ;
a. if the clot extend down the internal jugular vein , then perivenous inflammation 7
tenderness along its course with perivenous odema or even suppuration in the
internal jugular LN which press on the lower 3 cranial nerves causing their palsies .
b. increase the ICP cuasing papilloedema & blindness .
c. cavernous sinus thrombosis cause chemosis & proptosis .
d. lung & large joints , viscera (rare) .
2. After the antibiotic era ; ill persistant fever without violent rigor , otalgia , neck pain
& tenderness over the mastoid with softening along the sternomastoid muscle .
Rarely , subclavian vein thrombosis causing engorgement of the collateral veins over the
shoulder & thrombocytopenia (due to platelets mopped up within the vessels) .
Rarely Grissinger's sign which is pitting odema over the occipital region due to clots within
the large emissary mastoid veins .
The investigations are ;
1. General ; FBC (anaemia , leucocytosis , high ESR ..etc) , blood culture taken within
fever & LP .
2. Tobey-Ayer test (or Queckenstedt) ; measurement of the CSF pressure & observe its
changes on compression of one or both internal jugular veins by finger on the neck ,
rapid rise of CSF pressure 50-100 mmHg & decrease the pressure is normal .
The abnormal result when there is no rise or very slow one of 10-20 mmHg .
3. CT scan , increase in density (blood clot) , filling defect within the sinus (with convay
enhancement) , the septic thrombus show as intense inflammatory enhancement of the
sinus wall & the adjacent dura (Delta sign , empty ∆) , the other findings are decrease in
the ventricular size , tentorial enhancement & cerebral odema .
4. Angiography ; demonstrate the obstruction site & extent of the obstruction (risk of
displacing the infected thrombus) , also the carotid arteriography can show the venous
outflow .
5. MRI , the thrombus increase the signal intensity in T1& T2 weighted images ,
gadolinium enhancement show Delta sign .

Lecture notes in
6. Radioisotop scanning with gallium , show hot spot of sepsis .

7. Radioneucleotide scanning show blocked venous flow .
The management by ;
1. Antibiotics , i.v. Ampicillin , Chloramphenicol , Cephalosporine , Garamycine &
Flagyl .
2. Anticoagulant , Heparin (in past) .
3. Surgical , early intervension ; mastoidectomy with neurosurgical intervension .
They need chart for ; (1) response to medical Rx (2) 4 hr chart for temp. (3) 1-2 days
neurological examination , but if there is rapid detorioration , then mastoid exploration
within the 1st two days (cortical if follow ASOM , modified or radical if follow CSOM) ,
exposing the sinus plate by drilling reveal pus of the perisinus abscess (outflow) , the whole
sinus exposed from the sinodural angle down to the jugular pulp .
Normally the sinus soft , bluish & compressable , in the disease should open by instruments
, if the sinus is covered by granulation tissue , the sinus must be opened & the abscess &
necrotic tissue removed with ligation of the internal jugular vein (to prevent dissemination)
It is unnecssary to remove the organized clot or thrombus .
Meningitis
It is a major & serious complication of CSOM & still the commonest intracranial
complication (usually after the ASOM in children & CSOM in adults) .
It caused by extension through the necrotized bone (usually tegemn) or ruptured brain
abscess .
Bacteriologically in ASOM ; H. influenza , Str. pneumonia , in CSOM ; Proteus ,
Pseudomonas & Bacteroid .
The spread ; (1) along the Virchow-Robins spaces causin brain abscess (2) irritate the
upper cervical nerve roots causing neck stiffness & (3) exudate around the exit foramina of
the cranial nerves causing their paralysis .
The clincal features are ;
1. Bursting localized headache & neck stiffness .
2. Malaise & pyrexia (39o ) which remain high .
3. Restlessness & fretfullness (in children) , anexity with periods of drowsiness (in
adults) .
4. Exagurated tendon reflexes .
5. Photophobia , characteristic constant feature .
6. Vomiting due to increased ICP .
With preceeding the symptoms become more severe with positive kernig's sign , the
reflexes decrease & the abdominal reflex lost .
7. Finally , delirium , stupor & coma with cranial nerves palsy .
8. Chyne-stokes respiration with fixed dilated pupils , coma & death .
9. in Complicated meningitis there are fits .
The diagnosis by ;
1. LP ; increase in CSF pressure , cloudy , turbid , increased protien , decrease glucose
, decrease chloride , increase in the polymorph leucocytes , also do gram stain &
C&S .
2. CT scan to exclude brain abscess .
3. MRI show typical signal changes , exudate & adhesion in the basal cistern , also
increase intensity on T2 weighted & abnormal gadolinium enhancement .

Lecture notes in
4. Polymerase chain receptor to detect the bacterial DNA .

The management by ;
1. Surgical Rx ; only done if we expect no response yo antibiotics (deterioration)
leading to mastoiditis , in ASOM do myringotomy with grommet & cortical
mastoidectomy (if there is mastoiditis) , in CSOM do radical mastoidectomy .
2. Medical Rx ;
a. Repeated LP to decrease the ICP with intrathecal antibiotics (crystaline pencillin
1000/5ml of saline) .
b. High dose systemic antibiotics (i.v. for at least 10 days) .
c. Decadrone to decrease the neurological sequelly .
Failure of medical Rx may due to ; (1) M.O. resistanec (2) persistant leakage of infected
material into the CSF (3) presence of unidentified other complications (solved by CT)
(4) leakage into CSF from unrecognized brain abscess .
Brain abscess
Otologenic brain abscess almost always develope in the temporal lobe or cerebellum (2:1) .
In children , 25% of brain abscesses are otologenic , in adults 50% of it caused by dierct
extention of the infection through an osteitic tegmen tympani causing extradural abscess ,
then thrombophelibitis extending to the brain cortex or through periarteriolar Virchow-
Robin space to the white matter .
Cerebral abscess is encapsulated which need 2-3 weeks to form , it is due to preceeded lat.
sinus thromnophilebitis .
The pathology ; the encephalitis & cerebral odema causing abscess contained in the
capsule , the central part of the affected brain liquifies & then period of abscess
enlargement leading to the formation of space occupying lesion features ( increased ICP ,
focal neurological damage , in the cerebellum cause rapid increase in ICP leading to
coning i.e. impaction of the flocculus & brainstem into the foramen magnum leading to fatal
disruption of vital centres in the brainstem) .
Further brain softening causing secondary brain abscess which is multilocular abscess ,
finally the rupture of the abscess lead to meningitis or death (the mortality rate decline to
6%) .
Bacteriliology ; Staph. aureus , Str. pneumonia & haemolytius , G –ve Proteus , E. coli ,
Pseudomonas , & Bacteroids .
N.B. : some report brain abscess with intact tympanic memberane .
The clinical presentation are ;
1. Stage I ; localized encephalitis , headache , fever , malaise , vomiting , drowsiness
which should provoke suspecion .
2. Stage II ; rare , generalized encephalitis , stupor , then coma & death from tentorial
herniation .
3. Stage III ; latent period , more often 10 days – weeks , develope after localized
encephalitis , the pus contained within fibrous capsule is asymptomatic .
4. Stage IV ; enlarging abscess , features of CSF dynamic changes & vocal
neurological impairment (decrease pulse rate , hypothermia , papillodema leading to
death) , malaise , lethargy & anorexia .
5. Stage V ; rupture of the abscess , either intraventricular or subarachenoid causing
meningitis leading to death .

Lecture notes in
The cerebral-tempore-sphenoidal abscess ; usually in the left side (dominant side) , nominal
aphasia (patient can't name the common everyday objects) , hemianopia , paralysis of upper
& lower limbs .
The cerebellar abscess ;
(1) weakness & muscle incoordination on the same side of lesion .
(2) ataxia with tendency to fall towards the side of the lesion .
(3) nystagmus (spontaneous) to the side of the lesion .
(4) dysmetria , dysdiadokokkinesia & intention tremor .
(5) rapid increase in the ICP with its sign & symptoms .
1. Radiology ;
a. CT scan with contrast shows the abscess or the localized encephalitis .
b. MRI distinguish pus , abscess , capsule & odema .
c. Previously use carotid artery Angiography , upward & medial displacement of
middle cerebral artery .
d. Plain x-ray of no value (displacement of the calicified Penial body) .
2. LP ; risk of coning , show increased CSF pressure & protien with normal glucose .
3. Burr-hole needling give the definit Dx (not used now) .
The differentila diagnosis are ; (1) meningitis (2)subdural abscess (3)lat. sinus
thrombophelibitis (4) otitic hydrocephalus & (5) brain tumors .
The management are ;
1. Management of the ear disease .
2. Medical Rx ; urgent consultation to neurosurgery .
a. large dose of systemic antibiotics ,Chloramphenicol ,Garamycin , Flagyl for 3 weeks
b. Decadrone 4 mg i.v. /6 hr to decrease the ICP or 20% manitol .
3. Surgical Rx
a. Repeated needle aspiration under GA through a burrhole , the aspirate sent for C&S
(Bacteroid fragilis , sterile abscess) , nowaday do aspiration under CT scan (Rx of
choice) , the disadvantages are ; 40% multilocular abscess , collapsed the capsula lead
to damage to the white mater by the needle & canula , little to decrease the mass effect
of the abscess .
b. Primary excision with its capsule (cause extensive damage to the brain tissue leading
to residual neurological deficit) , the sequella ; epilepsy , so need anticonvulsant drugs .
Otitic hydrocephalus
Syndrome of increased ICP during & following the middle ear infection , it is benign IC
hypertension , usually affect the children (s.t. called pseudotumor cerebri) , the cause of it
unknown .
The pathogenesis ; the obstruction to the lat. sinus affect the cerebral venous outflow or
extebtion of the thrombus to the superior sagital sinus will impade the CSF resorption by
pacchionian bodies .
It is presented as ; headache , drowsiness , blurred vision , nausea , vomiting , & s.t.
diplopia , the onset may be over many weeks after ASOM & many years after CSOM .
O/E ; papillodema & VI cranial nerve palsy (false localizing sign) .
We should do CT scan to exclude the other possibilities , normal ventricles while in this
disease there is abnormal ventricles .

Lecture notes in
It is managend by ; steroids , diuretics & hyperosmolar dehydrating agents , also repeated

LP , long term thecopertopneal shunting , the prognosis good , recurrence reported .
Facial palsy
In ASOM , <10% , there is congenital dehiscence of the horizontal part of the canal ,
infection of the mucosa will cause inflammatory reaction in adjacent epineurium &
perineurial spaces .
The diagnosis , striaght forward , DDx from Ramsay Hunt syndrome .
Managed by antibiotics , occasionally myringotomy & rarely do cortical mastoidectomy ,
the operative nerve decompression is unnecessary .
The prognosis is very good , full recovery because it is neuropraxia .
In CSOM , the facial berve trunk may be exposed (either by eroding cholesteatoma or by
granulation tissue & osteitic disease) .
The diagnosis is from the clinical picture (pain , discharge) & microear & CT scan .
The management is urgent exploration of the middle ear (radical mastoidectomy) , then the
berve exposed (espicially the horizontal & vertical mastoid segments) , the attached
granulation tissue is untouched .
The prognosis is good with more than 70% full recovery .
Lanyrinthine complications
Pathogenesis
1. ASOM ; through the thin , permeable round window to the labyrinth (serous) , the pus
then enter to the perilymph by diapedesis from inflammed labyrinthine vessels .
Fibrillary percipitate in the peri- & endo-lymphatic spaces causing endolymphatic hydrops
& destruction of the memberaneous labyrinth , then irreversible suppurative labyrinthitis .
2. Chronic destructive ear disease ;
a. erodes the bone by cholesteatoma or osteitis causing simillar inner ear destruction
(which preceeded by thining of the bony labyrinthine wall & developement of the
labyrinthine fistula).
b. inflammation close to the endosteum of bony labyrinth lumen , then vestibular
irritation leading to paralabyrinthitis .
c. rarely chronic osteitis around the bony labyrinthin causing necrosis of the whole
otic capsule (perilabyrinthitis) leading to sequestration of the labyrinth .
These complications are ;
A. Suppurative & serous labyrinthitis
Charcterized by violent attacks of prostrating vertigo , vomiting & severe SNHL , the
patient lie on the side when the affected labyrinth is upward .
Nystagmus , sponatneous irritative jerky one with slow component toward the affected ear
(serous labyrinthitis) , then paralytic jerky nystagmus toward healthy side .
The direction of the nystagmus dictate the preference for lying on the unaffected ear ,
turning the eye toward the damaged labyrinth (3rd degree intially , then 2 nd degree , & then
1 st degree , then abscence of nystagmus on fixation) .
This take 2-3 weeks , then the patient have good balance , but still unsteady on dark walking
or with eye closed or sudden head movement .
The diagnosis from ;
1. History of underlying middle ear disease .

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2. Examination under microscope to see the whole attic & remove the obscuring crusts
, secretions & debris . (bulous or haemorrhagic myringitis with varicella zoster
infection can cause sudden vestibular failure)
3. Radiology , mastoid x-ray & CT scan .
The sequellae are ; meningitis (extention through the subarachenoid space) , SNHL , loss of
balance .
The management by ;
1. Bed rest & avoid head movement (vestibular function test postponds) .
2. i.v. or i.m. prochloreperazine or cinnirazine (stugeron) .
3. i.v. fluid & antibiotics (for ASOM & to prevent meningitis) , Claforan ,
Chloramphenicol for 7-10 days .
4. Myringotomy & cortical mastoidectomy .
5. Vestibular head excercises (Cawthorne-Cooksey) , the regimen are ;
a. Stage I ; head kept still in bed or sitting .
b. Stage II ; head & eyes movement while sitting .
c. Stage III ; head & body movement while still sitting .
d. Stage IV ; standing excercise .
e. Stage V ; moving about .
The future advances of labyrinthitis treatment are ;
1. Growth factors ;
a. Brain derived neurtophic factor , gene of Herps simplex virus (vector) injected
into the cochlea with dead hair cells which are more susceptable to damage than
the vestibular receptors .
b. Glial cell line neutrophic factor ; osmotic pump infusion into the perilymph .
2. Antioxidants ; decrease the sensory hair loss due to cisplatinum & protective
function to gentamycine ototoxicity & acoustic trauma .
Both provide protection to the labyrinth from progressive damage due to injury or any
aetiology & allow the regeneration of vestibular receptors .
B. Labyrinthine fistula
The most important complication , it is a complication of CSOM , the endosteum of the
labyrinth has been exposed by bony erosion , threatened by suppurative labyrinthitis .
Most commonly in the dome of the lateral SSC (the promontory also may be eroded) .
It could be silent (discovered at the operation) or CSOM with brief episodes of vertigo or
unsteadiness & proved by CT scan .
Fistula sign , an important physical sign depend on transmission of the air pressure
changes from the EAC to a fistula in the labyrinth causing perilymphic movement , it is
done either by finger press on the tragus or pneumatic otoscope (air-tight seal) , the
increased pressure lead to conucate deviation of the eyes away from the examination side ,
if the pressure maintained then jerky nystagmus developed beating toward the examinated
& affected ear , as the pressure released the eye return to the midline .
The lateral canal fistula anterior to the ampulla lead to deviation toward the side of the
fistula , while an erosion into the vestibule is indicated by rotatory horizontal deviation
toward the diseased ear .
Vertical deviation of the eyes indicate fistula in the posterior canal .
Fistula test should be done in every case of CSOM or any vertigenous patient , also +ve
fistula sign with intact TM (Henebert sign , found in Meinnier's disease & syphilis) .

Lecture notes in
Tullio-phenomenon which is the transmission of the pressure through a subluxated stapes

footplate to the otolith organ of the saccule .
False –ve fistula sing can be due to ; (1) inadequate seeling of the speculum (2)
cholesteatoma protect the inner ear (3) the diseased vestibular labyrinth not stimulated .
the management of the fistula by ;
1. Surgical exploration of the middle ear , peeling the cholestatoma matrix off with great
care , dissection carried out slowly under high power magnification , slightly changes in
colour may be possible fistula , then small sheeth of cholesteatoma matrix over the fistula
isolated (if break result in dead ear) .
2. Radical mastoidectomy ; the matrix of cholesteatoma left safely undisturbed , closed by
new bone growth , while if the matrix removed , the defect closed with temporalis fascia or
perichondrium .
3. Intact canal wall tympanoplasty ; matrix over the fistula need secondary exploration
after 6-12 months , so the matrix have epithelial pearl which is easily removed , so here the
patient should accept a 2 nd exploration & the other ear has good hearing & free from the
disease .
C. Perilabyrinthitis (Cawthorne -1957)
It is a problem caused by a fistula into the labyrinth after mastoid surgery (so called
syndrome after mastoid surgery) , the fistula may preceed mastoidectomy or caused by it .
Giddiness provoked by pressure changes near the fistula & cold air blow into the ear at
windy street corners (can be prevented by occulde the external ear) .
Opeartive management by exploration , removal of the skin from the fistula & protection by
connective tissue graft .
Sometimes we need vestibular nerve section or labyrinthine destruction to prevent vertigo .
Vertigo after mastoid surgery
1. Middle ear ; Persisting middle ear disease with further bony erosion .
2. Inner ear ;
a. Untreated vestibular disease .
b. Perilabyrinthitis .
c. Delayed endolymphatic hydrops .
3. CNS
a. Breakdown of central compenstaion after loss of labyrinth function .
b. Cerebellar abscess .
c. Vestibular nerve neuroma activity after labyrinthectomy .
Cochlear complications
Usually high frequency sensorineural hearing loss due to ;
1. Penetration of the cochlea by bacteria through the round window memberane
causing hair cells damage .
2. Transmission of the macrophages & macromolecular toxic substances through the
round window to the basal turn of the cochlea .

Lecture notes in
Chronic suppurative otitis media in children

Clues for serious middle ear disease ;
1. Otitis media with effusion .
2. Multiple ventilation tubes .
3. Myringostpedopexy .
4. Posterior retraction pockets .
5. Marginal granulations .
6. Accumulation of sequamous debris .
Aetiology
Incidence ; from 0.6 – 8% , male equal female .
Possible relations ;
1. Smoking parents ; increase glue ear in their children , smoking cause mucous
secretion & oedema .
2. Systemic conditions ;
a. Bronchiactesis .
b. Cystic fibrosis .
a & b especially postural drainage technique , there is pus in the nasopharynx
means CSOM .
c. Immunosuppression ; decrease . the resolution of active ear sepsis .
3. Otitis media with effusion is the precursor for cholesteatoma (OME & chronic tubal
dysfunction , frequently in children , this predispose to perforation & cholesteatoma .
The virtuous cycle ; acute OM cause discharge & healing of the perforation , there are
many things that assist in the healing like ;
1. Adenoidectomy for chronic nasopharyngitis , keep the ear dry , while an acute
perforation heals .
2. Managing the early infection with drops may prevent the CSOM .
3. Grommet & excision of the retraction pockets , this arrest the development of
cholesteatoma .
4. Universal vaccination against measles & H. Influenza type B , reduce the incidence
of CSOM & its sequelae .
The vicious cycle ; exist when the incomplete healing occur ;
1. Repeated attacks of acute OM secondary to adenoid hypertrophy .
2. Scar tissue found in a wrong place lead to tympanosclerosis instead of repairing the
perforation .
3. Contaminated water enter the middle ear through the perforation before healing .
4. Virulence of the microorganisms like streptococci infection or low host immunity
(malnutrition & measles) or both , lead to large areas of tympanic membrane lost
which lead to perforation remains .
5. Poor Eustachian tube function lead to retraction pockets with deeper retained
keratin which lead to accumulation of sequamous debris lead to cholesteatoma .
Bacteriology
Culture from chronic middle ear reveal about 6 X 106 – 6 X 109 bacteria of ;
1. Pseudomonas aeroginosa , characteristic odour "like sweaty feet" .
2. Monilia , new backed bread odour .
3. Streptococcal , characteristic cellulitis & oedema .
4. Aspergllosis , characteristic black deposit .

Lecture notes in
5. Bacteroid (anaerobes) .
Clinical assessment
A. Symptoms
There may be any combination of discharge , deafness , bleeding , tinnitus , vertigo &
pain ;
(1) Discharge & HL are usually & pain .
(2) Bleeding comes from a polyp or granulation tissue .
(3) Tinnitus ; if pulsatile , it is associated with blood flow through granulation .
while if hissing means cochlear damage , which may be precede .
(4) Vertigo which indicated invasion of vestibular labyrinth by bacteria or
cholesteatoma or both .
(5) Deep unremitting pain , associated with serious complications .
B. Ear examination
(1) 1 st ; examine the mother's ear to gain the child trust .
(2) 2 nd ; we must remove the wax & debris by ring probe or forceps to clear the
view of the drum head .
(3) Examine by head mirror to see whether the perforation is in pars tensa or pars
flaccida , sometimes , easy & other is difficult to seen .
(4) Auroscope examination , the small structures like lentiform process of the incus
, chorda tympani , perforations , also we can see the tympanic plexus , ossicular
chain , wispd of dry cholesteatoma or wet debris & sometimes polyps .
(5) Seiglization to see the mobility of the tympanic membrane , occasionally
retraction pockets can be temporarily everted , fistula test also performed & if
+ve cause vertigo .
Nowadays the tympanometry elects much more information about the middle ear
function .
(6) Microscope with X6 power for cleansing the meatus & X10 power for
examination , 1st we can lift the child to the eye piece & shown a magnified view
of coin to gain his confidence , it can show ;
- Detailed examination of the ear , polyps to be removed & put betadine wick .
- Crust on pars flaccida removed to see cholesteatoma .
- Sometimes can suck the whole cholesteatoma lead to dry ear .
C. Classification of the disease
(1) Tubotympanic disease "safe" , perforation in the pars tensa with preservation of
the fibrous annulus (central perforation) usually associated with bacterial
infection of the middle ear .
(2) Atticoantral disease "unsafe" , the defect in pars tensa & associated with
cholesteatoma .
(3) Marginal perforation or tympanic sinus disease , posterior defect in the fibrous
annulus associated with cholesteatoma , so unsafe .
(4) Cholesteatoma in a safe perforation , central defect of the pars tensa with
cholesteatoma curling under the edge of the perforation & accumulating in the
middle ear , so unsafe .

Lecture notes in
D. Clinical tests of hearing

(1) Whisper test ; the tragus of nontested ear depressed by the examiner & the
ability of the child to discriminate whisper conversational voice or shout may be
determined from behind .
(2) Tuning fork test ; usually –ve Rinne & Weber lateralized to the affected ear , the
Barany noise pox used in the non tested ear to remove the false response .
E. Clinical tests of balance
(1) Romberg's test with closed eyes , sometimes the patient sway towards the site of
the lesion which indicate recent paralytic lesion , or sway to the other side
which indicate irritative lesion .
(2) Heel-Toe walking test , if abnormal means recent lost of labyrinth function
because of surgery or tight packing .
(3) Unterberger's test , marching on the spot with closed eyes & arms stretched out
infront , the patient rotate towards the weak labyrinth .
The upset of vestibular system either from the disease , surgery or suction or packing
F. Other points in examination
(1) Eye examination , in advanced disease , nystagmus , rectus palsy &
papilloedema .
(2) Neck examination , cervical LAP or abscess in the sheath of sternomastoid
muscle (Bezold's abscess) .
(3) Cranial nerves palsies , especially facial palsy .
(4) Cerebellar signs must not be missed .
G. Investigations
(1) Audiological
- In young children , behavioral tests .
- In older children ; PTA .
The surgeon must know which is the better ear , the proportion of loss (which is
conductive) & the cochlear function that remains in octave between 0.5-1 KHz ,
which is necessary to discriminate speech , either by Glasco plot & 1530 dB rule of
the thumb .
(2) Radiological
- Plain x-ray of the mastoids , it indicate the position of the tegmen , sigmoid sinus &
degree of pneumatization .
- CT scan (axial plain usually) indicated if the patient refuse surgery , if there is
threat of complications or if the patient refred from another ENT surgeon as a
difficult case .
Cholesteatoma usually shown to cause bony erosion of the facial nerve canal , the
lateral SCC or the cochlea (non-enhancing mass) .
- MRI show the relationship to brain more clearly than CT .
Both MRI & CT required GA in children <8 years old & are not often essential in
management .
Differential diagnosis from Langerhan's cell histiocytosis which present with the
temporal bone & may erode into the mastoid or ear canal causing aural polyp
(usually children) , the diagnosis made by biopsy & characteristic bone defect seen
in x-ray . Management by systemic steroids (partial control) with chemotherapy in

Lecture notes in
extensive disease . The disease in the ear responds to intralesional steroid injection
& mustine ear drops if meatal skin is involved .
Conservative management
Aimed to remove the debris , identify & eliminate the associated microorganism &
ventilating the middle ear if required .
1. Removing debris ; under microscope ;
a. The larger masses of debris can be removed with crocodile microforceps .
b. Suction is required to clean the deeper recess of the canal , using 18 sura caliber
sucker tip to reduce the level of the noise & less likely to damage if it is
accidentally applied to a dehiscent facial nerve or a fistula in the membranous
labyrinth .
2. Identify the organism , by swab taken from the depths of the ear canal & send for
culture & sensitivity to choose the antibiotics or antifungal agents .
So if the bacteria identified , the elimination of a specific microorganism from the
chronic ear will not be curative , but it greatly reduce the symptoms & render the ear
quiescent (especially in safe perforation) .
Uninfected dry ear is a better starting point for tympanoplasty surgery than wet one
The therapeutic options are ;
a. Oral antibiotics
- For aerobes use ciprofloxacin 750 mg twice daily with ciprofloxacin drops , the
cure rate about 85% (40-60% in oral alone) , especially as pseudomonas .
- Others , amoxil or septrin (for H. Influenza) or erythromicyin or flucloxacillin
(in case for Staph. aureus) .
- For anaerobes (bacteroids) use flagyl (but the management dose not cure the
CSOM) .
b. Topical antibiotics
- Garamycin 0.3% , the cheapest especially for pseudomonas , drop into the deep
meatus using the tragus as a piston .
- Neomycin with polymixin drops .
- Antibiotic powders applied by the otologist after microsuction (uneffective in
messy ear at home) .
c. Topical antiseptics
- Chlorhexidine cream , potent against Staph. but it is neurotoxic , so not deposit
on cranial nerves or meninges .
- BIPP , effective against all microorganisms , clean up the infection within 10
days .
- Mercurochrome stain applied by a wool dressed probe , occasionally toxicity to
the ear & need several weeks to absorbed .
- Acetic acid or aluminum acetate drops (not used now) .
d. Intravenous antibiotics ; the most rigorous non-operative management that can
be offered to the patient with a resistant symptomatic chronic diseased ear is ;
daily suction toilet , dressings & high dose i.v. antibiotics (especially garamycin)
Antibiotics useful for CSOM which threatened complications in immune
compromised patients like leukaemias or when OM become otitis interna with
loss of balance as pus entered the labyrinth .

Lecture notes in
e. Antifungal agents , 49% of CSOM "with itching" reveal fungal infection , so

managed by nystatine drops or miconazole creams or packs or suction with
antiseptics .
f. Anti T.B. therapy , if C/S reveal T.B. (with avoiding ototoxic streptomycine) .
g. The prophylactic antibiotics for ear surgery not necessary .
h. Immunosuppression , patient with DM , AIDS & drug induced
immunosuppression in transplantee , need especial care & control of DM with
strenuous antibiotics therapy
3. Management of hearing loss ;
- Conservative management with daily suction & i.v. antibiotics may be needed to
control the sepsis , so aids may be worn in dry clean ear , with antiseptic smear on
the moulds or use swimmer moulds .
- In patient under management of otorrhea , use a bone conduction aids on a spring
steel head band , give excellent results .
- In bilateral active CSOM can't be controlled , use bone anchored hearing aids
attaching an ear level bone conductor aid to a tintanium 4X4 mm screw threaded
fixture , which gives gain of 15-20 dB over the conventional bone conductor aid
(more than the age of 4 years child) .
Clinical presentations & management
A. CSOM with cholesteatoma
1. Posterior retraction pockets accumulating debris
- Symptoms , usually absent , but seen accidentally when examining child with
history of many grommet insertions or Eustachian tube dysfunction .
- Signs ; pars tensa hollow (pocket) , site ; above the lateral process of malleus
(attic) or area near the stapes (posterior) .
The question which must be asked is the pocket selfcleansing & passing keratin into
the ear canal or is there any accumulation of matter in the pocket ?
- Conservative management , if debris is present & has to be removed by suction or
forceps under microscope , so if left untreated it will lead to cholesteatoma sac
formation . So the patient choose either lifelong attendance for microear or
operation .
The use of Indian ink applied to the depth of the retraction lead to stained
epithelium seen to be migrating down the walls of the canal over 6 weeks , so
indication that the pocket is still selfcleansing . If ink remaining in the pocket over
this period , so the disease will progress & need surgical management by excision
of the retraction pocket & grafted the perforation by temporalis fascia by the
underlay technique with grommet placed in the unaffected part of the tympanic
membrane & adenoidectomy .
2. Attic retraction pockets accumulating debris
The site of the pocket is Sharpnell's membrane , with the same signs & symptoms as
for posterior pockets .
Management ;
- Conservative by microsuction , sometimes with time the outer attic wall (scutum)
necrosd causing the natural attic cavity to be broad & the bottom shallow lead to
selfcleansing ear .

Lecture notes in
- Atticotomy ; converts the retraction pockets into bottle neck , shallow bowl . This
done through the postaural , enaural or canal approach .
3. Posterior marginal perforation
- Symptoms ;
(1) Foul smelling purulent discharge .
(2) HL ; conductive with dry ear occasionally .
(3) Polyp filling the ear canal .
(4) Complications like vertigo or facial palsy .
- Signs ;
(1) Perforation in the posterior half of the pars tensa (the annulus is missing) , the
defect lack the sharp crescent like edge that the annulus provide with debris
(which can be sucked) .
All the above may be hidden behind pus , fleshy granulation or aural polyp .
(2) Siegle's speculum , +ve fistula test causing vertigo & nystagmus .
- Management ;
(1) If there is a doubt about the diagnosis , examination under GA needed .
(2) Once the diagnosis of cholesteatoma has been made , plans are made for
surgery to eradicate the disease by modified radical mastoidectomy is the safest
& most reliable operation for cholesteatoma with meatoplasty (to make the
subsequent cleaning of the cavity easy) .
4. Attic cholesteatoma
- Symptoms ; the same as in posterior marginal disease .
- Signs ; the mouth of the cholesteatoma sac is found in the pars flaccida above the
short process of malleus , may be obscured by pus , debris or granulation tissue
(removed by suction) .
- Management ;
(1) If there is cholesteatoma is suspected , but not seen in out patient then
examination under GA is required .
(2) Assessment completed , audiological , radiological & bacteriological .
(3) Modified radical mastoidectomy with removal of the posterior bony canal wall
& meatoplasty .
5. Cholesteatoma arising in a safe perforation
- Symptoms ; HL with discharge .
- Signs ; there is feather like appearance at the healing edge of the safe pars tensa
perforation & occasionally sequamous epithelium accumulates on the underside of
the margin of the perforation which can't escape because it is wedged under the
tympanic membrane remnants lead to a new cholesteatoma exists & will enlarged
in the usual way .
- Management ;
(1) Suction clearance to remove the thread of progressive disease .
(2) Surgery , excision of the drum edges & accumulated disease leaving an open
middle ear .
(3) 2 nd stage operation to restore the hearing , when the surgeon can be sure that
there is no residual or recurrent disease .
6. Cholesteatoma in a radical cavity (mastoid misery)
- Symptoms ; characteristic purulent offensive discharge .

Lecture notes in
- Signs ; sequamous debris is seen clinging to white cholesteatoma matrix in the

depths of the surgical cavity (the ear is resistant to cleansing by outpatient
management) .
- Management
(1) The simplest , meatoplasty to give access to the cavity .
(2) Revision mastoidectomy with lower the facial ridge excentrating all the mastoid
ear cells & excising all diseased lining which is more successful .
(3) Mastoid reconstruction , tympanomastoid reaeration & obliteration with
autologus bone plate behind a new posterior meatal wall .
7. Cholesteatoma behind an intact tympanic membrane
- Symptoms ; silent at childhood , HL presented at the middle life with a serious
complication like facial palsy & brainstem complication .
- Signs ; intact tympanic membrane or sometimes bulged from pressure of the
disease .
- Management is surgery after CT scan , to show the extent of the disease (petrous
apex cholesteatoma is the 3rd common CPA tumor after vestibular Schwannoma &
meningioma) , the surgery either ; permeatal tympanotomy or combined approach
tympanoplasty or translabyrinthine approach (in extensive disease) which is the
best .
B. CSOM without cholesteatoma
1. Dry central perforation
- Symptoms ; HL with discharge after a swimming or colds .
- Signs ; perforation with sharp curved edges most easily seen inferiorly , sometimes
tympanosclerotic patch at the rim of the perforation misdiagnosed as
cholesteatoma .
- Management ; myringoplasty , especially underlay with fresh temporalis fascia
give the excellent results (97%) which improve the hearing & give safe swimming .
2. Subtotal perforation
- Symptoms ; HL & discharge after swimming or respiratory infections , vertigo may
occur in cold winds due to caloric stimulation .
- Signs ; the drum head is absent & often difficult to see the rim of the perforation in
the anterior recess of the ear canal & usually with missing ossicles (especially
incudostapedial joint) with tethered short handle of malleus (usally tethered to the
promontory by fibrous band) .
Some patients has no middle ear structures , other by the presence of masses of
tympanosclerosis which feel hard by probing , other show mountain floor of the
middle ear . Not know why there is necrosis in some & tympanosclerosis in others
- Management either ;
(1) Surgery like ossiculoplasty with myringoplasty which lead to some improvement
to the hearing .
(2) In bilateral loss , hearing aid is the safe alternative to surgery .
3. Burunt out disease with tympanosclerosis
- Symptoms ; HL with past history of ear discharge .
- Signs ; large white rough patches over the tympanic membrane remnants (rigid on
probed) .

Lecture notes in
- Management ; hearing aids , as the myringoplasty failed because has no tympanic

membrane to get blood supply to the graft & ossiculoplasty lead to damage to the
inner ear .
4. Active wet perforation
- Symptoms ; complains more of discharge than HL , unless the problem is bilateral ,
usually the discharge offensive which make the patient isolated socially , usually
the disease associated with secondary otitis externa (itching & pain) .
- Signs ;
(1) In the ear ;
Pus & granulation tissue usally obscure the tympanic membrane , so do
suction clearance or dry mopping to see the source of the discharge , usually
pulsatile one which distinguish it from otitis externa .
Polyps fill the external auditory canal .
(2) In the nose & throat ; chronic rhinosinusitis , chronic infected adenoids , cleft
palate , all fuelling the flames cause unremitting discharge .
- Management ; three visits to the outpatient to dry up most ears ;
(1) At the 1st visit ;
The nose & sinuses assessed & the bad habits like probing or frequent wetting
the ears are corrected .
Microsuction & take ear swab for C/S to give the antibiotic (preferably ear
drops)
(2) At the 2nd & 3 rd visits , microsuction again with antibiotics according to C/S .
Techniques of cholesteatoma surgery
The versatile approach ; small cavity mastoidectomy , beginning the bone work from the
inside of the bony meatus rather than the outside & stopping the dissection as soon as the
posterior limit of the disease is reached . It is more stable than the large cavity approach .
This technique ignored in the debate about wall down mastoidectomy in which the posterior
wall is removed for access of the disease .
The place of combined approach tympanoplasty in the management of the paediatric
cholesteatoma (wall up operation) ; it is technically a more demanding procedure than
modified radical mastoidectomy & take more time to learn in the temporal bone room &
longer too performed in the operating theatre .
The principles ;
(1) Disease is removed from the mastoid & attic & then from the sinus tympani through
a slot cut in the posterior canal wall (the facial recess approach) with access down
the canal via a Rosen's tympanomeatal flap .
(2) The ear drum is returned to its normal position , so the cavities in the mastoid &
middle ear remain sealed of from the outside & can't collect wax .
(3) The ear canal left a normal size & shape & its posterior bony wall preserved .
This operation is suitable for those patients who are settled in area & have no intention of
moving & understand the necessity of close follow up .
Advantages are ;
(1) The ear stay dry even with swimming .
(2) The hearing aid may be worn without provoking discharge .
(3) There is no mastoid cavity exist but hidden behind the tympanic membrane &
carefully preserved bony canal wall .

Lecture notes in
Disadvantages ; the cholesteatoma may persist or retained or reoccur behind the tympanic
membrane & its associated fascia graft .
Complications (contraindications) are ;
(1) Patients with complications of CSOM .
(2) Patients who likely to move out at areas or fail to comprehend the need for follow up
(3) If the surgeon has a short term contact , or if the ENT department show that this
approach not wisest option (so wall down mastoidectomy) .
(4) If the disease recurs is possible , nothing to see with auroscope or microscope .
(5) Persistent Eustachian tube dysfunction causing retraction of the tympanic membrane
which form new corners for debris to accumulate behind .
Adult & Paediatric results compared on relative effectiveness of wall up & wall down
mastoidectomy for cholesteatoma
90% success rate for removing cholesteatoma in wall down procedure & 45% success rate
for wall up procedures , required revision operation .
To discover wheteher cholesteatoma has recurred behind the drum head or posterior canal
wall
(1) Reopening the postaural wound at the 2 nd stage of a combined approach
tympanoplasty .
(2) Hopkin's rod rigid endoscope of <3mm diameter passed into the middle ear cleft via
the drum or mastoid .
(3) One millimeter flexible endoscope pass through the Eustachian tube .
Bony overgrowth in younger children & adhesions in older children lead to poor view for
Endoscopy which less practical than it seems .
Causes of discharging mastoid cavity are ;
(1) Technical ; high facial ridge or narrow meatoplasty .
(2) Growth of bon or adhesions which decrease aeration .
(3) Virulent microorganisms or decreased host immunity .
Problems & solutions with open cavity techniques
1. Mastoid misery ; revision operation & meatoplasty ;
Years of suppuration despite outpatient visits , indicates for 2nd operation , if the child &
the parents are willing . By use of Mare's scale , a mastoid misery score 8 or more ,
should be undergo revision surgery
Never Some of the time Most of time Always
0 1 2 3
Preoperative ;
- Pain (discomfort) .
- Wax .
- Discharge .
- Smell (odour) .
- Giddiness (vertigo) .
Postoperative
- Same as preoperative
The typical preoperative score ; 2+1 +3+3+1= 10 .
The typical postoperative score ; 0+1+0+0+1= 2 .

Lecture notes in
2. Meatoplasty
Sometimes the only needed for mastoid misery , by increasing the ventilation with he
volume of air circulating in the cavity .
Revision mastoidectomy include , lowering of the facial ridge , exenterating all the
mastoid air cells & excising all the diseased lining .
Alternative , tympanomastoid re-aeration with a long graft reaching from the
Eustachian tube to the posterior limit of the cavity , by grafting the cavity with autologus
epithelium (buccal epithelium) .
3. Obliteration techniques
Unwise , the material may contaminated by cholesteatoma .
(1) Obliterate the cavity with soft tissue ;temporalis muscle , connective tissue from the
back of the auricle , the wound healed by 1 st intention (no postoperative pack or
dressings) .
(2) Cavity obliteration with hydroxyl apatite ; the posterior canal wall reconstructed
with a performed hydroxyl apatite prosthesis & granules which is the mineral of the
natural bone , invaded by osteoblasts & osteoclasts , by time converted to the living
bone . Advantages are new strong posterior canal wall with good middle ear space
for prosthetic ossicular reconstruction .
(3) Cavity obliteration with autologus bone chip ; cut the fresh bone chips by burr , 2
teaspoonful required to fill the cavity , usually pate made of bone chips .
(4) Mastoid & middle ear obliteration in dead ear ; the cavity filled with abdominal fat ,
the Eustachian tube blocked off & the ear canal closed as a blind pit . It need long
term follow up , unlikely to be needed in a child but sometimes manage the dead wet
ear .

Lecture notes in
Mastoid surgery
Relevant anatomy
Posterior wall of the tympanic cavity : wider from above than below .
- At the upper part ; aditus opening , which
lead to the mastoid antrum .
- Below the aditus a small depression call
fossa incudis which contain the short process
of incus & a ligament between them .
- Below the fossa incudis & medial to the
opening of the chorda tympani , there is a
small hollow conical bony projection , called
the Pyramid with its apex pointing anteriorly
, within the pyramid there is a canal curves
downwards & backwards to join the
descending part of the facial nerve canal .
- Scutum , thin plate of bone constitute lateral
wall of the epitympanum .
- The long process of incus , the facial canal
lies deep to it , so its important landmark for
the nerve .
- Between the pyramid & the tympanic
annulus , there is the Facial recess which is
bounded medially by the facial nerve &
laterally by the tympanic annulus .
- Stapedius & stapedial tendon , immediately anterior to the 2nd of the facial nerve .
- Chorda tympani , medial to the tympanic membrane , the angle between the facial
nerve & chorda tympani is the access to the middle ear from mastoid without
disruption to the tympanic membrane , this angle may be large or small depending
on the site of origin of chorda tympani of facial nerve .
- Sinus tympani , it is posterior extension of the mesotympanum , lies deep to both
pyramid & facial nerve , extension of air cells may be extensive which may be
measured from the tip of the pyramid into the mastoid bone about 9 mm , the medial
wall of sinus tympani become continuous with posterior part of the medial wall of the
tympanic cavity where it is related to the two openings of the promontory .
- Antral threshold triangle , bounded by fossa incudis , facial recess & chorda
tympani .
- The facial nerve turn 90o to leave the middle ear just above the pyramid & slightly
lateral to it forming 3 rd portion (mastoid & descending) .
Aditus: large irregular opening leading from the posterior epitympanum to the air filled
mastoid antrum , also called aditus ad antrum , it is bounded ;
- Medially : lateral SCC prominence .
- Below & medially : facial nerve canal .
- The short process of incus closely related .
The average distance between ;
- Facial nerve & SCC : 1.77 mm .
- Facial nerve & short process of incus : 2.36 mm .

Lecture notes in
- Short process of incus & SCC : 1.25 mm .

Mastoid antrum ; air filled space within the petrus part of the tempral bone , connected to
the middle ear by aditus , well developed at birth , the adult volume about 1 ml , being 14
mm from front to back , 9 mm from top to bottom & 7 mm from side to side .
Mastoid air cells , lined with flattened non-cilliated sequamous epithelium , like mastoid
itself , according to its degree of pneumatization , the mastoid divided into ;
- Cellular type "well pneumatized" .
- Acellular or sclerotic "20%" type .
The mastoid air cells separated from the sigmoid sinus , posterior & middle cranial fossa
by thin bone which occasionally dehiscent .
The groups of air cells are ;
1. Retrofacial , medial to the descending portion of the facial nerve .
2. Tip cells , down to the diagastric muscle .
3. Perisinus cells , around the sigmoid sinus .
4. Zygomatic cells , at the root of the zygoma .
5. Sinodural cells , at the angle between the sigmoid sinus & middle cranial fossa .
6. Perilabyrinthine , under the basal turn of the cochlea .
7. Apical cells , at petrus apex .
Spine of Henele , lies postero-superior to the bony EAM , has irregular contours & varies
in size , cause tethering of the overlying skin .
Squamo-matoid suture , run longitudinally along the floor of the EAM , also cause
tethering to the overlying skin .
Suprameatal (McEwin's) triangle ; it is posterior superior to the EAC , identified by
pressure on cymba concha , bounded by suprameatal crest , posterior meatal wall &
tangential line between them .
Cortical mastoidectomy
Complete dissection of the mastoid cavity, maintaining an intact posterior canal wall.
During the dissection, the tegmen antri , sigmoid sinus, labyrinth, incus, and facial nerve
are identified.
It affords access to the antrum , attic, labyrinth, and endolymphatic sac region.
Indications
1. Preliminary step to otologic procedures requiring exposure of structures within and
medial to the temporal bone
2. Complications of acute otitis media, including mastoiditis and subperiosteal abscess
3. Cholesteatoma
4. Chronic otitis media including secretory OM .
5. Cerebrospinal fluid otorrhea
6. Facial nerve trauma
7. Temporal bone neoplasm
8. Acute mastoiditis , if ; symptoms & signs not controlled by adequate course of
appropriate antibiotics or in patient present with complications .
9. T.B. mastoiditis which should be suspected in patient with T.B. , pale granulation found
in the mastoid antrum or air cells .
Special Considerations
1. Reconstruction of scutal defects
2. Total canal wall reconstruction

Lecture notes in
3. Mastoidectomy in children
Preoperative Preparation
1. Audiometry .
2. Laboratory and radiographic studies, as indicated .
3. Neurological examination .
4. Examination of the facial nerve .
5. Ear swab for C & S .
6. Appropriate antibiotic at induction .
Special Instrumentation, Position, and Anesthesia
1. Operating microscope
2. Otologic drill system with assorted cutting and diamond burs
3. Suction-irrigation system
4. General anesthesia
Tips and Pearls
1. Precise identification of tegmen antri , sigmoid sinus, labyrinth, ossicular chain, and
facial nerve is essential.
2. Efficient dissection is facilitated by altering the pressure on the bur, not the drill
speed.
3. Proper use of the suction-irrigation system allows irrigant to flow over the path of the
bur, preventing bone dust from obscuring the view or collecting in the flutes of the bur.
4. Adequate epitympanic exposure
Operative Procedures
1. The Position & incision ; patient is placed in a supine position, with the operated
ear facing up. Hair above and behind the ear is shaved approximately
2 cm behind the hairline for the postauricular approach; endaural
incisions may also be used, but exposure is compromised. In children
younger than 3 years of age, the mastoid tip may not be fully
developed, and the incision must be placed more posteriorly .
2. The ear is undermined at the level of the temporalis fascia, and a
transverse incision is made along the inferior edge of the temporalis
down to the bone , avoid cutting the belly of the muscle to prevent
bleeding . The remaining postauricular soft tissue is divided by
creating a vertical limb toward the mastoid tip. The periosteum is
reflected away from underlying mastoid cortex. Mollison's self
retaining retractors are used to maintain exposure.
Several bony landmarks may be identified , including the extension of
the root of the zygoma (suprameatal crest) and the spine of Henle
External landmarks cannot be relied on to predict the position of
deeper structures. Safe mastoid surgery depends on precise
identification of internal structures.
3. Before beginning the dissection ;
a. The surgeon should have a mental image of the completed
cavity, which resembles a kidney bean.
b. Bone removal must proceed evenly from lateral to medial
positions, across a broad plane to avoid making ‘‘potholes.''

Lecture notes in
Cortical bone removal requires a moderate amount of pressure to be placed on

the burr.
c. As important structures are approached, pressure on the drill is minimized to
prevent injury.
d. Dissection parallel to a given landmark facilitates its identification.
e. The sound produced by the bur contacting bone increases in pitch as the bone is
thinned, but a change in pitch cannot be recognized if the surgeon is not
dissecting along a broad plane.
f. An eggshell-thin layer of bone along the middle fossa dura, sigmoid sinus, and
facial nerve should be preserved.
4. Begin drilling with a cutting bur that is 6.0 mm in diameter or larger and with a 12-
Fr or larger suction-irrigator. Use each bur to its
fullest extent before switching to a different size, and
limit the number of times the bur is changed.
5. Landmarks within the mastoid bone should be
identified in a manner that defines the borders of the
cavity and allows rapid bone removal between
known areas. Bone removal begins superiorly, at or
above the level of the temporal line. The initial
landmark is the tegmen antri and the underlying
dura of the middle cranial fossa. The dura is easily
identified on its lateral aspect and then followed
further inferiorly and medially. The dura appears
white and has a lattice of small blood vessels on its
surface. Continue to develop the tegmen from anterior to posterior aspects; the
tegmen should form an acute angle with the sigmoid sinus at its posterior limit.
6. Bone removal continues inferiorly and posteriorly to identify the sigmoid sinus. The
sinus sets the posterior limit of the dissection. The distance from the cortical bone to
the lateral aspect of the sinus varies. The sinus
appears blue and is usually readily identified.
Follow the tegmen medially and posteriorly into
the sinodural angle to avoid difficulty in identifying
the sinus. After the sinus is found, begin to thin the
bone on its lateral and anterior aspects. The sinus
gently curves medially as it is followed inferiorly.
The posterior semicircular canal is encountered by
dissecting anterior and medial to the sinus.
7. The antrum is then opened , the tegmen is followed
anteriorly and medially. The air cells seem to
enlarge as Korner's septum is breached and the antrum is entered.
The thick, white bone of the lateral semicircular canal may be seen
on the medial wall of the antrum. The incus lies more anterior. As
the opening to the antrum is enlarged, the incus may be seen as a
reflection in the irrigant. To fully expose the incus, open the
epitympanum from lateral to medial aspects. Continue following
the tegmen into the root of the zygoma while thinning the canal

Lecture notes in
wall on its superior aspect. If indicated, the anterior extension may be continued to
the supratubal space, anterior to the head of the malleus. If the epitympanum is
approached posteriorly, damage to the incus may occur because the bur may block
the path of vision.
8. The inferior limit of the dissection is the digastric ridge. Follow the
sigmoid sinus inferiorly on its lateral aspect to identify the
digastric ridge. The digastric ridge appears slightly lighter than
the sinus and is oriented in a horizontal direction just lateral to the
sinus. Mastoid tip air cells lateral to the digastric may be removed
without risk to important structures. The facial nerve is found
anteriorly at the level of the digastric ridge.
The canal wall may be thinned rapidly by staying lateral to the incus superiorly and
the digastric ridge inferiorly. Avoid creating a defect in the canal by listening to the
pitch of the burr, examining the thickness from within the canal, or placing the burr
in the canal to see if its shadow is visible. A significant overhang at the lateral aspect
hinders visibility during subsequent dissection.
Open the retrofacial air cell tract, dissecting anterior to the sigmoid sinus, inferior to
the posterior semicircular canal, and medial to the digastric ridge. The jugular bulb
soon becomes apparent.
9. The final objective is identification of the facial nerve. Multiple landmarks should be
available for safe and rapid identification.
a. The tympanic segment of the nerve may be visible medial to the incus, and the
second genu is just inferior to the lateral semicircular canal.
b. The vertical segment is lateral to the retrofacial air cells and at the level of
the digastric ridge.
Continue thinning the posterior canal wall medially, and the nerve is encountered on
its posterolateral aspect. Use a diamond bur, ample irrigation, and broad strokes
parallel to the course of the nerve to ensure safety during delineation of the nerve. In
patients with extensive mastoid pneumatization, it is desirable to maintain an intact
canal wall.
10. Small defects of the canal wall or scutum may be repaired with autogenous or
homograft cartilage or bone. Tragal cartilage is widely used for
this purpose, because it can be harvested with ease and trimmed to
fit the defect. The tragus is injected with local anesthetic. An
incision is made on the medial aspect, transecting skin and
cartilage. The lateral 5 mm of cartilage is preserved for better
cosmetic . The skin is dissected away from the perichondrium
medially and laterally, and a piece of cartilage is removed.
Minimal bleeding is encountered in most cases and controlled with
bipolar cautery.
11. The wound is irrigated and closed with interrupted, simple, 5-0 fast-absorbing plain
sutures.
Pitfalls and Complications
1. Common areas of incomplete dissection are the sinodural angle, epitympanum, and
inadequate thinning of the posterior canal wall.
2. Facial nerve injury .

Lecture notes in
3. Sensorineural hearing loss or vertigo secondary to labyrinthine injury .

4. Cerebrospinal fluid leak secondary to dural tear .
5. Vascular injury .
6. Persistent deafness due to , incus damage or removal or persistent infection in the
mastoid cells .
7. Meatal stenosis , occur if the bony meatal wall taken down & the skin dissected off the
bony wall .
Postoperative Care Issues
1. Mastoid dressing overnight is advised.
2. Severe pain postoperatively is infrequent and may portend hematoma or wound
infection.
3. The routine use of antibiotics is not indicated and is determined by the indication for
surgery.
4. Audiometry to document outcome, usually approximately 2 months after the
procedure.
Radical mastoidectomy
The radical mastoidectomy technique is the basis for the open cavity mastoid
procedures. The classical radical mastoidectomy entails a canal-wall-down mastoidectomy
combined with complete removal of the tympanic membrane, annulus, malleus, incus, and
middle ear mucosa. The Eustachian tube is stripped of mucosa and the remaining mucosa
inverted into the Eustachian tube orifice. The Eustachian tube is then blocked with a fascia
plug. The goal of radical mastoidectomy is to establish a dry, open cavity devoid of
secretory epithelium.
Indications
1. Cholesteatoma with chronic or recurring otorrhea, with adequate cochlear reserve for
possible future reconstruction
2. Incompletely resected or exteriorization of Cholesteatoma.
3. Poor compliance or follow-up
4. Unreconstructable posterior canal wall
5. Contracted mastoid (relative indication)
6. Disease in the only hearing ear or dead ear
7. Medical illness
8. Severe otologic and central nervous system complications
9. Neoplasms .
10. Nonfunctioning Eustachian tube
11. Neoplastic disease
12. Cavity obliteration is rarely indicated because of a high failure rate, but it is used
when other forms of treatment have failed to dry mastoid bowl.
13. Skin grafting is rarely indicated. It may apply 2 to 3 weeks after a healthy granulation
layer has developed.
Contraindications
1. Benign chronic mucoid , secretory, or allergic otorrhea
2. Acute otitis media with coalescent mastoiditis
Thin-cut (1.5-mm) non-contrast computed tomography scan of the temporal bone, with
axial and coronal views .

Lecture notes in
Check for labyrinthine fistula; position and dehiscence of the facial nerve; position,
height, and erosion of tegmen and sigmoid sinus; and condition of the ossicles .
Tips and Pearls
1. Use periosteum or perichondrium (tragal or conchal) if fascia is unavailable for the
graft.
2. Identify the middle fossa dura and sigmoid sinus, and enter the middle ear from the
attic. Identify the facial nerve.
3. Cholesteatoma that extends onto the medial aspect of malleus head and incus requires
their removal
4. Save dissection over the labyrinthine fistula or stapes for last. Dissect along the
stapedial tendon from posterior to anterior.
5. Matrix firmly adherent to the dura, sigmoid sinus, or facial nerve is left exteriorized.
6. Matrix covering the footplate is left exteriorized, rather than risk opening the vestibule
and causing labyrinthitis.
7. No packing is used. Fill the cavity with antibiotic ointment (e.g. Polysporin).
8. Adequate meatoplasty requires a smooth, open, accessible mastoid bowl.
Operative Procedure
1. General anesthesia is induced, and preoperative antibiotics are given, if indicated.
Electrodes are applied to monitor the facial nerve. The Betadine prep includes the ear
canal .
2. Sterile drapes are applied, and the postauricular sulcus and tragus are injected with a
2% solution of Xylocaine with a 1:100,000 dilution of epinephrine. The canal is
injected in a four-quadrant fashion with 2% Xylocaine and 1:50,000 epinephrine.
Vascular strip incisions are made, followed by a postauricular incision 0.5 cm from
the sulcus . A large piece of preareolar fascia (or periosteum) is harvested and set
aside to dry.
3. A T-shaped incision is made over the mastoid fascia, the tissue is elevated along with
the vascular strip out of the canal and held in place with a self-retaining retractor . If
a previous mastoid defect is present, the bony rim is palpated, and the incision follows
the lateral margin of the rim to avoid injury to the dura and sigmoid sinus. Canal flaps
are elevated and rotated anteriorly. The middle ear is entered, and the cholesteatoma
is dissected from the mesotympanum and off the ossicular chain . Polyps and
granulation are removed, unless they are over the stapes or facial nerve. Disease in
the posterosuperior quadrant of the mesotympanum is approached last. Atrophic
tympanic membrane is resected.
4. A complete simple cortical mastoidectomy is performed ;
a. All plates are smoothed .
b. The facial nerve is identified, leaving a thin layer of bone over it. The facial recess
is opened.
c. The cholesteatoma sac is decompressed, and dissection proceeds always from
known to unknown features .
d. The malleus head is removed to expose the anterior epitympanum .
e. If the incus is involved, the incudostapedial joint is separated, and the incus is
removed.
f. The lateral canal and facial nerve are palpated through
the matrix to determine if a dehiscence or fistula exists.

Lecture notes in
g. The facial ridge is lowered, and the chorda tympani is sacrificed.

h. The inferior limit of the mastoid cavity is drilled to the level of the hypotympanum,
confluent with the mastoid tip.
i. The anterior epitympanum is drilled down to the level of the
anterior external auditory canal wall .
j. The tympanic membrane and malleus are removed, leaving a
thin anterior rim and annulus .
k. Cholesteatoma is dissected off the lateral semicircular canals
and facial nerve last . If a fistula exists, it may be grafted
quickly or left with the overlying matrix exposed into the
cavity.
5. The final product should be a smooth-walled, rectangular
cavity without edges. The facial ridge should be low, with a
smooth transition into the hypotympanum. The stapes is the
only ossicular remnant, if not destroyed by disease. An anterior
rim of tympanic membrane is left. Gelfoam soaked with
epinephrine is placed in the middle ear and mastoid while a
meatoplasty is performed.
6. Meatoplasty ;
a. The conchal skin is injected with a 2% solution of
Xylocaine with a 1:100,000 dilution of epinephrine, and the
ear is placed in retraction with dural hooks.
b. The soft tissue medial to the conchal cartilage is removed,
exposing the conchal cartilage .
c. A 1.5- to 2-cm section of cartilage is removed, leaving the
conchal skin for the Koerner flap .
d. The conchal skin is incised superiorly between the tragus
and anterior helix and incised inferiorly.
e. All exposed cartilage is trimmed or covered.
f. Hemostasis of the flap is confirmed.
7. Grafting ;
a. Gelfilm is placed over denuded mucosal areas.
b. Pressed Gelfoam soaked in Tis-U-Sol (Ringer lactate) is placed into the
eustachian tube and middle ear.
c. The graft is tucked firmly under the anterior annulus and draped over the
stapes, facial ridge, and mastoid .
d. Exposed perilabyrinthine, retrofacial, zygomatic, and peritubal air cell
tracts are also covered with grafts.
e. If the stapes is lower than the facial ridge, the malleus head (autoclaved),
tragal cartilage, or a partial ossicular replacement prosthesis (PORP) may
be used to augment .
f. Polysporin ointment is placed over the graft, filling the medial one half of
the cavity.
g. The Koerner flap is then tacked with a superior and inferior 3-0 Vicryl
suture to maintain an adequate meatoplasty;

Lecture notes in
8. The postauricular incision closed in tow layers , it should not be over tightened ., the
remainder of the cavity filled with ointment, and a Glasscock dressing is applied .
Complications
1. Poor meatoplasty and scar bands
2. High facial ridge
3. Infection, perichondritis, and brain abscess
4. Facial nerve, dural, or sigmoid sinus injury
5. Vertigo
6. Recurrent or residual cholesteatoma
7. Mucous or chocolate cysts
Postoperative Care
1. On the first postoperative day, the dressing is removed, and the cotton ball is changed.
The patient is instructed to avoid nose blowing and water in the ear.
2. Pain medication and stool softeners are dispensed.
3. The patient returns to the office in 3 weeks and gentian violet and silver nitrate are
applied during the next month, as required, on a weekly basis. The cavity is usually
healed in 2 months, after which water activity is permitted.
Modified radical mastoidectomy
The radical mastoid operation has been modified to construct a tympanic membrane and an
ossicular chain with or without mastoid obliteration.
The modified radical mastoidectomy procedure generally begins with a complete
mastoidectomy with or without a facial recess approach . After the extent of the disease is
established, the decision on whether to proceed with a canal-wall-down procedure can be
made . At this point, the posterior and superior external auditory canal wall may be
removed . The removal of the canal wall is most safely performed lateral to the attic area
and the incus . Since the facial nerve is medial to the incus, this affords a safe area of bone
removal .
The scutum is removed flush with the anterior canal wall . The posterior and inferior
portions of the remaining ear canal wall should then be removed . This wall is sometimes
termed the facial ridge , since it is the bone that lies lateral to the fallopian canal and facial
nerve . To have a well-aerated , dry mastoid cavity, this posterior canal remnant must be
removed down to about the level of the fallopian canal . The facial nerve generally travels
from its medial location near the incus to the stylomastoid foramen in an oblique, slightly
lateral direction.
Once the bulk of the posterior part of the ear canal has been removed with cutting burrs, the
diamond burr with constant suction-irrigation should be used in approaching the fallopian
canal in its vertical or descending portion. Once the bone over the fallopian canal is thin,
the remainder of the facial nerve region can be smoothed to facilitate reconstruction .
Actual exposure of the facial nerve should be avoided, since it puts the nerve at greater risk
during the rest of the procedure and in any possible future operations .
Open versus closed techniques
In contrast to the intact canal wall procedures, in the canal-wall-down and radical
procedures the cortex completely surrounding the mastoid should be well saucerized to a
smooth contour . In addition, the mastoid tip must be removed . Failure to remove the
mastoid tip after exenteration of its air cells may lead to a dependent pocket within the
mastoid defect, which will accumulate debris and harbor infection. Air cells over the

Lecture notes in
sigmoid sinus (lateral venous sinus) should be removed completely and that region
saucerized as well.
Extensive saucerization of the mastoid and removal of the mastoid tip may lead to an
alteration in the position of the pinna after closure. The hypotympanic air cells may be
exposed more widely by removal of part of the tympanic bone forming the inferior portion
of the external auditory canal. It is advisable to identify the exact location of the facial
nerve before lowering the floor of the ear canal. Lowering the floor of the ear canal also
helps to widen the external auditory canal and lessen the likelihood that the air cells near
the mastoid tip will become dependent. If possible, the digastric ridge marking the lowest
extent of the mastoid cavity and the lower part of the external auditory canal should be at
the same level, creating a smooth, easily cleansed mastoid bowl.
The anterior canal wall may obscure the anterior most part of the tympanic cavity and may
be sculpted to allow better anterior exposure. If removal of the anterior wall overhang is
required, an incision is made with a canal knife along the anterior canal just lateral to the
tympanic annulus. The skin of the external auditory canal is then raised in a retrograde
manner to the bony cartilaginous junction. The laterally based flap thus created is
preserved while the anterior ear canal is sculpted. It is advisable to use a large diamond
burr with constant suction-irrigation in this area, since entry into the glenoid fossa should
be avoided . Entry into the glenoid fossa may allow herniation of the contents of the glenoid
fossa into the ear canal at a later time, with the potential, although unusual, for
temporomandibular joint problems.
After mastoid surgery has been completed, middle ear reconstruction, including tympanic
membrane reconstruction and ossicular reconstruction, may be performed .
Advantages Disadvantages
Intact wall Physiologic tympanic membrane Residual cholesteatoma may be
occult
position
Deep middle ear Recurrent cholesteatoma may occur
in attic
No mastoid bowl Delayed canal breakdown
Incomplete exteriorization of facial
recess
2nd stage often required
Canal-wall- Residual cholesteatoma visible Mastoid bowl maintenance can be a
down lifelong problem
on follow-up
Recurrent cholesteatoma is rare Middle ear is shallow and difficult
to reconstruct
Total exteriorization of facial Position of pinna may be altered
recess
2nd stage sometimes required
Mastoid obliteration
Following canal-wall-down mastoidectomy, the patient is left with a mastoid cavity and its
inherent problems. The bowl generally needs to be cleansed on a routine basis every 6 to 12

Lecture notes in
months. The cavity is prone to collection of debris and consequent infection, and this
necessitates caution with regard to water contamination.
Various techniques have been used to minimize the potential complications following canal-
wall-down procedures. Wide saucerization, avoidance of a dependent pocket in the mastoid
tip, lowering of the facial ridge, and a generous meatoplasty are the cornerstones of a
healthy mastoid bowl, as described previously. Despite these precautions, mastoid cavity
complications can still occur.
Further modifications of the mastoid cavity have been suggested to minimize the size of the
bowl and consequent complications . The postauricular musculoperiosteal flap (the Palva
flap) has been used quite successfully in obliterating mastoid cavities .
Other flaps used to obliterate mastoid cavities include temporalis muscle pedicled
anteriorly or temporalis fascia pedicled on the superficial temporal artery (Hong Kong
flap) , the vascularized temporalis fascia pedicled flap serves many purposes. The flap helps
cover exposed bone together with providing a smooth surface upon which the epithelium
can migrate. It also provides additional blood supply to facilitate the healing process. In
patients with large, well-pneumatized mastoids, the cavity often is incompletely obliterated
with these flaps alone.
The paté is placed deep to the postauricular musculoperiosteal flap or deep to the
temporalis fascia flap or graft. The addition of bone paté may resolve the problem of
subsequent cavity enlargement due to atrophy of the flap. It is important to collect the bone
paté before entering the diseased mastoid to avoid the possibility of collecting any
cholesteatoma matrix or infected tissue with the bone dust.
Bone paté contouring of the mastoid cavity, together with a Palva or temporalis fascia flap,
consistently results in dry mastoid cavities.
Grote and Blitterswijk have described reconstructing the posterior canal wall with a
porous hydroxyapatite prosthesis that is covered by a temporalis fascia flap.
Montandon et al. have recommended combining the canal-wall-up procedure with mastoid
obliteration with a fat graft to avoid recurrent disease. They also exteriorize the attic into
the ear canal.
Complications Mastoid surgery
A . Facial nerve injury
- The tortuous course of the facial nerve through the temporal bone, together with
areas of bony dehiscence and possible anomalous courses, places this important
structure at risk.
- The heat generated by a diamond burr may injure the facial nerve even without
direct mechanical trauma to the nerve. Heat damage may be minimized by the use of
constant suction-irrigation during dissection with diamond burrs.
- In reoperated ears or in anomalous temporal bones such as in congenital atresia, the
normal landmarks may be absent or misleading . In addition, sclerotic new bone
deposition can distort the normal anatomy. Intraoperative electromyographic facial
nerve monitoring can be helpful in these situations.
If the facial nerve is traumatized during surgery ;
- The extent of the injury should be assessed by direct observation and electrical
testing , the region of the suspected injury should be examined by exposing the nerve
above and below the injury site by 5 to 10 mm, using the diamond burr and constant
suction-irrigation for bone removal.

Lecture notes in
If facial muscle contraction can be elicited by stimulation (at 0.5 mA) of the nerve
above and below the injured area, further treatment is unnecessary.
- Systemic corticosteroids may be helpful in the postoperative period to minimize
swelling .
- If facial movement can be elicited by stimulation of the distal nerve but not proximal
to the injury, a more thorough exposure of the injured nerve should be performed by
removing the bone over the injured segment over its lateral 180 degrees. If only a
few fibers are damaged, they may be returned to their anatomic position; recovery
with synkinesis is likely.
- If the nerve is severely injured or completely severed, reanastomosis is required. If
enough length can be obtained by mobilization of the nerve, primary reanastomosis
should be performed. Reapproximation in the groove of the fallopian canal is usually
sufficient; suture support with two or three 8-0 nylon sutures may be used to stabilize
the anastomosis. In most cases of severe injury to the facial nerve within the
temporal bone, direct reanastomosis is not possible. In such cases, the traumatized
segment will require cable grafting. The great auricular nerve (from C2 and C3) can
be an excellent source for a cable graft. A great auricular nerve graft can be
harvested as it travels over the sternocleidomastoid muscle in the upper neck.
- Facial paralysis in the postoperative period when injury was not suspected requires
prompt attention. Lidocaine administered in the preoperative injections may be
responsible for some cases of immediate postoperative facial palsy; consequently,
surgical reexploration should be deferred for a few hours and the patient reassessed
at that time. If complete paralysis is present, early reexploration is indicated. On
exploration, decompression of any traumatized region should be performed and
direct anastomosis or cable grafting of the nerve undertaken if a laceration is
identified . If, on the other hand, the facial palsy is delayed or paretic, conservative
management is indicated and would include a tapering course of systemic steroids.
B. Sensorineural hearing loss
Iatrogenic hearing loss and vertigo resulting from cochlear or labyrinthine injury are
inherent risks in all otologic surgery . Due to these risks, guidelines have been
established for decision making with operations on an only hearing ear .
C. Vestibular complication
Injury to the labyrinth during tympanomastoid surgery can result from direct trauma or
subsequent infection. A severe vestibular injury may lead to complete loss of vestibular
function in the operated ear. Complete loss of unilateral vestibular function, if the
opposite ear is intact, results in acute vertigo with slow resolution over weeks to months.
Chronic dysequilibrium or vertigo may occur.
D. Postoperative infection
Postoperative infection continues to pose a potential obstacle in otologic surgery.
Infection may result in failure of the tympanoplasty, dissolution of the grafts and bone
paté, and necrosis of the external auditory canal skin flaps, as well as the myriad of
potential complications of any mastoid infection. In an attempt to minimize these risks,
perioperative oral antibiotics have been administered according to preoperative culture
and sensitivity results. Intraoperative irrigation with bacitracin solution may also be of
benefit. Perichondritis can occur in the immediate postoperative period. Debridement of

Lecture notes in
necrotic cartilage and the administration of systemic, parenteral antibiotics are often
necessary.
E. Cerebrospinal fluid leakage
Iatrogenic CSF leaks can occur when a rent is created in the middle or posterior
cranial fossa dura . Dura matter thins with aging and consequently places elderly
patients at greater risk for this complication. Lacerated dura must be sutured and
covered by a fat, fascia, or muscle graft to prevent a CSF fistula. Dural lacerations can
usually be prevented by using diamond burrs once the dural plate has been skeletonized.
F. Bleeding
Laceration of the sigmoid sinus or jugular bulb results in bleeding, which is generally
easily controlled by the application of Gelfoam covered by a small cotton pledget .
However, a significant laceration places the patient at risk for secondary complications,
including air embolism and thrombosis of the sigmoid sinus . If a large laceration of the
sigmoid sinus or jugular bulb occurs, hemostasis should be attained by direct pressure
over the injury site.
Once bleeding is controlled, the potential for air embolism should be considered. Severe
air embolism can lead to the formation of an air bubble within the right ventricle,
making effective circulation impossible. The early signs of air embolism are increased
end-expiratory carbon dioxide, hypotension, and abnormal cardiac sounds. If air
embolism is detected, the patient should be placed in the Trendelenburg’s (head-down)
position to minimize the further ingress of air into the vascular system. The patient may
be put into the left lateral position in an effort to reposition the air bubble into the right
atrium or vena cava. If cardiovascular compromise is still present after these
maneuvers, air must be aspirated from the vena cava promptly.
Injury to the carotid artery during tympanomastoid surgery must first be managed by
direct occlusion of the injured artery. Once bleeding is controlled, proximal and distal
ligation of the internal carotid artery is necessary.
G. Dysgeusia
H . Brain herniation
If larger areas of dura are exposed, brain herniation into the mastoid cavity and
epitympanum can occur . This situation is potentially hazardous in the event of
reexploration , Cerebritis, meningitis, and CSF leakage may occur years later.
I. Delayed complications
Other complications of mastoid surgery include delayed posterior canal wall
breakdown, perichondritis, blue-domed cyst or cholesterol granulomas, mucosalization
of the mastoid bowl, and external auditory canal stenosis.

Lecture notes in
Reconstruction of the middle ear cavity

Historical review
Perthold (1878) in Germany repair the tympanic membrane with full thickness skin by
operation called "Myringoplastik" .
Nylen in Stockholm (1921) introduce monocular operating microscope .
Holmgreen (1922) introduce binocular operating microscope .
Lembert (1938) in USA , carried out one stage fenestration operation .
Wullstein & Zolliner (1953) introduce their tympanoplasty method at the 5th international
congress of otolaryngology in Amsterdam .
Zolliner (1956) successfully use autologous fascia lata .
Shea (1956) perform the 1st stapedectomy & replace the stapes with Teflon replica . He
later introduce the vein graft , polyethylene tube method of stapes replacement .
Shea (1960) accidentally introduce underlay technique .
Chalet (1964) was the 1st to use tympanic membrane allograft .
Marquet(1966) introduced the use of homograft tympanic membranes.
Definition
Tympanoplasty ; It is operation performed to eradicate the middle ear disease &
reconstruct it.
Myringoplasty ; It is an operation performed to repair or reconstruct the tympanic
membrane , often incorrectly referred to as type I tympanoplasty .
he hearing mechanism with or without myringoplasty (tympanic membrane graft) , & it may
be combined with mastoid surgery when there is concomitant mastoid disease or CSOM .
Ossiculoplasty ; It is an operation performed to repair or reconstruct the ossicular chain .
Classification of tympanoplasty
Over years , classification of tympanoplasty have been proposed by various authors , but
the one presented by Wullstein (1953) is still used today by most otologic surgeon ;
 Type I ; Reconstruction of the tympanic membrane (ossicular chain intact & mobile)
 Type II ; Malleus handle is absent , reconstruction of the tympanic membrane over
the malleus remnant & long process of incus .
 Type III ; Malleus & incus are absent , reconstruction of the tympanic membrane
over an intact & mobile stapes (myringostapediopexy) with stapes acting as a
columella .
It was categorized as one in which the tympanic membrane graft lies right on the
stapes.
 Type IV ; Mobile stapes footplate exteriorized with reconstruction of the tympanic
membrane as a round window baffle .
 Type V ; Stapes is fixed , the graft is placed over a fenestration of the horizontal SCC
.
Paparella –modified type V tympanoplasty is subdivided into ;
- Type Va , fenestration of the horizontal SCC .
- Type Vb , stapedectomy in cases of tympanoplasty type IV with stapes fixation
 Type VI , added by Garcia (1961) ; The round window is left uncovered &
reconstruction of the tympanic membrane , so that the inferior edge lies on the
promontory above the round window there by creating an oval window baffle .
With advent of the interposition of ossicular prosthesis , multiple attempts have been made
to modify the over the years .
Lecture notes in
Farrior proposed the types of tympanoplasties according to the basic pathologic anatomy at
the completion of the surgery rather than classify them according to the method of
reconstruction , Farrior sub-classified tympanoplasty type III as follows ;
- Type III ; Drum on stapes .
- Type III (IG) , Incus graft .
- Type III (IGM) ; Incus graft to malleus .
- Type III (MR) ; Malleus repositioned .
- Type III (MG) ; Malleus graft .
- Type III (BG) ; Bone graft .
- Type III (SSMS) ; Stainless steel malleus to stapes .
Austien addressed the issue by proposing a separate classification scheme for
ossiculoplasties , he described four ossicular defect replacement types using letters A to D .
- Type A ; Has a malleus –stapes assembly , the malleus handle present & stapes
superstructures present .
- Type B ; A graft footplate assembly , malleus handle absent , stapes superstructures
present .
- Type C ; A short columella tympanic membrane-stapes assembly , , malleus handle
present , stapes superstructures absent .
- Type D ; A long columella tympanic membrane-footplate assembly , , malleus handle
absent , stapes superstructures absent .
Rare defects ;
- E ; Isolated loss of the malleus handle , reconstruction of the tympanic membrane
& malleus , removal of the incus & its reconstruction .
- F ; Isolated loss of the stapes superstructures , reconstruction of the tympanic
membrane & reconstruction of the superstructures of the stapes .
Fixed stapes ;
- G ; , malleus handle present , incus & stapes fixed , reconstruction of the tympanic
membrane & when possible removal of the stapes , sealing of the oval window with a
vein or tragal perichondrium autograft & reconstruction of the ossicular chain from
oval window to the malleus handle (malliolabyrinthopexy) .
- H ; , malleus handle absent , incus absent & stapes fixed , reconstruction of the
tympanic membrane & malleus & when possible removal of the stapes , sealing of
the oval window with a vein or tragal perichondrium autograft & reconstruction of
the ossicular chain from the oval window to the neo-malleus handle .
Nodal & Schuknecht divided type III tympanoplasty into 3 subtypes ;
- A : Stapes columella , in which the tympanic membrane graft is laid on an intact
stapes head .
- B : Minor columella , in which a strut is placed between the tympanic membrane
graft & stapes capitulum .
- C : Major columella , in which the strut is placed between the tympanic membrane
graft & footplate .
Grafts used in tympanoplasty & mastoidectomy
Generally , 4 types of grafts can be defined according to the genetic relationship between
the donor & the host , which are ;\
A. Autograft ; tissue transplant from one part of the body to another in the same
individual.

Lecture notes in
B. Isograft ; tissue transplant between genetically identical individuals .

C. Allograft ; tissue transplant between genetically non-identical members of the same
species , e.g. preserved human cadaver incus used to repair an ossicular chain
defects.
D. Xenograft ; tissue transplant between members of different species , e.g. preserved
bovin vein graft used to repair the human tympanic membrane .
Grafts of any genetic origin may be further defined according to their ;
- New anatomical site ;
(1) Orthotopic graft ( ortho=correct) ; graft placed in an anatomical position
normally occupied by such tissue , e.g. tympano-ossicular allograft . .
(2) Hetrotopic graft (hetro=different) ; graft placed in an unnatural recipient
location .
- Pattern of vascularization ;
(1) Vascularized graft ; graft placed directly in a vascular pedicle (kidney transplant)
.
(2) Non-vascularized graft ; free graft vascularized indirectly from recipient bed
(preserved dural matter) .
- Functional capacity
(1) Vital grafts ; graft expected to fulfill their normal physiology .
(2) Static grafts ; graft serve a mechanical function that does not require
physiological viability .
At present , all tissue grafts used in tympanoplasty & tympanoplasty with mastoidectomy
are free , non-vascularized grafts .
Grafts currently used in the middle ear & mastoid reconstruction surgery are ;
Autografts Allografts Xenografts
Myringoplasty Temporalis fascia Dura matter Bovine jugular vein
Tragal Tympanomeatal Calf caecal serosa
perichondrium
Tragal
perichondrium &
cartilage
Fat
Vein
Ossiculoplasty Ossicular bone Tympanoossicular
Cortical bone Incorporating malleus handle
Cartilage Malleus & incus
Malleus , incus & stapes
Ossicular bone
Cartilage
Canal wall Cartilage bone Cortical bone
reconstruction Cartilage Cartilage
Cartilage & Composite graft (tympano-
perichondrium ossicular)with/without
posterior bony canal wall
Cavity Cortical bone Cortical bone
obliteration Cancellous bone Cancellous bone

Lecture notes in
Biomaterials
Also known as alloplastic materials , subdivided into 4 groups based on their interface
reaction with bone
1. Bio-tolerant .
a. Metals ; stainless steel , Tantalum , Platinum & Titanium .
b. Polymers ; solid , porous , light harness stain , weave carbon fibers .
2. Bio-inert .
3. Bio-reactive .
4. Bio-active .
The most recent materials available for ossiculoplasty & posterior canal wall & outer attic
wall reconstruction & mastoid obliteration are the bioceramic , these are classified as
follows ;
1. Bio-inert Alluminum oxide ceramics .
2. Bio-reactive glass ceramics .
3. Bio-active calcium phosphate ceramics .
Most ear surgeons prefer to use healthy , fresh autologous tissue whenever possible , their
2 nd choice have been preserved for allogenic tissue , the polymer biomaterials have enjoyed
wide spread usage , but have not gained universal acceptance & ceramics have yet to prove
their superiority over autografts & preserved allografts in the middle ear & mastoid
reconstruction .
Indications of tympanoplasty
It is indicated to eliminate the middle ear infection or to restore the sound conducting
mechanism .
Contraindications to tympanoplasty
1. Malignancy of the temporal bone .
2. Invasive uncontrolled life threatening infections .
3. The following conditions should be left alone ;
a. Only hearing ear (or much better one) .
b. Repeated surgical failure .
c. Non-functioning Eustachian tube .
d. Recurrent protrusion of the prosthesis .
4. Age
- Old patient , there is no contraindication in general condition , then no problem
- There is controversy in children , arguments against tympanoplasty are ;
a. Dysfunction of the Eustachian tube .
b. Increased incidence of URTI .
c. Small diameter of child’s ear canal .
These are strong arguments for postponing the operation in children .
Preoperative evaluation & workup
Preoperative preparation is to maximize the rates of take for a graft , the infection should
brought under control at least 30 days before surgery is performed .
1. Analysis of the symptoms & signs
By this allows physician to determine the need for surgery , its urgency & anticipated
results , otorrhea , hearing loss , pain , vertigo & paralysis or paresis of the facial
nerve.

Lecture notes in
2. Otological examination
Otoscopical & microscopical , to look for perforations , size & site , also special
attention should be paid to the pars flaccida where not rarely small perforations may
be covered with dried crusts .
Also look for the status of mucosa of the middle ear , normal or near normal mucosa
is favorable for prognosis , sequamous epithelium or granulation tissue in the middle
ear represent more aggressive disease .
3. Complete otolaryngological clinical examination .
4. Audiological evaluation ; PTA , speech reception level & discrimination score .
5. Radiological evaluation
Should be adopted according to the clinical findings ;
a. Lateral (Schuller) plain view of mastoid .
b. CT scan , high resolution .
c. MRI with Gadolinium differentiate granulation tissue (enhanced on T1-
weighted) from cholesteatoma which does not enhance , while cholesterol
granuloma results in bright signals in all spin-echo pulse sequence .
CT & MRI of temporal bone to detect ; complications , large masses of
granulation tissue , suspicion of tumor & atypical evolution .
6. Investigations apart from radiological & audiological
CBP , platelets , PTT , PT , medical evaluation (above 40yeras) ..etc .
Approaches & techniques
- Anesthesia ;
1. GA ; hypotensive technique with LA /adrenaline infiltration to the external meatus .
2. L A ; 2% lignocaine with 1:200000 adrenaline , with sedation (Midazolam) .
- Position ; supine , reverse Trendelenberg , sandbag under shoulder (5 cm) & head ring .
- Incision & approaches ;
a. Permeatal .
b. Endaural .
c. Postauricular .
Every case needed to be evaluated on the basis of whether disease excision require a
purely transcanal operation or whether in addition some form of mastoidectomy was
needed together with tympanoplasty .
When mastoidectomy is necessary , two basic surgical techniques have been evolved
namely ;
1. Canal wall down , in which we have either small cavity which epitheliaze rapidly or
large cavity which prone to recurrent infection (need for either obliteration
technique or posterior canal wall & attic reconstruction) .
2. Canal wall up , in which we will face residual disease or recurrent disease , so all
closed operations need to be staged & second look operation (revision surgery)
indicated .
- Surgical technique ;
1. Myringoplasty
a. Onlay graft
Positioned lateral to the tympanic membrane remnant & malleus handle after
removing all sequamous epithelium (refreshing the edges) .
b. Underlay graft

Lecture notes in
Medial to the tympanic membrane remnants & malleus handle or medial to the
tympanic membrane remnants & lateral to the malleus handle .
c. Tympanomeatal allograft
Underneath the deep meatal skin cuff & lateral to the malleus handle .
d. Popin underlay technique
For small central perforations , autologous graft , fat , tragal perichondrium or
temporalis fascia inserted through the perforation onto gelfoam bed after
excising the perforation margins & scarifying the undersurface of the adjacent
tympanic membrane .
2. Ossiculoplasty
Used ;
1. Homograft , risk of Cruetzfeldt –Jacob disease (not used now) .
2. Autograft , use cortical bone or remodeled incus .
3. Alternatives ;
a. Implant materials like stainless steel , Titanium , Platinum , Tantalum , ..etc
, but they appear to be unstable & become displaced in the middle ear , so
their use abandoned
b. Biodegradabl porous hydroxyapetite tricalcium phosphate ceramic , which
replaced by osteogenic cells & host connective tissue .
c. Porous polyethylene prosthesis , by Shea 1976 , side effect is late fracture of
ceramic
Technique ;
a. Total ossicular replacement prosthesis (TORP)
When there is stapes footplate remnant with malleus , then do
myringostapediopexy or malliostaediopexy using autograft or ceramic .
b. Ceramic partial ossicular replacement prosthesis (PORP)
Stapes superstructures is intact & absent long process of incus , autograft
malleus to stapes or ceramic .
c. Incudostapediopexy
Using cortical bone or ceramic , prosthesis (incus to stapes assembly used
for incudostapedial joint discontinuity secondary to an absent lenticular
process or/& stapes head) .
To decrease the extrusion of the ceramic use autograft (tragal cartilage
interpositioned between the tympanic membrane & the prosthesis) .
Air-bone gap about 20 dB in 80% of PORP & 50% of TORP
Follow up & care ;
1. Dressing for 7-14 days .
2. Nasal decongestant used .
3. Valsalva maneuver in early postoperative period .
4. Avoid flying & diving for 4-6 weeks .
5. Swimming is contraindicated until healing .
There is an incudostapedial joint instability caused by absent long process of incus ,
a malliostapediopexy is performed , after removing & refashioning the incus to creat
a malleus to stapes assembly .
Disadvantages of ossicular autografts

Lecture notes in
1. Failure to control infection in CSOM after surgical removal of the disease

which may be due to retained ossicles in the middle ear .
2. The use of diseased autologous ossicle in tympanoplasty may prejudice the
results of reconstruction .
Advantages of allografts
1. The need to find a new material to reconstruct the ossicular chain in patient
without a malleus &/or incus &/or stapes superstructures or with severe
infection or cholesteatoma involving the ossicles
2. It is able to remain in the middle ear without resumption , this encourage the
surgeon to use ossicles bone allograft preserved in alcohol or by autocaving
from ossiculoplasty when healthy ossicle autograft is not available .
3. Apparent lack of immune or inflammatory response
Postoperative care
After completing the operation
 The canal is packed firmly with gelfoam & BIPP .
 The external dressing is fashioned according to the magnitude & procedure &
applied for 24 hours .
 Examine the facial nerve after recovery .
 Before discharge , Weber test is performed to exclude dead ear .
 The patient after 3 days can wash his hair without allowing water to enter into the
ear .
 Sutures removed after 5 days .
 BIPP is removed after 3 weeks under microscopy .
 Scheduled future visits until the ear heal completely
 Repeat PTA after 3 months .
Complications
1. Graft failure ; it caused by :
a. Inadequate Eustachian tube function .
b. Persistent mucosal disease .
c. Recurrent or residual cholesteatoma .
d. Extrusion of the prosthesis .
e. Poor surgical technique , badly placed graft or bulky graft .
f. Fibrous adhesion between the graft & the promontory .
g. Bulky (skin) graft which continue to secret sebum & lead to infection & necrosis .
h. Perforation & epithelia cyst & graft cholesteatoma .
2. Decreased hearing .
3. Facial nerve palsy .
4. Vertigo .
5. External canal stenosis .

Lecture notes in
OTOSCLEROSIS
It is an autosomal dominant disease of incomplete penetrance affecting the bone drived
from the otic capsule in which mature lamellar bone replaced by woven bone of greater
thickness , cellularity & vascularity .
It is charcterized by an alternating phases of bone resorption & formation
The primary pathological changes occurs in part of the periotic capsule (bony labyrinth)
which has secondary effects upon middle & inner ear audiotry function .
The primary changes is one of irregular ossification occur in the region of the fissula ante
fenestrum principaly & the main secondary effect is the ankylosis of the stapes .
Aetiology
- The exact cause of the disease is unknown; however, a heterogeneous group of genetic
disorders affecting the development of the endochondral bony labyrinth is generally agreed
responsible .
- Reports implicate the measles virus plays an important role in gene activation of
otosclerosis. This hypothesis is supported by a declining incidence of otosclerosis since
measles vaccinations became widespread.
- Otosclerotic changes may appear as a result of interaction between bone growth
promoting substances circulating in blood (late pregnancy , after fractures of other bones
...etc) & the unstable cartilagenous elements in the capsule of the labryinth .
- There were many theories (with unproved suggestions yet) of causation & promotion of
otosclerotic changes , inculding ;
(1) Inflamatory process (2) Disturbance of blood supply
(3) Skull stress factors ; anatomical & histological abnormalities in the temporal bone .
(4) Collagen diseases , increase in the anticollagen type II in otosclerosis .
(5) Osteoblastic dysfunction ; Paget's disease & osteogenesis imperfecta .
(6) Unstable nest of embryonic cartilage within the otic capsule & enzyme activity drived
from the inflamatory monocytes , recruited by immune reaction in these nests leading to the
disease .
(7) Cell degeneration in the labyrinthine bone releasing Ag in the circulation causing
intolerance leading to the disease .
(8) Trauma . (9) Metabolic .
- As a result of advanced studies using electrom microscopy & biochemical studies , it also
has been suggested that (1) release of lysosomal enzymes derived from histiocytes within the
otosclerotic foci results in lysis & resorption of bone (2) high concentration of oestrogen
are known to increase the fragility of lysosomal membranes (another explanation for
deafness progression in pregnancy) (3) otosclerosis is a connective tissue disorder in which
the primary changes affect the bony ground substance .
Incidence
- It was commonly accepted to be one of the most frequent causes of deafness in active
adults , its incidence in the general population (western world) is about 1% (0.5-2%) .
- Histological changes of the disease have been found in about 13% of caucasean temporal
bones (only 10% of them have clinical defects in hearing) .
- It is found more in fair –haired races (generally limited to the white population) .
- It is rare in the Mongoloid or Negroid ( Caucasean : Others 10:1) .

Lecture notes in
- It is believed to be twice as common in women as in men (probably in fact no difference

in incidence in between sexes) , the apparent female predominance may be due to
noticeable deterioration of hearing during pregnancy .
- Female have 3 times Air-Bone gap of 30 dB or greater
- 70% of cases the deafness noticed between 11 and 30 years old .
- Deafness due to otoseclerosis initiated or made worse by ; pregnancy , menopause &
those undergone stress associated with trauma as in major operations & accidents .
- Tendency for otosclerosis to run in famillies are ; (1) thought to have secondary cases in
70% of patients (2) the disease can be traced through several generations (3) 30% of cases
appears to be sporadic (degree of penterance vary from case to case) (4) almost 50% of
those carry the abnormal gene develope clinical disease .
The effect of prolonged noise exposure in patient with otosclerosis ; (1) it make the cochlea
more sensitive to the damaging effect of the noise in the early stages of the disease with
minimal hearing loss (2) marked conductive deafness not protect the patient from the
damaging effect of the high level of industerial (3) those with conductive loss caused by
otosclerosis show a high frequency of sensorinueral deafness which is typical of noise
induced hearing loss .
Otosclerosis and pregnancy ; 50% have no effect , 42% have associated hearing loss , the
risk of hearing loss from any pregnancy in women with stapedial otosclerosis about 1:24 ,
pregnancy aggrevated deafness in 33% in one pregnancy to 63% after six pregnancies in
bilateral cases , while in unilateral cases the pregnancy related deterioration of hearing
loss less common .
Pathology
- Macroscopical ;
1. Any part of the bony labyrinth can be affected , but , the commonest site is fissula ante
fenestrum (immediately infront of the oval window) which is the 1 st site of residual cartilage
into adult life , other sites of residual cartilage are (1) fissula post fenestrum (2)
intracochlear (3) cochlear (round) window (4) semicircular canal (5) petrosequamous
suture & capsula beneath (6) base of styloid process .
2. Approximately 2% of patients display both labyrinthine and ossicular chain involvement
, In 8% of patients the process involves the cochlea and parts of the labyrinth (labyrinthine
otosclerosis) , resulting in sensorineural hearing loss , In 80-90% of patients, lesions are
limited to the anterior oval window and affect its pathology by calcification of the annular
ligament or by involving the stapes .
3. 70-80% are bilateral & 10-15% unilateral .
4. The otosclerotic exostoses clearly seen under the operating microscope , they are whiter
& softer to instrumental touch than bone of the promontory, it appears most often to have
erupted like lava from the fissula & to have encroched in a variable degree upon the
anterior region of the stapedial footplate (less frequently arise in the footplate itself) .
5. The gross appearances may be classified by thier ankylosing effect into four types , on
the basis of appearance & the technique required to remove the stapedial footplate ;
a. Type 1 ; the stapes minimally fixed in the oval window niche , so they can removed in
total without fenestration .
b. Type 2 ; the footplate appear to be thin having milky opalescence , it can be removed
piecemeal after bieng perforated with needles .

Lecture notes in
c. Type 3 ; the footplate are thick , chalky & opaque , but can still be removed
piecemeal with perforating picks .
d. Type 4 ; the footplate are very thick & tightly fixed & have to be drilled before removal
are possible , in extreme variant , the fossa may be totally obliterated by otosclerotic
bone (obliterative otosclerosis , in which the oval window is filled with a mass of
unusually dense new bone ) with only the head , neck & upper part of the crura of the
stapes visible , s.t. the foot plate rim can't be identified & the crura enveloped , here
the cobductive hearing loss appear in childhood or adolescence due to low levels of
fluorine in dinking water (especially south of Austeralia) .
6. The borders of the round window , 2nd important site where otosclerotic bone can be
found , have a significant relation regarding the deafness & otosclerotic closure of the
round window may occur in 2% of cases .
7. More than one focus in one labyrinth is present in half of cases & bilateral , often
asymmetrical foci occur in three quarters of cases .
- Microscopical ;
1. The normal endochondral bone of the labyrinthine capsule is compact in type .
2. The lamellae composed of fine fibrils lying in a ground substance ,
are concentrically disposed around Haversian canals containg the
blood vessels & connective tissue , between the lamellae are the
branched osteocytes which lies in lacunae connected by countless
minute canaliculi whithin it the branched processes of the osteocytes &
small blood vessels .
3. In otosclerotic foci , the new bone formation could be differentiated
from normal bone by thier marked enlargement of bone spaces & Haversian canals , these
appearance may be summarized as showing three distinctive departures from normal ;
a. focal or diffuse replacement of the normal compact bone by an irregular , losser
cancellous structure of new , more deeply staining lamellae .
b. increase in the size of Haversian canals , cell spaces , caniliculi & marrow spaces
with corresponding increase in vascularity , the blood vessels frequently being surrounded
by marrow margin or mantle of blue staining material .
c. increase in osteocytes & appearance of osteoblast & osteoclast cells .
4. The lesion is a pleomorphic replacement of normal bone with spongiotic or sclerotic
bone. The histiologic disease not orderly progressed in stages. Bony resorption and
replacement with new spongy bone characterize early lesions. Osteolytic osteocytes appear
at the leading edge of the lesion, and sheets of connective tissue can be observed replacing
the bone. Formation of dense sclerotic bone in areas of previous resorption signifies the
late phase of otosclerosis. The result is disorganized bone, increased population of
osteocytes, and enlarged marrow spaces containing vessels and other connective tissue.
Spaces are later replaced by dense sclerotic bone with narrow vasculature and few
recognizable haversian systems. Pleomorphism is largely due to normal coexistence of both
stages of otosclerosis in any single temporal bone.
5. More recent studies of living otosclerotic bone have provided further histopathological
details of the activity & extent of the disease ;
a. Early focal otosclerosis ; the abnormalities localized to one or two small areas of
otherwise normal footplate section , this areas shows an enlarged marrow spaces
surrounded by blue-staining area in which fibrillar material can't be seen .

Lecture notes in
b. Diffuse active otosclerosis ; the abnormal vascularity with great increase in size &
number of marrow spaces , most of the spaces are lined by osteoblasts , in palces around
the circumference of marrow spaces there is a scalloped appearance where the bone may be
recently absorbed , inbetween the marrow spaces the ground substance stains blue or dark
bluish-red & the cement between plates of bone are increased & vary greatly in size ,
staining intensity & orientation toward each other.
The active disease charcterized by the presence of ; (1) vascular spaces containg highly
cellular fibrous tissue (2) mononuclear histiocytes together with osteocytes & osteoclasts
are prominent (3) finger like projections which are spaces produced by resoprption of
perivascular bone (4) clearly defined boyndaries between normal & abnormal bone .
c. Quiescent otosclerosis ; there may be some increase in size & number of marrow
spaces with no evidence of recent bone formation or destruction , the osteoblasts &
osteoclasts are only occasionally seen , the ground substance is markedly irregullar & not
difficult to seen , the least active areas may be difficult to distinguished from normal , very
sclerotic bone being relatively avascular with homogeneous , pale pink , staining ground
substance & few cells .
When the otosclerotic process start , as a phase of activity , with very vascular lesion
within which a new , woven , irregular bone is being laid down , this activity is more
vigorous the younger the age at onset , later , there is healing as the disease become
quiescent with reduction in vascularity & no sign of recent bone resorption or of new bone
formation .
The final inactive stage consist of ; (1) highly mineralized bone with mosaic appearance (2)
osteoblasts &/or osteocytes still in peripheral area (osteoclasts disappear) (3) vascular
spaces are narrowed or obliterated by new bone formation & the lamellar bone which is
formed thicker & more cellular than normal bone .
d. Cochlear otosclerosis ; the otosclerotic foci do occur in the otic capsule without the
involvement of stapedial footplate , usually near to one or other window , but occasionally
in the cochlear capsule , there were recognizable atrophy of the spiral ligaments in parts of
the cochlea adjacent to otosclerotic activity .
N.B: The histological variants of otosclerosis can be staged into (1) active (2) intermediate
(3) final inactive .
Clinical features
- Often this process reveals a family history of otosclerosis.
- The presenting Symptoms are ;
1. Deafness
- 1 st noticed in most cases between the ages of 11 & 30 years , a small proportion occur
before the age of 5 & a smaller proportion after the age of 50 .
- Onset is insidious & the deafness affect only one ear may pass unnoticed .
- Progress ; is inexorable , but often uneven , in some cases an early period of rapid &
contineous deterioration followed by long period of stability , in others there may be a
steady decline in hearing acuity .
- presence of Paracusis Willisii , the ability to hear conversation better in the noisy
surrounding (public transports , machine shops , engine rooms & like ) is a feature of
deafness seen in 80% of cases , this due to the fact that in this places speakers
automatically raise their voices .

Lecture notes in
- the Deafness unnoticed until the loss reach 25-30dB when there is difficulty in
understanding the speech .
- s.t. hearing loss equal in each ear , but , in the others could show greater loss in one
ear , in unilateral cases (15%) the deafness confined to one ear & the other may affected
late .
- patient with pure conductive loss shows SNHL in later years more than that expected
in ageing .
2. Tinnitus ; it is common (80% of cases) , occasionally the presenting feature , tend to
worse in patients with associated cochlear loss & during episodes of rapid progression , it
s.t. seen without cochlear degeneration & it is more indicate SNHL , it may be unilateral or
bilateral , roaring , hissing or pulsatile charcter (varies in charcter & its subjective effect
upon the patient) , more common in the early stages & disappear as the lesion mature
(spongy vascular bone replaced by hard sclerotic bone) .
3. Vertigo ; transient in nature , thought to be due to toxic ebzymesinto the vestibular
labyrinth , experienced commonly as slight momentary dizziness after head movements ,
especially after stooping down , it is an associated symptoms in 25% of cases , the cause is
uncertain & caloric tests are normal .
Other variety of vertigo could be due to vestibular hydrobs secondary to capsular
otosclerosis or s.t. the coexistance of Miniere's disease .
4. History of episodes of ear disease , head injury , noise exposure , ototoxic drugs , bone
& joint diseases , must be taken seriously as these factors important in the Dx & Rx .
- Signs ;
1. Patients often exhibit low-volume speech.
2. Otoscopy ; fails to reveal any abnormality , in just 10% (or over) the memberane has a
pink tinge (flamingo-tint of Schwartze) , imparted to it from dilated vessels on the mucosa
covering the promontory which accompanied the increased vascularity over the active
otosclerotic foci .
It may show thick or atrophid TM , rigid or immobile due to prior inflamtry diseases .
3. Hearing tests
a. Simple speech tests , using conversational & whispered voice , Barany noice box can
used to mask the other ear , the effect of trying hearing aid , the patient not shows
recruitment & are able to hear the amplified sound clearly .
b. Tunning forks tests ; the commonly employed Rinne & Weber test shows in most
cases pure conductive deafness .
c. Pure Tone Audiometry ; this is an essential test for pre- & post-operative hearing
assessment , shows initially pure cobductive deafnesss , sometimes later there will be
deterioration of cochlear function , measurments for both air & bone conduction , the
gap between the two provide a measure of the deafness & results of Rx .
d. Speech audiometry ; it is valuable preliminary to Rx , since by the ration of
intelligibility to amplification of sounds ,when the deafness conductive the score can
reach 100% with higher intensities , but never reach so in senorineural deafness (the
intelligibility affectted with high intensity) .
e. Impedence audiometry ; usefull investigations in the DDx , tympanometry usually
reveals the normal (type A) tympanogram, compliance usually reduced , but there is
great an overlap between the normal & the otosclerotic patients , when the stapes

Lecture notes in
fixation present the stapedial reflex is abscent in the probe in the ear under test (as
expected in conductive deafness) .
4. Radiological demonstration of otosclerosis ; the conventional radiography &
tomography have a little value in the Dx & doesn't give adequate informations , while
multidirectional poly tomography may be of value (capsular changes may be idenified) , &
high resolution Computed tomography scanning of the temporal bone can often
demonstrate foci of demineralization in the otic capsule in cases of cochlear otosclerosis.
Stages of deafness in otosclerosis
- Stage I (no cochlear impairment)
Rinne Test ; negative at all frequencies .
Weber Test ; lateralized to the affected ear .
Schwabach's Test ; normal showing no loss of absolute bone conduction .
audimetry ; Air conduction shows loss on all frequencies , greater on low tones (slope to
left) , never exceeds 60 dB .
audiometry ; Bone conduction may be normal or in low tones it may better than normal ,
characteristic finding is a dip centred at 2000 Hz "Carhart's notch" .
Speech curve is parallel to normal .
- Stage II (slight cochlear impairment)
Rinne Test ; always negative at all frequencies .
Weber Test ; lateralized to the more affected ear .
audimetry ; Air conduction loss may exceed 60 dB , the curve is flattened .
audiometry ; Bone conduction remains better than air , but the dip at 2000 Hz
accentuated .
Speech curve still shows 100% intelligibility on adequate amplification (parallel to or a
slight slope from normal) .
- Stage III (moderate cochlear impairment)
Rinne Test ; still negative in low frequencies only .
Weber Test ; may not be lateralized to the better ear due to sensorineural loss .
audimetry ; Air conduction shows marked loss at high frequencies , curve slope to right &
loss may reach 90 dB .
audiometry ; Bone conduction indicates unmistakeable high tone loss & impairment of
cochlear acuity .
Speech curve is variable , may slope away from normal with low intelligibility score .
- Stage IV (severe cochlear impairment)
Rinne Test ; still negative in low frequencies only .
Weber Test ; generally lateralized to the better ear .
audimetry ; Air conduction shows severe loss at all frequencies , high tones may not be
registered .
audiometry ; Bone conduction shows severe loss , the signal may not be heard at any
frequency .
Speech curve shows poor intelligibility with shift to the right beyond 70 dB & score
seldom exceeding 70% .

Lecture notes in
In summary otosclerosis can Diagnosed from th following

A. History ; (1) Progressive hearing loss (present) (2) Tinnitus (present/absent) (3)
Vestibular symptoms (present/absent) (4) Otitis media/otorrhea (absent) (5) Head trauma
(absent) .
B. Physical examination;(1)Tympanic membrane(normal) (2)Schwartze’s sign
(present/absent) (3) Rinne test (negative) (4) Weber’s test (lateralizes to conductive
hearing loss)
C. Ancillary studies ; (1)Audiogram (conductive, mixed, or rarely pure sensorineural
hearing loss; Carhart’s notch) (2)Tympanometry (reduced tympanic membrane
(3)compliance, absent or “on-off” stapedial reflex) (4)Imaging (radiolucent areas around
cochlea)
Differential Diagnosis
1. Secretory otitis media (OM with Effusion) ; absent tinnitus & vertigo , translucent
TM (fluid may or may not seen) , typical tympanometry (flat) , x-ray shows reduced
pnuematization , in adults usually unilateral due to pathology in the postnasl space .
2. Middle ear fibrosis (Chronic adhesive OM) ; the TM normal shaped but usually
retracted or thickened , immobile , affected one or all ossicles & the tympanogram & x-ray
will establish the diagnosis .
3. Tympanosclerosis ; with only minor changes in the TM severe conductive deafness ,
if the deposits immobilize the stapes or malleus or incus , tympanometry shows reduced
compilance , x-ray shows lack of translucency of mastoid air cells .
4. Congenital footplate fixation ; important to distinguish this disease as stapedectomy
carries a risk of perilymph floading (gusher) causing SNHL , the deafness is not progressive
& the PTA shows upsloping curve & best air conductive at 2 kHz (suggestive) , if bilateral it
will affect the speech , unilateral usually diagnosed in late childhood or early adulthood .
5. Ossicular discontinuity ; traumatic dislocation of the incus as a result of RTA
(bleeding from ear & facial palsy) , head injury & blow on the ear , or unskilled attempt to
remove F.B. pushing the TM , tympanometry shows abscent stapedial reflex with abnormal
compliance & low impedence , in polytomography ossicular chain abnormality .
6. Fixed malleus –incus syndrome ; 2% of tympanotomies shows fixation of the incus
or malleus or both , but stapes not immediately involved , with stapedectomy no
improvement , so we meust check the mobility of malleus & incus intraoperatively ..
7. Congenital cholesteatoma ; primary cholesteahead behind intact TM causing
conductive deafness , with careull examination we can see the cholesteatoma , tympanotomy
with removal of the cholesteatoma with or without mastoidectomy which if needed ossicular
chain reconstructon .
8. Fluid in the middle ear (CSF or Perilymph) ; head injury or congenital
communication between subarachnoid & mastoid air cells (Hyrtl's fistula) , CSF (clear fluid
in the middle ear which refill after aspiration) , this faced during the operation .
Perilymph in the middle ear leaking from the scala vestibuli fracture or stapes fracture , or
in ruptured round or oval window secondary to explosive forces affecting the labyrinthine
fluid , also can occur with Mondini deformity & congenital middle ear deformities .
9. Persistant stapedial artery ; large rtery my cover the footplate & immobilize the
stapes leading to conductive hearing loss without footplate fixation (operation
contraindicated) .

Lecture notes in
10. Paget's disease ; rarely causing conductive hearing loss , occur after the age of 45 ,
in early stage CHL with high tone SNHL , the cause of CHL is ossicular fixation (esp.
malleular head) , the operation are illogical as there is no histological evidence of stapedial
fixation .
11. Osteogenisis imperficta ; there will be progressive SNHL & CHL , abscence of
Schwartze sign , abscence vertigo , tympanometry shows abscence of stapedial reflex with
very high compliance , here the defness Rx surgically but this must be delay untill the
spontaneous fractures ceased , floating footplate found at the operation
Treatment
1. conservative Medical Rx
- Medical therapy for otosclerosis should be considered for patients in the following
categories:
1. Those who for any reason are not surgical candidates .
2. Those who decide against surgery .
3. Those who have only sensorineural hearing loss or vestibular symptoms believed to be
due to otosclerosis .
- Sodium Fluride ; reduce the osteoclastic bone resorption & increase osteoblastic bone
formation , also it have an antienzymatic action on proteolytic enzymes which are cytotoxic
to the cochlea & produce sensorineural deafness .
So it will cause recalicification of the active foci (inactivation) , fading og the Schwartze
sign , stabilization of the progressive SNHL & reduce tinnitus & improve the mild vestibular
symproms .
There is radiographic evidence of recalicification of diffuse otosclerotic lesions following
the adminstration of Na-fluride 50mg /d for 2 years (can increased to 75mg in active cases)
with daily maintenance of 25mg for the rest of life . This could be given in an enteric coated
tablets supplemented with calcium & vitamin D (BPC) .
It is recommended in some centres for ; (1) very active disease -+ve Schwartze sign- (2)
delay the progress of cochlear otosclerosis (3) surgically confirmed disease with
progressive sensorineural deafnees disproportionate to age (4) patient with pure
sensorineural deafness with criteria sugessting cochlear otosclerosis (5) patient in whom
CT shows spongiotic changes in cochlear capsule .
It contraindicated in ; (1) chronic nephritis with nitrogen retension (2) chronic rheumatoid
artheritis (3) pregnancy & lactation (4) children before completing full skeletal growth (5)
allergy to fluride (6) patient with skeletal flurosis (rare condition in certain area of India) .
Adverse effect of the Rx are ; (1) gastric upset (2) flare up of symptoms of DU (3) increase
in joint symptoms in those with chronic artheritis (4) skeletal flurosis .
Hearing aids ; All patients with conductive hearing loss caused by otosclerosis may use
hearing aids as an alternative to surgery; this should be discussed with the patient as an
option. If the patient has a significant sensorineural component to the hearing loss, a
hearing aid may be required even after successful stapedectomy. A patient with far-
advanced otosclerosis requires a hearing aid at all times, but with a successful surgery, the
patient can use a much less powerful hearing aid. Many require time to adjust to the new
hearing level and are sensitive to the sound of the hearing aid. It may take as long as 4
months before these patients can tolerate and benefit from the hearing aid .

Lecture notes in
2. Surgical Rx
Surgical therapy remains the mainstay of treatment for conductive hearing loss from
otosclerosis , surgery has developed through 3 distinct eras;
1. The Mobilization era began in the late 1800s when Kessel attempted stapes
mobilization without ossicular chain reconstruction in cases where it was noted to be fixed.
Later, Jack removed the stapes, leaving the oval window open. Both techniques allowed
increased transmission of sound through the oval window but did not use middle ear
amplification structures. Furthermore, fatal cases of meningitis from intraoperative
exposure of perilymph to bacteria occurred, and any gains in hearing frequently were
temporary because any remaining stapes footplate often refixed.
2. The Fenestration era began in 1923, when Holmgren created a fistula in the
horizontal semicircular canal and sealed it immediately with periosteum. This procedure
allowed sound conduction preferentially through the fistula, rather than the ossicular chain.
Sourdille popularized the procedure when his 3-stage technique was widely published
during the 1930s. Lempert developed a 1-stage technique for horizontal semicircular
fenestration, which went on to gain worldwide acceptance after it proved to enhance
hearing. Results, however, were short-lived because the fenestra often resealed with bone.
3. The Stapedectomy era began before the fenestration era closed. Rosen revisited stapes
mobilization in 1952. Later, Shea removed the stapes, sealed the oval window with an
autograft vein wall, and then reconstructed the sound-conducting mechanism with an
artificial prosthesis. This technique gained wide acceptance and has been improved since
inception. In the 1970s, Myers conducted stapedotomy using a piston prosthesis. In the
early 1980s, Perkins began using the laser for stapedotomy in a procedure in which a small
hole is made in the footplate, as opposed to complete or subtotal removal. Several
techniques and approaches are commonly used today, with largely excellent results. A few
challenges remain, such as those patients enduring sensorineural hearing loss and
unsteadiness, but many think surgical treatment for otosclerosis has reached perfection.
The Operations ;
Stapedectomy is the removal of one half or more of the footplate to position a prosthesis
into the vestibule & ellviate the conductive hearing loss , advantages of stapedectomy ; (1)
easier technique & give good results , disadvantages ; difficult in obtaining accurate
followup .
Stapedotomy is the removal of 0.8 mm segment of the posterior portion of the footplate to
bypass the otosclerotic footplate fixation & alleviate the conductive loss , advantages of
stapedotomy ; (1)Cochlear trauma is greatly reduced (2) Great reduction of the
stimulation of the otosclerotic foci which may lead to release of cryptolitic enzyme into the
vestibule , the disadvantage ; tendency of disarticulation of the prosthesis .
LASER in stapedotomy
Perkin's in 1980 introduce the argon Laser for stapes operations
The advantages are ; (1) better ability to prepare the bloodless fenestra (2) reduce risk of
footplate subluxation (3) equally good hearing results with other techniques .
The disadvantages are ; (1) postop. vestibular symptoms in 39% of cases due to increase
perilymph temperature (2) over all serious inner ear trauma has not yet been reported .
Indications
1. Average patient bone conduction level of 0 to 25 dB in the speech range and air
conduction of 45 to 65 dB .

Lecture notes in
2. Minimum air-bone gap of 15 to 20 dB and word recognition of 60% or better .

3. Unilateral or bilateral otosclerosis .
4. Preferably, a negative (absent) stapes reflex .
5. Criteria may be expanded for advanced otosclerosis; a patient with a bone conduction
level of 45 dB or lower and an air conduction level as high as 95 to 100 dB may be
candidate if he is not suitable for stabedotomy (to enable then to wear hearing aid) .
6. Preferably, a negative Rinne on tuning forks 256 Hz and 512 Hz .
Contraindications
1. Active Meniere's disease .
2. Better-hearing ear or only hearing ear .
3. Avoid spongiotic phase of “active” otosclerosis , Rx medically then plan for surgery .
4. External otitis or otitis media , should managed 1 st .
5. Unfit for surgery .
6. Age more than 70 , risk of fistula formation & 40% chance to worsen discrimination .
7. Children .
8. Conductive deafness for other causes .
9. Early fixation with small hearing loss .
10. Unilateral otosclerosis .
11. Poor air – bone gap (benifit from hearing aid) .
12. Vertigo & fluctuating hearing loss (dead ear) .
13. Pregnancy ( delay to after labour) .
14. Occupations demands physical starin , sports & airman .
15. Revision stapedectomy (fine adhesion between the footplate & saccule & cochlear duct .
16. Poor eustachian tube fubction in one ear & bilateral otosclerosis (operate the better) .
17. 2nd ear surgey still contraversial , risk of immediate or delayed SNHL or vestibular
damage , it has advantage of restoration of binaural hearing & the ability to localized
sound direction
1. Informed consent and probability of surgical success carefully explained , the patient
should informed about ;(a) 85% chance of improved hearing (b) 10% chance of slight
improvement (c) 5% chance of some degree of SNHL which may become total (dead ear
may result & the incidence by expert otologist is 1-4%) (d) ear may fail after good result
years later & further 10% have no benifit from surgery (e) also tinnitus may not improve &
may be more intense after surgery (f) vertigo may present immediately postop. & in
minority may be perminant sense of imbalance , also (g) transient weakness of facial
muscles (h) taste loss due to damage of chorda tympani (bilateral surgery) .
2. The alternative of a hearing aid is discussed .
3. Reasonable medical status for local anesthesia with sedation .
Intraoperative Problems
1. Various footplate anomalies require experience in management, such as a biscuit
deformity or drill out procedure for obliterative otosclerosis.
2. Surgeons performing stapes surgery should be prepared to do malleus to oval window
(ie, incus bypass) techniques , the narrow oval window niche is be exposed & the
overhanging bone removed .
3. Unexpected cerebrospinal fluid gushers may require management , this occur in patent
choclear aqueduct , most commonly occur with congenital fixation of footplate .

Lecture notes in
4. A floating or subluxed footplate is best left alone , with the prosthesis positioned over a
mobilized footplate .
5. there is a small chance that the facial n. will run an anomalous course (0.5%) , either
splitting around or coursing inferior to oval window & may be injured .
6. Persistant stapedial artery (0.2%) causing troublesome bleeding , avoided by
stapedotomy.
7. Presence of blood in the vestibule .
8. TM tear , small tear can underlied with gelatin spong , large one we rotate the flape &
cover with gelatin spong , if not enough do grafting , healing almost always occur .
9. Obliterative otosclerosis , carry high risk of damaging the cochlea , stapedotomy more
safe .
1. Vertigo, which is most commonly the result of hydrops, responds to bed rest. If
prolonged, consider a long prosthesis or slipped prosthesis. If delayed, evaluate the patient
for a reparative granuloma or fistula.
2. Facial paralysis is unusual but can occur, usually because of an aberrant mucosa-
covered nerve.
3. Cochlear hearing loss may be the result of vascular phenomena or caused by a foreign
body reaction or intralabyrinthine disruption.
4. Dysgeusia secondary to chorda tympani generally is temporary and disappears in a few
months.
5. Late complications may include hearing loss with incus necrosis; wire loop problems, a
perilymph fistula, and others causes are rare.
6. Meningitis is rare.
7. Tympanic membrane perforation
8. Cholesteatoma may be prevented by scrupulous attention to surgical procedures.
9. The patient should avoid ; (1) diving or swimming , lifting heavy objects (2) agressive
nose blowing (3) flying for the 1st 3 weeks postop. (4) closing the mouth on coughing or
sneezing .
10. Postoperative hearing results reveal closure of the air-bone gap to within 10 dB of the
preoperative bone-conduction level in about 90% of patients .
Complications
1. Peropeartive ; (a) tympanic membrane tear (b) chorda injury (c) overhanging facial
nerve (d) persistant stapedial artery (e) tympanosclerosis arthrodesing the incudostapedial
joint (f) perilymph floading (g) floating footplate (h) depressed footplate (i) injury to
saccule .
2. Postopeartive ;
(a) Early ; (1) detached prosthesis from the incus (2) displaced prosthesis from oval
window (3) loose attachement of incus & prosthesis (4) footplate granuloma (5)
persisting primary perilymph fistula .
(b) Late ; (1) secondary perilymph fistula (2) necrosis of the long process of incus (3)
late detachement or displacement of the prosthesis .
- Perilymph fistula ; the most common single complication , it is potentially dangerous
because it carry risk of meningitis & may rise to vertigo & hearing loss .
The aetiology of it could be , primary fistula could be created by the surgeon in every
stapedectomy & relise on the natural process of healing or use of a graft of soft tissue to

Lecture notes in
seal the openening , the secondary fistula could be acquired due to barotrauma which
break the fragile seal & can occur at any time postoperatively .
It can be prevented by ; (1) use of vien graft to avoid the thin memberane that develope to
close the oval window if fat or gelfoam is used (2) if greater part of the footplate removed
then increase the chance of fistula (3) perform a stapedotomy with small openening .
The clinical features are ; (1) TM usually normal , rarely retracted or fluid in the middle
ear (2) audiometric tests ; PTA show SNHL in low frequency followed curve with
fluctuation , speech discrimination score are fluctuant & then become poor , caloric test
shows canal paresis or hypoactive response (3) electronystagmography ; directional fixed
positional nystagmus (not relied upon as indication of fistula) (4) fistula test ; -ve in 1/3rd
of cases .
Dx is by radioactive tracer method ; injection of of radioactive Indium –III DTRA into
lumbar subarachenoid space , then detect the increase in the radioactivity in the
nasopharyngeal secretion strongly support the Dx .
In primary type the vertigo stay for days & weeks postop. until vestibular paralysis &
compensation occur , while the secondary type the change in hearing for months or years
after successful operation associated with fullness , tinnitus & dysequilibrium .
The proper Rx is by tympanotomy at the earliest possible moment & attempt to close it ,
the fistulous tract excised , prosthesis removed & put soft tissue graft to cover the
openening & new prosthesis .
- Immediate SNHL ; occur in 0.5-4% in the best expert hands , it may be due to ; (1)
acoustic trauma from drilling (2) excessive movement of the stapes produce hydrolic effect
damaging the memberanous structers (3) rupture of the memberanous labyrinth (4) rapid
loss of perilymph (5) footplate fragment or bone dust in the vestibule (6) floating footplate
(7) presence of blood in the vestibule .
The mangement depends on the technique , vien graft or small fenestra , carefull
monitoring of hearing postop. is important & the final speech score & PTA is done in the
20th day postop. , also mangement include bed rest , diuretics , H.C. in gradual tappering
dose , inhalation of 5% Co 2 & 95% o2 , NaFl therapy .
- Delayed SNHL ; although stapedotomy significantly reduce the loss of high tone
response with time , it certainly doesn't eleminate the problem .
Stapedotomy frequently doesn't provide better bone conduction at 0.5 kHz & provide less
satisfactory threshould at 1&2 kHz than does stapedotomy .
This lack of uniformity in result may be explained by ; the energy transmission to the
cochlea & the effect on the sensory apparatus .
Operative Technique
A. Stapedectomy .
- While the local anesthesia is working in the ear canal, a small amount of 1% lidocaine
with 1:100,000 epinephrine is injected above the ear, and a small incision is made in the
hairline and continued down to the temporalis fascia .
- A small amount of lidocaine is then injected underneath the fascia, and a small piece of
fascia roughly the size of a pencil tip eraser is removed , this wound is closed with
interrupted 3-0 Vicryl sutures in the subcutaneous tissues and a running 4-0 Vicryl
subcuticular stitch, this graft is placed in a press and then dried underneath a heating lamp.
This graft will be placed over the oval window before the prosthesis is put in
position.

Lecture notes in
- Using microscopic magnification, the ear canal incisions are made (endaural or
permeatal incision) . A #64 Beaver blade is used to make a curvilinear incision, starting
roughly at 6:00 o'clock, a few millimeters above the bony annulus, and reaching its apex at
3:00 o'clock, around the bony cartilaginous junction. A roller knife is used to continue the
incision back down toward the bony annulus near the neck of the malleus .
- After the fibrous annulus is raised, a gimmick is used to separate any
adhesions and lift the flap. If there is an overhang of the bony annulus
obstructing the oval window, a ‘‘super'' curette (eg, Xomed) is used to remove
part of the bony annulus .
- The curette is always used in the axis of the stapedial tendon to allow
posterior visualization of the stapes footplate, because this is the limit of the
dissection. No curetting over the incus prevents possible dislocation or subsequent
depression of the tympanic membrane. A larger right-angle pick can be used to open the iter
of the chorda tympani nerve to allow displacement for increased visualization .
- After adequate exposure is achieved, the amount of stapes fixation is assessed. This is
done by palpating the underside of the malleus to ensure there is no malleolar fixation.
Stapes fixation is usually made evident by a gentle rotary motion at the incudostapedial
joint. This ensures that there is no malleolar fixation and that the conductive hearing loss is
caused by the stapes fixation.
- Using standard measuring devices, the incus to footplate distance is measured . a
controlled fenestra is opened in the oval window footplate. An argon laser set at
1.5-A intermittent pulse is used. A small rosette is made in the center portion of the
oval window. A ‘‘skeeter drill'' using a diamond tip is used to finish the fenestra.
Care is taken to support the drill hand against the patient's head. The fenestra is enlarged
using a Farrior rasp .
- After the controlled fenestra is achieved, the stapes superstructure is
removed. Initially the incudostapedial joint is cut with a joint knife, and a
laser is used to cut the stapedial tendon and to mark the anterior and
posterior crura. These are then fractured, and a triangular pick and a cup
forceps are used to remove the capitulum of the stapes .
- Fascia graft is then placed over the controlled fenestra. As the fascia is
placed, it is initially laid in over the incus to allow it to form a cup in the oval window,
allowing the prosthesis to sit nicely.
- A piston-type prosthesis (eg, McGee, Robinson) can be used. The usual measurement is
0.6 mm X 4.0 mm. This is placed into the oval window fenestra .
- Once in place, the lenticular process is placed in the trough of the prosthesis,
and the hook is pulled up over or the hook is crimped. Positioning is ensured by
palpation of the prosthesis to check that it is in the oval window on fenestra. The
tympanomeatal flap is then laid back down.
- Because the patient is under local anesthesia, the hearing can be assessed. Usually, the
hearing is tested by normal speech and a barely perceptible soft whisper.
- After this is done, the ear canal is packed with strips of Owens gauze and a string
of pearls, which is small cotton balls sewn onto a long silk suture. The pearls are
placed in the Owens gauze, and the Owens gauze is folded over the top of these in the
canal. A cotton ball then is placed in the ear. This packing is usually removed in 1
week.

Lecture notes in
B. Stapedotomy
- The same exposure as above .
- Having gain visual access to the footplate , a defect is created 1 mm larger in its diameter
than that of the prosthesis 9using penteration needle , small diamond drill or laser) .
- The prosthesis placed so that it enter the fenestra & encircle the incus simultaneosly .
- Sectioning of the stapedious tendon , posterior crus is at its midpoint using crurotomy
scissor , the anterior crus fractured with mobilization needle .
- Stapes head & the remaining crura are severed using microscissors to seperate them from
the lenticular process .
- Two small pledget of gelatin spong placed around the fenestra .
Results of the surgery
Reports published over 20 years ago indicate that not all initially successful stapedectomy
results were likely to be maintained indefinitely , inspite of the excellent chance of an
immediate successful outcome , a hearing aid may be needed for many patients .
The requirements for patients benifit from surgery were assessed by Belfast (rule of the
thumb) for significant benifit to be acheived the postop. air conduction average over the
speech frequencies should be close to 30 dB or the interaural difference reduced to <15 dB
, this figure of 15dB correspond to the cross –attenuation effect of the skull .
In a study of 750 patients , the following categories of failure are concluded ;
a. immediate severe SNHL in 1.5% of stapedectomy , but not in any stapedotomies due
to the traumatic events during surgery .
b. delayed SNHL , with sudden onset 2% in stapedectomy , 0.6% stapedotomy (due to
surgically confirmed fistula) , or chronic progressive in 26% stapedectomy , 10%
stapedotomy .
c. immediate & delayed conductive loss causes due to ; incus necrosis , disarticulated
prosthesis , medially displaced prosthesis & lossely articulated prosthesis .
The hardly surprising findings in the study is the reassuring to know that stapedotomy can
on average effectively postpone the need for a hearing aid for longer than 20 years , a
period which can be extended by sodium fluride therapy .
Sensorineural hearing loss in otosclerosis
The deafness usually conductive , but the possible causes of cochlear degeneration are ;
1. Bony invasion of the scala tympani of the cochlea (Nager's theory) ; the main changes
occur in the labyrinthine capsule with minor alteration of the inner ear exam. , the
extensive bone formation in the sacla tympani then filled with new bone & the cause of
this is the otosclerotic focus in the wall of the labyrinth producing a certain alteration or
irritation of the endosteal layer & perilymphatic spaces resulting in circumscribed fibrosis
& bone production which found only in otosclerosis .
2. Circulatory changes in the cochlea secondary to the abnormal bony foci (Rnedi's
theory) ; this is only applicable in some cases ; (a) actively growing foci causing
thrombosis of the blood vessels adjacent to it , walled blood vessels lead to sharp
demarkation between the newly blood vessels in the otosclerotic foci & the old blood
vessels at otic capsule (b) connection between wide capillary of old otic capsule &
vascular spaces at the cative foci (c) flamingo flush which is shunt between the blood
vessels of the foci & the mucosa of the promontory (d) vascular shunt between the blood
vessels of the foci & the spiral capillaries leading to congestion of the modiolus resulting

Lecture notes in
in lamellar bone fromation secondary to this stasis (due to stimulation of the endosteal
capsule) .
3. Damage to the cochlea by toxic metabolites from abnormal bone ; (a) the foci erode
the endosteum & come in clos relation ship with the perilymph in the scala tympani which
then after mixing to enter the spaces of otosclerotic foci (b) across Reissner's memberane
& basal membrane to the scala media causing damage to the organ of Corti (c) there is a
correlation between the activity of perilymph proteolytic enzyme & SNHL in 75% in
stapedial otosclerosis
The otosclerosis is a localized disease due to the balance in between the activity of
ebzymes & antienzymes in the microfoci of the disease , this give a variable clinical
picture (stapedial foci cause CHL , cochlear cause SNHL , vestibular cause vertigo ..etc) ,
so Rx with antiebzymes or enzyme inhibitor is important .
Diagnosis of SNHL in otosclerosis
SNHL may preceed stapedial fixation , but usually associated with it , Shambaugh gave 6
reasons for suspecion that otosclerosis is the cause of SNHL ;
1. positve Schwartze' sign in one or both ears .
2. Family history of surgically confirmed stapedial otosclerosis .
3. presence of Symmetrical SNHL in both ears , one of which has stapes fixation .
4. A flat , rising or a Cookie-bite audiometric air conduction curve with usually good
speech discrimination test with pure SNHL .
5. Pure SNHL begiening insideously in early , middle adult life & progressing with no
appearent cause .
6. the demonstration of stapes fixation in patient with previous pure SNHL of no
appearent cause .
Adir-Dightton (Van Der Hoeve) Syndrome
It is a familial symptom complex charcterized by fragility of the bones , blue sclera &
deafness , deafness due to stapedial fixation by a disease process resembling , but not
identical to otosclerosis induced by the circulation of excess bone-growth-promoting
substances as a result of recurrent fractures .
The otosclerosis is always very active in charcter , the bone formation being soft & friable
& the flamingo tint is commonly present .
The attempts at mobilization have very frequently resulted in fractured stapedial crura
without gain in hearing , stapedectomy made difficult by unusually excessive bleeding but
good results from the operation can be expected .

Lecture notes in
FACIAL NERVE PARALYSIS

Embryology
By the third week of gestation, the fascioacoustic primordium gives rise to cranial nerves
VII and VIII. During the fourth week, the chorda tympani can be discerned from the main
branch. The former courses ventrally into the first branchial arch and terminates near a
branch of the
trigeminal nerve that eventually becomes the lingual nerve. The main trunk courses into the
mesenchyme, approaching the epibranchial placode.
The geniculate ganglion, nervus intermedius, and the greater superficial petrosal nerve are
visible by the fifth week.
The second branchial arch gives rise to the muscles of facial expression in the seventh and
eighth week . To innervate these muscles, the facial nerve courses across the region that
eventually becomes the middle ear.
By the eleventh week, the facial nerve has arborized extensively. In the newborn, the facial
nerve anatomy approximates that of an adult, except for its location in the mastoid, which is
more superficial (Development of the mastoid occur between 1-3 years of age & displace
the facial nerve medially & inferiorly) . .
The facial nerve develops within the 2nd pharyngeal arch adjacent to the derivative of the 1st
arch & 1 st external groove & internal pouch which the external & middle ear region , so
anomalies of the facial nerve should be anticipated in association with malformed external
or middle ear .
The facial nerve arrangement , the nerve may course with the chorda tympani , bifurcate ,
trifurcate or take aberrant pattern within the temporal bone , the nerve may be dehiscent &
may herniated into the middle ear .
The main pattern of the nerve complex course , branching pattern & relationships are
established during the 1st three months of prenatal life , during this period , the muscles of
expression also differentiated .
The nerve is fully developed by the age of 4 years .
Anatomy
The facial nerve, or cranial nerve (CN) VII, is the nerve of facial expression. The pathways
of the facial nerve are variable, and knowledge of the key intratemporal and extratemporal
landmarks is essential for accurate physical diagnosis and safe and effective surgical
intervention in the head and neck.
The facial nerve is composed of approximately 10,000 neurons, 7,000 of which are
myelinated and innervate the nerves of facial expression. Three thousand of the nerve fibers
are somatosensory and secretomotor and comprise the nervus intermedius. The course of
the facial nerve and its central connections can be roughly divided into 6 segments,Altered
function of the facial nerve following injury .
The facial nerve is a mixed nerve (motor , sensory & parasympathetic fibers) , it has 4
functional components (2 efferent & 2 afferent) ;
1. Efferent fibers
- Motor fibers ; to the posterior belly of the digastric muscle , the stylohyoid
muscle & the stapedius muscle & muscles of facial expression .
- Parasympathetic ; for lacrimation & salivation , by greater superficial
petrosal nerve (GSPN) & chorda tympani nerve .

Lecture notes in
2. Afferent fibers
- Taste fibers from anterior 2/3 rd of the tongue (to nucleus solitarius) through
the lingual , chorda tympani & nervus intermedius .
- Sensation from the concha , EAC , ear lobule & supratonsiller fossa .
Facial nerve segments ; are
1. Intracranial segment ; 23-24 mm , from the brainstem to the IAC , (i) cortex &
midbrain , (ii) extrapyramidal system (iii) midbrain (iv) pontine nucleus & (v) CPA .
2. Meatal segment ; 8-10 mm from the porus of IAC to the meatal foramen (to fundus) .
3. Labyrinthine segment ; 3-5 mm , from the meatal foramen to geniculate ganglia , the
fallopian canal is narrowest here (0.68 mm) give the GSPN .
4. Tympanic segment ; 8-11 mm , at the geniculate ganglia , the nerve makes 40-
80oturn to proceed posteriorly across the tympanic cavity to the pyramidal eminence
5. Mastoid segment ; 10-14 mm , from the pyramidal process to the stylomastoid
formen , here gives 3 branches ; nerve to stapedius , chorda tympani & nerve to
auricular branch of the vagus .
6. Extrapyramidal segment ; 15-20 mm , from the stylomastoid foramen to the muscles
of facial expression .
The total length of the facial nerve about 80 mm .
Surgical landmarks to the facial nerve ;
- Extratemporal ; tragal pointer , tympanomastoid suture (6-8 mm below the inferior drop
of the tissue) , posterior belly of digastric muscle , identification of the peripheral
branches .
- Intratemporal ; short process of incus (fossa incudis) , process chochleoformis ,
horizontal & posterior canals & the digastric ridge .
Blood supply of the facial nerve
The cortical motor area of the face is supplied by the Rolandic branch of the middle
cerebral artery . Within the pons, the facial nucleus receives its blood supply primarily from
the anterior inferior cerebellar artery (AICA) .
The AICA, a branch of the basilar artery, enters the internal auditory canal with the facial
nerve , the AICA branches into the labyrinthine and cochlear arteries.
The superficial petrosal branch of the middle meningeal artery is the second of 3 sources of
arterial blood supply to the extramedullary (ie, intrapetrosal) facial nerve .
The posterior auricular artery supplies the facial nerve at and distal to the stylomastoid
foramen . Venous drainage parallels the arterial blood supply.
Communications of the facial nerve
1. 8 th nerve within the internal auditory canal .
2. Otic ganglion & sympathetic fibers in the area of geniculate ganglia .
3. Intra-axial connection within the CNS .
4. Auricular branch of the vagus .
5. 5 th , 9th , 10th , 12th & cervical cutaneous nerves .
Facial nerve sheath
The sheath consist of ; periosteum , epineurium & perineurium .
Pathophysiology
Wallarian degeneration ; start within the 24 hours of injury & progress towards the
periphery over few days .
Injury to the facial nerve can be one of the following ;

Lecture notes in
1. Neurpraxia ; due to local compression of the nerve , no wallarian degeneration ,

normal function tests .
2. Axontemesis ; axon disintegrated , wallarian degeneration occur distal to the lesion ,
complete recovery occur .
3. Neurotemesis ; axons & the surrounding is distracted , wallarian degeneration ,
unpredictable potential regeneration .
Degeneration occur in the distal & proximal parts of the nearest Ranvier node with
changes seen in cells bodies (Nissl bodies) .
Regeneration ; shortly after degeneration , regeneration occur , it involve changes in
neuronal body & axons , at the site of the lesion , neurofibrils produce neurolemmal tracts
which either find way & establish a continuity or gap is large , so the end pulp neuron or
stump . Regeneration about 1.5 mm/day .
Nerve stimulation electrically immediately after trauma may be normal , but 3-5 days at the
stylomastoid foramen there is evidence of degeneration .
Plasticity hypothesis
It propose ; connections between groups of cells & reinforced by multiplication of terminal
branches of the protoplasmic appendices & nerve collaterals , thus bringing about function
transformation of particular system of neuronal as the result of appropriate stimuli or
combination of the stimuli .
It often explanation not only for repair of nerve after trauma , but , also for spontaneous
recovery of function after trauma .
Altered function of the facial nerve following injury
Hypo- or hyperfunction "hyperkinesis" is due to :
1. Distance between the node of Ranvier is altered .
2. Thin myeline over the new axon .
3. Crossing & splitting of the axons .
4. Changes at the myoneural junction .
5. Alterations in central connections & changes around & within facial nerve nucleus .
6. Ephatic transmission .
Types of altered function :
- Synkinesis : an abnormal synchronization of the movement occurring with voluntary &
reflex activity of the muscles that normally don't contract together like blinking with
opening the mouth .
- Crocodile tears : increased unilateral lacrimation with eating , the site of the lesion is at
or above the geniculate ganglion or along the greater superficial petrosal nerve , it is due
to faulty regeneration of parasympathetic nerve fibers (lacrimal instead of salivary gland)
- Stapedial tendon contraction : causes fullness or roaring in the ear noted with facial
movement or spasm , Dx from tympanometry with electroacoustic bridge , managed by
tympanotomy & stapedial tendon sectioning .
- Facial myokymia : continuous , fine , fibrillary or undulating movement of the facial
muscles , associated with multiple sclerosis & brainstem tumors (bag of worms) .
Supranuclear facial palsy
1. Facial weakness .
2. Varies greatly in degree
3. In complete weakness , lower part suffering more .

Lecture notes in
4. There is return of function after a variable interval usually quicker than that of
accompanying parlysis of the limbs of the same side .
5. There is dissociation between emotional & voluntary movement paralysis .
6. Recovery : greater & quicker than in the upper than in the lower parts of the face .
7. Facial expression & forehead wrinkles remain intact .
Lower motor neuron palsy
1. Facial weakness .
2. Equally distributed between the upper & lower parts of the face .
3. Complete paralysis cause asymmetry of the face at rest .
4. Sagging of the lower lid , angle of the mouth on the affected side .
5. Mouth pulled to the active side .
6. Tears over flow & saliva dribble out in the affected side .
7. Collection of food in the checks due to paralyzed beccinator muscle .
8. Platysma fail move skin over the neck .
Level of the lesion

Involved Cause
1. Pons Motor & sensory fibers CVA , Poliomyelitis ,
Taste & lacrimation not involved Tumors
2. Before entering 5 th , 7th & 8th nerves Meningitis , CPA
the IAM Taste & lacrimation not involved tumors
3. After entering the 8 th nerve & nevus intermedius Trauma , Tumor
IAM
4. In the fallopian Loss of taste over the anterior 2/3rd of the Bell's palsy
canal tongue
May associated with hyperacusis due to
involvement of nerve to stapedius
5. Below the Motor paralysis only
stylomastoid Intact taste , lacrimation & salivation
foramen
Causes of facial nerve palsy

1. Idiopathic ; Bell's palsy , recurrent facial palsy .
2. Congenital ; Moebius'syndrome , congenital unilateral lower lip paralysis ,
Melkersson – Rosenthal syndrome & dystrophic myotonia .
3. Traumatic ; temporal bone fracture , intrauterine compression , birth trauma , facial
contusion & laceration , penetrating wounds of the face & temporal bone & iatrogenic
injury .
4. Neoplastic ; cholesteatoma , carcinoma , acoustic neuroma , meningioma , facial
nerve neuroma , glomus jugulare & tympanicum , Schwannoma of the lower cranial
nerve , leukaemia , haemangioblastoma , osteopetrosis , rhbdomyosarcoma &
histioocytosis .
5. Infection ; Herpes zoster oticus , OME , acute mastoiditis , malignant otitis externa ,
ASOM , CSOM , T.B. , lyme disease , HIV , IMN , influenza , sarcoidosis &
encephalitis .
6. Metabolic ; DM , hyperthyroidism , pregnancy & autoimmune diseases .

Lecture notes in
7. Neurologic ; Gullian – Barre syndrome , MS & Millard – Gubler syndrome .

Causes of facial palsy according to the onset ;
1. Acute ;
a. Polyneuritis ; Bell’s palsy , Herpes Zoster , HIV , ..etc .
b. Trauma .
c. Otitis media .
d. Melkersson – Rosenthal syndrome .
e. Neurological disorders ; CVA , HIV , ..etc .
2. Chronic or progressive paralysis .
a. Malignancies ; Primary & secondaries .
b. Benign tumors .
c. Cholesteatoma .
Facial nerve palsy grading system (House –Brackmann)
I. Normal : noram facial function in all areas .
II. Mild dysfunction :
- Gross : slight weakness noticeable on close inspection , may have very slight
synkinesis .
- Symmetry : normal symmetry & tone at rest .
- Motion :
 Forehead ; moderate to good function .
 Eyes ; complete closure with minimal effeort .
 Mouth ; slight asymmetry .
III. Moderate dysfunction
- Gross : obvious but not disfiguring difference between the two sides, noticeable but
not severe synkinesis , contracture or hemifacial spasm .
- Motion :
 Forehead ; slight to moderate movement .
 Eyes ; complete closure with effort .
 Mouth ; slightly weak with maximum effort .
IV.Moderately severe dysfunction
- Gross : obvious weakness &/or disfiguring asymmetry .
- Motion :
 Forehead ; none .
 Eyes ; incomplete closure .
 Mouth ; asymmetric with maximum effort .
V. Severe dysfunction
- Gross : only barely perceptible motion.
- Symmetry : Asymmetry at rest .
- Motion :
 Forehead ; none .
 Eyes ; incomplete closure .
 Mouth ; slight movement .
VI.Total paralysis : no movement .
Evaluation of facial nerve paralysis
Lecture notes in
Evaluation of the patient with facial paralysis begins with a careful history and physical
examination.
A. History
A thorough history includes onset, initial degree of paralysis, and associated symptoms.
These details often can help identify the etiology , for example, a slowly progressive
paralysis is suggestive of malignancy, while a sudden onset of complete paralysis
suggests Bell palsy. The workup, treatment, and prognosis of these 2 disorders are vastly
different from one another.
1. Onset ; complete or incomplete , sudden or delayed , are suggestive criteria , the
typical scenario is unilateral facial weakness over 2-3 weeks .
2. Progression ; beyond three weeks or lack of improvement after 6 months , suggest
Neoplastic process especially if associated with facial twitching , CNS involvement ,
SNHL & ipsilateral recurrence .
3. Numbness in the middle & lower face , otalgia , hyperacusis , diminished tearing &
altered taste could be due to Bell's palsy or Ramsy Hunt syndrome .
Ramsy Hunt syndrome will also manifests vesicular eruption of the face & ear with
SNHL & vertigo .
4. Recurrence occur in Bell's palsy (1/3 ipsilateral & 2/3 contralateral) , Melkersson-
Rosenthal syndrome (characterized by 2 or more recurrent attacks of alternating
facial palsy , recurrent oedema of the lips , face & eyelids , chelitis , fissured tongue
or family history) .
5. Bilateral simultaneous paresis is caused by Gullian – Barre syndrome , Bell's palsy ,
Leukaemia , Sarcoidosis , skull fractures , Moebius'syndrome, Rabies , lyme disease
& IMN .
6. History of medical conditions ; DM , pregnancy , HL , ear disease , previous ear
surgery , cancers (thyroid , kidney , lungs ovary or prostate) & risk factors of HIV .
B. Physical examination
1. Motor function "Grading system" ; physical examination of the patient with facial
paralysis requires observation of the face at rest and during voluntary and reflex
emotional movement.
Determine total versus partial paralysis and unilateral versus bilateral involvement.
Assess symmetry at rest and during movement and the presence and degree of
synkinesis.
Note the severity of brow ptosis, ectropion, and oral commissure incompetence.
2. Otoscopy ; signs of CSOM , ASOM , or trauma , signs of Bell's palsy (red chorda
tympani , vascular flaring in the posterior superior aspect of the tympanomeatal
area).
3. severe pain & vesicles , ear canal , pinna , face or neck (Ramsy Hunt syndrome) .
4. Initial intraoral examination ; fissured tongue or oedema , pharyngeal lesion , mass
in the parotid gland , submandibular region or neck .
5. Ocular examination (optic & abducent nerves) ; uveitis , Schrmer's test ,
ophthalmoplegia (MS) , ptosis , laryngeal & facial weakness (Mysthenia gravis) .
6. Identify other cranial nerve or neurologic deficits and significant soft-tissue volume
deficits in addition to the paralysis.
C. Investigations
To reach the diagnosis , on which the Rx depends , we should identify the :

Lecture notes in
1. Site of the lesion , topognostic tests & clinically .

2. Severity of the lesion , electrophysical tests .
3. Patholoical causes of the lesion ; history , examination & radiology .
4. Duration of paralysis (the prognosis) .
1. Site of the lesion ; can be identified clinically or by topognostic test .
- Clinically
Supranuclear : intact upper face with neurological deficit (CVA , trauma ..etc) .
Nuclear : involvement of the 6th & 7 th nuclei & nerves (MS , vscular , Neoplastic ,
encephalitis & poliomyelitis) .
CPA : involve the 8th nerve , s.t. the 5th , 9th , 10 th & 11th nerves , there is altered
taste , salivation & lacrimation (neuromas , meningioma & cholesteatoma) .
Geniculate ganglia : hyperacusis , altered taste & salivation , lower motor facial
palsy with altered TSL (neuromas , fractures , herpes zoster oticus , Bell's palsy &
cholesteatoma) .
Tympanomastoid : intact lacrimation while lower motor palsy , normal taste , with
normal TSL (fractures ,infection , Bell's palsy & cholesteatoma) .
External segment : facial palsy & deviation of the jaw to the normal side with
normal TSL (trauma , parotid & pharyngeal tumors) .
- Topognostic tests
 Schirmer's test (lacrimation) ; evaluate the greater superficial petrosal nerve ,
reduction of less than 30% of the total amount of both eyes or reduction less than
25 mm in the affected side after 5 minutes .
 Acoustic impedance test (stapedial reflex) ; evaluate the nerve to stapedius
muscle , the stapedius muscle contract with contralateral ear stimulation altering
the compliance of the middle ear , measured by impedance audiometry , if the
lesion proximal , no contraction .
 Salivary flow testing ; salivary flow measurement after gustatory stimuli ,
reduction of 25% as compared to the normal side is suggestive .
 Blink reflex ; percutaneous stimuli of the supraorbital nerve lead to blink reflex
(seen by electrode in the orbicularis oculi muscle) because of the central
connection between the trigeminal & facial nerves .
 Electrogustography "rarely performed" ; electrical stimulation of the tongue
cause metallic taste , we compare both sides .
2. Severity of the lesion "electrophysiological tests"
Not needed in all patients , but in acute palsy or for follow up in persistent palsy, so
determine the time of surgical intervention .
 Nerve excitability test (NET) ; minimal nerve excitability test (NET) determines
the threshold stimulation required for muscle contraction, which is compared to
the unaffected side .
It measured in mA , a difference of 3.5 mA or greater is significant & suggest
degeneration .
 Maximal stimulation test (MST) ; maximum nerve excitability test (maximum
stimulation test [MST]) is a modification of the NET in which the amount of
muscle twitch in response to a supramaximal stimulus is compared to the
contralateral side.

Lecture notes in
In this test stimulation is begin with 1 mA DC current 7 increased slowly to 5 mA

or until discofort & recording the amount of muscle twitching .
The response of the involved side is compared with normal side for each area
tested & recorded as absent , markedly diminished , minimally diminished or
equal .
Because MST elicit a response from the entire nerve , there fore it is a prognostic
indicator of facial nerve degeneration .
The subjective nature of the measurements and lack of recorded data limit both
methods.
 Electromyography (EMG) ; s a measure of volitional muscle response, in contrast
to the evoked responses of NET, MST, and ENog.
This test determine the activity of the muscle itself .
Needle electrodes are used to monitor activity of the facial muscles(during rest &
voluntary movement) .
Normal muscle exhibits activity upon needle insertion, electrical silence at rest,
and diphasic or triphasic action potentials during voluntary contraction.
Fibrillation potentials are observed in the denervated muscle (appear after 10-12
dyas after injury) , and polyphasic potentials are observed in muscle undergoing
reinnervation (at 6-12 weeks prior to clinical return of nerve function) , complete
electrical silence is observed in denervated muscle with significant fibrosis.
EMG is useful in evaluating the patient with an acute or traumatic nerve injury
and in assessing the viability of the facial musculature when evaluating patients
for reinnervation procedures.
So the presence of voluntary action potentials indicate the the lesion is
incomplete which is important to know in trauma aetiology to obviate the need for
surgical exploration .
It is the most reliable test available follow up the course of severe denervation , it
offers the earliest evidence of recovery of facial nerve function .
 Evoked EMG (EEMG) ; an objective measure of facial nerve function that
records an evoked muscle response.
The nerve is stimulated at the stylomastoid foramen, and a skin electrode, usually
at the nasolabial fold, records the compound action potential of the muscle. Use
increasing current to achieve a maximum response.
The compound action potential is compared between the 2 sides of the face, and
the response of the affected side is expressed as a percentage of the response of
the unaffected side.
A percentage of nerve fiber degeneration is calculated; use this to determine
prognosis and plan treatment in the patient with facial nerve paralysis.
It is the most accurate prognostic indicator , poor prognosis if the response lost
within the 1 st 5 days , but favorable if maintained beyond 10 days (especially 14
days)
 Magnetic stimulation of the facial nerve (magnetic evoked neuromyography) ; it
is experimental test , stimulate the facial nerve intracranially by magnetic coil
placed over the scalp (it has the advantage of having a potential intracranial
stimulation) .
3. Pathology of the lesion "identification"

Lecture notes in
 Imaging , which depend on history & examination .

- Plain views of mastoid & internal auditory meatus .
- Tomography of temporal bone .
- CT scan of the brainstem , CPA , temporal bone & skull base .
- MRI with gadolinium enhancement , proximal & distal lesions , Bell's palsy
shows enhancement of labyrinthine segment , also enhancement shown in
Ramsy Hunt syndrome , facial nerve in neuroma in the CPA is
indistinguishable from vestibular Schwannoma .
Erosion & expansion in the labyrinthine segment & geniculate ganglia are
classic for these tumors .
- CXR , to detect sarcoidosis , lymphoma & carcinoma .
 Special laboratory tests
- LP : to detect meningitis , encephalitis , MS , Gullian-Barre syndrome .
- WBC , complete & differential : IMN & leukaemia .
- Monospot test for IMN (also hetrotrophilic titers) .
- ESR : for sarcoidosis .
- Urine & stool examination : evaluate porphyrins & urinary porphobilinogen ,
increase urinary calcium in sarcoidsosis , toxins in stools .
 Serum tests
- Serum cryoglobuline & immune complexes : lyme disease .
- Serum globuline to detect sarcoiosis .
 Bone marrow examination : Leukaemia & lymphoma .
 Glucose tolerance test : forDM .
 Audiological : Audiometric testing, including acoustic reflexes and
tympanometry, may be useful in identifying the etiology of facial palsy secondary
to retrocochlear pathology or mass lesions of the middle ear.
Causes of facial palsy
According to the incidence ; Bell's palsy (60%) , ATYPICAL Bell's palsy , trauma (20%) ,
tumor , suspected tumor , Herpes zoster oticus , infection , present at birth , hemifacial
spasm & CNS lesion .
# Bell's palsy "Sir Charles Bell 1821"
It is an acute , sudden , unilateral facial palsy due to a viral inflammatory immune
mechanism , resolve spontaneously , non-progressive , not life threatening , neither
preventable nor curable .
Diagnosis made by exclusion (LMNL , acute , no signs of CNS disease or ear disease or
CPA disease) .
It is self limiting disease usually improves within 4-6 months & always by 12 months after
onset
Incidence : 15-40/100000 population , 3 rd decade , 12% recurrence & 14% with family
history. Charcterized by viral prodrome (60%) , pain around the ear (50%) , facial
numbness (40%) , altered taste (50%) & numbness of tongue (20%) .
Aetiology : idiopathic , but , theory suggest ;
1. Viral inflammatory immune mechanism lead to swelling , neuronal
entrapment in the fallopian canal causing ischemia & then nerve injury
(stylomastoid area & pyramidal eminence) . Which is the most widely

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accepted theory depending on clinical observations & changes in the viral

antibody titer
2. Microcirulatory failure of the vasnervorum .
3. Ischemic neuropathy .
4. Autoimmune reactions .
Types
1. Incomplete palsy ; evaluated within 14 days , am appointment is given to return in 3
weeks for further evaluation (daily checking , if palsy worsen , patient return) , usually
recover in 6 weeks , if not or worsen , a tumor is suspected .
2. Complete palsy ; needs MST or EEMG & evaluation for recovery appearance , if
recovery start within 3 weeks & response to EEMG remains more than 11% of normal
up to day 14 after onset , then recovery .
If delayed recovery & response to EEMG < 11% , then the prognosis recovery drops to
30%. Facial function re-evaluated 3 months , 6 months , 1 year & 2 years after the onset
of the paralysis .
Management
Controversial , Peterson's managed 1011 patients with Bell's palsy , recovery without
medical or surgical treatment . The aim of management is to prevent complications &
manage the sequel .
Complete otologic , audiometric & radiographic workup is needed .
For partial palsy , no management needed , while for complete palsy we should determine
the level of involvement & daily electrical testing until ;
- Threshold of the involved side increased to 4 mA >healthy side .
- Evidence of some return of the facial function .
1. Medical
- Physical : heat , massage & facial exercise daily .
- Drugs : steroids , vitamins , acyclovir & sodium chromglycate , the steroids prevent
denervation , decrease pain , prevent progression from incomplete to complete palsy
& dyskinesis .
Indications for steroid therapy ; recent (1-2 days) , complete , associate with pain &
electrogustrometric threshold > 100 A above that of the normal tongue side .
- Psychological : encouragement , relieve depression by reassuring the patient &
group therapy , also use pain killers (NSAID , steroids & s.t. narcotics) , & eye care
by keeping the affected eye moist to prevent keratitis & corneal ulcers (closure ,
drops , ointments) , also by tarsorraphy & amplantation of gold weights .
2. Surgical
Needed for cases of complete palsy & evidence of extensive nerve degeneration , if the
hearing is good , then use middle cranial fossa approach (should be done if the GSPN is
involved) , if HL , then use translabyrinthine approach .
But , decompression still controversial , decompression of the nerve from the
stylomastoid foramen to the level of the blockage .
Indications (bad signs)
a. Ineffective medical therapy .
b. Dry eye & corneal anesthesia .
c. Patient lacks Bell's phenomenon .
# Traumatic facial nerve palsy "2nd commonest cause"

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- Iatrogenic injury
 Otologic surgery ; uncommon (1%) , the commonest site is the tympanic segment ,
when there is unexpected facial palsy postoperatively .
Rule out the effect of local anesthesia & the overlying tight mastoid packing .
Management :
3. Partial ; usually minor trauma & oedema , with good prognosis & managed
by steroids & removing the wick .
4. Complete ;
a. Delayed onset ; remove the wick & steroid & observation with frequent
EEMG , if deterioration , then surgical decompression .
b. Immediate ; let the patient recover completely from anesthesia , remove the
wick (which may press on dehiscent section of facial nerve) , the decision
will depend on the surgeon confidence of nerve status :
- If the nerve don't identified in operation or injury felt to be a possibility ,
then explore as soon as possible (not before the sunset) , discuss the
condition with the patient family & this wait allow the surgeon to regain
his composure , so if the nerve is intact then remove any bony compression
or pieces , but if the nerve transected then do nerve graft or end to end
anastamosis .
- If the surgeon convinced that the nerve was not compromised , follow the
paralysis with electrical tests & explore only if there is a signs of
degenerations .
Good prognostic signs are ;
1. Response to electrical stimulation is maintained beyond 10 days .
2. Visible facial movement is maintained or begin to appear within 3 weeks .
3. Voluntary motor unit AP or EMG persist or return after 14 days .
 Parotid gland surgery ; stimulate the main trunk before closure , if nor response then
inspect carefully for area of disruption , if muscle jump briskly , then no nerve injury
& even if the patient awake with paralysis nothing needed & recovery within 4-6
weeks .
- Non-iatrogenic injury
 Intratemporal injury ; due to temporal bone fracture which is either ;
1. Longitudinal (temproparietal trauma) ; 80-90% , involve the middle ear leading
to facial nerve paralysis in 20% of cases , mostly due to compression & ischemia
, characterized by bleeding from the ear , perforated tympanic membrane &
conductive hearing loss .
2. Transverse (occipitomastoid trauma) associated with facial nerve palsy due to
nerve transection (involve the inner ear) , characterized by haemotympanum ,
vestibular symptoms & a dead ear .
Management ;
1. Partial ; conservative Rx , serial electrical tests to exclude degeneration , the
use of steroid here is controversial .
2. Complete ; do CT , MRI , EEMG , arteriography (in case of penetration injury)
, if >90% degeneration after 6 days , so need decompression surgery either
transmeatal or middle fossa approach , s.t. need end to end anastamosis or

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nerve graft (after resection) , the best nerve graft is from sural nerve or greater
auricular nerve .
 Extratemporal injury ; need full assessment of the surrounding structures (globe ,
duct , mouth ..etc) .
Trauma distal to the line between the lateral canthus & mouth angle , then leave it .
Immediate repair give good results without synkinesis which is contraindicated in
significant tissue loss & extensive tissue contamination .
# Infections
- Viral
 Ramsy Hunt syndrome (Herpes zoster oticus) ; by Hunt 1907 who describe the
syndrome
It is a viral prodrome , severe pain , vesicles involving the pinna , SNHL , tinnitus &
vertigo , the incidence increased after the age of 60 years due to decreased cell
mediated immunity .
Diagnosis from clinical picture confirmed by rising titer of antibodies to Varicella
zoster virus & enhancement of on gadolinium MRI .
There is no correlation between the enhancement level , electrophysiological &
intraoperative findings & prognosis of paralysis .
Prognosis for recovery is worse due to significant nerve degeneration .
Differential diagnosis from Bell's palsy :
1. Significant nerve degeneration , so worse prognosis (60% recovery) .
2. Rarely recure .
3. Diminished response to electrical tests by 10-14 days , while in Bell's palsy
more earlier "6-10 days") .
Treatment ;
1. Acyclovir , 800 mg , 5 times daily for 10 days .
2. Steroids , controversial , reduce pain & vertigo & minimize the post-herpetic
neuralgia .
3. Analgesia & topical ointment .
 EBV "IMN" , CMV , HIV & influenza virus .
- Bacterial ; ASOM , CSOM & malignant otitis externa , the dehiscent fallopian canal
serves as portal of direct bacterial infection ,
ASOM managed by antibiotics (G+ve & haemophilus) with wide myringotomy & cortical
mastoidectomy .
CSOM managed by tympanomastoidectomy & nerve decompression .
Malignant otitis externa by Claforan & surgical debridment .
# Tumors
Involving the facial nerve & the surrounding structures , features suggesting aetiology are ;
a. Slowly progressing paralysis .
b. Persistent paralysis (>6 months) .
c. Ipsilateral recurrence .
d. SNHL .
e. Cranial nerves deficits .
f. History of Malignancy .
- Intracranial lesions ; mostly benign , frequently Schwannoma , half of them are vestibular
one located at the CPA or IAM , others include menigiomas , angioma , intraosseous

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haemangioma , A-V malformation , congenital cholesteatoma , arachnoid cyst & adenoid

cyctic carcinoma .
The diagnosis by MRI & otological workup .
The treatment by surgical excision , the approach depend on hearing status & tumor site .
- Extracranial lesions ; almost exclusively of parotid origin .
Benign , especially pleomorphic adenoma , slowly growing , nontender mass , causing
compression of soft tissue causing facial nerve dysfunction & salivary flow obstruction ,
managed by surgery .
Malignant , especially adenoid cystic carcinoma or mucoepidermoid carcinoma or s.t.
facial nerve tumor causing facial nerve paralysis (poor prognostic sign) , managed by
excision for a tumor free margin , nerev graft , adjunctive radiotherapy & chemotherapy .
# Melkersson –Rosenthal syndrome
Recurrent unilateral or bilateral facial palsy of unknown aetiology associated with facial
oedema & fissured tongue , the peak age is 20 years .
Histologically ; dilated lymphatics channels , giant cells & inflammatory cells .
# Paediatric facial nerve disorders (1:2000)
Causes
1. Birth trauma ; forceps delivery , unilateral complete facial nerve palsy , echymosis &
haemotympanum .
Management for traumatic facial palsy in children is controversial , but it has
indications for surgical intervention ;
a. Unilateral complete palsy at birth .
b. Haemotympanum & displaced fracture of the temporal bone .
c. No evoked or voluntary motor response for 3-5 days .
d. No return of facial nerve function by 5 weeks .
2. Congenital syndromes ; poor prognosis
 Moebius syndrome ; bilateral facial palsy , unilateral or bilateral 6 th nerve
palsy , extremities anomalies , absent of pectoralis muscle , also involvement
of hypoglossal nerve .
 Congenital unilateral lower lip paralysis ; a brainstem lesion leading to a
lack of development of the depressor angularis muscle , usually unilateral &
associated with other congenital anomalies (CVS or otological) .
# Hyperkinetic disorders
1. Hemifacial spasm ; intermittent spasm of the orbicularis oculi muscle which may
spread to other facial muscles , it caused by compression of the facial nerve by artery
in the posterior cranial fossa .
Diagnosed by MRI & angiography .
Managed by ;
a. Retromastoid vascular decompression , if not ;
b. Intracranial selective peripheral neurolysis . or ;
c. Injection of Botulinium A toxins (last for 6 weeks – 6 months) .
2. Blepherospasm ; unilateral or bilateral involving spasmodic eye closure , managed by
a. Peripheral selective neurolysis .
b. Selective muscle resection in or around the eye lid .
c. Injection of Botulinium A toxins .

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3. Aberrant regeneration (like crocodile tear) ; lacrimation with eating occur in facial
nerve injury above or at the geniculate ganglia or along the GSPN , due to faulty
regeneration of the parasympathetic fibers innervating the lacrimal gland instead of
salivary gland .
Managed by Botulinium A toxins .
Surgical management of the facial nerve paralysis (Decompression)
# Decompression
The decompression means slitting the nerve sheath vertically on its posterior aspect with
Bearer knife .
Indications
1. Absolute ;
a. Facial nerve transection .
b. Tumor infiltration .
2. In certain cases of ;
a. ASOM .
b. Malignant otitis externa .
c. Trauma .
3. Controversial ;
a. Bell's palsy .
b. Ramsy Hunt syndrome .
Time
1. Before electrical denervation (for better recovery) .
2. Not delay , if incomplete , convert to complete within hours or days .
3. Response to EEMG < 25% or decreased after 3rd day .
Approaches
1. Middle cranial fossa approach (Neurosurgeon) .
2. Transmastoid sublabyrinthine approach (Otologist)
- Cortical mastoidectomy at 1 st with thinning of the bony posterior meatal wall to
identify the facial nerve canal from the stylomastoid foramen to the tip of the incus
above (vertical segment) .
- Thinning of the bone between the stylomastoid foramen & lateral semicircular canal
which is parallel to the nerve course , here the nerve will be seen as a pink streak .
- If the horizontal segment involved also , decompression done in the triangle of facial
nerve medially , chorda tympani laterally & short process of incus superiorly
(preserve the incus or dislocate & round it) .
# Repair of the facial nerve
1. Approximation (neurorraphy) , freed the nerve & reanastamosed end to end , avoid
tension to guarantee successful repair .
2. Graft (interpositional) , usually sural nerve (10 cm) or greater auriculat nerve , use
10/0 nylon & then covered by vein graft .
Best results with epineural anastamosis , no need for suture with the temporal bone .
3. Reanimation , should be within 6 months , not beyond 2 years , it is excellent
technique to provide neural input into intact distal nerve part , it is done in cases of ;
a. Proximal damage preclude neurorraphy .
b. Conservative management failure to obtain reasonable long out come (>18
months) , so need intact muscles .

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Hypoglossal – facial nerve anastamosis , only one with good results , facial
hypertonia & synkinesis expected after surgery .
4. Neuromuscular transfer & facial slings , done as alternative for the above
procedures when facial muscles are atrophied .
It is cosmetically inferior to the neural reconstruction surgery , but provide
protection to the eyes & mouth . Usually use temporalis muscle .
N.B.:
I. Facial palsy not involving the GSPN give a tearing eye because ;
a. Paralysis of the Horner muscle that dilate the nasolacrimal orifice .
b. Ectropia that produce end position of the punctum .
c. Absence of the blinking (lack of pumping action) .
II. Histselberger's signs ; decreased sensitivity in the posterosuperior aspect of the concha
corresponding to the sensory distribution of the facial nerve suggest space occupying
lesion in the internal auditory canal .
III. The degree of facial nerve paralysis
- 1 st degree : Compression , complete recovery .
- 2 nd degree : Interruption of the axonplasm & myelin , satisfactory recovery .
- 3 rd degree : Disruption of the endoneurium , incomplete recovery .
- 4 th degree : Disruption of the endoneurium & perineurium , weak recovery .
- 5 th degree : Transection of the nerve , no recovery .
IV. Facial paralysis of central origin characterized by ;
a. Intact frontalis & orbicularis oculi .
b. Intact mimetic function .
c. Absence of Bell's phenomenon (the globe turns up & out during an attempt to close
the eyes) .
d. Bilateral , simultaneous facial palsy is a sign of central generalized disease ,
especially Gullian – Barre syndrome .

Lecture notes in
LABYRINTHITIS
Definitions
- Labyrinthitis ; it is an inflammation of the labyrinth .
- Labyrinthine fistula ; bony erosion of the labyrinth capsule to expose , but not breach
the endosteum of the labyrinth .
- Tullio phenomena ; vertigo as a result of loud sound, occur in fenestration operation
(fistula) & in endolymphatic hydrops .
- Fistula sign ; occur in the prescence of labyrinthine fistula , raising the external ear
canal pressure of the affected side may cause conjucate deviation of the eyes away
from the affected ear .
Pathology
Labyrinthitis are either
A. Viral
The viruses are ; mumps , influenza & adenovirus .
Vertigo & nystagmus lasting for 3-5 days with gradual lessening of the spontaneous
nystagmus .
Various degrees of prominent vestibular & auditory loss may bee seen .
Viral agent will affect structures located within the scala media & sense organs of the
vestibular labyrinth . Hair cells of organ of Corti , stria vascularis & spiral ganglia may
be affected by infection .
B. Bacterial
Occur as an extension of the infection from the middle ear space or intracranial cavity .
Stages are :
1. Acute , toxic or serous .
2. Acute suppurative .
3. Chronic supporative .
4. Fibrosseous .
Acute , serous labyrinthitis ; chemical changes in the perilymphatic space caused by
suppurative process which impinges on a membrane barrier of the labyrinth .
Vertigo & nystagmus occur in this stage , but these disturbances are reversible if the
adjoining toxic process is controlled medically or surgically .
Acute suppurative labyrinthitis ; invasion of the perilymph space by bacterial organism
& host response in the form of inflammatory cells infilteration & fibrocytes .
Irreversible destruction of the labyrinth has occurred & the treatment aim to prevent
intracranial extension .
Chronic suppurative labyrinthitis ; involvement of the labyrinth by bacterial organisms
with inflammatory tissue response has occurred over a long period of time usually as an
extension of chronic inflammatory middle ear disease or mastoid disease .
Complete irreversible loss of the labyrinth function invariably occur & treatment aims to
prevent intracranial extension .
Fibrosseous stage ; final or heald stage , it is a response that is generated by the host as
an inflammatory process has been successfully controlled .
Fibrous tissue completely obliterate the labyrinth space with resultant complete loss of
the labyrinth function , followed by calcification & ossification of the labyrinth .
The microorganism are :
1. Acute ; Pneumococci , Streptococci & H. influenza .

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2. Chronic ; mixture of gram negative (Psuedomonas , Proteus & E. coli)

Serous & Suppurative labyrinthitis
The distinction between these depend on retrospective recognition of the recovery of
cochlear & vestibular function .
Spread of infection mostly from the infected middle ear or mastoid , rarely from meningitis
through the internal auditory meatus or cochlear or vestibular aqueducts , much more
rarely infection spread through the blood (blood born infection) .
Clinical features
- A patient with acute or chronic middle ear infection presents with violent prostrating
vertigo & vomiting .
- Severe hearing loss of sensorinueral type , but the greatest attention given to the
severe disabiling vertigo especially if has been a preceding conductive loss from
middle ear disease .
- The patient lies immobile , on the side of the infected labyrinth upward avoiding any
head movement .
- On examination ; there is evidence of the preceding middle ear disease accompined
by pyrexia & leucocytosis .
At 1 st there is spontaneous irritative jerky nystagmus beating “with quick component”
toward the infected ear .
This is soon replaced by paralytic jerk nystagmus beating toward the healthy side .
At beginning there is retained cochlear function & mastoid bone conduction test , this
means serous labyrinthitis , but when the cochlear function lost , this means suppurative
labyrinthitis .
- During 2-3 weeks , the condition start to subside gradually , nystagmus start to
convert from 3rd degree to 2nd & 1st degree & then disappear .
- After that , the patient had good balance , but still unsteady when walking in dark or
with closed eyes & he is unhappy with sudden head movement .
- Hearing loss in the damaged ear is inevitably total & permanent
- Diagnosis
- Mainly depend on the clinical pattern .
- Suspected suppurative labyrinthitis augmented by recognition of the middle ear
infection .
- Examination of the ear with binocular microscope & sometimes under GA needed to
inspect the attic fully .
- Haemorrhagic or bulous myringitis with varicella zoster virus can cause sudden
vestibular failure with acute pain & inflammatory changes on otoscopic examination
- In cases of doubt , one should treat as suppurative labyrinthitis .
Differential diagnosis ; from Cerebellar abscess in which ;
1. The patient more ill .
2. Cerebellar signs on neurological examination .
3. Nystagmus persisting longer .
4. Nowadays , CT scan will provide a definitive distinction .
Sequelae ;
- During the acute course continuing danger of intracranial spread leading to
meningitis .

Lecture notes in
- Long term effect , the labyrinth remain filled with sequestrated pus which
occasionally need surgical drainage .
Management ;
1. Complete bed rest ;
- Head movement should be avoided .
- Hearing tests should be carried at bed side .
- Vestibular function tests should be avoided .
2. Parenteral prochlorperazine to control vertigo & vomiting .
3. i.v. fluids to prevent dehydration “severe vomiting” .
4. Parenteral antibiotics ;
The choice of antibiotics depend on bacterial examination of any available secretions ,
during that time use broad spectrum antibiotics .
- Used to traet acute OM as a cause .
- It is doubtfull whether its penetration in to the labyrinth will affect the course of
labyrinthitis .
- It may prevent the development of the meningitis .
5. Observation of any early sign of meningitis .
6. Treatment of ear infection
- Acute ear infection ;
 Mostly with antibiotics therapy .
 Sometimes , myringotomy .
 Rarely , need mastoidectomy
- Chronic ear infection ;
 Mastoid exploration to make the ear safe .
 In acute labyrinthitis , mastoid exploration should be deffered until 7-10 days
course of antibiotics , otherwise there may be dissemination of infection .
7. Vestibular head excersizes which will accelerate central compensation .
Perilabyrinthitis
Denotes the problem caused by labyrinthine fistula after mastoid surgery in the presence of
retained vestibular function .
The fistula precede mastoidectomy or caused by it , vertigo provoked by pressure changes
near the fistula , cold air blown into the ear (Tullio phenomena) .
Prevention by occluding the external meatus . Surgical treatment by grafting the fistula with
temporalis fascia , sealing the graft with fibrin glue & temporalis muscle flap .
Occasionally deliberate labyrinthine destruction or vestibular nerve section may be needed
to prevent vertigo .
Paralabyrinthitis
Vertigo occuring in the presence of CSOM when inflammation close to the endosteum of the
labyrinth cause irritative nystagmus toward the affected ear .
Future advances
Growth factors & antioxidants may provide protection to the labyrinth from progressive
damage & may allow regeneration of the vestibular receptors after injjury of any aetiology .
Growth factors of particular interest are Brain Derived Neurotrophic Factor “BDNF” &
Glial cell line Derived Neurotrophic factor “GDNF” .

Lecture notes in
Experimental autoimmune labyrinthits

Systemic sensitization of Guinea pigs with single intradermal injection of bovine inner ear
antigens , lead to ;
- Lymphocytes & polymorphonucleocytes appeared mainly in the scala tympani on day
7-14
- Thickening & cellular infiltration of the round window membrane at day 14
- They noted that ; spontaneous remission & cellular clearance occur after day 28 .
- Improved hearing threshold can occur spontaneously .

Lecture notes in
MENIER'S DISEASE
In 1861 Dr. Prosper Menier described a series of similarly affected patients in a series of
six articles , Dr. Menier was the 1st to suggest that the symptoms complex he was seeing in
his patients was due to a disturbance of the inner ear "episodic vertigo , sensory hearing
loss & tinnitus" .
In 1926 , Dr. Cacarges Portmann published a paper documenting the 1st endolymphatic sac
drainage operation for the Rx of vertigo , he think that patient with Menier's triad of
symptoms was due to intralabyrinthine hypertension (auricular glaucoma) , there is
amprovement in the symptoms after the drainage operation .
In 1927 , Guild produced the 1st description of the longitudinal flow of endolymph (stria
vascularis) as the principle source of endolymph & the endolymphatic sac as the site of
endolymphatic outflow .
In 1928 , Dandy , treat Menier's disease "MD" in 9 patients by sectioning the 8th cranial
nerve (an operation by Parry 1904) .
The endolymphatic hydrops , the principle pathological feature of MD , was the 1st
described by Hallpike & Cairus in 1938 , they demonstrate the increase in volume of
endolymph in the scala media in two patients .
Vincent Van Gogh suffer from MD .
It is defined as a disease of the membranous labyrinth "inner ear" , characterized by
deafness , vertigo & usually tinnitus , which has as its pathological correlate hydropic
distension of the endolymphatic system (aural fullness usually added) .
Atypical MD , is a term which has been suggested to describe patient who complain of some
, but not all the classical symptoms of MD .
Cochlear MD , the patient complain from auditory symptoms , while in vestibular MD , the
patient complain from vestibular symptoms .
Lermoyez syndrome , which describing characteristic sudden sensorineural hearing loss
which improves during or immediately after the attack of vertigo .
Tumarkin's otolithic catastrophe or drop , attack MD , which is a variant of abrupt falling
attacks of brief duration without loss of consciousness .
Incidence
Vary significantly ;
- 157 per 100000 population , in UK is 100:100000 .
- MD is responsible of 10% of visits to dizziness units .
- Racial variation : the same .
- Sex : female to male ratio is 3:2 .
- Familial tendency , +ve family history up to 20% .
- Age of onset ; before the age of 60 & rare under 10 years , peak at the 5 th & 6th
decade .
- Frequency of bilateral MD range from 2-78% , 31% of patients is bilateral (British
survey of 610 patients with MD) , 72% of patients develop bilateral MD within 5
years .
Pathophysiology
Theories of controversies ;
1. The basic pathology is endolymphatic hydrops , which is the end result of variety of
insults lead to the causation of fluctuating HL , episodic vertigo & usually tinnitus .

Lecture notes in
The endolymphatic hydrops is a physical distortion of the membranous labyrinth affect

mostly the cochlea (bowing of the Reissner membrane) , saccule & uncommonly the
utricle
So the endolymphatic space will expand on the exposure of Perilymph space ,
endolymphatic space bulge at the helicotrema & footplate & semicircular canal "SCC"
lead to fibrous adhesions especially between the saccule & footplate (which explain
the Henebert sign & Tullio phenomena) .
Henbert sign , subjective vertigo & nystagmus observe during a pressure induced to an
intact tympanic membrane .
Tullio phenomena , vertigo , tonic eye movement & nystagmus observed in response to
loud , low frequency noise exposure .
2. Endolymphatic hydrops occur due to defect in the longitudinal flow of the endolymph ,
especially endolymph malabsorption (in the sac) .
Histologically , there is hypoplasia of the vestibular aqueduct , narrowing of the
endolymphatic duct , perisaccular fibrosis & loss of epithelia integrity & atrophy of
the sac .
The endolymphatic circulation , either longitudinal , where the endolymph produced in
stria vascularis & then circulate through the scala media , then to the ductus Reunieus
, then saccular duct , vestibular aqueduct & then absorbed in the sac , or radial ,
where it produced from dark cells & planum semiluminal with local absorption .
3. Other , high endolymph pressure alone can produce MD .
4. MD occur due to rupture of the membranous labyrinth , cause sudden mixing of the
toxic endolymph (high K + ) with Perilymph , lead to sustained depolarization &
inactivation of the hair cells & neurons of the 8 th nerve , leading to symptoms then
subsequent healing , which lead to return of the endolymph-perilymph barrier return
to normal inner ear function , relieving the symptoms .
5. Recent , 3 possible mechanisms , viral labyrinthitis , altered glycoprotein metabolism
& fibrosis of the endolymphatic sac .
Studies on temporal bone , shows , small Trautmann triangle which is between the lateral
sigmoid sinus , bony labyrinth & the superior petrosal sinus or vein .
Aetiology
1. Primary hydrops
a. Genetic , autosomal dominant , 14-20% with family history .
b. Anatomical , small endolymphatic duct & sac with small aqueduct .
c. Traumatic , release of debris cause obstruction of the endolymphatic duct .
d. Viral infection , neurptropic one cause damage to the endolymphatic sac & duct .
e. Allergy , doubtfull because fail to found high IgE .
f. Autoimmunity , high ESR , autoantibodies (high IgG) , the presence of of Ig &
lymphocytes in the sac lead to strong association between MD & autoimmunity .
g. Psychosomatic & personality may associate with MD .
2. Secondary hydrops
a. Developmental insult like Mondini dysplasia , dysplasia of endolymphatic sac .
b. Metabolic & endocrine disease , DM , hypothyroidism , hypoprotienaemia , adrenal
insufficiency & premenstrual period .
c. Abnormal fluid balance , haemdialysis of the patient with MD lead to endolymphatic
hydrops of the other ear due to sudden change of the plasma osmolarity .

Lecture notes in
d. Syphilitic , congenital or acquired one , 7% due the disease .

e. COM , secondary to the effect of the toxic products & enzymes which migrate
through the round window membrane which lead to sensory cell degeneration &
endolymphatic hydrops , also due to osteitis of the otic capsule & inner ear .
f. Viral , mumps & measles cause viral labyrinthitis .
g. Autoimmune disease , Rh. Arthritis & Cogan syndrome .
h. Otosclerosis , the cause of this association is ; physical impingment of otosclerotic
bone with the vestibular aqueduct & biochemical alteration of the Perilymph &
endolymph .
i. Others , leukaemia , Shy-Drager syndrome & temporal arteritis .
Clinical picture
The typical presentation is episodic attack of rotatory vertigo (96%) , with tinnitus (91%) &
SNHL (88%) & aural fullness (74%) .
This vertigo preceded by aura , 5-60 minutes , the patient feels of aural fullness , increasing
tinnitus & HL , s.t. it may suddenly awake the patient from deep sleep .
The length of the attack , mostly 2-3 hours (usually 24 min. – 24 hrs) , then the patient go to
sleep , the frequency of the attack , from day – years , the vertigo subside , but the SNHL &
tinnitus continue .
- Episodic vertigo ; is the most distressful & disabling symptom of the MD , associated with
nausea & vomiting .
It start suddenly as severe spinning sensation associated with pallor , diaphoresis , nausea
& vomiting , diarrhea & aggravated by head movement , during the attack , the patient
has normal level of consciousness & orientation with no focal neurological symptoms .
After minutes to hours , the patient sleep , then he often fells entirely normal .
86% of patients with MD have BPPV between the attacks . Also , nystagmus associated
with vertigo is classically horizontal one beating toward the affected ear .
Generally , in MD , vertigo has gradual increase in frequency over years until it reach
maximum then it will decreased in frequency when the disease lead to irreversible damage
of the inner ear .
- SNHL ; typically fluctuant & progressive , during the attacks , auditory acuity always
diminished & may remain so for sometimes after the vertigo has subsides .
It is low frequency fluctuant HL or or low frequency HL occurring with high frequency HL
(inverted V diagram , centered at 2 KHz) , less frequent audiometric figure are h-shaped
or down-ward slopping .
The average pure tone HL over the long term is 50dB & average speech discrimination
drop to 53% .
Most patients experience dysacusis (sounds perceived to have abnormal tinny nature) .
Diplacusis , 43% of patient with MD , the same sound frequency is perceived as different
pitches in the two ears & the affected ear had the higher pitch .
Recruitment , 56% of patients have oversensitivity to suprathreshold acoustic stimuli , due
to hair cells injury & absent in lesions of auditory nerve .
- Tinnitus ; variable in characteristics & may be the 1 st symptom , it is always present
during the spell if the patient can listen to it & often present between the attacks .
It may be continuous or intermittent & it non-pulsatile , early in the disease , when
hearing diminished , the tinnitus increased & vice versa , later on , it is more constant , it
is the main complaint in later stages of the disease .

Lecture notes in
- Aural fullness ; mostly pressure sensation limited to the ear , other patients fell pressure
else where in the head & neck .
Differential diagnosis
1. Conditions with vertigo without auditory symptoms
a. Vestibular neuritis , here the vertigo & vegetative symptoms disappear after 1-2 days
, s.t. vertigo continue for 2-6 months , the patient generally ill & it lack the auditory
symptoms & aural fullness , ENG reveal reduced caloric response on the affected
side & paralytic nystagmus .
b. BPPV , vertigo evoked by head movement , latent period of some seconds (<1min) ,
triggers by lying back on the affected side & then rolls over onto that side , then sit
up quickly & tilt the head back while looking up . Dix-Hallpike +ve with rotatory
nystagmus
2. Conditions with auditory symptoms without vertigo
a. Sudden HL , absent aural fullness .
b. Vestibular Schwannoma , progressive SNHL & tinnitus without vertigo , absence of
recruitment & stapedial reflex , very poor speech discrimination .
3. Conditions with combination of vertigo & auditory symptoms
a. Cogan syndrome , interstitial keratitis.
b. Craniovertebral junction abnormalities , carniocervical dysplasia (Dx by x-ray &
MRI) .
c. Vertebrobasilar insufficiency , transient vertigo , associated with focal neural deficit
.
d. Migraine , adolescent & postmenpausal women .
e. Non-specific cochleovestibulopathies , progressive non-fluctuating unilateral HL ,
attacks of vertigo &/or disequilibrium & abnormal ENG .
Investigations
1. Assessment of the cochlear function
a. Standard auditory assessment
- PTA ; flat audiogram in 42% , peaked pattern in 32% , down-ward slopping in
19% & rising pattern in 7% , serial PTA reveal fluctuant SNHL at 250-1000 Hz with
average amplitude 20-30dB .
- Alternate binaural loudness balance test (Fowler test) , show complete recruitment
.
- Speech discrimination score , variable & resemble the PTA in most of cases .
b. Evoked response audiometry, which is a mean of determining the electrical activity
within the cochlea & central auditory pathway in response to sound stimuli .
As , ECochleogram which evaluate the evoked potential activity of the cochlea & 8th
nerve , the transtympanic ECochleogram , obtained from the middle ear promontory
near the round window niche .
It show the following finding in MD ;
(1) small distorted cochlear microphonic potential .
(2) increased SP/AP ratio >1/3 (normal 1/3) .
(3) widened SP/AP complex >2ms (normal 1.2-1.8 ms) .
ECochleogram used for Dx of MD , in preoperative selection of the patients (those
with normal SP/AP complex) , & as a postoperative prognostic value in patients
undergone surgery .

Lecture notes in
While brainstem ERA , which evaluate the electrical activity of the central
connections .
Cochlear microphonic potential (CM) , the sound energy tranduced in the inner ear
from mechanical vibration of the basilar membrane into an electrical waveform by
the outer hair cells within the 1st few millimeters of the basal turn of the cochlea .
Summating potential (SP) , is a compound action potential (complex) representing
the sum of various electrical events occurring within the cochlea .
Action potential (AP) , represent the firing of multiple cochlear neurons
synchronously , at the basal turn of the cochlea .
Transtympanic ECochleogram during glycerodehydration , we give oral or i.v.
glycerol 200 ml of 10% solution , this will lead to significant improvement of the HL
by decreasing the endolymphatic hydrops & intralabyrinthine pressure with decrease
in the width of the SP within 2 hours of oral route (also can use urea & lasix) .
Reverse glycerol test , use diamox (carbonic anhydrase inhibitor) , increasing the
endolymphatic hydrops , cause deterioration of PTA & speech discrimination making
the Dx of MD .
Intraoperative ECochleography to assess the progress of surgery (the improvement
of SP/AP during surgery) .
c. Audiometric tests under investigations ; Brainstem ERA , to exclude retrocochlear
pathology .
2. Assessment of the vestibular function
a. Caloric test , show hypoactive reflex , 94% of MD show abnormal reaction to the test
which is either canal paresis or directional preponderance .
b. Galvanic stimulation of the vestibular system differentiate between MD &
retrocochlear disease .
c. Rotational chair test , wide variety of responses .
d. Romberg & Unterburger test , useful .
3. Metabolic & other screening tests , aimed to exclude causes of secondary hydrops ,
which include , GTT , FBS , ESR , urea & electrolytes , VDRL , TPHA , lipid profile ,
thyroid function test & immunological assay .
Management
Since the cause of MD is unknown , then no cure exist , the medical Rx improve the
symptoms of MD 60-80% & failure in 10-20% (go to surgery) .
In patients refusing any management , 57% complete resolution of vertigo at 2 years , 71%
at 3 years .
A. Medical therapy
- General considerations ;
1. Good patient – doctor relationship .
2. Explanation of the nature of the disease .
3. Psychological support .
- Symptomatic relief during the acute attack , which achieved by vestibular
suppressants which have anticholenergic , antiemetic & sedative effects like ;
Phenothiazines (Prochlorperazine) , Benzodiazepines (Valium & Lorazepam) ,
Antihistamines (Cinnarizine, astemazole & cyclazine) .
- Prophylaxis between the acute episodes ;
1. Management of vertigo

Lecture notes in
 Salt restriction & diuretics , to decrease the endolymph volume .

 Hyperosmolar dehydration , glycerol , urea & mnnitol .
 Anti or carbonic anhydrase inhibitors like acetazolamide "Dimox®" .
 Vasodilators , betahistin (which is antihistamine precursor) , papaverine , Co 2
& nitroglyceride .
 Steroids & cytotoxic drugs , for the autoimmunity of the disease .
 Hyperbaric pressure champers & herbal preparations .
2. Management of tinnitus & HL , use tinnitus maskers & hearing aids .
B. Surgical therapy
Surgery indicated as a treatment modality in MD for ;
(1) Failure of medical therapy .
(2) Special findings like ; good or normal SP/AP complex & +ve glycerol test .
- Procedures involving hearing & vestibular preservation , aim is to reverse the
1. Procedures on the endolymphatic sac
 1926 , Portmann , the 1st one who did simple opening of the endolymphatic
sac .
 Shambaugh , dod decompression of the sac by removing the overlying bone .
 Shea , use Teflon film & insert it into the sac for drainage .
 The use of one way valve to evacuate the sac ; the success rate about 80% .
It may had complications like ; severe postoperative HL , complications of
mastoidectomy , CSF leak & meningitis .
It has the advantages of being with less complications , with good success rate
(50-80%) & suitable for bilateral MD (it will preserve hearing) .
 Procedures of decompression of the endolymphatic sac , we do postaural
incision & then do formal cortical mastoidectomy , then we drill posteriorly to
delinate the lateral sinus (do not remove the overlying bone) because it is the
1 st landmark .
Then expose the antrum as the 2nd landmark , then expose the lateral SCC as
the 3 rd landmark & continue drilling deeper & posterior to it to expose the
posterior SCC (Trautmann triangle) .
The endolymphatic sac located infront of the lateral sinus & below & behind
the posterior SCC , so drilling there by cutting burr to remove the bone (2 cm
high & 1 cm wide) to expose the sac .
The sac is identified by its white colour than gray colour dura , it is then
incised (by Beaver knife from posterior forward ) , the endolymph is flowing
through the opening which remain open by applying gelfoam in the incision .
Then we close the wound in two Layers
The results are good ; 50-80% with complete resolution , 12-25% substantial
relief for 2 years , 60-70% with hearing improvement or stable & 40-60%
with improvement of tinnitus .
2. Procedures on the other ear structures
 Grommet insertion in the tympanic membrane (by Tumarkin 1966) , who
assume that MD is due to –ve middle ear pressure .
 Osmotic agents used in the scala tympani to decrease the fluid .

Lecture notes in
 Fistula creating via oval window which lead to decompression of the

endolymphatic hydrops , but cause HL , so it is abandoned , so instead of we
do round window cochleosacculotomy (80% with HL , so useful in old
patients)
- Procedures involving hearing preservation & vestibular ablation
1. Ablation of the 8th nerve
 Sectioning of the 8th nerve , the 1st to do is R.H. parry 1904 , through the
suboccipital approach .
 Sectioning of the vestibular components of the 8th nerve alone done by
McKenzie 1936 , either through , the infracranial approach (dangerous) or
total osseous labyrinthectomy , which is easier & with less side effects & has
greater accuracy , with less facial nerve injury or damage to the cochlear
nerve .
 Selective incomplete supralabyrinthine transtemporal bone vestibular
neuroectomy , by Bohmer & Fisch 1995 , through which we section the
superior vestibular nerve & singular (posterior ampular) nerve & preserve
the inferior vestibular nerve .
 Posterior vestibular nerve section .
 Transtemporal supralabyrinthine approach of the 8th nerve section , by Fisch
1984 , remove the root of zygoma & roof of the epitympanum & as much as
bone as possible from above the labyrinth itself , so better visualization of the
IAC .
 Suboccipital vestibular nerve section , by Silvestein 1987 , sectioning of the
superior vestibular nerve .
 Advantages , (1) famillar dissection to the otologist (2) good exposure of the
7 th & 8th nerves (3) less risk of injury to the facial nerve , labyrinth &
temporal lobe .
 Results ; (1) stabilization or improvement in hearing in 55-85% (2) tinnitus
improvement 31-36% .
 Complications ; (1) rarely facial nerve injury (2) CSF leak in 5% (3)
meningitis 3% (4) wound infection 20% (5) severe postoperative headache 9%
due to drilling of the posterior lip of IAC .
2. Chemical ablation of the vestibular end organ
 Neomycine & Streptomycine & Kanamycine & Gentamycine
(Aminoglycosides) .
 Neomycine & Kanamycine are cochleotoxic .
 Gentamycine & streptomycine are vestibulotoxic .
 Schuknecht 1956 , the 1st who use intratympanic streptomycine , 63% cured
(all have increase in HL) .
 Indications ; active unilateral MD with frequent disabling attacks of vertigo
irrespond to medical management .
 Contraindications ; (1) active OM (2) allergy (3) impairment of renal function
(4) MD in only hearing ear .
 Method ;
- T-tube inserted in the tympanic membrane , the tube attached to the
external ear to prevent movement .

Lecture notes in
- a solution containing 26.4 mg//ml of gentamycine instilled (0.8 ml) in

the middle ear .
- the patient then lie for 20 min. to make pooling to the round & oval
windows .
- this repeated for 3 times daily for 4 days.
- management stops if develop nystagmus /unsteadiness or significant
hearing deterioration .
 The results ; (1) 100% vertigo relief (2) 89% decreased caloric excitability &
(3) 10% with total deafness .
 Parenteral streptomycine used in bilateral MD , so cause bilateral vestibular
ablation (20 gm titration with monitoring to the vestibular function during
therapy) , this is the preferable method nowadays .
3. Non-chemical ablation of the vestibular end organs
 Ultrasonic irradiation applied to the capsule of the horizontal SCC or to the
round window causing irritative nystagmus , then no nystagmus & then
paralytic nystagmus . , when no irritative nystagmus , then there be total
vestibular ablation , it cause recurrent vertigo as a long term results .
 Cryosurgery ; transmastoid application of cryoprobe of – 160 C o to the lateral
SCC for 3 cycles of 2 minutes each .
The results are ; (1) 73% control of vertigo (2) 5-8% delayed facial nerve
palsy &(3) recurrent vertigo (high rate) .
- Procedures involving hearing & vestibular ablation
This is by labyrinthectomy which is destructive procedure with total & irreversible
destruction of the sensory cells of the inner ear with complete relief of MD symptoms
Indicated in patients with MD & poor hearing (>60dB HL) .
It is either through the transcanal approach or transmastoid approach , the
neuroepithelium destroyed by mechnical or chemical means , most patients need
revision surgery due to incomplete removal of the neuroepithelium .

Lecture notes in
OTOTOXICITY
Many drugs may cause damage to the inner ear leading to deafness , tinnitus & vertigo ,
some drugs appear to have central effects on the brainstem , these effects can be transient
or permenint .
Hearing loss ; the classical effect is usually initial high frequency HL which progress until
become noticeable HL . Follwing withdrawal of the drug , there will be some recovery of
the auditory function & recovery partially damaged hair cells , other drugs may produce
flat SNHL which also recover .
Tinnitus ; it represent the initial manifestation of the cochlear changes , which include
direct neural element involvement or damage in the outer hair cells , tinnitus is of high
frequency , often continuos .
Vertigo ; some drugs are vestibulotoxic causing vertigo & nystagmus , darkness or poor
vision make the symptoms worse (peripheral cause) , in caloric test , absent or decreased
bilaterally .
There aremany drugs that are known to be ototoxic to the inner ear (cause damage to either
the auditory or/& the vestibular systems) .
The most significant drugs are ;
1. Aminoglycosides
It affect the neural tissue , kidney & inner ear , in inner ear it affect the sensory cells in
the cochlea , it affects preferentially the outer hair cells in the basal coil & the damage
spreads apically from the high frequency & then to the lower frequencies .
The damage start at the outer hair cells & then to the adjacent supporting cells & later
the inner hair cells nave been lost .
Studies of aminoglycosides showed that the drug enter the perilymph slowly within 4
hours after injection following the drug entry the stereocillia may be the primary site of
drug action where the cationic aminoglycoside will distrupt the negatively charged cell
coat over the stereocilliary surface , so the membrane of the adjacent stereocillia come
closely together leading to fusion of the stereocillia .
Another hypothesis , is that the aminoglycosides interact specifically & irreversibly with
the phospholipids of the cell membrane causing activation of the biochemical pathways
that control various aspects of cellular physiology .
Aminoglycosides may affect organ of Corti & stria vascularis which become thinner &
atrophid , there are 3 stages of interaction of aminoglycosides with the hair cells ;
a. Initial reversible binding of the drug with the phospholipids .
b. Selective uptake into the hair cells .
c. Irreversible binding of the drug to the phospholipids , which increase the
permibility of the membrane , increasing the entry of the drug .
2. Cisplatin
It is chemotherapeutic agent which is predominantly cochleotoxic & less vestibulotoxic .
It cause loss of the hair cells which resembles that of aminoglycosides & the outer hair
cells in the basal turn are preferentially affected , it enter the perilymph causing
blockage of the transduction channels , affecting the compound action potential .
It may affect also stria vascularis causing strial atrophy .
3. Salicylate
It is ototoxic even within therapeutic dose , it cause hearing loss , tinnitus & vertigo .
Hearing loss is mild-moderate , symmetrical , usually flat , sometimes variable .

Lecture notes in
Tinnitus is of high frequency .

The cation is in the cochlear blood supply where there is construction of the blood
vessels in the stria vascularis due to the effect of the drug on prostoglandines causing
ischemia & anoxia which affect the action potential .
It may enter the perilymph also , effecting on the outer & inner hair cells , but mainly the
outer cells leading to flat HL .
It can affect the permeability of the cellular membrane which lead to increase the
potassium ion (neurotoxic) & decrease the chloride conduction blocking the channels .
4. Quinine
Its action is similar to that of salicylate , it causes construction of the cochlear
capillaries (ischemia) , another effect is that its perilymphatic perfusion will affect the
compound action potential effect on the outer hair cells .
It may affect the intracellular calcium .
5. Loop diuretics
It interfere with the normal ion transport process in the endolymph which decrease the
compound action potential causing HL .
It may affect also the ion transport through the vestibular cells , it affect the stria
vascularis causing extensive oedema in it which is due to the fact that loope diuretics
may cause inhibition of Na/K ATPase & adenyl cyclase in the stria , so affect Na/K/Cl
transport .
6. Erythromycine
It is rare & reversible , some times permanent , it is seen in patients with poor renal or
hepatic function .
Topical ototoxicity
1. There is potential of ototoxicity of aminoglycosides containing ear drops , only 2% of
patient used antibiotics ear drops develop SNHL .
So these should be used cautionsly in patient with tympanic membrane perforation .
2. Also , alcohol containing antiseptics solutions like chlorhexidine which may be used
for cleaning before surgery are though to be cochleotoxic .
The route of absorption is the round window although its membrane is thick which
provide partial protection .
Ototoxic synergism
- There is several drugs that are administrated concurrently , which may lead to
potentiation of the ototoxicity even in recommended dose limit , e.g. loop diuretics &
aminoglycosides .
- Noise exposure seems to increase the susceptibility to drug –induced cochleotoxicity
especially after high intensity noise , this is synergestic effect rather than additive .
Management of ototoxicity
The aim is to prevent or decrease the adverse effects of the ototoxic drugs , this can be
achieved by ;
1. Avoiding or discontinuing the ototoxic drug if satisfactory alternative is available .
2. Performing baseline audiometric & vestibular tests .
3. Beraing in mind the high risk patients .
4. Limiting the drug dose within the safe therapeutic levels .
5. Using tinnitus masking fro patients with severe tinnitus .

Lecture notes in
Methods for evaluation of the ototoxicity

A. Preyer reflex : It is a twitching of the pinna in response to sounds of different
frequencies & intensities so with HL the reflex decreased .
B. Behavioral response audiometry : It is experimental method where the animal learn to
do some tasks when hearing the sounds .
C. Brainstem eveoked potential : Stimulation of the auditory nerve by sounds lead to
stimulation of the centers along the auditory neural pathways in the brainstem & the
cortex .
This electrical activity can be recorded by electrodes placed on the skull , it is non-
invasive & can be used repeatedly .
D. Otoacoustic emissions : The sound stimuli can elicit active mechanical responses
which cause emission of sounds within the ear called cochlear echo or otoacoustic
emission which can be detected in the EAM .
It is non-invasive & can be used repeatedly .
E. Structural examination : Examination of the iner ear structures by light or electron
microscope can be used to evaluate the ototoxic injury & histological assessment of
the hair cells (both loss & regeneration) .
Regeneration & appearance of new hair cells appear both in the auditory & vestibular
portions of the inner ear , they arise spontaneously through damage –induced
stimulation , this regeneration cause functional recovery .
F. Compound action potential : This can be achieved by placing electrodes close to the
round window which detect the neural excitation following sound stimuli , it is invasive
technique

Lecture notes in
HEARING LOSS
The diagnostic approach to hearing loss is as follow :
1. History ; onset , duration , progression , otalgia , ottorrhea , vertigo , tinnitus , ear
diseases in childhood , obstetric & neonatal history , family history , noise exposure , ,
ototoxic drugs & history of trauma .
2. Examination ; through out ENT examination & neurological examination .
3. Investigations
- Haematological ; FBC , ESR , VDRL , FBS , triglyceride , thyroid function test .
- Radiology ; mastoid x-ray , middle ear tomography , internal auditory meatus x-ray ,
temporal bone CT , MRI , sinus x-ray .
- Audiology ; PTA , speech audiometry , tympanometry , acoustic reflexes & tone decay ,
Bekesy , evoked response audiometry , vestibular function studies .
Conductive hearing loss
Causes
1. Congenital
a. Syndrome related ; e.g. Treacher Collins syndrome .
b. Isolated ; Otosclerosis ,Ossicular defects , Meatal atresia ..etc .
2. Acquired
a. Traumatic ; barotrauma , head injury , iatrogenic ..etc .
b. Neoplastic ; benign (osteoma) & malignant (SCCa of the middle ear) .
c. Infective ; otitis externa , ASOM , CSOM , T.B. , …etc .
d. Miscellaneous ; wax , keratitis obturans , middle ear effusion , …etc .
Sensorineural hearing loss
Causes
1. Congenital
a. Genetic :
- Syndrome related ; e.g. Penard's syndrome .
- Chromosomal ; trisomy 18 .
- Isolated ; familial progressive , Sensorineural deafness , inner ear apllasia ,
congenital Cholesteatoma , …etc .
b. Intrauterine ;
- Infective ; Rubella , Syphilis , Toxoplasmosis , CMV , ..etc .
- Toxins ; Hypoxia , Kernicterus ,& drugs .
c. Perinatal ; birth injury , hypoxia & anoxia .
2. Acquired
a. Traumatic ; noise , head injury, iatrogenic ..etc .
b. Neoplastic ; benign (vestibular Schwannoma) & malignant (SCCa of the middle ear)
.
c. Infective ; measles , mumps , influenza , syphilis , suppurative labyrinthitis & herpes
zoster oticus .
d. Degenerative ; presbyacusis .
e. Metabolic ; MD .
f. Toxins ; Ototoxic drugs .
g. Vascular ; cardiac by pass surgery .
h. Miscellaneous ; in association with other systemic disease (DM) or idiopathic .

Lecture notes in
History
1. When did the 1st notice of HL by the patient .
2. Onset ; sudden or gradual .
3. Site ; unilateral or bilateral .
4. Course ; progressive , static or fluctuant .
5. Associated symptoms ; discharge , tinnitus , vertigo …etc .
6. Duration ; short history , or long one .
Examination
1. Otoscopic examination ; to show tympanic membrane & external auditory canal
"EAC" .
2. Tuning fork tests , Weber & Rinne's tests (256 & 512 Hz) .
Audiometry
1. PTA ; to show the degree of HL & at which frequency .
2. Speech discrimination score test ; based on 25 phonically balanced monosyllables
presented at 40 dB above the average PTA threshold for 0.5 , 1 & 2 KHz .
3. Stapedial reflex & tympanometry .
4. Other , BERA , radiology …etc .
According to audiogram , SNHL divided into 3 groups ;
A. Bilateral SNHL
- Symmetrical
1. Presbyacusis ; it is the commonest cause of bilateral symmetrical SNHL , it is
slowly progressive , the patient over 60 years old .
Sensory presbyacusis , due to loss of hair cells secondary to initial loss of
supporting cells , the loss of outer hair cells mainly at the apical & basal turns of
the cochlea , while the inner hair cells less marked & occur at the basal turn only
, loss of the hair cells in the 10 mm region of 4 KHz frequency (mainly due to
acoustic trauma) .
At 1st , loss of sterocilia , distorted & flattened organ of Corti & loss of
supporting cells .
Neural presbyacusis , due to loss of cpchlear neurons , characterized by
progressive loss of word discrimination with stable PTA threshold , the whole
length of the spiral ganglion is affected especially at the basal turn , so the high
frequency is more affected .
Metabolic presbyacusis , atrophy of the stria vascularis , lead to flat audiogram
with good speech discrimination score , the organ of Corti & spiral ganglion
appear to be normal .
Mixed presbyacusis , combination of any of the above .
Inner ear conductive deafness , cochlear conductive presbyacusis , characterized
by Ski-slope audiogram with only slightly impaired speech discrimination , it is
due to the resonance characteristics of the cochlea , here there is atrophy of the
spiral ganglion & basilar membrane (lipidosis of the basilar membrane) .
Indeterminate presbyacusis , there is no microscopically evidence of of cochlear
damage , but there is bilateral symmetrical SNHL which increased with age .
2. Industrial noise induced deafness ; occurs when there is exposure to the noise of
85-90 dB for average of 40hrs/week .

Lecture notes in
3. Ototoxic hearing loss ; the diagnosis by history of ingestion of drugs , causing

irreversible HL , but for drug causing reversible HL like aspirin , need further
inquiry .
4. Dish-shaped audiogram , moderately severe loss for the middle frequencies &
good hearing for the high & low frequencies , it is due hereditary causes .
- Asymmetrical
1. Weapons firing ; especially firing from the shoulders , other weapons like
antitank , rockets & launchers .
2. Head injury & explosion , due to uneven blast pressure wave .
3. Menier's disease , congenital or late syphilis & bilateral vestibular Schwannoma
.
B. Unilateral SNHL
Usually it is of sudden onset & due to :
1. Trauma , like head injury , blast injury , acoustic accident & damage at surgery .
2. Vascular , interference with cochlear blood supply .
3. Viral infection , like mumps .
4. Vestibular Schwannoma .
5. Reissiner's membrane rupture .
6. Perilymph leak .
7. Perinatal causes .
Diagnosis done by CT scan , MRI & BERA .
C. Deafness with normal PTA ; 5% , with excellent speech discrimination & it is called
obscure audiometry disorder (OAD) , it may be due to ; (1) anxiety (2) multiple sclerosis
(3) psychoacoustic (4) tumors causing pressure on the central auditory pattern .
Mixed HL ; conductive – Sensorineural HL , caused by ; otosclerosis , CSOM & secretory
OM , usually due toxins which damage the inner ear together with altered mechanism of
sound transmission .
Immune SNHL
The autoimmune diseases can cause deafness which may reverse with immunosuppressive
therapy , it is common with middle aged females with other autoimmune diseases with high
ESR & Ig & C-reactive proteins .
Suspected malingering HL
It is suspected after exclusion of other causes , which arise in the 1st few minutes of
interview of the patient , in audiometry , he attempts to exaggerate the severity of the loss ,
the recorded hearing level inconstant with his ability to hear the spoken words .
General management of HL
The extent of deafness should be explained to the patient , explaining that high frequency
HL is increased with noise & most SNHL are irreversible , hearing aid is the main help for
the patient
Sudden and Fluctuating HL
Fluctuating HL :
1. Middle ear pressure changes lead to CHL .
2. Inner ear function fluctuation lead to SNHL , like in MD , syphilitic labyrinthitis &
Perilymph fistula .
Sudden HL : presents a therapeutic dilemma .
The causes for sudden CHL are ;

Lecture notes in
A. External ear canal occlusion with wax or foreign body .

B. Infection ; like otitis externa , AOM or CSOM .
C. Trauma , like surgery (iatrogenic) or direct blow , barotrauma & acoustic trauma
(non-surgical) .
The causes for sudden SNHL are ;
A. Cochlear causes
1. Inflammatory
a. Bacterial
- Acute OM ; small proportion of the AOM lead to SNHL , which may only become
apparent in later life (can't use phone) .
- Typhoid fever ; at the 2nd -3 rd week , cochleovestibular lesion may lead to SNHL ,
either bilateral or unilateral , mostly female , with abnormal caloric test .
- Brucellosis ; after 10 weeks with +ve blood culture , neurobrucellosis affecting the
8 th nerve causing SNHL which is irreversible by tetracycline & rifampicine .
- Other bacterial infections may lead to SNHL .
b. Spirochates
- Syphilis ; congenital or acquired can cause SNHL , usually bilateral with features
of MD .
- Lyme disease ; reversible SNHL with vertigo & abnormal ABR results .
c. Riekettsiae , Typhus ; gram –ve bacilli causing early serious SNHL .
d. Mycoplasma
- Mycoplasma Pneumonoae , affect the CNS causing SNHL with tinnitus & vertigo .
- Bullous myringitis , with sudden SNHL .
e. Chlamydia , like C. trachumatis & C. psittaci , one case report of sudden SNHL
with interstitial keratitis , uveitis & CV lesions .
f. Viral
- Mumps ; uncommon cause of SNHL , 0.1% of cases , usually unilateral & of
gradual onset , usually seen in adults .
- Measles ; more common . 5-10% , abrupt bilateral SNHL .
- Chicken pox (Varicella) , CNS complications , SNHL , cerebellar ataxia , aseptic
meningitis & transverse myelitis .
- Varicella zoster , 7th nerve palsy with SNHL (Ramsy Hunt syndrome) .
- Others ; IMN , Lassa fever & HIV causing SNHL .
g. Protozoal , like toxoplasmosis , causing reversible SNHL with total loss of
vestibular function .
2. Traumatic
a. Electricity ; like lightening , sonic wave shock may lead to acoustic rupture of the
tympanic membrane (uni-or bi-lateral) & transient bilateral SNHL .
b. Iatrogenic
- Radiotherapy ; the total radiation dose related to the inner ear damage , especially
the organ of Corti may lead to SNHL , the degree of which increased with the
increase in the dose of radiation .
- Postoperative , microembolism involving the cochlear division of the internal
auditory artery may cause SNHL .
- Anesthesia ; nitrous oxide lead to middle ear damage & SNHL .
- Spinal anesthesia , transient SNHL with vestibular symptoms .

Lecture notes in
- Dental surgery , 4 cases reported causing unilateral SNHL .

3. Vascular
a. Hypertension ; cause vascular obstruction of the inner ear with atherosclerosis &
aneurysm which decrease the cochlear blood supply & flow , it cause
vestibulobasilar occlusion disease .
b. Burger's disease ; thrombangitis obliterans , it cause intermittent claudication &
HL . The use of vasodilators may amprove the leg blood supply but not the ear
(HL) .
c. Thrombophilia ; thrombosis may cause stasis of the blood flow leads to SNHL .
d. Viscosity ; it cause ischemia .
4. Haematological
a. Anaemia ; with Fe ++ deficiency , megaloblastic anaemia , aplastic & pernicious
anaemia , all may cause marked decrease in blood flow lead to ischemia & SNHL .
b. Sickle cell disease , it lead to hypoxemia (stasis , anoxia of the cochlear blood flow)
, increase incidence of bacterial meningitis & neurological involvement .
c. Thalasaemia , it lead to ; low Hb level with resultant hypoxemia , ototoxicity of
desferrioxamine & haemochromatosis & haemosiderosis leading to neurological
involvement causing SNHL .
d. Cryoglobulinamia ; the cryglobuline precipitate in the cold & redisolve in worm , it
cause diminished cochlear blood flow .
e. ALL , it can affect ;
- The middle ear through infiltration, infection & haemorrhage , destroying the
ossicles & also the bone marrow of the petrous bone .
- Inner ear ; uncommon , sudden SNHL &/or vertigo .
5. Autoimmune disease
a. Systemic vasculitis ; characterized by +ve ANCA (antineutrophil cytoplasmic
antibodies) .
b. SLE ; characterized by high ESR , C3 , C4 , antibodies to double stranded DNA ,
autoantibodies leading to SNHL . Also it may be due to CNS involvement ,
immunosuppressive drugs or without any cause .
c. Cogan syndrome ; characterized by non-syphilitic keratitis lead to vestibular &
cochlear disorders causing fluctuation HL with remission & exacerbations .
d. Relapsing polychondritis ; involve the Eustachian tube causing OME & SNHL .
Wegner's granulomatosis ; it is differ from lethal midline granuloma , it has 3
components ;
- Necrotizing granulomatosis ;esion in the upper & lower respiratory system .
- Generalized focal necrotizing vasculitis of both artery& vein almost in the lungs .
- Glomerulonephritis .
The hearing loss either due to involvement of paranasal sinuses or OME .
e. Others ; like polyarteritis nodosa , Giant cell arteritis (temporal arteritis) ,
Kawasaki disease , Takayasu disease & Behçet disease & endolymphatic hydrops .
6. Metabolic disorders
a. Renal failure ; it is due ether to ; hyponatraemia , dialysis or transplantation , or
DM .

Lecture notes in
b. Alport's syndrome ; characterized by nephritis , SNHL & +ve family history (x-
linked recessive M>F) , the SNHL due to degeneration of the stria vascularis , loss
of hair cells & cochlear neurons .
c. Renal transplantation ; the HL due to dialysis , lasix & immunosuppressive drugs
may cause thromboembolism .
d. DM ; the HL due to neural complications (peripheral & central neuropathy) &
vascular complications (retinopathy & nephropathy) . The degree of HL depends on
the duration of the DM & the control .
e. Others ; like renal tubular acidosis , IgA nephropathy , hyperlipidaemia ,
hypothyroidism & Refsum's disease .
7. Skeletal system & otic capsule ; metastatic carcinoma & osteoma of IAM lead to
SNHL .
8. Ototoxicity ; interferon , contraceptive pills (thrombotic effect) , Co toxicity (which
cause carboxy Hb , deoxygenation of the vital organs) & vaccinations like tetanus
toxoids & vaccine for small pox , rabies & whooping cough .
9. Endolymphatic hydrops & MD , cause SNHL , 5% of sudden SNHL eventually
develop MD .
10. Miscellaneous
a. Ulcerative colitis , due to immune complex vasculitis .
b. Scleroderma , the SNHL due to management by cyclophosphamide .
c. Sarcoidosis , due to granulomatous meningitisor 8 th nerve involvement .
B. Retrocochlear causes (vestibulocochlear nerve or CNS)
1. Meningitis , like bacterial & viral meningitis lead to sudden bilateral total or
subtotal SNHL .
2. Multiple sclerosis , multiple areas of demyelination of the CNS may lead to SNHL at
the 1 st 4 years of the disease .
3. Friedreich's ataxia ; affect the peripheral; nerves causing SNHL .
4. Amyotrophic lateral sclerosis ; involvement of the 8th nerve may lead to bilateral
severe SNHL .
5. Xeroderma pigmentosa , central SNHL .
6. Tumors
a. Vestibular Schwannoma lead to SNHL .
b. Metastasis in the CPA lead to SNHL .
c. Carcinomatous neuropathy especially with lung Ca. , ovary & stomach &
Hodgken's disease .
7. Central deafness ; like in cortical encephalitis & Alzheimer's disease .
C. Idiopathic
It is due to (pathogenesis) :
1. Viral infections (thrombosis) .
2. Viral & vascular causes (thrombosis) .
3. Cochlear membranes break or rupture or disrupted lead to sudden SNHL with
marked tinnitus .
It has the following symptoms ;
- Sudden onset HL , or deafness occur for short period of time , from hour to 3 days .
- The age ; 75% of patients more than 40 years old .
- Precipitating factors ;

Lecture notes in
 30-40% with viral infections which can be divided into 3 groups ; (1) URTI
viruses like Influenza , Parainfluenza , RSV & Rhinovirus , (2) Poliovirus ,
Coxsakie virus , Rubella virus , EBV , adenovirus & HSV , (3) Mumps ,
Measles & Varicella zoster virus .
 Noise ; can cause acute deafness .
- Other symptoms are ; (1) pain or feeling of pressure in the ear , (2) tinnitus "80%" of
favorable prognosis because it indicates that the cells are still functioning & may
recover , (3) vertigo , which is of vascular aetiology & it carry poor prognosis &
indicates the need to exclude vestibular Schwannoma .
Investigations
1. Haematology ; CBP , ESR , PT , plasma viscosity , sickle cell test , GTT , LFT , renal
function test , Paul Bunnell test , serology for syphilis & viral studies .
2. ECG .
3. Radiology ; CXR , MRI , CT scan (if MRI not available) , the MRI is important to
exclude vestibular Schwannoma & to show the vestibulocochlear & facial nerves &
any labyrinthine changes .
4. Audiometry ; PTA , tympanometry , tone decay , stapedial reflex , fistula test , ABLB ,
ABR & otoacoustic emission .
The patient with upwards slopping audiograph means low frequency HL (good
recovery) , while patients with downwards slopping audiographs with poor
prognosis , the benefit of the PTA is to assess the level of HL , , the type of HL &
determine the site of the lesion
5. Lumbar puncture ; for CSF examination .
Management
Unfavourable prognosis seen in : (1) High frequency loss , (2) Severe HL , & (3) Presence
of vertigo , there is 50-60% of cases improvement within 15 days . The management include
1. Increasing the cochlear blood flow (for cochlear HL)
- Vasodilators ; increase the inner ear oxygenation , like Betahistine (induce
vasodilatation , due to its histamine effect on H receptors in the cochlea , therefore
increasing the cochlear blood flow) , Glycerol (increase cerebral & cochlear blood
flow) , Ca + antagonists (cause peripheral vasodilatation) .
- Low molecular weight dexran 40 (decrease the coaguability of the blood) .
- Inhalation of 5% Co2 & 95% O2 (Carbogen cause vasodilatation) .
- Anticoagulants like Heparin (decrease serum lipids) .
2. Steroids (for retrocochlear HL)
It is the management of choice for the retrocochlear deafness , the patient receiving
steroids should be examined regularly for the side effects by checking the blood
pressure & ECG & electrolytes , the dose regimen is Prednisolone for 20 days as
follow ;
- 60 mg for 1 day .
- 50 mg for 1 day .
- 40 mg for 3 days .
3. Bed rest , avoid excersion which is important if the cause is membranous rupture .

Lecture notes in
4. Management of the cause , if possible .

Noise induced hearing loss
The noise are of many types ;
- Psychological : any sound which is unpleasant or unwanted .
- Physical : which is a complex sound having little or no periodicity which can be
measured or its characteristics analyzed .
- Physiological : a signal that bears no informations & whose intensity varies
randomly in time .
The noise has intensity (in dB) , frequency (in Hz) & a duration , it is also either continuous
, intermittent or impulsive .
The white noise defines as a random sound with a spectrum containing mixture of all
frequencies .
The pink noise , is a fabricated sounds which contain a constant power .
The damaging effect of noise depend on ; the characteristics , frequency , intensity ,
duration , time interval between the exposure & the individual susceptibility (nature &
previous SNHL) .
It is 1st described by Haberman , 1890 , as partial displacement of organ of Corti with
destruction of the hair cells , practice exposure is 90 dB for 8 hours/day for 5 days/week .
Noise induce HL is either ; insidious (chronic noise exposure) , explosive (single exposure
to an intense sound stimulus) or accidental (abrupt HL after certain period of noisy work at
an intensity level not higher than that previously exposed to) .
Effects of sound stimulation
A. Functional changes
- Adaptation ; prestimulatory fatigue , it is immediate phenomenon which occur when a
sound is presented to the ear , somewhat elevating the threshold , for fatiguing sound
of up to 80 dB , the greatest adaptation is produced for an identical test tone of
identical frequency or reduction in sensitivity with time due to prolonged stimuli (not
depend on the duration) .
- Temporary threshold shift "TTS" , post stimulatory fatigue , occur due to prolonged
duration or stronger (intensity) exposure to noise , TTS last > 2 min. recover
completely within 16 hours , TTS lasts more with > 40 dB , recovery within 2 weeks
(long lasting TTS) , which is pathological & frequently associated with some degree of
residual perminat threshold shift "PTS" .
- Permanent threshold shift ; Irreversible elevation of the auditory threshold associated
with pathological changes in the cochlea , not recover after 2 weeks & then continue ,
it may called occupational HL , industrial noise induce deafness , NIHL , or stimulated
deafness , so the acoustic notch (or dip) at 4 KHz .
- Asymptomatic threshold shift " ATS" , the length of sound exposure at a given intensity
above which no further TTS occur , 74 dB at 4 KHz , 78 dB at 2 KHz & 82 dB at 0.5
KHz (the lower frequency of sound stimulus , the higher the basal level above TTS
occur) .
B. Structural changes of noise
- Dynamic phase ; during the sound stimulus , the inner row of outer hair cells
damaged more than inner rows , then the inner pillar cells , inner hair cells ,
associated with degeneration of organ of Corti , spiral ganglia & auditory nerve
changes .

Lecture notes in
In temporary threshold shift , there is shortening of the supracuticular rootlets , while

in permanent threshold shift , the rootlets fractured or damaged leads to less auditory
sensitivity & cells death .
- Static phase ; when the noise cease , either full recovery , partial recovery & scarring
or destruction occur .
All changes are encountered more prominently at 4 KHz because the sense of that
frequency located at the basal turn of the cochlea which is firmly fixed & more
susceptible to torsion & damaging eddies & vascular vulnerability of this are &
increased amplitude of the sound waves between 2-3.5 KHz due to the resonance of the
EAC .
There is also what called heat shock protein produced in noise exposure .
Natural history of NIHL patients
Noise induce HL start around 4 KHz & gradually worsens at that frequency , then spread
into neighboring frequencies , at 1st it is asymptomatic , but if spread into the lower
frequency of 3 or 2 KHz , then the complaint begins , initially poor speech discrimination
(espec
ially if there is any background noise) with spreading to lower frequencies , there will be
difficulty with sounds being too quite , after a time there will be a flat audiogram at the
high frequency .
Hearing loss at 4 KHz , progress rapidly at 1st (15-20 dB/1-2 yrs) , with 90 dB daily
exposure for 8 hours , the loss continuous to worsen fair swiftly for 10 years & then slow
down athough , it doesn't stop completely (presbyacusis increase the loss) .
85 dBA/8hrs , protect 90% of the population , the rate of progress depends on ;
a. Type of noise .
b. Intensity of noise .
c. Repeated exposure .
d. Individual susceptibility .
Tinnitus presents for some hours , after noise exposure , usually but not always disappear
, chronic tinnitus in prolonged exposure found in 50-60% , characterized by ; tonal ,
relieved by hearing aid , worse with worsen hearing , greater in those exposed to impact
noise .
Synergistic effects of oto-traumatic agents
1. Drugs ; garamycine , kanamycine (dose related) , also salicylate & cisplatine.
2. Vibration ; those with white hands (Raynoud's Phenomenon) & exposed to explosive
sounds , more hearing loss .
3. Noise & Age ; in younger persons there will be greater damage for noise exposure ,
in premature infants more with noisy incubator & garamaycine Rx , but old age they
had presbyacusis .
4. Previous noise induced HL ; ripe ear , it is affected less than the grean ear (that is
not exposed to previous noise) .
5. Degree of melanization ; melanin protect from noise , so black < white , while
albinos or blue-eye people are more susceptible to damage .
6. Acoustic reflex ; stapedius muscle contraction , after 30 dB sounds , if higher
frequency then this cause fatigue to the muscle (no protective effect) .

Lecture notes in
7. Environmental hydrocarbons ; jet fuel & styrene cause psycho-organic syndrome

which affect the auditory & vestibular systems . Also toluene (paints , printing inks &
leather tanning) & Co poisoning (central deafness) .
Some types of noise
1. Acoustic trauma like explosion & telephone or bombs & shells .
2. Otitic blast injury .
3. Non-industrial noise hazards ; like ;
a) Guns .
b) Sociacusis .
c) Community noise exposure (air craft & underground trains) .
d) Compression champers & diving .
e) Recreational noise exposure : (a) fire works & cap pistols (b) snowmobiles (c) sports
, motor cycles riding , boxing ..etc (d) air crafts (e) hobbies , gardening equibments ,
leaf blowers , edger's & chain saws (f) pop music (g) recorders & radio (h) classical
music .
f) Medical noise ; hazards from hearing aids , hospital noise (MRI , Lab. , Kitchen &
ICU) , drills , dental drills & suction units (large burrs > small burrs , sound :107
dB ) , vibration & U/S .
Noise & Health
- Increased mental hospital admission in those subjected to high levels of air crafts
noise .
- Noise sensitivity associated with further psychiatric disorders & it is a secondary
symptom of depression .
- Associated with increased risk of heart diseases .
- Effects on children & their behavioural development lead to learning hopelessness
(non auditory effects of noise) .
Diagnosis
- History ; occupational , personal , familial , recreational , accidental noise exposure
, head injury , Ototoxic drugs , military service , disease like MD , otosclerosis ,
CSOM , acoustic neuroma …etc .
- Examination ; throughout ENT examination & cranial nerves .
- Investigations ; haematological , serological , radiological , audiological (PTA ,
usually 4 KHz dip , under water sounds , notch at 1-2 KHz) , other like behavioural
threshold audiometry , Bekesy , ERA , ABR , SUR , EcochG .
Management
- Reassurance & rest .
- Hyperbaric oxygen .
- Carbogen ; 10% C02 + 90 O 2 , which is vasodilator & prevent NIPTS .
- Rehabilitation :
a. Assisting listening devices .
b. Hearing aids (high frequency aids) .
c. Management of psychological aspects .
N.B.: asymmetrical HL , due to other ear deafness , asymmetrical noise exposure or
unexplained asymmetry , Dx by find the same PTA but lower in one ear & by ABR .
Hearing conservation programs
It needs engineering , managerial , audiological & medical skills , it has 8 phases :

Lecture notes in
1. Noise hazards identification .

2. Engineering control .
3. Personal hearing protection .
4. Monitoring audiometry .
5. Records keeping .
6. Health education .
7. Enforcement .
8. Programmes evaluation .
Sounds measurements
Sound pressure level (SPL) at different typical works , need special equipments, worker
exposure to sounds must not be 85 dB not more
Sounds control need personal protection & engineering control (redesigning machinery) .
The hearing screening aims to ; identify those with HL , identify those whose hearing
altered & determine whether the hearing conservation program is effective .
The new employers should retested every 3 months , then every year (Dx the tender ear) ,
test after 16-48 hours out of work , a shift of 15 dB or more with 2 frequencies , then
referral .
Personal hearing protection
Used when noise level remain hazardous & the workers can't be isolated ;
1. Passive protection ; ear plugs (25 in lower frequency & 40 in high frequency) & ear
muffs (30 lower frequency & 50 in higher frequency) , this can be modified by adding
acoustic filters .
2. Active protection ; incorporate electronic circulatory akin to a hearing aid with a
good automatic gain control , they are fitted to a muff which has a microphone &
amplifier which allow low intensity sounds to pass , but which cut out at a
predetermined intensity usually 85 dB to act as a passive muff .

Lecture notes in
Deafness in children
The accurate assessment of hearing in young children is the highly specialized work of a
team of experts , but much valuable information can be obtained from a careful and detailed
history.
The defective speech of the partially hearing child is essentially a vowel speech, defective in
the fainter, high-pitched consonant sounds . the extent of the defect will depend very largely
on the nature and severity of the deafness (which also determine the age at which it is likely
to be noticed) and may vary from a very marked defect , almost entirely devoid of
consonants and usually noticed during the second year of life , to a minimal disturbance
which may go quite unnoticed or be passed as normal childish speech until the child enters
school. Particularly does this apply to cases of abrupt high – tone deafness , in which the
cause of the speech disorder may not be recognized until the child is 7 or 8 years old , and
in exceptional cases several years older .
The more severe the deafness , the earlier is it likely to be detected by the parents. And in
cases of total or sub-total deafness it is not uncommonly suspected within the first year –
usually because the child shows none of the normal reactions to the many loud noises of
everyday life ; sometimes because ،he has always been so placid, or ،he seemed too good ,
. As in all things , experience counts for much , and any mother will tend to recognize a
relatively slight degree of deafness in her third or fourth child earlier than she would
suspect a severer one in her first – born.
Many children who are born partially deaf learn to lip – read quite spontaneously . They "
listen with their eyes" , and deafness should always be suspected in the child who looks with
rapt attention at the speaker's lips.
When a mother thinks her child is deaf , she is very rarely wrong and it is unforgivable to
dismiss a mother 's convictions without a most careful and thorough examination of the
hearing.
With the rare exception of congenital atresia of the external auditory canal , physical
examination of the ears is entirely negative and X – rays are of limited value . Since the
deafness is the sensorineural type in the vast majority of children born deaf their handicap
can be diagnosed only by the functional examination of their hearing.
GENETIC FACTORS AND DEAFNESS
There are 46 chromosomes, 44 are autosomal and 2 sex chromosomes.
The 44 autosomes comprise 22 chromosomes pairs, one of maternal and one of paternal
origin. Within a chromosome pair the order of the gene is exactly alike. Alternative forms of
the gene are known as alleles and may or may not be interfere with function of the gene.
If both alleles of the pair are the same, then the individual is homozygous at that gene locus
and if two different allelic forms of the gene exist within the pair, the individual is
heterozygous.
When a gene is expressed (i.e. apparent in the phenotype) in the heterozygous state, that
allele is said to be dominant.
Mendelian Genetics
Autosomal dominant, if an allele undergoes a disease causing dominant mutation, the
individual will manifest the disease even though there is a normal allele present at the same
locus on the paired chromosome.
• 50% chance of passing the normal allele to the offspring and a 50% chance of passing
the disease-bearing allele to the offspring.

Lecture notes in
• The family tree will show vertical transmission from one generation to the next.
• E.g. Marfan's syndrome.
Autosomal recessive, the individual must have disease causing mutation on both maternal
and paternal alleles before the disease manifests itself clinically.
• The risk of transmitting the disease to the next generation is much smaller.
• Recurrence rate 25%.
• Increase with consanguinity.
• E.g. sickle cell disease.
Pseudodominance, autosomal recessive disease is usually seen in a single generation,
unless there is consanguinity in successive generation which would facilitate the emergence
of the disorder in several generations of the same family.
X-linked recessive, if a gene involved in a mutation on the X chromosome, then the
condition will be apparent in males who are hemizygous for most loci on this chromosome.
• The females (heterozygous) will be asymptomatic (carrier).
• Male offspring: 50% affected 50% unaffected
Female offspring: 50% carrier 50% non carrier •
• E.g. haemophilias A and B
X-linked dominant, generally lethal in male as the normal allele is required for the patient
to survive.
• Females have dominant mutation on one of the X chromosome which are fully expressed
on the heterozygous state and are compatible with life due to presence of normal allele.
• E.g. focal dermal hypoplasia (Goltz syndrome)
Mitochondrial genome, a single circular chromosome within the mitochondrion, several of
which are present within each cell. It is almost exclusively maternal in their transmission.
Multifactorial model of inheritance, it attributes phenotypic variation between individual to
a large number of causes, each in itself having only a small effect but when acting together,
producing a disorder with the clinical phenotype.
Principles of Genetic Counseling In deafness
It is the process by which patient or relatives at risk of a disorder that may be hereditary
are advised of the consequences of the disorder, the probability of developing and
transmitting it and the ways in which this may be prevented or ameliorated.
Estimation of risks ;
o Specific risks , occur in Mendelian disorders which give a specific risk of recurrence
and transmission to offspring.
o Modified Mendelian risks, used when an individual is at a known risk of having
inherited a mutant gene, but some other information available which changes the
overall risk of having inherited the condition.
o Empiric risks, are based on observed data of recurrence in siblings involving several
families with same clinical problem, but where a simple Mendelian pattern of
inheritance does not apply.
Prevalence of Genetic deafness
o Deafness in genetic term refers to sensorineural deafness.
o 50% of all childhood deafness is genetic.
o Incidence is 1\2000 live-births.
Other Definitions
Malformations: the developmental process was always abnormal. E.g. Polydactyl.

Lecture notes in
Deformations: developmentally normal process is modified by mechanical forces to produce

an abnormal outcome. E.g. plagiocephaly.
Disruption: an extrinsic breakdown or interference with an originally normal
developmental process leads to altered morphology. E.g. the phocomelia of thalidomide
embryopathy.
Syndrome: "running together ", describes one of the relationships which may exist between
observed abnormalities of morphology in a patient (i.e. consist of multiple abnormalities
thought to be causally related.)
Classification of Genetic Deafness
This classification according to the underlying aetiology:
1) Monogenic (i.e. single gene disorder)
a. undifferentiated (non syndromic) deafness.
o Autosomal dominant
o Autosomal recessive
o X-linked recessive
b. Syndromic
o Autosomal dominant
o Autosomal recessive
o X-linked
c- Miscellaneous single gene disorders which may be associated with deafness.
2) Mitochondrial mutation causing deafness.
3) Chromosomal disorders associated with deafness.
4) Deafness due to aetiologically heterogeneous disorders of development.
Monogenic
Undifferentiated (non-syndromic) deafness
o 70% of monogenic deafness is said to be undifferentiated.
o More than 75% are autosomal recessive…..10-20% are autosomal dominant…….2-
3% X-linked recessive.
Autosomal dominant undifferentiated deafness:
o The number of genetic loci which cause this type of deafness is unknown.
o Molecular pathology of this form of deafness remains undetermined.
Autosomal recessive undifferentiated deafness:
o The distinction between genetic and environmental causes of the deafness is
obscured, unless consanguinity in the family tilts the balance of the suspicion
towards this aetiology.
o The recognition of the second affected child is usually confirmatory.
X-linked recessive undifferentiated deafness:
o Male preponderance.
o There are at least 2 distinct forms: the more common of these characterized by
stapes fixation and perilymphatic gusher at surgery →→ mixed pattern of deafness.
o There is a range of disturbance of other otoneurological parameters.
Syndromic deafness
Autosomal dominant syndromic deafness:
1) Waardenburg syndrome;
o Probably the single most recognized form of syndromic deafness.

Lecture notes in
o Pigmentary disturbance (classical white forelock or iris heterochromia), lateral

displacement of the inner canthi of the eye (dystophia canthorum) and deafness.
o Type 1 and type 2 according to the presence or absence of dystophia canthorum
respectively.
o Deafness is observed in approximately 25% of all cases of Waardenburg syndrome.
2) LEOPARD Syndrome;
o Acronym signifies Lentigines, ECG abnormalities, Ocular hypertelorism, Pulmonary
stenosis, Abnormalities of genitalia, Retardation of growth and sensorineural
Deafness.
o Numerous small dark brown spots on the skin over the arms and the trunk and may
involve the face.
o ECG abnormalities is said to be unique and characterized by a superiorly oriented
mean QRS axis in the frontal plane, generally between – 60º and –120º.
3) Brachio-oto-renal syndrome;
o Auricular or preauricular pits in association with ear malformations, branchial
sinuses and renal abnormalities.
o Branchial signs are present in approximately 60% of patients, otological signs in
80%, deafness in 66% and renal anomalies in 10%.
4) Treacher Collins syndrome;
o Also known as mandibulofacial dysostosis.
o Recognizable facial appearance: downslanting palpebral fissures, marked malar
hypoplasia, small mandible causing receding chin appearance.
o The pinna is frequently deformed or misplaced.
o Deafness may be conductive, mixed or sensorineural.
5) Neurofibromatosis type II;
o Also known as Central neurofibromatosis OR Bilateral acoustic neurofibromatosis.
o The cardinal feature; bilateral acoustic neuroma →→ pressure on the VIII cranial
nerve →→ deafness.
o The age of onset of deafness; most commonly the 2nd or 3rd decade.
o Other neural tumors are common in the patients and their families.
o Café-au-lait patches are fewer in number than in type I, between 1 and 5 patches.
6) Stickler syndrome;
o Many patients with Pierre-Robin sequence are affected by one of the conditions
grouped under the stickler syndrome.
o Features in infancy: flattening of the midface, prominence of the eyes and early onset
of high myopia.
o High tone sensorineural deafness of a progressive nature is common" ~ 70-80% of
cases".
o Retinal degenerative changes are a fundamental part of the syndrome. 50% have
cataract.
o The biological basis of the deafness is not understood at present.
Autosomal recessive syndromic deafness
1) Usher's syndrome;
o Two types: both are characterized by deafness and retinitis pigmentosa.
o Type I: severe to profound deafness, absent vestibular responses and prepubertal
onset of retinitis pigmentosa.

Lecture notes in
o Type II: less severe form of deafness, normal vestibular responses and later onset of
retinal changes.
o Mental retardation in up to 25% of cases.
2) Jervell and Lange Nielsen syndrome;
o Fainting and deafness.
o Fainting is due to cardiac conduction disturbance, prolonged Q-T interval on ECG.
o 50% of all cases reported died before adolescence.
3) Pendred's syndrome;
o Deafness and goiter.
o Deafness is usually sensorineural + abnormal vestibular responses.
o Goiter is due to dyshormonogenesis in the thyroid gland.
X-linked syndromic deafness
1) Alport's syndrome;
o Nephritis with or without deafness.
o It is X-linked recessive inheritance with male being affected more severely and no
male to male transmission being recorded.
o The clinical course in male: haematuria in early childhood + progressive
sensorineural deafness developing at school years →→→
o Chronic renal failure by the early 20s →→→
o Characteristic ophthalmic signs of anterior lenticonus and macular flecks
manifesting in late teenage years.
o The course in female is much milder.
o The carrier female is asymptomatic with microscopic haematuria.
2) Otopaltodigital syndrome;
o Rare condition.
o Distinctive facies, cleft palate, widely separated toes, short stature and CHL .
o Mild degree of mental retardation.
Miscellaneous single gene disorders which may be associated with deafness
1) Osteogenesis imperfecta;
o There are two classes of collagen mutation.
o In the first, the quantity of type I collagen produced is reduced but of normal quality.
o In the second, the structure of collagen produced is abnormal.
o It is autosomal dominant or recessive varying from mutation to mutation.
o Deafness is most common in osteogenesis imperfecta type I and III.
o Type I, patient is normal stature, little or no bony deformity and blue sclera.
o Type III, progressive skeletal deformity, short stature and dentinogenesis imperfecta.
2) Saethre-Chotzen syndrome;
o Autosomal dominant condition.
o Comprising: craniosynostosis, facial asymmetry, ptosis, brachydactyly with or
without syndactyly and several skeletal anomalies.
o Mild to moderate hearing loss thought to be result of compression of the VIII nerve.
3) Crouzon's syndrome;
o Maxillary hypoplasia, shallow orbit and proptosis.
o Deafness of an unspecified nature has been documented in 55% of cases and external
auditory canal atresia in 13%.

Lecture notes in
4) Apert's syndrome;
o Craniosynostosis, midfacial flattening and syndactyly (typical mitten hands and feet).
o Mental retardation.
o Otitis media is common, perhaps related to the high prevalence of cleft palate. Also,
a congenitally fixed stapes footplate is a frequent observation.
Mitochondrial mutation causing deafness
Three particular reports specifically correlated deafness with mitochondrial mutations.
1) Higashi (1989) noted that familial streptomycin-induced deafness appeared to be
transmitted predominantly through females, compatible with mitochondrial inheritance.
2) In a large Arab-Israeli pedigree maternally inherited sensorineural deafness was
described suggested that the deafness represented a two-locus model due to simultaneous
inheritance of the mitochondrial mutation and an autosomal recessive gene.
3) Ballinger (1992) observed deafness of an unspecified nature in association with diabetes
mellitus in a family shown to have a deletion of the mitochondrial DNA.
Chromosomal disorders associated with deafness
Specific chromosomal disorders and, in particular, Down's syndrome (triosomy 21) may be
significantly associated with deafness.
There are over 150 discrete chromosomal abnormalities documented which have been
associated with deafness.
Deafness due to aetiologically heterogeneous disorders of development
Many of the conditions are not strictly 'genetic' in that they are not related to a
chromosomal disorder nor are an identifiable pattern of inheritance.
Examples are; oculoauriculovertebral phenotype (Goldenhar's syndrome) and Klippel-Feil
syndrome.
Goldenhar's syndrome;
o Hemifacial microsomia, vertebral anomalies and epibulbar dermoids.
o Autosomal dominant or autosomal recessive.
o Deafness is common, perhaps a feature of 50% of cases, and not associated with any
particular aetiology. The ear pathology may be extensive, involving the external
auditory canal, ossicular development in the middle ear and occasionally
sensorineural deafness.
Klippel-Feil syndrome;
o Fusion of two or more cervical vertebrae.
o Most commonly, autosomal dominant inheritance.
o The association of Klippel-Feil syndrome, congenital deafness and Duane syndrome
(abducens palsy with retraction bulbi) comprises the Wildervanck syndrome, also
known as cervico-oculo-acusticus syndrome.
o The condition has observed almost exclusively in females.
Causes of deafness in children
1. Conductive deafness
a. Congenital disorders
(1) Gongenital disorders with external & middle ear abnormalities .
- At birth
1. Down's syndrome ; trisomy 21 , narrow EAC , OM both suppurative &
with effusion , stapes abnormalities .

Lecture notes in
2. Crouzon's syndrome , atresia or stenosis of the EAC , absent tympanic

membrane , malleus fused with the epitympanum bony wall .
3. Marfan's syndrome ; conductive deafness .
4. Treacher cholin's syndrome , microtia , stenosed or atretic EAC , tympanic
membrane replaced by bony plate , s.t. absent middle ear cleft , managed
by bone-anchored hearing aid .
5. Pierre Robin syndrome , low seated cup shaped ear , , middle ear cleft may
be absent , thickened footplate of stapes , poorly developed modulus or
narrow IAC .
6. Achondroplassia , dwarfism , fused ossicles , deformed cochlea , OME .
7. Duane syndrome , microtia , tresia of the EAC , closed oval window &
fused ossicles .
8. Apert's syndrome , fixation of the stapes footplate , OM secondary to the
cleft palate .
9. Otopalatodigital syndrome , small low seated pinna , ossicles deformity .
- During childhood
1. Osteogenesis imperfecta , similar tom otosclerosis .
2. Otosclerosis .
(2) Congenital disorders which predispose to OME or infection , including cystic
fibrosis , immotile cilia syndrome , cleft palate & immune-deficiency diseases .
(3) Miscellaneous disorders , congenital cholesteatoma , rhabdomyosarcoma ,
fibrous dysplasia , Golderhar's syndrome & isolated malformations of the
external & middle ear .
b. Acquired disorders
(1) Inflammation , OE , ASOM , CSOM , AOM with effusion & CSOM with effusion .
(2) Trauma
(3) Foreign body & wax .
2. Sensorineural deafness
(1) Genetic
- At birth , either presented with deafness alone or syndromes associated with
deafness ;
1. Klippel-Feil syndrome , microtia , preauricular appendages , atresia of the
EAC , fused ossicles .
2. Turner's syndrome , low seated large lobule poorly developed mastoid air
cells system & stapes abnormalities .
3. Fanconi syndrome , high frequency SNHL .
4. Pili-Torti , SNHL .
5. Usher's syndrome , SNHL & vertigo .
6. Pendrad's syndrome , goiter & SNHL .
7. Cretinism , congenital hypothyroidism & SNHL .
8. Waardenburg's syndrome .
9. Jervell & Lange –Nielsen syndrome , bilateral profound SNHL .
- During childhood , either presented with deafness alone or syndromes
associated with deafness ;
1. Alport's syndrome , high frequency SNHL .

Lecture notes in
2. Renal tubular acidosis , profound SNHL .

3. Refusm's disease , SNHL from 10-20 years .
4. Cogan's syndrome , SNHL & vertigo .
5. Norrie's syndrome , X-linked recessive .
(2) Non-genetic , deafness
- Due to intrauterine disease ;
1. Infections ; TORCHES , toxoplasmosis , rubella , CMV , herpes simplex &
congenital syphilis .
2. Ototoxic drugs .
3. Irradiation .
4. U/S cause cochlear hair cell damage .
5. Maternal DM .
6. Fetal alcohol syndrome .
- Peripheral disorders ; hypoxia , hyperbilirubinaemia , low birth weight &
preterm children .
b. Acquired disorders
(1) Infection , viral labyrinthitis (mumps , measles) & OM complications .
(2) Immunization .
(3) Autoimmune disease .
(5) Trauma .
(6) Metabolic disease .
(7) Neoplastic disease .
3. Mixed deafness
- At birth , ear –pits deafness syndrome .
- During childhood , osteopetrositis , langerhans cell histiocytosis &
mucopolysacharodosis .
b. Acquired disorders , infections .
4. Non organic deafness (Psychogenic deafness)
a. Functional deafness (hysterical) .
b. Malingaring .
c. Organic deafness with psychogenic overlay , deaf child & increasing his symptoms .
N.B.: sudden deafmness ;
1. Infection ; mumps , measles , meningitis & varicella .
2. Trauma , concusion , fractured temporal bone , perilymph fistula .
3. Idiopathic , vascular with spasm , thrombosis , embolism , haemorrhge causing cell
anoxia & death .
Management of hearing impared child
- The importance of the early diagnosis ;
1. Normal speech & language development .
2. Normal communication , social & emotional development .
3. provision of suitable support & aid .
- The detection by ;
1. Screening tests .
2. at Risk children registers .

Lecture notes in
3. Parental suspicion (50% of cases) .

4. Children who fail to develop speech (HL , specific language disorders , emotional
problems & mental retardation) .
- The management of the child refferd for assessment (otolaryngologist & audiologist
"Hospital Clinic" ) , the aims of hospital clinic are ;
1. Determine whether the HL present or not .
2. The type of HL .
3. The severity of the HL .
4. The age of onset (prelingual cause serious complications) .
5. Looks for the other relavant handicaps .
A. History
Usually a brief history is taken & audiological tests are started to prevent the child
becoming anxious ;
1. What to worry the parents .
2. Pregnancy & postulated development .
3. ENT symptoms .
4. Family history .
The symptoms are ;
1. Severe , deaf , mute , only one ear affected (5-10 years) .
2. Less degree , late or defects of speech development , backwardness at school (with
normal intelligence)
B. Examination
In which include ENT , neural & general examination , there is difficult to examine the
child with otoscope because of ;
1. Narrow EAC "& filled with with debris" .
2. Thick oblique tympanic membrane .
3. Irritability.
4. Engorged tympanic membrane especially in crying .
C. Audiological assessment
- The environment (room) ; it should be acoustically accepted (30dB) , comfortable , ,
inviting , good space for caregiver & child & the tester can move freely , also need
good quality (no shadow) & have no large windows & no distracting features (like
moving objects & pictures)( & no two way mirror .
- The stimulus ;
a. Frequency ; cup / spoon "wide frequency" , human voice " OO -500 Hz , MM- 1 KHz
, S-3KHz) , Rattle 3-4KHz , instruments producing warble tones .
b. Intensity , sound level meter , should record down to 20 dB SPL , factor affecting
intensity , distance , position & level .
- Subjects ; we should use approperaitae test method for the child over all
developmental age (not chronological age) , the application of wrong method will lead
to lack of cooperation from the child & unreliable results .
a. Neonatal response ;
- Startle reflex , aural palpebral reflex .
- Change in heart rate & respiratory pattern .
- Moro reflex , backward head jerk & body movement .

Lecture notes in
b. Infant < 4 months , stilling & listening (loud sound) at 4 months , stilling 7 smiling ,
even if the source is not within the visual field .
c. 4 -6 months , turn the head toward sound source .
d. 7-9 months , localize sound in horizontal plane , copy sounds & babbling tunefully .
e. 10-12 months , localize sounds in any plane source .
f. 13-24 months , localize & search for sound source & need more distraction .
g. > 2 years , can inhibit the earlier ready response to sound (ignore the sound) .
Subjective Audiological tests
In testing the hearing of adults , we ask them to tell us whether or not they hear certain
sounds . It is obviously impossible to do this with infants and young children , and we must
employ a variety of "play" techniques in which the child is taught to do something , not to
say something , every time he hears a sound . Before we can begin to undertake any such
test , we must have a clear understanding of the development of hearing and speech in the
normally hearing child.
The first requirement of all hearing test in young children is a natural and friendly
atmosphere , as far removed as possible from the hum – drum and hurly – burly of a busy
hospital clinic. A separate room is essential and must also be available , together with a
good selection of toys and testing apparatus.
No child will co – operate fully until he has been allowed to settle in and one must be
prepared to allow at least a half , often three- quarters , of an hour for each child at each
attendance . It is of the utmost importance to establish rapport with every child and the first
lesson to be learnt by those who are not familiar with the hand line of children is that one
must be prepared , quite literally , to get down to the child is own level – if necessary , on
bended knees.
Some of the children who attend audiology clinics have already had experience of hospitals
, and every doctor or nurse is likely to be associated with pain or discomfort. It is not
surprising that the child is confidence in the "man in white " is almost certainly under –
mined , and the team of an audiology unit should dress normally . " no white coats" should
be the rule.
It is rarely to train a child to perform a purposeful conditioned respone to sound before the
age of about 2-3 . In children under this age we must therefore look for simpler responses .
In testing the small child , it is of the utmost importance that he should not be able to see or
feel the source of the testing sound . the child who is deprived of hearing at , or soon after ,
birth will often develop his other senses to a remarkable degree and we must be careful not
to cast shadows over him as we approach , nor to walk too heavily towards him lest he feel
the vibrations fromour feet . He may even turn to the odour of a highly scented hair - cream
or face powder .
If the child is too young to walk , he should be seated on his mother's lap and allowed to
settle down. Before the testing is begun , he must be distracted by his rattle or some other
toy. If he is not distracted at all , he will tend to look round and watch the person who is
going to test him ; if he is distracted too much , he may become so engrossed in the game he
is playing that he will not respond to sounds which are well within his hearing capacity . It
is never easy to distract an infant just enough – not too little , not too much – but it is
pointless to begin any formal testing until this point has been reached.
Children with defective vision should be allowed to feel the testing objects , and they may
tend to incline rather than turn their heads merely cease to do whatever he is doing –

Lecture notes in
kicking , smiling chuckling – at the moment when he hears the testing sound , or a few
seconds later . Furthermore , at about the age of 1 year, many children will respond only
once to any particular sound and the examiner must be prepared to change rapidly from
one sound to another as the child loses interest in each of them , one by one . Perhaps the
easiest time to test the infant is that short period of half – awareness when he is just a bout
to wake from natural sleep.
From the age of 5 or 6 months onwards , the alert baby is able , not only to detect a sound
stimulus , but also to localis it , by turning his eye or his head towards its source.
There can be little doubt that the most difficult age is the age at which the child has just
begun to walk and is beginning to explore his widening horizon . At this stage in his
development , the examiner must be prepared to follow closely on his heels through all his
wanderings , banging a drum or calling his name at any suitable moment that offers itself.
The child can be seated at a small table and distracted by the teacher or other observer .
Both drums and xylophone bars are capable of producing either faint or loud sounds ; but
these instruments should always be struck softly at first, because many of the children who
are referred nowadays to audiology clinics may have no deafness at all . A variety of testing
sounds will have to be used before one can gain a fairly accurate impression of the hearing
capacity and no test of hearing can be regarded as complete until some attempt has been
made to assess the child's reaction to the human voice. If severe deafness is present , a very
loud sound may have to be used and , although it is open to many objections, the drum is
useful for attracting attention . if he responds to the drum , a series of xylophone bars can
be substituted and his reactions noted again . The examiner then moves further and further
behind the child until there is no longer any response at all.
From the age of about 2 or 3 onwards , attempts can be made to ' condition ' the child to
carry out some simple act every time he hears a sound. The principle of these conditioning
techniques can best be illustrated by a series of action shone taken during an actule test.
The child is seated at a small table with a nest of coloured beakers. Opposite him sits the
observer (in this case a teacher of the deaf) and beside her the examiner . The child is
encouraged to look and to listen as a xylyophone bar is struck and after the teacher has
picked out the beakers two or three times , she holds the child's hand on the top remaining
beaker and helps him to lift it out when he sees and hears the xylophone as often as
necessary until he appears to understand what is required of him . He is then allowed to do
it himself. As soon as has leant this ' look and listen ' game , the examiner goes behind him
and the observer beckons him to listen . Every time he hears the sound , he will now pick out
another cup and the examiner can go further and further away from him until he finds the
greatest distance at which the child responds to this particular testing sound . Thereafter
other frequencies and other sounds can be used.
'The assessment of hearing in children demands a variety of approaches which will vary
with the age of the child. The choice of lest will depend on the child's age, intellect and
motor abilities. Screening tests, subjective hearing tests and objective tests are all available.
Nearly all subjective testing will require two testers. The best results are achieved in
multidisciplinary paediatric assessment centres where the environment and organization
arc geared for children.
- Behavioral audiometry
Hearing is important for normal speech development, and it is important that moderate
and severe hearing losses are diagnosed early. This will allow the provision of suitable

Lecture notes in
support and aid, which will help facilitate the development of speech and communication.
In an effort to achieve this aim, children are subject to regular screening tests, at 7
months. 2-4 years and again shortly after school entry. Any child who persistently fails
screening test will be referred for a full assessment. In addition, children may be referred
for assessment from other sources because of concern about their hearing, e.g. parental
concern, post meningitis, family history, intensive care units, etc. Most health authorities
maintain an at-risk register of families in whom possible prenatal and perinatal causes
exist. Listed below arc the current screening method;, of choice for the three age groups
at which testing occurs.
1. Behavioural techniques (0 -6 months)
This method is based on the presentation of a loud sound und observation of the baby's
response. Some experience is needed in interpreting the variety of possible responses,
which include startle, blinking, crying or the cessation of activity. A positive response
is one in which there is a significant alteration in activity.
2. Distraction test (6-18 months).
Done in horizontal plane , with 1 meter distance with the child sitting comfortably on
his or her mother's lap, an assistant attracts the attention of the child. The tester then
distracts the child by making sounds of various intensity, behind and to one side of the
child, without giving any visual cues. A positive response is when the child turns to the
sound. the procedure is repeated on both sides, Test sounds include conversational
voice for low frequency. sibilant s for higher frequency or a high – frequency rattle in
younger children. A hand-held audiometer may be used with older children.
The normal response at 25-30 dBA
3. Visual reinforcement audiometry (9-36 months)
This technique is relatively uncommon in the UK but more frequently used in USA and
Australia. In essence it is a free field audiogram. The child sits in an acoustic room at
a table (usually with a parent) and is allowed to play with some toys. Sounds (warbles
or pure tones) are produced from one of two loudspeakers placed at 30" either side of
the child. if the child turns to the correct speaker at signal presentation a visual
(reinforcing) stimulus is presented adjacent to the speaker (e.g. a flashing light) to
reinforce the turning response. The tester sits outside the test room and observes the
procedure through a one-way mirror. In this way a reasonably accurate tree field
audiogram may be obtained .
The normal response at 20-25 dBA .
4. Conditioned audiometry "Performance testing " (24-60 months)
This technique involves training the child to perform a specific task such as putting a
narble in a cup, or giving a toy to the mother, after hearing a specific auditory
stimulus. The stimulus may be the spoken word or a lone produced by a hand-held
audiometer. With this method it is important to avoid any visual cues. This technique
may also be used with older children to obtain a pure tone audiogram.
5. Pure tone audiometry (>5years) .
This technique is discussed in detail elsewhere (pure lone audiometry). Most children
of around 5 years can with a little encouragement be persuaded 10 perform an
audiogram, even if only at three frequencies in each ear.
6. Toy discrimination test "McCormick TDT"

Lecture notes in
There are seven pairs with names that are acoustically very similar, e.g. cup/duck,
key/tree. Only those toys that are recognized by the child are used and the aim is to
establish the speech level that gives an 80% correct response rate.
7. Speech discrimination tests (24-60 months}
These tests involve asking the child 10 point to or handle a variety of toys. The toys
arc selected so that their names cover a range of speech patterns.
- Objective tests
1. Auditory response cradle (0—6 months)
This device monitors four behavioural responses to the production of sound. Head
turning. startle responses and body movements are recorded by pressure transducers
in the head rest and mattress. Respiratory changes are monitored by a transducer in a
band around the baby's chest.
The stimulus is 5-sccond bursts of 85 dB sound pressure level (SPL) sound made into
earphones. A microprocessor analyses die responses to the sound stimuli, taking
account of the baby's overall level of arousal, and makes an objective verdict of pass
or fail.
2. Otoacoustic emissions (0-12 months)
Much of the recent work with otoacoustic emissions is related to their feasibility as a
screening tool for sensory hearing loss. Distortion-product otoacoustic emissions have
been shown to be particularly effective at 4 and 8 kHz.
Here the low intensity sound energy generated by the cochlea could be recorded in the
ear canal , used now routinely as a screening test in neonates (for assessment) ,
handicaps & those children on an ototoxic drug & to identify the site of hearing
impairment (absent in CHL & peripheral audiotory diseases & present in central
auditory disease) .
The result , delayed OAE are generated only in healthy cochlea (active outer hair
cells) .
In case of HL > 40 dBA , the test is not useful (absent typically used in 25-35 dB loss) ,
the middle ear must be mobile & free from effusion .
3. Evoked response audiomeiry
This is indicated if there is any difficulty or uncertainly in the results of conventional
distraction techniques, or if the child is too young for conventional testing and there
are doubts as to the child's hearing ability.
- Electroccochleography, fast , few milliseconds (cochlear nmicrophonics , action
potential & summating potential) .
- ABR , fast , 10 milliseconds , ECOLI (used in practice)
- Middle latency response (10-75 milliseconds) , thalamus & primary auditory cortex .
- Slow vertex response
- (75-300 milliseconds) , slow threshold estimation in cooperative alert adult .
- P300 > 300 milliseconds )late) .
- Period evoked potential .
ABR may be affected by MS , Kernicterous & high CSF pressure , the interview
latencies decrease with age , the wavwes increase with age from birth , with wave I
reaching adult size by 6 months & wave II by 2 years , wave III become prominent at 2
weeks of age .
4. Impedance audiometry

Lecture notes in
a. Tympanometery , monitor the middle ear pressure , A : norma , B: decreased peak (in
otosclerosis & tympanosclerosis) , C: high peak (in ossicular discontinuity) , D: peak
shifted to the left (-ve middle ear pressure) , E: flat curve (OME) .
If the tympanic membrane move with respiration , patent Eustachian tube , if pulsatile
then AOM or glomus tumor .
Causions should be taken for false +ve , pathologies can coexist , less than 7 months
age with W shaped tympanogram .
b. Acoustic stapedial reflex , is the lowest signal intensity at which the stapedius muscle
contract , normal response at 85 dB (+/- 10 dB) , above normal hearing threshold .
It is used for ;
1. CHL , 10 dB , ART , absent in 80% .
2. SNHL , cochlear , +ve 9% if hearing threshold less than 60dB , while
retrocochlear , -ve if hearing threshold less than 60dB .
3. ART decay indicate retrocochlear pathology .
4. Brainstem lesion , both ipsilateral & bilateral reflex absent .
5. Facial nerve lesion .
6. threshold estimation .
c. New related techniques ;
1. Tympanic membrane displacement measurement , fluctuating in HL in child with
high CSF pressure .
2. Acoustic reflectometry , by use acoustic otoscope which not required air-tight seal
& can use in crying child the speaker of the instrument emits a multifrequency (2-4
KHz) tone at 80dB SLP & a microphone pick up any sound reflected from the
tympanic membrane .
Testing a difficult child , include those with ;
1. Visulal problems .
2. Below 3-4 months .
3. Cerebral palsy .
4. Hyperactive child & those with autistic feature .
5. Those with attention problems .
Screening tests
1. ABR " auditory brainstem response" .
2. OAE " otoacoustic emission" .
3. ARC " auditory response cradle" .
4. Utilizing parental suspicion (20%) .
5. Distraction test " trained health visitors" .
6. Behavioral tests .
7. Toy discrimination test " McCormick" .
8. Performance test .
9. PTA .
D. Vestibular tests
To determine the response or absence of vestibular disease ; (1) caloric test & (2)
rotation test .
E. Serological investigations , Rubella (IgM & IgG) , CMV , Toxoplasmosis , Syphilis
(FTA) .

Lecture notes in
F. Other tests
1. Urine ; CMV (viral culture or IgG) , Alpert's syndrome (renal disease & SNHL) .
2. ECG ; prlonged Q-T interval in Jervell & Lange-Nelson syndrome .
3. Guthric test ; +ve , T4 & TSH to detect Pendard syndrome & cretinism .
G. Radiology
1. Skull x-ray , intracranial calcification in toxoplasmosis .
2. Tomography .
3. CT scan , useful in child with fluctuating HL , perilymphatic fistula or to assess
child with cochlear inflammation
H. Assessment by other specialties
1. Ophthalmologist ; visual acuity & fundoscopy (rubella : retinopathy) .
2. Paediatrician , if there is head & neck abnormalits , delayed growth &
development .
3. Medical genetics , if there is no obvious environmental factors .
I. Treatment
1. Prophylactic
- Avoidance of the predisposing factors ; exposure to ototoxic agents or infections,
vaccination , detection of Rh-incompitability , intermarriage of bone deaf .
- Screening test ; 7 months (distraction test) , 2-4 years (distraction test or
conditioned response audiometry) & 5 years & above (PTA) .
2. Therapeutic
- Management the underlying causes .
- Subsequent management of hearing impaired child (SNHL) by ; appropriate
hearing aid selection , cochlear implant , promotion of language development &
communication skills & if possible speech development .
Hearing aid
- Types
1. Entirely worn by the patient ;
a. Body worn .
b. Behind the ear .
c. In the ear .
2. Not-entirely worn by the listener ;
a. Speech trainer , patient connected to the parents & teacher .
b. Group hearing aid , patient connected to the parents & teacher & with several
children .
c. Radio hearing aid , FM radio system .
d. Infrared hearing aid , affected by bright sun light .
e. Loop system "electromagnetic loop" .
It is rare for a child to be born totally deaf & every attempt should be made to reach the
residual hearing by the use of high powered hearing aid , residual hearing with low
frequency .
- Problems with hearing aid selection in children ;
1. Limited information about the exact extent of hearing loss .
2. young child can't say with aid or setting on the aid they prefer .
- Methods

Lecture notes in
1. The empirical "selective" method , try different aid .

2. The theoretical "prescriptive" method , consider some parameters ;
a. Child's threshold at each frequency .
b. Most comfortable listening level .
c. Speech discrimination scores .
- Advantages of the binaural fitting
1. Impacted localization of sound source .
2. Improved hearing in background noise .
3. Better amplifications .
Cochlear implantation
- By passing the damaged hair cells & stimulate the nerve fiber directly electrically .
- Component
1. External worn on the body (microphone , processor , decoding unite & coil) .
2. Internal implanted to the cochlea (electrode & receiver) .
- Factors affecting the success of implantation in children are ;
1. Postlingual onset of deafness .
2. Implantation in preschool age .
3. Shorter period of auditory deprivation .
4. Participitation in communication therapy programs .
5. Psychological & motivational suitability .
- Indications
1. Profound total bilateral SNHL with no significant useable hearing (this means HL
>90dB) with this there should be no benefit from preoperative training period with
hearing aid .
2. Age ; not less than 2 years , 50% of skull growth occur in the 1st 2 years , & not more
than 6-7 years , for prelingual deafness .
Education & Communication methods
- Auralism , speech with lip readimg , the child can understand significant amount of
language by one year .
- Finger spelling , need speech , MPB or KDL use different hand shapes in four different
positions close to the speaker's mouth .
- Signing systems "Manualism"
1. British sign language , separate language with its own vocabulary , grammar &
syntax .
2. Paget – Groman sign system , with grammatical structures .
3. Maketon , simple signd , used for children with learning difficulties .

Lecture notes in
TABLE
Causes of deafness in paediatric group
Onset of
Condition Inheritance Deafness deafness Other features
Waardenburg White forelock & iris
syndrome AD SND At birth heterochromia
Usher's syndrome AR SND At birth Retinitis pigmentosa
Pendred's syndrome AR SND At birth Goiter at 5-10 years

Klipple-Feil Fusion of 2 or more of
syndrome AD SND At birth cervical vertebrae
Turner's syndrome XO pattern SND At birth

Cong. Anaemia, skin
pigmentation &skeletal
Fanconi's syndrome AR SND At birth deformities
Pili torti AR SND At birth Dry brittle hair

Mental and physical
Cretinism SND At birth abnormalities
Neurofibromatosis 2nd -3rd Bilateral Acoustic neuroma
type II AD SND decade + café-au-lait patches
around 10
Alport syndrome X-linked R SND years Nephritis
Renal tubular
acidosis AR SND At 3 years
Retinitis pigmentosa
,peripheral neuropathy&
Refsum's syndrome AR SND 10-20 years cerebellar ataxia
Interstitial keratitis &
Cogan's syndrome Autoimmune SND Adolescence vertigo
LEOPARD syndrome AD SND Acronym

Retinal degenerative
Stickler's syndrome AD SND changes
Seather-Chotzen Facial asymmetry,
syndrome AD SND brachydactyly & ptosis
Norrie's syndrome X-linked R SND Progressive blindness

Recognizable facial
Treacher Collins appearance & small
syndrome AD CD At birth mandible

Lecture notes in
Otopalatodigital Cleft palate & widely

syndrome X-linked CD At birth separated toes
Maxillary hypoplasia &
Crouzon's syndrome AD CD At birth proptosis
Mitten hands & feet + cleft
Apert's syndrome AD CD At birth palate
Down's syndrome Triosomy 21 CD At birth Distinctive facies

Tall,scoliosis,hypotonia,long
Marfan's syndrome CD At birth fingers& toes
Pierre Robin Cleft palate,glossoptosis&
syndrome AD CD At birth small mandible
Short limbs, large head&
Achondroplasia AD CD At birth prominent forehead
Short neck,VI cranial nerve
Duane syndrome AD CD At birth paralysis & enophthalmus
6 - 51years,
Osteogenesis peak at 3rd Skeletal abnormalities &
imperfecta AD or AR CD decade blue sclera
Otosclerosis AD CD 11 - 30 years
Goldenhar's Hemifacial microsomia&
syndrome AD or AR CD vertebral anomalies
Cystic fibrosis AR CD
Immotile cilia Sinusitis, bronchiectasis&
syndrome CD situs inversus
Cleft Palate CD Otitis media with effusion

Branchio-oto-renal Branchial sinuses & renal
syndrome AD Mixed abnormalities
Jervel & Lange Fainting (prolonged Q-T
Nielsen syndrome AR interval )

Lecture notes in
HEARING AIDS
It has been estimated that every year, two-million people throughout the world obtain
hearing aids. Hearing loss (predominantly it is sensorineural hearing loss) which is not
response to medical or surgical management , so it is response to or can only be alleviated
by some rehabilitation programs , the major component of it is the hearing aids .
Characteristically all the hearing aids devices had the same characteristics & degree of
functionality . Hearing aid usually thought as they are appropriate management of both
SNHL & CHL & the hearing aids are more successful in CHL .
It has a simple job that required to overcome the attenuation due to conductive conditions
by providing amplification .
SNHL , the majority are due to damage of the hair cells in the cochlea which are essential
for auditory abilities to process different frequencies as well as sounds of different
intensities . This have effect of indistinguishable adjunct frequencies with confused
information or intense frequency may physically mask the perception of another frequency .
Making that all the hearing aids . make no attempt to overcome the various physiological
deficit that accompany SNHL , so it is clear that they can’t return all auditory abilities that
enjoy the patient , but only for listening conditions .
With suitable amplification most of hearing impaired listener can function quite well , but
this can’t be make with background noise or other competing speakers are present .
One of the important circumstances for the consideration with hearing aid , is the noisy
background , no attempt to separate the speech from the noise .
That would we like to present to the impaired auditory system are 3 aspects ; intensity ,
frequency & temporal changes in acoustic signals .
The primary rule of hearing aid are the understanding of the speech & making the speech
signal available .
Historical
The oldest aid to hearing is the hand cupped behind the ear, but this is of value only in the
very slightest degree of deafness .Non electric hearing aids have in used for at least two and
a half centuries and they still find a limited usefulness in elderly persons who take unkindly
to the mechanics of an electrical aid and cannot tolerate the distortions imposed on their
hearing by recruitment phenomena.
Ear trumpets, auricles and speaking tubes have all been used, but the most powerful of
these is the speaking tube which brings the speakers voice acoustically nearer to the listener
s ear.
The first commercial electric aid was made in America about 85 years ago, and great
advances followed the invention of radio valve in the 1920.The substitution, in 1948,of the
transistor for the radio valve led to a minor revolution in hearing aid design, and
transistors are now used exclusively
Definition
A hearing aid is any device that amplifies sound or assists the hearing –impaired individual
, but in present context will be taken to mean an electro-acoustic device used to amplify
sounds. Cochlear implants can be included in this definition .
Aim
To help a person with a hearing impairment to identify desired sounds, including speech
(and especially his own), by selective amplification.

Lecture notes in
Design
Basically any aid consist of ;
1. Receiver / Microphone &/or Induction coil.
2. Amplifier / Processor .
3. Sound transmitter ; earphone , bone conductor ..etc .
4. Ear mould ; vital part of the aid , usually manufactured individually from casts of the
external meatus . Ill –fitting mould lead to:-
a. Acoustic leakage—loss of low frequency
b. Acoustic feedback—whistling sound
If the amplification is too high , then use venting mould (making a hole in the mould) .
5. Power source .
6. Signal processing system which is of two types , either
a. Analogue system ;
Acoustic signal converted to electric analogue at the microphone stage of the
aid , that is acoustic signal is constantly varying the sound pressure when it is
converted electrical signal , the varying sound pressure is changed to varying
voltage .
To avoid the problem of excessive amplification of loud sounds which cause
discomfort to the patient , we can use one of the 2 methods of decreasing sudden
peaks of sounds ;
 Peak clipping ;basically chops the tops off the peaks of sound waves , it is
simple & instant , but may result is some distortion of sounds .
 Automatic gain control ; involve some complicated circulatory that picks up
the signal & compress it , so that the maximum sound peak is never above a
certain maximum value , it produce less distortion , but it is little more
complicated .
It is of 2 modalities ;
(1) External controller ; Usually a selector switch & volume controller ,
selector switch with 3 markings ; O for off , T for TV or telephone coil
& M for microphone .
(2) Internal controller ; on the amplified /processor , used to alter the
frequency response & spread of volume controller available to the
user .
b. Digital (signal processing) system
Defined as mathematical representation of sounds , when used the acoustic
signal converted to electrical signal at the microphone stage of the aid , after
this conversion a frequency filter introduced to decrease the possible distortion
of the input signal (simplified as a defined fraction of times /second which is
normally 10000 times /sec. or more) .
Analogue signal converted to digital signal at the digital stage (A/D) , binary
numbers (0&1) used to represent the digital value of each sample .
The advantages of this system ; there are unlimited ways in which the signal can
be processed & manipulated , so that a number of parameters that can be
utilized significantly greater than those found in the analogue system , so that
the ability to manipulate the signal to acoustic need of patients is greatly
enhanced & this without excessive battery current demand .

Lecture notes in
Characteristics of the hearing aids

1. Amplification
Is the acoustic gain or amount of increase of sound available (the difference in the
sound pressure level (in dB) between output and input)
It must be over 25 dB for weak sound to be heard.
The electrical gain of an amplifier must be 85 dB to obtain an acoustic gain of 50 dB.
Some modern individual aids provide a gain as high as 81 dB in a post-aural aid and
91dB in a pocket-aid . In order to avoid feedback, the gain limited to 55-65 dB in the
middle range of frequencies.
2. Output
The maximum intensity that the aid can deliver. The most powerful aid is made to
deliver is 148 dB and such aid with this very high output should be used with caution
and for limited periods.
Limitation of output ; the severely deaf person requires high acoustic gain over a wide
frequency range. Loud sounds cause loss of intelligibility or discomfort.
It is important to select a hearing aid with an output which not exceed the maximum
comfortable listening level of the patient.
An automatic volume control (AVC) device is needed which automatically limit the total
output of a hearing aid . Three main methods of providing AVC.
a. Peak clipping ; An electrical circuit is included in the amplifier system which
ensures that the voltage fed from the output of the amplifier to the earpiece will
never exceed a definite fixed maximum level which represents a safe limit of
intensity for the deaf ear.
b. Compression amplification .
c . Automatic gain control (AGC) .
3. Frequency range
The average requirement is 500-4000 Hz. many variations are required and can be
provided.
4. Frequency response
For selective amplification the best response curve is one rising gradually from 500 Hz
by 6dB per octave. Modification of responses are effected by:-
1. Changing the receivers.
2. Continuously adjustable tone controls.
3. Varying the length and diameter of polythene tube to the earpiece.
4. Design of ear mould.
5. Filters placed in ear mould or tubing.
Types of the hearing aids
1. Body worn hearing aid
Ugly aids are worn with a strap around the neck and the body of the aid on the patient’s
chest . It precede the development of the ar level devices .
Their rule declined over the last years except in 2 conditions ;
1) very high gain , some users need to overcome a deficit .
2) Very limited manipulative conditions as in arthritis , in elderly ..etc.
It considered to be as available alternative in ;
1) Patients with large conductive components to their hearing loss (anatomical
deficit making difficult ear-mould fitting like canal stenosis) .

Lecture notes in
2) Individuals with appropriate training & counseling can’t cope with small
controllers on post-aural device , however this rare & body worn devices only
usually fitted following an unsuccessful trial with ear level device .
Advantages
1) Great power available.
2) Maximum amplification with minimum feedback ; due to
a. They are made very powerful .
b. Distance between the microphone & the earphone .
3) Ability to incorporate induction coil and provide variable setting of input, gain,
output, frequency response, peak clipping and AGC.
4) Space to have many transistors to give better sensitivity or higher fidelity.
5) Ideal for patients without manual dexterity to manipulate the miniature controls
of an ear level aid.
6) They are prone to picking up the sounds of rustling clothes.
Available in BW 60 and BW 80 series.
Disadvantages ; Physical a awkwardness, psychological disfavour, inconvenience of
flex, clothes-rub and inability to produce stereophonic effect.
2. Post-aural hearing aid
Most common usage are the standard behind- the- ear (BE) aids, available on the NHS.
The body of the aid sits behind the wearer’s ear is normally connected by a hollow
plastic tube to an ear mould , which allows sound passage to the ear.
Three main groups
1) BE10 series are medium gain (45-47dB)
2) BE30 series –higher gain instruments (53-57 dB)
3) BE50 series-power post aural (63-64 dB)
With each series are a number of models with differing pattern of frequency response ,
all contain induction coil which can be used with TV , telephone & in theater , cinema
fitted with induction loop to bypass much of unwanted background noise .
Advantages
1) Smallness of size.
2) Inconspicuousness.
3) Freedom from flex and clothes-rub.
4) Stereophonic effect when binaural reception used.
3. In the ear or in the canal hearing aid
Commonly available commercial aids sit in the concha or in the canal. Their external
shell is usually of acrylic and conforms to the shape of the wearer’s ear.
Less obtrusive than the standard BE aids but are expensive and occasionally prone to
feedback problems (proximity of the microphone & speaker) . They are ;
1) Smaller .
2) Less conspicuous .
3) Less obvious wearing prosthesis .
4) Technically & manufacturely develop that the simple linear hearing aid can be
manufactured as in the ear hearing aid device .
5) Cosmetic advantage .
6) Wide spread application .
7) Suitable for mild & moderate HL .

Lecture notes in
Problems with the device ;

1) The need to customize it to each individual ear which overcome by manufacturing
2 standard housing .
2) Contain microphone & earphone arc closer together than that of the post-aural
or body worn devices , so they are ;
a. Always more susceptible to feedback problem .
b. The gain the can be delivered from the device will continue to be more limited
than that of post-aural device .
4. Bone conductive hearing aid
Similar to the BW aid but feed their output to a bone conductor (mechanical vibrator)
rather than an earphone.
Here the attenuation is bypass the middle ear & directly stimulate cochlea via the
temporal bone (the transducer “bone conductor” held contact firmly with temporal
bone via the mastoid process) .
Indicated in the following:-
1) Meatal discharge or stenosis (or any problem with wearing the air conduction
device)
2) Subjective preference for bone conduction reception.
3) Impractical air conduction device , like abnormalities lead to feedback problems
or lead to exacerbation of any present middle ear or external ear pathology .
Problems with this type ;
1) Bone conduction testing in clinical audiometry .
2) High pressure from contact which lead to irritation & discomfort from prolonged
use .
Maximum out put is about 40 dB HLat low frequencies & 75-80 dB HL at high
frequencies .
5. Osseo-integrated hearing aid
Conventional bone conduction aids have drawback, such as bulkiness and discomfort. In
addition, the skull cannot be vibrated directly, but only through the energy absorbing
skin and soft tissues. Bone -anchored hearing aids largely overcome these problems.
Two devices transmits mechanical vibrations to bone of the skull ;
1) Bone –anchored hearing aid (BAHA) ; Percutaneous titanium abutment is fixed
to titanium screw implanted in the mastoid.
2) Xomed audiant bone conductor , consist of encased rare earth magnet implanted
completely under the skin & fixed into the bone with Titanium screw , also
another external magnet .
6. Implantable hearing aid
Symphonix sound bridge works on similar principles of Xomed audient except that the
external magnet vibrates a coil that is attached to the patient incus .
7. Spectacle hearing aid
Modification of standard spectacle frames to incorporate a hearing aid & deliver the
acoustical signal via conductional ear piece , it is no longer necessary . Can used in a
number of ways ;
- As a standard hearing aid.
- As a bone conductor.

Lecture notes in
- Contralateral routing of signal (CROS) .In this variation, sound is picked up from
one side of the head and fed to the contralateral side, which is the good side
Choice of the aid
Factors influence the choice of hearing aid are ;
A. Actual degree and nature of hearing loss (Amplification characteristics).
B. Cause of deafness.
C. Available finance (cost) .
1. According to the type of hearing aid
A spectacle- type aid.
Useful for those people who regularly wear glasses.
When there is one very deaf ear and a requirement for contralateral signal routing.
A bone conduction aid.
Ideal in those cases where a hearing loss exists in association with active outer ear or
middle ear inflammatory pathology.
A body –worn aid.
Useful for anyone with a profound hearing loss .
For most NHS patients an ear –level aid found to be suitable.
2. According to the amplification characteristics
The pattern of frequency response chosen depends very much on the shape of the
audiogram.
A hearing aid must function in a narrow dynamic range (Providing adequate
amplification to overcome the hearing loss, but not over amplifying sound and causing
recruitment and consequent discomfit and intolerance.
To over come this problems there is a number of formulate developed such as ; ½ gain
rule , Perger’s procedure , PoGo2 , NAL ..etc , all formulate give differing importance
of differing frequencies with maximum important for hearing loss at the main speech
frequency of 1000-2000 Hz . Most hearing aids can be adjusted to alter their frequency
response .
3. According to ear mould
Modifications made to ear mould for both auditory and medical reasons.
Venting the mould will reduce the low frequency response and useful for aeration in-
patient with otitis externa (also to skeletonized the mould) .
Unfortunately feedback becomes more likely with a high-power aid and if the mould is
vented.
4. General
In which the ear to fit the aid depends on the number of factors include
a. Patient preference .
b. Available dynamic range .
c. Discrimination score in each ear .
d. Presence of active inflammatory process in either ear .
e. Medical factors such as ; arthritis , stroke , amputation ..etc .
5. Physical parameters of the hearing aid , such as ;
a. Lay out of the components .
b. Type of transduction .
c. Processing involved .
d. How & where the sound going to be peaked by hearing aid .

Lecture notes in
e. How the sound is processed or amplified before delivery to the impaired ear .
f. How & where the processed acoustical signal is delivered to impaired auditory
system .
The requirement of an ideal aid are ; (1) High amplification , (2) High fidelity (3) Small
size and low weight (4) Low power consumption & (5) Low cost .
How to provide a hearing aid for patient with bilateral hearing loss ?
It is preferable to provide binaural aids ,this rarely possible in the NHS on the ground of
cost.
Follow up & after care
After fitting a period of support & rehabilitation , it is important to get the patient
confidence .
An initial period of euphoria (when the patient finds that he can hear sounds again), a
period of depression follow when he realizes that many of the sounds that he hears are
distorted for instant recognition.
Auditory training is an essential supplement to the aid, both in children and in adults.
A better progress can be made when a hearing therapist can see the patient regularly, to
help him to come to terms with his handicap and to make the best use of his hearing aid.

Lecture notes in
COCHLEAR IMPLANT
It is a device used to stimulate the residual neural tissue in patient with profound hearing
loss .
Also it defined as an electronic device that convert sound energy to electrical signals to
stimulate ganglion cells & the cochlear nerve thus transmits the information to the brain .
Djourno , Eyries & Valancien (1957) published the 1st description of the cochlear implants
inserted in totally deaf patients .
House (1961) , implanted a single electrode into the cochlea .
Simmon (1964) , implant 6 stainless steel electrodes directly into the auditory nerve .
William House (1969) , human implantation by single wire .
Clark & coworkers (1987) in Australia developed a multi-electrode intracochlear implant .
Basics of cochlear implants
The cochlear implant prosthesis consist of 2 main parts ;
A. The implant ; is the internal part which is placed surgically beneath the scalp , with an
array of the electrodes placed inside the cochlea , the body of the implant contains a
receiver/stimulator that decodes the signals from the external prosthesis & send the
electrical charges to the individual electrode .
B. The external part ; consist of :
(1) Microphone ; receive sound & transduces it to an electrical wave-form which send
to the ;
(2) Speech processor ; which alters the electrical signals to emphasize the speech
signals & divide the signals into components for each of the electrodes through ;
(3) Magnet transmitting coil .
Nowadays , use high electrode stimulation rate by speak (spectral peak processing) , use 20
filters in this strategy to cover a frequency range from 150 Hz to 10 KHz (up to 10
maximum) , the rate of stimulation on each electrode varies from 180-300 Hz .
Selection of the candidates
The deaf people are completely normal , some can overcome the disability aspect of
deafness by becoming fluent in sign language & joining the other deaf groups , so the word
"Patient" best avoided (except for the period when the person in the hospital & recovering
from surgery) , so during the assessment period use the term "Candidate" & after surgery
use the term "Implantee" .
Candidacy categories
The main factor influencing candidacy for a cochlear implant is whether the person has
already acquired speech before becoming completely deaf (postlingual) or become deaf
before learning speech (prelingual) .
Sometimes the patient become deaf at the time of beginning speech (perilingual) which can
categorized with the prelingual for clinical purposes .
Categorization of the candidates
- Postlingual ; onset of deafness has occurred after completion of speech development
which can subdivided into ;
(1) Postpubertal group (adults & teenagers) , they are excellent candidates especially
after 13 years of age (speech appear to lose all plasticity by puberty) .
(2) Prepubertal group (children 2-12 years of age) , plasticity still present (the younger
the child , the more likely speech will be lost) , they develop incorrectable
articulation errors
Lecture notes in
- Perilingual ; onset of deafness occurred while speech development was occurring .

- Prelingual ; onset of deafness occurred prior to any development of speech , it is either ;
(1) Primary candidate ; have no acquired language by any other means of
communication (usually young children) , so the key to success appears to the ability
to establish an effective cochlear implant at early age as possible & then teaching
the child to hear & speech (habilitation) , or use (education) in older children which
is rare .
(2) Secondary candidates ; have used another mode of communication (usually sign) to
develop language , they seek an implant to improve their oral skills (which
sometimes be minimal) , this occur especially after 5 years of age , poor prognosis &
disappointing the parents .
(3) Change over candidates ; have developed auditory skills using a hearing aid , this
excellent for implants .
Medical selection of candidates
- History
1. Extent , timing & cause of HL .
2. Whether the hearing aid has been useful .
3. How the patient communicate .
4. Language level .
5. Any major health problems .
6. Any evidence of developmental delay .
7. Past otological history ; OM , ear surgery & OME .
8. Family history ; how does the family communicate .
9. Social history ; does the patient understand & want the implant .
- Examination ; the appearance including congenital stigmata , any abnormal behaviour ,
state of meatus , tympanic membrane & middle ear , presence of a cavity or atticotomy ,
also nose , throat & general examination .
- Preoperative investigations
1. Blood tests ; CBP , LFT , renal function (in indicated patients) & serology for
syphilis .
2. Audiological ; in adults do PTA , impedance & speech testing & in children do aided
PTA & special speech test to measure the discrimination .
Others like ABR , electrocochleography , promontory stimulation testing .
3. Vestibular function tests ; caloric test in adults .
4. Radiology ;
CT scan ; detect bony obliteration within the cochlea , to detect mineralization in
otosclerosis & to detect any congenital abnormalities of the otic capsule .
MRI ; can confirm the presence of acoustic nerve & reveal any degeneration by
brightness of the T2 weighted .
PET ; show if the auditory areas of the brain can still respond to auditory input .
CXR ; for GA routinely .
5. ECG for those with history of cardiovascular problems .
- Referral ; audiologist , speech therapist , teacher of the deaf . language assessment ,
developmental pediatrician , ophthalmologist , physician & implant support group (visit
the implantee & parents of already implantee) .
The final assessment meeting is held after the completion of all preoperative testing & visits

Lecture notes in
A. Postlingually deaf adult or teenagers , in meeting ;

1. The results are explained & the likely benefits of the implant outlined .
2. The candidate usually will decide whether or not to have surgery , the otologist
now has a surgical patient , explain the possible complications of surgery .
3. The choice of the ear to be implanted is made ; implant the more recently
deafened ear or that with better threshold & result of promontory electrical
stimulation & results of the radiology .
B. For children , more complex ;
1. Professional staff involved with the 10 weeks assessment with the parents &
itinerant teacher if possible .
2. Each professional tables a written report about the assessment & explained to the
parents .
3. Then the parents will decide , if yes , then (by consent) .
4. the otologist explain the surgery & the possible complications .
The importance of the neural plasticity , it is the ability of the CNS to be
programmed to learn a task (there is specific neurons with normally available for
these , which lost to adopt in period of time & lost the plasticity to adopt) , the neural
plasticity of speech articulation is more severe than that of listening , fade between 6-
8 years , speech articulation , fade excellent (if learn before age of 2-3 years) .
Surgery
- Anesthesia ; under GA .
- Incision ; either
(1) Vertical ; suitable for children , most females & some males , placed close behind
the attachment of the pinna , so it crosses the mastoid cavity anteriorly where the
electrode array should be medially placed .
The upper end is 3 cm above the pinna , a step incision is performed 1 cm posterior
to the skin incision to prevent postoperative fistula .
The advantages : rapid postoperative healing , lack of scalp numbness & minimal
need for hair shaving .
(2) Vertical with posterior upper limb ; needed when there is thick scalp , so the
transmitter magnet coil difficult to contact with the buried receiver/stimulator , so
the scalp can hinged backward & thinned .
(3) Others "forbidden now" ; C-shaped postaural incision & transverse incision .
- Approach to the middle ear
(1) Cortical mastoidectomy , the usual technique of rounding the edges avoided for
leaving overhanging edges useful for containing the electrode array after insertion .
(2) Limited posterior tympanotomy through the facial recess leaving incus & superior
bridge of bone intact .
(3) The facial nerve shouldn't be exposed & a thin layer of bone should be left covering
it , since change-over will be needed in future , so protection of the facial nerve is
important
If the surgeon uncovers the facial nerve sheath , the site of exposure should be
carefully documented (preferably with photographs) .
(4) Exposure of the round window niche , by drilling of the edge of the bone on the
medial rim of the posterior tympanotomy , if difficult , the angle of viewing can be

Lecture notes in
improved by removing some of the external end of the posterior meatal wall (mouse
nibble) .
Drilling of the anterior lip of the round window niche may give a nice view .
The cochlea should not be opened until all drilling has finished to prevent fluid &
bone chips entering the duct .
- Drilling the site of cochlear implant package
The current cochlear implant is 6 mm in width , so need to expose the dura to get
significant depth in children . We should fashioning the niche to exact proportions , so
that the implant fits snugly .
- Insertion of the electrode array Special
(1) We should know the round window anatomy & the basal coil must be identified , the
window lie superiorly in the niche , there is inferior ridge of bone called crista
semilunaris (around with the cochlear duct hooks) .
The main trap that fool the inexperienced surgeon is extensively pneumatized
mastoid with large cells parallel to the basal coil .
(2) Drill the crista semilunaris 1st , direct view down the basal turn of the cochlea (using
xomed microdrill) .
Some surgeon prefer to fashion cochleostomy through the promontory immediately
infront of the round window (good access) .
(3) Immediately before the electrode insertion , check for any bleeding vessels & the
thickness of the skin over the expected implant site (<5 mm) .
The monopolar diathermy is removed & replaced with bipolar one because the
monopolar one can damaging the implant .
(4) The implant then given to the surgeon to check that the body will fit snugly into the
drilled out site .
(5) The implant array is inserted gently to prevent buckling after 10-15 electrodes are
inserted , then the body of the device can be rotated to encourage the passage of the
tip around the bend of the cochlea .
All active electrodes should be inserted plus a few of the stiffening rings .
(6) After the implant is positioned , the rest of the electrode lead has to be gently
manipulated into the mastoid cavity without the electrode falling out the cochlea .
The lead can be placed under the bony rim has been left behind around the mastoid
cavity , some surgeons place a special tie , others use an adhesive to prevent
electrode array extrusion .
(7) The electrode insertion rechecked & the number of the stiffening rings outside the
cochlea is noted , usually take a picture for the records & to aid in any future
revision .
(8) Next ; the round window is sealed with muscle covering the entire electrode array in
the middle ear , the posterior tympanotomy & attic also obliterated with muscle to
decrease the risk of infection .
(9) The round window is closed with clips or nonabsorbable suture .
(10) Postoperatively ;
Antibiotics ; amoxil or erythromycin for 7-10 days .
The patient stay in hospital for 12-24 hours postoperatively .
Pain killer for pain , due to surgical trauma to sternomastoid muscle .
Some patient develop vertigo even in normal vestibular test prior to surgery .

Lecture notes in
Tinnitus , 76% of patient will relieved or improved .

- Special consideration
Very young children
1. In children < 2 years care should be taken to avoid facial nerve damage .
2. Monopolar diathermy used with caution for fear of burning the intracranial content
3. The mastoid very small & may still contain marrow cells cause bleeding .
4. Special care taken to avoid facial nerve exposure which may required for further
update .
5. Middle ear packed with muscle or fibrous tissue to prevent OM to spread to the
implant .
Osteogenesis ( prediagnosed by CT scan)
1. No contraindication for implant , but less optimal results .
2. If osteogenesis obstruct the round window , then attempt to drill out the new bone
without straying outside the cochlea .
If the disease extends around the bent of the basal turn , attempt to insert the
electrode through the scala vestibule by removing the stapes superstructures &
drilling into the cochlea anteriorly & slightly inferior to the anterior crus of the
stapes (better method) , can insert 17-22 electrodes .
3. If both the scala tympani & vestibule are obstructed , then join the 2 openings
together & then develop a cleft in the promontory along the site of the basal coil &
under the facial nerve , 15 electrodes can be inserted into this cleft (good results) .
Surgery on discharging ear
1. First ; managed vigorously with aural toilet & antibiotics until the ear is
completely clear of infection & stable .
If perforation is present then it must be closed preoperatively .
2. At surgery , advocate blind sac closure of the external meatus to decrease the risk
of breakdown at a future date , this done by removing the tympanic membrane &
the medial half of the external meatus (and remove all the epithelial tissue) & the
bony margins polished with a burr , the external half of the meatus is then raised &
delivered out through the meatus , also the external cartilaginous & middle ear are
filled with abdominal fat & the meatus is closed by careful suturing .
Surgery on mastoid cavity
We need two stage procedure , but 1st the cavity is rendered as free from infection as
possible (by aural toilet& antibiotics) .
At the 1st operation , the mastoid cavity is obliterated with fat & blind sac procedure
(closure) of the external meatus is done with removal of all epithelial tissue from the
mastoid cavity .
The 2nd operation done 4-6 months later , the ear is reopened & careful inspection is
made of any skin pockets or infection , if the ear free , then insert the cochlear implant
in the usual fashion .
- Postoperative care
1. i.v. antibiotics given during surgery & postoperative fro 1 week .
2. The wound inspected 12 hours postoperatively for haematoma .
3. The tight dressing removed & replace. d by loser dressing .
4. Patient discharged 1 day postoperatively .
5. Use simple analgesia .

Lecture notes in
6. The stitches removed 7 days postoperatively & the external meatus checked &
cleaned if necessary .
7. Children usually quarantined for 14 days , no visitors & no playing & no school .
8. The initial programming of the implant usually start 14-28 days postoperatively .
when all swelling over the device has subsides .
- Complication of the surgery
1. Immediate
a. Facial paralysis , usually temporary , rarely permanent .
b. Infection of the wound , need antibiotics & if continue , the scalp swollen & the
implant extruded .
c. Skin necrosis (especially C- shaped) especially in children & in elderly .
d. Misplacement of the electrodes array , especially in pneumatized bone or in too
drilling requiring like in labyrinthitis ossificance (need simple mastoid x-ray for
checking) .
e. Short term increase in tinnitus .
2. Long term
a. Gradual hearing deterioration .
b. Device failure (replaced by another one) .
c. Extrusion of the electrode array from the cochlea , difficult to reinserted due to
fibrosis.
d. Extrusion of the device through the scalp (very rare) .
e. Facial nerve twitching on stimulation , especially in otosclerosis .
f. Progressive partial facial nerve paralysis .
g. Long term balance disturbances & tinnitus (not reported) .
h. Numbness of the scalp (in transverse incision) .
i. Taste disturbances , due to division of the chorda tympani .
j. Non-users , especially in prelingual adults & teenager .
k. OM in children .
Problems at the "switch on" of the device
This done by audiologist after 12-28 days , when swelling decreased over the implant , if
with no swelling & the implantee can hear nothing , then the possibilities are :
1. Misplaced electrode array (seen by mastoid x-ray) .
2. No survival spiral ganglion cell , helpful to Dx by implant evoked brainstem potential
3. Unrecognized response to hearing sensation (children) .
4. Nonfunctioning device , electrode integrity test can done to prove it . .
After the initial switch on , the implantee has to return several times to have the map , the
map is the stimulation threshold & maximum comfort levels of each of the electrode .
It can take several months before a stable map is achieved , which is a problem if the
implantee lives far away from the implant centre .
N.B.:
- IMPlant Evoked Brainstem Auditory Potential "IMPEBAP" : done for every child under
the age of 8 years under GA prior to switch on .
- The electrically elicited stapedial reflex , done during surgery , if visible muscle
contraction after the electrode array is stimulated at the level above the comfort settings

Lecture notes in
TINNITUS
The 1 st known writings on the management of tinnitus found in the 16th century B.C. in
Egyptian papyruses , the tinnitus defined as conscious experience of a sound that originates
in an involuntary manner in the head of its owner , or may appear to him to do so .
The term tinnitus refers to the sensation & not to any externally detectable correlates , so an
objective tinnitus or somato-sounds like bruit or acoustic emissions not included .
Classification
1. Physiological
Humming , buzzing or ringing heard in normal hearing threshold in silent , due to
circulatory hum , or muscular tremor or Brownian movement at of air at the tympanic
membraneor fluid within the cochlea , sometimes oulsatile tinnitus due to partial arterial
occlusion when the patient lie on hard pillow .
2. Pathophysiological
- Temporary
a. Noise-induced ; loud sound lead to tinnitus (in some patients) , which lasts for
seconds up to days after exposure .
b. Drug-induced ; like some antidepressants & antihistamines , B-blockers &
caffeine & alcohol , other drugs cause permanent tinnitus like aspirin , NSAID ,
quinine , loop diuretics , aminoglycosides & antineoplastics .
c. Drug withdrawal , like sedatives & addictive drugs .
d. Toxaemia may lead to tinnitus which sometimes being permanent .
- Ongoing , like spontaneous otoacoustic emissions , sometimes it classified as
physiological , usually due to reduction in the efferent inhibitory control of the
cochlear function or intensity instability preventing normal adaptation to these
sounds .
3. Pathological
Here the tinnitus associated with definitive disorder (physical or psychological) , it has 5
subdivisions ;
- Extra-auditory, associated with somatosounds
a. Muscular
- Palatal dysfunction , there is irregular episodic twitching of the soft palate
muscles , pharynx & tensor tympani muscle , this cause unpleasant clicking
sensation .
It diagnosed from history & observation of the synchronous twitching of the
tympanic membrane , pharynx & soft palate by nasoendoscopy , the cause usually
due to neurological abnormality .
It managed with tinnitus masker & injection of Botulinium toxins into the palatal
muscles .
- Middle ear muscles myoclonus, either spontaneously or with eyelid blinking ,
acoustic stimulation , cutaneous stimulation of the pinna or phonation, treated by
division of the stapedius tendon .
- TM joint abnormalities & jaw clenching .
b. Respiratory , like patulous Eustachian tube causing complains of blowing sounds
coincident with respiration (it associate with weight loss) , it appear in drivers ,
playing of wind or brass instruments .

Lecture notes in
Diagnosed from history (disappear on bending or lying down) , examination , by

observing the tympanic membrane movement with respiration or by do
tympanometry
Managed by chemical or electrical cauterization of the Eustachian tube orifice ,
or by surgical closure of the tube , or by peritubal injection of paraffin or Teflon
paste or gelatin sponge .
c. Vascular , like in arterial turbulence by atheromatic plaque or arteriosclerosis ,
hypertension , glomus jugulare tumor , arteriovenous fistula & aneurysm .
- Conductive , it is tinnitus associated with middle ear disorders &/or CHL , it is either
;
a. Enhancement , due to decrease of the normal masking effect of the ambient noise
due to CHL , decrease auditory nerve activity , SNHL coincident to or consequent
middle ear disease or physiological or extra-auditory tinnitus .
b. Movement , middle or external ear disorders .
- Sensorineural , orginate from disorders within the cochlea , it is subdivided into ;
a. Sensory "cochlear" , usually above 20 years (age associated hearing loss) , head
or ear trauma , endolymphatic hydrops , noise induced hearing loss , cochlear
vascular insufficiency , viral infection , we must note that tinnitus increased with
increased HL
b. Peripheral neural "cochlear nerve" , described as coarse , buzzing , seen in
vestibular Schwannoma & MS , affecting the 8 th nerve (due to decrease nerve
conduction) .
c. Central neural , the patient says that the tinnitus in the head , its onset , offset &
fluctuation occur in stress (precipitating & relieving factors) , it is quite unlike an
external sounds .
- Associated , like TM joint disorders (& bite disorders) , cervical spondylosis , nearby
muscle spasm (masseter & temporalis) , neck manibulation (especially during
anaesthesia) , tinnitus lead to intratympanic muscle tension which cause otalgia
leading to tinnitus again .
- Psychological
a. Hallucination , serious mental disorders .
b. Imaginary , music or singing especially in elderly musician (psychosis) , Rx by
Flupenthixol .
4. Pseudotinnitus
- Environmental , like the voice of refrigerator , underground , gas , distant traffic ,
heavy machines or water piping , so tinnitus stimulated by external sounds (ask if
other hear it)
- Feigned , here the patient exaggerate tinnitus for medicolegal context , for
functional gain (N.B.: if the general impression of the patient give idea about the
severity of the disease + PTA + tinnitus measurement "pitch matching & tinnitus
loudness match") .
Mechanisms of generation of tinnitus
- Associated with cochlear lesion
The cochlear mechanism of tinnitus generation , due to disturbance of resting pattern of
afferent nerve firing , which interpreted by the brain as tinnitus .

Lecture notes in
The onset of tinnitus a; all slowly progressive cochlear disorders associated with tinnitus ,
but , it can occur in little (or normal) hearing loss & may be absent in severe hearing loss .
The triggering factors are ;
1. Acute or increasing psychological stress (domestics , marital & occupational)
account for 26% .
2. Noise exposure & ear surgery (over 90dB) .
3. Mild head injury .
4. Acute TM joint disorders or injuries .
5. Ear syringing & acute OM .
6. Acute neck injury (within 4 weeks of whiplash injury)
7. Barotrauma , even following tympanometry .
8. Thyrotoxicosis & hypoglycaemia or hyperlipidaemia .
9. Drugs like aspirin & NSAID .
10. Rapid withdrawal of benzodiazepines drugs .
The hypothesis of tinnitus ;
1. Altered auditory firing rate (decreased or increased) , so tinnitus is due to decreased
cochlear neural activity .
2. Cross talk ; noise or MD may cause damage to the myelin sheath "insulation" of the
auditory nerve between the axons in the peripheral auditory system leading to cross
talk in between these structures causing tinnitus .
3. Central processing , emotions & model causing tinnitus (emphasis at the central
auditory cortex) .
Cochlear disorder
Abnormal spontaneous Reduction of sensitivity Other hearing dysfunctions (of

rate or rhythm of (hearing threshold level frequency & temporal resolution , over
cochlear nerve elevation) recruitment , distortion)
discharge
Hearing disability
Tinnitus perception
Hearing handicap
Suffering
- Associated with psychological stress & with hyperacusis

Lecture notes in
Hearing disorder Increase in brain

attention to auditory
normal activity
Abnormal rate or
rhythm of background
auditory neural activity
Decrease tolerance to
Tension every day noises
"hyperacusis"
Tinnitus
Anxiety recause & progress

Unrealistic beliefs & attributes Increased intrusiveness of
Obssessive attension tinnitus
Recruitment Hyperacusis
Abnormal build up of loudness Loudness discomfort from every day
sounds , that not bother the patient
previously
Cochlear site of origin Brainstem site of origin
Associated with HL May or may not associated with HL (in
the frequency of 500-4000 dB)
The phonophobia , is an actual fear of or/ aversion to loud sounds , due to hyperacusis
leading to increased loudness of tinnitus .
Epidemiology
- Prevalence in adults
35% of persons have an attacks of tinnitus .
10% experienced spontaneous tinnitus > 5 minutes lasting .
5% has tinnitus interfere with sleep .
0.5% has tinnitus affecting on their normal life .
The site usually at the left > right , F:M 3:2 , 88% of patient has aural disorders , 70% in
hyperacusis , 50% in sudden deafness , 40% in MD , 30-90% in intoxication .
- Tinnitus in children , lead to
Confusion in audiometry (wrong results in PTA) .
Reluctant to wear hearing aid .
Disturbance in concentration & behavior .
- The clinical prevalence
1 st indicator of some pathologies like acoustic neuroma .
Warning sign of developing impairment & risk of future disability .
Can cause suffering &/or anxiety , so it is like the pain .
- The effect of tinnitus
Effects on hearing , understanding speech & television .
Effects on life style , can't sleep , avoid quite situations .
Effects on general health , dependence on drugs , pain , headache & dizziness .
Emotional problems , lespian , frustration , depression , inability to relax , fear ,
confusion & warriness
- Severity of tinnitus
Lecture notes in
Loudness , correlates with severity , but difficult to measured .

Quality , may have tonal element , pitch matching tell us little about the actual tinnitus ,
sounds or about its unpleasantness .
Temporal characteristics , continuous tinnitus more troublesome than intermittent , but
fluctuating one cause fear from bad spells .
Lateralization , worsen tinnitus , if affect both ears , if it is previously unilateral .
Psychological reaction , the patient usually upset .
Associated stress , the patient says that the tinnitus worsen if become tired or tense .
Management
A. History
- The time & severity course of tinnitus , triggers or exacerbating factors , including
starting or sudden stopping of drugs .
- The characteristics & the site of tinnitus .
- The effect of tinnitus (same heading above) .
- Whether the tinnitus is greater , equal or lesser problem to the patient than any HL
or hyperacusis .
- The effect of environmental sounds in masking or decreasing the loudness of
tinnitus when it is quite .
- The time(s) of the day or night when the tinnitus is more troublesome .
- Otological examination
- Check the general health , neurological examination , TM joint function & neck
mobility .
- Where there is pulsating , check the pulse & blood pressure , auscultation for head
& neck & ears & see the effects on the tinnitus of neck turning & jugular vien
compression .
C. Investigations
- General investigations
X-ray &/or MRI of the brain especially CPA .
Blood tests , Hb% , ESR , LFT , RFT , thyroid FT , FBS , lipids profile ,
immunological screen & serology for syphilis .
- Hearing testing
The purpose is to ; (1) assess the patient hearing threshold , (2) provide baseline
for tinnitus tests & (3) measure the extent of any associated hyperacusis .
These tests include ; PTA , tympanometry , acoustic reflex , tone decay & speech
audiomtry .
- Tinnitus testing
The aim to ; (1) gain ata of the pitch & loudness of tinnitus , (2) provide quantative
data for comparison post-therapy & (3) provide background for the subsequent
visits .
We have 3 tests ;
Pitch-match frequency ; use pure tone threshold , it should select the tone mostly
closely match the pitch of the most troublesome tinnitus sound .
Tinnitus loudness match ; is best obtained with pure tone from an audiometer at
the pitch-match frequency & in the ear with troublesome tinnitus sound .

Lecture notes in
In tinnitus , patient , especially at pitch-match frequency , means SNHL ,

Yamashita & Yasuda 1992 enter the air-conduction threshold , but , if there is
air-bone gap , enter the bone conduction threshold .
Minimal masking level ; measured by gradually increasing the level , usually in
dB (5 dB steps) of the masking ground until the tinnitus is no longer audible
(delivered to one or both ears) .
D. Treatment options
- Option 1 ; "prevent" hearing loss due to maternal rubella & excessive noise , to
decrease the incidence of tinnitus .
- Option 2 ; "pathological" , management of the underlying cause ;
Management of the conductive HL ; wax , MD & otosclerosis .
Drugs , foods & liquids , avoided , drugs like quinine , aminoglycosides , aspirin ,
cytotoxics & alcohol , foods like cheese & chocolate & liquids like coffee , red
wine & ports .
Benzodiazepines reinstatement (for rapid withdrawal) .
Management of hypertension & hyperlipidaemia & anaemia .
Management of transient hypoglycaemia (especially immediatelynafter sleep , do
the patient drinks glucose rich inerals 1/2 cup to decrease tinnitus after 10-20
minutes .
- Option 3 ; "psychological" , reassurance .
Professional counseling , for ENTist , giving & explaining most probable
reasonable diagnosis , once a harmless Dx reached , so tinnitus not due to tumors
, explain that the tinnitus is symptoms not a disease itself , also any apparent
trigger for onset or increase the tinnitus needs comments , show PTA to the
patient & explain how HL cause tinnitus , the general favorable prognosis even
without Rx should be outlined & learn the patient to live with the tinnitus
Counseling by literature , start with booklets & information sheets .
 Lay counseling , advice to how to live with tinnitus & by local self-help groups ,
give a good data on tinnitus (also by national telephone helpline) .
Relaxation training therapy , take relaxations as a way of life & remove the stress
& tension , need frequent relaxation training sessions .
Psychological counseling & management , important to the patient to understand
that referral is not psychotic one .
- Option 4 ; " prosthetic" .
Tinnitus retraining therapy ; it is a combination of prosthetic avenues , gradually
to learn to develop the ability to ignore the tinnitus as a sound , the instruments
are
a. Hearing aids ; for one or both ears , must be associated with some degree of
HL &/or hearing difficulties , the HL must be 10 dB as lower limit , hearing aid
should be wear for many hours/day especially in the quite periods (at night) .
b. Tinnitus maskers , monoaural or binaural , used if , too small or to great HL
for hearing aid to be appropriate , or with insufficiency of hearing aid or dislike
of it due to recruitment or hyperacusis .
It may be in the ear canal , in the ear , or behind the ear (with fitted in an open
ear mold) , for 6 waking hours/day for one year .

Lecture notes in
Hyperacusis desensitization therapy ; with tinnitus maskers , used if the

hyperacusis more disturbing than tinnitus & if there is hyperacusis without
tinnitus .
The starting level of therapeutic noise is slightly higher level than just clearly
audible , this level is maintained for 6 or more hours a day , after a month , the
level of the noise in increased progressively , the aim to increase the level
gradually to higher level of tolerance .
Tinnitus masking either ;
(1) Complete masking , making the noise is increased in level until the
tinnitus become inaudible .
(2) Partial masking , better , provide background sound against which the
loudness of tinnitus is reduced , alternatively , the masker can be turned
up until its loudness is almost equal to that of tinnitus .
- Option 5 ; "pharmacological" , to reduce the tinnitus
Clonazepam , carbamazipine , depakin , oxazepam & mexiletine , benefit 1/3rd of
patients , the dose of clonazepam is 0.5 mg at night for week , if no benefit then
0.5 mg twice daily or 1 mg at night for 4 week , if no benefit , then 1 mg twice
daily for 2 weeks , if no benefit , then stop the drug .
Carbamazepine , 100 mg at night for one week , the maximum dose is 200 mg
t.d.s .
Nimadipine , 30 mg twice daily for 3 weeks & then increase to 30 mg q.d.s for
further 3 weeks .
- Option 6 ; "surgery/ablative" , the surgery not advisable when tinnitus is the
primary indication , it is the option for ; (1) Glomus tumor (2) MD (3) Perilymph
fistula (4) Vascular loop on 8th nerve .
- Option 7 ; "suppression"
Electrical , electrical stimuli , of the cochlea , decrease the tinnitus partially or
completely in 60% of patients (by round window electrode) & 43% (with
promontory electrode) , use 20 Hz sinusoidal electrical stimulation .
Magnetic ,small powerfull magnet placed deep in the ear canal with its north
(+ve) pole oriented medially & the results is questionable .
Electromagnetic stimulation , some benefit in 45% of cases .
U/S stimulation & pillow speaker or pillow radio .
- Option 8 ; "suppression of spontaneous otoacoustic emission-tinnitus" ; aspirin &
quinine used to decrease the OAE .
- Fringe medicine
Acupuncture , sometimes beneficial , but not change the hearing threshold in
SNHL .
Ginkgo biloba extract , vegetable extract from the leaves of the maidenhair tree
for the management of cerebrovascular insufficiency which decrease vertigo &
tinnitus .
E. Prognosis , there is a model for the effect of tinnitus on the patient ;
- The majority of people who have tinnitus do not complain of it .
- The decreased number of problems caused by tinnitus , we must say to the patient
that the majority do infact learn to live with their tinnitus & our aim to help the
patient to do this (habituation model) .

Lecture notes in
- Tinnitus that come suddenly seldom increased in loudness & 1/3 rd of cases comes
on gradually .
- If the tinnitus is still increasing when the patient is 1st seen or increased again , he
can be reassured that it is unlikely to go on & on increasing .
- The patient refers to untreated tinnitus , with management , the prognosis is better
still.

Lecture notes in
VERTIGO
Anatomy & Physiology
Membranous vestibular portion of the inner ear consist of three SCC at approximately right
angles to each other (lateral , superior & posterior) , & also has two otolothic organs
(utricle & saccule) .
Neuroepithelium of the utricle & saccule found in a specialized region called the macula
which contain the otolothic membrane .
Otolothic membrane is sensitive in changes of motion relative to gravity (saccule) while the
utricle is sensitive to linear acceleration .
The three SCC , set at right angles to each other to provide response to angular
acceleration in all planes & they sense head rotation acceleration .
Within the membranous duct , a dilated portion contains the Neuroepithelium responsible
for the translation of mechanical stimuli to electrical one known as the ampulae
The crista supported within the ampula at a right angle to its long axis , this saddle shaped
organ support the mechanically sensitive hair cells that are responsible to initiate neural
messages from the vestibular apparatus .
Suspended above the crista is a gel like network called the cupula , this snail-like structure
is exquisitely sensitive to motion .
The hair cells that subserve the vestibule are of two types ;
1. Type I hair cells , Chalice shaped .
2. Type II hair cells , Boutonnière shape ending .
Both has a numerous stereocilia embedded im surrounding cuticular plate . Jextaposing the
tallest stereocilia but not fixed in the cuticle is a singular kinocilium which determine the
direction of depolarization .
There is a resting basal discharge rate from the hair cells within the ampulae of the
vestibular apparatus . When the kinocilium deflected away from the stereocilia , the resting
discharge rate is increased & the reverse is true .
Therefore in the lateral SCC , ampulopetal (utriculopetal) endolymphatic flow cause
displacement of the kinocilium toward the utricle & away from the stereocilia , thus
increasing discharge rate . Conversely ampulofugal (utriculofugal) direct the kinocilium
toward the stereocilia caused decrease the firing rate .
Because the orientation of the kinocilia & stereocilia in the vertical canals ampulofugal
movement cause increase firing rate & ampulopetal cause decrease basal firing .
The nerve impulse from the labyrinth gone to the vestibular nuclei in the brainstem , here
they integrated with other two inputs that enable us to balance (vision & proprioception"
the neck & ankle are the most proprioceptive inputs") .
Seventy percent of balance is due to visual input , 15% proprioceptive & 15% from the
vestibular system .
The brainstem computerized these three inputs & with the help of the cerebellum maintain
the balance & coordination of the head & body .
Definitions
Vertigo : Hallucination of movement of the patient body or the patient environment , or it is
subjective sense of imbalance or it is hallucination of movement .
Dizziness : Non-painful discomfort related to the head which could be cerebral , visual ,
GIT or vestibular in origin .

Lecture notes in
Unsteadiness: Loss of equilibrium in relation to one's environment , or defined as a

sensation of being off balance & it occur only on walking , it is the cardinal symptoms of the
diseases of the vestibular system & its central connections .
Lightheadedness : Loss of equilibrium within one's head .
Drop attack : Loss of extensor powers & falls suddenly with no loss of consciousness .
Vertigo has a Latin root of the word which means sensation of turning (but this not implies
clinically .
Incidence
Dizziness & vertigo are among the most common symptom causing the patient to visit the
physician . The over all incidence of dizziness , vertigo & imbalance 5-10% & it reach 40%
in patient older than 40 years .
Migraine more prevalent (10%) than Menier's disease (<1%) , about 40% of patients with
migraine have vertigo , motion sickness & mild hearing loss , therefore differentiating
migraine from primary inner ear disorders is sometimes difficult .
Classification of vertigo
A. Based on history :
1. Rotational ;
a. Episodic ;seconds or hours .
b. Prolonged ; for weeks .
2. Unsteadiness ;
a. Episodic ; seconds or hours to days .
b. Prolonged ; for weeks to months .
B. Other classification :
i. Physiological vertigo , by stimulation of normal & intact sensory structures like in
heights , spinning movement …etc .
ii. Pathological vertigo , by disease process which affect one of the many functions used
in balance .
C. Aetiological classification
1. Otological
a. Infection ; labyrinthitis (bacterial or viral like mumps) .
b. Trauma ; fractured temporal bone or iatrogenic .
c. Ototoxicity ; drugs .
d. Tumors like vestibular Schwannoma .
e. Idiopathic like Mennier's disease (MD) & benign paroxysmal positional vertigo
(BPPV) .
2. Non-otological
a. Medical
- Haematological ; anaemia , migraine …etc .
- CVS ; heart failure & hypotension .
- Metabolic ; DM , renal failure & alcoholism .
- Psychological
b. Neurologial
- Epilepsy .
- Multiple sclerosis (MS) & brainstem disease .
- CVA .
- Brain tumors especially cerebellar tumors .

Lecture notes in
- Head injury .
c. Miscellaneous
- Cervical vertigo (OA changes) .
- Ocular vertigo .
D. Classification (by letters)
- V : Vascular causes ; anaemia , migraine , hypotension , heart failure , CVA &
cervical vertigo .
- E : Epilepsy & elderly .
- R : Rx (therapy) , ototoxicity & alcohol .
- T : Trauma (head injury) or fractured temporal bone) , Tumors (vestibular
Schwannoma) , Thyroid (hypothyroidism) .
- I : Idiopathic (MD or BPPV) , Iatrogenic (post mastoidectomy or stapedectomy) ,
Inflammation (labyrinthitis & vestibular neuritis) .
- G : Glial causes like MS which associate with vertigo , nystagmus & associated with
other focal signs .
- O : Ocular causes .
Management
A. History
- Ask the patient to describe their symptoms by using words other than dizzy to
differentiate the vertigo from unsteadiness , generalized weakness ..etc .
- Detailed history should be directed to the possible causes of vertigo , start from the
age of the patient , the onset of vertigo , duration of the disease , duration of the
attack , frequency of the attack .
- Associated symptoms (deafness , tinnitus , nausea , vomiting , diplopia , blurred
vision , parasthesia of the face , headache , sudden fall & loss of consciousness) .
- Precipitating & relieving factors .
- Neurological symptoms like headache , weakness , sensory disturbances .
- Psychological history .
- Past history of medical disease (like DM , renal failure or hypertension or thyroid
diseases) .
- Any history of trauma or previous surgery , family history & drug history (ototoxic
drugs or alcoholism) .
1. General examination
- Starting from the way that the patient come in it like walk by himself or assisted by
others or by wheel chair .
- Vital signs , blood pressure , pulse rate …etc .
- Evaluate the cardiovascular system .
2. Otological examination
- Inspection , for vesicles of herpes zoster , any scars for previous surgeries .
- Otoscopy ; any discharge , tympanic membrane perforation ..etc .
- Fistula test , by tragal massage or Siegel speculum .
- Tuning fork , to assess the hearing .
3. Cranial nerves examination , all cranial nerves should be examined separately .
4. Eye examination , for visual field , acuity , fundoscopy & for nystagmus .
5. Cerebellar function ; gait , finger to nose test & dysdiadochokineis .

Lecture notes in
6. Vestibular function tests ;

- Vestibulo-ocular ; Saccades eye movements , smooth pursuit eye movement ,
nystagmus .
- Vestibulo-spinal ; Romberg's test , Unterburger's test , Gait & Posturography .
C. Investigations
1. Haematological ; CBP , FBS , ESR , urea & electrolytes .
2. Audiological ; PTA , Tone decay , Fowler's test & SISI , Tympanometry & Acoustic
reflex test .
3. Vestibular tests
The results of these tests are not diagnostic alone , for example unilateral
vestibular loss can be due to vestibular neuritis or an acoustic tumor , therefore
clinician must avoid interpretating the results as pathological entities , so
background in neurophysiology & electrophysiology is important to use the results
effectively .
- ENG testing , standard ENG test battery is composed of ;
Saccadic test ; used to evaluate the voluntary fast eye movement , it should be
performed for each eye separately , abnormalities include ; dysmeteria , slow
saccadic velocity & dysconjucate saccades .
Gaze test ; used to evaluate the ability to generate & hold a steady gaze
without drift or gaze evoked nystagmus .
Pursuits eye movement ; prevent slipping of an image on the retina while the
patient tracking moving objects .
Test for optokinetic nystagmus ; is a complex CNS reflex initiated by moving
images on the retina , OKN abnormalities seen in deep parietal lobe lesions .
Test for head shake nystagmus ; is seen with uncompensated unilateral
vestibular hypofunction of any cause .
Positional test ; by recording eye movements without visual fixation in three
cardinal positions (supine , head right & head left) , an objective sign of
vestibular asymmetry
Dix – Hallpike positioning test , classical finding in patients with BPPV .
Bithermal caloric test , only in failure of fixation suppression is indicative of
central cerebellar disease , while other abnormality indicate peripheral
vestibular disease .
- Rotating chair test ; this test most useful in determining residual vestibular
function & the degree of central vestibular compensation .
- Dynamic Posturography ; used to evaluate both sensory and motor components
of balance , especially in peripheral lesions .
4. ABR & ECG .
5. Radiological test , plain film (mastoid & cervical spine) , CT scan & MRI .
D. Treatment
1. Eliminate the cause
- Vascular like anaemia , correct it , manage the HF & renal failure , also cervical
spine vertigo managed by rheumatologist .
- Epilepsy managed by anticonvulsant drugs .
- Avoid (Rx) ototoxic drugs & alcoholism .

Lecture notes in
- Tumors should be removed surgically , with trauma patch the defect or wait for
compensation & in thyroid disorders give T4 supplements.
- Inflammations like labyrinthitis should managed by rest & antibiotics , in
iatrogenic cases either patch the defect surgically or wait for compensation & in
idiopathic cases , for MD & BPPV either anthorane Kawasaki or singular nerve
neuroectomy .
- Glial tumors referred to neurosurgeon .
- Ocular cases referred to ophthalmologist .
2. Suppress the vestibular symptoms
- Those to decrease the vegetative symptoms , like Stugeron , Plasil , Stemetil ,
Valium & Steroids .
- Those used in episodic vertigo , like Astimazole , Betahistine , Largectil &
Flurnarazine .
3. Suppress the emotional reaction , reassurance , explanation about the nature &
progress of the disease & give minor tranquilizer (in small doses) .
4. Wait for compensation , in early stage , there is cerebellar clumping of activity of
vestibular nuclei , with time , gradual restoration of comfortable balance .
5. Eliminate the offending labyrinth , although nature can compensate readily for
complete loss of function of labyrinth , it may have some difficulty in compensating in
; complete loss & fluctuating loss .
To Rx the fluctuating loss or failure of the nature to compensate by ; labyrinthectomy
or vestibular nerve section & the result will be loss of all the auditory function of the
affected ear .
6. Acceptance of the problem , sometimes despite the application of appropriate
management , there is a persistent imbalance , so that the physician should explain to
the patient that there is some degree of imbalance is acceptable with explanation of
the appropriate aids like walking with sticks , & in severe cases walking frame &
placed hand rails will be needed .
Surgery for vertigo
It is occasionally needed in vertigo management .
- In BPPV , do singular neuroectomy or posterior SCC occlusion .
- In perilymph fistula , repair through tympanotomy , usually combined approach .
- CSOM , mastoidectomy .
- MD , convert the underling problem like saccus decompression through
mastoidectomy or cervical sympathectomy , or ablation of the vestibular function in
an offending labyrinth like labyrinthectomy , vestibular neuroectomy or Garamycin
injection through the round window .
Prognosis
The best overall prognosis is unilateral peripheral & in BPPV , while poor prognosis in
CNS lesions & elderly patients .
1. Vertigo alone ; MD , Drugs & Vestibular neuritis .
2. Positional vertigo ; BPPV & Central causes .
3. Vertigo with syncope ; CNS diseases , Ischemia & Migraine .
4. Vertigo with tinnitus & SNHL ; MD , Vestibular Schwannoma , Labyrinthitis ,
Syphilis & Labyrinthine trauma .

Lecture notes in
Pathological correlates
The suggested pathological correlates for different types of vertigo are ;
A. Rotatory
1. Episodic
- Seconds ; , short livid stimulation or inhibition of vestibular system (labrynth) , like
caloric effects , BPPV , alternobaric vertigo , labyrinthine fistula , post-concussional
syndrome , vestibulobasillar insufficiency , cervical vertigo & coriolis phenomenon
.
- Hours , physiological or metabolic failure of the labyrinth or central connections ,
like MD , Syphilitic labyrinthitis , delayed endolymphatic hydrops , decompensation
of previous vestibular lesion & following middle ear surgery .
2. Prolonged , , destructive lesions of the labyrineth or central connections , like
vestibular neuritis , labyrinthitis(bacterial or viral) , trauma (head injury , ear
surgery , labyrinthectomy & vestibular neuroectomy) , vascular lesions & secondary
tumors in the CPA .
B. Unsteadiness
1. Episodic
- Seconds , physiological overload of vestibular system , like Rapid movement &
Abnormal input (especially visual) & minor inadequaties (visual , vestibular &
properioceptive) .
- Hours to days , temporary impairment of the central connections or decompensation
of the vestibular system , like Drugs (self inflected or iatrogenic) , Travel sickness ,
Perilymph fistula , Decompensation of the pre-existing lesion , hyperventilation ,
functional & active CSOM .
2. Prolonged , vestibular inadequacy , like Elderly & Drugs either through its
metabolic effect like anticonvulsants or destructive effect like garamycine , CNS
lesions , Floating females (psychogenic) & Toxins from CSOM .
Cause of vertigo in head trauma
1. Post concussional syndrome . 2. BPPV .
3. Destructive labyrinthine lesion . 4. Perilymph fistula .
5. Delayed endolymphatic hydrops (MD) . 6. Functional .
Benign paroxysmal positional vertigo
Characterized by sudden episodes od vertigo , precipitated by head movement & lasts for
seconds , it is resolves spontaneously over weeks to months . It is due to the presence of
heavily particles in one of SCC possibly otoliths that have been displaced from the utricle .
The movement of these particles with gravity cause stimulation to the canal .
It is managed by ; therapeutic head maneuvers like Epley maneuver (Canalith
repositioning procedure) , which is useful with success rate of about 90% , if fails , then do
surgical ablation of the ear or blockage of the affected canal or singular neuroectomy will
stop the spells .
Management of viral labyrinthitis
- If hearing normal , give diazepam , meclazine & promethazine to control vomiting ,
these drugs should be discontinued after a week due to their interference with the
normal process of compensation to vestibular injuries , then if still symptomatic , the
patient will be candidate for vestibular rehabilitation .
- If hearing deteriorate ; give steroids to prevent deafness .

Lecture notes in
NYSTAGMUS
It is a disturbance of ocular posture characterized by a non-voluntary rhythmical oscillation
of the eyes , the posture of the eyes depend on visual or vestibular afferent impulses .
The speed of eye movement may be , same in both directions or quicker in one than others .
Nystagmus may be ; horizontal , vertical or rotatory . Nystagmus & eye posture depend on 2
sets of afferent impulses ; visual & vestibular .
1. The visual impulses ; regulate the eye position in relation to the object of visual
interest .
2. The vestibular impulses ; regulate the eye position in relation to the position &
movement of the head & remainder of the body .
The eye posture controlled by central mechanism which receive their afferent impulses &
central efferent impulses to the ocular muscles .
Nystagmus may result from any lesion affecting the afferent pathways , their central
connections or to less extent the efferent pathways .
Two types of nystagmus "depend on the appearance of movement" ;
1. Pendular "horizontal" nystagmus , characterized by ocular oscillation that there are
approximately equal in velocity in both directions & there may be jerk movement on
extreme lateral gaze .
2. Phasic nystagmus , characterized by rhythmic oscillation in which the movement in
one direction is significantly faster than the other , the pathological one is the slow
one , but the fast or corrective used to denotes the direction of the nystagmus
(position in which the nystagmus is least marked is called null point) .
Duration of common causes of nystagmus ;
- Seconds : BPPV .
- Minutes : migraine & vestibulobasillar insufficiency .
- Hours : MD .
- Days : vestibular neuritis & infection of the labrynth .
Other classification of the nystagmus ;
1. Gaze evoked nystagmus , if the nystagmus begins when the patient looks to the left &
right or up & down .
2. Positional nystagmus , occur with certain head or body postures .
3. Spontaneous , occur without stimulation .
4. Induced , which is elicited by stimulation with caloric or rotational tests .
Factors affecting nystagmus
1. State of arousal , if increased , increase the nystagmus .
2. Habituation , like dancers & ice-skater .
3. Optic fixation , increase nystagmus in peripheral disease & not affect it in central
lesions .
4. Other sensory stimuli like auditory & tactile input .
5. Age .
6. Drugs .
Characterization of nystagmus
Nystagmus whether spontaneous , gaze induced , or positional , must be completely
characterized for correct interpretation & this should include provocative factors , latency ,
directions , effects of gaze , fatigability . Failure to fully characterized nystagmus can lead
to misdiagnosis .

Lecture notes in
Examination for nystagmus

Nystagmus found in examination either ;
- Pathological , spontaneous , which is either acquired , vestibular (due to disorders ,
toxic (alcoholic & anticonvulsants) , CNS lesions)& ocular(pendular) , or
congenital , it is present when there are rhythmical eye movement on frontal gaze .
- Physiological , induced , which is end-point nystagmus , caused (induced) by ; tests
like positional tests or investigations like caloric test .
- Intermittent nystagmus or gaze nystagmus , demonstrated by altering gaze to the
right or to the left or up or down , it may be considered under the heading
spontaneous nystagmus .
When examine for nystagmus ;
- The patient in good light .
- Objects at which the patient asked to look must be ; in comfortable range (40o& 60
cm) , at infinity but few feet away will suffice , so that no need for extensive
accommodation .
- The nose doesn't impinge on the field of vision & on looking upwards (objects remain
in comfortable view) , otherwise searching or nystagmoid movement may be
mistaken & interpretated as nystagmus .
Causes of nystagmus
A. Spontaneous
1. Labyrinthine "phasic"
It has 4 main characteristics ; (1) usually associated with sensation of vertigo (2)
usually unidirectional (3) more marked when looking in the direction of the fast
component & (4) enhanced by removal of fixation by eye closure or Frenzel glasses
or darkness .
It follow destructive labyrinthine lesion , decreased with time & caloric disappears
entirely within 4 weeks , however , even then it may be still detected after removal of
visual fixation .
2. Vestibular
In normal subject the tone of the extra-ocular muscles is to same extent controlled by
vestibular nuclei .
The vestibular nuclei tend to drive eyes to the opposite side , so that the vestibular
nuclei on the right side influence the left lateral & right medial recti moving the eyes
to the left side , normal ocular posture maintained by correct balance between the
vestibular nuclei on both sides .
So that if there is abnormal function of the vestibular nuclei on one side , there will
be a change in the tone of corresponding muscles .
Consequently , stimulation of the vestibular nuclei on one side result in eye
movement to the opposite side , while unilateral inhibition of the vestibular nuclei ,
result in movement of the eyes toward that side .
The effect is to move the eyes from the point of visual interest , so that there is a
correcting movement to restore the eyes to original position , this repeated deviation
of the yes & repeated correction it means nystagmus , e.g. destructive lesion in the
right labyrinth results in lesion of the right vestibular nuclei , causing slow right
deviation of right eye & quick corrective movement on the left side & this called left
beating nystagmus .

Lecture notes in
In describing uni-directional nystagmus , we should mention ;

a. Direction of nystagmus .
b. Degree of nystagmus .
- 1 st degree nystagmus , when phasic eye movement detected only when
looking in the direction of the quick phase .
- 2 nd degree nystagmus , phasic movement also seen on looking straight ahead
- 3 rd degree , phasic movement seen even when looking in a direction away
from nystagmus (any direction) .
Alexander's law ; in general if vestibular nystagmus is present , it can be enhanced
by moving the eyes in the direction of the fast phase & diminished by moving the eyes
away from the fast phase .
3. CNS lesion
Nystagmus due to CNS lesion present in multitude of different forms , some of which
not clearly understood , it is ;
a. Bidirectional which is not like the labyrinthine .
b. Produce vertical nystagmus which not occur in labyrinthine nystagmus , this
is good rule , but it is not implicated in excitation of the posterior canal crista
as in BPPV may cause up beat nystagmus , & transudation of posterior
ampulary nerve may cause a down beat nystagmus .
c. Vary in amplitude & velocity .
d. Not decreased with removal of fixation .
Sometimes one eye up & the other down .
4. Toxic
Drugs like alcohol , barbiturates , anticonvulsants & tranquilizers , they are a
potential cause of nystagmus , the effect of drugs is on the CNS , they are the most
common cause of vertical nystagmus . However , the positional nystagmus associated
with alcohol may well be peripheral in its action .
Positional alcoholic nystagmus of 2 phases in opposite directions , the 1st occur
shortly after ingestion of alcohol & pass off after few hours & the 2nd occur 8 hours
later .
It is due to partial replacement by alcohol of water containing components of the
SCC ampulae followed later metabolites .
5. Ocular
Any lesion affect the macula , especially when the peripheral vision is maintained ,
nystagmus which is usually pendular , this may occur in amblyopia . .
Minor nystagmus may be one of this type , neurosis may maintain the disorder &
CNS lesion affect the ocular pathways cause ocular nystagmus .
6. Congenital
The congenital nystagmus is present from birth but may be not noticed until school
age or adulthood and sometimes it is only documented at an occupational medical or
after the patient has presented with neurological or opthalmological symptoms.
Congenital nystagmus is included under the category of disorders of fixation because
it can frequently present as a severe gazeevoked nystagmus, and because it is
increased by attempts at fixation.
Congenital nystagmus is universal in albinism and also occurs in achromatopsia.

Lecture notes in
It present only on eccentric gaze and there is a wide neutral zone or null position
(This is a position of the eyes in the orbit where the eyes are nearly still) in which
nystagmus is absent.
people with congenital nystagmus adopt a head posture which allows them to put
their eyes into this "null", to improve their visual acuity
It consists of very high frequency,up to 6 Hz,oscillations of the eyes.
It can be associated with sensory pathology,e.g, ocular albinism .
The direction of congenital nystagmus is horizontal,but it may be torsional or
vertical.
The waveforms consist of pendular and jerk nystagmus.
It characterized by an exponentially increasing or decreasing slow phase or by
unidirectional or bidirectional jerks and each subject display several waveforms, e.g
a pendular nystagmus may convert to a jerk nystagmus with gaze in the direction of
the fast phase.
Congenital nystagmus may associated with concomitant squint.
The subject with congenital nystagmus report some failure to stabilize the visual
target suggesting that the vestibular response not fully suppressed.
It always dependent on optic fixation, so disappears when this removed by asking the
patient to wear Frenzel s glasses.
It attenuates with convergence, with eye closure and in sleep.
congenital nystagmus, contrary to vestibular nystagmus, is generally increased by
fixation and reduced in the dark. This is an important distinguishing feature.
Subjects with congenital nystagmus display saccadic,optokinetic and smooth pursuit
abnormalities.
(Saccades are rapid eye movements, which correct errors in the direction of gaze,
and bring the desired object of fixation to the fovea in the shortest possible time.)
In congenital nystagmus saccadic abnormalities are mild and involve their initiation
and accuracy though not their velocity.
( the smooth pursuit system, responsible for maintaining gaze on a moving target, by
comparing the eye velocity with that of target velocity.)
In congenital nystagmus, pursuit eye momvements are impaired,revesed pursuit, a
sign is strongly suggestive of congenital nystagmus.
(optokinetic nystagmus is the name given to the rhythmical series of slow then rapid
eye movements, the function of this response is to stabilize the eyes relative to space
during slow head movement.)
Reversal of optokinetic nystagmus is a characteristic feature of a significant
proportion of cases of congenital nystagmus.
The pathophysiology of congenital nystagmus is uncertain.
Hypothesis suggests that the congenital nystagmus may be the result of an abnormal
decussation of temporal retinal fibres.
B. Induced
1. Caloric tests
a. Positional test (Dix-Hallpike maneuver) , it is useful in Dx of positional vertigo &
in differentiating between BPPV & uncommon positional vertigo of central origin
b. Fistula test , nystagmus induced by altering pressure in the EAC , produce both
nystagmus & sensation of dizziness .

Lecture notes in
Tullio phenomena is a variant of this cause of nystagmus & it is induced by

acoustic stimuli of high intensity .
2. Caloric investigations
a. Optokinetic drum b. Pendular tracking . c. Caloric test . d. Rotational test .
Comparisons tables
Peripheral Central
Severity More severe Less severe
Onset Sudden Non-paroxysmal
Nausea & vomiting Common Uncommon
Nystagmus Always present Present or not
Tinnitus & HL After Vary "rare"
Visual fixation Inhibit Not affect
Peripheral Central
Direction Usually horizontal & may have Any direction (pure vertical : central)
rotatory component
Symmetry Always symmetrical Dissociation between the yes possible
between the eyes
Lesion side Fast components away from No relation between the direction &
injured labyrinth the lesion site .
Duration Minutes to weeks Days to years
Visual fixation Inhibit Not affect
BPPV CNS
Latency period Few seconds (5-10) Nil
Fast component Under most ear Variable
Distress Present (may be severe) Nil
Direction of nystagmus Usually rotatory (anticlock Variable
wise) , if horizontal , towards
the undermost ear .
Duration of nystagmus Less than 30 seconds Persist while the position
maintained
On sitting up again Similar events with Nystagmus stops
nystagmus in opposite
direction
Fatigability Nystagmus & dizziness stop Nystagmus persist with
with repeated testing repeated testing .

Lecture notes in
VESTIBULAR DISORDERS in paediatric

Embryology
Vestibular apparatus starts its formation on the 1st month of development (intrauterine life)
& at 49 days complete morphogenesis occur .
Between 12 -24 weeks of gestation connection of the labyrinth to the occulomotor nuclei in
the brainstem .
At 16 weeks the vestibular nuclei complete myelination , at 8-9 months, the vestibular
system become active , so that it is the 1 st sensory system developed .
Anatomy
Labyrinth consist of 3 semicircular channels , utricle & saccule , the peripheral vestibular
nerve ending in the ;
1. Hair cells of the maculae of the utricle & saccule .
2. Cristae of the ampulae of the SCC .
Rotational head movement "angular acceleration" sensed by the SCC , while the linear
acceleration "gravitational movement" sensed by the maculae of the utricle & saccule
(otoliths)
Development & maturation of vestibular nuclei
At birth the labyrinth morphologically is complete , but functionally immature .
Development of the vestibular function divided into 2 types ;
1. General motor development ( posture) .
2. Specific development of stable vision in the presence of head movement .
History
- History placed upon an observation parents for description of the attacks .
- History taking ;
a. History taking can't overemphasized as physical examination because reveal no
abnormality .
b. Attacks of vertigo may start before 2 years age .
c. Child suddenly crying out & dropping to the floor & crawling or clinging to parent leg
for support until the acute attack finished .
d. Rapid resumption to play or ataxia may be observed .
e. Pallor , sweating or vomiting occur with severe attacks .
f. Vertigo suspected when child lies face down wedged against the side of the cot with
eye closed , nor wanting to be moved .
- Full description of the attack including ;
a. Age & speed of onset .
b. Frequency .
c. Periodicity .
d. Duration .
e. Speed & manner of recovery .
f. Associated loss of consciousness , amnesia , lassitude , sleep or drowsiness , wetting
..etc .
g. Precipitating or aggravating factors .
h. Complications .
- Exploration of specific areas ;
a. Ear symptoms
- Are the attacks associated with hearing loss or tinnitus .

Lecture notes in
- Has been recent episodes of ASOM or an exacerbation of serous OM or glue ear .

- Is there any history of recent ; otorrhea , exertion barotrauma , head injury involving
the ear resulting in clear or bloody discharge from it .
- Has the child have recent measles or mumps with otological involvement .
b. Eye symptoms
- Photophobia .
- Ocular palsies .
- Nystagmus .
- Visual aura .
c. CNS symptoms
- Motor or speech problems or hemiparesis or parasthesia .
- Child development is normal or there is a delay .
- Learning abilities in the school .
- Orientation in dark room .
- Recent head injury .
d. Infection
- History of meningitis .
- Reluctance to mobilized following the acute attack , suggesting viral labyrinthitis
which usually occur in relation to acute phase .
e. Past history
- Renal or endocrine disease .
- Physical deformity .
- Serious medical illness .
- Psychological disturbances .
- Is the child taking certain drugs (phenytoin for epilepsy , imitryptaline for enuresis ,
peprazin for intestinal worms , aminoglycoside taken by the mother during
pregnancy) .
f. Family history of
- Migraine .
- Epilepsy .
- Deafness .
- Endocrine or renal disease .
- Infection cross the placenta , such as syphilis .
g. Developmental history ; motor milestones , social & speech development , school
performance ….etc .
Physical examination
- This should include through out otolaryngological examination , neurological
examination & developmental examination .
- Neurological examination include ;
a. Hand – eye coordination test .
b. Cranial nerves .
c. Tendon reflexes .
d. Tone .
e. Developmental abnormality & congenital defects & syndromes & abnormal
movements .
- Vision & eye movement ; acuity , ophthalmoscopy …etc .

Lecture notes in
- Postural control ;
a. Rightening rflexes .
b. Postural nystagmus .
c. Hell –toe walking .
d. Romberg's test .
e. Kicking a ball .
f. Gait .
g. Stance .
- General examination ; congenital defects , pigmentation , musculoskeletal defects , heart
sounds , …etc .
- Developmental examination .
Investigations
- Auditory tests ; PTA , speech discrimination , tympanometry …etc .
- Electrophysical tests ;
a. EEG , should done in all children presented with persistent & progressive
dysequilibrium .
b. Evoked response audiometry .
- Blood tests ;
a. Serology ;
- For screening for congenital syphilis , in child with progressive cochlear or
vestibular dysfunction , 1st – 2nd decade of life .
- Viral screening , if congenital deafness present .
- CBP & ESR routinely .
- Autoimmune profile , if fluctuating HL is present .
b. Blood biochemistry ; RBS , Creatinine , electrolytes , thyroid function , …etc .
- Radiological ;
a. Skull x-ray , sinus x-ray, mastoid x-ray , as indicated .
b. CT scan & MRI , to exclude any intracranial pathology & its localization .
- Urine analysis ; for protein , sugar , RBCs , …etc .
- Vestibular tests
Most of the lesions cause vertigo are due to lesion in the inner ear , so that need vestibular
tests such as ENG , this to permit evaluation of the vestibular function without influence
of visual & properioceptive input , also it can give a mathematical calculation of the
frequency , amplitude & velocity of the nystagmus .
Factors affecting the vestibular testing in infants & children ;
1. Eyes closure ; this inhibits nystagmus & it results from Bell's phenomena (vertical
eye ball deviation) .
2. Mental tasking ; e.g. mental arithmetic which release the affect in the horizontal
nystagmus .
3. Maintenance of attention during test procedure , difficult to maintain the child in
constant state of alertness .
4. Anatomical , narrow external canal can cause inequalities in caloric irrigation .
5. Neurological immaturity of eye movement control ; cause :
a. Defective stability of gaze .
b. Saccadic movement are present at birth , but not accurate until later (infant
need more than one saccade to reach the target) .

Lecture notes in
c. Foveal immaturity .
d. Infant optokinetic movement differs from that of adults .
e. Visual stimulation alone cause sensation that is identical to that produced by
rotation .
f. Inexperience with test procedure & difficulties in cooperation .
1. Calibration , gaze & ocular Dysmetria .
2. Persistent testing ; can be performed in infants & children as in adults & the method
of testing depends on the age .
3. Optokinetic tracking (OKN) .
4. Per-rotational tests ; rotational response either sinusoidal harmonics or rapid
acceleration , or per-rotational nystagmus regardless age (CNS origin) .
It represent the vestibular response to the threshold physiological bilateral
labyrinthine stimulation .
It is best done by Torsion swing test (TST) .
5. Caloric test ; unpleasant for infants , so that it done for serious vestibular disorders
such as in ;
a. Abnormal response in TST .
b. Ototoxic drugs exposure .
c. Delayed head & postural control .
d. Congenital deafness .
With age , there will be higher , frequency of nystagmus , amplitude of beat of
nystagmus & speed of the slow component of nystagmus .
This reaching plateau between 18 to 24 months .
Ice caloric test done in infants (5 cofor 10 seconds) , it is +ve (eye deviation towards
the opposite side) in full term infants & 20% of premature infant in the 1st three
months .
Unilateral depressed response due to ipsilateral hypoactive labyrinth , while
bilateral suppression lead to sleep or drowsiness , in middle ear infection there is
exaggeration of the response .
In very premature infants , ice caloric test response cause lateral deviation of the
ipsilateral eye toward the stimulated ear with medial deviation of the contralateral
eye which may present which may called disconjugate movement suggesting
internuclear ophthalmoplegia which is secondary to immature medial longitudinal
fasiculus .
Ice caloric test can be done until 3 years .
Three years age , most children accept bithermal caloric test , according to Jonkees
formula (> 14% labyrinthine preponderance & >18% directional preponderance) .
The presence of directional preponderance is strongly suggestive central - vestibular
pathology , while the presence of labyrinthine preponderance suggest peripheral
organic disorder (hypoactive labyrinth) or 8th nerve lesion , while combination of
both in young patient suggest central lesion with or without peripheral lesion .
6. Other 3 tests , can't done (used) in paediatric , include ;
a. Vestibular spinal stability tests .
b. Dynamic posturography .
c. Harmonic acceleration .

Lecture notes in
Causes of vertigo in childhood

1. Peripheral
a. Congenital vestibular defects
Frequently accompanies SNHL in childhood , while vestibular hypofunction may
contribute to the Down's syndrome .
Vestibular dysfunction suspected in child with vertigo & reveal anatomical
abnormalities in CT scan .
Every child with SNHL should have vestibular investigations .
There is no significant correlation between the auditory brainstem response &
vestibular tests during the 1st year of life .
Delay in motor development suggest variety of disabilities such as ; cerebral palsy ,
mental retardation & minimal brain dysfunction .
Failure in identify correctly the peripheral vestibular lesion will increase the anxiety
of parents & to avoid this , they emphasized all deaf child should undergo vestibular
investigations .
Syndrome associated with vestibular dysfunction :
- Waadenburg's syndrome ; 30% of patients have congenital vestibular failure .
- Hurler's syndrome ; the lesion affects the 8 th nerve .
- Usher syndrome ; congenital severe SNHL with no vestibular response & early
onset of retinitis pigmentosa (TYPE I) , but (TYPE II) no retinitis pigmentosa with
normal vestibular response .
b. Wax
Impacted wax may cause dysequilibrium of unknown cause & its relieved after the
removal of wax .
c. OME
Occurrence of vertigo related to ; Eustachian tube dysfunction or middle ear
effusion (50% of children with OME may have a balance disease) .
Episodes may take forms ;
- Falling all over the place or walking clumsy or walking into things .
- Child may trip easily or fall when walking on flat surface .
Dizziness accompanying glue ear settles following myringotomy & grommet
insertion in cases of OME , if it is not wattle following grommet insertion , we should
suspect another aetiology .
Unsteadiness with OME may be due to ;
- Negative (transient) middle ear pressure with displacement of the round window
membrane which lead to secondary movement of the Perilymph .
- Serous labyrinthitis which is secondary to superadded in the middle ear .
d. Infection
Occurrence of acute suppurative labyrinthitis may be due to ;
- Secondary to ASOM by transmitting bacterial infection from the middle ear to the
labyrinth .
- Invasion of the labyrinth by cholesteatoma , causing fistula (pain may present) .
- Bacterial infection transmitted to the labyrinth from meningitis via the cochlear
aqueduct .
- Viral labyrinthitis .

Lecture notes in
So that , any child with persistent discharging ear or attic disease & vertigo should
do fistula test .
Also early exploration should performed if there is no rapid response to antibiotics .
Meningitis (strepto or pneumococcal meningitis) associated with 20-30% with
purulent OM with deafness occur in 30% .
Infection with congenital syphilis may present with deafness , tinnitus & vertigo .
Viral labyrinthitis , more common than bacterial one , 2 general pattern of viral
labyrinthitis can occur :
- Endolymphatic labyrinthitis l secondary to viraemia in stria vascularis , occur in
mumps , rubella & CMV .
- Perilymphatic labyrinthitis ; secondary to perineural or endneural meningial
spread , occur in Varicella zoster .
Mumps , measles & Varicella zoster may cause sudden HL , diagnosis of viral
labyrinthitis may be missed at the time of original viral disease .
Vertigo may be subsided in a few days without diagnosis of labyrinthine involvement
Viral labyrinthitis histologically characterized by early involvement of cochlea &
vestibule (saccular degeneration with sloughing of the otolithic membrane)
especially the vestibular labyrinth .
In the future CMV may consider to be the most common cause of viral labyrinthitis
due to vaccination against the other viruses .
In children with sustained HL due to viral infection , routine vestibular testing should
be done in children who are deaf as a result of rubella infection (caloric test may be
normal , but impaired rotational test) .
e. Trauma
Head injury can cause peripheral HL with vertigo , either with or without temporal
bone fracture which is of 2 types :
- Longitudinal ; usually bypass the inner ear , but crosses the middle ear causing
CHL due to haemotympanum , ruptured tympanic membrane &/or injury to the
ossicular chain which usually involve incus dislocation or fracture of the stapes
crura .
- Transverse ; involve the inner ear producing SNHL which seen shortly after the
accident which occur due to inner ear haemorrhage , intracranial pressure waves
spread through the open cochlear aqueduct into the inner ear (this not occur in
adults after 4th decade of life because of cochlear aqueduct closure) .
Persistent vertigo of central origin it is uncommon following head injury in children ,
but if it is occur (continuous vertigo) ; then peripheral causes susbected like the
possibility of Perilymph fistula particularly if associated with HL , & BPPV nature of
vertigo present
f. Benign paroxysmal positional vertigo "BPPV"
It is purely peripheral phenomena , while benign paroxysmal vertigo "BPV" central .
Peripheral , may be due to either trauma or neurolabyrinthitis . Characterized by
burst of nystagmus (fast component) .
Vertigo elicited by rapid alteration of head position from up right position to a
hanging position & affected ear is undermost (directed towards the floor) .
Nystagmus , burst , rotatory , fast component toward the floor , continue for 30-
40seconds .

Lecture notes in
Commonly seen after head trauma & settles with time due to ability of the child to
adapt & compensate its more rapid than adult .
The condition due to ; cupulolithiasis & rarely in children surgical Rx of posterior
ampulary nerve which is commonly in adult .
Maneuver of Semont useful in refractory cases of childhood BPPV , but should
performed with caution .
g. Perilymph fistula
Abnormal communication between the fluid surrounding the membranous labyrinth
& the middle ear space , can occur in ; SCC , vestibule & cochlea .
Commonly appear with permanent HL with occasionally in capacity vestibular
symptoms , early recognition & repair is mandatory .
Diagnosis is from
- History , history of meningitis with/without labyrinthitis , sudden fluctuating or
progressive SNHL & symptoms of dysequilibrium .
Certain features in history ; history of head injury with/without skull fracture ,
history of penetrating injuries to the ear , history of slapping injury & history of
barotrauma including exercise , straining , laughing , sneezing , jumping ,
blowing a wind instrument , valsalva or airflight & history of sudden ear popping
- Examination of the middle ear .
- Audiometry with vestibular tests & radiology .
Pathogenesis of Perilymph fistula ; it could be due to both +ve & -ve changes in the
intracranial pressure , this changes transferred from the cranial cavity to the
perilymphatic space via the cochlear aqueduct & this may cause rupture of the round
window membrane causing of fistula .
Cochlear aqueduct originate internally in an orifice on the medial wall of the scala
tympani & terminate on an undersurface of the petrous portion of the temporal bone
in the superior border of the jugular fossa between the jugular bulb & inferior
surface of the IAC .
Cochlear aqueduct in children & fetus open , then in elderly closed by meshwork of
arachnoid connective tissue .
Specific abnormalities related to the development of fistula in children ;
- Anatomical
(1) Abnormal stapes ; straight anterior crus of stapes joining central portion of
footplate rather than anterior edge given anterior fistula .
Straight posterior crus joining the central portion of the footplate giving a
posterior fistula .
(2) Fistula situated centrally between the crura .
(3) Funnel shaped round window .
(4) Angulated round window .
(5) Fistula in geniculate ganglion .
(6) Fistula in Hyrtl's fissure (bony cleft below the round window niche which
extend under the cochlea toward the cranial fossa) .
(7) Radiological finding ; short cochlear coil with dilated SCC & wide vestibule .
(8) Syndromes like ; Klippel-Feil syndrome , Pernard's syndrome ,
Craniocyntosis & Mondini-dysplasia .

Lecture notes in
- Physiological ; barotrauma which is either implosive (alteration of tubotympanic

pressure) or explosive (alteration of the CSF pressure) .
Diagnosis , definitively only by the tympanometry , clinically by tests include ;
(1) Tullio-phenomena ; patient develop vertigo or loss of balance after exposure
to 95 dB tone at 500 Hz for 3 seconds .
(2) Postural audiometry ; minimum hearing gain (10 dB at least in 2 frequencies
in PTA) & it is consider +ve after the patient lain horizontally with affected
ear upper most for 30 minutes .
(3) Fistula test ; +ve strongly indicate fistula , but it is –ve in surgically induced
fistula .
(4) MRI ; not significant in human .
(5) Electrocochleography , changes give a clear cut of diagnosis .
(6) Fibro-optic & rigid endoscope ; to visualize the middle ear .
(7) Combination of ENG & tympanometry , it is the most effective method of
diagnosis .
(8) Vestibulo-ocular reflex & vestibulo-spinal response , the most newly fistula
tests .
h. Ototoxic drugs & irradiation
Exposure to irradiation , most vulnerable time , 12-13 days of gestational age , more
severe associated with malformation of crista ampularis , less severe malformation
occur following exposure on 16 days of gestation .
Ototoxic drugs , like ; kanamycine (primarly affecting hearing) , garamycine ,
amikacine tobramycine (vestibulotoxic) & streptomycine (hearing & vestibulotoxic) .
Risk factors of developing SNHL & vestibular disorders in preschool child :
(1) Hereditary tendency for deafness .
(2) Malformation of ear-face syndrome .
(3) Low birth weight .
(4) Rubella /viral infection in pregnancy .
(5) Neonatal sepsis / meningitis .
(6) Asphyxia .
i. Vestibulo-neuritis
Due to a lesion in the vestibular pathways at some points centered to the labyrinth ,
characterized by ; major attack of vertigo , vomiting & autonomic disturbances &
the caloric testing show bilateral or unilateral canal paresis , while the cochlear
function is normal & caloric return to normal with resolution of the condition .
There is also history of febrile illness , 50% of patient have one attack only & other
50% have subsequent attacks , but they are decreased over 6-12 months .
There is an association between epidemic labyrinthitis , vertigo & neuronitis , they
suppose that it represent a form of polyneuritis .
It is a disease of young adults & also affect children .
j. Menier's disease
Traditionally is a disease of adults , 75% between the age of 30-40 years , but it is
reported in children & adolescent .
Clinical features are ; recent attacks of rotational vertigo accompanied by nausea &
vomiting , progressive SNHL & fluctuating HL of cochlear type , tinnitus ,

Lecture notes in
progressive feeling in the affected ear prior to the attack & nystagmus may be
present during the attack or certain after word depend on the severity of the attack .
Pathogenesis ; it is associated with endolymphatic hydrops & low frequency HL .
Suggestive treatment ; low salt diet , diuretics , labyrinthine sedative , vasodilators ,
anticholenergic & antihistamine , in failure of medical Rx , then surgical intervention
by mastoidectomy & endolymphatic sac drainage .
2. Central
a. Congenital skull anomalies
Vertigo may result from pressure on or stretching of cerebellum , brainstem &/or
lower cranial nerves , by structural anomalies of upper cervical vertebrae & foramen
magnum including ;
- Platybasia ; narrowing of the foramen magnum with upward displacement of
posterior cranial fossa , associated with other CNS abnormalities such as Chiari
malformation .
- Chiari malformation ; herniation of the cerebellum through the foramen magnum
. characterized by cerebellar elongation & protrusion through the foramen
magnum into the spinal cord , it is of 3 types ;
(1) Type I ; cerebellar herniation exist alone or with malformation of base of the
skull such as platybasia , basilar impression , Klippel Feil syndrome ,
asymptomatic in childhood , apparent in adolescent with hydrocephalus ,
signs of cervical cord decompression , suboccipital headache , vertigo ,
laryngeal paralysis , progressive cerebellar signs & nystagmus (down beating
vertical , thus are not diagnostic) .
(2) Type II ; common than type I , consist of type I malformation & non-
communicating hydrocephalus & lumbosacral spina bifida .
(3) Type III ; may have features of type I & II with occipital cranium bifida or
cervical spina bifida .
- Klippel – Feil syndrome ; characterized by reduction & fusion of numbers of
cervical vertebrae causing variable neurological syphilis & associated with
congenital deafness .
b. Migraine related disorders
Migraine is uncommon in children , 3-6% , but it is common in adulthood & it is of 2
types ; common (without aura) & classical (with aura) .
Classical migraine is a vascular disease associated with disturbed cerebellar blood
flow , intracranial vasospasm lead to neurological symptoms (aura) followed by
extracranial vasodilatation (headache) , this disruption of unknown cause .
Certain clinical symptoms produce the development of classical migraine in children
; motion sickness , cyclic vomiting , recurrent abdominal pain , limb or growing pain
, dizziness , sleep troubles & hyperactivity , this called risk factors of vertigo .
c. Paroxysmal torticollis of infancy
Uncommon , the onset is in early infancy & present frequently on waking & last for
minutes-days , it appear when the head tilted to one side & associated with nausea &
vomiting , F>M m aetiology , unknown , but the site of dysfunction either in the
brainstem or cerebellum .
d. Benign paroxysmal vertigo

Lecture notes in
Central , Sudden brief attack of dizziness occur when standing or lying & it is
unrelated to position .
Underestimated in its frequency due to difficult evaluation & classification of
dizziness in children .
Attacks occur in 4-6 weeks cycles , it is benign settle wth months or few years.
Usually seen in the 1 st four years of life up to the age of 10 years . Investigation
invariably normal , include ; neuro-otological tests , audiometry , ENG ,
haematology & serology .
Caloric test , abnormal information of moderately sever or complete canal paresis in
those children with vestibular disease either unilateral or bilateral paresis .
Recent reports demonstrate normal caloric test in percentage of patients , so that
variable responses indicates difficulty in obtaining standardized results from
children with developed vestibular disorders .
There may be progression from paroxysmal torticollis of infancy to BPV in childhood
Close observation needed for Dx , food allergies should be considered in all cases ,
migraneous pathophysiology are the most likely cause (vascular disturbances of the
posterior circulation & ischemia of the labyrinth & vestibular nuclei) .
e. Basilar artery migraine
Syndrome of sudden episodes of visual manifestation , vertigo , gait ataxia ,
dysarthria , tinnitus with various combination of headache , usually occipital &
follow disappearance of other symptoms & in many patient , more typical vascular
headache between the episodes .
Frequently affect females (adolescent) , diagnosed with some difficulty because it
relies on history which is neglected from child , so that objective manifestation such
as (head hanging , cyclic vomiting , recurrent abdominal pain …etc) this provide
necessary clue to a migraneous pathophysiology .
In infant , attacks started with progressive lethargy , anorexia & photophobia ,
followed by period of disturbed sleep & infant choose to stabilize himself maintains
against the side of the cot (picking up the child lead to vomiting) .
Headache , demonstrated by seeing the child pull his hair in desperation .
Investigation ; vestibular test on bithermal caloric , audiological (normal) .
Pathophysiology ; ischemia in the territory of the posterior temporal branch of the
posterior cerebral artery & then give visual symptoms & vertigo , also ischemia of
the internal auditory artery causing hearing involvement & if no visual or hearing
involvement this means brainstem involvement .
f. Infection
Mode of spread ;
(1) From meningies (meningitis) to labyrinth through the cochlear aqueduct .
Meningitis either bacterial (H. influenza , pneumococcal ) gives central
symptoms as ataxia , or viral , usually associated with perilabyrinthitis lead to
vertigo .
(2) Ascending infection through the IAC .
(3) In the blood to the acoustic-vestibular organs .

Lecture notes in
g. Trauma
Post-traumatic vertigo & dizziness , rare in children because of difference between
children & adult tissue such as bone flexibility & plasticity of vestibular system &
ready ability to compensate .
h. Neoplasia
Benign CPA tumors give asymmetrical progressive SNHL or imbalance .
Posterior cranial fossa tumors give progressive persistent vertigo , ataxia with
associated audiological symptoms (MRI strongly indicated) .
i. Demyelination
Multiple sclerosis , rarely in children , but it occur post- or pre-puberty .
j. Seizer disease
It give rise to vertigo in 3 ways ;
- Aura of grandmal fit , common & easily diagnosed .
- Two specific vestibulogenic & vertiginous .
Vestibulogenic epilepsy ; rare , precipitated by stimulation of the labyrinth
producing activation of the hyper excitable neurons of brainstem & reticular system
lead to convulsion (this can be seen during caloric test) .
Vertiginous epilepsy (temporal lobe epilepsy) ; common , dizziness is the aura
precedes the occurrence by few years , characterized by vertigo , headache , nausea
& vomiting & may progress to loss of consciousness with or without seizers .
k. Hereditary cerebellar ataxia
Hereditary degenerative disorder of the cerebellum , uncommon , presented with
slowly progressive ataxia .
Most frequent ;
(1) Ataxia telangectasia .
(2) Friedrich's ataxia .
(3) Refusm's disease , cerebellar ataxia , deafness , retinitis pigmentosa &
polyneuritis , night blindness lead to progressive difficult walking .
l. Hereditary disease of peripheral & cranial nerves
Charcot – Marie - Tooth disease , usually presented with peroneal muscular atrophy
, sometimes with SNHL .
Neurofibromatosis , affect both peripheral & cranial nerves , optic nerve is the
commonest & earliest nerve affected & less commonly affected the acoustic nerve .
Also there is epilepsy with Café de au liat spot with/without subcutaneous
Neurofibroma means intracranial tumor .
Congenital nystagmus , fine rapid pendular nystagmus .
3. Other
a. Metabolic
DM , hyperinsulinism , adrenal insufficiency , hyperthyroidism , anaemia ,
hyperlipidosis & hyperprotienaemia type II , Pendred's syndrome (hypothyroidism &
congenital deafness) ..etc , if there is episodes of vertigo , tinnitus & vomiting suggest
Menier's disease .
b. Psychosomatic dizziness & hyperventilation
Two risk groups :
- These under excessive social pressure .
- Adolescent female .

Lecture notes in
c. Vestibular disease associated with abnormal development , behavior & learning

abilities
Down's syndrome & cerebral palsy , abnormal nystagmus in girls with scoliosis ,
abnormal post rotatory nystagmus , & schizophrenia .
d. Motion sickness
It is a form of physiological vertigo , occur when the brain receive conflicting
information about the body motion from visual & vestibular receptors &
properioceptors
Female > male , 2-12 years , more frequent with classical migraine , rare before 2
years because any travel supine & with limited visual input .
It is more in female because of less degree of vestibular stimulation or adaptation .
Differential diagnosis of vertigo in children
A. Subtle seizers & various forms of syncope
Epilepsy ; differentiated by EEG & clinical evaluation .
B. Breath – holding spells & seizers
Peak incidence 2-3 years .
1 st type ; sudden fear , trauma may precipitate the attack , attacks last for 2-20 seconds
initiated by valsalva maneuver & consist of crying , exhalation , cyanosis , limpness ,
regain conscious gradually , transiently confused child .
2 nd type ; less common , painful stimuli precipitate sudden limpness , pallor , loss of
consciousness & apneoa & the child quickly regain consciousness .
Diagnosis by ; the ocular compression test which induce cardiac asystole which last
for > 2 seconds , +ve fetal heart , & EEG shows normal pattern between the attacks .
C. Recurrent syncope
Seen in infants & adolescent , usually it is a reaction to emotional stress ,
hypoglycemia & environmental factors & possibility of cardiac syncope .
Sudro-Cardiac syndrome ; congenital deafness , prolonged QT interval , fainting &
sudden death (attack begins in infancy) .
D. Infantile spasm
Occur in mentally handicapped child associated with abnormal EEG which is
diagnostic .
E. Myoclonic astatic epilepsy of early childhood
Similar to infantile spasm , but occur in children > 2 years .
F. Night terrors
May be confused with positional vertigo or basilar artery migraine occurring at night .
Night terrors occur in the 1st three hours of deep non-REM sleep , the child suddenly
sits upright screaming with terror & remain un-ware of surroundings for 10-20
minutes before drop to deep sleep .
Management of vertigo
A. Medical
- Motion sickness , because it result from mismatching of inputs from sensory system
& dynamics & posture orientation , so that ;
oPositioning of the child in clear view to the surroundings .
oVestibular sedatives ; dimenhydrinate , transdermal hyoscine ..etc .
- Benign paroxysmal vertigo by ; reassurance & dimenhydrinate .

Lecture notes in
- Migraine ; avoid precipitating factors (diet ; cheese , orange & tomato) ,

antihistamine & B-blockers .
- Seizers disorders by antiepileptic .
- Meneir's disease ; difficult to Rx in children , use low salt diet , antihistamine ,
betahistadine & diuretics .
B. Surgical
Indications are ;
1. Persistent Glue ear in which the grommet correct the fluctuation in middle ear
pressure .
2. Labyrinthine fistula with fluctuating & deteriorating SNHL .
3. Post-traumatic labyrinthine dysfunction with non-hearing ear & recurrent
vertigo
4. Operable CPA , brainstem , posterior fossa tumors or lesions .
5. Explorating mastoid &/or middle ear surgery in a child which a suspected
which labyrinthine lateral SCC fistula secondary to cholesteatoma or
meningitis or labyrinthitis & meningitis .
6. Endolymphatic sac surgery , in Menier's disease .
C. Psychological support
Include reassurance of both parents & child especially adolescent females .

Lecture notes in
TUMORS of the ear

Route of spread
1. Medial
a. Promontory of the middle ear with facial nerve exposure .
b. Petrous apex & petrous pyramid .
c. Oval & round windows .
d. Below & behind the labyrinth .
2. Superior ; tumor may spread through the tegmen tympani .
3. Inferior ; to the base of the skull particularly to the jugular foramen & this explain the
paralysis of the 9th , 10th & 11th cranial nerves .
4. Anteriorly ; the medial bony wall of the Eustachian tube & associated bony wall of the
middle ear cavity which are separated from carotid canal by thin layer of bone , this is a
frequent route of spread of tumor to the carotid canal .
5. Posteriorly ;
a. Into the mastoid air cells .
b. Via the thin bony wall of the posterior wall into the internal auditory meatus .
6. Local invasion ; remnants of the ossicles , stapedius muscle & facial canal .
7. Lymphatics ;
a. From the external auditory meatus & auricle ;
- Anteriorly ; to the parotid gland especially to the gland infront of the tragus .
- Inferiorly ; LN along the external jugular vein under the sternomastoid muscle .
- Posteriorly ; to the mastoid LN .
b. Of the middle ear & mastoid
- Lymphatics less well defined anatomically .
- Lymphatics arranged like blood vessels in 2 sets on lateral & medial surface of
the tympanic membrane .
- Lymphatics from the tympanic cavity drain to the retropharyngeal LN & parotid
LN .
Pathology
A. Benign Tumors
1. Epithelial tumors ; like primary cholesteatoma , choristeoma , adenoma ..etc .
2. Mesenchymal tumors
a. Paragangilioma ; glomus tumors …etc .
b. Schwannomas ; of facial nerve , of jugular foramen ….etc .
c. Other like ; Osteoma , Xanthomas , Gaint cells tumors , Benign osteoblastomas
& Haemengioma
3. Other tumors
a. Chordoma ; rare tumor derived from notochord remnants in relation to the axial
skeleton , 40% in clivus & petrous .
They are locally malignant , but can metastasize following surgery .
They produce symptoms of pressure on the inner ear or cranial nerves with pain ,
CT scan shows irregular bony erosion with central areas of calcification .
b. Meningioma ; the commonest benign intracranial tumor arise from the
arachnoid’s villi , meningioma of the petroclival region & CPA constitutes 5-10%
of all meningiomas .
Treated by surgery & postoperative radiotherapy .

Lecture notes in
c. Direct extension from ; nasopharynx , external ear , parotid & intracranial

meningiomas .
d. Granulomas of temporal bone ;
- Wegner’s granulomatosis ; sometimes seen in the middle ear with granulation
tissue .
- Histiocytosis X ; 3 types of unknown aetiology .
Eosinophilic granuloma ; young adult with male predominance , it is more
common in middle ear & EAM leading to secondary infection , on x-ray they
appear as osteolytic lesion , treated by local resection with postoperative
radiation (low dose) .
Hand-Schuller-Christian disease ; seen in children with recurrent URTI ,
hepatosplenomegally , DM & lymphadenopathy . Treated by chemotherapy .
Letter-Siwe disease ; affect children under 3 years , with diffuse
granulomatous deposit , death from inercurrent infection & bleeding .
B. Malignant tumors
- Primary ;
1. Epithelial ; seq. cells Ca. , Adenocarcinoma , Melanoma , BCC , Sebaceous cell Ca.
2. Mesynchymal ;
a. Sarcoma , Haemangio-endothelioma , malignant xanthoma .
b. Rhabdomyosarcoma ; rare , common in children , there is granulation tissue with
rapid growth & extensive destruction , the main modality of treatment is
radiotherapy & chemotherapy , also surgery for debulking is possible .
c. Chondrosarcoma ; derived from cartilaginous rests in foramen lacerum , it is
rarer than those in the nasal cavity .
- Distant metastasis from Kidney , lung , prostate , thyroid & breast .
Epithelial tumors of the external & middle ear
Pathogenesis
There is possible link between CSOM with SCC of the middle & external ear in 38% .
SCC of the EAM may arise separately or independently from epithelial tumor of the middle
ear cleft , it caused by ;
1. Chronic infection ; chronic otitis externa (SCC of external ear) & CSOM (SCC of the
middle ear) .
2. Radiotherapy .
3. Speculative un-investigated caused such as production of crcinogens within cermun
4. Azoxy-methane induce SCC of sebaceous gland of the EAM in 15% .
5. Carcinogens , aflatoxins B produced by Asperigillus flavus .
Epidemiology
 1:1000000 / year in female
 0.8/1000000/year in male . So M:F 1:1.2
 Increased with age in male & decreased with increased age in female .
 Mortality decreased with age in male & increased with age in female .
 More common in adult male
Pathology :
Majority is SCC or BCC , uncommonly adenoma . Usually appears as a warty lesion in the
auricle or ulcer lesion , biopsy required to differentiate it from benign tumor such as
epithelioma , adenoma cysticum , molluscum contiagiosum & navous .
Lecture notes in
BCC don’t metastasis , but SCC spread to involve pre-a7 post-auricular LN .

External ear ;
1. Hidradenoma (Hidradenocarcinoma , Cerminoma)
Wax is secreted by 2 glands ; cerminous glands (apocrine sweat glands which
responsible for the odour of cerumon)& the eccrine pilosebaceous glands (which
secrete the wax) . Hidradenoma are more often malignant tumor , so it is divided into
a. Benign tumors ; adenoma similar to benign tumor of salivary gland .
b. Malignant tumor ; adenoid cystic carcinoma , mucoepidermoid ,
adenocarcinoma (Their secretion are watery fluid devoid of lipids & don’t
secrete wax of the meatus which produced by sebaceous gland ) .
2. Basal cell carcinoma (BCC) , sebaceous tumor , malignant melanoma
Rare , BCC usually arise in the pinna & then invade the EAM , once bony invasion
occur , it will behave like SCC , it rarely metastasize .
Middle ear : Majority SCC , sometimes adenoma , adenocarcinoma , BCC .
Behavior of SCC of the middle ear & EAM
1. Carcinoma of the middle & external ear
Difficult to determine the site of origin because one may involve the other at the 1 st visit .
So determination depend on history & extent of the involvement of the area . If
carcinoma of the meatus arise adjacent to the tympanic membrane , it can easily &
quickly spread beneath the fibrous annulus of the tympanic membrane & invade the
middle ear & destroy the tympanic membrane .
The same situation seen in carcinoma of the middle ear cleft , majority of cases of SCC
are associated with CSOM & perforation which would accelerate the spread of the
tumor from the middle ear to the EAM or vice versa .
2. Seq. Cell carcinoma of the EAM
Constitute 90% of all malignant tumors , originate at any portion especially the bony
portion Slow growing & later on it may extend toward the junction of the cartilaginous
& bony meatus or outward to the concha or extend anteriorly to the parotid gland , TM
joint & posteriorly to the retroauricular sulcus .It may weakens the tympanic membrane
& may invade middle ear with facial nerve paralysis. 20% may present with cervical LN
3. Carcinoma of the middle ear & mastoid
It may extend superiorly to the tegmen tympani & middle cranial fossa dura or
posteriorly to the mastoid antrum & mastoid process & posterior cranial fossa dura &
sigmoid sinus . It may extend inferiorly to the jugular bulb & the last 4 cranial nerves , it
may extend anteriorly to the Eustachian tube & peritubal cells & bony septum between
the Eustachian tube & carotid canal & then to the ITF . Destruction of the facial nerve
& fallopian canal is common especially the horizontal segment .
4. Cervical LN
In carcinoma of the EAM is not uncommon , in carcinoma of the middle ear is rarely
metastasize to the pre- & postauricular LN , then to the LN in the posterior triangle at
the anterior border of the trapezius muscle .
Clinical features
- Symptoms
1. Deep seated boring pain , due to invasion of both the bone & the dura .
2. Discharge especially in patients with history of CSOM & this may be blood stained
(highly suspicious of Ca.) , also history of chronic otitis externa in tumors of EAC

Lecture notes in
3. Hearing loss , is deteriorating CHL if the middle ear or external ear is involved ,
while SNHL is due to invasion of the inner .
4. Vertigo & unsteadiness due to vestibular involvement (rare) .
5. When the tumor infiltrate to reach the dura this followed by rapid deterioration &
then death .
- Signs
a. Identify the extension of tumor .
b. Facial palsy , commonly in the middle ear carcinoma but also seen in carcinoma of
EAM through the parotid gland .
c. Trismus due to involvement of the pterygoid muscle & ITF .
d. Fullness of the parotid region & ITF .
e. Perichondritis of the auricle .
f. Regional LN in 20% , especially pre-& post-auricular group .
g. Lower cranial nerves paresis ; indicate extension of the tumor to the skull base .
Investigation
A. Biposy
1. Tumors of the pinna by incisional biopsy under LA .
2. Tumors of the ear canal & middle ear by punch biopsy under LA or GA .
B. Radiology
1. Plain x-ray of the mastoid bone .
2. CT scan ;
Sign of chronic mastoiditis .
Erosion of the labyrinth which is a late sign , because the labyrinth is avascular
bone & resist invasion .
Bony destruction of the EAM .
Loss of the outer attic wall .
Destruction of the tegmen tympani .
Erosion of the mastoid ear cells .
Erosion of the carotid canal (the greater radiological feature) .
3. MRI
 Ascertain whether the dura is thickened or penetrated .
 Ascertain the respectability of the tumor .
 Delineate small nonpalpable LN (1cm or >) .
 Spread in the prevertebral region .
4. Angiography in major blood vessels involvement .
5. Retrograde jugular veinography , useful to demonstrate the extension of the disease .
Staging (UICC & AJCC)
T1 : tumor limited to the site of origin without facial palsy or bone destruction .
T2 : tumor extend beyond the site of origin indicated by facial palsy or bone destruction ,
but the tumor not extend beyond the organ of origin .
T3 : tumor extending to the surrounding structures like dura , skull base , parotid gland TM
joint .
Tx : patient with insufficient data for classification including patient previously treated
elsewhere .
Treatment
Combination of surgery & radiotherapy for the best results , because :
Lecture notes in
- Reaction are lessened & the patient feel more comfortable .

- High dose can be given with less complications .
- Five years survival is about 35% in EAM Ca. , results are about 10% better than these
from tumor of the middle ear & mastoid .
1. Surgery aims to ;
Allow the surgeon to confirm the findings on radiology .
Exenterate all or most of the disease .
Provide a useful information to the radiotherapist .
Remove large block of sclerotic bone which facilitate the access for radiotherapist .
Bad prognostic signs seen are ;
a. Invasion of the brain , dural involvement per se not a contraindication .
b. Facial palsy .
c. Involvement of the ITF , can’t be controlled by surgery (inoperable) .
The extension of the tumor outward along the EAM into the pinna , retroauricular
sulcus & parotid gland which not prevent satisfactory results .
Surgery of the tumor ;
- Disease confined to the EAM , middle ear & mastoid treated by radical
mastoidectomy .
- Small tumor confined to the EAM treated by core excision with drilling &
removal of the underlying bone with skin graft .
- Escape of the disease to a limited scale , large operation of subtotal
petrosectomy , by drill & microscope .
- Facial nerve involvement , ablation of the facial nerve with hypoglossal –
facial nerve anastamosis .
- Middle ear & EAM Ca. extending to the pinna & parotid gland , treated by
pinnaectomy & parotidectomy & excision of the preaural & postaural skin .
Surgery of the cervical LN : Radical neck dissection for overt metastasis .
Complication of surgery ;
1. CSF leak & meningitis .
2. Damage to the last 4 cranial nerves ; hoarseness , dysphagia & aspiration .
3. Bleeding from nearby major blood vessels .
4. Dead ear with imbalance for several months due to petrosectomy .
2. Radiotherapy
It is usually used postoperatively , its dose :
- Ca. of the pinna ; 10 Mev electrons , 45 Gy in 10 fractions over 2 weeks to 55 Gy in
20 fractions over 4 weeks .
- Ca. of EAM & middle ear & mastoid ; 66 Gy in 20-33 daily fractions over 4-6
weeks .
Its complications are ;
a. The EAM become dry & stenotic .
b. Conductive deafness .
c. Wax become hard .
d. Radiation to the labyrinth cause decreased hearing & imbalance .
e. Damage to the brainstem & eyes especially in elderly .
f. Osteonecrosis cause pain , discharge & sequestration of bone for long period .

Lecture notes in
VESTIBULAR SCHWANNOMA
Anatomy
The cerebellopontine angle "CPA" is a triangular area bounded by the followings
- Laterally by the medial portion of the posterior surface of the temporal bone .
- Medially by the pones .
- Posteriorly by the cerebellar hemisphere & floccules .
- Superiorly by the trigeminal nerve as it crosses the petrous apex .
- Inferior limit by lower cranial nerves (IX , X , XI & XII) .
Its contents are ; anterior inferior cerebellar artery , 7th & 8th cranial nerves .
The internal auditory meatus "IAM" , its length about 1 cm , width 2-8 mm (4.5 mm
average) . pass from the posterior portion of the temporal bone to the vestibule .
- Medially , it has porus or inlet .
- Laterally , fundus separated from the vestibule by thin plate of bone , the fundus
separated by transverse crest (falciform crest) , into superior & inferior halves & the
superior halve in turn divided into anterior & posterior halves by Bill's bar .
The inferior vestibular nerve supply the saccule & the superior vestibular nerve supply the
utricle , superior & lateral SCC , while the singular nerve supply the posterior SCC .
The anterior inferior cerebellar artery is a branch of the basilar artery , the main branches
are internal auditory & subarccuate artery .
Pathology
- Site of origin ; from Schwann cells which envelops the distal portion of the 8th nerve in the
internal auditory canal , mainly superior vestibular nerve , then the inferior vestibular
nerve & rarely the cochlear nerve (Glial neurolemmal junction , zone of Glial instability)
- Aetiology
1. Defects in chromosome 22 .
2. Neurofibroma type II .
3. Irradiation for enlarged adenoids & tonsils (Freedman 1983) .
- Pattern of growth ;
Increased pressure rather than invasion , the growth from medial part of the internal
auditory canal lead to double layer of arachnoid .
increased growth lead to increased CSF production forming arachnoid cyst , invasion of
porus may occur , contact to the fifth nerve , when the tumor reach 2 cm intracranial
diameter lead to diminished corneal reflex .
- Obstructing hydrocephalus ; obstruction of the aqueduct with dilatation of the 3rd &
lateral ventricle , but compression of the 4th ventricle .
- Communicating Hydrocephalus , as a result of high protein level in the CSF , lead to
dilatation of the 4 th ventricle .
- Tumor growth factors ; slowly (2 cm/year) , the young has higher rate of growth .
- Age & sex ; F>M , 50-60 year old , in neurofibromatosis 20-30 years .
- Effect on the inner ear ; degenerative changes with biochemical changes , due to the
pressure interfering with blood supply , increasing protein in Perilymph lead to
degeneration changes .
- Gross appearance ; firm , well encapsulated tissue with nodular surface , well defined line
of separation between the arachnoid & tissue , sometimes adhesions .
- Histological appearance ; Antoni type A & B .
Type A : fasciculate type whorls of parallel cells with dark nuclei .
Lecture notes in
Type B : more common , reticular in pattern , losser reticular arrangement with areas of
degeneration may be seen with foamy appearance due to lipid containing cells , the
malignant changes are rare .
- Otological stage "stage I"
1. Unilateral HL with tinnitus , gradual & slowly progressive .
2. Poor speech discrimination , especially in telephone , sudden HL because of
bleeding (vascular) with sensitive cochlea (barotrauma) .
3. The tinnitus is non pulsatile with or precede the HL .
4. Imbalance , CNS compensation because tissue (Schwannoma) is slowly growing ,
total loss of caloric response on the affected side without experiencing any
disequilibrium , s.t. slight imbalance on change of head or body position .
5. Facial nerve involvement ; uncommon , because motor fibers more resistant to
pressure & severe facial weakness means facial nerve Schwannoma .
Positive Histiberg's sign in 25% means facial nerve involvement .
Altered lacrimation in 85% due to involvement of nervus intermedius .
Defective nasolacrimal reflex , the most superficial clinical evidence of CPA
pathology .
- Trigeminal nerve involvement "stage II"
Sensory changes occur when the tumor size reach 2-2.5 cm , lead to irritation of the eye
, pain-tingling or numbness in any or all the three divisions & altered thermal sensation
on face or tongue edges .
- Brainstem & cerebellar involvement (compression) "stage III"
1. Ataxia – Dysmetria –Dysdiadochokinesis –Dysnergia .
2. Intension tremor , decreased with tension unlike Parkinson's which increased with
tension .
3. Involvement of the lower cranial nerves .
4. Lean of the patient on the side of the tumor .
5. Nystagmus , vertical , horizontal or rotatory .
- Increase intracranial pressure "stage IV"
1. Increasing headache , mainly suboccipital & upper neck associated with nausea &
vomiting , the patient when flex the head decrease the pressure .
2. Titubation , rhythmic side to side or nodding movement of the head due to extreme
distortion of the brainstem .
3. Dementia from hydrocephalus .
4. Failure of vision due to papilloedema .
- Terminal stage "stage V" , coma & multiple organ failure .
Examination
- General ; Café de au Lait spot (Neurofibromatosis) .
- Ear ; normal tympanic membrane , look for cholesteatoma , on tuning fork unilateral
SNHL , s.t. CSOM coexist with Schwannoma makes the surgery difficult due sclerotic
mastoid .
- Cranial nerves
a. Trigeminal ; pricking & touching test , corneal reflex .
b. Facial nerve ; delayed blinking in one side (tapping on forehead by finger) , +ve
Histilberger's sign (unreliable) , parasthesia in postero-superior part of the EAC ,

Lecture notes in
lacrimation from involvement of nervus intermidus by Shimmer's test & test over the
2/3 rd of the tongue .
c. Nasolacrimal reflex (the most important) .
d. Tongue ; electrogustography .
e. Palatal examination .
- Eyes ;
a. Ophthalmoscopy , for papilloedema .
b. Lens opacities & retina hamartomas (Neurofibromatosis II) .
c. Nystagmus , to the contralateral side : fine , ipsilateral side : course with high
amplitude , also do electronystagmography .
d. Brun's nystagmus .
- Cerebellar function test ; coordination , gait , posture , finger nose test , dysmetria ,
dysdiadochokinesia , Romberg's test , Unterburger's test (deviation toward the side of the
lesion , more sensitive) .
Investigation
- Audiological – Vestibular
a. PTA ; descending curve or flat .
b. Speech discrimination test ; recruitment (ABLB) & tone decay (unreliable & has no
place here) .
c. Speech audiometry ; needed in hearing preservation surgery .
d. Stapedial reflex , reliable .
e. Electric response audiometry (ERA) , the most reliable test for vestibular
Schwannoma , consist of 2 techniques ;
Electrocochleography , for endolymphatic hydrops .
Brainstem ERA , records the elective events which occur in the 8th nerve &
brainstem following acoustic stimulation referred as ABR (Auditory Brainstem
Response) using scalpel electrodes .
Grades (Jewette) "ECOLI" ; JI: E. 8th nerve wave , JII: C. cochlear nucleus wave ,
JIII: O. superior Olivary complex wave , JIV: L. lateral Leminiscus wave , & JV: I.
Inferior colliculus wave .
Abnormalities seen in vestibular Schwannoma ;
- Latency of I-V .
- No recognizable wave form despite adequate hearing level due to loss of synchrony
of the neural firing necessary to produce identifiable wave form .
- Delay in the contralateral ABR , due to distorted brainstem by large tumor , return
to normal when the tumor removed .
Disadvantage of the ABR , lack of specificity , waveform is reliable when hearing
level of 75 dB , in higher threshold reflect the severity regardless the cause .
ABR remains the single most useful audiological test currently available & still has a
key role in Dx especially centers where access to MRI restricted .
f. Caloric test ; canal paresis , 100% in large tumors , while 20% of the patients with <
2cm tumor size the test may be normal , because the test produce a maximum
stimulus on horizontal SCC (supplied by superior vestibular nerve) , small tumor
arising within inferior vestibular nerve produce normal caloric test .
So the Dx of vestibular Schwannoma suggested when there is abnormal caloric test
without history of dizziness .

Lecture notes in
- Radiological
a. Temporal bone radiology (tomography) , poor technique .
b. CT scan , has many disadvantage ; it is can't demonstrate a small tumor & need
contrast , to which the patient may be sensitive & it is ionizing radiation .
c. MRI ; advantage
1. High intrinsic contrast between tissue .
2. An ability to image directly in the coronal , sagital & axial planes .
3. Absence of bone artifact .
4. Brainstem distortion can be seen easily (2-3 mm) .
5. Intracanilicular component of the large tumors are rapidly demonstrated (lesion
< 2 cm can be seen quit clearly) .
MRI can demonstrate the tumor from brain tissue by Gadolinium enhancement .
When there is no MRI , then the protocol ; ABR , CT with contrast & caloric test.
1. Meningioma , erosion of the temporal bone , but uncommon expansion of the internal
auditory meatus , on MRI isodense with brain on T1 .
2. Primary cholesteatoma ; Progressive 7th nerve paralysis & hemifacial spasm , x-ray
shows destruction of the tempral bone & on CT no enhancement withcontrast (avascular
lesion) .
3. Posterior fossa arachnoid cyst ; due to infection , trauma , congenital malformation &
increased ICP , they are thin walled & hypointense (because contain CSF) .
4. Lesions of the cranial nerves IX , X , XI , XII ; with HL & expansion of the Jugular
foramen , in Neurofibromatosis the involvement of the 5th nerve in addition to the 8th
nerve .
5. Others ; lipoma , MD , choroids plexus papilloma , glomus jugulare , Ca. of the middle
or external ear .
CPA syndrome ; is a vascular cause include basilar artery ectasia , aneurysm &
compression of the 8th nerve by vascular loop of the anterior inferior cerebellar artery .
Management
A. Conventional surgery
- Results of surgery improved because ;
1. Depend on skilled base specialist like otoneurologist .
2. Advance diagnostic tools like MRI up to 2-3 mm tumor size .
3. Advances in neuroanasthesia .
4. Intraoperative monitoring of the vital signs , facial nerve .
5. the Introduction of the operating microscope .
- Preoperative mortality about 1% or less , related to the size of the timor , all patients with
intracanalicular tumor should be treated conservatively , also infirm or old aged with
small tumor , then annual MRI monitoring .
- Factors influencing surgery ; age , tumor growth , characteristic hearing levels opposite
ear , the risk of death , the cost of the prolonged follow up .
- Approaches
1. Superior (middle fossa approach) ; has advantage of hearing preservation ,
disadvantages , the facial at risk & temporal lobe epilepsy .
2. Posterior (retrosigmoidal technique) , advantage , hearing preservation &
disadvantage , temporal lobe epilepsy .

Lecture notes in
3. Lateral (translabyrinthine approach) , advantage , early identification of facial nerve

& avoid temporal lobe retraction & the disadvantage is total hearing loss .
4. Transotic approach ; an extension of the translabyrinthine approach in which the
cochlea drilled out & the IAM skeletinized through 360 o, it gives better control over
the whole length of the facial nerve .
- Postoperative care
1. Patient kept in ICU for regular neurological & CVS monitoring .
2. Ventilation should be avoided as it mask the neurological signs .
3. N/G tube not used unless risk of lower cranial nerve damage (rare) .
4. Tracheostomy unnecessary unless 10th nerve damaged .
5. Put a cathter & i.v. fluid (input & output monitoring) .
6. i.v. antibiotics .
7. Steroids , in case of cerebral oedema , but of no benefit for facial nerve function after
tumor excision .
8. Corneal protection , artificial tears & lateral tarsoraphy .
9. CSF fistula , if not healed spontaneously , then repeated LP or lumbar drain or
return the patient to the theatre .
10. In case of large tumor , hydrocephalus , so Rx by daily LP or ventriculo-peritoneal
shunt
11. Tinnitus is rare complication .
12. Vestibular function is rehabilitated .
13. In non recovering facial nerve , in severed facial nerve , do immediate repair , if
not possible XII – VII anastamosis should be carried .
14. Patient go home on 10th day postoperatively .
B. Stereostatic radiosurgery (Gamma knife)
- The delivery of highly focused high dose of ionizing radiation from a Zol-Cobalt 60 source
in one session (20 minutes) to the tunor , the location of which identified stereostatically .
- The dose about 15 -25 Gy in the center & 10-15 Gy in the periphery .
- The aim is not total destruction of the tumor , but the longterm arrest the growth with
hearing preservation & facial nerve preservation .
Neurofibromatosis type 1 & 2
The criteria for diagnosing the neurofibromatosis type 1 , it may be Dx in Caucasians when
2 or more of the following are present :
1. Six or more Café de au Lait macules whose greatest diameter is > 5 mm in
prepubescent patients & > 15 mm in postpubescent patients .
2. Two or more Neurofibromas of any type or one plexiform neurofibroma .
3. Freckling in the axillary or inguinal region .
4. Destructive osseus lesion as sphenoid dysplasia or thining of the long bone cortex
with or without pseudoarthrosis .
5. Optic glioma . 6. Tow or more Lisch nodules (iris hanartomas) .
7. A parent , sibling or child with neurofibromatosis type 1 in the base of the above .
The criteria for diagnosing the neurofibromatosis type 2 ; when 1 of the following is present
1. Bilateral 8 th nerve masses seen by MRI with Gadolinium .
2. A parent , sibling or child with neurofibromatosis type 2 & either unilateral 8th nerve
mass or any one of the following ; neurofibroma , glioma , meningioma ,
Schwannoma , posterior capsular cataract or opacity at young age .

Lecture notes in
GLOMUS TUMORS
Also called chemodectoma or extra-adrenal paragangliomas , which are derived from the
neural crest (they are the precursors of Schwann cells which give neurofibromas &
neurolemmomas , & sympathicoblast which give the paraganglionic cells) .
Paragangliomas found widely distributed in the autonomic nervous system , the sites are :
1. Carotid body tumor.
2. Glomus vagale (vagal body tumor) .
3. Glomus jugulare .
4. Glomus tympanicum ( 3& 4 called glomus temporale) .
Histologically & according to the chroaffin reaction ;
- Chromaffin ganglia ; +ve chromaffin stain & secrete hormones (adrenalin &
noradrenalin) .
- Non chromaffin ganglia ; -ve chromaffin stain & don’t secrete hormones , the nerve
supply is mainly sensory .
Carotid body , physiologically active chemoreceptors which responds to changes in
PH & PO2 , while glomus jugulare is inactive .
Glomus jugulare tumor
Glomus jugulare lies in the temporal bone . Average of 3 glomus bodies in each temporal
bone , the anatomical positions ;
1. Usually is close relationship with either tympanic branches of the IX nerve or
auricular branch of X nerve (both 25%) .
2. Fifty percent found in the adventitia of jugular bulb .
3. Twenty five percent found in the mucosa of the promontory .
The nerve supply from the sensory fibers of the adjacent nerves .
The blood supply from the ascending pharyngeal artery .
The size is variable , ovoid in shape .
Histologically ;
1. Similar to carotid body .
2. With epithelial cells (epitheloid cells) interspaced in highly vascular stroma of
capillary vessels .
3. Two groups ;
a. Cellular glomus bodies (cells >vessels) .
b. Vascular glomus bodies (vessels>cells) .
Pathology ;
- Has similar histological appearance to normal glomus jugulare .
- Cytologically ; not very active with only rare mitotic fingers .
- Usually have a well defined fibrous capsule .
- Clinically ; locally invasive & destructive to bone or facial nerve .
- Sex ; female 6 : male 1 .
- Age ; 5 th decade , sometimes with +ve family history .
- No endocrine function , but 10% has normal activity which lead t increased vanilly
mandelic acid & 5HT (so should be measured if patient develop flushing , sweating
or headache) .
- Sometimes , it is multicentric (10%) , 10% malignant & 10% of +ve family history .
- Bilateral , 25% if +ve family history & 3% if –ve family history .
The natural history of presentation ;

Lecture notes in
- Late Dx , average 6 years from the original symptoms , extreme 2 weeks – 42 years .
- Symptoms are ;
Pulsatile tinnitus (55%) & CHL (69%) , the commonest .
Otalgia & aural bleeding , also common symptoms .
Not uncommon , red mass like sun rising behind the tympanic membrane .
Thirty percent presented with facial nerve palsy .
Headache & visual disturbances .
Vertigo & SNHL , due to inner ear involvement .
Cranial nerves deficit , X , XII , V & VI nerves lead to hoarseness & dysphagia .
Avellis syndrome , IX & XI cranial nerves pressed on the jugular foramen lead to
dysphagia & shoulder drop .
Cerebellar dysfunction , if extend to the posterior cranial fossa .
- On examination
Examining the tympanic membrane under microscopy shows ;
 Aural polyp or obstruction of the tympanic membrane by the tumor .
 Red , purple or bulging mass , Pulsatile swelling (rising sun sign) .
Hearing loss usually CHL .
Cranial nerve examination is very important to determine the extension of the
disease .
Classification ; by Oldering & Fisch (1979) :
A : Tumor localized to the middle ear cleft (glomus tympanicum) .
B : Tympanomastoid tumor with no destruction of bone in the infralabyrinthine
compartment of temporal bone .
C : tumor invading infra-labyrinthine compartment of temporal bone & extending towards
the petrous apex with destruction of the infra-labyrinthine compartment of the temporal
bone .
D : Tumor with intracranial extension ; De (Extradural) & Di (intradural , Di1<2cm , Di2
>2cm & Di3 large & irresectable) .
1. Otitis media .
2. Glomus jugulare .
3. High jugular bulb .
4. Aberrant carotid artery .
5. Idiopathic haemotympanum .
6. Ca. of middle ear (otalgia & bloody otorrhea & progressive deafness) .
7. Neuromas of the last 4 cranial nerves .
Diagnosis by ;
1. History .
2. Examination ; full otological examination (by microscopy) & neurological .
3. Laboratory ; FBC , 24 hours urine for VMA (normal 7mg/24hrs) .
4. Audiological investigations ;
- PTA ; either normal , or CHL (more common) or asymmetrical SNHL (cochlear
invasion or retrocochlear compression) .
- Impedence audiometry ; decreased compliance & pulsation synchronize with
heart beats .
-
Lecture notes in
Acoustic reflex ; abnormal findings indicate facial palsy , involvement or pressure on

ossicular chain .
- Caloric test ; canal paresis which mean involvement of the labyrinth .
- ABR , to differentiate between cochlear from retrocochlear .
5. Radiology ;
- Plain skull x-ray & polytomography , show the Phelp’s sign (absence of the
normal bony crest between the carotid canal & the jugular fossa on lateral
tomography) which is diagnostic .
By plain –ray , type A & B (clouding of the middle ear & mastoid cells) & type C
(bone erosion & unilateral enlargement of the jugular foramen)
- CT scan , is the technique of choice , can enhanced the lesion , show bone
destruction & differentiate tumor types .
Axial CT scan ;
 Enlarged Jugular fossa ; cortex eroded (glomus jugulare) , while normal
cortex (high jugular bulb) .
 Normal jugular fossa ; normal carotid canal (glomus tympanicum) , while
laterally displaced carotid canal (aberrant carotid artery) .
- MRI ; can detect tumor of > 8 mm , by enhancement T1 with Gadolinium or
unenhanced T1&T2 weighted .
Also MRA for preoperative detailed assessment of the extent of the disease &
blood supply .
Recently ; subtraction MRAngiography (non-invasive) , extension towards
petrous apex & cavernous sinus , used for follow up .
- Angiography ; can demonstrate all glomus except very early glomus tympanicum
, it can identify the blood supply to the tumor (usually ascending pharyngeal
artery , or occipital artery or internal maxillary artery) .
Lyre sign , bowing & displacement of the external & internal carotid arteries by a
tumor at the bifurcation of the common carotid artery .
6. FNA ; useful & safe & accurate (especially for carotid paragangilioma) .
7. Biopsy , contraindicated (because the risk of bleeding) , used for tumors in the EAM
to exclude sequamous cell Ca. (if bleeding occur , stop with BIPP) .
Retrograde venography by catheterization of the internal jugular vein (invasive
technique) now CT scan .
In past used to differentiate between glomus tympanicum & glomus jugulare tumor
which will show a filling defect .
Management
The current management options for glomus jugulare tumor are ;
1. No active management .
2. Primary radiotherapy .
3. Surgical resection .
4. Surgery with adjunct chemotherapy .
1. NO treatment
The tumor is extremely slow growing & have long history , indications of no Rx ;
a. Minimal symptoms .
b. Age of 6th-7 th decade .
c. Repeated CT scan do not show very extensive spread or rapid growth .

Lecture notes in
2. Radiotherapy
It is rarely curative , has some effects on slowing tumor growth , so tumor shrink ,
bleeding cease & tinnitus& vertigo diminished (but deafness & cranial nerve palsies will
persist) , the tumor vascularity decreased (tumor not sensitive to radiation) .
Histopathologically after radiotherapy , radiation fibrosis appear 6-12 months later .
Improvement may take several years . The epitheloid cells & Chief cells broken up into
nests of tumors & fibrous tissue .
Nowadays ; megavoltage & tumor localization by 3 dimensionalimages give few
complications , 40% continue to grow , deliver 4000-5000 cGy/3-4 weeks .
Radiotherapy indicated in ;
a. Elderly .
b. Inoperable tumors .
c. Asymptomatic growing tumor .
d. Patient refuse surgery .
e. Inexperienced team .
f. Recurrence after surgery .
g. Bilateral tumors .
3. Postoperative radiotherapy
Subtotal resection with postoperative radiation , when the tumor invades the cancellous
bone or cells of the petrous apex around the internal carotid artery & those presented
with limited neurological deficits (surgery may increase it) .
4. Surgery
- Type A ; permeatal approach or postauricular .
- Type B ; combined approach (intact canal wall) .
- Type C ; infratemporal fossa (or skull base) approach utilizing upper cervical
dissection & transmastoid .
- Type D ; skull base approach & posterior fossa craniotomy (some prefer 2 stages
surgery) .
Complications of surgery ;
a. Cranial nerve palsies ; VII , IX , XII & X nerves , patient may need
tracheostomy or medialization of the vocal cords .
b. CSF leak ; when the subarachenoid space opened , managed by compression
dressing & lumbar drain .
c. Pulmonary embolism .
d. Hearing loss .
e. Wound infection , due prior surgery , pre-existing infection , necrosis of fat
grafts or muscle grafts & infection of haematoma .
Surgical techniques
Reducing the tumor vasculature by ;
- Preoperative Irradiation by inducing stromal fibrosis & decreased vascularity
which made dissection easier .
- Preoperative embolization ; sometimes lead to stroke , selective angiography is
performed & embolization achieved either with gelfoam or polyvinyl alcohol
sponge (Ivalin) 4-8 hours prior to surgery .
Anaesthesia ; prolonged hypotensive technique used , controlled by intra-arterial
monitoring decrease bleeding & dissection of gauze soaked with 1:1000 adrenaline .

Lecture notes in
Approaches
A. Transmeatal approach
Simple tympanotomy for removal of very small glomus tympanicum tumors , if all
their branches can be visualized .
Addition exposure by
- Dissection of malleus handle free tympanic membrane .
- Lowering of the annulus (Shambaugh hypotympanic approach) .
- Removing the mastoid tip & mobilization of vertical portion of facial nerve
(Farrior).
B. Extended facial recess approach
For large type A & moderate size type B glomus jugulare tumor , by ;
- Removing bone of the tympanic recess posteromedial to the fallopian canal .
- Skeletonizing of the vertical portion of the facial nerve & sigmoid sinus &
posterior SCC .
- Total tumor removal can be done with preservation of the ossicular function .
C. Infra-temporal fossa approach (lateral approach) .
The essential features of this approach ;
- Resection of the jugular bulb after ligation of the internal jugular vein in the
neck .
- Packing of the sigmoid sinus superiorly .
- Anterior transposition of the facial nerve to allow direct access to jugular bulb
region & resection of the jugular bulb .
- Preserve the medial wall of the sinus , to protect the neural component of the
bulb region & intact dura of the posterior fossa & radiotherapy for extensive
tumor .
The basic steps of Fisch’s approach (ITF) ;
- Postaural incision extended to the neck .
- Facial flap & pinna are raised & reflected anteriorly .
- Transaction of the cartilaginous portion of the of the EAM & closed off as a
blind ending sac .
- The parotid region is dissected to mobilize the peripheral branches of the facial
nerve .
- Nerves & veins of the upper neck mobilized carefully up to the skull base .
- Ligatures placed around the internal jugular vein & internal carotid artery , but
not tied at this stage .
- Complete mastoidectomy (subtotal petrousectomy) , removal of the all air cells ,
posterior meatal wall , the drum , ossicles .
- The outer wall of the hypotympanum is drilled away .
- The facial nerve skeletonized along both its horizontal & vertical portions &
dissected free from the canal .
- If the facial nerve invade by the tumor , either removal of the nerve sheets or
resection of the involved segment of the nerve & cable graft using sural nerve
placed between the cut ends .
- The sigmoid sinus is ligated at the sinodural angle & the internal jugular vein is
ligated in the neck .
- The tumor is mobilized .

Lecture notes in
- Packing of the lumen with surgical gauze , to control the bleeding occur from
petrosal sinus where it enters the bulb medially .
- Any dural defects repaired with fascia .
- The Eustachian tube is closed with bone wax & the whole cavity filled free fat
graft
- Temporary paresis of facial nerve due to anterior transposition 2-3 months
recovery in 85% .
Intracranial extension > 2 cm best managed by 2nd stage procedure to decrease the
chances of CSF leak & meningitis .
D. Posterolateral approach
Modification of Fisch’s approach , achieve total resection of type C & D without
facial nerve transposition , it allows preservation of the posterior meatal wall .
Used for large C & D tumors , the steps are ;
- Upper neck dissection & posterior reflection of the sternomastoid muscle to
show the lateral process of atlas .
- Cortical mastoidectomy or suboccipital exposure .
- Complete resection with preserved neural compartment with packing of the
inferior petrosal sinus .
It need postoperative irradiation to enable more conservative resection .
E. Management of secretory glomus jugulare tumors
Preoperatively ;
- VMA estimation in 24 hours urine collection .
- Localization of pheochromocytoma .
- Management hypertension by a- & B- blockers .
After embolization & surgery , circulatory collapse due to loss of vasoconstrictor
tone , managed by massive i.v. fluid & antigravity suit to increase venous return .
Other paragangliomas
Glomus vagale
Clinical features are ;
1. Hoarseness or breathing voice .
2. Aspiration , due to inadequate glottic closure .
3. Vagal paralysis .
4. Extensive ;
- Jugular foramen ; tinnitus & Avellis syndrome (IX & XI) .
- Anaesthesia of palate & nasal reflux .
- Hypoglossal palsy .
On examination ;
1. Solitary mass in the neck closely associated with carotid artery .
2. I/L show vocal cord palsy .
3. No pulsation , no thrill & no bruits .
Managed by surgical resection .
Carotid body tumors
Clinical features ;
1. 65% of head & neck paragangliomas .
2. 4 th – 5 th decade of life , male = female .
3. Slowly growing , painless swelling with labile hypertension & headache .

Lecture notes in
4. Swelling in the neck at the carotid artery bifurcation .

5. If large , dysphagia , cough & hoarseness .
6. Pain & syncope (pressure effect) .
On examination ;
1. Sometimes , mass behind the posterior pillar (10%) .
2. Poorly defined neck mass at the anterior border of the sternomastoid at the level of
the hyoid bone , mobile from side to side (not vertically) .
3. Transmitted carotid pulsation (with bruit in 50%) .
Glasscock – Jackson classification
A. Glomus tympanicum
- Type I : at promontory , managed by permeatal approach .
- Type II : completely filling the middle ear space , managed by post-auricular
extended facial recess .
- Type III : type II + mastoid , managed same as type II .
- Type IV : type III + EAC through the tympanic membrane or anterior to the
internal carotid artery , managed same as type II .
B. Glomus Jugulare
- Type I : jugular bulb , middle ear , mastoid , massaged by skull base dissection .
- Type II : extended under IAM , manage same as type I .
- Type III : extend under to petrous apex , may have intracranial extension ,
managed by modified ITF exposure .
- Type IV : ITF or clivus , may have intracranial extension . managed as type III or
extended ITF exposure .
C. Carotid body tumors
Based on size & difficulty of resection .
- Group I ; small tumor , easily dissected .
- Group II ; medium size , intimately associated with vessels , but can be separated
with careful subadventitial dissection .
- Group IV ; large , enclosed the carotid , require partial or complete vessels
resection & replacement .
Other tumors of the petrous apex
Rare , usually presented by erosion of the IAM or inner ear & mimic CPA tumors ,
diagnosed by CT & MRI , these are ;
A. Chordoma ; management by wide resection with postoperative irradiation , either by
brachytherapy usuing I 125 implant or stereotatic radiotherapy .
B. Chondrosarcoma ; arise from the cartilaginous nests in the foramen lacerum ,
locally malignant , managed by surgery & radiotherapy .
C. Meningioma ; arise from arachenoid villi , managed by surgery & postoperative
radiotherapy .
D. Others ; epidermoid , lipoma , facial neuroma , arachenoid cyst , choroids plexus
papilloma , secondaries , lymphomas & cholesterol crystals .
E. Epithelial tumors ; adenoma , SCC & adenid cystic carcinoma .
Surgical approach to the petrous apex & clivus
1. Infratemporal fossa route to lateral skull base & petroclival region (Fisch 1982) .
- Type B approach for chordoma of clivus , cholesteatoma of petrous apex &
meinigioma , by removing bone of posterior zygomatic arch (for access) , then

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working along the Eustachian tube with dividing the mandibular & middle
meningeal artery , access to clivus anterior to internal carotid artery .
- Type C approach to the posterior aspect of the maxillary antrum , parasellar
region , nasopharynx & sphenoid sinus , used for angiofibromas , SCC of
nasopharynx & adenoid cystic Ca.
2. Anterior approach to the petroclival region
By doing Lefort I osteotomy lead to clival region .
Horizontal Lefort I osteotomy , using midline sagital split to separate the 2 maxillae
with intraoperative implant of radioactive Gold or Iodide .

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Examination of the nose

The nose can be examined in three steps ;
- Examination of the external nose
a. Inspection , to detect ;
(1) congenital deformities like clefts , sinuses …etc .
(2) Acquired deformities .
(3) Shape .
(4) Swelling , inflammatory , cysts , tumors …etc .
(5) Ulceration , trauma , neoplastic , infective …etc.
b. Palpation , carried for ;
(1) Tenderness (over the tip due to boil , while over the dorsum due to trauma) .
(2) Crepitus .
(3) Deformities .
- Anterior rhinoscopy
Consist of the following steps ;
a. Examination of the vestibule , skin lined part of the nose
Carried out by tilting the tip of the nose upwards , the lining is skin & has all the skin
appendages , all the diseases affecting these adenxae can occur in the vestibule .
Boil causes swelling in the roof & lateral wall , ulceration may be neoplastic , infective
& some times find excoriation due to discharge .
b. Examination of the nasal cavity using Thudichum’s speculum
Look at roof , floor , lateral & medial wall of the cavity , notice the sptum , position ,
spurs , deviation , color of mucosa , ulcers , crusting , perforation , vessels ..etc .
Lateral wall ; look to the inferior & middle turbinates , size , color , shape & for meatii
to see for discharge & polyps .
Middle meatus is situated higher up , so tilt the head backwards at an angle of 45 , if
any growth or polyp is suspected confirm by probe test .
c. Patency test
By placing a cold tongue depressor or wick of cotton below the nostril , nasal patency
can be assessed (compare the two sides) .
d. Probe test
Carried out by spraying the nose with 4% lidocaine with adrenalin or 10% cocaine ,
the lesion or area is palpated to determine its character & mobility .
- Posterior rhinoscopy
It is carried out to examine the postnasal space , it is a difficult space to be examined , so
the disease may be hidden for quite a long time , different methods of examining the area
are ;
(1) Postnasal mirror .
(2) Nasopharyngoscope .
(3) Examination under GA .
(4) Radiological evaluation .
- Radiological examination
A. Conventional radiology
(1) Occipitomental (Water’s) view
- Maxillary antra .
- Frontal sinus .

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- Sphenoid sinus .
(2) Lateral view
- Sphenoid sinus .
- Frontal sinus .
- Ethmoid sinus .
- Post nasal space .
- Nasal bones .
(3) Submentovertical view
- Sphenoid sinus .
- Ethmoid sinus .
- Maxillary antra .
(4) Occipitofrontal (Caldwell) view
- Frontal sinus .
- Ethmoid sinus .
- Nasal cavity .
- Orbital margins .
B. Tomography
- Fractures .
- Bony destructions .
- Tumors .
C. CT scan
- Tumors .
D. Carotid arteriography
- Nasopharyngeal angiofibromas .
- Epistaxis .

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Nasoendoscopy
The nasendoscopes of two types ;
1. Rigid ; we have 4 or 2.7 mm diameter , which is a rigid glass rod with various angles
of deflections (0o or 30o angle) , it has superior image quality & angular viewing
ability (the flexible need to bent the tip) .
2. Flexible "fibreoptic" ; fibreoptic flexible fiberglass , can reach deeply to the larynx
or trachea , used when there is difficulty to pass the rigid type .
Technique
1. Nasal mucosa sprayed with LA & vasoconstrictors , ribbon gauze soaked with 5%
cocaine (or 4% xylocaine + 1:10000 adrenaline) placed against the middle &
inferior turbinates for 10 minutes .
2. Position ; the patient in recumbent or semirecumbent position , the examiner sits on
the right side allowing a stable base for the head of the patient , let the patient
relaxed , then use suction to clear the nasal cavities & to offer a good field of vision
which is necessary to avoid mucosal injury .
Also we can examine in sitting position .
3. Some precautions , when we deal with secretions & blood , gloves , mask & eye
protection are needed & the endoscope lens treated with a thin film of antifug
solution .
The endoscope held lightly the shaft with the thumb & first two fingers & introduce
slowly under direct vision .
4. The nasal vestibule inspected first & we have three passes through the nasal cavity ;
a. Along the floor of the nasal cavity , the anatomy , pathology , secretions , polyps
& nasal mucosa , we examine the inferior meatus , nasolacrimal duct , the
nasopharyngeal end of Eustachian tube , previous nasoantral window & to note
large several submucosal vessels at the posterior edge of the hard palate , also
we can examine the contralateral Eustachian tube by rotating the telescope .
b. The 2nd pass ; between the middle & inferior turbinates . while the scope directed
posteriorly , the inferior portion of the middle meatus , fontanelles & accessory
maxillary ostia can be examined , the scope pass medial to the middle turbinate &
advanced posteriorly to examine the sphenoethmoidal recess , rotating the scope
superiorly & slightly laterally allows for visualization of the superior turbinate &
meatus as well as the slit like or oval ostia of the sphenoid sinus .
c. The 3rd pass ; is made as the scope is withdrawn as the scope is brought back
anteriorly , it can frequently be rotated laterally under the middle turbinate into
the posterior aspect of the middle meatus .
The bulla ethmoidalis , hiatus semilunaris & infandibular enterance are inspected
, withdrawing of the scope further can provide an excellent view of the middle
turbinate uncinate process & surrounding mucosa .
We can examine by anterior approach if the anatomy favourable (no visible
uncinate process , pneumotized ethmoidal bulla , pneumatized middle turbinate
head , reversal curvature ..etc) all will obscure the view .
5. Look for ;
a. The middle meatus is the area of where most of the pathologies identified in
inflammatory sinonasal diseases ; abnormal purulent secretions , inflammatory
polyps , odematous mucosa , fungal accumulation should be recorded .

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b. The ostia are frequently visible in the lateral wall & may be sufficiently large to
inspect the maxillary antrum .
c. It is vital to monitor "Key areas" as frontal recess & maxillary sinus ostium .
Conditions where endoscopy contribute to diagnosis & treatment
1. Congenital atresia .
2. Cleft palate .
3. Adhesions .
4. Neoplasms .
5. Recent epistaxis .
6. Fungal sinus diseases & Sinusitis .
7. Forign bodies .
8. Eustachian tube dysfunction .
9. Septal perforation .
10. Polyps .
11. CSF leak .
Complications
Rare injury to the nasal mucosa , Eustachian tube , nasopharynx by the improper maneuver
, even following deep biopsy bleeding require blood transfusion is very rare .
Nasendoscopic surgery
History of the Procedure
Rhinology and sinus surgery have undergone a tremendous expansion since the discourses
of Messerklinger and Wigand in the late 1970s .
Imaging advances, increased understanding of the anatomy and the pathophysiology of
chronic sinusitis, and image-guided surgery have allowed surgeons to perform more
complex procedures with increased safety .
Although functional endoscopic sinus surgery is the primary approach used today for the
surgical treatment of chronic sinusitis, the time-honored external approaches still play a
role , therefore, familiarity with both approaches, in conjunction with a precise
understanding of the anatomy, ensures optimal patient care and outcome.
Relevant Anatomy
Knowledge of the anatomy of the lateral nasal wall and the sinuses is critical for
performing safe and complete endoscopic sinus surgery .
This description of endonasal anatomy is roughly based on the order of dissection during
nasal endoscopy and surgery.
Immediately upon entering the nasal cavity, the first structures encountered are the nasal
septum and the inferior turbinate , the nasal septum consists of the quadrangular cartilage
anteriorly, extending to the perpendicular plate of the ethmoid bone posterosuperiorly and
the vomer posteroinferiorly .
Recognizing deflections of the nasal septum preoperatively is important because they may
significantly contribute to nasal obstruction and limit endoscopic visualization during
surgery. As appropriate, patients with septum deflections may be counseled regarding the
need for septoplasty in conjunction with functional endoscopic sinus surgery.
The inferior turbinate extends along the inferior lateral nasal wall posteriorly toward the
nasopharynx. In patients with a significant allergic component to their problems, the
inferior turbinates may be edematous .

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These patients may benefit from a turbinate reduction at the same time as the endoscopic
sinus surgery. The inferior meatus, where the nasolacrimal duct opens, is located
approximately 1 cm beyond the most anterior edge of the inferior turbinate.
As the endoscope is further advanced into the nose, the next structure encountered is the
middle turbinate. The middle turbinate is a key landmark in endoscopic sinus surgery.
It has both a vertical component (lying in the sagittal plane, running from posterior to
anterior) and a horizontal component (lying in the coronal plane, running from medial to
lateral). Superiorly, the middle turbinate attaches to the skull base at the cribriform plate.
As such, care should always be taken when manipulating the middle turbinate .
The horizontal component of the middle turbinate is referred to as the basal lamella, and it
represents the dividing point between anterior and posterior ethmoid air cells .
Posteriorly and inferiorly, the middle turbinate attaches to the lateral nasal wall at the
crista ethmoidalis, just anterior to the sphenopalatine foramen.
The uncinate process is the next key structure to be identified in endoscopic sinus surgery.
This L-shaped bone of the lateral nasal wall forms the anterior border of the hiatus
semilunaris, or the infundibulum .
The infundibulum is the location of the ostiomeatal complex, where the
natural ostium of the maxillary sinus opens .
For patients with sinus disease, a patent ostiomeatal complex is critical for an
improvement of symptoms . Anteriorly, the uncinate process attaches to the lacrimal bone,
and, inferiorly, the uncinate process attaches to the ethmoidal process of the inferior
turbinate. Once the uncinate process is removed, the natural maxillary ostium can be seen,
typically just posterior to the uncinate process, roughly one third of the distance along the
middle turbinate from its anterior edge .
It lies at approximately the level of the inferior border of the middle turbinate, superior to
the inferior turbinate .
The natural maxillary ostium is the destination for the mucociliary flow within the
maxillary sinus , therefore, for optimal results, the surgically enlarged maxillary antrostomy
must include the natural ostium .
In fact, failure to include the maxillary ostium in endoscopic surgical antrostomy is one of
the key patterns of failure in functional endoscopic sinus surgery .
The maxillary sinus, approximately 14-15 mL in volume, is bordered superiorly by the
inferior orbital wall, medially by the lateral nasal wall, and inferiorly by the alveolar
portion of the maxillary bone.
The next structure to be encountered is the ethmoid bulla, which is one of the most constant
anterior ethmoidal air cells . It is just beyond the natural ostium of the maxillary sinus and
forms the posterior border of the hiatus semilunaris .
The lateral extent of the bulla is the lamina papyracea . Superiorly, the ethmoid bulla may
extend all the way to the ethmoid roof (the skull base) .
Alternatively, a suprabullar recess may exist above the roof of the bulla. A careful
preoperative review of the patient's CT scan clarifies this relationship .
The ethmoid sinus consists of a variable number (typically 7-15) of air cells , the most
lateral border of these air cells is the lamina papyracea , and the most superior border of
these cells is the skull base. Supraorbital ethmoid cells may be present .
A review of the patient's CT scan alerts the surgeon to these variations. The basal lamella
of the middle turbinate separates the anterior ethmoid cells from the posterior ethmoid cells

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Anterior ethmoid cells drain to the middle meatus, and the posterior cells drain into the
superior meatus.
Exenteration of the posterior ethmoid cells leads to the face of the sphenoid. The sphenoid
sinus is the most posterior of the paranasal sinuses, sitting just superior to the nasopharynx
and just anterior and inferior to the sella turcica .
The anterior face of the sphenoid sits approximately 7 cm from the nasal sill on a 30° axis
from the horizontal .
Several important structures are related to the sphenoid sinus. The internal carotid artery
is typically the most posterior and medial impression seen within the sphenoid sinus. In
approximately 7% of cases, the bone is dehiscent .
The optic nerve and its bony encasement produce an anterosuperior indentation within the
roof of the sphenoid sinus .
In 4% of cases, the bone surrounding the optic nerve is dehiscent.
Therefore, controlled opening of the sphenoid sinus, typically at its natural ostium, is
critical for a safe outcome. The location of the natural ostium of the sphenoid sinus is
variable; approximately 60% are located medial to the superior turbinate, and 40% are
located lateral to the superior turbinate.
The frontal recess, or the frontal outflow tract, is the tract that leads from the frontal sinus
into the nasal cavity .
Often, the ethmoid bulla is the posterior border of the frontal sinus outflow tract.
Anteriorly, the frontal sinus outflow tract is bordered by the uncinate process or the agger
nasi cells (frontal anterior ethmoid air cells) . If any of these cells are enlarged or if
scarring is present from a previous surgery, resultant outflow tract obstruction, leading to
frontal sinusitis, may occur .
Typically, the medial wall of the frontal recess is formed by the lamina papyracea.
Intimate knowledge and understanding of the anatomy, in conjunction with a careful
preoperative review of CT scans, are paramount in the safe and complete performance of
endoscopic sinus surgery.
Indications
Endoscopic sinus surgery is most commonly performed for inflammatory and infectious
sinus disease . The most common indications for endoscopic sinus surgery are as follows ;
1. Chronic sinusitis refractory to medical treatment
2. Recurrent sinusitis
3. Nasal polyposis
4. Antrochoanal polyps
5. Sinus mucoceles
6. Excision of selected tumors
7. Cerebrospinal fluid (CSF) leak closure
8. Orbital decompression (eg, Graves ophthalmopathy)
9. Optic nerve decompression
10. Dacryocystorhinostomy (DCR)
11. Choanal atresia repair
12. Foreign body removal
13. Epistaxis control

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Typically, endoscopic sinus surgery is reserved for patients with documented rhinosinusitis,
based on a thorough history and a complete physical examination including CT scans if
appropriate, and in whom appropriate medical treatment has failed .
Patients with nasal polyposis commonly have poor results with medical therapy alone;
therefore, surgical intervention may be considered earlier in the course of treatment .
Similarly, antrochoanal polyps require surgical removal .
Increasingly, selected nasal masses and tumors are being removed endoscopically.
Endoscopic removal of inverted papilloma is controversial .
Endoscopic surgery can be performed for limited lesions in which definitive control and
margins can be obtained endoscopically ; this circumstance can be predicted preoperatively
via nasal endoscopy and imaging .
More extensive lesions should be approached externally with use of either a lateral
rhinotomy method or a midfacial degloving method in order to perform en bloc tumor
removal , further research with long-term monitoring in this area will better delineate the
optimal treatment for these patients.
CSF leaks associated with CSF rhinorrhea can be managed endoscopically. Success rates
of 80% have been reported in the literature with primary endoscopic attempts; success rates
increase to 90% if revision endoscopic closures are included .
With endoscopic repair of CSF leaks, the more extensive neurosurgical external
approaches via craniotomy can be avoided .
In certain clinical settings, endonasal encephaloceles are repaired via endoscopic
approaches , endoscopic approaches may also be applied for ophthalmologic procedures,
including orbital decompression, endoscopic DCR, and optic nerve decompression for
traumatic indirect optic neuropathy . Traditionally, these procedures were performed
through external approaches , but, with increasing experience in nasal endoscopic
techniques, they are now performed endoscopically .
Only surgeons with extensive training in and expertise with endoscopic techniques should
perform these procedures .
Contraindications
Certain conditions may require an external approach for complete treatment of disease;
these include intraorbital complications of acute sinusitis, such as orbital abscess or frontal
osteomyelitis with Potts puffy tumor .
An open approach in these instances, with or without additional endoscopic assistance,
may be preferable .
A careful review of preoperative CT scans or MRI films helps to guide the surgeon.
After 2 failures to endoscopically manage CSF leaks associated with CSF rhinorrhea,
patients should be referred to a neurosurgeon for closure using a neurosurgical approach.
Likewise, after failure to endoscopically manage frontal sinus disease, open approaches
should be considered .

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CONGINTAL ANOMALIES
The nose charcterize the outstanding feature of the face , the abnormalities of the nose are
either ;
1. Minor ; cause no functional abnormalities or disabilities , even though the parents
observe & comment on them .
2. Major ; induce parental dismay & occasionally reject the child .
The Developement of the nose
At the 3rd week of fetal life , paired thickening (olfactory or nasal placodes) appear in the
cranial ectoderm near the embryonic anterior neuropore .
Invagination of the placodes , consequent on growth of the surrounding mesoderm resulting
in the formation of the nasal pits which as they deepen serve to delinate
the medial & lateral prominence of the frontonasal process .
The medial prominence fuse to form the central portion of the upper lip ,
the premaxilla & primitive nasal septum .
The floor of the nose (at 1st) formed by medial growth of the maxillary
process of the mandibular arch , as the nasal pits deepen , they become
slit-like .
Progressive thinning of the mesoderm , dorsally & caudally results in
formation of the bucconasal memberane seperating the lumen of the nose
from the buccal cavity .
The bucconasal memberane eventually breakdown forming the primitive posterior nasal
aperatures which lie horizontally in the roof of the buccal cavity or stomatodeum , at this
stage the lower free border of developing nasal septum lies in contact with dorsum of the
tongue .
Meanwhile , paired lateral palatal processes are formed , one on each side of the tongue ,
fusion of these with each other with an unpaired , ventrally sited , median process & with
the caudal border of the septum give rise to the definitive palate which finally seperate the
nasal & nasopharyngeal cavities from the mouth .
Choanal atresia
Choana means funnel which is the posterior apeartures of the nose , the atresia of the
choana 1st described by Roederer 1775 , it is an autosomal recessive trait .
It occur in 1:8000 live birth , bilateral choanal atresia still a frequently unrecognized cause
of death in a neonatal period , female:male about 2:1 .
The aetiology explained by 3 theories which has been reported ;
1. Persistance of the buccopharyngeal memberane .
2. Failure of the bucconasal memberane to undergo involution .
3. Persistance of the epithelial cells which proliferate within the nasal cavities during
the 6 th-8th week of intrauterine life .
The pathology ;
The atresia are bony in 90% (mostly easily perforated) & 10% memberanous , it is
unilaterally in 2/3 rd of cases & bilateral in the other 1/3rd .
The site is infront of the posterior end of the nasal septum , there is associated asymmetry of
the facial skeleton (espicially in unilateral cases) ; high arched palate , deformed or abscent
teeth , or transverse maxillary compression .
CT findings are ; thickening of the vomer , bowing of lateral wall of the nasal cavity &
fusion of the bony elements in the choanal region .
Lecture notes in
Sometimes only choanal stenosis present (bony stenosis) .

The clinical features are ;
1. Unilateral ; appear at later childhood or even adulthood as unilateral nasal
discharge , sometimes during feeding of child espicially breast feeding , the non-
affected side occluded by contact with the breast .
2. Bilateral ; it is respiratory emergency (need urgent management) because the infant
is obligatory nose breathers (because the reflexes which make the breathing through
the mouth in response to nasal obstruction need weeks to months to be developed) .
So the patient present at birth & the infant demonstrate cyclical changes in
oxygenation , on quite cynosed , but when cry (the mouth opened , or when insert an
airway) the child returning normal colour .
60-70% of cases associated with one or more other congenital anomalies (CHARGE)
; Colobomatous blindness , Heart disease , Atresia of the choana , Retarded growth
(including mentally) , Genital hypoplasia in males , Ear deformities including
deafness .
The diagnosis by ;
1. Examination which determine the patency of the nasal cavities in newborn infant ;
a. Pass a soft red-rubber catheter through each side of the nose into the oropharynx ,
failure to pass the catheter is not exclusive evidence for atresia (as the tip may
become impacted in the adenoid or may be deflected by minor abnormalities of the
turbinates) .
b. Stethoscope with removal of the bell & held over each nostril , the presence or
abscence of air-blast noted .
2. Investigations ;
a. CT scan , give informations whether the obstruction is memberanous or bony , with
associated finding maintained in the pathology (we can see the atretic plate) . The
presence of mucous within the nasal cavities can misleading the Dx , so we must
gives vasoconstructors drops with suction of the mucous prior to doing the CT scan .
b. Choanography (in past) , contrast medium is held up at the choanae .
The management by ;
The main aim of the management is the aeration of the patent nasal airways .
A. In unilateral atresia , surgery done as planned or cold "elective" procedure .
B. In bilateral atresia , always present as a respiratory emergency & so the management ;
(1) Primary or emergency Rx , we planned to proseed to definitive surgery within 24
hours usually insert a standard neonatal waters airway (taping it security into position) .
If the child general condition is precarious , usually due to additional pathology , delay
the surgery , so wiser to do endotracheal tube or tracheostomy .
(2) Secondary or definitive Rx , best carried out as soon as possible , there are 4
approaches ; transnasal , transapalatal , transseptal & transantral (the 1st two is the
commonest) .
Preparation , we need microscope for illumination & to make the operation easier & safer ,
some prefers to do transnasal endoscopic repair to provide better visualization & to do exact
surgery , the operation done under GA with orotracheal tube .
In thin bony or membearnous atreisa , use the transnasal route by different ways;
a. The simplest , perforation of the atretic lamina followed by dilatation , the perforation
done either by Lichtwitz's trocar & canula to achieve the primary puncture (which

Lecture notes in
carry risk of serious damage to the cervical spine & spinal cord) or by female urethral
dilators (which is curved) , so directing the perforator to the lumen of the nasopharynx
safely .
The site of puncture should be at the thinnest & weakest point which is at the junction of
the floor of the nose & posterior end of the septum .
Once the puncture has been achieved , the opening may be widened using progressive
dilators up to 5 mm , then some surgeons use portex or silastic tubes to prevent restenosis
of the choana (some prefers to dilate the choana once a week for 4-6 weeks) .
b. Drilling out the bony atresia with diamond paste burrs .
c. Vaporizing the obstruction by Co 2 laser , it is important to use aural speculum to
protect the skin of nasal vestibule otherwise damage to the anterior nares causing
stenosis .
If the atresia is thick , transpalatal approach is preferable & the position ass used for cleft
palate repair (tonsillectomy position with head on the surgeon lap) , then insert Boyl-Davis
mouth gag which give better exposure of the hard palate .
An incision is made around the summit of the alveolar ridge (or at the gingivopalatal margin
if the teeth are present) , the mucous memberane of the hard palate is elevated by Cottle
septal elevator & the flap developed posteriorly until the edge of the hard palate is reached
(care taken to avoid greater & lesser palatine vessels & nerves in the bone close to the
posterior edge) .
The nasopharynx is entered by seperation of the muscle fibers from the posterior edge of the
hard palate & the incision of the superior mucosal layer of the soft palate .
Then by dimaond paste or cutting burr of suitable size , the posterior end of the hard palate is
removed to expose the bony atresia , continuity of the nasal cavity can more be restored by
drilling away the obstructing bone (with the removal of the posterior end of the vomer at the
same time) , care must be taken to avoid damage the vessels & nerves at the lateral nasal wall
Then soft silastic tube inserted & anchored in position with an anterior septal transfixation
suture , then replace & suture the palatal flap (the tube removed 4-6 weeks later) .
The complications of such approach are ;
1. Risk of palatal perforation if the palatal flap is too short .
2. Subsequent maldevelopement of the upper dental arch .
There is another approach recommended by Koltai & Baily in 1992 , external rhinoplasty
approach in children which also used for septal deviation , nasal dermoid , sphenoid sinus
problems as well as unilateral choanal atresia , it give good exposure to the posterior vomer
as the transpalatal approach without the risk of palatal growth .
Septal deviation
Some degree of septal deviation is found in 58% of all newborn babies (& 4% has associated
external nasal deformity) , there are two mechanisms proposed that explain how it arise ;
1. Difference in the rate of growth of septum as compared to other midface structures ,
too big septum for the space it has to occupy .
2. Trauma to the nose , during labour of long contact with the uterine wall .
It is frequently concommitant with cleft lip & palate .
So the deviated septum results which leads to nasal obstruction which present in the neonates
as difficult or slow feeding with colic due to air swallowing with resulatant nasal infection
causing snuffly & s.t. obstruction (s.t. severe which mimic choanal atreisa) .

Lecture notes in
The examination to estimate the patency by comparing the air-blast heard over each nostril
(as in choanal atresia) .
The management , both the external pyramidal & internal septal deformities may be
corrected within the 1st few days of life using espicially designated neonatal nasal septum
forceps .
The external rhinoplasty approach give good access to the nasal septum .
At 6 years of age , septoplasty can performed with minimal tissue removal (otherwise
jeopardize growth of the nose) .
Congenital nasal masses
The causes are ;
1. Cystic ;
a. Congenital , meningoencephalocele , meneingocele , dermoid cyst , epidermoid cyst &
nasolacrimal duct mucocele .
b. Acquired , sebaceous cyst , lacrimal duct cyst & mucocele .
2. Solid ;
a. Congenital ; glioma , haemangioma , teratoma , lymphangioma , congenital
angiofibroma , neurofibroma , hamartoma , hairy polyp , neuroblastoma , chordoma ,
craniopharyngioma & rhabdomyosarcoma .
b. Acquired , lipoma , papiloma , lymphoma , nasopharyngeal carcinoma , angifibroma ,
abscess , ethmoidal & antrochoanal polyps .
Nasal dermoids
These are solid tumors , cysts or sinuses occuring anywhere in the midline of the nose from
the glabella to the columella , whose wall contain skin adenxae .
It can be found at the nasopharynx as a hairy polyp (the mass covered with hair-bearing skin)
It is due to sequestration of epithelial elements during the fusion of the midline nasal
structures .
The Dx usually delayed untill adolescent (s.t. untill it get infection) , it is done by contrast
sinography , showing the extent & configuration of the sinus tract .
The clincal freatures of it are ; it can be multiple , charcterized by dimple or minute
openening , s.t. it has single hair , which may extend deeply in the nasal septum , s.t. reach
the cribriform plate .
It is managed by ; external rhinoplasty approach (complete excision, facillated by canulation
of the punctum & methylin blue instillation) with intracranial approach (if has intracranial
extension) .
Nasal glioma
It about 5% of all nasal congenital anomalies (swellings) , M>F , 60% occur entirely outside
the nasal cavity , 30% entirely within the nasal cavity & 10% combination of both .
It is due to fautly closure of the anterior neuropore (same as meningoencephalocele) .
The pathology is ; glioma detached from the intracranial cavity by closure of the skull suture ,
s.t. fibrous tract remain connecting the glioma to the skull base (while in
meningoencephalocele retain their connection with subarachenoid space) .
Macroscopically ; are smooth , rubbery with grey , yellow or purple surface .
Microscopically ; there is aggregates of mature glial cells , predominantly astrocytes ,
interspread with fibrous tissue .
The Dx , mostly seen after birth , the presentation is s.t. as lump to one side of the nasal
bridge or obstructing intranasal mass which not increase in the size of the nose with straining

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or crying , the tomography or CT af the anterior skull base will be helpfull , & confirm the Dx
by biopsy (1st check for CSF by needle) .
It is slow growing with age , but s.t. with rapid expansion .
The management is by excision (intranasal mass need laser excision or lateral rhinotomy) ,
s.t. in dural connection , anterior craniotomy needed , we must note that incomplete removal
lead to recurrence .
Nasal meningoencephalocele
It is local herniation of glial tissue & meninges through a defect in the skull , it is classified
according to the size & site of the herniation to ; (1) occipital (2) cranial vault (3)
frontoethmoidal (4) basal (5) cranioschisis (large bony defect in the skull) .
The most one that seen by ENTist are frontoethmoidal or basal cyst .
The pathology ; the frontoethmoidal type share a common origion with nasal gliomas , others
depend upon local developemental abnormalities .
It is a sac like protrusion of meninges contain brain tissue & the subarachenoid space with
CSF filling it , communicate freely with the cranial cavity , so any injury will cause CSF
rhinorrhea & meningitis .
Its presentation depend on the type ;
- Frontoethmoidal as soft cystic mass over the root of the nose .
- Basal type as pedunculated intranasal swellings , crying or straining increase the size &
tension of the mass .
Radiology needed to detect the exact site & size of the cranial defect , this by plain film ,
tomography , CT scan & MRI , the MRI can distinguish between the brain paranchyma &
inflammed nasal mucosa .
The management , either by ;
1. Local lateral excision with careful plugging of the cranial opening . or
2. Craniotomy needed sometimes , with removal of the herniated brain tissue followed by
closure of the bony defect using tantalum mesh & repair of the meninges with fascia .
Congenital nasolacrimal duct mucocele
May prolapse or expand into the nose lead to resiratory distress & feeding difficulties .
It managed by endoscopic marsupilization of the mucocele with lacrimal duct probing &
insertion of the lacrimal duct drainage tube .
Nasal hamartomas
Presented as nasal obstruction , epistaxis & chronic rhinorrhea .
It managed with excision by FESS .
Nasopharyngeal angiofibroma
Occur in later childhood & late adult life .
Haemangioma
It is a vascular hamartoma , it is common in childhood (in head & neck) , but rare in the nose
Histologically it is either ; capillary , cavernous , mixed or hypertrophied , it usually progress
spontaneously .
If the growth continue , surgery is needed (it associated with arteriovenous shunt if persist) .
Agenesis of the nose
Two cases reported only with com plete agenesis , it associated with abscence of the
nasopharynx & no evidence of any nasal developement .
It managed by ; (1) learn the child to mouth breath (2) surgery to establish nasal airway (3)
nasal prosthesis which is better than surgical reconstruction .

Lecture notes in
Partial agenesis with falted developement of one nasal cavity also reported .
Cleft nose
It vary from minor notching of the nasal tip to total midline division of the nose , widely
seperated nasal cavities , s.t. associated with median cleft of the upper lip & palate or
notching of the alar margin leading to bifid nose & hypertelorism & mental retardation .
Management by surgery with assisstant with faciomaxillary surgeon & s.t. neurosurgeon .
Proboscis lateralis
Consist of a tube of skin & soft tissue arising at the inner canthus of the eye , the nasal cavity
on the affected side may be completely normal or abnormality (including total agenesis) .
It is due to embryological defect result from imperfect fusion of the lateral nasal & maxillary
process , so associated with failure of developement of the nasolacrimal duct .
It managed by dacryocystorhinostomy .
Table summary of some

Congenital anomalies of the nose
Diagnosis Treatment Complications

Dermoid Fistulous tract on nasal dorsum, Complete Infection
with or without cyst located from surgical Cosmetic deformity
nasal tip to glabella excision Meningitis (rare)
Protruding hair, cheesy contents
typical
CT scan may show bifid septum
or patent foramen cecum
Glioma Smooth , firm intra- and/or Surgical Cosmetic deformity

extranasal mass not attached to excision Nasal obstruction
skin Meningitis
Encephaloceles Soft , pulsatile mass Surgical Progressive expansion
Swell with straining or crying excision Cosmetic deformity
Probe cannot be passed between Meningitis
septum and intranasal mass Associated congenital
abnormalities possible
CT scan shows bony skull base

defect

Lecture notes in
Fractures of the facial skeleton

Aetiology
RTA , Suicide , Playing , Sprot injery , Dental surgery & Pathological lesions of the jaws .
Primary care of the maxillofacial injuries
The primary considerations are ;
1. Ensure adequate airway , to prevent hypoxia & hypercapnea .
2. Establish effective breathing & ventilation ;
- posterior displacement of the tongue secondary to the mandibular fractures which
compropize the airway .
- also oropharyngeal odema may deteriorate the airway .
- feature suggesting fracture of the larynx are ; loss of voice , dysphagia , surgical
emphysema in the neck & increasing stridor & this may need immediate
tracheostomy .
3. Maintain the circulation ;
- Bleeing into the airway from the nose or mouth is serious , it must be controlled by
nasal packing or arterial ligation .
- Shock with fractured facial skeleton is rare & if occur it may be due to intrabdominal
or intrathoracic injury , so the source of bleeeding must be recongnized , controlled
& replaced .
4. Assess the level of consciousness & neurological dysfunction , aftre control of the
previous complications , we should assess the head injury including the level of
consciousness , speech , response to commands & painful stimuli .
5. Assessment of the other injuries ;
- examination of the eye , pupil size & reaction to light .
- abscence of the limb movement may mean cerebral damage .
- look for CSF rhinorrhea & otorrhea .
- the cranium must be papated to detect depressed fractures , scalp laceration must be
carefully cleaned & disinfected .
- prophylactic antibiotics espicially in scalp laceration & CSF rhinorrhea & otorrhea.
- Tetanus prophylaxis should be adminstred in patient with contaminsted wound .
Clinical examination of facial injury
1. Eyes ;
- Look for penterating injuries , corneal abrasion , lense dislocation & lacerations ,
subconjunctival haemorrhage .
- Examine the eye for light reflexes , eye movement & diplopia , displacement of the
globe , periorbital odema .
- Forced duction test , after application of LA to the conjunctiva , the inferior rectus
muscle is grasped with foreceps , so any limitation of upward rotation indicate
herniation of the orbital contents through the orbital floor .
2. Nose ;
- It is not possible to make accurate assessment of nasal injury untill all soft tissue
odema has subside 5-7 days later .
- Septal haematoma is not recognized & evacuated , it may get infection causing septal
abscess , cartilage necrosis & saddle nose , when increased pain & nasal obstruction
persist for few days with/without pyrexia , then suspect septal abscess .

Lecture notes in
- Carefull inspection of the external deformity & displacement of the nasal bones or
abnormality of the septal anatomy .
- CSF rhinorrhea should be kept in mind .
- Unilateral epistaxis in the abscence of direct nasal injury suggest fracture of the
maxillary antrum .
3. Middle 1/3 rd of the face (maxilla)
- Odema , ecchymosis , swelling should be checked for .
- Check the jaw occlusion looking for posterior displacement of the maxilla .
- Palpate for step deformity & surgical emphysema & the bony contour of the face .
- Evaluate the sensory function & facial nerve function
4. Mandible
- Feeling of step deformity .
- Observation for asymmetry of the face & mivement of the jaw .
- Examine for TM joint by placing the little finger of each hand in the EAM .
- Examine for any sensory deficite of the lip .
5. Mucosa & dentation
- Missing or fractured teeth .
- Inspection for asymmetry of the dental arch .
- Palpation for abnormal mobility or crepitus .
- Blood stained saliva which indicate compound fracture which the oral cavity .
Sings of maxillofacial fractures
1. Mandibular fracture
a. Condylar neck fracture ; tenderness over the TM joint , trismus , deviation of the
jaw towards the injured side on opening & at rest , inable to move the mandible ,
symmetrical anterior open bite in bilateral fracture .
b. Fracture of the body , angle & symphysis ; step deformity , assymmetry of the
dental arch , pain , crepitus & pardoxiacal movement , haematoma of the buccal
sulcus , blood stained saliva , mental nerve anaesthesia .
2. Mixillary fracture (middle 1/3rd fracture)
a. Central middle 1/3 rd fracture ; epistaxis , facial odema & surgical emphysema ,
circuorbital ecchymosis (Panda facies) , infraorbital nerve deficit , anterior open
bite & oral respiration & haematoma at the junction between the hard & soft
palate .
b. Lateral middle 1/3rd fracture ; proptosis & subconjuctival haemorrhage ,
increase interpupillary distance , decrease eye movement & decrease visual
acuity , step deformity of the orbital margin , epiphora , decrease mandibular
movement , flattening of the check with step deformity , haematoma of the buccal
sulcus & infraorbital nerve deficit .
Radiological examination
1. Plain x-ray , for ;
a. Skull , chest & cervical spine for associated injuries .
b. Facial skeleton ;
- Nose ; lateral view of the nose showing the nasal bones .
- Orbit , OMW 45o .
- Maxillary sinus , by the standard viewa , it may show , fracture line (of little help)
, fluid level in the sinus (meanable) , airwithin the cranium (aerocephlus or

Lecture notes in
pneumocephlus , mean CSF fistula) , tear drop sign in blow-out fracture of the
orbit & pathological fracture .
- Mandible by OMV 30o , Town's anteroposterior view , submentovertical view &
orthopantomography .
2. Orthopantomography ; it is a per-oral tomography with occlusal film , it gives
panoramic view & used in dental surgery .
3. CT scan used to ;
- assess cerebral damage .
- show the fracture line .
- localize the site of CSF fistula , if occur .
N.B.: vascular markings & suture lines may be misinterpretted as fracture line ,
radiological evaluation & reports should be made by the radiologist for medicolegal
purposes .
Principles of treatment
General principles in the management must include ;
1. The fractured segement must be reduced accurately , & immobilized absoultely &
maintained free from infection .
2. It is essential to restore the correct functional position of the jaw & dentation .
3. Facial fracture are all compound either ;
- directly through the mouth , nose & paranasal sinuses .
- indirectly with the mouth through the peridontal ligaments .
4. The realibility of the fractured segments of the nose & jaws is better than elsewhere
in the body , so it should be maintained .
5. The period of fixation ;
- 7 days for simple nasal fracture .
- 10 days for condylar fracture .
- 6 weeks for angle , body fracture & Le Fort fracture .
Examples of maxillofacial fractures
1. Nasal bones fracture ( discussed in detail in seperate topic) .
2. Mandibular fracture
- Surgical anatomy ; the mandible composed of symphysis , body , lateral chin ,
angle & ramus with coroniod & condylar processes .
The weakest part of it is the subcondylar area which is the commonest site of
fracture , the next most frequent site is the angle which is weakened by unerupted
3 rd molar tooth , then the next site is the body , lateral chin & symphysis .
The type of fracture of the mandible is determined by direction of the trauma ,
magnitude , age of the patient , state of his jaws & dentation .
- Mechanism ;
a. there is favourable & unfavourable (displaced) fractures .
b. single & multiple fracture may occur .
c. displacement of the angle fracture is determined by two factors ; (1) muscles that
pull the posterior segment upward & forward (e.g. masseter , temporalis &
medial pterygoid muscles) & (2) direction of the fracture line .
d. fracture dislocation of the TM joint posteriorly & centrally into the middle
cranial fossa may also seen .
e. fractures of the ramus & coronoid process are stabilized .

Lecture notes in
f. multiple or comminuted fracture are usually grossly displaced , like all fracture
through the tooth bearing areas , they are usually compound into the mouth
directly or indirectly .
- Treatment ;
a. Closed reduction technique ;
i. Intermaxillary fixation , by using interdental wiring (stainless steel wire) ,
the wires are fixed to group of teeth by encircling the free ends of the wires
around the neck of the teeth .
ii. External pin fixation , the advantages of that it can be used in those
patients with ; (1) combined fracture of both mandible & maxilla (2)
fracture with comminution or bone loss & (3) osteomylitis .
The pins are linked by screws into the fragements of the mabdible .
b. Open reduction technique ;
i. Transosseus wiring ; simple & the advantage is that is used in comminuted
or multiple fractures .
Holes are made on either side of the fracture line by burr & stainless steel
wire is passed & tightened to approximate the fractured segments .
ii. Bone plates ; particularly useful when prolonged immobilization of jaws
are avoided because of epilepsy , aged , body fracture & fracture around
the TM joint .
It is contraindicated only in gross contamination of the wound .
Stainless steel or Tetanium plates used (length 3-7 cm) with holes for
fixation of the fracture .
In case of open reduction , wiring or plate can be done directly & so the
trunk of the facial nerve is at risk of surgical trauma .
Fixation for 10 days is sufficient which should be followed by gradual
mobilization of the joint .
3. Middle 1/3 rd fracture
a. Central middle 1/3rd ; it resulted from blow to the front of the face , it can be
classified into ;
i. Alveolar fracture , through the alveolar process only .
ii. Le Fort I fracture ; run above the floor of the nasal cavity , passing through
the nasal septum , maxillary sinus & inferior part of both medial & larteral
pterygoid plates .
iii. Le Fort II fracture ; run from the floor of the maxillary sinuses to the
infraorbital rin passing through the zygomatico-maxillary suture , it pass a
cross the lacrimal bone & nasion .
iv. Le Fort III fracture ; disconnection of the facial from the skull base , the
fracture extend from the medial wall of the orbit to the superior orbital fissure
& pass across the greater wing of the sphenoid & zygomatic bone (arch of
zygoma) & to the zygomatico-frontal suture .
Posteriorly it extend to the optic foramen , lesser wing of the sphenoid &
sphenopalatine foramen .
All these fracture may lead to chronic dish-face deformity .
It is treated by ;

Lecture notes in
i. External fixation technique , this has less popularity due to ; bulky external
frames , unsightly frames , interference with the patient visual field & sleep ,
can not be used if there is possibility of craniotomy & also can not be used if
the patient is likely to have epiliptic fits .
The steps of the procedure ;
(1) Disimpaction & reduction of the maxilla may need some force
Walsham's or Rowe's foreceps , can be used to grip the maxillary .
(2) then the maxilla rocked gentely laterally & forwards into its correct
position .
(3) intermaxillary fixation is then applied .
e.g. of external fixation ; plaster head cap , Levant frame or Box frame .
ii. Internal skeletal fixation technique , the fractured maxilla segment can be
suspended from various ponits of craniofacialskeleton by using internal wire
suspension .
Direct wiring can be done easily as for mandibular fracture .
The site of the internal suspension of Le Fort fracture are ; pyriform
apearture , lateral frontal , central frontal , inferior orbital rim or circum-
zygomatic process .
b. Lateral middle 1/3 rd fracture (zygomatic complex) , the zygomatic bone
constitutes the lateral midddle 1/3 rd , depressed fracture of the zygomatic bone
are called tripod fracture due to the bone breaks in 3 places , zygomatocofrontal
suture , zygomatic buttress & infraorbital rim .
In all types of fracture there is distruption of the orbital floor .
Treatment , is unlike other facial fractures , reduction of the zygomatic complex
can performed only by open reduction technique .
Many zygomatic complex fracture may not require reduction , there is a risk of
iatrogenic blindness following reduction .
The procedure of open reduction (by Gillies)
i. the skin incision is done just behind the hair line , anterioposterior to the
pinna , the incision is deepened through the temporalis fascia .
ii. Rowe's elevator can be passed deep to the fascia (on the temporalis
muscle) to lie behind the body of the zygomatic bone .
iii. Controlled elevation is then applied to the bone .
iv. Great care is taken to avoid pressure on the parietal bone & the eye ball .
v. Fractures found to be unstable following reduction need to be wired or
plated .
Some times , the orbital floor with some contents are collapsed into the antrum ,
so called blow-out fracture , it is better to explore & repair the orbital floor .
The post operative care ;
i. good oral hygien .
ii. wash the mouth three times daily with normal saline or diluted H2 o2 .
iii. careful monitoring of the visual acuity or pupilary reflex .
iv. regular checking of the intermaxillary fixation .
The complications are ; facial assymetry , dental injury , nasal injury (epistaxis ,
nasal onstruction , cosmetic problems) , orbital injury , CSF rhinnorhea , other
systems injury & scarring .

Lecture notes in
Fractures of the nasal bones

Nasal fractures are the most common types of facial fractures (accounting for
approximately half of all facial fractures . Zygomatic (22%), blowout (12%), mandibular
bone (8%), and maxillary bone (9%) fractures follow in frequency) , they are the third most
common types of fractures ; however, they are often unrecognized and untreated at the time
of injury . the central position and anterior projection on the face predisposes the nose to
traumatic injury.
Fractures can be classified as open or closed, depending on the integrity of the mucosa ,
prompt identification and management of the injury in the early postinjury period is
imperative to avoid the potential complications of nasal and septal fractures , longer-term
follow-up allows the surgeon to assess for both early and late sequelae of injuries to the
nasal complex , surgical intervention may be appropriate in the early postfracture period or
much later, after the fracture has healed.
Relevant Anatomy
Nasal skin has an abundant blood supply and tends to be thinner over
the rhinion and thicker over the nasion. Nasal skin thickness varies
among individuals.
The nasal pyramid is composed of 2 nasal bones and the frontal
process of the maxilla. The thickness of the bones decreases toward
the tip of the nose; as a result, most fractures occur in the lower half.
Upper lateral cartilages form the middle nasal vault . They are
attached to the nasal bones superiorly, the quadrangular cartilage of
the septum medially, and the lower lateral cartilages (ie, tip
cartilages) inferiorly.
Sesamoid cartilages are less important and lie in the fat pad between
lower lateral cartilages and the piriform aperture.
The nasal septum has a cartilaginous and bony component that is lined
with mucoperichondrium and mucoperiosteum, from which the
cartilage and bone receive their blood supply. Interruption of the
opposition of perichondrium to cartilage (as with septal hematoma)
may interrupt the blood supply and lead to resorption of septal
cartilage and possibly subsequent saddle-nose deformity.
Aetiology ; Most commonly, nasal bone fractures are sustained in fights (34%), accidents
(28%), and sports (23%) , with increasing use of air bags in automobiles, a shift in the
mechanism of injury and the type of nasal fractures has occurred ; therefore, the incidence
of septal injury in nasal fractures, without concurrent nasal bone fracture, has increased.
In children, nasal fractures are most commonly due to falls , the possibility of child abuse
should be considered in every child presenting with a nasal fracture.
Pathophysiology ; The direction of force to the nose during injury determines the pattern of
the fracture (also the extent of the nasal deformities after trauma determined by the force) ;
1. Frontal force causes damage ranging from simple fracture of the nasal bones to
flattening of the entire nose.
2. Lateral force may depress only one nasal bone; however, with sufficient force, both
bones may be displaced , lateral force can cause severe septal displacement, which can
twist or buckle the nose , septal fragments may interlock, creating difficulty in reduction.

Lecture notes in
3. Superior-directed force (from below) rarely occurs . It may cause severe septal
fractures (C- shaped) and dislocation of the quadrangular cartilage.
Clinical findings in patients with a history of trauma to the nose or face may include the
following:
1. Epistaxis, which is common in nasal fractures due to mucosal disruption
2. Change in nasal appearance
3. Nasal airway obstruction
4. Infraorbital ecchymosis
There are three classes of fractur nasal bone ;
Class I
Also called Chevalet fracture , the depressed fracture is the simplest form of class I , little
force required (25-75 pounds , about 173-518 Kpa) , the fracture line run parallel to the
dorsum of the nose & nasomaxillary suture oining at the point when the nasal bones
become thicker (2/3rd the way along it's length) .
The fractured segment usually re-gain its position as it's attached along the lower border of
the upper lateral cartilage which gives it some recoil .
The bony nasal septum not involved , but involved in severe variant when both nasal bones
involved (fractured) .
The fracture line , on the side of the blow runs parallel to the nasomaxillary suture , while
in the contralateral side parallel to the dorsum & ust below it , also they oin together across
the dorsum at the point when the nasal bones become thick .
The cartilagenous septum , fracture about 0.5 cm below the dorsum , this may extend
posteriorly to involve the perpendicular plate of the ethmoid .
There is no gross lateral displacement of the nasal bones .
In children , it is of green stick variety , subsequent deformity developed at the time of
puberity when the nasal growth accelarated .
Class II
Also called Jarjavay fracture , it cause significant cosmetic deformity , it involve the nasal
bones , septum & frontal process of the maxilla .
The deformity determined by the direction of the blow .
- Frontal impact may communate nasal causing gross flatening & widening of the dorsum
- Lateral blow cause high deviation of the nasal skeleton .
- C- shaped septal fracture with inevitably involve the perpendiculare plate , the fracture
begins just beneath the nasal tip in the quadrilateral cartilage , extending posteriorly &
caudally through the perpendicular plate of ethmoid into the inferior part of the
quadrilateral cartilage .
Class III
The most severe nasal injury & are usually caused by high velocity trauma , in past called
by variety of terms include ; ethmoidal fracture , naso-orbital fracture & naso-lacrimal
fracture , more recentally called naso-orbito-ethemoidal fracture .
So there is orbital component in this type of injury , which is of two types , both often
acquired in association with a Le Forte fracture ;
- First type ; no injury to the ; anterior skull base , posterior frontal wall or the optic
canal , the external butresses of the nose which give way .
Collapse of the ethmoid labyrinth or telescope on itself , as a consequence , the
perpendicular plate of the ethmoid is rotated , the quadrilateral cartilage is pulled

Lecture notes in
backward , these movement gives pig-like appearance of the patient whose nose
foreshortened & saddled & nostrils facing forward .
Telecanthus (increase the space between the eyes) which may be exagurated due to
distruption of the medial canthal ligaments from the crest of the lacrimal bone .
- Second type ; distruption of the posterior frontal sinus , multiple fractures of the roof of
the ethmoid & orbit , s.t. extending as far back as the sphenoid & parasellar region .
Because the dura adherent closely to the roof of the ethmoid , so this type of injury
complicated by ;
1) Multiple dural tears .
2) CSF leak .
3) Pneumocranium .
4) Cerebral herniation .
Surgical correction of the nasal fractures
At 1st elevation of the head and use of cold compresses in the periorbital and nasal region
can be helpful while waiting for edema to subside , even in the presence of significant
edema, a nasal deformity often may be obvious .
In a patient with no apparent abnormality at the initial visit, reassessment of the nose after
the edema subsides may reveal findings necessitating repair . Surgical intervention may
then be undertaken.
Significant number of patient may not need reduction because there is no deformity or
displacement , its correction indicated in ;
1) Correct the cosmotic deformity .
2) Correct septal haematoma whic need urgent intervention .
3) Correct simple injury with car allowed 7-10 days to allow the odema subside .
4) Abnormal nasal function .
5) Presence of early postinjury complications.
Several methods of reduction and repair can be performed to achieve good cosmetic and
functional results ;
A. Closed reduction may be performed under local anesthesia or local anesthesia with mild
sedation. Indications include the following:
1. Simple fracture of nasal bones
2. Simple fracture of nasal-septal complex
B. Open reduction requires deeper sedation or a general anesthetic. Indications include the
following:
1. Extensive fracture-dislocation of nasal bones and septum
2. Fracture dislocation of caudal septum
3. Open septal fractures
4. Persistent deformity after closed reduction
5. Relative indications, eg, septal hematoma, inadequate bony reduction due to septal
deformity, cartilaginous deformities, displaced nasal spine, & recent intranasal surgery.
Contraindications ; Some fractures do not need correction, providing the patient is satisfied
with the appearance and function of the nose. In more severe injuries, one must entertain
the option of deferring a nasal procedure until the patient has become stabilized.
At 1 st oedemal cause difficult breathing through the nose T distort the appearance , so we
wait for 7-10 days allowing the odema to subside & then do 2nd examination to reassesse

Lecture notes in
the fracture & be sure that there is no significant damage (we use vasoconstroctor drops to
improve airflow through the nose) .
Great care should be taken to distinguish between recent acquired deformity & old one .
Pre-operative management
A) History ; to assess the direction of trauma (fracture applied in 3 different direction) ,
depend on the extent of the force (either nasal bone , septum or orbit will occur) , some
details about previous injuries , deformities , surgeries may be helpfull in assessing the
current injury .
B) Examination ;
1. Nasal pyramid ; laceration , bruizing , lateral deviation or deppression , tenderness &
astep deformity localize the fracture line , cosmetic deformity which best assessed by
standing the behind the seated patient & looking down the nasal contour .
2. Nasal septum ; anterior rhinoscopy reveal ; swelling caused by septal haematoma ,
caudal dislocation of quadrilateral cartilage OFF maxilary groove , also angulation of
the septal fracture .
3. Orbital structures ; orbital movement , visual acuity , lacrimal duct obstruction & CSF
fluid leak (by testing of glocose) .
C) Imaging Studies:
1. The use of radiography is controversial , old fractures, vascular markings, and suture
lines can lead to false-positive results. A Water's view can be used to evaluate the bony
septum, dorsal pyramid, and lateral nasal walls . However, studies have shown that
radiographs are not helpful in the diagnosis or management of nasal fractures.
2. CT is more useful to assess for other associated injuries, as well as extent of nasal
injury. Septal fractures may be more obviously depicted on these films. Because the
nose occupies such a prominent and accessible position, careful examination is
possible and may obviate any need for radiographic study.
3. Photographs are useful and necessary for documentation and for comparison with
preinjury photos. Photographs should include the standard angles used in facial
analysis: frontal, left and right lateral, left and right oblique, base view, and often a
bird's eye or partial base view. A smiling lateral view can also be helpful to evaluate
depressor septae nasalis function. While 35 mm film and cameras still allow a superior
resolution, digital photography is quickly becoming more prevalent.
Management options can be according to the fracture class (I, II or III) .
- Class I , managed with closed reduction under LA after the subside of odema & before
significant fixation of bone fragment take place (5-7 days in adults , a little sooner in
children) , if after 2 weeks of injury the patient then will need osteotomies for reduction .
It can be reduced under LA or GA , with LA we infilterate the dorsum of the nose & spray
the nasal mucosa (or pasted) with 5% cocaine .
Mostly it need only digital pressure , but if there is impacted fracture , then Walsham's
forceps used to elevate this fragment (it cause considerable damage nasal mucosa causing
brisk haemorrhage) , after that we apply nasal packs for 3 days to help to maintain the
reduction & external splint applied if the reduction partially unstable .
- Class II , closed manipulation of the nasal bones should be accompanied by open
reduction of septal deformity .
Only closed reduction of this type rarely give a satisfactory results of final position of the
dorsum of the nose because the underlying deformity of the septum .

Lecture notes in
50% of those fractures remain displaced due to the overlaping segment of the fractured
perpendicular plate of the ethmoid or septal cartilage which are not reposioned be closed
reduction , so we do the following ;
a. Killian's incision , elevation of the mucoperichondrial flap on both sides .
b. Elevation of the overlaping parts of the nasal septum .
c. Distrubtion of the bony –cartilagenous junction .
d. Removal of the narrow cartilagenous strips from just beneath nasal bones to the
maxillary crest .
e. Maintance of the nasal septum by nasal packs or by 4/0 catgut suturing .
f. Maintance of the nasal bones by POP splint which removed after 1 week .
g. Nasal packs removed after 3 days .
- Class III , nasoorbital fracture , need open reduction & internal fixation , the major
problem here is that even if the nasal bones can be easily disracted from the skull base ,
the adjacent structures which normally support them (fracture bones & medial wall of the
orbit) have also been comminuted & are unstable .
So that one of the primary aims of the management is to reconstruct & stabilize the
fractured table of the fractured bones , so the other parts of the nasal skeleton can drive
support from it .
In past , a reduced frontonasal complex supported by a transnasal wires tied externally
over either silicon or lead plates & the comminuted medial orbital wall left to reattach &
recognize itself .
Recently , replacement of the medial orbital wal; with splint rib bone grafts , so its
essential to have good exposure which usually provided by a sequence of surgical
procedure steps done by Ellis (not neccessarly needed in every case) ;
a. Adequate surgical exposure ; by combination of coronal & medial canthal
incision , to provide an unobstructed veiw of all component of the fracture .
b. Identification of the medial canthal ligaments ; rarely avulsed , attached to long
fragement of bone , once identified should be reattached or secured to avoid
subsequent telecanthus .
c. Reduction & reconstruction of medial orbital wall ; by transnasal 26 gauge wires
, if plate used it should be as thin as possible otherwise they conspicious when the
tissue heald .
d. Reconstruction of the medial orbital wall & floor with bone grafts .
e. Transnasal canthopexy , for those with persistant canthal displacement despite
reattachment of medial canthal ligaments .
f. Realignment of the nasal septum .
g. Augmentation of the nasal dorsum &/or collumela with bone grafts .
h. Accentuate soft tissue readaptation with splint to avoid post-surgical thickening .
Operative technique (Gelleez approach)
- Anasthesia ; either local or general anasthesia ;
LA to the mucos memberane of the nose can be done by ;
1) Soaked pledgets with coccain & lignocaine placed superiorly to anasthize the
anterior & posterior ethmoidal nerves , & placed at the posterior end of the middle
turbinate to anasthize the sphenopalatine ganglion .
2) Local infilteration of lignocaine to block the sensation applied by the infratrochlear
nerve , infraorbital nerve & external nasal nerve .

Lecture notes in
While GA with intubation can be used which is the safest method to control fracture &
septal deviation correction .
No antibiotics or steroids are needed as premedications
- Position and prepeartion ; prone position with head tilted up slightly , skin
preparation needed with proper draping .
- The procedure ;
1. Nasal bones ;
a. Clinical assessment , looking down the nasal countour .
b. Walsham's forceps , a small blade inserted under the individual nasal bone , rotated
lateral fracture intial outfracturing the nasal bone .
c. Infracturing of nasal bones by applying external thumb pressure to narrow 7
medialize the nasal bones .
d. Nasal bones elevation by intranasal packing usuing , BIPP or antibiotics' soaked
pack .
e. If the fractured is stable , skin tape applied to the skin overlying the dorsum , if
fracture unstable then POP or plastic external cast applied over the nasal bones to
protect against further minor trauma .
2. Nasal septum ;
a. Minor septal deviations we use Asch's forceps introduced on either side of the septum
b. Severe angulations need septoplasty with resection of small area of bone or cartilage
(Frieer's incision) .
c. Drainage of septal haematoma by ; anterior mucoperichondrial incision (Killian's
incision) , sucker introduced for evacuation & suturing wit 4/0 catgut or vicryle ,
small rubber tube drain inserted at the most dependant part of the incision &
bilateral nasal packing with BIPP or other nasal dressings for 24 hours .
- Postoperative management ; all patients with septal haematoma should had oral
antibiotics for 5 days , also nasal packs should be removed at the 1-2 days .
- Complex nasoethmoidal fracture require open surgical exposure via ; either
bicoronal nasal incision or External nasal incision .
Fracture can be reduced & plated or wired to support the nasal pyramid .
Follow-up care
1. Treat nasal crusting, remove splints and packing, and carefully reassess the cosmetic
result as routine postoperative care.
2. Assess airway patency.
3. Assess the need for further intervention (eg, septorhinoplasty).
Complications from nasal fractures include cosmetic deformity and airway obstruction.
Problems arising from nasal fracture complications may be mitigated by adequately
recognizing and treating the injury at the time it occurs.
Most of these cosmetic & functional airway problems can be delt with by elective formal
septorhinoplasty .
1. Cosmetics & nasal function ; most common complication is the unsatisfactory
cosmetic results , hanges in the shape of the nose atributeable to fracture may continue
for several years after the incident (e.g. saddle nose & hump formation) .
The same degree of stenosis may develope which need surgical repair , factors of
unsatisfactory cosmetic results are ; (1) degree of initial replacement (2) previous nasal
trauma (3) delay in reduction (4) inapproperate surgical technique .

Lecture notes in
Conventional medial & lateral osteotomies should not be used on nasal bones that have
heald after trauma because this technique usually produce irrigular fracture running
along the old fracture line , so that a triple osteotomy technique is used for this group (
medial , intermediate & lateral) which effectively shatter the nasal bones & render the
nasal bones completely manipulated .
2. Hematoma (may require drainage to avoid septal necrosis and superinfection that
exacerbates septal deterioration) .
3. Complications of nasal packing , it could displace the corrected nasal bones or
fractured septal line , also it should be avoided if there is CSF leak suspecion .
4. Unremitting epistaxis , also may complicate the correction due to the use of
Walsham's forceps & can be controlled with simple nasal packing .
5. Failure of adequate correction of deformity may be due to ; (a) inadequate
stabilization of fractured bone (b) previously heald nasal fracture & displacement & (c)
difficult correction of septal deformity .
6. CSF rhinorrhea ; common immediately after the nasoorboethmoidal fracture (class
III) , the vast majority stopped after reduction & fixation of the fracture .
Any leak persist for > 2 weeks after injury should be considered for formal repair.
Meningitis , it is of constant risk to develope in those patients & thesymptoms suggestive
incipient meningitis should be taken very seriously in this group of patients .
Delayed complications
1. Airway obstruction
2. Scar contracture
3. Nasal deformity
4. Saddle-nose deformity (due to injury or ischemic necrosis of nasal septum secondary
to hematoma formation, followed by loss of dorsal nasal support)
5. Septal perforation
6. Orbital complications ;
(a)Telecanthus , can be acquired despite every effort at the initial reduction .
(b) Epiphora , due to damage to the lacrimal duct , infrequent complication ,
usuallyresolved by dacryocystorhinostomy .

Lecture notes in
Epistaxis
Epistaxis, or bleeding from the nose, is common in its frequency and varied in its
manifestation , the true prevalence of epistaxis is not known because most episodes are self-
limited and thus are not reported , when medical attention is needed, it is usually because of
either the recurrent or severe nature of the problem .
Epistaxis is a risk factor of spread of HIV , Hepatitis & other blood born infections .
Vascular anatomy of the nose
The nose has a rich vascular supply with contribution from the internal and external carotid
arteries.
The external carotid system supplies blood to the nose via the facial and internal maxillary
arteries. The superior labial artery is one of the terminal branches of the facial artery. This
artery subsequently contributes to the blood supply of the anterior nasal floor and anterior
septum through a septal branch. The internal maxillary artery enters the pterygomaxillary
fossa and divides into 6 branches: posterior superior alveolar, descending palatine,
infraorbital, sphenopalatine, pterygoid canal, and pharyngeal. The descending palatine
artery descends through the greater palatine canal and supplies the lateral nasal wall. It
then returns to the nose via a branch in the incisive foramen to provide blood to the anterior
septum. The sphenopalatine artery enters the nose near the posterior attachment of the
middle turbinate to supply the lateral nasal wall. It also gives off a branch to provide blood
supply to the septum.
The internal carotid artery contributes to the nasal vascularity through the ophthalmic
artery. This artery enters the bony orbit via the superior orbital fissure and divides into
several branches. The posterior ethmoid artery exits the orbit through the posterior ethmoid
foramen, located 2-9 mm anterior to the optic canal. The larger anterior ethmoid artery
leaves the orbit through the anterior ethmoid foramen. Both of these vessels cross the
ethmoid roof to enter the anterior cranial fossa and then descend into the nasal cavity
through the cribriform plate. Here, they divide into lateral and septal branches to supply the
lateral nasal wall and the septum.
The Kiesselbach plexus, or Little area, is located on the anterior cartilaginous septum and
is the location of most anterior epistaxis. Many of the arteries supplying the septum have
anastomotic connections at this site.
Vascular physiology of the nose
The dynamics of the nasal circulation depends to large extent on the prescence of arterio-
arterial anastamosis between the various arteries which contributes to the vascular supply
of the nose .
The upper 1/3rd of the nose anastamosis between the anterior & posterior ethmoidal arteries
, while above the middle turbinate the branches from the sphenopalatine artery with the
ethmoidal arteries .
The arteriovenous anaastamosis present at the anterior end of the septum & inferior
turbinate is at microscopical level , it is of little important in the aetiology of persistant
epistaxis .
Pathology of the nasal arteries
1. Examination of the middle & smaller arteries of persons dying in the middle & old
age reveal progressive replacement of the muscular tissue in the tunica media by
colllagen & these changes varies from interstitial fibrosis to complete replacement of
muscles by scar tissue , so this give a discription why the arterial bleeding is
Lecture notes in
prolonged ; due to the failure of the artery to contract because of no muscles in the
tunica media .
2. Large vessles (macillary arteray) are prone to calicification (Monckeberg sclerosis)
leading to loss of elasticity .
3. Dissecting anurysm of nasopalatine arteries branches due to unknown cause .
4. Localized ischemia or trauma occur on the retrocollumelar vein which appear as a
localized ballooning overlying the vein which signify the area of vessl wall weakness
due to this trauma .
Epidemiology
- Age ; a ffect all age groups , the anterior epistaxis more in child & younger age (15-25 y)
, while the posterior more in older age group (45-65 y) with hypertension or arterial
sclerosis .
- No sex predilaction .
- Incidence , more common in clder – winter months due to URTI is more frequent &
fluctuation in both temperature & humidity , also common in hot dry climate with low
humidity .
Aetiology
A . Local
1. Congenital
a. Unilateral choanal atresia .
b. Meningocele .
c. Encephalocele .
d. Glioma .
2. Acquired
a. Infective ;
- Acute due to viral infections , fungal or bacterial .
- Chronic ; specific like TB , syphilis , leprosy , rhinoscleroma , or nonspecific like
ozena .
b. Inflamatory ; rhinosinusitis (allergic , vasomotor ...etc) & nasal polyposis .
c. Trauma ; iatrogenic , facial trauma , F.B. , surgery & nose picking .
d. Idiopathic ; Little's area , superior part of the nose , middle turbinate & Woodruff's
plexus .
e. Neoplastic ; benign like transitionalk cell papilloma & angiofibroma or malignant
like sequamous cell ca. , adenocarcinoma , adenoid cystic ca. , olfactory neuroblastoma
, melanoma , lymphoma .
f. Drug induced ; rhinitis medacmentosa (topical decongestant , cocain ...etc) .
g. Inhalants ; tobacco , carrabis , heroin , chrome , mercury , phosphorus , wood dust .
B. General
1. Bleeding disorders
a. Coagulopathies , factors (8& 9) deficiencies , vitamin K difficiency & DIC .
- Inherited coagulation factors deficiences ; i.e. factor VIII (haemophilia A & B) &
factor IX deficiency .
- Acquired ; anticoagulants , liver diseases , vitamin K deficiency , DIC , acquired
inhibitors ... etc .

Lecture notes in
b. Platelets disorders ;
- Decrease platelets account could be congenital or acquired , the acquired due to
bone marrow failure (infilteration , drugs aplasia) , blood loss & increased
consumption (hypersplenism , DIC , massive blood loss) .
- Platelets dysfunction ; congenital like Von-Willbrand's disease , Bernard Saulier
syndrome , Glanzmann's thrombasthenia syndrome , or acquired like
myloproliferative disorders ( leukemia , uraemia , dysparaprotienaemia) , drugs
(aspirin , NSAID) & acquired storage disease .
c. Blood vessl disorders
- Congenital ; osteogenesis imperficta , heridatory haemorrhagic telangectasia ..etc .
- Acquired ; amyloid , vasculitis , vitamin C dificiency .
d. Hyperfibrinolysis ;
- Congenital ; a2 – antiplasmin deficiency .
- Acquired ; malignancy , DIC , fibrinolytic therapy (streptokinase) .
2. Drugs ; aspirin , anticagulants , chloramphenicol , methotrexate , immunosuppression
, alchol , dysprimadole ...etc .
3. Neoplasms .
4. Idiopathic ; inflammatory disorders , sarcoidosis , wegner's granuloma , lethal
midline granuloma .
5. Others ; liver failure , HIV , hypothyroidism .
Clinical managemnt
A. Of spontaneous epistaxis
1) Young patient with recurrent bleeding .
a. Careful history , to establish that the bleeding may be secondary to systemic disease .
b. Examination of the nose for signs of recent bleeding &/or local abuse .
The examination should be extended as possible including the rigid & fibroptic flexible
nasoendoscope in the abscence of any obvious local disease .
Also attention to the septum which often shows the engorged veins at the anterior end
of the Little's area ust behind the collumela .
If the bleeding is recent , microanuerysm seen in the mucosa overlying the vein .
Also see the prominant vasculateure of Little's area .
c. Treatment (contravesial) ;
- LA with 5% cocaine .
- Chemical cauterization with silver nitrates sticks .
- 7 days course of naseptin cream , recently they said given naseptin alone for 4 weeks
is effective .
- Advising the patient ; regarding nose picking & blowing , application of vasaline to
the vestibular & Little's area twice daily , the vasaline decrease recent nose bleeding by
keeping the vessels moist & preventing them becoming dry & friable .
- Sometimes need to applicate trichloroacetic acid with great care that ensure non of
the acid comes in contact with the vestibule because it will cause painful burn .
- If still bleeding , coagulation diathermy UGA or galvano-cautry ULA which is not
recomended in children .
2) Adult – person with recurrent bleeding
a. History & examination (the same as above) , important to ask about alchol , current
medications , blood pressure problems & bleeding disorders .

Lecture notes in
b. Recent epistaxis is less frequent in eldery , but some have one major bleed which is of
no benifit from cauterization to Little's area unless its certain that the bleeding from this
area .
c. Assess the cardiovascular system , then refer the patient to physician for any
abnormalities such as hypertension thats to protect the patient from harmful effect of
hypertension , but not prevent epistaxis .
d. Treatment ;
- Chemical cauterization with silver nitrates sticks ULA .
- Weeks course of naseptin cream , unlike children ineffective hen used alone .
- Electrocautary for anterior epistaxis in resistant cases either ULA or UGA .
- Alteranative Rx like ; SMR , transection of varicose vessels , diathermy & excision of
haemorrhagic nodules .
- SMR –Septoplasty indicated in ; transesction of varicose vessels , interuption of blood
supply to the haemorrhagic nodule , septal turbinates removal of any spurr .
B. Of acute epistaxis
1) In Young patients
a. Resuscitate the patient .
b. Establish the site of bleeder .
c. Stope the bleeding .
- Pinching the nostrile to stop the bleeding from caudal end of the septum .
- Cocain application with causterization of the venous & arterial bleeders .
- Sometimes bleeding persist espicially in children with haematological disorders ,
packing of the nose with either ; vasaline pack , BIPP , nasal baloons (useful in
children & easily inserted) or Ca-Na-alignate which is useful in very young patients
(it can inserted without LA , atraumatic & absorbed locally) .
- Persistant bleeding we use ; posterior packing , causterization UGA , arterial
ligation , replacement therapy (factor VIII) &/or subsequent Rx with DDAVP .
d. Treat the cause .
2) In elderly
a. Resuscitate the patient with observation of BP , PR & general condition , in order
to gauge the extent of blood loss .
b. Estimation of packed cell volume in conucation with Hb% will guide the clinician
from blood transfusion (early blood transfusion should be approached with caustion) .
c. If suspecion of blood dyscrasia , then do bleeding time & clotting time & platelet
count .
d. Examination of the nose in upright position is important , inspect the nose for
spurting blood vessels on the nasal seotum but usually the site of bleeding is
smoothred in blood .
e. Cocaonization of the nose by 5% spray for 3 purposes ;
- Allow the contruction of the cathters so the blood cane sucked away .
- Stop the bleeding by vasoconstruction .
- Give apportunity to localize the bleeding site .
f. Further examination by using nassopharyngoscope , rigid endoscope or microscope .
g. Cauterization of any accessible bleeding point & if the bleeding point is not
accessible , situated back in the septum or bleeding behind the spurr so the use of
nasopharngoscope .

Lecture notes in
h. Stope the bleeding

- For anterior bleeding use anterior packing & admit the patient to the hospital .
- If it is not sure about the site of the bleeding then do bilateral anterior packing
(vasialin pack imprignated with antiseptics or BIPP) , the pack shouldn't left for
more than 48 hours without antibiotics cover but the advantage of BIPP is that it can
be left for several days without fear of complications .
- For the posterior bleeding we use ; Baloon-foley's cathetet as an additional
posterior packing , push along the floor of the nose untill the tip of the cathter visible
below the soft palate , then inflate the baloon with 15 ml of sterile water or air , then
with drawn it to be impacted at the posterior choana , prevent deflation by using
umbilical clamps placed on the cathter at the anterior nares , placing a dental role
between the clamp & the skin to prevent ulceration & scarring , then do anterior
packing to both nasal cavities .
- There is an old method (Trotter's method) in which we sit the patient up with cork
held between the teeth and allow him to bleed untill the patient become hypotensive
& then stop bleeding , but this method may lead to death from coronary thrombosis
secondary to hypotension .
- Old patients with chronic diseases can't tolerate severe & prolonged bleeding .
- The complications of packing are ; (1) uncomfortable (2) life-threatening hypoxia
Nasal ballooning associated with increased efficacy & few complications (headache ,
Eustachian tube obstruction...) , this occur because the balloon expand along the pathways
of least resistance & plolapse into the nasopharynx .
The advantages of balloon are ; easily inserted , less painful , less sedative need , less
hypoxic , while its disadvantages are ; necrosis (nasal mucosa , nasal septum & alar
necrosis) , respiratory obstruction & its cost (expensive) .
The most usefull baloon is the triple lumen type due to the combined anterior & posterior
compression with central canal for both breathing & suction .
Posterior packing indicated in failure of anterior packing (also in haemorrhage following
adenoidectomy) , it is performed either under GA or LA by passing a small cathters into
both nostiles backwards to the oropharynx , then drawn out from the mouth & tied to two
taps which are secured to the pack & then pulling forward of the cathter through the nose &
tied a cross the dental roll to protect the collumela .
BIPP anterior pack inserted , then cover with broad spectrum antibiotics , then after 2-3
days remove the anterior pack , and cut the taps over the collumela & then remove the
posterior pack through the mouth .
Rebleeding occur in patients with aspirin therapy , alchol ingestion & hypertension , these
patient & patients with prlonged bleeding & elderly & unfit patients must be admitted to the
hospital & nursed at sitting position , given an ice pack with sedation to decrease anxity &
decrease blood pressure .
Sedation shouldn't be used with overdose because this will cause increase risk of confusion
& allow blood to drip unnoticed into the pharynx , larynx & trachea causing
bronchopneumonia .
The choice of sedation ; either morphin which is the most popular but cause vomiting , or
diazepam orally or by injection , or when a blood pressure is a problem use nifidipine .
Surgical intervention
When the bleeding is persist inspite of all above measures then we do

Lecture notes in
- Indications ;
1. Patient continues to bleed with or without anterior pack .
2. Patient continues to bleed more than 4-5 days .
3. Profuse haemorrhage .
- The principle is to interrupt the external carotid system which supply 90% of nasal
mucosa .
- Arterial ligation is the method of choice to Rx surgically persistant epistaxis , the arteries
which can be ligated are ; external carotid artey , internal maxillary artery & anterior &
posterior ethmoidal arteries .
- The drop in the local pressure which occur following ligation of the internal maxillary
artery is greater than that following ligation of the external carotid due to the fact that the
maxillary artery lies nearer the source of bleeding .
- Continous bleeding after the ligation of the internal artery may be due to retrograde blood
flow by way of arterio-arterial anastamosis between the branches of the maxillary artery
in the pterygo-palatine fossa , the descending branch of the sphenopalatine artery may be
the possible source of retrograde bleeding into the final portion of the maxillary artery .
- Failure to stop bleeding may be due to ;
a. Ligation of the non dominant maxillary artery .
b. Failure to identify the maxillary artery in the pterygo-maxillary space .
c. Blood flow through the partially closed clips .
d. Bleeding from the posterior ethmoidal arteries .
e. Revascularization of the nasal blood supply .
- Ligation of the external carotid artery less effective because it doesn't produce the same
reduction of local blood pressure as in internal maxillary artery ligation .
- Ligation of the external carotid artery easier & quicker to perform than the internal
maxillary artery ligation , so it is the method of choice in elderly & deblitated patients .
- If the bleeding persist after ligation of the internal maxillary artery it preceeds to ligation
of the anterior ethmoidal artery which is more effective than ligation of anterior ethmoidal
& external carotid artery because the cause of the persistant bleeding its due ti
inadequate drop of pressure in distal external carotid artery with displacement of blood
from one area of the nose to another .
- In case of hypertension , ligation of the internal maxillary artery & anterior ethmoidal
artery at the same time .
- It is better to ligate anterior & posterior ethmoidal arteries at the same time when there is
protracted severe or/& recent bleeding .
The surgical techniques of arterial ligation
- External carotid artery ;
1. Neck curved incision lies over the bifurcation of the common carotid artery (upper
border of the thyroid cartilage) .
2. Exposure of the carotid sheath by dissection of the deep cervical fascia from its
attachment to the sternomastoid muscle , so can expose the carotid sheath lying
between the sternomastoid & the infrahyoid muscles .
3. Open the carotid sheath & identify the carotid bulb & carotid bifurcation .
4. Identify & preserve the hypoglossal nerve , cross lateral to the arteries .
5. identify the external carotid artery by one of its branches , the greater cornue of the
hyoid bone is landmark for facial & lingual arteries .

Lecture notes in
6. ligate the artery in continuity to the ascending pharyngeal artery using 3/0 silk or
linen thread .
7. Closure of the wound in layers with vaccum drain .
- Internal maxillary artery ;
1. UGA , sublabial incision (Caldwell-Luc's) 3 mm at the canine fossa .
2. Elevate the flap , opening the anterior antral wall & avoid compressing the
infraorbital nerve .
3. Penterate the thin posterior wall of the antrum with gauge & remove a peice with
puch forcepes to reveal the periosteum of the posterior wall of the maxilla , this
periosteum incised horizontally from side to side & remove fat of the pterygo-
palatine fossa untill reach tortuos maxillary artery .
4. Divide the artery with clips placed on the larger branches .
5. Antrostomy is optional .
- Anterior ethmoidal artery ;
1. External ethmoidectomy incision .
2. ligate branches of the angular vein , continue the incision down untill reach the
periosteum which is incised in the line of incision .
3. Posterior elevation of the periosteum , 1st at the lacrimal fossa & 2nd at the lamina
papyracea of ethmoid .
4. Lateral retraction of the medial orbital periosteum together with lacrimal sac by self
retaining retractor (Tolbot or Kwango) .
5. Identify the arteries as funneling of orbital periosteum into ethmoid labyrinth at the
junction of the medial & superior walls of the orbit about half way back from the
orbital margin , coagulate it & divide .
6. the Posterior ethmoidal artery 1 cm behind the anterior one .
7. Closure of the incision without drain .
Other surgical methods of treatment
A. Angiography & Embolization ;
- Indications ;
1. Epistaxis due to congenital arterio-venous malformations .
2. Aberrant arterial vessel .
3. Rebleeding after arterial ligation .
4. Nasal tumors .
5. Facial trauma .
6. Interactable cases especially those with posterior bleeding .
- Embolization after localization can't be used for anterior epistaxis because the arterial
supply is from the anterior & posterior ethmoidal artery (mostly) which are branches from
the internal carotid artery .
- Advantages are ;
1. Visulization of the bleeding site close to the source .
2. Occlusion of the vessel close to the site of bleeding which can cause decrease in the
collateral blood flow .
3. repeatable technique & 90% or more successful in expenced hands .
4. Less complications (<0.1%) such as CVA , facial palsy ..etc .
- Contraindications ;
1. Angiographic evidence of a significant anastamosis with internal carotid system .

Lecture notes in
2. severe atheromatous disorders .

3. Allergy to contrast material .
- Angiography technique of two types , direct (through percutaneous route) or indirect
(digital substraction technique) .
- Material used for embolization are ; gelfoam of different size , polyvinyl –alchol &
coiled springs .
B. Submucous resction of the septum ;
Indicated when there is ;
1. Bleeding orginates behind a prominant spurr to improve the access of the inspection
for cautary , packing & interupt the blood supply to the Little's area .
2. Haemorrhagic nodule .
3. Septal turbinate .
4. Patient not respond to nasal packing for >2 days .
C. Endoscopic cautary & ligation ;
Using rigid endoscope , this facillitate greater diagnostic accuracy regading the bleeding
site & facillitate both endoscopic cautary & ligation .
Unusual causes of epistaxis
A. Osler's disease (Haemorrhagic familial telengectasia)
- Autosomal dominant disease , clinically as red spots on lips & mucous memberane of
the mouth , espicially the tongue as well as face & nose , lesions in the nose causing
epistaxis (more liable to bleed) which is commonly bilateral .
- The condition may be complicated by the prescence of a bleeding lesions in the lung ,
gut & genitourinary system .
- Treatment by ;
1. Oestrogen , decrease the frequency & severity of the bleeding by inducing sequamous
metaplasia of the mucosa of the nose but it is unsuitable for males .
2. Radiotherapy . 3. Diathermy cautary or LASER cautary .
4. Cryosyrgery 5. Microembolization .
- In mild cases packing & repeated transfusion .
- More severe cases may need septal-dermoplasty or alternative is Young's procedure
(bilateral nasal closure which stop bleeding by preventing repeated trauma) , this
operation also indicated for epistaxis due to atrophic rhinitis or large septal perforation
, some said that Young's operation is the Rx of choice of Osler's disease .
B. Bleeding diatheses ;
- Epistaxis may be caused due to clotting defects , increased capillary fragility or platelet
deficiency , when these suspected the patient should have ;
1. Full clinical examination with careful search for ; purpura , brusing , swellen joints .
2. Investigations ; Hess's test , Clotting time , bleeding time , platelets count & specific
test for coagulation factors to exclude Chrismas disease & haemophilia .
- Treatment by blood transfysion with avoidance of traumatic packing of the nose .
C. Nasopharyngeal angiofibroma ;
- Mainly in adolescent male , due to vascular malformation , charcterized by severe
epistaxis & local sepsis with disability .
- Diagnosis by anatomical imaging ; MRI followed by arteriography .
- Treatment by surgical removal by external incision or midfacial degloving approach ,
also embolization may be helpful prior to surgery or in recurrent cases .

Lecture notes in
RHINITIS
Allergic rhinitis
An IgE mediated hypersensitivity disease (Type I) of the mucous memberane of the nasal
airways charcterized by sneezing , itching , watery nasal discharge & sensation of nasal
obstruction , it is associated with allergic conjunctivitis & asthma .
Incidence
- Occur in 30% of the population , it is occur in atopic individual , it is either seasonal
(summer hay fever) or perennial .
- Sex ; Males and females tend to be affected by allergic rhinitis in fairly equal proportions.
- Age ; Allergic rhinitis appears mainly to affect individuals younger than 45 years , the
condition may begin to appear in patients as young as 2 years and usually reaches a peak in
those aged 21-30 years , it then tends to remain stable or slowly decrease until patients are
aged 60 years, when again the prevalence may increase slightly.
Aetiology
1. Allergy is a hypersensitivity reaction of the tissue to certain substances called
allergens like pollens , moulds , house dustmite , animal epithelia ...etc , they cause
seasonal or perennial rhinitis .
2. Atopy , in which there elevated total IgE (or +ve skin test) or elevated allergens
speciefic IgE concentrations , so the patients have a tendency to develope an exagurated
IgE antibody response (reflected by +ve skin prick test) .
3. Food & drug induced rhinitis , the patient here atopic with sensitivity to aeroallergens
causing nasal , mouth , tongue & digestive tract symptoms , while foods like milk , eggs &
cheese , nuts , fish , shellfish & citrus fruits , Drugs like aspirin , tenormin & inderal .
4. Pollution can play role , like perfumes , tobacco , traffic fumes & domestic sprays .
Pathophysiology
After initial exposure to an antigen, antigen-processing cells (macrophages) present the
processed peptides to T helper cells . Upon subsequent exposure to the same antigen, these
cells are stimulated to differentiate into either more T helper cells or B cells. The B cells
may further differentiate into plasma cells and produce immunoglobulin E (IgE) specific to
that antigen . Allergen-specific IgE molecules then bind to the surface of mast cells,
sensitizing them.
Further exposures result in the bridging of 2 adjacent IgE molecules (at the Fab portion of
the allergen , the Fc portion attache to the mast cell& basophils) , leading to disruption of
the mast cells & degranulation of the lysosomes which lead to the release of preformed
mediators from mast cell granules . These mediators (ie, prosteoglandins , histamine,
leukotrienes , kinins) cause the cappilaries to be more permeable , decrease the viscosity of
the ground substance by hyaluronidase , eosinophils infilteration leading to the early-phase
symptoms such as sneezing , irritation , rhinorrhea , odema and congestion . Late-phase
reactions begin 2-4 hours later and are caused by newly arrived inflammatory cells .
Mediators released by these cells prolong the earlier reactions and lead to chronic
inflammation .

Lecture notes in
Clinical features
- History
A. Allergy history ; For the physician who treats patients with allergic rhinitis, nothing is
more crucial than the allergy history. It is important not only in identifying an allergy but
also in guiding the treatment plan.
B. Family history ; children of individuals with allergies have been shown to have a
higher incidence of allergies than that of other children , if both parents have allergies,
their child has a 50% chance of having the same problem.
C. Past medical history ; In children, a history of recurrent otitis media, upper
respiratory tract infection, asthma, chronic rashes, and formula intolerance are
suggestive of allergies . Other pertinent medical problems (eg, asthma, aspirin
hypersensitivity) and the use of medications (eg, beta-blockers, tranquilizers) that could
interfere with the treatment for allergies should be evaluated. Inquire about the results of
previous allergy tests and treatment.
D. Symptoms ; 2 out of 3 ; (1) sneezing due to histamine release (2) rhinorrhea which is
the response of seromucous glands to mast cells /basophils derived mediators (3) nasal
blockage or obstruction due to vascular engorgement with resultant vasodilatation &
odema formation (4) others ; itching of the eyes , nose & palate due to histamine release
& s.t. even red eye (esp. in hay fever) (5) s.t. burning sensation in the throat & asthma
symptoms like wheezing & chest tightness .
- Examination
A. Face ; patients with allergic rhinitis frequently grimace and twitch their face, in
general, and nose, in particular, because of itchy mucus membranes , chronic mouth
breathing secondary to nasal congestion can result in the typical adenoid facies.
B. Eyes ; patients may have injected conjunctiva; increased lacrimation; and long, silky
eyelashes , Dennie-Morgan lines (creases in the lower eyelid skin) and allergic shiners
(dark discoloration below the lower eyelids) caused by venous stasis may be present.
C. Ears ; ears are frequently unremarkable , eczematoid otitis externa and middle ear
effusion may be present.
D. Nose ; a transverse nasal crease may be present because of the patient's repeated
lifting of the nasal tip to relieve itching and open the nasal airway , the turbinates are
frequently hypertrophic and covered with a boggy pale or bluish mucosa , nasal
secretions can range from clear and profuse to stringy and mucoid , presence of polyps
does not necessarily indicate that the affected individual has allergic rhinitis.
E. Mouth ; a high arched palate, narrow premaxilla, and receding chin may be present
secondary to long-term mouth breathing , the posterior oropharynx may be granular
because of irritation from persistent postnasal discharge.
Investigations
1. Skin prick test ; inexpensive , accurate , rapid & can be undertaken with a wide variety
of allergens at a single skin prick testing session , they diagnose or exclude the atopy &
support the history , if the patient has allergy then the response will be wheal & flare
within 20 min. .
The skin test may be invalid in patient on antihistamines , patient with severe eczema or
patient with dermatographism , it always include a positive control (histamine 10 mg/ml)
& a negative control test (allergen diluted) .

Lecture notes in
If an adverse reaction occurs , a tourniquet should be placed proximally to contain it &

give i.v hydrocortisone , allermine & adrenaline .
In general, the acute phase starts within 2-4 minutes and reaches a maximum in 10-20
minutes. It may be followed by a late phase 4-6 hours later.
A number of factors affect the responses; these include the following ; (1)Volume and
potency of the antigen (2) Reactivity of the skin (3) Age and race of the patient (4) Area
of body tested (5) Distance between the injections and time of day of testing (6)
Medications (eg, antihistamines and tricyclic antidepressants) .
2. Blood tests ; (a) Total serum IgE level measured in the plasma radioimmunosorbant
test , or in the radioallergosorbant test to speciefic allergen (b) ELISA (Enzyme Linked
ImmunoSorbant Assay) which depend on the developement of colour reaction .
3. Nasal smear ; taken by scrubing of the lateral nasal wall , put the smear on the slide &
stain with Gimsa , this shows eosinophils , neutrophils , mast cells , epithelial cells &
bacteria (not Dx) , swab should also taken for bacteriology .
4. Provocation test ; a drop of suspected allergen put in the nose resulting in rinorrhea &
sneezing , this effect measured objectively by rhinomanometry .
Treatment
1. Avoidance of the percipitating allergen which is obviously helpful ,but always possible ,
this done by mattress covers , pillows covers & bedding (which is the major source of house
dustmite) , vaccuming , liquid nitrogen , acaricides , humidity of the home (regulation of
ventilation) .
2. Oral antihistamines , once daily , like asetamazole , cetrizine , terfenadine & oratidine ,
these cause no drowsness .
3. Total topical steroid sprays & drops ; the corner stone in the Rx of rhinitis (safe &
effective) , like beconase spray (S/E crusting & bleeding) .
4. I.M injection of steroid (Depot like Depomedrol) , if the symptoms interfer with special
events like exam. in schools .
5. Sodium cromoglycate for prophylaxis (4-6 times /d) , it is mast cell stabilizer .
6. Desensitization , use in pollen allergy , we inject small amount of pollen in purified form
in the hope that blocking IgG antibodies (immunotherapy) , S/E anaphylaxis , so need
resuscitation by i.v H.C. , allermine & adrenaline .
7. Surgical mangement ; turbinate surgery like SMD or even turbinectomy .
Complications
1. Allergic rhinitis is frequently associated with otitis media with effusion (not an allergic
disease per se , but a frequent complication of nasal allergy especially in children) ,
rhinosinusitis (due to obstruction of the sinus ostea & also the perennial rhinitis has
features of sinusitis), and asthma, either as a precipitating and/or aggravating factor or a
symptomatic comorbid condition.
2. Allergic rhinitis can significantly decrease the quality of life and impair social and work
functions, either directly or indirectly, because of the adverse effects of medications taken to
relieve the symptoms.
Intrinsic rhinitis
Definition
Non infectious , non allergic condition of the nasal mucosa charcterized by nasal
obstruction & watery rhinorrhea of unknown aetiology .

Lecture notes in
Idiopathic nasal congestion & rhinorrhea that is not associated with sneezing or nasal
itching , after the other causes of rhinitis are ruled out .
It is a symptom complex produced by several pathological conditions .
Terminology
o Intrinsic rhinitis .
o Vasomotor rhinitis .
o Non-allergic , non-infectious perennial rhinitis
o Intrinsic rhinopathy ; as some of the causes had no pathological evidence of
inflammation
Nasal Physiology
Nasal function include ; temperature regulation , olfaction , filtration & humidification of
inspired air .
Also the nasal lining produce secretions that contain immunoglobulins (mainly IgA) ,
protiens , enzymes which provide lubrication & protection .
Secretions traps particles matter & then propel them (by ciliary movement) towards the
natural ostea (mucus blanket stream in a rate of 2.5-7.5 ml/min.) .
The innervations of the nasal mucosa highly organized & complex , regulating the mucosal
vasculature & glandular secretions by autonomic nervous system ;
o Sympathetic half of the efferent arc causing vasoconstriction .
o Parasympathetic half of the arc causing glandular secretion
The sensory innervations from the trigeminal nerve , which its sensory ending stimulated by
inflammatory mediators (e.g. histamine) & inhalated irritants (e.g. smoke) .
Pathophysiology
Disorder of any components of the nasal mucosa will produce the disease .
Hyper-responsiveness of the afferent sensory limb will cause an exaggerated efferent
response to neural stimuli . The result is over secretion of the mucus & increased nasal
congestion as a result of cappillary plasma exudation . The same seen with normal sensory
& hyperactive efferent response .
Generally it though to be due to imbalance in between the parasympathetic ( increased)
&/or sympathetic (decreased) .
Pathology
It is divided into two types on the basis of the numbers of eosinophils found in the nasal
secretions & to some extent the clinical features ;
o Non-eosinophilic rhinitis ; it is twice as common as the eosinophilic type , it is due to
imbalance in the autonomic nerve supply , it is due to ; decrease in the sympathetic
system activity causing nasal obstruction , while increase the activity of the
parasympathetic system causing rhinorrhea which is severe here (Rhinorrhea
syndrome).
o Eosinophilic rhinitis ; it is an intrinsic mucosal disorder of prostaglandin
metabolism , usually associated with aspirin hypersensitivity , asthma & nasal
polyposis (Nasal obstruction syndrome).
Microscopically ; there is glandular hyperplasia & submucosal vascular dilation
Macroscopically ; the nasal mucosa becomes hyperaemic & hypertrophic & inferior
turbinate hypertrophy with nasal polyposis (commoner than in allergic rhinitis) .

Lecture notes in
Predisposing factors
1. Family tendency (some authors regards this –ve) .
2. Preceding infection ; viral or bacterial rhinitis .
3. Psychological & emotional factors .
4. Endocrine ; puberty , menstruation & pregnancy .
5. Drugs ; beta blockers , aldomet , oral CCP , aspirin ..etc
6. Pollution ; fumes , dust , industrial detergents , car engine & other pollutants .
7. Atmospheric condition ; change in humidity & temperature .
8. Alcohol & Smoking .
Clinical assessment
It account for about 40-70% of all cases of perennial rhinitis .
The symptoms are ;
1. Nasal obstruction .
2. Watery rhinorrhea & postnasal drip .
3. Itching & sneezing are not marked like in allergic rhinitis (mostly absent) .
The signs are ;
1. Diminished nasal patency .
2. Red , angry , injected & odematous mucosa .
3. Copicious watery mucoid secretions .
4. Hypertrophid , both middle & inferior turbinates .
5. Polyps & lymphoid hyperplasia may be seen .
Eosinophilic Non-eosinophilic
- Symptoms
1 Obstruction Moderate / severe Mild
2 Rhinorrhea Mild / Moderate Severe
3 Sneezing / Pruritis Minimal Minimal
4 Hyposmia Usual Rare
- Signs
1 Mucosal swelling Marked Mild
2 Inf. Turbinate hypertrophy Marked Mild
3 Polyps Frequent Never
4 Sinus mucosal thickening Frequent Rare
Investigations
1. Serum testing ; IgE estimation by PRIST & RAST .
2. Skin testing can be used to indicate an allergy .
3. Radiological exam. of the sinuses may Diagnose sinusitis .
4. Nasal cytology brushings to assess the proportion of eosinophils & neutrophils
(suggest infection) .
5. Acoustic rhinometry ; objective measure of nasal patency .
Diagnosis
Intrinsic rhinitis are diagnosis of exclusion & the aim is to identify the other causes of
rhinitis .
o History must show the pattern & timing of symptoms , aggravating & relieving
factors , environmental triggers , exclusion of allergies & systemic diseases (e.g.
collagen disease , endocrine disorders ..etc) .
o Examination ; thorough head & neck exam .

Lecture notes in
o Investigations .
Treatment
A. Medical treatment
1. Patient education to avid triggers & have regular exercises (help to decrease nasal
obstruction) .
2. Rinsing the nose with normal saline will cleansing the nose , improving the ciliary
function & the mucociliary clearance .
3. Topical nasal steroids ; like beconase or methadine drops , sometimes short course
of systemic steroids .
4. Systemic & local decongestant ; topical like xylometazoline (short course) &
systemic like psuedoephdrine .
5. Systemic antihistamine ; used in some cases .
6. Topical anticholinergic ; like ipratropium bromide (for non-eosinophilic type) .
7. Interluekien antagonists ; not totally proved .
8. Mast cell stabilizers , topical sodium cromoglycate (Intal) & systemic Ketotifin (oral)
B. Surgical treatment
Useful for the control of symptoms especially nasal obstruction & rinorrhea when the
medical mangement become ineffective .
oMangement of nasal obstruction
1. Turbinate reduction ;SMD , linear diathermy , LASER cautery & multiple out
fractures , all these are successful in the short term but recurs after 1-2 yrs .
2. Turbinate resection ; partial turbinectomy , submucosal turbinectomy & total inf.
turbinectomy , this more successful for long term symptoms control , but with higher
morbidity (i.e. haemorrhage postop.) .
In the Rx of nasal obstruction it is neccessary to manage the concomitant causes of
obstruction like septal spurs & nasal polyps .
o Mangement of rhinorrhea ; by vidian neurectomy in which we divide the
parasympathetic nerve supply to the nose as the nerve of pterygoid canal (vidian n.)
enters the pterygopalatine fossa , but >50% of patients relapsed within one year due to
reinnervation .
Infective rhinitis
Atrophic rhinitis
It is a chronic nasal disease charcterized by progressive atrophy of the nasal mucosa & the
underlying bone of the turbinates & the presence of viscid secretions which rapidly dries &
forms crusts which emit a charecteristic foul odour (called ozena) , there is also an
abnormal patency of the nasal passages .
Aetiology ; unkown :
1) in the past , MO like Coccobacillus , Bacillus mucous , Coccobacillus foetidus ozena ,
Diphtheroid bacilli & Klebsiella ozaena , founds in clusters with little evidence that they
cause the disease .
2) other factors "possible causes" ; chronic sinusitis , excessive surgical destruction of
the nasal mucous membrabes & Syphilis causing secondary atrophic rhinitis .
3) it is commonest at puberty , much more in female than male , so accepted that the
endocrine imbalance may play a rule .
4) heridity & racial influence (yellow , latin & american negros) .

Lecture notes in
5) auto-immune disease , percipitated primarly by viruses , malnutrition or

immunedeficiency , all trigoring the destructive autoimmune process which relase the Ag
of nasal mucosa into the circulation .
6) poor nutrition ( i.e. iron deficiency disease) .
Pathology ; all authors agree that :
1) there is a patches of metaplasia from col. Cilliated to seq. epithilium .
2) there is decrease in the no. & size of the compound alveolar glands .
3) dilated cappilaries .
Taylor & Young in 1961 are demonstrate the disease according to
A.Presence or abscence of the endarteritis & periarteritis of the terminal arteries ,
dividing it into 2 types;
Type I ; charcterized by the prescence of the endarteritis & periarteritis of the terminal
arteries which is due to chronic infection , so it get benifit from the vasodilatation effect of
oestrogen therapy .
Type II ; there is vasodilatation of the cappilaries which might be worse with oestrogen
therapy .
B.Endothelial cells of the dilated capillaries have more cytoplasm than normal , shows
+ve reaction to the Alk. Phosphatase "active bone resorption" which is a feature of the
disease .
Clinical features
- The presenting Symptoms are ;
1. nasal obstruction sensation despite the wide nasal cavity .
2. epistaxis .
3. ansomia (s.t.) , foul stench (don't demonstrated by the patient) .
4. chocking (s.t.) due to pharyngitis sicca when the detached crusts slip from the
nasopharynx into the oropharynx .
- Signs ;
1. O/E we find simillar atrophic changes seen in the nose , pharynx & larynx .
2. foetor in all patients .
3. the mucosa lined with green , yellow & black crusts .
4. enormous capacity of the nasal cavity .
5. detachment of the crusts reveals bleeding & ulcerated mucosa & shrivelled
turbinates .
Investigations
- Plain X-ray of paranasal sinuses or even proof puncture to exclude the presence of
sepsis in the sinuses .
- Swab from the nasal secretions send for culture " not important ".
- Serological tests to exclude Syphilis .
- CBP , S. Protiens & iron should be checked .
Treatment
1. conservative Medical Rx
- douche the nose twice daily with an alkaline solution prepared by disolving a
teaspoonful of powder (sodium bicarbonate 28.4 g or sodium chloride 56.7 g) in a
half pint (280 ml) of warm water .
- regular nasal cleansing is the basis of the conservative Rx " freedom of ozaena" .

Lecture notes in
- removal of the crusts by forceps or suction , then apply either ; (1)25% glucose in
glycerin which inhibit the proteolytic organisms , or (2)oestradiol in arachis oil
10000 unit/ml , or (3)kemicetive antiozaena solution , each ml containing
chloramphenicol 90 mg , oestradiol diprpionate 0.64 mg , vit. D2 900 IU & propyle
glycole .
- use of potassium iodide by mouth which object of increasing the nasal secretion .
- autogenous vaccines ; (1) tissue therapy with systemic human placental extract
shows 80% improvement within 2 years , or (2)submucosal intranasal injection of
human placental extract which shows 93% relief .
- refampicin 600 mg orally once daily for 12 weeks
2. Surgical Rx
- Lantense stage ; submucous injection of parrafin to replace the lateral nasal wall
medially .
- Recently ; teflon strips , polythelene & cartilage have been inserted after flaps of the
mucoperiosteum .
- By Wilson at 1964 ; submucousal injection of a suspention of powdered teflon in
50% glycerin paste .
- Young at 1967 ; closure of one or both nostrils by plastic surgery ,then after months
to years the nostrils have been reopened & shows abscence of the crusts & normal
mucosa .
- Partial nostril closure leaving 3 mm hole well tolerated & gave simillar results with
no recurrence of the disease over 2 years period .
- Chatteri at 1980 ; autologous medullary cancellous bone graft as a single long piece
of bone .
- Repeated stellate ganglion blocks " cervical sympathectomy – 1st line of Rx "
Rhinitis Sicca
Ill defined crusting condition affecting the anterior 1/3rd of the nasal cavities of the patient
who works in dusty surroundings .
Periglandular fibrosis & metaplasia of the cilliary epithelium result in a viscid & stagnant
mucous blanket which forms crusts .
These are not foeted but , blood stained & may lead to a septal perforation , there is no
generalized atrophic changes or any increase in the calibre of the airways .
Managed by the correction of the occupational surroundings & lubrication by sprays ,
paints or ointments .

Lecture notes in
SINUSITIS
Anatomy
Several bones that surround the nose are hollow and the spaces contained within, the
paranasal sinuses, are named for the skull bone in which they lie.
The paranasal sinuses are air-filled bony cavities that extend from the skull base to the
alveolar process and laterally from the nasal cavity to the inferomedial aspect of the orbit
and the zygoma. They are lined with pseudostratified columnar epithelium that is
contiguous, via ostia, with the lining of the nasal cavity .
This epithelium contains a number of mucous-producing goblet cells. The arterial supply of
the paranasal sinuses is from branches of the internal and external carotid arteries, while
the venous and lymphatic drainage path is through the sinus ostia into the nasal cavity
plexus. In addition, venous drainage occurs through valveless vessels corresponding to the
arterial supply. The focal point of sinus drainage is the ostiomeatal complex, which is
located in the middle meatus and is composed of the maxillary, frontal, and anterior
ethmoid ostia. The posterior ethmoids empty into the superior meatus, and the sphenoids
empty into the sphenoethmoidal recess .
The roots of the upper premolar and molar teeth project into the maxillary sinus, often
separated from the contents of the sinus only by the mucous membrane that lines the sinus
cavity.
The exact function of the paranasal sinuses is not well understood. The possible roles of the
sinuses may include reducing the weight of the skull; dampening pressure; humidifying and
warming inspired air; absorbing heat and insulating the brain; aiding in sound resonance;
providing mechanical rigidity; and increasing the olfactory surface area.
The sinus mucosa has less secretory and vasomotor function than the nasal cavity does.
Cilia are concentrated near and beat toward the natural sinus ostia. Blockage of the ostium
results in stasis of mucous flow, which can lead to development of disease.
Embryology
The development of the paranasal sinuses begins in the third week of gestation and
continues until early adulthood .
During the third week of embryonic development, proliferation and medial migration of
ectodermal cells form the notochord. After the heart tube and pericardium have rotated
from the cranial position to lie anteriorly, the notochord, which is initially in the caudal
region of the embryonic disc, rotates to lie posterior to the primitive foregut. The paraxial
layer of mesenchyme, which lies adjacent to the notochord, differentiates into the somite
ridges, intermediate cell mass, and lateral plate mesoderm. From these mesodermal
structures the branchial arches develop, the first of which gives rise to internal nasal
structures.
The paranasal sinuses develop in conjunction with the palate from changes in the lateral
wall of the nasal cavity .
At 40 weeks' gestation, 2 horizontal grooves develop in the mesenchyme of the lateral wall
of the nasal cavity .
Proliferation of maxilloturbinate mesenchyme between these grooves results in an
outpouching of tissue medially into the nasal lumen. This outpouching is the precursor of

Lecture notes in
the middle and inferior meatus as well as the inferior turbinate. Ethmoidoturbinate folds
develop superiorly to give rise to the middle and superior turbinates. Once the turbinate
structures are established, sinus development begins and continues until early adult life.
Pathophysiology
The contributory factors in the development of chronic sinusitis either ;
1. Local ; whenever two mucosal surfaces came into direct contact , localized disrubtion
of the mucocilliary clearance leading to retention of secretion the area of contact
preventing or slowing the drainage predispo\sing to infection & leading to inflamation &
odema leading to further increase in contact (vicious circle) .
There are anatomical variants , usually one or more of them presented in 60% of patients
with chronic rhinosinusitis , these are ;
(a) Concha bullosa (b) Enlarged ethemoid bullae (c) everted uncinate process
(d) paradoxical middle turbinate (e) Agger nasi pneumotization
(f) Haller cells (g) septal deflection .
But , the important factor is whether or not narrowing of the OMC is present .
2. Systemic
(a) Mucocilliary abnormalities ;
1. Primary , as ; primary cilliary dyskinesia , cystic fibrosis , Young’s syndrome , these
lead to secondary bacterial infection .
2. Secondary , as ; allergy , found in the 2/3 rd of patient with chronic sinusitis , bacterial
infection which is either acute like Strp. Pneumonia & H. influenza , or chronic like
anaerobes & the above .
(b) Immune-deficiency ;
. Primary , common variable immune diffeiciency , IgG subclass difficiency , selective
antibody difficiency , IgA difficiency & C4 difficiency ( it is unclear whether these arise
as a consequence of chronic sinusitis , or are a contributory factor in the development of
chronoc infection ) .
2. Secondary , HIV infection & immunosuppressant drugs .
(c) Allergy .
Acute sinusiitis
Acute sinusitis may be defined as a bacterial or viral infection of the sinuses of fewer than 4
weeks duration that resolves completely with appropriate treatment.
Subacute sinusitis represents a temporal progression of symptoms for 4-12 weeks.
Recurrent acute sinusitis is diagnosed when 2-4 episodes of infection occur per year with at
least 8 weeks between episodes, and, as in acute sinusitis, the sinus mucosa completely
normalizes between attacks.
Pathophysiology
The sinuses are normally sterile under physiologic conditions.
Purulent sinusitis can occur when ciliary clearance of sinus secretions decreases or when
the sinus ostium becomes obstructed, which leads to retention of secretions, negative sinus
pressure, and reduction of oxygen partial pressure. This environment is then suitable for
growth of pathogenic organisms.
Factors that predispose the sinuses to obstruction and decreased ciliary function are ;

Lecture notes in
1. Allergic, nonallergic, or viral insults, which produce inflammation of the nasal and sinus
mucosa and result in ciliary dysmotility and sinus obstruction.
Approximately 90% of patients who have viral upper respiratory tract infections (URTIs)
have sinus involvement, but only 5-10% of these patients have bacterial superinfection
requiring antimicrobial treatment.
2. Anatomical variations that narrow the ostiomeatal complex, including septal deviation,
paradoxical middle turbinates, and Haller cells, make this area more sensitive to
obstruction from mucosal inflammation.
3.Mechanical obstruction of the ostiomeatal complex from foreign bodies, polyps, or tumors
can also result in acute sinus disease.
4. Systemic diseases that result in decreased mucociliary clearance, including cystic fibrosis
and Kartagener syndrome, can be predisposing factors for acute sinusitis in rare cases.
5. Patients with immunodeficiencies (eg, agammaglobulinemia, combined variable
immunodeficiency, and immunodeficiency with reduced immunoglobulin G [IgG]– and
immunoglobulin A [IgA]–bearing cells) are also at increased risk of developing acute
sinusitis.
Acute sinusitis in the intensive care population is a distinct entity, occurring in 18-32% of
patients with prolonged periods of intubation, and is usually diagnosed during the
evaluation of unexplained fever. Cases in which the cause is obstruction are usually evident
and can include the presence of prolonged nasogastric or nasotracheal intubation.
Moreover, patients in an intensive care setting are generally debilitated, predisposing them
to septic complications, including sinusitis.
6. Ciliary function is also reduced in the presence of low pH, anoxia, bacterial toxins,
smoking, dehydration, foreign bodies, and drugs (eg, atropine, antihistamines,
phenylephedrine).
7. Approximately 10% of cases of acute sinusitis result from direct inoculation of the sinus
with a large amount of bacteria.
8. Dental abscesses or procedures that result in communication between the oral cavity and
sinus can produce sinusitis by this mechanism. Facial trauma or large inoculations from
swimming can produce sinusitis as well .
Causes
The bacteria most commonly involved in acute sinusitis are part of the normal nasal flora.
These bacteria can become sinus pathogens when they are deposited into the sinuses by
sneezing, coughing, or direct invasion under conditions that optimize their growth.
The most common bacterial pathogens in acute sinusitis are Streptococcus pneumoniae (30-
40%), Haemophilus influenzae (20-30%), and Moraxella catarrhalis (12-20%).
Staphylococcus aureus and Streptococcus pyogenes are isolated in rare cases.
Sixty-six percent of patients with acute sinusitis grow at least 1 pathogenic bacterial
species on sinus aspirates, while 26-30% percent of patients have multiple predominant
bacterial species. Anaerobic organisms have been found in fewer than 10% of patients with
acute bacterial sinusitis, despite the ample environment available for their growth. The
exceptions are in sinusitis resulting from a dental source and in patients with chronic sinus
disease, in whom anaerobic organisms are usually isolated.

Lecture notes in
Gram-negative organisms, including Pseudomonas aeruginosa (15.9%), Escherichia coli

(7.6%), Proteus mirabilis (7.2%), Klebsiella pneumoniae, and Enterobacter species,
predominate in nosocomial sinusitis, accounting for 60% of cases. Polymicrobial invasion
is seen in 25-100% of cultures. The other pathogenic organisms found in nosocomial
patients are gram-positive organisms (31%) and fungi (8.5%). Viruses are the most
common trigger of acute sinusitis. Rhinovirus, influenza, and parainfluenza viruses are the
primary pathogens in 3-15% of patients with acute sinusitis.
Diagnosis
(1) History
Acute sinusitis is a clinical diagnosis; thus, an understanding of its presentation is of
paramount importance in differentiating this entity from allergic or vasomotor rhinitis and
common URTIs. No specific clinical symptom or sign is sensitive or specific for acute
sinusitis, so the overall clinical impression should be used to guide management.
A history of purulent secretions, facial or dental pain, symptoms that last beyond 7-10 days,
and/or a poor response to nasal decongestants suggest a diagnosis of acute sinusitis. In a
patient in intensive care, acute sinusitis should be suspected in the presence of sepsis of
unknown origin.
(2) Physical
- Anterior rhinoscopic examination, with or without a topical decongestant, is important to
assess the status of the nasal mucosa and the presence and color of nasal discharge.
Predisposing anatomical variations can also be noted during anterior rhinoscopy.
- Sinus transillumination and palpation are of little predictive value.
- A basic evaluation of ocular and neurological function is also necessary in order to rule
out potential complications.
(3) Endoscopic examination may reveal the origin of the purulent discharge from the
middle meatus and may provide information about the nature of ostiomeatal obstruction.
The use of endoscopy may also aid in the etiologic diagnosis of acute sinusitis by allowing
the careful attainment of purulent secretions from the sinus ostia for culture.
(4) Lab Studies
- laboratory tests including sedimentation rate, white blood cell counts, and C-reactive
protein levels help to diagnose acute sinusitis. These tests appear to add little to the
predictive value of clinical findings in the diagnosis.
- Cultures are not routinely obtained in the evaluation of acute sinusitis but should be
obtained in a patient in intensive care or with immunocompromise, in children not
responding to appropriate medical management, and in patients with complications of
sinusitis.
- Because the nose is colonized with multiple nonpathogenic species of bacteria, care must
be taken when evaluating culture results. A specific organism is considered pathogenic
when more than 104 colony-forming units of the species are grown on culture or when
polymorph counts are greater than 5000 cells/mL.

Lecture notes in
(5) Imaging Studies

- Imaging studies are not necessary when the probability of sinusitis is either high or low
but may be useful when the diagnosis is in doubt, based upon a thorough history and
physical examination.
- Plain sinus radiographs may demonstrate mucosal thickening, air-fluid levels, and sinus
opacification. Limitations of plain films include interobserver variability, inability to
distinguish infection from a polyp or tumor disease, and poor depiction of the ethmoid and
sphenoid sinuses.
- CT scanning has poor specificity for the diagnosis of acute sinusitis, demonstrating sinus
air-fluid levels in 87% of individuals with simple URTIs and 40% of asymptomatic
individuals. CT scanning is the modality of choice, however, in specific circumstances such
as in the evaluation of a patient in intensive care, when complications are suspected, or in
the preoperative evaluation of surgical candidates. CT scanning can give valuable
information regarding the anatomical and mechanical contributions in the development of
acute sinusitis. Coronal views with bone windows are the preferred sinus study for
evaluating each of the sinuses as well as the ostiomeatal complex.
- Magnetic resonance imaging (MRI) is excellent for evaluating soft tissue disease within
the sinuses, but it is of little value in the diagnostic workup for acute sinusitis.
Treatment
Medical Care
- The primary goals of management of acute sinusitis are to eradicate the infection,
decrease the severity and duration of symptoms, and prevent complications.
- Most patients with acute sinusitis are treated in the primary care setting.
- Further evaluation is recommended when (1) continued deterioration occurs with
appropriate antibiotic therapy, (2) episodes of sinusitis recur, (3) symptoms persist after 2
courses of antibiotic therapy, or (4) comorbid immunodeficiency, nosocomial infection, or
complications of sinusitis are present.
- The goals of management of acute sinusitis are the provision of adequate drainage and
appropriate systemic treatment of the likely bacterial pathogens.
- Drainage of the involved sinus can be achieved both medically and surgically .
Aggressively treat patients in intensive care who develop acute sinusitis in order to avoid
septic complications.
- Consider removal of nasotracheal and nasogastric tubes and promote drainage either
medically or surgically.
- Medications ;
A. Medical drainage is achieved with ;
1. Topical and systemic vasoconstrictors. Oral alpha-adrenergic vasoconstrictors,
including pseudoephedrine and phenylephrine, can be used for 10-14 days to allow
for restoration of normal mucociliary function and drainage. Because oral alpha-
adrenergic vasoconstrictors may cause hypertension and tachycardia, they may be
contraindicated in patients with cardiovascular disease. Oral alpha-adrenergic
vasoconstrictors may also be contraindicated in competitive athletes because of
rules of competition. Topical vasoconstrictors (eg, oxymetazoline hydrochloride)

Lecture notes in
provide good drainage, but they should be used only for a maximum of 3-5 days,
given the increased risk of rebound congestion, vasodilatation, and rhinitis
medicamentosa when used for longer periods.
2. Mucolytic agents (eg, guaifenesin, saline lavage) have the theoretical benefit of
thinning mucous secretions and improving drainage. They are not, however,
commonly used in clinical practice in the treatment of acute sinusitis.
3. Intranasal steroids have not been conclusively shown to be of benefit in cases of
acute sinusitis.
4. Antihistamines are beneficial for reducing osteomeatal obstruction in patients
with allergies and acute sinusitis; however, they are not recommended for routine
use for patients with acute sinusitis. Antihistamines may complicate drainage by
thickening and pooling sinonasal secretions.
B. Antibiotics ; In cases of suspected or documented bacterial sinusitis, the second
principle of treatment is to provide adequate systemic treatment of the likely bacterial
pathogens (ie, S pneumoniae, H influenzae, M catarrhalis). The physician should be aware
of the probability of bacterial resistance within their community. Approximately 44 % of H
influenzae and almost all of M catarrhalis strains have beta-lactamase–mediated resistance
to penicillin-based antimicrobials in children. As many as 64% of S pneumoniae strains are
penicillin-resistant because of altered penicillin-binding proteins. Multiple drug–resistant S
pneumoniae strains are also found in substantial numbers of children in daycare settings.
1. Initial selection of the appropriate antibiotic therapy should be based on the likely
causative organisms given the clinical scenario and the probability of resistant strains
within a community.
2. The course of treatment is usually 14 days .
3. Criteria of antibiotic selection are (1) current sinus puncture study results
demonstrating bacteriologic response; (2) knowledge of changing antimicrobial resistance
in a community; (3) history of medication allergy, especially the sulfa drugs and
cephalosporins; (4) adverse effect profile of the medication; (5) cost of the medication and
the economic status of the patient; and (6) other factors that affect compliance, such as
dosing and formulation.
4. First-line therapy at most centers is usually amoxicillin or a macrolide antibiotic in
patients allergic to penicillin because of the low cost, ease of administration, and low
toxicity of these agents. Amoxicillin should be given at double the usual dose (80-90
mg/kg/d), especially in areas with known S pneumoniae resistance.
Surgical Care
- Sinus puncture and irrigation techniques allow for a surgical means of removal of thick
purulent sinus secretions.
- The purpose of surgical drainage is to enhance mucociliary flow and provide material for
culture and sensitivity.
- A surgical means of sinus drainage should be used when appropriate medical therapy has
failed to control the infection and prolonged or slowly resolving symptoms result or when
complications of sinusitis occur.

Lecture notes in
- Another indication for sinus puncture is to obtain culture material to guide antibiotic
selection if empiric therapy has failed or antibiotic choice is limited. This is particularly
important in patients who are immunocompromised or in intensive care.
- Sinusitis can be a prominent source of sepsis in these patients. In adults, sinus puncture
can usually be achieved using local anesthesia; however, in children, a general anesthetic
is usually necessary.
- In today's era of minimally invasive surgical techniques, sinus endoscopy is commonly
used to achieve sinus drainage. It offers the advantages of (1) being able to open multiple
sinuses or to decompress the orbit in cases of complications and (2) allowing the surgeon to
open the natural ostia of the involved sinuses.
Chronic sinusitis
Chronic sinusitis is characterized by persistent suppuration lasting beyond the acute stage
of infection. An arbitrary temporal definition has little value, although sinus symptoms
lasting longer than 6-12 weeks can be considered chronic.
Sinusitis is rarely life-threatening, although serious complications can occur because of
proximity to the orbit and the cranial cavity.
Approximately 75% of all orbital infections are directly related to sinusitis.
Intracranial complications secondary to sinusitis remain comparatively rare, with a
prevalence rate of 3.7-10%.
Sinusitis is more common in the pediatric population than in the adult population. This is
because of an increased frequency of exposure to upper respiratory tract infections in the
pediatric population.
Pathophysiology
The key to normal sinus function is the mucociliary transport system. The nose and
paranasal sinuses are lined with ciliated, pseudostratified, columnar epithelium. Epithelial
goblet cells and submucosal seromucous glands produce a secretory blanket that has 2
components: a surface mucous layer and a deeper aqueous layer. Ciliary action moves the
mucous layer toward the natural sinus ostia and then to the nasopharynx. An alteration in
sinus ostia patency, ciliary function, or the quality of secretions causes disruption of the
system and leads to sinusitis.
The most important factor in the pathogenesis of sinusitis is the patency of the sinus ostia.
Partial or complete obstruction of the sinus ostia results in stagnation of secretions,
decreased pH, and lowered oxygen tension within the sinus. These changes create a
favorable environment for bacterial growth. Stagnant secretions and bacterial infection, in
turn, cause mucosal inflammation.
Causes
Anaerobes play a significant role in chronic sinusitis in adults, predominantly anaerobic
cocci, bacteroid and streptococcal species, and Staphylococcus aureus.
Diagnosis
(1) History
- The primary symptom reported by persons with chronic sinusitis is nasal congestion or
obstruction.
- Secondary symptoms include pain, pressure, and postnasal discharge.

Lecture notes in
- Because symptoms are poorly localized and mild, chronic sinusitis may be extremely
difficult to recognize.
- Chronic sinusitis in children usually manifests as purulent rhinorrhea with or without
postnasal drip.
- Cough and occasional wheezing episodes are also reported.
(2) Physical
- Physical examination usually reveals a mucopurulent discharge in the region of the
middle meatus that can be secondary to maxillary, ethmoid, or frontal sinusitis.
- Pus in the region of the superior meatus implicates the posterior ethmoid or sphenoid
sinuses.
- The sinus mucosa is diffusely congested.
- The paranasal sinuses may be tender to palpation.
(3) Lab Studies
- Nasal swab and culture may help in selecting the proper antibiotic. Taking the swab from
the middle meatus under endoscopic visualization is the method of choice.
- Endoscopically directed middle meatus aspiration culture appears to be a valuable
alternative to antral puncture for guiding organism-specific antibiotic therapy in persons
with sinusitis.
(4) Imaging Studies
- Plain x-ray films are not recommended for the evaluation of chronic sinusitis because
visualization of the ethmoid sinuses, which are usually the seat of disease and from where
inflammation extends into the frontal and maxillary sinuses, generally is inadequate.
Usually, the clinical role of plain films is limited to documentation of acute maxillary or
frontal sinusitis.
- CT scan is the modality of choice to identify and evaluate the details of sinus anatomy and
pathology. This imaging technique provides the operating surgeon with the road map for
surgery.
- Ultrasonography provides variable results and is not recommended.
(5) Other Tests
- Transillumination lacks sensitivity but may have value in experienced hands.
- Nasal endoscopy complements the CT scan because it displays the surface mucosa of the
ethmoid air cells. Perform this diagnostic procedure first.
- Maxillary sinus irrigation–inferior meatus puncture is performed for diagnostic and
therapeutic purposes.
- Biopsy samples from the maxillary sinus mucosa of patients with chronic and/or
recurrent sinusitis show basement membrane thickening, atypical gland formation, goblet
cell hyperplasia, mononuclear cell infiltration, and subepithelial edema. Rarely, squamous
cell metaplasia may be seen. The endoscopic appearance and nature of the sinus fluid do
not correspond to any specific histologic pattern .
Treatment
Medical Care ; The principles involved in the treatment of recurrent and chronic sinusitis
are as follows :
- Make every attempt to identify and treat the underlying cause.

Lecture notes in
- Therapeutic entities include antibiotics, mucolytics, nasal irrigation, corticosteroids, and

antiallergic therapies, depending on the clinical picture and associated manifestations.
- When present, treat underlying factors such as allergy, vasomotor instability, immune
deficiency, and mucociliary dysfunction.
- Reestablishing sinus ventilation and correcting mucosal opposition allows restoration of
the mucociliary clearance system. Irreversibly damaged mucosa is rare. Strive to restore
the functional integrity of the inflamed mucosal lining.
- Currently, first-line antibiotics for patients with chronic sinusitis include amoxicillin-
clavulanate, second-generation cephalosporins, and erythromycin-sulfasoxazole. Beta-
lactamase–mediated resistance to the early second-generation cephalosporins is high
among strains of Haemophilus influenzae and Moraxella catarrhalis. Cefixime, the third-
generation cephalosporin, may be selected for infections caused by H influenzae or M
catarrhalis, but it has a poor spectrum of activity against Streptococcus pneumoniae. The
newer-generation macrolides, clarithromycin and azithromycin, achieve excellent mucosal
levels but should be considered backup drugs. Azithromycin appears more potent against H
influenzae, whereas clarithromycin may be slightly better against intermediate-resistant S
pneumoniae. Clindamycin should be reserved for culture-documented–resistant S
pneumoniae. Clindamycin has little efficacy against H influenza infection.
Surgical Care ; Medical treatment is most appropriate for obstruction resulting from
physiological abnormality ; reserve surgery for anatomical obstruction.
Fungal sinusitis
Asperigillosis
It is the commonest fungal infection of the nose & paranasal sinuses , it occur anywhere &
at any age .
The causative M.O. is the Asperigellus spp. ; A. fumigatus (90% of them) , A. niger & A.
flavus (isolated in Sudan & Saudia Arabia) .
The Morphology ; it occur as a sapt\rophyte in soil & fruit , spread by air-borne
transmission , it reproduces as sexual conidium & is recognized by septate hyphae &
discohotomous branching .
Types
1. Asperigelloma (fungal ball or mycetoma) ; which behave as a chronic sinusitis & should
be suspected in any refractory cases , it is benign in nature charcterized by green-brown
sludge which is found filling the sinus cavity (esp. the maxillary antrum) .
The CT scan & x-ray will show calcium deposite & wall destruction .
2. Allergic aspergillus sinusitis ; the inhaled dust infected with fungus activate type I & III
reaction , usually affect young patients with asthma & polyps .
Charcterized by thick (ckay) mucous found in the sinuses contains eosinophils & charcoat-
Leydem crystals , the fungus hyphae santy (which identified by Grocott-silver stain) .
The x-ray shows thickemned mucosa & the CT show hyperattenuated signal , MRI T1&2
(shows dense in T2 & hypointense in T1) .
3. Invasive form ; it is uncommon , behave like a malignant neoplasm & spread to the
adjacent structures (check & orbit) causing proptosis , it is slowly progressive & locally
destructive to the bony walls .

Lecture notes in
The x-ray shows destruction to the bone , also serology & skin test for asperigella will be
+ve , H/P will show fiprosis & granulomatous response to the asperigillous hyphae which
are seen in gaint cells (by fungus stain) .
4. Fuliminant form ; it is a rapid progressive angioinvasive , destructive infection with high
mortality & usually affect the immunocompromized patients , the intracranial extention
(direct or by blood) will lead to death even with Rx , it can arise from the invasive form .
H/P shows infilterating aspergillus hyphae with little inflammatory response (contrast to
invasive form) .
Other classification by (Rowe-Jones)
1. Non-invasive ; either aspergilloma or allergic .
2. Semi-invasive ; locally destructive without tissue invasion .
3. Invasive ; representing true fungal tissue invasion either fulminant or non-fulminant in
course .
Diagnosis
1. Fresh nasal scrubing & mucous .
2. Mucosal biopsy .
Treatment
1. Non-invasive disease , surgical debridement & sinus ventilation , topical &
systemic steroids used for the allergic type .
2. Semi-invasive disease , surgery & antifungal (itraconazole) .
3. Invasive disease & fulminant form , radical surgery (exentration of the
affected area) craniofacial resection & orbital clearance with i.v.
amphotericin or liposmal amphotericin (Ambisome) which is less toxic , or
oral antifungal like itraconazole & ketoconazole .
Mucormycosis (rhinocerebral phycomycosis)
The causative M.O. is order Mucorales which include Rhizopus oryzae , Mucor
circinelloides & Mucor javanicus .. all behave in simillar manner causing aggressive
opportunistic infection , they are saprophytic found in soil , fruit & starchy foods , they can
be isolated from the nose & GIT of the normal people .
They become pathogenic when the patients general resistance has been altered (DM ,
Leukaemia , Uraemia , malnutrition , steroid , antimetabolic & antibiotics Rx)
Pathogenesis ; the fungus has great affinity to the arteries , it dissect the internal elastic
lamina from the media causing extensive endothelial damage & thrombosis .
Pathologically there is a mixed picture of inflammation & necrotic changes , later the vein
& lymphatics are involved .
Clinical forms
1. Rhinocerebral disease ; rhinomaxillary & rhinoorbitocerebral (highly fatal) .
2. Cerebral & ocular .
3. Pulmonary form .
4. Disseminated form .
Course of infection ; the disease in the nose then extended by direct extention & by
intravascular propagation to involve the sinuses , orbit , cribriform plate , meninges &
brain .

Lecture notes in
Clinical features
1. the Characteristic black necrotic turbinate (like blood clot when dried) .
2. Unilateral gangren & perforation of the hard & soft palate (secondary to
palatine arteries involvement) .
3. Proptosis , ophthalmoplagia & blindness due to CNS involvwment .
Investigations
1. Sinus x-ray shows thickening of the lining of the sinuses , no fluid level , spotty
destruction of the bony walls .
2. MRI to detect the early vascular & intracranial invasion .
3. Biopsy to confirm the disease . .
The early detection of the disease is essential before irreversible changes occur .
Treatment
1. Control the percipitating factors .
2. Heparinization .
3. Systemic amphotericin or Ambiosome or oral ptassium iodide .
4. Local drainage & debridement .
5. Orbital exenteration manditory in case of blindness or ophthalmoplagia .
Rhinophycomycosis
It is caused by Conidiobolus coronatus which manifisted by prominent nasal polyps &
granulomas in the nasal cavity .
The incidence ; male more than female , found in central Africa , India , Brazil & west
Indies (uncommon disease) .
It is charcterized by nasal obstruction & swelling over the nose & later checks & upper lip .
Pathogenesis ; the disease start in the inferior turbinate & then spread in the submucosa
through the natural ostia to the paranasal sinuses , H/P shows granulomatous reaction with
collection of multinucleated gaint cells in the centers of which hyphae can be seen .
Treatment ; removal of the tumor mass with i.v. amphotericin .
Blastomycosis
The causative M.O. is Blastomyces dermatidis , it is either ;
1. Nasal disease ; the mucosal lesion near the vestibule or alar rim consist of papillary
hyperplasia with cysts which contain polymorphoneuclear leucocytes surrounding the M.O.
2. Disseminated disease ; can be fatal , the skin , lungs are involved , at the room
temperature the mold form which produce spores which inhaled into the lungs , at body
temperature they form thick walled round budding yeast .
It is diagnosed from examination H/P of Gomori stained or PAS stained section & from
fungal serology for blastomycosis .
Treatment ; in severe disease use i.v. amphotericin , in less severe use oral ketoconazole .
Rhinosporidiosis
It is caused by Rhinosporidium seeberi which predominantly affect the mucous memberane
of the nose & nasopharynx , also affect the lips , maxillary sinus , conjunctiva , lacrimal sac
, epiglottis , trachea , bronchus , ear , scalp , skin , penis , uvula & vagina .
Charcteristic pathology id the formation of papillomatous & polypoidal lesions (bleeding
polyps) , in H/P the polyp has a vascular fibromyxamatous structure , unique round

Lecture notes in
structure soform sporangia (redesignated nodular bodies , spores as spheres of cellular

waste) .
Its incidence ; found in India & Sri Lanka , usually affect young males , the mode of
infection is dust from the dung of the infected horses & cattle .
1. in the early stages there will be viscid nasal discharge with irritation &
partial obstruction due to polyps .
2. epistaxis which is rarely symptoms , esp. when the polyp increased in size .
3. the lesion is friable , strawberry (in shape & colour) with greyish under
surface studded with sporangia showing as white dotts , it start in the
vestibule & usually attach to the septum , when the polyp increased in size it
may hang in the naso- & oro-pharynx & interfere with the swallowing .
4. swollen nasal mucosa , hyperaemic , covered with copious viscid secretion ,
containing spores , but no pus .
5. no lymphadenopathy .
The diagnosis from ; the examination of the discharge under LM identifying the spores ,
also by biopsy & H/P of polyps to show the charcteristic pathological picture .
Treatment
1. Surgical ; wide excision with cutting diathermy & cautery to the base of the
lesion (because excessive bleeding may occur) .
2. Medical ; local injection of depot corticosteroids into the polypoidal masses ,
also give amphotericin i.v. with dapsone .
Staging of Rhinosinusitis
5. Preoperative CT scan findings ; scoring for each sinus (maxillary , ant. & post.
Ethemoid , frontal & sphenoid) 0-2 , 0 means no abnormality , 1 partial opacification & 2
total opacification (OMC is 0 or 2) , the maximum score of 24 possible (anatomical variants
, also scored 0 or 1 , but not included into the CT score) .
6. Symptoms evaluated on a visual analogue score (VAS) of 0-10 (0 for none till 10 the
most severe) , for nasal congestion , headache , facial pain , sense of smell , nasal discharge
& over all symptomatic assessment .
7. Surgical score ; for each manouver of endoscopic operation (0 means not performed , 1
undertaken) , the maximum score of 14 .
The procedures ; uncinatectomey , reduction of the middle tyrbinate , middle meatal
antrostomy , ant. Ethemoidectomy , post. ethemoidectomy , sphenoidotomy & frontal recess
surgeries .
8. Endoscopic appearance , qualified on 0-2 point basis for the presence of polyps ,
discharge , odema , scaring or adhesion & crusting , this performed pre- & post- therapy
(like the VAS) .
Management of sinusitis (General)
- Diagnosis
1. History ; careful clinical history remains the corner stone of the Dx , i.e. sign &
symptoms like facial pain & tenderness over the maxillary antrum or between the eyes or
above the eyes & postnasal discharge .

Lecture notes in
2. Examination ; Full ENT examination .

3. Investigations ;
a. Nasoendoscope ; to exclude the aetiological factors & obtain accurate material for
bacteriological examination , topical vasoconstrictors may be required (it should be
postpond until the nasal mucocilliary clearance test & rhinomanometry performed)
b. Radiology ;
1. Sinus x-ray ; useful to assess patient with acute rather than chronic inflammation ,
air fluid level or thickening of the mucosal lining or opacification .
2. CT scan ; optimum to demonistrate the extent & distribution of the mucosal
disease together with any anatomical variants , also used in staging of sinusitis .
c. U/S ; it is diagnostic & free from hazard of radiation on the orbit caused by CT scan
, it can be repeated freely .
d. Proof Puncture ; used in the past .
e. Sinoscope ; it provide the only certain method of providing accurate information
about the nature of the mucosal changes .
f. Blood tests ; CBP , WBC , ESR , biochemistry , LFDT , immunological tests , all these
needed to detect the underlying disease predisposing to the infection .
- Treatment
A. For Maxillary sinus
1. Conservative ; AWO or antrostomy (either endoscopic middle meatus or inferior
meatus) .
2. Radical ; Caldwell-Luc’s operation .
B. For Frontoethemosphenoid
1. Conservative ; trephenination of the frontal or sphenoidal washout , intranasal
ethemoidectomy , FESS & transantral ethemoidectomy .
2. Radical ; external frontoethemoidosphenoidectomy (Lynch-Howarth-Paterson) &
osteoplastic flap (with or without obliteration) .
In general the management either medical or surgical .
I.Medical treatment
1) Antibiotics ; Amoxil for 2 weeks (s.t. for 6 weeks) or augmentin (both effective against
Strp. Pneumonia & H. influenza) & flagyl .. or Keflex , Claforan , Ciprodar .
2) Analgesia ; 79% of patient cure spontaneously with analgesics alone , Aspirin & Codein
for 2 weeks are effective .
3) Decongestant ; as nasordin drops (shrink the mucosal , improve the airway & assist
sinus drainage) .
In chronic sinusistis , preferable to give the antibiotics according to the C&S results or use
Amoxil & Flagyl , s.t. it is due to fungal infection , so use antifungals , also use mucolytics
as the chronic infection cause the secretion to be viscid & thick (like Guaiphensin) , nasal
toilet by dooshing or irregation with salin using Higginson’s syringe lead to cleansing of
the thick secretions , also steroids may used to decrease the mucosal swelling associated
with the inflamatory response of the infection (use Neodexon drop or spray for 3-4 weeks
maximum , if fail to heal the disease , then surgery) .

Lecture notes in
II. Surgical treatment

1) Antral washout (AWO)
- Indications ; Dx & Rx of sinusitis .
- Contraindications ; children under 3 years , hypoblastic maxilla , acute febrile sinusitis
(AWO lead to septecaemia) & truma to the orbital floor .
- Anasthesia ; LA (use Moffatt’s solution or cocaine) or GA .
- Technique ; a Tilly-Lichtwitz trocar & canula inserted usually in the inferior meatus (at
the middle avascular portion) , s.t. we insert indwelling catheter for repeated irrigation .
- Complications ;
a. mild haemorrhage at the puncture site may occur .
b. incorrectly piercing the anterior wall causing pain & swelling of the check .
c. perforation of the orbital floor causing pain & bulging of the eye .
d. perforation of the lateral or posterior wall of the antrum .
In all complications above , the AWO should stop & antibiotics given .
2) Inferior meatal antrostomy
- Indications ; acute & chronic sinusitis unresolved by medical Rx , it depends on the
gravititional drainage , so it is usually usueful only in case of primary mucocilliary
abnormality like cystic fibrosis .
- Anasthesia ;perfectly done under GA .
- Technique ; the inferior turbinate is elevated with a Hill elevator , then by also the
elevator we perforate the inferior meatus at the highest point under the genu of the
turbinate (thinne bone) , then enlargement done in all directions by many instruments
(posteriorly with Grunwald nasal turbinate forceps , anteriorly with sSeymour-Jones
antrum forceps, superiorly & inferiorly with Hagek antrum punch forceps) , so 2X1cm
window is fashioned , then the inferior turbinate repositioned .
- Complications ;
a. severe bleeding occur if the antrostomy extend too posterior damaging the lateral
sphenopaltine artery .
b. altered dental sensation occur if the procedure extend anteriorly damaging branches of
ant. superior alveolar n. plexus .
3) Caldwell-Luc’s procedure ;
- Indications ;
a. chronic maxillary sinusitis .
b. closue of oroantral fistula .
c. removal of F.B. (amalgum or dental root) .
d. dental cyst in the antrum .
e. accesss to the pterygomaxillary fissure & sphenopalatine fossa .
f. antrochoanal polyp (recurrent) .
g. orbital floor fracture (for elevation & stabilization) .
- Contraindications ; children as it damage the secondary dentation .
- Anasthesia ; GA or LA (using maxillary n. block) .
- Technique ; incision done in the canine fossa 3 mm above & parallel to the gingivolabial
fold (3cm from the posterior edge of the lateral incisor to the 2 nd molar tooth) , the

Lecture notes in
mucoperosteal flap is then elevated superiorly to expose the anterior wall of the sinus , then
the anterior antral wall is opemed in the canine fossa (the bone here is thin) by gauge or
drill , then enlarged by Hajek punch forceps (1-1.5cm diameter) , then the entire lining of
the sinus is dissected & removed completely (which is difficult in the roof & inferolateral
angle) , the a large inferior meatal antrostomy (2X1 cm) is fashioned then packing of the
nasal cavity & occasionally of the antrum needed , then we suture the buccal incision with
absorbable suture (must be loose to allow drainage of the blood) .
- Complications ;
a. pain & swelling , can be decreased by good surgery .
b. haemorrhage ; either from the anterior bony wall or from the antrostomy .
c. parasthesia due to damage of the infraorbital n. (s.t. significant neuralgia) .
d. damage to the teeth & their innervation , change in sensation , devitalization &
discoloration .
e. oroantarl fistula , require subsequent surgical intervention .
f. retention cyst which will fill the antrum .
4)Intranasal ethemoidectomy ;
- Indications ; chronic sinusitis associated with polyposis (it provide ainadequate approach
for complete exenteration of the ethemoid) .
- Contraindications ; we usually use endoscopic surgery to provide good visualization of
the area .
- Anasthesia ; GA .
- Technique ; the ethemoidal labyrinth is cleared between the vertical attachement of the
middle turbinate medially & the lamina papyracea using a small Tilly-Henckel forceps , the
posterior cells may entered through the grand lamella also the sphenoid entered (all
materials removed should be examined for the presence of orbital fat – float in watre-)
- Complications ;
a. injury to the lamina papyracea , haemorrhage , periorbital hamatoma & then proptosis
with risk of visual loss , so we remove the pack & do orbital decompression via an external
approach .
b. direct injury to the orbital periosteum revealing fat in the surgical field , it may cause
damage to the medial rectus & optic n.
c. dural injury .
d. penteration to the medial ethemoidal roof & CSF leak .
e. Meningitis & blindness may be a sequale to other complications .
5) Transantral ethemoidectomy (Jansen –Horgan operation)
- Indications ; chronic antroethemoiditis & for orbital decompression .
- Anasthesia ; GA .
- Technique ; Caldwell-Luc approach done , then the posterior ethemoidal cells are opened
through the antrum by pushing a closed Tilly-Hunckel forceps upward medially &
posteriorlyat the upper & inner angle of the antrum (might combined with intranasl
ethemoidectomyto clear the anterior cells) .
- Complications (the same as for Caldwell-Luc’s operation & intranasl ethemoidectomy) .
6) External frontoethemoidectomy

Lecture notes in
It is designed to offer access , illumination & perception of depth .

- Indications ;
a. chronic sinusitis not respond to conservative Rx .
b. complications of acute ethemoiditis like orbital cellulitis .
c. recurrent polyposis (esp. if previous surgeries destroy the landmarks) .
d. frontoethemoidal mucocele .
e. access to ; ethemoidal artery (ligation in epistaxis), dacrocystrhinostomy ,
transethemoidal hypophysectomy , repair of CSF leak & decompression of the orbit for
malignant exophthalmos .
f. it has no place in the definitive oncologocal Rx of sinus malignancy .
- Anasthesia ; GA .
- Technique ;
a. Lynch-Howarth procedure ; the incision concave & medially curved towards the medial
canthus striaght down to the bone , then extended under the eye brow to facilitate access to
the frontal sinus .
the periosteum elevated reveal the nasl process of the maxilla & frontal bone & medial wall
of the orbit , the lacrimal sac elevated & displaced laterally , the dissection continue
posteriorly reveal the anterior ethemoidal b.v. which are ligated & then ligate the posterior
ethemoidal vessels .
the thin medial wall of the orbit perforated entering the ethemoidal system , excenturated
under direct vision (not pierec the cribriform plate) , s.t. extended to the sphenoid removing
all the diseased mucosa , also the frontal sinus entered after cleaning the frontal recess (the
patency of the frontal recess is the key to successful Rx , usually by using stent with silastic
tube & left in place up to 3-5 months , when removed it cause circumferntial scarring & the
canal resulted has rarely functioning respiratory epithelial lining) , s.t. it combined with
endoscopy in selected cases , not do stenting if there is sufficient bony support to the recess .
The periosteum , subcutaneous tissue & skin sutured with catgut & silk, at the end of the
operation the eye washed with saline (to remove blood) , & apply chloramphenicol ointment
to prevent conjunctivitis , then apply pressure bandage for 24 hours .
b. Paterson’s procedure ( transorbital ethemoidectomy) ; the incision 2 cm in length in the
natural crease line below the inferior orbital margin , the orbicularis oculi muscle is split &
the periosteum incised & elevated for the orbital margin (care taken to avoid periosteal tear
& the inferior oblique also care taken to preserve the lacrimal sac & duct) .
The orbital floor is removed laterally as far as the infraorbital n. (s.t. lateral to the nerve) ,
the bone is removed posteriorly from behind the nasolacrimal duct as far as the hard bone
of the sphenoid surround the optic apex .
The ethemoid can be removed under direct vision & endoscopy to clear the frontonasal
recess (which is difficult by the operation) .
- Complications ;
a. Lynch-Howarth procedure ;
1. incision problems , odema, infection , parasthesia , damage to the medial palpebral lig.
& webbing of the wound .
2. haemorrhage , self limiting associtaed with ethemoidal vessels retraction .

Lecture notes in
3. damage to the supraorbital n. due to the incision extension laterally .

4. dural exposure , by surgery or pathology itself leading to CSF leak .
5. damage to the periorbital with fat prolapse , sould managed immediately to avoid fat
prolapse in the surgical field .
6. mucocele due to failure to maintain the patency of the frontal recess , s.t. lead to
recurrence of the initial disease .
7. periorbital swelling , minimized by pressure bqandaging .
8. temporary diplopia , due to surgical decompression .
9. disturbed trochlea which should be reattached at the end of the operation by catgut
suture , this causing diplopia also .
b. Paterson’s procedure ; same as above and ; transient diplopia , odema of the orbicularis
oculi &/or streaching of the nasolacrimal duct , parasthesia (due to infraorbital n. damage)
, diplopia (due to inferior oblique muscle detachement) .
7) Frontal sinus washout
- Indications ; acute supporative frontal sinusitis not relieved by antibiotics (should done
under AB cover) , radiological examination should preceed the operation (Dx) .
- Anasthesia ; GA .
- Technique ; temporary tarsorraphy to protect the eyes , small incision done 1 cm below
the medial end of th eyebrow striaght down to the bone , then the sinus entered easily using
a drill or gauge & hammer , this will release the purulent content .
The entry hole may be enlarged further more by Hajek forceps to allow adequate
visualization , then drainage tube inserted & sutured in place , regular lavage through the
tube for 48-72 hours with postop. AWO (because it is usually pansinusitis).
- Complications ;
a. dural dehiscence .
b. supraorbital & supratrochlear nerve damage (avoided by careful incision) .
8) Osteoplastic flap procedure
- Indications ; chronic suppurative frontal sinusitis failed all other method of treatment ,
also for large osteomas & repair of trauma in this region & management of mucocele .
- Contraindications ; extensive ethmoiditis in association with frontal sinusitis , fail to
access the ethmoids by this procedure .
- Anasthesia ; GA .
- preoperative preparations ; x-ray of the frontal regionn taken to determine the extent of
the sinuss & the pathological changes , from the x-ray , a template of the sinus can made
using silastic sheet , prophylactic antibiotics according to the C&S used .
- Technique ; the skin shaved in a 2.5 cm strip within the hairline then painting with
hibitane , temporary tarsorraphy & infilterate of cocaine & adrenaline .
A coronal incision is made through the skin , subcutaneous tissue & frontalis muscle behind
the hairline (but not incise the pr\eriosteum) , the flap is elevated inferiorly in the plane
between the frontalis & the periosteum down to the supraorbital rim & glabella , use
neurosurgical clips for haemostasis .
By fissue burr or saw , a cut is made round the outline , cutting just inside the line to ensure
the incision is within the sinus & the entire margin is cut around including the supraorbital

Lecture notes in
rim , it is necessary to cut through the intersinus septum with chisel to face the anterior wall
& the flap hanged along the floor of the frontal sinus .
All the diseased mucosa can be removedd , if attempt of obliteration of the sinus adapted ,
fat from the abdominal wall removed as traumatically as less as possible & then placed in
the sinus cavity which should be filled completely , the bony flap is replaced & the
periosteal layer repaired , the skin is sutured & pressure bandage for 24 hours .
Alternative incision , just above or below the eyebrows & connected across the glabella
(spectacle incision) , this suitable in small sinus or in men with male-pattren baldness (the
eyebrow should never be shaved) , also sometimes we open one sinus (unilateral) .
- Complications ;
a. cosmetic problems ; nasal skin necrosis , incision healed with ugly scar & haematoma
collection .
b. frontal bossing & depression of the bone flap .
c. osteomylitis in the bone flap .
d. dural tear (if the template is incorrectly drawn, then CSF leak) .
e. recurrence of the disease .
9) FESS
- Indications ;
a. chronic sinusitis .
b. acute recurrent sinusitis .
c. nasal polyposis .
d. frontoethmoidal mucocele .
e. allergic fungal sinusitis & mycetoma .
f. repair of the CSF leak .
g. orbital & optic n. decompression .
h. dacrocystorhinostomy .
i. Choanal atresia .
k. hypophysectomy .
j. septal & turbinate surgery .
l. control of epistaxis .
m. drainage of periorbital abscess .
n. benign tumo excision .
o. removal of foreign body .
- Contraindications ;
a. orbital extention of the acute sinusitis with suggesion of intracranial complication like
meningitis , epidural abscess , cavernous sinus thrombosis , or blindness , here the
Messerklinger technique is contraindicated .
b. malignant tumors .
c. mycotic mass in the antrum , not use Messerklinger technique .
- Anasthesia ;
a. LA ; if the disease is minimal or the patient unfit to GA , 3 ways should given collectively;

Lecture notes in
1. topical ; applied 0.05 % xylometazoline & lidocaine directed at the middle meatus ,
sphenopalatine artery & nerve , posterior part of the inferior turbinate & the anterior
ethmoid artery & nerve .
2. intranasal infilteration ; 1% lodocaine with 1:200000 adrenaline at the uncinate process
, greater palatine foramen & middle turbinate (up to 4 ml) .
3. external injection occasionally to the greater palatine foramen , block the sphenopalatine
nerve .
b. GA ; keep the patient comfortable & not anexious , we use Moffatt’s solution instilled in
the Anasthetic room , 2 ml of 2% Naco3 , 2 ml of 10% cocaine & 1 ml of 1:1000
adrenaline… total 5 ml , give half in each nostril .
The patient head is left hyperextended for 10 min. before he is transferred to the theatre ,
put him in supine position , further vasoconstruction achieved with ribbon gauze soaked in
1:1000 adrenaline packed around the middle meatus & surgical cavity .
The CT scan always found in the theatre ( when the patient dicharged postop. After 24 hrs ,
no pack kept in the nose , but s.t. telfa pack placed in the surgical cavity) .
- Technique ;
A. use zero degree 4 mm Hopkin’s rod telescope , doing infundibulotomy by incising the
anterior attachement of the uncinate process with a sickle knife , then use freer elevator to
lift the uncinate process , then it grasped with forceps , the upper & lower attachements cut
with fine scissor & the process detached with twisting motion , any residual rim can be
removed secondarly with forceps (care taken to avoid damage to the nasolacrimal duct) .
B. the bulla ethmoidalis is opened with finestraight forceps & removed piecemeal , we can
see the yellow orbital fat through the thin lamina papyracea , behind the bulla , enter a
variable space , superiorly the base of skull should be visible & the anterior ethmoidal
artery may be identified .
In many cases , this is all required , then depending upon the CT finding we ecide whether
to continue or open the maxillary sinus , explore the frontal recess , the posterior ethmoid &
sphenoid .
C. the posterior ethmoid entered by oiercing the ground lamella , the lateral attachement of
the turbinate , they are larger & pyramidal in shape , the optic nerve can be prominent in
the lateral wall covered by extremely thin bone .
D. the sphenoid can opened from the posterior ethmoid by entering it as ainferior &
medially as possible from the last cell , here , the great care must taken because the sinus is
of variable size & closely related to the carotid artery & optic nerve .
E. checking the superior meatus , clear any pathology , free access into the posterior
ethmoidal system .
F. middle meatus antrostomy , is unnecssary if the ostium is patent when uncovered by
removal of the uncinate process , if accessory ostium is present , then joined to the natural
one to avoid abnormal mucous circulation .
Usually enlarge the ostium into the anterior fontanelle , if the ostium is invisible after
uncinatectomy , palpation by blunt probe , J curette or curved sucker identify its postion or
see the bubles of mucous .
G. it is advisable to limit removal of mucosa in the frontal recess to avoid scaring .

Lecture notes in
To avoid bleeding this tep postpond to the end of the procedure.

S.t. the uncinate process attached laterally onto the lamina papyracea , so that the
infanudibulum leads into the blind-ending terminal recess .
When the uncinate process attached superiorly or rarely medially to the middle turbinate ,
so visualize the frontal recess with a 30 degree scope .
Care must be taken in the frontal recess to avoid damage to the anterior ethmoidal artery &
enterance to the anterior cranial fossa .
- Postoperative management ;
a. the patient discharged home in the next day .
b. kept on antibiotics for one week & systemic decongestant & local steroid drops (if the
patient has diffuse polyposis , kept on systemic steroids like prednisolone 30mg/d for one
week , then 20mg/d one week , 10mg/d for another weeek) .
c. the patient usually seen after one week postoperatively , then weekly for one month , then
monthly fo9r one year , in each visit ; the cavity cleaned by endoscope under LA , remove
the debris & divide any adhesions , remove of further polyposis & granulation tissue &
additional medication prescribed .
- Complications ;
a. Major ; meningitis , brain abscess , blindness , diplopia , orbital haematoma , nasal &
intracranial haemorrhage , carotid artery injury , epiphora , stroke & anosmia .
b. Minor ; periorbital ecchynosis , headache , dental pain , epistaxis , adhesions , postop.
Sinusitis , hyposmia , asthma exacerbation & ostial stenosis .
- Suggestions ;
a. the operator experience , 100 diagnostic endoscope before attempting surgery .
b. the surgeon shoul attend a course or workshope that allows hands on experience .
c. the initial operation should done under supervision of an experienced surgeon .
d. follow up & assessment clinics should seperated from the general clinics & should used
for audit & training .
e. Ct scan facilities should be available .
- Advantages of FESS ;
a. no surgical trauma to the external skin & intervening bone & the ability to minimize
intranasal & intrasinus trauma .
b. preservation of the bony framework within the frontal recess .
c. visualization of nasal antomy .
d. preservation of mucosa for the restoration of normal mucocilliary clearance .
Sinusitis in children
Radical surgery are avoided in children due to the longterm effect on dentation , if the
medical Rx fail , then AWO with tonsillectomy/adenoidectomy .
We should remmeber that congenital abnormalities of immune & mucocilliary function
present at young age in addition to allergy , they lead to infection .
FESS in paediatrics has many effects ;
1. periodental complications .
2. need subsequent GA to perform postoperative clearance (abunded in children) .
3. may lead to mucocele & affect the facial growth .

Lecture notes in
FESS must done by expert surgeon if it is necessary .

Complications of sinusitis
Routes of spread
A. Local ; the majority of complications associated with acute bacterial infection where the
natural dehisences & weaknesses of the surrroundings bone are found , when the
inflamation blocks the drainage routes , outflow obstruction lead to abscess in the bony wall
1. Direct ; causing osteitis , osteomylitis & osteoporosis .
2. Venous ; causing septic vein thrombosis (diploic bone osteomylitis) , thrombosis of
minute veins in the sinus mucosa & septaceamia & pyemia .
3. Lymphatics ; carry infection through the vessels .
4. Perineural ; olfactory nerve to the subarachenoid space .
B. Distal ; rare , leading to generalized septicaemia .
The Pathogens are ;
a. Orbital
1. Aerobes ; Staph. Aureus , H. influenza , Strep. Pneumonia , Moraxella caterrhalis .
2. Anaerobes like bacteroids .
b. Intracranial
1. Aerobes ; Staph. Aureus , H. influenza , Strep. Pneumonia , Pseudomonas aerogenosa ,
Strep. Spp. (B-haemolytic & non-B haemolytric) .
2. Anaerobes .
A 5-7 days course of oral antibiotics Rx may be wholly or partially ineffective , as bacteria
has resistance (espicially staph. Aureus & H. influenza) .
Complications of sinusitis
A. ACUTE
1. Local
 Orbital ; usually the left orbit , in children under 6 years due to an ethmoiditis , while in
adults due to frontal & sphenois sinusitis are frequently responsible .
The incidence between 21-90% , higher during winter & spring .
Route of spread ; through areas of weakness ; lamina papyracea which is thin & may
be dehiscent leading to orbital complications (usually from ethmoiditis) like abscess .
The infraorbital canal also another weak area leading to orbital complications (rare – from
maxillary sinusitis) .
Chandler , Langenbrunner & Stevens classification (1970) :
1. Preseptalcellulitis ; charcterized by odema of the lids without pain or tenderness , no
visual loss or limitation of the extraocular motility , if not Rx seriously then lead to more
dangerous complication .
2. Orbital cellulitis without abscess formation ; charcterized by diffuse odema of the
adipose tissue , pain & tenderness over the eye , when this cellulitis increase , proptosis
occur which is difficult to distinguished from odema of the lids .
3. Orbital cellulitis with subperiosteal (extra periosteal) abscess ; charctrized by pain &
tenderness with severe proptosis which may limit the extraocular movement & associated
with visual loss , pus already collected between the sinus & the orbit striping the periosteum

Lecture notes in
from the lamina papyracea , also there is colour vision impairement , when the patient
unable to distinguish red from brown & blue from black .
Occassionally , preseptal abscess forms in the upper eyelid & may discharge through a
fistula .
4. Orbital cellulitis with intraperiosteal abscess ; the displacement of the globe is severe
with obvious limitation of the extraocular movement & visual loss due to optic neuropathy
(in 13%) , additional cranial nerves may be affected as an orbital apex system , so there will
be parasthesia in the distribution of the V1 , V2 branches of the trigeminal nerve .
5. Cavernous sinus thrombosis ; in which , thrombophelobitis extends posteriorly from the
orbit & can cross the basilar venous plexus to affect the opposite side & spread
intracranially , usually it associated with posterior ethmoiditis or sphenoiditis & carry
serious morbidity (bilateral blindness) & mortality .
It usually affect youngs (under 20) , charcterized by fever , headache & painful parasthesia
in the area of V nerve distribution , then II & VI n. also involved leading to perminant
ophthalmoplegia , the sudden development of bilateral orbital signs should alert the
clinicial to this complication , the mortality are 50% before the antibiotics & now 10-27% .
Mangement of orbital complications
1. History ; patient usually unwell , pyrexial with neutrophil leucocytosis , in addition
to past history of events & medications .
2. ENT exam. ; include the anterior & posterior rhinoscopy & s.t. rigid endoscopy
(under LA & decongestant , also therapeutic) which reveal inflamation & odema of
the middle meatus , also take bacteriological speciemens (s.t. indicate other
pathology like sinonasl malignancy) .
3. Eye exam. ; by an ophthalmologist , assess the displacement of the globe as distinct
from the lid odema , ocular movement & regular checking of the visual acuity .
In patient faced with already lossing vision , surgical decompression should not be
delayed , CT scan is of great advantage in determining the location of the abscess (done
if the clinical situation is stable) .
In general , generalized orbital odema will cause symmetrical axial proptosis , while
speciefic collection will displace it away from the quaderent with asymmetrical
restriction of movement (usually extraperiosteal collection) .
Changes in the visual acuity must be distinguished from diplopia (due to restricted
muscle movement or mass) & bluring of conjunctivitis .
The optic neuropathy due to nerve compression (its dural sheeth or bllod supply)
accompained by relative afferent pupilary defect , the patient reports that the aimage is
darker (if looking only through the affected eye) , also examination shows small amount
of pupil dilatation by tourch .
The mucocele s.t. cause rapid compression of the central retinal artery & ophthalmic
artery causing immediate effect on vision , by fundoscopy odema of the optic disc &
retinal vein engorgement .
The compression must be relieved within 100 min. if vision to be restored .
4. Neurological exam. ; to exclude cavernous sinus thrombosis .

Lecture notes in
5. Treatment ;
a. Admition to the hospital for observation & i.v. antibiotics (claforan + flagyl or
amoxyclav) with intranasal decongestants & analgesia , this may resolve the problem
b. If there is evidence of visual loss , surgical decompression should be performed
(genuine surgical emergency) .
Assymetrical displacement & limitation of the eye movement will strongly indicate an
extraperiosteal abscess .
AWO may resolve the problem , but formal surgical drainage under GA either ;
endoscopic approach (need expert personell) or external approach of modified Lynch-
Howarth incision is preferable resulting in complete decompression & pus drainage at
any site , this approach may be accompiend with middle meatus antrostomy performed
endoscopically .
Sometimes do trephination of the frontal sinus as an alternative , but the formal
decompression offers the most reliable solution .
Also give 8-12 mg of dexamethasone (in adults) helpful pre- & per-operatively when
the vision is compromized
c. If there is no danger to the vision , Rx by i.v. antibiotics for 24 hrs during which
CT scan can be obtained (looks for the adjacent anterior cranial fossa for collection) .
CT scan should be done for any patient with orbital complication after 2 months if he
has residual headache & malaise .
If the patient has signs of meningitis , CT should performed prior to the LP to
eleminate the possibility of intracranial abscess .
An emergency CT is required when suspect cav. sinus thrombosis , Rx by high dose i.v.
antibiotics (with speciefic antistaph.) & surgical drainage .
6. Long term sequelae of orbital complications ;
a. Perminant vision loss .
b. Ophthalmoplagia .
c. Anasthetic cornea due to exposure keratitis & ulcers .
d. Infection of the sclera , choroid & retina .
e. Uveitis , choroiditis & glucoma .
f. Rupture of the globe & iris prolapse due to increased intraorbital pressure .
 Intracranial ; less common & it can coexist with orbital complications , occur most
commonly in adolescent & young adults , mailnly male (more vascularity of the diploic
system in adolescent , but unknown why M>F) .
Route of spread ; due to associated thrombophelibitis espicially diploic veins of the frontal
bone or from the sphenoid affecting the bone itself & spreading to the adjacent cranial fossa.
The venous connection between the sinuses & the orbit have no valves allowing free
infection communication .
It divided into ;
1. Abscess ; epidural , subdural or intracerebral abscess , 2/3rd of brain abscess are due to
otitis media & sinusitis , usually affect children below 10 years , acute or chronic ,
commonly it is subdural (2nd commonest is frontal lobe abscess) .

Lecture notes in
It begin as cerebritis (localized) with necrosis & liquification within the capsule leading to
multiple abscesses due to septic thrombophelibitis .
In acute stage abscess in the frontal lobe gives few symptoms unless large size reached
(clinical picture masked by the orbital complications) , fever , leucocytosis & headache . s.t.
seizures , nuchal rigidity or focal neurological signs (which found at the other site of the
abscess like temporal) .
Chronically , papilodema , nausea & vomiting , decrease level of consciousness (due to
increased intracranial pressure) .
2. Cav. Sinus or superior sagital sinus thrombosis ; s.t. associated with brain abscess .
3. Meningitis /encephalitis ; associated with acute sphenoiditis due to direct venous spread
or due to parameningeal inflamation of the cavernous sinus .
Mangement of intracranial complications
1. History & neurological evaluation .
2. If suspect an abscess , CT scan should be done urgently prior to proceed to LP , CT
with contrast give the image of choice to demonstrate localized intracranial infection
, but if available MRI offer an excellent alternative as it will define very small
collection & more general cerebritis , if no abscess then do LP to Dx meningitis .
3. Treatment ;
a. Admition to the hospital for observation & i.v. antibiotics (high dose ) that
cross the blood brain barrier like claforan & flagyl or chloramphenicol &
oxacillin or methacillin & claforan & flagyle for 4-6 weeks .
b. Serial CT scan done to see if localized collection found , then drainage by
simple burr hole by neurosurgeon (If there is multiple abscesses then need
craniotomy) .
c. Steroids has a contraversial role , as it decrease the inflammation , but also
interfere with the antibiotics penteration .
d. Any patient with severe frontal sinusitis need to be followed by CT scan ,
espicially if complicated by orbital spread or if frontal abscess is suspected .
4. Long term sequelae of Intracranial complications ;
a. Mortality still high (15-43%) & increased with age .
b. The worse prognosis found with multiple subdural abscesss with associated
cortical thrombophelibitis .
c. Perminant disability like conulsion s & hemiparesis .
d. The earlier the medical & surgical intervention , the better the likely outcome .
 Bony ; this called Pott’s puffy tumor (after sir Percival Pott 1760) is a complication of
frontal sinusitis in which the overlying frontal bone becomes involved .
The frontal bone is diploic bone with a marrow cavity & so iti is capable of developing
osteomylitis , the anterior & posterior walls may be affected , the infection spread anteriorly
onto forehead or posteriorly to form subdural abscess (need CT to see if there is abscess) .
It appears as fluctuant swelling over the forehead which might be painful or not .
The affecting M.O. are Staph. Aureus , Strep. & anaerobes .

Lecture notes in
Treatment by ; i.v. antibiotics & surgical intervention through bilateral coronal or spectacle
incision to drain the pus & the affected bone is debrided , the cosmetic defect then managed
later on (when the infection completely resolved) by bone grafts or exogenous materials .
 Dental ; acute maxillary sinusitis may produce dental pain (which confuse the Dx) due
to close relationship between the 2 nd premolar & 1st molar to the floor of the antrum .
Route of spread ; through the roots of the 2nd premolar & 1st molar (they are intimately
related to the floor of the antrum) & s.t. direct contact with the mucosa of the sinus , this
spread suggested when the patient has pain & swelling of the check .
In dental abscess there is great swelling of the gum which may rarely complicate the
sinusitis as they may coexist .
2. Systemic ; toxic shock syndrome is rare , but potentially fatal sinusitis complications ,
usually due to Staph. Aureus infection , there will be f, hypotension , rash with
desequamation & multisystem failure .
B. CHRONIC
1. Mucocele ; frontoethmoidal mucocele occur in 25% of frontoethmoidal sinusitis .
2. Pyocele ; forms when a mucocele become secondarly infected , when a +ve C&S
obtained it shows Staph. Aureus , H. influenza & Strep. Pneumonia as the commonest M.O.
In both the above , if the optic nerve displaced rapidly (it can tolerate streaching up to 2 cm
of axial proptosis) vision is rapidly compromized .
Both treated by ; i.v. antibiotics & surgical decompression
C. ASSOCIATED diaseases ; otitis media , adenotonsilitis , bronchiectasis may coexist , so
we exclude the prescence of mucocilliary clearance disorders or immune difficiencies .

Lecture notes in
Nasal obstruction and Rhinorrhea in paediatric

The sight of a snuffy baby or a child with blocked running nose is so common as to be
considered normal , in most of cases ; the symptoms are not that serious & can easily be
disregarded , but if investigated appropriately & managed ; these young patients can enjoy
a signifcantly improved quality of life .
The infants relay on a patent nasal airways to survive , obligate nasal breather , because
has no reflexes that make the breathing peroral when facing a nasal obstruction conditions ,
so the nasal discharge can obstruct an already small airway .
Older children are seldom at risk merely through nasal obstruction , though severe sleep
apnoea will occur if nasal obstruction is combined with significant oropharyngeal
obstruction .
Nasal discharge is the ploblem of parents more than the child , the causes of nasal
obstruction & rhinnorhea in infants & older children are ;
1. Congenital
a. Skeletal abnormalities ; choanal atresia/stenosis , nasal agenesis/stenosis , cleft
palate/nose , Down's syndrome , Apert-Crauzon's syndrome .
b. Nasal masses ; dermoid cysts , mucous cysts , meningoencephalocele , nasal glioma ,
nassopharyngeal teratoma , haemengioma , rhabdomyosarcoma & angiofibroma (in
boys) .
2. Acquired
a. Septal deviation/haematoma .
b. Infective ; viral (cold) , snuffles (AIDS) , rhinosinusitis ,...etc .
c. Allergic ; rhinitis , polyps ,...etc .
d. Non allergic rhinitis .
e. Adenoid hypertrophy .
f. Foriegn bodies .
3. Idiopathic
a. Neonatal rhinitis ; most snuffy babies have it .
b. Pubertal rhinitis .
4. Associated with general paediatric diseases ; cystic fibrosis , sickle cell anaemia ,
immotile cillia syndrome & immune difficiency .
Most of the snuffy babies have idiopathic neonatal rhinitis , while most of the catarrhal
children have a mixture of allergic rhinitis & adenoid hypertrophy , but it is important to
exclude the other causes , in older children , allergy is the commonest cause of catarrah
History
In infancy , there are 3 parameters which distinguish infants with significant nasal
obstruction from many snuffy babies whose nasal obstruction & rhinorrhea are benign ,
these are ;
1. Sleep disturbances ; parent describe waking , struggling to breath & inability to
settle , apnoeas , soft tissue recession , stertor & snoring .
Sleep disturbances & snoring in older children are often due to combination of nasal
, nasopharyngeal & oropharyngeal obstruction .
2. Feeding difficulties , disturbed feeding if the infant keeps coming up for air during
feeding , nasal obstruction which may be associated with air swallowing & colic .

Lecture notes in
3. Poor growth , severe airway obstruction can result in failure to thrive due to
increased energy expenditure rather than any disturbance of growth hormone
secretion , as growth in this age group is relatively independant of growth hormone .
In older children , the symptoms are often less dramatic ;
1. Sleep disturbances & snoring , can occur due to a combination of nasal ,
nasopharyngeal & oropharyngeal obstruction .
An audio-tapes can be computer analysed to provide objective evidence of sleep
disturbance without admitting the child .
2. Mouth breathing during the day is due to nasal obstruction , which concerned by the
parents & teachers more than the child .
Fixed nasal obstruction means a septal deviation .
3. Nasal discharge (rhinorrhea) is of little concern to the children , thein clear
discharge usually from a viral common cold or due to allergic or perennial rhinitis .
Thick discoloured secretions not always mean bacterial infection .
Foul smelling unilateral discharge strongly suggest foreign body .
4. Inability to blow nose for 4-5 years old children .
Examination
In infants ;
1. Observe (inspect) ; assess the respiratory pattern , soft tissue recesion , use of
accessory muscles & the timing & charcteristics of any stertor (even an infant with
bilateral choanal atresia can breath well if he is crying enthusiastically) .
2. Assess the airflow , suction of the nasal secretions is very helpful prior to
examination , there are 3 methods ;
a. Auscultation with stethoscope bell .
b. Spatula test , observing misting pattern on a cold spatula .
c. Watching wisps of cotton wool move in the airfstream .
3. Examination ;
a. Nose ; by fibreoptic otoscope , if no obvious cause seen , pass N/G tube for
choanal patency .
b. Oropharynx ; occasionally nasopharyngeal polyps may be seen hanging behind
the palate .
In children ;
1. Nose examination ; by elevation of the nasal tip with head mirror illumination .
2. Otoscope used to obtain a magnified view .
3. Video-otoscope used to examine the anterior nares & has the advantage that the
child's cooperation is improved & abnormalities can demonstrated to the parents .
Investigations
Fourtunately , a provisional diagnosis can ofetn be arrived at from the history &
examination , so no need for investigations , and the management started in the bases of this
1. Radiology
a. Sinuses ;
i. Sinus x-ray ; Water's view , clear view provide reassurance for parents & doctor
alike this intervention is required .
Mucosal thickening means allergic rhinosinusitis .
Opaque antrum due in 70% to infection .

Lecture notes in
ii. CT scan provide much more informations & is essential if FEES is being
considered .
iii. U/S of sinuses has advantage of avoiding ionizing radiation & easier patient
cooperation .
b. Adenoids ; x-ray examination of the postnasal space to determine the adenoid
size & postnasal airway correlates poorly with the size of adenoids at opearation
2. Nasal smears & swabs
- Swab for bacteriology , is not usually useful in Dx & Rx .
- Smear from the turbinates , eosinophilia which doesn't confirm allergy i.e. non-
allergic eosinophilic rhinitis .
3. Cillial function ; brushing for cilliary motility & saccharine transport test (for child
> 6 years) .
4. Blood tests
a. Full blood count is seldome helpfull .
b. Radioallergosorbant test , less sensitive "RAST" .
c. Immunoglobuline assay , espicially immunoglobuline subclass estimation , very
valuable in children leading to successful management with prophylactic
antibiotics & provide an explanation for parents as to why their child has
repeated infection .
5. Skin tests ; quick , easy & effective in adults , but not popular in children .
6. Rhinomanometry , anterior rhinomanometry correlate well with the size of the
adenoids at operation , as does the acoustic rhinomanometry , it is of no clinical use
in children as it is difficult & time consuming .
7. Sleep studies
a. Polysomnography , is routinely used to detect periods of apnoea & oxygen
desaturation .
b. Sleep nasendoscopy is useful for revealing the site of an obstruction .
Management
A. Neonatal conditions
While most infants will have ideopathic neonatal rhinitis , some will have obvious
congenital abnormalities ;
1. Congenital syndromes ; craniofacial syndromes (hypoblastic maxilla , hypoblastic
nares , micrognathia ..etc) , usually associated with nasal obstruction & even
choanal atresia .
The initial management is to insert an oral airway , subsequently , the placement of
nasopharyngeal airway or even long nasal stent .
2. Congenital masses ; like nasopharyngeal cysts , hairy polyps ,
meningoencephalocele , gliomas , dermoids , capillary haemangiomas , fibromas ,
fibromyxoma , mucocele , granuloma , lipoma , nasal aplasia , nasal cleft & web .
CT & MRI manditory prior to surgery to assess the intracranial connection .
Surgical management of all these conditions except for the haemangiomas which
resolve spontaneously by the time of 5 years of age with use of steroids .
3. Nasal septum ; there is no difference between a group of neonates whose septa were
strightened after birth (by surgery) & a group who were left alone (corrected
spontaneously with growth and moulding) .

Lecture notes in
Surgery of the septum either via sublabial approach or simple replacement in the
midline without anaesthesia .
4. Choanal atreisa ; patient with bilateral atresai need oral airway prior to surgery ,
diagnosis by CT scan after nasal suction & vasoconstruction , managed by
transnasal drilling under video control (drilling done even if the stenosis is
memberanous) provides the best success rate & stent left in place for at least 6 weeks
to prevent restenosis .
5. Nasal stenosis ; by using CT scan can Dx what is called congenital nasal pyriform
apearture stenosis .
6. Syphilitic neonatal rhinitis ; rare , there is thin discharge starts in the 3rd week , then
become purulent with crusting around the nares , so mothers preinatal screening will
usually rule out this rare cause of snuffly babies .
7. Chlamydial rhinitis ; C&S shows intracellular parasites Chlamydia trachomatis
found during vaginal delivery .
8. Idiopathic neonatal rhinitis ; the possible causes are ; allergic , bacterial , deficiency
in autonomic control , associated with gastroesophageal reflux .
Managed by simple extraction of nasal mucous by sucker , betamethazone nasal
drops (with/without neomycine) , occasionally there is turbinate odema & excessive
secretions needing nasal stent to provide an airway .
B. General childhood conditions
1. Immune deficiency ; can cause rhinitis/rhinosinusitis , so in relactant sinusitis we
have to do immunoglobulines & immunoglobulines subclasses assay .
Managed by prophylactic antibiotics in less severe cases , & in severe cases
replacement of the gamma-globuline .
2. Cystic fibrosis ; it affect primarly the lungs & sinuses & to lesser extent the ears , it
charcterized by ; polyps with CT scan evidence of sinusitis .
Managed by steroids nasal drops in mild polyposis , in the sever cases surgery in the
form of simple nasal polypectomy with external or internal ethmoidectomy or
CaldWell-Luc's operation or FEES (endoscopic polypectomy better than simple one).
3. Immotile cillia syndrome ; there is inability to transport mucous by the cillia leading
to bronchectasis , sinuisits , ototis media & nasal polyposis , situs inversus also may
occur (which is a feature of kartegner's syndrome) .
Diagnosed by sacchrine transport time (done in clinic) & managed by medical
management for cilliary dyskinesia & FEES .
4. Sickle cell disease ; adenotonsillar hypertrophy causing obstructive sleep apnoea
leading to vasculo-occlusive disease .
Managed by blood transfusion & adenotonsillectomy .
5. Down's syndrome ; all patients show sleep abnormalities with true obstructive sleep
apnoea with crniofacial anomalies .
Managed by adenotonsillectomy for those without craniofacial anomalies .
6. Pubertal rhinitis ; during puberty , there is intermittent nasal obstruction & even
rhinorrhea .
Managed by reassurance & ipratripium bromide for rhinorrhea (not the obstruction)
C. Specific childhood conditions of the nose & sinuses

Lecture notes in
1. Adenoids ; most adenoids removed at operations are infected by H. influenza ,

usually the sized of adenoids is not imporatnt , but the size relative to the postnasal
space & the airway that is remaining is the important .
Diagnosis from ;
a. History ; parents say that nasal obstruction , mouth breathing & s.t. nocturnal
apnoea & snoring .
b. Postnasal mirror examination (for child >6 y) .
c. Sleep nasendoscopy , most closely correlates with the clinical situation .
Indications of surgery , patiet usually fall somewhere between snoring without nasal
obstruction & significant obstructive sleep apnoea .
Management is by ; suction diathermy technique (to decrease bleeding) , blind
adenoidectomy (risk of choanal adenoids which is obstructive tissue leaves at the
choana) , adenoidectomy contraindicated for , bifid uvula , significant history of
nasal regurgitation in infant ,& intercurrent URTI .
Adenoidectomy is also effective in controlling rhinorrhea , parents usually more
impressed with the improvement in obstruction than with cessation of rhinorrhea .
2. Nasal polyps ; occur in the presence of non-allergic eosinophilic rhinitis (not only in
cystic fibrosis) , managed by nasal steroids (good response in most of cases) or
surgical removal for unresponds & for large antrochoanal polyps .
3. Nasal septal deformities ; previously , it is taboo to do corrective septoplasty in
children because of possible damage to the growth centres .
Where there is severe nasal obstruction or in social & psychological difficulties ,
limited surgery accepted for > 5 years old child (also external septorhinoplasty is
same surgery to access nasal masses in infants & children) .
4. Rhinitis
- Allergic rhinitis ; it is due to house dust mite faeces & pollution play adjuvant role
in allergic rhinitis (with traffic density) , 90% of children with rhinitis are allergic
with pollen being the commonest caustive factor .
The prognosis is very poor (with poor compliance rather than change in the disease).
- Infective rhinosinusitis ; we can not distinguish between rhinitis & sinusitis by
history , examination , x-ray , U/S & even by AWO , it is either viral rhinitis (adeno ,
rhino & coxackie virus A&B) or bacterial sinusitis .
- Eosinophilic non-allergic rhinitis ; congestion , rhinorrhea , itching & sneezing
which not fluctuate with allergy exposure & skin tests are negative .
Nasal smears shows eosinophils with low or normal IgE , it is associated with nasal
polyps & interensic asthma .
Management of childhood rhinitis ;
a. Medical ;
- After history & skin tests , recommended allergen avoidance like ; avoid contact
with pets , damp dusting , plastic covers for mattress , ascarides (chemicals to kill
house dust mite) & freeze duvents , pillowa & toys for 6-24 hours .
- Course of oral hyposensitization (effective) .
- Use of non sedative antihistamines like acetamazole , loratadine & terfenadine ,
useful for rhinorrhea .
- The use of vasoconstructors usefull for rhinorrhea , like topical (cause rhinitis
medicamentosa) & systemic (safe & effective) .

Lecture notes in
- Topical nasal steroids (if both nasal obstruction & rhinorrhea) , is the back bone in
the management of adults , but with caution in paediatric (because of the effect in the
axial growth) , in the correct dose the children take once a day preparation
(fluticasone) is not at risk .
- Inhaled cromoglycate though effective , but with low compliance , because it given
in 4 seperated doses per day .
- Nasal suction & saline nasal drops are very usefull for snuffly infants .
- Short courses of antibiotics used if discharge recurres .
- Homeopathic medicine used by some keen parents .
- Immunoglobuline replacement rarely necessary .
b. Surgical ; if medical Rx fail , then surgery in the form of turbinectomy (if there is
turbinate hypertrophycausing nasal obstruction) , types are ;
- Simple submucous diathermy "SMD" may cause severe bleeding .
- Total turbinectomy , may lead to rhinitis sicca , crusting & bleeding (s.t. do
trimmig turbinectomy) .
- Cryosurgery to the turbinates , effective & without the risk of bleeding .
- Laser turbinectomy .
5. Sinusitis
a. Acute bacterial sinusitis , manage it by decongestant & antibiotics (without AWO) .
b. Chronic sinusitis ; signs & symptoms with long radiological sinus abnormalities
(on x-ray & CT) with rhinnorhea & minor pain & headache .
Management by prolonged antibiotics & topical nasal steroids with AWO , now
use paediatric FEES , with more efficacy & safety in skilled hands espicially for
cystic fibrosis & in few cases of medically resistant symptomatic sinusitis .

Lecture notes in
Nasal polyps
It is the pudenculated portion of the oedematous mucosa of the nose & paranasal sinuses
(ethemoid or maxillary sinuses).
They are result from the prolapsed lining of the ethemoid sinuses & block the nose to a
variable degree depending on thier size .
It is classified either according to thier aetiology & pathology or thier site .
According to the aetiology & patholgy , they divided into ;
1. Simple mucous polyps , which results from the polyps of the mucosa of the ethemoid
or antrum , they block the nose to avariable degree depends on the size .
a. Allergic polyps ; due to uncomplicated sensitivity to one or more allergin , usually
multiple .
b. Vasomotor polyps ; simillar to allergic polyps , but , there is no allergin to be
adentified .
c. Inflamatory polyps ; due to bacterial or vira infection , uncommon , the acute type
occur recently & usually associated with influenza , usually single , very soft ,
uncommon & slightly haemorrhagic , the chronic non-speciefic are long standing &
multiple , while the chronic speciefic (i.e. Rhinospordiosis) usually single , friable ,
bleeding polyps resembling strawberry .
d. Mixed inflamatory allergic polyps ; represent secondary inflamation in allergic or
vasomotor polyps .
2. Neoplastic polyps , which are ;
a. Benign polyps ;like bleeding polyps of the septum , DDx are fibroneuroma ,
grsnuloms , neurofibroma , transient cells tumor , fibroma , glioma (in children)
meningioma (in adults) .
b. Malignant polyps ; carcinomatous , lymphomatous (usually solid , friable , extremely
haemorrhagic) , or sarcomatous (simulate mucous polyps) .
According to the site , they divided into ;
1. Ethemoidal polyps ; ethemoidal cells are the commonest site , inferior turbinate is
the next in frequency , these polyps tend to grow forwards towards the anterior
nares.
The ethemoidal polyps are easily diagnosed clinically ;(1) the polyp insensitive due to
poor nerve supply (this is against probing of the middle turbinate) (2) Pale colour of the
polyp due to poor blood supply, s.t. it become reddish due to trauma or inflammation (3)
most commonly bilateral , but may be unilateral this indicate histopathological
examination (biopsy also indicated in haemorrhagic polps) to exclude transient cells
papiloma (Ringert's tumor , inverted papiloma) & malignancy, & (4) unusual before the
age of 10 years , but if occur we should suspect cystic fibrosis which excluded by sweat
test .
2. Antral polyps ; may be single or multiple , emerges from the sinus anteriorly then
extends backward to the posterior choana (ACP) .
Antrochoanal polyp (ACP) are simillar in colour to the ethemoidal polyps , but, are
disease affecting the maxillary antrum where the polyp prolapse through the middle
meatus backwards to the post-nasal space , it is single polyp may arise at any time after
the age of 2 years , if seen before this age we should exclude meningocele or
encephalocele & should examine the anterior cranial fossa radiologically.

Lecture notes in
Although polyps are disease of ethemoidal sinuses , the mucosal changes frequently
affect the maxillary sinus commonly than the frontal or sphenoidal sinuses which may be
seen radiologically .
Pathogenesis of polyps are ; (1) mucosal reaction at the cellular level (2) poorly developed
blood supply to the ethemoid sinus & (3) complex anatomy of the ethemoid labryinth .
Five THEORIES of pathogenesis :
1. Bernonilli's phenomenon ; result in pressure drop next to construction which suck
the mucosa of the ethemoid sinus into the nose & this cause the mucosa nearest the
nasal valve will be polypoidal .
2. Polysaccharide changes ; alteration of polysaccharide of the ground substance &
less mature collagen formed in the polyps .
3. Vasomotor imbalabce ; it's applied to majority of cases aren't atopic & no obvious
allergen to be found , the poor nerve supply & blood vessles are infrequent & are
usually cappilaries , the larger polyps have little smooth muscles within them .
4. Infection ; sinusitis usually of 2 types , either purulent or hyperplastic , the purulent
sinusitis usually results from secondary bacterial infection following viral infection
(URTI) & the inflammatory changes may extend into the ethemoid sinus causing the
mucosa to become polypoidal . While the hyperplastic sinusitis associated with mucous
hypersecretion in which the organism may be found & cultured .
Inapproperate surgery on the maxillary sinus (such as intranasal antrostomy) through
which new mucosa which undergoes the same changes & subsequently polyps through
artificial ostia .
The cause of the inflamtory is uncertain , the commonest organism is the non-capsulated
Haemophilis influenza which is the commonest commensal MO in the nose &
oropharynx & frequently cultured from sputum of patient with chronic bronchitis .
It is difficult to implicate a role of this theory because of the role of antibiotics &
steroids on treatment .
5. Allergy (hypersensitivity) ; this theory implicated due to 3 factors ; (1) 90% of
histological picture of nasal polyps which have eosinophilia (2) association with asthma
& (3) nasal findings may mimic allergic symptoms & signs .
Allergy means hypersensitivity , immune reactions cause tissue damage , mainly
mediated by IgE which so attached to the mast cells(they also triggered by IgG ,
complement activation , drugs , chemicals & non-speciefic factors) causing thier
degranulation (releasing ; histamine , heparin & other vaso-active & chemo-tactic
factors) which is rapid event (within 30 min.) , the Arachodonic acid which manfuctired
in the cell memberane to produce PGs , slow reacting substance of anaphylaxis(SRS-A)
& Leukotrines mediators , other mediators comes from the cytoplasm .
The early phase of allergy is nasal blockage , sneezing & running nose (attachment of
the cells to the sote of the reaction) , this followed by amplification of lymphocytes &
eosinophilis release more mediators & this phase causing mucous hypersecretion &
nasal blockage .
There may be local allergy in the nose causing polyps .
Clinically as attacks of rhinorrhea , sneezing , nasal blockage & the patient may have
one or more +ve skin tests .

Lecture notes in
The conditions associated with polyps are ;

1. Asthma
- 20-40% of patients with polyps have existing asthma mainly in the late onset asthma
rather than childhood asthma .
- surgery has little effect on asthma .
- most commonly asthmatic pathient with polyps are female (polyps alone occur more
in males) .
2. Aspirin hypersenstivity
- nasal polyps + asthma + aspirin hypersenstivity about 8% .
- mechanism for both aspirin hypersenstivity & asthma are unclear .
- it's not allergic reaction , but, thier may be alteration of PGs synthesis .
3. Cystic fibrosis
- multisystemic disease affecting the exocrine glands in about 1:2000 live births , M:F
5:1 , there is abnormality in the 7 th chromosome in 75% of cases .
- exocrine sweat glabds unable to produce diluted sweat & values of above 60 mmol of
Na+ in sweat test (diagnostic) & the electrolyte transport in the respiratory
epithelium (esp. Cl-) is defective causing thick & dry sticky airway secretion .
- GIT symptoms are ; failure to thrive , failure to pass muconium .
- Respiratory symptoms are ; recurrent RTI , severe lung damage due to persistant
colonization of Staph. & Pseudomonas .
- It is coomon in children bellow 2 years to develope polyps with cystic fibrosis .
- True incidence is uncertain ( 3 – 48%) .
- Muconium illeus is the commonest presenting symptoms , but, not in patients
associated with polyps which have less GIT problems
- Lung function detoriorate with age in all cases , but, the child may live to adulthood
with lung-heart transplantation .
- X-ray of the sinuses shows opaque sinuses , but, it is not diagnostic because 1/3rd of
normal children with thick mucosa .
- Sinuses act as a reservior for the decending infection , this hypothesis supported by
different culture & senstivity of MO from sinusitis , but not supported by presence of
sterile sinusitis .
4. Other respiratory diseases ; rare in adults but more in children.
- Kartinger's syndrome ; primary immotile cillia syndrome (cilliary dyskinasia)
causing polyps due to stasis of mucous .
- Young's syndrome ; hyperviscous mucous charecterized by bronchitis , sinusitis &
azospemia .
The Incidence
- Age ;it is disease of adullts 30-60 years , may developed in children with cystic
fibrosis or in teenagers , simple ethemoidal polyps occur at any age , ACP common
in children & young adults (mostly Males) , also atopic & asthmatic patients
develope polyps at later age .
- 1 in 1000 – 20 in 1000 of adult population have nasal polyps once or more in life .
- Sex ; male prodomenance 2:1 – 4:1 in adults & also in children with cystic fibrosis .
- Race ; all racial groups could be affected .
- Animals ; seen in champanzii , cattle & cats .

Lecture notes in
- Genetic predisposition ; unknown , but, (1) patient with cystic fibrosis is autosomal
rescesive of chromosome No. 7 , (2) mutation of G55ID associated with nasal polyps
more , (3) HLA-A (A1/B8) associated with nasal polyps, asthma & aspirin
hypersenstivity more , & (4) family history not supportes by genetic predisposition .
Pathological features
- Macroscopical
 Site ; may arise from the respiratory mucosa of the nasal lining , it may arise from
the inferior & middle turbinates , but, classically & commonly developed from the
ethemoid sinus from ; either beneath the middle turbinate (anteriorly) or above
middle turbinate (posteriorly) , also it may occur in the otjer sinuses ,particularly
maxillary sinus following antrostomy .
 Colour ; translucent , white in colour ( poor blood supply) , it may be red due to
trauma or infection .
 May prolapse through the anterior nares .
 Usually Multiple & about 1/4th regress spontaneously without Rx .
 Size & side ; variable size & usually bilateral , but in ACP usually unilateral .
- Microscopical
 Usually have respiratory epithelium with cilliated columnar & goblet cells .
 If there is repeated trauma , the epithelium converted into sequamous type .
 As the polyp shrinks , this lead to loss of surface epithelium to avariable degree &
this called cobblestones .
 Basement membrane is thick which will be vary from area to area & from polyp to
polyp .
 Submucosal tissues , grossly odematous & contains (1)few blood vessels which are
mainly cappillaries & (2)occusional nerve fibers , also there were be cellular
infilterate of plasma cells , small lymphocytes , macrophages, neutrophils & the most
stricking feature is the eosinophilia(found in 90% of polyps) which vary inbetween
the patients & polyps .
 Sensitized eosinophils believed to be important in intrusion of mucosal odema in
patients with aspirin hypersenstivity .
 High levels of IgE can be identified in polyp odema which may be due to presence of
allergic elements .
 Culture ; it shows the followings :
- Streptococci ; frequently more common cultured from asthmatic patients .
- Completely –ve culture for ; Mycobacteria , Mycoplasma & Viruses .
- Bacterial speciefic IgE ; present in polyp's odema & most commonly increased with
Proteus .
Clinical features
- Symptoms ; slow incidious onset , but, may be sudden after acute infection .
1. Nasal blockage ;(1) the commonest symptom , occur in all patients without exception
(2)constant althogh it vary in size & position of the polyp (3)the mildest form is
congestion (4)it causes ansomnia , epiphora , postnasal catarrh (irritation & drip),
headache , snoring & speech defects, & (5)after surgery there may be some nasal
breathing & there is humidification of air & that those patients with asthma notice
an improvement of thier chest symptoms .

Lecture notes in
2. Running nose & sneezing ; (1)half of patients suffer from this symptom, which may
be helped with surgery when large area of odematous mucosa improved (2) patients
with this symptom usually they say that they have hay fever (3)common in patient
with aspirin hypersensitivity .
3. Partial loss of smelling & alteration of taste ; common , not improved following Rx
except in some cases treated by corticosteroids espicially when taken orally .
4. Pain ; (1)not frequent (2)occur it is over the nasal bridge , forehead & checks (3)
worst when the nose congested , the sinuses infected & when the postnasal drip
changes in colour .
5. Post-nasal drip ; (1)mostly occur (2)usually white in colour , but, may become yellow
or green , particullary associated with maxillary pain or after exacerbation of nasal
symptoms & there is alteration due to inflamation or severe eosinophilia which may
change the colour of secretions & this called the allergic pus & (3)may improved
following surgery , if it is green in colour it improved after Rx with AB.
6. Epistaxis ; infrequent , follows extensive clearing of the nose , if it occur may
indicate a more sensiter underlying pathology .
7. Purulent rinorrhea ; common in the inflamatory type , associated with headache .
- Signs
1. Hyponasal speech (Rhinolallia clauza) if the blockage is severe .
2. Polyps can be seen externally .
3. Mouth breathing .
4. Flair out of alar cartilage which occur with complete obstruction .
5. Hypertelerosis , if the polyp develope before the facial bones fuse (seen in child with
cystic fibrosis) , this cause expansion of the nasal bones & broadening of the of the
nasal bridge (occur in longstanding cases –frog face)
6. intranasal sings ; the polyp appears as pale bag which arise most commonly from
the middle meatus & are relatively insensitive when probed , usually bilaterally .
Investigations
- There is no speciefic haematological , biochemical or immunological tests .
- Skin test widely used to investigate nasal causes .
- If patients with anterior mucoid rhinorrhea or develope polyp early we should
investigate for : (1)cystic fibrosis (2) cilliary dysfunction (3)immune deficiency.
- Radiology ;
1. Plain X-ray of paranasal sinuses , demonsiterated by 3 conventional views ;
(1)Occiptomental view (water's view) (2)Occiptofrontal view (Cadwell lock view)
(3)Lateral view .
This will show the extent of the disease in the nose & paranasal sinuses to some extent .
2. CT – scan ; give more information particularly the anatomical details , the other
features are ; (1)loss of radiotranslucency in the nose (2)hypertrophy of the
turbinates (3) deviation of the boney septum & intra-nasal masses (4)ethemoid
complex opaque in the side of polyp (5)change in the mucosal thickening , fluid level
which is due to either retained secretions alone or purulent secretions due to
blockage of the ostea (6)ethemoidal expansion in patients with polyps developed
before the bone fused (7)boney erosion suggest malignancy , polyps due to previous
surgeries which is implicated for mucocele which is more common in the frnotal or
ethemoid & rare for sphenoid sinuses .

Lecture notes in
The anatomical variations :

 Some surgeons consider the variations in the osteomeatal complex are the most
important factors in the development of the polyps , so that the correction of this
variations is the main stay of Rx .
 Osteomeatal complex ; agger nasi cells , borders of the uncinate process , over
pneumotized ethemoidal bullae , coancha bullosa , parodoxical middle turbinate .
 Area of junction between the nose & the ethemoid sinus which is the area where the
polyps start .
Treatment
- Medical ; start first & when fail progress to surgical Rx .
1. indicated where the polyps not obstruct the nose completely .
2. in cases of anatomical variations , they not respond to medical treatment .
3. it is divided into (1)inducing remission (2)prevent recurrence .
4. Pre-operative ; use intranasal corticosteroids for one month (Mecca position , spray
use is very important for position of spray to reach the posterior parts of the cilliary
epithelium , althogh the cilliary action transport the spray posteriorly & cover the
lining) , Betamethasone drops (2 drops to each side per day) or acqueous
Beclomethasone (twice daily) , this prevent surgery in 50% of patients .
5. post-operative ; intranasal corticosteroids indicated in patients with severe recurrent
symptoms (Beclomethasone twice daily) , if not we give oral corticosteroids
(prednesolon 5-10 mg daily for 10 days with continuation of the topical Rx) , cushing's
syndrome may occur with the abuse of Beclomethasone , also the patient may develope
steroid resistance .
6. Diet ; help those with aspirin hypersensitivity .
7. Allergy control .
- Surgical
 Anatomical consideration & complication :
1. the middle turbinate is the key point for surgery , if the surgery performed medially
we may breach the cririform plate & then enter the anterior cranial fossa , if
performed laterally we will enter the ethmoid complex .
2. extensive intranasal operations on ethemoids causing unstable middle turbinate ,
also may cause injury to medial rectus (anteriorly) or optic n. (posteriorly) .
3. if remove the middle turbinate , subsequent orientation will be difficult .
4. endoscopic surgery could be lead to stenosis of the middle meatus .
5. if do vigrous ethemoidal surgery this will lead to enter the orbit easily by piercing
the thin Lamina Papyracea .
6. herniation of the orbital fat which is the simplest complication .
 Pre-operative preparations ; keys of good surgery are ; good illumination & minimal
bleeding , so prepare the nose by vasoconstruction & shrinkage of mucosa by the use
of LA to provide drier nose which done by several methods :
1. 10% cocaine – spray given 15 min. Before LA .
2. 25% cocaine –paste used on cotton wool loaded wires & the mucosa painted
throughly , this used for middle turbinate posteriorly & anteriorly between the nasal
bones & the septum , if the inferior meatus need to be entered use a probe .

Lecture notes in
 Surgical procedures
- Simple polypectomy ; removal of the polyps either by avulsion , cutting snare or
forceps (Tilly Hienkells foceps) , also care must be taken when use a forceps not to
go either too medially or to laterally , we remove all prolapsed mucosa & inspect the
ipsilateral eye before pulling the material .
- Intranasal ethemoidectomy
1. preoperatively we see the site of the disease accurately by the nasoendoscope & CT-
scan of the nose & paranasal sinuses .
2. the endoscope can be used to (1)undertake more through endonasal ethemoidectomy
(2)monitor the postoperative course .
3. oral corticosteroids can srunck the polypoidal mucosa if used preoperatively , 30 mg
prednesolon/d in reducing dose for 10 days before surgery .
4. it is not a safe procedure because it may make the middle turbinate unstable or lost .
- External ethemoidectomy
1. incision ; Howarth's incision medial to the inner canthus or Patterson's incision
through the natural skin crease below the infraorbital margin .
2. displace the orbit & the lacrimal apparatus laterally .
3. find the anterior ethemoidal vessels ( land mark for the cririform plate) & divid
them & ligate it .
4. remove all the ethemoid cells & sphenoid sinus .
5. care should be taken to open the osteum of the frontal sinus widely to prevent
mucocele (which is late complication) .
6. no trail said that ext. Ethemoidectomy prevent recurrence , but, it may delay it
several years .
- Jansen-Horgan procedure ; indicated when the mucosal changes extend to the
maxillary sinus , it is a combination of Caldwell-Luc & Post. ethemoidectomy
through the antrum & the intranasal anterior & middle ethemoidectomy .
- Caldwell-Luc operation ;
1. the operation designed to remove the irreversable damaged diseased mixillary sinus
mucosa & to facilitate the gravitional drainage & aeration via the inferior meatal
antrostomy.
2. may be undertaken alone for maxillary sinus mucosal disease , but, prolapse of the
polypoidal mucosa through the antrostomy in the inferior meatus may occur which is
exceptimally difficult to Rx .
3. it is predominantly used for chronic persistant sinusitis when the medical Rx , lavage
& antrostomy failed , so indicated for ; (1)chronic maxillary sinusitis (2)removal of
recurrent ACP (3)removal of F.B. such as dental root or amulgum (4)closure of oro-
antral fistula (5)dental cyst involving the antrum (6)access to the pterygomaxillary
fissure & pterygo-palatine fossa (7)elevation & stabilization of the orbital floor fracture
or removal of the orbital floor in decompression (8) Maxillary sinus fracture (9) Fungal
sinusitis (10) Maxillary sinus tumor (11) Empyema of the maxillary sinus resistant to
conservative therapy (12) Symptomatic maxillary mucocele .
4. don't recommended as a route for biopsy of antral malignacy .
5. It is contraindicated in (1)children because it cause damage to the secondary
dentation (2) Uncontrolled bleeding disorder (3)Aplastic maxillary sinus .

Lecture notes in
6. operative technique
a. head light or illuminated speculum .
b. supine position , reverse Trendelenberg , 15o head flexion .
c. can be done under LA (maxillary n. block) or usually under GA (cuffed ETT ,
pharyngeal pack , topical LA within the inferior meatus , injection of 1:200000 into
gingivolabial sulcus & soft tissue of canine fossa .
d. incision ; 3 mm above & parallel to the gingivolabial fold from the posterior edge
of the lateral incisor to 1st or 2 nd molar tooth (3-4cm) .
e. continue down to the bone of gum margine , it is advisable that the incision doesn't
directly overlie the opening in the anterior face of the maxilla to decrease risk of
fistula .
f. muco-perosteal flap dissected superiorly with periosteal elevator to expose anterior
wall of the maxilla , take care to avoid damage to the infraorbital n. which arise in
the foramina just below the orbital rim either directly or indirectly by retraction .
g. the anterior wall opened in canine fossa where the bone relatively thin with a drill
or with a 5 Jenkin's gauge .
h. enlarged the openeing by Hayek or Kerrison punch forceps to produce a hole
suffeciently large to allow removal of sinus mucosa (approximatly 1-1.5 cm in
diameter) .
i. inferior extension lead to damage to the teeth & thier nerve supply , laateral
extension cause bleeding due to injury to the anterolateral branch of spheno-
palatine artery , the boney bleeding controlled by either crushing of the bone by
punch forceps or by diathermy or usually settls once the mucosa removed .
j. removal & dissection of the entire lining of sinus mucosa , the success of the
operation depend on complete extirpation of the mucosa which can be difficult to
done in the inferolateral angle & the roof .
k. large inferior meatal antrostomy (2X1 cm) through the sinus .
l. packing of the nose & occasionally the antrum via antrostomy & care should be
taken when want to remove it (that no strands are caught on boney edge of the
antrostomy) .
m. suturing the buccal mucosa incision with absorbable suture to decrease the
incidence of fistula , but, it should be suffeciently loose to allow drainage of blood .
7. advice the patient ;(1) not over enthusastic blowing of the nose for 1 week (2)should
replace upper teeth dentures within 24 hours to avoid obliteration of the labio-alveolar
sulcus .
8. complication of the operation
a. pain & soft tissue swelling which decreased by attention on surgical procedure .
b. haemorrhage ; can occure from both ant. bony wall or inferior meatal antrostomy
c. parasthesia due to damage of the infraorbital n. , not occure in careful dissection
& retraction , also in long term patient complain from neurolagia in the
distribution of the infraorbital nerve .
d. altered sensation to the teeth & occasionally devitalization & tooth discoloration
due to damage to the teeth innervation .
e. oro-antral fistula which occasionally occure espicially when care not taken with
the sitting of the incision , it could be temporary or perminant & require surgical
closure .

Lecture notes in
f. abnormal mucosa grows in the maxillary sinus both histologically & functionally .
g. retention cysts which particularily large to fill the sinus .
 Complications of surgery
1. Haemorrhage ; it is the main immediate complication , occure at the time of surgery ,
can be minimized by good preoperative preparation & pscking , in the next few days
slight serangious discharge occure from the raw areas .
2. Crusting ; due to driness of blood & mucous 2 weeks after the surgery & this should
follow up for removal .
3. Damage to the cribriform plate ; causing CSF rhinorrhea , meningitis (more
important) , complete ansomia (rare) due to damage of the olfactary bulb .
4. Damage to the orbit which entered through the lamina papyrecea or through
posterior ethemoidal cells .
5. Damage to orbital periosteum ; lead to ; herniation of the periorbital fat , med.
Rectus palsy , damage to the ant. & post. ethemoidal arteries & division of the optic n.
6. Endoscopic surgery associate with increased rate of complication , so that before
surgery we should be famillar with anatomy .
N.B : recurrence of the polyps is not a complication because it is a feature of the disease .
 Post-operative medical care
1. ten days course of decongestant & stem inhalation for all patient undergone nasal
surgery .
2. long term of corticosteroids spray suggest that it is (1)control the reccurence &
prevent it (2)control symptoms of rhinitis .
3. patient with rhinitis & polyps noy means that he is more prone to recurrence .
4. antihistamis had no place in the mangement of recurrence due to (1)sedative effect of
antihistamins (2)non-sedative antihistamins cause liver enzyme induction after 6
weeks , but, short can be prescribed if rhinitis difficulty controlled .
5. diet ; patient with aspirin hypersensitivity should exclude tartazine dyes from thier
diet due to its pharmacologically linked with aspirin .
Recurrence of the nasal polyps
- one of the pronlems facing the otolaryngologist , variable rate from 40% presented
for the 1st time & 5% had 5 or more previous polypectomy .
- factors associated with recurrence ; (1)female (2)long history of nasal complaints
(3)association with asthma (4)young (5)aspirin hypersensitivity .
Treatment of polyps in patient with cystic fibrosis
1. intranasal steroids is the 1st line , spontaneous resolution even without the use of
steroids .
2. extensive sinus surgery which associated with severe blood loss .
3. both 1&2 can control 60% of the patients , but each line depend on ; age of the
patient , compliance & family .
4. if there has been improved , Betamethasone with or without neomycin drops used for
2 months , this could be followed by long term corticosteroids spray (Beclamethasone).
5. simple polypectomy associated with high rate of recurrence , FESS under LA have a
place in older children with compramized pulmonary function .
6. the avearage time between recurrence is 1-5 years , age of the 1st operation 2-15
years ( 7.5 years) .

Lecture notes in
Antrochoanal polyps (Killian's polyp)

- arise in the maxillary antrum & prolapse through the ostium of maxillary sinus in the
middle meatus .
- hangs either in the nose or if it is larger into the posterior choana , the choanal
portion of the polyp may be seen in the oropharynx where it pushes the soft palate
forward .
- aetiology , unknown , not associated with allergy , lower RTI or sinsusitis , it could
be due to faulty developement of the maxillary sinus ostium since it always large ,
but, the ostium may be large due to the expansion by the polyp , this is unlikely
because there is no expansion of the posterior choana by the polyp & no erosion or
displacement of the middle turbinate .
- occure equally in all racional groups , male > female .
- onset before 40 years , but, may occure at any age .
- dumb bell in shape because of construction where they pass through the maxillary
ostium or accessory ostium .
- usually unilateral (rarely bilateral) & arise from the floor & lateral wall of the
maxillary antrum , although the site of origin frequently can't determind .
- simillar in colour to the simple type of polyp (pale , white or translucent) .
- histologically ; respiratory epithelium over normal basement , odematous
interstitium & cellular infilterate (the same as simple polyp but with no eosinophilia)
- symptoms ; causing unilateral nasal obstruction , but, when large , bilateral nasal
obstruction , greater in expiration than inspiration (ball valve effect) , other nasal
symptoms are rare except mucoid anterior nasal discharge .
- it may be not visible in anterior rhinoscopy , but, usually seen by posterior
rhinoscopy occasionally without aid of mirror , the rigid endoscope shows the polyp ,
also radiograph of the sinus shows mucosal thickening or completely opaque antrum
, the sinus never appear normal on the affected side , the lateral view shows the
polyp at the postnasal space .
- Treatment
1. no medical Rx pre- or post-operative .
2. pre-operative nasal priping is not essential .
3. it is neccessary to remove both parts of the polyp .
4. approaches dedicated by the age of the patient ;
(1)simple intranasal polypectomy alone which result in recurrence.
(2)Caldwell- Luc procedure ; not introduced in young patients with incomplete
dentation .
(3) Antral washout ; straw coloured fluid , should be done because it may be help the
dissection of antral mucosa in simple polypectomy.
(4) deliver the polyp through the oropharynx because it is impossible to remove it
through the nose .
(5) blunt dissection ; done in case of larger polyp which can't or difficult to remove it
due to adhesions in the nose , so do broken of the polyp by blunt disection
(6) Caldwell –Luc Antrostomy ; indicated in adult to decrease recurrence rate .

Lecture notes in
Nasal SEPTUM
The nasal septum is an integral part of the nose with

functional and aesthetic significance. The septum divides
the nasal chamber into two cavities, lends shape and
support to the middle nasal vault, aids in the regulation of
air flow through the nose, and helps to support the
columella and nasal tip.
he nasal septum is composed of cartilage and bone that is
primarily covered by respiratory mucous membrane. The
septum is commonly divided into anterior (dorsal), posterior, caudal, and cephalic parts .
The components of the nasal septum include the nasal spine of the frontal bone, the keel-
shaped undercarriage of the joined nasal bones, the perpendicular plate of the ethmoid, the
vomer and crest of the sphenoid, the nasal crest of the palatine bone, the nasal crest of the
maxilla and premaxilla, the quadrangular cartilage, the upper
lateral cartilage, the membranous septum, and the columella .
Unlike the external nose, where most anatomic structures are
paired, the septal components are largely singular except for
the vomer, which may be bilaminar owing to its embryologic
origin. The vomer and the perpendicular plate of the ethmoid
and maxillary crest are the components of the bony septum of
principal interest to the surgeon. Most of the remainder of the
septum, the anterior and caudal portion, is cartilaginous and is
formed by the quadrangular cartilage.
Septal Haematoma
When the septum subjected to a sharp buckling strees , tear of the submucosal vessels
results , if the mucosa remain intact , unilateral heamatoma formed & if the septal cartilage
fractured (very severe trauma) then the blood pass to the other side causing bilateral
haematoma .
As the cartilage depend on perchondrium for its nutrition , then when blood accumulate
subperichondrially , this will affect the cartilage vitality (remain viable for 3 days) , if more
than that , then death of the chondrocytes & absorption of the cartilage ( by collagenase
action) .
Small haematoma not cause necrosis of the cartilage ,but may be slowly absorbed leads to
perminant thickening of the septum with gross fibrosis
The major symptoms are nasal obstruction & initialy may be some discofort .
The major signs (examination best without sepeculum) reveal a smooth rounded bilateral
septal swelling often extended to the lateral wall causing obstruction .
The major complications ;
(1) Septal abscess ; the haematoma may easily become infected forming abscess , there will
be increase in the severity of pain , constitutional symptoms ( fever & rapid pulse..etc) , this
will result in extensive caltillage necrosis , Rx by drainage (75% abscess due to trauma , the
rest as a complication to ethemoid & sphenoid surgeries or to AIDS) , the abscess can
spread to the orbit , brain , meninges & cavernous sinus .
(2) External nose deformity ; either supratip saddling or maxillary hypoplasia (children) .
(3) perminant thickening of the nasal septum .

Lecture notes in
The condition Treated by early surgical drainage (reduce the risk of cartilage necrosis) ,
this done by ; (1) long hemitransfixation incision –Free's incision- (2) aspirate the blood
with any other necrotic tissue (3) assess the status of the cartilage , if defect then patch by
homograft cartilage (4) insert small drain into the bottom of the cavity (5) anterior nasal
packing to maintain the mucosa .
Septal Deviation
Extremely common condition , but, are not severe enough to affect nasal function , more in
Caucasean races (leptorrhine type of nose) .
Aetiology :
(1) Traumatic ; direct trauma usually subjected to the nose associated with fracture &
damage to the other parts of the nose .
(2) Non-traumatic ; birth moulding theory , abnormal intrauterine posture lead to
compression force acting on the nose & upper jaws causing displacement of septum , also
more torsion forces added by labour depending on the type of delivery (minimal in
elective C/S , moderate with normal vertex presentation , severe with persistant occipital
posterior presentation .
(3) Genetic & enviromental factors are seen in identical twins ; 21% had anterior septal
deviation which mostly due to external cause (trauma) , 74% had posterior septal
deviation which mainly due to genetic factors .
The incidence of neonatal septal deviation about 4% either due to trauma or genetic factor.
Pathological anatomy : the deformity of nasal septum devided into ;
(1) Spurs ; sharp angulation occur at the junction of the vomer below with the septal
cartilage &/or ethemoid bone above , it is due to vertical compression forces (fracture of
the cartilage can lead to spur also causing fibrosis which lead to difficulty in flap
elevation) .
(2) Deviations ; charcterized by a more generalized bulge , the cause is vertical or
horizontal plane involving both the cartilage & the bone ( C-shaped deviation or S-shaped
deviation .. both are boney) .
(3) Dislocations ; here the lower border of the septal cartilage is displaced from its
medial position projecting into one of the nostrils (caudal dislocation) .
The associated anatomical abnormalities in the adjacent areas are ;
- the lateral nasal wall , there will be compensatory hypertrophy of the turbinates &
bulla ethmoidalis on the side of concavity .
- the maxilla ; flatening of the check , elevation of the floor of the affected nasal cavity
, smaller antrum on the affected side , distortion of the palate & orthodontic
abnormalities (because the compression forces are often asymmetrical) .
- the external nasal pyramid ; deviation in the external nasal pyramid caused in the
anterior septal deviations .
Types of deviations :
(1) Cartilagenous deviations ; the upper bony septum & the bony pyramid are central .
(2) C- deviations ; displacement of the upper bony septum & the pyramid to one side &
the whole cartilagenous septum & vault to the opposite side .
(3) S- deviations ; the deviation of the middle 1/3rd (upper cartilagenous vault &
associated septum) is opposite to the upper & lower 1/3rd .
As the septum goes , the nose goes , so the 1st step in manegement of a twisted nose is to
straighten the septum , so do septorhinoplasty .

Lecture notes in
The effects of septal deviation : only severe one causing effects on the nasal function & so
need manegement , these effects are ;
(1) Nasal obstruction ; on both sides usually due to the disease & the compensation ,
causing snoring .
(2) Mucosal changes ; deviation causing concetration of the inspired air currents on a
small area leading to dryness & crustation , ulceration & bleeding causing loss of
the protective mucous memberanes decreasing the resistance to infection & as a
result of Bernonilli's principle leading to oedematous mucosa around the septal
deviation causing further nasal obstruction .
(3) Neurological changes ; (a) pain due to pressure by deviation ( 1st described by
Sluder & called anterior ethemoidal n. syndrome) , (b) reflex changes affect the
nasopulmonary & nasal reflexes & (c) the pressure in the lateral wall sensitive
structers causing referred trigeminal pain & chronic headache .
Clinical features :
- Symptoms ; (1) nasal obstruction ( not severe usually) . (2) snoring (3) anosmia (4)
epistaxis ( esp. If the deviation at the valve area) .
- Signs ;
(1) Anterior Rhinoscopy (without speculum , because the blade can easily straighten the
septum & thus hidden the caudal dislocations) under LA ; septal deviation & look for the
lateral nasal wall .
N.B. : paradoxical nasal obstruction , the patient complain of unilateral obstruction & by
rhinoscopy the deviation on the other side , this due to long standing fixed obstruction will
become accustomed & the mucosal swelling associated with the nasal cycle & result in
additional intermittant nasal obstruction on the wider side .
(2) Cottle test ; small deviation in the area of nasal valve can cause greatest obstruction
because it is the narrowest part of the nosal cavity ; +ve confirm the fact that the obstruction
in the valve area .
N.B.: small devaiation at the anterior part of the nose cause obstruction while the large
deviation in the posterior part can't affect the airflow resistance .
(3) Examination of the external nasal pyramid , the palate , the teeth must be included .
(4) In newborn ; can be associated with ; assymetry of the nostrils (flattened on the affected
side) , oblique collumella & tip points in a direction opposite to the deviation .
This could be diagnosed by ; (a) anterior rhinoscopy shows assymmetry of the nostrils (b)
Gray's struts ; 4 mm wide & 2 mm thick strut lubricated & inserted into the floor of the
nostrils , normally introduced for a distance of 4-5 cm , if deviation then 1.5-2 cm back from
the nostril) (c) compression test ; +ve , the nasal tip is pushed backwards , if there is septal
dislocation , it will collapse against the philtrum of the upper lip .
Septal perforation & ulceration
The commonest cause is traumatic (esp. Iatrogenic) , usually the perforation preceded by
ulceration (except traumatic) , so a successful mangement of a septal ulcer will prevent the
developement of perforation (esp. in children , as it cause growth retardation for the nose &
midthird of the face) .
Causes are ;
(1) Trauma ; (a) iatrogenic ; surgery (SMR & septoplasty) & repeated cautery (b) nose
picking ; self induced digital trauma (c) injury ; RTA , sport injuy & assult .

Lecture notes in
(2) Neoplasm ; (a) malignant tumors ; SCC , BCC , Adenocarcinoma & T-cell
lymphoma (b) malignant granuloma .
(3) Chronic inflammation ; like Wegener's granulomatosis , SLE , rheumatoid artheitis ,
candidiasis , T.B. & syphilis ( usually cause posterior perforations) .
(4) Poisons ; (a) industrial (occupational) ; Chrome , Arsenic & Alkaline dust (b) cocain
addicts (snuff) (c) topical corticosteroids or decongestant .
(5) Idiopathic .
Clinical features ;
The majority are a symptomatic , in symptomatic patient the main complaints are (1)
recurrent epistaxis (2) dryness of the nose (3) crusting (4) nasal obstruction , the severity of
symptoms depend on the site & size of the perforation , the more anterior & larger one , the
worst symptoms , the small perforation cause whistling on nasal breathing .
There are 4 well demarkated stages (for non-traumatic type) ;
A. Redness & congestion of the mucosa leading to irritation & rhinorrhea .
B. The mucosa then become blanched & anaemic leading to dryness .
C. Late , it undergoes necrosis which revealed by adherent crusts over the affected area
D. The crust extends into the cartilage causing perforation .
The diagnosis from ;
1. History ; espcially for traumatic & occupational causes .
2. Examination ; if the lesion looks raised or hypertrophid , biopsy taken to exclude
malignancy , also done in susbected cases of Wegener's granulomatosis (CXR may
needed to show the lung lesion & urinolysis also needed for this disease) .
3. Serology for syphilis (FTA) esp. if the perforation in the bone .
4. Recently we use CT scan & MRI to assess the size & extent of the perforation .
The mangement is by ;
1. treating the causative pathology before any speciefic Rx .
2. medical Rx ; to prevent further crustation & to encourge the natural history of
healing (perforation never heal spontaneously) & this by ; avoiding trauma & toxic
materials , 25% glucose in glycerol drops will loosen the crusts & silver nitrate
cautery can be applied to bleeding & granulation tissue .
3. surgical closure of the perforation by the use of ; (a) split –skin graft (b) septal
muco-perichondrial flaps (c)silastic septal button (silastic obturator , this can patch
the perforations up to 3 cm , the patient here should be seen at regular 4-6 months
interval to decrust & clean the prosthesis) .
Indications of the SubMucous operations on the nasal septum :
A. Septal deviation ; Cottle classify the septal lesions into 3 types ;
1. Simple deviation ;mild deflection of the septum will not cause obstruction & not require
any surgical Rx .
2. Obstructive deviation ; more severe deviation which may touch the lateral nasal wall but,
with vassoconstruction the turbinates shrinck away from the septum, this need surgery(s.t)
3. Impaction ; very marked angulation with a spur which lies in contact to the lateral nasal
wall even after vasoconstruction , this need surgery (because it cause skeletal septal
obstruction) .
We must differentiate the cause of nasal obstruction whether it is from septal deviation or
from perennial rhinitis .
B. Closure of septal perforations (most technique) .

Lecture notes in
C. Source of grafting materials ; for rhinoplasty & tympanoplasty (use cartilage or s.t.
vomerine bone) .
D. To obtain surgical access ; for hypophysectomy & for vidian neurectomy .
The developement of septal surgery
- Langenbeck in 1843 did shaving the convexity , Rubrecut in 1868 did complete removal of
the deviated septum by punch forceps , both above procedures lead to septal perforation .
- Killian's in 1904 ; describe the technique which is most commonly practiced today (for
SMR) , leave anterior strut .
- Freer in 1902 ; more radical approach , remove the whole septal cartilage , he say that the
saddle nose postop. is due to rough surgery that destroy the lateral cartilage leading to
cartilage contracture (supratip depression) & collumellar retraction .
- Metzenbaum in 1929 (USA) ; put a part of the excised cartilage in its place forming
compound flap ( applied to caudal dislocation onlywithout fragmountation or gross
fibrosis) .
The principles of septal surgery :
- the septum devided into anterior & posterior segment by vertical line drawn between the
nasal process of the frontal & maxillary bones , so the posterior deviation Rx by classical
Killian's SMR , while the anterior deviation Rx by conservative septoplasty .
- the anasthesia ;
(1) LA ; by ; (1) postural nerve block technique (best) , it is more effective & done by puting
the patient in Proetz position which are the chin & the external auditory meatus in the
same vertical plane , then 2 ml of 4% cocaine introduced into each nostril using a special
angulated needle , so the cocaine gravitates into the superior & middle meatus where it
blocks both the ethmoid & sphenopalatine n. ( keep the patient in the positon for 10 min.) ,
then small quantity of ligocaine injected into the coumella . (2) moffett technique .
(2) GA ; for children & nervous adults , the nose should be sprayed with a decongestant
about 10-15 min. Before the induction of GA to decrease the amount of bleeding .
Septoplasty & SubMucosal Resection (SMR) :
Indications
1. Nasal obstruction secondary to deviated or obstructing nasal septal cartilage or bone
2. Sleep apnea with contributing nasal obstruction
3. Relief of recurrent septal epistaxis
4. Cosmetic correction of the deviated or twisted nose in conjunction with rhinoplasty.
5. Chronic sinusitis in cases of septal deviation
6. Septal neoplasms (rare).
7. Augmentation of saddle nose .
8. Alteration of naso-labial angle .
9. Insertion of dorsal spreader graft for valve insuffeciency syndrome .
10. Donar site fot cartilage graft .
11. Repair of septal perforation .
1. Patients with rhinitis medicamentosa (must first be treated medically)
2. Patients who abuse cocaine (should not be operated on)
3. Previous septal or nasal surgery
4. Specific sites of deviation: quadrilateral cartilage, vomer, perpendicular plate of ethmoid,
anterior nasal spine, and various combinations

Lecture notes in
5. Whether one or both sides are obstructed

6. Posterior deflection, anterior deflection, or both
7. Concomitant nasal disease (eg, sinusitis)
8. Bleeding or clotting abnormalities
9. Other causes or contributing factors to nasal obstruction, such as nasal valve collapse or
enlarged turbinates
10. Prior septal perforations or trauma
1. Routine laboratory studies
2. Consider allergy studies if allergic disease exists.
3. Consider sleep study if the history suggests sleep apnea.
4. Consider computed tomography scan if sinus disease exists.
Special Instruments, Position, and Anesthesia
1. Headlight
2. Septorhinoplasty tray should include Freer elevator, Cottle elevator, swivel knife, small 6-
to 10-mm Frazier suction tips, 4-mm straight osteotome, Takahashi biting forceps, scalpel,
double-action biting Jansen-Middleton forceps, bayonet forceps
3. Slight reverse Trendelenburg position
4. Preoperative vasoconstriction: cocaine, oxymetazoline, or another decongestive agent 10
minutes before beginning the operation
Tips and Pearls
1. Take the time to get in the correct surgical plane, which is bloodless, white, and has a
slightly gritty feel. In the correct plane, the operation can be performed extremely rapidly and
without mucosal tears.
2. If the mucoperichondrial flap does not elevate easily, the surgeon is in the wrong plane.
3. Small unilateral tears in the mucoperichondrial flap usually heal without sequelae and
need not be repaired
Complications
1. Through-and-through mucosal tears must be avoided and should be repaired when they
occur.
2. Septal perforation
3. Loss of septal support and saddle nose deformity (rarely immediate saddling occure as a
result of scar contracture of septum) .
4. Postoperative bleeding may occasionally require packing
5. Cerebrospinal fluid (CSF) rhinorrhea can occur from damage to the cribriform plate
during resection of the bony septum.
6. Recurrent or persistent nasal obstruction
7. Septal hematomas should be drained and the nose packed.
8. Collemullar retraction & supratip depression .
9. Deviation of the proximal & dorsal struts .
1. Persistent clear rhinorrhea suggests a CSF leak.
2. Persistent obstruction may be caused by enlarged turbinates.
3. Nasal packing may be required for 24 hours then removed .
4. Splints, when used, are usually removed 5 to 7 days postoperatively.

Lecture notes in
5. Antistaphylococcal antibiotics should be prescribed if packing or

splints are used.
Operative Procedure
A. Septoplasty ; the steps are ;
1. Incision ; Freer incision (at the lower border of the septal
cartilage) , also unilateral hemitransfixation incision (for right
handed surgeon , made in the left side) , the advantages are : (1)
placed in a relatively avascular plane (2) thck & tough mucosal edges which decrease the
risk of tear (if tear happened can be repaired easily) (3) provide easy access to the whole
area of the septum , including the caudal septal border , anterior septal spine region with its
associated premaxillary crest (4)easy to extends the incision to the opposite side with full
transfixation ( if rhinoplasty needed) .
2. Exposure;the cartilagenous & bony septum exposed by
complete elevation of the mucosal flap on the concave side ,
there may be difficulty in flap elevation due to fibrosis &
searing of previous trauma , also the anatomy must be
understood to avoid mucosal tear .
It is easy to elevate mucosal flaps across the ethmoid
vomerine suture & the ethmoid-septal cartilage suture , the
difficulty in flap elevation occure at the junction of the septal
cartilage (above) with the anterior nasal spine , premaxillary crest & vomer (below) , this
because the perichondrium encloses the cartilage in a complete envelope which doesn't fuse
with the periosteum , so the subperichondrial plane is not contineous with the subperiosteal
plane , the difficulty in uniting these two planes may lead to tear easily .
Cottle use technique that started the elevation over the septal
cartilage & worked upwards & backwards , always keeping
above the chondrovomerine junction (the anterior channel) , then
attention directed to the pisterior end of the incision & the
periosteum over the anterior nasal spine was incised & then
elevated backwards on both sides over the maxillary crest , then
the vomer (keeping below the chondrovomerine suture) , so
called the inferior tunnels , then the difficult elevation done which involve uniting the
anterior & inferior tunnels using knife (under direct vision) , so called Maxilla-Premaxilla
approach of cottle .
3. Mobilization & Straightening ; the 1st step is to seperate the lower border of the septal
cartilage from its osseous base .
N.B: in many cases , the lower border is dislocated from its
osseous grove , so continue the subperichondrial elevation
downwards over the concave side of the septum , so the cartilage
freed , attempt to reposition it back in its osseous grove which is
impossible , so best we remove a strip of cartilage 3-4 mm wide
from its lower border which is ideal autograft needed later .
Also neccessary to straighten & lower the vomerine crest to make a suitable bed to
accomodate septal cartilage .
When the anterior spine is deviated , fractured & repositioned in the midline (inadequate
for the angulated spure) , so vertical incision is made through the septal cartilage just

Lecture notes in
behind the line joining the nasal prosses of the frontal & maxillary bone , then a mucosal
flap elevated & the deviated cartilage & bone removed back to the face of sphenoid .
If the external nasal pyramid twisted , so we seperate the skin & subcutaneous tissue off the
underlynig upper lateral cartilage , so skin drap over the strightened cartilagenous dorsum
(without the risk of cutaneous traction which lead to recurrence of the deviation) , this done
through the cartilagenous incision .
Sometimes when there is severe septal lesion (due to haematoma) or where extremely
radical surgery is needed to correct the deviation , the residual septal cartilage can be
supported with a free bone graft (from the perpendicular plate of ethmoid or thicker vomer)
& sutured in position through a 2 hole drilled in the bone .
4. Fixation ; at the end of operation , the septum should be freely at the midline (neither
suture nor splinting will prevent subsequent failure) , then through & through mattress
suture is used to fix the septum (N.B.: in some instances a figure of 8 suture immobilize the
lower border of the septum to the anterior nasal spine).
Finally , the septoculumellar incision is closed with a few sutures .
Insertion of splints &/or packs used in the past , the splints prevents the nasal adhesion
especially if combined turbinectomy is necessary .
B. Submucosal resection ; the steps are ;
1. Incision ; killian's incision (5mm above the caudal border of the septal cartilage) .
2. elevation of the mucosal flaps ( easier than in septoplasty) , the exposure the same as in
septoplasty .
3. then about 1 cm above & parallel to the lower border, the incision is made in the septal
cartilage , then the mucoperchondrium can be elevated off the far side through the incision .
4. then by Hyman scissors , cut through the septal cartilage in a direction which is parallel
to & at least 1cm posterior to the nasal dorsum , then remove the cutted cartilage & bone
leaving that dorsal & caudal struts of cartilage to support the nasal dorsum & the
collumella ( the cartilage removed by Luc's forceps or Balenger's swivel knife) .
5. then elevate the flaps off the maxillary crest & vomer , the crest removed by Hammer &
gauge .
N.B.: they founr that an insertion of bone or cartilage again in the septum because the flaps
prevent ( & manege) the risk of septal perforation which can occure even in perfectly
performed Killian-type operations .
Septal surgery in growing nose
- as the nasal septum plays an important role in the developement of the facial skeleton &
the nose , so surgery is avoided & can carry a risk of growth retardation , so no less than
16 years of age to be operated .
- in necessary surgery under the age of 16 , should be of a very conservative nature
(confind to the reposiyioning of the septum) .
- experimental studies on children , broadening of the nose & supratip depression & septal
abscess (any septal abscess during childhood may lead to saddling deformity) .
Reduction of septal fracture in the newborn (3 – 9 months)
This is should be done as early as possible because it will become very difficult with the
passage of time , this is done by Gray's technique without anasthesia by the insertion of
neonatal nasal septal forceps (Gray's modification of Walsham's forceps) in the nose , then
the middle of the forceps firmly pressed downwards for 15-20 sec. to pull the septum
straight & then manipulate it in the midline .

Lecture notes in
The septum in Rhinoplasty

The septum should considerd in rhinoplasty because it is of great importance ;
1. in the deviated nose ; play a role in every external deviation .
2. in reduction rhinoplasty .
3. as a source of graft material for augmentation .
4. as a support to the nasal dorsum .
5. there may be an unrelated septal problem requiring surgery .

Lecture notes in
Rhinoplasty
It is a procedure alter the appearance of the nose while maintaining or improving the
physiological function of the nose .
Nasal plastic surgery is necessary in otorhinolaryngolgogy because ;
A. the external nasal shape may be associated with septal deformity .
B. correction of nasal airways linked with rhinoplasty .
Septoplasty aims to repositioning of the septum in the midline with mininmal excision of the
cartilage & bone , also it could be binded with rhinoplasty if there is an obvious nasal
deformity .
The standard surgical steps is by the seperation of the upper lateral cartilage from the
septum which may cause collapse of the nasal dorsum & saddling of the nose .
Rhinoplasty after SMR lead to no satisfactory results to be achieved .
Analysis & selection of the patients for rhinoplasty ;
1. Aesthetics sense & common sense ; the main cause of patients dissatisfacation
following rhinoplasty its failure of surgeon to understand what the patient wishes ,
let the patient define the complaint before we analyse the detailed medical &
psychlogic evaluation .
2. Good pre-operative photography for ; demonistrates the changes occure postop. to
the patient & give excellent concept for the surgeon , they are
daylight film with blue back ground , six standard 5 X 7 inches
photographs ; side or lateral view (2 photograph) , three quarter
vertical or oblique view (2 photograph) , midsagital or frontal view
& basal view .
3. Sex of the patient ; female done for beuty , male for give rise of
ridcule .
4. Pre-operative psychatric assessment ; necessary , in male they
found some of them presenting with psychatric disturbances , so it is
important to detect thier disturbed personality because 8 surgeons was killed by
mentally retarded patients after rhinoplasty .
5. Age of the patient ; not to operate before the age of 15-16 , in older
patients less radical alteration should be aimed , & in eldery after
rhinoplasty appear unnatural & less skin elasticity make folds over
the dorsum of the nose .
6. Hight of the patient ; small nose suitable for small patient .
7. Degree of deformity ; moderate nasal deformity easy to correct .
8. Assessment of skin thickness & texture before rhinoplasty ; thick skin
is a thick blanket for rhinoplasty , while thin skin has minimal
changes & any irrigularity appear , also after rhinoplasty telengectasia & tethearing
of skin may affect the appearence after rhinoplasty .
Surgical anatomy
- The supporting structure of the nose are bony in the upper 1/3rd & caltilagenous for lower
2/3 rd , the bony skeleton composed of the 2 nasal bones , nasal process of the frontal bone
(project superiorly) , frontal process of the maxilla (projects laterally) & these bones
supported in the midline by the bony nasal septum (perpendicular plate of ethmoid&
vomer) .
- The nasion is the depression of the profile at the root of the nose where the nasal bones
meet the basal glabella of the frontal bone .

Lecture notes in
- The nasal floor formed by palatine bone posteriorly & the maxilla anteriorly , these 2
structures fuse at the midline to form a crest which support the bony & cartilagenous
septum .
- Too far can make nasolabial angle more obtuse & appear of tethered & shut upper lip .
- The cartilages of the nose are ; middle 1/3rd of the nose formed by cartilage of the nasal
septum & paired upper lateral cartilages (triangular shape) overlaped superiorly by the
nasal bones & frontal process of maxilla & inferiorly by lower lateral cartilages , so that
these lateral forming a groove called Limen-nasi which is the land mark for
intercartilagenous incision .
- It is important to note that the upper lateral cartilages lies below the nasal bones
superiorly & they are easy to seperate (disarticulated) when try to elevate the skin &
periosteum forming unsight deformity .
- Lower 1/3 rd of the nose formed by lower lateral cartilages
(alar cartilages) which are made up of 2 crura ; medial crura
forming the collumella & lateral crura form the framework of
the tip of the nose preventing the alar collapse during
inspiration , the lower margin of the lateral crus doesn't
follow the margin of the nostril but ascend away from it
(travel laterally) 1 cm from the nostril laterally & 1 mm
medially .
- Highest point of the lower lateral cartilage called the dome ,
usually at the junction of the medial & lateral crura , but may
be at a variable distance along the lateral crus .
- Facit ; is the line between the collumella & the lat. rim of the
nostril , it reffered as soft triangle & not backed by cartilage ,
should be avoid surgical interference here because of
impossibility to corrected postoperatively .
- Seasamoid cartilages ; several cartilages lies between the upper & lower lat. cartilages .
- Collumella ; formed by ; caudal end of the septum , nasal spine & medial crura of the
lower lat. cartilage .
- Naso-labial angle ; it is the angle formed between the collumella & the upper lip , about
90o in male & 110o in female .
- Muscles of the nose are ; procerous , nasalis & depressor septi muscle .
- Anatomic evaluation of the face & nose should concerne with ; (1) quality of the skin
(2)inherent strenghth & support of the nasal tip (3) size , shape , altitude & resilience of
alar cartilages (4) internal vestibula (5) internal examination (6) the position &
inclination of the nasofrontal & nasolabial angles (7) relation of the nose with other
structures in face (8) equal distance between hairline & glabella , subnasale & menton .
- The ideal distance between the inner canthi should be one eye width .
- In The ideal nose vertical line from the inner canthus touch the lateral aspect of the
lateral crura .
- The width of rhinion should ideally one half the distance between the vertical line dropped
from the inner canthi ( important to decide if the nose deviated or not) .
- Determine the proper depth of thenasofrontal angle , imaginary line from sellion to the tip
, anything overthis line hump to be removed & below this have to be augmented .
- Vertical line tanged to the nasion & upper lip , just touch the chin in male , in female
record few mm from this line .
Anasthesia of the rhinoplasty
- GA with ETT (cuffed) with pharyngeal pack (moist ribbon gauze) & tube should be in the
midline .
Lecture notes in
- Bleeding controlled by ; (1) local infilteration of vasoconstrectors (2)hypotensive GA

technique .
- Anasthetist should addmite the patient before GA & take history , exam. , Investigations
pre-operatively to evaluate for any contraindications for GA .
- Fasting minimally 4-5 hrs before the operation & the usual premedication given .
- As the nose infilterated with vasoconstructor , tell the anasthetist who avoid Halothan &
B-blockers , because this may cause cardiac arrythemia .
- Monitoring ECG throughout the operation .
- Position ; supine position with head up on a head ring & rotate the table 15-30o .
- Operating light , (1) one directed above the nose (2) one directed at the nose from the foot
– starlight- (3) headlight or fibro-optic illuminated instrument .
- In addition to local vasoconstructor application , inject the nose with 1% lignocaine
contain 1:80000 adrenaline , care must be taken to inject small bleb per a time , maximum
amount 6 ml & inject the following sites ; (1) between the upper & lower nasal cartilages
(2) along the nasal dorsum (3) lateral towards the infraorbital n. (4) along the site of the
lateral osteotomy (5) collumella (6) lower margin of the lower lateral cartilage .. after the
injection wait for 10 min. For vasoconstruction to have maximum effect .
Osteo – cartilgenous vault
- The bony& cartilage vault is a single unite because ; (1) nasal bones overlap with upper
lat. cartilage & firmly united with them (2) dorsal hump always include bony &
cartilagenous elevation .
- The dorsal hump is themost commonest cause of patient dissatisfaction with thier
appearance , so 2 step taken theoretically Dehump & Infracture .
- Secondary hump (polybeak) ; results from ; (1) inadequate removal of the cartilage in the
supartip region (2) hypertrophic scar .
- Osteotomy ; exessive bony hump removal leading to more unsatisfactry
appearance , while if incomplete lateral osteotomy this will prevent proper
infracture of nasal bone causing open – roof deformity .
- How much hump can be removed ? This depend on ; (1) thickness of the skin
(2) amount of cartilagenous hump in relation to bony hump (3) width of the
hump (4) angulation of the tip of the nose (5) inclination of the naso-frontal
angle .
- Should be decraese the nose in harmony with other facial features & remebering its
always better to remove too little than too much .
- Why we should correct the tip 1 st ? This because ; (1) less bleeding occure (2) landmark ,
hump is the nasion , so correct tip 1st to know howmuch hump removed (degree of tip
modification) (3) require introduction of large & cumbersome saws .
N.B.: some authors tends to take profile correction 1 st followed by tipoplasty , this favoured
in cases of patient with ; (1) short collumella (2) tip – projection is the main aim .
Steps of Rhinoplasty
- 1st step after step after suitable arrangement of the patient (position , clensing of the nose
& infilteration of vasoconstructor) is the trimming of the vibrissae of the nasal vestibula
because thes tend to cake with blood clot afterward causing discomfort .
- 2 nd step incision along the limen nasi (intercartilagenous
incision) continue this incision medially to become
continues with transfixation incision with seperation of
collumella from the caudal end of the septum & some do
high transfixation incision to prevent pollybeak deformity

Lecture notes in
- elevate the skin overly the upper lateral cartilage & little beyond the osteo-cartilagenous
junction of the nasal bones & upper lateral cartilages & then elevate the skin &
periosteum overly the nasal bones .
- be carefull no to disaticulate upper lateral cartilage from the pyramid appearture.
- Elevation continues up wards to glabella & lateral which shouldn't be continued too far
especially in multiple osteotomy , but if no need for multiple osteotomy continue more
laterally because wider elevation may be helped in redraping the skin in radical reduction
- Divide the upper lateral cartilage from the nasal septum ;
keeping it as close as possible to nasal septum to prevent
the formation of T-shaped structure which is difficult to
lowered at later stages (occasionally the patient may have
V-shaped deformity when the upper lateral cartilage &
nasal septum join) which can be confused .
- Lowering of the upper lateral cartilage & nasal septum each by the same amount up to
nasal bones using Foman's scissors .
- Hump reduction by osteotome or chisel , also the bony & cartilagenous hump can be
removed by large artery forceps ,but should always pushed further into the nose before
withdrawal to detach any adhesions remain between the mucous membrane , periosteum
& bone . Alternative methode of hump lowering is using Bull's nasal saw which has ; (1)
single fine blade allowing the surgeon to remove even a small hump (2) rounded blunt end
which prevent damage to overlying skin .
- Further Lowering of ; (1) nasal bones with Rasp (2) nasal cartilages by scalpel or scissors
- Infracturing of the lateral nasal wall to close the flat (open bridge) in order to acheive this
lateral , medial , & superior osteotomies which done if lateral & medial osteotomies not
curved on each other .
- Few surgeons now use the saw , require elevation of the skin & periosteal tunnel laterally
along the line of osteotomy , this lead to (1) marked postop. laborious swelling (2) dust
may become infected .
- Some use introduction of small osteotome (2-3 mm) intranasally at the lateral aspect of
the pyramid aperature .
Whichever the methode used its important to lower the osteotomy as possible to prevent
astep deformity which felt or seen postoperatively .
- Rechecking of the hight of the nasal septum & lower lateral cartilage ; ideally (1) should
lowered equally & remove too little cartilage (2) reduction of caudal end of the septum &
lowering of the lower lateral cartilage & tipoplasty ti acheive shut nose (3) excessive
removal of caudal septal cartilage may lead to collumellar retraction or excessive obtuse
angle of nasolabial angle .
Indications of septorhinoplasty
1. purely cosmetic .
2. traumatic nose .
3. saddle nose .
4. septal deviation with external deformity .
Surgical Indications of hump rhinoplasty
1. Lowering of the nasal hump .
2. Alteration in shape of bony & cartilagenous dorsum .
3. Angulation of the dorsum .
Methods of hump reduction
1. Hump removal .
2. Backward dispacement of hump .
3. Hump removal & then displacement .
Lecture notes in
Nasal tip rhinoplasty

- It was ignored & attention was given to hump removal , then finer tip technique
elaborated , but have disadvantages such as tip asymmetries & deformities if wrongly
applied technically & the nasal tip deformity is more conspicuous than other site on the
nose & face .
- Problems in the nasal tip are ; (1) Bulbosity ; fullness over the upper or cephalic aspect of
the alar cartilage (2) Tip rotation (3) narrowing of cephalic portion of the alar cartilage ;
achieved by excision of the cephalic part of the alar cartilage & by visoring of caudal rim
of alar cartilage .
- Access to the cephalic aspect of the alar cartilage ;
(1) Intercartilagenous incision with retrograde dissection ,but its not easy to acheive
accurate & symmetrical cartilage excision .
(2) Cartilage splitting incision & delivery of the cephalic aspect of the alar cartilage is
performed but not sufecient when more radical changes in tip anatomy needed .
Whichever the technique used its important to preserve the vestibular skin , because if
excesive skin excised then pinching & the alar collapse occure which is unsatisfactory
problem both cosmetic & functionally (airway) . & if failure to preserve a sufficient rim of
alar cartilage to support the lateral wall this lead to pinching & alar collapse , about 3-
4mm of cartilage should preserved to prevent this , but in thin walled nose – thin skin – lax
cartilage more than 3-4 mm required , but in thick skin 2 mm required .
This lateral alar collapse determind by texture of skin & cartilage .
Excessive removal of skin & cartilage from the lateral wall of vestibula cause pinching or
knock – kneed tip deformity .
(3) Rim incision , we use this incision when more radical changes in the tip anatomy
needed , we use it with complete delivery of the cartilage which is necessary to ; (a)
correct bifid or flat nasal tip (b) lenghthening of the collumella (c) reduce the
marked tip projection (d) cleft nasal tip .
Rim incision & delivery of the cartilage given almost complete exposure to the lateral
crus , medial crus & dom of the cartilage , it is better to avoid deviding the lower lateral
cartilage at the dom or cartilage itself because this lead to alter tip anatomy (spring
crura irrigularity , sharp edge) esp. in resielent cartilage underlying this skin .
(4) Goldman technique (1965) ; if it is necessary to devide the
alar cartilage seperating teh medial & lateral crura
completely from each other to increase the tip projection
(i.e. suturing of the medial crura & medial portion of
lateral crura back to back to increase tip projection) .
Rarely increase tip projection >2-4mm .
(5) Sheen technique (1978) ; cartilage graft & strut insertion between the medial crura ,
these certainly proved in revision rhinoplasty .
(6) Transdomal suture procedure (4-0 PDS suture) ; aim to preserve & reorient the
nasal tip structures & conserve the straight anatomy of the alar cartilages , this is
suitable for broad boxy or bifid nasal tip with firm strong alar cartilage & thin skin
& with little intervewing subcutaneous tissue , also it relies on the repositioning of
the existing cartilage & removal of the interdomal soft tissue .
In nasal tip which require less marked narrowing not necessary to suture alar dome
together , but suture each individual dome near the apex between medial & lateral crura
with 4-0 plain cat gut .
Saddle nose

Lecture notes in
- The cause of it could be due to abscess or fibrosis of the cartilagenous part of the
septum (the cartilagenous septum & maxillary crest is the major support to the lower
2/3 rd of the nose) .
- It is of variable degree & could follow ; (1) septal haematoma (2) septal abscess (3)
septal injury (4) septal surgery .
- loss of the septal support to the dorsum occure due to ; (1) Taruma – mostly- (2)
chronic inflamatory conditions involving the cartilage – T.B. , sarcoidosis , syphilis &
polychondritis - (3) malignant disease (4)familial or racial .
- Considering the mangement of the deformity ;
(1) thought about suitable graft material .
(2) should remember that small saddle are accentuated by anormal hump , so hump
removal will solve the problem resulting in small nose especially in female aged 17-18
, in some cases it is possible to removethe dorsal hump & use it to graft the deformity.
(3) In more severe deformity , implant is required , when the saddling due to loss of
cartilage support then soft cartilage graft is preferable than hard graft , if the entire
dorsum involved (bone & cartilage) then one of harder implant is preferable (bone or
synthetic .
- Grafts are ;
(1) Bone ; commonly iliac crest bone graft used , but ; (a) Doubtful long term survival
(b) Unsatisfactory for cartilagenous deformity & producing rigid – wide unnatural
appearance (c) Donor site produce pain & scar tissue .
(2) Cartilage ; according to the deformity size ;
(a) Small saddle ; autograft , the most useful obtained from the septum (cartilage) , but
not vomer & ethmoid bone are unsatisfactory for graft because they are thin .
(b) Large saddle ; either
1. Rib cartilage (disadvantages are ; pneumothorax postop. , pain & scar , twisting of
rib cartilage whatever the manouver are taken)
or 2. Aural – conchal cartilage (advantages ; majorly used , shape of it lends itself
restoring good countor to saddle deformity& its viable graft & change in shape & bulk
may occure & can be used for saddling related to chr. inflammatory or malignant
disease) .
or 3. Irradiated preserved cartilage .
(3) Synthetic implants ; like synthetic meshs such as supramid , it has disadvantages ;
extrusion of the implant to either outside or through the sinus to inside the nose (due
to the implant is near the exterior & nasal cavity , but this could avoided if certain
precautions taken) & the implant may move & cause asymemetry of the outline &
unaccepted aesthetic results .
- Technique ;
a. implant inserted through a midline – vertical –collumellar incision into a pocket
underlying the dorsum of the nose with few or no other rhinoplasty steps undertaken &
carefully remain in situ (telengectasia & displacement from midline could occure) .
b. surgical removal of the implants (complete removal) is impossible with mesh implants
& bony & cartilage grafts .
c. firm synthetic implant are useful in ; saddling involving bone & cartilage & in racial
saddling , but , it is avoided in thin , scarred or blanching skin .
d. there is no single ideal implants for all deformities , but, conchal cartilage for
moderate deformity & synthetic implant or ribs or iliac crest graft for gross deformity .
The Deviated Nose
- Correction of deviated nose is one of the more difficulties in rhinoplasty , because 2/3rd
of the nose is cartilage which is unlike bone it doesn't (stay put) but tend to sping back
Lecture notes in
to its former position , so that in many cases extensive septal surgery is required &
there is no guarantee can be given that the nose will be perfectly straighten , but
certainly one hopes to acheive an improvement .
- Technique required to correct a deviated nose considered under 4 headings ;
A. Correction of septum & upper lateral cartilage ;
- when the septum although deviated is itself resnobly straight i.e. may bend at one
particular position only or its straight within the nose , but both nose & septum
deviated to one side of the face so called septoplasty technique & the
mucoperichondrial flap elavated from both sides or completely from one side with
superior & inferior tunnels , if its left attached to one side it decraese the chance of
cartilage resorption , but rarely seems in practice because it may leads to unequal
scarring & then contracture leading to further destruction later on , so that should be ;
a. septum seperated from that above .
b. devide the septum at the band posteriorly .
c. repositioning of the septum onto maxillary crest below .
d. repositioning of the crest itself following osteotomy if its not in the midline .
e. repocket the septum into a slot incised behind the collumella .
f. elevation of the skin overlying the upper lat. cartilage via intercartilagenous incision .
g. detach the upper lat. cartilage from the septum & any inequality can be corrected by
lowering the long side & possinly augmenting the shut side of cartilage graft .
1. When the deviation is maximum in valve area , so that septoplasty is less satisfactory
because it lead to generalized ballooning of the septum towards one side .
- When it is buckling & distortion of the nasal septum , in these cases better to do SMR
or complete replacement by autograft from ear or homograft of banked septal
cartilage , in such cases there is a risk of supratip depression & saddling , so if it is
possible not seperate the upper lateral cartilage from the septum .
- Sometimes the septum may dislocated to one side of collumella anteriorly , but the
remaining septum is in a satisfactory position , this checked by pressing a finger in the
collumella or excise the cartilage parallel to the septum , if it is excised at aright angle
this lead to too much caudal border may be removed causing collumellar retraction .
B. Dealing with deviation & asymmetry of nasal bones (upper 1/3rd ) ;
- Theoritacally it is not a problem because of the refracturing & manipulation &
immobilization of the nasal bones .
- Practecally residual deviation in this area is not uncommon because medial , lateral &
superior osteotomes not correct the deformity .
- With gross deviation of the nasal bones , a standard medial & lateral osteotomes leads
to Banana-shaped fragments , so transverse intermediate osteotoem are required using
2 or 3 osteotomes intranasaly & completed before any other osteotomes done .
C. The Nasal tip ;
- Corrected by cartilage splitting technique either by (1) removing more cartilage from
one side than the other , or (2) reduction the tip on the side to which the nose is
devided & occasionally the tip reduced & the cartilage removed used to augment the
other side .
- When the tip deviate & also required a projection then use Goldman's technique ; rim
incision with elevation of the overlying skin & incize the cartilage & skin 2 mm lateral
to the dome with suturing both sides back to back leads to projection of the tip & twist
the tip to midline .
D. Augmentation i.e. filling the depression to give an appearance of straighten nose .

Lecture notes in
Deviation associated with gross deformity of the nose

- Where there is gross deviation associated with severe septal deformity , then external
rhinoplasty is indicated which gives excellent exposure to the septum & direct
visualization of the nasal anatomy .
- Alar collapse ; a phenomenon where the alae collapsed inwards with inspiration in a
valve like manner causing nasal obstruction .
Most commonly in eldery patients with ; (1) dropping tip (2) loss of elasticity of cartilage
(3) atrophy of dialtor muscles .
Also it may occur after rhinoplasty if ; (1) too much lower lateral cartilage had been
excised (2) loss of vestibular skin lead to scarring causing contracture in the valve area .
Diagnosis reserved to those patients unable to achieve inspiration at a physiological flow
rates .
Pathophysiology of this ; (1) small cahnges in the width of nostrils will remarkedly affect
the flow (2) as air pass inward through the nose there will be inward drawn of nostril due
to Bernollul's principle (3) small decrease in the diameter of airway will greatly increase
the resistance .
The alar collapse results from ; (1) septal deviation at the valve area (2) wide collumella
(3) medial crus herniate of lower lateral cartilage (4) lateral crus herniate of lower
lateral cartilage .
Correction of medial crus herniation by excision of skin to include herniation porter of
medial crus & the skin then gently undermind & closed with suture .
Lateral crus herniation can't corrected by simple excision , but need Free – dissection &
repositioned in a new pocket slightly more lateral & superior to its former position .
The methods used to correct Alar collapse of 3 groups ; (1) prosthesis (2) modification of
existing cartilage (3) grafting additional materials .
External Rhinoplasty
Indications
1. certain gross deformity such as cleft tip with severe deviation .
2. marked deviation .
3. revision technique .
4. for insertion of composite cartilage .
5. as access for repair septal cartilage .
6. open valve augnebtation .
7. small cyst or tumor affect nasal inspiration .
Incisions
1. Transcartilagenous incision across the collumella linking the cartilage rim ( ugly) .
2. Inverted V- shaped incision ( impercitible scar) .
3. Vertical collumellar incision (borely percitible) .
Advantages
1. Clearly demonstrating the anatomy .
2. Excellent access for excision with minimal scarring .
- Skin elevation over the lower & upper lateral cartilage & gently retracted by Cottle
alar retractor will clearly visualize underlying nasal skeleton .
- Alar cartilage sculptured & refashioned under direct vision if there is any asymmetry
as in cleft tip nose cartilage taken from one side & augment the other side .
- Suturing ; interdomal suturing of cartilage .
- Cartilage graft from ; septum or conchal cartilage .
2. High-quality photographs
Lecture notes in
3. Discontinue all aspirin and nonsteroidal antiinflammatory agents at least 2 weeks

before surgery.
4. Contraindicated to use skin incisions with caution in keloid-forming patients.
External fixation
- Materials ;
1. Plastics ; light & easy to keep clean .
2. Metal splints ; advantage easy to apply but may expand with swelling of the nose
leading to loose fit if unsequized tight again few days postoperatively .
3. Plaster of Paris ; although it is the oldest but still applied , 6-8 layers of POP dipped
in warm water & sequized out in a gauze & applied over the nose .
- The external fixation should cross the nasion up onto forehead , some fell this due to
postoperative odema & swelling at the nasal root .
- bolster 1/2 a gauze eye –pad strapped under the nose .
Postoperative care
1. Recovery , the patient should be completely awake & conscious but if he is drowsy ,
may inhale the blood , once fully conscious transfered to the ward , this type of
surgery not cause much pain , so no need for strong analgesia .
2. Local wound care to discourage crust formation at the suture lines.
3. Use packing only if needed .
4. Ward , nursed in sitting position , BP, PR , Temp. (sign of bleeding) & swallowing .
5. Antibiotics , no need for prophylactic antibiotics but needed in patient with splints
(should stay for >1wk) & implants , the commonest MO is Staphcoccus strain which
resistant to pencillins , so that speciefic antibiotics given .
6. Dressing , splints & packing ;
a. Before dressing should ensure ; (1) suturing of any cartilage spliting incision (2)
mucoperichondrial flap replaced & secured (3) not usually necessary to suture the
intercartilagenous incision .
b. Splints ; required immobilization of the nasal septum & maintain in the midline , it
should be thick enough to provide rigid support & with sufficient length to support
the entire length of the septum , but it shouldn't too wide to avoud causing pain due
to pressure between septum & middle turbinate & should secured with transfixation
suture securing the 2 sides & not suture one to other across the front of collumella
because this will annoying the patient & cut the skin cause perminant scar which is
difficult to correct ... it should removed after one week .
c. Packs with doule layer – telfa dressing or simple vassaline pack which should
applied carefully because any vassaline entering the wound will cause granuloma ,
it should removed at 12-24 hrs , strap the nose with 0.5 inch strips , moulding the
nose in desired position & ensure the tip hold well up & approximate the
transfixation incision & keeping the tip suitable pinched in , also it is important to
keep the supratip strapped down to prevent any haematoma forming which may
cause pollybeak , avoid leaving any small area unstrapped because the risk of
herniation through lead to skin necrosis & ugly scarring .
Complications
1. External ; occure due to excessive removal of tissue at the time of surgery or over
correction of the deformity , they are ;
a. Polly beak appearance ; due excessive removal of tissue , caused by using of wide
saw instrument (lower lateral cartilage portion) .
b. Ski –slope appearance ; due to excessive removal of nasal bones & nasl dorsum ,
these changes may be unsatisfactory in eldery because skin may not take up &
avoidance of gross changes in nasal countour .
Lecture notes in
c. Pig – Snout appearance ; excessively open nasolabial angle >90-100 o, exision of

caudal end of the septum is the standard step in rhinoplasty , but it is unnecessary if
the angle is 90-100 .
d. Knock – Kneed nasal tip appearance ; due to excessive removal of lateral crus of the
alar cartilages wich is predisposing steps from pinching & collapse .
e. Open – Roofed deformity (wide nose bridge) ; due to failure to obtain good lateral
osteotomy of nasal bones with infracture , this most commonly occure with the use of
saw because it is most inffective & traumatic instrument for the lateral osteotomy , so
that osteotome is to be performed .
f. Bossing or asymmetry of the nasal tip ; due to asymmetrical exision of the alar
cartilage & the rim of cartilage remain too narrow .
g. Tip irrigularities or High-lights ; due to division of the medial & lateral crura the
overlying skin is thin or division of one side or asymmetrical division .
2. Intra-nasal complication ;
a. Vestibular stenosis which follows revision rhinoplasty or excessive incisionm inside
the nasal vestibula especially if coupled with excision of vestibular skin leading to
narrowing & obstruction of the airways .
b. Prjection of caudal portion of the upper lateral cartilage into the vestibula with an
area of vestibula due to failure to exise the caudal portion of the cartilage .
c. Synachiae ; due to trauma to the lateral wall mucosa & skin with instruments .
d. Webbing of the nasal valve & nasal obstruction predisposed by exessive lowering of
the upper lateral cartilage along its dorsal margin .
Patient instructions after rhinoplasty
1. Don't blow nose until instructed .
2. The nasal plaster cast removed in the office .
3. avoid foods that require prolonged chewing .
4. Avoid extreme activity ( athletics & sexual intercourse) .
5. Brush teeth gently
6. Avoid smiling , graining & excessive facial movement for 1 week .
7. Absolutly avoid sun , heat may cause nose swelling .
8. Don't wear regular glasses rest on the bridge of the nose for 4 months .
9. must know physician phone number .

Lecture notes in
Snoring and Sleep apnoea

Historical review
- Charles Dickens (1836) , observe association between day time sleep & obesity .
- William Hill (1889) , add to the above association the symptom of snoring & restless sleep
- Burwell (1956) , pickwickian syndrome , obesity , hypersomnolence , alveolar
hyperventilation & cor pulmonale & Gastalit (1965) relate this syndrome to sleep .
- Guilleminanlt & Dement (1973) , describe sleep apnoea syndrome & established the 1st
sleep clinic to investigate the patients with sleep complaint .
- In USA , clinical polysomnographer "sleep disorder specialist" with need to chest
physician , cardiologist , ENTist , neurologist , anasthesiologist & maxillofacial surgeons
to assess & investigate & manage sleep apnoea .
Definations
- Snoring ; noise generated as a result of partial upper airways obstruction during sleep , if
during wakes called sterter .
- Apneoa ; cessation of airflow at the nostrils & mouth for at least 10 seconds .
- Apneoa index (AI) ; the number of apnoeas per hour of sleep .
- Hypoapnoea ; less than 50% reduction in tidal volume .
- Sleep apnoea syndrome ; diagnosis made when more than 30 apnoeas per 7 hours of sleep
or AI > 5 , grades of sleep apnoea syndrome are ;
a. Mild ; AI 5 – 20 . b. Moderate ; 20 – 40 . c. Severe ; > 40.
- Respiratory disturbance index ; apnoea & hypoapnoea per 1 hour of sleep .
- High upper airway resistance syndrome ; partial upper airway obstruction with marked
respiratory effort , but able to maintain O2 saturation , microarousals lead to excessive
day time sleepiness .
- Nocturnal hypoventilation & hypoxia ; hypoventilation & hypoxia in patients with normal
sleep rhythm & no apnoea .
Types of sleep apnoea
1. Obstructive sleep apnoea (OSAS) ; apnoea in the prescence of respiratory effort
(movements of the ala nasi & intercostal ressesion) .
2. Central sleep apnoea ; apneoa with cessation of all respiratory effort (may or may
not snore) .
3. Mixed sleep apnoea ; starts as central sleep apnoea with no respiratory effort
followed by forceful respiratory effort with no airflow until the airflow clear the
airways .
Prevalance ; habitual snoring occur in 24% of males (10% < 30 y , 60% >60 y) & 14% of
female , this occur espicially in obese patients .
Aetiology ; risk factors for sleep apnoea syndrome are ;
1. Weight ; more in obese .
2. Age ; more above 40 years .
3. Sex ; male : female about 2-10:1 .
4. Snoring .
5. Alchol & tobacco .
6. Sedatives .
7. Familial & genetic risk .
8. Any obstruction from the nose to glottis , nose (polyps , septal deviation , rhinitis ,
septal haematoma , nasal packs , congenital disease "choanal atresia" , neural

Lecture notes in
tumors) , pharynx (nasopharyngeal tumor , enlarged tonsils/adenoids , lingual

tonsils , large tongue "myxodema , acromegaly , Down's syndrome ..etc" &
retropharyngeal mass) , Larynx ( tumor & odema) , facial skeleton anomalies
(Alport's , Cruzon's , Pierrs Robin's & Trecher Collin's syndrome) .
Pathophysiology
Sleep apnoea occur when there is negative intrauminal pressure exceed that of pharyngeal
dilators lead to pharyngeal obstruction which cause ;
1. Hypoxia which lead to cardiac arrhythmias , systemic & pulonary hypertension .
2. increased intrathoracic pressure due to decraese cardiac refilling .
Clinical features
- Symptoms ; snoring , excessive daytime sleepiness , obstruction episods , morning
headache , personality changes , intellicutual deterioration "poor memory" , depression ,
abnormal body movements , frequent awaking , nocturnal chocking & impotence .
- Signs ; nasal obstruction , tonsil/adenoid hypertrophy , macroglossia , reflux laryngitis ,
hort collar size ">17 inhes" , goiter , trunckal obesity , hypertension , congested heart
failure "pitting odema" & acromegally .
- In children ; growth retardation , developmental delay , failure in the shool , nocturnal
enuresis , upper lip often coated with nasal secretions , , streter , underweight , chest
abnormalities "ribsulcus & pectus excavatus" .
Complications ; systemic & pulmonary hypertension , right heart failure , cardiovascular
morbidity & arrhythmias .
Differential diagnosis (of excessive daytime sleepiness)
1. Sleep apnoea syndrome .
2. Narcolepsy .
3. Nocturnal Myoclonus .
4. Depression .
5. Drugs .
6. Sleep deprivation .
7. Idiopathic hypersomnolence .
8. Hypoglycaemia .
9. Severe anaemia .
10. Hypothyroidism .
11. Cerebral tumors .
Mangement
- Diagnosis
A. History ;
1. The partener must be present , parents for children .
2. History of any above symptoms & signs .
3. History of drugs , alchol intake ..etc .
4. Social history , snoring use as excuse by the spouse to leave the marrital bed .
B. Examination ;
1. General ; obesity , myxoedema, acromegaly ...etc .
2. Hight & weight ; 70% of sleep apnoea syndrome are obese , the morbid obesity when
45 Kg > ideal weight , the BMI "body mass index" = Weight in Kg/(Hight in m) 2,
normal BMI , in male <27.8 & in female <27.3 .

Lecture notes in
Obesity can encourage sleep apnoea by ; decreasing lung compliance , fautly inflation
of the diaphram & intercostal muscles , depression of the genoglossus muscle reflex ,
decrease in hypercapnia & hypoxia ventilatory response & also increase fat deposition
at the soft palate & pharyngeal wall .
3. Neck circumference .
4. Nasal airway , tongue size , tonsils/adenoids & uvula .
5. Craniofacial morphology like micrognathia ...etc .
6. Nasopharynx ; adenoids , tumors , polyps & cysts .
7. Hypopharynx ; lingual tonsils , vallecula , supraglotic cysts .
8. Larynx ; vocal cords mobility & tumors .
C. Investigations ;
1. Those assess the general condition of the patient
a. Full blood count ; anaemia , polycythemia ...etc .
b. Thyroid function test ; hypothyroidism .
c. CXR ; cardiomegaly , pulmonary disorders ..etc .
d. ECG ; cardiac diseases .
e. Blood gas analysis ; PO2 & PCo2 in daytime hypoxia & hypoventilation .
f. Pulmonary function test ; OSAS shows saw-tooth pattern .
2. Those differentiate between simple snoring & sleep apnoea & determining the
prescence of & type & severity of the sleep apnoea attacks
a. Polysomnography ; this is done in special labrotory , simulaneous & continuous
recording of the relaevant physiological measures during sleep .
The patient spend a night or more in sleep labrotory connected to a variety of monitors
, the parameters measured at polysomnography are ;
(1) EEG ; detect REM & non-REM .
(2) EMG ; differentiate between REM sleep & arousal .
(3) EOG ; detect REM sleep .
The above tests are for sleep staging .
(4) Pulse-oxymeter ; O2 saturation .
(5) ECG ; to detect any arrhythmias .
(6) Nasal & oral airflow ; no flow for 10 seconds , this mean apnoea .
(7) Chest & abdominal movement (by belt) ; differentiate between central & OSAS .
(8) Tracheal microphone .
(9) Oesphageal baloon .
(10) Sleep position detector .
(11) Anterior tibialis EMG ; Dx periodic movements during sleep which lead to
excessive daytime sleepiness .
The EEG , EMG & EOG used to detect the indicating cases for use of REM
shortening drugs (Protriptyline) , also it can used preoperatively to determine
objectively the operation success . , it might be used to monitor the effectiveness of
nasal continuous postive airway pressure (CPAP) .
b. Overnight pulse-oxymetry , is cheeper , simpler & alternative screening test to
polysomnography , it detects 100% of severe OSA & only 60% of mild OSA .
c. Acoustic recording devices used in paediatric to record the repiratory sounds while
the patient is sleep .

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d. Multiple sleep latency test (MSLT) ; Nap study , it measures daytime sleepiness
objectively , it is not necessary to diagnose OSAS , it document sleepiness in a patient
with normal polysomnography , the patient given 4 or more chances to nap throughout
a day at 2 hours interval & the latency to sleep onset & REM sleep are evaluate .
3. Those assessing the site of obstruction
a. Awake patient ;
(1) Muller manoeuver ; reverse valsalva , awake patient i sitting position , we
introduce the flexible nasoendoscope pernasally to the level of the tongue base ,
then ask the patient to inhale forcefully against closed mouth & nose , so the degree
of the hypopharyngeal collapse noted , then repeated with the endoscope just above
the soft palate (velopharyngeal level) .
(2) CT & MRI ; costy & not always available , can , measure the pharyngeal cross
section , if CT of upper respiratory tract shows that the patient with minimum cross
sectional area < 1cm located 20 mm below the hard palate had high chance of
successful U3P operation .
(3) Lateral cephalometry ; by x-ray to the head & neck on which the relationship
between various soft tissue & bony points ;
- PNS –P (the length of softpalate) .
- PAS (posterior airway space) which is the narrowest diameter of the entire
hypopharynx .
- MP-H (mandible plane hyoid) .
If MP-H > 24 mm & PAS < 5 mm , then increased chance of OSAS , it is essential
if considering maxillofacial surgery .
There is no correlation between it & the success of U3P operation .
b. Sleeping patient
(1) Fibroptic nasoendoscope ; sleep nasendoscopy , done as an outpatient procedure
by inducing sleep by small dose of sedatives , then examine the upper airways
during an obstruction episode by nasendoscope or done at polysomnography , it
done for already diagnosed patient by an overnight sleep study .
(2) Somnofluoroscopy ; during polysomnography the patient with OSAS who is sleep
visualize the upper airway during the obstruction episodes by using image
intensifier , the results recorded on videotape & later analysed ;
- Type I ; soft palate only .
- Type II ; soft palate & more distal airway .
- Type III ; distal to soft palate & the soft palate may closed or remained open .
(3) Pharyngeal manometry ; measure the upper airway pressure at the soft palate &
tongue base , by using series of 3 cathters records .
(4) Cine-CT scan ; rapid CT can take slices throughtout an obstruction episode , the
results either soft palate obstruction (respond to U3P) or multisegemental
obstruction (not respond to U3P) .
But it is costy with hazards of radiation exposure.
All the above test will show the obstruction ; either (1) velopharyngeal (benfit from
U3P) or (2) Multisegmental or (3) toungue base (2&3 not had benifit from U3P) .
4. Others (Intubation) ; used in children with cynotic heart disease & upper airway
obstruction (Down's syndrome) to detect the pulmonary artery pressure & systemic
PO2 saturation , so if the pulmonary artery pressure decreased & O 2 saturation

Lecture notes in
increased , so the patient can't benifit from the surgery which aim to the correction of
the obstruction .
- Treatment
It depends on the level of obstruction , severity of the obstruction , prescence of the
complications (cardiac , respiratory ..etc) , what the patients want & if it simple snoring or
OSA , then the Rx modalities are ;
A. No treatment ; if it is just snoring , no daytime sleepiness , or investigation shows no
OSA or its complications .
B. Behavioural therapy ; like decrease weight , avoid alchol or sedative drugs , use of
devices for tongue & mandible to get them protruded , use of electerical devices to
detect position (positional therapy) .
C. Medical therapy ;
1. Diagnosis & management of systemic diseases like hypothyroidism .
2. relief of nasal obstruction by antiallergic drugs & nasovent (elastic splints) which
dilate the nasal valve .
3. Drugs ; Protriptyline which increase the muscle tone , respiratory stimulant &
supress REM sleep , other drugs like acetazolamide , theophylline , doxapram ,
medroxy progesterone & nicotine .
4. Nasal continuous positive airway pressure (CPAP) which is the gold standard
management , it prevent the apnoea in 99% of patients who can tolerate it .
It cosist of tight mask over the nose , tube connecting the mask to a pump (pressure
7-15 cm H2o) acts as pneumatic splint , so hold the pharynx opened .
The 1 st night should be in sleep labrotory because it could induce intense &
prolonged REM sleep leading to low aeronasal level causing dangerous hypoxaemia
, also the correct air pressure can be determined .
The advantages of CPAP are ; non-invasive , 99% successful & could be
disconnected at any time .
The disadvantages are ; the patients compliance 50-90% , nasal mucosal irritation ,
noise from the machine , mask discofort , air leak causing sore eyes , abdominal
bloating & impractical to those need for travel .
5. Nasopharyngeal airways (nasal spong) ; used for 3 months then disconnected .
i. In Pierre Robin syndrome ; just above the epiglttis because the site of obstruction is
at the tongue base .
ii. In Apert syndrome ; at free edge of the soft palate , because the obstruction is in
the nasopharynx .
D. Surgery ;
There are many anaesthetic considerations ;
1. They are sensitive to sedatives & narcotics , so should be avoided in premediacation
2. Difficult intubation , short neck & collapsed upper airways during intubation may
increased the obstruction , so mask ventilation is inadequate , so use nasopharyngeal
intubation which is manditory .
3. Decrease the ventilatory drive due to paralysing agents & associated COAD .
4. Postoperatively should extubate when fully awake , leave the nasopharyngeal airway
in place , avoid narcotics & need constant PO2 monitoring .

Lecture notes in
The surgical procedures are ;

1. Nasal surgeries ; like correction of the septal deviation , polypectomy , or SMD , the
nasal obstruction cause contonuous negative intrapharyngeal pressure leading to
muscle laxity , so for any pharyngeal surgery to correct OSAS we should correct any
nasal obstruction at first .
2. Oropharyngeal surgeries ;
a. Uvulopalatopharyngoplasty (U3P) ; done either by No. 12 blade , electrocautory
or Co2 laser , in which we remove the tonsils , trimming the faucial pillars & if
required removing the uvula & variable amount of the soft palate , also suturing
the anterior pillar to the posterior pillar .
Indicated in ; (1) socially disrupting snoring "success 85-90%" (2) OSA when the
obstruction is at the velopharyngeal or upper oropharyngeal levels "success 50-
60%" , the success will be cure of snoring .
Contraindicated in ; (1) velopharyngeal insufficiency (2) submucosal cleft palate
& (3) special voice & swallowing considerations .
Complications are ; (1) Pain , 1 week , decreased by wound infilteration with
mercaine at the end of the prodcedure (2) nasal regurgitation of food & fluid "2-3
weeks" (3) dry throat (4) taste disturbances (5) hypernasal speech & (6)
velopharyngeal stenosis .
So never did adenoidectomy & U3P simultaneously , U3P not fully defined to
improve the snoring in the Rx of OSA , but doesn't decrease the mortality .
b. Palatal procedures ; attempt to stiffen the soft palate by ;
(1) Laser assissted uvulopalatoplasty (LAUP) ; we enlarge the oropharyngeal
airspace by successive vaporization of the uvula (by Co2 laser) , sof palate ,
posterior tonsillar pillar & any redundant posterior pharyngeal mucosa , this
is done on successive occasion under LA in outpatient clinic .
(2) Use of Nd-YAG laser to remove longitudinal strip of mucosa from the oral
surface .
(3) Somneplasty , low temperature radifrequency energy is delivered via a needle
placed into the soft palate lead to scarring & stiffening of the soft palate (used
for simple snoring ) .
(4) Full-thickness excision of the horizontal strip fromoropharyngeal mucosa .
c. Adenotonsillectomy & lingual tonsillectomy , espicially for children , cure rate
about 90% of patients with snoring & sleep apnoea .
d. Midline laser glossectomy (Fujita 1991) ; it can manage the problem of
hypopharyngeal collapse (an alternative to maxillofacial procedures) .
Technique ; we did covering tracheostomy 1st , then Co2 laser used to excise
rectangular area of the tongue base down to the valeculla , further tongue base ,
hypertrophied lingual tonsil & redundant aryepiglottic fold are also excised .
3. Maxillofacial surgeries ; at which we widen the hypopharynx by advancing the
tongue base by many prodcedures ;
a. Infrahyoid myotomy ; with suspension of the hyoid bone through a strip of fascia
lat wraping around the hyoid bone & fix it to the inferior border of the mandible ,
we displace the hyoid 15 mm anterosuperiorly (if > 15 mm this cause dysphagia)
b. Mandibular osteotomy & genoglossus muscle advancement , usually it combined
with the above procedure or with U3P if there is soft palate obstruction , the

Lecture notes in
segment of mandible (genial tubercle) freed from its attachement (to genoglossus
& genohyoid muscles) & advanced forward (8 mm) & fix it with tetanium screw
& wires .
c. Bimaxillary & mandibular advancement , in severe OSA who fail other forms of
medical & surgical managements , use this procedure (BMI >30), the procedures
(1) Lefort I osteotomy & advancement .
(2) Sagital split ramus osteotomy & advancement .
(3) Maximise the distance that the segment is moved & filling the defect with bone
graft .
The response rate > 90% , the over all advancement of genial tubercle is 21 mm .
4. Tracheostomy ; carry 100% cure , it is indicated when there is severe apnoea with
life threatening complications like corpulmonale , chronic alveolar hypoventilation ,
serious cardiac arrhythmias & disabiling daytime sleepiness .
Problems are ;
a. difficult technique (short thick neck & deep trachea) .
b. Usual complications of tracheostomy .
c. Psychological problems .
d. Excessive fat lead to granulation tissue around the stoma , so must remove the
excessive fat & create a skin flap & suture it to the edge of the tracheal defect.
e. Postoperatively ; speaking valve & educate about care .

Lecture notes in
Non – healing granulomas

Wegner's granulomatosis
Heinz Klinger (1931) is the 1st who report patients death from dissemintated vasculitis .
Wegener (1936) describe the rhinological grnulomatosis .
Aetiology ; unknown , but some say that it is the cause of hypersensitivity reaction with an
autoimmune response to unknown stimuli .
Clinical features
Usually the patient under the age of 25 , with generalized form of the disease , it is serious
& lethal disease with patients frequently dying within 6-8 months .
The classical presentation ; vasculitis of the respiratory tract & fulminating
glumerulonephritis with rapid progression with fatal outcome can occur in as little as 48
hours , wee might reach the diagnosis after year in some cases .
1. Nasal symptoms ; the nose & sinuses involved in 80% of patients , epistaxis , nasal
obstruction & appearance of bloody crusts in the nose , this continue leading to
destruction of the intranasal structures including the septum causing nasal collapse
(minor nasal surgeries & biopsies during this period may add to the problem) .
Many patients present with a short history of progressive malaise , pyerexia , weight
loss & feel unwell .
The misdiagnosis result in delay of the treatment allowing considerable progression .
2. Pulmonary symptoms ; cough , haemoptysis & plueritic pain , the pulmonary lesions
often cavitate & seen radiologically (which may be the presenting symptom) , the Dx
aided by flexible endoscopy & lung biopsy , also the lung abscess can occur .
3. Renal symptoms ; 30-90% of patients develope it , limited form of the disease ,
segmental or diffuse GN , the early management is vital as the lesion irreversible .
GUE microscopically there are blood & casts (renal biopsy not essential) .
4. Ocular symptoms ; orbital involvement in about 20% causing proptosis due to
orbital mass or extension from the surrounding sinuses .
Optic neuropathy , retinal artery occlusion , conjunctivitis , dacrocystitis ,
episcleritis & corneal ulceration , delay in mangement lead to loss of vision .
5. Oral symptoms ; hyperplastic granular lesions of the gingiva (at the interdental
papillae) , so when the tooth lost , the socket fails to heal .
Also may be there extenssive ulcerative stomatitis .
6. Otological symptoms ; 1/3 rd of patients has OM or OME , also facial nerve paralysis
can occur (both CHL & SNHL can occur) , also affect the temporal bone leading to
necrotizing granulation tissue filling the tympanic cavity .
7. Laryngeal & tracheal symptoms ; unusual , s.t. serious laryngotracheal obstruction ,
other times localized disease with +ve ANCA test .
8. Neurological symptoms ; direct nervous system involvement (in 10-15%) due to
granulomatous invasion of the neural tissue , intracranial or meningeal
granulomatosis & neuritic vasculitis , also any cranial nerve may be involved .
9. Other symptoms ; generalized vassculitis cause ulceration of the skin (espicially at
the distal arms & legs) , polymyalgia & polyarthritis .
Investigations
1. High ESR & ANCA (antineutrophil cytoplasmic antibodies) .
2. GUE ; red cells & casts .
3. CXR & sinus x-ray .

Lecture notes in
4. Renal biopsy ; glumerulonephritis .

5. Nasal biopsy ; several biopsies taken from the septum & turbinates , it should be
adequate & minimally traumatic , it should be represantive (taken from area of
crustation which may cover an ulcer) , the crust is large greenish & often bloody
with bad odour .
The diagnosis with high ESR & ANCA with CXR changes & +ve nasal findings should
managed urgently with steroids & cytotoxic drugs .
Treatment
Prednisolone 60-80 mg/day with cyclophosphamide 2 mg/kg (or azathioprine 200mg/day)
will result in 100% control , the gradual decrease in the dose started after clinical &
laboratory assessment (ESR & ANCA) , late recurrance espicially after immunological
chalange like influenza & pregnancy .
Sarcoidosis
It is a systemic disease of unknown aetiology , may affect the any part of the body but most
frequently LN , skin , lungs , eyes , liver , spleen & small bones of the hands & feet .
Incidence ; high in coloured races , USA & Scandinavia .
Sarcoid lesion may affect the nose in 3 different ways ;
1. Skin of the nose ; affected by sarcoid lesion , deep granulomatous plaques which may
occupy the full thickness of the dermis , bulbous red or violet skin lesion .
2. Nasal bone ; the nasal bridge may become swellen & plain x-ray show translucent
deposite .
3. Nasal mucosa ; most common , espicially in the nasal septum & the inferior
turbinates , yellow or greyish , slightly raised nodules causing nasal obstruction ,
mucopurulent discharge & s.t. bloody –stained discharge & crusting (smaller than
that of Wegner's) , saddling of the nose & stenosis & syneachiae may present .
Investigations
1. ESR , S. Calcium , S. Angiotension converting enzymes .
2. CXR & sinus x-ray ; show mucosal thickening .
3. Kviem test , which is intradermal injection of filtered extract of spleen from a case of
sarcoid , followed 6 weeks later by skin biopsy shows +ve histology in 90% of cases
charcterized by the presence of epithelial cell tubrcles without caseation which
converted into hyaline fibrous tissue (with central necrosis) .
Treatment
Alkaline douches & betamethazone nasal drops .
Oral corticosteroids used in systemic disease , also can improve the nasal lesion .
Sinonasl Lymphoma (non-healing midline granuloma)
Also known as lethal midline granuloma or midfacial detructive granuloma , whatever the
name it is due to Malignant Lymphoma & should be treated as such , 3 forms of malignant
lymphoma ;
1. Generalized lymphoma ; involving the sinonasal tract , Hodjken or non-Hodjken
lymphoma , in which the nose & sinuses rarely involved (although Waldeyer's ring
often involved) , Dx by the LN biopsy (already) espicially from Waldeyer's ring to
assess the clinical stage of the disease .
2. Malignant Lymphoma of Waldeyer's ring ; all form of malignant lymphoma may
occur (mostly large cell histiocytic type) , most of them of B-cell , can be extended to
the nose & sinuses causing nasal obstruction, epistaxis or swelling of maxillary area

Lecture notes in
3. Peripheral , sinonasal T-cell lymphoma ; it is responsible for the classical

destruction of the midface , there is little systemic disturbances (in complete contrast
with Wegner's , no evidence of pulmonary or renal involvement) .
It still present a diagnostic problem because the atypical cell infilterate are often
disappear in necrotic areas ,.
Good quality biopsy material from the tissue beneath the crust is essential (the
formaline fixed biopsy is insufficient , so arrange for fresh tissue biopsy) , in good
quality biopsy material , abundant of atypical lymphocytes which show +ve
immunohistochemical reactivity to T-cell markers .
Histologically the infilterate are polymorphic & atypical cells tend to be arranged in
a necrotizing angioinfilterative growth pattern , the infilterate consist of neoplastic
atypical T-lymphocytes mixed with plasma cells , small lymphocytes , histiocytes ,
eosinophills & some immunoblasts , thrombosis & necrosis are common findings .
Treatment
Low dose radiotherapy lead to dramatic response , but no longterm cure , but nowadays ,
radical dose of radiotherapy of 5500 cGy or more with wide field coverage including nose ,
sinuses & palate .
Prognosis ; the recurrence or developement of disseminated lymphoma worsen the
prognosis , so need chemotherapy (classified as high grade) .
Specific (infective) granulomas
- T.B. ; rare & almost always associated with primary pulmonary T.B. .
Macroscopically ; the lesion in the nose in the form of ulcers (also may occur as
polyps) on the anterior part of the septum , inferior turbinate & anterior choanae .
Microscopically ; epithelial granuloma , Langerhan's gaint cells , extensive
caseation (charcteristic) , AFB are present in the granulomas which confirm the
diagnosis .
Lupus vulgaris (the name of T.B of the skin of the nose) which misdiagnosed as
seqamous cell Ca. (due to its causing epitheliomatous reaction of the sequamous
epithelium) .
- Leprosy ; the nose is frequently involved in the leprosy (often the site of the 1st
manifestation) although the disease is best known for its effects on skin & peripheral
nerves , it is caused by bacillus called Mycobactrium lepra & Mycob. tuberculosis .
Macroscopically ; nodular thickening of the mucous memberane & perforation of the
cartilagenous septum .
Management by Dapsone 44 for many years , espicially in lepramatous leprosy .
- Aspergillosis ; fungal infection , four clinical groups ;
1. Fungal ball (myocetoma) in the maxillary antrum associated with low grade
inflammation (aspergellosis) .
2. Slowly progressive disease with fibrosis of the nasal & paranasal sinus mucosa
spreading externally into the suncutaneous tissue of the nose orbit &
nasopharynx , this caused by zygomycete .
3. Fulminating disease (in DM patients) which spread rapidly from the nose to the
skull base & brain (caused by zygomycete lead to rhizopus oryzae) .
4. Chronic granulomatous lesions of the nose & sinus cavities caused by
Rhinosporidium seeberi (Candidiosis may rarely also become chronic & cause
candidial granuloma) .

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- Syphilis ; it may be transmitted venereally or congenitally (congenitally the nose is

always involved) .
1. Congenital syphilis ; after several weeks after birth , acute inflammation &
persistant catarrh , then within 3-4 years charcteristic saddle nose .
2. Acquired syphilis ;
a. Primary chancre of the nose (rare) involve the anterior part of the septum or
skin of the vestibule .
b. Secondary lesions , white mucous patches associated with oral & cutaneous
lesions .
c. Tertiary lesions occur any time following secondary one (can delay for > 20
years) , destructive lesions causing collapse of the bridge of the nose
(involve the nasal bone) lead to saddle deformity .
The sites are ; septum , inferior turbinates & the floor of the nasal cavity , nasal
obstruction & bloody stained discharge is a common presentation , the anterior nares
may involved causing indolent browny ulcerating granulations .
Localized gummatous form produce ulceration & posterior septal perforation , diffuse
syphilitic infilteration may cause swelling & extensive necrosis of nasal & facial tissue
Microscopically ; there is area of necrosis alternating with granulation tissue which
ranges from non-specific appearance to epithelial manifestations including
multinucleated gaint cells minmiking a T.B. granuloma .
To confirm the diagnosis we need for serological tests of syphilis .
- Actinomycosis ; bacteria not mycosis , caused by Actnomyces israelii , more than
50% occur in the head & neck with rare nose & sinus involvement .
The usual site is the maxillary antrum usually , irrigation may reveal foul pus
containing the microrganism ,.
Glandular lesions may be seen in the nose , diagnosed by tissue sections )erosion of
bone may occur) , macroscopically there ia sulpher granules surrounded by a
purulent exudate , also fistula through the checks is reported .

Lecture notes in
Cerebrosinal fluid rhinorrhoea

Leakage of the CSF from the nose which is a symptom of failed containment of the CSF to
its subarachenoid compartment , it indicates a communication with the subarachenoid
space & therefore , an opening of the arachenoid , dura & bone to permit exist of the CSF
to the nose .
Defects in the floor of the anterior cranial fossa can lead to the leakage of CSF into the
nasal cavity, because of the nature of the nasal cavity and its exposure to the rest of the
upper aerodigestive tract, communication with the intracranial contents can lead to
meningitis and otherintracranial complications, including serious and sometimes lethal
medical problems.
The pathways of CSF leakage to the nose are ;
1. Anterior cranial fossa via ; frontal sinus , ethmoid sinus , cribriform plate &
sphenoid sinus .
2. Middle cranial fossa via ; sphenoid sinus , mastoid aircells , middle ear &
eustachian tube .
3. Posterior cranial fossa via ; sphenoid sinus , mastoid aircells , middle ear &
eustachian tube .
The actual loss of CSF itself is of no particular consequence , but persistanat dural fistula
represents persistant hazard for a potentially fatal purulent meningitis & death complicate
most cases of unrecognized CSF rhinorrhoea .
Historical background
- The earliest theories suggest that there is normal communication between the spinal fluid
space & the nose , this was from the 2nd century A.D. untill the 17th century A.D.
- Willis – 1676 ; described a case thought to be the 1st recorded instance of CSF
rhinorrhoea.
- Miller – 1826 ; the 1st comperhensive description of CSF rhinorrhoea , describe the
finding , at necropsy , a fistula between the nasal cavity & subarachenoid space in
hydrocephalic child who had suffered an inttermittant clear nasal discharge .
- St. Clair Thompson – 1899 ; the 1st who use term rhinorrhoea for the nasal CSF discharge
, he published his findings on 20 patients which include chemical analysis CSF & suggested
diagnostic criteria for differentiating CSF from other clear fluid nasal discharge .
Aetiology
1. Traumatic
a. Accidental ; acute (within 48 h) or delayed , ( 80% secondary to head injury with
skull base fracture) , it complicate about 2% of all head injuries & 5% of fractures of
the skull base , most of which through the anterior cranial fossa .
Trauma to the floor of the anterior cranial fossa may cause disrubtion of the
arachenoid , tear of the dura , fractured bone , tear of the periosteum & mucosa
leading to fistula .
The most common location of the anterior fossa is the region of fovea ethmoidalis
(roof of ethmoid) & the posterior frontal sinus wall , followed by the cribriform plate
& sphenoid sinus . The cribriforn are is more common location for a traumatic
fistula through the olfactory tract .
Middle cranial fossa fracture lead to CSF rhinorrhoea through the sphenoid sinus
or Eustachian tube .

Lecture notes in
The posterior cranial fossa fracture of clivus or petrus temporal bone may lead to
CSF rhinorrhoea through the sphenoid sinus or Eustachian tube .
Most post-traumatic CSF rhinorrhoea are immediate , if delayed 95% appear within
3 months , at the time of injury there is oedema & inflammation which cause
temporary obstruction to the flow of CSF , as this resolves in the 1 st week after injury
, the fistula appear , but in delayed fistulae ; resorbtion of bone & soft tissue in the
fracture site probably occur secondary to the distrupted blood supply , this gradually
weakens the pia-arachenoid seal untill elevation of the intracranial pressue (ICP)
initiate a leak
b. Iatrogenic ; acute or delayed , 16% secondary to nasal , paranasal & skull base
surgeries , it may follow skull base surgery , excision of sinus neoplasm , intradural
procedure (mucocele excision) , excision of acoustic neoroma , trans-sphenoidal
hypophysectomy & endoscopic ethmoid surgery .
2. Non –traumatic (spontaneous) , it is uncommon , 3-4% , mostly occur in adults , 4th
decade of life , F:M 2:1 , it may occur after an episode of sneezing , coughing or minor
URTI , so it is often mistaken as a feature of rhinitis .
a. Normal pressure ; most commonly in cribriform plate or sella turcica , 90% orginate
from the potential &/or congenital pathways & 10% due to direct erosion of the skull
base by tumor or infections .
The potential pathways of leak are ; the prolongations of the subarachenoid space
along the olfactory nerve & stalk of the hypophysis .
The minor degree of maldevelopemental anomalies of cribrifrom plate or
diaphramatic sella lead to further extension of subarachenoid space in these regions
, most cases in the cribriform plate area .
Congenital pathways can be through the oseous defects in the skull base which can
occur as a meningocele (rare) or congenital defects in the tegmen or through &
around the stapes (Mondini dysplasi) occasionally .
The direct erosion of skull base are very rare , could be due to osteoma of the
frontoethmoid region , nasopharyngeal angiofibroma & Ca. & also osteomyelitic
erosion of skull base due to local sinus infection .
b. High pressure ; 45% of non-traumatic fistulae , 75% of these fistulae are in the
cribriform area (fragile) with prolongation of subarachenoid space follow the
olfactory filaments .
84% of these cases assocaited with slow growing intracranial tumors (most
commonly pitutary neoplasms) , 16% associated wit hydrocephalus .
Direct invasion of the skull base is not the usual cause mechanism of the leak .
These fistulae act as a safety valve , so closure of the leak will worsen the patient
condition if the causative lesion is not treated .
Pathophysiology
1. Traumatic ; two factors are responsible for the CSF fistulae ;
a. Distruption of the arachenoid-dura & bony defects .
b. CSF pressure gradient that is either contineuosly of intermittently higher than
healing tensile strength (gradient) of distrubted tissue lead to seperation of the dura
fibers & then CSF leak .
These 2 factors occur after the trauma , but difficult to acheive in non-traumatic type ,
the mechanism begin by increased ICP & even transient nature could start a leak , if

Lecture notes in
potential pathways present & this occur , if there is no increase in ICP because the leak
may act as a safety valve .
2. Non-traumatic ; onset usually in adults due to high ICP (normally 140 mm while in
infant 40 mm) , the normal ICP +ve in many head positions with subject to recurring
fluactuation , the normal arterial & respiratory rate also affect the CSF pressure .
There is some theories to describe the CSF leak ;
- Omaya's theory ; normal contents of the cribriform plate or sella turcica areas can
become reduced in bulk , possibly because of ischemia , the empty space become
pouch filled with CSF , the normal pressure pulse causes this pouch to exert a focal
& contineous errosion effect , this possibaly lead to CSF fistula .
- Theories of non-traumatic leaks in the anterior cranial fossa which include ; focal
atrophy , rupture of the arachenoid sleeves passing through the cribriform plate with
the olfactory nerve filaments & persistance of an embryonic olfactory lumen .
Diagnosis
1. Confirm the presence of leak
a. History ;
- In cases of trauma , any persistant rhinorrhoea should be considered to be CSF
untill proven other wise , the possibility of delayed fistulae should be kept in mind .
- Cases of spontaneous CSF rhinorrhoea may escape Dx untill complications presents
i.e. repeated attacks of meningitis .
- Patients presentation usually as ; unilateral , clear , nasal discharge which may be
persistant or intermittant .
- There may be salty taste .
- Rate of flow will increased by bending the head forward , valsalva manoevere & by
compression of both jugular veins .
- Headache due to either low or high CSF pressure , low pressure headache relieved
by reclining or straining , while high pressure headache relieved by rhinorrhoea .
- Anosmia suggest cribriform fracture & olfactory trauma .
b. Examination ;
- Positional changes or jugular compression can increase the flow & confirm the Dx .
- Reservoir sign ; after being supine for sometime , the patient brought to an upright
position with neck flexed , a sudden rush of clear fluid idicates CSF fistula , it's also
useful for collecting fluid for analysis .
- Handkerchief test ; mucous stiffen the handkerchief while CSF not .
- Halo sign ; the blood stained CSF rhinorrhoea dried out with a central blood
surrounded by a clear ring .
- Nasal endoscopy ; it is mandatory , used alone or in conjucation with intrathecal
flurecien , it confirm & localize the presence of leak .
- CSF otorrhoea lead to effusion & then conductive deafness .
- If labyrinthine capsule fractured , then sensorineural deafness & lower motor neuron
facial palsy .
c. Investigations ;
- Glocose concentration ; a concentrations of 30 mg/dl is confirmatory of CSF if the
patient has normal blood glocose level , active meningitis can lower the CSF glocose
concentrations & if CSF is contaminated with blood then the test is invalid .

Lecture notes in
- B2 transferrin ; protien electrophoresis show one transferrin band (B1 fraction) ,

while CSF protien electrophoresis show two transferrin bands (B 1&B2 fractions) , so
B2 transferrin is pathogenomic to CSF .
The method of the test is ; cellulose acetate strips containing an antitransferrin
serum applied at the B-area , if the sample contain CSF , stained immunoprecipitates
appear both in B 1&B2 fractions zones .
Moderate contamination with other body fluids doesn't invalidate the method , if
doubt persist then localize the leak .
2. Confirm (demonsitrate) the cause (whenever possible) ; CT scan & MRI are important
investigations to exclude the intracranial tumors especially in high pressure non-
traumatic leaks .
3. Confirm (identify) the exact site of leak if surgical repair is necessary
a. Radiology ; it confirm the presence of CSF leak , may identify the underlying cause ,
may determine the exact antomical site , side , size of fistula & assisst in planning the
surgical approaches .
The finding in radiology are ; bone defect , air-fluid levels & erosion .
- Plain films ; can shows pneumocephalus , air-fluid levels , fractured skull base &
fluid in the adjacent sinuses which is suggestive of fistula , in the absence of a history
of trauma, plain radiographs are of little value.
- CT scanning , extermely helpful .
CT scans can reveal the fracture site that underlies a traumatic leak, reveal an
underlying anatomic or developmental abnormality in the case of nontraumatic leak,
and provide information on the brain parenchyma in the vicinity of the leak . At
present, it is the criterion standard in the evaluation of craniofacial trauma.
Especially helpful are thin-section (1-mm) coronal CT scan , these thin sections can
depict small defects of the cranial base that are not visible on standard CT scans or
reconstructed images.
For the anterior cranial fossa we do coronal CT to show the cribriform plate , fovea
ethmoidalis , planus sphenoidale , the floor of the frontal sinus , pitutary fossa &
orbital roof , also fluid collection in any sinus can be examined .
Axial CT for the anterior & posterior tables of the frontal sinus , medial orbital walls
& perpendicular plate of ethmoid .
CT scan should be included in the investigations for nontraumatic fistula , views to
the anterior , middle & posterior carnial fossae should be taken (including the inner
ear) with intracranial CT to exclude tumors or hydrocephalus .
Metrizamide CT cisternography which is the most helpful & reliable method for
identifying & localizing the CSF leaks , but only if there is active leak at the time of
study , the success rate 22-100% depending on the presence of active leak .
The findings are ; the metrizamide pass through the bony defect , bony defect &
metrizamide outside the cranium .
Sometimes it need artificial elevation of the ICP by valsalva manouvere or
intrathecal infusion of saline .
Recently (Byrne 1990) combined CT cisterngraphy with digital substraction of
fluroscopy images . It is useful in ; large defects associated with postoperative
rhinorrhoea , demonsitration of multiple fistulae .

Lecture notes in
Metrizamide is associated with little morbidity like mild headache & some reports of
neurotoxicity , how it has been replaced by the next generation of Iodine-based
contrast media such as Iohexol .
- MRI , it is not used in investigating CSF rhinorrhoea due to its ineffectiveness
(compared with CT) in demonstrating the bone windows , although it has advantage
of lacking exposure to ionizing radiation . However, a heavy T2-weighted image can
reveal a brisk CSF leak , also can be useful when trying to determine the extent of an
encephalocele.
- Pneumoencephalography; this is an obsolute procedure that is also uncomfortable
because patients are required to be in a head-hanging position , this study provides
poor contrast with the paranasal sinuses and nasal airway.
b. Isotope studies ;
- Used in cases of inactive , intermittent , small or questionable leaks .
Different tracers, including radioactive iodine-131, radioactive iodinated serum
albumin (RISA), ytterbium-169, diethylenetriamine pentaacetic acid (DTPA), indium-
111 DTPA, technetium-99m human serum albumin, and 99mTc pertechnetate, can be
used , despite their relative safety, studies based on these tracers have several
limitations; (1) They do not help in precisely identifying the location of the leak (2)
The isotope is absorbed into the circulatory system and can contaminate extracranial
tissue (3) Patient positioning can cause distal pledgets to incorrectly take up the
isotope (4) Readings of radioactivity should be high to determine a true leak;
borderline readings are not reliable. False-positive results are present in as many as
33% patients.
- Radioneuclide cisternography is more effective in identifying the presence of the
leaks , although often not give precise anatomical localization .
- Indium 111 –DPTA is now used , with half life 2-8 days , much lower radiation
absorption , higher quality images & lower neurotoxicity
c. Intrathecal dyes ;
- It is used as early as 1933 , but it falls into disrepute due to the reports about
neurological complications .
- Messerklinger – 1972 , use combination of intrathecal fluricien dye (stain CSF with
bright yello-green colour) & nasal endoscopy to Dx the anterior cranial fossa leaks .
- Technique ( Stammberger -1992) ; through a lumber puncture 1 ml of CSF is
withdrawn & 1 ml of 5% Na-fluricien injected intrathecally , then the patient kep in
prone position with the head down slightly lower than the rest of the body to allow
the dye to distrebuted throughout the entire dural space (it has a higher speciefic
gravity than the CSF) .
If there is large fistula , then bright yellow-green coloured CSF drippling from the
nose few minutes after the injection .
The patient then placed in supine position for endoscopic examination , the nose
sprayed with topical anasthetic (xylocain 4% + 1:1000 adrenaline) , after a minute ,
endoscopy done using 4 mm 30 o endoscope , if the fluricien test is strongly positive
white light will show the stained CSF clearly & allow it to be followed back to its
source (SCF otorrhoea , the CSF leak through the nasopharynx from the Eustachian
tube orifice during swallowing) .

Lecture notes in
If fistula is small & difficult to recognized , then use blue light source , even in a
tracer of CSF appear under blue light as a bright whitish-green streak , while simple
nasal secretions remain colourless , the blue light technique is extermely sensitive , if
this test negative , then useful to place a small Merocel sponges into the nose for 6
hours & then absorpe nasal secretions & examined under blue light .
The intrathecal dyes method infrequently has complications .
Management
- It need close coooperation in between neurosurgeon , neuroradiologist &
otorhinolaryngologist , the plan divided into mediacal management & surgical management
- The Rx plan depend on ; severity & extent of the injury , the aetiology & the anatomical
site of the CSF leak .
1. Medical treatment ; the majority of acute traumatic fistulae will seal spontaneously , the
leakage stops within 1 week in 70% of patients, within 3 months in 20-30%, and within 6
months in most patients; leakage rarely recurs , the opposite is true for nontraumatic leaks;
only one third stop spontaneously, and they tend to persist for several years, with
intermittent leakage, this line include ;
- Bed rest in the head-up position .
- Patient should avoid coughing , sneezing & nose blowing & straining due to physical
activity .
- Measures that reduce the CSF production rate like ; medications (acetazolamide ,
fruseamide "minimally effective") , repeated removal of CSF by repeated lumber taps or
an indwelling lumber-subarachnoid drain "most effective" .
All these lead to approximation of the dural tears & then healing by primary intention .
- Objections ;
a. Indwelling lumber drains may lead to increased risk mof developing meningitis , so
need antibiotics cover .
b. The use of prophylactic antibiotics (when not use a drain) is controversial ;
proponets that antibiotics prevent the developement of meningitis because of the
exposure of the CSF to potentially pathogenic M.O. of the upper airways , the
opponents ; the prophylactic antibiotics expose the patients to potentially resistant
organism & more serious infections .
- If the medical Rx failed after 10-14 days , if the leaks reoccurs , if the leak persistant &
chronic , then localization needed & surgery indicated .
2. Surgical treatment ;
- It involve ; the closure of fistula & removal of the cause (nontraumatic cause) .
- The operative approaches either intracranial (intradural or extradural) or extracranial ,
the approach depends on preoperative localization of the fistula , poor localization need
wide approach & vice versa .
- Recurrence rates are high as 20% & can be decreased by the use of postoperative
placing of indwelling subarachnoid-lumbar drain (controversial) .
Intracranial approach
- The 1st successful intracranial repair of CSF leak was done by Dandy at 1926 , it is the
pocedure of choice in non-identified CSF leak .
- Technique ; craniotomy through the region of leak exposing the floor of one or more
cranial fossae , this approach either intradural (preferred) or extradural , the

Lecture notes in
subarachnoid dehiscence identified & intradural repair with suture permit water-tight
seal .
- The advantage of it ; direct visulazation of the dural tear & inspection & treatment of
the adjacent cortex , there will be better chance at tamponding a leak in the face of
increased ICP .
- The disadvantages are ; greater morbidity , brain retraction & frequent loss of olfaction
in surgeries of the anterior cranial fossa .
Extracranial approach
- Dohlman – 1948 & Hirsch – 1952 the 1st to describe this approach & developed by
Montagomery – 1966 & 1973 .
- Preoperative localization of the fistula needed in this type , the technique depends on the
site , size & nature of the leak .
- It offers a reasonable chance to success & minimal morbidity & mortality .
- In all approaches the use of fibrin glue by its adgesive sealing properties inhance the
results of the repair .
- CSF leaks through the frontal sinus ;
a. Anterior osteoplastic flap procedure using eyebrow or coronal incision .
b. Removal of the entire mucous memberanes lining the frontal sinus .
c. Removal of the inner cortical lining of the sinus with a rotatory cutting burr .
d. Subcutaneous fat used to fill the sinus completely .
e. Fascia lata may be ised to repair dural defects .
- CSF leaks through the cribriform plate & roof of the ethmoid ;
a. Repair via external ethmoidectomy approach .
b. All the ethmoidal cells cleared up at the level of the cribriform plate .
c. The middle turbinate is removed to facilitate exposure .
d. Superior incision extended along the anteroposterior dimension & the superior
nassal septum at the junction of the septum & olfactory slit .
e. Inferior incision 1.5 cm below & parallel to the superior one .
f. Anterior incision connect the anterior ends of the two .
g. Septomucosal flap is rotated 90o to civer the point of leakage & adjacent dura of
the olfactory & ethmoid region .
- CSF leaks through the sphenoid sinus ;
a. External ethmoidectomy is used (Trans-septal appraoch provide less visibility) .
b. Septal mucosal flap must be fashioned before entering the sphenoid sinus as the
mucosa covering its anterior wall make the base of the flap .
c. Mucosal flap carefully elevated & reflected into the nasopharynx , then anterior
wall of the sphenoid removed .
d. To provide wide exposure it is better to remove the intersphenoidal septum & part
of the posterior nasal septum .
e. Mucosal lining of the sphenoid is removed & the flap placed over the point of
leakage , if the dural defect is large , fat or fascia lata placed before the flap .
- CSF leaks through the mastoid & middle ear ;
a. All the dura surrounding the petrous bone can be approached extracranially from
below , so this leak can be successfully stopped by obliteration technique .
b. Pedicled sternocledomastoid muscle or in larger leaks free fat graft may be used .

Lecture notes in
c. The flap or graft packed tightly against the point of leakage , mastoid incision
tightly closed in layers without drainage .
Endoscopic repair of CSF fistula
- CSF leak is a potential complication of endoscopic ethmoidectomy & immediate
endoscopic repair of such leaks should be considered by any surgeon performing
endoscopic nasal surgeries , if the leak discovered intraoperatively .
- Delayed onset leaks which are visible endoscopically are amenable to endoscopic repair
- Technique ;
a. Identify the defect accurately .
b. Mucosa elevated from the surroundings bone .
c. Abdominal fat or fascia lata or temporalis fascia is tucked in above the bony skull
base , muscle or mucoperiosteum (from septum) placed over the defect .
d. The edged are tucked under the mucosal edges around the defect , tissue glue or
microfibirillar collagen help to secure with further support using gelfoam .
- The advantages of this approach ; excellent field of vision lead to exact localization of
the leak , the ability to clean the mucosa precisely from the bony defect without
significantly increasing the size of the defect , & accurate position of the graft material
over the defect .

Lecture notes in
Trans-sphenoidal hypophysectomy
Operations in the pitutary gland are for the removal of the pitutary tumors & it is not
complete removal of the gland (not complete hypophysectomy) because the remaining
pitutary tissue is not removed .
We have ywo imporatant approaches ;
1. Transethmoidal approach ; advantage of it is wider access & better exposure , but it
leave a bad facial scar (disadvantage) , this approach performed by otolaryngologist
2. Sublabial (trans-septal) performed by neurosurgeon .
The trans-sphenoidal approach hypophysectomy is long & narrow approach , can not used
two instruments at the same time , & can not use microscope .
It is the most popular approach because ; it is direct route with low morbidity & mortality
& rarely postoperative complications occur such as seizure or brain damage , also the
convalscent period usually quite short & can comletely remove the tumor as its most
effective treatment in acromegally .
Traetment of pitutary tumors by surgery & radiotherapy (by external beam x-ray & proton
radiotherapy or by implication of gold or Yttrium become very effective) .
Both surgery & radiotherapy are non-selective & just destructive , also the radiotherapy
nonselective & doesn't completely destroy the tumor & leave the normal gland intact
espicially in case of well differentiated carcinoma , but it does have a useful & effective role
It is possible to shrink the pitutary tumor medically by Bromocriptine (so Rx of pitutary
tumor by surgery + radiotherapy + medication) .
Sphenoid sinus anatomy
It is small before the age of 3 years , fully developed at the age of 12-15 years , it situated in
the body of the spenoid bone (the paranasal sinuses, are named for the skull bone in which
they lie) the sphenoid sinus drains into the space above the superior concha called the
sphenoethmoidal recess . It related posteriorly to the pons , inferiorly to the nasopharynx &
superiorly to the optic nerve
The sphenoid sinus drains into the space above the superior concha called the
sphenoethmoidal recess , the size of the ostia is 0.5 -4 mm , the site 10-20 mm above the
floor of the sinus , capacity about 7.5 ml .
Sensory innervation of the sphenoid sinus is by the ethmoidal branches of the ophthalmic
division of the trigeminal nerve , by the pterygopalatine brabch .
The blood supply is from the sphenopalatine artery & pterygomaxillary artery , the
lymphatic drainage is to the retropharyngeal LN .
Degree of pneumatization is 1% conchal (central) , 40% pre-sphenoidal & 60% post-
sphenoidal .
The bone overlying the internal carotid artery & optic nerve is extremely thin & dehiscent
in significant percentage of population ; 6% optic nerve & 25% internal carotid artery .
Indications of the removal of the pitutary tumors
I. Surgical Indications ; due to local effect of the tumor extension ;
1. External upward causing ;
a. Bitemporal hemi-anopia with restriction of the visual field , then complete
blindness .
b. Increase intracranial pressure causing headache & papilloedema .
2. Lateral extension into the cavernous sinus affecting the cranial nerves III , IV & VI .

Lecture notes in
3. Downward extension present in nasopharynx & s.t. cause CSF leak with recurrent
meningitis .
II. Medical indications ;
1. Acromegally & gigantism ; the most effective is complete removal of the tumor by
trans-sphenoidal hypophysectomy which give 80% cure (decrease growth hormone
to normal) .
Partially effective Rx is radiotherapy (protone therapy) & porly effective Rx is
medical therapy as it lead to shrinkage of the tumor size , but in the future may
become more effective espicially in prolactine producing tumors .
2. Cushing's disease & Nelson's syndrome ;
Cushing's syndrome may be caused by ; pitutary tumor , adrenal gland tumor ,
ectopic ACTH producing tumor & adminstration of steroid & other certain drugs .
The diagnosis of cause is not stright forward , however the Rx of Cushing's syndrome
is s.t. by removal of pitutary tumor which are ; micro-tumors & can not seen on plain
x-ray , but may be identified on CT or MRI , and these microtumor cures with
surgical removal .
Sometimes the tumor may be large invasive tumor which are difficult to cure
surgically or any other way .
Nelson's syndrome , if an adrenalectomy done for Cushing's syndrome primarly due
to small pitutary tumor , then few months or years after that developement of the
pitutary tumor occur , this result in increased level of ACTH & melanocyte
stimulating hormone (MSH) causing generalized pigmentation .
So that trans-sphenoidal hypophysectomy is more satisfiable solution for this seious
condition .
3. Prolactinaemia ; before discover prolactine hormone , these tumor included in
chromophobe tumor & they thought that they didn't have any hormonal effect .
Prolactine –secreting hormone , tumor secreting prolactine in high quantity ,
however any suprasellar tumor secretion or interfere with secretion & control of
prolactine , but the level is not as high as with prolactine secreting tumor .
Hyperprolactinaemia , in female cause amenorrhea , infertility & galactorrhea , in
male it cause impotence , gynacomasia & skin changes .
Prolactine secreting tumor treated now greatly with medical therapy , if medical Rx
is not tolerated by the patient , then surgery indicated .
4. Chromophobe tumors (adenoma & germinoma in children) ; these tumors not have
direct hormonal effect , but they elevate the prolactine level indirectly by pressure on
the prolactine controlling mechanism .
Germinoma rare , surgery done for diagnosis & radiotherapy is the choice for treatment
5. Other pitutary tumors ; rare pitutary tumor produce mixture of hormones .
Contraindication of trans-sphenoidal hypophysectomy
1. Presence of nasal or sinus infections .
2. Partial or non-pneumatization of sphenoid sinus .
3. Upward extension of >few mm anteriorly or 1 cm posteriorly (not accessable from
below) , except dumb bell tumor which need surgery from below & from above &
better to staging this operation starting with transphenoidal approach .

Lecture notes in
Preoperative investigations
I. Medical investigations ;
1. Measuring all pitutary hormones level .
2. Measuring GH (serum level) .
3. Measuring insulin .
4. Glocose tolerance test (oral or i.v.) .
5. Blood sugar .
6. Serum electrolyte level , in some conditions such as Cushing's disease K + level
dangerously low for GA .
7. Blood group & cross match may be needed , if there is serious bleeding from
cavernous sinus or carotid artery .
II. Imaging studies ;
1. Plain x-ray ;
a. Skull x-ray shows outline of the pitutary fossa , pneumatization of the sphenoid &
size of the frontal sinus .
b. Sinus x-ray needed to exclude infection .
2. Encephalography ; to show the outline of the gland in the pitutary tumor , but its
risky investigation , so it is now subsided by CT scan & MRI .
3. CT scan ; shows the gland very satisfactory & shows the extension of the tumor to
decide the type of operation .
4. MRI shows pitutary tumor better than CT , espicially where there is empty sella-
turcica with a rim of the tumor or a lateral extension of the tumor .
It will show the site of the tumor ; GH secreting tumor inthe lateral-inferior aspect ,
prolactine secreting tumor in the superior aspect & ACTH secreting tumor centrally.
5. Arteriography of the internal carotid artery to show position of the tumor & there is
certainly this can be more informative & that is if the tumor has been treated
medically & has apparently regressed , so that the carotid artery can be move
toward the midline & space between them become a few mm , also the carotid artery
can be identified during surgery .
III. Visual field ; visual field defects start to appear where the tumor extends upward to
optic chiasma , this is an important signwhich is usually means that trans-sphenoidal
operation is not indicated & the surgery better done from above .
The visual field better to done routinely & compare the results in case of recurrence .
The procedure
- Preoperative drug therapy
1. Adequate dose of steroids , should be given to cover the operation & postoperative
period .
2. Prophylactic antibiotics , to decrease the risk of infection , pack removal from the
nose after 9 days & to prevent infection we give combination of broad spectrum
antibiotics with effective distribution to the CSF , it should be continued untill the
pack is removed .
3. Desmopressin (DDAVP) , should be available for the 1 st few days postoperatively to
treat diabetes insepidus , water intoxication is more dangerous than diabetes
insepidus , so that this drug should be given only when necessary by using urine
osmolarity as a guide , urine specific gravity (low) with UOP >500ml/hr for 3

Lecture notes in
consuctive hours (indicate DDVAP injection 2 mg) & total UOP of > 5 letters/24hrs
(indicate diabetes insepidus , should be treated) .
Some patients should told that they become thirsty & because of this they drink much
mimiking the diabetes insepidus .
- Anasthesia
1. Intubation ; may be difficult due to acromegally in some patient , so that the large
laryngoscopy & long ETT should be available .
2. Ventilation ; spontaneous or controlled , should provide low venous pressure .
3. Air embolism is not a problem because under direct vision it is possible to see if the
blood come from cavernous sinus or air entry to it & ventilation pressure can be
adjusted accordingly .
4. So that , it is not necessary to assess the neck viens for air embolism by doppler
prob.
5. Blood pressure ; should be kept at early stage of the operation at normotensive
levels to control all superficial bleeders & prevent haematoma , then after
hypotensive technique is employed during dissection of the pitutary gland .
- The operation
1. Trans-ethmoidal approach
- Operation table & Patient position ; tripped 25 o head up with slight flexion of neck
- Surgeon ; stnds on the right side of the patient .
- SMR ; performed to access the right side of the nose .
- External curved incision around the medial side of the orbit & deepened towards
the nose to avoid the lacrimal sac .
Strightening the upper 1 cm of the incision to avoid the supratrochlear nerve .
- Division of the periosteum & seperate it from the bone & dissected back the orbital
rim to expose the anterior ethmoidal artery which runs through the frontoethmoidal
suture & represent the upper limit of the roof the ethmoid , seal the artery from
above & below using unipolar diathermy (not bipolar, because it not effective) ,
usually there is no bleeding but there is small fat extravasation .
- Continue dissection to the posterior ethmoidal artery which left as a landmark .
- Lacrimal sac lifted from its groove & mobilized to avoid tousim .
- Luogo retractor placed in position , remove the paper plate of the ethmoid either to
anterior or posterior ethmoidal artery .
- Take the orbital rim with drill or gauge .
- Position of the intersphenoidal sinus can be seen by submento-vertical x-ray &
always necessary to removed .
2. Trans-sphenoidal approach
- Gingival incision .
- Elevate the mucosa & periosteum (mucoperiosteal flap) to expose the mucosa of
the pyriform opening & floor of the nose .
- Continue dissection to the front of the septum .
- Firm retraction to elevate the upper lip & tip of the nose by right angled retractors.
- Seperate the mucosa from the fllor of the nose & nasal septal cartilage .
- SMR of the nasal septum & holding the flap with large Killian speculum with hard
bivalve speculum inserted .

Lecture notes in
- Exposure of the anterior wall of the sphenoid & retract it laterally as far as
possible .
N.B.: in transethmoidal approach use stright instruments , while in trans-sphenoidal
approach use angled instrument is better .
- Opening the pitutary fossa & dissection
1. Zeiss-operative microscope with 300 mm objective lens viewing through the
external incision (transethmoidal approach) .
2. Drill out the bone over the pitutary fossa by small burr because it doesn't damage
the dura & remove a layer of bone to reach the top of the sphenoid sinus .
3. Not remove the floor of the sinus ehich needed to support the bluge of muscle at the
end of the operation .
Postoperative care
1. Patient temperature increased in the 1st 12 hours which is not due to infection , but
due to hypothalamic disturbances & from the 2 nd – 8th day the temperature decreased
due to the sane cause .
2. After the 9th day , remove the pack & same treatment of ant intranasal surgery .
3. For 2-3 weeks use saline sniffe to clean the nose .
4. 1 month postoperatively look inside the nose for pulsation of the pitutary .
5. Steroids continue untill normal patient function had been tested (6 weeks) .
6. repeat preoperative test , to assess the effectiveness of the operation & whether
necessary to continue steroids &/or thyroxine .
7. Replacement hormone therapy , about 25% of patient have some pitutary hormone
deficit .
Complications
1. Superficial haematoma or black eye , but this is outside the orbital periosteum , settle
within 5 days .
2. Excessive intraorbital pressure , complete eye closure , so should examine the eye for
vision movement .
3. Temporary diabetes inspedius in 1/3 rd of patients .
4. CSF leak following removal of the pack & the Rx should be conservative with
continuation of antibiotics , this leak usually settle within 3 weeks & very rarely
complicate with meningitis .
5. Frontal sinusitis , occur espicially in acromegalic patients when the frontonasal duct
has been too widely opened .
6. In experienced hands the mortality less than 1% .
Conclusion
Trans-sphenoidal hypophysectomy is the most effective method of treating the pitutary
tumors which extend downwards into the sphenoid sinus .
Neurosurgeon approach usually through the septum , but the otolaryngologist usually
through the external ethmoidal approach .
CT scan & MRI localize the micro-tumors which can be dissected & leave the normal
pitutary tissue .

Lecture notes in
The Orbit
The importance of the orbital anatomy in ENT mainly lies in its content & relationships .
These relatioships are ;
- Superiorly ; anterior cranial fossa .
- Medially ; nasal cavity & ethmoidal labyrinth .
- Laterally ; infratemporal fossa & middle carnial fossa .
- Inferiorly ; maxillary sinus & occasionally ethmoidal cells .
- Apex of the orbit leads to the middle cranial fossa directly .
The orbit , it is a quadrilateral pyramid with base facing laterally , its volume about 30 ml
in adults , 70% of which occupied by the retrobulbar & peribulbar structure as it constitues
a fixed bony cavity , increase in orbital volume only 4 ml produce 6 mm of proptosis .
The orbit is formed by seven bones of the skull ; the frontal, zygomatic, maxillary, greater
and lesser wings of the sphenoid, palatine, lacrimal, and ethmoid .
In this bony compartment sits the globe and its contents: the first, third, fourth, fifth, and
sixth cranial nerves (CN) and their associated vessels; the periorbital fat ; the muscles that
control movement of the globe and lids; and the lacrimal apparatus and drainage system .
Within the orbit, the greatest diameter is found approximately 1.5 cm posterior to the
inferior orbital rim.
The orbital roof has an upward convexity that places it approximately 5 to 7 mm above the
superior orbital rim , and the orbital floor is concave, with a depth of approximately 3 mm
in relation to the inferior orbital rim .
The globe itself rests within this concavity. Posteriorly the floor is convex, and
posteromedially it slopes upward into the medial orbital wall without a sharp demarcation
Laterally and posteriorly the floor is separated from the greater sphenoid wing by the
inferior orbital fissure .
The optic foramen actually lies posteriorly in the plane of the medial orbital wall, thus
placing it medial and superior to the true orbital apex.
The bony orbit consists of the medial wall occupied largely by the ethmoid bone, lacrimal
bone, and a portion of the nasal process of the maxilla .
The floor of the orbit consists of the roof of the maxilla.
The inferior orbital fissure is at its lateral extent.
The zygomatic bone and greater wing of the sphenoid form the lateral orbital wall and join
the frontal bone superiorly to complete the pyramidal bony orbit.
On its medial aspect are the paired ethmoidal foramina, which provide a route to the orbit
for the anterior and posterior ethmoidal arteries.
The optic canal posteriorly transmits the optic nerve and ophthalmic artery.
The superior orbital fissure transmits cranial nerves III, IV, V, and VI and provides an
aperture for the ophthalmic vein.
The orbit of considerable importance in otorhinolaryngology due to ;
1. Adveancement of the endoscopic sinus surgery .
2. Overlap of the pathologies between the orbit & the nose & the paranasal sinuses .
3. Surgery may involve the orbit .
The changes of the orbit with the age are ;
Orbital exploration in child is rare .
Orbital growth occurs with the developement of the facial skeleton .

Lecture notes in
Orbital index = orbital hight /orbital breadth X 100 , it is high in children & with
great volume , so that a little change occur in over all size after age of 7 years .
Orbital fissures relatively large .
Infraorbital foramine usually present at birth .
infraorbital canal , not fully formed but remain dehisent for some years .
Female orbit in general larger & longer than male orbit .
The periorbital (orbital periosteum) charcterized by ;
1. Able to protect all the orbital contents .
2. Resist inflammation & malignancy .
3. Adherent to the orbital margins , sutures , foramina , fissures & lacrimal sac .
4. Continous with dura through the optic canal , superior orbital fissue & ethmoidal
canals .
5. Enclose the lacrimal fossa & surround the duct as far as inferior meatus .
So that during surgery we must do carefull dissection to avoid complicatios as prolapse of
the orbital fat into the surgical field .
The canthal ligaments , are strong fibrous structure attached to the extermities of the tarsal
plates in the eyelids to the orbital margins .
The medial tarsal ligaments made up by preseptal & pretarsal heads of the orbicularis oculi
muscle , each of this consist of ;
 Deep head ;attached to the posterior lacrimal crest .
 Superfacial head ; fuse medially to the frontal part of the medial canthal ligaments
which attached to the anterior lacrimal crest , may be detached during surgery
without serious complication , but may result in deformity ; remding of the medial
canthus , disappearance of the caruncle & increased intercanthal distance .
Tenon's capsule (Fascia bulbi) ; it is a thin memberane surround the globe from cornea to
the optic nerve , inferiorly is thickened to form suspensary ligamnets of Lockwood , it is
important in radical maxillectomy .
Radiological evaluation of the orbit
1. Plain x-ray ; may show adjacent sinus pathology (frontoethmoidal mucocele) , but
with high false negative results .
2. Hypocyclodial tomography .
3. CT scan , the most useful one , allow evaluation of the soft tissue & bone depending
in the window width , both coronal & axial sections should be performed .
4. MRI ; most useful , but lower than CT scan .
5. Orbital venography .
6. Carotid arteriography .
7. Orbital Ultrasound .
Sino-nasal pathologies & the orbit
Infection & inflammation ; the commonest inflammatory & infective conditions are ;
complications of bacterial sinusitis , polyposis & fungal sinusitis .
The bacterial sinusitis & polyposis produce significant hypertelorism with widenening of
the intercanthal distance .
Fungal sinusitis cause widening of the ethmoidal complex when allergic poluypoids occur
in its more aggressive forms , it may invade the orbit directly & gain an access to the
cavernous sinus & middle cranial fossa through the orbital apex .

Lecture notes in
The orbital complications of sinusitis ; antibiotics altered the frequency of complications ,

but if they occur they are disasterous , 20% of the complications result in complete visual
loss & 10% with perminant visual damage .
Acute maxillary & ethmoidal sinusitis , confind in children < 5 years .
Frontal sinusitis , the commonest cause of orbital cellulitis in adults .
Acute sphenoiditis , by direct effect on optic nerve & cavernous sinus in indvidual with
dehiscent intervenening lateral sphenoidal wall .
In children & adolescent ;
 Minor URTI produce orbital complications suddenly , but in adults the situation may
become more chronic or contribute developement of mucocele .
 Congenital dehiscent or open suture lines in childdren facillitate the spread through
the superior , inferior or middle orbital wall .
 Orbital odema can occur even in early stages of sinusitis due to the thin lamina
papyracea .
 Intraorbital but extraperiosteal abscess due to readly stripped periosteum .
 Spread of the infection through the suture lines can results from direct invasion
through thr bone or retrograde thrombophelibitis because the complex venous
drainage & because of no valve in ophthalmic viens allows direct communications
between the cavernous sinus , orbit & pterygoid plexus .
In 1937 , Hubert's classification of orbital complication of sinusitis (5 groups) ;
I. Inflammatory odema of eyelids with/without odema of orbital contents .
II. Subperiosteal abscess with ; (a) odema of the lids , or , (b) spread of pus to lids .
III. Abscess of the orbital tissue .
IV. Mild & severe orbital cellulitis with phelibitis of ophthalmic vein .
V. Cavernous sinus thrombosis .
The spread of infection , into the superior orbital fissure causing ophthalmoplegia ,
anaesthesia of the ophthalmic division of the 5 th cranial nerve & in combination with the
optic nerve it can produce , orbital apex syndrome .
The subperiosteal abscess or extraperiosteal abscess of medial orbit can cause ;
1. Push the globe forwards & laterally (displacement) .
2. Pain & Diplopia .
3. Chemosis of the cornea .
4. Visual loss primarly due to compression of the central retinal artery .
It is treated by rapid high dose of i.v. broad spectrum antibiotics with intranasal
decongestant & constant careful monitoring of the visual acuety which may be difficult to
assess due to lid swelling , the 1 st to affected is the colour vision & ocular mobility (should
be assessed carefully & if occur , then surgical intervention) , CT scan shows the localized
site of collection .
Orbital complications of sinusitis are an emergency in ENT because it may results in
perminant visual loss , surgery should not delayed if there is deterioration of vision .
Sometimes spontaneous discharge may occur through the upper eyelid from the frontal
sinus or near the medial canthus from the ethmoidal sinus .
Surgery in past ; trephening of the frontal sinus with insertion of external drain through
which irrigation done , nowadays ; external frontoethmoidectomy with maxillary sinus
drainage , it is more definitive procedure , alternatively endoscopic drainage &
decompression , but this require extensive experience .
Lecture notes in
In young children , may develope orbital complication , but with little effective antibiotics &
improved surgically .
Orbital cellulitis
More serious complication with odema of retrobulbar structures enclosed by periorbita ,
presented with ; (1) restriction of the eye movement (2) axial proptosis (3) ophthalmoplegia
(4) rapid visual deterioration (5) papilloedema & risk of cavernous sinus thrombosis , & (6)
there may be association with subperiosteal abscess &/or intraperosteal abscess may be
formed . Treated by aggressive antibiotics with orbital decompression .
Periorbital cellulitis (perseptal abscess) in the upper eyelid
Less common complication , presented with ; opened eyelids , normal undisplaced glob with
normal movement & vision . Treated by abtibiotics & surgical drainage .
Frontoethmoidal mucocele
Epithelial lined mucous containing sac completely filling the sinus & capable of expansion .
All paranasal sinuses can develope mucocele , but commonly in the frontal & ethmoidal
sinuses , followed by sphenoid & maxillary sinuses .
Uncommon condition & rarely bilateral (4%) , can reach to the orbit from any paranasal
sinus , expanded may take many years or rapidly occur when secondary infected causing
pyocele .
Male > female , age 40-70 years , Japaneis commonly presented with maxillary mucocele .
It is formed (aetiology) due to obstruction & inflammation of the affected sinus , this protect
that the frontoethmoidal regio is commonly affected , the developement of the mucocele
depend on ;
1. Degree & duration of the obstruction .
2. Abscence of alternative routs of drainage .
3. Bone resorption & expansion possibly intiated by infection .
Histologically , bone remodelling between the mucocele & sinus wall , recently studies on
bone resorbing factors , presence of PGE2 – collagenase –cytokines such as IL I & tumor
necrosis factor (TNF) .
1. Globe displacement due to expansion of the mucocele into the least restricted areas .
2. Proptosis (91%) , 1-17 mm , lateral 55% 2-13 mm , inferior 59% 1-10 mm .
3. Diplopia , 95% , it is minimal in condition developed over many years .
4. Limited upward gaze due to a mass felt in the upper medial aspect of the orbit (55%)
, s.t. with egg-shell crackle sensation due to thinnest overlying bone .
5. Epiphorea , occur in anterior ethmoidal mucocele , espicially in young children due
to compression on the nasolacrimal duct .
6. Compromise vision & occasionally discharging upperlid (4%) , this due to
conversion to a pyocele with additional infection .
7. Retro-orbital headache with facial pain & orbital symptoms such as diplopia &
proptosis , ophthalmoplegia & visual loss , these occur in mucocele & pyocele
posterior ethmoidal & sphenoid sinuses .
8. meningitis & increased intracranial pressure , in severe cases due to intracranial
extension .
Radiologically ;

Lecture notes in
1. Plain x-ray ; signs of frontoethmoidal mucocele are ; expansion of the frontal sinus ,
loss of scalloped margin of the frontal sinus (only seen by vertical view) &
depression or erosion of supraorbital ridge .
2. CT scan , direct coronal or axial sections , the above features (in 1) & homogenous
smooth mass , sinus expansion & thin or less bone , it may show new bone formation
or sclerosis .
CT scan with i.v. contrast show charcteristic ring enhancement if pyocele present .
3. MRI , show higher signal or T2 –weighted spin , low signal T1 , mixed signal intensity
appear when there is haemorrhage or associated with attempts at drainage .
N.B.: the ethmoidal mucocele , in early stage can be missed with plain x-ray , although
lateral x-ray shows expansion of the sphenoid with elevation & erosion of the floor of the
pitutary fossa .
The ethmoidal , sphenoidal & maxillary mucocele , better seen on CT & distinguish thier
mucocele from other pathologies as acute & chronic sinusitis , polyps , retension cyst ,
dermoid , cholesterol granuloma , benign & malignant tumors .
The treatment are ;
1. Surgical ; external modified Lynch-Howarth approach & radical
frontoethmoidectomy .
Stripping of all lining mucosa , except where there is bony erosion exposing the dura
Insertion of suitable silastic tube from the frontal sinus to the nasal cavity which left
in place for 5 months to prevent recurrence .
2. Endoscopic approach , to avoid external incision & associated morbidity ,
displacement of the globe may take several months to occur .
While bone remodelling occur which have a postoperative advantage of decreasing
postoperative excerbation of diplopia which may occur with rapid decompression of
the orbit .
Endoscopic approach suitable for ethmoid , maxillary & sphenoid mucocele in ypung
patients , but not all frontoethmoidal mucocele .
3. Combined external & endoscopic approach to preserve frontonasal recess & to
avoid stenting .
4. External frontoethmoidectomy ; indicated fro recurrence cases which is about 100%
in frontoethmoidal mucocele .
5. Osteoplastic flap , few advantages over the endoscopic & external approach .
Trauma to the orbit
Eye is vulnerable to trauma because it enclosed with an incomplete bony box & trauma may
occur accidently associated with facial trauma or sinus surgery .
The orbital margins , provide a protective boundary to globe because it is stronger than the
orbital walls .
Compression of the orbital contents produce blow-out fracture of the inferior & medial wall
of the orbit .
The zygoma frequently with stand the direct blow except in the zygomatofrontal suture &
zygomatomaxillary suture which are areas of potential weakness & clinically present with ;
1. Depression or flattening of the orbital rim .
2. Inferior deviation of the lateral canthus .
3. Localized step deformity of the inferior rim of the zygomaticomaxillary suture .
4. Tenderness over the zygomatic arch .

Lecture notes in
5. Pain with mastication .

6. Echymosis of buccal mucosa .
This fracture produce significant facial & cosmotic deformity , so it is important to early
diagnosis & repair .
The clinical features are ; (blow-out fracture of the orbital floor)
1. Restriction of the orbital movement in upward gaze .
2. Infraorbital parasthesia including the canine teeth .
3. Orbital swelling & echymosis.
4. Patients with nasoethmoidal fracture presents with ;
a. Periorbital echymosis secondary to the ethmoidal artery damage .
b. Traumatic telecanthus (not seen usually established when the odema obscure the
medial palpebral angle) , an alternative , measure the interpupilary width which is
normally twice the intercanthal distance .
c. Globe displacement , indicate retrobulbar haemorrhage (exophthalmus) .
d. Epiphora , it is not a realible sign of nasolacrimal damage .
e. Facial fracture may also associated with CSF leak .
5. Fracture of lamina papyracea , can occur alone or with floor fracture , more often
seen with complex midfacial fracture , it may accombined with CSF leak with
lacrimal damage & visual loss & epistaxis (severe) due to damage to the anterior
ethmoidal artery .
The radiology is important to determine the site & extent of the trauma , it will show ;
1. Plain x-ray , 70% of the orbital frctures diagnosed by Water's view (OMV) &
Calwell view (OFV) , but with common false positive results .
2. CT , recomended if blow-out fracture suspected , it shows ; classical tear-drop sign
in the antral roof which is due to entrapment of fat & inferior rectus muscle .
The treatment success judged by ;
1. Preservation of the binocular vision .
2. Prevention of the enophthalmus resolution .
3. Restoration of ocular morbidity .
A. Orbital floor exploration , indicted when there is ;
1. Hyperasthesia .
2. Irrigularity of the orbital rim .
3. Periorbital odema .
4. Diplopia .
Not indicated if there is no extraocular muscle restriction & no diplopia .
Immediate exploration is indicated when diplopia & enophthalmus , once exclude other
causes of diplopia such as haematoma of the inferior rectus muscle which eliminated by
forced duction test .
The surgical managemnt depend on the extent of the injury , collapse of the anterior wall
of the maxilla or orbital floor need intra-antral manipulation which achievd by either
commercial stents & baloons or white head varnish on ribbon gauze inserted via
Caldwell-Luc's operation & removed after 2-3 weeks via sublabial incision or inferior
meatal antrostomy .
Reconstruction of the orbital floor indicated in ;
1. Significant enophthalmus & prolapse of fat .
2. Comminuted , hinged or inferiorly displaced bone .

Lecture notes in
Patterson's approach to the inferior orbital rim allows ;

1. Careful dissection of the orbital periosteum .
2. Insertion of the orbital supporting material which may become at the site of
inferior or be absorbed extroded .
The matterials used , bone , cartilage , fascia lata , teflon & silicone , artificial
matterials such as silastic sheath & hydroxyapatite are best tolerated & most successful
for long term .
B. Surgical management of the medial orbital wall
1. Open repair , indicated when there is postrolateral displacement of the lacrimal
bone with its attached medial canthal ligamnets .
2. Bilateral exploration & wiring of the fractured bone , indicated in bilateral
traumatic telecanthus .
3. Insertion of silastic tube indicated when there is damage to the nasolacrimal
appratus .
N.B.: in this type of injury , early exploration is mandatory for late construction , late
complications are ; one eye being lower , diplopia , enophthlmus , dacrocystitis & epiphora
Iatrogenic orbital trauma
1. Endoscopic sinus procedures .
2. Sino-nasal surgeries including ; polypectomy , conventional ethmoidectomy & Caldwell-
Luc's operation ...etc .
3. Sinus procedures ;
a. Antral lavage , particularly under GA when ;
i. Incorrect angle of the entery lead to penteration of the floor .
ii. Dehiscent infraorbital canal .
iii. Excessive pressure .
So that for these causes the eye should not covered during the procedure & always
observed closely , so that the operation can be abandoned with the 1st sign of proptosis .
b. Intra-nasal ethmoidectomy ; this operation was without illumination & visualization ,
so it was difficult operation so they perform the endoscopic sinus surgery .
c. Endoscopic sinus surgery ; in this area make the operation neither safer nor more
dangerous & it is the anatomical & pathological knowlodge of the surgeon .
The anatomy may be disturbed by pathological process or by previous surgeries in
addition to the various anatomical variations , so that CT is mandotary preoperatively
both the coronal & axial sections if surgery in the posterior ethmoid or sphenoid sinus.
Some surgeons may use LA rather than GA to increase safety , but if there is pain ,
may indicate penteration of the orbit .
GA , should ask the patient preoperatively about visual acuety , strabismus &/or
epiphora which may be excerbated by muscle relaxant .
During the procedure , the eyes should not covered & under direct observation .
d. Middle meatal antrostomy ; may cause damage to the nasolacrimal duct because of
that the bone which surround the duct is thicker than that of the uncinate process & so
that it is difficult to remove it with back-bitting-Osrium type forceps , the resistance
should alarm the patient about hazard , so if the duct is damaged , so that conservative
approach because the majority have no more sequlae .

Lecture notes in
e. Damage to the anterior ethmoidal artery causing orbital haemorrhage which occur
with retraction of this vessel & may cause developement of orbital heamatoma which
required immediate decompression .
f. Posterior ethmoidectomy associated with serious compolications which damage the
orbital apex & optic nerve particularly with Ondoni cells which lies lateral to the
sphenoid or within the sphenoid itself .
g. Caldwell-Luc's operation may cause damage to the infraorbital nerve & penteration of
the orbit if transnasal ethmoidectomy is done via this route .
h. Lynch-Howarth & Patterson's external frontoethmoidectomy , associated with minor
orbital complications , the most significant one is ;
i. Diturbance of the trochlear occurance after Lynch-Howarth approach .
ii. Damage to the nasolacrimal duct in Patterson's approach & this combined with
odema of the orbicularis oculi muscle which render the epiphora .
iii. Detachement of the inferior oblique & both anterior & posterior components of the
medial canthal ligaments .
i. Lateral rhinotomy & cranio-facial resection frequently cause transection of the
nasolacrimal duct .
j. Mid-facial-degolving approach cause epiphora due to the streaching of the
nasolacrimal duct .
Tumors of the nose & sinuses may affect the orbit
A. Benign
1. Angifibroma ; young male exclusively , arised from the sphenopalatine foramina &
present as vascular mass in the nasal cavity & nasopharynx , as it is enlarged it
expands to the pterygopalatine fossa & dumb-bell into the infratemporal region
when it can compromise the important structures in the orbital apex & impings on
the inferior orbital fissure & consequently occasionally present with visual loss .
2. Inverted papilloma ; commonest , arised in the middle meatus & invade the maxillary
sinus , intimately related to the nasolacrimal duct & may spread extraperiosteal to
the orbit , rarely intraperiosteal & intra-orbital which had difficult Rx problem .
3. Osteomas ; benign bony lesions arise in the frontoethmoidal region , it can achieve
large percent making difficult to determine thier point of origion , but said they arise
at the junctional point between the mucous memberane & cartilage & bone & are
usually composed of cancelous core with varying amount of compact bone
peripherally . The patient usually have proptosis with osteomas usually diagnosed by
plain x-ray , small & asymptomatic need no Rx , but when the mass associated with
mucocele formation , external frontoethmoidectomy indicated or lateral rhinotomy or
craniofacial approach .
B. Malignant
- Orbital symtoms due to invasion from malignant sinosoidal tumors are ;
1. Unilateral epiphora .
2. Proptosis .
3. Diplopia .
- Different ways of the invasion of sinonasal malignant tumors into the orbit ;
1. through thin or dehiscent bone of lamina papyracea .
2. through infraorbital canal .

Lecture notes in
3. through the orbital periosteum when it is breached by the disease because the orbital
periosteum is resistant to the tumor & disease .
- Fifty percent of the patients need orbital clearance except those with local superficial
invasion of the lid because no lymphatic drainage at this area .
- Once the tumor transversed the lamina papyracea , it may spread intraorbitally , but
extraperiosteally to the orbital apex , then escape into the middle cranial fossa , in simillar
way meningioma & chondrosarcoma of sphenoid sinus leading to bilateral optic canal
compression .
- Adenocystic Ca. through the perineural –lymphatic spread , both directly & by
embolization which may compromise the optic nerve .
- Skin tumors of the medial canthus particularly when the ethmoid & cribriform plate
involved .
Proptosis
Abnormal forward protrusion of the globe (eye ball) , it has to be differentiated from
Pseudoproptosis which is a condition in which the eye ball appears to be proptosed like in ;
1. abnoromal enlagement of the eye (Bphthalmos) lead to infantile glucoma .
2. high degree of axial type of myopia .
3. any cause producing lid retraction .
4. anterior staphyloma & facial asymmetry
The proptosis either ;
1. Acute ;
a. Orbital emphysema , in the fracture of the medial orbital wall .
b. Orbital haemorrhage .
c. Orbital injection (in AWO) .
2. Intermittent ;
a. Varicose of the orbital veins .
b. Highly vascular orbital tumors , periodic congestion .
c. Recurrent orbital haemorrhage .
d. Sinusmucocele .
3. Pulsating
a. Carotid artery –cavernous sinus anurysm or fistula .
b. Saccular anurysm of ophthalmic artery .
c. Cerebral pulsation transmitted to the orbit due to erosion of the orbital roof as in
neurofibromatosis .
4. Positional ; it is a sign of orbital varicose , occur with valsalva maneuver , straining
or coughing .
Aetiology of unilateral proptosis
1. Infective ;
a. Acute ; either bacterial (orbital cellulitis , panophthalmitis) or fungal
(mucormycosis & aspergelosis) .
b. Chronic ; like osteoperiosteitis , tuberculoma & gumma .
2. Inflammatory ;
a. Pseudotumors , idiopathic orbital inflamatory disease , it is a non-neoplastic ,
non-infective space occupying orbital lesion , in children in 30% bilateral .
It is a disease of exclusion , diagnosed after the other causes of inflammation or
rapidly developing proptosis has been ruled out .

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Histologically range from granuloms to vasculitis & fibrosis .

Clinically there is unilateral painful proptosis with conjunctival irritation ,
diagnosed by increased ESR & extraocular muscle inflammatory changes in MRI
& CT , management by prednisolone 60-80mg/day for 2 weeks (50% relieve) , if
less response to steroids , then open biopsy & if there is no response , then
radiotherapy .
b. Orbital myositis ; one or more of the extraocular muscles are primarly
inflammation by immunologically induced inflammation causing mild proptosis .
c. Orbital apex syndrome ; Tolosa-Hunt syndrome , non-specific granulomatous
inflammation of the cavernous sinus , superficial orbital tissue &/or orbital apex
causin mild proptosis .
d. Wegner's grnulomatosis ; 25% of cases , secondary to sinusitis &
nasopharyngeal Wegner's granulomatosis , commonly cause bilateral proptosis .
3. Vascular lesion ;
a. Orbital venous anomalies ; varices , congenital enlargement of one or more of
the venous chanales causing intermittent proptosis (& positional one) .
b. Crotid artery-cavernous sinus fistula ; pulsating proptosis with bruit & thrill ,
diagnosed by angiography & managed by selective intraarterial embolization .
4. Cystic lesions ;
a. Dermoid & epidemoid cysts .
b. Parasitic cyst .
c. Encephalocele ; by herniation of the intracranial contents through a congenital
defect in the base of the skull , so give pulsatile proptosis (communicate with the
CSF) but no bruit .
d. Mucocele ; it is an epithelial lined mucous containing sac completely filling the sinus
& capable of expansion , it is commonly in the frontal & ethmoidal sinuses , expand
slowly or rapidly (if pyocele occur) , caused by combination of obstruction &
inflammation , its developement depend on ;
i. Degree & duration of the obstruction .
ii. Abscence of alternative drainage routes .
iii. Prescence of bone resorption (& expansion possibly indicated by infection) .
Clinical feaures are ;
i. Proptosis in 91% (55% lateral displacement & 50% inferior) .
ii. Diplopia in 95% , minimal chronic condition .
iii. Limited ocular mobility "ophthalmoplegia" .
iv. Mass felt in the upper medial quaderent of the orbit with charcteristic egg
shell cracking sensation due to thin overlying bone .
v. Epiphora due to compression of the nasolacrimal duct .
vi. Visual impairment .
vii. Pyocele causing rapid expansion .
viii. Discharging sinus through the upper eyelid .
ix. Retro-orbital pain & headache .
x. Meningitis & increased ICP .
Diagnosis from ;
i. Plain x-ray shows ; expanded frontal or sphenoid sinus , elevation or erosion
of the sella turcica & suprameatal ridge

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(loss of scaloped margins & translucence , erosion or depression) .

ii. CT scan shows ; expanded sinus with very thin bone , homogenous smooth
walled mass & new bone formation or sclerosis , if the contrast used , ring
enhancement in the prescence of pyocele .
iii. MRI shows ; high signal in T1 , low in T2 & mixed in haemorrhage .
Managemnt by ;
i. Extended modified Lynch-Howarth approach , so extended radical
frontoethmoidectomy .
ii. Endoscopic approach "FESS" .
iii. Combined external & endoscopic approach (to avoid stenting & to preserve
frontonasal recess) .
iv. Osteoplastic flap (for frontal mucocele) .
5. Tumors ;
a. Primary ;
i. Orbital tissue ;
(1) Benign ; osteoma , lymphoma , haemangioma , fibroma & neurofibroma .
(2) Malignant ; adenocarcinoma , lymphosarcoma of the lacrimal gland .
ii. Neural ; optic berve glioma & meningioma .
iii. Eye ball ; retinoblastoma & malignant melanoma .
iv. Vascular ; Capillary & cavernoushaemangioma & lymphangioma .
b. Secondary ;
i. Metastasis from distant sites (lung in male & breast in female) .
ii. Invasion from adjacent structures like angiofibroma , nasopharyngeal Ca. ,
maxillary antrum Ca. & inverted papilloma .
6. Craniostenosis ; like Croazon & Apert syndromes in which there is shallow orbit
lead to prptosis .
7. Trauma ; like haemorrhage , odema & proptosis resulted (usually delayed except in
haemorrhage which is immediate) .
8. Paralysis of extraocular muscles ; as in complete ophthalmoplegia .
9. Systemic diseases ; cellular deposites as in leukaemia & endocrine like graves
orbitopathy .
N.B.: the most common non-traumatic causes of unilateral proptosis in order of frequency
are ; in adults ; Graves disease , infection , psuedotumors , paranasal tumors , in children ;
infection , psuedotumors , dermoid , heamorrhage , rhbdomyosarcoma , lymphoma &
leukaemia .
Aetiology of bilateral proptosis
1. Endocrine exophthalmos ; in both hypothyroidism & hyperthyroidism .
2. Developemental anomalies of the skull & orbit as in oxycephaly .
3. Cavernous sinus thrombosis .
4. Neoplasms like lymphosarcoma & malignant tumors of the nasopharynx affecting the
bony orbit .
5. Xanthomatosis of the orbits as in Hand-Schuller Christian syndrome .
Mangement of proptosis
- History
1. Age & sex & race ; some tumors almost entirely found in children like
neuroblastoma & retinoblastomas .

Lecture notes in
Meningioma are tumors of middle age white female , while nasopharyngeal Ca.
affect Chines male .
2. Past history ; tumor elsewhere in the body (skin , lungs & breast) .
3. Presentation ;
a. Onset & duration ;
- Rapid ; haematoma , odema & injury in AWO , infection &
rhabdomyosarcoma in children .
- Delayed ; benign tumors & low grade malignancy .
b. Pain ; in rapid expansion & in exposure keratitis .
c. Trauma ; bleeing , odema & infection .
d. Intermittent in orbital varices .
e. Bilateral , secondary to hyperthyodism , pseudotumors & cavernous sinus
thrombosis , commonly in adults (Grave's disease) , children (leukaemia or
metastatic hypernephroma) .
f. Drop in vision & diplopia mean maligancy .
g. Other ENT symptoms like ;
- Nose ; blood stained rhinorrhea , nasal obstruction , epistaxis & signs of
sinonasal disease .
- Ear ; otalgia , hearing loss & tinnitus .
- Throat ; difficult swallowing , trismus & hoarsness .
4. Family history , Von-Reckling housen's disease or retinoblastoma of the eyes .
- Examination ;
1. Consistency of the mass , obtained by retropulsion of the eyes , very soft in benign
tumors or difficult to retropulsed in malignant lesion .
2. Lid signs ; ecchymosis in neurolastoma , mass involving the lid means tumor in the
anterior part of the orbit (dermid cyst or lacrimal gland tumor) .
3. Vascular signs ; odema of the lid & conjunctiva , pulsation in carotid –cavernous
fistula , bruit in vascular tumors or anurysm or in graves disease .
4. ENT examination & cranial nerve examination .
5. Opthalmic consultation , manditory ;
a. Visual acuity & field .
b. Colour vision .
c. Mobility of the extraocular muscles .
d. Fundoscopy for fundus & retinal veins .
e. Measurement of the intra-ocular pressure .
f. Measuring the degree of proptosis by
- Clinical observation , looking to the patient from behind to see proptosis .
- Hertel's exophthalmometer , normal up to 16 mm .
- Investigations
1. Labrotary ; CNP , ESR (inflammatory lesions) & TSH (Graves disease) .
2. Radiology ;
- Plain x-ray ; Caldwell-Luc's view (orbital lesion) , Water's view (orbital floor
fracture) .
- CT scan , MRI & tomography .
3. Others ; U/S , angiography , orbital venography , metastatic work up (serology &
radiography) .

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4. Needle aspiration or open biopsy ; FNA obtained under CT guidence using a 23

gauge needle , it is useful in ;
- Orbital metastasis .
- Secondary neoplasm from the adjacent structures
- Treatment (according to the cause)
1. Medical ; steroid , antibiotics & nasal decongestant .
2. Surgery ; for proptosis proper , orbital decompression .
3. Radiotherapy in some cases
Multidiscpilnary approach id sometimes required for conditions involving the adacent
structure .
Orbital decompression
Indicated in ;
1. Thyroid eye diseases ; charcterized by significant global displacement which depend
on pattern of muscle & fat hypertrophy .
CT scan of the thyroid eye diseases show hypertrophy of the muscles & fat (global
displacement) with clssical Coca-cola sign appear on axial section .
Treated by stabilization of the thyroid function , oral steroids &/or radiotherapy , also
do surgical decompression of orbit indicated in optic neuropathy , severe exposure
keratopathy & for cosmetic causes .
2. Psuedotumors of the orbit .
3. Wegner's grnulomatosis infilterating the orbit .
4. Paliation of Metastatic deposits .
5. endoscopic decompression of traumatic compression to the optic nerve by fracture or
foreign body .
Aims ; to relieve the optic neuropathy , severe exposure keratitis & s.t. for cosmotic results
The approaches are ;
1. Dollinger approache , lateral approach , decompression by removal of the lateral
wall of the orbit & allow the orbital contents to herniate into the temporal fossa , this
produce few mm of improvement .
2. Naffziger approach , trans-corneal route (superior approach) , decompression into
the anterior cranial fossa , indicated in extreme cases with visual compromization .
3. Sewell approach , medial approah through the paranasal sinus route , removal of
the medial orbital wall .
4. Hirsch approach , inferior approach , into the maxillary antrum .
5. Ogura , transantral approach , combination of medial & inferior approaches .
6. Harrison , Patterson's external ethmoidectomy approach , provide removal of the
entire medial wall from the level of ethmoid vessels , it may combined with lateral
orbitotomy .
7. Endoscopic approach , it is need middle meatal antrostomy to reach successfully
posteriorly to the sphenoid sinus & it is of great benifit in orbital apex
decompression .
8. Combination of endoscopic & external approaches .
9. Dacryocystorhinostomy , removal of the hard maxillary bone overlying the lacrimal
sac by drill , currate or laser .

Lecture notes in
Olfacation & its doisorders

Embryology of the nasal cavity
The nose develop from number of mesenchymal processes
around the primitive mouth .
The nasal cavity is first recognizable in the 5.6 mm embryo
in the fourth intrauterine week as the olfactory or nasal
placode, a thickenng of the ectoerm above the
stomatodaeum. This placode sinks to fom the olfactory pit
lying between the proliferating mesoderm of the medial and
lateral nasal foldsof the frontonasal process. This deepens
to form the nasal sac by the fifth week.
In the 12.5 mm embryo the maxillary process of the first
branchial arch grows anteriorly and medially to fuse
anteriorly with the medial nasal fold and the frontonasal
process which closes the nasal pits off to form widely
seperated primitive nasal cavities.
The primitive nasal cavity and mouth are seperated initially
by a bucconasal membrane. This gradually thins as the
nasal sac extend posteriorly and eventually breaks down at
the 14-15 mm stage to form the primitive choanae.
The olfactory neuroepithelium is well develop in the human fetus and by 11 weeks' gestation
there is complete differentiation of olfactory cells. The human olfactory system is operative
at birth and neonates respond preferentially to maternal odour.
Vomeronasal Organ :As in other mammals, the human fetus also possesses a well developed
vomeronasal organ with a cellular configuration similar to olfactory epithelium, on each
side of the nasal septum. However the vomeronasal organ in man regresses in late fetal life
and only remnant are found in the adult.
It can be found as small pit on the nasal septum in about 20% of the population and has no
neurological connection with the CNS.
Anatomy
The olfactory neuroepithelium is a pseudostratified columnar epithelium situated on the
cribriform plate and segments of the superior septum and both the superior and middle
turbinates and comprises receptor cells, sustentacular (supporting) cells, basal cells,
microvillar cells, and cells that line the ducts extending from Bowman’s glands (the primary
source of mucus in the olfactory region) .
The bipolar receptor cells, which serve both as the receptor cell and the first-order neuron,
project directly from the nasal cavity into the brain without an intervening synapse, and are
a well-known route of invasion for viruses and other agents into the central nervous system .
Unlike most other neurons, these cells have the propensity to regenerate from basal cells
after being damaged.
The dendritic knob of each receptor cell has a dozen or more cilia of considerable length (
30 Mm), which lack dynein arms, have a 9+2 microtubule arrangement, and have combined
surface area of nearly 9 square inches .
The supporting cells, whose apices contain microvilli, span the distance from the basal
lamina to the epithelial surface .

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These cells appear to (a) mechanically isolate the bipolar receptor cells from one another,
(b) secrete mucopolysaccarides, (c) transport molecules across the neuroepithelium, and (d)
detoxify and degrade odorants . Flask-like microvillar cells, located at the surface of the
mucosa, send tufts of microvilli into the nasal mucus .
Within the lamina propria, the unmyelinated axons of the olfactory receptor cells coalesce
into bundles of about 200 axons surrounded by ensheathing or Schwann cell mesoaxons.
These bundles, after combining with others to form the olfactory fila, traverse the cribriform
plate through 50 or so foramina.
The fila then exit into the anterior cranial fossa and form a dense layer of axons on the
surface of the olfactory bulb. From the olfactory bulb, the receptor cell axons branch and
synapse with second order neurons within the glomeruli of the bulb.
Olfactory Bulb and Projections , The ovoid-shaped olfactory bulbs are located on the
ventral surface of each frontal lobe dorsal to the cribriform plate. Each bulb contains a
number of cell types, including neurons, afferent and efferent nerve fibers, microglia,
astrocytes, and blood vessels, all surrounded by a thin layer of pia-arachnoid cells . The
bulb’s compartments are arranged in six concentric layers: the olfactory nerve layer
(ONL), the glomerular layer (GL), the external plexiform layer (EPL), the mitral cell layer
(MCL), the internal plexiform layer (IPL), and the granule cell layer (GCL). The GCL is the
largest of these layers, constituting about half the volume of the bulb. In humans, the
anterior olfactory nucleus (AON) lies within a segment of the core of the olfactory bulb as
well as within the rostral olfactory peduncle near the anterior perforated substance. This
nucleus, an element of the primary olfactory cortex, contains pyramidal cells whose
dendrites receive synapses from mitral and tufted cells, central brain structures, and the
contralateral AON (via the anterior commissure; AC). The axons of the latter cells project
to ipsilateral bulb neurons (mainly granule and periglomerular cells) as well as to the
contralateral AON, bulb, and rostral olfactory cortex via the AC .
An olfactory bipolar receptor neuron makes its first synapse with the dendrites of the
second-order neurons (mitral and tufted cells) within a glomerulus, a globe-like structure
located within the bulb.
Central Connections , The olfactory tract, which contains both afferent and efferent fibers,
is relatively flat posteriorly and becomes the olfactory trigone just rostral to the anterior
perforated substance. There appears to be no medial olfactory tract in mammals, as
previously believed. All mitral and tufted cell axons leave the olfactory bulb via the lateral
olfactory tract to synapse on structures collectively termed the primary olfactory cortex.
The structures include (a) the anterior olfactory nucleus, (b) the olfactory tubercle, (c) the
prepiriform cortex, (d) the piriform cortex, (e) the periamygdaloid cortex (a region
contiguous with the underlying amygdala), (f) the cortical nucleus of the amygdala, and (g)
the entorhinal area. Reciprocal connections are present between the olfactory cortex and
the orbitofrontal cortex, the dorsomedial and submedial thalamic nuclei, the amygdala, the
lateral hypothalamus, and the hippocampus. A major pathway exists between the olfactory
cortex and the orbitofrontal cortex via the mediodorsal nucleus of the thalamus.
Histology
The olfactory epithelium spreads down from the cribriform plate
onto the upper septum. It is composed of receptor cells, supporting
cells with microvilli and basal stem cells conferring on olfactory
epithelium the capacity for regeneration. Each receptor cell has

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approximately 17 cilia, but these differ from their respiratory counterpart in their radial
arrangement, greater length and poorly developed ultrastructure.
Dynein arms are not present preventing linking between the microtubule and conventional
beating. The sensory endings have a characteristic knob-like vesicular structure from which
olfactory fibres join the axonal bundle.
There is a sharp transition zone between the olfactory and respiratory epithelium.
Secretion for the olfactory epithelium is provided by Bowman's glands
Physiology
 Odours ; are complex mixture of different compounds, each one at a low concentration.
Olfactory compounds must contact the nasal mucosa in order to produce a smell and
have to be soluble in water and lipids. Man is able to discriminate between a large
number of different smells. The olfactory mucosa and pathway is rapidly fatigued but
recovers quickly.
Classification of odours , there is no satisfactory classification of odours, but Amoore
(1969) has suggested that there are as many as 30 primary odours which are recognized
by human , basing his theory on the stereochemistry of compounds and variations of
anosmia to substances which are present in man.
There is no obvious discriminatory mechanism in the nose at the receptor site or in the
olfactory bulb. Some cells in the olfactory bulb increase their discharge rate while
others decrease their discharge rate on stimulation.
 Sniffing ; maximum exposure of the olfactory area to smell is acieved by sniffing which
causes turbulent air flow. During normal tidal breathing, only 5-10% of the nasal
inspired air reaches the region of the olfactory mucosa. Sniffing increases this to 20%.
 Stimulus ; odours are absorbed into the water fraction of the mucus and the lipid react
with lipid bilayer of the receptor cell at specific sites →→ K+ and Cl- flow out→→→
depolarizes the sensory cells. After a latent period of up to 400 ms a slow compound
action potential may be recorded from the olfactory mucosa.
 Receptors ; olfaction appears to be mediated by G-protein coupled receptors in the cells.
These interact with a specific adenyle cyclase (type III) within the neuroepithelium.
 Threshold ; olfactory response exhibits variation in threshold and adaptation.
The threshold of perception is lower than identification i.e. a smell is sensed before it is
recognized. Threshold values vary widely between studies and they reflect the nature of
smell and the different methods of detection.
Some animals particularly dogs have a much lower threshold than man.
Factors affecting threshold ,
o Changes in the nasal mucus and its PH will alter olfactory perception.
o Threshold decreases with age.
o Threshold increases and altered by hormons, particularly sex hormons.
o Genetic variation is present which is similar to colour blindness, there is familial
lack of perception to certain odours which is more common in males.
 Adaptation ; The olfactory response shows marked adaptation, the threshold increases
with exposure and recovery is rapid when the stimulus is withdrown.
Adaptation is both central and peripheral phennmenon. Cross adaptation is present
between odours at high concentration.
 Discrimination ; man appears to be better at detecting the pleasantness of an odour
rather than recognizing it. If two odour are mixed the resulting intensity is always less
Lecture notes in
than the sum of the two individually perceived intensities and is dominated by the
stronger componant.
 Olfactory Transduction ;
o At the first stage of olfactory transduction, odorants, most of which are hydrophobic,
move from the air phase of the nasal cavity into the aqueous phase of the olfactory
mucus.
o They then diffuse or are transported through the mucus by small water-soluble
proteins (termed odorant binding proteins) .
o They then bind to the proteinaceous olfactory receptors located mainly on the cilia,
leading to the production of generator potentials and subsequent action potentials of
the receptor cells.
Theories of smell
It is a general scientific rule that if there is no single theory of function then no one really
knows or has proven the mechanism involved. However there is a number of hypotheses
which have been advanced to explain the nature of smell.
1) Molecular structure , Moncrieff (1967) suggested that molecular structure is
important, however, no stereospecific olfactory receptors have been demonstrated.
2) Electrochemical reaction , Briggs and Duncan (1962), some cells contain carotenoids
similar to the eye and these could give rise to photochemical reactions similar to those
that take place in the eye.
3) Stereospetial patterns , Mozell (1970), certain receptors could have stereospatial,
lock and key form, and receptor cells fire when the surface membrane is altered.
4)Molecular properties , Laffort, Patte and Ecmeto (1974), a modification of the
previous theory would hold that basic molecular properties account for receptor
specificity and include molecular volume at boiling point, proton affinity and donation
and local polarization within the molecule.
5) Olfactory mucosa morphology , Holley and Doving (1977), the pattern of the stimulus
within the mucosal configuration of receptor cells detect the nature of the smell. This
theory of discrimination is based partly on specific receptor sites and partly on their
position within the olfactory mucosa.
6) The wave theory , it is suggested that by analogy with light and sound odorant
substances emit waves which then stimulate the olfactory organ.
Olfaction & behaviour
Smell is used in four main areas of behaviour: the detection and consumption of food,
recognition, territorial markings and sexual behaviour.In human eating and sexual
behaviour are important.
a. Eating , olfaction is related to two aspects of eating, recognition of food types and
initiation of digestion. Initiation of digestion is mediated via the hypothalamus: it
causes salivation and increases the output of gastric acid and enzymes.
b. Sexual behaviour , Pheromones : a term describe chemicals which are produced by
glands and are sexually attractive . The degree of involvement in human behzviour is
uncertain.
Terminology
Olfactory dysfunction can be either bilateral or unilateral (sometimes termed binasal or
uninasal). Loss of olfaction on both sides of the nose is referred to as bilateral anosmia, or,
as noted above total anosmia.

Lecture notes in
- Anosmia refers to loss of the ability to smell .

- Hyposmia , or microsomia , refers to decreased ability to smell .
Total anosmia denotes an inability to smell all odorants on both sides of the nose . Partial
anosmia implies an inability to smell certain odorants.
In some cases, partial anosmia is indicative of decreased sensitivity to a broad spectrum of
odorants (general hyposmia) .
Specific anosmia, the lack of ability to smell one or a few odorants in the presence of an
otherwise normal sense of smell, is rarely a reason for medical consultation .
- Hyperosmia reflects abnormally acute smell function , this condition occurs only rarely
(e.g., in some unmedicated epileptic patients and occasionally during pregnancy) .
- Dysosmia is distorted or perverted smell perception, with parosmia and cacosmia
denoting a change in the quality of an olfactory cue (e.g., a flower smelling rancid), and
phantosmia denoting odor perception in the absence of an olfactory stimulus (e.g.,
olfactory hallucinations).
Olfactory dysfunction
Possible aetiologic categories are
1. Lesions of the nose/airway
a. Structural abnormality : Deviated septum , Weakness of alae nasi , Nasal polyps .
b. Rhinitis : Allergic rhinitis (Seasonal , Perennial) , Vasomotor rhinitis , Atrophic
rhinitis , Hypertrophic rhinitis , Chronic inflammatory rhinitis (Syphilis ,
Tuberculosis , Sarcoidosis , Rhinoscleroma , Leprosy , Wegener’s granulomatosis ,
Midline granuloma) , Rhinitis medicamentosa
c. Adenoid hypertrophy
d. Sjögren’s syndrome
e. Infections and viral : Influenza or acute viral rhinitis , Acute viral hepatitis ,
Bacterial rhinosinusitis , Bronchiectasis , Infected teeth and gums , Infected tonsils .
f. Others : Fungal , Rickettsial , Microfilarial .
2. Nutritional/metabolic
a. Vitamin deficiency : Vitamin A , Vitamin B6 , Vitamin B12.
b. Trace metal deficiencies : Zn , Cu .
c. Protein calorie malnutrition .
d. Total parenteral nutrition (without adequate replacement) .
e. Cystic fibrosis
f. Abetalipoproteinemia
g. Chronic renal failure
h. Cirrhosis of liver
i. Gout
j. Whipple’s disease
3. Neoplasms
a. Intracranial : Osteomas , Olfactory groove and cribiform plate , meningiomas ,
Frontal lobe tumors (esp. gliomas) , Paraoptic chiasma tumors , Pituitary tumors
(esp. adenomas) , Craniopharyngioma , Suprasellar meningioma , Aneurysms ,
Suprasellar cholesteatoma , Temporal lobe tumors , Midline cranial tumors ,
Parasagittal meningiomas , Tumors of the corpus callosum .
b. Intranasal : Neuroolfactory tumors , Esthesioneuroepithelioma ,
Esthesioneuroblastoma , Esthesioneurocytoma , Esthesioepithelioma

Lecture notes in
c. Other benign or malignant nasal tumors ; Conductive effect (e.g., adenocarcinoma)

Perceptive effect (e.g., Schwannoma ; neurofibroma) .
d. Nasopharyngeal tumors with extension .
e. Paranasal tumors with extension .
f. Leukemic infiltration .
g. Carcinomas : Lung , Gastrointestinal tract , Ovary , Breast
4. Neurologic :
a. Amyotrophic lateral sclerosis
b. Familial dysautonomia
c. Refsum’s syndrome
d. Multiple sclerosis
e. Parkinson’s disease
f. Progressive supranuclear palsy
g. Temporal lobe epilepsy
h. Mesial temporal sclerosis(ammons horn sclerosis)
i. Scars/previous infarcts
j. Myesthenia gravis
k. Retinitis pigmentosa
5. Vascular insufficiency and anoxia
a. Small multiple cerebrovascular accidents
b. Transient ischemic attacks
c. Subclavian steal syndrome
6. Endocrine : Adrenal cortical insufficiency–Addison’s disease , Congenital adrenal
hyperplasia , Cushing’s syndrome , Hypothyroidism, Diabetes mellitus , Primary
amenorrheas , Chromalin negative gonadal dysgenesis– , Tumer’s syndrome,
Hypogonadotropic hypogonadism , Kallmann’s syndrome , Hypergonadotropic
hypogonadism , Pseudohypoparathyroidism , Panhypopituitarism , Gigantism ,
Adiposogenital dystrophy–Froelich’s syndrome .
7. Congenital/hereditary :
a. Syndrome of hypogeusia and hyposmia .
b. Triad of :Submucous cleft of dorsal hard palate , Facial hypoplasia , Stunted
growth , “Red haired disease” with pigmentary abnormality .
c. Complete and specific anosmias of genetic origin .
d. Multiple lentigines syndrome
8. Trauma (Most common ) proposed mechanisms:
a. shearing of olfactory nerves .
b. hemorrhage of the basal frontal lobes and bruising of the olfactory bulbs and
tracts) .
c. Frontal fracture (esp. fronto-ethmoidal fracture) .
d. Occipital contrecoup injury.
e. Nasal fracture .
9. Drugs : Adrenal steroids (chronic usage) , Amino acid excess , Histidine , Cysteine ,
Anesthetics ( local Procaine HCl , Cocaine HCl , Tetracaine HCl) , Anticancer agents
(e.g., methotrexate) , Antihistamines (e.g., chlorpheniramine maleate) , Antimicrobials
(Griseofulvin , Lincomycin , Streptomycin , Tetracyclines , Intranasal tyrothricin , Local
neomycin) , Neoarsphenamine , Antirheumatics , Mercury or gold salts , D-

Lecture notes in
Penicillamine , Antithyroids (Methimazole , Propylthiouracil , Thiouracil) ,

Hyperlipoproteinemia medications ( Clofibrate , Cholestyramine) , Intranasal saline
solutions with (Acetylcholine , Acetyl, ß-methylcholine , Menthol ) , Strychnine , Zinc
sulfate , Opiates , Codeine , Hydromophone HCl , Morphine , Psychopharmaceuticals
(e.g., psilocybin, LSD) , Sympathomimetics , Amphetamine sulfate , Phenmetrazine
theoclate , Fenbutrazate HCl , Antipyrine , Oral ETOH , Local vasoconstrictors ,
Cimetidine , L-dopa .
10. Chemical pollutants : gaseous , Sulfuric acid , Hydrogen selenide , Phosphorus
oxychloride , Pepper and cresol mixture , Benzene , Benzol , Butyl acetate , Carbon
disulfide , Ethyl acetate , Ethyl acrylate , Hydrazine , Oil of peppermint , Hydrogen
sulfide , Paint solvents , Chlorine , Benzine , Nitrous gases , Industrial dusts
(particulate) , Coke/coal , Grain , Silicone dioxide , Spices , Flour , Cotton , Paper ,
Cement , Cadmium , Ashes , Lead , Chromium , Nickel , Chalk , Potash , Iron carboxyl .
11. Medical intervention : Laryngectomy , Rhinoplasty , Anterior craniotomy Surgical
interruption of olfactory tract , Frontal lobotomy , Temporal lobotomy , Paranasal sinus
exenterationPostanesthesia , Radiation therapy , Arteriography , Influenza vaccination ,
Maintenance hemodialysis , Thyroidectomy , Hypophysectomy , Adrenalectomy ,
Orchiectomy , Oophorectomy , Gastrectomy
12. Psychiatric : Schizophrenic disorders , Olfactory reference syndrome , Depressive
disorders , Hysteria , Malingering , Presbyosmia .
13. Physiologic processes : Circadian variation , Menses , Pregnancy
14. Others : Cerebral abscess (especially frontal or ethmoidal regions) , Meningitis ,
Syphilis , Syringomyelia , Paget’s disease , Korsakoff’s disease , Hydrocephalus ,
Migraine .
15. Idiopathic
Or other classification are ;
Anosmia and hyposmia
1) Nasal obstruction, due to polypi, enlarged turbinate, severe septal deflection and
septal swelling→→→temporary anosmia.
2) Vasomotor rhinitis→→permanent anosmia.
3) Peripheral neuritis from influenza →→→ usually permanent anosmia.
4) Atrophic rhinitis , degeneration of the nasal mucosa .
5) Trauma, especially base skull fracture involving the anterior cranial fossa.
6) Intracranial lesion, may cause compression of the olfactory tract.
7) exposure to noxious gasses, e.g, bromine.
Cacosmia
1) Maxillary sinusitis, usually of dental origin.
2) Foreign bodies in the nose.
3) The presence of foetid pus in chronic infection of middle ear cleft.
Parosmia
1) Functional
2) Organic
a. of central origin
i-influenzal neuritis
ii- epileptic aura
iii- uncinate fits, in temporal lobe lesion.

Lecture notes in
iv- drugs, streptomycin, arsphenamine.

b. of peripheral origin
i- nasal disease, as above.
ii- drugs, topical application of tyrothricin.
Management
1. Clinical History
- Most patients present with complaints of both smell and taste loss, few (<5%) have
identifiable whole-mouth gustatory deficits .
- Assessment of the patient’s past medical and surgical histories, with an emphasis on
such areas as endocrinologic state, history of radiation therapy, and medications
taken before symptom onset (such as thyroid supplementation or antineoplastic
agents) .
- Delayed puberty in association with anosmia (with or without midline craniofacial
abnormalities, deafness, and renal anomalies) suggests the possibility of Kallmann’s
syndrome .
- Importantly, associated events are critical for establishing an etiologic diagnosis
(e.g., viral or bacterial respiratory tract infections, head trauma, exposure to toxic
fumes, systemic diseases, and signs of early dementia, parkinsonism, or central
tumors) .
- In patients complaining of anosmia or hyposmia, it is useful to ask whether smell
function is diminished or completely absent, whether it is localized to one or the
other nasal chamber (or both), and whether the dysfunction is for all odorants or
only a few . Patients with loss resulting from nasal or paranasal sinus disease are
more likely to indicate a gradual loss of function than those whose loss is
attributable to a prior upper respiratory infection or to head trauma (Some patients
with olfactory dysfunction secondary to nasal or paranasal sinus disease report
temporary recovery of function under circumstances in which nasal patency is
increased) .
- Smoking history should be explored in light of evidence that olfactory ability
decreases as a function of cumulative smoking dose and that cessation of smoking
can result in improvement in olfactory function over time .
- A history of allergy should be sought, as should a history of current or past nasal or
paranasal sinus infection .
- Inquiry should be made about previous nasal or paranasal sinus surgery.
- Importantly, the association of nasal obstruction, headache, facial pain, postnasal
discharge, purulent or clear rhinorrhea, otologic symptoms, and throat symptoms
should be sought with specific questioning.
- The order in which symptoms appeared and regressed is at times helpful.
- The duration of the problem is of importance in relation to the possibility of
spontaneous recovery ( minimal after 6 months if damage to the olfactory epithelium
is implicated) .
2. Physical Examination
- Complete otolaryngologic examination with an emphasis on anterior rhinoscopy and
nasal endoscopy .
- Complete neurologic evaluation is also necessary, emphasizing cranial nerve
function and attention to possible skull base and intracranial lesions.

Lecture notes in
3. Olfactory Testing
Accurate assessment of olfactory function is essential to ;
(a) Establish the validity of a patient’s complaint .
(b) Characterize the specific nature of the problem .
(c) Reliably monitor changes in function over time .
(d) Detect malingering .
(e) Establish compensation for permanent disability.
It should be noted that many patients who complain of anosmia or hyposmia actually
have normal function relative to their age and gender. Others may be unaware of their
deficits (about 90% of patients with idiopathic Parkinson’s disease have a demonstrable
smell loss, and yet fewer than 15% are aware of their problem until tested objectively) .
Olfactory evaluation often has both medical and legal consequences .
Traditionally examine the ability to smell by asking a patient to sniff a few odorous items
(e.g., coffee, cinnamon, or tobacco in small vials) and to report whether an odor is
perceived . Asking the patient to identify the odor does not correct the situation, because
even normal subjects have difficulty identifying some odors without cueing .
Although most olfactory problems are bilateral, and bilateral testing reflects the better
functioning side of the nose, in some instances unilateral testing is warranted. To assess
accurately olfaction unilaterally, the naris contralateral to the tested side should be
occluded to prevent or minimize crossing of inhaled or exhaled air at the rear of the
nasopharynx to the opposite side (so-called retronasal stimulation) . An easy way to do
this is to seal the contralateral naris using a piece of Microfoam tape (3M Corporation,
Minneapolis, MN) cut to fit the naris borders . The patient is instructed to sniff the
stimulus normally and to exhale through the mouth.
4. Olfactory biopsies
In rare instances, biopsies of the olfactory neuroepithelium can be obtained to assess
damage to this region of the olfactory system . In this procedure, a small amount of
olfactory neuroepithelial tissue is removed from the superior nasal septum by the
rhinologist and analyzed histologically . This procedure must be performed by a surgeon
who is experienced in the technique, and multiple biopsies usually are needed to obtain
true neuroepithelium, given the considerable age-related metaplasia of respiratory-like
epithelium within the region of the olfactory neuroepithelium .
5. Psychophysical Tests
Despite the fact that a wide range of psychophysical olfactory tests are available for
accurately assessing olfactory function, most have unknown reliability and validity , are
cumbersome, and suffer for lack normative data. Fortunately, six reasonably practical
clinical psychophysical tests of known reliability are now commercially available ;
- The most widely used of these tests is the University of Pennsylvania Smell
Identification Test (UPSIT), also known as the Smell Identification Test , which can
be self-administered in 10 to 15 minutes by most patients in the waiting room and
scored in less than a minute by nonmedical personnel, consists of four booklets
containing ten odorants apiece .
The stimuli are embedded in 10- to 50-Mm-diameter microencapsulated crystals
located on “scratch and sniff” strips on the bottom of the pages of the test booklets .
Above each strip is a multiple choice question with four response alternatives .

Lecture notes in
The patient is required to choose an answer, even if none seems appropriate or no

odor is perceived (i.e., the test is forced choice) .
This encourages the patient to sample all the stimuli carefully and provides a means
for detecting malingering; because chance performance is 10 out of 40, low scores
reflect avoidance, and hence recognition, of the correct answer .
- Three-item forced-choice microencapsulated Pocket Smell Test (which is only a brief
screen) .
- 12-item Cross-Cultural Smell Identification Test (CC-SIT) .
- The five-odorant Takagi & Toyota (T&T) olfactometer threshold test .
- A squeeze bottle odor threshold test kit .
- Recently developed “Sniff ‘n Sticks” test, which incorporates inexpensive felt-tip
pen-like odor-dispensing devices .
6. Electrophysiological Tests
Several electrophysiological procedures are available for assessing olfactory function .
Of these procedures, only one, chemosensory event-related potentials (CSERPs) , has
been used in the clinical setting .
- Chemosensory Event-Related Potentials “CSERPs” are derived from the EEG after
intranasal chemical stimulation .
They consist of synchronized central nervous system (CNS) activity recorded from
the surface of the scalp following brief presentations of odorants .
To obtain accurate potentials, stimuli are presented in a precise manner (e.g., with
rise times <20 ms) using equipment that produces stimuli embedded within a warmed
and humidified airstream .
Odor-evoked responses are useful in detecting malingering and are sensitive to
alterations in olfactory function due to nasal polyposis, temporal lobe epilepsy,
parkinsonism, and multiple sclerosis .
Furthermore, in anosmic patients CSERPs can be used to distinguish differences in
electrophysiological responses to olfactory versus trigeminal stimulants . To test the
integrity of the olfactory afferents, evoked potentials have been elicited by electrical
stimulation of the nasal mucosa alone .
- The Electro-Olfactogram ; assessment of peripheral olfactory function is possible
with the EOG , which is believed to represent summated generator potentials of
olfactory receptor neurons , and presumably reflects the degree of damage to such
cells; however, the recording of EOGs is more difficult than the recording of
CSERPs .
- Neurophysiological testing ; Given the close association between olfactory loss and
several forms of dementia, including Alzheimer’s disease and multiinfarct dementia,
brief neuropsychological testing is warranted in some cases to determine the
presence of dementia . The Mini-Mental State Examination is a widely used brief
screening instrument for dementia and can be administered in the otolaryngologist’s
office in a few minutes to determine whether further referral is necessary . More
extensive dementia assessment is time consuming and best left in the hands of the
neuropsychologist .
7. Neuroimaging
- Computed tomography (CT) has proven invaluable in identifying soft-tissue disease
and bony changes within the sinonasal cavities .

Lecture notes in
Olfactory dysfunction of idiopathic etiology warrants CT imaging of the nasal cavity,

paranasal sinuses, anterior skull base, and if central causes of olfactory dysfunction
are suspected, the brain as well .
Coronal scans are particularly valuable for assessment of the paranasal anatomy, and
may help identify such entities as limited polypoid disease in the olfactory cleft .
Contrast enhancement is useful to identify vascular lesions, neoplasms, abscesses, and
meningeal or parameningeal processes . Currently, high-resolution CT appears to be
the most useful and cost-effective screening tool to assess sinonasal tract inflammatory
disorders.
- Magnetic resonance imaging (MRI) is the technique of choice to evaluate the olfactory
bulbs, olfactory tracts, and intracranial causes of olfactory dysfunction .
8. Patient management
- Conductive Olfactory Loss
Treatment to relieve the edema or physical obstruction can be undertaken , examples
of treatments that have restored olfactory function include allergy management,
topical and systemic corticosteroid therapies, antibiotic therapy, and various surgical
interventions, including functional endoscopic sinus surgery .
- Sensorineural Olfactory Loss
For sensorineural loss related to presbyosmia, no current treatment regimen has been
developed as yet to reestablish complete olfactory function.
For patients with dysosmia, a careful review and systematic cessation of drugs
potentially associated with the dysfunction may be fruitful in some instances, although
this process can take months, depending on the mode of action of the drugs involved
and the number of medications being taken by the patient .
Treatment of patients with anosmia due to sensorineural problems is challenging.
Although there are a few advocates of zinc and vitamin therapies , sound empirical
evidence of their efficacy is lacking. In cases where olfactory loss has been present for
a long time and can be attributed to neural damage within the olfactory
neuroepithelium, prognosis is poor and no treatment is possible.
Nevertheless, simply providing such patients with accurate information about their
disorder, establishing objectively the degree and nature of the deficit, and ruling out
the possibility of a serious disorder as the cause of their problem can be very
therapeutic.
Malingering
Malingering sometimes occurs in patients seeking insurance settlements or other restitution
for negligence claims.
On forced-choice psychophysical tests, such as the UPSIT, malingering appears as the
reporting of fewer incorrect responses than expected on the basis of chance. The theoretical
probability of a true anosmic having an UPSIT score of 5 or lower is below 0.05.
The theoretical probability of a true anosmic scoring 0 on the UPSIT is less than 0.00001.
Evidence for a general tendency to malinger also can be obtained using neuropsychological
tests specifically designed for this purpose .

Lecture notes in
Oro-antral fistula
Problems following dental extraction are ;
1. Post extraction bleeding .
2. Dry socket (alveolar ostetitis) .
3. Oro-antral fistula .
Fistula are abnormal communication between two epithelia surfaces , so oro-antral fistula
is a communication between the oral cavity & the maxillary antrum .
Incidence probably higher than recognized cases because many fistulae escape the
diagnosis following dental extraction & heal spontaneously without complications .
Its aetiology are ;
(1) Dental extraction , fistula formed through ;
a. Tooth socket following extraction particularly of 1st upper molar & 2nd upper
premolar , the root of which may penetrate the antral floor
b. Fistula also follow search for the retained root after been broken .
(2) Surgery (Caldwell-Luc's operation or sublabial radical antrostomy) when sublabial
incision fails to heal (this is called sublabial fistula) .
(3) Trauma , fracture maxilla , penetrating wound such as gunshot & injury to the hard
palate (extent of damage proportional to the size & velocity of missile) .
(4) Neoplasm , especially lower lateral malignant tumor of the maxillary antrum , the
malignant disease may occasionally cause erosion into the oral cavity .
Clinical features
(1) Symptoms of maxillary sinusitis (chronic) .
(2) Purulent discharge may collect in the nose or mouth of foul smelling or taste is often
noticed .
(3) Patient with previous inferior antrostomies may notice air of fluid & food particle
can be sucked through the fistula into the nose .
(4) Diagnosis can be established by passing a probe through the fistula into the antrum ,
but it is dangerous because it may induce fistula by tearing intact palate mucosa
retained through the tooth socket .
Investigations
(1) Radiological examination of sinus by plain x-ray & orthopantogram (plain x-ray to
all upper & lower teeth) .
Radiology shows ; retained root fragment (foreign body) with signs of erosion if
neoplastic disease & infection in case of sinusitis .
(2) CT scan will improve delineation , especially in neoplastic disease .
(3) Injection of contrast media into the defect help in confirming the presence of fistula
in doubtful cases .
(4) Endoscopy (sinus endoscope) .
Treatment
Two important features determine the treatment ;
a. Length of the time of fistula has been present .
b. Presence or absence of infection .
The treatment are ;
(1) Treatment for those fistulae following dental extraction by immediate suturing at the
time of extraction .
(2) If there is retained root must be removed or the treatment will be unsuccessful .

Lecture notes in
(3) When the fistula is discovered later , there will be always granulation tissue in the
tract & possibility of antral infection which should be treated 1st & the pus sent for
C/S & generous inferior meatal antrostomy done under antibiotics cover in order to
correct the sinus condition & allow drainage of pus & secretions .
(4) Patient should be reviewed 4 weeks later .
(5) If the fistula is not healed , it will need formal surgical closure by flap which are of 3
types ;
a. Buccal advancement flap ; wide based flap based on buccal sulcus , a
transverse releasing incision of flap periosteum will allow advancement of the
flap over the socket to be sutured without tension to the palatal mucosa .
If necessary a small amount of socket removed to facilitate this maneuver .
b. Palatal flap ; has the advantage that it does not interfere with the depth of
buccal sulcus . It involve ; raising a finger shaped flap of palatal mucosa based
on anterior palatine artery , then transposed over the oro-antral communication
& sutured to the mucoperiosteum & leave a small area of exposed bone in the
palate which is left to granulate .
c. Buccal fat-pad flap ; a new technique , through which the buccal fat pad
mobilized through a gingival flap & again based on buccal sulcus . The fat pad
is brought into the mouth & sutured across the open socket .
Within few weeks the mucosa has seeded into the flap & give an excellent
healing results .
(6) The formal surgical closure
 Any foreign body must be removed & the bony edges of the alveolus reduced .
 The fistula tract is incised circumferentially around the margins of the fistula &
turned inwards .
 If the adjacent tooth cause a problem , should be removed & the patient should be
give a consent for this .
 If there is evidence of chronic sinusitis an antrostomy done . If not present ,
should be fashioned at the same time of fistula closure .
(7) Follow up & after care ;
a. 1 st postoperative week give nasal decongestant with broad spectrum antibiotics
(choice revised according to the results of C/S) .
b. Patient should be reviewed monthly in the outpatient department until healing is
complete .

Lecture notes in
Tumors of the nose and sinuses

It accounts for 0.2 -0.8% of all carcinoma & only 3% of those in the upper aerodigestive
tract .
The Risk factors are ;
1. Wood dust , hard for adenocarcinoma , while the soft for sequamous cell Ca. (SCC) .
2. Nickle & Chromium worker .
3. Boot & shoe & textile worker .
4. Isopropyl oil & volatile hydrocarbones .
5. Snuff .
6. Human papioma virus (HPV) .
7. Smoking .
8. Recurrent sepsis .
The male : female ratio is 2:1 , the mean age is 55 years , in the UK & USA the incidence
about 10:1000000 population , in Japan 20:1000000 , 44% of which attributed to
occupational exposure , the site of origion is from ; lateral nasal wall in 45% , maxillary
sinus in 30% .
Benign tumors
1. Everted papiloma ; arise from the septum , usually single or occasionally diffuse in the
vestibular region , the stratified sequamous epithilium range from basal cells to
keratinized form .
2. Osteoma ; slowly growing tumor , containing mature bone , most frequently on the
mandible & then frontoethmoidal region .
In the frontal sinus it is either silent when it is away from the osteum or block the sinus
drainage causing mucocele which require removal of the osteoma with an osteoplastic
flap or external frontoethmoidectomy or it fill the entire frontal sinus , extend into the
ethmoid .
In the ethmoid sinus , proptosis & invade the orbit & when extend posteriorly go to the
sphenoid bone & close to the optic nerve , managed by full frontoethmoidectomy , if very
large need craniofacial approach .
Gardener's syndrome , autosomal dominant inheritence charcterized by the presence of
osteoma with other soft tissue tumors & intestinal polyposis .
3. Chondroma ; develope anywhere , they are potentially malignant espicially if
metastasized , management by extensive resection (because it is aggressive & tend to
reccure) .
4. Fibrous dysplasia ; usually female & usually diagnosed in infancy or childhood & the
growth cease after puberty , charcterized by painless , slowly growing swelling of the
maxilla leading to deformity , ossifying fibroma is variant of it , female = male at the 3rd -
4 th decade .
5. Hamangioma ; usually on the nasal septum causing epistaxis , it is cavernous one with
increased recurrence rate when removed inadequately , the patient usually female at 20-
50 years age & always benign , the x-ray shows soap bubble appearance (gaint cell
tumor of the jaw) with sun rays appearance & smaller lacunae .
6. Leiomyoma ; rare causing nasal obstruction & not reccure when removed .
7. Schwannoma ; 4% , 12-80 years , all show +ve S-100 protien staining , usually lack a
capsule , so diagnosed as malignant by pathologist .

Lecture notes in
Intermediate tumors
1. Inverted papilloma (transitional cell tumor) ; up to 4% of all nasal neoplasms ,
4:1000000 , very rare in black , M:F 3-10:1 , usually in the 6 th decade , 60% symptoms
less than 1 year & 20% syptoms >5 years , 25% misdiagnosed at the intial consultation.
The papilloma is present as firm , bulky , red & vascular mass usually on one side of the
nose , histologically show patterns of invasion or papilliferous outgrowth & covered
with sequamous or transitional epithelium with intact basement memberane &
microcyste suggesting low grade SCC .
The incidence of metchronous malignancy is only 1% but the synchronous malignancy
up to 15% .
2. Cylindric cell papilloma ; arise in the antrum & lateral nasal wall , appear by nacked
eye as finely granular surface , microscopically it is columnar epithelium (like inverted
one in malignant predilaction) .
3. Haemorrhagic pericytoma ; it is found whenever there is capillaries , histologically
there is perivascular hyalinization , cellular processes arise from the pericyte alongside
the long axis & grip the vessel like fingers .
Usually , it is rare of low grade malignant potential , painless , grey to tan coloured
polypoidal spongy haemorrhagic mass , present with epistaxis , nasal obstruction ,
facial swelling & proptosis , the mean age about 55 years & F:M 1:1 , occasionally
cause parneoplastic syndrome , the recurrence rate is 18% , metastasis 2.5% , death 3%
4. Extracranial meningioma ; arise from ectopic arachenoid tissue & can spread to the
frontal sinus , they are locally recurrent & difficult to managed surgically , radiation is
useful .
5. Oncocytoma ; oncocytic adenoma of minor salivary glands , rare , in the nasal cavity ,
have abundant acidophilic granular cytoplasm & many mintochondria .
Malignant tumors
1. Basal cell Ca. (BCC) ; nose is the most common site for BCC in the head & neck , it is
30 times more common than SCC , equalt F:M , usually in the 6 th -8th decades .
It is either circumscribed or infilterative , the clinical appearance vary from small
nodular growth to chronic ulcers or ulceronodular lesion , the border of the ulcer rolled
of flat , recurrence 4/10 with possible gross destruction of the face .
2. Sequamous cell Ca. (SCC) ; lateral wall or antrum or ethmoid sinuses is the site of
origin , 50% in the antrum , usually male & show bony destruction , usually affect
elderly male , usually localize (6% node +ve) , management by excision & radiotherapy.
Carcinoma of the collumela usually aggressive form , high recurrence rate & slow bony
destruction .
The direct spread of the antroethmoidal tumors into ;
- antrum to the ; nasal cavity , ethmoid , orbit via the inferior orbital fissure , soft
tissue of the check by anterior antral wall erosion , buccal sulcus , infratemporal
fossa & palatal or alveolar ridge through the dental foramina .
- ethmoid to the ; antrum , orbit , nose , sphenoid by direct extension & anterior
cranial fossa through the fovea or cribriformplate .
Dissemination of the antroethmoidal tumors ; 5% have LAP at presentation (if the
tehmoid tumor had +ve LAP at presentation then it is incureable , while that of the floor
of the antrum had small chance of cure) , 1/3rd of patients dies from metastasis espicially

Lecture notes in
abdominal viscera , lungs & bones , and 1/5th of the patients have second primary
usually in the bronchus .
The T(tumor) classification & staging of the paranasal sinuses are ;
Maxillary sinus
T1 : tumor limited to the antral mucosa with no bony erosion or destruction .
T2 : tumor causing bone erosion or destruction , except for the posterior wall , including
extension into the hard palate & /or middle nasal meatus .
T3 : tumor invades any of the followings ; bone of the posterior wall of the antrum ,
subcutaneous tissue , skin of the check , floor of the medial wall of the orbit .
T4 : tumor invades the orbital contents byeond the floor of the medial wall including the
apex &/or any of the following ; cribriform plate , base of the skull , nasopharynx ,
sphenoid & ethmoid sinuses .
Ethmoid sinus
T1 : tumor limited to the ethmoid with or without bony erosion .
T2 : tumor extend to the nasal cavity .
T3 : tumor extend into the anterior orbit &/or antrum .
T4 : tumor with intracranial extension , orbital extension , including the apex , sphenoid
&/or frontal sinuses , &/or skin of the nose .
Stage grouping
Stage 0 : Tis No Mo
Stage I : T1 No Mo
Stage II : T2 No Mo
Stage III : T1 N1 Mo
T2 N1 Mo
T3 No-1 Mo
Stage IV A : T4 No-1 Mo
Any T N2 Mo
Stage IV B : any T N3 Mo
Stage IV C : any T any N M1
3. Tumors of minor salivary glands ;
a. Adenocystic Ca. ;solid areas of the maligant cells , vascular invasion , distant
metastasis frequent & death more likely , also has perineural invasion espicially V2 ,
infraorbital nerve & the greater palatine nerve , also can spread intracranially
through the olfactory nerve & to the pterygoid space through the posterior dental n.
b. Mucoepidermoid carcinoma .
4. Sarcoma ;
a. Osteogenic sarcoma ; enlarging firm mass , 10-20% with 5 years survival rate .
b. Chondrosarcoma , rare , septal lesion , ringform calcification (in CT) .
c. Rhbdomyosarcoma ; soft tissue tumor .
d. Malignant fibrous histiocytome ; occur in areas of previous boe disorders like
Paget's disease & fibrous dysplasia .
5. Adenocarcinoma ; rare except in people working in the hardwood industry & isopropyle
alchol & chrome inhalation , classify into high & low grade .
The high grade is of bad prognosis (80% die) , more in male with pain 7 deformity ,
while low grade , 90% cureable , at the 6th decade causing nasal obstruction .

Lecture notes in
6. Malignant melanoma ; 1% , not related to Clarck's skin classification , histologically ,

orginate commonly from septum & lateral nasal wall , with slight male preponderance ,
the peak age 5th-8 th decades espicially in Japanese "orientals" , 50% with 3 years
survival , but 0% with 10 years survival .
It present as grey , blue or black polypoidal swelling , only 5% secondary from
cutaneous lesion , regional satelites frequent , <40% have LN in the neck .
Management by (85% relapses) ;
a. discrete lesions ; need wide local excision via lateral rhinotomy .
b. late presentation ; need radical surgery (partial or total maxillectomy & orbital
exnteration) .
c. elderly ; via simple debulking through lateral rhinotomy .
d. elective radiation for primary &/or neck disease , improve the local control not
the survival .
e. combination of chemotherapy & immunotherapy for mucosal melanoma .
f. palliative radiotherapy induced by hyperthermia to inhance the tumor response to
radiation , for those unwish surgery .
7. Esthesineurobastoma ; rare , presented with mass causing nasal obstruction , all ages
are affected (20-50 y) , usually undetectable vanillymandilic acid , two peaks ;
- 20 years peak , less local recurrence & more metastasis .
- 50 years peak , more local recurrence & less metastasis .
It is slowly growing tumor , may become very large & destructive , the clinical staging ;
Group A : tumor confind to the nasal cavity .
Group B : extend to the nasal cavity & one or more paranasal sinuses .
Group C : tumor extend byeond the above limits .
8. Extramedulary plasmocytoma ; usually solitary , well differentiated B-lymphocyte , it
replace rather than invade tissue , only 20% progress to generalized multiple
myelomatosis .
9. Malignant neurogenous tumor ; rare involve the nose like paragangilioma &
schwannoma .
10. Non-Hodgkin's lymphoma ; very rare , espicially in Asia , two types ;
- B-cell lymphoma ; predominant in the paranasal sinuses & in Waldeyer's ring ,
espicially the antrum & ethmoid , with good prognosis .
- T-cell lymphoma ; male at the age of 50 years , worse prognosis , usually
associated with EBV , adverse prognostic factors are , Asian . more than 60 years
& advance stage .
Clinical features
Antral tumors cause nasal obstruction , epistaxis , infraorbital anaesthesia , tooth ache ,
facial swelling & pain & trismus .
Ethmoidal tumors cause nasal obstruction , epistaxis , proptosis or diplopia
Examination , look for ; fullness , numbness of the check , proptosis , ptosis (Horner's
syndrome) & ophthalmoplegia , evidence of tumor in the nose , mouth or nasopharynx ,
loose teeth or illfitting dentures , persistant oroantral fistula , numbness of the hard palate ,
trismus , LAP , evidence of IX & X paralysis in the laryngopharynx , palpable disease in the
hard palate , buccal sulcus or anterior antrum .

Lecture notes in
Investigations
1. Radiology ;
a. CT scan ; bone destruction , cribriform plate , fovea , posterior wall of the antrum ,
optic foramina , medial orbital wall & sphenoid sinus (in coronal & axial sections) .
b. MRI ; has advantages over CT in being ; more soft tissue resolution for extensions
in the deep face , orbit & intracranial , to distinguish tumor from sinusitis (T1, 2 &
contrast ) , weighted image of sinusitis , isointense image , while T1 enhanced & T2
give high intensity image , & inverted papilloma give isotense image on T1 with
contrast but with T2 tumors are isotense .
2. Labrotory ;
a. CBP & biochemistry .
b. Plasma protien electroporesis & urine for Bence-Jones protien if myeloma is
suspected .
c. B2 – transferrin estimation (in watery nasal discharge) from CSF .
3. Biopsy ; FNA for LN & biopsy taken endoscopically .
Management policy
A. Benign Tumors
1. Osteoma ; frontal , osteoplastic flap or frontoethmoidectomy , while ethmoidal
tumors by lateral rhinotomy or craniofacial approach if close to the optic foramina .
2. Chondroma ; wide local excision , because it is aggressive disease with reccurence .
3. Ossifying fibromas ; easily sheld out .
4. Fibro-osseus dysplasia ; drilling away the excess tissue .
B. Intermediate tumors
1. Transitional cell papilloma ; best Rx by lateral rhinotomy after the intial diagnostic
polypectomy , because of the high recurrence rate of other procedures , 80%, ^0% &
30& for intranasal removal , Caldwell-Luc's & medial maxillectomy , also
endoscopic medial maxillectomy can used ( no scar , shorter hospitalization , lower
nmorbidity & less blood loss) .
2. Meningioma & haemingiopericytoma ; wide excision .
C. Malignant tumors
Need team managemnt , surgery alone or with radiotherapy is the management of choice .
The chemotherapy given either ;
a. as part of the triple therapy like in rhabdomyosarcoma .
b. in combination with radiotherapy like in lymphoma .
c. or for palliation like in poorly differentiate SCC with disseminated disease .
Topical chemotherapy (5-FU) with repeated surgical debulking for SCC & adenocarcinoma
Endoscopic resection have a palliative role .
The causes of incurability ;
a. involvement of the nasopharynx & wide spread intracranial & pterygoid involvement
b. poor surgical risk .
c. distant metastasis .
d. refusal to undergo surgery .
3/10 patients loss thier eyes ( cure compromize by blindness) .
1. Lymphomas ; radiotherapy & chemotherapy .
2. SCC ; partial maxillectomy (leave the orbit) , if involve the ethmoid do craniofacial
resection .

Lecture notes in
3. Adenocarcinoma ; craniofacial resction with orbit excutiration (as it always involve

the ethmoid) .
4. Malignant melanoma ; if lie discretely on the turbinates , wide local resection & wait
& see policy , if present as a polyp , then lateral rhinotomy (if neck LAP , so add
RND) .
5. Esthesioneuroblastoma ; surgery with adjuvant radiotherapy .
The adjuvant radiotherapy ;
a. every patient has maxillectomy should has postop. radiotherapy .
b. chemotherapy for melanoma (5-FU) & mainly used for the lymphomas , study in
Japan , debulking of the tumor with postop radiotherapy & the cavity is then packed
with 5-FU on a weekly bases , debridment & packing for several weeks .
Radiotherapy technique ; usually the radiotherapy is postoperatively , it is either by
hyperfraction or intracavitary , include the primary site which are usually the maxilla on
the affected site with the alveolus , the whole nasal cavity & the ethmoid complex , the
pterygopalatine fossa & the orbit with epsilateral neck (if there is LN disease) & we should
spare the contralateral eye , brainstem & the upper cervical cord .
Dose about 50-55 Gy in 20 fractions over 4 weeks using megavoltage x-ray (4-6 MV) or 60-
65 Gy in 30-33 fractions over 6-6.5 weeks , for lymphoma , 40 Gy in 20 fractions in 4 weeks
D. Vestibular and septal tumors
30% of anterior nasal tumors invade the cartilage & neck , so in the management need
RND (even N0 need elective ND) , in high rsik group , the over all survival rate is 20-30% .
The management is by surgical excision including the upper lip (total thinectomy with
upper 2/3 rd upper lip excision) , so need reconstruction by forehead flap (for only soft tissue
replacement) , while sometimes need dental prosthesis & osteointegrated nasal
replacenment with bilateral perrialar cresentic advancement .
E. Sinus tumors in children
Usually benign , rhabdomyosarcoma is the commonest malignant tumor , managed with
biopsy to confirm the diagnosis & then surgery .
Contravesies in management
1. Is transitional cell papilloma a premalignant condition ?
If the lesion doesn't show any focus of malignancy at biopsy , so there is 1% only chance
for carcinoma developement .
2. What if the pathologist reports as undifferentiated Ca. ?
Should ensure that the pathologist use a tumor markers to determine whether the
epidermis is the site of the origion , treatable tumor (those appearantly untreatable) .
3. CT shows wide spread infilteration of the tumor ?
Odema indistiguishable from the tumor extension (30%) need MRI .
4. Is it ever worthwile rehabilitating the orbit with skin flap ?
Very little place for flap to make a prosthesis site correctly .
5. Preoperative or poatoperative radiotherapy ?
Preoperative radiotherapy used when there is doubt about resectibility of the tumor ,
while surgery for those operable disease & radical radiotherapy fro patient refuse or
unfit to major surgery .
The advantages of preopearative radiotherapy are ; shrinks the tumor (convert it to
operable one) , decrease the chance of distal metastasis & avoid management delay .

Lecture notes in
The disadvantages of preoperative radiotherapy are ; increase the complications of

surgery , directly or indirectly through malnutrition , less well defined tumor extent ,
impaired wound healing & those with initial response may refuse the surgery .
Surgical procedures
1. Total rhinectomy
- Indications ; SCC of the skin of the external nose including the vestibula &
collumela .
- The excision ; remove the nose with wide margin if possible leave some or all
nasal bones to facillitate the placement of the osseointegrated implants at the
pyriform apearture , s.t. the septum removed .
2. Lateral rhinotomy/medial maxillectomy
- Anaesthesia ; oroendotracheal tube with head up position (15o ) , cover th eyes ,
the wound area infilterated with 1% lidocaine with 1:200000 adrenaline .
- Incision ; Moure's incision ; it may extend to divide the lip or superior onto the
glabellar region (craniofacial resection) .
- Performance of the medial maxillectomy ; enblock resection of the lateral wall
including the bone at the lateral & superolateral aspect of the pyriform
appearture & the medial 30% of the orbital floor & orbital rim with lamina
papyracea & the lacrimal sac .
- Elevation & rotation of the nasal bones , medial & lateral rhinoplasty
osteotomiesnperformed .
- Creation of a defect into the anterior maxilla , perforating the anterior wall of the
antrum & enlarge it by Hajek's forceps .
- Removal of the speciemen using a 9 mm osteotome , access anterior osteotome ,
also superior & inferior resection osteotomies .
- Mobilization of the speciement done .
- Opening & suturing of the lacrimal sac with canulation of the inferior lacrimal
punctum .
- Nasal pack with BIPP , the incision closed with 3/0 cat gut & 5/0 nylon , POP or
splint aid cosmetic recovery .
- Complications of the lateral rhinotomy ;
a. early ; haemorrhage , blepharitis , lid odema , meningitis , wound infection &
CSF leak .
b. Late ; crusting (Rx: removed with Na-bicarbonate douch) , eoiphora ,
diplopia , telecanthus , facial paraesthesia , frontonasal recess obstruction
with secondary mucocele , cosmetic (alar lift , vestibular stenosis & webbing).
Alternative to Lateral rhinotomy :
3. Midfacial degloving approach
- the buccogingival sulcus & nasal vestibules infilterated with xylocaine &
adrenaline .
- the incison done in the gingivolabial sulcus striaght down to bone linking the 2
maxillary tuberosities & the soft tissue elevated over the nasal spine from below
& bilaterally intrecartilagenous incison with full septal transfixation incsion .
- Complications of the midfacial degloving ; facial bruising , malar paraesthesia ,
vestibular stenosis , crusting of the cavity , thickening of the glabella , telecanthus
, hetrotopia , nasal deformity (over-removal of the frontal process of maxilla)

Lecture notes in
4. Maxillextomy
- Preparation ; eyebrow not ahaved (because it regrow in irregular fashion) ,
supine position with head extended , temporary tarsorraphy by 5/0 silk & also
tracheostomy is performed .
- Incision ; (1) Weber-Fergusson incision (2) Midfacial degloving (3) Fergusson
incision .
- Excision ;
a. the upper central incisor on the side of operation removed ,.
b. by Gigli saw , the hard palate is divided through the floor of the nasal cavity
c. with the stryker saw or fissure burr , the nasal process of the maxilla is
divided .
d. Stout Mayo scissors , division between the superior & inferior turbinates &
mobilization of the lateral nasal wall .
e. Division of the temporalis muscle .
f. Division & removal of the maxilla by osteotomes .
g. Packing of the cavity by BIPP & suture (stay suture if no dentures) .
- After care ;
a. general care .
b. Pack removed after 10-14 days .
c. Temporary denture made .
d. Final prosthesis , one or two piceses .
- Complications ; general complications , notching of the lip (need z plasty) ,
granuloma formation if the obturator is too large , do biopsy for recurrence , if
grnuloma then need to adjust the obturator .
5. Craniofacial resection
- Done by ENTist & neurosurgeon .
- Anaesthesia , 200 ml of 20% mannitol within 20 minutes & 150 mg of H.C. with
hyperventilation , this will cause brain shrinkage to ease the manipulation .
- Incision ; bicoronal incision (lateral rhinotomy incision with midline forehead
incision) , may be combined with midfacial degloving 0r Weber-Fergusson
incision .
- Craniotomy ;
a. Shield shaped segment is removed from the frontal bone , care not cut or tear
the dura , the frontal lobe retracted .
b. Or ; across the brow level & through the frontal sinus .
- Further surgery is contraindicated if there is tumor extension ; (1) into the frontal
lobe (2) beyond the posterior margins of the cribriform plate (3) to involve both
optic nerves (4) laterally outside the boundaries of the fovea .
- The maxilla removed , possiblity to retain the palate & even the orbital floor .
- Occular preservation , successfully applied even in bony involvement , the eye
included in the resevtion if obvious extension through the periosteum seen , if not
wait a frozen section from the area of the optic foramina .
- After care ;
a. general care .
b. supine bed rest .
c. antibiotics (flagyl 10 days + augmentine for 3 weeks) .

Lecture notes in
d. neurological observation .
e. anticonvalsant used for 1 year postoperatively .
f. managing any CSF leak .
- Complications ;
a. sudden death (if the patient mobilized prematurely) .
b. persistant CSF leak .
c. meningitis .
d. venous bleeding .
e. convulsion .

Lecture notes in
Facial pain and Headache

The patient with facial pain present a diagnostic challange because the frequency of the
reffered pain & overlap in symptoms between the diseases , the patient may consult ENTist ,
neurologist , ophthalmologist , G.P. or maxillofacial surgeon to resolve his problem .
It is essential to take a structural history , as history is often the only source of informations
on the nature of the pain & the patient discription & affect are vital clues in the diagnosis .
It has a special emotional significance , it may remain constant for many months or years or
which extends either across the midline or dermatome , less likely to have a physical bases ,
while that associated with clear exacerbating or a relieving factors & onset clearcut & site
not vary (organic cause) .
The pain stimuli of the face mainly transmitted by 5th cranila to the spinal tracts in the
brainstem , also by 7th , 9th, 10th & 11th cranials , the majority of these fibers are
unmyelinated , so producing a poorly localized dull ache .
In general we have 12 questions to reduce the D.Diagnosis ;
1. Where the pain & does it radiate anywhere ? the patient point to the site of pain by
finger.
2. It is deep or superficial ? skin , not deep , causing sharp , well defined , while the
deep pain is dull & poorly localized .
3. Is the pain contineuous or intemittent ? the pain over long period & not responds to
analgesia , non organic , while that last 2 hours waken the patient is cluster
headache .
4. How did the pain begin ? nagging ache under nasal nasal bridge due to URTI cause
rhinological pain , while aura of nausea & vomiting then unilateral facial pain is
charcteristic for migraine .
5. How did often does the pain occur ? recurrent bouts of ache in the ear & upper neck
may be due to TM joint disease , while migraine charcterized by monthly
premenstrual headache .
6. What is the pattern of the attacks & are they progressing ? progressing associated
nausea & vomiting "effort one" may be due to intracranial cause .
7. How long is each episode "duration" ? in frontoethmoidal sinusitis with variable
duration , while trigeminal neuralgia may had sharp multiple attacks of facial pain
in chronic paroxysms hemicranial last for 15 minutes .
8. What precipitate the pain ? chewing mean TM joint pain , special triggor points
means trigeminal neuralgia .
9. What relieves the pain ? Aspirin with sleep in dark room decreasing migraine , while
tension headache not responds to anashthesia .
10. Are there any associated symptoms ? nausea & vomiting usually ocurr with migraine
11. What effect does it have on daily life & sleep ? history of severe pain with normal life
is atypical facial pain , facial pain with early morning walking in male usually due to
cluster headache .
12. What management has been tried & with what effect ? tension headache & atypical
facial pain unrelieved by analgesia , while trigeminal neuralgia decreased with
tegritol , migraine relieved with indomethacine .

Lecture notes in
Classifications
A. Rhinological pain
1. Sinusitis ; chronic sinusitis is painless , while the acute variety associated with dull
ache around the medial canthus , lower part of the forehead or under the nasal
bridge , with tender maxillae , while those of frontal sinuses causing frontal pain
(obstruction of the frontoethmoidal recess) the pain is increased when the patient
bending forward .
High calvarium or temple pain due to posterior ethmoid & sphenoid sinusitis ,
symptoms of blockage under the nasal bones may be due to mucosal swelling &
obstruction of the osteomeatal complex .
The Diagnosis from history , outpatient nasoendoscopy , CT scan , although 30-40%
of asymptomatic people show changes on CT scan . When full course of medical
Treatment has failed , surgery either AWO , antrostomy or FESS .
2. Ca. of the maxialla ; rare & the pain is a late feature , ussually associated with
unilateral bloody purulent discharge .
3. Nasopharyngeal Ca. ; involve 5th & 6th cranial nerves cuasing facial pain & diplopia
& when spread posteriorly , so involve 9 th & 12th cranials the tumor may cause ;
a. Trotter's triad ; unilateral middle ear effusion , elevation & immobility of the
ipsilateral soft palate & pain in the ear , jaw or tongue .
b. Intracranial extension ; Godtfredsen's syndrome , ophthamoplegia , pain in the 5th
nerve distribution , tongue paralysis .
c. Pterygopalatine fossa syndrome ; maxillary dental pain , infraorbital & palatal
anasthesia with pterygoid muscle paralysis & blindness .
d. Foix's syndrome ; ophthalmoplegia & 5th nerve without tongue sign , it is due to
anurysm abulting , a tumor invading or a thrombosis of the cavernous sinus .
e. Tolsa Hunt syndrome ; recurrent painful ophthalmoplegia , affect any age for both
sex , charcterized by growing unilateral orbital pain with relapsing & remitting
paralysis of the 3 rd , 4th & 6th cranial nerves occasionally there is parasthesia of the
forehead .
It is caused by lesion in the region of the cavernous sinus or superior orbital fissure ,
managed by steroids (but not diagnostic) .
B. Dental pain
1. Dental pulp ; poorly localized pain because unmyelinated , while dentino-enamel
defect cause sharped , well localized pain followed by dull ache due to cold or hot or
mechanical stimuli .
2. Pulpitis ; acute with dull ache pain , chronic with dull pain worse when lying flat .
3. Once the periodontium is involved , pain is more localized , usually due to periapical
abscess or infection in pocket around the tooth causing erythema & swelling of the
gingiva , not affected by hot or cold stimuli .
4. Percoronitis ; around the wisdom teeth leading to TM joint dysfucntion .
5. Unerupted impacted tooth ; erode the adjacent root causing pain .
6. Dry socket ; pain which is progressive usually start 48 hours after extraction & take
10 days to be settled .
7. Phantom tooth pain ; following dental extraction , incomplete osseous repair ,
necrotic bone & neural elements may found , s.t. cause neuroma whihc need LA to

Lecture notes in
cause temporarly block , but usually such pain is due to oral infection or adjacent
dental erosion .
8. Tempromandibular(TM) joint dysfunction ; 90% unilateral , young adult with history
of bruxism trauma , clenching , recent dental work , anexity , kissing , handle the
telephone between the shoulder & jaw , poor occlusion & inappropriate denture , all
the above may lead to deep dull ache (toothache or earache) due to pterygoid spasm
, radiate to the neck or over the side of the face & temple (chewing increase the pain)
, stress & clicking of the TM joint id unreliable sign while tenderness over the lateral
pterygoid muscle insertion is definit sign , also the x-ray had a little help .
Trismus & deviation of the jaw from the midline on opening (sign) .
Costen's syndrome (1934) ; dull pain at TM joint + trismus + intermittent or
continuous hearing loss + vertigo (intermittent) .
9. Myofacial pain ; wide spread poorly defined aching in the neck , jaw & ear , F:M 5:1
increased by distress , tender point on the sternomastoid & trapizius , percipitated by
malocclusion or poor deltopectoral posture .
Management by reassurance , local heat , U/S & massage helpful , also inection of
local anasthetics (long acting types) .
C. Vascular pain
1. Migraine ; affect 8-10% of adults , include prodromal symptoms like nausea
(common not preceeded by nausea , classical preceeded by nausea "aura") ,
parasthesia & visual disturbances (blurred vision , scotoma & fortification) , usually
has +ve family history .
It is due to vasoconstruction of the cerebral vessels folowed by vasodilatation , it is
induced by stress , diet , menstruation & barometric changes .
The pain charcterized by hemifacial , frontal , temporal or parietal ache , 90% at the
same side , throbbing in nature .
Managed by aspirin , paracetol or codien with rectal or oral largeactil in nausea , if
not respond give ergotamine (but it increase the nausea) during the attack (not
prophylactic) , for prophylaxis give pizotifen (cause weight gain) .
2. Cluster headache ; periodic migranous neuralgia , severe unilateral stabbing or
burnning pain which may be frontal , temporal , occular , maxillary teeth or over the
checks , so it is facial pain & not a headache .
There is no nausea , but rhinorrhea , conjunctival injection & lacrimation with
unilateral nasal obstruction & myosis with flushing , it is common in men from 20-50
years old , awaking the patient in early hours & lasts for 30 minutes – 2 hours , up to
3 bouts/day , percipitated by alchol & managed by ergotamine & methylsergide use
for prophylaxis , avoid alchol during the attack & give O2 .
3. Chronic paroxismal hemicranial ; multiple attacks of excruciating pain by day or
night , in the frontal , temporal or occular region , common in female , each episode
lasts 5-10 minutes , also there is nasal obstruction & ptosis , managed by analgesics
(Indocid) .
4. Temporal arteritis ; affect female over 50 years age with malaise , anorexia & a deep
boring temporal pain , associated with low grade fever , tender temporal artery &
feel thickened with increased ESR .
If untreated , 40% develope visual loss due to ophthalmic artery involvement ,
histopathological examination of the artery shows intimal hyperplasia &

Lecture notes in
fragmentation of the internal elastic lamina (biopsy taken within 72 hours of starting
Treatment) .
Managed by prednisolone 60 mg/day .
5. Carotidynia ; unilateral ache involving the upper neck , face & ear & often occurs
with athrobbing headache , worse by compressing the carotid artery below its
biforcation , it has two subtypes ; (1) young-middle age patients ; normal ESR &
relived by aspirin (2) elderly ; throbbing pain in the area feeded by external carotid
artery , pain lasts for several minutes & hours & respond to ergotamine & to stellate
ganglia block .
6. Causalagia ; reflex sympathetic dystrophy , following trauma or surgery , incomplete
peripheral lesion causing constant diffuse pain with burnning charcter with skin
autonomic changes , managed by sympathetic block .
7. Sphenopalatine neuralgia ; Sluder's neuralgia , charcterized by paroxismal pain in
the forehead , eyebrows & over the nasal bridge bone , about 3 episodes/day , also
may be rhinorrhea , lacrimation , injected conjunctiva , swollen nasal mucosa ,
facial flushing & photophobia , so like sinusitis but without nasal pathology & the
use of decongestant not work , the Diagnosis by touching the middle turbinate , this
will induce pain & cocaine application decrease this pain , managed by SMR &
cryosurgery .
8. Raede;r's paratrigeminal syndrome ; associated red corneal reflex , charcterized by
intense sharp pain or ache in the area of ophthalmic division of the 5th nerve due to a
lesion near the base of the middle cranial fossa (Gasserian's ganglia) , it may be due
to secondary or carotid anurysm .
D. Neuralgias
1. Trigeminal neuralgia ;Tic douloureux ,
a. Primary ; the incidence about 5:100000 per year , common in female > 40 years
old (50-60 y) , charcterized by paroxism of agonizing lanciting pain with
triggered points (D.Diagnosis from dental pain) , has refractory period of > 30
seconds , in > 1/3 rd of patients the pain occur in both the maxillary & mandibular
division (1/5 th in the mandibular alone , 3% at the ophthalmic division) the
patients can localize the trigger zone but it reluctant to demonstrate it
with/without flushing .
Trigger points ; lips , nasolabial folds but pain may be triggered by touching the
gingiva , but firm pressure over the triggor point may delay the bout .
Histology shows proliferation & disorganized changes in the myeline sheath of
the involved nerve .
Also large percent has a vascular compression of the 5 th nerve (so need MRA) .
Managemnt by carbimazipine & phynetoin or antidepressant , s.t. sugery
indicated which is by thermocoagulation of the sensory root or divisions .
b. Secondary ; under 40 years , usually due to multiple sclerosis , while > 40 years
is due to tumor , anurysm , meningioma & tabes dorsalis .
2. Glossopharyngeal neuralgia ; uncommon , stabbing pain at the tonsillar area "rarely
at the base of the tongue" , associated with ipsilateral earache pecipitated by
swallowing or talking & lasts for weeks or months with high recurrence .

Lecture notes in
Management by tegritol tablets with avulsion of the nerve (temporal , tonsillar bed ,
or posterior fossa approach) , tympanic pluxes neuralgia (earache) Treatment by
tympanic plexus neuroectomy .
3. Greater auricular neuralgia ; uncommon , it follow parotidectomy (neuroma of the
sectioned nerve) , managed by steroid injection & LA .
4. Post-herpetic neuralgia ; occur in 1/8th of cases of herpes zooster infection , 2/3rd of
the patient occur in the 1st year , charcterized by intense burnning persistant pain
for more than one month after the eruption , decreased by early use of acyclovir ,
common in elderly , if persist >1year , unlikely to be resolved , also there is
dysathesia , depression & irritability , histologically there is demyelination .
Managed by tegretol with anxiolytic , TCDA , transcutaneous nerve stimulation &
acue puncture , need pain clinic .
5. Mental nerve neuralgia ; mimic 5th nerve neuralgia , sharp pain in the lower lip &
chin , when the lower premolar area is touched in the edentoulous patient due to
exposure & irritation of the mental nerve , managed by bone grafting or re-eouting
of the nerve .
E. Central pain
1. Space occupying lesions like meningioma , angioma & intracranial metastasis , all
cause headache .
2. Streaching of the arterial tree which supply the proximal portion of the cranial
nerves & the dura within 1 cm of any venous sinuses induce headache .
3. Syphilis , multiple sclerosis & syringobulbia , lead to headache .
4. Increase the intracranial pressure lead to headache worsed by coughing or straining
& vomiting .
5. CVA lead to headache .
F. Ophthalmic pain
1. Uncorrected refraction errors , visual acuety is tested .
2. Optic neuritis & scleritis lead to pain on occular movement .
3. Acute glucoma lead to severe headache with nausea & vomiting .
4. Orbital haemorrhage .
5. Periorbital cellulitis .
6. Polyarteritis nodosa & vasculitis , inflammed orbital tissue leads to pain & proptosis
& decreased eye movement with swelling .
7. Uveitis , keratitis & dry eye syndrome .
G. Iatrogenic pain
Scar tissue from any surgery can cause neuroma , it is rare & last thing to be explained .
H. Miscellaneous facial pain
1. Von – Frey's syndrome ; gustatory sweating occur in 25-95% of patients following
superficial parotidectomy , it cause burnning pain in the temple , need no
management , now use drugs to decrease sweating like topical 20% aluminum
chloride hexahydrate.
2. Tension headache ; charcterized by feeling of tightness , pressure or construction
which varies in intensity , frequency & duration , usually at the vertex or forehead ,
eyes or temple , usually has suboccipital component .
It last for hours – several days , associated with anexity & depression .
Managed by analgesia & amitryptaline .

Lecture notes in
3. Eagle syndrome ; pain felt in the lateral wall of the pharynx , floor of the mouth ^
side of the neck , charcterized by nagging discomfort lasting for seconds – minutes
percipitated by opening the mouth or head turning .
It is due to elongated styloid process & calicified subhyoid ligament , diagnosed by
palpation of the tonsillar area or externally , this cause pain , or by x-ray (lateral
oblique film) showing the elongated styloid process .
Management by fracturing the styloid process or remove it surgically .
4. Glossodynia ; unknown aetiology , burnning sensation in the toungue , disordered
taste or sensation of dry mouth , usually affect females > 50 year with caucer phobia
& history of emotional disturbances or percipitating major life events .
Diagnosed by throughout history & examination of the oral cavity to exclude other
pathology (iron deficiency , DM & candidia , local irritation , lichen planus ,
irritatnt mouth wash , ulceration , dentures , galvanism , drug reactions &
erythroplakia) .
5. hypochondrriosis ; there is a coexisting symptoms elsewhere in the body & the
patient express exagurated concern about the function of the body .
6. Atypical facial pain ; occur in female > 40 years , Diagnosis when organic causes
are excluded , there is often psychological factor or unpleasant life event .
The pain ; deep , ill defined , changes location , unexplainable on anatomical bases ,
occur daily , s.t. fluctuating & s.t. continuous , not awake the patient & last many
months , some patients have depression or anexity neurosis , so psychatric support is
helpful . Managed by tricyclic antidepressants .
7. Hysterical pain ; ill defined with unusual neurological symptoms like weakness &
paraesthesia , no physical lesion can be found & the distribution of the neurological
loss not follow the anatomical bases , the pain occur without delay with fluctuation
in severity .
It is enable the patient to obtain some personal benifit by avoiding an unwanted tasks
I. Otological causes
1. Acute otitis media .
2. Otitis externa .

Lecture notes in

Lecture notes in
Examination of the throat

The throat consist of ; oral cavity , , oropharynx , larynx & hypopharynx .
The oral cavity includes the following structures ;
1. Lips ; the common site for Ca. herpes & primary syphilis .
2. Teeth &Gums ; bleeding form gums , state of dentition , foul discharge from tooth ,
sensation …etc .
3. Tongue includes ; anterior 2/3rd , posterior 1/3rd , tip , dorsum & the margins
4. Hard & soft palate .
5. Floor .
6. Cheecks .
The oropharynx includes ;
1. Uvula .
2. Soft palate .
3. Anterior & posterior tonsillar pillars .
4. Tonsils .
5. Posterior pharyngeal wall .
The hypopharynx includes ;
1. Posterior pharyngeal wall .
2. Pyriform fossae .
3. Postcricoid area .
Check for ;
1. The tongue .
a. Common & taste sensation .
b. Size , macroglossia in acromegaly & Down's syndrome .
c. Ulcers ; traumatic , dental , aphthus , malignant , tuberculus & syphilitic .
d. Movement ; restricted in hypoglossal palsies or tumor inflteration .
e. Fasciculation ; motor neuron disease .
f. Depapillation in vitamin deficiencies .
g. Furrowing as a geographic tongue .
h. Coating ; thrush , black hairy tongue , …etc .
i. Hypoglossal palsy ; tongue deviates toward the lesion .
2. Checks ; parotid duct opening opposite the upper 2nd molar , red or white patches ,
ulcers , moisture .
3. Palate ; swelling , ulcer , movement , perforations , clefts …etc.
4. Uvula ; position , deviations (towards the normal side in palsies) , ulcers , ..etc.
5. Tonsillar pillars ; linear congestion , ulcers , patches ,..etc .
6. Tonsils ; presence , size , crypts , ulcers , express the contents of crypts by pressing
on the pillars to see whether purulent .
7. Posterior pharyngeal wall ; lymphoid follicles . ulcers , ..etc .
8. Floor of the mouth ; Wharton duct openings , ulcers & bimanual palpation .
9. The upper & lower vestibule of the checks .
10. Larynx & hypopharynx , examination carried out by ;
a. Indirect laryngoscopy ;
- The mirrod is plane on a straight handle .
- Mirror is held like a pen in the right hand with the glass pointing downwards .
- Warm the mirror & test the temperature on the the back of the hand .

Lecture notes in
- The patient asked to stick out the tongue which is held with a piece of gauze .
- The patient is asked to breath through the mouth .
- The mirror is introduced into the mouth to the uvula which is gently pushed
back to get a view of the larynx & the pyriform fossae .
- The patient is asked to say "Aaa" & "Eee" .
b. Flexible or rigid endoscope ;
c. Direct laryngoscopy ;
d. X-ray ;
Examination of the neck form an integeral part on the examination of the throat ;
1. Inspection ; position , shape , thyroid angle , movement with swallowing , retraction
of the suprasternal notch on inspiration .
2. Palpation ; cartilages for irregularity , scars , tenderness , subcutaneous emphysema
, laryngeal crepitus .

Lecture notes in
Radiography of the head & neck

Head & neck radiographes divided into ;
A. Conventional radiography ;
Best views that describe the skull bones & formina & its contents .
1. Transorbital view ; chin slightly flexed until the orbito-frontal line became
perpendicular to the film , this view magnifying the orbit & visualize the internal
auditory canal , lateral SCC , cochlea & vestibule .
2. Town's view ; AP projection with 30 otilt , allow comparison of the patient
pyramid & mastoid , identify petrus apex , internal auditory meatus , arcuate
eminence , mastoid antrum & mastoid process .
It evaluate the apical petrositis , acoustic neuroma , CPA tumors .
3. Water's view (occipitomental) ; chin-nose position .
PA –OMV show maxillary sinus , frontal sinus , ethmoidal sinus , best shown in
order , but not for sphenoid unless mouth opened .
Maxillofacial structures also shown ; nasal bones , frontal process of maxilla ,
zygomatic arch , mandible , others (superior orbital fissure , oblique orbital line ,
orbital rim & floor , foramina rotundum , formina oval) .
4. Lateral view ; best for sphenoid sinuses .
5. Submentovertical .
6. AP view & Lateral view for larynx & neck .
7. Facial bone injury ;
a. Nasal fracture by left & right lateral , Water's or superior axial view .
b. Facial bone series ; exagurated Town's view & Submentovertical view .
B. Cross sectional anatomy & imaging ; CT scan & MRI .

Lecture notes in
Oral cavity conditions

Anatomy
The mouth is bounded by the palate above, the mylohyoid muscle below, the buccinator
muscles in the cheek on each side, and the palatoglossal arches behind. In addition to the
oral cavity proper, the mouth includes the vestibule, which is the space between the cheek
and the teeth.
PALATE ; hard palate is formed by the palatal process of the maxilla and the horizontal
process of the palatine bone, which are covered by a mucous membrane. The soft palate is
formed by contributions from a number of muscles ;
- The tensor veli palatini arises from the scaphoid fossa of the sphenoid bone and
descends in the lateral wall of the nose, narrowing to a tendon that turns medially
around the pterygoid hamulus. It then fans out to become the palatine aponeurosis
and attaches to the muscle of the opposite side. Together, the two muscles tense the
soft palate for other muscles to act upon it.
- The levator veli palatini arises from the petrous part of the temporal bone near the
base of the styloid process and from the cartilage of the eustachian tube. It passes
between the lowest fibers of the superior pharyngeal constrictor muscle and the
highest fibers of the middle pharyngeal constrictor muscle, attaching to the upper
surface of the palatine aponeurosis. It helps to elevate the soft palate and, together
with the palatopharyngeus and superior pharyngeal constrictor muscles, it closes off
the nose from the oropharynx during swallowing.
- The palatoglossus muscle arises from the lower surface of the palatine aponeurosis
and passes down, in front of the palatine tonsil, to attach to the side of the tongue. It
pulls the back of the tongue upward and approximates the soft palate to the tongue,
closing off the mouth from the pharynx.
- The palatopharyngeus muscle also arises from the lower surface of the palatine
aponeurosis and passes down, behind the palatine tonsil, to blend into the
longitudinal muscle layer of the pharynx. It helps to pull the pharyngeal wall upward
during swallowing and, together with the levator veli palatini and superior
pharyngeal constrictor muscles, it closes off the nose from the oropharynx.
- The musculus uvulae is a small muscle that helps to elevate the uvula.
The blood supply of the palate is from the ascending palatine branches of the facial artery
as well as from the palatine branch of the maxillary artery, both of which drop down to the
palate from the pterygopalatine fossa by passing through the palatine canal.
TONGUE , the anterior two thirds of the tongue develop separately from the posterior third,
and the two parts come together at the sulcus terminalis. The surface of the anterior two
thirds of the tongue is covered by filiform, fungiform, and vallate papillae. The posterior
third of the tongue contains collections of lymphoid tissue, the lingual tonsils.
The mass of the tongue is made up of intrinsic muscles that are directed longitudinally,
vertically, and transversely; these intrinsic muscles help to change the shape of the tongue.
The extrinsic muscles help to move the tongue.
- The genioglossus, which arises from the genial tubercle on the inside surface of the
front of the mandible and passes upward and backward into the tongue, acts to
protrude and depress the tongue.

Lecture notes in
- The hyoglossus, which arises from the hyoid bone and passes upward to attach to the
side of the posterior part of the tongue, acts to depress and retract the back of the
tongue.
- The styloglossus, which arises from the styloid process and passes downward and
forward through the middle pharyngeal constrictor muscle to attach to the side of
the tongue, acts to elevate and retract the tongue.
- The palatoglossus muscle (described previously) acts on the tongue but is considered
a muscle of the palate.
The blood supply of the tongue is from the lingual branch of the external carotid artery. The
lingual artery reaches the tongue by passing behind the posterior edge of the hyoglossus
muscle and turning forward into the substance of the tongue, thus coursing medial to the
hyoglossus. In contrast, all the other nerves and vessels of the tongue pass lateral to the
hyoglossus before entering the tongue.
FLOOR OF MOUTH , the floor of mouth is formed by the mylohyoid muscle upon which lie
the geniohyoid muscles. The digastric muscle lies immediately below the mylohyoid muscle.
Both the geniohyoid and the digastric muscles are discussed with the suprahyoid muscles of
the neck. The mylohyoid arises from the similarly named line on the inside surface of the
mandible and attaches to the front of the hyoid bone. It is the main support of the structures
in the mouth. It helps to elevate the hyoid bone during movements of swallowing and
speech. Also, with the infrahyoid muscles holding the hyoid bone in place, the mylohyoid
and digastric muscles help to depress the mandible and open the mouth.
The deep part of the submandibular gland and the duct that emerges from it lie above the
mylohyoid muscle. The sublingual gland also shares this relationship. The hypoglossal
nerve (CN XII) enters the mouth from the neck by passing lateral to the hyoglossus muscle
and above the free posterior edge of the mylohyoid muscle. It continues in the mouth,
inferior to the submandibular duct, and enters the substance of the tongue at its side. The
lingual branch of the mandibular division of the trigeminal nerve enters the mouth from the
infratemporal fossa by passing medial to the lower third molar. It initially lies above and
lateral to the submandibular duct and then spirals under the duct as it comes to lie above
and medial to the duct, where it gives off its terminal branches to the tongue and the floor of
mouth. The glossopharyngeal nerve passes from the pharynx to the mouth, lies lateral to the
bed of the palatine tonsil, and courses into the posterior third of the tongue.
SENSORY INNERVATION
Sensation from the palate is carried by branches of the maxillary division of the trigeminal
nerve. From the front of the hard palate, just inside the incisors, sensation is carried by the
incisive branch of the nasopalatine nerve. From the rest of the hard palate and the mucosa
lining the palatal aspect of the upper alveolar margins, sensation is carried by the greater
palatine nerve. From the soft palate, sensation is carried by the lesser palatine nerve.
Sensation from the tongue is carried by nerves predicated upon the development of the
tongue. There are general sensory fibers that carry sensations of touch, pressure, and
temperature. In addition, there are special sensory fibers that carry the sensation of taste.
General sensation from the anterior two thirds of the tongue is carried by the lingual
branch of the mandibular division of the trigeminal nerve. General sensation from the
posterior third of the tongue is carried by the glossopharyngeal nerve. Taste sensation from
the anterior two thirds of the tongue is carried by the chorda tympani branch of the facial

Lecture notes in
nerve. Taste sensation from the posterior third of the tongue is carried by the
glossopharyngeal nerve.
Sensation from the floor of mouth and the mucosa lining the lingual aspect of the lower
alveolar margins is carried by the lingual branch of the mandibular division of the
trigeminal nerve. Sensation from the buccal mucosa and the mucosa lining the buccal
aspect of the upper and lower alveolar margins is carried by the buccal branch of the
mandibular division of the trigeminal nerve. Sensation from the mucosa lining the anterior
part of the vestibule, inside the upper lip, and the adjacent mucosa lining the labial aspect
of the upper alveolar margins is carried by the infraorbital branch of the mandibular
division of the trigeminal nerve. Sensation from the mucosa lining the anterior part of the
vestibule, inside the lower lip, and the adjacent mucosa lining the labial aspect of the lower
alveolar margins is carried by the mental branch of the inferior alveolar branch of the
mandibular division of the trigeminal nerve.
MOTOR INNERVATION
All the muscles of the palate are innervated by branches of the vagus nerve (CN X), except
the tensor veli palatini, which is innervated by the mandibular division of the trigeminal
nerve. All the muscles of the tongue, extrinsic and intrinsic, are innervated by the
hypoglossal nerve, except the palatoglossus muscle, which is considered a muscle of the
palate and is therefore innervated by the vagus nerve. The mylohyoid muscle and anterior
belly of the digastric muscle are innervated by the nerve to the mylohyoid muscle, a branch
of the mandibular division of the trigeminal nerve. The geniohyoid muscle is innervated by
fibers from the cervical spinal cord (C1), which are carried to it by the hypoglossal nerve.
Congenital anomalies ; the most important are ;
1. Cleft lip & palate .
2. Congenital abnormalities of the jaw .
Mucosal abnormalities
1. Dyskeratosis congenita ; rare ectodermal abnormality , dyskeratotic white patches in
the mouth , also abnormality of skin , nails , cornea & hair which may be absent .
2. Fordyce's spots ; atopic sebaceous gland in the buccal & labial mucosa , it is small
yellowish lesion of no significance .
3. White sponge naevus ; autosomal dominant disease , characterized by white raised
lesion of no significance .
4. Hereditary hemorrhagic telangectasia ; (Osler-Weber-Rendue disease) , autosoaml
dominant , telangectasia present in the lips & oral mucosa .
Congenital lesions of the tongue
1. Macroglossia ; in Down's , Beckwith's syndrome & cretinism ( also in lymphangioma ,
but not congenital) , also occur with acromegally & amyloidosis .
2. Ankyloglossia , tongue tie , due to short lingual frenulum , rarely it severe enough to
affecting suckling or later speech , managed by horizontal incision of the frenulum &
vertical repair .
3. Median rhomboid glossitis ; of no significance , area in the dorsum of the tongue ,
anterior to the circuvellate papillae which is devoid of papillae appear flat & pink .
It due to failure of lateral halves of the tongue to fuse in the midline with tuberculum
impar .
4. Lingual thyroid ; occur in the posterior 1/3 rd of the tongue behind the circuvellate
papillae in the oropharynx , need Rx if only enlarging causing changes in speech ,
swallowing & airway patency.
Lecture notes in
Radioneuclic scan (Tc or I) establish the nature of the tissue & determine whether this
is the only thyroid tissue in the body , also it may be the site of thyroid neoplasm .
Stomatitis & oral ulceration
Diagnosis mainly from , history & physical examination (may be enough) , bacteriological
examination of the smear , blood film , serological tests & biopsy .
It classified into ;
1. Oral manifestation of systemic disease
a. Haematological
(1) Agranulocytosis ; may be due to drugs hypersensitivity (sulphanomide ,
chloramphenicol , carbimazole , isoniazide) , or normal response to
bleomycine or methotrexate therapy , it is characterized by acute ulceration of
the oral cavity with sloughing inside it , this associated with fever & illness ,
diagnosed from blood picture .
(2) Acute leukaemia ; ulceration & bleeding from the gums .
(3) AIDS ; hairy leucoplakia , oral candidiasis , herpetic stomatitis & Kaposi
sarcoma .
b. Acute exanthemes ; chichen pox (vesicles in the oral cavity) , acute strep.
tonsillitis (strawberry tongue) , measles (Koplik spots) , IMN (petechial rash on
the hard palate) …etc .
c. Drug reactions ; phenytoin cause gingival hypertrophy , Gold cause gingivitis ,
pencillins , sulphonamide , barbiturates , all cause agranulocytosis & erythema
multiforme .
d. Vitamin deficiencies ; vitamin C cause gingivitis , iron , folate & B12 cause
glossitis & B2 & nicotinic acid cause angular chelitis & glossitis
e. Autoimmune diseases ; chronic discoid lupus & SLE cause vesicular eruption &
ulcerative lesions , scleroderma & PAN cause oral ulceration , Sjogren's
syndrome & Rh. arthritis cause xerostomia , Behcet's disease , pemphegus &
pemphegoid cause ulceration .
2. Oral pigmentation
a. Not ulcerative lesion , found normally in blacks .
b. Neurofibromatosis .
c. Haemochromatosis.
d. Albright syndrome .
e. Peutz-Jegher syndrome .
f. Von-Recklinghaussen's disease .
g. Addison's disease .
h. Melanoma .
i. Mercury , bismuth & lead poisoning .
3. Infection
a. Viral ; primary herpetic gingivostomitis , herpes zoster , hand-foot & mouth
disease , herpangina ..etc .
b. Bacterial ; Vincent angina (acute necrotizing gingivitis) , cancrum oris
(gangerenous stomatitis) , syphilis , T.B. …etc .
c. Fungal infections ; candidiasis , histoplasmosis …etc .
4. Trauma ; hard food , rough dentures , sharp rough dentition , patient bitting his buccal
mucosa or tongue .

Lecture notes in
Many patients with oral carcinoma relate this to ill fitting dentures or to trauma ,
traumatic ulcers heal within 2 weeks & if not , then biopsied .
5. Miscellaneous ; aphthus ulcer , necrotizing sialometaplasia , lichen planus , Behcet
syndrome , pephegus vulgaris , pemphegoid , eryhthema multiforme , leucoplakia ,
geographic tongue , hairy tongue …etc .
- Primary herpetic gingivostomatitis ; mostly in children, must be differentiated from (DDx)
herpangina , chicken pox , hand foot & mouth disease , acute erythema multiforme
It is used by Herpes simplex virus , frequently occur in children & adult not s
Exposed to the virus before .
Presented as fever , malaise , vesicular lesions , 2-4 mm in size , when break forming
ulcers with yellowish base & erythematous halo , similar to aphthus ulcer , the condition
lasts 2-4 weeks .
Diagnosed from scraping's or smear , then the virus identified by immunoflurecent
staining , or by exofolative cytology showing multinucleated giant cells , or by culture .
We must note that recurrent oral herpes is very unusual , but recurrent herpes labialis
(cold sore) is very common .
- Herpes zoster , the virus affect the trigeminal nerve leading to intraoral lesion , always
unilateral , often painful , cervical LAP may be present , also , there may be associated
facial nerve palsy (Ramsy Hunt syndrome) .
- Hand , foot & mouth disease . caused by group A coxsackie virus , cause vesicles on the
hands , feet , & buttocks with intraoral vesicles & later ulcers .
Presented as fever , malaise , the incubation period about 1 week & it last about 1 week .
- Herpangina , mainly in children , caused by different viruses (coxsackie , ECHO ..etc) ,
similar herptic eruption , but the lesions in the oropharynx (rather than oral cavity) .
- Acute necrotizing gingivitis , caused by spirochete Bomelia Vincenti & anaerobic bacillus
fusiformis , occur in adults , debilitated with poor oral hygiene .
It is gingivitis of the interdental papillae leading to ulceration & necrotic membrane .
Presented with pain , foeter , fever (s.t.) & cervical LAP , the lesion may spread to the
tonsils & nasopharynx , dignosis confirmed by stained smear with genition violet to
identify the microorganism , treated by local mouth washes & systemic penicillin & flagyl
(i.v.) .
- Gangrenous stomatitis , affect children , mostly debilitated , rapidly enlarging ulcer &
necrosis in the oral cavity & upper & lower jaws , caused by mixed bacterial infection .
Managed by local oral hygiene with i.v. penicillin & flagyl .
- Syphilis , caused by spirochete Trepanoma pallidum , it could be acquired (sexual
intercourse) or congenital .
The pathology are ; endarteritis , increased adventitial cells , proliferation of endothelial
cells & inflammatory cells infiltrate with lymphocytes , plasma cells & monocytes , in the
tertiary phase , granulomatous reaction with giant cells encircling a necrotic center , the
organism can be isolated from the primary & secondary stages .
The stages are ;
(1) Primary stage ; which is at the site of initial inoculation , the lesion called
Chancre , ainly found in the genital area .
Extragenital sites are ; lips , buccal mucosa , tongue & tonsils , the incubation
period for 3 weeks . There is papule , then painful ulcer heals within 2-6 weeks ,
may be painless LAP .

Lecture notes in
(2) Secondary syphilis ; is the one mostly affect the oral cavity , it occur 4-6 weeks
after the primary stage , 30% of it have healing chancre .
Presented as malaise , headache , fever , generalized LAP , mucocutaneous rash
& sore throat , in the oral cavity mainly in the tongue & palate , the ulcers are
covered with grayish membrane called snail-truck ulcers or mucous patches
(circular) , the secondary stage lasts for few weeks .
Tertiary syphilis ; develop many years after the initial infection , lesions affect
any organ or restricted to 1 or 2 organs , in the URT , the lesion is Gumma start
as nodule which break to form necrotic ulcer , in the palate it cause oronasal or
oroantral fistula .
Palate , nasal septum , tonsils , posterior pharyngeal wall or larynx , the gumma
is painless due to tissue destruction (including the nerve endings) .
The diagnosis in the primary or secondary stages by ; smear of the lesion (spirochete) ,
biopsy (using silver nitrate or immunoflurecent technique) , biopsy in the tertiary stage not
found the spirochete (but show the typical histopathological appearance) .
Serology , fall in 2 groups ;
(1) Those identify non-specific antibodies to cardiolipin (VDRL) , uses beef heart
Ag , +ve 1-2 weeks after development of the chancre (99% +ve in the secondary
& tertiary syphilis) , false +ve in non-syphilitic treponemal diseases (Yaws ,
Pinta ..etc) , infections (atypical pneumonia , malaria , leprosy , small pox) & in
autoimmune diseases (SLE & Rh. arthritis) .
(2) Those detect specific treponemal antibodies , Treponema pallidum
immobilization test (TPI) , which depend on specific Ab in the patient serum
which immobilize the spirochete observed by dark ground illumination , 100%
+ve in the secondary & tertiary syphilis , 100% specific .
Also florescent treponemal antibodies (FTA) test , involve absorption of Ab onto
dried treponema preparation identified by fluorescent labeled antihuman
gamma globulin , 100% +ve in secondary & tertiary syphilis , but not 100%
specific (false +ve in SLE & Rh. arthritis)
The management by single or 2 deep intramuscular 2.4 megaunits of benzathine penicillin
separated by 1 week , the 3rd injection (2.4 MU) at weekly or 2 weekly intervals .
- Tuberculosis , only affect the oral cavity in +ve pulmonary T.B. sputum , found as
multiple superficial ulcers , painful in the tongue & other areas .
- Candidiasis , candida albicans is a normal commensal flora in the mouth , become
pathogenic when , debilitating illness (AIDS) , antibiotics , anticancerous cheotherapy , &
steroids (local or systemic) .
Acute Candidiasis present as multiple , small , white patches when wiped off shows
erythematous patch , they are painful , the diagnosis by smear stained with periodic acid
Schiff method (PAS) .
Managed by correcting the underlying condition , using local Nystatin or amphortercin .
Chronic Candidiasis presents as whithe lesions can't be removed or rubbed off , it give the
appearance of leucoplakia (candidial leucoplakia) , the site mainly inside the corners of
the mouth , managed by local or systemic antifungals (ketoconazole , may be of benefit) &
excision is the only way to remove it .
- Histoplasmosis , due to Histoplasma capsulatum , cause granular –looking ulcers usually
in wide spread systemic histoplasmosis , managed by ketoconazole .

Lecture notes in
- Aphthus ulcer , very common , unknown aetiology , suggested causes are ; hypersensitivity
reaction , hormonal , vitamin deficiencies & stress .
It is single or multiple ulcers , 2-10 mm in size , lasrs few weeks , each ulcer heal in about
10 days , biopsy may be done to distinguish from Ca. (if > 10 days) , treated by local
steroids to decrease the inflammation & assist healing .
- Behcet disease , unknown aetiology , oral ulcer, genital ulcer , uveitis , vasculitis of the
skin , synovitis & meningoencephalitis , it is relapsing disease & treated with steroids .
- Pemphegus Vulgaris , bullae in the skin & oral cavity (palate , buccal mucosa & tongue) ,
affect late middle age & elderly , relapses is common , the bullae in the oral cavity when
reptured forming irregular painful ulcers .
Diagnosed from histological examination which shows acantholysis in the epithelium ,
also immunofluroscence test can demonstrate IgG .
Nikolysky's sign ; strok the mucous membrane will cause vesicle or bullae .
Management by systemic steroids .
Benign mucous membrane pemphigus vulgaris , less serious than pemphigus vulagaris ,
causing chronic scarring of the conjunctiva , affecting older age groups & F>M , vesicles
in the oral cavity , pharynx , larynx & conjunctiva , skin lesions are rare , less painful .
Histologically there is no acantholysis , there is only subepithelial clefts ,
immunofluroscence show IgG & complement C 3 in the basement membrane .
No need for any sort of Rx , but sometimes use steroids .
- Erythema multiforme , unknown aetiology , affect young people (10-30 y) , it could be
secondary to infection (HSV & Mycoplasma) , drugs (penicillin , sulphanoamide ,
barbityrate) , it is present as nodular lesion with bluish centre , bullae & vescles in the
skin , the oral lesion more common in the major form of the disease (Steven-Johnson's
syndrome) than in minor form . in 1/4 th of the patients , the only lesion is in the oral cavity
It lasts for 2-3 weeks , relapses common , in Steven-Johnson's syndrome pyrexia & the
patient ill , the patient lips covered with haemorrhagic crusts (characteristic of the
disease) .
- Necrotizing sialometaplasia , uncommon , ulceration to the hard palate or oropharynx ,
histopathological exam show ductal metaplasia or hyperplasia of the salivary tissue with
extensive inflammatory changes .
The diagnosis from histopathology & biopsy differentiate it from Ca. , it is self limiting
disease within few weeks .
- Lichen planus , lesions in the skin & oral cavity , affect middle aged people , F>M , it has
unknown aetiology , the most common types are reticular & erosive .
The reticular type ; slightly raised lesion , white , bluish with reticular pattern of striae .
The erosive type ; erythematous lesion , ulcerated & painful , biopsy done to distinguish it
from other types & diseases (leucoplakia , erythroplakia , early Ca.) .
Histologically there is keratosis , parakeratosis with pointed or saw-toothed rete pegs &
accumulation of fluid along the basement membrane .
Treatment by local steroid for erosive type with observation & biopsy due to increased
incidence of Ca. in this type .
- Leucoplakia , white patches (keratinizing epithelium) , it is precancerous , with unknown
aetiology , the importance of it due to its relationship with Ca.
Histopathological changes are ; keratosis (accumulation of keratin) , hyperkeratosis
(thickening of the stratum corneum) , parakeratosis (increased nucleated cells) &
acanthosis (elongation of the rete pegs of st. corneum) .
Lecture notes in
The most important factor is the degree of abnormality or dyskeratosis with nuclear
hyperchromatism , nuclear pleomorphism , mitosis & loss of normal maturation of the
cells (loss of polarity with intercellular adherence) .
Vary from mild atypia to frank carcinoma .
Management policy for leucoplakia , by doing biopsy using orascreen , show little or no
dysplasia , then no Rx or laser destruction with follow up & stop drinking & smoking &
treat the dental caries .
- Erythroplakia , mucosal abnormality with erythematous changes represent dysplasia
without keratosis , severe dysplasia may lead to high malignant potential .
Candidial leucoplakia ; chronic Candidiasis with dysplasia .
Management for erythroplakia , dyskeratosis or carcinoma in situ , by laser excision with
several histological examination .
- Geographical tongue ; also called migratory glossitis or erythema migrans , benign
condition of unknown cause , the tongue usually appear map like with loss of papillae , it
is asymptomatic or may be with mild burning pain , the loss of papillae also may be
progress & increased , so it is migratory , no need for any sort of treatment .
- Hairy tongue , coated tongue due to elongation & accumulation of keratin associated with
filiform papillae , usually white , it blackened in smokers , the aetiology unknown & the
treatment is by scraping the keratin with brush .
- Xerostomia , dry mouth , it could be due to ;
1. Sjogren's syndrome ; an autoimmune disease of the salivary glands , 50% may be
associated with other connective tissue diseases (Rh. arthritis , SLE , PAN or
polymyositis) .
2. Radiotherapy ; due to the effect on the major & minor salivary glands .
3. Drug interaction ; atropine like drugs (tricyclic antidepressant , antibiotics like
tetracycline , sulphonamide , others like thiouracil or phenobutazone) .
Benign swelling in the oral cavity
1. Cyst in the mouth
a. developmental cysts ; they may be midline or lateral where the maxilla &
premaxilla elements fuse .
b. Cyst associated with the tooth .
c. Nasopalatine cysts .
d. Dermoid cyst ; it may be submental or in the floor of the mouth & tongue .
e. Cysts & tumors of the jaws .
f. Retention cyst (Ranula) ; it is uni- or multi-locular mucous filled cyst in the floor of
the mouth & classified into two types ;
(1) Simple ranula ; which has epithelial lining & confined to the floor of
mouth .
(2) Plunging & burrowing ranula ; which is lined by connective tissue & not
epithelium & it can be confined to the floor of the mouth or may extend
through the mylohyoid muscle in the neck .
It may arise from damaged & obstructed sublingual salivary gland & s.t.
submandibular gland , other theories of origin is it due to embryonic epithelial
nests , Submucosal bursa , or from dermoid cyst , also plunging type may results
from extravasations of cyst contents into the tissue .
There is no age limit , but generally seen in children & young adults , it is abluish
translucent cyst in the floor of the mouth on one side of the frenulum of the tongue lead to
Lecture notes in
frog belly appearance , sometimes may reach large size or may burst & recur , the wall
composed of fibrous capsule .
Treatment is by marsupilization which is effective for simple ranula , s.t. failed in plunging
ranula because of the remaining salivary tissue will continue to secrete , so Rx plane is ; if
it confined to the mouth , then Rx by excision , but if extending to the neck , then by
marsuplization & excision of the sublingual salivary gland .
2. Inflammatory swellings
Most of the inflammatory swelling are associated with the teeth , dental caries & gingivitis
are all predisposing factors , these lead to destruction of the enamel & dentine & dental
abscess leading to chronic inflammatory disease of the gums , treated by removal of the
swelling & Rx the causative infection .
3. Benign tumors of the oral cavity
a. Odentogenic tumors & cyst .
b. Papilloma ; sequamous Papilloma arise from the stratified sequamous epithelium
of the oral cavity .
c. Pleomorphic adenoma ; the most common benign salivary glands tumor , within the
oral cavity , the majority occur in the hard palate , also in the tongue & floor of the
mouth , it is soft , irregular , bluish or purple , treated by complete excision which
should be as conservative as possible .
Oral cavity tumors
Spread of the tumor
1. Along the spaces created by passage of the normal anatomical structures .
a. Inferior alveolar nerve , Ca. of lower alveolus cause anaesthesia of an area of skin to
one side of the chin , it enter through the mandibular canal , inferior dental canal ,
then mental foramen .
b. Small bony canals in the hard palate ;
- Greater palatine foramen , transmit the anterior palatine vessels & nerve , through it
spread to the pterygopalatine fossa & ganglia .
- Lesser palatine foramen , there are 2 in each side of the hard palate , transmit the
middle & posterior palatine vessels & nerves .
- Incisive foramen , connect the oral cavity to the nasal cavity , it transmit the terminal
branches of the greater palatine vessels & nasopalatine nerve .
2. Along muscles & mucosal planes , like medial & lateral pterygoid muscle causing trismus
(which is bad prognostic sign) , or the muscles of the floor of the mouth like myelohyoid ,
genihyoid & genioglossus muscles , close the opening of the submandibular gland leading
to swelling of the gland .
Types of the tumors
1. Ectodermal origin
- Benign , like neural tumors 1% & benign salivary gland tumors .
- Malignant , SCC 85% , verrocus Ca. 5% , malignant salivary Ca. 5% , melanoma 5% .
2. Mesodermal origin ;
- Benign , haemangioma 1.5% , others 1% .
- Malignant , non-Hodgin's lymphoma 1% , Hodgkin's 0.1% , sarcoma 1% .
3. Metastatic ; about 1% .
Site of the tumor
1. Tongue , 35%, lateral border 31% , tip 2% & dorsum 2% .
2. Floor of the mouth , 30% , anterior 25% & lateral 5% .
Lecture notes in
3. Buccal mucosa , 10% .

4. Lower alveolus , 5% .
5. Upper alveolus 3% .
6. Retromolar trigon , 2% .
Risk factors
Smoking , high alcohol intake , dental caries , alcoholic mouth washes , hot spices ,
leucoplakia , avitamenosis , chronic glossitis , malnutrition , syphilis , cirrhosis , iron
deficiency anaemia , lichen planus , HIV , xeroderma , chronic hyperplastic candidiasis &
submucosal fibrosis .
The only premalignant lesion in the oral cavity is leucoplakia , which is white lesion due to
abnormal kertainization , 6% of it developed to Ca. , the clinical variant of leucoplakia are ;
lecoplakia simpley , verrocus leucoplakia & erythroleucoplakia .
Eighty percent of AIDS patients develop hairy oral leucoplakia .
Sequamous cell carcinoma (SCC)
Pathology
It is either exophytic , ulcerative or infiltrative , when the depth of the tumor increased , this
increase the incidence of cervical metastasis , other variant of SCC ;
1. Verrocus Ca. , which is well differentiated SCC , rare , it is flat warty tumor composed
of sequamous cells covered by keratin layer .
2. Sarcomatoid or spindle cell Ca. , resemble sarcoma cells .
Other oral cavity tumors are ; malignant salivary gland tumors (10%) which is either adenoid
cystic Ca. (50%) or adenocarcinoma (30%) .
Site of the oral carcinoma
1. Buccal mucosa ; 10% usually old age male (M>F) , common in Africa & southeast Asia ,
it occur in the region of the chewing of betal nut . mostly well differentiated , leucoplakia
is common .
The commonest sites are the commissure of the mouth , occlusal plane & Retromolar area
, there are 3 distinct types , exophytix , ulcerative , infiltrative & verrocus .
It extends posteriorly to the pterygomaxillary fissure & anterior tonsillar pillar , in 15%
palpable nodes & 5% microscopical nodes .
Management policy ;
- Small T1 tumors (<2 cm) , removed with safe margin or interstitial radiotherapy .
- Tumors > 2 cm , by radiotherapy (if no bony invasion) , or surgery (upper & lower lip
incision or Weber fergesson's) .
- Large tumors by wide resection involving the skin with reconstruction be deltopectoral
or pectoral or temporalis or cervicofacial flaps .
2. Ca. of the tongue ; 35% , usually middle age male , or young female , mostly well
differentiated , high LN occult metastasis , 40% arise from anterior 2/3rd , 85% of which
from lateral borders .
It is either infiltrative or exophytic , it infiltrate the tongue muscle restricting its mobility .
LN metastasis , N0 50% , N1 20% , N2 20% & N3 10% , it is proportional to staging ,
depth & grading .
Management policy ;
- Tip , V-shaped excision of the tip .
- Dorsum , if < 1 cm , ellipse excision of the lesion with primary closure or
radiotherapy, while for large tumors we Rx by radiotherapy to preserve the tongue .

Lecture notes in
- Lateral borders , if no LN , by radiation or surgery (partial glossectomy) , while large

tumors (T2 , > 2cm) by hemiglossectomy or radiation , if LN present , then do
hemiglossectomy with RND .
3. Ca. of the floor of the mouth ; 30% it is either arising from the anterior part "common"
around the papilla of the duct of the submandibular duct opening , or arising laterally .
It spread medially & laterally , the teeth form some barrier preventing the spread from the
lingual to Buccal surface , in edentulous mandible , the tumor can readily spread into the
mandible & medullary cavity , to inferior alveolar nerve to the ptergoid fossa & skull base
The myelohyoid muscle acts as barrier anteriorly , it may spread to submandibular area
causing a palpable lump .
Management policy of the anterior floor lesions ;
- No mandibular invasion , then resect the lesion & soft tissue reconstruction .
- Mandible invasion with no previous radiotherapy , then conservative surgery &
reconstruction .
- If the patient previously irradiated or with extensive invasion , then resection of the
anterior mandibular segment with reconstruction to prevent Audy-Gump deformity .
So management is by removing the floor & segment of the mandible with bilateral neck
dissection , bur radiotherapy may be used early .
If the LN are palpable , then bilateral selective supraomohyoid (level I-III) ND , or
extended supraomohyoid (level I – IV , anterolateral) ND (palpable LN , ND + postop.
Radiotherapy)
Management policy for lateral floor tumors ;
- By surgical resection , if the mandible involved , then rim resection .
- In extensive invasion or previous radiation , then COMMANDO operation with
reconstruction .
4. Ca. of the lower alveolus ; 15% , it affects the anterolateral part & spread to the floor of
the mouth , 30% shows bony destruction (by x-ray) , Ca. of the gingiva generally affect the
premolar & molar areas .
It is either leucoplakia , exophytic or ulcerating , 50% invade the underlying bone , spread
through the lymphatic & nerves by infiltration & emboli (spread through the mandible
either neural spread or medullary spread) .
5. Ca. of the upper alveolus & hard palate , 5% & 3% , uncommon , usually salivary gland
tumor , usually in India (habit of smoking chuttas with burning end inside the mouth) ,
often leucoplakia , usually elderly male .
Staging of the oral carcinoma
Tx : tumor can't be assessed .
T0 : no evidence of primary tumor .
Tis : carcinoma in situ .
T1 : tumor < 2 cm in greater diameter
T2 : tumor measures > 2 cm , but not >4 cm in greater diameter.
T3 : tumor > 4 cm in greater diameter .
T4 : tumor invade adjacent structures like tongue muscles , maxillary sinus , bone & skin .
Stage 0 : Tis N0 M0
Stage I : T1 N0 M0
Stage II : T2 N0 M0
Stage III : T1 N1 M0 or T2 N1 M0 or T3 N0-1 M0
Stage IV : A (T4/anyT N0-1/N2 M0) or B (anyT N2 M0) or C (anyT anyN M1)
Lecture notes in
Prognostic factors
1. Site of the tumor & depth of it (size) , large one increase the possibility of LN
metastasis .
2. Type of histopathology , high grade , high chance of LN metastasis .
3. Presence of perineural spread .
4. Level & size of Metastatic LN .
5. Mandibular invasion .
Management
- History ; small painful ulcer , the pain radiate to the ear , other features , toothache , loose
teeth , ill fitting dentures & s.t. presented as palpable LN .
- Examination ; with head mirror & two tongue depressors , we examine the teeth , alveolar
margins , retromolar trigon , sulci , duct of the parotid , tongue , floor of the mouth , also
we palpate the oral cavity & neck .
- Investigations ;
1. Routine preoperative work up ; CBP , blood biochemistry , …etc .
2. Investigations for HIV & syphilis .
3. Biopsy , under LA or GA , it is unwise to do it under LA because this will increase the
metastasis , if less than 1 cm , then excisional biopsy under GA with clearance of the
margins of the lesion to the depth of < 5mm , then wait & see if greater thckness , then
do prophylactic neck dissection & postoperative radiotherapy .
4. Radiology ; we assess the state of the dentition , site & size & extent of the primary
tumor , the tumor depth , mandibular invasion & assess the neck , this is done via CT ,
MRI , bone scan & U/S , also we do CXR , U/S for the liver (to discover the metastasis)
- Treatment policy , the planning of Rx depends on ;
1. Size & site of the tumor .
- T1 & T2 , either by surgery or radiotherapy(either interstitial implanted or external
beam) , the survival rate about 80% , anterior lesion by mplanter radiation ,
posterior lesion by surgery (preferable) .
- Large T2 & small T3 , by surgery .
- T4 , high dose of palliative radiation +/- chemotherapy or just palliation .
- T1, T2 N0 by surgery or radiation , T3, T4 N0 by surgery , T1-4 N1-3 by surgery or
radiation .
- Wide excision of the anterior floor lesion may cause Andy Gump deformity , the soft
tissue defect managed by free tissue transfer .
- Lymphoma by chemotherapy & radiotherapy .
- Sarcoma by wide resection with radiation & chemotherapy .
2. Status of dentition .
3. Mandibular invasion ; large tumor increase the possibility of mandibular invasion
(assessed by CT , MRI & bone scan) , this need wide excision & postoperative
radiation .
4. Age of the patient .
5. Elective neck management .
- Palpable neck LN should be Rx by surgery .
- T1 & T2 + N0 ;
a. if the primary lesion Rx by radiation , then the neck irradiated prophylactically
b. in midline tumor , give radiation to both sides of the neck .

Lecture notes in
c. if the primary tumor managed by surgery , then the neck should be managed by
surgery .
d. also , tumors > 5mm , do selective omohyoid (level I-III) ND , or extended
supraomohyoid (level I – IV , anterolateral) ND .
6. Appropriate for of reconstruction .
- Access to the oral cavity
We should excise 2 cm safe margin which may affect the function especially speech &
deglutition (although the surgery is simple for early accessible lesion) , in compared to
radiotherapy that there is no impairment of function , the surgery composed of exposure ,
excision & reconstruction ;
1. Exposure
The most important factor in determining the survival of the patient with surgery is
adequate exposure & excision of the tumor , adequate exposure is achieved by many
ways ;
- Peroral approach ; advantage ; without external incision , disadvantage is the
limited access , it indicated in ; suitable for small anterior lesions (anterior lesion of
the tongue , upper jaw & lower alveolus) .
- Pull through procedure ; external & peroral approach , the tumor can be excised by
combination of peroral approach 7 external approach in which the check & upper neck
flap is elevated but the mandible & lip are intact & not divided .
It suitable for lateral tongue lesions & tumors of the floor , its advantage in good
cosmetic results (intact lip & mandible) , but its disadvantage are the division of the
mental nerve causing chin anesthesia , in this primary tumor excised after neck
dissection
- Lip split , it involve splitting of the lower lip in the midline & the check flap is
elevated which can be combined with hemimandibelectomy (if the mandible is involved
& should be resected) or mandibulotomy (if not involved) .
It is indicated for more posterior lesions , & its disadvantage is the scar at lower lip .
2. Excision
- Adequate exposure is the key for adequate excision .
- The minimum for surgical resection is 2 cm safe margin .
- The tumor should be visualized in 3 dimensions & the margins of the normal tissue
should be excise in 3 dimensions .
- The tumor may be deeply infiltrated & so palpation of the tumor is the most
important in assessing this deep extent .
- Frozen section is helpful to determine the adequacy of the safe margins .
- Fixation of the tumor to the mandibular periosteum or minimal invasion may allow
marginal resection with preservation of the mandibular arch .
- When there is radiological evidence of bone erosion , full thickness segment should
be taken .
3. Reconstruction of the defect
- It should not interfere with the excisional surgery .
- The function should be quickly restored .
- It should not increase the morbidity & mortality .
- No cosmetic defect , should be completed as quick as possible .
- Should be avoided when prosthesis are available .
- The options in reconstruction include ;
Lecture notes in
a. Split skin graft ; it is of limited use , only used if there is vascular bed on which
the graft can be sutured e.g. superficial tumors of the tongue , Buccal tumors &
floor of the mouth tumors .
b. Primary closure of the defect following excision ; in small tongue tumors ,
reasonable primary closure , in large tongue tumors with big defect , so the
primary closure compromise the function .
c. Flap repair ;
(1) Local flaps ;
- Buccal flaps , local flap constructed from the Buccal mucosa & rotated
into small defects .
- Lingual flap , flap taken from the tongue on one side & rotated to close a
large defect .
- Nasolabial flap , of limited value .
(2) Distant flaps ; like temporal & deltopectoral flaps .
(3) Myocutaneous flaps ; like pectoralis major flap , trapezius flap or
latissmus dorsi flaps .
(4) Free flaps ; with microvascular anastamosis .
d. Reconstruction of the mandible ; difficult , when do hemimandibulectomy, the
defect best left not reconstructed , full thickness mandibulectomy need
reconstruction (which may be immediate or later on) , there are 5 mathods ;
(1) Replacement with iliac crest flap or graft .
(2) Cancellous bone graft .
(3) Using AO plate .
(4) Using osseomyocutaneous flap .
(5) Free microvascular bone graft .
- Salivary gland tumors ;
90% of the minor salivary gland tumors in oral cavity are malignant , managed by surgical
excision with postoperative radiotherapy , especially for adenocystic Ca. , neck dissection
only if there is palpable LN .
- Melanoma ; managed by wide surgical excision with ND if palpable LN
N0 N1-3
T1 Surgery + implanted radiation Surgery + postop. Radiation
T2 Surgery + postop. Radiation Surgery + postop. Radiation
Or implanted brachytherapy
- Other modalities of treatment are ;

a. Cryotherapy , difficult to control the depth with freezing , so imprecise margin of
excision
b. Electrocoagulation ; same critism .
c. Co2 laser , helpful in remove superficial dysplasia & to Rx osteoradionecrosis of bone
Lip cancer
It include mucosal or vermilion surface of the anterior limit with the junction of the mucosa
& skin , the epithelium is sequamous epithelium containing accessory salivary glands .

Lecture notes in
The bllod supply from the facial artery (superior & inferior labial branches) , the lymphatics
drains the upper lip into the submental , submandibular , preparotid & parotid LN , & the
lower lip into submental & submandibular LN .
Its incidence about 25-30% , the majority of it are SCC , small percentage is salivary gland
tumors , keratoacanthoma , basal cell ca. & melanoma may be seen in the lip , also dysplasia
(premalignant)may be seen .
The presentation as ;
1. Visible ulcer with bleeding & crustation .
2. LN , superficial or deep cervical LN .
3. The upper lip tumors are more aggressive with poor prognosis .
Diagnosis is by incisional biopsy & the staging is the same as oral carcinoma .
Management ;
- T1 & T2 by surgery or radiotherapy .
- Large T4 , by surgery & radiation , especially if with ; Metastatic neck disease , doubtful
margin of excision (which should be 2 cm) , extracapsular spread , or more than one LN
involved .
- Also require reconstruction .

Lecture notes in
Salivary glands
Developemental Anatomy
The major salivary glands develop in the sixth to eighth weeks of embryonic life as
outpouchings of oral ectoderm into the surrounding mesenchyma . The primordia originate
at the sites of the eventual duct orifices, and as they grow, they develop into elaborate
tubuloacinar systems. The parotid anlage grows posteriorly as the facial nerve advances
anteriorly and eventually surrounds the nerve with glandular tissue. As the mesenchymal
capsule surrounds the gland, it entraps lymph nodes and sends projections into the gland
itself. The minor salivary glands arise from oral ectoderm and nasopharyngeal endoderm
and form simple tubuloacinar systems.
Surgical anatomy
The parotid gland is the largest of the major salivary glands and lies in the preauricular
region deep to skin and subcutaneous tissues . Its acinar cells are mainly of the serous
secreting type. The facial nerve divides the gland, by definition, into a large supraneural
gland and a smaller infraneural component. The parotid compartment is the triangular
space that contains the parotid gland and its associated vessels, nerves, and lymphatics. The
parotid compartment is bounded superiorly by the zygoma, posteriorly by the external
auditory canal, and inferiorly by the styloid process, the styloid muscles, and the internal
carotid and jugular vessels. The anterior margin of the gland forms a diagonal from the
gland’s superior to posterior boundaries superficial to the masseter muscle. In addition, a
small tail of parotid tissue extends posteriorly toward the mastoid process and overlays the
sternocleidomastoid muscle.
Stensen’s duct arises from the anterior border of the gland, 1.5 cm below the zygoma. The
duct, which courses approximately 4 to 6 cm, runs anteriorly across the masseter muscle,
turns medially and pierces the buccinator muscle, and ultimately opens intraorally just
opposite the second upper molar. The buccal branch of facial nerve travels with the duct.
The parotid fascia is a continuation of the superficial layer of deep cervical fascia and is
divided into superficial and deep layers. The dense superficial fascia extends from the
surrounding musculature, from the masseter anteriorly and the sternocleidomastoid
posteriorly, and extends superiorly to the zygoma. The fascia sends septa into the glandular
tissue, which prevents separation of a surgical plane between the gland and its fascia.
Because of the presence of this inelastic capsule, a suppurative or other expansive process
in the parotid gland requires surgical drainage.
The deep layer of parotid fascia extends from the fascia of the posterior portion of the
digastric muscle and forms the stylomandibular membrane . The membrane separates the
parotid gland from the submandibular gland and stretches from the mandible anteriorly,
from the stylomandibular ligament inferiorly, and from the styloid process posteriorly.
Occasionally, parotid tissue can herniate through a weakness in the stylomandibular
membrane and lie in the lateral pharyngeal wall. For this reason, tumors deep in the
parotid gland can present as parapharyngeal masses.
The facial nerve exits the skull base from the stylomastoid foramen, which lies lateral to the
styloid process and medial to the mastoid tip. The facial nerve gives off three motor
branches as it exits the stylomastoid foramen: (a) to the stylohyoid muscle, (b) to the
postauricular muscle, and (c) to the posterior belly of the digastric muscle. The nerve can
be identified by its relationship to the surrounding structures. The “tragal pointer” is a

Lecture notes in
projection of conchal cartilage that points medially toward the stylomastoid foramen. The
nerve lies approximately 6 to 8 mm anteroinferior to the tympanomastoid suture line.
After it exits the stylomastoid foramen, the facial nerve then turns laterally to enter the
parotid gland posteriorly. It branches at the pes anserinus (goose’s foot) into an upper
temporofacial and lower cervicofacial division. The pes is usually about 1.3 cm from the
stylomastoid foramen. The two subdivisions then branch to form the five major branches:
temporal, zygomatic, buccal, marginal mandibular, and cervical. There are often small
internerve communications among the buccal, zygomatic, and temporal branches, as well as
normal anatomic variations in the branching patterns .
When the normal anatomy is distorted, as when tumor is present, the facial nerve can be
identified from several constant relationships. The buccal branch of the facial nerve follows
the course of the parotid duct and lies either superior or inferior to the duct3. The temporal
branch crosses the zygomatic arch parallel with the superficial temporal vessels. The
marginal mandibular branch runs along the inferior border of the gland superficial to the
posterior facial vein (retromandibular vein). Each of these branches can be identified
distally, then followed proximally through the gland to the main trunk of the nerve.
Occasionally, if the main nerve trunk cannot be identified by the usual landmarks, a
mastoidectomy can be performed to identify the nerve as it exits the stylomastoid foramen.
The great auricular nerve supplies sensation to the posterior surface of the pinna and the
ear lobule. It is the largest branch of the cervical plexus and is often divided during
parotidectomy. It passes around the posterior border of the sternocleidomastoid muscle and
then travels superiorly toward the pinna. This nerve can be harvested and used, if needed,
for facial nerve grafting.
The auriculotemporal nerve is a branch of the mandibular (third) division of the trigeminal
nerve. It exits by way of the foramen ovale, turns superiorly, anterior to the external
auditory canal, and parallels the superficial temporal vessels to innervate the scalp. The
nerve carries postganglionic parasympathetic fibers from the otic ganglion to the parotid
gland, which stimulates secretion. When injured during parotidectomy, aberrant
innervation to the skin can result in gustatory sweating (Frey’s syndrome).
The external carotid artery provides the major blood supply to the parotid gland. The artery
runs cephalad, parallel with the mandible, and bifurcates into its two terminal branches
(maxillary and superficial temporal arteries) at the level of the mandibular condyle. The
transverse facial artery, a branch of the superficial temporal artery, supplies the parotid
gland, Stensen’s duct, and the masseter muscle. It is accompanied by the transverse facial
vein and travels anteriorly between the zygomatic arch and the parotid duct.
The superficial temporal vein joins the maxillary vein to form the posterior facial
(retromandibular) vein. The posterior facial vein is the major venous drainage of the
parotid and lies deep to the facial nerve. The vein runs lateral to the carotid artery and
emerges at the lower pole of the gland. It then joins the postauricular vein to form the
external jugular vein. Also, the posterior facial vein joins the anterior facial vein to form the
common facial vein, which ultimately empties into the internal jugular system .
The parotid gland is the only salivary gland with two layers of nodes. The superficial layer,
consisting of approximately 3 to 20 nodes, lies between the gland and its capsule. These
nodes drain the parotid gland, external auditory canal, pinna, scalp, eyelids, and lacrimal
glands. The second layer of nodes lies deep in parotid tissue and drains the parotid gland,
external auditory canal, middle ear, nasopharynx, and soft palate. More lymph nodes are

Lecture notes in
present in the superficial lobe of the parotid as compared to the deep lobe . The two systems
empty into the superficial and deep cervical lymph systems.
The second largest major salivary gland is the submandibular (submaxillary) gland. It
comprises both mucous and serous cells. The gland lies in the submandibular triangle,
which is formed by the anterior and posterior bellies of the digastric muscle and the inferior
margin of the mandible . The gland lies medial and inferior to the mandibular ramus and
wraps around mylohyoid muscle in a C-shaped fashion to produce a superficial & deep lobe
The superficial lobe of the submandibular gland lies in the lateral sublingual space. The
deep lobe of the gland (actually first encountered during a routine submandibular gland
excision) lies inferior to the mylohyoid muscle and constitutes the bulk of the gland. The
superficial layer of deep cervical fascia splits to envelop the gland. Wharton’s duct exits
from the medial surface of the gland and travels between the mylohyoid and hyoglossus
muscles onto the genioglossus muscle. It then opens intraorally lateral to the lingual
frenulum at the floor of the mouth. The duct is approximately 5 cm in length. As the duct
exits the gland, the hypoglossal nerve lies inferiorly and the lingual nerve superiorly.
The submandibular gland is innervated by the sympathetic and parasympathetic nervous
systems, which stimulate the gland to produce mucoid and watery saliva, respectively. The
parasympathetic supply is from the chorda tympani nerve, which is a branch of the facial
nerve. The chorda carries preganglionic parasympathetic fibers to the submandibular
ganglion by means of the lingual nerve. At the submandibular ganglion, the fibers synapse
onto postganglionic parasympathetic fibers that stimulate the gland to produce saliva. The
sympathetic fibers originate in the superior cervical ganglion and travel with the lingual
artery to the gland.
The facial artery provides the major blood supply to the gland. The artery, which is a major
branch of the external carotid artery, grooves the deep portion of the submandibular gland
as it courses superiorly and anteriorly. At the superior aspect of the gland, it passes
laterally and curves around a notch in the mandible to supply the face. The anterior facial
vein drains the gland. The marginal mandibular branch of the facial nerve lies superficial
to the anterior facial vein. Ligation of the vein and retraction superiorly are one technique
used to protect the nerve during submandibular gland excision.
Lymph nodes are present between the gland and the capsular fascia but not deep in
glandular tissue. The nodes drain into the deep cervical and jugular chains.
The sublingual gland is the smallest of the major salivary glands and lies just below the
floor of mouth mucosa . It contains primarily mucus-secreting acinar cells. The gland is
bordered by the mandible and genioglossus muscle laterally and the mylohyoid muscle
inferiorly. The submandibular duct and lingual nerve travel between the sublingual gland
and the genioglossus muscle. In contrast to the parotid and submandibular glands, no true
fascial capsule surrounds the sublingual gland. Approximately ten small ducts (ducts of
Rivinus) exit the superior aspect of the gland and open intraorally along the sublingual fold
or plica of the floor of the mouth. Occasionally, several of the ducts may join to form a
major sublingual (Bartholin’s) duct, which then empties into Wharton’s duct.
Like the other major salivary glands, the sublingual gland is innervated by both the
sympathetic and parasympathetic nervous systems. The lingual nerve carries postganglionic
parasympathetic fibers to the gland from the submandibular ganglion. The facial artery
carries the sympathetic fibers from the cervical ganglion. The sublingual branch of the
lingual artery and the submental branch of the facial artery provide the blood supply to the

Lecture notes in
sublingual gland. The venous drainage is by the corresponding veins. The major lymphatic
drainage is to the submandibular nodes.
The minor salivary glands are mucous, serous, or mixed glands that line the entire oral
cavity and number about 600 to 1,000. Each gland has its own simple duct that empties
directly into the oral cavity. The glands are concentrated in the buccal, labial, palatal, and
lingual regions. They can also be found in the superior pole of the tonsils (Weber’s glands),
tonsillar pillars, and base of the tongue. Minor salivary gland tumors most often arise in
glands located in the palate, upper lip, and cheek.
The blood supply, venous drainage, and lymphatic drainage of the glands correspond to
those of the region of the oral cavity in which the glands are located. Most of the glands
receive parasympathetic innervation from the lingual nerve; however, the glands located in
the palate receive their supply from the sphenopalatine ganglion by way of palatine nerves.
Physiology
The major function of the salivary glands is the production of saliva. Saliva is secreted in
the oral phase of swallowing, where it lubricates and moistens foods to facilitate
mastication. Saliva cools hot foods, buffers chemicals, and continuously lavages the oral
cavity. In addition, salivary mucins concentrate on the mucosal surfaces and protect against
desiccation and chemical irritation. Saliva is important in the prevention of dental caries
and has been shown to play an active role in the enamel formation of maturing teeth by
providing a rich supply of inorganic ions (calcium, fluoride, phosphate, magnesium).
Saliva also contains antibacterial compounds such as lysozyme, secretory IgA, and salivary
peroxidase (thiocyanate dependent factor). Lysozyme agglutinates bacteria and activates
autolysins. Secretory IgA, the major immunoglobin found in exocrine secretions, interferes
with microorganism adherence. Salivary peroxidase is involved in the breakdown of
salivary thiocyanate, whose breakdown products interfere with bacterial cell metabolism by
oxidizing the enzymes involved in glycolysis.
Suggest that salivary flow rate actually is more important in oral hygiene than any of
antimicrobial factors identified.
Changes in the body’s volemic status are reflected in salivary gland secretion. Hypovolemia
causes glandular dehydration and therefore thirst. In addition, mercury, lead, sulfa, iodine,
morphine, antibiotics, and some viruses are actively excreted in saliva; however, their
excretion does not play an important role in homeostasis. Mercury poisoning can manifest
as stomatitis and lead poisoning by the gingival deposition of lead. The rabies and
poliomyelitis viruses are excreted into saliva and can be transmitted in this manner.
Secretory IgA antibodies to the human immunodeficiency virus (HIV) have also been
isolated from the saliva of infected persons; however, it is unclear whether the virus is
transmissible by this route.
The production of saliva is an active process that begins proximally in the acinus and is
modified distally by the ducts. The secretory unit refers to the acinus, secretory tubules, and
collecting duct . The acinar cells and proximal ducts are surrounded by myoepithelial cells
that contract to expel preformed secretions from the glandular cells. The acini secrete
saliva, which travels by the intercalated ducts to intra- and interlobular ducts, which
ultimately empty into larger collecting ducts. The intralobular and interlobular ducts make
up the secretory tubules, which are involved in salt and water transport. As previously
described, the parotid and submandibular glands have elaborate tubuloacinar systems,

Lecture notes in
whereas the sublingual glands have simple systems in which the interlobular ducts empty
into 10 to 12 separate collecting ducts.
Because the parotid gland has only serous acinar cells, it secretes a thin, watery saliva,
devoid of mucins. The sublingual gland has only mucous acinar cells and thus produces a
more viscous saliva. The submandibular gland contains acinar cells of both types and
produces a mixed (serous and mucous) saliva. The minor salivary glands contain acini that
are serous, mucous, or mixed.
The Secretory Process ; although once thought to be a passive ultrafiltration process, the
production of saliva is now known to be an active process involving cell synthesis and
active transport. The secretion of saliva involves two interrelated processes: primary
secretion and ductal secretion. The primary secretion is produced by the acinar cells and
has an electrolyte composition and osmolality similar to that of plasma. As the secretion
moves distally through the tubule, modifications on the primary secretion are made,
producing a hypotonic fluid.
Histologic examination of the acinar cells reveals marked similarity with other protein-
secreting cells. The secretory (zymogen) granules contain most of the organic components
of the primary secretion. Serous acinar cells produce secretory granules with amylase,
whereas mucous cell granules contain mucin.
Electrochemical studies of acinar cells reveal that active transport of sodium, potassium,
and chloride ions is also involved in production of the primary secretion10. Resting acinar
cells show a membrane potential of -20 to -35 mV. Upon stimulation by the autonomic
nervous system, the cells hyperpolarize (become more negative) as a result of the efflux of
K+ and the influx of Cl . This hyperpolarization, which occurs contrary to other excitable
cells that depolarize upon stimulation, is known as the secretory potential.
As the fluid moves distally, the ducts alter its composition by the secretion of electrolytes,
water, and organic solutes and by the resorption of water and electrolytes. The degree of
modification of the primary secretion by the ducts is dependent on the rate of salivary flow.
At rapid flow rates, there is little time for secretion and resorption of water and ions, so the
final fluid produced is much like the primary secretion (but always hypotonic to plasma). At
slower flow rates, there is ample time for modification of the fluid; therefore, the fluid
produced is increasingly hypotonic. The net effect of ductal transport is a decrease in
sodium and an increase in potassium concentrations.
Autonomic Innervation ; stimulation of salivary gland secretion by the parasympathetic
nervous system (PNS) produces an abundant, watery saliva. Preganglionic parasympathetic
neurons originate in the salivary nuclei of the brainstem, synapse in autonomic ganglia, and
enter the salivary glands by their sensory nerves. The parotid gland receives its PNS
innervation from the glossopharyngeal nerve (cranial nerve IX). The parasympathetic fibers
are carried to the otic ganglion by the lesser superficial petrosal nerve. The postganglionic
fibers are then directed toward the parotid gland by the auriculotemporal nerve (branch of
cranial nerve V 3). The submandibular and sublingual glands receive PNS fibers from the
chorda tympani nerve (branch of cranial nerve VII), which travels with the lingual nerve.
The fibers synapse at the submandibular ganglion. Postganglionic parasympathetic fibers
release acetylcholine in close proximity to the glands, and stimulation occurs by way of
passive diffusion of neurotransmitter; that is, no true synapse exists between the
postganglionic nerves and the glands.

Lecture notes in
Acetylcholine is the primary neurotransmitter of the PNS. Acetylcholine receptors can be

nicotinic or muscarinic, although only the latter appear to be involved in salivary gland
stimulation. Anticholinesterases, which block the breakdown of acetylcholine, prolong the
action of acetylcholine at the receptor sites and sustain glandular stimulation. Alternatively,
atropine, which competes with acetylcholine for postganglionic receptor sites, retards
glandular stimulation and has been used as a potent antisialagogue. Because of the
bothersome anticholinergic side effects of atropine, scopolamine and methscopolamine have
similarly been used as antisialagogues.
The sympathetic nerve fibers arise in the superior cervical ganglion and travel with the
arteries that supply the salivary glands. The sympathetic nervous system (SNS) nerves travel
with the external carotid artery to supply the parotid gland, with the lingual artery to supply
the submandibular gland and with the facial artery to the sublingual gland. Norepinephrine
is the major neurotransmitter of the SNS, and all synapses are adrenergic. Stimulation of
the gland by the SNS produces a scant, viscous saliva rich in organic and inorganic solutes.
Garrett12 showed that stimulation of the salivary glands by the PNS produces acinar fluid,
whereas stimulation of the SNS causes the release of preformed organic components.
Historically, the SNS was believed to antagonize the PNS stimulation of salivary secretion,
but Emmelin has proved that SNS stimulation actually augments the PNS-stimulated
secretion. Salivary Flow Rates ; when the salivary glands are not being stimulated by the
autonomic nervous system, they produce saliva at a rate of approximately 0.001 to 0.2
mL/min/gland. Flow rates can rise to 0.18 to 1.7 mL/min/gland when stimulated. The 24-
hour volume of salivary secretion has been estimated to be 1,000 to 1,500 mL, or an
average flow of 1 mL per minute.
Salivary flow in the unstimulated glands is produced primarily by the submandibular glands
(69%), with the parotid and sublingual glands providing 26% and 5% of the flow,
respectively . Once stimulated, the relative contributions of the parotid and submandibular
glands are reversed, with the parotid gland supplying two-thirds of the flow. The minor
salivary glands, independent of stimulation, produce about 7% to 8% of the total flow.
Hypersecretion of saliva can be secondary to excessive salivary flow rates (as high astwice
normal) or caused by flow rates that surpass the patient’s ability to swallow. Bilateral
tympanic neurectomies (bilateral parasympathetic denervation) have been used for patients
with ptyalism (drooling), with good initial results . Others, however, advocate bilateral
parotid duct rerouting with or without bilateral submandibular gland excision for long-term
management of drooling .
It has been assumed that salivary glands undergo ultrastructural changes during the aging
process that result in hypofunction and xerostomia. Salivary flow rates are independent of
age. While the acinar cells do undergo a degenerative process, the rate of saliva production
remains constant . Xerostomia in the elderly is probably the result of systemic disease or
medication side effects. The submandibular glands, which provide the majority of salivary
volume at rest, have been found to be more sensitive to metabolic and physiologic
alterations than the parotid gland .

Lecture notes in
Non-Neoplastic disorders
1. Pseudoparotomegaly ; hypertrophy of the masseter m. , aging , dental causes , tumor in
the PPS , tumor of the ITF , mandibular tumors , mastoiditis , intraparotid lesion .
2. Parotitis .
3. Metabolic parotomegaly ; obesity , bulimia .
4. Drug induced parotomegaly .
5. Radiotherapy & parotid gland .
6. Parotomegaly & HIV infection .
7. Sialectasis .
8. Sjogren syndrom .
9. Cysts .
10. Fistulae .
 Pseudoparotomegaly ; the gland contain 2ndary L.N. & 5-10 on its surface , related
to the skin , masseter m. & PPS .
Hypertrophy of the masseter ; occur in women exclusively causing square shape face (
young female) , 1stly appear as bilateral parotid eblargement & when the patient asked
to clench her teeth , bulging rippling masseter , it must be distinguished from true
parotomegaly due to bulimia .
It is caused by ;
1. Bruxism , grinding of the molar teeth , were seen on the cusps of the molars .
2. Long term orthodontic fracture due to the masseter setting jaw in the new position .
3. Kissing .
The treatment is difficult but it is necessary due to the distress of the patient ;
a. External appraoch ; leave a scar , required unnecessary parotidectomy & puts the
facial n. At risk , so remove the masseter m. .
b. Intraoral appraoch ; treatment of choice , the jaw splinted open & cut is made
along the asending ramus of the mandible , identification of the outer heads of the
masseter & remove the inner 2 heads , leaving the outer head protecting the facial n.
 Aging ; we can palpate the gland in the submandibular area in the elderlies due to
absorption of the adipose tissue .
 Dental causes ;
1. Infection ; spread to the LN within or around the parotid & LN in the submandibular
triangle .
2. Drainage of the lower incisor or canine below the myelohyoid line , sometimes
Ludwig's angina which involve the submandibular glands .
3. Tissue odema in the ITF & between the masseter heads cause facial swelling .
 Tumors of the PPS ; any tumor in this space like chemodectoma , glomus vagale
tumor , schwanomas of vagus or symp. Trunk LN enlargement , T.B or secondaries
will push the parotid outwards (fullness) .
 Tumor of the ITF ; this space lies anterior to the PPS , so tumor within it push the
parotid by escaping through the mandibular notch or under the zygomatic arch .
 Mandibular tumors ; osteosarcoma , chondrosarcoma of the mandinle (ascending
ramus .... parotid , body .... submandibular) .
 Mastoiditis ; subperiosteal abscess drains into the sternomastoid or digastric m.
Lifting the tail of the parotid (like enlargement) .

Lecture notes in
 Intra parotid lesions ; facial n. Neuroma , anurysm of the temporal artery , parotid
cyst , LN enlargement in or around the gland (ear infection or 2 ndary) , this can be
memiked by Warthin's tumor , branchial cyst , hydiated cyst or cystic mixed cell
tumor .
 Parotitis
Pathogenisis ;
1. Viral parotitis ; Mumps (commonest infection in childhood) , Echo or Coxakie virus
(in toung adults the incidence increased) .
2. Bacterial parotitis ; staphylococcal ascend along the duct in the dehydrated postop.
patient who lack resistance to infection .
3. Fungal parotitis ; uncommon due to ascending from oral Candidiasis .
4. Secondary to duct obstrubtion parotitis ; due to epithelial debris or stones in the
submandibular gland or stenosis of the duct secondary to ductal infection , if the
supervene by infection will lead to parotid abscess .
5. Secondary to lymphangitis ; within the parotid the were 10-20 LN , around 5-10
draining the skin of the scalp , face , ears , eyes & posterior parts of the oral cavity ,
infected pireced ears is the commonest & preauricular pits , this nodes may resolved
or proceed to abscess formation .
6. Chronic parotitis ; like T.B of the LN surrounding the parotid , sarcoid of the parotid
& submandibular , actinomycosis & leprosy ... symptoms produced when the patient
eat causing salivation to occur with the obstructed duct causing the tense gland to
swell more with severe pain (in case of parotitis prior to abscess formation) .
Clinical features ; severe pain & fever (this incresed by eating) , painfull swelling
cause spasm of the m. Of mastication & masseter causing trismus which inturn increase
the chance of opportunistic bacterial infection following viral parotitis due to poor oral
hygien .
Tenderness over the parotid area & pain when ask the patient to sip a little lemon juice
(parotitis rather than LN infection) , the oral cavity examined for dental infection (by hot
& cold stimuli) , the secretion looked from the duct (type of it) , the external ear
examined for signs of infection or COM .
Investigations ;
1. Labrotary ;
a. Blood ; increased WBC which is lymphocytosis (viral) , neutrophilia
(bacterial) , increase ESR (if very high ESR the could be Sjogren's syndrom) ,
also viral titer for mumps should be neasured (if +ve then mumps , if –ve then
echo or coxsakie) .
b. Bacteriology ; secretions from the duct cultured to identify the causative agent
, if T.B or sarcoidosis suspected we ask for the opinion of the ophthamologist
for uveitis (Heerford's syndrom) .
2. Radiology ;
a. Plain radiographs ; to see if there is submandibular gland stone .
b. Sialography ; contraindicated in the acute phase , 1-2 weeks later it is
therapuetic in washing out the duct system , it is useful be gives idea of duct
blockage & Dx for the sialectasis & duct distoration .
c. Scanning , scan with Tc99 , but this abandond due to false +ve & -ve results .
3. FNA ; not required , but may carried out , if +ve helpful .

Lecture notes in
Treatment ;
A. Medical (conservative) Rx ;
1. Bed rest , oral hygein (inspit of trismus) , & high caloric intake , milk drink without
any flavour to support the nutrition .
2. Analgesia & local heat application .
3. adrinaline applied to the duct to decrease the odema & promote the secretion &
saliva .
4. Clindamycine , the only one which is secreted through the saliva ,but , cause
psuedomemberanous colitis as side effect .
5. If T.B or leprosy proved then Rx with anti T.B or anti leprotic .
6. Rx the lymphadenitis by Rx the primary cause either by antibotics or surgically .
B. Surgical Rx ; this applied on stone blocks the submandibular duct with secondary
sialadenitis , the stone can be removed perorally allowing the abscess to drain & the
condition resolved with antibiotics .
In parotid abscess the facial flap lifting with multiple incision over the gland .
 Metabolic parotomegaly ; gout cushing's syndrome myxodema & DM all associated
with parotomegaly , also it closely related nutritional abnormalities , those who
undergo starvation the fat arround the gland disappear leading to parotomegaly
(which show alveolar hypertrophy histologically .
 Obesity & the parotid ; carbohydrate diet causig increase the salivary amylase
activity leading to parotomegaly , bulk diet lead to compensatory enlargement of the
parotidby increase in acinar cell size due to increased functional activity of the
parotid , also fatty infilteration of the parotid & when the obese get weight loss the
parotid remain large .
 Bulimia nervousa ; associated with parotomegaly (when binge eating followed by
self induced vomiting) , the aetiology unknown , but they suggest is due to
compensatory salivary gland hypertrophy or due to associated malnutrition .
There is decrease in the salivary flow rate but, increase in amylase level.
 Drug induced parotomegaly ; Dextropropoxyphane & high oestrogen CCP which
cause epithelial shedding within the duct causing epith. mud & blockage of the duct
forming stone in the submandibular duct leading to painful parotomegaly &
submandibular enlargement .
 Radiotherapy & the parotid gland ; DXT of the head & neck causing perminant
damage to the salivary gland according to the dose –time- volume , leading to dry
oral cavity with subsequent complications like candidiasis .
Radiotherapy (100 CGY) leading to damage to the acinar cells , the regeneration
occur when the dose is low & then following high doses loss of acinar regeneration
& dut proliferation become marked .. also it affect the blood vessele & nerves ,
inturn affect gland function .
 Paotomegaly & HIV infection ; AIDS cause bilateral parotid gland enlargement
with multiple cysts (on MRI & CT scan) , caposi sarcoma & Malignant lymphoma ,
this should be confirmed by US guided needle biopsy .
 Salivary gland cyst ; they are benign swellings mostly secondary to sialectasis or
dermoid tumors (pleomorphic adenoma , warthin's tumor , mucoepidermoid tumor ,
adenocarcinoma) .

Lecture notes in
The majority are minor salivary gland mucocele (80%) , parotid duct cyst(10%) ,
lymphoepithelial cysts (6%) , ranulae (<1%) .
Mucocele ; extravasation type (80%) following repeated minor mucosal trauma ,
affect young adults , it lies at lower lip (80%) , check & floor of mouth (15%) , palat ,
tongue & upper lip (5%) ... while retention one (20%) due to duct obstruction by
microlith or bend in the duct , affect older patients , both are Rx by excision .
Ranulae ; bluish swelling sublingually , affecting the sublingual gland , treated by
marsubilization or excision .
 Salivary fistula ; usually of the parotid , inernal or external , congenital or acquired
, the internal one drain into the mouth & not noticed , the conginital are rare & arise
from aberrant or accessory salivary tissue or associated with branchial cleft
abnormalities .
The acquired parotid fistulae due to surgery , facial truma or parenchymal sepsis .,
those developed after lumpectomy or parotiectomy usually arise from the gland
parenchyma drain through the suture line which will close spontaneously (minimal
leakage occur during meals , then closed) , to prevent it's occurance , the duct must
be divided well foreward & ligated , saliva may be collected under the flap , this
should be aspirated & apply pressure dressing .
Fistula which arise from the main duct causing profuse leak even at thought of food
& need operation to close it , it is usually due to deep facial wound & the facial n.
may also damaged , it is difficult to control & there are 3 lines of Rx ;
1. reduction of saliva production ; by drugs , irradiation (wihich carry risk of
later Ca) , tympanic nuerectomy & duct ligation .
2. Operation on the fistula ; excision , diversion into the mouth , reconstruction
of the damaged duct (which may be demonestrated by sialogram) , it may
need parotiectomy due to uncertain outcome .
3. Removal of the gland ; partial or total conservative parotidectomy .
Fistula of submandibular gland closed spontaneously , if not gland should be excised
 Sialectasis ;
Pathogenesis ; the cause is unknown , it is the analouge of bronchiectasis , progressive
necrosis & distengration of the alveoli which then coaleses forming cysts & the debris from
the cysts pass along the duct causing block leading to hypertrophy , stenosis & duct
dilatation .
The parotid is serous gland & low in calcium , remain mud lead to block the duct (but , not
like stone) by soft easy removeable by build up of saliva (s.t. radiolucent stones)
The submandibular gland is mixed seromucinous & high in calcium , so the epithelial
debris calcified (radiopaque one) .
The symptom usually start when the duct blocked causing swelling of the gland in response
to secretomotor stimuli like eating or drinking .
The gland usually clear itself , s.t. swelling stays for minutes or hours , s.t. for days which
become secondarly infected forming abscess which either fibrosed or ruptured or drained .
Clinical features ;
1. History ; pain , swelling of the gland during meal , remain for minutes , hours or days ,
no fever , in children Dx wrongly as mumps more than once , 50% resolved & only few
adults need surgery .

Lecture notes in
2. O/E ; stone in the submandibular gland may be felt in bimanual palpation , odematous
mouth of the duct , the same appearance seen in parotid , do massage to see if there is
any drainage of saliva from the gland .
Investigations ;
1. Labrotary ; useless .
2. Radiology ; sialogram is Dx , plain film also useful to see any stone , CT scan with
sialogram is of little value (but attractive film) , sialogram may show 6 appearances;
a. may be normal .
b. overfilled ; sialectasis .
c. fail to canulate the duct ; odematous duct with cannulation insisting , difficult
to cannulate so leading to stenosis which is iatrogenic .
d. obstruction duct ; stone in the submandibular & mud in the parotid
obstructing the duct .
e. true picture of sialectasis ; cystic sialectasis in which the alveoli coalesce &
form large spaces together with duct stenosis & dilatation .
f. false picture of sialectasis ; glandular or saccular sialectasis in which the
lipidol or radioopaque medium lie in stroma outside the alveoli .
(e) & (f) are the classical pictures of sialectasis .
Treatment ;
1. No Rx ; ny sialogram , therapuetic by washing out the duct & alveolar system , so
we advice the patient to finish the meal by citrus drink which increase salivation
& then massage the gland , washout any debris & stop collection (successful in
majority of patients) .
2. Peroral removal of the calculus (in submandibular gland) ; the stone looked &
the duct blocked proximally then the stone removed & the duct marsupialized .
3. Marsupialization of the duct ; either like above or in case of parotid duct stenosis
of dental origin .
4. Ligation of the duct , illogical & inadequate .
5. Duct dilatation ; illogical .
6. Tympanic neurectomy ; divide the Jacobson's n. which cross the promontory , s.t.
combined with division of corda tympani , this work for 6 months then alternative
pathway develope & symptoms recure .
7. Removal of submandibular gland ; in case of sialectasis & stones , this is difficult
in the presence of sailadenitis , we should certain that the stone removed with the
gland & take care to the mandibular branch of facial n.
8. Total parotidectomy ; Rx of choice inspite of the risk on the facial n. , due to
recurrent sialadenitis , if we did superficial parotidectomy this lead to fistula
formation from the deep lobe .
 Sjogren's syndrome ;
In 1933 , Henrik Sjogren , Finnish ophthalmologist describe a syndrome of
xerostomia & keratoconjuctivitis sicca in 33 patients with rheumatoid arthritis in 23
of them but don't mention a parotid gland enlargement .
Classification ;
1. Primary Sjogren's syndrome (sicca complex) ; xerostomia & xerophthalmia
with no connective tissue component, charcterized by dry mouth ,

Lecture notes in
psychological upset , seldom have salivary gland involvemebt , 1/6 of patients

develope lymphoma .
2. Secondary Sjogren's syndrome ; w xerostomia & xerophthalmia with
connective tissue component (50% RA , other are SLE , scleroderma &
polymyositis , also primary biliary cirrhosis , autoimmune liver dis. & ch.
graft versus host dis.) , 30% have reccurent attacks of parotitis , small
minority develope lymphoma .
3. Benign lymphoepithelial lesion (myoepithelial sialadenitis); localized to the
parotid , some regard as prelymphomatous condition .
4. Aggressive lymphocytic behaviour ; disease of the parotid which regarded as
pseudolymphoma .
Epidemiology ; common in the northern Europe , it is the second most common
autoimmune disease following RA , many elderlies have many of syndrome
symptoms without the immunological profile , 30% of RA have Sjogren's
syndrome .
Clinical features ; it is dease of multisystems , but especially the oral cavity , eyes
, parotid & other salivary apparatus .
1. Oral symptoms ; dry mouth with 2nd ary candidiasis , stomatitis , glossitits
& subsequent dental carries .
2. Eye symptoms ; F.B sensation in the eye , burning , redness , itching ,
photosensitivity & inability to tolerate a contact lens (due to keratoconj.
Sicca) .
3. 2/3 rd of the patients have no parotid enlargement , 10% feel it , 20% show
it clinically with high chance to develope lymphom.
4. Associated systemic problems , primary biliary cirrhosis , ch. Hepatitis ,
vasculitis , ch. graft versus host disease , cryoglobulinaemia , polyarthritis
& hypergammaglobulinaemic purpura , thyroiditis (15%) & pancreatitis ..
Also achlrohydria , disease of the oesophageal motility & web formation ,
go to the otolaryngologist for nasal crusting , epistaxis , serous OM ,
laryngitis sicca & persistant cough with tenacious sputum & sticky
secretion in the nasopharynx .
5. General exam . ; for the presence or abscence of connective tissue
disorders & abnormalities of other organs .
Investigations ;
1. Blood exam. ; ESR usually increased , increase in all immunoglobulin esp.
IgG , RF & ANF with many autoantibodies .
2. Specific immunological tests ; class 2 Ag like HLA A1 &B8 & DR3 are
examined (in primary dis. Three times more than in 2 ndary dis.) , specific
Ag for the syndrome are SSA & SSB (common in 1ary than 2ary) .
3. Schirmer's test ; putting special strips into the lower fornix for 5 min ,
wetting of less than 5 mm in 5 min will be Dx for xerophthalmia .
4. Salivary flow rate ; measured by Carlesson-Crittenden cups which are
suction cups placed over the parotid duct , ask the patient to suck a lemon ,
flow less than 0.5 ml in a min Dx for xerstomia .
5. Labial biopsy ; Dx for the syndrome , under LA 4 globules of fat obtained
from the back of lower lip , four grades results ;

Lecture notes in
a. Grade 1 ; slight lymphocyte infilteration .

b. Grade 2 ; less than 50 lymphocytes per 4 mm .
c. Grade 3 ; 50 lymphocytes per 4 mm .
d. Grade 4 ; more than 50 lymphocytes per 4 mm .
The distribution of the lymphocyte is important periductally than diffused .
6. Radiology ; not Dx , either normal or globular sialectasis , but indicate
that there is an abnormality in the duct allowing leakage of lipiodol into
the gland stroma .
Natural history ; CMV infects the salivary ducts & ducts elsewhere in the body , the
ducts act as Ag & the B-lymphocyte proliferate as well as lymphoma & anaplastic
Ca present (non-Hodgkin's lymphoma) .
Treatment ;
1. steroids ; for bouts of parotid swelling & seldom so severe that require
the immunosuppressive drugs .
2. arrificial tears & synthetic saliva ; limited comfort .
3. bromohexine ; 40 mg/d , s.t. help the tenacious cough .
4. put those patient on a lympoma follow up (important) .
5. diagnostic parotidectomy for those with parotomegally to exclude
lymphoma .
 Salivary gland disorders in children
A. Evaluation ;
1. History ; onset , duration of the symptoms , periodicity , the presence or
abscence of swelling , characteristics of secretions ,& the presence of
associated systemic disorders .
2. Examination ;
a. Bimanual exam. ; exam any mass at the anatomical site of salivary glands ,
should be DDx from cervical adenitis (preceeded by fever , URTI or dental ) .
b. Massage of the salivary glands , clear secretion from the duct .
c. Any salivary swelling should distinct ;
1. is the entire gland enlarged or just part of it .
2. if part , is the mass in or adjacent to the gland .
3. if in the gland , is the mass cystic or solid in nature .
d. associated signs like tenderness , facial n. weakness , skin involvement , or
fixity of the mass to the surrounding structures .
e. Salivary gland swelling either unilateral discrete , unilateral diffuse or
bilateral diffuse .
3. Examination of saliva ;
a. culture ; simple swabing shows mixed flora & misleading data , needle
aspiration after skin preparation (valid data) , intraoral aspiration via
catheter (valid data) .
b. cytology ; FNA & saliva collection .
c. sialochemistry (of little use in children) .
B. Radiological exam. ;
1. Plain x-ray ; dental causes & radioopaque caliculi detection .
2. Sialography ; caliculi detection , inflamatory lesion detection , assess parotid
gland trauma , obstructive & discrete swelling .

Lecture notes in
3. US ; to distinguish intrinsic from extrinsic lesion , inflamatory lesion , to

guide needle drainage of abscess or FNA for cytology .
4. CT scan ; evaluate interinsic & etrinsic masses (study of choice) , sharply
circumscribed mlesions (benign) & irregular & infilterative lesion
(inflamatory or malignant) .
5. MRI ; excellent evaluating soft tissue definition , advantage is able to provide
sagital , axial & coronal planes , avoid radiation exposure .
DDX of parotid gland mass
1. Discrete parotid gland enlargement (CT / Sialogram / FNA)
1.1. Fluctuant (aspiration / needle biopsy)
1.1.1. Haemangioma ( observe).
1.1.2. Lymphangioma ( observe then excise) .
1.2. Firm ( wide local excision)
1.2.1. Benign ( no further Rx) .
1.2.2. Low grade malignancy ( no further Rx) .
1.2.3. High grade malignancy ( rRadiotherapy / Chemotherapy) .
2. Unilateral diffuse parotid gland enlargement (CT / Sialogram / Biopsy)
2.1. Inflamatory disease
2.1.1. Acute
2.1.1.1. Bacterial sialadenitis ( antibiotics analgesia)
2.1.1.2. Abscess (antibiotics & drainage)
2.1.2. Chronic (Sialogram)
2.1.2.1. Obstructive ; stone or stricture ( dilate , remove ,
parotidectomy)
2.1.2.2. Non-obstructive ; antibiotics (if reccurent then do
parotidectomy)
2.2. Trauma ; Observe or Explore .
3. Bilateral diffuse parotid gland enlargement (CT / Sialogram / Biopsy)
3.1. Systemic disease (Rx the primary cause) .
3.2. Viral sialadenitis
3.3. Benign lymphoepithelial disease ; either controlled by autoimmune Rx
then only observe , if not (reccurent sialadenitis) & the medical Rx not enough then
could do parotidectomy .
Neoplastic disorders
Salivary gland neoplasms are a diverse group of benign and malignant tumors with a wide
range of biologic behaviors. Management requires accurate pathologic diagnosis because
the degree of aggressiveness and patterns of spread of these lesions depend on their
histologic profiles. The surgeon must understand the pathologic behavior of each tumor
type to develop an appropriate treatment plan.
About 80% of salivary gland neoplasms originate in the parotid gland, 10% to 15% develop
in the submandibular glands, and the remaining tumors arise in the sublingual and minor
salivary glands. The smaller the salivary gland, the more likely the salivary gland neoplasm
is malignant. About 80% of parotid neoplasms are benign , and about 50% of
submandibular tumors are benign , but fewer than 40% of the sublingual and minor
salivary gland neoplasms are benign .

Lecture notes in
Ninety-five percent of salivary gland neoplasms occur in adults. The most common benign
mesenchymal tumor in children is the hemangioma, and the most common benign epithelial
tumor is the pleomorphic adenoma . The probability of malignancy in a child is increased if
a solid nonvascular salivary mass is found. About 85% of salivary gland malignancies
found in children originate in the parotid gland. Mucoepidermoid carcinoma is the most
frequently encountered (50%) tumor type found in this age group.
An accurate histopathologic diagnosis is important for a rational approach to the
management of salivary gland neoplasms , the theories of the histogenesis of salivary gland
are ;
1. The multicellular theory states that salivary gland neoplasms arise from the
adult differentiated counterpart of the salivary gland unit. In this theory,
oncocytic tumors arise from the striated duct cells, acinous cell tumors arise
from the acinar cells, squamous cell and mucoepidermoid carcinomas develop
from the excretory duct cells, and mixed tumors arise from the intercalated
duct cells and the myoepithelial cells.
2. The bicellular theory states that the basal cells of the excretory duct and
intercalated duct act as stem cells for the mature cells in the salivary gland
unit. In this hypothesis, the mixed tumor, Warthin’s tumor, oncocytoma, acinic
cell carcinoma, adenoid cystic carcinoma, and oncocytic carcinoma arise
from reserve cells of the intercalated duct. Squamous cell carcinoma and
mucoepidermoid carcinoma arise from the reserve cells of the excretory duct.
According to this theory, neoplasms originate from the two undifferentiated
reserve cells, and the state of differentiation of the stem cell determines
whether the tumor is benign or malignant.
3. Single nueroectodermal stem cell theory ; benign & malignant tumor cell
cluster has led to a SNSC .
4. The lymphoepithelial Ca (in Asian) ; associated with EBV which gains entery to
the cells via surface C3d receptors (also for warthin's tumor) .
The world health organization’s histologic classification of salivary gland tumors
I. Adenomas
Pleomorphic adenoma
Myoepithelioma (myoepithelial adenoma)
Basal cell adenoma
Warthin’s tumor (adenolymphoma)
Oncocytoma (oncocytic adenoma)
Canalicular adenoma
Sebaceous adenoma
Ductal papilloma
Inverted ductal papillomas
Intraductal papilloma
Sialadenoma papilliferum
Cystadenoma
Papillary cystadenoma
Mucinous cystadenoma
II. Carcinomas
Acinic cell carcinoma
Lecture notes in
Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Polymorphous low-grade adenocarcinoma (terminal duct adenocarcinoma)
Epithelial-myoepithelial carcinoma
Basal cell adenocarcinoma
Sebaceous carcinoma
Papillary cystadenocarcinoma
Mucinous adenocarcinoma
Oncocytic carcinoma
Salivary duct carcinoma
Adenocarcinoma
Malignant myoepithelioma (myoepithelial carcinoma)
Squamous cell carcinoma
Small cell carcinoma
Undifferentiated carcinoma
Other carcinomas
III. Nonepithelial tumors
IV. Malignant lymphomas
V. Secondary tumors
VI. Unclassified tumors
VII. Tumor-like lesions
Sialadenosis
Oncocytosis
Necrotizing sialometaplasia (salivary gland infarction)
Benign lymphoepithelial lesion
Salivary gland cysts
Chronic sclerosing sialedenitis of submandibular gland (Kuttner tumor)
Cystic lymphoid hyperplasia in patients with AIDS .
Benign Tumors & Non-neoplastic swellings
Pleomorphic Adenoma ; the most common tumor of major salivary gland , F:M equal ,
4oyrs old , 90% of benign parotid tumors & 50% of submandinular tumor , a few
bilateral tumors have been described .
It is mixed cell tumor arise from the intercalleted duct cells & myoepithelial cells , the
tumor grows slowly & usually asymptomatic apart from lump & the facial n. never palsy
Nearly all arise in the tail of the parotid just anterior to the lobe of ear , s.t. in the
retromandibular part as either solitary deep lobe tumor or dumb bell tumor .
The tumor is smooth , superficial , round & mobile , the capsule lobulated & vary in
thickness , while the cut surface of the tumor usually greyish –white (s.t. have blue tings)
with secondary cyst formation & haemorrhage , the reccurence rate about 5% after
primary surgery & 20-30 after simple enucleation .
Warthin's tumor (Adenolymphoma) ; 6-8% of salivary gland tumor , M:F 7:1 , arise in
the hetrotrophic parotid tissue occuring within the parotid LN , the average age is 70 yrs
old , 10% bilateral & usually in the parotid tail ( the most common benign bilateral
tumor) , it is fluctuant , slow growing , smooth , soft , compressable , it is cystic once
contain mucoid fluid , solid white areas are s.t. seen due to lymphoid tissue .
Lecture notes in
Oncocytoma (oxyphil cell adenoma) ; 1% of all salivary gland tumors , F=M , rare
under 50 yrs , painless slowly growing lump arise from the striated duct cells ,
malignant variant are exceedingly rare .
Vascular tumors ;
1. Haemangioma ; usually Dx durig the 1st year of life , over half of childhood salivary
gland tumors ,F>M ,50% of patients have a cutaneous haemangioma in head & neck
It appears as soft painless mass , pathologically the parenchyma is replaced by
vasoformative elements but normal glandular lobulation is maintained .
No mangement attempt until the age of 10-12 yrs due to chance of spontaneous
regression & surgery done only if the tumor enlarging .
2. Lymphangioma ; presented at birth , F>M , the thin-walled lymph spaces invade the
parotid & adjacent tissues but don't replace the glandular parenchyma , it is either
simple lymphangioma , cavernous lymphangioma or cystic hygroma .
It is soft , fluctuant , usually transilluminated , they should removed if causing
disfiguring .
Granulomatous disease ;
1. Sarcoidosis ; usually bilaterl & diffuse , presented as salivary gland swelling ,
lacrimal gland swelling , chorioretinitis & progressive C.N. involvement (Heerford's
disease) .
2. T.B. ; rare , affect LN within or out the gland .
3. Actinomycosis ; can follow dental extraction or other oral tumors .
4. Cat – scratch disease ; wid or domestic animals to human by scratch (due to G -ve
bacilli) .
Cysts ;
1. simple retention cyst ; within the parotid are rare .
2. hydiated cyst or HIV related cyst.
3. warthin's tumors & area of pleomorphic adenoma ( the commonest cystic lesion) .
4. branchial cyst within the LN in the gland & in its surface .
Other benign tumors ;
1. Lipoma ; sually lateral to the parotid gland , it is usually unilateral & cystic .
2. Benign lymphoepithelial lesion ; arise in the intralobular ducts like punctate
parotitis , the duct dilated & thier cells disrupted & epidermoid metaplasia begins ,
the lymphocyte aggregates around the duct the duct obliterated .
3. Sjogren's Syndrome(mention above).
Malignant Tumors
They comprise about 12 per million of population , about 3-4% of all head & neck
malignancies , F=M , at the 5th decade , high risk : black , eskemo , scot , post DXT
survivors .
The parotid malignancy are ; 40% involve the lateral lobe , 10% the deep lobe , 27% both
lobes , 20 extend beyond the glandular tissue.
Prsentation of malignant tumor with facial palsy as follow ; 23-26% poorly diff. Ca. , 23-
26% adenoid cystic Ca. , 9-14% pleomorphic adenoma , 8% mucoepidermoid Ca. & 3%
acinic cell Ca. .
Prognostic factors in salivary gland malignancy ; tumor histology , grade & staging ,
anatomical site of origin , age of the patient , facial n. involvenent & experience of the
surgeon .
Lecture notes in
Staging system for major salivary gland malignancies

Primary tumor (T)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
T1 Tumor 2 cm in greatest dimension
T2 Tumor >2 cm but 6 cm in greatest dimension
T3 Tumor >4 cm but 6 cm in greatest dimension
T4 Tumor >6 cm in greatest dimension
All categories are subdivided: (a) no local extension; (b) local extension. Local extension is
clinical or macroscopic evidence of invasion of skin, soft tissue, bone, or nerve.
Microscopic evidence alone is not local extension for classification purposes.
Regional lymph nodes (N)
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension
N2 Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm
in greatest dimension, or in 6 cm in greatest dimension, or in bilateral or contralateral
lymph nodes, none more than 6 cm in greatest dimension
N2a Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm
in greatest dimension
N2b Metastasis in multiple ipsilateral lymph nodes, none more than 6 cm in greatest
dimension
N2c Metastasis in bilateral or contralateral lymph nodes, none less than 6 cm in greatest
dimension
N3 Metastasis in a lymph node, more than 6 cm in greatest dimension
Distant metastasis (M)
MX Presence of distant metastasis cannot be assessed
M0 No distant metastases
M1 Distant metastasis
Stage grouping
Stage I T1a N0 M0
T2a N0 M0
Stage II T1b N0 M0
T2b N0 M0
T3a N0 M0
Stage III T3b N0 M0
T4a N0 M0
Any T (except T4b) N1 M0
Stage IV T4b Any N M0
Any T N2, N3 M0
Any T Any N M1

Lecture notes in
Types of malignant tumors ;

Mucoepidermoid tumor ; 4-9% of salivary gland tumors , M=F , more than 90% arise
in the parotid , 8% in the submandibular &1% in the sublingual , while it is more
common in the minorsalivary glands (71% in the palate , 14% in the buccal , 9% in
the tongue & 5% in the lips )
It is the commonest salivary gland tumors in childhood (in adult it presented at 5th
decade) . it presented as solid or cystic mass usually not encapsulated , 40% have
lymphoadenopathy .
Histologically there are several types of cells presented ; epidermoid , columnar ,
clear & mucinous , s.t. it misDx as Sq. Cell Ca .
Acinic cell Ca ; 2-4% of salivary gland tumors ,, the 2 nd commonest salivary gland
tumor in childhood , M=F , usually in the 5th decade , s.t bilateral , often
encapsulated & arise from the terminal tubular intercalated duct cells , most behave
like pleomorphic adenoma & some have an aggressive malignant course , propensity
for late recurrance (even after 30 yrs after excision) .
5 year survival about 90% , 20 year about 50-60% , the recurrence rate 10% have
LN & about 15% have distant metastasis .
Adenoid cystic Ca. ; 40% of salivary gland tumors , F>M , 6th decade , unencapsulated
but appear circuscribed , have many pathological patern (types) ; cribrform ,
tubuloglandular , solid cellular & cylindromatous .
It arise from the intercalated duct with marked tendency to invade nerves with pain .
It lies (site) ; 60% minor glands(70% in oral) , 25% parotid , 15% submandibular &
1% sublingual .
Lymphadenopathy ; 8% at presentation & 7% late node appearance (15%
metastasis), distant metastasis about 40% & 70% in patient dying from the disease .
Characterized by moist & grey-pink on section .
Pleomorphic adenoCa ; malignant mixed cell tumor , originated at 1% from abinito&
the rest from pre-existing adenoma (after 10 yrs) , charcterized by still grossly
encapsulated , suspecious features are ; pain , rapid growth & infilterative to the
periphery, in about 25% metastasis to the regional LN , & 30% to the distant organs
5 year survival rate about 40% while 15 year about 19% .
Adenocarcinoma ; 3% of parotid & 10% of submandibular & minor glands , F=M , at
any age , common in children .
Charcterized by being asymptomatic mass or with typical malignant features , it is
highly malignant with high metastasis rate & low 5 year survival rate (only 10%).
Sq. Cell Ca. ; rare tumor (1%) , M :F 2:1 , 7th decade with very bad prognosis with any
Rx , charcterized by ; aggressive behaviour , no capsule , rapid growth , pain , skin
fixation ,facial n. palsy , & ulceration , 50% with LN metastasis at presentation .
Malignant lymphoepitheloid lesion ; rare tumor , occur in major & minor salivary
glands , in Eskemo & Chinies , associated with EBV ,
Sarcoma ; very rare .
Lymphoma ; arise in the intraparotid LN (swelling) , managed as other lymphomas .
Metastatic tumors ; deposited either in the LN in the gland or within the gland , 80%
orginated from the skin (melanoma or SCC) or from infraclavicular sites .
Recurrent pleomorphic adenoma ; two categories ;

Lecture notes in
1. when the recurrence can be expected after invadequate lumpectomy

for pleomorphic adenoma .
2. when the recurrence unexpected after a superficial lobectomy for
pleomorphic adenoma .
The possible causes for recurrence are ; bursting the capsule &/or inadequate
lumpectomy .
This manged with total parotidectomy with facial n. preservation .
Mangement
History ;
1.
usually unilateral (except warthin's tumor bilateral) .
2.
tumor in the tail usually pleomorphic adenoma .
3.
benign tumors grows slowly over a period of years .
4.
malignant tumors growth is rapid with pain , skin can be involved with facial
nerve palsy .
5. the inflamitory condition usually with marked fluctuation of the disease with
pain & tenderness which increase with eating .
6. in parotomegally ; usally ask about systemic disease like DM , Myxoedema ,
Cushing's disease , Cirrhosis & alcholism , drugs like pills & thiouracil .
Examination ;
1. tumors present as discrete mass (swelling) while inflamation as wholegland
enlargement .
2. tumor usually affect single gland while sialectasis , lymphoepithelial benign
lesion , Sjogren's syndrome , calculus & endocrine disease affect more than one
gland .
3. Key points of examination of major salivary gland ;
a. salivary or extra-salivary .
b. whole gland swellen or swelling within the gland .
c. one gland is affected or multiple .
d. firm or cystic .
e. finding of bimanual exam. (calculus in the submandibular ?!) .
f. medial displacement of the pharynx (deep lobe tumors ?!) .
g. pus can be expressed from the duct (infection) .
h. is there associated lymphadenopathy .
4. examination of condition outside the parotid that mimic parotomegally ;
a. masseter hypertrophy .
b. dental cyst
c. mastoiditis .
d. branchial cyst .
e. myxoma of the masseter .
f. facial n. neuroma .
g. temporal a. anurysm .
h. mandibular tumor .
i. lymphadenitis of parotid LN .
j. sebaceous cyst .

Lecture notes in
Investigations ;
1. Laboratory test ; CBP , biochemistry , ESR , protien electropheresis ,
antinuclear & rheumatoid factors .
2. Radiology ;
a. plain film ; intraoral can Dx submandibular stones (radioopaque) & can
differentiated other causes of parotomegaly , CXR in suspected sarcoidosis
or in malignant lesion like Adenoid cystic tumor .
b. Sialography ; for non-neoplastic lesion .
c. U/S ; to assesst the cystic nature of the tumor , neoplastic appear as solid
mass (except warthin's) .
d. CT scan ; the gold standard for parotid tumor investigation , assess the
extension in the deep lobe & it's relation to the 7th C.N. (with sialography) .
e. MRI ; to differentiate between & malignant by contrast film (less eficient) .
3. FNAC ; used in Dx of the salivary gland mass (depend on the access to the
pathologist & his skills) .
If the tumor is obviously malignant & involving the skin (incisional biopsy) .
4. Open biopsy ;
a. in discrete mass ; 90% pleomorphic adenoma , so incisional biopsy lead to
tumor implantation .
b. in diffuse enlargement of the salivary gland ; the incisional biopsy may be
necessary (by sublabial biopsy) to Dx Sjogren's syndrome .
c. in obeveously malignant lesion (diffuse fungating mass).
d. Inconclusive FNA .
Treatment policies ;
A . Benign tumors ;
 For parotid gland the mangement is by superficial parotiectomy (while can do
complete surgical excision for warthin's tumor) .
Technique of superficial parotidectomy ; the patient lies supine with reverse
trendelenburg position , extended neck & the head turned away , the incision begin
in the preauricular skin crease which inclines backwards ,downwards & then into
the cervical skin crease below the mandible , the skin flap elevated & the posterior
extermity of the gland is seperated from the EAC , the facial n. is founded & then
followed by using the tempromastoid sulcus as standing point , the part of the gland
which lies supeficial to the n. is pealed off together with the tumor & then the wound
closed with drain tube .
 For submandibular gland ; remove the gland through transverse incision made just
above the hyoid bone , then the flap elevated & the facial b.v. ligated , the gland
mobilized , the mylohyoid m. Retacted & the duct is severed , then remove the gland
 For sublingual gland ; remove the gland through incision done medial to the line of
the warton's duct , the lingual n. retracted medially together with the submandibular
duct , then remove the gland with the tumor .
The indication of submandibular gland removal are ; sialectasis , stones , duct
stenosis , tumors , part of RND , part of access to the para pharyngeal space .
 For minor salivary glands ; like the pleomorphic adenoma of the hard palate ; the
patient lies in the tonsillectomy position , Boyle-Davis MG applied , incision through
the mucous membrane down to the bone (hard palate) by cutting diathermy with

Lecture notes in
enuculation of the tumor by dissection from the underlying & the bone should be
drilled away through the whole thickness to ensure complete removal of the tumor ,
the patient may need denture or obturator postoperatively .
B. Malignant tumors ;
1. Surgery
 For parotid gland the mangement is by total parotiectomy (conservative)with
preservation of the facial n. (all or part) or total radical parotidectomy with
hemimandibulectomy , sacrify the facial n. , petrosectomy & RND (indicated when
there is palpable neck disease , strong evidence of LN & to facilitate myocutaneous
flap repair – if the defect large-) with/or without postop. radiotherapy .
For patients with an operable tumor or those ubfit for surgery or advanced age , the
mangement will be by radiotherapy alone .
Total conservative parotidectomy , like partial parotidectomy when the superficial
lobe removed & then the branches & the main trunk of the facial n. dissected from
the attachement to the adjacent structures , the b.v. (retromandibular v. , External
carotid a. , intenal maxillary a. & superficial temporal a.) are ligated , then the deep
lobe together with the tumor is mobilized (take care not to rupture the neoplasm)
Indications ; recurrent pleomorphic adenoma , certain malig. Tumors , recurrent
suppurative parotitis & even 1st branchial arch abnormalities .
 For submandibular gland ; resect the gland with all the nerves in close proximity to
the tumor with suprahyoid LN with postop. radioRx .
 For minor salivary glands ; partial maxillectomy with postop. radiotherapy .
Comlication of surgery ;
A. Parotidectomy
1. Early complications
a. Facial nerve weakness or paralysis ; due to pressure or retraction on the n. or due to
suction tubes or heat from diathermy (temporary weakness affecting the temporal or
frontal branch)
b. Hemorrhage or hematoma ; due to the dead space resulting from gland removel , can
be prevented by large suction tube away from the n. with adequate pressure will
decrease this .
c. Infection .
d. Skin flap necrosis .
e. Trismus (temporary for short period) .
f. Salivary fistula or sialocele ; due to over production of the saliva in the remaining
glandular tissue , Rx by suction & pressure pandaging ..
g. Seroma .
2. Long-term complications
a. Frey’s syndrome ; gustatory sweating due to misrouting of the parasympathetic
secretomotor n. fibers into the cutaneous n. fibers during healing , during meal the
patient develope sweating into the preauricular & subparotid region .
b. Hypoesthesia of the greater auricular nerve ; numbness of the ear in the pinna , this
is temporary .
c. Recurrent tumor .
d. Cosmetic deformity ;Soft tissue deficit & hypertrophic scar or keloid .
e. Xerostomia .

Lecture notes in
B. Submandibular excision
1. Hemorrhage
2. Infection
3. Marginal mandibular branch of facial nerve injury ; paralysis of depressor anguli
oris .
4. Hypoglossal nerve injury
5. Lingual nerve injury
6. Scar
2.Radiotherapy
RadioRx as adjuvent to surgery , it is indicated in ;
1. palliation of inoperable tumors with pain .
2. lymphomas .
3. locally aggressive tumor .
4. residual disease after surgery .
5. patient undergo surgery for recurrence .
It's contraindication are ;
1. low grade & early stage .
2. benign tumor( increase the incidence of malignancy) .
Side effect of it ; xerostomia , eustachian tube dysfunction .
Complications of radiation therapy for major salivary gland malignancies are
uncommon40. Unilateral radiation therapy portals are sufficient for most major salivary
gland malignancies, and because this spares the contralateral parotid gland and most of the
mucosa of the pharynx, xerostomia is uncommon. Complications include hearing loss,
xerostomia, hair loss, skin ulceration, osteoradionecrosis of the mandible, fibrosis, and
brain stem necrosis48.
Complications of radiation therapy for minor salivary gland malignancies involving the
oral cavity include xerostomia and osteoradionecrosis of the mandible. A dental
consultation before radiation therapy and preventative dental care can avert radiation-
related dental complications. Irradiation of the sinonasal region can be complicated by
radiation injury of the eye, optic nerve, brainstem, and the pharynx. Dosage ; 6000 cGy
Mangement of the recurrent pleomorphic adenoma
Adenoma seems as multiple nodules , may be seen on the parotid gland or in the overlying
tissue .The cause of recurrence ;
1. enculation without safety margin .
2. the tumor is breached accidently .
3. spillage of the tumor espicially in large tense tumor through incomplete capsule .
Managed by superficial partial or total conservative parotiectomywith radioRx (4000-5000
Gy) , if the neoplastic nodule is empaded within the facial n. , so that by radical
parotidectomy with radioRx .
The operation aim to remove the major bulk of the tumor mass while radioRx sterilize the
microscopic residue of the tumor , so we do total conservative parotidectomy to remove all
the macroscopic disease & radioRx .It is immpossible to conserve the facial n. , so we have
to preserve as much as possible of the n. ( if cut the n. , then immediate n. graft) .
N.B. ; low grade tumor (Acinic cell Ca. , Pleomorphic adenoCa. , BCC , AdenoCa. ,
Myoepithelial Ca.) , High grade tumor ( Mucoepidermoid Ca , Adenoid cystic Ca. ,
AdenoCa. , Undifferintiated Ca. , SCC , Small cell Ca. , & Oncocystic Ca.)

Lecture notes in
Drooling "Sialorrhea"
Over flow of saliva from the mouth . It is classified into :
A. Physiological drooling ; occurs in most normal infants , may increased during teething ,
stops by 18-24 month of age .
B. Acute drooling , occurs in any painful or inflammatory condition of the mouth &
pharynx, especially acute epiglottitis & post-tonsillectomy .
C. Chronic drooling , occurs in
oMental retardation .
oCongenital or acquired muscle spasticity or incoordination (or due to drugs , used in
management of the above disease like anticonvulsant & tranquilizer with cholinergic
effect) .
osometimes in Oesophageal obstruction .
oAudy gump deformity , after partial resection of the lower jaw which cause damage to
the muscles of the tongue & floor of the mouth .
Aetiology
1. Overproduction of saliva like in cholinergic drugs (tranquilizers or anticonvulsants) .
2. Inadequate disposal of saliva ;
oOutflow obstruction .
oFailure to initiate swallowing .
oFaulty head & jaw posture .
oMuscular incoordination .
oInappropriate muscle activity .
Clinical features
Drooling is a sign . The typical appearance of drooling child ; head hanging , open mouth
attitude , drooling with everted lower lip , it leads to ;
1. Excoriation of the skin over the chin & upper chest .
2. Dehydration & electrolytes disturbances .
3. Burden on the family , frequent clothes chang , serious drain on family financial
resources .
4. Social problems , signs of mental enfeeblement & slovenly behavior , also withdrawal
from the social contact .The child shunned by their peers .
Management
Most people are unaware of the possibility of management & regard it as a problem of little
or no consequences , especially when it associate with multiple handicaps , the quality of
life of those people can be improved dramatically by simple means .
The aim of management ;
1. Improve swallowing .
2. Reduce the flow of saliva to the point where the patient's own defective clearance can
cope . If the salivary flow decreased below 5% of normal , this will cause xerostomia
which is unpleasant & affect the oral hygiene .
Also avoid management modality which cause damage to other structures .
Modalities of management
According to the ; (1) Age (2) Type of the problem & (3) Results of investigations , they are
A. Non-surgical methods
- Swallowing improvement (increase outflow)

Lecture notes in
o Physiotherapy ; carried by speech & language therapist . The aim id to improve

the oral phase of deglutition by specific exercises for the lips , tongue , palate &
mandible .
The gain is ; jaw closure & stability are improved , better closure of lips ,
especially during swallowing & enhance the mobility , posture & coordination of
the tongue & palate .
Many patients get great benefit from physiotherapy , but those with severe mental
disability or excessive drooling get little improvement .
6 months trial of physiotherapy should be undertaken before any surgery .
o Biofeedback & behavioral modification ; conditioning the patient with drooling to
respond to auditory stimuli , EMG activity in the orbicularis oris & strap muscles
is used to enhance the awareness of swallowing activity , this lead to achievement
of proper motor response triggers an auditory signals .
After training to the patient , he is supplied with a timer which beeps at a pre-set
intervals , these supplying an auditory clue for swallowing to begin .
- Reduction of salivary flow (decrease the inflow)
o Drugs ; use anticholinergic like atropine & hyocine to decrease salivation , the
disadvantages are ;
Side effects like xerostomia , constipation , urinary retention , restlessness &
glaucoma .
Management continue indefinitely.
o Radiotherapy ; irradiation of the parotid , sublingual & submandibular glands , it
is too risky to be useful & too uncertain , its disadvantages are ;
Difficult to determine the dosage that achieves reduction in flow without causing
xerostomia .
Cause very thick viscid saliva , because the serous elements of the glands are
more radiosensitive than the mucinous , this lead to infection & bad oral hygiene
.
Painful mucositis .
Dysplasia or neoplasia .
B. Surgical methods
1. Improvement of the jaw posture
By mylohyoid myotomy , poor posture is related to hypertonicity of the muscles of the
floor of the mouth rather than weakness of jaw muscles .
2. Redistribution of the salivary outflow
By relocation of the submandibular & parotid ducts from oral cavity to the tonsillar
fossae . The aim ; when saliva projected to the oropharynx , in addition to
redistribution , it will stimulate swallowing reflex .
Tonsillectomy can be done prior to the procedure (Crystale remove the tonsil only
when they fill the fossae) .
Some in the past place the duct in the anterior pillar without removing the tonsils ,
but it is a difficult procedure & the accurate position can not be guaranteed .
oParotid duct relocation , by Wilkie 1967 , the parotid duct at the anterior border of
the masseter , lies in close proximity to the upper & lower buccal branches of the
facial nerve & to the buccal branch of the trigeminal nerve . The risks are ;
Injury to the nerves .

Lecture notes in
Duct stenosis .
Painful parotid swelling .
Septic parotitis .
oSubmandibular duct relocation , by Ekedahl 1974 , the steps are ;
Routine tonsillectomy with good haemostasis .
Infiltration of the floor of the mouth with 1:80000 adrenaline .
Horizontal elliptical incision is made to enclose both papillae , but not
separate the papillae at this stage .
The duct , so easy to identified as it runs backwards & laterally & dissected
out by sharp & blunt dissection we separate the ducts from the surrounding
sublingual tissue (especially the gland , which if damaged lead to ranula
formation) . Freeing of the duct is carried backwards as far as possible ,
beyond the midpoint of the distance between the tonsillar fossae & frenulum
The lingual nerve & hypoglossal nerve may be seen lying on either sides of
the duct .
A tunnel is then created sublingually on each side using long straight artery
forceps with the finger in the tonsillar fossa , the tip of the forceps is aimed to
exit as low down in the fossa as possible .
A thin red rubber catheter introduced in the pharynx , is grasped by the
forceps & drawn forwards through the tunnel .
The duct papillae are separated in the midline & each sewn to the tip of its
corresponding catheter with along tail on the surface fixing the duct to the
catheter , this in order to restore the duct to its normal position if there is
tension in the relocated duct , so further dissection done .
The duct pulled by the catheter to the tonsillar fossa avoiding twisting &
tension , so the duct in its new place .
The tonsil gag reinserted & the end of the duct is sutured to the posterior
aspect of the anterior faucial pillar & the catheter & retrieved suture are
removed .
Finally ; the wound in the floor of the mouth is closed .
Postoperatively ;
The same comfort following tonsillectomy .
May have swelling of the floor of the mouth .
Sometimes submandibular gland swelling , transient & subside within 1-2
days .
Ranula in 10% , excision of the sublingual gland will decrease the incidence
Submandibular duct calculi (not proven) .
Contraindications are ;
Very small mouth .
Restricted jaw opening .
High arched palate
3. Reduction of secretions
(1)Excision of the salivary glands
- Submandibular gland excision simple & safe .
- Parotid gland excision , risky to the facial nerve .

Lecture notes in
(2) Ligation of the ducts ; safe & simple , with significant postoperative morbidity ,
like tender swelling of the glands ( in parotid within weeks or months) .
4. Interruption of the parasympathetic nerve supply
It is a procedure to the ENTist & it is the ideal solution to the problem , especially
chronic one . The glands will continue to secrete at their basal or resting level (thus
decrease xerostomia) .
(1)Tympanic neuroectomy & division of the chorda tympani .
Lempert 1946 , tympanosympathectomy for management of tinnitus aurium .
Golding-Wood (1962) rename the operation as a tympanic neurectomy , for
the management of Frey's syndrome & chronic tympanic neuralgia .
Superior salivary nerve gone with the chorda tympani to the submandibular
ganglia (submandibular & sublingual glands) supplying the parasympathetic
& secretomotor fibers .
Variation in location of the chorda tympani in the middle ear ;
- Normally lie between the long process of incus & handle of malleus .
- Plastered onto the posterior wall of the middle ear just deep to the bony
annulus .
- Within the facial recess .
- Absent .
Inferior salivary nerve gone with the glossopharyngeal nerve to give the
Jackobson nerve .
The tympanic plexus is a single trunk running upwards in an oblique fashion
over the promontory just anterior to the round window niche , variations ;
- Main trunk lies within the substance of the promontory bone .
- 50% , anterior or hypotympanic branch (below the curve of the
promontory in the hypotympanum) .
Steps of the procedure ;
Anaesthesia ; GA with hypotensive technique .
Approach ; either postaural (if small external canal) or endaural
(endomeatal) tympanotomy , more inferiorly based flap give good access
to the hypotympanum .
Chorda tympani ; free the nerve from its mucosal fold with a Rosen needle
, then sever it at its point of exit from the posterior wall with microscissor
& then avulse the remainder of the nerve with fine crocodile forceps . By
this way we protect the facial nerve & ensures that long segment is
removed .
Tympanic plexus ; elevate the mucosa from the promontory after dividing
it around the anterior rim of the round window niche (a lot of mucosa
covering the promontory & the hypotympanum is removed) .
The nerve is identified , usually in shallow groove on the promontory &
avulsed & the side branches are removed .
If the nerve is covered by thin bone , then remove the bone by pick or
needle . If within the substance of the promontory , use a small diamond
paste burr (take care to the basal turn of the cochlea) .

Lecture notes in
The anterior & inferior aspects of the promontory should be cleansed with
a small house curette or by careful drilling with a diamond pasate burr
(with higher magnification) for anterior or hypotympanic branch .
Risks are ;
Hearing , in 1% , preoperative hearing assessment (PTA or ABR if the
patient is mentally retarded) , 6 weeks should elapse before operation on
the other side , if only one hearing ear , then consider other method .
Taste , if preserve chorda tympani in one side , no worthwhile outcome .
Usually there is no evidence of loss of appetite & exploration for this is
olfaction , taste buds on the posterior 1/3rd of the tongue & the texture of
the food all contribute to the remaining sense of smell .
(2)Division of the auriculotemporal nerve .
(3)Extirpation of the submandibular ganglion .
Results of surgery
Rough guid based on direct observation of ;
1. Parents .
2. Nursing staff .
3. Estimation of decrease in the number of bib or clothing changes required .
The criteria for assessment are ;
1. Unchanged .
2. Improved , means noticeable improvement but drooling still a problem .
3. Good , means noticeable improvement & drooling no longer a problem .
4. Excellent , means drooling has ceased all together .
In surgical management , 85% with good or excellent results (tympanic neurectomy with
50-80% & relocation of the submandibular duct 80-100%) .

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Cysts , granulomas & tumors of the jaw

Cyst defined as pathological cavity filled with fluid or semi-fluid , lined by an epithelium &
it is more common in the jaws than other bone in the body . The residual epithelial tissue is
of 3 sources ;
1. Reduced enemal tissue .
2. Cells rests of Malasse .
3. Epithelial cells remaining following dissolution of the dental lamina & called cells
rests of Serres .
It can be divided into ;
A. Epithelial cysts
1. Developemental cysts
oOdontogenic
a. Gingival cyst of infants ; small keratinized cyst seen on alveolar ridge of infants
, containing white or cream coloured nodules . Treatment ; some times need
marsupilization , but usually spontaneous resolution at the age of 3 months .
b. Gingival cyst of adults ; gingival swelling without any bony involvement , it is
slowly growing , painless swelling lined by cuboidal epithelium . Treated by
excision .
c. Lateral periodontal cyst ; swelling on the lateral aspect or between the roots of
teeth especially the canine or premolar . It may be asymptomatic or there is
gingival swelling lined by non-keratinized sequamous or cuboidal epithelium .
Treated by enuclation .
d. Glandular odontogenic cyst ; it is sialo-odontogenic cyst , it is ntraosseous
multilocular cyst , it contain non-keratinized sequamous epithelium with
glandular mucinous epithelium . Treated by resection .
e. Eruption cyst ; it results when the teeth impeded withing the soft tissue during
its eruption , seen during childhood & it is painless soft fluctuant swelling .
Treated by marsupilization .
f. Odontogenic keratocyst ; arise from the remnants of dental lamina ,
characterized by pain , swelling & if infected then it discharged , it has
malignant potential & treated by excision .
oNon-odontogenic (source rather than the tooth forming organ)
a. Nasopalatine duct cyst ; the commonest of all non-odontogenic cyst , arise from
the epithelial remnants of the nasopalatine duct which connect the oral & nasal
cavities . Presented as asymptomatic or slowly growing swelling in the palate
just behind the incisors or in the midline of the oral cavity & the protuberance
is in the floor of the nose , if secondary infected then mucoid discharge .
x-ray show ovoid radiolucent area with sclerotic margin . It is lined by
pseudostratified sequamous or cuboidal epithelium with goblet cells &
characterized by presence of neurovascular bundle . Treated by enuclation .
b. Nasolabial or nasoalveolar cyst ; rare , seen in the upper lip below the lar
margin , it arise from the epithelial remnants of the nasolacrimal duct .
Clinically presented as swelling , pain , nasal obstruction , fluctuant swelling
withing the labial sulcus . x-ray show radiolucent swelling above the root of the
incisor teeth . Histology show noncilliated pseudostratified columonar
epithelium with goblet cells . Treated by removal through labial sulcus .

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c. Midpalatal cyst of infants .

d. Fissural cyxts ; midalveolar , median mandibular cysts .
2. Inflammatory cysts
They are radicular cysts arise from the odontogenic remnants as a result of chronic
inflammation , commonly seen at the apices of the teeth . Presented as cystic lesion in
the maxilla (commonest one) especially the anterior teeth .
It is slowly enlarging swelling with egg shell cracking , sometimes there is sinus
discharging into the oral cavity . x-ray show radiolucent , rounded area with
sclerotic margins . Histologically ; non-keratinized stratified sequamous epithelium
with cholesterol crystals & cheesy brownish paste .
Treated by enculation of the cyst & treating the inflammation .
B. Non-epithelial cysts
1. Solitary bone cysts ; nonepithelial cyst seen in long bones & jaws in children ,
especially the mandible . Presented as bony cyst with expansion of the mandible with
labial parasthesia . x-ray show irregular radiolucent area .
It may be due to trauma which cause blood to clot which fail to resolve resulting in
cavity . Treated by spontaneous resolution & sometimes need surgical excision .
2. Anurysmal bone cyst ; non-epithelial , non-neoplastic bone cyst , seen in female child
mainly , it is firm painful swelling with displacement of the teeth & erosion of the
cortical bone with egg shell cracking .
x-ray show radiolucent ovoid area which is unilocular or multilocular appearance
(characteristic soap bubble like appearance) .
It may be seen with other benign lesions as a cause (gaint cell granuloma ,
nonossifying fibroma , fibrous dysplasia) .
Histologicallly ; multiple blood filled spaces with flat spindle cells . Treated by
currettgae & if recur , then resection .
Odontogenic tumors of the jaws
A. Benign odontogenic tumors
1. Epithelial tumors
oAmeloblastoma ; benign , but locally invasive neoplasm , the most common
odontogenic tumor seen in the 4th & 5 th decade , it is of 2 types ;
(1) Unicystic ameloblastoma .
(2) Extraosseous ameloblastoma .
It is slowly growing , may cause bony expansion with egg shell cracking & facial
deformity , it may extend to the maxillary sinus or adjacent soft tissue , it cause lost
teeth , ill fitting dentures , malocclusion , nasal obstruction , ulceration , discharge.
x-ray show multilocular radiolucencies with well defined borders .
Histologically of 5 types ; (1) Follicular (2) Plexiform (3) Acanthomatous (4) Basal
cell , & (5) Granular .
Treated by curettage , if recur then radical excision .
oSequamous odontogenic tumor
Rare , both jaws are equally affected , presented as local tenderness & tooth
mobility x-ray show radiolucency with sclerotic margins , histological examination
show well differentiated sequamous epithelium cells with connective tissue stroma
with cystic degeneration or calcification . Treated by curettage .
oCalcifying epthilial odontogenic tumors

Lecture notes in
Affect the mandible & maxillary antrum , slowly growing , painless swelling ,
epistaxis , nasal obstruction . x-ray show radio-opaque irregular mass ,
Histologically there is epithelial cells with fibrous stroma which may be calcified .
Treated by curettage .
oClear cell odontogenic tumor
Rare tumor with intraosseous mass in the maxilla or mandible , seen in female >50
years age , x-ray shows radiolucent areas , Histologically ; epithelial cells with
clear cytoplasm . Treated by local resection .
2. Epithelial & mesenchymal tumors
oAmeloblastic fibroma .
oAmeloblastic fibrodentinoma .
oAmeloblastic fibroodontoma .
oCalcified odontogenic cyst .
oComplex odontoma .
oCompound adontoma .
B. Malignant odontogenic tumors
It has various origions , it arise from ;
(1) Malignat transformation of ameloblastoma .
(2) Directly from th epithelial remnants of the odontogenic epithelium .
(3) Malignant transformation of the odontogenic cyst .
oMalignant ameloblastoma ; seen mainly in male over 40 years , has primary
growth & metastatic growth to the LN & lungs . Histologically shows all the
cytological features of malignancy .
Treated by radical excision of the primary lesion with radical neck dissection &
irradiation to the sites of distant metastasis .
oPrimary intraosseous carcinoma ; seen within the maxilla & mandible ,
characterized by pain , swelling , discharge , parasthesia & pathological fracture .
x-ray shows radiolucent area with poorly defined margins .
Histologically it is characterized by sequamous metaplasia & it is indistinguishable
from sequamous cell carcinoma . Treated by radical resection with radiotherapy .
oMalignant changes in odontogenic cyst ; clinically & radiologically diagnosed as
odontogenic cysts , but Histologically it is carcinoma , it result from malignant
transformation of benign cysts .
oAmeloblastic fibrosarcoma ; resemble ameloblastic fibroma but with features of
sarcoma , characterized by pain , swelling , parasthesia , bleeding & ulceration .
x-ray shows radiolucent area with thinned cortex . Treated by radical surgery .

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Lecture notes in
Pharyngitis
An infection or irritation of the pharynx and/or tonsils . The etiology is usually infectious,
with 40-60% of cases being of viral origin and 5-40% of cases being of bacterial origin.
Other causes include allergy, trauma, toxins, and neoplasia.
A. Acute pharyngitis
It is the most common cause of sorethroat in adults , iy may be associated with URTI ,
nasal obstruction , mouth breathing . The affecting micro-organism , the same as
tonsillitis , except viruses form a higher proportion .
1. Bacterial pharyngitis
(1) Group A beta-hemolytic streptococci (15% of all pharyngitis)
The classic clinical picture includes a fever of greater than 101.5°F,
tonsillopharyngeal erythema and exudate, swollen tender anterior cervical
adenopathy, elevated WBC count, headache, emesis in children, palatal
petechiae, midwinter to early spring season, and absent cough or rhinorrhea,
which are associated with viral pharyngitis.
A scarlatiniform rash also is associated with GABHS infection (scarlet fever),
ie, a sandpaperlike erythematous rash over the trunk and extremities with
circumoral pallor and a strawberry tongue.
(2) Group C, G, and F streptococci (10%)
May be indistinguishable clinically from GABHS infection but do not cause the
immunologic sequelae of GABHS infection. They may be associated with food-
borne outbreaks. Group C streptococci have been reported to cause meningitis,
endocarditis, and subdural empyemas.
(3) Arcanobacterium (Corynebacterium) haemolyticus (5%)
Is more common in young adults and is very similar to GABHS infection,
including a similar scarlatiniform rash. Patients often have a cough.
Occasional outbreaks have been reported.
(4) Mycoplasma pneumoniae in young adults presents with headache, pharyngitis,
and lower respiratory symptoms. Approximately 75% of patients have a cough,
which is distinctive from GABHS infection.
(5) Acute gonococcal pharyngitis
Characterized by transient sorethroat with tender enlarged cervical LN with
(sometimes) exudative gonococcal tonsillitis . May be complicated by
septicaemia , septic arthritis , iritis ..etc .
Treated by ; 4.8 megaunits of procaine pencillin or oral tetracycline for patients
not improved with pencillin .
(6) Chlamydia pneumoniae (5%)
Has a clinical picture similar to that of M pneumoniae. Pharyngitis usually
precedes the pulmonary infection by about 1-3 weeks.
(7) Corynebacterium diphtheriae is rare in the western world . A foul smelling
gray-white pharyngeal membrane may result in airway obstruction.
2. Viral pharyngitis
Start as nasal infection with common cold or coryza after which there is fever
malaise & pharyngitis .
Most children & adults have 3-4 viral infections/year, the virus may be prevented by;
(1) Specific secretory antibodies in the mucous blanket (IgG , IgA) .

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(2) Non-specific antiviral mucoprotiens .

(3) Mechanical effect of cilliary function .
The systemic effect are due to haematogenous & systemic spread of the virus or by
release of the intracellular factor from the necrosed epithelial cells .
The viruses are ; Rhinovirus , Corona virus , Influneza A & B viruses , Para virus ,
Adenovirus & RSV .
The symptoms are ;
- Rhinitis , pharyngitis & conjunctivitis .
- Painful , difficult swallowing .
- Pain may radiate to the ear .
- Hoarseness with cough .
- Acute OM .
The signs are ;
- Hyperaemic congested turbinates .
- Rhinitis with hayperaemic mucosa covered by mucopus .
- Posterior pharyngeal wal with hyperaemic islands of lymphoid tissue .
- Tonsils may be inflamed .
Treatment by
- The disease is self limited , lasting for 3-4 days .
- Bed rest , analgesia , oral fluid & other supporting measures .
- Antibiotics administrated if secondary bacterial infection is developed .
Complications
- Local ; (1) sinusitis (2) OM (3) Laryngitis (4) Pneumonia (5) Tracheobronchitis .
- General ; (1) Meningitis (2) Encephalitis (3) Myocarditis .
(1) Adenovirus (5%)
The distinguishing feature of an adenovirus infection is conjunctivitis associated
with pharyngitis (pharyngoconjunctival fever). It is the most common etiology in
children younger than 3 years.
(2) Herpes simplex (< 5%)
HSV type I affect the oral cavity & oropharynx , while type II affect the genital
tract .
In the primary hepetic infection there will be ; ulcerative stomatitis of the lips ,
gums , tongue , buccal mucosa & soft palate . The virus can be identified by
flourscent antibodies or by intranuclear inclusions in the scrabings .
In the secondary herepetic infection (occur due to the viral residue in the
posterior root ganglia) , intercurrent illness lead to appearance of the herpetic
vesicles , it is commonly seen in immunocompromised patients .
Treated by Acyclovir (local & systemic) , analgesia & fluid .
(3) Herpes Zooster
Arises by reactivation of virus particles which have remained in the cranial nerve
nuclei , ganglia or spinal root ganglia , following previous attacks of chicken pox
It lead to eruption in the distribution of the 5th , 7th , 9th & 10th cranials , so
affect the palate , tonsils & posterior pharyngeal wall , together with the Herpes
zoster oticus

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(4) Coxsackieviruses A and B (< 5%)

These infections present similarly to herpes simplex and also may have vesicles.
If vesicles are whitish and nodular, it is known as lymphonodular pharyngitis.
Coxsackie A16 may cause hand-foot-and-mouth disease, which presents with 4-
to 8-mm oropharyngeal ulcers and vesicles on the hands and feet, and,
occasionally, on the buttocks. The oropharyngeal ulcers and vesicles resolve
within one week.
(5) Epstein-Barr virus (EBV)
Clinically known as infectious mononucleosis, it is extremely difficult to
distinguish from GABHS infection. Exudative pharyngitis is prominent.
Distinctive features include retrocervical or generalized adenopathy and
hepatosplenomegaly. Atypical lymphocytes can be seen on peripheral blood
smear. Viral cultures from washings are about 20% sensitive in adults.
(6) CMV
Presentation of CMV is similar to the presentation of infectious mononucleosis.
Patients tend to be older, are sexually active, and have higher fever and more
malaise. Pharyngitis may not be a prominent complaint.
3. Other causes include dry air, allergy/postnasal drip, chemical injury,
gastroesophageal reflux disease (GERD), smoking, neoplasia, and endotracheal
intubation.
4. Vesicular & bullous eruption of the pharynx
- HSV , HZV , Stevens-Johnson syndrome , CMV …etc .
- Permiphigus or permiphigoid ; may affect the mucous membrane & skin of the
mouth & the oropharynx .
- Herpangina ; self limiting vesicular eruption of the oropharynx caused by
entrovirus & Coxasackie virus .
- Hand – Foot & Mouth syndrome ; vesicular eruption of the oropharynx , hands ,
& feet caused by Coxasackie virus .
B. Oedema of the uvula
1. Quinke’s disease ; acute oedema of the uvula characterized by tickling sensation or
irritation or gagging .
Eitiology unknown , may related to inhaled or ingested allergen or it may be part of
allergic reaction (angioneurotic oedema) .
Treatment ; mostly it settles down by its own self , sometimes need I.V hydrocortisone
injections .
2. Trauma ; Foreign bodies , intubation , surgery ..etc.
3. Acute infections ; viral pharyngitis , quinsy .
4. Chronic infections ; T.B. , syphilis .
5. Tumors ; SCC .
6. Radiotherapy .
7. Allergic ; angineurotoc oedema .
8. Blood diseases ; Acute leukaemia , agranulocytosis ..etc.
9. Miscellaneous ; aphthus ulceration & Behcet disease .
C. Chronic pharyngitis
1. Chronic non-specific pharyngitis

Lecture notes in
Chronic sorethroat with generalized diffuse hypertrophy of the pharyngeal lymphoid

tissue of the lateral pharyngeal bands , sometimes it called chronic granular
pharyngitis . It has unknown aetiology , other factors may cause it like chronic
sinusitis with postnasal drip , dental carries & irritation (tobacco & alcohol) &
excessive use of voice (refered otalgia usually dangerous sign “malignancy”) .
Clinically presented as irritation of the throat , constant hawking , snoring & tiring
of voice .
Treated by ; analgesia , gargle s antiseptics , reassurance , exclusion of malignancy
& removing of the predisposing causes .
2. Chronic specific pharyngitis
(1) Syphilis
The secondary form is the most commonly affecting the pharynx , the pathology is
endarteritis with lymphocyte & plasma cell infilteration & healing is with fibrous
tissue , also granulomatous lesion seen in the tertiary form .
- Primary syphilis ; the incubation period about 3 weeks , it affect the lips ,
tongue , buccal mucosa & tonsils .
The lesion start as papule which break to painless ulcer with indurated margins
, this painless chancre is characteristic .
It may associate with painless cervical LAP (if secondary infected become
tender) , the ulcer persist for 2-6 weeks during which the patient can transmit
the disease .
- Secondary syphilis ; occur 4-6 weeks after the primary lesion , characterized by
fever , headache , malaise , generalized LAP & mucocutaneous rash &
sorethroat (pharynx & soft palate are hyperaemic with mucous patches or snail
track ulcer , covered with gray-white membrane which can be scraped with no
bleeding) . It may last for few weeks (30% of patients go to the tertiary form) .
- Tertiary syphilis ; develop 5-25 years after the primary lesion . Characterized
by gumma which is granulomatous necrotic lesion which begins as nodule &
then break down to form ulcer .
It occur in the hard palate , septum , tonsils , posterior pharyngeal wall or
larynx , the gumma typically painless (whether ulcerated or not) , there is no
LAP unless there is secondary bacterial infection .
The diagnosis of syphilis by ;
a. Smear examined by dark field illumination microscope for the primary &
secondary lesions only .
b. Biopsy for tertiary syphilis using silver stain & immunoflourscent
technique .
c. Serological tests (for secondary & tertiary)
Non-specific (VDRL) ; this test using antigens extracted from beef heart
in a slide flocculation test , it is +ve in the 1st & 2nd weeks in 99% .
Other diseases may give +ve test like Yaws , Begils or Penta
(nonsyphilitic trepanomas) , atypical pneumonia , malaria , leprosy ,
small pox , SLE & RA .
Specific tests

Lecture notes in
TPI (Trepomema Pallidum Immune test) ; depends upon the ability of the
antibodies in the patient serum to immobilize spirochetes & seen by
direct ground illumination . It is the most specific with 100% +ve .
FTA (Flourscent Treponemal Antibody test) ; involve the absorption
from patient serum of cross reacting antibodies using nonpathogenic
treponemas & then absorption of the specific antibodies by treponema
pallidun preparations . The absorbed antibody identified by flourscent
labeled antihuman gammaglobulin , the test is sensitive with 100% +ve
with small flase +ve (sometimes in patients with SLE or RA) .
Treatment by ;
- Primary & secondary syphilis ; 2.4 megaunits of benzathine pencilllin in 1 or
2 I.M. injections .
- Tertiary syphilis ; 2.4 megaunits of benzathine pencilllin in 3 I.M. injections
with 7 & 14 days intervals .
(2) T.B.
It is the site of primary infection nearly always in children which may be
asymptomatic primary focus in the pharynx (usually in the tonsils or adenoids)
with cervical LAP .
Secondary T.B. of the pharynx usually seen in adults with massive sputum +ve
with cavitating pulmonary T.B. , some times the pharynx may be involved in
milliary T.B. (blood borne) .
Presented as painless discrete , slowly progressive , yellow – pink nodule which
may ulcerate & coalesce forming pale yellow granular area lead to scarring &
then the uvula shrink & soft palate stiffened .
Diagnosis from clinical picture & radiology .
Treatment by anti-T.B. drugs (INH , Rifampcine , Pyrazinamide ..etc) .
(3) Toxoplasmosis
(4) Leprosy
Pharynx may get infection from the nasal cavity , tuberculoid leprosy is low
grade infection of the skin & its nerves , while lepramatous leprosy is an
extensive form of the disease which affect the skin , nose & pharynx .
It is a granulomatous lesion which ulcerate & heal with fibrosis . Diagnosed by
biopsy & drug of choice (treatment) is Dapson© .
(5) Scleroma
(6) Fungal infection
Candida albicans ; of the normal flora in 30-40% of normal individuals , the
organism amy become pathogenic in patients with systemic diseases , the
predisposing factors are ;
a. Lacal diseases ; Lichen planus , Leukoplakia ..etc .
b. Systemic antibiotics .
c. Radiotherapy .
d. Immunocomporomized patients ; DM , AIDS , Lymphoma , ..etc .
Presented as white patches in the oropharynx , when removed it leaves an
erythematous ulcer & reccur in the next day .

Lecture notes in
Treatment by ; antifungal , Nystatin 100000 units fourtimes daily , Amphotricin B

100000 I.U. X4/day , Meconazole 125 mg X 4/day . Also we must treat the
predisposing factors .
D. Pharyngeal symptoms of blood diseases
1. Agranulocytosis
Decreased number of the polymorphonuclear cells , mostly it is due to
hypersensitivity to drugs (Chloramphenicol , Sulphonamides , Phenylbutazone ,
Cytotoxic drugs ..etc.) . Occasionally it is idiopathic .
Presented as ; fever , headache , severe pain on swallowing with pharyngeal necrotic
ulcer with sloughing that are usually multiple & coalescent , associated with severe
halitosis , there is no cervical LAP , also there is flase membrane .
Diagnosed by Full blood count & blood film which should be always performed in
any patient with sorethroat .
Treatment by ; withdrawalling the drug , high dose of steroids , systemic antibiotics
& blood transfusion (sometimes needed) .
2. Acute leukaemia
Pharyngeal manifestation may be the 1st symptom of the disease , it presented as
ulcer with slough & membrane formation which is severe & associated with bleeding
& bilateral cervical LAP .
Diagnosed by blood film & bone marrow examination .
E. Pharyngeal manifestation of AIDS
40-60% of patients with AIDS have symptoms refer to head & neck , these include ;
1. Hairy leukoplakia
Affect the oral cavity , soft palate , lateral & dorsal surface of the tongue .
2. Opportunistic infection
Candidiasis : may be oral , pharyngeal or oesophageal , it cause severe dysphagia &
odynophagia , treated by systemic & local antigungals .
Viruses : CMV , HSV , ..etc , it cause pharyngeal mucosal ulceration with pain &
dysphagia , treated by analgesia & acyclovir .
3. Lymphoid hyperplasis
May occur in the nodal & extranodal lymphoid tissue , it cause adenoid hypertrophy
, tonsillar hypertrophy & cervical LAP .
Presented with nasal obstruction , OME , massive adenotonsillar hypertrophy which
may lead to airway obstruction .
Treated by ; adenoid removed to exclude malignancy (although it is benign disease) ,
extensive surgical removal of the lymophoid tissue not indicated & it is important to
take biopsy from the unilateral hypertrophid palatine or lingual tonsils to exclude
neoplasia in HIV infected patients .
OME need myringotomy with ventilation tube .
4. Neoplasia
Benign tumors ; papilloma , verruca vulgaris & condyloma acuminate .
Malignant tunors ; Lymphomas (NHL of high grade extranodal B- cell type) &
Kaposi sarcoma (affect the pharyngeal mucosa , nasopharynx , tonsils , posterior
pharyngeal wall & hypopharynx , it cause dysphagia with ulceration & pain &
odynophagia with airway obstruction , treated by chemotherapy , cryotherapy , laser
& surgical resection) .

Lecture notes in
F. Vincent angina
Also called trench mouth & acute necrotizing gingivitis . Caused by spirochete Borrelia
vincentii & anaerobic Bacillus fusiformis .
Occurs in patients with poor oral hygein & debilitated conditions , it is a necrotizing
gingivitis with ulceration & bleeding with necrotic membrane & the lesion is painfull
with pyrexia , foetor & tender cervical LAP .
Diagnosed by scraping the ulcer & staining with genition violet . Treated by ; H2o 2
mouth wash , benzathine pencillin with metronidazole & good oral hygein .
G. Pharyngeal stenosis
It is fibrous tissue formation with adhesions covered by mucous membrane , it occurs in
the nasopharynx affecting the nasal respiration & eustachian tube function , or affecting
the oropharynx & soft palate & posterior pharyngeal wall leading to distortion of the
speech , or affecting the hypopharynx causing dysphagia , or affecting the larynx
causing dysphonia .
Treatment rarely necessary or successfull , sometimes dilatation .
Causes of pharyngeal stenosis are ;
1. Trauma ; surgical like adenoidectomy & tonsillectomy , cleft palate repair ,
pharyngoplasty , laryngectomy , pharyngolaryngectomy . Or inhalation of
corrosives .
2. Radiation .
3. Infections ; acute (septic tonsillitis , acute diphtheria ..etc) or chronic (syphilis ,
T.B. , leprosy , scleroma ..etc) .
4. Miscellaneous ; Wegner’s granulomatosis , Behcet disease , Aphthus ulcer,
permphegous , permphigoid , ..etc .
Diagnostic work up
Lab Studies
GABHS rapid antigen detection test
o This is the preferred method for diagnosing GABHS infection in the ED because of
difficulties with culture follow-up.
o A throat swab should follow a negative result.
o Rapid antigen detection is not sensitive for Group C and G streptococci or other
bacterial pathogens.
Throat culture
o This is the criterion standard for diagnosis of GABHS infection (90-99% sensitive).
o Positive cultures are clinically important only in patients with a related clinical
illness less than 10 days old.
Antistreptolysin-O (ASO) is a highly sensitive test but it is not practical in the ED
because of the need for acute and convalescent titers.
Mono spot is up to 95% sensitive in children (less than 60% sensitivity in infants).
Peripheral smear may show atypical lymphocytes in infectious mononucleosis.
Perform gonococcal culture, as indicated by history.
Routine labs usually are not available for A hemolyticus, M pneumoniae, or C
pneumoniae.
Fluorescent monoclonal antibody test exists for C pneumoniae.
A complete blood count (CBC), erythrocyte sedimentation rate (ESR), and C-reactive
protein have a low predictive value and usually are not indicated.
Imaging Studies:
Lecture notes in
Imaging studies generally are not indicated for uncomplicated viral or streptococcal
pharyngitis.
Lateral neck film should be taken in patients with suspected epiglottitis or airway
compromise.
A chest x-ray can elucidate pneumonia in M pneumoniae or C pneumoniae infection or
in other clinically suspected lower respiratory infection.
Complications:
General complications of pharyngitis (mainly seen in cases of bacterial pharyngitis)
include sinusitis, otitis media, epiglottitis, mastoiditis, and pneumonia.
o Recurrence is usually due to patient noncompliance but may be due to bacterial
resistance/treatment failure or a new exposure.
o Suppurative complications of bacterial pharyngitis result from spread of infection from
pharyngeal mucosa via hematogenous, lymphatic, or direct extension (more common
with GABHS), peritonsillar abscess, retropharyngeal abscess or suppurative cervical
lymphadenitis.
In addition to the above general complications, nonsuppurative complications (3%
incidence) specific to GABHS infection include acute rheumatic fever (3-5 weeks
postinfection), poststreptococcal glomerulonephritis, and toxic shock syndrome.
Complications of infectious mononucleosis include splenic rupture (contact sports
should be avoided for 6 weeks), hepatitis, Guillain Barré syndrome, encephalitis,
hemolytic anemia, agranulocytosis, myocarditis, B-cell lymphoma, and nasopharyngeal
carcinoma. Use of penicillin in cases of infectious mononucleosis results in 100%
incidence of rash.
Prognosis:
Most cases of pharyngitis resolve spontaneously within 10 days, but it is important for
the clinician to be aware of potential complications listed above.
Treatment failures are frequent and are attributed mainly to poor compliance, antibiotic
resistance, untreated close contacts, carrier states, and antibiotic-related or
copathogenic suppression of host immunity and necessary flora.
Patients should expect improvement in symptoms in penicillin-sensitive streptococcal
pharyngitis within 24 hours of initiation of treatment. Contagious and often the febrile
periods also are reduced to one day.
With erythromycin therapy, patients should expect improvement in 72 hours. The
incidence of streptococcal resistance to erythromycin consistently exceeds 25%.
Therefore, patients on erythromycin therapy should be more closely monitored for
treatment failure.

Lecture notes in
Pharyngeal pouch
Anatomy
There are 3 constrictor muscles ;
- Superior constrictor muscle
oOrigin ; pterygoid plate & hamulus , pterygomandibular raphe , mylohyoid ridge &
mucosa of the floor of the mouth .
oInsertion ; median raphe & posterior pharyngeal wall above the level of the vocal cords
oNerve supply ; pharyngeal plexus (IX) .
- Middle constrictor muscle
oOrigin ;greater cornu of the hyoid & stylohyoid ligament at the level of the vocal cords .
oInsertion ; median raphe & posterior pharyngeal wall .
oNerve supply ; pharyngeal plexus , recurrent laryngeal nerve & external branch of the
superior laryngeal nerve .
- Inferior constrictor muscle
oOrigin & Insertion ;
a. Thyropharyngeus ; from the oblique line of the thyroid ala & fibrous arch between
the thyroid & cricoid cartilage . The upper fibers overlap with the superior & middle
one & the lower fibers lie edge to edge with cricopharyngeus .
b. Cricopharyngeus ; thicker & bulkier, pass from one side to other side around the
back of the pharynx , recurrent nerve enter the larynx under the lower border of it .
oNerve supply ; recurrent laryngeal & superior laryngeal "external branch" nerves .
The weak areas ;
- Lateral ;
(1) Above the superior constrictor muscle ; sinus of Morgangi .
(2) Between the superior & middle constrictor muscles .
(3) Between the middle & inferior constrictor muscles .
(4) Below cricopharyngeus (Killian-Jamieson's area) , entrance of the recurrent nerve .
- Posterior ;
(1) Killian dehiscence .
(2) Laimer-Hackerman area .
Classification
1. Lateral diverticuli
a. Congenital ; rare affect children , 1st & 2nd decade , it attributed to branchial cleft
remnant . There is protrusion through all muscle & mucous membrane lead to
recurrent swelling in the anterior triangle of the neck which is tender with fever ,
mild stridor & mild dysphagia .
Diagnosis from plain x-ray of the neck which show air in the diverticulum & by
barium swallow which give better view .
Management ; in the acute episodes by antibiotics & incision & drainage , also we
do surgical excision of the diverticulum & the tract .
b. Acquired ; commoner affect adult , it is protrusion of the mucous membrane through
the muscle layer .
oNormal bulge ; orginate in the tonsillar or pyriform fossae , it is due to decreased
muscle tone & loss of tissue elasticity (in elderly) , usually asymptomatic &
bilateral . x-ray & barium swallow show smooth , hemispherical prominence arise
from these fossae called the pharyngeal ear "seen clearly on valsalva maneuver" .

Lecture notes in
Management ; nothing required because it is asymptomatic .

oTraumatic , iatrogenic , created between the superior & middle constrictor muscles
& disappear rapidly (in the tonsillar fossa) .
oPharyngocele ; due to increased intrapharyngeal pressure in previous pharyngeal
ear (due to aging) .
Presented as ;
(1) Usually unilateral , asymptomatic , M:F 8:1 .
(2) Symptoms ; intermittent mild dysphagia , regurgitation of food (undigested)
halitosis , nocturnal cough & chocking & dysphonia (due to recurrent nerve
compression & spillage into the larynx) .
(3) On examination ; lump in the anterior border of the sternomastoid muscle ,
compressible which gurgle due to mixture of air & fluid .
Investigation ;
(1) Plain x-ray show transcelucency lateral to the pyriform fossa .
(2) Contrast study (barium) show round contrast lined opacity communicating with
the pyriform fossa or tonsillar fossa by a neck .
(3) U/S may be helpful .
(4) Direct pharyngoscopy ; find the opening of the diverticulum .
Management ;
oNo treatment for asymptomatic (just follow up) .
oSymptomatic excised by external approach .
Postoperative N/G feeding for 3-5 days to ensure healing & prevent fistula formation.
2. Posterior pouch "common"
a. Congenital ; rare , in which it arise above the cricopharyngeus & the whole pouch
covered with muscle & lined with mucosa .
Barium study show elongated smooth walled pouch lies posterior to the oesophagus
& extends into the posterior mediastinum . treated by excision .
b. Acquired ;
oTraumatic pharyngeal pseudodiverticulum ; rare , seen in newborn infants due to ;
(1) Obstetrician finger in the breech delivery .
(2) Bilnd passage of suction tube or endotracheal tube .
(3) Spontaneous rupture of retropharyngeal abscess .
Presented with dysphagia with excessive oropharyngeal secretions , coughing ,
chocking (due to spillage into the trachea) which may develop cyanosis &
aspiration pneumonia with toxic & fever & may progress to mediatenitis .
Diagnosis by plain x-ray which show air in the stomach excluding the oesophageal
atresia , while the contrast study show irregular elongated tract originating in the
pharynx & pass behind the oesophagus into the posterior medistinum .
Management by abtibiotics , N/G nutritional support , if deteriorate , then surgical
drainage either through cervical or thoractotomy incision .
oDiverticulum form increased intrapharyngeal pressure ; rare , occur through the
Laimer-Hackerman are in elderly . It is asymptomatic & so require no management
oPosterior pharyngeal pulsion diverticulum , also called Zenker diverticulum . It is a
circumscribed acquired pouch caused by protrusion of mucosa of the pharynx
through the muscle layer at Killian dehiscence , there are 4 theories for aetiology ;

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(1) Negus ; tonic spasm of the cricopharyngeus secondary to inflammation ,

stenosis & neurological deficit .
(2) Dohlman's ; lack of inhibitory stimuli to the cricopharyngeus , sphenictor fail
to relax .
(3) Wilson ; 2nd swallow due to pharyngeal muscle laxity .
(4) Korkis ; neuromuscular incoordination & congenital weakness .
Incidence ; 1:200000 & 1:800 of routine barium study , M:F 2:1 , >50 years old ,
usually white race .
Pathogenesis ; it start as a small bulge at the Killian dehiscence , which enlarge to
lie between oesophagus & vertebral column , then pass into the posterior
mediastinum , most sacs are covered by stratified sequamous epithelium .
Presented as ;
(1) Symptoms ; 3 stages according to the size ;
- Stage I ; intial stage , small mucosal protrusion , just sensation of ffod
sticking in the throat .
- Satge II , defined pouch but oesophagus & hypopharynx still in line lead to
regurgitation , gurgling from the pouch .
- Stage III , large pouch with the hypopharynx in line with the neck of the
diverticulum & the oesophagus & the oesophageal inlet pushed anteriorly .
So symptoms ;
oDysphagia ; progressive , from solid & then liquid & event lately the
patient can not swallow his own saliva .
oRegurgitation of undigested food into the mouth , coughing , chocking ,
foul taste & gargling sound during swallowing .
oWeight loss due to dysphagia & malnourishment .
oHoarseness , due to spillage irritation , recurrent nerve compression or
vocal cord palsy from carcinoma development .
oPulmonary embolism , aspiration pneumonia , pneumonitis , lung abscess ,
bronchiactesis & collapse .
oOthers ; pain (Ca. in the pouch) , bleeding (ulcer in the pouch) , fistula
(cough on eating "parapharyngeal") .
(2) Signs ;
oSevere emaciation .
oSoft cystic lesion in the neck , usually the left side , in the lower part of the
anterior triangle .
oGurgle on palpation "Boyce's sign" .
oI/L ; laryngitis & pooling of saliva with undigested food particles .
Investigations ;
(1) Radiography ;
oPlain x-ray ; translucency with its apex towards the cricoid with air-fluid
level .
oContrast videofluroscopy , demonstrate the upper & lower lips of the neck
near the end of the 2 nd stage of swallowing (lower lip is cricopharyngeus
sphincter) .

Lecture notes in
Small filling defect in the contrast study means that ; in the bottom &
stable suggestive of carcinoma & in the neck & unstable suggestive of food
particles .
(2) U/S & Endoscopy .
(3) Biopsy of suspicious areas within the diverticulum .
Management
1. No management , for asymptomatic disease & those unfit to surgery (elderly & chronic
medical diseases) .
2. Endoscopic management ;
a. Dilatation , of the cricopharyngeal sphincter to alleviate dysphagia , now used only
for postoperative dilatation of stenosis .
b. Endoscopic diathermy , in past use scissors to divide the septum between the pouch
& the oesophagus lead to severe haemorrhage .
Now use diathermy , short operation (5-10 min.) under LA (the recurrence rate
about 7% , in external approach only 0.5%) , complications are haemorrhage ,
mediastenitis , stenosis & emphysema .
Advantages (over external approach) , can done under LA , short time , no external
scar & can be repeated easily if recurrence occur & fluid can given orally after 24
hours . The patient stay 4-5 days postoperatively , after 5 days , Barium study done
to decide the success of the operation .
3. External approach
a. One stage diverticulectomy ;
oThe patient admitted 1-2 days preoperatively , to empty the sac from food , restrict
for only clear fluid & to do preoperative investigations & management of any
concomitant URTI .
oIt is done under GA , N/G tube passed to the oesophagus , the pouch inspected for
Ca. & food , then the pouch packed with ribbon gauze soaked in proflavin .
oIncision ; collar at the upper boarder of the cricoid , from midline to half a cross
the sternomastoid muscle .
oDissection carried out medial to the carotid sheath .
oGreat care taken to avoid tearing the neck of the pouch .
oThe pack removed & stay suture inserted into the neck of the pouch inferiorly &
superiorly .
oExcision & suturing in 2 layers , drain is put & the wound closed .
oNo antibiotic is recommended unless complications .
oDrain removed 2-3 days postoperatively , N/G tube feeding for 5-7 days , then
removed & start fluid diet , normal diet at the 10th day postoperatively .
b. Inversion ; The pouch is invaginated into the oesophagus & its neck over sewn with
interrupted can gut instead of being excised .
Advantages ; low complication rate (Especially fistula & mediastinitis) , short
hospitalization (2-3 days) & early nutrition (drink within 24 hours) .
c. Cricopharyngeus myotomy ; indicated in neurological disorders (done alone) & with
diverticulectomy procedure .
The muscle divided as posterior as possible (to avoid damaging the recurrent nerve)
& it extended 3-4 cm caudally into the oeosphagus musculature as high pressure

Lecture notes in
zone can be at least that long , the patient can drink in the following day , go home 2-
3 days eating normally .
The complication ; damage to the recurrent nerve & fistula .
Complications of the external approach ;
(1) Immediate ; Haemorrhage , pneumothorax & surgical emphysema .
(2) Intermediate ;
o Infection (wound infection) & abscess , lead to fistula (1-5%) & secondary
bleeding .
o Hoarseness due to recurrent nerve damage (3-5%) .
o Mediastinitis ; due to leak , treated by antibiotic & suturing of the leak & put a
drain , occasionally thoracotomy needed .
o airocele between the superior mediastinum & the pharynx .
(3) Late ;
o Persistent hoarseness , division of the recurrent nerve .
o Stricture , need repeated dilatation (occasionally surgery needed) .
o Recurrence , high in endoscopic management , if myotomy no done , high
recurrence rate .
Mortality between 0.5 – 3% .
Carcinoma of the diverticulum
Incidence about 0.5-1% of all diverticuli , male > female (5:1) , occur in longstanding
disease . The predisposing factors are ; chronic irritation & inflammation from food .
The symptoms indicating carcinoma are ;
(1) Increased dysphagia & Pain .
(2) Weight loss .
(3) Occasionally blood in the regurgitated food .
(4) LN or mass in the neck , usually SCC .
(5) Hoarseness with vocal cord palsy .
Diagnosis by ;
(1) Oesophagoscopy & biopsy .
(2) Barium study shows filling defect (contrast) usually in the distal 2/3rd of the pouch .
Management by diverticulectomy with postoperative radiotherapy .

Lecture notes in
Nasopharyngeal carcinoma
Anatomy
The nasopharynx is large space , 4 cm high , 4 cm wide & 2 cm deep . It is opened
anteriorly into nasal fossa , above by the base of skull , below by the soft palate , posteriorly
the 1 st cervical vertebrae seperated from its posterior wall by prevertebral fascia &
underlying longus capitis & cervicis muscle .
The lower end of Eustachian tube situated in the lateral wall about 1-1.5 cm behind the
posterior end of the inferior turbinate , its bounded above & behind by tubal elevation
“Torus Tubarius” which is formed by tubal cartilage covered by mucous memberane .
The anatomical relation of Fossa of Rosenmuller :
- Anteriorly : Eustachian tube & levator palatini .
- Posteriorly ; pharyngeal wall mucosa overlying the pharyngeobasilar fascia &
retropharyngeal space containing the lateral pharyngeal wall of “Rouviere” .
- Medially ; nasopharyngeal cavity .
- Superiorly ; foramen lacerum & floor of carotid canal .
- Post-laterally ; tensor palatini & mandibular nerve & pre-styloid compartment of
parapharyngeal space .
The epithelial lining of the nasopharynx ; actual surface area in adult 50 cm2 , during fetal
life gradual transition of respiratory cilliated epithelium to sequamous type in the lower &
posterior part , true sequamous epithelium occur in the post-fetal life & completed by 10
years .
The choana & roof cover with cilliated respiratory epithilium with patches of sequamous &
transitional epithelium , cover the rest of the roof & lateral wall , the posterior wall cover
with sequamous epithelium .
The nasopharyngeal mucosa has distinict basement memberane & differ from the rest of
repiratory epithilium by subepithelial connective tissue is rich with lymphoid tissue which
form together with aggregate of lymphoid tissue & tonsil “ the internal Waldayer ring” .
The blood supply ; all from branches of the external carotid artery ; ascending pharyngeal
artery , ascending palatine & tonsillar branches of facial artery , descending palatine from
internal maxillary artery & dorsalis linguae from lingual artery .
The venous drainage via plexuses communicated above with ptyrigoid plexus & drain to
common facial & internal jugular vein .
The nerve supply derived from pharyngeal plexus which formed by branches of IX & X
cranial nerves with autonomic fibers , the motor part mainly by XI nerve which distributed
through pharyngeal branch of vagus , it supply all muscle of the pharynx except the
stylopharngeous (IX nerve) & tensor palati (V nerve) , the sensory part by IX & X nerves ,
the nasopharynx supply mainly by Vth nerve .
The lymphatic drainage ; it has extensive submucosal lymphatic plexus , the 1st order
drainage site is retropharyngeal nodes situated in the retropharyngeal space between the
posterior pharyngeal wall , pharyngobasilar fascia & prevertebral fascia , the node of
Ranvier from the main lateral group anterior to the lateral mass of the atlas at the lateral
border of the longus capitis . Efferent vessels drain to the deep internal jugular chain at the
skull base deep to the upper end of sternocledomastoid then drain posteriorly to the
accessory nerve node & anteriorly jugulodiagasteric group .
The nasopharynx is midline structure so cross drainage & bilateral spread of the tumor is
not uncommon .

Lecture notes in
Epidemiology
- It is the most common tumor of the nasopharynx , irrespective of geography &
race , it is 75-95% in low risk population , all in high risk population & in
southeast Asia 99:1 with respect to other types .
- Race ; Higher among Chinese (18% of all malignant neoplasm , 80% of head
& neck cancer) & other southeast Asian (the 2 nd most common tumor in
Singapore) , about 10-50 times than other countries (in Europe < 6% of Head
& neck cancer) . In HongKong , Vietnam , Malysea , Indonesia . Common in
Chinese born in USA 20 times higher than Caucasian . Also high in Eskimo &
Tunisian . Higher among Cantones other than people in the south of China .
- Age ; in Chinese in the 4th decade , in non-Chinese in the 6th decade .
- Sex ; M:F about 3:1 (in Chinese) 2:1 (in non-Chinese) .
Predisposing factors
1. Enviromental factors
a. Smoking ; active & passive .
b. Drugs ; Chinese herbal medicine .
c. Diet ; Chinese foods like salted fish , preserved meat (containg volatile
nitrosamines) , alsom dried fish , salted duck eggs , salted mustard green &
fermenated soybean paste . Also the above foods are diffecient in vitamin C .
d. Babies during weaning that feeding salted fish increase the risk of carcinoma .
e. House hold smoke & fums .
f. Religious practice ; incense smoke .
g. Occupation ; wood dust , metal , formaline dye …etc .
h. Socio-economic ; poor .
i. Nutritional deficiencies .
2. Immunological factors
a. More than 90% of patients high titre of antibodies to EBV Ag .
b. These antibodies in response to viral capsid Ag (VCA) , early Ag (EA) & EB
nuclear Ag (EBNA) .
c. Only undifferentiated & poorly differentiated type have high titre of EBV .
d. Increased IgA & IgM in related to VCA which is useful diagnostic marker & for
screening in high risk patients (Chinese) & for follow up in family history of
carcinoma .
3. Genetic factors
a. High incidence in southern Chinese .
b. HLA A & B associted with nasopharyngeal carcinoma .
- HLA A2 without BW 46 or B17 associated with long term survival.
- HLA BW6 allel asociated with intermediate term survival .
- HLA B17, Bw58 have high prevalence , HLA B17 associated with short term
survival
c. Deletion in chromosome 3p14-21 , 9p21-22 .
d. Translocation in 5q .
Tumor types
Sequamous cell carcinoma represent 85% of all malignant tumors of the nasopharynx .
The WHO classification ;
1. Type I ; Keratinizing sequamous carcinoma , well , moderate or poor
differentiation , -ve EBV , 25% of cases , 5 year survival 10% .
Lecture notes in
2. Type II ; Non-keratinizing carcinoma , EBV +ve , 12% of cases , 5 years

survival 50% .
3. Type III ; Undifferentiated carcinoma (lymphoepithelioma carcinoma & also
called transitional cell carcinoma) , high lymphocyte infilteration & may miss
Dx from lymphoma unless immunohistochemical technique with lymphocyte
marker done , EBV +ve , 63% of cases , 5 years survival 50% .
The site of orign mainly from the fossa of Rosenmuller , its impossible to determine exact
site of origin . The tumor extension are ;
1. Anteriorly ; nasal cavity , paranasal sinuses , pterygopalatine fossa & apex of
the orbit .
2. Posteriorly ; retropharyngeal space , node of Rouviere & lateral mass of atlas
3. Laterally ; to parapharyngeal space ; (a) prestyloid compartement , to the
mandibular nerve , pterygoid muscle & deep lobe of the parotid (b) post-
styloid compartement , vascular compression of the carotic sheath , last 4
cranial nerves & cervical sympathetic trunk .
4. Superiorly ; sphenoid body & sinus , parasellar structure , optic nerve ,
petrous apex , foramen lacerum , III , IV , V , nerves & the brain .
5. Inferiorly ; oral cavity & retrotonsillar region .
Management
The history reveal ;
1. The onset is insidous .
2. Cervical LAP (60% in Scott , 20% in Maran) , it is painless , 1 st palpable node is
jugulodigastric &/or apical node under sternocledomastoid , bilateral node not uncommon ,
in 1/3rd unilateral & in 1/5th bilateral .
3. Epistaxis (40% Scott , 1/3 rd Maran) in advances cases , blood stained mucous secretions
, nasal obstruction is late presentation , erosion to the antrum (mimic sinusitis) & ozena due
to necrosis of tumor .
4. Respiratory symptoms .
5. Tinnitus & aural symptom , OME (30%) , unilateral CHL in most cases .
6. Neurological palsy (20%) ; involve V, IX & X account 50% of nerve palsies , next III , IV
& VI .
7. Horner’s syndrome .
8. Pain & headache in terminal disease when the skull base & sphenoid sinus involvement.
9. Diplopia , trismus , facial numbness , ptosis & hoarsness .
10. Second malignancy in 9% of patient .
11. Metastasis ;
a. Locoregional ; paranasal sinuses , parapharyngeal space , infratemporal fossa ,
orbit , parotid gland .
b. Distant ; thoracolumbar spine , lungs & liver .
The Trotter’s triad ; (1) Conductive deafness (2) Elevation & immobility of homolateral
soft palate & (3) headache “homolateral” due to 5th cranial nerve involvement .
The examination reveals ;
A. Nasopharynx ;
1. With out anasthesia ; mirror examination inadequate & may miss the lesion &
can be done under GA .
2. Under LA ; Rhinoscope ; rigid (0o , 30o , 10 o ) or flexible (fibroptic) , 5% of
patient have normal endoscopy (submucosal disease) .
Lecture notes in
3. Under GA ; by using Yankauer speculum (direct) or laryngeal mirror (indirect) .

B . Ear examination ; serous OM with retracted tympanic memberane .
C. Eyes ; diplopia or Horner syndrome .
E . Cranial nerve examination ; loss of facial , palatal & pharyngeal sensation (5th nerve
palsy) .
F . Neck examination ; +ve node in 70% of cases which may be the presenting feature .
G. Oral cavity examination ; shows s.t. paralysis or pushed down soft palate , vocal cord
paralysis & tongue paralysis , also trismud (indicate parpharyngeal space invasion) .
The investigation
1. Full blood count & ESR , increased ESR in lymphoma .
2. Audiometry & impedence test ; CHL with flat tympanogram ..
3. Eye ; field test .
4. EBV related Ag titre ; VCA speciefic IgA increased , the polymerase chain relation
to EBV genome used for Dx of the carcinoma if the patient with occult primary .
The imaging study ;
1. CT scan ; is the investagation of choice , do coronal & axial sections , it will
show ;
a. Any evidence of destruction of ptyrigoid plate , foramen lacerum , foramen
ovale , spinosum & jugular .
b. Tumor extension ethemoid & sphenoid sinuses .
c. Presence of deep impalpable node in deep retropharyngeal & rest of the neck .
2. MRI ; with its superior density , shows ;
a. Tumor edge & its vascular nature very clearly .
b. Intracranial extension .
c. With Gadolinium enhancement can differentiate between trapped secretion
within sinus from tumor extension .
3. CXR , plain x-ray to bones , abdominal U/S to detect distal metastasis .
The Biopsy ;
- Done under GA , if the mass seen , the palate can be held by 2 catheters , visualize by
postnasal mirror & biopsy performed transnasally by Tilly forceps , or by Yankaur’s
speculum or rigid endoscopic control .
- If no mass can be seen use adenoid currate or take blind biopsy .
- Full upper aerodaigestive tract endoscopy to exclude any 2nd primary .
- Flexible endoscope can be used in the contralateral side of the nose & Henckel
forceps through the diseased site to obtain biopsy , the advantages of this method ;
a. Tiny tumor can be visualized & biopsy .
b. To detect & biopsy post radiation tumor recurrence beneath the necrotic scab the
persist long after radiotherapy .
The Staging (TNM)
T (primary tumor)
Tx : primary tumor can’t be assessed .
T0 : No evidnce of primary tumor .
Tis : carcinoma in situe .
T1 : tumor confid to the nasopharynx .
T2 : tumor extend to soft tissue of the oropharynx &/or nasal fossa
T2a :without invasion to the parapharyngeal space .
T2b : with invasion to the parapharyngeal space .
Lecture notes in
T3 : tumor invade bony structure &/or paranasal sinus .

T4 : tumor with intracranial extension &/or involvement of cranial nerves , infratemporal
fossa , hypopharynx or orbit .
N (regional LN)
Nx : LN can’t be assessed .
N0 : No LN metastasis .
N1: unilateral LN , 6 cm or less , above the supraclavicular fossa .
N2 : bilateral LN , 6 cm or less , above the supraclavicular fossa .
N3 : metastasis in LN ; (a) greater than 6 cm (b) in the supraclavicular fossa .
M ( distant metastasis)
Mx : metastasis can’t be assessed .
M0 : No distant metastasis .
M1 : distant metastasis .
Stage 0 : Tis N0 M0
Stage I : T1 N0 M0
Stage II A : T2a N0 M0
Stage II B : T1 N1 M0
: T2a N1 M0
:T2b N0 M0
Stage III : T1 N2 M0
: T2a,T2b N2 M0
: T3 N0,N1,N2 M0
Stage VI A : T4 N0,N1,N2 M0
Stage VI B : any T N3 M0
Stage VI C : any T any N M1
Treatment
1. Radiotherapy
Is the primary Rx modality , the radiation field must be large including , nasopharynx , base
of skull , cranial foramenia , sphenoid sinus , posterior ethemoidal sinus , posterior orbit ,
posterior maxillary antrum & posterior nasal cavity & perhapse the oropharynx &
retropharyngeal nodes & neck radiation if the cervical neck involved .
Because the nasopharynx is midline structure , both sides of the neck must be radiated ,
patient without clinically involved cervical LAP should undergo elective radiation , for both
side the neck because high incidence of occult disease at presentation .
Brachytherapy ; transnasal intracavitory brachytherapy with afterload Iridium –192
use to localized residual or recurrent tumor to preserve neighbouring structures & brain
Technique of radiotherapy ; large dose are required which necessate to include spinal cord
which is dose limited structure , so 2 phase technique are used ;
I . Phase I ;
a. Lateral field are used including from the level of the eyebrows to below the clavicle
with head extension to keep anterior part of oral cavity out of the field .
b. The anterior limit include the upper neck , oropharynx & posterior part of the nasal
cavity & orbit .
c. The posterior border pass to the suboccipital area with sparing of the upper
posterior area (brainstem , optic chiasma) .
d. Additional block shield the eyes & anterior orbits .
e. Sometimes additional blocks may shield mandible & oral mucosa .
Lecture notes in
The lower part of the neck can’t be Rx with lateral field , so anterior field required with
block shield the spinal cord . The 1 st phase giving 40 Gy in 20 fractions over 4 weeks during
this the patient replane for the 2 nd phase immediately after the 1st phase .
II. Phase II ; smaller lateral field ; nasopharynx , base of skull , parapharyngeal , sphenoid
& posterior ethemoid & any extension into nasal cavitory or oropharynx .
The posterior border move anteriorly so not cover the spinal cord , the neck treated by
single anterior field from the lower side of the lateral field .
Phase II giving 26 Gy in 13 fractions over 2.5 weeks .
The Patient care ;
1. Approperiate analgesia with morphine .
2. Nutritional support by percutaneous endoscopic gastrostomy .
3. continue the course because any interruption even in short gap will decrease
the cure rate .
The Complications are ;
1. Mucositis , xerostomia , dental caries .
2. Radiation OME .
3. Lhermittes’ sign ; cevical spinal cord radiation , electerical sensation spread
to both arms & legs on neck flexion .
4. Mylitis , encephalitis & Temporal lobe necrosis .
5. Hypopitutarism .
The 5 years survival ;
1. Stage I : 90% . 2. Stage II : 70% . 3. Stage III : 60% .
4. Stage VI : without distant metastasis 40% , with distant metastasis 0% .
2. Chemotherapy ; limited data with the use of chemotherapy as adjuvant with
radiotherapy , common used chemotherapuetic agents are cisplatin & flurouracil , the
survival rate (in combination with radiotherapy) about 76% .
3. Surgery ; of limited role , persistant recurrent disease in the nasopharynx LASER can
be used , while in persistant neck disease we can do radical neck dissection .
The surgical apprache to the nasopharynx are ; (a) Transoral (b) Tranpaltal (c) Endoscopic
transnasal (d) Transmaxillary (e) Transnasoantral (f) Maxillary swing .
Salvage surgery can be done in nasopharyngeal carcinoma recurrence .
The Rx of recurrent carcinoma are ;
a. Further radiotherapy which will increase the rate of complications , so use
intracavitary or brachytherapy (with little value if the disease extend byeond the
nasopharynx) .
b. Surgery which of limited place , combined craniofacial procedures , radical neck
dissection may be performed .
c. LASER may be used to exicise the superficial disease .
d. Chemotherapy which is disappointing .
The follow up ;
1. Review of the patient , montly at the 1st year , bimonthly at the 2nd year , 3
months for the 3rd year & 6 months for the 4th & 5th year .
2. Follow up for another 5 year because of suspecion of 2nd primary carcinoma .
The Prevention by ;
1. In high risk individuals , screening by nasopharyngeal biopsy & for viral
genome is useful for detrmination of the high risk person .
2. A vaccin based on EBV envelope glycoprotien (GP 340) .
Lecture notes in
Tumors of the oropharynx

Anatomy
The hypopharynx extends from its juncture with the oropharynx at the level of the hyoid
bone to the inferior border of the cricoid cartilage .
It is divided into three anatomic sites: the piriform fossa, or sinus; the postcricoid region;
and the posterior hypopharyngeal wall
A comprehensive description of the anatomy of this region is not appropriate for this
chapter, but several important anatomic features must be emphasized in relation to the
treatment of hypopharyngeal cancers.
The vasculature of the hypopharynx is derived directly from the great vessels of the neck,
which are, in themselves, positioned adjacent to its lateral walls. Any incision or excision of
the hypopharynx therefore requires careful isolation of the parent vessels to avoid injury.
Tumor also may spread directly from the lateral walls of the piriform fossae to these
structures.
The nerve supply to the hypopharynx is mixed. Sensory fibers are derived from the
glossopharyngeal nerve and the internal branches of the superior laryngeal nerves. The
motor supply to the region is from the pharyngeal plexus for the inferior constrictors and
the recurrent laryngeal nerves for the cricopharyngeus muscle.
The lymphatic drainage of the hypopharynx is of major importance in cancer therapy. Most
of the lymphatic flow from this region is directed toward the upper deep cervical lymph
nodes. There are, however, channels that extend superiorly from the hypopharynx into the
retropharyngeal nodes as high as the nodes of Rouvier at the skull base. Inferiorly, there is
a varied and extensive lymph drainage system from the piriform apex and postcricoid
regions. Here the lymphatics extend laterally to the juguloomohyoid nodes and inferiorly to
the paratracheal, paraesophageal, and thyroid nodes. In the medial aspect of the piriform
fossa, there is crossover with the lymphatics of the larynx at the aryepiglottic folds and the
arytenoids. Extensive submucosal lymphatics are found in the hypopharynx, particularly in
the inferior portions.
Physiology
The hypopharynx is an important component of both respiration and deglutition.
Hypopharyngeal cancers alter these physiologic functions in several ways.
Pure obstruction to swallowing or respiration may occur but only from very large or
pedunculated tumors.
In most cases of obstruction, edema occurs secondary to lymphatic invasion or infection.
Obstruction to swallowing also may occur from neural invasion that causes alterations in
the delicate neuromuscular balance between the inferior constrictor and the
cricopharyngeus muscles.
Pain from neural invasion, or secondary infection, also may produce a physiologic
obstruction. Invasion of the arytenoid or the recurrent laryngeal nerve also can cause
airway obstruction and aspiration as a result of vocal cord paralysis.
Pathology
The main tumor of the hypopharynx is sequamous cell Ca. (SCC) , it is found in 40% in the
postcricoid area , 10% in the posterior pharyngeal wall & ½ -2/3 rd of patients in the
pyriform sinus .

Lecture notes in
It is of poor prognosis (less than 30% 5 years survival) , the hypopharyngeal Ca. may
metastasis early 1st to the cervical LN especially pyriform fossae tumor , many patients
presented with occult primary (30-40%) .
The most common is the pyriform sinus , ½-2/3rd of cases , it is either involving the medial
wall or lateral wall primarily .
I. Medial wall tumor ; more extensive , extends through the aryepiglottic space to invade
the paraglottic space , fix the hemilarynx & can also extnd into the pre-epiglottic space ,
then to the postcricoid area & then invade the cricoarytenoid joint fixing it leading to
vocal cord fixation .
II. Lateral wall tumors ; extends through the thyroid cartilage & thyrohyoid membrane
causing palpable mass in the neck (25% involve the carotid sheath & thyroid gland) .
Other tumors are ;
- Benign ; lieomyomas is the most common , usually affect the male > female in the 3rd -5th
decade of life , causing rubbery & firm intramural swelling (when small) , when increased
in size it dragged down into the oesophagus by swallowing , it managed by pharyngotomy
with removal of the tumor .
Others like lipoma & fibrolipoma causing dysphagia & chocking sensation (managed as
liemyosarcoma) .
- Malignant , usually lieomyosarcoma , psuedosarcoma & adenoid cystic Ca. &
plasmacytoma .
Epidemiology
- Sex ; female > male (especially postcricoid tumors) .
- Age ; >70 years .
- Precipitating factors ; alcohol & smoking .
- Risk factors ; tea , vitamin A deficiency , iron deficiency & decrease S. cholestrol
- Dysphagia ; mechanical , often persistent & progressive , patient who complaint that food
sticks on swallowing need investigation , it could result in aspiration & lung infection .
- Pain ; usually lateralized & more prominent on swallowing , may radiate to the ipsilateral
ear .
- Hoarsness ; if occur in association with dysphagia or referred otalgia , usually means
extension into the larynx .
- Neck mass ; likely to be due to nodal metastasis , but it may represent direct extension
through the thyrohyoid membrane .
- Haemoptysis ; unusual , occur with tumors of the pyriform fossa & postcricoid area .
- Weight loss ; suggest serious disease , loose several Kgs with dehydration & protein loss
especially in elderly .
The causes of advanced tumor at presentation ;
1. Large space of hypopharynx allow considerable growth before dysphagia development
2. The important adjacent structures are already involved .
3. Rich lymphatics , early LN metastasis .
The prognostic factors of hypopharungeal Ca. are ;
1. Tumor size ; less or more than 5 cm .
2. Site ; pyriform fossa & poterior pharyngeal wall do the best .
3. Vocal cord paresis .
4. Presence or absence of LN metastasis .

Lecture notes in
5. Size & number of LN involvement .

6. Distant metastasis , absence or presence .
Staging
To decide the type of management & the prognosis .
T1 : tumor limited to one subsite of the hypopharynx & < 2 cm in greater diameter
T2 : tumor invade more than one subsite of the hypopharynx or an adjacent site , or
measures > 2 cm , but not >4 cm in greater diameter without fixation of the hemilarynx .
T3 : tumor > 4 cm in greater diameter or with fixation of the hemilarynx .
T4 : tumor invade adjacent structures like thyroid & cricoid cartilage , carotid artery , soft
tissue of the neck , prevertebral fascia , muscles , thyroid gland or esophagus .
Stage 0 : Tis N0 M0
Stage I : T1 N0 M0
Stage II : T2 N0 M0
Examination
Need full ENT & general examination .
- Pharynx & larynx , examined in outpatient by indirect laryngeal mirror examination ,
rigid endoscope through the mouth or a flexible nasopharyngoscope .
Look for swelling or ulceration & pooling of saliva in the pyriform fossa (Chevalier
Jackson’s sign) & odema of the arytenoids (unilateral odema in the pyriform fossa tumor
& bilateral in postcricoid tumor) , also assess the larynx for vocal cord movement ,
airway, supraglotic or subglottic disease .
The remainder of theupper aerodigestive tract examined to exclude 2nd tumor .
- Neck ;
a. LN : specially the upper deep cervical LN , systemic LN , examine for the site , size ,
texture , contour , tenderness & mobility , if it is fixed to the sternomastoid , larynx ,
carotid sheath or prevertebral muscles .
b. Laryngeal crepitus ; if absence , indicates postcricoid or posterior pharyngeal wall
involvement .
- General examination ; cachexic , anaemic , cyanosed , dyspnoeic , skin wrinkled , angular
stomatitis & chelosis .
Investigations
1. Laboratory ; CBP ,(B12 & folate level) , iron stores , urea & electrolytes , LFT , S.
Calcium , thyroid function test …etc .
2. Radiology ;
a. Plain x-ray ; lateral soft tissue of the neck (show widening of the retropharyngeal
space) & CXR for secondary tumor or metastasis of fitness .
b. Barium swallow ; Barium videofluroscopy , to assess tumor length , to exclude the
2 nd tumor in the esophagus , exclude aspiration , assess the tumor mobility or the
vertebral column during deglutition .
c. CT & MRI ;
- To assess the extent of the tunor , its relation to the larynx , extension into the
paraglottic space & postcricoid region & direct extension into the surrounding
structures to include the neck & pulmonary function .

Lecture notes in
- To exclude a 2nd primary tumor or distant metastasis (skull base to liver CT) .
- To assess the absence or presence of cartilage invasion .
- To assess the neck .
- To assess the stomach prior to gastric transposition .
- To confirm or refute the presence of pharyngeal pouch .
3. Endoscopy ; to assess the following areas ;
- Superio & inferior spread , larynx , pharynx , trachea & esophagus , tongue base
& tonsils .
- Posterior pharyngeal wall , prevertebral muscles involvement .
- Lateral extension into the neck & thyrohyoid membrane .
- Assess the submucosal skipped lesions extending beyond the apparent limit of the
tumor .
- Visualization of the bronchus by bronchoscope .
- Before awaking the patient , do ; examination to the neck LN , examination to the
base of the tongue , posterior pharyngeal wall by finger & assess the vocal cord
mobility .
4. Biopsy ; either by endoscopy , from the tumor mass , or for LN by FNA with U/S guide .
Management
The determinant for Rx planning
- Tumor factors ; anatomical subsites , staging & grading .
- Patient factors ; general condition , nutritional status & immunity .
- External factors ; the availability of expert surgeons , ethnic consideration , family
understanding about the outcome of management .
The benign tumors ; pedunculated managed usually by surgery , either by lateral
pharyngotomy or endoscopic excision .
The malignant tumors (SCC) ; many points should be taken in consideration 1st ;
1. Tumor , patient & external factors should be taken in consideration .
2. There must be aware of changes in life .
3. Meeting other laryngectomies patients to understood by the patient .
4. They should know whether the Rx is curative or palliative .
5. In incurable lesion , do N/G tube or gastrostomy tube .
6. 25% of patients are not manageable at the presentation .
7. The prognosis is about 60% die in the 1st year of diagnosis .
The causes of untreatability & incurability ;
1. Advanced age & poor general condition .
2. Local tumor inoperability , like pyriform fossa tumor extended into the tongue base ,
or postcricoid tumor fixed to the prevertebral fascia .
3. Extensive neck disease , fixed , bilateral & size >3 cm .
4. Vocal cord paralysis due to extension of the tumor outside the esophagus to invade
the recurrent laryngeal nerve at the tracheosephageal groove .
The neck diseases are ;
- 60% of piriform fossa tumors associated with +ve LN in the neck .
- 30-40% of clinically healthy LN harbour occult disease .
- management modalities depends on the stage of the primary tumor ;
a. N0 ; radiation is the main Rx , especially in T1&T2 or RND (id Rx of the primary
tumor is surgery) .

Lecture notes in
Surgery here has advantage over radiotherapy in providing staging , used in

decision regarding the postoperative radiation .
Sometimes , the ipsilateral or contralateral (in large primary) paratracheal LN
should be removed to reduce risk of stomal recurrence .
b. N1 ; if small primary , Rx by radiation , if the primary managed bt surgery
(T3&T4) , then surgery with postoperative radiation if there is extranodal spread
Advantages of surgery over radiation (in N1) is that no delay which is needed in
radiotherapy postoperatively .
c. N2-3 ; extranodal invasion , surgery (RND) with postoperative radiation
The management modalities are ;
1. Radiotherapy
- Used for the primary tumors , pre- & postoperative & prphylactically & for
palliation .
- Field of radiotherapy cover the primary tumor , both sides of the neck , from the
skull base to the clavicles & to trapezius muscle posteriorly .
- Combined radiation & surgery , either pre- or postoperatively .
- Radiotherapy has 2 forms ;
a. Hyperfractionated , smaller fractions , increase the number of fractions &
increase the total dose .
b. Accelerated hyperfractionated , smaller fractions , increase numbers of
fractions & shorter duration of radiation .
- The criteria for primary radiation are ; N0 , mobile vocal cords & vertical length
of tumor < 5 cm .
- The dose (conventional dose) , 60-74 Gy , hyperfractionation consist of 2 fractions
per day (separated by 3-6 hours) to a total dose of up to 60 Gy .
- The preoperative radiation given to a dose of 50 Gy in 20 daily fractions & surgery
after 6 weeks .
- In postoperative radiation , start within 6 weeks of surgery (better control) , 50-60
Gy for LN in 20 fractions .
2. Resection of the tumors
a. Endoscopic pharyngectomy .
b. Partial pharyngectomy(PP) .
c. Partial pharyngectomy & supraglotic laryngectomy (PP&SL) .
d. Total laryngectomy & pharyngectomy pharyngectomy (TLPP) .
e. Total pharyngectomy (TP) .
f. Total pharyngolaryngoesophagectomy (TPLO) .
Laser or diathermy used to resect locally small accessible tumors along with the small
recurrence , especially posterior pharyngeal wall via oral or lateral pharyngotomy .
3. Pharyngeal reconstruction
a. Partial pharyngeal reconstruction ; by ; split skin graft , pectoralis major
musculcutaneous flap , radial forearm flap or free jujenal transfer .
b. Total pharyngeal & pharyngo-esophageal reconstruction ; by ; pectorlais
major flap , deltopectoral flap , gastric transposition (when the lesion extend
to the thorax) , or free jujenal transfer .
The free jujenal transfer has success rate of about 90% with 2-3 weeks of
hospitalization , the mortality 6-17% , the swallowing restored in 2-3 weeks .

Lecture notes in
While in gastric transposition , the mortality 11% with the same period of
hospitalization .
4. Nutrition
- The nutritional status of the patient should be assessed , > 10% of body
weight loss , we do total paraentral nutrition ; 5-7 days preoperatively & 7-10
day postoperatively (for jujenal transfer) .
- Entral feeding started after starting bowel sound , by N/G tube or direct
percutaneous route , continuous infusion or bolus feeding .
- Oral intake begin between 7-14 days .
- In case of postoperative fistula or following radiotherapy , also we use total
paraentral nutrition
- The assessment of nutritional status carried out by ; regular weighting ,
monitoring of S.albumin , Hb% & S. prealbumin & transferrin .
- Feeding protocol “postoperative entral feeding” ;
(1) Day 1 ; full strength standard polymeric feed (nutrism) , i.e. glucose +
electrolytes at 50 ml/hr & increased in 6 hour rate as the patient tolerate
(increase 25 ml) up to 100 ml/hr , if feeding over 20 hours , additional i.v.
fluid usually required .
(2) Day 2 ; adjust the feed rate to meet fluid & nutritional requirement .
(3) Day 3 ; when fill feed rate is achieved , monitor the nutritional status by ;
fluid balance (daily) , bowel habbit (daily) , S. biochemistry & urea ,
electrolytes , LFT & glucose (twice weekly) & weight (twice weekly) .
5. Rehabilitation ; for breathing , swallowing & speech (tracheosphageal puncture) ,
gastric transposition achieve higher scores than other reconstruction group.
6. follow up ; patient should reviewed at regular intervals for ;
a. Evidence of recurrence (local or regional) , small local recurrence can be Rx
b. Development of 2 nd primary tumor .
7. Complications of management ;
A . Radiation
(4) Weight loss due to mucositis , dysphagia & odynophagia , so the patient need
admission & N/G tube feeding .
(5) Delayed speech rehabilitation , especially if surgery precede radiation .
(6) Stenosis of the pharyngeal repair & tracheal stoma .
(7) Xerostomia due to salivary gland affection , so the patient always carry a bottle
of water to lubricate the mouth .
(8) Hypothyroidism .
(9) Difficult early detection of the nodal recurrence (neck radiation) & less
readilycontrolled by neck dissection after radiation .
B. Surgery
(1) Short term ;
a. Problems in swallowing , breathing , talking & feeding .
b. Pharyngocutaneous fistula , delay oral intake .
c. Aspiration , in patient with intact larynx .
(2) Late complications ;
a. Stenosis of the pharynx .
b. Local recurrence or regional recurrence .

Lecture notes in
c. Pain & discomfort on shoulder , in those with trapezius muscle loss .

The palliative care , used when the tumor is advanced & beyond management ;
2. Pain ; managed by pain killers (without surgery or radiation) .
3. Dysphagia ; gastrostomy feeding .
4. Dyspnoea ; tracheostomy .
The curative management of hypopharyngeal tumor
N.B.:
1. If the lesion not reach to the apex of the pyriform fossa or postcricoid area , we can
preserve the larynx .
2. If the lateral wall of the pyriform fossa involved alone (rare) , then the Rx is by
partial pharyngectomy with resection of the upper thyroid ala .
Surgical procedures
1. Partial pharyngectomy
- Indications ;
a. Small tumor (T1) .
b. Confind to the posterior pharyngeal wall .
c. Confind to the lateral wall of the pyriform fossa .
Pyriform sinus Post. Pharyngeal wall Postcricoid
Stage I R or S (PP or PPPL) R or S (PP) R or S (TLP)
Stage II R or S (PPPL or TLP) R or S (PP or TLP) R or S (TLP)+ postop. R .
Stage III S (TLPP or TLP) + postop. R . S (Ppor TLP)+postop. R S (TLP or TLPO)+ postop. R
Stage IV S (TLPP or TLP)+ postop. R . S (TLP)+ postop. R . S(TLPO) + postop. R .
d. Advanced node disease renderin primary Rx by radiation alone (T1N2-3) .
- Approaches ; either through the thyrohyoid membrane or transhyoid approach .
- In pyriform fossa tumor , the inferior constrictor muscle must be separated from
the thyroid ala , so that portion of thyroid ala can be removed with the specimen .
- Pharyngeal closure , easy in pyriform fossa through the lateral approach , while
for the posterior pharyngeal wall tumor , revascularized radial forearm flap used
2. Partial pharyngectomy & Partial laryngectomy , Indications are ;
a. Tumors of the superior aspect of the medial wall of the pyriform fossa &
doesn’t extend into the apex , partial pharyngectomy & supraglotic
laryngectomy (including the aryepiglottic fold , ipsilateral vocal cord & the
epiglottis) through lateral pharyngeal approach .
b. Tumors involve the medial wall & the apex of the pyriform fossa with normal
vocal cords mobility , partial pharyngectomy with vocal cord & false cords &
aryepiglottic fold through lateral pharyngeal approach .
3. Partial pharyngectomy & near total laryngectomy (or total laryngectomy) , indicated
tumor of the hypopharynx & fixed vocal cords .
4. Total pharyngeosphagoectomy & replacement with stomach transposition
- Anaesthesia & preparation ; GA with ETT , the patient cleaned from the chin to
suprapubic area .
- Neck incision ; classical Gluck-Sorenson incision with side arm extension to
facilitate neck dissection , the specimen is left attached at this stage & then the
pharynx , larynx & the whole throid gland are mobilized from the carotid sheath ,
the uperior & inferior laryngeal neurovascular pedicle divided & a tracheostome
created .

Lecture notes in
- Abdominal incision ; left upper paramedian incision done , stomach & esophagus
mobilized with preservation of the right gastric & right gastroepiploic arteries ,
the 1 st two parts of the duodenum are freed & pyloroplasty is done .
The thoracic esophagus mobilized by blunt dissection from above downwards , then
stomach is pulled into the neck & the pharynx then divided above the level of the
hyoid & the esophagus divided from the upper stomach & close to the opening
lefted , then an incision is made in the fundus of the stomach which is anastamosed
to the base of the tongue , then we take CXR postoperatively to exclude
pneumothorax (if present , do chest tube) .
Sometimes we do jujenal transfer (free flap) instead of stomach in which we need
also two teams , the jujenal flap is removed (10-12 cm) from abdomen .
In the neck operation , suitable blood vessel for icrovascular anastamosis should
be preserved (external carotid artery or superior thyroid artery or facial artery) ,
also venous anastamosis using external or internal jugular veins , the graft is
transferred to the neck , a feeding gastrostomy is fashioned before the abdomen
closed .
The microvascular anastamosis done before sewing the flap to the pharyngeal
defect , the carotid artery on the side of the neck dissection is covered with
mesentry of the flap for prortection in case of fistula .
5. The Gastric transposition , when resection below the thoracic inlet .
- Advantage ;
1. Single anastamosis .
2. Rapid swallowing restoration .
3. Elasticity of the stomach allow easy extension to the neck .
4. Getrid of risk of second primary in the esophagus or potential skip lesion
5. Good perfusion of the stomach , no need for vascular anastamosis .
- Disadvantages ;
1. Not used in patients with previous gastric surgery .
2. Reflux & dumping syndrome in 55% of patients .
3. High mortality , about 11% .
4. Post operative radiotherapy lead to gastric haemorrhage .
6. Free jujenal flap , when the resection above the thoracic inlet
- Advantage ;
1. mucosal surface , easily lubrication .
2. 90% success rate .
3. the lumen is of appropriate diameter .
- Disadvantages ;
1. mortality rate about 6% .
2. high rate of complications .
3. fistula at the site of anastamosis .

Lecture notes in
Tumors of the hypopharynx

Anatomy
The hypopharynx extends from its juncture with the oropharynx at the level of the hyoid
bone to the inferior border of the cricoid cartilage .
It is divided into three anatomic sites: the piriform fossa, or sinus; the postcricoid region;
and the posterior hypopharyngeal wall
A comprehensive description of the anatomy of this region is not appropriate for this
chapter, but several important anatomic features must be emphasized in relation to the
treatment of hypopharyngeal cancers.
The vasculature of the hypopharynx is derived directly from the great vessels of the neck,
which are, in themselves, positioned adjacent to its lateral walls. Any incision or excision of
the hypopharynx therefore requires careful isolation of the parent vessels to avoid injury.
Tumor also may spread directly from the lateral walls of the piriform fossae to these
structures.
The nerve supply to the hypopharynx is mixed. Sensory fibers are derived from the
glossopharyngeal nerve and the internal branches of the superior laryngeal nerves. The
motor supply to the region is from the pharyngeal plexus for the inferior constrictors and
the recurrent laryngeal nerves for the cricopharyngeus muscle.
The lymphatic drainage of the hypopharynx is of major importance in cancer therapy. Most
of the lymphatic flow from this region is directed toward the upper deep cervical lymph
nodes. There are, however, channels that extend superiorly from the hypopharynx into the
retropharyngeal nodes as high as the nodes of Rouvier at the skull base. Inferiorly, there is
a varied and extensive lymph drainage system from the piriform apex and postcricoid
regions. Here the lymphatics extend laterally to the juguloomohyoid nodes and inferiorly to
the paratracheal, paraesophageal, and thyroid nodes. In the medial aspect of the piriform
fossa, there is crossover with the lymphatics of the larynx at the aryepiglottic folds and the
arytenoids. Extensive submucosal lymphatics are found in the hypopharynx, particularly in
the inferior portions.
Physiology
The hypopharynx is an important component of both respiration and deglutition.
Hypopharyngeal cancers alter these physiologic functions in several ways.
Pure obstruction to swallowing or respiration may occur but only from very large or
pedunculated tumors.
In most cases of obstruction, edema occurs secondary to lymphatic invasion or infection.
Obstruction to swallowing also may occur from neural invasion that causes alterations in
the delicate neuromuscular balance between the inferior constrictor and the
cricopharyngeus muscles.
Pain from neural invasion, or secondary infection, also may produce a physiologic
obstruction. Invasion of the arytenoid or the recurrent laryngeal nerve also can cause
airway obstruction and aspiration as a result of vocal cord paralysis.
Pathology
The main tumor of the hypopharynx is sequamous cell Ca. (SCC) , it is found in 40% in the
postcricoid area , 10% in the posterior pharyngeal wall & ½ -2/3 rd of patients in the
pyriform sinus .

Lecture notes in
It is of poor prognosis (less than 30% 5 years survival) , the hypopharyngeal Ca. may
metastasis early 1st to the cervical LN especially pyriform fossae tumor , many patients
presented with occult primary (30-40%) .
The most common is the pyriform sinus , ½-2/3rd of cases , it is either involving the medial
wall or lateral wall primarily .
III. Medial wall tumor ; more extensive , extends through the aryepiglottic space to invade
the paraglottic space , fix the hemilarynx & can also extnd into the pre-epiglottic space ,
then to the postcricoid area & then invade the cricoarytenoid joint fixing it leading to
vocal cord fixation .
IV. Lateral wall tumors ; extends through the thyroid cartilage & thyrohyoid membrane
causing palpable mass in the neck (25% involve the carotid sheath & thyroid gland) .
Other tumors are ;
- Benign ; lieomyomas is the most common , usually affect the male > female in the 3rd -5th
decade of life , causing rubbery & firm intramural swelling (when small) , when increased
in size it dragged down into the oesophagus by swallowing , it managed by pharyngotomy
with removal of the tumor .
Others like lipoma & fibrolipoma causing dysphagia & chocking sensation (managed as
liemyosarcoma) .
- Malignant , usually lieomyosarcoma , psuedosarcoma & adenoid cystic Ca. &
plasmacytoma .
Epidemiology
- Sex ; female > male (especially postcricoid tumors) .
- Age ; >70 years .
- Precipitating factors ; alcohol & smoking .
- Risk factors ; tea , vitamin A deficiency , iron deficiency & decrease S. cholestrol
- Dysphagia ; mechanical , often persistent & progressive , patient who complaint that food
sticks on swallowing need investigation , it could result in aspiration & lung infection .
- Pain ; usually lateralized & more prominent on swallowing , may radiate to the ipsilateral
ear .
- Hoarsness ; if occur in association with dysphagia or referred otalgia , usually means
extension into the larynx .
- Neck mass ; likely to be due to nodal metastasis , but it may represent direct extension
through the thyrohyoid membrane .
- Haemoptysis ; unusual , occur with tumors of the pyriform fossa & postcricoid area .
- Weight loss ; suggest serious disease , loose several Kgs with dehydration & protein loss
especially in elderly .
The causes of advanced tumor at presentation ;
1. Large space of hypopharynx allow considerable growth before dysphagia development
.
2. The important adjacent structures are already involved .
3. Rich lymphatics , early LN metastasis .
The prognostic factors of hypopharungeal Ca. are ;
1. Tumor size ; less or more than 5 cm .
2. Site ; pyriform fossa & poterior pharyngeal wall do the best .
3. Vocal cord paresis .

Lecture notes in
4. Presence or absence of LN metastasis .

5. Size & number of LN involvement .
6. Distant metastasis , absence or presence .
Staging
To decide the type of management & the prognosis .
T1 : tumor limited to one subsite of the hypopharynx & < 2 cm in greater diameter
T2 : tumor invade more than one subsite of the hypopharynx or an adjacent site , or
measures > 2 cm , but not >4 cm in greater diameter without fixation of the hemilarynx .
T3 : tumor > 4 cm in greater diameter or with fixation of the hemilarynx .
T4 : tumor invade adjacent structures like thyroid & cricoid cartilage , carotid artery , soft
tissue of the neck , prevertebral fascia , muscles , thyroid gland or esophagus .
Stage 0 : Tis N0 M0
Stage I : T1 N0 M0
Stage II : T2 N0 M0
Examination
Need full ENT & general examination .
- Pharynx & larynx , examined in outpatient by indirect laryngeal mirror examination ,
rigid endoscope through the mouth or a flexible nasopharyngoscope .
Look for swelling or ulceration & pooling of saliva in the pyriform fossa (Chevalier
Jackson’s sign) & odema of the arytenoids (unilateral odema in the pyriform fossa tumor
& bilateral in postcricoid tumor) , also assess the larynx for vocal cord movement ,
airway, supraglotic or subglottic disease .
The remainder of theupper aerodigestive tract examined to exclude 2nd tumor .
- Neck ;
a. LN : specially the upper deep cervical LN , systemic LN , examine for the site , size ,
texture , contour , tenderness & mobility , if it is fixed to the sternomastoid , larynx ,
carotid sheath or prevertebral muscles .
b. Laryngeal crepitus ; if absence , indicates postcricoid or posterior pharyngeal wall
involvement .
- General examination ; cachexic , anaemic , cyanosed , dyspnoeic , skin wrinkled , angular
stomatitis & chelosis .
Investigations
1. Laboratory ; CBP ,(B12 & folate level) , iron stores , urea & electrolytes , LFT , S.
Calcium , thyroid function test …etc .
2. Radiology ;
a. Plain x-ray ; lateral soft tissue of the neck (show widening of the retropharyngeal
space) & CXR for secondary tumor or metastasis of fitness .
b. Barium swallow ; Barium videofluroscopy , to assess tumor length , to exclude the
2 nd tumor in the esophagus , exclude aspiration , assess the tumor mobility or the
vertebral column during deglutition .
c. CT & MRI ;

Lecture notes in
- To assess the extent of the tunor , its relation to the larynx , extension into the
paraglottic space & postcricoid region & direct extension into the surrounding
structures to include the neck & pulmonary function .
- To exclude a 2nd primary tumor or distant metastasis (skull base to liver CT) .
- To assess the absence or presence of cartilage invasion .
- To assess the neck .
- To assess the stomach prior to gastric transposition .
- To confirm or refute the presence of pharyngeal pouch .
5. Endoscopy ; to assess the following areas ;
- Superio & inferior spread , larynx , pharynx , trachea & esophagus , tongue base
& tonsils .
- Posterior pharyngeal wall , prevertebral muscles involvement .
- Lateral extension into the neck & thyrohyoid membrane .
- Assess the submucosal skipped lesions extending beyond the apparent limit of the
tumor .
- Visualization of the bronchus by bronchoscope .
- Before awaking the patient , do ; examination to the neck LN , examination to the
base of the tongue , posterior pharyngeal wall by finger & assess the vocal cord
mobility .
6. Biopsy ; either by endoscopy , from the tumor mass , or for LN by FNA with U/S guide .
Management
The determinant for Rx planning
- Tumor factors ; anatomical subsites , staging & grading .
- Patient factors ; general condition , nutritional status & immunity .
- External factors ; the availability of expert surgeons , ethnic consideration , family
understanding about the outcome of management .
The benign tumors ; pedunculated managed usually by surgery , either by lateral
pharyngotomy or endoscopic excision .
The malignant tumors (SCC) ; many points should be taken in consideration 1st ;
1. Tumor , patient & external factors should be taken in consideration .
2. There must be aware of changes in life .
3. Meeting other laryngectomies patients to understood by the patient .
4. They should know whether the Rx is curative or palliative .
5. In incurable lesion , do N/G tube or gastrostomy tube .
6. 25% of patients are not manageable at the presentation .
7. The prognosis is about 60% die in the 1st year of diagnosis .
The causes of untreatability & incurability ;
1. Advanced age & poor general condition .
2. Local tumor inoperability , like pyriform fossa tumor extended into the tongue base ,
or postcricoid tumor fixed to the prevertebral fascia .
3. Extensive neck disease , fixed , bilateral & size >3 cm .
4. Vocal cord paralysis due to extension of the tumor outside the esophagus to invade
the recurrent laryngeal nerve at the tracheosephageal groove .
The neck diseases are ;
- 60% of piriform fossa tumors associated with +ve LN in the neck .
- 30-40% of clinically healthy LN harbour occult disease .

Lecture notes in
- management modalities depends on the stage of the primary tumor ;

a. N0 ; radiation is the main Rx , especially in T1&T2 or RND (id Rx of the primary
tumor is surgery) .
Surgery here has advantage over radiotherapy in providing staging , used in
decision regarding the postoperative radiation .
Sometimes , the ipsilateral or contralateral (in large primary) paratracheal LN
should be removed to reduce risk of stomal recurrence .
b. N1 ; if small primary , Rx by radiation , if the primary managed bt surgery
(T3&T4) , then surgery with postoperative radiation if there is extranodal spread
Advantages of surgery over radiation (in N1) is that no delay which is needed in
radiotherapy postoperatively .
c. N2-3 ; extranodal invasion , surgery (RND) with postoperative radiation
The management modalities are ;
8. Radiotherapy
- Used for the primary tumors , pre- & postoperative & prphylactically & for
palliation .
- Field of radiotherapy cover the primary tumor , both sides of the neck , from the
skull base to the clavicles & to trapezius muscle posteriorly .
- Combined radiation & surgery , either pre- or postoperatively .
- Radiotherapy has 2 forms ;
a. Hyperfractionated , smaller fractions , increase the number of fractions &
increase the total dose .
b. Accelerated hyperfractionated , smaller fractions , increase numbers of
fractions & shorter duration of radiation .
- The criteria for primary radiation are ; N0 , mobile vocal cords & vertical length
of tumor < 5 cm .
- The dose (conventional dose) , 60-74 Gy , hyperfractionation consist of 2 fractions
per day (separated by 3-6 hours) to a total dose of up to 60 Gy .
- The preoperative radiation given to a dose of 50 Gy in 20 daily fractions & surgery
after 6 weeks .
- In postoperative radiation , start within 6 weeks of surgery (better control) , 50-60
Gy for LN in 20 fractions .
9. Resection of the tumors
a. Endoscopic pharyngectomy .
b. Partial pharyngectomy(PP) .
c. Partial pharyngectomy & supraglotic laryngectomy (PP&SL) .
d. Total laryngectomy & pharyngectomy pharyngectomy (TLPP) .
e. Total pharyngectomy (TP) .
f. Total pharyngolaryngoesophagectomy (TPLO) .
Laser or diathermy used to resect locally small accessible tumors along with the small
recurrence , especially posterior pharyngeal wall via oral or lateral pharyngotomy .
10. Pharyngeal reconstruction
a. Partial pharyngeal reconstruction ; by ; split skin graft , pectoralis major
musculcutaneous flap , radial forearm flap or free jujenal transfer .

Lecture notes in
b. Total pharyngeal & pharyngo-esophageal reconstruction ; by ; pectorlais

major flap , deltopectoral flap , gastric transposition (when the lesion extend
to the thorax) , or free jujenal transfer .
The free jujenal transfer has success rate of about 90% with 2-3 weeks of
hospitalization , the mortality 6-17% , the swallowing restored in 2-3 weeks .
While in gastric transposition , the mortality 11% with the same period of
hospitalization .
11. Nutrition
- The nutritional status of the patient should be assessed , > 10% of body
weight loss , we do total paraentral nutrition ; 5-7 days preoperatively & 7-10
day postoperatively (for jujenal transfer) .
- Entral feeding started after starting bowel sound , by N/G tube or direct
percutaneous route , continuous infusion or bolus feeding .
- Oral intake begin between 7-14 days .
- In case of postoperative fistula or following radiotherapy , also we use total
paraentral nutrition
- The assessment of nutritional status carried out by ; regular weighting ,
monitoring of S.albumin , Hb% & S. prealbumin & transferrin .
- Feeding protocol “postoperative entral feeding” ;
(1) Day 1 ; full strength standard polymeric feed (nutrism) , i.e. glucose +
electrolytes at 50 ml/hr & increased in 6 hour rate as the patient tolerate
(increase 25 ml) up to 100 ml/hr , if feeding over 20 hours , additional i.v.
fluid usually required .
(2) Day 2 ; adjust the feed rate to meet fluid & nutritional requirement .
(3) Day 3 ; when fill feed rate is achieved , monitor the nutritional status by ;
fluid balance (daily) , bowel habbit (daily) , S. biochemistry & urea ,
electrolytes , LFT & glucose (twice weekly) & weight (twice weekly) .
12. Rehabilitation ; for breathing , swallowing & speech (tracheosphageal puncture) ,
gastric transposition achieve higher scores than other reconstruction group.
13. follow up ; patient should reviewed at regular intervals for ;
a. Evidence of recurrence (local or regional) , small local recurrence can be Rx
.
b. Development of 2 nd primary tumor .
14. Complications of management ;
A . Radiation
(4) Weight loss due to mucositis , dysphagia & odynophagia , so the patient need
admission & N/G tube feeding .
(5) Delayed speech rehabilitation , especially if surgery precede radiation .
(6) Stenosis of the pharyngeal repair & tracheal stoma .
(7) Xerostomia due to salivary gland affection , so the patient always carry a bottle
of water to lubricate the mouth .
(8) Hypothyroidism .
(9) Difficult early detection of the nodal recurrence (neck radiation) & less
readilycontrolled by neck dissection after radiation .
B. Surgery
(1) Short term ;

Lecture notes in
a. Problems in swallowing , breathing , talking & feeding .

b. Pharyngocutaneous fistula , delay oral intake .
c. Aspiration , in patient with intact larynx .
(2) Late complications ;
a. Stenosis of the pharynx .
b. Local recurrence or regional recurrence .
c. Pain & discomfort on shoulder , in those with trapezius muscle loss .
The palliative care , used when the tumor is advanced & beyond management ;
1. Pain ; managed by pain killers (without surgery or radiation) .
2. Dysphagia ; gastrostomy feeding .
3. Dyspnoea ; tracheostomy .
The curative management of hypopharyngeal tumor
N.B.:
1. If the lesion not reach to the apex of the pyriform fossa or postcricoid area , we can
preserve the larynx .
2. If the lateral wall of the pyriform fossa involved alone (rare) , then the Rx is by partial
pharyngectomy with resection of the upper thyroid ala .
Pyriform sinus Post. Pharyngeal wall Postcricoid
Stage I R or S (PP or PPPL) R or S (PP) R or S (TLP)
Stage II R or S (PPPL or TLP) R or S (PP or TLP) R or S (TLP)+ postop. R .
Stage III S (TLPP or TLP) + postop. R . S (Ppor TLP)+postop. R S (TLP or TLPO)+ postop. R
Stage IV S (TLPP or TLP)+ postop. R . S (TLP)+ postop. R . S(TLPO) + postop. R .
Surgical procedures
1. Partial pharyngectomy
- Indications ;
a. Small tumor (T1) .
b. Confind to the posterior pharyngeal wall .
c. Confind to the lateral wall of the pyriform fossa .
d. Advanced node disease renderin primary Rx by radiation alone (T1N2-3) .
- Approaches ; either through the thyrohyoid membrane or transhyoid approach .
- In pyriform fossa tumor , the inferior constrictor muscle must be separated from
the thyroid ala , so that portion of thyroid ala can be removed with the specimen .
- Pharyngeal closure , easy in pyriform fossa through the lateral approach , while
for the posterior pharyngeal wall tumor , revascularized radial forearm flap used
2. Partial pharyngectomy & Partial laryngectomy , Indications are ;
a. Tumors of the superior aspect of the medial wall of the pyriform fossa &
doesn’t extend into the apex , partial pharyngectomy & supraglotic
laryngectomy (including the aryepiglottic fold , ipsilateral vocal cord & the
epiglottis) through lateral pharyngeal approach .
b. Tumors involve the medial wall & the apex of the pyriform fossa with normal
vocal cords mobility , partial pharyngectomy with vocal cord & false cords &
aryepiglottic fold through lateral pharyngeal approach .
3. Partial pharyngectomy & near total laryngectomy (or total laryngectomy) , indicated
tumor of the hypopharynx & fixed vocal cords .
4. Total pharyngeosphagoectomy & replacement with stomach transposition

Lecture notes in
- Anaesthesia & preparation ; GA with ETT , the patient cleaned from the chin to
suprapubic area .
- Neck incision ; classical Gluck-Sorenson incision with side arm extension to
facilitate neck dissection , the specimen is left attached at this stage & then the
pharynx , larynx & the whole throid gland are mobilized from the carotid sheath ,
the uperior & inferior laryngeal neurovascular pedicle divided & a tracheostome
created .
- Abdominal incision ; left upper paramedian incision done , stomach & esophagus
mobilized with preservation of the right gastric & right gastroepiploic arteries ,
the 1 st two parts of the duodenum are freed & pyloroplasty is done .
The thoracic esophagus mobilized by blunt dissection from above downwards , then
stomach is pulled into the neck & the pharynx then divided above the level of the
hyoid & the esophagus divided from the upper stomach & close to the opening
lefted , then an incision is made in the fundus of the stomach which is anastamosed
to the base of the tongue , then we take CXR postoperatively to exclude
pneumothorax (if present , do chest tube) .
Sometimes we do jujenal transfer (free flap) instead of stomach in which we need
also two teams , the jujenal flap is removed (10-12 cm) from abdomen .
In the neck operation , suitable blood vessel for icrovascular anastamosis should
be preserved (external carotid artery or superior thyroid artery or facial artery) ,
also venous anastamosis using external or internal jugular veins , the graft is
transferred to the neck , a feeding gastrostomy is fashioned before the abdomen
closed . The microvascular anastamosis done before sewing the flap to the
pharyngeal defect , the carotid artery on the side of the neck dissection is covered
with mesentry of the flap for prortection in case of fistula .
5. The Gastric transposition , when resection below the thoracic inlet .
- Advantage ;
1. Single anastamosis .
2. Rapid swallowing restoration .
3. Elasticity of the stomach allow easy extension to the neck .
4. Getrid of risk of second primary in the esophagus or potential skip lesion
5. Good perfusion of the stomach , no need for vascular anastamosis .
- Disadvantages ;
1. Not used in patients with previous gastric surgery .
2. Reflux & dumping syndrome in 55% of patients .
3. High mortality , about 11% .
4. Post operative radiotherapy lead to gastric haemorrhage .
6. Free jujenal flap , when the resection above the thoracic inlet
- Advantage ;
1. mucosal surface , easily lubrication .
2. 90% success rate .
3. the lumen is of appropriate diameter .
- Disadvantages ;
1. mortality rate about 6% .
2. high rate of complications .
3. fistula at the site of anastamosis .

Lecture notes in
ANGIOFIBROMA
It is vascular swelling arising in the nasopharynx of prepubertal & adolescent males &
exhibiting a strong tendency to bleed .
It is common middle east & India males of 7-19 years , 1-2/2000 patients , with age the
swelling shrinkage & harden with loss of its vascularity .
Grossly ; it is firm , slightly spongy lobulated swelling , colour from pink (in the
nasopharynx because of mucous memberane covering) to white (in the extrapharyngeal
areas) .
On section ; spongy appearance or reticulated whorled & lack a true capsule , but sharply
demarkated edges .
Microscopically ; there is picture of vascular spaces (large thin walled sinusoidal vessels
lined by flattened epithelium unsupported by muscular coat , the nearer to the surface are
the smaller they become) of varying shape & size abounding in a stroma of fibrous tissue .
Early tumor has vascular predominant , while in more longstanding one there is collagen
predominant .
With age there is gradual compression of the sinusoids & s.t. thrombosed the stroma ,
composed of coarse parallel weavy or interlacing bundles of collagen in the stromal cells
seen to radiate outward from the vessels .
The pathogenesis unknown , but there are many theories to explain the origion of
angiofibroma ;
1. Ringertz theory ; nasopharyngeal periosteum .
2. Som & Neffson theory ; inequalities in the growth of bones of skull base leading to
hypertrophy of the underlying periosteum due to hormonal influence .
3. Ewing theory ; embryonic fibrocartilage between the basioccipt & basishenoid .
4. Brunner theory ; the conoined pharyngobasilar & buccopharyngeal fascia .
5. Osborn theory ; hamartoma or residues of fetal erectile tissue secondary to hormonal
effect .
6. Girgis & Fahmy theory ; paragangiloma .
7. Vestiges of the atrophied stapedial artery .
8. In past ; from the vault of the nasopharynx or concha (fail to precise the point of
origion) .
9. Modern ; sphenopalatine formena region is the site of origion (which explain the
subsequent behaviour of angiofibroma) , this based on the observation that larger tumors
present as bilibed dumb-bell swelling straddling the sphenopalatine foramena with one
component filling the nasopharynx & the other extending out into the ptyrgopalatine &
infratemporal fossae , the central stalk joining the two portions occupies the
sphenopalatine foramena at the upper end of the vertical plate of the palatine bone .
The seeding swelling arising from the sphenopalatine formena migrate ;
- Medially beneath the mucos memberane of the nasopharynx , displacing it
downwards & growing to fill the postnasal space , which continue growing leading
to erosion to the anterior face of the sphenoid sinus & the sinus invaded , then the
swelling follow the lines of least resistance & grows forwards into the nasal fossa
(may acquired secondary attachment) , so displace the septum to the unaffected side ,
so blocking thehealthy side also .
- Laterally ; from the sphenopalatine foramena to the sphenopalatine fossa which
invaded & once filled it causing forward bowing of the posterior wall of the antrum

Lecture notes in
(on x-ray called Holman-Miller sign or antral sign) , eventually occupy the
infratemporal fossa , then encroach the orbital fissures causing proptosis .
we must note that not all lesions behave like that , it may extend to the nasopharynx
with unilateral extension .
Also from the infratemporal fossa to erode the anterior face of the greater wing of the
sphenoid making contact with the dura of the middle fossa .
It may displace the maxillary nerve upwards & also the optic nerve .
The main blood supply to angiofibroma are ; (1) Enlarged maxillary artery (mainly) &
others (2) Ascending pharyngeal artery (3) Vidian artery (4) unnamed branch of internal
carotid artery (5) vertebral artery (rarely) .
The clinical picture are ;
- The symptoms are two cardinal symptoms ;
1. Nasal obstruction , which may be complete leading to stasis of secretions & sepsis
followed by anosmia .
2. Intermittant spontaneous , s.t. life threatening epistaxis which lead to chronic
anaemia .
3. Others ; like : (a) nasal speech with plummy quality (b) deafness & otalgia
secondary to Eustachian tube blockage (c) headache due to secondary sinusitis or
dural compression (d) blindness due to optic nerve tenting or proptosis secondary to
orbital fissures invasion .
- The signs are ;
1. Anterior rhinoscopy shows abundant mucopurulent secretions with bowing of the
nasal septum towards the normal side .
2. Posterior rhinoscopy of cooperative relaxed patient shows pink or red mass filling
the nasopharynx .
3. Gross signs ; when extensive disease has involved the nose & infratemporal fossa ;
(a) widening of the nasal bones "splayed out" (b) obvious swelling in the temple &
check (c) fullness of the interval between the ascending ramus of the mandible & the
side of the maxilla (intraoral palpation) .
4. Extreme sign , the disease in the infratemporal fossa , trismus & bulging of the
parotid gland leading to typical frog face .
1. Plain film , sinus x-ray , sunmentovertical & lateral views , soft tissue shaddows in the
postnasal space with sinusitis (misleading with antrochoanal polyp) with antral sign .
2. Tomography in the fronto-occipital plane to : localize the position of the mass , show
the area of bone destruction & invasion of the sphenoid sinus , the lateral view will show
the antral sign which indicate that the lesion in the sphenopalatine fossa .
3. CT scan & MRI shows ; invasion of the sphenoid sinus , erosion of the greater wing of
the sphenoid & extension into the sphenopalatine & infratemporal fossae .
4. Selective angiography using subtraction method for Dx the recurrent disease or if
there is doubt of imaging , it gives an idea about site & size of the lesion & the size of
the feeding vessels .
The staging are ;
- Stage I ; tumor confind to the nasopharynx .
- Stage II ; tumor extend to the nasal cavity &/or sphenoid sinus .

Lecture notes in
- Stage III ; extension into the antrum , ethmoid sinus , pterygomaxillary or

infratemporal fossa , orbit , checks or any combinations .
- Stage IV ; intracranial extension .
The Differential diagnosis ; from the antrochoanal polyp , large adenoids , tumor of the
postnasal space & chordoma .
The Management are ;
The angiofibroma should be managed surgically , otherwise it expands into the adjacent
cavities especially the orbit causing blindness .
1. Hormonal therapy & Radiotherapy ; as a preoperative measures based on that they
promot collagen formation & there by reduce the vascularity causing shrinkage of the
mass , the hormon used are the Estrogen , or Testosteron or both .
The use of radiation is for selective patients like those with inoperable , intracranial
extension & recurrent tumors , the radiation cause shrinkage & hardening of the tumor
which reduce its vascularity , the radiation foreiden because it increase the risk of later
on malignant tumors & also affect the growth of bones of the face of the patient which
are usually adolescent .
The radiation given in 5 fractions over three weeks with total dose of 30Gy using the
three-field technique including the anterior field .
2. Preoperative emoblization may reduce the bleeding provided that the timing is right .
3. Surgery ; the management of choice ;
a. Tumors in the nasopharynx should be removed transpalatally or transorally , they
need access to the tumor in such way thet we gain safe dissection of the tumor from the
adjacent structuresto ensure that the tumor paranchyma is not breached in the process
& need suffuicient room to ligate the principle feeding vessels to the tumor , also can
use endoscopic transnasal approach .
b. Tumors in the nasal fossa & just spillover into the pterygopalatine fossa by lateral
rhinotomy combined with resection of the medial antral wall .
Larger tumors which invade the infratemporal fossa which need transantral
approach to access the lesion .
48 hours prior to surgery we use embolization to decrease the vascularity of the lesion
The Complications are ;
1. palatal fistula (in transpalatal approach) especially if the incision lies between the
hard & soft palate .
2. Anasthesia of the check (with Wber-Ferguson approach) .
3. Slight ectropion of the lower lid .
4. Crusting of the nose .
5. Recurrence which depends on the adequacy of the approach , the condition at
operation , the experience of the surgeon & the extent of the lesion .
The recurrent angiofibroma need another approach "facial disassembly approach" ,
s.t. use doxurobicin & decabazine (chemotherapuetic agents) .
The surgical approaches to the nasopharynx are ;
1. Transnal "endoscopic" approach ; used following embolization for the disease
confined to the nasopharynx (stage I) with very limited extension to the sphenopalatine
fossa & sphenoethmoid sinus , it may be used following transantral maxillary artery
ligation to enhance the effect of embolization .

Lecture notes in
The pedicle approached both lateral & medial & the ligaclips applied before avulsion of
the lesion , the tumor then delivered through the mouth .
2. Transoral approach ; used for nasopharyngeal biopsy , removal of adenoid &
masopharyngeal cysts , it is of no value in removing the angiofibroma .
3. Transpalatal approach ; used formerly to remove the angiofibroma , has access to the
lateral nasopharynx , so inadequate access for angiofibroma , palatal fistula occur in 40%
of cases postoperatively .
The incision started just inside the upper alveolus to provide a large flap & reach to the
bone (the incision) , the bony hard palate removed by cutting burr or nibbling forceps , it
is important that always there is bone underneath the incision line otherwise lead to
fistula , so the incision must be as far anterior as possible.
4. Transnasoantral approach ; this achieved by either Ferguson incision or facial
digloving approach (no facial scar postoperatively) .
The objective of that is expose the maxillary antrum , so the anterior , lateral , posterior
& medial walls of the antrum can be removed , leaving the orbital floor & upper alveolar
arch , so the nasal cavity , antrum , infratemporal fossa , sphenopalatine fossa &
nasopharynx are converted into one large continous space , so access to both compatment
of the swelling & its central stalk .
Then starting laterally , the infratemporal fossa part of the swelling is 1 st identified & the
maxillary artery found & ligated , then the tumor mobilized in a medial & forward
direction towards the antrum & the nasopharynx , then removing the vertical plate of
palatine bone serves to uncap the central stalk of the dumb-bell which previously occupy
the sphenopalatine foramena , so facillitate the subsequent mobilization of the
nasopharyngeal component of the tumor which dissected then freed from the base of skull
& from within sphenoid sinus & the mucous membrane covering its undersurface is
divided at its periphery in order to complete the removal of the tumor .
No attachment is made to strip the mucous memberane of the inferior aspect of the
swelling because of the close attachment between the two .
5. Transmaxillary approach ; the maxilla is approached with alveolar degloving incision
from tuberosity to tuberosity , then Lefort I osteotomies carried out & the alveolus is
fractured downwards .
It need intramaxillary fixation postoperatively , it is contraindicated below 12 years
(dentation) , it has alot of tissue damage leading to odema .
6. Maxillary swing ; required exposure of the whole face except for the contralateral eye
through a Weber-Fergusson incision (the horizontal limb extend to the zygoma , while the
vertical limb extend to the inner surface of the upper lip along the hard palate between the
two medial incision) , then turn laterally at the junction of the hard & soft palate to run
behind maxillary tuberosity .
The soft tissue externally remains attached to the underlying maxilla except at a narrow
strip of bone for osteotomy below the infraorbital margin keeping the floor of the orbit
intact , the tuberosity of maxilla seperated from the pterygoid plates by the transoral
insertion of curved osteotome exposing the whole mucosa of the nasopharynx , so en block
resection of the lesion with cartilagenous portion of the Eustachian tube , the internal
carotis artery must be identified & preserved .

Lecture notes in
Tonsillectomy & Adenoidectomy

Tonsillectomy & adenoidectomy , like all other surgical procedures should never be advised
unless it is virtually certain that the patient will benefit .
Large numbers of operations performed each year . It is the responsibility of every surgeon
to be certain that every one of these operations is performed for the correct indication .The
morbidity & mortality associated with such surgery are not to be taken lightly .
Tonsillectomy & adenoidectomy should be regarded as entirely separate procedures with
separate indications , on occasion with tonsils & adenoid will need to be removed at the
same time .
The decision to perform tonsil or adenoid surgery in most patients still based on a careful
history & examination .
Indications
A. Tonsillectomy
1. Infection
a. Recurrent, acute tonsillitis (more than six episodes per year or three episodes per
year for 2 years)
b. Recurrent acute tonsillitis associated with other conditions:
- Cardiac valvular disease associated with recurrent streptococcal tonsillitis
- Recurrent febrile seizures
- Recurrent attacks of acute rheumatism & some cases of acute
glomerulonephritis .
c. Chronic tonsillitis that is unresponsive to medical therapy associated with:
- Halitosis
- Persistent cervical adenitis (especially when suspect T.B.) .
- Tender cervical adenitis
- Streptococcal or Diphtheria carrier state unresponsive to medical therapy .
- Peritonsillar abscess ; which not absolute indication for tonsillectomy , a 2nd
quinsy is probably the point at which decide absolutely on tonsillectomy .
- Tonsillitis associated with abscessed cervical nodes
- Mononucleosis with severely obstructing tonsils that is unresponsive to medical
therapy.
2. Obstruction
a. Excessive snoring and chronic mouth-breathing
b. Obstructive sleep apnea or sleep disturbances
c. Adenotonsillar hypertrophy associated with:
- Cor pulmonale
- Failure to thrive
- Dysphagia
- Speech abnormalities
- Craniofacial growth abnormalities
- Occlusion abnormalities
3. Other
a. Suspected neoplasia–asymmetric tonsillar hypertrophy (biopsy purposes) .
b. To give access to other structures as gloosopharyngeal nerve in the treatment of
Glossopharyngeal neuralgia or styloid process for Eagle's syndrome .

Lecture notes in
B. Adenoidectomy
1. Infection
a. Purulent adenoiditis
b. Adenoid hypertrophy associated with:
- Chronic otitis media with effusion
- Chronic recurrent acute otitis media
- Chronic otitis media with perforation
- Otorrhea or chronic tube otorrhea .
2. Obstruction
a. Adenoid hypertrophy associated with excessive snoring and chronic mouth-
breathing
b. Sleep apnea or sleep disturbances
c. Adenoid hypertrophy associated with:
- Cor pulmonale
- Failure to thrive
- Dysphagia
- Craniofacial growth abnormalities
- Occlusion abnormalities
3. Other
a. Suspected neoplasia
b. Adenoid hypertrophy associated with chronic sinusitis
Contraindications
A. Tonsillectomy
1. Bleeding disorders , this should be investigated , diagnosed & treated before the
operation .
2. Recent infection , a recent within 4 weeks episodes of tonsillitis makes the surgery
more difficult & increase the incidence of haemorrhage . A recent URTI probably
increase the risk of pulmonary complications of GA & the operation should be
postponed for 2-3 weeks .
3. Oral contraceptives .
4. Local or national epidemic of poliomyelitis .
5. Cleft palate .
6. Uncontrolled systemic disease as DM , heart disease , seizure disorders ..etc .
B. Adenoidectomy
1. Recent URTI .
2. Bleeding tendency .
3. Cleft palate ; the adenoids assist in closure of the nasopharynx from the
oropharynx during swallowing & speech , the removal of adenoids may impair
speech , so the adenoid should never be removed in a child who has had cleft
palate repair , one who has congenitally short palate or in one who has a
submucous cleft palate .
Adenoidectomy should be regarded as a major operation with significant risk &
complications , 60-70% of blood loss during adenotonsillectomy is due to

Lecture notes in
adenoidectomy & the control of excessive bleeding following it is more difficult than
after tonsillectomy .
Preoperative consideration
1. Careful history & physical examination .
2. Recent URTI , bleeding tendency , coincidental anaemia or heart murmer must be
ruled out .
3. State of the patient dentition must be assessed & in particular carious or loose front
teeth or capped teeth must be looked for & the patient suitably informed of the risk .
4. Preoperative investigations ; CBP , ESR , CXR , PT & PTT , B.T. , C.T. & GUE .
5. Premedication ; ideally the patient should arrive the anaesthetic room drowsy or a
sleep , especially in children .
In adults single I.M. injection of 75 mg pethidin 1 hour before the operation with 25
mg promethazine , while in children between 6-10 years , papaveretum 15 mg & 0.8
mg scopolamine I.M. 1 hour before the operation .
Anaesthesia & Position
A. Tonsillectomy
GA is the routine for tonsillectomy with naso- or oro-tracheal cuffed intubation for
maintenance of the air way . After induction with thiopentone , the anaesthesia is
continued with nitrous oxide , oxygen & halothane .
The patient lies supine with the head extended slightly (sandbag under shoulders ,
excessive extension should be avoided .
B. Adenoidectomy
GA with cuffed orotracheal tube using halothane , nitrous oxide & oxygen to control the
depth of anaesthesia .
The child lie supine & flat on the table & the Boyle-Davis mouth gag is inserted , a
small wet pharyngeal pack should be put around the anaesthetic tube to prevent blood
entering the larynx .
Operative procedure
Before starting the operation the checking should be done for the instruments , light source
& counting the gauze swabs (before & after the operation) .
A. Tonsillectomy
- A Boyle-Davis mouth gag is introduce & open with the tongue blade in the midline
with care not to damage the lips , teeth , tongue & posterior pharyngeal wall . The
gag is secured in the optimum position with Draffin bipods .
- Incision ; the mucosa of the anterior & posterior tonsillar pillars should be incised in
such a way as to preserve as much mucosa as possible . The incision should start
half way between the upper & lower poles of the tonsil & carried downwards to the
base of the tongue & upwards to the upper pole .
- Dissection ; when the capsule of the tonsil has been identified a Gwyne Evan's or
similar blunt dissector is used to separate the tonsil . The plane of dissection is in the
loose areolar tissue between the capsule & the superior constrictor muscle .
- Mobilization of the upper pole ; it must be mobilized 1st , care being taken to keep the
dissection as close as possible to the capsule throughout the dissection ,Digging into
the fossa cause more bleeding & more postoperative scarring .

Lecture notes in
Gripping the tonsil by its upper pole , the surgeon continue to draw the tonsil toward
the midline & dissection continues towards the lower pole (triangular fold should be
cut with scissor) & the base of the tongue .
- Removal of the tonsil ; a cold wire snare is threaded over the tonsil which is finally
removed by closing the snare at the level of the tonsillolingual sulcus or Negus artery
forceps is used to cut & ligate the lower pedicle .
- Haemostasis ; bleeding points are identified & ligated .
It is usual to pack the fossa with gauze immediately following the removal of the
tonsil while the other tonsil removed . Much bleeding will have stopped by the the
gauze pack is removed .
- Recovery ; recovery from GA must be smooth , coughing & retching are liable to
cause bleeding , patient recovered on his side with his head down so that if bleeding
does begin , the blood will flow out of the nose & mouth . The airway must be
maintained all the time & noisy respiration may indicate that there is blood in the
airways .
B. Adenoidectomy
It is a blind procedure & great care must be taken to ensure that the curette engages the
upper end of the adenoids . The surgeon should select the broadest curette that will span
the width of the postnasal space without encroaching the Eustachian tubes orifice . If the
curette is toothed , the surgeon must check the number & stability of its teeth .
- Palpation of the postnasal space with index finger to ;
(1) Assess the width of the nasopharynx & size of the adenoid so as to choose
the appropriate curette .
(2) Exclude vascular lesions such as angiofibroma or aneurysm .
(3) Check for the Eustachian tube opening
- Insertion of the curette ; exerting a steady pressure on the curette , the adenoid is
shaved away with a firm sweeping movement of the wrist until the curette emerges
from behind the soft palate .
Similar lateral masses are removed in a V shaped movement using a smaller curette
controlled by careful palpation of any remnants .
- Pack is then placed in the nasopharynx for 5-10 minutes , if bleeding continue after
removal of the pack an adenoid remnants may be the cause , which should be
removed & a 2nd pack should be inserted & left for further 5 minutes , if bleeding still
continue , mirror examination of the nasopharynx may reveal bleeding point which
can be diathermized . If at this point bleeding continues , some advise the use of
diluted topical adrenaline on a swab & if the bleeding continues , then insertion of
postnasal pack remain for 24 hours .
There must be absolutely no bleeding from the nasopharynx before GA is terminated.
Postoperative care
- Postoperative care directed towards the detection of any bleeding as early as possible
by regular observation of pulse every 15 minutes for 4 hours , then every 30 minutes for
further 4 hours & then hourly . Blood pressure check hourly for 12 hours .
- Vomiting of blood or rise of PR means the tonsillar fossa must be examined for signs of
haemorrhage .
- Analgesia like paracetemol to reduce postoperative pain & the patient should
encouraged to eat & drink as much as possible .

Lecture notes in
- Antibiotics are indicated only if the temperature is persistently raised or the fossa
appear to be infected , in certain conditions antibiotics are given as prophylaxis .
Complications
A. Tonsillectomy
1. Perioperative
a. Heamorrhage ; primary , the amount of bleeding during tonsillectomy varies with
individual patients & surgeons , recent infection , previous quinsy , rough surgery
& previous scarring are the factors which increase the tendency to bleed in any
patient . Excessive haemorrhage from both fossae raises the question of
coagulation defect .
Control of heamorrhage ;
(1) Ligation & diathermy .
(2) Undersewing & ligating a difficult bleeding point .
(3) Pack in the fossa & oversewing the pillars .
(4) Uncontrolled haemorrhage due to large tonsillar branch of facial artery
may require external carotid ligation .
(5) Occasionally an aberrant internal carotid artery will be encountered in the
tonsillar fossa & this lead to massive haemorrhage which can be controlled
by ligation of the internal carotid artery .
b. Trauma ;
(1) Rough insertion of the mouth gag may damage the teeth , tongue , lips &
posterior pharyngeal wall .
(2) Damage to arterial supply of the uvula bilaterally may lead to loss it .
(3) Rough opening of the mouth gag may lead to dislocation of the TM joint .
2. Postoperative
a. Immediate
(1) Haemorrhage(reactionary) ; that occurs in the 1 st 24 hours postoperatively ,
but the vast majority in the 1st 8 hours . It occurs in about 0.5-1% of
operations . The signs of it are ; bleeding form mouth , a gurgling sound in the
throat on respiration , repeated swallowing , rising PR & falling BP &
tachycardia .
A crossed matched blood should be prepare & a look to the fossa to identify
the bleeding point , any clot should be removed & a swab soaked with 1:1000
adrenaline applied to the fossa , if bleeding continue or there is any doubt ,
then prepare the patient for anaesthesia to ligate the bleeding point .
(2) Anaesthetic complications .
b. Early
(1) Haemorrhage (secondary) ; occur some 5-10 days postoperatively & it is due
to an infection I n the fossa , if significant the patient must be admitted for
observation , CBP & crossed match blood should be prepared .
It is usually settle with infection when treated with antibiotics .
It is usual to remove the unstable blood clot (blood ooze around its margins) from
the tonsillar fossa & hold a swab soaked in diluted adrenaline in the fossa .
Its most unusual for secondary haemorrhage to be severe & prolonged to require
ligation under GA , if this occurs a coagulation defect which didn't cause the
problem at initial surgery can still cause a problem at the secondary stage .

Lecture notes in
In a tonsillar fossa which is infected & friable it is difficult to find & ligate a
bleeder so diathermy or suturing of a bleeding point will be necessary .
(2) Haematoma & oedema of the uvula .
(3) Infection of the tonsillar fossa which lead to parapharyngeal abscess .
(4) Pulmonary complications like atelectasis , pneumonia & lung abscess .
(5) Subacute bacterial endocarditis .
(6) Acute otitis media .
c. Late
(1) Postoperative scarring .
(2) Tonsillar remnants .
B. Adenoidectomy
1. Haemorrhage ; postoperative bleeding from the adenoid bed is serious & the child
should be returned to the theatre immediately & postnasal pack inserted .
2. Surgical trauma to the uvula , soft palate & Eustachian tubes .
3. Effect of speech (Rhinolalia aperta) .
4. Acute otitis media , retropharyngeal abscess &/or sinusitis .
5. Scarring .
6. Recurrence ; either due to incomplete removal or inherent tendency for re-growth of
lymphoid tissue in certain children , further removal may be indicated .
7. Subluxation of atlanto-occipital joint .

Lecture notes in
Tumors of the infratemporal fossa & parapharyngeal space

A. Anatomy
The space nelow the skul base & lateral to the pharynx can be divided into infratemporal
fossa & parapharyngeal space , they are separated anteriorly by the medial ptyrigoid
muscle & communicates posteriorly behind the muscle .
The infratemporal fossa is an inverted pyramid filled with muscles , nerves & blood vessels
& communciates with fissures & openenings , its boundaries are
- Roof ; formed by the greater wing of the sphenoid bone & sequama of the temporal
bone , it communicates seperiorly with the temporal fossa .
- Inferiorly ; it is formed by the medial Pterygoid muscle (upper surface) , behind with
it communicates with the parapharyngeal space .
- Medial wall ; formed by the lateral Pterygoid plate , superior constrictor muscle &
tensor palati muscle .
- Lateral wall , formed by the zygomatic arch , ascending ramus of the mandible ,
temporalis muscle , masseter muscle & deep lobe of the parotid gland & the styloid
apparatus .
- Anterior wall ; formed by the posterolateral wall of the maxillary antrum .
- Posterior margin ; formed by the inner surface of the tympanic plate .
It communicates with ;
1. Temporal fossa .
2. Parapharyngeal space .
3. Ptyregopalatine fossa through the pterygomaxillary fissure which is the junction
between the anterior & medial walls .
4. Orbit through the inferior orbital fissure (junction between the roof & anterior wall)
5. Oral cavity through the gap between the ascending ramus of the mandible & the
posterolateral wall of the maxilla .
Its contents are ;
1. Muscles ; medial & lateral ptergoid muscles & temporalis muscle .
2. Maxillary artery cross the fossa with its 5 branches .
3. Pterygoid venous plexus .
4. Mandibular branch of the trigeminal nerve .
The parapharyngeal space has the boundaries ;
- Roof ; it lies between the medial pterygoid muscle & the superior constrictor muscle .
- Medially ; lateral wall of the pharynx .
- Laterally ; by under surface of the medial pterygoid muscle , styloid process & deep
lobe of the parotid gland .
The parapharyngeal space is narrow anteriorly & broad posteriorly , it communicates with;
1. Superiorly ; anterior half separated from the ITF by the medial ptergoid , posterior
half continues with the ITF .
2. Posteriorly ; with the retropharyngeal space .
3. Inferiorly ; it descend to the neck medial to the carotid sheath & the fascia
surrounding the submandibular gland .
Its contents ;
1. Prestyloid compartment ; two muscles ; tensor palati & levator palati , two arteries ;
ascending pharyngeal & ascending palatine arteries & one nerve ; mandibular nerve

Lecture notes in
2. Poststyloid compartment ; carotid sheath (internal carotid artery , internal jugular

& vagus nerve) , last 4 cranial nerve & sympathetic , styloid group of muscles &
some LN & islands of salivary gland & losse fibroareolar tissue .
It traversed at the lower extremity by the superior laryngeal muscle nerve & pharyngeal
branch of vagus nerve .
Pathology
- Primary ;
Paraphryngeal space ; more frequent , mainly pleomorphic adenoma .
Infratemporal fossa ; less frequent , extracranial meningioma , lymphoma &
angioma , fibro- & chondrosarcoma .
- Secondary ; invade the PPS & ITF from adjacent structures ;
Benign swelling ; for both spaces ; angiofibroma , ameloblastoma , chordoma , for
PPS ; carotid body tumor , glomus & neurofibroma .
Cancer from oral cavity , nasopharyngeal & maxillary antrum .
C. Specific common tumors
- Angifibroma ; it arise close to the sphenopalatine foramen , then either pass medially
to the nasopharynx , or pass outward to the ITF through the pterygo-maxillary fissure ,
pushing the posterior wall of the maxillary sinus causing bowing of the posterior wall .
It also may extends to the orbit through the inferior orbital fissure or to the sphenoid
bone & attached to the dura .
- Ameloblastoma ; either ;
Benign , the majority , which arise from the maxilla (ITF) or from the mandible (PPS) .
Or malignant , minority which infiltrate cause destruction .
- Chordoma ; derived from the primitive notochord cause swelling in the ;
1. Prevertebral region pushing the posterior wall .
2. Nasopharynx causing small non ulcerating swelling in the roof or posterior wall of
the nasopharynx which may extend to the ITF .
- Menigioma ; extension of the intracranial meningiomas (more common) , it extends
through the base of the skull by more than one orifice extends to the ITF then to then
PPS .
The last 4 cranial nerves invaded & the internal carotid artery usually fused with the
cranial nerves (which the growth) , so impossible to preserve them .
- Pleomorphic adenoma ; it is the most common primary tumor of the PPS , then
secondaries invade the ITF .
It arise from ;
1. Either detached islands of the normal salivary gland which lies in the
parapharyngeal space medial to the deep lobe of the parotid gland which displace
the medial pterygoid muscle upward , parotid gland laterally & the palatofaucial
region of the oropharynx medially .
2. Arise from the deep lobe of the parotid gland which pass to the PPS through the
stylomandibular tunnel which is a hiatus bounded by the ascending ramus of the
mandible , styloid process & the stylomandibular ligaments .
- Neurogenic tumors , neural crest ; Schwann cells (neurofibroma & Schwannoma) &
sympatheoblast (ganglionic cell “ganglioneuroma” & paraganglionic cells like
carotid body tumor , glomus jugulare , glomus vagale & glomus tympanicum) .

Lecture notes in
- Neurofibroma ; arise from perineurium of Schwann cells , so it can’t be separated

from the nerve , the nerve should be sectioned above & below the tumor , it resemble
Schwannoma (macroscopically) .
- Schwannoma ; the most common , but with rare malignant variety , it arise from
Schwann cells along the length of the nerve , fusiform without affection on the nerve ,
so can be separated , it is firm or hard swelling which arise with areas of cystic
degeneration .
- Carotid body tumor ; arise from the paraganglionic cells within the carotid bifurcation
& grow upward between the internal & external carotid arteries causing displacement
of one vessel anteromedially & the other laterally .
It extends to the PPS & ITF , then to the base of the skull , the XII & X & superior
laryngeal nerve & the pharyngeal branch of the vagus close to the tumor will fused
with the capsule .
Charcterized by the rich blood supply with small blood on the surface which lead to
made it easily bleed in touch , it is pulsatile one .
Microscopically , it arise beneath the advantitia , firmly embeded in the wall of the
carotid bifurcation causing tear of the wall .
- Glomus vagale ; arise from the inferior vagal ganglia , it is indistinguishable from the
carotid body tumor , & it may push the internal carotid artery forward & the internal
jugular vein laterally , the surface vasculature is less evident , so excision is straightly
froward .
- Glomus jugulare ; in high altitude , arise from the superior vagal ganglion at the
jugular bulb , charcterized by lack of the distinct capsule .
It affect the petrous bone , extending to the base of the skull & ITF .
- Invasion of the PPS & ITF by SCC ;
1. Nasopharyngeal Ca , pass along the mandibular nerve laterally .
2. SCC of the maxillary antrum , along the posterior suprerior dental nerve to the
pterygomaxillary fissure & sphenopalatine fossa , along the maxillay nerve to ITF .
3. Tonsillar artery through the medial pterygoid muscle , mandibular nerve & vagus
nerve to the PPS .
4. Oral Ca. along the lingual nerve to the ITF .
Clinical features
Infratemporal fossa tumors
1. Benign tumors ; asymptomatic until expand through the channels , causing dull ache
pain or minimal discomfort .
On examination , bulging in the temple above the zygomatic arch which indiacte the
extension deep to to the temporalis muscle & fascia .
The lateral wall of the nasopharynx may be pushed inward which indicate
displacement of the superior constrictor muscle .
Proptosis due to orbital invasion , palpation if the oral cavity may reveal a tumor mass
in the gap between the ascending ramus of the mandible & the maxilla
(retromandibular) .
OME , which indicate eustachian tube dysfunction due to pressure of the tumor mass .
2. Malignant tumors ; primary or secondary , may cause pain & tenderness , swelling
in the ITF , trismus & anaesthesia in the distribution of the mandibular branch .

Lecture notes in
Parapharyngeal space tumors

1. Benign tumors ; may be presented as painless swelling , if large size with sign of the
ITF tumors .
Ballotment elicited by bimanual palpation .
Swelling of the parotid gland (only in PPS) .
It may be misdiagnosed as quinsy (but no trismus here) .
In carotid body tumor there is cranial nerve palsy (due to stretching ot distortion of
the nerves especially 10 th & 12th ) .
Sometimes there is headache & syncope (secretion of catacholamines) .
2. Malignant tumors ; presented as swelling , trismus , pain & loss of nerve function .
Investigations
A. Radiology
1. Plain x-ray ; of little benefit , it may show soft tissue mass & bone destruction .
2. CT scan ; with or without enhancement , it permit precise assessment of the size ,
shape , consistency & extent of the tumor , its margins & relationship with adjacent
structures & can assess the possibility of removing the tumor without dissecting the
facial nerve (like in pleomorphic adenoma) .
3. MRI ; better for soft tissue .
4. Angiography ; like digital suntraction & carotid angiography , useful in
angiofibroma & neurogenic tumors , it demonstrate the full extent of the tumor ,
proximity to the skull base & outline , the carotid system & defined the feeding
vessels .
Sometimes use venography in glomus jugulare tumor .
B. Doppler U/S ; to assess the adequacy of the circulation of the circle of Willis & the risk
of sacrificing the ineternal carotid artery .
C. FNAC ; done because the open biopsy is contraindicated , the open biopsy discouraged
because ;
- Obvious Dx ; unnecessary to open biopsy .
- Inaccessable lesion .
- Dangerous haemorrhage like in angiofibroma .
- Spread of malignant disease .
Management
Complete resection only in limited involvement .
All treated by surgery except lymphoma which Rx by radio & chemo-therapy .
Infratemporal fossa tumors approached by temporal , palatal , maxillary & oral approach .
Parapharyngeal space tumors approached by transparotid , submandibular & midline
transmandibular oropharyngeal approach .
Surgical techniques
A. Transpalatal approach
Suitable for patient with pleomorphic adenoma within the deep lobe of the parotid gland
1. Total conservative parotidectomy ;
- Classical incision done .
- The superficial lobe excised completely & the facial nerve dissected off from the
underlying deep lobe & the deep lobe is removed as a separate specimen &
separated from the posterior border of the ascending ramus of the mandible , TM
joint , styloid process , EAM & digastric muscle .

Lecture notes in
- The posterior facial vein (retromandibular vein) is divided at its exist from the deep
lobe of the gland & the external carotid artery is divided at its entry .
- Superficial temporal artery , maxillary artery & transverse facial artery are ligated
- Mobilization of the tumor is done now which lies medial to the deep lobe of the
gland , the stylomastoid ligament should be divided & the styloid process should be
fractured .
- Care should be taken to ; not breach its contents , once the tumor is free ,
mobilization & extraction in the lateral & downward direction from beneath the
facial nerve .
Not to damage the exposed facial nerve , temporary weakness due to stretching .
- The wound washed throughoutly .
- Skin sutured .
2. Radical lateral approach
It is suitable for Ca of the parotid reaching the ITF & Ca of the external or middle
ear reaching the parotid & ITF .
Excision of the parotid gland , facial nerve , ascending ramus of the mandible &
zygomatic arch .
Resection of the external & middle ear & the eustachian tube .
Obliteration of the large dead space by myocutaneous flap or muscle transposition .
3. Conservative lateral approach
Suitable for benign tumors of the ITF in patient related to lip splitting incision &
also for extracranial extension meningioma , deep lobe tumor & recurrent
pleomorphic adenoma .
Extended parotidectomy incision done .
Superficial parotidectomy done
The branches of the facial nerve are traced & freed .
The zygomatic arch is divided anteriorly & removed .
The ascending ramus of the mandible is sectioned in Y trifurcate manner
The encapsulated mass is freed , the assisstant finger’s is pushed in the nasopharynx
to push the lateral nasopharyngeal wall outwards .
The zygomatic arch & mandible rewired .
The postoperative complications ; (1) neuropraxia of the facial nerve (2) damage to
the lingual nerve & inferior dental nerve (3) trismus .
B. Anterior transantral approach
It is designated for removal of the benign well circumscribed mass & angiofibroma .
Incision either Weber-Ferguson (leave scar, lateral reflection check flap) or facial
degloving (no scar , superior reflection flap) .
Both expose the anterior antral surface , the anterior , posterior , lateral & medial
antral walls are removed by drilling leaving the superior (orbital floor) & the inferior
parts (superior alveolar) intact .
Removal of the inferior & middle turbinates & lateral nasal wall .
Angiofibroma so identified & mobilized by blunt dissection from lateral to medial .
The internal maxillary artery is identified & ligated .
Mobilization of the tumor continued toward the nasopharynx .
Removal of the vertical plate of the palatine bone (essential) with separation of the
nasopharynx composed of tumor from the base of skull .

Lecture notes in
Complications are ; (1) infraorbital anaesthesia & (2) temporary ectropion of the lower
lid .
C. Superior transtemporal approach
It provid good access to the upper lateral part of the ITF , useful for ;
1. Removal of the osteoblastoma of the skull base .
2. Lower grade malignant tumors .
3. Biopsy .
The incision behind the pinna extending up to the temporal fossa & down below the
mandible .
The pinna reflected downward & forward together with division of the EAM
The temporalis muscle is detached & reflected downwards & forwards , the temporalis
fascia then separated .
Arch of the zygoma & infratemporal crest is drilled .
Now good access to the ITF is achieved .
D. Inferior submandibular approach
It provides good access to both PPS & ITF , but can’t reach to the superior part of ITF .
Horizontal incision at the level of the hyoid bone which extend from the midline to a
point which overlap the sternomastoid muscle . The submandibular gland excised .
The superior separation of the tumor is difficult especially if it is large & reach the skull
base because the upper part of the tumor hidden , so blind dissection is done .
So access to the upper part is helped by the division of the medial pterygoid muscle
&horizontal ramus of the mandible . Secure any bleeding especially the inferior dental
artery . After removal of the tumor , the mandible rewired & the wound closed in layers .
Complications are ; (1) damage to the mandibular branch of the facial nerve (2)
permanent mental anaesthesia & (3) instability of the bone fragments .
E. Midline transmandibular oropharyngeal approach
Suitable for both ITF & PPS & very large primary PPS , pleomorphic adenoma .
An incsion is done through the lower lip by vertical line down to the upper part of the
protuberance of the chin , then curves around the contour of the hyoid bone level to the
anterior border of the sternomastoid muscle .
The submandibular gland is removed , to release the lingual nerve .
The mandible & the mylohyoid muscle are divided & evertion of the horizontal ramus of
the mandible .Incision of the mucous membrane done & continued to the anterior pillar
& soft palate , then opening the superior constrictor muscle & PPS .
The osteoplastic flap containing the mandible is retracted & the medial pterygoid
muscle is divided .The tumor separated & excised
.The muscles & mucous membranes should be repaired & the mandible plated .
Complications are ; (1) lingual nerve damage & (2) trismus .
F. Extended anterolateral approach
Suitable for Ca of the antrum extending to the ITF & mouth cancer extending to the ITF
(like tonsillar & faucial Ca) . The lower incision may split the lip , mandible & extend
back to the submandibular triangle . The mucosa of the floor of the mouth & mylohyoid
muscle are incised . The medial pterygoid muscle & the mandible are divided .
The upper incision is classical Weber-Ferguson , but surround the eye & extend upward
& slightly outwards in the midline of the forehead .

Lecture notes in

Lecture notes in
Congenital disorders of the larynx , trachea & bronchi

Larynx
A. Supraglottis
1. Laryngomalacia
It is the commonest cause of congenital stridor , 60-70% , characterized by
flaccidity of the the supra-larynx , incidence equale in both sex .
Pathophysiology :
- Softness , flobbiness or lack of consistency of the laryngeal tissue .
- Thining & hypocellularity of the laryngeal cartilage .
- Wrinkled , loose or redundant mucosa , especially over the arytenoids .
Clinically the majority of cases are asymptomatic , also it may presented as ;
- Inspiratory stridor , high pitched within the 1st few days of birth or when the
child get his 1st URTI , the stridor increased in severity during the 1st 8 months
to be maximum in the 9-12 month , then start to resolved .
- It is intermittent , appearing only during feeding or crying & when the child lie
on his back , hyperextension of the head , sometimes decrease the stridor .
- Difficulties in feeding & failure to thrive .
- Rarely , respiratory distress , which may need active management like
tracheostomy , excision of the redundant mucosa or division of the aryepiglottic
fold .
Endoscopy done to see the appearance & movement of the laryngeal structures
(during recovery from anasthesia) , the stridor become more noticeable during the
early stages of anaesthesia because the child is supine position & this increase the
respiratory effort , the endoscopic findings (separately or in combination) are ;
- Tall tubular , in -rolled epiglottis with tendency to prolapsed , omega-shaped .
- Short flaccid medially prolapsing aryepiglottis aryepiglottic fold .
- Prominent , elongated arytenoid , covered by loose redundant mucosa &
separated by a deep interarytenoid cleft .
- Deepened narrowed supraglottic , so the vocal cords difficult to be seen .
Bifid epiglottis has similar presentation & course & often associated with other
congenital anomalies especially of digits .
2. Lartyngeal cyst (saccular cyst)
It is a mucous filled dilatation of the larynx saccule which may distort the
aryepiglottic fold , the false fold or the laryngeal ventricle .
There is no communication with the airway & the contents are fluid rather than gas
It is a symptomatic & noticed incidentally during hoarse stridor & increasing the
airway obstruction . Endoscopy , show large bluish swelling in the aryepiglottic
fold & sometimes totally obscuring the vocal cords .
Managed by endotracheal excision or wide masupulization & in case of severe
distress do tracheostomy .
Extensive cystic hygroma , involve the posterior tingue , valleculae & epiglottis ,
may lead to airway obstruction & managed by Co2 laser wide excision , sometimed
need tracheostomy .
3. Congenital laryngocele
It is air-filled dilatation of the ventricular sinus of Morgangi , sometimes extends
beyond the thyroid cartilage piercing the thyrohyoid membrane (external type) .

Lecture notes in
Diagnosed by papation of the neck finding a soft , fluctuant swelling above the
thyroid cartilage .
Clinically presented as , intermittent hoarseness or respiratory distress which
increased on crying or straining .
Diagnosis by x-ray of the nech which show air-filled sac .
B. Glottis
1. Laryngeal web
75% in the glottis & 25% in the supra- & sub-glottis .
It caused by partial canalization of the vestibulotracheal & pharyngeotracheal
canal during 5 th week of intrauterine life (total failure lead to atresia) .
Characteristics ; usually anteriorly located , involving variable length of the vocal
cords , it is either thin (membranous) or thick (fibrous , majority) , extending to the
supraglottis .
Clinically presented as ; biphasic stridor , hoarseness on crying & respiratory
distress .
Management ;
- Thin web ; formation of epithelial lined tract (in intial stage) , or insertion of
keel (by endoscopy or laryngofissure) .
- Small one , leave well alone .
Other posterior web (interarytenoid) , difficult to diagnosed , may cause ankylosis
of the cricoarytenoid joints or subglottic stenosis .
2. Cri – Du – Chat syndrome
Characterized by high pitched mewing stridor , endoscopy show diamond shaped
rima glottis , narrow vocal cords , the subglottis is curved & elongated .
Chromosomal studies show partial deletion of the short arm of the 5th chromosome
Management , rarely required tracheostomy (in respiratory distress) .
3. Vocal cords paralysis
It is the 3 rd most common cause of congenital stridor (6-13% of all cases) .
It has many types ;
- Unilateral ; 4 times commoner than the bilateral type , characterized by breathy
crying or weak , stridor uncommon with little tendency to airway obstruction .
- Bilateral ; normal crying , stridor & respiratory distress which nor appear until
the child becomes more active .
Diagnosis confirmed at laryngoscopy which is difficult especially in small child due
to ; (1) incorrectly placing the tip of the laryngoscope posterior to the epiglottis ,
distorting the glottis , (2) From deep anasthesia causing inhibition of the laryngeal
reflexes . During recovery from anaesthesia the best view , also we must distinguish
between true vocal cord paralysis & fixation of the cricoarytenoid joint (by gentle
palpation of the arytenoids cartilage) .
Many of infants has other congenital defects involving the CNS , CVS ,or
respiratory system , so a case of meningocele , encephalocele , Arnold-Chiari
syndrome (stridor with abnormal cry) , should inspect their vocal cords .
Differential dignosis
- Congenital myasthenia gravis ; characterized by ptosis , inability to suck , or
intermittent facial paralysis , sometimes present with progressive weakness of
cry & stridor .

Lecture notes in
- Cardiomegally & great vessels abnormalities , cause stretching of the left

recurrent laryngeal nerve .
- Trachea , bronchus & oesophageal anomalies , associated with recurrent
laryngeal nerve palsy .
- Benign congenital hypotonia & other muscle disease , associate with recurrent
laryngeal nerve palsy .
Management ;
- Unilateral ; Teflon paste injection .
- Bilateral ; tracheostomy to protect the airways & vocal cord lateralization
postponded because there is late recovery of one or both cords at the age of 9
years . Alternative , reduction of one cord by laser +/- arytenoidectomy .
C. Subglottis
1. Subglottic stenosis
Either congenital or acquired , the diagnosis present if the diameter of the
subglottic space <3.5 mm as measured by failure of unforced passage of
bronchoscope of this size .
The abnormality (pathology) is thickened & oval shaped cricoid cartilage with
concomitant increase in the thickness of the submucosa causing characteristic
cresenteric narrowing of the anterior subglottic space (2-3 mm below the true
cords, sometimes extend to involve the anterior commissure of the cords) .
Clinically , mild cases are asymptomatic , but after 1 st URTI or after traumatic
intubation , inspiratory stridor or biphasic (in severe) .
Diagnosed by plain x-ray of the neck or thoracic inlet which is unrealiable ,
bronchoscopy (gentle) otherwise precipitate the need for tracheostomy .
Management ; in mild cases only reassurance (spontaneous improvement) , while
in severe cases may need tracheostomy , serial dilatation which is less valuable in
congenital type or do laryngotracheoplasty .
The acquired type , there is autoimmunity to type III collagen & precipitated by
prolonged intubation .
2. Subglottic haemangioma
It is hamartoma of blood vessels origin , associated with skin haemangiomas .
Sturge-Weber syndrome ; portwine stains at the area of the distribution of the
trigeminal nerve with haemangioma of the cerebral cortex , eyes & abdomen &
skeleton .
Mostly at the subglottis with capillary navi of the face & neck . Presentd as
inspiratory or biphasic stridor , dyspeneoa , harsh cry & sometimes haemoptysis .
Diagnosis by Laryngoscopy ; bluish bear shaped swelling on the lateral wall of the
subglottis , unilateral , undersurface of the cords , occasionally bilateral , it is
compressable , not bleed easily & so can take a biopsy (histology : capillary type) .
Management ; either spontaneous resolution , steroids , tracheostomy & laser
excision is the management of choice .
3. Laryngotracheal cleft
Pathogenesis ; failure of tracheo-oesophageal septum formation or arrest of its
rostral advancement lead to open communication between the laryngotracheal
airway & the oesphageal lumen . Patterson (1955) classification ;
(1) Laryngotracheal cleft .

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(2) Partial laryngotracheo-oesophageal cleft .

(3) Total laryngotracheo-oesophageal cleft .
Clinically presented as aspitation , stridor & toneless cry .
Diagnosis is difficult , by ; barium swallow ( so difficult to precise the site &
associated with aspiration) , MRI , endoscopy & palpation of the interarytenoid
cleft by blunt hook .
Management by repairing the defect by lateral pharyngectomy approach .
Trachea & Bronchi (26% of congenital stridor )
A. Agenesis
Either partial or complete , it is incompatiable with life , agenesis of the main
bronchus lead to weak infant with increased recurrent chest infections .
B. Stenosis
Either in the form of membranous web , segmental or whole organ stenosis , if at the
lower trachea or main bronchi , management by gentle dilatation with bronchoscope .
If at the upper , management by tracheoplasty , vertical incision in the anterior
tracheal wall & inserting an elliptical wedge of costal cartilage.
C. Tracheomalacia
Has associated with laryngomalacia , either localized (commoner) or generalized .
Presented as high pitched expiratory stridor like expiratory wheeze of asthma , harsh
barking cough (in the localized form) .
Diagnosis by bronchoscopy , anteroposterior tracheal compression increased with
expiration (flattened cartilaginous ring) .
Must be differentiated from laxity of trachealis muscle .
Management by complete spontaneous resolution which is the rule , few cases may
need tracheostomy (using tube reach the carina , sometimes segemental resection &
reconstruction with rib cartilage graft) .
It may be cause from ;
(1) Compression from without (vascular ring) .
(2) Longstanding tracheostomy .
D. Vascular compression
Desnos classification into ;
- Vascular ring
(1) double aortic arch , compression ring on trachea & oesophagus .
(2) Neuhauser’s anomaly , the aorta pass to the right of the trachea , so the
ligamentum arteriosus compress the trachea .
- Vascular sling ; the left pulmonary artery pass between the trachea & oesophagus
causing compression .
- Anterior compression ;
(1) Anomalous innominate artery , sloping compression of the lower trachea 1-2
cm above carina .
(2) Larger than normal pulmonary artery , compress the trachea & bronchi just
below the carina .
(3) Left atria enlargement , compress the left main bronchus anteriorly .
- Posterior compression ; aberrant right (sometimes left) subclavian artery passing
posterior to the oesophagus .

Lecture notes in
Clinically presented as ; stridor , dyspneoa , harsh brassing cough & oesphageal

compression .
Diagnosed by ; barium swallow , high reolution U/S , CT scan , MRI & arteriorgraphy
(conclusive) .
Management ; in severe symptoms with inadequate tracheal airway , them do surgical
decompression . Tracheostomy should be avoided , because bypassing the obstruction
result in intubation of the right main bronchus with fatal risk of erosion of the blood
vessels by the tip of the tracheostomy tube .
Complications ; localized tracheomalacia for years postoperatively .
E. Anomalous bronchial bifurcation (asymptomatic) .
F. Congenital cysts & tumors
It cause non-pulsatile compression of the trachea & main bronchi .
Tracheogenic & bronchogenic cysts contain thick mucous & when inflamed increased
in size wbhic cause compression .
Management by thoracotomy & excision .
Cervical & mediastinal cysts & tumors (thymomas , teratomas & branchia arch
anomalies) may cause compression of the trachea .

Lecture notes in
Acute laryngeal infections in children

There are important points to been considered in the child larynx ;
1. The larynx in infant is smaller , higher , narrower & more difficult to see than
in adults , also it is more brittle physiologically .
2. The epiglottis is surrounded by loose connective tissue (pre-epiglottic &
paraepiglottic spaces) & inflammation may spread quickly from epiglottis within
these spaces , so rough instrumentation or even toungue depression may
encourage inflammatory odema to surround the laryngeal inlet completely .
3. The mucosa of the subglottis within the cricoid ring is lax & full of mucous
glands & easily become oedematous leading to biphasic stridor & laryngeal
spasm ocurr more easily .
The management of acute laryngeal infections in the childhood has aimed to ;
1. Arrive swiftly at the correct diagnosis .
2. Manage the child safely (from the child's airway obstruction) .
In order to acheive these must be an admission policy & special protocol should be
adapted , there must be essential cooperation between the anasthetist , ENTist &
paediatrician , there must be a special resuscitation room near an operating theatre .
The personnel involved in the management should be as senior as possible (not a
situation for training) .
The equipment in the resuscitation room needs to be checked daily like bulbs , fibro-
light cables & suckers .
Enough space at the resuscitation room to house the mother & her child with
anasthetist , ENTist & paediatrrician .
The resuscitation trolly should have full range of naso- & oro-tracheal tubes (2.5 mm
upwards) , introducers , two laryngoscopes with straight blades , bronchoscope
(Storz rigid fibre light bronchoscope) , various foriegn body forceps , paediatric
tracheostomy set , suction tubes (pharyngeal ; Yankauer fine catheters for
bronchoscopic suction & Magill sucker which used to intubate the patient & provide
a temporary airway) .
The most important consideration is to distinguish epiglottitis & laryngeal foriegn
body (F.B.) from croup .
The choice & care of an alternative airway in the inflammatory laryngeal
obstruction could be either personal or depends upon local nursing services , the
endotracheal intubation is the choice over the tracheostomy inspite that
tracheostomy need less care & need less specialist facilities & carry no death .
In ideal situation , endotracheal intubaton is preferable to tracheostomy as an
alternative airway in acute inflammatory obstruction in childhood .
1. Endotracheal intubation
- The most common complications are (1) tube obstruction & (2) extubation , so
multiple intubations needed to replace the obstructed tube . The tube if pass
through the affected site , need a good fixation to prevent stryggling which cause
movement which cause (3) further damage to the inflammed mucosa , also the (4)
vocal cords splinted apart by the tube , preventing talk & cough .
- N/G tube needed for feeding & fixed by brace on the forehead .

Lecture notes in
- Expert nursing care required to (1) prevent the above complications & to (2)
provide adequate humidity & (3) regular aspiration (by suction catheter) to prevent
obstruction
- The size of the tube should be small to prevent trauma to already damaged tissue
, use polyvinyl chloride (PVC) .
- The tube size formula = child's age/4 + 4.5 mm .
- In epiglottitis , apply CPPP circuit to the endotracheal tube as there is no lower
airway involvement .
- In croup secretions lead to lower airway occlusion & pneumonia , so require
mechanical ventilation .
- Humidification is necessary to get the secretions less tenacious , either by warm
nebulizer attached with the tube or by instilation of 2 cc N/S prior to aspiration .
- The suction tube should be go beyond the endotracheal tube , but not so far
because this could cause damage to the carina causing granuloma .
- Regular physiotherapy needed to prevent bronchopneumonia .
- The extubation within 48 hrs (epiglottitis) & 6 days (croup) , or when there is a
leak which indicate the decrease of odema , then extubate with corticosteroids (6
hrs prior) to prevent odema & racemic adrenaline nebulizer prior for the same
purpose , then observed for 2 hours after extubation & need humidity .
- The parents should reassured about post extubation weak husky voice of the child
which will return to normal within 24 hours .
2. Tracheostomy
- The advantages are ; (1) disease process is bypassed (2) child not need sedation
& require less skills for nursing (3) normal feeding is usually possible (4) can talk
or cough by occlusion of the tube with finger on expiration or with the use of valve .
- The disadvantages are ; (1) increase the moratality rate (2) increase the length of
time before extubation (3) leave a scar on the neck (4) risk of accidental extubation
, disastrous event in which there is difficulty to replace the tube .
- The complications are ; pneumothorax & surgical emphysema in the neck .
- After tracheostomy we do; (1) CXR to demonistate pneumothorax early &(2)
lateral neck x-ray to see if the tube within the trachea & not causing backward
displacement of the anterior tracheal wall just above the tracheostomy site , so
need to change the tube or otherwise cause tracheal stenosis which will cause
difficulty in extubation .
- Types ; (1) polyvinyl chloride & (2) silastic (preferable) , become soft at the body
temperature & moulds itself to the correct shape of the trachea .
Acute epiglotitis
Acute supraglottic laryngitis or acute supraglottitis , it is themost frightening of
paediatric emergencies , if unrecognized may lead to death .
The aetiology are ; H. influenza (mainly type B) , B-haemolytic streptococci . ,
Pneumococci & staphylococci .
The incidence ; it is rare , occur usually at winter months , affect children from 1-6
years (peak 3&4) , as children more than 5 years have protective antibodies against
H. influenza (HIB) & also immunity exist below the age of 2 years .
The introduction of HIB vaccin has reduce the incidence of acute epiglottitis .

Lecture notes in
The pathology ; the disease maximally on the epiglottis but the whole supraglottic
compartment may involved in the inflammation , the infection spread in the losse
connective tissue anteriorly & posterolaterally to the epiglottis , the laryngeal
surface of the epiglottis is largely spared .
Clinical presentation are ;
The most stricking feature is the transformation of a fit child into one a deperately ill
.
- The classical presentation is ; (1) a fit child (2) aged 3 years (3) complain from
sore throat , within 1/2 hour (4) dysphagia (5) rapidly worsening inspiratory
stridor , & within 2 hours (6) a critically ill child present to the ER , the child sit up
& leaning forward (because if lie may be suffocated) & using his arms to fix his
chest (to use the accessory muscles of respiration) , also he had (7) dribbling , due
to dysphagia (8) muffled voice , when the child become (9) quiet , floopy &
decrease the respiratory distress , there will be imminent cardiopulmonary arrest .
Also there is (10) marked cervical LAP (which may be the only physical sign) ,
examination of the pharynx is contraindicated & may cause asphaxia . Also 90% of
patients has (11) odynophagia & stridor , 64% has (12) drooling .
In the above picture , no further investigations needed untill an alternative airway
has been established (even x-ray) because any thing can agitate the child
increasing the likehood of obstructing the airway & waste of valuable time , so the
only time to con firm the Dx is as the child is being provided with an alternative
airway .
- The unclassical presentation are ; 1/3rd of patient has history of URTI during the
previous 24 hours or some had surprisingly long history of stridor prior to
admission.
The management ; the following protocol should be adopted ;
1. The terrified child is comforted & his mother allowed to hold him upright ,
avoiding undress him , venuncture him , x-ray or any further examination
because this lead to let the child crying & perticipitate immediate respiratory
arrest & also not do throat examination by using a tongue depressor (the same
reason) , but if there is radiology room at the casuality & we are in doubt of the
Dx , then do lateral view to the neck which will reveal the classical thumb sign .
2. The child is carried by his mother to the resuscistation room where the team
prepare to secure an akternative airway , the anasthetist introduce a tube in
patient with upright position (if fail , the ENTist do rigid bronchoscope followed
by tracheostomy onto the bronchoscope through with anasthesia is maintained) ,
the mask fright the child , so cupped hands used as a mask & not use muscle
relaxant which can lead to apneoa , also the i.v. induction avoided because it let
the child cry & aggrevate the condition .
3. When the child sleep , the mother shown from the room & the child laid on his
back ready to be intubated , anasthesia then deepened using a partially closed
system to allow application of continueous positive airway pressure (CPAP) as a
pneumatic splint .
We must know that early intubation may provok laryngospasm .
4. A laryngoscope is inserted to confirm the Dx by showing a red cherry swollen
epiglottis & oftenly the aryepiglottic folds are grossly oedematous (supraglottitis)

Lecture notes in
, here pharyngeal Yankaur sucker needed to clear all the secretions (the anterior
nature of the odema , the inverted V of the epiglottis & obliterate the view of the
laryngeal inlet) . So , anterior displacement of the epiglottis bu the use of semi-
rigid intriducer or stylet (like portex) within the endotracheal tube is required ,
an approperiately sized orotracheal tube is inserted & hopefully the airway is
fully & suddenly restored .
5. If the 1 st attempt at intubation fails , the ENTist insert a rigid bronchoscope
behind the epiglottis & into the trachea , if the bronchoscope not available , the
intubation done by Magill sucker which has the advantage of being rigid , hollow
& readily available .
6. Once the airway is secured (by any method) , then immediate danger is over ,
so start i.v. canula insertion to allow anasthesia better control .
7. The decision now is what is the type of airway to stay in place for the next 24-
48 hours , some prefer nasotracheal tube & other prefer orotracheal tube (if easy
put orotracheal tube & minimal odema , stay the orotracheal tube) .
So the nasotracheal tube can be inserted via the nose to a position adjacent to the
oral tube behind the epiglottis & the oral tube removed then with the immediate
placement of the nasotracheal one .
If the bronchoscope necessary , safer to do tracheostomy onto the bronchoscope .
8. At this stage ; (a) swab for C&S taken from the epiglottis (b) take blood
culture sample (c) i.v. infusion line for fluid replacement & antibiotics therapy (d)
N/G tube to decompress the stomach , which may be inflated during the bagging
in anasthesia (e) sedation to avoid swallowing movement (advantage of
tracheostomy to endotracheal tube is that free moving & swallow normally) .
N.B.: the moratlity rate ; with tracheostomy about 0.86% , with endotracheal
tube about 0.92% which is not significant , while if the airway not secured it be
about 6.1% whic is a significant percentage .
9. Fixation of the endotracheal tube prior to transfer , by elastoplast stripping
around the tube to the face .
10. Then the child transfered from the ER to a paediatric intensive care unit ,
sedate the child before transfer (to avoid risk of extubation during transfer) by
Morphin & i.v. Midazolam 0.1 mg/kg as bolus followed by contineous infusion of
0.1 mg/kg/hr , this also control the pain of epiglottiitis.
The antibiotic choice will be ; Claforan (HIB resist pencillin & chloramphenicol)
200mg/kg/day in divided 6 hourly doses .
The steroids used to allow earlier extubation (6 hrs after intubation) , 1 mg/kg of
dexamethasone .
Care of the endotracheal tube need highly trained nurses & enough of them , in
the ICU , while tracheostomy being safer & require less intense nursing skills .
11. Extubation , possible within 48 hrs , if leak is present so need immediate
extubation , we use corticosteroids half hour prior to extubation to decrease the
subglottic oedema caused by the irritant nature of the tube (extubation within 48
hrs , fully active child) .
When there is doubt that the child can extubated , inspect the epiglottis 1st (after
spraying the nose & use of flexible fibroptic laryngoscope) .

Lecture notes in
The complications are ; (a) accidental extubation (b) pulmonary oedema which
exhibited after the relief of the obstruction airway , due to hypoxia with negative
intrathoracic pressure , this increase the pulmonary arterial presuure & damage
to the alveolar capillaries with transudation .
In certain cases , management without intubation , the Dx confirmed by lateral
neck x-ray , the management with antibiotics in the ICU .
We must note that HIB is contagious , so prophylactic antibiotics (Rifampicin)
given to the siblings , also HIB vaccin can decrease the infection possibilty , &
when there is slight suspicion of epiglottitis , immediately transfer to the hospital .
Laeyngotracheobronchitis
Croup , acute subglottic laryngitis , acute laryngotracheatis , it is the commonest
infectious cause of upper respiratory tract obstruction in children (40 times
commoner than acute epiglottitis) .
The aetiology are ; Parainfluenza virus type I mainly , also Parainfluenza virus type
II & III , influenza virus & RSV & Rhino virus may also responsible , also it may
follow measles .
The incidence ; the age peak 18 months , M>F , espicially winter .
The pathology ; the subglottis area is the maximum , the vocal cords are inflammed
& may be ulcerated with gross odema & ulceration of the subglottis , seperated
bacterial infection may arise .
1. Always preceded by URTI of 48 hrs , sometimes stridor .
2. The initial symptoms are ; hoarsness followed by croupy cough (musical
cough of crowing quality) or (bark of a seal) .
3. Then signs of respiratory distress appear often at night .
4. Stridor , intially inspiratory then biphasic .
5. Associated symptoms & signs ; pyrexia , flarring of the ala nasae ,
suprasternal & intercostal recession & the child become very restless &
prefer to lie down , exhausion & respiratory failure , crying & cough which
worse by stridor (so we sedate the child) .
The management are ; 50% need hospitalization of with 1% require intubation , the
main reason for admission is to observe & to secure the airways .
1. Radiology ; lateral x-ray of the neck , narrow subglottis (steeple sign) &
ballooning of the hypopharynx .
2. Reassurance for the child & parents , s.t. need to sedate the patient by
chloralhydrate 30 mg/kg .
3. Humidification of the inspired air , in croup room , high humidity room , at
home use steam kettle , s.t. use warm moist air delivered via head box (in
young children) or in a tent (for older children) .
4. Careful monitoring , by croup scoring hopping for , stridor lessening ,
decrease restlessness , decraese pulse rate & blood pressure , pink colour .
This include PR , BP , blood gas analysis , need 1/4 hour PR chart done by
trained nurse sitting for 2-3 hours .
If an alternative airway needed , manage like epiglottitis , but extubation after
6 days .
5. Others ;

Lecture notes in
a. O 2 therapy ; not used in mild cases as it mask the early signs of hypoxia ,
but used when alternative airway needed & secured , we can use O2 which
will help to prevent reflex bronchospasm .
b. Steroids ; need only hoping to avoid intubation or prior to extubation .
c. Antibiotics ; used in the intubated child & when there is bacterial
bronchitis supervenes .
d. Racemic adernaline nebulized & delivered by IPPB (s.t. contraindicated) .
Bacterial laryngotracheobronchitis
Pseudomemberanous croup , it may be seperated disease or secondary bacterial
infection of viral croup , it involve the trachea predominately . It is more severe than
croup , rare , older children affected .
The aetiology ; Staph. aureus is the causative microorganism .
The pathology ; sloughing of the respiratory epithilum & more severe obstruction ,
often need artificial airway , easily obstructed with crusts of sloughed epithilum .
1. Insidious disease with history of URTI , brassy cough & high fever , toxic
child with increased WBC , respiratory distress then occur needing an alternative
airway
2. If bronchoscopy used , show ulcerated sloughed epithilum , aspirated for C&S
, so need approperiate antibiotics .
The management are ; the major problem for the nursing is the marked tendency to
endotracheal tube obstruction , tracheostomy safer & with less risk of obstruction .
The management line in general the same as croup (if need intubation manage like
epiglottitis) .
Spasmodic laryngitis
Spasmodic croup , acute subglottic odema , laryngismus stridulus .
Clinical presentation are charcterized by recurrent , sudden bouts of cough at night
without predominate features & disappear rapidly often at the morning , the attack
responds to the Mist therapy & may stop after vomiting , the bronchoscopy shows
subglottic odema , some children develope asthma or other allergic state .
The management are by antiasthmatic topical steroids or sodium cromoglycate , s.t.
use dexamethasone 0.6 mg/kg as single dose , most cases not need alternative airway
Diphtheria
Rare , laryngeal diphtheria nearly always follow pharyngeal infection .
The aetiology ; the causative M.O. is Corynebacterium diphtheiae gravis .
The pathology ; mortality due to laryngeal obstruction & endotoxins in the blood
leading to myocarditis & perineuropathy , the initial lesion is at the tonsils as
necrotic greyish memberane (mixture of necrotic tissue & rich fibrinous exudate with
bacteria in large numbers) , when remove the memberane bleeding ocurr . The
membrane become thicker in late disease & easily seperated from the underlying
mucosa .
Clinical presentation are ; insidious onset with barking cough followed by
inspiratory stridor with chest wall recession (as the disease progress from pharynx to
the larynx) other signs are ; pyrexia , malaise & sorethroat (at early stage of the
disease) .

Lecture notes in
Signs are ; at the early stage ; memberane over the faucial pillars , then general
signs of toxaemia appear , bull neck appearance due to regional LAP & cellulitis ,
exhausion occur due to toxaemia & barking cough .
The cause of death is the acute toxic myocarditis at the 2 nd week .
Neuropathy usually involve the palate leading to paralysis of the muscles causing
nasal regurgitation of the food & nasal speech .
The management are ;
1. Bed rest for 2-4 weeks untill the danger of myocarditis gone .
2. i.v. Benzyl-pencilline 600 mg/6hrs .
3. Antitoxins i.v. 10000-100000 unit .
4. Remove the memberane from the larynx with endotracheal intubation (if
conservative management failed) .
5. Humidified O2 .
Conditions mimic laryngeal infections
A. Foreign bodies
History shows apyrexial child who has been playing with small objects , then begins
to have paroxysms of coughing , this increase suspicion of F.B. inhalation .
Management by remove the F.B. by endoscopy .
B. Infectious mononeucleosis
Occasionally cause airway obstruction , the memberane is less adherent than in
diphtheria , charcterized by tonsillar hypertrophy (massive) causing inspiratory
stridor
The management by i.v. dexamethasone to prevent the need for an alternative airway
, we should avoid ampicillin & amoxil .
C. Quinzy
Rare in infancy , charcterized by trismus , dribbling & airway obstruction due to
displacement of tonsils medially .
It is managed by surgical drainage which lead to rapid improvement of the symptoms
, also we use antibiotics .
D. Retropharyngeal abscess
Common in infancy , it is caused by ;(1) URTI (2) uninspected F.B. (3) syphilis (4)
T.B. of the cervical spine .
The pathology ;
- Tonsillitis causing inflammation of the retropharyngeal LN through
lymphatics leading to abscess .
- T.B. of the cervical spine causing retrophryngeal extension leading to abscess
- Cervical LAP & inspiratory stridor (due to laryngeal odema or anterior
displacement of the hypopharynx) .
- Examination difficult , palpation may lead to rupture of the abscess (risk of
pus inhalation) , or strip the abscess to the mediastinum .
The diagnosis confirmed by ;
1. Lateral soft tissue of the neck x-ray plain film ; the soft tissue exceed the width
of the vertebrae .
2. Ct scan , show the extent of the abscess cavity to decide the route used for
drainage .

Lecture notes in
3. CXR ; to exclude spread from the neck to posterior mediastinum .

The management ;
1. Combined pencillin , flucloxacillin & flagyl (or use clindamycine) therapy .
2. If not respond or there is compression on the airway , drainage which is via
either internal or external approaches under GA with intubation which should
continue for 24 hrs after aspiration or incision of the abscess or untill there is
clinical improvement(fever subside , & x-ray findings) .
Table summary of the commones acute laryngeal infection in children
Epiglottitis Croup Laryngeal Retropharyngeal

F.B. abscess
Pathology HIB (bacterial) Parainflunza ----- Staph aureus
virus type I
Age 2-6 y Below 3 y Any 1-4 y
History
Onset Rapid < 6 hrs Slow within 48 Rapid Slow usually Hx of
hrs tinsillitis or URTI
Previous attacks Not reported Quite often occasional Not reported
Symptoms
Cough Abscent Barking Paroxysmal Abscent
Dysphagis Severe None occasional Severe
Stridor Inspiratory Biphasic Inspiratory Inspiratory
Signs
Temp. Elevated Elevated Apyrexial Elevated
Posture Sitting Lying on back Variable Sitting , stiff
leaning forward neck
Drooling Marked None Occasional Marked
Cervical LN Large Small None Large
Behavior Quiet & Struggling Variable Restlessness
terrified
Colour Pale or grey Pink .... cynotic Usually Normal Flushed
Voice Muffled Hoarse Hoarse Hoarse
x-ray Thumb sign Steeple sign F.B. visible Widening of the
if opaque retropharyngeal space

Lecture notes in
Recurrent respiratory papillomatosis

The 1 st description of it by Mackenzie (1880) who describe papillomas in the larynx of a
child call it juvenile laryngeal papillomas , but recurrent is a better description as it affect
the adult population , the whole of respiratory tract may be involved from the lips to the
terminal bronchi .
Aetiology
The causative microorganism is Human Papilloma Virus (HPV) , a DNA virus , has 70
types , but type 6 & 11 is the main causative agents (these are the same viruses that cause
warts in the penis , vulva , cervix & perianal areas) .
The disease may be transmitted at the time of delivery (60%) due to mother genital warts at
the time of delivery . So advice to have subsequent children by C. section .
After the infection , the virus remain in the basal layer of the mucosa & replicating by
episomal maintenance , then transcribed the viral particles identified in the stratum
granulosum & cornum .
Epidemiology
It is worldwide disease , found in all socio-economic groups , incidence about 7
million/year in the USA .
In children female > male (before the age of 10) , while in adult male > female .
Clinical features
The presenting symptoms are ;
1. Present before the age of 4 years in majority of children , some during the 1st 6
months of life .
2. Initial symptoms ; hoarseness or abnormally increasing stridor & acute respiratory
obstruction which occur usually late in the disease .
The papillomas formed initially in the vocal cords themselves , this interfere with the
laryngeal function early in the disease .
Endoscopy is a must to established the disease , hoarseness in a child should not
dismissed as due to vocal abuse .
There is tendency of papillomas to occur at the anterior aspect of the glottis & on
anterior commissure .
3. The interarytenoid mucosa involved later in the disease , because the thickness of the
mucous blanket & the more rapid movement of it which exert a protective role in this
situation . But when the larynx extensively involved , the normal mucous blanket
disrupted causing involvement .
4. The disruption of the tracheal mucous blanket that occur after tracheostomy lead to
explosive increase in the tracheal papillomatosis , so tracheostomy should be
avoided if it is possible to establish a normal airway by endoscopic removal of the
papillomas .
Characteristics of the disease
1. The papillomas of the recurrent respiratory papillomatosis are benign sequamous
papillomas , occur in clusters on the involved mucosa , the fronds of papillomas may
be sessile & spread over a wide area of mucosa or pedunculated & localized .
2. The lesion characteristically multiple , occasionally single , recurrent even after the
most radical extirpation , recurrence may be as early as 2 weeks or after 5-20 years .
3. Mostly the larynx is the site of the greatest involvement & is often the only site .

Lecture notes in
4. On some occasionally removal of the papillomas enhancing effect on growth rate of

the lesion & recurrence larger than the original lesion .
5. Respiratory papillomatosis is a diffuse diathesis of the mucous membrane of the
upper respiratory tract & food passages , it may encountered in the nostrils (at the
mucocutaneous junction) , gingival , lips , soft palate , tonsillar pillars , larynx ,
tracheobronchial tree & occasionally pulmonary parenchyma & oesophageal inlet .
6. The lesion has predilection on points of airway construction , where there is increase
in the rate of airflow , drying , crusting & irritation , especially around the
tracheostomy site & at the tip of the tracheostomy tube .
Remission
- Remission of recurrent respiratory papillomatosis can take place at any age & at ant
time .
- The chance of remission is greatest if the disease present between the age of 6&10 years
- Remission in patients < 10 years at the time of presentation about 46% if followed for 1
year & managed by Endoscopy & laser destruction , while 26% remission if the disease
manifested > 16 years .
- The remission in the larynx is 48% , while in the tracheobronchial tree is 27% & in the
lung 0% . . The duration of remission ;
(1) It varies from 2 years to life long .
(2) Relapses may occur at ant time & for no reason , so the hope is for prolonged
remission rather than cure .
(3) Unfortunately , respiratory papillomatosis have the potential to spread (in same
case) from the larynx to the bronchiotracheal (11%) & to the lung parenchyma in
3% of cases , so produces cystic spaces (on x-ray) timed with sequamous
epithelium & filled with air or fluid , the pulmonary spread is multicentric ,
progressive & eventually fatal .
- Malignant degeneration ; is extremely low unless radiotherapy used , so it is
contraindicated here . In adults only 2 cases of sequamous cell Ca. & 3 cases of
verrucous Ca. recorded (in smokers) .
Management
A. Co2 laser vaporization with Endoscopy is the management of choice , with care to the
surrounding tissue not to damaged , especially anterior & posterior commissure lead to
scarring , also we avoid exposure of vocalis muscle , then awaiting for spontaneous
remission .
The use of low power intermittent mode Co2 laser minimize the risk of scarring & web at
the anterior commissure (prefer to do one side at a time) . Hazards of laser are ;
(1) Damage to the adjacent structures & to the theatre staff .
(2) Also inhalation of the smoke generated by laser in which HPV DNA found .
B. Medical management ; because the disease has dormant viral episomes in the basal
layer , so definitive management is medical in form of immunomodulating agents &
antiviral agents which include ; inosine pranobex , adenine arabenoside , lysozyme
chlrhydrate , acyclovir & ribavirin . Non of the above agents has established as having a
major role in the management of the disease .
Some use the interferone in the management of the disease , acting by producing
enzymes to prevent viral replication & stimulation of the host defense by increasing
lymphocytotoxic activity or killer lymphocytes .

Lecture notes in
Trauma & Stenosis of the larynx & trachea

Classification of the laryngeal injuries depend on ;
A. Sites ; supraglottic , glottic , subglottic or mixed .
B. Tissue ; internal soft tissue or laryngeal framework (hyoid , thyroid , cricoid &
tracheal rings) .
Epidemiology ; about 1:30000 in emergency room , especially those due to RTA , because
of several safety measures in cars & streets , usually young male .
1. Direct injury
(1) Acute laryngeal trauma
It occurs mostly in young males due to sport , RTA & fighting , it is of 2 types ;
1) Penterating wounds ; knives , bullets , wires & aggrucultural implantes .
Penetration of the thyrohyoid membrane , bleeding in paraglottic space leading
to obstruction , but not affect the voice .
If little bleeding & oedema this will resolved , if significant , it will organized &
lead to supraglottic stenosis .
Penetration of the cricothyroid membrane ;
- Air will leak from the respiratory tract (surgical emphysema) .
- Bleeding fill the subglottic space lead to respiratory obstruction .
- Bleeding rum in the trachea causing cough .
- Affect the vocal cords causing dyspneoa & hoarsness .
2) Blunt injuries ;
- Low velocity blunt injury "mostly affect the soft tissue" , by manual
strangulation , blow with fist & sport injury & inhalation of smoke & fumes , it
cause ;
a. Fracture of the hyoid bone , movement during swallowing lead to pain &
dysphagia & swellen of the base of the tongue .
b. Soft tissue injury cause bleeding within the paraglottic space & Reinke’s
space & supraglottic space causing stenosis .
- High velocity blunt injury "mostly affect skeletal framework"; by RTA & work
injuries , sometimes high velocity lead to compound fractures .
a. Thyroid cartilage ; depend on the age of the patient & degree of
calcification , if elastic cartilage , no fracture , if rigid , then splitting ,
disruption of the anterior commissure , the vocal cords roll on themselves
& the epiglottis falls backwards with posterior displacement with bleeing
in the pre-epiglottic space . If calicified , it is the important one , it will
shatter like an egg lead to flattened neck (loss of laryngeal prominence) .
b. Cricoid cartilage ; it is the most important one because it is the only
complete ring cartilage , so any trauma or disruption may lead to linear
fracture causing resorption of the cartilage & decrease airway caliber
causing stenosis .
Also high velocity injury may cause damage to the integrity of the cricoid ,
it rarely damage the soft tissue within it .
c. Tracheal rings , there may be damage to the trachea or cricoidtracheal
membrane & sometimes separation of the trachea from the cricoid lead to
death (sometime small patent lumen allow the patient to reach hospital) .

Lecture notes in
Pathological consequences of the injury

- Soft tissue ;
1. Oedema of the vocal cords or Reinke’s space lead to laryngeal polyps , also
it may affect the tongue base leading to dyspneoa & dysphagia .
2. Haematoma either supraglottic "most common" , paraglottic space or
Reinke’s space .
3. Anterior commissure may be detached .
4. Web due to abrasion of the anterior commissure .
5. Glottic incompetence due to ; arytenoids fixation , resorption of the
thyroarytenoid muscle , atrophy of the vocal cords & recurrent laryngeal
nerve palsy (subglottic injury) .
- Skeletal injuries ;
1. Hyoid bone ; may heal with out any discomfort .
2. Thyroid cartilage , may heal by fibrous union .
3. Cricoid cartilage , disruption may lead to resorption of the cartilage &
tracheal rings lead to weak trachea (tracheomalacia) causing dyspneoa in
excercize .
The subglottic space in children more important than adults because it is narrower
& has lax mucosa which may lead to marked obstruction with any mild oedema .
- History ;
1. Awareness of the possibility in every upper body trauma victim .
2. Symptoms ; dyspneoa , dysphonea , dysphagia , pain , cough &
haemoptysis .
- On examination ;
1. Stridor , if obstruction above the level of the larynx , then low pitch
stridor with andrawing of the cheecks during inspiration & blowing out
during expiration .
If the obstruction at the level of the larynx , then high pitch with
suprasternal retraction & decreased respiratory drive .
2. Cervical bruising .
3. Abdomen ; gastric dilatation .
4. Surgical emphysema confind to the neck (pathogenomonic) .
5. Loss of thyroid prominence (diagnostic) .
6. Be aware of the risk of the associated damage ; great vessels , cervical
spine & chest (haemothorax/pneumothorax, emphysema) & abdomen
(distant oesphageal tears) .
- Radiology ;
1. Plain cervical x-ray , helpful in emergency , show fracture or air in the
soft tissue (deep cervical or perivertebral tissue) .
2. CXR , shows ;
- Incomplete bronchial transaction shows collapsed lung at the level of
hilum .
- Deep cervical emphysema .
- Peribronchial air .

Lecture notes in
- Sudden obstruction along the course of the air filled bronchus .

- Fracture of the 1st rib , scapula or sternum , this suggest severe injury
& possibility of airways trauma .
3. CT scan may be helpful in suspected fracture but clinically not obvious .
4. Laryngoscopy , flexible should be done in all patients , direct rigid
laryngoscopy contraindicated here because it may exacerbate the injury .
Treatment ;
1. Protection of the airways , the most important aspect , if there is oedema
with no signs of intralumeninal bleeding , then advice bed rest at sitting
position & jaw kept forward to clear secretions with steroids with or
without steam inhalation .
If the airway at risk (bruising , odema with no major mucosal lacerations
& arytenoids displacement) , then intubate or do tracheostomy .
Laryngeal lacerations with subcutaneous emphysema , then do
tracheostomy (avoid cricothyroidotomy because it may lead to late
stenosis) .
If there is bronchial injury , then do emergency thoracotomy preceded by
elective intubation to stabilize the patient condition .
If associated with great vessels damage , then do emergency
tracheostomy.
N/G tube to prevent inhalation from gastric dilatation (for few days) .
Inflate the cuff of the endotracheal tube to prevent the blood aspiration .
If there is any significant endolaryngeal bleeding , then do midlaryngeal
laryngofissue to evacuate the spaces & qualited with 3/0 vicryl suture .
2. Protection of the laryngeal function , the function of the larynx is
breathing , speaking take priority with swallowing .
Breathing ; no need for permenant tracheostomy , minimal or no
dyspneoa & the patient undertaken normal daily activities .
Speaking , the out come depends on ; type of injury (vocal cords damage
cause prominent voice changes) .
Bleeding within the larynx , need laryngofissure to evacuate the
haematoma & quilted with 3/0 vicryle & leave drain in the space .
Skeletal damage need debridment & reconstruction or stenting .
N/G tube used in all cases to bypass dysphagia secondary to the
arytenoids oedema & to stop inhalation from glottic incompetence .
3. Surgery according to the type ;
a. Penterating injuries ; open the larynx , drainage & guilted (in bullet ,
require surgical exploration & debridment of the cartilage &
exploration of the neck blood vessels) .
Sometimes severe laryngeal injury need total laryngectomy .
b. Blunt injury ;
Low velocity injury , the majority of the patient has reasonable voice
& airway , so they need observation for oedema & airway
obstruction . If the voice or airway are disturbed , then intubate &
explore then reconstruct the larynx .
High velocity injury , like in RTA , need exploration & reconstruction

Lecture notes in
Skeletal damage need reconstruction using a stent , while soft tissue

injury need to stop the bleeding , spaces evacuated & quitting sutures
inserted . In cricoid injury we should do primary repair , if fail so
manage it by one of the technique of cricoid stenosis management .
Separation of the cricothyroid membrane approached by dropping
the larynx in the neck , freeing the trachea down to the carina with
end to end anastamosis & excising any damaged trachea rings
Most high bvelocity blunt injuries involve the glottis & subglottis , so
lead to chronic subglottic stenosis .
Indications for laryngeal stenting are ;
(1) To maintain the shape of the cartilaginous framework ;
- Posterior displacement of the epiglottis .
- Fracture of the arytenoids .
- Depressed cricoid fractures .
- Markedly displaced thyroid cartilage .
(2) To separate mucosal lacerations .
(2) Chronic laryngeal stenosis (see the separate topic laryngeal stenosis)
Differs in paediatric age group than the adults .
In paediatrics ; it is more frequent than tracheal stenosis , most commonly occur in
subglottic area within that part of the larynx from the lower aspect of the cricoid
cartilage to the insertion of conus elasticus fibers in the vocal cords above .
It is of 2 types ;
1. Acquired , increased incidence of subglottic acquired stenosis related to
increasing survival rate of preterm infants ventilated for brochopulmonary
dysplasia & hyaline membrane disease , true incidence 1-8% .
2. Congenital , due to soft tissue abnormality (responds to dilatation) or
abnormality of the cricoid cartilage (not respond to dilatation , so
contraindicated here) . It is the 3rd most common congenital laryngeal
anomaly & it is the most common cause of tracheostomy in child <1 year .
Histopathology ; abnormal submucosal lesion , abnormal shape of cricoid cartilage ,
normal shape of cricoid but with small diameter & posterosuperior displacement of
the tracheal rings .
Clinical features ; asymptomatic at birth (usually appear in the 1st few weeks or
months after URTI) , M:F about 2:1 , stridor which is either inspiratory or
expiratory with normal voice & crying .
In adults , established if the airways unsatisfactory after injury , it is important
because it interfere with speaking , breathing & ability to clear secretions , it caused
by ;
1. Failed management or non-recognition of acute trauma .
2. As a complication of tracheostomy , intubation & partial laryngectomy .
3. Scleroma , most common cause in the middle east .
4. rarely , Wegner’s granuloma , polychondritis & autoimmune thyroiditis .
There is a disruption of the supporting skeleton usually of the cricoid & tracheal
rings , usually occur in the subglottic area .

Lecture notes in
Pathological considerations ; the soft tissue dmage is due to mucosal loss , mucosal
adhesions , & organization of the haematoma in the paraglottic , pre-epiglottic &
interarytenoid space , all these cause soft tissue narrowing .
Glottic compitance is affected by ;
1. Web formation anteriorly .
2. Arthrodesis of the arytenoids posteriorly .
3. Recurrent laryngeal nerve injury , either at the time of trauma or in the ensuing
management .
Arytenoidectomy or codopexy almost always forms part of the management of
chronic laryngeal stenosis .
- History ;
1. The cause of condition is important , if it is as a result of systemic
disease or partial laryngectomy , then no enough tissue found for
augment the lumen of the larynx .
2. Need good surgeon-patient relationship to decide what is must be done
& the timing of the operation .
3. No attempt should be made to increase the laryngeal lumen until 18
months have been passed from the time of the initial injury .
4. The patient objective is to improve the voice & get rid from tracheostomy
, sometimes end with permanent tracheostomy .
- On examination ;
1. Flexible endoscopy is performed to gauge the extent of the stenosis .
2. Assess the length of the neck & howmuch cervical trachea is available
for mobilization .
- Rigid endoscopy , to assess ;
1. The extent of the laryngeal damage ;
o1 st degree : 50% of the lumen lost .
o2 nd degree : 50-75% of the lumen lost .
o3 rd degree : 75-95% of the lumen lost .
o4 th degree : complete obstruction .
2. The lower extent of the subglottic stenosis is shown .
3. Examine the state of the tracheal rings .
4. Assess the arytenoids (fixed or not) .
Oesphagoscopy should be done in every case .
- Radiography
1. CT scan , should be carried in all cases if possible .
2. Laryngography , only used if the subglottic space can’t be evaluated .
3. MRI show all soft tissue nature .
Management ;
1. Airway , most of the patients have tracheostomy already .
2. Warn the patient that ;
a. Tracheostomy may be permanent .
b. Postoperative N/G tube required at least for few days until the oedema
settles .

Lecture notes in
c. If function of the glottis involved , then unlikely postoperative voice will be

normal .
3. Surgical management according to the site ;
- Supraglottic stenosis , two options ;
(1) Laryngeal widening ; the larynx opens in the midline & as much as
possible the mucosal scarred tissue removed , the remaining mucosa is
stiched back against the laryngeal framework with quilting suture (or
areas of scarred tissue are grafted with skin or buccal mucosa) .
(2) Laser excision of the soft tissue .
- Glottic stenosis ;
(1) Anterior stenosis ; usually due to web , managed by ;
oLaser excision or repeated endoscopic excision , if the web limited to the
glottis .
oExternal excision & separation of the anterior glottis with a silastic or
tantalum keel (Mc Naught keel) for at least 5 weeks .
(2) Posterior stenosis , fixation of the arytenoids , difficult to managed
because it lies between the arytenoid cartilages & fixation of at least one
of them ;
oIf the arytenoids are mobile , then arytenoids separation by modified keel
or silastic stent .
oSuperior mucosal flap from the interarytenoid area above the stenosis .
oIf the arytenoids are immobile , then do laryngofissure & the arytenoids
are removed & the vocal cords stiched laterally with stenting to prevent
adhesions .
- Cricoid stenosis ; remove the narrowed scarring of the cricoid & swung down
the body of the hyoid bone with muscle pedicle & then wired into the arch of
the cricoid to keep it open & the scar tissue must be removed & replaced with
skin graft & a stent applied .
In greater degree of cricoid cartilage stenosis , then remove the cricoid
leaving part of the posterior lamina on which the arytenoids sit , then the
larynx is dropped & the trachea is pulled up & joined to the lamina anteriorly
& to the arch of the cricoid posteriorly .
- Tracheal stenosis ;
(1) Minor degree , treated by dilatation .
(2) Severe degree , excision of 4-5 cm of the weak tracheal wall & join the
trachea to the cricoid .
2. Burn & Scalds
It is caused by ; inhalation of irritant fumes or gases , swallowing of corrosive fluids &
inhalation of steam .
Pathology ; oedema of laryngeal inlet & vestibule .
Clinical features ; dyspneoa , pain & dysphagia .
Management ; usually conservative
(1) Bed rest , voice rest & sedatives .
(2) Parenteral steroids & analgesics .
(3) Antibiotics to prevent secondary infection .
(4) Tracheostomy or laryngectomy , if the airway is compromised .

Lecture notes in
(5) If stenosis follows , then need local management .

3. Radiation reaction
The radiotherapy cause severe local laryngeal reaction which exacerbated by smoking ,
alcoholism & local infection (including common cold) .
It causes ; dypneoa (use cover with dexamethasone) , discomfort on swallowing
secondary to membrane reaction with tenacious mucous increased with discofort & pain
due to Perichondritis & cartilage necrosis .
Management ;
(1) Manage the oral sepsis prior to irradiation .
(2) Tracheostomy sometimes needed for dyspneoa .
(3) Antibiotics for Perichondritis .
(4) Aspirine mucilage to decrease pain & swallowing discomfort .
(5) Laryngectomy for cartilage necrosis .
4. Inhalated forign bodies
Especially sharp forign bodies like pins or glasses which impacted in the larynx (large
forign body usually fatal) .
Clinically the presented as ; dyspneoa (urgent) , violent bouts of coughing followed by
quiescent phase , hoarseness or aphonia secondary to oedema , & Perichondritis &
stenosis follow in the forign body causing severe trauma .
Management
(2) Bear hug , Heimlich’s maneuver , from behind with hand clasped just below the
xiphisternum , will lead to expel the forign body .
(3) Removed by D/L as soon as possible , sometimed removed by laryngofissure .
(4) Tracheostomy or laryngotomy may be necessary in an emergency .
(5) Systemic antibiotics given to prevent infection .
5. Intubation injury
Due to prolonged intubation in ICU & it is caused by ;
(1) Rough intubation , especially if it is blind (the use of relaxant reduce it) .
(2) Prolonged intubation (berween the vocal cords) .
(3) The use of too large tube .
Pathology
(1) Superficial abrasion .
(2) Granulomatous formation usually occurs over the vocal prominence of the
arytenoids (50% bilateral , F:M 4:1) .
(3) Subglottic oedema especially in children .
Clinical features ; hoarseness & sometimes dyspneoa .
Management ;
(1) Voice rest .
(2) If persist , endoscopic removal of the granulomas .
(3) Tracheostomy for dyspneoa .
Prevented by avoiding blind intubation , use of relaxant & prepare for tracheostomy in
the intubated patients .
6. Acute haemorrhagic laryngitis
Due to haemorrhage secondary to sudden violent & forcefull approximation of the vocal
cords , usually seen after coughing , shouting , weight lifting & injuries to the larynx .
Clinically presented as ; hoarseness occur suddenly after vocal strain with pain .

Lecture notes in
On examination there are haemorrhage either single or multiple , sometimes the whole
cord involved , this may organized into granulation or fibrous nodule .
It must be differentiated (DDx) from ; acute laryngitis , leukaemia , external injury ,
purpura & carcinoma .
Management by ; voice rest & if there is organized nodule need endoscopic removal .
7. Singer’s nodules (vocal nodules)
The condition occur in excessive use of voice with straining & faulty production .
It is affect ; singers , teachers , actors , & mothers of young children , commonly in
females .
Pathology ; localized hyperkeratosis , usually at the junction of the anterior 1/3rd &
posterior 2/3rd of the free edge of one or usually both vocal cords .
Presented as ; increasing hoarseness (sudden or insidious) & vocal fatique , on
examination (D/L) bilateral symmetrical nodules , vary in size .
Management ;
(1) Voice rest , cures the recent & small nodules .
(2) Removed by D/L if the condition persist .
(3) Speech therapy to re-educate voice production .
(4) Elimination of the focal sepsis (teeth , sinuses & tonsils) .
8. Contact ulcers
Not true ulcers because the mucosa intact , occur in males & street venders due to vocal
abuse & coughing lead to hammering of one vocal process of the arytenoids to the other
Pathology ; thickening of the tissue around one vocal process & saucer shaped
depression over one vocal process .
Presented as discomfort in the throat , huskiness & vocal fatique with referred otalgia
(when ulcer occur) .
On examination ; kissing ulcers (on I/L) , granuloma on one side fitting in ulcer crater
of the other .
Management ;
(1) Total voice rest for 2-3 weeks with systemic steroids .
(2) Removal of the thickened epithelium by microlaryngeal surgery .
(3) Vocal rehabilaitation .

Lecture notes in
Foreign bodies in the larynx & trachea

Degree of difficulty of foreign body removal endoscopically depends on many factors ;
1. Age of the patient .
2. Type of the foreign body .
3. Interval between inhalation & removal .
4. Anaesthetist skills .
5. Equipment available .
Modern technique of foreign body removal by Endoscopy made by Chevaller-Jakson who
decrease the mortality of foreign body inhalation from 20% to 2% & the removal done
under LA . Then (nowadays) removal done under GA with Hopkins rod lens system &
advent ventilatory bronchoscope will greatly decrease the mortality & facilitate the use of
endoscopes .
Other technique of removal by postural drainage by Heimlich maneuver & introduction of
finger into the pharynx to remove the foreign body & because the manipulation may
dislodge the foreign body & cause total respiratory obstruction , this maneuver is
deprecated .
Incidence
- Maximum foreign body inhalation incidence between 1-3 years of age .
- The must common cause of death in home in children under 6 years is the inhalated
foreign body .
- Boys > Girls 2:1 because of unknown cause .
- Mainly these objects impact in the larynx .
- Foreign body in the larynx ; if they are too large , or they are triangular in shape or
they have a sharp edge which can catch on the laryngeal mucosa .
Clinical assessment
A. History
1. In most cases of inhalated foreign body there is definite history of chocking followed
by paroxysmal cough which then subside because after the paroxysm of coughing the
tracheal mucosa become tolerant of foreign body & the cough stopped , so this
feature responsible of delayed diagnosis .
2. One symptom of a triad chocking , wheezing & coughing was present in 91% of
patients with foreign body inhalation .
Wheeze is the most common symptom resemble to that in asthma & of sudden onset
in child with no past history of asthma , then we should suspect foreign body
inhalation as the cause especially if the wheeze unilateral ;
a. Unexplained persistent fever .
b. Fever associated with persistent respiratory symptoms in spite of treatment .
c. Persistent or recent pneumonia demand diagnostic bronchoscopy to exclude
foreign body .
3. Acute respiratory distress is uncommon but it is the most alarming presentation .
4. Pain at the route of the neck or over the larynx suggest foreign body .
5. Oesophageal foreign body , if large compress the trachea & cause repiratory
symptoms , if small , sharp longstanding then may cause fistula between the
oesophagus & trachea causing respiratory symptoms .

Lecture notes in
B. Clinical examination
1. Clinical examination is essential , but if respiratory distress or cyanosis , this need
immediate action with a special care during anaesthesia because the foreign body
may change the position & completely obstruct the airways .
2. Inhaled foreign body common in children with URTI cause by mouth breathing &
cough , which may lead to inhalation of peanuts with the sharp intake of breath
which follows the cough .
3. Laryngeal foreign body presented with hoarse or stridelous crying or excessive
salivation .
4. In the 1 st few hours after aspiration there will be ;
a. Signs present due to change in the airflow through the tracheobronchial tree .
b. Click heard by the stethoscope due to movement of the foreign body down &
up & fluttering noise heard also due to rapid oscillation of the object in the
air stream in the trachea or bronchi .
5. Unilateral expiratory wheeze with diminished air entry which may indicate foreign
body in the bronchus .
6. Obstructive emphysema , detected by mediastinal shift , easily detected by x-ray &
produced by valvular obstruction of the expiratory air stream due to the presence of
foreign body in the lumen of air passage .
7. If the foreign body not removed within 24 hours , pneumonia symptoms appears . The
severity of these symptoms depends on ;
a. Reaction of the bronchial mucosa .
b. Size of the foreign body .
c. Type of the foreign body (organic or non-organic) .
If the foreign body of vegetable origin , then ;
Severe intense inflammatory reaction occur .
Production of granulation tissue .
Atelectasis of distal lung due to mucosal swelling & inflammatory exudates
which obstruct the bronchial lumen .
Lung abscess may occur but this takes several months .
Unusual complication : brain abscess .
If the foreign body of dry vegetable type (beam) , it cause ;
Very rapid obstruction changes due to combination of mucosal irritation &
swelling of the beam itself by hydroscopic action .
Atelectasis of occluded segment of the lung with rapid onset in this type of
foreign body .
If the foreign body of ferrous metal or rough surface , it will cause the same
bronchial irritation , but the occlusion take longer time .
If the foreign body inert & has a smooth surface , it will cause very little
irritation & no pneumonia changes .
8. Haemoptysis , due to presence of flurried granulation tissue around the foreign body
C. Radiological findings
1. Plain x-ray " soft tissue of the neck " taken with neck extension , AP & lateral views
& AP view with inspiratory & expiratory .
2. CXR , lateral view because sometimes difficult to diagnose in young child & this
view complete the examination .

Lecture notes in
3. CT scan help to show the foreign body not seen with conventional radiography .
4. isotopes scanning , demonstrate changes in the ventilation & perfusion of the scar
tissue .
Abnormal x-ray finding not seen within the 24 hours of inhalation which changed
dramatically noted after 24 hours , this applied in case of obstructive emphysema .
The majority of the foreign bodies rest in the right bronchial tree because the right side
is wider & more vertical than the left & the projection of the interbronchial septum to
the left . In young children the difference is less pronounced , so there is more equal
distribution of the foreign body between the right & left bronchi .
Management of foreign body in the respiratory tract
Diagnosis from clinical features , radiology & endoscopic examination (which is the
method of choice for removal) .
A. Laryngeal or large tracheal foreign body
Tracheal foreign body should be removed as an emergency procedure ;
- If the airway compromised immediately perform Endoscopy & tracheostomy urgently
, large tracheal foreign body may be delivered through the tracheostomy .
- If the airway not compromised , the procedure performed within hours to allow the
stomach to empty .
Laryngeal foreign body , removed by D/L ;
- Majority easy to remove .Rarely large foreign body cause total respiratory
obstruction which treated by tracheostomy which is necessary here .
- Commonly encountered difficulty of the foreign body is the delay of diagnosis .
B. Tracheal & bronchial tree
Better removed using rigid bronchoscope & in absence of respiratory distress should
consider as elective procedure . Efficacy & safety of rigid bronchoscope performed by
doing conservative measures include ;
(1) Bronchodilators .
(2) Chest physiotherapy (thoracic percussion & postural drainage) .
Indeed this postural drainage is the cause of complete respiratory obstruction & even
hypoxic cardiac arrest , if the foreign body is moved & impact in the subglottis .
Preoperatively physiotherapy with antibiotics may be useful in patients with peripherally
situated foreign body (usually organic) for long time because there is usually ;
atelectasis or pneumonia or even lung abscess .
Postoperatively physiotherapy also help to treat the atelectasis .
In cases where there is granulation tissue , then application of 10% adrenaline will
shrink the granulation tissue & decrease the bleeding to minimum .
Rarely the foreign body can't removed by endoscope , then it need thoracotomy &
bronchotomy .
Technique of removal
- The majority are elective procedures .
- Instruments ;
(1) Complete set of ventilating bronchoscope .
(2) Hopkins rod lens system manufactured by Karl-Storz , Storz endoscopes with
different diameters & lengths ;
Diameter (mm) 2.5-3 3-3.5 4-5-6
Length (cm) 20 25 30

Lecture notes in
In children 3.5 or larger can be used .

(3) Grasping forceps , used in children & combined with bronchoscope (in infants can't
be combined with the bronchoscope) .
(4) In infants & neonates use a set of open tube bronchoscope of Negus pattern suckling
& infant sizes with a swing arm magnifier which provide magnification of X4 .
The forceps used call Chevaller-Jakson foreign body forceps .
(5) In some cases , Fogorty balloon-catheter designed for arterial embolectomy used for
removal of the peanuts .
- Size of the catheter 3-4 passed down to the side of the Storz bronchoscope .
- The tip of the catheter pass beyond the foreign body & the balloon inflated with
saline .
- Telescope withdrawn 1 cm , to allow a space for a presenting part of the peanuts .
- Traction exerted on Fogorty catheter .
- Catheter , bronchoscope & foreign body are removed together .
Fogorty catheter also useful in removal of foreign body with holes (beads) , the
catheter threaded through the hole & inflated & the foreign body removed .
(6) Dormia basket used by urologist can be used by the same procedure (as Fogorty
Catheter) .
- Before commencing the procedure , the surgeon must check ;
(1) Jaws of the Chevaller-Jakson forceps .
(2) Patency of suckers .
(3) Length of sucker to be long enough to protrude beyond the bronchoscope .
(4) Selection of the suitable size & shape bronchoscope & forceps , by passing the
forceps through the chosen bronchoscope & open the blades of the forceps .
The emergence of the tip of the forceps is felt but not seen , because of no
stroboscopic vision in bronchoscope . Opening of the tip of the forceps beyond the
end of the bronchoscope is the correct position for grasping of the foreign body .
(5) In cases where there is particular difficulty is likely to be encountered , e.g. open
safety pins or other sharp objects .
- Special care must be taken in young children to keep the bronchoscope in line with the
trachea to ensure adequate ventilation .
- The ventilation may be difficult when the bronchoscope passed deeply into the obstructed
bronchus .
- Adequate ventilation is maintained if the holes in the side of the bronchoscope remain
unobstructed & directed toward the normal main bronchus .
- Following removal ;
(1) 2nd look is taken while the child still anaesthetized to ensure a 2nd foreign body has
not been over locked .
(2) Remove any remaining small fragments in case of peanuts .
(3) Aspiration of pus & mucous from the distal bronchus will speeding the resolution of
atelectasis & pneumonia .
(4) Inspection of all bronchpulmonary segments including the upper lobe orifice
inspected .
If the bronchoscope prolonged or noted to be tight fit in the subglottis , use systemic
corticosteroids (dexamethasone 0.5 mg/kg) to decrease the incidence of laryngeal oedema
postoperatively .

Lecture notes in
Stenosis of the larynx

It is commoner than tracheal stenosis .
Aetiology & Pathology
1. Intubation ; subglottic stenosis , due to many factors , like the material from which the
tube is made , shape & size of the tube , method of fixation , the skill & care .
2. Infection (cause subglottic stenosis) .
3. Blunt trauma (cause subglottic stenosis) .
4. Iatrogenic , prolonged management of juvenile laryngeal papilomatosis & the use of
Co2 laser .
Acquired laryngeal stenosis
Has two varities ;
2. Soft stenosis
Acute oedema (inflammation) of the mucosa & submucosal connective tissue , then
mucosal ulceration supervene (due to mucosal abrasion resulting from posterior
fixation of the endotracheal tube , or due to pressure if the tube is large) .
The ulceration process accelerated by infection (which can be prevented by good
aseptic technique) , chemical irritation from rubber , this process of ulceration then
expose the perichondrium of the cricoid causing Perichondritis & chondritis , it is
associated with formation of the granulation tissue & fibrosis .
3. Hard stenosis
Stenosis associated with infection & it is of 2 types ;
- Fibrous stenosis , can be dilated but tend to restenosed .
- Cartilagenous stenosis , can’t be dilated .
Investigations ; endoscopy , CT scan , MRI & Barium swallow .
Management of laryngeal stenosis ; it is one of the most controversial topics in paediatric
laryngology , it is range from repeated dilatation , prolonged laryngeal stenting with
steroids , Co2 laser +/- tracheostomy , to early tracheostomy & open surgical operation on
the child’s larynx .
Management of laryngeal stenosis in infants & young children should be conservative
because the majority the stenosis will improve with laryngeal growth & need gentle
endoscopic evaluation . Open surgery done when careful endoscopic assessment said that
the laryngeal lumen has not increased in size .
Congenital subglottic stenosis
Less severe than acquired one , most of them managed by Co2 laser , others required
tracheostomy & then decanulate within 2-5 years without requiring any operation on the
larynx .
Histopathological nature of the cricoid of the preterm infant ; it is hypercellular with scanty
gell like matrix which is more distensible , that is why those babies tolerate endotracheal
intubation for several weeks without great damage to the subglottis .
It is difficult to distinguish between the acquired & congenital causes (congenital has more
tendency to heal spontaneously) , it can be distinguished by failure to pass 3.5 mm
bronchoscope through the airway (means stenosis <3.5 mm) .
It resolved spontaneously with laryngeal growth with conservative treatment , surgeru may
be indicated to assess the stenosis (Endoscopy) or for laryngeal grafting or
laryngotracheoplasty .
The management of the 2 types of the subglottic stenosis (congenital) ;

Lecture notes in
- For the soft tissue abnormalities : Due to intubation with submucosal fibrosis ,
hyperplasia of the submucosal glandular tissue (submucosal retension cysts) managed
by deroofing with Co2 laser , cup forceps or diathermy .
- Abnormalities of the cricoid : large anterior lamina with very small posteriorly sited
airway (1.9 mm in diameter) & oval cricoid , managed by dilatation or Co2 laser is
unsuccessful , so the management by open procedure on the larynx which is the
management of choice for acquired subglottic stenosis also .
Dilatation : Used only for soft tissue stenosis , may respond
Steroids : Used as adjuvant to dilatation , simple excision of scar by Co2 laser or cup
forceps , & to aid the decanulation (stop fibroplasias & development of granulation
tissue) . Side effects are ; delay wound healing ,& increased susceptibility to infections .
Dose ; 0.5 mg/kg to reduce oedema after bronchoscopy .
Endoscopic resection : many types
(1) Infant urethral resectoscopes .
(2) Cryogenic probes .
(3) Co2 laser endoscopic resection .
It can be unsuccessful due to (need open surgery) ;
(1) Combined laryngeal & tracheal stenosis (with significant loss of cricoid or
tracheal cartilage) .
(2) Abundant scar tissue (at least 1 cm of larynx or trachea) .
(3) Bacterial infection , Perichondritis , so wait for 6-12 months , then do open surgery
on the larynx .
Open surgery : Many procedures , using autologus graft from the hyoid bone ,
sternohyoid myo-osseous flap & nasal septal cartilage .
- Laryngotracheoplasty
Indications ;
1. Congenital subglottic stenosis , hard type .
2. Laryngeal web with cricoid cartilage abnormalities .
Incision , midline incision (castellated incision) , through the thyroid & cricoid
cartilage & tracheal ring .
Procedure ; open the larynx , vocal cords separated at the anterior commissure ,
submucosal dissection & remove the scar tissue (by microscissors) , then the thick
cricoid cartilage cored from its internal surface to increase the lumen , then insertion
of internal stent (Swiss-roll of silastic sheathing) & fixed , suturing of the displaced
tracheal & laryngeal cartilages , the silastic roll removed after 6 weeks by endoscope .
- Laryngotracheal reconstruction
Indication ; in Acquired stenosis with loss of cartilage due to perichondritis or
chondritis .
Incision ; laryngeal fissure incision .
Procedure ;
(1) If the stenosis anteriorly , insert the cartilage graft anteriorly (free costal
cartilage) , trimmed until it exactly fits the defect , sutured by 0/5 polypropyline .
(2) If the scarring at the posterior part with interarytenoids fixation , division of the
posterior lamina of the cricoid & small graft of the costal cartilage inserted .
(3) Combination of anterior & posterior stenosis or complete stenosis , then anterior
& posterior graft used .

Lecture notes in
Stenting : Many types ;

1. Silastic –roll , advantage ; self adjusting .
2. Rigid stent like Montogomry silastic laryngeal stent , Motogomry T-tube or
Aboulker Teflon stent (do not have the above advantage) , it may cause further
damage because it is large .
The silastic stents usally retained for 6 weeks (6-24 months in severe cases) .

Lecture notes in
Stertor & Stridor

Stertor defined as noisy breathing caused by partial obstruxtion of the respiratory tract
above the larynx (low pitch snoring sound) .
Stridor defined as noisy breathing caused by partial obstruxtion of the respiratory tract at
or below the larynx (low-high pitch) .
Aetiology
A. Stertor
1. Congenital
- Nose ; agenesis , or hypogenesis or stenosis of the anterior nares , choanal atresia
or stenosis , dermoid cyst , nasoalveolar cyst , dentigerous cyst , meningocele
encephalocele .
- Nasopharynx ; craniofacial abnormality (Apert’s & Crouzon’s syndromes) .
- Oropharynx ; micrognathia secondary to a craniofacial abnormality ,
macroglossia (Down’s syndrome) , lingual thyroid & thyroglossal cyst .
2. Acquired
- Trauma ; septal haematoma & secondary abscess , nasal & septal & midfacial
fractures .
- Inflammation ; adenoids , tonsillitis , pharyngitis & retropharyngeal abscess .
Ludwig’s angina , acute epiglottitis , Wegner’s granulomatosis .
- Allergy ; allergic rhinitis & angio-oedema of the mouth .
- Tumors ; benign (polyps & angiofibroma) or malignant (nasopharyngeal ,
oropharyngeal Ca. & lymphomas) .
- Iatrogenic ; synaekia & adhesions postnasal & tonsillectomy surgeries .
B. Stridor
1. Congenital
- Larynx ;
a. Supraglottic ; laryngomalacia , web , cystic hygroma & saccular cyst .
b. Glottic ; web , vocal cord paralysis .
c. Subglottic ; web , stenosis , haemangioma .
- Trachea & bronchi ; web , stenosis , tracheomalacia , other mediastineal cysts &
tumors (thymic cyst) , tracheo& bronchogenic cysts , vascular compression .
2. Acquired
- Trauma ; thermal , chemical , iatrogenic , external (blunt or sharp) .
- Inflammation ; acute laryngitis , laryngotracheobronchitis & diphtheria .
- Forign bodies ; laryngeal , brinchia or tracheal or compression from oesophageal
forign bodies .
- Allergy ; angioneurotic oedema of the larynx or trachea & allergic alveolitis .
- Tumors ; papilomatosis , Ca. of larynx & bronchus .
N.B.:
1. Supraglottic cause inspiratoy stridor, because of infantile freely mobile supraglottic is
drawn into the glottis during inspiration .
2. Glottic & subglottic , usually biphasic stridor , the relatively rigid wall of the rima
glottides , subglottis & trachea prevent the collapse , so the stridor result from airflow
turbulence alone .
3. Small bronchi & brinchioles , the stridor expiratory , as in expiration the tissue
collapse the airway causing expiratory stridor .

Lecture notes in
Clinical features
1. History
a. Characteristic described by the parents as noisy breathing , sometimes whistling ,
snoring , rowing or wheezing , either continuos or intermittent .
b. Severity ; loud sound associated with cynosis or apneoa .
c. Age of the onset ; congenital start shortly after birth or after 1st week , while in
acquired start later on .
d. Relationship with feeding , crying & excersize , with sleep the sound decreased
because of decreased respiration while in crying , feeding or increased activity there
is increased respiration & increased sound .
Except in laryngomalacia when the stridorincrease during sleep because of laxity of
the laryngeal mucosa .
e. Related disease , associated with other congenital anomalies like respiratory , CVS
& CNS , it may be percpitated by URTI .
f. Related symptoms ;
- Dyspneoa ; always a manifestations of airway obstruction , respiratory
embrassement lead to hypoxia & increased Co2 leading to cor-pulmanale &
pulmonary odema causing vomiting & aspiration leading to pneumonia & death .
- Cough ; especially in subglottic inflammation or tracheal disease .
- Hoarseness , vocal cord paralysis , inflammation & infections or tumors .
- Noisy breathing (symptoms not diagnostic) .
- Feeding difficulties , stridor & stertor increased with feeding , so the child poorly
feed & failure to thrive .
2. Physical examination
a. General appearance ;
- Active , well feed , happy child unlikely to have serious pathology .
- Pectus excavetus (some times) may be seen .
- Extension of the neck lead to decrease the stridor (in laryngomalacia) .
- Flaring of the ala nasi , intercostals , suprasternal , subcostal recession which
indicate acute respiratory embrassement .
- Tracheal tug , phenomena of marked suprasternal recession which pulling down
the trachea into the chest during inspiration .
- Cynosis , tachypneoa , rising pulse rate which means increased distress .
- Pallor , bradycardia & hypotension are late signs .
b. Nose , oral cavity & pharynx
- Nose ; comngenital or acquired causes (polyps , septal deviation ..etc.) .
- Nasopharynx , postnasal discharge , adenoids hypertrophy , tumors , ..etc.
- Oral cavity & oropharynx ; large tongue , micrognathia , tonsillitis & peritonsillar
abscess & IMN .
d. Nutritional status ; over weight child liable to develop croup or airway obstruction
due to increased breathing effort & high oxygen requirement .
e. Larynx ; stridor we do indirect laryngoscopy .
f. Palpation , like congenital thyroglossal cyst & other swellings .
g. Tape recording , to show the change in quality during sleep .

Lecture notes in
h. Auscultation timing of the sound in relation to the respiration , quality , pitch

(inspiratory “glottic & supraglottic” & expiratory “tracheal & bronchial” , biphasic
“subglottic”) .
i. Vital signs ; pulse rate , blood pressure , temperature , …etc .
j. Other examination ; CNS , CVS , ..etc .
3. Investigations
a. Laboratory ;
- Biochemival , like serum proteins , blood urea , ..etc .
- Haematological ; Hb , PCV , ..etc .
- Immunological ; VDRL .
- Physiological ; blood gases , PH & ECG .
b. Radiological
- Plain x-ray , lateral view of the neck soft tissue during expiration with extended
head on the neck .
- AP view of the chest .
- Polysomnography .
- CT scan & MRI .
- Fluroscopic screening (with contrast) .
- Angiography .
c. Endocopy
- Stertor ;
 Cottle’s speculum , examine the nasal cavity .
 Hopkin’s rod telescope .
 Fibrooptic flexible nasoendoscope .
 Boyle-Davis mouth gag to examine the oropharynx .
 Postnasal mirror to examine the nasopharynx .
- Stridor ;
 Laryngoscopy & microlaryngoscopy .
 Bronchoscopy .
 Oesophagoscopy .
 Flexible endoscopy .
Management
According to the cause .

Lecture notes in
Voice disorders
The phonatory system has 3 levels ;
1. The voice activating air system (Respiratory system) , the deficient air pressure above ,
below the glottis provide energy that overcome the resistance of the adducted cords
causing its vibration .
In cord dysfunction , the air pressure & the air system are not usually controlled during
phonation , then the vocal cords not be closed fully during phonation & will allow
passage of large air flow (seen by I/L as triangular shape aperture of the glottis) .
2. The vibrating glottis (voice generator) , the air system , vocal cords vibration , the
human voice results from ;
o Cricothyroid articulation movement by muscles , straighten or shorten the vocal
ligament .
o The movement of the arytenoids cartilages .
o The tendinous membrane that cover the inner surfaces of the intrinsic muscle of the
vocal cords .
The hyoid bone & larynx are suspended because the between the bone of the skull &
thorax & move up & down infront of the cervical spine by muscles (sternohyoid ,
omohyoid & geniohyoid muscles) , the highest position in swallowing & lowest position
in yawing , also it attached to the cricopharyngeus .
The voice resonators are ;
o The oropharyngeal resonators .
o The velopharyngeal valve (middle) .
o The (outer most part) between lips .
3. Integration & control by CNS , all the muscles especially the intrinsic muscles , soft
palate , floor of the mouth , neck , diaphragm & pelvis integrated by CNS which sends
out signals to adjust the muscle tone .
Management
A. History
Chief complain , date of onset (gradual or sudden) , the course , previous management ,
swallowing troubles , patient job , general health , review of systems , hypernasality ,
alcohol & smoking .
B. Examination
1. The quality of voice should be recorded , look for facial expression & eye contact .
The voice may be low or high , loud or soft , powerful or weak , clear or breathy ,
hoarse , sharp or dull , thin or sonorous , resonant or falsetto , periodic or raw ,
harsh relaxed or tense strained .
The voice production either ;
oHyperkinetic lead to tense voice with forceful closure of the glottis & high
subglottic air pressure .
oHypokinetic , the voice with little energy & air waste .
2. Voice alteration in response to coughing , phonation & yawing .
3. Examination of the ear , nose & throat & evaluate the voice during examination ,
also examine oral cavity , pharyngeal isthmus & nasal patency .
4. Indirect laryngoscopy , the vocal cords seen in quite & deep breathing , low voice ,
coughing , producing high falsetto & sharp loud voice .
The vocal cords closed completely on coughing , but not on phonation .

Lecture notes in
C. Special methods of examination

1. Magnetic tape recording of voice .
2. Phonogram or pitch-intensity profile , the examiner subjective assessment of the
loudness , pitch , quality of voice can be supplemented by objective measurements .
3. Stroboscopy , mirror examination of the vocal cords under intermittent light give
excellent clinical tool to deserve details of epithelial & the deeper structures during
phonation . It show the vibratory motion , different phases of opening & closure of
the vocal cords .
4. EMG , of the intrinsic laryngeal muscles , either through the mouth (electrode placed
in the vocalis muscle) or through the skin of neck (the needle electrode inserted into
various layers of the laryngeal musculature) .
5. Recording of air flow during phonation (efficient voce use by using low air flow) .
6. EGG (electroglottogram) , recording changes in electrical impedance over the glottis
Voice disorders of primary organic origin
Like congenital web , neuromuscular disorders , trauma , cyst , polyps , inflammation ,
tumors , endocrine disorders , congenital anomalies (sulcus glottides) .
1. Vocal cord paralysis
Laryngeal stroboscopic examination shows hypotonia of the paralyzed side with the
amplitude of vibration is more than normal side (flutter like a flag in the wind) .
In bilateral abductor paralysis , paramedian position impair the breathing causing
inspiratory stridor .
If the cord in intermediate position , little resistance to the respiratory air , sometimes
hyperventilation , light headedness , dizziness , headache , irritability & emotional
liability .
Management by ;
a. Exercise to improve the glottic closure (short well controlled expiratory thrust) .
b. The Bernoulli (suction) effect will narrow the glottis .
c. External pressure by 2 fingers to the side of the larynx
d. For parmedian position , widening of the glottis by straightening of the vertebral
column & increasing the pull by the diaphragm .
2. Voice disturbances caused by the endocrine disorders
The child voice . adult women & adult man voice differs due to ; different size of the
vocal cords & resonant tubes (small in child , median in women & large in man) .
a. Intersexuality ; in Turner & Klienfilter syndromes the differentiation of voice is
absent or incomplete .
Three common mutation occur at adolescent ;
o Mutation falsetto voice , during lough & coughing , the voice drops into heavy
register .
o Prolong mutation , the heavy & light register alternate .
o Incomplete mutation , no question of split registered , the pitch of voice too
high , the tone dull , it lacks the low resounding quality of the metal or heavy
register .
b. Sexual orientation & gender identity ; homosexuals have high pitch voice , trans-
sexual may wish to change their physical sexual characteristics by surgery or
hormonal therapy .

Lecture notes in
c. Virilization of voice in females ; musculinization in female called perverse mutation

before oval puberty , the cause is ovarian tumor .
Postmenopausal , critical period for female voice , the decrease in hormone lead to
changes in elastic & collagenous fibers .
Anabolic steroids cause voice changes before other symptoms of Virilization occur.
d. Laryngopathia grvidarum ; it is a disorder of pregnancy due to high estrogen , also
premenstrual hoarseness due to mild vocal cords oedema .
The voice lower than normal , may be complete aphonia (dysphonia & stridor) .
Predisposed women with more serious , red oedematous vocal cords epithelium ,
ventricular bands , aryepiglottic folds lead to haemorrhage & loss of epithelium or
crust formation . The condition resolved when the pregnancy over .
e. Hypothyroidism ; there is thickening of the subcutaneous tissue . monotonous voice
, low , dull slow speech & laborious articulation .
Managed by replacement therapy .
f. Hyperthyroidism ; the voice clear , high , animated , but poor control (respiratory
& laryngeal control) lead to hoarseness . Goiter may cause compression &
displacement of the pretracheal membrane lead to voice complaint .
3. Congenital abnormalities of the larynx
a. Webbing of the anterior commissure ; affect the vocal cords leading to high ,
breathing sound & can't produce a powerful tone , managed by surgery .
b. Asymmetry of the vocal cords ; unequal vocal cords length , difference in vocal
cords level & unequal vocal cords mobility .
c. Sulcus glottides , there is groove along the length of one or both vocal cords due to
connective tissue hypoplasia .
d. Ehler-Danlos syndrome ; over elasticity of the vocal cords ligaments lead to
hyperexcitable ligament , lead to low monotonous voice which managed by Teflon
injection .
4. Others
a. Senile atrophy ; elderly female may have low pitch due to oedema of the vocal
cords or hypothyroidism , while elderly male may have high pitched , temper &
high voice due to the ability to phonate in chest registers due to shrinkage of
muscle mass of the cords or stiffening of the vocal cords membrane ligaments .
b. Inflammation ; like T.B. , syphilis & granulomas .
c. Vocal cords cyst ; either mucinous retention cyst r epithelial inclusion cyst as a
result of laryngitis .
Signs are according to the site , usually halfway along the membranous cord , I/L
show unilateral nodule (or hind under moncorditis) .
The small cyst can cause diplophonia , management by removal & voice therapy .
d. Papillomatosis of the larynx ; gradual progressive dysphonia , I/L shows warty
mass on the vocal cords (in adult unlikely recurred , while in children recur) .
The prognosis ; improved with age .
e. Trauma to the larynx ; RTA direct trauma may cause fracture of the cartilage ,
ligamantous tear or rupture of the trachea , mucosal adhesion , interference with
Cricothyroid or cricoarytenoid joints lead to huskiness of the voice .
Prognosis ;

Lecture notes in
o Adhesion ; removal with Teflon injection lead to regulat voice & further
improvement .
o Prognosis depends on I/L findings ; position & mobility of the arytenoids ,
aperture & closure of the glottis & difference in levels of both cords .
Stenosis of the larynx in children before the onset of speech lead to buccal voice
(frog's speech) .
Plastic reconstruction lead to satisfactory lumen with remaining lumen fitted with
an acrylic tube & tracheostomy tube to produce voice .
f. Vocal cord cancer ;hoarseness for more than 6 weeks refer to throat specialist .
constant not intermittent , not improved , nor worsen .
Stroboscopy show the vocal cords not vibrate (used for diagnosis & follow up) .
g. Hyperplasia of the epithelium ; the improper use of voice & smoking & alcohol ,
reflux gastric contents , all cause epithelial changes , chronic irritation also cause
such changes with inflammation , acanthosis & hyperkeratois .
The voice changed & the patient can't phonate at low level intensity .
On examination ;
o I/L & D/L , see the extent & degree of thickness .
o Stroboscopy , beneficial in checking for movement (absence of vibration if the
vocal cords infiltrated) .
Management by removing the causative factor , because the epithelium hyperplasia
is reversible , sometimes need phonosurgery to correct voice .
Psychogenic voice disorders
1. Voice reaction to stress
The common reaction to frustration is crying , turn to primitive behavioral pattern or
withdrawal or flight . Showed crying , then conversion symptoms developed ;
o The whispered voice of psychogenic aphonia (female) .
o Vocal stuttering , spastic dysphonia in male .
It need behavioral therapy .
2. Habitual dysphonia
When a person in normal circumstances nearly always using poor voice , following
questions should be asked ;
a. The quality of voice always been poor ?
b. Has the voice problem had very gradual onset ?
c. Is the quality of voice nearly constant ?
d. Has the voice failed repeatedly after prolonged speech ?
If all are yes so the diagnosis is habitual dysphonia , if the following question answered
yes , so the diagnosis is psychogenic dysphonia ;
a. Before the voice problem began , was the voice quality normal ?
b. Has the changes in voice quality are seen abruptly ?
c. Is the quality of voice inconstant , changes with certain instances ?
d. Has the voice failed repeatedly in situation of stress ?
Disorders of voice in adolescence
At the age of 12-15 years , the voice changes , low voice in male as chest & falsetto
requester as a result of laryngeal & vocal cords affected by testosterone & decreased
gonadotrophins , after a year the 8 semitones lead to 256 Hz & then to 873 Hz .
Adam's apple indicates sexual maturation of the larynx .

Lecture notes in
Abnormal functional adjustment to changes in size of the vocal cords

Hyper- & Hypo-kinetic form of habitual dysphonia & resulting organic laryngeal
abnormalities ;
1. Vocal cord nodules ; singer nodule , it affect adults & children , the cause is the over
laxity of the vocal cords with incorrect use of voice (habitual dysphonia) , if the
nodule persist for longtime it will be permanent .
Sequences ; submucous transudation , then growth of blood vessels & then fibrous
organization . The site always symmetrical on both sides , in children & adolescence
spindle shaped thickening of the edges of the vocal cords , while in adults more
localized thickening , nodule at the junction of the anterior 1/3rd & posterior 2/3rd .
Managed by voice rest which indicated when the cause of the trouble short lived or
when preliminary to voice therapy .
2. Vocal cord oedema & laryngeal polyps ; the polyp is hypertrophied oedematous
mucosa , here there is accumulation of the fluid in the subepithelial space of Rienke
called vocal cords oedema . If the accumulation is concentrated at one point &
balloons of the epithelium out infront of it , then lead to vocal cords polyp .
The site mostly the whole membranous part of the vocal cords especially the anterior
commissure .
The cause ; Mostly unknown aetiology .But excessive subglottic pressure with
incompletely closed cords , then the mucosa sucked in & ballooned anteriorly with
accumulation of the subepithelial fluid & ingrowth of the new connective tissue &
later firm consistency .
The oedema is symmetrical after acute laryngitis , when the voice not spared , pale
appearance . Stroboscopy show floppy wave edge with enlarged ventricle
components of the vibrating system .
If slight oedema managed by vice rest (resolved) , but if polyp , then it need excision .
Phonosurgery
Indications are ;
1. Vocal cord nodules ; when decreased in the duration by fibrosis & covered by
hyperkeratosis .
2. Cyst giving serious voice complaints .
The aim to ;
1. Surgery to congenital defects like sulcus vocal cords (atrophic patch) to restore the
mucosa & prevent adhesions of the mucosa into the ligaments which lead to normal
vibration .
2. In multiple papillomatosis , saving the epithelium .
3. Surgery to improve the voice in pseudospasmodic dysphonia , to paralyze one vocal
cord , the replace the voice stuttering by a paralytic dysphonia .
Thyroplasty of 4 types ;
- Type I ; vocal cord nedialization .
- Type II ; vocal cords laterlization .
- Type III ; vocal cords shortening .
- Type IV ; vocal cords elongation .
The advantage of the procedure is to delicate interior of the larynx not touch & the
procedure is reversible .

Lecture notes in
Vocal cord paralysis

Surgical anatomy
Phonation initiated by area 4 in the Sylavian fissure of the cerebrum , the fibers pass down
to the internal capsule & lower pons , some fibers decussate to the opposite side before
entering the medulla , in which they go to the nucleous ampigus (so the vagus nuclei
inervated bilaterally) .
The peripheral vagus nerve comes out of the lower pons & upper medulla , passing through
the Jugular formen to the neck , gives the superior laryngeal nerve (which is usually mptor
to the cricothyroid muscle & sensory to the laryngeal mucosa above the vocal cords) , then
the vagus pass through the neck in the carotid sheath (between the carotid artery & the
jugular vien) entering the chest where it give rise the recurrent laryngeal nerve which is
motor to all internsic muscles of the larynx & sensory to the mucosa below the vocal cords .
On the left side the recurrent laryngeal nerve pass anterior under & then behind the aorta
(beside the ligamentum arteriosum ) , then in the tracheo-oesophageal groove to enter the
larynx near the cricothyroid joint .
In the right side , it pass anterior to the right subclavian artery & loop around it & return to
the neck & follow the same course as the left side .
The glottis ; 60% membraneous vocal cord (soft & mobile) & 40% vocal process & medial
border of the arytenoids (hard & cartilaginous) .
Relations of the recurrent laryngeal nerve ;
- Right ; right subclavian artery , supraclavicular LN & apex of the right upper lung lobe
- Left ; aortic arch , oesophagus , left atrium , mediastienal LN & left bronchus .
Surgical pathology
A. Superior laryngeal nerve palsy
Wheather unilateral or bilateral , it is often clinically unrecognized .
In unilateral palsy , the voice not severely affected & compensation occur rapidly , on
examination , there is asymmetrical tilt & shift of the larynx & the affected vocal cord
appear bowed , flabby & long & the arytenoids movement unimpaired .
While in bilateral palsy , the voice is lower & weaken , breathy & lack inflection due to
leakage of air during phonation . On examination the larynx appear symmetrical during
rest & phonation , absence of anterior tilt which make the epiglottis to hang over the
endolarynx & the vocal cords slightly flaccid , bowed , hyperaemic (difficult to see) .
The main causes of it ;
1. Thyroid surgery , to avoid this , ligation of the superior pole vessels immediately
adjacent to the capsule of the upper pole of the gland .
2. Trauma to the neck ; e.g. RTA .
B. Recurrent laryngeal nerve palsy
Vocal cord paralysis either unilateral or bilateral , abductor or adductor , the vocal
cords either in the median position or lateral cadaveric position depending on the
degree & permanency of the denervation & the degree of the associated muscle & joint
atrophy & fibrosis .
No theory describe fully the position of the paralysed vocal cord ;
1. Semon's theory ; proposes that the motor fibers innervating the adductor &
abductor muscles lay in separate bundles in the recurrent nerve & they exhibit
different susceptibility to an advancing lesion (the abductor fibers are more
susceptabile to pressure) , so postcervical surgery , haematoma cause abductor

Lecture notes in
palsy lead to adducted cords , while transected nerve lead to adductor palsy lead
to abducted cords .
2. Wagner & Grossman theory ; implies that the superior laryngeal nerve has an
adductive effect through the cricothyroid muscle , this mean lesion of the
recurrent nerve only keep the cord in the midposition , while if the vagus
paralysed high in the neck then the adductive effect will lost & the cord will be in
the cadavaric position .
In practice , show that this theory is not always correct , since clinically some
patients with intrathoracic lesion give rise to a vocal cord in the lateral position ,
the explanation of this is either ;
a. Streaching of the nerv by the intrathoracic lesion thus pulling the vagus
down from the skull base & injuring the superior laryngeal nerve .
b. Possible retrograde atrophy of the vagus fibers to the nucleus ambigus .
Consequence of vocal cord paralysis
Dual effect ;
- If the laryngeal sphenicter is open , then poor phonation & aspiration is possible .
- Also loss of sensation , undetected aspiration lead to aspration pneumonia .
- The inability to obtain positive subglottic pressure affect the swallowing reflex &
difficulties to cough to clear the lower respiratory tract .
- Because of the longer course of the left recurrent laryngeal nerve , then paralysis more
(4:1) & 15% with bilateral palsy .
- Male most commonly affected ; M:F 8:1 .
Causes of the vocal cord paralysis (recurrent laryngeal nerve palsies)
1. Malignant diseases ; 25% , half of them belong to the Ca. lung , 20% to oesophageal
Ca. , 10% to thyroid Ca. , 20% to nasopharyngeal Ca. & lymphoma .
2. Surgical trauma ; 20% , due to surgery on the the lung , oesophagus , thyroid , heart
, larynx , mediastimum & pharyngeal pouch .
3. Non-surgical trauma ; 15% , Ortner's syndrome (paralysis of the recurrent laryngeal
nerve due to pressure by cardiomegally) & neck trauma (RTA) .
4. Idiopathic ; 15% , influenza & IMN .
5. Neurological causes ; 15% , CVA , Parkinsonism , multiple sclerosis , amyotrophic
lateral sclerosis , DM , alcoholic neuropathy , head injury & Gullian-Barre
syndrome .
6. Inflammatory causes ; 5% , pulmonary T.B. & syphilitic aortitis .
7. Miscellaneous causes ; 5% , Rhuematoid arthritis , Haemolytic anaemia & collagen
diseases .
N.B.: Bilateral vocal cord palsy due to ; (1) Direct blow on the neck (2) Surgery (3)
Traumatic endotracheal intubation (4) Infilteration , by T.B. , sarcoid & amyloid (5)
Parkinson's disease & (6) Amyotrophic lateral sclerosis .
Management
A. Diagnosis
1. History
- Voice quality :
1) Faint whisper ; functional adductor paralysis .
2) Forced whisper ; organic adductor paralysis .
3) Voice which tires with use ; unilateral abductor paralysis .

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4) Stridor & aspiration ; bilateral abductor paralysis .

- Other symptoms ; hoarseness , dysphagia , sorethroat , pain in the ear , cough ,
haemoptysis & neck mass .
- Smoking & occupational history of the patient .
- Past medical history like recent viral infection .
- Past surgeries like thyroidectomy or radical neck dissection ..etc .
2. Examination ;
- Careful examination of the neck & thyroid gland .
- The standard head and neck examination should include careful evaluation of the
larynx . Evaluate the following: (1) Mucosal color and condition (2) Stenosis or
scarring of the posterior glottis (3) Mobility of the arytenoids (4) Muscle mass and
tone of each vocal cord & (5)Length of each vocal cord .
- Laryngoscopy ; fibroptic &/or videolaryngoscopy(stroboscopy) , for the vocal
cords position & the mucosal phonating wave .
The paralysed cord being bowed & atrophic & lies at a lower level than the normal
one with an anterior rotation of the arytenoid .
- EMG , is the only test that provide information on the integrity of the laryngeal
innervation .
3. Investigations
- Haematological ; CBP , ESR , serology , viral study & GTT .
- Radiology ;
1) CT scan with contrast is the investigation of choice (from skull base to the
midthorax) .
2) Plain radiographes ; CXR ,skull base x-ray , soft tissue of the neck ,
nasopharynx (lateral view) .
3) Tomography of the chest , especially for the left lung upper lobe & left hilum .
4) Barium swallow & thyroid scan .
5) Thyroid scan , if there is palbable thyroid mass .
6) Laryngogram , of limited value , paralysis of the cord may give an laryngogram
with : rotated arytenoids , change in the level of the cord & cord atrophy .
- Endoscopy ; panendoscopy with rigid & flexible instruments , biopsy taken from
the fossa of Rosenmuller & tracheal carina even they are look normal , also the
arytenoids must be palpated to differentiate between the palsy & cricoarytenoid
joint fixation .
- Pulmonary function tests: Although diagnosis is based on clinical findings, results
of pulmonary function tests performed with flow volumeloops help support a
diagnosis of upper airway obstruction. Also, they are used to provide an indicator
of the severity of the obstruction and to monitor change after treatment.
- Acoustic analysis: Voice quality usually is not significantly altered. Assessing the
voice with acoustic analysis as a baseline test can be helpful in evaluating recovery
over time.
- Neurologic tests: In certain patients, a neurologist may perform a more thorough
examination to assess central disorders or neuromuscular disorders that may result
in bilateral vocal fold (cord) immobility.
B. Treatment
1. Unilateral Abductor paralysis (voice tires with use)

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Here the vocal cord is fixed in the paramedian position , asymptomatic or slight
symptoms "hoarseness" , with time the hoarseness disappear spontaneously as the
mobile vocal cord compensate .
If the left recurrent laryngeal nerve paralysed , often due to Ca. of the lung & which
mean that the Ca. is inoperable .
Line of treatment ;
(1) Only speech therapy .
(2) Surgical , indicated for ; (a) Voice changes "when distressing professional
voice users" (b) Disorders in protective mechanism "especillay in those with
short life span" .
The surgical modalities are ;
(1) Teflon injection (produce good results) .
(2) Arytenoids rotation .
(3) Recurrent laryngeal nerve reinnervation .
(4) Medialization (laryngoplasty) .
(5) Nerve-muscle pedicle reinnervation .
(6) Combination of the above .
2. Unilateral adductor paralysis
Here the flaccid cord lie in the lateral position lead to weak husky voice (whisper)
with aspiration of food (because the mucosa are insensitive & the sphenictor is
incompetent) . Caused by damage affecting the vagus nerve or both superior &
recurrent laryngeal nerves .
If it is due Ca. lung , use Teflon injection or fat injection (short period because it is
absorbable) . Teflon injection fail to close the posterior part of the glottis between
the arytenoids & always there is air wastage .
The disadvantages of medialization by injection are ;
(3) Cord changes in mass , stiffness & volume .
(4) Hard to estimate amount , distribution .
(5) Irreversible .
(6) Local reaction ; Teflon granuloma & hypersensitivity (30% with ZCl collagen ).
If it is due to cause other than carcinoma , wait for at least 2 months to allow for
compensation or evidence of recovery , speech therapy attempted at this time .
If it is due to laryngeal trauma ; lead to scarring , especially of the thyroarytenoid
muscle , which can't be medialize the vocal cord by Teflon injection , so use collagen
(ZCl collagen injection to augment an atrophic vocal cord by injection superfascially
which soften the scar tissue) .
If the posterior commissure gap more than 2-3 mm , this need combination of the
medialization thyroplasty & arytenoids adduction or reinnervation .
Also thyroplasty still can't resolve the problem of chronic aspiration as it is medialize
the membranous part of the vocal cord leaving a persistent posterior glottic chink (it
is done through external approach) . Advantages are ; (1) LA (2) Reversible "no
tissue reaction" (3) Correct level of implant & (4) Unaffected vocal cord volume &
stiffness .
Arytenoids adduction can manage the posterior glottic chink & as adjunct to
thyroplasty .

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3. Bilateral adductor paralysis

If due to psychogenic disturbances & causing severe dysphonia , then managed by
speech therapy & sometimes psychiatric referral .
If due to organic cause like CNS disease , tumors affecting the medulla , base of the
skull or neck , then lead to aphonia with inability to cough & incoordinated
swallowing , this is lifethreatening & aspiration may lead to aspiration pneumonia .
So the initial management is tracheostomy with cuffed tube & N/G tube for feeding ,
then either need ;
(1) Total Laryngectomy (For protection) .
(2) Teflon injection .
(3) Closure of the glottis by suturing of the vocal cords .
(4) Epiglottis plication .
4. Bilateral abductor paralysis
Usually it is due to bilateral recurrent laryngeal nerve paralysis at thyroidectomy ,
presented with good voice but poor airway , the vocal cords lies in the paramedian
position (1-2 mm) , this lead to stridor , especially if the patient develop a respiratory
infection , so it may need tracheostomy .
If the lesion diagnosed soon after thyroidectomy , then reexplore & find the nerve &
ligate it , otherwise we will wait for 2 months for possible spontaneous recovery .
Any procedure for management will result in good airway with bad voice (except
with tracheal speaking valve we have good voice) .
We must do vocal cord lateralization by ;
(1) laser arytenoidectomy/cordectomy .
(2) Cordopexy with/without arytenoids removal .
(3) Woodman's operation .
(4) Reinnervation .
Phonosurgery
Any surgey designed primarily for the improvement nor restoration of the voice . This term
cover all laryngeal injection techniques , microlaryngeal surgery , laser surgery , laryngeal
framework surgery & laryngeal reinnervation techniques .
Variety of material used for injection ; formly they use paraffin , but its use abandond
because it may cause paraffinoma or embolization . Other materials used for injection ;
cartilage particles , silicon , bone paste , tantalum , oxid powder & teflon (perminant , low
tissue reactivity & lack of carcinogenesis) .
Laryngeal framework surgery 1st described by Payer (1915) who use anteriorly based
rectangular thyroid cartilage flap for vocal cord medialization . At 1952 , Meurman use rib
cartilage implantation lateral to the vocal cord for medialization .
At 1980 Isshiki , use silastic implant for medialization .
A. Vocal cord medialization ; By :
1. Injection
a. Teflon injection
- Transoral laryngoscopic injection
Done under LA or GA , a Brunning –Arnold syringe is charged with collagen or
Teflon , the syringe have a very long needle & it is controlled by a pistole grip

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with a retractor handle , closure of one notch on the handle which lead to
deliver 0.1 ml of collagen paste .
The larynx then exposed by D/L , on the paralysed side the upper surface of the
vocal cord is exposed by retracting the false cord laterally with the end of the
needle , then the needle is pushed into the soft tissue immediately lateral to the
vocal cord & the handle close on notch , the operator waits for several seconds
as the paste extrudes slowly & during this period the vocal cord seen to move
slowly towards the midline .
After that the patient asked to say "ee" , if the mobile vocal cord doesn't
approximate to the paralysed one , another 0.1 ml injected & again the surgeon
wait (the upper limit is threetimes) .
Two important points ;
oWe must know how slowly the paste excruded , so need to close the hand for
several times .
oThe injection must put in the exact site (just lateral to the vocal cord) .
- Transcutaneous injection
The Brunning needle introduced in the midline through the cricothyroid
membrane & angled upwards & laterally into the cord (angled 30o in female &
45o in male) , then enter the vocal cord under endoscopic control or direct
lateral penetration through the thyroid ala .
The success of Teflon injection depends on ;
o Injection in the proper plane .
oThe presence of of adequate glottic soft tissue .
Poor result suspected when there is ;
oPrevious severe laryngeal trauma with extensive scarring .
oThose who had cordectomy for sequamous cell Ca.
oPrevious arytenoidectomy .
After injection , the mass walled by forign body reaction lead to formation of
hard mass (perminantly) , it is removal by Co 2 laser is difficult & preservation
of vocal cords anatomy is impossible .
Cautions during injection ;
o Avoid placing paste in the Rienke's space .
oToo far injection laterally into the floor of ventricle .
oToo deeply in the subglottis .
Complications of injection ;
oMild pain & forign body sensation which subsides within few days &
managed by analgesia .
oInfection (laryngitis)occasionally occur 7-10 days postoperatively &
managed by antibiotics .
oAcute progressive odema which may require tracheostomy , it is respond to
steroids , antibiotics & humidification of air allowing decanulation within
several days .
oLaryngeal obstruction due to too collagen injection superadded by infection
, managed by antibiotics , steroids & humidification & sometimes by
tracheostomy which done if necessary .
b. Collagen injection

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Purified dermal bovin collagen , has too low viscosity & allow to be injected with
fine needle & placed precisely into an atrophid vocal cord . The collagen implant
slowly resorbed & it is replaced to some extent by loose connective tissue .
The material is placed superficially in the plane of vocal ligaments , not that to
the arytenoids muscle , usually the injection done by single injection into the
posterior 1/3rd of the membraneous vocal cord .
The amount of collagen to be injected between 0.2-0.8 ml provided that there is
no serious scarring , the collagen spread forwards as the injection continues .
Sometimes , there may be need for 2 nd or 3rd injection in other points (presence of
extreme scarring) , the collagen soften the scar tissue achieving a good results .
The most important parameters of success of injection are ;
(1) Subsequent quality & strength of voice .
(2) Recently , laryngeal videostroboscopy is a good indication of the success .
(3) Acoustic measures , simple measurement of the increased maximum phonation
time is a clinical test which can indicate improvement after or during an
injection procedure .
c. Steroid injection by the collagen device for management of rheumatoid arthritis ,
granulomatosis & inflammatory lesions .
2. Thyroplasty
Indicated in : (1) Unilateral vocal cord paralysis (2) Vocal cord atrophy & (3)
Sulcus vocalis .
Isshiki's classical type 1 thyroplasty involve displacing the paralysed vocal cord
medially by means of medial displacement of a small rectangular
musculcartilagenous flap of the thyroid cartilage with attached perichondrium &
thyroarytenoid muscle .
The thyroid cartilage is exposed through a small transverse incision & the point
midway between the superior notch & the inferior border is identified & marked . A
horizontal line is then drawn across the ala parallel to its inferior border begin 5-6
mm from midline .
The window measured 5X12 mm in male & 4X10 mm in female , this window should
be not closer to midline & the rectangular window is created in the thyroid cartilage
using a fine perforating burr & completed using a small periosteal elevator .
This procedure is difficult when the cartilage is calcified , but we can freely mobilize
the window , then obtain satisfactory mobilization & gain space for insertion of
silastic plug .
The cartilage is advanced inwards to a distance approximately equal to the thickness
of the thyroid ala & the results monitored by a flexible fibroptic endoscope attached
to a video monitor , the window mobilized & the patient asked to phonate .
Complications : (1) Airway obstruction (2) Extrusion & (3) Late failure .
3. Arytenoid adduction
Done under LA with sedation , it is a procedure of choice when the glottic apertus is
wider (in unilateral adductor paralysis) , by which the arytenoids cartilage rotated
by pulling the muscular process in the direction of the force of the adductor muscle
(difficult technically) , bringing the tip of the vocal process towards the midline .
The incision , the same as in thyroplasty but the skin incsision extended laterally
several centimeters to expose the posterior edge of the thyroid ala , the cricothyroid

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joint is dislocated & the posterior edge of the thyroid ala reflected anteromedially ,
the muscular process reflected anteromedially inferiorly with 3/0 nylon suture , then
fixed to the thyroid ala through two small drilled holes .
The necessary tension on the suture is determined by phonation & monitored by
flexible fibroptic endoscope .
4. Reinnervation
By ansa hypoglossi-recurrent nerve anastamosis .
A collar incision is made from the midline at the level of cricoid cartilage across the
sternomastoid muscle , then retracted laterally & the nerve stimulation is used
around the internal jugular vein , when strong twitching of the strap muscles occur ,
then this means identifying the ansahypglossi nerve , the most inferior branch cut
immediately proximal to its entry into the sternothyroid muscle & anastamose the
distal segment of the recurrent nerve with it .
B. Vocal cord lateralization
1. Laser cordectomy/arytenoidectomy
Co2 laser resection of part of the vocal cord &/or arytenoids with laser on 4-10 watt
superpulse mode .
It is precise & quick to perform , removal of the posterior half of the vocal cord &
the anterior 2/3rd of the arytenoids , the important is short , it is the management of
choice . complications like ; postoperative odema & graniulation tissue formation .
Traditional cordectomy ; removal of wedge of the posterior half of the cord .
2. Cordopexy
By endoscopic laterofixation , better success than Woodman's procedure .
It is done under GA by twom surgeons (ideally) , one working endoscopically & the
other working on the laryngeal framework .
Three centimeters collar incision over the thyroid ala , the point 4 mm anterior & 2
mm below the midpoint of the oblique line identified .
The position of the needle insertion at this point is checked by the endoscopist , it
should be above the tip of the vocal process .
Then a second needle is inserted 5 mm below it , A 0 nylon or prolene is inserted
down the inferior needle & the end retrieved internally by endoscopist who
manipulate it into the lumen of the upper needle .
The suture is then tightened by the external surgeon & knotted , when the endoscopist
is satisfied with the internal configuration , then the skin incision closed in 2 layers .
3. Woodman's operation
Through tracheostomy anaesthesia , the head slightly extended & turned away from
the paralysed side . A horizontal skin crease incision is made at the level of the
cricoid cartilage , then access to the cricothyroid membrane .
Skin flap raised & the sternomastoid retracted , then surgeon cut through the
constrictor muscles on the back of the thyroid cartilage , then rotate the larynx by
finger behind the lamina , then disarticulate the cricothyroid joint .
Then enter the cricoarytenoid joint & disarticulate it , then fixed the vocal process by
3/0 nylon suture , then remove the body of arytenoids . Another 2 stiches done to
lateralize the cord (4-5 mm posterior gap) .
4. Reinnervation
By using the pherenic nerve lead to abducted cords .

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Controversies in management
- How do you know where the cord is ?
In half of cases it is difficult to say exactly where the cord lies , best method , by
videoendoscopy (even hardly) .
In lateral cord paralysis , we can see how far the arytenoids is drapped forward &
howfar the vocal process lie below the glottic line , so it is possible to design the best
rehabilitation measures .
- How does one know whether the arytenois is fixed ?
It is difficult to move any arytenoids when the patient is a sleep , gross degree of fixation
can be identified but can't be said that the arytenoids is fixed or mobile in every case .
- How long should one wait to operate ?
It depends on the cause of the paralysis , 6-12 months for potentially reversible or
selflimiting paresis .
For patients with lung Ca. , do the surgery as soon as possible to emhance voice quality
& improve the cough .
- What can be done when a collagen injection goes wrong ?
Tracheostomy is required if too much collagen has been injected .
In wrong placing , diplophonia arise , so in either case the collagen has been to be
removed , preceeded by tracheostomy , then removed by doing laryngofissure & to enter
the thyroarytenoid muscle , this cause gross scaring & worsen the dysphonia .

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Tumors of the LARYNX

I. Pseudo-tumors
1. Cyst ; the most common site is the vocal cords (55%) , ventricular bands (2.5%) &
epiglottis (20%) , the lining usually sequamous or columnar epithelium .
a. Congenital ; rare , most common in ventricular bands or aryepiglottic fold , may
be diagnosed in the neonatal period as a consequence of breathing difficulties .
They may originate from sequestration of embryonic cells in the saccule or
laryngeal ventricles or arise from the serimucinous glands .
Incision of the cysts may be sufficient or excision can be performed if possible , if
the airway is secured , the intubation may be removed , otherwise it has to be left
in place throw repeated laryngoscopies . However , if the clinical coarse is
prolonged , a tracheostomy is necessary .
b. Acquired
(1) Mucous retention cyst ; sequamous or columnar , both of them originate from
obstructed seromucinous salivary glands .
The sequamous variant is common in the lingual surface of the epiglottis , in
vallecula & on the aryepiglottic fold , minor cysts diagnosed by routine
otolaryngological examination or may reach considerable size before being
diagnosed .
If possible the cyst should be excised completely . Sequamous cyst also present
on the sequamous lined portion of the vocal cords , most commonly on the
undersurface of the anterior part of the cords .
Minor cyst on the vocal cord are filled with clear mucous , while larger cysts
contain yellowish thick fluid , which sometimes includes cholesterol .
The laryngoscopic examination of the vocal cord cyst & polyps may be very
similar & its microscopic examination is that reveal true nature of the lesion .
Larger cysts are easier to diagnosed with their yellow color & localize under
the thin translucent epithelium .
Treatment by excision of the minor one & marsuplization of the large one
(cysts of the ventricular bands may be confused with neoplasms & must be
differentiated from them) .
(2) Subhyoid bursa , enlargement of the normal bursa "inflammatory" .
(3) Cysts resulting from degenerative changes ; as in haematoma or fibroma of
the cord or in polypus (localized oedema of the larynx) .
2. Polyps ; Rienkes' space is a potential space under the epithelium of the vocal cord
separate it from the underlying ligaments & muscles .
It is a thin layer of loose connective accumulation of fluid in this space (vocal fold
oedema) . If accumulation is concentrated at one point & balloon the epithelium out
infront of it , lead to vocal cord polyp . It is the most common laryngeal mass with
unknown aetiology .
It may arise from the area of unresolved infection or it is a response to traumatic
abrasion or haematoma .
The site almost exclusively on the vocal cords from the subepithelial connective
tissue of the Rienkes' layer .
The commonest site is the anterior commissure which is overlooked by epiglottis , so
ask the patient to lower the larynx during mirror examination by yawing & falsetto

Lecture notes in
phonation . Or from the subglottic surface & extend to the glottic area & act as valve
like action & this may lead to stridor .
Causes ;
- Unknown .
- The most common due to phonation with excessive subglottic air preesure with
incomplete closure of cords , cause the mucous membrane of the anterior
commissure to be sucked in & bllooned out .
- After acute laryngitis , especially when the voice is not spared .
- Chronic over use of voice .
- Proffessional speakers when speaking with incomplete closed glottis .
- As organic compensation , an attempt to close chink , so better to advice them to
speak with a clear voice of low intensity & to avoid noisy places & not let the
patient to whisper during inflammation in order to save their cord from damage .
Clinical features ;
- Voice is deeper than usual , high tone & falsetto tones become impossible .
- Usually men .
- I/L show ; oedematous vocal folds , usuallt affect both sides symmetrically , pale ,
swellen , oedematous , usually near the anterior commissure .
- Stroboscopic examination show ; flappy , wave edge & enlarged vertical
component of vibratory pattern .
- Bilateral polyps , means Rienkes' oedema , these polyps are along the whole
length of the cords & it is an oedema of the submucosal space , it is the same seen
in myxoedema .
Treatment ; for biopsy & relieve hoarseness .
- Slight oedema will resolve with time .
- Large colloidal oedema usually take long time to resolve during surgical removal
of the swollen mucosa , healthy epithelium grow over the bare area .
- Voice therapy to control breath flow & ensure sufficient glottic closure
preventing recurrence .
- Vocal cord polyps can be remove by microlaryngeal surgery with punch forceps
(polyp never resolve spontaneously) .
- Spontaneous resolution of the polyps occur at very early stage when epithelial
ruptured & the contents escaped out .
3. Granulomata
a. Specific ; like T.B. or syphilis .
b. Non-specific ; nearly always caused by trauma .
(1) Postoperative ; after laryngeal endoscopy , post-partial laryngectomy , stitch
granuloma , laser , excessive granulation tissue formation during healing
process .
treatment by microlaryngoscopy , especially to rule out recurrence in patient
treatment of malignant disease .
(2) Intubation granuloma , long term intubation with prolonged pulmonary
ventilation , usually occur on the vocal process "posterior commissure" .
It is due to de-epithelization of the cartilage leading to low grade
perichondritis & granuloma formation . Occasionally seen after traumatic
blind intubation , but must commonly after long operation with light

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anaesthesia when the arytenoids & posterior ends of the vocal cords vibrate
against the tube causing abrasion lead to granulation tissue formation .
Granuloma formation depends on ; duration of intubation (not >48-72 hours)
, size & type of the tube & degree of relaxation .
Diagnosis usually within few weeks after extubation .
Clinically presented with ; hoarseness , irritation , pain , & F:M 4:1 .
Treated by microlaryngoscopy with excision , tracheostomy if stridor ,
recurrence may occur . It is very common , but most of these may be coughed
up & the base heal spontaneously .
(3) Contact granuloma ; nearly always unilateral , localized granuloma at the
medial or superior surface of the vocal process of the arytenoids , often
confused with contact ulcers .
It is typical polypoid appearance which is local reaction to trauma ,
granulation tissue develop if the perichondrium is damaged wither by trauma
or endotracheal tube .
Presented as slight hoaseness , diagnosed by I/L which show small lesion
(sometimes large) partially obstruct rge laryngeal lumen , mostly restricted to
one side & usually attached to the superior edge . It can be pedunculated ,
move up & down between the cords with red color & sometimes stained with
dark area (haematoma) .
Treated by simple removal by microlaryngoscopy , the local recurrence is
common , also could be treated by laser or wait & see policy (conservative) .
(4) Contact ulcer ; it is saucer shaped lesion in the medial edges of the vocal
cords , exactly on the vocal process with no epithelial defect & granuloma
formation often occupies ulcer crater on one side .
Its aetiology multifactorial ; nearly always male > 30 years old , with
emotional stress , vocal abuse (most important cause) & other causes like
hiatus hernia , gastroesophegeal reflux .
Presented with low pitch quality of voice (vocal fatigue) , irritation & pain in
the larynx with cough to clear the throat .
It is difficult to know whether oesophageal dysfunction is an aetiology or
concomitant factor for contact granuloma .
Treated by ; biopsy taken to exclude malignancy , voice rest , surgery for
excessive granulom a(take with it part of the vocal process of the arytenoid)
& antireflux measures .
(5) Granuloma gravidarum ; during pregnancy , leave it to resolve spontaneously
after pregnancy .
(6) Pyogenic granulomas .
4. Amyloidosis ; 1% of all benign tumors of the larynx , unknown aetiology ,
characterized by extracellular deposition of protienaceous substance , it has two
types ; (a) Generalized ; Primary "rare in the larynx" , type B & Secondary , type B
& (b) Localized . Male > female , between 40-60 years old .
The amyloid is an eosinophilic hyaline material with a strong affinity to certain dyes
such as congo red .
Mostly deposit at the flse cords , aryepiglottic folds & subglottic , the types of
amyloidosis in the larynx are ;

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(1) Tumor like .

(2) Displaying diffuse infiltration .
Symptoms depends on the site ;
- Vocal cords ; hoarseness .
- Subglottis ; increased inspiratory problems .
- Supraglottic ; uncharacteristic & diffuse symptoms .
Must be differentiated from ; hayalinized myxomatous polyps , benign & malignant
tumors , retention cysts & laryngocele , & plasmacytoma with amyloid deposit .
Diagnosis done by biopsy from the lesion & biopsy from the rectal mucosa to exclude
generalized form .
Treated (amyloidosis of the larynx) by ; excision of the localized disease , if diffuse ,
then repeated excision , laryngofissure may indicated , also Co2 should not be
overlooked . Also immunosuppressive therapy & cytotoxics (Amyloid of Ig origin) .
II. Benign tumors
1. Ectodermal
a. Papilloma ; of 2 types ;
(1) Juvenile ; which is multiple & usually regress after puberty & recurrent in
nature , 40% associated with genital papillomas in the mother .
More in female . Mainly found on the true & flase vocal folds (anterior
commissure) , sometimes extend to epiglottis, trachea , subglottis & bronchi .
It though to be due to abnormal response to virus , there is no inclusion
bodies under light microscopy .
Caused by Human papillomas virus (small DNA virus) type 6 & 11 ,
malignant transformation rarely occur unless radiotherapy is used .
(2) Adult ; usually single & not regress , rarely recur after removal , 5-10% show
malignant changes , more in male .
There is no histological difference between the two types .
b. Adenoma ; tumor of the seromucinous gland of the larynx , causing obstructive
symptoms , it must be differentiated from any expansile , smooth mass with
overlying mucosa such as ; retention cyst , internal laryngocele , angioma , &
adenoid cystic carcinoma .
Treated by surgery & the approach depend on the size & site of the tumor .
c. Neurogenic tumor ; neurolemmoma , benign tumor arising from the Schwan cells
of the axon sheath , well encapsulated , slowly growing , may reach large size .
Treatment by surgery which depend on the size & site of the tumor ; e.g. small
tumor endoscopically , while large tumor either by laryngofissure or lateral
laryngectomy .
d. Paraganglioma ; both sexes affected equally , common in the 6th decade , usually
in the supraglottic area with no symptoms until reach an advanced stage .
Diagnosis by MRI & CT scan to assess the extent , if arise from the inferior
paragangilion , then thyroid like tumor .
Histopathology ; typical zellaballen pattern on light microscope demonstrated by
reticulin staining , presence of argyrophilic granules (on Grimelius stain) .
It should be differentiated from ; haemingioperucytoma , carcinoid tumor ,
granular cell tumor , salivary gland tumor , haemangioma & thyroid carcinoma .

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High percentage of laryngeal paragangliomas have malignant behaviour with

regional & distant metastasis . Treated by conservative surgery .
2. Mesodermal
a. Vascular ; arise from the blood vessel or lymph vessel .
(1) Haeamangioma ; in adult supraglottis , rare . It occur as a telangectatic
vocal cords polyp filled with thin walled blood vessel , must be differentiated
from pyogenic granuloma (which often located at the posterior part of the
cord & related to previous intubation) .
(2) Lympahngioma .
b. Chondromata ; presented between 40-70 years age , M:F about 4:1 , the site of
origin mostly the cricoid cartilage (70%) at the posterior plate .
Presented with non-specific hoarseness & dyspneoa , their degree depends on the
site & size of the tumor . The tumor arising from the cricoid cartilage extend to
subglottic causing progressive inspiratory stridor , if the vocal cord mobility
impaired it will lead to hoarseness , if extend posteriorly to the hypopharynx will
cause dysphagia , while see external swelling if the tumor in the cricoid ring or
thyroid cartilage . I/L show mass covered by intact mucosa .x-ray show coarse
irregular calcification is the rule (pathognomic) , found in 75% of cases .
The tumor is so hard , so the biopsy is difficult , also it is difficult to differentiate
it from highly differentiated chondrosarcoma . Treated by conservative surgery
to both chondroma & sarcoma , because they are slow growing & low incidence
of metastasis . Also radiotherapy has a little value in treatment .
c. Myogenic tumors
(1) Lieomyoma ; one of the most common benign tumors in human being , most
common in the supraglottic region , varies in size from pea to pigeon egg .
Treated by removal by laryngoscopy or external approach .
(2) Rhabdomyoma ; mostly originate in the vocal cords , appears as polypoidal
mass , may extend above or below the cord , the adult type appears as vocal
cord polyp (fetal after birth) , treated by microlaryngoscopy .
(3) Granular cell tumor (Myoblastic myoma) ; occur in the vocal cord ,
Histologically show profuse pseudoepitheiomatous hyperplasia , treated by
endoscopical removal .
d. Fibromata ; could be soft pedunculated to round firm , smooth & sessile , treated
by microlaryngoscopy .
e. Lipomata ; found in the flase cords & hypopharynx (extends to the larynx) , it is
encapsulated , light color & lobulated . Treated by endoscopic removal or
external approach , depending on the size & location .
III. Malignant tumors
1. Ectodermal
a. Sequamous cell carcinoma . b. Anaplastic carcinoma .
c. Carcinosarcoma . d. Verrucus carcinoma .
e. Adenocarcinoma . f. Adenoid cystic carcinoma .
g. Mucoepidermoid carcinoma .
2. Mesodermal
a. Chondrosarcoma . b. Non-Hodgken's lymphoma
c. Melanoma . d. Fibrosarcoma .

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Carcinoma of the LARYNX

Anatomy
The larynx is located at the very top of the trachea and functions not only to produce voice,
but also to divide and protect the respiratory from the digestive tracts. It acts as a sphincter
during deglutition, protecting against the penetration of bypassing food by closing off the
trachea at two sites: the epiglottic flap and the closure
of the vocal cords. The larynx consists of a framework
of cartilages connected by ligaments, membranes, and
muscles covered by a respiratory and stratified
squamous mucosal epithelium .
Spraglottis, the glottis, and the subglottis.
The supraglottic larynx extends from the tip of the
epiglottis and vallecula superiorly to the ventricle and
undersurface of the "false" cords inferiorly; it includes
the arytenoid cartilages, the aryepiglottic folds, the
false vocal cords, and the epiglottis. The glottic larynx
encompasses the "true" vocal cords, extending from
the ventricle between the true and false cords to 0.5
cm below the free edge of the true cords, including the
anterior commissure and interarytenoid area. The
subglottic larynx extends from the inferior extent of the
glottis to the inferior edge of the cricoid cartilage.
Understanding the embryologic origin of these regions
of the larynx helps to explain the difference in clinical
behavior between cancers arising from these laryngeal subsites. The supraglottis derives
from the midline buccapharyngeal primordium and branchial arches 3 and 4 with rich,
bilateral lymphatics. The glottis, on the other hand, forms from the midline fusion of lateral
structures derived from the tracheobronchial primordium and arches 4, 5, and 6.
There is a paucity of lymphatics and, in comparison to supraglottic primary neoplasms,
malignant glottic growths have less of a tendency for
bilateral regional lymphatic spread and remain
confined to the glottis for longer periods of time.
Fibroelastic membranes and ligaments further divide
the larynx into the preepiglottic ( fibrofatty filled
space bounded ; superiorly : hyoepiglottic lig. ,
posteriorly : epiglottis , anteriorly :thyrohyoid lig. ,
Apex : inferior limit by the attachment of epiglottis to
the thyroid cartilage through thyroepiglottic lig.) and
paraglottic spaces ( potential space lies laterally to
the true & false cords filled by fibrofatty tissues &
bounded ; superiorly : vallecula & aryepiglottic fold ,
medially : vestibular fold , quadringular membrane & conus elasticus , laterally :mucosa of
the medial wall of the pyriform fossa posteriorly & thyroid cartilage anteriorly ,
inferiolaterally ; cricothyroid lig. ).
These structures, including the conus elasticus, the quadrangular and thyrohyoid
membranes, and the hyoepiglottic ligament, act as barriers to spread of tumor . The thyroid

Lecture notes in
and cricoid cartilages and their perichondrium are further barriers to tumor spread. The
anterior commissure tendon and thyroepiglottic ligaments are not effective barriers to
tumor spread, and tumors involving the anterior commissure are more likely to have direct
regional spread.
The muscles of the larynx are divided into intrinsic and extrinsic groups. The intrinsic
muscles are those of the vocal cords and cartilages contained within the larynx itself. The
extrinsic muscles, the strap muscles and constrictors, help with laryngeal elevation and
pharyngeal constriction. Innervation of the intrinsic muscles is from the recurrent laryngeal
branches of the vagus nerve on both sides. Arterial blood supply is off the external carotid
artery and off the thyrocervical trunk via the superior and inferior thyroid arteries. Venous
drainage is into the internal jugular vein. Lymphatic drainage is to levels II, III, and IV, as
well as sometimes to level VI of the neck.
Rienke's space ; lies beneath the laryngeal mucosa ( superficial to the vocal lig.) .
Incidence & Epidemiology ;
- Each year, 11,000 new cases of larynx cancer will be diagnosed in the United States
(1% of new cancer diagnoses) and approximately one-third of these patients will die
of their disease.
- incidence in the UK 4/100000 (Brazil >10/100000 , Japan 2/100000) , 90% in men
(3-4:1) , more common in the people lived in the cities than in rural areas , at the
present time & for no fully explained reason the incidence increased in women &
earlier years of live .
- Ca. Of larynx is the most common primary head & neck in men (excluding skin
malignancy) , Sequamous cell Ca. represent the fast majority of the laryngeal Ca.
(85%) , other forms are ; undifferintiated Ca. (5%) , verrucous Ca. (3%) ,
carcinoma in situ (3%), Adenocarcinoma (0.5%), Sarcoma (2%) , & miscellaneous
(1.5% ; adenocystic , spindle cell , ...etc.) , this incidence increased with age but the
peak for it is the 7th decade age (60-62 yrs) .
- Malignant disorders of the glottic larynx outnumber those of the supraglottis 1.5:1.0
(This ratio does not hold worldwide) , Malignant disorders arising in the subglottis
are universally rare
- The risk factors ; geographycal , social class V , urban , alchol & radiation .
Aetiology ;
the cause is unknown , but smoking ( smooker had 20 time risk than non-smooker) &
alchol are predisposing to the disease , also exposure to asbestos , therapuetic radiation
& formaldyhide , also genetic predisposition & premalignant condition (e.g.
leukoplakia).
Pathogenesis ;
- More than 90% of patients with larynx cancer have a history of heavy tobacco and
alcohol use , The combination of smoking and alcohol use has a more than additive
carcinogenic effect on the larynx.
- Laryngeal infection with the human papilloma virus (HPV) results in laryngeal
papillomatosis, which is usually benign, but subtypes 16 and 18 are known to
degenerate into SCC .
- Gastroesophageal reflux can lead to larynx cancer.

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- Various occupational exposures and toxic inhalations (such as asbestos and mustard
gas), nutritional deficiencies, and previous neck irradiation have all been linked to
larynx cancer as well.
- Genes and gene products being investigated for their link to larynx cancer include
p53, the Bcl-2 family of genes and other markers of apoptosis, proliferating cell
nuclear antigen (PCNA), Ki67, cyclin D1, the ras gene and other oncogenes, tumor
suppressor genes, and the loss of heterozygosity and changes in the DNA content of
tumors.
- Many studies address the protective effect of retinoids, -carotene, and other
antioxidants against the development of larynx cancer. A reversal of laryngeal
leukoplakia after treatment with retinyl-palmitate has been demonstrated.
Histological types ;
Squamous Cell Carcinoma ; represents > 90% of larynx cancers and is linked to tobacco
and excessive alcohol use. Histologically, the carcinogenesis of SCC is viewed as a
continuum of change from normal phenotype, to hyperplasia, to dysplasia, to carcinoma in
situ, to invasive carcinoma. Invasive SCC can be well, moderately, or poorly differentiated
and is characterized by nests of malignant epithelial cells in a surrounding desmoplastic,
inflammatory stroma , Varying degrees of mitoses and necrosis are seen. Keratin pearls are
a pathognomonic feature seen in well- and moderately differentiated SCC. SCC can invade
blood and lymphatic vessels as well as nerves. Immunohistochemical staining is positive for
keratin proteins , Variants of SCC include verrucous carcinoma, spindle cell carcinoma,
basaloid squamous cell carcinoma, and adenosquamous carcinoma .
Verrucous Carcinoma ; 1% of the laryngeal Ca. ,72% at the glottis & the rest in the
supraglottis , not aggressive , viral DNA detected in 85% (Herpes v. Infection) , usually
presented as hoarseness , s.t. misDx as benign , but, rarely have LN metastasis , slow
growing & locally invasive .
Endoscopy shows it as fungating , papilomatous , shaggy greyish-white & has warty
papilary surface , histologically ; well differentiated keratinizing sequanous epithelium .
Infilteration is on abroad base with pushing margins against the stroma.
Rx of small tumor by endoscopic resection , partial laryngectomy , or radical laryngectomy
, large tumors with airway obstruction treated by radical surgery , Radiotherapy if used will
cause anaplastic changes in the lesion which lead to more aggressiveness .
Adenosquamous carcinoma ; is a high-grade malignant neoplasm with features of both SCC
with epithelial differentiation and adenocarcinoma with glandular differentiation.
Kaposi Sarcoma ; Previously rare in Europe & America , recently more common due to
increase the HIV infection , presented as skin lesion & later involving the larynx .
Sequamous intraepithelial neoplasia ; keratosis , para keratosis , dyskeratosis , dysplasia ,
carcinoma in situ (cells of malignant cytology but confined to the surface & not invade the
basement memberane .
Other tumors ; that can occur in the larynx include neuroendocrine tumors such as
carcinoid tumors, lymphoma, and metastases from other primary sites. Malignant tumors of
the thyroid can invade into the larynx with or without vocal cord paralysis.
Epithelial lesions ; leucoplakia , erythroleucoplakia , hyperkeratosis , modern terminology ;
1. Grade I ; Seq. Cell hyperplasia with mild dysplasia & keratosis ( benign but
premalignant) .
2. Grade II ; keratosis with dysplasia with/without nueclear atypia .

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3. Grade III ; Seq. Cell hyperplasia or Ca. in situ (course abnormality to

diffirentiation & nueclear atypia in almost all areas & epithelium with basal cell
proliferation & mitosis) .
Micro carcinoma ; the maximal size 10X10X3 mm .
Microinvasive carcinoma ; has not yet infilterate the submucosa of the vocal cords .
- Carcinoma in situ in the vocal cords : three clinical types ;
1. white patch on the vocal cords ; examine , remove , stop smoking & then review , if
recurrence then do vocal cord stripping or laser vaporization (repeated) .
2. wide spread , white –grey changes in the laryngeal epithelium .
3. wide spread white-grey & reddish ting(erythroleucoplakia) , has worse prognosis
than T1, treated aggressively with external radiotherapy .
Staging ;
Cancers of the larynx are staged according to the TNM (tumor, node, metastasis) system of
the American Joint Committee on Cancer , for staging purposes, positive neck nodes are
considered locoregional metastases; metastases to other parts of the body (such as lung,
mediastinum, liver, and bone) are considered distant.
- Tumor size (T)
Supraglottic tumor
Tis Carcinoma in situ
T1 Tumor confined to one sub-site with normal v.c. mobility .
T2 Tumor involving > 1 subsite of supraglottis or glottis with impaired v.c. mobility .
T3 Tumor limited to the larynx with v.c. fixation ; tumor may invade postcricoid area ,
medial pyriform sinus , or pre –epiglottic space .
T4 Massive tumor invading beyond thyroid caltilage &/or with extralaryngeal spread .
Glottic tumor
T1 Tumor confined to v.c. with normal mobility .
T1A Tumor confined to one v.c. .
T1B Tumor confined to both v.c.
T2 Tumor extend to the supraglottis &/or sub glottis with/without impaired v.c. mobility .
T3 Tumor limited to the larynx with v.c. fixation .
Subglottic tumor
T1 Tumor confined to the subglottis .
T2 Tumor extend to the v.c. with/without impaired v.c. mobility .
T3 Tumor limited to the larynx with v.c. fixation .
N.B : T4 tumors are divided into resectable (T4a) and unresectable (T4b) tumors.
- Nodal involvement (N)
Nx Minimum requirement to assess regional nodes cannot be met
N0 No clinically positive node
N1 Single clinically positive homolateral node 3 cm or less in diameter
N2 Single clinically positive homolateral node more than 3 cm but not more than 6
cm in diameter or many clinically positive homolateral nodes, none more than
6 cm in diameter

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N2a Single clinically positive homolateral node more than 3 cm but not more than 6
cm in diameter
N2b Multiple clinically positive homolateral nodes, none more than 6 cm in
diameter
N3 Massive homolateral node(s), bilateral nodes, or contralateral node(s)
N3a Clinically positive homolateral node(s), one more than 6 cm in diameter
N3b Bilateral clinically positive nodes (in this situation, each side of the neck
should be staged separately; i.e., N3b; right, N2a; left, N1)
N3c Contralateral clinically positive node(s) only.
- Distant metastasis (M)
Uncommon for patients of laryngeal Ca. to presented with distant metastasis as the main
symptom , the incidence for this is about 5% , 44% of glottic & subglottic ca has distant
metastasis , N stage has a greater influence in the distant metastasis than T stage , the most
common site for this is lung & bones .
Mx Minimum requirements to assess presence of distant metastasis cannot be met
M0 No known metastasis
M1 Distant metastasis present
Stage grouping
Stage O T0 N0 M0
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T1 N1 M0
T2 N1 M0
T3 N0,N1 M0
Stage IV A T4 N0,N1 M0
Any T N2 M0
B Any T N2 M0
C Any T Any N M1
Prognostic factors ;
1. Histologic characteristics of the tumor, such as extracapsular spread in nodal
metastases, angiolymphatic invasion, perineural spread, and a high histologic grade
2. Various chromosomal and molecular markers, such as p53 mutations, Ki67 or PCNA
overexpression, DNA content, and loss of heterozygosity .
3. Presence of patient comorbidities.
4. Site ; glottic tumor better Px .
5. N & M stage ; inversly related .
6. Biological Px factors ; aneuploid tumor worse Px .
7. Tissue eosinophilia ; good Px .
8. Radiotherapy ; adverse effect ; mass recurrence of the tumor , affect patren of spread
, affect healing follows surgery .
Clinical Findings;
1. History ( sign & synptoms) ;
a. proggressive contineous hoarseness(common) .
b. dyspnoea & stridor (less common) , supraglottis ; presenting feature , glottis &
subglottis ; dysphonia (proggressive neglected) .

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c. pain (throat or ear) ; late symptom , typically of supraglottic & transglottic ,

radiate to the ear (means extension of the disease & invasion of the cartilage) .
d. dysphagia ; rare , may be the presenting feature of transglottic ca due to
extension to the medial wall of the pyriform fossa , through paraglottic space
(marginal lesion)
e. neck swelling ; LN , thyroid involvement or thyroid cartilage invasion .
f. cough , irritation , haemoptysis , aspiration & later foeter , cachexia or anorexia .
g. A significant weight loss often accompanies the diagnosis of an advanced larynx
cancer because of swallowing difficulties.
2. Physical examination ;
a. General exam. ; for the chest , abdomen ...etc .
b. Complete head and neck examination is performed, focusing on the larynx and
the neck ; indirect laryngoscopy , nasopharyngoscopy ; Malignant laryngeal
lesions can appear to be fungating, friable, nodular, or ulcerative, v.c. thickening ,
nodule , warty lesion , hyperkeratosis ...etc or simply as changes in mucosal color,
also assess the v.c. mobility
c. The quality of the voice is noted. A breathy voice may indicate a vocal cord
paralysis; an irregular voice, a glottic lesion; and a muffled voice, a supraglottic
lesion.
d. Videostrobolaryngoscopy ; parameters are ; fundamental frequency , bilateral
symmetery , periodicity of successive vibration , glottal closure , ampilitude of
vibration , mucosal wave , & non vibratory portion .
Some areas are difficult to be examined like ; subglottis (examined by flexible scope
under LA by injecting 2-3 ml of xylocaine through the cricothyroid memberane in the
midline & cough then vaporize the anaesthetic after 5 min) , posterior surface of the
epiglottis , laryngeal ventricle (can be examined under GA by rigid laryngoscopy) .
e. The neck is examined by careful palpation, feeling for enlarged lymph nodes and
noting the location, size, firmness, and mobility of these nodes. Restricted laryngeal
crepitus (the "clicking" movement from side to side across the pharynx and
prevertebral fascia) can reveal postcricoid or even retropharyngeal invasion , and
also for visceral mobility , tracheal mobility, thyroid cartilage thickening ...etc .
f. Nutritional status should also be assessed and supplementation discussed .
3. Endoscopy & Biopsy ; Biopsy of a laryngeal lesion is necessary to establish the
diagnosis of a malignant disorder. Biopsy of the larynx is best accomplished in the
operating room with the patient under general anesthesia and paralyzed. Direct
laryngoscopy is performed , With the patient anesthetized and paralyzed, an even
better neck examination is obtained. Esophagoscopy and bronchoscopy can also be
performed at this setting as part of a cancer staging workup , for patients who cannot
tolerate a general anesthetic, the biopsy of laryngeal lesions can be performed as an
office procedure. Under fiberoptic guidance, with generous topical anesthesia
(typically using lidocaine or Cetacaine), a flexible biopsy forceps passed through the
fiberoptic scope is used.
a. endoscopy for supraglottic tumor ; size , site , extent (vallecula , preepiglottic space ,
tongue base , lateral pharyngeal wall , medial wall of the pyriform fossae...etc) , v.c.
mobility , para glottic space involvement , check the hypopharynx , take biopsy .

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b. endoscopy for glottic tumor ;Hopkin's rods with a 30o angle-viewing telescope , ant.
commissure laryngoscope , assess the size , site , extent (to the ant. commissure ,
posteriorly to the vocal process , may be exophytic , infilterative ..etc) , check the
ventricles , paraglottic space , hypopharynx & take biopsy .
c. endoscopy for subglottic tumor ; paediatric laryngoscope or Hopkin's rods can be
used , assess v.c. mobility , assess the size , site , extent (paraglottic , post. tracheal
wall , cervical oesophageus ) & take biopsy( when take it take care to not crush the
spiecemen) .
In the future microlaryngoscopy & contrast videoendoscopy using methyle-blue dye .
4. Investigations ;FBC , Blood biochemistry (urea , creatinine , electrolyte ...etc) , LFT
...etc .
5. Radiology ;
a. CXR ; important in the screening for metastitic lesions ( the 1st site for it is the
lungs, then liver , then bone) , This test should be repeated once or twice yearly ,
If there are any abnormalities noted on the chest x-ray, a CT scan of the chest
should be performed .
b. Ultrasound of the neck ; used to identify cervical metastases and even to
characterize laryngeal abnormalities .
c. CT scan & MRI , ; to assess the size & extent of the lesion , it is important to aid
with staging and treatment planning for clinically advanced larynx cancers , also
useful in identifying preepiglottic or paraglottic space invasion, laryngeal
cartilage erosion, and cervical nodal metastases, it sometimes recommended to
obtain neck imaging in early-stage supraglottic cancer due to the risk of occult
nodes is high , and If there is any suspicion of impaired vocal cord mobility.
d. Positive emission tomography (PET) scanning uses fluorescence-tagged glucose
and the increased metabolic rate of malignant tissues to identify cancers.
Application of PET in the head and neck has focused on (1) identifying occult
nodal metastases, (2) distinguishing the recurrence of malignant growth from
radionecrosis and other sequelae of prior treatment, and (3) identifying the
location of an unknown primary cancer.
Definitive tissue diagnosis must be obtained prior to starting treatment for a laryngeal
cancer because lesions that appear malignant may be benign.
These benign conditions include infectious, inflammatory, and granulomatous diseases
such as tuberculosis, sarcoidosis, blastomycosis, papillomatosis, and granular cell tumors.
Supraglotic Carcinoma
40% of Ca. larynx in UK , 30% north America , the most common , occur in the center of
the infrahyoid epiglottis , 90% invade the epiglottic fenestra in the calrtilage , 50% invade
the thyroid cartilage & 50% the preepiglottic space , 5% invade the floor of the ventricle &
vocal cords .
lateral supraglottic (ventricular bands , invade the paraglottic space & spread
superficially) , extend cranially to the valeculae & the tongue base , extend posteriorly to
the arytenoids .
invasion of the preepiglottic space is a prominant feature esp. After the involvement of the
posterior laryngeal surface of the epiglottis then through the fenestra .

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Glottic Carcinoma
The most frequent site for Ca & for hyperkeratosis & leucoplakia (in north America 60% of
laryngeal neoplasm are glottic & 50% in the UK).
In the glottis either localozed small tumor (restricted to the glottis) or involve large part of
the larynx (transglottic).
Glottic cancers are slowly growing , well differentiated & extend in predictable way to
Rienke's space , superficially (10% to supraglottis & subglottis) , through the ant.
Commisure to the opposite v.c. ,subglottis or ant. Supraglottis , & invasion may involve
thyroartenoid memberane .
Deep spread of the glottic Ca. is to ; post. Cricoartynoid m. & laterally to the artynoid
cartilage .
The causes of v.c. fixation ; (1) involvement of the thyroartenoid m. (2) involvement of the
cricoartynoid joint , cricoid cartilage , artenoid or combination of this & (3) perineuronal
invasion .
The lymphatic spread fortunatly rare due to the limited lymphatic drainage of the area .
The transglottic tumor may came from ; ventricles via the paraglottic space , 50% involve
the ipsilateral lobe of the thyroid gland , strap m. , pharyngeal mucosa ( LN in transglottic
tumor ; N0 70% , N1 20% , N2,N3 7%) .
Subglottic Carcinoma
Uncommon (5%) , unilateral , ulcerated or fungating , silent & poorly differintiated &
extend through the cricothyroid memberane , conus elasticus & cricoid cartilage to involve
the paratracheal & cervical lymphatics in a large number of the cases .
The tumor arise primarly in the subglottis or it arise on or under the v.c. & extend into the
subglottis .
True subglottic Ca. can cause stridor & v.c. Fixation in 30% of cases , with 20% LN
metastasis .
Stomal recurrence
Incidence after total laryngectomy about 5-15% .
Causes are ;
1. Inadequate removal with positive margins .
2. Residualt disease in the paratracheal LN .
3. Subglottic extention of the Ca.
4. Tracheostomy performed close to the tumor prior to resection .
Patient with N0 : 3% develop stomal reccurence , N1 : 8% , N2: 33% , the risk of stomal
reccurence after emergency tracheostomy 8-26% , but this risk decreased if suspect
laryngectomy within 48 hours . Classification "Sisson classification ;
- Type I ; discrete nodule at the superior aspect of the stoma (good prognosis) .
- Type II ; involvement of the oesophagus (posterior) but without inferior extension (fair
to good prognosis) . In type I & II radical surgery justified in carefully selected cases .
- Type III ; originate at the inferior aspect of the stoma & usually has direct extension to
the mediastinum (no benefit of surgery) .
- Type IV ; lateral extension & usually under either side of clavicle (no benefit of surgery)
The 5 years survival are ; 24% for type I & II , while 9% for type III & IV . They
accompanied by miserable life .
Surgery is the only viable option which they should be medically fit for surgery , with
negative metstasis & the local extension of the disease should be evaluated by CT & MRI .

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Carcinoma of the LARYNX Treatment OPTIONS

More then 95% of the laryngeal tumor are treatable , the remaineder which are untreatable
could be due to ; distant metastasis (<1%), extremely poor general health & rarely the
refusal by the patient , the over all 5 years survival rate about 55 – 60% in UK .
General considerations
- In many centers in the UK is to Rx by radiotherapy for all tumors then the recurrence
Rx by total laryngectomy .
- while in Europe & North America use conservative surgery followed by partial or
total laryngectomies for recurrence .
- In UK T1-T3 N0 of glottic & supraglottic Rx by radiotherapy .
- In UK T4 N0 there are contraversy in Rx (organ preservation with/without postop.
radiotherapy) .
- The choice of Rx modality should be made according to ; likely modality to control
the disease , general health of the patient & the relative consequence of the Rx .
- Early-stage larynx cancer (Stages I and II) can be treated with either surgery or
radiation in single-modality therapy.
- Advanced-stage larynx cancer (Stages III and IV) is treated with dual modality
therapy, traditionally surgery and radiation.
- The advantages of surgery compared to radiation are a shorter treatment period
(compared with 6–7 weeks for radiation) .
- In addition to the risks inherent in any surgical procedure, surgery results in a
poorer voice quality and, for external surgical approaches, a worse cosmetic
outcome.
- The advantages of radiation are better voice quality and the avoidance of surgical
risks.
Treatment modalities
A. No Treatment ; for those with extremely advanced disease (pain free) , or with
another intercurrent chronic disease which will kill the patient .
B. Radiotherapy
- Radiation given as the primary treatment for larynx cancer or as an adjuvant
treatment following surgery .
- done using an external-beam technique; a dose of 6000–7000 cGy is administered to
the tumor site(s).
- If the risk of locoregional nodal metastasis in a clinically negative neck exceeds 20–
30%, 5000 cGy is delivered prophylactically to the neck as well.
- The indications for adjuvant postoperative radiation include ; (1) advanced-stage
disease (T4) , (2) microscopically positive margins, (3) an extracapsular spread of
tumor in a lymph node, (4) the perineural or angiolymphatic spread of tumor, (5) the
subglottic extension of tumor, (6) T3 supraglottic Ca. Rxed by supraglootic
laryngectomy , and (7) the involvement of nodes in multiple neck levels (in
particular, levels IV or V, or the mediastinum).
- Newer protocols using hyperfractionation, such as twice-daily administration of
radiation, have shown some promise in limiting side effects while achieving cure
rates equal to those of traditional once-daily fractions.
- Prior to undergoing radiation, patients should have a thorough dental examination.
When the field will encompass the oral cavity, carious teeth are extracted prior to

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starting radiation due to the radiation-induced increased risk of further dental decay
and osteoradionecrosis.
- The short-term side effects of radiation, lasting up to 6 weeks after the conclusion of
therapy, include mucositis, odynophagia, dysphagia, skin breakdown, a loss of taste,
and edema.
- The long-term side effects include xerostomia, fibrosis, edema, impaired taste,
chondroradionecrosis and osteoradionecrosis, hypothyroidism, and an increased
risk for radiation-induced sarcoma.
- Radiation necrosis of 2 types ; 1st ; pain in the larynx with odema for 3 months after
the DXT ( Rx ; admition , antibiotics , steroid , Rx the airway rarely tracheostomy) ,
2 nd ; when there is ulceration of the mucosa , foeter , difficult to distinguish from
recurrence (Rx by antibiotics , steroid , if not ; total laryngectomy).
C. Surgery
- Many types of operation are included
1. Microendoscopic or LASER surgical removal .
2. Vertical partial resection
(a) cordectomy .
(b) hemilaryngectomy (frontal , lateral & fronto-lateral).
3. Horzinontal partial resection
(a) epiglottectomy .
(b) supraglottic laryngectomy .
4. Near-Total laryngectomy.
(a) supracricoid partial laryngectomy.
(b) Vertical subtotal laryngectomy.
5. Total resection
(a) Total laryngectomy.
(b) Extended Total laryngectomy.
- Mangement by surgery can be done in ;
1. Doubtfull malignancy ( keratosis , ca. in situ in glottis & supra glottis by
microscopical removal with the help of LASER .
2. Small tumors of the marginal zones ( supraglottic epiglottis , aryepiglottic fold &
s.t. false cords) Rx as (1) .
3. Supraglottic tumors esp. Those arising from the false cords & the base of the
epiglottis , Rx by horizontal partial laryngectomy .
4. Large T3 & T4 Rx by total laryngectomy.
5. T3 glottic cancer Rx by Radiation & salvage surgery .
6. For secondary LN we use surgery primarily which is more appropriate .
7. Other less common forms of cancer (AdenoCa. , Verrocus Ca. , ..etc) Rx by
laryngectomy .
8. Recurrence after Radiotherapy treated by laryngectomy .
9. Radical neck dissection on one or both sides may used with any procedure ,
partial or total thyroidectomy may be obligatory in the major resection .
- Complication of surgery in general are ;
1.pharyngocutaneous fistula ; develope at 4-10 days postop. with collection under
the skin , Rxed by frequent dressing with good nutrition , antibiotics & most of them
closed spontaneously after days or weeks , It can be prevented by good technique ,

Lecture notes in
antisepsis , good haemostasis & well preparation of the patient , large fistulae need
repair by full thickness flap.
2. haemorrhage & wound infection .
3. stenosis of the tracheostome .
4. stenosis of the pharynx ; Rx by repeated dilatation under GA by boughues or
baloon , s.t. need use of flaps for augmentation of the pharynx .
5. recurrence within the pharynx ; Rx by neopharyngectomy & free jujenal transfer .
6. stomal recurrence ; which is due to (1) implantation into the tract of the
preoperative tracheostomy (2)inadequate excision of the tumor (3)tumor in the
paratracheal LN & (4)second tumor in the cervical trachea .
If the recurrence at the anterior part of the stoma , then the iceberg wrapped around
the great blood vesseles in the mediastinum & therefore untreatable , but , if the
recurrence at the upper posterior part of the stoma we do tracheostomal resection .
7. pulmonary & cereberal embolism & MI .
8. respiratory tract infection .
9. thyroid & parathyroid insufficiency ; replacement as thyroxin 0.1-0.3 mg/d (1-2
weeks after surgery) & vitamin D with Calicium .
D. Chemotherapy
- Chemotherapy had not traditionally been part of larynx cancer primary treatment
protocols.
- Chemotherapy has also been used concurrent with radiation as a sensitizer to
enhance the effectiveness of external beam radiation.
- organ-preserving protocols using chemotherapy in conjunction with radiation for
advanced-stage laryngeal cancer have been compared to standard surgery and
radiation treatment. Comparable survival rates have been shown with differing
treatment morbidities.
- Cisplatinum and 5-fluorouracil are the two agents found to be the most effective
against larynx cancer. Recently, taxane and docetaxel (eg, Taxotere) are showing
some usefulness without the side effects of cisplatinum .
- Chemotherapy is not considered a first-line treatment or standard of care for early-
stage (Stages I and II) larynx cancer.
E. Photodynamic therapy
- an emerging modality of treating larynx cancer, as well as cancer arising from other
primary mucosal sites of the head and neck.
- A photosensitizing agent (a chemical preferentially taken up by tumor tissue and
sensitive to specific wavelengths of light) is administered intravenously. A laser is
then used to activate the photosensitizing agent and induce the destruction of tumor
tissue.
- This treatment has been shown effective in treating cancers as deep as 5 mm, with
similar local control and survival rates as traditional treatment modalities.
- The side effects of photodynamic therapy include light sensitivity that can linger for
several weeks after the administration of the photosensitizing agent. For this reason,
patients must wear sun-protective clothing during this period of time and avoid being
outside during the hours of maximal sun intensity.

Lecture notes in
Treatment Policy
A. Curative Rx ;
2. Supraglottic tumors ;
- Single-modality treatment of supraglottic cancer is preferable to other treatments
because it is easier on the patient, less expensive, and, for early cancers, as effective
as combined therapy.
- Neck metastasis is the major problem with early supraglottic cancer; both sides of
the neck are at risk.
- The key to a safe, successful supraglottic partial laryngectomy is patient selection.
Most complications can be avoided or diminished by proper patient selection. The
patient who is likely to suffer a major complication based on his or her general
health is best treated some other way( patient more than 70 years age & unfit
patient with bronchitis shouldn't Rx by this modality) .
- Patient selection criteria for supraglottic laryngectomy ; No v.c. involvement ,
normal v.c. mobility , No cartilage invasion , No paraglottic space involvement , No
significant preepiglottic space involvement , No tongue base involvement , NO
previous DXT & Surmountable nodal metastasis .
- Possible complications of Supraglottic laryngectomy ; major ; Airway obstruction ,
Pneumonia , speech alteration & aspiration , minor ; Delayed feeding tube removal ,
wound infection & fistula .
- Although radiation with laryngectomy for salvage is offered as an alternative to
supraglottic laryngectomy, more voices are preserved with the supraglottic
operation. Some very early supraglottic cancers high on the epiglottis can be treated
safely by endoscopic laser surgery (supraglottic Tis , improve the airways , T2 , T3
advanced Ca.-recurrence rate 20%-) . Extending endoscopic laser excision is being
used, but comparisons to the classic operation are lacking. Careful selection is the
key to successful treatment with endoscopic and open conservation operations. Safe
margins must be managed by the surgical pathologist.
- Safe supraglottic laryngectomy depends on margin control by a pathologist skilled in
fresh-frozen tissue section diagnosis.
- Attention to the technical details of the surgical technique is important to the
execution of a predictable operation.
- stage I by partial laryngectomy or radioRx , in the UK cure rate 80-90% 5 year
survival .
- T3 N0 , in UK Rx by radioRx , if N1 the radioRx had a contraversial rule .
- T1& T2 epiglottic should be Rx with radioRx & salvage surgery for recurrence ,
alternative supraglottic laryngectomy, if there are LN then supraglottic
laryngectomy(partial or total) . .
- Tumor of the aryepiglottic fold Rx by supraglottic laryngectomy with excision of one
v.c. , the alternative total laryngectomy .
- Horizental supraglottic laryngectomy may be used for T1,T2 supraglottic tumors
(high volume >3cm) without extension to v.c.
- Tumors of the false cords ; total laryngectomy ., best Rx by DXT with follow up & LN
examination , if recurrence ; neck surgery & total laryngectomy .
- Advanced supraglottic tumor (T3, T4) ; total laryngectomy .

Lecture notes in
- In certain instances ; one v.c. not involved , so do near total laryngectomy , the
appropriate alternative supracricoid partial laryngectomy .
- Stage III , IV ; this is not suitable for surgery , so Rx by DXT & chemotherapy .
- In supraglottic tumor T2 & above we Rx the neck due to high incidence of occult
metastasis .
3. Glottic tumors ;
- Laryngeal cancer arises on the vocal cords 75% of the time, and hoarseness is an
early warning symptom suggesting cancer when it persists more than 2 weeks.
- Laryngeal lymphatic anatomy underlies the effective surgical treatment of early
glottic carcinoma.
- Laryngeal function includes airway protection, respiration, phonation, and
sphincteric activity, and surgical procedures to treat laryngeal cancer must consider
all four functions.
- Most membranous vocal cord (glottic) carcinomas extend to the supraglottic region
(20%), to the subglottic region (20%), or to the anterior commissure (25%).
- Early glottic carcinoma limited to the membranous portion of the vocal fold can be
cured using endoscopic surgical excision, thyrotomy with cordectomy,
hemilaryngectomy, vertical partial laryngectomy with laryngoplasty, and/or
radiation therapy.
- About one in six patients with severe dysplasia or carcinoma in situ will develop
invasive carcinoma if the only therapy used is a single vocal cord stripping or
biopsy.
- Microinvasive carcinoma of the true vocal fold can be managed by sequential
endoscopic excisional biopsy, endoscopic laser excision, or radiation therapy.
- The goals of treatment for early glottic carcinoma are (a) complete removal of all
malignant disease, (b) preservation of function, and (c) predictable and reliable
rehabilitation of the patient.
- Indications for vertical partial laryngectomy and laryngoplasty are ; anterior
commissure involvement, extension to the vocal process of the arytenoid, selected
superficial transglottic lesions, and recurrent cancer after radiation therapy.
- Partial laryngectomy for recurrent cancer after radiation therapy must meet the
following criteria:
1. Lesion limited to one cord (may involve the anterior commissure)
2. Body of arytenoid free of tumor.
3. Subglottic extension no more than 5mm.
4. Mobile cord.
5. No cartilage invasion.
6. Recurrence correlating with initial tumor.
- Early complications after partial laryngectomy including subcutaneous emphysema,
bleeding, and tracheotomy tube occlusion.
- T1 & T2 ; DXT , 90% cure rate & 5 years survival , DXT cause cartilage necrosis
especially for those who smoke heavily , chronic laryngitis , nasal sepsis , chronic
bronchitis , in this situation ; surgery by endoscopic laser or scissors .
- T1b ; DXT or endoscopic laser excision , best voice result after DXT than endoscopic
surgery or cordectomy .
- T2 ; DXT or surgery , cure rate 80-90% 5 year survival .

Lecture notes in
- Prognostic values ; T volume (<3cm) , mobile v.c. , No ventricle involvement , No

deep ulceration , No spread to subglottis or supraglottis , only one side involvement ,
stop smoking .
- Alternative for T2 ; primary surgery , vertical hemilaryngectomy with tracheostomy
& postop. DXT (contraversial) .
- T1 +N1 (rarely) ; low volume (<2cm) , DXT to the LN & salvage surgery in
recurrence , alternative Rx ; surgery with modified radical neck dissection (type I,II,
III or seldom RND with/without postop. DXT) .
- Recurrence after DXT ; vertical laryngectomy if ; mobile v.c. , No >5mm of
subglottic spread , No intrusion , No LN involvement , NO arytenoid involvement
,NO involvement of 1/5 – 1/3 of v.c. (few patient following DXT had
hemilaryngectomy ) .
- T3 ; contraversial ;
1. small glottic tumor with mobile v.c. ; surgical (extended partial or total laryngectomy)
or DXT .
2. transglottic T3 tumor ; surgery (total laryngectomy) with RND , s.t. extended vertical
laryngectomy or subtotal laryngectomy with cricoid epiglotopexy (remove the cartilage ,
false & true cords , paraglottic space & epiglottis , preserve the cricoid , one artynoid &
hyoid bone) .
3. advanced glottic cancer (T3, T4) ;total laryngectomy , alternative is near total
laryngectomy (complication ; aspiration & shunt stenosis) .
4. advanced laryngeal Ca. ; don't want surgery then do DXT alone or with adjuvent or
neoadjuvent chemotherapy , the DXT either fractional or CHART(Contineous ,
Hyperfractional , Accelerated , Radiation Therapy) .
The survival rate about 50% 3 years for DXT , 30-40% expected for survival with
neoadjuvant chemotherapy .
Selected surgical procedures for glottic cancer ;
a. Microlaryngoscopy partial cordectomy with or without carbon dioxide laser
(excisional biopsy) ; Indications ; T1 midcord leukoplakia, Tis/microinvasion .
b. Cordectomy complete with or without carbon dioxide laser (endoscopy) ; T1
midcord .
c. Cordectomy (laryngofissure) ; T1 midcord
d. Frontolateral partial laryngectomy ; T1 with extension to anterior commissure
e. Hemilaryngectomy and extended hemilaryngectomy ; T1-T2 with extension to
arytenoid, without anterior commissure fixation (minimal)
f. Anterior partial laryngectomy with epiglottoplasty or with keel ; T1-T2 with
extension to anterior commissure (without arytenoid)
g. Subtotal laryngectomy with cricohyoidoepiglottopexy; T1b-T2 bilateral anterior
involvement, may include removal of one arytenoid
h. Three quarter laryngectomy ; T3.
4. Subglottic tumors ;
- treated by total laryngectomy with partial thyroidectomy , prefered in Rx of T1&T2
are DXT & follow up with salvage surgery .
- advanced disease with LN involvement ; extended total laryngectomy with RND &
postop. radioRx .

Lecture notes in
Diagnosis of recurrence ; if odema persist & not settle after 6 months , the recurrence & do
open biopsy , if negative , recurrence should be suspected in the deep paraglottic space (Rx
by total laryngectomy) .
B. Palliative Rx ;
- Therapy to ameolirate symptoms without any chance to cure .
- Radiotherapy or chemotherapy with pain relif , tracheostomy may be required , also
insertion of percutaneous feeding tubes .
- Pain relive ; by psychological (Tender loving care with intensive support to thier
family & friends) , electerical , pharmaceutical or combination of radiation &
surgery & chemotherapy .
- Tracheostomy to relive airway obstruction .
- Radiotherapy used locally for the primary lesion or distant metastasis , it is simpler
than that used for curative Rx , usually use radioactive implants of gold especially at
the secondary deposite .
- Chemotherapy ; adjuvant partial response .
T1 T2 T3 T4
Glottic radioRx (80-9-% cure) or endoscopic Advanced glottic Ca. Rx , either by ; total
removal , or by LASER (1) . laryngectomy , near-total laryngectomy(
T1N1 (rare) ; low volume Rx by radioRx voice preservation surgery) ,
to the neck with salvage surgery in the raidotherapy (3), or Neo-adjuvant
reserve(2). chemotherapy(30-40% survive)
Supraglottic radioRx + prophylactic ND + savage radioRx . Lryngectomy + ND
surgery for recurrence . even N1 ;
or partial laryngectomy + selective ND .radiRx + ND .
Subglottic Radiotherapy & follow up with Advanced disease Rx with extended
salvage surgery . total laryngectomy + ND + partial
thyroidectomy + postop. radioRx .
(1)
best result with radioRx than surgery , the choice for surgery is in cartilage necrosis ,
chronic laryngitis , nasal sepsis & ch. bronchitis , alternative for T2 is primary surgery
(hemilaryngectomy with tracheostomy) with postop. radiation .
(2)
if recurrence after radiotherapy ; vertical laryngectomy .
(3)
to those want voice preservation & not prefer surgery , radiotherapy , either
conventionally fractionated or CHART , can give 3 years local control .
Surgical PROCEDURES
A . Endoscopic Partial Laryngectomy at the Glottic Level
Indications
1.Squamous cell carcinoma, limited to the midportion of a mobile vocal fold
2.Verrucous carcinoma
1.Adequate surgical margins for histologic inspection
2.Extensive resection produces an inadequate postoperative voice
3.Vocal fold anatomy and histology
4.Laser safety for patient and operating room staff
Preoperative Evaluation
1.Routine laboratory studies
2.Electrocardiogram
Lecture notes in
3.Photographic documentation
4.Endostroboscopic evaluation
Special Instrumentation, Position, and Anesthesia
1.Binocular microlaryngoscope
2.Suspension device
3.Microsurgical instrumentation
4.Laser-safe endotracheal tube
5.Patient eye and skin protection
6.Neck flexion, with head extension
7.Total patient paralysis and relaxation
8.Decreased fraction of inspired oxygen (FI02) with helium, nitrogen, or room air
Tips and Pearls
1.Exposure with a suitable laryngoscope and suspension device
2.Define the extent of resection before surgical retraction, which distorts the field.
1.Extension to the anterior commissure
2.Extension to the vocal process
3.Lateral extension into the ventricle
4.Subglottic extension
5.Overaggressive resection leading to loss of postoperative voicing
6.Intraoperative and postoperative bleeding
1.Airway observation
2.Humidification after large resection
Operative Procedure
1. The largest-caliber laryngoscope possible is placed, and a suspension device is used.
2. The glottis is inspected with a 0‫؛‬telescope. This provides excellent monocular
visualization and can be coupled with a video or still camera for teaching or
documentation purposes.
3. The operating microscope is then aligned with the visual field. The 400-mm focal length
lens provides an acceptable working distance. Precision is enhanced by using the
microscope on 16X magnification.
4. The lesion is visualized and palpated to determine if it can be separated from the vocal
ligament. Neoplasms arise within the mucosa. By incising the vocal fold membrane
lateral to the lesion, a blunt elevator may be inserted into Reinke's space, and used to
separate the vocal fold cover, consisting of the mucosa and superficial lamina propria,
from the underlying ligament.
5. Specially designed microlaryngeal scissors are then used to excise the mucosal flap.
6. If it is not possible to separate the lesion from the vocal ligament, a superficial biopsy is
taken.
7. The carbon dioxide laser is attached to the operating microscope with the
micromanipulator. The newer-generation microspot micromanipulators provide a laser
spot size of 250 to 300 µm at a 400-mm focal length working distance.
8. The portion to be excised is retracted with cup forceps or a microlaryngeal suction while
the laser in a repeat pulse mode of approximately 2000 watts/cm2 is used to excise the
portion of vocal fold previously outlined.

Lecture notes in
9. It is possible to excise the entire membranous vocal fold in this manner. However, voice
results may worsen as more aggressive resection is pursued. Resection limited to mobile
middle-third vocal fold lesions usually result in the formation of a scar band during
healing. Although this scar band does not develop normal vibratory characteristics, it
usually provides a surface for the normal vocal fold to vibrate against during phonation.
Voice results are comparable to those obtained after radiation therapy.
B . Vertical hemilaryngectomy
Indications
1. Cancer involving the anterior commissure
2. Cancer involving the vocal process of the arytenoid cartilage
3. Bilateral glottic cancer
4. Early, ‘‘superficial'' transglottic cancer
5. Recurrent glottic cancer after radiation therapy
Contraindications
1. Cord fixation
2. Posterior commissure involvement
3. Involvement of both arytenoids
4. Bulky transglottic cancer
5. Thyroid cartilage invasion
1. Encroachment or involvement of anterior commissure
2. Encroachment or involvement of vocal process arytenoid cartilage
3. Assessment of cord mobility
4. Extension to ventricle or false cord
5. Status of mucosa adjacent to obvious tumors
6. Prior treatment
7. Pulmonary status; general medical problems
8. Communication needs in work and other activities
9. Reliability for follow-up
10. Neck node status
2. Computed tomography scan, if concerned about occult nodes or cartilage invasion
3. Careful mapping DL
4. Fiberoptic endoscopy with or without videostroboscopy
1. Headlight
2. Small, delicate plastic surgery instruments
3. Senn retractor, bipolar cautery
4. Shoulders on roll, neck extender, head stabilized in foam doughnut
5. Deepen anesthesia when entering larynx
Tips and Pearls
1. Explore the neck to detect occult metastatic nodes that were missed preoperatively.
2. Enter the larynx at a safe distance from the tumor.
3. Resect the tumor with close margins, and then send margin strips for frozen-section
confirmation of the adequacy of the excision.

Lecture notes in
4. Attempt to spare the posterior segment of the arytenoid cartilage, because it will
enhance postoperative glottic function.
5. Avoid extending the resection into the epiglottis; otherwise, postoperative problems with
aspiration are likely.
6. ‘‘Severe dysplasia'' has almost the same long-term prognosis as carcinoma in situ.
7. Preserve a central strip of midline thyroid cartilage if the cancer involves the anterior
commissure.
8. Techniques that limit granulation tissue formation yield more predictable outcomes.
9. The safety and efficacy of partial laryngeal surgery for cancer has been documented.
1. Aspiration may occur during the first 2 weeks after surgery, but it should not persist
beyond the fifth week.
2. Granulation tissue may develop in the surgical field and should be excised
endoscopically.
3. Laryngeal stenosis is a rare complication and should raise the suspicion of recurrence.
4. Recurrence usually is associated with voice changes as an early sign.
5. Regular follow-up examinations are important during the first 3 to 5 years after surgery.
1. When a Silastic keel is used to separate raw surfaces, my colleagues and I prefer to
remove the keel at 3 weeks.
2. Liquids may be swallowed 5 to 7 days after surgery, and a soft diet may be initiated 10
to 14 days postoperatively.
3. Decannulation is usually accomplished about 3 weeks postoperatively, after it has been
possible to plug the tracheostomy tube for extended periods.
4. The speech pathologist is a key individual in assisting the patient to regain maximum
voice quality.
Operative Procedure
1. The patient is positioned on the operating table in a prone position with the head
extended. Oral endotracheal intubation or tracheotomy under local anesthesia may be
performed to allow the induction of anesthesia.
2. A transverse incision is made, passing one fingerbreadth below the inferior margin of
the cricoid cartilage and curving outward and superiorly in the natural skin folds of the
neck.
3. As the incision passes lateral to the anterior jugular veins, it is curved superiorly toward
the mastoid tip and carried up to a level just inferior to the greater cornua of the hyoid
bone.
4. A vertical midline incision is dropped from the midpoint of the transverse incision and
extends about 2 cm inferiorly, and through this incision, a tracheotomy can be performed if
it was not accomplished initially.
5. The anterior cervical flap of skin and platysma muscle is elevated superiorly until the
entire hyoid bone is exposed. Care is taken to avoid injury to the superior laryngeal
neurovascular bundle( this innervation is important for postoperative function) .
6. The inferior skin flap is elevated laterally for a distance of several centimeters to allow
access to the tissue of the neck for direct palpation along the jugular lymphatic chains
bilaterally.

Lecture notes in
7. These chains of lymph nodes are palpated to identify any suspicious nodes to confirm the
absence of metastatic carcinoma. Any suspect nodes are sent for frozen-section evaluation.
8. The sternohyoid, sternothyroid, and thyrohyoid muscles (ie, strap muscles) and the larynx
from the level of the hyoid bone down to the cricoid cartilage are clearly visible.
9. The external thyroid perichondrium is incised in the midline and along the superior and
inferior margins of the thyroid alae bilaterally.
10. The external thyroid perichondrium is then elevated, being careful to avoid tearing the
perichondrium. The perichondrium is sutured to the overlying strap muscles to prevent
shrinkage of the injury.
11. The plane between the external thyroid perichondrium and the overlying strap muscles
is not entered, because these tissues will be repositioned to lie deep to the thyroid ala to
provide bulk and to stabilize the thyroid cartilage. The external thyroid perichondrium and
muscle flap are the essential ingredients for the laryngeal reconstruction (ie, laryngoplasty)
phase of the procedure. The external thyroid perichondrium is elevated back to the
posterior margin of the thyroid ala.
12. The thyroid cartilage is divided in the midline using an oscillating surgical saw, being
careful to avoid injury to the underlying soft tissue. As the internal thyroid perichondrium is
reached, it is elevated carefully from the thyroid cartilage, and the dissection is carried
three quarters of the way back in the direction of the superior and inferior thyroid cornua.
13. The airway is entered below the level of the glottis by employing a transverse incision
through the cricothyroid membrane. This incision is extended on both sides approximately 1
cm from the midline. At this point, the surgeon employs a headlight to permit visualization
in a superior direction and progressively enlarges the opening into the airway by extending
the incision superiorly so that it passes through the anterior commissure and up to the
superior thyroid notch.
14. With the tumor directly in the vision of the surgeon, the incision is then extended
laterally across the midportion of the false vocal fold (ie, ventricular band). The inferior
line of resection is then extended along the superior margin of the cricoid cartilage as it
begins to curve superiorly and posteriorly).
15. Then arbitrarily select the posterior resection line, often at about the point where the
vocal process of the arytenoid cartilage joins the body of the arytenoid cartilage. My
colleagues and I make a strong effort to preserve the body of the arytenoid cartilage to have
dynamic glottic tissue involved in the rehabilitation of larynx postoperatively.
16. For the unilateral lesion, the specimen comprises all of the tissue from the midline of
that side back to the body of the arytenoid cartilage posteriorly. In the vertical dimension, it
extends from the level of the cricoid cartilage up to a point superiorly that includes one half
to one third of the false vocal fold. The internal perichondrium of the thyroid cartilage
forms the deep margin of the tumor specimen.
17. Care is taken to avoid resection of substantial portions of the epiglottic cartilage,
because experience has shown that this invites postoperative aspiration. On some
occasions, we have employed the surgical operating microscope to visualize epithelial
changes under higher-powered magnification, especially in patients with patchy dysplasia
or carcinoma in situ.
18. Having ensured the adequacy of the tumor resection, we begin the laryngoplasty or
reconstructive phase of the operation. We employ a bipedicle muscle flap consisting of most
of the sternohyoid, sternothyroid, and thyrohyoid muscles. This strap muscle bundle is

Lecture notes in
separated from its posterolateral tissue attachment by a vertical incision made arbitrarily
so as to develop a pedicle muscle flap about the size of the small finger or index finger,
depending on the size of the surgical defect. The flap appears excessively large initially, but
experience has shown that there will be muscular atrophy of about 30%.
19. The incision that isolates the bipedicle muscle flap is made from a point about 1 cm
above the superior margin of the thyroid cartilage to a similar point about 1 cm below the
inferior margin of the thyroid cartilage. The bipedicle muscle flap preserves its attachment
to the external thyroid perichondrium on its deep or under surface and is also intact
superiorly and inferiorly. This tissue complex is then repositioned so that it comes to lie
deep to the thyroid ala, which is still attached posteriorly to its muscular insertion by the
inferior pharyngeal constrictor.
20. The muscle flap tends to flatten out along the inner surface of the thyroid ala, and the
external perichondrium forms the lining of the laryngeal lumen. The perichondrium is
sutured to the adjacent mucosa with a few loose tacking sutures.
21. The thyroid alae are then sutured together, and the wound is drained using a 0.5-in (1-
cm) Penrose rubber drain or a small flap drain.
22. A #5 or #6 tracheotomy tube replaces the endotracheal tube, and a light compression
dressing is applied over the skin.
Surgical Variations
Laryngofissure
The laryngofissure procedure represents the earliest form of vertical partial laryngectomy
and consists of either a midline or paramedian vertical incision in the thyroid cartilage to
afford access to the anterior of the larynx. Through this incision, a limited resection (ie,
cordectomy) of one true vocal cord can be performed for a small, early-stage glottic
carcinoma involving the mobile portion of the true cord . An upward extension of the
operative field allows the laryngeal ventricle and the lower half of the false vocal cord to be
included with the specimen. The resection stops short of the arytenoid cartilage, and its
deepest layer is the internal perichondrium of the thyroid ala .
Hemilaryngectomy
The hemilaryngectomy procedure is indicated for the management of T1 or T2 glottic
carcinoma, and it is appropriate for lesions that arise on the true cord and extend to the
false cord. The technique involves a full-thickness incision from the laryngeal epithelium
through the entire soft tissue depth, including most of the thyroid ala on the same side as an
en bloc resection of one half of the larynx ). The posterior resection line can be extended to
the midline of the posterior commissure .
Anterior Commissure Partial Laryngectomy
Anterior commissure partial laryngectomy is used for lesions involving the anterior
commissure and extending a significant distance posteriorly along both true vocal cords.
There may also be superior extension toward the petiole of the epiglottis. The anterior one
third to two thirds of the true vocal cord is excised en bloc with a smaller amount of the
midline portion of the thyroid cartilage.
The defect can be reconstructed by advancing a triangular segment of the epiglottis
superiorly to inferiorly into the defect, or it can be allowed to fill in with granulation tissue
if a keel is left in place for 4 to 6 weeks postoperatively

Lecture notes in
C . Supraglottic Laryngectomy (Horizontal Hemilaryngectomy)

Indications
1. T1, T2 supraglottic carcinomas, eg, cancers involving laryngeal surface of the epiglottis,
infrahyoid and suprahyoid epiglottis, ventricular folds, and aryepiglottic folds
2. Supraglottic carcinomas that are T3 by virtue of pre-epiglottic space involvement
Contraindications
1. Fixation or impaired motion of vocal fold
2. Poor medical condition, especially extreme age, poor pulmonary reserve, or both
3. Tumor within 5 mm of anterior commissure
4. Thyroid cartilage involvement
5. Prior radiation therapy is a relative contraindication
1. The Jackson ‘‘anterior commissure'' laryngoscope is a useful tool in the detection of
vocal fold involvement
2. A bulky supraglottic tumor makes it difficult to assess by endoscopy inferior extension
toward the ventricle and the vocal fold. Preoperative CT may help
3. Bilateral selective neck dissection should be done concomitantly
4. Enter the airway as far away from the tumor as possible
1. Preoperative barium esophagogram and upper GI series are helpful in detecting
esophageal motility disorders and reflux, which may delay or interfere with
postoperative swallowing rehabilitation
2. Consent must always be obtained for total laryngectomy
1. Headlight
2. Skin hooks
3. Oscillating saws
4. Shoulder roll with neck extended
5. If there is no danger of airway compromise, anesthesia may be initiated by endotracheal
intubation, with a tracheotomy performed after general anesthesia induction
6. Local tracheostomy followed by induction of general anesthesia is required in cases of
bulky tumor
7. Deepen anesthesia and make certain the patient is paralyzed when the larynx is entered
Tips and Pearls
1. The line of transection in supraglottic laryngectomy is the valleculae superiorly and
both ventricles inferiorly
2. The inferior margin must be free of tumor for at least 2 to 3 mm
1. Aspiration and pneumonia are the most common complications of supraglottic
laryngectomy
2. Fistula
3. Postoperative edema, particularly if the field has been radiated
4. Airway obstruction
1. If the nasogastric tube is dislodged during the early postoperative period, it should be
replaced with extreme care to avoid disrupting the suture line

Lecture notes in
2. Bedside evaluation by the swallowing team prior to oral feeding is helpful. Diet should
start with semi-solids.
3. Be sure the airway is adequate prior to the removal of the tracheotomy tube.
Operative Procedure
1. An apron type incision from mastoid tip to mastoid tip is preferred .
2. Bilateral selective neck dissection is carried out in the usual fashion.
3. The neck specimen can be left attached to the thyrohyoid membrane or be totally
removed , the hyoid bone is skeletonized from the greater horn of the involved
side to the lesser horn of the uninvolved side. The infrahyoid muscles are divided
just inferior to the hyoid bone, and the suprahyoid muscles are also detached
from the hyoid bone. The neurovascular bundle of the involved side is identified
near the superior horn of the thyroid cartilage and ligated. On the uninvolved
side, the hyoid bone is transected just lateral to the lesser horn. The superior
laryngeal nerve on this side is preserved if possible. Incision of the
perichondrium is carried out along the superior border of the thyroid cartilage
and the perichondrium is carefully elevated inferiorly to just below the middle of
the thyroid cartilage.
4. On the involved side, the cartilage is cut horizontally with the oscillating saw at
the middle of the thyroid cartilage in male patients, and at the junction of the
upper and middle third in females. This level should be above the level of the
vocal folds.
5. On the uninvolved side, the cartilage cut sweeps upward to the superior edge of
the thyroid cartilage, intersecting at a point midway between the thyroid notch
and the superior horn ).
6. The pharynx is now entered, either through the piriform sinus of the uninvolved
side or through the valleculae just above the hyoid bone. Once the pharynx is
entered, the epiglottis is grasped with an Allis clamp (the patient should be fully
paralyzed at this point) so the full extent of the tumor can be determined. After
ensuring no involvement of the lingual surface of the epiglottis, the incision is
continued across the valleculae.
7. The arytenoid prominence and the laryngeal ventricle should be clearly
identified. The mucosal cut is carried along the aryepiglottic fold toward the
anterior end of the arytenoid into the laryngeal ventricle. The mucosa overlying
the arytenoid may be removed, but the cartilage should not be exposed.
8. If tumor extent requires removal of the arytenoid, the vocal fold should be sutured
to the cricoid.
9. Using the scissors, one blade is engaged in the ventricle and the other blade cuts
along the cartilage incision on the uninvolved side. Care must be taken to avoid
injury to the thyroid perichondrium. Once the uninvolved side has been incised,
then the remnant of the larynx with the tumor can be exposed like an open book.
The incision on the involved side is carried along the aryepiglottic fold through
the posterior part of the false cord into the ventricle continuing anteriorly to the
midline of the thyroid cartilage
10. . The rest of the supraglottic structures should be removed with at least a 2- to 3-
mm margin (inset). Frozen section is mandatory to determine the adequacy of the
margin.

Lecture notes in
11. A generous cricopharyngeal myotomy is carried out by inserting the index finger
into the lumen of the esophagus and then dividing the inferior constrictors.
12. Before beginning closure, a nasogastric tube is inserted through the nose into the
stomach. The shoulder roll should be removed and the neck flexed to facilitate
closure. Mucosa-to-mucosa closure is not achievable and should not be
attempted. Some mucosa approximation from tongue base to piriform sinus is
achievable with 3-0 atraumatic absorbable sutures , the rest of the closure is
achieved by suturing the base of the tongue to the perichondrium of the thyroid
cartilage. Interrupted sutures are first placed without tying.
13. Later all are tied at the same time after placement of a suspension suture of 0-
nylon from the remnant of the thyroid cartilage midline to the soft tissue adjacent
to the genial area of the periosteum of the mandible.
14. The wound is thoroughly irrigated, and a closed suction drainage device is
placed. The skin is closed in two layers. A cuffed size 8 tracheostomy tube
replaces the endotracheal tube. A retention suture with 0-Prolene is placed from
the chin to the chest wall to prevent extension of the neck.
D . Near Total laryngectomy
Indications
1. Near-total laryngectomy
a. Lateralized glottic or transglottic cancers with impaired movement, fixation, or
subglottic extension, for which conventional vertical partial laryngectomies or
supracricoid partial laryngectomy would be unsafe
b. Lateralized supraglottic or aryepiglottic fold cancers with impaired movement,
fixation, or glottic extension, for which conventional supraglottic partial
laryngectomy, partial laryngopharyngectomy, or supracricoid laryngectomy would
be unsafe
c. Most supraglottic cancers in patients physiologically unfit for supraglottic or
supracricoid partial laryngectomies, obviating escalation to a total laryngectomy
2. Near-total laryngopharyngectomy
a. Piriform cancers with impaired movement (indicating paraglottic space invasion) or
supraglottic and aryepiglottic cancers with pharyngeal wall spread or tongue base
extension such that partial laryngopharyngectomy or extended supraglottic partial
laryngectomy would be unsafe
3. Extended near-total laryngopharyngectomy
a. All that remains of the hypopharynx after adequate resection of large piriform and
hypopharyngeal wall cancers is the contralateral piriform fossa and the postcricoid
region. The piriform can serve as the usual recipient of the voice shunt, but the rest
of the swallowing tube depends on reconstruction with extrapharyngeal tissues.
Contraindications
1. Previous irradiation failure or partial laryngectomy failure is a relative
contraindication.
2. Bilateral anterior ‘‘horseshoe'' glottic/transglottic cancers infiltrating both ventricles
3. Primary subglottic cancers
4. Posterior cancer, such as postcricoid cancer
1. The concept of continuing diagnosis

Lecture notes in
2. Neck dissections are often indicated.

3. Postoperative irradiation is tolerable.
1. Suspicion of the likely diagnosis of cancer before biopsy
2. Mapping the surface extent of the tumor
3. Use videolaryngoscopy, and document the tumor extent with prints.
4. Imaging studies, if they help demonstrate the depth of invasion
5. Speech pathology consultation
6. Tracheotomy demonstration by a nurse
7. Appropriate educational materials for the patient and family
1. A small (5.5 or 6), cuffed initial endotracheal anesthesia tube
2. Lindholm vallecular laryngoscope and 0° and 70° telescopes (Storz)
3. The neck is extended. The anesthesia tube is accessible and can be removed when the
tracheotomy is made.
4. A fiberoptic headlight, preferably xenon
5. Light bone shears; nasal perichondrial elevators; bipolar cautery
6. A 14-Fr catheter to size the voice shunt
Tips and Pearls
1. The more subglottic mucosa is preserved, the more favorable to voice production is the
internal taper of the eventual tracheopharyngeal shunt.
2. A chalice-shaped configuration of the upper (pharyngeal) opening of the shunt is
undesirable; it catches food and favors aspiration.
3. Sometimes, supraglottic cancer is found beyond the supraglottis, and a supraglottic
laryngectomy may need to be extended beyond the expected pulmonary tolerance of the
patient. In these situations, a near-total laryngectomy should be considered before a
total procedure.
1. Regional and distant metastases, second primaries, and local recurrences (rare)
2. Near-total laryngectomy was primarily designed for untreated, well-defined, relatively
predictable cancers centered in the paraglottic space. Beware of radiation treatment
failure.
3. Delayed acquisition of voice is probably the most common complication of near-total
laryngectomy.
4. Aspiration will ensue if the recurrent laryngeal nerve to the shunt is destroyed or if the
muscle in the laryngeal remnant is overcauterized.
5. The anterior tracheal wall stoma is slower to stabilize than the usual end-on stoma that
follows a total laryngectomy.
1. The dressing is removed on postoperative day 1.
2. Closed wound suction for approximately 3 days.
3. Feed through a nasogastric tube for about 10 days.
4. Speech pathology plays an integral role.

Lecture notes in
Operative Procedures
Direct Laryngoscopy and Biopsy
Carefully examine the column of laryngeal tissue slated for preservation. The ventricle to
be entered should be free of tumor. The surgeon should not overlook submucosal extension
or satellitosis, especially in pharyngeal cases. The center of the lesion should be biopsied,
taking care not to obscure the lesion's borders. The surgeon must communicate her or his
exact suspicions, the specimen site and orientation, and the history of previous treatment
directly to the histopathologist performing the frozen-section analysis. Conclude by
inserting the nasogastric feeding tube.
Tracheotomy
The trachea is approached through the transverse segment of the future apron flap incision.
The surgeon separates the straps, and divides and ligates the inferior thyroid veins. The
trachea is exposed below the thyroid isthmus. The operator again checks the transoperative
tube's cuff and the sterile anesthetic hose. An aliquot of local anesthetic is instilled into the
trachea without puncturing the balloon. After stabilizing the trachea with a hook, an
opening incision is made. The band retractors are placed into the tracheal lumen, and the
new tube is inserted as the anesthetist pulls out the old one. Careful placement prevents
excessive advancement and ventilation of one lung. After the new tube is connected, it
should be anchored to the skin.
Neck Dissection
After elevating the flaps in the subplatysmal prevenous plane, all the fat, fascia, and lymph
nodes of the submental, submandibular, carotid, muscular, and posterior triangles of the
neck are removed. The accessory, phrenic, vagus, hypoglossal, and marginal mandibular
nerves, as well as the brachial plexus and the carotid arterial system, are preserved. In the
neck of a high-risk patient, the internal jugular vein, the omohyoid and digastric muscles,
and the submandibular gland and cervical plexus should be included in the resection. For
elective surgery on a node-negative neck, these components are often preserved.
Near-Total Laryngectomy
The neck dissection exposes the strap muscles over the larynx on the principal side of the
tumor. These are transected low, exposing the thyroid lobe to be included in the resection.
The fascia is incised along the anterior border of the contralateral straps so the midline
prelaryngeal soft tissues stay with the specimen. The contralateral straps are preserved. The
surgeon divides and oversews the union between the contralateral thyroid lobe and the
isthmus. The isthmus will accompany the specimen.
The surgeon next rolls away the larynx and the ‘‘specimen side'' lobe of the thyroid. The
superior, middle, and inferior thyroid veins are visualized and divided. (They may have
already been released by a neck dissection.) The superior and inferior neural and arterial
pedicles are identified as they cross to the specimen. The surgeon divides and ligates the
superior thyroid artery and laryngeal nerve and similarly transects the inferior thyroid
artery and recurrent nerve. The posterior border of the thyroid ala and the hyoid are
skeletonized and freed from the inferior constrictor muscle . The suprahyoid muscles are cut
free to release the hyoid to be removed with the specimen. The operator shadows the upper
border of the hyoid across the midline to the opposite lesser horn, taking care to evade the
nearby hypoglossal nerve and the loop of the lingual artery.
The surgeon identified the column of the larynx to be preserved for the shunt on the side of
least tumor involvement. It was previously confirmed during laryngoscopy that the ventricle

Lecture notes in
on that side was tumor free. It is safe to enter there to begin the separation between the
laryngeal elements of the composite shunt and the anterolateral margin of the resection
specimen.
A middle ‘‘column'' or wedge is removed from the ala of the thyroid cartilage on the
conserved side after releasing the hyoid origin of the sternohyoid covering it and dividing
the hyoid. The hyoid body stays with the specimen. A periosteal elevator is insinuated under
the deep surface of the middle third of the thyroid ala, starting at the superior margin to
prepare the overlying wedge of cartilage or bone (alotomy) for removal between saw cuts.
The operator must be careful not to traumatize the outer fibers of the underlying
thyroarytenoid muscle or to enter yet into the ventricle just above it. The laryngeal lumen is
entered through the fibroglandular tissue that caps the ventricle on the noninvolved side.
The mucosal edges of the ventriculotomy are retracted with hooks, and the larynx is entered
with the outstretched blade of a scissors. An upward cut is made across the false cord.
Turning toward the tumor side, the vallecula is transected . The specimen is folded forward
as the headlight shines into the open larynx, enabling a good look at the cancer. The
surgeon determines where to safely transect the ‘‘good'' true cord and cuts down from
above through this point and on into the anterior subglottis. The posterior cricoid plate is
cut in the midline and broken to open the cricoid ring, and then the anterior and posterior
cuts are joined at a safe distance under the tumor. The surgeon continues cutting up
through the break in the posterior cricoid plate and divides the interarytenoid . The
specimen, attached only by pharyngeal mucosa, is lifted and removed completely.
Samples of the surgical margins are sent with the specimen for histopathologic review
While waiting for the pathologist's report, the surgeon carries out a submucosal resection of
the residual cricoid cartilage. The remaining recurrent laryngeal nerve is essential to
aspiration prevention and must be preserved, but the surgeon should ensure that the shunt
becomes flaccid. After a report of tumor-free surgical margins, the reconstruction
commences.
Reconstruction With the Composite Shunt
The surgeon stretches out the hypopharyngeal mucosa remaining on the newly cleared
tumor side and makes a simple backcut to develop an inferiorly based pennant-shaped flap
from the margin. The base is level with the residual corniculate. The tip is high enough on
the pharynx to give a flap that can rotate down and lie alongside the entire length of the
shunt . The width is whatever size is needed to form an appropriate shunt diameter after it is
combined with the laryngeal component. In cases with much residual larynx, a flap may be
minimal or unnecessary.
The surgeon next forms the tubular shunt. The flap and the laryngeal remnant are united in
parallel to create the posterior wall. The composite is tubed, and the anterior wall is
completed by sewing the vertical anterior seam that completes the tubular configuration
A 14-Fr catheter is a useful temporary gauge for the diameter.
The remaining pharyngotomy is closed and the permanent stoma in the anterior tracheal
wall is completed . Suction drains are placed in the neck, and the skin flaps are closed with
an airtight deep layer of running chromic suture and a well-aligned skin closure of staples.
To complete the operation, the surgeon dresses the stoma and the neck as necessary (eg,
Xeroform around the tracheal tube and bulky gauze around the neck). The physician makes
sure the bladder is not distended, and the patient is transported to the recovery room.

Lecture notes in
E . Total Laryngectomy
Indications
a. Malignant disease
1. Advanced tumors with cartilage destruction and anterior extralaryngeal spread;
2.Posterior commissure or bilateral arytenoid tumor distribution.
3.Circumferential submucosal disease with or without bilateral vocal cord paralysis .
4.Subglottic extension, either longitudinal or circumferential, sufficient to preclude near-
total, tracheopharyngeal shunt formation or cricohyoidpexy.
5.Completion laryngectomy for failed conservation or extensive endoscopic surgery;
6.Hypopharyngeal tumor originating at or spreading to the postcricoid mucosa;
7.Massive neck metastases or thyroid tumors (usually recurrent) invading both sides of the
larynx from outside the laryngeal skeleton;
8.Advanced tumors of certain histologic types that are incurable by endoscopic resection,
chemotherapy, or radiotherapy, e.g.,
adenocarcinoma, spindle cell carcinoma, sarcomas, minor salivary gland tumors, and
large cell neuroendocrine tumors;
9.Total pharyngectomy for those with tumors that also necessitate either sensory or motor
denervation of the larynx;
10.Radiotherapy failures;
11.Extensive recurrent cancer after conservation surgery and radiotherapy.
12.Circumferential endolaryngeal malignancy, persistent or recurrent after definitive
radiotherapy .
b. Benign disease
Although infrequent, the following indications may necessitate total laryngectomy.
1.Radiation necrosis of the larynx, despite tumor control, unresponsive to adequate
antibiotic and hyperbaric oxygen management; and
2.Severe irreversible aspiration, with the laryngectomy used for complete separation of
the air and food passages.
1. Early ; (1) Drain failure (2) Hematoma. (3) Infection. (4) Pharyngocutaneous fistula.
& (5) Wound dehiscence .
2. Late ; (1) Stomal stenosis (2) Pharyngoesophageal stenosis and stricture (3) Chronic
pharyngocutaneous fistula & (4) Hypothyroidism & Hypoparathyroidism .
1. Monitoring: systemic vital signs, fluid balance, oxygenation, wound drain vacuum
retention and output, and neck flap viability.
2. Postoperative treatment includes ventilator assistance , as per respiratory status;
tracheostomy tube care (cleaning, cuff pressure checks); airway humidification;
bronchodilator treatments or chest physical therapy; suture line care 3 times daily; and
nasogastric or tracheoesophageal fistula tube feeding once bowel sounds are present .
3. Drains are removed when output is below 25 ml/day for two consecutive days, and oral
feeding normally is begun 7 days after surgery in the nonirradiated patient.
Laryngectomees previously radiated are fed 12 to 14 days after surgery to allow a
longer healing time for the pharyngeal repair .

Lecture notes in
Operative Procedure
A. Resection
1. Proper patient positioning provides access to the anterior part of the neck for the surgeon
and the assistant. Positioning is best achieved by placing the patient on a table fitted with a
head holder, allowing the head to be cantilevered out but remain well supported.
2. A curved, horizontal neck skin incision is preferred because of its minimal intersection
with the pharyngeal closure and its potential for extension laterally into a neck dissection
incision. The laryngectomy incision is made from sternomastoid to sternomastoid, at or
above the level of the cricoid such that a 2- to 3-cm bridge of skin is preserved between the
main incision and the upper stomal verge .
3. Once the incision is deepened through, but not beyond, the platysma, flaps are elevated
superiorly and inferiorly in the subplatysmal plane until there is exposure above to the
upper border of the hyoid bone and below to the cervical trachea.
4. The anterior jugular veins and the prelaryngeal Delphian node are left undisturbed on
the specimen, as are the strap muscles. The sternocleidomastoid muscle then is identified
along its anterior border on each side.
5. The investing layer of cervical fascia is incised longitudinally from hyoid to clavicle .
6. The omohyoid then is divided , which allows entry to the loose areolar compartment
bounded laterally by the sternomastoid muscle and carotid sheath and medially by the
pharynx and larynx contained in the visceral compartment of the neck.
7. The strap muscles then are divided inferiorly from their sternal origins and elevated to
expose the thyroid gland. The isthmus and the lobe ipsilateral to the laryngeal tumor are
often left attached to the larynx and trachea for en bloc resection.
8. The ipsilateral superior and inferior thyroid vascular pedicles are therefore ligated and
divided, as is the middle thyroid vein.
9. After dividing the thyroid isthmus, the contralateral lobe then is dissected off the
laryngotracheal skeleton from medial to lateral, thereby preserving blood supply to the
remaining thyroid and parathyroid parenchyma via superior and inferior thyroid vessels.
10. after dividing and ligating the upper and lower extent of the anterior jugular veins, the
superior aspect of the hyoid bone is skeletonized by detaching the mylohyoid, geniohyoid,
digastric sling, and hyoglossus in sequence from medial to lateral.
11. blunt dissection should be used lateral to the lesser cornu, avoiding excess electrical
stimulation or direct damage to the hypoglossal nerve.The posterior border of the thyroid
cartilage lamina is rotated anteriorly by traction with a double hook, allowing sharp
release of the constrictor muscles from the inferior to the superior cornu.
13. The pharyngotomy incisions and definitive laryngeal removal now are performed. To
avoid contact with the neoplasm or cutting through its submucosal extensions, the pharynx
is entered contralateral to the tumor. If superior extension to the tongue base is present,
lateral pharyngotomy behind the thyroid cartilage is performed, and using a headlight, the
extent of tumor is inspected. A safe 2-cm margin of normal-looking mucosa then is
preserved with further cuts from below, progressing superiorly behind the thyrohyoid
membrane, around the hyoid bone, and then transversely across vallecula or tongue base.
14. A view of the endolarynx and pharynx now is possible to assess tumor extent and to plan
appropriate mucosal cuts .Using Mayo scissors, bilateral, inferiorly direct cuts are made,
releasing the lateral pharynx from the larynx. The inside scissors blade is on mucosa, and
the outside blade is on constrictor musculature. As these vallecula-to-pyriform sinus

Lecture notes in
incisions are made, the larynx is further angled anteriorly out of the wound until it is
released to the apices of the pyriform sinuses. The postcricoid mucosa is exposed and is
incised sharply in the transverse direction connecting the inferior extent of both lateral
incisions across the lower half of the cricoid lamina.
15. A plane of blunt dissection—initially behind the posterior cricoarytenoid muscle, but
from there down between the trachealis and longitudinal esophageal muscle then is opened
until the desired level of tracheal transection is reached. Optimum exposure of the trachea
at this stage is achieved by further lateralization of the preserved thyroid lobe and then
followed by knife transection of the trachea itself.
16. The wound is thoroughly irrigated; all clots are removed, and hemostasis is achieved.
17. If a primary tracheoesophageal puncture is to be performed, the permanent tracheal
stoma is created before pharyngeal repair. This technique enables definitive positioning of
the trachea relative to the esophagus and skin before a puncture site is selected. A pair of
right-angled forceps then is passed into the esophagus with the tip elevating the posterior
tracheal wall at the intended puncture site . A tracheoesophageal stab incision is made,
exposing the forceps tip, and with these, a 14-French gauge feeding tube is grasped, pulled
into the pharynx, and then fed down the esophagus until its end is positioned in the stomach .
B. Repair and reconstruction
1. Pharyngeal reconstruction is currently performed by direct closure or flap augmentation.
Configurations for a direct repair are T-shaped or linear (horizontal or longitudinal) ,
Selection of closure type is based on an assessment of the shape and size of the pharyngeal
defect, elasticity of remaining tissue, and simulated wound approximation before suturing.
The least-tensioned apposition of wound edges is the best and usually is T-shaped and
results in minimal or no horizontal pharyngeal shelf formation.
2. The pharyngeal wall is closed in two layers, the first being mucosal and submucosal and
the second being muscle. A running or interrupted closure, according to the surgeon’s
preference, is used with particular attention to inversion of the mucosal edges into the
pharynx. This inversion is achieved with an absorbable stitch that runs horizontally through
the submucosa, without penetration of the mucosal surface , muscle layer closure requires
advancement of the cut constrictor margins over the mucosal closure for reinforcement.
3. If there is insufficient pharyngeal wall to close over a 36 French dilator, a flap repair
should be considered to increase the circumferential dimension of the neopharynx.
C. Tracheal stoma
1.The permanent end-tracheal stoma is created before or after pharyngeal repair.
2. An appropriate shield-shaped skin button is removed from the lower neck flap in the
midline, just above the sternal notch . Any excess adipose tissue or bulky sternomastoid
muscle or tendon is excised deep to the skin flap to minimize tracheostenosis.
4. The tracheal end then is passed through the hole and secured with several stay stitches.
5. The circumferential suture line should provide support for the trachea and accurate skin-
mucosal apposition without cartilage exposure. This is best achieved by a modified vertical
mattress suture that traverses (1) skin (peripherally), (2) cartilaginous tracheal wall
(extramucosally), and (3) skin (centrally). It is advisable to place all eight sutures in
position before any are tied.

Lecture notes in
Voice rehabilitation after laryngectomy

The appropriate time to begin speech training depends on ;
1. The local condition of the wound , which should be healed & mirror examination
should show no trace of fiber in the pharynx .
2. The general condition of the patient , the patient encouraged to walk & do other
exercises , check & teeth condition , an audiogram recorded as preliminary to voice
& speech training .
There are four types of voice restoration post-laryngectomy :
1. Oesophageal speech
It is the earliest form by which the patient soon or later develop intelligible speech , but
only in patient with no external pharyngeal fistula .
It is pseudo-whispered speech after laryngectomy the patient turn to move the floor of
the mouth & the roof of the tongue in such way that some air is displaced enough to
produce shout sibilant & plosive sounds .
The pseudo-whisper speech is a pharyngeal speech which is unsatisfactory , they so be
avoided when learn to produce the oesophageal speech which is the correct maneuver
in which the air enter the oesophagus .
It produces by ;
a. Drawing "compressing" air into the oesophagus by inhalation .
b. Pumping "releasing" air into the oesophagus by injection causing pharyngo-
oesophageal segment to vibrate producing oesophageal tone used for speech .
Carbonated water may be used to help the patients .
The pharyngo-oesophageal segment replace the larynx as a generator of vibrating
column of air upon which the articulators & resonators in the oral cavity , nose &
sinuses superimpose the individual voice quality .
Basically the sound produced within 1-2 days , it takes 2-10 weeks before the patient can
use his newly acquired voice .
Methods of oesophageal speech ;
(2) Consonant injection method ; it is more efficient one , inject air during speech
rather than just during rest or breaks because phrases the typical consonants are
the plosive one (Pa , Ka , …etc) .
(3) Glossopharyngeal press method ; the patient pumps the tongue by moving the
posterior tongue against the hard palate until it approximately the pharyngeal wall
(4) Inhalation method ; can be use to supplement oesophageal speech air , it depends
on a principle that air will enter the oesophagus when the pharyngo- oesophageal
segment relaxed during pulmonary inhalation .
Difficulties & disadvantages of oesophageal speech ;
(1) Complex method , only 50% of patients are able to develop adequate oesophageal
speech , especially difficult for female & elderly .
(2) The most frequent problem for beginners is that the oesophagus opening does not
relax at the moment that the air must pass through it on the way in or out , this
cause the sound produced is tense , high-pitched & short duration (which is
unsuitable) , sometimes the patient succeed to inject air into the oesophagus , but
fail to return it back , so the air pushed in the stomach & lost of phonation . To
solve this problem , active relaxation training of neck muscles & jaw muscles
which indirectly relax the oesophageal sphincter .

Lecture notes in
(3) Diverticulum of the pharyngeal wall , have adverse effect on the sound which may
be moist & bubbling , this diverticulum prevented by stitching of the pharyngeal
wall & avoid the swallowing in the 1st days postoperatively .
(4) Hissing sound , it is a distracting symptom , made by air passing through the stoma
or through the tracheostomy tube .
(5) Too weak voice caused by flaccidity of the pharyngeal wall at the level of vibrating
structures . Improved by fitting of special neck band above the tracheostome .
Advantages ;
(1) Increase intelligibility .
(2) Increase fluency .
(3) Enhanced intensity .
(4) Easier to acquired .
(5) Improved fundamental frequency .
At the present time , every laryngectomized patient should have a course of voice
restoration (rehabilitation) immediately after the wound healing & feeding tube has
been removed .
2. Primary tracheo-oesophageal puncture
Introduced by Singer & Blom at 1980 , it is a surgical method of choice for voice
restoration .
The method ; at laryngectomy , a small fistula created between the posteror tracheal
wall & the oesophagus prior to pharyngeal repair , a heavy curved artery forceps
inserted into the oesophageal lumen & used to indent the posterior tracheal wall & an
assistant can then cut down onto the artery forceps , then a stomogastric tube pass
through this fistula (can be used for feeding purposes until the wound healing) .
At this point or 1-2 weeks later , a small silicon valve prosthesis is inserted , this allows
diversion of the pulmonary air from the trachea , so that the vibrating pharyngo-
oesophageal segment generated is lung powered rather than powered by a small volume
of insufflated air .
3. Secondary tracheo-oesophageal puncture
It is carried out after wound healing using special designed endoscope , the principle
complication for both primary & secondary punctures is the leakage (occur in 10%)
which improved by insertion of larger valve .
The choice of valve ; the original Blom-Singer valve was a handmade with a slit in its tip
forming one way duckbill valve with outer retention coil .
The 1st available was 16 FG duckbill (every one FG equal to 3 mm) device , followed by
prosthesis of similar diameter with beveled tip incorporating an internal one way hinged
flap valve , then followed by 20 FG nowadays .
The latest development is an extended wear indwelling device which incorporates a
larger or longer tracheal & oesophageal retention collars .
Tracheo-oesophageal puncture need preliminary dilatation of 22 FG prior to insertion
of the indwelling valve , the indwelling device , there is no strap , so that it is a neck seal
& decrease in skin irritation , available in length ranging from 1.4-3.3 cm , replaced at
6 months interval (or earlier if needed) & can be cleaned insitu by twizors .
Valve failure indicated by air leakage through the valve .
Recently develop , is the use of a tracheostome valve which eliminate the manually
needed closure off tracheostome with a finger during speech .

Lecture notes in
Provox now produce a low resistance indwelling voice prosthesis system which contain
one way hinged valve moulded in one piece with a prosthesis to form the integral part of
the device , it is available in 3 length (6, 8 & 10 mm) & can inserted transorally .
Valve care ;
(1) Prevention of fungal infection , one of the commonest problems is the candida
colonization of the indwelling valve which can damage the prosthesis causing
incomplete closure & leakage through the prosthesis decreasing the lifespan .
This prevented by ;
- Oral nystatin suspension twice daily . OR 10 mg lozenge of amphotricin
dissolved slowly in the mouth 4 times daily .
- Some patients benefit from soaking their denture with 3% hydrogen peroxide to
eliminate denture yeast .
- Buccal bio-adhesive slow released tab contain miconazole nitrate .
(2) Prevention of pharyngeal spasm (hypertonicity) , by ;
- Cricopharyngeus myotomy at the time of surgery , but this carry risk of mucosal
dehiscence & fistula formation .
- Peripheral denervation by identification of the pharyngeal plexus by dirct
electric stimulation , the neurectomy preserve the blood supply to the
pharyngeal wall & may enhance the quality of phonation due to residual elastic
tone & resulting increased fundamental frequency .
(3) Heat-moisture exchange , the use of external heat-moisture exchange will decrease
cough & sputum , the exchanger is a disposable filter cassette contain heat-
moisture exchange foam & may include speech valve with spring for air tight
digital closure to the stoma .
Kapitex Trachi-Naze system act as source of moist warmth & improve oxygenation by
increase the fundamental airway resistance .
Voice outcome of tracheo-oesophageal puncture ;
- High successful rates for it (70% of patient achieve functional spoken
communication)
- Predictors of voice outcome are ;
a. Prelaryngectomy communication status , patients major pre-existing disease
most unlikely to achieve any postlaryngectomy oral communication .
b. Age ; younger age more likely to acquired good communication .
c. Acute local xomplications , occur in 50% of patients which is consider as
adverse prognostic factors for long term tracheo-oesophageal speech .
4. Other aid ;
a. Electrolarynx (cervical vibrator)
Until recently (artificial larynx) was considered to be the method of choice in patient
unable to learn oesophageal speech .
Transcervical (servox) vibrator include immediate & intelligible speech . It uses
temporarily & gives a higher intensity noise environment , it is a useful fallback for
patient with acute problems of a valve .
b. Lip reading classes
Use for the relatives of the patient who perform total laryngectomy , it is of benefit
especially during the early phases of rehabilitation .

Lecture notes in
Endoscopic Management of Benign & Malignant laryngeal disease

History of endoscopic laryngeal surgery
- In 1807 Philipp Bozzini (father of minimally invasive surgery) was the 1st to suggest
visually controlled endoscopic surgery .
- He described the light conductor (Lichtleiter) which consisted of a univaersal handle that
incorporated a candle & a reflector as an extracorporeal light source , to that handle he
attach a variety of cannulas to examine the natural passages , the laryngeal canula consist
of an additional mirror that allowed for visualization of the lower part of the pharynx &
larynx .
- The reports of mirror laryngoscopy in the 1st half of 19th century were not widely accepted
- Horace Green (father of American laryngology) was the 1st throat & respiratory diseases
specialist in USA , he described the transoral application of causatics to the larynx to treat
the infectious inflamatory disorders of the laryngeal memberanes .
- He was , however maligned by his contemporaries who didn't believe that his transoral
interventions where possible . Later , Green resolved this by placing a wholebone probang
transorally through the glottis of a patient with a tracheostomy until it could be visualized
at the tracheostomy site .
- In 1852 , Green describe the 1st direct laryngoscopy & visually controlled excision of
laryngeal neoplasm .
- Manual Garcia reported autolaryngoscopy to the Royal society of London in 1855 .
- Czermak & Turck were the 1st who concentrated on educating the physician the technique
of laryngoscopy throughout Europe .
- In 1859 , Stoerk reported the 1st laryngoscopically controlled manipulation , which involve
the topical application of silver nitrate to the larynx .
- In 1861 , Lewin was the 1 st to report the laryngoscopically guided management of
laryngeal tumors .
- In 1886 , Fraenkel punlished the 1st report of transoral resection of laryngeal cancer .
- At the end of 19th century , Kirstein reintroduce the direct laryngoscopy (call it autoscopy)
- In 1925 , Jacson use the Kirstein head & neck position for direct laryngoscopy in the
supine position .
- Killian introduce the inverted V laryngoscope blade to conform to the anterior glottal
commisure & designed the laryngeal suspension that facillitate the bimanual surgery .
- Haslinger with his bivalve laryngoscope , introduce the internal distension in the
anteroposterior dimension .
- Jacson with his laryngostat introduce the internal distension in mediolateral dimension .
- Brunings was describe the external counterpressure .
- Zeitels & Vaughan combined all the above concepts together .
- In 1960 , Scalco , Jako & Kleinsasser introduce the surgical microscope in the
endoscopic laryngeal surgery .
- Jako also designed the 1st set of microlaryngeal hand instruments .
- At the same time , Priest & Wesolowski introduce the concept of general endotracheal
anasthesia to laryngoscopy .
- In early 1970s , Polanyi worked with Jako , strong & Vaughan , and coupled the Co2 laser
to the surgical microscope .
- In 1990s , the understanding of the physiological principles of laryngeal sound
production & the use of stroboscopy to analyze vocal cord oscillation , producing a

Lecture notes in
sunstantive innovations in the endoscopic surgey , which termed Phonomicrosurgery which

based on maximally preserving the vocal fold's layered microstructure .
General endoscopic technique & principles
- Anasthesia ; general endotracheal anasthesia with paralysis .
- External counterpressure & internal distension are routinely used .
- A laser –safe endotracheal tube provide a stable point from which the largest –lumened
laryngoscope is intercalated between the tube & the infrapetiole region of the supraglottic
(for glottic surgery) to internally distend the surgical field .
- For supraglottic surgery , the upper blade of bivalved laryngoscope is placed against the
tongue base or the epigottis .
- Position ; classic Boyce – Jackson position with the neck flexed & the head extended at
the atlanto-occipital joint , the position is maintained with modified Killian gallows (Pilling
Co.) in true elevated –vector suspension .
- External laryngeal counterpressure is 1st applied manually to determine its value for
improving exposure & then applied with silk tape that streached from the lower laryngeal
framework to the operating table , the magnitude of the pressure & vector of the force are
adjusted to optimize the exposure of the lesion & the anterior of the glottis .
- If Co2 laser used , both patient & endotraheal tube are protected in the appropriate fasion.
- An operating microscope fitted with 400 mm front lens is used to examine the glottal field
at 15X , 25X & 40X .
- The lesion is palpated with a blunt probe to assess the texture of the lesion & the depth of
deep tissue involvement .
- Submucosal infusion of saline & 1:10000 epinephrine into the superficial laminal propria
is used in the majority of glottal lesions , if the epithelial lesion has not invaded &/or
obliterated the superficial laminal propria , the infusion will hydrodissect under the lesion
& lift it from the vocal ligament .
- Pre-exisional knolodge about the depth of penteration of the lesion is important for
selecting instrumentation (cold vs laser) , as well as for adjusting the deep margin precisely
, both these factors are crucial to the patient's postoperative vocal outcome .
- During superficial glottal procedures , haemostasis is achieved by topical application of
epinephrine soaked cotton , for deeper lesions & supraglottal lesions , laser is used with
defocused spot or electrocoagulation is used .
- When surgery completed , any residual blood or secretions that are in the laryngeal
introitus or hypopharynx are suctioned & the larynx is sprayed with plain lidocaine to avoid
laryngo spasm during extubation .
- Postoperatively , the patient recieves humified room air & managed for
laryngopharyngeal reflux as necessary
- Antibiotics , steroids &/or analgesics are prescribed selectively according to surgeon
preference & extent of surgery .
- After vocal fold surgery , complete voice rest is adviced for 1 week & modified voice use
for 2 weeks .
- The patient has pre- & post-operative appointment with speech pathologist for objective
voice assessment & vocal hygiene discussion .
- Diet restrictions are instituted after wide-field supraglottil resections because of concern
of aspiration , swallowing therapy instituted as necessary .

Lecture notes in
Glottic surgery
- Select the glttoscope that provide the widest aperture for visualizing the surgical field , it
sometimes need hardwork to admit the largest size , but the use of smaller size which placed
easily may compromise the operative procedure by limiting the exposure & then detection
of the lesion & its extent & also limiting the manpulation of the instrument used for
retraction or excision .
- The use of smaller size laryngoscope is less important when laser is used because only one
hand instrument requires angulation .
- Many laryngologist believe that for most glottal pathology , precise micridissection is
optimally performed by exclusive use of cold instruments .
- In recent study , it was noted that 77% of 263 glottal procedures were done with cold
instruments alone , the thermal trauma of laser was found to be detrimental to delicate ,
lossely arranged elastic tissue of the superficial laminal propria .
- Laser optimally used in more vascular lesions because bleeding would oscure the
operative field & larger lesions that couldn't effectively retracted within the lumen of the
laryngoscope .
Supraglottil surgery
- It is undertaken fer less than glottal surgery .
- The surgical field is typically much larger , therefore requires different laryngoscopes &
hand instrumentation .
- Specially designed bivalved adustable supraglottiscope was designed to facillitate the
endoscopic surgery , this instrument was a modifiction of Steiner's laryngoscope .
- Larger & more sturdy hand instruments from premicroscope era can still purchased or
can obtained from the mediastinoscopy set .
- If the airway is stable , there are different primary functional concerns in endoscopic
surgery of the glottis & supraglottis .
- In the glottal surgery the most common functional concern is preservation of voice & in
the supraglottal surgery , it is swallowing .
- Microspot Co2 laser is very effective instrument for supraglottal surgery , thermally
induced fibrosis of the residual supraglottsl tissue results in benificial cicatricial scarring &
reestablishment of complete supraglottic swallowing valve .
Glottis (General comment)
- Endoscopic surgery mostly indicated for treatment of benign larngeal disorders .
- Most frequently the initial symptom of these disorders is hoarsness .
- Benign lesions typically occur in the vocal overdoers & seldomely occur in individuals
who are shy & reticent , so many of the former individual need pre-& post-operative voice
therapy , which is either to unload the habits that predispose the orginal lesion , or remove
the compensatory mechanism that produced as a result to the lesion , also the time of
deciding surgery is influenced by the speech therapy & its results .
- Preoperatively , we must do ;
1. Flexible & rigid (telescopic) laryngostroboscopy ; the flexible instrument is superior
in assessing the general laryngeal configration during sound production which is
necessary for assessing the magnitude of muscular tension accompanies the lesion ..
while the telescopic variant is superior in analyzing the anterior of the vocal folds ,
details of the lesion & the charcteristics of the mucosal wave oscillation .

Lecture notes in
2. Accoustic & Aerodynamic assessment ;they should be performed for normal & loud
voice task , aerodynamic efficiency (pressure , flow & resistance) is an excellent
indicator of the patient's work & effort of phonation .
The visual informations along with acoustic & aerodynamic data provide the surgeon with
objective informations about laryngeal sound production .
This assessment should be repeated after 1 month postoperatively to analyze the results
providing ;
1. valueable information to the surgeon for postoperative discussions with the patient
about what to expect from his voice .
2. information to the speech therapist who may instituting the speech therapy .
3. documentation of the results , as many patients may prone to new lesions .
- Pathophysiology ; the lesion along the glottal introitus impair the entrained oscillation by
creating stiffness in the diseased vocal fold & by preventing the smooth vocal fold edge
closure , these factors result in aerodynamic ineffecient glottic valve .
- Phonomicroscopical surgery ; usually designed to improve aerodynamic efficiency &
vocal quality by creating smooth vocal fold edge that is not excavated with overlying
epthelium that is flexible .
It requires maximal preservation of normal superficial laminal propria & epithelium ,
therefore assessing the microlaryers involvement of the lesion , this involving both high
magnification visual inspection as well as gentle retraction & palpation , given the choice
of sacrificing or destrurbing the normal superficial laminal propria or normal epithelium .
There is little difficulty in the growth & regeneration of the normal epithelium (regenerated
epithelium reflect the oscillation charcteristics of the underlying tissue) , as is seen after
cordectomy that is left to heal secondarily .
Furtherly noted that the normal superficial laminal propria doesn't regenerate if it has been
removed , postoperative stroboscopy reveal that if extensive dissection of superficial
laminal propria is performed to raise a wide micro flap , stiffness will be noted in the field
of dissection (wise to preserve the superficial laminal propria) .
Benign glottic lesions
Vocal polyps
It varies in size , the lesion may ne sessile or pedunculated .
It resulted from the trauma to the microvasculature of the superficial laminal propria , most
commonly found in the mid-musculo-memberanous region due to the aerodynamic induced
shearing forces on the microvasculature of the laminal propria are greatest at this region .
Subepithelial saline & epinephrine infusion enhance the precision of resection of the lesion ,
the sessile lesion can be removed by means of micrpflap & subepithelial resection of the
polyp component , while the pedunculated lesion can be removed by retraction &
amputation , care should be taken to palpate the component of the polyp that is in the
superficial laminal propria , so it is adequately excised .
Small (0-3mm) & medium (3-6mm) lesion can usually removed with greatest precision by
cold instruments , when these lesions are removed , small feeding vessel may be
encountered & the bleeding can be stoped after application of saline/epinephrine soaked
cotton , occasionally laser is necessary to microcaurrize the vessel .
Large sessile lesion (>6mm) best managed by microspot Co 2 laser (bleeding that occur after
incising the lesion with cold instruments will usually obscure the operative field) .

Lecture notes in
Vocal nodule
It is manifested visually in varied manner , there are dvergent opinions as to the value of
phonomicroscopical surgery ,
There is a little disagreement that these lesion are result of vocal abuse or inapproriate
vocal use , therefore irrespective of the decision to excise vocal nodules , virtually all these
individuals will require vocal therapy .
It is adviseable in most cases to use surgery as a secondary management , an intial trial of
vocal therapy should unload hyperfunctional behaviour & reduce the generalized edema of
the superficial laminal propria that typically accompanies these lesion .
Even the nodules not resolve & disappear visually , patients may satisfied with the quality
stamina of thier voice ,such that surgical intervention is not necessary .
If further improvement is desired by the patient & clear nodules are seen ,
phonomicrosurgical excision will benifit the patient during the postoperative patient
rehabilitation may prevent injury & reccurence .
Patient who are not typically surgical candidates will have what has been termed nodular
swelling , anatomically the vocal folds have fusiform swelling of the superficial laminal
propria that is usually in the midmusculomemberanous region , a discreet mass is not seen
on telescopic laryngostroboscopy .
Simillary to the techniques of vocal polyps , the vocal nodules can be excised either by
means of microflap or by amputation , cold instrumentation provide improved precision in
view of the small size of the lesions & the need for palpation during the procedure , the
subepithelial infusion technique must be used selectively , nodules that are less well defined
visually & by palpation may come obscured by infusion –induced distension of the
superficial laminal propria .
Subepithelial Cyst
It is variable in size , it arise in the superficial laminal propria , may attached to the vocal
ligaments &/or the epithelium basement memberane , small cyst also suspended freely
within the superficial laminal propria which can be confused with vocal nodules if visual
examination done without stoboscopy .
Stroboscopy reveal the charcteristic asymmetric disordered oscillation of the mucosa due to
the well circumscribed stiffness of the area of the cyst , a nodule may ne noticed in the
contralateral vocal cord .
It probably arise from the obstructed ducts within the superficial laminal propria , may
contain mucous or composed of an epithelial rest (simillar to cholesteatoma) .
Occasionally , small subepithelial mass that are thought preoperativel to be a cyst within
the superficial laminal propria are found at microsurgery to be a fibrous mass , this mass
usually firm to palpation & may be the result of old microvascular injury or rheumatoid
lesion .
The submucosal infusion technique is extermely helpful in well-defined cyst & firm mass
within the superficial laminal propria , the infusion can obscure the boundaries of small
cyst & lead to unnecessary dissection & trauma to the normal superficial laminal propria .
Masses within the superficial laminal propria should be resected with cold instruments with
few exceptions , the need for extremely delicate tangential dissection precludes effective use
of the Co2 laser , great care should be taken to minimally disturbe any normal superficial
laminal propria & epithelium , this approach will optimize the postoperative mucosal wave
oscillation & vocal quality .

Lecture notes in
Granulomas
Occur anywhere when there will be a traumatic disruption of the mucosa , but , mostly it
arise in the arytenoid region , these lesions arise in the patients who have
laryngopharyngeal reflux , reflux creates an environment of generalized mucositis &
traumatic distruption of the glottal epithelium predisposes to a hypertrophic inflammatory
reaction .
There are classical descriptions of posterior glottal granulomas that occur after
endotracheal intubation , in this instance , the posteriorly situated endotracheal tube has
disrupted the periartytenoid epithelium , these patients will frequently have simultaneous
endotracheal & N/G tubes , & the later predisposes to extraesophageal reflux .
The typical outpatient posterior glottal granuloma is the result of vocally induced trauma in
a reflux environment , these patients demonstrate vocal hyperfunction that causes high
impact oscillation forces of the artynoids during phonation .
Videolaryngoscopy reveal hyperfunction of the lateral cricoarytenoid that result in
hyperrotation of the arytenoids & abnormal concussion , this in turn leads to epithelial
trauma .
It is common to see a granuloma that show a bilobed configuration , this reflects the
confirmation of the contralateral arytenoid to closure pattern of the arytenoids during
phonation , these patients requires vocal therapy as adjunct to thier treatment , which
include antireflux management & possible microlaryngeal resection .
Granulomas are frequently exophytic with surprisingly narrow base , when they are small
or medium in size they may not impair glottal closure , however large one will result in a
substantial glottal chink in the musculomemberanous region that leads to further glottal
insufficiency during laryngeal sound production & increased vocal hyperfunction .
Phonomicrosurgical resection should be performed when behaviour modification &
medication have not led to resolution &/or there is concern about a neoplastic process , on
rare occasion , granuloma need excision due to the airway compromisation , espicially in
older patients , use of laser or cold instruments alone is individualized according to surgeon
preference & the anatomical charcteristics of the lesion .
The critical surgical principle is to remove the mass without disturbing the arytenoid
perichondrium , injecting the base of the granuloma with small amount of aqueous-based
steroids (methylprednisolone) may help to prevent recurrence .
Unloading vocal hyperfunction , a predisposing traumatic behaviour , can't be overstated ,
abusive vocal behavior is usually the culprit with recurrent , recalcitrant artynoid
granuloma , if the hyperfunctional activity of the lateral cricoartynoid is still observed , low
dose botulinum toxin (botox) can be used to chemically unload this closure pattern ,
adminstration of about 1.5 IU is good initial dose , based on the severity of the
hyperfunctional activity , one or both cords injected , the injection can be placed at the time
of the endoscopic exceision of the granuloma .
The botox should be directed toward the lateral cricoartyenoid rather than the
thyroarytenoid muscle , this will help to minimize the vocal insufficiency that the patient
must be prepared for .
Polypoid corditis (Reinke's edema)
It is manifestied as extensive swelling of the superficial laminal propria (Reinke's space) ,
the swelling usually situated on the superior surface of the musculomemberanous vocal fold

Lecture notes in
, it is pathogenisis multifactorial , Zeitels demonstrated that these patients typically smoke

extensively , have larygopharyngeal reflux & demonstrate vocal hyperfunction .
The swelling probably occurs from the increased aerodynamic pressure that drive vocal
fold mucosal oscillation in general environment of glottal mucositis which is secondary to
smoking & reflux .
Individuals with polypoid corditis have abnormally low-pitched voices (the mass loaded
folds oscillateat inordinately low frequency) , females are affected more than males &
undergo phonomicrosurgical management more frequently due to the greater discrepancy
from their normal foundmental voice frequency .
These individuals should discontinue smoking , having their reflux controlled & undergo
preoperative vocal therapy before any surgery .
The technique for the procedure is based on raising a thin epithelial microflap , after
incising the mucosa near the vestibular fold , microscissors are used for the initial incision
unless there is prominent subepithelial vascular injection , the gelatenous hypertrophid
superficial laminal propria should then be carefully countered & reduced to more normal
volume , this can be done by suctioning or by direct removal , great care must be taken to
not overreduce the superficial laminal propria which results in an inordinately stiff vocal
system , the vocal ligaments should never be visualized directly .
Overreduction of the superficial laminal propria can result in severely starined harsh voice
because these patient use high subglottial pressure to drive their floppy –mass loaded folds ,
vocally , it is preferable to leave larger fold than to create a visually pleasing small fold .
Once the superficial laminal propria has been reduced , the epithelium is redraped and
trimmed appropiately , if there is keratotic or dysplastic epithelium , it should be excised &
sent to histopathological analysis .
After an initial period of voice rest (10 days) , patient should receive vocal therapy &
should be mointored closely , preventing recurrence is dependent on modification of the
predisposing factors , especially smoking .
Respiratory papilloatosis
Patients most frequently complain from hoarsness , most commonly the glottal disease is
confind to the musculomemberanous region , although unusual to find extension into the
ventricle & subglottis .
Adults disease tend to be more plaque-like than juvenile variety , because the disease
confind to the epithelium , graet care should be taken to maximally preserve the underlying
superficial laminal propria .
In all cases , the initial occurrence & in most recurrent cases , the subepithelial infusion
technique with cold instruments dissection is best suited for this goal .. An en block
resection by means of microflap can frequently be accomplished , every attempt to perform
a narrow margin excision should be made , even if this includes serial procedures (to
preserve the integrity of the anterior commissure) .
Preliminary findings suggest that resecting this disease at the initial evaluation is likely to
be curative & that completely resecting previously recurrent disease will be curative in
approximately 30% of patients .
Premalignant vocal fold epithelium & early glottic cancer
It is initially smoking induced diseases , they are (geographically) frequently confind to the
superior ventricular surface of the vocal fold , this allowing for complete preservation of the
layered microstructures of the medial valving surface of the glottis .

Lecture notes in
Keratotic (white) lesions of the vocal folds constitutes most of the dysplastic lesions of the
glottis , the magnitude & appearance of keratosis don't belie the severity of the cellular
atypia or the presence of microinvasive carcinoma .
Erythroplasia (red lesion) typically contain carcinoma in situ & is an infrequent finding .
Isolated ulceration of the vocal fold in an immunocompetent smoking host who does not
have an infectious process typically reflects carcinoma .
Because any adequate treatment for T1 glottic cancer (endoscopic excision , transcervical
excision , radiation therapy) result in a cure rate of about 85-90% , a primary parameter by
which the clinician should judge the success of the treatment is the resulting quality of voice
Recently laryngologist have incorporated physiologic principles of laryngeal sound
production into the design of oncologic procedure , the surgeon , however must not foreget
that there are a variety of circumstances that might dictate a dofferent teratment approach
& that "no treatment exist to the exclusion of the others" .
A primary goal of the endoscopic management of the T1 glottic cancer is to narrow the
cancer-free margin & decrease patient morbidity while not altering the cure rate .
Phonomicrosurgical procedures can precisely accomodate the narrow deep resection
margin of the T1 focal fold cancer to the depth of invasion (invisible 3 rd dimension) , a small
amount of the extra tissue that is excised with the deep margin can have a profound effect
on vocal outcome , although it doesn't necessarily improve the cure rate , this is especially
so for lesions that are confind to the epithelium of that minimally invade the superficial
laminal propria .
Reinke's space infusion has helped to precisely determine the depth of invasion of T1 cancer
before committing to the depth of the excision , there are a number of patients with T1
cancers in whom the infusion has allowed preservation of all of vocal ligament & vocalis
muscle as well as part of the deep portion of the superficial laminal propria .
Endoscopic resection is associated with very low complication rate , which consist of minor
postoperative bleeding & granuloma formation , an en block excisional biopsy provide an
accurate diagnosis as well as an effective treatment & does so with minimal morbidity ,
whole-mount-section histopathological examination of the resected speciemen prevents
overtreatment or undertreatment of small glottic lesions .
All treatment options are preserved after endoscopic excision , including further transoral
excision , unlike radiotherapy , endoscopic esection treats only the lesion without ablating
the remaining normal glottial tissue , postradiotherapy videostroboscopic examination
suggest that both normal & cancerous tissue reflect fibrotic changes & impaired mucosal
oscillation , the use of radiotherapy for early cacers precludes its further use for tumor
recurrence or for new primaries & may even induce carcinogenesis in atypical epithelium .
The cost of endoscopic excision is significantly less than that for open laryngeal surgery or
irradiation because both of these latter procedures are typically preceded by a staging
endoscopy , also the patient sustain the increased burden of time & travel commitment
required in radiotherapy .
Disease in the anterior commissure
The anterior commissure tendon , or Broyle's ligament , is a confluence of the vocal
ligament , the thyroepiglottic ligament, the conus elasticus & the internal perichondruim of
the thyroid ala , there is a misconception that T1 cancers at the anterior commissure have a
great predilaction for understaging & that many of these lesions have occult invsion of the
thyroid cartilage (T4 stage) .

Lecture notes in
This is based on the misunderstanding that the anatomy of the dense anterior commissure
ligament is a less resilient tumor barrier than the adjacent thin thyroid perichondrium .
Kirchner has made clear that T1a & T1b carcinomas rarely transgress Broyle's ligament to
invade the thyroid cartilage .
Anterior commissure tumors that have thyroid cartilage invasion of the infrapetiole region
of the supraglottis (both T2 by surface staging criteria)
There has been divergent opinion as to whether cancer can be endoscopically eradicated
from the anterior commissure , the proscription imposed by some are based primarily on
the difficulty of obtaining adequate surgical exposure in this area .
The rate limiting factors for resection of early glottic cancer in the anterior commissure are
the true extent of the tumor & the endoscopic exposure required to encompass the lesion .
It required a great skill to excise the lesion without vaporizing the specimen , vaporizing
cancer without clear en block resection margin is inadequate surgical technique .
The problem with any surgical approach to the anterior commissure is that these
procedures disturbe the structural integrity of the anterior commissure & result in poor
voice .
Endoscopic exploration of the infrapetiole region of the supraglottis allows a definetive
determination about whether a presumed T1 lesion exhibits cartilage invasion (T4 , Rx by
open surgery) , this procedure facilitates precise staging (without disarticulating Broyle's
ligament) , commensurate management & optimal posttreatment voice quality .
Endoscopic technique
The goal of the treatment of an isolated T1 lesion of the musculomemberanous vocal fold is
eradication of the disease with maximal preservation of the normal layered microstructure .
This approach results in an optional postoperative voice without compromising oncological
cure , there are four basic procedures that are based on the depth of excision ;
1. Dissection ust deep to the epithelial nasement membrane & superficial to the lamina
properia for atypical epithelium & microinvasive cancer .
2. Dissection within the lamina properia of microinvasive cancer that not attached to
the vocal ligament .
3. Dissection between the deep lamina properia (vocal ligament) & the vocalis muscle
for lesions that attached to the ligament , but not through it .
4. Dissection within the thyroartynoid muscle for lesions penterating the vocal ligament
& invading the vocalis muscle , this approach can be fine-tuned further by
performing partial resections of any layered microstructure , the speciemen always
oriented for histological analysis , & frozen section margin assessment is used
selectively to verify a complete excision .
If dissection is performed in the superficial laminal propria , cold instruments facilitate
precise tangential dissection around the curving vocal fold , this allows maximal
preservation of the superficial laminal propria & enhance the pliability of the regenerating
epithelium .
Dissection between the vocal ligament & the vocalis muscle can be performed equally well
with cold instruments alone or with assisstance by laser .
Dissection through the muscle is perrformed most precisely with Co2 laser which allows
improved visualization because of its hemostatic cut cutting properties .

Lecture notes in
In addition to improving preexicisional assessment of lesion depth , subepithelial

saline/epinephrine infusion into Reinke's space assisst the surgeon's technical excution of
the surgery in a number of ways ;
1. the infusion facilitate mucosal incisions by improving visulization of the lateral
border of the lesion & by distending the superficial laminal propria , so that the
overlying epithelium is under tension .
2. the infusion also increases the depth of the superficial laminal propria which
facilitate less traumatic dissection in this layer & leads to regenerated epithelium
that is more flexible .
3. the epinephrine & hydrostatic pressure of the infusion vasoconstrict the
microvasculature in the superficial laminal propria & this improve visualization &
precise dissection .
4. if laser used , the saline acts as a heat sink which decrease thermal trauma to the
normal vocal fold tissue .
Vocal outcome after endoscopic resection of the musculomemberanous region
We can preciesely accomodate a microcontrolled excision to the three dimensional
charcteristics of the vocal cord cancer , in this approach , unlike radiation , we avoid
trauma to the contralateral fold during treatment of unilateral lesion , as expected ,
increasing the magnitude of the resection , especially depth , leads to deteriorating the
vocal function , therefore , a graded resection is suggested .
The mucosal microflap technique that is useful for resection of epithelial atypia &
microinvasive cancer can sometimes be confind to the superior surface of the vocal cord ,
after reepithelization , typically the patient can comfortably increase subglottic driving
pressures to achieve a perceptually & objectively measured normal voice at conversational
levels , maximal range task reveal some mild limitation of the frequency variation &
loudness capability , these vocal findings show mild progression in simillar pattern with
extension of the resection to the medial vocalizing surface of the vocal fold .
When surgical dissection limited to the superficial laminal propria in one fold , perceptual
assessment of resulting voice is usually normal , stroboscopy reveals mild impairment of the
mucosal wave propogation with regard to both ampilitude & magnitude wherever there has
been dissection in the superficial laminal propria .
As the deep resection margin extends to include the vocal ligament , there isfurther acoustic
, aerodynamic & stroboscopic impairment .
When the superficial laminal propria is excised as a component of cancer resection , the
regenerated epithelial surface is adherent to the underlying body of the vocal cord , this
results is unavoidable stiffness in the regenerated epithilium .
We have not seen evidence that pliable superficial laminal propria regenerate after removal
in the way that epithelium does , however , after resection of the vocal fold epithelium &
underlying laminal propria , the healed neocord is usually smooth & straight & glottal
closure is usually normal .
Vocal limitation may still not be perceptable at conversational levels in some patients if
glottal closure is complete , obvious hoarsness usually observed when complete glottal
closure doesn't occur because of tissue loss & resulting vocal edge excavation .
When a significant amount of vocalis muscle is removed as part of the deep margin , the
healed neocord is usually concave , the excavated neocord is result in incomplete glottal

Lecture notes in
closure during phonation , this lead to a stiff , leaking glottal valve & hoarse , disordered
voice , as the depth of an excision leads to valvular incompetence of the glottis , there is ;
1. increased acoustic instability (jitter & shimmer) .
2. increased subglottic pressure & flow .
3. increased supraglottal muscle strain patterns .
Stroboscopy reveals no substantive mucosal wave oscillation , but rather a mass vibration
of the stiff neocord body .
Vocal outcome after endoscopic resection of the anterior commissure
The resulting configration of the glottal valve reflects the magnitude & location of the soft
tissue that is excised , there has not been substantive information regarding the vocal
results after these varied procedures .
Visually the glottal aperature is smaller & accompained by a web (s.t.) , glottal closure can
be incomplete & there is often evidence of the supraglottal strain pattern .
Stroboscopy reveal stiffness wherever the superficial laminal propria has been disturbed ,
perceptually the voice is strained & hoarse with air leakage , the patients have some
difficulty with pitch variation & modulation , this finding of instability are confirmed by
acoustic measurements that reveal increased jitter & shimmer with normal & loud voice ,
the foundmental frequency is usually elevated with restricted dynamic range , the stiffer ,
smaller glottal valve require elevated subglottal driving pressure that is accompained by
elevated airflow .
Generally , voice quality after these operation is disappointing , although serviceable , if the
T1 diagnosis is accurate , the voice result after irradiation is probably superior to that
results from any type of surgical excision to this small volume , soft tissue disease .
It is empirical that significant transmural alteration to the anatomical insertion of both
cords results in a severely disorderd voice .
Although there is certain indication for endoscopic surgery such as previous irradiation
(with minimal recurrence or new primary disease) & patient choice .
Benign supraglottal diseases
The microspot Co2 laser is a precise cutting & vaporizing instrumnt for the use in the
supraglottis , the most common lesion here is papilomatosis , these lesion managed quite
well with microspot laser because mild thermal trauma in the supraglottis doesn't result in a
substantive changes in the laryngeal function .
Laser vestibular fold resection can be performed to marsupilize saccular cysts or to
improve exposure of the superior surface of the true cords , valecular cysts are not
infrequently noticed in examination & the larger ones are sometimes resected because of
suspicion of neoplasia or because they cause throat discomfort .
Large fibroepithelial polyps that ball valve into the airway are occasionally encountered ,
they usually arise from a narrow stalk & are easily resected .
Chronic odema after irradiation that not respond to medical management can often ne
vaporized to avoid a tracheostomy .
On rare occasion , Sarcoid is manifested as a mass in the epiglottis & can be resected with
little difficulty , vascular malformations are better managed with Nd-YAG laser .
Cancer of the supraglottis
At the early 20 th century direct laryngoscopic resection of supraglottic cancer described by
the use of tubed laryngoscope (by Jackson) & punch biopsy forceps for resecting
suprahyoid epiglottic cancer , the lesion was resected by cutting around the lesion with the

Lecture notes in
punch , & if the tissue specimen with the punch were without cancer , the resection was
considered curative .
In 1941 New et al performed transoral ablation of several supraglottic cancers (by the
means of diathermy) by the use of Lynch suspension laryngoscope which was a modification
of Killian system .
Vaughan 1 st describe the use of laser in the endoscopic resection of supraglottic Ca. at 1971
Curative endoscopic resection
It can performed as a single modality treatment , small lesions are excised during the
staging endoscopy & the resection is both diagnostic & therapuetic , therefore any further
treatment such as open surgery & irradiation become cost effective , with this endoscopic
approach there has not been significant loss of laryngeal function , most patients return to
normal diet within several days & no patient has required artificial airway intervention .
Transoral excision of supraglottic cancer as a single modality is successful when the lesions
are selected for small size & endoscopic accessability , small volume lesions that arise on
the suprahyoid epiglottis , aryepiglottic fold & the vestibular fold are amenable to en block
endoscopic resection because they are more perpendicular to the distal lumen of the
laryngoscope .
Specimen margins are ideally established through multiple section analysis of the en block
resected specimen rather than by means of frozen section , decisions about postoperative
radiotherapy & treatment of the necks should be based on pathological assessment of the
lesion , controlling the neck metastasis is critical for curing the patients .
Consideration should be given to the volume of the cancer , depth & location of its
penetration & the pattern of invasion , even small lesions of aryepiglottic fold & vestibular
fold will demonstrate early invasion of the paraglottic space , this place the neck at risk of
occult metastasis , in contrast early suprahyoid epiglottic cancer rarely invade the
preepiglottic space & rarely metastasize to the neck if there is no occult tongue base
invasion .
Endoscopic resection followed by radiotherpy
Transoral resection of lsrger supraglottic cancer followed by full course radiotherapy to the
primary site & the neck offers a more aggressive treatment approach for these indicviduals
who otherwise would have undergone radiotherapy as a sole treatment .
The endoscopic resection is a neoadjuvant therapy with a histopatholpgically controlled
results , this approach stresses laryngeal function preservation rather than organ
preservation .
These endoscopic supraglottic resections are considered excisional biopsies because
margins are frequently close & the deep compartments are not excised completely .
The patient however has no clinical evidence of cancer they commence radiotherapy , the
success of gaining a clear margins on these excisional biopsies is based on the typical
pattern of invasion ,which is broad & pushing with psuedocapsule (arise fro the epiglottis
perichondrium & the quadrangular memberane) .
Surgical technique
Lesions that are larger & those arising in the infrahyoid epiglottis & upper vocal fold are
more difficult to resect transorally because the visualized tangentially .
The surgeon must decide whether the neoplasm will be excised en block or in a piecemeal
fashion , the phylosophy of endoscopic en block excision maintains a more standard

Lecture notes in
surgical oncologic approach , however , larger lesions gradually fill the laryngoscope
lumen as they are mobilized , this make the en block excision technichally difficult .
With larger lesion , some prefer to excise in piecemeal fashion which make the operation
easier , also transecting the lesion facilitate the precise assessment of the depth of invasion ,
but also noticed an increased rate of local , regional & distant failure .
Laryngeal function after endoscopic excision
The airway & voice are not typically impaired by endoscopic supraglottic resection ,
however , the airway is improved when an exophytic lesion is excised , on occasion , a
patient may require a late tracheostomy secondary to late stenosis from severe
gastroesphageal reflux .
Laryngeal protective function may ne impaired temporarily depending on the extent of the
tissue excised , there has not been permenant swallowing impairment in patients who have
otherwise normal swallowing mechanism , previous impairment such as that sustained from
strock or previous head & neck surgery is a relative contraindication to any partial
resection .
Limited resections of the suprahyoid epiglottis , aryepiglottic fold or vestibular fold didn't
impair swallowing function because most of the sphenectric action of the supraglottis is
unaffected , but more extensive resections may predispose to aspiration that may last from
several days to 6 weeks depending on the magnitude of the resection .
Although patients require N/G feeding during this time , none have sustained an aspiraion
pneumonia during swallowing rehabilitation or from salivary soilage .
Favourable swallowing rehabilitation after resection occurs for several reasons ;
1. the superior laryngeal nerve are not disturbed proximal the larynx , therefore , the
neosupraglottis become fully sensate .
2. laryngeal elevation is not impaired either by disturbing the suprahyoid musculature
or by performing a tracheostomy .
3. the supraglottic defect heals completely by secondary fibrosis & reepithelization ,
there is a favourable cicaterization that results in a new supraglottic valve .
4. Hospitalization from this procedure usually last for 1 to 3 days .

Lecture notes in
Tracheostomy
Creation of a surgical opening in the trachea & converting the opening to a stoma on the
skin surface , it is indicated to :
A. Relief of upper airway obstruction , causes :
1. Congenital
a. Bilateral choanal atresia .
b. Laryngeal web or cyst .
c. Upper tracheal stenosis .
d. Tracheo-oesophageal anomalies .
2. Traumatic
a. External ; blow on the larynx or gun shot or cut throat .
b. Internal ; inhalation of steam or irritant fumes , forign bodies , or swallowing of
corrosives .
3. Infections
a. Acute laryngo-tracheo-bronchitis .
b. Acute epiglottitis .
c. Diphtheria .
d. Ludwig's angina .
4. Tumors ; malignant tumors of the tongue , pharynx , larynx & upper trachea &
thyroid gland .
a. In advanced stage .
b. Oedema from radiotherapy causing respiratory embrasement .
c. As adjunct to surgery .
5. Other causes of glottic obstruction like haemophilia , angioneurotic oedema , ..etc .
6. Bilateral laryngeal nerve palsies
a. After thyroidectomy .
b. Bulbar palsies .
7. Cord fixation due to rheumatoid arthritis .
B. Protection of the tracheobronchial tree , in condition leading to :
 Inhalation of saliva , food , gastric contents or blood .
 Stagnation of bronchial secretions .
These conditions includes ;
1. Bulbar palsies .
2. Polyneuritis .
3. Tetanus .
4. Mysthania gravis .
5. Coma ; head injury , drug overdose , ..etc.
6. Cervical cord lesion & injuries .
7. Burns of the face & neck .
8. Multiple fractures of the mandible .
C. Treatment of conditions lead to respiratory insufficiency :
1. Pulmonary diseases ;
a. Chronic bronchitis & emphysema .
b. Post-operative pneumonia .
c. Any condition in A & B which may lead to respiratory insufficiency.
2. Severe chest injury (flial chest) .

Lecture notes in
3. Neuromuscular incoordination , causing condition leading to ;

a. Stagnation of bronchial secretion .
b. Need artificial or intermittent PPV .
Tracheostomy aids respiration by ;
1. Reducing the dead space by 50% .
2. Bypassing resistannce to air flow in the nose , mouth & glottis .
3. Easy toilet of bronchi .
4. Using PPV .
Procedure
- Anasthesia
Preferably GA with endotracheal tube , if not LA with lignocain infilteration , avoid
paratracheal injection because this may lead to recurrent laryngeal nerve paralysis , also
avoid intratracheal injection because it will lead to severe paroxysmal coughing which
may lead to turn the semiemergency operation into an absolute emergency procedure , for
elective operation GA almost always .
- Position
The head extended over a small sandbag under shoulders & held exactly in the sagital
plane , & the head is prevented from rolling by using head ring .
This position adapted to ;
1. Increase the distance between chin & the suprasternal notch .
2. To smooth out any redundant skin in the neck .
3. To bring the trachea & larync close to the skin surface & pull as much trachea as
possible into the operative site .
- Incision
Either midline vertical incision (paediatric & emergency procedures) or transverse in the
elective procedure (less scar) .
Advantages of the vertical incision in paediatric age group ;
1. It is in the line of trachea .
2. Less vascular .
3. Produce nearly the similar scar .
It begins from the level of the cricoid cartilage downward to the maniburium sterni using
the cricoid as a guide & feel with finger , avoid large dilated veins or dividing & clamping
them . The incision should be carried deep & including deep cervical fascia .
Horizontal incision about 2 cm from the lower border of the cricoid or 2 finger breadth
above the suprasternal notch .
- Operative steps ;
1. Midline separation of the strap muscles through the linea alba using a blunt scissors
(vertical separation) . In elective procedures all bleeding vessels should be ligated or
cauterized at this step .
After separation of the strap muscles , they held apart using retractors , then the
pretracheal fascia is identified .
2. Thyroid isthmus divided usually or may be separated & retracted superiorly or
inferiorly , but if retracted , the 1st change of the tracheostomy tube should be done by
the surgeon who did it .
The thyroid isthmus is good landmark for the site of the tracheal incison (2nd , 3 rd & 4th
tracheal rings) .

Lecture notes in
3. Trachea exposed & opened ; incison through the trachea either vertical (especially in
paediatric , because of less incidence of stenosis & less scarring & less airways
resistance) , or removal of circular disc cut out of the anterior tracheal wall at the
level of the 2nd , 3 rd & 4th tracheal rings & sometimes if large , incision required 5th
tracheal ring is involved .
Incision should be done from below upward after pulling the index finger of surgeon
into the cricoid cartlage & 1st tracheal ring as incising those structures lead to
subglottic stenosis .
Disadvantages of removal of piece of tracheal ring ;
a. Tracheal stenosis .
b. Delayed healing after removal of the tube .
c. Tracheo-cutaneous fistula , which need formal surgical repair .
4. Insertion of the tube ; the tracheostomy tube should have been previously selected &
the cuff checked for leaks before insertion .
Once the tube has been inserted into the trachea , the obturator is removed
immediately & blood & mucous aspirated from the tracheal lumen .
If any difficulty is experienced in introducing the tube , the following points may be
helpful ;
a. The incision of the trachea may need to be lengthened .
b. If the tube is metal one , the introducer should be properly in place , while if it is
platic one , the end can be compressed in an artery forceps & inserted through
the incision .
The anasthesist asked to withdraw the tube just proximal to the upper end of the
tracheal incision under the guidance of surgeon .
The tracheostomy tube inserted under direct vision & done in calm unhurried way
since the anasthesist still control the airway .
Once the tube inserted & the anasthetesist satisified that both lungs are being
ventilated , the endotracheal tube is fully withdrawn .
The tracheostomy tube is fixed in position by stiching it by silk suture to the skin in
both sides & by using the tape tied around the neck in flexion position to avoid
loosening when tied in extention .
5. Closure of the wound ; the wound then inspected for any bleeding & for proper
haemostasis , the wound loosely closed , for the fear of surgical emphysema .
Gauze pad surrounding the tube should be avoided as it may obscure signs of bleeding
& may even encourage surgical emphysema , as neck tissue become swellen , this is
advised for the 1st 24 hours .
Criteria for elective tracheostomy in patients having endotracheal tube in the RCU
1. With paralyzing disease & normal lungs , if the vital capacity falls less than 1/4th
ofnormal , or if with deep breathing , the patient can only count to 20 (not 60) .
2. With pulmonary diseases , if patient losses consciousness or PCo2 exceeds 70 mm Hg
3. With crushed chest , clinical judgement is usually sufficient , but Co 2 measurement is
valueable .
Criteria for emergency tracheostomy
1. Recession of the suprasternal notch & intercostals spaces .
2. Anxious , pale , sweating facies , cynosis indicate a late & grave stage .

Lecture notes in
Postoperative care
1. As soon as the patient arrive the ward , an x-ray of the chest & neck should be arranged
for 2 reasons ;
a. To confirm the the tip of the tube not so low that it impinges on carina or enter
the right main bronchus specially in paediatric age group .
b. To demonstrate surgical emphysema .
2. Monitoring of the patient , includes ; PR , RR & BP every 15 minutes until the patient
awake , alert & aware of the situation & then every hour for the 1st 24 hours .
3. Nursing , constant attention is essential for the 1 st 24 hours , nurse should provide
materials for the patient to write & bell to ask for assistance . Initially children feeding
is via the i.v. drip which is established at operation, but within few hours , they are able
to feed by mouth , hydration is also important to prevent tracheal crusting .
4. Position , the patient must be sitting upright in the bed .
5. Humidification , as the nose is bypassed , so the air came in contact with the trachea &
bronchi become dry which eventually lead to crustation & blockage of the tube , so
humidification is vital , this is done by the following ways ;
a. Special humidifier .
b. Mosturized gauze over the tube .
c. Instillation of normal salin or sodium bicarbonate at the rate of 1-2 ml/hr , help
to reduce crusting & aids clearance of secretions .
6. Suction , applied regularly , because the tube act as a forign body & stimulate the
formation of secretions , loss of cough reflex also lead to accumulation of secretion , in
addition the secretions are profuse in the 1st 24 hours .
No special time interval can be set & suction is required when indicated . Aspectic
technique should be followed , washing of hands , wearing gloves & using sterile &
disposable suction cathter . Suction done as follows ;
a. The cathter inserted without suction .
b. The negative pressure is exerted as the cathter is withdrawn .
The cathter size is important & its external diameter should be less than the half of the
internal diameter of the tracheostomy tube , if not hypoxia may occur . Each act of
suction should not exceed 10 seconds to avoid hypoxia .
7. Prevention of apneoa , in cases of longstanding obstruction , apneoa may follow
restoration of the airway , with lowering of PCo2 , Co 2 (5-7%) is given via a flowmeter
through the tracheostome if this occur .
8. Changing & care of the tube , in adult changing the tube for the 1st time should be done
at least after 36-48 hours postoperatively , at this time the tract will have become
established & the opening in the trachea will usually be readily found , it should be done
by surgeon who has performed the tracheostomy .
In paediatrics , it should be done at least one week after surgery & 1st change should be
done in operating room with availability of endotracheal tube , spare tracheostomy tube
& tracheal dilators .
Inner tube should be project 0.25 cm beyond the distal end of the outer tube to collect
mucous & prevent blockage of the outer tube , the inner tube is taken out & cleaned
whenever necessary , the outer tube must be held firmly while withdrawing the inner one
Cuffed tube need firm attachment of the cuff to prevent it overriding the end of the tube ,
the cuff should be adequate length & not inflated too much to avoid pressure necrosis of

Lecture notes in
the tracheal mucosa & periodic deflation (hourly for 2 minutes) , so low pressure high
volume cuffed tube is used .
9. Care of the wound , dressing is done , should be sterile & must be changed frequently
or more often if secretions are copicious as a soiled dressing is a bacterial reservoir &
can cause the wound to became infected .
The sutures used to stabilize the tracheostomy tube need to be cared for , the crust need
to be removed with hydrogen peroxide or salin soaks , the tape if used should be
changed when soiled .
10. Weaning & decanulation , this present no problem in adults , the tube is removed once
the patient can sleep a night with the tube corked , this is for short standing
tracheostomy . If the tracheostomy is longstanding "weeks , months or years" difficulty
may arise in decanulation , so careful assessment is mandatory before removal for
detection of any tracheal narrowing or granulation tissue around the stoma & above it .
So gradual reduction of the size of the tube until smaller size tube is crocked & left for
few days before the final removal , sometimes the wound may need to be surgically
closed .
Weaning & decanulation in children , especially in long standing tracheostomy , the
child should be assessed before decanulation , this includes ;
(1) Child should appear to be well & show no signs of aspiration during eating or
drinking .
(2) Temporary occlusion of the tube with finger permits respiration to continue
adequately through the glottis .
(3) Good voice or cry in the absence of valved tube .
(4) CT scan or MRI if possible taken during tube in & during extubation will
determine any narrowing of the trachea .
(5) Physiological assessment by using peak inspiratory flow through the
tracheostomy is compared with that through the mouth .
(6) Endoscopy is carried out & the larynx , trachea & bronchi are examined with
special attention to the site of original lesion & tracheal stoma .
Procedure of decanulation , two ways ;
(1) Most common is to remove the tube & allow the track to close down & heal ,
specially in short standing tracheostomy .
(2) Other way , is to excise the track & allow it to heal by primary intention .
During decanulation the child should be at hospital for a period of observation which is
about 2-3 days .Trials of decanulation should precede the final decanulation , this is
done either by using a fenestrated tube or small plastic tube allows adequate airway
around it , blocking it during the day , if well tolerated , then it should be continued at
night as long as there are enough qualified nursing staff to provide constant watch , if
there are still no problem during night , the tube is removed & the stoma is covered by
sterile dressing , then the child kept under observation for few days before discharged .
Before decanulation all the essential emergency equipment must be at the bed side .
Decanulation problems , they are ;
(1) Dead space , due to increased dead space , airway resistance will increased
because the child's airway are smaller than adult , this factor should be assessed
before decanulation , although it is doubtful whether they could be very
significant after decanulation .

Lecture notes in
(2) Tracheal narrowing above the stoma , this is most common problem of
decanulation , it caused by ;
a. Significant granulation tissue above the stoma , should be removed by
using endoscope before decanulation .
b. A flap or fibrous tissue or displaced anterior tracheal wall , this flap can
be sutured forwards or removed surgically .
c. The trachea may be weakened in the vicinity of the stoma by low grade
chondritis , so it lead to collapse of the trachea during inspiration .
d. Repeated interference with larynx , during periodic assessment &
decanulation , this lead to subglottic oedema .
(3) Repeated movement of the vocal cords due to loss of reflex abduction of the cords
during inspiration , practical experience show it has no real clinical significance
Surgical decanulation , here the tracheostomy tract is excised & the tracheal stoma is
examined under direct vision .
Endoscopy is performed prior to excision to confirm presence of any granulation tissue
& remove it . Suitable endotracheal tube introduced for GA , a horizontal , elliptical
incision is formed around the stoma & the island of skin grasped by tissue forceps .
The tract with its surrounding cuff of fibrous is freed down to the trachea with cutting
diathermy , it is important not to pull to much on the fibrous tract as the weakened
trachea may be tent upward & damaged when the track is incised horizontally at the
tracheal stoma . The tracheal lumen & the intralumenal endotracheal tube can now be
clearly seen & any visible granulation tissue or excessive fibrous tissue are excised .
A small triangular piece of anterior tracheal wall tissue about 2 mm long is now excised
from the superior border of the tracheal stoma , this piece is made up of fibrous tissue
which may displaced posteriorly into the tracheal lumen & it carries on its internal
surface the suprastomal granulation tissue .
Now using vicryl suture to reconstruct the tubular structure of the trachea at this level &
repeat Endoscopy to ensure no residual granulation tissue or displace anterior tracheal
wall . Excessive narrowing of the trachea by suturing should be avoided .
The wound then closed in layers , the endotracheal tube remain in the trachea after the
child is sedated & taken back to the ICU , the tube is removed after 24 hours to allow
the postoperative oedema to settle .
The child is observed for further 5 days in the ENT ward before suture removal & the
child discharged .
Emergency situations in tracheostomy
1. Obstruction , the most common cause of such airway obstruction is narrowing of the
lumen by crusted secretions , instillation of salin & frequent suction should clear this
problem .
2. Acute total obstruction , it may occur when ;
a. Trying to pass too long cathter .
b. Mucous plug .
c. Displaced tube .
d. Displaced cuff .
This condition is managed by placing the patient's neck in extended position , cuff
deflated , saline solution instilled in to the tracheostomy & suction attempted , if all

Lecture notes in
these failed , then remove the tube & reinsertion of another one or even endotracheal
tube if not possible when it difficult to insert the tracheostomy tube .
3. Accidental decanulation , causes ;
a. Severe bouts of coughing .
b. During chest physiotherapy .
c. During suction .
d. During change of the tracheostomy tube tapes .
In early postoperative period the tissue around the tracheostomy site are oedematous &
soft , so it is very difficult to locate the opening of the trachea , so accidental
decanulation can be prevented by suturing the tube in place ubtil the tract has developed
4. Haemorrhage , specially in the 1st 24 hours , causes ;
a. From wound edges .
b. Thyroid isthmus or thyroid gland .
c. Divided strap muscles .
d. Anterior jugular vein .
e. Brachiocephalic vein .
The wound must be opened & inspected in the theatre & any bleeding point should be
dealt by ligation or cautery .
Complications of tracheostomy
1. Immediate
a. Haemorrhage ; during operation bleeding either from the anterior jugular veins or
thyroid gland , it should be controlled by ligation or diathermy . If the bleeding is
profuse & difficult to control , digital pressure should be applied & wound extended
for further visualization .
b. Air embolism ; during surgery large neck veins may be opened & air sucked in
rapidly in right atrium , if not recognized it may cause temponade & death .
c. Apneoa ; due to rapid wash out of Co 2 & this managed by allowing the patient to
breath a mixture of 95% O2 & 5% Co2 .
d. Cardiac arrest ; caused by ;
(1) Excessive adrenaline production in anxious patient .
(2) Rapid rise of PH due to washing of Co2 .
(3) Hyperkalaemia due to respiratory alkalosis .
e. Local damage ;
(1) Due to extension of tracheal incision through the 1st ring or cricoid with
subsequent tracheal stenosis .
(2) Unilateral or bilateral vocal cord palsy from inadvertent cutting of recurrent
laryngeal nerve .
2. Intermediate
a. Dislodgement of the tube ; this is prevented by suturing the tube flanges to the neck
skin & tying the tube in flexion rather than extension of the neck .
b. Surgical emphysema ; causes ;
(1) Too tight closure of the subcutaneous tissue & skin around the stoma "most
common"
(2) Too large incision in the trachea .
(3) Depression of the superior flap of the trachea above the incision .
(4) Obstruction of the exist of air by glottic or pharyngeal obstruction .

Lecture notes in
(5) Partial obstruction of the tube which direct air into the soft tissue of the neck .
(6) Excessive coughing .
Usually present in the 1st 24 hours & it is self limiting & disappear around the 7th day
unless the precipitating factors persist , expansion of the soft tissue due to surgical
emphysema may increase the risk of dislodgement of the tube .
c. Pneumothorax & Pneumomediastinum ; occur due to injury to the apex of the lung
especially during LA in anxious , struggling , gasping patient with excessive cough ,
the dyspneoa in those patients is not improved & the CXR will confirm the diagnosis
& the chest tube should be done .
d. Scabs & crusts ; a tracheostomy alter the physiology of the inspired air from filtered
, warm & humidified to dry , cold air coming into direct contact with the trachea ,
this lead to formation of thick tenacious mucous scabs & crusts , if not carried it may
increase in size causing infection , obstruction , atelectasis & pneumonia .
So , humidification is vital for prevention , either by using steam tent or more simply
by installation of saline (15 drop/min) via a small bore cathter or instillation of 5
ml/hr of saline by syringe in the trachea .
e. Infections ; all tracheostomy wound become locally infected within hours of their
creation , prevention of infection by ;
(1) Local dressing applied around the tube to reduce pressure on the neck skin .
(2) Frequent changing of dressing as secretions & blood accumulate .
(3) Barrier cream to the skin help to reduce the risk of infection .
f. Tracheal necrosis ; causes ;
(1) Oversize tracheostomy tube .
(2) Improper curve of the tube .
(3) Impingement of the tip of the tube .
(4) Pressure of the cuff on the trachea .
Tracheal necrosis lead to ; ulceration , stenosis , tracheo-oesophageal fistula &
tracheo-arterial fistula .
Signs of necrosis are ; signs of bleeding , pain & obstruction .
Treated by ; eliminating the pressure factors , careful inspection of the ulcer , either
allowing the ulcer to heal by secondary intention or excise it & attempt primary
closure , also large ulcers , the great vessles at risk & need to be protected with a
muscle flap with withdrawal or change the position of ventilating approach .
g. Tracheo-arterial fistula ; occur in 0.4% , mortality rate 80-90% , signs , the so called
sentinel bleeding which if occur through fibroptic examination of the trachea
indicated . it caused by ;
(1) Improper positioning of the tube .
(2) Improper curve of the tube .
(3) Pressure of the cuff .
Warning signs is slight bleeding of the trachea at any time from 3rd day to 3rd week
before catastrophe .
h. Tracheo-oesophageal fistula ; two factors contributing to this fistula formation ,
which result from necrosis of the posterior tracheal wall & anterior oesophageal
wall , these factors are ;
(1) Over inflated or improperly fitting cuffed with an indwelling N/G tube in the
oesophagus .

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(2) Positive pressure ventilation .

Clinically the patient shows violent coughing during eating , chronic coughing
associated with swallowed saliva & air escaping through the hypopharynx .
Endoscopic examination is the best method to confirm the diagnosis , while contrast
study is not helpful because it can't differentiate between aspiration of contrast
through the fistula or aspiration in the larynx as a result from loss of swallowing
reflex . The best treatment is surgical closure .
i. Dysphagia ; cause ;
(1) Original causes of tracheostomy .
(2) Tethering of the larynx , so can't move during swallowing .
(3) Pressure of the inflated cuff on the oesophagus .
(4) Rarely , ulceration of the trache-oesophageal wall leading o fistula .
3. Late
a. Stenosis of the trachea ; may occur at the ; stoma , cuff site or tip of the tube , it
caused by ;
(1) Inflatable cuff .
(2) Improper placed incision lead to scar contracture .
(3) Repetitive incision .
(4) Tracheal resection & trauma .
(5) Tracheal infections or organic disease of the trachea .
b. Difficulty in decanulation ; occur specially in longstanding tracheostomy due to
suprastomal granulation tissue & fibrous mass , so patient need to be carefully
examined before the tube removal using Endoscopy & radiography , alos the
tracheal lumen need to be inspected directly .
This problem overcomed by graded reduction of the tube size until the patient is able
to breath through the glootis , then the smaller tube may be closed by plug for
several days before final removal .
Any granulation tissue or fibrous tissue masses may need to be removed surgically ,
if the wound is of long duration , closure of the stoma done surgically .
c. Tracheo-cutaneous fistula & scars ; most of the incision & tracheal wounds closed
by secondary intention , bur occasionally fistula persist especially in longstanding
tracheostomy , fistula causes tracheal secretions with sometimes irritant , disturbing
phonation & frequent infection & poor cosmoses .
The scar of tracheostomy incision become attached to the tracheal wall by fibrous
tissue & moves up & down during swallowing , most of fistulae heal spontaneously ,
but if persist >16 weeks , need surgical closure .
Tracheostomy tubes
Selection of the tube depend on the requirement of the operation & the postoperative care .
If patient need ventilator , so cuffed tube (plastic) is required with low pressure high volume
cuff system .
A fenestrated tube permit the passage of air upward through the glottis there by allowing
the patient to speak .
Criteria for the ideal tracheostomy tube are ;
1. Design of the tube should permit an optima airflow , which is favored by shorter
shaft , greater radius of curvature & a smooth inner surface .

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2. Material of the tube should be nontoxic , nonirritant & should passes minimal tissue
reactivity .
3. Tube should be comfortable , easy to clean & easy to change .
4. It must be easily connected to ventilation equipment .
5. It is advisable to put a chain restrainer which will prevent the chin of the child from
occluding the tube .
6. It is desired that the measurement of the tube were easily accessible & expressed
clearly .
Types of the tracheostomy tubes are ;
1. Metal tubes
Common principles are ; an inner tube , an obturator & an outer tube .
Inner tube slightly longer than the outer tube , so that crusts can collected on the
protruding end . Removal of the inner tube allowing the frequent cleansing of the
tube while the outer tube in place .
Disadvantages of this type ;
a. Doesn't have a cuff , therefore can't be used for artificial ventilation or
prevention of aspiration .
b. If it not fit properly , the end of the tube may erode the anterior tracheal wall .
The metal tube supplied a set , incomplete set should not be used .
Metal tubes like ; Silver-Jakson's , Durham's with adjustable flanges for very thick or
thin neck & Koenig's tube for extensive & low narrowing of the trachea …etc .
2. Non-metal tubes
Advantages are ;
a. They can be made with an inflatable cuff , so it can be connected to
respiratory machine & prevent aspiration .
b. Available also in non-cuffed tube .
c. They don't produce some degree of mechanical damage to the trachea .
Disadvantages are ;
a. Main disadvantage is the tracheal necrosis from pressure by the inflatable
cuff , so it is advisable to monitor the cuff & it should be deflated 5 min/hour .
b. Absence of the inner tube which make the cleansing more difficult than metal
tubes .
Examples of it ; Salpeker double cuff tube .

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Embryology and Anatomy

• Thyroid Gland: two pear-shaped lobes, isthmus (connect the left and right lobes), and a
pyramidal lobe (may present as a superior extension of the embryological thyroid duct)
• each parathyroid weighs 20–40 mg, the normal thyroid gland weighs approximately 20
gms
• Superior Parathyroids: most commonly located in the posterolateral aspect of the superior
pole, 1 cm above the intersection of the recurrent laryngeal nerve and the inferior thyroid
artery
• Inferior Parathyroids: more variable location, most commonly located 1–2 cm from the
entrance of the inferior thyroid artery into the lower thyroid pole (may also be associated
with the superior thymus)
• Berry’s ligament (lateral suspensory ligament): attaches thyroid lobes to the trachea
• C-cells (parafollicular cells): cells within thyroid gland that secrete calcitonin
Embryology
• Thyroid Embryology: endoderm between the first and second branchial arch on the floor
of pharynx (foramen cecum) invaginates around the fourth week and descends into
mesenchymal tissue along the path of the thyroid duct (anterior to the hyoid bone) forming
a ventral diverticulum that differentiates at the distal end into the thyroid anlage, the
proximal portion typically atrophies by the sixth week
• Parathyroid Embryology: the third dorsal branchial pouch . inferior parathyroids and
thymus; the fourth dorsal branchial pouch . superior parathyroids and C-cells of the thyroid
• Embryological Pathology: Athyreosis (rare), Ectopic Thyroid (may be found anywhere
along the thyroid duct from the tongue as a lingualthyroid to the sternal notch),
Thyroglossal Duct Cyst Supernumery Parathyroids, Aberrant Parathyroids (most common
location at the anterior superior mediastinum) Vasculature
• external carotid artery . superior thyroid artery . superior pole of the thyroid
• subclavian artery . thyrocervical trunk . inferior thyroid artery . lateral lobes of the
thyroid and the inferior and superior parathyroid arteries (superior parathyroid arteries
may also arise from superior thyroid artery)• aortic arch or innominate artery . thyroidea
ima artery . the
thyroid isthmus
• venous drainage from the superior, middle, inferior (largest) veins into
the internal jugular and innominate veins
Nerves
• Superior Laryngeal Nerve (SLN): the external branch (motor fibers) parallels the superior
thyroid artery and descends to innervate the cricothyroid muscle; the internal branch
parallels the superior thyroid artery then pierces the thyrohyoid membrane (may
anastomose with the sensory branch of the RLN to form the loop of Galen)
• Recurrent Laryngeal Nerve (RLN): ascends 1 cm lateral to the tracheoesophageal groove,
closely associates with the inferior thyroid artery, near the middle 1/3 of the gland the nerve
crosses posterior or superficial to the inferior thyroid artery, continues superior and medial
along the posterior thyroid capsule, then enters the larynx between the cricoid cartilage and
the inferior cornu of the thyroid cartilage (at the articulation)
Lymphatics

Lecture notes in
• isthmus and median lateral lobes . upward to the delphian (prelaryngeal), and digastric
nodes
• inferior lateral lobes . pretracheal and cervical nodes
Thyroid Hormone Physiology
Thyroid Hormone (TH) Synthesis and Release
• anterior pituitary secretes TSH . increases thyroid iodide uptake (stored in lumen)
• iodination of thyroglobulin forms monoiodotyrosine (MIT) and diiodotyrosine (DIT)
molecules (organification)
• MIT and DIT molecules link together to form triiodothyronine (T3) or thyroxine (T4),
stored within the “colloid”
• released into blood after endocytosis and fusion with lysosome to release T3 and T4 (T4 is
90% of thyroid output)
• Thyroid Hormone Transport: Thyroxine-Binding Globulin (TBG, made from the liver,
increased with increased estrogen and pregnancy, binds 75% of T4); Thyroxine Binding
Pre-Albumin (TBPA, binds 15% of T4); and Albumin (binds 5% of T4)
• liver, kidneys, muscle, and anterior pituitary convert T4 to T3 via 5’ monodeiodinase (T3
is four times more active than T4 and binds with higher affinity to TBG) and reverse T3
(inactive form)
Regulation
• Thyrotropin-Releasing Hormone (TRH): released from supraoptic and paraventricular
nuclei of hypothalamus (not affected by TH)
• Thyroid Stimulating Hormone (TSH): secreted by anterior pituitary, stimulates iodide
trapping, increases release of thyroid hormone, activates growth of thyroid gland (inhibited
by TH for negative feedback)
• Wolff-Chaikoff Effect: excess iodine inhibits thyroid hormone (usually temporary)
Thyroid Hormone Effects
• elevates metabolic rate (thermogenesis, increases oxygen consumption)
• essential for normal neural and skeletal development (stimulates
chondrocytes, bone reabsorption, growth of neuronal tissue)
• increases sympathetic activity (increases heart rate and contractility)
• releases steroid hormones
• stimulates erythropoiesis
Pharmacology
• Thinamides: Propylthiouracil (PTU), Methimazole (Tapazole), inhibits T3 conversion and
the oxidation and organification of iodine; may cause hepatitis, agranulocytosis,
parotiditis; Methimazole is contraindicated in pregnancy
• Iodine, Lugol’s solution: excess iodine inhibits thyroid hormone (Wolff-Chaikoff Effect);
contraindicated in rheumatoid arthritis
• Glucocorticoids: suppress the hypothalamic–pituitary–thyroid axis
• Lithium: inhibits thyroid hormone release; contraindicated in renal failure and
cardiovascular disease
• Propanolol, Metoprolol: (B-blockers) used to control the peripheral manifestation of
sympathetic overactivity (inhibits thyrotoxicosis)
Thyroid Function Tests
• Total T4: radioimmunoassay measures free and bound T4
• Free T4: measures unbound T4, more specific for hypo- and hyperthyroidism

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• TSH: radioimmunoassay measures TSH, most sensitive test for primary hypo- and
hyperthyroidism
• Total T3: radioimmunoassay measures free and bound T3, useful for toxic nodules and
toxic multinodular goiters (higher increase in T3 than T4)
• TRH Stimulation Test: measures TSH after infusion of TRH, tests pituitary secretion of
TSH and hypothalamic response
Thyroid function test results
Condition TBG Total T4 RT3U Free T4
Normal Normal Normal Normal Normal
Pregnant ↑ ↑ ↓ Normal
Liver/Renal disease ↓ ↓ ↑ Normal
Hyperthyroid Normal ↑ ↑ ↑
Hypothyroid Normal ↓ ↓ ↓
• Radioactive Iodide Uptake (RAIU): measures the percentage of radiolabeled iodine taken
up by the thyroid, assess metabolic status
• Calcitonin: elevated in medullary thyroid carcinoma
• Resin T3 Uptake (RT3U): measures the binding capacity of existing TBG, indirect
measurement of TBG, an increased RT3U suggests a decreased total TBG (pregnancy or
estrogen from oral contraceptives increases TBP and therefore increases total T4, however
will have a normal euthyroid state (normal free T4)
Calcium Physiology
• calcium is 46% ionized and 46% bound to albumin (H+ competes with protein binding of
calcium, therefore acidosis increases more ionized calcium)
• 99% of calcium is stored in bone
• Vitamin D: stimulates calcium and phosphate absorption in the intestine (minor effect of
bone reabsorption and kidney reabsorption)
• Parathyroid Hormone (PTH): increases serum calcium and decreases serum phosphate by
stimulating osteoclastic reabsorption of bone, calcium absorption in the kidney, vitamin D
production, and phosphate excretion
• Calcitonin: produced by parafollicular cells (C-cells), inhibits calcium reabsorption from
bone and increases kidney clearance of calcium and phosphate
Thyroid Nodules and Cysts
Evaluation of the Thyroid Nodule
History and Physical Exam
• Associated Symptoms: rate of growth of nodule, hoarseness, pain, dysphagia, symptoms of
hypo- or hyperthyroidism
• Contributing Factors: radiation exposure, family history of thyroid disorders
• Physical Exam: palpation of nodule (consistency, mobility, size, tenderness), cervical
adenopathy, vocal fold mobility (nasopharyngoscope), stridor
Fine Needle Aspiration (FNA)
• indicated to identify benign nodules, malignant nodules, metastasis, and lymphoma
• 1–10% false-negative, depending on size of needle, experience of pathologist and
technician
• fine needle biopsies are preferred over large-bore needles to reduce the risk of malignant
seeding and to allow for multiple biopsies

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• larger needle biopsies may be considered for failed fine needle aspiration
• Interpretation and Management
o requires adequate specimen and a well-trained pathologist
o cysts tend to reduce after aspiration (may be cystic degeneration in malignancy)
o Benign: consider observation
o Uniform Follicular Epithelium and Abundant Colloid: suggests nodular or
adenomatous goiters
o Inflammatory Cells: suggests thyroiditis
o Papillary Cells (psammoma bodies, giant cells): suggests papillary
o carcinoma since adenoma is exceedingly rare
o Follicular Cells: may be adenoma or carcinoma, requires a hemithyroidectomy to
examine architecture for differentiation
o (extracapsular spread, lymph or vascular invasion, or metastasis indicate
carcinoma)
o Amyloid Deposits (stained with Congo red): suggests medullary carcinoma
o Undifferentiated, Bizarre Cells: suggests anaplastic carcinoma
Thyroid Radionucleotide Studies/Scintigraphy
• Indications: to determine function of thyroid gland or nodule, identify ectopic thyroid
tissue (including retrosternal goiter, lingual thyroid, and metastasis), determine size, shape,
and symmetry of gland
• Radionucleotides
o 131I: high radiation burden, results available in 48–72 hours, tracer of choice to
evaluate metastasis, also used to induce local tissue damage for hyperthyroidism
o 123I: expensive, must be delivered daily, testing requires 2 visits at 4 and 24 hours
(shorter half-life)
o 99mTc pertechnetate: trapped by follicular cells, does not measure uptake, low dose
radiation, less expensive, image obtained in single visit within 30 minutes
• Interpretation and Management
o hypofunctioning (“cold”) nodules have a 5–20% malignancy rate, consider
lobectomy and isthmusectomy, decision of completion of thyroidectomy based on
accuracy of pathology (may consider a frozen section)
o hyperfunctioning (“hot”) nodules may be observed, 4% malignancy rate
Other Tests
• Screening Thyroid Function Tests: TSH, free T4
• Ultrasound: indicated to distinguish cysts, guide FNAs, and identify nonpalpable lesions
• CT/MRI: evaluates substernal goiter, nodal involvement, airway and vascular
displacement, tumor invasion
• Chest X-ray: metastasis work-up, tracheal displacement
Thyroid Cysts
Pathophysiology;Typically arises from degenerated nodules, may result from cystic
degeneration of malignancy
Symptoms and signs : smooth, round mass
Diagnosis : FNA, ultrasound, CT
Treatment: may observe for regression, fine needle aspirate relieves pain and acquires
cells for cytology, may consider lobectomy for recurrent cysts that are recalcitrant to
drainage or bloody aspirates

Lecture notes in
Thyroid Nodule
Ultrasound
Fine-Needle Aspiration Follicular Cells (Size & Number)
Nodules
Multiple
Single, Large (Low Risk)
Malignant Benign Cystic (>2cm)
Evacuate & reassess +/- U/S
Surgery U/S Follow
Cystic Surgery
Solid
No recurrence Recurrence
History
+ve family history of
Radioneuclide scan thyroid carcinoma
Follow Re-aspirate
+ve history of
radiotherapy
Surgery Follow Age and Gender
Hot Not Hot Physical exam.
Sclerosing agent Hardness , Fixation , LN
Laryngeal exam.
C-spine flexibility
Toxic Non-toxic T4 suppression Chvostic sign
No regression
Large Small Regression
I 131 or
Follow Continue T4 Surgery or Follow
surgery
. Flow Diagram of the evaluation of the solitary nodule.

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Euthyroid Goiter
Diffuse Colloid Goiter (Adenomatous Goiter, Multinodular Colloid Goiter)
• more common in women
• Pathophysiology: iodine deficiency cause TSH hypersecretion which stimulates chronic
thyroid hyperplasia and involution lead to multinodularity
• Toxic Nodular Goiter: variation of diffuse colloid goiter in which one nodule is
hyperfunctional resulting in hyperthyroidism
• Types
1. Endemic Goiter: iodine deficiency, extrinsic goitrogens (soybeans, lithium, iodides,
etc.)
2. Sporadic: uncertain etiology
• Symptoms & signs : multiple nodules of varying size, may present with compressive ,
stridor, dysphagia .
• Diagnosis: FNA of a prominent nodule, TFT to confirm euthyroid state (may be
hypothyroid), consider radionuclear scanning to evaluate functional status
• Treatment: iodine replacement (reverses goiter), hormonal suppression (controversial),
radioactive iodine therapy or surgical excision (subtotal thyroidectomy) may be considered
for cosmesis, decompression, concern of malignancy, or toxicosis
Mediastinal Goiter
• Pathophysiology: intrathoracic extension of thyroid gland (inferior extension is the path of
least resistance)
• Symptoms & signs : dyspnea, stridor, dysphagia, choking, superior vena cava syndrome
• Diagnosis: CT/MRI of neck and chest, radionuclear scanning
• Treatment: surgical excision, typically accessed from collar incision although a
sternotomy may be required
Hyperthyroid Disease
Symptoms
• Elevated Metabolic Rate: weight loss, fatigue, sweating, heat intolerance
• Increased Sympathetic Activity: palpitations, tachycardia, tremor
• Increased Protein Degradation: weakness, fine hair
• Neurologic Effects: increased deep tendon reflex, nervousness
• Reproductive Effects: abnormal menstrual cycle, decreased libido
Most Common Causes
• Graves’ Disease
• Multinodular Toxic Goiter
• Subacute Thyroiditis
• Exogenous from medications, iodine induced
• Uninodular Toxic Goiter
• Thyroid Cancer
• Pituitary tumors
Graves’ Disease
• Pathophysiology: thyroid receptor autoantibody (IgG) . stimulates glandular hyperplasia
via TSH receptor . goiter and increased T3 and T4 secretion
• Risks: radiation exposure, women (adolescence or 30-40), genetic disposition
• Histopathology: hyperplasia, increased colloid material, papillary projections

Lecture notes in
• Symptoms & signs: diffuse goiter, hyperthyroid symptoms (see above), infiltrate
dermopathy, exophthalmos (autoimmune . extraocular muscle deposition), blindness from
optic neuropathy, pre-tibial myxedema
• Diagnosis: thyroid-stimulating autoantibodies; elevated T3, T4, RAIU, and
thyroglobulins; decreased serum TSH; radioactive iodine scan reveals diffuse uptake
• Treatment;
• Propylthiouracil and Methimazole: (see above) may be considered for small goiter and
moderate disease
• Propanolol: (see above) may be supplemented for severe symptoms
• Radioactive Iodine (131I): indicated for more severe symptoms or failed medical
therapy; there is risk of hypothyroidism and is contraindicated in pregnancy
• Subtotal Thyroidectomy: indicated for failed medical therapy, pregnancy (especially in
second trimester), noncompliance, suspicious nonfunctioning (“cold”) nodule,
compressive symptoms
Management for Exophthalmos and Optic Neuropathy
• Ophthalmology evaluation
• artificial tears, taping retracted lids, protective eyewear
• if optic neuropathy persists despite medical therapy, a trial of corticosteroids is used for
2 weeks, if no improvement then surgical decompression is performed
• if exophthalmos persists after 6 months despite adequate therapy, radiation therapy or
surgical correction (orbital decompression, eyelid retraction release, and strabismus
surgery) is performed
Hypothyroid Disease
Symptoms
• Reduced Metabolic Rate: weight gain, cold intolerance, lethargy
• Decreased Sympathetic Activity: bradycardia, constipation
• Decreased Protein Degradation: weakness, fine hair, hoarseness
• Decreased Neurologic Response: slowed deep tendon reflex, depression
• Myxedema: nonpitting edema
• Creatinism: hypothyroidism in children; mental retardation, impaired physical growth,
macroglossia, protruberant abdomen
• Myxedema Coma: severe hypothyroidism; hypothermia, hypoglycemia, hypoventilation,
ileus, death; Treatment: parenteral levothyroxine, corticosteroids
Causes
• Radiation Therapy
• Chronic Thyroiditis
• Idiopathic Atrophy
• Hashimoto’s Thyroiditis
• Surgical or Radioiodine Ablation Therapies
• Secondary Hypothyroidism (pituitary or hypothalamic dysfunction)
• Iodine Deficiency
• Congenital Hypothyroidism: from maternal iodine expectorants, anti-thyroid medications,
and anti-thyroid antibodies
Thyroiditis
Subacute Thyroiditis (de Quervain’s)
• Pathophysiology: viral (mumps, Coxsackivirus) . decreased iodine

Lecture notes in
uptake (unlike Grave’s)

• Symptoms and signs: painful enlarged thyroid, self limiting, malaise, associated upper
respiratory infection
• Diagnosis: clinical history, TFT (may be transient hyperthyroid)
• Treatment: symptomatic therapy, observation
Hashimoto’s (Chronic Autoimmune Thyroiditis)
• associated with lymphoma, neoplasms, other autoimmune disease
• Pathophysiology: anti-thyroglobulin & anti-microsomal Ab . anti- TSH receptor .
transient hyperthyroid then hypothyroidism
• Risks: women, genetic susceptibility (HLA-DR3), Sjögren’s, DM, pernicious anemia
• Histopathology: fibrosis, lymphocytic infiltration
• Symptoms and signs: slowly enlarging goiter, painless
• Diagnosis: antimicrosomal antibodies, ESR, TFT (may have elevated, normal, or low
serum levels of T4 and TSH), FNA only for prominent nodules suspicious of carcinoma
or lymphoma that do not resolve with medical therapy)
• Treatment: long term thyroxine therapy with TFT monitoring; surgical excision for
compressive symptoms, suspicious nonfunctioning (“cold”) nodule, and pregnancy
Other Thyroiditis
• Painless Thyroiditis: like subacute (self-limiting hyperthyroid) but painless, common in
women postpartum
• Riedel’s Thyroiditis: thyroid fibrosis of unknown origin, “rock hard” thyroid, produces
local pressure and hypothyroidism; Treatment: hormone replacement, may consider
surgical release at isthmus
• Acute Supporative Thyroiditis: uncommon; Treatment: systemic antibiotics, consider
drainage for abscess formation
Clinical Differences Between Thyroiditis Conditions

Condition Subacute Hashimoto’s Riedel’s Suppurative
Incidence Common Common Rare Rare
Thyroid hormone hyper- then hyper- then hypothyroid -----
status hypothyroid hypothyroid
Onset Acute Gradual Gradual Rapid
Pain Common None Rare Common
Goiter Rare Common Hard gland Rare
Thyroid Neoplasia
Introduction
• High Risks
1. Age: males =41 years old, females =51 years old
2. Metastasis: presence of metastasis suggests malignancy
3. Extent: extrathyroidal, major capsular involvement
4. Size: nodule =5 cm
5. Other: radiation therapy, autoimmune thyroiditis, more common in women (children
and males have a higher risk of malignancy if presents with a thyroid nodule)
• Staging: I: thyroid only; II: nonfixed cervical node; III: fixed cervical
node; IV: metastasis

Lecture notes in
Adenomas
• 70% of solitary nodules
• follicular adenomas are the most common
• papillary adenomas are exceedingly rare
Papillary Carcinoma
• most common
• more common in young females
• Risks: radiation exposure, Gardner’s syndrome
• 30% palpable regional nodes (70% occult nodes)
• Diagnosis: FNA (see above)
• Histopathology: papillary and follicular structures, psammoma bodies (calcific),
intranuclear vacuoles (“Orphan Annie” eyes), multicentric
• Prognosis: 95% 5-year survival; poor prognostic indicators include tumors >1.5 cm or
extracapsular spread (cervical metastases have increased cervical recurrence rates
without affecting survival)
• Treatment
1. total or near total thyroidectomy (multicentric)
2. lobectomy and isthmusectomy (hemithyroidectomy) with
radioactive iodine (I131)may be considered if <1.5 cm or in younger patients
3. modified neck dissection (MND) for palpable nodes only (elective neck dissection
[END] has not been shown to improve survival)
4. thyroid suppression therapy
Follicular Carcinoma
• more common in the elderly and in females
• 50% hematogenous spread with distant metastasis (lymphatic spread rare)
• Diagnosis: requires open biopsy (unable to distinguish adenoma from carcinoma from
FNA)
• Histopathology: unifocal; extracapsular spread, invasion of lymphatics or vasculature,
or metastasis required for diagnosis
• Prognosis: 70–85% 5-year survival (20% with distant metastasis), worse prognosis for
angioinvasion, extracapsular spread
• Treatment
1. lobectomy and isthmusectomy (hemithyroidectomy) for low risk groups (may
consider intraoperative frozen section with completion total thyroidectomy (or
subtotal) for carcinoma)
2. subtotal or total thyroidectomy with radioactive iodine (I131) for high-risk groups
(angioinvasion, extracapsular spread)
3. lateral neck dissection for clinical nodes
4. thyroid suppression therapy
Hürthle Cell Tumors
• variation of follicular carcinoma (Hürthle cells predominate)
• difficult to distinguish adenoma from carcinoma (assume malignancy)
• Histopathology: Hürthle cells (large granular eosinophilic cells, trabecular pattern)
• Treatment: same as follicular carcinoma
Medullary Thyroid Carcinoma
• Pathophysiology: derived from parafollicular or C-cells (produce calcitonin)

Lecture notes in
• Types
1. Familial: 20%, Multiple Endocrine Neoplasia IIA/B , multicentric, bilateral
2. Sporadic: 80%, unifocal, unilateral, worse prognosis
• 50–60% lymph node involvement (late vascular involvement), approximately 8% distant
metastasis
• secretory granules of malignant C-cells release calcitonin and also secrete gastrin,
adrenocorticotropin hormone (ACTH), substance P, carcinoembryonic antigen (CEA),
and others
• Prognosis: 50–80% survival; worse prognosis if unilateral, sporadic type, younger
patient, or with metastasis
• Diagnosis: FNA or biopsy, elevated serum calcitonin, elevated CEA, presence of Ret-3
oncogene
• Histopathology: small round cells, amyloid stroma, may have calcification and fibrotic
strands
• Treatment
1. patient and family should be screened for MEN syndromes , examine for mucosal
neuromas, marfanoid habitus, serum calcium levels, urine catecholamines and
metabolites (vanillylmandelic acid, metanephrine)
2. total thyroidectomy with elective or modified neck dissection and medical thyroid
suppression therapy
3. screen with calcitonin levels to monitor for recurrence NOTE: radioactive iodine
(I131) is not effective because parafollicular cells do not take up I131
Multiple Endrocrine Neoplasms

MEN I MEN II MEN IIB/III
(Werner’s Syndrome) (Sipple Syndrome)
Parathyroid hyperplasia Medullary thyroid carcinoma Medullary thyroid carcinoma
Pancreatic tumors Pheochromocytoma Pheochromocytoma

(insulinomas , gastrinomas) Parathyroid hyperplasia Mucosal neuromas
Pituitary adenomas Marfanoid habitus
Anaplastic Carcinoma
• most commonly seen in the elderly
• Pathophysiology: may be from transformation of a well-differentiated carcinoma (may
find coexistent follicular or papillary carcinoma)
• uniformly fatal (5-year survival), often found with metastatic disease
• Histopathology: giant and spindle cells variation, undifferentiated “bizarre cells”
• Treatment: no adequate therapy, tracheotomy (protect airway), consider radiation and
chemotherapy, surgical resection may be considered (controversial)
Lymphoma
• associated with chronic lymphocytic thyroiditis and Hashimoto’s thyroiditis
• Diagnosis: difficult to distinguish lymphoma from chronic lymphocytic thyroiditis by
FNA alone, therefore a conformational open biopsy is required along with lymphoma
staging work-up

Lecture notes in
• Treatment: radiotherapy to neck and superior mediastinum, surgical excision considered

if tumor is confined to the thyroid
Thyroidectomy
Introduction
• preferable for patient to be euthyroid at time of surgery to avoid thyroid storm
• may consider preoperative potassium iodine to reduce vascularity of thyroid gland
Indications
• suspicion of malignancy
• compression symptoms (airway compromise, dysphagia)
• extension into mediastinum
• cosmesis
• failed medical management for Graves’ disease or hyperthyroidism
• pregnancy in Graves’ disease or Hashimoto’s Thyroiditis
• documented metastasis from thyroid carcinoma
Postoperative Complications
• Hematoma: may present as respiratory compromise from compressive effect; Treatment:
for respiratory distress immediately remove sutures and open wound, for large
hematomas control bleeding in operating room and place suction drains; for smaller
hematomas may be observed (place on antibiotics) and aspirate contents after
liquification (7–10 days)
• Vocal Fold Paralysis: RLN or SLN injury (SLN injury more common), prevent by
identifying nerve and avoiding ligation of inferior thyroid artery; Treatment: if
discovered interoperatively may consider primary anastomosis
• Transient or Permanent Hypocalcemia: if parathyroid is removed interoperatively, cut
into fragments and replace into adjacent muscle bed (sternocleidomastoid or
brachioradialis muscles), prevent by identifying glands and avoid ligation of inferior
thyroid arteries
• Thoracic Duct Injury: rare, results in chyle leak or fistula .
Thyroid Storm
• Etiology: surgery, trauma, childbirth, infection
• 50% mortality
• Symptoms and signs: fever, profuse sweating, tachycardia, nausea, abdominal pain,
tremors, restless, psychosis, coma, stupor
• Diagnosis: clinical history and exam
• Treatment:
1. immediate administration of inorganic iodine, propylthiouracil, propanolol, and
corticosteroids
2. supportive measures (glucose-containing IV fluids, cooling blanket, supplemental
oxygen, pyrogens)
3. intensive care admission (cardiac monitoring)
Hyperparathyroidism and Hypercalcemia
Types of Hyperparathyroidism
Primary Hyperparathyroidism
• elevated serum PTH
• Benign Adenoma: most common, single adenomatous gland.

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• Parathyroid Hyperplasia: associated with MEN I & IIA , familial hypocalciuric

hypercalcemia (autosomal dominant, increased renal calcium absorption), familial
hyperparathyroidism
• Carcinoma of the Parathyroid Gland: rare tumor, suspect with a palpable, gray mass,
vocal fold paralysis, or severe hypercalcemia; Treatment: en bloc resection including
thyroid lobectomy, monitor for recurrence with serial serum calcium levels
• must differentiate hyperparathyroidism from other causes of hypercalcemia Causes of
Hypercalcemia “CHIMPANZEES “
1. Calcium: exogenous
2. Hyperparathyroidism
3. Immobility
4. Metastasis to bone
5. Paget’s disease
6. Addison’s disease
7. Neoplasms: typically solid tumors (prostate, lung, colon, breast cancers)
8. Zollinger-Ellison syndrome (hypergastrinemia)
9. Excess: vitamin A or D, thiazides, lithium, estrogens, milk-alkali syndrome
10. Endocrine disorders: familial hypocalciuric hypercalcemia, hyperthyroidism,
pheochromocytomas
11. Sarcoidosis: also other granulomatous diseases (tuberculosis and berylliosis)
Secondary Hyperparathyroidism
• compensatory parathyroid hyperplasia secondary to malfunction of other organ system
• Causes: chronic renal disease, osteogenesis imperfecta, Paget’s disease, multiple
myeloma, bone metastasis, pituitary adenomas
Tertiary Hyperparathyroidism
• autonomous or irrepressible PTH production (parathyroid hyperplasia from secondary
parathyroidism, persistent hyperfunction despite correction)
• may have normal or low calcium
Evaluation
History and Physical
• Contributing Factors: family history of MEN disorders, radiation exposure
• “stones, bones, groans:” nephrolithiasis, osteitis fibrosa cystica, cholelithiasis
• Renal: polyuria, nephrolithiasis, nephrocalcinosis
• Gastrointestinal: constipation, dyspepsia, pancreatitis
• Musculoskeletal: muscle weakness, bone and joint pain (osteitis fibrosa cystica, calcific
tendonitis)
• Central Nervous System: slow mentation, fatigue, depression, poor memory, psychosis
• Cardiovascular: heartblock, hypertension
Diagnosis of Hyperparathyroidism
• Serum Electrolytes: ionized calcium (should be elevated at 3 different times), magnesium
(usually low), chloride (usually elevated from PTH induced bicarburia), and phosphate
(usually low)
• PTH levels: immunoradiometric assay
• Plain Films: brown tumors (osteitis fibrosis cystica), loss of lamina, resorption of
terminal phalanges, soft-tissue calcification, chest x-ray (granulomatous diseases or
metastasis), abdominal film (renal calculi)

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• Others: alkaline phosphatase (suggests bone disease), BUN/creatinine (renal function),

urine calcium (elevated in primary hyperparathyroidism, low levels with familial
hypocalciuric hypercalcemia), TFT, ACE levels (sarcoidosis), serum prolactin and gastrin
and urine catecholamines and metabolites (evaluate for MEN syndromes)
Localization
• Thallium-Technetium Subtraction: thallium uptake by thyroid and parathyroid,
technetium uptake by thyroid gland only, parathyroid glands identified by computer
subtraction; up to 90% accurate (less accurate for multiple gland hyperplasia, associated
thyroid disease, or small glands)
• High-resolution Ultrasound: can not locate mediastinal, retrotracheal, retroesophageal,
or small nodes
• Selective Venous Catheterization for PTH: reserved after exploration has failed
• CT/MRI: poor resolution, MRI more useful in identification of glands
Surgical Management
• surgery is the only definitive cure, avoids long-term complications of nephrocalcinosis
and bone demineralizations
• parathyroidectomy is indicated for symptomatic (bone pain, pathological fractures,
ectopic calcifications, intractable itching, etc) or persistently
elevated serum calcium
• Surgical Theory: must first remove pathologic gland (adenoma), hyperplasia versus
adenoma can not be distinguished grossly, therefore, must identify one “normal” gland to
evaluate hyperplasia, if other gland is also hyperplastic then assume parathyroid
hyperplasia and perform a subtotal (31/2 glands) or total parathyroidectomy with
autotransplantation, if gland is normal may either assume adenoma and terminate case or
further biopsy other contralateral glands (controversial)
• autotransplantation requires 20 mg into muscle bed (usually to forearm)
• pregnant women should undergo surgery during second trimester to avoid miscarriage
Complications
• Persistent Hypercalcemia: most commonly from missed adenoma (the most commonly
missed location is the posterior mediastinum), also from supernumerary gland, second
adenoma, failed recognition of parathyroid hyperplasia, incorrect diagnosis, and residual
adenoma
• Postoperative Hypocalcemia and Hypomagnesmia: usually temporary until replacement
of low bone calcium stores (increased risk with elevated alkaline phosphatase)
• Nerve Injury and Hematomas .
Medical Management of Hypercalcemia
• Saline Diuresis: restores extracellular fluid volume and promotes calcium excretion,
loop diuretics can also be given (thiazides impair calcium excretion)
• Biphosphonates: inhibit bone resorption, calcium serum levels reduce over several days
• Plicamycin: inhibits bone resorption; toxic side effects include thrombocytopenia,
hepatic dysfunction, and renal failure, therefore used only for malignant hypercalcemia
• Calcitonin: rapid onset (serum calcium falls within hours)
• Glucocorticoids: inhibit calcium intestinal absorption, may be effective for
hypercalcemia secondary to malignancy
• Gallium Nitrate: inhibits bone resorption, used for parathyroid carcinoma
• Hemodialysis: indicated for life-threatening conditions

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Radiography of the head & neck

Head & neck radiographes divided into ;
C. Conventional radiography ;
Best views that describe the skull bones & formina & its contents .
1. Transorbital view ; chin slightly flexed until the orbito-frontal line became
perpendicular to the film , this view magnifying the orbit & visualize the internal
auditory canal , lateral SCC , cochlea & vestibule .
2. Town's view ; AP projection with 30 otilt , allow comparison of the patient
pyramid & mastoid , identify petrus apex , internal auditory meatus , arcuate
eminence , mastoid antrum & mastoid process .
It evaluate the apical petrositis , acoustic neuroma , CPA tumors .
3. Water's view (occipitomental) ; chin-nose position .
PA –OMV show maxillary sinus , frontal sinus , ethmoidal sinus , best shown in
order , but not for sphenoid unless mouth opened .
Maxillofacial structures also shown ; nasal bones , frontal process of maxilla ,
zygomatic arch , mandible , others (superior orbital fissure , oblique orbital line ,
orbital rim & floor , foramina rotundum , formina oval) .
4. Lateral view ; best for sphenoid sinuses .
5. Submentovertical .
6. AP view & Lateral view for larynx & neck .
7. Facial bone injury ;
a. Nasal fracture by left & right lateral , Water's or superior axial view .
b. Facial bone series ; exagurated Town's view & Submentovertical view .
D. Cross sectional anatomy & imaging ; CT scan & MRI .

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Mass in the neck

Mass in the neck could arise from any tissue in the neck , so a variety of masses could be
identified
Anatomy
Cervical Triangles
The prominent landmarks of the neck are the hyoid bone, the thyroid cartilage, the trachea,
and the sternocleidomastoid muscles.
The sternocleidomastoid muscles divide each side of the neck into two major triangles,
anterior and posterior. The anterior triangle of the neck may be further delimited by the
strap muscles into the superior and inferior carotid triangles. The posterior triangles or
lateral triangles of the neck are formed by the posterior border of the sternocleidomastoid
muscle anteriorly, the clavicle inferiorly, and the anterior border of the trapezius
posteriorly.
The omohyoid muscle divides this triangle of the neck into a small inferior subclavian
triangle and a larger posterior occipital triangle. Deep to these muscles are the scalenes,
which form much of the muscle mass of the posterior and lateral portions of the neck. The
brachial plexus and subclavian artery course between the anterior and middle scalenes. The
subclavian vein courses anterior to the anterior scalene muscle.
Inferior Neck
In the inferior root of the neck, closely associated with the brachial plexus, are the paired
phrenic nerves that course medially to innervate the diaphragm.
Their origins are in the ventral rami of the cervical plexus of the third, fourth, and fifth
cervical nerve rootlets. The subclavian artery gives rise to the thyrocervical trunk.
Typically, the transverse cervical and suprascapular arteries course laterally over the
surface of the phrenic nerve. This relationship allows identification of these structures.
The vagus nerve lies further medial, contained within the carotid sheath. It shares the
sheath with the common, internal, and external carotid arteries and jugular vein. Posterior
to the carotid sheath lies the cervical sympathetic nerve.
On the surface of the carotid sheath lie the ansa hypoglossi nerves.
Lateral Neck
The dominant structure of the lateral cervical triangle is the spinal accessory nerve. It
emanates from the posterior border from the sternocleidomastoid muscle in close
association with the splay of nerves of the cervical sensory plexus.
It innervates the trapezius muscle on its inferior aspect in close association with the
transverse cervical artery or suprascapular artery, which variably supplies the trapezius
muscle.
Arterial Supply
The two common carotid arteries differ in length, because the right carotid usually arises
from the brachycephalic artery behind the sternoclavicular joint, and the left arises from the
arch of the aorta . Both arteries end by bifurcating into the internal and external carotid
arteries .
Over the lateral aspect of these arteries course the paired hypoglossal nerves. The internal
carotid artery is situated more posteriorly and has no branches.
The external carotid artery has branches and lies slightly anteriorly. This information can
be crucial in differentiating the two vessels for ligation. From its origin, the internal carotid
artery ascends directly toward the carotid canal and is crossed laterally, in ascending

Lecture notes in
order, by the hypoglossal nerve, occipital artery, posterior belly of the digastric and
associated stylohyoid muscle, and the posterior auricular artery.
Still higher and close to the base of the skull, the external carotid artery is situated
anterolateral to the internal carotid artery, and the stylopharyngeus muscle and associated
glossopharyngeal nerve, the pharyngeal branch of the vagus, and the stylohyoid ligament
all pass lateral to the internal carotid, between it and the external carotid artery.
After its origin in the carotid triangle, the external carotid artery passes upward, deep to
the posterior belly of the digastric and the stylohyoid muscle, crosses the styloglossus and
the stylopharyngeus muscles on their lateral side, and paralleling the ramus of the
mandible, passes into the deeper portion of the parotid gland. The external carotid artery
has branches to the superior thyroid, lingual, facial, ascending pharyngeal, occipital,
posterior auricular, maxillary, transverse facial, and superficial temporal arteries.
Venous Supply
The veins of the neck vary considerably in their connections with each other and in their
relative size . Those conducting blood downward from the head and face include the
external jugular, anterior jugular, internal jugular, and vertebral veins.
At the base of the neck are the suprascapular and transverse cervical veins and the
subclavian vein that unites with the internal jugular vein to form the brachycephalic or
innominate vein.
The subcutaneous veins and the external and anterior jugular veins are especially variable
in size and course.
Lymphatics
The lymphatic system of the neck consists of numerous lymph nodes intimately connected
with each other by lymphatic channels and the terminations of the thoracic and right
lymphatic ducts. The deep cervical lymph nodes are numerous and prominent, and many of
them are large. They form a chain embedded in the connective tissue of the carotid sheath.
Most are in that portion of the sheath around the internal jugular vein. They extend from the
base of the skull to the base of the neck. Two nodes that deserve particular attention are the
superior jugulodigastric node at the junction of the internal jugular vein and the posterior
belly of the digastric and the inferior jugulo-omohyoid node at the junction of that muscle
and the internal jugular vein. Block resections of the neck in a standard radical or modified
fashion rely on reproducible and consistent lymphatic drainage pathways for their success.
Viscera
The visceral structures of the neck include the thyroid and parathyroid glands, a portion of
the pharynx, the larynx, the trachea, the esophagus, and sometimes portions of the thymus .
The thyroid gland lies below and on the side of the thyroid cartilage covered anteriorly by
the infrahyoid muscles. A pyramidal lobe of the thyroid may extend superiorly from the
isthmus that connects the two lobes of the thyroid gland. On the posterior surface of the
thyroid gland lie the paired parathyroid glands. Successful parathyroid exploration and
thyroidectomy depend on accurate identification and preservation of the recurrent
laryngeal nerves and identification of the parathyroid glands. Landmarks that are used
successfully to locate these structures include the trachea, common carotid artery, and
inferior thyroid artery, which form a triangle within which the surgeon will usually find the
recurrent laryngeal nerve. Lymphatic drainage occurs along the peritracheal nodes. Venous
drainage similarly is directed inferiorly along the inferior thyroid veins.
The four or more parathyroid glands develop from the dorsal extremities of the third and
fourth pharyngeal pouches. As the thyroid and thymus and their associated parathyroid
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glands move caudally from the region in which they originate, the thymus normally
descends beyond the level at which the thyroid halts.
The parathyroids from the fourth pouches (i.e., superior parathyroid glands) are typically
located more cranially than the thyroid gland, and those derived from the third pouches
(i.e., inferior parathyroid glands) are typically freed from the thymus and become
associated with the thyroid gland at its lower pole.
Both sets of parathyroid glands are usually located on the posterior aspect of the lateral
lobes of the thyroid gland, but there are many exceptions. Because of the manner in which
they arise and migrate into the neck, the glands are often displaced and may be located in
other portions of the thyroid gland or lie above or below it.
We will divide the causes of mass in the neck according to the triangles of the neck &
according to its pathology .
So that mass could be congenital or acquired (which could be inflammatory " acute or
chronic" , neoplastic "benign or malignant" or miscellaneous) .
A. Midline masses
1. Congenital
a. Thyroglossal cyst
Embryology ; at the forth week of intrauterine life , the thyroid gland formed &
enlarged between the tuberculum impar of the posterior 1/3rd of the tongue , forming
bilobed diverticulum which moves downwards across the hyoid bone which
developed later on .
This forming the thyroglossal tract which atrophied & disappear at the 5 th – 10th
week , but caudal attachment may remains as the thyroglossal (pyramidal) lobe of
the thyroid gland .
Pathogenesis ;it account about 40% of all primary swellings in the neck , both sexes
affected equally .
The age presentation as follow ; 31.5% at the 1 st decade , 20.4% at the 2nd decade ,
13.5% at the 3rd decade & 34.6% at the forth decade & above .
The site ; 90% at the midline , 10% at one side (90% at left & 10% at right) , it is
either intralingual (2.1%) , suprahyoid (24.1%) , thyrohyoid (60.9%) , or
suprasternal (12.9%) .
The cyst may be formed on both sides of the hyoid bone as double bell lesion ,
multiple cysts may be found , or pseudocyst .
Sinus always secondary due to spontaneous rupture , or surgical drainage or after
lumpectomy operation , thyroid tissue found in 60% of cases in the cyst wall with
active thyroid function .
Differential diagnosis ;Dermoid cyst , infected LN , lipoma , minor salivary gland
tumor , sebaceous cyst , cartilaginous tumor , hypertrophic pyramidal lobe , lingual
thyroid & thyroid adenoma .
3. Painless . soft , mobile , fluctuant , tense mass in the midline or at the left
side , rehyoid or infrahyoid , contain viscous mucous .
4. Move with swallowing & deglutition & on protruding the tongue .
5. When infected , painful odynophagia & redness .
6. Tract , sometimes seen .
7. Death from respiratory obstruction from intralingual cyst .
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Diagnosis
1. Clinical presentation .
2. I131 scan for all suprahyoid & infrahyoid lump . 65-75% of lingual thyroid
there is no other thyroid tissue .
3. U/S , thyroid tissue .
Management
1. Sistrunk procedure
- Horizontal incision at the inferior border of the mass .
- Separation from the skin (s.t. difficult) , follow the tract (or tracts) .
- The hyoid body between the lesser horns is divided with Mayo scissors , the
core is removed in aline drawn at 45o to the body of hyoid (removal of a
core of tissue between the hyoid bone & the formen caecum) .
- Infected cyst , aspirated with antibiotics & later on removed by Sistrunk
procedure
2. Management of recurrence
If the hyoid bone is not removed , then 85% will reoccur . while if removed ,
the recurrence rate are 2-8% , operation , the body of the hyoid removed
along with the core . The possible causes of reoccurrence ;
a) Missing dumb-bell cyst in the back of the hyoid bone .
b) Ruptured cyst (thin walled) , causing pseudocyst .
c) Rupturing cyst leaving part of the wall .
d) Failing to realize that the tract may be multiple .
3. Management of sinus ; Sistrunk operation is performed with elipse of the skin
is removed around the sinus (so the incision is elliptical) .
Thyroglossal carcinoma ;of two types ;
(1) Thyroid elements (common) .
(2) Sequamous elements .
Seven percent have metastatic LN in the neck , the age is 6-81 years (average 39) ,
both sexes affected equally , in 85% papillary adenocarcinoma & 15% follicular
adenoma , adenocarcinoma & SCC .
Managed by Sistrunk operation with suppressant doses of thyroxin .
b. Dermoid cyst
28% of all midline masses , it is either epidermoid cyst or true dermoid cyst or
teratoid cyst.
They are midline swelling between the suprasternal notch & submental region ,
either cystic or solid mass .
It is painless swelling , not move with swallowing or tongue protrusion .
Managed by complete surgical excision .
2. Acquired
a. Ranula
It is an extravasations cyst arise from the obstructed & damaged sublingual (s.t.
submandibular gland) , it forms translucent bluish swelling in the floor of the mouth
at one side of the frenulum of the tongue (called frog belly) .
The wall composed of fibrous tissue capsule , if ruptured , it may reoccur .
Managed by removal of the sublingual gland with marsuplization of the cyst .
b. Ludwig's angina

Lecture notes in
Submandibular space infection , infection of the soft tissue of the floor of the mouth
due to ; mostly dental origin (80% of causes , the M.O. are E. coli & Strp. viridens)
or tonsillar infection or soft tissue infection .
It is firm brownish swelling in the submental & submandibular areas , tender , hot ,
associated with fever , trismus , dysphagia & even dyspnoea , the tongue is elevated
(causing respiratory obstruction) , & also there is excessive salivation .
Managed by antibiotics , delay the drainage as much as possible , if no response then
we do surgical drainage .
c. Perichondritis of the thyroid cartilage
Occur after trauma or radiotherapy , it is firm , tender swelling , associate with fever
, dysphagia , dyspnoea with bad odour .
Managed by antibiotics & steroids , if no response then total laryngectomy .
d. Thyroid gland carcinoma
It is of two types , thyroid element (common) & sequamous element .
7% have metastasis LN in the neck , the age is 6-81 years (average 39 years) , both
sexes affected equally .
85% papillary adenocarcinoma & 15% follicular adenoma , adenocarcinoma &
SCC .
Management by Sistrunk operation with suppression doses of thyroxin .
e. Chondroma & chondrosarcoma
Chondroma , M:F 4:1 , age 40-70 years , 70% in the cricoid cartilage ,
characterized hoarseness , dyspnoea & dysphagia & on examination there is hard
painless swelling of the cricoid or thyroid cartilage .
On I/L , smooth mass covered by intact mucosa .
The diagnosis , by x-ray which show peripheral or central calcification (coarse
irregular calcification , which is pathognomic) in 75% of cases , the biopsy not
preventative .
Managed by complete excision .
Chondrosarcoma , extremely rare , managed by total laryngectomy .
f. Advanced laryngeal tumor (cause widening of the laryngeal frame work) .
g. Thyroid isthmus swelling (painless , smooth , solid or cystic , move with deglutition) .
h. Lymph nodes
Especially prelaryngeal LN , it drains the larynx , also the submental LN which drain
the tip of the tongue & floor of the mouth .
i. Skin associated structures
(1) Boil & abscesses ; show all signs & symptoms of inflammation , it is tender , hot ,
red skin , swollen & fluctuant , managed by drainage with antibiotics according
to the C&S.
(2) Sebaceous cyst ; cystic swelling due to the obstruction of the sebaceous gland
duct , especially occur in the greasy skin .
It is cystic , painless , not tender (unless infected) , soft & with presence of
punctuation (characteristic) , managed by complete excision .
(3) Lipoma ; slowly growing tumor composed of fat cells , encapsulated or diffuse ,
they are among the commonest tumors .
It is lobulated , painless swelling , managed by excision if symptomatic .
(4) Actinomycosis ; managed by i.v. Benzyle pencillin with drainage .

Lecture notes in
(5) Melanoma ; pigmented navus or mole , it is benign tumor of the melanocytes ,

either junctional navus or dermal navus or compound (mixed) or lentigo (within
the basal layer of the epidermis) .
It is brown , flat or slightly raised , painless & s.t. contain hair . Managed by
simple excision with biopsy (indicated in ; cosmetic , repeated trauma &
malignant changes) .
(6) Neurofibromatosis ; arise from the connective tissue of the nerve sheath .
Local , smooth , firm swelling which may move in lateral direction but otherwise
fixed by nerve sheath , parasthesia & pain occur due to pressure on the affected
nerve .
Generalized , Von-Rechlinghausen's disease , associated with caffee du au laite
pigmentation on the skin .
Plexiform , occur in connection with 5 th cranial nerve branches .
Managed by local excision , s.t. with the affected nerve .
B. Lateral masses
1. Congenital
Branchial cyst ; also called lateral cervical cyst , present in the lateral part of the
anterior triangle at the junction in between the upper 1/3 rd & lower 2/3rd of the
sternomastoid muscle (deep to the muscle) some cysts have tract into the posterior
pillar . It orginate from the reminant of the 2nd pharyngeal pouch , it may be in the
midline .
Branchial sinus or pit open along the line between the tragus & the sternoclavicular
joint at the anterior border of the sternomastoid muscle . They reflect failure of
development to the 1st,2nd , 3 rd & 4th arches . Sinus may occur with internal opening
only .
Branchial fistula , rare , the pits demonstrated clinically &/or radiologicallyto have an
internal opening at the posterior pillar to form a fistula .
Embryology ; In 2 nd week embryo , there is 6 branchial arches 5 branchial clefts & 5
pharyngeal pouch . The 2nd arch grows downwards on its lateral side to meet the 5th
arch to form cervical sinus of His . In 6 week embryo , the branchial apparatus form
the ear , tongue , hyoid , larynx , tonsils & parathyroids .
The 1st arch "Meckel's cartilage"
- The upper part give malleus & incus , intermediate give amterior malleular
ligament & sphenomandibular ligament , lower give the mandible .
- The mesoderm give the tensor tympani . muscle of mastication , tensor palate ,
anterior belly of the digastric muscle .
- Its nerve is the mandibular branch of the trigeminal nerve , its artery degenerate ,
the remaining form the maxillary artery .
The 2nd arch "Hyoid arch , Reichert's cartilage"
- Give stapes , styloid process , stylohyoid ligament , lesser cornu of the hyoid ,
upper part of the hyoid body .
- Mesoderm ; platysma , stapedius muscle & tendon , muscle of facial expression ,
auricular muscle , posterior belly of diagastric & stylohyoid muscle .
- Nerve ; facial nerve (geniculate ganglion) . Artery ; degenerate (stapedial artery)
.
The 3rd arch "Glossopharyngeal artery"
- Cartilage bar ; greater cornu of the hyoid & lower part of the body .
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- Mesoderm ; stylopharyngeus muscle .

- Nerve ; Glossopharyngeal nerve . Artery ; common & internal carotid arteries .
The 4th arch "Thyroid arch"
- Cartilaginous part ; Thyroid & cuneiform cartilages .
- Mesoderm ; constrictor muscles , Cricothyroid muscle & cricopharyngeus muscle
.
- Nerve ; superior laryngeal nerve (vagus nerve) . Artery ; left (aorta) & right
(right subclavian artery) .
The 5th arch "6th arch ??"
- Cartilage bar ; cricoid , arytenoids & corniculate cartilages .
- Mesoderm ; intrinsic muscle of the larynx (except Cricothyroid)& trachea .
- Nerve ; recurrent laryngeal nerve (vagus nerve). Artery ; left (pulmonary trunck
give ductus arteriosus) & right (pulmonary trunck) .
Theories of origin
- Branchial apparatus theory ; the cyst though to be originate from the pharyngeal
pouches or branchial clefts or fusion of these 2 elements , the internal opening at
the upper part of the posterior pillar or supratonsillar recess (2nd branchial
pouch)
- The fistula & sinus ; the 2nd pouch pass between the external & internal carotid
artery , while the 3rd & 4th pouches unlikely pass over the hypoglossal nerve to
reach the skin to the internal opening below that of the 3rd , the 1st pouch cyst
usually under the parotid gland , the internal opening between bony &
cartilaginous meatus .
- Cervical sinus theory ; represented the remnants of cervical sinus of His which
formed by 2nd arch growing to meet the 5th one .
- Thymo-pharyngeal duct theory ; remnants of the original connection between the
thymus & the 3rd branchial pouch from which it originate .
- Inclusion theory ; the cyst epithelium arise from LN epithelium , this supported by
; (1) lymph tissue in the wall (2) most cysts have no internal opening (3) less
known in neonates & (4) peak at late ages .
Pathogenesis
- Cysts & fistula lined by stratified epithelium or occasionally by non-ciliated
epithelium , contain straw colored fluid containing cholesterol crystals & the
wall contains lymphoid tissue (80%) .
- Branchial sinus & fistula are present at birth , while the cyst at the 3rd decade .
- Site ; 60% on the left , 75% at the upper lateral neck , while 25% in the lower
neck , parotid , pharynx & posterior triangle .
Clinical features
(1) The peak incidence in the 2nd or 3rd decade .
(2) 60% male & 40% females .
(3) Presented as well demarcated cystic swelling (70% cystic & 30% firm) ,
continuous in 80% & intermittent in 20% , lies at the upper neck .
(4) Not move with swallowing .
(5) Painless (Painful in 30%) unless infected (15%) , pressure symptoms (5%) .
(6) Sometimes presented as infected mass with overlying skin erythema , the infection
either blood born or from the internal opening or chemical reaction within a
sequamous lined cyst .
Lecture notes in
Diagnosis
(1) Clinical examination & FNA .
(2) CT scan , sonogram for sinuses & fistulae .
(3) Carotid angiography for pulsatile swelling .
Lymphangioma , dermoid cyst , rhabdomyosarcoma , lipoma , T.B. , lymphoma ,
Schwannoma , metastatic LN , normal LN .
Management
(1) Cyst ; transverse incision , sternomastoid retracted , find the tract , pass between
the external & internal carotid artery . If infected , then aspiration & antibiotic ,
then excision .
(2) Sinus & fistula ; elliptical incision around the mouth of the sinus & follow the
tract (thick like medium size artery) .
(3) Periauricular pit ; the tract either go up toward the temporal region or junction
of the bony & cartilaginous external meatus or goes downward facial nerve .
Branchiogenic carcinoma ; Before it be clinical , 4 postulates had be attained ;
- Carcinoma should be demonstrated as a rising in the wall of the branchial cyst .
- It should a line running from just anterior to the tragus long the anterior border
of the sternomastoid , to the clavicle .
- Histology ; should be compatible with bronchial vestige .
- No other primary , in 5 years follow up .
Management is by radical neck dissection with postoperative radiotherapy or
excisional biopsy with postoperative radiotherapy .
2. Acquired
b. Skin & associated structures (as mention above) .
c. Neck spaces infections
(1) Retropharyngeal abscess ; in infants , it is due to lymphadenitis , while in adults ,
usually due to T.B. of cervical spine .
It presented with fever , dysphagia , swelling of the posterior pharyngeal wall &
in severe cases there is respiratory obstruction .
Managed by drainage & antibiotics (antiT.B. in adults) .
(2) Parapharyngeal space infection ; occur more in adults after tonsillitis or
infection of the 2 nd molar tooth .
Presented as fever , trismus , the tonsil pushed medially , but looks normal ,
swelling is tender & hot , especially at the posterior part of the middle 1/3 rd of the
sternomastoidmuscle .
Managed by drainage & antibiotics .
(3) Submandibular space infection "Ledwig's angina" ; 80% due to dental cause ,
spread to the submandibular triangle & floor of the mouth .
It present as swollen floor of the mouth , elevated tongue which may lead to
respiratory obstruction , also there is fever & trismus with excessive salivation ,
on examination firm brownish swelling in the submandibular triangle .
Management by antibiotics & postpond drainage as possible .
d. Lymph nodes
(1) Non-neoplastic LN enlargement
- Acute Lymphadenitis ; especially of the upper cervical LN due to infection
elsewhere in the head & neck (like cute tonsillitis) .
Lecture notes in
Presented as tender swelling medial to the angle of the mandible , fever &
odynophagia.
Management by antibiotics & analgesia .
- Chronic lymphadenitis ; either
Non-specific ; like chronic pharyngitis & chronic tonsillitis , managed by Rx the
underlying condition .
Or Specific ; like T.B. , brucellosis , AIDS , toxoplasmosis , IMN , sarcoidosis ,
actinomycosis & cat scratch disease .
T.B. lymphadenitis ; 50% reach the LN through the tonsils , the LN affected
mostly upper deep cervical LN then submandibular group .
Presented as painless , low grade fever & night sweating , 5% has cough & +ve
CXR Diagnosed by +ve tuberculin test & +ve biopsy (caseation) , management
by excisional biopsy with antiT.B. drugs for 9-12 months .
Sarcoidosis ; rarely affect the cervical LN alone , diagnosed by Kveim test &
biopsy (no caseation) , managed by steroids .
AIDS ; multiple LN , may be associated with parotid swelling , cutaneous & oral
lesions , hairly leukoplakia & candidiasis .
Diagnosed by +ve serological test for HIV .
Toxoplasmosis ; presented as generalized aching pain , fever , cough &
maculopapular rash with simple LAP , diagnosed by serology & biopsy ,
managed by dapson or methprime with folic acid .
Brucellosis ; present as drenching sweating , chills , fever , malaise , then
undulant fever , 20% has cervical LAP , diagnosed by brucella agglutinine test or
culture of the microorganism , managed by combination antibiotics for 6 weeks
(tetracycline & streptomycin) .
Infectious mononucleosis ; present as triad of fever , sore throat & LAP , when
give ampicilline , rash developed , it caused by EBV .
Diagnosed by monospot test , managed by supportive measures .
(2) Neoplastic LN enlargement
- Primary
Lymphoma ; either Hodgkin's or non-Hodgkin's , presented as weight loss ,
anorexia , low grade fever & s.t. cervical LAP (multiple , discrete & rubbery in
consistency , not tender) , diagnosis by FNA & excisional biopsy , managed by
chemoRx & radioRx .
Sarcoma ; rare & diagnosed by FNA or excisional biopsy , managed by RND .
Leukaemia ; usually associated with other signs of leukaemia like anemia ,
scattered echmosis , bleeding tendency & oropharyngeal manifestations .
Diagnosed by BM biopsy & CBP , managed by chemotherapy (infection by
antibiotics) .
- Secondary
Mostly in the deep cervical LN , the LN appear firm to hard , not tender , s.t. fixed
, even fungating tumor with involvement of the overlying skin , also signs &
symptoms of the primary tumor may be evident .
Diagnosis by FNA or frozen section biopsy , if +ve then either RND or
radiotherapy with management of the primary tumor if present .
e. Neurogenic tumors

Lecture notes in
(1) Schwannoma , nerve sheath tumor , either , neurofibroma (outer sheath of the
nerve) or neurolemmoma (inner sheath of the nerve) .
Presented as parapharyngeal mass , at the angle of the jaw , pushing the
sternomastoid muscle laterally , painless , ill defined , it has anterior border , but
no superior border , rarely cause nerve paralysis , it push the posterior pillar
anteriorly .
Diagnosis by CT , angiography & FNA . Managed by surgical excision (via
transparotid , transmandibular or transcervical approach) .
(2) Paraganglionic tumors , arise from the sympathetic cells , divided into ;
- Carotid body tumors ; arise in the bifurcation of the common carotid artery , 10%
with malignant transformation , 10% with distant metastasis , 10% with +ve
family history .
It present as parapharyngeal mass , F=M , pushing the pharyngeal wall medially
, with common cranial nerve palsies .
It is painless mass , hot , pulsatile , move side to side but not up & down ,
diagnosed by CT & angiography (Dx biopsy avoided) .
Managrd by surgical excision if techniqueally possible (when 2.5 cm of the
carotid artery free of tumor at the skull base) or by radiation which used when ;
poor risk patients , inoperable tumors , refuse surgery & malignant
transformation ,
- Glomus vagale ; arise from parapharyngeal tissue in the inferior vagus ganglion ,
it grows along the vagus nerve & distort the skull base causing bleeding , so
dissection extremely difficult .
It present as vagus nerve palsy , high neck mass under the sternomastoid muscle ,
painless , move side to side but not up & down . also it push the posterior pillar
anteriorly .
It diagnosed by CT with FNA & angiography . Managed by surgery if possible .
- Glomus tympanicum & jugulare (not present in the neck) .
(3) Postoperative neuroma ; results from the uncontrolled growth of the axons from
proximal stump of a nerve that has been cut , it attempt by the damaged nerve to
repair itself , presented as localized pain & tendeness , on palpation , electric
shock type sensation will result , also +ve history of neck surgery (like
parotidectomy or RND) .
f. Salivary glands masses
(1) Non-neoplastic
- Parotitis
Acute parotitis , either bacterial (due to dehydration , duct obstruction by stone ,
duct stenosis or LN inflammation of the gland) or viral (like mumps) , or fungal
(like candidiasis) .
Chronic parotitis ; like T.B , leprosy & sarcoidosis , presented as severe pain ,
fever , made worse by eating (& increased in size) , trismus , tender gland .
On examination , the oral cavity may show dental infection or on pressure on the
duct may reveal pus , diagnosis by investigations which shows leukocytosis , high
ESR , C&S for pus if present .
Managed by ; good oral hygiene, good nutrition , analgesia , local heat
application , antibiotic (clindamycine in acute infection) , if pus present then we

Lecture notes in
must drain it , if T.B use antiT.B. , also local adrenaline application on the
affected duct to decrease edema .
- Sialectasis ; the cause is unknown , it is similar to bronchiectasis , there is
progressive necrosis of alveoli which ultimately coalesce to form cysts , these
debris pass from the cyst to the duct causing obstruction leading to hypertrophy ,
stenosis & dilatation (s.t. stone in the submandibular gland & mud in the parotid
gland duct is the causative factor) , it presented as typical pain & swelling during
meal , this swelling can remain for minutes , hours or days , during swelling the
gland is painful , painless when the swelling decreased , no fever , 50% resolved
spontaneously especially in children .
Palpation of the duct of submandibular gland & floor of the mouth may reveal
stone (bimanual palpation) , the mouth of the duct may be oedematous .
Diagnosis by sialogram which may show stone in the duct , overfilled sialogram ,
stenosed duct normal or cystic or globular dilatation .
No Rx is need as the sialogram will wash the duct .
Sometimes peroral removal of the stone , marsuplization , duct dilatation ,
tympanic neuroectomy , removal of the submandibular gland & total
parotidectomy .
- Sjogren's syndrome ; an autoimmune multisystemic disease , but especially affect
the oral cavity , eyes & salivary apparatus .
It classified into ; primary , secondary (associated with connective tissue disease ,
50% Rh. arthritis) , benign lymphoepithelial lesion (prelymphoma) & aggressive
lymphocytic behaviour (pseudolymphoma) .
Presented , primary disease as xerostomia & xeroophthamia , while the
secondary present as xerostomia & xeroophthamia with connective tissue disease
.
The oral symptoms are , dry mouth , stomatitis , glossitis & dental caries .
The eye symptoms are ; keratoconjunctaitis sicca , F.B. sensation , burning
redness , itching with photosensitivity .
Only 20% have clinically palpable mass (in parotid) , there is also ; epistaxis &
crusting in the nose , otitis media with effusion , cough , tenacious sputum &
laryngitis .
The diagnosis by ;
i. Blood examination ; high ESR , high IgG , +ve Rh. factor.
ii. Specific immunological tests , the patient have HLA A1, B8 , DR3 > seven
times than other HLA types , also specific Ag called SSA & SSB for
Sjogren's syndrome
iii. Schirmer's test ; < 5 mm in 5 minutes is diagnostic .
iv. salivary flow rate , if flow rate < 0.5 ml /min , diagnostic for xerostomia .
(2) Neoplastic , either benign or malignant .

Lecture notes in
Table summary of D.Dx of neck mass

Lateral Midline
A. History
1. Age Newborn Sternomastoid tumor
Infancy Cystic hygroma Thyroglossal cyst
Childhood Lymphadenitis Sublingual dermoid
Adults Lymphadenitis Goiter
Salivary gland
Retivulosis
Caroyid body tumor
Older adults 2o malignancy Goiter
2. Duratiaon Days Salivary calculus Heamorrhage in
Lymphadenitis thyroid cyst
Weeks Chronic
Lymphadenitis
Months Chronic
Lymphadenitis
2o malignancy
Reticulosis
Years Branchial cyst Goiter
Ph. Pouch
3. Pain Inflammation Inflammation
Salivary calculus
4. Associated symptoms Regurgitation Ph. Pouch
Dysphagia 2o malignancy Goiter , particulary
Dyspnoea retrosternal or
Dysphonia malignant
Horner's syndrome
Facial n. lesion Parotid Ca.
Brachial plexus
lesion
Raynoid's Cervical rib
phenomenon Subclavian anurysm
Hemiparesis Carotid body tumor
Exopthalmus
Excessive sweating
Tremor Toxic goiter
Nervousness
Weight loss
B. Local examination
1. Number Multiple Lymphadenitis
Reticulosis
2o malignancy
2. Site Behind mandible Parotid gland
ramus Preauricular LN
Level of greater Tonsillar LN Subhyoid bursa
Cornu Branchial cyst Laryngocele
Lecture notes in
Behind chin Submental LN

Plunging ranula
Sublingual dermoid
Level of thyroid Carotid body tumor Goiter
cartilage Thyroglossal cyst
Supraclavicular Supraclavicular LN
Cervical rib
Subclavian anurysm
3. Size Large Hodgkin's Goiter
4. Shape May conform to an anatomical structures , e.g. thyroid ,
bifurcation of common carotid , parotid & submandibular gland
5. Surface Smooth with cysts , lipomata , LN .
Irregular & nodular with malignancy
6. Swallowing Midline swelling moving with swallowing are usually thyroid or
thyroglossal in origin
7. Tenderness Indicates inflammation , e.g. lymphadenitis , infected branchial
cyst , subacute thyroiditis ..etc
8. Temperature Indicates inflammation , but also may be present in highly
vascular tumors
9. Transillumination Of little value in neck , cystic hygromas are brilliantly
translucent , as are plunging ranula
10. Tethering To skin consider sebaceous cyst , T.B. , lymphadenitis
To muscle consider sternomastoid tumor & malignancy
To carotid artery consider carotid body tumor
11. Thrill Vascular goiter , Anurysm
12. Colour Reddened skin over lump indicates inflammation , consider
sebaceous cyst , lymphadenitis , branchial cyst , thyroglossal cyst
13. Consistency Hard – calcified LN , malignancy .
Tens – cyst
Rubbery – branchial cyst Hodgkin's disease
Soft – lipoma
14. Fluctuation Some cysts
15. Pulsation Expansile pusation may be eleciated with vascular goiters ,
subclavian or innominate anurysm
Transmitted pulsation will occur with lumps situated over major
vessels
16. Percussion Some laryngocele may be tympanatic
17. Protrusion of A thyroglossal cyst usually move upwards when the tongue is
tongue protruded as it attached by fibrous cord to the hyoid bone
18. Pressur over lump If lump disappears with pressure , consider pharyngeal pouch ,
laryngocele or branchial cyst with a pharyngeal communication
19. Auscultation A bruit may be heard over vascular goiter or over a stenotic
carotid artery bifurcation
20. Aspiration This may be considered if a cystic swelling is present
Pus – suppurative adenitis or cyst , Pus like – branchial cyst
Straw coloured or clear – cystic hygroma
Tooth-paste like – sebaceous cyst
Lecture notes in
Metastitic neck disease

Anatomy
The prominent landmarks of the neck are the hyoid bone, the thyroid cartilage, the trachea,
and the sternocleidomastoid muscles.
The sternocleidomastoid muscles divide each side of the neck into two major triangles,
anterior and posterior.
The anterior triangle of the neck may be further delimited by the strap muscles into the
superior and inferior carotid triangles.
The posterior triangles or lateral triangles of the neck are formed by the posterior border of
the sternocleidomastoid muscle anteriorly, the clavicle inferiorly, and the anterior border of
the trapezius posteriorly. The omohyoid muscle divides this triangle of the neck into a small
inferior subclavian triangle and a larger posterior occipital triangle. Deep to these muscles
are the scalenes, which form much of the muscle mass of the posterior and lateral portions
of the neck. The brachial plexus and subclavian artery course between the anterior and
middle scalenes. The subclavian vein courses anterior to the anterior scalene muscle.
The fascia of the neck ; several layers ;
- Superficial fascia , single layer of fibrofatty tissue which lies superficial to the platysma
muscle .
- Deep cervical fascia , vary in thickness from very thin layer to dense fibrous tissue (like
in carotid sheath) surrounding the various structures & allowing movement between
these structures , it is divided into ;
1. Outer investing layer ; surrounding the whole neck & split to surround the trapezius
& sternomastoid muscles , it also split to provide a fascial sheath for the parotid &
submandibular glands & to form the carotid sheath (which surround the internal &
external carotid artery , common carotid artery , internal jugular vien & vagus
nerve) . Also it surround the 9 th , 11th & 12th cranial nerves & the ansa hypoglossi
(which supply the strape mauslces) .
It attached ; superiorly to the superior nuchal line , mastoid process & the mandible
Inferiorly to the spine of the 7 th cervical vertebra , spine of acromion , clavicle &
manibrium .
2. Middle , visceral layer ; siurround the pharynx , larynx , oesophagus & trachea , the
thyroid & parathyroid gland (by the prevertebral fascia) .
3. Internal , prevertebral layer ; surround the deep muscles of the neck (erector sinae ,
levator scapula & 3 scalene muscles , the longus capitis & longus coli) , the
structures related to it are ; sympathetic trunk (superficial to the fascia) , branches of
the cervical plexus (deep to it & then pierce it) , pherenic nerve & brachial plexus
(deep to it) .
The lymphatic system of the head & neck ;
1. Waldeyer's internal ring ; lies within the pharynx at the skull base , it is circular
connection (collection) of lymphoid tissue including the adenoids , tubal & lingual
tonsils , palatine tonsils & posterior pharyngeal wall lymphoid tissue . It plays role
in the immunological development .
2. Waldeyer's external ring "superficial LN" ; they drain skin & subcutaneous tissue of
the scalp & face & neck , sinuses & oral cavity .

Lecture notes in
In the head ; occipital , postauricular , preauricular & buccal nodes . In the neck ;
superficial cervical , submandibular , submental & anterior cervical nodes , along
the external & anterior jugular viens .
3. Deep "cervical LN proper" ; the deeper tissue of the head & neck drain either
directly or indirectly through the superficial then to the deep . The levels of the deep
cervical LN as follows ;
- Level I ; submental & submandibular , bounded by the anterior belly of the
digastric muscle , the hyoid bone , the posterior belly of the digastric muscle & the
body of the mandible .
- Level II ; upper jugular or upper deep cervical , consist of LN located around the
upper 1/3rd of the internal jugular vien & adjacent spinal accessory nerve ,
extending from the level of the carotid bifurcation to the skull base , contain the
junctional & sometimes the jugulodigastric LN .
- Level III ; middle jugular , consist of LN around the middle 1/3rd of the internal
jugular vien , from the carotid bifurcation to the upper part of the cricoid cartilage
, contain the jugulo-omohyoid LN .
- Level IV ; lower jugular group , consist of LN located around the lower 1/3 rd of the
internal jugular vien , extending from the cricoid cartilage down to the clavicle ,
sometimes contain the jugulo-omohyoid LN .
- Level V ; posterior traiangle group , LN located along the lower half of the spinal
accessory nerve & the transverse cervical artery , includes supraclavicular LN .
- Level VI ; visceral or anterior compartement nodes , LN surround the midline
visceral structures , extending from the hyoid bone to the suprasternal notch . It
contains the parathyroid , paratracheal & pretracheal , perilaryngeal & precricoid
nodes .
- Level VII ; anterior mediastinal nodes .
Clinical staging of cervical metastasis
Nx : Regional nodes can not be assessed .
No : No regional LN metastasis .
N1 : Single ipsilateral LN less than 3 cm in diameter .
N2 a: Single ipsilateral LN > 3cm < 6cm .
b: Multiple ipsilateral nodes > 3cm < 6cm .
c: Bilateral or contralateral LN > 3cm < 6cm .
N3 : Nodes more than 6 cm in greatest diameter .
Assessment of cervical lymph nodes
1. History
The patient may be aware of the swelling in the neck or detected by the clinician .
2. Clinical examination
Should be from behind & don't miss any region , limitation of the examination ;
a. Retropharyngeal & parapharyngeal LN .
b. Supraclavicular LN .
c. Short neck patient .
There is structures in the neck may be mistaken for enlarged LN ; transverse procees of
atlas , submandibular gland & carotid bifurcation .
The false +ve & false –ve rate about 20-30% , also there is what called individual
variation .
3. Radiology
Lecture notes in
a. Computerized tomography (CT scan) ; 80% accuracy rate , CT criteria are ;

Size ; 1 cm & 1.5 cm in the jugulodigastric & submandibular nodes .
Rim enhancement following i.v. contrast .
Central necrosis .
Spherical in shape .
CT has the same sensitivity & specificity of the clinical examination , but when use in
conjucation with clinical examination , improve the sensitivity & specificity ,
especially for that difficult to be examined (short neck , those suspected carotid
artery & base of the skull metastasis , those tumors with high possibility of bilateral
disease "midline primary & extensive ipsilateral disease") .
b. MRI ; normal nodes are rarely demonstrated by MRI , but enlarged nodes & those
with central necrosis are well demonstrated .
With small nodes (less than 13 mm) prefer CT , for larger nodes use CT or MRI ,
both comparable , but MRI differentiate nodes from the surrounding tissue more
clearly than CT .
c. U/S ; size dependant , difficult to distinguish between the normal & metastatic nodes
, but it is more sensitive than examination to detect cervical LAP & it demonstrate
the relationship of these metastatic disease to the major vessels in the neck & used in
conjucation with FNA .
d. Radioisotopes ;
- Radionuclides scan & gamma camera with Gallium & Cobalt labeled bleomycin ,
do noty label the normal nodes , it has advantage over the CT & MRI , but LN to be
demonstrated must be > 2cm .
- Technetium – labeled DMSA .
- PET sacn (Positron Emission Tomography) .
4. FNA
Indicated in difficult situations like unknown primary with metastatic neck disease , -ve
results should be ignored . Histology reporting ;
- Prepare speciment on board .
- Report number of nodes .
- Report nodal levels .
- Is there any extracapsular spread ?
- Draw a diagram of results .
Management
The option in general either radiotherapy , surgery or both .
Treatment controversies are ;
1. Management of N0 .
2. Role of selective neck dissection in N1 disease .
3. Role of radiotherapy in the management of neck disease .
4. Role of radical neck dissection , modified radical neck dissection & extended radical
neck dissection .
5. Management of neck disease in patient has occult primary .
6. Management of suspected or established bilateral neck disease .
7. management of difficult , unmanageable or inoperable neck .
8. Role of slvage surgery in the management of the recurrent neck disease .
9. Role of chemotherapy .
- N0 , management options :
Lecture notes in
1. Elective , prophylactic neck dissection .

2. Elctive radiotherapy .
3. Elective neck investigations (CT & MRI) .
4. Adopt a policy of wait & see .
The risk factors for occul nodes are ; size , site & the histological grade of the primary
tumor , so if the primary tumor with high incidence of occult nodes (nasopharynx , tonsils
,tongue base , pyriform fossa & supraglottis) , then do prophylactic neck dissection or
elective radiotherapy according to the management of the primary tumor .
So arguments for elective neck surgery are ;
1. High incidence of occult neck metastasis .
2. If limited neck dissection has a low morbidity & mortality .
3. If the neck has to be entered to remove the primary lesion , it is better to perform
neck dissection at that time .
It is impossible to provide the clinical follow up necessary to detect the earliest conversion
of the neck from N0 to N1 . Allowing neck metastasis to develop increase the incidence of
distant metastasis , cure rate for neck dissection is decreased if the gland enlargement
occurs or multiple LN appear .
Arguments against th elective neck surgey are ;
1. Cure rates are no lower , if the surgeon waits for the neck to convert from N0 to N1
2. Careful clinical follow up will allow detection of the earliest conversion from N0 to
N1 .
3. Radiotherapy is as effective as neck dissection for nonpalpable disease .
4. Elective neck dissection results in a large number of unnecessary surgical
procedures associated with inevitable morbidity .
5. Elective neck dissection remove the barrier to spread of the disease &may have a
detrimental immunological effect .
Indications for elective neck management ;
1. Greater than 20-25% chance of subclinical neck disease .
2. Vigilant follow up is not impossible .
3. Clinical evaluation of the neck is difficult .
4. Surgery is being performed for access or reconstruction .
5. Imaging suggest possible occult nodal spread .
- N1 ; nodes less than 2 cm managed by radiotherapy , if the primary tumor managed as the
same , some surgeons prefer modified radical neck dissection which give better results
(not for extranodal spread)
- N2a & N2b ; managed by modified or radical neck dissection due to the high incidence of
extranodal spread it conjucated with radiotherapy (if there is extranodal spread in the
specimen) .
- N2c ; staged bilateral neck dissection or modified radical neck dissection on the least
invaded side .
- N3 ; incurable if invade the base of the skull or internal jugular vien or the brachial
plexus . In fixation to the skin it managed by surgical removal of the skin , pectoralis
major myocutaneous flap . While in invasion to the carotid artery , it managed by bypass
operation with resection .
Role of radiotherapy
Indications are ;
1. Palpable metastatic disease .
Lecture notes in
2. Post or pre-operative .
3. Prophylactically "N0" in tumors of high risk of occult metastasis .
4. Palliative treatment .
5. Recurrence ; nodal metastasis in unmanaged neck , nodal metastasis in managed
(surgery) neck & recurrence after combined management .
Once the disease is palpable in the neck , surgery is better than radiation , the cure of
radiation depends on ;
1. Size of the nodes (<3cm) .
2. Dose of radiation (6500 cGy) .
When the primary tumor treatment is radiotherapy , then we prefer it as management to the
neck metastasis . The use of high dose radiation (5000-6000 cGy) postoperatively is better
than surgery alone or surgery & preoperative radiation (2000 cGy) .
Postoperative radiotherapy should be reserved for patients with advanced disease in the
neck (ECS , large nodes , multiple nodes ; N2b , N2c & N3) .
The mostwidely accepted role of radiotherapy is for N0 of highly aggressive tumor like oral
cavity , oro-naso-hypopharyngeal & supraglottic Ca. larynx .
The use of radiotherapy does not improves the survival figures .
Primary of unknown origin "occult primary"
It means that there is cervical metastatic disease with an occult primary , it needs a careful
search which may reveal the primary tumor in the skin or mucosa of the head & neck or
rarely in an area below the clavicles (like lungs) .
Search includes , history, examination , imaging , panendoscopy & selective biopsies from
the high risk sites (nasopharynx , ipsilateral tonsil , base of the tongue & pyriform fossa) ,
3-11% remain elusive , so the primary of unknown origin .
Prognosis varies from 30-70% five years survival . It depends on the stage & position of the
LN (supraclavicular nodes has the worse prognosis , because may involve non-head & neck
sites) , patient managed by radical neck dissection & radiotherapy may have better & the
use of chemotherapy can improve the prognosis .
Radical neck dissection
It is an operation performed to remove the lymph nodes containing levels in the neck (I-V)
& all three non-lymphatic structures ; accessory nerve , sternomastoid muscle & internal
jugular vien . It is indicated for ;
1. Operable palpable neck disease in the presence of primary tumor in the upper
aerodigestive tract (N2a, N2b , N3) .
2. Operable palpable disease in the neck when the primary tumor has previously
controlled (for salvage) .
3. More controversial indications are ;
a. Large primary tumor with size , site & nature carrying high risk of microscopic
deposite , although no LN are palpable .
b. Patient with extensive primary lesion which is being treated surgically .
c. When the metastatic disease is present in the neck though no primary can be
found (unknown primary) .
d. Occultr metastasis .
Contraindications are (relative) ;
1. Patient unfit for major surgery .
2. Untreatable primary tumor .
3. Extensive bilateral neck disease .
Lecture notes in
4. Unresectable neck disease .

5. Patient with distant metastasis .
Types of neck dissection are ;
1. Classical radical neck dissection .
2. Extended radical neck dissection .
3. Modified radical neck dissection .
4. Selective neck dissection .
The limits of radical neck dissection are ;
- Superiorly : the mandible .
- Inferiorly : the clavicle .
- Anteriorly : Strap muscles .
- Posteriorly : trapezius muscle .
Preoperative preparations ;
Advice the patient about the risk & complications of radical neck dissection .
The patient with unilateral neck dissection not need tracheostomy , while elective
tracheostomy indicated in : (1) Bilateral neck dissection (2) 2nd neck dissection & (3) Neck
dissection with previous radiotherapy .
The procedure ;
- The patient lie supine with sandbag beloow shoulders .
- General anesthesia with premedications (decided by the anasthetesist) .
- Skin painting , drapping , skin incison marked by pen (then make the incision) .
- Incision ; the decision to use incision depends on ;
(1) Patient preference .
(2) Number of levels required for access purposes .
(3) Any previous surgical incision .
(4) Site of the primary tumor .
(5) Previous radiotherapy .
If the patient not irradiated , Y-shaped incison (with lazy S in the vertical limb to
decrease the scar) called Circle or Shobinger incision .
If the patient irradiated ;
(1) McFee incision , difficult dissection with limited access & there is bleeding under the
bridge flap which is difficult to controlled .
(2) Horizontal T (Hetter) .
(3) Utility incision
The incison should provide access to the 4 corners of condensation which are ;
(1) The lower end of the internal jugular vein .
(2) The junction of the lateral border of the clavicle with the lower edge of trapezius .
(3) The upper end of the internal jugular vein .
(4) Submandibular triangle .
Once the incion made , dots of ink made on the skin in 3 or 4 sites to facilitate placement
of critical sutures .
- We keep the platysma on the skin flap (to increase the strength of the wound
postoperatively & to provide important blood supply to the flap) , af the platysma
invaded by the tumor , then removed with the overlying skin (usually it is inoperable in
this case) .
- The marginal mandibular nerve & its cervical branch (which supply the muscles around
the mouth & part of the platysma that cross the mandible) are in danger of division
Lecture notes in
causing weakness of the lower lip , they lies one finger breadth bellow the mandible ,
there are many ways to protect these nerves ;
(1) Cut the investing layer of the fascia at the level of hyoid bone , then expose the
capsule of the lower part of the submandibular gland , then the fascia elevated as a
flap over the mandible .
(2) Ligate & divide the facial vessels on the submandibular gland & lift them over the
mandible (less reliable method) .
- The flap are elevated , the neck is exposed with access to the corners of consternation ,
the flaps sutured to the towels by strong silk sutures .
- Lower end of the internal jugular vein "usually 1st" , the basic principle of cancer
surgery is that the main vein draining the tumor that being removed should be divided 1st
, this step reduces the number of systemic metastasis because small tumor emboli
released by manipulating the tumor are unable to find their way into the circulation
(some prefer to late the ligation as much as possible to decrease bleeding) .
The lower end usually approached early in te operation by dividing the sternomastoid
muscle , this allows the blueness of the vein to be identified (one or two small arteries in
the muscle need to be diathermed) .
The carotid sheath is opened to expose the vein (adentify at least 2 cm length to facilitate
ligation with adequate control by silk or vicryl) . Make sure that the vagus is not
included in the ligature (two ligature around the lower end & one at the upper end , then
both ends are transfixed) .
The lower transfixed suture called Houseman suture , because if it fail in the early
postoperative hours , the houseman who know about it 1st .
If tear of the internal jugular vein occur (easily to occur) , the bleeding identified &
occluded temporarly by pressure or arterial clamps & the defect then repaired using 6/0
ethilon (with tear there is danger of air embolism not from bleeding , so the head should
tilted downwards) .
When there is extensive neck disease we need to get gain to the junction between the
internal jugular & subclavian veins .
On the left side the thoracic duct pass medially to the jugular vein , then posterior to it
& finally curves around to enter the junction of internal jugular & subclavian vein
Once the internal jugular vein tied , the dissection extend laterally to approach
Chaissaignac's triangle (triangle between longus coli & scalenus anterior & subclavian
artery as the base) , the contents of this triangle is sclene nodes (should be removed) &
also main jugular lymph duct which terminate here on the left side with the thoracic duct
The thoracic duct should be isolated & oversewn with fine silk (at the end of the
operation we should check that there are no futher leaks) .
The critical steps in radical neck dissection at low neck are ;
1. Divid the lower end of the sternomastoid in corner one .
2. Isolate & ligate the internal jugular vein .
3. Avoid thoracic duct &/or jugular lymph duct .
4. Divide & retract the omohyoid muscle upwards .
5. Mobilize the fat pad overlying prevertebral fascia.
6. Identify & preserve of the brachial plexus & phrenic nerve .
7. Deal with corner two .
- Supraclavicular dissection "2nd corner"

Lecture notes in
After ligating the internal jugular vein , move to the bottom end of the trapezius muscle
& begin the dissection behind the omohyoid muscle , divide it (through the tendon) , at
this stage the transverse cervical vessels encountered & ligated .
The fascia between the omohyoid & the internal jugular vein should be incised & the
prevertebral fascia exposed by sharp or blunt dissection with a swab in an upward
direction , here , the pherenic nerve seen as it runs over scalenus muscle anteriorly from
the lateral to medial (lie behind the prevertebral fascia) . Also the brachial plexus lies
here (so we use bipolar diathermy to avoid damage to the nerves) .
At this point we clear the Chaissaiguac's triangle (contains branches of the
thyrocervical trunk , vertebral vein , thoracic duct & scalenus LN) .
After clearing the supraclaviculr dissection towards the anterior border of the scaleus
anterior muscle , then continue in upward direction to dissect the posterior triangle .
Also the external jugular vein divided & the fat in the supraclavicular fossa can be
removed with minimal bleeding .
- Posterior triangle dissection
With continue up the anterior border of the trapezius muscle to the mastoid tip (all
important structureslie below the accessory nerve) .
The accessory lies in the roof (not floor) of the posterior triangle , so can damaged early
in the dissection . So the 1st thing is to identify the nerve which is done by the following ;
(1) Erb's point , 1 cm above the point above where the great auricular nerve wind
around the sternomastoid muscle on its way to supply the parotid gland .
(2) The nerve exit the sternomatoid muscle lateral border at the junction of its upper
1/3 rd & lower 2/3rd
(3) Dissect upwards the anterior border of the trapezius muscle in the posterior
triangle until the nerve is encountered (may confirmed by stimulation) .
(4) Draw a line laterall from the laryngeal prominence through the posterior triangle ,
the nerve will usually cross this line as it is run from Erb's point to the lower
posterior corner of the posterior triangle .
Ligate the ascending branches of the transverse cervical vessels .
Division of the accessory nerve with preservation of the branches to the trapezius
muscle (from C3&C4)
Dividing the fascia from the anterior border of the trapezius muscle up to the mastoid tip
& then follow the accessory nerve on the sternomastoid muscle reaching the upper end
of the internal jugular vein , retracting the digastric muscle , so the upper end of the
internal jugular vein identified .
- Division of the upper end of the internal jugular vein
After dividing the upper end of the sternomastoid muscle , the position may be located by
palpating the transverse process of the C2 over which it lies .
The vien is mobilized , ligature (silk sutures , 2 above & 1 bellow) with transfixing
sutures (if the disease extend to the digastric muscle , it must be removed with specimen)
Before tying any ligature , 10 th & 12th should be identified & preserved .
Ligation of the venae nervi hypoglossi comitantes . Ligation of the occipital artery as it
cross the internal jugular vein . Also ligation of the posterior branch of the posterior
facial vein (0.5 inch anterior to the internal jugular vein) , so the specimen is now
mobilized both top & bottom . Division of the lower portion of the parotid gland .
- Dissection of the submandibular triangle

Lecture notes in
The fat in this area divided , display the anterior belly of digastric muscle . The
submandibular gland identified , ligation of the facial vessels (that cross the lower
border of the mandible) .
The mylohyoid muscle is retracted in a forward direction to reveal the submandibular
duct & at this point the lingual nerve is pulled down in a curve which gives branch to the
submandibular ganglion (which accompanied by blood vessels , ligated) , then divide the
branch to the gland & so the lingual nerve spring back upwards behind the body of the
mandible . Then the submandibular duct tied & divided .
Ligation of the facial vessels at 2nd point (as they wind over the posterior border of the
gland) , then mobilize the gland .
Once the dissection is completed , a warm pack is placed in the wound , haemostasis
secured , irrigation with saline done .
- Closure
The early instruments discarded & new gloves worn to close the wound . Two large
drains placed through the posterior flap & securely tied (drains should be never cross
the carotid sheath) .
Check made for any chylous leak & any bleeding .
Closure in 2 layers & the check for any air leak (disasterous results) . Either uncover
the wound or dress it .
Radical neck dissection as a part of combined procedure
1. Laryngeal cancer
Radical neck dissection never done in hemilaryngectomy , but when done with
supraglottic laryngectomy , it is pedicled on the thyrohyoid membrane .
In total laryngectomy the radical neck dissection should be left attached along the whole
length of the larynx to include the superior & inferior lymphatic pedicles .
2. Pharyngeal cancer
With pharyngectomy , the pedicle must be as broad aspossible , left along the whole
length of the pharynx .
3. Oral cancer
Oral cancer drain to level I, II & III , so the specimen remains attachesd along the lower
boredr of the mandible & the inner layer of the periostium is included to preserve
continuity .
4. Oropharyngeal cancer
This drain to the levels II , III & IV , so the specimen should remain in continuity
attached near to the tail of the parotid gland .
Complications
A. Immediate
1. haemorrhage , due to slip ligatures .
2. Chyle leak , due to damage to the thoracic duct .
3. Nerve palsies , pherenic , vagus , marginal mandibular , lingual , hypoglossal ,
sympathetic trunk & brachial plexus .
B. Intermediate
1. Facial oedema .
2. Cerebral oedema , after synchronus or stage bilateral neck dissection .
3. Wound infections .
4. Wound breakdown . due to poor surgical technique , previous radiotherapy , DM &
poor nutritional status .
Lecture notes in
5. Rupture of the carotid artery (to protect the carotid artery , use levator scapula
muscle flap & swang like a page of a book anteriorly over the artery) .
C. Late
1. Frozen shoulder , less likely when the C3& C4 preserved .
2. Skin or gland recurrence
Extended radical neck dissection otid artery
This operation consist of removal of all the structures resected in the radical neck & one or
two of the additional LN groups (like retropharyngeal LN , parotid nodes or LN at level VI
& VII) &/or non-lymphatic structures (part or all the mandible , the parotid gland , part of
the mastoid tip , prevertebral fascia & muscles , the digastric muscle , the external carotid
artery & skin) . Indicated in ;
1. When the neck disease involve the above .
2. When the disease arise in the parotid gland or the pharynx (primary) .
3. For transglottic & subglottic cancers .
4. Cancer of the cervical oesophagus & thyroid .
Modified radical neck dissection
Consist of the removal of all LN groups (Level I to V) with preservation of one or more of
non-lymphatic structures ;
- Type I ; removal of all LN groups (I-V) with preservation of the spinal accessory nerve ,
it is indicated for operable palpable neck disease (usually N1 , N2a & N2b) not involve
the accessory nerve , occasionally can be done for N0 neck .
- Type II ; removal of all LN groups (I-V) with preservation of the spinal accessory nerve
& the internal jugular vein , it is indicated for ; some time the same as type I , or when
the internal jugular vein not need to be resected (as in differentiated thyroid cancer) .
- Type III "called comprehensive or functional selective neck dissection" ; removal of all
LN groups (I-V) with preservation of the spinal accessory nerve , internal jugular vein &
sternomastoid muscle , it is indicated for ; (1) Managing N0 neck (2) Managing of
differentiated thyroid cancer & (3) Skin tumors like melanoma & SCC & Merkle cell
carcinoma .
Operative technique ;
- Preservation of accessory nerve (not ligate by retract upward) .
- Preservation of the internal jugular vein , by dissection of the carotid sheath along with
the deep investing layer of fascia & the contents of the posterior triangle , the relevant
branches of the vein identified & tied up .
- Preservation of the sternomastoid muscle which make the operation time consuming
(danger for elderly) . So we dissect along the fascia anterior to the muscle , then retract
upwards , other method , divide the muscle at its lower end , follow it upward , complete
dissection & then resuture the muscle .
Selective neck dissection
Consist of the preservation of one or more of LN groups & all the 3 non-lymphatic
structures ;
1. Supraomohyoid neck dissection ; dissect LN level I, II & III , indicated in T1-T4 N0
SCC oral cavity .
2. Extended Supraomohyoid neck dissection (anterolateral) ; dissect LN level I , II , III
& IV , indicated in skin cancer (SCC & melanoma) anterior to the line of tragus ,
usually performed in conjunction with superficial parotidectomy .

Lecture notes in
3. Lateral neck dissection ; usually carried bilaterally as the nature of the disease
associated with bilateral metastasis , dissect LN II , III & IV , indicated in T2-T4 N0
(or T1-T2 N1) SCC of larynx , oropharynx & hypopharynx .
4. Posterolateral neck dissection ; dissect LN II , III & V with postauricular &
suboccipital LN , indicated in skin cancer posterior to the line of tragus .
5. Anterior or central neck dissection ; dissect LN level VI , indicted for differentiated
thyroid Ca. , subglottic & hypopharyngeal SCC .
6. Superior mediastinum ; dissect Ln level VII , indicated in differentiated thyroid Ca. &
medulary Ca. , subglottic laryngeal & hypopharyngeal SCC & oesophageal Ca (if the
diseaseis completely respectable) .
Figure shows the diagnostic approach to patient with unknown primary in the neck
Neck swelling
Node
Characterize lump
ENT exam
Reactive
Tumor FNAC
Benign Malignant Infective screen

SCC
Suspicious AdenoCa. Reticuloendothelial
Other thyroid
Repeat FNA Reexamine
MRI
"Coffin corners" Observe
Incisional biopsy
Frozen section
-ve
CT scan
Head & neck , Chest , Abdomen & pelvis
-ve Chest , abdomen ,

Head & neck +ve Pelvis +ve
Biopsy from PNS ,
tongue base , Tonsil
Thoracic or general
Stage & treat +ve surgeon opinion
-ve
Manage the neck &
ORL , Head & Neck surgery probable primary site
650
Lecture notes in
LASER in otorhinolaryngology
LASER means ; Light Amplification by Stimulated Emision of Radiation .
All uses of the laser , all depend on basic characteristics of the laser beam ;
- Intense beam of pure monochromic light .
- Does not diverge .
- All the light of the same length .
- Travel in the same direction & are in phase .
- Can be focused to a fine point to produce very light energy levels .
This means ; monochromic (same colour) , collimated (parallel & unidirectional) &
coherent (intense & in phase) .
Development of laser
- Before laser physicists believed that there could be only two interaction between matter &
light (absorbtion & emission) .
- Albert Enistein 1916 , suggest third possibility (stinulated emission) , form the bases of
laser , he state that " under certain circumstance a photon could stimulate an excisted
atom or molecule to emit another photon with the same energy traveling in exactly the
same direction " .
- 1930s , stimulated emission was refered to as ; negative absorption , but obsessed with the
principle of the thermodynamic equilibrium .
- 1940 , Fabrikant said that a population invension was necessary for molecular
amplification (stimulated emission) .
- Schawlow & Townes 1953 , the 1st published detailed proposed for the production of laser
call it an " mivrowave amplification bt stinulated emission of radiation (optical maser)" .
- Townes Basov & Prokhorov 1964 , awarded a Nobel price for the maser .
- Maiman 1960 , made the 1st Ruby laser despite the widely held belief that the ruby was
unsuitable for laser .
- Gensic Marcos & Van Vitert 1964 , Patel 1965 , Nd-YAG , Co2 , diode , ion , chemical ,
dye & metal vapour lasers were produced shortly after .
- Recently excimer laser has been developed (Argon-Fluride laser) , the medium composed
of two atoms .
LASER in surgery & medicine
- Meyer Schwickerath 1956 , use xenon –arc photogoagulator in ophthalmology to treat the
threatened retinal detachement & other disorders .
- Kapang et al 1963 Flock & Zweng 1964 , produce more powerful pulsed ruby laser
(superior for retinal photocoagulation) , but later demonsitrate that viable cancer cells in
the debris ejected explosively during pulsed irradiation which could disseminate the
malignancy .
- Patel 1965 , produce Co 2 laser precise & bloodless field , there may be viable cancer cells
on viral particles in the vapour produced by tissue destruction .
- Breidmeir 1969 developed endoscopic coupler for the Co2 laser can remove vocal cord
lesions with bloodless & excellent healing , then it coupled to Zeiss operating microscope
in vocal cord microsurgery .
- Argon laser blue-green light produced readily absorbed by vascular tissue in diabetic
retinopathy .
- Nd-YAG laser continueous wave could be transmitted by fibreoptics for control of
bleeding in the GIT .
Lecture notes in
Development of photodynamic therapy

- Far from new , Raab 1900 describe killing the Paramecium sensitive with acridine dye &
exposed to light .
- Jessonel & Tappenier 1905 , used to pical eosin & white light to treat skin tumors .
- Policard 1924 demonstrate number of tumors exhibited area fluorescence & attributed
this to accumulation of endogenous porphyrins (secondary bacterial wall) .
- Recently haemato-porphyrin derivative (HPD) used to demonsitrate fluorescence in
malignant tissue & to treat tunors in combination with with filtred light .
- HPD , selectively retained with in malignant tissues & also in liver , spleen , kidneys &
skin , but the exact mechanism is uncertain .
- Light with wave length 630 nm optimal & best produced by an argon-pumped dye laser ,
using rhodamine dye & transmitted by flexible fiber .
- When HPD activated by light single oxygen is created , this is cytotoxic acting at several
sites by the oxidation of sensitive bonds .
- Has diagnostic & therapeutic uses .
- It has been shown HPD bearing tumor fluorescence when exposed to blue light .
- Many tumor which has failed all other treatment modalities , also usefull in palliation with
encouraging results reported for small tumors for cure .
The production of coherent laser light
- The lasing medium contained in laser tube , has
fully reflective mirror at one end & partially
reflective mirror at the other end to allow exist of
laser beam .
- The lasing medium excited either electronically or by
light energy light source to creat a population
inversion of atoms in high laser energy state .
- Stimulated emission then occurred as atoms
spontaneously emit photons which on collision with other excited atoms stimulate these to
emit identical photon traveling in the same direction as the orginal stimulating photons .
- Photons released in exactly the same axis of the tube
- Reflected back atoms into the media , excited atoms
to release photons , by this mean there is a rapid
built up of light energy in the laser tube .
- As this whole process results in the production of
heat , the optical chamber is surrounded by a water-
jacket cooling system .
Beam transmission
- Coherent light visible & low infrared lasers can be transmitted by fine flexible fibers .
- No flexible fiber can transmit Co2 laser energy efficiently .
- Now laser tube is mounted in a separate consule & the beam transmitted to the
microscope , handipiece or bronchoscope .
Beam aiming
- The laser beam must be aimed accordingly at the target before activation .
- Laser in visible wave length an attenuated beam is used to define the beam path & target
area .

Lecture notes in
- With invisible near infrared laserws (low power ) , visible Helium-Neon laser is used &
either a concave mirror or zinc senide lens focuses the beam .
- Most microscopic laryngeal surgery use 400 mm focal length produce wide defocused
beam of 2 mm in diameter .
- The argon laser beam can be transmitted to a slit lamp operating microscope , hand piece
or flexible endoscope .
- Design of the end of the endoscopic delivery fibre appear to be critical , the laser fibers
has to be surrounded by metal tipped Teflon sheath down which compressed air is blown
to keep the tip free from debris & secretions .
Laser beam parameters
- Beam power , range from milliwatts of power for low level laser therapy to 100 watts in
high power Co2 or Nd-YAG lasers .
- Power density , the laser energy has generator effect of delivered to a small spot rather
than spread over large area , the power density measured in watts or milliwatts per cm2 .
- The energy distribution within the beam , inspite of the parallel nature of the laser beam ,
there may be profound difference in the energy distribution within the beam resulting from
differences in the optical cavity .
- The total energy delivered measured in joules (watts/seconds) & is calculated from the
output power & exposure time .
Laser tissue interaction
- The pattern of laser absorption is determined by its wave length .
- The effect on the tissue depends on :
1. intensity of the radiation .
2. total energy delivered .
3. the rate of delivery of the energy .
Biostimulation
Very low levels of laser energy is thought to be a biostimulative & has been used to improve
wound healing & to relieve pain .
This effect offerd by many lasers , ranging from red Helium-Neon laser , infrared Gallium-
Arsenide , Co2 laser , Argon laser , Nd-YAG laser .
Thermal effects
- The temperature of tissues increased as they absorbe energy & no change in tissue
structure between 37-60 Co, but above this the tissue coagulate .
- The protein in collagen fibers denatures & results in tissue contraction which imparts
haemostatic properities when laser applied to blood vessels .
- When soft tissue temperature raised to 100 Co , the intracellular water converted to a
steam , once water has been removed from the tissues , residual cellular debris is burnt at
the temperature of 400-500 Co, but doesn't cause significant damage to the surrounding
tissues as there is poor theramal contact betweemn debris and the adjacent normal tissues
Non-thermal effects
It is of two types ;
1. Photomechnical ; example of it , pulsed Nd-YAG laser for destruction of opaque
bodies within the eye , & longer pulses for this laser used to destroy renal & gall
stones .

Lecture notes in
2. Photochemical effect , by direct interaction between laser photons & molecules ,

example of it , is photoactivation of heamatoporphyrin derivitaves within malignant
tumors .
Surgical lasers
Laser derive its name from its lasing medium , in clinical practice there is considerable
overlap in the role of the three most commonly used lasers .
Co2 laser has high presicision light scalpel .
Argon laser mainly to coagulate blood vessels .
Nd-YAG lase , superior to Co2 for haemostasis .
Co2 Laser
- Produces continuous wave far infrared coherent light at wave length 10600 nm , invisible
beam , so the surgeon use aiming beam , red or green dot to direct the laser .
- Several studies show no viable cells in the debris released by cell vapourization , also
recent studies unable to find any viral particles during destruction of viral laryngeal
papilloma .
- There is no shock impact when strike the tissues , so no tendency to force cells to adjacent
normal tissues .
- 90% of Co2 laser energy absorped in the depth of 100 micrometer .
- Two techniques used to remove the lesions ;
1. Vapourize the whole lesion .
2. Used as scalpel to excise the lesion .
- Advantages of Co2 laser ;
1. Immediate tissue destruction ; by instant vapourization , so pain , edema & slough
are minimum or abscent as compared to cryosurgery .
2. Bloodless dissection ; focused Co2 laser beam seal blood vessels up to half mm in
diameter , while larger blood vessels can be controlled by defocused beam .
3. Minimal instrumentation ; no instruments needed to driver the beam when the laser
used with the operating microscope , but efficient suction is required .
We use rigid straight endoscope & mirrors (steel mirrors) to focus the laser to
inaccessible areas (under surface of vocal cords , laryngeal surface of the epiglottis
& nasopharynx) because we can't transmit the Co2 laser by fibreoptic cable .
4. Precise dissection, because of the specific wave length & coherence .
In modern machines the spot size can be varied , small one for endolaryngeal work ,
while wider spots appropriate for intraoral resection .
5. Minimal damage to the adjacent normal tissues , there is exteremly thin layer of
damaged cells only few microns in width between the laser & adjacent normal
tissues .
So less oedema & heal with minimal inflammation & scarring or deformation of the
tissues is most unusual .
6. Their absorption no dependant on the colour of the tissue & is strongly absorped by
all solids & by liquids (notably water) .
- Disadvantages of Co2 laser ;
1. Fibreoptic transmission is not possible because it is absorped by glass & water .
2. Most delivery systems are capable of 7000 micrometers minimum spot size at 400
mm focal length .
3. Poor tissue penetration (not coagulate blood vessels > 0.5 mm) .

Lecture notes in
4. Conact lenses or acrylic lenses are not protective (need special protective lens) .
Argon laser
- The argon laser produce coherent light which transmitted by a flexible fibers & the laser
has number of discret wave length , but most energy at 488 & 514 nm .
- Not absorped by water or clear colourless structures & is selectively absorped by tissues
which are red .
- It is visible blue-green light .
- It is used in blood vessles coagulation , to bipolar coagulator , it perform precise
coagulation & without spread of energy to adjacent tissues .
- Argon laser 1st used for photocoagulation of retinal lesions , the laser beam was delivered
to avascular area of the retina were photocoagulated attempt to reduce new vessels
formation .
- It is selective absorption offered a unique advantages like it could be used to coagulate
small vessels lying on vital structures such as vasa nervorum .
- Amber colour glasses protection must be used all the time during the procedure .
- Advantages of argon laser ;
1. Can be used in fibreoptic fibers (not absorped by glass) with a beam size as a small
as 0.15 mm .
2. Selective absorption .
3. Precise minimum penetration (1 mm) , so minimum oedema & scarring .
- Disadvantages of argon laser ;
It is operate on 220 volts energizers & open cooling system require both voltage
adaptors & an exterior blumping & cooling system .
Nd-YAG ( Neodenium - Yetterium-Aluminuim-Garnet) laser
- Emit an invisible beam of light , 1060 nm , the beam also transmitted through non-red
tissues & glass , it is absorped by water & dark pigments .
- Green glasses worn fro protection & like argon laser , it utilize 220 volts energizers &
need an exterior cooling device .
- It doesn't has a gas lasing medium , but a crystal rod made of YAG , it is the most
powerful surgical laser in current use with power level up to 100 watts .
- It can be transmitted by fibreoptic cable & aimed by a visible low powered helium-neon
laser .
- Absorped by tissues of considerable depth without colour or tissue specificity , so it was
obvious that damage can be sustained in the tissues beyond the organ being treated .
- High power Nd-YAG laser destroy tissues relatively slow , but with better haemostatic
control than is possible with Co2 & can control vessels up to 1.5 mm in diameter .
- It is an excellent photocoagulator & also used for vascular tumors .
- In general Nd-YAG laser not used frequently in the larynx (not a precise) .
KTP (Pottasium –Titanyl-Phosphate) laser
- A modification of Nd-YAG laser in which the crystals stimulated by krypton arc lamp to
produce a beam of 532 nm visible green light can be transmitted by fibreoptic cable with
more energy available .
- It is less precise with higher temperature with superior haemostasis .
The dye laser
- Has two main clinical areas ;
1. Photoactivation of intratumoral haematoporphryine derivative .

Lecture notes in
2. Selective destruction of blood vessels within the skin .

- It use organic Rhodamine dye as the lasing medium & can be transmitted by a flexible
fibers .
Metal-vapour lasers
- Has a wave length of 630 nm required to photoactivate intratumoral HPD .
- An alternative light source for this is the gold vapour laser .
Excimer laser
- The lasing medium substance only combined in the excited state , example argon-floride .
- The coherent light in the violete/ultraviolet range .
- Has a precise microlaryngeal use , but too costy .
Erbium & Holium –YAG lasers
- Coherent light wave length 2 & 3 micrometers .
- Can be used to cut both soft & hard tissue with great precision with a little damage to the
adjacent normal tissues.
- Its main use in laser skin resurfacing .
Diode lasers
- The wave length 630-1000 nm .
- May be used with optical fibers & have properties similar to those of the Nd-YAG lasers
with respect to coagulating tissues in the non-contact mode & hot knife in contact mode .
Photodynamic therapy
New & exciting approach to the management of many forms of localized tumors , we have ;
1. Haematoporphyrine derivative activated by red light 630 nm (by tunable dye or gold
vapour laser) .
2. Phthalocyanines which seem to incorporate better to malignant cells .
This activation lead to release of single oxygen atom which is extremely cytotoxic & result
in tumor necrosis , this technique not found a significant application in ENT , although its
potential for treating laryngeal cancers & papillomatosis has been investigated .
It could offer a significant advantages to aid in palliation & local control for late staged
head & neck carcinomas .
Safety of laser use
Laser use require extreme caution , the protective measures are ;
1. Environment ;
a. laser localized area & warning signs displayed .
b. remote door locks to prevent non-essential personnel to enter during use .
2. Personnel ;
a. access only to essential personnel .
b. all of them require to wear eye protection .
3. Anaesthetic ;
a. potential explosion risk with volatile anaesthetic agents & oxygen .
b. protecting the endotracheal tube (metal tubes , coated aluminum tubes & even
jet venturi system are used) .
4. Patient ; all exposed parts of the patient adjacent to the operating area are covered
with damp swabs to prevent burns .
Clinical uses of laser in otorhinolaryngology
Laser only used when it offers a significant advantages over established conventional
techniques .

Lecture notes in
Laryngeal surgery
Most common application of laser in ENT , it cause minimal injury to the tissues &
minimal oedema , so less airway obstruction & scar tissue postoperatively .
Co2 is the method of choice to excise benign lesions from the vocal cords like ;
papillomas , polyps , nodules , webs' division , also can be used in the management
of vocal cords palsy by doing laser arytenoidectomy & cordectomy , also cordectomy
for T1 SCC with good voice preservation .
KTP laser may be used to debulk obstructing laryngeal & tracheobroncheal tumors
& even completely excise small one .
Laser , also used to manage congenital & acquired subglottic stenosis .
Oro-pharyngeal surgery
Mostly , we use Nd-YAG & KTP lasers with ;
1. less damage to adjacent structures .
2. less bleeding & postoperative morbidity .
3. reduce inflammatory reaction & contracture .
4. submandibular duct can be cut with less risk of stenosis (postoperative).
Than when we use conventional scalpel
Laser used to excise many benign & malignant oropharyngeal tumors & even to
excise pharyngeal pouch (Dohlman's) .
Ear surgery
KTP laser used as a weight less knife for work around the ossicles minimizing
cochlear trauma & defocused beam used to reduce the incidence of residual
cholesteatoma .
Argon laser used in stapedectomy & also to spot weld tympanoplasty graft in place .
Co2 laser could be used to remove lesions from the pinna , open soft tissue meatal
stenosis & also can be used for simple myringotomy .
Argon & Co2 lasers have been used to remove acoustic neuroma & other CPA
tumors .
Nasal surgery
Co2 laser can be use to treat choanal atresia & variety of nasal cavity lesions like
papilloma , granuloma , nasal polyps , adhesion & also rhinophyma .
Argon & Pulse dye lasers used to treat cutaneous vascular malformations like ; port-
wine stain & intranasal teleangectasia …etc .
Argon & KTP lasers used to reduce the turbinate or turbinectomy , but limited by the
cost .
Advantages of lasers
1. Precise excision .
2. Rapid tissue destruction .
3. Reach inaccessible sites .
4. Excellent haemostasis .
5. Minimal postoperative oedema , pain & scarring .
6. Avoid tracheotomy .
7. Minimize hospitalization time .
Disadvantages of lasers
1. Costy .
2. Time consuming .

Lecture notes in
3. May be harmefull to the patients & operating room personnel if proper precautions
are not taken .
Complications of lasers
1. Co2 laser microlaryngeal surgery associate with strocking unprotected material in
the airway & tissues & room personnel .
2. Precautions taken to avoid endotracheal tube ignition involve use of specialized laser
retardant ETT , wrapping the tube with reflective aluminum .
Endotracheal tube ignition managed by ;
a. remove the damaged tube & reintubate .
b. i.v. steroids & antibiotics .
c. intraoperative bronchoscopy to remove debris .
d. delayed extubation with re-examination of the subglottis & trachea .

Lecture notes in
AIDS in otorhinolaryngology
The AIDS epidemic
AIDS first received public attention in 1981 when several authors described clusters of
cases of Kaposi’s sarcoma (KS) and Pneumocystis carinii pneumonia in otherwise healthy
homosexual men in New York and California .
AIDS was rapidly discovered to be a problem of epidemic proportions. Although early
attention focused on the homosexual population, it became quickly apparent that
intravenous drug abusers (IVDAs), hemophiliacs, and blood transfusion recipients were
also particularly prone to the development of this syndrome.
This immune disorder was characterized by a progressive deficiency of helper T
lymphocytes; in 1983 and again in 1984, a virus was isolated that appeared to be
responsible for the development of AIDS. This retrovirus has been designated the human
immunodeficiency virus (HIV), and as a result of its isolation and characterization, serum
antibody titers to HIV were quickly identified. Tests that identify these antibody markers
(ELISA, Western blot) continue to serve as major serologic markers of HIV infection.
Approximately 50% of HIV-infected patients will develop AIDS within 10 years of their
initial infection . Given this long incubation period, as well as the continuing trend toward
longer survival with medical interventions, the far-reaching impact of AIDS will clearly
continue well into the next century.
HIV virus & host response
The identification of HIV structure, mechanisms, and host interactions enabled the
development of strategies for potential drugs and vaccines and facilitated the institution of
clinical trials to evaluate agents possibly effective in combating HIV.
The HIV virus particle has ;
- An outer lipid bilayer with distinct glycoproteins
(designated gp120 and gp41) protruding from its
surface that allow it to bind with appropriate host cells.
- Within this capsule is the viral core, consisting of
structural proteins, two identical strands of RNA, and
the important enzyme reverse transcriptase.
Upon contacting a compatible host cell :
- Viral surface glycoproteins bind to host cell membrane
receptors ; these host receptors (CD4 receptors) are present in high concentrations
on helper T- lymphocytes and account for the predilection of HIV for these cells
(several other cell types also have low concentrations of CD4 receptors , e.g.,
monocytes, macrophages, central nervous system [CNS] dendritic cells , and they
can also be infected) .
- Following initial binding, the viral and host cell membranes fuse, and the viral core
is injected into the host .
- The viral enzyme reverse transcriptase immediately begins to synthesize DNA from
the viral RNA template .
- This DNA migrates to the host cell nucleus, becomes incorporated into the host cell
DNA, and thus permanently infects the host cell with HIV. This incorporated HIV
DNA, referred to as a provirus, is now an integral part of the host cell genome; as
the host cell multiplies, the HIV provirus also multiplies “zidovudine [AZT],

Lecture notes in
dideoxyinosine [DDI]) acted by inhibiting the action of reverse transcriptase,

thereby interfering with the synthesis of DNA “ .
- The provirus remains latent until activated by unknown cellular or environmental
influences, and the second part of its life cycle begins .
- Using host cell enzymes, the provirus directs the synthesis of new HIV particles,
which attach to the inner surface of the host cell membrane, causing cell lysis and
freeing HIV particles to reinfect other cells with CD4 surface receptors “
antiretroviral drugs, the “protease inhibitors,” acts at this stage in the HIV life cycle
, these agents (saquinavir, ritonavir) interfere with the activity of enzymes needed to
assemble new virus particles” .
Immunodeficiency resulting from HIV infection is due to the loss of helper T lymphocytes.
Since these cells play an important role in the cellular-mediated immune system , HIV-
infected patients are susceptible to opportunistic infections from viral, bacterial,
protozoal, and mycobacterial sources and are prone to develop unusual malignancies .
As the population of helper T lymphocytes gradually diminishes, the morbidity and
mortality of this disease increase “ absolute helper T lymphocyte count (CD4 count) is
commonly used as a quantitative marker of HIV disease stage” . The normal CD4 count is
usually well above 1,000; however, HIV-infected patients display a steadily decreasing
count. Counts below 200 are associated with a level of immunosuppression that allows the
clinical manifestations classically used to define AIDS .
The CDC has established specific criteria to define and classification of AIDS , three
clinical categories have been identified ;
A. Asymptomatic HIV infection , persistent generalized LAP , or acute HIV infection (a
mononucleosis type syndrome) .
B. Symptomatic conditions such as oral thrush , oral hairy leukoplakia & fungal
sinusitis that are attributed to HIV infection , but do not fall into category A or C .
C. AIDS , defined by the presence of one of several defining opportunistic infections
(e.g., P. carinii pneumonia, toxoplasmosis, Cryptococcus) or malignancies (e.g., KS,
non-Hodgkin’s lymphoma [NHL]) in patients with no other defined cause for
immunosuppression , also broadened to include other noninfectious, noncancerous
HIV-associated conditions such as AIDS dementia complex and HIV wasting
syndrome.
Patient in each category can be further classified according to their CD4+ counts ; (1)
500 or more cells/ML , (2) 200-499 cells/ML & (3) fewer than 200 cells/ML .
Most HIV-infected patients mount a substantial antibody response ; antibodies are
produced primarily against the glycoprotein components of the external envelope ,
regions that are highly variable and subject to a high rate of genetic mutation (this has
been a major obstacle to the development of effective vaccines against HIV) . The other
major reason that HIV vaccines may be ineffective in preventing infections is that vaccines
are aimed primarily at neutralizing free virus particles . Evidence suggests that infection
with HIV can occur by cell-to-cell transmission of HIV, thus bypassing the effects of
neutralizing antibodies .
Clinical manifestation
Patients infected with HIV can present with many different problems in the head and neck,
including frequent acute infections with the usual human pathogens, opportunistic
infections, neurologic complaints, and certain specific neoplastic processes .

Lecture notes in
Throughout the natural progression of HIV disease, each new phase brings about certain
types of manifestations .
During the early stages of infection, as the CD4 count is gradually decreasing, patients
experience more frequent viral and bacterial infections as well as candidiasis .
As the CD4 count drops below 200 and AIDS fully develops, infections with unusual
opportunistic organisms as well as the occurrence of HIV-associated neoplasms begin to
predominate .
Dermatologic
- The incidence of fungal and viral infections of the skin, such as candidiasis, tinea
versicolor, and molluscum contagiosum, increases as the CD4 count decreases.
- The clinical response to medical therapy also decreases , often necessitating prolonged
treatment with more potent medications .
- Molluscum contagiosum is extremely common in patients with symptomatic HIV disease.
These pearly umbilicated papules usually measure from 2 to 5 mm and often have a
predilection for the eyelids , occasionally grow very large, forming giant molluscum
bodies and often requiring excision or cryosurgery .
- Cutaneous histoplasmosis and Cryptococcus (indicates systemic infection and should
trigger a search for pulmonary or CNS cryptococcosis) lesions have also been reported
in AIDS patients but are extremely uncommon .
- Seborrheic dermatitis , often involving the face and scalp. Although this process can
present in a variety of ways, the inflammatory and hyperkeratotic forms predominate .
- Other hyperproliferative dermatoses have also been associated with AIDS .
- Bacillary angiomatosis is an uncommon infectious condition found primarily in
immunosuppressed patients, although this condition can affect multiple organ systems,
the skin seems particularly susceptible .
Skin lesions may appear as subcutaneous nodules or as friable vascular papules .
- Herpes zoster infections with typical dermatomal distribution or the Ramsay Hunt
syndrome have been reported in up to 16% of AIDS patients .
Permanent cranial nerve palsies are occasionally unavoidable, and disseminated
disease (primary chickenpox) has also been reported .
- Idiopathic multiple sarcoma of the skin, better known as Kaposi’s sarcoma (KS), is the
most common neoplasm associated with AIDS .
Not all AIDS patients are equally affected by KS. Although 43% of homosexual or
bisexual AIDS patients have KS, only 4% of IVDAs, and essentially no hemophiliacs
with AIDS have evidence of this neoplasm .
Unlike the traditional form, AIDS-associated KS can be very aggressive, often
appearing over the face, neck, upper trunk, and lower extremities, as well as the oral
and pharyngeal mucosa. KS can also present as neck masses secondary to lymph node
infiltration. The typical KS lesion is pink to purplish in color and slightly raised or
nodular.
Otologic
- Primary dermatologic conditions such as KS and seborrheic dermatitis can also occur
in the external auditory canal of AIDS patients , become symptomatic when there is
secondary infection or obstruction of the canal.
- Cutaneous P. carinii infection can present as a subcutaneous cyst ; it has also been
reported to cause external auditory canal obstruction .

Lecture notes in
- Serous and acute otitis media are the most common otologic conditions seen in HIV-
infected patients. This is particularly true in pediatric patients in whom eustachian tube
dysfunction, typical of this age group, combined with depressed cell-mediated immunity
increases the susceptibility to infection .
- In adults, eustachian tube dysfunction resulting from nasopharyngeal lymphoid
hypertrophy, a common finding in HIV-infected adults, also contributes to middle ear
disease (usual middle ear pathogens are similar for both HIV-infected and non–HIV-
infected patients, infections with unusual organisms can occur , Staphylococcus and
Pseudomonas acute or chronic otitis media is more common in these patients, and P.
carinii and Candida have been cultured from middle ear aspirates of AIDS patients with
otitis media).
- Mild to moderate sensorineural hearing loss is often reported in HIV-infected patients.
Although the etiology of this loss is unclear, a viral infection of either the CNS or the
peripheral auditory nerve is suspected. Although the increased latencies found on the
auditory brainstem testing suggest central demyelination consistent with such an
infection, other possible causes such as ototoxic antibiotics, other CNS infections, and
neoplasms must always be considered .
Nose and Paranasal Sinuses
- Giant herpetic ulcers can extend from the nasal vestibule onto the adjacent facial skin
and are often resistant to oral antiviral agents .
- KS and NHL usually result in nasal obstruction and occasionally involve the paranasal
sinuses and nasopharynx.
- Recurrent and chronic sinusitis often develops despite medical therapy. Complaints of
nasal obstruction and thick postnasal rhinorrhea are very common in HIV-infected
patients . Persistent low-grade viral or bacterial infection of the nasal ostiomeatal
complex or edema secondary to the active allergic response of the nasal mucosa may
contribute to this predilection for paranasal sinus infection.
Chronic sinusitis is a common problem as immune function diminishes , three
pathogenic mechanism contribute to the high incidence of sinusitis ;
(1) Impaired systemic & local immunity .
(2) Decreased mucocilliary clearance resulting in mucous stasis in the sinuses .
(3) Increased atopy in patient with AIDS .
Although many unusual organisms have been reported, the usual bacterial pathogens
causing HIV-related chronic sinusitis include Staphylococcus species, Streptococcus
pneumoniae, Haemophilus influenzae, and anaerobic bacteria. Pseudomonas
aeruginosa has also been implicated in up to 20% of patients with HIV-related chronic
sinusitis .
These patients often respond to surgical drainage, though most continue to have some
nasal symptoms postoperatively. For individuals with pain out of proportion to findings
on examination and radiographic imaging despite being on empiric antibiotics, the
clinician should consider the possibility of invasive fungal sinusitis .
Oral Cavity and Pharynx
- Mucosal candidiasis, or thrush is the most common oral and oropharyngeal
manifestation of AIDS.

Lecture notes in
- Although this infection typically presents as tender white pseudomembranous or

plaquelike lesions with an underlying erythematous raw mucosal surface, the less typical
atrophic or chronic hypertrophic form can also be seen .
- The diagnosis is easily confirmed with a potassium hydroxide (KOH) smear of scrapings
from a lesion, revealing typical candidal budding yeast forms or hyphae.
- When thrush is accompanied by severe odynophagia, hypopharyngeal or esophageal
candidiasis should be considered .
- If initial medical therapy does not produce symptomatic improvement, a barium swallow
or esophagoscopy can help to establish this diagnosis. Systemic antifungals such as
ketoconazole, fluconazole, and amphotericin B are often necessary in these cases.
- Herpetic ulcers of the oral mucosa are common in HIV-infected patients . These usually
start as a small group of extremely painful vesicles over the palatal, labial, buccal, or
gingival mucosa and coalesce to form large ulcerative lesions measuring up to several
centimeters .
- These slow-healing ulcers usually respond to acyclovir; topical steroids are often
helpful to control local symptoms.
- Giant aphthous ulcers, not of viral origin, are also commonly seen. Although usually
difficult to manage, these lesions can respond to topical and occasionally to
intralesional or systemic steroid therapy.
- Adenotonsillar hypertrophy is usually asymptomatic , histopathologic examination
reveals severe follicular hyperplasia similar to that seen in the cervical
lymphadenopathy of HIV-infected patients.
- The oral and oropharyngeal mucosa is a common site for KS . Unlike the dermatologic
lesions, oral KS frequently ulcerates or becomes secondarily infected, resulting in severe
odynophagia or dysphagia.
- Ulcerative lesions of the tongue or oropharynx, especially the tonsils, can also be
caused by NHL . This is the second most common neoplasm associated with AIDS .
- Hairy leukoplakia is a white, vertically corrugated lesion that appears along the
anterior lateral border of the tongue and occurs almost exclusively in HIV-infected
patients , probably caused by the Epstein-Barr virus and is a reliable prognostic
indicator of AIDS .
- Aggressive periodontal disease is a common early finding in the HIV-infected patient.
The associated necrotizing ulcerative gingivitis can be very painful and result in marked
gingival recession .
Larynx
- When the HIV-infected patient presents with hoarseness, several etiologies in addition to
the typical causes of hoarseness must be considered : Fungal, viral, and mycobacterial
infections of the larynx can cause throat discomfort or hoarseness if the vocal folds are
involved . When laryngeal symptoms persist, biopsy and culture must be considered so
that appropriate therapy can be instituted .
- KS and NHL can also occur in the larynx and, when associated with obstructive
symptoms, may necessitate surgical intervention.
Neck
- Salivary gland disease is often encountered in HIV-infected patients ;
a. Xerostomia is a common complaint in AIDS patients, and histopathologic findings
similar to Sjögren’s syndrome have been described in salivary gland tissue .

Lecture notes in
b. Generalized parotid enlargement has been reported in 30% of HIV-infected

children and is caused by a lymphocytic infiltration of the gland parenchyma .
c. In adults, parotid masses can result from the usual parotid neoplasms, KS, NHL,
or lymphoepithelial cysts.
d. Lymphoepithelial cysts in HIV-infected patients, which have been well described,
usually involve the tail of the parotid and are often bilateral .
- The incidence of second branchial cleft cysts also increases in AIDS patients.
- Lymphadenopathy in HIV-infected patients ;
(1) Infections ;
a. Tuberculous, atypical mycobacterial infections .
b. Pneumocystis lymphadenitis .
c. Pneumocystis thyroiditis .
d. Viral lymphadenitis ; CMV , EBV , toxoplasmosis ..etc
e. Bacterial lymphadenitis or abscess secondary to oropharyngeal infection .
f. Cat-scratch disease .
(2) Neoplastics
a. Lymphoma ; HL & NHL .
b. Metastatic Kaposi sarcoma .
c. Metastatic carcinoma .
d. Metastatic melanoma .
e. Salivary gland tumors .
f. Thyroid tumors .
(3) Idiopathic
a. Persistant generalized LAP .
b. Lymphoepithelial cysts of the parotid .
- evaluation of cervical masses can be difficult. Previous experience with excisional
biopsy of cervical lymph nodes revealed follicular hyperplasia in the majority of cases.
Despite the higher incidence of NHL and KS in AIDS patients, stable lymphadenopathy
requires observation only.
- Fine-needle aspiration biopsy can often provide valuable information without the need
for formal open biopsy . Indications for cervical LN biopsy are ;
1. Marked constitutional symptoms
2. Localized lymphadenopathy
3. Single disproportionately large node in a patient with persistent generalized
lymphadenopathy
4. Cytopenia or elevated erythrocyte sedimentation rate or both in a patient with
otherwise negative evaluation
5. Patient (or physician) reassurance of an ambiguous tissue diagnosis
Universal precautions for otolaryngologist
The risk of developing HIV infection following a needlestick from an infected source is
approximately 1 in 300. Treatment with AZT is currently recommended by the CDC for
postexposure HIV prophylaxis following high-risk exposures.
Some precautions to be taken by the ENTist as ;
1. Use gloves during office exam (oral, nasal, laryngeal); double gloving during
surgical procedures is recommended. Thorough handwashing between patients is
also important.
Lecture notes in
2. Refrain from patient care if exudative or weeping skin lesions or dermatitis is

present.
3. Protect the eyes during any procedure in which splashes may occur (laryngeal and
oral exam, endoscopy, or surgical procedures).
4. Wear a gown when contamination of clothing is anticipated.
5. Prevent needlestick injury by proper disposal of needles and syringes; never recap
or bend needles. Exercise careful handling of scalpels and other sharps during
surgical procedures.
6. Properly dispose of potentially contaminated materials (office and surgical suite).
7. Thoroughly and carefully clean and disinfect all instruments (e.g., laryngeal mirrors,
nasal specula, fiberoptic scopes).

Lecture notes in
Chemotherapy in head & neck cancers

Cytokinetics means the study of the life cycle of the cells at cellular level .
The cell cycle is a dynamic process represent the fundamental to the understanding of the
growth & division of normal & malignant cells , it consist of four phases ;
- G1 phase "Gap 1" ; the majority of slow growing cell population spend their time in this
phase .
- S phase "synthetic" ; DNA transcription & replication as well as protein synthesis take
place .
- G2 phase ; RNA & protein synthesis continue .
- M phase "mitosis" ; segregation of genetic material & cells division take place .
Tumor growth
Both normal tissue & tumors grow by ;
1. Net increase in cells numbers .
2. Net increase in cell size .
3. Net increase in intracellular substances or products
These composed of 3 distinct population of cells ;
1. Stem cells , take an active part in the cell cycle & so most sensitive to drugs or
radiation , they are capable to proliferate , renew themselves , differentiate & be
regulated .
2. Dormant cells , they left the cell cycle temporarily but may re-enter & proliferate
when signaled to do so .
3. Differentiated cells , they passed through several maturation stages after existing
from the cell cycle & usually have a limit function .
The dynamics of any population of tumor cells is governed by the following 3 indices ;
1. Cell cycle time , differ between different normal tissue & between normal &
malignant cells . Normal bone marrow : 18 hours & basal cell Ca. : 68 hours .
2. Growth fraction , the percentage of the proliferating cells in a tumor (those actually
passing through the cell cycle) at a given point in time .
3. Cell loss , occur by unsuccessful division , death , desquamation , metastasis &
migration . Lymphoma : 30% & poorly differentiated bronchial Ca. : 90% .
Doubling time is an observation depends on all three of the above indices . Bone sarcoma
20 days to double in volume while breast Ca. need 100 days for this .
Concepts in chemotherapy
- Cells kill hypothesis ; cells destruction by drugs followed the 1st order kinetics , i.e. a
given dose of drug kills a constant fraction of cells not a constant number .
Once a "cure volume" is reached , anatomical & immunological factors may supervene
to destroy the remaining tumor cells .
- Drug scheduling & dosage ; Gompertzian growth curve , suggest that maximum growth
fraction achieved when the tumor reaches 37% of its expected volume .
The timing of the 1st treatment & the timing of the successive treatment is important for
successful outcome .
The objective of ant cytotoxic drug regimen is to achieve maximum tumor cell kill with
minimum effects on normal stem cells .
- Selective toxicity ;
Class I drugs ; non-specific like nitrogen mustard , affect both proliferating & resting
cells equally , affect tumor & normal cells in an equal dose related manner .

Lecture notes in
Class II drugs , phase specific , like methotrexate , these mainly kills proliferating cells
during specific part or parts of the cell cycle .
Class III drugs , cell specific , like cyclophosphamide , kills both resting &
proliferating cells , but the later is much more sensitive
- Combinations of drug therapy
The practical benefits are ;
1. Drug resistance .
2. Biochemical blockade ;
a. Sequential blockade ; develop when enzymes are blocked at various steps in
the production of essential metabolites .
b. Concurrent blockade , present when the parallel pathways affected .
c. Complementary inhibition , achieved when drug that block the biosynthesis of
macrooulcules combined with drug that damage it .
3. Cell cycle complementation ; combination of the agent affective against bon
cyclic cells with cycle specific agent producing synergism .
4. Pharmacological considerations ;
a. Prolongation of action , e.g. probincid .
b. Facilitation of membrane transport , e.g. vitamin D .
c. Reversal of toxic effects following great cytotoxic dosage , e.g. folinic acid
after methotrexate .
Definitions
Chemotherapy schedules
- Adjunctive chemotherapy ; use of cytotoxic agent with intent to improve survival before ,
during or after standard local treatment by radiotherapy , surgery or both .
- Induction chemotherapy "neoadjunctive" ; use of cytotoxic agents with intention of
improving survival before progression to standard local treatment .
- Concurrent chemotherapy "concommitent" ; the use of cytotoxic agent with intention of
improving survival during a course of radiotherapy.
- Adjuvant chemotherapy "maintenance" ; use of cytotoxic agent following definitive local
treatment to improve survival .
- Palliative chemotherapy ; use of cytotoxic agent , usually single agent in an attempt to
relieve symptoms in an incurable disease process .
Response ; usually measured 3-4 weeks after the administration of the induction
chemotherapy which may consist of one or more cycles .
- Complete response ; there is total tumor regression , some tissue destruction or mucosal
scarring may be allowed , it should be maintained for at least 4 weeks .
- Partial response ; there is 50% or greater reduction in the products of the 2 largest
perpendicular diameters of all measurable lesions .
- No response ; no change in the size of the tumor or less than 50% reduction .
- Progressive disease ; a growth of measurable tumor of 25% or more , or the appearance
of new lesions .
- Major response ; complete or partial response .
- Minor response ; less than 50% reduction in the bidimentional product .

Lecture notes in
Induction chemotherapy
Its advantages are ;
1. Effective drug level obtained because tumor vascularity unaffected by radiotherapy
or surgery .
2. Better drug tolerance allows full effective course to be given .
3. Micrometastasis eradicated .
4. Unresectable tumor renders resectable .
5. Radiotherapy field & dose may be reduced decreasing the morbidity .
6. Chemotherapy predicts response to radiotherapy .
7. Radiotherapy alone may be sufficient after major response .
Its disadvantages are ;
1. Time spent giving chemotherapy delays surgery & radiotherapy which may be more
beneficial .
2. Toxicity .
3. Immune suppression promotes survival of Micrometastasis .
4. Tumor shrinkage confuse the surgical margin .
5. Potentiation of the side effects of radiotherapy , e.g. mucositis .
6. Complete responders occasionally refuse further treatment until too late .
7. Prolonged hospital stay .
The significance of complete response with induction chemotherapy is that those patients
appear to have better prognosis overall regardless of treatment modality than those who do
not response . But several studies showed that it is generally accepted that induction
chemotherapy , even with the most active combination of drugs , is unlikely to improve
survival significance & should either be investigated or abandoned completely .
The major reasons for failure are ;
1. Delay in the progress to the standard local treatment .
2. Inadequate cells kill .
3. Reduction in the surgical margin or radiation field .
4. Reduction in radiosensitivity after chemotherapy .
Synchronous chemotherapy/radiotherapy
Interactions are ;
1. Drugs & radiation active against different tumor cells subpopulations .
2. Increase tumor cells recruitment from G0 into therapy response with cell cycle phase
3. Cell cycle synchronization .
4. Improved drug delivery with shrinkage of the tumor .
5. Early eradication of the tumor cells preventing drug&/or radiation resistance .
6. Eradication of cell resistant to one treatment modality by the other .
7. Inhibition of repair of radiation damage .
Two types of schedules ;
1. Add single agent at a low or moderate dose to the standard radiation treatment .
2. Multiple agents were given at higher doses & in more intensive schedule which
require regular interruption of radiation treatment .
Studies showed encouraging rates of local & regional control & survival in comparison
with induction chemotherapy & with radiation alone .
These beneficial effects may be due to the added toxic effect of the two modalities .

Lecture notes in
N.B.:
- Recruitment means that following the treatment with non cycle specific drug , most
tumor show a substantial increase in their growth fraction , e.g. hormonal dependant
tumor in response to giving the appropriate hormone .
- Chemoprevention ; is the administration of drugs to suppress carcinogenesis & prevent
the development of invasive cancer

Lecture notes in
Radiotherapy for head & neck cancer

Radiotherapy involve the use of various form of ionizing radiation to treat benign &
malignant tumors . It includes 2 forms ;
1. Photons ; deeply penetrating radiation .
2. Electrons ; superficial radiation .
these forms of radiation can be given in one of 2 ways ;
1. External beam radiation therapy "EBRT" , the delivery of radiation from external
source to the patient , linear accelerators or cobalt machine & directed at a target
tissue within the patient .
2. Brachytherapy ; implantation of the permanent or temporary radioactive source into
the tumor or tissue at risk .
3. Systemic ; like radioactive iodine used for thyroid carcinoma .
How does radiotherapy work ?
Ionizing radiation causes damage to the DNA of the target cells through a complicated
series of atomic interactions .
Radiation with water molecules lead to release of free radicals & DNA , causing nuclear
damage . Normal cells in the body are better able to repair DNA damage .
Types of radiation
- Orthovoltage ; the most basic form of radiotherapy & rarely used now .
Orthovoltage machine produce x-ray with energy below one million electron volts .
Poor penetration , so used in superficial skin lesions . The radio-efficacy of orthovoltage
is higher than that of supervoltage , 1 Gy orthovoltage = 1.15 Gy supervoltage .
Orthovoltage causes bone & cartilage necrosis (radionecrosis) .
- Supervoltage ; most frequently used to treat head & neck cancer , advantages are ;
(1) Greater penetration .
(2) Skin sparing .
(3) Homogenous dose distribution .
The higher energy of linear accelerators , the more its skin sparing effects .
The source , long distance radioactive cobalt 60 machine which produce gamma rays .
The disadvantage ; lack of sharp edge to the beam which is risky when treating close to
the spinal cord or lens .
Linear accelerators produce x-ray from a point source & have an extremely sharp fall
off at the edge of the field .
Homogenous dose distribution avoid cartilage & bone damage .
- Electron beam ; x-ray produced when accelerated electron bombard a target , it is
possible to remove the target in a linear accelerator & treat the patient with electron
instead . Electron energy is largely absorbed at a limited depth depends on the energy of
electrons , so there is sharp fall of dose at depth .
It is poorly penetrating beam like orthovoltage with difference that absorption of beam
independent of density of material absorbing the radiation .
It is useful in treating primary skin tumors around the cartilage of nose & pinna , no
cartilage risk & better cure with better cosmotic results , e.g. anteriorly placed tumors
of the frontal & ethmoidal sinuses & superficial tumor of the scalp (angiosarcoma) .
- Neutrons ; used by Stone in 1926 , heavily uncharged particles can be produced by high
energy machine , they produce a beam of high energy transferred with a low oxygen
enhancement ratio .

Lecture notes in
Cells that are well oxygenated are approximately 3 times more sensitive to irradiation
with x-ray than poorly oxygenated cells (OER of 3) . Neutrons beam has OER of 1.5 , so
cells whether well oxygenated or anoxic are similarly affected by radiation .
Disadvantages ; late damaging effect on normal tissue .
In UK , the use of neutrons is now reserved for management of parotid gland tumor .
- Protons ; heavily positively charged proton beam , advantage ; Braggy peak which is an
area of deposition of maximum energy at a depth in tissue , leaving much lower dose at
the entry & exit point of the beam .
It does not relay on oxygenation of tissue for its effect . In some centers excellent results
obtained in treating some radioresistant lesions like chondrosarcoma of base of the skull
or chordoma of the clivus .
- Hyperbaric oxygen ; using concentrated radiation therapy under hyperbaric oxygen &
1 st used by Van Den Brenk in 1969 .
The patient put in a cylinder at 3 atmosphere oxygen .
The disadvantages are ; (1) Using extermly heavy apparatus (2) Fire risk (3)
Barotrauma & (4) Difficulty in planning of radiation field .
- Brachytherapy ; short distance radiotherapy . It has the advantage of giving a very high
dose to the target tissue with a rapid fall off of isodoes at a distance .
Disadvantages ; only a small volume may be raised to the target dose.
It is either endocavitory or interstitial
oEndocavitory ; used for nasopharyngeal carcinoma in primary treatment or for
recurrence . Advantage for recurrence ; does not have the same dose-depth
distribution as EBRT & does not added to skin toxicity .
It have poor penetration , so used at the end of EBRT .
oInterstitial ; frequently used in carcinoma of the anterior 2/3 rd of the tongue , these
needles inserted in the target tissue under GA in 2 planes , so as to the radiation
delivered will be homogenous .
It lead to cold & hot spots . The dose is 70 Gy in 5 days in a protected room with
lead screen .
The advantages of brachythearpy ; implants in head & neck are will make the isodoses
packed closely together around the linear source & so the radiation at distance from the
source will be minimal .
- Hyperfractionation ; 1st used by Wang 1986 , traditional dose 60-70 Gy in 6-7 weeks of
daily treatment . Radiation can be given in several fractions each day , because normal
tissue take 4-6 hours to repair .
The dose limiting factors are late responding normal tissue against actually responding
tumor tissue .
If the dose/fraction is decreased , it is possible to spare the late reaching tissue
(Hyperfractionation) . In Hyperfractionation the same dose given but broken down into
smaller fraction over the same period .
Accelerated fractionation give the standard number of treatment , but in a shorter period
The aim is to enhance therapeutic difference between the fast responding tumor tissue &
slowly responding normal tissue .
- Hyperthermia ; tumor cells are more sensitive to radiation if the tumor temperature is
raised , even anoxic cells seem to be sensitive to radiation when heated .

Lecture notes in
Treatment planning
A. Initial assessment
- Patient with head & neck cancer should be seen in joint clinic where pathology &
radiology can be demonstrated & reviewed , where the help of dentist , speech
therapist , dietitian , social workers & counselor as well as medical & surgical
oncologist is available .
- Biopsy should be establish the diagnosis of malignancy .
- Agreement of the patient , then the patient referred to planning department .
- Patient dental condition should be assessed , because irradiation will cause
xerostomia , leading to change in PH of the environment & less salivary cleansing
causing erosion at the bases of the teeth . The pre- radiotherapy dental evaluation
include ;
o Routine dental & oral hygiene .
o Daily fluoride treatment .
o Dental treatment or extraction , this depends on the time of healing . If
prognosis > 6 months , then treat , If prognosis < 6 months then extraction .
o Following radiotherapy healing is impaired & any dental extraction or
invasive surgical procedure post radiotherapy will lead to chronic & painful
bone exposure & tissue necrosis .
B. Treatment volume
- Clinical oncologist , surgical oncologist & radiologist should determine the best
treatment approach .
- Aim of treatment of cancer & any extension of the disease .
- Treatment volume depends on ; extension of the disease & general condition of the
patient , e.g. maxillary antrum tumor , treatment volume should be include ; 1 cm
across the midline , ipsilateral frontal sinus (superiorly) , palate (inferiorly) ,
posterior margin of the maxillary sinus , 1 cm anterior to the external auditory
meatus (posteriorly) .
If the orbit involved , radiotherapy should include it & if not , then use lead block .
C. Preparation for treatment
- Aim ; to put the patient in an immobilization position , so the radiation field with its
sharp cut off may be positioned close to sensitive organs like spinal cord & lens .
- An immobilization shell should be constructed .
- The patient should be positioned supine & spinal cord straight & horizontal .
- The mouth position at rest or gag used to displace the lower jaw & tongue , tissue
below palate involved or not .
- CT planning scan performed in treatment position , offer the anatomical
registration of the patient tumor in this position .
- According to that , clinical oncologist will outline the treatment volume , type of
radiation & dose required .
D. Care during treatment
- Clinical oncologist should see the patient regularly .
- There should be no systemic symptoms .
- In the 2nd half of treatment , skin erythema & a soft palate mucositis .
- Care for oral hygiene , like antifungal wash .
- Avoid radiation to both parotids .

Lecture notes in
- Dose should be in correct time , because dose/time relationship & its effect on
normal tissue is critical .
- Treatment of node metastasis .
- Advice the patient about loss of hair .
E. Response to the treatment ; it depends on :
1. Cell type ; lymphoma better than carcinoma , carcinoma better than sarcoma .
2. Mitotic index ; Well differentiated tumor ; less radiosensitive & more
radiocurable .
F. Assessing the response ; 4-6 weeks after complete treatment .
Advantages of radiotherapy in comparison with surgery
1. Out patient therapy ; allowing the patient to continue daily activities without
interruption .
2. The overall medical condition of the patient does not contraindicate radiotherapy
because there is no concern to the risk of anaesthesia , bleeding , …etc .
3. When radiotherapy is the primary modality of treatment , it is less physically deforming ,
no large scar or organ resection .
4. Organ preservation & hence function , improve the quality of life ; Ca. larynx .
Disadvantage of radiotherapy
1. Longer time commitment than surgery ; 4-6 weeks on daily basis .
2. Tumor control depend on site of the tumor & maximum tolerable dose .
Indications of radiotherapy
1. As a sole treatment modality
oNearly all carcinoma that are T1- T2 & N0-N1 .
oException : nasopharyngeal Ca (EBRT) , salivary gland & floor of the mouth (surgery)
2. As a postoperative modality ;
oPrimary tumor > 4 cm involving bone or beyond the primary site (T3-T4) .
oMultiple positive neck nodes .
oExtracapsular nodal extension .
oPositive resection margins of either primary or neck disease .
oRecurrent disease .
Contraindications for radiotherapy
1. Patient with collagen vascular diseases .
2. Pregnant women .
3. Those who have previously received radiotherapy to head & neck region .
Side effects of radiotherapy
1. Acute ; appear in 2nd -3 rd week of therapy & resolve 4-6 weeks after completing the
radiotherapy .
a. Skin ; erythema , dryness , pruritis & mild desquamation .
b. Hoarseness , serous otitis media , mucositis , odynophagia & xerostomia (which is
permanent if the major salivary glands included in the radiotherapy field) .
Management of the side effects during radiotherapy ;
oSkin care ; lanoline based & other moisturizers .
oOdynophagia ; anesthetic mouth rinses .
oMucositis ; oral analgesics .
2. Long-term (<10%) ; depends on :
oTotal dose of radiation delivered .

Lecture notes in
oTime over which it was given .

oAnatomic site included .
a. Xerostomia ; the most common & bothersome , long term side effect , when major
salivary glands treated to dose > 2000 Gy .
Treatment by intake of large amount of liquid between & during meals , use of
artificial saliva preparation & use of pilocarpine can improve salivary function .
b. Skin changes , osteonecrosis , bone exposure , laryngeal oedema & induction of
secondary cancers .
Will the radiotherapy make the patient radioactive ?
Patient undergoing EBRT are not radioactive .
Certain brachytherapy procedures where radioactive source of sufficient energy are
implanted into the patient , they will be radioactive , so ; the implant will be temporary &
the patient treated in a single bed rooms fro duration of brachytherapy treatment .
Once the implant is removed , the patient no longer radioactive .

Lecture notes in
Paediatric Endoscopy
Endoscopy means visual examination of body cavities , hollow viscus or spaces through a
specially designed instrument . Basically it is a tube with an optical & lightening system .
In otolaryngology , three principle forms of endoscopes ;
1. Fibero-optic , flexible endoscope .
2. Hopkin's rod , rigid telescope endoscope .
3. Direct , rigid , endoscope .
In adults the larynx can be examined by indirect laryngoscope , through illumination of the
larynx by light reflected from a laryngeal mirror hold against the soft palate . Most children
will not tolerate I/L because of fear or sensation of chocking .
Flexible endoscope
1. Offers great diagnostic capabilities because they can be used to visualize the sub-
segmental bronchi which beyond the reach of the rigid endoscope .
2. Can be used under LA .
3. Provide more physiological examination
Advantage of rigid Endoscopy
It is far superior in the use for ; (1) Biopsy (2) Obtaining culture (3) Removal of foreign
body & (4) Surgical intervention .
Indications of paediatric endoscopy & bronchoscopy
(1) Diagnostic & (2) Therapeutic , in the following conditions ;
1. Stridor ; for treatment & diagnosis . When scope a child with congenital stridor
(stridor at 1st week of birth) we look for ; stridor at rest with sever recession ,
expiratory component , previous intubation , feeding difficulties , apnoeas , stridor
increased rather than resolved , stridor present after 12 months , general problems
(respiratory or neurological) & failure to thrive .
2. Bronchial lavage ; for cytology , microbiology & treatment .
3. Aspiration ; to exclude vocal cord paralysis , laryngeal cleft , tracheo-oesophageal
fistula .
4. Apneoa ; to exclude laryngomalacia .
5. Hoarseness ; to exclude & treat laryngeal lesions .
6. Cough ; rarely indicated .
7. Foreign body removal & exclusion .
8. Haemoptysis ; for cytology & microbiology , to exclude tracheo-bronchial lesion .
Assessment of paediatric airways
1. History
a. To determine the cause
(1) Stridor most be distinguished from stertor which are noisy breathing due to
partial obstruction in the respiratory tract .
Stridor Stertor
Site of obstruction At or below the larynx Above the larynx
Worsening During feeding , exercise & upset At sleep
st
(2) Laryngomalacia , developed within the 1 few weeks of life .
(3) History of previous prolonged intubation , give suspicion of subglottic stenosis ,
interarytenoids scarring & tracheal stenosis .
(4) History of abnormal voice or cry , suggest pathology at the laryngeal level , e.g.
papillomatosis or congenital web .

Lecture notes in
(5) Patient with history of repaired tracheo-oesophageal fistula may have

tracheomalacia or laryngeal cleft .
(6) Patient with previous thoracic surgery may have vocal cords palsy .
b. To assess the severity of the airways obstruction
(1) Recession .
(2) Poor growth .
(3) Apnoeic episodes .
(4) Cyanosis .
(5) Effect of obstruction on feeding .
2. Examination
oStridor ; if inspiratory means laryngeal cause , while expiratory means intrathoracic
cause .
oDon't be mislead by children whose stridor become improved as this may be due to
worsening of airflow .
oGeneral examination may reveal a features of ; craniofacial syndrome , isolated
maxillary or mandibular hypoplasia .
oChildren with Down's syndrome have increased risk of subglottic stenosis .
oHaemangiomas , presents in 30% of patients with subglottic stenosis .
3. Preoperative investigations
(1) Lateral neck x-ray .
(2) Cincinnati view , penetrating CXR , AP view to show major airways .
(3) Barium swallow , for tracheomalacia .
Contraindications of paediatric endoscopy
1. Cervical spine disorders (congenital) .
2. Coagulopathies (releative C/I) .
3. Seriously debilitated patient .
4. Patient with significant airway compression , should not undergoes endoscopy unless
rigid equipments is available .
Laryngoscopy
Visualization of the voice box (larynx) . Adults range (Kleinsusses) can be safely used for
children & smaller one can be even used in neonates .
It is important that ;
1) Not pinched the lower lip between the instrument & the teeth or gum .
2) Protection of the upper teeth .
It is indicated in ;
1) For identifying a lesion in the glottis or subglottis .
2) For assessment of vocal cord & laryngomalacia (laryngoscope placed in the
vallecula to avoid fixation of the glottis & supraglottic structures) .
Laryngomalacia easily distinguished by indrawing of the arytenoids , vocal cord
movement difficult to identified (dynamic laryngoscope) .
Subglottic stenosis , identified when vocal cords are not in spasm .
3) Full examination of the respiratory tract .
4) Examination of the hypopharynx , oropharynx & mouth .
Laser laryngoscopy ;
- The most useful for ; (1) Postintubation granuloma & (2) Laryngeal papillomatosis .
- Unsuccessful use for ; (1) Anterior web or (2) Subglottic stenosis .

Lecture notes in
- Laser safe-tube need to be used .

- Greater care must be taken because of ; (1) Postoperative damage to tissue & (2)
Secondary stenosis .
Dynamic laryngoscope ; the gold standard to dynamic assessment is to insert a laryngeal
mask with fibroptic bronchoscope passed through this to just above the larynx .
Laryngo-tracheo-bronchoscopy
Most paediatric airway endoscopy used for investigating stridor , we have a standardized
technique which is the 1st described & also used for examination & modification of this used
in foreign body removal or vocal cord palsy .
Laryngo-tracheo-bronchoscopy technically need a team of surgeons , anaesthetist &
nursing assistant with a good experience to do examination safely .
If the examination for assessment , so accurate records kept to allow comparison with
future examination , this facilitated by use of standardize form (Video record) .
Endoscopy of respiratory system commonly carried by otolaryngologist , while paediatric
oeosphagoscope commonly performed by paediatric surgeon .
There is increased used of Hopkin's rod telescope with video which are excellent for ;
teaching , clinical reporting & follow up examination .
Key equipments are ;
1) Xenon light source with feed back intensity control .
2) Undamaged light leads .
3) Laryngoscopes ;
oBenjamin for anterior pathology .
oLindham for posterior pathology .
oKleisasson for general pathology . .
4) Laryngeal probe & forceps .
5) Full range of ventilating bronchoscopes to accept standardized Hopkin's rod .
6) Spaghatti sucker .
7) Side arm forceps & peanut extraction forceps .
8) Video-camera attached to microscope .
9) Video-camera attached to bronchoscope .
10)Video-printer /video-recorder .
11)Neurosurgical micro-patties soaked in 1:100000 adrenaline (excellent for
controlling oedema & bleeding) .
12)Hopkin's rod ; Optic endoscope used to magnify tracheo-broncheal tree , in which
the former air space is replaced by a serial of glass rodes & then replace the former
lens with small air space . This is to allow much large viewing angle , a greater
illumination & resolution .
Surgical technique ;
1) Anaesthesia ;
oIM atropine is vital for ; provide a dry field & to ensure that the LA is affective .
oIV induction is preferable for older children .
oGas induction is preferable for infants & those with precarious airways .
oIV suxamethenium is given ; if the patient stable , before lignocaine spray to avoid
laryngeal spasm & to facilitate intubation .
oHalothane & oxygen which maintain the level of anaesthesia .
oPreoperative steroids which is a good safe guard if stenosis suspected .

Lecture notes in
2) Microlaryngoscopy ;
o A small sandbag under shoulders with great neck extension .
o In the neonates may need a sandbag laterally to support the head .
o Mayo-table support to clear larynx from the chest .
o Prepare & check the equipment ;
a. Microscope ; 400 mm lens for standard laryngeal instrumentation & 350 mm
lens to aid manipulation of the larynx .
b. Bronchoscope size & telescope .
c. Anti-fug solution , freshly applied to lens to be effective .
3) Laryngeal examination ;
o With endotracheal intubation ;
a. Insert lubricated laryngoscope .
b. Protecting teeth & lips .
c. Keeping the tongue central .
d. Check overall appearance of supraglottis & laryngo-pharynx during
introduction of the scope .
e. Follow the endotracheal tube , as a rail road , to the tip of the epiglottis .
f. Gently lift the epiglottis forward (easiest with Benjamin) .
g. Make sure that epiglottis not infront of the laryngoscope prevent a complete
view of the anterior commissure .
h. Check if in doubt by gently withdrawing the laryngoscope .
i. Don't insert laryngoscope so far into the larynx that ; the arytenoids splinted
preventing assessment of the aryntenoid movement .
j. A child with laryngomalacia tend to have aryepiglottic fold tall transversely
but short antero-posteriorly .
k. Use a probe to check vocal cord & ventricle .
o With endotracheal removal ; using a probe for ;
a. Gentle checking of crico-arytenoid fixation by moving the arytenoid
inadequately .
b. Exclude interarytenoid scar by trying separate the 2 arytenoids .
c. Exclude posterior laryngeal cleft by passing a probe between the arytenoid .
d. Move the cords a part to inspect the epiglottis .
Complications of laryngoscopy ;
1) Laryngospasm in response to an irritant & act to protect the respiratory tree .
Usually occur when the patient start breath spontaneously & treated by intubation &
muscle relaxant .
2) Laryngo-cardiac reflex ; due to pressure on the larynx , lead to bradycardia &
cardiac arrest , the use of LA to the larynx prior to the procedure prevent this .
3) Injuries to the lips , teeth & tongue .
4) Anterior laryngeal webbing , in case of stripped cords , so care should be taken to
the mucosa of the anterior commissure of both side .
Bronchoscopy
Endoscopic examination of the trachea & tracheo-bronchial tree . Most cases of paediatric
endoscopy involve the use of (of 2 types) ;
1. Open bronchoscopy (rigid) ; the tube inserted from the larynx into the
tracheobronchial tree

Lecture notes in
2. Closed bronchoscopy (flexible) ; the tube inserted from the larynx into the lungs .
In normal patient the carina can be seen as soon as the instrument pass through the glottis ,
inability to see the carina indicate that there is something press from out side as in vascular
ring & tracheomalacia .
Complications of bronchoscopy ;
1) Injuries to the lip , gums , teeth & tongue not uncommon .
2) Laryngeal oedema due to rough insertion or prolonged examination , treated by
parentral steroids (10 mg dexamethasone) , followed by 2 further doses & put the
patient on airway & oximetric monitoring in the ward .
3) Haemorrhage controlled by ;
a. tamponade & peanut gauze soaked in 1:200000 adrenaline ,.
b. electrocautary or by laser .
c. Also Fogarty venous cathter used in severe bleeding .
4) Penetration of the trachea & bronchi wall which cause ;
a. Sudden development of surgical emphysema .
b. Oxygen desaturation .
c. Lung collapse can occur , this require urgent chest tube & ventilating support .
Nasoendoscopy
1. Fibroptic .
2. Rigid , recently developed , it represent an advanced in rhinology diagnostic capability .
It is of 3 types ;
a. 0-degree .
b. 30-degree , 2.4 mm endoscope .
c. 30-degree , 4 mm endoscope , the most useful one due to its ; supreme illumination ,
ample viewing & well tolerated by most patients .
It is ;
1) More sensitive to diagnose accessible disease than CT .
2) Provide essential complementary information for diagnosis .
3) Permits detailed evaluation of the critical areas for sinuses , osteomeatal complex &
sphenopalatine recess .
4) It is superior to anterior rhinoscopic examination , because it provide more accurate
& through out diagnostic evaluation in patient with sinonasal complaint .
Patients with nasal pathology diagnosed by endoscopic examination , 40% of them are
normal in traditional nasal examination .
Equipment of the endoscope ;
1) Freer elevator . 2) Light source .
3) Fibro-optic cable . 4) Assortment of suction tip .
Procedure of diagnostic endoscopy ;
- Patient sitting or supine position .
- Sprayed of the nasal cavities with topical decongestant or LA which applied to the
inferolateral surface of the middle turbinate & to the other sites where passing of the
endoscope may exert pressure .
- Examine precaution when dealing with secretions & blood ; gloves , masks ..etc should be
recommended .
- Successful examination can be recorded with 3 passages of the endoscope ; 1st select 30-
degree 4 mm telescope , then endoscope lens treated with a thin film of anti-fug solution ,

Lecture notes in
then held the instrument lightly in the left hand by the shaft with thump & 1 st 2 fingers &
introduce slowly under direct vision .
o1 st pass
a. Along the floor of the nose to identify ;
- The overall anatomy . - Presence of pathological secretions or polyps .
- Condition of the mucosa . - Sometimes , identify the nasolacrimal duct within
the inferior meatus .
b. The scope advanced through the nasal cavity towards the nasopharynx , entire
nasopharynx including contralateral Eustachian tube orifice by rotating telescope .
o2 nd pass
- Between the middle turbinate & inferior turbinate .
- While the scope directed posteriorly , we can examine ; the inferior portion of the
middle meatus , fontanel & accessory maxillary ostea .
- Pass scope medial to the middle turbinate & advance posteriorly to examine the
sphenopalatine recess .
- Rotate the scope superiorly & slightly lateral to examine the superior turbinate &
meatus & the slit like or oval shaped ostea of the sphenoid sinus .
rd
o3 pass
- Is made as the telescope is withdrawn .
- By frequent rotation laterally examine ; posterior aspect of the middle meatus , bulla
ethmoidalis , hiatus semilunaris & infadibular entrance .
- Further withdrawing the telescope , see ; middle turbinate , uncinate process &
through mucosa .
oExamination of the middle meatus done by ;
- Sublexation of the middle turbinate medially .
- Using a cotton tipped applicator moistened with topical anaesthesia & then insert
the telescope into the middle meatus .
Diagnostic & therapeutic applications of nasendoscope
1. Initial identification of the disease .
2. Evaluate patient response to medical treatment such as ; topical steroids , antibiotics
, systemic steroids & antihistamine .
Through serial endoscopic examination , we evaluate ; resolution of polyps ,
pathological secretions , oedematous mucosa , inflammatory changes …etc .
Can be followed through the objective data from endoscope combined with subjective
response of the patient are valuable in determining the need for further treatment .
3. Endoscopy greatly decreased & many cases eliminate the need for repeated
radiological examination during & after medical or surgical treatment .
4. Especially important diagnostic applications of the scope is to identify the causative
organisms of sinusitis , by C&S of swab taken from the middle meatus or other sites
of origin of purulent drainage .
5. Diagnostic nasoendoscpe especially useful in follow up after FESS .
6. Endoscopy provide early objective data including recurrence of polyp , hypertrophic
mucosa & chronic infection , often long before symptoms occur .
7. Diagnostic scope originally used for diagnosis of sinusitis , but also can be used to
postoperative surveillance following intranasal resection & for evaluation of CSF
rhinorrhea .

Lecture notes in
ENT manifestations of systemic diseases

Sarcoidosis
Sarcoidosis is a chronic systemic granulomatous disease capable of involving almost any
organ in the body. It is of interest to the otolaryngologist because of its predilection to
involve many head and neck organs, including the eye (episcleritis, uveitis), various
neuropathies (sudden deafness, unilateral or bilateral facial palsy), salivary glands (parotid
swelling), the oropharynx (tonsillar hypertrophy), and larynx (epiglottic swelling and
subglottic stenosis).
Pathophysiology
Idiopathic systemic granulomatous disease of unknown etiology, mononuclear cells
accumulate in affected organs followed by formation of granulomas, may lead to
irreversible fibrosis of tissue
More common in African-American women .
There are 2 theories of aetiology ;
1. Atypical mycobacterium .
2. Unidentified micro-organism .
Histopathology
Non-caseating granulomas, accumulation of T-cells, epitheloid cells , mononuclear
phagocytes, derangement of normal tissue architecture
(1) Nasal manifestation
A. External
1. Present as a raised, papular lesion on the nose. Several of these lesions may
coalesce to form bluish-red swellings. The lesions are firm and elastic when
palpated and extend deeply to involve the entire thickness of the dermis .
2. Lupus pernio ; this describes chronic, violoceous cutaneous lesions with a
predilection for cold-sensitive areas such as the nose, cheeks, ears, and
fingers.
3. widening of the nasal bridge due to involvement of the nasal bones .
B. Internal ;
1. Diffuse nasal crusting .
2. A vasomotor-like appearance to the nasal mucosa, causing diffuse mucosal
swelling (chronic rhinitis) .
3. Cobblestoning of sinonasal mucosa from granulomatous inflammation .
4. Dryness, crusting , epistaxis or mucopurulent or seranguinoes discharge .
5. Septal nodules or perforation .
(2) Oral manifestation in sarcoidosis ;
1. Occasionally, appears with masses on the tongue, lips, mandible, and maxilla.
2. Painless nodule , white , brown or blue with injected areola in the palate .
(3) Laryngeal manifestation in sarcoidosis
1. Larynx may be involved in 3% to 5% of patients, usually in the region of the
epiglottis.
2. Cough , shortness of breath & haemoptysis .
3. Initial stages of laryngeal involvement may be relatively benign; the affected
mucosa is often described as being covered with one or more white or brown
nodules that eventually coalesce to produce a pale, edematous epiglottis .

Lecture notes in
4. Lesser changes being seen in other supraglottic structures such as the

arytenoepiglottic folds and false cords .
5. The true cords are rarely involved, possibly because of a lack of lymphatics . The
lesions are rarely painful, and thus hoarseness or partial airway obstruction may
be the first sign of laryngeal involvement.
(4) Cervical lymphadenopathy (25–50%, most common H&N presentation)
(5) Salivary Glands: parotid mass, uveopartoid fever or Heerfordt’s
Uveoparotid Fever (Heerfordt’s Syndrome)
More common in women
Pathophysiology: extrapulmonary form of sarcoidosis
Symptoms & signs: self-limited uveitis , non-suppurative parotid enlargement, SNHL,
facial palsy, malaise , mild fever .
Diagnosis: based on clinical history and exam and evidence of sarcoidosis in
salivary gland tissue
Treatment : corticosteroids
(6) Otological manifestation of sarcoidosis
1. The facial nerve is the most commonly affected cranial nerve; it is usually involved
as part of the triad of uveoparotid fever of Heerfordt’s syndrome, parotiditis,&
cranial nerve palsy.
2. Involvement of the temporal bone may include facial, auditory, or vestibular nerve
dysfunction.
3. Sudden SNHL ; 20% have eighth cranial nerve findings. This eighth cranial nerve
involvement may present as sudden SNHL , although it only rarely is an isolated
finding.
4. Vestibular dysfunction .
5. Granulomatous lesion of the external & middle ear .
Evaluation
Clinical picture .
Biopsy of lung or affected organ .
Chest x-ray, anergy skin tests, ECG .
CBC, serum protein electrophoresis (hypergammaglobulinemia), LFT, electrolytes
(hypercalcemia), ESR, ACE level .
Complications
Progressive interstitial lung disease, blindness (progression of uveitis), airway obstruction
(rare)
Treatment
Corticosteroids for significant exacerbations, do not treat asymptomatic lesions, may
require surgical excision of obstructing laryngeal lesions .
Infectioes mononeucleosis syndrome “Glandular fever syndrome , chronic fatigue
syndrome “
Is a systemic infection caused by EBV , it is a disease of young adults & adolescent
transmitted by oral contact (kissing) , incubation period of 5-7 weeks .
Clinical manifestations
A. General ; a prodromal phase (4-14 days) of malaise , fatigue , headache , fever (up to
40 c) .
B. ENT ; sorethroat and cervical LAP .
Lecture notes in
C. Signs
1. Acute follicular enlargement of tonsils .
2. A membrane on the oropharynx .
3. maculopapular rash between the soft palate and hard palate .
4. Severe enlargement of tonsils with grayish-white memebrane .
5. Enlarged pharyngeal & base of the tongue lymphoid tissue .
6. Generalized LAP ; cervical , postauricular , suboccipital , inguinal & axillary ,
which may persist for several months .
7. Spleenomegally (50%) .
8. Hepatomegally (10%) & jaundice (10%) .
9. Periorbital oedema involving the lower eyelid mistaken with acute sinusitis .
Rare manifestations ;
A. facial palsy . B. Gullian –Berre C. Encephalitis .
syndrome
D. Myocarditis . E. Mylitis . F. Pericarditis .
G. Pneumonitis H.
Diagnosis
1. Clinical picture .
2. CBP ;
a. Lymphocystosis with atypical lymphocytes (40% of lymphocytes) .
b. Occasionally ; haemolytic , aplastic & thrombocytopenia .
c. WBC may be normal in the 1st week but increased later up to 10-20 x 10 9/L .
3. Serological test ; Paul-Bunnel & monospot test , depending on development of
hetrophil antibodies , the most useful being agglutinin to sheep & hoarse red cells .
These test +ve in the 1 st week , up to 105 –ve especially in children .
4. LFT ; abnormal .
5. ECG ; myocarditis .
6. Viral culture .
Treatment
1. Rest .
2. Intravenous fluids .
3. Analgesics .
4. Steroids for severe cases , 60 mg/day predinisolone for 4 days then rapidly tapering .
5. Never use ampicillin which lead to rubelliform rash .
Complications
1. Airway obstruction due to enlarged tonsils , treated by steroid , nasopharyngeal or
nasotracheal entubation or tracheostomy .
2. Peripheral neuropathy ; laryngeal & eye muscle affected .
3. Hepatitis & myocarditis .
4. Persistant cervical LAP .
5. Abnormal blood picture & serology reaction .

Lecture notes in

Lecture notes in
Appendix A
Commonly asked questions in oral examination
1. Indications of posterior tympanotomy ?
(1) CSOM .
(2) Resistant secretory OM .
(3) Cochlear implant .
2. Regarding PTA ?
Mixed deafness exist when the gap between the AC & BC is > 20 dB , while ossicular
disconnection exist when the gap > 40 dB .
3. Three main causes of poor speech discrimination & severe SNHL of young ?
(1) Mumps ; unilateral cochlear deafness .
(2) Measles ; bilateral severe necrotizing otitis externa .
(3) Meningitis .
4. Caffin’s corners ?
(1) Fossa of RosenMuller . (2) Retromolar .
(3) Base of the tongue . (4) Floor of the mouth .
(5) Laryngeal surface of the epiglottis (6) Anterior commissure .
(7) Ventricles . (8) Subglottis
5. Differential diagnosis of cavity in mastoid “osteolytic lesion” ?
(1) cholesteatoma ; irregular shape surrounded by sclerotic margins .
(2) Mastoid cavity .
(3) Large air cells .
(4) Tumors .
(5) Granulations ; not surrounded by sclerosis .
(6) Eosinophilic granuloma ; osteolytic lesion .
6. Surgical landmarks to identify facial nerve ?
(1) Deep to the short process of the incus (Mastoid) .
(2) Posterior to the chorda tympani (Tympanic) .
(3) Lateral to the ampullary end of the posterior SCC (Mastoid) .
(4) Deep to the tympanic suture (Parotid) .
(5) Anterior & lateral to the sigmoid sinus (Mastoid) .
(6) Behind process cochleoformis (Tympanic) .
(7) Lateral & posterior to pyramid (Tympanic) .
7. Why sagging occur postero-superior ?
(1) It’s close to the antrum ; invasion of the posterior meatal wall .
(2) Adhesion of skin is less .
8. Malignancy in mastoid x-ray ?
(1) Unusual site ; e.g. more posterior .
(2) Large cavity .
(3) Rugged margins , not well defined .
9. Types of meatoplasty ?
(1) Korner ; remove part of the conchal cartilage .
(2) Superior pedicle flap .
(3) Inferior pedicle flap .
(4) Sebilmann .
10. Poor prognostic factors in sudden SNHL ?

Lecture notes in
(1) Old age .

(2) High ESR .
(3) Associated vertigo .
(4) Not showing improvement within 2 weeks .
11. Local antibiotics in ear can cause ?
(1) Resistance of MO .
(2) Allergy .
(3) Cochlear toxicity .
(4) Others ; caloric effect if it’s cold & moistering of the ear (otomycosis) .
12. Limitations of caloric test ?
(1) OM & OE .
(2) Mastoid cavity .
(3) Tympanic membrane perforation .
(4) Sedations .
(5) Wax or any mass .
(6) Congenital nystagmus & squint .
(7) IHD .
13. During mastoid surgery ?
If cholesteatoma on the facial canal , remove it .
If granulation tissue ; contraindication to remove it because it invade deeply inside the
canal . To diagnose it we apply local anaesthesia , if weakness or paralysis occurs ,
then invasion of the nerve +ve .
14. Chronic discharging ear ?
Discharge
(1) Bloody ; granulation tissue or malignancy .
(2) Clear .
(3) Purulent ;
a. Otitis externa ; otomycosis , chronic otitis externa , malignancy .
b. Otitis media ; atticoantral ( attic & marginal perforation) , tympanomastoid
(central perforation) .
Radiological assessment
(1) Lateral oblique of mastoids .
(2) PNS & postnasal space plains .
(3) CT scan .
Audiology
(1) Tuning fork .
(2) PTA .
(3) Tympanometry “Eustachian tube function” .
15. Assessment of hearing loss ?
The least amount of energy required to intiate auditory sensation is 0.00024 dyne/cm2 =
10 -16 watt/cm2 .
Average HL – label
0-15 Normal
16-25 Slight HL
26-40 Mild HL
41-55 Moderate HL
Lecture notes in
56-70 Moderately severe HL

71-90 Severe HL
>90 Profound HL
(1) Conductive HL ; soft sound due to autophony because of loss of ambient noise ,
voice directed from vocal cords to the cochlea .
SNHL ; shouting .
(2) Voice test ; whisper ; 16 feet – 30 dB , conversational ; from the side of the
patient to avoid lip reading .
Each ear tested separately , masking by moving tragus or close the ear by a
finger . Test the better ear 1 st & test in quite room .
Whisper ; at the ear ; 75 dB , at 30 cm ; 55 dB , at 100 cm ; 45 dB , at 300 cm ;
35 dB & at 360 cm ; 30 dB .
Conversational ; at the ear ; 90 dB , at 30 cm ; 70 dB , at 100 cm ; 60 dB , at 300
cm ; 50 dB .
From 60-90 dB called the most comfortable level .
Above 90-100 dB , loudness discomfort level (DL) .
Above 120 dB ; painfull .
Above 140 dB ; rupture of the tympanic membrane .
N.B.: always subsract 25 dB ambient noise .
(3) Tuning fork ;
Rinne assess each ear separately .
Weber ; both ears at the same time .
Absolute bone conduction test . “ABC” .
(4) PTA
Advantages ;
a. Threshold of hearing .
b. Determine the type of deafness .
c. Follow up .
d. Assessment of hearing aid or speech therapy .
e. Determine the disability & compensation .
f. For further testing of asymmetrical SHL e.g. acoustic neuroma .
Basic tests in PTA ;
a. Air and bone conduction .
b. Speech audiometry
c. We strat from 1000 Hz , because it more sensitive at that frequency .
d. Recruitment ; abnormal rapid growth of loudness with increasing intensity .
(5) Tympanometry
We use low frequency 220 Hz , because middle ear is very sensitive to low
frequency sounds , flat curve seen in ;
a. Glue ear .
b. Wax .
c. Probe advanced & struck the tympanic membrane .
d. Tympanic membrane perforation & obstructed Eustachian tube .
16. Causes of air bone gap > 10 dB after stapedectomy ?
(1) Immediate SNHL .
(2) Disarticulation of the prosthesis .

Lecture notes in
(3) Fistula .
(4) Predicted delayed SNHL .
17. Systemic disease associated with CSOM ?
(1) Chronic lung diseases .
(2) Immune suppression .
18. Examination of the eye in CSOM ?
(1) Nystagmus .
(2) Occular muscle palsy .
(3) Papilleodema .
(4) With congenital HL , note for ; hypertelorism , coloboma , blue sclera &
interstitial keratitis .
19. Indications of facial nerve exploration ?
(1) Immediate facial palsy after trauma .
(2) Delayed facial palsy following trauma .
(3) Immediate facial palsy following surgery .
(4) Delayed facial palsy , may due to tight pack or mild contusion of the nerve .
(5) If , referred after 8 weeks of complete paralysis , it is worthy to wait &
performing EMG to identify any polyphasic action potential indicating re-
innerveation , if no recovery after 4 months , then exploration .
(6) Facial nerve neuroma .
(7) Selective neuroectomy for hemifacial spasm & blepharospasm .
20. Classification of CSOM ?
(1) Tubotympanic ; perforation of pars tensa with preservation of fibrous annulus
(safe) .
(2) Atticoantral ; defect in pars flaccida associated with cholesteatoma (unsafe) .
(3) Marginal perforation or T-sinus disease (posterior defect in the fibrous annulus ,
cholesteatoma “unsafe”) .
(4) Cholesteatoma in a safe perforation .
21. Intra-operative with stapes avulsion , what to do ?
(1) Ask the anaesthetist to give hypotensive technique .
(2) Head up .
(3) Avoid sucker near the site .
(4) Use fat pad to seal the defect .
22. Risk factors for middle ear effusion ?
(1) Cleft palate .
(2) Adenoids .
(3) Chronic infective & obstructive conditions of the nose & sinuses .
(4) Congenital syndromes affecting the morphology of the nasopharynx & skull base.
(5) Any condition affecting the mucocilliary function of the upper respiratory tract .
23. When you do myringotomy in middle ear effusion ?
When the condition is persistent for more than 3 months with significant HL causing
symptomatic morbidity .
24. Cholesteatoma on the lateral SCC , removed or not ?
There are 2 opinions , either remove it or preserve it , this depends on the status of
hearing of the other ear & if there is mastoid cavity (leave it) .
25. How dose tympanic membrane perforation produce HL ?

Lecture notes in
(1) Reduce the effective area of the drum in contact with the sound wave .
(2) Reduce the pressure differential across the tympanic membrane .
(3) Reduce the mechanical coupling between the remaining intact portions of the
membrane & malleus .
26. Value of pack in mastoid surgery ?
(1) Mastoid bony cavity not collapsible , allows blood , pus to accumulate continuously .
(2) Encourage re-epithelization .
27. Why you do incision few millimeter from the post-auricular sulcus in mastoidectomy ?
(1) To avoid damage to the cartilage .
(2) Better exposure of the mastoid air cells .
28. Indications of tympanic neuroectomy ?
(1) Drooling child .
(2) Frey’s syndrome .
(3) Chronic tympanic neuralgia .
(4) Salivary fistula .
(5) Sialectasia .
29. Uses of Seigle speculum ?
(1) Diagnostic
a. Otoscopy ; magnification .
b. Mobility .
c. Fistula test .
(2) Therapeutic
a. Insufflations of antibiotic powder .
b. Suction
30. Why posterior marginal perforation of the tympanic membrane usually associated with
granulation tissue with/without cholesteatoma ?
Because there is crowding of anatomical structures ; incus , malleus , stapedius tendon ,
chorda tympani which all may impede the drainage .
31. In CSOM , why granulation tissue found most commonly near ossicular chain ?
 Due to mucosal fold directing the spread of inflammation .
 Due to position of the antrum where even a mild degree of oedema will block
secretion within the mastoid air cells .
32. How you prove nystagmus in patients with unsteadiness in dark ?
(1) Infra-red light .
(2) Frenzeel glass .
(3) Electronystagmography .
33. Causes of bilateral HL ?
A. Symmetrical
(1) Presbyacusis .
(2) Noise induced deafness .
(4) Hereditary (dish shape) .
B. Asymmetrical
(1) Head injury .
(2) Explosion .
(3) Bilateral acoustic neuroma .

Lecture notes in
(4) Late Menier’s disease .

34. Surgery for vertigo ?
(1) Glue ear , insert grommet .
(2) Labyrinthine fistula , do explorative tympanotomy .
(3) Post-traumatic labyrinthine dysfunction with non-hearing ear & recurrent
troublesome vertigo , 3 canal labyrinthectomy leads to resolution of vertigo .
(4) Operable cerebellopontine angle , brainstem or posterior fossa tumors .
(5) Exploratory mastoid +/- middle ear surgery with suspected or lateral SCC fistula
secondary to cholesteatoma or in whom recurrent meningitis or combination of
labyrinthitis or meningitis occur due to communication between the mastoid or
middle ear & the meninges or between the inner ear (IAM) & the meninges .
(6) Endolymphatic sac surgery .
(7) Surgery for BPPV (singular neuroectomy) .
35. To what age you do transverse incision in cortical mastoidectomy ?
Till the age of 2 years .
36. What is the importance of suprameatal crest ?
It demarcate the level of the dural of the middle cranial, fossa .
37. Hearing aids ?
Composed of ; microphone “pick up the sound” , amplifier , receiver & battery source .
Gain of the aid = difference of the input & out put .
Problems in the hearing aids ;
(1) Limited frequency range .
(2) Small distortion of sound wave , so acceptation of hearing aid take time till
the adaptation of the patient occur .
Types are ;
a. Ear level aid
1. BTE “behind the ear” ; which is the most common type attached to the ear tip
(mould) which is most important & must be very perfect , but this may cause
distortion , so the patient need to make a hole (vent) to reflect part of the energy
going to the ear to go to the outside or by decreasing the volume .
2. ITE “in the ear” , CIC “completely in the canal” which pulled by small piece of
wire for extortion or cleansing ..etc . & half conchal type & on the concha in
the EAM .
3. Spectacle ; air conduction or bone conduction .
4. BAHA , bone anchoring hearing aid , used in persistent discharge & congenital
anomalies of the EAC or middle ear , by implantation of hearing inside the bone
& directly connected either fitted by screw or magnetic or by FM .
b. Body level ; air conduction & bone conduction .
Advantages of ear level hearing aid ;
(1) Nearly non conspicuous .
(2) Light in weight .
(3) Direction of sound .
(4) No extra noise from rubbing of clothes .
Disadvantages ;
(1) Expensive .
(2) Easily broken .

Lecture notes in
(3) Acoustic feedback ; treated by ear-mould fit well .

Advantages of body level hearing aids ;
(1) Greater power availability .
(2) Maximum amplification with minimum feedback .
(3) Better sensitivity .
Disadvantages ; the advantages of the ear level aids .
Problems ;
(1) Sensitivity ; with CHL great benefit (linear HL) , while in SNHL less & difficult .
The aid supplied by volume control , adjustable gain control .
(2) Recruitment , solved by ; adjustable aid & peak clipping .
(3) Lack of discrimination in neural hearing loss .
Uses of hearing aid ;
(1) Sensitivity loss
o According to the aspect of HL , quantitive & qualitative or both .
o Volume knob , in crowded places he must decrease the volume & then
increase in quite room .
o IN CHL with intact cochlea he talk very quietly , because no ambient noise .
o Adjustable maximum gain also used in sensitivity HL (quantitive) .
(2) Frequency dependence ; Low to High by screwing .
(3) Recruitment ; we use 2 system & managed by peak clipping or automated gain
control .
(4) Discrimination loss ; by rehabilitation ; lip reading , signals ..etc .
How to prescribe the hearing aid ?
(1) CHL ; like 60 dB loss , give 60 dB or more (+10-15dB) .
(2) SNHL ; if the loss 60 dB , then amplification cause recruitment , so we have tow
methods ;
a. Hearing threshold ; Half gain rate (60/2=30) + 10 dB = 40 dB .
b. Discomfort level – threshold ; 100 – 60 = 40 dB .
38. Why you didn’t use high frequency or low frequency tuning fork to perform Rinne test ?
High frequency ; due to it’s decay quickly , so there is insufficient time to perform it .
Low frequency ; tends to enhance perception by vibration sensation .
39. Uses of speech audiometry ?
(1) Assessment of actual disability produced by deafness .
(2) Predict the usefulness of the hearing aid .
(3) Help in localizing the lesion causing SNHL , cochlear with good speech
audiometry or retrocochlear with poor speech audiometry .
40. Difficulties associated with treatment of OM in children from 4-10 years old ?
(1) Chronic nasopharyngeal source of infection ; adenoids , tonsils ..etc .
(2) Allergy .
(3) Mastoid reservoir of infection .
(4) Antibiotics resistance .
(5) Care of radical mastoidectomy is difficult postoperatively .
(6) Cholesteatoma
41. Regarding CSOM ?
Outcome Safe Unsafe
1. Perforation Anterior or central Attic or marginal

Lecture notes in
2. Discharge Mucoid , profuse , odourless Thick , fetid , scanty

3. Granulation Uncommon Common
4. Deafness Conductive CHL >50 dB or mixed
5. Polyp Unusual , pale oedema Fleshy & hyperaemic
6. Cholesteatoma Very uncommon Very common
7. x-ray Cells size & number normal Absence “sclerotic”
42. Criteria of congenital cholesteatoma ?

(1) Intact tympanic membrane .
(2) No history of ear infection .
(3) Origin ; inclusion of squamous epithelium during embryonic development .
The sites are ; petrous apex , mastoid , external canal , CPA , middle ear , jugular fossa .
The clinical features are ; facial palsy , CHL , with intracranial complications .
43. Indications of systemic antibiotics in furnculosis of EAC ?
(1) Marked oedema .
(2) Marked lymphatics .
(3) Multiplicity .
44. Causes of Carhat’s notch ?
Mechanical interference with cochlear hydrodynamics due to loss of inertia of the
ossicles , seen in ;
(1) Otosclerosis .
(2) Complete fracture of the stapes .
(3) OME .
(4) Tympanosclerosis .
(5) Paget’s disease .
(6) Post-mastoidectomy .
45. Attic perforation is dangerous because ?
(1) Lack of fibrous layer .
(2) Crowded area by ossicles (mucosal folds) .
(3) Poor aeration .
(4) Poor drainage .
46. Advantages of radial incision in myringotomy ?
(1) Less bleeding .
(2) Less scarring & good healing .
(3) Delayed extrusion of Grommet by heaping of epithelium around the Grommet .
47. Diplacusis ?
Apparent difference in the pitch & tone of the sound between the two ears & associated
with endolymphatic hydropes .
48. Difference between osteoma & exostosis ?
Single cancellous osteoma Multiple exostosis
Cancellous bone Ivory bone
Usually arise from the outer part of Usually from deep parts of the meatus
the meatus near the tympanic membrane
Attached to the posterior wall of the Arise from the anterior & posterior
osseous meatus by narrow base meatal wall
Continuous & rapid growth which Complete closure is unusually

Lecture notes in
may completely fill the canal

Usually unilateral Bilateral & symmetrical
Treatment is mandatory Treat if symptomatic
49. Causes of red tympanic membrane ?

(1) Acute OM .
(2) Schwartz’s sign .
(3) Vascular tympanic membrane .
50. Causes of red rising mass behind an intact tympanic membrane (blue membrane) ?
(1) Glomus jugulare . (2) High jugular bulb .
(3) Aberrant carotid artery . (4) Acute otitis media .
(5) OME . (6) Haemytympanum .
(7) Cholesterol granuloma (8) Myringitis bullosa haemorrhagica
51. What are the advantages of external ethmoidectomy ?

(1) Provide an excellent access .
(2) Perception of depth .
(3) Good illumination .
52. How you maintain the patency of frontal recess ?
(1) Stenting for 3-5 months .
(2) Mucoperiosteal flap .
(3) Combined endoscopic & external approach .
53. What is blow out fracture ?
It is fracture of the medial & inferior wall of the orbit .
54. What is the advantages of Freer’s incision ?
(1) Avascular plane .
(2) Tears less , mucosa tough & thick .
(3) Access .
(4) It can extend into full transfixation in septorhinoplasty .
55. Define cholesteatoma ?
It is keratinizing squamous epithelium surrounded by granulation tissue .
56. Intact wall operation ?
Advantages are ;
(1) Physiologic tympanic membrane position .
(2) Deep middle ear with good potential for reconstruction .
(3) No mastoid bowl .
(4) Can use hearing aids .
Disadvantages are ;
(1) Residual cholesteatoma “16%” .
(2) Recurrent cholesteatoma “16-36%” .
(3) Risk of incomplete extentration of the facial recess .
(4) Delayed canal breakdown may occur .
(5) Second stage operation required after one year .
57. Canal wall down operation ?
Advantages are ;
(1) Residual cholesteatoma visible in follow up .

Lecture notes in
(2) Recurrent cholesteatoma visible in follow up .

(3) Total exteriorization of the facial recess .
Disadvantages are ;
(1) Open cavity .
(2) Middle ear shallow & difficult to reconstruct .
(3) Second stage operation sometimes required .
58. Advantages of MRI ?
(1) No radiation .
(2) Multi-plain imaging .
(3) Differentiate tumor from mucosa & fluid in the paranasal sinuses .
59. Why angiofibroma with intracranial extension need angiography before surgery ?
(1) To know the blood supply from intracranial circulation .
(2) Large high incidence of recurrence or incomplete excision .
(3) Embolization CT for intracranial artery sometime needed .
60. What is Costen’s syndrome ?
Wear in the glenoid fossa & pressure of the the auriculotemporal nerve leads to pain &
fullness in the ear with tinnitus & vertigo .
61. Why cut the perpendicular plate of ethmoid in septal surgery ?
To avoid dipping (fibrous tissue between the cartilaginous & bony septum) .
62. If do antrostomy , where to do it ?
According to pathology , if it is high up do middle meatal antrostomy , if it is lower do
inferior meatal antrostomy .
63. How can be sure of patent osteomeatal complex ?
By antral washout & pay attention on backflow of fluid .
64. What is concha bullosa ?
It is an excessive pneumotized & enlarged middle turbinate .
65. How to remove concha bullosa ?
By using No. II knife we split it into 2 parts & we remove the lateral part .
66. What are the complications of tonsillectomy in summary ?
(1) Airway .
(2) Bleeding .
(3) Infection
67. In mastoid surgery , where we do incision ?
Do it within the hairline making a flap & try to avoid doing the incision over the cavity
with subsequent complication which leads to fistula .. etc .
68. What are the mastoid air cells ?
(1) Middle ear
a. Mesotympanic area .
b. Epitympanic area .
c. Hypotympanic area .
d. Protympanic area .
e. Posttympanic area .
(2) Mastoid region
a. Mastoid antrum area .
b. Peripheral mastoid area ; tegmental , sinodural , sinal , facial , & tip cells .
(3) Perilabyrinthine region

Lecture notes in
a. Supralabyrinthine area .
b. Infralabyrinthine area .
(4) Accessory
a. Zygomatic .
b. Squamous .
c. Occipital .
d. Styloid .
(5) Petrous apex .
69. How to remove the posterior end of the inferior turbinate ?
Via anterior rhinoscopy using long Killian speculum & Tilley-Henkle forceps pushing it
backwards & then forwards .
70. How to learn speech therapy to the patient ?
Allow him to speak , so that stream of air no stop the fire of flame .
71. How to do SMR for turbinate ?
L-shaped incision at the anterior end of the turbinate , long incision under the turbinate
72. Bleeding mainly posteriorly due to sphenopalatine artery .
73. If the mucosa above do linear cauterization .
74. After turbinectomy do diathermy .
75. Soft tissue abduction SMD .
76. Apply silastic sheeth before diathermy .
77. What are recent treatment for glomus tumor ?
Stereostatic radiosurgery using Gamma knife .
78. What are the treatment of 1st stage zero in Ca. larynx ?
Laser & follow up .
79. Precaution is to use metallic tube plus normal saline (corrosive effect) .
80. Soaked pack ? precaution on the medial side to avoid trauma to the trachea .
81. Treatment of the postnasal tumors ?
Radiotherapy with prophylactic irradiation of the cervical LN , because the 1 st step or 1st
station of metastasis is to retropharyngeal nodes .
82. In glue ear , in case of nasopharyngeal Ca. , what is the fluid ?
It is mucous & pulsatile , so always put Grommet .
83. What is indirect laryngoscopy ?
Means mirror examination & flexible endoscopy .
84. Superior view of the base of the tongue ? Valleculae & anterior surface of the epiglottis .
85. What is measures can used to treat web of vocal cords during laser surgery ?
a. Open only the anterior end leaving a bridge at the posterior edge with later divided
when the anterior end has been epithelized .
b. Remove the fibrin from the heating cord endoscopically at regular intervals to
prevent adhesions .
c. Use cover for vocal cords using absorbable gelatin sponge or fibrin glue .
86. What are local anaesthetics ?
Cocaine ; heat labile , used only locaaly because it is too toxic to used systemically . It
is anesthetic & vasoconstrictor .
Act by blocking the re-uptake of catecholamine release at adrenergic nerve ending .
Also it sensitize the myocardium to adrenaline which leads to ventricular fibrillation .
Available solution 4-20% or 20% paste .

Lecture notes in
Dose 3 mg/kg (Max. <200mg) , duration of action about 60 minutes .

Xylocaine ; heat stable , rapid onset of action , available in 0.5% , 1% , 4% & 10% .
Dose 3 mg/kg (Max.<200 mg) .
87. What are the benefit of adding vasoconstrictor to LA ?
(1) Reduce bleeding .
(2) Delay rate of absorption .
(3) Prolong action .
(4) Decrease toxic effect .
88. What is the concentration of adrenaline ? 1/80,000 or 1/200,000 .
89. What is Ventur principle ?
Entrainment of air by means of a tube within a tube , large tube being the trachea or
laryngoscope . The gas in the inner tube being under pressure & thus expand at a point
of exit producing suction effect which entrains the surrounding gas (air) in the large
tube . Contraindications in ;
(1) Gross obesity .
(2) Contracted abdomen during the procedure , surgery between them .
(3) Injured part of tissue downward .
(4) Subglottic can not protected .
(5) COAD .
90. Compare between the CT scan & MRI ?
CT MRI
Better for bone view High level of contrast
Excellent for cartilages Absence of artifact
Excellent for airway Relationship of mass to various major abdominal vessels
Ideal for deep infiltration T1 : Normal & T2 : contrast .
Non invasive
91. Differential diagnosis of granulation tissue in the posterior commissure of vocal cords ?
(1) T.B.
(2) Pachyderma .
(3) Intubation injury .
(4) Tumor .
92. What are the advantages & disadvantages of laryngoscopy ?
Advantages are ;
(1) Physiology clearly demonstrated .
(2) Mucosal surface can be studied in minute detailed .
(3) Subglottic area well delineated .
(4) Excellent for pyriform sinuses & laryngeal ventricles .
Disadvantages are ;
(1) Invasive procedure .
(2) Deep infiltration are not demarcated .
93. Complications of adenoidectomy ?
(1) Immediate ; bleeding , inhalation of blood , debris or teeth , fracture of the TM
joint .
(2) Intermediate ; otitis media & secondary haemorrhage .

Lecture notes in
(3) Late ; recurrence , palatal scarring . Eustachian tube dysfunction , hypernasality

& subluxation of the atlanto-axial joint .
94. Compare between the uni- & bi-polar diathermy ?
Unipolar Bipolar
Current passes through the body to Current only pass between the tips of
exit through the attached plate forceps
Risk of burn More accurate control
95. Uses of Luc’s turbinate forceps ?

(1) Remove bone /cartilage , soft tissue .
(2) Biopsy from oral & oropharynx .
(3) Caldwell Luc’s .
(4) Nasal polypectomy .
(5) Removal of adenoid tags .
(6) Intranasal antrostomy .
(7) Substitute Dennis-Brown in tonsillectomy .
(8) Turbinectomy .
96. Uses of Hill’s elevator ?
(1) In-fracturing of the inferior turbinate .
(2) Initial opening of the antrostomy .
(3) Dissection of the mucoperichondrial flap in Caldwell Luc’s operation .
97. Uses of Tilley-Henckel punch forceps ?
(1) Nasal polypectomy which include simple & antrochoanl .
(2) Removal of septal cartilage .
(3) Turbinectomy .
(4) Intranasal ethmoidectomy .
(5) Biopsy .
(6) Widening the posterior wall of the intranasal antrostomy .
98. Uses of Sickle knife ?
(1) Separation of the incudostapedial joint .
(2) Cutting the stapedial tendon .
(3) Quinsy .
(4) Uncinectomy .
99. Uses of Freer’s separator & elevator ?
(1) SMR / Septoplasty .
(2) External frontoethmoidectomy .
(3) Taking graft during myringoplasty .
(4) Separation of the posterior meatal wall .
(5) FEES .
(6) Subperchondrial dissection of the inferior constrictor muscle during
laryngectomy .
100. Uses of Tilley dressing foceps ?
(1) Dressing .
(2) Removal of foreign body , crust , ..etc .
(3) Open synchea .
(4) Insertion of the nasal pack after nasal surgery .

Lecture notes in
101. Uses of Siegle speculum ?

(1) As an auroscope .
(2) Checking of the mobility of the tympanic membrane .
(3) Fistula test .
(4) Suction .
(5) Insufflations of powder .
(6) Delineation periphery by pushing powder .
102. What is Schwartz’ sign ?
It is used in active otosclerosis where there is hyperaemic promontory blood vessels ,
it fade during positive Sieglization & return to normal in negative Siegalization .
103. Uses of Gruber’s aural speculum ?
(1) Examination .
(2) Removal of wax , F.B. , …etc .
(3) Polypectomy .
(4) Myringotomy .
(5) Used with Siegle’s .
104. Uses of Eusachian catheter ?
(1) Catheterization of the Eustachian tube .
(2) F.B. removal .
(3) Washing of the antrostomy .
(4) Opening of choanal atresia .
(5) Insufflation of drugs into the middle ear .
105. Disadvantages of microlaryngoscopy ?
(1) Time consuming & coasty .
(2) Static .
(3) Must use wide laryngoscope .
106. What are the precautions during laryngoscopy in children ?
(1) Inserted to the vallecula leading to damage of the epiglottis .
(2) Must be used in neutral position due to high larynx .
107. What is the risks of cardiovascular patients ?
(1) Hypertension .
(2) Dysarrythmia .
(3) Ischemia .
(4) Cardiac arrest .
108. Uses of direct laryngoscopy ?
 Diagnostic like hoarseness , suspicion of tumors (occult biopsy) .
 Therapeutic ;
(1) Removal of benign lesions , F.B. .
(2) Injection of Teflon or Sclerosing agents (haemangioma) .
(3) Removal of membrane in diphtherial laryngitis .
(4) For cautery/cryo – laset surgery .
(5) Insertion of endotracheal tube .
(6) Preliminary to bronchoscope .
109. What is the complications of direct laryngoscopy ?
(1) Trauma to the teeth , alveolus (in edentulous patient) , lips .
(2) Haematoma formation over the posterior pharyngeal wall .

Lecture notes in
(3) Stridor due to oedema .

(4) Webbing of the anterior commissure .
(5) Pulmonary complications .
110. What are the advantages & disadvantages of Portex tracheostomy tube ?
Advantages are ;
(1) Can be used during course of radiotherapy .
(2) Inflatable cuff can be used during +ve pressure ventilation .
(3) Associated with less granulation tissue .
(4) Lighter & more acceptable cosmetically .
Disadvantages are ;
(1) It has inflatable cuff leading to ischemia of the mucosa . Prevented by
deflation every 5 minutes .
(2) Can’t used during laser surgery .
111. What are the tubes used with extensive & lower narrowing of the trachea ?
(1) Koenig’s flexible silver tracheostomy tube .
(2) Cuffed tracheostomy tube called Salpeker tube .
(3) Durham’s lobster tube used in Ca. thyroid , after total laryngectomy ; adjustable
flanges , so can be used in thin or very fat neck .
(4) Tail tracheostomy tube which has adjustable flanges .
112. What are the complications of using tracheostomy tubes ?
(1) General .
(2) Local ;
a. Perforation of the oesophagus .
b. Laryngeal spasm & mucosal haemorrhage & oedema .
c. Trauma .
d. Damage to the cervical spine .
113. What are the advantages & disadvantages of Silver tube ?
Advantages are ;
(1) Easily cleaned .
(2) Smooth surface allowing a laminar airflow (wide lumen) .
(3) Re-useable .
(4) Some have a speaking valve .
(5) Can be used in patient who need laser surgery .
Disadvantages are ;
(1) Not used during courses of radiotherapy .
(2) Not used during positive ventilation (no cuff) .
(3) Can erode the posterior tracheal wall .
(4) Cosmetically less satisfies .
(5) Associated with more granulation tissue .
(6) Susceptible to fracture due to erosion between the plate & the tube .
114. Define oesophagoscope ?
It is stainless instrument graduated blunt oval shaped . Used for ;
(1) Diagnostics ;
a. Evaluate patient with dysphagia .
b. Seeking of occult primary .
c. F.B.

Lecture notes in
d. Biopsy .
(2) Therapeutics
a. Removal of F.B. .
b. Dilatation of stricture .
c. Uses of ND-YAG laser .
d. Endioscopic insertion of oesophageal stent .
e. Induction of sclerotic agents .
f. Insertion of packs in Zenker’s diverticulum .
g. Application of endoluminal Irridium .
It is contraindicated in ;
(1) Unfit patient .
(2) Severe stenosis .
(3) Marked Kyphosis .
(4) Pulmonary hypotension .
(5) Cervical spine injury .
(6) Aortic aneurysm .
(7) Haemorrhage .
115. Describe , anaesthesia for bronchoscopy ?
Inhalational anaesthesia .
Short acting myoneural blocking agents .
We can use jet ventilation of low frequency & high frequency .
We can use the eye piece to produce closed anaesthetic system (disadvantage is
preventing any surgical maneuver) .
116. Describe the openings in the bronchoscope ?
(1) One for visualization & instrumentation .
(2) 2 nd for venting .
(3) 3 rd for anaesthesia .
(4) 4 th ; Prism .
117. What are the advantages of side hole in the bronchoscope ?
(1) Ventilation .
(2) If enter to one side the ventilation maintained through the other .
118. Indications of bronchoscope ?
(1) Diagnostic
a. Persistent cough & haemoptysis .
b. Biopsy as lavage for cytology .
(2) Therapeutic
a. Lavage .
b. F.B. removal .
c. Securing the airway when intubation is impossible .
119. What to check in bronchoscope ?
(1) Mucosa .
(2) Secretions .
(3) Any mass .
(4) Mobility of the carinal blunting .
120. What are the complications of bronchoscope ?
(1) Haemorrhage .

Lecture notes in
(2) Laryngospasm .
(3) Bronchial rupture .
(4) Pneumothorax .
(5) Trauma .
(6) Cardiac arryhtmias .
121. Purpose of tympanoplasty ?
To eradicate the pathology from the middle ear cleft with reconstruction of the
hearing mechanism , it is done to prevent the complication (main aim to ventilation
& drainage) .
122. What for myringoplasty to be successful ?
(1) No oedema .
(2) No extravasations .
(3) Tense .
(4) Not atrophic .
(5) Moveable .
(6) Not retracted .
(7) Eradication of the neighboring infections (tonsillitis , sinusitis ..etc) .
123. Before myringoplasty , what must to see ?
(1) The perforation all around .
(2) The tympanic membrane all around which include pars tensa & flaccida , the
posterior superior part start to be sucked lead to retraction pocket causing
necrosis , tethering & then cave development & increased bone destruction .
(3) Middle ear cavity which include ;
a. Mucosa ; which is normally pinkish in color , so must see the mucosa is it
healthy or not i.e. color , swollen or not , inflamed or not , granular or not ,
boggy or not , polypoidal or not .
b. Retained secretions ; which is very important to seek for the cause (important
to diagnose) & treat it .
c. Glistening or not , the glistens of the middle ear mucosa is due to the presence
of mucous blanket which normally present .
d. Any sign of adhesion or fixity or calcium deposit (tympanosclerosis) .
124. Mention the classification of Glottic carcinoma ?
125. Postoperative complications of external auditory meatus surgery ?
(1) Become smaller “stenosis” .
(2) Crumbling .
(3) Easily damaged .
(4) Irregular shaped .
126. Causes of postoperative orbital oedema ?
(1) Oedema of manipulation .
(2) Decompression effect of longstanding mass .
(3) Dislodgement of the superior oblique muscle trochlea .
127. Causes of oral breathing after adenoidectomy ?
It is habitual & disappeared gradually with time .
128. Do we do Caldwell Luc to antral tumor ? NO , at all .
129. Assessment of patient with chronic discharging ear ?
(1) History ;

Lecture notes in
a. To know the chief complaint & duration .

b. Must know the HL ; conductive or sensorineural .
c. Discharge ; is it from the middle or external ear .
d. Tinnitus , . most likely means inner ear ”discharge from the inner ear
regarded serious otorrhea (CSF) or perilymph fistula” .
e. Vertigo , most likely means inner ear or local cause or referred .
(2) Clinical examination ;
a. Otoscopy .
b. Tuning fork .
(3) Investigations ;
a. Laboratory ; blood , bacteriology , histopathology , ..etc .
b. Radiology ; x-ray , CT , MRI .
c. Audiology .
d. Brainstem .
e. Caloric test .
(4) Management ;
a. Medical .
b. Surgical .
130. What are the levels of lymph node in the neck ?
 Level I : submental & submandibular .
 Level II : along the internal jugular vien (superior 1/3rd of it) , from the skull base
to the hyoid bone .
 Level III : between the hyoid bone & the lower cartilage of the cricoid .
 Level IV : between the lower border of the cricoid & the clavicle .
 Level V : posterior triangle of the neck .
 Level VI : pretracheal & paraoesophageal .
 Level VII : superior mediastinuem .
131. Notes on tympanoplasty ?
 Any retraction pocket must put the patient under observation .
 Usually the retraction pocket appears in pars flaccida due to narrow situation &
a limited area in the aditus .
 Perforation of the tympanic membrane means fistula between two epithelial
surfaces (middle & external ears) , so treated like any fistula (Fistulectomy)
starting by removing the margins of the perforation by end-aural incision or post-
aural incision put at the defect of the cartilage .
 Key area ; is the junction in between the bony & cartilaginous parts .
132. Describe the sound characteristics ?
(1) Frequency ; measured by Hz , psychacoustically called pitch .
(2) Intensity ; measured by decibel & called loudness .
133. Anything below 20 dB
134. means hearing loss .
135. Define decibel “dB” ?
It is a logarithmic ratio between 2 intensities (out put & reference) .
Measurement of energy by power (watt/cm2 ) or by (Dyne , Paskal , Joul , Neutron ,
..etc) . The last feeling of auditory sensation is 10-16 watt/cm2 , the range of intensity is
from 10-16 – 1 watt/cm2 .
Lecture notes in
136. Describe the cochlea ?

It is about 35 mm in length (2 ½ cycle) & is consist from apex & base , it’s a frequency
analyzing organ & its range 20-20,000 Hz while the speech level 500-2,000 Hz .
137. What is the audiometric zero ?
138. Any hearing loss up to 20 dB without air-bone gap is considered normal (normal gap
not more than 10 dB) .
139. Define decade audiogram ?
In which the hair cells start to degenerate at the 2nd decade of life .
140. Presbyacusis ? Start after the age of 65 years .
141. Vowels ? Like a o y u , called low frequency , high energetic .
142. Consonants ? Give the meaning of speech & have high frequency , low energetic .
143. Lack of speech discrimination means loss of part or all the consonants in addition to
other complaint like tinnitus .
144. Hearing assessment ?
 History
o Of noise exposure is very important .
o Pre-& post-natal history of viral infection of rubella , CMV ..etc or drug
history like cytotoxic & others , DXRT , history of labor , jaundice , cyanosis ,
obstructed labor , prematurity (<1.5 Kg) , all these called risk factors .
o APGAR scoring < 4 , also risk factor .
o Prelinguisted 0-3 months .
o Postlinguistic 3-6 months at which the child start to say Bibb or Didd ..etc
means normal .
o The most common cause of prelinguistic period HL is meningitis (12%) in
which the sensory nerve affected more than the motor .
o History of trauma , Eustachian tube dysfunction (recurrent OME) , snoring .
o At 8-10 years the most common cause of SNHL is mumps in which 4:9 the
parotid is normal & 5:9 the parotid enlarged .
o History of Herpes zoster oticus .
 Examination
o Inspection of both ears .
o Voice test ; in which sit behind the patient in a distance of 4-8 m (3-6 m for
conservation) & occlude the unexamined ear by its tragus , so whisper means
30 dB , its voiceless sound (no vocal cord mobility) & if the patient hear 50%
of words or more means test +ve .
Rubbing by a finger means a lose of 30-35 dB in 1 m distance .
o Start to examine the better ear at 1 st .
o Threshold of speech is 60 dB .
o The most comfortable level of speech is 60-90 dB .
o Loudness discomfort level “LDL” is 90-110 dB .
o Pain > 110 dB .
o 130 dB or more will cause rupture of the tympanic membrane .
o Hearing loss
20-30 dB Slight HL
30-45 dB Mild HL
45-60 dB Moderate HL

Lecture notes in
60-90 dB Severe HL
> 90 dB Profound or Nill HL
o Pure tone average , in which take a reading of 500 , 1000 & 2000 Hz &
dividing the dB by 3 .
o Linear HH HL present in CHL (Quantitative) .
o Slope HL present in SNHL (Quantitative & qualitative) .
o Tuning fork exam ; must start from 128 Hz up to 4096 Hz in which 128
rapidly decaying while 4096 prolonged decay , the low frequency tuning fork
give us vibrotactile sensation which is not suitable for examination .
512 Hz fork is the most suitable one because it is within the speech range .
1) Rinne test ; it is qualitative & subjective test , normally air conduction
better than bone conduction (also SNHL) which called +ve Rinne test ,
while if BC > AC & in which the air bone gap more than 20 dB then called
Rinne test –ve , this called intensity method of Rinne test .
While duration method of Rinne test , in which put the tuning fork on the
mastoid bone then after disappearing of sound change it to the opposite to
the EAM & ask the patient if still hear or not (if hear +ve , if not –ve) .
2) Weber test ; assess both cochlea at the same time using , usually it is
central , lateralization occur when the difference more than 5 dB & go to
the good ear in SNHL & to the bad ear in CHL , some times still central in
longstanding SNHL .
False negative test in which must use Barany noise box to know flase
negative from genuine SNHL .
3) Schwabach’s test ; in which compare the examiner bone conduction with
the bone conduction of the patient .
o Normal tympanic membrane thickness is 0.07 mm & have 0.8- 1 cm2 surface
area & 56 mm 2 vibrate physiologically .
o The oval window have a diameter of 4 mm2 , so 56/4 = 14 which is the times of
amplification of sound by the tympanic membrane .
o Amplification of the ossicles 1.3 , so 14 X 1.3 = 18 , the amplification power
of the middle ear .
o Disrupted ossicles give HL of 60 dB .
o Disrupted tympanic membrane give HL of 30 dB .
 PTA ;
o Is a subjective & qualitative test of single sinusoidal wave of frequency of 125
– 12000 Hz .
o Masking used in all the bone conduction ( >10 dB loss) & in 40 dB air
conduction or more loss .
o Give + 5 dB of the difference of the 2 ears , like Rt ear BC 40 dB , Lt ear BC
10 dB , 40-10=30 + 5 = 35 dB .
o Recruitment is an abnormal growth of intensity & frequency & tested in
suprathreshold levels .
1. Suprathreshold response
a. Alternate binaural loudness balance test “ABLB” Fowler test .
b. Alternate monoaural loudness balance test “AMLB” Reger test .

Lecture notes in
c. Short increment sensory index “SISI”

2. Auditory adaptation
a. Tone decay test ; decay less than 1 minute means +ve .
b. Bekesy audiometry .
3. Additional special auditory test ;
a. Brainstem evoked response audiometry “BERA” .
b. Acoustic reflex test “ART” .
c. Acoustic reflex decay test “ARDT” .
 Sieglization ; objective & qualitative test used to evaluate the function of the
middle ear in a normal tympanic membrane .
Negative Sieglization seen in ; (1) OME (2) Ruptured drum (3) Otosclerosis .
 Floppy tympanic membrane seen in disrupted ossicular chain .
 Tympanometry ; the only test in which recording the reflected sound , it is
objective & quantitive test , the reflected sound depends on ;
(1) Integrity of the tympanic membrane .
(2) Physiological state of the middle ear .
(3) Air pressure of the EAM .
Use 80 dB SPL , 220 Hz frequency , we have many types of tympanograms ;
o Type A ; peak at zero point ( -100 - -150 normal in children) .
o Type B ; in immobile or ruptured drum .
o Type C ; in –ve middle ear pressure (Eustachian tube dysfunction) .
o Type A d ; in ossicular disarticulation , compliance +200 , > 0.24 .
o Type A s ; compliance -200 , <0.28 .
 Stapedial reflex ; a protective mechanism of the inner ear from high intensity
sounds , the stapedial arc afferent is the 8th nerve & the efferent is the 7th nerve
causing contraction of the stapedial muscle leading to stiffness of the ossicles
leading to blockage sensation of the ear & tinnitus (brief deafness) , it depends on
(1) Latency of sound which is the speed of sound (63 milisec.) .
(2) Attenuation of the sound which is 10-15 dB .
The reflex start in 82+/- 10 dB above the threshold (0 dB) , so in any patient with
CHL of 30 dB we can expect –ve reflex (A-B gap 30 dB) .
The advantages of the stapedial reflex are ;
(1) Differentiation between cochlear & retrocochlear HL .
(2) Facial nerve integrity where it +ve in the level below intratympanic level &
where it is –ve in the level above the intratympanic level .
(3) In inorganic HL .
(4) In cortical level HL .
(5) In peripheral myogenic disease , it is –ve like myasthenia gravis .

145. What are the contents of the internal auditory meatus ?
(1) Sleeve of dura .
(2) CSF .
(3) 7 th & 8th cranial nerves .
(4) Internal auditory artery .
146. What are the types of tympanoplasty ?
 Type I ; only the tympanic membrane removed .
Lecture notes in
 Type II ; only the tympanic membrane + malleus is removed .

 Type III ; only the tympanic membrane + malleus + incus rami is removed .
 Type IV ; only the footplate is preserved .
 Type V ; fenestration of the SCC .
147. Complication of tympanoplasty ?
(1) Vertigo ; due to lateral SCC fistula , removal of the cholesteatoma & irritation of
the inner ear .
(2) Injury .
148. Ligation of both external carotid arteries are possible , also ligation of one internal
carotid artery are possible , but ligation of both external & internal carotid artery are
risky in young patient than in the elderly due to decreased anastamosis .
149. Enumerate the common types of polyps in the ear ?
(1) CSOM .
(2) T.B.
(3) Eosinophilic granuloma .
(4) Glomus jugulare .
150. In total laryngectomy , how to differentiate between the hyoid bone & the greater
cornue of the thyroid cartilage ?
(1) Hyoid bone lateral & posterior to the cartilage .
(2) Freely mobile .
(3) Easily removed .
151. What to check in the 1st & 2 nd day post-laryngectomy ?
(1) The most dangerous complication is pneumothorax not emohysema .
(2) 1 st day check ; airway , pulse , position (must be in semisitting) , analgesia .
(3) 2 nd day check ; auscultation , admit to the ICU , fluid input & output .
152. What is the treatment of OME ?
Adenoidectomy (if adenoid hypertrophied) & myringotomy (with grommet if glue) .
153. What is the complications of myringotomy & grommet insertion ?
(1) Trauma ;
- To the EAC , lead to blood clot in the grommet & blockage .
- To ossicles , commonly the long process of incus , stapes , dislocation of
incudostapedial joint .
- To the promontory , facial nerve injury if dehiscent (not common) .
- To jugular bulb (if high) .
(2) Large incision cause dislodgement of the grommet .
(3) Persistent otorrhea , treat infection by systemic & local antibiotics & avoid
wetting of the ear .
If not settled (20% of cases) , then remove the grommet .
(4) Implantable cholesteatoma (1.7%) .
(5) Persistent perforation , tympanosclerosis & early extrusion .
154. Indications & contraindications of adenoidectomy ?
Indications are ;
(1) Nasal obstruction .
(2) OME .
(3) Chronic adenoiditis .
(4) OSA .

Lecture notes in
(5) Recurrent AOM , repeated attacks of sinusitis .

(6) As biopsy for neck mass , either by curette (large tissue for biopsy) or from the
mass .
Contraindications are ;
(1) Cleft palate , submucous cleft , bifid uvula .
(2) Acute infection .
(3) Bleeding tendency (not absolute) .
155. Acute tonsillitis not responds to treatment for 2 weeks ? Either IMN or T.B. .
156. Indications for mastoid exploration ?
Indications are ;
(1) Cholesteatoma .
The mastoid exploration for cholesteatoma contraindicated in ; increase age ,
small localized attack & early leaving ear which is not contraindicated because it
will end with destruction .
(2) Failure of medical management (after 3 months) , either due to mastoid reservoir
of infection (C&S : Proteus in 85%) or presence of cholesteatoma .
Program of treatment are ; 2 weeks visits , suction clearance & local antibiotics .
(3) Complications of CSOM ; the sinister signs are pain (aggressive infection or
meningeal irritation) & vertigo (labyrinthitis) .
(4) Acute mastoiditis ; can be treated with hospital admission , antibiotics , drainage
(as emergency) +/- myringotomy , after the condition settle then mastoid
exploration .
(5) Revision mastoid surgery .
(6) As a route for other surgery ; cochlear implant , acoustic neuroma , petrositis &
endolymphatic decompression .
(7) Suspicion of malignancy ; otalgia , bleeding , severe disturbances not related to
time .
(8) Granulomatous diseases ; eosinophilic granuloma .
(9) Glomus tumor ; glomus tympani .
(10) Refractory cases of OME .
157. Indications(limited) of septoplasty ?
(1) Caudal dislocation with anterior deviation .
(2) Twisted nose , need undermine & cut from ULC .
(3) In children .
(4) As part of rhinoplasty .
158. In USA do laryngoplasty as a treatment for laryngeal stenosis .
At 1 st do SMR for cartilaginous graft , then Laryngofissure & cricoid splitting &
fibrous tissue remoal with grafting & stenting (T-tube still for 6 months) .
Subglottic stenosis more if intubation > 2weeks due to ; small & narrow area , the
cuff press on the mucosa causing necrosis & fibrosis & the movement causing
friction & leads to injury .
159. Treatment of laryngeal trauma ?
- Antibiotics .
- The early laryngoplasty better (when cord settled) .
- Emergency angiography is very important in head & neck injury ; traumatic
aneurysm (rupture even after 5 days) , A-V shunt .

Lecture notes in
160. α- interferon used in ; GORRP , haemangiomas , intrinsic rhinitis .

161. Treatment of CSOM ?
- Admission to the hospital .
- Treat the underlying cause .
- Start local antibiotics & steroids (use systemic steroids later) .
- Suction clearance for 2-3 weeks .
- If this fail , then mastoid exploration .
162. Myringoplasty not done in children because of high URTI which cause failure of the
grafting .
163. Surgery of CSOM = tympanomastoid surgery .
164. Postoperative mandatory investigations after oesophagoscopy is CXR to exclude any
complication (mediastinitis is an early sign) .
165. Disadvantages of partial laryngectomy ?
(1) Recurrence , because of microscopic invasion .
(2) Aspiration lead to pneumonia especially in old age due to weak cough reflex .
166. Conservative surgery ; endoscopic debulking or removal . In Germany they found it
has same outcome survival life .
167. Treatment of GORRP ?
(1) Co2 laser ; small (vaporization) , large (cut the pedicle & cauterize its end &
remove the mass) .
(2) Interferon .
168. Fungal sinusitis ?
- Recently they found that nasal polyposis cause by fungal infections .
- Surgery means debridement & exteriorization of the sinus cavity to the nose .
- Canazole less toxic than Amphotricin –B (IM injection) .
- Now use drops (locall) of ictranozole .
169. Tracheostomy prior to total laryngectomy may cause ;
(1) Infection by resistant MO like Pseudomonas Spp.
(2) Recurrence .
170. Haematoma auris (spontaneous) ?
- Apsiration ; 80% serous (no blood) .
- Better no hospital admission (nosocomial infection) .
- Frequent aspiration (better than incision which increase the risk of infection) .
- Moulding by vasalin pack for 72 hours .
171. Epistaxis ?
- ECA ligation ; ligation with division better than ligation in continuity because
increased pressure will lead to recirculation , so ligation , division &
transifixation .
- Maxillary artery ligation with anterior ethmoidal artery is much effective than
ECA ligation .
- Rare but dangerous ECA ligation complicated by blindness because ligating the
middle meningeal artery which is the only supply of the ophthalmic artery .
172. Differential diagnosis of Angiofibroma ?
a. Antrochoanal polyp .
b. Inverted papilloma .
c. Bleeding polyps of the septum .

Lecture notes in
d. Benign & malignant tumors of the nasopharynx .

173. Mass in the postnasal space in adult , biopsy better by punch biopsy or curette ?
If suspect tumor , punch biopsy to avoid tumor , if suspect adenoid hypertrophy then
curettage (diagnostic & therapeutic) .
174. To do not biopsy angiofibroma ? NOT .
175. Treatment of recurrent angiofibroma ?
(1) Surgery ; facial degloving approaches .
(2) Gamma knife for small intracranial recurrences .
(3) Radiotherapy especially for intracranial extensions but with risk of DXT on child
growing period .
(4) Hormonal (??) .
(5) Highly selective Embolization . For intracranial extension supplied by middle
meningeal , accessory meningeal & foramen rotundum arteries supplying the
cranial nerves in the cavernous sinus , so for treatment to highly selective
embolization for the maxillary artery beyond the origin of the accessory
meningeal artery .
(6) Chemotherapy (Doxorubcin) .
176. Is it routine to perform angiography (angiofibroma) ?
No , it is mainly indicated in ;
(1) Pre-embolization .
(2) For recurrence (pre-revision surgery) .
(3) As a complementary to diagnosis .
177. What are the methods of tonsillectomy ?
(1) Conventional dissection .
(2) Laser .
(3) Coagulation diathermy .
(4) Guillotine .
(5) Cryosurgery .
178. Postoperative (tonsillectomy0 precaution of bleeding ?
(1) Vital signs ; PR , BP , sweating ..etc .
(2) Frequent swallowing .
(3) Relevant bleeding with vomiting of fresh blood .
Treated by ; children (early return the theater) & adults (according to severity ,
conservative or theater) .
179. Laryngeal carcinoma ?
- CT scan important in ; partial laryngectomy , assessing the vertical extent of the
tumor (sagittal & coronal sections) & assess LN metastasis .
- In elective postoperative DXT give less than the salvage dose for neck in Ca.
supraglottis .
- T3N1 supraglottic tumor , best treatment ; combined modality like total
laryngectomy & modified RND with postoperative DXT for the neck (supraglottis
has high degree of occult neck metastasis) .
180. Postauricular swelling in children ?
(1) Skin lesions ; eczema , infection , insect bite , ..etc .
(2) Subcutaneous lesion ; lipoma , sebaceous cyst , LN , dermoid , mastoid
abscess(70% of AOM associated with mastoiditis , but not all develop abscess) .

Lecture notes in
(3) Otitis externa with furunclosis .

181. Differentiate between furunclosis & acute mastoiditis ?
Furunclosis Acute mastoiditis
History of ear disease - +
Toxicity Mild High
Signs of postauricular tenderness Diffuse Max. over tip
Sagging of the posterior meatal wall - +
Pressure on tragus Painful -ve
Mastoid x -ray Clear aircells or Cloudy or loss of
haziness of soft aircell
tissue trabeculation
W.B. count Increased Highly increased
182. Types of mastoiditis ?

(1) Acute coalescent .
(2) Masked mastoiditis .
(3) Chronic reservoir ; when production of mucopus by large number of aircells is
greater than the discharge power .
183. What is the treatment of the following ?
- Mastoid abscess ;
a. Admission .
b. Drainage of abscess , during drainage look for the cortex of the mastoid , if
there is erosion , then confirm the diagnosis of abscess .
c. Systemic antibiotics till the condition settled (48 hours) .
d. Cortical mastoidectomy even in very young child because of high possibility of
cholesteatoma formation if mastoidectomy not done .
- Mastoid cellulites ;
a. Admission .
b. Systemic antibiotics .
c. Close observation , if no improvement or signs of complications , then mastoid
exploration .
- Masked mastoiditis ;
a. admission .
b. mastoid exploration .
184. Role of myringotomy in acute mastoiditis ?
No role accept in ;
(1) Bulging tympanic membrane due to AOM .
(2) Facial nerve palsy to get relieve of tension .
185. Patient with bilateral objective (audiable) tinnitus , O/E can heard tinnitus which is
not correlated with pulse & mobile or synchronous twitching of the tympanic
membrane ?
This is caused by muscular sounds ;
- Palatal myoclonus ; irregular twitching of the soft palate , pharynx & tensor
tympani muscle .

Lecture notes in
Diagnosed from history , observation of movement of the soft palate , posterior

pharyngeal wall or tympanic membrane through nasopharyngoscopy which is
better to avoid inhibition of twitching .
Tinnitus heard by auscultation tube , intrameatal microphone & amplifier or
observe with oto-admittance meter .
Unknown aetiology & may associated with serios neurologiacal disorders .
Treated by ; maskers , boutlinium toxins into the palatal muscles .
- Middle ear muscle myoclonus (stapedius) ; occur either spontaneous or with eye-
blinking , acoustic stimuli , cutaneous stimulation or phonation .
Treated by division of the stpedius muscle
186. What is the important symptoms in T.B. laryngitis ?
They are ; pain & referred otalgia .
187. Which tumor can get important from steroid therapy ?
Lymphoid tumors .
188. Local anesthesia For larynx ;
- Gargle with 5-10 ml of 2% xylocaine for 10 min. , the 4% lignocain or swab
inserted with the aid of Krause’s laryngeal forceps into both pyriform fossae (for
internal laryngeal anesthesia .
- Subcutaneous injection of xylocain 4-5 ml at the greater horn of hyoid bone for
superiorlaryngeal nerve .
189. Tonsillectomy is also effective as a treatment of OME because the chronically inflamed
tonsils affect swallowing diminished the opening of the Eustachian tube opening .
Also in severe resistant cases can do cortical mastoidectomy to enhance aeration .
OME has a genetic predisposition .
190. Recent theory regarding the nasal polyposis suggest that there is fungal infection
predisposition due to high eosinophilia .
191. In OME (GLUE ear) can use N/S or urea solution instilled through the EAC then
aspirated .
192. Indications of External frontoethmoidectomy ?
(1) Chronic sinusitis not respond to treatment (medical or FEES) .
(2) Recurrent nasal polyposis when surgical landmarks are lost .
(3) Frontoethmoidal mucocele , small osteoma removal .
(4) Access for ; ethmoidal artery ligation , orbital decompression (for malignant
thyrotoxicosis , when remove the medial orbital wall , floor & nasal process of
frontal bone & lamina papyracea) & CSF leak repair .
193. Indications of FEES ?
(1) Pansinusitis .
(2) Chronic headache due to osteal closure by mucosal hypertrophy .
Don’t widen the frontal recess circumferentially .
194. Glioma ?
Hetrotrophic brain tissue , they are not continuous with subarachenoid space or CNS .
If so it is encephalocele , but 15% of glioma do have fibrous connection to
subarachenoid space .
It appears as red polypoidal masses that are firm & non-compressible , must be
differentiated (DDx) from ; dermoid cyst , antrochoanal polyp .
It is not a true neoplasm .

Lecture notes in
195. Indications of fenestration operation in Otosclerosis ?

(1) Abnormally situated facial nerve .
(2) Persistent stapedial artery .
(3) Obliterative Otosclerosis where reclosure has followed stapedectomy .
The fenestra of LSSC covered by the tempromeatal flap .
196. Drainage of the tonsils into the jugulodigastric LN which lies below the posterior belly
of the digastric muscle between the angle of the mandible & the anterior border of the
sternomastoid muscle .
197. Ranula ?
- A bluish translucent cystic swelling in the floor of the mouth to one side of the
lingual frenelum .
- Latin name ranula means frog , so it looks like underbelly of frog .
- In children & young adults .
- Two types, both from the sublingual or salivary gland duct ;
a. Simple ranula , confined to the floor of the mouth .
b. Plunging ranula , with cervical extension through or behind the mylohyoid
muscle .
- Surgical excision ; incision along the gingival margin on the lingual side from the
1 st molar to the canine on the opposite side (mucoperiosteal flap) .
198. Differential diagnsosis of neck mass in children ?
(1) In the midline
a. Thyroglossal cyst ; cystic , sometimes hard (infected) move with swallowing &
tongue protrusion .
b. Dermoid ; cystic & sometimes hard , can pinch skin over it .
c. LN ; infection , malignancy (primary or secondary) .
(2) In the lateral
a. Lymphadenitis ; infection (acute & chronic) or tumors .
b. Cystic hygroma ; not well localized mass , spongy .
c. Branchial cyst ; cystic or firm , under sternomastoid & filled with cholesterol
crystals .
d. Congenital laryngocele .
e. Lipoma .
f. Vascular tumor .
g. Neurogenic tumor .
To differentiate inbetween neck mass & normal structures palpate bilaterally .
To differentiate inbetween submandibular gland & LN palpate bimanually .
199. Laryngeal mass ?
Investigations ;
- CBP & ESR .
- VDRL .
- Sputum for AFB for 3 successive days .
- Radiology ; CXR (for pulmonary T.B. or milliary T.B. , fitness for GA & primary
& secondary tumor) & CT scan (helpful bu endoscopy is superior) .
- MRI ; T1 with Gadolinium best assessment for the tumors margins , while T2 for
nodal staging
200. Hidden areas of the larynx ?

Lecture notes in
- Area of pyriform fossae .

- Ventricles .
- Subglottic areas .
- Laryngeal surface of the epiglottis .
201. Chemotherapy in the treatment of Ca. larynx ?
(1) Used for cure as adjunct with surgery or DXT so increase survival rate .
(2) Used for palliation .
202. Fibroptic nasopharyngoscope ?
- Disadvantages ; limited view that can’t be magnified .
- Advantages ; for patients with overhanging epiglottis .
203. Investigations for Ca. larynx ?
(1) CBP ; anaemia , blood disease .
(2) ESR ; if >100 think of T.B. or lentic disease because it will affect surgery lead to
fistula .
(3) Serological test ; Wassermann test .
(4) LFT , RFT , ECG .
(5) Radiology ;
a. Lateral neck x-ray ; show widening of the potential test .
b. CXR ; to assess the cardiopulmonary status preoperatively & to check for
secondaries .
c. CT scan & MRI ; better both , MRI is the best choice if only one of them , but
LN detection is better by CT (central necrosis) , MRI provide good assess to
margins of the tumor (differentiating it from oedema) , also MRI for blood
vessels involvement (vascular surgeon may be needed) .
d. PET ; it is the precise way for LN detection .
What want to check with radiology ?
I. Paraglottic space ; same as I .
II. Cartilaginous skeleton invasion ; difficult to be assessed because no homogenous
calcification & sometimes the tumor itself result in calcification .
204. In Ca. larynx , there is cartilaginous invasion , what will do ? Is total laryngectomy is
contraindicated ?
Total laryngectomy can be done but be careful during flap elevation , so try to left
platysma with the spciemen , also not take the perichondrium of the thyroid with the
constrictors for repair .
Also postoperative DXT is mandatory or can use it preoperatively to decrease the
tumor volume .
205. In Ca. larynx ; D/L should be done few days before surgery or a the time of operation
to check the ; pyriform fossae , vallecula , postcricoid area , base of the tongue , vocal
cord mobility .
206. Right pharyngeal swelling with apin & dysphagia for few months ?
Investigations ;
- CBP & ESR ; relative lymphocytosis , but no increased WBC , High ESR >90 (in
tumor ESR <50) .
- Radiological ; increase prevertebral space in lateral view of the neck (>80% of
vertebral body , 7 mm at C2 & 22 mm at C6) .
Differential diagnosis ;

Lecture notes in
- T.B. spine ; retropharyngeal abscess .

- Posterior pharyngeal wall tumors including lymphomas .
- F.B. ; e.g. old fish bone .
- FNAC ; cytology , AFB , C&S .
Treatment ; incision & drainage , either ;
- Peroral approach ; better horizontal incision at the lower dependant site , but
there is high risk of fistula formation & to avoid this & other
complications(fistula , T.B. enteritis , ..etc) , should did anesthetic precaution
(cuffed tube) , preoperative (2-3 weeks) of triple anti.T.B. therapy which will
serve for ; stabilize the critical vertebra (destructed) , sterilize the area , decrease
the risk of fistula & therapeutic trial .
In case of T.B. swelling , not open over the swelling directly , but take along tract
of normal tissue & drain it & it is preferable not to leave drain to avoid T.B. skin.
-
207. COG ?
It is bony specula extends down from the anterior part of the tegmen tympani to form
with the anterior middle ear wall the anterior epitympanic recess where cholesteatoma
may be hide , so it is mandatory to remove it if expose the anterior epitympanic recess
during mastoidectomy .
208. Tympanic membrane perforation ?
(1) Central ; anterior , posterior & subtotal .
(2) Marginal ; attic & postero-superior .
209. Cupullolithiasis ?
It is basophilic deposit embedded into the cupula of the posterior SCC of the
undermost ear in the provocative position .
These otoconia dislodged from utricular macula as a result of ; head trauma , acute &
chronic inflammatory conditions , ageing , & surgical insult to the labyrinth .
210. Dehiscence of Fallopian canal usually in the horizontal segment , facial nerve palsy
due to CSOM is almost always affect the nerve in the tympanic segment .
211. Congenital anomalies of the auricle ?
(1) Darwin’s tubercle ; small elevation on the poster-superior surface part of helix .
(2) Mozart’s ear ; fusion of the helix & antihelix .
(3) Fused lobule ; to the side of the head , more common in female .
(4) Bat ear ; lop ear (underdevelopment of crus antihelix) & cup ear
(underdevelopment of most of antihelix) .
(5) Auricular appendages or accessory auricles ; small elevation of skin anterior to
the tragus contain an elastic cartilage .
(6) Preauricular sinus .
(7) Collaurial fistula between the EAC & open at the anterior border of the
sternomastoid muscle .
212. Management of the laryngeal carcinoma ?
- Staging ; N1 (III) & pre-epiglottic involvement (T3) .
- Chemotherapy ; 5FU +cisplatine , given concomittent with DXT , then give
another course with surgery .
For stage III & above about 68% success rate (2 ways chemo-/Radio-therapy &
surgery) .

Lecture notes in
- DXT postoperative with 2 weeks not more than 6 weeks .

- DXT with partial laryngectomy ; 4500 Rad , if salvage DXT ; 6500 Rad .
- Field cancerization ; on the hospital find a lot of malignant changes in mucosa
for that who smoke & drink .
- Free tissue transfer sutured by 10/0 nylon via the facial artery or superior thyroid
artery .
213. 45 years male presented with vertigo (severe rotatory) associated with repeated
attacks of vomiting , left patient immobile in bed aggravated by any head movement ,
become less with lying on the left side , where the right side with CSOM for 20 years ,
during the attack increased HL , tinnitus , ear fullness , headache , but no otalgia ,
with history of infrequent attacks of unsteadiness since last year , last one was 2 weeks
which end with this attack .
- History of left CSOM treated surgically 15 years ago , now dry .
- O/E ;
oDrowsy , supported by relative , temp. 37 c .
oEar ; right with polyp & granulation tissue obscuring the tympanic membrane
, while the left with radical mastoidectomy , dry .
oFistula test ; -ve .
oFacial nerve ; intact .
oRinne test ; -ve bilaterally , Weber central , ABC prolonged .
oEyes ; 3rd degree nystagmus to the right , more in looking to the right .
oCerebellar tests ; normal .
oBalance tests ; acute vertigo status (not done) .
oNeck ; no abnormality .
- Differential diagnosis
oIntratemporal complications of CSOM ; labyrinthitis (serous , purulent ,
circumscribed) .
oIntracranial complications of CSOM ;meningitis , cerebellar abscess .
oVestibular neuronitis .
oSecondary endolymphatic hydropes .
- Investigations ; before doing a lot of investigations put the patient on
symptomatic supportive measures ; bed rest , antibiotics (systemic & local) wick ,
labyrinthine sedative & antiemetic & i.v. fluid if recurrent vomiting .
oSequential PTA for follow up & for ; type of the HL , severity of the HL , state
of the 2nd ear , cochlear reserve , baseline for follow up , medicolegal aspect .
oRadiological ;
a. Lateral oblique x-ray for ; anatomical landmarks for surgery , degree of
pneumatization & identify pathology .
b. CT scan for precise identification of pathology , erosion & bony distortion
, intracranial complications …etc .
oEar swab for C&S .
oFBC & ESR ; increased WBC means infection & ESR to exclude T.B. ,
malignancy , …etc .
- Provisional diagnosis ; right serous labyrinthitis secondary to CSOM mostly with
labyrinthine fistula (occur in the last year “infrequent attacks of unsteadiness”)
- What goes with the diagnosis ?

Lecture notes in
oIncreased HL , but not dead ear (purulent) .

oVertigo for many days (destructive lesion in the inner ear) .
oNystagmus towards the diseased ear . In contrast with the purulent
labyrinthitis which start to the affected ear , but sonly changes to the good ear
oNo pyrexia ; goes with labyrinthitis in general .
oCaloric test ; done after the acute phase ; show hypofunction , but its canal
parasthesia in purulent type .
N.B. : serous labyrinthitis “called catarrhal labyrinthitis” is non purulent
inflammation of the labyrinth occasionally with fibrinous or serous exudates , it is
reversible & recover with some of vestibular & cochlear function .
Purulent labyrinthitis with polymorph cell infiltration , destruction of vestibular
& cochlear structure (irreversible) occasionally the bony capsule , its symptoms
more severe .
Although there is differences between the two types , but diagnosis is usually
retrospective ; after the condition settle , so if dead ear it is purulent & if some
function recover then serous .
- What against other differential diagnosis ?
oMeningitis ; no fever , no neck stiffness .
oCerebellar abscess ; no pyrexia , no neck stiffness , normal cerebellar
function , no focal neurological signs or fits .
oVestibular neuronitis ; there is HL .
oSecondary endolymphatic hydropes ; usually vertigo with hours (not days) .
- Treatment ;
oSupportive systemic treatment for labyrinthitis .
o7-10 days later , mastoid exploration for CSOM (need radical usually) .
oCooksey-Cawthorne exercise to accelerate central compensation (many
exercise with closed eyes) ;
a. Stage I ; head kept still in bed , eye movement .
b. Stage II ; head & eyes movement while sitting .
c. Stage III ; head & body movement while sitting .
d. Stage IV ; standing exercise .
e. Stage V ; moving out .
214. Notes on CSOM management ?
- Middle ear 7 mastoid cavity is a good media for the MO growth because the
body temperature & debris , so treatment by ; cleansing , betadine or antibiotic
wick which give a dramatic response .
- Period of preoperative prepare for CSOM before mastoidectomy is better & it
can take 2 weeks to decrease infection .
- Surgery of the ear ; (1) soft tissue work (2) bone work & (3) plastic work .
- Postauricular incision is 1 cm behind the sulcus to avoid stenosis of the EAC .
- Graft used is temporalis fascia & other is cartilage graft used since 1960 .
- For bony work eccenturate aircells as much as possible .
- Facial nerve is posterior to the perifacial cells , so thining of the facial ridge is
mandatory .
- CAT ; anterior & posterior tympanotomy = extended cortical ;
o Used for CSOM in adults .

Lecture notes in
o Use postauricular & permeatal approach to clear aircells from anterior to

posterior .
o Clear zygomatic , sinodural angle & especially the anterior epitympanum
because cholesteatoma commonly hidden their , 50% of residual & recurrence
is there & that call now anferior epitympanic recess .
- Tympanotomy = viewing middle ear from outside ;
o Permeatal approach .
o Anterior = above Eustachian tube .
o Superior = above ossicles .
o Posterior = for posterior mesotympanum .
- In mastoid surgery to prevent postoperative stenosis ;
o Canal plasty , by drilling i.e. shaving superior & posterior & anterior wall .
o Suture of periosteal layer .
o 1 cm incision behind sulcus .
- Tympanoplasty = myringoplasty + ossiculplasty .
- Level of bridge = level of annulus .
- Meatoplasty ;
o Elevation map ; incision from 12 o’clock to 6 o’clock .
o Remove good amount of cartilage .
o Lowering of the facial ridge till floor .
- In revision mastoid surgery sometimes you will find dural herniation +/- brain
tissue , treatment , recently they amputate the herniation even with brain tissue
because they found it is non-functioning , then repair with temporalis fascia .
215. Differential diagnosis of nasal mass in children ?
(1) Congenital
a. Cystic ; Meningoencephalocele , Dermoid , Epidermoid , Nasolacrimal duct
mucocele .
b. Solid ; Glioma , Haemangioma , Lymphangioma , Teratoma ,
Rhabdomyosarcoma , Craniopharyngioma .
(2) Acquired
a. Cystic ; sebaceous cyst , lacrimal duct cyst .
b. Solid ; lipoma , papilloma , lymphoma , polyp , abscess .
216. Nasal dermoid ; anywhere in the midline of the nose between the glabella to the
collumella may extend to septum , to cribriform plate or intracranial extension .
Treated by surgical excision , comined intracranial & extracranial approaches if there
is intracranial extension .
217. Nasal glioma ; neural tissue trapped by skull closure i.e. hetrotopic brain tissue
outside the brain without any connection to the brain , but sometimes fibrous stalk with
dura . Outside the cranial cavity , inside it or mixed .
Smooth rubbery mass with grey, yellow or purple surface , diagnosis by examination ,
CT (not distend with crying) & FNA (NO CSF) .
Treated by ; intracranial (lateral rhinotomy) & dural connection (anterior craniotomy) .
218. Nasal meningoencephalocele ; local herniation of glial tissue & meninges through
skull defect (brain tissue +subarachenoid space + CSF) .
Treatment in few cases , where small skull defect ; excision of the plugging defect .

Lecture notes in
In most cases ; craniotomy , removal of the herniated brain tissue , tantalum mesh for
bony defect & fascia for meninges .
219.

Lecture notes in
Appendix B
BRANCHIAL APPARATUS
Components of the Branchial Apparatus
o Branchial Arch: composed of a cartilaginous bar, brachiometric nerve, muscular
component, and aortic arch artery
o Branchial Grooves or Clefts: external, lined with ectoderm
o Branchial Membrane: formed between branchial groove and pouch
o Branchial Pouches: internal, lined with endoderm, contains a ventral and dorsal
wing
Branchial Arches
I (Mandibular Arch)
o Meckel’s Cartilage: malleus head and neck, incus body and short process, anterior
malleal ligament, mandible (formed from intramembraneous ossification)
o CN V3: muscles of mastication, tensor tympani, tensor veli palatini, mylohyoid, and
anterior digastric muscles
o Maxillary Artery
o Hillock of His: 1. tragus; 2. helical crus; 3. helix
II (Hyoid Arch)
o Reichert’s Cartilage: manubrium of malleus, long process and lenticular process of
the incus, stapes (except vestibular part of footplate), styloid process, stylohyoid
ligament, lesser cornu and upper half of hyoid
o CN VII: muscles of facial expression, stapedius, stylohyoid, and posterior digastric
muscles
o Stapedial Artery (degenerates)
o Hillock of His: 4. antihelix crus; 5. scapha; 6. lobule
III
o Cartilage: greater cornu and lower half of the hyoid
o CN IX: stylopharyngeus muscle, superior and middle constrictors
o Common Carotid and Internal Carotid Arteries
IV
o Cartilage: thyroid and cuneiform cartilage
o Superior Laryngeal Nerve: cricothyroid muscles and inferior pharyngeal
constrictors
o Aorta (left); Proximal Subclavian Artery (right)
V/VI
o Cartilage: cricoid, arytenoid, and corniculate cartilage
o Recurrent Laryngeal Nerve: intrinsic laryngeal muscle (except cricothyroid muscle)
o Ductus Arteriosus and Pulmonary Artery (left); Pulmonary Artery (right)
Branchial Pouches
I: eustachian tube, middle ear (mastoid air cells), inner tympanic membrane
II: supratonsillar fossa, palatine tonsils, middle ear
III: epithelial reticulum of thymus, inferior parathyroids
IV: parafollicular cells (C-cells) of thyroid, superior parathyroids
Branchial Clefts (Grooves)
I: external auditory canal, outer tympanic membrane (dorsal part)
II-V: obliterates

Lecture notes in
Appendix C
CRANIAL NERVES
CN I — Olfactory
Olfaction
o neurosensory cells (in olfactory epithelium) . lateral olfactory stria lateral olfactory
area of temporal bone
o neurosensory cells (in olfactory epithelium) . medial olfactory stria (lesser
contribution) . frontal lobe (limbic system)
CN II — Optic
Vision
o ganglion cells of the retina — optic nerve . lateral geniculate body (thalamus),
pretectal area (midbrain), primary visual cortex (occipital lobe)
CN III, IV,VI — Oculomotor,
Trochlear,Abducens
Somatic Motor
o CN III: levator palpebrae superioris, superior rectus, medial rectus, inferior rectus,
and inferior oblique rectus muscles (oculomotor nucleus)
o CN IV: superior oblique muscle (trochlear nucleus)
o CN VI: lateral rectus muscle (abducens nucleus)
Parasympathetic
o Edinger-Westphal nucleus — preganglionic parasympathetic fibers (CN III) . ciliary
o ganglion — postganglionic parasympathetic fibers ciliary muscles and sphincter
pupillae muscles
NOTE: sympathetic fibers to the globe and sensation from V1 also pass through the
ciliary ganglion
CNV — Trigeminal
Branchial Motor
o CNV3 (foramen ovale) . muscles of mastication, tensor tympani, tensor veli palatini,
mylohyoid, and anterior digastric muscles (masticator trigeminal nucleus)
Sensory
o CN V1: lacrimal (also carries parasympathetic fibers from facial nerve), frontal,
nasociliary, and meningeal branches
o CN V2: zygomatic, infraorbital, pterygopalatine, and meningeal branches
o CN V3: buccal, auriculotemporal, lingual, inferior alveolar, and meningeal
branches
o trigeminal ganglion (Meckle’s cave in middle cranial fossa) trigeminal nucleus
CNVII — Facial Nerve (mentioned in detailed in lectures) .
CNVIII — Vestibulocochlear Nerve
Balance
o vestibular nerve . ipsilateral and contralateral pontomedullary (4) vestibular nuclei
Hearing
o cochlear nerve . cochlear nucleus . superior olivary nuclei . lateral lemniscus .
inferior colliculus . thalamus (medial geniculate body) . auditory cortex at sylvian
fissure of temporal lobe (Brodmann’s area 41)

Lecture notes in
CNIX — Glossopharyngeal
Taste
o taste from posterior 1/3 . nucleus solitarius
Branchial Motor
o stylopharyngeus muscle (ambiguus nucleus)
Parasympathetic
o inferior salivatory nucleus (medulla) — glossopharyngeal nerve (Jacobson’s nerve)
— lesser (superficial) petrosal nerve . otic ganglion . postganglionic
parasympathetic fibers . parotid gland
Sensory
o visceral sensation from carotid body (chemoreceptors for oxygen tension) . nucleus
of the tractus solitarius
o sensation from posterior 1/3 of tongue, external auditory canal, and tympanic
membrane
CN X — Vagus
Branchial Motor (ambiguus nucleus)
o Recurrent Laryngeal Nerve: all intrinsic laryngeal muscles except cricothyroid
muscle (also sensory to laryngeal mucosa inferior to glottis)
o Superior Laryngeal Nerve (External Branch): cricothyroid and pharyngeal
constrictors
o muscles of the pharynx (except stylopharyngeus), levator veli palatini, uvulae,
palatopharyngeus, palatoglossus, salpingopharyngeus, and pharyngeal constrictors
muscles
Parasympathetic
o dorsal motor nucleus — preganglionic parasympathetic fibers . smooth muscle
innervation to thoracic and abdominal viscera, secretory glands of the pharynx and
larynx
Sensory
o Superior Laryngeal Nerve (Internal Branch): sensory to laryngeal mucosa above
glottis
o Auricular Branch (Arnold’s Nerve): sensory from postauricular skin, external
auditory canal, tympanic membrane, and pharynx
o visceral sensory from pharynx, larynx, and viscera . nucleus of the tractus solitarius
CN XI — Accessory
Branchial Motor
o sternocleidomastoid and trapezius muscles (accessory nucleus)
CN XII — Hypoglossal
Somatic Motor
o intrinsic muscles of the tongue (except palatoglossus muscle), styloglossus,
hyoglossus, and genioglossus muscles (hypoglossal nucleus)


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Lecture notes in

Part One Otology and Neurotology

ORL , Head & Neck surgery 2

Fracture of the facial skeleton 248

Stenosis of the larynx 531

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Examination of the ear

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- Cochlea & semicircular canals .

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o Conduct sounds energy to the inner ear .

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FUNCTIONAL EXAMINATION OF HEARING

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- CHL , the sound heard towards the deafened ear .

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4. Short increment sensitivity test (SISI)

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The acoustic reflex

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The diagnostic importance of acoustic reflex measurement should be considered in tow

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3. CT with i.v. contrast , if normal .

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VESTIBULAR FUNCTION TESTS

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Congenital malformation of the ear

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(2) Autosomal dominant (20%) .

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Theories which explain these symptoms ;

6. Not necessary beat toward the involved ear .

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c. CT scan to see whether there is pus collection .

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