Clinical Methods in ENT by P. T. Wakode

Clinical Methods
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Clinical Methods
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(Second Edition)
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PT Wakode
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Dean
Indira Gandhi Government Medical College
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Nagpur University
Nagpur, Maharasthra, India
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Clinical Methods in ENT
First Edition : 2002

Reprint : 2005
Second Edition : 2013
ISBN 978-93-80704-97-5
Printed at
Foreword.............................................................
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It is a great delight for me to write a brief introduction to Professor Wakode’s excellent textbook
Clinical Methods in ENT. It was my great pleasure in 1988 to welcome Professor Wakode to Southampton
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on a Commonwealth Medical Fellowship sponsored by the British Council and Association of
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Commonwealth Universities. My particular expertise is in medical laser applications in ENT and
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certain other specialties and I very much enjoyed teaching him “all I know about lasers” and he was
also a most valuable member of our Clinical Department. I have followed his career since his return
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to India and I am delighted to know of his appointment as Professor of ENT in Yavatmal.
This textbook is designed for undergraduate students and will also be of great value to any doctor
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in any grade wishing to improve his knowledge of clinical methods in otolaryngology. I wish this
book every success.
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John Carruth MA MB PhD FRCS
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Southampton, UK
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Preface to the Second Edition ..........................
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I am really happy to write preface for the second edition of our book “Clinical Methods in ENT” in a
span of 8 years. But at the same time I am also anxious because of explosion of knowledge through
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internet, the virtual reality of the matter and the speed with which our medical science is changing
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every day, it is difficult to keep pace with it. Moreover, contradictory opinions and research results
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are likely to confuse the undergraduate students. Hence, an attempt is made to stick to the old and
Gold standard whatever possible. But at the same time, the new entrant in the medicine should not be
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unknown to the fastly expanding knowledge in the field. Hence, an attempt is made to keep the
golden median of the two. With this intent we have added a chapter on ‘Thyroid’ in this edition, and
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also brief notes on “Nasal Endoscopy”.
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New and newer investigative tools are coming to the market and medical treatment is becoming
more and more expensive day by day. In these days of evidence based Medicine, it has become
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mandatory to keep evidence of everything a clinician is doing for the patient. However, the
investigation may be sophisticated or costly, the last sentence does mention, “Please co-related clinically”;
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itself is self evident and need no overemphasis for the value of Clinical Judgment.
I am really thankful to Dr RB Deshmukh, a consultant ENT Surgeon, Nagpur for his contribution
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on Nasal Endoscopy and providing beautiful photographs on a very short notice. My residents Dr
Ranjan Mahajan and Aatish Gujrathi were all the time ready to help me, whatever help I needed.
I hope this edition to stands true to the expectations of readers and proves to be the first milestone
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in the achievement of their medical carrier.
PT Wakode
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Preface to the First Edition ..............................
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It would not be an exaggeration if I say that otolaryngology is the specialty, which has grown spell
and bound, in the last 25 years. Few years’ back ENT was supposed to be a branch of surgery for
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tonsil and submucous resection of septum. This is no longer true. ENT has made inroads, which
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comprise from dura to pleura. With the advent of newer technologies like micro ear surgery, laser
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surgery and functional endoscopic sinus surgery, otolaryngology is usurping the newer records of
state of art. A medical student, who is going to treat the patients in 21st century cannot afford to lag
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behind.
While teaching undergraduate students, I always felt the necessity of a book based on clinical
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teaching in ENT. There are large numbers of textbooks on ENT written by senior authors. But they do
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not satisfy the need of students as to “ How to examine an ENT patient?” Books to this effect are
written for General Surgery and Medicine. Even though the basic principles of examining the patient
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remain the same, the specialty of otolaryngology differs in many respects. There was a gap between
a novice student and field of otolaryngology. It was my desire to fill up this gap.
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I am sure that this book would be immensely useful to the undergraduate students who are doing
clinical posting in ENT. It would give them insight to patient examination. The book would be
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equally useful to residents who are working in ENT. The book is illustrated nicely with 163 coloured
photographs of various clinical conditions. Diagrams and charts given in the book should be useful
to the students in clinical learning. An attempt is also made to teach the relevant radiology to the
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student.
I owe beyond words to my wife Mrs Bharati Wakode, who could tolerate my masterly inactivity in
household matters due to pre-occupation in this book. Dr Surendra Gawarle, Associate Professor, in
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ENT has all the time helped me in giving positive criticism on various aspects of the book. Dr Samir
Joshi, Lecturer in my department was always ready to help me in preparing the photographs, text
and any other help needed to me from time to time. Dr Dilip Sarate, a Pathologist has drawn beautiful
diagrams for the book and definitely needs to be mentioned. Dr Pawan Tekade, my House Officer has
given his co-operation in digital photography.
It would be my pleasure to see this book in the hands of students attending the ENT clinics.
PT Wakode
Contents .............................................................
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Part I: Basics of History Taking
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1. Introduction ......................................................................................................................... 3
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2. History Taking .................................................................................................................. 11
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3. Examination of Swelling, Ulcer and Fistula ............................................................. 15
Part II: Otology

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4. Examination of Ear .......................................................................................................... 29
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Part III: Rhinology
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5. Examination of Nose and Paranasal Sinuses ........................................................... 73
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Part IV: Head and Neck
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SECTION A
6. Oral Cavity and Oropharynx ...................................................................................... 117
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7. Examination of Larynx and Laryngopharynx ......................................................... 136
8. Thyroid Gland ................................................................................................................ 148
SECTION B
9. Examination of Neck ..................................................................................................... 157
10. Examination of Salivary Glands ................................................................................ 173
X Clinical Methods in ENT
SECTION C
11. Diseases of Oesophagus .............................................................................................. 179
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12. Tracheo-bronchial Tree ................................................................................................ 187
Part V
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13. Examination of Cranial Nerves .................................................................................. 197
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Index ................................................................................................................................... 217
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Basics of HistoryiTaking
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• Introduction
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• History Taking
• Examination of Swelling,
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Introduction
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Dear students, by the time you are posted in ENT you have already completed your clinical posting
in General Surgery and General Medicine. So, you are well acquainted with patient’s history
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taking. Let me tell you that though basic principles remain the same, the clinical examination in
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ENT is a bit different from what you have learnt so far. And this is so because Ear, Nose and Throat
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are small darker cavities in the human body. They are partially hidden and to examine them you
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need good illumination. Not only that but these are very sensitive parts of the body and while
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examining them one has to have a “feathery touch” and some patience also. Because many a times
even with utmost care, patient does not co-operate in the examination. One more difference is that the
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teacher can teach you how to examine a tumor on hand, foot or even abdomen and more than one
student can see it simultaneously. But this is not the case in ENT. It is very difficult to examine the
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patient by two people simultaneously because of small and relatively inaccessible anatomical areas.
And hence, one has to put more efforts to be proficient in the ENT examinations. Let me say that it is
a scientific art.
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So, before we actually embark on the clinical examination it is better, if we get acquainted with
various instruments commonly needed to examine a patient.
Bull’s Eye Lamp (Figure 1-1)

This is the most important instrument for proper illumination of the relatively darker cavities like ear,
nose and throat. It consists of a heavy base, stand and a cylindrical box. This box contains an
electrical bulb and a powerful convex lens. Electrical bulb should be milky white so that you get a
good circular focus.
4 Clinical Methods in ENT
Figure 1-1: Bull’s eye lamp
Head Mirror (Figure 1-2)

This is another important equipment needed. It has a circular concave mirror and a headband attached
to it. It has a central hole of diametre of approximately 2 cm through which examiner can see. The
concave mirror has focal length of approximately 23.6 cm. The headband is fixed to the head and then
the concave mirror is held close to the right eye completely covering it. Examiner closes his left eye and
focuses the light on the patient’s body. Then he sees with his right eye through the central hole. Once he
Figure 1-2: Head mirror

Introduction 5
gets a good focus he opens his left eye and examines the patient by keeping both eyes open. With little
practice this becomes a routine. Light coming from the Bull’s eye lamp is reflected from the head mirror
on the patient’s body. As the rays focussed on the patient are parallel to visual axis of examiner you get
very good illumination. Your both hands are free for various manipulations like syringing or removal
of foreign body, etc. This illumination system is best in the present circumstances. Torch, or otoscopes
are in the use but these instruments keep your hand engaged and manipulations like removal of wax,
FB, etc. are not possible. Hence, this lighting system is popular all over the world.
Aural Speculum (Figure 1-3)

This instrument is used to examine the ear canal and tympanic membrane. They are polished from
outside but having dull finish inside so that they do not reflect much light to cause glare. Black finish
ear speculums are used in operation theatre for the same reason. Aural speculum of appropriate size
should be chosen and negotiated in the ear canal. It should pass easily the junction of bone and
cartilage. It should be snugly fitting, not too large or too small for the ear under examination.
Figure 1-3: Aural speculum
Nasal Speculum (Figure 1-4)

Thudicum’s nasal speculum is in the common use. It has blades and a U-shaped metallic strip to
hold the instrument. Nasal speculum of appropriate size should be chosen. It is usualy held in the
left hand with the blades of the instrument facing the patient. Index finger and thumb hold the
instrument and middle and ring finger control the movements of blades. Slowly it is negotiated in the
patient’s nostril without hurting the patient. You can examine nasal septum, turbinates and any
Figure 1-4: Nasal speculum
abnormality in the nose with the help of this instrument. Long bladed instrument may be painful and
should not be used without anaesthesia.
Laryngeal Mirrors (Figure 1-5)

These are small plane mirrors fixed in a circular metallic bracket. They are used to examine the larynx
and pharynx, which is otherwise inaccessible for examination. They have a small handle to hold the
instrument. The mirror surface is gently heated before doing the examination. This is to prevent
condensation of patient’s breath on the mirror. As you do not see the actual larynx but a mirror
image. The procedure is known as Indirect Laryngoscopy.
Figure 1-5: Laryngeal mirror
Post-nasal Mirrors (Figure 1-6)

These mirrors are similar to laryngeal mirrors but smaller in size and the handle is not straight. It is
having two bends in it. This is to suit the instrument in the post-nasal space and to keep the hand of
clinician away from the visual field while examining. This examination is called as Posterior
Rhinoscopy, popularly known as PR examination.
Introduction 7
Figure 1-6: Post-nasal mirror
Siegle’s Pneumatic Speculum (Figure 1-7)

This instrument is having a rubber bulb, rubber tubing and an adapter that can be attached to an ear
speculum. The adapter has fitted in it a convex lens having a magnification of 2X.
USES
1. To see a magnified view of the tympanic membrane
2. To elicit the mobility of tympanic membrane
3. To elicit fistula test.
Tuning Forks (Figure 1-8)

Tuning forks of 256, 512 and 1024 Hertz are used in ENT practice. They are different from the tuning
forks used by physicist. Medical tuning forks have a strong metallic base, stem and prongs. They are
used to perform hearing tests like Rinnie test, Weber test, etc.
Figure 1-7: Siegle’s speculum Figure 1-8: Tuning forks

Wire Vectis with Cerumen Spud (Figure 1-9)

This instrument is used for removal of FB/wax in clinical practice.
Figure 1-9: Wire vectis
Tongue Depressor (Figure 1-10)

This is used to depress the tongue during oral cavity and oropharynx examination. It is also used
during posterior rhinoscopy. Cold spatula test is also possible with it.
Figure 1-10: Tongue depressor
Cotton Wool Carrier (Figure 1-11)

This instrument is used to clean the cavity if it is full of discharge, wax or pus. It has serration at one
end. Surgical cotton is wrapped to that end and the instrument is negotiated in the nose or ear to wipe
out the secretions. This is superior over various buds available in the market. Ring end can be used to
remove foreign bodies also.
Figure 1-11: Cotton wool carrier

Introduction 9
Nasal Packing Forceps (Figure 1-12)
It is used for the nasal/aural packing, removal of FB or crusts.
Figure 1-12: Nasal packing forceps
Suction Cannula
To clear the secretions from the ear nose or throat.
Spirit Lamp
It is used to warm the mirror in indirect laryngoscopy and posterior rhinoscopy. Few people also use
hot air blasts instead of spirit lamps.
Sitting Arrangement (Figure 1-13)

It is better to have a small cubicle arrangement rather than a big hall for examination. Patient is sitting
on a revolving stool or a chair at a distance of approximately 1.5 feet away from the clinician.
Patient’s head and neck and clinician’s eyes should preferably come in same horizontal plane. Bull’s
eye lamp is kept on the left side of the patient approximately one foot away and behind, at a little
higher level so that the heat generated does not cause discomfort to patient. Clinician should sit on a
chair with an instrument trolley available on his right hand side. Parallel rays coming from the Bull’s
eye lamp are reflected from the concave mirror, on the patient’s body and we get a good circular focus.
With the help of this illumination, examination of relatively darker cavities of nose, ear and throat
becomes easier.
Figure 1-13: Sitting arrangement
Otoscope (Figure 1-14)

This is one more useful instrument in ENT. It is used to examine the ear. It has disposable black
coloured ear speculum, magnifying lens having magnification power X 2. It is battery or electrically
operated. It gives bright-magnified view of the tympanic membrane. Some of the otoscopes have
facility for changing ear canal pressure. This helps to test mobility of tympanic membrane and fistula
test. However, removal of wax, FB is very difficult when the instrument is in ear canal and clinician’s
one hand gets engaged in holding the instrument.
Figure 1-14: Otoscope

2
History Taking
The importance of good history taking is beyond doubt. With a careful history taking you can help
yourself to come to more accurate diagnosis which at times may not be possible even with
sophisticated investigation. You have already learnt this art during your posting in General Medicine
and General surgery. Here I would narrate few points related to ENT. Otherwise it is more or less
same as taught to you in medicine/surgery.
Name
It is a good practice to call the patient by name. This gives a feeling of closeness to the patient. This
may at times help you to know the religion of the patient without asking him. For example, you can
guess the religion of a person having name Yussuf Khan or George De’silva.
Age
There are few problems, which are age related. Tonsil, adenoid hypertrophy is commonly seen in younger
patients. Nasopharyngeal angiofibroma is usually seen in puberty age. Congenital anomalies are usually
seen in early childhood. Cancer is usually seen after the age of 40, however, no age is immune from it.
Sex
Nasopharyngeal angiofibroma is exclusively seen in males in puberty age group. It is almost non-
existent in female. Atrophic rhinitis is more common in young female. Otosclerosis is more commonly
seen in female. Carcinoma of larynx is more common in male while post-cricoid malignancy is more
common in female. This information is necessary to avoid certain blunders that can be made in the
beginning of one’s carrier.
Occupation
It is very important to know the exact nature of work the patient does. This not only helps in the
diagnosis but also gives an idea about his/her socioeconomical status. The job he/she is doing may
itself be directly or indirectly responsible for his/her present problem. For example, teachers, preachers,
hawkers, singers who use their voice to the maximum are likely to suffer from chronic laryngitis,
vocal nodule, etc. People working in wood industry, petroleum refineries are prone to develop
malignancy of nose and paranasal sinuses. People working in noisy industry may develop noise
induced hearing loss after prolong exposure.
Similarly the treatment policy may have to be changed taking into account the occupation of the
patient. For example, a person whose bread and butter depends upon his voice may be advised
radiotherapy instead of total laryngectomy in case of carcinoma larynx.
Residence
Rhinosporidiosis is common in some pockets of Madhya Pradesh, Chhattisgarh and along the coastal
border of our country. But it is very rare in the European community to develop it without visiting the
Southeast Asia. People living in damply atmosphere are prone to develop otitis externa or otomycosis
frequently. Proper record of postal address helps us to trace out the patient when needed for
follow-up.
Complaints
Majority of the patients do not know what exactly the clinician needs, and they beat round the bush.
It is true even for educated patients. Hence, clinician has to have a patient hearing towards the
patient’s complaints and give some hints to the patient to extract proper history. All the complaints
should be noted down in chronological order.
For example:
Otorrhoea right ear 2 years
Hearing loss same ear 1 year
Headache 7 days
Fever 2 days
If the complaints arise at the same time then more severe complaint should be written first.
History taking 13
History of Present Illness
As far as possible this should be narrated in patient’s own language or style. Each and every complaint
should be properly analysed. The mode of onset, severity of the complaint and laterality should be
asked. For example, if the patient complains of otorrhoea he should be asked as to How it started or
what made it to start, because it may be an attack of acute otitis media to begin with or a history of
trauma. Severity of the complaint should always be asked as it gives you an information whether it
needs urgent intervention or not.
God has given us bilateral organs to compare. Hence, always compare the diseased ear
with normal one, if only one is diseased.
• Leading questions should be avoided
• Negative history may be very helpful at times. For example, perforation in nasal septum with no
history of surgery on septum suggests some heavy metal poisoning or chronic granulomatous
condition.
Past History
The diseases, patient suffered prior to the present problem should be narrated in this history in
chronological order. The doctors who have treated, duration and details of the treatment received
should be asked for. Same is true for operative procedures. Chronological record of operative
procedures with details of operation may be mentioned. This may have some bearing on the present
problem. For example, a hypertensive patient on methyldopa may have stuffy nose and instead of
trying a nasal decongestant, it is better to change the antihypertensive if possible. A large number of
drugs like streptomycin, diuretics, anti-inflammatory drugs and antimalarial drugs are ototoxic.
This history in a patient of deafness may give clue in the diagnosis.
Personal History
Patient may be asked about his/her habits, like smoking, tobacco chewing, intake of alcohol, etc. in
details. His/Her lifestyle, food habits, bowel habits be enquired. Marital status and obstetrical history
in case of female patient, is important.
Family History
Certain diseases do run in families. And few diseases even if they are not genetic in origin, run in
families. Hence, family history should be asked particularly in case of deafness in early childhood,
epistaxis, nasal allergy, etc.
Physical Examination
Surgeon thinks locally, acts locally. Physician thinks globally and forgets locally.
A good clinician finds a golden median of the two.
After adequate history, physical examination should be carried out. This includes:
1. General examination
2. Local examination
3. Systemic examination.
1. In the general examination vital parameters like pulse, blood pressure, temperature, respiration
are noted down. In addition to this pallor, clubbing, icterus, hydration, built and nutrition, height
and weight, mental status, oedema over feet if any, and condition of lymph nodes in neck, axillae,
groin are noted down.
2. Local examination is the most important examination. On the basis of this examination clinician
can come to a definitive diagnosis. Affected part should be examined thoroughly. The opposite
side should also be examined.
3. Systemic examination includes physical examination of cardiorespiratory system, gastrointestinal
system, and nervous system. This examination is essential to know fitness for anaesthesia, any
associated disease and systemic involvement of various ENT diseases.
3
Examination of Swelling,
Ulcer and Fistula
You must have learnt by heart the methods of examining a swelling, ulcer and fistula during your
posting in General Surgery. In ENT the basic pattern remains the same, with little modifications here
and there. Examination of these lesions is so important that even with the charge of repetition I
would like to discuss it.
History
DURATION
Patient should be asked, How long he is having the swelling. The swelling may be there since long but
the patient may not have noticed it or being painless might have neglected it. Swellings of acute onset
may be inflammatory or post-traumatic in origin. Swellings of very long duration are usually benign
in nature.
MODE OF ONSET
Ask the patient how the swelling progressed? A swelling may progress very fast in traumatic condition
or may progress very slowly in benign condition. Certain swellings are slow in progress for a long
period and then suddenly they increase in size or initiate pain. This is usually seen with malignant
change in mixed parotid tumour or sudden haemorrhage in thyroid.
ASSOCIATED SYMPTOMS
Swellings in head and neck region due to their anatomical location may cause change in voice. A
peritonsillar abscess may give rise to plummy voice. A large tumour over neck may compress the
vessels and nerves of the neck and may cause loss of function of the nerves involved. Say for example,
there may be 9, 10, 11 or 12th cranial nerve palsy when a large tumour compresses over the nerve
trunk, giving rise to various symptoms. Compression over cervical sympathetic chain may result into
Horner’s syndrome. Compression over trachea/oesophagus may cause respiratory distress or
dysphagia. Dysphagia of long duration may cause weight loss in a patient. All these symptoms need
to be analysed properly. Swelling may be associated with pain. In that case details of pain like nature
of pain, site, time of onset, severity, spread, aggravating factors, ameliorating factors all should be
asked in details. At times it may be fever with or without rigors. And details of it should be taken.
At times patient’s main concern is swelling in the neck. But he may have primary malignancy
somewhere in nose/nasopharynx or laryngopharynx. And this possibility should always be kept in
mind while examining a patient and relevant symptoms should be asked.
EXACT SITE
To begin with, swelling may be very small arising from one site and then gradually enlarges to cover
up a large area. Patient should be asked the exact site where from the swelling started. This may give
information about the tissue of origin of the swelling.
OTHER SWELLINGS OVER BODY

Patient may be asked that whether there is any swelling elsewhere on body. Examples, Multiple
neurofibroma, Hodgkin’s disease, etc.
General Examination
The built, attitude and look of the patient may be given proper attention in addition to vital parameters
like temperature, pulse, respiration, BP, pallor, oedema feet, etc.
Local Examination
Local examination of swelling is very important and it helps the clinician to come to a clinical
diagnosis. Hence, this part of examination should be done very carefully and meticulously. The
number of swellings should be noted. The pattern of examining a swelling is universal and is followed
here with relevance to otolaryngology.
Examination of swelling is done in the following manner:
A. Inspection
B. Palpation
Examination of Swelling, Ulcer and Fistula 17
C. Percussion
D. Auscultation.
Inspection
SITE
Site of the swelling may give you clue about its origin and hence, careful inspection about exact
location of the swelling is must.
SIZE
Size of the swelling should be noted down in vertical and horizontal directions. Say for example, the
swelling is 4 cm × 4 cm located between tragus and angle of mouth in horizontal direction and
between zygomatic arch to lower alveolus in vertical direction.
SHAPE
The swelling may be spherical, ovoid or irregular. Shape may not be clear in some swellings where it
is called as diffuse.
SURFACE
Surface of the swelling may be smooth, globular or irregular.
MARGINS
Margins of a swelling may be well-defined or poorly-defined.
SKIN OVER SWELLING

The skin overlying the swelling may be red, oedematous in inflammatory swellings. It may be tense
glossy with prominent blood vessels over it, in case of sarcoma. A punctum may be seen on skin in
sebaceous cyst. Scar mark over the swelling indicates previous operation or application of irritants to
the swelling or burst abscess.
PULSATIONS
Swellings that arise from arteries may be pulsatile. The swelling that is in close vicinity of blood
vessel may transmit the vascular pulsations.
COLOUR
Haemangiomas give a reddish colour to the tumour mass and black colour may be imparted by
melanoma.
CHANGE IN SIZE OF SWELLING ON COUGHING/STRAINING OR VALSALVA

Few swellings do change in size on coughing/straining or after performing a Valsalva manoeuvre.
Examples, Meningocoele, Laryngocoele.
Palpation
In palpation, the findings noted down in inspection are confirmed and additional findings are
searched, if any.
• Local temperature: This is the first thing to be noted in palpation of swelling. It should be done by
dorsum of the hand. Local temperature is raised in inflammatory swellings.
• Tenderness: When a patient experiences pain on pressing the swelling gently it is known as
tenderness. It is usually seen in inflammatory swellings.
• Size: Size of the swelling observed in inspection is confirmed by palpation and dimensions in
vertical and horizontal direction are noted down.
• Shape: Shape can be better delineated by palpation.
• Surface: Surface of a swelling may be smooth (e.g. cyst) lobular (e.g. lipoma) or nodular (multi-
nodular goitre) or irregular (malignancy). Pulp of fingers/palm is used to know the surface of
swelling.
• Margins: Margins of a swelling may be well-defined or poorly-defined and should be palpated
with tips or margins of fingers. Inflammatory and neoplastic swellings may have poorly-defined
margins.
• Consistency: The consistency of a swelling is:
Soft: when it is comparable to consistency of your lips.
Firm: when it is comparable to consistency of tip of nose.
Hard: when it is comparable to consistency of your forehead.
Cystic: when it is comparable with water filled balloon.
The consistency of a swelling may be homogenous throughout the swelling or may change at
different places. This variable consistency may be seen in malignancy.
FIXITY TO SKIN
Some of the swellings do arise from skin appendages itself, like sebaceous cyst. One cannot move the
overlying skin in such lesions. But overlying skin can be moved when the swelling is deeply situated.
If the overlying skin is involved in malignant process, it cannot be moved.
MOBILITY OF SWELLING
Swelling should be grasped in the hand and moved in vertical and horizontal direction to see
whether it is mobile or fixed to deeper structures. Fixity is an important feature of advanced malignancy,
which may contraindicate surgical intervention.
Then there are certain signs, which can be elicited to get additional information about the swelling.
These signs are:
Fluctuation (Figures 3-1A and B)

Sign of fluctuation is an important clinical sign, which can be elicited as follows.
Fix both the poles of the swelling between thumb and fingers of both the hands and press one pole
of swelling by index finger. The fingers used to fix the swelling appreciate the change in the pressure.
In case of a very small swelling, it is pressed at the centre and pressure changes are felt at the
periphery of the swelling. Example, neck abscess, or any swelling containing fluid.
A B
Figures 3-1A and B: (A) Showing swelling on right side of neck, and
(B) Showing how to elicit fluctuation
Transillumination Test (Figure 3-2)
This test can be carried out when you suspect fluid in the swelling. It should preferably be done in a
dark room. Clinician should sit in the dark room with his eyes closed for 10 minutes to get ‘dark
adaptation’. A small pencil torch is applied close to the swelling at one end and swelling is observed
through a paper roll at other end. If the swelling contains clear fluid it would be brightly
transilluminant. If the fluid inside the swelling is turbid or thick, the swelling may be translucent or
opaque. Swellings in head and neck region that are brilliantly transilluminent are cystic hygroma and ranula.
Figure 3-2: Showing how to elicit transillumination test

Reducibility
The reducible swelling disappears completely or partly on compression. This happens because the
swelling has a connection with the body cavity. And on compression swelling gets pushed in the
cavity. Examples, external laryngocoele, meningocoele.
Compressibility (Figures 3-3A and B)

Swellings, which decrease in size on firm pressure or compression, are called compressible swellings.
Example, lymphangioma/haemangioma.
Pulsatile Swelling
A swelling in close vicinity of artery or arising from wall of the artery may transmit pulsations of the
underlying vessel or may itself be expansible. If you keep two fingers on such a swelling as wide
A B
Figures 3-3A and B: Compressibility in haemangioma
apart as possible, the fingers are lifted up with every stroke of pulse (e.g. carotid body tumour). When
the swelling is expansible the fingers are not only lifted up but they are also separated from each
other with every stroke of pulse (e.g. aneurysm).
Percussion
This may not be that useful in examination of swellings.
Auscultation
Bruit may be heard over the swellings arising from a blood vessel or a highly vascular lesion or when
the swelling compresses the blood vessel. Example, thyroid nodule.
REGIONAL LYMPH NODES

In any head and neck swelling the regional lymph nodes should be palpated to know whether they
are enlarged, tender or otherwise. If one group of lymph node is affected the other groups of nodes
should also be examined.
EXAMINATION OF SINUS OR FISTULA

Sinus
A blind tract lined by the epithelium that communicates the inner tissues with skin. Example,
tuberculous neck sinus.
Fistula (Figure 3-4)
A fistula is an open tract communicating two epithelial surfaces, e.g. oroantral fistula.
While examining a Fistula or Sinus following aspects do need attention:
A. Position: Many sinuses or fistulae have a typical position and thus help in diagnosis.
• Branchial fistula is usually situated at lower third of the neck in front of sternomastoid muscle.
• Thyroglossal fistula is located in midline.
• Preauricular sinus is located at the root of helix.
B. Number: Usually fistula is single in number. But may be multiple in tuberculosis and actinomycosis.
C. Discharge: Character of the discharge may be noted. It may be thin whitish discharge in tuberculosis,
frank pus in osteomylitis, ‘sulphur granules’ in case of actinomycosis.
D. Surrounding skin: May show scarring in case of tuberculous fistula. Repeated infections in the
sinus may cause scarring and thinning of surrounding skin.
E. The sinus or fistula should be palpated for tenderness. Thickness of wall should be noted down.
Probing of the sinus/fistula may be done to know the depth and direction of tract.
Fistulography: Radio-opaque dye may be injected in the fistula and X-rayed to delineate the tract.
At times the opening of sinus may be closed and form a cystic swelling.
Figure 3-4: Showing multiple fistulae over face.

A probe entering in oral cavity through fistula
EXAMINATION OF ULCER (FIGURE 3-5)
Definition: Ulcer is a breach in the continuity of skin or mucous membrane.
Figure 3-5: A diagrammatic representation of an ulcer

History
Ask the patient How the ulcer started? Is there any history of trauma or surgery or it developed
spontaneously?
Is there history of local pain, fever prior to ulcer formation?
Are there patches of hypoesthesia over body?
Is there history of diabetes, tuberculosis or malnutrition?
How long the ulcer is there? This would tell you whether the ulcer is acute or chronic in nature.
Aphthous ulcer, traumatic ulcer is an example of acute ulcer. However, ulcer due to tuberculosis and
malignancy may be chronic in nature.
Is the ulcer painful? Aphthous ulcers are highly painful, while malignant ulcers may not be painful.
Is ulcer discharging? The nature of discharge should be enquired.
“Are the ulcers increasing in number or size?”
“Are there ulcers over other parts of body, e.g. genitals.”
Examination of Ulcer
A. Inspection:
1. Number—Note whether the ulcer is single or multiple.
2. Site—Note down where the ulcer is located? It would give you idea about the tissue of origin.
3. Size—Note down the vertical and horizontal dimensions of the ulcer.
4. Shape—Aphthous ulcers are oval or round. Syphilitic ulcers are serpiginous and malignant
ulcers are irregular.
5. Discharge:
i. Serous—discharge may be seen in non-healing ulcer.
ii. Serosanguinous—discharge may be seen in healing ulcer or at times in malignant ulcer.
iii. Purulent—discharge may be seen in spreading ulcer.
iv. ‘Sulphur granules’ discharge may be seen in actinomycotic ulcer.
6. Floor—This part of ulcer contains granulation tissue, discharge and/or slough. Granulation
tissue may be pink (pinhead size) in healing ulcer. Pale flat granulation tissue in chronic non-
healing ulcer and unhealthy granulation tissue with slough in spreading ulcer.
7. Edges—Edge is the type of union between floor and margin of ulcer (Figure 3-6).
• Punched out edges, e.g. syphilitic ulcers.
• Undermined edges, e.g. tuberculous ulcers.
• Everted edges, e.g. malignant ulcer.
• Slopping edges, e.g. healing ulcer.
Figure 3-6: Type of edges

8. Margin:
• Healing margin: This may show outer white zone of epithelisation. Middle blue zone of
regenerating epithelium and inner red zone of healthy granulation tissue.
• Inflammed margin: It shows signs of inflammation and seen in spreading ulcer.
• Fibrotic margin: This ulcer shows evidence of fibrotic tissue in the margin. It is seen in chronic
non-healing ulcer.
9. Surrounding area: Area surrounding the ulcer should be inspected for any scar, excoriation of
skin, oedema, sinus formation, dilated blood vessels, etc.
B. Palpation: Palpation of the ulcer should be done carefully for-
• Local temperature
• Tenderness
• Edges of the ulcer should be palpated and findings of inspection are confirmed.
• Base of the ulcer should be palpated for any induration. It should be noted whether ulcer bleeds
on touch or not? And fixity of the ulcer to the structures down below may be tested by mobility
test. Moving the base of ulcer in two directions checks the mobility of the ulcer. One along the
direction of underlying muscle and one perpendicular to it. This mobility may be tested by
contracting the underlying muscle against resistance and without contracting the muscle.
NB: If the ulcer moves freely before and after the contracting the underlying muscle, it is superficial.
If the mobility is reduced after contracting the muscle, ulcer has infiltrated the muscle. If the ulcer is
immobile even without contracting the muscle, it is fixed to underlying bone.
Otology
• Examination of Ear
4
Examination of Ear
Before we actually start clinical examination of ear it is quite in order if we understand the various
symptoms related to ear diseases. Ear disease may cause one or more than one of the following symptoms.
1. Ear discharge (otorrhoea)
2. Hearing loss (deafness)
3. Ringing in ear (tinnitus)
4. Pain in ear (otalgia)
5. Giddiness/vertigo
6. Itching in ear
7. Blocking/wooly or FB sensation in ear
8. Autophony/hyperacusis
9. Swelling in pre and post-auricular area
10. Bleeding from ear.
Some of the symptoms are not dedicated to ear diseases, but they may be closely associated. They
are:
• Nausea
• Vomiting
• Light headedness
• Headache
• Fever
• Retro-orbital pain
• Diplopia
• Inability to close the eye
• Deviation of angle of mouth.
A patient may have one or more than one symptoms mentioned above. Each symptom should be
analysed minutely to get more insight into the patient’s problem. It is usually observed that a relative
accompanying the patient starts giving information, which many of the times is not accurate. Hence,
it is always better to elicit the history from the patient himself unless he is a child or unable to give
history due to illness.
Otorrhoea
DURATION
Patient should be asked How long he is suffering from the present complaint? This gives you clue whether
disease is of acute onset or chronic or acute exacerbation of chronic disease. Patient should be asked
whether he recalls the first attack of otorrhoea? How and when it started? What were the preceding
or associated symptoms that time? Usually upper respiratory tract infection, either bacterial or viral
precedes first attack of acute otitis media and patient may develop fever, pain in ear. As soon as
discharge starts, the pain disappears. This initial otorrhoea may be blood stained.
SEVERITY
Patient should be asked What way it [symptom] disturbs you and/or your work? It would give an idea as
to how much troublesome it is, to the patient. Discharge may be so profuse that it may not be possible
for the patient to work.
LATERALITY
Patient should be asked Is ear discharge unilateral or bilateral? Many of the times patient has bilateral
disease. But the disease on one side is quiescent or inactive and patient is concerned with the ear that
is troubling him at present (active ear) and hence may not mention about inactive ear.
PERIODICITY
Patient may be asked Is this complaint constant or intermittent? If it is intermittent, how much is the time
duration between two episodes. Is it seasonal? Some patients develop upper respiratory tract infection
with every change in season and this is followed by otorrhoea. Such a relationship—if existing—
should be noted down.
Examination of Ear 31
CHARACTER OF THE DISCHARGE
Colour, quantity, consistency and smell of the discharge should be noted.
Otorrhoea may be watery, mucoid, mucopurulent, purulent, thick inspissated, cheesy or blood stained.
i. Watery: Watery discharge is colourless, thin, and transparent. It may be seen after head injury
[CSF otorrhoea] or in the beginning of viral myringitis.
ii. Mucoid: This is colourless but not thin. It is tenacious mucous gland secretion, coming
from middle ear. May be seen in acute otitis media after drum is perforated, or in chronic otitis
media.
iii. Mucopurulent: Mucopurulent ear discharge is a coloured ear discharge. It may be whitish,
yellowish or greenish or mixture of the three. It is tenacious and usually seen in acute or chronic
otitis media.
iv. Purulent: Here the discharge is thick, but less tenacious. Usually it is scanty, and may be
foul smelling. A scanty foul smelling ear discharge is usually due to ‘Pseudomonas’
infection. The underlying pathology of bone necrosis or cholesteatoma may be responsible for
foul smelling ear discharge. Discharge in furunculosis is thick purulent but without tenacious
character.
v. Blood stained: At times the ear discharge shows frank blood. This may be seen after trauma, or in
cases of baro-otitis media, haemangioma or glomus jugular tumour. In skull base, there can be
bleeding from both the ears. But sometimes it is only blood stained (dirty red colour fluid). This
may be seen in aural myiasis or bullous myringitis or in cases of chronic suppurative otitis
media (CSOM) associated with ear granulation. Acute otitis media patients may present with
serosanguinous discharge in its stage of suppuration.
NB: Yellowish, whitish, blackish discharge may be seen in fungal infection of ear canal (Otomycosis).
At times, discharge may show a soaked blotting paper appearance due to ‘Candida’ infection.
Hearing Loss
This complaint should also be analysed in the same pattern. Duration, severity, laterality and
periodicity may be asked. History suggestive of suppurative otitis media, exanthema, consumption
of ototoxic drugs or trauma to head, history of familial deafness should be asked. In case of
deafness since childhood detailed history of antenatal, perinatal and postnatal causes like TORCH
group of infection in ANC period should be ruled out. Exposure to loud sounds should be taken into
account.
DURATION
This may give information whether the problem is acute or chronic in nature. Patient may be asked
When he noticed it first? Hearing loss due to congenital malformation in hearing apparatus may be
there since birth. Post-traumatic hearing loss like exposure to bomb blast may have very short history.
SEVERITY
Patient may be asked What way it disturbs you or your work? Significance of hearing loss may be
different in different ages, occupations and also depends upon sensitivity of an individual. Mild
hearing loss to a manual labour may not matter much but it matters a lot for a telephone operator or
cardiologist. So while analysing this complaint age, sex, occupation may be taken into account.
LATERALITY
Localisation of sound source is best when both the ears are functioning normally. Moderate hearing
loss in one ear may be less troublesome than mild hearing loss in both ears.
PERIODICITY
Patient may be asked Is your hearing loss constant or intermittent?
Hearing loss due to congenital defects in ear like fixed malleus syndrome, canal atresias remain
constant. If it is intermittent how often it is? Has it any relationship with change of season, upper
respiratory infection (URI), pain in ear or otorrhoea? Is it static or progressive?
In degenerative heredofamilial deafness, otosclerosis and Meniere’s disease deafness is progressive.
Hearing loss due to secretory otitis media or chronic Eustachian tube block may be intermittent and
usually seen during change of season or attack of URI.
NATURE OF DEAFNESS
Patients having conductive type of deafness may get improvement in speech perception on
amplification of sound. However, patients having sensory neural type of deafness may not get any
improvement in speech perception on amplification as speech discrimination is poor in these patients.
Tinnitus
Tinnitus means ringing in ear. It may be tickling, whistling, fussing or roaring. It may be soft or very
harsh. The exact mechanism of tinnitus is not clear. But any pathology in ear starting from wax to
acoustic neuroma can give rise to tinnitus. It may be subjective, i.e. patient only perceives it. It may be
objective, i.e. it is heard by other person also. Enquire about duration, laterality, severity, periodicity
and associated symptoms.
Duration: Tells you, how long the patient is suffering?
Laterality: Unilateral tinnitus usually indicates local pathology. Bilateral tinnitus may be due to
central pathology.
Severity: Tinnitus may be of mild nature and patient may neglect it. Or it may be so severe that patient
is unable to sleep in the night or unable to concentrate on his work. Usually tinnitus is more felt
during quiet hours of night-time.
Periodicity: Tinnitus may be continuous or intermittent. Tinnitus due to Meniere’s disease is
aggravated at the time of attack. Associated symptoms like hearing loss /vertigo should be asked and
analysed.
Otalgia
DURATION
Patient should be asked How long he is having pain in ear? Is it constant or intermittent? How it is
aggravated and how it is ameliorated? How long it lasts? Pain due to otitis externa usually aggravates by
chewing movements or touching the pinna may be painful.
CHARACTER
Whether it is dull aching, stabbing, cutting or pinpricking should be asked.
SEVERITY
Pain due to furuncle in external auditory canal is usually severe. This is because skin is tightly
adherent to underlying perichondrium and perichondrium is stretched during inflammation and
compresses over the nerve endings. Pain in acute otitis media (AOM) is very severe in stage of
suppuration.
Uncomplicated chronic otitis media is usually painless.
LATERALITY
Bilateral pain in ear may be due to wax impaction, Eustachian tube block or after tonsillectomy.
PERIODICITY
Pain due to chronic Eustachian tube block may be experienced during winter or rains as exposure to
cold may cause spasm of the tensor tympani muscle.
Following nerves supply external auditory canal:
1. Auriculo temporal nerve (Vth)
2. Auricular branch of vagus nerve (Xth)
3. Great auricular nerve (C2,C3)
4. Branch of glassopharyngeal nerve (IX)
5. Lesser occipital nerve (C2)
When there is pain in the ear the cause usually lies in the ear. However at times, it may not be so.
Tonsillitis, adenoiditis, sinusitis, impacted tooth, cervical spondylosis, nasopharyngitis, malignancy
of larynx and laryngopharynx and oropharynx may present with pain in ear. And ear examination
may be normal. This is known as referred otalgia. This occurs due to common nerve supply to the ear
and the organs mentioned above. Treatment of the primary cause should be contemplated in such
cases (Figures 4-1A and B).
Figure 4-1A: Nerve supply of pinna (lateral part) Figure 4-1B: Nerve supply of pinna (medial part)
Giddiness
This symptom should be screened very carefully because the terminology used by the patient may be
very vague and interpreted wrongly. Sense of unsteadiness is termed as giddiness. This may be
experienced in ‘postural hypotension’ while standing from lying down position, in cervical
spondylosis or mild ischaemia of the brain. Vertigo is a sense of rotation of body or surrounding. Inner
ear pathology may give rise to true vertigo. In true vertigo patient may feel that he is moving in
relation to his surrounding or his surrounding is moving around him. This sensation of whirling is
very unpleasant, and patient may even vomit during the attack of vertigo. Example, labyrinthitis or
Meniere’s disease.
Patient should be asked to recall his first attack of giddiness. How and when it started? How long
it lasted? What was the severity? Is this symptom recurrent and how frequently? Are there some
associated symptoms like tinnitus, hearing loss, heaviness in ear or vomiting? Meniere’s disease is a
triad of symptoms consisting of vertigo, deafness and tinnitus. Vertigo is severe, recurrent and disabling
and, may be followed by vomiting. Hearing may reduce with every attack. In contrast vestibular
neuronitis presents with vertigo and vomiting without hearing loss.
Positional vertigo: Some patients do complain of vertigo/giddiness on particular neck position or
change of posture. This may be seen after head trauma.
Itching in the Ear

This symptom may be seen in patients having wax, otomycosis or some dermatological conditions
affecting canal skin.
Blocking/wooly or FB Sensation in Ear

This is usually a vague complaint and patient is unable to describe it properly. It may be a blocking
sensation or wooly sensation or FB sensation in ear canal. It may be experienced in cases of secretory
otitis media, ET block or in early phase of acute otitis media. Details of the complaint are noted down.
Autophony and Hyperacusis

Autophony: This is a very peculiar symptom in which the patient experiences his own voice, as if he
is speaking in his ears. This can happen when there is abnormal patency of Eustachian tube or when
there is fluid in middle ear.
Hyperacusis: Here patient has undue sensitivity of loud sounds. This is also known as phonophobia.
Seen after stapedial nerve paralysis [facial nerve paralysis]. In normal situation loud sounds are not
allowed to enter the inner ear by reflex contraction of stapedius muscle. This protective function of
stapedius muscle is lost in facial nerve paralysis. And hence patient experiences loud sounds more
severely.
Swelling in pre- and post-auricular Area

Pre-auricular area: The most common swelling in this area is viral lymphadenopathy and cyst. But
mixed parotid tumours or diseases of temporomandibular joint may present in this area as
swelling.
Post-auricular area: Most of the time it is a subperiosteal mastoid abscess. But tumours of muscles and
bone may be rarely seen in the post-aural area.
Bleeding from Ear

This is an important clinical symptom. It may be seen after trauma or as a consequence of disease.
Any injury to external ear, temporomandibular joint, baro-trauma may cause bleeding from ear.
Particularly head injury may cause bleeding from both the ears and is an important sign of middle
cranial fossa. Diseases like haemangioma, glomus jugular tumour can cause significant bleeding
from ear, while aural myiasis, bullous myringitis results into serosanguineous discharge.
There are few symptoms closely associated with ear diseases and require prompt action. Hence an
enquiry to that effect should always be made. These symptoms are:
i. Nausea: This symptom may be associated with motion sickness or labyrinthitis, Meniere’s disease
or vestibular neuronitis.
ii. Vomiting: Vomiting is associated with acute labyrinthitis. It is non-projectile and copious in
amount. Patient is usually unable to walk during the attack. However, one should be suspicious
because vomiting may be a symptom of raised intracranial tension.
iii. Light headedness: Patients of Meniere’s disease may have this vague complaint.
iv. Headache: May be caused in ear diseases when there is intracranial complication like meningitis,
extradural abscess, subdural abscess, brain abscess and otitic hydrocephalous. Hence, the
symptom of headache in patients of CSOM should not be taken lightly.
v. Fever: Acute otitis media may give rise to high-grade fever in children but not in adults. Fever
due to lateral sinus thrombophlebitis may be associated with rigors. Fever with severe headache,
vomiting, papilloedema suggest raised intracranial tension.
vi. Retro-orbital pain: This is a peculiar complaint seen in patients who have developed ‘petrositis’
as a complication of SOM.
vii. Inability to close the eye.
viii. Deviation of angle of mouth: These two complaints are seen in any patient of facial nerve
palsy and hence may be seen in patient who has developed 7th nerve palsy as a complication
of SOM.
Past History (History of Major Illnesses)

History of tuberculosis/diabetes/hypertension/trauma/allergy should be asked. A patient of
tuberculosis might have used ototoxic drugs for the treatment, resulting into hearing loss. Diabetes
and hypertension do have an impact in the management of the patient and also cause changes in
inner ear. Patients who had contracted enteric fever in the past may develop hearing loss. Similarly
previous history of ear surgery, trauma or head injury may cause vertigo or hearing loss.
Family History
Chronic suppurative otitis media (CSOM) is not a hereditary disease. Still, more than one member in
the family may be having CSOM. And this is because the same environmental and social factors are
operating. Poverty, crowding and malnutrition is the basic triad in the genesis of CSOM. And hence
history of ear disease in other members of family should always be asked. Few heredo-familial
degenerative disorders run in families.
Personal History
People working in noisy industry are likely to develop noise induced hearing loss. People having
reduced immune response, cleft palate are notorious to develop SOM. Patients with allergic diasthesis
like allergic rhinitis are prone to develop ET block which acts as precursor for all sorts of otitis media.
People having renal problem or patients on anti TB treatment may develop ototoxicity.
General Examination
In general examination, apart from vital signs, look of the patient, general built, icterus, pallor,
lymphadenopathy, oedema feet (if any) are noted down. Patient with serious intracranial
complications or severe headache may not co-operate in the history taking and/or examination.
Patient having labyrinthine affection may have ‘nystagmus’ and may not be able to walk properly.
They may tend to fall on one side while walking.
Blood pressure should be taken in supine and standing position.
Local Examination
EXAMINATION OF EAR
The following pattern may be followed:
1. Examination of pinna, pre and post-aural area
2. Examination of external auditory canal
3. Examination of tympanic membrane
4. Fistula test
5. Tuning fork tests
6. Examination of nose, nasopharynx Though this is not a part of ear examination,
PNS, oral cavity and throat it should be carried out after ear examination
7. Examination of facial nerve
8. Examination of other cranial nerves. Described elsewhere.
Examination of Pinna, Pre- and Post-aural Area (Figures 4-2 to 4-5)

Pinna: Should be examined for any obvious abnormality in size, shape or position.
Size: May be small and located at lower position, e.g. Down’s syndrome.
Shape: May be abnormal since birth or after surgery/trauma.
Movements of pinna and tragus are very painful in cases of otitis externa.
Figure 4-2: Showing mastoid fistula Figure 4-3: Showing post-aural granulation
Figure 4-4: Showing lipoma in incisura terminalis Figure 4-5: Showing sebaceous horn grown
on tip of pinna
Microtia: is a poorly developed pinna since birth.
Anotia: is absence of pinna since birth.
Accessory tragus, lop ear, pre-auricular sinus are other congenital malformations seen in clinical
practice.
Post-aural area: should be examined without fail.
It may show swelling [e.g. mastoid abscess], scar of previous mastoid surgery or mastoid fistula.
Tenderness should be elicited in post-aural area, by giving firm pressure over mastoid tip or mastoid
bone corresponding to cymba concha, which corresponds to McEven’s triangle, a bony landmark for
mastoid antrum. Tenderness at this area suggests infection in mastoid bone. Normally when you
move your finger along the mastoid bone the bony unevenness is palpated. However, in some cases
of CSOM with mastoiditis and emissary vein thrombosis palpation of post-aural area gives a very
smooth ‘cat’s fur’ feel. When pitting oedema is extending to occipital area it is known as “Griesinger’s
sign”.
Pre-auricular area: may show a sinus, swelling due to cyst, accessory tragi or lymphadenitis.
EXAMINATION OF EXTERNAL AUDITORY CANAL

External auditory canal is not a straight canal. It is sigma-shaped. It is 24 mm in length. Outer 8 mm
part is cartilaginous and inner 16 mm is bony. Cartilaginous part contains hair preventing proper
visualisation of drum. Pinna is pulled upwards, backwards and outwards to make this sigma-
shaped canal straight. Roof, floor, anterior and posterior walls of EAC are examined for any deviation
from normality. Pus, foreign body, wax, debris are the common findings in ear canal. Polyps, granulation,
furuncle, osteoma and laceration may be found at times. There may be stenosis of EAC due to disease
or trauma or the EAC might not have developed since birth [atresia]. Pus in the canal should be
cleaned with the help of cotton wool carrier. Wax should be removed carefully with cerumen spud, so
that drumhead can be examined. Wide EAC can be examined without the help of ear speculum. But
in case of narrow EAC or in presence of excessive hair, ear speculum examination becomes necessary.
Examination of Ear with Aural Speculum (Figure 4-6)

Proper size ear speculum is chosen. It should not be too large or too small for the ear under examination.
Speculum is gently negotiated in the ear canal with rotatory movements and passed just beyond the
junction of bony and cartilaginous ear canal, and eardrum is examined.
Figure 4-6: Showing method of holding ear

speculum during ear examination
EXAMINATION OF TYMPANIC MEMBRANE

Tympanic membrane is located at the medial end of ear canal. It is pearly grey in colour. The most
prominent part of the drum that attracts the attention is handle of malleus. The terminal part of
which ends in a knob like structure called as ‘umbo’. Running down antero-inferiorly from the umbo
is ‘cone of light’. This is a triangular area—a reflection of light with its base towards periphery. From
the annular rim to the handle of malleus runs anterior malleolar fold and similar fold posteriorly
called posterior malleolar fold. The part of the tympanic membrane above these two folds is called
“pars flaccida” and part below this is known as “pars tensa”. One or two blood vessels running
along the handle of malleus may be seen even in normal drumhead. In some patients having thin
tympanic membrane long process of incus may be visible. Short process of malleus is seen projecting
laterally.
For the purpose of understanding and description, tympanic membrane is divided into four
unequal quadrants by drawing a line along the long axis of handle of malleus and other line passing
through umbo perpendicular to the previous one. This divides pars tensa into 4 quadrants. Antero-
superior quadrant (ASQ), antero-inferior quadrant (AIQ), postero-superior quadrant (PSQ), and
postero-inferior quadrant (PIQ). These quadrants have clinical significance.
Mobility of TM (Figures 4-7 and 4-8)

Mobility of TM should be elicited as follows:
• Siegalization: In this test Siegle’s speculum is snugly fitted to ear speculum and negotiated in ear
canal. Air pressure in EAC is increased/decreased alternately with the help of inflatable bulb.
This causes movement of the tympanic membrane. If the tympanic membrane is normal and
middle ear pressure is normal the drum is fully mobile. In ET block, secretory OM, tympanosclerosis,
atelectasis, adhesive otitis media mobility of TM may get hampered or lost totally.
• Valsalva manoeuvre: It also tests the mobility of TM. Patient is asked to close his mouth and nose
and inflate cheek. While patient is doing this manoeuvre, his eardrums are observed otoscopically.
If the eardrum moves laterally it is said that TM is mobile and ET is patent. These movements may
be restricted or absent in middle ear dysfunction.
Valsalva manoeuvre raises the pressure in nasopharynx, which is transmitted via ET to middle
ear cavity and causes movement of TM.
Figure 4-7: Right TM and left TM

Figure 4-8: Division of Pars tensa
Note: TM mobility cannot be tested when it is perforated. Some patients cannot perform valsalva even
if their middle ear function is normal.
Abnormalities of Tympanic Membrane

1. Colour
i. Pink: Seen in acute otitis media or active stage of otosclerosis [flamingo tint]. “Rising sun”
appearance seen in glomus jugular tumour. Warm water irrigation may impart pink colour to
the drumhead. In small children even crying can cause pink colouration and may be mistaken
as a sign of inflammation.
ii. Red: In acute otitis media, bullous myringitis, baro-otitis media.
iii. Bluish: When there is collection of blood in middle ear after trauma/head injury or baro-otitis
media and known as Haemotympanum.
iv. Chalky white patches: Seen in tympanosclerosis.
2. Cone of light: Distortion or loss of cone of light is the earliest sign of middle ear pathology. Hence
drum is called face of middle ear. Cone of light is distorted/lost in acute/chronic Eustachian tube
block and atelectasis. It occurs due to displacement of drum from its normal position or due to
inflammation of drum.
3. Pars tensa: Pars tensa may show retraction, granulation tissue, blebs, tympanosclerotic patches or
perforation.
a. Retraction: Most common and important cause of retracted tympanic membrane is acute or
chronic Eustachian tube block. The whole drum or a small quadrant of the drumhead may be
retracted. Retracted drum looks dull, lusterless. There may be distortion of cone of light, even it
may be completely lost. The drumhead is displaced medially towards middle ear, resulting into
foreshortening of handle of malleus and prominence of lateral process of malleus. Retracted
tympanic membrane moves poorly or doesn’t move at all on Siegalisation. At times the retraction
pocket may be confused with a perforation in drumhead.
Some times otoscopy may show dull tympanic membrane, fluid level and few air bubbles
behind intact tympanic membrane. This is a classical picture of otitis media with effusion also
called as Secretory otitis media.
b. Perforation in TM
It is a breech in the continuity of drumhead.
It is a sign of recent or past suppurative otitis media. Perforation should be described taking
into account type, location, size, shape, margins, residual drum and structures seen through
perforation.
i. Type: Perforations in pars tensa may be (Figures 4-9A and B):
A B
Figures 4-9 and B: Diagrammatic representation of
central and marginal perforation in TM
a. Central: A perforation, which shows residual drum on all sides of perforation, is a central
perforation.
b. Marginal: A perforation, which does not show residual drum on all sides, but is deficient
at some place, is a marginal perforation.
ii. Location: Perforation may be situated in one of the quadrants of the tympanic membrane, for
example, antero-superior, postero-inferior. At times it may occupy more than one quadrant
and it should be described accordingly.
iii. Size: Size of the perforation may be described as small, moderate or large. You need not tell
it in millimetres or centimetres. There are no specific guidelines to call a perforation as
small, moderate or large. It is a clinical judgement. However, grossly you can label a
perforation as small if it occupies less than one quadrant of the drumhead. Moderate—if it
occupies area equivalent to two quadrants of the drumhead. If the perforation is occupying
3/4 of drum surface, it may be called large. And when a small rim of drum is left behind and
Figure 4-10: Diagrammatic Figure 4-11: Figure showing large Figure 4-12: Showing irregular
representation of moderate central/subtotal perforation perforation due to trauma
central perforation
rest is perforation, it can be labeled as subtotal perforation. Total loss of pars tensa or very
large marginal perforation is called as “total perforation” (Figures 4-10 to 4-12).
iv. Shape: It is usually oval, round or at times kidney, shaped. Irregular perforation is seen in
traumatic lesion.
v. Margins: Margins of the perforation may be regular in chronic otitis media but irregular and
red in traumatic perforation.
vi. Edge: Edge of the perforation may be thick in CSOM and thin in ASOM. Edge may be red in
active state of disease.
vii. Residual drum: A comment on residual drum is must. Condition of residual drum may be
congested, atrophic or having tympanosclerotic patches. It may also contain granulation
tissue.
viii. Structures seen through perforation: Structures of middle ear may be seen through perforation.
In case of anterior perforation it is the Eustachian tube crater that may be visible. Promontory
is visible in most of the perforations. In posterior perforations round window niche, oval
window, incudo-stapedial joint or stapedius tendon may be visible. Middle ear mucosa
needs to be mentioned. It may be normal, congested or edematous. There may be a polyp or
granulation seen through perforation.
Condition of ossicles seen, should be commented. There can be erosion of handle of
malleus or destruction of incudo-stapedial (I-S) joint or other ossicles.
ix. Postero-superior retraction pouch with cholesteatoma: At times there is no perforation in the
tympanic membrane. But postero-superior quadrant shows retraction pocket in which
there is collection of whitish, foul smelling debri, which is difficult to remove. This may be
a case of retraction pocket with cholesteatoma. And needs proper examination under
operating microscope.
x. Granulation: They are dark red in colour, bleed on touch. They develop as a part of healing
r/
process. They may arise from middle ear or drumhead.
.i
xi. Polyps: They are pale in colour, arise from middle ear mucosa and do not bleed on touch.
They are lined by respiratory epithelium.
s
xii. Tympano-sclerotic patches: They are small, chalky white
s
patches seen on the drum. They may be of any size and
n
shape. They are suggestive of old healed middle ear
pathology. And are caused by hyaline degeneration of
is a
collagen tissue with deposition of calcium salts in it. Similar
patches may be there in middle ear resulting into ossicular
r
fixation.
Figure 4-13: Diagrammatic
4. Pars flaccida: This part of tympanic membrane is also known as
e
representation of attic
‘Attic’ or Sharpnell’s membrane. It may show retraction pouch perforation
p
with accumulation of whitish foul smelling debris, (Cholesteatoma)
.
which is difficult to remove. At times perforation or granulation may be seen. Attic perforation is
iv p
a dangerous perforation (Figure 4-13).
NB: Central perforation is ‘safe’ while marginal/attic perforation is ‘unsafe’.
/: /
Marginal perforation is usually seen in postero-superior quadrant.
Mobility of the tympanic membrane is then tested as already described.
tt p
FISTULA TEST
This is an important clinical test to diagnose a fistula in the labyrinth. (Horizontal semicircular
h
canal). Cholesteatoma may cause this fistula.
Procedure: Patient is explained the test and tragus is pressed repeatedly against ear canal, or pressure
in EAC is alternately increased/decreased by siegalisation.
Interpretation: If a patient has fistula in horizontal semicircular canal, the air currents by repeated tragus
pressure or siegalisation would stimulate the labyrinth and patient would experience giddiness, vertigo,
nausea or vomiting. At the same time examiner may notice nystagmus in the patients. This is a fistula
test positive. It indicates that surgical exploration of mastoid should be done at the earliest.
Fallacy
1. False negative test: There can be a fistula without fistula test positive. This happens in dead
labyrinth, or when fistula is temporarily blocked by cholesteatoma flakes.
r/
2. False positive test: There can be fistula test positive without actually having a fistula. This happens
.i
when thinning of bony labyrinth occurs. This may happen in syphilis, cholesteatoma.
s
Tips
s
1. Examination of the other ear should be done on similar lines. It is preferable that you examine a
n
normal ear first. This helps the clinician and patient both. If you examine the diseased ear first, it
may be painful and may hurt the patient and he/she may loose confidence in you. Secondly it is
is a
possible that you may transfer the infection from diseased ear to normal ear. Hence, it is a good
practice to examine the normal ear first.
r
2. While examining or cleaning the ear canal one should be very gentle lest patient can develop vaso-
vagal attack due to stimulation of vagus nerve.
e
3. Examination of ear is never considered complete unless you perform posterior rhinoscopy.
p
4. Examination of ear is never complete unless you examine the facial nerve.
.
5. If you suspect hearing loss in a patient, cover your face with a mask so that patient can’t make ‘lip
p
reading’. And you get correct assessment of his conversational level.
iv
6. The room in which you examine a suspected deaf patient should be relatively quiet.
/: /
TUNING FORK TESTS
Tuning fork tests assess type and amount of the hearing loss a patient is having. There is a long list
tt p
of various TF tests given in textbooks, however, there are mainly three tests that are in common use:
• Rinnie’s test
h
• Weber’s test
• Absolute bone conduction test (ABC test).
All these tests need medical type of tunning forks, which are different from the one used by
physicists. Medical tunning forks have foot piece, stem and prongs. Tunning forks of 256, 512 and
1024 cps are used. It is better if you start the test from 512 cps as this tuning fork has less decay rate.
Rinnie’s Test (Figure 4-14 and Table 4-1)

It is a commonly performed tuning fork test based on the fact that in a normal individual air
conduction is better than a bone conduction and the ratio of air: bone is 2:1.
r/
s .i
n s
is a
Figure 4-14: Diagrammatic representation of Rinnie’s test
Table 4-1: Rinnie’s test and its interpretation
r
Test details Result Interpretation
e
AC > BC Rinnie +ve Normal or SN loss
BC > AC Rinnie -ve Conductive deafness
.p
AC = BC Rinnie = Mild conductive deafness
BC > AC? Rinnie false negative This is seen when a patient has severe SN deafness on test side and
iv p
normal hearing on non-test side. On application of vibrating tuning
fork to deaf side the sound is transmitted to the non-test ear by
bone and patient perceives this bone conduction and presumes
/: /
that it is perceived by test ear, thus interpreting it as BC > AC. Bone
conduction level should be confirmed by Weber test
tt p
Procedure: Test is explained to the patient. A tuning fork of 512 cps is taken. It is set into vibration by
striking against a surface like thinner eminence or elbow joint, and vibrating fork is placed lateral to
ear canal approximately at a distance of 2 cm. Hold the fork in such a way that axis of sound waves
h
should be in the same axis that of ear canal. Patient is asked to listen the sound. Foot piece of the fork
is then immediately kept over mastoid process or its tip. Patient listens the same fork by bone and
again it is transferred in front of ear canal. This is continued till patient stops listening at one place.
Here we are testing duration of sound heard. But we can test loudness of sound also by asking the
patient which sound (air or bone) is louder. The test is repeated by using 256 and 1024 Hz. Similar
testing is done on opposite ear and findings are noted down.
You can also quantify the hearing loss with the help of Rinnie’s test (Table 4-2).
Table 4-2: Quantification of HL using Rinnie’s test

256 cps 512 cps 1024 cps Interpretation
- + + Mild conductive deafness
- - + Moderate conductive deafness
- - - Severe conductive deafness
Figure 4-15: Photograph showing method of

performing Weber test
Weber Test (Figure 4-15)

Tuning fork is set into vibration and kept either on vertex, forehead, chin or upper incisor teeth and
patient is asked to hear the fork sound by both ears. Patient may listen it on both sides with equal
loudness or not at all, on either side. This is a normal response. And the side to which patient listens
the sound more loudly is labeled as ‘lateralisation’ to that side.
Right Left
Normal or equal hearing on both sides
No lateralisation /Central Weber
Left conductive deafness/or (R) SND
Lateralised to Left
Right conductive deafness/or (L) SND
Lateralised to Right
Weber is a sensitive test and a difference of even 5 dB is sufficient to lateralise the Weber.
Figure 4-16: Showing—Absolute bone conduction test
Table 4-3: Showing interpretation of ABC test

Test details Result Interpretation
Clinician listens longer than patient ABC reduced SN deafness
Clinician listens equal to that of patient ABC normal Normal
Patient listens longer than clinician. ABC lengthened Conductive deafness
Absolute Bone Conduction (ABC) Test (Figure 4-16 and Table 4-3)
In this test the bone conduction level of the patient is compared to that of clinician. During test
ambient noise in the surrounding is reduced by pressing the tragus of the EAC. This is a modification
of ‘ Shwabach’s Test’.
Pre-requisite: Clinician should have normal bone conduction level or at least he should know his
bone conduction level.
Procedure:
• Patient is explained the test.
• Test ear is closed by gently pressing the tragus against ear canal.
• Foot piece of vibrating tuning fork is kept over mastoid bone and patient listens to the fork till
sound disappears completely.
• Immediately same fork is transferred over mastoid bone of the clinician and simultaneously ear
canal is closed by pressing the tragus. Clinician listens whether he can appreciate the sound
stimulus or not. If the clinician does not listen the sound after transferring it from mastoid of the
patient, the procedure may be reversed, i.e. clinician listens the vibrating Tuning fork and the
moment the sound disappears it is transferred to the mastoid of the patient to know whether
patient can still listen it. And thus the bone conduction level of the patient is determined.
Tuning fork test done carefully can give you a sufficiently reliable information about the hearing
loss. It is a qualitative and quantitative test comparable to audiometry.
NB: After you complete the ear examination, nose, throat, nasopharynx and neck examination
should be completed. Facial nerve and other cranial nerve examination should be carried
out.
Systemic Examination
CVS, RS, CNS and abdominal examination should be carried out as usual. And evidence of any
systemic disorder is noted.
Majority of ear conditions can be diagnosed on the basis of history and clinical examination.
However you may need few investigations to confirm the diagnosis or to have additional assessment
of patient for management.
A large number of sophisticated investigations are available now a days but all are not needed in
every case. More over it is beyond the scope of this book to give all the possible details of each test.
And hence only important investigations would be discussed.
The investigations commonly needed for ear diseases are:
1. Microbiology of pus discharge
2. Radiology of mastoid and PNS
3. Pure tone audiometry
4. Impedance audiometry
5. Caloric testing.
Other investigations that may be needed in specific case are:
a. High resolution CT scan
b. Fundoscopy when you suspect intracranial extension of disease
c. Evoked response audiometry
d. Electronystagmography
e. Craniocorpography.
Radiological Examination of the Ear
Views advised for temporal bone study are:
1. Laws position
2. Schuller’s position
3. Mayer’s position
4. Stenver’s position
5. Chausse III position.
Out of these Schuller’s view is most commonly advised view (Figures 4-17 and 4-18).
Position: Patient’s head is placed in lateral position. The beam is directed 30–35° caudally and film is
taken.
This view gives adequate information about mastoid air cells, lateral sinus plate, dural plate and
aditus ad antrum. On the basis of pneumatisation mastoids are divided into:
Cellular: If cells are plenty, hexagonal and arranged in honeycomb pattern. This is a normal mastoid
(Figure 4-19).
Figure 4-17: Showing sketch diagram of Schuller’s view

Figure 4-18: X-ray—Left mastoid Schuller’s view. Showing well-pneumatised mastoid
Figure 4-19: X-ray—Right mastoid Schuller’s view. Showing sclerotic mastoid

Sclerotic: If no cells are visible and radio-opaque shadow covers the air cell area. This is considered as
diseased mastoid particularly when the X-ray of opposite mastoid is penumatised. Bilateral non-
development of mastoid air cells is seen in 4 percent of otologically normal individuals.
Diploeic: Cells are present but few in numbers and smaller in size. This is usually seen in poorly
developed mastoid.
Apart from air cells, dural plate (tegmen antri) and lateral sinus plate may be visible in Schuller’s
view. It is more visible when the mastoid cells become sclerotic. Angle formed between lateral sinus
plate and tegmen plate is known as ‘sinodural angle’.
• In acute mastoiditis the disease may destroy the intervening bony walls of the mastoid air cells
and this gives a picture called “clouding” of air cells.
• Low lying dura and forward lying sinus may be seen in some cases and this alerts the surgeon and
prevents intraoperative catastrophe.
• Cholesteatoma may cause erosion, and destruction in attic/antrum area. It may also erode the
lateral sinus plate or dural plate.
Audiometry
Audios = Hearing
Metrios= Measuring
It is a sophisticated way to measure the hearing. Today different types of audiometries are available.
They can be subdivided as:
Subjective Pure tone audiometry
Speech audiometry
Objective Impedance audiometry
Brainstem evoked response audiometry
Bekesy audiometry
Electrocochleography.
Out of all the above pure tone audiometry is in common use. With the help of PTA we can find out
the exact hearing threshold as well as type of the hearing loss. In audiometry, symbols are also being
used (Table 4-4).
PURE TONE AUDIOMETRY (PTA)

It is performed in sound treated room. Speech frequencies ranging from 250 to 8000 Hz are measured.
The audiometer is adjusted in such a way that in an audiologically normal individual sound stimulus
at 0 dB level should be just audible in all frequencies.
Procedure: Patient is sitting in a sound treated room. Test is explained to him. Headphones are
applied and sound is fed. Level of sound that is just audible for each frequency is measured and
plotted on a graph called ‘audiogram’.
Advantages:
1. Easy and reliable method
2. Permanent record is maintained.
Disadvantages:
Subjective test and hence not of much help in unco-operative children and malingerer.
Audiograms of common conditions may be as follows (Figures 4-20 to 4-24).
Few Ear Conditions

Conditions of external ear may be divided into:
1. Congenital • Absence of pinna (anotia)
• Small poorly developed pinna (microtia)
• Darwin’s tubercle
Figure 4-20: Showing air and bone conduction in

left ear
Figure 4-21: Audiogram showing A-B gap
Figure 4-22: Pure tone audiometry showing

SN deafness
Figure 4-23: Showing deep at 4000 Hz seen in

acoustic trauma
Figure 4-24: Showing deep at 2 kHz in BC seen

in otosclerosis
Table 4-4: Symbols used in audiometry
Air conduction Bone conduction

Ear Colour code
Masked Unmasked Masked Unmasked
Left X > Blue
Right < Red
No response Dwon arrow below respective symbol

• Low set and small pinna (Down’s syndrome)
• Atresia of EAC
• Pre-auricular sinus
• Treacher Collin’s syndrome
• Dermoid cyst
• Accessory tragus.
2. Traumatic • Laceration, haematoma auris.
3. Infective • Bacterial Furunculosis
Diffuse otitis externa
Impetigo contagiosa
Retroauricular intertrigo
Cellulitis of auricle
Malignant otitis externa
• Fungal Otomycosis
• Viral Herpes simplex
Herpes zoster (Ramsay Hunt syndrome)
Otitis externa haemorrhagica.
3. Reactive • Eczema
• Seborrhoeic dermatitis
• Keratosis obturans
• Neurodermatitis
• Psoriasis.
4. Neoplastic—osteoma, haemangioma, squamous cell carcinoma.
5. Miscellaneous—FB in ear, keloid, aural myiasis, etc.
CONGENITAL
Anotia
It is complete absence of pinna on one or both sides. It is associated with severe conductive deafness.
Usually associated with atresia of EAC. Middle ear defects may be there. Severe hearing loss needs
fitting of hearing aid and correction of defect by plastic surgery. Middle ear abnormality may need
various middle ear reconstructive procedures.
Microtia
Here few appendages of pinna are developed but poorly (Figure 4-25). It may be unilateral or bilateral
condition. It may be associated with atresia of EAC. It can be surgically corrected, but primary aim is
Figure 4-25: Showing—poorly developed pinna.

Absence of ear canal operation scar seen
to give useful hearing to the child at the earliest possible, by prescribing suitable hearing aids.
Reconstruction of ear canal and middle ear should
be contemplated later on.
Meatal Atresia (Figure 4-26)

First branchial groove deepens to form primitive exter-
nal auditory meatus. At the same time evagination
from pharynx [1st pharyngeal pouch] starts pressing
outward in the direction of branchial groove. At the
end of 2nd foetal month a solid core of epithelial cells
grows inwards from primitive funnel shaped meatus
towards pharyngeal pouch. This core of epithelial
cells remains solid upto 7th month of foetal life. And Figure 4-26: Showing
then starts dissolving. Failure of this dissolution development of ear
Figure 4-27: Showing accessory Figure 4-28: Showing treacher Collin’s syndrome
tragi + atresia of EAC
results into atresia of external auditory canal. Treatment is canalisation of EAC after hearing
assessment (Figure 4-27).
Treacher Collin’s Syndrome (mandibulo-facial dysostosis) (Figure 4-28)

Occurs due to maldevelopement of 1st and 2nd branchial arches.
Features
• Hypoplasia of mandible
• Hypoplasia of middle part of face
• Microtia and atresia of EAC
• Notching of lower eyelid
• Antimongoloid palpabral fissures.
Treatment: Correction of anatomical defect for functional improvement.
Pre-auricular Sinus (Figure 4-29)

The auricle develops around first branchial groove from six knob like outgrowths from first and
second branchial arch which appears in 6th week of embryonic life then gradually fuse by 3rd month
Figure 4-29: Showing pre-auricular cyst
to form an adult auricle. If this fusion is not proper a sinus persists infront and above meatus. This is
known as ‘pre-auricular sinus’.
Treatment: Surgical excision.
Dermoid Cyst (Figure 4-30)

Dermoid cysts may be congenital or acquired. In conge-
nital variety cysts develop at the site of embryological
fusion such as root of the nose, external angular dermoid
or at the root of helix.
TRAUMATIC
Traumatic conditions are quite common and it is beyond
the scope of this book to mention them in details.
INFECTIVE
Perichondritis, furunculosis, diffuse otitis externa,
otomycosis, dermatitis are common.
Figure 4-30: A case of post-aural dermoid
Diffuse Otitis Externa (Figure 4-31)
Common in all climatic conditions but heat, humidity and trauma aggravates. Staphylococcus aureus,
Pseudomonas aeruginosa and Bacillus proteus are common invaders. It is non-specific inflammatory
reaction with oedema and polymorph infiltration in dermis.
Treatment: Avoid swimming, keep ear dry, care of dandruff, meticulous cleaning of ear, local antibiotics.
Post-aural Intertrigo (Figure 4-32)

Retroauricular sulcus is site of predilection for occurrence of fissures. If these fissures get infected
with Staphylococcus aureus or Streptococcus pyogenes, a form of impetigo contagiosa develops
accompanied with weeping and crusting.
Otomycosis
It is fungal infection of EAC, caused by, Aspergillus fumigatus, Aspergillus niger or Candida albicans.
Peak incidence seen in rainy season when atmosphere is humid. Diabetics, patients on prolong
antibiotics and debilitated are more susceptible. Ear discharge, itching, discomfort and hearing loss
are common symptoms. On examination whitish, blackish, yellowish discharge may be seen in ear
canal. Sometimes whitish sheets like soaked blotting paper due to Candida infection may be seen.
Treatment: Aural toilet, gentian violet application, candid ear drops.
Figure 4-31: A case of diffuse otitis externa Figure 4-32: A case of post-aural intertrigo
Malignant Otitis Externa
Seen in elderly, debilitated or diabetic people. Caused by Pseudomonas infection. Condition is
characterised by destruction of surrounding tissues like pre and post-auricular area, facial nerve
and even base of skull.
Treatment: Control of infection by heavy antibiotics, control of diabetes, debridement. If not treated
promptly may prove fatal.
FB ear: Foreign bodies in ear are quite common. They may be metallic, non-metallic, vegetative, non-
vegetative, living, non-living. Common in children due to their basic nature of inquisitiveness. Beads,
stones, pencils, buttons, insects and other house hold things commonly seen.
Symptoms: Pain in ear, bleeding, blocking/FB sensation in ear.
Treatment
• Living insects—Instill edible oil in ear canal and suffocate the insect. Then it can be removed by
syringing or manually.
• Non-living things—Can be removed either by syringing or with the help of wire vectis or with the
help of micro-ear forceps. All care should be taken not to injure the ear canal and tympanic membrane.
Keloids (Figure 4-33)
Keloids: These are benign fibrous proliferation developing in predisposed persons, at the sites of
cutaneous injury. Ear lobe piercing can give rise to Keloid formation.
Treatment: Core excision and steroid injection.
Aural myiasis (Figure 4-34)
Patients having uncontrolled diabetes, Hensen’s disease, or debilitated patients or those who do not
care properly the chronically discharging ear may develop maggots in the ear. Flies enter the ear, lay
eggs. Larval stage of housefly is called maggots.
Treatment: Manual removal after suffocating the maggots by putting in liquid paraffin. Hygiene care
of the discharging ear and treatment of underlying disease like, Hensen, diabetes, etc.
Viral infection (Figures 4-35A to C)
Herpes zoster may affect external and middle ear at times. Usually it shows shingles as cutaneous
lesions, which may be seen on pinna or in post-aural area. Zoster has predilection for neural tissue
and so it may affect the geniculate ganglion resulting into facial nerve palsy. This condition is called
as “Ramsay Hunt syndrome” (Figure 4-36).
Figure 4-33: Showing keloid at Figure 4-34: Case of ‘Aural myiasis’

ear piercing site
Treatment: Antiviral agents and supportive therapy for facial nerve.
Common Conditions of Middle Ear

1. Suppurative otitis media
a. Acute
b. Chronic
2. Non-suppurative otitis media
a. Acute
b. Chronic
1. Adhesive otitis media
2. Tympanosclerosis
3. Otitis media with effusion
4. Traumatic conditions (Baro-otitis, bomb blast, slapping the ear, etc.).
A B
C
Figures 4-35A to C: Few benign tumours of external ear: (A) osteoma EAC,
(B) haemangioma EAC, and (C) pyogenic granuloma
Figure 4-36: Ramsay Hunt syndrome
SUPPURATIVE OTITIS MEDIA

Acute
A very common ear condition in children, follows upper respiratory tract infection. Infection enters
through Eustachian tube. Pain in ear may be followed by discharge and pain disappears after
discharge. Group B hemolytic Streptococcus or H. influenzae are common invaders.
Treatment: Antibiotics, analgesics, decongestants, steam inhalation. Myringotomy, if no response to
medical treatment.
NB: Rarely ASOM may culminate into acute mastoiditis and also facial nerve palsy if it is uncovered.
Such patient needs urgent intervention.
Chronic Suppurative Otitis Media

Common condition in India and developing countries.
Pus discharge from ear and hearing loss are presenting symptoms. A painless condition unless
complicated. Hence, patient comes late to clinician. Pus in external auditory canal and perforation of
drumhead are common findings. Depending upon its characteristics it may be divided into ‘safe’
and ‘unsafe’ varieties.
1. Safe ear (Tubo-tympanic disease)
Criteria:
1. Drum perforation is central
2. ET usually diseased
3. Mastoid is usually healthy
*Complications are rare.
2. Unsafe ear (Attico-antral disease)
Criteria:
1. Drum perforation marginal/attic
2. ET may be normal
3. Disease [Cholesteatoma/granulation] may extend to attic-aditus and antrum.
* Intracranial complications are common.
Safe ear (Tubo-tympanic disease)
Symptoms:
1. Otorrhoea
2. Hearing loss.
Signs:
• Pus discharge in EAC usually present in active stage
• Central perforation in pars tensa
• Conductive deafness on tunning fork tests.
Depending upon the disease activity the safe CSOM can be further subdivided into:
• Active ear
• Quiescent ear
• Inactive ear.
Active ear: Characterisitis
1. Profusely discharging ear
2. Polyp/granulation in middle ear
3. Congested drum margins or middle ear mucosa.
Quiescent ear 1. Ear discharge intermittent. Not profuse
2. Otorrhoea has recently stopped.
Inactive ear: No ear discharge since last 6 months.
Investigations:
Pus culture may be done to know organisms and sensitivity to drugs.
X-ray mastoids to know the condition of mastoid air cells.
Treatment:
Objectives
• To stop ear discharge
• To make the ear infection free
• To improve hearing by reconstructive procedures like tympanoplasty/myringoplasty.
This can be achieved by:
• Aural toilet—dry/wet
• Antibiotics to control infection
• Control of allergy in nose if existing
• Eliminating the source of infection in nose/nasopharynx/sinuses/tonsil.
Prerequisites for tympanoplasty
1. Ear should be dry
2. Good air—bone gap on PTA
3. ET should be patent
4. Good cochlear reserve.
Note: Some patients may require cortical mastoidectomy before tympanoplasty
Unsafe ear (attico-antral disease)

It is usually associated with cholesteatoma.
Cholesteatoma
Cholesteatoma is most common condition in chronic suppurative otitis media of unsafe
variety.
Definition: It is a bag like structure lined by keratinising stratified squamous epithelium containing
desquamated epithelium having erosive property and mostly seen in temporal bone.
Aetiology: Exact aetiology not known.
Varieties: Congenital Due to embryonic cell rests
Acquired Primary
Secondary
Pathology: Columnar ciliated epithelium in the middle ear is replaced by stratified squamous
epithelium which may have migrated from the external ear or caused by metaplasia of middle ear
mucosa due to repeated infection. Persistently blocked ET results into a retraction pocket formation,
which may act as a precursor for cholesteatoma formation. Cholesteatoma causes destruction of bone
or whatever structure comes in its way eroding aditus and or antrum. Horizontal semicircular canal,
facial nerve may be similarly injured. It may erode lateral sinus plate resulting into lateral sinus
thrombosis. If the dural plate is eroded the disease may travel intracranially resulting into extradural
abscess, subdural abscess, brain abscess, meningitis and otitic hydrocephalus.
Symptoms:
1. Otorrhoea—usually scanty and foul smelling
2. Hearing loss
3. Symptoms due to complications.
Signs:
1. Attic or postero-superior marginal perforation or retraction pocket with cholesteatoma
debri.
2. Fistula test may be positive, if disease erodes lateral semicircular canal.
Investigations:
1. Pus culture may be positive for Pseudomonas pyocynes.
2. X-ray mastoid may show sclerosis in mastoid bone with erosion.
Treatment:
Objectives
1. To make the ear safe, disease free and prevent intracranial spread of disease
2. To conserve/improve residual hearing.
Medical: Not useful.
Surgical: Aim of the surgical treatment is to make the ear, disease free, prevent complications and to
give useful hearing if possible. Depending upon extent of the disease, modified or radical
mastoidectomy may be done.
NON-SUPPURATIVE OTITIS MEDIA
Synonyms: (serous otitis media, secretory otitis media, glue ear, otitis media with effusion)
Patient may have history of URI in recent past, which is not resolved completely or may have recurrent
attacks. Upper respiratory allergy may be pre-disposing factor.
Complains of wooly sensation in ear, discomfort in ear or blocking sensation or hard of hearing.
School going children may have poor language acquisition or poor performance in school due to
hearing loss.
On examination: EAC may be normal.
TM-lustreless, cone of light distorted or lost. Mobility of TM may be reduced or lost. Fluid level may
be seen on otoscopy as ‘hair line’ with air bubbles in middle ear. Tympanometry may show negative
middle ear pressure.
Treatment:
i. Opening up of ET by valsalva, nasal and systemic decongestants
ii. Antibiotics and antihistaminic
iii. Myringotomy and insertion of grommet if conservative line fails
iv. Enlarged adenoids or infection in throat or sinuses needs treatment.
Adhesive otitis media tympanosclerosis may be considered as different end results of the same
underlying pathology, i.e. chronic ET block. In adhesive otitis media adhesions develop between
medial wall of middle ear and tympanic membrane due to chronic retraction. In tympanosclerosis
the hyaline degeneration of collagen fibres is followed by calcium salt deposition in the fibrous layer
of drum, and also in other tissues of middle ear.
OTOSCLEROSIS (TABLE 4-5)

• A condition common in Caucasians, rare in Negroes
• Females are more commonly affected
• Exact aetiology not known
• Remnants of endochondral bone thought to be responsible
• Deficiency of alpha1-antitripsin seen in few
• Tinnitus, hearing loss [progressive] are presenting symptoms
• Flamingo-tint (pink hue of drum) may be seen in 1 per cent patients
• T-F tests often show—conductive hearing loss, which may later on go worse and land up into SN
loss
• Audiogram may show a dip at 2 kHz in bone conduction. This is known as “Carhart’s notch”.
• Impedance audiometry may help in diagnosis
• Stapedectomy is the treatment of choice. Hearing aids when patient not willing for surgery unfit
for surgery or has sensorineural hearing loss due to cochlear otosclerosis.
Common Conditions of Inner Ear

1. Meniere’s disease
2. Labyrinthitis
Table 4-5: DD of conductive deafness with intact TM
Disease EAC TM PTA Impedance Audiometry
General Cone o’ light Mobility MEP curve
ET block Normal Retracted Distorted Reduced Conductive Negative ‘C’ type
Lustreless lost deafness +
Secretory OM Normal Lustreless Distorted Reduced Conductive Negative ‘B’ type
Retracted lost Absent deafness +/++
Adhesive OM Normal Dull Distorted Absent Conductive Negative ‘B’ type
Retracted lost deafness+++
Tympano- Normal Chalky Distorted Normal Conductive Normal/ Variable
sclerosis Patches lost Absent deafness Negative
Otosclerosis Normal Normal Normal Normal Conductive/ Normal ‘As’ type
flamingo- SN deafness
tint ±
3. Presbycusis
4. Acoustic neuroma
5. Noise induced hearing loss.
Few Common Procedures

SYRINGING (FIGURES 4-37A AND B)
Wax is brown/black collection of ceruminous and sebaceous gland secretion, along with
desquamated canal skin epithelium. In normal process this wax is extruded from ear canal. It is
considered abnormal only when it gets accumulated and causes symptoms (impacted wax). It may
cause pain in ear and hearing loss. It can be removed by cerumen spud manually or by syringing.
Impacted wax needs wax solvents before attempting syringing.
A B
Figures 4-37A and B: Showing method of syringing of ear
Requirement:
1. 20 ml glass syringe with rubber nozzle
2. Kidney tray and bowl
3. Luke warm water/saline.
Procedure: Patient is in sitting position. Luke warm water is taken in 20 ml glass syringe and forced in
the ear canal in the antero-superior direction. The fluid strikes the drum and returns back. While
returning back it brings with it the softened wax.
Complications:
1. Vaso-vagal attack: When auricular branch of vagus gets stimulated. To prevent this complication
force of fluid should be directed towards antero-superior canal wall.
2. Perforation of drum: If the force of fluid is more, it may perforate the drum.
3. Spread of infection: If the drum is perforated the fluid may carry infection in the middle ear and
hence syringing should not be done in perforated drum.
4. Caloric stimulation: If the water temperature is very much above or below body temperature
labyrinth may get stimulated resulting into vertigo and vomiting.
Rhinology
• Examination of Nose and Paranasal Sinuses
5
Examination of Nose and
Paranasal Sinuses
Let us first consider the symptoms related to nose and paranasal sinuses. Symptoms of nose and
symptoms of paranasal sinuses are many of the times inseparable.
Nasal and Paranasal Sinuses (PNS) Symptoms

1. Nasal obstruction
2. Nasal discharge (rhinorrhoea)
3. Bleeding per nose (epistaxis)
4. Sneezing
5. Nasal mass
6. Crusting
7. Disturbances of smell
8. Itching in nose
9. Nasal regurgitation
10. FB in nose
11. Swelling over nose/face
12. Pain in or around nose.
Some other symptoms associated with nasal disease are:
• Headache
• Eye symptoms like watering from eye (epiphora), itching, diplopia, proptosis, etc.
• Alteration in voice
• Snoring
• Fever.
Your patient may have one or more than one of the above symptoms. Let us analyse these symptoms
one by one.
Nasal Obstruction
DURATION
Ask the patient How long you are suffering from nasal obstruction? This would tell you whether the
disease is acute or chronic.
LATERALITY
Ask the patient Whether the nasal obstruction is unilateral or bilateral or changes side? Unilateral nasal
obstruction may be due to deviated nasal septum, nasal foreign body, or some mass in nose like
polyp. Bilateral nasal obstruction may be due to conditions like nasal allergy, septal haematoma or
ethmoidal polyposis.
LATENCY
It should be asked whether the symptom is constant or intermittent, nasal obstruction, which is
constant, may be due to some nasal mass. Intermittent nasal obstruction may be seen in allergic rhinitis.
SEVERITY
Patient should be asked, How severe the obstruction is? It may be just noticeable or severe enough to
prevent routine work of the patient. It may be even progressive in case of a polyp or malignancy.
CHARACTER
It should be asked whether nasal obstruction is during inspiration or expiration. In Antro-choanal
polyp nasal obstruction may be more during expiration. This is because the polyp allows air to
breathe in but at the time of expiration it corks the posterior choana and hence patient experiences
obstruction more during expiration.
In allergic rhinitis patient may experience nasal obstruction on one side at a time. And then
changes to other side. This is so because even in the normal individual, only one nostril is patent at
a time. After a period, other nostril opens and the previous one blocks. This is a normal process called
Examination of Nose and Paranasal Sinuses 75
as Nasal cycle and it is under autonomic control. A person with allergic rhinitis has swollen turbinates
and hence he becomes aware of this nasal cycle.
In allergic rhinitis if a patient lies on a bed in lateral position with blocked nostril on upper side,
the obstruction disappears. This is because the blood collected in the cavernous tissue of nasal
turbinates drains away as soon as turbinate occupies the position above the heart level.
Factors aggravating and ameliorating the nasal obstruction should be asked, particularly the
seasonal variation, emotional stress, food or drugs.
Nasal Discharge (Rhinorrhoea)

DURATION
Ask the patient How long he is suffering from nasal discharge. Short duration rhinitis may be due to
simple disease like acute viral rhinitis. Long standing nasal discharge may be seen in allergic rhinitis,
sinusitis, atrophic rhinitis, etc.
LATERALITY
Ask the patient Is nasal discharge unilateral or bilateral. Unilateral nasal discharge may be seen in case
of foreign body in the nose or some mass in the nose like polyp, malignancy.
NB: Unilateral foul smelling nasal discharge in a child is almost

diagnostic of retained foreign body in the nose.
SEVERITY
Nasal discharge may be scanty, moderate or copious so much, so that it may not be possible for a
person to work.
LATENCY
It should be asked whether the symptom is constant or intermittent. Perennial nasal allergy manifests
round the clock while seasonal allergy manifests in particular season when allergen is predominant
in the environment.
CHARACTER
Character of nasal discharge should be asked in details. The nasal discharge may be watery, mucoid,
mucopurulent, purulent, or blood stained.
Watery
Watery nasal discharge is seen in viral rhinitis. It may be confused with CSF rhinorrhoea.
Mucoid
The discharge is tenacious but transparent. This is seen in early rhinitis or allergic rhinitis.
Mucopurulent
Here the discharge is coloured and tenacious. It is seen in chronic rhinitis, sinusitis and any nasal
mass or in malignancy.
Purulent
This is thick coloured nasal discharge, which is less tenacious. It may be seen in chronic sinusitis or
atrophic rhinitis.
Blood Stained Discharge

This may be seen in infected nasal mass, nasal myiasis or in malignancy.
Bleeding Per Nose (Epistaxis) (FIGURE 5-1)

It should be confirmed whether it is a fresh blood, clotted blood or blood stained discharge.
• Amount of blood loss may be enquired.
• History of trauma should be excluded/confirmed.
• History of taking any drugs particularly anticoagulants should be taken.
• History of bleeding from any other site should be asked.
• History of bleeding disorder in the family should be asked.
• History of similar episodes in the past may be asked.
Cause of epistaxis may be local or systemic.
• Local: Trauma, acute rhinitis, acute sinusitis, angiofibroma, haemangioma, rhinosporidiosis,
malignancy, etc.
• Systemic: Severe hypertension, bleeding disorder, leukaemia, uraemia, and vitamin K deficiency or
some physiological causes like pregnancy, etc.
• Most common site for bleeding in nose is little’s area.
1. Anterior ethmoidal artery

2. Posterior ethmoidal artery
3. Septal branch of sphenopalatine artery
4. Septal branch of superior labial
5. Great palatine artery
6. Little’s area
Figure 5-1: Showing blood supply of nasal septum
Children have a tendency to scratch the nose, which causes bleeding from Little’s area. This is
commonly known as “epistaxis digitorum”. In case of profuse epistaxis angiofibroma, haemangioma,
bleeding disorders and hypertension should be preferably kept in mind.
Sneezing
Sneezing as such is a protective reflex. It prevents entry of any obnoxious material into the nose.
Sneezing is also elicited during nasal mucosal irritation. Hence in allergic rhinitis when patient gets
up from bed he gets a cascade of sneezing which amounts in tens. Occasional sneezing is normal.
However, more than 8 to 10 sneezing at a time without any obvious provocation should be seen
carefully.
Nasal Mass
Any abnormal tissue in the nose is called as nasal mass.
Many of the times patient looks into the mirror and confuses his inferior turbinate as a nasal mass.
Antrochoanal polyp, rhinosporidiosis, angiofibroma, nasal glioma, malignancy may present as nasal
mass. Patient should be asked.
1. When he has noticed this nasal mass?
2. Is it unilateral/ bilateral?
3. Does it cause nasal obstruction?
• If the answer is yes, how severe it is?
• Is it more during inspiration/expiration or both.
4. Is the mass enlarging, static or regressing?
5. Are there some associated symptoms like headache, fever, epistaxis, hyposmia, etc.
Crusting
It is usually due to drying up of nasal secretions. Seen in atrophic rhinitis, rhinitis sicca and in nasal
scleroma. Roomy nostril, DNS or dry weather may also predispose to excessive crusting in nose.
Disturbances of Smell
Anosmia—Total loss of sense of smell (e.g. head injury, functional)
Hyposmia—Reduced sense of smell (e.g. rhinitis, nasal polyp, nasal allergy)
Parosmia—Altered sense of smell (e.g. allergic rhinitis)
Cacosmia—Any smell is experienced as foul (e.g. chronic sinusitis).
Itching in Nose
Nasal allergy, beginning of viral rhinitis can cause itching in and around nose.
Nasal Regurgitation
It may be the first symptom in diphtheria. Palatal palsy, perforated palate due to any cause and
velopharyngeal insufficiency can also result into nasal regurgitation.
Foreign Body in Nose

A child is usually brought by parent with a history of FB in nose. However, many a times there may
not be any history and retained FB may be detected on clinical examination accidentally. It may
present as unilateral foul smelling nasal discharge. It may be seen in adults who are mentally retarded.
Usual household articles like pencils, rubber, beads, needles, sponges, seeds are commonly seen.
They may be classified as living and non-living, vegetative and non-vegetative, metallic and non-
metallic, etc.
Swelling over Nose and Face

Ask the patient When he noticed swelling over nose/face for first time? Ask about history of trauma. Is the
swelling static, progressive or regressive? Associated nasal symptom like nasal obstruction, rhinorrhoea,
anosmia, epistaxis should be enquired.
Swellings following trauma may be due to soft tissue injury or nasal bone or facial bones. Swellings
since birth may be dermoid or meningocoele. Inflammatory and neoplastic conditions can also give
rise to swelling in this area.
Pain in and Around Nose

1. Ask the patient When it started?
2. Has it started spontaneously or induced after trauma or any other way?
3. How long the pain lasts?
4. Are there any aggravating and/or ameliorating factors?
5. Is there associated fever, e.g. furunculosis of nasal vestibule?
6. What is the nature of pain? Is it stabbing, cutting, dull aching, etc.?
7. Does it spread any where, e.g. neuralgias?
8. Are there any associated symptoms like vomiting or coloured hallos infront of eye, nasal obstruction, etc.?
9. Has it any postural or diurnal variation?
10. Ask the patient about his dental hygiene.
HEADACHE
Headache is very important and common symptom for large number of different disease conditions.
Some of the causes for headache are beyond the scope of otolaryngology and this book. Upper
respiratory infections, various types of facial neuralgias, migraine, refractory error, cervical
spondylosis, severe anaemia, raised intracranial tension, all can give rise to headache. Following
questionnaire may give you a guideline.
1. When he noticed it? And how it started?
2. Is it constant or intermittent?
3. What is the exact site?
4. How severe it is?
5. Does he have fever?
6. What is the character of pain? Is it sharp shooting, cutting or dull aching?
7. How it is aggravated?
8. How it is relieved?
9. Is there any diurnal variation?
10. Are there any associated nasal symptoms or nausea, vomiting or giddiness?
11. Are there any colour hallos in front of eyes?
12. Does the patient have a normal vision? Or he uses glasses?
13. Does he have restricted painful neck movements?
Patient may be referred to proper specialty to rule out causes other than ENT causes.
Headache may be sharp shooting during acute sinusitis and dull aching during chronic
sinusitis. Headache due to particular sinus may have typical features, which help us to recognise
the sinus involed in the patient. When all the sinuses are involved, the condition is called as
Pan-sinusitis.
Frontal sinusitis: Headache of frontal sinusitis is usually located in frontal area, superciliary area and
looking down at the feet is not comfortable for the patient. The headache of frontal sinusitis is more
when patient wakes up in the morning. Headache lasts for few minutes/hour and then
gradually disappears. This is so because during sleep the secretions are accumulated in the
sinus. When patient wakes up in the morning, retained secretions try to drain through the fronto-
nasal duct. Stretching of this duct results into headache. Moment secretions are drained headache is
relieved.
Maxillary sinusitis: Pain of maxillary sinusitis is more in the region of upper jaw teeth or spread over
cheek. It may be experienced in temple area. Usually dull aching.
Ethmoidal sinusitis: It is more marked in small children. The upper and lower eyelids may be oedematous
and eye movements may be painful. Pain is more in the region of medial canthus.
Sphenoid sinusitis: Malaise and bodyaches are the predominant features in sphnoidal sinusitis. The
patient may experience headache on the vertex.
• Significant deviated nasal septum may cause pressure over turbinate and cause headache or pain
over dorsum of nose. This is named as anterior ethmoidal nerve syndrome.
EPIPHORA (WATERING FROM EYES)
When there is obstruction to naso-lacrimal duct due to any big nasal mass or anterior nasal packing
the tears cannot pass through naso-lacrimal duct and they overflow from eyes. This is known as
epiphora.
ALTERATION IN VOICE
The nose and paranasal sinuses give timber to our voice. Hence, whenever there is fluid collection in
the sinuses or mass in the nose or sinuses, it alters the quality of voice. For example, “flat voice”
during rhinitis. Mass in nasopharynx may also alter the quality of voice. A big adenoid in the
nasopharynx may give rise to “rhinolalia clausa”. Similarly a perforated palate/cleft palate or removal
of adenoid may result into alteration of voice called as Rhinolalia aperta.
Snoring
A partial obstruction to naso/oropharyngeal air passage during sleep resulting into a peculiar noise is called as
snoring.
This symptom has a peculiarity that patient may never complain about it. It is usually the other
family member who complains about it. The obstruction may be in nose, nasopharynx, oropharynx
due to enlarged tonsils, adenoid, deviated nasal septum or due to lax/bulky oropharyngeal tissues
in an obese individual. Elongated uvula, macroglossia, retrognathia may be contributory. During
sleep these patients develop hypotonia of musculature maintaining airway. This leads to collapse of
oropharyngeal airway and negative oropharyngeal pressure.
If this obstruction is prolong and severe, it may result into sleep apnoea. This condition has
deleterious effects over heart. When a patient develops 30 apnoeic spells of longer than 10 seconds
duration in a 6-hour sleep, may be considered a case of Sleep apnoea and needs treatment.
Clinical Examination of Nose and PNS

INSTRUMENTS
1. Bull’s eye lamp
2. Head mirror
3. Thudicum nasal speculum
4. Postnasal mirror
5. Jobson horne probe
6. Tongue depressor
7. Nasal dressing forceps.
Examination of nose and PNS may be done as follows:

a. Examination of external nose and face
b. Anterior rhinoscopy
c. Posterior rhinoscopy
d. Sinus tenderness
e. Cold spatula test (if needed)
f. Transillumination test
g. Examination of both ears, pharynx, larynx and neck.
Examination of External Nose and Face

INSPECTION
Look whether the nose is appropriate for the face or not. Few noses are too small or too big for the face.
Look for any obvious deformity like flattened dorsum of nose, bulbous nasal tip, columellar retraction,
supra tip depression, nasal hump, crooked nasal tip, swelling in the region, increase in intercanthal
distance, sinus, ulcer or any obvious scar mark on the nose due to previous injury or surgery.
Even by the smell, conditions like atrophic rhinitis and retained foreign body can be guessed, as both these
conditions emit a very foul smell (Figures 5-2A to C).
Figure 5-2A: Showing fall of nasal Figure 5-2B: Lateral view Figure 5-2C: Huge rhinophyma
bridge on nasal tip
PALPATION
In case of swelling, ulcer, sinus findings of inspection are confirmed by palpation. In case of trauma,
nasal pyramid should be palpated for any tenderness and crepitus.
One should utilise this opportunity to examine rest of the face also. This may give good information
about the sinus conditions. For example, expanding lesion in maxillary, frontal or ethmoidal sinus
may result into swelling in the affected region or deviation, proptosis or even chemosis of eyeball, e.g.
malignancy of paranasal sinuses.
Anterior Rhinoscopy
Support the head with left hand fingers and retract the nasal tip with the help of left thumb. This
simple examination shows anterior part of nasal septum, nasal cavity and anterior end of inferior
turbinate. It is particularly useful in children who get alarmed on seeing that some instrument is
being put into their nose.
Take thudicum nasal speculum in left hand. Hold it with left index finger, supported by thumb,
and press the fangs of the speculum by left middle finger and ring finger and slowly negotiate it in the
nostril of the patient and release the blades. This should not cause any discomfort to the patient. You
can see the nasal septum, inferior turbinate, inferior meatus, middle turbinate and middle meatus in
this examination. Superior turbinate and meatus are not seen in normal conditions (Figure 5-3).
Figure 5-3: Clinical photograph showing how to hold nasal speculum.

Anterior end of inferior turbinate seen in photograph
STRUCTURES TO BE SEEN IN ANTERIOR/RHINOSEOPY
• Nasal vestibule
• Nasal septum
• Colour of the mucosa
• Lateral nasal wall
• Inferior turbinate
• Middle turbinate
• Inferior meatus
• Middle meatus
• Nasal floor
• Nasal roof (usually not seen).
Findings of clinical examination should be drawn diagrammatically as follows (Figure 5-4).
Figure 5-4: Diagrammatic representation of anterior/rhinoscopy

• Nasal vestibule: It is an anteriormost part of nasal cavity lined by skin, having vibrissae (hair). It can
be easily examined without nasal speculum. It is the site for foreign body, fissures and furuncles.
Infection in the nasal vestibule is known as vestibulitis and may complicate as facial cellulitis, orbital
cellulitis and cavernous sinus thrombophlebitis and hence infection in this area is considered as dangerous
and treated promptly. This area of the face including upper lip is called danger zone of face.
• Nasal septum: It is cartilaginous in the caudal segment and bony in the deep part. It divides the nose
into two compartments. Mild deviations here and there are not clinically significant. Deviation of
septum may be ‘C’ or ‘S’ shaped. When the anterior end of nasal septum juts out of nasal cavity on
retraction of nasal tip, it is called as “caudal dislocation” of the nasal septum. Acute buckling of
nasal septum over maxillary crest is called as ‘spur’. There can be perforation in nasal septum due
to disease or surgery. Trauma to nose may result into septal haematoma formation, which may lead
to septal abscess if not treated. Benign tumours like haemangioma (bleeding polypus of septum)
rhinosporidosis may be seen over septum. Little’s area should be examined in a case of epistaxis.
• Colour of nasal mucosa
Pink—Normal
Bright red—Infection
Bluish, wetty—Nasal allergy.
• Lateral wall
• Inferior turbinate: This is the largest turbinate which attracts attention of everyone including
patients. Inferior turbinate is highly sensitive to touch and firm on touch. It may get
hypertrophied in nasal and sinus infections. It may get enlarged, wetty and bluish in allergic
nasal conditions.
• Inferior meatus: This is not easily visible unless vasoconstrictor spray is used. It may be the site
where a FB may be lodged. Naso-lacrimal duct opens into it.
• Middle turbinate: This is the second largest turbinate in the nose and one has to extend the neck
of the patient to have a better view of the turbinate.
• Middle meatus: It lies below middle turbinate. All anterior group of sinuses, i.e. frontal, maxillary,
anterior and middle ethmoidal open into the middle meatus and hence is the common site
where from pus may be seen trickling down. Look for polyp in this area.
• Superior turbinate: This is usually not seen in A/R examination. One should not attempt to see
superior turbinate except when patient is under general anaesthesia.
• Nasal floor: It should be looked for secretions, FB, antrochoanal polyp or malignancy.
• Nasal roof: Examination of nasal roof is painful and hence should be done under GA if
needed.
Abnormalities that are commonly encountered in anterior rhinoscopy are nasal secretions, nasal
mass, foreign body, hypertrophy or atrophy of turbinates.
Secretions should be wiped out by cotton wool carrier or electrical suction. This would give you a
clear vision of nasal cavities. After identifying normal nasal structures, abnormal findings should be
identified.
If there is abnormal mass in nose its exact location, size and colour is noted down. It is touched with
a cotton wool carrier to know whether it is sensitive to touch or not. Consistency of the mass is
confirmed by pressing the swelling with the help of cotton wool carrier. Attachment of mass is
assessed by passing the jobson horne probe, with cotton wool firmly wrapped on its tip, on all sides
of the swelling. Probe can’t be passed from the side where it is attached to nasal structure. During this
manipulation you can also decide whether the mass bleeds on touch or not.
Turbinates: These are pinkish in colour. Highly sensitive to touch and firm on probing.
Polyps: Polyps in nose are greyish masses, soft in consistency and poorly sensitive to touch. They do
not bleed on touch.
FB: Foreign bodies are easily identified on A/R. However, a retained FB may be difficult to identify
due to deposition of calcium layer on it. The retained FB has a gritty sensation on probing and may
bleed due to surrounding granulation tissue.
Malignancy: Malignant lesions are reddish masses, friable and bleed on touch.
• After visualising the nose in the manner described above findings are noted down
diagrammatically.
Posterior Rhinoscopy (Figure 5-5)

Examination of posterior nares and nasopharynx by a postnasal mirror is known as posterior
rhinoscopy. It is very sensitive examination and lot of co-operation from the patient is needed. This
examination is not possible in small children and anxious adults.
Figure 5-5: Diagramatic representation of

posterior rhinoscopy examination
PROCEDURE
The test should be explained to the patient. Then postnasal mirror is gently heated on spirit lamp to
prevent condensation of patient’s breath on the mirror. It is tested on our own body to see that it is not
too hot to scald the patient. Tongue depressor is taken in left hand, tongue is depressed, and postnasal
mirror is gently negotiated along left angle of mouth, holding like a pen, beyond the soft palate to
visualise various structures in nasopharynx. Mirror is rotated in various angles without touching
the posterior pharyngeal wall or base of tongue to prevent gag reflex.
One can see roof of the soft palate, posterior end of nasal septum, two posterior choanae, posterior
ends of inferior and middle turbinates. You cannot see superior turbinate in this examination. Roof
of nasopharynx is seen and may show tuft of adenoid tissue in children. At the posterolateral wall of
nasopharynx one can see nasopharyngeal end of Eustachian tube. This is also known as torus
tubaris. There is a small gutter formed between posterior nasopharyngeal wall and torus, which is
popularly known as fossa of Rosenmuller.
In some patients it may not be possible to visualise all the structures in posterior rhinoscopy. In
such patients nasopharyngoscopy can be done by using fibreoptic flexible scope.
Clinical significance: The fossa of Rosenmuller has a great clinical significance. Malignancy may be
hidden in this area and not detected easily even after posterior rhinoscopy examination. But the
secondaries from this site may develop in the neck in the form of enlarged lymph nodes. This situation
is known as secondaries in neck with primary unknown. In such a situation, it is customary to take
biopsy from fossa of Rosenmuller, emperically.
Sinus Tenderness (Figures 5-6A to C)

Tenderness over sinuses may be elicited as follows:
1. Maxillary sinus: firm pressure is given over canine fossa.
2. Ethmoid sinus: pressure given medial to medial canthus.
3. Frontal sinus: pressure given at the roof of orbit, above medial canthus, in the floor of frontal sinus.
4. Sphenoid sinus: tenderness cannot be elicited.
5. Sinus tenderness indicates infective pathology in affected sinus.
A B C
Figures 5-6Ato C: (A) Ethmoid sinus tenderness, (B) Frontal sinus tenderness, and
(C) Maxillary sinus tenderness
Cold Spatula Test (Figure 5-7)
One can examine the patency of each nostril separately by cold spatula test. In this tongue depressor is
/
held just below the anterior nares and patient is asked to blow gently on it. Two distinct areas on the
r
tongue depressor would show fogging due to exhaled air. Absence or less fogging indicates
.i
obstruction on that side.
s s
n
is a
e r
.p
iv p
Figure 5-7: Showing cold spatula test
/: /
Transillumination Test
tt p
This test is done to know the status of frontal and maxillary sinuses. The procedure is done in a dark
room. Clinician gets himself dark adaptation by sitting in a dark room with eyes closed for 10
minutes. A small but bright light source is kept in oral cavity. In a normal sinus the light is transmitted
h
through the maxillary sinus and seen as “pupillary glow” or “infra-orbital crescent”. When there is
fluid, mass or polyp in the sinus the Transillumination test would be negative. In the advent of recent
investigative tools, this test has a very limited utility.
After examining the nose, PNS and postnasal space, ears, pharynx, larynx
and neck examination should be done without fail.
After clinical examination one may need the help of investigations for confirmation of diagnosis.
The most common investigation done for nose and PNS diseases is radiological examination.
Nasal Endoscopy
The nasal endoscopy has revolutionised the diagnosis and management of many nasal disorders. It
/
comparatively a new weapon in the hands of otolaryngologists. Its most important utility is excellent
r
vision of all the parts of nose which are otherwise difficult to visualise with anterior rhinoscopy. It is
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also easier to take photographs with the help of nasal endoscope to keep the records of the patients.
Management of many nasal and PNS disorders can be done with this new weapon. It also helps to
s
manage some of orbital and neurological disorders like orbital abscess, CSF rhinorrhoea, pituitary
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tumours, etc.
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INDICATIONS
is a
1. To assess the degree and located the site of nasal obstruction.
2. To evaluate patients complaining of Headache.
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3. To evaluate patients with Epistaxis.
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4. To monitor the progress in the treatment of nasal and Para nasal sinus infections.
5. To locate the site of Cerebrospinal, Rhinorrhoea.
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6. To monitor nasal fossa after resection of tumours.
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INSTRUMENTS REQUIRED (FIGURES 5-8 AND 5-9)
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Figure 5-8: Showing nasal endoscope
1. 0 Degree and 30 degree nasal endoscopes.

2. Light source—halogen or xenon.
3. Fibreoptic cable.
4. Television or medical grade monitor.
5. Endoscopic camera and its attachements.
6. Freer’s elevator.
7. Suction tips.
8. Ball Probe.
9. Straight forceps.
10. Savlon or defogging solution.
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s .i
n s
is a
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Figure 5-9: Showing various forceps required for nasal endoscopy
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PROCEDURE
Diagnostic nasal endoscopy is usually done under local anaesthesia as an OPD procedure in either
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sitting position with head support or in laying down position. Good nasal decongestion and surface
anaesthesia is required which is achieved by placing cottonoids/patties made of soft roll/ribbon
tt p
gauze strips soaked in 4% xylocaine + adrenaline solution (30 ml xylocaine with 2 ampoules of
1:1000 adrenaline). The strips are squeezed well before inserting into the nostrils. The packing is
repeated two or three times to achieve good result.
h
The surgeon stands on the right side of the patient, holding the endoscope in right hand and
guides and support the scope with the left hand. The routine nasal endoscopy is done in three passes.
1st pass: The endoscope is passed along the floor of the nostril posteriorly upto the posterior choana
an then into nasopharynx. The parts examined are the nasal septum, inferior turbinate and the
inferior meatus, middle turbinate as also the nasopharynx including the Eustachian tube opening,
the tubal fold and the fossa of Rossenmuller and the opposite side Eustachian tube opening. The
opening of the nasolacrimal duct may be seen in the inferior meatus.
2nd pass: At the level of the posterior choana, endoscope is directed up between the middle turbinate
and the septum first and then between the superior turbinate and the septum to visualise the ostium
of sphenoid sinus in the sphenoethmoid recess.
3rd pass: Endoscope is introduced in the middle meatus (space below the middle turbinate) from the
posterior aspect to visualise the infundibulum, the bulla ethmoidalis, uncinate process and the
maxillary ostium or the accessory ostia.
Advantages of Diagnostic Nasal Endoscopy

1. All parts of the nasal cavity, meatii and the postnasal space can be visualised directly under better
illumination and clarity, thus detecting may pathologies, which would be missed during the
routine anterior rhinoscopy.
2. The efficacy of medical or surgical treatment can be followed up by subsequent repeat nasal
endoscopy.
3. It is an OPD procedure.
4. Finding can be documented and recorded in the form of CDs or DVDs. This can be useful for the
medico-legal purposes.
5. It is an excellent teaching aid as students can watch the TV screen.
Disease like chronic sinusitis, polyps, benign tumours, epistaxis and even angiofibroma are also
managed by using nasal endoscopy. However it requires a good amount of practice on cadavers
before venturing on patients. Complications like epistaxis, CSF rhinorrhoea and orbital injuries are
also seen if the procedure is not done carefully.
The following figures (Figures 5-10 to 5-14) are taken with the help of nasal endoscope:
Figure 5-10: Angiomatous polyp of inferior turbinate Figure 5-11: Antrochoanal polyp
Figure 5-12: Concha bullosa Figure 5-13: Ethmoid polypii
Figure 5-14: Nasopharynx with adenoid hypertrophy
RADIOLOGICAL EXAMINATION OF NOSE AND PARANASAL SINUSES

The radiological views commonly used to assess nose and PNS are:
1. Occipito-mental view (Water’s view)
2. Occipito-frontal view (Caldwell view)
3. Base skull (Submento-vertical view)
4. Lateral view
5. X-ray for nasal bones.
Occipito-mental View (Water’s View) (Figures 5-15 and 5-16)

This view is taken mainly to demonstrate maxillary sinuses. However, it shows nasal cavity, septum,
frontal sinuses, anterior ethmoid sinuses and sphenoid sinuses [when mouth is kept open]. Hence,
it is also known as ‘screening view’.
Patient is facing the X-ray plate and X-rays are passed from occipital area directing to chin. This
view avoids the superimposition of temporal bones over maxillary sinuses.
Occipito-frontal View (Caldwell View) (Figures 5-17 and 5-18)

This view focuses mainly on the frontal sinuses. Patient’s forehead and nasal tip are kept in contact
with X-ray film. This view shows frontal sinuses, part of maxillary antrum and nasal cavity.
Figure 5-15: Diagrammatic representation of Water’s Figure 5-16: X-ray PNS Water’s view
view
1. Frontal sinus 5. Maxillary antrum 9. Middle turbinate

2. Orbit 6. Upper jaw 10. Ethmoidal sinuses
3. Nasal cavity 7. Lower jaw (not shown)
4. Inferior turbinate 8. Nasal septum
X-ray Base Skull (Submento-vertical View) (Figures 5-19A and B)
The neck and head are fully extended so that vertex faces the film and rays are passed beneath the
mandible. This view shows sphenoid sinus, ethmoid sinuses, nasopharynx and posterior wall of
maxillary sinus.
Figure 5-17: Occipito-frontal (Caldwell view): Figure 5-18: X-ray base skull (occipito-frontal
diagrammatic representation view)
Showing Caldwell view skull

1. Frontal sinus
2. Orbit
3. Nasal cavity
5. Maxillary sinus
10. Ethmoid sinuses
11. Petrous bone
Lateral view (Figure 5-20): Patient’s head is placed in lateral position against the film and the rays are
directed behind the outer canthus of eye. This view is useful to show posterior table of frontal sinus,
maxillary sinus, middle and posterior group of ethmoid sinuses. But for better visualisation of ethmoid
sinuses lateral oblique view is preferred. To visualise adenoid tissue or nasopharyngeal mass soft
tissue exposure is required.
Usually clinical examination and X-rays give sufficient clue to keep a clinical diagnosis in the
nose and paranasal sinus diseases. However, in some cases one may need specialised investigations
like—
1. Greater wing of sphenoid

2. Ethmoid sinus
3. Sphenoid sinus
4. Foramen ovale
5. Foramen spinosum
6. Foramen lacerum
7. Internal auditory meatus
8. Foramen magnum
9. Mastoid bone A B
Figures 5-19A and B: (A) Skull submento-vertical view (Diagrammatic),

(B) X-ray submento-vertical view
1. Cranial cavity
2. Frontal sinus
3. Orbit
4. Sphenoid sinus
5. Maxillary sinus
6. Upper jaw
7. Postnasal space
‘White arrow’—posterior wall of maxilla.
Figure 5-20: Lateral view skull showing
• CT scan: To know the extent of the disease and consistency of the lesion.
• Carotid angiography: Lesions like naso-pharyngeal angiofibroma do need carotid angiography to
know the blood supply to the tumour particularly the intracranial blood supply, and may show
beautiful “tumour blush” .
• Biopsy/Cytology: To confirm the diagnosis, e.g. malignancy.
• Microbiological: Investigations may prove useful to know type of organisms, e.g. fungal infections.
FEW CONDITIONS OF NOSE AND PARANASAL SINUSES

1. Congenital
e.g. bifid nose, dermoid, meningocoele, choanal atresia.
2. Traumatic
e.g. nasal bone, maxilla, septal haematoma, etc.
3. Inflammatory
Rhinitis
• Acute
• Specific
• Non-specific
• Chronic
• Specific—tuberculous rhinitis
• Non-specific—atrophic rhinitis
Sinusitis
• Acute
• Chronic
4. Miscellaneous
• Deviated nasal septum,
• Foreign bodies, rhinolith
• Adenoiditis
• Polyps
• Antrochoanal polyp
• Ethmoidal polyposis
• Nasal myiasis
• Cysts of nasal/dental origin
• Granulomas—rhinosporidiosis, rhinoscleroma, leprosy, syphilis, midline granulomas,
Wegener’s granuloma.
5. Neoplastic
Benign: fibroma, lipoma, neurofibroma, melanoma, angioma, angiofibroma, glioma, haemangioma,
osteoma, chondroma, inverted papilloma (Ringertz’s tumour).
Malignant: malignant melanoma, neurofibrosarcoma, squamous cell carcinoma, adenoid cystic
carcinoma, basal cell carcinoma, olfactory neuroblastoma, chondrosarcoma are few malignant
lesions in nose and paranasal sinuses.
Atrophic Rhinitis (Figure 5-21)

A condition characterised by nasal crusting, obstruction, foul smell, pale mucosa and roomy nostrils
seen mostly in young girls.
• Aetiology: Endocrine, infective, nutritional deficiency and extensive nasal surgery are thought to
be responsible factors.
• Symptoms: Nasal obstruction, headache, yellowish greenish nasal discharge crusting and
occasional epistaxis.
• On examination: Nasal cavities are roomy, filled with yellowish greenish crusts, mucosa is pale
and atrophic, and emits foul breath.
Figure 5-21: Showing a case of atrophic rhinitis

• Treatment:
1. Nasal douching with sodium bi-carbonate and salt solution.
2. Correction of nutritional deficiencies like vitamin and iron deficiency.
3. Surgical treatments like Young’s operation, transplantation of Stenson’s duct and submucosal
implants.
NB: In some patients due to poor nasal hygiene and loss of sensations in nose Houseflies enter the
nose and lay eggs. The eggs hatch and larvae are produced. This condition is called Nasal Myiasis
and is quite common in developing countries. Underlying cause is usually atrophic rhinitis or
Hensen’s disease. Maggots are removed manually by suffocating them with instillation of liquid
paraffin. After complete removal of maggots nasal douching and treatment of primary nasal disease
is carried out.
Rhinolith
Foreign body retained in nose for a longer time may
form a rhinolith. Seen commonly in children and
mentally retarded people.
Pathology: FB in the nose of child may go undetected
for a longer time resulting into deposition of calcium
salts on the FB. This gives whitish/blackish
discolouration and a gritty/stony feel. As a part of
mucosal reaction granulation tissue may be formed
in close vicinity of FB which may cause occasional
epistaxis (Figure 5-22).
Symptoms: Unilateral, foul smelling nasal discharge,
nasal obstruction and occassional epistaxis.
Signs: Foul smelling nasal discharge [unilateral].
Evidence of obstruction on affected side, whitish/ Figure 5-22: X-ray PNS water’s view
blackish mass in nasal cavity having stony/gritty showing FB in nasal cavity
feel. On probing granulation tissue may bleed.
Investigations: X-ray PNS Water’s view usually shows retained FB in nose.
Treatment: Surgical removal of retained FB under anaesthesia.
Adenoiditis (Figure 5-23)
Adenoid is collection of lymphoid tissue in postnasal space. It may get infected and hypertrophied in
school going age, resulting into a cascade of symptoms and signs.
Aetiology: As a result of chronic infection in nose and sinuses/allergy or it may be non-specific
reaction of Waldeyer’s ring to various infections in childhood.
Symptoms: Nasal obstruction, nasal discharge, mouth breathing, snoring.
Signs: High arch palate, crowding of teeth, pinched up nose, open mouth, loss of malar prominence
and anxious look. These changes are called as ‘adenoid facies’. Evidence of ET block/secretory otitis
may be seen on otoscopy.
Diagnosis: By history, clinical examination and radiological examination.
X-ray nasopharynx lateral soft tissue exposure may show large amount of adenoid tissue in
postnasal space.
Treatment
Conservative: Systemic and local decongestants, antiallergic drugs and antibiotics
Surgical: Removal of adenoid tissue.
1. Adenoid gland
2. Cervical vertebrae
3. Mastoid bone.
‘White arrow’ showing narrowing of air way in
nasopharynx.
Figure 5-23: X-ray skull lateral view showing enlarged adenoid
Sinusitis
It is an inflammation of mucous lining of one or more paranasal sinuses. It may be
A. Acute
B. Chronic
• Aetiology: Str. pneumonae, H. influenzae, and Sta. aureus. And at times anaerobes like bacteroids.
• Symptoms: Nasal discharge, headache and nasal obstruction.
• Signs: A/R shows pus or crusting in the middle meatus. Oedema and congestion near natural
osteum of the sinus seen. Tenderness on affected sinus may be present on firm pressure.
• Investigation: X-ray PNS be present show haziness in the affected sinus. It may show even air fluid
level, if X-ray is taken in standing position (in maxillary sinusitis) (Figure 5-24).
• Treatment
Acute: Antibiotics, steam inhalation, decongestants (local and systemic). Antral puncture is avoided
as far as possible.
Chronic:
• Medical: Antibiotics, steam inhalation, mucolytics if secretions are thick.
• Other surgical: Treatment of underlying cause like DNS, nasal polyp, and dental caries.
• Surgical: If no relief after conservative treatment then, antral puncture, intranasal antrostomy or
Caldwell-Luc operation may be done. Recently functional endoscopic sinus surgery (FESS) is
usurping the role of Caldwell-Luc procedure.
Figure 5-24: X-ray PNS Water’s view

showing right antral haziness
Deviated Nasal Septum (Figures 5-25A and B)
Aetiology
• Traumatic
• Congenital/developmental
Symptoms: Unilateral/bilateral nasal obstruction, headache, crusting and nasal discharge may be there.
Signs: ‘C’ or ‘S’ shaped deviation of nasal septum/maxillary crest or spur/caudal dislocation of
septum may be present. As a consequence of DNS unilateral/bilateral sinusitis and even polyp
formation may occur. Sinusitis so developed may predispose to secondary tonsillitis/pharyngitis or
middle ear infection.
Treatment: Surgical correction, septoplasty/SMR.
A B
Figures 5-25A and B: Showing diagrammatic representation of deviated

nasal septum (A) C shaped, (B) S shaped
Nasal Polyps
a. Antrochoanal polyp
b. Ethmoidal polyposis
ANTROCHOANAL POLYP
Aetiology:
1. Nasal allergy and/or infection.
2. Faulty development of maxillary sinus osteum.
Figure 5-26: Diagrammatic representation of Figure 5-27: Showing hazy maxillary antrum
antrochoanal polyp
Pathology: Polyp is a prolapsed oedematous respiratory mucosa. It arises from maxillary osteum or antrum
and comes out of osteum, usually the accessory osteum. Enters into middle meatus and goes
posteriorly towards choana and hence it is called as antrochoanal polyp. It is trifoliate structure.
Common in young adults (Figures 5-26 and 5-27).
Symptoms: Nasal obstruction, more during expiration, nasal discharge, headache, change in voice if
polyp is huge.
AR examination: AC polyp is a single, pearly grey,
glistening mass, soft in consistency, insensitive
to touch and attached to lateral wall of nose, i.e.
coming from middle meatus. It doesn’t bleed on
touch (Figure 5-28).
PR examination: Same polypoidal mass may be
seen in posterior rhinoscopy as a solitary
glistening mass in choana.
Differential diagnosis:
• Nasal glioma
• Angiofibroma Figure 5-28: Photograph showing AC polyp
• Inverted papilloma protruding out of nasopharynx
Treatment:
1. Surgical excision (Polypectomy, Caldwell-Luc operation).
2. Treatment of underlying allergy.
3. Functional endoscopic sinus surgery (FESS) has become more popular in last few years.
ETHMOIDAL POLYPOSIS
Bilateral condition, common in middle aged people. Allergic factor predominates.
Symptoms: Bilateral nasal obstruction, nasal discharge, sneezing, headache, nasal broadening, (in
long standing cases).
AR: Small multiple greyish whitish masses, soft in consistency, do not bleed on touch, insensitive to
touch and attached to lateral nasal wall.
PR: Polyps not seen in posterior rhinoscopy.
Treatment:
• Medical: Antihistaminic, steroids locally or systemically. Systemic steroids used cautiously.
• Surgical:
• Excision by functional endoscopic sinus surgery technique (FESS)—This technique has
surpassed all older technique and is reliable and popular.
• Intranasal polypectomy
• Ethmoidectomy—intranasal or external.
RHINOSPORIDIOSIS
• Aetiology: Fungal infestation by Rhinosporidium seeberi and R kineyali. Seen along the coastal border
or ponds where source of drinking water for men and cattle is same. Balaghat district in Chattisgarh
state is an endemic area.
• Symptoms: Commonly present as nasal mass, epistaxis, nasal discharge and headache. At times
conjunctiva, skin, respiratory tract, genitals, bones may be involved.
• AR: Reddish fleshy mass, firm to touch, bleeds on touch, attached to floor, septum or lateral wall of
nose. Under surface of mass studded with whitish yellowish sporangia.
• Treatment: Wide surgical excision and cauterisation of base. Recurrence is known.
RHINOSCLEROMA (FIGURE 5-29)
It is less common nasal condition. Caused by Klebsiella rhinoscleromatis. Disease may spread to
nasopharynx, trachea and bronchi. Histologically it shows Mikulicz cells and Russell bodies.
Figure 5-29: A case of rhinoscleroma
Stages
1. Catarrhal stage—Difficult to diagnose.
2. Atrophic stage: It simulates atrophic rhinitis in this stage.
3. Nodular or granulomatous stage: Nodules may be seen at muco-cutaneous junction.
4. Cicatrising stage: Extensive fibrosis seen in affected part. Usually patient comes in last stage. The
nasal tip has ‘woody’ feel. There is progressive narrowing of the nostril. Crusting may be present.
Extensive cicatrisation may cause destruction of uvula and soft palate, which may get adhered to
posterior pharyngeal wall. Lesion may spread to larynx, trachea and bronchi causing progressive
narrowing of lumen.
Treatment: Medical: Streptomycin, tetracycline, rifampicin, etc.
Surgical: Recanalisation of blocked respiratory passage.
JUVENILE NASOPHARYNGEAL ANGIOFIBROMA (FIGURE 5-30)

It is a benign highly vascular tumour arising from sphenopalatine foramen exclusively seen in
puberty age males.
Figure 5-30: Photograph showing big mass in post-nasal

space hanging down in oropharynx (angiofibroma)
Aetiology: Not exactly known. Hormonal theory, haemartoma theory exists.

Pathology: After its origin it may spread to nasal cavity, pterygopalatine fossa, infratemporal fossa
maxillary sinus, orbit, cheek and even intracranially.
Symptoms: Epistaxis, nasal obstruction, nasal mass, deformity of face, proptosis, headache, etc.
Signs: A firm pinkish mass in nose/nasopharynx, which bleeds on touch.
Investigations:
• X-rays skull: (Lateral view/Water’s view/base skull) may show soft tissue shadow in nasopharynx,
nasal cavity, maxillary sinus, ethmoid sinus and even sphenoid sinus. Destruction of sinus wall
may be there.
• Carotid angiography: It is confirmatory investigation. It may show typical “tumour blush” in
nasopharynx. Feeders to the tumour are visualised.
• CT scan: This may show the extent of the disease. Particularly whether disease has spread
intracranially or not.
Diagnosis: Clinically and by carotid angiography. Biopsy not advised as it may bleed profusely.
Treatment: Wide surgical excision, by using lateral rhinotomy/transpalatine or Caldwell-Luc
procedure or any other modification to remove mass completely. Sufficient amount of blood should
be ready at the time of surgery.
Some Tumours Seen in Nose and PNS
See Figures 5-31 to 5-37.
Figure 5-31: Nasal Figure 5-32: Right frontal Figure 5-33: X-ray PNS Water’s view
haemangioma osteoma with cellulitis showing osteoma R frontal sinus
Figure 5-34: A case of chondroma Figure 5-35: A photograph showing nasal malignancy
nasal septum
Figure 5-36: Mucocele on coronal CT Figure 5-37: CT coronal view showing enhancing mass
in nasal cavity and extending to infratemporal fossa
CARCINOMA OF MAXILLARY ANTRUM (FIGURES 5-38 AND 5-39)
This is relatively common malignant lesion of paranasal sinuses. Seen in middle aged people.
• Aetiology: Chronic mucosal irritation by:
• Smoking
• Air pollution
• Workers in wood industry/nickel/mustard gas industry.
Figure 5-38: A case of carcinoma Figure 5-39: Clinical photograph showing lympho-
of maxilla reticular malignancy involving right maxilla
• Pathology: Squamous cell carcinoma is most common. Adenocarcinoma, adenoid cystic carcinoma
muco-epidermoid carcinoma are the varieties seen.
• Maxillary antrum has 5 walls. Superior, inferior, anterolateral, medial, posterior. At a given time
one or more than one wall may be involved. Symptoms and signs depend upon which wall is
involved. For ease of understanding we would discuss it as per wall of involvement.
• Symptoms and signs: See Table 5-1.
Table 5-1: Showing symptoms and signs depending upon involvement of wall of maxilla
Wall of maxlla sinus Symptoms Signs
involved
Anterolateral wall Swelling over face, pain Swelling in maxillary area
Medial wall • Nasal obstruction • Lateral nasal wall pushed medially
• Nasal mass • Friable, fleshy, nasal mass
• Nasal discharge/ which bleeds on touch
Serosangious discharge • Serosangious discharge
• Hyposmia/Anosmia
Superior wall • Blurring of vision • Blunting of inferior orbital margin
• Pain in and around the eye • Eyeball pushed upwards and laterally
• Inability to move eyeball • Eccentric proptosis
• Double vision • Chemosis, 3,4,6 cranial nerve palsy
• Diplopia
Inferior wall • Swelling over hard palate • Loosening/falling of teeth
• Pain in tooth/teeth • Increase in inter-dental gap
• Loosening/falling of teeth • Swelling in gingivo-labial sulcus
• Perforation of palate • Swelling/ulceration over hard palate
• Ill fitting denture
Posterior wall • Inability to open mouth • Trismus
• Difficulty in chewing • Sensations over hard palate may be
reduced
Investigations:
X-ray PNS (Figure 5-40)
Water’s view
Dead lateral view to visualise posterior wall of maxilla
Base skull
Figure 5-40: X-ray showing mass in antrum and

destruction of post wall of maxilla
May give useful information

• Biopsy from most accessible site
• CT scan to know extent of disease.
Treatment:
1. Surgery: Total/partial maxillectomy. Radical surgery may be needed to remove disease from eye,
ethomid sinus or sphenoid.
2. Radiotherapy: 5000 to 6000 rads 200 rads/day, 5 days a week regimen.
3. Chemotherapy: As palliative therapy.
SOME COMMON PROCEDURES IN NASAL DISEASES

1. Antral puncture
2. Anterior nasal packing
3. Posterior nasal packing
4. FB removal.
Local Anaesthesia for Nasal Procedures

For detailed nasal examination in depth and also for minor surgical procedures one needs local
anaesthesia in nose. It can be carried out by one or more ways given below:
For surface anaesthesia one of the following is used:
• Ten per cent lignocaine spray
• Five per cent lignox jelly
• Four per cent xylocaine (by cotton wool nasal packing)
• Xylocaine + Adrenaline (1: 100 000) used cautiously gives good visualisation and minimises
bleeding during surgery.
Infiltration Anaesthesia
One or two per cent xylocaine with or without adrenaline used prior to surgery.
ANTRAL PUNCTURE (ANTRAL LAVAGE) (FIGURE 5-41)

In this procedure maxillary antrum is approached through inferior meatus. It is diagnostic as well as
therapeutic procedure to diagnose maxillary sinusitis, to know the causative organisms in the
sinusitis, to diagnose early malignancy by aspirating the fluid in the sinus for malignant cells. And
to treat maxillary sinusitis by repeated antral puncture.
Anaesthesia: Local anaesthesia (4% Xylocaine surface application).
Instruments: Tilley Lichtwitz trocar and cannula (Figure 5-42), kidney tray, Higginson’s syringe,
nasal speculum, nasal dressing forceps.
Figure 5-41: A diagrammatic representation

showing site for antral puncture
Figure 5-42: Lichtwitz trocar and cannula
Procedure: Trocar and cannula is negotiated in the inferior meatus approximately 1 to 1.2 cm posteriorly
from anterior end of inferior turbinate to reach genu. Then it is directed laterally and upwards
towards tragus of the same side and pierced firmly to enter maxillary sinus. A ‘click’ is heard, a
sensation of loss of resistance is felt and trocar/cannula is in the antrum. Trocar is taken out keeping
cannula in situ. With the help of 5 ml syringe fluid if any is aspirated and sent for culture/sensitivity
or cytology.
Patient is asked to lean forward. Then with the help of Higginson’s syringe or ordinary glass
syringe Luke warm saline is irrigated in the maxillary antrum which comes out of natural osteum of
the maxillary sinus. Irrigation is continued till clear fluid returns.
The procedure may be repeated every week 2 to 3 times if needed. If the returning fluid is
still turbid or shows pus flakes Caldwell-Luc operation may be advised. With the advent of
FESS (functional endoscopic sinus surgery) need for Caldwell-Luc surgery has drastically
reduced.
Complications
1. False passage
2. Bleeding
3. Vaso-vagal attack
4. Injury to eyeball
5. Air embolism.
NB: Antral puncture should be avoided in acute maxillary sinusitis. This may lead to osteomylitis. If
the procedure is must, then IV antibiotics may be started 24 hours prior to procedure.
ANTERIOR NASAL PACKING (FIGURE 5-43)

Indications: When epistaxis is not controlled by simple measures like pinching of nose, application of
ice or cauterising the bleeder, etc. Nasal packing is also needed after nasal operations.
Figure 5-43: Showing anterior nasal packing
Instruments: Bull’s eye lamp and head mirror or head light, nasal speculums, nasal packing forceps,
liquid paraffin, tape ribbon gauze.
Procedure: Nasal cavity is inspected under good light and blood if any is sucked out. Only anterior
2/3 of nasal cavity is packed. Application of pack in posterior part causes gag reflex and soft palate
movements may dislodge the pack in oral cavity.
Ribbon gauze soaked in liquid paraffin is negotiated along the nasal floor and heaped up in the
cavity layer by layer till nasal cavity is nicely packed as shown in the Figure 5-43. Packing is removed
after 48 hours. During this period patient is given antibiotics to prevent infection.
Complications:
1. Infection
2. Adhesion formation
3. Acute otitis media.
POST-NASAL PACKING (FIGURE 5-44)

Indications: Severe bleeding from posterior part of nares or nasopharynx.
Instruments: Head light, mouth gag, long bladed nasal speculums, ribbon gauze, liquid paraffin,
postnasal pack, fine rubber catheters, artery forceps, etc.
Figure 5-44: A post-nasal pack
Procedure: It is preferably done under GA. Patient is put on oral endotracheal intubation with
pharyngeal pack. Two small rubber catheters are introduced through nostrils. One end of catheter is
taken out from oral cavity. Proper size postnasal pack (already sterilised) is taken and its tapes are
tied to rubber catheters and catheters are pulled up through nose. As soon as post-nasal pack enters
into the nasopharynx it is adjusted by finger and snugly fitted in the area. Guide tapes are tied
around the collumela lightly. Anterior nasal packing is done as described previously. Patient is put
on antibiotics to prevent infection. Post-nasal pack is removed after 48 hours.
Foley’s catheter can also be used for post-nasal packing.
Complications: Acute otitis media, sinusitis, drying up of mouth due to mouth breathing.
FB REMOVAL (FIGURE 5-45)

Usually they are small children who put foreign bodies in nose. If the child is small enough that can
be held firmly then FB can be removed without anaesthesia. If the child cannot be held firmly it is
better to remove the foreign body under anaesthesia.
Instruments: Wire vectis, nasal speculum and illumination.
Figure 5-45: Showing how to hold a child

for ENT examination and removal of FB
Procedure: Child is held firmly as seen in the photograph. Foreign body is inspected for its size, shape,
consistency, location and lie in the nose. A wire vectis is negotiated in the nostril beyond the foreign
body and FB is pulled along with it. It is a very simple procedure in expert hands.
Complications:
1. Injury to surrounding structures
2. Bleeding
3. FB may slip down into nasopharynx, oesophagus or bronchus.
Head and Neck
Section A
• Oral Cavity and Oropharynx
• Examination of Larynx and Laryngopharynx
• Thyroid Gland
Section B
• Examination of Neck
• Examination of Salivary Gland
Section C
• Diseases of Oesophagus
• Tracheo-bronchial Tree
SECTION A
6
Oral Cavity and Oropharynx
Oral cavity: It includes inner surface of lips, cheeks, teeth, gums, anterior 2/3 of tongue, upper jaw,
lower jaw, upper and lower gingivo-labial and gingivo-buccal Sulci, retromolar area, hard palate,
soft palate and floor of mouth.
Oropharynx: Its superior limit is the level of hard palate and where the soft palate touches the posterior
pharyngeal wall. Inferior limit is at the level of tip of the epiglottis. It includes tongue posterior to
vallate papillae, velleculae, lingual surface of epiglottis, anterior pillars, posterior pillars, faucial
tonsils, posterior pharyngeal wall, free margin of soft palate and uvula.
The symptoms related to this part of the body are quite common and may be as follows:
1. Pain in throat (sore throat)
2. Difficulty in swallowing/chewing, pain during swallowing
3. Irritation in throat
4. Swelling/mass in oral cavity/throat
5. Ulcers in mouth
6. Trismus
7. Change in voice
8. Cough
9. Burning sensation
10. Foul breath
11. Foreign body
12. Dysarthria
13. Dental symptoms (excluded).
Associated symptoms:
14. Swelling over face
15. Painful/painless neck swelling
16. Nasal regurgitation
17. Fever with/without rigors.
It is usual observation that the symptoms related to throat are vaguely described by the patient and
poorly understood by the clinician [if he is not careful enough]. Hence, these symptoms should be
asked in greater details to understand the exact problem of the patient. Each symptom should be
analysed in proper manner, so as to come to clinical conclusion.
PAIN IN THROAT (SORE THROAT)

Patient should be asked, “Is it pain, or discomfort? Is it at rest or during movement of oral cavity or during
chewing/swallowing. How long he is suffering from this complaint? How it started? Is it progressive. Is it a
constant or intermittent. What is exact site of pain? How it starts, How it aggravates and how it gets relieved?
How severe is the symptom? Is it just a discomfort or is it sufficient to disturb his work. Is it localised or spreads
to the surrounding area. Is it sharp shooting or dull aching?” Associated symptoms like fever, change in
voice, swelling should be asked.
Common causes of pain in throat are pharyngitis, tonsillitis, quinsy, trauma, malignancy,
neuralgias, etc. Pain of acute infection like tonsillitis starts suddenly. It is severe and constant in
nature. Pain due to apthous ulcers is very severe and aggravated by taking solids or liquids. Pain
may be initiated by the act of swallowing [odynophagia] in pharyngitis, tonsillitis, stylalgia, or
malignancy. Pain due to salivary gland stone usually starts at the time of meals and shows swelling
in the submandibular area, which gets relieved after sometime. Patients having quinsy/ulcers may
locate a specific site for pain.
DIFFICULTY IN SWALLOWING
This symptom needs proper evaluation. Ask the patient, Is it pain during swallowing or food does not
pass down below or is it both?
Oral Cavity and Oropharynx 119
Causes
• Congenital, e.g. cleft palate.
• Traumatic, e.g. injury to tongue and pharynx.
• Inflammatory, e.g. acute tonsillitis, pharyngitis, quinsy.
• Nutritional, e.g. cheilitis, glossitis.
• Neoplastic, e.g. malignancy of tongue, tonsil or pharyngeal wall.
• Miscellaneous, e.g. neurological affections of pharynx.
Difficulty in chewing may be experienced by the patient when he has painful lesion in oral cavity,
trismus, temporomandibular pathologies and dental conditions.
IRRITATION/ITCHING IN THROAT
Some patients having allergic manifestation may particularly complain of irritation in throat.
Exposure to dust or smoke can also cause irritation in throat. Post-nasal drip may be responsible for
irritation or itching.
SWELLING/MASS IN THROAT
Haemangioma, lymphangioma, lingual thyroid, ranula, ectopic salivary tumours, parapharyngeal/
peritonsillar abscess and malignancy are some of the swellings seen in the oral cavity and throat.
Proper history should be obtained by following the pattern described in ‘examination of swelling’.
Patient should be asked, “How long he has noticed the swelling?” It may be congenital like torus palatinus
or may be acquired due to trauma, infection or malignancy. He should be asked whether the swelling is
constant or intermittent. Swelling due to stone in submandibular gland duct or parotid gland duct may
arise at the time of meals only and may disappear after some time. Swelling may be painful or painless.
Peritonsillar abscess is very painful so much, so that patient cannot swallow his own saliva and may
drool over cheek. Pain may be aggravated by the act of swallowing in malignant or inflammatory
lesions. Radiation of pain to the ear may be seen in tonsillar/base tongue malignancy.
ULCERS IN MOUTH
Mode of onset: Patient should be asked, How the ulcer/s developed. The ulcer may develop after trauma
or spontaneously. Tongue bite may result into an ulcer, which heals within few days. However, if the
teeth are sharp and cause repeated trauma to tongue, may give rise to chronic non-healing ulcer and
even granuloma. Aphthous ulcers develop suddenly and are very painful.
Duration: Ulcer of acute onset may heal spontaneously after few days. However, chronic ulcer like
tuberculous ulcer, syphilitic ulcer and malignant ulcer may not heal.
Pain: Syphilitic ulcers are painless while aphthous ulcers are highly painful. Malignant ulcers may
be painless to begin with.
Discharge: History of any discharge associated with ulcer may be asked.
Associated diseases: Diseases like uncontrolled diabetes, tuberculosis may develop ulcers in the head
and neck region. In Behcet syndrome, oropharyngeal ulceration is associated with genital ulceration.
Oral ulcerations are seen in pemphigus vulgaris and Stevens-Johnson syndrome. And these conditions
should be kept at the back of mind while examining the oral ulcers.
TRISMUS: TRISMUS IS INABILITY TO OPEN THE MOUTH

It may be seen in a case of tetanus [lockjaw], oral submucous fibrosis, quinsy, cheek malignancy or
lesions involving pterygopalatine fossa, muscles of mastication or temporomandibular joint. History of
trauma to temporomandibular joint or history of chewing pan masala, tobacco, betel nut must be
asked when you suspect oral submucous fibrosis.
CHANGE IN VOICE
Oral cavity lesions like quinsy, cleft palate, palatal palsy or a big mass in oral cavity/oropharynx can
cause change in voice.
COUGH
Usually it is dry cough due to irritation of throat. Particularly postnasal drip may cause dry irritating
cough. Allergen, elongated uvula, drying up of mucosa due to exposure to hot/dry air too can cause
cough. Some patients do have acid regurgitation in the throat, which causes dry cough and irritation.
BURNING SENSATION
Commonly complained by the patient in oral submucous fibrosis or severe anaemia, glossitis,
stomatitis, etc.
FOUL BREATH (HALITOSIS)

Bad oral/dental hygiene, chronic illness, patients who are nil by mouth for a long period can emit
foul breath.
FB IN THROAT
Foreign body is quite common in oral cavity and oropharynx. Though children are commonly affected,
it is equally common in adults. Particularly fish bones, pins, clips (in female) needles (in tailors) and
during influence of alcohol. Old age also predisposes for FB lodgement due to loose teeth and dentures.
DYSARTHRIA
This is a disorder of articulation. Speech may be slurred and labored or it may be monotonus. Lesions
of joints, muscles, ligaments of oral cavity and oropharynx may cause dysarthria, e.g. bilateral
corticobulbar tract lesions. Lesions of 7th 10th and 12th cranial nerves. Myasthenia gravis, lesions of
extrapyramidal system and cerebellar affections are known to cause affections of articulation.
SWELLING OVER FACE

Lesions related to teeth like dental cyst, dentigerous cyst, adamantinoma, malignancies of cheek/
alveolus may give rise to swelling over face.
PAINFUL/PAINLESS NECK SWELLINGS

Lesions in oral cavity and oropharynx may extend in neck, e.g. Ludwig’s angina, parapharyngeal
abscess/tumours, etc. In inflammatory conditions of oral cavity and oropharynx, the draining lymph
nodes may become enlarged and tender. In malignant lesions, it may be secondary deposits in neck
nodes.
NASAL REGURGITATION
Conditions like palatal palsy, perforated palate can cause nasal regurgitation.
Examination of Oral Cavity and Oropharynx

INSPECTION
In the examination of oral cavity one should examine lips, teeth, mucosa lining the cheeks, gingivo-
buccal and gingivo-labial gutters, gums, dorsum of tongue, under surface of tongue and floor of
mouth for any obvious congenital defect, swelling, foreign body, ulcer or sinus. Later hard palate,
soft palate, uvula, anterior pillars, posterior pillars, tonsils, posterior pharyngeal wall may be examined
similarly. Movements of soft palate, uvula and tongue should be observed.
Lips should be looked for any fissures, clefts, angular stomatitis, etc. (Figure 6-1A).
Figure 6-1A: Showing growth on

vermilion surface of lip
Tongue
Patient is asked to open the mouth widely.
Anterior 1/3 of the tongue may be examined without using tongue depressor.
Size: Note the size of the tongue. It may be too large (macroglossia) due to lymphangioma or
haemangioma or even congenitally and teeth marks may be seen on the margins of the tongue. In
long-standing paralysis of tongue, the affected side may show atrophy and wrinkling (Figure 6-1B).
Figure 6-1B: Lymphangioma on tongue

Appearance: Tongue is normally pink in colour. But may become pale in severe anaemia or may show
white patch ‘leucoplakia’ in patients having chronic tobacco/betel nut use. It is considered as pre-
malignant condition. Black hairy tongue may be seen in few patients. Patients having B-complex
deficiency may show red, smooth tongue with loss of normal papillae. Fissures may be seen over
tongue in nutritional deficiencies.
Swelling: Note down the number, site, size, shape, surface and other features of the swelling.
Ulcer: Size, shape, number margins and base of the ulcer should be described in details.
Mobility: Ask the patient to protrude out his tongue. If the patient has ‘tongue tie’ he cannot protrude
out his tongue properly. In case of hypoglossal nerve injury or malignancy, the affected side may
show wrinkling due to fibrosis of the tongue on that side and may be deviated to the same side.
Ask the patient to touch the palate with his tip of tongue. This gives you an opportunity to examine
undersurface of tongue and floor of mouth.
Floor of mouth is the part extending from innerside of arch of lower jaw to the attachment of
tongue. Floor of mouth may have swelling, mass, ulcer or foreign body and should be carefully
inspected. Wharton’s duct openings should be seen. Posterior part of floor of mouth unto tonsillo
lingual sulcus is not easily visible and you have to retract the side of the tongue with tongue depressor
to see it (Figure 6-1C).
Figure 6-1C: Showing ‘floor of mouth’. (1) Tongue,

(2) Floor or mouth, and (3) Warton’s duct
Teeth and Gums
While examining oral cavity a definite look at the teeth and gum condition is needed. There may be
carious teeth, loosening or absence of teeth. Patient may be using artificial teeth or dentures, which
should be removed before examination. Diseases of teeth give rise to many oral cavity manifestations.
Ulcers, epulis or growth in the vicinity of gums and teeth may be looked for.
Cheeks and Gingivo-labial Gutters

Patient is asked to open his mouth and cheeks are retracted with tongue depressor to see mucosal
surface. Gingivo-labial and gingivo-buccal gutters on right and left side in upper and lower jaw are
examined carefully with the help of tongue depressor upto the last molar tooth. Stenson’s duct
[parotid gland duct], which opens in the close vicinity of 2nd molar tooth, is carefully examined on
both sides.
This part of oral cavity should be looked for any swelling, ulcer, congestion or foreign body.
Mucosa lining the cheeks may show typical Koplik’s spots in measles. Cheek mucosa may be stained
dark due to chronic tobacco use. Or may show white patch (leucoplakia) red patch (erythroplakia).
Upper gingivo-buccal sulcus may be obliterated in carcinoma maxilla.
Hard Palate, Soft Palate, Uvula (Figure 6-1D)

Patient is asked to open the mouth while his head is tilted back. Patient is asked to say “aha” to see
palatal and uvula movements.
Figure 6-1D: Showing perforation in hard palate

Patient may have congenital cleft palate, bifid uvula, or fibrous swelling over palate called “torus
palatinus”. Chronic smokers may show prominent mouth of salivary glands over hard palate. In
case of diphtheria or vagal palsy, movements of soft palate and uvula may be restricted or lost. Soft
palate and uvula deviates to normal side on saying “aha” (Figure 6-2).
‘ Arrow’ – Uvula
1. Posterior pillar
2. Anterior pillar
3. Trigone
4. Tongue
5. Soft palate
6. Hard palate
Figure 6-2: Photograph of oropharynx
Anterior Pillars, Tonsils and Posterior Pillars

Lateral surface of the tongue is depressed with the help of tongue depressor, to visualise tonsil and
its pillars. Tongue depressor should not be put too posteriorly, otherwise patient would get gag
reflex. Neither it should be kept too anteriorly lest, middle part of the tongue would bump up preventing
proper vision.
• Anterior pillars: These are basically muco-muscular folds containing the palatoglossus muscle.
They cover the anterior surface of tonsil partly. In normal condition they are pink in colour.
Congestion along anterior pillar suggests infection in tonsil.
• Tonsils: Colour—(normal-pink infection-congested, red
Size of the tonsil is graded by few as follows:
Grade I Medial surface of tonsil hidden behind anterior pillar
Grade II Medial surface of tonsil just at the level of anterior pillar
Grade III Size in between Gr II and Gr IV
Grade IV Tonsils touching each other (Kissing tonsils).
Any other abnormalities—like follicles, membrane, cyst, FB, keratosis, ulcer, growth, etc. may be
noted.
• Post pillars: They too are muco-muscular folds housing palato-pharyngeus muscle. They may not
be properly seen particularly when tonsils are enlarged.
• Posterior pharyngeal wall:
It should be examined for any congestion, bulging, postnasal drip, granulations, Aphthous ulcer
or malignant ulcer. Posterior pharyngeal wall may show bulge in cases of retropharyngeal abscess.
Patients having chronic sinusitis may show prominent lymphoid tissue in lateral pharyngeal gutter.
NB: At times tonsils and post-pharyngeal wall may show multiple whitish, yellowish horny outgrowth
called as keratosis pharyngis. This is benign condition but may alarm the patient and novice clinician
both.
• Post 1/3 of tongue:
A small part of post 1/3 of tongue may be seen during this examination. But for complete vision of
base tongue indirect laryngoscopy is needed.
PALPATION
Surgical gloves should always be used while palpating the oral cavity.
Tongue
Tongue should be palpated, if it shows ulcer or swelling. In suspected case of malignancy induration
around and deep to lesion should be particularly palpated.
Floor of Mouth (Figure 6-3)

Floor of mouth may be palpated if it shows ulcer or swelling. The submandibular gland should be
palpated by keeping gloved finger in the mouth and fingers of other hand over the skin in
submandibular triangle and the gland is bimanually palpated. Normally the gland is soft. But may
become firm or hard in chronic infections and malignancy respectively. Similarly the submandibular
gland duct (Wharton’s duct) should be palpated for any stone in it. Finger palpation should be
extended posteriorly upto tonsillo lingual sulcus and induration if any is noted. This area is considered
as ‘grave yard’ for the surgeon as lesion in this area may be easily missed.
Tonsils and its Bed

In a suspected case of chronic tonsillitis the tonsil may be squeezed or compressed with the help of
tongue depressor. A cheesy material may be expressed out from crypts. In a suspected case of styloid,
Figure 6-3: Showing method of

palpating floor of mouth
enlargement the styloid is palpated in the bed of the tonsil. Any unusual enlargement of tonsil, ulcer
over tonsil should be palpated for induration, which may be a feature of malignancy.
Base of Tongue
Malignant lesion at the base of tongue may not be properly visualised in mirror examination and
hence, in all suspected base tongue malignancies it should be palpated for any induration. A small
transparent fish bone that is not visualised may be detected by palpation method.
Swelling in Oral Cavity

Should be palpated using rubber gloves. And the findings of inspection, i.e. size, shape, surface
should be confirmed. Consistency of the swelling should be assessed. It may be soft, cystic, firm or
hard. Mucosa over the swelling should be moved by finger to know whether it is free or fixed to the
underlying mass. Expanding cystic lesion in maxilla and mandible cause thinning of bone cortex
and this may be responsible for “egg shell crackling” on palpation. The feel of various swelling may
be as follows:
• Soft swellings, e.g. lipoma
• Cystic swellings, e.g. dermoid cyst, cystic hygroma, ranula
• Firm swellings, e.g. chronic siloadenitis, neurofibroma
• Hard swellings, e.g. mixed parotid tumour
• Compressible swellings, e.g. haemangioma.
PERCUSSION AND AUSCULTATION

These do not contribute much in the examination of oral cavity, except one that is tapping over teeth
may be tender in dental and alveolar conditions.
Some common conditions:
1. Pharyngitis
2. Tonsillitis
2. Quinsy
3. Retropharyngeal abscess
4. Parapharyngeal abscess
5. Ludwig’s angina
6. Aphthous stomatitis
7. Leucoplakia
8. Oral submucous fibrosis
9. Cleft palate
10. Malignancy
11. Submandibular siloadenitis
12. Foreign body.
Pharyngitis
Inflammation of mucosa lining the pharynx is known as pharyngitis. It may be acute or chronic in
nature.
Acute pharyngitis:
Aetiology: Viral infection, smoking, exposure to dust, bacterial infection.
Symptoms: Sore throat, hawking cough, odynophagia.
Signs: Pharyngeal mucosa inflamed, congested. Prominent blood vessels may be seen on posterior
pharyngeal wall.
Treatment: Soothing lozenges, saline gargles, antipyretics if needed. Stop smoking, avoid dusty
environment. Antibiotics may be needed if bacterial infection sets in.
Chronic pharyngitis:
Aetiology: Smoking, alcohol, acid regurgitation in mouth, chronic infection in nose, sinuses or teeth.
Symptoms: Raw sensation in throat, odynophagia, desire to remove sticky secretions, cough/irritation
Signs: Diffuse congestion with prominent blood vessels over posterior pharyngeal wall. When
prominent granulation tissue is seen over posterior pharyngeal wall, it is called as ‘granular
pharyngitis’.
Treatment: Avoid smoking/alcohol. Avoid dusty area. Infection in nose, sinuses may be treated. Acid
peptic disease, dental caries to be taken care of.
Tonsillitis
Inflammation of faucial tonsils proper is known as tonsillitis. Common in children below 10 years.
May persist in some adults. Infection in nose, sinuses may give rise to secondary tonsillitis.
Aetiology:  haemolytic Streptococci, Staphylococci, H. influenzae, Pneumococci are common infecting
organisms.
It may be acute or chronic in nature.
Acute tonsillitis (Figure 6-4):
Symptoms: Discomfort or pain in throat, pain during swallowing, painful neck glands, malaise, fever
may be seen in children.
Figure 6-4: A case of acute tonsillitis

Signs: Tonsils enlarged, swollen, congested (acute parenchymatous), a membrane may be seen (mem-
branous tonsillitis) or follicles may be seen (follicular tonsillitis). Jugulo-diagastric lymph nodes may
be enlarged and tender. Patient may have high grade fever.
Treatment: Bed-rest, plenty of oral fluids, analgesics and antibiotics. Warm saline gargles are quite
soothing.
Chronic tonsillitis:
When acute tonsillitis recurs frequently or symptoms are not controlled even after giving adequate
antibiotics, chronic tonsillitis might have set in.
Symptoms: Discomfort in throat, unpleasant taste in mouth (cacagus), bad smell from mouth (halitosis),
constant irritating cough, and desire to expectorate sticky throat secretions.
Signs: Tonsils may/may not be enlarged. Congestion along anterior pillars, on squeezing tonsils
debri can be expressed out. Jugulo-diagastric lymph nodes are persistently enlarged.
Treatment: Usually do not respond to conservative treatment. Tonsillectomy should be considered.
Source of infection in nose and/or sinuses may be cleared before thinking of tonsillectomy.
Quinsy (Synonyms: paratonsillar abscess, peritonsillar abscess) (Figure 6-5)

Collection of pus between tonsillar capsule and its bed is known as quinsy.
It is usually a sequel of recurrent/chronic tonsillitis.
Figure 6-5: A case of peritonsillar abscess

Symptoms: Severe pain in throat, odynophagia, fever, inability to open mouth.
Signs: Patient may be febrile, toxic. He may have tachycardia, dry tongue, tonsil and its surrounding
peritonsillar area is red congested and oedematous. Due to collection of pus in the potential space
between tonsillar capsule and its bed, tonsil is pushed downwards and medially. Uvula shifted to
opposite side and is congested, but its tip may be pointing towards same side. Due to pain and
swelling in mouth patient may not be able to swallow his own saliva and may even cause drooling.
Treatment: Hospitalisation, bed-rest, IV fluids, antibiotics, incision and drainage of abscess. Interval
tonsillectomy 6 weeks after the control of disease, to prevent recurrence.
Retropharyngeal Abscess (Figure 6-6)

It is collection of pus between buccopharyngeal fascia and prevertebral fascia.
Types: Acute and chronic.
Acute:
Common in children. Limited to one side of midline. Caused by suppuration of retropharyngeal
lymph nodes. Infection in tonsils, adenoid or sinuses may cause it.
Figure 6-6: (1) Retropharyngeal abscess, (2) Airway,

(3) Cervical vertebrae, and (4) Mandible
Symptoms: Fever, malaise, difficulty in swallowing, difficulty in breathing, cough and neck stiffness.
Signs: Patient is ill, toxic, torticollis may be seen, posterior pharyngeal wall may show bulging. X-ray
/
lateral view neck may show increase in prevertebral space.
.i r
Treatment: Antibiotics, hydration, I and D of abscess and Tracheostomy, if respiratory obstruction
predominates.
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Chronic:
s
This is usually secondary to tubercular infection of retropharyngeal LN or caries of cervical spine.
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Common in adults.
is a
Symptoms: Dysphagia, cough, sore throat.
Signs: Posterior pharyngeal wall may show bulging, cervical LN may be enlarged.
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Treatment: I and D by neck route. Anti TB treatment.
Parapharyngeal Abscess
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.
Infection from tonsil, wisdom tooth, or gums may spread to this area.
p
Symptoms: Fever, swelling in neck, pain in throat, dysphagia.
iv
Signs: Patient may be toxic, lateral pharyngeal wall bulging, tonsils may be pushed medially. Trismus
/: /
may be present.
Treatment: Antibiotics, I and D of abscess, anti-inflammatory drugs.
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Ludwig’s Angina
Cellulitis of the floor of mouth resulting into hard brawny swelling in submandibular area is known as
h
Ludwig’s angina. It may be due to spread of dental infection. Common in children and debilitated
patients. Pushing of tongue posteriorly or spread of infection in superior mediastinum may result
into respiratory distress. It is a potentially dangerous condition and should be handled
enthusiastically.
Aphthous Stomatitis
Aetiology: Not known. Possibly it is an autoimmune disorder.
Symptoms: Painful ulcers in mouth.
Signs: Multiple ulcers are seen over tongue, cheek, floor of mouth, or anterior pillar. Ulcers have
sloughy base with marked hyperaemia around the margin of ulcer. They are highly painful and
usually take 7 to 10 days to heal completely (Figure 6-7).
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Treatment: Steroid lozenges, local astringents, antiseptic mouth wash, treatment of underlying
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anaemia, cauterisation of ulcer.
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Figure 6-7: Showing aphthous ulcer on tongue
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Leucoplakia (Figure 6-8)
Leucoplakia is a white patch in mouth commonly seen over cheek or tongue. In Indian subcontinent,
/: /
the habit of keeping tobacco mixed with lime in gingivo-buccal sulcus is an important cause for this
tt p
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Figure 6-8: A case of leucoplakia
condition to develop. This condition is considered to be pre-malignant. And hence every case of
leucoplakia should be followed up carefully. Local irritants should be removed. And lesion should
be biopsied. Histologically it may be simple keratosis, hyperkeratosis or acanthosis or classical
dysplasia. This last variety may progress to carcinoma in situ in 5 per cent of the affected.
Treatment: Stop irritants, follow-up. Excision of patch if histologically dysplasia.
Cleft Palate
This is a congenital condition caused due to failure of fusion of primitive palate. A large defect is seen
in hard and/or soft palate. Nasal structures may be seen through the defect. Patient has feeding and
speech problems. It is also a precursor for chronic Eustachian tube dysfunction. It needs repair by
plastic surgical procedures.
Malignancy (Figure 6-9)

Malignancy in oral cavity is very common in India. Basic underlying cause is chronic mucosal
irritation in the form of tobacco, alcohol, and repeated trauma by sharp tooth. Syphilis or sepsis was
considered as important factors in the past. The common sites involving malignancy are cheek,
gingivo-buccal and gingivo-labial gutters, alveolus, tongue, floor of mouth, tonsil, etc. It may present
as cauliflower growth, non-healing ulcer or neck mass. Patient may have pain in throat, excessive
salivation, fetor and even bleeding in advanced cases. Usually the patients come in a very late stage.
All the patients need biopsy/aspiration cytology to confirm the diagnosis. And depending upon the
size, site, operability, morbidity and willingness of the patient, he may be submitted for surgery,
radiotherapy, chemotherapy, or the combination of these.
Figure 6-9: Malignant lesion of gingivo-labial sulcus

Submandibular Sialoadenitis (Figure 6-10)
This is chronic inflammatory condition of submandibular salivary gland. It may be due to stone in
the Wharton’s duct or in gland proper.
Calculus in submandibular gland is more common than parotid gland because:
1. Submandibular duct has a long tortuous course.
2. It is wide, and it has to work against the gravity to expel its contents.
3. Quality of submandibular gland secretions is thicker as compared to parotid gland secretion.
Hence, stone formation is more common in submandibular gland.
Figure 6-10: A case of chronic submandibular sialoadenitis
Symptoms: Patient would complain of swelling in submandibular area particularly during taking
meals.
Signs: On bi-manual palpation the gland is firm to hard in consistency and stone in the gland or duct
may be palpated.
Treatment:
Stone present: Antibiotics, analgesics, anti-inflammatory drugs. Removal of stone either by milking
the duct or opening the duct. If stones are multiple or in close vicinity of gland, excision of gland may
be needed.
Stone absent: Antibiotics, analgesics, anti-inflammatory drugs. If there is no relief then sialoadenectomy
may be needed.
7
Examination of Larynx and
Laryngopharynx
Larynx is devided into supraglottis, glottis and subglottis.

It includes epiglottis, aryepiglottic folds, arytenoid cartilages, false cords, true cords, ventricles and
subglottic area.
Laryngopharynx includes pyriform fossae, posterior pharyngeal wall and post-cricoid area.
Symptoms related to this part may be:
• Change in voice
• Difficulty in breathing
• Stridor
• Difficulty in swallowing
• Pain in throat
• FB inhalation/ingestion
• Cough
• Neck swelling.
Change in Voice
Patient should be asked, what exactly has gone wrong with his voice? Is it hoarse, is it feeble, is it crowing,
is it husky, or is it throaty? And when he noticed it first? Was the first episode sudden in onset or gradual?
Was it following some neck surgery? Is there history of trauma to neck? Is it following fever or exanthema?
What is total duration of this symptom? Is it constant or intermittent? Has it any diurnal variation, i.e.
Examination of Larynx and Laryngopharynx 137
is it more during fag end of the day or early in the morning? Does it become hoarse after speaking for
some time? If it is intermittent, how much is the time duration between two attacks? Is the symptom
progressive? Is it any way associated with other symptoms like rhinitis or catching of cold? Does the
patient have any respiratory allergy or chronic sinus infection? Is the patient smoker? Few professions
like teachers, hawkers, preachers, singers are more prone for change in voice due to vocal abuse.
Enquiry should be done about the environment where patient is working. People working in industries
where atmosphere is dry, hot or have irritating gas fumes are more prone for change in voice.
Difficulty in Breathing
Difficulty in breathing may be caused by FB, infections like acute epiglottitis, acute laryngotrac-
heobronchitis, mass in larynx, obstruction in airway due to congenital defects in larynx and by
neurological affections of larynx. It may be sudden after trauma or progressive. It may be mild in
nature or severe. It may be manifested during rest or only after exertion. It may land up in stridor. All
these points should be noted.
Stridor
It is a noisy respiration produced due to obstruction in air passage. It may be inspiratory, expiratory, or
mixed. Commonly seen in children. Patient or relatives accompanying the patient should be asked,
• “How long the patient has stridor”? “Is it since birth or acquired?”
• “How it started?”
• Is it associated with fever?
• Is it associated with dysphagia?
• Is there history of recent upper respiratory tract infection?
• Is there any history of aspiration or FB inhalation?
• Is there any history of injury to larynx or chest?
• Does it change with posture?
• Is it more after exertion or present even at rest?
Congenital conditions like laryngomalacia, bifid epiglottis, laryngeal web, subglottic stenosis or
vallecular cyst can give rise to stridor. Trauma resulting into haematoma in laryngeal inlet or injury
to vocal cord, injury to vagus nerve resulting into cord palsy can give rise to stridor. Acute
laryngotracheobronchitis, laryngeal oedema too can cause stridor. FB inhalation in larynx proper or
trachea/bronchi can also result into stridor. It may be following thyroid surgery due to injury to
recurrent laryngeal nerve. Big masses in neck like malignancy or cystic hygroma may compress over
trachea or recurrent laryngeal nerve resulting into stridor. Primary malignancy of larynx/
laryngopharynx is the most common cause of stridor in adults in ENT practice.
Difficulty in Swallowing
Apart from other routine questions, patient should be asked, Is it painful swallowing? (Odynophagia)
or, is it inability to swallow due to obstruction down below (Dysphagia) or both. Or is it spill over of
liquids and solids into respiratory tract, due to which patient is unable to eat. Proper history should be
asked.
CAUSES
• Congenital, e.g. tracheo-oesophageal fistula, stricture oesophagus.
• Traumatic, e.g. external injury to larynx/laryngopharynx may cause painful swallowing.
• Inflammatory, e.g. acute epiglottitis, tuberculous laryngitis, retro-pharyngeal abscess.
• Neurological, e.g. vocal cord palsy, pharyngeal paralysis and neurasthenia.
• Neoplastic, e.g. malignancy of larynx or laryngopharynx.
• Miscellaneous, e.g. Patterson Brown Kelly syndrome, globus hystericus, FB impaction.
Pain in Throat
This may be a predominant symptom. Patient should be asked when it started? How it started, Is there
history of URI, trauma, fever or FB ingestion/inhalation? Is it constant or intermittent? How it is aggravated
and ameliorated.
CAUSES
• Traumatic: Injury to larynx/laryngopharynx, corrosive ingestion.
• Inflammatory: Laryngitis, retro-pharyngeal abscess, acute epiglottitis.
• Neurological: Glassopharyngeal neuralgia.
• Neoplastic: Carcinoma larynx, carcinoma pyriform fossa.
• Miscellaneous: FB in larynx/hypopharynx.
Foreign Body (FB)

Any substance either exogenous or endogenous found in the body, where it is not present anatomically may be
considered as a foreign body.
When a foreign body enters respiratory passage, it is called as FB inhalation and when it enters in
digestive tract, it is known as FB ingestion. Treatment differs in both.
FB INHALATION
Ask the patient [if he can answer] or to relative What is inhaled by the patient? When? Did the patient have
cyanosis, choking spells after inhalation? Can relatives provide the duplicate of FB or details of FB? Is patient
febrile? History of any attempt to remove FB should also be asked.
Usually it is a small child who may be brought in a severe hypoxic state. He may have cyanosis,
respiratory urge and urgent tracheostomy may be needed.
FB INGESTION
Patient or his relative should be asked the same array of questions that are mentioned above, as it is always
better to rule out FB in larynx. Then he may be asked, Whether patient had any vomiting after ingestion of
FB? Can patient swallow solids or liquids? Is patient febrile?
Causes
In children: Routine household things like coins, buttons, pencils, rubber, hairpins, safety pins, stones,
may get lodged in laryngopharynx. They are more commonly stucked at C6 level in cricopharynx.
However, sharp, pointed objects can get lodged in mucosa in any place.
In adults: In adults, it is more commonly seen in mentally weak people or while under the influence of
alcohol. However in old people due to poor propelling capacity of oesophageal musculature, large
food bolus, or inadvertent bone [fish bone or chicken bone] impaction in pyriform fossa or cricopharynx
is possible. Professionals like tailors are habituated to keep needles in mouth, which may slip down
in larynx or laryngopharynx.
Cough
Cough is a protective reflex. It can be initiated whenever there is irritation in larynx, laryngopharynx,
trachea or bronchi. Hence, all the situations where irritation in larynx /hypopharynx occurs cough
is the result.
Neck Swelling
Details are given in Chapter 9 on Examination of Neck.
Indirect Laryngoscopy
For the examination of larynx and laryngopharynx in OPD Bull’s eye lamp, head mirror, laryngeal
mirror, spirit lamp, gauze square pads are needed. In this procedure, clinician does not see the larynx
directly but a mirror image and hence this procedure is known as Indirect laryngoscopy.
Procedure: Patient is sitting on a revolving stool in front of clinician at a distance of approximately one
foot. The procedure is explained to the patient to reduce his anxiety. Head mirror is adjusted and a good
circular focus is obtained on the patient’s face. Mirror part of laryngeal mirror is gently heated to
prevent condensation of patient’s breath on the mirror. Spirit lamp or air warmers may be used to warm
the mirror. Then it is tested by the clinician himself to make sure that it is not too hot to scald the patient.
Patient is asked to lean forward a little and to pop out his tongue. It is held firmly with the help of
gauze square pad in between left thumb and middle finger. With the help of left index finger upper
lip is retracted. Warmed laryngeal mirror is held like a pen in the right hand and it is negotiated in
oral cavity along left angle of mouth and held at base of uvula without touching posterior pharyngeal
wall. Various parts of larynx are seen in the mirror. One has to change the position of laryngeal
mirror in different directions and formulate a mental picture of the larynx and laryngopharynx.
Various structures that should be identified during indirect laryngoscopy, from above downward
are (Figure 7-1):
All these structures should be seen carefully for any congestion, oedema, ulcer, growth, foreign
body, loss of function or any other obvious lesion.
Figure 7-1: Diagrammatic representation of indirect laryngoscopy

Later on patient is asked to say “EE”. This visualises the glottic area and one can observe the
movements of true vocal cords. Anterior commissure, posterior commissure, and sometimes part of
subglottic area may be seen in co-operative patients.
Indirect laryngoscopy is technically difficult procedure and requires co-operation on the part of
patient and experience on the part of clinician, to obtain maximum information. However, in some
unco-operative patients 4 per cent xylocaine may be spread over posterior pharyngeal wall to blunt
the gag reflex.
The structures that are not seen in the indirect laryngoscopy are:
• Laryngeal ventricles
• Subglottic area
• Post-cricoid area.
In some sensitive or anxious patients, it may not be possible to examine the larynx even after
xylocaine spray. Such patients may require fiberoptic flexible laryngoscopy under local or direct
laryngoscopy under general anaesthesia.
NB: Neck should always be examined after completing Indirect Laryngoscopy. Laryngeal crepitus should be
elicited laryngeal widening and tenderness if any should be looked for (See neck examination).
Laryngeal examination can also be done using 700 Hopkin Rod and magnified view can be seen on
monitor, which can be recorded for documentation and it could be shown to the patient and reiatives also.
Common Conditions Involving Larynx and Laryngopharynx

1. Laryngotracheobronchitis
2. FB in larynx and laryngopharynx
3. Juvenile laryngeal papillomatosis
4. Laryngomalacia
5. Vocal nodules
6. Vocal cord palsy
7. Malignancy of larynx and laryngopharynx.
LARYNGOTRACHEOBRONCHITIS
Common in children below 3 years. Caused by parainfluenza virus 1 and then secondarily invaded
by Streptococci, Staphylococci, Pneumococci and H. influenzae.
Symptoms: Child is febrile, toxic, hypoxic, inspiratory stridor +. This is due to oedema, congestion
and narrowing in the subglottic area due to deposition of thick secretions, which results into
respiratory distress.
Treatment: Hospitalisation, O2 tent and humidification (if needed), IV fluids, antibiotics, endotracheal
intubation or tracheostomy may be considered if obstructive element does not respond to conservative
treatment. Child may die of asphyxia if not treated properly.
FB IN LARYNX AND LARYNGOPHARYNX (FIGURES 7-2A TO 7-3D)

Symptoms and signs: Common symptoms of FB larynx and laryngopharynx may be pain in throat,
difficulty in swallowing, pain in neck movements. However, stridor is a predominant feature of
laryngeal FB. At times patient may die due to laryngeal spasm.
Diagnosis: On history, clinical examination and radiological evidence.
Treatment: Removal of FB by direct laryngoscopy and FB removal forceps.
NB: Prevention of FB inhalation is the best form of treatment.
JUVENILE LARYNGEAL PAPILLOMATOSIS (FIGURE 7-4)

Juvenile laryngeal papillomatosis is a disorder presenting with change in voice or huskiness, which
may develop gradually. Patient may have difficulty in respiration so much so that some may need
urgent tracheostomy. Indirect/direct laryngoscopy may show multiple papillomas studded in larynx
over AEF, arytenoid, ventricles, cords and subglottic area.
A B
Figures 7-2A and B: X-rays showing FB in pharynx of a small child
Aetiology: Exact aetiology not known. It is closely associated with human papilloma virus (HPV)
infection in mothers.
A B
C D
Figures 7-3A to D: (A) X-ray PA view neck and chest showing radio-opaque shadow in coronal
plane, (B) X-ray neck lateral view showing radio-opaque FB in cricopharynx, (C) X-ray neck PA view
showing inverted safety pin in pharynx, (D) X-ray neck lateral view showing pin in cricopharynx
Figure 7-4: Endoscopic view of laryngeal papillomatosis
Treatment: Large number of treatment modalities are available.

1. CO2 lasers
2. Photodynamic therapy
3. Surgical excision
4. Interferon therapy
5. Indole-3-carbinol
6. Endoscopic micro-debridement.
LARYNGOMALACIA
Newborn and small children present with inspiratory stridor more so on exertion or during sleep.
Flexible nasopharyngolaryngoscopy reveals that there is abnormal laxity of supraglottic structures
resulting into, pulling of tissues, in inlet of larynx during every attempt of inspiration.
The condition is self-limiting. Laryngeal framework gets rigidity by 2 years of age. No specific
treatment needed. Parent assurance essential. Still due care should be exercised during upper
respiratory tract infection.
VOCAL NODULE (FIGURE 7-5)

These are hyperkeratotic nodules seen over both true cords at the junction of anterior 1/3 with
posterior 2/3.
Aetiology: Vocal abuse, seen in voice users like hawkers, singers, teachers, preachers and children
who shout often.
Symptoms: Change in voice, tiredness of voice, discomfort in throat.
Signs: Indirect laryngoscopy shows—classical vocal nodules.
Treatment
1. Voice rest.
2. Remove source of infection in nose/sinuses if any.
3. Microlaryngeal surgery if conservative therapy fails.
4. Voice therapy to reduce the vocal strain.
VOCAL CORD PALSY

It may be congenital or acquired. In acquired variety, the causes may be:
• Trauma to neck
Figure 7-5: Diagrammatic representation of vocal nodule
• Surgery over thyroid gland

• Viral infections
• Tumour compressing over recurrent laryngeal nerve
• Tumours of larynx, trachea, oesophagus or thyroid.
Paralysis of the cord may be complete/incomplete, unilateral/bilateral.
Symptoms: Change in voice, spill over of liquids, dysphagia, difficulty in respiration depending upon
type of paralysis.
Signs: Indirect laryngoscopy would reveal unilateral or bilateral cord fixed in paramedian or cadaveric
position. Glottic chink may be compromised.
Treatment:
Temporary cord paralysis: removal of cause, wait and watch.
Permanent cord palsy:
Resulting into airway obstruction: tracheostomy, lateralisation of cord, cordopexy, may be done.
Resulting into air waste: medialisation of cord, Teflon paste injection in cord.
MALIGNANCY OF LARYNX
Carcinoma of larynx is a common condition in India.
Aetiology: Smoking, alcohol, irritating fumes in industry.
Pathology: Squamous cell carcinoma most common variety. Glottic malignancy has good prognosis
as symptoms are early, diagnosis is early and no lymphatic spread, as compared to supraglottic and
subglottic areas.
Symptoms: Change in voice, pain in throat, respiratory difficulty. Difficulty in swallowing, neck
nodes and rarely haemoptysis.
Signs: Exophytic or ulcerative lesion affecting either epiglottis, AEF, arytenoids, false cords or true
cords. Cord movements may be restricted due to involvement of laryngeal muscles, cricoarytenoid
joint or recurrent laryngeal nerve.
Investigations and diagnosis: Direct laryngoscopy to know extent of disease and to take biopsy. Radiology
and CT scan to know extent and metastasis.
TNM classification of larynx:
Tumour status:
TiS Carcinoma in situ
T0 No evidence of malignancy
T1 Tumour confined to the region with normal mobility
T1a Tumour confined to one anatomical site
T1b Tumour spreading to surrounding area but not crossing region
T2 Tumour extending to adjacent region but without fixation of cord and not extending beyond
larynx
T3 Tumour confined to larynx but with evidence of cord fixation or deep invasion
T4 Tumour with direct extension beyond larynx
TX Minimum requirement to assess the primary cannot be met with
Nodal status:
N0 No evidence of regional lymph node involvement
N1 Single, homolateral clinically + lymph node < 3 cm diameter
N2a Single, homolateral, clinically + lymph node between 3 to 6 cm diameter
N2b Multiple, homolateral clinically + lymph nodes none > 6 cm diameter
N3a Single/multiple, homolateral clinically + lymph node/s one > 6 cm diameter
N3b Bilateral clinically positive nodes. (Each side of neck should be staged separately)
N3c Contralateral clinically + lymph nodes.
Distant metastasis:
M0 No evidence of distant metastasis
M1 Evidence of distant metastasis
MX Minimum requirement to assess the presence of distant metastasis can’t be met with.
Staging:
Stage I : T1 N0 M0
Stage II : T2 N0 M0
Stage III : T3 N0 M0/Any T N1 M0
Stage IV : T4 N0 M0/Any T N2 M0/Any T Any N M1
Treatment:
• Surgery, radiotherapy, chemotherapy and combinations are the treatment modalities available.
• Surgery offers better chance for elimination of disease. Treatment depends upon age, sex,
occupation, extent of the disease, operability, facilities available and willingness of the patient.
• Total laryngectomy results into permanent loss of voice. Post-laryngectomy vocal rehabilitation is
a ray of hope for ‘a laryngeal’ patients.
• In selected cases ‘conservative laryngectomy’ procedures, which preserve voice are gaining
popularity.
• Involvement of neck nodes requires radical neck dissection, along with total laryngectomy and
partial pharyngecotmy.
8
Thyroid Gland
Introduction
Thyroid gland is one of the most important endocrine glands of the body. It is a bilobed structure
connected by isthmus in the anterior part of neck. It is located anterior to 2nd 3rd and 4th tracheal
rings and its lobes are related laterally. Its average weight is 25 grams and is normally not visible
externally.
The gland secretes thyroxin and tri-iodothyronine. These substances regulate tissue metabolism.
In infants, adequate supplies of thyroid hormone are necessary for normal development of central
nervous system. Deficiency of thyroid hormone in this period results into irreversible mental
retardation known as cretinism. Excessive secretion of the thyroid gland is known as hyperthyroidism
and reduced secretion is known as hypothyroidism.
Average daily intake of dietary iodine is 150–300 g/day.
History Taking
A patient having hyperthyroidism may have one or more of the following complaints:
1. Swelling in thyroid region (Goitre)
2. Weight loss (however appetite is usually good)
3. Palpitation
4. Heat intolerance
5. Muscle weakness
Thyroid Gland 149
6. Fatigability
7. hyperdefecation
8. Amenorrhoea or oliguria
9. Pruritus
10. Gynaecomastia (in males)
11. Symptoms of compression
a. Change in voice
b. Difficulty in swallowing
c. Stridor
12. Eye symptoms
a. Stare
b. Protruding eyes
c. Easy tearing
d. Photophobia
e. Gritty eye sensation
f. Diplopia
g. Periorbital oedema.
A patient having hypothyroidism may have one or more of the following symptoms:
• Cold intolerance
• Constipation
• Lethargy
• Dry skin
• Arthralgia.
Goitre, exopthalmos, and tremors may be the presenting features of hyperthyroidism that can be
noted without asking the patient.
Patient should be asked:
• Place of his residence
• Food habits (excessive use of goitrogenic food)
• Cooking habits (using table salt or not)
• Duration of swelling
• Similar swelling in other family members or other people in locality or village.
• Pain in swelling
• Sudden increase in size
• Change in voice
• Dysphagia
• Dyspnoea
• Use of anti thyroid drugs
• Surgery on thyroid.
Patient should be asked the history similar to history asked for other swellings in body. In addition
to that his residence should be carefully noted. People living in hilly area may have iodine deficiency
in their diet. And if this is not supplemented by fortified salt, may present with clinical symptoms of
Iodine deficiency disease. Duration of swelling, rate of growth should be specifically asked. Thyroid
swelling is usually a painless swelling. However, pain may start in the swelling if sudden
haemorrhage occurs. Sudden increase in size may suggest malignant change or sudden haemorrhage.
History should be asked about taking any anti-thyroid drugs and details should be noted. History of
any previous surgery should also be noted.
General Examination
General examination of the patient with thyroid disease gives large number of clues and information.
A patient may be restless and nervous; he may have tremors in hyperthyroid state. His skin may be
warm and moist. On the other hand patient having hypothyroidism may be lethargic and have dry
skin.
PULSE RATE
There is obvious tachycardia in a hyperthyroid status. However, pulse rate does increase due to
anxiety. To confirm this, sleeping pulse rate is counted. Any sleeping pulse rate above 90 in an adult
is considered to be significant. There may be irregularity in the pulse rate if paroxysmal atrial
tachycardia or atrial fibrillation has developed.
BLOOD PRESSURE
There may be rise in systolic blood pressure. This is due to positive inotropic effect of circulating T3
and T4. Diastolic blood pressure may be decreased. This is due to reduction in peripheral vascular
resistance.
Venous hum may be heard over external jugular vein and bruit over carotid vessels.
Thyroid Gland 151
Spleenomegaly and/or liver enlargement may be seen if patient lands into congestive cardiac
failure.
Proximal muscle weakness may be noted. Mental clouding and depression are the features of
hypothyroid status. Deep tendon reflexes may be delayed.
Swelling in Thyroid Region

Majority of times this swelling is painless and hence patient does not come to doctor in early stage
unless he/she is cosmetically concerned. Usually swelling takes a very insidious course. It may be
solitary or multinodular swelling. Rarely haemorrhage occurs inside the swelling and swelling size
increases suddenly giving rise to pain. This may also result into change in voice due to compression
over recurrent laryngeal nerve.
Swelling in thyroid region is seen many a times in young puberty age girls. This is not necessarily
abnormal. It is due to increased demand of thyroid hormone in growing age. Similar swelling may be
observed in pregnant women. This is known as physiological goitre.
Similarly other complaints should be asked in details and noted down in case history.
Examination of Thyroid Gland

INSPECTION
Patient should be sitting comfortably in a chair or stool. Neck and upper part of chest should be
exposed.
Inspect the neck of the patient from front and side. Note down the swelling in thyroid region
whether it is solitary or multiple, generalised or localised. Note down exact site, size, surface and
margins of the swelling, any obvious pulsations and condition of overlying skin. Note down any
neck scar of previous thyroid surgery or any other neck surgery.
Ask the patient to swallow his/her own saliva or water and observe whether swelling moves with
the act of deglutition or not. Observe whether lower limit of swelling is visible or not. A thyroid
swelling and thyroglossal duct cyst moves with the act of deglutition. Ask the patient to protrude out
the tongue. A thyroglossal duct cyst moves up with protrusion of tongue.
At times pressure of swelling or malignant change in thyroid gland may cause involvement of
cervical sympathetic chain, giving rise to Horner’s syndrome.*
* Horner’s syndrome—due to involvement of cervical sympathetic chain results into ptosis, miosis,
enophthalmos and unhydrosis.
PALPATION
This should be done from front and also from behind. Neck should be flexed to relax neck muscles.
Give gentle pressure over swelling and observe whether it is tender to touch.
Ask the patient to swallow and palpate the swelling during the act of swallowing. Slight
enlargement of gland and tenderness can be better appreciated by this method. Note down whether
you can reach the lower limit of swelling or not. Then palpate each lobe of thyroid separately. Make
the lobe prominent by pushing it from other side. Confirm findings of inspection like size of thyroid
gland.
Shape—is the gland uniformly enlarged or irregular?
Surface—is it smooth or nodular ?
Nodules—if you detect any nodules on palpation, note down their number, site, size, consistency,
mobility and tenderness.
Consistency: soft (normal). Firm/rubbery (goitre). Hard-suspected malignancy.
Thrill may also be palpated in toxic state.
Position of trachea should be ascertained. Trachea may be central or shifted to one side or it may
not be palpable due to thyroid enlargement and or retrosternal extension of goitre.
Cervical lymph nodes should be palpated at this stage to know any metastasis. At the same time
do not forget to palpate carotids.
PERCUSSION
This is particularly useful to know whether goitre has extension in superior mediastinum or not.
Start percussion from lower end of thyroid gland down to the superior mediastinum and hear the
percussion note. It is dull if there is retrosternal extension of goitre.
AUSCULTATION
Should be done over the thyroid swelling and bruit may be heard in toxic state due to increased blood
flow in the gland.
Eye Signs
some of the patients develop eye signs. Every attempt should be made to find out the early eye sings.
These are as follows:
Thyroid Gland 153
Lid lag sign—Lagging of the upper eyelid on downward rotation of the eye, indicating toxic goitre.
Upper lid retraction (Dalrymple sign)—Mechanisms for upper lid retraction include proptosis,
sympathetic drive of Müller muscle, upgaze restriction, fibrosis of the levator, and contralateral
ptosis (myasthenia).
The other signs include—Wide palpabral fissure, chemosis, periorbital swelling, proptosis. These
changes occur due to lymphocytic infiltration of eye tissue and release of cytokines. Increase in
hyaluronic acid contents increases osmotic load causing osmotic damage which results into muscle
oedema and proptosis.
It is not sure that these changes occur due to thyroid hormone imbalance. But these are
many a time associated with thyroid hormone imbalance. Hence, these are called as thyroid
associated ophthalmopathy.
Systemic Examination
Should be carried out in usual manner.
On the basis of history and clinical examination you will get a fairly good idea whether your
patient is having goitre or not, whether your patient is in euthyroid, hyperthyroid or hypothyroid
status.
To confirm your findings and to get additional information for diagnosis patient needs to be
submitted to set of investigations. These are as follows:
1. Thyroid function tests
2. Thyroid ultrasonography
3. Fine needle aspiration cytology
4. Thyroid scan
5. Radioactive iodine uptake
6. Basal metabolic rate
Thyroid function test: Here we study the serum levels of TS4, T3 and T4, and this gives us an idea
whether patient is having euthyroid status or otherwise. Normal values of T3 are 80–120 ng/dL and
normal values of T4 are 5–11 µg/dL in a normal individual. However, free thyroid hormone estimation
gives more accurate idea. Measurement of serum TS4 is the most sensitive test to detect primary
hypothyroidism or subclinical hypothyroidism.
Thyroid ultrasonography: It detects whether thyroid mass is solid or cystic. Even the nodules of size
2–3 mm not palpable clinically are also detected in USG.
Fine needle aspiration cytology: It is reliable and simple investigation, particularly to confirm the
diagnosis of malignancy.
Thyroid scan: In this study I123 or I131 are used. It is used to know the functional status of palpable
thyroid nodule.
Radioactive iodine uptake: This is not a popular test as the results are not clinically reliable and the test
is contraindicated during pregnancy.
Types of Goitre (Figures 8-1 and 8-2)

i. Sporadic goiter: This refers to thyroid enlargement in a small fraction of given population. The
cause for thyroid enlargement may be different from patient to patient.
ii. Endemic goitre: This is seen in much larger fraction of population mostly due to iodine deficiency.
Diseases associated with thyrotoxicosis:
a. Graves’ disease
b. Toxic multinodular goitre
c. Toxic adenoma
d. Subacute thyroiditis
e. Iodine-induced hyperthyroidism.
Diseases/conditions which can lead to Hypothyroidism
a. Hashimoto’s thyroiditis
Figure 8-1: Showing thyroid nodule

Thyroid Gland 155
Figure 8-2: X-ray chest PA view showing

retrosternal extension of goitre
b. Total thyroidectomy
c. Drug induced
d. Irradiation
e. Neoplasm.
GRAVE’S DISEASE
In 1835, Robert Grave described clinical syndrome constituting hypermetabolism, thyroid enlargement
and exophthalmos. In Europe, it is known as Besedow’s disease. It is considered to be an autoimmune
disorder in which TSH levels are low. A non TSH thyroid stimulator possibly a family of gamma
globulin acts as thyroid stimulator. Exact cause of exophthalmos is not clear. There may be strong
family history. Pretibial myxoedema may be observed. Natural remissions are known. Patient is
treated by anti-thyroid drugs, surgery or radio iodine depending upon the need of the patient and
facilities available in the centre.
HASHIMOTO’S DISEASE
First described by Hakaru Hashimoto in 1912. There is destruction of thyroid cells by cell-mediated
and antibody-mediated immune response. Histology shows diffuse lymphocytic and plasma cell
infiltration with formation of lymphoid follicles and damage to follicular basement membrane.
Antibodies block TSH receptors resulting into reduced T3 and T4 circulation.
More common in female. Hypothyroidism is very insidious and hence morbidity results due to
failure to make early diagnosis and institute replacement therapy. There may be goiterous changes in
thyroid but goitre is not large in size. Early compensatory raised TSH levels tends to maintain nearly
normal thyroid function and keeps patient in euthyroid state. Long standing hypothyroidism may
present with myxoedema coma. Treated by life time levothyroxine. Surgery on thyroid may be needed
if pressure symptoms develop or malignant change develops in nodule.
BENIGN NEOPLASMS
Follicular adenoma : Most common benign thyroid tumour. Many of these tumours do not possess
the capacity to concentrate iodides and hence called non functioning or “cold“ nodules. Thyroid
function tests may be normal but USG shows cystic cavity within the nodule and iodine uptake
studies may show non functioning “ cold” nodule. Confirmation is done by FNAB. Functional
lesions that have suppressed TSH synthesis and caused hyperthyroidism are called “ HOT” nodules.
Treatment depends upon the age of the patient, size of the nodule and whether patient is in euthyroid
state or hyperthyroid status.
MALIGNANT THYROID TUMOURS

Various types of carcinoma found in thyroid are papillary, follicular, medullary and poorly
differentiated. Papillary carcinoma is more common in young female. The differential diagnosis of a
solitary non functioning nodule (cold nodule) includes carcinoma, colloid nodule, non-functioning
adenoma and cyst. Chances of thyroid nodule being malignant are more in previous irradiation of
neck, rapid growth, sudden recurrent nerve palsy, cervical lymphadenopathy and fixation of thyroid
nodule. Depending upon the histological type of malignancy, stage, age and facilities available
treatment can be planned.
To consolidate treatment plan following classification is applied.
Low risk patient =  =Female under 45 years of age
High risk patient =  =All males and females above 45 years of age
Low risk tumour =  = Papillary carcinoma less than 1 cm
High risk tumour =  = Papillary or follicular more than 1cm, multicentric, local or distant spread
 +  = Lobectomy
 + = Lobectomy or total thyroidectomy
 +  = Lobectomy or total thyroidectomy
 +  = Total thyroidectomy
SECTION B
9
Examination of Neck
Some of the diseases are primarily diseases of neck organs, and majority of inflammatory and
neoplastic diseases in oral cavity, oropharynx, nasopharynx, larynx and laryngopharynx do manifest
in neck, as the lymphatics from these areas ultimately drain into neck nodes. Diseases originating in
oral cavity, oropharynx, larynx or laryngopharynx may also extend to neck. Hence, one has to
examine the neck very carefully.
ANATOMICAL CONSIDERATIONS
For better understanding of underlying structures and ease of description the neck is divided into
various triangles. It is better to memorise them.
Anatomical Map of Neck (Cervical triangles) (Figures 9-1A, B and 9-2)

1. Muscular triangle: Outlined anteriorly by midline of neck, superolaterally by superior belly of
omohyoid, inferolaterally by lower part of anterior border of sternomastoid.
2. Carotid triangle: Outlined by anterior border of sternomastoid, superior belly of omohyoid, and
posterior belly of diagastric muscle.
3. Diagastric triangle: Upper boundary by lower border of mandible, anterior boundary by anterior
belly of diagastric muscle, posteriorly by posterior belly of diagastric muscle.
4. Submental triangle: Its base is formed by hyoid bone, sides by anterior bellies of diagastric muscles
of either side, apex lies at symphysis menti.
A B
Figures 9-1A and B: Showing cervical triangles. (1) Muscular triangle, (2) Carotid triangle,
(3) Diagastric triangle, (4) Submental triangle, and (5) Posterior triangle
5. Posterior triangle: It is formed by posterior border of sternomastoid, middle part of clavicle bone and
anterior border of trapezius muscle.
Lymphatic drainage of neck

1. Pre-auricular LN
2. Retro-auricular LN
3. Suboccipital LN
4. Superficial cervical LN
5. Superior deep jugular
6. Middle deep jugular
7. Spinal accessory LN
8. Inferior deep jugular
9. Supraclavicular LN
10. Antereior scalene LN
11. Delphian LN
12. Submandibular LN
13. Submental LN
14. Facial LN
Figure 9-2: Diagrammatic representation of lymphatic chain of neck

Examination of Neck 159
The lymph nodes draining head and neck are submental, submandibular, superficial cervical,
retropharyngeal, paratracheal, spinal accessory, anterior scalene and supraclavicular and deep
jugular chain.
• Submental—receive drainage from skin of the chin, mid portion of lower lip, tip of the tongue,
anterior oral cavity and the nasal vestibule.
• Submandibular nodes—receive drainage from submental area, lower nasal cavity, upper lip, lateral
part of lower lip, anterior oral cavity and skin of mid face. They drain into superior deep jugular chain.
• Superficial cervical—they are located along external jugular vein, receive cutaneous lymphatic
from face, retro-auricular region, parotid nodes and occipital nodes. They ultimately drain into
superior deep jugular chain.
• Retropharyngeal nodes—receive drainage from nasopharynx, posterior nasal cavity, paranasal
sinuses, posterior oropharynx and hypopharynx and drain into deep jugular chain.
• Paratracheal nodes—receive drainage from lower larynx, hypopharynx, cervical oesophagus,
upper trachea, thyroid and drain into inferior deep jugular chain.
• Spinal accessory—located along the spinal accessory nerve and receives drainage from parietal and
occipital regions of scalp, nape of the neck, upper retropharyngeal and parapharyngeal nodes. Upper
spinal accessory nodes drain into upper deep jugular chain and lower drain into supraclavicular nodes.
• Anterior scalene (Virchow’s nodes) receive drainage from thoracic duct, and are situated at the
junction of thoracic duct and left subclavian vein. They may get involved from infraclavicular
malignancy.
• Supraclavicular nodes—receive drainage from spinal accessory and infraclavicular malignancy.
Deep jugular chain: This extends from base of skull to clavicle, and divided into superior, middle and
inferior group.
Superior deep jugular chain: Receive primary drainage from soft palate, tonsils, tonsillar pillars, base of
tongue, pyriform fossa and supraglottic larynx, and secondary drainage from retropharyngeal, spinal
accessory, parotid, superficial cervical and submandibular nodes.
Middle deep jugular chain: Receives primary drainage from supraglottic larynx, lower pyriform sinus
and postcricoid area. They receive secondary drainage from superior deep jugular chain and lower
retropharyngeal nodes.
Inferior deep jugular chain: Receives primary drainage from thyroid, trachea and cervical oesophagus.
Secondary drainage from superior and middle deep jugular chain and paratracheal nodes.
Clinical Application (Figure 9-3)
Malignancy in nose, sinuses, oral cavity, oropharynx, larynx and laryngopharynx ultimately drain
into neck nodes as secondary deposits. Level of the involved neck node has a clinical significance.
Figure 9-3: Diagrammatic representation of neck node levels, AJC (1997)
There is no unaminouness in various organisations like AJC, AAD-HNS and others. To prevent any confusion
in the minds of undergraduate students more simple AJC classificaion of 1997 is given below:
Level I Lymph node involvement in submental and submandibular triangles.
II Upper jugular lymph nodes from skull base to hyoid.
III Mid jugular lymph modes from hyoid to cricothyroid membrane.
IV Lower jugular LN from cricothyroid membrane to clavicle inferiorly.
V Lymph node involvement in posterior triangle.
VI Lymph node in anterior compartment from hyoid bone to suprasternal notch inferiorly.
VII From suprasternal notch to upper mediastinum.
INSPECTION (FIGURES 9-4A AND B)

NB: It is presumed that you have already carried out the detailed examination of nose, PNS,
nasopharynx, oral cavity, oropharynx, larynx and laryngopharynx.
• Neck should be exposed upto the level of nipples for proper examination. Look for any swelling,
ulcer, sinus, fistula or scar mark in the neck.
• Location: Note down the exact location of lesion as to which triangle/s the lesion is situated.
• Look for the size, shape, surface, margin and overlying skin in case of swelling. Look for appropriate
findings in case of ulcer/fistula or sinus.
NB: It should be noted whether swelling moves with deglutition or not. Swelling attached
to larynx or trachea moves upward with the act of swallowing.
Figure 9-4A: Showing permanent tracheal Figure 9-4B: Showing scar mark on neck due to
stoma after total laryngectomy old healed tuberculosis
Palpation
It is a fair practice to identify various normal landmarks in neck from above downwards like hyoid
bone, thyroid notch, cornua of thyroid, cricoid cartilage, trachea, its position, tracheal rings,
suprasternal notch, etc.
For proper palpation of neck, clinician should stand behind the patient, flex the neck so that neck
muscles are relaxed and fingers are slipped along various triangles of neck. This examination may
notice any small swelling not observed during inspection.
• Look for local temperature and tenderness.
• Findings of inspection (size, shape, surface and margins) are confirmed on palpation.
• In case of swelling look for consistency, transillumination, mobility, fluctuation or other relevant
sign.
• Examination of ulcer, fistula or sinus should be done in appropriate way as described elsewhere.
The deep cervical chain of lymph nodes lies below the sternomastoid and cannot be palpated
without getting underneath the muscle:
1. Insert your fingers under the anterior edge of the sternomastoid muscle.
2. Ask the patient to bend his neck towards the side you are examining.
3. Move the muscle backward and palpate the deep nodes underneath.
Note the size and location of any palpable nodes and whether they are soft/hard, tender/non-
tender, mobile or fixed.
In
Tuberculosis more than one lymph nodes may be affected, firm in consistency. The glands
may be clustered together due to periadenitis. This is known as ‘matting’.
Lymphoma lymph nodes may be small, multiple, discrete, mobile and rubbery in consistency.
Malignancy single or multiple, nodes are involved. They are hard in consistency or even
fungated. They may be fixed to deeper structures.
Inflammatory lymphadenitis lymph nodes are enlarged and tender.
Tenderness over Laryngeal Cartilages

Laryngeal cartilages are held between the thumb and fingers and gentle pressure is given all over the
cartilages to test the tenderness. This test may be positive if the cartilages are involved in inflammatory,
traumatic, malignant or tuberculous process.
Laryngeal Widening
Alae of thyroid cartilage get wide open whenever there is expanding lesion in larynx, e.g. laryngeal
malignancy.
Laryngeal Crepitus (Figure 9-5)
Laryngeal cartilages are held in between thumb and fingers and rubbed against vertebral column
side to side. In a normal individual it gives a gritty sensation. This is known as Laryngeal Crepitus.
It is lost in post cricoid growth or retropharyngeal abscess.
To Test Relationship of Swelling with Sternomastoid Muscle (Figures 9-6A and B)

It can be determined whether swelling is above or below the sternomastoid muscle as follows:
• Mobility of the swelling in vertical and horizontal direction is tested.
Figure 9-5: Showing how to elicit laryngeal crepitus
• Patient is asked to turn his neck opposite to the side of lesion.

• Firm pressure is applied to the chin of the patient with hand on opposite side.
• Patient is asked to counteract the pressure. This contracts the sternomastoid muscle. Mobility of
the swelling is again tested in vertical and horizontal directions.
Interpretation
1. If the swelling is above the sternomastoid muscle, it becomes prominent on contracting the muscle.
Mobility remains unaffected.
2. If the swelling is below the sternomastoid muscle, it disappears partly or completely. Mobility of
the swelling would be reduced.
3. If the swelling is arising from muscle, the size may change and mobility restricted on contraction
of muscle.
A B
Figures 9-6A and B: Method to test relationship of swelling with sternomastoid
Neck swellings can be classified as:

1. Midline neck swellings
2. Lateral neck swellings.
Midline neck swellings: e.g. dermoid cyst, thyroglossal duct cyst, sublingual dermoid, thyroid swelling,
Ludwig’s angina, pyramidal lobe goitre, enlarged lymph node.
Lateral neck swellings: e.g. branchial cyst, carotid body tumour, cystic hygroma, pharyngeal pouch,
laryngocoele, lymphadenopathy of any aetiology in lateral part of neck, submandibular sialoadenitis,
benign and malignant tumours of submandibular gland, oral malignancy extending to neck. Parotid
gland tumours, parapharyngeal space tumours and abscesses. Lateral thyroid swellings.
ECTOPIC THYROID (FIGURE 9-7)

• Aetiology: Developmental defect in descent of thyroid gland in the neck. It may remain at the
lingual site or at any site from tongue to level of normal gland.
• Diagnosis may be done by ultrasound scanning, tomographic scanning and radionuclide thyroid
scanning.
• Treatment:
• Euthyroid/asymptomatic patient—No treatment.
Figure 9-7: Photograph showing ectopic thyroid
• Hypothyroid state + obstructive symptoms—Thyroid

hormone replacement.
• Euthyroid state + obstructive symptoms—Thyroid tissue
transplant to neck, chest or abdomen.
THYROGLOSSAL DUCT CYST (FIGURE 9-8)

Aetiology: The thyroid gland develops from epithelial
proliferation in the floor of foregut between tuberculum impar
and hypobranchial eminence during 3rd week of foetal
development. The thyroid premordium forms a tubular
structure the thyroglossal duct, which descends anteriorly
infront of hyoid bone and larynx. The thyroglossal duct becomes
bilobed distally to become thyroid gland. The duct solidifies
and later atrophies.
Failure of the duct to close gives rise to thyroglossal duct
cyst. Majority of them are seen in midline just beneath the hyoid
bone. Few are suprahyoid and rarely in suprasternal area. Figure 9-8: A case of thyroglossal
duct cyst
Age: Noticed in second decade of life.
This is a midline cystic neck swelling which moves with act of deglutition and also on protrusion
of tongue.
Treatment: Excision of the cyst, and duct along with middle part of hyoid bone and core of tongue
tissue upto foramen caecum (Sistrunk operation).
DERMOID CYST
This develops in the line of embryonic fusion. And hence may be seen in midline of the body or in the
area where two embryonic processes meet each other.
Clinical Features
• Cystic swelling in the neck
• Margins well defined
• Fluctuation postive
• Overlying skin can be lifted up
• No punctum.
• Transillumination may be negative
• Not fixed to underlying structures.
THYROID SWELLING (FIGURE 9-9)

Detailed description of symptoms and Signs are given in Chapter
on Thyroid.
LUDWIG’S ANGINA
This is an infection in the submandibular facial plane. Usually
occurs secondary to dental infection. Children are commonly
affected.
Symptoms
• Fever, malaise, difficulty in swallowing Figure 9-9: Photograph showing
• Swelling in submental and submandibular area huge thyroid
• Floor of mouth swollen and oedematous
• Due to elevated tongue child may develop respiratory obstruction.
Treatment
/
• Antibiotics, anti-inflammatory and antipyretic drugs
.i r
• Incision and drainage of abscess
• Tracheostomy if respiratory distress develops.
SEBACEOUS CYST
This arises due to obstruction of sebaceous gland in the skin.
s s
Clinical Features
a n
is
• A slowly growing, painless smooth cystic swelling
• Margins well defined.
r
• Overlying skin cannot be lifted up
e
• Punctum [opening of the gland] seen over skin
p
• Not fixed to deeper structures.
.
BRANCHIAL CYST (FIGURES 9-10A TO C)
ivp
/: /
Exact aetiology is not known. However, branchial apparatus theory states that they represent fusion
of remains of pharyngeal pouches and branchial clefts.
tt p
Cyst arising from:
• 1st pouch: Has an internal opening at junction of bony and cartilaginous external auditory canal.
• 2nd pouch: Internal opening at posterior pillar near base of tonsil.
h
1st branchial defect:
Cysts are lined by stratified squamous epithelium and have lymphoid tissue in the wall. They contain
straw coloured fluid. Commonly seen in third decade. Two per cent are bilateral.
Symptoms: Cystic swelling in lateral part of neck
r/
s .i
s
A B C
n
Figures 9-10A to C: Showing different position of branchial cysts
LIPOMA (FIGURE 9-11)
is a
r
It is a common benign subcutaneous tumour. May be seen over any part of body. Solitary or multiple.
It is soft, nonfluctuant, lobulated, freely mobile structure. The
e
edge of the swelling slips under the finger. It usually has no
p
symptom except for cosmetic purpose.
.
iv
CYSTIC HYGROMA (LYMPHANGIOMA) (FIGURE 9-12)
p
/: /
Cystic hygroma is usually present at birth and presents as
lobulated soft translucent swelling in the posterior triangle and
tt p
may spread to other parts of neck. It is developed due to
maldevelopment of jugular lymphatics. It may increase in size
at the time of upper respiratory tract infection.
h
Symptoms: Cosmetic deformity or respiratory distress if the
swelling compresses trachea.
Figure 9-11: A case of lipoma in
Signs: It is soft, cystic, multilobulated, transilluminant swelling. neck
Overlying skin is free.
r/
s .i
n s
is a
Figure 9-12: Photograph showing a case of cystic hygroma
r
CAROTID BODY TUMOUR (CHEMODECTOMA) (FIGURE 9-13)
e
The tumour arises from chemoreceptor cells of carotid bulb. There is usually a long history of slowly
. p
growing painless swelling in the region of carotid bulb.
On palpation they are small, firm, oval, pulsatile masses which
iv p
reduce on compression and then refill synchronous with pulse.
A bruit may be heard over swelling. They can be moved in
/: /
horizontal but not vertical direction.
Diagnosis: By carotid angiography and CT scan.
tt p
Treatment:
• If growth is slow and no symptoms wait and watch policy.
• Surgical excision if lesion extends in oral cavity or causes
h
symptoms.
LYMPHOMAS
Lymphoma is a term used to describe primary lymphoreticular
malignancy. It can affect head and neck region.
Figure 9-13: A case of carotid
body tumour
Types
1. Hodgkin
2. Non-Hodgkin lymphomas.
Patient may have weight loss, night sweats and other systemic symptoms.
Neck glands are multiple, discrete, firm, rubbery in consistency. Tonsils, liver/spleen may be
enlarged.
Diagnosis: By aspiration cytology/biopsy. Dorothy reed cells seen in Hodgkin lymphoma.
Treatment: Radiotherapy/chemotherapy.
SECONDARY DEPOSITS IN NECK (FIGURE 9-14)

They may arise from malignancy of any organ in head and neck region. They may present as solitary
or multiple hard mass/es in neck, which may be mobile/fixed to the deeper structures. Fungation is
quite common in malignant lesion of neck. They may compress over trachea, oesophagus or cranial
nerves and result into dyspnoea, dysphagia, or various types of cranial nerve palsies.
Diagnosis: By aspiration cytology. Primary should be searched and diagnosed. If needed Pan-
endoscopy is done. When primary is not detected, biopsy may be taken empirically from base of
tongue, fossa of Rosenmuller, pyriform sinus Tonsillectomy may be done. If this too does not confirm
the primary, the case is labeled as ‘occult primary’ with secondaries in neck.
Figure 9-14: Showing fungated secondaries

Treatment: Radical neck dissection if growth is resectable + excision of primary lesion, if detected.
Radiotherapy± chemotherapy if growth is not operable.
Chemotherapy if the growth is fungating/inoperable.
LARYNGOCOELE (FIGURES 9-15 TO 9-17)

• It is air containing sac arising from laryngeal ventricles.
• Unilateral or bilateral.
• The air sac comes out of larynx through thyro-hyoid membrane.
• Aetiology: Not exactly known. More common in blowers.
• Types: Internal/external or mixed laryngocoele.
• Symptoms: Hoarseness, neck swelling, stridor or dysphagia if pressure symptoms develop.
• Signs: Air containing sac coming out of thyro-hyoid membrane may become prominent after
performing valsalva. Sac can be emptied on compression. X-rays show air filled sac.
• Treatment: Surgical excision.
Figure 9-15: Clinical photograph—laryngocoele Figure 9-16: X-ray laryngocoele

Figure 9-17: Laryngocoele—lateral view X-ray
CLINICAL FEATURES OF COMMON NECK LESIONS

Site Shape Edge Pulsa- Moves with Moves with Over- Consis- Fluctua- Transillu- Impulse Reduci- Compressi- Any other
tions deglutition protrusion lying tancy tion mination on cough bility bility
of tongue skin
Dermoid Midline Spherical Distinct Ab No No N Cystic P No Ab No No
Sebaceous Any Spherical Distinct Ab No No Punctum+ Cystic P No Ab No No

cyst
Lipoma Any Any Distinct Ab No No N Soft Ab No Ab No No
Thyroglossal Midline Spherical Distinct Ab Yes Yes N Cystic P Yes Ab No No

cyst
Siloadenitis SM area Ab No No N Firm Ab No Ab No No Bimanually

palpable
Carotid Carotid Tri Spherical Present No No N Firm Ab No Ab No No Moves

body vertically
tumour only
Cystic Post. Tri Ab No No N Soft/cystic P Yes Possible No Yes hygroma
Pharyngeal Post. Tri Ab No No N Soft Ab No Ab Yes No Gurgling

pouch on pressure
Laryngocoele Carotid Tri Ab No No N Soft Ab No Yes Yes No Size - on

valsalva
Aneurysm Post. Tri Expansile No No N Variable Ab No Ab No No Bruit heard
Haemangioma Any Ab No No Reddish Soft Ab No Ab No Yes
Lymphangioma Any Ab No No N Soft Ab No Ab No Yes
Branchial cyst Carotid Tri Ovoid Distinct Ab No No N Soft/firm P No Ab No No
Abbreviations Ab Absent
N Normal
P Present
10
Examination of Salivary
Glands
Parotid Gland
Lesions in the region of parotid gland may be either swelling, ulcers, fistulas related to parotid itself,
or lesions of temporomandibular joint, soft tissue tumours arising from skin, muscle, nerve, lymph
node or blood vessel. Clinician has to use his knowledge to identify whether the lesion belongs to
parotid gland itself or to other structures.
A swelling in the region of parotid gland, which is in the close vicinity of ear lobule and even lifts
the ear lobule upwards, is likely to be due to parotid gland itself. Painless enlargement of parotid for
a very long duration is a typical feature seen in pleomorphic adenoma of parotid.
Symptoms: Swelling in parotid region, pain in swelling, symptoms of facial nerve palsy (if present),
fever, malaise, dry mouth are some of the symptoms related to parotid gland.
Once you suspect that it is a parotid pathology, examination may be carried out as follows:
Inspection: Swelling should be examined in the same way other swellings in the body are examined,
i.e. extent, size, shape, surface, etc.
Palpation: Findings of inspection are confirmed on palpation including local temperature and tender-
ness, consistency of the swelling. Mobility of the swelling should be seen in normal situation and
with clenched teeth position (Figure 10-1). This would tell whether the gland is fixed to masseter
muscle or not.
Deep lobe of the parotid may be palpated by bimanual palpation after keeping one finger in the
mouth in front of anterior pillar pressing laterally and other finger externally behind the angle of
mandible.
Figure 10-1: Testing mobility of

parotid with clenched teeth
Opening of parotid duct (Stensen’s duct) can be seen after retracting the cheek by tongue spatula.
It lies in the cheek mucosa opposite the upper 2nd molar tooth. It may be red congested in inflammatory
conditions of parotid and may express few drops of pus in pyogenic conditions. The Stensen’s duct
can be palpated bimanually between thumb and index finger.
Examination of facial nerve: This should be carried out without fail in all swellings of parotid. Paralysis
of facial nerve in presence of parotid swelling usually indicates malignant lesion in the gland.
Examination of lymph nodes: The parotid gland drains into pre-auricular, post-auricular and
submandibular lymph nodes which ultimately drain into deep cervical group of lymph nodes. Hence
in all cases of parotid disease the lymph node palpation in the above mentioned areas should be
done.
Common conditions affecting parotid glands:
1. Acute parotitis
• Viral ( Mumps)
• Bacterial (Suppurative parotitis)
2. Parotid tumours
• Benign, e.g. pleomorphic adenoma (mixed parotid tumour), Warthin’s tumour
Examination of Salivary Glands 175
• Malignant, e.g. adenoid cystic carcinoma, adenocarcinoma, malignant pleomorphic adenoma,
squamous cell carcinoma, etc.
Acute parotitis may be due to viral infection and is known as mumps. Common in children. There
is a short history of swelling in parotid region usually bilateral. Pain may be associated. In some
cases, submandibular glands are also inflammed. Symptoms and signs of toxaemia, i.e. fever,
tachycardia, dry coated tongue, malaise may be there. Mumps is self-limiting disease. It subsides
within 7 to 10 days. Few males may develop orchitis.
Suppurative parotitis may be seen in elderly diabetic, chronically ill or immuno-compromised
patients. There may be swelling in parotid region with symptoms and signs of toxaemia. Pus may be
collected below the parotid fascia, but fluctuation is a late symptom as the fascia is very tough.
Treatment: Antibiotics, anti-inflammatory drugs and I and D.
Pleomorphic Adenoma (Figure 10-2)

This is a benign painless growth arising from myoepithelial cells in parotid gland. It may progress
very slowly. It is a firm lobulated structure seen in parotid region. Malignant transformation is
known. When parotid swelling changes its size suddenly or becomes painful or facial nerve palsy
develops or gets fixed to the masseter muscle or skin, malignant change should be suspected.
Figure 10-2: Showing pleomorphic

adenoma of parotid
Treatment: No medical treatment. Superficial parotidectomy if tumour is in superficial lobe. Total
parotidectomy if deep lobe is involved or facial nerve is involved. Few patients may develop recurrence
after surgical removal.
Submandibular Gland (Figures 10-3A and B)

Submandibular gland lies in the submandibular triangle. Lesions that affect this gland may be acute
and chronic sialoadenitis, stone in the submandibular gland, malignancy or salivary fistula. Swelling
in the submandibular area may be due to lymph node enlargement in that area or lesions of
submandibular gland or other structures in that area. For proper diagnosis, examination of the
submandibular gland should be done carefully.
Inspection: Submandibular area can be inspected by asking the patient to extend his neck. One can
look for fistula, sinus or ulcer in this area. Then the patient is asked to open his mouth and lift his
tongue towards the hard palate. This shows two openings of submandibular ducts along both the
sides of frenulum lingue. In infective conditions, the openings may show congestion and/or discharge.
If you suspect a stone in the gland give the patient a lemon or vitamin C tablet to chew. This would
give rise to a painful swelling in the submandibular area. Because of obstruction of stone the salivary
secretion of gland remains collected in the gland itself.
A B
Figures 10-3A and B: (A) Submandibular swelling, and
(B) Palpation of submandibular gland and duct
Examination of Salivary Glands 177
Palpation:
Procedure: Left hand’s finger is kept over the skin of submandibular triangle and index finger of right
hand is passed below the tongue in the floor of mouth and submandibular gland is palpated
bimanually. It is normally a soft structure and can be easily differentiated from submandibular
lymph node. A stone may be palpated in the Wharton’s duct by palpating along the duct in the floor
of mouth.
Submandibular Gland Calculus (Figure 10-4)

Calculus is more common in the submandibular gland as compared to parotid gland.
Reasons:
1. Secretions of submandibular gland contain more calcium and magnesium.
2. The duct is long tortuous in course and has to work against the gravity to drain the secretions.
For these reasons stasis of secretions is more common in submandibular gland which may result into
stone formation.
Symptoms: Painful swelling in the submandibular area, which may increase in size at the time of
taking food.
Signs: Swelling in the submandibular area. Stone may be palpated in the gland itself or in the course
of the Wharton’s duct.
Figure 10-4: Sialography showing submandibular duct

Investigations: Apart from routine investigations submandibular gland silography may be advised,
which gives an idea about the size, shape of the Wharton’s duct and stone if any.
Treatment:
1. Milking of the stone.
2. Removal of stone surgically.
3. Removal of the gland itself if stone formation is recurrent or more than one stones are found or
stone found in the gland.
NB:
• Tumours arising from deep lobe of parotid gland may present as parapharyngeal swelling.
• Ectopic salivary tumours from minor salivary glands may arise anywhere in oral cavity but
particularly over hard palate.
SECTION C
11
Diseases of Oesophagus
Oesophagus is a fibromuscular tube approximately 25 cm in length starting from hypopharynx and

ending in stomach. This structure is not available for clinical examination and hence one has to rely
more on the investigations to diagnose diseases of this organ.
Symptoms
1. Dysphagia/odynophagia/burning sensation
2. Regurgitation
3. Bleeding
4. Respiratory symptoms
5. Foreign body impaction.
Dysphagia
Patients vaguely describe this complaint. One should try to elicit the correct information. It may be
difficulty during swallowing, pain during swallowing or burning sensation during swallowing or just
a retrosternal burning. And one can get various permutations and combinations of these symptoms.
Any disease affecting tongue, oral cavity, floor of mouth, tonsil, etc. may cause dysphagia and
hence the symptom of dysphagia may not point us towards oesophagus. However, if one goes into
the details of the history of dysphagia some clue may be obtained. Say for example, inflammatory
lesions of oral cavity give rise to dysphagia in the beginning of act of swallowing. Lesion in upper
part of oesophagus may cause sense of obstruction to food passage along with pain and to pass the
food bolus down, patient has to make voluntary acts of swallowing. Lesion in the lower part of
oesophagus may cause sense of discomfort while food is passing down.
Strictures in the oesophagus may cause sense of obstruction during swallowing but usually there
is no pain. Stricture in upper part of oesophagus may result into spill over of the food to larynx,
resulting into severe bout of cough. Patients with neuromuscular disorders experience more difficulty
to liquids than to solids, as liquids may spill over. Total obstruction may result into malnourishment
and cachexia.
Candidial oesophagitis may cause painful swallowing.
Regurgitation
Undigested food may return to mouth due to obstruction in the oesophagus down below. The amount
of regurgitation may be copious and foul smelling in achalasia cardia and small in quantity in
pharyngeal pouch. Acid regurgitation from stomach may cause burning sensation in throat, chest
and back.
Bleeding
Bleeding from oesophagus may be scanty due to injury and malignancy but copious in amount in
case of oesophageal varices. One should also keep in mind the bleeding disorders and leukaemia.
Respiratory Symptoms
Liquid/solid regurgitation may result into spill over to the larynx and may even be aspirated. This
may give rise to severe bout of cough. Recurrent regurgitation or neurological lesion of larynx like
cord palsy may accelerate the process of aspiration pneumonia.
Congenital oesophageal atresias are usually associated with tracheo-oesophageal fistulas. And
these children do present with aspiration pneumonia, which may be fatal.
FB in Oesophagus
• Common in children.
• May be seen in old people due to dental factors.
Diseases of Oesophagus 181
CLINICAL EXAMINATION
• When you suspect that the disease is oesophageal in origin look for evidence of wasting or
dehydration.
• Complete ENT examination comprising of oral cavity, pharynx, indirect laryngoscopy, examination
of neck and thyroid should be done carefully. Look for laryngeal crepitus, which may be lost in
postcricoid malignancy.
• General examination should be carried out specially looking for weight loss, anaemia, dehydration,
hypotension, nutritional deficiency, etc. This can also give clue about severity and duration of
obstruction.
Patient should be observed while taking liquids/solids.

This would give much more additional information.
INVESTIGATIONS
For diagnosis and confirmation of oesophageal diseases the following two investigations are routinely
carried out.
a. Radiography
b. Oesophagoscopy.
Radiography
i. X-ray neck AP and lateral
ii. X-ray chest PA and lateral
iii. Barium swallow.
Out of these the barium swallow is the most common and useful investigation. Barium study may
give information about site of obstruction, severity of obstruction, type of obstruction and also gives
a chance to study peristaltic waves.
X-rays of neck may help to diagnose conditions like retropharyngeal abscess, cervical spondylosis,
kyphoscoliosis which may be responsible for dysphagia in some cases.
X-ray chest may show cardiac hypertrophy, mass in lung fields which also contribute to
dysphagia.
Oesophagoscopy
This is a procedure to examine the oesophagus by rigid or flexible oesophagoscope.
Indications:
X. Diagnostic
• To investigate dysphagia
• To investigate haematemesis
• To confirm FB in oesophagus.
Y. Therapeutic
• To remove FB
• Control of bleeding oesophageal varices
• To dilate oesoephageal strictures.
Contraindications: Today, there are as such no contraindications except corrosive poisoning and
severe trismus. One can safely perform flexible oesophagoscopy even in debilitated patients and in
patients having spine lesions and aortic aneurysm.
Anaesthesia: General or local.
Position:
Boycee’s position: Patient is in supine position on operation table. Patient’s head is raised by 15 cm
above table level and head end of table is dropped. This flexes the neck. Extension is given at atlanto-
axial joint. The first assistant sits on a stool on left side of patient winding his right arm around the
patients neck and at the same time retracting the lips of patient as and when required. He supports
his hand on the crossed legs.
The second assistant is standing on the right side of patient and pressing the shoulders of patient
against operation table as and when needed.
The surgeon is standing at head end of table and trolley is kept on right side of surgeon. Anaesthetist
is standing beside the first assistant along with his anaesthesia equipment.
This position is standard position for all peroral rigid endoscopies. Because this position brings
the inlet of larynx and pharynx in the direct visual axis of the surgeon, it gives best possible vision.
Procedure (Figure 11-1):
Oesophagoscope is held like a pen in right hand and negotiated from right side of mouth along the
tongue till pyriform fossa is identified. At the cricopharyngeal opening one should wait till sphincter
is relaxed and then scope is furthered. Scope should be negotiated further without using force in a
‘feathery touch’ manner. When oesophagoscope enters cardiac end of stomach, the colour of mucosa
is changed to pink, the mucosal rugosity is increased and gush of liquid is noticed from stomach.
During the journey of oesophagoscope through oesophagus, one should look for congestion of mucosa,
Figure 11-1: Diagrammatic representation showing OT

personnel arrangement during peroral endoscopy
ulcer, growth, foreign body or stricture as the case may be. Scope should be removed slowly and
mucosa should be examined while removing the scope.
Complications: (common with rigid oesophagoscopy)
1. Perforation of oesophagus.
2. Injury to teeth, lips, gums and cheek.
3. Cardiac arrest.
4. Rupture of aneurysm of aorta.
Diseases of Oesophagus
A. Congenital
• Atresia of oesophagus
• Tracheo-oesophageal fistula
• Oesophageal stenosis
• Short oesophagus.
B. Traumatic
C. Inflammatory
• Fungal
• Non-specific oesophagitis.
D. Miscellaneous
• Hiatus hernia
• Achalasia cardia
• Pharyngeal pouch
• Strictures
• Foreign body in oesophagus.
E. Neoplastic
• Carcinoma oesophagus.
Common oesophageal conditions in ENT practice are:
Foreign bodies in oesophagus (Figures 11-2 and 11-3):
Age: Common in children and old age. In old age due to poor peristaltic power food bolus may get
impacted in oesophagus. Dentures used by old people may get dislodged and result into foreign
body in oesophagus.
Figure 11-2: Photograph showing irregular Figure 11-3: Barium swallow showing
bone removed from oesophagus ‘ Mega’ oesophagus
Food: Fish bones, bony pieces in minced meat are notorious to cause foreign body in oesophagus.
Site: The usual site where the FB gets impacted is cricopharynx, but in oesophagus FB may stuck up
at the site of stricture or at the site of natural constrictions, i.e. at the level of crossing of aorta, left main
bronchus, diaphragm.
Symptoms: Dysphagia is the predominant symptom. It may be minimal to begin with however as
surrounding tissue oedema develops due to FB, dysphagia progresses. It may progress to the level
that patient cannot swallow his own saliva.
Signs: Neck movements may be painful and tender spot may be located.
Diagnosis: Usually confirmed by X-rays.
Treatment: Oesophagoscopy and FB removal.
Achalasia cardia: (cardiospasm)
Aetiology: Not exactly known.
Pathology: Degeneration of Auerbach’s plexus in lower part
of oesophagus, resulting into unco-ordinated peristaltic
movements. Lower sphincter of oesophagus fails to relax
in response to food bolus. This results into retention of food
and distension of oesophagus, producing mega
oesophagus.
Symptoms: Sense of fullness in epigastrium, dysphagia,
regurgitation of food, loss of weight.
Barium swallow may show dilated oesophagus and
smooth narrowing at the lower end. Barium picture is
typically known as Parrot beak appearance (Figure 11-4).
Oesophagoscopy shows large dilated and at times
ulcerated oesophagus
Treatment: Figure 11-4: Barium swallow showing
• Conservative: Regular dilatation of stricture with the help mucosal irregularity and obstruction in
of mercury bougies. Various other methods of dilatation 1lower 1/3 of oesophagus giving a typical
“rat tail appearance”
are in use.
• Operative: Heller’s operation—a longitudinal incision at cardio-oesophageal junction in muscular
coat of oesophagus which is done without cutting mucosa of oesophagus.
Carcinoma of oesophagus:
Aetiology: Not exactly known. However, chronic oesophagitis, fibrous stricture, achalasia cardia and
Paterson Brown Kelly syndrome are considered as predisposing factors.
Age: Usually after the age of 50 years.
Pathology: Squamous cell carcinoma is most common. Adenocarcinoma may be seen at cardiac end
of oesophagus.
Symptoms: Progressive dysphagia. Dysphagia, initially for the solids may end up with total dysphagia.
Signs: Dehydration, cachexia, weight loss are evident.
Barium swallow study may show hold up and irregularity of lumen.
Oesophagoscopy should be done in all suspected cases. And biopsy obtained from suspected
tissue should be sent for histopathological examination.
Treatment:
1. Surgery
2. Radiotherapy
3. Chemotherapy
4. Combination therapy.
Food intake should be maintained either by Ryle’s tube or Souttar’s tube. If negotiation of feeding
tube is not possible then feeding gastrostomy/jejunostomy is done. Palliative radiotherapy is all that
is possible in late cases. However in operable cases, oesophagectomy with gastric pull up can be
done. Chemotherapy can be advised in combination with radiotherapy or independently. Overall
prognosis of carcinoma oesophagus is gloomy.
12
Tracheo-bronchial Tree
ANATOMY
Trachea is cartilaginous and membranous tube measuring about 10 to 11.5 cm in length in adults.
Trachea starts from C6 level and ends at T5 level where it divides into right and left main bronchi.
This bifurcation is at a distance of 25 cm from upper incisor teeth in adults.
Right main bronchus (RMB) is further subdivided into right upper lobe (RUL) bronchus, right
middle lobe (RML) bronchus and right lower lobe (RLL) bronchus. Similarly, left main bronchus
(LMB) is subdivided into left upper lobe (LUL) bronchus, lingular lobe and left lower lobe (LLL)
bronchus. Further ramification of bronchi is shown in Figure 12-1.
Examination of Trachea and Bronchi

PALPATION OF TRACHEA IN NECK (FIGURE 12-2)
Only a small part of trachea in the neck is accessible for clinical examination. Patient is sitting
comfortably in chair or lying in bed with his head straight. Extension of neck is avoided as far as
possible. Index and ring fingers are kept over sternoclavicular joints of both sides and middle finger
enters gently in suprasternal space of burn. The finger palpates trachea, tracheal rings and its relation
with lower ends of sternomastoid muscle. This gives you information whether trachea is central or
not. Normally it is centrally located. But may be slightly shifted to right side. Conditions that pull or
push the mediastinum may shift the position of trachea.
Part of trachea behind sternum is not available for clinical examination and should be assessed
by:
RMB (Right main bronchus) – RUL (Right upper lobe)
1. Apical
2. Posterior
3. Anterior
RML (Right middle lobe)
4. Lateral
5. Medial
RLL (Right lower lobe)
6. Apical
7. Medial basal
8. Anterior basal
9. Lateral basal
10. Posterior basal
LMB (Left main bronchus) – LUL (Left upper lobe)
1 & 2. Apico posterior
3. Anterior
Lingular
4. Superior
5. Inferior
LLL (Left lower lobe)
6. Apical
7. Medial basal (absent )
8. Anterior basal
9. Lateral basal
10. Posteior basal
Figure 12-1: Showing broncho-pulmonary segments
Figure 12-2: Showing how to palpate

trachea in neck
Tracheo-bronchial Tree 189
1. Radiography
2. Bronchoscopy
3. Mediastinoscopy.
Symptoms related to trachea and bronchi may be:
1. Dyspnoea
2. Cough ± expectoration
3. Cyanosis
4. Stridor
5. Apnoea
6. FB in trachea/bronchi
7. Haemoptysis.
• Dyspnoea is uncomfortable respiration. It may be due to obstruction in respiratory passage or due
to metabolic disorders causing air hunger.
• Cough may be dry or wet. When it is with expectoration, details of expectoration should be asked.
It may be scanty in acute bronchitis. It may be coloured, copious and foul smelling in bronchiectasis.
It may be blood stained in malignancy and frothy in allergic bronchitis.
• Stridor ( described elsewhere).
• Apnoea: It is complete stoppage of respiration. Usually it is central in origin. However it may be
seen during tracheostomy.
• Haemoptysis: Bleeding or blood stained sputum is known as haemoptysis.
Causes: Tuberculosis of lungs, bronchial malignancy, carcinoma of larynx, etc.
Diseases of Trachea and Bronchi

A. Congenital—Stenosis, tracheo-oesophgeal fistula, tracheomalacia.
B. Traumatic—Road accidents, throttling, etc.
C. Inflammatory—Tracheitis, bronchitis, laryngotracheobronchitis, bronchiectasis.
D. Neoplastic—Multiple papillomas, carcinoma bronchus.
E. Miscellaneous—Scleroma of trachea and bronchi, FB, etc.
FOREIGN BODIES IN TRACHEA AND BRONCHI

Foreign body is more common in bronchus as compared to trachea.
It is more common in children as compared to adults.
It is more common in right main bronchus than left.
Because
1. Right main bronchus is direct continuation of trachea.
2. It is wider than left bronchus.
FACTORS FOR FB LODGEMENT IN RESPIRATORY TRACT

• Children put non-edible things like button, pencil, and rubber in the mouth.
• In children seeds of watermelon or custard fruit slip easily in respiratory tract while eating the
fruit.
• Some toys have a valvular whistle. Children blow the whistle by sucking in air through it. In this
manoeuvre whistle dislodges from the toy and enters respiratory tract of child.
• In adults dentures, loose teeth and dental material may slip into respiratory passage inadvertently.
• Road accidents may cause FB lodgement in respiratory tract.
• It is also common when person is under the influence of alcohol.
PATHOPHYSIOLOGY
A. When a FB is hygroscopic or large, air can neither enter in (ingress) nor can escape out (egress).
This is known as STOP VALVE mechanism. It may result into collapse of concerned lung. When
infection sets in, consolidation may be seen (Figure 12-3A).
B. When a FB is small enough or FB is having a lumen [whistle, broken tracheostomy tube], it may
allow ingress and egress both. This is known as BYPASS VALVE. This causes wheeze or rales. But
usually no lower respiratory tract changes (Figure 12-3B).
C. During inspiration the bronchi are dilated and may allow ingress of air. But during expiration the
lumen of bronchi is narrowed and egress is not possible. This is known as BALL VALVE mechanism.
It causes air to be trapped in the lower respiratory tract and may result into emphysema or
pneumothorax (Figure 12-3C). And thus depending upon size, site and duration of FB, collapse,
consolidation, emphysema or pneumothorax may develop.
Symptoms: Dyspnoea, cough, stridor, cyanosis, tachypnoea, fever are the common symptoms in FB
respiratory tract.
Depending upon pathophysiological changes one would get the clinical picture.
Figure 12-3A Figure 12-3B Figure 12-3C

No ingress Ingress positive Ingress positive during inspiration
No egress Egress positive Egress negative during expiration
( STOP VALVE ) ( BYPASS VALVE) ( BALL VALVE )
The picture may be deceptive and mimic lower respiratory tract infection, like tracheobronchitis,
tuberculosis and lung abscess. Utmost care is taken to elicit the history of FB inhalation.
It may be old history, which child has forgotten or is afraid of telling it.
Hence with the slightest doubt, FB should be suspected and child investigated for FB.
A duplicate of FB should always be asked if available.
Investigations (Figures 12-4 to 12-8)

1. X-rays chest lateral and PA views.
2. Diagnostic bronchoscopy.
Treatment: Removal of FB by bronchoscopy.
Position: Boycee’s position.
Anaesthesia: Usually general anaesthesia.
Procedure: Though flexible fibreoptic bronchoscope can remove some of the foreign bodies, rigid
bronchoscope should be preferred over the flexible. Ventilating bronchoscopes with telescopes
give good illumination, vision and safety during anaesthesia. Appropriate sized bronchoscope is
taken.
Figure 12-4: Showing FB in right main

bronchus (white arrow)
Figure 12-5: Showing fish removed from the RMB
Patient’s mouth is opened and appropriate sized bronchoscope is negotiated through right side of
mouth along the tongue till you reach posterior 1/3 of tongue. Bronchoscope is then taken in the
centre and negotiated further. Epiglottis is identified and crossed. Inlet of larynx is seen and
A B
Figures 12-6A and B: (A) Rigid bronchoscopy set, (B) Flexible bronchoscope
Figure 12-7: X-ray chest PA view showing hair-pin Figure 12-8: FB seen after removal
in right main bronchus
bronchoscope is negotiated through the cords in trachea. As you reach to the lower end of trachea, a
vertical ridge is seen. It is carina and you can locate right and left main bronchi on its two sides.
Scope is negotiated in main bronchus and looked for any foreign body, pus discharge, secretions,
bleeding, tumour, ulcer, etc. depending upon the clinical diagnosis. Secretions may be sent for culture
and sensitivity or AFB culture, or even for cytology. Biopsy may be taken in suspected cases and sent
for histopathology. If the tumour mass is very small even brush biopsy may be useful. Foreign body
is removed with the help of foreign body removal forceps. Tracheostomy trolley should be kept ready
during the procedure.
Complications
1. Cardiorespiratory arrest—more common in hypoxic children.
2. Injury to teeth, tongue, palate or pharynx and cervical vertebrae.
3. Difficulties in removal of FB may be experienced.
BRONCHIECTASIS
It may be associated with ‘Kartagener’s syndrome’ a triad of bronchiectasis, chronic sinusitis and
dextrocardia. It may be associated with retained FB, strictures or tumours.
Copious foul smelling cough with expectoration is the classical picture.
CARCINOMA BRONCHUS
Aetiological factors: Chronic mucosal irritation by smoking, environmental pollution, radioactive
substances in working place, arsenic, chromate and nickel exposure, pneumoconiosis, chronic
bronchitis, etc.
Pathology: Squamous cell carcinoma, adenocarcinoma, anaplastic carcinomas are commonly found.
Symptoms: Cough, discomfort in chest, pain in chest, haemoptysis, dyspnoea, weight loss, pyrexia
are commonly seen.
Investigations:
1. X-ray chest PA and lateral views are most important
2. Bronchoscopy
2. CT scans
3. FNAB (Fine needle aspiration biopsy)
4. Exploratory thoracotomy.
Treatment:
1. Lobectomy or pneumonectomy
2. Radiotherapy
3. Chemotherapy.
• Examination of Cranial Nerves
13
Examination of Cranial
Nerves
Diseases like cholesteatoma, temporal bone, can give rise to facial nerve palsy. Similarly large
neck masses can cause compression over cranial nerves resulting into palsy. Hence, it is mandatory
for the student posted in ENT to know about various cranial nerves and method of examining these
nerves.
Olfactory Nerve
Basic function of olfactory nerve is sense of smell or olfaction. The olfactory system is made up of the
olfactory epithelium, bulbs, and tracts, together with the olfactory areas in the brain.
Olfactory nerve is not tested in routine course of cranial nerve examination. However in case of
anosmia after a head trauma, it should be examined.
CLINICAL EXAMINATION (FIGURES 13-1A TO C)
• Examine the nose for nasal patency. Rule out any DNS, polyp, turbinate hypertrophy or
any other local nasal disease.
• Ask the patient to close his eyes.
• Each nostril is tested separately for peppermint, camphor, and rose-water to test the
sense of smell.
Causes of anosmia: Blocked nasal passage due to any cause, head trauma, Parkinson’s disease, and
frontal lesion like glioma or meningioma.
Figure 13-1A: Bottles containing aromas Figure 13.1B: Blind folding of patient
Figure 13-1C: Testing sense of smell
Optic Nerve
It is beyond the scope of this book to give detailed optic nerve testing. A brief outline is given here
Visual acuity: Can be tested with the help of a Snellen’s eye chart.
• Position the patient 20 feet in front of the Snellens’s eye chart (or hold a Rosenbaum
pocket card at a 14-inch “reading” distance).
• Ask the patient to cover one eye at a time with a card.
• Ask the patient to read progressively smaller letters until he can go no further.
• Record the smallest line the patient reads successfully (20/20, 20/30, etc.)
• Repeat the test in other eye.
Examination of Cranial Nerves 199
Visual field:
• Ask the patient to look at your eyes.

• Put your hands out, on both sides approximately 50 cm apart and 30 cm above eye
level.
• Slowly move your finger medially till patient can see your finger. Thus map out the
visual field.
• Repeat the test with fingers 30 cm below eye level.
The examiner can interpret his own field of vision when he sees the finger entering in his view.
And based on the results given by patient, clinician can localise the defects in field of vision.
Colour vision: This can be tested by Ishihara’s chart (Figures 13-2 and 13-3).
Figure 13-2: Ishihara’s chart Figure 13-3: Showing effects of lesions in visual
pathway
Pathological Lesions
1. A pre-chiasmatic lesion results in ipsilateral blind eye.
2. A chiasmatic lesion can result in bitemporal hemianopia.
3. Post-chiasmatic lesions proximal to the geniculate ganglion can result in left or right homonymous
hemianopia.
Lesions distal to the geniculate ganglion can result in upper (4) or lower (5) homonymous
quadrantopia.
The Pupillary Light Reflex
• Ask the patient to look at distance.

• Shine a bright light obliquely into each pupil in turn.
• Look for both the direct (same eye) and consensual (other eye) reactions.
• Record pupil size in mm and any asymmetry or irregularity.
Light shown in the ipsilateral eye will cause constriction of both pupils provided both IInd and
IIIrd cranial nerves are functioning properly.
Pupillary Accommodation
• Hold your finger about 10 cm from the patient’s nose.

• Ask him to look at your finger and at distance alternately.
• Observe the pupillary response in each eye.
Oculomotor Nerve
As the name implies, the oculomotor nerve plays an important role in eye movements. In addition to
the general motor component that innervates extraocular muscles, the third nerve also contains
visceral efferents (parasympathetic) that innervate intrinsic ocular muscles. The nerve also innervates
the levator palpebrae superioris that elevates the upper eyelid.
PUPILLARY LIGHT REFLEX

Light entering the eye causes signals to be sent along the optic nerve to the pretectal region of the
midbrain to elicit pupillary constriction. Light shown in either eye causes constriction of the pupil in
the same eye (direct light reflex) and also in the other eye (consensual light reflex). When the
parasympathetic fibres in the third nerve are damaged, light shown in the affected eye does not cause
constriction of its pupil (loss of direct light reflex). However, the light causes pupillary constriction of
the opposite, unaffected eye (preservation of consensual light reflex).
Symptoms: Ptosis, diplopia,
Signs: Infero-lateral displacement of ipsilateral eye, mydriasis.
Clinical Examination (Figure 13-4)
• Observe for ptosis

Tests for extraocular muscles
• Stand in front of the patient at 3 to 6 feet distance.
• Ask the patient to follow your finger with eyes without moving his head.
• Check gaze in the six cardinal directions using a cross or “H” pattern.
• Check convergence by moving your finger towards the bridge of the patient’s nose.
Oculomotor nerve lesions:
Causes:
• # Base skull
•  Intracranial pressure
• Aneurysm or tumours compressing the nerve.
Figure 13-4: Diagrammatic representation of

testing extraocular muscles
Trochlear Nerve
The trochlear nerve is a motor nerve that innervates a single muscle in the orbit, the superior oblique.
Since the trochlear nerve crosses to the opposite side, each superior oblique muscle is innervated by
the contralateral trochlear nucleus.
Symptoms:
• Extortion of the ipsilateral eye
• Severe diplopia with attempted downgaze, which improves when head turned to contralateral
side.
Clinical examination: Already described in tests for extraocular muscles.
Causes for lesion:
• Fracture of the sphenoid wing
• Intracranial haemorrhage
• Neoplasm or aneurysm.
Trigeminal Nerve (Figure 13-5)

INTRODUCTION
As the name implies “trigeminal” has three major
divisions, the ophthalmic, maxillary and mandibular.
It is the major sensory nerve of the face but also has a
motor component. The trigeminal nerve emerges on the
midlateral surface of the pons as a large sensory root
and a smaller motor root. Its sensory ganglion, the tri-
geminal ganglion sits in a depression in the floor of the
middle cranial fossa. The three divisions of V nerve arise
from the ganglion.
APPLIED ANATOMY
• Ophthalmic branch (V1)
Passes forward in dura mater on lateral wall of
cavernous sinus and then subdivides into frontal, Figure 13-5: Sensory distribution of
lacrimal and naso-ciliary branches as it passes trigeminal nerve
through superior orbital fissure. It supplies to the skin of upper nose, eyelid, forehead and scalp.
It also supplies cornea, conjunctiva, mucosa of frontal, ethmoidal and sphenoidal sinus, upper
part of nasal cavity.
• The maxillary nerve (V2)
Arises from the gasserian ganglion and exits the skull base through foramen rotundum into
pterygopalatine fossa. It innervates lower eyelid, dura of middle cranial fossa, temple area, upper
cheek and adjacent part of nose and upper lip, mucosa of upper mouth and nose, roof of pharynx,
maxillary, ethmoid and sphenoid sinuses, gums teeth and palate.
• Mandibular division (V3)
It arises from gasserian ganglion and exits the skull base through foramen ovale into infratemporal
fossa. It divides and lingual branch receives pre-ganglionic fibres from chorda tympani of facial
nerve. The parasympathetic fibres enter the submandibular ganglion as secretomotor fibres for
submandibular gland.
• Sensory—Branches of V3 supply dura of middle and anterior cranial fossa, teeth and gums of
lower jaw, mucosa of cheek and floor of mouth, epithelium of anterior 2/3 of tongue, temporo-
mandibular joint (Figure 13-6)
• Motor—Muscles of mastication, i.e. masseter, temporalis, medial and lateral pterygoid. It also
supplies anterior belly of diagastric mylohyoid, tensor veli palatini and tensor tympani. These
muscles are responsible for initiation and co-ordination of act of swallowing.
Figure 13-6: Showing testing of

trigeminal nerve (sensory)
Sensory Functions
• Light touch and pain.
• Sit in front of the patient. Explain the test. Ask him to close the eyes.
• Take cotton wool and touch the various parts of the face supplied by V1, V2 and V3.
• Ask the patient to count every time he perceives a “touch”.
• Compare it with opposite side.
• Similar test done with the help of pinprick for pain sensation.
• Deficit if found, is mapped.
• Temperature can be similarly tested.
Corneal Reflex
Afferent for corneal reflex is naso-ciliary branch of V1 and efferent is the facial nerve. Touching the
cornea evokes a brisk contraction of orbicularis oculi (blinking). Because of interneural connections
the corneal reflex is bilateral, direct and consensual.
• Ask the patient to look up and away from you.

• Without the knowledge of patient, touch the cornea by twisted cotton wool, by
bringing it from temporal side.
• Watch both the eyes.
• Repeat on the other side.
Interpretation
Both eyes blink Normal
No blink on either side V1 lesion
No blink on one side 7th nerve lesion
Motor Function
• Inspect the muscles of mastication for wasting, and compare with opposite side.
• Ask the patient to clench his teeth and palpate masseter muscle bulk and compare it
with opposite side.
• Ask the patient to open the jaw against resistance.
• Unilateral pterygoid weakness causes the jaw to deviate to the weak side when mouth is opened.
• When patient tries to move the jaw from side to side, there is difficulty in moving it to the contralateral
side.
Trigeminal neuropathy:
Aetiology
• Skull #
• Tumour of the nerve
• Surgery on the face
• Lesions in cavernous sinus
• Lesions at petrous apex.
TRIGEMINAL NEURALGIA (TIC DOLOUREUX)

Aetiology: Not known. May be demylinating plaque, tumour, or post-herpetic lesion.
Symptoms: Sudden severe lanceting pain in lips, gums, cheek or chin. Brushing, washing of mouth
may provoke the attack. No sensory loss.
Treatment (if no precipitating cause found)
Medical—Carbamazepine 100 mg BD to begin with
Surgical—Phenol injection in the nerve. Radiofrequency rhizotomy.
Abducent Nerve
Abducent fibres originate from the brainstem at the anterior junction of the pons and medulla. It
passes through the cavernous sinus and exits through the superior orbital fissure where it innervates
the lateral rectus muscle. Contraction of lateral rectus muscle results in abduction of eye.
Symptom: Diplopia
Signs: Medial deviation of ipsilateral eye. No lateral movement of eye.
Diplopia improves if contralateral eye is abducted.
Causes of lesion:
• # Skull base
• Mass in cavernous sinus
• Aneurysm of vessel
• Raised intracranial tension due to any cause (This acts as false localising sign)
• Petrositis as a complication of CSOM (Gradenigo’s syndrome—otorrhoea, diplopia and retro-
orbital pain).
Facial Nerve
Facial nerve has following functions:
1. Motor function (supplies muscles of facial expression)
2. Secreto-motor function (lacrimal gland and submandibular gland)
3. Sensory function (taste function in anterior 1/3 of tongue).
MOTOR FUNCTIONS
Upper part of the face has motor supply from contralateral and ipsilateral motor cortex whereas lower
part has supply only from contralateral motor cortex. Motor fibres course dorsally from
the nucleus towards the floor of the fourth ventricle and then they loop around (from medial to lateral)
the abducent nucleus to form a slight bulge in the floor of the fourth ventricle (the facial colliculus).
Upper motor neuron lesions affect voluntary control of only the lower muscles of facial expression
contralateral to the lesion. Upper muscles of facial expression continue to function because the part
of the facial nucleus that innervates them still receives input from the ipsilateral motor cortex. Lower
motor neuron lesion results in paralysis of all the ipsilateral muscles.
Secreto-motor function: This is the parasympathetic component of the VIIth nerve which is responsible
for control of the lacrimal, submandibular, and sublingual glands, mucous glands of the nose pre-
ganglionic fibres come from superior salivary nucleus.
Sensory function: Taste sensation from anterior 2/3 of tongue is carried via chorda tympani nerve. A
small part in EAC is also having sensory supply from facial nerve.
• Observe the face at rest for any facial asymmetry

• Observe any facial tics, symmetry of eye blinking or eye closure
• Observe the patient during smiling.
Action: 1. Ask the patient to close his eyes
2. Ask the patient to wrinkle the forehead
3. Ask the patient to show his teeth
4. Ask the patient to blow out his cheek with lips closed
5. Ask the patient to whistle.
Action 1: Normal person can close his eyelids effectively, which cannot be opened up by using mild
force to open them. In infranuclear palsy, eyelid is not completely closed. Instead the eyeball rolls up.
This is known as Bell’s phenomenon (Figure 13-7)
Action 2: On the side of facial palsy patient cannot wrinkle his forehead (Figure 13-8A)
Action 3: Angle of mouth deviates towards normal side while showing teeth (Figure 13-8B)
Action 4: Patient cannot blow out his cheek as air escapes from affected side (Figure 13-8C)
These tests indicate the muscular weakness if any in facial nerve.
Figure 13-7: Action 1 Figure 13-8A: Action 2

Figure 13-8B: Action 3 Figure 13-8C: Action 4
SENSORY FUNCTION TESTING

Taste function testing:
• Close the eyes of the patient.
• Ask the patient to protrude out his tongue.
• Place sweet, salt, bitter and sour substances on one side of tongue one by one.
• Test the opposite side also.
Electrogustometry is used nowadays.
SECRETO-MOTOR FUNCTION
Schirmer’s test: Put a small piece of blotting paper under the lower eyelid on affected and non-affected
side. Remove blotting paper within 5 minutes. On affected side blotting paper may not be damped at
all or damped much less as compared to normal side.
Causes for lesion:
• Traumatic
Accidental—Temporal bone
Surgical—Surgery of middle ear, parotid and skull base.
• Inflammatory
• Viral (Herpes zoster oticus {Ramsay Hunt syndrome})
• Malignant otitis externa
• Cholesteatoma.
• Neoplastic—Cerebellopontine angle tumours, parotid tumours.
• Miscellaneous—Brainstem infarction, multiple sclerosis, idiopathic facial palsy (Bell’s palsy).
Vestibulo-cochlear Nerve
NB: It is beyond the scope of this book to give detailed examination of vestibulo-cochlear nerve. A
brief account is given. The tests given below are meant to assess vestibular and cochlear functions.
Figure 13-9: Diagrammatic representation of

facial nerve and its lesion at different sites GG—
geniculate ganglion, PC—pterygoid canal,
SPG—spenopalatine ganglion, ZN—
zygomatic nerve, GSPN—greater superficial,
petrosal nerve, LSPN—lesser superficial
petrosal nerve, OG—otic ganglion, V3—
mandibular nerve, NTS—nerve to stapedius,
CT—chorda tympani, LN— lingual nerve,
SMF—stylomastoid foramen, SMG—
submandibular ganglion
Effect of lesion at
1. No Lacrimation
No taste
2. Lacrimation intact This testing has a topographic value.
Taste lost It indicates the site of lesion clinically.
3. Lacrimation intact
Taste intact
This nerve has two different functions to perform:
A. Vestibular—Balancing of the body
B. Cochlear—Hearing.
Vestibular function is a complex function carried from vestibular apparatus (i.e. semi-circular
canals and labyrinth) to vestibular nerve, which enters, in vestibular nucleus in the floor of 4th
ventricle.
Pathology: Vestibular nerve may be affected by:
• Infection: Vestibular neuronitis, purulent labyrinthitis
• Trauma: # Skull base, surgery over labyrinth
• Toxic: Use of drugs like streptomycin, kannamycin
• Tumors: Acoustic neuroma.
Major symptoms of vestibular nerve affection are:
• Vertigo
• Vomiting
• Nausea.
Clinical Examination
• Ask the patient to stand errect with eyes open and eyes closed and observe whether patient is
waving to one or the other side.
• Ask the patient to walk in a straight line keeping minimum distance in two steps (eyes open and
closed) and observe waving.
• Romberg’s test
Originally described for patients with tabes dorsalis, is positive in patients with dorsal columm or
severe afferent polyneuropathy. A positve Romberg means that the patient shows a tendency to
actually fall on eye closure. Almost all patients with balance problems show a small to moderate
increase in body sway on eye closure. In acute phase of a peripheral vestibular disorder, Romberg
test will be positive, usually with an ipsilateral fall.
• Unterberger test
Patient’s eyes are closed and hands are stretched in front and he is asked to lift his left and right
foot alternately off the ground. Approximately 80 to 90 steps are repeated in a minute. During the
process patient deviates from his original position. This deviation is measured and concluded.
Rotation of more than 30°or forward/backward displacement of more than 1 metre is considered
as abnormal.
Normally a person gets feedback of his position from 3 receptors. One is labyrinth, other is eyes
and third is stretch receptor. Because of constant foot lifting, stretch receptors are eliminated and
with the eyes closed, these too do not give feedback about one’s position in the space and hence
patient has to rely totally on his vestibular apparatus. If there is defect in the vestibular apparatus
the patient deviates more.
• Positional testing
In this, patient is explained the test. He wears Frenzel’s glasses and then made to sit errect on an
examination table. Patient is asked to look at the clinician’s forehead and not to close the eyes.
Then suddenly patient’s head is lowered down by 30° and tilted to one side by 30° to 45°.
Patient’s eyes are observed for 15 seconds for any nystagmus. The test is repeated for other neck
position and the position that gives rise to vertigo/nystagmus or giddiness is noted down. Based
A B
C
Figures 13-10A to C: Showing different types of caloric responses
on this test a patient may be labeled as having “Benign Positional Nystagmus” or “Central
Positional Nystagmus”.
• Caloric testing (Hallpike and Dix test) (Figure 13-10A to C)
This is very important vestibular function test. Herein the cold and hot water is irrigated in the ear
canal to stimulate the labyrinth.
Pre-requisite: There should not be a drum perforation or wax in ear.
Procedure: Patient is lying in supine position on a table, and head is elevated by 30° so as to make
the horizontal semi-circular canal, vertical in position. Ear canal is irrigated with water having
temperature of 30°C and 44° C respectively. This causes change in the temperature of endolymph
and sets up convection currents in endolymphatic fluid, thereby stimulating the labyrinth and
vestibulo-ocular reflex is elicited. Nystagmus thus evoked has a slow and fast component and is
labeled by the direction of fast component. Cold water causes nystagmus to the opposite side and
warm water to the same side. This is popularly known as “COWS RESPONSE”. Duration of
nystagmus is noted and plotted on a graph called ‘calorigraph’. Normal duration of nystagmus is
1.5 to 2.5 minutes. A reduced response is known as canal paresis. Exaggerated response to one
side is known as directional preponderance.
• Tests like Electronystagmography (ENG) or Videonystagmography (VNG) Cranio-corpography,
Posturography, Vestibular Evoked Myogenic Potentials (VEMP) can be done whenever necessary.
COCHLEAR NERVE
Cochlear nerve testing can be done by:
• Whispering test, tuning fork tests.
• Pure tone audiometry, evoked response audiometry (ERA), cochleography
All these tests except ERA are given in chapter on ear examination.
Glossopharyngeal Nerve
Glossopharyngeal nerve exits the brainstem medulla at the post-olivary sulcus. It then travels with
vagus nerve and accessory nerve and exits the cranium through the jugular foramen.
Motor nuclei are located in the nucleus ambiguus in the medulla and supply to stylopharyngeus muscle.
Sensory supply lining of middle ear cavity, Eustachian tube, mucosa of pharynx, tonsil and conveys
taste sensation from post 1/3 of tongue.
Secreto-motor supply for the parotid gland.
Gag reflex: (IXth nerve afferent, Xth nerve efferent)
Touching the tonsil or pharynx with swab stick causes reflex contraction of palatal and pharyngeal
muscles leading to elevation of palate and pharynx.
• Take a cotton swab stick and look for tactile sensation over palate, upper pharynx
and tonsil.
• Touch tonsil or pharynx with cotton swab each side separately and elicit ‘gag reflex’.
• Taste sensation over posterior 1/3 of tongue is usually not tested.
• Oculocardiac reflex (slowing of heart rate on orbital compression) is usually not tested.
• Carotid reflex (slowing of heart rate and pulse on carotid bulb massage) usually not
tested.
Due to its close proximity with vagus nerve and accessory isolated lesions of IXth cranial nerve are
rare.
Symptoms: Numbness of ipsilateral pharynx—Dysphagia
Signs: Absence of gag reflex [ on touching affected side].
Vagus Nerve
Arise as rootlets from post-olivary sulcus of lateral medulla and exit the skull through jugular foramen.
Motor supply: To muscles of upper pharynx and soft palate and intrinsic muscles of larynx including
cricothyroid.
Sensory supply: Dura mater of posterior cranial fossa and posterior wall of external auditory canal.
It acts as efferent in gag reflex, oculocardiac reflex and carotid reflex.
Symptoms: Change in voice, hoarseness and dysphagia, nasal regurgitation, cough during swallowing
due to aspiration.
• Ask the patient to open his mouth and say ‘aah’. Observe the movement of soft
palate and uvula.
(Normally both sides of palate elevate symmetrically and uvula remains in midline.)
• Touch tonsil or pharynx with cotton swab each side separately and elicit ‘gag reflex’.
RESULTS
• Uvula and soft palate moves to one side (contralateral side) in upper and lower motor neuron
lesion of vagus.
• Uvula/palate does not move on saying ‘aah’ or gag in bilateral palatal muscle paralysis.
• Uvula/palate moves on saying ‘aah’ but does not gag in IXth nerve palsy.
• Indirect laryngoscopy is done and vocal cords palsy if any is assessed.
Spinal Accessory Nerve

ANATOMY
It is a purely motor nerve arising from two nuclei. One is intimately related to the caudal part of
nucleus. The much larger spinal nucleus arises from a- and g-motoneurons in anterior horn cells of
C1-C3. The nerve runs upwards in subarachnoid space and enters the cranial cavity through foramen
magnum, and exits the skull through jugular foramen. Upon leaving the cranium it crosses the
transverse process of the atlas and enters the sternomastoid muscle. It emerges from posterior border
of sternomastoid, crosses posterior triangle of the neck to reach the trapezius.
The ipsilateral cerebral hemisphere supplies the contralateral trapezius and ipsilateral
sternomastoid muscle.
• Inspect the trapezius muscle from behind.
• Ask the patient to shrug the shoulders, maintain them in elevation and apply
downward pressure to shoulders to check the paresis of trapezius muscle.
• Inspect and palpate the size and tone of sternomastoid muscle.
• Ask the patient to turn his head to one side against pressure, and examine the
strength of sternomastoid muscle.
Causes for Lesion

In radical neck dissection spinal accessory is cut by choice.
In skull base tumours.
In progressive bulbar palsy.
Hypoglossal nerve
It arises from motor nucleus located beneath the floor of 4th ventricle. It exits the skull through
hypoglossal canal in occipital bone. It passes to the root of tongue and supplies intrinsic and extrinsic
muscles of tongue.
Clinical Examination
• Observe the tongue (while in floor of mouth) for fasciculation. Fasciculation may
indicate peripheral 12th nerve dysfunction.
• Ask the patient to protrude out and move his tongue in all directions.
• Ask the patient to make rapid movements of tongue in and out and side to side to
assess the motor activity.
In unilateral supranuclear lesion in first few hours or days, tongue deviates towards [opposite]
side because of stronger pull of healthy genioglossus. Later on tongue may not deviate. After a long
gap the tongue muscles atrophy and on protrusion of tongue, it deviates to the side of lesion.
12th cranial nerve palsy may be seen in:
• Skull base tumours.
• Medullary infarct.
• Vertebral artery aneurysm.
• # Base skull.
• Motor neuron disease.
• Iatrogenic—during surgery of submandibular gland and radical neck dissection.
Index 217
Index
Page numbers followed by f refer to figure and t refer to table
A Alteration in voice 73, 81
Abducent nerve 205 Amenorrhoea 149
Abnormalities of tympanic membrane 42 Angiofibroma 103, 105f
Absolute bone conduction test 46, 49, 49f Angiomatous polyp of inferior turbinate 91f
Accessory tragus 56 Anosmia 78
Achalasia cardia 184, 185 Anotia 39, 56
Acid peptic disease 129 Anterior
Acoustic basal 188
neuroma 69 ethmoidal
trauma 55f artery 77
Acute nerve syndrome 81
otitis media 33, 113 nasal packing 109, 111, 112f
parotitis 174, 175 pillars 125
tonsillitis 119, 129f rhinoscopy 82, 83
Adenoid scalene 159
gland 99 Antero-superior quadrant 41
hypertrophy 92f Antimongoloid palpabral fissures 58
Adenoiditis 97, 99 Antral puncture 110, 110f, 111
Adhesive otitis media 62 Antrochoanal polyp 91f, 96, 101, 102f
Air Aphthous
embolism 112 stomatitis 128, 132
pollution 109 ulcer on tongue 133f
Apnoea 189 Brainstem infarction 209

Arthralgia 149 Branch of glassopharyngeal nerve 34
Aspergillus fumigatus 60 Branchial
Atresia of oesophagus 183 cyst 167
Atrophic rhinitis 96, 97, 97f, 105 fistula 22
Attic perforation 45f Bronchiectasis 194
Attico-antral disease 65 Broncho-pulmonary segments 188f
Aural speculum 5, 5f Bronchoscopy 189, 194
Auricular branch of vagus nerve 34 Bull’s eye lamp 3, 4f, 81, 112, 140
Auriculo temporal nerve 34 Burning sensation 118, 120
Auscultation 17, 21, 152 Bypass valve 191
Autophony 29, 35 C
B Cacosmia 78
Ball Caloric testing 50, 212
probe 90 Carcinoma
valve 191 bronchus 194
Baro-otitis 62 in situ 146
Basal metabolic rate 153 oesophagus 184
Base of tongue 127 of maxilla 107f
Behcet syndrome 120 of maxillary antrum 107
Bell’s phenomenon 207 of oesophagus 186
Benign neoplasms 156 Cardiac arrest 183
Bleeding 112, 114, 179, 180 Carotid
from ear 29, 36 angiography 96, 107
per nose 73, 76 body tumour 169, 169f
Blood reflex 213
pressure 150 triangle 157, 158f
stained discharge 76 Catarrhal stage 104
supply of nasal septum 77f Causes of anosmia 197
Bottles containing aromas 198f Cellulitis of
Boycee’s position 182, 191 auricle 56
Index 219
floor of mouth 132 Corneal reflex 204
Cerebellopontine angle tumours 209 Cotton wool carrier 8, 8f
Cervical Cough 117, 120, 139
sympathetic chain 151 Cranial cavity 95
triangles 158f Craniocorpography 50
vertebrae 99 Crusting 73, 78
Chemotherapy 186, 194 CT scan 96, 107
Cholesteatoma 209 Cyanosis 189
Chondroma nasal septum 106f Cystic
Chorda tympani 209f hygroma 168, 169f
Chronic swelling 127
siloadenitis 127 in neck 166
submandibular sialoadenitis 135f Cysts of nasal 97
suppurative otitis media 31, 37, 64 D
Cleft palate 119, 128, 134
Darwin’s tubercle 53
Cochlear nerve 212
Deep jugular chain 159
Cold
intolerance 149 Delphian LN 158
spatula test 82, 88, 88f Dermoid cyst 56, 59, 127, 166
Colour Development of ear 57f
of mucosa 84 Deviated nasal septum 97, 101, 101f
of nasal mucosa 85 Deviation of angle of mouth 30, 37
vision 200 Diagastric triangle 157, 158f
Combination therapy 186 Difficulty in
Common conditions of breathing 137
inner ear 69 swallowing 117, 118, 138
middle ear 62 Diffuse otitis externa 56, 60, 60f
Compressibility in haemangioma 21f Diplopia 29, 149
Compressible swellings 128 Diseases of
Concha bullosa 92f oesophagus 179, 183
Cone of light 42 trachea and bronchi 189
Constipation 149 Disturbances of smell 73, 78
Division of pars tensa 42f larynx and laryngopharynx 136
Dry skin 149 lymph nodes 174
Dysarthria 118, 121 neck 157
Dysphagia 150, 179 nose and paranasal sinuses 73
Dyspnoea 150, 189 oral cavity and oropharynx 121
E salivary glands 173
sinus or fistula 21
Ear discharge 29
swelling, ulcer and fistula 15
Ectopic thyroid 164, 165f
thyroid gland 151
Electronystagmography 50
trachea and bronchi 187
Elicit transillumination test 20f
tympanic membrane 40
Endemic goitre 154
ulcer 23
Endoscopic
Exploratory thoracotomy 194
camera 90
micro-debridement 144 F
Enlarged adenoid 99f Facial
Epiphora 81 LN 158
Ethmoid nerve 206, 209f
polypii 92f Fatigability 149
sinus 94, 95 FB
tenderness 87f in larynx and laryngopharynx 141, 142
Ethmoidal in nose 73
polyposis 97, 102, 103 in oesophagus 180
sinuses 93 in right main bronchus 192f
sinusitis 80 in throat 121
Evoked response audiometry 50 in trachea/bronchi 189
Examination of ingestion 139
cranial nerves 197 inhalation 139
ear 29, 38 removal 114
with aural speculum 40 Fever 12, 29, 36, 74
external auditory canal 39 Fibreoptic cable 90
external nose and face 82 Fibrotic margin 24
facial nerve 174 Fine needle aspiration
Index 221
biopsy 194 Greater
cytology 153, 154 superficial 209f
Fistula 22 wing of sphenoid 95
test 45 Griesinger’s sign 39
Flexible bronchoscope 193f Gritty eye sensation 149
Floor of mouth 126 Gynaecomastia 149
Fluctuation 19 H
Foramen
Haemoptysis 189
lacerum 95
Hair-pin in right main bronchus 193f
magnum 95
Hard
ovale 95
palate 124, 125
spinosum 95
swellings 128
Foreign body
Hashimoto’s
impaction 179
disease 155
in nose 78
thyroiditis 154
in oesophagus 184
Hazy maxillary antrum 102f
Fracture of sphenoid wing 202
Headache 12, 29, 36, 73, 79
Freer’s elevator 90
Hearing loss 29, 31, 65, 67
Frontal
Hensen’s disease 61
sinus 93-95
Herpes
tenderness 87f
simplex 56
sinusitis 80
zoster 56
Functional endoscopic sinus surgery 101, 103
oticus 208
G Hiatus hernia 184
Gag reflex 213 Horner’s syndrome 16, 151
Geniculate ganglion 209f Huge thyroid 166f
Glossopharyngeal nerve 212 Hyperacusis 29, 35
Granulomas 97 Hypoglossal nerve 215
Grave’s disease 154, 155 Hypoplasia of
Great mandible 58
auricular nerve 34 middle part of face 58
palatine artery 77 Hyposmia 78
I Laryngeal
Impetigo contagiosa 56 crepitus 163
Indirect laryngoscopy 140, 140f mirror 6, 6f
Inferior papillomatosis 144f
ventricles 141
deep jugular 158, 159
widening 162
meatus 84, 85
Laryngocoele 171, 172f
turbinate 84, 85, 93
Laryngomalacia 141, 144
Inflammatory lymphadenitis 162 Laryngotracheobronchitis 141
Interferon therapy 144 Latency 74, 75
Internal auditory meatus 95 Lateral
Intracranial haemorrhage 202 nasal wall 84
Inverted papilloma 103 neck swellings 164
Iodine-induced hyperthyroidism 154 Lesions in visual pathway 199f
Ishihara’s chart 199f, 200 Lesser
Itching in occipital nerve 34
ear 29, 35 superficial petrosal nerve 209f
nose 73, 78 Lethargy 149
J Leucoplakia 128, 133, 133f
Lichtwitz trocar and cannula 111f
Jobson Horne probe 82
Lid lag sign 153
Juvenile Light headedness 29, 36
laryngeal papillomatosis 141, 142 Lingual nerve 209f
nasopharyngeal angiofibroma 105 Lipoma 127, 168
K in incisura terminalis 39f
Kartagener’s syndrome 194 in neck 168f
Keloid formation 61 Lobectomy 194
Keratosis obturans 56 Ludwig’s angina 128, 132, 166
Klebsiella rhinoscleromatis 104 Lymphangioma 168
on tongue 122f
L Lymphatic
Labyrinthitis 69 chain of neck 158f
Lacrimation intact 209 drainage of neck 158
Index 223
Lymphoma 162, 169 deep jugular chain 159
M meatus 84, 85
turbinate 84, 85, 93
Malignancy 86, 128, 134, 162
Midline neck swellings 164
of larynx 146
Miosis 151
and laryngopharynx. 141
Mixed parotid tumour 128
Malignant
Mobility
lesion of gingivo-labial sulcus 134f
of swelling 19
otitis externa 56, 61, 209
of tympanic membrane 45
thyroid tumours 156
test 25
Mandibular nerve 209f
Moderate central perforation 44f
Mandibulo-facial dysostosis 58
Motor
Mastoid
neuron disease 215
bone 95, 99
nuclei 212
fistula 38f
Multiple fistulae over face 22f
Maxillary
Muscle weakness 148
antrum 93
Muscular triangle 157, 158f
nerve 203
Myasthenia gravis 121
sinus 94, 95
Myringotomy 68
tenderness 87f
sinusitis 80 N
Mayer’s position 51 Nasal
McEven’s triangle 39 and paranasal sinuses symptoms 73
Meatal atresia 57 bridge 82f
Mediastinoscopy 189 cavity 93, 94
Medullary infarct 215 discharge 73, 75
Mega oesophagus 184f dressing forceps 82
Meniere’s disease 33, 69 endoscope 89, 89f
Method of floor 85
performing Weber test 48f glioma 103
syringing of ear 70f haemangioma 106f
Microtia 39, 56 malignancy 106f
Middle mass 73, 78
obstruction 73, 74 Otomycosis 56, 60
packing forceps 9, 9f Otorrhoea 29, 30, 65, 67
polyps 102 right ear 12
regurgitation 73, 78, 118, 121 Otosclerosis 55f, 68
roof 84, 85 Otoscope 10, 10f
septum 84, 93 P
speculum 5, 6f
Pain in
vestibule 84
ear 29
Nature of deafness 32
swelling 150
Nausea 29, 36
throat 117, 118, 138
Neck swelling 139
Palpate trachea in neck 188f
Nerve supply of pinna 34f
Palpation of
Neurodermatitis 56
submandibular gland and duct 176f
Non-Hodgkin lymphomas 170
trachea in neck 187
Non-suppurative otitis media 68
Pan-sinusitis 80
Notching of lower eyelid 58
Parapharyngeal abscess 128, 132
O Paratonsillar abscess 130
Oculocardiac reflex 213 Paratracheal nodes 159
Oculomotor nerve 200 Parotid gland 173, 174
Odynophagia 179 Pars
Oesophageal stenosis 183 flaccida 45
Oesophagoscopy 181 tensa 42
Olfactory nerve 197 Perforation
Oliguria 149 in hard palate 124f
Ophthalmic branch 202 of oesophagus 183
Optic nerve 198 Periorbital oedema 149
Oral submucous fibrosis 128 Peritonsillar abscess 130, 130f
Orbit 93-95 Petrosal nerve 209f
Oropharynx 117 Petrous bone 94
Otalgia 29, 33 Pharyngeal pouch 184
Otic ganglion 209f Pharyngitis 128
Otitis externa haemorrhagica 56
Index 225
Photodynamic therapy 144 Pterygoid canal 209f
Photophobia 149 Ptosis 151
Pleomorphic adenoma 175 Pulsatile swelling 20
of parotid 175f Pupillary
Pneumonectomy 194 accommodation 200
Position of branchial cysts 168f light reflex 200
Positional Pure tone audiometry 50, 53
testing 211 Pyogenic granuloma 63f
vertigo 35 Q
Post-aural
Quiescent ear 65
dermoid 59f
Quinsy 128, 130
granulation 38f
intertrigo 60 R
Posterior Radiological examination of ear 51
ethmoidal artery 77 Ramsay Hunt syndrome 56, 61, 64f, 208
nasal packing 110 Rat tail appearance 185f
pharyngeal wall 126 Regional lymph nodes 21
pillars 125 Regurgitation 179, 180
rhinoscopy 82, 86 Retroauricular
triangle 158f intertrigo 56
wall of maxilla 95 LN 158
Post-nasal Retro-orbital pain 29, 36
mirror 6, 7f Retropharyngeal
packing 113 abscess 128, 131, 131f
space 95 nodes 159
Pre-auricular Retrosternal extension of goitre 155f
cyst 59f Rhinitis 96
sinus 22, 58 Rhinorrhoea 73, 75
Presbycusis 69 Rhinoscleroma 97, 104, 104f
Pruritus 149 Rhinosporidiosis 97, 104
Pseudomonas aeruginosa 60 Right
Psoriasis 56 lower lobe 188
main bronchus 187, 188 swellings 127
upper lobe 187 Sore throat 117, 118
Rigid bronchoscopy set 193f Spenopalatine ganglion 209f
Rinnie’s test 46, 47f, 47t, 48t Sphenoid
Romberg’s test 210 sinus 95
Rupture of aneurysm of aorta 183 sinusitis 80
S Spinal accessory nerve 214
Spirit lamp 9
Schirmer’s test 208
Sporadic goiter 154
Schuller’s position 51
Squamous cell carcinoma 146
Sclerotic mastoid 52f
Staphylococcus aureus 60
Sebaceous cyst 167
Stenson’s
Seborrhoeic dermatitis 56
duct 98
Secondary deposits in neck 170
position 51
Secreto-motor function 206, 208 Stevens-Johnson syndrome 120
Sensory Stop valve 191
distribution of trigeminal nerve 202f Straight forceps 90
function testing 208 Streptococcus pyogenes 60
Septal branch of Stridor 137, 189
sphenopalatine artery 77 Stylomastoid foramen 209f
superior labial 77 Subacute thyroiditis 154
Serous otitis media 68 Submandibular
Short oesophagus 184 duct 177f
Siegle’s ganglion 209f
pneumatic speculum 7 gland 176
speculum 7f calculus 177
Sinus tenderness 82, 87 nodes 159
Sinusitis 100 sialoadenitis 128, 135
Skull base tumours 215 Submental triangle 157, 158f
Sneezing 73, 77 Submucosal implants 98
Snoring 74, 81 Suction
Soft cannula 9
palate 124, 125 tips 90
Index 227
Superficial cervical 158, 159 swelling 166
Superior ultrasonography 153
deep jugular 158, 159 TNM classification of larynx 146
turbinate 85 Tongue 122, 126
Suppurative depressor 8, 8f, 82
otitis media 64 Tonsillitis 128, 129
parotitis 174, 175f Total thyroidectomy 155
Supraclavicular nodes 159 Toxic
Swelling 123 adenoma 154
in oral cavity 127 multinodular goitre 154
in pre-and post-auricular area 29, 36 Tracheo-bronchial tree 187
in thyroid region 148, 151 Tracheo-oesophageal fistula 183
over Transillumination test 20, 82, 88
face 118, 121 Treacher Collin’s syndrome 56, 58, 58f
nose and face 79 Treatment of underlying allergy 103
T Trigeminal
nerve 202
Taste function testing 208 neuralgia 205
Tenderness over laryngeal cartilages 162 neuropathy 205
Testing Trochlear nerve 202
extraocular muscles 201f Tuberculosis 162
mobility of parotid with clenched teeth Tuberculous rhinitis 96
174f Tubo-tympanic disease 65
of trigeminal nerve 203f Tumour of nerve 205
sense of smell 198f Tuning fork tests 7, 46
Thyroglossal Turbinates 86
duct cyst 165, 165f Tympanosclerosis 62
fistula 22 Tympano-sclerotic patches 45
Thyroid Types of goitre 154
function test 153
gland 148 U
nodule 154f Ulcer 123
scan 153 in mouth 117, 119
Upper nodule 144, 145f

jaw 93, 95 Vomiting 29, 36
jugular lymph nodes 160 W
respiratory infection 32
Wall of maxilla 108f
Uvula 124
Warthin’s tumour 174
V Weber’s test 46, 48
Vagus nerve 213 Wharton’s duct 123
Valsalva manoeuvre 41 Wire vectis 8f
Vaso-vagal attack 112 X
Vermilion surface of lip 122f
X-ray
Vertebral artery aneurysm 215
base skull 94, 94f
Vestibulo-cochlear nerve 209
laryngocoele 171f
Viral infection 61
skull 107
Virchow’s nodes 159
Visual acuity 198 Z
Vocal Zygomatic nerve 209f
cord palsy 141, 145

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Clinical Methods

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

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Clinical Methods in ENT

First Edition : 2002

Part II: Otology

Bull’s Eye Lamp (Figure 1-1)

Figure 1-1: Bull’s eye lamp

Head Mirror (Figure 1-2)

Figure 1-2: Head mirror

Aural Speculum (Figure 1-3)

Figure 1-3: Aural speculum

Nasal Speculum (Figure 1-4)

Figure 1-4: Nasal speculum

Laryngeal Mirrors (Figure 1-5)

Figure 1-5: Laryngeal mirror

Post-nasal Mirrors (Figure 1-6)

Figure 1-6: Post-nasal mirror

Siegle’s Pneumatic Speculum (Figure 1-7)

Tuning Forks (Figure 1-8)

Figure 1-7: Siegle’s speculum Figure 1-8: Tuning forks

Wire Vectis with Cerumen Spud (Figure 1-9)

Figure 1-9: Wire vectis

Tongue Depressor (Figure 1-10)

Figure 1-10: Tongue depressor

Cotton Wool Carrier (Figure 1-11)

Figure 1-11: Cotton wool carrier

Figure 1-12: Nasal packing forceps

Sitting Arrangement (Figure 1-13)

Figure 1-13: Sitting arrangement

Otoscope (Figure 1-14)

Figure 1-14: Otoscope

OTHER SWELLINGS OVER BODY

SKIN OVER SWELLING

CHANGE IN SIZE OF SWELLING ON COUGHING/STRAINING OR VALSALVA

Fluctuation (Figures 3-1A and B)

Figure 3-2: Showing how to elicit transillumination test

Compressibility (Figures 3-3A and B)

REGIONAL LYMPH NODES

EXAMINATION OF SINUS OR FISTULA

Figure 3-4: Showing multiple fistulae over face.

Figure 3-5: A diagrammatic representation of an ulcer

Figure 3-6: Type of edges

Itching in the Ear

Blocking/wooly or FB Sensation in Ear

Autophony and Hyperacusis

Swelling in pre- and post-auricular Area

Bleeding from Ear

Past History (History of Major Illnesses)

Examination of Pinna, Pre- and Post-aural Area (Figures 4-2 to 4-5)

EXAMINATION OF EXTERNAL AUDITORY CANAL

Examination of Ear with Aural Speculum (Figure 4-6)

Figure 4-6: Showing method of holding ear

EXAMINATION OF TYMPANIC MEMBRANE

Mobility of TM (Figures 4-7 and 4-8)

Figure 4-7: Right TM and left TM

Figure 4-8: Division of Pars tensa

Abnormalities of Tympanic Membrane