Nose and Paranasal Sinuses

Christian Vion B. Guzman, MD, DPBO-HNS | 03-13-2022

Trans by: Hipolito, Pontila, Sibalon

OUTLINE • The nasal septum divides the nasal cavity into symmetrical air
passages. Each passage begins anteriorly at the naris and
I. Anatomy XI. Epistaxis widens into a vestibule before passing into a high, narrow
II. Physical Examination XII. Rhinosinusitis
passage that communicates posteriorly with the nasopharynx by
III. Imaging XIII. Acute Rhinosinusitis
an oval orifice, the choana. The septum is a vertical plane, while
IV. Congenital anomalies XIV. Chronic Rhinosinusitis
the lateral nasal surface has three horizontal, parallel, downward
V. Cyst XV. Allergic Fungal
curving bony plates, the superior, middle, and inferior turbinates
VI. Allergic Rhinitis Rhinosinusitis
or conchae
VII.Non-allergic rhinitis XVI. Complications of
VIII. Atrophic rhinitis Rhinosinusitis
IX. Wegener XVII. Common Causes of
granulomatosis ER Consultations
X. Rhinoscleroma XVIII. Reference

I. ANATOMY

Figure 1. External Nose

• The external nose is a triangular pyramid with one side adjoining
the face. The upper angle of the facial side is the root, connected
with the forehead. The two lateral sides join in the midline to form
the dorsum nasi; its superior portion is the bridge of the nose.
The free angle or apex forms the tip of the nose. The triangular
base is pierced on either side by an elliptic orifice, the naris (plural
nares), separated in the midline by the columella, which is
continuous internally with the nasal septum. Lining the margins
of the nares, still hairs, the vibrissae, inhibit inhalation of foreign
bodies. The lateral nasal surface ends below in a rounded
eminence, the ala nasi (plural, alae nasi).
• The upper third of the lateral nasal wall is supported medially by
the nasal bone and laterally by the nasal process of the maxilla.
The lower two-thirds is supported by a framework of lateral
cartilage, the greater alar cartilage, and several lesser alar
cartilages. The nasal passages are separated anteriorly by the
cartilaginous nasal septum and posteriorly by bone, the vomer. Figure 3. Lateral nasal wall.
• The nasal cavity is bounded laterally by the lateral nasal walls,
which are formed by the ethmoid bone and maxilla, and
posteriorly by the palatine bone and the pterygoid process of the
sphenoid bone. Several functionally important structures are
located on the lateral nasal wall: the nasal turbinates and their
associated passages (meati), sinus ostia, and the orifice of the
nasolacrimal duct.
• The inferior turbinate consists of a separate bone that is attached
to the medial wall of the maxillary sinus. The opening of the
nasolacrimal duct is located in the corresponding inferior meatus.
The middle and superior turbinates are part of the ethmoid bone.
In rare cases, a rudimentary “supreme turbinate” is also present
above the superior turbinate. The middle turbinate has by far the
greatest functional importance, because most of the drainage
tracts from the surrounding paranasal sinuses open into the
middle meatus
• The nasal cavity is bounded superiorly by the cribriform plate of
the ethmoid bone. This thin bony plate has numerous openings
for the passage of the fila olfactoria and also forms the boundary
of the anterior cranial fossa. The floor of the nasal cavity is
formed mostly by the hard palate, which is formed in turn by the
two palatine processes of the maxilla and the horizontal laminae
Figure 2. Nasal Septum of the palatine bone.

Trans # 7 Nose and Paranasal sinuses 1 of 12

 A. ARTERY BLOOD SUPPLY but except for the ethmoid air cells, they do not develop into
bony cavities until after birth.
• The frontal sinus and sphenoid sinus reach their definitive size in
the first decade of life.
• The maxillary sinus is present at birth but remains very small until
the second dentition, because the presence of tooth germs in the
maxilla limit the extent of the sinuses. The maxillary sinus, frontal
sinus, and anterior ethmoid cells drain into the nasal cavity
through the middle meatus—i.e., below the middle turbinate. The
posterior ethmoid cells drain into the nasal cavity through the
superior meatus. The ostium of the sphenoid sinus is located in
the anterior wall directly above the choanae. The anatomical
connections between the nasal cavity and paranasal sinuses are
functionally important and play a key role in the pathogenesis of
many rhinologic diseases that involve the paranasal sinuses.
C. VENOUS DRAINAGE
• Venous system is valveless.
• Sphenopalatine vein drains via sphenopalatine foramen into
pterygoid plexus.
• Ethmoidal veins drain into superior ophthalmic vein.
• Anterior facial vein drains through common facial vein to internal
jugular vein; also communicates with cavernous sinus via
ophthalmic veins, infraorbital and deep facial veins, and the
Figure 4. Artery blood Supply of Nose pterygoid plexus.
• External nose: • Angular vein drains external nose via ophthalmic vein to
cavernous sinus.
→ Primary supply from external carotid artery to facial artery
→ Superior labial artery: columella and lateral nasal wall
→ Angular artery: nasal side wall, nasal tip, and nasal dorsum
• Nasal cavity:
→ Both external and internal carotid artery
→ External carotid artery system
• Kiesselbach’s plexus (Little’s area)
→ Confluence of vessels along the anterior nasal septum where
the septal branch of sphenopalatine artery, anterior
ethmoidal artery branches, greater palatine artery, and septal
branches of superior labial artery anastomose
• Woodruff’s plexus (naso-nasopharyngeal plexus)
→ Anastomosis of posterior nasal, posterior ethmoid,
sphenopalatine, and ascending pharyngeal arteries along
posterior lateral nasal wall inferior to the inferior turbinate
B. PARANASAL SINUSES Figure 6. Venous Drainage
• Anterior facial vein drains through common facial vein to
internal jugular vein; also communicates with cavernous sinus
via ophthalmic veins, infraorbital and deep facial veins, and
the pterygoid plexus.

D. LYMPHATIC DRAINAGE
• Anterior portion of nose drains toward external nose in the
subcutaneous tissue to the facial vein and submandibular nodes.
• Others pass posterior to tonsillar region and drain into upper
deep cervical nodes.
• Most drain into pharyngeal plexus and then to the
retropharyngeal nodes.
E. NASOCILIARY NERVE
• Branch of ophthalmic division of cranial nerve (CN) V (CNV1).
• Arises in the lateral wall of cavernous sinus and enters orbit and
gives off two branches:
→ Infratrochlear nerve -Supplies skin at the medial angle of
eyelid
→ Anterior ethmoidal nerve -Leaves orbit with anterior ethmoidal
artery,supplies anterior superior nasal cavity, anterior ends of
middle and inferior turbinate and corresponding septum; also
region anterior to the superior turbinate, leaves nasal cavity
and supplies skin on dorsum of the tip of nose
• Maxillary nerve (CN V2)
→ Exits middle cranial fossa via foramen rotundum
Figure 5. Paranasal Sinuses • Pterygopalatine (sphenopalatine) ganglion: contains
• The paranasal sinuses are air-filled cavities that communicate parasympathetic, sympathetic, and sensory nerves
with the nasal cavities. All but the sphenoid sinus are already → Lateral posterior superior nasal branch
present as outpouchings of the mucosa during embryonic life,
Trans # 7 Nose and Paranasal sinuses 2 of 12
 → Supplies posterior portion of superior and middle turbinates,
posterior ethmoid cells
→ Medial posterior superior nasal branch
→ Cross anterior surface of sphenoid; roof of nasal cavity;
posterior septum
→ Nasopalatine nerve
▪ Supplies anterior hard palate
→ Greater palatine nerve
▪ Supplies mucous membrane over posterior portion of
inferior turbinate and middle and inferior meatus
• Infraorbital branch
→ Supplies portion of vestibule of the nose; anterior portion of
Figure 8. Nasal Cycle
inferior meatus; part of the floor of nasal cavity
F. AUTONOMIC INNERVATION
H. PHYSIOLOGY OF THE NOSE
• Derived from pterygopalatine ganglion
• Functions of the Nose
• Parasympathetic fibers of the nose
→ Airway: conduit for air
→ Derived from CN VII
→ Filtration: trap and remove airborne particulate matter
→ Preganglionic fibers
→ Humidification: increases relative humidity
▪ From superior salivatory nucleus in medulla oblongata
→ Heating: provides radiant heat of inspired air
▪ Located in the nervus intermedius portion of facial nerve
▪ Leave CN VII at the geniculate ganglion with greater → Nasal reflex: multiple that causes periodic nasal congestion,
superficial petrosal nerve and become vidian nerve and rhinorrhea, or sneezing
head to pterygopalatine ganglion • Postural reflex: increased congestion with supine position;
→ Postganglionic fibers congestion on the side of dependence upon lying on the side
▪ Arise in ganglion and join sympathetic and sensory fibers • Hot or cold temperature reflex: sneezing upon sudden exposure
▪ Travel with branches of sphenopalatine nerve and provide of skin to dramatic temperature extremes
secretomotor fibers to mucous glands in nasal mucosa • Chemosensation: detects irritants and temperature changes
▪ Vasodilation • Olfaction: see later
• Sympathetic fibers of the nose
→ From thoracic spinal nerves (T1-T3) I. NASAL AIRFLOW RESISTANCE
→ Postganglionic fibers • Contributes up to 50% of total airway resistance.
▪ From superior cervical ganglion and travel with internal • Mucosal vasculature is under sympathetic tone; when tone
carotid artery; leave this plexus as deep petrosal nerve and decreases, vessels engorge, airflow resistance increases;
join the greater superficial petrosal nerve to form vidian change in tone is part of normal nasal cycle occurring every 2 to
nerve (nerve of pterygoid canal) 7 hours.
▪ Mediate vasoconstriction
G. MUCOUS BLANKET J. OLFACTION
• Two layers: gel and sol phase • Olfactory epithelium.
→ Gel phase: superficial layer, produced by goblet and → It is located in upper edge of nasal chamber adjacent to
submucosal glands; layer to trap particulate matter cribriform plates, superior nasal septum, and superior lateral
→ Sol phase: deep layer, produced by microvilli; provides fluid nasal wall.
that facilitates ciliary movement → Pseudostratified neuroepithelium containing primary olfactory
• Other components: mucoglycoproteins, immunoglobulins, receptors.
interferon, and inflammatory cells → Two layers separated by basement membrane.
▪ Olfactory mucosa
▪ Lamina propria
• Different cell types:
1) Bipolar receptor cell
2) Sustentacular cell
3) Microvillar cell
4) Cells lining Bowman gland
5) Horizontal basal cell
6) Globose basal cell

Figure 7. Mucociliary transport.

• The “nasal cycle” is a physiologic phenomenon marked by an

alternation between luminal narrowing and widening of the nasal
cavities.

Figure 9. OE Cell types

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 II. PHYSICAL EXAMINATION The rhinologic examination itself begins with anterior
rhinoscopy to evaluate the nasal vestibule and the anterior
• The clinical examination begins with a visual inspection.
portions of the nasal cavity.
→ Findings such as mouth breathing may direct the examiner to Technique: The examiner holds the nasal speculum in
suspect nasal airway obstruction. The shape of the external the left hand and braces the index finger on the patient’s right
nose may suggest intranasal abnormalities (e.g., a nostril. The speculum is inserted into the nose with the blades
cartilaginous nasal deviation with a tension septum). closed. During the examination, the physician uses the right
• Palpation is most useful for detecting bony discontinuities. hand to position the patient’s head and gently opens the
• In patients with suspected neuralgias, it is also done to check speculum to spread open the nostril to allow inspection of the
for tenderness over the supraorbital, infraorbital, or mental nasal cavity.
foramina. In patients with a recent trauma history, palpation of The speculum should not be opened too far, as this would
the external nose will disclose any mobility or crepitus cause discomfort. The head should be tilted slightly forward for
suggesting a fracture of the nasal pyramid. evaluating the nasal floor, inferior turbinate, and the anterior
Table 1. Differential Diagnosis of nasal airway obstruction portions of the septum. The head is tilted backward to obtain a
limited view of the middle meatus and middle turbinate.
Often this region cannot be adequately assessed by
anterior rhinoscopy alone due to anatomical constraints.
As a result, endoscopy is commonly used to examine this
region as well as the posterior portions of the nasal cavity and
the nasopharynx. When anterior rhinoscopy has been
completed, the
speculum is carefully withdrawn with the blades slightly open to
avoid avulsing hairs from the nasal vestibule. In many cases the
nasal mucosa should be decongested with vasoconstrictors
prior to the examination, as this makes it easier to examine the
interior of the nose. At the same time, it is also important to
assess the “original” condition of the nasal mucosa, and so the
nose should be examined before and after decongestion of the
mucosa.

First the examiner advances the endoscope into the

nasopharynx and inspects the eustachian tube orifice, torus
tubarius, posterior pharyngeal wall, and roof of the nasopharynx
While the transnasal nasopharyngeal inspection can provide
very detailed views (e.g., for early detection of nasopharyngeal
cancer), it should still be supplemented by transoral
postrhinoscopic endoscopy
Nasal endoscopy is particularly useful for evaluating the
ostiomeatal unit, as this pathophysiologically important region
generally cannot be adequately evaluated by anterior
rhinoscopy alone. To inspect the middle meatus, the endoscope
is first advanced toward the head of the middle turbinate. This
should provide a good overview of the middle meatus.

Figure 10. Anterior Rhinoscopy

Figure 11. Nasal Endoscopy

• Active anterior rhinomanometry-most standardized procedure for

the assessment of nasal patency (The accuracy of this test is
most limited in patients with severe nasal airway obstruction, and
the test cannot be performed when one nasal cavity is completely
obstructed.)
• Acoustic rhinometry -does not assess the patency of nasal
airflow.

Trans # 7 Nose and Paranasal sinuses 4 of 12

• Skin tests-The most widely used method is the prick test, in which
the skin is superficially pricked with standard test substances that
contain the suspicious antigens
• Serologic tests

Table 2. Causes of olfactory disturbances

Figure 14. Waters view

III. IMAGING OF THE NOSE AND PARANASAL SINUS

Figure 12. Paranasal sinuses

Figure 15. CT scan of paranasal sinuses

CT Scan is used when we are not contented with routine

radiographs and the patient cant afford more expensive imaging
modality. It is more specific and detailed.

Figure 13. Caldwell view

Trans # 7 Nose and Paranasal sinuses 5 of 12

 IV. CONGENITAL ANOMALIES
A. CHOANAL ATRESIA

Figure 16. Choanal atresia

• One in 5000 to 8000 live births. Figure 17. Dermoid
• Female to male ratio is 2:1. • During development, projection of dura protrudes through
• Unilateral greater than bilateral; right side more common in fonticulus frontalis or inferiorly into prenasal space; the
unilateral. projection normally regresses and if it does not, the dura can
• The ratio of bony and membranous bony is 30%:70%. remain attached to the epidermis, causing trapping of
• “The main problem with this is that you will get referral from pedia. ectodermal elements.
Usually, hindi dila makapagpasok ng OGT or NGT tapos may • Have tendency for repeated infections, ranging from cellulitis
resistance pag nagpasok sila sa nostril ng mga newborns. They to abscess.
would refer the patient to you for evaluation of choanal atresia. • CT and magnetic resonance imaging (MRI) important for
So, usually ang atresia is close or walang opening yung airway. determining extent of lesion.
”[Doc Guzman]
• Surgical excision is treatment of choice; incision and drainage
• Bilateral choanal atresia usually presents with airway distress are discouraged. Entire cyst and tract with bone and cartilage
at birth since newborns are obligate nasal breathers; classic should be removed.
presentation is cyclic cyanosis relieved by crying (paradoxical
cyanosis). C. GLIOMA
• Unilateral choanal atresia presents usually between 5 and 24
months with unilateral obstruction and nasal discharge.
• Diagnosis:
→ Definitive diagnosis established by computed tomography
(CT) scan.
• Treatment:
• Bilateral: immediate management—airway stabilization with oral
airway, McGovern nipple, intubation if ventilation is required
• Surgical correction:
→ Transpalatal approach
→ Transnasal approach: puncture, most commonly with Fearon
dilator
→ Endoscopic approach
• Four basic theories are:
a. Persistence of buccopharyngeal membrane Figure 18. Glioma
b. Abnormal persistence of bucconasal membrane • Comprised of ectopic glial tissue; 15% to 20% have intracranial
c. Abnormal mesoderm forming adhesions in connection.
nasochoanal region • Abnormal closure of the fonticulus frontalis can lead to an ectopic
d. Misdirection of neural crest cell migration rest of glial tissue if left extracranially.
• 20% to 50% with other associated congenital anomalies. • Sixty percent external; 30% unilateral intranasal; 10% combined.
a. CHARGE (coloboma, heart disease, choanal atresia, • Mass is firm, nontender, noncompressible, does not
mental retardation, genital hypoplasia, ear anomalies) transilluminate.
b. Apert syndrome, Crouzon disease, Treacher-Collins • Need to rule out intracranial connection by radiology.
syndrome • Complete surgical excision also is the treatment of choice.
B. DERMOID D. ENCEPHALOCELE
• Epithelium-lined cavities or sinus tracts filled with keratin debris,
hair follicles, sweat glands, and sebaceous glands.
• May present as intranasal, intracranial, or extranasal masses
along the nasal dorsum.
• May also present as pit or fistulous tract.
• Mass is nontender, noncompressible, and firm; do not
transilluminate.

Figure 19. Encephalocele

• Congenital herniation of central nervous system (CNS) tissue
through skull base defect
A. Meningoceles: contain only meninges

Trans # 7 Nose and Paranasal sinuses 6 of 12

 B. Meningoencephaloceles: contain meninges and glial • Benign cyst in the sella turcica
tissue • Usually present in fifth or sixth decades of life; females greater
• “Hindi mo ooperahan yung mga ganitong pasyente agad without than males
requesting for imaging. You check if meron siyang • Usually asymptomatic but may compress adjacent structures
communication intracranially.” [Doc Guzman] such as the pituitary gland or optic chiasm
• Mass is often bluish or red, soft, compressible, and • MRI is modality of choice
transilluminate • Tumor of Rathke’s pouch is craniopharyngioma.
• Mass pulsatile, expand with crying or straining
B. THORNWALDT’S CYST
• Furstenberg test: expand with compression of internal jugular
veins
• CT and MRI important for diagnosis and surgical planning
• Should be surgically resected and repaired to prevent
cerebrospinal fluid (CSF) leak, meningitis, or herniation.
•

E. TERATOMA
•

Figure 22. Thornwaldt’s cyst

• Benign nasopharyngeal cyst
• Develops from remnant of notochord
• Symptoms: postnasal drainage, aural fullness, serous otitis
media, and cervical pain
• Examination: smooth submucosal midline mass in nasopharynx
• Treatment: none if asymptomatic; if symptomatic,
marsupialization through surgical correction via endoscopic
approach
C.INTRA-ADENOIDAL CYST
Figure 20. Teratoma
• Rare developmental tumors that comprise of all three germ
layers.
• Head and neck teratomas account for 2% to 3% of all teratomas.
• Most common is cervical teratoma, followed by nasopharyngeal
teratoma.
• Antenatal diagnosis by ultrasound is available in the United
States.
• Secure the airway in cases of airway obstruction.
• Plain film radiograph showing calcification is pathognomonic.
• CT helpful in delineation of lesion extent and rule out intracranial
connection.
V. CYSTS
A. RATHKE’S POUCH CYST Figure 23. Intra-adenoidal cyst
• Occlusion of adenoid crypts, leading to retention cyst in
adenoids; asymptomatic; in midline; rhomboid shape on imaging

D. BRANCHIAL CLEFT CYST

Figure 21. Rathke’s pouch cyst

• Rathke’s pouch is an invagination of the nasopharyngeal
epithelium in the posterior midline; the anterior pituitary gland
develops from this in fetal life.
• Remnants of this pouch may persist forming cyst or tumor.
Figure 24. Branchial cleft cyst
Trans # 7 Nose and Paranasal sinuses 7 of 12
• Can be formed by either the first or second branchial arch a. Infectious rhinitis: most common is viral (rhinovirus,
• Relative lateral position in nasopharynx respiratory syncytial virus, parainfluenza virus, adenovirus,
• Treatment is surgical excision influenza virus, enterovirus)
b. Vasomotor rhinitis: imbalance in the autonomic system
VI. ALLERGIC RHINITIS where the parasympathetic system predominates leading to
vasodilation and mucosal edema. Cold air, strong odors
• Nasal symptoms: nasal congestion, rhinorrhea, nasal pruritus, exacerbate symptoms
palate pruritus, postnasal drainage, anosmia, or hyposmia c. Hormonal rhinitis: associated with hormonal imbalance;
• Ocular symptoms: ocular pruritus, watery eyes usually due to pregnancy, puberty, menstruation, or
• Pathophysiology: hypothyroidism
• Gel and Coombs type I hypersensitivity. d. Occupational rhinitis: rhinitis at the workplace; usually due
• Sensitization: After initial exposure to an antigen, antigen- to inhaled irritant; frequently associated with concurrent
processing cells (macrophages, dendritic cells) present the occupational asthma
processed peptides to T-helper cells. e. Drug-induced rhinitis:
▪ Antihypertensives: angiotensin-converting enzyme (ACE)
inhibitors, beta blockers
▪ Nonsteroidal anti-inflammatory drugs (NSAIDs)
▪ Oral contraceptives
f. Rhinitis medicamentosa: tachyphylaxis associated with
prolonged use of nasal sympathomimetics, over 5 to 7 days;
alpha receptors in the nose are desensitized; rebound
congestion due to overuse of decongestants; treat with
intranasal steroids and stop decongestant
g. Gustatory rhinitis: watery rhinorrhea due to vasodilation after
eating, especially with spicy or hot foods
Figure 25. Allergic rhinitis h. Nonallergic rhinitis of eosinophilia syndrome (NARES)
▪ Rhinitis with approximately 10% to 20% eosinophils on
nasal smears
▪ Symptoms of nasal congestion, rhinorrhea, sneezing,
pruritus, and hyposmia
VIII. ATROPHIC RHINITIS

Early phase response starts within 5 minutes to 15 minutes.

1. Mast cells degranulate, releasing histamine, heparin, and Figure 26. Atrophic rhinitis
tryptase; they producesymptoms of sneezing, rhinorrhea, • Also called as rhinitis sicca or ozena
congestion, and pruritus. • Mucosal colonization with Klebsiella ozaenae and other
2. Degranulation also triggers formation of prostaglandin organisms
PGD2, leukotrienes LTC4, LTD4, LTE4, and platelet • Nasal mucosa degenerates and loses mucociliary function
activating factor (PAF). • Presents with foul smell as well as yellow or green nasal
Late phase response begins 2 to 4 hours later. crusting with atrophy and fibrosis of mucosa
1. Caused by newly arrived inflammatory cells recruited by
→ Primary atrophic rhinitis
cytokines.
→ Secondary atrophic rhinitis
2. Eosinophils, neutrophils, and basophils prolong the earlier
▪ Secondary to trauma or nasal surgery (empty nose
reactions and lead to chronic inflammation.
syndrome)
• Seasonal allergies: particular time of the year according to
seasonal allergens (grass, trees, pollen, ragweed) IX. WEGENER’S GRANULOMATOSIS
• Perennial allergies: symptoms present all year around (insects,
dust mites, dogs, cats)

VII. NON-ALLERGIC RHINITIS

• Chronic symptoms of nasal congestion, rhinorrhea, posterior
nasal drainage, may be distinguished from allergic rhinitis by
consistent presence of symptoms, lack of nasal or ocular
pruritus
• Possible triggers
→ Strong fragrances, tobacco smoke, changes in temperature,
cleaning products
• Subclassification
Figure 27. Wegener granulomatosis
Trans # 7 Nose and Paranasal sinuses 8 of 12
• Triad of necrotizing granulomas of respiratory tract, vasculitis,
and glomerulonephritis
• Sinonasal symptoms usually manifest early with severe nasal
crusting, epistaxis, rhinorrhea, and secondary rhinosinusitis
• Nasal biopsy usually nondiagnostic
• Cytoplasmic pattern (+C-ANCA) strongly associated with
Wegener’s granulomatosis (WG)
• Anti-Myeloperoxidase (MPO) and anti-Proteinase 3 (PR3) testing
for WG
• Consultation with rheumatology for systemic treatment
• Nasal treatment
→ Saline irrigation, nasal moisturization, topical antibiotics

X. RHINOSCLEROMA

Kiesselbach’s plexus (Little’s area)

→ Confluence of vessels along the anterior nasal septum where
the septal branch of sphenopalatine artery, anterior ethmoidal
artery branches, greater palatine artery, and septal branches of
superior labial artery anastomose
• Management:
Figure 28. Rhinoscleroma
→ Airway breathing circulation (ABC); patient stabilization
• Chronic granulomatous disease due to Klebsiella
rhinoscleromatis → Cauterization under direct visualization
• Endemic to Africa, central America, or Southeast Asia → Nasal packing:
▪ Anesthetic: vasoconstrictor–solution-soaked cotton
• Usually affects nasal cavity, but may also affect the larynx,
▪ Vaseline gauze
nasopharynx, or paranasal sinuses
▪ Merocel
• Three stages of disease progression
▪ Epistaxis balloon
→ Catarrhal or atrophic: rhinitis, purulent rhinorrhea, and nasal ▪ Topical tranexamic acid application
crusting ▪ Gelfoam or Surgicel in coagulopathic patient
→ Granulomatous or hypertrophic: small painless ▪ Posterior packing (balloon or gauze) requires close
granulomatous lesions in upper respiratory tract monitoring. All patients with nasal packing.
→ Sclerotic: sclerosis and fibrosis narrowing nasal passages → Control of hypertension
• Key pathologic findings: → Correction of coagulopathies
→ Mikulicz cells: large macrophage with clear cytoplasm → Greater palatine foramen block
containing bacilli → Saline sprays
→ Russell bodies in plasma cells → Humidity or emollients
• Treatment: long-term antibiotics, biopsy, and debridement → Surgical ligation
→ Saline irrigation, nasal moisturization, topical antibiotics ▪ Continued bleeding despite nasal packing
XI. EPISTAXIS ▪ IMAX ligation
− Caldwell-Luc to enter maxillary sinus; enter posterior
• Over 90% of bleeds can be visualized anteriorly. wall, vessels clipped
• Causes: ▪ Endoscopic sphenopalatine ligation
A. Local − Follow middle turbinate to posterior aspect
1. Trauma: digital, foreign body, fracture, surgery − Make vertical incision approximately 7 to 8 mm anterior
2. Dessication to the posterior end of middle turbinate
3. Drug-induced: cocaine, nasal steroids − Crista ethmoidalis seen and marks anterior
4. Infectious: bacterial sinusitis sphenopalatine foramen; vessels posterosuperior; clip
5. Inflammatory: allergic rhinitis, granulomatous disease or cauterize
6. Neoplastic: angiofibroma, papillomas, carcinoma ▪ Ethmoid artery ligation
B. Systemic
− Lynch incision; frontoethmoid suture line identified
1. Intrinsic coagulopathy: von Willebrand disease, hemophilia,
▪ External carotid artery ligation
hereditary hemorrhagic telangiectasia (HHT)
− Approach via anterior border of sternocleidomastoid
2. Drug-induced coagulopathy
(SCM) muscle. Identify bifurcation between internal and
3. Hypertension
external arteries
4. Neoplastic
→ Embolization
▪ Most commonly embolized vessel is IMAX (Internal
maxillary artery)

Trans # 7 Nose and Paranasal sinuses 9 of 12

 • Symptoms last for less than 14 days
• Symptoms are self-limited
B. ACUTE NONVIRAL RHINOSINUSITIS
• Increase in symptoms after 5 days or persistent symptoms after
10 days
• Sudden onset of two or more symptoms
→ Nasal blockage or congestion
→ Anterior or posterior nasal drainage
→ Facial pain or pressure
• Palpation of maxillary and frontal sinuses
→ Hyposmia or anosmia
C. ACUTE BACTERIAL RHINOSINUSITIS
• Haemophilus influenza, Streptococcus pneumonia, and
Moraxella catarrhalis are the most common agents
• Three cardinal symptoms for diagnosis
→ Purulent nasal discharge
• Check the characteristic of the discharge: color, odor (foul
smelling or non-foul smelling), location (where is it coming
from), consistency.
→ Face pain or pressure
→ Nasal obstruction
→ Facial pain or pressure
• Secondary symptoms that further support diagnosis
→ Anosmia
→ Fever
→ Aural fullness
→ Cough
→ Headache
XII. RHINOSINUSITIS
D. PATHOPHYSIOLOGY OF ARS
• Inflammation of the nose and the paranasal sinuses
• Anatomic abnormalities may predispose one to ARS
• Symptoms (two or more symptoms)
→ Septal deviation and spur
a. One of which should be nasal blockage or obstruction or
congestion or nasal discharge (anterior or posterior nasal → Turbinate hypertrophy
drip) → Middle turbinate concha bullosa
b. ± Facial pain or pressure → Prominent agger nasi cell
c. ± Hyposmia or anosmia → Haller cells
→ Prominent ethmoid bulla
→ Pneumatization
→ Inversion of uncinate process
• Acute viral respiratory infection affects nasal and sinus mucosa
leading to obstruction of sinus outflow
• Other factors: allergies, nasal packing, sinonasal tumors,
trauma, and dental infections
E. TREATMENT
• Goals of treatment
→ Decrease time of recovery
→ Prevent chronic disease
Figure 29. Rhinosinusitis
→ Decrease exacerbations of asthma or other secondary
• Classification of Rhinosinusitis diseases
→ The Rhinosinusitis Task Force (RSTF) in 2007 proposed a • Objectives
clinical classification system: → Reestablish patency of ostiomeatal complex
a. Acute rhinosinusitis (ARS): symptoms lasting for less → Reduce inflammation and restore drainage of infected
than 12 weeks with complete resolution sinuses
b. Subacute RS: duration between 4 and 12 weeks → Eradicate bacterial infection and minimize risk of
c. Chronic RS (CRS) (with or without nasal polyps): complications or sequelae
symptoms lasting for more than 12 weeks without
complete resolution of symptoms Medical Treatment
d. Recurrent ARS: ≥ 4 episodes per year, each lasting ≥ A. Initial management should be symptomatic
7 to 10 days with complete resolution in between B. Analgesics, decongestants, and mucolytics (saline irrigation)
episodes are recommended
e. Acute exacerbation of CRS: sudden worsening of
C. Antibiotics and topical corticosteroids shown to be effective
baseline CRS with return to baseline after treatment
D. Mild disease (Mild pain and temp less than 38 deg C)
XIII. ACUTE RHINOSINUSITIS 1. Deferring antibiotics for up to 5 days in patients with
nonsevere illness at presentation
A. ACUTE VIRAL RHINOSINUSITIS 2. Follow-up needs to be ensured
• Common cold 3. Reevaluate patient if illness persists or worsens
• Rhinovirus and influenza are the most common agents

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 E. Moderate to severe disease ( symptoms persist or worsening XV. ALLERGIC FUNGAL RHINOSINUSITIS
after 5 day and temp > 38 deg C)
1. Empiric oral antibiotics A. FIVE CRITERIA OF BENT AND KUHN
2. First line: amoxicillin or amoxicillin/clavulanate for 7 to 14 A. Eosinophilic mucin (Charcot-Leyden crystals)
days; if penicillin allergic: TMP/SMX, doxycycline, and B. Noninvasive fungal hyphae
macrolide C. Nasal polyposis
3. Switch to respiratory quinolones (levofloxacin, moxifloxacin, D. Characteristic radiologic findings:
1. CT: rim of hypointensity with hyperdense central
high dose amoxicillin/clavulanate if no improvement in 72
material (allergic mucin)
hours or if recent antibiotic use 2. CT: speckled areas of increased attenuation due to
4. Nasal corticosteroids ferromagnetic fungal elements
5. Decongestants should be used for less than 5 days 3. MRI: peripheral hyperintensity with central
6. Oral antihistamines in patients with allergic rhinitis hypointensity on both T1 and T2
4. MRI: central “void” on T2
XIV. CHRONIC RHINOSINUSITIS E. Type I hypersensitivity by history, skin tests, or serology
A. FOUR CARDINAL SYMPTOMS OF CRS B. CLINICAL FEATURES
• Anterior or posterior purulent nasal discharge • Dermatiaceous fungi (Alternaria, Bipolaris, Curvularia,
• Nasal obstruction Cladosporium)
• Face pain or pressure • Typically unilateral but sometimes bilateral
• Hyposmia or anosmia • Dramatic bony expansion of paranasal sinuses
• High association with asthma
B. DIAGNOSIS OF CRS
• At least two of the cardinal symptoms plus one of the XVI. COMPLICATIONS OF RHINOSINUSITIS
following: • Hematogenous spread: retrograde thrombophlebitis through
A. Endoscopic evidence of mucosal inflammation: purulent valveless veins (veins of Breschet)
mucus or edema in middle meatus or ethmoid region • Direct spread: through lamina papyracea, osteomyelitis
B. Polyps in nasal cavity or middle meatus • Mucoceles
C. Radiologic evidence of mucosal inflammation → Collection of sinus secretions trapped due to obstruction of
C. SUBTYPES OF CRS sinus outflow tract
• CRS with nasal polyps (20-33%) → Expansile process
→ Predominantly neutrophilic inflammation → Mucopyoceles: infected mucocele
• CRS without nasal polyps (60-65%) → Treatment: endoscopic marsupialization
→ Predominantly eosinophilic inflammation
→ IL-5 and eotaxin involvement Ophthalmologic
• Chandler’s classification
D. FACTORS ASSOCIATED WITH CRS
A. Preseptal cellulitis: inflammatory edema, no limitation of
• Ostiomeatal complex compromise: the common drainage
extraocular movements
pathway for frontal, anterior, ethmoid, and maxillary sinuses
B. Orbital cellulitis: chemosis, impairment of EOM, proptosis,
• Blockage by inflammation or infection can lead to obstruction of
visual impairment
sinus drainage, resulting in sinusitis
C. Subperiosteal abscess: pus, collection between medial
• Mucociliary impairment: ciliary function plays important role in periorbital and bone, chemosis, exophthalmos, EOM
clearance of sinuses; loss of ciliary function may result from impaired, visual impairment worsening
infection, inflammation, or toxin D. Orbital abscess: pus collection in orbital tissue, complete
• Kartagener syndrome (situs inversus, CRS, bronchiectasis) ophthalmoplegia with severe visual impairment
may be associated • Superior orbital fissure syndrome (CN III, IV, V1, VI)
• Up to 50% of CRS patients have asthma • Orbital apex syndrome (CN II, III, IV, V1, VI)
• Osteitis: area of increased bone density and thickening may be • Cavernous Sinus Thrombosis
a marker of chronic inflammation
• Treatment for ophthalmologic complications:
• Biofilms: 3D structures of living bacteria encased in
→ Mild preseptal cellulitis: outpatient antibiotics, topical
polysaccharide have been found on sinus mucosa in CRS
decongestants, saline
patients
→ Irrigation with close follow-up
• ASA or Samter’s triad: Nasal polyposis, aspirin (ASA)
→ Hospital admission with low threshold for IV antibiotics
sensitivity, and asthma
→ Topical decongestants
• Granulomatous vasculitis
→ Ophthalmology consultation
E. SURGICAL TREATMENT → Surgical exploration if no improvement with IV antibiotics
• Endoscopic sinur surgery is reserved for small percentage of → Endoscopic decompression
patients with CRS who fail medical management
Neurologic
• Patients with anatomical variants often benefit from surgery to
• Meningitis: severe headache, fever, seizures, altered mental
correct the underlying abnormality, re-establishing sinus
status, and meningismus
drainage
• Epidural abscess: pus collection between dura and bone
• Massive polyposis rarely responds to medical treatment and
surgery will relieve symptoms and establish drainage as well as • Subdural abscess: pus under dura
allow for use of topical corticosteroids • Brain abscess: pus within brain parenchyma
• Other indications for surgery include mucocele formation, and Bone
suspected rhinosinusitis
• Osteomyelitis: thrombophlebitic spread via diploic veins
• Ostiomeatal complex compromise: the common drainage • Pott’s puffy tumor: subperiosteal abscess (frontal bone
pathway for frontal, anterior, ethmoid, and maxillary sinuses
osteomyelitis to erosion of the anterior bony table)
Blockage by inflammation or infection can lead

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 XVII. COMMON CAUSES OF ER CONSULTATIONS
RELATED TO NOSE
• Nasal foreign body
→ Pebbles, slate pencils, beads, marbles, peas, beans, nuts,
button batteries, paper wads
• Nasal bone fracture
→ Xray: soft tissue lateral of the nose
• Most nasal bone fracture are diagnosed clinically, most of
the time diagnostic tests are not needed
→ Treatment: REDUCTION
→ Complications: Septal hematoma, septal abscess

Figure 33. Inverted papilloma

• Nasopharyngeal tumor
→ Presents with lateral neck mass due to drainage of
nasopharynx into upper jugular and posterior group of lymph
nodes
→ Treatment: Radiation

XVIII. REFERENCE
• Doc’s Lecture

Figure 30. Nasal bone fracture with deviation of nasal structure and
presence of hematoma
• Nasal furuncles
→ Painful, tender, erythematous swellings about the nasal tip
and nares
→ There may be concomitant edematous swelling of the upper
lip
→ The changes are confined to the outer skin and do not involve
the mucosa

Figure 31. Nasal furuncles

• Le Fort fractures
→ Classification
I. Isolated detachment of the alveolar process
II. Pyramidal fracture with detachment of the maxilla
III. Craniofacial disjunction

Figure 32. Le Fort Classification

• Inverted papilloma
→ Nonspecific clinical manifestations: nasal airway obstruction,
headache, occasional epistaxis
→ Polyp-like appearance when inspected by nasal endoscopy
→ In many cases, only histologic examination can establish the
diagnosis
→ Imaging (CT) is helpful in defining tumor extent
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