Chapter 23

Muscles of
Anatomy of Nose
nose

1.
Process
2. Natalis
g. levator labii superiors alaqve nasi

u Dilator nares cant & Post

s .

Depressor septi
EXTERNAL NOSE (transverse and alar parts), levator labii superioris alaeque
nasi, anterior and posterior dilator nares and depressor
It is pyramidal in shape with its root up and the base septi.
directed downwards. Various terms used in its descrip-
tion are shown in Figure 23.1. Nasal pyramid consists of
osteocartilaginous framework covered by muscles and NASAL SKIN
skin. The skin over the nasal bones and upper lateral cartilages
is thin and freely mobile while that covering the alar carti-
OSTEOCARTILAGINOUS FRAMEWORK lages is thick and adherent, and contains many sebaceous
glands. It is the hypertrophy of these sebaceous glands
Bony Part which gives rise to a lobulated tumour called rhinophyma
Upper one-third of the external nose is bony while lower (see p. 162).
two-thirds are cartilaginous. The bony part consists of
two nasal bones which meet in the midline and rest on
the upper part of the nasal process of the frontal bones INTERNAL NOSE
and are themselves held between the frontal processes of
the maxillae (Figure 23.2). It is divided into right and left nasal cavities by nasal
septum. Each nasal cavity communicates with the exte-
Cartilaginous Part rior through naris or nostril and with the nasopharynx
It consists of: through posterior nasal aperture or the choana. Each nasal
cavity consists of a skin-lined portion—the vestibule and
1. Upper lateral cartilages. They extend from the under- a mucosa-lined portion, the nasal cavity proper.
surface of the nasal bones above, to the alar cartilages
below. They fuse with each other and with the upper
border of the septal cartilage in the midline anteriorly. VESTIBULE OF NOSE
The lower free edge of upper lateral cartilage is seen Anterior and inferior part of nasal cavity is called vesti-
intranasally as limen vestibule, nasal valve or limen nasi bule. It is lined by skin and contains sebaceous glands,
on each side. hair follicles and the hair called vibrissae. Its upper limit
2. Lower lateral cartilages (alar cartilages). Each alar on the lateral wall is marked by limen nasi (also called
cartilage is U-shaped. It has a lateral crus which forms nasal valve).
the ala and a medial crus which runs in the columella.
Lateral crus overlaps lower edge of upper lateral carti- 1. Nasal valve. It is bounded laterally by the lower bor-
lage on each side. der of upper lateral cartilage and fibrofatty tissue and
3. Lesser alar (or sesamoid) cartilages. Two or more in anterior end of inferior turbinate, medially by the
number. They lie above and lateral to alar cartilages. cartilaginous nasal septum, and caudally by the floor
The various cartilages are connected with one anoth- of pyriform aperture. The angle between the nasal ¥
er and with the adjoining bones by perichondrium septum and lower border of upper lateral cartilage is
and periosteum. Most of the free margin of nostril is nearly 30°.
formed of fibrofatty tissue and not the alar cartilage. 2. Nasal valve area. It is the cross-sectional area bounded
4. Septal cartilage. Its anterosuperior border runs from by the structures forming the valve. It is the least cross-
under the nasal bones to the nasal tip. It supports the sectional area of nose and regulates airflow and resist-
dorsum of the cartilaginous part of the nose. In septal ance on inspiration.
abscess or after excessive removal of septal cartilage as
in submucosal resection (SMR) operation, support of
NASAL CAVITY PROPER
nasal dorsum is lost and a supratip depression results.
Each nasal cavity has a lateral wall, a medial wall, a roof
and a floor.
NASAL MUSCULATURE
Osteocartilaginous framework of nose is covered by mus- Lateral Nasal Wall
cles which bring about movements of the nasal tip, ala Three and occasionally four turbinates or conchae
and the overlying skin. They are the procerus, nasalis mark the lateral wall of nose. Conchae or turbinates are

149

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150 SECTION II — Diseases of Nose and Paranasal Sinuses 80hr9
fpontonasal Nasal process
q%0%te
¥*
I basal bones
frontal
provesMaxthe
of
Figure 23.1. Various parts of nose and related facial structures.

Figure 23.2. Osteocartilaginous framework of nose. (A) Lateral view. (B) Basal view.

scroll-like bony projections covered by mucous mem- which open posterior and superior to it form the posterior
brane. The spaces below the turbinates are called mea- group.
tuses (Figures 23.3 and 23.4).
→ Largest
INFERIOR TURBINATE. It is a separate bone and below
MIDDLE MEATUS. It shows several important structures
which are important in endoscopic surgery of the sinuses
it, into the inferior meatus, opens the nasolacrimal duct (Figure 23.5).
guarded at its terminal end by a mucosal valve called Uncinate process is a hook-like structure running in
Hasner’s valve. from anterosuperior to posteroinferior direction. Its pos-
terosuperior border is sharp and runs parallel to anterior
MIDDLE TURBINATE. It is an ethmoturbinal—a part of border of bulla ethmoidalis; the gap between the two is
ethmoid bone. It is attached to the lateral wall by a bony called hiatus semilunaris (inferior). It is a two-dimensional
lamella called ground or basal lamella. Its attachment is space of 1–2 mm width.
not straight but in an S-shaped manner. In the anterior The anteroinferior border of uncinate process is at-
third, it lies in sagittal plane and is attached to lateral tached to the lateral wall. Posteroinferior end of unci-
edge of cribriform plate. In the middle third, it lies in nate process is attached to inferior turbinate dividing the
frontal plane and is attached to lamina papyracea while membranous part of lower middle meatus into anterior
in its posterior third, it runs horizontally and forms roof and posterior fontanelle. The fontanel area is devoid of
of the middle meatus and is attached to lamina papyracea bone and consists of membrane only and leads into max-
and medial wall of maxillary sinus. illary sinus when perforated. Upper attachment of unci-
The ostia of various sinuses draining anterior to basal nate process shows great variation and may be inserted
lamella form anterior group of paranasal sinuses while those into the lateral nasal wall, upwards into the base of skull

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 Chapter 23 — Anatomy of Nose 151

Figure 23.3. Structures on lateral wall of nose.

Base of skull

Figure 23.4. Lateral wall of nose with turbinates removed showing openings of various sinuses.
me
LYÑÑ
Bulla ethmoidal
or medially into the middle turbinate (Figure 23.6). This it is called suprabullar or retrobullar recesses, respectively
also accounts for variations in drainage of frontal sinus. (Figure 23.8). The suprabullar and retrobullar recesses to-
The space limited medially by the uncinate process gether form the lateral sinus (sinus lateralis of Grunwald).
and frontal process of maxilla and sometimes lacrimal The lateral sinus is thus bounded superiorly by the skull
bone, and laterally by the lamina papyracea is called in- base, laterally by lamina papyracea, medially by middle
fundibulum. turbinate and inferiorly by the bulla ethmoidalis. Posteri-
Natural ostium of the maxillary sinus is situated in the orly the sinus lateralis may extend up to basal lamella of
lower part of infundibulum. Accessory ostium or ostia of middle turbinate. The cleft-like communication between
maxillary sinus are sometimes seen in the anterior or pos- the bulla and skull base and opening into middle meatus
terior fontanel (Figure 23.7). is also called hiatus semilunaris superior in contrast to hia-
tus semilunaris inferior referred to before.
BULLA ETHMOIDALIS. It is an ethmoidal cell situated be-
hind the uncinate process. Anterior surface of the bulla ATRIUM OF THE MIDDLE MEATUS. It is a shallow depres-
forms the posterior boundary of hiatus semilunaris. De- sion lying in front of middle turbinate and above the na-
pending on pneumatization, bulla may be a pneumatized sal vestibule.
cell or a solid bony prominence. It may extend superiorly
to the skull base and posteriorly to fuse with ground la- AGGER NASI. It is an elevation just anterior to the attach-
mella. When there is a space above or behind the bulla, ment of middle turbinate. When pneumatized it contains

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152 SECTION II — Diseases of Nose and Paranasal Sinuses

Figure 23.5. Lateral wall of nose. Middle turbinate is reflected upwards to show structures of the middle meatus.

Figure 23.6. Upper attachment of uncinate process: (A) into lamina papyracea, (B) into skull base and (C) into middle turbinate thus affecting
drainage of frontal sinus.

- Hiatus semilunar

Infundibulum
-

Figure 23.7. (A) Coronal section through middle meatus. Uncinate process forms the medial wall and floor of the infundibulum. (B) Coronal
section showing relationships of uncinate process, bulla ethmoidalis, middle turbinate, maxillary sinus, orbit and cribriform plate.

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 Chapter 23 — Anatomy of Nose 153

Medial Wall
Nasal septum forms the medial wall and is described on

NÉEsphenoid
p. 165.

Roof
Anterior sloping part of the roof is formed by nasal bones,
posterior sloping part is formed by the body of sphenoid
bone and the middle horizontal part is formed by the
cribriform plate of ethmoid through which the olfactory
nerves enter the nasal cavity.

Floor
It is formed by palatine process of the maxilla in its an-
terior three-fourths and horizontal part of the palatine
bone in its posterior one-fourth.

LINING MEMBRANE OF INTERNAL NOSE

1. VESTIBULE. It is lined by skin containing hair, hair fol-

Figure 23.8. Axial view showing middle meatus and its structure. licles and sebaceous glands.
Note also the retrobullar recess.
2. OLFACTORY REGION. Upper one-third of lateral wall

dnevmalnjed
air cells, the agger nasi cells, which communicate with
the frontal recess. An enlarged agger nasi cell may en-
(up to superior concha), corresponding part of the nasal
septum and the roof of nasal cavity form the olfactory
region. Here, mucous membrane is paler in colour.
croach on frontal recess area, constricting it and causing
mechanical obstruction to frontal sinus drainage.
3. RESPIRATORY REGION. Lower two-thirds of the nasal
Pneumatization of middle turbinate leads to an en-
cavity form the respiratory region. Here mucous mem-
larged ballooned out middle turbinate called concha bul-
brane shows variable thickness being thickest over nasal
losa. It drains into frontal recess directly or through agger
conchae especially at their ends, quite thick over the na-
nasi cells. Haller cells are air cells situated in the roof of
sal septum but very thin in the meatuses and floor of the
maxillary sinus. They are pneumatized from anterior or
nose. It is highly vascular and also contains erectile tissue.
posterior ethmoid cells. Enlargement of Haller cells en-
Its surface is lined by pseudostratified ciliated columnar
croaches on ethmoid infundibulum, impeding draining
epithelium which contains plenty of goblet cells. In the
of maxillary sinus.
submucous layer of mucous membrane are situated se-
rous, mucous, both serous and mucous secreting glands, Olfactory
SUPERIOR TURBINATE. It is also an ethmoturbinal and

€-77m
the ducts of which open on the surface of mucosa.
is situated posterior and superior to middle turbinate. It .

may also get pneumatized by one or more cells. It forms

an important landmark to identify ostium of sphenoid NERVE SUPPLY
sinus which lies medial to it. olfactory FLYFobes]
1. OLFACTORY NERVES. They carry sense of smell and
SUPERIOR MEATUS. It is a space below the superior tur- supply olfactory region of nose. They are the central fila-
binate. Posterior ethmoid cells open into it. Number of ments of the olfactory cells and are arranged into 12–20
posterior ethmoid cells varies from 1 to 5. Onodi cell is a nerves which pass through the cribriform plate and end
posterior ethmoidal cell which may grow posteriorly by in the olfactory bulb. These nerves can carry sheaths of
the side of sphenoid sinus or superior to it for as much dura, arachnoid and pia with them into the nose. Injury
distance as 1.5 cm from the anterior surface of sphenoid. to these nerves can open CSF space leading to CSF rhinor-
Onodi cell is surgically important as the optic nerve may rhoea or meningitis (Figure 23.9).
be related to its lateral wall.
2. NERVES OF COMMON SENSATION. They are:
SPHENOETHMOIDAL RECESS. It is situated above the supe-
1. Anterior ethmoidal nerve.
rior turbinate. Sphenoid sinus opens into it.
2. Branches of sphenopalatine ganglion.
3. Branches of infraorbital nerve. They supply vestibule
SUPREME TURBINATE. It is sometimes present above the
of nose both on its medial and lateral side.
superior turbinate and has a narrow meatus beneath it.
The ostium of sphenoid sinus is situated in the sphe- Most of the posterior two-thirds of nasal cavity (both
noethmoidal recess medial to the superior or supreme septum and lateral wall) are supplied by branches of sphe-
turbinate. It can be located endoscopically about 1 cm nopalatine ganglion which can be blocked by placing a
above the upper margin of posterior choana close to the pledget of cotton soaked in anaesthetic solution near
posterior border of the septum. the sphenopalatine foramen situated at the posterior

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154 SECTION II — Diseases of Nose and Paranasal Sinuses

Sphene palatine
g- foramen

Figure 23.9. Nerve supply of nose. (A) Lateral wall. Sphenopalatine ganglion situated at the posterior end of middle turbinate supplies most of
posterior two-thirds of nose. (B) Nerves on the medial wall.

extremity of middle turbinate. Anterior ethmoidal nerve nerve of pterygoid canal (vidian nerve) and reach the sphe-
which supplies anterior and superior part of the nasal nopalatine ganglion where they relay before reaching the
cavity (lateral wall and septum) can be blocked by placing nasal cavity. They also supply the blood vessels of nose
the pledget high up on the inside of nasal bones where and cause vasodilation.
the nerve enters. Sympathetic nerve fibres come from upper two thoracic
segments of spinal cord, pass through superior cervical
3. AUTONOMIC NERVES. Parasympathetic nerve fibres ganglion, travel in deep petrosal nerve and join the
supply the nasal glands and control nasal secretion. They parasympathetic fibres of greater petrosal nerve to form
come from greater superficial petrosal nerve, travel in the the nerve of pterygoid canal (vidian nerve). They reach the

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 Chapter 23 — Anatomy of Nose 155

nasal cavity without relay in the sphenopalatine ganglion. LYMPHATIC DRAINAGE

Their stimulation causes vasoconstriction. Excessive rhi-
norrhoea in cases of vasomotor and allergic rhinitis can be Lymphatics from the external nose and anterior part
controlled by section of the vidian nerve. of nasal cavity drain into submandibular lymph nodes
while those from the rest of nasal cavity drain into upper
jugular nodes either directly or through the retropharyn-
BLOOD SUPPLY geal nodes. Lymphatics of the upper part of nasal cavity
Both the internal and external carotid systems supply the communicate with subarachnoid space along the olfac-
nose. Details of blood supply are given on p. 197. tory nerves.

pins
Greater petrosal sphenopalatine
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 Chapter 24
Physiology of Nose

Functions of the nose are classified as: while nasal mucus traps particles as fine as 0.5–3.0 µm.
Particles smaller than 0.5 µm seem to pass through the
1. Respiration.
nose into lower airways without difficulty.
2. Air-conditioning of inspired air.
2. Temperature control of the inspired air. It is regulated
3. Protection of lower airway.
by large surface of nasal mucosa which is structurally
4. Vocal resonance.
adapted to perform this function. This mucous mem-
5. Nasal reflex functions.
brane, particularly in the region of middle and inferior
6. Olfaction.
turbinates and adjacent parts of the septum, is highly
vascular with cavernous venous spaces or sinusoids
which control the blood flow, and this increases or de-
RESPIRATION creases the size of turbinates. This also makes an efficient
“radiator” mechanism to warm up the cold air. Inspired
Nose is the natural pathway for breathing. Mouth breath-
air which may be at 20°C or 0°C or even at subzero tem-
ing is an acquired act through learning. So natural is the
perature is heated to near body temperature (37°C) in
instinct to breath through the nose that a newborn infant
one-fourth of second, the time that the air takes to pass
with choanal atresia may asphyxiate to death if urgent
from the nostril to the nasopharynx. Similarly, hot air is
measures are not taken to relieve it. The nose also permits
cooled to the level of body temperature.
breathing and eating to go on simultaneously.
3. Humidification. This function goes on simultaneously
During quiet respiration, inspiratory air current pass-
with the temperature control of inspired air. Relative
es through middle part of nose between the turbinates
humidity of atmospheric air varies depending on cli-
and nasal septum. Very little air passes through inferior
matic conditions. Air is dry in winter and saturated
meatus or olfactory region of nose (Figure 24.1). There-
with moisture in summer months. Nasal mucous mem-
fore, weak odorous substances have to be sniffed before
brane adjusts the relative humidity of the inspired air
they can reach the olfactory area.
to 75% or more. Water, to saturate the inspired air, is
During expiration, air current follows the same
provided by the nasal mucous membrane which is rich
course as during inspiration, but the entire air current is
in mucous and serous secreting glands. About 1000 mL
not expelled directly through the nares. Friction offered
of water is evaporated from the surface of nasal mu-
at limen nasi converts it into eddies under cover of infe-
cosa in 24 h.
rior and middle turbinates and this ventilates the sinuses
through the ostia. Moisture is essential for integrity and function of the
Anterior end of inferior turbinate undergoes swelling ciliary epithelium. At 50% relative humidity, ciliary func-
and shrinkage thus regulating inflow of air. tion stops in 8–10 min. Thus, dry air predisposes to infec-
tions of the respiratory tract. Humidification also has a
NASAL CYCLE. Nasal mucosa undergoes rhythmic cyclical significant effect on gas exchange in the lower airways.
congestion and decongestion, thus controlling the air- In nasal obstruction, gaseous exchange is affected in the
flow through nasal chambers. When one nasal chamber lungs, leading to rise in pCO2, causing apnoeic spells dur-
is working, total nasal respiration, equal to that of both ing sleep; it also decreases pO2.
nasal chambers, is carried out by it. Nasal cycle varies
every 2½–4 h and may be characteristic of an individual.
PROTECTION OF LOWER AIRWAY
1. Mucociliary mechanism. Nasal mucosa is rich in
AIR-CONDITIONING OF INSPIRED AIR goblet cells, secretory glands both mucous and se-
rous. Their secretion forms a continuous sheet called
Nose is aptly called the “air-conditioner” for lungs. It fil-
mucous blanket spread over the normal mucosa. Mu-
ters and purifies the inspired air and adjusts its tempera-
cous blanket consists of a superficial mucus layer and
ture and humidity before the air passes to the lungs.
a deeper serous layer, floating on the top of cilia which
1. Filtration and purification. Nasal vibrissae at the en- are constantly beating to carry it like a “conveyer belt”
trance of nose act as filters to sift larger particles like towards the nasopharynx (Figure 24.2). It moves at
fluffs of cotton. Finer particles like dust, pollen and a speed of 5–10 mm/min and the complete sheet of
bacteria adhere to the mucus which is spread like a mucus is cleared into the pharynx every 10–20 min.
sheet all over the surface of the mucous membrane. The inspired bacteria, viruses and dust particles are
The front of the nose can filter particles up to 3 µm, entrapped on the viscous mucous blanket and then

157

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158 SECTION II — Diseases of Nose and Paranasal Sinuses

Figure 24.1. Physiology of nasal airflow. (A) Inspiration. (B) Expiration.

So efficient are the functions of nose that 500 cubic

feet of air, that we breathe every 24 h, is filtered, humidi-
fied, adjusted to proper temperature and cleared of all the
dust, bacteria and viruses before reaching the lungs.

VOCAL RESONANCE
Nose forms a resonating chamber for certain consonants
Figure 24.2. “Conveyor belt” mechanism of mucus blanket to en- in speech. In phonating nasal consonants (M/N/NG),
trap and carry organisms and dust particles. sound passes through the nasopharyngeal isthmus and
is emitted through the nose. When nose (or nasophar-
ynx) is blocked, speech becomes denasal, i.e. M/N/NG
carried to the nasopharynx to be swallowed. Presence
are uttered as B/D/G, respectively. It is to be remem-
of turbinates almost doubles the surface area to per-
bered that in Hindi alphabets, last letter of a “varga”
form this function. About 600–700 mL of nasal secre-
( ) is sub-
tions are produced in 24 h.
stituted by its third letter. Thus, an affected person utters
In mammals, cilia beat 10–20 times per second at
for and for . Reverse is true in velopharyngeal
room temperature. They have a rapid “effective stroke”
insufficiency where is substituted for .
and a slow “recovery stroke.” In the former, the extend-
ed cilia reach mucus layer while in the recovery stroke,
they bend and travel slowly in the reverse direction in
the thin serous layer, thus moving the mucous blanket NASAL REFLEXES
in only one direction. In immotile cilia syndrome, cil-
Several reflexes are initiated in the nasal mucosa. Smell
ia are defective and cannot beat effectively, leading to
of a palatable food cause reflex secretion of saliva and
stagnation of mucus in the nose and sinuses and bron-
gastric juice. Irritation of nasal mucosa causes sneezing.
chi causing chronic rhinosinusitis and bronchiectasis.
Nasal function is closely related to pulmonary functions
Movements of cilia are affected by drying, drugs (adren-
through nasobronchial and nasopulmonary reflexes.
aline), excessive heat or cold, smoking, infections and
It has been observed that nasal obstruction leads to in-
noxious fumes like sulfur dioxide and carbon dioxide.
creased pulmonary resistance and is reversed when nasal
2. Enzymes and immunoglobulins. Nasal secretions
obstruction is surgically treated. Nasal packing in cases
also contain an enzyme called muramidase (lysozyme)
of epistaxis or after nasal surgery leads to lowering of
which kills bacteria and viruses. Immunoglobulins IgA
pO2 which returns to normal after removal of the pack.
and IgE, and interferon are also present in nasal secre-
Pulmonary hypertension or cor pulmonale can develop
tions and provide immunity against upper respiratory
in children with long-standing nasal obstruction due to
tract infections.
tonsil and adenoid hypertrophy and can be reversed after
3. Sneezing. It is a protective reflex. Foreign particles
removal of the tonsils and adenoids.
which irritate nasal mucosa are expelled by sneezing.
Copious flow of nasal secretions that follows irritation
by noxious substance helps to wash them out.
OLFACTION
The pH of nasal secretion is nearly constant at 7. The
cilia and the lysozyme act best at this pH. Alteration in Sense of smell is well-developed in lower animals to give
nasal pH, due to infections or nasal drops, seriously im- warning of the environmental dangers but it is com-
pairs the functions of cilia and lysozyme. paratively less important in man. Still it is important for

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 Chapter 24 — Physiology of Nose 159

pleasure and for enjoying the taste of food. When nose necessary are the healthy state of olfactory mucosa and
is blocked, food tastes bland and unpalatable. Vapours the integrity of neural pathways, i.e. olfactory nerves,
of ammonia are never used to test the sense of smell as olfactory bulb and tract and the cortical centre of
they stimulate fibres of the trigeminal nerve and cause olfaction.
irritation in the nose rather than stimulate the olfactory Anosmia is total loss of sense of smell while hyposmia
receptors. is partial loss. They can result from nasal obstruction due
to nasal polypi, enlarged turbinates or oedema of mucous
1. OLFACTORY PATHWAYS. Smell is perceived in the ol- membrane as in common cold, allergic or vasomotor rhi-
factory region of nose which is situated high up in the na- nitis. Anosmia is also seen in atrophic rhinitis, a degener-
sal cavity. This area contains millions of olfactory recep- ative disorder of nasal mucosa; peripheral neuritis (toxic
tor cells. Peripheral process of each olfactory cell reaches or influenzal); injury to olfactory nerves or olfactory bulb
the mucosal surface and is expanded into a ventricle with in fractures of anterior cranial fossa; and intracranial le-
several cilia on it. This acts as a sensory receptor to re- sions like abscess, tumour or meningitis which cause pres-
ceive odorous substances. Central processes of the olfac- sure on olfactory tracts.
tory cells are grouped into olfactory nerves which pass Parosmia is perversion of smell; the person interprets
through the cribriform plate of ethmoid and end in the the odours incorrectly. Often these persons complain
mitral cells of the olfactory bulb. Axons of mitral cells of disgusting odours. It is seen in the recovery phase of
form olfactory tract and carry smell to the prepyriform postinfluenzal anosmia and the probable explanation is
cortex and the amygdaloid nucleus where it reaches con- misdirected regeneration of nerve fibres. Intracranial tu-
sciousness. Olfactory system is also associated with auto- mour should be excluded in all cases of parosmia.
nomic system at the hypothalamic level. Sense of smell can be tested by asking the patient to
smell common odours such as lemon, peppermint, rose,
2. DISORDERS OF SMELL. It is essential for the percep- garlic or cloves from each side of the nose separately, with
tion of smell that the odorous substance be volatile and eyes closed. Quantitative estimation (quantitative olfac-
that it should reach the olfactory area unimpeded. Also tometry) requires special equipment.

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 Chapter 26
Nasal Septum and Its Diseases

also the site for origin of the “bleeding polypus” (hae-

ANATOMY
mangioma) of nasal septum.
Nasal septum consists of three parts:

1. COLUMELLAR SEPTUM. It is formed of columella con-

taining the medial crura of alar cartilages united together
FRACTURES OF NASAL SEPTUM
by fibrous tissue and covered on either side by skin. AETIOPATHOGENESIS
2. MEMBRANOUS SEPTUM. It consists of double layer of Trauma inflicted on the nose from the front, side or be-
skin with no bony or cartilaginous support. It lies be- low can result in injuries to the nasal septum. The sep-
tween the columella and the caudal border of septal car- tum may buckle on itself, fracture vertically, horizontally
tilage. Both columellar and membranous parts are freely or be crushed to pieces as in a smashed nose. The frac-
movable from side to side. tured pieces of septum may overlap each other or project
into the nasal cavity through mucosal tears. Fracture of
3. SEPTUM PROPER. It consists of osteocartilaginous the septal cartilage or its dislocation from the vomerine
framework, covered with nasal mucous membrane. groove, can result from trauma to the lower nose without
Its principal constituents are (Figure 26.1): associated fractures of nasal bones. Septal injuries with
mucosal tears cause profuse epistaxis while those with
1. the perpendicular plate of ethmoid,
intact mucosa result in septal haematoma which, if not
2. the vomer and
drained early, will cause absorption of the septal cartilage
3. a large septal (quadrilateral) cartilage wedged between
and saddle nose deformity.
the above two bones anteriorly. Other bones which
“Jarjaway” fracture of nasal septum results from blows
make minor contributions at the periphery are crest
from the front; it starts just above the anterior nasal spine
of nasal bones, nasal spine of frontal bone, rostrum of
and runs horizontally backwards just above the junction
sphenoid, crest of palatine bones and the crest maxilla,
of septal cartilage with the vomer (Figure 26.2A).
and the anterior nasal spine of maxilla.
“Chevallet” fracture of septal cartilage results from
Septal cartilage not only forms a partition between the blows from below; it runs vertically from the anterior na-
right and left nasal cavities but also provides support to sal spine upwards to the junction of bony and cartilagi-
the tip and dorsum of cartilaginous part of nose. Its de- nous dorsum of nose (Figure 26.2B).
struction, e.g. in septal abscess, injuries, tuberculosis or
excessive removal during septal surgery, leads to depres- TREATMENT
sion of lower part of nose and drooping of the nasal tip.
Septal cartilage lies in a groove in the anterior edge Early recognition and treatment of septal injuries is essen-
of vomer and rests anteriorly on anterior nasal spine. tial. Haematomas should be drained. Dislocated or frac-
During trauma, it may get dislocated from anterior nasal tured septal fragments should be repositioned and sup-
spine or vomerine groove causing caudal septal deviation ported between mucoperichondrial flaps with mattress
or septal spur, respectively. This compromises the nasal sutures and nasal packing. Fractures of nasal pyramid are
airway. Septal cartilage is also intimately related to the often complicated with fractures of the septum and both
upper lateral cartilages of nose and is in fact fused with should be treated concomitantly.
them in the upper third. For this reason septal deviation
may be associated with deviation of cartilaginous part of COMPLICATIONS
external nose.
Blood Vessels of Nasal Septum (see Chapter 33). Septum is important in supporting the lower part of the
Nerve Supply of Nasal Septum (see Chapter 23). external nose. If its injuries are ignored, they would result
in deviation of the cartilaginous nose, or asymmetry of
LITTLE’S AREA OR KIESSELBACH’S PLEXUS. This is the nasal tip, columella or the nostril.
vascular area in the anteroinferior part of nasal septum
just above the vestibule. Anterior ethmoidal, sphenopala-
tine, greater palatine and septal branch of superior labial DEVIATED NASAL SEPTUM (DNS)
arteries and their corresponding veins form an anastomo-
sis here. This is the commonest site for epistaxis. This is This is an important cause of nasal obstruction.

165

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 166 SECTION II — Diseases of Nose and Paranasal Sinuses

Figure 26.3. DNS associated with high-arched palate.

MCC -

B) 5th trauma C 58
-

Figure 26.1. Anatomy of nasal septum.

often overlooked. Even the history may not be forthcom-
ing. Trauma may also be inflicted at birth during difficult
labour when nose is pressed during its passage through
the birth canal. Birth injuries should be immediately at-
tended to as they result in septal deviation later in life. Tectosepkl
from Pucks
Blows
µ
2. DEVELOPMENTAL ERROR. Nasal septum is formed by
front the tectoseptal process which descends to meet the two
halves of the developing palate in the midline. During
→ C
the primary and secondary dentition, further develop-
ment takes place in the palate, which descends and wid- 2 halves
ens to accommodate the teeth. older
Unequal growth between the palate and the base of in
-
skull may cause buckling of the nasal septum. In mouth
palate
- -
midline
breathers, as in adenoid hypertrophy, the palate is often
-

highly arched and the septum is deviated (Figure 26.3).

-

Similarly, DNS may be seen in cases of cleft

-
lip and palate
and in those with dental abnormalities. -

3. RACIAL FACTORS. Caucasians are affected more than

black Americans.
from
Blows 4. HEREDITARY FACTORS. Several members of the same
below family may have deviated nasal septum.

☒ TYPES OF DNS (FIGURE 26.4)

Deviation may involve only the cartilage, bone or both
the cartilage and bone.

1. ANTERIOR DISLOCATION. Septal cartilage may be dislo-

E-
-

cated into one of the nasal chambers. This is better appre-

ciated by looking at the base of nose when patient’s head
Figure 26.2. Septal fracture showing: (A) Jarjaway type. (B) Chevallet
type.
is tilted backwards (Figure 26.5).

2. C-SHAPED DEFORMITY. Septum is deviated in a simple

curve to one side. Nasal chamber on the concave side of
AETIOLOGY
y
=
the nasal septum will be wider and may show compensa-
Trauma and errors of development form the two impor- -
=
tory hypertrophy of turbinates.
tant factors in the causation of deviated septum.
3. S-SHAPED DEFORMITY. Either in vertical or anteropos-
1. TRAUMA. A lateral blow on the nose may cause dis- terior plane. Such a deformity may cause bilateral nasal
placement of septal cartilage from the vomerine groove obstruction.
and maxillary crest, while a crushing blow from the front
may cause buckling, twisting, fractures and duplication 4. SPURS. A spur is a shelf-like projection often found at
of nasal septum with telescoping of its fragments. Inju- the junction of bone and cartilage. A spur may press on -

ries to the nose commonly occur in childhood but are the lateral wall and gives rise to headache. It may also

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 Chapter 26 — Nasal Septum and Its Diseases 167

Figure 26.4. Types of deviated nasal septum.

CIF
, Nasal obstructs
2 Sinusitis Dois ① Cold
Figure 26.6. spatula
Cottle
test
test: On pulling the cheek away from the mid-
line, the ②
nasal 's test
valve opens,
Cattle increasing the airflow from that side of the
3 Nasal discharge nasal cavity.
4 AOM ③ CT scan

5 Headache [Link] neuralgia]

6
Hyposmie (choanal atresia or a choanal polyp). Unilateral choanal
atresia may be missed in infancy and childhood. Choanal
7- epistaxis polyp may be missed on the anterior rhinoscopy unless
• Eat deformity posterior rhinoscopy or nasal endoscopy is done.
Cottle test. It is used in nasal obstruction due to abnor-
mality of the nasal valve. In this test, cheek is drawn later-
ally while the patient breathes quietly. If the nasal airway
improves on the test side, the test is positive and indicates
abnormality of the vestibular component of nasal valve
Figure 26.5. Anterior dislocation. Caudal border of septal cartilage (Figure 26.6).
projects into right naris.
2. HEADACHE. Deviated septum, especially a spur, may
press on the lateral wall of nose giving rise to pressure
predispose to repeated epistaxis from the vessels stretched headache.

=
on its convex surface.
3. SINUSITIS. Deviated septum may obstruct sinus ostia
5.-THICKENING. It may be due to organized haematoma resulting in poor ventilation of the sinuses. Therefore, it
or overriding of dislocated septal fragments. forms an important cause to predispose or perpetuate si-
nus infections.
CLINICAL FEATURES
4. EPISTAXIS. Mucosa over the deviated part of septum
DNS can involve any age and sex. Males are affected more is exposed to the drying effects of air currents leading to
than females. formation of crusts, which when removed cause bleeding.
Bleeding may also occur from vessels over a septal spur.
1. NASAL OBSTRUCTION. Depending on the type of septal
deformity, obstruction may be unilateral or bilateral. Res- 5. ANOSMIA. Failure of the inspired air to reach the olfac-
piratory currents pass through upper part of nasal cavity, tory region may result in total or partial loss of sense of
therefore, high septal deviations cause nasal obstruction smell.
more than lower ones.
When examining a case of nasal obstruction, one 6. EXTERNAL DEFORMITY. Septal deformities may be as-
should ascertain the site of obstruction in the nose. It sociated with deviation of the cartilaginous or both the
could be (i) vestibular (caudal septal dislocation, synechi- bony and cartilaginous dorsum of nose, deformities of
ae or stenosis), (ii) at the nasal valve (synechiae, usually the nasal tip or columella.
postrhinoplasty), (iii) attic (along the upper part of na-
sal septum due to high septal deviation, (iv) turbinal (hy- 7. MIDDLE EAR INFECTION. DNS also predisposes to mid-
pertrophic turbinates or concha bullosa) and (v) choanal dle ear infection.

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 168 SECTION II — Diseases of Nose and Paranasal Sinuses
Granger ⑥
TREATMENT Examination reveals smooth rounded swelling of the
septum in both the nasal fossae. Palpation may show the
Minor degrees of septal deviation with no symptoms are mass to be soft and fluctuant. man

work
commonly seen in patients and require no treatment. It

¥
is only when deviated septum produces mechanical nasal
TREATMENT
aot%kʰ
*
obstruction or the symptoms given above that an opera-
tion is indicated. Small haematomas can be aspirated with a wide bore ster-
Submucous Resection (SMR) Operation ile needle. Larger haematomas are incised and drained
↑ by a small anteroposterior incision parallel to the nasal
It is generally done in adults under local anaesthesia. It floor. Excision of a small piece of mucosa from the edge
'sconsists of elevating the mucoperichondrial and muco-
Killianperiosteal flaps on either side of the septal framework by a of incision gives better drainage. Following drainage,
⑨ nose is packed on both sides to prevent reaccumulation.
incisionsingle incision made on one side of the septum, removing ⑨Systemic antibiotics should be given to prevent septal
the deflected parts of the bony and cartilaginous septum, abscess.
and then repositioning the flaps (see section on Operative
Surgery for details).
COMPLICATIONS
Septoplasty
Septal haematoma, if not drained, may organize into fi-
's It is a conservative approach to septal surgery. In this op- CO
freer eration, much of the septal framework is retained. Only
brous tissue leading to a permanently thickened septum. fibrosis
②If secondary infection supervenes, it results in septal ab-
incision the most deviated parts are removed. Rest of the septal scess with -necrosis of cartilage and depression of nasal
omw framework is corrected and repositioned by plastic means.
Mucoperichondrial/periosteal flap is generally raised only
dorsum. ③ñ
end G
_

on one side of the septum, retaining the attachment and

prop blood supply on the other. Septoplasty has now almost
Septa replaced SMR operation (see Chapter 88). SEPTAL ABSCESS
Septal surgery is usually done after the age of 17 so
AETIOLOGY
as not to interfere with the growth of nasal skeleton.
However, if a child has severe septal deviation causing Mostly, it results from secondary infection of septal hae-
marked nasal obstruction, conservative septal surgery matoma. Occasionally, it follows furuncle of the nose or
(septoplasty) can be performed to provide a good airway. upper lip. It may also follow acute infection such as ty-
phoid or measles.

SEPTAL HAEMATOMA CLINICAL FEATURES

AETIOLOGY There is severe bilateral nasal obstruction with pain and
tenderness over the bridge of nose. Patient may also com-
It is collection of blood under the perichondrium or peri- plain of fever with chills and frontal headache. Skin over
osteum of the nasal septum (Figure 26.7). It often results the nose may be red and swollen. Internal examination of
from nasal trauma or septal surgery. In bleeding disorders, nose reveals smooth bilateral swelling of the nasal septum
it may occur spontaneously. (Figure 26.8). Fluctuation can be elicited in this swelling.
Septal mucosa is often congested. Submandibular lymph
CLINICAL FEATURES Mardy mnaeperieb both sides nodes may also be enlarged and tender.
④ ~
Bilateral nasal obstruction is the commonest presenting
②
symptom. This may be associated with frontal headache
and a sense of pressure over the nasal bridge.
③

Figure 26.7. Septal haematoma. Figure 26.8. Septal abscess.

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 Chapter 26 — Nasal Septum and Its Diseases 169

Figure 26.10. Septal button for closure of perforation.

Figure 26.9. Septal perforation.

TREATMENT 4. Chronic granulomatous conditions like lupus, tuber-

Abscess should be drained as early as possible. Incision culosis and leprosy cause perforation in the cartilagi-
is made in the most dependent part of the abscess and a nous part while syphilis involves the bony part. In
piece of septal mucosa excised. Pus and necrosed pieces these cases, evidence of the causative disease may also
of cartilage are removed by suction. Incision may require be seen in other systems of the body.
to be reopened daily for 2–3 days to drain any pus or to 5. Wegener’s granuloma is a midline destructive lesion
remove any necrosed pieces of cartilage. Systemic antibi- which may cause total septal destruction.
otics are started as soon as diagnosis has been made and
continued at least for a period of 10 days. 3. DRUGS AND CHEMICALS
1. Prolonged use of steroid sprays in nasal allergy.
COMPLICATIONS 2. Cocaine addicts.
3. Workers in certain occupations, e.g. chromium
Necrosis of septal cartilage often results in depression of plating, dichromate or soda ash (sodium carbonate)
the cartilaginous dorsum in the supratip area and may manufacture or those exposed to arsenic or its
require augmentation rhinoplasty 2–3 months later. compounds.
Necrosis of septal flaps may lead to septal perforation.
Meningitis and cavernous sinus thrombosis following 4. IDIOPATHIC. In many cases, there is no history of
septal abscess, though rare these days, can be serious trauma or previous disease and the patient may even be
complications. unaware of the existence of a perforation.

CLINICAL FEATURES
PERFORATION OF NASAL SEPTUM ⑧
(FIGURE 26.9) Small anterior perforations cause whistling sound dur-

AETIOLOGY
⑧
ing inspiration or expiration. Larger perforations
,
develop
crusts which obstruct the nose or cause severe epistaxis
1. TRAUMATIC PERFORATIONS. Trauma is the most com-
mon cause. Injury to mucosal flaps during SMR, cauteri-
when removed.
Large
-
flapiupoircaimkupnose
crustfhll
siatistie Mauna
TREATMENT snallpesfod
-

zation of septum with chemicals or galvanocautery for oinhmt

epistaxis and habitual nose picking are the common
button whereas
An attempt should always be made to find out the cause
forms of trauma. Occasionally, septum is deliberately per-
before treatment of perforation. This may require biopsy
forated to put ornaments.
from the granulations or biopsy of the edge of the per-
foration. Inactive small perforations can be surgically
2. PATHOLOGICAL PERFORATIONS. They can be caused by:
closed by plastic flaps. Larger perforations are difficult to
1. Septal abscess. close. Their treatment is aimed to keep the nose crust-free
2. Nasal myiasis. by alkaline nasal douches and application of a bland oint-
3. Rhinolith or neglected foreign body causing pressure ment. Sometimes, a thin silastic button can be worn to
necrosis. get relief from the symptoms (Figure 26.10).

[Link]
 Chapter 30
Allergic Rhinitis

It is an IgE-mediated immunologic response of nasal mu- Nonspecific nasal hyper-reactivity is seen in patients of
cosa to airborne allergens and is characterized by watery allergic rhinitis. There is increased nasal response to nor-
nasal discharge, nasal obstruction, sneezing and itching mal stimuli resulting in sneezing, rhinorrhoea and nasal
in the nose. This may also be associated with symptoms congestion. Clinically, allergic response occurs in two
of itching in the eyes, palate and pharynx. Two clinical phases:
types have been recognized:
1. Acute or early phase. It occurs immediately within
1. Seasonal. Symptoms appear in or around a particular 5–30 min, after exposure to the specific allergen and
season when the pollens of a particular plant, to which consists of sneezing, rhinorrhoea nasal blockage and/
the patient is sensitive, are present in the air. or bronchospasm. It is due to release of vasoactive
2. Perennial. Symptoms are present throughout the year. amines like histamine.
2. Late or delayed phase. It occurs 2–8 h after exposure
to allergen without additional exposure. It is due to
infiltration of inflammatory cells—eosinophils, neu-
AETIOLOGY
trophils, basophil, monocytes and CD4 + T cells at the
INHALANT ALLERGENS. They may be seasonal or peren- site of antigen deposition causing swelling, congestion
nial. Seasonal allergens include pollens from trees, grasses and thick secretion. In the event of repeated or con-
and weeds. They vary geographically. The knowledge tinuous exposure to allergen, acute phase symptoma-
of pollen appearing in a particular area and the sea- tology overlaps the late phase.
son in which they occur is important. Their knowledge
also helps in skin tests. Perennial allergens are present
throughout the year regardless of the season. They in- CLINICAL FEATURES
clude molds, dust mites, cockroaches and dander from
animals. Dust includes dust mite, insect parts, fibres and There is no age or sex predilection. It may start in infants
animal danders. Dust mites live on skin scales and other as young as 6 months or older people. Usually the onset
debris and are found in the beddings, mattresses, pillows, is at 12–16 years of age.
carpets and upholstery. The cardinal symptoms of seasonal nasal allergy include
paroxysmal sneezing, 10–20 sneezes at a time, nasal ob-
GENETIC PREDISPOSITION. plays an important part. Chanc- struction, watery nasal discharge and itching in the nose.
es of children developing allergy are 20 and 47%, respec- Itching may also involve eyes, palate or pharynx. Some
tively, if one or both parents suffer from allergic diathesis. may get bronchospasm. The duration and severity of
symptoms may vary with the season.
Symptoms of perennial allergy are not so severe as that
of the seasonal type. They include frequent colds, persis-
PATHOGENESIS tently stuffy nose, loss of sense of smell due to mucosal
oedema, postnasal drip, chronic cough and hearing im-
Inhaled allergens produce specific IgE antibody in the ge-
pairment due to eustachian tube blockage or fluid in the
netically predisposed individuals. This antibody becomes
middle ear.
fixed to the blood basophils or tissue mast cells by its Fc
Signs of allergy may be seen in the nose, eyes, ears,
end (Figure 30.1 ). On subsequent exposure, antigen
pharynx or larynx.
combines with IgE antibody at its Fab end. This reaction
produces degranulation of the mast cells with release of • Nasal signs include transverse nasal crease—a black
several chemical mediators, some of which already exist line across the middle of dorsum of nose due to con-
in the preformed state while others are synthesized afresh. stant upward rubbing of nose simulating a salute (al-
These mediators (Figure 30.2) are responsible for symp- lergic salute), pale and oedematous nasal mucosa which
tomatology of allergic disease. Depending on the tissues may appear bluish. Turbinates are swollen. Thin, wa-
involved, there may be vasodilation, mucosal oedema, in- tery or mucoid discharge is usually present.
filtration with eosinophils, excessive secretion from nasal • Ocular signs include oedema of lids, congestion and
glands or smooth muscle contraction. A “priming affect” cobble-stone appearance of the conjunctiva, and dark
has also been described, i.e. mucosa earlier sensitized to circles under the eyes (allergic shiners).
an allergen will react to smaller doses of subsequent spe- • Otologic signs include retracted tympanic membrane
cific allergen. It also gets “primed” to other nonspecific or serous otitis media as a result of eustachian tube
antigens to which patient was not exposed (Figure 30.3). blockage.

187

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188 SECTION II — Diseases of Nose and Paranasal Sinuses

Figure 30.1. (A) Structure of IgE antibody. Fc end is attached to the mast cell or blood basophil while Fab end is the antigen binding site. (B) Release
of mediator substances from mast cell producing symptoms of nasal allergy. One antigen bridges two adjacent molecules of IgE antibody.
Scan to play Allergic Rhinitis.

• Pharyngeal signs include granular pharyngitis due to subdivided into intermittent or persistent and severity of
hyperplasia of submucosal lymphoid tissue. A child disease into mild, moderate or severe.
with perennial allergic rhinitis may show all the fea- This new system of classification helps in treatment
tures of prolonged mouth breathing as seen in adenoid guidelines.
hyperplasia. A detailed history and physical examination is helpful,
• Laryngeal signs include hoarseness and oedema of and also gives clues to the possible allergen. Other causes
the vocal cords. of nasal stuffiness should be excluded.

DIAGNOSIS INVESTIGATIONS
NEW ALLERGIC RHINITIS AND ITS IMPACT ON ASTHMA 1. Total and differential count. Peripheral eosinophilia
(ARIA) CLASSIFICATION (TABLE 30.1). It is based on du- may be seen but this is an inconsistent finding.
ration and symptoms of disease. Duration of symptoms is 2. Nasal smear. It shows large number of eosinophils in
allergic rhinitis. Nasal smear should be taken at the
time of clinically active disease or after nasal chal-
lenge test. Nasal eosinophilia is also seen in certain

Figure 30.3. Both allergic and nonspecific stimuli act on mast cells or
Figure 30.2. Release of mediators from mast cell when challenged blood basophils releasing several mediator substances responsible for
by allergic or nonspecific stimuli. symptomatology of allergy.

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 Chapter 30 — Allergic Rhinitis 189

TABLE 30.1 CLASSIFICATION OF ALLERGIC TREATMENT

RHINITIS (ARIA)
Treatment can be divided into:
• Duration of disease
• Intermittent: Symptoms are present 1. Avoidance of allergen.
– Less than 4 days a week or 2. Treatment with drugs.
– For less than 4 weeks 3. Immunotherapy.
• Persistent: Symptoms are present
– More than 4 days a week or
1. AVOIDANCE OF ALLERGEN. This is most successful if
– For more than 4 weeks
• Severity of disease the antigen involved is single. Removal of a pet from
• Mild: None of the following symptoms are present the house, encasing the pillow or mattress with plastic
– Sleep disturbance sheet, change of place of work or sometimes change of
– Impairment of daily activities, leisure and sport job may be required. A particular food article to which
– Impairment of school or work the patient is found allergic can be eliminated from the
– Troublesome symptoms diet.
• Moderate to severe: One or more of the above symptoms are
present 2. TREATMENT WITH DRUGS
1. Antihistaminics. They control rhinorrhoea, sneezing
and nasal itch. All antihistaminics have the side effect
nonallergic rhinitis, e.g. NARES (nonallergic rhinitis
of drowsiness; some more than the other. The dose
with eosinophilia syndrome).
and type of the antihistaminic has to be individual-
3. Skin tests. These tests help to identify specific allergen.
ized. If one antihistaminic is not effective, another
They are prick, scratch and intradermal tests.
may be tried from a different class.
a. Skin prick test. This is an excellent method to dem-
2. Sympathomimetic drugs (oral or topical). Alpha-adren-
onstrate the allergen. A drop of concentrated aller-
ergic drugs constrict blood vessels and reduce nasal
gen solution is placed on the volar surface of the
congestion and oedema. They also cause central
forearm or back and a sharp needle pricked into the
nervous system stimulation and are often given in
dermis through the drop. It introduces the allergen
combination with antihistaminics to counteract
into the dermis. A positive reaction is manifested
drowsiness. Pseudoephedrine and phenylephrine are
by the formation of a central wheal and a surround-
often combined with antihistaminics for oral admin-
ing zone of erythema (flare) within 10–15 min.
istration.
Simultaneously a control test is performed with his-
3. Corticosteroids. Oral corticosteroids are very effective
tamine and the diluent used in allergen solution.
in controlling the symptoms of allergic rhinitis but
b. Specific IgE measurements. It is an in vitro test to find
their use should be limited to acute episodes which
the specific allergen. There is a good correlation
have not been controlled by other measures. They
between the skin tests and specific IgE measure-
have several systemic side effects.
ments. However both false positive and false nega-
4. Sodium cromoglycate. It stabilizes the mast cells and
tive results can occur. It is therefore recommended
prevents them from degranulation despite the forma-
to correlate the two tests with clinical symptoms.
tion of IgE-antigen complex. It is used as 2% solution
4. Radioallergosorbent test (RAST). It is an in vitro test
for nasal drops or spray or as an aerosol powder. It is
and measures specific IgE antibody concentration in
useful both in seasonal and perennial allergic rhinitis.
the patient’s serum.
5. Anticholinergics. They block rhinorrhoea both of the
5. Nasal provocation test. A crude method is to chal-
allergic and nonallergic rhinitis. Ipratropium bromide
lenge the nasal mucosa with a small amount of aller-
has been used as nasal spray to control rhinorrhoea.
gen placed at the end of a toothpick and asking the
There are no systemic side effects.
patient to sniff into each nostril and to observe if al-
6. Leukotriene receptor antagonists. They include montelu-
lergic symptoms are reproduced. More sophisticated
kast, pranlukast and zafirlukast. They block cysteinyl
techniques are available now.
leukotriene type receptors. They are well-tolerated
and have few side effects.
7. Anti-IgE. It reduces the IgE level and has an anti-
COMPLICATIONS inflammatory effect. Omalizumab is such a drug.
It is indicated in children above 12 years who have
Nasal allergy may cause:
moderate to severe asthma. It is not yet approved for
1. Recurrent sinusitis because of obstruction to the sinus allergic rhinitis.
ostia.
2. Formation of nasal polypi in about 2%. 3. IMMUNOTHERAPY. Immunotherapy or hyposensitiza-
3. Serous otitis media. tion is used when drug treatment fails to control symp-
4. Orthodontic problems and other ill-effects of pro- toms or produces intolerable side effects. Allergen is
longed mouth breathing especially in children. given in gradually increasing doses till the maintenance
5. Bronchial asthma. Patients of nasal allergy have dose is reached. Immunotherapy suppresses the forma-
four times more risk of developing bronchial asthma. tion of IgE. It also raises the titre of specific IgG antibody.
Twenty to thirty per cent of patients with rhinitis have Immunotherapy has to be given for a year or so before
asthma. significant improvement of symptoms can be noticed.

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190 SECTION II — Diseases of Nose and Paranasal Sinuses

It is discontinued if uninterrupted treatment for 3 years • For severe symptoms, combination therapy with oral
shows no clinical improvement. nonsedating antihistamines and intranasal steroids is
Subcutaneous immunotherapy is often used but now used.
sublingual and nasal routes are also being employed. The • For severe and persistent symptoms in spite of the
latter can be used with doses 20–100 times greater than above treatment a short course of oral steroids and im-
used by the subcutaneous route. munotherapy is recommended.
A step-care approach is recommended by ARIA for • If nasal obstruction persists a short course of intranasal
allergic rhinitis treatment. decongestant can be used. Oral decongestant can be
combined with antihistamines.
• Oral antihistamines or intranasal cromolyn sodium is
• Avoid allergen and irritants in all forms of disease.
recommended for mild intermittent disease.
Nonallergic rhinitis can coexist with allergic rhinitis.
• For allergic symptoms of moderate severity or for per-
Nonspecific stimuli produce allergic rhinitis-like symp-
sistent disease intranasal corticosteroids can be used as
toms due to hyper-reactivity of nasal mucosa.
monotherapy.

[Link]
 Chapter 31
Vasomotor and Other Forms
of Nonallergic Rhinitis

VASOMOTOR RHINITIS (VMR) TREATMENT

It is nonallergic rhinitis but clinically simulating nasal al- Medical
lergy with symptoms of nasal obstruction, rhinorrhoea 1. Avoidance of physical factors which provoke symp-

I
E-
and sneezing. One or the other of these symptoms may toms, e.g. sudden change in temperature, humidity,
predominate. The condition usually persists throughout blasts of air or dust.
the year and all the tests of nasal allergy are negative. 2. Antihistaminics and oral nasal decongestants are help-
ful in relieving nasal obstruction, sneezing and rhinor-
PATHOGENESIS rhoea.
3. Topical steroids (e.g. beclomethasone dipropionate,
Nasal mucosa has rich blood supply. Its vasculature is budesonide or fluticasone), used as spray or aerosol,
similar to the erectile tissue in having venous sinusoids are useful to control symptoms.
or “lakes” which are surrounded by fibres of smooth 4. Systemic steroids can be given for a short time in very
muscle which act as sphincters and control the filling or severe cases.
emptying of these sinusoids. Sympathetic stimulation 5. Psychological factors should be removed. Tranquilliz-
causes vasoconstriction and shrinkage of mucosa, while ers may be needed in some patients.
parasympathetic stimulation causes vasodilation and en-
gorgement. Overactivity of parasympathetic system also Surgical
causes excessive secretion from the nasal glands. ①
1. Nasal obstruction can be relieved by measures which
Autonomic nervous system is under the control of hy-
reduce the= size of nasal =

=%_
turbinates (see hypertrophic
pothalamus and therefore emotions play a great role in
-

rhinitis). Other associated causes of nasal obstruction,

vasomotor rhinitis. Autonomic system is unstable in cases
e.g. polyp, deviated nasal septum, should also be cor-
of vasomotor rhinitis. Nasal mucosa is also hyper-reactive
rected.
and responds to several nonspecific stimuli, e.g. change
2. Excessive rhinorrhoea, not corrected by medical ther-
in temperature, humidity, blasts of air, small amounts of
apy and bothersome to the patient, can be relieved by
dust or smoke.
-

sectioning the parasympathetic secretomotor fibres to

nose (vidian neurectomy).
SYMPTOMS
1. Paroxysmal sneezing. Bouts of sneezing start just af-
ter getting out of the bed in the morning. OTHER FORMS OF NONALLERGIC RHINITIS
2. Excessive rhinorrhoea. This accompanies sneezing
or this may be the only predominant symptom. It is Nasal mucosa responds to several different stimuli pro-
profuse and watery and may even wet several hand- ducing symptoms of rhinitis. Some of these conditions
kerchiefs. The nose may drip when the patient leans have acquired specific eponyms. Some authorities cat-

=÷
forward and this may need to be differentiated from egorize them under the catch-all term of vasomotor
CSF rhinorrhoea (see p. 183). rhinitis.
3. Nasal obstruction. This alternates from side to side. 1. DRUG-INDUCED RHINITIS. Several antihypertensive
Usually more marked at night. It is the dependent side drugs such as reserpine, guanethidine, methyl dopa and
of nose which is often blocked when lying on one side. propranolol are sympathetic blocking agents and cause
4. Postnasal drip. nasal stuffiness. Some anticholinesterase drugs, e.g. ne-
ostigmine, used in the treatment of myasthenia gravis,
have acetylcholine like action and cause nasal obstruc-
SIGNS
tion. Contraceptive pills also cause nasal obstruction
Nasal mucosa over the turbinates is generally congested
- because of oestrogens.
=
_

and hypertrophic. In some, it may be normal. 2. RHINITIS MEDICAMENTOSA. Topical decongestant na-
sal drops are notorious to cause rebound phenomenon.
Their excessive use causes rhinitis. It is treated by with-
COMPLICATIONS
① ② drawal of nasal drops, short course of systemic steroid
therapy and in some cases, surgical reduction of turbi-
Long-standing cases or VMR develop nasal polypi, hyper-
trophic rhinitis and sinusitis. nates, if they have become hypertrophied.
③ 191

[Link]
192 SECTION II — Diseases of Nose and Paranasal Sinuses

3. RHINITIS OF PREGNANCY. Pregnant women may de- predominance of parasympathetic activity causing nasal
velop persistent rhinitis due to hormonal changes. Nasal stuffiness and “colds.” Replacement of thyroid hormone
mucosa becomes oedematous and blocks the airway. relieves the condition.
Some may develop secondary infection and even sinusi- 7. GUSTATORY RHINITIS. Spicy and pungent food may
tis. In such cases, care should be taken while prescribing in some people produce rhinorrhoea, nasal stuffiness,
drugs. Generally, local measures such as limited use of lacrimation, sweating and even flushing of face. This
nasal drops, topical steroids and limited surgery (cryosur- is a cholinergic response to stimulation of sensory re-
gery) to turbinates are sufficient to relieve the symptoms. ceptors on the palate. Spicy food, particularly the red
Safety of the developing fetus is not established for newer pepper, contains capsaicin which is known to stimu-
antihistaminics and they should be avoided. late sensory nerves. It can be relieved by ipratropium
4. HONEYMOON RHINITIS. This usually follows sexual bromide nasal spray (an anticholinergic), a few minutes
excitement leading to nasal stuffiness. before meals.
5. EMOTIONAL RHINITIS. Nose may react to several 8. NONAIRFLOW RHINITIS. It is seen in patients of lar-
emotional stimuli. Psychological states like anxiety, ten- yngectomy and tracheostomy. Nose is not used for air-
sion, hostility, humiliation, resentment and grief are all flow and the turbinates become swollen due to loss of
known to cause rhinitis. Treatment is proper counselling vasomotor control. Similar changes are also seen in naso-
for psychological adjustment. Imipramine, which has pharyngeal obstruction due to choanal atresia or adenoi-
both antidepressant and anticholinergic effects, has been dal hyperplasia, the latter having the additional factor
found useful. of infection due to stagnation of discharge in the nasal
6. RHINITIS DUE TO HYPOTHYROIDISM. Hypothyroid- cavity which should otherwise drain freely into the na-
ism leads to hypoactivity of the sympathetic system with sopharynx.

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Chapter 32
Nasal Polypi pathvayofair-mucosalautpauchn.
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disease
Nasal polypi are non-neoplastic masses of oedematous DIFFERENTIAL DIAGNOSIS
nasal or sinus mucosa. They are divided into two main
varieties: 1. A blob of mucus often looks like a polypus but it would
disappear on blowing the nose.
1. Antrochoanal polyp. 2. Hypertrophied middle turbinate is differentiated by its
2. Bilateral ethmoidal polypi. pink appearance and hard feel of bone on probe testing.
3. Angiofibroma has history of profuse recurrent epistax-
is. It is firm in consistency and easily bleeds on probing.
ANTROCHOANAL POLYP 4. Other neoplasms may be differentiated by their fleshy
pink appearance, friable nature and their tendency to
(SYN. KILLIAN’S POLYP)
bleed.
This polyp arises from the mucosa of maxillary antrum X-rays of paranasal sinuses may show opacity of the in-
near its accessory ostium, comes out of it and grows in volved antrum. X-ray (lateral view), soft tissue nasophar-
the choana and nasal cavity. Thus it has three parts. ynx, reveals a globular swelling in the postnasal space. It
1. Antral, which is a thin stalk. is differentiated from angiofibroma by the presence of a
2. Choanal, which is round and globular. column of air behind the polyp. Non-contrast CT scans
3. Nasal, which is flat from side to side. and paranasal sinuses show the extent of the polyp.

TREATMENT
AETIOLOGY
The treatment of choice for antrochonal polyp is endo-
Exact cause is unknown. Nasal allergy coupled with sinus
scopic sinus surgery. It has superseded earlier operations
-

infection is incriminated. Antrochoanal polypi are seen

of
-
simple polypectomy and Caldwell–Luc operation per-
in children and young adults. Usually they are single and
formed for recurring cases.
unilateral.
An antrochoanal polyp is easily removed by avulsion
either through the nasal or oral route. Recurrence is un-
SYMPTOMS common after complete removal. In cases which do recur,
⑧
a -

Caldwell–Luc operation may be required to remove the

Unilateral nasal obstruction is the presenting symptom. polyp completely from the site of its origin and to deal
Obstruction may become bilateral when polyp grows into with coexistent maxillary sinusitis. These days, endo-
the nasopharynx and starts obstructing the opposite cho- scopic sinus surgery has superceded other modes of polyp
②
ana (Tables 32.1 and 32.2). Voice may become thick and removal. Caldwell–Luc operation is avoided.
③Nasal discharge, mostly mucoid,
dull due to hyponasality.
may be seen on one or both sides.
BILATERAL ETHMOIDAL POLYPI
SIGNS AETIOLOGY
As the antrochoanal polyp grows posteriorly, it may be
Aetiology of nasal polypi is very complex and not well-

←
missed on anterior rhinoscopy. When large, a smooth
understood. They may arise in inflammatory conditions
⑨mobilegreyish mass covered with nasal discharge may be seen. of nasal mucosa (rhinosinusitis), disorders of ciliary mo-
It is soft and can be moved up and down with a probe.
tility or abnormal composition of nasal mucus (cystic fi-
A large polyp may protrude from the nostril and show a
brosis). Various diseases associated with the formation of
to pink congested look on its exposed part (Figure 32.1). nasal polypi are:
Due Posterior rhinoscopy may reveal a globular mass filling
air the choana or the nasopharynx. A large polyp may hang 1. Chronic rhinosinusitis. Polypi are seen in chronic rhi-
down behind the soft palate and present in the orophar- - nosinusitis of both allergic and nonallergic origin. Non-
ynx (Figure 32.2A–B ). allergic rhinitis with eosinophilia syndrome (NARES) is
Examination of the nose with an endoscope may re- a form of chronic rhinitis associated with polypi.
veal a choanal or antrochoanal polyp hidden posteriorly 2. Asthma. Seven per cent of the patients with asthma of
in the nasal cavity (Figure 32.3). atopic or nonatopic origin show nasal polypi.
See Table 32.3 for differences between antrochoanal =
3. Aspirin intolerance. Thirty-six per cent of the patients
and ethmoidal polypi. with aspirin intolerance may show polypi. Samter’s

193

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194 SECTION II — Diseases of Nose and Paranasal Sinuses

TABLE 32.1 COMMON CAUSES OF UNILATERAL

NASAL OBSTRUCTION
• Vestibule
• Furuncle
• Vestibulitis
• Stenosis of nares
• Atresia
• Nasoalveolar cyst
• Papilloma
• Squamous cell carcinoma
• Nasal cavity
• Foreign body
• Deviated nasal septum (DNS) Figure 32.1. An antrochoanal polyp projecting through the left
• Hypertrophic turbinates nostril in a 14-year-old patient.
• Concha bullosa
• Antrochoanal polyp
• Synechia 9. Nasal mastocytosis. It is a form of chronic rhinitis in
• Rhinolith which nasal mucosa is infiltrated with mast cells but
• Bleeding polypus of septum few eosinophils. Skin tests for allergy and IgE levels are
• Benign and malignant tumours of nose and paranasal sinuses normal.
• Sinusitis, unilateral
• Nasopharynx
• Unilateral choanal atresia PATHOGENESIS
Nasal mucosa, particularly in the region of middle mea-

EI
tus and turbinate, becomes oedematous due to collection
triad consists of nasal polypi, asthma and aspirin of extracellular fluid causing polypoidal change. Polypi
intolerance. which are sessile in the beginning become pedunculated
4. Cystic fibrosis. Twenty per cent of patients with cystic due to gravity and excessive sneezing.
fibrosis form polypi. It is due to abnormal mucus.

E
5. Allergic fungal sinusitis. Almost all cases of allergic PATHOLOGY
fungal sinusitis form nasal polypi.
6. Kartagener syndrome. This consists of bronchiectasis In early stages, surface of nasal polypi is covered by ciliat-
sinusitis, situs inversus and ciliary dyskinesis. ed columnar epithelium like that of normal nasal mucosa
7. Young syndrome. It consists of sinopulmonary dis- but later it undergoes a metaplastic change to transitional
ease and azoospermia. and squamous type on exposure to atmospheric irrita-
8. Churg–Strauss syndrome. Consists of asthma, fever, tion. Submucosa shows large intercellular spaces filled
eosinophilia, vasculitis and granuloma. with serous fluid. There is also infiltration with eosino-
phils and round cells.

TABLE 32.2 COMMON CAUSES OF BILATERAL SITE OF ORIGIN

NASAL OBSTRUCTION
Multiple nasal polypi always arise from the-lateral wall of
• Vestibule
• Bilateral vestibulitis nose,
-
usually from the middle meatus. Common sites are
• Collapsing nasal alae uncinate process, bulla ethmoidalis, ostia of sinuses, me-
• Stenosis of nares dial surface and edge of middle turbinate. Allergic nasal
• Congenital atresia of nares polypi almost never arise from the septum or the floor of
• Nasal cavity nose.
• Acute rhinitis (viral and bacterial)
• Chronic rhinitis and sinusitis
• Rhinitis medicamentosa SYMPTOMS
• Allergic rhinitis
1. Multiple polypi can occur at any age but are mostly
• Hypertrophic turbinates
seen in adults.
• DNS
• Nasal polypi 2. Nasal stuffiness leading to total nasal obstruction may
• Atrophic rhinitis be the presenting symptom.
• Rhinitis sicca 3. Partial or total loss of sense of smell.
• Septal haematoma 4. Headache due to associated sinusitis.
• Septal abscess 5. Sneezing and watery nasal discharge due to associated
• Bilateral choanal atresia allergy.
• Nasopharynx 6. Mass protruding from the nostril.
• Adenoid hyperplasia
• Large choanal polyp
• Thornwaldt’s cyst SIGNS
• Adhesions between soft palate and posterior pharyngeal wall
• Large benign and malignant tumours On anterior rhinoscopy, or endoscopic examination,
polypi appear as smooth, glistening, grape-like masses

[Link]
 Chapter 32 — Nasal Polypi 195

Figure 32.2. (A) An antrochoanal polyp seen hanging in the oropharynx from behind the soft palate on the right side of uvula. (B) Polyp after
removal.
Scan to play Posterior Rhinoscopy.

often pale in colour (Figure 32.4). They may be sessile or

pedunculated, insensitive to probing and do not bleed
on touch. Often they are multiple and bilateral. Long-
standing cases present with broadening of nose and in-
creased intercanthal distance. A polyp may protrude from
the nostril and appear pink and vascular simulating neo-
plasm (Figure 32.5 ). Nasal cavity may show purulent
discharge due to associated sinusitis.
Probing of a solitary ethmoidal polyp may be neces-
sary to differentiate it from hypertrophy of the turbinate
or cystic middle turbinate.

DIAGNOSIS
Diagnosis can be easily made on clinical examination.

¥
Computed tomography (CT) scan of paranasal sinuses is
essential to exclude the bony erosion and expansion sug-
gestive of neoplasia. Simple nasal polypi may sometimes
be associated with malignancy underneath, especially in
people above 40 years and this must be excluded by histo-
logical examination of the suspected tissue. CT scan also
Figure 32.3. An endoscopic view of a choanal polyp on the right
side.
helps to plan surgery.

TABLE 32.3 DIFFERENCES BETWEEN ANTROCHOANAL AND ETHMOIDAL POLYPI

Antrochoanal polypi Ethmoidal polypi
Age Common in children, can occur in adults Common in adults
Aetiology Infection Allergy or multifactorial
Number Solitary Multiple
Laterality Unilateral Bilateral
Origin Maxillary sinus near the ostium Ethmoidal sinuses, uncinate process, middle
turbinate and middle meatus
Growth Grows backwards to the choana; may hang down behind the Mostly grow anteriorly and may present at
soft palate the nares
Size and shape Trilobed with antral, nasal and choanal parts. Choanal part Usually small and grape-like masses
may protrude through the choana and fill the nasopharynx
obstructing both sides
Recurrence Uncommon, if removed completely Common
Treatment Endoscopic sinus surgery Endoscopic sinus surgery

[Link]
196 SECTION II — Diseases of Nose and Paranasal Sinuses

Surgical
Endoscopic sinus surgery. These days, ethmoidal polypi
are removed by endoscopic sinus surgery more popularly
called functional endoscopic sinus surgery (FESS). It is done
with various endoscopes of 0°, 30° and 70° angulation.
Polypi can be removed more accurately when ethmoid
cells are removed, and drainage and ventilation provided
to the other involved sinuses such as maxillary, sphenoi-
dal or frontal.
Prior to the advent of endoscopic sinus surgery, follow-
ing operations were commonly done:
1. Polypectomy. One or two polyps which are peduncu-
lated can be removed with snare. Multiple and sessile
polypi require special forceps.
2. Intranasal ethmoidectomy. When polypi are multi-

Figure 32.4. An endoscopic view of multiple nasal polypi.

E-ple and sessile, they require uncapping of the ethmoi-
dal air cells by intranasal route, a procedure called
intranasal ethmoidectomy.
3. Extranasal ethmoidectomy. This is indicated when
polypi recur after intranasal procedures and surgical
landmarks are ill-defined due to previous surgery. Ap-
proach is through the medial wall of the orbit by an
external incision, medial to medial canthus.
4. Transantral ethmoidectomy. This is indicated when
infection and polypoidal changes are also seen in the
maxillary antrum. In this case, antrum is opened by
Caldwell–Luc approach and the ethmoid air cell ap-
proached through the medial wall of the antrum.
This procedure is also superceded by endoscopic sinus
surgery.

Figure 32.5. A polyp protruding from the left nostril in a patient with SOME IMPORTANT POINTS TO
bilateral ethmoidal polypi.
Scan to play Nasal Polypi.
REMEMBER IN A CASE OF NASAL POLYPI
1. If a polypus is red and fleshy, friable and has granular sur-
TREATMENT face, especially in older patients, think of malignancy.
2. Simple nasal polyp may masquerade a malignancy
Conservative underneath. Hence all polypi should be subjected to
1. Early polypoidal changes with oedematous mucosa histology.
may revert to normal with antihistaminics and control 3. A simple polyp in a child may be a glioma, an encepha-
of allergy. locele or a meningoencephalocele. It should always be
2. A short course of steroids may prove useful in case of aspirated and fluid examined for CSF. Careless removal
people who cannot tolerate antihistaminics and/or in of such polyp would result in CSF rhinorrhoea and
those with asthma and polypoidal nasal mucosa. They meningitis.
may also be used to prevent recurrence after surgery. 4. Multiple nasal polypi in children may be associated
Contraindications to use of steroids, e.g. hypertension, with mucoviscidosis (cystic fibrosis).
peptic ulcer, diabetes, pregnancy and tuberculosis 5. Epistaxis and orbital symptoms associated with a pol-
should be excluded. yp should always arouse the suspicion of malignancy.

Polyp c- malignancy
•
Red & fleshy
•
forcible & granular
Epistaxis
•

•
Orbital symptoms
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 Chapter 33
Epistaxis

Bleeding from inside the nose is called epistaxis. It is fairly sphenopalatine and the greater palatine, anastomose here
common and is seen in all age groups-children, adults and to form a vascular plexus called “Kiesselbach’s plexus.”
older people. It often presents as an emergency. Epistaxis This area is exposed to the drying effect of inspiratory
is a sign and not a disease per se and an attempt should current and to finger nail trauma, and is the usual site for
always be made to find any local or constitutional cause. epistaxis in children and young adults.

RETROCOLUMELLAR VEIN. This vein runs vertically down-

BLOOD SUPPLY OF NOSE (FIGURES 33.1 wards just behind the columella, crosses the floor of nose
AND 33.2) and joins venous plexus on the lateral nasal wall. This is a
Nose is richly supplied by both the external and internal common site of venous bleeding in young people.
carotid systems, both on the septum and the lateral walls.
WOODRUFF’S PLEXUS
NASAL SEPTUM It is a plexus of veins situated inferior to posterior end
of inferior turbinate. It is a site of posterior epistaxis in
Internal Carotid System adults.
1. Anterior ethmoidal artery Branches of ophthalmic
2. Posterior ethmoidal artery artery
CAUSES OF EPISTAXIS
External Carotid System They may be divided into:
1. Sphenopalatine artery (branch of maxillary artery) gives 1. Local, in the nose or nasopharynx.
nasopalatine and posterior medial nasal branches. 2. General.
adult
2. Septal branch of greater palatine artery (branch of 3. Idiopathic. MC in
-

maxillary artery).
3. Septal branch of superior labial artery (branch of facial A. LOCAL CAUSES
artery).
mi ctulduhs
Nose Me
LATERAL WALL 1. Trauma. Finger nail trauma, injuries of nose, intrana-
sal surgery, fractures of middle third of face and base of
Internal Carotid System skull, hard-blowing of nose, violent sneeze.
2. Infections
1. Anterior ethmoidal

É=
Branches of ophthalmic artery (a) Acute: Viral rhinitis, nasal diphtheria, acute sinusitis.
2. Posterior ethmoidal (b) Chronic: All crust-forming diseases, e.g. atrophic
rhinitis, rhinitis sicca, tuberculosis, syphilis septal
External Carotid System perforation, granulomatous lesion of the nose, e.g.
rhinosporidiosis.
1. Posterior lateral nasal From sphenopalatine 3. Foreign bodies
branches artery (a) Nonliving: Any neglected foreign body, rhinolith.

gdnlts
2. Greater palatine artery From maxillary artery (b) Living: Maggots, leeches.
3. Nasal branch of anterior From infraorbital branch 4. Neoplasms of nose and paranasal sinuses.
superior dental of maxillary artery (a) Benign: Haemangioma, papilloma. Young
4. Branches of facial artery
to nasal vestibule 5.
(b) Malignant: Carcinoma or sarcoma.
Atmospheric changes. High altitudes, sudden decom- Angiofibroma
pression (Caisson disease).
6. Deviated nasal septum.
LITTLE’S AREA Nasopharynx
It is situated in the anterior inferior part of nasal septum, 1. Adenoiditis.
just above the vestibule. Four arteries-anterior ethmoi- 2. Juvenile angiofibroma.
dal, septal branch of superior labial, septal branch of 3. Malignant tumours.

197

[Link]
198 SECTION II — Diseases of Nose and Paranasal Sinuses

Woodruff's pleas
Dcs Potstenor epistaxis

Figure 33.1. Blood supply of the nasal septum.

Scan to play External and Internal Carotid Artery.

B. GENERAL CAUSES C. IDIOPATHIC

1. Cardiovascular system. Hypertension, arteriosclero- Many times the cause of epistaxis is not clear.
sis, mitral stenosis, pregnancy (hypertension and hor-
monal). SITES OF EPISTAXIS
2. Disorders of blood and blood vessels. Aplastic
anaemia, leukaemia, thrombocytopenic and vascular 1. Little’s area. In 90% cases of epistaxis, bleeding occurs
purpura, haemophilia, Christmas disease, scurvy, vi- from this site.
Inherited
tamin K deficiency and hereditary haemorrhagic tel- 2. Above the level of middle turbinate. Bleeding from
angectasia. above the middle turbinate and corresponding area on
3. Liver disease. Hepatic cirrhosis (deficiency of factor II, the septum is often from the anterior and posterior
VII, IX and X). ethmoidal vessels (internal carotid system).
4. Kidney disease. Chronic nephritis. 3. Below the level of middle turbinate. Here bleeding
5. Drugs. Excessive use of salicylates and other analgesics is from the branches of sphenopalatine artery. It may
(as for joint pains or headaches), anticoagulant thera- be hidden, lying lateral to middle or inferior turbinate
py (for heart disease).
Elvrtkdlsiow
and may require infrastructure of these turbinates
6. Mediastinal compression. Tumours of mediastinum for localization of the bleeding site and placement of
(raised venous pressure in the nose). packing to control it.
7. Acute general infection. /
B
A Influenza, measles, chick- 4. Posterior part of nasal cavity. Here blood flows di-
rsneiaeag
enpox, whooping cough, rheumatic fever, infectious
mononucleosis, typhoid, pneumonia, malaria and)
rectly into the pharynx.
5. Diffuse. Both from septum and lateral nasal wall. This
dengue fever. aspirin NSAIDs
, cranhplehlt is often seen in general systemic disorders and blood
8. Vicarious menstruation (epistaxis occurring at the dyscrasias.
time of menstruation). 6. Nasopharynx.

[Link]
 Chapter 33 — Epistaxis 199

Figure 33.2. Blood supply of the lateral wall of the nose.

TABLE 33.1 DIFFERENCES BETWEEN ANTERIOR

CLASSIFICATION OF EPISTAXIS AND POSTERIOR EPISTAXIS
Anterior epistaxis Posterior epistaxis
Anterior Epistaxis
Incidence More common Less common
When blood flows out from the front of nose with the
- Site Mostly from Little’s Mostly from posterosuperior
patient in sitting position. area or anterior part part of nasal cavity; often
of lateral wall difficult to localize the
Posterior Epistaxis bleeding point
Mainly the blood flows back into the throat. Patient may Age Mostly occurs in After 40 years of age
swallow it and later have a “coffee-coloured” vomitus. children or young
This may erroneously be diagnosed as haematemesis. adults
Cause Mostly trauma Spontaneous; often due
The differences between the two types of epistaxis are
to hypertension or
tabulated herewith (Table 33.1).
arteriosclerosis
Bleeding Usually mild, can be Bleeding is severe, requires
MANAGEMENT easily controlled by hospitalization; postnasal
local pressure or pack often required
In any case of epistaxis, it is important to know: anterior pack

v 1. Mode of onset. Spontaneous or finger nail trauma.

2. Duration and frequency of bleeding.
FIRST AID
3. Amount of blood loss.
4. Side of nose from where bleeding is occurring. Most of the time, bleeding occurs from the Little’s area
5. Whether bleeding is of anterior or posterior type. and can be easily controlled by pinching the nose with
6. Any known bleeding tendency in the patient or family. thumb and index finger for about 5 min. This compresses
7. History of known medical ailment (hypertension, leu- the vessels of the Little’s area. In Trotter’s method patient
kaemia, mitral valve disease, cirrhosis and nephritis). is made to sit, leaning a little forward over a basin to spit
8. History of drug intake (analgesics, anticoagulants, etc.). any blood and breathe quietly from the mouth. Cold

[Link]
200 SECTION II — Diseases of Nose and Paranasal Sinuses

compresses should be applied to the nose to cause reflex the whole nasal cavity is packed tightly by layering the
vasoconstriction. gauze from floor to the roof and from before backwards.
Packing can also be done in vertical layers from back to
the front (Figure 33.3). One or both cavities may need to
CAUTERIZATION
be packed. Pack can be removed after 24 h, if bleeding
This is useful in anterior epistaxis when bleeding point has stopped. Sometimes, it has to be kept for 2-3 days; in
has been located. The area is first topically anaesthetized that case, systemic antibiotics should be given to prevent
and the bleeding point cauterized with a bead of silver sinus infection and toxic shock syndrome.
nitrate or coagulated with electrocautery.
POSTERIOR NASAL PACKING
ANTERIOR NASAL PACKING
It is required for patients bleeding posteriorly into the
In cases of active anterior epistaxis, nose is cleared of throat. A postnasal pack is first prepared by tying three
blood clots by suction and attempt is made to localize the silk ties to a piece of gauze rolled into the shape of a cone.
bleeding site. In minor bleeds, from the accessible sites, A rubber catheter is passed through the nose and its end
cauterization of the bleeding area can be done. If bleeding brought out from the mouth (Figure 33.4). Ends of the
is profuse and/or the site of bleeding is difficult to local- silk threads are tied to it and catheter withdrawn from
ize, anterior packing should be done. For this, use a rib- nose. Pack, which follows the silk thread, is now guided
bon gauze soaked with liquid paraffin. About 1 m gauze into the nasopharynx with the index finger. Anterior na-
(2.5 cm wide in adults and 12 mm in children) is required sal cavity is now packed and silk threads tied over a dental
for each nasal cavity. First, few centimetres of gauze are roll. The third silk thread is cut short and allowed to hang
folded upon itself and inserted along the floor and then in the oropharynx. It helps in easy removal of the pack

Figure 33.3. Methods of anterior nasal packing. (A) Packing in vertical layers. (B) Packing in horizontal layers.

Figure 33.4. Technique of postnasal pack.

[Link]
 Chapter 33 — Epistaxis 201

Caldwell-Luc operation. Posterior wall of maxillary si-

nus is removed and the maxillary artery or its branches
are blocked by applying clips. This procedure is now
superceded by transnasal endoscopic sphenopalatine
artery ligation.
3. Ethmoidal arteries. In anterosuperior bleeding above
the middle turbinate, not controlled by packing, an-
terior and posterior ethmoidal arteries, which supply
this area, can be ligated. The vessels are exposed in
the medial wall of the orbit by an external ethmoid
(Lynch) incision.

Transnasal Endoscopic Sphenopalatine

Artery Ligation (TESPAL)
The procedure can be done with rigid endoscopes under
Figure 33.5. Epistaxis balloon for posterior epistaxis. Posterior bal- topical anaesthesia with sedation or under a general an-
loon (A) is inflated with 10 mL and anterior balloon (B) with 30 mL. aesthesia. A mucosal flap is lifted in posterior part of lat-
Catheter provides nasal airway. eral nasal wall, sphenopalatine artery (SPA)is localized as
it exits the foramen and closed with a vascular clip. Distal
branches of the artery can be additionally cauterized and
the flap then reposited. Anterior ethmoidal artery can
later. Patients requiring postnasal pack should always be
also be ligated by Lynch incision as an adjunctive proce-
hospitalized. Instead of postnasal pack, a Foley’s catheter
dure. SPA ligation gives high success in control of refrac-
size 12-14 F can also be used. After insertion balloon is
tory posterior bleed.
inflated with 5-10 mL of saline. The bulb is inflated with
saline and pulled forward so that choana is blocked and
then an anterior nasal pack is kept in the usual manner. Embolization
These days nasal balloons are also available (Figure 33.5). It is done by an interventional radiologist through femo-
A nasal balloon has two bulbs, one for the postnasal space ral artery catheterization. Internal maxillary artery is lo-
and the other for nasal cavity. calized and the embolization is performed with absorb-
able gelfoam and/or polyvinyl alcohol or coils. Both
ipsilateral or bilateral embolizations may be required for
ENDOSCOPIC CAUTERIZATION
unilateral epistaxis because of cross circulation. Emboliza-
Using topical or general anaesthesia, bleeding point is lo- tion is generally a safe procedure but may have potential
calized with a rigid endoscope. It is then cauterized with risks like cerebral thromboembolism, haematoma at local
a malleable unipolar suction cautery or a bipolar cau- site. Ethmoidal arteries cannot be embolized.
tery. The procedure is effective with less morbidity and
decreased hospital stay. The procedure has a limitation
when profuse bleeding does not permit localization of GENERAL MEASURES IN EPISTAXIS
the bleeding point.
1. Make the patient sit up with a back rest and record
ELEVATION OF MUCOPERICHONDRIAL any blood loss taking place through spitting or vom-
iting.
FLAP AND SUBMUCOUS RESECTION (SMR)
2. Reassure the patient. Mild sedation should be given.
OPERATION 3. Keep check on pulse, BP and respiration.
In case of persistent or recurrent bleeds from the septum, 4. Maintain haemodynamics. Blood transfusion may be
just elevation of mucoperichondrial flap and then reposi- required.
tioning it back helps to cause fibrosis and constrict blood 5. Antibiotics may be given to prevent sinusitis, if pack is
vessels. SMR operation can be done to achieve the same to be kept beyond 24 h.
result or remove any septal spur which is sometimes the 6. Intermittent oxygen may be required in patients with
cause of epistaxis. bilateral packs because of increased pulmonary resist-
ance from nasopulmonary reflex.
7. Investigate and treat the patient for any underlying lo-
LIGATION OF VESSELS cal or general cause.
1. External carotid. When bleeding is from the external
carotid system and the conservative measures have HEREDITARY HAEMORRHAGIC TELANGIECTASIA. It occurs
failed, ligation of external carotid artery above the on the anterior part of nasal septum and is the cause of re-
origin of superior thyroid artery should be done. It is current bleeding. It can be treated by using Argon, KTP or
avoided these days in favour of embolization or liga- Nd: YAG laser. The procedure may require to be repeated
tion of more peripheral branches of sphenopalatine several times in a year as telangectasia recurs in the sur-
artery. rounding mucosa. Some cases require septodermoplasty
2. Maxillary artery. Ligation of this artery is done in where anterior part of septal mucosa is excised and re-
uncontrollable posterior epistaxis. Approach is via placed by a split-skin graft.

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 Chapter 34
Trauma to the Face

Injuries of face may involve soft tissues, bones or both. 2. Middle third. Between the supraorbital ridge and the
The majority of facial injuries are caused by automobile upper teeth.
accidents. Others result from sports, personal accidents, 3. Lower third. Mandible and the lower teeth.
assaults and fights. The management of facial trauma can
The various fractures encountered in these regions are
be divided into:
listed in Table 34.1.
1. General management.
2. Soft tissue injuries and their management.
3. Bone injuries and their management. I. FRACTURES OF UPPER THIRD OF FACE
A. FRONTAL SINUS
GENERAL MANAGEMENT Frontal sinus fractures may involve anterior wall, poste-
rior wall or the nasofrontal duct.
1. Airway. Maintenance of airway should receive the
highest priority. Airway is obstructed by loss of skeletal 1. Anterior wall fractures may be depressed or commi-
support, aspiration of foreign bodies, blood or gastric nuted. Defect is mainly cosmetic. Sinus is approached
contents or swelling of tissues. Airway is secured by through a wound in the skin if that is present, or
intubation or the tracheostomy. through a brow incision. The bone fragments are el-
2. Haemorrhage. Injuries of face may bleed profusely. evated, taking care not to strip them from the perios-
Bleeding should be stopped by pressure or ligation of teum. The interior of the sinus is always inspected to
vessels. rule out fracture of the posterior wall.
3. Associated injuries. Facial injuries may be associated 2. Posterior wall fractures may be accompanied by dural
with injuries of head, chest, abdomen, neck, larynx, tears, brain injury and CSF rhinorrhoea. They may
cervical spine or limbs and should be attended too. require neurosurgical consultation. Dural tears can
be covered by temporalis fascia. Small sinuses can be
obliterated with fat.
SOFT TISSUE INJURIES AND THEIR 3. Injury to nasofrontal duct causes obstruction to sinus
MANAGEMENT drainage and may later be complicated by a mucocele.
In such cases, make a large communication between
FACIAL LACERATIONS the sinus and the nose. Small sinuses can be obliterated
Wound is thoroughly cleaned of any dirt, grease or for- with fat after removing the sinus mucosa completely.
eign matter. The lacerations are closed by accurate ap-
proximation of each layer. B. SUPRAORBITAL RIDGE
Ridge fractures often cause periorbital ecchymosis, flat-
PAROTID GLAND AND DUCT tening of the eyebrow, proptosis or downward displace-
ment of eye. Fragment of bone may also be pushed into
Parotid tissue, if exposed, is repaired by suturing. Injuries
the orbit and get impacted. Ridge fractures require open
of parotid duct are more serious. Both ends of the duct are
reduction through an incision in the brow or transverse
identified and sutured over a polyethylene tube with fine
skin line of the forehead.
suture. The tube is left for 3 days to 2 weeks.

C. FRACTURES OF FRONTAL BONE

FACIAL NERVE
They may be depressed or linear, with or without separa-
If severed, the facial nerve is exposed by superficial pa- tion. They often extend into the orbit. Brain injury and
rotidectomy and cut ends are approximated with 8–0 or cerebral oedema are commonly associated with each oth-
10–0 silk under magnification. er and require neurosurgical consultation.

BONE INJURIES AND THEIR II. FRACTURES OF MIDDLE THIRD OF FACE

MANAGEMENT
A. NASAL BONES AND SEPTUM
The face can be divided into three regions:
Fractures of nasal bones are the most common because of
1. Upper third. Above the level of supraorbital ridge. the projection of nose on the face. Traumatic forces may

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204 SECTION II — Diseases of Nose and Paranasal Sinuses

TABLE 34.1 FRACTURES OF THE FACE 2. ANGULATED. A lateral blow may cause unilateral de-
pression of nasal bone on the same side or may fracture
Upper third Middle third Lower third
both the nasal bones and the septum with deviation of
Frontal sinuses Nasal bones and septum Alveolar process nasal bridge.
Supraorbital Naso-orbital area Symphysis Nasal fractures are often accompanied by injuries of
ridge nasal septum which may be simply buckled, dislocated
Frontal bone • Zygoma • Body or fractured into several pieces. Septal haematoma may
• Zygomatic arch • Angle
form.
• Orbital floor • Ascending
• Maxilla ramus Clinical Features
• Le Fort I (transverse) • Condyle
• Le Fort II (pyramidal) • Temporoman- 1. Swelling of nose. Appears within few hours and may
• Le Fort III (craniofacial dibular joint obscure details of examination.
dysjunction) 2. Periorbital ecchymosis.
3. Tenderness.
4. Nasal deformity. Nose may be depressed from the front
or side, or the whole of the nasal pyramid deviated to
act from the front or side. Magnitude of force will deter- one side (Figure 34.2).
mine the depth of injury. 5. Crepitus and mobility of fractured fragments.
6. Epistaxis.
Types of Nasal Fractures (Figures 34.1
7. Nasal obstruction due to septal injury or haematoma.
and 34.2) 8. Lacerations of the nasal skin with exposure of na-
1. DEPRESSED. They are due to frontal blow. Lower part sal bones and cartilage may be seen in compound
of nasal bones which is thinner, easily gives way. A severe fractures.
frontal blow will cause “open-book fracture” in which na-
sal septum is collapsed and nasal bones splayed out. Still, Diagnosis
greater forces will cause comminution of nasal bones and Diagnosis is best made on physical examination. X-rays
even the frontal processes of maxillae with flattening and may or may not show fracture (Figure 34.3). Patient
widening of nasal dorsum. should not be dismissed as having no fracture because
X-rays did not reveal it.
X-rays should include Waters’ view, right and left lat-
eral views and occlusal view.

Treatment
Simple fractures without displacement need no treat-
ment; others may require closed or open reduction. Pres-
ence of oedema interferes with accurate reduction by
closed methods. Therefore, the best time to reduce a frac-
ture is before the appearance of oedema, or after it has
subsided, which is usually in 5–7 days. It is difficult to
reduce a nasal fracture after 2 weeks because it heals by
that time. Healing is faster in children and therefore ear-
lier reduction is imperative.

1. CLOSED REDUCTION. Depressed fractures of nasal

bones sustained by either frontal or lateral blow can be
reduced by a straight blunt elevator guided by digital ma-
nipulation from outside.
Laterally, displaced nasal bridge can be reduced by firm
digital pressure in the opposite direction. Impacted frag-
ments sometimes require disimpaction with Walsham
or Asch’s forceps before realignment. Septal fractures are
also reduced by Asch’s forceps. Septal haematoma, if pre-
sent, must be drained.
Simple fractures may not require intranasal packing.
Unstable fractures require intranasal packing and exter-
nal splintage.

2. OPEN REDUCTION. Early open reduction in nasal frac-

tures is rarely required. This is indicated when closed
methods fail. Certain septal injuries can be better reduced
Figure 34.1. Types of fractures. (A) Normal. (B) Frontal blow causing by open methods. Healed nasal deformities resulting
depressed fracture or open-book fracture. (C) Lateral blow causing from nasal trauma can be corrected by rhinoplasty or
deviation of the nasal bridge or depression of one nasal bone. septorhinoplasty.

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 Chapter 34 — Trauma to the Face 205

Figure 34.2. (A) Fracture of the nasal bones with displacement of the bridge to the right. (B) Fracture after manual correction.

B. NASO-ORBITAL FRACTURES Diagnosis

Direct force over the nasion fractures nasal bones and dis- Various facial films will be required to assess the extent
places them posteriorly. Perpendicular plate of ethmoid, of fracture and injury to other facial bones. Computed
ethmoidal air cells and medial orbital wall are fractured tomography (CT) scans are more useful.
and driven posteriorly. Injury may involve cribriform
Treatment
9 distance
medial
plate, frontal sinus, frontonasal duct, extraocular mus-
1. CLOSED REDUCTION. In uncomplicated cases, fracture
cles, eyeball and the lacrimal apparatus. Medial canthal
b/w ligament may be avulsed. is reduced with Asch’s forceps and stabilized by a wire
canthi passed through fractured bony fragments and septum
Clinical Features and then tied over the lead plates. Intranasal packing is
a 1. Telecanthus, due to lateral displacement of medial or- given. Splinting is kept for 10 days or so.
bital wall.
2. Pug nose. Bridge of nose is depressed and tip turned 2. OPEN REDUCTION. This is required in cases with ex-
up. tensive comminution of nasal and orbital bones, and
3. Periorbital ecchymosis. those complicated by other injuries to lacrimal apparatus,
4. Orbital haematoma due to bleeding from anterior and medial canthal ligaments, frontal sinus, etc.
posterior ethmoidal arteries. An H-type incision gives adequate exposure of the frac-
5. CSF leakage due to fracture of cribriform plate and tured area. This can be extended to the eyebrows if access
dura. to frontal sinuses is also required.
6. Displacement of eyeball. Nasal bones are reduced under vision and bridge height
is achieved. Medial orbital walls can be reduced. Medial can-
thal ligaments, if avulsed, are restored with a through and
through wire. Intranasal packing may be required to restore
the contour. When bone comminution is severe, restoration
of medial canthal ligaments and lacrimal apparatus should
receive preference over reconstruction of nasal contour.

C. FRACTURES OF ZYGOMA (TRIPOD

FRACTURE)
After nasal bones, zygoma is the second most frequently
fractured bone. Usually, the cause is direct trauma. Lower
segment of zygoma is pushed medially and posteriorly re-
sulting in flattening of the malar prominence and a step
deformity at the infraorbital margin. Zygoma is separated
at its three processes (Figure 34.4). Fracture line passes
through zygomaticofrontal suture, orbital floor, infraor-
bital margin and foramen, anterior wall of maxillary si-
nus and the zygomaticotemporal suture. Orbital contents
may herniate into the maxillary sinus.

Clinical Features
1. Flattening of malar prominence.
2. Step deformity of infraorbital margin.
Figure 34.3. Fractured nasal bone (arrow) as seen in a radiograph. 3. Anaesthesia in the distribution of infraorbital nerve.

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206 SECTION II — Diseases of Nose and Paranasal Sinuses

Clinical Features
Characteristic features are depression in the area of zygo-
matic arch, local pain aggravated by talking and chewing,
trismus or limitation of the movements of mandible due
to impingement of fragments on the condyle or coronoid
process.

Diagnosis
Arch fractures are best seen on submentovertical view of
the skull. Waters’ view is also taken.

Treatment
A vertical incision is made in the hair-bearing area above
or in front of the ear, cutting through temporal fascia.
An elevator is passed deep to temporal fascia and carried
under the depressed bony fragments which are then re-
duced. Fixation is usually not required as the fragments
remain stable.

E. FRACTURES OF ORBITAL FLOOR

Figure 34.4. Fractured left zygoma. Zygomatic and Le Fort II maxillary fractures are always
accompanied by fractures of orbital floor. Isolated frac-
tures of orbital floor, when a large blunt object strikes the
4. Trismus, due to depression of zygoma on the underly- globes, are called “blow out fractures.” Orbital contents
ing coronoid process. may herniate into the antrum (Figure 34.5).
5. Oblique palpebral fissure, due to the displacement of
lateral palpebral ligament. Clinical Features
6. Restricted ocular movements, due to entrapment of in- 1. Ecchymosis of lid, conjunctiva and sclera.
ferior rectus muscle. It may cause diplopia. 2. Enophthalmos with inferior displacement of the eye-
7. Periorbital emphysema, due to escape of air from the ball. This becomes apparent when oedema subsides.
maxillary sinus on nose blowing. 3. Diplopia, which may be due to displacement of the
Diagnosis eyeball or entrapment of inferior rectus and inferior
oblique muscles.
Waters’ or exaggerated Waters’ view shows the fracture 4. Hypoaesthesia or anaesthesia of cheek and upper lip, if
and displacement the best. Maxillary sinus may show infraorbital nerve is involved.
clouding due to the presence of blood. Comminution
with depression of orbital floor and herniation of orbital Diagnosis
contents cannot be seen on plain X-rays. CT scan of the Waters’ view shows a convex opacity bulging into the an-
orbital will be more useful. trum from above (tear-drop opacity). CT scans may con-
Treatment firm the diagnosis (Figure 34.6). Entrapment of inferior
rectus and inferior oblique muscles is diagnosed by asking
Only displaced fractures require treatment. Open reduc- the patient to look up and down, or by the traction test.
tion and internal wire fixation gives best results. Fracture The latter is performed by grasping the globe and passive-
is exposed at the frontozygomatic suture through lateral ly rotating it to check for restriction of its movements.
brow incision and reduced by passing an elevator behind
the zygoma. Wire fixation is done at frontozygomatic su- Treatment
ture and infraorbital margin. The latter is exposed by a Indications for surgery include enophthalmos and persis-
separate incision in the lower lid. Fracture of orbital floor tent diplopia due to entrapment of muscle. Orbital floor
can also be repaired through this incision.
Transantral approach is less favourable. Antrum is ex-
posed as in Caldwell–Luc operation, blood is aspirated,
fracture reduced and then stabilized by a pack in the an-
trum. Fractures of orbital floor can also be reduced. An-
tral pack is removed in about 10 days through the buccal
incision, which is left open at the end of operation, or
through the intranasal antrostomy route.

D. FRACTURES OF ZYGOMATIC ARCH

Zygomatic arch generally breaks into two fragments
which get depressed. There are three fracture lines, one at Figure 34.5. Blow out fracture with herniation of orbital contents
each end and third in the centre of the arch. into the maxillary sinus.

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 Chapter 34 — Trauma to the Face 207

The fracture line passes through root of nose, ethmo-

frontal junction, superior orbital fissure, lateral wall of
orbit, frontozygomatic and temporozygomatic sutures
and the upper part of pterygoid plates.

Clinical Features
1. Malocclusion of teeth with anterior open bite.
2. Elongation of midface.
3. Mobility in the maxilla.
4. CSF rhinorrhoea. Cribriform plate is injured in Le Fort
II and Le Fort III fractures.

Diagnosis
X-rays, helpful in diagnosis of maxillary fractures are
Waters’ view, posteroanterior view, lateral view and
the CT scans. They help to delineate fracture lines and
the displacement of fragments.
Figure 34.6. A CT scan showing blow out fracture of the right orbital
floor.
Treatment
Treatment of maxillary fractures is complex. Immediate
attention is paid to restore the airway and stop severe
fractures can be satisfactorily reduced by a finger passed haemorrhage from maxillary artery or its branches. For
into the antrum through a transantral approach. A pack good cosmetic and functional results, fractures should be
can be kept in the antrum to support the fragments. In- treated as early as the patient’s condition permits. Asso-
fraorbital approach, through a skin crease of the lower ciated intracranial and cervical spine injuries may delay
lid, can also be used either alone or in combination with specific treatment.
transantral approach. Badly comminuted fractures of or- Fixation of maxillary fractures can be achieved by:
bital floor can be repaired by a bone graft from the iliac
crest, nasal septum or the anterior wall of the antrum. 1. Interdental wiring.
Silicon or teflon sheets have also been used to reconstruct 2. Intermaxillary wiring using arch bars.
the orbital floor but autogenous grafts are preferable. 3. Open reduction and interosseous wiring as in zygo-
matic fractures.
4. Wire slings from frontal bone, zygoma or infraorbital
F. FRACTURES OF MAXILLA (FIGURE 34.7) rim to the teeth or arch bars.
They are classified into three types:
1. Le Fort I (transverse) fracture runs above and paral-
lel to the palate. It crosses lower part of nasal septum,
III. FRACTURES OF LOWER THIRD
maxillary antra and the pterygoid plates. FRACTURES OF MANDIBLE
2. Le Fort II (pyramidal) fracture passes through the
root of nose, lacrimal bone, floor of orbit, upper part of Fractures of mandible have been classified according
maxillary sinus and pterygoid plates. This fracture has to their location (Figure 34.8). Condylar fractures are
some features common with the zygomatic fractures. the most common. They are followed, in frequency, by
3. Le Fort III (craniofacial dysjunction). There is com- fractures of the angle, body and symphysis (mnemonic
plete separation of facial bones from the cranial bones. CABS). Fractures of the ramus, coronoid and alveolar pro-
cesses are uncommon.
Multiple fractures are seen as frequently as single ones.
Most of the mandibular fractures are the result of direct
trauma; however, condylar fractures are caused by indi-
rect trauma to the chin or opposite side of the body of
mandible. Displacement of mandibular fractures is de-
termined by (i) the pull of muscles attached to the frag-
ments, (ii) direction of fracture line and (iii) bevel of the
fracture.

Clinical Features
In fractures of condyle, if fragments are not displaced, pain
and trismus are the main features and tenderness is elicit-
ed at the site of fracture. If fragments are displaced, there
is in addition, malocclusion of teeth and deviation of jaw
to the opposite side on opening the mouth.
Most of the fractures of angle, body and symphysis can
Figure 34.7. Fractures of maxilla. (A) Le Fort I, (B) Le Fort II and be diagnosed by intraoral and extraoral palpation. Step
(C) Le Fort III. deformity, malocclusion of teeth, ecchymosis of oral

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208 SECTION II — Diseases of Nose and Paranasal Sinuses

Figure 34.8. Fractures of mandible (Dingman classification). Condylar fractures are the most common, followed by those of the angle, body and
symphysis of the mandible. Remember CABS.

mucosa, tenderness at the site of fracture and crepitus 2. Failure of sublabial incision to heal after Caldwell–Luc
may be seen. operation.
3. Erosion of antrum by carcinoma.
Diagnosis 4. Fractures or penetrating injuries of maxilla.
X-rays useful in mandibular fractures are PA view of the 5. Osteitis of maxilla, syphilis or malignant granuloma.
skull (for condyle), right and left oblique views of mandi-
ble and the panorex view. Clinical Features
1. Regurgitation of food. Food or fluids pass from oral
Treatment cavity into the antrum and thence into the nose.
Both closed and open methods are used for reduction and 2. Discharge. Antrum is always infected. Foul-smelling
fixation of the mandibular fractures. discharge is seen, filling the nose or exuding from the
In closed methods, interdental wiring and intermaxil- fistulous opening into the mouth.
lary fixation are useful. External pin fixation can also be 3. Inability to build positive or negative pressure in
used. the mouth. Patient will have difficulty to blow the
In open methods, fracture site is exposed and frag- wind instruments or drink through a straw. To drink
ments fixed by direct interosseous wiring. This is further through a straw, negative pressure has to be created in
strengthened by a wire tied in a figure of eight manner. the oral cavity. This cannot be done in the presence of
These days, compression plates are available to fix the an oroantral fistula as air gets drawn from nose to an-
fragments. With their use, prolonged immobilization and trum to oral cavity. Reverse is true when blowing wind
intermaxillary fixation can be avoided. instruments; instead of building a positive pressure in
Condylar fractures are also treated by intermaxillary the oral cavity, air is blown out from the oral cavity to
fixation with arch bars and rubber bands. Sometimes, antrum and out through the nose.
open reduction and interosseous wiring may be required
in adult edentulous patients with bilateral condylar frac- Diagnosis
tures or in fractures of children. A probe can be passed from the fistulous opening in the
Immobilization of mandible beyond 3 weeks, in con- oral cavity into the antrum.
dylar fractures, can cause ankylosis of temporomandib-
ular joints. Therefore, intermaxillary wires are removed Treatment
and jaw exercises started. If occlusion is still disturbed, RECENT FISTULA. When fistula is discovered immediately
intermaxillary wires are reapplied for another week and after tooth extraction and there is no infection or a re-
the process repeated till the bite and jaw movements are tained tooth in the antrum, conservative treatment with
normal. suturing of gum margins and a course of antibiotics is
effective.

OROANTRAL FISTULA CHRONIC FISTULA OR A LARGE FISTULA. It requires sur-

gical repair by a palatal or a buccal flap. Maxillary sinusi-
It is a communication between the antrum and oral cav- tis is first treated by repeated irrigations and antibiotics.
ity. The fistulous opening may be situated on the alveolus Squamous-lined fistulous track is excised, bony edges of
or gingivolabial sulcus. the fistula are smoothened and prepared for the flaps
to sit properly. Caldwell–Luc operation may be required
Aetiology to remove a retained tooth root or a foreign body, clear
1. Dental extraction is the most important cause. Roots the antrum of diseased mucosa and to provide a nas-
of second premolar and upper molars (first and some- oantral window for free drainage. Some fistulas are bet-
times second and third) are closely related to the antral ter closed by a dental obturator. The latter also permits
cavity and their extraction may lead to fistula forma- observation of antral cavity particularly in those treated
tion. Presence of apical tooth abscess predisposes to it. for cancer.

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 Chapter 35
Anatomy and Physiology
of Paranasal Sinuses

at birth
Absent
M
ANATOMY OF PARANASAL SINUSES Frontal Sinus
Each frontal sinus is situated between the inner and outer
Paranasal sinuses are air-containing cavities in certain
tables of frontal bone, above and deep to the supraorbital
bones of skull. They are four on each side. Clinically, par-
margin. It varies in shape and size and is often loculated
anasal sinuses have been divided into two groups:
by incomplete septa. The two frontal sinuses are often
1. Anterior group. This includes maxillary, frontal and asymmetric and the intervening bony septum is thin and
anterior ethmoidal. They all open in the middle mea- often obliquely placed or may even be deficient. Frontal
tus and their ostia lie anterior to basal lamella of mid- sinus may be absent on one or both sides or it may be
dle turbinate. very large extending into orbital plate in the roof of the
2. Posterior group. This includes posterior ethmoidal orbit. Its average dimensions are: height 32 mm, breadth
sinuses which open in the superior meatus and the 24 mm and depth 16 mm (remember code 8, i.e. 8 × 4,
sphenoid sinus which opens in sphenoethmoidal re- 8 × 3 and 8 × 2).
cess. Anterior wall of the sinus is related to the skin over
the forehead; inferior wall, to the orbit and its contents;
Maxillary Sinus (Antrum of Highmore) and posterior wall to the meninges and frontal lobe of the
It is the largest of paranasal sinuses and occupies the body brain.
of maxilla. It is pyramidal in shape with base towards lat- Drainage of the frontal sinus is through its ostium into
eral wall of nose and apex directed laterally into the zygo- the frontal recess. In fact frontal sinus, its ostium and the
matic process of maxilla and sometimes in the zygomatic frontal recess form an hour glass structure. Frontal recess is
bone itself (Figure 35.1). On an average, maxillary sinus situated in the anterior part of middle meatus and is bound-
has a capacity of 15 mL in an adult. It is 33 mm high, ed by the middle turbinate (medially), lamina papyracea
35 mm deep and 25 mm wide. (laterally), agger nasi cells (anteriorly) and bulla ethmoida-
→ Earliest to develop lis (posteriorly). It may be encroached by several anterior
RELATIONS ethmoidal cells, which may obstruct its ventilation and
• Anterior wall is formed by facial surface of maxilla and drainage and lead to sinusitis. Frontal recess drains into the
is related to the soft tissues of cheek. infundibulum or medial to it, depending on the superior
• Posterior wall is related to infratemporal and pterygo- attachment of the uncinate process (refer to Figure 23.6).
palatine fossae. Due to encroachment of small air cells in the frontal
• Medial wall is related to the middle and inferior mea- recess, the drainage pathway may be reduced to a straight
tuses. At places, this wall is thin and membranous. It or more often tortuous pathway which was earlier called
is related to uncinate process, anterior and posterior nasofrontal duct. It is an erroneous term as no true duct
fontanelle, and inferior turbinate and meatus. exists.
• Floor is formed by alveolar and palatine processes of
the maxilla and is situated about 1 cm below the level Ethmoidal Sinuses (Ethmoid Air Cells)
of floor of nose (Figure 35.1). Usually it is related to Ethmoidal sinuses are thin-walled air cavities in the lat-
the roots of second premolar and first molar teeth. eral masses of ethmoid bone. Their number varies from
Depending on the age of the person and pneumatiza- 3 to 18. They occupy the space between upper third of
tion of the sinus, the roots of all the molars, some- lateral nasal wall and the medial wall of orbit. Clinically,
times the premolars and canine, are in close relation ethmoidal cells are divided by the basal lamina into an
to the floor of maxillary sinus separated from it by a anterior ethmoid group which opens into the middle mea-
thin lamina of bone or even no bone at all. Oroan- tus and posterior ethmoid group which opens into the supe-
tral fistulae can result from extraction of any of these rior meatus and into supreme meatus, if that be present.
teeth. Dental infection is also an important cause of Roof of the ethmoid is formed by medial extension of
maxillary sinusitis. the orbital plate of the frontal bone, which shows depres-
• Roof of the maxillary sinus is formed by the floor of sions on its undersurface, called fovea ethmoidalis. The
the orbit. It is traversed by infraorbital nerve and lateral wall is formed by a thin plate of bone called lamina
vessels. papyracea.

209

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210 SECTION II — Diseases of Nose and Paranasal Sinuses

ANTERIOR GROUP. Important ethmoid cells in the ante-

rior group include:
1. Agger nasi cells – present in the agger nasi ridge.
2. Ethmoid bulla – forms the posterior boundary of the
hiatus semilunaris.
3. Supraorbital cells.
4. Frontoethmoid cells – situated in the area of the fron-
tal recess and may encroach the frontal sinus.
5. Haller cells – situated in the floor of the orbit.

POSTERIOR GROUP. The posterior group of ethmoid si-

nuses lies posterior to the basal lamina of middle concha.
They are 1–7 in number and open into superior meatus
or in the supreme meatus, when present. One important
cell of this group is sphenoethmoid cell, also called the
Onodi cell. It is the most posterior cell of this group and
extends along the lamina papyracea, lateral or superior to
the sphenoid and may extend 1.5 cm behind the anterior
face of sphenoid. Optic nerve and sometimes the carotid
artery are related to it laterally and are in danger during
endoscopic surgery.
Figure 35.1. Coronal section showing relationship of maxillary and At birth anterior ethmoids are 5 × 2 × 2 mm and pos-
ethmoidal sinuses to orbit and the nasal cavity. Floor of maxillary sinus
terior ethmoids are 5 × 4 × 2 mm. They attain their adult
is about 1 cm below the floor of nose.
size by the 12th year.

Sphenoid Sinus
It occupies the body of sphenoid. The two, right and left
sinuses, are rarely symmetrical and are separated by a thin
bony septum which is often obliquely placed and may
even be deficient (compare frontal sinus) (Figures 35.2
and 35.3). Ostium of the sphenoid sinus is situated high
up in the anterior wall and opens into the sphenoethmoi-
dal recess, medial to the superior or supreme turbinate. It
may be slit like, oval or round and can be seen endoscopi-
cally. In adults, it is situated about 1.5 cm from the upper
border of choana. The average distance from the anterior
nasal spine to the ostium is about 7 cm.
An adult sphenoid sinus is about 2 cm high, 2 cm deep
and 2 cm wide, but its pneumatization varies. In some
cases pneumatization may extend into greater or lesser
wing of sphenoid, pterygoid or clivus, i.e. basilar part of
occipital bone.

RELATIONS OF THE SPHENOID SINUS. Lateral wall of the

sphenoid is related to the optic nerve and carotid artery.
The opticocarotid recess can be seen in between the two.
Figure 35.2. Coronal section of sphenoid sinuses. Note the reliefs
It may extend laterally when the anterior clinoid process-
made by various structures in the cavity of sphenoid sinus. Optic nerve
forms the superolateral ridge.
es are also pneumatized. Maxillary nerve may be related
to lower part of the lateral wall of sphenoid. The optic
nerve and internal carotid artery are usually covered by
a thin bone, but sometimes this bony covering may be
dehiscent, and then these structures lie exposed, covered
only by mucosa.
Floor of the sinus is related to the Vidian nerve. Rela-
tion of the roof can be divided into two parts. Anterior
part of the roof is related to the olfactory tract, optic chi-
asma and frontal lobe, while posterior part is related to
the pituitary gland in the sella turcica and laterally to the
cavernous sinus. Posterior wall of the sphenoid forms the
clivus.
Relations of the sphenoid sinus are important in endo-
Figure 35.3. Relations of sphenoid sinus. scopic skull base surgery.

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 Chapter 35 — Anatomy and Physiology of Paranasal Sinuses 211

MUCOUS MEMBRANE OF PARANASAL is transported by the cilia to the natural ostium and then
SINUSES through it into the middle meatus (Figure 35.4A). Mucus
always drains from the natural ostium, even though ac-
Paranasal sinuses are lined by mucous membrane which cessory ostia be present in the fontanelle. It is also ob-
is continuous with that of the nasal cavity through the served that inferior meatal antrostomy made in Caldwell–
ostia of sinuses. It is thinner and less vascular compared Luc operation provides ventilation to the sinuses, but it
to that of the nasal cavity. Histologically, it is ciliated co- does not help in mucociliary clearance which still takes
lumnar epithelium with goblet cells which secrete mucus. place through the natural ostium.
Cilia are more marked near the ostia of sinuses and help
in drainage of mucus into the nasal cavity.
a
F RONTALS . Mucociliary clearance of the frontal si-
INUS
nus is unique (see Figure 35.4B). Mucus travels up along
DEVELOPMENT OF PARANASAL SINUSES the interfrontal septum, along the roof of the lateral wall,
along the floor and then exits through the natural ostium.
Paranasal sinuses develop as outpouchings from the mu-
At two points, one just above the ostium and other in the
cous membrane of lateral wall of nose. At birth, only the
frontal recess, part of the mucus recycles through the si-
maxillary and ethmoidal sinuses are present and are large
nus and this may carry infection of the frontal recess and
enough to be clinically significant.
sinuses draining into it, towards the frontal sinus. Circu-
Growth of sinuses continues during childhood and
lation is anticlockwise in the right and clockwise in the
early adult life. Radiologically, maxillary sinuses can be
left frontal sinus.
identified at 4–5 months, ethmoids at 1 year, frontals at
6 years and sphenoids at 4 years (Table 35.1).
SPHENOID SINUS. Mucociliary clearance is towards its os-
tium into the sphenoethmoidal recess.
LYMPHATIC DRAINAGE
The lymphatics of maxillary, ethmoid, frontal and sphe- ETHMOID SINUS. Mucus from anterior group of ethmoid
noid sinuses form a capillary network in their lining mu- sinuses joins that from the frontal and maxillary sinuses
cosa and collect with lymphatics of nasal cavity. Then and travels towards eustachian tube, passing in front of
they drain into lateral retropharyngeal and/or jugulodi- torus tubarius into the nasopharynx. Mucus from pos-
gastric nodes. terior ethmoids drains into superior or supreme meatus
and then joins the mucus from the sphenoid sinus in the
sphenoethmoidal recess, passes above and behind the to-
PHYSIOLOGY OF PARANASAL SINUSES rus tubarius into the nasopharynx (Figure 35.4C).
It is noted that infected discharge from the anterior
VENTILATION OF SINUSES group of sinuses, passes behind the posterior pillars and
causes hypertrophy of lateral pharyngeal bands. Dis-
Ventilation of paranasal sinuses takes place through their
charge from posterior group of sinuses spreads over the
ostia. During inspiration, air current causes negative pres-
posterior pharyngeal wall.
sure in the nose. This varies from −6 mm to −200 mm
H2O, depending on the force of inspiration. During ex-
piration, positive pressure is created in the nose and this FUNCTIONS OF PARANASAL SINUSES
sets up eddies which ventilate the sinuses. Thus, ventila-
It is not clear why nature provided paranasal sinuses.
tion of sinuses is paradoxical; they are emptied of air dur-
Probable functions are:
ing inspiration and filled with air during expiration. This
is just the reverse of what takes place in lungs which fill 1. Air-conditioning of the inspired air by providing large
during inspiration and empty during expiration. surface area over which the air is humidified and
warmed.
2. To provide resonance to voice.
MUCOCILIARY CLEARANCE OF SINUSES 3. To act as thermal insulators to protect the delicate
structures in the orbit and the cranium from variations
MAXILLARY SINUS. Mucus from all the walls of the maxil- of intranasal temperature.
lary sinus—anterior, medial, posterior, lateral and roof— 4. To lighten the skull bones.

TABLE 35.1 DEVELOPMENT AND GROWTH OF PARANASAL SINUSES

Status at birth Growth First radiologic evidence
Maxillary Present at birth Rapid growth from birth to 3 years and from 7–12 years 4–5 months after birth
Volume 6–8 mL Adult size – 15 years
Ethmoid • Present at birth Reach adult size by 12 years 1 year
• Anterior group: 5 × 2 × 2 mm
• Posterior group: 5 × 4 × 2 mm
Frontal Not present Invades frontal bone at the age of 4 years. Size increases 6 years
until teens and complete development by 20 years
Sphenoid Not present Reaches sella turcica by the age of 7 years, dorsum sellae 4 years
by late teens and basisphenoid by adult age Reaches
full size between 15 years to adult age

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212 SECTION II — Diseases of Nose and Paranasal Sinuses

f- Anticlockwise ✓ clockwise

Figure 35.4. Mucociliary clearance of paranasal sinuses. (A) Maxillary sinus. (B) Frontal sinus. (C) Anterior and posterior group of sinuses. See
text for details.

5. To provide extended surface for olfaction; olfactory 7. To act as buffers against trauma and thus protect brain
mucosa is situated in the upper part of nasal cavity and against injury, e.g. frontal, ethmoid and sphenoid
extends over ethmoid as well. sinuses.
6. To provide local immunologic defence against
microbes.

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 Chapter 36
Acute Rhinosinusitis

DEFINITION Complications are uncommon, as the disease is self-

limiting. However, if bacterial infection supervenes or if
Earlier the term sinusitis was used to describe inflamma- the patient is immunocompromised, it can convert to
tion of the mucosa of sinuses. However, as this condition bacterial RS, and also cause pharyngitis, bronchitis, pneu-
is invariably associated with inflammation of the nasal monia or otitis media.
mucosa, hence the term rhinosinusitis (RS) has been
preferred.
ACUTE BACTERIAL RHINOSINUSITIS
CLASSIFICATION This usually follows viral upper respiratory infection. The
virus damages the cilia and epithelium, and causes oede-
Rhinosinusitis Task Force (2007) gave the clinical classi- ma of the mucosa membrane and obstruction of sinus
fication as: ostia with stasis of sinus secretion and subsequent bacte-
• Acute RS: Symptoms lasting for less than 4 weeks with rial infection.
complete resolution. The most common bacteria responsible for RS are
• Subacute RS: Duration 4-12 weeks. Streptococcus pneumoniae, Haemophilus influenzae, Morax-
• Chronic RS: Duration 12 weeks. ella catarrhalis and Staphylococcus aureus.
• Recurrent RS: Four or more episodes of RS per year; Pathophysiology is depicted in Figure 36.2. It is an in-
each lasting for 7-10 days or more with complete reso- terplay of forces between pathogens and the host's im-
lution in between the episodes. mune responses and other structural predisposing factors.
Clinical features include nasal obstruction and pu-
Acute exacerbation of chronic RS is the sudden worsen- rulent rhinorrhoea. Facial pain/pressure are the cardinal
ing of chronic RS with return to baseline after treatment. symptoms. Hyposmia/anosmia, cough, fever, headache,
Symptoms associated with RS include: fullness of ear, dental pain or halitosis may be other as-
• Nasal obstruction. sociated symptoms.
• Nasal discharge/congestion, anterior, or posterior in Diagnosis of acute bacterial RS is made when symp-
the form of postnasal drip. toms of acute viral RS persist or worsen beyond 10 days.
• Facial pain or pressure. However, bacterial infection can set in earlier if the host is
• Alteration in the sense of smell, hyposmia or anosmia. immunocompromised. CT scans are not required to make
• Other symptoms include cough, fever, halitosis, a diagnosis unless complications are suspected or the dis-
fatigue, dental pain, pharyngitis, headache or ear ease is refractory to medical treatment. Some structural
fullness. deformities are thought to be responsible for the persis-
tence of infection.
Nasal endoscopy may reveal purulent discharge in the
ostiomeatal complex. A swab can be taken from middle
ACUTE VIRAL RHINOSINUSITIS meatus to establish culture and sensitivity of bacteria.
It is caused by respiratory viruses, usually the common Treatment strategies for acute bacterial RS include the
cold viruses such as rhinoviruses, influenza and parainflu- following:
enza. They spread by aerosolised droplets through cough- 1. Analgesics: NSAIDs can be used to relieve headaches
ing and sneezing. Incubation period is 1-4 days. and sinus or dental pain.
Pathophysiology is depicted in Figure 36.1 . 2. Antibiotics: A short course of antibiotics can cut down
Clinical features include nasal congestion (block- the course of disease, but wait and watch is recom-
age), rhinorrhoea, sneezing and low-grade fever. Unless mended by some and antibiotics are prescribed if the
complicated by bacterial infection, the patient improves patient's condition worsens. CCAMOXICLAV
within a week or 10 days. It is a self-limiting disease. Amoxicillin with or without clavulanic acid is ef-
Treatment is symptomatic with use of topical nasal fective and is the first line of treatment. Those allergic
decongestants and antihistamines. Analgesics are useful to penicillin can be given doxycycline, levofloxacin or
to relieve headache, fever and myalgia. Aspirin should other antibiotics that can be chosen on the basis of
be avoided, as it causes increased shedding of the virus. suitable antimicrobial culture and sensitivity tests.
Plenty of fluid intake should be encouraged. Nasal saline 3. Saline irrigations: They help to thin the mucus, wash
sprays are useful. Antibiotics are not needed. out bacteria and give symptomatic relief.

213
214 SECTION II — Diseases of Nose and Paranasal Sinuses

ACUTE MAXILLARY SINUSITIS

AETIOLOGY
1. Most commonly, it is viral rhinitis which spreads to
involve the sinus mucosa. This is followed by bacterial
invasion.
2. Diving and swimming in contaminated water.
3. Dental infections are important source of maxillary
sinusitis. Roots of premolar and molar teeth are re-
lated to the floor of sinus and may be separated only
by a thin layer of mucosal covering. Periapical den-
tal abscess may burst into the sinus; or the root of
a tooth, during extraction, may be pushed into the
sinus. In case of oroantral fistula, following tooth ex-
traction, bacteria from oral cavity enter the maxillary
sinus.
4. Trauma to the sinus such as compound fractures, pen-
etrating injuries or gunshot wounds may be followed
by sinusitis.

Predisposing factors
One or more of the predisposing factors enumerated for
sinusitis in general may be responsible for acute or recur-
Figure 36.1. Pathophysiology of acute viral rhinosinusitis.
rent infection.

CLINICAL FEATURES
Clinical features depend on (i) severity of inflammatory
process and (ii) efficiency of ostium to drain the exudates.
Closed ostium sinusitis is of greater severity and leads
more often to complications.
1. Constitutional symptoms. It consist of fever, general
malaise and body ache. They are the result of toxaemia.
2. Headache. Usually, this is confined to forehead and
may thus be confused with frontal sinusitis.
3. Pain. Typically, it is situated over the upper jaw, but
may be referred to the gums or teeth. For this reason
patient may primarily consult a dentist. Pain is aggra-
vated by stooping, coughing or chewing. Occasionally,
pain is referred to the ipsilateral supraorbital region
and thus may simulate frontal sinus infection.
4. Tenderness. Pressure or tapping over the anterior wall
of antrum produces pain.
5. Redness and oedema of cheek. Commonly seen in
Figure 36.2. Sequence of acute viral to acute bacterial rhinosinusitis.
children. The lower eyelid may become puffy.
6. Nasal discharge. Anterior rhinoscopy/nasal endos-
copy shows pus or mucopus in the middle meatus.
Mucosa of the middle meatus and turbinate may
appear red and swollen.
4. Antihistamines should be used if there is concurrent 7. Postnasal discharge. Pus may be seen on the upper
allergy. Antihistamines make the mucus thick. soft palate on posterior rhinoscopy or nasal endoscopy.
5. Decongestants give relief from nasal obstruction.
Topical use of xylmetazoline should be limited only
for a few days, as prolonged used can cause rhinitis
DIAGNOSIS
medicamentosa.
Oral nasal decongestants can be used if there are • Transillumination test. Affected sinus will be found
no contraindications such as hypertension or peptic
ulcer.
opaque. Oceipin mental view
• X-rays. Waters’ view will show either an opacity or a
6. Intranasal steroids. They are anti-inflammatory in na- fluid level in the involved sinus. Computed tomogra-
ture and are used to relive oedema and associated al- phy (CT) scan is the preferred imaging modality to in-
lergy and cut down the course of the disease. vestigate the sinuses.
Pierre's view → waters view
c- mouth open
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 Chapter 36 — Acute Rhinosinusitis 215

TREATMENT i.e. comes up on waking, gradually increases and

reaches its peak by about mid day and then starts sub-
Medical siding. It is also called “office headache” because of its
1. Antimicrobial drugs. Ampicillin and amoxicillin are presence only during the office hours.
quite effective and cover a wide range of organisms. 2. Tenderness. Pressure upwards on the floor of frontal
Erythromycin or doxycycline or cotrimoxazole are sinus, just above the medial canthus, causes exquisite
equally effective and can be given to those who are pain. It can also be elicited by tapping over the ante-
sensitive to penicillin. β-lactamase-producing strains rior wall of frontal sinus in the medial part of supraor-
of H. influenzae and M. catarrhalis may necessitate the bital region.
use of amoxicillin/clavulanic acid or cefuroxime axetil. 3. Oedema of upper eyelid with suffused conjunctiva
Sparfloxacin is also effective, and has the advantage of and photophobia.
single daily dose. 4. Nasal discharge. A vertical streak of mucopus is seen
2. Nasal decongestant drops. One per cent ephedrine or high up in the anterior part of the middle meatus. This
0.1% xylo- or oxymetazoline are used as nasal drops may be absent if the ostium is closed with no drainage.
or sprays to decongest sinus ostium and encourage Nasal mucosa is inflamed in the middle meatus.
drainage.
X-rays. Opacity of the affected sinus or fluid level can
3. Steam inhalation. Steam alone or medicated with
be seen. Both Waters’ and lateral views should be taken.
menthol or Tr. Benzoin Co. provides symptomatic re-
CT scan is the preferred modality.
lief and encourages sinus drainage. Inhalation should
be given 15–20 min after nasal decongestion for better
penetration. TREATMENT
4. Analgesics. Paracetamol or any other suitable analge-
sic should be given for relief of pain and headache. Medical
5. Hot fomentation. Local heat to the affected sinus is This is same as for acute maxillary sinusitis, i.e. antimi-
often soothing and helps in the resolution of inflam- crobials, decongestion of the sinus ostium for drainage
mation. and analgesics. A combination of antihistaminic with an
oral nasal decongestant (phenylephrine hydrochloride)
Surgical
is useful. Placing a pledget of cotton soaked in a vaso-
Antral lavage. Most cases of acute maxillary sinusitis re- constrictor in the middle meatus, once or twice daily,
spond to medical treatment. Lavage is rarely necessary. It helps to relieve ostial oedema and promotes sinus drain-
is done only when medical treatment has failed and that age and ventilation. If patient shows response to medical
too only under cover of antibiotics. treatment and pain is relieved, treatment is continued for
full 10 days to 2 weeks.
COMPLICATIONS
Surgical
1. Acute maxillary sinusitis may change to subacute or
chronic sinusitis. Trephination of frontal sinus. If there is persistence
2. Frontal sinusitis. Due to obstruction of frontal sinus or exacerbation of pain or pyrexia in spite of medical
drainage pathway because of oedema. treatment for 48 h, or if the lid swelling is increasing
3. Osteitis or osteomyelitis of the maxilla. and threatening orbital cellulitis, frontal sinus is drained
4. Orbital cellulitis or abscess. Infection spreads to the externally. A 2 cm long horizontal incision is made in
orbit because of oedema either directly from the roof the superomedial aspect of the orbit below the eyebrow
of maxillary sinus or indirectly, after involvement of (Figure 36.3). Floor of frontal sinus is exposed and a hole
ethmoid sinuses. drilled with a burr. Pus is taken for culture and sensitiv-
ity, and a plastic tube inserted and fixed. Sinus can now

ACUTE FRONTAL SINUSITIS

AETIOLOGY
1. Usually follows viral infections of upper respiratory
tract followed later by bacterial invasion.
2. Entry of water into the sinus during diving or swimming.
3. External trauma to the sinus, e.g. fractures or penetrat-
ing injuries.
4. Oedema of middle meatus, secondary to associated ip-
silateral maxillary or ethmoid sinus infection.
Predisposing factors, pathology and bacteriology are
the same as in acute sinusitis in general.

CLINICAL FEATURES
1. Frontal headache. Usually severe and localized over
the affected sinus. It shows characteristic periodicity, Figure 36.3. Trephination of right frontal sinus.

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216 SECTION II — Diseases of Nose and Paranasal Sinuses

be irrigated with normal saline two or three times daily Visual deterioration and exophthalmos indicate ab-
until frontonasal duct becomes patent. This can be de- scess in the posterior orbit and may require drainage of
termined by adding a few drops of methylene blue to the ethmoid sinuses into the nose through an external
the irrigating fluid and its exit seen through the nose. ethmoidectomy incision.
Drainage tube is removed when frontonasal duct be-
comes patent. COMPLICATIONS
1. Orbital cellulitis and abscess.
COMPLICATIONS 2. Visual deterioration and blindness due to involvement
of optic nerve.
1. Orbital cellulitis.
3. Cavernous sinus thrombosis.
2. Osteomyelitis of frontal bone and fistula formation.
4. Extradural abscess, meningitis or brain abscess.
3. Meningitis, extradural abscess or frontal lobe abscess,
if infection breaks through the posterior wall of the
sinus. ACUTE SPHENOID SINUSITIS
4. Chronic frontal sinusitis, if the acute infection is ne-
glected or improperly treated. AETIOLOGY
Isolated involvement of sphenoid sinus is rare. It is often
a part of pansinusitis or is associated with infection of
ACUTE ETHMOID SINUSITIS posterior ethmoid sinuses.

AETIOLOGY CLINICAL FEATURES

Acute ethmoiditis is often associated with infection of 1. Headache. Usually localized to the occiput or vertex.
other sinuses. Ethmoid sinuses are more often involved Pain may also be referred to the mastoid region.
in infants and young children. 2. Postnasal discharge. It can only be seen on posterior
rhinoscopy. A streak of pus may be seen on the roof
CLINICAL FEATURES and posterior wall of nasopharynx or above the poste-
rior end of middle turbinate.
1. Pain. It is localized over the bridge of the nose, medial
and deep to the eye. It is aggravated by movements of X-rays. Opacity or fluid level may be seen in the sphe-
the eye ball. noid sinus. Lateral view of the sphenoid sinus is taken in
2. Oedema of lids. Both eyelids become puffy and swol- supine or prone position and is helpful to demonstrate
len. There is increased lacrimation. Orbital cellulitis is the fluid level. CT scan is more useful.
an early complication in such cases.
3. Nasal discharge. On anterior rhinoscopy, pus may be DIFFERENTIAL DIAGNOSIS
seen in middle or superior meatus depending on the Mucocele of the sphenoid sinus or its neoplasms may
involvement of anterior or posterior group of ethmoid clinically simulate features of acute infection of sphenoid
sinuses. sinus and should always be excluded in any case of iso-
4. Swelling of the middle turbinate. lated sphenoid sinus involvement.

TREATMENT TREATMENT
Medical treatment is the same as for acute maxillary Treatment is the same as for acute infection of other
sinusitis. sinuses.

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 Chapter 47
Anatomy and Physiology of Pharynx

PHARYNX IN GENERAL fibres. Between these two parts exists a potential gap called
Killian’s dehiscence. It is also called “gateway of tears” as
Pharynx is a conical fibromuscular tube forming upper perforation can occur at this site during oesophagoscopy.
part of the air and food passages. It is 12–14 cm long, This is also the site for herniation of pharyngeal mucosa
extending from base of the skull (basiocciput and basis-
phenoid) to the lower border of cricoid cartilage where it
in cases of pharyngeal pouch.
Zcekd 's diverticulum
becomes continuous with the oesophagus. The width of
pharynx is 3.5 cm at its base and this narrows to 1.5 cm at WALDEYER’S RING (FIGURE 47.2)
pharyngo-oesophageal junction, which is the narrowest Scattered throughout the pharynx in its subepithelial layer
part of digestive tract apart from the appendix. is the lymphoid tissue which is aggregated at places to
form masses, collectively called Waldeyer’s ring. The mass-
es are:
STRUCTURE OF PHARYNGEAL WALL
(FIGURE 47.1) 1. Nasopharyngeal tonsil or the adenoids
2. Palatine tonsils or simply the tonsils
From within outwards it consists of four layers: 3. Lingual tonsil
1. Mucous membrane 4. Tubal tonsils (in fossa of Rosenmüller)
2. Pharyngeal aponeurosis (pharyngobasilar fascia) 5. Lateral pharyngeal bands
3. Muscular coat 6. Nodules (in posterior pharyngeal wall).
4. Buccopharyngeal fascia
PHARYNGEAL SPACES
1. MUCOUS MEMBRANE. It lines the pharyngeal cavity
and is continuous with mucous membrane of eustachian There are two potential spaces in relation to the pharynx
tubes, nasal cavities, mouth, larynx and oesophagus. The where abscesses can form.
epithelium is ciliated columnar in the nasopharynx and 1. Retropharyngeal space, situated behind the pharynx
stratified squamous elsewhere. There are numerous mu- and extending from the base of skull to the bifurcation
cous glands scattered in it. of trachea (see p. 299).
2. Parapharyngeal space, situated on the side of pharynx.
2. PHARYNGEAL APONEUROSIS (PHARYNGOBASILAR It contains carotid vessels, jugular vein, last four cra-
FASCIA). It is a fibrous layer which lines the muscular coat nial nerves and cervical sympathetic chain (see p. 301).
and is particularly thick near the base of skull but is thin
and indistinct inferiorly. It fills up the gap left in the mus-
I

cular coat near the base of skull.

DIVISIONS OF PHARYNX
3. MUSCULAR COAT. It consists of two layers of muscles Anatomically, pharynx is divided into three parts
with three muscles in each layer. (Figure 47.3):
(a) External layer. It contains superior, middle and infe- 1. Nasopharynx
rior constrictor muscles. 2. Oropharynx
(b) Internal layer. It contains stylopharyngeus, salpin- 3. Hypopharynx or laryngopharynx.
gopharyngeus and palatopharyngeus muscles.

4. BUCCOPHARYNGEAL FASCIA. It covers outer surface of NASOPHARYNX (EPIPHARYNX)

the constrictor muscles and in the upper part, it is also
Applied Anatomy
prolonged forwards to cover the buccinator muscles.
Above the upper border of superior constrictor, it blends Nasopharynx is the uppermost part of the pharynx and
with pharyngeal aponeurosis. therefore, also called epipharynx. It lies behind the nasal
cavities and extends from the base of skull to the soft pal-
ate or the level of the horizontal plane passing through
KILLIAN’S DEHISCENCE the hard palate (Figure 47.4).
Inferior constrictor muscle has two parts: thyropharyngeus 1. Roof of the nasopharynx is formed by basisphenoid
with oblique fibres and cricopharyngeus with transverse and basiocciput.

aryrophangngeu Killian's dehiscence

=-→oicophayngg-
→

269

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270 SECTION IV — Diseases of Pharynx

Figure 47.4. Rathke’s pouch is represented by a dimple, high in

nasopharynx. Inferior to this, within the adenoid mass, is the naso-
pharyngeal bursa.
Figure 47.1. Structure of pharyngeal wall. From within outwards it
consists of (a) mucous membrane, (b) pharyngobasilar fascia, (c) mus-
cular coat and (d) buccopharyngeal fascia. 2. Posterior wall is formed by arch of the atlas vertebra
covered by prevertebral muscles and fascia. Both the
roof and the posterior wall imperceptibly merge with
each other.
3. Floor is formed by the soft palate anteriorly but is de-
ficient posteriorly. It is through this space, the naso-
pharyngeal isthmus, that the nasopharynx communi-
cates with the oropharynx.
4. Anterior wall is formed by posterior nasal apertures or
choanae, separated from each other by the posterior
border of the nasal septum. Posterior ends of nasal tur-
binates and meatuses are seen in this wall.
5. Lateral wall. Each lateral wall presents the pharyngeal
opening of eustachian tube situated 1.25 cm behind
the posterior end of inferior turbinate. It is bounded
above and behind by an elevation called torus tubarius
raised by the cartilage of the tube. Above and behind
:&
¥☒j•ir÷
the tubal elevation is a recess called fossa of Rosenmül-
Figure 47.2. Waldeyer’s ring. ler, which is the commonest site for origin of carcino-
" ma (Figure 47.5). A ridge extends from the lower end
of torus tubarius to the lateral pharyngeal wall and is
:&

:P
called -salpingopharyngeal fold (Figure 47.9). It is raised
✓
-
appear :*
by the corresponding muscle.
a Nasopharyngeal Tonsil (Adenoids)
It is a subepithelial collection of lymphoid tissue at the
junction of roof and posterior wall of nasopharynx and
causes the overlying mucous membrane to be thrown
into radiating folds (Figure 47.1). It increases in size up to
the age of 6 years and then gradually atrophies.

Nasopharyngeal Bursa (Figure 47.4)

It is an epithelial-lined median recess found within the
adenoid mass and extends from pharyngeal mucosa to
the periosteum of the basiocciput. It represents the at-
tachment of notochord to the pharyngeal endoderm dur-
ing embryonic life. When infected, it may be the cause
of persistent postnasal discharge or crusting. Sometimes
an abscess can form in the bursa (Thornwaldt’s disease).
Rathke’s Pouch
Figure 47.3. Divisions of pharynx and the vertebrae related to their It is represented clinically by a dimple above the adenoids
posterior wall. and is reminiscent of the buccal mucosal invagination, to

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 Chapter 47 — Anatomy and Physiology of Pharynx 271

2. Through the eustachian tube, it ventilates the middle

ear and equalizes air pressure on both sides of tympan-
ic membrane. This function is important for hearing.
3. Elevation of the soft palate against posterior pharynge-
al wall and the Passavant’s ridge helps to cut off naso-
pharynx from oropharynx. This function is important
during swallowing, vomiting, gagging and speech.
4. Acts as a resonating chamber during voice production.
Voice disorders are seen in nasopharyngeal obstruction
and velopharyngeal incompetence (see Chapter 63).

- 5. Acts as a drainage channel for the mucus secreted by

nasal and nasopharyngeal glands.

Opening OROPHARYNX
of
Eustachian
tube
Applied Anatomy
Oropharynx extends from the plane of hard palate above
Figure 47.5. Endoscopic view of nasopharynx showing torus tubari-
us in the lateral wall of nasopharynx. Note also the fossa of Rosenmül- to the plane of hyoid bone below. It lies opposite the oral
ler which lies behind it. Fossa of Rosenmüller is the commonest site for cavity with which it communicates through oropharynge-
the origin of carcinoma nasopharynx. al isthmus. The latter is bounded above, by the soft palate;
below, by the upper surface of tongue; and on either side,
by palatoglossal arch (anterior pillar).
form the anterior lobe of pituitary. A craniopharyngioma
may arise from it. Boundaries of Oropharynx
Tubal Tonsil 1. POSTERIOR WALL. It is related to retropharyngeal
space and lies opposite the second and upper part of the
It is collection of subepithelial lymphoid tissue situated at
third cervical vertebrae.
the tubal elevation. It is continuous with adenoid tissue C2 ,
and forms a part of the Waldeyer’s ring. When enlarged
2. ANTERIOR WALL. It is deficient above, where oropharynx
due to infection, it causes eustachian tube occlusion.
communicates with the oral cavity, but below it presents:
Sinus of Morgagni (a) Base of tongue, posterior to circumvallate papillae.
It is a space between the base of the skull and upper free (b) Lingual tonsils, one on either side, situated in the base
border of superior constrictor muscle. Through it enters of tongue. They may show compensatory enlarge-
(i) the eustachian tube, (ii) the levator veli palatini, (iii) ment following tonsillectomy or may be the seat of
tensor veli palatini and (iv) ascending palatine artery— infection.
branch of the facial artery (Figure 47.1). (c) Valleculae. They are cup-shaped depressions lying
between the base of tongue and anterior surface of ep-
Passavant’s Ridge iglottis. Each is bounded medially by the median glos-
It is a mucosal ridge raised by fibres of palatopharyngeus. soepiglottic fold and laterally by pharyngoepiglottic
It encircles the posterior and lateral walls of nasopharyn- fold (Figure 47.6). They are the seat of retention cysts.
geal isthmus. Soft palate, during its contraction, makes
firm contact with this ridge to cut off nasopharynx from 3. LATERAL WALL. It presents:
the oropharynx during the deglutition or speech.
(a) Palatine (faucial) tonsil (for details, see p. 291).
Epithelial Lining of Nasopharynx (b) Anterior pillar (palatoglossal arch) formed by the pala-
toglossus muscle.
Functionally, nasopharynx is the posterior extension of
(c) Posterior pillar (palatopharyngeal arch) formed by the
nasal cavity. It is lined by pseudostratified ciliated colum-
palatopharyngeus muscle.
nar epithelium.
Both anterior and posterior pillars diverge from the soft
Lymphatic Drainage palate and enclose a triangular depression called tonsillar
Lymphatics of the nasopharynx, including those of the fossa in which is situated the palatine tonsil (Figure 47.7).
adenoids and pharyngeal end of eustachian tube, drain Boundary between oropharynx above and the hy-
into upper deep cervical jugular nodes either directly or popharynx below is formed by upper border of epiglottis
indirectly through retropharyngeal and parapharyngeal and the pharyngoepiglottic folds.
lymph nodes. They also drain into spinal accessory chain
of nodes in the posterior triangle of the neck. Lymphatics Lymphatic Drainage
of the nasopharynx may also cross midline to drain into Lymphatics from the oropharynx drain into upper jugu-
contralateral lymph nodes. lar chain particularly the jugulodigastric (tonsillar) node.
The soft palate, lateral and posterior pharyngeal walls and
Functions of Nasopharynx the base of tongue also drain into retropharyngeal and
1. Acts as a conduit for air, which has been warmed and parapharyngeal nodes and from there to the jugulodigas-
humidified in the nose, towards its passage to the tric and posterior cervical group. The base of tongue may
larynx and trachea. drain bilaterally.

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272 SECTION IV — Diseases of Pharynx

Figure 47.8. Normal pyriform fossae right and left (arrows). They
show better when patient phonates.

Figure 47.6. Base of the tongue and valleculae.

HYPOPHARYNX (LARYNGOPHARYNX)
Applied Anatomy
Hypopharynx is the lowest part of the pharynx and lies be-
hind and partly on the sides of the larynx. Its superior lim-
it is the plane passing from the body of hyoid bone to the
posterior pharyngeal wall, while the inferior limit is lower
border of cricoid cartilage where hypopharynx becomes
continuous with oesophagus. Hypopharynx lies opposite
the third, fourth, fifth, sixth cervical vertebrae. Clinically,
it is subdivided into three regions—the pyriform sinus,
postcricoid region and the posterior pharyngeal wall.
1. Pyriform sinus (fossa). It lies on either side of the lar-
ynx and extends from pharyngoepiglottic fold to the
upper end of oesophagus.
It is bounded laterally by the thyrohyoid membrane
and the thyroid cartilage and medially by the aryepi-
glottic fold, posterolateral surfaces of arytenoid and cri-
coid cartilages (Figure 47.8). It forms the lateral channel
for food. Foreign bodies may lodge in the pyriform fos-
sa. Internal laryngeal nerve runs submucosally in the
Figure 47.7. Various structures seen in the oropharynx. lateral wall of the sinus and thus is easily accessible for
local anaesthesia. It is also through this nerve that pain
is referred to the ear in carcinoma of the pyriform sinus.
Functions of Oropharynx
2. Postcricoid region. It is the part of the anterior wall of
1. As a conduit for passage of air and food.
laryngopharynx between the upper and lower borders
2. Helps in the pharyngeal phase of deglutition.
of cricoid lamina. It is a common site for carcinoma
3. Forms part of vocal tract for certain speech sounds.
in females suffering from Plummer–Vinson syndrome
4. Helps in appreciation of the taste. Taste buds are pre- ← d Iron deficiency
(Figure 47.9).
sent in the base of tongue, soft palate, anterior pillars Oesophageal webs Glossitis
3. Posterior pharyngeal wall. It extends from the level
anaemia

and posterior pharyngeal wall.

of hyoid bone to the level of cricoarytenoid joint.
5. Provides local defence and immunity against harmful
intruders into the air and food passages. This function
is subserved by subepithelial masses of lymphoid tis- Lymphatic Drainage
sues scattered as Waldeyer’s ring. They are strategically Pyriform sinus is richly supplied by lymphatics which
placed at the portals of air and food entry and act as exit through the thyrohyoid membrane and drain into
protective sentinels. B-lymphocytes in the germinal the upper jugular chain.
centres of the follicles produce secretory antibodies of Lymphatics of the posterior wall terminate in the lat-
IgA class whereas T-lymphocytes in parafollicular re- eral pharyngeal or parapharyngeal nodes and thence to
gion produce cell-mediated immunity against various the deep cervical lymph nodes.
viruses, bacteria and fungi. Pathogens which happen Lymphatics of postcricoid region also drain into the
to enter into these lymphoid masses are dealt by IgM parapharyngeal nodes but may also drain into nodes of
and IgG antibodies secreted by plasma cells. supraclavicular and paratracheal chain.

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 Chapter 47 — Anatomy and Physiology of Pharynx 273

Figure 47.9. Pharynx opened from behind showing structures related to nasopharynx, oropharynx and laryngopharynx. Source. RL Drake,
AW Vogl, AWM Mitchell, 2017. Gray’s Anatomy for Students, 1SEA edition. Elsevier.

Rich lymphatic network of pyriform fossae explains certain speech sounds and helps in deglutition. There is
the high frequency with which nodal metastases are seen coordination between contraction of pharyngeal muscles
in carcinoma of this region. and relaxation of cricopharyngeal sphincter at the up-
per end of oesophagus. Lack of this coordination, i.e.
Functions of Hypopharynx failure of cricopharyngeal sphincter to relax when phar-
Laryngopharynx, like oropharynx, is a common pathway yngeal muscles are contracting causes hypopharyngeal
for air and food, provides a vocal tract for resonance of diverticulum.

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 Chapter 49
Tumours of Nasopharynx

BENIGN TUMOURS 4. Orbits giving rise to proptosis and “frog-face deform-

ity.” It enters through the inferior orbital fissure and
Benign and malignant tumours of the nasopharynx are also destroys apex of the orbit. It can also enter the
listed in Table 49.1 . orbit through superior orbital fissure.
5. Cranial cavity. It can extend into:
NASOPHARYNGEAL FIBROMA (JUVENILE (a) Anterior cranial fossa through roof of ethmoids or
NASOPHARYNGEAL ANGIOFIBROMA) cribriform plate.
(b) Middle cranial fossa through erosion of floor of
It is a rare tumour, though it is the commonest of all be- middle cranial fossa or indirectly by invading the
nign tumours of nasopharynx. sphenoid sinus and sella turcica. In the former
case, tumour lies lateral to internal carotid artery
Aetiology and in the latter case medial to the artery.
The exact cause is unknown. As the tumour is predomi-
nantly seen in adolescent males in the second decade Clinical Features
of life, it is thought to be testosterone dependent. Such 1. Age and sex. Tumour is seen almost exclusively in
patients have a hamartomatous nidus of vascular tissue males in the age group of 10–20 years. Rarely, it may
in the nasopharynx and this is activated to form angiofi- be seen in older people and females.
broma when male sex hormone appears. 2. Profuse, recurrent and spontaneous epistaxis. This is
the most common presentation. Patient may be mark-
Site of Origin and Growth edly anaemic due to repeated blood loss.
The site of origin of the tumour is still a matter of dispute. 3. Progressive nasal obstruction and denasal speech. It
Earlier it was thought to arise from the roof of nasophar- is due to mass in the postnasal space.
ynx or the anterior wall of sphenoid bone but now it is be- 4. Conductive hearing loss and otitis media with effu-
lieved to arise from the posterior part of nasal cavity close sion. It occur due to obstruction of eustachian tube.
to the superior margin of sphenopalatine foramen. From 5. Mass in the nasopharynx. Tumour is sessile, lobu-
here the tumour grows into the nasal cavity, nasopharynx lated or smooth and obstructs one or both choanae.
and into the pterygopalatine fossa, running behind the It is pink or purplish in colour. Consistency is firm but
posterior wall of maxillary sinus which is pushed forward digital palpation should never be done until at the time of
as the tumour grows. Laterally, it extends into pterygomax- operation.
illary fossa and thence to infratemporal fossa and cheek. 6. Other clinical features like broadening of nasal bridge,
proptosis, swelling of cheek, infratemporal fossa or in-
Pathology volvement of IInd, IIIrd, IVth and VIth cranial nerves
Angiofibroma, as the name implies, is made up of vascu- will depend on the extent of tumour (Figure 49.2 ).
lar and fibrous tissues: the ratio of the two components
may vary. Mostly, the vessels are just endothelium-lined
spaces with no elastic or muscle coat. This accounts for
TABLE 49.1 BENIGN AND MALIGNANT TUMOURS
the severe bleeding as the vessels lose the ability to con-
OF THE NASOPHARYNX
tract; also the bleeding cannot be controlled by applica-
tion of adrenaline (Figure 49.1). Though benign, angiofi- Benign Malignant
bromas do not have a capsule. • Angiofibroma • Carcinoma nasopharynx
• Choanal polyp • Lymphoma
Extensions of Nasopharyngeal Fibroma • Squamous papilloma • Rhabdomyosarcoma
Nasopharyngeal fibroma is a benign tumour but locally • Thornwaldt’s cyst • Chordoma
invasive and destroys the adjoining structures. It may ex- • Pleomorphic adenoma • Plasmacytoma
• Craniopharyngioma • Haemangiopericytoma
tend into:
• Paraganglioma • Malignant salivary gland
1. Nasal cavity causing nasal obstruction, epistaxis and • Hamartoma tumours
nasal discharge. • Congenital tumours • Melanoma
2. Paranasal sinuses. Maxillary, sphenoid and ethmoid • Hairy polyp
sinuses can all be invaded. • Teratoma
• Epignathi
3. Pterygomaxillary fossa, infratemporal fossa and
cheek. Scan to play Benign Tumours of Nasopharynx.

279

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 280 SECTION IV — Diseases of Pharynx

Figure 49.1. Angiofibroma. Section shows multiple dilated vessels surrounded by fibrous stroma. (A) H&E, ×100. (B) H&E, ×200.

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Figure 49.2. (A) Specimen of an extensive angiofibroma in a 32-year-old male. (B&C) CT scans of the same. Note destruction of bone and
extension into pterygopalatine fossa.
Scan to play Nasopharyngeal Fibroma.

Diagnosis Investigations
It is mostly based on clinical picture. Biopsy of the tumour
-

1. Computed tomography (CT) scan of the head with

is attended with profuse bleeding and is, therefore, avoid- contrast enhancement is now the investigation of
ed. If it is essential to differentiate it from other tumours, choice (Figure 49.3). It has replaced conventional radi-
biopsy can be done under general anaesthesia with all ar- ographs. It shows the extent of tumour, bony destruc-
rangements to control bleeding and transfuse blood. tion or displacements. Anterior bowing of the poste-

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 Chapter 49 — Tumours of Nasopharynx 281

Figure 49.3. Embolization of angiofibroma to decrease vascularity: (A) & (B) pre-embolization and (C) after embolization.

intracranial

:^*
for
rior wall of maxillary sinus, often called antral sign or
Holman-Miller sign, is pathognomic of angiofibroma.
2. Magnetic resonance imaging (MRI) is complementary
Treatment
TY
SURGERY. Surgical excision is the treatment of choice
extension

*
though radiotherapy
- and chemotherapy singly or in
to CT scans and shows any soft tissue extensions pre-
combination have also been used. Spontaneous regres-
sent intracranially in the infratemporal fossa or in the
sion of the tumour with advancement of age, as thought
orbit.
previously, does not occur and no wait and watch policy
3. Carotid angiography shows the extent of tumours, its
should be adopted. Surgical approaches used to remove
vascularity and feeding vessels which mostly come
angiofibroma, depending on its origin and extensions,
from the external carotid system. In very large tumours
are listed below.
or those with intracranial extension vessels may also
come from internal carotid system. Embolization of 1. Transpalatine (Figure 49.4)
vessels can be done at this time to decrease bleeding at 2. Transpalatine + Sublabial (Sardana’s approach)
operation. Feeders from only the external carotid sys- 3. Lateral rhinotomy with medial maxillectomy
tem can be embolized. Resection of tumour should not (a) Via facial incision
be delayed beyond 24–48 h of embolization to = avoid (b) Via degloving approach
revascularization from the contralateral side. 4. Endoscopic removal
4. Arrangement for blood transfusion. Though blood 5. Transmaxillary (Le Fort I) approach
may not be required during surgery if successful 6. Maxillary swing approach or facial translocation ap-
embolization is done, 2–3 units of blood should be proach, or Wei’s operation
available and kept in reserve after grouping and cross- 7. Infratemporal fossa approach
matching. 8. Intracranial–extracranial approach

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282 SECTION IV — Diseases of Pharynx

Preoperative embolization of the tumour reduces its

blood supply and causes less bleeding, if tumour remov-
al is performed within 24–48 h of embolization before
collaterals have time to develop. Preoperative angiogra-
phy also helps to find any feeders from internal carotid
system.
Before the era of tumour embolization, oestrogens
were used systemically to reduce blood supply. Similarly
cryotherapy was also used.
Recurrence of juvenile angiofibroma is not uncommon
and has been reported in up to 35%.
MANAGEMENT OF RECURRENT TUMOUR. Various options
used are:
(a) Observation. The tumour may spontaneously regress.
(b) Revision surgery and removal. If it recurs even after revi-
sion surgery, radiotherapy may be considered.
(c) Radiation. Reduces the blood supply and the tumour
Figure 49.4. Nasopharyngeal fibroma as seen after transpalatal subsides over time. It is also used when tumour recur-
exposure. rence is surgically inaccessible.
RADIOTHERAPY. Radiotherapy has been used as a pri-
mary mode of treatment, thus avoiding surgery. A dose
Transpalatal approach is used for tumours confined to of 3000 to 3500 cGy in 15–18 fractions is delivered in
the nasopharynx. It can be extended into Sardana’s ap- 3–3.5 weeks. Response is not immediate. Tumour regress-
proach if the tumour
- = extends laterally. These days such es slowly in about a year, sometimes even up to 3 years.
tumours can be removed endoscopically. Wide access to Radiotherapy is also used for intracranial extension of
pterygomaxillary fossa can also be obtained by removing disease when tumour derives its blood supply from the
the anterior wall of maxillary sinus along with parts of internal carotid system.
pyriform aperture of nose through osteotomies and later Recurrent angiofibromas have also been treated by ra-
reconstruction at the end of operation with plates. This diotherapy. Intensity modulated radiotherapy—a newer
avoids depression and deformity of the face (Table 49.2). mode of treatment—may be employed.
Transmaxillary Le Fort I approach has also been used Treatment with radiotherapy is controversial. Some
to give a wider access to remove tumours which extend believe that all large tumours with intracranial extension
into maxillary and ethmoid sinuses and pterygopalatine should be treated with radiation while others reserve it
fossa. For tumours of infratemporal fossa maxillary swing for recurrent inoperable tumours. Radiation to nasophar-
approach also called facial translocation has been used. ynx in the young has the risk of development of malig-
Here an osteoplastic flap with entire cheek and maxilla is nancy at a later age.
raised as a single unit, which is later reconstructed. Most HORMONAL THERAPY. Since the tumour occurs in young
of the intracranial extensions are extradural and can be males at puberty, probably activated by testosterone, hor-
removed easily with the extracranial approaches but tu- monal therapy as the primary or adjunctive treatment
mours extending intradurally or to the cavernous sinus has been used. Diethylstilbestrol and flutamide (an an-
require help of the neurosurgeon. drogen blocker) have been used in the past to arrest the

TABLE 49.2 EXTENT OF JUVENILE NASOPHARYNGEAL ANGIOFIBROMA AND SURGICAL APPROACH

Location Approach
A. Nose and nasopharynx Transpalatal or endoscopic
B. Nose, nasopharynx maxillary antrum and pterygopalatine fossa Lateral rhinotomy with medial maxillectomy
OR
Endoscopic
OR
Le Fort I
C. As in B + Infratemporal fossa Extended lateral rhinotomy
OR
Infratemporal fossa approach
OR
Maxillary swing approach
D. As in C + Cheek extension Extended lateral rhinotomy
E. As in B + C + Intracranial Combined intracranial and extracranial approach (craniotomy + one
of the extracranial approaches)
OR
Radiation if intracranial part is inaccessible
F. Residual or recurrent disease (extracranial) Observation OR repeat surgery or radiation if inaccessible
G. Intracranial residual or recurrent Stereotactic radiation (X or gamma knife)

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 Chapter 49 — Tumours of Nasopharynx 283

growth but no significant regression has been observed born in America have lesser incidence than those born
in practice. in China. Burning of incense or wood (polycyclic hydro-
CHEMOTHERAPY. Very aggressive recurrent tumours carbon), use of preserved salted fish (nitrosamines) along
and residual lesions have been treated by chemotherapy. with vitamin C deficient diet (vitamin C blocks nitrosi-
Doxorubicin, vincristine and dacarbazine have been used fication of amines and is thus protective) may be other
in combination. factors operative in China.
Chemotherapy and radiotherapy can arrest the growth Nasopharyngeal cancer is uncommon in India and
and cause some tumour regression but not total tumour constitutes only 0.41% (0.66% in males and 0.17% in
eradication. females) of all cancers except in the North East region
where people are predominantly of Mongoloid origin.
People in Southern China, Taiwan and Indonesia are
OTHER BENIGN TUMOURS more prone to this cancer.
OF NASOPHARYNX Aetiology
They are very rare and arise from the roof or lateral wall The exact aetiology is not known. The factors responsible
of nasopharynx. They include: are:
1. Congenital tumours. They are seen at birth and are 1. Genetic. Chinese have a higher genetic susceptibility
six times more common in females than males. Vari- to nasopharyngeal cancer. Even after migration to oth-
ous types include: er countries they continue to have higher incidence.
(a) Hairy polyp. A dermoid with skin appendages. 2. Viral. Epstein–Barr (EB) virus is closely associated
(b) True teratoma. Having elements derived from all with nasopharyngeal cancer. Specific viral markers are
the three germ layers. being developed to screen people in high-incidence
(c) Epignathi. Having well-developed fetal parts. areas. EB virus has two important antigens: viral cap-
2. Pleomorphic adenoma. sid antigen (VCA) and early antigen (EA). IgA anti-
3. Chordoma. Derived from the notochord. bodies of EA are highly specific for nasopharyngeal
4. Hamartoma. Malformed normal tissue, e.g. haeman- cancer but have sensitivity of only 70–80% while IgA
gioma. antibodies of VCA are more sensitive but less specific.
5. Choristoma. Mass of normal tissues at an abnormal AgA antibodies against both EA and VCA should be
site. done for screening of patients for nasopharyngeal
6. Paraganglioma. cancer.
3. Environmental. Air pollution, smoking of tobacco
and opium, nitrosamines from dry salted fish, smoke
MALIGNANT TUMOURS from burning of incense and wood have all been
incriminated.
NASOPHARYNGEAL CANCER
Pathology
Epidemiology and Geographic Distribution Squamous cell carcinoma in various grades of its differ-
Nasopharyngeal cancer is a multifactorial disease. Its in- entiation or its variants such as transitional cell carcino-
cidence and geographic distribution depends on several ma and lymphoepithelioma is the most common (85%).
factors such as genetic susceptibility, environment, diet Lymphomas constitute 10% and the rest 5% are rhabdo-
and personal habits. myosarcoma, malignant mixed salivary tumour or malig-
Nasopharyngeal cancer is most common in China par- nant chordoma.
ticularly in southern states and Taiwan. On the basis of histology, as seen on light microscopy,
Its incidence in North American whites is 0.25% of all WHO has lately reclassified epithelial growths into three
cancers, while it is 18% in American Chinese. Chinese types (see Table 49.3).

TABLE 49.3 WHO CLASSIFICATION BASED ON HISTOPATHOLOGY

Present WHO terminology Former terminology
Type I (25%) Keratinizing carcinoma Squamous cell carcinoma
Type II (12%) Nonkeratinizing differentiated • Transitional cell carcinoma
carcinoma • Intermediate cell carcinoma
• Lymphoepithelial carcinoma (Regaud type is tumour with malignant
tissues in nests)
Type III (63%) Nonkeratinizingundifferentiated • Anaplastic carcinoma
carcinoma • Clear cell carcinoma
• Lymphoepithelial carcinoma (Schminke type is tumour with diffusely
distributed malignant tissue)
• Spindle cell carcinoma

Note: All the types are squamous cell carcinoma when seen under electron microscope. Special stains for epithelial and lymphoid markers are required to
differentiate them from lymphomas.

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 Chapter 51
Acute and Chronic Tonsillitis

2nd Pharyngeal pouch

Gloryology
→

APPLIED ANATOMY OF PALATINE BLOOD SUPPLY

(FAUCIAL) TONSILS The tonsil is supplied by five arteries (Figure 51.3).
Palatine tonsils are two in number. Each tonsil is an ovoid 1. Tonsillar branch of facial artery. This is the main artery.
mass of lymphoid tissue situated in the lateral wall of oro- 2. Ascending pharyngeal artery from external carotid.
pharynx between the anterior and posterior pillars. Ac- 3. Ascending palatine, a branch of facial artery.
tual size of the tonsil is bigger than the one that appears 4. Dorsal linguae branches of lingual artery.
from its surface as parts of tonsil extend upwards into 5. Descending palatine branch of maxillary artery.
the soft palate, downwards into the base of tongue and
anteriorly into palatoglossal arch. A tonsil presents two
surfaces—a medial and a lateral, and two poles—an upper VENOUS DRAINAGE
and a lower. Veins from the tonsils drain into paratonsillar vein which
Medial surface of the tonsil is covered by nonkerati- joins the common facial vein and pharyngeal venous
nizing stratified squamous epithelium which dips into plexus.
the substance of tonsil in the form of crypts. Openings
of 12–15 crypts can be seen on the medial surface of
LYMPHATIC DRAINAGE
the tonsil. One of the crypts, situated near the upper
part of tonsil is very large and deep and is called crypta Lymphatics from the tonsil pierce the superior constrictor
magna or intratonsillar cleft (Figure 51.1). It represents and drain into upper deep cervical nodes particularly the
the ventral part of second pharyngeal pouch. From jugulodigastric (tonsillar) node situated below the angle
the main crypts arise the secondary crypts, within the of mandible.
substance of tonsil. Crypts may be filled with cheesy
material consisting of epithelial cells, bacteria and food
NERVE SUPPLY
debris which can be expressed by pressure over the an-
terior pillar. Lesser palatine branches of sphenopalatine ganglion (CN V)
Lateral surface of the tonsil presents a well-defined fi- and glossopharyngeal nerve provide sensory nerve supply.
brous capsule. Between the capsule and the bed of tonsil
is the loose areolar tissue which makes it easy to dissect
FUNCTIONS OF TONSILS
the tonsil in the plane during tonsillectomy. It is also the
site for collection of pus in peritonsillar abscess. Some fi- They act as sentinels to guard against foreign intruders
bres of palatoglossus and palatopharyngeus muscles are like viruses, bacteria and other antigens coming into
attached to the capsule of the tonsil. contact through inhalation and ingestion. There are two
Upper pole of the tonsil extends into soft palate. Its mechanisms:

[Link]
medial surface is covered by a semilunar fold, extending
1. Providing local immunity.
between anterior and posterior pillars and enclosing a po-
2. Providing a surveillance mechanism so that entire
tential space called supratonsillar fossa.
body is prepared for defence.
Lower pole of the tonsil is attached to the tongue. A tri-
angular fold of mucous membrane extends from anterior Both these mechanisms are operated through humoral
pillar to the anteroinferior part of tonsil and encloses a and cellular immunity.
space called anterior tonsillar space. The tonsil is separated
from the tongue by a sulcus called tonsillolingual sulcus 1. LOCAL IMMUNITY. Tonsils and adenoids are lined by
which may be the seat of carcinoma. squamous epithelium, surface area of which is further in-
Bed of the tonsil. It is formed by the superior constric- creased by several crypts of tonsils and folds of adenoid.
tor and styloglossus muscles. The glossopharyngeal nerve This epithelium is specialized and contains M-cells, an-
and styloid process, if enlarged, may lie in relation to the tigen processing cells and micropores. Through them 2
lower part of tonsillar fossa. Both these structures can be antigenic material is brought into contact with subepi-
surgically approached through the tonsil bed after tonsil- thelially situated lymphoid follicles. Follicles have a ger-
lectomy. Outside the superior constrictor, tonsil is related minal centre rich in B-cells and a mantel zone rich in
to the facial artery, submandibular salivary gland, posteri- large lymphocytes. B-cells when stimulated change to
or belly of digastric muscle, medial pterygoid muscle and plasma cells and produce antibodies. Bacteria and viruses
the angle of mandible (Figure 51.2). are also phagocytosed by the macrophages and destroyed.

291

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292 SECTION IV — Diseases of Pharynx

Low-dose antigens and chronic infections are dealt with play with antigen processing cells, memory cells, den-
in this manner. dritic cells, macrophages, T-helper and T-suppressor
cells. Antibodies produced by the plasma cells prepare
2. SURVEILLANCE MECHANISM. It identifies the in- the antigen to be phagocytosed by neutrophils and
truder and alerts the body for wider response. If the other phagocytes. The antibodies also get attached to
dose of antigen is high, B-cells of the germinal centre macrophages and give them enhanced ability to catch
proliferate and undergo hyperplasia and also enter the the antigens.
blood stream. Complex immune system comes into Tonsils are most active from 4 to 10 years of age. In-
volution begins after puberty resulting in decrease of B-
cell production and relative increase in ratio of T to B
cells.
There has been a common notion that removal of
tonsils and adenoids will impair the integrity of immune
system and make the patient susceptible to poliovirus or
increase the incidence of Hodgkin disease in them. This
has not been substantiated by clinical and epidemiologi-
cal observations. Removal of tonsil and adenoid has also
not affected general immune surveillance function. Ton-
sil and adenoid, however, should only be removed on
specific indications.

Figure 51.1. Primary and secondary crypts of tonsils. ACUTE TONSILLITIS

Primarily, the tonsil consists of (i) surface epithelium
which is continuous with the oropharyngeal lining,
(ii) crypts which are tube-like invaginations from the sur-
face epithelium and (iii) the lymphoid tissue. Acute in-
fections of tonsil may involve these components and are
thus classified as:
1. Acute catarrhal or superficial tonsillitis. Here tonsil-
litis is a part of generalized pharyngitis and is mostly
- svpf
seen in viral infections.
2. Acute follicular tonsillitis. Infection spreads into the
crypts which become filled with purulent material, - crypts
presenting at the openings of crypts as yellowish spots
(Figure 51.4). whole
3. Acute parenchymatous tonsillitis. Here tonsil a
Figure 51.2. Relations of tonsil. Tonsil is related laterally to its capsule substance is affected. Tonsil is uniformly enlarged and
subprime
(1), loose areolar tissue containing paratonsillar vein (2), superior con- red.
strictor muscle (3), styloglossus (4), glossopharyngeal nerve (5), facial
artery (6), medial pterygoid muscle (7), angle of mandible (8) and
4. Acute membranous tonsillitis. It is a stage ahead of
acute follicular tonsillitis when exudation from the •
Membrane
submandibular salivary gland (9), pharyngobasilar fascia (10), buc-
copharyngeal fascia (11).
crypts coalesces to form a membrane on the surface of
tonsil.
font

Figure 51.3. Arterial supply of tonsil. Figure 51.4. Acute follicular tonsillitis.

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 Chapter 51 — Acute and Chronic Tonsillitis 293

AETIOLOGY 4. The jugulodigastric lymph nodes are enlarged and ten-

der.
Acute tonsillitis often affects school-going children, but
also affects adults. It is rare in infants and in persons who
are above 50 years of age. TREATMENT
Haemolytic streptococcus is the most commonly infect- 1. Patient is put to bed and encouraged to take plenty of
ing organism. Other causes of infection may be staphylo- fluids.
cocci, pneumococci or H. influenzae. These bacteria may 2. Analgesics (aspirin or paracetamol) are given according
primarily infect the tonsil or may be secondary to a viral to the age of the patient to relieve local pain and bring
infection. down the fever.
3. Antimicrobial therapy. Most of the infections are due to
SYMPTOMS Streptococcus and penicillin is the drug of choice. Pa-
tients allergic to penicillin can be treated with erythro-
The symptoms vary with severity of infection. The pre- mycin. Antibiotics should be continued for 7–10 days.
dominant symptoms are:
1. Sore throat. COMPLICATIONS
2. Difficulty in swallowing. The child may refuse to eat
anything due to local pain. 1. Chronic tonsillitis with recurrent acute attacks. This
3. Fever. It may vary from 38 to 40 °C and may be associ- is due to incomplete resolution of acute infection.
ated with chills and rigors. Sometimes, a child presents Chronic infection may persist in lymphoid follicles of
with an unexplained fever and it is only on examina- the tonsil in the form of microabscesses.
tion that an acute tonsillitis is discovered. 2. Peritonsillar abscess.
4. Earache. It is either referred pain from the tonsil or 3. Parapharyngeal abscess.
the result of acute otitis media which may occur as a 4. Cervical abscess due to suppuration of jugulodigastric
complication. lymph nodes.
5. Constitutional symptoms. They are usually more 5. Acute otitis media. Recurrent attacks of acute otitis me-
marked than seen in simple pharyngitis and may in- dia may coincide with recurrent tonsillitis.

f-Systems
clude headache, general body aches, malaise and con- 6. Rheumatic fever. Often seen in association with tonsil-
stipation. There may be abdominal pain due to mes- litis due to Group A beta-haemolytic Streptococci.
enteric lymphadenitis simulating a clinical picture of 7. Acute glomerulonephritis. Rare these days.
acute appendicitis. 8. Subacute bacterial endocarditis. Acute tonsillitis in a pa-
tient with valvular heart disease may be complicated
by endocarditis. It is usually due to Streptococcus viri-
SIGNS dans infection.
1. Often the breath is foetid and tongue is coasted.
2. There is hyperaemia of pillars, soft palate and uvula. DIFFERENTIAL DIAGNOSIS OF MEMBRANE
3. Tonsils are red and swollen with yellowish spots of OVER THE TONSIL
purulent material presenting at the opening of crypts
(acute follicular tonsillitis) or there may be a whitish 1. Membranous tonsillitis. It occurs due to pyogenic or-
membrane on the medial surface of tonsil which can ganisms. An exudative membrane forms over the medial
be easily wiped away with a swab (acute membranous surface of the tonsils, along with the features of acute
tonsillitis, Figure 51.5). The tonsils may be enlarged tonsillitis.
and congested so much so that they almost meet in 2. Diphtheria. Unlike acute tonsillitis which is abrupt
the midline along with some oedema of the uvula and in onset, diphtheria is slower in onset with less local dis-
soft palate (acute parenchymatous tonsillitis). comfort, the membrane in diphtheria extends beyond the

Eg ⑧
tonsils tonsils, on to the soft palate and is dirty grey in colour.
kiss
It is adherent and its removal leaves a bleeding surface.
Urine may show albumin. Smear and culture of throat
swab will reveal Corynebacterium diphtheriae.
3. Vincent angina. It is insidious in onset with less fe-
ver and less discomfort in throat. Membrane, which usu-
ally forms over one tonsil, can be easily removed reveal-
ing an irregular ulcer on the tonsil. Throat swab will show
both the organisms typical of disease, namely fusiform
bacilli and spirochaetes. Ante
Necrotizing Ulcerative
4. Infectious mononucleosis. This often affects young
Gingivitis
adults. Both tonsils are very much enlarged, congested
and covered with membrane. Local discomfort is marked.
Lymph nodes are enlarged in the posterior triangle of
neck along with splenomegaly. Attention to disease is
Figure 51.5. Acute follicular tonsillitis. Note pus beads on the surface attracted because of failure of the antibiotic treatment.
of left tonsil. On the right pus beads have coalesced together to form Blood smear may show more than 50% lymphocytes,
a membrane. of which about 10% are atypical. White cell count may

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294 SECTION IV — Diseases of Pharynx

be normal in the first week but rises in the second week. ularly the jugulodigastric, become enlarged and tender,
Paul–Bunnell test (mono test) will show high titre of het- sometimes presenting a “bull-neck” appearance. Patient
erophil antibody. is ill and toxaemic but fever seldom rises above 38 °C.
5. Agranulocytosis. It presents with ulcerative necrot-
ic lesions not only on the tonsils but elsewhere in the
COMPLICATIONS
oropharynx. Patient is severely ill. In acute fulminant
form, total leucocytic count is decreased to <2000/cu Exotoxin produced by C. diphtheriae is toxic to the heart
mm or even as low as 50/cu mm and polymorph neutro- and nerves. It causes myocarditis, cardiac arrhythmias and
phils may be reduced to 5% or less. In chronic or recur- acute circulatory failure.
rent form, total count is reduced to 2000/cu mm with less Neurological complications usually appear a few weeks
marked granulocytopenia. after infection and include paralysis of soft palate, dia-
6. Leukaemia. In children, 75% of leukaemias are phragm and ocular muscles.
acute lymphoblastic and 25% acute myelogenous or In the larynx, diphtheritic membrane may cause air-
chronic, while in adults 20% of acute leukaemias are lym- way obstruction.
phocytic and 80% nonlymphocytic.
Peripheral blood shows TLC >100,000/cu mm. It may
TREATMENT
be normal or less than normal. Anaemia is always present
and may be progressive. Blasts cells are seen on examina- Treatment of diphtheria is started on clinical suspicion
tion of the bone marrow. without waiting for the culture report. Aim is to neutral-
7. Aphthous ulcers. They may involve any part of oral ize the free exotoxin still circulating in the blood and to
cavity or oropharynx. Sometimes, it is solitary and may kill the organisms producing this exotoxin. Dose of anti-
involve the tonsil and pillars. It may be small or quite toxin is based on the site involved and the duration and
large and alarming. It is very painful. severity of disease. It is 20,000–40,000 units for diphthe-
8. Malignancy tonsil (see p. 305) ria in less than 48 h, or when the membrane is confined
9. Traumatic ulcer. Any injury to oropharynx heals to the tonsils only; and 80,000–120,000 units, if disease
by formation of a membrane. Trauma to the tonsil area has lasted longer than 48 h, or the membrane is more
may occur accidently when hit with a toothbrush, a pen- extensive. Antitoxin is given by i.v. infusion in saline in
cil held in mouth or fingering in the throat. Membrane about 60 min. Sensitivity to horse serum should be tested
appears within 24 h. by conjunctival or intracutaneous test with diluted anti-
10. Candidal infection of tonsil toxin and adrenaline should be at hand for any immedi-
Diagnosis of ulceromembranous lesion of throat thus ate hypersensitivity. In the presence of hypersensitivity
requires: reaction, desensitization should be done.
Antibiotics used are benzyl penicillin 600 mg 6 hourly
1. History.
for 7 days. Erythromycin is used in penicillin-sensitive in-
2. Physical examination.
dividuals (500 mg 6 hourly orally).
3. Total and differential counts (for agranulocytosis, leu-
kaemia, neutropenia, infectious mononucleosis).
4. Blood smear (for atypical cells).
5. Throat swab and culture (for pyogenic bacteria, CHRONIC TONSILLITIS
Vincent angina, diphtheria and Candida infection).
6. Bone marrow aspiration or needle biopsy. AETIOLOGY
7. Other tests. Paul–Bunnell or mono spot test and biopsy 1. It may be a complication of acute tonsillitis. Pathologi-
of the lesion. cally, microabscesses walled off by fibrous tissue have
been seen in the lymphoid follicles of the tonsils.
2. Subclinical infections of tonsils without an acute attack.
FAUCIAL DIPHTHERIA 3. Mostly affects children and young adults. Rarely oc-
curs after 50 years.
AETIOLOGY 4. Chronic infection in sinuses or teeth may be a predis-
posing factor.
It is an acute specific infection caused by the Gram-pos-
itive bacillus, C. diphtheriae. It spreads by droplet infec-
tion. Incubation period is 2–6 days. Some persons are TYPES
“carriers” of this disease, i.e. they harbour organisms in
1. CHRONIC FOLLICULAR TONSILLITIS. Here tonsillar
their throat but have no symptoms.
crypts are full of infected cheesy material which shows
on the surface as yellowish spots.
CLINICAL FEATURES
2. CHRONIC PARENCHYMATOUS TONSILLITIS. There is
Children are affected more often though no age group hyperplasia of lymphoid tissue. Tonsils are very much en-
is immune. Oropharynx is commonly involved and the larged and may interfere with speech, deglutition and res-
larynx and nasal cavity may also be affected. piration (Figure 51.6). Attacks of sleep apnoea may occur.
In the oropharynx, a greyish white membrane forms Long-standing cases develop features of cor pulmonale.
over the tonsils and spreads to the soft palate and pos-
terior pharyngeal wall. It is quite tenacious and causes 3. CHRONIC FIBROID TONSILLITIS. Tonsils are small but
bleeding when removed. Cervical lymph nodes, partic- infected, with history of repeated sore throats.

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 Chapter 51 — Acute and Chronic Tonsillitis 295

Figure 51.6. Parenchymatous tonsillitis. The two tonsils are almost Figure 51.7. A tonsillar cyst left side in a 55-year-old male (arrow).
touching each other causing problems of deglutition, speech and
respiration.
Tonsilloliths (calculus of the tonsil). It is seen in chronic
tonsillitis when its crypt is blocked with retention of de-
CLINICAL FEATURES bris. Inorganic salts of calcium and magnesium are then
deposited leading to formation of a stone. It may gradu-
1. Recurrent attacks of sore throat or acute tonsillitis. ally enlarge and then ulcerate through the tonsil.
2. Chronic irritation in throat with cough. Tonsilloliths are seen more often in adults and give rise
3. Bad taste in mouth and foul breath (halitosis) due to to local discomfort or foreign body sensation. They are
pus in crypts. easily diagnosed by palpation or gritty feeling on prob-
4. Thick speech, difficulty in swallowing and choking ing. Treatment is simple removal of the stone or tonsillec-
spells at night (when tonsils are large and obstructive). tomy, if that be indicated for associated sepsis or for the
deeply set stone which cannot be removed.
EXAMINATION Intratonsillar abscess. It is accumulation of pus within
the substance of tonsil. It usually follows blocking of
1. Tonsils may show varying degree of enlargement. the crypt opening in acute follicular tonsillitis. There is
Sometimes they meet in the midline (chronic paren- marked local pain and dysphagia. Tonsil appears swollen
chymatous type). and red. Treatment is administration of antibiotics and
2. There may be yellowish beads of pus on the medial drainage of the abscess if required; later tonsillectomy
surface of tonsil (chronic follicular type). should be performed.
3. Tonsils are small but pressure on the anterior pillar ex- Tonsillar cyst. It is due to blockage of a tonsillar crypt
presses frank pus or cheesy material (chronic fibroid type). and appears as a yellowish swelling over the tonsil.
4. Flushing of anterior pillars compared to the rest of the Very often it is symptomless. It can be easily drained
pharyngeal mucosa is an important sign of chronic (Figure 51.7).
tonsillar infection.
5. Enlargement of jugulodigastric lymph nodes is a reli-
able sign of chronic tonsillitis. During acute attacks, DISEASES OF LINGUAL TONSILS
the nodes enlarge further and become tender.
1. Acute lingual tonsillitis. Acute infection of a lingual
TREATMENT tonsil gives rise to unilateral dysphagia and feeling of
lump in the throat. On examination with a laryngeal
1. Conservative treatment consists of attention to gen- mirror, lingual tonsil may appear enlarged and con-
eral health, diet, treatment of coexistent infection of gested, sometimes studded with follicles like the ones
teeth, nose and sinuses. seen in acute follicular tonsillitis. Cervical lymph
2. Tonsillectomy is indicated when tonsils interfere with nodes may be enlarged. Treatment is by antibiotics.
speech, deglutition and respiration or cause recurrent 2. Hypertrophy of lingual tonsils. Mostly, it is a com-
attacks (see Chapter 94). pensatory hypertrophy of lymphoid tissue in response
to repeated infections in tonsillectomized patients.
COMPLICATIONS Usual complaints are discomfort on swallowing, feel-
ing of lump in the throat, dry cough and thick voice.
1. Peritonsillar abscess (see p. 299, Figure 52.4). 3. Abscess of lingual tonsil. It is a rare condition but
2. Parapharyngeal abscess. can follow acute lingual tonsillitis. Symptoms are se-
3. Intratonsillar abscess. vere unilateral dysphagia, pain in the tongue, exces-
4. Tonsilloliths. sive salivation and some degree of trismus. Protrusion
5. Tonsillar cyst. of the tongue is painful. Jugulodigastric nodes will be
6. Focus of infection in rheumatic fever, acute glomerulo- enlarged and tender. It is a potentially dangerous con-
nephritis, eye and skin disorders. dition as laryngeal oedema can easily follow.

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