Dhingra Nose

Download as pdf or txt
Download as pdf or txt
You are on page 1of 82

DISEASES OF NOSE AND SECTION II

PARANASAL SINUSES

SECTION OUTLINE
23. Anatomy of Nose 32. Nasal Polypi
24. Physiology of Nose 33. Epistaxis
25. Diseases of External Nose and 34. Trauma to the Face
Nasal Vestibule 35. Anatomy and Physiology of
26. Nasal Septum and Its Diseases Paranasal Sinuses
27. Acute and Chronic Rhinitis 36. Acute Sinusitis
28. Granulomatous Diseases of Nose 37. Chronic Sinusitis
29. Miscellaneous Disorders of Nasal 38. Complications of Sinusitis
Cavity 39. Benign and Malignant Neoplasms
30. Allergic Rhinitis of Nasal Cavity
31. Vasomotor and Other Forms of 40. Neoplasms of Paranasal Sinuses
Nonallergic Rhinitis 41. Proptosis

133
23 Anatomy of Nose

3. Lesser alar (or sesamoid) cartilages. Two or more in


EXTERNAL NOSE number. They lie above and lateral to alar cartilages. The
various cartilages are connected with one another and
It is pyramidal in shape with its root up and the base directed
with the adjoining bones by perichondrium and peri-
downwards. Various terms used in its description are shown
osteum. Most of the free margin of nostril is formed of
in Figure 23.1. Nasal pyramid consists of osteocartilaginous
fibrofatty tissue and not the alar cartilage.
framework covered by muscles and skin.
4. Septal cartilage. Its anterosuperior border runs from
under the nasal bones to the nasal tip. It supports the
OSTEOCARTILAGINOUS FRAMEWORK dorsum of the cartilaginous part of the nose. In septal
BONY PART abscess or after excessive removal of septal cartilage as in
submucosal resection (SMR) operation, support of nasal
Upper one-third of the external nose is bony while lower two-
dorsum is lost and a supratip depression results.
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 and are themselves held NASAL MUSCULATURE
between the frontal processes of the maxillae (Figure 23.2).
Osteocartilaginous framework of nose is covered by muscles
CARTILAGINOUS PART which bring about movements of the nasal tip, ala and the
overlying skin. They are the procerus, nasalis (transverse
It consists of:
and alar parts), levator labii superioris alaeque nasi, anterior
1. Upper lateral cartilages. They extend from the undersur- and posterior dilator nares and depressor septi.
face of the nasal bones above, to the alar cartilages below.
They fuse with each other and with the upper border of
NASAL SKIN
the septal cartilage in the midline anteriorly. The lower
free edge of upper lateral cartilage is seen intranasally as The skin over the nasal bones and upper lateral cartilages
limen vestibuli or nasal valve on each side. is thin and freely mobile while that covering the alar carti-
2. Lower lateral cartilages (alar cartilages). Each alar cartilage lages is thick and adherent, and contains many sebaceous
is U-shaped. It has a lateral crus which forms the ala and a glands. It is the hypertrophy of these sebaceous glands
medial crus which runs in the columella. Lateral crus over- which gives rise to a lobulated tumour called rhinophyma
laps lower edge of upper lateral cartilage on each side. (see p. 144).

Root of nose

Dorsum
Naris
Alar groove

Columella
Naris

Columella Philtrum

Nasolabial fold Nasolabial


angle

Figure 23.1 Various parts of nose and related facial structures.

134
CHAPTER 23 — ANATOMY OF NOSE 135

Nasal bone

Alar cartilage
Frontal process
of maxilla Lateral crus
Medial crus
Lateral cartilage
Septal cartilage
Lesser alar
cartilages

Alar cartilage
Caudal border of
septal cartilage Fibrofatty tissue

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

Sup. turbinate and meatus

Agger nasi

Atrium
Middle turbinate
and meatus

Vestibule Inf. turbinate


and meatus

Figure 23.3 Structures on lateral wall of nose.

septum and lower border of upper lateral cartilage is


INTERNAL NOSE nearly 30°.
2. Nasal valve area. It is the cross-sectional area bounded
It is divided into right and left nasal cavities by nasal septum. by the structures forming the valve. It is the least cross-
Each nasal cavity communicates with the exterior through sectional area of nose and regulates airflow and resistance
naris or nostril and with the nasopharynx through posterior on inspiration.
nasal aperture or the choana. Each nasal cavity consists of a
skin-lined portion—the vestibule and a mucosa-lined por-
tion, the nasal cavity proper. NASAL CAVITY PROPER
Each nasal cavity has a lateral wall, a medial wall, a roof and
a floor.
VESTIBULE OF NOSE
Anterior and inferior part of nasal cavity is called vestibule. It LATERAL NASAL WALL
is lined by skin and contains sebaceous glands, hair follicles Three and occasionally four turbinates or conchae mark
and the hair called vibrissae. Its upper limit on the lateral the lateral wall of nose. Conchae or turbinates are scroll-
wall is marked by limen nasi (also called nasal valve). like bony projections covered by mucous membrane. The
spaces below the turbinates are called meatuses (Figures
1. Nasal valve. It is bounded laterally by the lower bor-
23.3 and 23.4).
der of upper lateral cartilage and fibrofatty tissue and
anterior end of inferior turbinate, medially by the Inferior turbinate. It is a separate bone and below it, into
cartilaginous nasal septum, and caudally by the floor the inferior meatus, opens the nasolacrimal duct guarded
of pyriform aperture. The angle between the nasal at its terminal end by a mucosal valve called Hasner’s valve.
136 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Hiatus semilunaris
Sphenoethmoid recess with
Uncinate process opening of sphenoid sinus
Bulla
ethmoidalis
Opening of frontal sinus

Opening of post. ethmoid

Opening of max. sinus

Opening of middle
ethmoidal sinuses

Opening of
nasolacrimal duct

Accessory opening
of max. sinus
Figure 23.4 Lateral wall of nose with turbinates removed showing openings of various sinuses.

Frontal sinus

Reflected middle
turbinate

Bulla ethmoidalis

Accessory ostium
of maxillary sinus

Uncinate process

Inferior turbinate

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

Middle turbinate. It is an ethmoturbinal—a part of eth- Middle meatus. It shows several important structures which
moid bone. It is attached to the lateral wall by a bony are important in endoscopic surgery of the sinuses (Figure
lamella called ground or basal lamella. Its attachment is not 23.5).
straight but in an S-shaped manner. In the anterior third, it Uncinate process is a hook-like structure running in from
lies in sagittal plane and is attached to lateral edge of crib- anterosuperior to posteroinferior direction. Its posterosu-
riform plate. In the middle third, it lies in frontal plane perior border is sharp and runs parallel to anterior border
and is attached to lamina papyracea while in its posterior of bulla ethmoidalis; the gap between the two is called hia-
third, it runs horizontally and forms roof of the middle tus semilunaris (inferior). It is a two-dimensional space of
meatus and is attached to lamina papyracea and medial 1–2 mm width.
wall of maxillary sinus. The anteroinferior border of uncinate process is
The ostia of various sinuses draining anterior to basal attached to the lateral wall. Posteroinferior end of unci-
lamella form anterior group of paranasal sinuses while those nate process is attached to inferior turbinate divid-
which open posterior and superior to it form the posterior group. ing the membranous part of lower middle meatus into
CHAPTER 23 — ANATOMY OF NOSE 137

Frontal
sinus
Middle
turbinate Lamina Uncinate
papyracea process

A B C
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.

Cribriform plate

Bulla ethmoidalis
Middle
turbinate Hiatus Lamina papyracea
semilunaris
Middle turbinate
Bulla Septum Uncinate process
ethmoidalis

Infundibulum Inferior
turbinate Max. sinus
Uncinate
process

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

anterior and posterior fontanelle. The fontanel area is


devoid of bone and consists of membrane only and leads
into maxillary sinus when perforated. Upper attach-
ment of uncinate process shows great variation and
may be inserted into the lateral nasal wall, upwards into
Nasolacrimal duct
the base of skull or medially into the middle turbinate
(Figure 23.6). This also accounts for variations in drainage
of frontal sinus.
The space limited medially by the uncinate process and
frontal process of maxilla and sometimes lacrimal bone, and Hiatus
laterally by the lamina papyracea is called infundibulum. semilunaris Uncinate
Natural ostium of the maxillary sinus is situated in the process
lower part of infundibulum. Accessory ostium or ostia of Middle
Infundibulum
turbinate
maxillary sinus are sometimes seen in the anterior or poste-
rior fontanel (Figure 23.7). Bulla
ethmoidalis
Bulla ethmoidalis. It is an ethmoidal cell situated behind
the uncinate process. Anterior surface of the bulla forms
the posterior boundary of hiatus semilunaris. Depend- Retrobullar
recess
ing on pneumatization, bulla may be a pneumatized cell (or sinus lateralis)
or a solid bony prominence. It may extend superiorly to
the skull base and posteriorly to fuse with ground lamella.
When there is a space above or behind the bulla, it is called
Figure 23.8 Axial view showing middle meatus and its structure.
suprabullar or retrobullar recesses, respectively (Figure 23.8).
Note also the retrobullar recess.
The suprabullar and retrobullar recesses together form
the lateral sinus (sinus lateralis of Grunwald). The lateral
sinus is thus bounded superiorly by the skull base, laterally
138 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

by lamina papyracea, medially by middle turbinate and


inferiorly by the bulla ethmoidalis. Posteriorly the sinus LINING MEMBRANE OF INTERNAL NOSE
lateralis may extend up to basal lamella of middle turbi-
nate. The cleft-like communication between the bulla and 1. Vestibule. It is lined by skin containing hair, hair follicles
skull base and opening into middle meatus is also called and sebaceous glands.
hiatus semilunaris superior in contrast to hiatus semilunaris 2. Olfactory region. Upper one-third of lateral wall (up to
inferior referred to before. superior concha), corresponding part of the nasal septum
Atrium of the middle meatus. It is a shallow depression lying and the roof of nasal cavity form the olfactory region. Here,
in front of middle turbinate and above the nasal vestibule. mucous membrane is paler in colour.

Agger nasi. It is an elevation just anterior to the attachment 3. Respiratory region. Lower two-thirds of the nasal cavity
of middle turbinate. When pneumatized it contains air cells, form the respiratory region. Here mucous membrane shows
the agger nasi cells, which communicate with the frontal variable thickness being thickest over nasal conchae espe-
recess. An enlarged agger nasi cell may encroach on frontal cially at their ends, quite thick over the nasal septum but
recess area, constricting it and causing mechanical obstruc- very thin in the meatuses and floor of the nose. It is highly
tion to frontal sinus drainage. vascular and also contains erectile tissue. Its surface is lined
Pneumatization of middle turbinate leads to an enlarged by pseudostratified ciliated columnar epithelium which
ballooned out middle turbinate called concha bullosa. It contains plenty of goblet cells. In the submucous layer of
drains into frontal recess directly or through agger nasi mucous membrane are situated serous, mucous, both serous
cells. Haller cells are air cells situated in the roof of maxil- and mucous secreting glands, the ducts of which open on
lary sinus. They are pneumatized from anterior or poste- the surface of mucosa.
rior ethmoid cells. Enlargement of Haller cells encroaches
on ethmoid infundibulum, impeding draining of maxillary NERVE SUPPLY
sinus.
1. Olfactory nerves. They carry sense of smell and supply
Superior turbinate. It is also an ethmoturbinal and is situ- olfactory region of nose. They are the central filaments of
ated posterior and superior to middle turbinate. It may also the olfactory cells and are arranged into 12–20 nerves which
get pneumatized by one or more cells. It forms an important pass through the cribriform plate and end in the olfactory
landmark to identify ostium of sphenoid sinus which lies bulb. These nerves can carry sheaths of dura, arachnoid and
medial to it. pia with them into the nose. Injury to these nerves can open
Superior meatus. It is a space below the superior turbinate. CSF space leading to CSF rhinorrhoea or meningitis (Figure
Posterior ethmoid cells open into it. Number of posterior 23.9).
ethmoid cells varies from 1 to 5. Onodi cell is a posterior eth- 2. Nerves of common sensation. They are:
moidal cell which may grow posteriorly by the side of sphe-
noid sinus or superior to it for as much distance as 1.5 cm (a) Anterior ethmoidal nerve.
from the anterior surface of sphenoid. Onodi cell is surgically (b) Branches of sphenopalatine ganglion.
important as the optic nerve may be related to its lateral wall. (c) Branches of infraorbital nerve. They supply vestibule of
nose both on its medial and lateral side.
Sphenoethmoidal recess. It is situated above the superior
turbinate. Sphenoid sinus opens into it. Most of the posterior two-thirds of nasal cavity (both sep-
tum and lateral wall) are supplied by branches of sphenopal-
Supreme turbinate. It is sometimes present above the supe- atine ganglion which can be blocked by placing a pledget of
rior turbinate and has a narrow meatus beneath it. cotton soaked in anaesthetic solution near the sphenopala-
The ostium of sphenoid sinus is situated in the spheno- tine foramen situated at the posterior extremity of middle
ethmoidal recess medial to the superior or supreme turbi- turbinate. Anterior ethmoidal nerve which supplies anterior
nate. It can be located endoscopically about 1 cm above the and superior part of the nasal cavity (lateral wall and sep-
upper margin of posterior choana close to the posterior bor- tum) can be blocked by placing the pledget high up on the
der of the septum. inside of nasal bones where the nerve enters.
MEDIAL WALL 3. Autonomic nerves. Parasympathetic nerve fibres supply
Nasal septum forms the medial wall and is described on p. 147. the nasal glands and control nasal secretion. They come
from greater superficial petrosal nerve, travel in the nerve
ROOF of pterygoid canal (vidian nerve) and reach the sphenopal-
Anterior sloping part of the roof is formed by nasal bones, atine ganglion where they relay before reaching the nasal
posterior sloping part is formed by the body of sphenoid cavity. They also supply the blood vessels of nose and cause
bone and the middle horizontal part is formed by the crib- vasodilation.
riform plate of ethmoid through which the olfactory nerves Sympathetic nerve fibres come from upper two thoracic
enter the nasal cavity. segments of spinal cord, pass through superior cervical gan-
glion, travel in deep petrosal nerve and join the parasympa-
FLOOR thetic fibres of greater petrosal nerve to form the nerve of
It is formed by palatine process of the maxilla in its anterior pterygoid canal (vidian nerve). They reach the nasal cavity
three-fourths and horizontal part of the palatine bone in its without relay in the sphenopalatine ganglion. Their stimula-
posterior one-fourth. tion causes vasoconstriction. Excessive rhinorrhoea in cases
CHAPTER 23 — ANATOMY OF NOSE 139

Olfactory bulb

Olfactory nerves

Ant. ethmoidal
nerve

Branches of
Infraorbital sphenopalatine
nerve ganglion

Olfactory nerves

Ant. ethmoidal
nerve

Nasopalatine
nerve

Infraorbital
nerve

Greater palatine
B nerve
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.

LYMPHATIC DRAINAGE
of vasomotor and allergic rhinitis can be controlled by sec-
tion of the vidian nerve. Lymphatics from the external nose and anterior part of
nasal cavity drain into submandibular lymph nodes while
those from the rest of nasal cavity drain into upper jugular
BLOOD SUPPLY
nodes either directly or through the retropharyngeal nodes.
Both the internal and external carotid systems supply the Lymphatics of the upper part of nasal cavity communicate
nose. Details of blood supply are given on p. 176. with subarachnoid space along the olfactory nerves.
24 Physiology of Nose

Functions of the nose are classified as: the surface of the mucous membrane. The front of the
nose can filter particles up to 3 μm, while nasal mucus
1. Respiration. traps particles as fine as 0.5–3.0 μm. Particles smaller
2. Air-conditioning of inspired air. than 0.5 μm seem to pass through the nose into lower
3. Protection of lower airway. airways without difficulty.
4. Vocal resonance. 2. Temperature control of the inspired air. It is regulated
5. Nasal reflex functions. by large surface of nasal mucosa which is structurally
6. Olfaction. adapted to perform this function. This mucous mem-
brane, particularly in the region of middle and inferior
turbinates and adjacent parts of the septum, is highly
RESPIRATION vascular with cavernous venous spaces or sinusoids which
control the blood flow, and this increases or decreases the
Nose is the natural pathway for breathing. Mouth breathing size of turbinates. This also makes an efficient “radiator”
is an acquired act through learning. So natural is the instinct mechanism to warm up the cold air. Inspired air which
to breath through the nose that a newborn infant with cho- may be at 20°C or 0°C or even at subzero temperature is
anal atresia may asphyxiate to death if urgent measures are heated to near body temperature (37°C) in one-fourth
not taken to relieve it. The nose also permits breathing and of second, the time that the air takes to pass from the
eating to go on simultaneously. nostril to the nasopharynx. Similarly, hot air is cooled to
During quiet respiration, inspiratory air current passes the level of body temperature.
through middle part of nose between the turbinates and 3. Humidification. This function goes on simultaneously
nasal septum. Very little air passes through inferior meatus with the temperature control of inspired air. Relative
or olfactory region of nose (Figure 24.1). Therefore, weak humidity of atmospheric air varies depending on cli-
odorous substances have to be sniffed before they can reach matic conditions. Air is dry in winter and saturated
the olfactory area. with moisture in summer months. Nasal mucous mem-
brane adjusts the relative humidity of the inspired air
During expiration, air current follows the same course as to 75% or more. Water, to saturate the inspired air, is
during inspiration, but the entire air current is not expelled provided by the nasal mucous membrane which is rich
directly through the nares. Friction offered at limen nasi in mucous and serous secreting glands. About 1000 mL
converts it into eddies under cover of inferior and middle of water is evaporated from the surface of nasal mucosa
turbinates and this ventilates the sinuses through the ostia. in 24 h.
Anterior end of inferior turbinate undergoes swelling and
shrinkage thus regulating inflow of air. Moisture is essential for integrity and function of the cili-
ary epithelium. At 50% relative humidity, ciliary function
Nasal cycle. Nasal mucosa undergoes rhythmic cyclical
stops in 8–10 min. Thus, dry air predisposes to infections
congestion and decongestion, thus controlling the airflow
of the respiratory tract. Humidification also has a signifi-
through nasal chambers. When one nasal chamber is work-
cant effect on gas exchange in the lower airways. In nasal
ing, total nasal respiration, equal to that of both nasal cham-
obstruction, gaseous exchange is affected in the lungs, lead-
bers, is carried out by it. Nasal cycle varies every 2½–4 h and
ing to rise in pCO2, causing apnoeic spells during sleep; it
may be characteristic of an individual.
also decreases pO2.

AIR-CONDITIONING OF INSPIRED AIR PROTECTION OF LOWER AIRWAY


Nose is aptly called the “air-conditioner” for lungs. It filters
1. Mucociliary mechanism. Nasal mucosa is rich in goblet
and purifies the inspired air and adjusts its temperature and
cells, secretory glands both mucous and serous. Their
humidity before the air passes to the lungs.
secretion forms a continuous sheet called mucous blanket
1. Filtration and purification. Nasal vibrissae at the entrance spread over the normal mucosa. Mucous blanket consists
of nose act as filters to sift larger particles like fluffs of of a superficial mucus layer and a deeper serous layer,
cotton. Finer particles like dust, pollen and bacteria floating on the top of cilia which are constantly beating
adhere to the mucus which is spread like a sheet all over to carry it like a “conveyer belt” towards the nasopharynx

140
CHAPTER 24 — PHYSIOLOGY OF NOSE 141

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

flow of nasal secretions that follows irritation by noxious


Mucus substance helps to wash them out.
layer
The pH of nasal secretion is nearly constant at 7. The cilia
and the lysozyme act best at this pH. Alteration in nasal pH,
Serous
layer due to infections or nasal drops, seriously impairs the func-
tions of cilia and lysozyme.
So efficient are the functions of nose that 500 cubic feet
of air, that we breathe every 24 h, is filtered, humidified,
adjusted to proper temperature and cleared of all the dust,
Figure 24.2 “Conveyor belt” mechanism of mucus blanket to entrap bacteria and viruses before reaching the lungs.
and carry organisms and dust particles.

(Figure 24.2). It moves at a speed of 5–10 mm/min and VOCAL RESONANCE


the complete sheet of mucus is cleared into the pharynx
every 10–20 min. The inspired bacteria, viruses and dust Nose forms a resonating chamber for certain consonants in
particles are entrapped on the viscous mucous blanket speech. In phonating nasal consonants (M/N/NG), sound
and then carried to the nasopharynx to be swallowed. passes through the nasopharyngeal isthmus and is emitted
Presence of turbinates almost doubles the surface area to through the nose. When nose (or nasopharynx) is blocked,
perform this function. About 600–700 mL of nasal secre- speech becomes denasal, i.e. M/N/NG are uttered as B/D/G,
tions are produced in 24 h. respectively. It is to be remembered that in Hindi alpha-
bets, last letter of a “varga” (
In mammals, cilia beat 10–20 times per second at room
) is substituted by its third letter.
temperature. They have a rapid “effective stroke” and a
Thus, an affected person utters for and for .
slow “recovery stroke.” In the former, the extended cilia
Reverse is true in velopharyngeal insufficiency where is
reach mucus layer while in the recovery stroke, they
substituted for .
bend and travel slowly in the reverse direction in the thin
serous layer, thus moving the mucous blanket in only one
direction. In immotile cilia syndrome, cilia are defec-
NASAL REFLEXES
tive and cannot beat effectively, leading to stagnation
of mucus in the nose and sinuses and bronchi causing
Several reflexes are initiated in the nasal mucosa. Smell of a
chronic rhinosinusitis and bronchiectasis. Movements of
palatable food cause reflex secretion of saliva and gastric juice.
cilia are affected by drying, drugs (adrenaline), excessive
Irritation of nasal mucosa causes sneezing. Nasal function is
heat or cold, smoking, infections and noxious fumes like
closely related to pulmonary functions through ­nasobronchial
sulfur dioxide and carbon dioxide.
and nasopulmonary reflexes. It has been observed that nasal
2. Enzymes and immunoglobulins. Nasal secretions also obstruction leads to increased p ­ ulmonary resistance and is
contain an enzyme called muramidase (lysozyme) which reversed when nasal ­obstruction is surgically treated. Nasal
kills bacteria and viruses. Immunoglobulins IgA and packing in cases of epistaxis or after nasal surgery leads to
IgE, and interferon are also present in nasal secretions lowering of pO2 which returns to normal after removal of the
and provide immunity against upper respiratory tract pack. Pulmonary hypertension or ­cor pulmonale can develop
infections. in children with long-standing nasal obstruction due to tonsil
3. Sneezing. It is a protective reflex. Foreign particles which and adenoid hypertrophy and can be reversed after removal
irritate nasal mucosa are expelled by sneezing. Copious of the tonsils and adenoids.
142 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

2. Disorders of smell. It is essential for the perception of


OLFACTION smell that the odorous substance be volatile and that it
should reach the olfactory area unimpeded. Also necessary
Sense of smell is well-developed in lower animals to give are the healthy state of olfactory mucosa and the integrity
warning of the environmental dangers but it is compara- of neural pathways, i.e. olfactory nerves, olfactory bulb and
tively less important in man. Still it is important for pleasure tract and the cortical centre of olfaction.
and for enjoying the taste of food. When nose is blocked, Anosmia is total loss of sense of smell while hyposmia is par-
food tastes bland and unpalatable. Vapours of ammonia are tial loss. They can result from nasal obstruction due to nasal
never used to test the sense of smell as they stimulate fibres polypi, enlarged turbinates or oedema of mucous membrane
of the trigeminal nerve and cause irritation in the nose as in common cold, allergic or vasomotor rhinitis. Anosmia
rather than stimulate the olfactory receptors. is also seen in atrophic rhinitis, a degenerative disorder of
nasal mucosa; peripheral neuritis (toxic or influenzal); injury
1. Olfactory pathways. Smell is perceived in the olfactory to olfactory nerves or olfactory bulb in fractures of anterior
region of nose which is situated high up in the nasal cav- cranial fossa; and intracranial lesions like abscess, tumour or
ity. This area contains millions of olfactory receptor cells. meningitis which cause pressure on olfactory tracts.
Peripheral process of each olfactory cell reaches the muco- Parosmia is perversion of smell; the person interprets the
sal surface and is expanded into a ventricle with several odours incorrectly. Often these persons complain of dis-
cilia on it. This acts as a sensory receptor to receive odor- gusting odours. It is seen in the recovery phase of postinflu-
ous substances. Central processes of the olfactory cells enzal anosmia and the probable explanation is misdirected
are grouped into olfactory nerves which pass through the regeneration of nerve fibres. Intracranial tumour should be
cribriform plate of ethmoid and end in the mitral cells of excluded in all cases of parosmia.
the olfactory bulb. Axons of mitral cells form olfactory Sense of smell can be tested by asking the patient to smell
tract and carry smell to the prepyriform cortex and the common odours such as lemon, peppermint, rose, garlic
amygdaloid nucleus where it reaches consciousness. Olfac- or cloves from each side of the nose separately, with eyes
tory system is also associated with autonomic system at the closed. Quantitative estimation (quantitative olfactometry)
hypothalamic level. requires special equipment.
Diseases of External Nose 25
and Nasal Vestibule

Aim of these operations is to correct not only the outer


DISEASES OF EXTERNAL NOSE appearance of nose but also its function.

CELLULITIS
TUMOURS
The nasal skin may be invaded by streptococci or staphylo-
cocci leading to a red, swollen and tender nose. Sometimes, They may be congenital, benign or malignant (Table 25.1).
it is an extension of infection from the nasal vestibule.
Treatment is systemic antibacterials, hot fomentation and 1. CONGENITAL TUMOURS
analgesics. (a) Dermoid cyst (Figure 25.3). It is of two types:
• Simple dermoid. It occurs as a midline swelling under the
NASAL DEFORMITIES skin but in front of the nasal bones. It does not have any
SADDLE NOSE external opening.
Depressed nasal dorsum may involve bony, cartilaginous or
both bony and cartilaginous components of nasal dorsum
(Figure 25.1). Nasal trauma causing depressed fractures is
the most common aetiology. It can also result from exces-
sive removal of septum in submucous resection, destruction
of septal cartilage by haematoma or abscess, sometimes by
leprosy, tuberculosis or syphilis. The deformity can be cor-
rected by augmentation rhinoplasty by filling the dorsum
with cartilage, bone or a synthetic implant. If depression is
only cartilaginous, cartilage is taken from the nasal septum
or auricle and laid in a single or multiple layers. If deformity
involves both cartilage and bone, cancellous bone from the
iliac crest is the best. Autografts (taken from the same indi-
vidual) are preferred to allografts (taken from other indi-
viduals or cadavers). Saddle deformity can also be corrected
by synthetic implants of silicone or teflon but they are likely Normal Saddle Supratip Humped
nose depression nose
to be extruded.
Figure 25.1 Deformities of nose.
HUMP NOSE
This may also involve the bone or cartilage or both bone
and cartilage. It can be corrected by reduction rhinoplasty
which consists of exposure of nasal framework by careful
raising of the nasal skin by a vestibular incision, removal of
hump and narrowing of the lateral walls by osteotomies to
reduce the widening left by hump removal.

CROOKED OR A DEVIATED NOSE


In crooked nose, the midline of dorsum from frontonasal
angle to the tip is curved in a C- or S-shaped manner. In a
deviated nose, the midline is straight but deviated to one
side (Figure 25.2).
Usually, these deformities are traumatic in origin. Inju-
ries sustained during birth, neonatal period or childhood,
but not immediately recognized, will also develop into these Crooked nose Deviated nose
deformities with the growth of nose. The deviated or crooked Figure 25.2 Nasal bridge is S-shaped in crooked nose. It is straight
nose can be corrected by rhinoplasty or septorhinoplasty. but deviated to one side in deviated nose.

143
144 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

• Dermoid with a sinus. It is seen in infants and children and the brain and repairing the bony defect through which her-
is represented by a pit or a sinus in the midline of the niation has taken place.
dorsum of nose. Hair may be seen protruding through
(c) Glioma. It is a nipped off portion of encephalocele
the sinus opening. In these cases, the sinus track may
during embryonic development. Most of them (60%) are
lead to a dermoid cyst lying under the nasal bone in front
extranasal and present as firm subcutaneous swellings on
of upper part of nasal septum or may have an intracra-
the bridge, side of nose or near the inner canthus. Some of
nial dural connection. In those with intracranial exten-
them are purely intranasal (30%), while 10% are both intra-
sion, sinus tract passes through the cribriform plate or
and extranasal. Extranasal gliomas are encapsulated and can
foramen caecum and is attached to dura or has other
be easily removed by external nasal approach.
intracranial connection. Meningitis occurs if infection
travels along this path. Treatment of such cysts may neces-
sitate splitting of the nasal bones to remove any exten- 2. BENIGN TUMOURS
sion in the upper part of the nasal septum. A combined They arise from the nasal skin and include papilloma (skin
neurosurgical–otolaryngologic approach is required in wart), haemangioma, pigmented naevus, seborrhoeic keratosis,
those extending intracranially so as to close simultane- neurofibroma or tumour of sweat glands.
ously any bony defect through which the fistulous tract Rhinophyma or potato tumour is a slow-growing benign
passed (Figure 25.4). tumour due to hypertrophy of the sebaceous glands of the
tip of nose often seen in cases of long-standing acne rosa-
(b) Encephalocele or meningoencephalocele. It is hernia- cea. It presents as a pink, lobulated mass over the nose
tion of brain tissue along with its meninges through a con- with superficial vascular dilation; mostly affects men past
genital bony defect. An extranasal meningoencephalocele middle age (Figure 25.4). Patient seeks advice because of
presents as a subcutaneous pulsatile swelling in the midline the unsightly appearance of the tumour, or obstruction to
at the root of nose (nasofrontal variety), side of nose (naso- breathing and vision due to large size of the tumour. Treat-
ethmoid variety) or on the anteromedial aspect of the orbit ment consists of paring down the bulk of tumour with sharp
(naso-orbital variety). knife or carbon dioxide laser and the area allowed to re-
Swellings show cough impulse and may be reducible. epithelialize. Sometimes, tumour is completely excised and
Treatment is neurosurgical; severing the tumour stalk from the raw area skin grafted.

Table 25.1 Tumours of external nose

Congenital Benign Malignant


•  ermoid cysts
D • R hinophyma • B asal cell
• Encephalocele • Haemangioma cancer
• Meningoencephalocele • Pigmented • Squamous
• Glioma naevus cell cancer
• Seborrhoeic • Melanoma
keratosis
• Neurofibroma
• Sweat gland
tumour

Figure 25.4 Rhinophyma.

Dura

A B C
Figure 25.3 Types of dermoids. (A) Simple dermoid beneath the skin. (B) Dermoid with an external pit or sinus. It lies in front of septum and
deep to nasal bones. (C) Dermoid with an intracranial connection to dura.
CHAPTER 25 — DISEASES OF EXTERNAL NOSE AND NASAL VESTIBULE 145

3. MALIGNANT TUMOURS Early lesions respond to radiotherapy; more advanced


(a) Basal cell carcinoma (rodent ulcer) (Figure 25.5). This lesions or those with exposure of bone or cartilage
is the most common malignant tumour involving skin of require wide surgical excision and plastic repair of the
nose (87%), equally affecting males and females in the defect. Enlarged regional lymph nodes will require block
age group of 40–60 years. Common sites on the nose are dissection.
the tip and the ala. It may present as a cyst or papulo-pearly (c) Melanoma. This is the least common variety. Clinically,
nodule or an ulcer with rolled edges. It is very slow growing it is superficially spreading type (slow growing) or nodular
and remains confined to the skin for a long time. Underly- invasive type. Treatment is surgical excision.
ing cartilage or bone may get invaded. Nodal metastases
are extremely rare. Treatment depends on the size, loca-
tion and depth of the tumour. Early lesion can be cured
by cryosurgery, irradiation or surgical excision with 3–5 DISEASES OF NASAL VESTIBULE
mm of healthy skin around the palpable borders of the
tumour. FURUNCLE OR BOIL (FIGURE 25.7)
Lesions which are recurrent, extensive or with involve-
ment of cartilage or bone are excised and the surgical defect It is an acute infection of the hair follicle by Staphylococcus
closed by local or distant flaps or a prosthesis. aureus. Trauma from picking of the nose or plucking the
nasal vibrissae is the usual predisposing factor.
(b) Squamous cell carcinoma (epithelioma). This is the The lesion is small but exquisitely painful and tender.
second most common malignant tumour (11%), equally Inflammation may spread to the skin of nasal tip and dor-
affecting both sexes in 40–60 age group. It occurs as an infil- sum which become red and swollen. The furuncle may rup-
trating nodule or an ulcer with rolled out edges affecting ture spontaneously in the nasal vestibule.
side of nose or columella (Figure 25.6). Nodal metastases Treatment of furuncle consists of warm compresses, anal-
are seen in 20% of cases. gesics to relieve pain, and topical and systemic antibiotics
directed against staphylococcus. If a fluctuant area appears,
incision and drainage can be done. In no case should the
furuncle be squeezed or prematurely incised because of the
danger of spread of infection to cavernous sinus through
venous thrombophlebitis.
A furuncle of nose may complicate into cellulitis of the
upper lip or septal abscess.

VESTIBULITIS
It is diffuse dermatitis of nasal vestibule. Nasal discharge,
due to any cause such as rhinitis, sinusitis or nasal allergy,
coupled with trauma of handkerchief, is the usual predis-
posing factor. The causative organism is S. aureus. Vestibuli-
tis may be acute or chronic.
In acute form, vestibular skin is red, swollen and tender;
Figure 25.5 Basal cell carcinoma of the nose. crusts and scales cover an area of skin erosion or excoria-
tion. The upper lip may also be involved (Figure 25.8).
In chronic form, there is induration of vestibular skin with
painful fissures and crusting.

Figure 25.6 Carcinoma nose. Figure 25.7 Furuncle right nasal vestibule.
146 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Figure 25.8 Acute vestibulitis (left side). Figure 25.9 Stenosis left naris following smallpox.

Treatment consists of cleaning the nasal vestibule of all


crusts and scales with cotton applicator soaked in hydrogen
peroxide and application of antibiotic-steroid ointment. The
latter should always be continued for a few more days, even
after the apparent cure, as the condition is likely to relapse.
A chronic fissure can be cauterized with silver nitrate. Atten-
tion should be paid to the cause of nasal discharge.

STENOSIS AND ATRESIA OF THE NARES


Accidental or surgical trauma to the nasal tip or vestibule
can lead to web formation and stenosis of anterior nares.
In Young’s operation, vestibular skin flaps are raised to cre-
ate deliberate closure of nares in the treatment of atrophic
rhinitis (see p. 153). Destructive inflammatory lesions of nose
also cause stenosis. Earlier, several cases of vestibular stenosis Figure 25.10 Nasoalveolar cyst as seen during operation.
resulted from smallpox (Figure 25.9).
Congenital atresia of anterior nares due to noncanalization excised by sublabial approach preserving the integrity
of epithelial plug is a rare condition. of vestibular skin (Figure 25.10).
Stenosis of nares can be corrected by reconstructive plas- 2. Papilloma or wart may be single or multiple, pedunculated
tic procedures. or sessile. Treatment is surgical excision under local
anaesthesia.
3. Squamous cell carcinoma arises from the lateral wall of the
TUMOURS
vestibule and may extend into nasal floor, columella and
1. Nasoalveolar cyst presents a smooth bulge in the lat- upper lip. It can metastasize to the parotid and subman-
eral wall and floor of nasal vestibule. The cyst can be dibular nodes. Treatment is surgical excision or irradiation.
Nasal Septum and 26
Its Diseases

depression of lower part of nose and drooping of the


ANATOMY nasal tip.
Septal cartilage lies in a groove in the anterior edge of
Nasal septum consists of three parts: vomer and rests anteriorly on anterior nasal spine. During
1. Columellar septum. It is formed of columella containing trauma, it may get dislocated from anterior nasal spine or
the medial crura of alar cartilages united together by fibrous vomerine groove causing caudal septal deviation or sep-
tissue and covered on either side by skin. tal spur, respectively. This compromises the nasal airway.
Septal cartilage is also intimately related to the upper lat-
2. Membranous septum. It consists of double layer of skin eral cartilages of nose and is in fact fused with them in
with no bony or cartilaginous support. It lies between the the upper third. For this reason septal deviation may be
columella and the caudal border of septal cartilage. Both associated with deviation of cartilaginous part of external
columellar and membranous parts are freely movable from nose.
side to side. Blood Vessels of Nasal Septum (see Chapter 33).
3. Septum proper. It consists of osteocartilaginous frame- Nerve Supply of Nasal Septum (see Chapter 23).
work, covered with nasal mucous membrane. Little’s area or Kiesselbach’s plexus. This is the vascular
Its principal constituents are (Figure 26.1): area in the anteroinferior part of nasal septum just above
(a) the perpendicular plate of ethmoid, the vestibule. Anterior ethmoidal, sphenopalatine, greater
(b) the vomer and palatine and septal branch of superior labial arteries and
(c) a large septal (quadrilateral) cartilage wedged between their corresponding veins form an anastomosis here. This
the above two bones anteriorly. Other bones which is the commonest site for epistaxis. This is also the site for
make minor contributions at the periphery are crest origin of the “bleeding polypus” (haemangioma) of nasal
of nasal bones, nasal spine of frontal bone, rostrum of septum.
sphenoid, crest of palatine bones and the crest maxilla,
and the anterior nasal spine of maxilla.
Septal cartilage not only forms a partition between the FRACTURES OF NASAL SEPTUM
right and left nasal cavities but also provides support
to the tip and dorsum of cartilaginous part of nose. Its AETIOPATHOGENESIS
destruction, e.g. in septal abscess, injuries, tuberculo-
Trauma inflicted on the nose from the front, side or below
sis or excessive removal during septal surgery, leads to
can result in injuries to the nasal septum. The septum
may buckle on itself, fracture vertically, horizontally or be
crushed to pieces as in a smashed nose. The fractured pieces
of septum may overlap each other or project into the nasal
Nasal spine of cavity through mucosal tears. Fracture of the septal cartilage
frontal bone or its dislocation from the vomerine groove, can result from
trauma to the lower nose without associated fractures of
Crest of nasal Perp. plate of nasal bones. Septal injuries with mucosal tears cause profuse
bone ethmoid epistaxis while those with intact mucosa result in septal hae-
Membranous matoma which, if not drained early, will cause absorption of
septum Septal cart. Vomer Rostrum of the septal cartilage and saddle nose deformity.
sphenoid “Jarjaway” fracture of nasal septum results from blows
Columellar from the front; it starts just above the anterior nasal spine
septum and runs horizontally backwards just above the junction of
Ant. nasal spine
septal cartilage with the vomer (Figure 26.2A).
of maxilla Crest of maxilla “Chevallet” fracture of septal cartilage results from blows
from below; it runs vertically from the anterior nasal spine
Crest of palatine bone upwards to the junction of bony and cartilaginous dorsum
Figure 26.1 Anatomy of nasal septum. of nose (Figure 26.2B).

147
148 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

High arched
DNS palate

A
Figure 26.3 DNS associated with high-arched palate.

Anterior dislocation C-shaped deflection S-shaped deflection

B
Figure 26.2 Septal fracture showing: (A) Jarjaway type. (B) Chevallet Nasal spur impinging Thickening of nasal
type. on turbinate septum
Figure 26.4 Types of deviated nasal septum.

TREATMENT
twisting, fractures and duplication of nasal septum with tele-
Early recognition and treatment of septal injuries is essen- scoping of its fragments. Injuries to the nose commonly occur
tial. Haematomas should be drained. Dislocated or fractured in childhood but are often overlooked. Even the history may
septal fragments should be repositioned and supported not be forthcoming. Trauma may also be inflicted at birth dur-
between mucoperichondrial flaps with mattress sutures and ing difficult labour when nose is pressed during its passage
nasal packing. Fractures of nasal pyramid are often com- through the birth canal. Birth injuries should be immediately
plicated with fractures of the septum and both should be attended to as they result in septal deviation later in life.
treated concomitantly.
2. Developmental error. Nasal septum is formed by the tecto-
septal process which descends to meet the two halves of the
COMPLICATIONS developing palate in the midline. During the primary and
secondary dentition, further development takes place in the
Septum is important in supporting the lower part of the
palate, which descends and widens to accommodate the teeth.
external nose. If its injuries are ignored, they would result
Unequal growth between the palate and the base of skull
in deviation of the cartilaginous nose, or asymmetry of nasal
may cause buckling of the nasal septum. In mouth breathers,
tip, columella or the nostril.
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
DEVIATED NASAL SEPTUM (DNS)
abnormalities.
This is an important cause of nasal obstruction. 3. Racial factors. Caucasians are affected more than black
Americans.
AETIOLOGY 4. Hereditary factors. Several members of the same family
may have deviated nasal septum.
Trauma and errors of development form the two important
factors in the causation of deviated septum.
TYPES OF DNS (FIGURE 26.4)
1. Trauma. A lateral blow on the nose may cause displacement
of septal cartilage from the vomerine groove and maxillary Deviation may involve only the cartilage, bone or both the
crest, while a crushing blow from the front may cause buckling, cartilage and bone.
CHAPTER 26 — NASAL SEPTUM AND ITS DISEASES 149

Figure 26.5 Anterior dislocation. Caudal border of septal cartilage


projects into right naris.

1. Anterior dislocation. Septal cartilage may be dislocated


into one of the nasal chambers. This is better appreciated Figure 26.6 Cottle test: On pulling the cheek away from the midline,
by looking at the base of nose when patient’s head is tilted the nasal valve opens, increasing the airflow from that side of the
backwards (Figure 26.5). nasal cavity.
2. C-shaped deformity. Septum is deviated in a simple curve
to one side. Nasal chamber on the concave side of the nasal patient breathes quietly. If the nasal airway improves on the
septum will be wider and may show compensatory hypertro- test side, the test is positive and indicates abnormality of the
phy of turbinates. vestibular component of nasal valve (Figure 26.6).
3. S-shaped deformity. Either in vertical or anteroposterior 2. Headache. Deviated septum, especially a spur, may press
plane. Such a deformity may cause bilateral nasal obstruction. on the lateral wall of nose giving rise to pressure headache.
4. Spurs. A spur is a shelf-like projection often found at the 3. Sinusitis. Deviated septum may obstruct sinus ostia result-
junction of bone and cartilage. A spur may press on the lat- ing in poor ventilation of the sinuses. Therefore, it forms an
eral wall and gives rise to headache. It may also predispose important cause to predispose or perpetuate sinus infections.
to repeated epistaxis from the vessels stretched on its convex
4. Epistaxis. Mucosa over the deviated part of septum is
surface.
exposed to the drying effects of air currents leading to
5. Thickening. It may be due to organized haematoma or formation of crusts, which when removed causes bleed-
overriding of dislocated septal fragments. ing. Bleeding may also occur from vessels over a septal
spur.
CLINICAL FEATURES 5. Anosmia. Failure of the inspired air to reach the olfactory
region may result in total or partial loss of sense of smell.
DNS can involve any age and sex. Males are affected more
than females. 6. External deformity. Septal deformities may be associated
with deviation of the cartilaginous or both the bony and car-
1. Nasal obstruction. Depending on the type of septal defor-
tilaginous dorsum of nose, deformities of the nasal tip or
mity, obstruction may be unilateral or bilateral. Respiratory
columella.
currents pass through upper part of nasal cavity, therefore,
high septal deviation cause nasal obstruction more than 7. Middle ear infection. DNS also predisposes to middle ear
lower ones. infection.
When examining a case of nasal obstruction, one should
ascertain the site of obstruction in the nose. It could be
TREATMENT
(i) vestibular (caudal septal dislocation, synechiae or ste-
nosis), (ii) at the nasal valve (synechiae, usually postrhi- Minor degrees of septal deviation with no symptoms are com-
noplasty), (iii) attic (along the upper part of nasal septum monly seen in patients and require no treatment. It is only
due to high septal deviation; (iv) turbinal (hypertrophic when deviated septum produces mechanical nasal obstruction
turbinates or concha bullosa) and (v) choanal (choanal or the symptoms given above that an operation is indicated.
atresia or a choanal polyp). Unilateral choanal atresia
may be missed in infancy and childhood. Choanal polyp SUBMUCOUS RESECTION (SMR) OPERATION
may be missed on the anterior rhinoscopy unless poste- It is generally done in adults under local anaesthesia. It con-
rior rhinoscopy or nasal endoscopy is done. sists of elevating the mucoperichondrial and mucoperios-
Cottle test. It is used in nasal obstruction due to abnormality teal flaps on either side of the septal framework by a single
of the nasal valve. In this test, cheek is drawn laterally while the incision made on one side of the septum, removing the
150 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

deflected parts of the bony and cartilaginous septum, and


then repositioning the flaps (see section on Operative Sur-
gery for details).

SEPTOPLASTY
It is a conservative approach to septal surgery. In this opera-
tion, much of the septal framework is retained. Only the Blood
most deviated parts are removed. Rest of the septal frame-
work is corrected and repositioned by plastic means. Muco-
perichondrial/periosteal flap is generally raised only on one
side of the septum, retaining the attachment and blood sup-
ply on the other. Septoplasty has now almost replaced SMR
operation (see Chapter 87).
Septal surgery is usually done after the age of 17 so as
not to interfere with the growth of nasal skeleton. However, Figure 26.7 Septal haematoma.
if a child has severe septal deviation causing marked nasal
obstruction, conservative septal surgery (septoplasty) can
be performed to provide a good airway.

SEPTAL HAEMATOMA

AETIOLOGY
It is collection of blood under the perichondrium or perios-
teum of the nasal septum (Figure 26.7). It often results from
nasal trauma or septal surgery. In bleeding disorders, it may
occur spontaneously.

CLINICAL FEATURES
Bilateral nasal obstruction is the commonest presenting
symptom. This may be associated with frontal headache and
a sense of pressure over the nasal bridge.
Examination reveals smooth rounded swelling of the sep- Figure 26.8 Septal abscess.
tum in both the nasal fossae. Palpation may show the mass
to be soft and fluctuant.
CLINICAL FEATURES
There is severe bilateral nasal obstruction with pain and
TREATMENT
tenderness over the bridge of nose. Patient may also com-
Small haematomas can be aspirated with a wide bore ster- plain of fever with chills and frontal headache. Skin over
ile needle. Larger haematomas are incised and drained by the nose may be red and swollen. Internal examination of
a small anteroposterior incision parallel to the nasal floor. nose reveals smooth bilateral swelling of the nasal septum
Excision of a small piece of mucosa from the edge of incision (Figure 26.8). Fluctuation can be elicited in this swelling.
gives better drainage. Following drainage, nose is packed on Septal mucosa is often congested. Submandibular lymph
both sides to prevent reaccumulation. Systemic antibiotics nodes may also be enlarged and tender.
should be given to prevent septal abscess.
TREATMENT
COMPLICATIONS
Abscess should be drained as early as possible. Incision is
Septal haematoma, if not drained, may organize into fibrous made in the most dependent part of the abscess and a piece
tissue leading to a permanently thickened septum. If sec- of septal mucosa excised. Pus and necrosed pieces of car-
ondary infection supervenes, it results in septal abscess with tilage are removed by suction. Incision may require to be
necrosis of cartilage and depression of nasal dorsum. reopened daily for 2–3 days to drain any pus or to remove
any necrosed pieces of cartilage. Systemic antibiotics are
started as soon as diagnosis has been made and continued
at least for a period of 10 days.
SEPTAL ABSCESS

AETIOLOGY COMPLICATIONS
Mostly, it results from secondary infection of septal haema- Necrosis of septal cartilage often results in depression of the
toma. Occasionally, it follows furuncle of the nose or upper lip. cartilaginous dorsum in the supratip area and may require
It may also follow acute infection such as typhoid or measles. augmentation rhinoplasty 2–3 months later. Necrosis of
CHAPTER 26 — NASAL SEPTUM AND ITS DISEASES 151

Figure 26.10 Septal button for closure of perforation.


Figure 26.9 Septal perforation.

septal flaps may lead to septal perforation. Meningitis 3. Drugs and chemicals
and cavernous sinus thrombosis following septal abscess,
(a) Prolonged use of steroid sprays in nasal allergy.
though rare these days, can be a serious complication.
(b) Cocaine addicts.
(c) Workers in certain occupations, e.g. chromium plating,
dichromate or soda ash (sodium carbonate) manufac-
PERFORATION OF NASAL SEPTUM ture or those exposed to arsenic or its compounds.
(FIGURE 26.9)
4. Idiopathic. In many cases, there is no history of trauma or
AETIOLOGY previous disease and the patient may even be unaware of the
existence of a perforation.
1. Traumatic perforations. Trauma is the most common
cause. Injury to mucosal flaps during SMR, cauterization of
septum with chemicals or galvanocautery for epistaxis and CLINICAL FEATURES
habitual nose picking are the common forms of trauma. Occa- Small anterior perforations cause whistling sound during inspi-
sionally, septum is deliberately perforated to put ornaments. ration or expiration. Larger perforations develop crusts which
2. Pathological perforations. They can be caused by: obstruct the nose or cause severe epistaxis when removed.

(a) Septal abscess.


TREATMENT
(b) Nasal myiasis.
(c) Rhinolith or neglected foreign body causing pressure An attempt should always be made to find out the cause
necrosis. before treatment of perforation. This may require biopsy
(d) Chronic granulomatous conditions like lupus, tubercu- from the granulations or biopsy of the edge of the perfora-
losis and leprosy cause perforation in the cartilaginous tion. Inactive small perforations can be surgically closed by
part while syphilis involves the bony part. In these cases, plastic flaps. Larger perforations are difficult to close. Their
evidence of the causative disease may also be seen in treatment is aimed to keep the nose crust-free by alkaline
other systems of the body. nasal douches and application of a bland ointment. Some-
(e) Wegener’s granuloma is a midline destructive lesion times, a thin silastic button can be worn to get relief from
which may cause total septal destruction. the symptoms (Figure 26.10).
27 Acute and Chronic Rhinitis

ACUTE RHINITIS form in the nose, which with attempted removal causes
bleeding.
Acute rhinitis can be viral, bacterial or irritative type. Secondary bacterial rhinitis is the result of bacterial infec-
tion supervening acute viral rhinitis.

VIRAL RHINITIS Diphtheritic rhinitis. Diphtheria of nose is rare these days. It


may be primary or secondary to faucial diphtheria and may
1. Common cold (coryza) occur in acute or chronic form. A greyish membrane is seen
• Aetiology. It is caused by a virus. The infection is usually covering the inferior turbinate and the floor of nose; mem-
contracted through airborne droplets. Several viruses brane is tenacious and its removal causes bleeding. Excoria-
(adenovirus, picornavirus and its subgroups such as rhi- tion of anterior nares and upper lip may be seen. Treatment
novirus, coxsackie virus and enteric cytopathic human is isolation of the patient, systemic penicillin and diphtheria
orphan virus) are responsible. Incubation period is antitoxin.
1–4 days and illness lasts for 2–3 weeks.
• Clinical features. To begin with, there is burning sensa- IRRITATIVE RHINITIS
tion at the back of nose soon followed by nasal stuffi-
ness, rhinorrhoea and sneezing. Patient feels chilly and This form of acute rhinitis is caused by exposure to dust,
there is low-grade fever. Initially, nasal discharge is watery smoke or irritating gases such as ammonia, formaline, acid
and profuse but may become mucopurulent due to sec- fumes, etc. or it may result from trauma inflicted on the
ondary bacterial invasion. Secondary invaders include nasal mucosa during intranasal manipulation, e.g. removal
Streptococcus haemolyticus, pneumococcus, Staphylococcus, of a foreign body. There is an immediate catarrhal reac-
Haemophilus influenzae, Klebsiella pneumoniae and Moraxella tion with sneezing, rhinorrhoea and nasal congestion. The
catarrhalis. symptoms may pass off rapidly with removal of the offend-
• Treatment. Bed rest is essential to cut down the course of ing agent or may persist for some days if nasal epithelium
illness. Plenty of fluids are encouraged. Symptoms can be has been damaged. Recovery will depend on the amount of
easily controlled with antihistaminics and nasal deconges- epithelial damage and the infection that supervenes.
tants. Analgesics are useful to relieve headache, fever and
myalgia. Nonaspirin containing analgesics are preferable
as aspirin causes increased shedding of virus. Antibiotics CHRONIC RHINITIS
are required when secondary infection supervenes.
• Complications. The disease is usually self-limiting and Chronic nonspecific inflammations of nose include:
resolves spontaneously after 2–3 weeks, but occasionally, 1. Chronic simple rhinitis.
complications such as sinusitis, pharyngitis, tonsillitis, 2. Hypertrophic rhinitis.
bronchitis, pneumonia and otitis media may result. 3. Atrophic rhinitis.
4. Rhinitis sicca.
2. Influenzal rhinitis. Influenza viruses A, B or C are respon- 5. Rhinitis caseosa.
sible. Symptoms and signs are similar to those of common
cold. Complications due to bacterial invasion are common. CHRONIC SIMPLE RHINITIS
3. Rhinitis associated with exanthemas. Measles, rubella AETIOLOGY
and chickenpox are often associated with rhinitis which
Recurrent attacks of acute rhinitis in the presence of predis-
precedes exanthemas by 2–3 days. Secondary infection and
posing factors leads to chronicity. The predisposing factors
complications are more frequent and severe.
are:
1. Persistence of nasal infection due to sinusitis, tonsillitis
BACTERIAL RHINITIS
and adenoids.
Nonspecific infections. It may be primary or secondary. 2. Chronic irritation from dust, smoke, cigarette smoking,
Primary bacterial rhinitis is seen in children and is usually snuff, etc.
the result of infection with pneumococcus, streptococcus or 3. Nasal obstruction due to deviated nasal septum, synechia
staphylococcus. A greyish white tenacious membrane may leading to persistence of discharge in the nose.

152
CHAPTER 27 — ACUTE AND CHRONIC RHINITIS 153

4. Vasomotor rhinitis. SIGNS


5. Endocrinal or metabolic factors, e.g. hypothyroidism, Examination shows hypertrophy of turbinates. Turbinal
excessive intake of carbohydrates and lack of exercise. mucosa is thick and does not pit on pressure. It shows little
PATHOLOGY shrinkage with vasoconstrictor drugs due to presence of
underlying fibrosis.
Simple chronic rhinitis is an early stage of hypertrophic Maximum changes are seen in the inferior turbinate. It
rhinitis. There is hyperaemia and oedema of mucous may be hypertrophied in its entirety or only at the anterior
membrane with hypertrophy of seromucinous glands and end, posterior end or along the inferior border giving it a
increase in goblet cells. Blood sinusoids particularly those mulberry appearance.
over the turbinates are distended.
TREATMENT
CLINICAL FEATURES
Attempt should be made to discover the cause and remove
1. Nasal obstruction. Usually worse on lying and affects the it. Nasal obstruction can be relieved by reduction in size of
dependent side of nose. turbinates. The various methods are:
2. Nasal discharge. It may be mucoid or mucopurulent,
thick and viscid and often trickles into the throat as post- 1. Linear cauterization.
nasal drip. Patient has a constant desire to blow the nose 2. Submucosal diathermy.
or clear the throat. 3. Cryosurgery of turbinates.
3. Headache. It is due to swollen turbinates impinging on 4. Partial or total turbinectomy. Hypertrophied inferior
the nasal septum. turbinate can be partially removed at its anterior end,
4. Swollen turbinates. Nasal mucosa is dull red in colour. inferior border or posterior end. Middle turbinate, if
Turbinates are swollen; they pit on pressure and shrink hypertrophied, can also be removed partially or totally.
with application of vasoconstrictor drops (this differen- Excessive removal of turbinates should be avoided as it
tiates the condition from hypertrophic rhinitis). Mid- leads to persistent crusting.
dle turbinate may also be swollen and impinge on the 5. Submucous resection of turbinate bone. This removes
septum. bony obstruction but preserves turbinal mucosa for its
5. Postnasal discharge. Mucoid or mucopurulent discharge function.
is seen on the posterior pharyngeal wall. 6. Lasers have also been used to reduce the size of turbinates.

TREATMENT COMPENSATORY HYPERTROPHIC RHINITIS


1. Treat the cause with particular attention to sinuses, ton- This is seen in cases of marked deviation of septum to one
sils, adenoids, allergy, personal habits (smoking or alco- side. The roomier side of the nose shows hypertrophy of
hol indulgence), environment or work situation (smoky inferior and middle turbinates. This is an attempt on the
or dusty surroundings). part of nature to reduce the wide space to overcome the ill
2. Nasal irrigations with alkaline solution help to keep the effects of drying and crusting that always attend wider nasal
nose free from viscid secretions and also remove superfi- space. Hypertrophic changes in these cases are not revers-
cial infection. ible with the correction of nasal septum and often require
3. Nasal decongestants help to relieve nasal obstruction and reduction of turbinates at the time of septal surgery.
improve sinus ventilation. Excessive use of nasal drops
and sprays should be avoided because it may lead to rhi- ATROPHIC RHINITIS (OZAENA)
nitis medicamentosa. A short course of systemic steroids
helps to wean the patients already addicted to excessive It is a chronic inflammation of nose characterized by atro-
use of decongestant drops or sprays. phy of nasal mucosa and turbinate bones. The nasal cavities
4. Antibiotics help to clear nasal infection and concomitant are roomy and full of foul-smelling crusts. Atrophic rhinitis
sinusitis. is of two types: primary and secondary.

PRIMARY ATROPHIC RHINITIS


HYPERTROPHIC RHINITIS
Aetiology (Remember Mnemonic HERNIA)
It is characterized by thickening of mucosa, submucosa,
The exact cause is not known. Various theories advanced
seromucinous glands, periosteum and bone. Changes are
regarding its causation are:
more marked on the turbinates.
1. Hereditary factors. Disease is known to involve more
AETIOLOGY than one member in the same family.
Common causes are recurrent nasal infections, chronic 2. Endocrinal disturbance. Disease usually starts at puberty,
sinusitis, chronic irritation of nasal mucosa due to smoking, involves females more than males, the crusting and foe-
industrial irritants, prolonged use of nasal drops and vaso- tor associated with disease tends to cease after meno-
motor and allergic rhinitis. pause; these factors have raised the possibility of disease
being an endocrinal disorder.
SYMPTOMS 3. Racial factors. White and yellow races are more suscep-
Nasal obstruction is the predominant symptom. Nasal dis- tible than natives of equatorial Africa.
charge is thick and sticky. Some complain of headache, 4. Nutritional deficiency. Disease may be due to deficiency
heaviness of head or transient anosmia. of vitamin A, D or iron or some other dietary factors.
154 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

crusts and the associated putrefying smell, and to further


The fact that incidence of disease is decreasing in west-
check crust formation.
ern countries and is rarely seen in well-to-do families
raises the possibility of some nutritional deficiency. (a) Nasal irrigation and removal of crusts. Warm normal saline
5. Infective. Various organisms have been cultured from or an alkaline solution made by dissolving a teaspoonful
cases of atrophic rhinitis such as Klebsiella ozaenae, (Perez of powder containing soda bicarbonate 1 part, sodium
bacillus), diphtheroids, Proteus vulgaris, Escherichia coli, biborate 1 part, sodium chloride 2 parts in 280 mL of
staphylococci and streptococci but they are all consid- water is used to irrigate the nasal cavities. The solution
ered to be secondary invaders responsible for foul smell is run through one nostril and comes out from the
rather than the primary causative organisms of the other. It loosens the crusts and removes thick tenacious
disease. discharge. Care should be taken to avoid pushing the
6. Autoimmune process. The body reacts by a destructive fluid into the sinuses and eustachian tube. Initially,
process to the antigens released from the nasal mucosa. irrigations are done two or three times a day but later
Viral infection or some other unspecified agents may once in every 2 or 3 days is sufficient. Hard crusts may
trigger antigenicity of nasal mucosa. be difficult to remove by irrigation. They are first loos-
ened and then mechanically removed with forceps or
Pathology suction.
Ciliated columnar epithelium is lost and is replaced by (b) 25% glucose in glycerine. After crusts are removed, nose
stratified squamous type. There is atrophy of seromucinous is painted with 25% glucose in glycerine. This inhibits
glands, venous blood sinusoids and nerve elements. Arter- the growth of proteolytic organisms which are respon-
ies in the mucosa, periosteum and bone show obliterative sible for foul smell.
endarteritis. The bone of turbinates undergoes resorption (c) Local antibiotics. Spraying or painting the nose with
causing widening of nasal chambers. Paranasal sinuses are appropriate antibiotics help to eliminate secondary
small due to their arrested development. infection. Kemicetine™ antiozaena solution contains
chloromycetin, oestradiol and vitamin D2 and may be
Clinical Features found useful.
Disease is commonly seen in females and starts around (d) Oestradiol spray. Helps to increase vascularity of nasal
puberty. There is foul smell from the nose making the mucosa and regeneration of seromucinous glands.
patient a social outcast though patient himself is unaware of (e) Placental extract injected submucosally in the nose may
the smell due to marked anosmia (merciful anosmia) which provide some relief.
accompanies these degenerative changes. Patient may com- (f) Systemic use of streptomycin. 1 g/day for 10 days has given
plain of nasal obstruction in spite of unduly wide nasal good results in reducing crusting and odour. It is effec-
chambers. This is due to large crusts filling the nose. Epi- tive against Klebsiella organisms.
staxis may occur when the crusts are removed. (g) Potassium iodide given by the mouth promotes and liq-
Examination shows nasal cavity to be full of greenish or uefies nasal secretion.
greyish black dry crusts covering the turbinates and sep-
tum. Attempts to remove them may cause bleeding. When 2. Surgical. It includes:
the crusts have been removed, nasal cavities appear roomy
(a) Young’s operation. Both the nostrils are closed com-
with atrophy of turbinates so much so that the posterior wall
pletely just within the nasal vestibule by raising flaps.
of nasopharynx can be easily seen. Nasal turbinates may be
They are opened after 6 months or later. In these cases,
reduced to mere ridges. Nasal mucosa appears pale. Septal
mucosa may revert to normal and crusting reduced.
perforation and dermatitis of nasal vestibule may be pres-
Modified Young’s operation. To avoid the discomfort of
ent. Nose may show a saddle deformity.
bilateral nasal obstruction, modified Young’s operation
Atrophic changes may also be seen in the pharyngeal
aims to partially close the nostrils. It is also claimed to
mucosa which may appear dry and glazed with crusts (atro-
give the same benefit as Young’s.
phic pharyngitis, p. 256).
(b) Narrowing the nasal cavities. Nasal chambers are very
Similar changes may occur in the larynx with cough and
wide in atrophic rhinitis and air currents dry up secre-
hoarseness of voice (atrophic laryngitis).
tions leading to crusting. Narrowing the size of the
Hearing impairment may be noticed because of obstruc-
nasal airway helps to relieve the symptoms. Among the
tion to eustachian tube and middle ear effusion.
techniques followed, some are:
Paranasal sinuses are usually small and underdeveloped
(i) Submucosal injection of teflon paste.
with thick walls. They appear opaque on X-ray. Antral wash
(ii) Insertion of fat, cartilage, bone or teflon strips
is difficult to perform due to thick walls of the sinuses.
under the mucoperiosteum of the floor and lat-
Prognosis eral wall of nose and the mucoperichondrium of
the septum.
The disease persists for years but there is a tendency to
(iii) Section and medial displacement of lateral wall of
recover spontaneously in middle age.
nose.
Treatment
SECONDARY ATROPHIC RHINITIS
It may be medical or surgical.
Specific infections like syphilis, lupus, leprosy and rhinoscle-
1. Medical. Complete cure of the disease is not yet possible. roma may cause destruction of the nasal structures leading
Treatment aims at maintaining nasal hygiene by removal of to atrophic changes. Atrophic rhinitis can also result from
CHAPTER 27 — ACUTE AND CHRONIC RHINITIS 155

long-standing purulent sinusitis, radiotherapy to nose or Treatment consists of correction of the occupational sur-
excessive surgical removal of turbinates. roundings and application of bland ointment or one with an
antibiotic and steroid to the affected part. Nose pricking and
Unilateral atrophic rhinitis. Extreme deviation of nasal sep-
forcible removal of crusts should be avoided. Nasal douche,
tum may be accompanied by atrophic rhinitis on the wider
like the one used in cases of atrophic rhinitis, is useful.
side.

RHINITIS CASEOSA
RHINITIS SICCA
It is an uncommon condition, usually unilateral and mostly
It is also a crust-forming disease seen in patients who work in affecting males.
hot, dry and dusty surroundings, e.g. bakers, iron- and gold- Nose is filled with offensive purulent discharge and
smiths. Condition is confined to the anterior third of nose cheesy material. The disease possibly arises from chronic
particularly of the nasal septum. Here, the ciliated columnar sinusitis with collection of inspissated cheesy material. Sinus
epithelium undergoes squamous metaplasia with atrophy of mucosa becomes granulomatous. Bony walls of sinus may be
seromucinous glands. Crusts form on the anterior part of destroyed, requiring differentiation from malignancy. Treat-
septum and their removal causes ulceration and epistaxis, ment is removal of debris and granulation tissue and free
and may lead to septal perforation. drainage of the affected sinus. Prognosis is good.
28 Granulomatous Diseases
of Nose

Various granulomatous lesions involving the nose are listed inclusion bodies found in the plasma cells. They occur
in Table 28.1. They are the result of bacterial or fungal infec- due to accumulation of immunoglobulins secreted by the
tions or due to causes not yet clear. Many of these lesions plasma cells. The causative organisms can be cultured from
may be manifestations of systemic diseases, which should the biopsy material.
always be looked for while making the diagnosis. Biopsy of
the lesion is also essential, not only to establish the c­ orrect TREATMENT
diagnosis of granulomatous disease but also to exclude a Both streptomycin (1 g/day) and tetracycline (2 g/day)
neoplasm, in which many of these diseases may clinically are given together for a minimum period of 4–6 weeks and
simulate. repeated, if necessary, after 1 month. Treatment is stopped

BACTERIAL INFECTIONS

RHINOSCLEROMA
It is a chronic granulomatous disease caused by Gram-
negative bacillus called Klebsiella rhinoscleromatis or Frisch
bacillus. The disease is endemic in several parts of the
world. In India, it is seen more often in the northern than
in the southern parts.

PATHOLOGY
The disease starts in the nose and extends to nasopharynx,
oropharynx, larynx (mostly subglottic region), trachea and
bronchi. Mode of infection is unknown. Both sexes of any
age may be affected.

CLINICAL FEATURES Figure 28.1 Rhinoscleroma nose.


The disease runs through the following stages:
1. Atrophic stage. It resembles atrophic rhinitis and is char-
acterized by foul-smelling purulent nasal discharge and
crusting.
2. Granulomatous stage. Granulomatous nodules form
in nasal mucosa. There is also subdermal infiltration
of lower part of external nose and upper lip giving a
“woody” feel (Figure 28.1). Nodules are painless and
nonulcerative.
3. Cicatricial stage. This causes stenosis of nares, distortion
of upper lip, adhesions in the nose, nasopharynx and
oropharynx. There may be subglottic stenosis with respi-
ratory distress.

DIAGNOSIS
Biopsy shows infiltration of submucosa with plasma cells,
lymphocytes, eosinophils, Mikulicz cells and Russell bod- Figure 28.2 Rhinoscleroma showing foamy Mikulicz cells (arrow)
ies. The latter two are diagnostic features of the disease and lymphocytic infiltration (arrowheads) (H&E, x400). Mikulicz cells
(Figure 28.2). Mikulicz cells are large foam cells with a contain Gram-negative bacteria which can be better appreciated in
central nucleus and vacuolated cytoplasm containing caus- sections stained with Giemsa stain and examined under oil immer-
ative bacilli. Russell bodies are homogenous eosinophilic sion lens.

156
CHAPTER 28 — GRANULOMATOUS DISEASES OF NOSE 157

only when two consecutive cultures from the biopsy material COMPLICATIONS
are negative. Steroids can be combined to reduce fibrosis. Syphilis can lead to vestibular stenosis, perforations of nasal
Surgical treatment may be required to establish the ­airway septum and hard palate, secondary atrophic rhinitis and
and correct nasal deformity. saddle nose deformity.

SYPHILIS TUBERCULOSIS
Nasal syphilis is of two types: acquired and congenital. Primary tuberculosis of nose is rare. More often it is second-
1. Acquired. It occurs as: ary to lung tuberculosis. Anterior part of nasal septum and
anterior end of inferior turbinate are the sites commonly
(a) Primary. It manifests as primary chancre of the vestibule
involved. First, there is nodular infiltration followed later by
of nose. It is rare.
ulceration and perforation of nasal septum in its cartilagi-
(b) Secondary. Rarely recognized. It manifests as simple
nous part.
rhinitis with crusting and fissuring in the nasal ves-
Diagnosis can be made on biopsy and special staining of
tibule. Diagnosis is suggested by the presence of
sections for acid fast bacilli and culture of organisms.
mucous patches in the pharynx, skin rash, fever and
Treatment is antitubercular drugs.
generalized lymphadenitis.
(c) Tertiary. This is the stage in which nose is commonly
involved. Typical manifestation is the formation of LUPUS VULGARIS
a gumma on the nasal septum. Later, the septum is
It is a low-grade tuberculous infection commonly affecting
destroyed both in its bony and cartilaginous parts.
nasal vestibule or the skin of nose and face. The skin lesions
Perforation may also appear in the hard palate. There
manifest characteristically as brown, gelatinous nodules
is offensive nasal discharge with crusts. Bony or car-
called “apple-jelly” nodules. In the vestibule, it presents as
tilaginous sequestra may be seen. Bridge of the nose
chronic vestibulitis. Perforation may occur in the cartilagi-
collapses causing a saddle nose deformity.
nous part of nasal septum.
It is difficult to isolate tubercle bacilli by culture, however,
2. Congenital. It occurs in two forms: early and late.
biopsy of the lesion is useful to make the diagnosis.
(a) Early form. It is seen in the first 3 months of life and Treatment is the same as for tuberculosis of nose.
manifests as “snuffles.” Soon the nasal discharge
becomes purulent. This is associated with fissuring and
excoriation of the nasal vestibule and of the upper lip. LEPROSY
(b) Late form. Usually manifests around puberty. Clinical pic- Leprosy is very common in the tropics and is widely preva-
ture is similar to that seen in tertiary stage of acquired lent in India. It is caused by Mycobacterium leprae. The nose
syphilis. Gummatous lesions destroy the nasal structures. is involved as a part of systemic disease, more often in the
Other stigmata of syphilis such as corneal opacities, lepromatous than tuberculoid or dimorphous forms of
­deafness and Hutchinson’s teeth are also present. disease.
Infection starts in the anterior part of nasal septum and
DIAGNOSIS anterior end of inferior turbinate. Initially, there is exces-
It is made on serological tests (VDRL) and biopsy of the sive nasal discharge with red and swollen mucosa. Later,
tissue with special stains to demonstrate Treponema pallidum. crusting and bleeding supervene. Nodular lesions on the
septum may ulcerate and cause perforation. Late sequelae
TREATMENT of disease are atrophic rhinitis, depression of bridge of nose
Penicillin is the drug of choice: benzathine penicillin and destruction of anterior nasal spine with retrusion of the
2.4 million units i.m. every week for 3 weeks with a total dose columella (Figure 28.3).
of 7.2 million units. Nasal crusts are removed by irrigation
with alkaline solution. Bony and cartilaginous sequestra
should also be removed. Cosmetic deformity is corrected
after disease becomes inactive.

Table 28.1 Granulomatous disease of nose

Bacterial Fungal Unspecified cause


Rhinoscleroma Rhinosporidiosis Wegener’s
granulomatosis
Syphilis Aspergillosis Nonhealing midline
granuloma
Tuberculosis Mucormycosis
Lupus Candidiasis Sarcoidosis
Leprosy Histoplasmosis Rare
Blastomycosis
Figure 28.3 Leprosy nose.
158 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Diagnosis can be made from the scrapings of nasal mucosa In India, disease is more common in the southern
and biopsy. Acid-fast lepra bacilli can be seen in the foamy states. It is prevalent in the states of Tamil Nadu, Kerala,
appearing histiocytes called lepra cells. Madhya Pradesh, Chhattisgarh, Puducherry and Andhra
Treatment is with dapsone, rifampin and isoniazid. Recon- Pradesh. A few cases are also reported from Punjab and
struction procedures are required when disease is inactive. Haryana.
Disease is also seen to involve animals such as cows, bulls,
horses, mules and dogs where men and animals share the
same infected ponds.
FUNGAL INFECTIONS
AETIOLOGIC AGENT (FIGURE 28.5)
RHINOSPORIDIOSIS (FIGURE 28.4)
It has long been considered to be a fungus but it has been
It is a chronic granulomatous disease caused by Rhinospo- difficult to classify this organism. It has not been cultured
ridium seeberi and affects both man and animals. so far. Some consider it to be a protozoa or a fish parasite
belonging to DRIP clade (Dermocystidium, Rosette agent,
EPIDEMIOLOGY Ichthyophonus and Psorospermum).
Most of the cases come from India, Sri Lanka and Pakistan
though cases have been reported from Africa (Kenya, Tanza- LIFE CYCLE
nia, Rwanda, Burkinafaso, Chad and Egypt), South America Three stages have been recognized in the life cycle of the
(Argentina, Brazil), North America, Europe and Canada. organism: trophic stage, development of sporangia and pro-
No case is reported from Australia. duction of endospores (Figure 28.6).

A B
Figure 28.4 Rhinosporidiosis presenting as (A) a polypoidal mass protruding through the naris and (B) multiple sites of involvement, viz. nose,
conjunctiva and tongue.

A B
Figure 28.5 (A) Histologic section showing rhinosporidiosis (blue arrow) evoking mixed inflammatory response (H&E, x40). (B) Histologic
section showing sporangium (blue arrow) which is fully packed with immature sporoblasts at the periphery and mature ones at the centre
(H&E, x200).
CHAPTER 28 — GRANULOMATOUS DISEASES OF NOSE 159

1. Trophic stage. The endospore is oval or rounded, 6–8 μm DIAGNOSIS


in size, clear cytoplasm, vesicular nucleus with a nucleo- This is made on biopsy. It shows several sporangia, oval or round
lus and a covering of chitin. It gradually increases in size, in shape and filled with spores which may be seen bursting
begins to divide cytoplasm and nucleus forming small through its chitinous wall. It has not been possible to culture
endospores by several divisions. Trophocyte becomes the organism or transfer the disease to experimental animals.
large filled with young endospores.
2. Development of sporangium. The mature trophocyte TREATMENT
then develops into sporangium. A sporangium is 200– Complete excision of the mass with diathermy knife and
250 μm in diameter, contains 12,000–16,000 endospores. cauterization of its base. Recurrence may occur after sur-
It has a thick wall consisting of two layers: outer chitinous gical excision. Not many drugs are effective against the
and inner cellulose layer. disease. Dapsone has been tried with some success.
Endospores mature with the formation of mucoid
and chitinous wall. Sporangium filled with thousands of
endospores develops a germinal pore ready to burst and ASPERGILLOSIS
liberate the endospores. The usual causative organisms are Aspergillus niger,
3. Production of endospores. Sporangium filled with endo- A. fumigatus or A. flavus. They invade nasal tissues when
spores develops high internal pressure and ruptures host’s defence mechanisms are compromised due to
liberating endospores into the surrounding tissue. If immunosuppressive drugs.
internal pressure is not high, spores are liberated one
by one without breaking the wall. After liberation endo- CLINICAL FEATURES
spores start their life as trophic stage. Some endospores Clinical features are those of acute or subacute rhinitis or
are carried by lymphatic channels to the blood stream to sinusitis. A black or greyish membrane is seen in the nasal
cause disseminated form of disease. mucosa. Exploration of maxillary sinus reveals a fungus ball
CLINICAL FEATURES containing semisolid cheesy-white or blackish material. The
organisms can be seen on special staining for fungus.
The disease mostly affects nose and nasopharynx; other sites
such as lip, palate, conjunctiva, epiglottis, larynx, trachea, TREATMENT
bronchi, skin, vulva and vagina may also be affected. Surgical debridement of the involved tissues and antifun-
The disease is acquired through contaminated water of gal drugs, e.g. Amphotericin B. Repeated irrigation of the
ponds also frequented by animals. In the nose, the disease involved area with application of 1% solution of gentian
presents as a leafy, polypoidal mass, pink to purple in colour violet is also useful.
and attached to nasal septum or lateral wall. Sometimes, it
extends into the nasopharynx and may hang behind the soft
palate. The mass is very vascular and bleeds easily on touch. MUCORMYCOSIS
Its surface is studded with white dots representing the spo- It is fungal infection of nose and paranasal sinuses which
rangia of fungus. may prove rapidly fatal. It is seen in uncontrolled diabetics
In early stages, the patient may complain of nasal dis- or in those taking immunosuppressive drugs. From the nose
charge which is often blood tinged and nasal stuffiness. and sinuses, infection can spread to orbit, cribriform plate,
Sometimes, frank epistaxis is the only presenting complaint. meninges and brain. The rapid destruction associated with
the disease is due to affinity of the fungus to invade the arter-
ies and cause endothelial damage and thrombosis. Typical
Chitinous wall finding is the presence of a black necrotic mass filling the
Trophocyte Clear cytoplasm nasal cavity and eroding the septum and hard palate. Special
Vesicular nucleus stains help to identify the fungus in tissue sections.
A with a nucleolus Treatment is by amphotericin B and surgical debride-
ment of the affected tissues and control of underlying
Chitinous layer

Cellulose layer
} Wall
­predisposing cause.
Sporangium
OTHER FUNGAL INFECTIONS
Other fungal infections of nose such as candidiasis, histoplas-
mosis, blastomycosis, etc. are rare.
B

GRANULOMAS OF UNSPECIFIED
Pore
Rupture of
AETIOLOGY
sporangium Endospores
and release of WEGENER’S GRANULOMATOSIS
endospores
AETIOLOGY
C It is a systemic disorder of unknown aetiology involving
Figure 28.6 Life cycle of rhinosporidiosis. mainly the upper airways, lungs, kidneys and the skin.
160 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

It should be differentiated from nonhealing midline granu- T-CELL LYMPHOMA


loma because the treatment of the two is quite differ­ent.
Earlier terms used to describe this lesion were midline malig-
CLINICAL FEATURES nant lesion and polymorphic reticulosis.
It is a destructive lesion usually starting on one side of nose
Early symptoms of Wegener’s granulomatosis include clear
involving the upper lip, oral cavity, maxilla and sometimes even
or blood-stained nasal discharge which later becomes puru-
extending to orbit. Histologically polymorphic lymphoid tis-
lent. The patient often complains of “persistent cold” or
sue with angiocentric and angioinvasive features is seen. There
“sinus.” Nasal findings include crusting, granulations, septal
is no vasculitis—a feature typical of Wegener’s granulomato-
perforation and a saddle nose. Destruction may also involve
sis. Unlike Wegener’s granulomatosis, it is rapidly destructive
eyes, orbit, palate, oral cavity or oropharynx. Middle ear can
and usually devoid of systemic involvement; there is absence
also be involved.
of involvement of lung and kidneys. Immunohistochemical
General systemic symptoms include anaemia, fatigue,
studies of biopsy material are necessary to establish diagnosis
night sweats and migratory arthralgias.
of T-cell lymphoma. Localized T-cell lymphoma is treated by
Involvement of lung is manifested by cough and some-
radiation while a disseminated disease requires chemotherapy.
times haemoptysis. X-ray chest may show a single or multiple
cavity lesions.
Sooner or later, kidneys are also involved. Urine examina- SARCOIDOSIS
tion will show red cells, casts and albumin. Serum creatinine It is a granulomatous disease of unknown aetiology resem-
level is raised. Renal failure is the usual cause of death in bling tuberculosis on histology but with the absence of case-
these patients. ation. It is a systemic disorder and the symptoms may refer to
involvement of lungs, lymph nodes, eyes or skin.
DIAGNOSIS In the nose, it presents with submucosal nodules involving
Biopsy from the nose is diagnostic. It shows necrosis and septum or the inferior turbinate with nasal obstruction, nasal
ulceration of mucosa, epithelioid granuloma and necrotiz- pain and sometimes epistaxis. Nodules may also form in the
ing vasculitis involving small arteries or veins. Erythrocyte nasal vestibule or skin of face.
sedimentation rate is raised. X-ray chest shows diffuse pulmonary infiltrate with hilar
adenopathy. Serum and urinary calcium levels are raised.
TREATMENT Biopsy of the lesions helps to establish the diagnosis.
It consists of systemic steroids and cytotoxic drugs. Cyclo- Treatment is with systemic steroids. For nasal symptoms,
phosphamide and azathioprine, both are found effective. steroids can be used locally as nasal spray.
Miscellaneous Disorders of 29
Nasal Cavity

FOREIGN BODIES RHINOLITH

AETIOLOGY AETIOLOGY
They are mostly seen in children and may be organic or It is stone formation in the nasal cavity. A rhinolith usually
inorganic. Pieces of paper, chalk, button, pebbles and seeds forms around the nucleus of a small exogenous foreign
are the common objects. Pledgets of cotton or swabs may be body, blood clot or inspissated secretions by slow deposition
accidentally left in the nose. of calcium and magnesium salts. Over a period of time, it
grows into a large, irregular mass which fills the nasal cavity
and then may cause pressure necrosis of the septum and/or
CLINICAL FEATURES
lateral wall of nose.
Patient may present immediately if the history of foreign
body is known. If overlooked, the child presents with unilat-
eral nasal discharge which is often foul smelling and occa- CLINICAL FEATURES
sionally bloodstained. It is a dictum that “If a child presents Rhinoliths are more common in adults. Its common pre-
with unilateral, foul-smelling nasal discharge, foreign body must sentation is unilateral nasal obstruction and foul-smelling
be excluded.” Occasionally, a radiograph of the nose is useful discharge which is very often bloodstained. Frank epistaxis
to confirm and localize a foreign body if it is radio-opaque. and neuralgic pain may result from ulceration of the sur-
In addition to overlooked foreign body in the nose, other rounding mucosa.
important causes for unilateral blood-stained discharge in a On examination, a grey brown or greenish-black mass
child are rhinolith, nasal diphtheria, nasal myiasis and acute with irregular surface and stony hard feel is seen in the nasal
or chronic unilateral sinusitis. cavity between the septum and turbinates. It is often brittle
and a portion of it may break off while manipulating. Some-
TREATMENT times it is surrounded by granulations.
Pieces of paper or cotton swabs can be easily removed with
a pair of forceps. Rounded foreign bodies can be removed TREATMENT
by passing a blunt hook (a eustachian catheter is a good
They are removed under general anaesthesia. Most of them
instrument) past the foreign body and gently dragging it
can be removed through anterior nares. Large ones need
forward along the floor. In babies and uncooperative chil-
to be broken into pieces before removal. Some particularly
dren, general anaesthesia with cuffed endotracheal tube is
hard and irregular ones require lateral rhinotomy.
used. Patient is placed in Rose’s position, a pack is inserted
into the nasopharynx and the foreign body retrieved with a
forceps or a hook. Foreign bodies lodged far behind in the
nose may need to be pushed into the nasopharynx before NASAL MYIASIS (MAGGOTS IN NOSE)
removal. A nasal endoscope is very useful to locate the for-
eign body and carefully remove it. Maggots are larval forms of flies. They are seen to infest
nose, nasopharynx and paranasal sinuses causing exten-
sive destruction (Figures 29.1 A, B, C and 29.2). Flies,
COMPLICATIONS
particularly of the genus Chrysomyia, are attracted by the
A foreign body left in the nose may result in: foul-­smelling discharge emanating from cases of atrophic
rhinitis, syphilis, leprosy or infected wounds and lay eggs,
1. nasal infection and sinusitis.
about 200 at a time, which within 24 h hatch into larvae.
2. rhinolith formation.
In India, they are mostly seen from the month of August to
3. inhalation into the tracheobronchial tree.
October.

161
162 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

A B C
Figure 29.1 Maggots nose. (A) Swelling of nose and puffy eyelids with serosanguinous nasal discharge. (B) Maggots have practically destroyed
the cheek and eye in this old and neglected lady. (C) Perforation of palate (arrow).

A B
Figure 29.2 (A) The maggot. (B) The fly responsible for maggots.

CLINICAL FEATURES slough, crusts and dead maggots. A patient with mag-
gots should be isolated with a mosquito net to avoid con-
In the first 3 or 4 days maggots produce intense irritation, tact with flies which can perpetuate this cycle. All patients
sneezing, lacrimation and headache. Thin blood-stained should receive instruction for nasal hygiene before leaving
discharge oozes from the nostrils. The eyelids and lips the hospital.
become puffy. Till this time patient is not aware of mag-
gots. He may present simply as a case of epistaxis. It is only
on the third or fourth day that the maggots may crawl NASAL SYNECHIA
out of the nose. Patient has foul smell surrounding him.
Maggots cause extensive destruction to nose, sinuses, soft Adhesion formation between the nasal septum and turbi-
tissue of face, palate and the eyeball. Fistulae may form nates by scar tissue is often the result of injury to opposing
in the palate or around the nose. Death may occur from surfaces of nasal mucosa. It can result from intranasal opera-
meningitis. tions such as septal surgery, polypectomy, removal of foreign
bodies, reduction of nasal fractures, endoscopic sinus sur-
gery or even intranasal packing. Severe infections which
TREATMENT
cause ulcerative lesions in the nose can also lead to synechia
All visible maggots should be picked up with forceps. Many formation.
of them try to retreat into darker cavities when light falls Nasal synechia (Figure 29.3) often cause nasal obstruction
on them. Instillation of chloroform water and oil kills or may impede drainage from the sinuses resulting in sinusitis,
them. Nasal douche with warm saline is used to remove headache and nasal discharge.
CHAPTER 29 — MISCELLANEOUS DISORDERS OF NASAL CAVITY 163

a
b

Figure 29.4 Sites of leakage: (a) frontal sinus, (b) ethmoid sinus,
Figure 29.3 Nasal synechia left. (c) sphenoid sinus, and (d) eustachian tube (temporal bone fracture).

Treatment is removal of synechia and prevention of the PHYSIOLOGY


opposing raw surfaces to come into contact with each other
by placing a thin silastic or a cellophane sheet between CSF forms a jacket of fluid round the brain and spinal cord
them. This is changed every two or three days till healing acting as a buffer against sudden jerks. It is secreted by cho-
is complete. roid plexuses in the lateral, third and fourth ventricles and
is absorbed into the dural venous sinuses by arachnoid villi.
Villi have one-way valve mechanism allowing CSF of the
CHOANAL ATRESIA subarachnoid space to be absorbed into the blood but not
vice versa. Total volume of CSF varies from 90 to 150 mL.
It is due to persistence of bucconasal membrane and may It is secreted at the rate of about 20 mL/h (350–500 mL/
be unilateral or bilateral, complete or incomplete, bony day). Thus total CSF is replaced three to five times every
(90%) or membranous (10%). Unilateral atresia is more day. Normal CSF pressure at lumbar puncture is 50–150 mm
common and may remain undiagnosed until adult life. H2O. CSF pressure rises on coughing, sneezing, nose blow-
Bilateral atresia presents with respiratory obstruction as the ing, straining on stools or lifting heavy weight―activities
newborn, being a natural nose breather, does not breathe which should be avoided in cases of CSF leak or after its
from mouth. Diagnosis of choanal atresia can be made by repair.
(i) presence of mucoid discharge in the nose, (ii) absence
of air bubbles in the nasal discharge, (iii) failure to pass a
AETIOLOGY
catheter from nose to pharynx, (iv) putting a few drops of
a dye (methylene blue) into the nose and seeing its pas- • Trauma. Most of the cases follow trauma. It can be
sage into the pharynx, or (v) flexible nasal endoscopy, (vi) accidental or surgical. Surgical trauma includes endo-
installing radio-opaque dye into the nose and taking a lat- scopic sinus surgery, trans-sphenoidal hypophysectomy,
eral film, and (vii) computed tomography (CT) scan in nasal polypectomy or skull base surgery. In endoscopic
axial plane is more useful. sinus surgery, CSF leak may be immediate or delayed in
Emergency management may be required in bilateral onset.
choanal atresia to provide an airway. A feeding nipple with • Inflammations. Mucoceles of sinuses, sinunasal polyposis,
a large hole provides a good oral airway (McGovern’s tech- fungal infection of sinuses and osteomyelitis, can all erode
nique) and obviates the need for tracheostomy. Definitive the bone and dura.
treatment consists of correction of atresia by transnasal or • Neoplasms. Tumours, both benign and malignant, invading
transpalatal approach. The latter is usually done at one the skull base.
and a half years. Choanal atresia can be corrected by using • Congenital lesions. Meningocele, meningoencephaloceles
nasal endoscopes and drill. Removal of a part of posterior and gliomas can have associated skull base defect.
nasal septum transnasally is another option to treat such • Idiopathic. Where cause is unknown and patient has
cases. spontaneous leak.

SITES OF LEAKAGE
CSF RHINORRHOEA
CSF from anterior cranial fossa reaches the nose via (i) crib-
DEFINITION riform plate, (ii) roof of ethmoid air cells or (iii) frontal
sinus. CSF from middle cranial fossa follows injuries to sphe-
Leakage of CSF into the nose is called CSF rhinorrhoea. noid sinus. In fractures of temporal bone, CSF reaches the
It may be clear fluid or mixed with blood as in acute head middle ear and then escapes through the eustachian tube
injuries. into the nose (CSF otorhinorrhoea) (Figure 29.4).
164 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Table 29.1 Differences between CSF and nasal secretions

Features CSF fluid Nasal secretion


History Nasal or sinus surgery, head injury or intracranial tumour Sneezing, nasal stuffiness, itching in the
nose or lacrimation
Flow of discharge A few drops or a stream of fluid gushes down when Continuous, no effect of bending forward
bending forward or straining; cannot be sniffed back or straining. Can be sniffed back
Character of discharge Thin, watery and clear Slimy (mucus) or clear (tears)
Taste Sweet Salty
Sugar content More than 30 mg/dL (Compare with sugar in CSF after Less than 10 mg/dL
lumbar puncture as sugar is less in CSF in meningitis.)
Presence of β2 transferrin Always present. It is specific for CSF Always absent

DIAGNOSIS Patient lies in 10° head down position for sometime. Dye
can be detected intranasally with the help of endoscope.
There is history of clear watery discharge from the nose on Dye appears bright yellow but when seen with a blue filter
bending the head or straining. It may be seen on rising in the it appears fluorescent green. One should examine olfac-
morning when patient bends his head (reservoir sign—fluid tory cleft (cribriform plate), middle meatus (frontal and
which had collected in the sinuses, particularly sphenoid, ethmoidal sinuses), sphenoethmoidal recess (sphenoid
empties into the nose). CSF rhinorrhoea should be differ- sinus) and area of torus tubarius (temporal bone frac-
entiated from nasal discharge of allergic or vasomotor rhi- ture) to localize the lesion.
nitis as the former is sudden, gushes in drops when bending Use of intrathecal radioactive substances has been
and cannot be sniffed back. Nasal discharge, because of its abandoned.
mucus content, also stiffens the handkerchief (Table 29.1). 4. CT cisternogram. It requires intrathaecal injection of
CSF rhinorrhoea after head trauma is mixed with blood iohexol and a CT scan to localize the site in cases when
and shows double target sign when collected on a piece of fil- beta-2 transferrin cannot be done. Now it is not favoured
ter paper. It shows central red spot (blood) and peripheral by many.
lighter halo.
Nasal endoscopy can help to localize CSF leak in some
cases. Otoscopic/microscopic examination of the ear may TREATMENT
reveal fluid in the middle ear in cases of otorhinorrhoea. Early cases of post-traumatic CSF rhinorrhoea can be man-
aged by conservative measures such as bed rest, elevating
LABORATORY TESTS the head of the bed, stool softeners, and avoidance of nose
blowing, sneezing and straining. Prophylactic antibiotics
Beta-2 transferrin is a protein seen in CSF and not in the can be used to prevent meningitis. Acetazolamide decreases
nasal discharge. Its presence is a specific and sensitive test CSF formation. These measures can be combined with lum-
and requires only a few drops of CSF. The specimen of nasal bar drain if indicated.
discharge is tested for this protein. Perilymph and aqueous Surgical repair can be done by the following:
humour are the only other fluids which contain this protein.
Another protein called beta trace protein is also specific for 1. Neurosurgical intracranial approach.
CSF and is widely used in Europe. It is secreted by menin- 2. Extradural approaches such as external ethmoidec-
ges and choroid plexus. Facilities to test these proteins are tomy for cribriform plate and ethmoid area, trans-septal
not easily available everywhere. Glucose testing by oxidase sphenoidal approach for sphenoid and osteoplastic flap
­peroxidase or biochemical estimation are no longer used. approach for frontal sinus leak.
3. Transnasal endoscopic approach. With the advent of
endoscopic surgery for nose and sinuses, most of the
LOCALIZATION OF SITE
leaks from the anterior cranial fossa and sphenoid sinus
1. High-resolution CT scan. Cuts are taken at 1–2 mm. Both can be managed endoscopically with a success rate of
coronal and axial cuts are important to see the bony 90% with first attempt. Principles of repair include:
defects. Axial cuts show any defects of frontal or sphe- (a) Defining the sites of bony defect (Figure 29.5). It can be
noid sinus. (i) Cribriform plate
2. MRI. T2-weighted image MRI is useful in depicting the (ii) Lateral lamina close to anterior ethmoid artery
site of leak. It requires that CSF leak is active at the time (iii) Roof of ethmoid
of scan. It is a noninvasive test. It is indicated also if (iv) Frontal sinus leak
encephalocele or intracranial pathology is suspected. (v) Sphenoid sinus
3. Intrathecal fluorescein study. It can be done preopera- (b) Preparation of graft site.
tively to diagnose the site or intraoperatively at the time (c) Underlay grafting of the fascia extradurally followed
of repair. It is an invasive procedure. Only 0.25–0.5 mL by placement of mucosa (as a free graft or pedicled
of 5% fluorescein diluted with 10 mL of CSF is injected. flap) (Figure 29.6).
CHAPTER 29 — MISCELLANEOUS DISORDERS OF NASAL CAVITY 165

(b) Ethmoid roof (a) Cribriform plate Brain


Pia mater
Arachnoid
Graft Dura
Orbit
Middle turbinate Bone
Mucosa

Surgicel
Septum Gelfoam

Figure 29.5 Sites of bony defect: (a) cribriform plate and (b) ethmoid Pack
roof. Figure 29.6 Repair of CSF rhinorrhoea.

Sometimes fat from the thigh or abdomen is used to


(d) If bony defect is larger than 2 cm, it is repaired with
plug the defect in place of fascia graft.
cartilage (from nasal septum or auricular concha)
(f) Lumbar drain if CSF pressure is high.
followed by placement of mucosa.
(g) Antibiotics
(e) Placement of surgicel and gelfoam further strength-
ens the area. This is followed by a high antibiotic CSF leak from frontal sinus often requires osteoplastic flap,
smeared nasal pack. operation and obliteration of the sinus with fat.
30 Allergic Rhinitis

It is an IgE-mediated immunologic response of nasal


mucosa to airborne allergens and is characterized by watery PATHOGENESIS
nasal discharge, nasal obstruction, sneezing and itching in
the nose. This may also be associated with symptoms of itch- Inhaled allergens produce specific IgE antibody in the geneti-
ing in the eyes, palate and pharynx. Two clinical types have cally predisposed individuals. This antibody becomes fixed to
been recognized: the blood basophils or tissue mast cells by its Fc end (Figure
30.1). On subsequent exposure, antigen combines with IgE
1. Seasonal. Symptoms appear in or around a particular antibody at its Fab end. This reaction produces degranulation
season when the pollens of a particular plant, to which of the mast cells with release of several chemical mediators,
the patient is sensitive, are present in the air. some of which already exist in the preformed state while oth-
2. Perennial. Symptoms are present throughout the year. ers are synthesized afresh. These mediators (Figure 30.2) are
responsible for symptomatology of allergic disease. Depend-
ing on the tissues involved, there may be vasodilation, muco-
AETIOLOGY sal oedema, infiltration with eosinophils, excessive secretion
from nasal glands or smooth muscle contraction. A “priming
Inhalant allergens. They may be seasonal or perennial. affect” has also been described, i.e. mucosa earlier sensitized
Seasonal allergens include pollens from trees, grasses and to an allergen will react to smaller doses of subsequent specific
weeds. They vary geographically. The knowledge of pol- allergen. It also gets “primed” to other nonspecific antigens
len appearing in a particular area and the season in which to which patient was not exposed (Figure 30.3). Nonspecific
they occur is important. Their knowledge also helps in nasal hyper-reactivity is seen in patients of allergic rhinitis.
skin tests. Perennial allergens are present throughout There is increased nasal response to normal stimuli result-
the year regardless of the season. They include molds, ing in sneezing, rhinorrhoea and nasal congestion. Clinically,
dust mites, cockroaches and dander from animals. Dust allergic response occurs in two phases:
includes dust mite, insect parts, fibres and animal dan-
ders. Dust mites live on skin scales and other debris and 1. Acute or early phase. It occurs immediately within
are found in the beddings, mattresses, pillows, carpets 5–30 min, after exposure to the specific allergen and
and upholstery. consists of sneezing, rhinorrhoea nasal blockage and/or
Genetic predisposition plays an important part. bronchospasm. It is due to release of vasoactive amines
Chances of children developing allergy are 20 and 47%, like histamine.
respectively, if one or both parents suffer from allergic 2. Late or delayed phase. It occurs 2–8 h after exposure
diathesis. to allergen without additional exposure. It is due to

Fab end Heavy chain Antigen

Light chain Antibody


SS
SS SS
Mast cell
SS
Mediator release

Tail Newly synthesized mediators


Preformed
mediators

A Fc end B
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.

166
CHAPTER 30 — ALLERGIC RHINITIS 167

infiltration of inflammatory cells—eosinophils, neutro- salute), pale and oedematous nasal mucosa which may
phils, basophil, monocytes and CD4 + T cells at the site appear bluish. Turbinates are swollen. Thin, watery or
of antigen deposition causing swelling, congestion and mucoid discharge is usually present.
thick secretion. In the event of repeated or continuous • Ocular signs include oedema of lids, congestion and cobble-
exposure to allergen, acute phase symptomatology over- stone appearance of the conjunctiva, and dark circles under
laps the late phase. the eyes (allergic shiners).
• Otologic signs include retracted tympanic membrane or
serous otitis media as a result of eustachian tube blockage.
CLINICAL FEATURES • Pharyngeal signs include granular pharyngitis due to
hyperplasia of submucosal lymphoid tissue. A child with
There is no age or sex predilection. It may start in infants as perennial allergic rhinitis may show all the features of pro-
young as 6 months or older people. Usually the onset is at longed mouth breathing as seen in adenoid hyperplasia.
12–16 years of age. • Laryngeal signs include hoarseness and oedema of the
The cardinal symptoms of seasonal nasal allergy include par- vocal cords.
oxysmal sneezing, 10–20 sneezes at a time, nasal obstruc-
tion, watery nasal discharge and itching in the nose. Itching
may also involve eyes, palate or pharynx. Some may get DIAGNOSIS
bronchospasm. The duration and severity of symptoms may
vary with the season. New Allergic Rhinitis and Its Impact on Asthma (ARIA) clas-
Symptoms of perennial allergy are not so severe as that of sification (Table 30.1). It is based on duration and symp-
the seasonal type. They include frequent colds, persistently toms of disease. Duration of symptoms is subdivided into
stuffy nose, loss of sense of smell due to mucosal oedema, intermittent or persistent and severity of disease into mild,
postnasal drip, chronic cough and hearing impairment due moderate or severe.
to eustachian tube blockage or fluid in the middle ear. This new system of classification helps in treatment
Signs of allergy may be seen in the nose, eyes, ears, phar- guidelines.
ynx or larynx. A detailed history and physical examination is helpful,
and also gives clues to the possible allergen. Other causes of
• Nasal signs include transverse nasal crease—a black line nasal stuffiness should be excluded.
across the middle of dorsum of nose due to constant
upward rubbing of nose simulating a salute (allergic
INVESTIGATIONS
Sensitized
mast cell
Antigen 1. Total and differential count. Peripheral eosinophilia may
be seen but this is an inconsistent finding.
Release of mediators
Specific allergic stimulus Nonspecific stimuli
(IgE-mediated) • Weather changes
Preformed Newly synthesized (Temp-humidity)
• Emotional stimuli
• Histamine • Prostaglandins, • Salicylates
• ECF-A e.g. PGD2 • Viral infections
• NCF-A • Leukotrienes, • Air pollution
• Heparin e.g. SRS-A
• Others • PAF
• Thromboxane A Mast cell or blood basophil
• TNF
Histamine Vasodilatation, bronchospasm
Drop in cAMP/cGMP ratio
ECF-A Eosinophil chemotactic factor of anaphylaxis—
attracts eosinophils to the site of reaction
NCF-A Neutrophil chemotactic factor—attracts
Release of preformed and
neutrophils
newly formed mediators
Heparin Enhances phagocytosis
Prostaglandins Vasoactive and bronchospastic
Leukotriene Vasoactive and bronchospastic Increased vascular Change in smooth Hyperactivity
permeability and muscle tone of glands
PAF Platelet aggregating factor. Histamine and vasodilatation
serotonin are released from platelets. Causes
chemotaxis of neutrophils and eosinophils
Thromboxane A Spasmogenic Tissue oedema Increased secretion

TNF Tumour necrosis factor. Helps transmigration


of neutrophils and eosinophils and attracts Nasal blockage Bronchospasm Rhinorrhoea
them to the site of reaction Figure 30.3 Both allergic and nonspecific stimuli act on mast cells
Figure 30.2 Release of mediators from mast cell when challenged or blood basophils releasing several mediator substances responsible
by allergic or nonspecific stimuli. for symptomatology of allergy.
168 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

5. Bronchial asthma. Patients of nasal allergy have four


Table 30.1 Classification of allergic rhinitis (ARIA) times more risk of developing bronchial asthma. Twenty
to thirty per cent of patients with rhinitis have asthma.
• D uration of disease
• Intermittent: Symptoms are present
– Less than 4 days a week or TREATMENT
– For less than 4 weeks
• Persistent: Symptoms are present
– More than 4 days a week or
Treatment can be divided into:
– For more than 4 weeks 1. Avoidance of allergen.
• Severity of disease 2. Treatment with drugs.
• Mild: None of the following symptoms are present 3. Immunotherapy.
– Sleep disturbance
– Impairment of daily activities, leisure and sport
– Impairment of school or work
1. Avoidance of allergen. This is most successful if the anti-
– Troublesome symptoms gen involved is single. Removal of a pet from the house,
• Moderate to severe: One or more of the above symptoms encasing the pillow or mattress with plastic sheet, change of
are present place of work or sometimes change of job may be required.
A particular food article to which the patient is found aller-
gic can be eliminated from the diet.
2. Nasal smear. It shows large number of eosinophils in 2. Treatment with drugs
allergic rhinitis. Nasal smear should be taken at the time
(a) Antihistaminics. They control rhinorrhoea, sneezing
of clinically active disease or after nasal challenge test.
and nasal itch. All antihistaminics have the side effect
Nasal eosinophilia is also seen in certain nonallergic rhi-
of drowsiness; some more than the other. The dose
nitis, e.g. NARES (nonallergic rhinitis with eosinophilia
and type of the antihistaminic has to be individualized.
syndrome).
If one antihistaminic is not effective, another may be
3. Skin tests. These tests help to identify specific allergen.
tried from a different class.
They are prick, scratch and intradermal tests.
(b) Sympathomimetic drugs (oral or topical). Alpha-adrenergic
(a)  Skin prick test. This is an excellent method to demon-
drugs constrict blood vessels and reduce nasal conges-
strate the allergen. A drop of concentrated allergen
tion and oedema. They also cause central nervous sys-
solution is placed on the volar surface of the forearm
tem stimulation and are often given in combination
or back and a sharp needle pricked into the dermis
with antihistaminics to counteract drowsiness. Pseu-
through the drop. It introduces the allergen into the
doephedrine and phenylephrine are often combined
dermis. A positive reaction is manifested by the for-
with antihistaminics for oral administration.
mation of a central wheal and a surrounding zone of
Topical use of sympathomimetic drugs causes nasal
erythema (flare) within 10–15 min.
decongestion. Phenylephrine, oxymetazoline and xylo-
Simultaneously a control test is performed with
metazoline are often used to relieve nasal obstruction,
histamine and the diluent used in allergen solution.
but are notorious to cause severe rebound congestion.
(b) Specific IgE measurements. It is an in vitro test to find
Patient resorts to using more and more of them to
the specific allergen. There is a good correlation
relieve nasal obstruction. This vicious cycle leads to rhi-
between the skin tests and specific IgE measure-
nitis medicamentosa.
ments. However both false positive and false nega-
(c) Corticosteroids. Oral corticosteroids are very effective in
tive results can occur. It is therefore recommended
controlling the symptoms of allergic rhinitis but their
to correlate the two tests with clinical symptoms.
use should be limited to acute episodes which have not
4. Radioallergosorbent test (RAST). It is an in vitro test
been controlled by other measures. They have several
and measures specific IgE antibody concentration in the
systemic side effects.
patient’s serum.
Topical steroids such as beclomethasone dipropio-
5. Nasal provocation test. A crude method is to challenge the
nate, budesonide, flunisolide acetate, fluticasone and
nasal mucosa with a small amount of allergen placed at
mometasone inhibit recruitment of inflammatory cells
the end of a toothpick and asking the patient to sniff into
into the nasal mucosa and suppress late-phase allergic
each nostril and to observe if allergic symptoms are repro-
reaction, are used as aerosols and are very effective in
duced. More sophisticated techniques are available now.
the control of symptoms. They have also been used
in rhinitis medicamentosa while withdrawing topical
use of decongestant nasal drops. Topical steroids have
COMPLICATIONS fewer systemic side effects but their continuous use may
cause mucosal atrophy and even septal perforation. It is
Nasal allergy may cause:
wise to break their use for 1–2 weeks every 2–3 months.
1. Recurrent sinusitis because of obstruction to the sinus They may also promote growth of fungus.
ostia. (d) Sodium cromoglycate. It stabilizes the mast cells and pre-
2. Formation of nasal polypi in about 2%. vents them from degranulation despite the formation
3. Serous otitis media. of IgE-antigen complex. It is used as 2% solution for
4. Orthodontic problems and other ill-effects of prolonged nasal drops or spray or as an aerosol powder. It is useful
mouth breathing especially in children. both in seasonal and perennial allergic rhinitis.
CHAPTER 30 — ALLERGIC RHINITIS 169

(e) Anticholinergics. They block rhinorrhoea both of the Subcutaneous immunotherapy is often used but now sub-
allergic and nonallergic rhinitis. Ipratropium bromide lingual and nasal routes are also being employed. The latter
has been used as nasal spray to control rhinorrhoea. can be used with doses 20–100 times greater than used by
There are no systemic side effects. the subcutaneous route.
(f) Leukotriene receptor antagonists. They include montelu- A step care approach is recommended by ARIA for aller-
kast, pranlukast and zafirlukast. They block cysteinyl gic rhinitis treatment.
leukotriene type receptors. They are well-tolerated and
• O ral antihistamines or intranasal cromolyn sodium is rec-
have few side effects.
ommended for mild intermittent disease.
(g) Anti-IgE. It reduces the IgE level and has an anti-
• For allergic symptoms of moderate severity or for per-
inflammatory effect. Omalizumab is such a drug. It is
sistent disease intranasal corticosteroids can be used as
indicated in children above 12 years who have moder-
monotherapy.
ate to severe asthma. It is not yet approved for allergic
• For severe symptoms, combination therapy with oral non-
rhinitis.
sedating antihistamines and intranasal steroids is used.
• For severe and persistent symptoms in spite of the above
3. Immunotherapy. Immunotherapy or hyposensitization treatment a short course of oral steroids and immuno-
is used when drug treatment fails to control symptoms or therapy is recommended.
produces intolerable side effects. Allergen is given in gradu- • If nasal obstruction persists a short course of intranasal
ally increasing doses till the maintenance dose is reached. decongestant can be used. Oral decongestant can be com-
Immunotherapy suppresses the formation of IgE. It also bined with antihistamines.
raises the titre of specific IgG antibody. Immunotherapy has • Avoid allergen and irritants in all forms of disease. Nonal-
to be given for a year or so before significant improvement lergic rhinitis can coexist with allergic rhinitis. Nonspe-
of symptoms can be noticed. It is discontinued if uninter- cific stimuli produce allergic rhinitis-like symptoms due to
rupted treatment for 3 years shows no clinical improvement. hyper-reactivity of nasal mucosa.
31 Vasomotor and Other Forms
of Nonallergic Rhinitis

TREATMENT
VASOMOTOR RHINITIS (VMR)
MEDICAL
It is nonallergic rhinitis but clinically simulating nasal allergy 1. Avoidance of physical factors which provoke symptoms,
with symptoms of nasal obstruction, rhinorrhoea and sneez- e.g. sudden change in temperature, humidity, blasts of
ing. One or the other of these symptoms may predominate. air or dust.
The condition usually persists throughout the year and all 2. Antihistaminics and oral nasal decongestants are helpful
the tests of nasal allergy are negative. in relieving nasal obstruction, sneezing and rhinorrhoea.
3. Topical steroids (e.g. beclomethasone dipropionate,
PATHOGENESIS budesonide or fluticasone), used as spray or aerosol, are
useful to control symptoms.
Nasal mucosa has rich blood supply. Its vasculature is similar 4. Systemic steroids can be given for a short time in very
to the erectile tissue in having venous sinusoids or “lakes” severe cases.
which are surrounded by fibres of smooth muscle which act 5. Psychological factors should be removed. Tranquillizers
as sphincters and control the filling or emptying of these may be needed in some patients.
sinusoids. Sympathetic stimulation causes vasoconstriction
and shrinkage of mucosa, while parasympathetic stimula- SURGICAL
tion causes vasodilation and engorgement. Overactivity of 1. Nasal obstruction can be relieved by measures which
parasympathetic system also causes excessive secretion from reduce the size of nasal turbinates (see hypertrophic rhini-
the nasal glands. tis). Other associated causes of nasal obstruction, e.g. polyp,
Autonomic nervous system is under the control of hypothal- deviated nasal septum, should also be corrected.
amus and therefore emotions play a great role in vasomotor 2. Excessive rhinorrhoea, not corrected by medical therapy
rhinitis. Autonomic system is unstable in cases of vasomotor and bothersome to the patient, can be relieved by sec-
rhinitis. Nasal mucosa is also hyper-reactive and responds tioning the parasympathetic secretomotor fibres to nose
to several nonspecific stimuli, e.g. change in temperature, (vidian neurectomy).
humidity, blasts of air, small amounts of dust or smoke.

SYMPTOMS OTHER FORMS OF NONALLERGIC RHINITIS


1. Paroxysmal sneezing. Bouts of sneezing start just after Nasal mucosa responds to several different stimuli produc-
getting out of the bed in the morning. ing symptoms of rhinitis. Some of these conditions have
2. Excessive rhinorrhoea. This accompanies sneezing or this acquired specific eponyms. Some authorities categorize
may be the only predominant symptom. It is profuse and them under the catch-all term of vasomotor rhinitis.
watery and may even wet several handkerchiefs. The nose
may drip when the patient leans forward and this may need 1. Drug-induced rhinitis. Several antihypertensive drugs
to be differentiated from CSF rhinorrhoea (see p. 163). such as reserpine, guanethidine, methyl dopa and propran-
3. Nasal obstruction. This alternates from side to side. Usu- olol are sympathetic blocking agents and cause nasal stuffi-
ally more marked at night. It is the dependent side of ness. Some anticholinesterase drugs, e.g. neostigmine, used
nose which is often blocked when lying on one side. in the treatment of myasthenia gravis, have acetylcholine
4. Postnasal drip. like action and cause nasal obstruction. Contraceptive pills
also cause nasal obstruction because of oestrogens.
SIGNS 2. Rhinitis medicamentosa. Topical decongestant nasal
drops are notorious to cause rebound phenomenon. Their
Nasal mucosa over the turbinates is generally congested and
excessive use causes rhinitis. It is treated by withdrawal of
hypertrophic. In some, it may be normal.
nasal drops, short course of systemic steroid therapy and
in some cases, surgical reduction of turbinates, if they have
COMPLICATIONS become hypertrophied.
Long-standing cases or VMR develop nasal polypi, hypertro- 3. Rhinitis of pregnancy. Pregnant women may develop
phic rhinitis and sinusitis. persistent rhinitis due to hormonal changes. Nasal mucosa

170
CHAPTER 31 — VASOMOTOR AND OTHER FORMS OF NONALLERGIC RHINITIS 171

becomes oedematous and blocks the airway. Some may parasympathetic activity causing nasal stuffiness and “colds.”
develop secondary infection and even sinusitis. In such Replacement of thyroid hormone relieves the condition.
cases, care should be taken while prescribing drugs. Gener-
ally, local measures such as limited use of nasal drops, topi- 7. Gustatory rhinitis. Spicy and pungent food may in some
cal steroids and limited surgery (cryosurgery) to turbinates people produce rhinorrhoea, nasal stuffiness, lacrimation,
are sufficient to relieve the symptoms. Safety of the devel- sweating and even flushing of face. This is a cholinergic
oping fetus is not established for newer antihistaminics and response to stimulation of sensory receptors on the palate.
they should be avoided. Spicy food, particularly the red pepper, contains capsaicin
which is known to stimulate sensory nerves. It can be relieved
4. Honeymoon rhinitis. This usually follows sexual excite- by ipratropium bromide nasal spray (an anticholinergic),
ment leading to nasal stuffiness. a few minutes before meals.
5. Emotional rhinitis. Nose may react to several emotional 8. Nonairflow rhinitis. It is seen in patients of laryngectomy
stimuli. Psychological states like anxiety, tension, hostility, and tracheostomy. Nose is not used for airflow and the tur-
humiliation, resentment and grief are all known to cause binates become swollen due to loss of vasomotor control.
rhinitis. Treatment is proper counselling for psychological Similar changes are also seen in nasopharyngeal obstruc-
adjustment. Imipramine, which has both antidepressant tion due to choanal atresia or adenoidal hyperplasia, the
and anticholinergic effects, has been found useful. latter having the additional factor of infection due to stagna-
6. Rhinitis due to hypothyroidism. Hypothyroidism leads to tion of discharge in the nasal cavity which should otherwise
hypoactivity of the sympathetic system with predominance of drain freely into the nasopharynx.
32 Nasal Polypi

Nasal polypi are non-neoplastic masses of oedematous nasal PATHOLOGY


or sinus mucosa.They are divided into two main varieties:
In early stages, surface of nasal polypi is covered by ciliated
1. Bilateral ethmoidal polypi. columnar epithelium like that of normal nasal mucosa but
2. Antrochoanal polyp. later it undergoes a metaplastic change to transitional and
squamous type on exposure to atmospheric irritation. Submu-
cosa shows large intercellular spaces filled with serous fluid.
BILATERAL ETHMOIDAL POLYPI There is also infiltration with eosinophils and round cells.

AETIOLOGY SITE OF ORIGIN


Aetiology of nasal polypi is very complex and not well- Multiple nasal polypi always arise from the lateral wall of
understood. They may arise in inflammatory conditions of nose, usually from the middle meatus. Common sites are
nasal mucosa (rhinosinusitis), disorders of ciliary motility or uncinate process, bulla ethmoidalis, ostia of sinuses, medial
abnormal composition of nasal mucus (cystic fibrosis). Vari- surface and edge of middle turbinate. Allergic nasal polypi
ous diseases associated with the formation of nasal polypi almost never arise from the septum or the floor of nose.
are:
1. Chronic rhinosinusitis. Polypi are seen in chronic rhino- SYMPTOMS
sinusitis of both allergic and nonallergic origin. Nonal- 1. Multiple polypi can occur at any age but are mostly seen
lergic rhinitis with eosinophilia syndrome (NARES) is a in adults.
form of chronic rhinitis associated with polypi. 2. Nasal stuffiness leading to total nasal obstruction may be
2. Asthma. Seven per cent of the patients with asthma of the presenting symptom.
atopic or nonatopic origin show nasal polypi. 3. Partial or total loss of sense of smell.
3. Aspirin intolerance. Thirty-six per cent of the patients 4. Headache due to associated sinusitis.
with aspirin intolerance may show polypi. Samter’s triad 5. Sneezing and watery nasal discharge due to associated
consists of nasal polypi, asthma and aspirin intolerance. allergy.
4. Cystic fibrosis. Twenty per cent of patients with cystic 6. Mass protruding from the nostril.
fibrosis form polypi. It is due to abnormal mucus.
5. Allergic fungal sinusitis. Almost all cases of fungal sinus-
SIGNS
itis form nasal polypi.
6. Kartagener syndrome. This consists of bronchiectasis On anterior rhinoscopy, polypi appear as smooth, glistening,
sinusitis, situs inversus and ciliary dyskinesis. grape-like masses often pale in colour. They may be sessile
7. Young syndrome. It consists of sinopulmonary disease or pedunculated, insensitive to probing and do not bleed on
and azoospermia. touch. Often they are multiple and bilateral. Long-standing
8. Churg–Strauss syndrome. Consists of asthma, fever, cases present with broadening of nose and increased inter-
eosinophilia, vasculitis and granuloma. canthal distance. A polyp may protrude from the nostril
9. Nasal mastocytosis. It is a form of chronic rhinitis in and appear pink and vascular simulating neoplasm (Figure
which nasal mucosa is infiltrated with mast cells but 32.1). Nasal cavity may show purulent discharge due to asso-
few eosinophils. Skin tests for allergy and IgE levels are ciated sinusitis.
normal. Probing of a solitary ethmoidal polyp may be necessary to
differentiate it from hypertrophy of the turbinate or cystic
middle turbinate.
PATHOGENESIS
DIAGNOSIS
Nasal mucosa, particularly in the region of middle meatus
and turbinate, becomes oedematous due to collection of Diagnosis can be easily made on clinical examination. Com-
extracellular fluid causing polypoidal change. Polypi which puted tomography (CT) scan of paranasal sinuses is essen-
are sessile in the beginning become pedunculated due to tial to exclude the bony erosion and expansion suggestive of
gravity and excessive sneezing. neoplasia. Simple nasal polypi may sometimes be associated

172
CHAPTER 32 — NASAL POLYPI 173

with malignancy underneath, especially in people above


40 years and this must be excluded by histological exami- ANTROCHOANAL POLYP (SYN. KILLIAN’S
nation of the suspected tissue. CT scan also helps to plan POLYP)
surgery.
This polyp arises from the mucosa of maxillary antrum near
TREATMENT its accessory ostium, comes out of it and grows in the choana
and nasal cavity. Thus it has three parts.
CONSERVATIVE
1. Antral, which is a thin stalk.
1. Early polypoidal changes with oedematous mucosa may 2. Choanal, which is round and globular.
revert to normal with antihistaminics and control of 3. Nasal, which is flat from side to side.
allergy.
2. A short course of steroids may prove useful in case of peo-
ple who cannot tolerate antihistaminics and/or in those AETIOLOGY
with asthma and polypoidal nasal mucosa. They may also Exact cause is unknown. Nasal allergy coupled with sinus
be used to prevent recurrence after surgery. Contrain- infection is incriminated. Antrochoanal polypi are seen
dications to use of steroids, e.g. hypertension, peptic in children and young adults. Usually they are single and
ulcer, diabetes, pregnancy and tuberculosis should be unilateral.
excluded.

SURGICAL SYMPTOMS
1. Polypectomy. One or two polyps which are pedunculated Unilateral nasal obstruction is the presenting symptom.
can be removed with snare. Multiple and sessile polypi Obstruction may become bilateral when polyp grows into
require special forceps. the nasopharynx and starts obstructing the opposite choana
2. Intranasal ethmoidectomy. When polypi are multiple (Tables 32.1 and 32.2). Voice may become thick and dull
and sessile, they require uncapping of the ethmoidal air due to hyponasality. Nasal discharge, mostly mucoid, may be
cells by intranasal route, a procedure called intranasal seen on one or both sides.
ethmoidectomy.
3. Extranasal ethmoidectomy. This is indicated when polypi
recur after intranasal procedures and surgical landmarks SIGNS
are ill-defined due to previous surgery. Approach is As the antrochoanal polyp grows posteriorly, it may be
through the medial wall of the orbit by an external inci- missed on anterior rhinoscopy. When large, a smooth grey-
sion, medial to medial canthus. ish mass covered with nasal discharge may be seen. It is soft
4. Transantral ethmoidectomy. This is indicated when infec- and can be moved up and down with a probe. A large polyp
tion and polypoidal changes are also seen in the maxillary may protrude from the nostril and show a pink congested
antrum. In this case, antrum is opened by Caldwell–Luc look on its exposed part (Figure 32.2).
approach and the ethmoid air cell approached through
the medial wall of the antrum. This procedure is also
superceded by endoscopic sinus surgery.
5. Endoscopic sinus surgery. These days, ethmoidal polypi Table 32.1 Common causes of unilateral nasal
are removed by endoscopic sinus surgery more popularly obstruction
called functional endoscopic sinus surgery (FESS). It is done
with various endoscopes of 0°, 30° and 70° angulation. • Vestibule
Polypi can be removed more accurately when ethmoid • Furuncle
• Vestibulitis
cells are removed, and drainage and ventilation provided
• Stenosis of nares
to the other involved sinuses such as maxillary, sphenoi- • Atresia
dal or frontal. • Nasoalveolar cyst
• Papilloma
• Squamous cell carcinoma
• Nasal cavity
• Foreign body
• Deviated nasal septum (DNS)
• Hypertrophic turbinates
• Concha bullosa
• Antrochoanal polyp
• Synechia
• Rhinolith
• Bleeding polypus of septum
• Benign and malignant tumours of nose and paranasal
sinuses
• Sinusitis, unilateral
• Nasopharynx
Figure 32.1 A polyp protruding from the left nostril in a patient with • Unilateral choanal atresia
bilateral ethmoidal polypi.
174 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Posterior rhinoscopy may reveal a globular mass filling


Table 32.2 Common causes of bilateral nasal the choana or the nasopharynx. A large polyp may hang
obstruction down behind the soft palate and present in the oropharynx
• V estibule
(Figure 32.3 A,B).
• Bilateral vestibulitis Examination of the nose with an endoscope may reveal
• Collapsing nasal alae a choanal or antrochoanal polyp hidden posteriorly in the
• Stenosis of nares nasal cavity (Figure 32.4).
• Congenital atresia of nares See Table 32.3 for differences between antrochoanal and
• Nasal cavity ethmoidal polypi.
• Acute rhinitis (viral and bacterial)
• Chronic rhinitis and sinusitis
• Rhinitis medicamentosa DIFFERENTIAL DIAGNOSIS
• Allergic rhinitis
1. A blob of mucus often looks like a polypus but it would
• Hypertrophic turbinates
• DNS
disappear on blowing the nose.
• Nasal polypi 2. Hypertrophied middle turbinate is differentiated by
• Atrophic rhinitis its pink appearance and hard feel of bone on probe
• Rhinitis sicca testing.
• Septal haematoma 3. Angiofibroma has history of profuse recurrent epistaxis.
• Septal abscess It is firm in consistency and easily bleeds on probing.
• Bilateral choanal atresia 4. Other neoplasms may be differentiated by their fleshy
• Nasopharynx pink appearance, friable nature and their tendency to
• Adenoid hyperplasia bleed.
• Large choanal polyp
• Thornwaldt’s cyst
• Adhesions between soft palate and posterior
pharyngeal wall
• Large benign and malignant tumours

Figure 32.2 Antrochoanal polyp projecting through the left nostril in


a 14-year-old patient. Figure 32.4 Endoscopic view of a choanal polyp right side.

Figure 32.3 (A) Antrochoanal


polyp seen hanging in the orophar-
ynx from behind the soft palate on
A B the right side of uvula. (B) Polyp
after removal.
CHAPTER 32 — NASAL POLYPI 175

Table 32.3 Differences between antrochoanal and ethmoidal polypi

Antrochoanal polypi Ethmoidal polypi


Age Common in children 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 Mostly grow anteriorly and may present at the nares
behind the soft palate
Size and Trilobed with antral, nasal and choanal parts. Usually small and grape-like masses
shape Choanal part may protrude through the choana and fill
the nasopharynx obstructing both sides
Recurrence Uncommon, if removed completely Common
Treatment Polypectomy; endoscopic removal or Caldwell–Luc Polypectomy. Endoscopic surgery or ethmoidectomy
operation if recurrent (which may be intranasal, extranasal or transantral)

X-rays of paranasal sinuses may show opacity of the involved


antrum. X-ray (lateral view), soft tissue nasopharynx, reveals SOME IMPORTANT POINTS TO REMEMBER
a globular swelling in the postnasal space. It is differenti- IN A CASE OF NASAL POLYPI
ated from angiofibroma by the presence of a column of air
behind the polyp. 1. If a polypus is red and fleshy, friable and has granular
surface, especially in older patients, think of malignancy.
2. Simple nasal polyp may masquerade a malignancy under-
neath. Hence all polypi should be subjected to histology.
TREATMENT
3. A simple polyp in a child may be a glioma, an encepha-
An antrochoanal polyp is easily removed by avulsion either locele or a meningoencephalocele. It should always be
through the nasal or oral route. Recurrence is uncommon aspirated and fluid examined for CSF. Careless removal
after complete removal. In cases which do recur, Caldwell– of such polyp would result in CSF rhinorrhoea and
Luc operation may be required to remove the polyp com- meningitis.
pletely from the site of its origin and to deal with coexistent 4. Multiple nasal polypi in children may be associated with
maxillary sinusitis. These days, endoscopic sinus surgery has mucoviscidosis.
superceded other modes of polyp removal. Caldwell–Luc 5. Epistaxis and orbital symptoms associated with a polyp
operation is avoided. should always arouse the suspicion of malignancy.
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.” This
older people. It often presents as an emergency. Epistaxis is area is exposed to the drying effect of inspiratory current
a sign and not a disease per se and an attempt should always and to finger nail trauma, and is the usual site for epistaxis
be made to find any local or constitutional cause. in children and young adults.
Retrocolumellar vein. This vein runs vertically downwards
BLOOD SUPPLY OF NOSE just behind the columella, crosses the floor of nose and joins
venous plexus on the lateral nasal wall. This is a common
(FIGURES 33.1 AND 33.2)
site of venous bleeding in young people.
Nose is richly supplied by both the external and internal
carotid systems, both on the septum and the lateral walls. WOODRUFF’S PLEXUS
It is a plexus of veins situated inferior to posterior end of
NASAL SEPTUM inferior turbinate. It is a site of posterior epistaxis in adults.
INTERNAL CAROTID SYSTEM
1. Anterior ethmoidal artery
2. Posterior ethmoidal artery } Branches
artery
of ophthalmic
CAUSES OF EPISTAXIS

They may be divided into:


EXTERNAL CAROTID SYSTEM
1. Sphenopalatine artery (branch of maxillary artery) gives 1. Local, in the nose or nasopharynx.
nasopalatine and posterior medial nasal branches. 2. General.
2. Septal branch of greater palatine artery (branch of max- 3. Idiopathic.
illary artery).
3. Septal branch of superior labial artery (branch of facial A. LOCAL CAUSES
artery).
NOSE
LATERAL WALL 1. Trauma. Finger nail trauma, injuries of nose, intranasal
surgery, fractures of middle third of face and base of
INTERNAL CAROTID SYSTEM skull, hard-blowing of nose, violent sneeze.
1. Anterior ethmoidal
2. Posterior ethmoidal }
Branches of ophthalmic artery 2. Infections
(a) Acute: Viral rhinitis, nasal diphtheria, acute sinusitis.
(b) Chronic: All crust-forming diseases, e.g. atrophic rhini-
tis, rhinitis sicca, tuberculosis, syphilis septal perforation,
EXTERNAL CAROTID SYSTEM 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.
2. Greater palatine artery → From maxillary artery (b) Living: Maggots, leeches.
3. Nasal branch of anterior → From infraorbital 4. Neoplasms of nose and paranasal sinuses.
superior dental branch of maxillary (a) Benign: Haemangioma, papilloma.
artery (b) Malignant: Carcinoma or sarcoma.
4. Branches of facial artery 5. Atmospheric changes. High altitudes, sudden decom-
to nasal vestibule pression (Caisson disease).
6. Deviated nasal septum.
LITTLE’S AREA NASOPHARYNX
It is situated in the anterior inferior part of nasal sep- 1. Adenoiditis.
tum, just above the vestibule. Four arteries—anterior eth- 2. Juvenile angiofibroma.
moidal, septal branch of superior labial, septal branch of 3. Malignant tumours.

176
CHAPTER 33 — EPISTAXIS 177

Internal carotid artery

Ophthalmic artery

Anterior Posterior
ethmoidal artery ethmoidal artery

Little’s area

Septal branch
Branches of
sphenopalatine
artery

Superior labial Greater palatine


artery artery

Facial artery Maxillary artery

External carotid
artery
Figure 33.1 Blood supply of nasal septum.

B. GENERAL CAUSES C. IDIOPATHIC


1. Cardiovascular system. Hypertension, arterioscle- Many times the cause of epistaxis is not clear.
rosis, mitral stenosis, pregnancy (hypertension and
hormonal).
2. Disorders of blood and blood vessels. Aplastic anaemia, SITES OF EPISTAXIS
leukaemia, thrombocytopenic and vascular purpura,
haemophilia, Christmas disease, scurvy, vitamin K defi- 1. Little’s area. In 90% cases of epistaxis, bleeding occurs
ciency and hereditary haemorrhagic telangectasia. from this site.
3. Liver disease. Hepatic cirrhosis (deficiency of factor II, 2. Above the level of middle turbinate. Bleeding from above
VII, IX and X). the middle turbinate and corresponding area on the sep-
4. Kidney disease. Chronic nephritis. tum is often from the anterior and posterior ethmoidal
5. Drugs. Excessive use of salicylates and other analgesics vessels (internal carotid system).
(as for joint pains or headaches), anticoagulant therapy 3. Below the level of middle turbinate. Here bleeding is
(for heart disease). from the branches of sphenopalatine artery. It may be hid-
6. Mediastinal compression. Tumours of mediastinum den, lying lateral to middle or inferior turbinate and may
(raised venous pressure in the nose). require infrastructure of these turbinates for localization
7. Acute general infection. Influenza, measles, chick- of the bleeding site and placement of packing to control it.
enpox, whooping cough, rheumatic fever, infectious 4. Posterior part of nasal cavity. Here blood flows directly
mononucleosis, typhoid, pneumonia, malaria and den- into the pharynx.
gue fever. 5. Diffuse. Both from septum and lateral nasal wall. This is
8. Vicarious menstruation (epistaxis occurring at the time often seen in general systemic disorders and blood dyscrasias.
of menstruation). 6. Nasopharynx.
178 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Internal carotid artery

Ophthalmic artery

Anterior Posterior
ethmoidal artery ethmoidal artery

Branches of
sphenopalatine
artery
Branches of
facial artery

Sphenopalatine
artery
Greater Lesser palatine
palatine artery
artery
Facial artery Maxillary artery

External carotid
artery
Figure 33.2 Blood supply of lateral wall of nose.

CLASSIFICATION OF EPISTAXIS Table 33.1 Differences between anterior


and posterior epistaxis
ANTERIOR EPISTAXIS
Anterior epistaxis Posterior epistaxis
When blood flows out from the front of nose with the patient
in sitting position. Incidence More common Less common
Site Mostly from Little’s Mostly from posterosu-
POSTERIOR EPISTAXIS area or anterior perior part of nasal
part of lateral wall cavity; often difficult
Mainly the blood flows back into the throat. Patient may
to localize the
swallow it and later have a “coffee-coloured” vomitus. This
bleeding point
may erroneously be diagnosed as haematemesis. Age Mostly occurs in After 40 years of age
The differences between the two types of epistaxis are children or young
tabulated herewith (Table 33.1). adults
Cause Mostly trauma Spontaneous; often
due to hypertension
MANAGEMENT or arteriosclerosis
Bleeding Usually mild, can be Bleeding is severe,
In any case of epistaxis, it is important to know: easily controlled requires hospitaliza-
by local pressure tion; postnasal pack
1. Mode of onset. Spontaneous or finger nail trauma. or anterior pack often required
2. Duration and frequency of bleeding.
3. Amount of blood loss.
4. Side of nose from where bleeding is occurring.
5. Whether bleeding is of anterior or posterior type.
6. Any known bleeding tendency in the patient or family.
CHAPTER 33 — EPISTAXIS 179

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

7. History of known medical ailment (hypertension, leukae- ties to a piece of gauze rolled into the shape of a cone. A rub-
mia, mitral valve disease, cirrhosis and nephritis). ber catheter is passed through the nose and its end brought
8. History of drug intake (analgesics, anticoagulants, etc.). out from the mouth (Figure 33.4). Ends of the silk threads
are tied to it and catheter withdrawn from nose. Pack, which
follows the silk thread, is now guided into the nasopharynx
FIRST AID
with the index finger. Anterior nasal cavity is now packed
Most of the time, bleeding occurs from the Little’s area and and silk threads tied over a dental roll. The third silk thread
can be easily controlled by pinching the nose with thumb is cut short and allowed to hang in the oropharynx. It helps
and index finger for about 5 min. This compresses the vessels in easy removal of the pack later. Patients requiring post-
of the Little’s area. In Trotter’s method patient is made to nasal pack should always be hospitalized. Instead of postna-
sit, leaning a little forward over a basin to spit any blood and sal pack, a Foley’s catheter size 12–14 F can also be used.
breathe quietly from the mouth. Cold compresses should be After insertion balloon is inflated with 5–10 mL of saline.
applied to the nose to cause reflex vasoconstriction. 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. These days nasal balloons are also avail-
CAUTERIZATION
able (Figure 33.5). A nasal balloon has two bulbs, one for
This is useful in anterior epistaxis when bleeding point has the postnasal space and the other for nasal cavity.
been located. The area is first topically anaesthetized and
the bleeding point cauterized with a bead of silver nitrate or ENDOSCOPIC CAUTERIZATION
coagulated with electrocautery.
Using topical or general anaesthesia, bleeding point is local-
ized with a rigid endoscope. It is then cauterized with a mal-
ANTERIOR NASAL PACKING leable unipolar suction cautery or a bipolar cautery. The
In cases of active anterior epistaxis, nose is cleared of blood procedure is effective with less morbidity and decreased
clots by suction and attempt is made to localize the bleed- hospital stay. The procedure has a limitation when profuse
ing site. In minor bleeds, from the accessible sites, cauteriza- bleeding does not permit localization of the bleeding point.
tion of the bleeding area can be done. If bleeding is profuse
and/or the site of bleeding is difficult to localize, anterior ELEVATION OF MUCOPERICHONDRIAL FLAP
packing should be done. For this, use a ribbon gauze soaked AND SUBMUCOUS RESECTION (SMR) OPERATION
with liquid paraffin. About 1 m gauze (2.5 cm wide in adults
and 12 mm in children) is required for each nasal cavity. In case of persistent or recurrent bleeds from the septum,
First, few centimetres of gauze are folded upon itself and just elevation of mucoperichondrial flap and then reposi-
inserted along the floor and then the whole nasal cavity is tioning it back helps to cause fibrosis and constrict blood
packed tightly by layering the gauze from floor to the roof vessels. SMR operation can be done to achieve the same
and from before backwards. Packing can also be done in result or remove any septal spur which is sometimes the
vertical layers from back to the front (Figure 33.3). One or cause of epistaxis.
both cavities may need to be packed. Pack can be removed
after 24 h, if bleeding has stopped. Sometimes, it has to be
LIGATION OF VESSELS
kept for 2–3 days; in that case, systemic antibiotics should be
given to prevent sinus infection and toxic shock syndrome. 1. External carotid. When bleeding is from the exter-
nal carotid system and the conservative measures have
failed, ligation of external carotid artery above the origin
POSTERIOR NASAL PACKING
of superior thyroid artery should be done. It is avoided
It is required for patients bleeding posteriorly into the these days in favour of embolization or ligation of more
throat. A postnasal pack is first prepared by tying three silk peripheral branches of sphenopalatine artery.
180 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Figure 33.4 Technique of postnasal pack.

2. Maxillary artery. Ligation of this artery is done in uncon-


trollable posterior epistaxis. Approach is via Caldwell–Luc
operation. Posterior wall of maxillary sinus 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, anterior B
and posterior ethmoidal arteries, which supply this area,
can be ligated. The vessels are exposed in the medial wall A
of the orbit by an external ethmoid (Lynch) incision.

TRANSNASAL ENDOSCOPIC SPHENOPALATINE


ARTERY LIGATION (TESPAL)
The procedure can be done with rigid endoscopes under
topical anaesthesia with sedation or under a general anaes-
thesia. A mucosal flap is lifted in posterior part of lateral Figure 33.5 Epistaxis balloon for posterior epistaxis. Posterior bal-
nasal wall, sphenopalatine artery (SPA)is localized as it exits loon (A) is inflated with 10 mL and anterior balloon (B) with 30 mL.
the foramen and closed with a vascular clip. Distal branches Catheter provides nasal airway.
of the artery can be additionally cauterized and the flap then
reposited. Anterior ethmoidal artery can also be ligated by 2. Reassure the patient. Mild sedation should be given.
Lynch incision as an adjunctive procedure. SPA ligation 3. Keep check on pulse, BP and respiration.
gives high success in control of refractory posterior bleed. 4. Maintain haemodynamics. Blood transfusion may be
required.
EMBOLIZATION 5. Antibiotics may be given to prevent sinusitis, if pack is to
It is done by an interventional radiologist through femoral be kept beyond 24 h.
artery catheterization. Internal maxillary artery is localized and 6. Intermittent oxygen may be required in patients with
the embolization is performed with absorbable gelfoam and/ bilateral packs because of increased pulmonary resis-
or polyvinyl alcohol or coils. Both ipsilateral or bilateral emboli- tance from nasopulmonary reflex.
zations may be required for unilateral epistaxis because of cross 7. Investigate and treat the patient for any underlying local
circulation. Embolization is generally a safe procedure but may or general cause.
have potential risks like cerebral thromboembolism, haema-
toma at local site. Ethmoidal arteries cannot be embolized. Hereditary haemorrhagic telangiectasia. It occurs on the
anterior part of nasal septum and is the cause of recurrent
bleeding. It can be treated by using Argon, KTP or Nd: YAG
GENERAL MEASURES IN EPISTAXIS laser. The procedure may require to be repeated several times
in a year as telangectasia recurs in the surrounding mucosa.
1. Make the patient sit up with a back rest and record any Some cases require septodermoplasty where anterior part of
blood loss taking place through spitting or vomiting. septal mucosa is excised and replaced by a split-skin graft.
Trauma to the Face 34

Injuries of face may involve soft tissues, bones or both. The


majority of facial injuries are caused by automobile acci- BONE INJURIES AND THEIR MANAGEMENT
dents. Others result from sports, personal accidents, assaults
and fights. The management of facial trauma can be divided The face can be divided into three regions:
into: 1. Upper third. Above the level of supraorbital ridge.
1. General management. 2. Middle third. Between the supraorbital ridge and the
2. Soft tissue injuries and their management. upper teeth.
3. Bone injuries and their management. 3. Lower third. Mandible and the lower teeth.
The various fractures encountered in these regions are
listed in Table 34.1.
GENERAL MANAGEMENT

1. Airway. Maintenance of airway should receive the highest


priority. Airway is obstructed by loss of skeletal support, I. FRACTURES OF UPPER THIRD OF FACE
aspiration of foreign bodies, blood or gastric contents or
swelling of tissues. Airway is secured by intubation or the A. FRONTAL SINUS
tracheostomy.
2. Haemorrhage. Injuries of face may bleed profusely. Frontal sinus fractures may involve anterior wall, posterior
Bleeding should be stopped by pressure or ligation of wall or the nasofrontal duct.
vessels. 1. Anterior wall fractures may be depressed or comminuted.
3. Associated injuries. Facial injuries may be associated with Defect is mainly cosmetic. Sinus is approached through
injuries of head, chest, abdomen, neck, larynx, cervical a wound in the skin if that is present, or through a brow
spine or limbs and should be attended too. incision. The bone fragments are elevated, taking care
not to strip them from the periosteum. The interior of
the sinus is always inspected to rule out fracture of the
SOFT TISSUE INJURIES AND THEIR posterior wall.
MANAGEMENT 2. Posterior wall fractures may be accompanied by dural tears,
brain injury and CSF rhinorrhoea. They may require
FACIAL LACERATIONS neurosurgical consultation. Dural tears can be covered
by temporalis fascia. Small sinuses can be obliterated with
Wound is thoroughly cleaned of any dirt, grease or foreign fat.
matter. The lacerations are closed by accurate approxima- 3. Injury to nasofrontal duct causes obstruction to sinus drain-
tion of each layer. age and may later be complicated by a mucocele. In such
cases, make a large communication between the sinus
PAROTID GLAND AND DUCT and the nose. Small sinuses can be obliterated with fat
after removing the sinus mucosa completely.
Parotid tissue, if exposed, is repaired by suturing. Injuries
of parotid duct are more serious. Both ends of the duct are
identified and sutured over a polyethylene tube with fine B. SUPRAORBITAL RIDGE
suture. The tube is left for 3 days to 2 weeks.
Ridge fractures often cause periorbital ecchymosis, flatten-
ing of the eyebrow, proptosis or downward displacement of
FACIAL NERVE
eye. Fragment of bone may also be pushed into the orbit
If severed, the facial nerve is exposed by superficial paroti- and get impacted. Ridge fractures require open reduction
dectomy and cut ends are approximated with 8–0 or 10–0 through an incision in the brow or transverse skin line of
silk under magnification. the forehead.

181
182 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Table 34.1 Fractures of the face

Upper third Middle third Lower third


Frontal Nasal bones and septum Alveolar process
sinuses
Supraorbital Naso-orbital area Symphysis
ridge
Frontal •  ygoma
Z • B ody A
bone • Zygomatic arch • Angle
• Orbital floor • Ascending
• Maxilla ramus
• Le Fort I (transverse) • Condyle
• Le Fort II (pyramidal) • Temporoman-
• Le Fort III (craniofa- dibular joint
cial dysjunction)

B
C. FRACTURES OF FRONTAL BONE
They may be depressed or linear, with or without separa-
tion. They often extend into the orbit. Brain injury and
cerebral oedema are commonly associated with each other
and require neurosurgical consultation.

II. FRACTURES OF MIDDLE THIRD OF FACE


C
A. NASAL BONES AND SEPTUM
Figure 34.1 Types of fractures. (A) Normal. (B) Frontal blow causing
Fractures of nasal bones are the most common because of depressed fracture or open-book fracture. (C) Lateral blow causing
the projection of nose on the face. Traumatic forces may act deviation of nasal bridge or depression of one nasal bone.
from the front or side. Magnitude of force will determine
the depth of injury.
DIAGNOSIS
TYPES OF NASAL FRACTURES (FIGURE 34.1) Diagnosis is best made on physical examination. X-rays may or
1. Depressed. They are due to frontal blow. Lower part of may not show fracture (Figure 34.2). Patient should not be dis-
nasal bones which is thinner, easily gives way. A severe fron- missed as having no fracture because X-rays did not reveal it.
tal blow will cause “open-book fracture” in which nasal sep- X-rays should include Waters’ view, right and left lateral
tum is collapsed and nasal bones splayed out. Still, greater views and occlusal view.
forces will cause comminution of nasal bones and even the
frontal processes of maxillae with flattening and widening TREATMENT
of nasal dorsum. Simple fractures without displacement need no treatment;
others may require closed or open reduction. Presence of
2. Angulated. A lateral blow may cause unilateral depression
oedema interferes with accurate reduction by closed meth-
of nasal bone on the same side or may fracture both the
ods. Therefore, the best time to reduce a fracture is before
nasal bones and the septum with deviation of nasal bridge.
the appearance of oedema, or after it has subsided, which is
Nasal fractures are often accompanied by injuries of nasal
usually in 5–7 days. It is difficult to reduce a nasal fracture
septum which may be simply buckled, dislocated or frac-
after 2 weeks because it heals by that time. Healing is faster
tured into several pieces. Septal haematoma may form.
in children and therefore earlier reduction is imperative.
CLINICAL FEATURES 1. Closed reduction. Depressed fractures of nasal bones sus-
1. Swelling of nose. Appears within few hours and may tained by either frontal or lateral blow can be reduced by a
obscure details of examination. straight blunt elevator guided by digital manipulation from
2. Periorbital ecchymosis. outside.
3. Tenderness. Laterally, displaced nasal bridge can be reduced by firm
4. Nasal deformity. Nose may be depressed from the front digital pressure in the opposite direction. Impacted frag-
or side, or the whole of the nasal pyramid deviated to one ments sometimes require disimpaction with Walsham or
side. Asch’s forceps before realignment. Septal fractures are also
5. Crepitus and mobility of fractured fragments. reduced by Asch’s forceps. Septal haematoma, if present,
6. Epistaxis. must be drained.
7. Nasal obstruction due to septal injury or haematoma. Simple fractures may not require intranasal packing.
8. Lacerations of the nasal skin with exposure of nasal bones Unstable fractures require intranasal packing and external
and cartilage may be seen in compound fractures. splintage.
CHAPTER 34 — TRAUMA TO THE FACE 183

Zygomaticofrontal fracture Zygomaticotemporal fracture

Infraorbital fracture
Figure 34.3 Fracture zygoma left.
Figure 34.2 Fractured nasal bone (arrow) as seen in radiograph.

2. Open reduction. Early open reduction in nasal frac- 2. Open reduction. This is required in cases with extensive
tures is rarely required. This is indicated when closed comminution of nasal and orbital bones, and those compli-
methods fail. Certain septal injuries can be better reduced cated by other injuries to lacrimal apparatus, medial canthal
by open methods. Healed nasal deformities resulting ligaments, frontal sinus, etc.
from nasal trauma can be corrected by rhinoplasty or An H-type incision gives adequate exposure of the frac-
septorhinoplasty. tured area. This can be extended to the eyebrows if access to
frontal sinuses is also required.
Nasal bones are reduced under vision and bridge height
B. NASO-ORBITAL FRACTURES is achieved. Medial orbital walls can be reduced. Medial can-
Direct force over the nasion fractures nasal bones and dis- thal ligaments, if avulsed, are restored with a through and
places them posteriorly. Perpendicular plate of ethmoid, through wire. Intranasal packing may be required to restore
ethmoidal air cells and medial orbital wall are fractured the contour. When bone comminution is severe, restoration
and driven posteriorly. Injury may involve cribriform plate, of medial canthal ligaments and lacrimal apparatus should
frontal sinus, frontonasal duct, extraocular muscles, eyeball receive preference over reconstruction of nasal contour.
and the lacrimal apparatus. Medial canthal ligament may be
avulsed. C. FRACTURES OF ZYGOMA (TRIPOD FRACTURE)
CLINICAL FEATURES After nasal bones, zygoma is the second most frequently frac-
tured bone. Usually, the cause is direct trauma. Lower seg-
1. Telecanthus, due to lateral displacement of medial
ment of zygoma is pushed medially and posteriorly resulting
orbital wall.
in flattening of the malar prominence and a step deformity at
2. Pug nose. Bridge of nose is depressed and tip turned up.
the infraorbital margin. Zygoma is separated at its three pro-
3. Periorbital ecchymosis.
cesses (Figure 34.3). Fracture line passes through zygomatico-
4. Orbital haematoma due to bleeding from anterior and
frontal suture, orbital floor, infraorbital margin and foramen,
posterior ethmoidal arteries.
anterior wall of maxillary sinus and the zygomaticotemporal
5. CSF leakage due to fracture of cribriform plate and dura.
suture. Orbital contents may herniate into the maxillary sinus.
6. Displacement of eyeball.
CLINICAL FEATURES
DIAGNOSIS
1. Flattening of malar prominence.
Various facial films will be required to assess the extent of 2. Step deformity of infraorbital margin.
fracture and injury to other facial bones. Computed tomog- 3. Anaesthesia in the distribution of infraorbital nerve.
raphy (CT) scans are more useful. 4. Trismus, due to depression of zygoma on the underlying
coronoid process.
TREATMENT 5. Oblique palpebral fissure, due to the displacement of lat-
1. Closed reduction. In uncomplicated cases, fracture is eral palpebral ligament.
reduced with Asch’s forceps and stabilized by a wire passed 6. Restricted ocular movements, due to entrapment of infe-
through fractured bony fragments and septum and then rior rectus muscle. It may cause diplopia.
tied over the lead plates. Intranasal packing is given. Splint- 7. Periorbital emphysema, due to escape of air from the
ing is kept for 10 days or so. maxillary sinus on nose blowing.
184 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

DIAGNOSIS 3. Diplopia, which may be due to displacement of the eye-


Waters’ or exaggerated Waters’ view shows the fracture and ball or entrapment of inferior rectus and inferior oblique
displacement the best. Maxillary sinus may show clouding muscles.
due to the presence of blood. Comminution with depres- 4. Hypoaesthesia or anaesthesia of cheek and upper lip, if
sion of orbital floor and herniation of orbital contents can- infraorbital nerve is involved.
not be seen on plain X-rays. CT scan of the orbital will be DIAGNOSIS
more useful.
Waters’ view shows a convex opacity bulging into the antrum
TREATMENT from above (tear-drop opacity). CT scans may confirm the
Only displaced fractures require treatment. Open reduc- diagnosis (Figure 34.5). Entrapment of inferior rectus and
tion and internal wire fixation gives best results. Fracture inferior oblique muscles is diagnosed by asking the patient
is exposed at the frontozygomatic suture through lateral to look up and down, or by the traction test. The latter is
brow incision and reduced by passing an elevator behind performed by grasping the globe and passively rotating it to
the zygoma. Wire fixation is done at frontozygomatic suture check for restriction of its movements.
and infraorbital margin. The latter is exposed by a separate TREATMENT
incision in the lower lid. Fracture of orbital floor can also be
repaired through this incision. Indications for surgery include enophthalmos and persis-
Transantral approach is less favourable. Antrum is tent diplopia due to entrapment of muscle. Orbital floor
exposed as in Caldwell–Luc operation, blood is aspirated, fractures can be satisfactorily reduced by a finger passed
fracture reduced and then stabilized by a pack in the antrum. into the antrum through a transantral approach. A pack can
Fractures of orbital floor can also be reduced. Antral pack be kept in the antrum to support the fragments. Infraor-
is removed in about 10 days through the buccal incision, bital approach, through a skin crease of the lower lid, can
which is left open at the end of operation, or through the also be used either alone or in combination with transan-
intranasal antrostomy route. tral approach. Badly comminuted fractures of orbital floor
can be repaired by a bone graft from the iliac crest, nasal
septum or the anterior wall of the antrum. Silicon or teflon
D. FRACTURES OF ZYGOMATIC ARCH sheets have also been used to reconstruct the orbital floor
but autogenous grafts are preferable.
Zygomatic arch generally breaks into two fragments which
get depressed. There are three fracture lines, one at each
end and third in the centre of the arch.

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. Figure 34.4 Blow out fracture with herniation of orbital contents into
the maxillary sinus.
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 reduced. Fixa-
tion is usually not required as the fragments remain stable.

E. FRACTURES OF ORBITAL FLOOR


Zygomatic and Le Fort II maxillary fractures are always
accompanied by fractures of orbital floor. Isolated fractures
of orbital floor, when a large blunt object strikes the globes,
are called “blow out fractures.” Orbital contents may herniate
into the antrum (Figure 34.4).

CLINICAL FEATURES
1. Ecchymosis of lid, conjunctiva and sclera.
2. Enophthalmos with inferior displacement of the eyeball.
This becomes apparent when oedema subsides. Figure 34.5 CT scan showing blow out fracture of right orbital floor.
CHAPTER 34 — TRAUMA TO THE FACE 185

F. FRACTURES OF MAXILLA (FIGURE 34.6) They help to delineate fracture lines and the displacement
of fragments.
They are classified into three types:
1. Le Fort I (transverse) fracture runs above and parallel to TREATMENT
the palate. It crosses lower part of nasal septum, maxil- Treatment of maxillary fractures is complex. Immediate
lary antra and the pterygoid plates. attention is paid to restore the airway and stop severe haem-
2. Le Fort II (pyramidal) fracture passes through the root of orrhage from maxillary artery or its branches. For good
nose, lacrimal bone, floor of orbit, upper part of maxil- cosmetic and functional results, fractures should be treated
lary sinus and pterygoid plates. This fracture has some as early as the patient’s condition permits. Associated
features common with the zygomatic fractures. intracranial and cervical spine injuries may delay specific
3. Le Fort III (craniofacial dysjunction). There is complete treatment.
separation of facial bones from the cranial bones. The Fixation of maxillary fractures can be achieved by:
fracture line passes through root of nose, ethmofrontal 1. Interdental wiring.
junction, superior orbital fissure, lateral wall of orbit, 2. Intermaxillary wiring using arch bars.
frontozygomatic and temporozygomatic sutures and the 3. Open reduction and interosseous wiring as in zygomatic
upper part of pterygoid plates. fractures.
CLINICAL FEATURES 4. Wire slings from frontal bone, zygoma or infraorbital rim
to the teeth or arch bars.
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 III. FRACTURES OF LOWER THIRD
and Le Fort III fractures.
FRACTURES OF MANDIBLE
DIAGNOSIS
Fractures of mandible have been classified according to their
X-rays, helpful in diagnosis of maxillary fractures are Waters’ location (Figure 34.7). Condylar fractures are the most com-
view, posteroanterior view, lateral view and the CT scans. mon. They are followed, in frequency, by fractures of the
angle, body and symphysis (mnemonic CABS). Fractures of
the ramus, coronoid and alveolar processes 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 indirect
trauma to the chin or opposite side of the body of mandi-
ble. Displacement of mandibular fractures is determined by
C (i) the pull of muscles attached to the fragments, (ii) direction
of fracture line and (iii) bevel of the fracture.
B
CLINICAL FEATURES
A
In fractures of condyle, if fragments are not displaced, pain
and trismus are the main features and tenderness is elicited
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.
Figure 34.6 Fractures of maxilla: (A) Le Fort I, (B) Le Fort II and Most of the fractures of angle, body and symphysis can be diag-
(C) Le Fort III. nosed by intraoral and extraoral palpation. Step deformity,

Coronoid
Condylar 2% process
process 35%
Alveolar process

3%
Ramus

5%
20%
Angle 20% Symphysis
15%

Body
Figure 34.7 Fractures of mandible (Dingman’s classification). Condylar fractures are the most common, followed by those of the angle, body
and symphysis of mandible. Remember CABS.
186 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

malocclusion of teeth, ecchymosis of oral mucosa, tender- formation. Presence of apical tooth abscess predis-
ness at the site of fracture and crepitus may be seen. poses to it.
2. Failure of sublabial incision to heal after Caldwell–Luc
DIAGNOSIS operation.
X-rays useful in mandibular fractures are PA view of the skull 3. Erosion of antrum by carcinoma.
(for condyle), right and left oblique views of mandible and 4. Fractures or penetrating injuries of maxilla.
the panorex view. 5. Osteitis of maxilla, syphilis or malignant granuloma.

TREATMENT CLINICAL FEATURES


Both closed and open methods are used for reduction and 1. Regurgitation of food. Food or fluids pass from oral cav-
fixation of the mandibular fractures. ity into the antrum and thence into the nose.
In closed methods, interdental wiring and intermaxillary 2. Discharge. Antrum is always infected. Foul-smelling dis-
fixation are useful. External pin fixation can also be used. charge is seen, filling the nose or exuding from the fistu-
In open methods, fracture site is exposed and fragments lous opening into the mouth.
fixed by direct interosseous wiring. This is further strength- 3. Inability to build positive or negative pressure in the
ened by a wire tied in a figure of eight manner. These days, mouth. Patient will have difficulty to blow the wind instru-
compression plates are available to fix the fragments. With ments or drink through a straw. To drink through a straw,
their use, prolonged immobilization and intermaxillary fix- negative pressure has to be created in the oral cavity. This
ation can be avoided. cannot be done in the presence of an oroantral fistula as
Condylar fractures are also treated by intermaxillary fix- air gets drawn from nose to antrum to oral cavity. Reverse
ation with arch bars and rubber bands. Sometimes, open is true when blowing wind instruments; instead of build-
reduction and interosseous wiring may be required in adult ing a positive pressure in the oral cavity, air is blown out
edentulous patients with bilateral condylar fractures or in from the oral cavity to antrum and out through the nose.
fractures of children.
Immobilization of mandible beyond 3 weeks, in con- DIAGNOSIS
dylar fractures, can cause ankylosis of temporomandibu- A probe can be passed from the fistulous opening in the oral
lar joints. Therefore, intermaxillary wires are removed cavity into the antrum.
and jaw exercises started. If occlusion is still disturbed,
intermaxillary wires are reapplied for another week and TREATMENT
the process repeated till the bite and jaw movements are Recent fistula. When fistula is discovered immediately after
normal. tooth extraction and there is no infection or a retained
tooth in the antrum, conservative treatment with suturing
of gum margins and a course of antibiotics is effective.
OROANTRAL FISTULA Chronic fistula or a large fistula. It requires surgical repair
by a palatal or a buccal flap. Maxillary sinusitis is first treated
It is a communication between the antrum and oral cavity. by repeated irrigations and antibiotics. Squamous-lined fis-
The fistulous opening may be situated on the alveolus or tulous track is excised, bony edges of the fistula are smooth-
gingivolabial sulcus. ened and prepared for the flaps to sit properly. Caldwell–Luc
operation may be required to remove a retained tooth root
AETIOLOGY or a foreign body, clear the antrum of diseased mucosa and
1. Dental extraction is the most important cause. Roots to provide a nasoantral window for free drainage. Some fis-
of second premolar and upper molars (first and some- tulas are better closed by a dental obturator. The latter also
times second and third) are closely related to the permits observation of antral cavity particularly in those
antral cavity and their extraction may lead to fistula treated for cancer.
Anatomy and Physiology of 35
Paranasal Sinuses

FRONTAL SINUS
ANATOMY OF PARANASAL SINUSES
Each frontal sinus is situated between the inner and outer
Paranasal sinuses are air-containing cavities in certain bones tables of frontal bone, above and deep to the supraorbital
of skull. They are four on each side. Clinically, paranasal margin. It varies in shape and size and is often loculated by
sinuses have been divided into two groups: incomplete septa. The two frontal sinuses are often asym-
metric and the intervening bony septum is thin and often
1. Anterior group. This includes maxillary, frontal and obliquely placed or may even be deficient. Frontal sinus
anterior ethmoidal. They all open in the middle meatus may be absent on one or both sides or it may be very large
and their ostia lie anterior to basal lamella of middle extending into orbital plate in the roof of the orbit. Its aver-
turbinate. age dimensions are: height 32 mm, breadth 24 mm and
2. Posterior group. This includes posterior ethmoidal depth 16 mm (remember code 8, i.e. 8 × 4, 8 × 3 and 8 × 2).
sinuses which open in the superior meatus and the sphe- Anterior wall of the sinus is related to the skin over the
noid sinus which opens in sphenoethmoidal recess. forehead; inferior wall, to the orbit and its contents; and pos-
terior wall to the meninges and frontal lobe of the brain.
MAXILLARY SINUS (ANTRUM OF HIGHMORE) Drainage of the frontal sinus is through its ostium into the
It is the largest of paranasal sinuses and occupies the body frontal recess. In fact frontal sinus, its ostium and the frontal
of maxilla. It is pyramidal in shape with base towards lateral recess form an hour glass structure. Frontal recess is situated
wall of nose and apex directed laterally into the zygomatic in the anterior part of middle meatus and is bounded by the
process of maxilla and sometimes in the zygomatic bone middle turbinate (medially), lamina papyracea (laterally),
itself (Figure 35.1). On an average, maxillary sinus has a agger nasi cells (anteriorly) and bulla ethmoidalis (poste-
capacity of 15 mL in an adult. It is 33 mm high, 35 mm deep riorly). It may be encroached by several anterior ethmoidal
and 25 mm wide. cells, which may obstruct its ventilation and drainage and
lead to sinusitis. Frontal recess drains into the infundibulum
Relations
or medial to it, depending on the superior attachment of
• Anterior wall is formed by facial surface of maxilla and is the uncinate process (refer to Figure 23.6).
related to the soft tissues of cheek.
• Posterior wall is related to infratemporal and pterygopala-
tine fossae.
• Medial wall is related to the middle and inferior meatuses.
At places, this wall is thin and membranous. It is related to Cribriform
uncinate process, anterior and posterior fontanelle, and plate
Roof of ethmoid
inferior turbinate and meatus.
• Floor is formed by alveolar and palatine processes of the
maxilla and is situated about 1 cm below the level of floor Orbit
of nose (Figure 35.1). Usually it is related to the roots of Olfactory
second premolar and first molar teeth. Depending on sulcus
the age of the person and pneumatization of the sinus, Uncinate Middle
the roots of all the molars, sometimes the premolars and process turbinate
canine, are in close relation to the floor of maxillary sinus
separated from it by a thin lamina of bone or even no Inferior
bone at all. Oroantral fistulae can result from extraction Maxillary turbinate
of any of these teeth. Dental infection is also an important sinus
cause of maxillary sinusitis. Floor of maxillary
  Ostium of the maxillary sinus is situated high up in medial sinus
wall and opens in the posteroinferior part of ethmoidal
infundibulum into the middle meatus. It is unfavourably
situated for natural drainage. An accessory ostium is also
present behind the main ostium in 30% of cases. Figure 35.1 Coronal section showing relationship of maxillary and
• Roof of the maxillary sinus is formed by the floor of the ethmoidal sinuses to orbit and the nasal cavity. Floor of maxillary
orbit. It is traversed by infraorbital nerve and vessels. sinus is about 1 cm below the floor of nose.

187
188 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Due to encroachment of small air cells in the frontal Superolateral ridge


recess, the drainage pathway may be reduced to a straight or
more often tortuous pathway which was earlier called naso-
frontal duct. It is an erroneous term as no true duct exists.

ETHMOIDAL SINUSES (ETHMOID AIR CELLS) Optic nerve

Ethmoidal sinuses are thin-walled air cavities in the lateral


masses of ethmoid bone. Their number varies from 3 to 18. Internal carotid
They occupy the space between upper third of lateral nasal artery
wall and the medial wall of orbit. Clinically, ethmoidal cells
are divided by the basal lamina into an anterior ethmoid
group which opens into the middle meatus and posterior eth- Maxillary nerve
moid group which opens into the superior meatus and into
supreme meatus, if that be present.
Roof of the ethmoid is formed by medial extension of the
orbital plate of the frontal bone, which shows depressions on Vidian nerve
its undersurface, called fovea ethmoidalis. The lateral wall is
formed by a thin plate of bone called lamina papyracea.

Anterior Group
Important ethmoid cells in the anterior group include: Figure 35.2 Coronal section of sphenoid sinuses. Note the reliefs
made by various structures in the cavity of sphenoid sinus. Optic
1. Agger nasi cells – present in the agger nasi ridge.
nerve forms the superolateral ridge.
2. Ethmoid bulla – forms the posterior boundary of the hia-
tus semilunaris.
3. Supraorbital cells.
III
4. Frontoethmoid cells – situated in the area of the frontal Pituitary IV
recess and may encroach the frontal sinus. Int. carotid VI
5. Haller cells – situated in the floor of the orbit.
Cavernous V1
Posterior Group sinus V2

The posterior group of ethmoid sinuses lies posterior to the V3


basal lamina of middle concha. They are 1–7 in number and
open into superior meatus or in the supreme meatus, when
Sphenoid sinus
present. One important cell of this group is sphenoethmoid
cell, also called the Onodi cell. It is the most posterior cell of
Figure 35.3 Relations of sphenoid sinus.
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 Relations of the Sphenoid Sinus
the carotid artery are related to it laterally and are in danger Lateral wall of the sphenoid is related to the optic nerve and
during endoscopic surgery. carotid artery. The opticocarotid recess can be seen in between
At birth anterior ethmoids are 5 × 2 × 2 mm and posterior the two. It may extend laterally when the anterior clinoid pro-
ethmoids are 5 × 4 × 2 mm. They attain their adult size by cesses are also pneumatized. Maxillary nerve may be related
the 12th year. to lower part of the lateral wall of sphenoid. The optic nerve
and internal carotid artery are usually covered by a thin bone,
SPHENOID SINUS but sometimes this bony covering may be dehiscent, and then
It occupies the body of sphenoid. The two, right and left these structures lie exposed, covered only by mucosa.
sinuses, are rarely symmetrical and are separated by a thin Floor of the sinus is related to the Vidian nerve. Relation
bony septum which is often obliquely placed and may even of the roof can be divided into two parts. Anterior part of
be deficient (compare frontal sinus) (Figures 35.2 and 35.3). the roof is related to the olfactory tract, optic chiasma and
Ostium of the sphenoid sinus is situated high up in the ante- frontal lobe, while posterior part is related to the pituitary
rior wall and opens into the sphenoethmoidal recess, medial gland in the sella turcica and laterally to the cavernous sinus.
to the superior or supreme turbinate. It may be slit like, oval Posterior wall of the sphenoid forms the clivus.
or round and can be seen endoscopically. In adults, it is situ- Relations of the sphenoid sinus are important in endo-
ated about 1.5 cm from the upper border of choana. The scopic skull base surgery.
average distance from the anterior nasal spine to the ostium
is about 7 cm.
MUCOUS MEMBRANE OF PARANASAL SINUSES
An adult sphenoid sinus is about 2 cm high, 2 cm deep
and 2 cm wide, but its pneumatization varies. In some cases Paranasal sinuses are lined by mucous membrane which is
pneumatization may extend into greater or lesser wing of continuous with that of the nasal cavity through the ostia
sphenoid, pterygoid or clivus, i.e. basilar part of occipital of sinuses. It is thinner and less vascular compared to that
bone. of the nasal cavity. Histologically, it is ciliated columnar
CHAPTER 35 — ANATOMY AND PHYSIOLOGY OF PARANASAL SINUSES 189

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 4–5 months after birth
Volume 6–8 mL years. 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 6 years
increases until teens and complete development
by 20 years
Sphenoid Not present Reaches sella turcica by the age of 7 years, dorsum 4 years
sellae by late teens and basisphenoid by adult age
Reaches full size between 15 years to adult age

A B

Posterior ethmoid sinuses

Sphenoid sinus
Agger nasi cell

Opening of
maxillary sinus
Torus tubarius

C Anterior ethmoid sinuses


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.

epithelium with goblet cells which secrete mucus. Cilia are Growth of sinuses continues during childhood and early
more marked near the ostia of sinuses and help in drainage adult life. Radiologically, maxillary sinuses can be identified
of mucus into the nasal cavity. at 4–5 months, ethmoids at 1 year, frontals at 6 years and
sphenoids at 4 years (Table 35.1).
DEVELOPMENT OF PARANASAL SINUSES
LYMPHATIC DRAINAGE
Paranasal sinuses develop as outpouchings from the mucous
membrane of lateral wall of nose. At birth, only the maxil- The lymphatics of maxillary, ethmoid, frontal and sphe-
lary and ethmoidal sinuses are present and are large enough noid sinuses form a capillary network in their lining
to be clinically significant. mucosa and collect with lymphatics of nasal cavity. Then
190 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

they drain into lateral retropharyngeal and/or jugulodi- may carry infection of the frontal recess and sinuses drain-
gastric nodes. ing into it, towards the frontal sinus. Circulation is anticlock-
wise in the right and clockwise in the left frontal sinus.
Sphenoid sinus. Mucociliary clearance is towards its ostium
PHYSIOLOGY OF PARANASAL SINUSES into the sphenoethmoidal recess.

VENTILATION OF SINUSES Ethmoid sinus. Mucus from anterior group of ethmoid


sinuses joins that from the frontal and maxillary sinuses and
Ventilation of paranasal sinuses takes place through their travels towards eustachian tube, passing in front of torus
ostia. During inspiration, air current causes negative pres- tubarius into the nasopharynx. Mucus from posterior eth-
sure in the nose. This varies from −6 mm to −200 mm H2O, moids drains into superior or supreme meatus and then
depending on the force of inspiration. During expira- joins the mucus from the sphenoid sinus in the sphenoeth-
tion, positive pressure is created in the nose and this sets moidal recess, passes above and behind the torus tubarius
up eddies which ventilate the sinuses. Thus, ventilation of into the nasopharynx (Figure 35.4C).
sinuses is paradoxical; they are emptied of air during inspi- It is noted that infected discharge from the anterior group
ration and filled with air during expiration. This is just the of sinuses, passes behind the posterior pillars and causes hyper-
reverse of what takes place in lungs which fill during inspira- trophy of lateral pharyngeal bands. Discharge from posterior
tion and empty during expiration. group of sinuses spreads over the posterior pharyngeal wall.

MUCOCILIARY CLEARANCE OF SINUSES FUNCTIONS OF PARANASAL SINUSES


Maxillary sinus. Mucus from all the walls of the maxillary It is not clear why nature provided paranasal sinuses. Prob-
sinus—anterior, medial, posterior, lateral and roof—is trans- able functions are:
ported by the cilia to the natural ostium and then through it
1. Air-conditioning of the inspired air by providing large
into the middle meatus (Figure 35.4A). Mucus always drains
surface area over which the air is humidified and warmed.
from the natural ostium, even though accessory ostia be pres-
2. To provide resonance to voice.
ent in the fontanelle. It is also observed that inferior meatal
3. To act as thermal insulators to protect the delicate struc-
antrostomy made in Caldwell–Luc operation provides ven-
tures in the orbit and the cranium from variations of
tilation to the sinuses, but it does not help in mucociliary
intranasal temperature.
clearance which still takes place through the natural ostium.
4. To lighten the skull bones.
Frontal sinus. Mucociliary clearance of the frontal sinus 5. To provide extended surface for olfaction; olfactory
is unique (see Figure 35.4B). Mucus travels up along the mucosa is situated in the upper part of nasal cavity and
interfrontal septum, along the roof of the lateral wall, along extends over ethmoid as well.
the floor and then exits through the natural ostium. At two 6. To provide local immunologic defence against microbes.
points, one just above the ostium and other in the frontal 7. To act as buffers against trauma and thus protect brain
recess, part of the mucus recycles through the sinus and this against injury, e.g. frontal, ethmoid and sphenoid sinuses.
Acute Sinusitis 36

Acute inflammation of sinus mucosa is called acute sinusitis. (e) Nasal polypi
The sinus most commonly involved is the maxillary followed (f) Structural abnormality of ethmoidal air cells
in turn by ethmoid, frontal and sphenoid. Very often, more (g) Benign or malignant neoplasm.
than one sinus is infected (multisinusitis). Sometimes, all 2. Stasis of secretions in the nasal cavity. Normal secretions
the sinuses of one or both sides are involved simultaneously of nose may not drain into the nasopharynx because of
(pansinusitis unilateral or bilateral). their viscosity (cystic fibrosis) or obstruction (enlarged
Sinusitis may be “open” or “closed ” type depending on adenoids, choanal atresia) and get infected.
whether the inflammatory products of sinus cavity can drain 3. Previous attacks of sinusitis. Local defences of sinus
freely into the nasal cavity through the natural ostia or not. mucosa are already damaged.
A “closed” sinusitis causes more severe symptoms and is also
likely to cause complications. GENERAL
• Environment. Sinusitis is common in cold and wet cli-
mate. Atmospheric pollution, smoke, dust and overcrowd-
AETIOLOGY OF SINUSITIS IN GENERAL ing also predispose to sinus infection.
• Poor general health. Recent attack of exanthematous
A. EXCITING CAUSES fever (measles, chickenpox, whooping cough), nutritional
deficiencies and systemic disorders (diabetes, immune
­
1. Nasal infections. Sinus mucosa is a continuation of nasal deficiency syndromes).
mucosa and infections from nose can travel directly by
continuity or by way of submucosal lymphatics. Most
common cause of acute sinusitis is viral rhinitis followed BACTERIOLOGY
by bacterial invasion.
2. Swimming and diving. Infected water can enter the sinuses Most cases of acute sinusitis start as viral infections fol-
through their ostia. High content of chlorine gas in swim- lowed soon by bacterial invasion. The bacteria most often
ming pools can also set up chemical inflammation. responsible for acute suppurative sinusitis are Streptococcus
3. Trauma. Compound fractures or penetrating injuries of pneumoniae, Haemophilus influenzae, Moraxella catarrhalis,
sinuses—frontal, maxillary and ethmoid—may permit Streptococcus pyogenes, Staphylococcus aureus and Klebsiella pneu-
direct infection of sinus mucosa. Similarly, barotrauma moniae. Anaerobic organisms and mixed infections are seen
may be followed by infection. in sinusitis of dental origin.
4. Dental infections. This applies to maxillary sinus. Infection
from the molar or premolar teeth or their extraction may
be followed by acute sinusitis. PATHOLOGY OF SINUSITIS

B. PREDISPOSING CAUSES Acute inflammation of sinus mucosa causes hyperaemia, exu-


dation of fluid, outpouring of polymorphonuclear cells and
LOCAL increased activity of serous and mucous glands. Depending on
1. Obstruction to sinus ventilation and drainage. Normally, the virulence of organisms, defences of the host and capabil-
sinuses are well-ventilated. They also secrete small amount ity of the sinus ostium to drain the exudates, the disease may
of mucus, which by ciliary movement, is directed towards be mild (nonsuppurative) or severe (suppurative). Initially,
the sinus ostia from where it drains into the nasal cavity. the exudate is serous; later it may become mucopurulent
Any factor(s) which interfere with this function can cause or purulent. Severe infections cause destruction of mucosal
sinusitis due to stasis of secretions in the sinus. They are: lining. Failure of ostium to drain results in empyema of the
(a) Nasal packing sinus and destruction of its bony walls leading to complica-
(b) Deviated septum tions. Dental infections are very fulminating and soon result
(c) Hypertrophic turbinates in suppurative sinusitis.
(d) Oedema of sinus ostia due to allergy or vasomotor Infections of individual sinuses are dealt within this
rhinitis chapter.

191
192 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

TREATMENT
ACUTE MAXILLARY SINUSITIS
MEDICAL
AETIOLOGY 1. Antimicrobial drugs. Ampicillin and amoxicillin are quite
1. Most commonly, it is viral rhinitis which spreads to involve effective and cover a wide range of organisms. Eryth-
the sinus mucosa. This is followed by bacterial invasion. romycin or doxycycline or cotrimoxazole are equally
2. Diving and swimming in contaminated water. effective and can be given to those who are sensitive to
3. Dental infections are important source of maxillary penicillin. β-lactamase-producing strains of H. influenzae
sinusitis. Roots of premolar and molar teeth are related and M. catarrhalis may necessitate the use of amoxicillin/
to the floor of sinus and may be separated only by a thin clavulanic acid or cefuroxime axetil. Sparfloxacin is also
layer of mucosal covering. Periapical dental abscess may effective, and has the advantage of single daily dose.
burst into the sinus; or the root of a tooth, during extrac- 2. Nasal decongestant drops. One per cent ephedrine or
tion, may be pushed into the sinus. In case of oroantral 0.1% xylo- or oxymetazoline are used as nasal drops or
fistula, following tooth extraction, bacteria from oral sprays to decongest sinus ostium and encourage drainage.
cavity enter the maxillary sinus. 3. Steam inhalation. Steam alone or medicated with men-
4. Trauma to the sinus such as compound fractures, pen- thol or Tr. Benzoin Co. provides symptomatic relief and
etrating injuries or gunshot wounds may be followed by encourages sinus drainage. Inhalation should be given
sinusitis. 15–20 min after nasal decongestion for better penetration.
4. Analgesics. Paracetamol or any other suitable analgesic
PREDISPOSING FACTORS should be given for relief of pain and headache.
One or more of the predisposing factors enumerated for 5. Hot fomentation. Local heat to the affected sinus is often
sinusitis in general may be responsible for acute or recur- soothing and helps in the resolution of inflammation.
rent infection. SURGICAL
Antral lavage. Most cases of acute maxillary sinusitis respond
CLINICAL FEATURES to medical treatment. Lavage is rarely necessary. It is done
only when medical treatment has failed and that too only
Clinical features depend on (i) severity of inflammatory
under cover of antibiotics.
process and (ii) efficiency of ostium to drain the exudates.
Closed ostium sinusitis is of greater severity and leads more
often to complications. COMPLICATIONS
1. Constitutional symptoms. It consist of fever, general mal- 1. Acute maxillary sinusitis may change to subacute or chronic
aise and body ache. They are the result of toxaemia. sinusitis.
2. Headache. Usually, this is confined to forehead and may 2. Frontal sinusitis. Due to obstruction of frontal sinus
thus be confused with frontal sinusitis. drainage pathway because of oedema.
3. Pain. Typically, it is situated over the upper jaw, but may 3. Osteitis or osteomyelitis of the maxilla.
be referred to the gums or teeth. For this reason patient 4. Orbital cellulitis or abscess. Infection spreads to the
may primarily consult a dentist. Pain is aggravated by orbit because of oedema either directly from the roof
stooping, coughing or chewing. Occasionally, pain is of ­maxillary sinus or indirectly, after involvement of
referred to the ipsilateral supraorbital region and thus ­ethmoid sinuses.
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 chil- ACUTE FRONTAL SINUSITIS
dren. The lower eyelid may become puffy.
6. Nasal discharge. Anterior rhinoscopy/nasal endoscopy AETIOLOGY
shows pus or mucopus in the middle meatus. Mucosa of the 1. Usually follows viral infections of upper respiratory tract
middle meatus and turbinate may appear red and swollen. followed later by bacterial invasion.
Postural test. If no pus seen in the middle meatus, it is 2. Entry of water into the sinus during diving or swimming.
decongested with a pledget of cotton soaked with a vaso- 3. External trauma to the sinus, e.g. fractures or penetrat-
constrictor and the patient is made to sit with the affected ing injuries.
sinus turned up. Examination after 10–15 min may show 4. Oedema of middle meatus, secondary to associated ipsi-
discharge in the middle meatus. lateral maxillary or ethmoid sinus infection.
7. Postnasal discharge. Pus may be seen on the upper soft
palate on posterior rhinoscopy or nasal endoscopy. Predisposing factors, pathology and bacteriology are the
same as in acute sinusitis in general.
DIAGNOSIS
CLINICAL FEATURES
• Transillumination test. Affected sinus will be found opaque.
• X-rays. Waters’ view will show either an opacity or a fluid level 1. Frontal headache. Usually severe and localized over the
in the involved sinus. Computed tomography (CT) scan is affected sinus. It shows characteristic periodicity, i.e.
the preferred imaging modality to investigate the sinuses. comes up on waking, gradually increases and reaches its
CHAPTER 36 — ACUTE SINUSITIS 193

peak by about mid day and then starts subsiding. It is also becomes patent. This can be determined by adding a few
called “office headache” because of its presence only dur- drops of methylene blue to the irrigating fluid and its exit
ing the office hours. seen through the nose. Drainage tube is removed when
2. Tenderness. Pressure upwards on the floor of frontal frontonasal duct becomes patent.
sinus, just above the medial canthus, causes exquisite
pain. It can also be elicited by tapping over the anterior
wall of frontal sinus in the medial part of supraorbital
COMPLICATIONS
region. 1. Orbital cellulitis.
3. Oedema of upper eyelid with suffused conjunctiva and 2. Osteomyelitis of frontal bone and fistula formation.
photophobia. 3. Meningitis, extradural abscess or frontal lobe abscess, if
4. Nasal discharge. A vertical streak of mucopus is seen high infection breaks through the posterior wall of the sinus.
up in the anterior part of the middle meatus. This may 4. Chronic frontal sinusitis, if the acute infection is
be absent if the ostium is closed with no drainage. Nasal neglected or improperly treated.
mucosa is inflamed in the middle meatus.
X-rays. Opacity of the affected sinus or fluid level can be
seen. Both Waters’ and lateral views should be taken. CT ACUTE ETHMOID SINUSITIS
scan is the preferred modality.
AETIOLOGY
TREATMENT
Acute ethmoiditis is often associated with infection of other
MEDICAL sinuses. Ethmoid sinuses are more often involved in infants
and young children.
This is same as for acute maxillary sinusitis, i.e. antimicrobials,
decongestion of the sinus ostium for drainage and analgesics.
A combination of antihistaminic with an oral nasal deconges- CLINICAL FEATURES
tant (pseudoephedrine or phenylephrine hydrochloride) is
1. Pain. It is localized over the bridge of the nose, medial
useful. Placing a pledget of cotton soaked in a vasoconstric-
and deep to the eye. It is aggravated by movements of the
tor in the middle meatus, once or twice daily, helps to relieve
eye ball.
ostial oedema and promotes sinus drainage and ventilation.
2. Oedema of lids. Both eyelids become puffy and swollen.
If patient shows response to medical treatment and pain is
There is increased lacrimation. Orbital cellulitis is an
relieved, treatment is continued for full 10 days to 2 weeks.
early complication in such cases.
SURGICAL 3. Nasal discharge. On anterior rhinoscopy, pus may be
seen in middle or superior meatus depending on the
Trephination of frontal sinus. If there is persistence or
involvement of anterior or posterior group of ethmoid
exacerbation of pain or pyrexia in spite of medical treat-
sinuses.
ment for 48 h, or if the lid swelling is increasing and threat-
4. Swelling of the middle turbinate.
ening orbital cellulitis, frontal sinus is drained externally. A
2 cm long horizontal incision is made in the superomedial
aspect of the orbit below the eyebrow (Figure 36.1). Floor TREATMENT
of frontal sinus is exposed and a hole drilled with a burr.
Pus is taken for culture and sensitivity, and a plastic tube Medical treatment is the same as for acute maxillary sinusitis.
inserted and fixed. Sinus can now be irrigated with nor- Visual deterioration and exophthalmos indicate abscess
mal saline two or three times daily until frontonasal duct in the posterior orbit and may require drainage of the eth-
moid sinuses into the nose through an external ethmoidec-
tomy incision.

COMPLICATIONS
1. Orbital cellulitis and abscess.
2. Visual deterioration and blindness due to involvement of
optic nerve.
3. Cavernous sinus thrombosis.
4. Extradural abscess, meningitis or brain abscess.

ACUTE SPHENOID SINUSITIS

AETIOLOGY
Isolated involvement of sphenoid sinus is rare. It is often a
part of pansinusitis or is associated with infection of poste-
Figure 36.1 Trephination of right frontal sinus. rior ethmoid sinuses.
194 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

CLINICAL FEATURES DIFFERENTIAL DIAGNOSIS


1. Headache. Usually localized to the occiput or vertex. Mucocele of the sphenoid sinus or its neoplasms may clinically
Pain may also be referred to the mastoid region. simulate features of acute infection of sphenoid sinus and
2. Postnasal discharge. It can only be seen on posterior rhi- should always be excluded in any case of isolated sphenoid
noscopy. A streak of pus may be seen on the roof and sinus involvement.
posterior wall of nasopharynx or above the posterior end
of middle turbinate.
X-rays. Opacity or fluid level may be seen in the sphenoid
TREATMENT
sinus. Lateral view of the sphenoid sinus is taken in supine or
prone position and is helpful to demonstrate the fluid level. Treatment is the same as for acute infection of other
CT scan is more useful. sinuses.
Chronic Sinusitis 37
CLINICAL FEATURES
CHRONIC SINUSITIS IN GENERAL
Clinical features are often vague and similar to those of
Sinus infection lasting for months or years is called chronic acute sinusitis but of lesser severity. Purulent nasal discharge
sinusitis. Most important cause of chronic sinusitis is failure is the commonest complaint. Foul-smelling discharge sug-
of acute infection to resolve. gests anaerobic infection. Local pain and headache are
often not marked except in acute exacerbations. Some
PATHOPHYSIOLOGY patients complain of nasal stuffiness and anosmia.

Acute infection destroys normal ciliated epithelium impairing


DIAGNOSIS
drainage from the sinus. Pooling and stagnation of secretions
in the sinus invites infection. Persistence of infection causes 1. X-ray of the involved sinus may show mucosal thickening
mucosal changes, such as loss of cilia, oedema and polyp for- or opacity.
mation, thus continuing the vicious cycle (Figure 37.1). 2. X-rays after injection of contrast material may show soft
tissue changes in the sinus mucosa.
PATHOLOGY 3. Computed tomography (CT) scan is particularly useful in
ethmoid and sphenoid sinus infections and has replaced
In chronic infections, process of destruction and attempts studies with contrast materials.
at healing proceed simultaneously. Sinus mucosa becomes 4. Aspiration and irrigation: Finding of pus in the sinus is
thick and polypoidal (hypertrophic sinusitis) or under- confirmatory.
goes atrophy (atrophic sinusitis). Surface epithelium may
show desquamation, regeneration or metaplasia. Submu-
cosa is infiltrated with lymphocytes and plasma cells and TREATMENT
may show microabscesses, granulations, fibrosis or polyp It is essential to search for underlying aetiological factors
formation. which obstruct sinus drainage and ventilation. A work-up for
nasal allergy may be required. Culture and sensitivity of sinus
BACTERIOLOGY discharge helps in the proper selection of an antibiotic.
Initial treatment of chronic sinusitis is conservative, includ-
Mixed aerobic and anaerobic organisms are often present. ing antibiotics, decongestants, antihistaminics and sinus

Pollution, chemicals, infections

Loss of cilia

Polypi, DNS,
adenoids, Impaired Mucosal
Allergy
tumours, drainage changes
allergy

Infection

Inadequate therapy of acute sinusitis


Figure 37.1 Causative factors and pathophysiology of chronic sinusitis.

195
196 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

irrigations. More often, some form of surgery is required CHRONIC SPHENOIDITIS


either to provide free drainage and ventilation or radical
surgery to remove all irreversible diseases so as to provide Sphenoidotomy. Access to the sphenoid sinus can be
wide drainage or to obliterate the sinus. obtained by removal of its anterior wall. This is accomplished
Recently, endoscopic sinus surgery is replacing radical by external ethmoidectomy or trans-septal approach, usu-
operations on the sinuses and provides good drainage and ally the former, because of the coexistence of ethmoid dis-
ventilation. It also avoids external incisions. ease with chronic sphenoiditis.

FUNGAL INFECTIONS OF SINUSES


SURGERY FOR CHRONIC SINUSITIS
Many different species of fungi are found to involve the
CHRONIC MAXILLARY SINUSITIS paranasal sinuses; the more common being the Aspergillus,
Alternaria, Mucor or Rhizopus. They may involve single or
1. Antral puncture and irrigation. Sinus cavity is irrigated multiple sinuses. Four different varieties of fungal infection
with a cannula passed through the inferior meatus. of sinuses are seen:
Removal of pus and exudates helps the sinus mucosa to
revert to normal. 1. Fungal ball. It is due to implantation of fungus into an
2. Intranasal antrostomy. It is indicated if sinus irrigations otherwise healthy sinus which on CT shows a hyperdense
fail to resolve infection. A window is created in the infe- area with no evidence of bone erosion or expansion.
rior meatus to provide aeration to the sinus and its free Maxillary sinus is the most commonly involved followed
drainage. by sphenoid, ethmoid and the frontal in that order. Treat-
3. Caldwell–Luc operation. In this operation, antrum is ment is surgical removal of the fungal ball and adequate
entered through its anterior wall by a sublabial incision. drainage of the sinus. No antifungal therapy is required.
All irreversible diseases are removed and a window is cre- 2. Allergic fungal sinusitis. It is an allergic reaction to the
ated between the antrum and inferior meatus. causative fungus and presents with sinunasal polyposis
and mucin. The latter contains eosinophils, Charcot-
Details of the above operations are described in the section Leyden crystals and fungal hyphae. There is no invasion
on Operative Surgery. of the sinus mucosa with fungus. Usually more than one
sinus are involved on one or both sides. CT scan shows
mucosal thickening with hyperdense areas. There may be
CHRONIC FRONTAL SINUSITIS expansion of the sinus or bone erosion due to pressure,
1. Intranasal drainage operations. Correction of deviated but no fungal invasion. Treatment is endoscopic surgical
septum, removal of a polyp or anterior portion of middle clearance of the sinuses with provision of drainage and
turbinate, or intranasal ethmoidectomy provide drainage ventilation. This is combined with pre and postoperative
through the frontonasal duct. Treatment of associated max- systemic steroids.
illary sinusitis also helps to resolve chronic frontal sinusitis. 3. Chronic invasive sinusitis. Here the fungus invades into
2. Trephination of frontal sinus (see p. 193). the sinus mucosa. There is bone erosion by fungus. Patient
3. External frontoethmoidectomy (Howarth’s or Lynch presents with chronic rhinosinusitis. CT scan shows thick-
operation). The frontal sinus is entered through its floor ened mucosa with opacification of sinus and bone erosion.
by a curvilinear incision round the inner margin of the Patient may have intracranial or intraorbital invasion.
orbit. Diseased mucosa is removed, ethmoid cells exen- Histopathology shows fungal invasion of submucosa and
terated and a new frontonasal duct created. granulomatous reaction with multinucleated giant cells.
4. Osteoplastic flap operation. It may be unilateral or bilat- Treatment consists of surgical removal of the involved
eral. A coronal or a brow incision is used. The anterior wall mucosa, bone and soft tissues followed by antifungal ther-
of frontal sinus is reflected as an osteoplastic flap, based apy with i.v. amphotericin B. Up to a total of 2–3 g of the
inferiorly. The diseased tissues are removed and the sinus drug is given. This is followed by itraconazole therapy for
drained through a new frontonasal duct. If it is desired to 12 months or more monitored by serial CT or MRI scans.
obliterate the sinus, all diseased as well as healthy mucosa 4. Fulminant fungal sinusitis. It is an acute presentation
are stripped off and the sinus obliterated with fat. and is mostly seen in immunocompromised or dia-
betic ­individuals. Common fungal species are Mucor or
CHRONIC ETHMOID SINUSITIS ­Aspergillus (Figure 37.2).
• Mucor causes rhinocerebral disease. Due to invasion of
1. Intranasal ethmoidectomy. This operation is done for the blood vessels, mucor fungus causes ischaemic necro-
chronic ethmoiditis with polyp formation. The ethmoid sis presenting as a black eschar, involving inferior turbi-
air cells and the diseased tissue are removed between nate, palate or the sinus. It spreads to the face, eye, skull
the middle turbinate and the medial wall of orbit by the base and the brain. Treatment is surgical debridement
intranasal route. The frontal and sphenoid sinuses can of necrotic tissue and i.v. amphotericin B.
also be drained by this operation. • Aspergillus infection can also cause acute fulminant
2. External ethmoidectomy. In this operation, ethmoid sinusitis with tissue invasion. Such patients present with
sinuses are approached through medial orbital incision. acute sinusitis and develop sepsis and other sinus com-
Access can also be obtained to sphenoid and frontal sinuses plications. Unlike Mucor infection, there is no black
and the operation is called fronto-spheno-ethmoidectomy. eschar. Treatment is antifungal therapy and surgery.
CHAPTER 37 — CHRONIC SINUSITIS 197

A B
Figure 37.2 Aspergillus fungus. Note septate hyphae with acute angle branching (arrow). (A) H&E stain, x200. (B) Gomori methenamine silver
stain, x200.

Figure 37.3 Functional endoscopic surgery of paranasal sinuses


without monitor and camera. Figure 37.4 Endoscopic surgery in progress. Endoscope and other
surgical instruments are passed through the nose and surgery per-
formed by looking at the monitor.

FUNCTIONAL ENDOSCOPIC SURGERY


OF SINUSES (FIGURES 37.3 AND 37.4) 2. Microsurgical instruments, which permit precise and lim-
ited surgery, directed at specific sites, to remove obstruc-
Better understanding of the pathophysiology of recurrent tion to the sinus ostia.
and chronic sinusitis and the fact that most of the changes are
Endoscopes can also be passed through a cannula into the
reversible, if proper drainage and ventilation is provided to
maxillary sinus to visualize its interior and take accurate
the sinuses has, in more recent years, led to the development
biopsies or deal with certain pathological conditions such as
of endoscopic surgery of sinuses. This has further been made
small cysts and polyps.
possible by advances in technology, such as development of:
With endoscopic surgery, it is now possible to cure selected
1. Rigid endoscopes, which provide better illumination and cases of chronic and recurrent infections of the frontal,
magnification and permit visualization of structures situ- maxillary, ethmoid and sphenoid sinuses without resort to
ated at different angles. external operations (see section on Operative Surgery).
38 Complications of Sinusitis

As long as infection is confined only to the sinus mucosa, it blocked. The sinus fills with mucus and its bony walls get
is called sinusitis. Complications are said to arise when infec- expanded due to expansile process. CT scan and MRI
tion spreads into or beyond the bony wall of the sinus (see can help in the diagnosis. A polyp, tumour or trauma in
Table 38.1 and Figure 38.1). the middle meatus may also obstruct the sinus ostium to
cause a mucocele.
Mucocele of sphenoid sinus or sphenoethmoidal mucocele arises
from slow expansion and destruction of sphenoid and poste-
I. LOCAL COMPLICATIONS rior ethmoid sinuses. Clinical features are those of superior
A. MUCOCELE OF PARANASAL SINUSES AND
MUCOUS RETENTION CYSTS Table 38.1 Complications of paranasal sinus
infection
The sinuses commonly affected by mucocele in the order of
frequency are the frontal, ethmoidal, maxillary and sphe- A. Local • M ucocele/Mucopyocele
noidal. There are two views in the genesis of a mucocele: • Mucous retention cyst
1. Chronic obstruction to sinus ostium resulting in accumu- • Osteomyelitis
• Frontal bone (more common)
lation of secretions which slowly expand the sinus and
• Maxilla
destroy its bony walls. B. Orbital • Preseptal inflammatory oedema of
2. Cystic dilatation of mucous gland of the sinus mucosa due lids
to obstruction of its duct. In this case, wall of mucocele • Subperiosteal abscess
is surrounded by normal sinus mucosa. The contents of • Orbital cellulitis
mucocele are sterile. • Orbital abscess
• Superior orbital fissure syndrome
Mucocele of the frontal sinus (Figure 38.2) usually presents in • Orbital apex syndrome
the superomedial quadrant of the orbit (90%) and displaces C. Intracranial • Meningitis
the eyeball forward, downward and laterally. The swelling • Extradural abscess
is cystic and nontender; egg-shell crackling may be elicited. • Subdural abscess
Sometimes, it presents as a cystic swelling in the forehead • Brain abscess
(10%). Patient’s complaints are usually mild and may include • Cavernous sinus thrombosis
headache, diplopia and proptosis. Imaging of the frontal D. Descending
sinus usually reveals clouding of the sinus with loss of scal- infections
E. Focal infections
loped outline which is so typical of the normal frontal sinus
(see Figure 38.3). Treatment is frontoethmoidectomy with
free drainage of frontal sinus into the middle meatus.
Mucocele of ethmoid sinuses causes expansion of the medial Skin Dura mater
wall of the orbit, displacing the eyeball forward and laterally. Periosteum
In addition, it may cause a bulge in the middle meatus of Arachnoid mater
nose. A mucocele of the ethmoid can be drained by an Frontal bone
Pia mater
intranasal operation, uncapping the ethmoidal bulge and Subdural abscess
establishing free drainage. Sometimes, it may require external
ethmoid operation. Pott’s puffy Brain abscess
tumour
Mucous retention cyst of the maxillary sinus presents as a
retention cyst due to obstruction of the duct of seromuci- Meningitis
nous gland and usually does not cause bone erosion. It is
Extradural
asymptomatic and is observed as an incidental finding on abscess
radiographs. No treatment is generally required for asymp-
tomatic retention cysts as most of them regress spontane-
ously over a period of time.
Mucocele of the maxillary sinus can occur as a complica-
tion of chronic sinus inflammation when its ostium is Figure 38.1 Complications of sinusitis.

198
CHAPTER 38 — COMPLICATIONS OF SINUSITIS 199

orbital fissure syndrome (involvement of CN III, IV, VI and Endoscopic surgery has replaced external operation of
ophthalmic division of V) or orbital apex syndrome which the sinuses for treatment of all mucocele or mucopyoceles
is superior orbital fissure syndrome with additional involve- of various sinuses.
ment of optic and maxillary division of trigeminal nerve.
Exophthalmos is always present and the pain is localized B. OSTEOMYELITIS
to the orbit or forehead. Some may complain of headache
in the occiput or vertex. Treatment is external ethmoidec- Osteomyelitis is infection of bone marrow and should be dif-
tomy with sphenoidotomy. Anterior wall of the sphenoid ferentiated from osteitis which is infection of the compact
sinus is removed, cyst wall uncapped and its fluid contents bone. Osteomyelitis, following sinus infection, involves either
evacuated. the maxilla or the frontal bone.
Pyocele or mucopyocele is similar to mucocele but its contents 1. Osteomyelitis of the maxilla. It is more often seen in
are purulent. It can result from infection of a mucocele of infants and children than adults because of the pres-
any of the sinuses. ence of spongy bone in the anterior wall of the maxilla.
Infection may start in the dental sac and then spread to
the maxilla, but less often, it is primary infection of the
maxillary sinus. Clinical features are erythema, swelling
of cheek, oedema of lower lid, purulent nasal discharge
and fever. Subperiosteal abscess followed by fistulae may
form in infraorbital region (Figure 38.4), alveolus or
palate, or in zygoma. Sequestration of bone may occur.
Treatment consists of large doses of antibiotics, drainage
of any abscess and removal of the sequestra.
Osteomyelitis of maxilla may cause damage to tempo-
rary or permanent tooth-buds, maldevelopment of maxilla,
oroantral fistula, persistently draining sinus or epiphora.
2. Osteomyelitis of frontal bone (Figure 38.5). It is more
often seen in adults as frontal sinus is not developed in
infants and children. Osteomyelitis of frontal bone results
from acute infection of frontal sinus either directly or
through the venous spread. It can also follow trauma or
surgery of frontal sinus in the presence of acute infec-
tion. Pus may form externally under the periosteum as
soft doughy swelling (Pott’s puffy tumour), or internally as
an extradural abscess. Treatment consists of large doses
of antibiotics, drainage of abscess and trephining of fron-
Figure 38.2 Mucocele of frontal sinus. Note swelling above the tal sinus through its floor. Sometimes, it requires removal
medial canthus of left eye (arrow).

Figure 38.3 CT scan of mucocele of the left frontoethmoid region.


Note the left eyeball has been displaced downwards and laterally Figure 38.4 Osteomyelitis of maxilla with fistula formation in infra-
(arrows) (different patient). orbital region (arrow).
200 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

of sequestra and necrotic bone by raising a scalp flap ethmoids forms on the medial wall of orbit and displaces
through a coronal incision (Figure 38.5). the eyeball forward, downward and laterally; from the
frontal sinus, abscess is situated just above and behind the
medial canthus and displaces the eyeball downwards and
II. ORBITAL COMPLICATIONS laterally; from the maxillary sinus, abscess forms in the
floor of the orbit and displaces the eyeball upwards and
Orbit and its contents are closely related to the ethmoid, forwards.
frontal and maxillary sinuses, but most of the complica- 3. Orbital cellulitis. When pus breaks through the perios-
tions, however, follow infection of ethmoids as they are teum and finds its way into the orbit, it spreads between
separated from the orbit only by a thin lamina of bone— the orbital fat, extraocular muscles, vessels and nerves.
lamina papyracea. Infection travels from these sinuses Clinical features will include oedema of lids, exophthal-
either by osteitis or as thrombophlebitic process of eth- mos, chemosis of conjunctiva and restricted movements
moidal veins. of the eye ball. Vision is affected causing partial or total
Orbital complications include: loss which is sometimes permanent. Patient may run high
fever. Orbital cellulitis is potentially dangerous because
1. Inflammatory oedema of lids. This is only reactionary.
of the risk of meningitis and cavernous sinus thrombosis.
There is no erythema or tenderness of the lids which
4. Orbital abscess. Intraorbital abscess usually forms along
characterises lid abscess. It involves only preseptal space,
lamina papyracea or the floor of frontal sinus. Clinical
i.e. lies in front of orbital septum. Eyeball movements
picture is similar to that of orbital cellulitis. Diagnosis
and vision are normal. Generally, upper lid is swollen in
can be easily made by CT scan or ultrasound of the orbit.
frontal, lower lid in maxillary, and both upper and lower
Treatment is i.v. antibiotics and drainage of the abscess
lids in ethmoid sinusitis.
and that of the sinus (ethmoidectomy or trephination of
2. Subperiosteal abscess. Pus collects outside the bone
frontal sinus).
under the periosteum. A subperiosteal abscess from
5. Superior orbital fissure syndrome. Infection of sphenoid
sinus can rarely affect structures of superior orbital fis-
sure. Symptoms consist of deep orbital pain, frontal
headache and progressive paralysis of CN VI, III and IV,
in that order.
6. Orbital apex syndrome. It is superior orbital fissure syn-
drome with additional involvement of the optic nerve and
maxillary division of the trigeminal (V2) (Figure 38.6).

III. INTRACRANIAL COMPLICATIONS

Frontal, ethmoid and sphenoid sinuses are closely related


to anterior cranial fossa and infection from these can cause:
1. Meningitis and encephalitis
2. Extradural abscess
3. Subdural abscess
Figure 38.5 Case of chronic frontal sinusitis presenting with a fistula 4. Brain abscess
in the floor of the sinus. 5. Cavernous sinus thrombosis.

Orbital
periosteum

Lamina
papyracea

A B C
Figure 38.6 Orbital complications of sinusitis. (A) Normal. (B) Subperiosteal abscess. (C) Orbital abscess.
CHAPTER 38 — COMPLICATIONS OF SINUSITIS 201

and orbital complications from these sinus infections can


Table 38.2 Source and route of infection in cause thrombophlebitis of the cavernous sinus(es). Other
cavernous sinus thrombosis sources of infection are listed in Table 38.2. The valveless
nature of the veins connecting the cavernous sinus causes
Source Disease Route
easy spread of infection.
Nose and danger Furuncle and Pharyngeal plexus Clinical features. Onset of cavernous sinus thrombophle-
area of face septal abscess bitis is abrupt with chills and rigors. Patient is acutely ill.
Ethmoid sinuses Orbital cellulites Ophthalmic veins Eyelids get swollen with chemosis and proptosis of eyeball.
or abscess Cranial nerves III, IV and VI which are related to the sinus
Sphenoid sinus Sinusitis Direct
get involved individually and sequentially causing total oph-
Frontal sinus Sinusitis and Supraorbital and
osteomyelitis ophthalmic
thalmoplegia. Pupil becomes dilated and fixed, optic disc
of frontal bone veins shows congestion and oedema with diminution of vision.
Orbit Cellulitis and Ophthalmic veins Sensation in the distribution of V1 (ophthalmic division of
abscess CN V) is diminished. CSF is usually normal. Condition needs
Upper lid Abscess Angular vein and to be differentiated from orbital cellulitis (Table 38.3). CT
ophthalmic scan is useful for this.
veins Treatment. It consists of i.v. antibiotics and attention
Pharynx Acute tonsillitis Pharyngeal plexus to the focus of infection, drainage of infected ethmoid
or peritonsillar
or sphenoid sinus. Blood culture should be taken before
abscess
starting antibiotic therapy. Role of anticoagulants is not
Ear Petrositis Petrosal venous
sinuses clear.

IV. DESCENDING INFECTIONS


Table 38.3 Differences between orbital cellulitis In suppurative sinusitis, discharge constantly flows into the
and cavernous sinus thrombosis pharynx and can cause or aggravate:
Cavernous sinus 1. Otitis media (acute or chronic).
Orbital cellulitis thrombosis 2. Pharyngitis and tonsillitis. Hypertrophy of lateral lym-
Source Commonly ethmoid Nose, sinuses, phoid bands behind the posterior pillars (lateral phar-
sinuses orbit, ear or yngitis) is indicative of chronic sinusitis. It may be
pharynx unilateral and affect the side of the involved sinus. Chronic
Onset Slow; starts with • Abrupt with high sinusitis may also cause recurrent tonsillitis or granular
oedema of eyelids fever and chills pharyngitis.
the inner canthus with near signs of 3. Persistent laryngitis and tracheobronchitis. Sinusitis may
→ chemosis → toxaemia be associated with recurrent laryngitis, bronchiectasis
proptosis • Oedema of and asthma but the latter are not necessarily caused by
eyelids, chemosis
sinusitis.
and proptosis
Cranial nerve Involved concurrently Involved individually
involvement with complete and sequentially
ophthalmoplegia V. FOCAL INFECTIONS
Laterality Often involves one eye Involves both eyes
The role of sinus infection to act as focus of infection is
doubtful. A few conditions such as polyarthritis, tenosy-
novitis, fibrositis and certain skin diseases may respond
CAVERNOUS SINUS THROMBOSIS
to elimination of infection in the sinuses. However, sinus
Aetiology. Infection of paranasal sinuses, particularly those infection, if present in these cases, is treated on its own
of ethmoid and sphenoid and less commonly the frontal, merit.
39 Benign and Malignant
Neoplasms of Nasal Cavity

Both benign and malignant tumours of the nasal cavity 3. Pleomorphic adenoma. Rare tumour, usually arises from
(Table 39.1) per se are uncommon. Very often their separa- the nasal septum. Treatment is wide surgical excision.
tion from tumours of paranasal sinuses is difficult except in
4. Schwannoma. Schwannoma is an uncommon benign
early stages. In addition to primary tumours, nasal cavity can
tumour arising from the nose or paranasal sinuses. The
be invaded by growths from paranasal sinuses, nasopharynx,
latter include ethmoid, maxillary and sphenoid sinuses. It
cranial or buccal cavity.
arises from the Schwann cells of nerve sheath.
Benign lesions are usually smooth, localized and covered
Clinically it presents a rounded mass, firm in consistency,
with mucous membrane. Malignant ones are usually friable,
yellowish in colour and may show blood vessels running on
have a granular surface and tend to bleed easily.
its surface. It can cause pressure necrosis of the surrounding
bones. Imaging techniques, CT and MRI, are useful to show
the extent. Diagnosis is made on biopsy. Treatment is surgi-
BENIGN NEOPLASMS
cal excision. They can be removed by endoscopic surgery or
by external approaches.
1. Squamous papilloma. Verrucous lesions similar to skin
warts can arise from the nasal vestibule or lower part of nasal
septum. They may be single or multiple, pedunculated or
sessile (Figure 39.1). Treatment is local excision with cauter-
ization of the base to prevent recurrence. They can also be Table 39.1 Tumours of nasal cavity
treated by cryosurgery or laser.
Benign Malignant
2. Inverted papilloma (Transitional cell papilloma or Ring-
•  quamous papilloma
S • C arcinoma
ertz tumour or Schneiderian papilloma). It is a tumour of the
• Inverted papilloma • Squamous cell carcinoma
nonolfactory mucosa of nose (Schneiderian membrane) and
• Pleomorphic adenoma • Adenocarcinoma
paranasal sinuses. Most common site of origin is lateral wall • Schwannoma • Malignant melanoma
of nose in the middle meatus; less commonly it arises from • Meningioma • Esthesioneuroblastoma
the maxillary, frontal or sphenoid sinus (Figure 39.2). It is so • Haemangioma • Haemangiopericytoma
named because hyperplastic papillomatous tissue grows into • Chondroma • Lymphoma
the stroma rather than in exophytic manner (Figure 39.3). • Angiofibroma • Solitary plasmacytoma
Human papilloma virus is thought to be responsible for its • Encephalocele • Various types of sarcoma
aetiology. Clinically, men are affected more than women in • Glioma
the age group of 40–70. It is almost always unilateral and pres- • Dermoid
ents with nasal obstruction, nasal discharge and epistaxis. It
can invade sinuses or orbit. Orbital involvement causes pro-
ptosis, diplopia and lacrimation.
On examination of nose or endoscopy, it presents as a pale
polypoidal mass resembling a simple nasal polypus or polypi.
Computed tomography (CT) and magnetic resonance
imaging (MRI) show the location and extent of the lesion.
MRI also helps to differentiate associated secretions in sinus
from the actual tumour mass. Biopsy is essential for diagnosis.
Care should be taken as simple nasal polypi may be associ-
ated with it or even the patient might have been operated
for their removal.
Treatment. Medial maxillectomy is the treatment of choice.
It can be performed by lateral rhinotomy or sublabial deglov-
ing approach. These days endoscopic approach is preferred.
In 10–15% of cases, it is associated with malignancy.
Wider external surgical approaches may be required for
tumour extending to the frontal sinus or orbit. Recurrence can
occur. Radiotherapy is not advised as it may induce malignancy. Figure 39.1 Squamous papilloma nose, left side.

202
CHAPTER 39 — BENIGN AND MALIGNANT NEOPLASMS OF NASAL CAVITY 203

5. Meningioma. It is an uncommon tumour found intrana- 8. Angiofibroma. It is included in nasal tumours because its
sally. Treatment is surgical excision by lateral rhinotomy. primary site of origin is supposed to be posterior part of
nasal cavity near the sphenopalatine foramen (see p. 246).
6. Haemangioma. It may be:
9. Intranasal meningoencephalocele. It is herniation of
(a) Capillary haemangioma (bleeding polypus of the septum). It is brain tissues and meninges through foramen caecum or
a soft, dark red, pedunculated or sessile tumour arising cribriform plate. It presents as a smooth polyp in the upper
from the anterior part of nasal septum (Figure 39.4). part of nose between the septum and middle turbinate, usu-
Usually it is smooth but may become ulcerated and ally in infants and young children. The mass increases in size
present with recurrent epistaxis and nasal obstruction. on crying or straining. Unless care is taken, it may be misdi-
Treatment is local excision with a cuff of surrounding agnosed as a simple polyp and mistakenly avulsed, resulting
mucoperichondrium. in cerebrospinal fluid rhinorrhoea or meningitis. For the
(b) Cavernous haemangioma. It arises from the turbinates on same reason biopsy should not be taken. CT scan is essential
the lateral wall of nose. It is treated by surgical excision to demonstrate a defect in the base of skull. Treatment is
with preliminary cryotherapy. Extensive lesions may frontal craniotomy, severing the stalk from the brain, and
require radiotherapy and surgical excision. repair of dural and bony defect. Intranasal mass is removed
as secondary procedure after cranial defect has sealed.
7. Chondroma. It can arise from the ethmoid, nasal cavity or
nasal septum. Pure chondromas are smooth, firm and lobu- 10. Gliomas. Of all the gliomas, 60% are extranasal, 30%
lated. Others may be mixed type fibro-, osteo- or angiochon- are intranasal and 10% both intra and extranasal. They are
dromas. Treatment is surgical excision. For recurrent or large seen in infants and children. An intranasal glioma pres-
tumours, wide excision should be done because of their ten- ents as a firm polyp sometimes protruding at the anterior
dency to malignant transformation after repeated interference. nares.

A B
Figure 39.2 (A) Inverted papilloma in a 79-year-old male (right side). (B) CT scan of the same.

Figure 39.3 Histological section of a Schneiderian papilloma show- Figure 39.4 Bleeding polypus arising from right side of nasal
ing ribbons of thickened epithelial proliferations growing downwards septum.
into the stroma (H&E, x40).
204 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

11. Nasal dermoid. It presents as widening of upper part


of nasal septum with splaying of nasal bones and hyper-
telorism. A pit or a sinus may be seen in the midline of nasal
dorsum with hair protruding from the opening.

MALIGNANT NEOPLASMS

1. Carcinoma of nasal cavity. Primary carcinoma per se is


rare. It may be an extension of maxillary or ethmoid carci-
noma. Squamous cell variety is the most common, seen in
about 80% of cases. Rest may be adenoid cystic carcinoma
or an adenocarcinoma.
(a) Squamous cell carcinoma. It may arise from the vestibule,
anterior part of nasal septum or the lateral wall of nasal
Figure 39.5 Rhabdomyosarcoma of the nose in a 2½-years-old
cavity. Most of them are seen in men past 50 years of age.
male child.
(i) Vestibular. It arises from the lateral wall of nasal
vestibule and may extend into the columella, nasal
orbital wall. MRI with enhancement will reveal extension
floor and upper lip with metastases to parotid
into the orbit or intracranially.
nodes.
Biopsy of tumour reveals true nature of the tumour. It
(ii) Septal. Mostly arises from mucocutaneous junc-
may be low grade with formation of pseudorosettes or high
tion and causes burning and soreness in the nose.
grade with nuclear pleomorphism but no rosette formation.
It has often been termed “nose-picker’s cancer.”
It may require special staining to differentiate from other
Usually, it is of low-grade malignancy.
tumours.
(iii) Lateral wall. This is the site most commonly
It should be differentiated from lymphoma, melanoma,
involved. Easily extends into ethmoid or maxillary
plasmacytoma, rhabdomyosarcoma, undifferentiated carci-
sinuses. Grossly, it presents as a polypoid mass in
noma and neuroendocrine carcinoma.
the lateral wall of nose. Metastases are rare. Treat-
Treatment. Treatment protocols differ between institu-
ment is combination of radiotherapy and surgery.
tions. They are:
(b) Adenocarcinoma and adenoid cystic carcinoma. They arise
from the glands of mucous membrane or minor sali- (a) Craniofacial resection with adjuvant radiation.
vary glands and mostly involve upper part of the lateral (b) Preoperative radiation followed by craniofacial resection.
wall of nasal cavity. (c) Preoperative chemotherapy and radiation followed
by craniofacial resection for advanced lesions extend-
2. Malignant melanoma. Usually seen in persons about 50 ing to orbit, cribriform plate and intracranially. Neck
years of age. Both sexes are equally affected. Grossly, it pres- nodes if present are also radiated.
ents as a slaty-grey or bluish-black polypoid mass. Within the
Craniofacial resection is done by osteoplastic flap expos-
nasal cavity, most frequent site is anterior part of nasal septum
ing the anterior cranial fossa while facial approach is
followed by middle and inferior turbinate. Amelanotic vari-
through lateral rhinotomy or midfacial degloving. En-block
eties are nonpigmented. Tumour spreads by lymphatics and
removal of tumour can thus be accomplished. Defect in the
blood stream. Cervical nodal metastases may be present at the
base of skull is repaired by pericranial flap.
time of initial examination. Treatment is wide surgical exci-
sion. Immunological defences of the patient play a great role 4. Haemangiopericytoma. It is a rare tumour of vascular
in the control of this disease. Radiotherapy and chemotherapy origin. It arises from the pericyte—a cell surrounding the
suppress the immune processes and are avoided. A 5-year sur- capillaries. It is usually seen in the age group of 60–70 and
vival rate of 30% can be expected after wide surgical excision. presents with epistaxis. Brisk bleeding may occur on biopsy.
The tumour may be benign or malignant but it cannot be dis-
3. Esthesioneuroblastoma (Syn. olfactory neuroblastoma).
tinguished histologically. Treatment is wide surgical excision.
Also called olfactory placode tumour as it arises from the
Radiotherapy is used for inoperable or recurrent lesions.
olfactory epithelium in the upper third of nose. Bimodal
peaks of incidence at 10–20 and 50–60 years are seen. 5. Lymphoma. Rarely a non-Hodgkin lymphoma presents
Most common symptoms are unilateral nasal obstruction on the septum.
and epistaxis. When tumour invades orbit and the sur-
6. Plasmacytoma. Solitary plasmacytoma without gener-
rounding structures, other symptoms like proptosis, head-
alized osseous disease may be seen in the nasal cavity. It
ache, epiphora, diplopia and blurred vision can also arise.
predominantly affects males over 40 years. Treatment is
Lymph node metastases in the neck can occur in 10–15%.
by radiotherapy followed 3 months later by surgery if total
Intranasal or endoscopic examination of nose reveals a fri-
regression does not occur. Long-term follow-up is essential
able cherry-red, polypoidal mass in the upper third of nasal
to exclude development of multiple myeloma.
cavity. It is a vascular tumour and biopsy should not be imme-
diately attempted unless imaging studies have been done. 7. Sarcomas. Osteogenic sarcoma, chondrosarcoma, rhab-
High-resolution CT scan shows the extent of lesion. It domyosarcoma (Figure 39.5), angiosarcoma, malignant his-
may show destruction or erosion of the cribriform plate or tiocytoma are other rare tumours affecting the nose.
Neoplasms of 40
Paranasal Sinuses

Paranasal sinuses may be affected by both benign and malig- 3. Histology. More than 80% of the malignant tumours are
nant neoplasms but the latter are much more common. of squamous cell variety. Rest are adenocarcinoma, adenoid
cystic carcinoma, melanoma and various types of sarcomas
(Figures 40.3 and 40.4).
BENIGN NEOPLASMS
CARCINOMA OF MAXILLARY SINUS
1. Osteomas. They are most commonly seen in the frontal
sinus followed in turn by those of ethmoid and maxillary. It arises from the sinus lining and may remain silent for a
They may remain asymptomatic, being discovered inciden- long time giving only vague symptoms of “sinusitis.” It then
tally on X-rays (Figure 40.1). Treatment is indicated when spreads to destroy the bony confines of the maxillary sinus
they become symptomatic, causing obstruction to the sinus and invades the surrounding structures.
ostium, formation of mucocele, pressure symptoms due to
CLINICAL FEATURES (FIGURE 40.5)
their growth in the orbit, nose or cranium.
Disease is common in 40–60 age group with preponderance
2. Fibrous dysplasia. In this condition, bone is replaced in males.
by fibrous tissue; mostly involves maxillary but sometimes
the ethmoid and frontal sinuses. Patient seeks advice for 1. Early features of maxillary sinus malignancy are nasal
disfigurement of the face, nasal obstruction and displace- stuffiness, blood-stained nasal discharge, facial paraes-
ment of the eye. Treatment is surgical resculpturing of the thesias or pain and epiphora. These symptoms may be
involved bone to achieve a good cosmetic and functional missed or simply treated as sinusitis.
result (Figure 40.2). 2. Late features will depend on the direction of spread and
extent of growth.
3. Ossifying fibroma. Seen in young adults. The tumour can
be shelled out easily.
4. Ameloblastoma (adamantinoma). It is a locally aggressive
tumour that arises from the odontogenic tissue and invades
the maxillary sinus. Treatment is surgical excision.
Other rare tumours include inverted papilloma, meningioma
and haemangioma (see Chapter 39).

MALIGNANT NEOPLASMS

1. Incidence. Cancer of nose and paranasal sinuses consti-


tutes 0.44% of all body cancers in India (0.57% in males
and 0.44% in females). Most frequently involved are the
maxillary sinuses followed in turn by ethmoids, frontal and
sphenoid.
2. Aetiology. Cause of sinus malignancy is largely unknown.
People working in hardwood furniture industry, nickel
refining, leather work and manufacture of mustard gas have
shown higher incidence of sinunasal cancer. Cancer of the
maxillary sinus is common in Bantus of South Africa where
locally made snuff is used, which is found rich in nickel and
chromium.
Workers of furniture industry develop adenocarci-
noma of the ethmoids and upper nasal cavity, while those
engaged in nickel refining get squamous cell and anaplastic
carcinoma. Figure 40.1 Osteoma right frontal sinus (arrow).

205
206 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

A B
Figure 40.2 Fibrous dysplasia of maxilla in a 13-year-old girl. (A) As seen externally. (B) After retraction of the lip.

Fat spaces

Keratin pearl

Figure 40.3 Photomicrograph showing adenocarcinoma having


glandular pattern with neoplastic epithelial cells lining them. The cells
contain intracytoplasmic mucin (black arrow) (H&E, x200). Figure 40.4 Photomicrograph showing well-differentiated squa-
mous cell carcinoma with pearl formation (H&E, x200).

A B
Figure 40.5 Antroethmoidal carcinoma left side. Note (A) swelling of left cheek and (B) expansion of alveolus and palate.
CHAPTER 40 — NEOPLASMS OF PARANASAL SINUSES 207

3. Medial spread to nasal cavity gives rise to nasal obstruc- 3. Lederman’s classification (Figure 40.7). It uses two hori-
tion, discharge and epistaxis. It may also spread into zontal lines of Sebileau; one passing through the floors
anterior and posterior ethmoid sinuses and that is of orbits and the other through floors of antra, thus
why most antral malignancies are antroethmoidal in dividing the area into:
nature. (a) Suprastructure. Ethmoid, sphenoid and frontal sinuses
4. Anterior spread causes swelling of the cheek and later and the olfactory area of nose.
invasion of the facial skin. (b) Mesostructure. Maxillary sinus and the respiratory
5. Inferior spread causes expansion of alveolus with dental part of nose.
pain, loosening of teeth, poor fitting of dentures, ulcer- (c) Infrastructure. Containing alveolar process. This clas-
ation of gingiva and swelling in the hard palate. sification further uses vertical lines, extending down
6. Superior spread invades the orbit causing proptosis, diplo- the medial walls of orbit to separate ethmoid sinuses
pia, ocular pain and epiphora. and nasal fossa from the maxillary sinuses.
7. Posterior spread is into pterygomaxillary fossa, pterygoid
The student may note here that suprastructure and infra-
plates and the muscles causing trismus. Growth may also
structure of Lederman’s classification is not the same as in
spread to the nasopharynx, sphenoid sinus and base of
Ohngren’s classification.
skull.
8. Intracranial spread can occur through ethmoids, cribriform TREATMENT
plate or foramen lacerum.
Histologically, nature of malignancy is important in decid-
9. Lymphatic spread. Nodal metastases are uncommon and
ing the line of treatment as is the location and extent of
occur only in the late stages of disease. Submandibular
disease.
and upper jugular nodes are enlarged. Maxillary and
ethmoid sinuses drain primarily into retropharyngeal
nodes, but these nodes are inaccessible to palpation.
10. Systemic metastases are rare. May be seen in the lungs
(most commonly) and occasionally in bone.
Suprastructure
DIAGNOSIS Ohngren’s
1. Radiograph of sinuses. Opacity of the involved sinus with line
expansion and destruction of the bony walls.
2. Computed tomography (CT) scan. If available, this is the
best noninvasive method to find the extent of disease. CT Infrastructure
scan should be done both in axial and coronal planes. It
also helps in the staging of disease.
3. Biopsy. If growth presents in the nose or mouth, biopsy
can be easily taken. In early cases, with suspicion of malig-
nancy, sinus should be explored by Caldwell–Luc opera-
tion. Direct visualization of the site of tumour in the sinus
Figure 40.6 Ohngren’s line extends from medial canthus of eye
also helps in staging of the tumour.
to the angle of mandible. Growths anteroinferior to this plane (infra-
Endoscopy of the nose and maxillary sinus will provide structural) have a better prognosis than those posterosuperior to it
detailed examination. An accurate biopsy can also be taken. (suprastructural).
This route is preferred to Caldwell-Luc approach.

CLASSIFICATION
There is no universally accepted classification for maxillary
carcinoma.
1. Ohngren’s classification. An imaginary plane is drawn,
extending between medial canthus of eye and the angle Suprastructure Orbit
of mandible (Figure 40.6). Growths situated above this
plane (suprastructural) have a poorer prognosis than
those below it (intrastructural).
2. AJCC (American Joint Committee on Cancer) classifica-
tion (Tables 40.1–40.3). AJCC classification is only for
squamous cell carcinoma and does not include nonepi- Meso-
thelial tumours of lymphoid tissue, soft tissue, cartilage structure
and bone. Histopathologically, squamous cell carcinoma
is further graded into:
(a) Well-differentiated,
(b) Moderately differentiated and Infrastructure
(c) Poorly differentiated.
In histopathology, note should also be made of vascular
or perineural invasion. Figure 40.7 Lederman’s classification.
208 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Table 40.1 TNM classification and staging system of cancer of maxillary sinus

Maxillary sinus
T1 Tumour limited to maxillary sinus mucosa with no erosion or destruction of bone.
T2 Tumour causing bone erosion or destruction including extension into the hard palate and/or middle nasal meatus, except exten-
sion to posterior wall of maxillary sinus and pterygoid plates.
T3 Tumour invades any of the following: bone of the posterior wall of maxillary sinus, subcutaneous tissues, floor or medial wall of
orbit, pterygoid fossa and ethmoid sinuses.
T4a Tumour invades anterior orbital contents, skin of cheek, pterygoid plates, infratemporal fossa, cribriform plate, sphenoid or
frontal sinuses.
T4b Tumour invades any of the following: orbital apex, dura, brain, middle cranial fossa, cranial nerves other than maxillary division
of trigeminal nerve (V2), nasopharynx or clivus.

Regional lymph nodes (N)


Nx Regional lymph nodes cannot be assessed.
N0 No regional lymph node metastasis.
N1 Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension.
N2 Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm in greatest dimension; or in multiple ipsi-
lateral lymph nodes, none more than 6 cm in greatest dimension; or in bilateral or contralateral lymph nodes, none more than
6 cm in greatest dimension.
N2a Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm in greatest dimension.
N2b Metastasis in multiple ipsilateral lymph nodes, none more than 6 cm in greatest dimension.
N2c Metastasis in bilateral or contralateral lymph nodes, none more than 6 cm in greatest dimension.
N3 Metastasis in a lymph node, more than 6 cm in greatest dimension.

Distant metastasis (M)


Mx Distant metastasis cannot be assessed.
M0 No distant metastasis.
M1 Distant metastasis.

Source: AJCC, Cancer Staging Manual, fifth ed. Chicago, 2002.

Table 40.2 Stage grouping of cancer of maxillary Table 40.3 Classification of cancer of nasal cavity
and ethmoid sinuses and ethmoid sinuses (AJCC, 2002)

Stage I T1 N0 M0 T1 Tumour restricted to any one subsite, with or without


Stage II T2 N0 M0 bony invasion
Stage III T3 N0 M0 T2 Tumour invading two subsites in a single region or
T1 or T2 or T3 with N1 M0 extending to involve an adjacent region within the
Stage IV A T4 N0 M0 nasoethmoidal complex, with or without bony invasion
T4 N1 M0 T3 Tumour extends to invade the medial wall or floor of the
Stage IV B Any T N2 M0 orbit, maxillary sinus, palate or cribriform plate
Any T N3 M0 T4a Tumour invades any of the following: anterior orbital
Stage IV C Any T Any N M1 contents, skin of nose or cheek, minimal extension to
anterior cranial fossa, pterygoid plates, sphenoid or
Regional lymph nodes and distant metastasis. They are divided in frontal sinuses
the usual manner into N0, N1, N2 & N3 (see p. 228) and M0, M1. T4b Tumour invades any of the following: orbital apex, dura,
brain, middle cranial nerves other than (V2), nasophar-
ynx or clivus

Early cases with Stage I and II squamous cell carcinomas


are treated with surgery (Figures 40.8 and 40.9) or radiation
with equal results. T3 and T4 lesions are treated by combined
modalities of radiation and surgery. Radiation in such cases tumours by different workers with 5 year survival of more
may be given preoperatively or postoperatively. Preoperative than 60%. Intra-arterial infusion of 5-Fu or cisplatin and
dose of radiation is 5500 cGy. Similarly postoperative dose 5-Fu with concomitant radiation has also been used with
of radiation used is 5000–5500 cGy. Now three-dimensional good results in preference to deformities created by exten-
conformal radiotherapy and intensity-modulated techniques sive surgery associated with advanced malignancy.
of radiotherapy cover larger tumour volumes and help to
reduce side effects of radiation to optic nerves and lens by PROGNOSIS
providing accurate and homogenous radiation dose. Survival diminishes with the stage of tumour. Overall
Chemoradiation, i.e. chemotherapy and radiation con- 5 year survival is about 40–50%. However, advances are being
comitantly has also been used for large and inoperable made in the multimodal therapy with improved techniques
CHAPTER 40 — NEOPLASMS OF PARANASAL SINUSES 209

of radiation delivery with the hope to improve results and TREATMENT


protect injury to lens and optic nerve. CT scan is essential to know the extent of disease and intra-
cranial spread. In early cases, treatment is preoperative
ETHMOID SINUS MALIGNANCY radiation, followed by lateral rhinotomy and total ethmoid-
ectomy. If cribriform plate is involved, anterior cranial fossa
Ethmoid sinuses are often involved from extension of the is exposed by a neurosurgeon and total exenteration of the
primary growth of the maxillary sinus. Primary growth of growth in one piece is accomplished by what is called cranio-
ethmoid sinuses per se is not common. facial resection.
CLINICAL FEATURES PROGNOSIS
1. Early features include nasal obstruction, blood-stained Five-year-cure rate of about 30% can be expected.
nasal discharge and retro-orbital pain.
2. Late features are broadening of the nasal root, lateral dis-
placement of eyeball and diplopia (Figure 40.10). Exten- FRONTAL SINUS MALIGNANCY
sion through cribriform plate may cause meningitis. Frontal sinus malignancies are uncommon and are seen in
3. Nodal involvement is not common. Upper nodes may be the age group of 40–50 years with male predominance (5:1).
involved.

Figure 40.8 Weber–Fergusson’s incision used in maxillectomy.

Figure 40.10 Carcinoma ethmoid.

Figure 40.9 (A) Maxillectomy with orbital


exenteration on the right side. (B) Same
patient after rehabilitation with a maxillary A B
prosthesis and an artificial eye.
210 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

CLINICAL FEATURES with ethmoid and orbital exenteration. Neurosurgical


Pain and swelling of the frontal region are the presenting approach may be required to resect the dura of anterior
features. Growths may erode through the floor of frontal cranial fossa, if involved.
sinus and present as a swelling above the medial canthus.
Growths of frontal sinus may extend through the ethmoids
SPHENOID SINUS MALIGNANCY
into the orbit. Dura of anterior cranial fossa may be involved
if growth penetrates the posterior wall of the sinus. Primary malignancy of the sinus is rare. It has to be differ-
entiated from the inflammatory lesions in this area. Plain
TREATMENT X-rays, CT scan and biopsy through sphenoidotomy are
Frontal sinus malignancy is treated by preoperative radiation essential to know the nature and extent of disease. Radio-
followed by surgery. Surgery includes frontal sinusotomy therapy is the mainstay of treatment.
Proptosis 41
Orbit has rigid walls; any space occupying lesion of the orbit affected structures. An important feature is involvement
causes eyeball to protrude forward or also displace in some of muscle and its tendon attached to the globe and differ-
other direction, i.e. medial, lateral, up or down depending entiates it from thyroid-related disease where only muscle
on location in the orbit. Proptosis should be differentiated belly is involved but not its tendon. Biopsy shows nonspe-
from pseudoproptosis, i.e. apparently proptosed eyeball cific inflammation without evidence of vasculitis. Treat-
though it is normal in position. This happens with enoph- ment is oral steroids. In some cases, immunosuppression
thalmos of the contralateral eye due to previous forgotten with cyclophosphamide, cyclosporine or radiotherapy
trauma such as orbital blowout fractures. Lid retraction and may be required.
high myopia can also make the eyeball look proptosed. Pro- 2. Graves ophthalmopathy. This is the most common cause
ptosis can be measured by exophthalmometer. of bilateral and sometimes unilateral proptosis. Patient is
hyperthyroid but sometimes he is euthyroid or even hypo-
AETIOLOGY thyroid. Lid retraction and lid lag may be present with
chemosis and lid oedema. CT scan is useful to differenti-
Table 41.1 shows the various conditions causing proptosis
ate it from idiopathic orbital inflammation (vide supra).
and can be remembered by the acronym of VEIN.
Visual loss can occur. Extreme proptosis causes corneal
Various conditions of concern to the ENT surgeon
ulceration and may require orbital decompression which
include orbital cellulitis or orbital abscess, subperiosteal
nowadays can be done endoscopically through the nose.
abscess, fungal infections of sinuses, Graves ophthalmopa-
3. Haemangioma of orbit. It can be cavernous or capillary.
thy, benign and malignant neoplasms of nose and paranasal
Cavernous haemangioma is the most common benign tumour
sinuses, such as angiofibroma, inverted papilloma, nasal pol-
in adult. It is more common in females in the age group
yposis, mucoceles, esthesioneuroblastoma, paranasal sinus
of 18–67 years. It manifests as painless, progressive, uni-
malignancies and trauma following endoscopic surgery.
lateral proptosis. CT/MRI reveals a round or oval mass
Some important diseases are described below.
without associated inflammation or infiltration around
1. Idiopathic orbital inflammation. As the name indicates, it. It is an encapsulated mass. Intraconal in location and
cause is uncertain. It may be diffused or localized to enhances on i.v. contrast. Treatment is complete excision
specific structures in the orbit, e.g. muscles (myositis), with its capsule by lateral orbitotomy.
lacrimal gland, sclera (scleritis) or optic nerve (perineu- 4. Capillary haemangioma. Most common tumour of orbit
ritis). Patient complains of dull orbital pain especially on in infants and children. May be isolated or associated
eye movements. Proptosis is seen in 70–80% of patients. with a lesion on the upper lid or elsewhere on the skin.
CT scan with enhancement shows enlargement of the Most of them involute by age 7. CT/MRI with contrast

Table 41.1 Causes of proptosis (Remember the mnemonic VEIN)

Vascular. Venous varix, cavernous haemangioma, carotid-cavernous fistula


Endocrinal. Graves’ disease which may cause bilateral or sometimes even unilateral proptosis
Inflammations and infections. Idiopathic orbital inflammation (pseudotumour of orbit), orbital cellulitis or abscess, mucormycosis or
aspergillosis of sinuses, Wegener’s granulomatosis, inflammations of lacrimal gland.
Neoplastic. Tumours (both benign and malignant) or tumour-like conditions arising from the orbital contents or its adjoining structures.
Orbit contains eyeball, optic nerve, muscles, nerves, blood vessels and lacrimal gland and tumour and tumour-like conditions can arise
from them. They also arise from paranasal sinuses and cranial cavity and invade the orbit.
(a) Primary tumours of orbit, its walls or adnexa (lid, lacrimal gland and conjunctiva). Dermoid cyst, cavernous or capillary haemangioma,
schwannoma, glioma, retinoblastoma, fibrous dysplasia, osteoma, histiocytosis X, orbital meningioma, pleomorphic adenoma of lac-
rimal gland. Malignant tumours include rhabdomyosarcoma, lymphoma, leukaemic deposits, malignant tumours of lacrimal gland and
melanoma of choroid.
(b) Tumours of paranasal sinuses. Mucocele of frontal or ethmoidal sinuses, inverted papilloma, angiofibroma, malignant tumours of
sinuses.
Tumours from cranial cavity. Meningioma of the sphenoid ridge.
(c) Metastatic tumours. Carcinoma breast (most common), lung, prostate, kidney, thyroid, gastrointestinal tract.

211
212 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

is diagnostic. Tumour is nonencapsulated and infiltrates may show a cyst with pressure effects (Figure 41.1). Large
the surrounding structures. Local or systemic steroids cysts may communicate with temporal fossa, paranasal
help to involute the mass. Total excision is not possible. sinuses or the cranial cavity. Treatment is surgical excision.
5. Venous varix of the orbit. It presents with positional pro- 9. Tumours of optic nerve. Glioma of optic nerve is usually
ptosis and congestion. Proptosis can also be induced by seen in children and may be associated with neurofibro-
Valsalva manoeuvre. A carotid-cavernous fistula is either matosis. It causes progressive proptosis and visual loss.
spontaneous or traumatic; it presents with pulsatile pro-   Meningioma of optic nerve (from arachnoid sheath)
ptosis, bruit, visual loss, dilated and arterialized blood occurs mostly in the middle-aged women leading to pro-
vessels in the conjunctiva or limbus. ptosis and visual loss.
6. Lymphoma. It is the most common malignant tumour of
adults. It may be isolated or associated with systemic dis-
EVALUATION OF PROPTOSIS
ease. Most of the patients are between 50 and 70 years with
female preponderance. It presents as painless progressive A case of proptosis requires a detailed history including
exophthalmos. Usually lesions are located anteriorly and onset, duration and progression. Associated illnesses (thy-
can be palpated or seen under the conjunctiva. Most of roid disease, tumours of nose or paranasal sinuses, systemic
them are extraconal. CT shows a homogenous tumour disorders such as leukaemia, lymphoma, Wegener’s granu-
without bone involvement. Biopsy is necessary to differ- lomatosis) should be looked for. Pain is a feature of inflam-
entiate it from the benign lymphoid or other tumours. mation or infection. Visual loss may be present and should
Isolated lymphoma can be treated by radiation alone be documented.
while systemic ones require chemotherapy in addition to Physical examination should include type of proptosis
orbital radiation. (straight forward or with globe displacement), condition of
7. Rhabdomyosarcoma. It is the most common primary malig- the conjunctiva (swelling, chemosis), scleral appearance, ocu-
nant tumour of orbit in children and is usually seen at lar movements and vision. Note should also be made if the
6–7 years of age. It can occur even in the newborn. It pres- proptosis is pulsatile or associated with change in position of
ents as painless but progressive proptosis and can spread the head or appears on performing Valsalva (venous varix).
to the adjoining paranasal sinuses. It may be intraconal CT and MRI are important and give clue to the type of
or extraconal. CT is helpful in diagnosis. Biopsy should tumour (intraconal/extraconal), smooth or infiltrative,
be taken. Treatment is radiation and chemotherapy. Five- location in the orbit and its extent, any changes in the
year survival of 90% can be achieved in localized disease. adjoining bone or extension to sinuses or cranial cavity.
8. Dermoid cyst. It is the most common benign tumour of They can help to differentiate thyroid orbitopathy from the
orbit in children. It is due to the trapped ectoderm and idiopathic orbital inflammation.
occurs at suture lines. Deep dermoids of orbit arise from Ultrasonography may be required to find abscess or cystic
the sphenoethmoid or sphenozygomatic sutures. They may lesions.
remain asymptomatic till adult age. They present with pain- FNAC or biopsy of the lesion may be required for histo-
less, progressive proptosis with globe displacement. CT orbit logic diagnosis.

A B
Figure 41.1 Dermoid cyst of the right orbit: (A) axial view and (B) coronal view (arrows). Patient presented with a mild proptosis.
CHAPTER 41 — PROPTOSIS 213

Systemic diseases causing orbital lesions should be investi- radiation for malignancies and sometimes pseudotumour.
gated as mandated by history and clinical examination and Surgery of orbit includes debulking of lymphangioma or
relevant investigation. plexiform neurofibroma to relieve pressure on the optic
nerve orbital exenteration for mucormycosis and malignan-
cies. Endoscopic orbital decompression may be required
MANAGEMENT
in Graves ophthalmopathy. Lateral orbitotomy is required
Imaging techniques help to make a diagnosis. Biopsy of the for lesions of lacrimal gland or those situated intraconally.
lesion can be taken depending on its location in the orbit. Transcranial approach is used for lesions at the orbital apex
Anteriorly located lesions can be approached by lid or con- or those invading intracranially from the orbit or vice versa.
junctival incision. Excisional biopsy is useful in encapsulated
and well-circumscribed lesions such as dermoid, cavernous Remember
haemangioma and pleomorphic adenoma of the lacrimal In children, dermoid cyst of the orbit is the most common
gland. All cases causing proptosis do not require surgery. benign tumour and rhabdomyosarcoma the malignant one.
Medical treatment includes antibiotics in orbital cellulitis, In adults, cavernous haemangioma is the most common
steroids in pseudotumour, chemotherapy for lymphoma, benign tumour of orbit and lymphoma the malignant one.
This page intentionally left blank

     

You might also like