Dhingra Nose
Dhingra Nose
Dhingra Nose
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
Root of nose
Dorsum
Naris
Alar groove
Columella
Naris
Columella Philtrum
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.
Agger nasi
Atrium
Middle turbinate
and meatus
Hiatus semilunaris
Sphenoethmoid recess with
Uncinate process opening of sphenoid sinus
Bulla
ethmoidalis
Opening of frontal 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.
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.
140
CHAPTER 24 — PHYSIOLOGY OF NOSE 141
A B
Figure 24.1 Physiology of nasal airflow. (A) Inspiration. (B) Expiration.
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.
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.
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
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.
147
148 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES
High arched
DNS palate
A
Figure 26.3 DNS associated with high-arched palate.
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
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
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.
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.
152
CHAPTER 27 — ACUTE AND CHRONIC RHINITIS 153
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.
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.
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
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
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).
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
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
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.
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
(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.
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
172
CHAPTER 32 — NASAL POLYPI 173
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
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
176
CHAPTER 33 — EPISTAXIS 177
Ophthalmic artery
Anterior Posterior
ethmoidal artery ethmoidal artery
Little’s area
Septal branch
Branches of
sphenopalatine
artery
External carotid
artery
Figure 33.1 Blood supply of nasal septum.
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.
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
181
182 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES
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.
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
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.
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.
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
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
A B
Sphenoid sinus
Agger nasi cell
Opening of
maxillary sinus
Torus tubarius
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.
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
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.
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
Loss of cilia
Polypi, DNS,
adenoids, Impaired Mucosal
Allergy
tumours, drainage changes
allergy
Infection
195
196 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES
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.
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).
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).
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
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
MALIGNANT NEOPLASMS
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
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
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
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.
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)
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.
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