Dhingra Diseases of Ear Nose and Throat 6th Edition medgagcom

136 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Hiatus semilunaris

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

Opening of max. sinus Opening of post. ethmoid
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
lies in sagittal plane and is attached to lateral edge of crib- Uncinate process is a hook-like structure running in from
riform plate. In the middle third, it lies in frontal plane anterosuperior to posteroinferior direction. Its posterosu-
and is attached to lamina papyracea while in its posterior perior border is sharp and runs parallel to anterior border
third, it runs horizontally and forms roof of the middle of bulla ethmoidalis; the gap between the two is called hia-
meatus and is attached to lamina papyracea and medial tus semilunaris (inferior). It is a two-dimensional space of
wall of maxillary sinus. 1–2 mm width.

The ostia of  various sinuses draining anterior to basal The anteroinferior border of uncinate process is
lamella form anterior group of paranasal sinuses while those attached to the lateral wall. Posteroinferior end of unci-
which open posterior and superior to it form the posterior group. nate process is attached to inferior turbinate divid-
ing the membranous part of lower middle meatus into

CHAPTER 23 — ANATOMY OF NOSE 137

Middle Frontal Uncinate
turbinate sinus process
Lamina
papyracea

A BC

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

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

Infundibulum Inferior Max. sinus
turbinate
Uncinate
process

AB

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

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

138 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

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

CHAPTER 23 — ANATOMY OF NOSE 139

Olfactory bulb

Olfactory nerves

Ant. ethmoidal
nerve

Infraorbital Branches of
nerve sphenopalatine
ganglion
A
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.

of vasomotor and allergic rhinitis can be controlled by sec- LYMPHATIC DRAINAGE
tion of the vidian nerve. Lymphatics from the external nose and anterior part of
nasal cavity drain into submandibular lymph nodes while
BLOOD SUPPLY those from the rest of nasal cavity drain into upper jugular
Both the internal and external carotid systems supply the nodes either directly or through the retropharyngeal nodes.
nose. Details of blood supply are given on p. 176. Lymphatics of the upper part of nasal cavity communicate
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
1. Respiration. nose can filter particles up to 3 μm, while nasal mucus
2. Air-conditioning of inspired air. traps particles as fine as 0.5–3.0 μm. Particles smaller
3. Protection of lower airway. than 0.5 μm seem to pass through the nose into lower
4. Vocal resonance. airways without difficulty.
5. Nasal reflex functions. 2. Temperature control of the inspired air. It is regulated
6. Olfaction. by large surface of nasal mucosa which is structurally
adapted to perform this function. This mucous mem-
RESPIRATION brane, particularly in the region of middle and inferior
Nose is the natural pathway for breathing. Mouth breathing turbinates and adjacent parts of the septum, is highly
is an acquired act through learning. So natural is the instinct vascular with cavernous venous spaces or sinusoids which
to breath through the nose that a newborn infant with cho- control the blood flow, and this increases or decreases the
anal atresia may asphyxiate to death if urgent measures are size of turbinates. This also makes an efficient “radiator”
not taken to relieve it. The nose also permits breathing and mechanism to warm up the cold air. Inspired air which
eating to go on simultaneously. may be at 20°C or 0°C or even at subzero temperature is
During quiet respiration, inspiratory air current passes heated to near body temperature (37°C) in one-fourth
through middle part of nose between the turbinates and of second, the time that the air takes to pass from the
nasal septum. Very little air passes through inferior meatus nostril to the nasopharynx. Similarly, hot air is cooled to
or olfactory region of nose (Figure 24.1). Therefore, weak the level of body temperature.
odorous substances have to be sniffed before they can reach 3. Humidification. This function goes on simultaneously
the olfactory area. with the temperature control of inspired air. Relative
During expiration, air current follows the same course as humidity of atmospheric air varies depending on cli-
during inspiration, but the entire air current is not expelled matic conditions. Air is dry in winter and saturated
directly through the nares. Friction offered at limen nasi with moisture in summer months. Nasal mucous mem-
converts it into eddies under cover of inferior and middle brane adjusts the relative humidity of the inspired air
turbinates and this ventilates the sinuses through the ostia. to 75% or more. Water, to saturate the inspired air, is
provided by the nasal mucous membrane which is rich
Anterior end of inferior turbinate undergoes swelling and in mucous and serous secreting glands. About 1000 mL
shrinkage thus regulating inflow of air. of water is evaporated from the surface of nasal mucosa
Nasal cycle. Nasal mucosa undergoes rhythmic cyclical in 24 h.
congestion and decongestion, thus controlling the airflow Moisture is essential for integrity and function of the cili-
through nasal chambers. When one nasal chamber is work- ary epithelium. At 50% relative humidity, ciliary function
ing, total nasal respiration, equal to that of both nasal cham- stops in 8–10 min. Thus, dry air predisposes to infections
bers, is carried out by it. Nasal cycle varies every 2½–4 h and of the respiratory tract. Humidification also has a signifi-
may be characteristic of an individual. cant effect on gas exchange in the lower airways. In nasal
obstruction, gaseous exchange is affected in the lungs, lead-
ing to rise in pCO2, causing apnoeic spells during sleep; it
also decreases pO2.

AIR-CONDITIONING OF INSPIRED AIR PROTECTION OF LOWER AIRWAY
1. Mucociliary mechanism. Nasal mucosa is rich in goblet
Nose is aptly called the “air-conditioner” for lungs. It filters
and purifies the inspired air and adjusts its temperature and cells, secretory glands both mucous and serous. Their
humidity before the air passes to the lungs. secretion forms a continuous sheet called mucous blanket
1. Filtration and purification. Nasal vibrissae at the entrance spread over the normal mucosa. Mucous blanket consists
of a superficial mucus layer and a deeper serous layer,
of nose act as filters to sift larger particles like fluffs of floating on the top of cilia which are constantly beating
cotton. Finer particles like dust, pollen and bacteria to carry it like a “conveyer belt” towards the nasopharynx
adhere to the mucus which is spread like a sheet all over
140

CHAPTER 24 — PHYSIOLOGY OF NOSE 141

AB

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

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

(Figure 24.2). It moves at a speed of 5–10 mm/min and VOCAL RESONANCE
the complete sheet of mucus is cleared into the pharynx Nose forms a resonating chamber for certain consonants in
every 10–20 min. The inspired bacteria, viruses and dust speech. In phonating nasal consonants (M/N/NG), sound
particles are entrapped on the viscous mucous blanket passes through the nasopharyngeal isthmus and is emitted
and then carried to the nasopharynx to be swallowed. through the nose. When nose (or nasopharynx) is blocked,
Presence of turbinates almost doubles the surface area to speech becomes denasal, i.e. M/N/NG are uttered as B/D/G,
perform this function. About 600–700 mL of nasal secre- respectively. It is to be remembered that in Hindi alpha-
tions are produced in 24 h. bets, last letter of a “varga” (

In mammals, cilia beat 10–20 times per second at room ) is substituted by its third letter.
temperature. They have a rapid “effective stroke” and a Thus, an affected person utters for and for .
slow “recovery stroke.” In the former, the extended cilia Reverse is true in velopharyngeal insufficiency where is
reach mucus layer while in the recovery stroke, they substituted for .
bend and travel slowly in the reverse direction in the thin
serous layer, thus moving the mucous blanket in only one NASAL REFLEXES
direction. In immotile cilia syndrome, cilia are defec- Several reflexes are initiated in the nasal mucosa. Smell of a
tive and cannot beat effectively, leading to stagnation palatable food cause reflex secretion of saliva and gastric juice.
of mucus in the nose and sinuses and bronchi causing Irritation of nasal mucosa causes sneezing. Nasal function is
chronic rhinosinusitis and bronchiectasis. Movements of closely related to pulmonary functions through ­nasobronchial
cilia are affected by drying, drugs (adrenaline), excessive and nasopulmonary reflexes. It has been observed that nasal
heat or cold, smoking, infections and noxious fumes like obstruction leads to increased p­ ulmonary resistance and is
sulfur dioxide and carbon dioxide. reversed when nasal ­obstruction is surgically treated. Nasal
2. Enzymes and immunoglobulins. Nasal secretions also packing in cases of epistaxis or after nasal surgery leads to
contain an enzyme called muramidase (lysozyme) which lowering of pO2 which returns to normal after removal of the
kills bacteria and viruses. Immunoglobulins IgA and pack. Pulmonary hypertension or ­cor pulmonale can develop
IgE, and interferon are also present in nasal secretions in children with long-standing nasal obstruction due to tonsil
and provide immunity against upper respiratory tract and adenoid hypertrophy and can be reversed after removal
infections. of the tonsils and adenoids.
3. Sneezing. It is a protective reflex. Foreign particles which
irritate nasal mucosa are expelled by sneezing. Copious

142 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

OLFACTION 2. Disorders of smell. It is essential for the perception of
Sense of smell is well-developed in lower animals to give smell that the odorous substance be volatile and that it
warning of the environmental dangers but it is compara- should reach the olfactory area unimpeded. Also necessary
tively less important in man. Still it is important for pleasure are the healthy state of olfactory mucosa and the integrity
and for enjoying the taste of food. When nose is blocked, of neural pathways, i.e. olfactory nerves, olfactory bulb and
food tastes bland and unpalatable. Vapours of ammonia are tract and the cortical centre of olfaction.
never used to test the sense of smell as they stimulate fibres
of the trigeminal nerve and cause irritation in the nose Anosmia is total loss of sense of smell while hyposmia is par-
rather than stimulate the olfactory receptors. tial loss. They can result from nasal obstruction due to nasal
1. Olfactory pathways. Smell is perceived in the olfactory polypi, enlarged turbinates or oedema of mucous membrane
region of nose which is situated high up in the nasal cav- as in common cold, allergic or vasomotor rhinitis. Anosmia
ity. This area contains millions of olfactory receptor cells. is also seen in atrophic rhinitis, a degenerative disorder of
Peripheral process of each olfactory cell reaches the muco- nasal mucosa; peripheral neuritis (toxic or influenzal); injury
sal surface and is expanded into a ventricle with several to olfactory nerves or olfactory bulb in fractures of anterior
cilia on it. This acts as a sensory receptor to receive odor- cranial fossa; and intracranial lesions like abscess, tumour or
ous substances. Central processes of the olfactory cells meningitis which cause pressure on olfactory tracts.
are grouped into olfactory nerves which pass through the
cribriform plate of ethmoid and end in the mitral cells of Parosmia is perversion of smell; the person interprets the
the olfactory bulb. Axons of mitral cells form olfactory odours incorrectly. Often these persons complain of dis-
tract and carry smell to the prepyriform cortex and the gusting odours. It is seen in the recovery phase of postinflu-
amygdaloid nucleus where it reaches consciousness. Olfac- enzal anosmia and the probable explanation is misdirected
tory system is also associated with autonomic system at the regeneration of nerve fibres. Intracranial tumour should be
hypothalamic level. excluded in all cases of parosmia.

Sense of smell can be tested by asking the patient to smell
common odours such as lemon, peppermint, rose, garlic
or cloves from each side of the nose separately, with eyes
closed. Quantitative estimation (quantitative olfactometry)
requires special equipment.

25Diseases of External Nose
and Nasal Vestibule

DISEASES OF EXTERNAL NOSE Aim of these operations is to correct not only the outer
appearance of nose but also its function.
CELLULITIS
The nasal skin may be invaded by streptococci or staphylo- TUMOURS
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. 1.  CONGENITAL TUMOURS
Treatment is systemic antibacterials, hot fomentation and (a) Dermoid cyst (Figure 25.3). It is of two types:
analgesics. • 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 Normal Saddle Supratip Humped
(Figure 25.1). Nasal trauma causing depressed fractures is nose depression nose
the most common aetiology. It can also result from exces-
sive removal of septum in submucous resection, destruction Figure 25.1  Deformities of nose.
of septal cartilage by haematoma or abscess, sometimes by
leprosy, tuberculosis or syphilis. The deformity can be cor- Crooked nose Deviated nose
rected by augmentation rhinoplasty by filling the dorsum
with cartilage, bone or a synthetic implant. If depression is Figure 25.2  Nasal bridge is S-shaped in crooked nose. It is straight
only cartilaginous, cartilage is taken from the nasal septum but deviated to one side in deviated nose.
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
to be extruded.
HUMP NOSE
This may also involve the bone or cartilage or both bone
and cartilage. It can be corrected by reduction rhinoplasty
which consists of exposure of nasal framework by careful
raising of the nasal skin by a vestibular incision, removal of
hump and narrowing of the lateral walls by osteotomies to
reduce the widening left by hump removal.
CROOKED OR A DEVIATED NOSE
In crooked nose, the midline of dorsum from frontonasal
angle to the tip is curved in a C- or S-shaped manner. In a
deviated nose, the midline is straight but deviated to one
side (Figure 25.2).

Usually, these deformities are traumatic in origin. Inju-
ries sustained during birth, neonatal period or childhood,
but not immediately recognized, will also develop into these
deformities with the growth of nose. The deviated or crooked
nose can be corrected by rhinoplasty or septorhinoplasty.

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- 2.  BENIGN TUMOURS
sitate splitting of the nasal bones to remove any exten- They arise from the nasal skin and include papilloma (skin
sion in the upper part of the nasal septum. A combined wart), haemangioma, pigmented naevus, seborrhoeic keratosis,
neurosurgical–otolaryngologic approach is required in neurofibroma or tumour of sweat glands.
those extending intracranially so as to close simultane-
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-
epithelialize. Sometimes, tumour is completely excised and
Swellings show cough impulse and may be reducible. the raw area skin grafted.
Treatment is neurosurgical; severing the tumour stalk from

Table 25.1  Tumours of external nose

Congenital Benign Malignant

• D ermoid cysts • R hinophyma • Basal cell
• Encephalocele • H aemangioma cancer
• Meningoencephalocele • P igmented
• Glioma • S quamous
naevus cell cancer
• S eborrhoeic
• Melanoma
keratosis
• Neurofibroma
• S weat gland

tumour

Figure 25.4 Rhinophyma.

Dura

AB C

Figure 25.3  Types of dermoids. (A) Simple dermoid beneath the skin. (B) Dermoid with an external pit or sinus. It lies in front of septum and
deep to nasal bones. (C) Dermoid with an intracranial connection to dura.

CHAPTER 25 — DISEASES OF EXTERNAL NOSE AND NASAL VESTIBULE 145

3.  MALIGNANT TUMOURS Early lesions respond to radiotherapy; more advanced
(a) Basal cell carcinoma (rodent ulcer) (Figure 25.5). This lesions or those with exposure of bone or cartilage
is the most common malignant tumour involving skin of require wide surgical excision and plastic repair of the
nose (87%), equally affecting males and females in the defect. Enlarged regional lymph nodes will require block
age group of 40–60 years. Common sites on the nose are dissection.
the tip and the ala. It may present as a cyst or papulo-pearly (c) Melanoma. This is the least common variety. Clinically,
nodule or an ulcer with rolled edges. It is very slow growing it is superficially spreading type (slow growing) or nodular
and remains confined to the skin for a long time. Underly- invasive type. Treatment is surgical excision.
ing cartilage or bone may get invaded. Nodal metastases
are extremely rare. Treatment depends on the size, loca- DISEASES OF NASAL VESTIBULE
tion and depth of the tumour. Early lesion can be cured FURUNCLE OR BOIL (FIGURE 25.7)
by cryosurgery, irradiation or surgical excision with 3–5 It is an acute infection of the hair follicle by Staphylococcus
mm of healthy skin around the palpable borders of the aureus. Trauma from picking of the nose or plucking the
tumour. nasal vibrissae is the usual predisposing factor.

Lesions which are recurrent, extensive or with involve- The lesion is small but exquisitely painful and tender.
ment of cartilage or bone are excised and the surgical defect Inflammation may spread to the skin of nasal tip and dor-
closed by local or distant flaps or a prosthesis. sum which become red and swollen. The furuncle may rup-
ture spontaneously in the nasal vestibule.
(b) Squamous cell carcinoma (epithelioma). This is the
second most common malignant tumour (11%), equally Treatment of furuncle consists of warm compresses, anal-
affecting both sexes in 40–60 age group. It occurs as an infil- gesics to relieve pain, and topical and systemic antibiotics
trating nodule or an ulcer with rolled out edges affecting directed against staphylococcus. If a fluctuant area appears,
side of nose or columella (Figure 25.6). Nodal metastases incision and drainage can be done. In no case should the
are seen in 20% of cases. furuncle be squeezed or prematurely incised because of the
danger of spread of infection to cavernous sinus through
venous thrombophlebitis.

A furuncle of nose may complicate into cellulitis of the
upper lip or septal abscess.

Figure 25.5  Basal cell carcinoma of the nose. 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;
crusts and scales cover an area of skin erosion or excoria-
tion. The upper lip may also be involved (Figure 25.8).

In chronic form, there is induration of vestibular skin with
painful fissures and crusting.

Figure 25.6  Carcinoma nose. Figure 25.7  Furuncle right nasal vestibule.

146 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

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

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

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

Stenosis of nares can be corrected by reconstructive plas-
tic procedures.

TUMOURS
1. Nasoalveolar cyst presents a smooth bulge in the lat-

eral wall and floor of nasal vestibule. The cyst can be

26Nasal Septum and
Its Diseases

ANATOMY depression of lower part of nose and drooping of the
nasal tip.
Nasal septum consists of three parts:
1. Columellar septum. It is formed of columella containing Septal cartilage lies in a groove in the anterior edge of
the medial crura of alar cartilages united together by fibrous vomer and rests anteriorly on anterior nasal spine. During
tissue and covered on either side by skin. trauma, it may get dislocated from anterior nasal spine or
2. Membranous septum. It consists of double layer of skin vomerine groove causing caudal septal deviation or sep-
with no bony or cartilaginous support. It lies between the tal spur, respectively. This compromises the nasal airway.
columella and the caudal border of septal cartilage. Both Septal cartilage is also intimately related to the upper lat-
columellar and membranous parts are freely movable from eral cartilages of nose and is in fact fused with them in
side to side. the upper third. For this reason septal deviation may be
3. Septum proper. It consists of osteocartilaginous frame- associated with deviation of cartilaginous part of external
work, covered with nasal mucous membrane. nose.

Its principal constituents are (Figure 26.1): Blood Vessels of Nasal Septum (see Chapter 33).
(a) the perpendicular plate of ethmoid, Nerve Supply of Nasal Septum (see Chapter 23).
(b) the vomer and Little’s area or Kiesselbach’s plexus. This is the vascular
(c) a large septal (quadrilateral) cartilage wedged between area in the anteroinferior part of nasal septum just above
the vestibule. Anterior ethmoidal, sphenopalatine, greater
the above two bones anteriorly. Other bones which palatine and septal branch of superior labial arteries and
make minor contributions at the periphery are crest their corresponding veins form an anastomosis here. This
of nasal bones, nasal spine of frontal bone, rostrum of is the commonest site for epistaxis. This is also the site for
sphenoid, crest of palatine bones and the crest maxilla, origin of the “bleeding polypus” (haemangioma) of nasal
and the anterior nasal spine of maxilla. septum.
Septal cartilage not only forms a partition between the
right and left nasal cavities but also provides support FRACTURES OF NASAL SEPTUM
to the tip and dorsum of cartilaginous part of nose. Its AETIOPATHOGENESIS
destruction, e.g. in septal abscess, injuries, tuberculo- Trauma inflicted on the nose from the front, side or below
sis or excessive removal during septal surgery, leads to can result in injuries to the nasal septum. The septum
may buckle on itself, fracture vertically, horizontally or be
Nasal spine of crushed to pieces as in a smashed nose. The fractured pieces
frontal bone of septum may overlap each other or project into the nasal
cavity through mucosal tears. Fracture of the septal cartilage
Crest of nasal Perp. plate of or its dislocation from the vomerine groove, can result from
bone ethmoid trauma to the lower nose without associated fractures of
nasal bones. Septal injuries with mucosal tears cause profuse
Membranous Septal cart. Vomer Rostrum of epistaxis while those with intact mucosa result in septal hae-
septum sphenoid matoma which, if not drained early, will cause absorption of
the septal cartilage and saddle nose deformity.
Columellar
septum “Jarjaway” fracture of nasal septum results from blows
from the front; it starts just above the anterior nasal spine
Ant. nasal spine Crest of maxilla and runs horizontally backwards just above the junction of
of maxilla septal cartilage with the vomer (Figure 26.2A).

Crest of palatine bone “Chevallet” fracture of septal cartilage results from blows
Figure 26.1  Anatomy of nasal septum. from below; it runs vertically from the anterior nasal spine
upwards to the junction of bony and cartilaginous dorsum
of nose (Figure 26.2B).

147

148 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

DNS High arched
palate

A Figure 26.3  DNS associated with high-arched palate.

Anterior dislocation C-shaped deflection S-shaped deflection

B Nasal spur impinging Thickening of nasal
on turbinate septum
Figure 26.2  Septal fracture showing: (A) Jarjaway type. (B) Chevallet
type. 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
Septum is important in supporting the lower part of the secondary dentition, further development takes place in the
external nose. If its injuries are ignored, they would result palate, which descends and widens to accommodate the teeth.
in deviation of the cartilaginous nose, or asymmetry of nasal
tip, columella or the nostril. Unequal growth between the palate and the base of skull
may cause buckling of the nasal septum. In mouth breathers,
DEVIATED NASAL SEPTUM (DNS) as in adenoid hypertrophy, the palate is often highly arched
This is an important cause of nasal obstruction. 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
AETIOLOGY abnormalities.
Trauma and errors of development form the two important 3. Racial factors. Caucasians are affected more than black
factors in the causation of deviated septum. Americans.
1. Trauma. A lateral blow on the nose may cause displacement 4. Hereditary factors. Several members of the same family
of septal cartilage from the vomerine groove and maxillary may have deviated nasal septum.
crest, while a crushing blow from the front may cause buckling,
TYPES OF DNS (FIGURE 26.4)
Deviation may involve only the cartilage, bone or both the
cartilage and bone.

CHAPTER 26 — NASAL SEPTUM AND ITS DISEASES 149

Figure 26.5  Anterior dislocation. Caudal border of septal cartilage
projects into right naris.

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

Cottle test. It is used in nasal obstruction due to abnormality
of the nasal valve. In this test, cheek is drawn laterally while the

150 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

deflected parts of the bony and cartilaginous septum, and Blood
then repositioning the flaps (see section on Operative Sur- Figure 26.7  Septal haematoma.
gery for details).

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

CHAPTER 26 — NASAL SEPTUM AND ITS DISEASES 151

Figure 26.9  Septal perforation. Figure 26.10  Septal button for closure of perforation.

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

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

27 Acute and Chronic Rhinitis

ACUTE RHINITIS form in the nose, which with attempted removal causes
Acute rhinitis can be viral, bacterial or irritative type. bleeding.

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

leading to persistence of discharge in the nose.

CHAPTER 27 — ACUTE AND CHRONIC RHINITIS 153

4. Vasomotor rhinitis. SIGNS
5. E ndocrinal or metabolic factors, e.g. hypothyroidism, Examination shows hypertrophy of turbinates. Turbinal
mucosa is thick and does not pit on pressure. It shows little
excessive intake of carbohydrates and lack of exercise. shrinkage with vasoconstrictor drugs due to presence of
PATHOLOGY underlying fibrosis.
Simple chronic rhinitis is an early stage of hypertrophic
rhinitis. There is hyperaemia and oedema of mucous Maximum changes are seen in the inferior turbinate. It
membrane with hypertrophy of seromucinous glands and may be hypertrophied in its entirety or only at the anterior
increase in goblet cells. Blood sinusoids particularly those end, posterior end or along the inferior border giving it a
over the turbinates are distended. mulberry appearance.
CLINICAL FEATURES
1. Nasal obstruction. Usually worse on lying and affects the TREATMENT
Attempt should be made to discover the cause and remove
dependent side of nose. it. Nasal obstruction can be relieved by reduction in size of
2. Nasal discharge. It may be mucoid or mucopurulent, turbinates. The various methods are:
1. Linear cauterization.
thick and viscid and often trickles into the throat as post- 2. Submucosal diathermy.
nasal drip. Patient has a constant desire to blow the nose 3. Cryosurgery of turbinates.
or clear the throat. 4. P artial or total turbinectomy. Hypertrophied inferior
3. Headache. It is due to swollen turbinates impinging on
the nasal septum. turbinate can be partially removed at its anterior end,
4. Swollen turbinates. Nasal mucosa is dull red in colour. inferior border or posterior end. Middle turbinate, if
Turbinates are swollen; they pit on pressure and shrink hypertrophied, can also be removed partially or totally.
with application of vasoconstrictor drops (this differen- Excessive removal of turbinates should be avoided as it
tiates the condition from hypertrophic rhinitis). Mid- leads to persistent crusting.
dle turbinate may also be swollen and impinge on the 5. Submucous resection of turbinate bone. This removes
septum. bony obstruction but preserves turbinal mucosa for its
5. Postnasal discharge. Mucoid or mucopurulent discharge function.
is seen on the posterior pharyngeal wall. 6. Lasers have also been used to reduce the size of turbinates.
TREATMENT
1. Treat the cause with particular attention to sinuses, ton- COMPENSATORY HYPERTROPHIC RHINITIS
sils, adenoids, allergy, personal habits (smoking or alco- This is seen in cases of marked deviation of septum to one
hol indulgence), environment or work situation (smoky side. The roomier side of the nose shows hypertrophy of
or dusty surroundings). inferior and middle turbinates. This is an attempt on the
2. Nasal irrigations with alkaline solution help to keep the part of nature to reduce the wide space to overcome the ill
nose free from viscid secretions and also remove superfi- effects of drying and crusting that always attend wider nasal
cial infection. space. Hypertrophic changes in these cases are not revers-
3. Nasal decongestants help to relieve nasal obstruction and ible with the correction of nasal septum and often require
improve sinus ventilation. Excessive use of nasal drops reduction of turbinates at the time of septal surgery.
and sprays should be avoided because it may lead to rhi-
nitis medicamentosa. A short course of systemic steroids ATROPHIC RHINITIS (OZAENA)
helps to wean the patients already addicted to excessive It is a chronic inflammation of nose characterized by atro-
use of decongestant drops or sprays. phy of nasal mucosa and turbinate bones. The nasal cavities
4. Antibiotics help to clear nasal infection and concomitant are roomy and full of foul-smelling crusts. Atrophic rhinitis
sinusitis. is of two types: primary and secondary.

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

154 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

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

CHAPTER 27 — ACUTE AND CHRONIC RHINITIS 155

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

RHINITIS SICCA RHINITIS CASEOSA
It is also a crust-forming disease seen in patients who work in It is an uncommon condition, usually unilateral and mostly
hot, dry and dusty surroundings, e.g. bakers, iron- and gold- affecting males.
smiths. Condition is confined to the anterior third of nose
particularly of the nasal septum. Here, the ciliated columnar Nose is filled with offensive purulent discharge and
epithelium undergoes squamous metaplasia with atrophy of cheesy material. The disease possibly arises from chronic
seromucinous glands. Crusts form on the anterior part of sinusitis with collection of inspissated cheesy material. Sinus
septum and their removal causes ulceration and epistaxis, mucosa becomes granulomatous. Bony walls of sinus may be
and may lead to septal perforation. destroyed, requiring differentiation from malignancy. Treat-
ment is removal of debris and granulation tissue and free
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 Figure 28.1  Rhinoscleroma nose.

RHINOSCLEROMA Figure 28.2  Rhinoscleroma showing foamy Mikulicz cells (arrow)
It is a chronic granulomatous disease caused by Gram- and lymphocytic infiltration (arrowheads) (H&E, x400). Mikulicz cells
negative bacillus called Klebsiella rhinoscleromatis or Frisch contain Gram-negative bacteria which can be better appreciated in
bacillus. The disease is endemic in several parts of the sections stained with Giemsa stain and examined under oil immer-
world. In India, it is seen more often in the northern than sion lens.
in the southern parts.
PATHOLOGY
The disease starts in the nose and extends to nasopharynx,
oropharynx, larynx (mostly subglottic region), trachea and
bronchi. Mode of infection is unknown. Both sexes of any
age may be affected.
CLINICAL FEATURES
The disease runs through the following stages:
1. Atrophic stage. It resembles atrophic rhinitis and is char-

acterized by foul-smelling purulent nasal discharge and
crusting.
2. Granulomatous stage. Granulomatous nodules form
in nasal mucosa. There is also subdermal infiltration
of lower part of external nose and upper lip giving a
“woody” feel (Figure 28.1). Nodules are painless and
nonulcerative.
3. Cicatricial stage. This causes stenosis of nares, distortion
of upper lip, adhesions in the nose, nasopharynx and
oropharynx. There may be subglottic stenosis with respi-
ratory distress.
DIAGNOSIS
Biopsy shows infiltration of submucosa with plasma cells,
lymphocytes, eosinophils, Mikulicz cells and Russell bod-
ies. The latter two are diagnostic features of the disease
(Figure 28.2). Mikulicz cells are large foam cells with a
central nucleus and vacuolated cytoplasm containing caus-
ative bacilli. Russell bodies are homogenous eosinophilic

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

Table 28.1  Granulomatous disease of nose

Bacterial Fungal Unspecified cause
Rhinoscleroma
Rhinosporidiosis Wegener’s
Syphilis granulomatosis
Aspergillosis
Tuberculosis Nonhealing midline
Lupus Mucormycosis granuloma
Leprosy Candidiasis
Histoplasmosis Sarcoidosis
Blastomycosis Rare

Figure 28.3  Leprosy nose.

158 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

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

AB

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.

AB

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

CHAPTER 28 — GRANULOMATOUS DISEASES OF NOSE 159

1. Trophic stage. The endospore is oval or rounded, 6–8 μm DIAGNOSIS
in size, clear cytoplasm, vesicular nucleus with a nucleo- This is made on biopsy. It shows several sporangia, oval or round
lus and a covering of chitin. It gradually increases in size, in shape and filled with spores which may be seen bursting
begins to divide cytoplasm and nucleus forming small through its chitinous wall. It has not been possible to culture
endospores by several divisions. Trophocyte becomes the organism or transfer the disease to experimental animals.
large filled with young endospores.
TREATMENT
2. Development of sporangium. The mature trophocyte Complete excision of the mass with diathermy knife and
then develops into sporangium. A sporangium is 200– cauterization of its base. Recurrence may occur after sur-
250 μm in diameter, contains 12,000–16,000 endospores. gical excision. Not many drugs are effective against the
It has a thick wall consisting of two layers: outer chitinous disease. Dapsone has been tried with some success.
and inner cellulose layer.
Endospores mature with the formation of mucoid ASPERGILLOSIS
and chitinous wall. Sporangium filled with thousands of The usual causative organisms are Aspergillus niger,
endospores develops a germinal pore ready to burst and A. fumigatus or A. flavus. They invade nasal tissues when
liberate the endospores. host’s defence mechanisms are compromised due to
immunosuppressive drugs.
3. Production of endospores. Sporangium filled with endo-
spores develops high internal pressure and ruptures CLINICAL FEATURES
liberating endospores into the surrounding tissue. If Clinical features are those of acute or subacute rhinitis or
internal pressure is not high, spores are liberated one sinusitis. A black or greyish membrane is seen in the nasal
by one without breaking the wall. After liberation endo- mucosa. Exploration of maxillary sinus reveals a fungus ball
spores start their life as trophic stage. Some endospores containing semisolid cheesy-white or blackish material. The
are carried by lymphatic channels to the blood stream to organisms can be seen on special staining for fungus.
cause disseminated form of disease.
TREATMENT
CLINICAL FEATURES Surgical debridement of the involved tissues and antifun-
The disease mostly affects nose and nasopharynx; other sites gal drugs, e.g. Amphotericin B. Repeated irrigation of the
such as lip, palate, conjunctiva, epiglottis, larynx, trachea, involved area with application of 1% solution of gentian
bronchi, skin, vulva and vagina may also be affected. violet is also useful.

The disease is acquired through contaminated water of MUCORMYCOSIS
ponds also frequented by animals. In the nose, the disease It is fungal infection of nose and paranasal sinuses which
presents as a leafy, polypoidal mass, pink to purple in colour may prove rapidly fatal. It is seen in uncontrolled diabetics
and attached to nasal septum or lateral wall. Sometimes, it or in those taking immunosuppressive drugs. From the nose
extends into the nasopharynx and may hang behind the soft and sinuses, infection can spread to orbit, cribriform plate,
palate. The mass is very vascular and bleeds easily on touch. meninges and brain. The rapid destruction associated with
Its surface is studded with white dots representing the spo- the disease is due to affinity of the fungus to invade the arter-
rangia of fungus. ies and cause endothelial damage and thrombosis. Typical
finding is the presence of a black necrotic mass filling the
In early stages, the patient may complain of nasal dis- nasal cavity and eroding the septum and hard palate. Special
charge which is often blood tinged and nasal stuffiness. stains help to identify the fungus in tissue sections.
Sometimes, frank epistaxis is the only presenting complaint.
Treatment is by amphotericin B and surgical debride-
Trophocyte Chitinous wall ment of the affected tissues and control of underlying
A Clear cytoplasm ­predisposing cause.
Vesicular nucleus
Sporangium with a nucleolus

}Chitinous layer
Wall
Cellulose layer

B OTHER FUNGAL INFECTIONS
Other fungal infections of nose such as candidiasis, histoplas-
mosis, blastomycosis, etc. are rare.

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

160 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

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

29Miscellaneous Disorders of
Nasal Cavity

FOREIGN BODIES RHINOLITH
AETIOLOGY AETIOLOGY
They are mostly seen in children and may be organic or It is stone formation in the nasal cavity. A rhinolith usually
inorganic. Pieces of paper, chalk, button, pebbles and seeds forms around the nucleus of a small exogenous foreign
are the common objects. Pledgets of cotton or swabs may be body, blood clot or inspissated secretions by slow deposition
accidentally left in the nose. of calcium and magnesium salts. Over a period of time, it
grows into a large, irregular mass which fills the nasal cavity
CLINICAL FEATURES and then may cause pressure necrosis of the septum and/or
Patient may present immediately if the history of foreign lateral wall of nose.
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
child are rhinolith, nasal diphtheria, nasal myiasis and acute On examination, a grey brown or greenish-black mass
or chronic unilateral sinusitis. with irregular surface and stony hard feel is seen in the nasal
cavity between the septum and turbinates. It is often brittle
TREATMENT and a portion of it may break off while manipulating. Some-
Pieces of paper or cotton swabs can be easily removed with times it is surrounded by granulations.
a pair of forceps. Rounded foreign bodies can be removed
by passing a blunt hook (a eustachian catheter is a good TREATMENT
instrument) past the foreign body and gently dragging it They are removed under general anaesthesia. Most of them
forward along the floor. In babies and uncooperative chil- can be removed through anterior nares. Large ones need
dren, general anaesthesia with cuffed endotracheal tube is to be broken into pieces before removal. Some particularly
used. Patient is placed in Rose’s position, a pack is inserted hard and irregular ones require lateral rhinotomy.
into the nasopharynx and the foreign body retrieved with a
forceps or a hook. Foreign bodies lodged far behind in the NASAL MYIASIS (MAGGOTS IN NOSE)
nose may need to be pushed into the nasopharynx before Maggots are larval forms of flies. They are seen to infest
removal. A nasal endoscope is very useful to locate the for- nose, nasopharynx and paranasal sinuses causing exten-
eign body and carefully remove it. sive destruction (Figures 29.1 A, B, C and 29.2). Flies,
particularly of the genus Chrysomyia, are attracted by the
COMPLICATIONS foul-s­melling discharge emanating from cases of atrophic
A foreign body left in the nose may result in: 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

AB 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).

AB

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

CLINICAL FEATURES slough, crusts and dead maggots. A patient with mag-
In the first 3 or 4 days maggots produce intense irritation, gots should be isolated with a mosquito net to avoid con-
sneezing, lacrimation and headache. Thin blood-stained tact with flies which can perpetuate this cycle. All patients
discharge oozes from the nostrils. The eyelids and lips should receive instruction for nasal hygiene before leaving
become puffy. Till this time patient is not aware of mag- the hospital.
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. Adhesion formation between the nasal septum and turbi-
Maggots cause extensive destruction to nose, sinuses, soft nates by scar tissue is often the result of injury to opposing
tissue of face, palate and the eyeball. Fistulae may form surfaces of nasal mucosa. It can result from intranasal opera-
in the palate or around the nose. Death may occur from tions such as septal surgery, polypectomy, removal of foreign
meningitis. 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
on them. Instillation of chloroform water and oil kills Nasal synechia (Figure 29.3) often cause nasal obstruction
them. Nasal douche with warm saline is used to remove or may impede drainage from the sinuses resulting in sinusitis,
headache and nasal discharge.

CHAPTER 29 — MISCELLANEOUS DISORDERS OF NASAL CAVITY 163

a
b

c

d

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

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

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

164 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Table 29.1  Differences between CSF and nasal secretions

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

DIAGNOSIS Patient lies in 10° head down position for sometime. Dye
There is history of clear watery discharge from the nose on can be detected intranasally with the help of endoscope.
bending the head or straining. It may be seen on rising in the Dye appears bright yellow but when seen with a blue filter
morning when patient bends his head (reservoir sign—fluid it appears fluorescent green. One should examine olfac-
which had collected in the sinuses, particularly sphenoid, tory cleft (cribriform plate), middle meatus (frontal and
empties into the nose). CSF rhinorrhoea should be differ- ethmoidal sinuses), sphenoethmoidal recess (sphenoid
entiated from nasal discharge of allergic or vasomotor rhi- sinus) and area of torus tubarius (temporal bone frac-
nitis as the former is sudden, gushes in drops when bending ture) to localize the lesion.
and cannot be sniffed back. Nasal discharge, because of its
mucus content, also stiffens the handkerchief (Table 29.1). Use of intrathecal radioactive substances has been
abandoned.
CSF rhinorrhoea after head trauma is mixed with blood 4. CT cisternogram. It requires intrathaecal injection of
and shows double target sign when collected on a piece of fil- iohexol and a CT scan to localize the site in cases when
ter paper. It shows central red spot (blood) and peripheral beta-2 transferrin cannot be done. Now it is not favoured
lighter halo. by many.

Nasal endoscopy can help to localize CSF leak in some TREATMENT
cases. Otoscopic/microscopic examination of the ear may Early cases of post-traumatic CSF rhinorrhoea can be man-
reveal fluid in the middle ear in cases of otorhinorrhoea. aged by conservative measures such as bed rest, elevating
the head of the bed, stool softeners, and avoidance of nose
LABORATORY TESTS 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
humour are the only other fluids which contain this protein. Surgical repair can be done by the following:
1. Neurosurgical intracranial approach.
Another protein called beta trace protein is also specific for 2. Extradural approaches such as external ethmoidec-
CSF and is widely used in Europe. It is secreted by menin-
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
p­ eroxidase or biochemical estimation are no longer used. approach for frontal sinus leak.
3. Transnasal endoscopic approach. With the advent of
LOCALIZATION OF SITE endoscopic surgery for nose and sinuses, most of the
1. High-resolution CT scan. Cuts are taken at 1–2 mm. Both leaks from the anterior cranial fossa and sphenoid sinus
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
of 5% fluorescein diluted with 10 mL of CSF is injected. by placement of mucosa (as a free graft or pedicled
flap) (Figure 29.6).

CHAPTER 29 — MISCELLANEOUS DISORDERS OF NASAL CAVITY 165

(b) Ethmoid roof (a) Cribriform plate Brain
Pia mater
Graft Arachnoid
Dura

Orbit

Middle turbinate Bone
Mucosa
Septum
Surgicel
Figure 29.5  Sites of bony defect: (a) cribriform plate and (b) ethmoid Gelfoam
roof.
Pack
Figure 29.6  Repair of CSF rhinorrhoea.

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

30 Allergic Rhinitis

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

Fab end Heavy chain Antigen
Light chain Antibody
SS SS SS
SS Mast cell
Mediator release

Tail Newly synthesized mediators
Preformed
mediators

A Fc end B

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

166

CHAPTER 30 — ALLERGIC RHINITIS 167

infiltration of inflammatory cells—eosinophils, neutro- salute), pale and oedematous nasal mucosa which may
phils, basophil, monocytes and CD4 + T cells at the site appear bluish. Turbinates are swollen. Thin, watery or
of antigen deposition causing swelling, congestion and mucoid discharge is usually present.
thick secretion. In the event of repeated or continuous • Ocular signs include oedema of lids, congestion and cobble-
exposure to allergen, acute phase symptomatology over- stone appearance of the conjunctiva, and dark circles under
laps the late phase. the eyes (allergic shiners).
• Otologic signs include retracted tympanic membrane or
CLINICAL FEATURES serous otitis media as a result of eustachian tube blockage.
• Pharyngeal signs include granular pharyngitis due to
There is no age or sex predilection. It may start in infants as hyperplasia of submucosal lymphoid tissue. A child with
young as 6 months or older people. Usually the onset is at perennial allergic rhinitis may show all the features of pro-
12–16 years of age. longed mouth breathing as seen in adenoid hyperplasia.
• 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 DIAGNOSIS
may also involve eyes, palate or pharynx. Some may get New Allergic Rhinitis and Its Impact on Asthma (ARIA) clas-
bronchospasm. The duration and severity of symptoms may sification (Table 30.1). It is based on duration and symp-
vary with the season. toms of disease. Duration of symptoms is subdivided into
intermittent or persistent and severity of disease into mild,
Symptoms of perennial allergy are not so severe as that of moderate or severe.
the seasonal type. They include frequent colds, persistently
stuffy nose, loss of sense of smell due to mucosal oedema, This new system of classification helps in treatment
postnasal drip, chronic cough and hearing impairment due guidelines.
to eustachian tube blockage or fluid in the middle ear.
A detailed history and physical examination is helpful,
Signs of allergy may be seen in the nose, eyes, ears, phar- and also gives clues to the possible allergen. Other causes of
ynx or larynx. nasal stuffiness should be excluded.
• Nasal signs include transverse nasal crease—a black line

across the middle of dorsum of nose due to constant
upward rubbing of nose simulating a salute (allergic

INVESTIGATIONS

Sensitized Antigen 1. Total and differential count. Peripheral eosinophilia may
mast cell 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)
• Histamine • Prostaglandins, • Emotional stimuli
• ECF-A e.g. PGD2 • Salicylates
• NCF-A • Leukotrienes, • Viral infections
• Heparin e.g. SRS-A • Air pollution
• Others • PAF
• Thromboxane A
• TNF␣ Mast cell or blood basophil

Histamine Vasodilatation, bronchospasm Drop in cAMP/cGMP ratio
ECF-A Eosinophil chemotactic factor of anaphylaxis—
attracts eosinophils to the site of reaction

NCF-A Neutrophil chemotactic factor—attracts Release of preformed and
neutrophils newly formed mediators

Heparin Enhances phagocytosis

Prostaglandins Vasoactive and bronchospastic

Leukotriene Vasoactive and bronchospastic Increased vascular Change in smooth Hyperactivity
permeability and muscle tone of glands
PAF Platelet aggregating factor. Histamine and vasodilatation
serotonin are released from platelets. Causes
chemotaxis of neutrophils and eosinophils

Thromboxane A Spasmogenic Tissue oedema Increased secretion

TNF␣ Tumour necrosis factor. Helps transmigration Nasal blockage Bronchospasm Rhinorrhoea
of neutrophils and eosinophils and attracts
them to the site of reaction Figure 30.3  Both allergic and nonspecific stimuli act on mast cells
or blood basophils releasing several mediator substances responsible
Figure 30.2  Release of mediators from mast cell when challenged for symptomatology of allergy.
by allergic or nonspecific stimuli.

168 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

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

ostia.
2. Formation of nasal polypi in about 2%.
3. Serous otitis media.
4. Orthodontic problems and other ill-effects of prolonged

mouth breathing especially in children.

CHAPTER 30 — ALLERGIC RHINITIS 169

(e) Anticholinergics. They block rhinorrhoea both of the Subcutaneous immunotherapy is often used but now sub-
allergic and nonallergic rhinitis. Ipratropium bromide lingual and nasal routes are also being employed. The latter
has been used as nasal spray to control rhinorrhoea. can be used with doses 20–100 times greater than used by
There are no systemic side effects. the subcutaneous route.

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

31 Vasomotor and Other Forms
of Nonallergic Rhinitis

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

SYMPTOMS OTHER FORMS OF NONALLERGIC RHINITIS
1. Paroxysmal sneezing. Bouts of sneezing start just after
Nasal mucosa responds to several different stimuli produc-
getting out of the bed in the morning. ing symptoms of rhinitis. Some of these conditions have
2. Excessive rhinorrhoea. This accompanies sneezing or this acquired specific eponyms. Some authorities categorize
them under the catch-all term of vasomotor rhinitis.
may be the only predominant symptom. It is profuse and 1. Drug-induced rhinitis. Several antihypertensive drugs
watery and may even wet several handkerchiefs. The nose such as reserpine, guanethidine, methyl dopa and propran-
may drip when the patient leans forward and this may need olol are sympathetic blocking agents and cause nasal stuffi-
to be differentiated from CSF rhinorrhoea (see p. 163). ness. Some anticholinesterase drugs, e.g. neostigmine, used
3. Nasal obstruction. This alternates from side to side. Usu- in the treatment of myasthenia gravis, have acetylcholine
ally more marked at night. It is the dependent side of like action and cause nasal obstruction. Contraceptive pills
nose which is often blocked when lying on one side. also cause nasal obstruction because of oestrogens.
4. Postnasal drip. 2. Rhinitis medicamentosa. Topical decongestant nasal
drops are notorious to cause rebound phenomenon. Their
SIGNS excessive use causes rhinitis. It is treated by withdrawal of
Nasal mucosa over the turbinates is generally congested and nasal drops, short course of systemic steroid therapy and
hypertrophic. In some, it may be normal. in some cases, surgical reduction of turbinates, if they have
become hypertrophied.
COMPLICATIONS 3. Rhinitis of pregnancy. Pregnant women may develop
Long-standing cases or VMR develop nasal polypi, hypertro- persistent rhinitis due to hormonal changes. Nasal mucosa
phic rhinitis and sinusitis.
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- 7. Gustatory rhinitis. Spicy and pungent food may in some
ally, local measures such as limited use of nasal drops, topi- people produce rhinorrhoea, nasal stuffiness, lacrimation,
cal steroids and limited surgery (cryosurgery) to turbinates sweating and even flushing of face. This is a cholinergic
are sufficient to relieve the symptoms. Safety of the devel- response to stimulation of sensory receptors on the palate.
oping fetus is not established for newer antihistaminics and Spicy food, particularly the red pepper, contains capsaicin
they should be avoided. which is known to stimulate sensory nerves. It can be relieved
4. Honeymoon rhinitis. This usually follows sexual excite- by ipratropium bromide nasal spray (an anticholinergic),
ment leading to nasal stuffiness. a few minutes before meals.
5. Emotional rhinitis. Nose may react to several emotional 8. Nonairflow rhinitis. It is seen in patients of laryngectomy
stimuli. Psychological states like anxiety, tension, hostility, and tracheostomy. Nose is not used for airflow and the tur-
humiliation, resentment and grief are all known to cause binates become swollen due to loss of vasomotor control.
rhinitis. Treatment is proper counselling for psychological Similar changes are also seen in nasopharyngeal obstruc-
adjustment. Imipramine, which has both antidepressant tion due to choanal atresia or adenoidal hyperplasia, the
and anticholinergic effects, has been found useful. latter having the additional factor of infection due to stagna-
6. Rhinitis due to hypothyroidism. Hypothyroidism leads to tion of discharge in the nasal cavity which should otherwise
hypoactivity of the sympathetic system with predominance of drain freely into the nasopharynx.

32 Nasal Polypi

Nasal polypi are non-neoplastic masses of oedematous nasal PATHOLOGY
or sinus mucosa.They are divided into two main varieties: In early stages, surface of nasal polypi is covered by ciliated
1. Bilateral ethmoidal polypi. columnar epithelium like that of normal nasal mucosa but
2. Antrochoanal polyp. later it undergoes a metaplastic change to transitional and
squamous type on exposure to atmospheric irritation. Submu-
BILATERAL ETHMOIDAL POLYPI cosa shows large intercellular spaces filled with serous fluid.
AETIOLOGY There is also infiltration with eosinophils and round cells.
Aetiology of nasal polypi is very complex and not well-
understood. They may arise in inflammatory conditions of SITE OF ORIGIN
nasal mucosa (rhinosinusitis), disorders of ciliary motility or Multiple nasal polypi always arise from the lateral wall of
abnormal composition of nasal mucus (cystic fibrosis). Vari- nose, usually from the middle meatus. Common sites are
ous diseases associated with the formation of nasal polypi uncinate process, bulla ethmoidalis, ostia of sinuses, medial
are: surface and edge of middle turbinate. Allergic nasal polypi
1. Chronic rhinosinusitis. Polypi are seen in chronic rhino- almost never arise from the septum or the floor of nose.

sinusitis of both allergic and nonallergic origin. Nonal- SYMPTOMS
lergic rhinitis with eosinophilia syndrome (NARES) is a 1. Multiple polypi can occur at any age but are mostly seen
form of chronic rhinitis associated with polypi.
2. Asthma. Seven per cent of the patients with asthma of in adults.
atopic or nonatopic origin show nasal polypi. 2. Nasal stuffiness leading to total nasal obstruction may be
3. Aspirin intolerance. Thirty-six per cent of the patients
with aspirin intolerance may show polypi. Samter’s triad the presenting symptom.
consists of nasal polypi, asthma and aspirin intolerance. 3. Partial or total loss of sense of smell.
4. Cystic fibrosis. Twenty per cent of patients with cystic 4. Headache due to associated sinusitis.
fibrosis form polypi. It is due to abnormal mucus. 5. Sneezing and watery nasal discharge due to associated
5. Allergic fungal sinusitis. Almost all cases of fungal sinus-
itis form nasal polypi. allergy.
6. Kartagener syndrome. This consists of bronchiectasis 6. Mass protruding from the nostril.
sinusitis, situs inversus and ciliary dyskinesis.
7. Young syndrome. It consists of sinopulmonary disease SIGNS
and azoospermia. On anterior rhinoscopy, polypi appear as smooth, glistening,
8. Churg–Strauss syndrome. Consists of asthma, fever, grape-like masses often pale in colour. They may be sessile
eosinophilia, vasculitis and granuloma. or pedunculated, insensitive to probing and do not bleed on
9. Nasal mastocytosis. It is a form of chronic rhinitis in touch. Often they are multiple and bilateral. Long-standing
which nasal mucosa is infiltrated with mast cells but cases present with broadening of nose and increased inter-
few eosinophils. Skin tests for allergy and IgE levels are canthal distance. A polyp may protrude from the nostril
normal. and appear pink and vascular simulating neoplasm (Figure
32.1). Nasal cavity may show purulent discharge due to asso-
PATHOGENESIS ciated sinusitis.
Nasal mucosa, particularly in the region of middle meatus
and turbinate, becomes oedematous due to collection of Probing of a solitary ethmoidal polyp may be necessary to
extracellular fluid causing polypoidal change. Polypi which differentiate it from hypertrophy of the turbinate or cystic
are sessile in the beginning become pedunculated due to middle turbinate.
gravity and excessive sneezing.
172 DIAGNOSIS
Diagnosis can be easily made on clinical examination. Com-
puted tomography (CT) scan of paranasal sinuses is essen-
tial to exclude the bony erosion and expansion suggestive of
neoplasia. Simple nasal polypi may sometimes be associated

with malignancy underneath, especially in people above CHAPTER 32 — NASAL POLYPI 173
40 years and this must be excluded by histological exami-
nation of the suspected tissue. CT scan also helps to plan ANTROCHOANAL POLYP (SYN. KILLIAN’S
surger y. POLYP)
TREATMENT
CONSERVATIVE This polyp arises from the mucosa of maxillary antrum near
1. Early polypoidal changes with oedematous mucosa may its accessory ostium, comes out of it and grows in the choana
and nasal cavity. Thus it has three parts.
revert to normal with antihistaminics and control of 1. Antral, which is a thin stalk.
allergy. 2. Choanal, which is round and globular.
2. A short course of steroids may prove useful in case of peo- 3. Nasal, which is flat from side to side.
ple who cannot tolerate antihistaminics and/or in those
with asthma and polypoidal nasal mucosa. They may also AETIOLOGY
be used to prevent recurrence after surgery. Contrain- Exact cause is unknown. Nasal allergy coupled with sinus
dications to use of steroids, e.g. hypertension, peptic infection is incriminated. Antrochoanal polypi are seen
ulcer, diabetes, pregnancy and tuberculosis should be in children and young adults. Usually they are single and
excluded. unilateral.
SURGICAL
1. Polypectomy. One or two polyps which are pedunculated SYMPTOMS
can be removed with snare. Multiple and sessile polypi Unilateral nasal obstruction is the presenting symptom.
require special forceps. Obstruction may become bilateral when polyp grows into
2. Intranasal ethmoidectomy. When polypi are multiple the nasopharynx and starts obstructing the opposite choana
and sessile, they require uncapping of the ethmoidal air (Tables 32.1 and 32.2). Voice may become thick and dull
cells by intranasal route, a procedure called intranasal due to hyponasality. Nasal discharge, mostly mucoid, may be
ethmoidectomy. seen on one or both sides.
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 Table 32.1  Common causes of unilateral nasal
superceded by endoscopic sinus surgery. obstruction
5. Endoscopic sinus surgery. These days, ethmoidal polypi
are removed by endoscopic sinus surgery more popularly • Vestibule
called functional endoscopic sinus surgery (FESS). It is done
with various endoscopes of 0°, 30° and 70° angulation. • F uruncle
Polypi can be removed more accurately when ethmoid • V estibulitis
cells are removed, and drainage and ventilation provided • S tenosis of nares
to the other involved sinuses such as maxillary, sphenoi- • A tresia
dal or frontal. • N asoalveolar cyst
• Papilloma
Figure 32.1  A polyp protruding from the left nostril in a patient with • Squamous cell carcinoma
bilateral ethmoidal polypi.
• Nasal cavity

• Foreign body
• Deviated nasal septum (DNS)
• H ypertrophic turbinates
• Concha bullosa
• Antrochoanal polyp
• S ynechia
• R hinolith
• B leeding polypus of septum
• Benign and malignant tumours of nose and paranasal

sinuses
• Sinusitis, unilateral
• Nasopharynx
• Unilateral choanal atresia

174 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Table 32.2  Common causes of bilateral nasal Posterior rhinoscopy may reveal a globular mass filling
obstruction the choana or the nasopharynx. A large polyp may hang
down behind the soft palate and present in the oropharynx
• Vestibule (Figure 32.3 A,B).
• B ilateral vestibulitis
• C ollapsing nasal alae Examination of the nose with an endoscope may reveal
• S tenosis of nares a choanal or antrochoanal polyp hidden posteriorly in the
• Congenital atresia of nares nasal cavity (Figure 32.4).
• N asal cavity
• A cute rhinitis (viral and bacterial) See Table 32.3 for differences between antrochoanal and
• C hronic rhinitis and sinusitis ethmoidal polypi.
• R hinitis medicamentosa
• A llergic rhinitis DIFFERENTIAL DIAGNOSIS
• Hypertrophic turbinates 1. A blob of mucus often looks like a polypus but it would
• DNS
• Nasal polypi disappear on blowing the nose.
• Atrophic rhinitis 2. H ypertrophied middle turbinate is differentiated by
• Rhinitis sicca
• S eptal haematoma its pink appearance and hard feel of bone on probe
• S eptal abscess testing.
• B ilateral choanal atresia 3. Angiofibroma has history of profuse recurrent epistaxis.
• Nasopharynx It is firm in consistency and easily bleeds on probing.
• A denoid hyperplasia 4. Other neoplasms may be differentiated by their fleshy
• L arge choanal polyp pink appearance, friable nature and their tendency to
• Thornwaldt’s cyst bleed.
• Adhesions between soft palate and posterior

pharyngeal wall
• L arge benign and malignant tumours

Figure 32.2  Antrochoanal polyp projecting through the left nostril in Figure 32.4  Endoscopic view of a choanal polyp right side.
a 14-year-old patient.

AB Figure 32.3 (A) Antrochoanal
polyp seen hanging in the orophar-
ynx from behind the soft palate on
the right side of uvula. (B) Polyp
after removal.

CHAPTER 32 — NASAL POLYPI 175

Table 32.3  Differences between antrochoanal and ethmoidal polypi

Age Antrochoanal polypi Ethmoidal polypi
Aetiology
Number Common in children Common in adults
Laterality Infection Allergy or multifactorial
Origin Solitary Multiple
Unilateral Bilateral
Growth Maxillary sinus near the ostium Ethmoidal sinuses, uncinate process, middle turbinate

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

X-rays of paranasal sinuses may show opacity of the involved SOME IMPORTANT POINTS TO REMEMBER
antrum. X-ray (lateral view), soft tissue nasopharynx, reveals IN A CASE OF NASAL POLYPI
a globular swelling in the postnasal space. It is differenti-
ated from angiofibroma by the presence of a column of air 1. If a polypus is red and fleshy, friable and has granular
behind the polyp. surface, especially in older patients, think of malignancy.

TREATMENT 2. Simple nasal polyp may masquerade a malignancy under-
An antrochoanal polyp is easily removed by avulsion either neath. Hence all polypi should be subjected to histology.
through the nasal or oral route. Recurrence is uncommon
after complete removal. In cases which do recur, Caldwell– 3. A simple polyp in a child may be a glioma, an encepha-
Luc operation may be required to remove the polyp com- locele or a meningoencephalocele. It should always be
pletely from the site of its origin and to deal with coexistent aspirated and fluid examined for CSF. Careless removal
maxillary sinusitis. These days, endoscopic sinus surgery has of such polyp would result in CSF rhinorrhoea and
superceded other modes of polyp removal. Caldwell–Luc meningitis.
operation is avoided.
4. Multiple nasal polypi in children may be associated with
mucoviscidosis.

5. Epistaxis and orbital symptoms associated with a polyp
should always arouse the suspicion of malignancy.

33 Epistaxis

Bleeding from inside the nose is called epistaxis. It is fairly sphenopalatine and the greater palatine, anastomose here
common and is seen in all age groups—children, adults and to form a vascular plexus called “Kiesselbach’s plexus.” This
older people. It often presents as an emergency. Epistaxis is area is exposed to the drying effect of inspiratory current
a sign and not a disease per se and an attempt should always and to finger nail trauma, and is the usual site for epistaxis
be made to find any local or constitutional cause. in children and young adults.
Retrocolumellar vein. This vein runs vertically downwards
BLOOD SUPPLY OF NOSE just behind the columella, crosses the floor of nose and joins
(FIGURES 33.1 AND 33.2) venous plexus on the lateral nasal wall. This is a common
Nose is richly supplied by both the external and internal site of venous bleeding in young people.
carotid systems, both on the septum and the lateral walls.
WOODRUFF’S PLEXUS
NASAL SEPTUM It is a plexus of veins situated inferior to posterior end of
inferior turbinate. It is a site of posterior epistaxis in adults.
INTERNAL CAROTID SYSTEM
CAUSES OF EPISTAXIS
} 1. Anterior ethmoidal artery Branches of ophthalmic They may be divided into:
1. Local, in the nose or nasopharynx.
2. Posterior ethmoidal artery artery 2. General.
3. Idiopathic.
EXTERNAL CAROTID SYSTEM
1. Sphenopalatine artery (branch of maxillary artery) gives A.  LOCAL CAUSES
NOSE
nasopalatine and posterior medial nasal branches. 1. Trauma. Finger nail trauma, injuries of nose, intranasal
2. Septal branch of greater palatine artery (branch of max-
surgery, fractures of middle third of face and base of
illary artery). skull, hard-blowing of nose, violent sneeze.
3. Septal branch of superior labial artery (branch of facial 2. Infections
(a) Acute: Viral rhinitis, nasal diphtheria, acute sinusitis.
arter y). (b) Chronic: All crust-forming diseases, e.g. atrophic rhini-

LATERAL WALL tis, rhinitis sicca, tuberculosis, syphilis septal perforation,
granulomatous lesion of the nose, e.g. rhinosporidiosis.
INTERNAL CAROTID SYSTEM 3. Foreign bodies
(a) Nonliving: Any neglected foreign body, rhinolith.
} 1. Anterior ethmoidal Branches of ophthalmic artery (b) Living: Maggots, leeches.
4. Neoplasms of nose and paranasal sinuses.
2. Posterior ethmoidal (a) Benign: Haemangioma, papilloma.
(b) Malignant: Carcinoma or sarcoma.
EXTERNAL CAROTID SYSTEM 5. Atmospheric changes. High altitudes, sudden decom-
pression (Caisson disease).
1. Posterior lateral nasal → From sphenopalatine 6. Deviated nasal septum.
branches artery NASOPHARYNX
→ From maxillary artery 1. Adenoiditis.
2. Greater palatine artery → From infraorbital 2. Juvenile angiofibroma.
3. Nasal branch of anterior branch of maxillary 3. Malignant tumours.
artery
superior dental

4. Branches of facial artery
to nasal vestibule

LITTLE’S AREA
It is situated in the anterior inferior part of nasal sep-
tum, just above the vestibule. Four arteries—anterior eth-
moidal, septal branch of superior labial, septal branch of

176

CHAPTER 33 — EPISTAXIS 177

Internal carotid artery

Ophthalmic artery

Anterior Posterior
ethmoidal artery ethmoidal artery

Little’s area

Septal branch Greater palatine Branches of
artery sphenopalatine
Superior labial
artery External carotid artery
artery
Facial artery Maxillary artery
Figure 33.1  Blood supply of nasal septum.

B.  GENERAL CAUSES C. IDIOPATHIC
1. Cardiovascular system. Hypertension, arterioscle- Many times the cause of epistaxis is not clear.

rosis, mitral stenosis, pregnancy (hypertension and SITES OF EPISTAXIS
hormonal). 1. Little’s area. In 90% cases of epistaxis, bleeding occurs
2. Disorders of blood and blood vessels. Aplastic anaemia,
leukaemia, thrombocytopenic and vascular purpura, from this site.
haemophilia, Christmas disease, scurvy, vitamin K defi- 2. Above the level of middle turbinate. Bleeding from above
ciency and hereditary haemorrhagic telangectasia.
3. Liver disease. Hepatic cirrhosis (deficiency of factor II, the middle turbinate and corresponding area on the sep-
VII, IX and X). tum is often from the anterior and posterior ethmoidal
4. Kidney disease. Chronic nephritis. vessels (internal carotid system).
5. Drugs. Excessive use of salicylates and other analgesics 3. Below the level of middle turbinate. Here bleeding is
(as for joint pains or headaches), anticoagulant therapy from the branches of sphenopalatine artery. It may be hid-
(for heart disease). den, lying lateral to middle or inferior turbinate and may
6. Mediastinal compression. Tumours of mediastinum require infrastructure of these turbinates for localization
(raised venous pressure in the nose). of the bleeding site and placement of packing to control it.
7. Acute general infection. Influenza, measles, chick- 4. Posterior part of nasal cavity. Here blood flows directly
enpox, whooping cough, rheumatic fever, infectious into the pharynx.
mononucleosis, typhoid, pneumonia, malaria and den- 5. Diffuse. Both from septum and lateral nasal wall. This is
gue fever. often seen in general systemic disorders and blood dyscrasias.
8. Vicarious menstruation (epistaxis occurring at the time 6. Nasophar ynx.
of menstruation).

178 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES
Internal carotid artery

Ophthalmic artery

Anterior Posterior
ethmoidal artery ethmoidal artery

Branches of
sphenopalatine

artery

Branches of Greater Lesser palatine Sphenopalatine
facial artery palatine artery artery
artery
Facial artery Maxillary artery

External carotid
artery

Figure 33.2  Blood supply of lateral wall of nose.

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

CHAPTER 33 — EPISTAXIS 179

AB

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
out from the mouth (Figure 33.4). Ends of the silk threads
8. History of drug intake (analgesics, anticoagulants, etc.). 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
CAUTERIZATION the usual manner. These days nasal balloons are also avail-
This is useful in anterior epistaxis when bleeding point has able (Figure 33.5). A nasal balloon has two bulbs, one for
been located. The area is first topically anaesthetized and the postnasal space and the other for nasal cavity.
the bleeding point cauterized with a bead of silver nitrate or
coagulated with electrocautery. ENDOSCOPIC CAUTERIZATION
Using topical or general anaesthesia, bleeding point is local-
ANTERIOR NASAL PACKING ized with a rigid endoscope. It is then cauterized with a mal-
In cases of active anterior epistaxis, nose is cleared of blood leable unipolar suction cautery or a bipolar cautery. The
clots by suction and attempt is made to localize the bleed- procedure is effective with less morbidity and decreased
ing site. In minor bleeds, from the accessible sites, cauteriza- hospital stay. The procedure has a limitation when profuse
tion of the bleeding area can be done. If bleeding is profuse bleeding does not permit localization of the bleeding point.
and/or the site of bleeding is difficult to localize, anterior
packing should be done. For this, use a ribbon gauze soaked ELEVATION OF MUCOPERICHONDRIAL FLAP
with liquid paraffin. About 1 m gauze (2.5 cm wide in adults AND SUBMUCOUS RESECTION (SMR) OPERATION
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 1. External carotid. When bleeding is from the exter-
given to prevent sinus infection and toxic shock syndrome.
nal carotid system and the conservative measures have
POSTERIOR NASAL PACKING failed, ligation of external carotid artery above the origin
It is required for patients bleeding posteriorly into the of superior thyroid artery should be done. It is avoided
throat. A postnasal pack is first prepared by tying three silk these days in favour of embolization or ligation of more
peripheral branches of sphenopalatine artery.

180 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Figure 33.4  Technique of postnasal pack.

2. Maxillary artery. Ligation of this artery is done in uncon- B
trollable posterior epistaxis. Approach is via Caldwell–Luc A
operation. Posterior wall of maxillary sinus is removed
and the maxillary artery or its branches are blocked by Figure 33.5  Epistaxis balloon for posterior epistaxis. Posterior bal-
applying clips. This procedure is now superceded by loon (A) is inflated with 10 mL and anterior balloon (B) with 30 mL.
transnasal endoscopic sphenopalatine artery ligation. Catheter provides nasal airway.

3. Ethmoidal arteries. In anterosuperior bleeding above 2. Reassure the patient. Mild sedation should be given.
the middle turbinate, not controlled by packing, anterior 3. Keep check on pulse, BP and respiration.
and posterior ethmoidal arteries, which supply this area, 4. M aintain haemodynamics. Blood transfusion may be
can be ligated. The vessels are exposed in the medial wall
of the orbit by an external ethmoid (Lynch) incision. required.
5. Antibiotics may be given to prevent sinusitis, if pack is to
TRANSNASAL ENDOSCOPIC SPHENOPALATINE
ARTERY LIGATION (TESPAL) be kept beyond 24 h.
The procedure can be done with rigid endoscopes under 6. Intermittent oxygen may be required in patients with
topical anaesthesia with sedation or under a general anaes-
thesia. A mucosal flap is lifted in posterior part of lateral bilateral packs because of increased pulmonary resis-
nasal wall, sphenopalatine artery (SPA)is localized as it exits tance from nasopulmonary reflex.
the foramen and closed with a vascular clip. Distal branches 7. Investigate and treat the patient for any underlying local
of the artery can be additionally cauterized and the flap then or general cause.
reposited. Anterior ethmoidal artery can also be ligated by Hereditary haemorrhagic telangiectasia. It occurs on the
Lynch incision as an adjunctive procedure. SPA ligation anterior part of nasal septum and is the cause of recurrent
gives high success in control of refractory posterior bleed. bleeding. It can be treated by using Argon, KTP or Nd: YAG
EMBOLIZATION laser. The procedure may require to be repeated several times
It is done by an interventional radiologist through femoral in a year as telangectasia recurs in the surrounding mucosa.
artery catheterization. Internal maxillary artery is localized and Some cases require septodermoplasty where anterior part of
the embolization is performed with absorbable gelfoam and/ septal mucosa is excised and replaced by a split-skin graft.
or polyvinyl alcohol or coils. Both ipsilateral or bilateral emboli-
zations may be required for unilateral epistaxis because of cross
circulation. Embolization is generally a safe procedure but may
have potential risks like cerebral thromboembolism, haema-
toma at local site. Ethmoidal arteries cannot be embolized.

GENERAL MEASURES IN EPISTAXIS

1. Make the patient sit up with a back rest and record any
blood loss taking place through spitting or vomiting.

34Trauma to the Face

Injuries of face may involve soft tissues, bones or both. The BONE INJURIES AND THEIR MANAGEMENT
majority of facial injuries are caused by automobile acci- The face can be divided into three regions:
dents. Others result from sports, personal accidents, assaults 1. Upper third. Above the level of supraorbital ridge.
and fights. The management of facial trauma can be divided 2. Middle third. Between the supraorbital ridge and the
into:
1. General management. upper teeth.
2. Soft tissue injuries and their management. 3. Lower third. Mandible and the lower teeth.
3. Bone injuries and their management. The various fractures encountered in these regions are
listed in Table 34.1.
GENERAL MANAGEMENT
1. Airway. Maintenance of airway should receive the highest I.  FRACTURES OF UPPER THIRD OF FACE
A.  FRONTAL SINUS
priority. Airway is obstructed by loss of skeletal support, Frontal sinus fractures may involve anterior wall, posterior
aspiration of foreign bodies, blood or gastric contents or wall or the nasofrontal duct.
swelling of tissues. Airway is secured by intubation or the 1. Anterior wall fractures may be depressed or comminuted.
tracheostomy.
2. Haemorrhage. Injuries of face may bleed profusely. Defect is mainly cosmetic. Sinus is approached through
Bleeding should be stopped by pressure or ligation of a wound in the skin if that is present, or through a brow
vessels. incision. The bone fragments are elevated, taking care
3. Associated injuries. Facial injuries may be associated with not to strip them from the periosteum. The interior of
injuries of head, chest, abdomen, neck, larynx, cervical the sinus is always inspected to rule out fracture of the
spine or limbs and should be attended too. posterior wall.
2. Posterior wall fractures may be accompanied by dural tears,
SOFT TISSUE INJURIES AND THEIR brain injury and CSF rhinorrhoea. They may require
MANAGEMENT neurosurgical consultation. Dural tears can be covered
FACIAL LACERATIONS by temporalis fascia. Small sinuses can be obliterated with
Wound is thoroughly cleaned of any dirt, grease or foreign fat.
matter. The lacerations are closed by accurate approxima- 3. Injury to nasofrontal duct causes obstruction to sinus drain-
tion of each layer. age and may later be complicated by a mucocele. In such
cases, make a large communication between the sinus
PAROTID GLAND AND DUCT and the nose. Small sinuses can be obliterated with fat
Parotid tissue, if exposed, is repaired by suturing. Injuries after removing the sinus mucosa completely.
of parotid duct are more serious. Both ends of the duct are
identified and sutured over a polyethylene tube with fine B.  SUPRAORBITAL RIDGE
suture. The tube is left for 3 days to 2 weeks. Ridge fractures often cause periorbital ecchymosis, flatten-
ing of the eyebrow, proptosis or downward displacement of
FACIAL NERVE eye. Fragment of bone may also be pushed into the orbit
If severed, the facial nerve is exposed by superficial paroti- and get impacted. Ridge fractures require open reduction
dectomy and cut ends are approximated with 8–0 or 10–0 through an incision in the brow or transverse skin line of
silk under magnification. the forehead.

181

182 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

Table 34.1  Fractures of the face

Upper third Middle third Lower third A

Frontal Nasal bones and septum Alveolar process
sinuses
Naso-orbital area Symphysis
Supraorbital
ridge • Zygoma • Body
• Zygomatic arch • A ngle
Frontal • Orbital floor • Ascending
bone • Maxilla
• Le Fort I (transverse) ramus
• L e Fort II (pyramidal) • Condyle
• Le Fort III (craniofa- • T emporoman-

cial dysjunction) dibular joint

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

II.  FRACTURES OF MIDDLE THIRD OF FACE C

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

CHAPTER 34 — TRAUMA TO THE FACE 183

Zygomaticofrontal fracture Zygomaticotemporal fracture

Figure 34.2  Fractured nasal bone (arrow) as seen in radiograph. Infraorbital fracture
Figure 34.3  Fracture zygoma left.
2. Open reduction. Early open reduction in nasal frac-
tures is rarely required. This is indicated when closed 2. Open reduction. This is required in cases with extensive
methods fail. Certain septal injuries can be better reduced comminution of nasal and orbital bones, and those compli-
by open methods. Healed nasal deformities resulting cated by other injuries to lacrimal apparatus, medial canthal
from nasal trauma can be corrected by rhinoplasty or ligaments, frontal sinus, etc.
septorhinoplasty.
An H-type incision gives adequate exposure of the frac-
B.  NASO-ORBITAL FRACTURES tured area. This can be extended to the eyebrows if access to
Direct force over the nasion fractures nasal bones and dis- frontal sinuses is also required.
places them posteriorly. Perpendicular plate of ethmoid,
ethmoidal air cells and medial orbital wall are fractured Nasal bones are reduced under vision and bridge height
and driven posteriorly. Injury may involve cribriform plate, is achieved. Medial orbital walls can be reduced. Medial can-
frontal sinus, frontonasal duct, extraocular muscles, eyeball thal ligaments, if avulsed, are restored with a through and
and the lacrimal apparatus. Medial canthal ligament may be through wire. Intranasal packing may be required to restore
avulsed. the contour. When bone comminution is severe, restoration
of medial canthal ligaments and lacrimal apparatus should
CLINICAL FEATURES receive preference over reconstruction of nasal contour.
1. T elecanthus, due to lateral displacement of medial
C.  FRACTURES OF ZYGOMA (TRIPOD FRACTURE)
orbital wall. After nasal bones, zygoma is the second most frequently frac-
2. Pug nose. Bridge of nose is depressed and tip turned up. tured bone. Usually, the cause is direct trauma. Lower seg-
3. Periorbital ecchymosis. ment of zygoma is pushed medially and posteriorly resulting
4. Orbital haematoma due to bleeding from anterior and in flattening of the malar prominence and a step deformity at
the infraorbital margin. Zygoma is separated at its three pro-
posterior ethmoidal arteries. cesses (Figure 34.3). Fracture line passes through zygomatico-
5. CSF leakage due to fracture of cribriform plate and dura. frontal suture, orbital floor, infraorbital margin and foramen,
6. Displacement of eyeball. anterior wall of maxillary sinus and the zygomaticotemporal
suture. Orbital contents may herniate into the maxillary sinus.
DIAGNOSIS CLINICAL FEATURES
Various facial films will be required to assess the extent of 1. Flattening of malar prominence.
fracture and injury to other facial bones. Computed tomog- 2. Step deformity of infraorbital margin.
raphy (CT) scans are more useful. 3. Anaesthesia in the distribution of infraorbital nerve.
TREATMENT 4. Trismus, due to depression of zygoma on the underlying
1. Closed reduction. In uncomplicated cases, fracture is
reduced with Asch’s forceps and stabilized by a wire passed coronoid process.
through fractured bony fragments and septum and then 5. Oblique palpebral fissure, due to the displacement of lat-
tied over the lead plates. Intranasal packing is given. Splint-
ing is kept for 10 days or so. eral palpebral ligament.
6. Restricted ocular movements, due to entrapment of infe-

rior rectus muscle. It may cause diplopia.
7. Periorbital emphysema, due to escape of air from the

maxillary sinus on nose blowing.

184 SECTION II — DISEASES OF NOSE AND PARANASAL SINUSES

DIAGNOSIS 3. Diplopia, which may be due to displacement of the eye-
Waters’ or exaggerated Waters’ view shows the fracture and ball or entrapment of inferior rectus and inferior oblique
displacement the best. Maxillary sinus may show clouding muscles.
due to the presence of blood. Comminution with depres-
sion of orbital floor and herniation of orbital contents can- 4. Hypoaesthesia or anaesthesia of cheek and upper lip, if
not be seen on plain X-rays. CT scan of the orbital will be infraorbital nerve is involved.
more useful.
TREATMENT DIAGNOSIS
Only displaced fractures require treatment. Open reduc- Waters’ view shows a convex opacity bulging into the antrum
tion and internal wire fixation gives best results. Fracture from above (tear-drop opacity). CT scans may confirm the
is exposed at the frontozygomatic suture through lateral diagnosis (Figure 34.5). Entrapment of inferior rectus and
brow incision and reduced by passing an elevator behind inferior oblique muscles is diagnosed by asking the patient
the zygoma. Wire fixation is done at frontozygomatic suture to look up and down, or by the traction test. The latter is
and infraorbital margin. The latter is exposed by a separate performed by grasping the globe and passively rotating it to
incision in the lower lid. Fracture of orbital floor can also be check for restriction of its movements.
repaired through this incision. TREATMENT
Indications for surgery include enophthalmos and persis-
Transantral approach is less favourable. Antrum is tent diplopia due to entrapment of muscle. Orbital floor
exposed as in Caldwell–Luc operation, blood is aspirated, fractures can be satisfactorily reduced by a finger passed
fracture reduced and then stabilized by a pack in the antrum. into the antrum through a transantral approach. A pack can
Fractures of orbital floor can also be reduced. Antral pack be kept in the antrum to support the fragments. Infraor-
is removed in about 10 days through the buccal incision, bital approach, through a skin crease of the lower lid, can
which is left open at the end of operation, or through the also be used either alone or in combination with transan-
intranasal antrostomy route. tral approach. Badly comminuted fractures of orbital floor
can be repaired by a bone graft from the iliac crest, nasal
D.  FRACTURES OF ZYGOMATIC ARCH septum or the anterior wall of the antrum. Silicon or teflon
Zygomatic arch generally breaks into two fragments which sheets have also been used to reconstruct the orbital floor
get depressed. There are three fracture lines, one at each but autogenous grafts are preferable.
end and third in the centre of the arch.
Figure 34.4  Blow out fracture with herniation of orbital contents into
CLINICAL FEATURES the maxillary sinus.
Characteristic features are depression in the area of zygo-
matic arch, local pain aggravated by talking and chewing,
trismus or limitation of the movements of mandible due
to impingement of fragments on the condyle or coronoid
process.

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

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

E.  FRACTURES OF ORBITAL FLOOR Figure 34.5  CT scan showing blow out fracture of right orbital floor.
Zygomatic and Le Fort II maxillary fractures are always
accompanied by fractures of orbital floor. Isolated fractures
of orbital floor, when a large blunt object strikes the globes,
are called “blow out fractures.” Orbital contents may herniate
into the antrum (Figure 34.4).

CLINICAL FEATURES
1. Ecchymosis of lid, conjunctiva and sclera.
2. Enophthalmos with inferior displacement of the eyeball.

This becomes apparent when oedema subsides.

CHAPTER 34 — TRAUMA TO THE FACE 185

F.  FRACTURES OF MAXILLA (FIGURE 34.6) They help to delineate fracture lines and the displacement
They are classified into three types: of fragments.
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
fracture line passes through root of nose, ethmofrontal Fixation of maxillary fractures can be achieved by:
junction, superior orbital fissure, lateral wall of orbit, 1. Interdental wiring.
frontozygomatic and temporozygomatic sutures and the 2. Intermaxillary wiring using arch bars.
upper part of pterygoid plates. 3. Open reduction and interosseous wiring as in zygomatic
CLINICAL FEATURES
1. Malocclusion of teeth with anterior open bite. fractures.
2. Elongation of midface. 4. Wire slings from frontal bone, zygoma or infraorbital rim
3. Mobility in the maxilla.
4. CSF rhinorrhoea. Cribriform plate is injured in Le Fort II to the teeth or arch bars.
and Le Fort III fractures.
DIAGNOSIS III.  FRACTURES OF LOWER THIRD
X-rays, helpful in diagnosis of maxillary fractures are Waters’
view, posteroanterior view, lateral view and the CT scans. FRACTURES OF MANDIBLE
Fractures of mandible have been classified according to their
C location (Figure 34.7). Condylar fractures are the most com-
B mon. They are followed, in frequency, by fractures of the
A angle, body and symphysis (mnemonic CABS). Fractures of
the ramus, coronoid and alveolar processes are uncommon.
Figure 34.6  Fractures of maxilla: (A) Le Fort I, (B) Le Fort II and
(C) Le Fort III. 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
(i) the pull of muscles attached to the fragments, (ii) direction
of fracture line and (iii) bevel of the fracture.
CLINICAL FEATURES
In fractures of condyle, if fragments are not displaced, pain
and trismus are the main features and tenderness is 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.

Most of the fractures of angle, body and symphysis can be diag-
nosed by intraoral and extraoral palpation. Step deformity,

Condylar 2% Coronoid
process process
35%
Alveolar process

3%

Ramus

Angle 20% 5%
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.