MPMSU ENT 2019 question paper with answers

Scattered throughout the pharynx in its subepithelial layer is the lymphoid tissue which is aggregated at places to form masses, collectively called Waldeyer’s ring. The masses are:

1. Nasopharyngeal tonsil or the adenoids
2. Palatine tonsils or simply the tonsils
3. Lingual tonsil
4. Tubal tonsils (in fossa of Rosenmüller)
5. Lateral pharyngeal bands
6. Nodules (in posterior pharyngeal wall)

Vocal nodules are benign growths on the vocal cords caused by chronic vocal abuse.

Etiology

Caused by vocal trauma from speaking at high intensities or in unnatural low tones for prolonged periods, commonly affecting teachers, actors, and singers.

Pathology

Trauma leads to edema, hemorrhage, hyalinization, and fibrosis in the submucosal space. Early nodules are soft and reddish, later becoming greyish/white and fibrous.

Clinical Features

Hoarseness, vocal fatigue, and neck pain on prolonged phonation are typical symptoms.

Management

Conservative: Voice rest and speech therapy are primary treatments, often effective in children.

Surgical: Excision may be needed for large or long-standing nodules in adults, followed by speech therapy to prevent recurrence.

It is the most common congenital abnormality of the larynx. It is characterized by excessive flaccidity of supraglottic larynx which is sucked in during inspiration producing stridor and sometimes cyanosis. Stridor is increased on crying but subsides on placing the child in prone position; cry is normal.

The condition manifests at birth or soon after, and usually disappears by 2 years of age. Direct laryngoscopy shows elongated epiglottis, curled upon itself (omega-shaped Ω), floppy aryepiglottic folds and prominent arytenoids. Flexible laryngoscope is very useful to make the diagnosis. Laryngomalacia cannot be diagnosed in a paralyzed patient.

Mostly, treatment is conservative. Tracheostomy may be required for some cases of severe respiratory obstruction. Supraglottoplasty is required in cases of severe laryngomalacia.

Maggots are larval forms of flies. They are seen to infest nose, nasopharynx and paranasal sinuses causing extensive destruction. Flies, particularly of the genus Chrysomyia, are attracted by the foul-smelling discharge emanating from cases of atrophic rhinitis, syphilis, leprosy or infected wounds and lay eggs, about 200 at a time, which within 24 h hatch into larvae. In India, they are mostly seen from the month of August to October.

CLINICAL FEATURES

In the first 3 or 4 days maggots produce intense irritation, sneezing, lacrimation and headache. Thin blood-stained discharge oozes from the nostrils. The eyelids and lips become puffy. Till this time patient is not aware of maggots. He may present simply as a case of epistaxis. It is only on the third or fourth day that the maggots may crawl out of the nose. Patient has foul smell surrounding him.

Maggots cause extensive destruction to nose, sinuses, soft tissue of face, palate and the eyeball. Fistulae may form in the palate or around the nose. Death may occur from meningitis.

TREATMENT

All visible maggots should be picked up with forceps. Many of them try to retreat into darker cavities when light falls on them. Instillation of chloroform water and oil kills them. Nasal douche with warm saline is used to remove slough, crusts and dead maggots.

A patient with maggots should be isolated with a mosquito net to avoid contact with flies which can perpetuate this cycle. All patients should receive instruction for nasal hygiene before leaving the hospital.

Sixty to seventy-five per cent of facial paralysis is due to Bell’s palsy. It is defined as idiopathic, peripheral facial paralysis or paresis of acute onset. Both sexes are affected with equal frequency. Any age group may be affected though incidence rises with increasing age. A positive family history is present in 6–8% of patients. Risk of Bell palsy is more in diabetics (angiopathy) and pregnant women (retention of fluid).

Aetiology

1. Viral Infection. Most of the evidence supports the viral aetiology due to herpes simplex, herpes zoster or the Epstein–Barr virus. Other cranial nerves may also be involved in Bell palsy which is thus considered a part of the total picture of polyneuropathy.

2. Vascular Ischaemia. It may be primary or secondary. Primary ischaemia is induced by cold or emotional stress. Secondary ischaemia is the result of primary ischaemia which causes increased capillary permeability leading to exudation of fluid, oedema and compression of microcirculation of the nerve.

3. Hereditary. The fallopian canal is narrow because of hereditary predisposition and this makes the nerve susceptible to early compression with the slightest oedema. Ten per cent of the cases of Bell palsy have a positive family history.

4. Autoimmune Disorder. T-lymphocyte changes have been observed.

Clinical Features

Onset is sudden. Patient is unable to close his eye. On attempting to close the eye, eyeball turns up and out (Bell phenomenon). Saliva dribbles from the angle of mouth. Face becomes asymmetrical. Tears flow down from the eye (epiphora). Pain in the ear may precede or accompany the nerve paralysis. Some complain of noise intolerance (stapedial paralysis) or loss of taste (involvement of chorda tympani). Paralysis may be complete or incomplete. Bell palsy is recurrent in 3–10% of patients.

Diagnosis

Diagnosis is always by exclusion. All other known causes of peripheral facial paralysis should be excluded. This requires careful history, complete otological and head and neck examination, X-ray studies, blood tests such as total count, peripheral smear, sedimentation rate, blood sugar and serology.

Nerve excitability tests are done daily or on alternate days and compared with the normal side to monitor nerve degeneration.

Localizing the site of lesion (topodiagnosis) helps in establishing the aetiology and also the site of surgical decompression of nerve, if that becomes necessary.

Treatment

General

1. Reassurance.
2. Relief of ear pain by analgesics.
3. Care of the eye as outlined on p. 108. Eye must be protected against exposure keratitis.
4. Physiotherapy or massage of the facial muscles gives psychological support to the patient. It has not been shown to influence recovery. Active facial movements are encouraged when there is return of some movement to the facial muscles.

Medical Management

Steroids. Their utility has not been proved beyond doubt in carefully controlled studies. Prednisolone is the drug of choice. If patient reports within 1 week, the adult dose of prednisolone is 1 mg/kg/day divided into morning and evening doses for 5 days. Patient is seen on the fifth day. If paralysis is incomplete or is recovering, dose is tapered during the next 5 days. If paralysis remains complete, the same dose is continued for another 10 days and thereafter tapered in next 5 days (total of 20 days). Contraindications include pregnancy, diabetes, hypertension, peptic ulcer, pulmonary tuberculosis and glaucoma.

Steroids have been found useful to prevent incidence of synkinesis, crocodile tears and to shorten the recovery time of facial paralysis. Steroids can be combined with acyclovir for Herpes zoster oticus or Bell palsy.

Other drugs. Vasodilators, vitamins, mast cell inhibitors and antihistaminics have not been found useful.

Surgical Treatment

Nerve decompression relieves pressure on the nerve fibres and thus improves the microcirculation of the nerve. Vertical and tympanic segments of nerve are decompressed. Some workers have suggested total decompression including labyrinthine segment by postaural and middle fossa approach.

Prognosis

Eighty-five to ninety per cent of the patients recover fully. Ten to fifteen per cent recover incompletely and may be left with some stigmata of degeneration. Recurrent facial palsy may not recover fully. Prognosis is good in incomplete Bell palsy (95% complete recovery) and in those where clinical recovery starts within 3 weeks of onset (75% complete recovery).

Normally, middle ear cleft is lined by different types of epithelium in different regions: ciliated columnar in the anterior and inferior part, cuboidal in the middle part and pavement-like in the attic. The middle ear is nowhere lined by keratinizing squamous epithelium. It is the presence of latter type of epithelium in the middle ear or mastoid that constitutes a cholesteatoma. In other words, cholesteatoma is a "skin in the wrong place." The term cholesteatoma is a misnomer because it neither contains cholesterol crystals nor it is a tumour to merit the suffix "oma." However, the term has been retained because of its wider usage.

Essentially, cholesteatoma consists of two parts: (i) the matrix, which is made up of keratinizing squamous epithelium resting on a thin stroma of fibrous tissues and (ii) a central white mass, consisting of keratin debris produced by the matrix. For this reason, it has also been named epidermosis or keratoma.

ORIGIN OF CHOLESTEATOMA

Genesis of cholesteatoma is a matter of debate. Any theory of its genesis must explain how squamous epithelium appeared in the middle ear cleft. The various views expressed are:

1. Presence of congenital cell rests.

2. Invagination of tympanic membrane from the attic or posterosuperior part of pars tensa in the form of retraction pockets (Wittmaack's theory). The outer surface of tympanic membrane is lined by stratified squamous epithelium which after invagination forms the matrix of cholesteatoma and lays down keratin in the pocket.

3. Basal cell hyperplasia (Ruedi's theory). The basal cells of germinal layer of skin proliferate under the influence of infection and lay down keratinizing squamous epithelium.

4. Epithelial invasion (Habermann's theory). The epithelium from the meatus or outer drum surface grows into the middle ear through a pre-existing perforation especially of the marginal type where part of annulus tympanicus has already been destroyed.

5. Metaplasia (Sade's theory). Middle ear mucosa, like respiratory mucosa elsewhere, undergoes metaplasia due to repeated infections and transforms into squamous epithelium.

CLASSIFICATION OF CHOLESTEATOMA

The cholesteatoma is classified into:

1. Congenital
2. Acquired, primary
3. Acquired, secondary

1. Congenital Cholesteatoma. It arises from the embryonic epidermal cell rests in the middle ear cleft or temporal bone. Congenital cholesteatoma occurs at three important sites: middle ear, petrous apex and the cerebellopontine angle, and produces symptomatology depending on its location.

A middle ear congenital cholesteatoma presents as a white mass behind an intact tympanic membrane and causes conductive hearing loss. It may sometimes be discovered on routine examination of children or at the time of myringotomy.

It may also spontaneously rupture through the tympanic membrane and present with a discharging ear indistinguishable from a case of chronic suppurative otitis media.

2. Primary Acquired Cholesteatoma. It is called primary as there is no history of previous otitis media or a pre-existing perforation. Theories include:

(a) Invagination of pars flaccida. Persistent negative pressure in the attic causes a retraction pocket which accumulates keratin debris. When infected, the keratin mass expands towards the middle ear.

(b) Basal cell hyperplasia. Proliferation of the basal layer of pars flaccida induced by subclinical childhood infections.

(c) Squamous metaplasia. Pavement epithelium of attic undergoes metaplasia due to subclinical infections.

3. Secondary Acquired Cholesteatoma. There is a pre-existing perforation in pars tensa. Theories include:

(a) Migration of squamous epithelium through the perforation into the middle ear.
(b) Metaplasia of middle ear mucosa due to recurrent infection.

EXPANSION OF CHOLESTEATOMA AND DESTRUCTION OF BONE

Once cholesteatoma enters the middle ear cleft, it invades surrounding structures via paths of least resistance and through enzymatic bone destruction.

An attic cholesteatoma may extend backwards into the aditus, antrum and mastoid; downwards into the mesotympanum; medially surrounding the incus and/or head of malleus.

Cholesteatoma destroys bone and may cause destruction of ossicles, erosion of labyrinth, canal of facial nerve, sinus plate or tegmen tympani, causing complications. Bone destruction is attributed to enzymes such as collagenase, acid phosphatase and proteolytic enzymes.

Vincent Infection (Acute Necrotizing Ulcerative Gingivitis). It is similar to Vincent’s angina. Causative organisms are the same (a fusiform bacillus and a spirochaete Borrelia vincentii). More often the disease affects young adults and middle-aged persons.

It starts at the interdental papillae and then spreads to free margins of the gingivae which get covered with necrotic slough. Gingivae also become red and oedematous. Similar ulcer and necrotic membrane may also form over the tonsil (Vincent’s angina).

Diagnosis is made by smear from the affected area. Treatment is systemic antibiotics (penicillin or erythromycin and metronidazole), frequent mouth washes (with sodium bicarbonate solution) and attention to dental hygiene.

Foreign Bodies of Ear

(a) Nonliving. Children may insert a variety of foreign bodies in the ear; the common ones often seen are: a piece of paper or sponge, grain seeds (rice, wheat, maize), slate pencil, piece of chalk or metallic ball bearings. An adult may present with a broken end of matchstick used for scratching the ear or an overlooked cotton swab. Vegetable foreign bodies tend to swell up with time and get tightly impacted in the ear canal or may even suppurate.

Methods of removing a foreign body include:

(i) Forceps removal
(ii) Syringing
(iii) Suction
(iv) Microscopic removal with special instruments
(v) Postaural approach

Soft and irregular foreign bodies like a piece of paper, swab or a piece of sponge can be removed with fine crocodile forceps.

Most of the seed grains and smooth objects can be removed with syringing. Smooth and hard objects like steel ball bearing should not be grasped with forceps as they tend to move inwards and may injure the tympanic membrane. In all impacted foreign bodies or in those where earlier attempts at extraction have been made, it is preferable to use general anaesthetic and an operating microscope. Occasionally, postaural approach is used to remove foreign bodies impacted in deep meatus, medial to the isthmus or those which have been pushed into the middle ear.

Unskilled attempts at removal of foreign bodies may lacerate the meatal lining, damage the tympanic membrane or the ear ossicles.

(b) Living. Flying or crawling insects like mosquitoes, beetles, cockroach or an ant may enter the ear canal and cause intense irritation and pain. No attempt should be made to catch them alive. First, the insect should be killed by instilling oil, spirit or chloroform water. Once killed, the insect can be removed by any of the methods described above.

Maggots in the ear

Flies may be attracted to the foulsmelling ear discharge and lay eggs which hatch out into larvae called maggots. They are commonly seen in the month of August, September and October. There is severe pain with swelling round the ear and blood-stained watery discharge. Maggots may be seen filling the ear canal.

Treatment consists of instilling chloroform water to kill the maggots, which can later be removed by forceps. Usually, such patients have discharging ears with perforation of the tympanic membrane and syringing may not be advisable.

It is the largest of paranasal sinuses and occupies the body of maxilla. It is pyramidal in shape with base towards lateral wall of nose and apex directed laterally into the zygomatic process of maxilla and sometimes in the zygomatic bone itself. On an average, maxillary sinus has a capacity of 15 mL in an adult. It is 33 mm high, 35 mm deep and 25 mm wide.

Technique

Patient sits facing the examiner, opens his mouth and breathes quietly from the mouth. The examiner depresses the tongue with a tongue depressor and introduces a warmed posterior rhinoscopic mirror. The mirror is held like a pen and carried behind the soft palate. Without touching the posterior third of the tongue to avoid gag reflex, light from the head mirror is focused on the rhinoscopic mirror, which illuminates the area to be examined. Patient’s relaxation is essential so the soft palate does not contract.

Look for the following:

(a) Choanal polyp or atresia.
(b) Hypertrophy of the posterior ends of inferior turbinates.
(c) Discharge in the middle meatus — seen in infections of maxillary, frontal or ethmoidal sinuses. Discharge above the middle turbinate indicates infection of the posterior ethmoid or sphenoid sinuses.