Long Answer Questions
Q.1 Discuss the classification, clinical features and management of Ca maxillary sinus
+Classification
There is no universally accepted classification for maxillary carcinoma.
1. Ohngren’s classification. An imaginary plane is drawn, extending between medial canthus of eye and the angle of mandible. Growths situated above this plane (suprastructural) have a poorer prognosis than those below it (intrastructural).
2. AJCC classification. AJCC classification is only for squamous cell carcinoma and does not include nonepithelial tumours of lymphoid tissue, soft tissue, cartilage and bone. Histopathologically, squamous cell carcinoma is further graded into:
(a) Well-differentiated,
(b) Moderately differentiated and
(c) Poorly differentiated.
In histopathology, note should also be made of vascular or perineural invasion.
3. Lederman’s classification. It uses two horizontal lines of Sebileau: one passing through the floors of orbits and the other through floors of antra, thus dividing the area into:
(a) Suprastructure. Ethmoid, sphenoid and frontal sinuses and the olfactory area of nose.
(b) Mesostrtructure. Maxillary sinus and the respiratory part of nose.
(c) Infrastructure. Containing alveolar process.
This classification further uses vertical lines, extending down the medial walls of orbit to separate ethmoid sinuses and nasal fossa from the maxillary sinuses.
The student may note here that suprastructure and infrastructure of Lederman’s classification is not the same as in Ohngren’s classification.
Clinical Features
1. Early features of maxillary sinus malignancy are nasal stuffiness, blood-stained nasal discharge, facial paraesthesias or pain and epiphora. These symptoms may be missed or simply treated as sinusitis.
2. Late features will depend on the direction of spread and extent of growth.
3. Medial spread to nasal cavity gives rise to nasal obstruction, discharge and epistaxis. It may also spread into anterior and posterior ethmoid sinuses and that is why most antral malignancies are antroethmoidal in nature.
4. Anterior spread causes swelling of the cheek and later invasion of the facial skin.
5. Inferior spread causes expansion of alveolus with dental pain, loosening of teeth, poor fitting of dentures, ulceration of gingiva and swelling in the hard palate.
6. Superior spread invades the orbit causing proptosis, diplopia, ocular pain and epiphora.
7. Posterior spread is into pterygomaxillary fossa, pterygoid plates and the muscles causing trismus. Growth may also spread to the nasopharynx, sphenoid sinus and base of skull.
8. Intracranial spread can occur through ethmoids, cribriform plate or foramen lacerum.
9. Lymphatic spread. Nodal metastases are uncommon and occur only in the late stages of disease. Submandibular and upper jugular nodes are enlarged. Maxillary and ethmoid sinuses drain primarily into retropharyngeal nodes, but these nodes are inaccessible to palpation.
10. Systemic metastases are rare. May be seen in the lungs (most commonly) and occasionally in bone.
Treatment
Histologically, nature of malignancy is important in deciding the line of treatment as is the location and extent of disease.
Early cases with Stage I and II squamous cell carcinomas are treated with surgery or radiation with equal results. T3 and T4 lesions are treated by combined modalities of radiation and surgery. Radiation in such cases may be given preoperatively or postoperatively. Preoperative dose of radiation is 5500 cGy. Similarly postoperative dose of radiation used is 5000–5500 cGy. Now three-dimensional conformal radiotherapy and intensity-modulated techniques of radiotherapy cover larger tumour volumes and help to reduce side effects of radiation to optic nerves and lens by providing accurate and homogenous radiation dose.
Chemoradiation, i.e. chemotherapy and radiation concomitantly has also been used for large and inoperable tumours by different workers with 5 year survival of more than 60%. Intra-arterial infusion of 5-Fu or cisplatin and 5-Fu with concomitant radiation has also been used with good results in preference to deformities created by extensive surgery associated with advanced malignancy.
Q.2 What are the various causes of conductive deafness? Discuss etiology, clinical features and management of otosclerosis.
+Causes of Conductive Deafness
Outer Ear
Excessive Earwax (Cerumen Impaction)
Foreign Objects: especially in children
Ear Canal Infections (Otitis Externa)
Abnormal Growths/Tumors
Congenital Malformations
Middle Ear
Fluid in the Middle Ear (Otitis Media with Effusion)
Ear Infections (Otitis Media)
Perforated Eardrum
Otosclerosis
Ossicular Dislocation/Discontinuity
Cholesteatoma
Eustachian Tube Dysfunction
OTOSCLEROSIS
Otosclerosis, more aptly called otospongiosis, is a primary disease of the bony labyrinth. In this, one or more foci of irregularly laid spongy bone replace part of normally dense enchondral layer of bony otic capsule. Most often, otosclerotic focus involves the stapes region leading to stapes fixation and conductive deafness. However, it may involve certain other areas of the bony labyrinth where it may cause neurosensory loss or no symptoms at all.
AETIOLOGY
Anatomical basis. Bony labyrinth is made of enchondral bone which is subject to little change in life. But sometimes, in this hard bone, there are areas of cartilage rests which due to certain nonspecific factors are activated to form a new spongy bone. One such area is the fissula ante fenestram lying in front of the oval window—the site of predilection for stapedial type of otospongiosis.
Heredity. About 50% of otosclerotics have positive family history; rest are sporadic. Genetic studies reveal that it is an autosomal dominant trait with incomplete penetrance and a variable expressivity.
Race. White races are affected more than black Americans. It is common in Indians but rare among Chinese and Japanese.
Sex. Females are affected twice as often as males but in India, otosclerosis seems to predominate in males.
Age of onset. Hearing loss usually starts between 20 and 30 years of age and is rare before 10 and after 40 years.
Effect of other factors. Hearing loss due to otosclerosis may be initiated or worsened by pregnancy, menopause, accidents or major operations.
Association with osteogenesis imperfecta. Triad of osteogenesis imperfecta, otosclerosis and blue sclera is called van der Hoeve syndrome.
Viral infection. Electron microscopy has shown RNA related to measles virus suggesting viral etiology.
SYMPTOMS
1. Hearing Loss – painless, progressive, usually bilateral and conductive.
2. Paracusis Willisii – hears better in noisy surroundings.
3. Tinnitus – more common in cochlear otosclerosis.
4. Vertigo – uncommon.
5. Speech – monotonous, soft speech.
SIGNS
1. Tympanic membrane normal; Schwartze sign may be present.
2. Eustachian tube function normal.
3. Tuning fork tests: Negative Rinne, Weber lateralizes to affected ear.
4. Audiometry: Air conduction loss; Carhart’s notch at 2000 Hz.
TREATMENT
Medical
No definitive medical cure. Sodium fluoride has been tried but is controversial.
Surgical
Stapedectomy/stapedotomy with prosthesis (teflon, stainless steel, platinum–teflon, titanium–teflon). 90% show good improvement in hearing.
Selection of Patients for Stapes Surgery
• Air conduction ≥ 30 dB
• Air-bone gap ≥ 15 dB
• Speech discrimination ≥ 60%
Contraindications
1. Only hearing ear
2. Ménière’s disease
3. Young children
4. High-risk professions (athletes, divers, construction workers)
5. Noisy workplace
6. Otitis externa, TM perforation, exostosis (relative)
Steps of Stapedectomy
1. Meatal incision and tympanomeatal flap elevation
2. Exposure of stapes
3. Removal of stapes superstructure
4. Stapedotomy or stapedectomy
5. Prosthesis placement
6. Repositioning the flap
Complications
• Flap tear, TM perforation
• Chorda tympani injury
• Incus dislocation
• Facial nerve injury
• Vertigo (early/late)
• Perilymph fistula/granuloma
• Prosthesis issues (short, loose, displaced)
• Sensorineural loss
• Dead ear (1 in 200 patients)
Other Treatments
Stapes mobilization and Lempert’s fenestration are outdated. Hearing aids are effective alternatives for non-surgical candidates.
Short Answer Questions
Q.1 Tonsilloliths (calculus of the tonsil)
+It is seen in chronic tonsillitis when its crypt is blocked with retention of debris. Inorganic salts of calcium and magnesium are then deposited leading to formation of a stone. It may gradually enlarge and then ulcerate through the tonsil.
Tonsilloliths are seen more often in adults and give rise to local discomfort or foreign body sensation. They are easily diagnosed by palpation or gritty feeling on probing. Treatment is simple removal of the stone or tonsillectomy, if that be indicated for associated sepsis or for the deeply set stone which cannot be removed.
Q.2 Examination of Nasopharynx
+EXAMINATION
Clinical examination of nasopharynx includes:
1. Anterior rhinoscopy.
2. Posterior rhinoscopy.
3. Other methods.
(a) Digital examination
(b) Endoscopy
(c) Retraction of soft palate with catheters and mirror examination
4. Cranial nerves.
5. Cervical lymph nodes.
1. Anterior Rhinoscopy
It is possible to see only a small part of the nasopharynx on anterior rhinoscopy. The view can be facilitated by decongestion of nasal and turbinal mucosa with vasoconstrictors.
2. Posterior Rhinoscopy
Structures to be examined are:
(a) Anterior wall. Posterior border of nasal septum, choanae, posterior ends of turbinates and their meatuses.
(b) Lateral walls. Torus tubarius, opening of eustachian tube, pharyngeal recess.
(c) Floor. Upper surface of soft palate.
(d) Roof and posterior wall.
Only a small part of nasopharynx can be seen in the mirror at one time. The examiner tilts the mirror in different directions to see all the walls of the nasopharynx and then mentally reconstitutes the entire picture.
Abnormal findings in the nasopharynx include:
(a) Discharge. It may be seen below the middle turbinate (anterior group of sinuses) or above the middle turbinate (posterior group of sinuses).
(b) Crusting. Atrophic rhinitis or nasopharyngitis.
(c) Mass
(i) Smooth pale mass — antrochoanal polyp.
(ii) Pink lobulated mass — angiofibroma.
(iii) Irregular bleeding mass — carcinoma.
(iv) Smooth swelling in the roof — Thornwaldt’s cyst or abscess.
(v) Irregular mass with radiating folds — adenoids.
(vi) Irregular mass filling the lower part of choana — mulberry hypertrophy of inferior turbinate.
(d) Bleeding. Due to posterior nasal or nasopharyngeal pathology.
3. Other Methods
(a) Digital Examination
It is a quick method to examine the nasopharynx by palpation but is uncomfortable for the patient. The examiner stands behind and to the right of the patient, invaginates patient’s cheek with his left finger and inserts right index finger behind the soft palate into the nasopharynx. He first examines the posterior border of the nasal septum, then the choana, lateral wall and finally the posterior wall of nasopharynx. Adenoids, antrochoanal polyp and other masses can be examined. Avoid this examination if angiofibroma is suspected.
(b) Endoscopy
A rigid nasal endoscope (zero degree, 4 mm) is passed through the nose after local anaesthesia and decongestion. It gives a bright and magnified view of the nasopharyngeal structures. Endoscopes with different angles allow visualization of angled structures. A flexible nasopharyngoscope can also be used for magnified viewing.
(c) Retraction of Soft Palate with Catheters and Mirror Examination
This method is reserved for difficult cases where the view of nasopharynx is not obtained by other methods. It requires good local or general anaesthesia.
A soft rubber catheter is passed through each nostril and retrieved from the oropharynx. Both ends are held together and clamped, retracting the soft palate forward. A mirror is then introduced to examine the nasopharynx. With the advent of endoscopy, this is rarely needed except for biopsy.
4. Examination of Cranial Nerves
Malignancy of nasopharynx can involve CN II to XII, more often CN IX, X and XI.
5. Examination of Cervical Lymph Nodes
Nasopharyngeal malignancy may present primarily as a lymph node mass in the neck. Commonly involved nodes are upper internal jugular nodes and nodes along the accessory nerve in the posterior triangle.
Q.3 Peritonsillar Abscess (Quinsy)
+Definition: It is a collection of pus in the peritonsillar space which lies between the capsule of tonsil and the superior constrictor muscle.
Aetiology
Peritonsillar abscess usually follows acute tonsillitis though it may arise de novo without previous history of sore throats. First, one of the tonsillar crypts, usually the crypta magna, gets infected and sealed off. It forms an intratonsillar abscess which then bursts through the tonsillar capsule to set up peritonsillitis and then an abscess.
Culture of pus from the abscess may reveal pure growth of Streptococcus pyogenes, S. aureus or anaerobic organisms. More often the growth is mixed, with both aerobic and anaerobic organisms.
Clinical Features
Peritonsillar abscess mostly affects adults and rarely the children though acute tonsillitis is more common in children. Usually, it is unilateral though occasionally bilateral abscesses are recorded. Clinical features are divided into:
1. General
- Fever (up to 104 °F)
- Chills and rigors
- General malaise
- Body aches
- Headache
- Nausea and constipation
2. Local
- Severe unilateral throat pain
- Odynophagia – patient cannot swallow saliva, leading to dribbling and dehydration
- Muffled “hot potato” voice
- Foul breath due to sepsis and poor hygiene
- Ipsilateral earache (referred via CN IX)
- Trismus due to spasm of pterygoid muscles
Examination
- Tonsil, pillars and soft palate on the involved side are congested and swollen. Tonsil may appear buried in oedematous pillars.
- Uvula swollen, oedematous and pushed to opposite side.
- Bulging of soft palate and anterior pillar above the tonsil.
- Mucopus may cover the tonsillar region.
- Cervical lymphadenopathy (jugulodigastric nodes).
- Torticollis – neck tilted to side of abscess.
Investigation
- Contrast-enhanced CT or MRI shows abscess and its extent.
- Needle aspiration provides pus for culture and sensitivity.
Treatment
- Hospitalization.
- Intravenous fluids to combat dehydration.
- Large dose IV antibiotics covering aerobic and anaerobic organisms.
- Analgesics like paracetamol for pain and fever; pethidine if needed. Avoid aspirin (risk of bleeding).
- Maintain oral hygiene with hydrogen peroxide or saline mouth washes.
The above conservative measures may cure peritonsillitis. If a frank abscess has formed, incision and drainage will be required.
Incision and Drainage of Abscess
A peritonsillar abscess is opened at the point of maximum bulge above the upper pole of tonsil or just lateral to the point of junction of anterior pillar with a line drawn through the base of uvula. With a guarded knife, a small stab incision is made and a sinus forceps inserted to open the abscess. The forceps may be reinserted the next day to drain any reaccumulation.
Interval Tonsillectomy
Tonsils are removed 4–6 weeks following an attack of quinsy.
Abscess or Hot Tonsillectomy
Some prefer “hot” tonsillectomy instead of incision and drainage. Abscess tonsillectomy carries the risk of rupture of abscess during anaesthesia and excessive bleeding at the time of operation.
Complications
- Parapharyngeal abscess (potential extension).
- Oedema of larynx – may require tracheostomy.
- Septicaemia, endocarditis, nephritis, brain abscess.
- Pneumonitis or lung abscess from aspiration of pus after spontaneous rupture.
- Jugular vein thrombosis.
- Spontaneous haemorrhage from carotid artery or jugular vein.
Q.4 CSF RHINORRHOEA
+DEFINITION
Leakage of CSF into the nose is called CSF rhinorrhoea. It may be clear fluid or mixed with blood as in acute head injuries.
PHYSIOLOGY
CSF forms a jacket of fluid around the brain and spinal cord, acting as a buffer against sudden jerks. It is secreted by choroid plexuses in the lateral, third and fourth ventricles and absorbed into the dural venous sinuses by arachnoid villi. The villi have a one-way valve mechanism allowing CSF to be absorbed into the blood but not vice versa.
Total CSF volume is 90–150 mL. It is secreted at about 20 mL/h (350–500 mL/day), so the total CSF is replaced three to five times daily. Normal CSF pressure at lumbar puncture is 50–150 mm H2O. CSF pressure rises during coughing, sneezing, nose blowing, straining or lifting heavy weights—activities that should be avoided in cases of CSF leak or after repair.
AETIOLOGY
• Trauma (accidental or surgical, including endoscopic sinus surgery, trans-sphenoidal surgery, nasal polypectomy, skull base surgery).
• Inflammations (mucoceles, sinonasal polyposis, fungal infections, osteomyelitis).
• Neoplasms (benign or malignant invading the skull base).
• Congenital lesions (meningocele, meningoencephalocele, gliomas).
• Idiopathic spontaneous leaks.
SITES OF LEAKAGE
• From anterior cranial fossa: cribriform plate, roof of ethmoid, frontal sinus.
• From middle cranial fossa: sphenoid sinus.
• In temporal bone fractures: CSF enters the middle ear and drains via the eustachian tube into the nose (CSF otorhinorrhoea).
DIAGNOSIS
Characterized by clear watery nasal discharge, particularly on bending the head or straining. The reservoir sign may occur on waking when fluid collected in sinuses drains out.
CSF rhinorrhoea is sudden, occurs in gushes on bending, and cannot be sniffed back, unlike nasal discharge which stiffens handkerchief due to mucus.
In traumatic leaks mixed with blood, a double target sign appears on filter paper.
Nasal endoscopy may help localize the leak. Ear examination may show fluid in the middle ear in cases of otorhinorrhoea.
LABORATORY TESTS
• Beta-2 transferrin: highly specific and sensitive for CSF.
• Beta trace protein: also specific for CSF; widely used in Europe.
• Glucose testing is no longer used.
LOCALIZATION OF SITE
1. High-resolution CT: coronal and axial 1–2 mm cuts showing bony defects.
2. MRI (T2-weighted): shows active leaks and detects encephaloceles.
3. Intrathecal fluorescein: invasive; dye seen as fluorescent green under blue filter via endoscope.
4. Radioactive studies are no longer used.
5. CT cisternogram: used when beta-2 transferrin testing is unavailable; now less preferred.
TREATMENT
Conservative Management
Includes bed rest, head elevation, stool softeners, avoidance of nose blowing, sneezing or straining, prophylactic antibiotics, and acetazolamide to reduce CSF production. A lumbar drain may be used when indicated.
Surgical Repair
1. Neurosurgical intracranial approach.
2. Extradural approaches such as external ethmoidectomy, trans-septal sphenoidal approach, and osteoplastic flap for frontal sinus leaks.
3. Transnasal endoscopic repair (success rate ~90%):
(a) Identify the bony defect:
– Cribriform plate
– Lateral lamina
– Roof of ethmoid
– Frontal sinus
– Sphenoid sinus
(b) Prepare graft site.
(c) Underlay fascia graft extradurally followed by mucosal graft (free graft or pedicled flap).
(d) For defects >2 cm: reinforce with cartilage, then cover with mucosa.
(e) Apply surgicel and gelfoam; place antibiotic-soaked nasal pack.
(f) Fat graft may be used instead of fascia in some cases.
(g) Lumbar drain if CSF pressure is high.
(h) Antibiotics.
Frontal sinus leaks may require an osteoplastic flap with sinus obliteration using fat.
Q.5 Complications of Tonsillectomy
+A. IMMEDIATE
1. Primary haemorrhage. Occurs at the time of operation. It can be controlled by pressure, ligation or electrocoagulation of the bleeding vessels.
2. Reactionary haemorrhage. Occurs within a period of 24 h and can be controlled by simple measures such as removal of the clot, application of pressure or vasoconstrictor. Presence of a clot prevents the clipping action of the superior constrictor muscle on the vessels which pass through it. If these measures fail, ligation or electrocoagulation of the bleeding vessels can be done under general anaesthesia.
3. Injury to tonsillar pillars, uvula, soft palate, tongue or superior constrictor muscle due to bad surgical technique.
4. Injury to teeth.
5. Aspiration of blood.
6. Facial oedema. Some patients get oedema of the face, particularly of the eyelids.
7. Surgical emphysema. Rarely occurs due to injury to the superior constrictor muscle.
B. DELAYED
1. Secondary haemorrhage. Usually seen between the fifth to tenth postoperative day. It results from sepsis and premature separation of the membrane. It may start with bloodstained sputum but can become profuse.
2. Infection. Infection of the tonsillar fossa may lead to parapharyngeal abscess or otitis media.
3. Lung complications. Aspiration of blood, mucus or tissue fragments may cause atelectasis or lung abscess.
4. Scarring in soft palate and pillars.
5. Tonsillar remnants. Tonsil tags or tissue left due to inadequate surgery may get repeatedly infected.
6. Hypertrophy of lingual tonsil. A late complication occurring as compensation for loss of palatine tonsils.
Q.6 FUNCTIONS OF TRACHEOSTOMY
+1. Alternative pathway for breathing. This circumvents any obstruction in the upper airway from lips to the tracheostome.
2. Improves alveolar ventilation. In cases of respiratory insufficiency, alveolar ventilation is improved by:
(a) Decreasing the dead space by 30–50% (normal dead space is 150 mL).
(b) Reducing the resistance to airflow.
3. Protects the airways. By using a cuffed tube, the tracheobronchial tree is protected against aspiration of:
(a) Pharyngeal secretions, as in bulbar paralysis or coma.
(b) Blood, as in haemorrhage from the pharynx, larynx or maxillofacial injuries. With tracheostomy, pharynx and larynx can also be packed to control bleeding.
4. Permits removal of tracheobronchial secretions. When the patient is unable to cough—as in coma, head injuries, respiratory paralysis—or when cough is painful, as in chest injuries or upper abdominal operations, secretions can be cleared by repeated suction through the tracheostomy, thus avoiding repeated bronchoscopy or intubation.
5. Intermittent positive pressure respiration (IPPR). If IPPR is required beyond 72 hours, tracheostomy is superior to intubation.
6. To administer anaesthesia. Useful when endotracheal intubation is difficult or impossible, as in laryngopharyngeal growths or trismus.
Q.7 NASAL MYIASIS (MAGGOTS IN NOSE)
+Maggots are larval forms of flies. They may infest the nose, nasopharynx and paranasal sinuses causing extensive destruction. Flies, particularly of the genus Chrysomyia, are attracted by foul-smelling discharge from conditions such as atrophic rhinitis, syphilis, leprosy or infected wounds and lay eggs (about 200 at a time) which hatch into larvae within 24 hours. In India, they are mostly seen from August to October.
CLINICAL FEATURES
During the first 3–4 days, maggots produce intense irritation, sneezing, lacrimation and headache. Thin blood-stained discharge oozes from the nostrils. Eyelids and lips become puffy. At this stage, the patient is usually unaware of the presence of maggots and may present as a case of epistaxis. By the third or fourth day, maggots may crawl out of the nose. The patient has a foul smell surrounding him.
Maggots may cause extensive destruction of the nose, sinuses, soft tissues of the face, palate and even the eyeball. Fistulae may form around the nose or in the palate. Death may occur due to meningitis.
TREATMENT
All visible maggots should be removed with forceps. Many retreat into darker cavities when exposed to light. Instillation of chloroform water and oil helps kill them. Nasal douche with warm saline helps to remove slough, crusts and dead maggots.
The patient should be isolated with a mosquito net to prevent flies from perpetuating the cycle. Before discharge, all patients must receive instruction on proper nasal hygiene.
Q.8 Foreign Bodies in Ear
+Foreign Bodies of Ear
(a) Nonliving. Children may insert a variety of foreign bodies in the ear; common ones include pieces of paper or sponge, grain seeds (rice, wheat, maize), slate pencil, piece of chalk or metallic ball bearings. Adults may present with a broken matchstick used for scratching the ear or an overlooked cotton swab. Vegetable foreign bodies tend to swell with time and become tightly impacted 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 paper, cotton swabs or sponge pieces can be removed with fine crocodile forceps.
Most seed grains and smooth objects can be removed with syringing. Smooth, hard objects like steel ball bearings should not be grasped with forceps, as they may slip inward and injure the tympanic membrane. In impacted foreign bodies or cases where previous attempts have failed, removal under general anaesthesia with an operating microscope is preferred. A postaural approach may be required for deeply impacted foreign bodies located medial to the isthmus or those pushed into the middle ear.
Unskilled attempts may cause laceration of the meatal lining, damage to the tympanic membrane, or injury to the ossicles.
(b) Living. Flying or crawling insects such as mosquitoes, beetles, cockroaches or ants may enter the ear canal and cause intense irritation and pain. They should not be caught alive. First, the insect should be killed by instilling oil, spirit or chloroform water. Once dead, the insect may be removed by any of the methods mentioned earlier.
Maggots in the Ear
Flies may be attracted to foul-smelling ear discharge and may lay eggs that hatch into larvae (maggots). These are commonly seen from August to October. There is severe pain, swelling around the ear and blood-stained watery discharge. Maggots may be visible filling the ear canal.
Treatment includes instilling chloroform water to kill the maggots, followed by removal with forceps. Such patients usually have discharging ears with tympanic membrane perforation, and syringing is generally not advisable.
Q.9 Tuning Fork Tests
+These tests are performed with tuning forks of different frequencies such as 128, 256, 512, 1024, 2048 and 4096 Hz, but for routine clinical practice, a tuning fork of 512 Hz is ideal.
(a) Rinne Test
In this test, air conduction (AC) of the ear is compared with its bone conduction (BC). A vibrating tuning fork is placed on the patient’s mastoid; when the patient stops hearing it, the fork is brought beside the meatus. If he still hears, AC is greater than BC.
Rinne test is positive when AC > BC — seen in normal persons or those with sensorineural deafness.
Rinne test is negative when BC > AC — seen in conductive deafness. A negative Rinne indicates a minimum air-bone gap of 15–20 dB.
Prediction of air-bone gap:
• Rinne equal/negative at 256 Hz but positive at 512 Hz → AB gap 20–30 dB.
• Rinne negative at 256 & 512 Hz but positive at 1024 Hz → AB gap 30–45 dB.
• Rinne negative at 256, 512 & 1024 Hz → AB gap 45–60 dB.
Negative Rinne at 256, 512 and 1024 Hz corresponds to minimum AB gaps of 15, 30 and 45 dB respectively.
False Negative Rinne
Occurs in severe unilateral sensorineural loss. Patient responds to BC, but actually hears through the opposite ear due to transcranial transmission. Masking the opposite ear prevents this. Weber test helps confirm.
(b) Weber Test
A vibrating tuning fork is placed on the midline (forehead or vertex). The patient reports where the sound is heard.
• Lateralizes to worse ear → conductive deafness.
• Lateralizes to better ear → sensorineural deafness.
Lateralization with 512 Hz indicates 15–25 dB conductive loss in same ear or sensorineural loss in opposite ear.
(c) Absolute Bone Conduction (ABC) Test
Compares patient’s BC with examiner’s BC (examiner must have normal hearing). Both meatuses must be occluded.
• Conductive loss → patient & examiner hear for same duration.
• Sensorineural loss → patient hears for shorter duration.
(d) Schwabach’s Test
Similar to ABC test but without occluding the meatus. Interpretation is the same.
• Reduced in sensorineural loss.
• Lengthened in conductive loss.
(e) Bing Test
Assesses effect of occluding the ear canal on BC.
• Normal or sensorineural loss → louder when canal occluded (Bing positive).
• Conductive loss → no change (Bing negative).
(f) Gelle’s Test
Assesses effect of increasing air pressure in ear canal on BC (using Siegel’s speculum).
• Normal or sensorineural loss → decreased hearing (Gelle positive).
• Ossicular fixation/discontinuity (e.g., otosclerosis) → no change (Gelle negative).
Previously used to detect stapes fixation; now replaced by tympanometry.
Q.10 RHINOSCLEROMA
+Rhinoscleroma
It is a chronic granulomatous disease caused by Gram-negative bacillus Klebsiella rhinoscleromatis or Frisch bacillus. The disease is endemic in several parts of the world and is more common in northern India.
Pathology
The disease starts in the nose and may extend to the nasopharynx, oropharynx, larynx (commonly subglottic region), trachea and bronchi. Mode of infection is unknown. It can affect both sexes at any age.
Clinical Features
The disease progresses through three stages:
(a) Atrophic stage. Resembles atrophic rhinitis. Characterized by foul-smelling purulent nasal discharge and crusting.
(b) Granulomatous stage. Granulomatous nodules develop in the nasal mucosa. Subdermal infiltration of the lower external nose and upper lip gives a “woody” feeling. Nodules are painless and do not ulcerate.
(c) Cicatricial stage. Leads to stenosis of nares, distortion of the upper lip, and adhesions in the nose, nasopharynx and oropharynx. Subglottic stenosis may develop, causing respiratory distress.
Diagnosis
Biopsy reveals infiltration of submucosa with plasma cells, lymphocytes, eosinophils, Mikulicz cells and Russell bodies, which are diagnostic.
Mikulicz cells: large foam cells with central nucleus and vacuolated cytoplasm containing bacilli.
Russell bodies: eosinophilic inclusion bodies in plasma cells, representing accumulated immunoglobulins.
The causative organism can be cultured from biopsy material.
Treatment
Streptomycin (1 g/day) and tetracycline (2 g/day) are given together for 4–6 weeks and repeated after one month if required. Therapy continues until two consecutive biopsy cultures become negative. Steroids may be used to reduce fibrosis.
Surgery may be required to secure the airway or correct nasal deformity.
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