ENT (Viva Answer Sheet)

ENT (Viva) – 4th &5TH Year Mohammad Shariful Alam (Shohan) Session: 2003-04 Shahabuddin Medical College & Hospital

Name ______________________________________________________________ Roll _______________ Batch ________________ Session __________________ College _____________________________________________________________

Mohammad Shariful Alam (Shohan) EAR

Q. Type of hearing loss in otitis media with effusion (OME). Medical management of acute otitis media. What is myringtomy?

Ans. OME is the commonest cause of non-suppurative conductive deafness in children. Causes of effusion: A. Middle ear: 1. Malfunctioning of Eustachian tube: (a) Adenoid hyperplasia (b) Chronic rhinitis and sinusitis (c) Chronic tonsillitis (d) Benign and malignant tumours of nasopharynx. (e) Palatal defects, e.g. cleft palate, palatal paralysis. 2. Allergy: Allergic oedema of middle ear cleft and subsequent effusion. 3. Unresolved acute otitis media: Inadequate antibiotic therapy stimulates mucosa to secret more fluid. The number of goblet cells and mucous glands also increase. 4. Viral infections: Various adeno- and rhino- viruses may cause middle ear effusion. 5. Immunological disorder of middle ear mucosa 6. Disturbance in muco-cilliary transport in middle ear 7. Barotraumas B. Inner ear:  Otitic labyrinthitis: When inner ear is infected from middle ear infection (diffuse purulent or serous labyrinthitis). 

Infective labyrinthitis: From meningeal or haematogenous route (e.g., by Salmonella typhi & Salmonella paratyphi)



Viral labyrinthitis: Following viral infections, such as measles, mumps, and influenza. (Severe and permanent seonsori-neural deafness).

The aims of treatment are: (a) (b) (c) (d)

To control infection of the middle ear cleft. To give symptomatic relief. To ensure patency of Eustachian tube for drainage and ventilation. To ensure complete resolution and full return of auditory functions.

Medical treatment of acute otitis media: 1. Bed rest and drink plenty of fluid. 2. Application of dry heat helps to relieve pain. 3. Analgesics to relieve earache e.g., Ibuprofen, Paracetamol or Nimusulide tablet. 2

Mohammad Shariful Alam (Shohan)

4. Systemic antibiotics to control of infection e.g., Amoxycillin, Tetracycline, Roxythromycin, Cephalexin, Co-trimazole etc. 5. Nasal decongestant to maintain patency of the Eustachian tube by 1% ephedrine in normal saline or decongestive nasal drop (e.g., Oxymetazoline), and antihistaminic tablet 6. Sedatives. Myringotomy: It is incision of the tympanic membrane with the purpose to drain suppurative or nonsuppurative effusion of the middle ear or to provide aeration in case of malfunctioning Eustachian tube. *For curiosity: Antibacterial agents and their dosage in acute otitis media Drug

Trade name

Total daily dose

Divided dose

Amoxicillin

Fimoxyl Moxacil

40 mg/kg

3

Ampicillin

Amblosin

50-100 mg/kg

4

Co-amoxiclav

Fimoxiclav Moxaclav

40 mg/kg

2-3

Erythromycin

Eromycin Etrocin

30-50 mg/kg

4

Cefaclor (II generation)

Ceflon Loracef

20mg/kg

2-3

Cefixime (III generation)

Cef-3 Triocim

8mg/kg

1 or 2

Cefpodoxime proxetil

Starin Taxetil

10mg/kg (max 400 mg/day)

2

(?)

9 mg/kg

1

Cotrim Fisat

8 mg (TMP) + 40 mg (SMZ)/kg

2

Ceftibuten (III generation) Co-trimoxazol (Trimethoprim + Sulphamethoxazole)

Q. 5 pathology of external ear causing conductive deafness.

Ans. External ear pathology causing conductive deafness are1. Congenital:  Atresia  Microtia  Treacher-Collins syndrome 2. Impacted wax or cerumen 3. Impacted foreign body 4. Otitis externa:  Diffuse otitis externa (when the auditory canal is obstructed)  Otomycosis (when mycotic plug is formed) 5. Neoplasm: (i) Benign - Osteoma, chondroma, exostosis. (ii) Malignant - Osteosarcoma, chondrosarcoma.

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Q. Sudden pain in the ear of a child after upper respiratory tract infections. What is your diagnosis? How you diagnosed?

Ans. Child is suffering from acute suppurative otitis media, its clinical features are1. Stage of tubal occlusion: Symptoms: i) Acute coryza ii) Mild earache iii) Fullness in the ear iv) Mild conductive deafness Signs: i) Tympanic membrane retracted & lusterless. 2. Stage of exudation or pre-suppuration: Symptoms: i) Severe earache (sharp & stabbing) ii) Deafness increases iii) Bubbling sound (due to serous exudates) iv) General illness: Rise of temperature, Malaise, Vomiting. Signs: i)

Tympanic membrane: Red & congested, dilated vessels radiating from the handle of the malleus gives Cart-wheel appearance.

3. Stage of suppuration: Pre-perforation: Symptoms: i) Pain is more acute (throbbing) ii) Deafness is more marked iii) High rise of temperature (101˚ - 103˚F) Signs: i) Bulged, congested & yellow spot on the tympanic membrane ii) Mastoid tenderness Perforation: Symptoms: i) ii) iii) iv)

Otorrhoea (pus or mucopus or may be blood stained) Pain diminishes Temperature comes down Conductive deafness is more marked

Signs: i) Perforation on the tympanic membrane ii) Pulsating discharge reflect light intermittently called “Light-house sign” iii) Mastoid tenderness disappears

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4. Stage of resolution: i) In early cases or in mild infection: Resolution occurs without perforation ii) In cases of perforation: Discharge subsides and perforation heals up or dry small perforation is left behind 5. State of complication: i) Persistence of otorrhoea & deafness ii) Vertigo & headache iii) Increase temperature iv) Facial paralysis. Q. Clinical features of otosclerosis. Treatment of otosclerosis.

Ans. Clinical features of otosclerosis: Symptoms: 1. Painless, progressive and bilateral hearing loss usually begins between the ages of 11-30. 2. Tinnitus due to high vascularity of spongiosum. 3. Paracusis willisii – the ability to hear better in noisy surroundings as people talk louder in noisy place. 4. Patients have a monotonous, well modulated soft speech. 5. Occasional vertigo or giddiness. Sign: 1. Otoscopy reveals - tympanic membrane is quite normal and mobile. - Flamingo‟s tint or positive Schwartze‟s sign. 2. Eustachian tube function is normal. 3. Tuning fork test: (a) Rinne is negative on both sides and Weber will be lateralized to the more deaf ear (conductive type o deafness) (b)Gelle‟s test is negative. Treatment: Though there are no medications that have been shown to work, the followings are the treatment optionsa) Conservative treatment: 1. Regular observation 2. When there is active stage or positive flamingo flash – Na fluoride 50-75 mg/day for 2 years. Then 25 mg/day for whole life. 3. Hearing aid –when operation is contraindicated or patient is not agreeable to operation. Hearing aids are effective for conductive hearing loss. b) Surgical treatment: 1. Stapedectomy under general anaesthesia is the most modern operation. 2. Other surgical procedures Fenestration operation  Stapes mobilisation  Small fensetra stapedotomy. 5


Q. What are the ototoxic drugs? Mention five.

Ans. Ototoxic drugs are1) Aminoglycoside antibiotics:  Streptomycin & gentamycin  mainly vestibulotoxic,  Neomycin, kanamycin, vancomycin & tobramycin  mainly cochleotoxic. 2) Diuretics: Ethacrynic acid, frusemide, etc. 3) Anti-malarial drug: Quinine, Chloroquine, etc. 4) NSAID: Salicylate, Aspirin, etc. 5) Tobacco and alcohol. Q. Treatment of furunculosis in ear.

Ans. Treatment: 1. The meatus is packed with wick soaked in 10% icthammol in glycerin or smeared with neomycin-steroid ointment. - Wick acts as a splint and prevents movement of cartilaginous part. It also relieves the tension of the furuncle into the canal by counter pressure and thereby relieves pain. - Icthammol is bacteriostatic and irritant. - Glycerin is hygroscopic and reduces oedema. The ribbon-gauze wick should be removed after 48 hours. Repacking may be necessary, if tenderness persists. 2. If furunculosis burst, canal should be cleaned and packed with gauze soaked in antibiotics and kept for 24 hours. 3. Analgesic is administered to reduce the pain. 4. Use of heat in the form of fomentation is soothing. 5. Systemic antibiotic e.g., Erythromycin, roxythromycin, cephalexin, or TrimethoprimSulphonamide group of drug, is administered in severe case or when there is spreading cullulitis. 6. Incision of furuncle is necessary if large boil and pus pointing. 7. In recurrent furunculosis, diabetes should be excluded and treatment should be done accordingly, if present. 8. If the patient is non-diabetic (with recurrent furunculosis), then ear swab culture is performed and a course of autovaccine should be considered. 9. Any other causative factor or focal sepsis should be looked into. Q. 5 pathologies of middle ear causing conductive deafness.

Ans. Middle ear pathology causing conductive deafness are1. Congenital: o Ossicular chain deformity o Fused ossicles 6


o Incudo-stapedial joint separation o Congenital otosclerosis 2. Traumatic o Haematomas o Ossicular dislocation 3. Inflammatory o Acute : ASOM o Chronic: - Non-specific: CSOM, Adhesive otitis media, secondary otitis media - Specific: Tubercular and syphilitic. 4. Neoplastic o Glomus jugularae o Carcinoma. Q. What are the causes of discharging ear?

Ans. Causes of discharging ear areA. Causes in the external ear: (a) Inflammatory: i. Bacterial inection- mainly by Staph. Aureus, Streptococcus, Haemophillus, Pseudomonas, Proteus  Localized otitis externa due to burst of furuncle (purulent discharge)  Diffuse otitis externa due to diseases like DM & the condition is called Otitis Externa Malignance characterized by perichondritis and formation of pus. ii. Fungal disease (Otomycosis)- Caused by  Aspergillus nigra → black discharge  Candida albicans → white discharge iii. Viral inflammation- Caused by Herpetic virus  Myringitis bullosa blood stained discharge  Herpes zoster oticus (due to blood vessel rupture) (b) Neoplastic:  Benign – osteoma, exostosis.  Malignant - squamous cell carcinoma, basal cell carcinoma. (malignant) (c) Impacted wax or foreign body in the ear. B. Causes in the middle ear: (i) Acute suppurative otitis media with perforation (ii) Chronic suppurative otitis media -

Discharge is thin mucoid or mucopurulent in safe variety Discharge is purulent in unsafe variety & CSOM with complication Discharge is blood stained in CSOM with infected polyp or granulation tissue Characteristics of discharge:  Foul smelling: in conditions like cholesteatoma, infection with gram negative organism (e.g., Pseudomonas, Proteus) → fishy smell.  Non foul smelling

(iii) Tympanic membrane perforation 7


(iv) Middle ear malignancy (e.g., carcinoma, glomus tumours, haemangioma etc.) (v) Following RTA, in secondary infection → blood stained discharge. C. Middle cranial fossa: C.S.F. otorrhoeaHead injury with temporal bone fracture Congenital defect Cholesteatoma Malignancy. Q. Intratemporal complications o CSOM. Intracranial complications of CSOM.

Ans. Complications of otitis media are classified into two main groups: Extra-cranial / Intratemporal Mastoiditis (*) Petrositis, (*) and Gradenigo‟s syndrome Facial paralysis (*) Labyrinthitis (*) Subperiosteal abscess: (a) Post-auricular (b) Zygomatic & Luc‟s (c) Bezold‟s abscess (d) Pharyngeal abscess (e) Citelli‟s abscess Osteomyelitis of the temporal bone Blood stream infection: Septicemia and pyemia Otogenic tetanus

1. 2. 3. 4. 5.

6. 7. 8.

1. 2. 3. 4.

5. 6. 7. 8.

Intracranial Extradural abscess Subdural abscess Meningitis (*) Brain abscess (a) Temporal lobe (b) Cerebellar abscess (*) Lateral sinus thrombophlebitis (*) Otitic hydrocephalus Peri-sinus abscess Encephalitis (*).

Q. Types of mastoidectomy. Indication of cortical mastoidectomy. Ans. Types of mastoidectomy: I. II. III. IV. V.

Cortical mastoidectomy* Radical mastoidectomy* Modified radical mastoidectomy* Mastoidectomy with cavity obliteration Canal-down & Canal-up technique in mastoidectomy.

Indication of cortical mastoidectomy: 1. 2. 3. 4. 5.

Acute mastoiditis where there is coalescence of the mastoid air-cells. Masked mastoiditis. Unresolved acute otitis media with persistent otorrhoea. In some cases of persistent or recurrent secretory otitis media. As an imitial step to perform: (a) Endolymphatic sac surgery (b) Decompression of facial nerve (c) Translabyrinthine or retro-labyrinthine procedures for acuostic neuroma.

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Q. 5 causes of sensory-neural deafness.

Ans. Causes of sensory neural deafness areCongenital or prenatal deafness (a) Hereditary group (Genetic):  Pendred syndrome  Waardenburg‟s syndrome  Klippel Fiel syndrome (b) Pregnancy group:  Rubella  Rh-factor  Congenital syphilis  Severe viral infection of the mother (c) Birth group or prenatal group:  Prolonged labour  Anoxia or hypoxia  Premature birth  Birth trauma  Phenylketonuria

Acquired or post-natal deafness I. Cause in cochlea or inner ear: i. Traumatic:  Fracture temporal bone (*)  Head injury  Blast injury (*) ii. Operative:  Post-stapedectomy (*)  Labyrynthectomy iii. Infective:  Bacterial: Labyrinthitis (*)  Viral: Measles, mumps, influenza, pox, etc. iv. Vascular:  Spasm  Thrombosis v. Toxic:  Streptomycin, quinine, gentamycin, and other ototoxic drugs. (*) vi. Degenerative:  Senile deafness or presbyacusis vii. Noise induced:  Acute noise trauma  Chronic noise trauma viii. Miscellaneous:  Diabetes  Meniere‟s disease (*)  Ramsay Hunt syndrome II. Causes in internal auditory canal and C.P. angle: i. Acuostic neuroma (*) ii. Meningioma iii. Cholesteatoma iv. Tuberculoma v. Basal meningitis III. Cause in central nervous system:  Dessiminated sclerosis  Vascular accidents  Tumours

Q. What is prebyacusis? Treatment of presbyacusis.

Ans. Presbyacusis (senile deafness): The term presbycusis refers to sensorineural hearing impairment associated with physiological aging process in the ear particularly after 60 years is called presbyacusis. 9


Characteristically, presbycusis involves bilateral high-frequency hearing loss associated with difficulty in speech discrimination and central auditory processing of information. Here degenerative process usually affects organ of Corti, spiral ganglion or stria vascularis. Treatment: Presbycusis is not curable, but the effects of the disease on patients‟ lives can be mitigated.  General nutrition should be improved including administration of Vit. B1, B6, and B12.  Amplification devices: Properly fitted hearing aids may contribute to the rehabilitation of a patient with presbycusis.  Lip reading and auditory training  Cochlear implants  Curtailment of smoking and stimulants like tea and coffee may help to decrease tinnitus. Q. What is deafness? What are the types of deafness?

Ans. Deafness: Partial or complete loss of hearing is called deafness. Types: 1. 2. 3. 4.

Conductive deafness Sensory-neural deafness Mixed Psychogenic deafness.

Q. What is cholesteatoma? Clinical presentation of cholesteatoma.

Ans. Cholesteatoma: The term cholesteatoma is a misnomer, because it neither contains cholesterol crystals nor is it a tumour to merit the suffix “oma”. *This is a sack or a pocket in the middle ear cleft lined by keratinized squamous epithelium and contains desquamated concentric sheets of keratin (and cholesterol crystals), usually associated with infections. In other words cholesteatoma is a “skin in the wrong place”. Essentially choesteatoma 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. Formation: 1. Congenital cholesteatoma: It arises from the embryonic epidermal cell and rests in th middle ear cleft or temporal bone. 2. Primary acquired cholesteatoma:  Retraction pocket theory (most accepted theory): 10


Auditory tube dysfunction/obstruction ↓ Hypoventilation of middle ear cleft & epitympanum ↓ Negative pressure of middle ear cavity produces pocket like depression in pars flaccid or posterosuperior region of pars tensa ↓ The pocket turns into pouch ↓ Self cleansing property of squamous epithelium is lost ↓ So, there is collection of sheets of squamous epithelium in concentric layers in the sac with formation of a tumour like mass called cholesteatoma. 3. Secondary acquired cholesteatoma: a. Migration theory: After perforation squamous cells migrate to the middle ear cavity & break into crystal keratin materials. b. Metaplastic theory: Chronic tonsillitis, adenoid ↓ Infection passes into middle ear cavity & break into crystal materials ↓ Inadequate treatment causes persistence of infection for years ↓ So, squamous cell metaplasia & shedding of cells are broken down to form cholesteatoma c. Implantation theory: Implantation of squamous epithelium from skin pedicle or remnant under the graft may lead to cholesteatoma formation. Q. What is tympanoplasty?

Ans. Tympanoplasty: A tympanoplasty is a surgical procedure that repairs or reconstructs the eardrum (tympanic membrane) to help restore normal hearing. This procedure may also involve repair or reconstruction of the small bones behind the tympanic membrane (ossiculoplasty) if needed. This procedure is usually not performed (or needed) in children under of age. A tympanoplasty is recommended when the eardrum is torn (perforated), (atelectatic), or otherwise abnormal and associated with hearing loss. Abnormalities drum and middle ear bones can occur through injury, otitis media, congenital deformities, or chronic ear conditions such as a cholesteatoma.

four years sunken in of the ear (at birth)

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Q. Causes of pain in ear (otalgia).

Ans. Local causes A. External ear  Furuncle  Perichondritis  Otitis externa  Impacted wax & FB  Herpetic lesions including bullous myringitis  Traumatic rupture of TM & myringitis  Malignant growth B. Middle ear  Acute otitis media  Acute salpingitis  Acute mastoiditis  Barotraumatic otitis media  Haemotympanum  Unsafe variety of CSOM with threatening complications  Malignant growth

Referred causes 1. Via Vth cranial nerve (a) Dental:  Caries tooth  Apical abscess  Impacted molar  Malocclusion (b) Oral cavity:  Benign or malignant ulcerative lesions of oral cavity or tongue (c) Temperomandibular joint disorder:  Bruxism  Osteoarthritis  Recurrent dislocation  Ill-fitting denture (d) Sphenopalatine neuralgia. 2. Via IXth cranial nerve (a) Oropharynx:  Acute tonsillitis  Peritonsillar abscess  Tonsillectomy  Benign or malignant ulcer of soft palate, tonsil and its pillars (b) Base of tongue:  Tuberculosis or malignancy (c) Elongated styloid process. 3. Via Xth cranial nerve  Malignancy or ulcerative lesion of- Vallecula - Epiglottis - Larynx or laryngopharynx - Oesophagus 4. Via C2 and C3 spinal nerves  Cervical spondylosis  Injuries to cervical spine  Caries spine

Q. Treatment of traumatic perforation of ear drums.

Ans. Treatment: 1. Immediate treatment: Should be conservative & preventive. Majority cases heal with this treatment alone:  Sterile cotton wool is applied at the external meatus. It is to be changed if soaked.  No ear drop should be given & syringing of the ear should be avoided.  Swimming & bathing in ponds or pools should be avoided.

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  

If there is chance of infection in traumatic perforation, then administer systemic antibiotic, either orally or perenterally in proper dose and duration. If associated with cold, then nasal decongestant and antihistaminic tablets are to be used. Application of trichlor-acetic acid or silver nitrate at the margin of perforation may help the healing process.

In majority of cases, healing of the TM occurs by epithelialization. 2. If patient attends late with purulent discharge following a perforation, then the case is to be treated like a case of ASOM with perforation. 3. If no healing within 3 to 6 months, myringoplasty operation is to be performed. In this operation, TM is repaired with temporal fascia. Q. Name qualitative hearing test (clinical test).

Ans. Qualitative hearing tests are1) Tuning fork test Rinne test  Weber test  Absolute Bone-Conduction 2) Impedance audiometry/Tympanometry 3) Stapedeal reflex test (SRT) 4) Vestbulo-cochleography. Q. Causes of tympanic membrane perforation.

Ans. Causes of tympanic membrane perforation are1. 2. 3. 4. 5. 6.

While picking the ear with matchstick, pencil, hair-pins, etc. Foreign body trauma or trauma during removal of F.B. Sudden fluid compression or water jet: Syringing, water polo game, diving, etc. Air compression: Slapping, blast, barotraumas. Forceful inflation of Eustachian tube Indirect way: By head injury and fracture of the petrous temporal bone.

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Mohammad Shariful Alam (Shohan) NOSE

Q. Nasal septoplasty/SMR – which one is functionally better? Complications of nasal septal surgery.

Ans. Septoplasty is functionally better because Conservation form of surgery to correct deviation with minimum resection of cartilage and repositioning in midline.  Most suitable in children and adolescence as it does not interfere with growth of the nose.  It is also preferred in females to avoid cosmetic deformity of nose.  Flappy Septum – never occurs.  Haematoma septum – does not occur.

Complications of nasal septal surgery are1. Septal perforation and crusting due to injury and tearing of the muco-periosteal flap of the intact side. 2. Haemorrhage 3. Septal haematoma 4. Septal abscess 5. Depression of the bridge of the nose 6. Retraction of columella 7. Persistance of deviation 8. Synechia between septum and turbinates 9. Flapping of the septum 10. Meningitis 11. Toxic shock syndrome

Q. Symptom and management of allergic rhinitis.

Ans. Symptoms: (1) (2) (3) (4) (5) (6)

Paroxysmal sneezing followed by watery nasal discharge Nasal obstruction Nasal irritation Anosmia Heaviness of head & headache Irritation and congestion of eyes, respiratory distress, and broncho-spasm.

Management: A. Prophylactic: (a) Avoidance of allergen (b) A course of desensitizing vaccine based on result of skin sensitivity test. (c) Hyposensitisation by vaccine (d) Immuno-therapy by gamma-globulin or immunoglobulin injection.

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B. Curative management: 1. Oral antihistamines: e.g., Pheniramine Terfanadine, Loratidine, Fexofenadine etc.

maleate,

Promethazine,

Cetrizine,

2. Symapthomimetic drugs: Topical use of sympathomymetic drugs cause nasal decongestion e.g., Phenylephrine, Oxymetazoline, Xylometazoline etc. 3. Steroid: Can be used as spray (e.g., Beclomethasone, Fluticasone) or as submucosal injection. 4. Sodium chromoglycate as nasal spray. 5. General body nutrition is to be improved. Vitamin C and B-complex is to be administered. Bowel is to be kept regular. C. Surgical management: (a) Minor surgery: Reduction of nasal turbinate‟s (inferior): (i) Surface electro-cautery (ii) Submucosal diathermy (S.M.D) (b) Other nasal surgery: (i) Submucosal resection (S.M.R) (ii) Fiber-optic endoscopic sinus surgery (FESS). Q. Epistaxis in a child of 3/4 years - cause and management.

Ans. Cause: In children commonest cause is epistaxis from Little‟s area either spontaneous or due to1. 2. 3. 4. 5. 6.

Picking of the nose Injury to the nose Exanthematous fever (e.g., measles, pox) Foreign body nose Diphtheric rhinitis Enlarged adenoids, etc.

Management: 1. Pinching of nose for 10-15 minutes, as pressure on nostril from outside compresses the vessels on the Little‟s area and stops bleeding. 2. Traumatic bleeding is often controlled by application of ice on bridge of the nose which causes reflex vaso-constriction. 3. In cases of persistent bleeding, the blood is sucked out including clots with suction machine under direct vision and spraying the nose with 4% xylocane. - If the actual bleeding point is found out, may be cauterized by chemical or electrocautery under G/A. - If bleeding point cannot be seen, then thick cotton wool pledget soaked in 4% Xylocaine solution should be inserted into the nasal cavity and it is removed after several minutes.

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Q. Causes of nasal obstruction with epistaxis.

Ans. Causes of nasal obstruction with epistaxis areInfected antro-choanal polyp Foreign body nose and rhinolith Rhinosporidiosis Diphtheric rhinitis DNS with acute rhino-sinusitis Back pressure from enlarged adenoid Juvenile nasopharyngeal angiofibroma Haemangioma Papilloma Carcinoma of nose, paranasal sinuses and nasopharynx Malignant garnuloma Q. Procedure of antral wash out.

Ans. Procedure of antral wash out/proof puncture/antral irrigation: 

Instruments & reagents: 1. Thudicum‟s nasal speculam 2. Lichtwitz antrum-punture trocar and cannula 3. Higgison‟s syringe or 50 cc syringe 4. A collecting kidney tray 5. Sterile normal saline or sterile water (at body temperature) 6. Tille‟s forceps or nasal dressing forceps 7. Cotton balls 8. Head light with mirror



Informed written consent of the patient



Steps of operation: 1. Anaesthesia - In adult local anaesthesia is preferred - In children & frightened patient general anaesthesia is required 2. Area of middle meatus should be decongested to open the maxillary ostium for easy return of fluid. 3. Position - Sitting position is preferred in all adults, when using local anaesthesia - When using general anaesthesia, patient is placed in tonsillectomy position 4. With the help of the nasal speculum, the Lichwitz trocar and cannula is introduced into the lateral wall of the inferior meatus at a point 1.5 – 2.0 cm from anterior end of inferior turbinate and near the attachment of concha with lateral wall. 5. The trocar is directed towards the outer canthus or rather zygoma with butt of the trocar in the palm of the hand. 6. The medial wall of the sinus is punctured and sense of entering cavity is felt by the surgeon. 16


7. The index finger acts as a guard to prevent double puncture. 8. The trocar is removed and cannula is advanced till it reaches the opposite antral wall and then withdrawn a little. 9. Now saline or sterile water is passed to the antrum by Higgison‟s syringe. 10. Syringing is continued until the return is clear. 11. The remaining water in the antrum is cleared out by withdrawing the syringe from saline and pumping-out air. 12. After the puncture is over, cannula is removed and a pack kept in the inferior turbinate to control bleeding. 13. Swab from antral pus may be taken for culture and sensitivity. Q.Types of nasal ployp. Difference between 2 types.

Ans. Nasal polyps are non-neoplastic pedunculated masses of hypertrophied oedematous nasal or sinus mucosa composed of loose fibro-oedematous tissue lined by ciliated columner epithelium. Types of nasal polyp: Nasal polyps are classified into 3 categories1. Simple mucous polyp: (commonest variety) (i) Antro-choanal polyp (ii) Bilateral ethmoidal polypi. 2. Fungal polyps 3. Neoplastic polyps: (i) Benign tumors such as papilloma, hemangioma, fibroma, inverted papilloma etc. may present as a polyp. (ii) Malignant tumours may present as solid polypoid mass, either of ethmoid or maxillary sinus origin or inverted papilloma with malignant change. Difference between Antrochoanal polypi and Ethmoidal polypi: Traits 1. Age 2. Aetiology 3. Number 4. Laterality 5. Origin

Antrochoanal Polyp Common in children and adolescents. Mainly allergic in origin; may be infective also. Solitary Unilateral Maxillary antrum near the ostium.

Grows backwards to the choana and best seen in P.N.S. by posterior rhinoscopy. May extend into the nasopharynx and 7. Extension oropharynx. Trilobed with antral, nasal and 8. Size & shape choanal parts. 9. X-ray of the sinuses Shows unilateral opacity of the maxillary antrum. 6. Growth

Ethmoidal Polyp Common in adults. Allergy or multifactorial Multiple Bilateral Arise from anterior, middle and posterior group of ethmoid cells. Grows forwards and best seen in A.N.S. by anterior rhinoscopy. No. Usually small and grape-like masses. Shows bilateral antral haziness and ethmoid cells are also hazy. 17


10. Treatment 11. Recurrence

Polypectomy; endoscopic removal or Caldwell-Luc operation if recurrent. Uncommon, if removed completely.

Endoscopic surgery or ethmoidectomy. Common.

Q. Treatment of chronic maxillary sinusitis.

Ans. Treatment: a. Conservative treatment: 1. Aggravating factors such as dust, smoke, alcohol and tobacco should be avoided. 2. Nutritious diet & Vit. C is helpful. 3. Dental sepsis is to be controlled. 4. Nasal decongestants and antihistamines to control allergy. 5. Steam inhalation helps to loosen mucoid secretion. 6. Broad spectrum antibiotic therapy e.g., with Cephalexin, amoxycillin with clavulanic acid, azythromycin, doxycycline. 7. Steroid nasal spray is helpful to reduce oedematous turbinate‟s and clearing ostiometal complex. b. Surgical treatment: 1. Eradication of sinus: a) Bilateral antral wash out b) Intra-nasal antrostomy or endoscopic maxillary antrostomy c) Caldwell-Luc operation d) Trephnine of frontal sinuses 2. Functional endoscopic sinus surgery (FESS) 3. Removal of associated cause e.g. DNS, polyp, HIT etc.

Q. What is FESS? Ans. FESS: Functional Endoscopic Sinus Surgery (FESS) is a term coined by an American ENT Surgeon, Dr David Kennedy in 1985 to describe the diagnosis and treatment of diseases of the nose and paranasal sinuses using endoscopes and CT scans. *FESS helps to maintain normal physiology, cilliary activity and drainage of the sinuses, thereby clears sinus pathology.ostio-meatal complex area is cleared of all obstructive pathology – mainly polypoid mucosa. Anterior end of polypoid middle turbinate is excised, uncinate process is trimmed, osteii of paranasal sinuses are freed from obstruction and helping proper drainage of sinuses. FESS is not one operation, but rather a range of diagnostic and treatment procedures carried out with the help of rigid nasal endoscopes.

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Q. Causes of nasal septum perforation.

Ans. Causes of nasal septum perforation are1. Traumatic perforation:  Following septal surgery  Repeated cautery  Habitual nose picking  To put ornaments 2. Pathological perforation: (a) Delayed drainage of septal abscess (b) Nasal myiasis (c) Rhinolith or neglected foreign body causing pressure necrosis (d) Chronic grnaulomatous condition  Catilagenous part – lupus, tuberculosis, leprosy  Bony part – syphilis (e) Wegener‟s granuloma 3. Chrome perforation (chemical): is an occupational hazard. 4. Idiopathic: No definite cause found. Q. Causes of unilateral nasal obstruction.

Ans. Causes of unilateral nasal obstruction areVestibule Furuncle Vestibulitis Stenosis of nares Atresia Nasoalveolar cyst Papilloma Squamous cell carcinoma Nasal cavity Foreign body DNS Hypertrophic inferior turbinate Concha bullosa Antro-choanal polyp Synechia Rhinolith Bleeding polypus of septum Benign and malignant tumours of nose and paranasal sinuses Sinusitis, unilateral Nasopharynx Unilateral choanal atresia

19


Q. What are complications of sinusitis?

Ans. Complications of sinusitis: a. Local spread of infection: 1. Cellulitis over sinuses 2. Abscess formation 3. Orbital cellulitis 4. Cellulitis of eyelid 5. Osteomyelitis. b. Distant spread of infection: 1. Pharyngeal infection 2. Laryngeal infection 3. Chronic suppurative otitis media (CSOM) 4. Dental sepsis 5. Intracranial :  Meningitis  Cavernous sinus thrombosis  Brain abscess  Extradural abscess.

THROAT

Q. Sign symptom and management of peritonsillar abscess.

Ans. Clinical features: Symptoms:  Local: i. Severe pain in the throat (usually unilateral) ii. Odynophagia iii. Muffled and thick speech iv. Foul breath v. Ipsilateral earache vi. Dribbling of saliva and mild trismus  General: i. Patient looks ill and anxious ii. High rise of temperature (103˚ - 104˚) iii. General malaise iv. Body aches v. Headache vi. Nausea vii. Constipation 20


Signs: 1. Buccal mucosa is dirty and foetor may be present. 2. There is marked congestion, bulging and oedema of the tonsilar, peritonsilar and palatal region on the affected site. 3. A diffuse swelling of the soft palate just superior to the involved tonsil is seen displacing the uvula medially. 4. In more advanced cases, there may be an area of pus pointing underneath the thin mucosa. 5. Tonsillar glands are enlarged and tender on the affected side. 6. If untreated, abscess may burst into pharynx, often through crypta magna. Treatment: a. Hospitalization b. Conservative treatment: In the early stages when no distinct abscess is pointingI. Intravenous fluids to combat dehydration II. Intravenous broad-spectrum antibiotics III. Analgesics like paracetamol, pethidine. IV. Maintenance of oral hygiene by hydrogen per-oxide or saline mouth washes. c. Surgical treatment: If there is frank abscess formationI. Incision and drainage of abscess under local anaesthesia, pt. in upright sitting position. 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 base of the uvula. II. Interval tonsillectomy: The tonsils are removed four to six weeks following an attack of quinsy. Abscess or hot tonsillectomy: It has the risk of rupture of the abscess during anaesthesia, and excessive bleeding at the time of operation. Q. Post-operative care immediately after tonsillectomy.

Ans. Postoperative care:  

  

  

Normal unaided respiration should be established before the patient leaves the operation theatre. The patient is placed in tonsil position until fully recovered from anesthesia which allows free respiration and permits any blood and secretions, which may collect, to run out of the nose and mouth. A strict watch should be kept on the pulse, respiration and blood pressure of the patient. A rising pulse indicates hemorrhage. Nothing is given orally for first 3/4 hours, and then liquid feed is allowed. Cold drinks (e.g. cold milk, ice cream or ice cubes) and soft diets are prescribed for the initial few days. Diet is gradually built from soft to solid food. Plenty of fluid should be encouraged. Analgesics are given for pain. Antiseptic mouth washes to keep the mouth clean. A suitable antibiotic can be given orally or by injection for a week. 21


Q. Causes of dysphagia.

Ans. Causes of dysphagia areA. Mechanical causes: 1. Oral causes:  Lock-jaw  Stomatitis, glossitis and angular stomatitis  Submandibular sialo-adenitis  Impacted molar, and other dental lesions  Inflammation of the floor of the mouth  Malignant growth of the tongue, ulcer tongue, etc.  Tumors of oral cavity, odontogenic tumours, palatal tumours, etc. 2. Pharyngeal and laryngeal causes:  Acute follicular tonsillitis  Peritonsillar abscess  Retro-pharyngeal and para-pharyngeal abscess  Cancer of the pharynx  Oedema larynx  Advanced laryngeal cancer  Foreign body pharynx  Pharyngeal diverticulum  Specific lesion e.g., koch‟s, syphilis etc.  Palatal and pharyngeal paralysis  Agranulocytic angina  Paterson-Brown Kelly syndrome 3. Oesophageal causes: (*) (a) Causes in the lumen:  Foreign bodies such as coins in the children  Meat bones or dentures in adult (b)Causes in the wall:  Congenital atresia and other abnormalities  Corrosive oesophagitis  Peptic oesophagitis (reflux)  Traumatic oesophagitis (operative)  Acquired strictures  Spasm and diverticulum  Cardio-spasm or Achalasia  Benign tumours : e.g., Adenoma or myoma, etc.  Cancer oesophagus  Tracheo-oesophageal fistula  Oesophageal varix  Scleroderma (c) Causes outside the wall:  Retro-sternal goiter and enlarged thymus in infants and young children  Pressure by mediastinal mass  Enlarged heart and aneurysm of the aorta  Bronchogenic carcinoma  Dysphagia lusoria 22


4. Cervical causes: o Enlarged thyroid and malignant thyroid o Metastatic, Hodgkin‟s or other neck node mass o Ludwig‟s angina o Parotitis o Temporo-mandibular arthritis B. Neuro-muscular causes: i. Central lesions causing vagal paralysis ii. Motor neuron disease iii. Peripheral neuritis iv. Jugular-foramen syndrome v. Myasthenia C. Psychological: Globus hystericus Q. 5 common causes of hoarseness of voice. Ans. Causes of hoarseness of voice: 1. Inflammations  Acute: Acute laryngitis, laryngo-tracheo-bronchitis, laryngeal diphtheria  Chronic:  Specific: Tuberculosis, syphilis, scleroma, fungal infections  Non-specific: Chronic laryngitis, atrophic laryngitis. 2. Tumors  Benign: Papilloma, haemangioma, chondroma, fibroma, leukoplakia.  Malignant: Carcinoma.  Tumour-like masses: Vocal nodule, vocal polyp, angiofibroma, amyloid tumour, contact ulcer, cysts, laryngocele. 3. Trauma:  External: Strangulation, injury neck, etc.  Internal: Instrumentation, fumes, operative. 4. Paralysis: Paralysis of recurrent, superior laryngeal or both nerves. 5. Fixation of cords: Arthritis or fixation of cricoarytenoid joints. 6. Congenital:  Laryngeal web, stenosis and atresia  Laryngeal malacia  Laryngeal arrhythmia 7. Miscellenious: Dysphonia plica ventricularis, myxoedema, gout 8. Functional: Hysterical aphonia Q. Causes and management of reactionary hemorrhage after tonsillectomy.

Ans. Reactionary hemorrhage occurs within 24 hours of the operation, but commonly within first 5/6 hours. Bleeding results from – (a) Failure to ligate all bleeding points; (b) Slipping of a loosely tied knot or clot following rise of B.P. after operation; 23


(c) Collapsed vessels opening up in the post-operative period; (d) Bleeding from vessels after relaxation of the stretched faucial tissue and muscle on removal of the mouth gag; (e) Failure of a vessel to contract and retract following crushing; and (f) In cases of local anesthesia, as the effect of adrenaline wears off, the vessels dilate. Management: After tonsillectomy operation in post-operative period when the patient is placed in tonsillar position if blood continuously accumulates in the mouth or dribbles through the mouth or repeated gulping specially in the children indicates reactionary hemorrhage.  I/V channel should be opened and saline infusion should be started.  Patient‟s blood is to be drawn and sent for grouping and cross matching.  A strict watch should be kept on the pulse, respiration and blood pressure of the patient. If features of shock develops than treatment of shock.  Airway is cleaned by giving suction and it is to be ensured that there is no obstruction or hypoxia.  Mouth is opened and tonsillar fossa is inspected. If a bleeding clot is seen, then it has to be removed with a Luc forceps and a piece of gauze soaked in hydrogen-per-oxide or adrenaline is held firmly against the fossa for 10-15 minutes. Usually in many cases bleeding stops by this measure.  If the bleeding persists - call the immediate senior consultant and anesthesiologist and make sure the operation theatre is ready - the patient is to be taken to operation theatre immediately and under G/A, the bleeding is controlled by ligation or electro-cauterization of bleeding vessel - a nasogastric tube is to be introduced before anesthesia and swallowed blood is to be sucked out to prevent aspiration  Blood transfusion is necessary in severe cases.  The patient is then kept under watch and follow-up is given accordingly. Q. Complication after adenoidectomy.

Ans. Complications of adenoidectomy are1. 2. 3. 4.

Haemorrhage : Primary, reactionary, & secondary. Eustachian tube injury and stenosis. Injury to pharyngeal musculature and vertebrae. Otitis media : i. Secretory otitis media ii. Acute otitis media. 5. Velopharyngeal insufficiency. 6. Nasopharyngeal stenosis due to scarring. 7. Incomplete removal and recurrence.

24


Q. What you know about achalasia cardia?

Ans. Achalasia cardia: Achalasia Cardia is a primary oesophageal motility disorder, characterized by a hypertensive lower oesophageal sphincter (LOS) which fails to relax on swallowing, and by aperistalsis of the body of the oesophagus. Incidence: The incidence of the disease is 1-2 per 200,000 per year, with both sexes equally affected. Onset of the disease is typically between the ages of 20 and 50. Aetiology: Exact aetiology is unknown. Some theories are1. Loss of ganglionic cells in the myenteric (Auerbach‟s) plexus 2. Abnormal pinch-cock action of right crus of diaphragm 3. Vagal disturbance 4. Aerophagy 5. Primary dilatation 6. Lack of integrated parasympathetic stimulation and non-propulsive motility in the body of the oesophagus. Pathology:  Marked dilatation of the lower two- third of the oesophagus  Lumen (diameter) 7.5 cm.  Muscular walls are hypertrophied  No hypertrophy of the cardiac sphincter  Histopathology of muscle specimens generally shows a reduction in the number of ganglion cells (and mainly inhibitory neurons) with a variable degree of chronic inflammation. Clinical features: Age- Young person of both sexes. Onset of disease is insidious. Symptoms: 1. Dysphagia – more liquid then solid. 2. Regurgitation of undigested food. 3. Discomfort or pain in the retrosternal or epigastric region. 4. Loss of weight. 5. Fullness after meal in retrosternal or epigastric area. 6. Night time cough. Differential diagnosis: 1. Carcinoma of oesophagus 2. Stricture 3. Hiatus hernia. Investigations: 1. Endoscopic examination shows a tight cardia and food residue in the oesophagus. 25


2. Barium swallow X-ray of the oesophagus shows - It usually shows a "bird‟s beak" narrowing at the GO junction and oesophageal dilatation proximal to the narrowing. - Gastric gas bubble is usually absent 3. Oesophagoscopy shows the dilated oesophagus with smooth narrowing of cardiac end containing undigested food. 4. Oesophageal Manometry :( In this test, a thin tube is passed into the esophagus to measure the pressure exerted by the esophageal sphincter.)

Typical manometrical findings are the absence of oesophageal peristalsis and a hypertensive LOS which fails to relax completely in response to swallowing. Treatment: 1. Medical treatment: Before meal- Nifedipine 2. Botulinum toxin injection. Injected into the sphincter, botulinum toxin paralyzes the muscle and allows it to relax. 3. Forceful dilatation of cardia under general anaesthesia: Oesophagoscopy & dilatation by Plastic balloons  Hydrostatic bag 4. Surgical treatments:  Hellar‟s myotomy under general anaesthesia  Anastomic operation – anastomosis between stomach & oesophagus. Q. Causes of white lesion in throat. Ans. Causes of white lesions in throat are1. 2. 3. 4. 5. 6. 7.

Acute follicular tonsillitis Faucial diphtheria Vincent‟s angina Agranulocytosis Infectious mononucleosis (Glandular fever) Oral thrush (cadidiasis) Leukaemia

Q. Causes of ulcer in the margin of the tongue.

Ans. Causes of ulcers of the oral cavity: 1. Infections  Viral: Herpengina; primary and secondary herpes simplex; hand, foot and mouth disease  Bacterial: Vincent‟s infection, TB, syphilis  Fungal: Candidiasis 2. Immune disorders:  Aphthous ulcer  Bechet‟s syndrome 3. Trauma  Physical: Cheek bite, jagged tooth, ill-fitting denture 26


 

Chemical: Silver nitrate, phenol, aspirin burn Thermal: Hot food or fluid, reverse smoking

4. Neoplasms 5. Skin disorders:  Erythema multiforme  Llichen planus  BMMP  Bullous pemphigoid  Lupus erythometosus 6. Blood disorders:  Leukaemia  Agranulocytosis  Pancytopenia  Cyclic neutropenia  Sickle cell anaemia 7. Drug allergy: Mouth washes, tooth paste, etc 8. Vitamin deficiencies 9. Miscellaneous:  Radiation mucositis  Cancer chemotherapy  Ddiabetes mellitus  Uraemia Q. Management of hemorrhage after adenoidectomy.

Ans. Management of hemorrhage after adenoidectomyHemorrhage usually seen in immediate post-operative period.  Nose and mouth may be full of blood  Vomitus of dark coloured blood which the patient had been swallowing gradually in post-operative period.  Rising pulse rate.  Primary hemorrhage always brisk and stops quickly.  Reactionary hemorrhage is common within 24 hours of operation. It is often due to remnant of adenoids.  Packing the area for sometimes  Conservative treatment: - Decongestive nasal drops - Coagulants and - Sedatives  Persistent bleeders are electro-coagulated under vision.  If bleeding still not controlled a postnasal pack is left for 24 hours under general anaesthsia.  If remnant of the adenoid tissue is present, then it should be removed.  Secondary hemorrhage is uncommon. 27


Q. What is adenoid facies?

Ans. Chronic nasal obstruction and mouth breathing due to enlarged adenoid lead to characteristic facial appearance of a child called adenoid facies. Features of adenoid facies are1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Elongated face with dull expression Open mouth Dribbling of saliva from angle of the mouth Prominent and crowded upper teeth Hitched up upper lip Pinched nose Highly arched hard palate Rounded shoulder Flat chest Abdomen is protuberant

Q. A woman of 45 years of age with anaemia complains dysphagia. What is your Dx?

Ans. The woman is probably suffering from Plummer-Vinson syndrome (Paterson-Brown Kelly syndrome). This is a precancerous lesion, commonly seen in woman whom there is chronic superficial pharyngo-oesophagitis. Aetiology:  Iron deficiency anaemia  Vitamin deficiency  Auto-immune disease. Clinical features: 1. Dysphagia – more to solids 2. Feeling of lump in the throat 3. Features of iron deficiency anaemia 4. Angular stomatitis, glossitis, and koilonychias. 5. Web formation or cicatrisation in post-carotid region. Diagnosis: (1) By clinical features, signs of vitamin deficiency (2) Hypochromic microcytic anaemia (3) Barium swallow X-ray shows a web at the post-cricoid region. (4) Hypopharyngoscopy and oesophagoscopy to confirm. (5) Serum iron and iron binding capacity to see prognosis after treatment. Treatment: 1. Iron and vitamins are given in large doses. 2. Endoscopic examination and dilatation relieves dysphagia. 3. Follow-up.

28


Q. Causes and management of primary hemorrhage after tonsillectomy. Ans. Causes of primary haemorrhage: Occurs at the time of operation 1. Faulty selection of the patient i.e. pt. with high blood pressure, DM, any bleeding disorders. 2. Injury to the surrounding structures 3. Tonsillar fibrosis. Management: It can be controlled by pressure, ligation or electrocoagulation of the bleeding vessels. Q. Types of hemorrhage after tonsillectomy.

Ans. The most common complication of tonsillectomy operation is haemorrhage which is of three types(i) Primary haemorrhage – occurs at the operation table. (ii) Reactionary haemorrhage – is due to rise of blood pressure in the post-operative period. (iii) Secondary haemorrhage – is due to infection. Q. What are the indications of tonsillectomy?

Ans. Indications of tonsillectomy are divided into: Absolute 1. Recurrent infections of throat(a) Seven or more episodes in one year, or (b) Five episodes per year for 2 years, or (c) Three episodes per year for 3 years, or (d) Two weeks or more of lost school or work in one year. 2. Peritonsillar abscess – tonsillectomy is done 4-6 weeks after abscess has been treated. 3. Tonsillitis causing febrile seizures. 4. Hypertrophy of tonsils causing  Airway obstruction (sleep apnoea)  Difficulty in diglutation  Interference with speech. 5. Suspicion of malignancy :  Lymphoma – in children  Epidermoid carcinoma – in adults.

Relative

As a part of another operation

1. Diphtheria carriers, who do 1. Palatopharyngoplasty not respond to antibiotics. 2. Glossopharyngeal neurectomy 2. Streptococcal carriers, who 3. Removal of styloid process. may be the source of infection to others. 3. Chronic tonsillitis with bad taste or halitosis which is unresponsive to medical treatment. 4. Recurrent streptococcal tonsillitis in a patient with valvular heart disease.

29


Q. Tell 5 contraindications of tonsillectomy operation.

Ans. Contraindications for tonsillectomy: 1. 2. 3. 4. 5.

Acute tonsillitis or acute upper respiratory tract infection. Blood dyscrasia and bleeding diathesis. Overt or submucous cleft palate. During epidemic of polio. Systemic infection and chronic debilitating disease (e.g. severe DM, gross HTN, severe asthma). 6. Children under 3 years of age. (They are at poor surgical risks)

HEAD-NECK

Q. Name parotid salivary gland tumor. Name surgical procedure of parotid.

Ans. Classification/Name of salivary gland tumors:

i.

Type Adenoma

ii. Carcinoma

Sub-group Pleomorphic Monomorphic

Common examples Pleomorphic adenoma (most common benign) Adenolymphoma (Warthin‟s tumor)

Low grade

Acinic cell carcinoma Adenoid cystic carcinoma Low-grade muco-epidermoid carcinoma

High grade

Adenocarcinoma Squamous cell carcinoma High-grade muco-epidermoid carcinoma Haemangioma Lymphangioma

iii. Non-epithelial tumors iv. Lymphomas

Primary lymphomas Secondary lymphomas

Non-Hodgekin‟s lymphomas Lymphomas in SjÖgren‟s syndrome

v. Secondary tumors

Local Distant

Tumors of head and neck specially Skin and bronchus

Solid lesions

Benign lymphoepithelial lesion Adenomatoid hyperplasia

Cystic lesions

Salivary gland cysts

vi. Unclassified tumors vii. Tumor like lesions

Surgical procedure of parotid: 1. Superficial parotidectomy - Incision and development of a skin flap (Incision is the „lazy S‟ pre-auricular-mastoid-cervical)

-

Mobilisation of the gland 30


- Location of the facial nerve trunk - Dissection of the gland off the facial nerve - Closure 2. Radical parotidectomy Q. What is Ludwig’s angina? Ans. Ludwig’s angina: This is a rare, virulent and often fatal septic inflammation of the soft tissue of the sublingual space with subsequent extension to the submandibular space and tissues of the neck.

Q. Symptoms of hyperthyroidism and hypothyroidism.

Ans. Symptoms of hyperthyroidism and hypothyroidism are      

Hypothyroidism Tiredness Mental lethargy Cold intolerance Weight gain Constipation Menstrual disturbance Carpal tunnel syndrome

     

Hyperthyroidism Tiredness Emotional lability Heat intolerance Weight loss Excessive appetite Palpitations

Q. Indication of tracheostomy.

Ans. Indications of tracheostomy areA. Respiratory obstruction 1. Infections - Acute laryngo-tracheo-brochitis, acute epiglottitis, diphtheria - Ludwig‟s angina, peritonsillar, retropharyngeal or parapharyngeal abscess, tongue abscess 2. Trauma - External injury of larynx and trachea - Trauma due to endoscopies, especially in infants and children - Fracture of mandible or maxillofacial injuries 3. Neoplasms - Benign and malignant neoplasms of larynx, pharynx, upper trachea, tongue and thyroid 4. Foreign body larynx 5. Oedema larynx due to steam, irritant fumes or gases, allergy, radiation 6. Bilateral abductor paralysis 7. Congenital anomalies - Laryngeal web, cysts, tracheo-oesophageal fistula - Bilateral choanal atresia 31


B. Retained secretions 1. Inability to cough - Coma of any cause, e.g. head injuries, cerebrovascular accidents, narcotic overdose - Paralysis of respiratory muscles, e.g. spinal injuries, polio, Guillain-Barre syndrome, myasthenia gravis - Spasm of respiratory muscles, tetanus, eclampsia, strychnine poisoning 2. Painful cough - Chest injuries, multiple rib fractures, pneumonia 3. Aspiration of pharyngeal secretions - Bulbar polio, polyneuritis, bilateral laryngeal paralysis C. Respiratory insufficiency - Chronic lung conditions, viz. emphysema, chronic bronchitis, bronchiectasis, atelectasis - Conditions listed in A and B* * In viva voce this point should not be told. Conditions listed in A and B means the points mentioned under the heading of respiratory obstruction and retained secretions.

Q. Post operative care after tracheostomy.

Ans. Post-operative management/after cares after tracheostomy: 1. Constant supervision:  Constant supervision for bleeding, displacement or blocking of tube and removal of secretions is essential.  A nurse or patient‟s relative should be attendance.  Patient is kept in propped up position.  Patient is given a bell or a paper pad and a pencil to communicate. 2. Suction:  Depending on the amount of secretion, suction may be required every half an hour or so.  Use sterile catheters with a Y-connector to break suction force. 3. Prevention of crusting and tracheitis: This is achieved by(a) Proper humidification by following methodsi. Humidifier ii. Steam-tent in children iii. Ultrasonic nebulizer or iv. Steam-kettle. (b) If crusting occurs, - A few drops of normal or hypotonic saline or Ringer‟s lactate are instilled into the trachea every 2-3 hours to loosen crusts. - A mucolytic agent such as acetylcysteine solution can be instilled to liquefy tenacious secretions or to loosen the crusts.

32


4. Care of tracheostomy tube:  Inner cannula should be removed and cleaned as and when indicated for the first 3 days.  Outer tube, unless blocked or displaced, should not be removed for 3-4 days to allow a track to be formed when the tube placement will become easy.  After 3-4 days, outer tube can be removed and cleaned every day. 5. Feeding: Proper nourishment is essential for recovery of the patient. If the patient is unable to eat, then naso-gastric feeding is to be started. 6. Physiotherapy and change of posture:  In ambulatory patient: Coughing out is encouraged and various breathing exercise to be taught.  In non-ambulant patient: Posture is to be changed frequently and lung care is to be taken to prevent lower respiratory tract infection. 7. Dressing: Water proof dressing should be applied to prevent maceration of surrounding skin. 8. Decannulation:  Tracheostomy tube is plugged and the patient closely observed. If the patient can tolerate it for 24 hours, tube can be safely removed. Q. Causes of midline neck swelling.

Ans. Causes of midline neck swelling are 

Solid Swelling of the thyroid isthmus and pyramidal lobe Enlarged lymph nodes (submental, prelaryngeal, pretracheal)

      

Cystic Ranula Ludwig‟s angina Sublingual dermoid Lipoma in the submental region Thyroglossal cyst Subhyoid bursitis Cold abscess in the space of Burns

Q. Causes of lymph node enlargement in neck.

Ans. Causes of cervical lymph adenopathy: Inflammatory  Reactive hyperplasia Infective  Viral For example, infectious mononucleosis, HIV  Bacterial Streptococcus, Staphylococcus Actinomycosis Tuberculosis Brucellosis 33




Protozoan Toxoplasmosis Neoplastic  Malignant Primary, e.g. lymphoma Secondary, e.g. squamous cell carcinoma Known primary Occult primary

Q. Causes of thyroid swelling. Name the investigations of thyroid enlargement.

Ans. Classification of thyroid swelling:  Simple goiter (euthyroid) Diffuse hyperplastic Physiological Pubertal Pregnancy Multinodular goiter  Toxic Diffuse Graves‟ disease Multinodular Toxic adenoma  Neoplastic Benign Follicular adenoma Malignant Primary Follicular epithelium – differentiated Follicular Papillary Follicular epithelium – undifferentiated Anaplastic Parafollicular cells Medullary Lymphoid cells Lymphoma Secondary Metastatic Local infiltration  Inflammatory Autoimmune Chronic lymphocytic thyroiditis Hashimoto‟s disease Granulomatous De Quervain‟s thyroiditis Fibrosing Riedels thyroiditis Infective Acute (bacterial thyroiditis, viral thyroiditis, „subacute thyroiditis‟) Chronic (tuberculous, syphilitic) 34


Other Amyloid Investigation: 1. Thyroid function Thyroid functional state Euthyroid Thyrotoxic Myxoedema Suppressive T4 therapy T3 toxicity

TSH (0.3-3.3 mU l-1) Normal Undetectable High Undetectable Low/undetectable

Free T4 (10-30nmol l-1) Normal High Low High Normal

Free T3 (3.5-7.5 μmol l-1) Normal High Low High (may be normal) High

2. Autoantibody titres Serum level of antibodies against thyroid peroxidase (TPO) and thyroglobulin are useful in determining the cause of thyroid dysfunction and swelling. Levels above 25 units‟ ml-1 for TPO antibody and titres of greater than 1:100 for anti-thyroglobulin are considered significant.

3. Isotope scan The uptake by the thyroid of a low dose of either radiolabelled iodine ( 132I) or the cheaper technetium ( Tc) will demonstrate the distribution of activity in the whole gland. In hyperthyroidism both the proportion of the tracer dose taken up and the rate at which this takes place are increased. 99m

4. Ultrasonography Ultrasongrapphy is used in determining the physical characteristics of thyroid swellings and to demonstrate subclinical nodularity and cyst formation.

5. Fine-needle aspiration cytology FNAC is the choice of investigation in discrete thyroid swellings. Thyroid conditions that can be diagnosed by FNAC include colloid nodules, thyroiditis, papillary carcinoma, medullary carcinoma, anaplastic carcinoma and lymphoma.

6. Radiology Chest and thoracic inlet radiograph may confirm the presence of significant retrosternal goitre and tracheal deviation, compression or retrosternal extension and are required when either clinical suspicion or FNAC indicates malignancy.

7. Ultrasound scan High-frequency ultrasound gives good anatomical images of the thyroid and surrounding structures.

8. Other scans Computed topography (CT), magnetic resonance imaging (MRI) and positron emission topography (PET) are used for the assessment of known malignancy and to assess the extent of retrosternal and, occasionally, recurrent goitres.

9. Laryngoscopy Flexible laryngoscopy is used preoperatively to determine the mobility of the vocal cord.

10. Core biopsy Core biopsy gives a strip of tissue for histological assessment. It is applied in assessment of locally advanced, surgically unresectable malignancy.

35


Q. Causes of unilateral neck swelling.

Ans. Causes of unilateral neck swelling areSite Submandibular triangle

Solid Tumor of submandibular gland Sialolithiasis Enlargement of lymph nodes

Cystic

Carotid triangle

Carotid body tumor Sternomastoid tumor Solidication of lymph nodes

Carotid aneurysm Branchial cyst Laryngoceal Cyst adenoma of thyroid (lateral lobe) Cold abscess of lymph nodes (e.g., TB lymphnodes)

Posterior triangle

Enlarged supraclavicular lymph nodes

Cystic hygroma Laryngoceal Pharyngeal pouch Subclavian aneurysm

Plunging ranula Sublingual dermoid

36

ENT (Viva Answer Sheet)

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