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ENT — Pharynx & Tonsils: Complete Study Guide

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1. EXAMINATION OF CHRONIC TONSILLITIS

Pharyngoscopic Picture (Local Signs on Pharyngoscopy)

• Tonsillar size — tonsils may be enlarged (hypertrophic type) or small and scarred (atrophic/fibrous type)
• Surface — irregular, nodular, or scarred surface; crypts visible
• Caseous/purulent plugs — white or yellowish caseous debris within tonsillar crypts (pathognomonic)
• Anterior pillar — hyperemia (redness) of the anterior faucial pillar is an important early sign; the pillar may be thickened and infiltrated
• Adhesions — fibrous adhesions between the tonsil and pillars or between the tonsil and posterior pillar
• Expressible pus — purulent or caseous material expressed from crypts on pressure
• Jugulodigastric (tonsillar) lymphadenopathy — palpable, sometimes tender lymph nodes at the angle of the jaw

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2. TYPES OF CHRONIC TONSILLITIS

A. Compensated (Simple) Chronic Tonsillitis

• Local signs of chronic inflammation present
• General reactivity of the body is sufficient to compensate; no systemic complications
• Patient has recurrent sore throats but recovers fully between episodes
• Symptoms: local signs on pharyngoscopy (crypts, debris, pillar hyperemia) with no signs of systemic disease or toxic damage to organs

B. Decompensated Chronic Tonsillitis

• Local signs present plus evidence that the infection is overwhelming the body's defenses
• Evidence of systemic involvement: tonsillogenic metastatic lesions (joint, heart, kidney, liver) — so-called "paired" or "associated diseases"
• Includes: recurrent peritonsillar abscess, parapharyngeal abscess, persistent cervical lymphadenitis, distant complications (nephritis, carditis, arthritis)
• May be subdivided into:
  • With recurrent exacerbations (angina)
  • Without exacerbations (toxic-allergic form)

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3. DIFFERENTIAL DIAGNOSIS: COMPENSATED vs. DECOMPENSATED TONSILLITIS

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4. CAUSES (AETIOLOGY) OF CHRONIC TONSILLITIS

• Primary pathogens: Group A β-hemolytic Streptococcus (S. pyogenes), S. pneumoniae, H. influenzae, staphylococci, anaerobes, adenoviruses, EBV
• Predisposing factors:
  • Recurrent acute tonsillitis inadequately treated
  • Anatomically deep crypts that trap debris and bacteria
  • Poor oral hygiene
  • Nasal obstruction leading to mouth breathing
  • Immunodeficiency states
  • Dental sepsis
  • Chronic sinusitis providing continuous bacterial seeding

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5. COMPLICATIONS OF CHRONIC TONSILLITIS

Local/Regional Complications

• Peritonsillar abscess (quinsy) — most common direct complication; collection between tonsil and superior constrictor muscle
• Parapharyngeal abscess
• Retropharyngeal abscess
• Cervical lymphadenitis/abscess
• Lemierre syndrome — thrombophlebitis of the internal jugular vein; caused by Fusobacterium necrophorum (anaerobic gram-negative bacillus); associated with spiking "picket fence" fevers, lateral neck tenderness, septic pulmonary emboli — K J Lee's Essential Otolaryngology

Distant (Tonsillogenic) Complications

• Rheumatic fever and rheumatic heart disease (most important — streptococcal sensitization)
• Glomerulonephritis (immune complex deposition)
• Reactive arthritis / joint pain
• Myocarditis / subacute bacterial endocarditis
• Psoriasis (guttate — triggered by streptococcal infections)
• PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections)
• Erythema nodosum
• Septicemia (rare)

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6. CONSERVATIVE TREATMENT OF CHRONIC TONSILLITIS

Local (Topical) Treatment

• Lacunae irrigation/washing with antiseptic solutions (furacillin, iodine-based solutions, antibiotics); removes caseous plugs and debris from crypts
• Tonsil surface lubrication with Lugol's solution, oil solutions of propolis, antibiotic-corticosteroid mixtures
• Ultraviolet irradiation (UVR) of tonsils — antiseptic effect
• UHF therapy / physiotherapy to the submandibular region — anti-inflammatory
• Aerosol therapy — spraying pharynx with antiseptics or antibiotics

Systemic Treatment

• Antibiotics during exacerbations — penicillin (drug of choice for streptococcal disease); amoxicillin-clavulanate or clindamycin for resistant cases
• Benzathine penicillin prophylaxis — monthly injections for prevention of rheumatic fever recurrence
• Immunocorrective therapy — immunomodulators, vitamins
• Antiallergic therapy — antihistamines for sensitization component
• Sanitation of other foci — dental caries, sinusitis

General Measures

• Hardening procedures, hydrotherapy
• Tonsil massage (bimanual)
• Therapeutic lacunae washing courses (10 sessions, 2× per year)

Conservative treatment is conducted in 2 courses per year for 2–3 years. If no improvement, tonsillectomy is indicated.

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7. COMPLICATIONS AFTER TONSILLECTOMY

Haemorrhage (most important)

• Primary — intraoperative
• Reactionary/early — within first 24 hours (slipped ligature, failed coagulation)
• Secondary (delayed) — days 5–10 postoperatively (most common); due to sloughing of clot/eschar as wound heals; accounts for majority of emergency readmissions
• Overall postoperative haemorrhage rate: 2–4%
• Mortality: approximately 1 in 25,000 — causes: haemorrhage, airway obstruction, anaesthesia — K J Lee's

Other Complications

• Airway obstruction — tongue/uvula oedema, haematoma, laryngospasm
• Velopharyngeal insufficiency (VPI) — hypernasality post-surgery (especially if large tonsils or adenoids removed)
• Nasopharyngeal stenosis — cicatricial scarring (rare, more with aggressive cautery)
• Atlantoaxial subluxation (Grisel syndrome) — ligamentous laxity from perioperative infection, mainly in children
• Eagle syndrome — calcified stylohyoid ligament causing pain after tonsillectomy
• Dental trauma — lip/tooth injury from mouth gag
• Anaesthetic complications — aspiration of blood, laryngospasm
• Infection / wound dehiscence
• Referred otalgia — common during healing (CN IX)
• Taste disturbance — glossopharyngeal nerve involvement

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8. INDICATIONS FOR TONSILLECTOMY

Absolute Indications

1. Hypertrophy causing obstructive sleep apnoea (OSA) or sleep-disordered breathing with adverse pulmonary/cardiovascular effects
2. Hypertrophy causing dysphagia and poor weight gain (especially children)
3. Hypertrophy causing malocclusion or facial bone malformation
4. Recurrent peritonsillar abscess — two or more, or failure of medical therapy
5. Tonsillitis causing febrile seizures
6. Suspicion of malignancy (unilateral enlargement, unknown primary tumour search)
7. Diphtheria carrier state

Relative Indications

1. Recurrent acute tonsillitis meeting the Paradise criteria:
   • ≥7 episodes in 1 year, OR
   • ≥5 episodes/year for 2 consecutive years, OR
   • ≥3 episodes/year for 3 consecutive years
   • Each episode must include: temperature >38.3°C, cervical lymphadenopathy, tonsillar exudate, or positive streptococcal test

2. 2 weeks of school/work missed in 1 year due to tonsillitis

3. PFAPA syndrome (Periodic Fever, Aphthous Stomatitis, Pharyngitis, Adenitis) unresponsive to medical management
4. Halitosis from chronic tonsillar disease
5. Decompensated tonsillitis — tonsillogenic complications (nephritis, carditis, arthritis)

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9. TECHNIQUE OF TONSILLECTOMY

Patient Positioning

• Supine with head extended (Rose position — head hanging off table OR on headrest)
• Mouth gag (Boyle-Davis or Crowe-Davis) inserted to hold mouth open and retract tongue
• Throat pack placed to prevent aspiration of blood

Extracapsular (Subcapsular) Dissection — Standard Technique

1. Incision of the anterior pillar mucosa along its full length using a curved tonsil knife
2. Grasp the tonsil with curved tonsillar tenaculum (Waugh's forceps)
3. Dissect the capsule from the superior constrictor muscle using blunt dissection (Mollison's dissector) or monopolar/bipolar electrocautery, proceeding from the superior pole downward
4. The tonsillar pedicle at the lower pole is divided using a tonsil snare (wire snare passed around the pedicle) or electrocautery
5. Haemostasis: by suture ligation (0 or 2-0 plain gut), electrocautery, or topical vasoconstricting agents
6. Key surgical landmark: superior and inferior poles are the primary vascular entry points — address these first if bleeding is brisk

Types of Tonsillectomy Technique

• Cold knife/snare — oldest method; sharp dissection, snare for lower pole; separate haemostasis required
• Electrocautery (monopolar) — most popular; provides haemostasis during dissection; may increase postoperative pain
• Coblation (bipolar radiofrequency ablation) — low temperature (60°C vs 400°C for electrocautery); reduces thermal damage; lower pain scores
• Harmonic (ultrasonic) scalpel — similar low-temperature advantages to coblation
• Intracapsular tonsillotomy — removes tonsil body only, leaves capsule; reduces pain and risk; higher recurrence rate

Anatomy of the Tonsil Bed

• Superior: soft palate
• Inferior: lingual tonsil
• Deep: superior constrictor muscle
• Anterior: palatoglossus muscle (anterior pillar)
• Posterior: palatopharyngeus muscle (posterior pillar)

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10. TECHNIQUE OF ADENOTOMY (ADENOIDECTOMY)

Classic Curette Technique

1. Patient supine, general anaesthesia (in children), mouth gag inserted
2. Soft palate retracted with a rubber catheter passed through the nose and out the mouth, to expose the nasopharynx
3. A adenoid curette (Beckmann or St Clair-Thompson) is introduced blindly through the mouth, placed against the posterior nasopharyngeal wall above the adenoid pad
4. Curette is swept downward with firm pressure to scrape the adenoid tissue off the posterior wall
5. Haemostasis by pressure with a postnasal pack for several minutes; electrocautery if needed
6. Inspection with a mirror or endoscope to confirm complete removal

Modern Endoscopic/Microdebrider Technique

• Rigid endoscope (0° or 30°) via the mouth or nose provides direct visualisation
• Powered microdebrider used to remove adenoid tissue under direct vision — allows more precise removal and better visualisation of residual tissue
• Electrocautery (monopolar or bipolar) can also be used under endoscopic guidance
• Advantage: precise removal, especially near Eustachian tube orifice

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11. INDICATIONS FOR ADENOTOMY (ADENOIDECTOMY)

Absolute Indications

1. Adenoid hypertrophy causing nasal obstruction with obstructive sleep apnoea
2. Recurrent or chronic otitis media with effusion (glue ear) — adenoidectomy reduces recurrence when grommets are inserted for second time
3. Recurrent acute otitis media (≥4 episodes in 6 months or ≥6 in 1 year) unresponsive to medical treatment
4. Adenoid hypertrophy with "adenoid facies" (open-mouth breathing, elongated face, retrognathia, dental malocclusion)
5. Chronic sinusitis with nasal obstruction from enlarged adenoids

Relative Indications

1. Chronic mouth breathing
2. Persistent nasal obstruction with rhinorrhoea
3. Repeated upper respiratory infections attributed to adenoid sepsis
4. Hyponasal voice

Contraindications

• Cleft palate (absolute — risk of velopharyngeal insufficiency)
• Submucous cleft palate — must rule out before surgery
• Bleeding disorders (relative)
• Active upper respiratory infection (defer 4–6 weeks)

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12. DIAGNOSIS AND CLINICAL FEATURES OF ADENOIDS

Definition

Clinical Features of Adenoid Hypertrophy

• Nasal obstruction — persistent, bilateral; worse at night
• Mouth breathing — open-mouth posture during sleep and at rest
• Snoring and sleep-disordered breathing / OSA
• Hyponasal ("adenoidal") voice — muffled, nasal quality
• Rhinorrhoea — mucopurulent, postnasal drip
• Recurrent otitis media — adenoids harbour bacteria near Eustachian tube orifice, causing tubal dysfunction
• Conductive hearing loss — secondary to chronic otitis media with effusion
• Adenoid facies (with longstanding obstruction):
  • Open mouth, elongated face
  • High arched palate
  • Dental malocclusion (overbite)
  • Hypoplastic maxilla
  • Pinched nostrils, dark circles under eyes

Diagnosis

• Clinical history and examination — characteristic facies, mouth breathing, hyponasal voice
• Flexible nasendoscopy — direct visualisation of adenoid pad; graded by percentage of choanal obstruction
• Lateral soft-tissue X-ray of nasopharynx — shows adenoid shadow (adenoid:nasopharynx ratio > 0.8 suggests significant hypertrophy)
• Audiometry + tympanometry — to assess middle ear status
• Polysomnography — if OSA suspected

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13. LOCAL SIGNS OF ACUTE PHARYNGITIS ON PHARYNGOSCOPY

• Diffuse hyperaemia of the posterior pharyngeal wall, soft palate, and pillars
• Mucosa appears bright red, oedematous, glistening
• Granular/follicular appearance if lymphoid follicles on posterior wall are engorged
• Mucous or mucopurulent secretion on posterior wall
• No membrane, no ulcers
• Uvula may be oedematous and elongated

• Marked hyperaemia of pharynx and tonsils
• Tonsillar exudate — white/yellow follicular or confluent exudate on tonsils
• Palatal petechiae — pinpoint haemorrhages on soft palate (characteristic of streptococcal infection)
• Tonsil hypertrophy ± exudate
• Large, tender jugulodigastric lymphadenopathy
• Possibly strawberry tongue (scarlet fever)

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14. FAUCIAL DIPHTHERIA

Aetiology

• Causative organism: Corynebacterium diphtheriae — gram-positive, non-spore-forming, non-motile rod
• Produces an exotoxin (encoded by β-phage) that inhibits protein synthesis by ADP-ribosylation of EF-2
• Disease rare where immunisation (DTP/DTaP) is practised

Clinical Features

• Incubation: 2–5 days
• Onset: insidious — begins with low-grade fever, sore throat, malaise
• Characteristic membrane: grayish-white or dirty grey pseudomembrane firmly adherent to tonsillar/pharyngeal mucosa; extends beyond tonsils onto soft palate and pillars
  • Membrane bleeds when forcibly removed (distinguishes from other membranes)
  • "Wet mouse" smell (characteristic)
• "Bull neck" — massive cervical lymphadenopathy with oedema of neck soft tissues
• Hoarse, croupy voice; stridor if larynx involved
• Systemic toxicity — pallor, tachycardia, prostration

Complications

1. Airway obstruction — leading cause of death; membrane extending to larynx/trachea causes respiratory failure
2. Myocarditis — diphtheritic cardiac toxin; arrhythmias, heart block; may be fatal
3. Peripheral neuropathy — demyelination from toxin:
   • Early: palatal palsy (nasal regurgitation, nasal voice)
   • Later: oculomotor palsies (diplopia, accommodation failure)
   • Late: generalised motor neuropathy (similar to Guillain-Barré)
4. Thrombocytopenia
5. Renal tubular necrosis

Treatment

1. Secure airway first — intubation or tracheostomy if needed
2. Diphtheria antitoxin (DAT) — administer immediately without waiting for culture confirmation; neutralises circulating toxin (not toxin already bound to cells); dose depends on severity (20,000–100,000 units IM/IV)
3. Antibiotics — penicillin G (drug of choice) or erythromycin × 14 days; eliminates organism, prevents transmission, reduces toxin production
4. Isolation — strict respiratory precautions
5. Contacts — trace, culture, booster immunisation; prophylactic antibiotics for unimmunised

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15. ATROPHIC PHARYNGITIS (Chronic Atrophic Pharyngitis)

Clinical Features

• Part of the spectrum of atrophic upper respiratory disease, often co-existing with atrophic rhinitis
• Complaints: persistent dryness and foreign body sensation in throat, tickling, hawking, difficult swallowing of dry food; crusting
• Pharyngoscopy:
  • Mucosa pale, thin, dry, glistening ("lacquered" appearance)
  • Reduced secretions; visible dry crusts or tenacious mucus
  • Submucosal vessels visible through thinned mucosa
  • Posterior pharyngeal wall appears "roomy" (paradoxically wider due to atrophy of lymphoid tissue and mucosal thinning)
  • Lymphoid follicles absent
• May be accompanied by ozaena (atrophic rhinitis with fetor)
• Worse in dry climates, low humidity, smokers, post-radiotherapy

Aetiology

• Idiopathic (primary)
• Post-infectious (repeated infections leading to mucosal atrophy)
• Post-radiotherapy
• Autoimmune (Sjögren syndrome)
• Iron deficiency (Plummer-Vinson syndrome)
• Hormonal changes (menopausal)
• Chronic irritants (smoking, alcohol, dust)

Treatment

• Alkaline inhalations/sprays — 1–2% sodium bicarbonate solution to soften and dissolve crusts
• Iodine-glycerine applications — 1% Lugol's solution in glycerine, stimulates mucous glands
• Oil sprays (olive oil, sea-buckthorn oil, vitamin A in oil) — moisturising and trophic effect
• Alkaline-oil inhalations — soften crusts and moisturise mucosa
• Humidification of environment
• Removal of crusts with suction and saline irrigation

• Iron supplementation if iron deficiency present
• Vitamin A and E — for mucosal regeneration
• Biostimulants — aloe vera injections, plasmol (tissue stimulation therapy)
• Thyroid hormones if hypothyroid
• Oestrogen therapy if post-menopausal

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16. CHRONIC HYPERTROPHIC PHARYNGITIS

Clinical Features

• Persistent sore throat, dryness, foreign body sensation, constant desire to clear throat
• Rhinopharyngitis sicca component if posterior nasal drip
• Pharyngoscopy:
  • Granular (follicular) form: prominent, rounded, red lymphoid follicles on posterior pharyngeal wall (cobblestone appearance); mucosa hyperaemic and thickened
  • Lateral hypertrophic form: lateral pharyngeal bands (posterior to posterior pillars) are hypertrophic and red
  • Mucosa oedematous, hyperaemic, with excess tenacious mucus
  • Uvula may be oedematous, elongated

Aetiology / Predisposing Factors

• Chronic nasal obstruction and mouth breathing
• Postnasal drip from chronic sinusitis
• Laryngopharyngeal reflux (GERD)
• Smoking, alcohol, dust, chemical irritants
• Vocal abuse
• Recurrent upper respiratory infections

Diagnosis

• Clinical pharyngoscopy
• Rule out systemic causes (sarcoidosis, Wegener's — by biopsy if in doubt)
• Endoscopy to exclude laryngopharyngeal lesion
• pH monitoring if GERD suspected

Treatment

• Treat underlying nasal obstruction (septoplasty, turbinate reduction)
• Treat GERD/LPR — proton pump inhibitors, dietary modification, elevation of head of bed
• Treat sinusitis
• Smoking cessation

• Alkaline saline gargles and sprays — reduce crusting, loosen mucus
• Astringent solutions — tannic acid, silver nitrate (10%) cauterisation of prominent follicles
• Cryotherapy or electrocautery of hypertrophic lymphoid follicles
• Aerosol therapy — antibiotics, anti-inflammatory agents
• Corticosteroid sprays — reduce mucosal inflammation

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17. CHRONIC CATARRHAL PHARYNGITIS

Clinical Features

• Mildest form of chronic pharyngitis
• Symptoms: persistent mild sore throat, rawness, tickling, moderate dryness, hawking of mucus, sensation of mucus running down the back of throat
• No marked systemic symptoms
• Pharyngoscopy:
  • Diffuse hyperaemia of posterior pharyngeal wall and pillars — not as vivid as acute pharyngitis
  • Mucosa oedematous, slightly thickened
  • Excess mucopurulent secretion visible on posterior wall
  • No ulcers, no membrane, no granules

Aetiology

• Most commonly: untreated/repeated acute pharyngitis
• Postnasal drip from chronic rhinosinusitis
• Smoking, alcohol
• Environmental irritants
• GERD/LPR (very common cause)

Treatment

• Eliminate causative factor first (most important)
• Alkaline gargles (warm saline, sodium bicarbonate)
• Antiseptic sprays (Hexetidine, Chlorhexidine)
• Posterior pharyngeal wall irrigation (saline, furacillin)
• Anti-reflux treatment if GERD/LPR is cause
• Smoking cessation, avoid alcohol and irritants
• Vitamins A, C, E — support mucosal regeneration

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18. ZENKER'S DIVERTICULUM (Pharyngeal Pouch/Sac)

Definition

Pathophysiology

• Results from incomplete relaxation of the upper oesophageal sphincter (UES) / cricopharyngeus muscle
• Also caused by: muscle fibrosis, failure of active dilatation due to inadequate laryngeal elevation
• Increased intraluminal pressure during swallowing herniates pharyngeal mucosa through Killian's dehiscence posteriorly

Clinical Features

• Oropharyngeal dysphagia — progressive difficulty swallowing, initially solids then liquids
• Regurgitation of undigested food — hours after eating (not digested, no acid taste)
• Halitosis
• Aspiration and chronic cough — risk of aspiration pneumonia
• Gurgling sensation in neck, sometimes visible/palpable neck swelling on left side
• Weight loss (if severe)
• Borborygmi in neck

Diagnosis

• Barium oesophagogram (lateral projection) — gold standard; shows contrast filling the diverticulum during swallowing; lateral view essential to see posterior herniation
• CT scan for pre-operative planning
• Flexible endoscopy (carefully — risk of perforation into diverticulum)

Treatment

• Cricopharyngeal myotomy — division of the cricopharyngeus (UES) to relieve the underlying dysfunction; essential component of treatment
• Combined with one of:
  • Diverticulectomy (excision of sac)
  • Diverticulopexy (suspension of sac — prevents filling)
  • Diverticulum inversion
• Endoscopic diverticulotomy (Dohlman procedure) — division of the common wall between diverticulum and oesophagus using endoscopic stapler (EndoGIA) or CO₂ laser; minimally invasive, preferred in elderly/high-risk patients

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19. LUDWIG'S ANGINA

Definition

Aetiology

• Most common (80–90%): dental origin — mandibular molar (2nd and 3rd) roots insert below the mylohyoid line, allowing infection to spread directly into submandibular space
• Other causes:
  • Mandibular fracture
  • Oral trauma (tongue piercing, lingual laceration, iatrogenic from intubation)
  • Secondary infection of oral malignancy
  • Suppurative parotitis
  • Adjacent head and neck infections
• Organisms: polymicrobial — mixed oral flora including Streptococcus viridans, Staphylococcus, anaerobes (Bacteroides, Peptostreptococcus)
• Risk factors: diabetes mellitus, immunocompromise, malnutrition, alcoholism

Mechanism of Spread

• Spreads rapidly through fascial planes (not via lymphatics — hence no fluctuation, no lymphadenopathy initially)
• Bilateral spread because submandibular spaces communicate posteriorly
• May spread into parapharyngeal space via styloglossus muscle → deep neck infections
• May spread into mediastinum (descending necrotising mediastinitis) — life-threatening

Clinical Features

• History: recent dental infection, dental caries, recent extraction
• Symptoms: dysphagia, odynophagia, drooling, trismus, muffled ("hot potato") voice, fever, neck pain and stiffness, progressive dyspnoea
• Signs:
  • Submental and bilateral submandibular indurated, brawny oedema — "woody" consistency (not fluctuant)
  • Floor of mouth elevated — tongue displaced superiorly and posteriorly ("tongue lifted to palate")
  • "Bull neck" — tense brawny oedema from submandibular region to hyoid
  • Erect posture, drooling, anxious
  • As progresses: stridor, progressive respiratory distress, cyanosis
  • Palpable fluctuation absent (cellulitis, not abscess)

Complications

1. Asphyxia / airway obstruction — leading cause of death
2. Descending necrotising mediastinitis — extension into mediastinum; very high mortality (40%)
3. Aspiration pneumonia
4. Septicaemia / septic shock
5. Internal jugular vein thrombosis (Lemierre syndrome)
6. Carotid artery erosion (rare)
7. Cavernous sinus thrombosis (via retrograde venous spread)
8. Osteomyelitis of mandible

Diagnosis

• Clinical — characteristic presentation
• Contrast-enhanced CT scan — delineates extent of infection, identifies any collections, airway calibre
• Blood cultures, FBC, CRP, glucose

Treatment

1. AIRWAY FIRST — most critical step:
   • Awake fiberoptic nasotracheal intubation — preferred if airway not critically compromised
   • Tracheostomy (awake, under local anaesthesia) if airway critically compromised or intubation fails
2. IV antibiotics — high-dose, broad-spectrum with anaerobic coverage:
   • Penicillin + metronidazole, OR
   • Clindamycin, OR
   • Ampicillin-sulbactam, OR
   • Piperacillin-tazobactam
3. Surgical drainage — wide drainage of bilateral submandibular and sublingual spaces through external neck incisions
   • Only if there is fluctuance or abscess formation (early Ludwig's is cellulitis — drainage alone without antibiotics insufficient)
4. IV corticosteroids — reduce oedema (adjunct)
5. Dental extraction of causative tooth after acute phase controlled
6. Hyperbaric oxygen — in refractory cases
7. ICU monitoring — continuous oximetry, vital signs

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20. ANGIOFIBROMA OF THE NASOPHARYNX (Juvenile Nasopharyngeal Angiofibroma — JNA)

Definition

Epidemiology

• Almost exclusively in males, ages 10–25
• Accounts for 0.05% of head and neck tumours
• More common in certain geographic areas (India, Egypt)

Pathogenesis

• Believed to arise from remnants of a branchial artery at Killian's dehiscence/sphenopalatine foramen area
• Epicentre of origin: pterygopalatine fossa / sphenopalatine foramen / base of pterygoid process
• Blood supply: primarily internal maxillary artery (sphenopalatine branch) + ascending pharyngeal artery; may have ICA contribution
• Molecular: androgen receptor expression; VEGF and FGFR pathway upregulation

Clinical Features

• Unilateral nasal obstruction — most common first symptom
• Recurrent, profuse, spontaneous epistaxis — characteristic, may be life-threatening; unilateral
• Facial deformity — "Holman-Miller sign" (anterior bowing of posterior wall of maxillary sinus on imaging)
• Nasal voice (rhinolalia clausa)
• Eustachian tube dysfunction → conductive hearing loss
• Proptosis, diplopia if orbital involvement
• Headache if intracranial extension

Staging (Fisch/Andrews staging commonly used)

• Stage I: limited to nasopharynx/nasal cavity
• Stage II: pterygomaxillary fossa involvement
• Stage III: skull base erosion
• Stage IV: intracranial extension

Diagnosis

• CT scan — bony erosion, Holman-Miller sign, extent
• MRI — soft tissue extent, intracranial involvement; characteristic "salt and pepper" appearance on T1 (flow voids + haemorrhage)
• Angiography — delineates blood supply; allows pre-operative embolisation
• Biopsy is contraindicated — risk of catastrophic haemorrhage
• Diagnosis is clinical + radiological

Treatment

1. Pre-operative embolisation — 24–48 hours before surgery to reduce intraoperative blood loss (embolise feeding vessels via interventional radiology)
2. Surgical resection — primary treatment:
   • Lateral rhinotomy, midfacial degloving, transpalatal, infratemporal fossa approaches depending on stage
   • Endoscopic resection — now preferred for lower-stage tumours (I–II); less morbidity, same local control rates
3. Radiotherapy — for unresectable or recurrent tumours, or significant intracranial extension; good local control (80–85%)
4. Hormonal therapy — flutamide (anti-androgen) used as adjunct pre-operatively in some centres
5. Watchful waiting — controversial; JNA may spontaneously involute after puberty but not reliably

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21. BENIGN TUMOURS OF THE PHARYNX

Oropharyngeal Benign Tumours

• Squamous papilloma — most common benign oropharyngeal tumour; caused by HPV (6, 11); sessile or pedunculated warty lesion; treatment: surgical excision
• Minor salivary gland tumours — most commonly pleomorphic adenoma; occurs on soft palate; treatment: wide local excision
• Fibroma / fibrous polyp — reactive lesion from chronic trauma
• Lipoma — rare; submucosal
• Lymphangioma / haemangioma — congenital; usually presents in childhood
• Lingual thyroid — ectopic thyroid tissue at base of tongue (failure of thyroid descent); may be the only functioning thyroid tissue — check technetium scan before excision

Nasopharyngeal Benign Tumours

• Angiofibroma (JNA) — see above (most important)
• Adenoid hypertrophy — technically physiological enlargement
• Thornwaldt's cyst — midline nasopharyngeal cyst arising from remnant of notochordal adhesion; causes postnasal drip, occipital headache, eustachian tube dysfunction; treatment: endoscopic marsupialization
• Craniopharyngioma — from Rathke's pouch remnants; compresses pituitary
• Chordoma — from notochordal remnants; locally aggressive; at clivus

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22. MALIGNANT TUMOURS OF THE PHARYNX

A. Nasopharyngeal Carcinoma (NPC)

• Most common nasopharyngeal malignancy
• Aetiology: EBV (Epstein-Barr virus) strongly associated; HLA types; nitrosamines (salted fish — Southern Chinese diet); genetic predisposition
• Histology: WHO types:
  • Type I: Keratinising squamous cell carcinoma
  • Type II: Non-keratinising differentiated
  • Type III: Undifferentiated (lymphoepithelioma) — most common; best radiosensitivity
• Clinical features:
  • Triad: unilateral nasal obstruction, epistaxis, cervical lymphadenopathy (often first presentation — often N2/N3)
  • Eustachian tube obstruction → unilateral secretory otitis media → conductive hearing loss
  • Cranial nerve palsies (III, IV, VI — cavernous sinus; V — Meckel's cave; XII — hypoglossal canal)
  • Trotter's triad: conductive deafness, ipsilateral immobile soft palate, trigeminal neuralgia
• Diagnosis: nasopharyngoscopy + biopsy; MRI for staging; EBV titres (VCA-IgA elevated)
• Treatment: Radiotherapy is primary treatment (radiosensitive tumour); concurrent cisplatin-based chemotherapy for advanced stages; surgery for neck nodes
• Prognosis: Stage I/II — 80–90% 5-year survival; Stage IV — 30–40%

B. Oropharyngeal Squamous Cell Carcinoma

• Two distinct subtypes:
  1. HPV-related (HPV-16 and HPV-18) — base of tongue, tonsillar fossa; typically non-smokers, younger patients; better prognosis; high p16 expression
  2. Standard variant — smokers/drinkers; worse prognosis
• Clinical features:
  • Sore throat, dysphagia, otalgia (referred via CN IX/X)
  • Neck mass (often first presentation — tonsil/base of tongue SCC metastasises early)
  • Unilateral tonsillar enlargement
• Diagnosis: biopsy; PET-CT for staging; EBV/HPV status
• Treatment: Surgery (transoral robotic surgery — TORS) ± radiotherapy; or definitive chemoradiotherapy; neck dissection for nodes
• Tonsil lymphoma (non-Hodgkin lymphoma) — presents as unilateral tonsillar enlargement; treat with chemotherapy ± radiotherapy

C. Hypopharyngeal Carcinoma

• Pyriform sinus most common (75%), posterior pharyngeal wall, postcricoid area
• Strongly associated with smoking and alcohol
• Postcricoid carcinoma — associated with Plummer-Vinson syndrome (iron deficiency anaemia, oesophageal web, dysphagia); predominantly in women
• Late presentation (silent area), poor prognosis
• Treatment: surgery (total pharyngolaryngectomy) ± chemoradiotherapy; often palliative

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• K J Lee's Essential Otolaryngology, 12th ed.
• Cummings Otolaryngology: Head and Neck Surgery, 7th ed.
• Pfenninger and Fowler's Procedures for Primary Care, 3rd ed.
• Rosen's Emergency Medicine, 10th ed.
• Sabiston Textbook of Surgery, 21st ed.
• Tintinalli's Emergency Medicine