GC219 Infections And Tumours In Pharynx And Oral Cavity
Infections and tumors of the pharynx and oral cavity encompass a spectrum of inflammatory, infectious, and neoplastic conditions—including pharyngitis, tonsillar abscess, oral candidiasis, and squamous cell carcinoma—that affect the mucosal surfaces of the mouth and throat.
Infections and Tumours in Pharynx and Oral Cavity
This lecture by Dr. Chung Chun Kit Joseph (ENT Consultant, HKU) sits within the Head & Neck Surgery subspecialty of ENT and covers two major domains: infections (acute tonsillitis → deep neck abscesses) and neoplasms (benign lesions → oral cavity / oropharyngeal / hypopharyngeal malignancies). It is one of the most directly examined GC lectures in the Fourth Summative — appearing in MCQ, EMQ, minicase, and SAQ formats. [1]
Learning Objectives (directly from slides): [1]
- Understand principles of treatment of different types of head and neck infections
- Medical and surgical management of head and neck infections
- Presentation and pathophysiology of tumours in the oral cavity and pharynx
- Investigation and management of tumours in the oral cavity and pharynx
Big-picture clinical relevance: Every doctor will encounter sore throats and oral ulcers. The critical skill is recognising when a benign-sounding complaint (sore throat, non-healing ulcer) represents a life-threatening infection (Ludwig angina, deep neck abscess) or a malignancy (SCC of oral cavity/oropharynx). The lecture trains you to triage correctly and refer early.
Part 1: Anatomy — Setting the Stage
Understanding exact anatomical boundaries is crucial because staging, lymphatic drainage, and treatment differ by subsite.
The upper aerodigestive tract includes: nasal cavity & paranasal sinuses, nasopharynx, oral cavity, oropharynx, larynx, and hypopharynx. [1]
| Oral Cavity | Oropharynx |
|---|---|
| Lip | Tonsils |
| Buccal mucosa (with parotid duct opening) | Soft palate |
| Gingival sulcus | Pharyngeal mucosa |
| Teeth | Tongue base (posterior 1/3) |
| Hard palate | |
| Oral tongue (anterior 2/3) | |
| Floor of mouth (with submandibular duct opening) |
What the floor-of-mouth photo shows: raised tongue exposing the lingual frenulum, sublingual veins, and bilateral floor mucosa — the surface you inspect and bimanually palpate for ranula, stones, and occult SCC. [1]
Why does the oral tongue vs tongue base distinction matter?
The junction of the anterior 2/3 (oral tongue) and posterior 1/3 (tongue base) marks the boundary between oral cavity and oropharynx. This has massive implications:
- Oral cavity SCC → surgery is preferred even in early stage
- Oropharynx SCC → RT or chemo-RT may be primary; HPV status matters
- Nerve supply differs: anterior 2/3 = CN V3 (sensation) + CN VII chorda tympani (taste); posterior 1/3 = CN IX (both)
- Lymphatic drainage differs → different neck dissection levels
- Upper aerodigestive tract
- Salivary glands (parotid, submandibular, sublingual, minor salivary glands)
- Thyroid
- Lymph nodes
- Skin and soft tissue of H&N region
Part 2: Clinical History and Examination
Key history points: Age, Sex, Duration (acute vs chronic), specific symptoms by site, systemic upset, risk factors (smoking, alcohol, family history), functional disturbances (breathing, chewing, swallowing, phonation, articulation), and comorbidities. [1]
| Site | Symptoms to Ask |
|---|---|
| Ear | Unilateral hearing loss, pain (referred otalgia) |
| Nose | Blood-stained discharge, unilateral nasal obstruction |
| Mouth | Non-healing ulcers, mass, blood-stained saliva, loose denture |
| Throat | Hoarseness, blood-stained sputum, shortness of breath |
| Pharynx | Globus, dysphagia, blood-stained saliva |
| Neck | Salivary gland swelling, lymph node |
Why ask about referred otalgia? The pharynx and tongue base are innervated by CN IX and CN X, whose tympanic branches (Jacobson's nerve from CN IX, Arnold's nerve from CN X) also supply the ear. A patient with persistent unilateral otalgia and normal ear examination should have the oropharynx and hypopharynx examined for malignancy.
Oral cavity and oropharynx: systematic inspection of all sub-sites + palpation for underlying mass/induration. Neck: assess location (region/level), shape + size (measure), consistency, mobility, inflammation. Also examine scalp and skin. [1]
Why palpation? Submucosal tumours (minor salivary gland, lymphoma) may look normal on surface but feel indurated. Always bimanually palpate the floor of mouth.
Part 3: INFECTIONS
3.1 Acute Tonsillitis [1]
Acute tonsillitis = infection and acute inflammation of the tonsils. [1]
| Category | Organisms |
|---|---|
| Virus | Influenza, parainfluenza, adenovirus, enterovirus, rhinovirus |
| Bacteria | β-haemolytic Streptococcus (Strep pyogenes) ← most important, Strep pneumoniae, H. influenzae, anaerobes, mixed |
| Others | Corynebacterium diphtheriae, Candida, syphilis, TB |
Why does Group A Strep (GAS) matter most? Because GAS pharyngitis is the only common bacterial cause that:
- Responds to antibiotics (shortening illness by ~1 day)
- Can cause acute rheumatic fever (prevented by penicillin within 9 days of symptom onset)
- Can cause post-streptococcal glomerulonephritis (not prevented by antibiotics but important to recognise)
Symptoms:
- Sore throat, odynophagia
- Fever
- Muffled voice / hot-potato voice
- Otalgia (referred via CN IX)
- Systemic: abdominal pain, vomiting (especially in children with GAS)
Additional EBV / infectious mononucleosis clinical features (body-diagram, slide): photophobia, fatigue, loss of appetite, malaise, headache, throat soreness and reddening, tonsillar reddening/swelling/white patches, lymph node swelling, cough, high fever, chills, aches, splenic enlargement with abdominal pain, nausea and vomiting. [1]
Signs:
- Hyperaemic tonsils with exudates/pus
- No or minimal trismus ← key discriminator from peritonsillar abscess
- Tender cervical lymphadenopathy
Investigations:
- CBP — WBC (usually elevated with neutrophilia in bacterial; lymphocytosis suggests viral/EBV)
- Throat swab for culture (gold standard for GAS; rapid antigen test in clinic)
Treatment:
- Bed rest, analgesics, fluid replacement, IV line
- Penicillin (first-line for GAS) or Erythromycin (if penicillin allergic)
Complications of acute tonsillitis: Local: Peritonsillar abscess, parapharyngeal abscess, retropharyngeal abscess, AOM General: Septicaemia, acute rheumatic fever, acute glomerulonephritis, meningitis [1]
Exam Discriminator: Trismus
No/minimal trismus = uncomplicated tonsillitis. Trismus present = suspect peritonsillar abscess or parapharyngeal abscess. Trismus occurs because inflammation irritates the medial pterygoid muscle adjacent to the tonsillar fossa.
3.2 Infectious Mononucleosis (Glandular Fever) [1]
Acute infection by EBV (Epstein-Barr virus). Young adult. Transmitted through saliva. Incubation period 5–7 weeks. Prodromal period 4–5 days. [1]
Pathogenesis (from first principles) [3][4]:
- EBV contacts oropharyngeal epithelial cells → viral replication
- EBV infects B cells in lymphoid-rich areas of oropharynx
- Infected B cells disseminate throughout the lymphoreticular system
- Immune system activates → EBV-specific cytotoxic T-lymphocytes (CD8+ T cells + CD16+ NK cells) = the "atypical lymphocytes" on blood smear
- Heterophile antibodies (mostly IgM, cross-react with horse/sheep RBCs) are produced → basis for monospot test
- EBV establishes latency with periodic reactivation; if immunocompromised → risk of EBV-related malignancy (Burkitt lymphoma, NPC, lymphoproliferative disease)
| Test | Finding | Why |
|---|---|---|
| CBP | Raised WCC, mononuclear cells | Reactive lymphocyte expansion |
| Blood smear | Atypical lymphocytes | Activated CD8+ T cells |
| Platelet count | Decreased | Immune-mediated consumption |
| LFT and clotting | Deranged | Hepatic involvement (~90% have mild transaminitis) |
| Monospot test | Positive | Detects heterophile antibodies; can be false-negative early or in young children |
Supportive: bed rest, fluid replacement, analgesics. AVOID AMPICILLIN → rubelliform rash. [1]
Why does ampicillin cause a rash in EBV? The exact mechanism is debated but involves aberrant immune activation — the atypical lymphocytes cross-react, causing a widespread maculopapular (rubelliform) rash in 70–100% of EBV patients given aminopenicillins. This is NOT a true penicillin allergy but is an important drug-disease interaction.
- Sepsis
- Hepatomegaly 10%
- Splenomegaly 50% → avoid contact sports for 1 month (risk of splenic rupture)
High Yield Exam Point
A young patient with severe tonsillitis, lymphadenopathy, and hepatosplenomegaly — do NOT give ampicillin/amoxicillin. If you suspect EBV, use penicillin V or erythromycin instead. The rubelliform rash from ampicillin in EBV is a classic exam trap.
3.3 Peritonsillar Abscess (Quinsy) [1]
Collection of pus between tonsillar capsule and superior constrictor muscle. Mixed aerobic and anaerobic organisms (Bacteroides, Peptostreptococcus). [1]
This is the most common deep neck space infection and often complicates acute tonsillitis.
Symptoms: Sore throat, fever, dysphagia, odynophagia, muffled voice, otalgia, airway obstruction
Signs (the classic triad):
- Unilateral peritonsillar swelling
- Deviation of uvula (away from the affected side)
- Trismus ← key differentiator from uncomplicated tonsillitis
Definitive: transoral incision and drainage + antibiotics. Symptomatic: analgesics, fluid replacement, chart I/O. Consider elective tonsillectomy (20% recurrence rate). [1]
Why incision and drainage? An abscess is a walled-off collection — antibiotics alone cannot penetrate adequately. The anterior tonsillar pillar is incised (or needle aspiration performed) to drain pus. If recurrent (20% chance), interval tonsillectomy prevents further episodes.
ENT emergency. Airway obstruction (stridor). Sore throat, odynophagia, and drooling. Management: Secure airway → IV antibiotics. [1]
Why is this an emergency? The epiglottis sits at the entrance of the larynx. When swollen, it can completely obstruct the airway — this progresses within hours. Do NOT examine the throat with a tongue depressor in a suspected case (especially in children), as this can provoke laryngospasm and complete obstruction.
Imaging: A lateral neck radiograph may show the "thumb sign" — an enlarged, thickened epiglottis silhouette — which is characteristic of acute epiglottitis. [1]
- Children: classically caused by Haemophilus influenzae type b (now rare due to Hib vaccine); presents with tripod position, drooling, toxic appearance
- Adults: often polymicrobial or GAS; less dramatic onset but still life-threatening [5]
Severe inflammation/abscess of floor of mouth. Dental origin. Airway obstruction (stridor). [1]
Management: Secure airway → Surgical drainage + IV antibiotics → Dental consultation. [1]
Why "angina"? The term derives from Latin angere (to strangle). Ludwig angina causes bilateral submandibular, sublingual, and submental space infection, pushing the tongue upwards and backwards, causing airway compromise. It is almost always of dental origin (infected lower molar teeth — the roots lie below the mylohyoid line, giving infection direct access to the submandibular space).
Why dental consultation? The source tooth must be dealt with (extraction or root canal), or the infection will recur.
Clinical features: fever, sore throat, neck swelling. Management: Secure airway → Surgical drainage → IV antibiotics → Dental consultation. [1]
| Type | Key Points |
|---|---|
| Retropharyngeal abscess | More common in children (retropharyngeal lymph nodes involute by age 6). Presents with neck stiffness, refusal to eat, stridor. CT scan is diagnostic. |
| Parapharyngeal abscess | Can arise from tonsillitis, dental infection, or spread from peritonsillar abscess. Lies lateral to pharynx → can involve carotid sheath → risk of internal jugular vein thrombosis (Lemierre syndrome) and carotid artery erosion. |
Deep neck space anatomy (axial cross-section) [1]: Key spaces to know include the retropharyngeal space, parapharyngeal space, masticator space, pharyngeal mucosal space, parotid space, carotid space (containing internal carotid artery, internal jugular vein, CN IX–XII), and prevertebral space. Understanding these compartments explains routes of infection spread (e.g., retropharyngeal space → posterior mediastinum; parapharyngeal space → carotid sheath).
Unifying Principle for Deep Neck Infections
For ALL deep neck infections: (1) Secure airway first, (2) Surgical drainage, (3) IV antibiotics, (4) Dental consultation if dental source suspected. The airway is ALWAYS the priority — these infections can progress to mediastinitis via the retropharyngeal space if untreated. [1]
Incidental finding. Presents during URTI. No trismus. 80% benign. [1]
This is included because parapharyngeal masses can mimic a parapharyngeal abscess — but the absence of trismus and fever suggests tumour rather than infection. Common benign tumours here include pleomorphic adenoma (deep lobe of parotid), schwannoma, and paraganglioma.
Part 4: BENIGN LESIONS OF ORAL CAVITY AND PHARYNX
Lipoma, papilloma, haemangioma, giant cell tumour. [1]
These are generally managed conservatively unless symptomatic. Important to differentiate from malignancy by biopsy if any doubt.
Bluish cystic swelling in the floor of mouth ("belly of a frog"). Mucus retention cyst arising from blocked sublingual gland. Definitive treatment: excision of pseudocyst together with resection of sublingual gland. [1]
Why excise the sublingual gland? Simple incision/marsupialisation has a high recurrence rate because the underlying obstructed gland continues to produce mucus. Removing the gland addresses the source.
A plunging ranula extends through the mylohyoid muscle into the neck — presenting as a neck mass. This is a classic exam scenario for "neck mass differential diagnosis."
Submandibular > Parotid > Sublingual. Colicky postprandial glandular swelling and pain. Treatment: marsupialization and calculus removal / submandibular gland excision. Recent advance: sialendoscopy. [1]
Why submandibular most common? Three reasons:
- Wharton's duct is longer and courses upward against gravity
- Submandibular saliva is more mucous (thicker) than parotid serous saliva
- Higher calcium content in submandibular saliva
Complication: sialadenitis — pus expressed from ductal orifice; ductal stone visible. [1]
Torus palatinus: bony outgrowth on hard palate, midline, smooth mucosa. Symptoms: pain, foreign body sensation, swallowing problem. Surgical removal if symptomatic (ulceration, affecting denture placement, associated periodontal disorder from food trapping). Torus mandibularis: bony protuberance on lingual aspect of mandible, commonly between canine and premolar areas. [1]
These are benign developmental bony exostoses — no malignant potential. Removal only if symptomatic.
May be ulcerative (mucosal origin) or have normal overlying mucosa (minor salivary gland tumour). May arise from nose or maxillary sinus (nasal symptoms). [1]
Minor salivary gland tumours of the palate are the most common intraoral salivary gland tumours. The most common malignant one is mucoepidermoid carcinoma or adenoid cystic carcinoma. They present as a submucosal swelling with intact overlying mucosa — this is an important exam discriminator from SCC which typically ulcerates.
Part 5: PRE-MALIGNANT LESIONS
Whitish patch on oral cavity mucosal membrane that cannot be wiped away. A clinical description with various pathological conditions (lichen planus, candidiasis, linea alba). Associated with malignancy (5%) → biopsy is needed. [1]
Key concept: Leukoplakia is a clinical term, not a histological diagnosis. It means "white patch that cannot be scraped off" (unlike candidiasis, which can). The 5% malignant transformation rate means all leukoplakias need biopsy.
Erythematous patch +/- granular or nodular lesion. Dysplasia without keratosis. HIGH malignant potential: 15 times increased risk of SCC. 90% CIS or SCC at time of biopsy. [1]
Leukoplakia vs Erythroplakia — Exam Comparison Table
| Feature | Leukoplakia | Erythroplakia |
|---|---|---|
| Appearance | White patch, cannot wipe off | Red patch, +/- granular/nodular |
| Pathology | Variable (hyperkeratosis → dysplasia) | Dysplasia without keratosis |
| Malignant potential | ~5% | ~90% already CIS/SCC at biopsy |
| Risk relative to SCC | Low-moderate | 15× increased risk |
| Management | Biopsy essential | Biopsy essential + excision |
Erythroplakia is far more dangerous than leukoplakia — this is a high-yield discriminator.
Causes: Aphthous, traumatic, dental-related, infective (bacterial, viral — Herpes, EBV), systemic (Behcet's disease, autoimmune, blood disease), malignant. Malignant ulcer features: irregular, rolled/everted edge, indurated, painless. May look 'same as benign' but persists. EARLY REFERRAL if persistent and/or suspicious. [1]
Clinical pearl: A painless, non-healing ulcer > 2 weeks in the oral cavity must be biopsied to rule out SCC. Most benign ulcers (aphthous, traumatic) heal within 2 weeks.
Part 6: MALIGNANCIES
90% of head & neck malignancies are squamous cell carcinoma (SCC) (not including nasopharynx and thyroid) — WHO Classification. [1]
Why SCC? The upper aerodigestive tract is lined by stratified squamous epithelium. Chronic carcinogen exposure (smoking, alcohol) causes field cancerization with stepwise mutations leading to SCC.
Risk factors:
- Smoking, smoking, smoking (primary risk factor)
- Alcohol — synergistic effect with smoking (especially hypopharyngeal carcinoma)
- Chewing betel nut (oral cavity carcinoma)
- Human papillomavirus / HPV (oropharyngeal carcinoma)
- Poor oral hygiene with chronic infection
- Previous irradiation/malignancy, immunocompromised [1]
| Risk Factor | Associated Subsite |
|---|---|
| Smoking alone | Floor of mouth, hypopharynx, larynx |
| Smoking + alcohol | Hypopharynx (synergistic — multiplicative risk) |
| Betel nut chewing | Oral cavity (buccal mucosa) |
| HPV (type 16, 18) | Oropharynx (tonsil, tongue base) |
| Non-smoker | Oral tongue, buccal mucosa, alveolar ridge |
HPV-related oropharyngeal SCC is a distinct entity [2]:
- Younger males, higher number of sexual partners, oral sex exposure
- Frequent LN metastasis at presentation
- Better prognosis than HPV-negative SCC
- Higher response to chemo/RT → de-intensification of treatment being explored
- HPV E6 and E7 oncoproteins inactivate p53 and Rb respectively
6.3 Oral Cavity Malignancy [1]
Oral tongue (commonest), buccal mucosa, floor of mouth, upper/lower alveolus, hard palate, lip.
- Epithelium (ulcerative): SCC / AdenoCa
- Underlying structure (smooth overlying mucosa): lymphoma / minor salivary gland
Exophytic mass. Non-healing ulcer. Painless at first, painful when infiltrating nerve. Surrounding leukoplakia/erythroplakia. Induration or fixation. Loosened tooth +/- non-healing tooth socket. Bleeding, swallowing/speech difficulty (ankyloglossia). 15–20% occult nodal metastasis → elective neck dissection. [1]
Why elective neck dissection even without palpable nodes? Because 15–20% of clinically N0 (node-negative) oral cavity cancers harbour occult micrometastases. Missing these significantly worsens prognosis. The threshold for elective neck dissection is usually tumour depth of invasion > 3–4 mm. [2]
Lymphatic drainage pattern [2]:
- SCC of oral cavity/lips → metastasize to Level I, II, III
- SCC of tongue can "skip" to Level III and IV
6.4 Oropharyngeal Malignancy [1]
Tonsil (commonest), tongue base, soft palate, posterior wall.
Histology [1]:
- Epithelium: SCC
- Underlying structure: lymphoma / minor salivary gland tumours
Symptoms:
- Sore throat, referred otalgia, dysphagia, odynophagia, muffled speech
- Risk factors: smoking, alcohol, oral sex (HPV-related)
Signs:
- Mass/ulcer, trismus, asymmetrical tonsil
- 50% cervical lymph node metastasis at presentation
Why is the node rate so high? The oropharynx has rich lymphatic drainage. Tonsil and tongue base tumours often present with a neck mass as the first symptom (CUP — cancer of unknown primary — think oropharynx/NPC). [2]
Metastatic pattern [2]:
- Most commonly to Level II, then III, IV, V
- Bilateral metastases common from tongue base and soft palate tumours
- Approximately 50% have nodal metastasis at presentation
6.5 Hypopharyngeal Carcinoma [1]
Level of hyoid to lower border of cricoid. Three sites: 60% piriform fossa, 30% postcricoid, 10% posterior pharyngeal wall. [1]
- Sore throat, globus → dysphagia, otalgia, hoarseness
- Risk factors: alcohol, smoking
- 30% LN metastases
- Loss of laryngeal crepitus (tumour fixes larynx to vertebral column)
- Paterson-Brown-Kelly syndrome (= Plummer-Vinson syndrome: iron deficiency anaemia + postcricoid web + dysphagia → predisposes to postcricoid carcinoma)
Paterson-Brown-Kelly / Plummer-Vinson Syndrome
Classic triad: iron deficiency anaemia + oesophageal/postcricoid web + dysphagia. More common in middle-aged women. The web is a pre-malignant condition for postcricoid SCC. Treatment: correct iron deficiency + endoscopic dilatation of web + surveillance.
10% risk of synchronous/metachronous tumour → panendoscopy required for all H&N SCC. [1]
Concept: Chronic carcinogen exposure (smoking/alcohol) causes widespread mucosal changes throughout the aerodigestive tract. This means:
- Synchronous tumour: second primary detected within 6 months
- Metachronous tumour: second primary detected > 6 months
- Oral/oropharynx cancer → increased risk of upper oesophageal cancer
- Laryngeal cancer → increased risk of lung cancer
Panendoscopy = direct laryngoscopy + bronchoscopy + OGD [2] — done to screen for second primaries.
History → Physical examination → Panendoscopy + biopsy (10% synchronous/metachronous tumour — field cancerization) → Tonsillectomy or EUA + Biopsy → USG neck +/- FNAC → CXR → CT/MRI → PET scan if necessary. [1]
| Investigation | Purpose |
|---|---|
| Panendoscopy + Bx | Tissue diagnosis + screen for synchronous tumours |
| Tonsillectomy / EUA + Bx | When tonsil is asymmetric or CUP with Level II node |
| USG neck + FNAC | Assess cervical LNs; FNAC for cytology |
| CXR | Screen for lung metastasis/second primary |
| CT scan | Bony invasion, LN staging, thorax/abdomen staging |
| MRI | Best for soft-tissue extent (especially oral cavity/oropharynx) |
| PET-CT | Distant metastasis, CUP workup, post-treatment surveillance |
6.8 Management Framework [1]
Based on TNM staging:
- Early stage (I, II): Single modality — surgery OR radiotherapy alone
- Late stage (III, IV): Combined modality — concurrent chemo-irradiation OR surgery with adjuvant RT +/- chemotherapy
General rule:
- Early stage → RT or minimally invasive surgery (laser/robotic)
- Late stage → Surgery with adjuvant treatment
BUT exceptions:
- Oral cavity and thyroid → SURGERY even in early stage
- NPC → Chemo-irradiation even in late stage [1]
Critical Exam Rule: Oral Cavity = Surgery First
Oral cavity carcinoma is preferentially treated with surgery as first-line at ALL stages because: (1) the oral cavity tolerates surgery well with acceptable functional outcomes, (2) post-RT complications in the oral cavity are severe (osteoradionecrosis of mandible, xerostomia), and (3) surgical margins are readily assessable intraoperatively (frozen section). This is a frequently tested point. [1]
Tumour clearance with long-term survival benefit + organ and function preservation. When surgery indicated: resection with adequate margins (1.5 cm radial margin, frozen section control) + reconstruction for form and function + rehabilitation (swallowing, voice, hearing). [1]
- Primary closure (for small defects)
- Flap reconstruction — may need microvascular anastomosis; restores form and function
- Options range from: minimally invasive surgery (laser/endoscopic/robotic partial pharyngectomy +/- reconstruction) to open major surgery (circumferential pharyngectomy + reconstruction, pharyngo-laryngo-oesophagectomy / PLO) [1]
Clinical presentations:
- Infective: acute and febrile
- Neoplastic (congenital/developmental/malignant): chronic and afebrile
- Airway issue in infections/abscesses
EARLY REFERRAL to ENT surgeons when suspecting malignancy:
- Persistent 2–4 weeks after conservative/empirical treatment
- Clinically suspicious: irregular, induration, > 2 cm, associated cervical LN enlargement [1]
Exam Intelligence
| Trap | Correct Thinking |
|---|---|
| Giving amoxicillin for suspected EBV tonsillitis | Causes rubelliform rash — use penicillin V or erythromycin |
| Treating oral cavity SCC with RT alone in early stage | Oral cavity = surgery first (unlike oropharynx/larynx) |
| Confusing leukoplakia with erythroplakia malignant risk | Erythroplakia (~90% CIS/SCC) >> leukoplakia (~5%) |
| Missing peritonsillar abscess because "it's just tonsillitis" | Trismus + uvula deviation + unilateral swelling = quinsy → needs I&D |
| Forgetting airway in deep neck infections | ALWAYS secure airway first in Ludwig angina, parapharyngeal/retropharyngeal abscess |
| Assuming painless oral ulcer is benign | Painless + non-healing + indurated = SCC until proven otherwise |
| NPC treatment = surgery | NPC = chemo-irradiation (NOT surgery in primary treatment) |
| Oral cavity SCC node-negative = no neck dissection | 15–20% occult nodal metastasis → elective neck dissection |
| Parapharyngeal mass + trismus = infection | Parapharyngeal TUMOUR → NO trismus, 80% benign |
| HPV-related oropharynx SCC = worse prognosis | HPV-positive = BETTER prognosis than HPV-negative |
| Feature | Acute Tonsillitis | Peritonsillar Abscess | Infectious Mononucleosis |
|---|---|---|---|
| Age | Any | Young adult | 15–24 years |
| Trismus | No/minimal | Yes | No |
| Uvula deviation | No | Yes | No |
| Lymphadenopathy | Anterior cervical | Anterior cervical | Posterior cervical + diffuse |
| Splenomegaly | No | No | 50% |
| Atypical lymphocytes | No | No | Yes |
| Treatment | Penicillin | I&D + antibiotics | Supportive; avoid ampicillin |
High Yield Summary
-
Infections
- Acute tonsillitis (GAS → penicillin; EBV → avoid ampicillin; complications → quinsy, deep neck abscess). Peritonsillar abscess = trismus + uvula deviation → I&D. Ludwig angina / deep neck abscess = secure airway first → surgical drainage + IV antibiotics + dental consultation. Acute epiglottitis = ENT emergency → do not examine throat → secure airway → IV antibiotics.
-
Pre-malignant
- Leukoplakia (5% malignant, biopsy needed). Erythroplakia (90% CIS/SCC at biopsy, 15× risk → always excise). Persistent non-healing oral ulcer > 2 weeks → refer and biopsy.
-
Malignancies
- 90% of H&N cancers are SCC. Risk factors: smoking (primary), alcohol (synergistic with smoking for hypopharynx), betel nut (oral cavity), HPV (oropharynx). Workup: panendoscopy + biopsy (field cancerization → 10% synchronous/metachronous tumours), USG + FNAC, CT/MRI, PET. Management: early stage = single modality; late stage = combined. BUT oral cavity/thyroid = surgery first at all stages; NPC = chemo-RT at all stages. Oral cavity SCC: 15–20% occult nodal metastasis → elective neck dissection. Oropharynx SCC: 50% nodal metastasis at presentation; HPV+ = better prognosis. Hypopharynx: piriform fossa commonest (60%); Paterson-Brown-Kelly syndrome for postcricoid carcinoma.
-
Cardinal rule
- Infective = acute + febrile. Neoplastic = chronic + afebrile. Early referral if persistent > 2–4 weeks, irregular, indurated, > 2 cm, or associated cervical LN.
Active Recall - Lecture Notes
[1] Lecture slides: GC 219. Infections and tumours in pharynx and oral cavity.pdf [2] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (H&N Diseases, CA Oropharynx chapters) [3] Senior notes: Adrian Lui Pediatrics Notes.pdf (p.479 — Infectious mononucleosis) [4] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.1811 — EBV pathogenesis) [5] Lecture slides: GC 220. Upper airway obstruction and tracheostomy.pdf (p.46, p.54)
GC 218 — I Have a Swelling in the Neck: Neck Mass
Combined notes from the GC 218 lecture slides and companion notes, covering the systematic assessment, investigation, and management of neck masses.
GC220 Upper Airway Obstruction And Tracheostomy
Upper airway obstruction is a partial or complete blockage of the airway above the tracheal bifurcation that may necessitate tracheostomy—a surgical opening in the anterior tracheal wall—to establish a secure airway and maintain ventilation.