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VINAYAKA MISSION'S — GENERAL SURGERY FINAL YEAR IA-2
ESSAY QUESTIONS
Q1. 60-year-old male, non-healing ulcer left buccal mucosa + hard ipsilateral neck swelling
Probable Diagnosis: Carcinoma of the Buccal Mucosa (Squamous Cell Carcinoma — Oral Cavity)
The combination of a non-healing ulcer in the buccal mucosa with a hard, ipsilateral cervical lymph node in a 60-year-old male is squamous cell carcinoma (SCC) of the buccal mucosa until proved otherwise.
Etiopathogenesis
Risk Factors (Predisposing causes):
| Factor | Mechanism |
|---|
| Tobacco — smokeless (pan, gutka, betel nut) | Nitrosamines → DNA adducts → p53 mutation |
| Smoking (bidi, cigarette) | Polycyclic aromatic hydrocarbons, oxidative damage |
| Alcohol | Acetaldehyde (carcinogen), potentiates tobacco |
| Betel nut (areca nut) | Arecoline → submucous fibrosis (premalignant) → SCC |
| Human Papillomavirus (HPV-16, 18) | E6/E7 oncoproteins inactivate p53 and Rb |
| Chronic irritation (sharp tooth, ill-fitting denture) | Repeated mucosal injury |
| Premalignant lesions | Leukoplakia (2% malignant transformation), erythroplakia (30–40%), oral submucous fibrosis |
| Nutritional deficiency | Iron, vitamins A & B complex deficiency → Paterson-Kelly syndrome |
Molecular Pathway:
- Loss of heterozygosity at 3p, 9p (p16), 17p (p53)
- Overexpression of epidermal growth factor receptor (EGFR)
- Field cancerization: entire oral mucosa exposed to carcinogens → multifocal disease
Spread:
- Local: Infiltrates buccinator, pterygoid muscles, mandible (bone invasion), skin
- Lymphatic: To submandibular (Level I), upper jugular (Level II) nodes — N2 bilateral involvement in advanced disease
- Haematogenous: Rare at presentation; lungs most common distant site
Clinical Features
History:
- Non-healing ulcer >3 weeks in buccal mucosa
- Pain (otalgia — referred via auriculotemporal nerve, V3)
- Trismus (invasion of pterygoid muscles — poor prognostic sign)
- Difficulty in chewing, altered speech
- Weight loss, dysphagia (advanced disease)
- History of tobacco/betel nut use
Examination of the primary:
- Ulcer: Irregular, indurated edges; raised, everted margins; hard base; floor covered with slough/necrotic tissue; bleeds on touch
- Surrounding mucosa: Leukoplakia, erythroplakia, submucous fibrosis may be present
- TNM assessment: Size (T), bone involvement, trismus
Regional lymph nodes (Neck):
- Hard consistency (stony hard, non-tender)
- Ipsilateral submandibular (Level I) or upper deep cervical (Level II) most common
- Fixed = extracapsular spread (N3)
- Bilateral nodes suggest advanced disease
Signs of advanced disease:
- Skin fixity, cutaneous fistula
- Mandibular involvement (panoramic X-ray shows "moth-eaten" bone)
- Trismus <3 cm = T4 disease
Staging (AJCC 8th ed — Oral Cavity SCC)
| Stage | Description |
|---|
| T1 | ≤2 cm, depth of invasion (DOI) ≤5 mm |
| T2 | ≤4 cm, DOI ≤10 mm |
| T3 | >4 cm or DOI >10 mm |
| T4a | Invades cortical bone, floor of mouth, skin; moderately advanced |
| T4b | Involves masticator space, pterygoid plates, skull base; very advanced |
Investigations
For diagnosis:
- Incisional biopsy (gold standard) — HPE confirms SCC; note degree of differentiation
- Fine needle aspiration cytology (FNAC) of neck node
Imaging:
3. OPG / Panoramic X-ray — mandible involvement
4. CT scan of neck with contrast — extent, bone erosion, node status, extranodal extension
5. MRI — soft tissue extent (preferred for tongue, floor of mouth); depth of invasion
6. CT chest / PET-CT — staging, distant metastasis
Baseline:
7. LFT, RFT, CBC, coagulation profile
8. Indirect laryngoscopy — second primary, vocal cord mobility
Management
Surgical (Mainstay for operable disease)
Primary tumor:
- Wide local excision — at least 1.5–2 cm clear margins (confirmed by frozen section intraoperatively)
- Composite resection (commando/pull-through) — if mandible involved: wide excision + marginal or segmental mandibulectomy
- Reconstruction:
- Small defects: Primary closure
- Medium: Pectoralis major myocutaneous flap (PMMF) — workhorse flap
- Large/complex: Free radial forearm flap, anterolateral thigh (ALT) free flap
Neck:
- Elective neck dissection (END): Indicated if DOI >4 mm (even N0 clinically) due to high occult nodal metastasis rate
- Therapeutic neck dissection: For clinically positive nodes (N+)
- Type: Selective (Levels I–III) for elective; Modified radical neck dissection (MRND) for N+; Radical neck dissection if structures involved
Radiation Therapy
- Post-operative radiotherapy (PORT): Indications — positive/close margins, perineural invasion, lymphovascular invasion, multiple nodes, extranodal extension, T3/T4 disease
- Dose: 60–66 Gy in 30–33 fractions
- Concurrent cisplatin with PORT if high-risk features (positive margins, extranodal extension)
Chemotherapy
- Cisplatin-based concurrent chemoradiotherapy for unresectable or recurrent disease
- Induction chemotherapy (TPF: docetaxel-cisplatin-5FU) for organ preservation or downstaging
- Cetuximab (anti-EGFR) for platinum-ineligible patients
Palliative
- Analgesics (WHO ladder), nutritional support (NG tube, PEG), tracheostomy for airway compromise
Q2. 58-year-old chronic smoker, cramp pain in right calf on walking, relieved by rest
Probable Diagnosis: Peripheral Arterial Disease (PAD) — Intermittent Claudication
The hallmark triad: effort-induced calf pain → relieves with rest → in a smoker = intermittent claudication due to PAD, almost certainly atherosclerotic.
Etiopathogenesis
Atherosclerosis is the underlying pathology in >90% of cases.
Pathological cascade:
- Endothelial injury → triggered by smoking, hypertension, hyperlipidaemia, diabetes, oxidative stress
- Lipid infiltration → LDL oxidized and taken up by macrophages → foam cells → fatty streak
- Smooth muscle cell migration from media to intima → fibrous cap formation
- Progressive plaque growth → stenosis → reduced luminal diameter
- When stenosis >50% → hemodynamic significance → reduced distal blood flow
- At rest, collateral circulation compensates; during exercise, oxygen demand increases, supply cannot match → ischemic pain (claudication)
- Muscle metabolites (lactate, H+, adenosine) accumulate → stimulate nociceptors → pain
- Pain resolves within 1–5 minutes of rest as metabolites clear
Risk factors for atherosclerotic PAD:
- Smoking (single most important modifiable risk factor; 4-fold increase)
- Diabetes mellitus (tibial vessels predominant; severe disease)
- Hypertension
- Dyslipidaemia (elevated LDL)
- Age >50, Male sex
- Chronic kidney disease
- Family history
Fontaine Classification:
| Stage | Description |
|---|
| I | Asymptomatic (ABI <0.9 but no symptoms) |
| IIa | Intermittent claudication >200 m |
| IIb | Intermittent claudication <200 m |
| III | Rest pain (Ischaemic rest pain — occurs at night, in forefoot) |
| IV | Tissue loss (ulceration, gangrene) |
This patient is Fontaine Stage IIb (claudication — requires further characterisation).
Clinical Features
Symptoms:
- Claudication distance: Distance at which calf cramp/pain begins (reproducible)
- Relief: Complete relief within 1–5 minutes of standing still (differentiates from neurogenic claudication which requires sitting/flexion)
- Affected limb: Right calf → right superficial femoral artery or popliteal stenosis likely
- No rest pain or ulceration (not critical limb ischemia — yet)
- History of smoking, possible diabetes, hypertension
Signs (Six Ps of arterial insufficiency):
- Pallor — on elevation (Buerger's angle <20° indicates severe ischemia)
- Pulselessness — reduced/absent popliteal, dorsalis pedis, posterior tibial pulses on right
- Pain — reproducible claudication
- Paraesthesia — in advanced disease
- Paralysis — in acute limb ischemia
- Perishing cold — limb cooler than contralateral
Additional findings:
- Buerger's test: Elevation blanching → dependent rubor (reactive hyperaemia)
- Capillary refill >3 seconds
- Venous guttering on elevation
- Skin: thin, shiny, hairless; toenail thickening (dystrophy)
- Bruits over iliac/femoral arteries
Investigations
Non-invasive:
- Ankle-Brachial Index (ABI) — gold standard screening
- Normal: 0.9–1.3
- Claudication: 0.6–0.9
- Rest pain: 0.3–0.6
- Tissue loss: <0.3
-
1.3 = non-compressible vessels (calcified — in diabetics)
- Duplex Doppler ultrasound — location, degree of stenosis, triphasic/biphasic/monophasic waveform
- Treadmill exercise test — objective claudication distance measurement, post-exercise ABI drop confirms PAD
- CT Angiography (CTA) — imaging of choice pre-intervention; maps entire aortoiliac-infrainguinal tree
- MR Angiography (MRA) — no contrast hazard; preferred in CKD
- Digital Subtraction Angiography (DSA) — gold standard for intervention planning (both diagnostic + therapeutic)
Bloods:
- FBC, fasting glucose, HbA1c, lipid profile, renal function
- ECG, echo (co-existing CAD common — 30–50% have significant CAD)
Management
1. Risk Factor Modification (Medical — ESSENTIAL in all patients)
- Smoking cessation: Single most important intervention — slows progression, reduces amputation risk
- Antiplatelet therapy: Aspirin 75–100 mg/day or Clopidogrel 75 mg/day (preferred in PAD per CAPRIE trial)
- Statin therapy: Atorvastatin 40–80 mg — reduces cardiovascular events AND improves claudication
- Antihypertensives: ACE inhibitors preferred (HOPE trial); β-blockers no longer contraindicated in mild PAD
- Diabetic control: HbA1c <7%
- Anticoagulation: Only if thrombotic events/AF
2. Supervised Exercise Programme (SEP)
- Most effective non-invasive treatment for claudication
- 30–45 minutes, 3×/week for ≥3 months
- Walk to near-maximum pain, rest, repeat
- Improves claudication distance by 100–150% via collateral development and metabolic adaptation
3. Pharmacotherapy
- Cilostazol (phosphodiesterase-3 inhibitor) — vasodilation + antiplatelet; improves walking distance by ~40%; contraindicated in heart failure
- Naftidrofuryl (5-HT2 antagonist) — second-line
- Pentoxifylline — modest benefit
4. Endovascular Intervention
Indications: Lifestyle-limiting claudication despite 3–6 months of conservative therapy, or critical limb ischaemia
- Percutaneous Transluminal Angioplasty (PTA) ± Stenting:
- Iliac arteries: Excellent long-term patency (5-year >80%); primary stenting preferred
- Femoral-popliteal: PTA ± drug-eluting stent (DES); covered stents (Viabahn) for long lesions
- Infrapopliteal: Balloon angioplasty for critical limb ischaemia
5. Open Surgical Revascularisation
Indications: Failed endovascular, long segment occlusions (TASC C/D), good operative risk
- Aorto-bifemoral bypass graft — aortoiliac disease (PTFE/Dacron; 5-year patency ~80%)
- Femoro-popliteal bypass — above-knee (PTFE or reversed saphenous vein), below-knee (vein preferred)
- Femoro-distal bypass — to tibial/peroneal for limb salvage
- Endarterectomy — for common femoral artery disease (profundoplasty)
6. Amputation
- Last resort for irreversible critical limb ischaemia, wet gangrene, failed revascularisation
- Below-knee amputation (BKA) preferred over above-knee (AKA) for mobility/rehabilitation
SHORT NOTES
SN 1. Dermatofibrosarcoma Protuberans (DFSP)
Definition: Low-grade, locally aggressive fibrohistiocytic sarcoma of dermis/subcutis with high local recurrence but rare metastasis.
Aetiology:
- Pathognomonic translocation: t(17;22) — fusion of COL1A1 (collagen gene) with PDGFB gene → constitutive activation of PDGFRβ → uncontrolled fibroblast proliferation
- May arise at sites of prior trauma, scarring, vaccination
Clinical Features:
- Slow-growing, painless, indurated plaque or nodule — usually on trunk (50%), proximal extremities (40%), head/neck (10%)
- Three morphological phases:
- Patch phase: Atrophic, violaceous/flesh-coloured skin plaque
- Plaque phase: Indurated, firm plaque
- Nodular phase: Multinodular, protuberant (hence the name), bluish-red, skin stretched taut
- Size: 1–5 cm typically; giant forms >20 cm described
- No regional lymphadenopathy (lymph node metastasis rare <1%)
- Aggressive fibrosarcomatous transformation (FS-DFSP) — 10–20% → higher metastatic potential
Investigations:
- Excisional/incisional biopsy + HPE
- Histology: Spindle cells in storiform (cartwheel/pinwheel) pattern; infiltration of subcutaneous fat in characteristic honeycomb/lace-like pattern
- Immunohistochemistry (IHC): CD34+, Factor XIIIa negative (differentiates from dermatofibroma)
- FISH or RT-PCR: Detection of COL1A1-PDGFB fusion gene (confirmatory)
- MRI: Assess deep extent before surgery
- CT chest for fibrosarcomatous transformation (metastasis screen)
Treatment:
- Wide local excision (WLE): 2–3 cm margins; historically standard; 20–50% local recurrence
- Mohs micrographic surgery (MMS): Treatment of choice — 1% recurrence rate vs 20% for WLE; tissue-sparing; maps all margins
- Imatinib mesylate (Gleevec): PDGFRβ inhibitor; neoadjuvant (to downsize before surgery), adjuvant, or for unresectable/metastatic disease — PDGFB fusion is predictive of response (90% response rate)
- Radiotherapy: Adjuvant if margins positive and re-excision not possible
- Prognosis: Excellent if completely excised; 5-year survival >95%
SN 2. Cardiac Tamponade
Definition: Life-threatening compression of the heart by accumulating fluid in the pericardial sac, impairing diastolic filling and reducing cardiac output.
Causes:
| Category | Examples |
|---|
| Trauma | Penetrating (stab, gunshot), blunt cardiac trauma |
| Neoplastic | Lung CA, breast CA, lymphoma — most common in medical tamponade |
| Infectious | Bacterial, viral (Coxsackie), TB pericarditis |
| Post-procedural | Post-cardiac surgery, post-pericardiocentesis, post-MI (Dressler's) |
| Renal | Uraemic pericarditis |
| Autoimmune | SLE, rheumatoid arthritis |
| Aortic dissection | Haemopericardium |
Pathophysiology:
- Normal pericardial fluid: 15–50 mL
- Rapid accumulation (even 150–200 mL) → rises above pericardial compliance threshold → intrapericardial pressure ↑ → diastolic filling impaired → stroke volume ↓ → CO ↓ → compensatory tachycardia → eventually decompensation → obstructive shock
Clinical Features — Beck's Triad (classic):
- Hypotension (reduced CO)
- Raised JVP (Kussmaul's sign — JVP rises on inspiration) / elevated CVP
- Muffled/distant heart sounds (fluid insulates sounds)
Additional signs:
- Pulsus paradoxus: >10 mmHg fall in SBP with inspiration (pathognomonic); exaggerated ventricular interdependence
- Tachycardia (compensatory)
- Tachypnoea, dyspnoea
- Cold, clammy extremities (shock)
- In chronic: Ewart's sign (dullness at left lung base from lung compression)
Investigations:
- ECG: Sinus tachycardia; electrical alternans (alternating QRS axis — pathognomonic of large effusion); low voltage complexes; PR depression in pericarditis
- CXR: Cardiomegaly — "water bottle" or "globular" heart shape (effusion >250 mL); clear lung fields (unlike LVF)
- Echocardiography (ECHO): Diagnostic gold standard
- Pericardial effusion
- RA collapse in systole (earliest sign)
- RV collapse in diastole (most specific sign of haemodynamic compromise)
- IVC plethora (non-collapsible on inspiration)
- Swinging heart motion
- CT/MRI: Characterise effusion, assess for malignancy
- Invasive: Right heart catheterization — equalisation of diastolic pressures
Treatment:
- Immediate: Pericardiocentesis (needle drainage) — emergency treatment; subxiphoid approach (Marfan's technique); ECG-guided or echo-guided; aspirate 50 mL may dramatically improve BP
- Surgical:
- Pericardiotomy/pericardial window — for recurrent effusions; subxiphoid or thoracoscopic (VATS)
- Pericardiectomy — for constrictive pericarditis (chronic)
- Treat underlying cause (antibiotics, chemotherapy, etc.)
- Do NOT give diuretics or vasodilators (they reduce preload and worsen tamponade)
SN 3. Deep Vein Thrombosis (DVT)
Definition: Thrombus formation in the deep venous system, usually of the lower limb, with potential for pulmonary embolism (PE).
Causes — Virchow's Triad:
| Component | Examples |
|---|
| Venous stasis | Prolonged immobility, long surgery, paralysis, obesity, heart failure, long-haul travel |
| Endothelial injury | Trauma, surgery, IV cannula, catheters |
| Hypercoagulability | Malignancy (Trousseau's syndrome), OCP/HRT, pregnancy, thrombophilias (Factor V Leiden, Protein C/S deficiency, antiphospholipid syndrome), nephrotic syndrome |
Clinical Features:
- Calf DVT (below-knee): Calf pain/tenderness, mild swelling, slight warmth
- Proximal DVT (popliteal, femoral, iliac): More significant swelling, pitting oedema, erythema, distended superficial veins
- Phlegmasia alba dolens ("white painful leg"): Massive DVT causing arterial spasm → white, cold, swollen, painful limb
- Phlegmasia cerulea dolens ("blue painful leg"): Massive DVT occludes venous drainage entirely → venous gangrene; blue, swollen, excruciating pain — limb-threatening
- Homan's sign: Calf pain on forced dorsiflexion — non-specific (only 50% sensitive)
- Moses sign: Calf tenderness on lateral compression
- Pyrexia, tachycardia
DVT can be asymptomatic in 50% of cases.
Investigations:
- Wells' DVT Score (pre-test probability):
- Active cancer (+1), immobility (+1), limb swelling (+1), calf asymmetry >3 cm (+1), pitting oedema (+1), collateral veins (+1), prior DVT (+1), alternative diagnosis as likely (−2)
- Score ≥2 = high probability
- D-dimer: High sensitivity (>95%), low specificity; elevated in DVT but also infection, trauma, malignancy; useful to RULE OUT DVT if negative in low/moderate probability
- Compression Duplex Ultrasonography: Non-invasive; diagnostic gold standard in clinical practice; shows non-compressible vein + absent flow Doppler
- Venography (ascending phlebography): Gold standard historically; invasive; reserved for equivocal duplex
- MRI venography: Useful for pelvic/iliac vein thrombosis
Treatment:
| Phase | Treatment |
|---|
| Initial anticoagulation (0–10 days) | LMWH (e.g. enoxaparin 1 mg/kg BD) or UFH (if renal failure/high bleeding risk) or fondaparinux; or DOAC (rivaroxaban/apixaban at therapeutic dose) — now first-line |
| Maintenance (3–6 months) | DOAC (rivaroxaban, apixaban, dabigatran) OR warfarin (INR 2–3); 3 months for provoked DVT, 6 months or longer for unprovoked or malignancy |
| Long-term | Reassess at 3 months; lifelong if recurrent DVT, antiphospholipid syndrome |
| Compression stockings | Class II (30–40 mmHg) — reduces post-thrombotic syndrome |
| Catheter-directed thrombolysis | For phlegmasia cerulea dolens, massive proximal DVT in young patient with low bleeding risk |
| IVC filter | Absolute contraindication to anticoagulation + proximal DVT; or massive PE despite anticoagulation |
| Thromboprophylaxis (prevention) | LMWH + early mobilisation + TED stockings in surgical/medical patients |
SN 4. Pleomorphic Adenoma of Parotid Gland
Definition: Most common benign tumour of the parotid gland (70–80%); "pleomorphic" because it contains a mixture of epithelial and mesenchymal (myxoid, chondroid) elements.
Clinical Features:
- Slow-growing (years), painless swelling in parotid region (pre-auricular or infra-auricular)
- Usually unilateral, solitary
- Rubbery to firm consistency; non-tender
- Mobile (not fixed) initially; bosselated/irregular surface
- Skin not involved; no skin ulceration
- Facial nerve intact (facial nerve palsy = malignancy)
- No pulsation or bruit
Complications:
- Malignant transformation → Carcinoma ex pleomorphic adenoma (5–10% with long-standing tumour; rises to 25% after 15 years)
- Recurrence after inadequate surgery (enucleation) → "seed deposits" of tumour — multinodular recurrence
- Facial nerve injury during surgery
- Frey's syndrome (auriculotemporal nerve syndrome) — sweating/flushing over cheek during eating post-parotidectomy; occurs in 40–60%
- Sialocele, haematoma (post-operative)
Investigations:
- FNAC — First-line; confirms pleomorphic adenoma (epithelial cells + stromal background); avoids excision for benign lesions; sensitivity ~80–90%
- MRI — gold standard imaging; shows characteristic intermediate T1/high T2 signal; defines extent, deep lobe involvement, nerve relationship
- CT scan — if bone involvement suspected
- Ultrasound — superficial lobe lesions; guides FNAC
Treatment:
- Superficial parotidectomy (standard operation) — removes superficial lobe with tumour, preserving facial nerve; never enucleation (high recurrence)
- Total conservative parotidectomy — if tumour in deep lobe or if uncertain about deep lobe involvement
- Extended parotidectomy ± facial nerve resection — for malignant transformation with nerve involvement
- Radiotherapy — for carcinoma ex pleomorphic adenoma post-operatively
SN 5. Thyroglossal Cyst
Definition: Cyst formed from persistence and secretion of the thyroglossal duct, the embryological tract of thyroid descent.
Embryology:
- Thyroid gland develops from foramen caecum at the junction of anterior 2/3 and posterior 1/3 of tongue (base of tongue) → descends in midline → passes anterior to/through hyoid bone → reaches final position in neck
- Thyroglossal duct normally obliterates by 7th–10th week; failure to obliterate → thyroglossal cyst, sinus, or fistula
Possible Sites:
- Intralingual (at foramen caecum) — rare
- Subhyoid (most common — 60–65%) — below hyoid bone, above thyroid cartilage
- Suprahyoid (24%)
- At the level of hyoid bone (15%)
- Suprasternal (few percent)
- Within thyroid (intrathyroidal)
Clinical Features:
- Usually presents in children <10 years; can present at any age
- Midline neck swelling (or slightly paramedian to the left)
- Moves upward on swallowing AND on protrusion of tongue — pathognomonic (because tract attached to tongue base via hyoid)
- Smooth, spherical, soft to firm, non-tender, transilluminant (if thin-walled)
- Skin not attached (unless infected)
- May become infected → thyroglossal fistula (external opening in midline below hyoid after infection/spontaneous drainage)
- Rarely: thyroglossal cyst carcinoma (1%) — papillary thyroid carcinoma most common; suspect if hard, irregular
Investigations:
- Ultrasound neck — first-line; confirms cystic nature, locates ectopic thyroid tissue in cyst wall
- Thyroid scan (Tc-99m) — BEFORE surgery: confirm normal thyroid tissue in normal position (cyst may contain the only thyroid tissue in 1–2% of cases)
- MRI — complex cysts, suspected carcinoma
- FNAC — if carcinoma suspected (thick wall, solid component)
- TFTs — to confirm euthyroid state
Treatment:
- Sistrunk's operation — standard surgery; resects:
- The entire cyst
- Central portion of body of hyoid bone
- Core of tissue from hyoid to foramen caecum (base of tongue)
- Critical: Hyoid bone central body removal reduces recurrence from 40% to <4%
- If ectopic thyroid is the only functioning thyroid → consider observation or thyroid supplementation
- Infected cyst → antibiotics first, then Sistrunk's after inflammation settles
SN 6. Retrosternal Goitre
Definition: Extension of thyroid tissue into the mediastinum such that >50% of the gland lies below the thoracic inlet.
Types:
- Primary (intrathoracic) — rare (<1%); develops from ectopic mediastinal thyroid tissue; has its own blood supply from intrathoracic vessels; no connection to cervical thyroid; harder to approach
- Secondary (descending/plunging) — majority (>95%); extension of enlarged cervical thyroid into the superior mediastinum; blood supply from inferior thyroid artery; usually anterior mediastinum
Depending on anatomical position:
- Anterior mediastinal (most common) — between trachea and sternum
- Posterior mediastinal — posterior to trachea/oesophagus; more prone to oesophageal compression
Clinical Features:
Symptoms of compression (triad of mediastinal compression):
- Tracheal compression → dyspnoea (especially on lying flat/supine), stridor, recurrent chest infections
- Oesophageal compression → dysphagia
- SVC compression → SVC syndrome: facial oedema, suffused conjunctivae, venous distension over chest wall, arm oedema, cyanosis
Additional:
- Pemberton's sign: Raising both arms above head → facial plethora, cyanosis, JVP rise (tightens thoracic inlet around goitre)
- Hoarseness (recurrent laryngeal nerve compression)
- Horner's syndrome (cervical sympathetic chain involvement)
- Plethoric facies
Investigations:
- CXR — mediastinal widening; tracheal deviation/compression; superior mediastinal mass
- CT neck and chest — imaging of choice; maps extent, vascularity, tracheal compression, relation to great vessels; plans surgical approach
- MRI — better soft tissue detail; useful to distinguish from other mediastinal masses
- Thyroid isotope scan (Tc-99m) — confirms functioning thyroid tissue in mediastinum
- TFTs — most are euthyroid; occasionally toxic or hypothyroid
- PFTs — flow-volume loop shows extrathoracic/intrathoracic obstruction
- Indirect laryngoscopy — vocal cord mobility pre-operatively
Treatment:
- Surgery is the definitive treatment — due to risk of progressive compression and malignancy (2–3%)
- Approach:
- Cervical approach alone in >90% — through standard collar incision; most secondary retrosternal goitres can be delivered digitally from mediastinum using "finger fracture" technique
- Median sternotomy — required if primary retrosternal (own blood supply), very large, malignant, cannot be delivered from above, or posterior mediastinal position
- Pre-operative preparation: Euthyroid state, vocal cord check
- Complications of surgery: Recurrent laryngeal nerve injury (1–2% bilateral = stridor/airway obstruction), hypoparathyroidism, bleeding, SVC injury, tracheomalacia (softened tracheal rings after long compression → tracheal collapse post-extubation)
- Radioiodine (I-131): For non-toxic retrosternal goitre if unfit for surgery; reduces size by 40–60%
BRIEF ANSWERS
BA 1. Clinical Features of Hyperthyroidism
Symptoms (caused by excess thyroid hormone → increased metabolic rate + sympathoadrenal activation):
Metabolic: Weight loss despite increased appetite, heat intolerance, sweating, fatigue
Cardiovascular: Palpitations, sinus tachycardia, atrial fibrillation (15%), exertional dyspnoea, angina
Neuromuscular: Nervousness, anxiety, irritability, tremor (fine, resting tremor of fingers), hyperreflexia, proximal myopathy (difficulty climbing stairs/rising from chair)
GI: Diarrhoea, increased bowel frequency
Reproductive: Oligomenorrhoea/amenorrhoea, gynaecomastia (male), reduced libido
Specific to Graves' disease:
- Exophthalmos/proptosis (thyroid eye disease — TED)
- Pretibial myxoedema (infiltrative dermopathy — skin plaques over shin)
- Thyroid acropachy (clubbing)
- Diffuse goitre with bruit
Signs:
- Warm, moist, smooth skin
- Stare and lid lag (von Graefe's sign)
- Onycholysis (Plummer's nails)
- Thyroid bruit (Graves')
- Tachycardia even at rest
- Broad pulse pressure
BA 2. Indications of Intercostal Drainage (ICD)
Drainage of:
-
Pneumothorax:
- Tension pneumothorax (immediate needle decompression first, then ICD)
- Large (>2 cm rim on CXR) spontaneous pneumothorax
- Secondary spontaneous pneumothorax (any size)
- Traumatic pneumothorax
- Persistent/recurrent pneumothorax after aspiration
-
Haemothorax — traumatic; significant (>300 mL)
-
Haemopneumothorax
-
Pleural effusion:
- Exudative effusion not responding to medical treatment
- Malignant pleural effusion (symptom relief; pleurodesis)
- Empyema thoracis (pus in pleural cavity) — free-flowing empyema; fibrinopurulent stage
-
Empyema/Pyothorax — frank pus (frank empyema)
-
Post-operative:
- After thoracotomy
- After oesophagectomy
- After cardiac surgery (mediastinal drains)
-
Chylothorax (thoracic duct injury)
Procedure: 5th intercostal space, mid-axillary line (safe triangle: anterior axillary line, posterior axillary line, 5th ICS); insert drain over upper border of lower rib (to avoid neurovascular bundle on inferior border); connect to underwater seal drain.
BA 3. Flail Chest
Definition: Paradoxical movement of a segment of chest wall due to fracture of ≥3 consecutive ribs in ≥2 places (anterior + posterior fracture of same rib), resulting in a "free-floating" segment.
Pathophysiology:
- The flail segment moves inward during inspiration (paradoxical — opposes normal outward movement) and outward during expiration
- This reduces tidal volume, causes hypoxia
- Main cause of respiratory failure is NOT the paradoxical movement but the underlying pulmonary contusion — alveolar haemorrhage, oedema, reduced compliance
- Splinting due to pain → hypoventilation → atelectasis → pneumonia
Clinical Features:
- History of severe chest trauma (RTA, crush injury)
- Dyspnoea, tachypnoea, hypoxia (SpO2 low)
- Paradoxical movement of chest wall segment (visible or palpable)
- Tenderness/crepitus over multiple rib fractures
- Associated injuries: pneumothorax, haemothorax, cardiac contusion
Investigations:
- CXR: Multiple rib fractures, pulmonary contusion (ground-glass opacity)
- CT chest: Superior — detects rib fractures, contusion, pneumo/haemothorax precisely
- ABG: Hypoxia, hypercapnia (type II respiratory failure in severe cases)
Management:
- Immediate: Oxygen (high flow), analgesia (pain relief crucial for adequate breathing)
- Analgesia: IV opioids, intercostal nerve block, epidural analgesia (gold standard for thoracic pain — allows deep breathing)
- Respiratory support: If SpO2 <90% or PaO2 <60 mmHg → CPAP/BiPAP; intubation + mechanical ventilation (IPPV) if severe respiratory failure — acts as "internal pneumatic stabilisation"
- Treat associated injuries: ICD for pneumo/haemothorax
- Surgical rib fixation (ORIF): Now increasingly used for severe flail chest — reduces ICU stay, ventilation duration, and long-term chest deformity
- Physiotherapy, nutritional support
BA 4. Clinical Types of Melanoma
Four main clinical-histological subtypes:
| Type | Frequency | Site | Key Features |
|---|
| Superficial Spreading Melanoma (SSM) | 70% (most common) | Back (male), legs (female) | Flat/slightly elevated; irregular pigmented plaque with notched border; variegated colour (brown, black, pink, white); prolonged radial growth phase |
| Nodular Melanoma (NM) | 15–20% | Trunk, head, neck | Rapidly growing blue-black or red-black nodule; may bleed/ulcerate early; NO radial growth phase — vertical growth only from start; worst prognosis |
| Lentigo Maligna Melanoma (LMM) | 5–10% | Face/sun-exposed areas; elderly | Arises in lentigo maligna (Hutchinson's freckle); large, flat, irregular brown lesion → central darkening/nodule; slow progression; best prognosis |
| Acral Lentiginous Melanoma (ALM) | 5–10% (most common in Asians/Africans) | Palms, soles, subungual | Irregular pigmented lesion; Hutchinson's sign: periungual pigmentation; often misdiagnosed as fungal nail; equal gender incidence across races |
Remember ABCDE criteria for clinical diagnosis:
- Asymmetry, Border irregularity, Colour variation, Diameter >6 mm, Evolution (change over time)
BA 5. Smoking Index and Pack Year Index
Smoking Index (SI):
- Used in India
- Formula: Smoking Index = Number of cigarettes/bidis smoked per day × Number of years of smoking
- SI ≥300 → significant risk; SI ≥600 → heavy smoker with high COPD/cancer risk
- Example: 15 cigarettes/day × 20 years = SI of 300
Pack Year Index (PYI):
- Used internationally (standardised)
- Formula: Pack Years = (Number of cigarettes per day ÷ 20) × Number of years smoked
- 1 pack = 20 cigarettes
- Example: 20 cigarettes/day (1 pack/day) × 30 years = 30 pack years
- 40 pack years = significant threshold for lung cancer risk
- Used for COPD staging, lung cancer screening (LDCT recommended if ≥20 pack years, age 50–80)
- Does not account for depth of inhalation, cigar/pipe smoking
BA 6. Shionoya's Criteria for Buerger's Disease (Thromboangiitis Obliterans)
Buerger's disease = non-atherosclerotic, segmental, inflammatory thrombotic occlusion of small/medium vessels in young male smokers.
Shionoya's Criteria (all 5 must be present for diagnosis):
- Smoking history — patient is a smoker (or recent ex-smoker)
- Onset before age 50 years — affects young men predominantly
- Infrapopliteal arterial occlusions — involvement of below-knee arteries (tibial, peroneal vessels); may also involve upper limb (radial, ulnar)
- Upper limb involvement OR phlebitis migrans — superficial migratory thrombophlebitis (hallmark); can affect arms (differentiated from atherosclerosis)
- Absence of atherosclerotic risk factors other than smoking — no diabetes, hypertension, hyperlipidaemia (to exclude atherosclerosis)
Clinical picture: Young male smoker, bilateral claudication, rest pain, digital ischaemia/gangrene of toes and fingers, migratory thrombophlebitis of superficial veins.
BA 7. Complications of Varicose Veins
Varicose veins = dilated, tortuous, superficial veins due to incompetent valves (saphenofemoral junction most common).
Complications:
- Haemorrhage — rupture of varicosity → severe bleeding (especially if standing); may be life-threatening; subdermal haemorrhage
- Superficial Thrombophlebitis — painful, tender, red, cord-like thrombosed varicosity; risk of proximal extension to deep veins
- Venous (varicose) Eczema — chronic inflammatory skin change over lower 1/3 of leg; itchy, eczematous, pigmented skin
- Lipodermatosclerosis — chronic fibrotic change of skin and subcutaneous fat; inverted champagne bottle appearance; precedes ulceration
- Haemosiderin pigmentation — brown discolouration from haemosiderin deposition (RBC extravasation)
- Venous/Varicose Ulcer — most serious complication; "gaiter area" (medial malleolus); shallow, large, sloping edges, painless, granulating base, surrounding lipodermatosclerosis; recurrent
- Atrophie blanche — white sclerotic patches over lipodermatosclerotic skin; avascular
- Calcification — phleboliths in thrombosed varicosities
- DVT — extension of thrombophlebitis; or de novo in venous stasis
BA 8. Premalignant Conditions of Oral Cavity
Potentially malignant disorders (WHO term):
| Condition | Description | Malignant Transformation Rate |
|---|
| Leukoplakia | White patch that cannot be wiped off; not attributable to any other disease; commonest (most frequent) | 2–4% overall; speckled/verrucous type ~10–15%; floor of mouth/ventral tongue = highest |
| Erythroplakia | Red velvety patch; less common but most sinister | 30–40% already carcinoma in situ at biopsy |
| Oral Submucous Fibrosis (OSMF) | Areca nut-induced fibrous bands; trismus; burning sensation; progressive stiffness | 5–7% (up to 10%) |
| Oral Lichen Planus (OLP) | Erosive/atrophic type; white striae (Wickham's striae) with erosions | 0.5–3% (erosive type) |
| Actinic cheilitis | Chronic sun damage to lower lip; scaling, blurring of vermilion border | 10–20% |
| Sideropenic dysphagia (Plummer-Vinson/Paterson-Kelly) | Iron-deficiency anaemia + dysphagia + angular stomatitis; post-cricoid web | Increased risk of post-cricoid carcinoma |
| Chronic hyperplastic candidiasis | Speckled leukoplakia; Candida infection | ~10% |
BA 9. Complications of Parotidectomy
Immediate:
- Haemorrhage / haematoma — reactionary haemorrhage most dangerous; may compress airway
- Airway obstruction (haematoma)
Early:
3. Facial nerve injury — most feared complication:
- Temporary palsy (neurapraxia) — 15–25%; recovers within 6 months
- Permanent palsy — 1–3% for benign disease; higher for malignancy
- Features: lagophthalmos, ectropion, inability to close eye → corneal exposure keratitis; drooping of corner of mouth; loss of forehead creases
- Sialocele — saliva pooling under skin flap; treated by aspiration ± pressure dressing; usually resolves
- Salivary fistula (if duct not properly ligated) — rare
- Wound infection
Late:
7. Frey's Syndrome (Auriculotemporal nerve syndrome) — most common late complication (40–60%):
- Aberrant reinnervation of sweat glands by parasympathetic secretomotor fibres (from auriculotemporal nerve)
- Gustatory sweating and flushing over cheek/preauricular area during eating
- Diagnosis: Minor's starch-iodine test (skin turns blue over sweating area when eating)
- Treatment: Botulinum toxin injection (effective); antiperspirant; tympanic neurectomy
- Tumour recurrence — especially with inadequate margins or after enucleation (for pleomorphic adenoma)
- Numbness of ear lobe (great auricular nerve division — inevitable in most cases)
- Trismus — rare; from fibrosis
BA 10. Stages of Tuberculosis Lymphadenitis
TB lymphadenitis is the most common form of extrapulmonary TB; cervical nodes (scrofula) most commonly involved, particularly posterior triangle.
Staging by Sharma and Mohanan (most widely used in surgical practice):
| Stage | Pathology | Clinical Features |
|---|
| Stage I — Reactive lymphadenitis | Hyperplastic reactive nodes; follicular hyperplasia | Discrete, firm, mobile, non-tender lymph nodes; no constitutional symptoms yet |
| Stage II — Periadenitis | Capsule involved; adjacent nodes begin to mat together | Matted nodes (nodes stuck together); rubbery; no fluctuation |
| Stage III — Caseation / Cold Abscess | Central caseation and necrosis within node; pus accumulation | Fluctuant, non-tender swelling ("cold abscess" — absent warmth/erythema); pus is cheesy/caseous; no signs of inflammation (hence "cold") |
| Stage IV — Collar Stud Abscess | Deep fascia is perforated; pus tracks through platysma/deep fascia → subcutaneous compartment | Bilocular abscess with "collar stud" or "shirt stud" configuration: deep component + superficial component connected by narrow neck through fascia; classic sign of tubercular abscess |
| Stage V — Sinus | Skin breaks down; abscess discharges spontaneously | Discharging sinus — chronic, non-healing; discharges thin, watery pus with cheesy material; edges are bluish-purple, undermined, indurated |
Diagnosis: Mantoux test, FNAC/biopsy (AFB stain, culture, CBNAAT/GeneXpert), CXR, CECT neck, LFT/RFT baseline before ATT.
Treatment: Anti-tubercular therapy (ATT) — 2HRZE + 4HR (6 months total); nodes may paradoxically enlarge initially (immune reconstitution phenomenon). Surgery only for diagnostic excision or persistent sinus — not routine.
All answers follow the Sabiston Textbook of Surgery, Bailey & Love's Short Practice of Surgery, and Cummings Otolaryngology content framework, cross-referenced with current surgical practice.