Here are comprehensive surgery exam notes covering all the topics you listed, drawn from Pye's Surgical Handicraft, Goldman-Cecil Medicine, Robbins Pathology, and Schwartz's Principles of Surgery.
SURGERY EXAM NOTES: VASCULAR DISEASES
SECTION 5: ARTERIAL DISEASE
a. Investigations in Arterial Disease
Non-invasive (bedside/outpatient):
- Ankle-Brachial Index (ABI): Ratio of highest systolic BP at ankle to highest systolic BP at arm. Measured with a hand-held Doppler probe.
-
0.90 = Normal
- 0.71-0.90 = Mild obstruction
- 0.41-0.70 = Moderate obstruction
- 0.00-0.40 = Severe obstruction
- Continuous-wave Doppler: Detects flow velocity, direction and quality of signal (triphasic = normal; monophasic = severe disease)
- Treadmill exercise testing: Exposes claudication; post-exercise ABI drop confirms PAD
- Duplex ultrasonography: Combines B-mode imaging with Doppler flow analysis; maps stenosis and occlusion; identifies false aneurysms and DVT
Imaging:
- Digital Subtraction Angiography (DSA): Gold standard for PAD; defines anatomy, site and extent of occlusion, collateral flow and "run-off" before surgery. Needs iodinated contrast; risk of contrast nephropathy (~0.1% severe allergy)
- CT Angiography (CTA): Non-invasive, high resolution 3D reconstruction of vessels
- MR Angiography (MRA): No ionizing radiation; good for renal failure patients (gadolinium, not iodine)
- Intraoperative arteriography / flow measurement: Confirms patency after repair
Other:
- Full blood count, ESR, lipid profile, blood glucose, HbA1c, renal function, coagulation screen
- ECG and echocardiogram (assess cardiac source of emboli)
- Chest X-ray
b. Assessment of a Case of Peripheral Vascular Disease (PVD)
History:
- Claudication: Pain in calf, thigh, or buttock on walking; relieved by rest (< 2 min). Note: walking distance, progression
- Rest pain: Severe, burning pain in foot/toes at night; relieved by hanging foot down
- Ulceration / gangrene
- Risk factors: smoking (2-3x more likely than for CAD), diabetes, hypertension, hyperlipidaemia, age >65, family history
- Co-existing disease: cardiac, cerebrovascular, renal
Examination:
- Inspect: skin - pallor, cyanosis, dependent rubor, loss of hair, trophic nail changes, ulcers, gangrene
- Palpate: temperature (cool), capillary refill, pulses (femoral, popliteal, posterior tibial, dorsalis pedis)
- Auscultate: bruits over aorta, iliacs, femorals
- Buerger's angle: limb raised - note angle at which pallor appears (<20° = severe ischaemia); dependent rubor on lowering = positive Buerger's sign
- ABPI measurement
Differential diagnosis of claudication:
- Lumbosacral root irritation
- Hip/knee arthritis (pain on weight-bearing, not walking distance-dependent)
- Chronic venous insufficiency
- Neurogenic claudication (spinal stenosis - walking distance variable, relieved by sitting/flexion not just rest)
Fontaine Classification:
| Stage | Features |
|---|
| I | Asymptomatic |
| IIa | Mild claudication (>200 m) |
| IIb | Moderate-severe claudication (<200 m) |
| III | Ischaemic rest pain |
| IV | Ulceration / gangrene |
c. Embolism
Sources (the 4 Hs):
- Heart (most common): Atrial fibrillation (mural thrombus in LAA), recent MI, dilated cardiomyopathy, rheumatic valve disease, prosthetic valves, infective endocarditis
- Proximal aorta/iliac: Atherosclerotic plaques, aneurysm thrombus ("cholesterol embolism")
- Paradoxical embolism: Via patent foramen ovale from venous system
- Fat/air/amniotic fluid embolism (non-thrombotic)
Clinical features of Acute Limb Ischaemia - The "6 Ps":
- Pain - sudden, severe
- Pallor - cold, white
- Pulselessness - distal pulses absent
- Paraesthesia - "pins and needles" = early neurological sign
- Paralysis - late, indicates irreversibility (muscle necrosis)
- Perishing cold (Poikilothermia)
Embolism vs Thrombosis (in situ):
| Feature | Embolism | Thrombosis |
|---|
| Onset | Sudden (seconds-minutes) | Gradual (hours-days) |
| Prior claudication | No | Yes |
| Contralateral pulses | Normal | Absent or reduced |
| AF / cardiac disease | Usually present | Absent |
| Collaterals | Absent | Developed |
Management:
- Emergency: IV heparin immediately (5000 units bolus)
- Surgical embolectomy: Fogarty balloon catheter via femoral arteriotomy (within 4-6 hours ideally)
- Thrombolysis: Intra-arterial tissue plasminogen activator (tPA) for thrombosis or emboli in poor surgical candidates
- Post-procedure: Warfarin / DOAC long-term; treat source
d. Thromboangiitis Obliterans (Buerger Disease)
Definition: Nonatherosclerotic, segmental inflammatory disorder affecting small and medium-sized arteries, veins, and nerves, predominantly of extremities - Robbins Pathology.
Epidemiology:
- Young males, typically <35 years
- Heavy cigarette smokers (strongly associated; direct EC toxicity or immune response to tobacco antigens)
- Increased prevalence in Israel, India, Japan; associated with certain MHC haplotypes
Pathology:
- Segmental, thrombosing acute and chronic inflammation of tibial and radial arteries
- Thrombus contains micro-abscesses (neutrophils surrounded by granulomatous inflammation) - pathognomonic
- Extends to contiguous veins and nerves (unique - not seen in other vasculitides)
- Eventually all three structures encased in fibrous tissue
Clinical Features (triad):
- Raynaud phenomenon
- Instep claudication (foot pain on exercise)
- Superficial migratory nodular phlebitis
- Progresses to rest pain, ulceration, and digital gangrene
- Microangiography shows "corkscrew" collateral vessels (characteristic finding)
Diagnosis:
- Clinical: young male smoker + distal ischaemia + migratory phlebitis
- Exclude atherosclerosis (lipid profile, normal in TAO)
- Arteriography: segmental occlusions in small vessels, corkscrew collaterals
- No reliable serology
Management:
- Absolute cessation of smoking - only proven effective intervention
- Sympathectomy - may provide some relief
- Prostaglandins (iloprost) - vasodilation, some evidence
- Amputation inevitable if smoking continues
e. Arteriosclerosis
Definition: Generic term for hardening and loss of elasticity of arterial walls. Three main types:
- Atherosclerosis - most common; intimal plaques
- Monckeberg medial calcific sclerosis: Calcium deposits in the media of muscular arteries (not intima); does not narrow lumen; vessels palpable as "pipestem"; not usually clinically significant
- Arteriolosclerosis: Affects small arteries/arterioles; two types:
- Hyaline arteriolosclerosis: homogeneous pink hyaline thickening of wall; associated with benign hypertension and diabetes
- Hyperplastic arteriolosclerosis: "onion-skin" concentric laminated thickening; associated with malignant hypertension
f. Atherosclerosis and Aneurysms
Atherosclerosis
Definition: Chronic inflammatory disease of large and medium arteries characterised by accumulation of lipid-laden plaques (atheromas) in the intima.
Risk factors:
- Non-modifiable: Age, male sex, family history
- Modifiable: Smoking, hypertension, hyperlipidaemia, diabetes mellitus, obesity, sedentary lifestyle
Pathogenesis (Response-to-injury hypothesis):
- Endothelial injury (shear stress, oxidised LDL, smoking, hypertension)
- LDL enters intima, oxidised by free radicals
- Monocyte recruitment → macrophages → engulf ox-LDL → foam cells → fatty streak
- Smooth muscle cell migration from media, proliferation, collagen deposition → fibrous cap
- Lipid core + fibrous cap = atheromatous plaque
Complications of plaques:
- Calcification (stable)
- Ulceration / rupture → thrombosis (acute MI, stroke, acute limb ischaemia)
- Haemorrhage into plaque
- Aneurysm formation (weakening of media)
- Embolisation of plaque fragments
Clinical manifestations:
- Coronary: Angina, MI
- Cerebrovascular: TIA, stroke
- Peripheral: Claudication, rest pain, gangrene
- Renal: Renovascular hypertension
- Mesenteric: Intestinal angina
Aneurysms
Definition: Pathological localised dilatation of an artery to >1.5x its normal diameter.
Types:
- True aneurysm: Involves all three layers (intima, media, adventitia) - e.g. AAA, popliteal
- False (pseudo) aneurysm: Breach in all three layers, contained by perivascular tissue - e.g. post-traumatic, anastomotic
- Dissecting aneurysm: Blood tracks between layers of media - e.g. aortic dissection
By shape:
- Fusiform (symmetric, circumferential)
- Saccular (asymmetric outpouching)
Abdominal Aortic Aneurysm (AAA):
- Defined as aorta >3 cm; >5.5 cm = indication for repair
- 90% are infrarenal
- Cause: Atherosclerosis + proteolytic degradation of elastin/collagen
- Risk: Rupture (5-year risk: 25% if >5 cm, 30-40% if >7 cm)
- Symptoms: Pulsatile, expansile mass; back/flank pain; rupture = "haemodynamic collapse + abdominal pain + pulsatile mass" = EMERGENCY
- Investigation: USS screening; CT for planning
- Treatment: Elective open repair or EVAR (endovascular aneurysm repair)
Popliteal Aneurysm:
- Most common peripheral aneurysm
- Complications: Thrombosis, embolisation, rupture
- Treatment: Bypass (with saphenous vein or Dacron)
Femoral Aneurysm:
- Similar natural history to popliteal
- Treatment: Primary repair with vein or Dacron interposition
g. Gangrene
Definition: Necrosis of tissue with superadded putrefaction (bacterial infection of dead tissue).
Types:
| Type | Features |
|---|
| Dry gangrene | Arterial occlusion only; tissue mummified, shrunken, black; clear line of demarcation; no infection; no smell |
| Wet gangrene | Arterial occlusion + venous obstruction + bacterial infection; swollen, blistered, foul smell; NO clear demarcation; spreads rapidly |
| Gas gangrene | Clostridium perfringens; crepitus due to gas in tissues; profound toxaemia; EMERGENCY |
| Diabetic gangrene | Mixed - neuropathy + ischaemia + infection; pressure points (toes, heel) |
| Hospital gangrene | Spreading necrotising fasciitis in wounds |
Pathophysiology:
- Critical limb ischaemia: Defined by rest pain + ulceration/gangrene; ABI typically <0.40
- Tissue hypoxia → cell death → liquefaction necrosis (wet) or coagulative necrosis (dry)
- Demarcation line forms between viable and non-viable tissue
Management:
- Dry gangrene: Allow to autoamputate OR elective amputation after demarcation; revascularise if possible
- Wet/gas gangrene: Emergency; IV antibiotics, debridement, possible amputation; gas gangrene requires hyperbaric oxygen + high-dose penicillin
h. Conservative Management of an Ischaemic Limb
Aims: Improve walking distance, prevent progression, reduce cardiovascular risk, control symptoms.
1. Risk factor modification:
- Stop smoking (single most important intervention)
- Control diabetes (target HbA1c <7%)
- Control hypertension (target <130/80)
- Statin therapy (lipid-lowering; also pleiotropic benefit on plaque stability)
- Control weight, encourage physical activity
2. Exercise therapy:
- Supervised exercise programme: 30-45 min walking 3x/week for 3-6 months
- Improves claudication distance by stimulating collateral development and muscle oxidative capacity
- First-line before revascularisation for stable claudication
3. Antiplatelet therapy:
- Aspirin 75-100 mg/day OR clopidogrel 75 mg/day
- Reduces MI, stroke and vascular death (not directly claudication)
4. Vasodilators / drugs for claudication:
- Cilostazol (phosphodiesterase-3 inhibitor): Improves walking distance; also antiplatelet (first-line drug for claudication)
- Naftidrofuryl (5HT2 antagonist): Modestly improves claudication
5. Anticoagulation:
- Only for acute limb ischaemia (heparin) or after bypass surgery
- Not routinely for claudication
6. Foot care (especially in diabetics):
- Regular inspection, nail care, avoid tight footwear
- Early treatment of infection
- Pressure-relieving footwear
7. Analgesia:
- Rest pain: Opioids (morphine) short term; gabapentin for neuropathic component
- Elevation of head of bed (dependent position of foot reduces rest pain by gravity-assisted perfusion)
8. Treatment of ulcers:
- Clean wound, offload pressure, control infection (systemic antibiotics)
- Wound debridement, silver dressings; negative pressure wound therapy
i. Surgical Management - Direct Arterial Surgery
Indications:
- Critical limb ischaemia (CLI) - rest pain, gangrene, non-healing ulcers
- Severe claudication unresponsive to conservative treatment
- Acute limb ischaemia
Principles:
- Adequate imaging (arteriography/CTA/MRA) to define inflow, stenosis and outflow ("run-off")
- Intraoperative angiography/flow measurements to confirm patency
Procedures:
1. Embolectomy
- Fogarty balloon catheter passed distal to embolus → balloon inflated → catheter withdrawn, extracting clot
- Done via femoral arteriotomy under local anaesthetic
- For acute embolic occlusion within 6 hours ideally
- Post-op heparin → long-term anticoagulation
2. Endarterectomy
- Surgical removal of atheromatous intima and media from within vessel
- Best for short segment stenosis, e.g. carotid (CEA) or common femoral
- Carotid Endarterectomy (CEA): For symptomatic carotid stenosis >70%; temporary shunt to maintain cerebral perfusion during clamping
3. Bypass Grafting
- A conduit is anastomosed proximal and distal to the occlusion
- Conduit options:
- Autologous vein (long saphenous vein) - preferred; best long-term patency; reversed or in-situ
- Synthetic grafts - Dacron or PTFE; used when vein unavailable or for large vessels
- Common operations:
- Aorto-bifemoral bypass: For aortoiliac occlusive disease (Leriche syndrome)
- Femoro-popliteal bypass: For superficial femoral artery occlusion (above or below knee)
- Femoro-tibial bypass: For distal tibial disease (limb salvage)
- Axillo-bifemoral bypass (extra-anatomical): For patients unfit for laparotomy
- Femoro-femoral crossover: For unilateral iliac occlusion
4. Percutaneous Transluminal Angioplasty (PTA) & Stenting
- Balloon catheter expands stenotic segment; stent may be placed
- First-line for short segment aortoiliac or iliac stenosis
- Drug-eluting stents / drug-coated balloons improve long-term patency
- Increasingly preferred over open surgery (lower morbidity)
5. Sympathectomy
- Lumbar sympathectomy: Destroys sympathetic chain (L2-L3) → vasodilation in skin
- Reduces rest pain, promotes healing of minor ulcers
- Does NOT improve claudication (muscle blood flow not sympathetically mediated)
- Chemical (phenol injection) or surgical
- Used in inoperable cases with rest pain
6. Amputation
- Last resort after failed revascularisation or non-viable limb
- Levels: Digital → Ray → Transmetatarsal → Syme's → Below-knee (preferred if possible) → Knee disarticulation → Above-knee → Hip disarticulation
- Below-knee amputation preferred when possible (better prosthetic rehabilitation)
- Guillotine amputation: Emergency, for septic gangrene; formal closure later
- Indication: Gangrene (dry - elective; wet - emergency), rest pain with no revascularisation option, failed bypass, malignancy
SECTION 6: VENOUS DISEASES
a. Varicose Veins
Definition: Dilated, tortuous, superficial veins of the lower limb resulting from incompetence of venous valves allowing retrograde (reflux) blood flow.
Anatomy:
- Long saphenous vein (LSV): Medial side of leg, joins femoral vein at saphenofemoral junction (SFJ) in groin
- Short saphenous vein (SSV): Posterior leg, joins popliteal vein at saphenopopliteal junction (SPJ) in popliteal fossa
- Perforating (communicating) veins: Connect superficial to deep system; valves normally direct flow superficial → deep
Pathophysiology:
- Primary varicose veins: Inherited valve weakness / wall weakness
- Secondary varicose veins: DVT (destroys deep vein valves → high deep venous pressure transmitted to superficial system), pelvic tumour, pregnancy
Clinical features:
- Unsightly dilated veins
- Aching, heaviness, cramps (worse in evening, better with elevation)
- Ankle oedema
- Complications: Superficial thrombophlebitis, varicose eczema, lipodermatosclerosis, haemorrhage, venous ulcer
Assessment:
- Trendelenburg test: Leg elevated to drain varices → tourniquet applied at suspected incompetent junction → patient stands up. If varices remain empty = incompetent junction correctly identified; release tourniquet → rapid filling confirms site
- Doppler: Demonstrates reflux in superficial system; identifies sites of incompetence
- Duplex USS: Maps SFJ, SPJ, perforators; confirms deep vein patency; pre-operative planning
Treatment:
Conservative:
- Graduated compression stockings (Class 2): For elderly/unfit; reduces symptoms, prevents progression
Injection Sclerotherapy:
- Sclerosant (e.g. ethanolamine oleate, sodium tetradecyl sulphate - STS, foam sclerotherapy) injected into vein → thrombosis and fibrosis
- Vein immediately compressed with bandage for ≥7 days
- Does NOT address source of incompetence → higher recurrence rate than surgery
- Best for: Thread veins, residual varicosities after surgery, short SSV incompetence
Surgical Treatment:
- Sapheno-femoral disconnection (Trendelenburg operation): Flush ligation of LSV at SFJ with all tributaries tied
- Long saphenous vein stripping: From groin to knee (below knee - risk of saphenous nerve injury)
- Multiple stab avulsions: Residual varices removed through tiny incisions
- Sapheno-popliteal disconnection: For SSV incompetence
Endovascular (modern):
- EVLA (Endovenous Laser Ablation): Laser fibre inserted into vein, thermal obliteration; day-case; equivalent outcomes to surgery
- Radiofrequency ablation (RFA): Similar mechanism
b. Superficial and Deep Vein Thrombosis
Superficial Vein Thrombosis (SVT) / Thrombophlebitis
Features:
- Tender, cord-like, red, inflamed vein
- Low risk of PE
- Treatment: NSAIDs, compression, elevation, early mobilisation; fondaparinux if extensive
Deep Vein Thrombosis (DVT)
Virchow's Triad (causative factors):
- Venous stasis: Immobility, surgery, long flights, cardiac failure
- Hypercoagulability: Malignancy, OCP, pregnancy, thrombophilia (Factor V Leiden, antiphospholipid syndrome)
- Endothelial damage: Trauma, surgery, IV catheter
Clinical Features:
- Calf pain, tenderness, swelling, pitting oedema
- Increased warmth, distended superficial veins
- Homans' sign (calf pain on dorsiflexion) - non-specific
- Phlegmasia alba dolens: Massive DVT with pale, oedematous, painful limb
- Phlegmasia cerulea dolens: Massive DVT + arterial spasm; cyanotic, extreme pain; may progress to venous gangrene
Diagnosis:
- Wells score to pre-test probability
- D-dimer: Sensitive but not specific; if low probability + negative D-dimer → DVT excluded
- Duplex ultrasonography: Investigation of choice; compressibility of vein = gold standard
- Venography (rarely used now; contrast-ascending venography)
Complications:
- Pulmonary embolism (PE) - most feared
- Post-thrombotic syndrome: Chronic venous insufficiency
- Venous gangrene
Treatment:
- Therapeutic anticoagulation: LMWH → DOAC (rivaroxaban/apixaban) or warfarin for 3-6 months
- Minimum 3 months for provoked DVT; 6+ months for unprovoked or cancer-associated
- Compression stockings to reduce post-thrombotic syndrome
- IVC filter: If anticoagulation contraindicated + recurrent PE
- Catheter-directed thrombolysis: For massive ilio-femoral DVT / phlegmasia
c. Chronic Venous Ulcers
Definition: Full-thickness skin loss above the medial malleolus due to sustained venous hypertension.
Pathophysiology:
- Venous valve incompetence → sustained venous hypertension → capillary leak → fibrin cuff around capillaries → tissue hypoxia → ulceration
- Site: Gaiter area (medial malleolus, medial lower 1/3 leg) - area of most perforator incompetence
Features:
- Shallow, irregular edges, sloping margins, pink granulation base
- Surrounding skin: Varicose eczema, haemosiderin pigmentation (brown), lipodermatosclerosis, atrophie blanche
- Painless (unless infected or arterial component)
- Cf. arterial ulcer: Deep, "punched-out," painful, toes/heel/pressure points, no oedema
Assessment:
- Exclude arterial component: Measure ABPI (>0.8 = compression safe; <0.5 = contraindication to compression)
- Ascending venogram / ambulatory venous pressure if deep vein damage suspected
Treatment:
- Bed rest with elevation of leg to reduce venous hypertension
- Wound care: Wound swab for culture; systemic (not topical) antibiotics for infection; debridement
- Compression bandaging: 4-layer bandage (Charing Cross technique) even ambulatory; emptying dilated veins, aiding muscle pump
- Once healed: Graduated compression stockings to prevent recurrence
- Surgical: Ligate incompetent perforating veins (once ulcer healed, demonstrated on venography); strip associated varicose veins
SECTION 7: LYMPHATICS AND LYMPH NODES
a. Lymphangitis and Lymphatic Obstruction (Filariasis)
Lymphangitis
Definition: Inflammation of lymphatic channels, usually due to bacterial infection (group A Streptococcus, Staphylococcus aureus).
Features:
- Red streaks running proximally from wound toward regional lymph nodes
- Tender, warm
- Fever, rigors, systemic toxicity
- Regional lymphadenopathy
- Can progress to septicaemia
Treatment:
- Rest, elevation of limb
- IV/IM penicillin (Streptococcal) or cloxacillin/flucloxacillin (Staphylococcal)
- Treat primary source of infection
Lymphoedema (Lymphatic Obstruction)
Types:
- Primary lymphoedema: Congenital abnormality of lymphatics
- Congenital (Milroy disease): Present at birth; autosomal dominant; lower limb
- Praecox: Onset at puberty/early adult life (most common); females > males
- Tarda: Onset after 35 years
- Secondary lymphoedema: Damage to lymphatics by:
- Filariasis (most common worldwide)
- Malignancy (direct invasion or nodal metastasis)
- Surgery (block dissection of lymph nodes, e.g. axillary clearance → arm oedema)
- Radiotherapy (fibrosis)
- Recurrent cellulitis / streptococcal lymphangitis
Filariasis
Cause: Wuchereria bancrofti (most common), Brugia malayi, Brugia timori
Transmission: Bite of Culex mosquito
Mechanism: Adult filariae live in lymphatics → inflammatory reaction → lymphatic obstruction → lymphoedema
Features:
- Acute: Filarial fever, acute lymphangitis, epididymo-orchitis
- Chronic: Elephantiasis - massive non-pitting lymphoedema of lower limbs, scrotum, labia
- Chyluria (milky urine), hydrocele, chylous ascites
Diagnosis: Night blood smear for microfilariae (W. bancrofti microfilariae are nocturnally periodic); immunochromatographic card test
Treatment:
- Diethylcarbamazine (DEC) - kills microfilariae and some adult worms
- Albendazole + ivermectin (single dose, annual) - for mass drug administration
- Doxycycline (targets Wolbachia endosymbiont of filariae)
- Surgical: Excision of redundant skin/tissue; scrotal surgery; lymphovenous bypass (specialised)
Investigation of lymphoedema:
- Isotope lymphography (lymphoscintigraphy): Gold standard for mapping lymphatic flow
- Lymphangiography (oil contrast): Defines lymphatic anatomy
- MRI: Differentiates lymphoedema from lipoedema
Clinical features of lymphoedema:
- Non-pitting oedema (early may be pitting; late = non-pitting due to fibrosis)
- Stemmer sign: Unable to pinch skin fold at base of second toe (pathognomonic)
- Hyperkeratosis, papillomatosis of skin
- Recurrent cellulitis
- Eventually skin becomes thick, tough, indurated
Conservative management of lymphoedema:
- Skin care + hygiene to prevent cellulitis
- Manual lymphatic drainage (MLD) - specialist physiotherapy
- Multilayer lymphoedema bandaging (MLLB)
- Compression garments (class 2-3)
- Exercise / weight loss
b. Diseases of Lymph Nodes
i. Acute Lymphadenitis (Acute Inflammation)
Causes: Bacterial infection (Streptococcus, Staphylococcus, TB in some regions), viral infections
Pathology:
- Reactive hyperplasia of lymphoid follicles
- Neutrophil infiltration
- If untreated: Abscess formation, necrosis (suppurative lymphadenitis)
Clinical features:
- Tender, enlarged, warm, soft/fluctuant nodes
- Overlying skin: Erythema, warmth
- Systemic: Fever, leucocytosis
- May progress to abscess, pointing and spontaneous discharge
Treatment:
- Treat underlying infection (antibiotics)
- If abscess: Incision and drainage
- Needle aspiration for Gram stain and culture
ii. Chronic Lymphadenitis (Chronic Inflammation)
Causes:
- Chronic bacterial infection: TB (most important), syphilis, cat-scratch disease (Bartonella)
- Chronic viral infection: HIV, EBV (infectious mononucleosis), CMV
- Fungal: Histoplasma
- Parasitic: Toxoplasma
Tuberculous Lymphadenitis (Scrofula):
- Most common cause of chronic cervical lymphadenopathy in developing countries
- Pathology: Central caseating granulomatous necrosis with Langhans giant cells
- Features: Rubbery, firm, initially discrete nodes → matting → collar-stud abscess (extension through deep fascia; can point through skin)
- Treatment: Standard ATT (2HRZE / 4HR); surgical drainage if abscess
General features of chronic lymphadenopathy:
- Non-tender or mildly tender
- Firm/rubbery
- May mat together
- Constitutional symptoms (fever, weight loss, night sweats = "B symptoms")
iii. The Reticuloses (Lymphomas)
Definition: Malignant proliferations of lymphoid tissue (lymphoma) or the broader reticuloendothelial system.
Classification:
- Hodgkin Lymphoma (HL)
- Non-Hodgkin Lymphoma (NHL)
- Leukaemias (when circulating)
- Myeloma (plasma cell)
Hodgkin Lymphoma
Epidemiology: Bimodal age distribution (20-30s and >55 years); males slightly more common
Pathology - Reed-Sternberg cell: Large binucleate or bilobed cell with prominent "owl-eye" nucleoli; positive for CD15 and CD30 - pathognomonic
Subtypes (WHO/Rye classification):
| Subtype | Frequency | Prognosis |
|---|
| Nodular sclerosis | 60-70% | Good |
| Mixed cellularity | 20-25% | Intermediate |
| Lymphocyte predominant | 5% | Best |
| Lymphocyte depleted | <5% | Worst |
Clinical features:
- Painless, rubbery cervical/supraclavicular lymphadenopathy (most common presentation)
- Mediastinal mass (especially nodular sclerosis)
- B symptoms: Fever (Pel-Ebstein fever - cyclical), night sweats, weight loss >10%
- Alcohol-induced lymph node pain (characteristic of HL)
- Pruritus
Staging (Ann Arbor):
- I: Single lymph node region
- II: Two or more regions, same side of diaphragm
- III: Regions on both sides of diaphragm
- IV: Extranodal involvement (bone marrow, liver, lung)
- A = No B symptoms; B = B symptoms present
Treatment:
- Chemotherapy: ABVD (Adriamycin, Bleomycin, Vinblastine, Dacarbazine) - standard
- Radiotherapy: For early-stage disease (ISRT - involved site)
- Highly curable (>85% 5-year survival early stage)
Non-Hodgkin Lymphoma (NHL)
Classification: Vast; broadly divided into:
- B-cell lymphomas: ~85-90% (e.g. Diffuse Large B-cell Lymphoma (DLBCL), Follicular, Burkitt, Mantle cell)
- T-cell/NK lymphomas: ~10-15%
- Indolent vs aggressive
Clinical features:
- Painless lymphadenopathy (peripheral ± central)
- Extranodal involvement more common than HL (GI tract, CNS, skin, bone marrow)
- B symptoms (less common than HL)
- NHL associated with: EBV (Burkitt, PTLD), H. pylori (gastric MALT), HIV (aggressive B-cell), HTLV-1 (T-cell)
Diagnosis (lymphoma in general):
- Excision biopsy of lymph node - essential for histological diagnosis (not just FNA)
- Immunohistochemistry (IHC): CD markers
- Flow cytometry, FISH/cytogenetics
- Staging: CT chest/abdomen/pelvis; PET scan; bone marrow trephine biopsy
Treatment:
- DLBCL: R-CHOP (Rituximab + Cyclophosphamide, Doxorubicin, Vincristine, Prednisolone)
- Follicular: Watch and wait (indolent) or rituximab ± chemo
- Burkitt: Intensive chemotherapy (highly aggressive but curable)
SUMMARY TABLE: ARTERIAL vs VENOUS ULCERS
| Feature | Arterial Ulcer | Venous Ulcer |
|---|
| Site | Toes, heel, pressure points | Medial gaiter (above medial malleolus) |
| Appearance | Deep, "punched-out," pale base | Shallow, sloping edges, pink base |
| Pain | Severe | Mild/painless (unless infected) |
| Surrounding skin | Pale, hairless, trophic changes | Haemosiderin pigmentation, eczema, lipodermatosclerosis |
| Pulses | Absent | Normal |
| ABPI | <0.5 | >0.8 |
| Oedema | Absent | Present |
| Treatment | Revascularisation | Compression |
Sources: Pye's Surgical Handicraft, 22e; Goldman-Cecil Medicine; Robbins, Cotran & Kumar Pathologic Basis of Disease; Schwartz's Principles of Surgery, 11e; Campbell's Operative Orthopaedics, 15e