Arterial disease a. Investigations b. Assessment of a case of peripheral vascular disease Embolism d. Thromboangitis obliterans e. Arterio selerosis f. Atherosclerosis and Aneurysms g. Gangrene h. Conservative management of an ischaemic limb i. Surgical management of an ischemic limb - direct arterial surgery (6. Venous diseases a. Varicose veins b. Superfical and deep vein thrombosis c. chronic venous ulcers Lymphatics and Lymphnodes: a. Lymphangitis and lymphatic obstruction (Filariasis) b. Diseases of lymphnodes i. Acute inflammation ii. Chronic inflammation Pcii. The Reticulosis For surgery exam

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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:
StageFeatures
IAsymptomatic
IIaMild claudication (>200 m)
IIbModerate-severe claudication (<200 m)
IIIIschaemic rest pain
IVUlceration / 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":
  1. Pain - sudden, severe
  2. Pallor - cold, white
  3. Pulselessness - distal pulses absent
  4. Paraesthesia - "pins and needles" = early neurological sign
  5. Paralysis - late, indicates irreversibility (muscle necrosis)
  6. Perishing cold (Poikilothermia)
Embolism vs Thrombosis (in situ):
FeatureEmbolismThrombosis
OnsetSudden (seconds-minutes)Gradual (hours-days)
Prior claudicationNoYes
Contralateral pulsesNormalAbsent or reduced
AF / cardiac diseaseUsually presentAbsent
CollateralsAbsentDeveloped
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):
  1. Raynaud phenomenon
  2. Instep claudication (foot pain on exercise)
  3. 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:
  1. Atherosclerosis - most common; intimal plaques
  2. 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
  3. 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):
  1. Endothelial injury (shear stress, oxidised LDL, smoking, hypertension)
  2. LDL enters intima, oxidised by free radicals
  3. Monocyte recruitment → macrophages → engulf ox-LDL → foam cells → fatty streak
  4. Smooth muscle cell migration from media, proliferation, collagen deposition → fibrous cap
  5. 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:
TypeFeatures
Dry gangreneArterial occlusion only; tissue mummified, shrunken, black; clear line of demarcation; no infection; no smell
Wet gangreneArterial occlusion + venous obstruction + bacterial infection; swollen, blistered, foul smell; NO clear demarcation; spreads rapidly
Gas gangreneClostridium perfringens; crepitus due to gas in tissues; profound toxaemia; EMERGENCY
Diabetic gangreneMixed - neuropathy + ischaemia + infection; pressure points (toes, heel)
Hospital gangreneSpreading 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:
  1. Adequate imaging (arteriography/CTA/MRA) to define inflow, stenosis and outflow ("run-off")
  2. 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):
  1. Venous stasis: Immobility, surgery, long flights, cardiac failure
  2. Hypercoagulability: Malignancy, OCP, pregnancy, thrombophilia (Factor V Leiden, antiphospholipid syndrome)
  3. 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:
  1. Hodgkin Lymphoma (HL)
  2. Non-Hodgkin Lymphoma (NHL)
  3. Leukaemias (when circulating)
  4. 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):
SubtypeFrequencyPrognosis
Nodular sclerosis60-70%Good
Mixed cellularity20-25%Intermediate
Lymphocyte predominant5%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

FeatureArterial UlcerVenous Ulcer
SiteToes, heel, pressure pointsMedial gaiter (above medial malleolus)
AppearanceDeep, "punched-out," pale baseShallow, sloping edges, pink base
PainSevereMild/painless (unless infected)
Surrounding skinPale, hairless, trophic changesHaemosiderin pigmentation, eczema, lipodermatosclerosis
PulsesAbsentNormal
ABPI<0.5>0.8
OedemaAbsentPresent
TreatmentRevascularisationCompression

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
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