General Surgery
Final Professional MBBS — General Surgery. Explanation-first answers that teach the reasoning behind every fact, with classifications, comparison tables, drug doses, clinical pearls and key-point recaps from Bailey & Love and SRB's Manual.
THE CONCEPT
Chronic limb ischaemia is a persistent reduction in the arterial blood supply to a limb, almost always caused by atherosclerosis of the lower-limb arteries. It represents a spectrum of severity — from pain only on exertion (intermittent claudication) at the mild end, through pain at rest, to tissue loss (critical limb ischaemia) at the severe end. Understanding it as a supply-versus-demand problem that worsens as the arteries narrow makes the whole clinical picture logical.
PATHOPHYSIOLOGY & RISK FACTORS
Atherosclerotic plaques narrow the arteries (aorto-iliac, femoro-popliteal, and tibial segments), reducing perfusion. When demand exceeds the limited supply on exercise, ischaemic muscle pain (claudication) occurs; as disease progresses, the supply is inadequate even at rest. The risk factors are those of atherosclerosis generally: smoking (the strongest), diabetes, hypertension, hyperlipidaemia, increasing age and male sex.
CLINICAL FEATURES — THE FONTAINE CLASSIFICATION
Severity is graded by the Fontaine classification:
Stage Features I Asymptomatic II Intermittent claudication — cramping calf/thigh/buttock pain on walking, relieved by rest III Rest pain (typically at night; relieved by hanging the foot out of bed) IV Tissue loss — ulceration or gangrene Critical limb ischaemia is defined as rest pain for more than 2 weeks, ulceration or gangrene, and is limb-threatening.
EXAMINATION
Signs of chronic ischaemia include absent or weak peripheral pulses, a cold and pale limb, hair loss, thin shiny skin, slow capillary refill, and arterial ulcers (painful, 'punched-out', on pressure points and toes). Buerger's test is positive — the leg goes pale on elevation (a low 'Buerger's angle' indicating poor perfusion) and shows reactive hyperaemia (a dusky red colour) on dependency.
INVESTIGATION & MANAGEMENT
The key bedside investigation is the ankle-brachial pressure index (ABPI): normal is ~1.0, <0.9 indicates PAD, and <0.5 indicates critical ischaemia — but it can be falsely high in diabetics because of calcified, incompressible vessels. Duplex ultrasound and CT/MR angiography map the disease before intervention. Management combines:
- Risk-factor modification — above all smoking cessation, plus control of diabetes, blood pressure and lipids (a statin), and an antiplatelet agent (aspirin or clopidogrel).
- Supervised exercise therapy for claudication (promotes collateral flow).
- Revascularisation — angioplasty ± stenting or bypass surgery — for critical ischaemia or severely disabling claudication.
- Amputation for an unsalvageable limb.
💡CLINICAL PEARL: Anchor the topic on the Fontaine classification and the ABPI (<0.9 = PAD; falsely high in diabetes). Smoking cessation is the single most important intervention. A useful clinical clue is that rest pain is relieved by hanging the foot out of bed (gravity aids perfusion), and critical limb ischaemia (rest pain or tissue loss) needs revascularisation to save the limb.ARTERIAL VS VENOUS ULCERS — THE KEY CONTRAST
A favourite exam distinction is between arterial and venous leg ulcers, and it follows from their pathology. An arterial (ischaemic) ulcer is painful, 'punched-out' with a well-defined edge, and lies over pressure points or the toes/heel, on a cold leg with absent pulses and a low ABPI. A venous ulcer is relatively painless, shallow with sloping edges, and lies in the 'gaiter area' around the medial malleolus, on a warm leg with skin changes of venous insufficiency and a normal ABPI. Getting this contrast right determines whether compression (safe for venous, dangerous for arterial) can be used.
BUERGER'S TEST EXPLAINED
Buerger's test is a valuable bedside sign worth understanding. The leg is elevated, and the angle at which it turns pale (the Buerger's angle) indicates the severity of ischaemia — a low angle (the leg going white when only slightly raised) means poor perfusion. The leg is then hung down over the edge of the couch: in significant ischaemia it turns first blue, then a dusky reactive hyperaemic red, as the ischaemic tissue reperfuses. A positive test confirms significant arterial insufficiency.
PROGNOSIS & THE SYSTEMIC PICTURE
It is important to appreciate that PAD is a marker of widespread atherosclerosis: a patient with limb ischaemia very often has coronary and cerebrovascular disease too, so their main risk is actually myocardial infarction and stroke. This is why 'best medical therapy' (antiplatelet, statin, blood-pressure and diabetes control, smoking cessation) is prescribed not just to save the leg but to reduce cardiovascular death — reframing claudication as a whole-body cardiovascular problem rather than a purely local one.
A NOTE ON THE ABPI PITFALL IN DIABETES
One practical pitfall deserves emphasis: in diabetic patients (and those with chronic kidney disease), the tibial arteries are often calcified and incompressible, so the cuff cannot occlude them and the ABPI reads falsely high or normal despite significant ischaemia. In these patients the ABPI is unreliable, and the circulation is better assessed with toe pressures (the digital vessels are usually spared calcification) or the Doppler waveform. Being aware of this prevents falsely reassuring a diabetic patient with a limb-threatening problem.
💊KEY POINTS / NUMBERS (viva)- Fontaine: I asymptomatic, II claudication, III rest pain, IV tissue loss; critical limb ischaemia = rest pain >2 weeks/ulcer/gangrene.
- ABPI: normal ~1.0, <0.9 = PAD, <0.5 = critical; falsely high in diabetics (calcified vessels).
- Manage: stop smoking (key) + statin + antiplatelet + risk factors; exercise for claudication; revascularise (angioplasty/bypass) for critical ischaemia.
🔑KEY POINTS TO REMEMBER- Chronic limb ischaemia = atherosclerotic reduction in limb arterial supply; spectrum from claudication to critical limb ischaemia.
- Risk: smoking (strongest), diabetes, hypertension, hyperlipidaemia, age, male.
- Fontaine: I asymptomatic, II claudication, III rest pain (relieved hanging foot down), IV tissue loss; signs — absent pulses, cold pale limb, arterial ulcers, positive Buerger's test.
- ABPI <0.9 = PAD, <0.5 = critical (falsely high in diabetes); duplex/CT-MR angiography for mapping.
- Stop smoking + statin + antiplatelet + risk-factor control; exercise for claudication; revascularise (angioplasty/bypass) for critical ischaemia; amputation if unsalvageable.
📚SOURCES: Bailey & Love's Short Practice of Surgery; SRB's Manual of Surgery.THE CONCEPT
Acute limb ischaemia is a sudden occlusion of the arterial supply to a limb, producing an acutely threatened limb — a surgical emergency. Unlike chronic ischaemia, there has been no time for collateral vessels to develop, so the tissue is rapidly deprived of blood and will become non-viable within a few hours if flow is not restored. Prompt recognition and revascularisation are what save the limb.
CAUSES — EMBOLISM VS THROMBOSIS
The two main causes must be distinguished because they differ in management:
Embolism Thrombosis Mechanism Embolus (often from the heart) lodges in a normal artery Thrombosis on a pre-existing atherosclerotic plaque Onset Very sudden Often less abrupt Source / history AF, recent MI (mural thrombus); no prior claudication History of claudication; signs of chronic PAD Other limb Normal pulses Signs of PAD Other causes include trauma and aortic dissection.
CLINICAL FEATURES — THE 6 Ps
The presentation is summarised by the 6 Ps: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, and Perishing cold (Poikilothermia). The last two — paraesthesia and paralysis — are ominous, indicating advanced ischaemia and a threatened, barely viable limb that demands the most urgent intervention.
INVESTIGATION & MANAGEMENT
It is largely a clinical diagnosis; a hand-held Doppler assesses flow, and angiography defines the anatomy if time permits, with an ECG to detect AF. Management is an emergency:
- Immediate measures — analgesia, oxygen, and intravenous heparin to prevent propagation of thrombus.
- Urgent revascularisation — surgical embolectomy (with a Fogarty balloon catheter) for an embolus, or thrombolysis, angioplasty or bypass for thrombosis, guided by the cause and limb viability.
- An irreversibly ischaemic limb (fixed mottling, muscle rigidity, paralysis) requires amputation.
- After revascularisation, watch for reperfusion injury — compartment syndrome (may need fasciotomy), hyperkalaemia, and myoglobinuria causing acute kidney injury.
💡CLINICAL PEARL: Remember the 6 Ps, and that paraesthesia and paralysis signal a threatened limb requiring immediate action. Distinguish embolus (sudden, AF or MI source, no claudication history, normal other limb) from thrombosis (claudication history, signs of chronic PAD). Give IV heparin immediately and arrange urgent revascularisation; anticipate reperfusion injury (hyperkalaemia, compartment syndrome).THE IMPORTANCE OF DISTINGUISHING EMBOLUS FROM THROMBOSIS
The embolus-versus-thrombosis distinction is not academic — it changes treatment. An embolus lodging in a previously healthy artery (a patient in AF with a suddenly white, pulseless leg and normal pulses elsewhere) is ideally treated by embolectomy with a Fogarty catheter. A thrombosis on chronic atherosclerotic disease (a patient with prior claudication and PAD signs) has collaterals and diseased vessels, so it is often better managed by angiography with thrombolysis, angioplasty or bypass. Misreading the cause leads to the wrong operation.
CATEGORIES OF LIMB VIABILITY
Management hinges on a rapid assessment of limb viability (the Rutherford categories). A viable limb (no sensory/motor loss, audible Doppler signals) allows time for imaging; a threatened limb (sensory loss, some muscle weakness, absent arterial Doppler) needs immediate revascularisation; an irreversibly ischaemic limb (profound sensory loss, paralysis, muscle rigidity, fixed skin mottling) is not salvageable and requires amputation. This triage decides speed and type of intervention.
REPERFUSION INJURY IN DEPTH
Restoring flow to a severely ischaemic limb brings its own dangers, which must be anticipated. As blood returns, accumulated potassium, hydrogen ions and myoglobin are washed into the circulation, causing hyperkalaemia (cardiac arrhythmia), metabolic acidosis, and myoglobinuria that can precipitate acute kidney injury. Swelling of the reperfused muscle within its fascial compartment can cause a compartment syndrome needing fasciotomy. This is why revascularised patients are monitored closely and why very late revascularisation of a dead limb can be more dangerous than amputation.
A NOTE ON THE 'GOLDEN' TIME WINDOW
As with other ischaemic emergencies, there is a narrow window in which the limb can be salvaged: skeletal muscle tolerates warm ischaemia for only about 6 hours before irreversible damage, so acute limb ischaemia is treated with the same urgency as acute coronary or cerebral ischaemia. Delay converts a salvageable limb into a dead one requiring amputation, which is why immediate senior vascular involvement, heparinisation and prompt revascularisation are stressed the moment the diagnosis is suspected.
💊KEY POINTS / NUMBERS (viva)- 6 Ps: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishing cold; paraesthesia/paralysis = threatened limb (urgent).
- Embolus (AF/MI, sudden, no history) vs thrombosis (claudication history, PAD signs).
- Immediate IV heparin + urgent revascularisation (embolectomy/Fogarty for embolus); watch for reperfusion injury (hyperkalaemia, compartment syndrome).
🔑KEY POINTS TO REMEMBER- Acute limb ischaemia = sudden arterial occlusion → threatened limb (emergency; non-viable within hours, no collaterals).
- Causes: embolism (AF/MI, sudden, no claudication history) vs thrombosis (on plaque, claudication history/PAD signs).
- 6 Ps: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishing cold; paraesthesia/paralysis = advanced/threatened.
- Immediate: analgesia, oxygen, IV heparin; urgent revascularisation (embolectomy/Fogarty for embolus; thrombolysis/angioplasty/bypass for thrombosis).
- Irreversible (fixed mottling, rigidity) → amputation; watch for reperfusion injury (compartment syndrome, hyperkalaemia, AKI).
📚SOURCES: Bailey & Love's Short Practice of Surgery; SRB's Manual of Surgery.THE CONCEPT & DEFINITION
An aneurysm is a permanent, localised dilatation of an artery to more than 1.5 times its normal diameter. An abdominal aortic aneurysm (AAA) therefore means an abdominal aorta of 3 cm or more (the normal aorta is ~2 cm), most commonly located below the renal arteries (infrarenal). It is a true aneurysm (involving all three layers of the wall) and is degenerative in origin. Its whole clinical importance lies in the risk of rupture, which is usually fatal.
RISK FACTORS
Risk factors are increasing age, male sex, smoking, hypertension, a family history, and connective-tissue disorders (e.g. Marfan syndrome). Smoking is a particularly strong association.
CLINICAL FEATURES
- Asymptomatic — the majority, found incidentally or on screening as a pulsatile, expansile abdominal mass.
- Symptomatic (unruptured) — abdominal or back pain (may herald expansion or impending rupture).
- Ruptured AAA — the classic triad of sudden severe abdominal/back pain, hypotension/collapse, and a pulsatile expansile abdominal mass — a catastrophic emergency with very high mortality.
SCREENING & INVESTIGATION
Because rupture is lethal but elective repair is safe, screening is offered (in the UK, a single ultrasound for men at 65). Ultrasound is used for diagnosis, screening and surveillance, while CT angiography gives precise size and anatomy for planning repair and is used to confirm rupture in the stable patient.
MANAGEMENT
- Small aneurysms (< 5.5 cm) — surveillance with ultrasound plus risk-factor control (stop smoking, control blood pressure), since the rupture risk is low.
- Large (≥ 5.5 cm), symptomatic, or rapidly expanding aneurysms — elective repair, either open surgical graft repair or endovascular aneurysm repair (EVAR — a stent-graft placed via the femoral arteries).
- Ruptured AAA — emergency repair (open or emergency EVAR) in those who reach theatre, though mortality remains high.
💡CLINICAL PEARL: Key numbers and facts: an AAA is an aorta ≥ 3 cm, usually infrarenal and asymptomatic; the repair threshold is 5.5 cm (or symptomatic/rapidly expanding). The ruptured AAA triad — pain + shock + pulsatile mass — is a surgical emergency, and screening men at 65 with ultrasound reduces deaths. A ruptured AAA can mimic renal colic, so consider it in any older man with acute abdominal/back pain and collapse.WHY SIZE DETERMINES REPAIR
The 5.5 cm threshold is not arbitrary but reflects the balance of two risks. Below ~5.5 cm the annual risk of rupture is low — lower than the risk of the repair operation itself — so surveillance is safer. Above 5.5 cm, or when the aneurysm is expanding rapidly (>1 cm/year) or causing symptoms, the rupture risk rises steeply and exceeds the operative risk, so repair becomes worthwhile. Wall tension rises with diameter (Laplace's law), which is the physical basis for this size-dependent rupture risk.
OPEN REPAIR VS EVAR
The two repair options have trade-offs worth knowing. Open repair replaces the aneurysmal segment with a prosthetic graft through a laparotomy — durable but with greater operative stress and a longer recovery. EVAR (endovascular aneurysm repair) deploys a stent-graft via the femoral arteries — less invasive with lower short-term mortality, but it requires lifelong surveillance for complications such as endoleak (persistent flow into the sac) and needs suitable anatomy. The choice depends on the patient's fitness and the aneurysm's shape.
THE RUPTURED AAA AS A MIMIC
A crucial clinical point is that a ruptured or leaking AAA is a great mimic — it can present like renal colic, an acute abdomen, or back pain, and a wrong diagnosis is fatal. Therefore any man over 60 with sudden abdominal or back pain, collapse, or a first presentation of 'renal colic' should have an AAA excluded (by examining for a pulsatile mass and prompt imaging). The stable patient gets a CT; the unstable one with a known/obvious AAA goes straight to theatre.
A NOTE ON THORACIC & OTHER ANEURYSMS
For completeness, aneurysms occur elsewhere and share the same principles. Thoracic aortic aneurysms (more often associated with connective-tissue disease or hypertension) and popliteal aneurysms (which tend to thrombose or embolise rather than rupture, threatening the limb, and are frequently bilateral) are the other important sites. A false (pseudo) aneurysm — a contained leak walled off by surrounding tissue, often after arterial puncture or trauma — differs from a true aneurysm in not involving all wall layers. Recognising these broadens the concept beyond the abdominal aorta.
💊KEY POINTS / NUMBERS (viva)- AAA = aorta ≥3 cm (aneurysm = >1.5× normal); usually infrarenal.
- Elective repair threshold ≈ 5.5 cm (or symptomatic/rapidly expanding); options = open graft or EVAR.
- Ruptured AAA triad: sudden abdominal/back pain + hypotension/collapse + pulsatile expansile mass (emergency).
🔑KEY POINTS TO REMEMBER- AAA = permanent localised dilatation of the aorta ≥3 cm (>1.5× normal); usually infrarenal, true aneurysm, degenerative.
- Risk: age, male, smoking, hypertension, family history, connective-tissue disorders.
- Usually asymptomatic (pulsatile expansile mass); ruptured AAA triad = pain + shock + pulsatile mass (emergency, high mortality).
- Ultrasound for diagnosis/screening/surveillance (screen men at 65); CT angiography for planning/rupture.
- <5.5 cm → surveillance + risk factors; ≥5.5 cm/symptomatic/rapidly expanding → elective repair (open or EVAR); ruptured → emergency repair.
📚SOURCES: Bailey & Love's Short Practice of Surgery; SRB's Manual of Surgery.THE CONCEPT
Varicose veins are dilated, tortuous, elongated superficial veins of the leg (in the long and short saphenous systems). They arise from incompetence of the venous valves, which allows blood to reflux backwards and pool in the superficial veins, raising the pressure within them (venous hypertension). This single mechanism — failed valves → reflux → venous hypertension → dilated veins and skin damage — explains the whole condition.
PATHOPHYSIOLOGY & CAUSES
Normally, valves and the calf muscle pump return blood upward against gravity. When valves become incompetent — at the saphenofemoral or saphenopopliteal junctions or the perforating veins — blood refluxes, distending the superficial veins. Incompetence may be primary (idiopathic, often familial) or secondary (to a previous DVT, pelvic mass, or pregnancy).
CLINICAL FEATURES & COMPLICATIONS
Patients have visible dilated tortuous veins with aching, heaviness, itching and swelling that worsen on standing and towards the end of the day. The important complications of chronic venous insufficiency are:
- Skin changes — haemosiderin pigmentation, venous eczema, lipodermatosclerosis (woody induration), and atrophie blanche.
- Venous ulceration — classically in the 'gaiter' area around the medial malleolus.
- Bleeding from a ruptured varix and superficial thrombophlebitis.
EXAMINATION & INVESTIGATION
The patient is examined standing. Traditional bedside tests (the Trendelenburg/tourniquet test to locate the level of incompetence, the tap test, and a cough impulse for a saphena varix) have largely been superseded by duplex ultrasound, which is the investigation of choice — it demonstrates the sites of reflux and, importantly, excludes deep venous obstruction (DVT) before any treatment.
MANAGEMENT
- Conservative — compression stockings, leg elevation, weight loss and exercise.
- Interventional — endovenous ablation (radiofrequency or laser), foam sclerotherapy, or surgery (saphenofemoral ligation and stripping).
- Venous ulcers — treated with graduated compression bandaging, but only after excluding arterial disease with an ABPI (compression on an ischaemic leg is dangerous).
💡CLINICAL PEARL: The essence: varicose veins result from valvular incompetence → venous hypertension, and their serious legacy is chronic venous insufficiency with skin changes and a venous ulcer in the gaiter area/medial malleolus. Duplex ultrasound is the key investigation, and a venous ulcer is treated with compression — but always check the ABPI first to exclude arterial disease.THE CALF MUSCLE PUMP & VENOUS HYPERTENSION
Understanding the calf muscle pump makes venous disease clear. During walking, calf muscle contraction squeezes the deep veins and, with competent valves, drives blood upward toward the heart while preventing backflow. When valves fail (or the deep veins are obstructed after a DVT), each contraction instead transmits high pressure back into the superficial system — sustained venous hypertension. It is this chronic pressure at the ankle that damages the skin and produces the pigmentation, lipodermatosclerosis and ulceration of chronic venous insufficiency.
CEAP & THE VENOUS ULCER
Venous disease is classified by the CEAP system (Clinical, Etiological, Anatomical, Pathophysiological), the clinical grades running from simple telangiectasia through varicose veins and skin changes to healed and active venous ulceration. The venous ulcer is the end-stage: a shallow, exudative ulcer in the gaiter area, treated by graduated compression bandaging (which counteracts the venous hypertension) once an ABPI has confirmed the arterial supply is adequate. Treating the underlying reflux (ablation) reduces recurrence.
A NOTE ON SECONDARY VARICOSE VEINS
It is important to identify secondary varicose veins, because they change management. Varicosities that follow a previous DVT (with deep venous damage), or that are caused by pelvic obstruction (a mass or pregnancy), must be recognised on duplex, since the deep system may be the patient's main venous drainage — stripping the superficial veins could then be harmful. This is another reason duplex ultrasound, which assesses both deep and superficial systems, is mandatory before intervention.
A NOTE ON SUPERFICIAL THROMBOPHLEBITIS
A common complication worth noting is superficial thrombophlebitis — thrombosis and inflammation of a superficial varicose vein, presenting as a tender, red, cord-like segment. Though usually self-limiting and treated with analgesia, compression and anti-inflammatories, extensive thrombophlebitis of the long saphenous vein near the saphenofemoral junction can propagate into the deep system and cause a DVT, so it is assessed with duplex and sometimes anticoagulated — a reminder that the superficial and deep systems are connected.
💊KEY POINTS / NUMBERS (viva)- Cause: valvular incompetence (saphenofemoral/saphenopopliteal junctions, perforators) → reflux → venous hypertension.
- Venous ulcer: gaiter area/medial malleolus; skin changes: haemosiderin pigmentation, lipodermatosclerosis, atrophie blanche.
- Duplex ultrasound is the investigation of choice; compression for venous ulcers only after checking ABPI (exclude arterial disease).
🔑KEY POINTS TO REMEMBER- Varicose veins = dilated tortuous superficial leg veins from valvular incompetence → reflux → venous hypertension.
- Primary (idiopathic/familial) or secondary (DVT, pelvic mass, pregnancy); worse on standing/end of day.
- Complications: skin changes (haemosiderin pigmentation, lipodermatosclerosis, atrophie blanche), venous ulcer (gaiter area/medial malleolus), bleeding, thrombophlebitis.
- Duplex ultrasound is the investigation of choice (also excludes DVT).
- Compression + elevation + exercise; endovenous ablation/sclerotherapy/surgery; venous ulcers need compression (check ABPI first to exclude arterial disease).
📚SOURCES: Bailey & Love's Short Practice of Surgery; SRB's Manual of Surgery.THE CONCEPT
Deep vein thrombosis (DVT) is the formation of a thrombus within a deep vein, usually of the leg or pelvis. Its great importance is that part of the clot can break off and travel to the lungs as a pulmonary embolism (PE) — the two together being called venous thromboembolism (VTE), a major, often preventable, cause of hospital death. So the topic is really about recognising, treating and — above all — preventing clot in the deep veins.
PATHOPHYSIOLOGY — VIRCHOW'S TRIAD
Thrombosis is driven by Virchow's triad of three contributing factors: venous stasis (immobility, surgery, long-haul travel), endothelial injury (trauma, surgery), and hypercoagulability (malignancy, pregnancy, the oral contraceptive pill, inherited thrombophilia, sepsis). Any clinical situation combining these raises VTE risk.
RISK FACTORS
Key risk factors are recent surgery (especially orthopaedic and pelvic), immobility, malignancy, pregnancy and the combined oral contraceptive pill, previous VTE, obesity, thrombophilia, and long-haul travel.
CLINICAL FEATURES
A DVT typically causes a unilateral, swollen, painful, warm, red leg with calf tenderness and dilated superficial veins — though it may be silent. A PE presents with pleuritic chest pain, breathlessness, haemoptysis and, if massive, collapse — always to be feared in a patient with a DVT.
INVESTIGATION
Assessment uses a clinical probability score (the Wells score) to guide testing. A D-dimer is sensitive but not specific — a normal D-dimer in a low-probability patient helps exclude VTE, but a raised one is non-specific. Duplex ultrasound of the leg confirms a DVT, and CT pulmonary angiography (CTPA) diagnoses PE.
MANAGEMENT & PREVENTION
- Anticoagulation is the mainstay — a direct oral anticoagulant (DOAC such as rivaroxaban or apixaban), or LMWH bridging to warfarin; the duration depends on whether the VTE was provoked or unprovoked.
- An IVC filter is used if anticoagulation is contraindicated.
- Prevention (thromboprophylaxis) is crucial in hospital patients — a combination of mechanical measures (graduated compression stockings, intermittent pneumatic compression) and pharmacological prophylaxis (LMWH), along with early mobilisation, based on individual risk assessment.
Complications of DVT are PE (life-threatening) and the post-thrombotic syndrome (chronic venous insufficiency of the leg).
💡CLINICAL PEARL: Remember Virchow's triad (stasis, endothelial injury, hypercoagulability) as the framework. A unilateral swollen painful leg is a DVT until proven otherwise — assess with the Wells score, D-dimer and duplex, and anticoagulate (DOAC). The overriding message for surgery is prevention: every hospitalised/surgical patient needs VTE risk assessment and appropriate mechanical + pharmacological prophylaxis.PROVOKED VS UNPROVOKED VTE
The distinction between provoked and unprovoked VTE guides the duration of anticoagulation. A provoked event has a clear transient cause (recent surgery, immobility, pregnancy) and, once the provoker resolves, may need only a defined course (e.g. 3 months). An unprovoked event, with no obvious trigger, carries a higher recurrence risk and may warrant long-term anticoagulation, and prompts consideration of an occult malignancy or thrombophilia. Tailoring duration to this distinction balances recurrence risk against bleeding risk.
MASSIVE PE — AN EMERGENCY
The feared complication, massive pulmonary embolism, is a distinct emergency: a large embolus obstructing the pulmonary circulation causes acute right heart strain, hypotension and collapse, and may be rapidly fatal. It is treated with resuscitation and, in the haemodynamically unstable patient, thrombolysis (or embolectomy), rather than anticoagulation alone. Recognising the shocked, breathless patient with a swollen leg as a possible massive PE is life-saving.
THE PRIMACY OF PREVENTION
The overarching message of VTE in a surgical setting is prevention, because most hospital-associated VTE is avoidable. Every admitted patient should undergo a VTE risk assessment balanced against bleeding risk, and receive appropriate prophylaxis — early mobilisation, mechanical measures (compression stockings, intermittent pneumatic compression), and pharmacological prophylaxis (LMWH) for those at risk. This systematic approach has substantially reduced deaths from hospital-acquired PE and is a routine part of surgical care.
A NOTE ON THROMBOPHILIA & MALIGNANCY
Two associations deserve mention. An unprovoked or recurrent VTE, VTE at a young age, or a strong family history prompts consideration of an inherited thrombophilia (such as factor V Leiden, protein C/S or antithrombin deficiency, or the antiphospholipid syndrome). Equally, an unprovoked VTE in an older patient can be the first sign of an occult malignancy (cancer causes hypercoagulability — Trousseau's sign of migratory thrombophlebitis), so appropriate assessment for an underlying cancer is considered. These links explain why the cause of a 'spontaneous' clot is always sought.
💊KEY POINTS / NUMBERS (viva)- Virchow's triad: stasis, endothelial injury, hypercoagulability.
- Investigate: Wells score → D-dimer (rule out if low probability) → duplex ultrasound (DVT)/CTPA (PE).
- Treat with a DOAC (rivaroxaban/apixaban); prevent with LMWH + mechanical prophylaxis + early mobilisation.
🔑KEY POINTS TO REMEMBER- DVT = thrombus in a deep vein (leg/pelvis); risk of PE (together = venous thromboembolism, VTE) — a preventable cause of death.
- Virchow's triad: stasis (immobility, surgery, travel), endothelial injury, hypercoagulability (malignancy, pregnancy/OCP, thrombophilia).
- Unilateral swollen, painful, warm leg; PE → pleuritic chest pain, dyspnoea, haemoptysis.
- Wells score + D-dimer (rule out if low probability) + duplex ultrasound (DVT)/CTPA (PE).
- Anticoagulate (DOAC); IVC filter if anticoagulation contraindicated; PREVENT with LMWH + mechanical prophylaxis + early mobilisation.
📚SOURCES: Bailey & Love's Short Practice of Surgery; Davidson's Principles and Practice of Medicine.THE CONCEPT
Gangrene is death (necrosis) of tissue with putrefaction, usually resulting from a loss of blood supply, often complicated by infection. Its clinical types are distinguished by whether infection is present and how the tissue looks, and this distinction determines urgency and treatment.
DRY GANGRENE
Dry gangrene follows a gradual arterial occlusion (chronic ischaemia, as in peripheral arterial disease or diabetes). The tissue slowly dries out, becoming shrivelled, mummified and black, with a clear line of demarcation between dead and living tissue and no significant infection. It progresses slowly and is comparatively less dangerous.
WET GANGRENE
Wet gangrene is necrosis complicated by infection (often with venous as well as arterial obstruction). The tissue is swollen, boggy, blistered, discoloured and foul-smelling, with no clear line of demarcation and rapid, spreading progression, causing systemic toxicity (sepsis). It is a surgical emergency.
GAS GANGRENE & MANAGEMENT
Gas gangrene is a life-threatening necrotising infection caused by Clostridium perfringens, producing crepitus (gas in the tissues), rapid myonecrosis and severe toxaemia. Management across the types involves treating the cause (revascularisation where possible), antibiotics, and surgical debridement or amputation — urgently for wet and gas gangrene — with a clean amputation through viable tissue.
A NOTE ON THE LINE OF DEMARCATION
The line of demarcation between dead and living tissue is a useful concept: in dry gangrene a clear line forms, and a stable, demarcated dry gangrene of a toe may be allowed to auto-amputate or be removed electively once demarcation is complete. In wet gangrene there is no clear line and the process spreads, so urgent debridement or amputation through healthy proximal tissue is required to control sepsis — the presence or absence of demarcation thus guides the urgency of surgery.
THE BOTTOM LINE
Gangrene is tissue necrosis with putrefaction: dry (chronic ischaemia, demarcated, may be watched), wet (necrosis + infection, spreading, an emergency), and gas gangrene (Clostridium, crepitus, life-threatening) — treated by revascularisation, antibiotics and debridement/amputation.
A NOTE ON PRESSURE SORES & DECUBITUS
Related to gangrene is the pressure sore (decubitus ulcer) — localised tissue necrosis over a bony prominence (sacrum, heel, ischium) from sustained pressure occluding the blood supply in an immobile patient. Like gangrene it reflects tissue death from ischaemia, and prevention (regular repositioning, pressure-relieving mattresses, good nutrition and skin care) is far better than treatment, which requires pressure relief, wound care and sometimes debridement — an important nursing and surgical concern in the bedbound patient.
🔑KEY POINTS TO REMEMBER- Gangrene = tissue necrosis with putrefaction, usually from loss of blood supply ± infection.
- Dry gangrene: gradual arterial occlusion (chronic ischaemia); dry, mummified, black, clear line of demarcation, no infection.
- Wet gangrene: necrosis + infection; swollen, boggy, foul, spreading, no demarcation, systemic toxicity — emergency.
- Gas gangrene: Clostridium perfringens; crepitus, myonecrosis, toxaemia — life-threatening.
- Treat: revascularise the cause, antibiotics, urgent debridement/amputation (esp. wet and gas gangrene).
📚SOURCES: Bailey & Love's Short Practice of Surgery.THE CONCEPT — A TRIAD OF PROBLEMS
The diabetic foot is a major cause of morbidity, and its complications arise from the combination of three factors produced by diabetes: neuropathy, ischaemia and impaired resistance to infection. Understanding this triad explains why a trivial injury can progress rapidly to ulceration, gangrene and amputation.
THE THREE FACTORS
- Neuropathy — sensory loss removes the protective pain that would normally warn of injury (so trauma goes unnoticed); motor neuropathy causes deformity and abnormal pressure points; autonomic neuropathy dries the skin (fissures) and alters blood flow.
- Ischaemia — accelerated peripheral arterial disease reduces the blood supply needed for healing.
- Infection — impaired immunity and hyperglycaemia allow infection to establish and spread rapidly.
CLINICAL FEATURES & MANAGEMENT
These produce ulcers (a neuropathic ulcer is painless and over a pressure point/sole; an ischaemic ulcer is painful and at the margins/toes), the Charcot foot (progressive bony destruction of an insensate foot), cellulitis, osteomyelitis and gangrene. Management is multidisciplinary: strict glycaemic control, meticulous foot care and patient education, pressure offloading, wound debridement, antibiotics for infection, and revascularisation for ischaemia, with amputation reserved for severe or unsalvageable disease. Prevention through regular foot screening in a diabetic foot clinic is central.
NEUROPATHIC VS ISCHAEMIC FOOT
Distinguishing the predominantly neuropathic from the predominantly ischaemic foot guides treatment. The neuropathic foot is warm and well-perfused with bounding pulses but insensate, developing painless ulcers over pressure areas and Charcot deformity — managed by offloading and foot care. The ischaemic (neuro-ischaemic) foot is cold with absent pulses and painful marginal ulcers — needing revascularisation. Many diabetic feet are 'neuro-ischaemic', combining both, which is why ABPI/Doppler assessment of the circulation is part of every diabetic foot review.
THE BOTTOM LINE
The diabetic foot results from neuropathy + ischaemia + infection, producing neuropathic (painless, pressure-point) or ischaemic (painful, marginal) ulcers and Charcot foot, managed by an MDT with glycaemic control, offloading, debridement, antibiotics and revascularisation.
A NOTE ON OSTEOMYELITIS & PROBING TO BONE
A crucial complication is osteomyelitis underlying a diabetic foot ulcer, which greatly complicates healing. A useful bedside sign is the 'probe-to-bone' test — if a sterile probe passed into the ulcer reaches bone, osteomyelitis is likely — supported by X-ray, MRI and inflammatory markers. Recognising bone infection matters because it usually requires prolonged antibiotics and often surgical debridement or partial amputation, and its presence changes the whole management plan.
🔑KEY POINTS TO REMEMBER- Diabetic foot complications arise from a triad: neuropathy (sensory loss, deformity, dry skin) + ischaemia (PAD) + impaired resistance to infection.
- Neuropathic ulcer: painless, over pressure points/sole; ischaemic ulcer: painful, at margins/toes; also Charcot foot, cellulitis, osteomyelitis, gangrene.
- Manage with a multidisciplinary team: glycaemic control, foot care/education, offloading, debridement, antibiotics, revascularisation.
- Amputation for severe disease; prevention by regular foot screening is central.
📚SOURCES: Bailey & Love's Short Practice of Surgery.THE CONCEPT
Intermittent claudication is cramping muscle pain brought on by walking (or exercise) and relieved by rest within a few minutes. It is the earliest symptomatic stage of chronic limb ischaemia, and results from chronic arterial insufficiency (atherosclerotic peripheral arterial disease): on exercise the muscle's demand for oxygen exceeds the supply a narrowed artery can deliver, producing ischaemic pain that resolves once demand falls at rest.
CLINICAL FEATURES — SITE INDICATES LEVEL
The pain is reproducible at a fairly constant 'claudication distance', and the site of pain indicates the level of arterial disease: calf claudication reflects femoro-popliteal disease, while thigh and buttock claudication reflects aorto-iliac disease. The classic Leriche syndrome (aorto-iliac occlusion) is the triad of buttock/thigh claudication, erectile dysfunction, and absent femoral pulses.
INVESTIGATION & MANAGEMENT
The key investigation is the ankle-brachial pressure index (ABPI), reduced below 0.9. Management is initially conservative and medical: smoking cessation, a supervised exercise programme, and 'best medical therapy' (a statin, an antiplatelet, and control of diabetes and blood pressure). Most patients stabilise or improve; revascularisation (angioplasty or bypass) is reserved for lifestyle-limiting claudication that fails conservative measures or for critical ischaemia.
DIFFERENTIAL — NEUROGENIC & VENOUS CLAUDICATION
Intermittent (vascular) claudication must be distinguished from its mimics. Neurogenic claudication (from lumbar spinal stenosis) causes leg pain on walking too, but it is relieved by sitting/bending forward rather than simply stopping, varies in distance, and is associated with back symptoms and preserved pulses. Venous claudication (a bursting pain after DVT) is relieved by elevation. Recognising these prevents misattributing a neurological or venous problem to arterial disease.
THE BOTTOM LINE
Intermittent claudication is exercise-induced muscle pain relieved by rest from PAD, its site indicating the level (calf = femoro-popliteal, buttock = aorto-iliac/Leriche), assessed by ABPI and treated with risk-factor control, exercise and best medical therapy.
A NOTE ON THE NATURAL HISTORY
Reassuringly, the natural history of stable intermittent claudication is relatively benign for the limb — with best medical therapy and exercise, most patients remain stable or improve and only a minority progress to critical ischaemia or amputation. The greater threat is to the patient's life from associated coronary and cerebrovascular disease. This is why counselling emphasises that treating risk factors protects the heart and brain as much as the leg, and why revascularisation is reserved for lifestyle-limiting or critical disease.
🔑KEY POINTS TO REMEMBER- Intermittent claudication = cramping muscle pain on walking, relieved by rest in minutes; from chronic arterial insufficiency (PAD).
- Reproducible claudication distance; site indicates level — calf (femoro-popliteal), thigh/buttock (aorto-iliac).
- Leriche syndrome (aorto-iliac): buttock/thigh claudication + erectile dysfunction + absent femoral pulses.
- ABPI <0.9; manage with smoking cessation, exercise, statin + antiplatelet + risk factors; revascularise only if lifestyle-limiting/critical.
📚SOURCES: Bailey & Love's Short Practice of Surgery.THE CONCEPT
Buerger's disease (thromboangiitis obliterans) is an inflammatory, thrombotic occlusive disease of the small and medium arteries and veins of the limbs. It is distinct from ordinary atherosclerosis, being an inflammatory 'vasculitic' process, and it has a very characteristic patient: the young male heavy smoker. Its defining and overwhelming association is with smoking, which both causes and drives the disease.
CLINICAL FEATURES
It presents with distal limb ischaemia — claudication (often of the instep/foot), rest pain, and digital ulceration or gangrene of the fingers and toes. Two associated features are characteristic: recurrent superficial thrombophlebitis (migratory, tender vein segments) and Raynaud's phenomenon. Because it affects distal vessels, the peripheral (digital) circulation is lost while proximal pulses may be preserved.
MANAGEMENT
The single most important intervention is absolute and complete cessation of smoking — this is essential and can halt progression, whereas continued smoking leads inexorably to further tissue loss and amputation. Other measures — analgesia, wound care and vasodilators — are supportive, and the distal nature of the disease means it responds poorly to revascularisation. Thus stopping smoking is not merely advice but the definitive treatment.
💡CLINICAL PEARL: The exam essence: Buerger's disease is the young male smoker with distal limb ischaemia, digital gangrene, migratory thrombophlebitis and Raynaud's, and the only effective treatment is complete cessation of smoking, which arrests the disease. Bypass surgery is usually not feasible because the affected vessels are small and distal.HISTOLOGY & DIAGNOSIS
Buerger's disease has a characteristic segmental, inflammatory thrombotic occlusion that, unlike atherosclerosis, spares the vessel wall's structure and affects both arteries and veins with a relatively cellular, inflammatory thrombus. Diagnosis is largely clinical (the young male smoker with distal ischaemia and the supporting features), supported by angiography showing distal, segmental occlusions with 'corkscrew' collaterals and by excluding atherosclerosis, embolic sources and autoimmune disease.
THE BOTTOM LINE
Buerger's disease is an inflammatory occlusive disease of the young male smoker causing distal ischaemia, digital gangrene, thrombophlebitis and Raynaud's, whose only effective treatment is absolute smoking cessation.
A NOTE ON PROGNOSIS WITH SMOKING
The prognosis of Buerger's disease is dictated almost entirely by smoking behaviour: patients who achieve complete, permanent cessation usually see the disease arrest, with no further tissue loss, whereas those who continue — even a few cigarettes — progress to repeated digital ulceration, gangrene and amputations. No drug or operation matches the effect of stopping smoking. This stark relationship makes intensive, sustained support for smoking cessation the entire foundation of management.
🔑KEY POINTS TO REMEMBER- Buerger's disease (thromboangiitis obliterans) = inflammatory thrombotic occlusion of small/medium limb arteries and veins.
- Classic: young male heavy smoker; strongly smoking-related.
- Distal ischaemia (instep claudication, rest pain, digital ulcers/gangrene) + migratory superficial thrombophlebitis + Raynaud's.
- Absolute smoking cessation is essential and can halt progression; poor response to revascularisation (distal disease).
📚SOURCES: Bailey & Love's Short Practice of Surgery.THE CONCEPT
Raynaud's phenomenon is episodic vasospasm of the digital arteries, usually triggered by cold or emotional stress, causing a characteristic sequence of colour changes in the fingers (more than toes). The exaggerated spasm transiently shuts off the blood supply to the digits and then releases, producing the classic triphasic colour change.
THE COLOUR CHANGES
The digits typically go white (pallor — from arterial spasm and ischaemia), then blue (cyanosis — as deoxygenated blood stagnates), then red (reactive hyperaemia — on rewarming and reperfusion), often with pain and numbness during the attack and tingling on recovery.
PRIMARY VS SECONDARY & MANAGEMENT
The crucial distinction is between primary and secondary Raynaud's. Primary (Raynaud's disease) is idiopathic, common in young women, symmetrical and benign, with no underlying disease. Secondary Raynaud's occurs as part of an underlying connective-tissue disease (especially systemic sclerosis/scleroderma, also SLE); it is more severe, may be asymmetrical, and can progress to digital ulceration or gangrene. Management is to keep warm, avoid triggers and stop smoking, with calcium-channel blockers (nifedipine) for troublesome cases, and to identify and treat any underlying connective-tissue disease.
DISTINGUISHING PRIMARY FROM SECONDARY
Distinguishing primary from secondary Raynaud's is the key clinical task, because secondary disease signals a serious underlying condition. Features suggesting secondary Raynaud's include onset at an older age, asymmetry, severe attacks with digital ulceration, abnormal nailfold capillaries, and positive autoantibodies (e.g. anti-centromere, anti-Scl-70). Such patients are investigated and monitored for an evolving connective-tissue disease, whereas primary Raynaud's in a young woman with a normal examination needs only reassurance and simple measures.
THE BOTTOM LINE
Raynaud's phenomenon is cold/emotion-triggered digital vasospasm with a white-blue-red colour change, benign when primary but a marker of connective-tissue disease when secondary, managed by warmth, trigger avoidance and calcium-channel blockers.
A NOTE ON DIGITAL ISCHAEMIA
In severe secondary Raynaud's (especially with systemic sclerosis), the repeated, prolonged vasospasm and associated small-vessel disease can lead to critical digital ischaemia — painful fingertip ulcers, and even gangrene of the digits. Such patients need more aggressive treatment (calcium-channel blockers, and agents such as intravenous prostacyclin (iloprost) for acute digital ischaemia), meticulous protection of the hands, and management of the underlying connective-tissue disease — a marked contrast to the benign, purely cosmetic-and-nuisance course of primary Raynaud's.
🔑KEY POINTS TO REMEMBER- Raynaud's phenomenon = episodic vasospasm of digital arteries triggered by cold/emotion.
- Triphasic colour change: white (ischaemia) → blue (cyanosis) → red (reactive hyperaemia).
- Primary (Raynaud's disease): idiopathic, young women, symmetrical, benign; secondary: connective-tissue disease (scleroderma, SLE), more severe, may ulcerate.
- Keep warm, avoid triggers, stop smoking; nifedipine for troublesome cases; treat any underlying disease.
📚SOURCES: Bailey & Love's Short Practice of Surgery.THE CONCEPT
Carotid artery stenosis is atherosclerotic narrowing at the carotid bifurcation (where the common carotid divides into internal and external carotid arteries). Its importance is as a source of emboli to the brain: fragments of platelet-thrombus or plaque break off and lodge in the cerebral or retinal circulation, causing transient ischaemic attacks (TIAs) and strokes. So carotid disease matters chiefly as a treatable cause of stroke.
CLINICAL FEATURES
It may be asymptomatic (found as a carotid bruit) or present with ischaemic neurological events in the territory supplied: amaurosis fugax (transient, painless monocular visual loss — 'like a curtain coming down' — from retinal artery embolism), and contralateral limb weakness or sensory loss and speech disturbance from cerebral emboli. A TIA is a warning of impending stroke.
INVESTIGATION & MANAGEMENT
The disease is assessed with carotid duplex ultrasound (to grade the stenosis), supplemented by CT or MR angiography. Management combines 'best medical therapy' — an antiplatelet, a statin, and control of blood pressure, diabetes and smoking — with, for symptomatic significant stenosis (generally > 50–70%), carotid endarterectomy (CEA) to remove the plaque and prevent future stroke (carotid stenting is an alternative in selected patients). The benefit of surgery is greatest when performed soon after a TIA/minor stroke.
TIMING & THE ROLE OF ENDARTERECTOMY
The timing of carotid endarterectomy is critical: the benefit is greatest when surgery is performed within about two weeks of a TIA or minor stroke, because the risk of a further, disabling stroke is highest in that early period. This is why a TIA is treated as an emergency ('brain attack') with urgent carotid imaging. Endarterectomy is offered for symptomatic significant stenosis; asymptomatic stenosis is more often managed medically, as the surgical benefit is smaller.
THE BOTTOM LINE
Carotid stenosis is atherosclerotic narrowing at the bifurcation causing embolic TIA/stroke (amaurosis fugax, contralateral weakness), assessed by duplex and treated with best medical therapy plus carotid endarterectomy for symptomatic significant stenosis, ideally early.
A NOTE ON STROKE PREVENTION IN CONTEXT
Carotid disease is only one cause of stroke, and its treatment fits within broader stroke prevention. A patient with a TIA is assessed for the full range of causes — carotid stenosis, atrial fibrillation (a cardioembolic source needing anticoagulation), and small-vessel disease — and given best medical therapy regardless. Carotid endarterectomy specifically addresses the embolic risk from a stenosed carotid; recognising which patients have surgically-treatable carotid disease, and acting quickly, is the key surgical contribution to preventing a disabling stroke.
🔑KEY POINTS TO REMEMBER- Carotid stenosis = atherosclerotic narrowing at the carotid bifurcation; a source of emboli → TIA/stroke.
- Asymptomatic (carotid bruit) or symptomatic: amaurosis fugax (transient monocular blindness), contralateral weakness/speech disturbance.
- Carotid duplex ultrasound (± CT/MR angiography) to grade stenosis.
- Best medical therapy (antiplatelet, statin, risk factors) + carotid endarterectomy for symptomatic significant stenosis (>50–70%), ideally soon after the event.
📚SOURCES: Bailey & Love's Short Practice of Surgery.THE CONCEPT
Lymphoedema is chronic swelling caused by impaired lymphatic drainage, leading to the accumulation of protein-rich interstitial fluid in the tissues. Because the lymphatic system normally returns this fluid and protein from the tissues to the circulation, its failure causes persistent, progressive swelling — usually of a limb — that differs from other oedemas in being high in protein and, over time, non-pitting.
CLASSIFICATION
- Primary lymphoedema — from a congenital or hereditary abnormality of the lymphatics (e.g. Milroy's disease), presenting at various ages.
- Secondary lymphoedema — from obstruction or damage to lymphatics: worldwide the commonest cause is filariasis (Wuchereria bancrofti); other causes are malignant infiltration, surgery or radiotherapy (classically arm swelling after axillary clearance for breast cancer), and recurrent infection.
CLINICAL FEATURES & MANAGEMENT
There is progressive limb swelling that is initially pitting but becomes non-pitting, with skin thickening and, in advanced disease, gross enlargement ('elephantiasis') and recurrent cellulitis. Management is largely conservative: compression (bandaging/garments), limb elevation, meticulous skin care to prevent infection, and exercise/manual lymphatic drainage, together with treating the cause (e.g. antifilarial drugs). Surgery is reserved for severe, refractory cases.
COMPLICATIONS & THE ROLE OF SKIN CARE
A key practical point is that lymphoedematous limbs are highly prone to recurrent cellulitis, and each infective episode further damages the lymphatics, worsening the swelling in a vicious cycle. This is why meticulous skin hygiene, prompt treatment of infection, and sometimes prophylactic antibiotics are central to management. Preventing infection is as important as compression in halting the progression from mild swelling to disabling elephantiasis.
THE BOTTOM LINE
Lymphoedema is chronic protein-rich swelling from impaired lymphatic drainage — primary (e.g. Milroy's) or secondary (filariasis, malignancy, surgery/radiotherapy) — managed mainly conservatively with compression, skin care and treatment of the cause.
A NOTE ON DIAGNOSIS & STEMMER'S SIGN
Lymphoedema is largely a clinical diagnosis, supported by a positive Stemmer's sign (inability to pinch and lift a fold of skin at the base of the second toe, because of skin thickening) which helps distinguish it from other causes of a swollen limb. Where the cause is unclear or intervention is planned, lymphoscintigraphy can demonstrate the abnormal lymphatic drainage. Excluding treatable causes — especially venous disease, cardiac/renal oedema, and (in endemic areas) filariasis — is an important part of the assessment.
🔑KEY POINTS TO REMEMBER- Lymphoedema = chronic swelling from impaired lymphatic drainage → protein-rich interstitial fluid (becomes non-pitting).
- Primary (congenital/hereditary, e.g. Milroy's) vs secondary (filariasis — commonest worldwide; malignancy; surgery/radiotherapy e.g. post-mastectomy; infection).
- Progressive limb swelling, skin thickening, 'elephantiasis', recurrent cellulitis.
- Mainly conservative: compression, elevation, skin care, exercise/lymphatic drainage; treat the cause (e.g. antifilarials); surgery rarely.
📚SOURCES: Bailey & Love's Short Practice of Surgery; SRB's Manual of Surgery.