Peripheral Arterial Disease & Limb Ischaemia

Peripheral arterial disease (PAD) is atherosclerotic narrowing of the lower-limb arteries causing chronic ischaemia, while acute limb ischaemia (ALI) is a surgical emergency from sudden arterial occlusion. This topic is heavily examined for the ABPI, Fontaine/Rutherford staging, the six P's, Fogarty embolectomy, and graft selection — pure vascular decision-making.

Definition & classification

Peripheral arterial disease denotes obstruction to arterial flow distal to the aortic bifurcation, almost always due to atherosclerosis in NEET PG questions. It produces a spectrum from asymptomatic disease → intermittent claudication → critical limb ischaemia (CLI, now called chronic limb-threatening ischaemia, CLTI) → tissue loss.

Anatomical levels of disease (high-yield correlation with claudication site):

Level of occlusion	Eponym	Claudication site	Classic feature
Aorto-iliac	Leriche syndrome	Buttock, hip, thigh	Triad: buttock claudication + impotence + absent femoral pulses
Femoro-popliteal (superficial femoral artery at adductor canal)	—	Calf	Commonest site of PAD
Infra-popliteal (tibial/peroneal)	—	Foot	Seen in diabetics, Buerger disease

High-yield: The superficial femoral artery in the adductor (Hunter's) canal is the single most common site of atherosclerotic occlusion in the lower limb, producing calf claudication.

Fontaine classification (chronic PAD)

Stage	Clinical picture
I	Asymptomatic (incidental, abnormal ABPI)
IIa	Intermittent claudication >200 m
IIb	Intermittent claudication <200 m
III	Ischaemic rest pain (esp. at night, relieved by hanging foot down)
IV	Ulceration / gangrene (tissue loss)

Rutherford classification (chronic)

Categories 0–6: 0 asymptomatic; 1–3 mild→severe claudication; 4 rest pain; 5 minor tissue loss; 6 major tissue loss. Stages III–IV Fontaine ≈ Rutherford 4–6 = chronic limb-threatening ischaemia.

High-yield: Rest pain + tissue loss = CLTI, requiring revascularisation within days, not weeks. Ankle pressure usually <50 mmHg (rest pain) or <30 mmHg with tissue loss.

Etiology & risk factors

• Atherosclerosis — by far the commonest cause.
• Smoking — the single strongest modifiable risk factor for PAD (stronger association with PAD than with coronary disease).
• Diabetes mellitus — causes infra-popliteal/tibial disease and medial calcification (Mönckeberg), giving falsely high ABPI.
• Hypertension, dyslipidaemia (high LDL, low HDL), hyperhomocysteinaemia, chronic kidney disease, age, male sex.
• Buerger disease (thromboangiitis obliterans): young male, heavy smoker, distal small/medium vessels of upper AND lower limbs, migratory superficial thrombophlebitis, corkscrew collaterals on angiography. Treatment = absolute smoking cessation.

Pathophysiology

Atherosclerotic plaque narrows the lumen → flow-limiting stenosis (>70% diameter). At rest, collaterals maintain perfusion; on exercise, oxygen demand outstrips supply → ischaemic muscle pain (claudication) relieved by rest. As disease progresses, resting perfusion fails → rest pain, ulceration, gangrene. Ischaemic rest pain is typically in the forefoot/toes, worse at night (loss of gravity assistance and reduced cardiac output) and relieved by dependency.

In acute limb ischaemia, sudden occlusion (embolus or in-situ thrombosis) gives no time for collateral development → rapid, profound ischaemia. Reperfusion after revascularisation risks compartment syndrome and reperfusion injury (hyperkalaemia, myoglobinuria, acidosis, acute kidney injury, arrhythmia).

Clinical features

Chronic PAD: intermittent claudication (cramping muscle pain on walking, reproducible distance, relieved by rest), rest pain, dependent rubor, elevation pallor (Buerger's test), trophic changes — shiny hairless skin, thickened nails, muscle wasting, cold pulseless foot, arterial ulcers (punched-out, painful, over pressure points/toes/heel/lateral malleolus).

High-yield: Buerger's angle = angle of leg elevation at which the foot turns pale. Angle <20°** indicates severe ischaemia. Vascular (capillary) **refilling time >15–20 s on dependency also indicates severe disease.

Acute limb ischaemia — the six P's

Pain → Pallor → Pulselessness → Paraesthesia → Paralysis → Perishing cold (Poikilothermia)

High-yield: Paraesthesia and paralysis are the ominous late signs — they indicate impending irreversible nerve/muscle damage. Loss of sensation and power = threatened limb demanding emergency revascularisation. The window for muscle viability is approximately 6 hours (golden period).

Embolus vs in-situ thrombosis (classic exam differentiation):

Feature	Embolic ALI	Thrombotic ALI
Source	Heart (AF, post-MI mural thrombus, valve)	Pre-existing atherosclerotic plaque
Onset	Sudden, dramatic	More gradual (collaterals exist)
Prior claudication	Absent	Often present
Opposite limb pulses	Normal	Often abnormal (generalised disease)
Commonest lodging site	Common femoral bifurcation	Site of existing stenosis
Treatment	Embolectomy (Fogarty)	Thrombolysis / bypass

High-yield: Commonest site for an arterial embolus to lodge in the lower limb = common femoral artery bifurcation. Overall the commonest peripheral embolism site is the femoral; saddle embolus lodges at the aortic bifurcation.

Investigation

Ankle–Brachial Pressure Index (ABPI / ABI) — the first-line bedside investigation.

ABPI = highest ankle systolic pressure (dorsalis pedis or posterior tibial) ÷ highest brachial systolic pressure, measured with a hand-held Doppler.

ABPI value	Interpretation
>1.3 (or >1.4)	Incompressible, calcified vessels (diabetes, CKD) — unreliable
0.9–1.3	Normal
0.8–0.9	Mild PAD
0.5–0.8	Moderate (claudication)
<0.5	Severe ischaemia
<0.3 (ankle pressure <50 mmHg)	Critical limb ischaemia

High-yield: Normal ABPI ≈ 1.0–1.2. In diabetics, medial calcinosis gives a falsely elevated ABPI; use toe-brachial index (TBI <0.7 abnormal) or toe pressures instead, as digital arteries are spared calcification.

Stepwise diagnostic approach:

1. History + examination + pulse palpation → 2. ABPI (screen/confirm) → 3. Duplex ultrasound (first-line imaging, non-invasive, locates stenosis) → 4. CT angiography / MR angiography (anatomical road-map before intervention) → 5. Digital subtraction angiography (DSA) — gold standard, now mainly therapeutic (combined with angioplasty).

• Exercise treadmill test: confirms claudication and reveals a post-exercise drop in ABPI when resting ABPI is borderline.
• Buerger disease → angiography shows "corkscrew collaterals."

High-yield: DSA = gold-standard imaging; Duplex ultrasound = best first-line/initial imaging modality.

Management

Conservative / medical (foundation for ALL patients)

• Risk factor modification: absolute smoking cessation (most important), statins (target LDL <70 mg/dL), BP and glycaemic control, antiplatelet (aspirin or clopidogrel; clopidogrel slightly superior per CAPRIE).
• Supervised exercise programme — first-line for intermittent claudication; promotes collateral formation.
• Cilostazol — phosphodiesterase-3 inhibitor; drug of choice to improve claudication walking distance. Contraindicated in heart failure. (Pentoxifylline is an alternative, weaker.)
• Foot care, avoid trauma; treat infection.

High-yield: Drug specifically to increase claudication distance = cilostazol. Contraindicated in congestive heart failure (all PDE-3 inhibitors increase mortality in CHF).

Revascularisation — indications

Reserved for lifestyle-limiting claudication refractory to medical therapy, and always for CLTI (rest pain, ulceration, gangrene) and acute limb ischaemia.

Endovascular (angioplasty ± stenting): preferred for short, focal, aorto-iliac lesions (TASC A/B). Lower morbidity; first choice in iliac disease.

Open surgical bypass: preferred for long-segment occlusions, diffuse disease, infra-inguinal disease (TASC C/D).

Graft choice — PTFE vs saphenous vein

Feature	Reversed/in-situ great saphenous vein	PTFE (Dacron) prosthetic
Patency below knee	Superior (best)	Inferior below the knee
Infection resistance	High (autologous)	Poor — avoid in infected fields
Use	Conduit of choice for infra-inguinal/below-knee bypass	Above-knee fem-pop, aorto-bifemoral

High-yield: The great (long) saphenous vein is the best conduit for infra-inguinal (especially below-knee femoro-popliteal/femoro-distal) bypass. Prosthetic (PTFE/Dacron) is acceptable for above-knee bypass where vein is unavailable, but vein patency is superior below the knee.

Named bypass procedures: aorto-bifemoral graft (Leriche/aorto-iliac disease), femoro-popliteal bypass (SFA occlusion), femoro-distal bypass, and extra-anatomical grafts (axillo-femoral, femoro-femoral crossover) for high-risk patients or hostile abdomen/infection.

Acute limb ischaemia management

Immediate: IV heparin bolus (prevent propagation), analgesia, fluids, keep limb dependent and warm (do not actively heat).

Rutherford classification of ALI (decides salvage vs amputation):

Class	Viability	Sensory loss	Motor deficit	Doppler (arterial/venous)	Action
I	Viable	None	None	Audible / Audible	Not immediately threatened; imaging then plan
IIa	Marginally threatened	Minimal (toes)	None	Inaudible / Audible	Salvageable, urgent revascularisation
IIb	Immediately threatened	More than toes, rest pain	Mild–moderate	Inaudible / Audible	Emergency revascularisation
III	Irreversible	Profound, anaesthetic	Paralysis, rigor	Inaudible / Inaudible	Primary amputation

Definitive:

• Embolus (Rutherford I–IIb): surgical embolectomy using a Fogarty balloon catheter via femoral cutdown — the classic answer for an embolic occlusion with a cardiac source.
• Thrombosis: catheter-directed thrombolysis (recombinant tPA/urokinase) for viable (I/IIa) limbs, or bypass/angioplasty.
• Class III (irreversible): primary amputation — revascularising dead muscle causes lethal reperfusion (hyperkalaemia, rhabdomyolysis).

High-yield: Fogarty (balloon embolectomy) catheter = device of choice to extract an arterial embolus. Invented by Thomas Fogarty.

Amputation — indications (the "three D's")

Dead (gangrene/irreversible ischaemia), Dangerous (spreading sepsis, gas gangrene), Damn nuisance (intractable rest pain, non-functional limb).

• Level chosen to balance healing (needs adequate perfusion) vs rehabilitation. Below-knee amputation (BKA) preserves the knee joint → far better prosthetic mobility than above-knee (AKA).
• Healing best predicted by toe pressure and tissue perfusion at the chosen level.

Reperfusion & complications

• Compartment syndrome post-revascularisation → prophylactic/therapeutic fasciotomy (4-compartment of the leg). Earliest reliable sign = pain on passive stretch; compartment pressure >30 mmHg or within 30 mmHg of diastolic = decompress.
• Reperfusion syndrome: hyperkalaemia, metabolic acidosis, myoglobinuria → acute kidney injury, cardiac arrhythmias.
• Disease progression: gangrene, limb loss, and high cardiovascular mortality (PAD is a coronary-risk equivalent — most patients die of MI/stroke).

Key differentials

Differential	Distinguishing feature
Neurogenic claudication (spinal canal stenosis)	Pain on standing/extension, relieved by bending forward/sitting, normal pulses, normal ABPI
Venous claudication	Bursting pain after exertion in post-DVT limb, relieved by elevation
Diabetic neuropathy	Burning pain, glove-stocking sensory loss, often palpable pulses, painless neuropathic (plantar) ulcer
Buerger disease	Young smoker, distal, upper + lower limbs, thrombophlebitis migrans

High-yield: Arterial ulcer = punched-out, painful, on toes/pressure points, ABPI low. Venous ulcer = gaiter area (medial malleolus), shallow, sloping edges, relatively painless, normal pulses. Neuropathic ulcer = painless, over plantar pressure points.

Recently asked / exam angle

• ABPI cut-offs: >1.3 = calcified (diabetic), <0.5 = severe, <0.3/ankle pressure <50 mmHg = CLI.
• Most common site of lower-limb atherosclerotic occlusion → SFA in adductor canal (calf claudication).
• Leriche syndrome triad — buttock claudication, impotence, absent femoral pulses.
• Six P's of acute limb ischaemia; paralysis + paraesthesia = late/ominous.
• Fogarty catheter for embolectomy; embolus lodges at common femoral bifurcation; AF is the commonest cardiac source.
• Best bypass conduit below knee = great saphenous vein.
• Drug to increase walking distance = cilostazol (avoid in CHF).
• Buerger disease = corkscrew collaterals; absolute smoking cessation.
• Rutherford class III ALI (anaesthetic, paralysed, no Doppler signal) → primary amputation, not revascularisation.
• Falsely high ABPI in diabetics → use toe-brachial index.
• Gold-standard imaging = DSA; first-line imaging = duplex ultrasound.

Rapid revision

1. Normal ABPI 1.0–1.2; <0.5 severe; <0.3 critical; >1.3 = incompressible/calcified vessels.
2. Cilostazol (PDE-3 inhibitor) improves claudication distance; contraindicated in heart failure.
3. SFA at adductor canal = commonest site of occlusion → calf claudication.
4. Leriche syndrome = aorto-iliac disease: buttock claudication + impotence + absent femoral pulses.
5. Six P's: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishingly cold — last two are late and limb-threatening.
6. Arterial embolus most commonly lodges at the common femoral bifurcation; commonest source = atrial fibrillation.
7. Fogarty balloon catheter = embolectomy; viability golden window ≈ 6 hours.
8. Great saphenous vein = best graft for infra-inguinal/below-knee bypass; PTFE for above-knee.
9. Duplex US = first-line imaging; DSA = gold standard.
10. Diabetics → falsely high ABPI (Mönckeberg medial calcinosis) → use toe pressures/TBI.
11. Rutherford III ALI (anaesthetic, paralysed, no Doppler) → primary amputation.
12. Post-revascularisation watch for compartment syndrome (fasciotomy) and reperfusion hyperkalaemia/myoglobinuria/AKI.