Peripheral Artery Disease — Causes, ABI Testing, Claudication & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Peripheral artery disease (PAD) is atherosclerotic narrowing or occlusion of the peripheral arteries — predominantly the aortoiliac and femoropopliteal-tibial segments supplying the lower limbs. It is a manifestation of systemic atherosclerosis and a powerful marker of cardiovascular risk. PAD affects approximately 200 million people globally, with prevalence rising steeply with age — affecting 5–10% of adults over 50 and up to 20% over 70 years. The condition ranges from asymptomatic (present in 50–60% of PAD patients), through symptomatic intermittent claudication (muscle cramping pain on walking, relieved by rest), to chronic limb-threatening ischaemia (CLTI) — rest pain, non-healing ulcers, and gangrene — which carries a high risk of amputation and mortality. PAD significantly predicts concurrent coronary and cerebrovascular disease — patients have a 2–4-fold increased risk of myocardial infarction and stroke.

Atherosclerosis is the underlying pathology in more than 95% of PAD cases. The same cardiovascular risk factors drive PAD as coronary and cerebrovascular disease. Smoking is the single most important modifiable risk factor for PAD — smokers have 3–4 times the PAD risk of non-smokers, and smoking cessation is the most effective intervention to halt progression. Diabetes mellitus: PAD affects 15–20% of diabetics; diabetic PAD is more distal (tibial and peroneal vessels), progresses more rapidly, and is associated with worse outcomes including higher amputation rates. Hypertension (doubles PAD risk); hypercholesterolaemia (elevated LDL); chronic kidney disease (CKD — independently associated with PAD and worse outcomes); age over 60; male sex; family history; and hyperhomocysteinaemia. Non-atherosclerotic causes of peripheral arterial disease (uncommon): thromboangiitis obliterans (Buerger's disease — affects young male smokers, involves small and medium vessels); vasculitis (Takayasu's arteritis, giant cell arteritis); fibromuscular dysplasia; popliteal entrapment syndrome.

Asymptomatic PAD (50–60%): low ABI without symptoms — detected on routine testing. Intermittent claudication (30–40%): reproducible cramping pain, aching, or tiredness in the calf, thigh, or buttock muscles occurring with walking a predictable distance (the 'claudication distance'), relieved within 2–10 minutes of rest. Aortoiliac disease (Leriche syndrome) causes buttock and thigh claudication plus erectile dysfunction in men. Femoropopliteal disease causes calf claudication. Chronic limb-threatening ischaemia (CLTI — 5–10%): ischaemic rest pain (constant burning pain in the foot or toes — worse at night when the limb is elevated, relieved by hanging the foot down or walking); non-healing ulcers or wounds (especially on the heel, toe tips, or areas of minor trauma); dry or wet gangrene. Signs: absent or reduced femoral, popliteal, or pedal pulses; pallor on elevation, dependent rubor; cool extremity; atrophic skin changes; hair loss on toes; nail changes.

Ankle-brachial pressure index (ABI or ABPI): the cornerstone diagnostic test — the ratio of the highest ankle systolic BP (dorsalis pedis or posterior tibial) to the highest brachial systolic BP measured by Doppler. ABI above 1.0 is normal; 0.9–0.7: mild PAD (claudication); 0.7–0.5: moderate PAD; below 0.5: severe PAD (CLTI). ABI above 1.4 (incompressible calcified vessels — common in diabetics and CKD) — use toe-brachial index (TBI) or pulse volume recordings instead. Exercise ABI (post-treadmill): ABI drop above 20% or below 0.9 after exercise confirms claudication in patients with normal resting ABI. Duplex Doppler ultrasound: maps the location and severity of stenoses and occlusions. CT angiography (CTA) or MR angiography (MRA): detailed vascular anatomy prior to revascularisation — identifies lesions suitable for endovascular versus surgical intervention. Digital subtraction angiography (DSA): the gold standard — used selectively, particularly when simultaneous intervention is planned. Transcutaneous oxygen pressure (TcPO2): assesses tissue perfusion in CLTI — values below 30–40 mmHg indicate critical ischaemia.

Medical management (all PAD patients): smoking cessation — most important intervention; antiplatelet therapy — clopidogrel 75 mg daily (preferred over aspirin per CAPRIE trial; rivaroxaban 2.5 mg BD + aspirin 100 mg daily in selected high-risk PAD patients — COMPASS trial, 24% reduction in MACE); high-intensity statin (atorvastatin 80 mg) — reduces MACE and PAD progression; ACE inhibitor or ARB; tight glycaemic control in diabetes (target HbA1c below 53 mmol/mol); blood pressure below 130/80 mmHg; cilostazol 100 mg BD (phosphodiesterase inhibitor — improves claudication walking distance by 40–60%; avoid in heart failure); wound care and podiatry in diabetic PAD. Supervised exercise therapy: 30–45 minutes walking 3 times weekly for 12 weeks — improves maximum walking distance by 50–200% in claudication; now a Class IA recommendation in ESC guidelines — as effective as angioplasty for claudication. Endovascular revascularisation (for CLTI or lifestyle-limiting claudication failing exercise therapy): percutaneous transluminal angioplasty (PTA) with or without drug-eluting stent; drug-coated balloon (DCB). Surgical revascularisation: aortobifemoral bypass (gold standard for aortoiliac occlusion); femoropopliteal bypass using autologous vein (great saphenous vein graft — best long-term patency) or prosthetic graft. Amputation (last resort in CLTI with non-reconstructable arterial anatomy or non-viable limb).

Untreated or inadequately managed PAD progresses to chronic limb-threatening ischaemia (CLTI) — characterised by ischaemic rest pain, non-healing ulcers, and gangrene. CLTI carries a 20–25% major amputation rate and 20–30% mortality within 12 months, predominantly from cardiovascular causes. Acute limb ischaemia — sudden arterial occlusion from thrombosis or embolism — is a surgical emergency requiring revascularisation within 4–6 hours to prevent irreversible limb loss. Non-healing diabetic foot ulcers frequently progress to osteomyelitis (bone infection), requiring surgical debridement or partial foot amputation. The leading cause of death in PAD patients is not limb loss but systemic cardiovascular events — myocardial infarction and stroke, which affect PAD patients at 2–4 times the rate of the general population due to coexistent coronary and cerebrovascular atherosclerosis. Post-amputation complications include phantom limb pain, impaired mobility, depression, and accelerated contralateral limb disease.

PAD prevention mirrors global cardiovascular disease prevention: stop smoking immediately and maintain cessation (most important single intervention); control LDL cholesterol to below 1.4 mmol/L in patients with established cardiovascular disease (high-intensity statin ± ezetimibe ± PCSK9 inhibitor — evolocumab, alirocumab); maintain blood pressure below 130/80 mmHg; achieve optimal glycaemic control in diabetes; maintain a healthy BMI and exercise regularly. Diabetic foot surveillance: all diabetic patients should have annual foot checks including ABI measurement, foot pulses, and sensation testing — early detection of PAD allows intervention before limb-threatening complications. Patients with established PAD should follow a structured walk-to-rest exercise programme, take antiplatelet therapy and a statin without interruption, and have regular vascular follow-up with ABI monitoring.

Seek emergency assessment immediately for: acute limb ischaemia — sudden-onset severe leg pain, pallor, pulselessness, paraesthesia, paralysis, and perishing cold ('six Ps') — this is a surgical emergency requiring revascularisation within 4–6 hours to save the limb. Consult your GP for: calf, thigh, or buttock pain that consistently occurs on walking a certain distance and resolves with rest; foot or toe ulcers that are not healing despite standard wound care; or cold, discoloured, or painful toes or foot at rest. All patients with diabetes should have annual ABI measurement and foot examination to detect silent PAD before it becomes limb-threatening. If you are diagnosed with PAD, ensure you are prescribed an antiplatelet agent and statin, and referred for supervised exercise therapy.