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Peripheral arterial disease

SNOMED: 8405800041001 words•Updated 03/03/2026
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Exam Tips

  • Differentiate vascular claudication (exercise-induced, relieved rapidly by rest, reduced pulses) from neurogenic claudication (posture-related, relieved by spinal flexion).
  • In OSCEs, always screen for limb threat: rest pain, tissue loss, infection, and the acute ischaemia 6 Ps.
  • ABPI interpretation is high-yield: <0.9 suggests PAD, while >1.4 may indicate calcified non-compressible arteries (especially diabetes/CKD) and requires toe pressure assessment.
  • For acute limb ischaemia, state immediate actions: urgent vascular referral plus IV unfractionated heparin unless contraindicated.
  • PAD is a cardiovascular risk equivalent conceptually in exams: management must include secondary prevention, not only limb symptom control.
  • See Figure: arterial lesion distribution and ABPI interpretation chart in your vascular surgery textbook/teaching atlas for viva-style anatomy correlation.

Definition

Peripheral arterial disease (PAD) is chronic arterial insufficiency of the lower limbs, most commonly due to atherosclerotic narrowing or occlusion of medium and large arteries. It exists on a spectrum from asymptomatic disease and intermittent claudication to chronic limb-threatening ischaemia (CLTI: rest pain, tissue loss, or infection with inadequate perfusion), and acute limb ischaemia is a separate emergency caused by sudden perfusion loss over less than 2 weeks.

Pathophysiology

In about 95% of cases, endothelial injury and lipid-driven inflammation produce progressive atherosclerotic plaque in lower-limb arteries (often aorto-iliac, femoropopliteal, and infrapopliteal segments), reducing flow reserve. During exercise, oxygen demand exceeds supply, causing reversible ischaemic muscle pain (claudication); with further progression, resting perfusion falls below tissue viability thresholds, leading to ischaemic rest pain, ulceration, gangrene, and impaired wound healing (CLTI). Acute limb ischaemia usually follows in-situ thrombosis on ruptured plaque (most common) or embolic occlusion, with rapid neuromuscular injury, then reperfusion-associated oxidative/inflammatory injury, compartment syndrome, rhabdomyolysis, acidosis, and hyperkalaemia if revascularization is delayed.

Risk Factors

  • Smoking (strongest modifiable risk; dose-response relationship and higher amputation risk if continued)
  • Diabetes mellitus (approximately 2- to 4-fold risk increase; worse outcomes with poor glycaemic control)
  • Hypertension
  • Hypercholesterolaemia (raised LDL, triglycerides, lipoprotein(a))
  • Older age (especially >60 years)
  • Established atherosclerotic disease elsewhere (coronary, carotid, aortic)
  • Chronic kidney disease (particularly advanced CKD/end-stage kidney disease)
  • Male sex for more severe/symptomatic disease
  • Raised homocysteine (association present, but treating homocysteine has not shown clear outcome benefit)
  • Multiple concurrent risk factors (risk rises markedly when several are present)

Clinical Features

Symptoms

  • Intermittent claudication: reproducible calf/thigh/buttock pain on walking, relieved by rest within minutes
  • Reduced walking distance and functional limitation
  • Ischaemic rest pain (often forefoot, worse at night, relieved by dependency) in CLTI
  • Non-healing ulcers, tissue loss, or gangrene in advanced disease
  • Sudden severe limb pain in acute limb ischaemia
  • Numbness/tingling or weakness in acute limb ischaemia

Signs

  • Reduced/absent peripheral pulses, arterial bruits
  • Cool limb, delayed capillary refill, pallor on elevation, dependent rubor
  • Trophic skin changes (shiny skin, hair loss), dystrophic nails, muscle wasting
  • Ulceration or gangrene (typically distal pressure points/toes) in CLTI
  • Acute limb ischaemia '6 Ps': pain, pallor, pulselessness, poikilothermia, paraesthesia, paralysis
  • Mottling/cyanosis; in embolic disease onset is abrupt with clearer demarcation, while thrombosis is often more gradual with background PAD signs

Investigations

Ankle-brachial pressure index (ABPI):ABPI <0.9 supports PAD; severe ischaemia often lower values; ABPI >1.4 suggests non-compressible calcified vessels (common in diabetes/CKD) and still implies high cardiovascular risk
Toe pressure/toe-brachial index:Useful when ABPI is falsely elevated from calcification; reduced toe pressures support distal arterial insufficiency/CLTI
Duplex arterial ultrasound:Localizes stenosis/occlusion and estimates haemodynamic severity; first-line imaging before intervention planning
CT angiography or MR angiography:Defines arterial anatomy and lesion length for endovascular vs surgical revascularization decisions
Digital subtraction angiography:Gold standard luminal imaging, usually when proceeding to endovascular treatment
Blood tests (FBC, U&E, HbA1c, lipid profile, CRP, coagulation):Characterizes risk factors/comorbidity and procedural risk; in acute ischaemia check lactate, CK, potassium, acid-base status for reperfusion/metabolic complications
ECG and cardiovascular assessment:Screens for concurrent atherosclerotic disease/arrhythmia sources (for example atrial fibrillation if embolic event suspected)

Management

Lifestyle Modifications

  • Urgent smoking cessation support (very high impact on limb and cardiovascular outcomes)
  • Supervised exercise programme for claudication (structured walking therapy)
  • Mediterranean-style cardioprotective diet, weight optimization, regular activity within symptom limits
  • Diabetes, blood pressure, and lipid optimization with primary/secondary prevention targets
  • Foot care education (daily inspection, protective footwear, early review of ulcers/infection)
  • Prompt same-day vascular referral for suspected CLTI or acute limb ischaemia

Pharmacological Treatment

Antiplatelet therapy (secondary prevention)

  • Clopidogrel 75 mg once daily
  • Aspirin 75 mg once daily (if clopidogrel is contraindicated or not tolerated)

Use single antiplatelet therapy for symptomatic PAD unless specialist indication for alternatives. Contraindications/cautions: active bleeding, recent haemorrhagic stroke, severe liver disease, peptic ulcer disease. Clopidogrel interacts with omeprazole/esomeprazole (prefer lansoprazole if PPI needed).

Lipid lowering

  • Atorvastatin 80 mg once daily (high-intensity statin, adjust if intolerance/drug interactions)

Check baseline and follow-up liver enzymes as clinically indicated; counsel on myalgia and rare myopathy/rhabdomyolysis risk, higher with interacting drugs.

Claudication symptom relief (when exercise therapy insufficient and revascularization not suitable)

  • Naftidrofuryl oxalate 100 mg three times daily

Consider trial with review of walking-distance benefit after 3-6 months; stop if ineffective. Caution in recurrent calcium oxalate renal stones.

Post-revascularization dual pathway inhibition (specialist decision)

  • Rivaroxaban 2.5 mg twice daily plus aspirin 75 mg once daily

May reduce major adverse cardiovascular/limb events in selected high-ischaemic-risk, low-bleeding-risk patients. Avoid in active bleeding, pregnancy, significant hepatic coagulopathy, and severe renal impairment; assess bleeding risk carefully.

Acute limb ischaemia anticoagulation (emergency)

  • Unfractionated heparin 5000 units IV bolus, then IV infusion adjusted to therapeutic APTT

Start immediately unless contraindicated while urgent vascular surgery/interventional radiology is arranged. Monitor for bleeding and heparin-induced thrombocytopenia.

Surgical / Interventional

  • Endovascular angioplasty with or without stent placement
  • Surgical bypass (for example femoropopliteal/distal bypass) for suitable anatomy
  • Endarterectomy in selected focal disease
  • Catheter-directed thrombolysis, thrombectomy, or embolectomy for acute limb ischaemia based on limb viability and timing
  • Fasciotomy if compartment syndrome after reperfusion
  • Primary or secondary amputation when limb is non-viable or salvage not possible

Complications

  • Progression from claudication to CLTI with rest pain, ulceration, gangrene, and infection
  • Major and minor lower-limb amputation
  • Severe chronic pain, reduced mobility, loss of independence, and depression
  • Myocardial infarction, stroke, and other systemic atherosclerotic events (high cardiovascular mortality burden)
  • Acute limb ischaemia complications: reperfusion injury, compartment syndrome, rhabdomyolysis, metabolic acidosis, hyperkalaemia, multiorgan failure

Prognosis

PAD is a systemic atherosclerotic marker with substantial long-term cardiovascular risk even when leg symptoms are mild or absent. In intermittent claudication over about 5 years, most remain stable, but roughly 10-20% deteriorate, 5-10% progress to CLTI, and cardiovascular death/non-fatal events are common; limb loss is uncommon in uncomplicated claudication but rises sharply in diabetes and CLTI. Without timely revascularization, CLTI has high 1-year amputation risk and poor survival (around half dead by 5 years in severe disease), while acute limb ischaemia has significant early mortality and amputation risk that increases with delay to reperfusion.

Sources & References

💊BNF Drug References(24)

✅NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 425, 426)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 535)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 531)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 425)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 534, 535)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 221)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 221)[context]
  • Netter F. Netter Atlas of Human Anatomy. A Systems Approach 8ed 2022.pdf(pp. 494, 495)[context]
  • Netter F. Netter Atlas of Human Anatomy. A Systems Approach 8ed 2022.pdf(pp. 493, 494, 495, 496)[context]
  • Netter F. Netter Atlas of Human Anatomy. A Systems Approach 8ed 2022.pdf(pp. 485, 486, 487, 488, 489, 490, 491, 492, 493, 494, 495)[context]
  • _OceanofPDF.com_Netters_Anatomy_-_8th_edition_-_Frank_H_Netter_MD.pdf(pp. 493, 494, 495, 496)[context]
  • _OceanofPDF.com_Netters_Anatomy_-_8th_edition_-_Frank_H_Netter_MD.pdf(pp. 494, 495)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 812, 813)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 578, 579)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 579)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 93)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 675)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 671, 672)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 670, 671)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 675)[context]

Sources

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