Peripheral Arterial Disease and Buerger's Disease — Claudication, ABI, Staging and Management

Peripheral arterial disease (PAD) develops from arterial narrowing and occlusion, most often in the aortoiliac, femoropopliteal or infrapopliteal vessels, which impairs blood flow to the lower limbs. The cause is atherosclerosis — a chronic, progressive accumulation of lipid-rich plaque; less common causes are vasculitis, injury and radiation. The spectrum runs from asymptomatic disease through intermittent claudication to chronic limb-threatening ischaemia (CLTI), which carries a high risk of limb loss and death.

Smoking is the strongest modifiable risk factor (it raises the risk of PAD about fourfold); others are diabetes, age 65 or more, hypertension, raised LDL, chronic kidney disease, obesity and a sedentary lifestyle. Patients with PAD have a raised risk of heart attack, stroke and cardiovascular death, so PAD is a marker of systemic atherosclerosis as well as a limb problem.

Intermittent claudication is muscle pain or cramping that occurs during exercise such as walking and is relieved by rest. It affects the calf, thigh or buttock depending on the level of atherosclerosis. During exercise the muscles need more blood than collateral flow can supply; the supply-demand mismatch causes temporary ischaemia. Lowering the energy demand (stopping) relieves the pain.

• Loss of palpable pulses or Doppler signals
• Pallor, cool or cyanotic skin, slow capillary refill, mottling
• Muscle atrophy and hair loss; distal paraesthesia or numbness
• Chronic foot wounds; wet or dry gangrene; black, necrotic toes
• Buerger's sign — pallor of the foot on elevation with dependent rubor on lowering — an examination sign of limb ischaemia (not specific to Buerger's disease)

The ankle-brachial index (ABI) is the ratio of the systolic pressure at the ankle to the systolic pressure in the arm, measured with a cuff and a handheld Doppler over the brachial artery and the dorsalis pedis and posterior tibial arteries. The commonly used ankle value is the highest of the ankle pressures. The patient should lie supine and rest; the ankle cuff sits above the malleoli.

Fontaine described his classification in the 1950s using clinical symptoms alone. Rutherford (1986) added objective haemodynamic criteria such as ABI and toe pressures, making it more reproducible.

1. Risk-factor control: stop smoking, treat hypertension, tight glycaemic control in diabetes.
2. Statins for every PAD patient, regardless of LDL level, targeting LDL-C below 70 mg/dL.
3. Antiplatelet therapy (aspirin or clopidogrel) to lower the risk of myocardial infarction, stroke and vascular death.
4. ACE inhibitors or ARBs for blood pressure control, associated with better outcomes.
5. Supervised exercise therapy — a core part of claudication treatment.
6. Cilostazol (phosphodiesterase III inhibitor) for symptom relief in patients without heart failure; benefit is seen within 8–12 weeks.
7. Revascularisation (endovascular or surgical bypass) for lifestyle-limiting claudication that fails therapy and for CLTI; the TASC morphological classification guides endovascular versus open surgery.

Prognosis: only about 1–3% per year of patients with claudication progress to critical limb ischaemia, but in CLTI the risk of amputation is about 25–40% at one year. Complications include gangrene, infection, osteomyelitis, acute limb ischaemia, compartment syndrome and amputation.

Chronic PAD builds over months to years and allows collaterals to develop. Acute limb ischaemia is a sudden drop in perfusion — from embolism, thrombosis, trauma or vasculitis — presenting with the classic features pain, pallor, pulselessness, paraesthesia, paresis and paralysis; the limb is cold, and mottling is a late sign. Rutherford's acute limb ischaemia classification grades the limb as viable (class I), threatened (IIa salvageable, IIb salvageable if treated promptly) or irreversible (III), according to capillary refill, sensory loss, motor loss and Doppler signals.

Buerger's disease, or thromboangiitis obliterans (TAO), is a progressive, non-atherosclerotic, segmental, inflammatory disease that most often affects small and medium-sized arteries (and veins) of the upper and lower limbs. It was first described by von Winiwarter in 1879; the eponym honours Leo Buerger, who reported the pathology of amputated limbs in 1908. It typically occurs at 20 to 50 years of age, more often in men who smoke, and the highest incidence is in Ashkenazi Jews and people of Indian, Korean and Japanese ancestry.

Tobacco exposure is required for both initiation and progression. The mechanism is unknown but may involve immune dysfunction and a hypersensitivity to tobacco. Disease begins in the distal vessels of the hands and feet and then moves proximally.

• Claudication of the foot, leg, arm or hand, often mistaken for joint or neuromuscular disease; progresses to calf claudication, ischaemic rest pain and ulcers of the toes, feet or fingers.
• Raynaud phenomenon and paraesthesias of the acral parts.
• Migratory superficial thrombophlebitis — a systemic inflammatory sign (StatPearls quotes up to 16% in one passage and almost half in another).
• The Allen test assesses the extent of hand involvement.
• No specific laboratory test; serology excludes mimics — thrombophilia, diabetes, autoimmune disease; echocardiography excludes a proximal embolic source.
• Angiography/CT angiography: segmental occlusions of small and medium arteries, with 'corkscrew' collaterals — but corkscrewing is not specific to TAO.

A precise diagnosis can be made only by histology: thrombosis of small and medium arteries and veins with dense polymorphonuclear leukocyte aggregation, microabscesses and multinucleated giant cells in the acute phase, then organised thrombus with recanalisation and fibrosis. The key distinguishing point from other vasculitides is that the internal elastic lamina is preserved and the vessel wall is relatively spared.

There is no cure; the cornerstone is complete and permanent cessation of tobacco. Even smoking one or two cigarettes a day can perpetuate the disease, and nicotine replacement can keep it active. In patients who stop, remission is impressive and amputation is avoided. If patients continue to smoke, 43% need one or more amputations within 7.6 years.

• Calcium channel blockers or other vasodilators for symptoms, especially with Raynaud phenomenon.
• Intravenous iloprost (prostacyclin analogue) for pain, trophic changes and to reduce amputation, most useful in the phase when the patient first quits.
• Sympathectomy or spinal cord stimulation have been used sporadically; VEGF therapy remains experimental.
• Surgical bypass has a minimal role because there is often no acceptable target vessel and vein conduits are limited by migratory thrombophlebitis.
• Analgesia and antibiotics for ischaemic pain and mild distal infection.