Peripheral Arterial Disease

Meet the patient

A 64-year-old, 40-a-day smoker with type 2 diabetes walks one bus stop before his left calf seizes "like a cramp", stops, and is right again in three minutes — every single time, at the same distance. Tonight his foot aches in bed and only hanging it over the edge lets him sleep.[2]

Two questions now live on this ward round, and they are the two that decide every PAD case: is the leg in danger? (the ABI and the 6 Ps answer that) and is the patient in danger? (the heart and brain answer that). Everything below is built to answer both, at consultant depth.[1]

PAD is a coronary risk equivalent — say it first, every time

The most important sentence on the page is not about the leg. PAD is atherosclerosis of the leg arteries, but it is also a window onto the whole vascular tree; the patient newly labelled PAD is, statistically, far more likely to die of a myocardial infarction or stroke than to lose a limb. That is why cardiovascular risk reduction sits at the centre of management, whether or not the leg is ever revascularised.[1][3]

Three chronic syndromes share one pathology and need different responses: asymptomatic PAD (an abnormal ABI, no symptoms), intermittent claudication (symptomatic but stable), and chronic limb-threatening ischaemia (CLTI) — rest pain, ulceration or gangrene. Sitting on top of these is acute limb ischaemia (ALI), a sudden occlusion that is a time-critical vascular emergency.[1]

Etymology for viva gold: claudication comes from the Latin claudicare, "to limp" — the Emperor Claudius was so named for his limp. The word has survived two millennia because the symptom is unchanged: walk, limp, stop, recover.[2]

Three syndromes, one pathology — the Fontaine ladder and the Rutherford mirror

Stage the limb before you treat it. PAD is classified by symptom severity (Fontaine in Europe, Rutherford in North America), by lesion anatomy (TASC II), and — for the threatened limb — by a combined Wound, Ischaemia and foot Infection (WIfI) stage that predicts amputation and sets the urgency of revascularisation.[3]

The Fontaine ladder is the classical exam answer, staging PAD by its clinical evolution: I asymptomatic, II claudication (IIa beyond 200 m, IIb within 200 m), III ischaemic rest pain, IV tissue loss — ulceration or gangrene. Rutherford mirrors it from 0 to 6 and adds treadmill data: 0 asymptomatic, 1–3 mild, moderate and severe claudication, 4 rest pain, 5 minor tissue loss, 6 major tissue loss. Rutherford 4–6 is chronic limb-threatening ischaemia.[2]

The number rule that earns marks: Fontaine 4 stages, Rutherford 7 categories, and both III / 4–6 = CLTI. Say it in one breath and the classification marks are yours.[3]

[3]

Everyone forgets: the TASC II classification does not stage symptoms — it grades lesion anatomy to choose the revascularisation strategy. Each bed (aortoiliac, femoropopliteal, infrapopliteal) is graded A (focal stenosis — endovascular first) through D (long, multilevel occlusion — bypass first); the 2015 supplement extended it below the knee.[6]

The leg pain that is claudication — and the relief that proves it

Claudication is reproducible, exertional, and relieved by rest alone within minutes. The cramping calf (or buttock or thigh) pain comes on after a predictable walking distance, stops within minutes of standing still, and recurs at the same distance. The relief is with rest only — not with sitting, leaning forward, or a change of posture. That single sentence separates PAD from every mimic.[2]

The site of pain localises the level of disease — a viva staple. Cluster it once:[2]

• Buttock and thigh with erectile dysfunction → aortoiliac (Leriche syndrome) — the "limping, impotent smoker".
• Calf → superficial femoral artery (SFA) — by far the commonest.
• Foot (rare) → infrapopliteal (tibial) — think diabetes, and think Buerger.[2]

Ischaemic rest pain is the limb-threatening threshold: severe, persistent forefoot pain, worse at night and relieved by hanging the leg out of bed or walking to the next room (gravity aids perfusion). When resting flow itself is inadequate, the limb is in danger.[3]

[3]

Chronic limb-threatening ischaemia (CLTI) — formerly "critical limb ischaemia" — is rest pain for more than two weeks despite optimal medical therapy, or ischaemic ulceration or gangrene, with no alternative cause. Ischaemic ulcers are punched-out, painful, dry, with a pale base — on the toes, lateral malleolus or pressure points.[3]

Leriche syndrome is chronic aortoiliac occlusion in a middle-aged male smoker: the triad of buttock and thigh claudication, absent femoral pulses, and erectile dysfunction. It is a perennial viva favourite and the classic aortoiliac clue.[2]

Acute limb ischaemia — the 6 Ps and the 6-hour clock

Acute limb ischaemia is a sudden drop in limb perfusion and a time-critical emergency. Capture it in the 6 Ps: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishing cold. The first three are early; the last three — sensory and motor loss with profound coldness — mark a threatened limb where minutes count. The order matters: a viable limb can wait for imaging; a threatened limb cannot.[1]

[1]

The classic trap: a threatened limb (paraesthesia or paralysis) is revascularised on clinical grounds, before cross-sectional imaging. Irreversible necrosis begins within 4 to 6 hours of occlusion. Imaging waits; the limb does not.[1]

Read the claudication like the cath lab does — the ABI is the whole exam

Two tests do almost all of the diagnostic work: the resting ABI, and the exercise ABI if the resting one is normal. With the patient supine, measure systolic pressures at both brachial and both ankle arteries (posterior tibial and dorsalis pedis) with a handheld Doppler and a manual cuff; the ABI is the higher ankle pressure divided by the higher brachial pressure for each leg.[2]

The three thresholds that decide a PAD answer — memorise them as a triplet:[2]

• ABI under 0.9 = PAD.
• ABI under 0.4 = chronic limb-threatening ischaemia.
• ABI over 1.3 = non-compressible calcified vessel — use the toe pressure.[2]

[2] [1]

Everyone forgets: in diabetes and chronic kidney disease, medial arterial calcinosis stiffens the vessel wall and renders it non-compressible — the ABI reads falsely high (over 1.3), and you will falsely reassure a sick patient. Measure the toe–brachial index (TBI): the digital vessels are spared by calcinosis, so a TBI under 0.7 is abnormal.[1]

If the history is classic but the resting ABI is normal, walk the patient. A treadmill or active plantar-flexion test with a re-measured ABI — a drop of over 0.15 — confirms PAD. Early disease normalises the resting ABI; the exercise test catches it.[2]

How common, who, and what drives it

PAD is enormous and growing. The Fowkes systematic review put the global burden at roughly 236 million adults aged 25 and over in 2010, up almost a quarter in a decade — driven by ageing populations and the spread of smoking and diabetes into low- and middle-income countries.[4]

[4]

The two drivers that decide prognosis and dominate the exam: smoking is the single strongest modifiable risk factor — dose-dependent, two- to five-fold, and the chief determinant of progression to amputation. Diabetes multiplies risk two- to four-fold, preferentially attacks the distal (infrapopliteal) arteries, and is the dominant driver of CLTI and major amputation.[4]

The rest of the risk profile is the standard atherosclerotic fingerprint: age, hypertension, dyslipidaemia (raised LDL, low HDL), chronic kidney disease, obesity, family history, and South Asian or Black ethnicity, which carries higher PAD risk at any given burden.[1]

Why the leg claudicates — supply, demand, and the fourth power of radius

Claudication is a supply–demand mismatch, and the maths is brutal. Atherosclerosis is the same smouldering inflammatory response to endothelial injury as in the coronaries: tobacco, hyperglycaemia, oxidised LDL, hypertension and turbulent shear injure the endothelium; LDL infiltrates the intima, oxidises, and recruits monocytes that become lipid-laden foam cells — the fatty streak.[1]

Over years, smooth-muscle cells migrate in and cap the lipid-rich necrotic core with collagen — the fibrous plaque. Positive (outward) remodelling hides the plaque early, but it encroaches on flow once it cuts the cross-sectional area by more than about 70 percent (a diameter stenosis over 50 percent). When the cap ruptures or erodes, tissue factor fires the coagulation cascade and the thrombus either narrows the lumen stepwise or, catastrophically, occludes it — acute limb ischaemia.[1][3]

The fourth power of radius is why a modest narrowing hurts so much. By Poiseuille's law, flow is proportional to the fourth power of the radius — halve the radius and flow falls sixteen-fold. At rest the leg demands little, so a moderate stenosis is silent; on exercise the calf needs a many-fold rise in flow that the stenotic vessel cannot deliver, and the patient claudicates. As stenosis deepens, perfusion fails even at rest — rest pain, then ulceration and gangrene.[3]

The molecular detail (viva depth, optional)

Atherosclerosis is a chronic inflammatory disease: endothelial dysfunction from nitric-oxide depletion and adhesion-molecule upregulation recruits monocytes that differentiate into pro-inflammatory M1 macrophages, scavenge oxidised LDL and become foam cells. The balance between matrix metalloproteinases (which thin the cap) and their tissue inhibitors (which stabilise it) decides whether a plaque matures quietly or becomes a thin-cap fibroatheroma — the lesion that ruptures.[1]

Not every leg pain on walking is claudication — the mimics face-off

The discriminating features are the pattern of relief and the ABI. A candidate who can separate PAD claudication from its mimics in a sentence earns the marks.[2]

[2]

The one-line discriminator examiners want: PAD claudication is relieved by standing still within minutes; neurogenic claudication is relieved by sitting down or leaning forward — the shopping-cart sign. And the ABI is normal in neurogenic, venous and musculoskeletal causes.[2]

Look, feel, listen — and never forget the abdomen and the other leg

The vascular examination is structured: look, feel, listen. Always include the abdomen (aortic aneurysm) and the contralateral limb.[2]

Inspection shows the chronic signs of ischaemia: hair loss on the lower leg, thin, shiny, dry skin, thickened, slow-growing nails, muscle wasting, and in advanced disease pallor on elevation, rubor on dependency, coolness, ulceration or dry gangrene of the toes. Buerger's test — elevate the leg to 45 degrees; pallor of the sole within 60 seconds is abnormal, and the Buerger's angle (where pallor appears) is a rough severity index: the lower the angle, the worse the perfusion.[2]

Palpation grades every lower-limb pulse — femoral, popliteal, posterior tibial, dorsalis pedis — from 0 (absent) to 2 (normal), with 3 a bounding, aneurysmal pulse. An expansile popliteal pulse is a popliteal aneurysm — and prompts screening for an abdominal aortic aneurysm. Compare skin temperature side to side; the level of the temperature drop localises the occlusion.[2]

Auscultation listens for bruits over the abdomen (aortic, renal), the femoral triangle (aortoiliac, common femoral) and the carotids (concomitant cerebrovascular disease). Exclude an abdominal aortic aneurysm in every PAD patient, especially a male smoker over 65.[2]

The ulcer tells you the territory. Cluster the three by where they sit and how they feel:[3]

• Arterial — punched-out, sharply demarcated, painful, dry; on the toes or lateral malleolus.
• Venous — shallow, exudative, mildly painful; in the gaiter area above the medial malleolus, with varicose eczema and lipodermatosclerosis.
• Neuropathic — painless, deep, at pressure points (under the metatarsal heads, heel); callused, in a warm, insensate foot.[3]

For acute limb ischaemia, the bedside grades the limb's viability — and that single judgement decides image-first versus theatre-now: viable (sensation and power intact, Doppler audible), threatened (sensorimotor deficit, arterial Doppler inaudible — revascularise now), irreversible (fixed mottling, anaesthesia with rigidity — primary amputation).[1]

Imaging — locate the lesion, plan the run

Investigation answers three questions: is PAD present, where is the disease, is the limb at threat? The ABI answers the first; anatomical imaging answers the second; toe pressure, TcPO₂ and WIfI answer the third.[2]

Segmental limb pressures and pulse-volume recordings (PVR) localise disease by the step-down in pressure between thigh, calf and ankle cuffs. Duplex ultrasound is the first-line anatomical test — safe, no contrast, it locates and grades stenoses by the peak systolic velocity ratio and maps the great saphenous vein for bypass.[1]

[1] [3]

CTA is the road-map for revascularisation — fast and widely available, at the cost of iodinated contrast and radiation. MRA avoids iodine and shows distal vessels beautifully, but gadolinium risks nephrogenic systemic fibrosis in advanced kidney disease and it overestimates stenosis. Digital subtraction angiography remains the gold standard, used when intervention is already planned.[1]

Transcutaneous oxygen pressure (TcPO₂) predicts wound healing — over 40 mmHg heals, under 30 mmHg fails — and guides the revascularise-or-amputate decision in CLTI. Bloods (lipid profile, HbA1c, fasting glucose, U&E, eGFR, FBC), an ECG (atrial fibrillation as an embolic source in ALI), and a one-off AAA ultrasound in male smokers complete the work-up.[1]

Treat the whole patient — four pillars plus an emergency

Two goals run in parallel: save the patient and save the leg. Best medical therapy (BMT) is the foundation for every PAD patient — including the asymptomatic one with an abnormal ABI; revascularisation is added on top of, never instead of, BMT.[1]

[1]

Pillar 1 — Lifestyle and risk-factor modification. Smoking cessation is the single most effective intervention to halt claudication progression and cut both cardiovascular events and amputation — offer varenicline, nicotine replacement or bupropion plus behavioural support to every smoker. Add a Mediterranean or low-salt diet, weight reduction toward a BMI under 25, and meticulous foot care.[1][3]

Pillar 2 — Supervised exercise therapy (SET). SET is first-line for claudication and matches or beats pharmacotherapy: 30 to 45 minutes of walking, three times a week, for at least 12 weeks, walking to near-maximal claudication each time. It improves both pain-free and maximal walking distance. Where SET is unavailable, a home-based programme with a step counter and coaching is the alternative.[1][5]

Pillar 3 — Cardiovascular pharmacotherapy. An antiplatelet goes to all symptomatic PAD (and asymptomatic PAD with a high-risk feature): aspirin 75 to 100 mg once daily, or clopidogrel 75 mg once daily — clopidogrel preferred by many after CAPRIE showed superiority in PAD. A high-intensity statin goes to every PAD patient regardless of baseline LDL — atorvastatin 40 to 80 mg or rosuvastatin 20 to 40 mg once daily, targeting LDL under 1.8 mmol/L (70 mg/dL). Control blood pressure to under 130/80 with an ACE inhibitor (ramipril up to 10 mg) or ARB, and diabetes to HbA1c under 53 mmol/mol, preferring SGLT2 inhibitors or GLP-1 receptor agonists for their cardiovascular-renal benefit.[1]

[1] [8]

Pillar 3b — Low-dose rivaroxaban plus aspirin (COMPASS). Rivaroxaban 2.5 mg twice daily plus aspirin 100 mg daily cut major adverse limb events and mortality in stable PAD — an option in patients without a high bleeding risk. It is not used in CLTI or right after revascularisation, where the evidence differs.[8]

Cilostazol — the drug, the dose, and the contraindication that kills

Cilostazol improves walking distance but is absolutely contraindicated in heart failure. It is a phosphodiesterase-3 inhibitor; the Cochrane review confirmed a modest benefit of roughly 25 to 30 percent over placebo. Dose 100 mg twice daily (50 mg twice daily if intolerant), 30 minutes before or two hours after food.[12]

The trap that costs marks — and patients: cilostazol is contraindicated in any degree of heart failure. All PDE-3 inhibitors increase mortality in heart failure (the milrinone / PROMISE lesson). In a PAD patient with heart failure, choose naftidrofuryl (a 5-HT₂ antagonist, 100 to 200 mg three times daily — NICE first-line in the UK) or supervised exercise. Never prescribe cilostazol to a heart-failure patient.[12]

Pillar 4 — Revascularisation. Offer it for disabling claudication that has failed BMT and SET for at least 3 months, and urgently for CLTI to salvage the limb. The choice of endovascular (angioplasty ± stent) versus surgical bypass is guided by the TASC II lesion class, the GLASS anatomic stage, the availability of a good autologous vein (great saphenous), and the patient's comorbidity and life expectancy.[1][6]

The territory rules for revascularisation:[1]

• Aortoiliac — angioplasty ± stenting for TASC A and B; aortobifemoral bypass for extensive TASC D occlusions in fit patients.
• Femoropopliteal — angioplasty with selective stenting (drug-eluting stents, drug-coated balloons cut restenosis) for TASC A–C; femoropopliteal vein bypass for long SFA occlusions in a fit patient with a good vein.
• Femorodistal (tibial/pedal) — reserved for CLTI; vein overwhelmingly preferred over prosthetic.[1]

Amputation is reserved for irreversible ischaemia, uncontrolled sepsis, intractable rest pain unsuitable for revascularisation, or a non-ambulatory patient — always aiming for the most distal amputation that will heal.[1]

Acute limb ischaemia — embolus versus thrombus, and the fork

The mechanism decides the operation. An embolus arises from the heart (atrial fibrillation, mural thrombus after MI, valvular vegetations) or an aneurysm (popliteal, abdominal aortic), lodges at a bifurcation (common femoral, popliteal, aortic), and strikes a patient without prior collaterals — a profoundly ischaemic limb, clear demarcation, no claudication history. Thrombosis rides on a ruptured plaque or an occluded graft in a patient with collaterals, and so may present less catastrophically.[1]

[1]

The Rutherford acute-limb-ischaemia grade decides image-or-operate. Cluster it as viable / threatened / irreversible:[1]

• I (viable) — sensation and power intact, arterial and venous Doppler audible; investigate urgently, hours to spare.
• IIa (marginally threatened) — minimal sensory loss, no motor deficit, arterial Doppler inaudible but venous audible; image then revascularise.
• IIb (immediately threatened) — marked sensory and early motor loss; operate now, do not image.
• III (irreversible) — fixed mottling, profound anaesthesia and rigidity, no venous Doppler; primary amputation.[1]

For an embolic occlusion, a Fogarty catheter embolectomy under general or regional anaesthesia — balloon passed through a transverse arteriotomy, inflated, withdrawn to extract clot — is both diagnostic and therapeutic, followed by an on-table angiogram and fasciotomies if ischaemia time is long. For a thrombotic occlusion on a known plaque or graft, catheter-directed thrombolysis (alteplase via an intra-arterial catheter over 12 to 24 hours, with heparin cover) lyses clot and exposes the lesion for angioplasty — preferred when the limb is viable and the occlusion subacute.[1]

Chronic limb-threatening ischaemia — WIfI, GLASS, and the angiosome

CLTI is the end of the chronic continuum, and it demands urgent vascular referral. Rest pain over two weeks, or ulceration or gangrene — refer now and plan revascularisation. The WIfI stage stratifies amputation risk; the GLASS anatomic stage guides endovascular-versus-surgical strategy and an angiosome-directed revascularisation.[9][1]

WIfI in practice. Each of Wound, Ischaemia, foot Infection is graded 0 to 3; the combination yields a clinical stage 1 to 4 predicting one-year amputation risk. A stage 1 limb (minor wound, mild ischaemia, no infection) carries an amputation risk under 10 percent and may heal with wound care alone; a stage 4 limb (extensive wound, severe ischaemia, severe infection) carries over 25 percent and demands urgent combined revascularisation and debridement.[1]

The angiosome concept refines the plan: the posterior tibial artery feeds the medial plantar surface, the anterior tibial (as dorsalis pedis) feeds the dorsum, and the peroneal feeds the heel and lateral border. Direct angiosome-targeted revascularisation — restoring flow to the specific artery feeding the ulcer — improves healing and limb salvage, especially in diabetics with distal disease.[1]

The diabetic foot — neuropathy, ischaemia, infection

The diabetic foot is the leading cause of non-traumatic amputation, and it sits where neuropathy, ischaemia and infection intersect. Three ulcer patterns: neuropathic (painless, on pressure points, in a warm, dry, callused, insensate foot with palpable pulses), ischaemic (painful, punched-out, in a cool, pulseless foot), and neuroischaemic (the commonest, combining both). Management is multidisciplinary — podiatry, diabetes, vascular surgery, orthotics, microbiology.[9][10]

The septic diabetic foot is an emergency: admit for broad-spectrum IV antibiotics, urgent surgical debridement, glycaemic control with an insulin infusion, and urgent vascular imaging to plan revascularisation. The IWGDF/IDSA grading sets antibiotic depth:[9][10]

• Grade 1 (mild) — cellulitis under 2 cm: oral amoxicillin–clavulanate 500 mg three times daily for one to two weeks.
• Grade 2 (moderate) — cellulitis over 2 cm or deep tissue: IV amoxicillin–clavulanate 1.2 g three times daily plus metronidazole 500 mg three times daily, with Gram-negative cover for chronic wounds.
• Grade 3 (severe) — systemic sepsis or critical ischaemia: broad-spectrum IV such as piperacillin–tazobactam 4.5 g three times daily, source control and ICU support.[9]

A positive probe-to-bone test over a necrotic ulcer base raises osteomyelitis — confirm with plain radiograph, MRI, and bone biopsy for culture. IWGDF 2023 prevention applies in full: examine the feet at every visit, offload plantar ulcers in a total-contact cast, and revascularise ischaemic and neuroischaemic ulcers. Never debride a dry, uninfected ischaemic ulcer without a perfusion plan — revascularise first.[9]

Buerger disease — the young smoker you must not miss

Buerger disease (thromboangiitis obliterans) is the one PAD phenotype that is not atherosclerosis — and it has only one treatment. It is a non-atherosclerotic, segmental inflammatory vasculitis of the small and medium arteries and veins of the distal extremities, in heavy tobacco users, onset before 45 (often under 35).[7]

The pathology is distinctive — an occlusive inflammatory thrombus with giant cells that preserves the internal elastic lamina, with skip lesions. The picture is distal ischaemia (foot or calf claudication, rest pain, digital ulceration or gangrene) plus superficial migratory thrombophlebitis and Raynaud's phenomenon. Proximal pulses are preserved while distal pulses are absent; arteriography shows segmental occlusions with corkscrew collaterals.[7]

The only effective treatment is absolute tobacco abstinence. Keep smoking and the disease marches to amputation; stop completely and it often halts. No drug, no bypass, no endovascular device substitutes for cessation.[7]

Leriche syndrome — the aortoiliac triad

Leriche syndrome is chronic aortoiliac occlusion in a middle-aged male smoker — the triad of buttock and thigh claudication, absent femoral pulses, and erectile dysfunction. CTA shows distal aortic and bilateral common iliac occlusion; revascularisation is endovascular recanalisation and stenting, or aortobifemoral bypass in fit patients with extensive occlusion.[2]

When PAD patients come to harm — the preventable list

The feared limb harms are progression to CLTI, major amputation, and — in ALI — limb loss when revascularisation is delayed past the salvage window. Infection of an ischaemic ulcer turns to wet gangrene and sepsis; osteomyelitis complicates deep diabetic foot ulcers (probe-to-bone, MRI, bone culture).[1]

But the lethal complications are not in the leg. Patients with PAD die predominantly of myocardial infarction and stroke — the systemic atherosclerosis the leg is signalling. That is why aggressive medical therapy is non-negotiable.[1]

[1]

Procedure-related harms: contrast-induced nephropathy (hydrate, minimise contrast, hold metformin and nephrotoxins), reperfusion injury and compartment syndrome (prophylactic fasciotomy after prolonged ischaemia), graft or stent thrombosis and restenosis (the rationale for antiplatelets and dual-pathway inhibition), pseudoaneurysm and bleeding at the puncture site, prosthetic graft infection, and the rare cholesterol embolisation syndrome (blue toes, livedo, renal failure, eosinophilia) after catheter manipulation in a diseased aorta.[3]

The recurring pitfalls every candidate must name:[1]

• Failing to measure an ABI in a patient with leg pain — PAD is missed.
• Trusting a normal ABI in diabetes without a toe pressure (medial calcinosis).
• Delaying heparin and revascularisation in a threatened limb while awaiting imaging.
• Prescribing cilostazol to a heart-failure patient.
• Treating the leg while neglecting the cardiovascular risk that will actually kill the patient.[1]

Prognosis — two stories, the limb and the life

Tell prognosis as two parallel stories. For the limb, claudication is relatively benign: with risk-factor modification and supervised exercise, around 70 to 80 percent of claudicants stay stable or improve, only 20 to 30 percent progress, and fewer than 5 percent need major amputation over five years. Most claudicants never need revascularisation.[1]

CLTI is the other country. Without revascularisation it carries a one-year major amputation rate of about 20 to 25 percent and a one-year mortality of about 20 to 25 percent — revascularisation improves but does not normalise those numbers. Acute limb ischaemia salvages over 90 percent of limbs if revascularised within 6 hours; delay collapses that number.[1]

For life, the dominant number is five-year mortality in symptomatic PAD of about 25 to 30 percent — and the deaths are overwhelmingly cardiovascular. Prognosis tracks smoking status, diabetes control, statin adherence, renal function and graft patency. Disposition: a vascular surgeon for every CLTI or ALI; stable claudication is managed in primary care with BMT and SET, referring for disabling or worsening symptoms.[1]

[1]

Special populations — diabetes and CKD change everything

Diabetes is the most important special population. PAD is two to four times more prevalent, preferentially attacks the distal (infrapopliteal) arteries, is masked by neuropathy, and progresses more often to ulceration and amputation. Medial calcinosis breaks the ABI — measure the toe pressure. Screen diabetics over 50 (or younger with risk factors) with an ABI, examine the feet every visit, and refer any ulcer to a multidisciplinary diabetic foot service.[9][10]

Chronic kidney disease and dialysis bring aggressive, often calcific, multilevel disease — minimise iodinated contrast (prefer CO₂ angiography or MRA), optimise hydration, and expect non-compressible vessels. The elderly attribute claudication to arthritis or immobility, present late, and tolerate revascularisation less well — the balance shifts toward BMT. Women are under-diagnosed, report claudication less often, and may present with atypical leg pain; ABI thresholds are the same.[1]

Buerger disease (young male smokers) is discussed above — absolute tobacco abstinence is the only effective treatment, and the prognosis is limb-threatening without it.[7]

Guidelines, trials, and the regional split

The contemporary global standards are the 2024 ACC/AHA PAD Guideline (Gornik) and the 2017 ESC Guideline (Aboyans), both resting on the foundational 2016 AHA/ACC Guideline (Gerhard-Herman) and the 2011 ACCF/AHA focused update (Rooke). The TASC II document (Norgren, 2007) and its 2015 supplement (Jaff) codify lesion classification. All agree: best medical therapy for every patient, supervised exercise for claudication, revascularisation for limb threat.[1][3][2][5][6]

The trials that shape practice: COMPASS established low-dose rivaroxaban 2.5 mg twice daily plus aspirin to cut major adverse limb events and mortality in stable PAD.[8] BASIL-2 and BEST-CLI refined the vein-bypass-first versus best-endovascular-first choice in severe limb ischaemia.[11] The Cochrane review of cilostazol (Brown, 2021) confirmed a modest but real gain in walking distance.[12]

The controversy worth naming: the 2018 paclitaxel-coated balloon and stent mortality signal (Katsanos meta-analysis) upended practice before larger, longer-term pooled analyses and 2024 vascular-society reviews showed no excess mortality — device-level monitoring continues. The role of dual antithrombotic therapy (rivaroxaban plus aspirin) in CLTI and after revascularisation remains under active study.[1]

The mantra

PAD is systemic atherosclerosis made visible in the leg. Measure the ABI, treat the whole patient, recognise the threatened limb, and act on time.[1]

Ward-round test — answer without another resource

Stem 1 — the claudicant on the ward round (answer)

A 60-year-old smoker gets left calf cramp after 100 metres, every time, relieved by standing still for three minutes. What is the diagnosis, the first test, and the single most important management step for his life (not his leg)? Model: Intermittent claudication from PAD — reproducible exertional calf pain relieved by rest within minutes. First test: ankle–brachial index (expect under 0.9). The most important step for his life is not the leg — it is smoking cessation, a high-intensity statin, an antiplatelet, and blood-pressure and glycaemic control, because PAD is a coronary risk equivalent and he is more likely to die of an MI than to lose the leg.[1]

Stem 2 — the ABI that lies (answer)

A 58-year-old diabetic with a foot ulcer has an ABI of 1.4. The registrar writes "no PAD". What is wrong, and what do you do? Model: The ABI is falsely high — over 1.3 means non-compressible calcified vessels (medial calcinosis, classic in diabetes and CKD). "No PAD" is the trap. Measure the toe–brachial index — a TBI under 0.7 is abnormal — because the digital arteries are spared by calcinosis.[1]

Stem 3 — the cold blue limb at 3am (answer)

A 72-year-old in atrial fibrillation wakes with a sudden cold, pale, painful right leg. She has paraesthesia in the foot but can still move it. What is the diagnosis, the first drug, and the next move? Model: Acute limb ischaemia — the 6 Ps, embolic (atrial fibrillation source). The limb is threatened (paraesthesia). Give IV unfractionated heparin 80 units/kg bolus then 18 units/kg/hr and analgesia, keep the leg dependent, and call the vascular surgeon now — proceed to Fogarty embolectomy on clinical grounds within 6 hours; do not wait for CT angiography in a threatened limb.[1]

Stem 4 — the claudication drug in a heart-failure patient (answer)

A 65-year-old with claudication and an ejection fraction of 30 percent is started on cilostazol. What is the error, and what do you prescribe instead? Model: The error is cilostazol in heart failure — it is absolutely contraindicated; all phosphodiesterase-3 inhibitors increase mortality in heart failure (the milrinone / PROMISE lesson). Prescribe naftidrofuryl 100 to 200 mg three times daily (NICE first-line in the UK) or supervised exercise therapy instead.[12]

Stem 5 — the young smoker with a painful toe (answer)

A 32-year-old man, 30 cigarettes a day, has digital ulceration, a superficial tender leg vein, and Raynaud's. Proximal pulses are normal. What is the diagnosis, and the one thing that will save his limb? Model: Buerger disease (thromboangiitis obliterans) — young heavy smoker, distal ischaemia with digital ulceration, superficial migratory thrombophlebitis, Raynaud's, preserved proximal pulses. The one thing that saves the limb is absolute tobacco abstinence — no drug, bypass, or device substitutes.[7]

References

1. [1]Gornik HL, Aronow HD, Goodney PP, et al. 2024 ACC/AHA/AACVPR/APMA/ABC/SCAI/SVM/SVN/SVS/SIR/VESS Guideline for the Management of Lower Extremity Peripheral Artery Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines Circulation, 2024.PMID 38743805
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