Cardiovascular · Full case

Peripheral Arterial Disease

NICE NG19CKS 2024
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Peripheral Arterial Disease · Clinical Reasoning Framework v2
GP & SCA · NICE NG19 / CG147 · CKS 2024
ABPI ≤0.9Diagnostic threshold for PAD
ABPI ≤0.5Critical limb-threatening ischaemia
<200 mClaudication distance: significant impairment
6 monthsSupervised exercise therapy minimum (NICE NG19)
6 PsAcute limb ischaemia: Pain · Pallor · Pulselessness · Paraesthesia · Paralysis · Perishingly cold
50–70%PAD patients die from MI or stroke — not limb loss
80 mgAtorvastatin dose for all PAD (NICE NG19)
>1.4ABPI falsely elevated: calcified vessels (DM/CKD) — use toe-brachial index
📋 Clinical Stem — Intermittent Claudication First Presentation
A patient presenting with bilateral calf pain on walking that resolves with rest
Brian Patel, a 62-year-old bus driver, attends with a 4-month history of bilateral calf cramping pain that comes on consistently after walking approximately 200 metres and is fully relieved within 5 minutes of standing still. He is a 40 pack-year smoker (currently 20/day), has Type 2 diabetes diagnosed 8 years ago (HbA1c 62 mmol/mol at last check), and is on amlodipine 5mg for hypertension (BP today 162/96). He has never had a heart attack or stroke. He mentions his uncle had his leg amputated due to "poor circulation" and is frightened that the same will happen to him. He is also privately worried about his HGV bus driver licence, on which his livelihood depends.
This stem covers the commonest PAD presentation in primary care — stable intermittent claudication in a patient with multiple cardiovascular risk factors. The critical skills are ABPI measurement, distinguishing vascular from neurogenic claudication, completing the secondary prevention cascade, and recognising when symptoms have progressed to critical limb-threatening ischaemia (CLTI). The hidden agenda (amputation fear, DVLA licence) drives the consultation's Relating to Others domain.
Scenario A — Claudication Progressing to Rest Pain 68-year-old smoker with 6-month claudication at 100m now developing night pain in the forefoot relieved by hanging leg out of bed. ABPI 0.42. Critical limb-threatening ischaemia — urgent vascular surgery referral.
Scenario B — Acute Limb Ischaemia 71-year-old with known AF presents with sudden onset severe left calf and foot pain, pallor, and inability to feel the foot. The 6 Ps present — embolic occlusion. 999 immediately; do not take a full history first.
Scenario C — Diabetic Foot with Ischaemia 65-year-old with T2DM, non-healing heel ulcer, absent pedal pulses, ABPI 0.6. Mixed ischaemic and neuropathic ulcer. Diabetic foot MDT referral; urgent vascular assessment; infection screen.
Scenario D — Leriche Syndrome 58-year-old male smoker, bilateral buttock and thigh claudication, absent femoral pulses, erectile dysfunction. Aortoiliac occlusion — needs CT angiography and vascular surgery; smoking cessation critical.
Scenario E — Neurogenic Claudication (DDx) 70-year-old with bilateral leg pain and weakness after walking, relieved by sitting or leaning on a trolley. No ABPI reduction. Lumbar spinal stenosis — MRI lumbar spine; orthopaedic/neurosurgery referral.
Key variables to adapt for ABPI value, Fontaine stage (IIa/IIb/III/IV), presence of rest pain or tissue loss, DM and neuropathy, AF as embolic source, previous vascular intervention, occupation (DVLA implications), and bilateral versus unilateral symptoms.
Steps:
1
Step 1
History Taking — Open Question First · Targeted Questions · ICE · Psychosocial Context
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PAD history is a story about the whole cardiovascular system, not just the legs. The most important fact in any PAD consultation is not how far the patient can walk — it is that 50–70% of PAD patients will die from a heart attack or stroke, not from limb loss. Every question about leg symptoms must be paired with questions about cardiovascular risk factors and systemic atherosclerosis. A patient who walks 400 metres before stopping has the same excess cardiovascular mortality as a patient who has had a recent MI. The legs are the diagnostic signal; the heart and brain are what we are protecting.
🎓 Consultation opener — use existing clinical information first
"I can see from your notes that you've come in about pain in your legs when you walk. Before I ask anything else, can you tell me in your own words what happens — describe it from the very beginning?"
Referencing the presenting complaint from the case notes acknowledges you've prepared, avoids wasting consultation time, and positions the open question as purposeful rather than vague. Asking for information already documented scores zero for Global Skills and wastes the 12-minute window.
1A — Start with an open question: let the patient lead, then move to targeted questions
Question to askWhy it matters clinicallyChanges what?
🟢 OPEN QUESTION — always start here"Can you describe exactly what happens — where does it start, what does the pain feel like, and what makes it go away?" The narrative contains the diagnosis: vascular claudication has a highly consistent pattern — cramping pain after a predictable distance that is completely relieved within 5–10 minutes of rest. No other condition has this predictable exertion–relief–exertion cycle. The spontaneous description reveals character (cramp vs ache vs heaviness), site (calf = SFA/popliteal; thigh = iliac; buttock = aortoiliac), and relief pattern (rest = vascular; sitting/flexion = neurogenic; unchanged = musculoskeletal).In SCA: a candidate who immediately asks "does your pain go away when you rest?" has led the witness and lost the diagnostic nuance. The open narrative is the examination. Vascular vs neurogenic vs musculoskeletal DDxABPI urgencyAmputation fear
Consistent claudication distance?"How far can you walk before the pain starts — and is it roughly the same distance every time, or does it vary?"Vascular claudication is characteristically reproducible — the same muscle mass requires the same cardiac output increase; the same arterial narrowing produces ischaemia at the same oxygen demand. Consistent onset distance is highly specific for vascular cause. Variable distance suggests neurogenic (worse with lumbar extension, better after sitting) or non-vascular cause. NICE classifies <200m as significant functional impairment warranting intervention.Claudication distance is the primary outcome measure for supervised exercise therapy — document it at baseline for comparison at 3 and 6 months.Vascular vs neurogenic claudicationExercise threshold for intervention
Exact site of pain?"Can you show me exactly where in your legs the pain is — is it mainly the calf, the thigh, the buttock, or everywhere?"Pain site localises the level of arterial occlusion: calf claudication = superficial femoral or popliteal artery disease (most common, 70%); thigh claudication = external iliac artery disease; buttock or hip claudication = aortoiliac occlusion. Bilateral buttock claudication + absent femoral pulses + erectile dysfunction in men = Leriche syndrome (aortic bifurcation occlusion). Each pattern directs the Doppler and angiographic imaging to the relevant vessel level.Leriche syndrome specifically: impotence is often the presenting complaint that brings the patient to the GP, not leg pain. Ask about erectile function in all male patients with bilateral proximal symptoms.Arterial level localisationDoppler target levelVascular surgery level decision
Rest pain or night pain?"Does the pain ever come on when you're sitting still or lying in bed at night? Do you ever need to hang your leg out of bed or get up and walk to relieve it?"This is the single most important question to distinguish stable claudication from critical limb-threatening ischaemia (CLTI). Rest pain that is persistent (>2 weeks), located in the forefoot (not calf), and relieved by dependency (hanging the leg down allows gravity-assisted perfusion) = CLTI until proven otherwise. ABPI will typically be ≤0.5. Night rest pain + dependent relief is pathognomonic of critical ischaemia and requires urgent vascular referral within 1–2 weeks.Patients often attribute night leg pain to cramp or arthritis — ask specifically. The dependent position relief sign is highly specific for ischaemic rest pain and is not present in musculoskeletal or neuropathic pain.CLTI: urgent vascular referralClaudication vs critical ischaemiaUrgency of specialist referral
Skin changes, ulcers, or wounds that aren't healing?"Have you noticed any sores, ulcers, or wounds on your feet or legs that aren't healing properly? Any colour change, skin breakdown, or areas that are black?"Tissue loss (ischaemic ulcers or gangrene) = Fontaine Stage IV = CLTI. Ischaemic ulcers are characteristically painful, at pressure points (heel, toe tips, malleolus), punched-out edges, pale/necrotic base, absent surrounding skin changes. Gangrene (dry = progressive necrosis; wet = superadded infection) requires same-day or emergency vascular referral. In DM, infection can mask ischaemia — warm infected tissue may maintain skin colour despite severe underlying arterial insufficiency.A non-healing wound on the foot in a diabetic patient with absent pedal pulses = ischaemic until proven otherwise. Never apply compression bandaging to an ischaemic limb without excluding PAD first — ABPI essential before compression.Tissue loss/gangrene: emergencyDiabetic foot MDT + vascularABPI mandatory before compression
Erectile dysfunction?"This might feel unrelated, but in men, problems with blood flow in the pelvis can sometimes cause difficulties with erections. Has that been an issue?"Erectile dysfunction in a male patient with bilateral thigh or buttock claudication is a diagnostic marker for aortoiliac disease (Leriche syndrome). The internal pudendal artery arises from the internal iliac, which is compromised in aortoiliac occlusion. This changes management from peripheral arterial work-up to aortic imaging and directly informs the level of vascular reconstruction required.Many male patients would never volunteer erectile dysfunction spontaneously, particularly in a GP setting. The specific, respectful framing "in men, blood flow problems can cause this" normalises the question and is essential for identifying Leriche syndrome before the femoral pulses are examined.Leriche syndrome (aortoiliac)CT aortogram rather than peripheral DopplerAortic reconstruction vs peripheral bypass
Acute worsening or sudden onset?"Has the pain changed suddenly — got much worse very quickly, or come on for the first time in one leg when it wasn't there before?"Acute limb ischaemia (ALI) can develop on a background of chronic PAD (acute-on-chronic) or de novo (embolic, usually from AF). Sudden severe worsening of symptoms in a known claudicant may represent acute thrombosis at a point of critical stenosis. Any suggestion of the 6 Ps (Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishingly cold) = limb-threatening emergency requiring 999 — not a clinic appointment.Acute-on-chronic ischaemia is harder to recognise than de novo ALI because the patient attributes the worsening to their known "bad circulation." Asking specifically about sudden change identifies the subset requiring emergency vascular intervention.Any 6 Ps features: 999 immediatelyAcute vs chronic ischaemia
Full cardiovascular history?"Have you ever had a heart attack, a stent in your heart, a stroke, or a TIA? Do you have angina?"PAD is a marker of systemic atherosclerosis — over 50% of PAD patients have coexisting coronary artery disease, and 20–30% have cerebrovascular disease. A patient with known PAD + angina + prior TIA has polyvascular disease and requires the most intensive secondary prevention strategy. Polyvascular disease is an independent predictor of CV mortality and drives more aggressive LDL and BP targets.The cardiovascular history is as important as the vascular history. PAD is the leg symptom of a systemic disease. Secondary prevention of MI and stroke is the primary clinical goal of PAD management.Statin and antiplatelet intensityCardiac work-up if symptomaticCardiology if uncontrolled CAD
Smoking history — detailed pack-year calculation?"How long have you smoked, how many per day? Have you ever tried to stop? Are you aware that smoking is the single most important factor driving your leg symptoms?"Smoking is the single most important modifiable risk factor for PAD — it increases PAD risk 2–4× and dramatically accelerates progression to critical limb ischaemia. Smokers who continue after PAD diagnosis have a 7× higher limb loss rate than those who stop. Cessation alone improves claudication distance more effectively than any drug intervention. Every consultation is an opportunity to deliver a brief motivational intervention.Pack-year calculation (cigarettes/day ÷ 20 × years smoked) documents tobacco exposure for surgical risk assessment. Post-vascular reconstruction patency rates are significantly worse in current smokers.Smoking cessation is the single most important interventionSurgical candidacy affected by smoking status
Diabetes — foot care, sensation, and glucose control?"Do you have diabetes? Do you check your feet regularly? Have you noticed any loss of sensation or numbness in your feet?"DM dramatically worsens PAD outcomes — neuropathy masks ischaemic pain (so patients present later, at more advanced disease), impaired immunity worsens infection, and microvascular disease compounds ischaemia. In DM, ABPI may be falsely elevated (calcified vessels) — toe-brachial index is required. Poor HbA1c is an independent predictor of amputation in PAD. Foot examination at every review is mandatory.The combination of neuropathy + ischaemia + infection in the diabetic foot is the leading cause of non-traumatic lower limb amputation in the UK. Each component must be assessed independently — treating infection without addressing ischaemia leads to non-healing.Toe-brachial index if ABPI >1.4HbA1c optimisation; foot care planDiabetic foot MDT if ulceration
Other vascular risk factors and drug history?"What medication are you taking? Do you take a blood pressure tablet, a cholesterol tablet, aspirin, or any blood thinners?"Establishes baseline secondary prevention status and identifies gaps. Absence of statin, antiplatelet, and antihypertensive in a patient with confirmed PAD = undertreated secondary prevention. Beta-blockers are NOT contraindicated in PAD (common misconception — NICE NG19 is explicit): they should be continued or started if there is concurrent angina or heart failure.Beta-blockers do not worsen claudication in controlled trials despite historical concerns. Stopping beta-blockers in a PAD patient who had an MI is more dangerous than the theoretical claudication worsening. State this clearly in SCA if it arises.Secondary prevention gaps identifiedBeta-blocker misconception corrected
1B — Red flags: must not miss · must ask · must act
🚨

Red Flags — act before continuing history

Red flagWhy dangerousAction
The 6 Ps — any combination: Sudden severe Pain · Pallor · Pulselessness · Paraesthesia · Paralysis · Perishingly cold limbAcute limb ischaemia (ALI) — the limb is threatened. Without revascularisation within 6 hours, irreversible muscle and nerve death occurs. Paralysis + paraesthesia = severely threatened limb requiring emergency surgical thromboembolectomy or catheter-directed thrombolysis.999 immediately — vascular surgical emergency
Sudden collapse + severe central/back/abdominal pain + pulsatile abdominal massRuptured or symptomatic abdominal aortic aneurysm (AAA). Rapidly fatal without emergency aortic repair. Can present with leg pain from malperfusion. In PAD patients with known AAA, any acute deterioration = AAA rupture until proven otherwise.999 immediately
Rest pain (forefoot) persisting >2 weeks, worse at night, relieved by dependencyCritical limb-threatening ischaemia (CLTI) — ABPI typically ≤0.5. Without urgent revascularisation, major amputation rate is 25–30% within 1 year. Prognosis is worse than many cancers. Early vascular referral is limb-saving and potentially life-saving.Urgent vascular surgery within 2 weeks
Non-healing ulcer or gangrene on foot or lower leg with absent pedal pulsesFontaine Stage IV CLTI — tissue loss with underlying ischaemia. In DM, infection can progress rapidly to septicaemia; gas gangrene can develop within hours. Compression bandaging applied without ABPI confirmation is potentially limb-threatening.Urgent vascular referral — same week
Rapidly progressive claudication (distance halved within weeks) with fever or raised inflammatory markersAcute-on-chronic ischaemia from thrombus propagation, plaque rupture, or vasculitis. May also represent infective aortitis (rare but life-threatening). Rapid deterioration outside of gradual atherosclerosis progression requires urgent imaging and specialist input.Same-day or next-day vascular review
Wet gangrene (blackened tissue + surrounding warmth + smell + systemic features: fever, rigors)Wet gangrene = ischaemia superimposed with gas-forming organisms (Clostridium spp.). Rapid progression to septicaemia and multi-organ failure. May require emergency digit or limb amputation within 24 hours to control sepsis source even before revascularisation.999 — surgical emergency
🛡️

Safeguarding Considerations — Consider in Every Consultation

PAD can be both a consequence of and a marker for harm and neglect. Inadequately treated foot ulcers in vulnerable people with DM and PAD are a common presentation of self-neglect, carer neglect, or inadequate system-level follow-up. Compression bandaging applied without ABPI by uninformed carers worsens ischaemia. Post-amputation patients are particularly vulnerable to depression, social isolation, and carer exploitation.
🏠 Domestic Abuse & Lower Limb Injury
  • Lower limb bruising, ulceration, or fractures inconsistent with history may represent physical abuse — particularly in older adults and people with mobility limitation
  • Partner-inflicted tying of limbs or improvised compression can cause acute ischaemia or exacerbate existing PAD — document mechanism carefully
  • Forced immobility (leaving a person unable to walk or access care) can cause rapid deterioration of claudication to critical ischaemia through reduced collateral formation
  • Ensure adequate privacy for PAD consultations — a controlling partner attending can prevent disclosure of worsening symptoms or limb injuries
👴 Older Adults & Carer-Related Concerns
  • Ischaemic foot ulcers in older adults with PAD can be misidentified as pressure ulcers — carers who apply compression bandaging to ischaemic limbs cause serious harm
  • Carer neglect: older person with PAD and dementia unable to self-report worsening symptoms; wet gangrene can develop over days in a person unable to communicate pain
  • Financial exploitation post-amputation: changes in mental capacity, mobility dependence, and social isolation increase vulnerability
  • Consider whether the patient can safely perform daily foot inspection — if not, ensure carer or community nurse foot checks are arranged
🧒 Young Adults / Self-Neglect
  • Heavy smoking and injecting drug use are causes of PAD in young patients — non-judgmental assessment of substance use is essential; intravenous drug use causes infected arterial pseudoaneurysm which mimics PAD
  • Self-neglect in alcohol dependence: the combination of alcoholic neuropathy + recurrent falls + ischaemia can lead to undetected limb injuries and rapid progression
  • Poor foot care in patients with intellectual disabilities or severe mental illness: advocate for regular chiropody and foot inspection to be included in CTPLD / CPA care plans
💊 Medication Misuse & Iatrogenic Harm
  • Ergotamine overuse (migraine treatment) causes lower limb vasospasm that mimics PAD — often presents as bilateral claudication in young women with migraine
  • Inadvertent compression of ischaemic limb by healthcare professionals without performing ABPI is a patient safety and potential medico-legal issue
  • Unnecessary anticoagulation changes (e.g. stopping warfarin for a procedure without LMWH bridging in AF + PAD) can precipitate acute limb ischaemia
  • Post-amputation opioid dependence: proactive pain management planning prevents iatrogenic opioid harm in patients with significant post-operative or phantom limb pain
If a safeguarding concern is identified: Document examination findings precisely — measure and photograph ulcers if consent given. For compression-related ischaemic harm: document who applied compression and when; report as patient safety incident. For older adult neglect: MASH referral; social care assessment; consider whether carer has capacity and insight. Safeguarding documentation must not delay assessment of limb viability.
1C — PMH · FH · Drug history · Social history: management impact
🧬 PMH / FH — changes management
FactorWhy it mattersManagement impact
Coronary artery disease / previous MIPAD is a marker of systemic atherosclerosis — 50–60% of PAD patients have coexisting CAD. MI in PAD patients is 3× more likely than limb loss as cause of deathDrives most intensive secondary prevention: atorvastatin 80mg + antiplatelet + ACEi. Cardiology review if uncontrolled angina or LV dysfunction before vascular surgery.
Previous TIA / stroke / carotid stenosisPolyvascular disease (PAD + CAD + cerebrovascular) = highest CV mortality risk. ABPI-confirmed PAD + prior stroke = very high-risk for recurrent eventAntiplatelet (clopidogrel preferred in PAD), statin, antihypertensive all mandatory. Carotid Doppler to screen for coexisting carotid stenosis.
Diabetes mellitusDM accelerates PAD progression, masks ischaemic pain via neuropathy, and impairs wound healing. ABPI falsely elevated (>1.4) if calcified vessels — toe-brachial index needed. Amputation risk 10× higher in DM + PADToe-brachial index instead of ABPI if DM + ABPI >1.4. HbA1c target <58 mmol/mol (or lower if tolerated). Diabetic foot MDT for any ulceration. SGLT2i for CV secondary prevention.
Chronic kidney disease (CKD)CKD is an independent predictor of PAD progression and cardiovascular mortality. Calcified vessels falsely elevate ABPI. Contrast nephropathy risk with CT angiography. Many PAD drugs require dose adjustment in CKD.Toe-brachial index if ABPI unreliable. MR angiography (no contrast) preferred over CT for pre-operative imaging. Check eGFR before ACEi; before contrast imaging; and DOAC dosing.
Atrial fibrillationAF is the most common cause of acute limb ischaemia (ALI) via embolism to the peripheral arteries. PAD + AF = dual antithrombotic therapy decision — DOAC for AF vs antiplatelet for PADDOAC for AF is primary; antiplatelet is secondary. Adding clopidogrel to DOAC increases bleeding — specialist decision. CHA₂DS₂-VASc calculation. Anticoagulation does not replace antiplatelet in PAD.
Abdominal aortic aneurysm (AAA)PAD and AAA share the same pathophysiology — diffuse atherosclerosis. PAD patients have 2–3× higher prevalence of AAA than general population. Any AAA in a PAD patient warrants surveillance.Abdominal examination + aortic palpation at every review. Refer for aortic ultrasound screening if not already performed. AAA >5.5cm → urgent vascular surgery referral.
Previous vascular intervention (stent, bypass, endarterectomy)Previous revascularisation changes anatomy, affects ABPI interpretation, and alters surgical options. Stent occlusion or bypass graft failure can cause acute deteriorationDocument previous procedures. Duplex graft surveillance post-bypass. Sudden deterioration in a patient with prior revascularisation = acute graft occlusion until proven otherwise — vascular emergency.
HyperlipidaemiaRaised LDL drives atherosclerotic plaque progression. LDL reduction is one of the most effective secondary prevention interventions in PAD — reduces major adverse limb events (MALE) as well as MACEAtorvastatin 80mg for all confirmed PAD regardless of LDL (NICE NG19). Target LDL <1.8 mmol/L in PAD (ESC 2019). Add ezetimibe if LDL not at target. PCSK9 inhibitor if still above target.
💊 Drug history · Social history — clinical impact
FactorWhy it mattersManagement impact
Smoking (current or ex-smoker)The single most important modifiable cause of PAD. Risk 2–4× in current smokers. Limb loss risk 7× higher in continuing smokers after PAD diagnosis. Post-bypass graft patency dramatically worse in smokersSmoking cessation is the most important single intervention — more effective than any drug. Every appointment: offer NRT + cytisine/varenicline + SMSC referral. Pack-year calculation for surgical risk. Current smoking affects candidacy for elective revascularisation.
Antiplatelets and anticoagulants already prescribedBreakthrough event on existing antiplatelet = treatment failure or non-compliance. Anticoagulant for AF + PAD requires specialist antiplatelet decision. Aspirin is less effective than clopidogrel in PAD specifically (CAPRIE trial)If already on aspirin 75mg → consider switching to clopidogrel 75mg (preferred in PAD, NICE NG19). Document compliance carefully. If already on DOAC → specialist decision on adding antiplatelet.
Beta-blockersCommon misconception: beta-blockers are NOT contraindicated in PAD. NICE NG19 is explicit — they should not be withheld if indicated for angina, post-MI, or heart failure. Multiple RCTs show no significant worsening of claudication distanceDo NOT stop beta-blockers because of PAD. If patient's cardiologist or GP has previously stopped a beta-blocker for PAD, consider restarting if there is a cardiac indication. State this clinical point explicitly in SCA.
NSAIDs / COX-2 inhibitorsNSAIDs increase cardiovascular risk, interfere with antiplatelet effect of aspirin, and worsen renal function in patients on ACEi. Should be minimised in PAD patients on maximal secondary preventionReview and stop NSAIDs where possible. Paracetamol preferred for analgesia. If NSAID essential: add PPI; monitor BP and renal function; avoid combination with antiplatelet + anticoagulant.
Occupation — driving, manual labourPAD with claudication <100m may affect safe vehicle operation. HGV/bus drivers: DVLA notification duty if exercise tolerance affects driving ability. Post-bypass or post-amputation: DVLA assessment required. Manual labourers may be unable to workDVLA Group 2: notify if exercise tolerance affected; vascular assessment may be required. Group 1: generally can continue if symptoms controlled. Document occupational impact and DVLA discussion at diagnosis and each review.
Alcohol (hazardous/harmful use)Heavy alcohol causes neuropathy (confounds ischaemic pain assessment), hypertension, and raises cardiovascular risk. Alcoholic neuropathy + PAD can cause rapidly progressing foot ulceration that is both neuropathic and ischaemicAUDIT-C screening. Brief intervention. Alcohol cessation improves BP, glycaemia, and neuropathy. SMSC referral if dependent. Neuropathic + ischaemic foot = referral to diabetic foot MDT regardless of DM status.
Depression and anxietyChronic pain and mobility limitation from claudication cause depression in 20–30% of PAD patients — comparable to post-MI depression rates. Depression independently predicts poor secondary prevention adherence and increased limb lossPHQ-9 screening at diagnosis and at each 3-month review. NHS Talking Therapies referral or SSRI for confirmed depression. Supervised exercise therapy has direct antidepressant benefit — this is an additional argument for exercise therapy beyond symptom management.
Diet and obesityObesity worsens claudication directly (increased cardiac output demand accelerates ischaemic threshold) and increases surgical risk. Mediterranean diet reduces cardiovascular events independently of cholesterol levelWeight reduction target: >5% body weight reduction improves claudication distance. Dietitian referral if BMI >35. Mediterranean diet counselling at every appointment.
1D — ICE: Ideas · Concerns · Expectations — in every consultation, not just SCA
💡 Why ICE matters in PAD — the gap between "bad circulation" and understanding systemic vascular risk

Most patients with PAD have a fundamentally different mental model of their disease from the clinical reality. They understand "bad circulation in the legs" but do not understand that they have systemic atherosclerosis that threatens their heart and brain. The amputation fear (the single most common and powerful concern) drives behaviour — patients who fear amputation more than they fear heart attacks are the most likely to engage with smoking cessation. The ICE framework is the only tool that reveals this hierarchy of concerns and allows you to harness it therapeutically.

💭 Ideas
"What do you think is causing this pain in your legs? Do you have any thoughts about what might be happening in the blood vessels?"
Most patients attribute claudication to "bad circulation," ageing, or sometimes DVT. Few understand the atherosclerotic mechanism or appreciate that their heart and brain arteries may be equally affected. The patient's explanatory model determines how you frame the diagnosis — "just like the arteries in your heart furing up, the same is happening in your legs" lands very differently from a clinical explanation of atherosclerosis.
😟 Concerns
"What's your biggest worry about these symptoms — is it about your walking, your legs, something you might have heard about what can happen?"
Amputation fear is the dominant hidden agenda in PAD consultations — and it is almost never volunteered until directly asked. A patient who is frightened of amputation (as Brian is, after his uncle) is far more likely to engage with smoking cessation, exercise, and medication if these are framed as "what keeps your legs and reduces your risk of amputation" rather than as cardiovascular risk reduction abstractions.
🎯 Expectations
"What were you hoping we could do today — were you hoping for a scan, a tablet, a referral to a specialist, or just to understand what's going on?"
Many PAD patients expect a referral for a stent or bypass operation. Understanding this expectation allows you to explain why supervised exercise therapy comes first (NICE NG19), and why it is genuinely more effective than they might expect. It also identifies the patients who need occupational support (e.g. the bus driver who can't walk 200m and is losing his livelihood) who require a faster pathway than the standard "try exercise first" approach.
1E — Psychosocial context: the person behind the PAD
🫂 Smoking, fear of amputation, and loss of independence — the lived experience of peripheral vascular disease

PAD is a disease of cumulative life choices, systemic vascular disease, and progressive functional limitation. By the time claudication develops, the atherosclerotic process has been developing for 20–30 years. The person in front of you is often already frightened, already limited by their walking, and often carrying an addiction (smoking) that they may have tried to stop many times. The psychosocial framework for PAD must address the fear of the future (amputation, disability), the shame and guilt of the lifestyle factors, and the practical consequences of mobility limitation — on work, relationships, and identity.

🚭 Smoking Addiction & Cessation

Smoking is the most powerful modifiable risk factor and simultaneously the hardest behaviour to change. Nicotine dependence is a medical condition, not a weakness. Patients who have tried and failed to stop multiple times carry significant shame and defeatism — which must be actively countered with a non-judgmental, evidence-based approach.

"I understand you've tried before — that's not failure, that's how most people eventually succeed. Each attempt gets you closer. The one thing I know for certain is that stopping smoking will do more for your legs than any tablet or operation I can offer."

Cytisine (Champix equivalent) + NRT combination has 26% 6-month quit rate in PAD populations. SMSC referral at every appointment. Document pack-years for surgical risk assessment.

😨 Fear of Amputation

Amputation fear is the most common and most powerful psychosocial driver in PAD consultations. It is often rooted in family experience (as with Brian, whose uncle lost a leg). Unaddressed, this fear causes catastrophising and paralysis rather than motivating action. Named and reframed, it becomes the most powerful engagement tool for secondary prevention.

"I want to be direct with you about your uncle — and I want to reassure you that the situation today is very different from what it was for him. We now know exactly what prevents that outcome: stopping smoking, the tablets I'm going to prescribe, and a structured exercise programme. Those things dramatically reduce the risk."

Acknowledge the fear explicitly before providing reassurance. Premature reassurance without acknowledgement is experienced as dismissal. Patients who feel heard are significantly more likely to engage with the management plan.

💼 Employment & DVLA Implications

Claudication affecting walking distance has direct occupational consequences. For bus, HGV, and professional drivers, DVLA Group 2 regulations require notification if symptoms affect safe vehicle operation. For manual workers, reduced walking tolerance may mean reduced earnings. Both situations require specific documentation and proactive management.

"I know your driving licence is central to your livelihood. I want to be upfront about what this means for your licence, and also what the treatment plan looks like in terms of getting your walking distance better — because that directly matters for whether you can keep driving."

DVLA Group 2: notify DVLA if exercise tolerance is affected; vascular assessment may be required. Document all DVLA discussions. The supervised exercise programme improves claudication distance and may directly resolve the driving restriction.

🦶 Diabetes, Foot Care & Amputation Prevention

In diabetic PAD, the combination of neuropathy (can't feel the injury), ischaemia (can't heal the injury), and infection (exacerbates both) creates the conditions for rapid progression to amputation. Daily foot inspection is a therapeutic intervention that prevents amputation — but requires patient education, ability to see and reach the feet, and a care plan for those who cannot.

"Looking at your feet every day is one of the most important things you can do — it's as important as taking your tablets. If you notice any redness, swelling, blistering, or a sore that isn't there the next day, please contact us immediately — don't wait. We can prevent a small problem from becoming a big one."

Prescribe foot care plan. Podiatry referral for all DM + PAD patients. Mirror for sole inspection if patient cannot see feet. Document who performs daily inspection if patient unable.

😔 Depression, Isolation & Quality of Life

Claudication causes progressive mobility limitation that leads to social withdrawal, loss of hobbies, reduced exercise (the most protective intervention), and depression. This creates a vicious cycle — depression worsens adherence, adherence worsening worsens PAD, worsening PAD worsens depression. PHQ-9 at diagnosis and every review is mandatory, not optional.

"I want to check in with how you're feeling in yourself — beyond the leg pain. Having pain that limits your walking can really affect your mood and your sense of independence. How has it been affecting your day-to-day life and your enjoyment of things?"

Supervised exercise therapy has direct antidepressant effects — beyond claudication improvement. NHS Talking Therapies referral if PHQ-9 ≥10. SSRI safe with antiplatelet (add PPI). Social prescribing for isolation.

🏠 Socioeconomic Deprivation & Health Inequalities

PAD has one of the strongest social gradients of any vascular condition — incidence 2× higher in the most deprived quintile, largely mediated through smoking rates, DM prevalence, and access to exercise facilities. Secondary prevention adherence is lower in deprived communities due to cost, access, and health literacy barriers. The supervised exercise programme requires transport, time, and physical capacity.

"I want to make sure the plan I'm suggesting actually works for your life. Is getting to a supervised exercise class something you'd be able to do practically? Are cost or transport a barrier? There are options we can look at to make this work."

Social prescribing link worker referral for transport, exercise access, and financial support. Home-based exercise programme if clinic attendance impossible. Document barriers to supervised exercise as these affect the threshold for referral for revascularisation (NICE NG19).

🎓 SCA Checkpoint — Step 1TasksRelating to OthersGlobal Skills
Key phrases that score
"I'd like to understand the pattern of the pain — does it come on at a predictable distance, and does it go completely within 5 minutes of stopping?"
"I want to ask about something that might feel unrelated — do you ever get pain in your legs when you're resting or at night?"
"I imagine one of your worries might be about your driving licence — let's make sure we talk about that today."
"Before I examine you, I want to be direct about something: stopping smoking will do more for your legs than any tablet or operation. Can I talk about what support is available?"
Deductions (examiner flags)
  • Not asking about rest pain or night pain — this distinguishes claudication from critical ischaemia
  • Not asking about skin changes, non-healing wounds, or gangrene — these define CLTI and change urgency
  • Failing to ask about erectile dysfunction in a male patient with proximal symptoms — Leriche syndrome
  • Not asking about DM and foot inspection status in a diabetic patient with PAD
  • Treating smoking as a lifestyle issue rather than an addiction requiring medical treatment and support
  • Not screening for depression — PHQ-9 is a mandatory component of PAD management
🔴 Red — failing
No rest pain question; ALI features not screened; smoking dismissed as lifestyle; DVLA not raised; amputation fear not explored despite obvious cue; DM foot care not asked
🟠 Amber — borderline
Rest pain asked but not explored; ICE only one or two components; smoking mentioned but without cessation support discussion; DVLA raised at end without proper exploration; no PHQ-9 screening
🟢 Green — passing
Open question; claudication pattern characterised; rest pain screened; skin changes/ulcers asked; smoking as medical treatment; ICE all three with amputation fear named; DVLA occupational impact explored; DM foot care checked; history complete by 6–7 min
2
Step 2
Triage Engine — Emergency · Urgent · Routine
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The PAD triage decision is binary at its most critical level: is the limb threatened right now? Acute limb ischaemia with the 6 Ps is a surgical emergency — the 6-hour revascularisation window determines whether the limb survives. Everything else is a gradient of urgency based on Fontaine stage, symptom trajectory, and the presence of tissue loss. The commonest triage error in primary care is sending a patient with critical limb-threatening ischaemia (CLTI) to a routine outpatient appointment when they needed a vascular surgical bed within days.
🔴 Emergency

999 / Immediate Vascular Surgery

Call 999 — 6-hour revascularisation window
  • Acute limb ischaemia (ALI) — any of the 6 PsSudden severe pain, pallor, pulselessness, paraesthesia, paralysis, perishingly cold limb; embolic or thrombotic occlusion; limb is threatened within hours
  • Paralysis or complete sensory loss in a limbSeverely threatened limb — irreversible muscle death if not revascularised within 6 hours; emergency thromboembolectomy or catheter thrombolysis
  • Wet gangrene with systemic sepsis (fever, rigors, haemodynamic instability)Gas gangrene or necrotising fasciitis of ischaemic limb — emergency surgical debridement and antibiotic therapy; life-threatening within hours
  • Ruptured or symptomatic AAA (collapse + pulsatile abdominal mass)Rapidly fatal — emergency aortic repair within minutes to hours; any PAD patient with sudden abdominal/back pain must have AAA excluded
  • Acute embolic occlusion in patient with known AF or recent MICardiac embolus to peripheral artery; cardioembolic ALI is more acute and more complete than thrombotic — 999 even if pulses partially preserved
🟠 Urgent

Same-Week Vascular Surgery Referral

Within 1–2 weeks
  • Critical limb-threatening ischaemia (CLTI): rest pain >2 weeksFontaine Stage III — ABPI typically ≤0.5; forefoot rest pain relieved by dependency; urgent revascularisation or amputation decision required
  • Non-healing ischaemic ulcer or early dry gangrene (Fontaine Stage IV)Tissue loss with underlying ischaemia; infection risk high; urgent vascular surgical assessment and diabetic foot MDT referral
  • Rapid deterioration in claudication distance (halved within weeks)Acute-on-chronic ischaemia; accelerated progression suggests plaque rupture or acute stenosis — urgent Doppler and vascular review
  • Bilateral claudication with absent femoral pulses (suspected Leriche)Aortoiliac occlusion; CT aortogram required; surgical reconstruction decision made with vascular surgery
  • Claudication + new AF with embolic riskAF increases risk of acute conversion to ALI — anticoagulation decision urgently needed; same-day cardiology or vascular input
🟢 Routine

GP-Led Primary Care Management

Weeks to months
  • Stable intermittent claudication (Fontaine IIa/IIb)ABPI confirmed; claudication distance consistent; no rest pain; supervised exercise therapy referral; secondary prevention cascade
  • ABPI measurement and baseline cardiovascular risk assessmentFirst presentation claudication — ABPI + fasting bloods + ECG + foot inspection + smoking cessation + medication review
  • Secondary prevention optimisation in known PADStatin, antiplatelet, antihypertensive, smoking cessation, HbA1c review — all should be initiated by GP without waiting for vascular referral
  • Claudication not responding to supervised exercise after 3–6 monthsElective vascular referral for angioplasty / stenting consideration after adequate exercise trial
  • Annual PAD review: ABPI, BP, LDL, HbA1c, foot inspection, PHQ-9Monitoring for progression; secondary prevention targets; early detection of CLTI
🎓 SCA Checkpoint — Step 2TasksGlobal Skills
Verbalising triage reasoning
"From what you've described, this sounds like stable claudication — your pain comes on walking and goes away at rest. That puts us in a routine management pathway where we start with exercise, tablets, and lifestyle changes rather than an operation."
"The situation I always need to rule out first is whether the pain is there at rest, especially at night, or whether there are any colour changes or wounds on your feet. If any of those are present, we'd need to act much more urgently."
Deductions
  • Not screening for rest pain or tissue loss before classifying as routine claudication
  • Referring stable claudication for emergency vascular assessment — misclassification wastes specialist capacity and frightens the patient unnecessarily
  • Sending a patient with the 6 Ps to a routine GP appointment instead of calling 999
  • Not considering ALI in a patient with known AF whose leg pain suddenly worsens
🔴 Red
Fails to recognise ALI features; treats CLTI as routine; does not screen for rest pain or tissue loss; does not connect AF to embolic limb risk
🟠 Amber
Correct triage category but reasoning not shared with patient; urgency not communicated; fails to explain why secondary prevention starts now, not after specialist review
🟢 Green
Rest pain and tissue loss screened; triage level communicated with reasoning; patient understands why exercise comes before surgery; 6 Ps safety-net given; secondary prevention starts today
3
Step 3
Do I Need This Examination?
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ABPI measurement is the most important examination in PAD and should be performed at every first presentation of claudication. It confirms the diagnosis, grades disease severity, establishes a baseline for monitoring progression, and is mandatory before applying any compression bandaging. The remaining examination answers the question "why does this patient have PAD and what else is the atherosclerosis affecting?" — pulse assessment, abdominal aortic palpation, and cardiac examination are essential components of the vascular survey.
ExaminationWhy it mattersWhat finding changes managementChanges management?
ABPI (Ankle-Brachial Pressure Index) — bilateralThe diagnostic test for PAD. Normal ABPI 0.9–1.3. ≤0.9 confirms PAD. ≤0.5 = critical limb ischaemia. >1.4 = falsely elevated (calcified vessels in DM/CKD — use toe-brachial index). Post-exercise ABPI (falls by >20% after exercise) can confirm PAD when resting ABPI is normal-borderline.ABPI must be performed bilaterally — a 10% inter-limb difference is significant and identifies the more affected side. Never apply compression bandaging without first confirming ABPI >0.8.ABPI ≤0.9 → PAD confirmed; secondary prevention cascade. ABPI ≤0.5 → CLTI; urgent vascular referral. ABPI >1.4 → use TBI (toe-brachial index). ABPI <0.8 → no compression bandaging.YES — diagnostic + determines management pathway
Peripheral pulse assessment (femoral, popliteal, dorsalis pedis, posterior tibial)Pulse assessment localises the level of occlusion and guides Doppler imaging. Absent femoral pulse = iliac disease. Absent popliteal = SFA/popliteal disease. Absent DP and PT = tibial disease. All pulses absent on one side = multi-level disease. Bilateral absent femoral pulses + absent ankle pulses = Leriche syndrome.Popliteal pulse: a pulsatile popliteal mass rather than a point pulse suggests popliteal aneurysm — a rare but important finding that requires urgent vascular referral (high thromboembolism and distal occlusion risk).All pulses absent → emergency (ALI vs very severe chronic). Absent femoral bilaterally → Leriche; CT aortogram. Pulsatile popliteal mass → popliteal aneurysm → urgent vascular referral.YES — localises disease level
Skin temperature, colour, and capillary refillCold skin below a point of occlusion identifies acute or severe chronic ischaemia. Pallor on elevation (Buerger's test positive) indicates significant ischaemia. Dependent rubor (reactive hyperaemia on lowering) occurs in critical ischaemia as capillaries maximally dilate to extract available oxygen.Buerger's test: elevate leg to 45° — pallor within 2 minutes = significant ischaemia (positive). On lowering: rubor developing within 2 minutes = severe ischaemia. Negative test does not exclude PAD.Buerger's positive + pallor <2 min → severe ischaemia; urgent vascular referral. Capillary refill >3 seconds → impaired perfusion; note bilaterally. Dependent rubor → CLTI features.YES — grades ischaemia severity
Skin inspection — hair distribution, skin texture, ulcerationIschaemic skin changes: sparse or absent hair on dorsum of foot and lower leg (ischaemia reduces keratin synthesis), thin/shiny skin, dystrophic toenails. Ischaemic ulcers: punched-out appearance, painful, at pressure points, pale necrotic base, no peripheral oedema. Venous ulcers: superficial, medial gaiter area, wet, surrounding lipodermatosclerosis — contrasting features help DDx.Infected ischaemic ulcer in a diabetic patient is a diabetic foot emergency. The absence of pain in an ulcer does not indicate a good prognosis — in DM, neuropathy removes the pain but the ischaemia is unchanged.Ischaemic ulcer present → CLTI; urgent vascular + diabetic foot MDT. Punched-out ulcer with absent pulses → do NOT apply compression. Venous ulcer pattern → ABPI before compression; refer leg ulcer clinic.YES — Fontaine staging
Blood pressure (bilateral arm measurement)Bilateral arm BP: difference >15 mmHg between arms = subclavian stenosis (also a marker of generalised atherosclerosis). Single arm BP misses this diagnosis and may underestimate true cardiovascular risk. BP control is the second most important secondary prevention target in PAD after smoking.Use the higher arm BP reading for clinical management. Subclavian stenosis also affects ABPI calculation — the brachial pressure used in the ABPI formula must be from the unaffected arm.BP >140/90 → antihypertensive treatment; target <140/90 (or <130/80 if DM). Inter-arm difference >15 mmHg → subclavian stenosis; use higher arm for ABPI. Hypertensive urgency (>180/120) → same-day management.YES — secondary prevention target
Abdominal examination (aortic palpation)Abdominal aortic aneurysm (AAA) is 2–3× more prevalent in PAD patients than the general population. A pulsatile expansile mass in the periumbilical region >3cm width = significant AAA. Symptomatic AAA (tender on palpation + back/abdominal pain) = vascular emergency regardless of size.AAA screening: men aged 65+ are offered NHS AAA screening (abdominal ultrasound). PAD patients of any age should be considered for opportunistic aortic screening given the shared risk factor profile. A ruptured AAA can mimic severe PAD with bilateral limb ischaemia from malperfusion.Pulsatile expansile mass → aortic ultrasound urgently. Tender mass + pain → 999 (symptomatic/rupturing AAA). AAA 3–5.5cm → USS surveillance programme. AAA >5.5cm → urgent vascular surgical referral.YES — AAA requires vascular referral
Cardiac auscultation and rhythmAF is the leading cause of acute limb ischaemia via peripheral embolism — detecting an irregular pulse at examination changes management from antiplatelet to anticoagulation. New cardiac murmur may indicate valvular disease or infective endocarditis as source of peripheral emboli.In a PAD patient with AF not yet anticoagulated: the CHA₂DS₂-VASc score is almost certainly ≥2 (PAD + age), making anticoagulation mandatory. Documenting the cardiac rhythm at every PAD review is essential.AF → DOAC anticoagulation; CHA₂DS₂-VASc calculation. New murmur → echocardiogram; blood cultures if IE suspected. Irregular rhythm in a PAD patient = most important finding for preventing ALI.YES — AF changes entire management
Neurological lower limb examination (sensation, reflexes, power)Peripheral neuropathy (in DM or alcohol dependence) masks ischaemic pain — a patient with both PAD and neuropathy may present later and with more advanced disease because they cannot feel the ischaemia developing. Distinguishes neurogenic claudication (dermatomal distribution, reproduce with lumbar extension) from vascular claudication.Absent ankle reflexes + stocking-distribution sensory loss = peripheral neuropathy. Combined with absent pedal pulses = highest risk for foot ulceration and amputation. Foot monofilament testing (Semmes-Weinstein) at every DM + PAD review.Neuropathy present → foot care plan; monofilament check; podiatry referral. Dermatomal pattern + positive femoral stretch test → lumbar spine pathology (spinal stenosis DDx). Normal sensation in non-DM patient → vascular aetiology more likely.Context — DDx neuropathy vs ischaemia
Venous insufficiency signs (varicosities, haemosiderin, lipodermatosclerosis)Venous claudication (thigh heaviness after walking, relieved by elevation not rest — the reverse of arterial claudication) and venous ulcers can coexist with PAD. Mixed arterial-venous ulceration requires ABPI before any compression. Misapplying full compression to an ischaemic leg causes devastating limb injury.ABPI ≤0.8 = compression bandaging is contraindicated. Modified compression (reduced pressure) may be possible with ABPI 0.6–0.8 with specialist leg ulcer service input. Below 0.6 = no compression.Venous ulcer + ABPI <0.8 → no compression; refer leg ulcer service + vascular. ABPI 0.8–1.0 + venous features → modified compression possible; leg ulcer nurse specialist. ABPI >1.0 + venous signs → standard compression safe.Context — compression safety decision
Foot inspection (in all diabetic patients) — interdigital spaces, heels, nail foldsThe diabetic foot examination must inspect all pressure points: heel, metatarsal heads, toe tips, interdigital spaces (fungal, fissures), and nail folds (ingrown toenails → portal of entry for infection). An ischaemic heel ulcer hidden in a shoe is a common source of late presentation with advanced limb-threatening disease.Arrange for full foot examination at the consultation — patients with DM + PAD often do not remove shoes and socks unless specifically asked. The risk classification (low/moderate/high/active diabetic foot problem) determines follow-up frequency.Any new ulceration, skin breakdown, or infection → diabetic foot MDT referral within 24 hours if high-risk features (redness, warmth, swelling, discharge). High-risk foot (previous ulcer/amputation, absent sensation, absent pulses) → 3-monthly podiatry.YES — determines diabetic foot risk stratification
🎓 SCA Checkpoint — Step 3TasksRelating to Others
Offering examination with clinical reasoning
"I'd like to do a test called the ABPI — ankle-brachial pressure index — which compares the blood pressure in your arms and ankles. It tells us how well blood is getting to your feet and confirms what's causing your symptoms."
"I'm going to feel all the pulses in your legs — from your groin down to your feet. This tells me exactly where in the blood vessel system the narrowing is."
"Because you have diabetes, I'd also like to look carefully at your feet — especially between the toes and under the heel. There are areas where problems can develop without causing pain."
Deductions
  • Not performing or arranging ABPI — this is the cornerstone diagnostic test and must be offered at first presentation
  • Not examining feet in a diabetic patient — missing a heel ulcer or interdigital infection is a patient safety failure
  • Not palpating the abdomen for aortic aneurysm in a patient with established PAD
  • Not assessing cardiac rhythm — missing AF changes the entire management pathway
🔴 Red
ABPI not performed or offered; feet not examined in DM; pulse assessment omitted; examination not explained to patient; no cardiac rhythm assessment
🟠 Amber
ABPI mentioned but rationale not explained; pulse assessment done but findings not linked to management; feet examined but findings not documented; aortic palpation omitted
🟢 Green
ABPI explained in plain language; bilateral pulses assessed with level localisation; feet inspected including hidden areas; aortic palpation with AAA explanation; BP both arms; cardiac rhythm; findings explicitly linked to management decisions
4
Step 4
Do I Need This Investigation?
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In PAD, investigations serve two purposes: confirming the diagnosis (ABPI) and profiling the risk factor burden that drives the secondary prevention cascade. Anatomical imaging (Doppler, CT angiography, MR angiography) is a specialist investigation — the GP role is to confirm the diagnosis with ABPI and initiate the secondary prevention blood tests. Imaging for revascularisation planning is arranged by the vascular surgery team, not requested from primary care.
InvestigationClinical question it answersWhat result changes management?
ABPI (Ankle-Brachial Pressure Index) — bilateralIs PAD present, and how severe? Confirms the diagnosis, grades severity (claudication vs CLTI), establishes a baseline for monitoring progression, and determines compression safety. ABPI is both a diagnostic test and a clinical examination finding — it takes 5–10 minutes with a hand-held Doppler and sphygmomanometer.ABPI ≤0.9 → PAD confirmed; secondary prevention. ABPI ≤0.5 → CLTI; urgent vascular. ABPI >1.4 in DM/CKD → use TBI (toe-brachial index). ABPI 0.6–0.8 → no full compression; modified compression with specialist input only. ABPI <0.6 → no compression of any kind.
Fasting lipid profile (TC, LDL, HDL, TG)LDL level guides statin intensity and response monitoring. NICE NG19 mandates atorvastatin 80mg for all PAD regardless of baseline LDL. A post-treatment LDL >2.0 mmol/L (or <50% reduction) indicates under-treatment and a need for ezetimibe addition.LDL >2.0 on atorvastatin 80mg → add ezetimibe 10mg. LDL still >2.0 on dual therapy → PCSK9 inhibitor consideration; refer lipid clinic. Baseline LDL before starting statin is required for monitoring response at 3 months.
HbA1cDM control is a major determinant of PAD progression and amputation risk. Undiagnosed DM is present in 15–20% of patients presenting with claudication. HbA1c >47.5 confirms new DM diagnosis and changes secondary prevention target (SGLT2i, lower BP target).HbA1c >47.5 → DM confirmed; SGLT2i for secondary CV prevention; foot care plan; podiatry. HbA1c 42–47 → pre-DM; intensive lifestyle; 6-monthly monitoring. HbA1c >70 on treatment → optimise DM therapy; endocrinology referral.
Full blood countAnaemia reduces oxygen-carrying capacity and dramatically worsens claudication symptoms — claudication distance may be substantially reduced by haemoglobin below 100g/L independently of ABPI. Polycythaemia (raised Hb/haematocrit) causes hyperviscosity and promotes thrombosis. Thrombocytosis drives arterial thrombosis in essential thrombocythaemia.Hb <100g/L → treat anaemia before evaluating true claudication severity; IDA → iron therapy; B12/folate deficiency → supplements. Polycythaemia (Hb >185 men, >165 women) → haematology; venesection. Thrombocytosis >600 → haematology; JAK2 mutation testing.
Urea, electrolytes, creatinine and eGFRCKD is an independent predictor of PAD progression and affects drug choices: ACEi dose-adjustment; contrast nephropathy risk with CT angiography; DOAC dose-adjustment in AF + PAD. Renal artery stenosis is 3× more common in PAD patients — significant renal failure without another cause warrants renal artery Doppler.eGFR <60 → MR angiography preferred over CT (contrast nephropathy risk); DOAC dose-adjustment; ACEi with monitoring. eGFR <30 → most DOACs need dose reduction or avoidance; haematology for anticoagulation choice. Unexpected creatinine rise on ACEi >25% → hold drug; investigate renal artery stenosis.
12-lead ECGAF detection — the most important cardiac rhythm finding in PAD (embolic ALI risk). LVH marker of longstanding hypertension (major PAD risk factor). Evidence of previous MI (mural thrombus source; guides secondary prevention intensity). Q-waves or regional wall motion changes on echo suggest polyvascular disease.AF → DOAC anticoagulation; CHA₂DS₂-VASc. STEMI pattern → cardiology review; LV thrombus imaging. LVH + HTN → optimise BP urgently. Frequent ectopics or conduction defect → cardiologist.
Duplex Doppler ultrasound (specialist investigation)Non-invasive localisation of stenoses and assessment of severity. Used by vascular surgery to plan revascularisation. In primary care: GP does not typically request this — it is arranged by the vascular surgery team. However, GP should understand the result: PSV ratio >4 = >70% stenosis; monophasic waveform = severe ischaemia.Stenosis >70% in proximal vessel → angioplasty / stenting consideration. Multi-level occlusion → bypass surgery may be more appropriate than angioplasty. Graft occlusion → emergency vascular review (acute graft thrombosis = ALI).
CT angiography (specialist investigation — pre-revascularisation)Definitive anatomical road map before bypass surgery or complex angioplasty. Shows full aorta-to-tibial vessel anatomy. Contrast required — check eGFR before requesting. Not a GP investigation but GP must understand the report: TASC A/B lesions = angioplasty; TASC C/D = surgery.TASC A/B → percutaneous transluminal angioplasty (PTA) ± stenting; lower surgical risk. TASC C/D → surgical bypass; higher risk but more durable. Aortoiliac occlusion (TASC D) → aortobifemoral bypass or axillobifemoral bypass.
Toe-brachial index (TBI) — when ABPI >1.4In DM, CKD, and elderly patients with calcified vessels, ABPI is falsely elevated (>1.4) because the calcified vessels cannot be compressed by the cuff. TBI (systolic pressure at great toe / brachial systolic) is not affected by vessel calcification — the toe vessels calcify last.TBI <0.7 → PAD confirmed despite normal/elevated ABPI. TBI <0.3 → severe ischaemia; urgent vascular. TBI-based management in DM with ABPI >1.4 prevents both under-treatment (missing PAD) and over-treatment (incorrectly reassuring).
Treadmill exercise test (specialist) + post-exercise ABPIConfirms PAD in patients with normal resting ABPI but typical claudication symptoms. Exercise increases oxygen demand — a stenosis that does not reduce resting ABPI to <0.9 may cause ABPI to fall >20% post-exercise. Also objectively measures claudication distance for baseline and post-exercise therapy documentation.Post-exercise ABPI fall >20% → exercise-induced PAD confirmed. Treadmill walking distance documents baseline for response to supervised exercise therapy. Abnormal treadmill + normal ABPI → further anatomical imaging; vascular referral.
🎓 SCA Checkpoint — Step 4TasksRelating to Others
Explaining investigations to the patient
"The most important test today is the ABPI — we measure blood pressure at your ankle and your arm and compare them. It tells us exactly how much blood is getting to your feet and confirms what we think is going on."
"Because you have diabetes, I want to be careful about one thing — in people with long-standing diabetes, the blood pressure test in the ankle can sometimes give an artificially normal reading because the arteries become harder. If that happens, I'd use a different test measuring blood pressure at the big toe instead."
"I'll also take some blood tests today — checking your cholesterol, blood sugar, kidney function, and blood count. These tell me what's driving the problem in your arteries and which tablets will help most."
Deductions
  • Ordering CT angiography from primary care — this is a pre-operative specialist investigation, not a GP blood test
  • Not acknowledging that ABPI may be falsely elevated in DM — toe-brachial index is needed
  • Not ordering lipid profile — statin initiation requires a baseline LDL for response monitoring
  • Not checking eGFR — CKD changes drug choices and investigation safety (contrast CT)
🔴 Red
ABPI not arranged; investigations ordered without rationale; CT angiography ordered from primary care; ABPI limitation in DM not acknowledged; no cardiovascular risk bloods ordered
🟠 Amber
ABPI offered; bloods ordered but explanation not given to patient; DM limitation not mentioned; TBI not offered if ABPI likely unreliable; results not linked to management changes
🟢 Green
ABPI explained in plain language; TBI mentioned for DM; bloods explained individually (lipids → statin, HbA1c → DM control, eGFR → drug safety, FBC → anaemia); ECG for AF; patient understands what will happen with results
5
Step 5
Reaching a Diagnosis & DDx — Explained in Plain Language
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The diagnostic task in PAD is twofold: confirming the vascular mechanism (ABPI-confirmed arterial insufficiency) and Fontaine-staging the severity to determine urgency and management pathway. But the equally critical task is translating the diagnosis into a coherent explanation that motivates lifestyle change. A patient who understands that their leg arteries are narrowing by the same process affecting their heart arteries is more likely to take their statin, stop smoking, and attend exercise therapy than one who understands only "bad circulation."
🗣️ Explaining the Diagnosis in Plain Language — say something like this

"The pain you're getting in your calves when you walk is called intermittent claudication — it means the artery supplying blood to your calf muscles is narrowed. Think of it like a garden hose with a partial kink in it: at rest, enough water gets through. But when you start walking, your muscles need much more blood — and the narrowed artery can't keep up. The muscle runs short of oxygen, cramps up, and forces you to stop. As soon as you rest, the demand drops and the pain goes. The same process — cholesterol and fatty deposits building up inside the artery walls over years — is happening in the arteries to your heart and brain as well. So treating this is about protecting your legs, your heart, and your brain all at the same time."

💬 Addressing the patient's own explanation

"It's probably just old age — my father had bad legs too."
"Ageing does affect blood vessels, but what you're describing isn't just age — it's a specific process called atherosclerosis, where fat and cholesterol deposits narrow the arteries. That process is strongly driven by smoking and diabetes — both of which are things we can actively treat. This isn't something you have to accept; it's something we can significantly improve."

"I thought it might be a DVT — my brother had a DVT in his leg."
"That's an understandable concern, and I'm glad you mentioned it. A DVT is a clot in a vein — which usually causes constant swelling, warmth, and pain even at rest. What you have is the opposite — pain only when you exercise, which goes quickly when you stop. That pattern is specific to the arteries, not the veins. The ABPI test I've done confirms this is arterial — poor blood supply rather than a clot."

A — Diagnosable in Primary Care
GP can diagnose with ABPI
Intermittent Claudication (Fontaine IIa/IIb)
ABPI ≤0.9 + consistent claudication distance + complete relief with rest. GP initiates secondary prevention and supervised exercise therapy without needing specialist input.
Venous Claudication (DDx — exclude)
Thigh heaviness after walking, worse with heat, relieved by elevation not rest. Prior DVT or IVC occlusion. ABPI normal. Venous Doppler confirms. Refer phlebology.
Musculoskeletal Pain (DDx — exclude)
Hip or knee OA, Achilles tendinopathy — site-specific, inconsistent claudication distance, not relieved predictably by rest, normal ABPI. Treat underlying MSK condition.
B — Suspected — Specialist Referral
Refer for confirmation + management

Neurogenic Claudication (Spinal Stenosis)

Bilateral leg pain/weakness after walking, relieved by sitting or forward flexion ("shopping trolley sign"). Worse on extension (lumbar stenosis narrows spinal canal). ABPI normal. MRI lumbar spine. Orthopaedic / neurosurgery referral.

Critical Limb-Threatening Ischaemia (CLTI)

Rest pain (Fontaine III) or tissue loss (Fontaine IV). ABPI ≤0.5. Urgent vascular surgery referral within 1–2 weeks — limb preservation requires revascularisation.

Popliteal Artery Entrapment / Adventitial Cystic Disease

Young, athletic male, unilateral claudication with normal ABPI at rest. Exercise Doppler confirms. Rare but important — surgical release or bypass required.

C — Emergency — Act Now
Diagnose & 999

Acute Limb Ischaemia (ALI) — The 6 Ps

Sudden severe pain, pallor, pulselessness, paraesthesia, paralysis, perishingly cold. Embolic (AF) or thrombotic (plaque rupture). 6-hour revascularisation window. 999 — vascular surgical emergency.

Ruptured Abdominal Aortic Aneurysm

Collapse + central/back pain + pulsatile mass. May cause bilateral limb ischaemia from malperfusion. Rapidly fatal without emergency surgery. 999 — do not delay for investigations.

📊 Fontaine Classification — PAD Staging (NICE NG19)
Fontaine StageClinical featuresTypical ABPIManagement pathwayUrgency
Stage I — Asymptomatic PADNo symptoms; ABPI reduced incidentally; cardiovascular risk factor profile0.7–0.9Secondary prevention + annual ABPI reviewRoutine
Stage IIa — Mild claudicationPain free walking >200m; not limiting daily activities significantly0.7–0.9Supervised exercise therapy × 6 months; secondary preventionRoutine
Stage IIb — Moderate–severe claudicationPain free walking <200m; significant functional impairment; work / lifestyle impact0.5–0.8Exercise therapy + consider vascular referral if exercise fails at 3–6 monthsWeeks
Stage III — Rest pain (CLTI)Constant forefoot pain at rest; worse at night; relieved by dependency (hanging leg down)<0.5Urgent vascular surgery referral within 1–2 weeksUrgent
Stage IV — Tissue loss (CLTI)Ischaemic ulceration, gangrene (dry or wet); active or healed tissue loss<0.5 (often <0.3)Urgent/same-week vascular + diabetic foot MDTEmergency
🎓 SCA Checkpoint — Step 5TasksRelating to OthersGlobal Skills
Diagnosis in plain language — key phrases
"What you have is called peripheral arterial disease — or 'PAD'. The arteries supplying blood to your legs are narrowed by a build-up of fatty deposits — the same process that narrows heart arteries. The ABPI test confirms this."
"The most important thing to understand is that this isn't just about your legs — it's a sign that the same process is affecting arteries throughout your body, including to your heart and brain. That's why the treatment is so important."
"The good news is you're at an early stage — claudication — not the more serious stage where pain is there all the time. That means exercise and lifestyle changes can make a real difference, and we can often avoid operations entirely."
Deductions
  • Using "PAD" or "peripheral arterial disease" without plain language explanation
  • Not framing PAD as a systemic vascular disease — patients who understand only "bad legs" miss the most important motivating fact
  • Not distinguishing claudication from CLTI — the patient who has rest pain needs urgency, not an exercise class
  • Not addressing the patient's DVT attribution — this common misattribution must be corrected specifically
🔴 Red
Diagnosis not shared; jargon only; systemic vascular context not explained; Fontaine stage not communicated; patient's DVT attribution unchallenged
🟠 Amber
Correct diagnosis named but no analogy or plain language; systemic nature mentioned briefly but not emphasised; Fontaine staging unclear to patient; DVT addressed generically
🟢 Green
PAD + "narrowed arteries" + garden hose analogy; systemic nature of atherosclerosis explained; Fontaine stage communicated with prognostic meaning; DVT specifically addressed; amputation fear reframed with positive messaging about current early stage
6
Step 6
If Referral Is Needed — What the GP Does Before & During
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The GP's role in PAD referral is to start secondary prevention now, not wait for the specialist to begin it. Clopidogrel, atorvastatin 80mg, and antihypertensive treatment should all be initiated at the GP consultation. NICE NG19 explicitly states that secondary prevention should not wait for vascular surgery review. The referral pathway depends on Fontaine stage — stable claudication referrals are routine; CLTI referrals are urgent; ALI is 999. The GP must document ABPI, Fontaine stage, risk factor profile, and secondary prevention medications in every referral letter.
ConditionUrgencyWhat GP does before referralWhat GP must NOT do
Acute limb ischaemia (ALI) — any of the 6 Ps999 nowCall 999 immediately. Document time of onset — vascular team need this for revascularisation timing. Do not give anticoagulant or antiplatelet without vascular team instruction. Keep the patient still and warm. IV access if available and trained.Do NOT delay for full history; do NOT give aspirin without instruction; do NOT apply elevation (worsens ischaemia — keep limb horizontal or slightly dependent); do NOT attempt to manage ALI in primary care.
Critical limb-threatening ischaemia (CLTI): rest pain or tissue lossWithin 1–2 weeksStart clopidogrel 75mg + atorvastatin 80mg + antihypertensive if not already prescribed. Arrange wound dressing if ulcer present. Document ABPI, Fontaine stage, and DM foot risk category. Refer to vascular surgery and diabetic foot MDT if DM. Analgesia for rest pain (opioids may be required — do not withhold).Do NOT apply compression bandaging to an ischaemic leg (ABPI <0.8). Do NOT debride an ischaemic ulcer in primary care without vascular input. Do NOT withhold analgesia for CLTI rest pain — opioids are appropriate.
Stable claudication not responding to supervised exercise (3–6 months)Elective — routineDocument claudication distance at referral (measured objectively if possible — treadmill or walking distance test). Confirm 3–6 months supervised exercise therapy completed. Confirm secondary prevention medications: clopidogrel, atorvastatin 80mg, antihypertensive. Include ABPI, Fontaine stage, and cardiovascular risk profile in referral letter.Do NOT refer before adequate trial of supervised exercise therapy (unless Fontaine IIb with severe lifestyle impact). Do NOT expect the vascular team to initiate secondary prevention — this is a primary care responsibility. Do NOT omit ABPI from the referral letter.
Suspected Leriche syndrome (aortoiliac occlusion)Urgent outpatientDocument: bilateral absent femoral pulses + bilateral claudication pattern + erectile dysfunction if present. Secondary prevention initiated. Expedited vascular referral — aortobifemoral bypass or endovascular aortoiliac reconstruction requires specialist planning. Do not arrange CT angiography from primary care — vascular surgery arranges this.Do NOT request CT aortogram from primary care. Do NOT delay referral pending MRI or further imaging — clinical diagnosis with femoral pulse findings is sufficient for urgent referral.
Diabetic foot ulcer with suspected ischaemiaWithin 24–48h if infected; within 1 week if notABPI (or TBI if ABPI unreliable). Wound photograph. Infection screen (swab, FBC, CRP, blood cultures if systemic features). Empirical antibiotics if infected (co-amoxiclav or alternative per local formulary). Refer to diabetic foot MDT + vascular surgery simultaneously — do not refer sequentially.Do NOT apply compression bandaging without ABPI. Do NOT debride an ischaemic ulcer. Do NOT delay referral to "see how it heals" — ischaemic ulcers do not heal without vascular intervention.
Popliteal aneurysm (pulsatile popliteal mass)Within 2–4 weeksConfirm finding on examination. Do not compress or manipulate the aneurysm. Arrange duplex ultrasound. Start antiplatelet and statin if not already prescribed. Refer to vascular surgery — popliteal aneurysms have high thromboembolism and distal occlusion rates and may require prophylactic repair even if asymptomatic.Do NOT attempt aspiration or compression of a pulsatile popliteal mass — may be an aneurysm and compression worsens distal ischaemia. Do NOT delay referral.
AAA discovered incidentally on abdominal palpation or imagingRoutine if asymptomatic <5.5cm; urgent if symptomatic or >5.5cmArrange abdominal USS for size confirmation. If tender or symptomatic: 999. Asymptomatic >5.5cm: urgent vascular referral. 3–5.5cm: USS surveillance every 3–12 months per size (3–4cm = 12-monthly; 4–5.5cm = 3–6 monthly). Smoking cessation critical — growth rate doubles in current smokers.Do NOT palpate a tender aortic aneurysm. Do NOT delay 999 for a symptomatic aneurysm. Do NOT ignore AAA finding in a PAD patient — shared risk factors make this a high-prevalence scenario.
🎓 SCA Checkpoint — Step 6TasksGlobal Skills
Explaining the referral pathway
"You don't need to see a vascular surgeon right away — at your stage, the evidence is clear that a structured exercise programme is more effective than an operation in the first instance. I'll start your tablets today so you're protected while we do that."
"If your walking doesn't improve after 3–6 months of the programme, or if your symptoms get worse, I'll refer you to the vascular team who can look at whether a procedure might help."
Deductions
  • Referring stable claudication urgently to vascular surgery without an exercise therapy trial
  • Not starting secondary prevention at the GP consultation — waiting for the specialist wastes weeks of protective treatment
  • Not explaining why the patient doesn't need immediate surgery — they expect it, and unexplained deferral causes anxiety
  • Applying compression to an ischaemic leg — ABPI must be checked first
🔴 Red
Urgent vascular referral for stable claudication; secondary prevention not started; compression applied without ABPI; CLTI sent to routine outpatient instead of urgent referral
🟠 Amber
Correct referral urgency but rationale not explained; secondary prevention partially started; exercise therapy mentioned but not specifically offered or booked; compression safety not addressed
🟢 Green
Correct referral urgency with explanation; all three secondary prevention medications started today; supervised exercise therapy specifically offered; ABPI before any compression; DVLA occupational impact addressed; patient understands pathway and what triggers escalation
7
Step 7
Management — Expectation · Goals · Lifestyle · Drug Selector · Drug Cards · Psychosocial · Follow-Up · Safety-Netting
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7A — Address the patient's expectation first: validate → explain → negotiate
🤝
Never dismiss the expectation — acknowledge it, share your reasoning, then agree a shared plan
1
Validate — name their expectation

Most PAD patients expect either a referral for a stent or an operation, or reassurance that "it's just ageing." Both expectations miss the evidence base. Validating the expectation before challenging it prevents the patient feeling dismissed or lectured.

"I can completely understand why you'd be expecting a referral for a scan or a stent — that's what many people hope for at this point. Can I explain why the evidence actually points in a different direction, and why I think you'll find the approach I'm suggesting more effective?"
2
Explain — share your clinical reasoning

Exercise therapy is more effective than angioplasty for stable claudication in terms of walking distance improvement and quality of life (CLEVER trial). Frame exercise as an active treatment, not a lifestyle suggestion — with a specific programme, a measurable outcome, and a follow-up plan.

"The evidence is quite clear that a structured exercise programme — walking to the point of pain and then pushing a little further — is actually more effective than a stent for your stage of the condition, and it has none of the risks of a procedure. We'll also start two important tablets today that protect your heart and brain as well as your legs."
3
Negotiate — offer something today

The patient must leave with concrete actions starting today — not just a referral for an exercise class in 6 weeks. Starting tablets, providing a walking plan, and booking the exercise referral all today gives the patient agency and momentum.

"Today I'm going to start your clopidogrel, your statin, and your blood pressure tablet. I'll also refer you to the supervised exercise programme — and I want you to know that I'm genuinely optimistic: most people at your stage see a significant improvement in how far they can walk within 3 months."
Key principle: Frame the amputation fear as a motivating factor rather than a threat. "These tablets, this exercise programme, and stopping smoking are exactly what keeps your legs — they're your best protection against your uncle's outcome." Linking every intervention to the patient's own named fear and values transforms compliance from obligation to purpose.
7B — Why treatment matters: goals tailored to this patient
Treatment goals
Prevent MI and stroke (primary cause of death in PAD)Reduce major adverse cardiovascular events (MACE) Increase claudication distance (doubled in 3–6 months with exercise)Prevent progression to CLTI or amputation LDL <1.8 mmol/L on atorvastatin 80mg ± ezetimibeBP <140/90 (or <130/80 if DM) Complete smoking cessation — most important single interventionHbA1c <58 mmol/mol if DM; foot care plan in place
Motivational language — tailored to this patient
"People at your stage who stop smoking, take their tablets, and complete the exercise programme have a dramatically lower risk of losing a limb. Your uncle's experience doesn't have to be yours — the treatments available now are much more effective."
"I know your driving and your job matter enormously to you. Getting your walking distance back — which this programme can realistically do — is directly connected to maintaining your licence and your livelihood. Let's treat this as the investment in your working life that it is."
7C — Non-medication management: mechanism + evidence + tailored advice
Supervised exercise therapy is the most effective first-line treatment for intermittent claudication and is mandated by NICE NG19. It is more effective than angioplasty for stable claudication in terms of claudication distance and quality of life (CLEVER trial). Each lifestyle intervention must be explained with a mechanism, a quantified benefit, and a specific, measurable target — never generic advice.
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Supervised Exercise Therapy
Target: 3× weekly × 6 months minimum
Mechanism

Walking to the point of moderate claudication pain and then resting stimulates collateral artery formation, improves endothelial function, increases skeletal muscle metabolic efficiency, and reduces systemic inflammatory markers. This is the most effective non-surgical intervention for claudication.

Practical

Supervised programme (NHS or community): walking to near-maximal pain, rest, repeat. 30–60 minutes per session, 3× per week, 3–6 months. Home walking programme if supervised unavailable: walk to pain, stop and rest for 5 minutes, continue. Track daily distance.

Doubles claudication distance in 3–6 months; superior to angioplasty (CLEVER trial)
🚭
Smoking Cessation
Target: complete cessation — not reduction
Mechanism

Smoking causes endothelial dysfunction, platelet activation, increased fibrinogen, and accelerated atherosclerosis. In PAD, smoking reduces collateral formation and dramatically accelerates progression to CLTI. Limb loss rate is 7× higher in smokers who continue after PAD diagnosis vs those who stop.

Practical

Combination NRT (patch + gum/lozenge) + cytisine or varenicline. NHS Stop Smoking Service (SMSC) referral at every appointment. Set quit date. Medication lasts 12 weeks. Each attempt increases probability of eventual success — "I know you've tried before; that's not failure."

↓ Limb loss risk by 7×; improves claudication distance independently of drugs
🥗
Mediterranean Diet
Target: daily dietary pattern change
Mechanism

Reduces LDL and systemic inflammation through olive oil polyphenols, omega-3 fatty acids (oily fish), and antioxidant-rich vegetables. PREDIMED trial: Mediterranean diet reduces major CV events by 30% independently of cholesterol level. Directly reduces atherosclerotic plaque progression.

Practical

Replace butter with olive oil. Two portions of oily fish per week. ≥5 fruit/vegetable portions daily. Replace red meat with legumes ×3/week. Reduce salt to <6g/day (BP benefit). Reduce ultra-processed foods. Dietitian referral if BMI >35 or diabetic.

↓ Major CV events 30% (PREDIMED); independent of statin effect
⚖️
Weight Management
Target: ≥5% body weight reduction if BMI >25
Mechanism

Obesity increases cardiac output demand at rest and on exercise, reducing the ischaemic threshold. Weight loss reduces both resting and exercise BP, improves insulin sensitivity in DM, reduces inflammatory burden, and allows greater benefit from the exercise programme. BMI >30 is an independent predictor of worse claudication outcomes.

Practical

5% weight loss target: SMART goals (e.g. "lose 4kg in 3 months"). Mediterranean diet as above. Referral to NHS weight management programme (Tier 2 if BMI >30). SGLT2i in DM provides ~2–3kg weight loss as a secondary benefit. GLP-1 agonist for obesity if indicated.

↑ Claudication distance; ↓ BP; ↓ CV risk; improves DM control
🍷
Alcohol Reduction
Target: <14 units/week; no binge drinking
Mechanism

Heavy alcohol (≥3 units/day) causes hypertension, exacerbates neuropathy (confounding ischaemia assessment), raises triglycerides, and destabilises diabetes. At PAD presentation, alcohol intake directly affects BP control — the second most important secondary prevention target. Binge drinking triggers AF episodes (embolic ALI risk).

Practical

AUDIT-C screen at diagnosis. Brief structured intervention. Track units using NHS Drink Free app. Target ≤14 units/week spread across days. Alcohol use disorder: SMSC referral; acamprosate/naltrexone consideration. Document Alcohol clearly in referral letters — affects surgical candidacy.

BP reduction of up to 8 mmHg; ↓ AF risk; improved DM control
🦶
Foot Care & Daily Inspection
Target: daily inspection; podiatry ×3–6 monthly in DM + PAD
Mechanism

In PAD (especially with DM neuropathy), minor foot trauma is the entry point for the cascade of infection, ischaemia, and tissue loss that leads to amputation. Early detection of skin breakdown allows intervention before irreversible tissue loss. Daily inspection by the patient or carer is equivalent to a clinical intervention in its preventive effect.

Practical

Inspect daily: between toes, heel, sole (use mirror if needed). Wash in warm (not hot) water — check temperature with elbow if neuropathy. Dry carefully between toes. Moisturise but not between toes. Wear well-fitting footwear (no barefoot at home). Podiatry referral — routine care of nails and callus prevents portals of entry.

Prevents up to 85% of DM + PAD amputations if combined with early intervention
7D — Prescribing guide: what to start, in what order, and why
Secondary prevention in PAD is a simultaneous cascade: antiplatelet + statin + antihypertensive. All three should be initiated at the GP consultation without waiting for specialist review. NICE NG19 is explicit: clopidogrel 75mg is preferred over aspirin in PAD (superior in CAPRIE trial specifically for PAD subgroup); atorvastatin 80mg for all confirmed PAD regardless of LDL; BP target <140/90 (or <130/80 if DM).
Start Immediately — All Confirmed PAD

Clopidogrel 75mg OD — preferred antiplatelet in PAD

  • Superior to aspirin in PAD subgroup (CAPRIE trial): relative risk reduction 23.8% over aspirin
  • NICE NG19: clopidogrel is the recommended antiplatelet for PAD
  • If clopidogrel not tolerated: aspirin 75mg OD as alternative
  • Do NOT use dual antiplatelet (clopidogrel + aspirin) routinely — no additional benefit for PAD, increased bleeding
CAPRIE trial: clopidogrel 75mg superior to aspirin 325mg for reducing MI, stroke, or vascular death specifically in PAD patients.
Start Immediately — Statin + ACEi

Atorvastatin 80mg OD + Ramipril 2.5mg (titrating to 10mg)

  • Atorvastatin 80mg: all confirmed PAD regardless of LDL (NICE NG19). Target LDL <1.8 mmol/L (ESC 2019). Add ezetimibe if >1.8 at 3 months.
  • Ramipril (HOPE trial): ACEi reduces CV events by 22% in PAD patients even without heart failure or LV dysfunction — specific additional benefit in PAD beyond hypertension control
  • If ACEi not tolerated (cough): ARB equivalent (candesartan, losartan)
  • Target BP: <140/90 or <130/80 if DM. Add CCB (amlodipine) as Step 2.
HOPE trial: ramipril 10mg reduced MI, stroke, and CV death by 22% in high-risk vascular patients including PAD — independent of BP-lowering effect.
Step 2 — Symptom Treatment if Exercise Insufficient

Naftidrofuryl oxalate 200mg TDS — only after supervised exercise

  • NICE NG19: first-line vasodilator for claudication in patients who prefer not to be referred for further treatment and have not had satisfactory improvement with exercise
  • Mechanism: serotonin antagonist; improves oxygen utilisation in ischaemic muscle
  • Trial period: 3–6 months; discontinue if no symptomatic improvement
  • NOT cilostazol — NICE does NOT recommend cilostazol due to cardiac side effect concerns
Naftidrofuryl oxalate improves claudication distance by ~20–30% vs placebo. NICE NG19 explicitly recommends naftidrofuryl over cilostazol.
High-Risk PAD — Rivaroxaban 2.5mg BD + Aspirin (COMPASS Trial)
  • NICE TA571 (2019): rivaroxaban 2.5mg BD + aspirin 75mg OD for PAD with high CV risk (symptomatic + prior MI, or polyvascular disease)
  • COMPASS trial: 28% reduction in MACE; also significantly reduced major adverse limb events (MALE) including amputation
  • Indicated when: symptomatic PAD + prior MI; or polyvascular disease (PAD + CAD + cerebrovascular). NOT routine for all PAD.
  • Contraindicated: stroke within 1 month, haemorrhagic stroke, high bleeding risk, concurrent DOAC for AF
  • If AF present: full-dose DOAC (apixaban 5mg BD) + specialist antiplatelet decision — do NOT add clopidogrel to DOAC without specialist input
Special Circumstances
  • Beta-blockers: NOT contraindicated in PAD (NICE NG19). Do not stop if indicated for angina, post-MI, or heart failure.
  • Diabetes: SGLT2i (empagliflozin, dapagliflozin) for secondary CV prevention; HbA1c target <58 mmol/mol
  • CKD: check eGFR before ACEi; dose-adjust or avoid DOAC if CrCl <15; TBI instead of ABPI
  • Analgesia for CLTI rest pain: regular paracetamol → neuropathic agents (gabapentin) → opioids if severe. Do not withhold opioids for genuine ischaemic rest pain.
  • Prophylactic antibiotics: NOT indicated for intermittent claudication; required if infected diabetic foot ulcer
7E — Medication selection tool — choose patient characteristics for tailored drug recommendations

Select patient characteristics — see drug cards and guidance below

PAD drug selection guide
All confirmed PAD: Clopidogrel 75mg + Atorvastatin 80mg + Ramipril 2.5mg (titrate). DM: add SGLT2i + TBI instead of ABPI. AF: DOAC replaces antiplatelet (specialist). High CV risk + prior MI: consider rivaroxaban 2.5mg BD + aspirin (COMPASS). Claudication not improving on exercise: naftidrofuryl oxalate 200mg TDS for 3–6 months. CLTI: urgent vascular surgery referral + analgesia. See drug cards below.
7F — Drug reference cards: antiplatelets · statins · ACEi · vasodilator · anticoagulant combo
Clopidogrel (Preferred Antiplatelet)
Clopidogrel 75mg tablets — generic
✓ Recommended
First-line antiplatelet in PAD75mg OD
✓ Prefer when
All confirmed PAD (ABPI ≤0.9) — NICE NG19 first-line; superior to aspirin in PAD subgroup (CAPRIE trial: 23.8% relative risk reduction)
Post-peripheral vascular intervention (angioplasty, stent, bypass) — antiplatelet essential for graft patency
Aspirin intolerance or previous GI bleed on aspirin — clopidogrel has lower GI side effect profile
Patient with prior MI or stroke on aspirin already — can switch to clopidogrel as superior antiplatelet for PAD specifically
✗ Avoid if
Active significant bleeding or high uncontrolled bleeding risk
Concurrent DOAC (for AF) without specialist haematology/cardiology input — adding clopidogrel to DOAC doubles bleeding risk without sufficient CV benefit in most cases
CYP2C19 poor metabolisers (genetic) — reduced efficacy; consider prasugrel or ticagrelor with specialist input post-stenting
⚠ Side effects
Bruising and prolonged bleeding — wound management pre-operatively (stop 5–7 days before elective surgery unless vascular; do not stop without vascular/cardiology advice)
GI upset — less than aspirin; add PPI if high GI risk or concurrent NSAID use
Thrombotic thrombocytopenic purpura (TTP) — rare; platelet drop + neurological symptoms = urgent haematology
🔬 Monitor
No routine monitoring required. FBC at baseline and if new bruising/bleeding. Annual review of indication, bleeding risk, and surgical status
Before any elective surgery: document antiplatelet status and discuss with vascular/surgical team — stopping clopidogrel post-stent or post-bypass can cause acute thrombosis
💬 Counselling

"This tablet prevents blood clots forming in your narrowed blood vessels — it's one of the most important things we can do to reduce your risk of a heart attack or stroke. You might bruise more easily and cuts take slightly longer to stop bleeding. If you need an operation of any kind, please tell the surgeon you're taking this tablet."

CAPRIE trial evidence: clopidogrel is superior to aspirin specifically in the PAD subgroup. Stating "clopidogrel is preferred over aspirin in PAD — the evidence specifically supports this" = Tasks domain mark. Prescribing aspirin instead of clopidogrel in confirmed PAD without explaining the choice = partial deduction.

Atorvastatin 80mg (High-Intensity Statin)
Atorvastatin 80mg tablets
✓ Recommended
All confirmed PAD80mg OD (evening)
✓ Prefer when
All confirmed PAD (ABPI ≤0.9) regardless of baseline LDL cholesterol — NICE NG19 mandates high-intensity statin at maximum tolerated dose for all PAD
Target LDL <1.8 mmol/L (ESC 2019 guidelines, adopted in UK practice) or ≥50% reduction from baseline
Polyvascular disease (PAD + CAD + cerebrovascular) — most intensive statin therapy required; PCSK9 inhibitor consideration if LDL not at target
✗ Avoid if
Active liver disease (LFTs >3× ULN) — do not start; investigate and treat liver disease first
Pregnancy and breastfeeding
Previous significant statin-induced myopathy — consider lower dose (rosuvastatin 20–40mg) with CK monitoring; avoid re-challenge with same statin
⚠ Side effects
Myalgia — most common (5–10%); check CK if severe; stop if CK >5× ULN + symptoms
Elevated transaminases — LFTs at 3 months; ALT >3× ULN persistently → reduce dose or switch statin
New onset DM — modest risk increase; outweighed by CV benefit in confirmed PAD
🔬 Monitor
Fasting lipids + LFTs + CK (if myalgia) at 3 months; then annually. LDL target <1.8 mmol/L
LDL >1.8 on 80mg → add ezetimibe 10mg OD. LDL still >1.8 on dual therapy → PCSK9 inhibitor (evolocumab or alirocumab); refer lipid clinic
💬 Counselling

"This tablet reduces the fatty deposits that are narrowing your arteries — and the evidence shows it protects your heart and brain as well as your legs. It works best taken in the evening. If you get unexplained muscle aches, let me know and we'll check a blood test. Most people tolerate it very well at this dose."

High-yield SCA pearl: Atorvastatin 80mg must be stated specifically in PAD — not just "a statin" or "a cholesterol tablet." Stating "NICE recommends high-intensity statin for all PAD regardless of cholesterol level" = Tasks mark. Omitting statin in PAD is one of the most common secondary prevention gaps identified in GP audits.

Ramipril (ACEi — Secondary Prevention)
Ramipril 1.25mg / 2.5mg / 5mg / 10mg capsules
✓ Recommended
All PAD with HTN or high CV risk2.5mg OD → titrate to 10mg
✓ Prefer when
All PAD patients with hypertension — HOPE trial evidence: ramipril 10mg reduces MI, stroke, and CV death by 22% in high-risk vascular patients including PAD, beyond BP-lowering effect
DM + PAD — renoprotective and cardioprotective; superior to other antihypertensives as first-line in DM
Post-MI, LV dysfunction, heart failure — mandatory alongside antiplatelet and statin in polyvascular disease
Titrate: 2.5mg OD for 2 weeks → 5mg → 10mg at monthly intervals if tolerated and eGFR stable
✗ Avoid if
Bilateral renal artery stenosis — ACEi can precipitate acute ischaemic nephropathy; renal artery stenosis is more prevalent in PAD (shared atherosclerotic risk)
Pregnancy — teratogenic; use amlodipine or labetalol instead
CKD (eGFR <30) — start at 1.25mg; monitor U&E carefully; nephrology input if creatinine rises >25% or K⁺ >5.5
⚠ Side effects
Dry cough (10–15%) — if persistent and troublesome, switch to ARB (candesartan 4–16mg or losartan 25–100mg); identical secondary prevention benefit
First-dose hypotension — start at 1.25mg at night; particularly in patients who are dehydrated, on high-dose diuretics, or have low sodium
Hyperkalaemia and AKI — check U&E at 2 weeks after initiation and after dose increases; stop if K⁺ >6.0 or creatinine rises >25%
🔬 Monitor
U&E at 2 weeks after initiation and each dose increase. Annual U&E and eGFR when stable. BP at 4 weeks
Renal artery stenosis screen: unexplained bilateral CKD deterioration on ACEi → renal Doppler. eGFR <60 → avoid iodinated contrast for CT angiography in these patients
💬 Counselling

"This blood pressure tablet does two important jobs: it lowers your blood pressure, and there's good evidence it also directly reduces the risk of a heart attack or stroke in people with your condition. A small number of people develop a dry cough on it — if that happens, please tell me and we can switch to a very similar tablet that doesn't cause the cough."

HOPE trial: ACEi in PAD has benefit beyond BP lowering. Stating "ramipril has specific evidence in PAD patients from the HOPE trial" = Tasks mark. Also: renal artery stenosis is more common in PAD — always check U&E at 2 weeks after starting ACEi and document in notes.

Naftidrofuryl Oxalate (Claudication Symptom Treatment)
Naftidrofuryl oxalate 200mg capsules (Praxilene)
✓ Recommended
After failed exercise therapy200mg TDS
✓ Prefer when
Claudication not improving after 3–6 months of supervised exercise therapy in a patient who does not wish to be referred for vascular intervention (NICE NG19 specific indication)
Patient unable to undertake supervised exercise programme (mobility limitation, comorbidities) — naftidrofuryl as bridge
Adjunct to exercise therapy in patients with severe functional limitation (<100m) while awaiting exercise programme referral
✗ Avoid if
Critical limb-threatening ischaemia (rest pain, ulceration) — vasodilators have no role in CLTI; urgent vascular referral required
Cilostazol — NOT recommended by NICE NG19 due to risk of serious cardiac events (tachyarrhythmia, worsening heart failure)
Liver impairment — metabolised hepatically; reduce dose or avoid in significant hepatic dysfunction
⚠ Side effects
Nausea, GI upset, headache — take with food
Hepatotoxicity (rare) — LFTs at baseline; stop if symptoms of jaundice
Dizziness, skin rash — less common
🔬 Monitor
Review at 3–6 months: has claudication distance improved? If no benefit, discontinue — do not continue indefinitely without demonstrated effect
Claudication distance before and after (treadmill or recorded walking distance) — document to assess treatment response
💬 Counselling

"This capsule helps improve blood flow to your leg muscles and can increase the distance you can walk before pain starts. It works over weeks to months rather than immediately. Take it three times a day with food. I'll review whether it's working in 3 months — if there's no improvement, we can stop it."

Critical NICE NG19 distinction: naftidrofuryl, NOT cilostazol, is recommended for claudication. Prescribing cilostazol = prescribing against NICE guidance (cardiac risk concerns). Stating "NICE recommends naftidrofuryl specifically and recommends against cilostazol" = high-value Tasks mark. This distinction is a known SCA examination topic.

Rivaroxaban 2.5mg BD + Aspirin 75mg (COMPASS Regimen)
Rivaroxaban 2.5mg BD + Aspirin 75mg OD (NICE TA571)
✓ Recommended
High-risk PAD onlyRivaroxaban 2.5mg BD + Aspirin 75mg OD
✓ Prefer when
Symptomatic PAD + prior MI (within 2 years) — NICE TA571 approved indication
Polyvascular disease (PAD + CAD + cerebrovascular disease) — COMPASS trial demonstrated reduction in MACE and major adverse limb events (MALE) including amputation
Symptomatic PAD who remain at high risk of MACE despite antiplatelet + statin + secondary prevention optimisation
✗ Avoid if
Stroke within previous month — increased intracranial haemorrhage risk
Previous haemorrhagic stroke
Concurrent full-dose anticoagulation (DOAC for AF) — do NOT combine full-dose DOAC with COMPASS regimen
High bleeding risk (recent GI bleed, active peptic ulcer, CrCl <15) — risk-benefit assessment required; add PPI
⚠ Side effects
Bleeding (GI most common) — add PPI (lansoprazole 30mg OD) to all patients on COMPASS regimen
Intracranial haemorrhage (lower rate than full-dose anticoagulation but higher than antiplatelet alone)
Bruising, epistaxis — standard anticoagulant/antiplatelet precautions
🔬 Monitor
Annual renal function (rivaroxaban dose-adjustment at CrCl <15). FBC and GI symptoms at 3 months
PPI co-prescription is mandatory with COMPASS regimen — do not prescribe without GI protection
💬 Counselling

"This combination — a low-dose blood thinner and a low-dose aspirin — has been shown in a large clinical trial to significantly reduce heart attacks, strokes, and the risk of losing a limb in people with your level of vascular disease. I'm also adding a stomach-protecting tablet alongside it. If you notice any unusual bleeding, please let me know straight away."

COMPASS trial (NEJM 2017): rivaroxaban 2.5mg BD + aspirin 75mg significantly reduced MACE and MALE in PAD. This is NOT standard anticoagulation for all PAD — only for high-risk patients (prior MI, polyvascular). Knowing the indication and the trial name = Tasks domain mark. Also: always co-prescribe PPI with COMPASS regimen.

SGLT2 Inhibitors (DM + PAD Secondary Prevention)
Empagliflozin 10–25mg OD · Dapagliflozin 10mg OD · Canagliflozin 100–300mg OD
✓ Recommended
DM + PAD — CV risk reductionEmpagliflozin 10mg OD
✓ Prefer when
DM + confirmed PAD (or any CV disease) — EMPA-REG OUTCOME, CANVAS, DECLARE trials show 14% reduction in 3-point MACE and 30–40% reduction in hospitalisation for heart failure
DM + PAD + CKD (eGFR >20) — DAPA-CKD trial: dapagliflozin reduces CKD progression by 39%
Additional benefits: weight loss 2–3kg, BP reduction 3–5 mmHg, HbA1c reduction 0.5–0.7%, diuretic effect
✗ Avoid if
eGFR <20 ml/min — reduced efficacy and risk of AKI; check renal function before starting and after illness
Recurrent genital tract infections or severe UTI history — SGLT2i dramatically increase mycotic genital infections
Foot ulceration or lower limb amputations — canagliflozin specifically associated with increased lower limb amputation risk (CANVAS); empagliflozin or dapagliflozin preferred if SGLT2i indicated in PAD
⚠ Side effects
Genital mycotic infections (thrush) — common (10–15%); advise hygiene; treat with topical antifungal
Euglycaemic diabetic ketoacidosis — rare but serious; typically in T1DM or perioperatively; hold SGLT2i 24–48h before major surgery
Fournier's gangrene (necrotising perineal infection) — very rare but life-threatening; any perineal pain, redness, or swelling = stop immediately and emergency surgical review
🔬 Monitor
HbA1c 3-monthly until stable; then 6-monthly. eGFR at baseline and 3 months (slight initial eGFR dip expected)
Hold during intercurrent illness, surgery, contrast imaging, or severe dehydration — sick day rules essential
💬 Counselling

"This tablet has two important jobs — it helps control your blood sugar, and it also significantly reduces your risk of heart attack and protects your kidneys. One side effect to be aware of: it can cause thrush infections in the genital area — good hygiene and staying well hydrated helps prevent this. I'll give you written information about when to stop it temporarily, for example if you become very unwell."

Canagliflozin and lower limb amputation: CANVAS trial showed increased amputation risk with canagliflozin. In DM + PAD, prefer empagliflozin or dapagliflozin — stating this specific drug choice distinction = high-value Tasks domain mark. Also: Euglycaemic DKA risk — hold peri-operatively; sick day rules essential.

7G — Psychosocial impact of the diagnosis: driving, work, relationships & daily life
🫂
Living with PAD — independence, amputation fear, and the long road to recovery
PAD is not just a vascular disease — it is a disease of progressive disability, fear, and identity loss. The patient who comes to the GP with claudication is often already living with the constant knowledge that a family member lost a limb, that walking is becoming dangerous, and that their livelihood may depend on mobility they are losing. Every aspect of daily life is affected: driving, employment, relationships, mood, and self-concept. The GP who addresses only the biochemistry and leaves the psychosocial consequences unaddressed has completed half the consultation.
🚗
Driving, DVLA & Occupation

Group 1 (cars): stable claudication that does not affect safe driving does not require DVLA notification. However, if claudication severely limits walking or if there is significant peripheral neuropathy affecting foot/leg control, DVLA notification and medical assessment may be required.

Group 2 (HGV/bus/PCV): DVLA must be notified. Medical standards require adequate cardiovascular fitness — recent MI, recent revascularisation, or severe PAD may temporarily or permanently affect Group 2 entitlement. Vascular assessment may be required before licence restoration.

For Brian: as a bus driver (Group 2), DVLA notification is required. The supervised exercise programme and secondary prevention treatment directly improve walking distance and cardiovascular fitness — both positively affecting the DVLA assessment outcome. Frame treatment as the pathway back to full licence status.

"I know your driving licence is your livelihood. I want to explain what the DVLA rules are — and more importantly, I want to tell you that the treatment plan we're starting today is exactly what maximises your chances of maintaining your licence."
😨
Amputation Fear & Family History

Amputation fear is the dominant psychosocial driver in PAD — and it is almost universally present, often rooted in family experience. This fear is simultaneously the greatest barrier to engagement (avoidance, catastrophising) and the most powerful motivator for change when correctly harnessed.

Reframe the family history not as inevitable fate but as the reason to act differently. Modern evidence-based management achieves outcomes radically different from the untreated disease of a previous generation. Early stage claudication with active management has a very low amputation risk with good outcomes.

Every intervention — clopidogrel, atorvastatin, exercise, smoking cessation — should be explicitly linked to the patient's stated fear of amputation. "This tablet reduces your risk of the outcome you're worried about" is a more powerful motivator than "this tablet reduces LDL."

"I want to be direct about your worry — and I want to reassure you with evidence, not just words. People who stop smoking, take these tablets, and do the exercise programme have a dramatically lower risk of amputation. You're at a stage where we can make a real difference."
💼
Employment, Sick Leave & Functional Capacity

Claudication with consistent onset distance <200m significantly limits occupational function in roles requiring sustained walking, standing, or physical activity. MED3 fit notes should document specific functional limitations ("unable to walk >100m without pain") to enable reasonable adjustments rather than blanket absence.

Supervised exercise therapy directly increases claudication distance — over 6 months, most patients double their pain-free walking distance. This occupational improvement should be explicitly communicated as a treatment goal that is personally relevant to the patient's employment.

Post-revascularisation (bypass or angioplasty): typically 4–6 weeks off work for desk-based roles; 8–12 weeks for manual work. Document and communicate return-to-work expectations proactively.

"I'll write you a fit note that explains your specific limitations — that should allow your employer to make adjustments rather than signing you off completely. And I want to be clear: the exercise programme we're starting is likely to significantly improve how far you can walk within 3 months."
😔
Depression, Chronic Pain & Quality of Life

PAD causes chronic pain that progressively limits activities previously taken for granted. This loss of mobility, independence, and pleasurable activity is a direct cause of depression (PHQ-9 screens positive in 20–30% of PAD patients). Depression then worsens secondary prevention adherence, creating a vicious cycle.

Exercise therapy has direct antidepressant effects through endorphin release, improved self-efficacy, and social engagement in group-based programmes. This dual benefit — improving claudication distance AND improving mood — makes supervised exercise therapy the most holistic intervention available for PAD.

CLTI with severe rest pain: opioid-level analgesia may be required. Do not withhold effective analgesia while awaiting vascular assessment. Chronic pain management referral for complex cases.

"I want to check in about how you've been feeling in yourself beyond the leg pain. Chronic pain that stops you doing the things you enjoy can really affect your mood. The exercise programme I'm recommending isn't just for your legs — many people find it lifts their mood significantly too."
👨‍👩‍👧
Relationships & Carer Impact

PAD progressively limits the patient's ability to participate in shared activities, household tasks, and family life. The partner of a PAD patient may take on increasing carer responsibilities while also managing their own anxiety about the patient's prognosis.

Partners often attend consultations for PAD and should be engaged in the management plan — particularly around smoking cessation (household smoking cessation dramatically improves individual quit rates), foot inspection support, and exercise programme encouragement.

Sexual dysfunction in men with aortoiliac disease (Leriche syndrome): impotence is a direct consequence of the arterial disease, not a medication side effect. Addressing this directly and sensitively is an important part of comprehensive PAD management. PDE5 inhibitors may be safe and effective once revascularisation has been performed.

"Is there someone in your life who should know about this — who might be able to support you with the exercise programme, or with the changes to your lifestyle? Having support at home makes a significant difference to how well the treatment works."
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Post-Amputation Rehabilitation & Identity

For patients who progress to major amputation, the psychological impact is profound. Phantom limb pain affects 60–80% of amputees. Body image disruption, loss of independence, and grief for the pre-amputation self require specific psychological support that is often not available in standard vascular follow-up.

Pre-amputation counselling: preparation for what to expect, prosthetic rehabilitation, and realistic expectations for recovery dramatically improve post-amputation outcomes. GP involvement in coordinating this preparation is important.

The post-amputation GP review should include: phantom limb pain assessment (gabapentin, pregabalin), prosthetic fitting progress, depression screening (PHQ-9), social care needs, driving and DVLA update, and ongoing secondary prevention (the CV risk does not resolve after amputation — these patients continue to need statin, antiplatelet, and antihypertensive).

"If you do end up needing a larger procedure, I want you to know that there's very active rehabilitation available, and the outcomes are much better than people often expect. But our goal right now is to avoid getting to that point."
7H — Follow-up schedule
1
4–6 Weeks — First Review

ABPI result review and interpretation. Secondary prevention medications started and tolerated (clopidogrel, atorvastatin 80mg, ramipril). Exercise therapy referral confirmed and patient attending. Smoking cessation update — SMSC attendance confirmed. BP target review — add amlodipine if needed. Foot inspection in DM. U&E if ACEi started. DVLA discussion documented.

ABPI result reviewMedication tolerance checkSmoking cessation
2
3 Months — Exercise Programme Review

Claudication distance at 3 months vs baseline. Fasting lipids (LDL target <1.8 mmol/L) — add ezetimibe if not at target. HbA1c if DM. PHQ-9 mood screen. Foot inspection. BP review. Smoking cessation update. If claudication distance improved ≥50% → continue programme to 6 months. If minimal improvement → review adherence; consider naftidrofuryl; reassess vascular referral.

LDL target checkClaudication distance measuredPHQ-9
3
6 Months — Exercise Programme Completion

Final claudication distance measurement. If adequate improvement: continue secondary prevention; annual review. If inadequate improvement (still functionally limiting, life or work impact): vascular surgery referral for angioplasty/stenting consideration. LDL, HbA1c, BP targets confirmed. Naftidrofuryl decision (start or review). Any CLTI features developing → urgent vascular referral — do not wait for next routine review.

Vascular referral decision pointNaftidrofuryl decision
4
Annual Review — Secondary Prevention Targets

Full cardiovascular risk review: BP, LDL, HbA1c, BMI, smoking status, alcohol. Repeat ABPI (progression monitoring). Foot inspection in DM — update podiatry referral if needed. PHQ-9 depression screen. DVLA status update. AAA surveillance if known AAA. Review for any rest pain or tissue loss developing (immediate upgrade to urgent management if present). Graft surveillance if post-revascularisation.

Annual ABPI — detect progressionFull CV risk reviewPHQ-9 + foot inspection
5
Ongoing — Post-Revascularisation Surveillance

Post-bypass graft: duplex surveillance at 3, 6, and 12 months then annually (graft failure is often asymptomatic until critical stenosis develops). Post-angioplasty: ABPI at 3 months; if falls back to pre-procedure level → re-occlusion; urgent vascular review. Continue full secondary prevention cascade permanently — revascularisation does not cure atherosclerosis. Antiplatelet mandatory post-intervention.

Graft surveillance mandatoryAntiplatelet continued lifelong
7I — Monitoring: the PAD secondary prevention targets

Memory rule — the PAD monitoring triad

At every PAD review: ABPI annually (detect progression to CLTI before it presents as emergency) · LDL <1.8 mmol/L on atorvastatin 80mg (add ezetimibe if >1.8) · BP <140/90 (or <130/80 in DM). Any rest pain or tissue loss developing = urgent vascular referral immediately — do NOT manage in the community. PHQ-9 at every review — depression is the most undertreated complication of PAD and the strongest predictor of poor adherence.

Drug / Risk factorTestTimingAction threshold
Clopidogrel (routine)FBCBaseline; if new bleeding symptomsTTP (platelet drop + neurological) → stop urgently + haematology. GI bleeding → PPI; endoscopy if significant.
Atorvastatin 80mgFasting lipids + LFTs + CK3 months; then annuallyLDL >1.8 → add ezetimibe. ALT >3× ULN → reduce or switch statin. CK >5× ULN + symptoms → stop urgently.
Ramipril (ACEi)U&E + eGFR2 weeks after each dose increase; annuallyCreatinine ↑ >25% → hold ACEi; investigate renal artery stenosis. K⁺ >6.0 → stop; urgent review.
ABPI monitoring (disease progression)ABPI bilateralAnnually; or if symptoms worsenABPI falls to ≤0.5 → CLTI developing; urgent vascular referral even if not yet symptomatic at rest.
Rivaroxaban 2.5mg + Aspirin (COMPASS)U&E + eGFR; FBC; GI symptoms3 months; then annuallyCrCl <15 → stop rivaroxaban. GI bleeding → stop; review with gastroenterology. PPI co-prescription mandatory.
Target / Patient groupBP target (mmHg)LDL / HbA1c target
PAD (all) — primary BP target<140/90LDL <1.8 mmol/L on atorvastatin 80mg
PAD + DM<130/80HbA1c <58 mmol/mol; LDL <1.8
PAD + CKD (eGFR <60)<130/80LDL <1.8; monitor eGFR closely on ACEi
Polyvascular disease (PAD + CAD + CVD)<130/80LDL <1.4 mmol/L (ESC 2019 very-high-risk target)
Post-revascularisation (ongoing)<140/90LDL <1.8; antiplatelet mandatory lifelong
Elderly (>80) — avoid over-treatment<150/90Tolerated statin dose; avoid muscular side effects
7J — Safety-netting: exact phrases + medico-legal rationale

⚠ Three scenario-specific phrases — use these verbatim

🔴 Emergency — acute limb ischaemia features (the 6 Ps)
"I need to tell you about the warning signs that would mean you need to go to A&E immediately — not a GP appointment, but 999. If your leg suddenly becomes very painful at rest, goes pale or cold compared to the other leg, if you lose feeling in it, or if you can't move it — those are emergency signs. It means the blood supply has suddenly been cut off and you have a few hours before permanent damage occurs. Call 999 immediately."
The 6 Ps of ALI (Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishingly cold) must be communicated verbally and in writing at every PAD consultation. A patient with known chronic PAD who develops ALI may attribute the worsening to their usual claudication and delay presentation fatally. Failure to provide this safety-net is a documented source of GP medico-legal liability in vascular surgery cases.
💊 Medication — clopidogrel and antiplatelet safety
"Your clopidogrel tablet keeps the blood from clotting in your narrowed arteries — so it's doing a really important job. It does mean you'll bruise more easily and cuts will take a little longer to stop. If you develop any unexplained bleeding — blood in your stools, black stools, or coughing up blood — come to us or go to A&E the same day. Please don't stop the tablet without telling me first — stopping suddenly could significantly increase your risk of a heart attack or losing a limb."
Premature cessation of antiplatelet therapy is a leading cause of acute vascular events post-PAD diagnosis. Patients stop for minor bruising or pre-procedure instructions without returning for advice. Pre-warning normalises expected side effects (bruising) while flagging the genuinely dangerous ones. Documenting antiplatelet safety counselling at every prescription is the medico-legal standard.
🟠 Disease progression — detecting CLTI early
"There are two things I want you to watch out for and contact us about immediately — don't wait for your next appointment. First: if you start getting pain in your foot or toes at rest, especially at night, that goes away when you hang your leg out of bed — that means we need to act urgently. Second: if you notice any sore, blister, or break in the skin on your feet that isn't healing within 1–2 weeks — contact us straight away. These are signs that your leg may need more urgent treatment."
Early detection of CLTI (rest pain, tissue loss) dramatically improves limb salvage rates — intervention before critical ischaemia is well-established versus emergency management. Rest pain with dependent relief is pathognomonic of CLTI and easily communicated. Non-healing wounds in DM are the commonest entry into the amputation cascade — patient education about early presentation is the most effective preventive intervention at this stage.
4–6 WeeksABPI result; medication tolerance; exercise programme attendance; BP; U&E on ACEi; foot inspection DM; DVLA confirmed
3 MonthsClaudication distance; LDL (add ezetimibe if >1.8); HbA1c DM; PHQ-9; smoking update; naftidrofuryl decision
AnnualABPI progression; full CV targets; foot inspection; PHQ-9; graft surveillance post-op; DVLA update
🎓 SCA Checkpoint — Step 7 (Final)TasksRelating to OthersGlobal Skills
Closing the consultation
"Today we've started three tablets: clopidogrel to protect against clots, atorvastatin for your arteries, and ramipril for your blood pressure. I've also referred you to the supervised exercise programme — that's your most important treatment."
"If you ever notice your leg becoming suddenly much worse — very painful at rest, going pale or cold — please call 999 immediately. And if you see any sores on your feet that aren't healing, contact us straight away."
"I want to come back to what you mentioned about your uncle. At the stage you're at, with active treatment and stopping smoking, your risk is much lower than his was. This isn't the same situation."
"About your driving licence — I'll document in your notes that we've discussed the DVLA notification. The good news is that improving your walking distance is directly connected to maintaining your licence."
"Is there anything else on your mind — anything we haven't covered today?"
Deductions — closing
  • Not giving the ALI safety-net (6 Ps) — the most important emergency safety-net in PAD
  • Not addressing the amputation fear explicitly, despite it being the patient's dominant concern
  • Prescribing aspirin instead of clopidogrel in confirmed PAD without acknowledging the NICE preference
  • Not mentioning supervised exercise therapy as the primary treatment — drugs alone without exercise is undertreating this patient
  • Not documenting DVLA discussion for a Group 2 (HGV/bus) driver
  • Closing without asking if patient has any remaining questions
Tasks domain — full criteria
  • ABPI measurement offered and interpreted at first presentation
  • Clopidogrel 75mg preferred over aspirin — CAPRIE evidence for PAD
  • Atorvastatin 80mg — all confirmed PAD regardless of LDL, NICE NG19
  • Supervised exercise therapy as primary first-line treatment — not optional
  • ALI safety-net (6 Ps) given verbally and in writing
Relating to Others — full criteria
  • Amputation fear explicitly acknowledged and addressed with evidence — not generic reassurance
  • Family history framed as motivation for action, not inevitable fate
  • Driving/DVLA concern addressed with empathy and positive treatment narrative
  • Smoking cessation framed as medical treatment, not lifestyle lecture — addiction acknowledged
  • ICE all three explored and referenced in the management plan
  • Closing question asked; patient agreement sought before ending
🔴 Red — failing
No ALI safety-net; aspirin instead of clopidogrel without CAPRIE acknowledgment; no supervised exercise referral; amputation fear unaddressed; DVLA not documented; no follow-up date
🟠 Amber — borderline
Clopidogrel prescribed but CAPRIE evidence not mentioned; exercise therapy mentioned but not specifically referred; ALI safety-net vague; amputation fear acknowledged but not specifically reframed; DVLA raised but not explored
🟢 Green — strong pass
Clopidogrel + CAPRIE evidence; atorvastatin 80mg + NICE NG19 rationale; supervised exercise as primary treatment; ALI 6 Ps written + verbal; amputation fear directly addressed with specific evidence; DVLA documented; smoking as addiction not choice; ICE all three; closing question; named follow-up
Peripheral Arterial Disease — SCA Consultation Scorecard
Based on the official SCA Consultation Tool · RAG self-assessment · Use after every practice consultation
0/ 33 pts
🌐
Global Skills
Structure, language, responsiveness
0/7
Tasks
Clinical reasoning, diagnosis, management
0/15
🤝
Relating to Others
Communication, rapport, shared decision making
0/11
RAG Self-Assessment Guide
🔴 Red — not achieved
Element absent or seriously erroneous. Examples: aspirin instead of clopidogrel; no ALI safety-net; compression without ABPI; CLTI managed as routine; cilostazol prescribed; amputation fear unaddressed.
🟠 Amber — partially achieved
Element present but incomplete. Examples: clopidogrel given but CAPRIE evidence not cited; exercise therapy mentioned but not specifically referred; ALI safety-net verbal only; CLTI features not screened; smoking mentioned without cessation support.
🟢 Green — fully achieved
Specific, evidence-based, patient-centred. CAPRIE cited for clopidogrel; NICE NG19 for statin; HOPE for ramipril; exercise therapy specifically referred; ALI 6 Ps written + verbal; amputation fear reframed with evidence; DVLA documented.
011172533
Fail
Borderline
Pass
Strong pass
📋
Complete the checklist above to see your score interpretation and personalised feedback
"I've been getting this pain in my calves when I walk — it started a few months back. It goes away when I stop. My mate said it might be a DVT like his brother had, so I thought I'd better get it checked. It's probably nothing — I'm not the sort to make a fuss."
Who you are

Brian Patel, 62-year-old bus driver for a major city bus operator. Married with two grown children. 40 pack-year smoker — currently 20/day, has tried to stop twice before without success. Type 2 diabetes diagnosed 8 years ago (HbA1c 62 mmol/mol at last check, 14 months ago). BP today 162/96 — on amlodipine 5mg. No other regular medication. Has never been told about "bad circulation" before. Uncle had his left leg amputated 12 years ago due to "poor circulation" — Brian was present during the hospital admissions. This is the central fact shaping his entire fear around these symptoms.

Hidden agenda (two layers)

Layer 1 — Amputation fear: Brian is quietly terrified he is going to lose a leg. He watched his uncle go through three operations and then a below-knee amputation. He attributes it to "the same thing in the family." He will not say this unless specifically asked about his concerns or unless the doctor asks about family history. If the amputation fear is not explored and directly addressed, Brian will seem compliant but will go home more anxious than he arrived.

Layer 2 — Driving licence: Brian drives a Group 2 bus licence (PCV). His job and mortgage depend entirely on keeping it. He has heard vague things about medical conditions and DVLA but doesn't know the specifics. If the doctor doesn't raise this, he will leave the consultation not knowing whether he can keep working. He may become defensive or evasive about symptom severity to protect his licence if he feels threatened.

Symptoms if asked directly
  • Bilateral calf cramping — left slightly worse than right
  • Starts consistently at around 200 metres of walking, sometimes a bit less if he has been walking quickly or uphill
  • Completely gone within 5 minutes of stopping and standing still
  • No rest pain — he sleeps fine; no night pain
  • No sores on his feet — hasn't looked recently ("I don't really check")
  • No chest pain or shortness of breath on exertion (he's noticed he can't do much exertion anyway due to the legs)
  • No visual symptoms, no headache, no speech problems
  • Erectile dysfunction: if asked about this specifically or about bilateral buttock/thigh symptoms — Brian has noticed some difficulty but will be embarrassed to volunteer it. He attributes it to "age and stress"
Lifestyle + bonus details
  • Smokes 20/day for 40 years — resistant initially ("I've tried twice, it doesn't work for me"). Responds to evidence-based framing about stopping smoking and leg/limb outcomes, especially linked to his uncle.
  • Alcohol: 14–16 units/week — doesn't think this is excessive
  • Diet: regular takeaways, skips breakfast; not actively trying to manage DM diet
  • Exercise: almost none beyond his working shifts (seated driving)
  • Foot care: checks his feet "occasionally" — doesn't inspect between toes or heel
  • DVT attribution: convinced this might be a DVT. Responds well to a specific explanation of why the pattern (goes away with rest) is arterial not venous. Needs direct comparison, not generic reassurance.
  • Clopidogrel vs aspirin: if asked, he already takes aspirin occasionally for headaches — this opens the discussion about switching to regular clopidogrel
  • Beta-blockers: if the candidate mentions beta-blockers, Brian will say "I was told I couldn't have those because of my legs" — creating an opportunity for the candidate to correct the misconception
"My mate had a DVT and his leg was swollen and painful all the time. Mine's only painful when I walk. Is it really the same thing? And look — I need to keep my bus licence. I can't afford to lose my job. What does this mean for my driving?"

Resolution: Brian will fully engage with the management plan if the candidate: (1) specifically explains why his symptoms are arterial and not a DVT — using the rest-relief pattern as the discriminating feature; (2) names his amputation fear directly ("I get the sense you're worried about losing a limb, like your uncle — let's talk about that") and reframes his uncle's outcome as motivating evidence rather than inevitable fate; (3) is honest and empathetic about the DVLA implications while framing the treatment as the pathway to maintaining his licence; (4) treats smoking as an addiction requiring medical treatment, not a choice; (5) includes a specific exercise programme referral rather than a vague "try to walk more." Brian will disengage if the doctor is dismissive about the DVT concern, avoids the amputation fear, or talks about "lifestyle" without acknowledging that stopping smoking is very hard.

🏥
Clinic Quick Reference
Peripheral Arterial Disease — Clinical Decision Framework
NICE NG19 (2020) · NICE CG147 (2024) · CKS PAD (2024) · First Presentation
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🚦 1 — Triage Algorithm
Patient with leg pain on walking or at rest
🔴 Emergency — 999
  • ALI — any of the 6 Ps: sudden severe pain, pallor, pulselessness, paraesthesia, paralysis, perishingly cold
  • Wet gangrene + sepsis: emergency debridement + antibiotics
  • Ruptured / symptomatic AAA: collapse + pulsatile abdominal mass
  • Paralysis or complete sensory loss → severely threatened limb
999 — 6-hour revascularisation window
🟠 Urgent — 1–2 weeks
  • CLTI: rest pain >2 weeks (forefoot, relieved by dependency)
  • Non-healing ischaemic ulcer or dry gangrene (Fontaine IV)
  • Rapid claudication deterioration (distance halved in weeks)
  • Bilateral absent femoral pulses (Leriche syndrome)
  • AAA >5.5cm or symptomatic
Start secondary prevention now; urgent vascular referral
🟢 Routine — weeks to months
  • Stable claudication (Fontaine IIa/IIb) — ABPI ≤0.9 confirmed
  • ABPI measurement and CV risk profiling at first presentation
  • Secondary prevention cascade: clopidogrel + atorvastatin 80mg + ramipril
  • Supervised exercise therapy referral × 6 months
  • Annual PAD review: ABPI, LDL, BP, HbA1c, foot inspection, PHQ-9
Start all three secondary prevention medications today
🔬 2 — ABPI Interpretation & Investigation Priority
ABPI Interpretation
>1.3: Normal
>1.4: Falsely elevated — calcified vessels (DM/CKD/elderly) → use Toe-Brachial Index (TBI)
0.9–1.3: Normal perfusion
0.8–0.9: Mild PAD
0.5–0.8: Moderate PAD — claudication range
≤0.5: Severe PAD — CLTI; urgent vascular
⛔ ABPI <0.8 = NO compression bandaging. TBI if ABPI >1.4 in DM/CKD.
Investigation Priority
🥇 ABPI bilateral — confirms diagnosis, grades severity, baseline for monitoring
🥇 Fasting lipids — baseline LDL before statin; 3-month response monitoring
🥇 HbA1c — DM diagnosis; guides glycaemic secondary prevention
🥈 U&E + eGFR — ACEi safety; DOAC dosing; renal artery stenosis screen
🥈 FBC — anaemia worsens claudication; polycythaemia/thrombocytosis thrombosis risk
🥈 ECG — AF detection (embolic ALI risk; anticoagulation decision)
📊 3 — Key Numbers
ABPI ≤0.9
Confirms PAD
ABPI ≤0.5
Critical limb-threatening ischaemia
<200 m
Significant claudication impairment
6 Ps
ALI: Pain · Pallor · Pulseless · Paraesthesia · Paralysis · Perishingly cold
6 months
Supervised exercise therapy minimum (NICE NG19)
80 mg
Atorvastatin — all confirmed PAD
50–70%
PAD patients die from MI or stroke — not limb loss
Higher limb loss if patient continues smoking
>1.4
ABPI falsely elevated (DM/CKD) → use TBI
23.8%
RRR: clopidogrel vs aspirin in PAD (CAPRIE)
22%
CV event reduction: ramipril in PAD (HOPE trial)
28%
MACE reduction: rivaroxaban 2.5mg + aspirin (COMPASS)
💊 4 — Secondary Prevention Cascade & Drug Choice
Start All Three Simultaneously at First Contact (NICE NG19)
1
Clopidogrel 75mg OD — preferred over aspirin in PAD (CAPRIE: 23.8% RRR in PAD subgroup)
2
Atorvastatin 80mg OD — regardless of LDL; target <1.8 mmol/L; add ezetimibe if not reached
3
Ramipril 2.5mg → 10mg — HOPE trial; target BP <140/90 or <130/80 if DM
+
Supervised exercise therapy — primary first-line treatment for claudication; 3× weekly × 6 months
⚠ Beta-blockers NOT contraindicated in PAD (NICE NG19) — do not stop if cardiac indication exists
Drug Choice by Scenario
All confirmed PAD — antiplatelet
Clopidogrel 75mg OD
Claudication unresponsive to exercise
Naftidrofuryl 200mg TDS
High CV risk (prior MI, polyvascular)
Rivaroxaban 2.5mg BD + Aspirin
DM + PAD — CV secondary prevention
Empagliflozin / Dapagliflozin
AF + PAD — anticoagulation
DOAC (specialist guidance)
⛔ Never cilostazol (NICE NG19) · Never canagliflozin in PAD (CANVAS amputation risk) · No compression without ABPI
⚠ 5 — Safety-Netting & DVLA
🔴 ALI — the 6 Ps
"Sudden severe pain · pallor · pulselessness · paraesthesia · paralysis · perishingly cold → 999 immediately. Written + verbal at every consultation."
🟠 CLTI developing — rest pain / tissue loss
"Pain at rest in feet/toes, especially at night, relieved by hanging leg down → contact us urgently. Any non-healing skin break or ulcer → contact within 24–48 hours."
💊 Antiplatelet safety
"Bruising expected. GI bleeding, black stools, coughing blood → A&E same day. Never stop without advice — acute thrombosis risk."
Follow-up timeline
1
4–6 weeks: ABPI result; medication tolerance; exercise programme; U&E on ACEi; foot inspection DM; DVLA
2
3 months: Claudication distance; LDL (add ezetimibe >1.8); HbA1c; PHQ-9; naftidrofuryl decision
3
6 months: Claudication distance final; vascular referral decision if inadequate improvement
4
Annual: ABPI progression; full CV targets; foot inspection DM; PHQ-9; DVLA update; graft surveillance post-op
📌 Any rest pain or tissue loss developing = upgrade to urgent vascular referral immediately — do not wait for scheduled review
🔬 6 — Monitoring Targets & Red Flags
Drug / TargetTestTimingAction threshold
Atorvastatin 80mgFasting lipids + LFTs + CK3 months; annuallyLDL >1.8 → add ezetimibe 10mg. ALT >3× ULN → switch. CK >5× + symptoms → stop urgently.
Ramipril (ACEi)U&E + eGFR2 weeks post-start; annuallyCr ↑ >25% → hold; investigate renal artery stenosis. K⁺ >6.0 → stop urgently.
ABPI (disease progression)ABPI bilateralAnnually; if symptoms worsenABPI ≤0.5 → CLTI developing; urgent vascular referral even if asymptomatic at rest.
COMPASS (rivaroxaban 2.5mg)U&E + eGFR; FBC; GI3 months; annuallyCrCl <15 → stop rivaroxaban. GI bleed → stop; endoscopy. PPI mandatory co-prescription.
Depression — PHQ-9PHQ-9Every reviewPHQ-9 ≥10 → NHS Talking Therapies; SSRI (safe with antiplatelet + PPI). PHQ-9 ≥20 → urgent psychiatric review.
🚨 Emergency flags: ALI (6 Ps — sudden pain, pallor, pulseless, paraesthesia, paralysis, cold) → 999; ruptured AAA → 999; wet gangrene + sepsis → 999; acute graft thrombosis (sudden deterioration post-revascularisation)
🛡️ Safeguarding: Compression without ABPI = patient safety incident — document and report. Older adult with carer neglect + ischaemic ulcer. DV: strangulation → carotid dissection (TIA mimic) in young adults. Post-amputation: increased vulnerability to exploitation and depression. Document DVLA discussion at every Group 2 consultation.
🎓
SCA Exam Quick Reference
SCA Consultation Blueprint
Tasks · Relating to Others · Global Skills · RAG guide
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🕐 12-Minute Consultation Flow — with Domain Scoring
0–1 min
Warm Opening + Open Question
"I can see you've come in about pain in your legs when you walk. Before I ask anything specific — can you describe in your own words exactly what happens, from the start?"
Do not repeat information from the case notes. Open question extracts the diagnostic narrative: character (cramp), site (calf), distance (consistent 200m), relief (gone in 5 min of rest). This is the vascular claudication pattern.
Global SkillsTasks
✗ Starting with closed questions ("Does the pain go when you rest?") · ✗ Repeating case note information verbatim
1–6 min
Targeted History + ICE + ALI Screen
"Is there ever pain in your legs when you're sitting or at night — especially in the feet or toes?"
"I imagine one of your worries might be about what this could lead to — is there anything specific you're concerned about?"
"What do you think is causing this — do you have any thoughts?"
Screen for rest pain (CLTI) first. Explore amputation fear when it arises. Ask about DVT attribution to set up the diagnostic explanation. DVLA concern should be proactively named for Group 2 drivers.
TasksRelating to Others
✗ Not asking about rest pain (misses CLTI) · ✗ Failing to proactively raise DVLA for a professional driver
6–8 min
Examination + Diagnosis in Plain Language
"I'd like to do an ankle pressure test — it compares blood pressure in your ankle and arm to tell us exactly how well blood is reaching your feet. It's the most important test for your symptoms."
"What you have is called peripheral arterial disease — or PAD. The arteries in your legs are narrowed, like a garden hose with a kink. At rest it's enough, but when you walk and your muscles need more blood, the narrowing can't keep up — hence the cramp. It's the same process that can affect the arteries to the heart and brain."
ABPI explained in plain language. Garden hose analogy is the most accessible for claudication. Systemic context (heart + brain) must be stated — it motivates secondary prevention beyond "bad legs."
TasksRelating to OthersGlobal Skills
✗ "PAD" without plain language · ✗ Not explaining the systemic vascular context · ✗ ABPI offered without rationale
8–11 min
Management: Three Tablets + Exercise + Smoking
"Today I'm going to start three tablets. First: clopidogrel — a blood-thinning tablet; the evidence specifically shows this is better than aspirin for your type of problem. Second: atorvastatin — a high-dose cholesterol tablet, for all patients with your condition. Third: ramipril — a blood pressure tablet that has specific evidence for protecting against heart attacks in people with your type of vascular disease."
"The most important treatment — more important than any tablet — is a supervised walking programme. I want to refer you to that today."
"I also want to talk about smoking — because stopping would do more for your legs than any of the tablets I've just described."
Three drugs each named with dose and specific evidence. Exercise therapy framed as more important than drugs — counterintuitive but correct (CLEVER trial). Smoking cessation as addiction, not lifestyle choice.
TasksRelating to Others
✗ Aspirin instead of clopidogrel · ✗ Generic statin without dose · ✗ Exercise not specifically referred · ✗ Smoking framed as choice not addiction
11–12 min
Safety-Net + DVLA + Amputation Fear + Close
"I want to come back to what you mentioned about your uncle. At the stage you're at, with these treatments, your risk is genuinely much lower than his was. The tablets, the exercise, and stopping smoking are exactly what prevents that outcome."
"One emergency sign: if your leg ever becomes suddenly very painful at rest, goes pale or cold, or you can't feel or move it — call 999 immediately. I've written this down for you."
"About your licence — I'll document that we've discussed DVLA. The good news is that improving your walking distance is directly connected to maintaining your licence."
"Is there anything else on your mind before we finish?"
TasksRelating to OthersGlobal Skills
✗ No ALI safety-net · ✗ Amputation fear unaddressed · ✗ No DVLA documentation · ✗ No closing question
🔴🟠🟢 RAG Scoring — All 3 Domains
Tasks Domain
🟢
ABPI explained with TBI caveat for DM; clopidogrel + CAPRIE evidence; atorvastatin 80mg + NICE NG19; ramipril + HOPE trial; supervised exercise as primary treatment; naftidrofuryl (not cilostazol) if needed; ALI 6 Ps written + verbal; CLTI safety-net; DVLA Group 2 documented
🟠
Clopidogrel prescribed but CAPRIE evidence absent; statin given but dose not confirmed as 80mg; exercise mentioned but not specifically referred; ALI safety-net verbal only; CLTI safety-net absent; DVLA mentioned but not documented
🔴
Aspirin instead of clopidogrel; no statin; no supervised exercise referral; no ALI safety-net; cilostazol prescribed; canagliflozin in DM + PAD; compression without ABPI; CLTI managed as routine claudication
Relating to Others
🟢
Amputation fear specifically named and reframed with evidence; family history linked to motivation; DVLA concern addressed empathetically with positive treatment narrative; DVT attribution specifically corrected; smoking as addiction; ICE all three; shared decision-making; closing question
🟠
Amputation fear acknowledged but not reframed; DVLA raised late without empathy; DVT corrected generically; smoking discussed as lifestyle; ICE only one or two components; plan imposed without patient agreement
🔴
Amputation fear unaddressed despite clear cue; DVLA not discussed; DVT attribution not corrected; smoking lectured about; no ICE; closes without checking understanding
Global Skills
🟢
Open question with claudication narrative; plain language throughout; garden hose analogy; signposting; responds to amputation fear cue without continuing clinical agenda; history complete by 7 min; closing question
🟠
Open question asked but interrupted; jargon (atherosclerosis, ABPI) without explanation; emotional cue noted but not responded to; takes >8 min for history; no signposting
🔴
Immediate closed questions; repeats case note information; medical jargon throughout; misses amputation fear cue; no plain language analogies; no signposting between phases
💬 Key Phrases — ICE, Diagnosis & Plan
💭 Ideas probe
"What do you think is causing the pain in your legs? You mentioned a DVT — what made you think that might be it?"
😟 Concerns probe (name amputation fear)
"I get the sense you might have a deeper worry — something like what happened to your uncle. Am I right? Can we talk about that directly?"
🎯 Expectations probe
"Were you expecting me to refer you for a scan or a stent today, or were you just wanting to understand what's going on?"
✓ DVT correction — specific
"What you're describing is actually the opposite of a DVT. A DVT causes constant pain even at rest. What you have goes away with rest — that's the specific pattern of an arterial problem, not a venous one. The ABPI test confirms this."
🗣️ Diagnosis + systemic framing
"It's PAD — peripheral arterial disease. Narrowed arteries in the legs: garden hose with a kink. Works at rest, fails under demand. Same process also affects heart and brain arteries — which is why the treatment protects all three."
🦿 Reframing amputation fear
"Your uncle's outcome was in a different era. Today, with clopidogrel, atorvastatin, supervised exercise, and stopping smoking, people at your stage do dramatically better. This plan is specifically designed to prevent what happened to him."
🚫 9 Danger Zones — Instant Deductions
Aspirin prescribed instead of clopidogrel for PAD→ NICE NG19: clopidogrel preferred. CAPRIE trial: 23.8% RRR in PAD subgroup specifically. State the preference and the evidence every time.
Cilostazol prescribed for claudication→ NICE NG19 does NOT recommend cilostazol (cardiac risk). Naftidrofuryl oxalate 200mg TDS is the NICE-approved drug for claudication.
Beta-blockers said to be contraindicated in PAD→ NICE NG19 explicitly states beta-blockers are NOT contraindicated in PAD. This is a common historical misconception. Correct it when it arises.
Compression bandaging without ABPI in a patient with possible PAD→ ABPI must be checked before any compression. ABPI <0.8 = no compression. ABPI 0.6–0.8 = modified compression only with specialist input.
Canagliflozin prescribed in DM + PAD→ CANVAS trial: increased lower limb amputation risk with canagliflozin. Use empagliflozin or dapagliflozin in DM + PAD.
CLTI (rest pain, tissue loss) sent for routine outpatient rather than urgent vascular referral→ CLTI = Fontaine III/IV = urgent vascular surgery within 1–2 weeks. Not a routine exercise therapy patient.
ABPI not offering TBI caveat in DM→ ABPI >1.4 in DM/CKD = falsely elevated (calcified vessels). TBI (toe-brachial index) is required for accurate PAD diagnosis in DM.
ALI safety-net not given verbally or in writing→ The 6 Ps must be given at every PAD consultation. If a patient re-presents with ALI and there is no documented safety-net, this is a medico-legal risk.
Secondary prevention deferred to vascular surgery specialist→ NICE NG19: clopidogrel, atorvastatin 80mg, and antihypertensive start at GP consultation. Not waiting for specialist review wastes weeks of protective treatment.
💊 Drug Quick-Pick
All confirmed PAD — antiplatelet
Clopidogrel 75mg OD
CAPRIE
All confirmed PAD — statin
Atorvastatin 80mg OD
NICE NG19
All PAD — ACEi
Ramipril 2.5→10mg
HOPE trial
Claudication + failed exercise
Naftidrofuryl 200mg TDS
NOT cilostazol
High CV risk + prior MI
Rivaroxaban 2.5mg BD + Asp
COMPASS
DM + PAD (SGLT2i)
Empagliflozin / Dapagliflozin
Not canagliflozin
⛔ Never cilostazol · Clopidogrel > aspirin in PAD · Beta-blockers NOT contraindicated · No compression without ABPI · No canagliflozin in PAD · Never ABPI alone in DM with calcified vessels
Reviewed: July 2026 · citations verified against current NICE / UK guidance