Lucan · Conditions

Peripheral arterial disease

Australian guidance: Australian guideline on diagnosis and management of peripheral artery disease (Diabetes Feet Australia / ADS, adapted from IWGDF) — covers PAD in diabetes and diabetes-related foot ulcer

1. Definition and epidemiology

Atherosclerotic narrowing of the arteries supplying the limbs, most often the lower limb. Shares its risk factors and its biology with coronary and cerebrovascular disease, so a patient with PAD should be assumed to have disease in the other beds until shown otherwise. Smoking and diabetes are the two dominant drivers; hypertension, dyslipidaemia, age, chronic kidney disease and male sex add to it. In Australia it matters most as the limb-threatening partner of diabetes-related foot disease.

2. Pathophysiology

Atherosclerotic plaque reduces the luminal cross-section; flow is adequate at rest but cannot rise to meet the demand of exercising muscle, producing reproducible exertional pain relieved by rest (intermittent claudication). As stenosis progresses, resting perfusion falls below the threshold for tissue viability: rest pain, then ulceration and gangrene (chronic limb-threatening ischaemia).

In diabetes the disease is distinctive in two ways. It is distal — tibial and pedal vessels rather than the aortoiliac and femoral segments — which makes it harder to bypass. And medial arterial calcification stiffens vessels so they resist compression, which falsely elevates ankle pressures and is why a normal ABI does not exclude PAD in a diabetic foot. Coexisting neuropathy removes the warning symptoms, so claudication and rest pain may simply never be reported.

See [[mechanisms/hyperglycaemia]] for the glucose-toxicity routes, [[mechanisms/smoking]] for the vasculotoxic route, and [[mechanisms/hypertensive-end-organ-damage]] for the pressure contribution.

3. Clinical presentation and diagnostic criteria

Intermittent claudication (calf, thigh or buttock pain on walking, relieved by rest); rest pain, classically nocturnal and relieved by hanging the foot down; non-healing ulcer or gangrene. Signs: absent or diminished pulses, cool pale limb, hair loss, dependent rubor, prolonged capillary refill, delayed venous filling.

The diabetic foot is the exception to all of it — the ulcer may be the first and only sign.

4. Investigations and AU-specific cutoffs

Grounded in the Australian PAD guideline (recommendation numbers given):

• Annual foot examination in every person with diabetes, even without ulceration — at minimum a relevant history and palpation of foot pulses (Rec 1, strong/low). Examine any patient with diabetes and foot ulceration the same way (Rec 2).
• Clinical examination does not reliably exclude PAD in a person with diabetes and a foot ulcer. Evaluate pedal Doppler arterial waveforms together with ankle systolic pressure and ABI, or toe systolic pressure and TBI. No single modality is optimal and there is no threshold that reliably excludes PAD (Rec 3).
• Healing-probability bedside tests — any one of these raises the pretest probability of healing by at least 25%: skin perfusion pressure ≥40 mmHg, toe pressure ≥30 mmHg, or TcPO₂ ≥25 mmHg (Rec 4, strong/moderate).
• Urgent vascular imaging and revascularisation when ankle pressure <50 mmHg, ABI <0.5, toe pressure <30 mmHg, or TcPO₂ <25 mmHg (Rec 6).
• The 4–6 week rule. Consider vascular imaging (Rec 7) and revascularisation (Rec 8) in any DFU not healing within 4 to 6 weeks despite good standard of care — irrespective of bedside test results. This is the single most useful trigger in the guideline.
• WIfI (Wound, Ischaemia, foot Infection) stratifies amputation risk and revascularisation benefit (Rec 5, strong/moderate).
• Anatomical imaging when planning revascularisation: colour duplex ultrasound, CTA, MRA or intra-arterial DSA, evaluating the entire lower-limb circulation with detailed below-knee and pedal visualisation (Rec 10).
• Do not blame microangiopathy for poor healing — always look for another cause (Rec 9).

5. Management

• Revascularisation aims to restore direct flow to at least one foot artery, preferably the one supplying the ulcer's angiosome, with objective post-procedure perfusion measurement (Rec 11). Evidence does not establish endovascular over open or hybrid technique; decide on disease distribution, availability of autogenous vein, comorbidity and local expertise (Rec 12).
• Do not revascularise where the risk–benefit from the patient's perspective is unfavourable (Rec 16) — poor healing likelihood, inevitable major amputation, prohibitive anaesthetic risk, unreconstructable tissue loss, or short life expectancy.
• PAD plus foot infection is a limb emergency — urgent assessment and treatment, because amputation risk is particularly high (Rec 15).
• Multidisciplinary care after revascularisation, as part of a comprehensive plan (Rec 14).
• Intensive cardiovascular risk management for any patient with diabetes and an ischaemic foot ulcer: smoking cessation support, treatment of hypertension, glycaemic control, a statin, and low-dose clopidogrel or aspirin (Rec 17).

Australian access adaptation (Rec 13). The IWGDF wording required on-site expertise in diagnosing and treating PAD including revascularisation at every centre treating DFU. The Australian panel judged that unfeasible given the country's geography, and adapted it to permit an alternative model using established rapid referral pathways for regional and rural centres. The guideline also flags culturally safe, community-linked care through Aboriginal Health and Medical Services and Aboriginal Health Workers as a priority, citing high uptake of preventive footcare when co-designed with community. Worth knowing for WA practice and for any question about rural service delivery.

6. Pharmacology and AU PBS notes

Statin, plus low-dose clopidogrel or aspirin, is the antithrombotic and lipid backbone named by the guideline for the ischaemic diabetic foot (Rec 17). Not verified here: general PAD antiplatelet choice, the role of rivaroxaban in vascular-dose combinations, cilostazol availability and PBS status in Australia. Capture a general PAD or cardiovascular-prevention guideline before drilling any of that.

7. Complications and monitoring

Non-healing ulceration, wet or dry gangrene, minor and major amputation, and the systemic consequence that matters most — PAD is a marker of widespread atherosclerosis, so these patients die of myocardial infarction and stroke more often than they lose a limb. Monitor healing trajectory against the 4–6 week rule, re-measure perfusion after revascularisation, and keep cardiovascular risk factors under active treatment.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.