01Purpose and principlesWhat the assessment is for and the core concepts behind it.
A neuroischaemic foot combines peripheral neuropathy with peripheral arterial disease. Sensory loss permits repetitive pressure and unnoticed trauma; motor neuropathy changes foot shape and loading; autonomic dysfunction dries and fissures skin. Reduced perfusion limits oxygen delivery, immune response and repair. Infection may then progress with few symptoms. The practical task is therefore not to label the foot from one finding, but to define tissue loss, infection, mechanical load, neurological deficit and perfusion in parallel.
Assessment begins with urgency. NICE requires immediate acute referral for ulceration with limb ischaemia, fever or sepsis, gangrene, or concern for deep soft-tissue or bone infection. Other active diabetic foot problems still require referral within one working day. After stabilisation, bedside assessment guides the next question: whether PAD is present, whether perfusion is adequate for healing, and whether anatomical imaging and revascularisation should be considered. No pulse examination or pressure threshold safely answers all three.
Key points
- Treat ulceration with suspected limb ischaemia as limb-threatening: refer immediately to acute services and alert the multidisciplinary foot care service rather than waiting for clinic tests.
- A normal or high ABPI does not exclude PAD in diabetes because medial arterial calcification can make ankle vessels incompressible; combine Doppler waveforms, ABPI and toe-based measurements.
- Loss of protective sensation removes pain as a reliable warning signal, so inspect the whole foot, footwear, wound depth, infection signs and perfusion even when the person reports little discomfort.
- Other active diabetic foot problems require referral within one working day for triage within one further working day under NICE pathways.
- Document ulcer site, dimensions and depth and use a structured system such as SINBAD; avoid using Wagner as the sole severity system in UK practice.
- Perfusion tests estimate different things: ABPI supports PAD detection, toe pressure or TcPO2 informs healing probability, and arterial imaging maps anatomy for revascularisation.
- Neuropathy and ischaemia often coexist; a warm foot or palpable pulse can be misleading, while autonomic neuropathy and oedema can obscure classic vascular signs.
- Assess the contralateral foot and cardiovascular risk because PAD and a prior ulcer signal high risks of recurrent tissue loss, myocardial infarction and stroke.
02Indications, selection and cautionsWhen it is useful, when urgency changes and important limitations.
Ask about numbness, burning, altered balance and previous painless injury. Test protective sensation at validated plantar sites with a 10 g monofilament and add another sensory modality such as vibration. Callus, clawing, prominent metatarsal heads and dry fissured skin indicate abnormal load and autonomic change.
Ask about claudication, rest pain and prior revascularisation, while remembering neuropathy can mask pain. Inspect colour, temperature, dependent rubor, pallor on elevation, delayed healing, tissue loss and gangrene; palpate femoral, popliteal, posterior tibial and dorsalis pedis pulses and assess Doppler signals.
Remove footwear and dressings. Record site, length, width, depth, wound bed, exudate, surrounding callus and skin, undermining and exposed structures. Plantar pressure-point ulcers suggest neuropathic loading; distal or marginal necrosis may suggest ischaemia, but mixed patterns are common.
Diagnose infection clinically when at least two local inflammatory findings are present, counting purulent discharge as one, rather than from bacterial growth alone. Define erythema extent, tenderness, warmth, swelling, discharge, fluctuance and systemic features; ischaemia or neuropathy can blunt inflammation.
An acutely warm, swollen, red foot with little pain and intact skin may be Charcot neuro-osteoarthropathy. Compare skin temperature with the other foot, protect from weight bearing and arrange urgent specialist review; infection, fracture and venous disease remain important alternatives.
03Method and interpretationA systematic approach to the test and its findings.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Pedal Doppler waveforms with ABPI and TBIFirst step - Why
- Identify PAD using complementary bedside measures rather than relying on pulse palpation or one pressure ratio.
- Interpretation and limitations
- Triphasic or biphasic waveforms with ABPI 0.9–1.3 and TBI at least 0.70 make PAD less likely but do not exclude it. ABPI above 1.3 suggests incompressibility; monophasic signals, low ABPI or low TBI support PAD and need vascular interpretation.
- 02
Toe pressure or transcutaneous oxygen pressure - Why
- Estimate the probability of wound healing when ankle pressures are unreliable or tissue loss is present.
- Interpretation and limitations
- A toe pressure at least 30 mmHg or TcPO2 at least 25 mmHg increases healing probability, while values below these levels increase amputation concern. Use them as prognostic evidence within the whole clinical picture, not absolute guarantees.
- 03
Structured neurological examination - Why
- Confirm loss of protective sensation and identify deformity, pressure points and functional risk.
- Interpretation and limitations
- Inability to perceive a 10 g monofilament at validated sites indicates loss of protective sensation. Combine with vibration or pinprick, reflexes and motor inspection; monofilament testing does not measure perfusion and a preserved response does not exclude PAD.
- 04
Wound and infection assessment - Why
- Stage tissue loss, detect infection and decide whether microbiology or imaging is needed urgently.
- Interpretation and limitations
- Document dimensions and depth using SINBAD or another accepted system. If infection is suspected, obtain tissue or bone from the debrided base before or close to antibiotics; surface colonisation alone does not define infection.
- 05
Arterial anatomical imaging - Why
- Map lesions when revascularisation is being considered or severe ischaemia or non-healing makes anatomy clinically decisive.
- Interpretation and limitations
- Duplex ultrasound, CT angiography, MR angiography or catheter angiography should visualise the circulation to the foot. Choice depends on renal function, calcification, local expertise and whether immediate intervention is contemplated.
04Clinical next stepsHow the result changes management or prompts escalation.
01Immediate triageThreatened neuroischaemic footFirst stepUlcer with ischaemia, gangrene, deep infection concern, fever, sepsis or rapidly deteriorating tissue.+
- 1Refer immediately to acute services and notify the multidisciplinary foot care service; institute sepsis assessment and resuscitation when systemic illness is present.
- 2Remove constricting footwear, protect the limb, document neurovascular status and wound extent, and obtain urgent senior surgical, vascular and infection assessment without delaying transfer.
- 3Coordinate source control, antimicrobial therapy, perfusion imaging and revascularisation planning; severe infection and ischaemia require parallel time-critical management.
02Active footStable active diabetic foot problemNew ulcer, blister, unexplained swelling, redness or suspected Charcot change without immediate limb- or life-threatening features.+
- 1Refer within one working day to the multidisciplinary foot care or foot protection service for triage within one further working day.
- 2Protect the area from further load, provide clear written and oral safety-netting, and assess both feet, footwear, neuropathy, perfusion and infection.
- 3Agree an individual plan for offloading, wound care, infection control, ischaemia management and monitoring frequency based on progress and deterioration risk.
03Perfusion pathwaySuspected PAD without immediate threatWeak pulses, abnormal Doppler signals, tissue loss or vascular symptoms in a clinically stable person.+
- 1Combine pedal Doppler waveforms, ABPI and TBI, recognising that no single normal value excludes PAD in a diabetic foot.
- 2Add toe pressure or TcPO2 to estimate healing probability and use WIfI when suitable specialist expertise is available to frame amputation risk and likely revascularisation benefit.
- 3Seek vascular imaging and specialist review if ischaemia is severe, the wound worsens, or meaningful healing fails despite good care; continue cardiovascular risk management.
05Risks, monitoring and follow-upComplications, safety checks and further assessment.
- At every review measure wound dimensions and depth, describe the wound bed and margins, and compare with a dated baseline rather than relying on a visual impression.
- Repeat pulse, Doppler and perfusion assessment when the foot deteriorates, after revascularisation, or when healing stalls; a previous reassuring result does not cover a new clinical state.
- Review offloading adherence, footwear fit, new pressure lesions, falls risk, contralateral foot injury and the person's ability to inspect the feet each day.
- Monitor glucose management, smoking, blood pressure, lipids, kidney function and cardiovascular symptoms because a neuroischaemic ulcer identifies systemic vascular risk.
- Escalate immediately for new fever, spreading erythema, severe or disproportionate pain, gangrene, coolness, colour change or systemic illness; do not wait for a scheduled appointment.
06Special situationsVariants, exceptions and circumstances that change the usual approach.
Calcification changes interpretation
Medial arterial calcification stiffens ankle vessels and can produce a high ABPI despite PAD. Toe arteries are often less affected, but toe pressure can also be technically limited; waveform quality and the full clinical picture remain necessary.
Healing tests are probabilistic
Toe pressure and TcPO2 modify the chance of healing but cannot promise it. Infection burden, wound depth, load, oedema, nutrition, renal disease and the feasibility of restoring direct foot perfusion also influence outcome.
Pain can mislead twice
Neuropathy may hide ischaemic rest pain and deep infection, while severe pain out of proportion may signal necrotising infection or acute ischaemia. Both absence and unexpected excess of pain require interpretation.
Classify for the right purpose
SINBAD supports communication and audit; WIfI combines wound, ischaemia and infection to estimate amputation risk and revascularisation benefit. A score supports, but never replaces, urgent clinical judgement.
Look beyond the index ulcer
The contralateral foot may already contain callus, deformity or poorly fitting footwear. Prevention work on the other foot begins during the acute assessment, not after the wound has healed.
07Common pitfallsFrequent interpretation and management errors.
- 01
Calling a foot well perfused because one pulse is palpable or ABPI is normal ignores the limited exclusion value of single bedside findings in diabetes.
- 02
Waiting for pain before escalating is unsafe because sensory neuropathy can make severe ischaemia, pressure injury and infection surprisingly painless.
- 03
Applying a rigid non-removable device before defining infection and ischaemia can prevent frequent inspection and be harmful in a complicated ulcer.
- 04
Taking a superficial swab from an unprepared wound often reflects colonisers; when infection is suspected, prefer aseptically collected tissue or bone from the debrided base.
- 05
Treating the wound while omitting cardiovascular risk and renal assessment misses the systemic implications of PAD and changes the safety of imaging and medicines.