Diabetic foot assessment, infection and ulceration

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Diabetic foot disease arises from the interaction of loss of protective sensation, pressure, deformity, peripheral arterial disease, tissue injury and infection. Annual examination is preventive only if its result changes care. NICE risk categories incorporate neuropathy, non-critical ischaemia, deformity, previous ulcer or amputation and renal replacement therapy. People need a clear explanation of their category, footwear and self-inspection advice, an interval for review, and immediate-access instructions for skin breaks or colour and temperature change. Someone with an active ulcer no longer belongs in a routine risk clinic: they need the active diabetic-foot pathway.

Assess every wound systematically. Record anatomical site, length, width and depth; edge, base, exudate, odour and surrounding skin; probe gently for deep structures where trained; and look for fluctuance, crepitus, lymphangitis, spreading erythema or systemic illness. Infection is clinical. Diabetes, renal failure and ischaemia may blunt fever, leucocytosis and pain, while all chronic wounds are colonised. After cleaning and debridement, obtain a tissue or bone specimen if microbiology will change care. Plain radiographs identify gas, foreign body, deformity or established bone destruction; MRI is preferred when osteomyelitis remains uncertain and the result will alter management.

Healing needs mechanical and vascular treatment, not a dressing competition. Offloading redistributes pressure and is central for neuropathic plantar ulceration; the device depends on site, infection, ischaemia, falls risk and ability to adhere. Debridement is performed by trained practitioners with perfusion and tissue viability in mind. Dressings manage exudate and protect the wound but should be chosen on clinical need and cost rather than an unsupported claim that one product heals all ulcers. PAD assessment and prompt revascularisation discussion are essential when perfusion is inadequate. Acute Charcot arthropathy presents with warmth, swelling and sometimes deformity in a neuropathic foot; immobilise and offload immediately while specialist imaging and care proceed.

Key points

Every diabetes foot review should inspect skin, nails, callus, deformity and footwear, test protective sensation and assess arterial supply in both feet.
Risk rises with neuropathy, PAD, deformity, callus, previous ulcer or amputation and renal replacement therapy; follow-up intensity follows the highest feature.
Active problems include ulceration, infection, ischaemia, gangrene and suspected acute Charcot arthropathy and require rapid foot-service referral rather than annual review.
Refer limb- or life-threatening problems immediately; refer other active diabetic foot problems to the multidisciplinary foot care service within one working day.
Clinical infection is diagnosed from local or systemic inflammatory features, not from a positive swab or the mere presence of an open ulcer.
Clean and debride before obtaining a deep tissue or bone sample when feasible; superficial swabs often describe colonisers and can misdirect antibiotics.
For mild diabetic foot infection in adults, NICE first-choice oral flucloxacillin is 500 mg to 1 g four times daily for 7 days; use the severity table, allergies, renal function and microbiology, and review intravenous therapy by 48 hours.
Ulcer treatment requires pressure offloading, perfusion review, debridement, appropriate dressing, infection control and glucose or nutrition optimisation as one coordinated plan.
A normal or raised ankle pressure can mislead in calcified diabetic arteries; combine Doppler waveforms, toe measures and vascular judgement when PAD is suspected.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Neuropathy and repetitive pressure

Loss of protective sensation allows ill-fitting footwear, deformity and repeated loading to damage skin without the pain that would normally limit activity.

Peripheral arterial disease

Reduced limb perfusion limits tissue resilience, oxygen delivery and healing, and may blunt inflammatory signs despite substantial infection or necrosis.

Tissue breach and infection

A blister, fissure, puncture or ulcer permits organisms to invade soft tissue and sometimes bone, particularly when diabetes and kidney disease impair host response.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Protective sensation is lost
Peripheral nerve injury reduces pressure, pain and temperature awareness, so local trauma continues and dry cracked skin may go unnoticed.
2
Pressure causes ulceration
Concentrated loading over deformity or a plantar prominence produces callus, tissue ischaemia and eventual breakdown unless pressure is redistributed.
3
Infection extends through tissue
Once the barrier fails, bacterial invasion can spread through fascial planes, joints or bone; ischaemia and impaired immunity limit containment and antibiotic delivery.
4
Healing stalls
Continuing pressure, inadequate perfusion, necrotic tissue, oedema and poor metabolic or nutritional reserve sustain inflammation and prevent durable closure.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Neuropathic ulcer

A plantar ulcer beneath a pressure point, surrounded by callus and with little pain, suggests neuropathic loading. Depth and infection still determine urgency.

Ischaemic tissue lossRed flag

Rest pain, pallor, coolness, absent pulses, delayed capillary refill, toe necrosis or a punched-out margin suggests PAD and requires urgent vascular assessment.

Spreading infectionRed flag

Expanding erythema, warmth, swelling, tenderness, purulent discharge, systemic illness, crepitus or disproportionate pain raises deep infection and surgical urgency.

Possible osteomyelitis

A deep, chronic or recurrent ulcer over bone, visible or probe-accessible bone and unexplained inflammatory change increase probability, but imaging and bone sampling may be needed.

Acute Charcot footRed flag

Unilateral warmth, oedema, erythema and shape change in a neuropathic foot can mimic cellulitis or gout. Normal early radiographs do not make weight-bearing safe.

Occult trauma

A nail puncture, foreign body, friction blister or thermal burn may be painless. Examine footwear and interdigital spaces and ask about walking barefoot or heat sources.

Systemic severity can hide

Older, immunosuppressed or renally impaired people may have serious infection without fever or marked inflammatory markers; physiology and tissue progression matter more than reassurance from one result.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

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
Full bilateral foot examinationFirst step
Why
Define wound severity, neuropathy, deformity, skin threat and arterial supply at the bedside.
Interpretation and limitations
Document wound dimensions and depth, monofilament sensation, pulses, callus, oedema, temperature and footwear. Compare both feet; a hot swollen intact foot may be Charcot rather than infection.
02
Doppler waveform, ankle and toe pressure assessment
Why
Estimate perfusion and identify PAD that limits healing or threatens the limb.
Interpretation and limitations
A high or apparently normal ankle–brachial pressure index may be falsely reassuring with medial arterial calcification. Toe pressure and waveform interpretation add information; no single bedside test excludes PAD.
03
Deep tissue or bone microbiology
Why
Identify pathogens in clinically infected tissue and guide narrowing of antimicrobial treatment.
Interpretation and limitations
Collect after cleansing and debridement, ideally before antibiotics when this will not delay urgent therapy. Superficial swabs detect colonisation; bone culture is the most specific sample for osteomyelitis.
04
FBC, CRP, renal profile, glucose and lactate
Why
Assess systemic infection, metabolic instability and medicine or imaging safety.
Interpretation and limitations
Normal markers do not exclude local osteomyelitis or severe ischaemia. AKI changes antibiotic selection and contrast planning, while hyperglycaemia may be a consequence as well as a healing risk.
05
Plain foot radiographs
Why
Look for foreign body, gas, fracture, deformity and established bone or joint destruction.
Interpretation and limitations
Early osteomyelitis and acute Charcot change can be radiographically occult. Gas or destructive change is important, but a normal film cannot end the urgent pathway.
06
MRI foot
Why
Define marrow, soft-tissue, joint and abscess involvement when diagnosis remains uncertain.
Interpretation and limitations
MRI is sensitive for osteomyelitis and deep collections, but Charcot marrow oedema can mimic infection. Interpret with ulcer site, examination, radiographs and MDT expertise.
07
Vascular imaging
Why
Map arterial disease when revascularisation could improve healing or prevent amputation.
Interpretation and limitations
Duplex, CT angiography, MR angiography or catheter angiography is chosen with renal function, anatomy and urgency in mind. Imaging should not delay emergency source control.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute Charcot arthropathy

A warm swollen neuropathic foot with little pain and initially subtle radiographs may represent Charcot change, requiring immediate immobilisation rather than routine cellulitis care.

Venous or pressure ulcer

Location, oedema, pressure history and vascular findings can indicate a non-diabetic ulcer mechanism, although neuropathy and diabetes may still modify healing.

Gout or inflammatory arthritis

Abrupt joint-centred pain, swelling and crystal or inflammatory evidence can mimic infection, but neither excludes a concurrent skin breach or septic process.

Deep vein thrombosis

Diffuse unilateral swelling without a focal wound may suggest venous thrombosis; vascular assessment helps separate it from cellulitis or Charcot inflammation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01PreventStratify and protectFirst stepA person with diabetes attends routine review without a current active foot problem.

1Inspect both feet and footwear, test protective sensation, assess pulses and identify deformity, callus, previous ulcer or amputation and renal replacement therapy.
2Assign the NICE risk category, explain it in practical language and refer to foot-protection services at the required interval rather than recording risk without action.
3Teach daily inspection, safe nail and skin care, correctly fitting footwear and avoidance of barefoot walking or direct heat, with an immediate contact route for new change.

02EscalateRoute an active problemEscalationThere is ulceration, clinical infection, ischaemia, gangrene or suspected acute Charcot arthropathy.

1Send sepsis, gangrene, critical ischaemia, deep infection or rapidly progressive tissue loss immediately to acute services with early surgical and vascular contact.
2For other active problems, arrange multidisciplinary foot care within one working day, protect the wound and pressure area, and avoid advising unsupported continued weight-bearing.
3If acute Charcot is possible, make the patient non-weight-bearing, provide safe immobilisation or transport and maintain offloading until specialist assessment excludes it.

03HealCoordinate ulcer treatmentThe multidisciplinary service confirms a diabetic foot ulcer with or without infection or PAD.

1Measure and photograph under consent, debride when appropriate, choose site-specific offloading and a dressing for exudate and tissue needs, and set an objective healing trajectory.
2First lineIf infection is clinical, grade severity, obtain a deep specimen where feasible and start antibiotics promptly. Use oral treatment first line when severity permits; for mild adult infection NICE first choice is flucloxacillin 500 mg to 1 g four times daily for 7 days, while moderate or severe infection follows the combination table and urgent specialist pathway.
3Assess perfusion early, involve vascular specialists when healing is compromised, and review glucose, nutrition, smoking, oedema, renal disease and social barriers at the same MDT.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

NICE first-choice oral antibiotic for mild diabetic foot infection in adults when penicillin is suitable.

Flucloxacillin for mild diabetic foot infection

Give immediate-release flucloxacillin 500 mg to 1 g orally four times daily for 7 days; clinical assessment may justify up to a further 7 days, with microbiology-guided narrowing when available.

Check immediate penicillin hypersensitivity, hepatic history, renal function, interactions and ability to absorb oral treatment. The 1 g four-times-daily dose is off label; reassess promptly if worsening or no improvement within 1–2 days.

NICE alternative oral treatment for mild infection when penicillin allergy or another reason makes flucloxacillin unsuitable.

Clarithromycin when flucloxacillin is unsuitable

Give clarithromycin 500 mg orally twice daily for 7 days for mild infection; clinical assessment may justify up to a further 7 days, guided by microbiology when available.

Check QT risk, macrolide interactions, hepatic and renal function and pregnancy. Verify the allergy phenotype and local resistance, and use microbiology to narrow or change treatment.

NICE alternative oral treatment for mild diabetic foot infection when flucloxacillin is unsuitable and doxycycline is appropriate.

Doxycycline when flucloxacillin is unsuitable

Give 200 mg orally on day 1, then 100 mg once daily, increased to 200 mg daily if needed, for 7 days; clinical assessment may justify up to a further 7 days.

Avoid in pregnancy and check swallowing, oesophageal risk, photosensitivity, antacid or iron timing and interacting medicines. Review microbiology and response rather than extending treatment automatically.

Provides broader empirical cover for selected moderate or severe diabetic foot infection while cultures, surgery and vascular assessment proceed.

Co-amoxiclav option for moderate or severe infection

Give co-amoxiclav 500/125 mg orally three times daily or 1.2 g intravenously three times daily as one NICE first-choice option; severe infection requires intravenous treatment for at least 48 hours until stabilised, then review oral switch.

Choose among the NICE combination options using severity, allergy, prior antibiotics, microbiology, renal and hepatic function and local resistance. Minimum treatment is usually 7 days; suspected osteomyelitis requires specialist duration and source control.

Adds Gram-negative cover to selected moderate or severe regimens pending microbiology and specialist review.

Gentamicin when added for moderate or severe infection

Give an initial 5 to 7 mg/kg intravenous dose once daily only when the selected NICE regimen includes gentamicin; determine subsequent doses from serum concentrations, renal function and the local aminoglycoside protocol.

This is a high-risk medicine requiring accurate weight, renal assessment, level-guided dosing and review for acute kidney injury, ototoxicity and interacting nephrotoxins. Stop or narrow promptly when results and clinical response allow.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Deep soft-tissue infection

Infection can form abscess, track along fascia or cause systemic sepsis, sometimes with muted fever and pain because of neuropathy and renal disease.

Osteomyelitis

A chronic or deep ulcer may seed adjacent bone, prolonging treatment and increasing the need for surgical debridement or resection.

Limb loss

Uncontrolled infection, critical ischaemia or non-healing tissue loss can culminate in amputation with major effects on mobility, independence and mortality.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

At every active-wound review, record dimensions, depth, tissue type, exudate, surrounding inflammation, pain, offloading use and whether progress matches the agreed trajectory.
Reassess infection within the interval dictated by severity; deterioration, spreading erythema, systemic illness or new necrosis needs immediate surgical and vascular escalation.
Review antimicrobial choice when culture and clinical response are available, narrowing or stopping appropriately and adjusting for renal function and interactions.
Repeat vascular assessment when healing stalls, tissue necrosis progresses or symptoms change; a previously reassuring ankle index should not override the wound course.
Monitor the contralateral foot and pressure created by offloading devices, because protective strategies can transfer injury to another site.
After healing, move the person into the appropriate high-risk foot-protection pathway with footwear, recurrence prevention and rapid-access arrangements.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Colonisation is universal

Micro-organisms on a chronic ulcer do not equal infection; inflammatory tissue signs and systemic context determine whether antibiotics are needed.

Pressure is treatment

A well-chosen dressing cannot overcome repetitive plantar loading, so offloading is a core biological treatment rather than an optional accessory.

Calcification distorts ankle tests

Medial arterial calcification can make ankle arteries poorly compressible and yield falsely high pressure ratios, especially with diabetes and CKD.

Charcot can be painless

Neuropathy removes protective pain while inflammation damages bone and joints; immediate offloading preserves architecture before radiographic collapse develops.

Healing speed informs diagnosis

Failure to reduce wound area despite adherence should reopen questions about perfusion, pressure, infection, malignancy, nutrition and the accuracy of the original diagnosis.

11Common pitfallsFrequent interpretation and management errors.

01
Leaving an active ulcer on the routine annual foot-review pathway instead of arranging rapid multidisciplinary care.
02
Treating every positive wound swab while ignoring clinical infection criteria and specimen quality.
03
Reassuring from a normal plain radiograph when acute Charcot or early osteomyelitis remains clinically plausible.
04
Relying on ankle–brachial pressure index alone to exclude PAD in a calcified diabetic circulation.
05
Selecting dressings repeatedly without effective offloading, debridement and perfusion review.
06
Continuing oral antibiotics for gangrene or deep abscess instead of obtaining source control and vascular or surgical assessment.