Diabetic Foot Management

Diabetic foot disease is the leading cause of non-traumatic lower limb amputation worldwide. The pooled global prevalence of diabetic foot ulceration is about 6.3%, highest in North America at 13% and lowest in Oceania at 3%, and the lifetime risk of an ulcer in a person with diabetes is estimated at 19-34% (Zhang 2017; Armstrong, NEJM 2017). Five-year mortality after an ulcer rivals that of several common cancers.

Why the ulcer is the target. Neuropathy means trauma without pain awareness, and peripheral arterial disease means impaired healing; together they create the chronic non-healing ulcer. In Pecoraro's dissection of the pathways to amputation, ulceration was a component cause in 84% of cases. The ulcer is the visible, interruptible step on the road to amputation, which is why screening and footwear target it.

The burden is unequal. Indigenous and lower-resource populations carry a disproportionately high amputation burden. Prevention and early intervention are cost-effective everywhere.

Four sibling pages carry the detail behind this overview: diabetic neuropathy for the mechanism and the screening examination, diabetic foot ulcers for wound care and offloading, diabetic foot infections for antibiotic selection and osteomyelitis, and Charcot neuroarthropathy for Eichenholtz staging, Brodsky anatomical patterns and reconstruction.

Three processes combine to produce the chronic non-healing ulcer: neuropathy, ischaemia and infection.

Neuropathy removes the warning. Sensory neuropathy causes loss of protective sensation (LOPS), so injuries go unnoticed; the 10 g monofilament is the diagnostic test. Motor neuropathy wastes the intrinsic muscles, and the imbalanced forces produce claw toes, prominent metatarsal heads and high plantar pressure. Autonomic neuropathy dries the skin (anhidrosis), and the resulting cracks and fissures are entry points for infection. Repetitive microtrauma without pain also destroys bone and joint, which is Charcot neuroarthropathy.

Ischaemia stops the healing. Peripheral arterial disease in diabetes preferentially involves the tibial vessels (anterior tibial, posterior tibial, peroneal) and spares the profunda femoris. Medial calcification (Mönckeberg sclerosis) deposits calcium in the arterial media: it is non-obstructive, but it reduces vessel compliance and makes the ABI falsely elevated. At the microvascular level a thickened capillary basement membrane reduces oxygen diffusion, and diabetic wounds have a reduced VEGF response with poor collateral formation. Ischaemia prevents healing even when infection is controlled.

Infection. Diabetic foot infection is polymicrobial and often involves anaerobes, and biofilm formation prevents healing.

Biomechanics of the plantar ulcer. Normal plantar pressure is 200-300 kPa. With neuropathy and motor imbalance, pressure at the metatarsal heads rises to 700-1000 kPa, seven to ten times higher. Callus forms as a protective response but, being thick and non-compressible, raises local pressure further. Repetitive high pressure plus loss of sensation produces an ulcer at the pressure point, and this is why offloading is critical: a total contact cast reduces plantar pressure by 80-90%, to below the ulceration threshold.

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Two systems are expected: Wagner, which grades depth alone, and the University of Texas system, which adds infection and ischaemia to depth and predicts outcome better. PEDIS is the research system, and WIfI and SINBAD are the modern tools for limb-threat stratification and audit. Know both classic systems, and be able to say which one guides treatment.

Wagner ClassificationTexas ClassificationPEDIS System

The original and most widely used system: simple, reproducible, and built on ulcer depth and tissue involvement. It guides treatment urgency and predicts amputation risk.

Grade 0

Definition

Intact skin at risk

Clinical Features

Callus, deformity, Charcot foot, prior ulcer

Treatment Approach

Prevention: custom orthotics, patient education, regular foot checks

Grade 1

Definition

Superficial ulcer

Clinical Features

Partial or full thickness skin loss, no deeper structures visible

Treatment Approach

Offloading (total contact cast), sharp debridement, moist dressing

Grade 2

Definition

Deep ulcer to bone/tendon

Clinical Features

Ulcer extends to ligament, tendon, joint capsule, or bone

Treatment Approach

Surgical debridement, probe-to-bone test, consider antibiotics

Grade 3

Definition

Deep with abscess/osteomyelitis

Clinical Features

Deep-tissue abscess, osteomyelitis, or septic arthritis

Treatment Approach

Urgent surgical debridement, IV antibiotics, prolonged therapy

Grade 4

Definition

Localised gangrene

Clinical Features

Necrosis of forefoot (toes, metatarsals), demarcated

Treatment Approach

Partial foot amputation (toe, ray, transmetatarsal)

Grade 5

Definition

Extensive gangrene

Clinical Features

Necrosis involving entire foot, not salvageable

Treatment Approach

Major amputation (transtibial, transfemoral)

Grade	Definition	Clinical Features	Treatment Approach
Grade 0	Intact skin at risk	Callus, deformity, Charcot foot, prior ulcer	Prevention: custom orthotics, patient education, regular foot checks
Grade 1	Superficial ulcer	Partial or full thickness skin loss, no deeper structures visible	Offloading (total contact cast), sharp debridement, moist dressing
Grade 2	Deep ulcer to bone/tendon	Ulcer extends to ligament, tendon, joint capsule, or bone	Surgical debridement, probe-to-bone test, consider antibiotics
Grade 3	Deep with abscess/osteomyelitis	Deep-tissue abscess, osteomyelitis, or septic arthritis	Urgent surgical debridement, IV antibiotics, prolonged therapy
Grade 4	Localised gangrene	Necrosis of forefoot (toes, metatarsals), demarcated	Partial foot amputation (toe, ray, transmetatarsal)
Grade 5	Extensive gangrene	Necrosis involving entire foot, not salvageable	Major amputation (transtibial, transfemoral)

What Wagner cannot tell you. It does not account for ischaemia or infection severity. A grade 2 ulcer can be clean, or it can have severe necrotising fasciitis, and perfusion status, critical limb ischaemia against adequate flow, dramatically affects healing. That gap is what the Texas and PEDIS systems were developed to fill.

Adds infection and ischaemia to Wagner's depth grading. It is a 4x4 matrix of 16 cells: a numeric grade for depth crossed with a lettered stage for what else is wrong with the wound. Wounds are written grade-then-stage, so a superficial clean ulcer is 1A and an infected ischaemic bone-deep ulcer is 3D.

The grade is the depth:

• Grade 0: pre-ulcerative or post-ulcerative lesion, completely epithelialised
• Grade 1: superficial wound, not through tendon, capsule or bone
• Grade 2: wound penetrating to tendon or capsule
• Grade 3: wound penetrating to bone or joint

The stage is the comorbidity:

• Stage A: clean wound, no infection, no ischaemia
• Stage B: infected, not ischaemic
• Stage C: ischaemic, not infected
• Stage D: infected AND ischaemic

Get the axes the right way round

Depth is the number and comorbidity is the letter - grade 1-3, stage A-D. Reversing them ("grade C, stage 2") is the commonest error made with this system, and it is self-evidently wrong once you notice that infection is a stage, never a depth: a wound cannot be "as deep as infected". The trial literature uses the correct form throughout - the offloading RCT cited below enrolled University of Texas grade 1A ulcers, meaning superficial and clean.

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1A

Clinical Scenario

Clean superficial ulcer, palpable pulses

Wagner Equivalent

Wagner 1

What the stage adds

Stage A is the group in which no amputation occurred at all in the validation cohort

2B

Clinical Scenario

Ulcer to tendon or capsule, infected, perfused

Wagner Equivalent

Wagner 2-3

What the stage adds

Infection without ischaemia - drain and debride, but the foot has the blood supply to heal

3C

Clinical Scenario

Probes to bone, ischaemic, not infected

Wagner Equivalent

Wagner 2-3

What the stage adds

Depth and ischaemia together - probing to bone alone raised midfoot-or-higher amputation from 2.0% to 18.3%

3D

Clinical Scenario

Probes to bone, infected AND ischaemic

Wagner Equivalent

Wagner 3-4

What the stage adds

The worst cell: in the validation cohort of 360 patients, 76.5% underwent midfoot-or-higher amputation within 6 months versus 3.5% in lesser stages, an odds ratio of 89.6

Texas Classification Worked Examples (grade then stage)

UT	Clinical Scenario	Wagner Equivalent	What the stage adds
1A	Clean superficial ulcer, palpable pulses	Wagner 1	Stage A is the group in which no amputation occurred at all in the validation cohort
2B	Ulcer to tendon or capsule, infected, perfused	Wagner 2-3	Infection without ischaemia - drain and debride, but the foot has the blood supply to heal
3C	Probes to bone, ischaemic, not infected	Wagner 2-3	Depth and ischaemia together - probing to bone alone raised midfoot-or-higher amputation from 2.0% to 18.3%
3D	Probes to bone, infected AND ischaemic	Wagner 3-4	The worst cell: in the validation cohort of 360 patients, 76.5% underwent midfoot-or-higher amputation within 6 months versus 3.5% in lesser stages, an odds ratio of 89.6

Texas 3D = Limb-Threatening Emergency

An infected AND ischaemic diabetic foot (stage D, and worst of all at grade 3 where it probes to bone) is a surgical emergency. Neither problem can be treated alone: antibiotics will not reach the tissue without perfusion, and revascularising an undrained abscess spreads it. Admit, IV antibiotics, urgent drainage and debridement, and a vascular opinion within 24 hours.

The International Working Group on the Diabetic Foot (IWGDF) system, used primarily in research. It grades each of five domains separately:

• Perfusion: grade 1 no symptoms or signs of PAD; grade 2 PAD without critical ischaemia; grade 3 critical limb ischaemia. Assessed by ABI, TBI, toe pressure and TcPO2.
• Extent: length × width in cm². Small is less than 1 cm², medium 1-3 cm², large greater than 3 cm²; larger ulcers have a worse prognosis.
• Depth: grade 1 superficial (skin only); grade 2 deep (to tendon, bone or joint); grade 3 all layers with abscess or osteomyelitis.
• Infection: grade 1 none; grade 2 involving skin and subcutaneous tissue; grade 3 systemic inflammatory response; grade 4 severe sepsis, life-threatening.
• Sensation: the 10 g Semmes-Weinstein monofilament. Loss of protective sensation is binary, present or absent.

PEDIS is comprehensive but complex for daily use. Most clinicians use Wagner or Texas for treatment decisions and then document the PEDIS components for research databases; its value is in standardising research outcomes and international communication.

WIfI and SINBAD. Wagner and Texas remain the classic exam systems, but two newer systems are now the international tools for limb-threat stratification and audit.

WIfI (Wound, Ischaemia, foot Infection) is the Society for Vascular Surgery threatened-limb classification:

• Each of the three components is graded 0-3 (0 none, 3 severe): W = wound/ulcer size and depth (and gangrene), I = ischaemia (by ABI, ankle or toe pressure, or TcPO2), and fI = foot infection (by the IDSA criteria).
• The combination places the limb in one of four clinical stages (1-4) that estimate the 1-year amputation risk and the likely benefit of revascularisation - higher stages mean greater amputation risk and greater revascularisation benefit.

SINBAD (Site, Ischaemia, Neuropathy, Bacterial infection, Area, Depth) is an IWGDF-endorsed audit and communication score:

• Each of the six items scores 0 or 1 for a total of 0-6; a higher score predicts poorer healing and higher amputation risk.
• It is deliberately simple and needs no special equipment, which suits it to inter-centre audit and resource-limited settings.

Quote Wagner and Texas for the classic answer. WIfI is the one to cite when the question is how badly the limb is threatened and whether revascularisation will help; SINBAD is the one for audit and international comparison.

History. Diabetes control (HbA1c, duration, complications) and the ulcer's timeline: when it was first noticed, how it has progressed, and any prior ulcers. Ask about pain, numbness and tingling, because a neuropathic ulcer is painless and an ischaemic one is painful; about walking ability and the distance before claudication; and about fever, rigors or confusion, the red flags of systemic infection. Living situation, mobility and the capacity to comply decide what treatment is realistic.

Examination. Inspect the ulcer: location (pressure points), size, depth, base (granulation, slough or necrosis) and edge (undermined, callused). Assess perfusion by the dorsalis pedis and posterior tibial pulses, capillary refill, temperature, ABI and toe pressure; sensation by the 10 g monofilament, vibration with a tuning fork and proprioception; and infection by the extent of erythema (measure and mark it), warmth, purulence, lymphangitis and crepitus. Always examine the contralateral foot for risk assessment.

Probe-to-bone. A sterile probe is passed into the ulcer after debridement; bone feels hard and gritty. Grayson et al (JAMA 1995) found that palpable bone on probing had a sensitivity of 66%, specificity of 85% and positive predictive value of 89% for osteomyelitis in a high-prevalence inpatient cohort, a positive likelihood ratio of roughly 4-5; later outpatient studies report a positive likelihood ratio of about 6, the 6.4 quoted in the summary. Bone felt on probing raises the probability of osteomyelitis substantially, but a negative test does not exclude it, and MRI is the gold standard if clinical suspicion remains high. The test is operator-dependent and requires adequate debridement first.

At the bedside. The 10 g Semmes-Weinstein monofilament is tested at 9 sites, and inability to feel it at 4 or more is loss of protective sensation. Probe-to-bone is done after debridement, as described above. Capillary glucose shows current control and guides insulin therapy. These three simple tests guide the immediate treatment decisions.

Vascular studies, within 24 hours. Whether the wound can heal at all depends on perfusion, so this assessment is essential:

• Ankle-brachial index (ABI): 0.9-1.3 is normal; less than 0.9 suggests PAD; greater than 1.3 suggests calcified vessels, common in diabetes, so use toe pressure instead
• Toe-brachial index: more reliable in diabetes; less than 0.6 suggests critical ischaemia
• Toe pressure: less than 30 mmHg is critical ischaemia and revascularisation is needed
• TcPO2 (transcutaneous oxygen): less than 30 mmHg suggests poor healing potential
• Duplex ultrasound: if the non-invasive studies are abnormal, to map the arterial disease for revascularisation planning

Imaging, within 48 hours. Plain radiographs (AP, lateral, oblique) are the first-line screen: look for gas in the soft tissues (necrotising infection), bone destruction (osteomyelitis) and Charcot change (fragmentation, dislocation). MRI is the gold standard for osteomyelitis, with sensitivity 90% and specificity 80%: infected marrow is dark on T1, bright on T2 and STIR, and enhances with gadolinium. CT with contrast is the alternative when MRI is contraindicated, less sensitive for osteomyelitis but good for surgical planning, and a labelled white-cell scan, in which the cells accumulate in infection, is for the case where MRI and CT are inconclusive.

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Laboratory, within 24 hours. HbA1c reflects control over three months, and the target for healing is below 7%. A full blood count shows the leukocytosis of systemic infection and the anaemia that is common in chronic disease. CRP and ESR are raised in infection, CRP the more specific and ESR the more sensitive, and are trended to assess response. Renal function matters because diabetic nephropathy is common and changes antibiotic dosing. Blood cultures are taken if there are systemic signs (fever, rigors, tachycardia, hypotension), and the culture that guides treatment is a deep tissue specimen taken after debridement, because swabs are unreliable.

Diagnosing osteomyelitis. Three clinical findings make the pre-test probability high:

1. A positive probe-to-bone test
2. ESR greater than 70 mm/h (sensitivity 28%, specificity 92%)
3. Bone destruction on the plain radiograph, a late sign that is only 50% sensitive

MRI is the gold standard, but all three clinical features are wanted for a high pre-test probability. Bone biopsy with culture is definitive but rarely needed.

Revascularisation and the Angiosome Concept

The vascular thresholds determine whether a wound can heal; the next question, and the one that decides the operation, is how revascularisation is targeted.

The angiosome concept. The foot and ankle are supplied by six angiosomes, three-dimensional blocks of tissue each fed by a source artery, derived from the three crural arteries: broadly, the posterior tibial (heel via the calcaneal branch, plus the medial and lateral plantar territories), the anterior tibial (dorsum of the foot via the dorsalis pedis), and the peroneal (lateral hindfoot and anterior ankle). Direct, angiosome-targeted revascularisation restores flow in the specific source artery feeding the angiosome that contains the wound; indirect revascularisation restores any line of flow and relies on collaterals. Direct revascularisation is associated with better wound healing and limb salvage in several series, although collateral quality and total flow also matter, so the principle is to re-establish in-line pulsatile flow to the wound's angiosome wherever feasible.

Strategy and timing. Control infection first: drain pus and debride or excise necrotic and infected tissue for source control before definitive revascularisation, then revascularise so that the now-clean wound (or amputation) can heal. An endovascular-first approach is common for focal disease and frailer patients, with distal bypass (for example to a tibial or pedal vessel using vein) reserved for long occlusions or failed endovascular treatment; the choice is individualised to anatomy, conduit availability and patient fitness. Either way, do not commit to a definitive amputation level until perfusion has been optimised.

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Algorithm

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The Wagner grade sets the urgency. Grades 0 and 1 are managed in the clinic with prevention, offloading and wound care; deep ulcers often need surgery, without delay if infection is present; grades 4 and 5 are decisions about amputation level and goals of care. Infection and perfusion, the Texas stage, set the intensity of treatment at every grade.

Infection, not colonisation. Every ulcer carries bacteria, so a positive swab means nothing on its own. The IDSA defines infection as purulence, or two or more of warmth, erythema (extending beyond the ulcer), lymphangitis (red streaking proximally), oedema and pain; an ulcer with bacteria on a swab but none of these signs is colonised, not infected, and gets no antibiotics. The culture that matters is a tissue specimen taken after debridement, because swab cultures are unreliable. The IDSA guidelines are the international standard for diabetic foot infection.

Empiric regimens (IDSA 2012). Mild, non-limb-threatening infection is treated orally:

• First line: cefalexin 500 mg QID or amoxicillin-clavulanate 875/125 mg BD
• MRSA cover: add TMP-SMX 160/800 mg BD or doxycycline 100 mg BD
• Penicillin allergy: moxifloxacin 400 mg daily (Gram-positive and Gram-negative cover)
• Duration 1-2 weeks, reassessed on clinical response

Moderate and severe infection are treated intravenously, and severe infection requires admission:

• Empiric broad-spectrum: piperacillin-tazobactam 4.5 g TDS or ticarcillin-clavulanate 3.1 g TDS
• MRSA suspected: add vancomycin 15-20 mg/kg BD (trough 15-20)
• Pseudomonas risk: add ciprofloxacin 400 mg BD or once-daily gentamicin
• Anaerobic cover: metronidazole 500 mg TDS if foul smell, crepitus or necrosis
• Duration 2-4 weeks, longer if osteomyelitis

Several international antibiotic guidelines recommend flucloxacillin plus metronidazole for mild-to-moderate infection, covering S. aureus and anaerobes, with piperacillin-tazobactam the common first-line broad-spectrum choice for severe infection. Always de-escalate on culture results and tailor to renal function, and avoid prolonged broad-spectrum therapy unless resistant organisms are culture-proven.

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Osteomyelitis. The diagnosis is confirmed by MRI or bone biopsy with culture, and there are three ways to treat it.

Antibiotics alone suit a small area of osteomyelitis with no abscess and no necrotic bone, or a patient who prefers to avoid surgery: pathogen-directed therapy for 6 weeks minimum, often 12, monitored by serial CRP and ESR (expect a 50% reduction by 2 weeks) and clinical healing. Success is 60-80% in the compliant patient and depends on the organism and extent.

Surgical debridement is for necrotic bone, abscess, failed conservative therapy, or the unstable patient who needs source control: resect all infected and necrotic bone until bleeding healthy bone, send the specimen for culture and histology, and give 2-6 weeks of antibiotics afterwards. Success is 85-90% if all infected bone is removed, and it is the definitive treatment for most cases because it removes the infected focus.

Amputation is for extensive osteomyelitis, a non-salvageable foot, life-threatening sepsis or patient preference, at the most distal level with viable tissue (toe, ray, transmetatarsal, Syme or transtibial). It gives immediate source control and a short course of 7-14 days afterwards, at the cost of function, so discuss goals of care.

Recurrence. Diabetic foot osteomyelitis recurs in 20-30% even after treatment. Inadequate debridement, resistant organisms, persistent neuropathy and pressure, and poor glucose control are the risk factors, so every patient needs lifelong foot surveillance and pressure offloading even after cure.

The rule is the most distal level with viable tissue. A higher level heals more reliably and functions worse, so the healing rates below are read against what the patient will be able to do afterwards.

Partial Foot AmputationsMajor Amputations

Toe (single)

Indications

Isolated toe gangrene, osteomyelitis confined to phalanx

Healing Rate

90%

Functional Impact

Minimal - great toe removal affects push-off slightly

Ray (toe + metatarsal)

Indications

Osteomyelitis involving metatarsal, web space infection

Healing Rate

80-90%

Functional Impact

Good if single ray; multiple rays cause transfer lesions

Transmetatarsal (TMA)

Indications

Forefoot gangrene, multiple ray involvement, salvageable hindfoot

Healing Rate

50-70%

Functional Impact

Requires orthotics, equinus deformity risk

Lisfranc (tarsometatarsal)

Indications

Extensive forefoot necrosis, Charcot midfoot

Healing Rate

40-60%

Functional Impact

Poor function, high revision to BKA rate

Partial Foot Amputation Levels

Level	Indications	Healing Rate	Functional Impact
Toe (single)	Isolated toe gangrene, osteomyelitis confined to phalanx	90%	Minimal - great toe removal affects push-off slightly
Ray (toe + metatarsal)	Osteomyelitis involving metatarsal, web space infection	80-90%	Good if single ray; multiple rays cause transfer lesions
Transmetatarsal (TMA)	Forefoot gangrene, multiple ray involvement, salvageable hindfoot	50-70%	Requires orthotics, equinus deformity risk
Lisfranc (tarsometatarsal)	Extensive forefoot necrosis, Charcot midfoot	40-60%	Poor function, high revision to BKA rate

Resect adequately. All infected and necrotic tissue until bleeding healthy bone, no exposed bone at the amputation site, a viable soft-tissue flap for coverage, and no tension on closure. Incomplete resection leads to failure.

Confirm perfusion. Toe pressure greater than 30 mmHg predicts healing, as does TcPO2 greater than 30 mmHg at the amputation level, and bleeding bone ends (the paprika sign) confirm it at operation. Ischaemic tissue will not heal, so if perfusion is borderline, revascularise first.

Transmetatarsal amputation. A TMA preserves weight-bearing on the plantar hindfoot but requires adequate perfusion, a toe pressure greater than 40 mmHg. Afterwards the Achilles is relatively stronger than the dorsiflexors and pulls the foot into equinus, so the patient needs a custom ankle-foot orthosis or a rocker-bottom shoe to prevent plantar ulceration at the stump. Failure to offload means a new ulcer, and a new ulcer means revision to a transtibial amputation.

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Syme (ankle disarticulation)

Indications

Hindfoot gangrene, failed TMA, Charcot ankle

Healing Rate

70-80%

Ambulation Rate

Good - end-bearing, no prosthesis needed for transfers

Transtibial (BKA)

Indications

Failed Syme, extensive foot necrosis, osteomyelitis to hindfoot

Healing Rate

80-90%

Ambulation Rate

Excellent - 60-80% ambulate with prosthesis

Knee disarticulation

Indications

Ischaemic BKA level, bilateral amputee (easier transfers)

Healing Rate

85-95%

Ambulation Rate

Good for transfers, limited prosthetic options

Transfemoral (AKA)

Indications

Failed BKA, critical ischaemia extending proximal

Healing Rate

90-95%

Ambulation Rate

Poor - 30-50% ambulate, high energy cost

Major Amputation Levels

Level	Indications	Healing Rate	Ambulation Rate
Syme (ankle disarticulation)	Hindfoot gangrene, failed TMA, Charcot ankle	70-80%	Good - end-bearing, no prosthesis needed for transfers
Transtibial (BKA)	Failed Syme, extensive foot necrosis, osteomyelitis to hindfoot	80-90%	Excellent - 60-80% ambulate with prosthesis
Knee disarticulation	Ischaemic BKA level, bilateral amputee (easier transfers)	85-95%	Good for transfers, limited prosthetic options
Transfemoral (AKA)	Failed BKA, critical ischaemia extending proximal	90-95%	Poor - 30-50% ambulate, high energy cost

Transtibial technique. A longer stump functions better but needs adequate perfusion, and careful bone preparation and soft-tissue technique prevent painful neuromas and skin breakdown.

1. Level and flaps. Target length 12-15 cm from the tibial plateau, which preserves knee function and allows prosthetic fitting. Flaps are a long posterior (gastrocnemius myocutaneous) or equal anterior-posterior (Burgess). Check perfusion by skin bleeding and toe pressure at the tibial level greater than 30 mmHg.
2. Bone. Divide the tibia 1 cm proximal to skin level and bevel the anterior crest at 45 degrees; divide the fibula 2 cm proximal to the tibia to prevent end impingement; file the sharp edges and round the borders.
3. Soft tissue. Divide the nerves sharply and let them retract proximally; ligate the tibial and peroneal arteries and veins individually; close the muscle by myodesis (sutured to bone) or myoplasty (antagonists sutured together); leave a deep drain for 24-48 hours.

Guillotine amputation. Open, without flap closure, it is for life-threatening sepsis needing urgent source control in an unstable patient: cut through soft tissue and bone at the same level, leave the wound open and pack it with gauze, and return to theatre in 48-72 hours for the definitive amputation with flap closure once the patient is stable. Modern ICU care has made it rare, and most severe infections are managed with debridement and antibiotics.

Mortality. These are sick patients, and the mortality after major amputation set out under Outcomes is the reason to optimise them medically and involve palliative care early for the goals-of-care discussion.

Recurrence is the norm, not the exception. Roughly 40% of healed ulcers recur within 1 year and around 65% within 5 years (Armstrong 2017), because the neuropathy, ischaemia and biomechanical abnormality that caused the first one persist, and continued neuropathy, poor offloading and non-compliance drive the next. Custom orthotics reduce recurrence but compliance is challenging, so every healed patient leaves with a prevention plan: lifelong surveillance, custom orthotics and education.

The Charcot foot. A warm, swollen, red foot in a neuropathic diabetic is easily mistaken for infection or DVT; the discriminators are in the differential table above. Early on the radiograph is normal and MRI bone oedema is the only sign, so a hot swollen neuropathic foot with a normal film is Charcot until proven otherwise, not a reason for reassurance. Management is non-weight-bearing in a total contact cast, typically 3-6 months, until the temperature difference falls below 2°C. Walking on an acute Charcot foot causes irreversible deformity, and a rocker-bottom midfoot then ulcerates over the prominence. Chronic deformity needs accommodative footwear or an AFO, and reconstruction (realignment arthrodesis) when bracing fails. The staging that governs the timing, Eichenholtz 0 to III for the disease process and Brodsky 1 to 3 for the anatomical pattern, is set out on the Charcot neuroarthropathy page.

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After debridement or a minor amputation the care is intensive and prolonged, and it requires the patient's commitment.

Days 0-3. The open wound is packed with gauze soaked in saline or antiseptic, and the foot is offloaded in a total contact cast or kept non-weight-bearing. Culture-directed antibiotics continue for a duration set by the severity of infection. Glucose is held at 6-10 mmol/L because hyperglycaemia impairs healing, the diet is high-protein with vitamin C and zinc supplementation, and LMWH is given if the patient is not ambulating. The first phase is infection control and wound preparation.

Days 4-14, granulation. Return to theatre or debride at the bedside if necrotic tissue appears; consider VAC for a deep wound, which promotes granulation and reduces oedema; change dressings daily to every 2-3 days by exudate; and record measurements, photographs and any sign of infection. Mobilisation is non-weight-bearing or protected weight-bearing with a device. Granulation tissue should appear by week 1-2.

Weeks 2-6, epithelialisation. Measure weekly. Small wounds heal by secondary intention; large wounds may need a skin graft or flap. Weight-bearing progresses from non-weight-bearing to protected, with range-of-motion exercises and gait training. Most wounds heal or are ready for closure by 4-6 weeks.

Weeks 6-12, maturation. Once healed, the patient moves into prevention mode: custom insoles, extra-depth shoes with rocker soles, monthly podiatry for the first 3 months and then every 3 months, and daily foot checks with immediate reporting of new problems.

After a major amputation the rehabilitation is long, and outcomes vary widely.

Days 0-7. The drain usually comes out on day 2-3 and dressings are changed daily. Analgesia is multimodal (paracetamol, NSAIDs, opioids as required), with gabapentin or pregabalin if phantom pain develops. Position the limb to avoid hip and knee flexion contractures, with frequent extension, and mobilise early: chair on day 1, bed exercises, and work to maintain contralateral limb strength.

Weeks 1-6. Keep the stump clean and dry and watch for infection or breakdown; shape it with an elastic bandage or shrinker sock. Physiotherapy strengthens the hip extensors and abductors in particular, with range of motion and balance work, and mobility progresses from wheelchair to a walking frame on the contralateral limb. Screen for depression and offer peer support.

Weeks 6-12. As stump volume falls and the scar matures, an interim prosthesis (adjustable socket, pneumatic limb) is used for gait training: weight-bearing, balance, stairs and outdoor walking. The definitive prosthesis is fitted once the stump volume is stable, at 3-6 months, and the functional goals are walking indoors, transfers and activities of daily living.

Months 3-12. Regular prosthetic reviews and socket modifications, contralateral limb protection by surveillance and offloading, cardiac rehabilitation because amputation increases cardiac workload, vocational assessment where return to work is realistic, and ongoing diabetes, psychological and peer support.

Functional outcome. The ambulation rates are in the Major Amputations table: after a transtibial amputation 20-40% remain wheelchair-bound, after a transfemoral amputation 50-70% do, and bilateral amputees have very poor ambulation rates, below 20%. Age, cardiac status, contralateral limb function and cognitive status are the key predictors. Set realistic expectations early.

Predictors of amputation or death. Five findings mark the patient at highest risk:

1. Texas stage D, infected and ischaemic, the worst cell of the grid
2. Chronic kidney disease with eGFR less than 30, which doubles mortality risk
3. Cardiac disease (prior MI, CCF), the major cause of death after amputation
4. Age greater than 75, with higher perioperative mortality and lower rehabilitation potential
5. Albumin less than 30 g/L, a marker of malnutrition and frailty

A patient with three or more of these has a very poor prognosis, and the palliative care discussion is essential.

Survival after major amputation. In Aulivola's 2004 series 30-day mortality was 5.7% after transtibial and 16.5% after transfemoral amputation, 8.6% overall; survival was 69.7% at 1 year and 34.7% at 5 years, falling to 30.9% with diabetes and 14.4% with end-stage renal disease; mortality at 3 years was 40%. The deaths are cardiac disease (50%), stroke (15%), renal failure (10%) and sepsis (10%), a survival similar to many stage III cancers. Major amputation is a marker of advanced systemic disease.

Quality of life. Independent living is maintained by 40-60%, and fewer than 20% of those working before the amputation return to work. 30-50% meet criteria for major depression, and psychological support is essential.

Offloading is treatment, not an adjunct. For a plantar diabetic foot ulcer it is the single most important intervention, and without it the ulcer does not heal whatever else is done. The total contact cast is the gold standard because it cannot be removed, which guarantees compliance. A non-removable walker is next best. Removable devices (CAM walker, half-shoe) fail because patients take them off at home; non-removable devices work.

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Sharp debridement. Remove all callus, slough and necrotic tissue down to bleeding healthy tissue, weekly or more often, and send deep tissue for culture if the wound is infected. Debridement converts a chronic wound into an acute one.

Moist wound healing. Dry gauze desiccates the wound bed. Use hydrogel, hydrocolloid, foam or alginate, selected by exudate level and changed per the manufacturer's instructions; a moist environment promotes epithelialisation.

Negative pressure. VAC therapy for deep wounds after debridement promotes granulation tissue and reduces oedema and bacterial load, changed every 48-72 hours. It is an adjunct to debridement, not a replacement for it.

Advanced therapies. Most have limited evidence:

• Hyperbaric oxygen: controversial, limited evidence
• Growth factors (becaplermin): modest benefit
• Bioengineered skin: Apligraf, Dermagraft
• Stem cells: experimental

Multidisciplinary diabetic foot clinics reduce major amputation rates by 50% compared with usual care, on evidence from multiple RCTs and cohort studies. The work is coordination between podiatry, vascular surgery, endocrinology, infectious disease, orthopaedics and rehabilitation, with weekly team meetings to review complex cases.

Who does what. The podiatrist assesses and debrides the wound and manages offloading; the vascular surgeon assesses for revascularisation; the endocrinologist optimises glucose control; infectious disease provides antibiotic stewardship; and the orthopaedic surgeon does the amputations and the Charcot reconstruction. Around them, the diabetes educator trains self-management, the dietitian optimises nutrition, the physiotherapist restores mobility and gait, the occupational therapist adapts activities of daily living, and the prosthetist fits the limb after amputation.

The system. Weekly multidisciplinary outpatient rounds, an inpatient service for acute admissions and surgical cases, home nursing for wound care and monitoring, community liaison to secure follow-up compliance, and a database that tracks outcomes for quality improvement. Organised systems deliver coordinated care.

Screen every patient with diabetes annually with the monofilament, the pulses, and a check for deformity, callus and footwear, and stratify by the IWGDF categories:

• Low risk: normal sensation and palpable pulses
• Moderate risk: loss of protective sensation or PAD, not both
• High risk: both, or a prior ulcer or amputation

Educate the high-risk patient. Structured education reduces the incidence of a first ulcer, and it comes down to four habits:

• Daily foot inspection, with a mirror for the plantar surface
• Shoes always, never barefoot, and check inside them daily for foreign objects
• Report any new wound, redness, warmth or drainage at once
• Nails cut straight across, with thick nails and callus left to podiatry rather than self-treated

Preventive podiatry every 4-12 weeks. Callus is debrided every 4-6 weeks, with nail care; custom orthotics redistribute pressure away from the high-risk areas; accommodative footwear means extra-depth shoes, cushioned insoles and rocker soles; and prophylactic Achilles lengthening is considered for persistent forefoot overload. Podiatry reduces ulcer incidence in the high-risk foot.

Control the diabetes. The HbA1c target is below 7% for most patients, relaxed to below 8% in the elderly to avoid hypoglycaemia, alongside multifactorial risk reduction: blood pressure, lipids and smoking cessation. Good control prevents neuropathy progression.

After a healed ulcer. The patient wears the prescribed orthotics and accommodative shoes, inspects daily for redness, blisters and cuts, and reports any new wound, pain, swelling or drainage. Professionally: podiatry every 3 months for callus debridement, nail care and a shoe check; an annual diabetic review with monofilament test, vascular assessment and risk stratification; orthotics replaced every 12-18 months or when worn; endocrinology input for control; and the multidisciplinary clinic coordinating all of it. Prevention works, but it requires sustained effort from the patient and the health system.