Diabetic Neuropathy

Distal symmetric sensorimotor polyneuropathy (95%). The most common type and the one that matters for orthopaedic complications. It is length-dependent, so it begins in the feet and progresses from distal to proximal before the hands are involved, and it mixes sensory and motor loss: vibration sense, protective sensation and pain and temperature discrimination fall away, the intrinsics waste into claw toes and the ankle reflex is lost early. It may be painless, which is the more dangerous form, or painful with burning and shooting pain.

Autonomic neuropathy (50%). Damage to the fibres controlling involuntary function shows itself in three systems that concern the foot surgeon:

• Sudomotor: anhidrosis, dry cracked skin and fissures that act as infection portals and add to ulcer risk
• Vasomotor: arteriovenous shunting, a warm foot despite neuropathy, and altered bone blood flow that may predispose to Charcot
• Cardiovascular: resting tachycardia, orthostatic hypotension and a perioperative risk factor, covered under Medical Management

Focal neuropathy (5-10%). A single nerve, often with acute onset. Femoral neuropathy is a true focal lesion and is not the same thing as diabetic amyotrophy, which is described below and is not a femoral neuropathy at all.

• Upper limb: carpal tunnel syndrome (median), the most common focal neuropathy; ulnar entrapment at the cubital tunnel; radial nerve palsy (rare)
• Lower limb: tarsal tunnel syndrome (tibial nerve behind the medial malleolus); peroneal nerve palsy with foot drop; femoral neuropathy
• Cranial: III, IV and VI (extraocular muscles, diplopia); VII (Bell's palsy)

Motor neuropathy. Usually part of the sensorimotor polyneuropathy rather than a separate entity. Its signs, the wasted first dorsal interosseous, the toes that cannot spread and weak toe extension, and its consequences, claw and hammer toes with prominent metatarsal heads and raised plantar pressures, are described under Pathophysiology.

Diabetic amyotrophy, properly diabetic lumbosacral radiculoplexus neuropathy (DLRPN, Bruns-Garland). Do not file this under focal neuropathy, and do not call it a femoral neuropathy. Nerve biopsy studies show a multifocal process involving the lumbosacral roots, plexus and peripheral nerves together, and the mechanism is not metabolic: it is an immune-mediated microscopic vasculitis of the epineurial vessels producing ischaemic nerve injury. That is why it behaves nothing like the length-dependent distal symmetric polyneuropathy.

The typical patient is older, with type 2 diabetes that is often well controlled and sometimes only recently diagnosed; it is not a complication of long duration or bad control. It starts with severe pain, unilateral and focal, in the thigh, buttock or leg, often worst at night and preceding the weakness. Profound proximal weakness of quadriceps, iliopsoas and hip adductors follows, spreads to other regions of the same limb and then to the opposite side, becoming bilateral and asymmetric. Marked weight loss, often 10 kg or more, is characteristic and is a diagnostic clue, and motor, sensory and autonomic fibres are all affected despite the "amyotrophy" name suggesting a pure motor problem. The course is monophasic, but the morbidity is prolonged and understated by the phrase "self-limiting": many patients become wheelchair-dependent during the illness, and recovery over one to three years is often incomplete.

Why this matters in an orthopaedic clinic: it is a spine referral in disguise. An older patient with severe thigh pain, quadriceps wasting and an absent knee jerk looks exactly like an L3/L4 radiculopathy, and an MRI of a degenerate lumbar spine will usually show something to blame. The discriminators are pain that is not positional and not eased by sitting, weight loss, weakness spreading beyond a single root territory and then to the other leg, and EMG showing a multifocal picture including paraspinal denervation with plexus involvement. Operating on the incidental disc will not help and will be blamed for the deterioration that follows. Management is analgesia for neuropathic pain, physiotherapy to prevent contracture and preserve function, and an explanation that the illness is monophasic. Immunotherapy (corticosteroid, IVIg) is used on the strength of the vasculitic mechanism, but its benefit remains unproven in controlled trials, which is exactly how it should be described in a viva.

Treatment-induced neuropathy of diabetes (TIND, historically "insulin neuritis"). An acute, severely painful small-fibre and autonomic neuropathy that appears within about eight weeks of a rapid improvement in glycaemic control, classically after starting insulin. It follows any fast fall in HbA1c, so the older name is misleading and the drug is not the culprit: the trigger is the rate of change, not the agent. Risk rises steeply with the magnitude of the HbA1c fall over three months, and a drop of more than 2-3 percentage points is the usual setting.

The patient has burning, allodynic pain out of proportion to the signs, often with new autonomic features (orthostatic hypotension, gastroparesis, erectile dysfunction), and has just been congratulated on their control. The trap is to read it as a failure of treatment or as worsening diabetic neuropathy and intensify further, which makes it worse; it is also mistaken for a psychiatric or functional presentation because the examination can be near normal early on. Manage the neuropathic pain, explain, and slow the rate of glycaemic correction rather than abandoning it. Most improve over months to a couple of years, though a retinopathy flare can accompany it. The counselling point: when taking someone from very poor control towards target, bring the glucose down gradually and warn them that transient worsening of pain or eye symptoms can happen and is not a reason to stop.

Clinical severity is staged by what the bedside tests show and whether complications have arrived. The stage sets the intensity of follow-up.

The Wagner grade describes depth and the presence of infection or gangrene, and each grade carries its own management.

Eichenholtz stages the process by the radiograph and the state of the inflammation. Stage 0, in which the foot is hot and swollen and the film is normal, is the one that is often misdiagnosed.

Sanders/Frykberg classifies by anatomical location, which carries the prognosis.

Only 20-30% of patients with diabetic neuropathy have pain, but when present it damages sleep and quality of life. Because the nerve damage is irreversible, treatment is symptom control. Three drug classes are first line.

Tricyclics. Amitriptyline has the most evidence. It inhibits serotonin and noradrenaline reuptake and blocks sodium channels. The anticholinergic effects (dry mouth, constipation, urinary retention in men with prostatic enlargement), drowsiness (use it at night, where it helps sleep), orthostatic hypotension in the elderly and weight gain limit it, and it is contraindicated after a recent myocardial infarction or with unstable angina, with conduction defects (prolonged QT, bundle branch block), in severe liver disease and in angle-closure glaucoma. Nortriptyline has fewer anticholinergic effects; imipramine is the other alternative.

Gabapentinoids. Pregabalin and gabapentin bind the alpha-2-delta subunit of voltage-gated calcium channels and reduce neurotransmitter release. They cause dizziness and somnolence (dose at night initially), peripheral oedema, weight gain (common, so warn the patient) and gait instability with a fall risk in the elderly. Their advantage is the absence of cardiac effects, so they are safe in heart disease; they are renally excreted and need dose adjustment in renal impairment.

Duloxetine. Inhibits serotonin and noradrenaline reuptake centrally. Nausea is the commonest side effect and is eased by taking it with food; dry mouth, constipation, dizziness and sexual dysfunction are the others. It is contraindicated in severe liver disease, uncontrolled hypertension and with a concurrent MAOI. In its favour: once-daily dosing, no weight gain and possible benefit for comorbid depression.

Second line. Tramadol, 50-100 mg up to QDS to a maximum of 400 mg daily, has an NNT of 4-5 but is reserved for patients who fail first-line treatment because of addiction potential, tolerance and falls in the elderly, and it risks serotonin syndrome combined with an SNRI or SSRI. Topical capsaicin 0.075% cream TDS-QDS depletes substance P from nerve endings, burns on first application (this improves with continued use), has minimal systemic absorption and can be used as an adjunct. Lidocaine 5% patches, up to 3 patches for 12 hours daily on localised painful areas, have minimal systemic absorption but are expensive and have limited evidence in diabetic neuropathy.

Combinations and what to avoid. If monotherapy is insufficient, combine mechanisms: amitriptyline with pregabalin, duloxetine with pregabalin, or a topical agent added to an oral one. NSAIDs and paracetamol are ineffective for neuropathic pain, and long-term opioids carry addiction risk with limited evidence and no superiority over other agents. TENS has limited evidence but is safe and patient-controlled, acupuncture has limited evidence and may be tried if the patient is interested, and cognitive behavioural therapy helps with coping strategies and sleep disturbance in chronic pain.

Tight glycaemic control is the only disease-modifying intervention: it prevents the development of neuropathy, slows the progression of established neuropathy and reduces the other microvascular complications, but it does not reverse damage already done. The trial evidence, and the difference between type 1 and type 2, is set out under Prevention and Screening.

Targets. The general target is HbA1c under 7%, individualised for age (less stringent in the elderly because of hypoglycaemia), duration of diabetes, comorbidity including cardiovascular disease, life expectancy and hypoglycaemia awareness. The elderly or frail are set under 8% to avoid hypoglycaemia; the young and motivated may aim under 6.5% if that is achievable without it.

Insulin strategies. A basal-bolus regimen pairs a long-acting basal insulin (glargine, detemir, degludec) with a rapid-acting bolus at meals (lispro, aspart, glulisine) and allows tight control with flexibility. Continuous subcutaneous insulin infusion is for type 1 patients with suboptimal control and improves glycaemic variability. Continuous glucose monitoring gives real-time levels with alerts for hypo- and hyperglycaemia and helps reach targets safely.

Oral agents. Metformin is first line for type 2 but can cause B12 deficiency, which can itself cause neuropathy, so check B12 annually. SGLT2 inhibitors bring cardiovascular and renal benefit and weight loss; GLP-1 agonists are injectable and bring weight loss and cardiovascular benefit.

Dry skin. Sudomotor failure is treated with a daily emollient, applied after bathing while the skin is still moist and never between the toes, where it macerates and invites fungal infection. Urea-based creams (10-25%) are for severe xerosis; sorbolene with glycerin, QV cream and Eucerin (both urea 10%) and CeraVe moisturising cream are the usual products. Avoid hot baths, which dry the skin, and inspect for early fissures and treat them aggressively.

Cardiovascular autonomic neuropathy. Damage to the autonomic fibres controlling the heart and vasculature is under-recognised but high-yield, because CAN is an independent predictor of mortality and the autonomic complication most relevant to the surgical patient. The vagal fibres go first, so resting tachycardia is the early sign, followed by exercise intolerance with a blunted heart-rate and blood-pressure response, a progressively fixed near-denervated heart rate as sympathetic involvement follows, and orthostatic hypotension later from sympathetic vasomotor failure. Loss of the cardiac afferents produces silent myocardial ischaemia and painless infarction, because the angina warning is gone, and QT prolongation carries a risk of malignant arrhythmia and sudden death.

Diagnosis and treatment. The cardiovascular autonomic reflex tests are the Ewing battery: heart-rate response to deep breathing, to standing (the 30:15 ratio) and to Valsalva, and blood-pressure response to standing and to sustained handgrip. Reduced beat-to-beat heart-rate variability is the earliest objective marker. Orthostatic hypotension is managed by education (rise slowly from lying or sitting), thigh-high compression stockings, increased salt intake and fludrocortisone if severe.

Why it matters to the orthopaedic surgeon. CAN brings greater intra-operative haemodynamic instability, with exaggerated hypotension on induction and impaired compensatory tachycardia; peri-operative myocardial events may be painless and missed; post-operative cardiovascular events are more frequent, so the threshold for cardiology assessment and intensive monitoring is lower; and neuraxial anaesthesia and positional changes need care.

Nerve decompression: the guideline position first, because it is the answer expected of you. The IWGDF states plainly: "we suggest not to use a nerve decompression procedure" for the prevention of foot ulceration, and neurological bodies have repeatedly judged the evidence insufficient to establish benefit. There is no randomised trial showing that decompressing peripheral nerves alters the course of diabetic polyneuropathy, and the published series are uncontrolled, in a condition with a fluctuating symptom burden and a large placebo response.

The theory, so you can argue against it. The double-crush hypothesis holds that a metabolically compromised nerve, already swollen from sorbitol accumulation, is unusually vulnerable to compression where it passes through a tight fibro-osseous tunnel: the tarsal tunnel (tibial), the fibular neck (common peroneal), the dorsum of the foot (deep peroneal) and the medial and lateral plantar nerves. Release the tunnel, the argument runs, and you restore perfusion and function. The reasoning fails as a justification because diabetic polyneuropathy is length-dependent, symmetrical and diffuse, precisely the pattern a focal entrapment cannot produce; improvement after surgery in an uncontrolled series is what you would expect from natural fluctuation and expectation alone.

What the series report. Case series of the Dellon triple decompression report sensory improvement in 60-80% of patients and pain improvement in 70-85%, with ulcer healing or prevention variable and amputation prevention claimed but unproven, all without randomised data. The limitations of that evidence are the absence of any high-quality randomised trial, selection bias in the case series, surgeon-dependent outcomes and an uncontrolled placebo effect, and the operation has not been widely adopted for lack of evidence.

Where decompression is legitimate. A genuine, separately diagnosed focal entrapment in a patient who also has diabetes: a carpal tunnel syndrome with confirmed median nerve conduction delay, or a true tarsal tunnel syndrome with localising signs that has failed conservative treatment. Diabetes makes entrapment more likely, not less treatable. The distinction is between operating on an entrapment and operating on the polyneuropathy itself, and only the first is defensible. If the viva asks "what is the role of nerve decompression in diabetic neuropathy?", the answer is that it is controversial and not first line: it may benefit selected patients with a demonstrable compressive neuropathy at an anatomical tunnel who have failed conservative treatment, and some studies show improvement in sensation and pain, but the evidence is limited.

Tarsal tunnel decompression. The steps:

1. Curvilinear incision posterior to the medial malleolus
2. Identify and protect the posterior tibial artery and veins
3. Release the flexor retinaculum completely
4. Decompress the tibial nerve and all its branches
5. Release the medial and lateral plantar nerve tunnels
6. Inspect for fibrous bands, lipomas or other compressive lesions
7. Careful haemostasis and closure

Full release of every compartment is what matters. Internal neurolysis is generally not required; an epineurotomy may be performed for a visibly swollen nerve; and the posterior tibial vessels are handled with care throughout.

Amputation. Surgery for diabetic neuropathy is surgery for its complications, not for the neuropathy, and amputation is the last of them. The indications are a non-healing ulcer with extensive gangrene, unreconstructable vascular disease, life-threatening sepsis such as necrotising fasciitis, extensive osteomyelitis not amenable to resection, and a non-functional limb with severe deformity. Below-knee is the most common major amputation; above-knee is chosen if below-knee healing is unlikely. The levels and their trade-offs:

Charcot reconstruction: when. Surgery is for the chronic Charcot foot in which bony prominences cause recurrent ulceration despite optimal footwear, the midfoot is unstable and cannot be braced, conservative treatment with casting and bracing has failed, or the deformity is too severe for footwear to fit; a motivated patient with good medical control may also choose it. Do not operate on acute Charcot unless there is an abscess or sepsis. Wait for the quiescent phase, Eichenholtz stage 3: a temperature differential under 2 °C between the feet, no oedema or erythema, and a stable radiographic appearance.

Charcot reconstruction: what. Exostectomy simply excises the bony prominence that is ulcerating; it suits a small isolated prominence, preserves the architecture of the foot, carries a lower complication risk and may allow better footwear fitting, but it corrects no deformity and does not address instability. Realignment and arthrodesis correct the deformity with an osteotomy that restores arch height, fuse the unstable midfoot or hindfoot joints and lengthen the Achilles if there is equinus, with the goal of a plantigrade, braceable foot. Fixation is by extensive internal fixation (multiple screws, plates, intramedullary beams) or by a circular external frame (Ilizarov), and soft-tissue coverage is planned at the same time. If the foot is unsalvageable, the infection will not respond, the reconstruction has failed or the limb is non-functional, the answer is a below-knee amputation.

Superconstructs. Extended fixation constructs follow four principles: use beams rather than screws (intramedullary bolts, plates), extend the fixation beyond the zone of injury, prepare the joints for fusion down to healthy bleeding bone, and consider external fixation as an alternative or adjunct. The options are intramedullary beams from hindfoot to forefoot, locking plates spanning multiple joints, a ring fixator or Taylor Spatial Frame, or internal and external fixation combined.

A high-risk operation. Before surgery, assess the vessels (ABPI, TBI, angiography: will the bone heal?), bring the HbA1c ideally under 8%, clear any active infection, check renal function because it affects antibiotic dosing, and obtain cardiac clearance for a high perioperative risk. During surgery, give prophylactic antibiotics and continue them post-operatively because the infection risk is high, handle the soft tissues carefully because their healing potential is poor, secure meticulous haemostasis and fix rigidly because the bone is poor. Afterwards, protected immobilisation for 8-12 weeks minimum with non-weight-bearing for 6-8 weeks and serial radiographs to monitor union. The patient must understand the complication rates before consenting:

• Wound infection 20-30%
• Delayed healing 30-40%
• Nonunion 20-30%
• Recurrent deformity 10-15%
• Amputation 5-10%

Only specialist foot and ankle surgeons should attempt Charcot reconstruction.

Ulcer debridement. Sharp surgical debridement removes all non-viable tissue back to bleeding margins and takes the callus around the ulcer with it. Probe for sinus tracts and undermining, assess the depth for exposed tendon, capsule or bone, take deep tissue cultures rather than a superficial swab, and biopsy bone if osteomyelitis is suspected.

Partial calcanectomy. For heel osteomyelitis with a non-healing ulcer: a curvilinear incision lateral to the Achilles, resection of infected bone back to healthy bleeding margins, preservation of the Achilles insertion if possible, and either primary closure or an open wound under a negative-pressure dressing.

The ulcer. Measure length, width and depth and photograph it for serial comparison. The location tells you the cause: the plantar metatarsal heads are neuropathic, the toes and heel ischaemic, and between the toes fungal or moisture-related. Depth is superficial (skin only) or deep with tendon or bone exposed, and the sterile probe settles the question of bone (see the probe-to-bone pearl under Investigations). Granulation tissue means healing, slough needs debridement and necrotic tissue means poor perfusion; serous discharge is normal, purulent means infection, and a malodorous discharge suggests anaerobes or necrotising infection.

The tissue around it. Callus indicates high pressure and needs debriding. Mark the extent of any cellulitis with a pen and track it daily. Probe any undermining or sinus tract, which may communicate with bone. A hot foot suggests infection or Charcot; a cool one suggests ischaemia.

Nerves and vessels. The 10 g monofilament will be abnormal in a neuropathic ulcer, and the ulcer is typically painless, whereas ischaemic ulcers hurt. The vascular assessment is critical: palpate the dorsalis pedis and posterior tibial pulses, remember the ABPI is unreliable above 1.3 because of medial calcification, and use the toe-brachial index, where above 0.7 is adequate perfusion for healing, below 0.5 means revascularisation may be needed and below 0.3 is critical ischaemia needing urgent vascular referral.

Infection. Grade it by extent and systemic effect, because the grade chooses the antibiotic route:

Record the Wagner grade (see Classification Systems) to complete the assessment.

Offloading, the pillar that matters most. You cannot heal what you do not offload. The total contact cast is the gold standard for the plantar neuropathic ulcer with adequate arterial perfusion: a custom-moulded plaster or fibreglass cast from the toes to below the knee that distributes pressure over the whole foot and leg and reduces plantar pressure by 30-50%, with protected weight-bearing allowed because the load is spread. It is changed weekly at first while the swelling settles, then every 2-3 weeks, and continued until complete epithelialisation, typically 6-12 weeks, healing 80-90% of ulcers by 12 weeks. It is contraindicated in active infection (severe cellulitis, abscess), critical ischaemia and fluctuating oedema.

The alternatives, and why they do worse. A removable cast walker has the same design but the patient can take it off, and they do: healing runs at 60-70% against 85% for the total contact cast. The remedy is the instant total contact cast, a walker wrapped in fibreglass so it cannot be removed; in the randomised trial by Armstrong and colleagues it healed 82.6% of grade 1A ulcers at 12 weeks against 51.9% for the removable walker (see Evidence Base). Felted foam cut to redistribute pressure away from the ulcer and changed every 3-7 days is less effective than a cast but useful where casting is unavailable. A wheelchair gives complete non-weight-bearing for extensive ulceration, if the patient will accept it.

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Debridement. Sharp debridement with a scalpel every 1-2 weeks removes callus, hyperkeratotic and non-viable tissue down to bleeding viable tissue; it reduces the bacterial load, stimulates the healing response and allows accurate assessment of depth. Surgical debridement is for deep infection, abscess and osteomyelitis, excising all non-viable tissue and sometimes taking a toe or ray. Enzymatic debridement with collagenase ointment is slow and less effective, reserved for patients who cannot tolerate sharp debridement.

Infection control. Most ulcers are not infected and get no antibiotics, to avoid resistance, and no topical antiseptics, which delay healing; the effort goes into offloading and moist healing. A mild or moderate infection is treated orally for 1-2 weeks with cephalexin 500 mg QDS or co-amoxiclav 875/125 mg BD to cover Staphylococcus aureus and Streptococcus, with a deep tissue sample for culture, never a superficial swab, which is always contaminated. A severe infection or osteomyelitis is admitted for intravenous antibiotics: empirically flucloxacillin 2 g QDS with metronidazole 500 mg TDS for anaerobic cover, or piperacillin-tazobactam 4.5 g TDS as the broad-spectrum alternative, adjusted to culture, for 2-4 weeks in severe soft-tissue infection and 6-12 weeks in osteomyelitis, switching to oral on response. Surgery is needed for an abscess (drainage), for necrotising fasciitis (an emergency demanding immediate extensive debridement) and for osteomyelitis with a sequestrum (remove the dead bone).

Moisture balance. Moist wound healing promotes epithelialisation and granulation and prevents desiccation and eschar. Choose the dressing by the exudate and change it 2-3 times a week, or more if the wound is heavily exudative:

• Hydrocolloid (Duoderm): low to moderate exudate, autolytic debridement
• Foam: moderate to high exudate
• Alginate: heavy exudate, haemostasis
• Hydrogel: dry wounds that need moisture added
• Silver: infected wounds, for the antimicrobial effect

Avoid dry gauze, which desiccates the wound, hydrogen peroxide, which is toxic to granulation tissue, and long-term povidone-iodine, which delays healing.

What normal looks like. Granulation begins in weeks 1-2, the wound should be 30-50% smaller by week 4, most neuropathic ulcers with a good blood supply are healed by weeks 8-12, and a mixed neuro-ischaemic ulcer may take 12-20 weeks.

The 4-week decision. If the wound has shrunk by 30-50%, continue, reassess weekly and maintain the cast. If it has shrunk by less than 30%, something is wrong and each pillar is re-examined in turn: is the patient adherent to offloading, and is an irremovable cast needed; what is the toe-brachial index, and is angiography needed; probe to bone again and consider MRI for osteomyelitis; check the HbA1c and optimise it; and check the serum albumin, because below 30 g/L healing is impaired.

Non-healing at 12 weeks. Investigate with MRI of the foot for osteomyelitis, deep abscess or sinus tract, formal angiography if the toe-brachial index is borderline, and a biopsy if the ulcer is atypical, to exclude malignancy, vasculitis and pyoderma gangrenosum. Then intervene: more aggressive surgical debridement if there is osteomyelitis, revascularisation if the TBI is below 0.5 or TcPO2 below 30 mmHg, a skin graft or flap for a large ulcer once granulation is complete, and amputation if the foot cannot be salvaged.

Red flags for admission. Severe infection with systemic signs (fever, rigors, hypotension); necrotising fasciitis (rapid progression, gas on the radiograph, crepitus); critical ischaemia (rest pain, ABPI below 0.4); osteomyelitis needing intravenous antibiotics; and social factors, such as homelessness or inability to offload.

Remission, not cure. 50-70% of healed diabetic ulcers recur within 5 years if the preventive measures lapse, so healing changes the phase of care rather than ending it. Footwear is lifelong: custom-moulded shoes with total contact insoles that redistribute pressure away from the old ulcer site and accommodate any residual deformity, with a wide deep toe box. Podiatry is monthly for the first year after healing and 3-monthly thereafter if the foot stays healed, for callus debridement, nail care and early detection of pre-ulcerative lesions. The patient monitors skin temperature at home with an infrared thermometer, inspects daily and reports any redness, warmth or breakdown at once; the rules of never barefoot, daily inspection, proper footwear and prompt reporting are reinforced at every visit; and the HbA1c is kept under 7-8% to slow the neuropathy.

Recognition. A hot, swollen, painless foot in a diabetic with neuropathy is Charcot until proven otherwise. There may be a minor trauma history, often forgotten or trivial. The foot is erythematous and oedematous and is often misdiagnosed as cellulitis or DVT; the hallmark is the absence of pain despite the swelling. Infrared thermometry shows the affected foot 3-5 °C warmer than the other, and a difference greater than 2 °C is diagnostic; the monofilament is abnormal because neuropathy is the prerequisite; and there may be palpable bony crepitus if the process is advanced.

Imaging. The initial radiograph may be normal in stage 0, before fragmentation. MRI is the early gold standard, showing bone marrow oedema and joint effusion before the film changes. Serial radiographs are taken monthly to follow progression or coalescence.

The differential. Cellulitis would bring pain and systemic signs such as fever; DVT would involve the calf and raise the D-dimer; gout would be severely painful, monoarticular and perhaps tophaceous; osteomyelitis needs a wound or ulcer as its source.

Treatment, the same day. Apply a total contact cast immediately, initially non-weight-bearing with crutches or a wheelchair, or protected weight-bearing in the cast, which distributes the forces; this prevents progressive fragmentation and collapse. Change the cast weekly at first because the swelling falls rapidly, then every 2-3 weeks once stable. Immobilise for a minimum of 3-6 months, and continue until the temperature has normalised to a difference of less than 2 °C for 2-4 consecutive weeks; some patients need 6-12 months, and removing the cast early causes recurrence. Monitor with weekly infrared thermometry of both feet, which guides the duration, monthly radiographs to watch fragmentation in stage 1 and coalescence in stage 2, and clinical assessment of swelling and erythema.

Medical adjuncts. Optimise glycaemic control to an HbA1c under 7-8% and supplement calcium and vitamin D. Bisphosphonates (pamidronate 90 mg IV monthly for 3-6 months) act by reducing osteoclastic bone resorption and may shorten the acute phase, but they are controversial and the evidence is limited.

What happens if it is not immobilised. Progressive fragmentation (stage 1), joint subluxation and dislocation, midfoot collapse into a rocker-bottom deformity, bony prominences, recurrent ulceration over them, osteomyelitis and infection, and amputation.

The consolidated foot. In Eichenholtz stage 3 the deformity is fixed, a rocker-bottom foot with medial column collapse; the temperature difference is under 2 °C, the radiograph shows consolidation, remodelling and sclerosis, and the foot is clinically stable, no longer hot or swollen. What remains is a lifelong risk of ulceration over the bony prominences.

Conservative management comes first. The foot lives in a CROW boot, a rigid total-contact ankle-foot orthosis custom-moulded to the deformity that distributes pressure over the whole lower leg, or in custom-moulded shoes with a total contact insole, extra depth for the deformity, a rocker-bottom sole to unload the forefoot and a high top for ankle stability. Podiatry reviews the foot 3-monthly, debriding callus over the prominences and catching ulcers early, and the patient checks skin temperature at home weekly, because a rise suggests recurrence. Activity is modified: no prolonged standing or walking, a wheelchair for long distances, no high-impact activity.

When surgery is considered. Recurrent ulceration despite optimal footwear, an unstable deformity that cannot be braced, a deformity too severe for footwear, or the preference of a motivated patient with good medical control. The operations, the timing and the risks are set out under Surgical Technique.

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The diabetic wound. Infection risk is higher and healing slower, so the sterile technique is meticulous, wounds are protected for longer and inspected regularly because the patient may not feel a problem developing, dressings are kept clean and dry and never tight enough to impair perfusion. The first inspection and a dry dressing are on day 2, wounds are checked daily for infection, and sutures or staples stay for 3-4 weeks rather than the 2 weeks of a non-diabetic; bone healing needs longer immobilisation too.

Perioperative glucose. The target is 6-10 mmol/L, not tight control, for major surgery, using a sliding scale or insulin infusion if required and avoiding hypoglycaemia, which causes falls and arrhythmia; check an HbA1c if it is unknown, to guide long-term management. The stress response raises glucose after surgery, usual diabetes medications resume once the patient is eating, poorly controlled patients need endocrinology input, and healing is impaired if glucose stays persistently above 12 mmol/L.

Offloading after surgery. After an amputation the residual limb is non-weight-bearing at first, with a soft dressing and elevation to reduce oedema, watched for dehiscence and haematoma, with early physiotherapy for conditioning, transfers and mobility aids, and prosthetic assessment once the wound has healed and the stump has matured. After ulcer debridement the foot goes into a total contact cast or removable walker, non-weight-bearing or protected, until fully epithelialised, then into therapeutic footwear.

Rehabilitation after amputation. The level sets the prosthetic need and the realistic mobility.

Prosthetics. A provisional prosthesis is fitted at 4-6 weeks if the wound has healed; the stump keeps maturing for 6-12 months and the definitive prosthesis waits until its volume is stable. The stump is inspected regularly, because the patient has neuropathy, and the other limb is protected with extreme vigilance, given the contralateral amputation risk set out under Outcomes: the remaining foot gets custom footwear, regular podiatry, education and aggressive treatment of any ulcer.

Preventing surgical infection. Clean surgery gets a single dose of prophylaxis; an existing infection or osteomyelitis gets an extended course covering Staphylococcus aureus and Gram-negatives, with anaerobic cover added for gangrene or deep tissue. Technique reduces the rest of the risk: sterile technique, minimal tissue trauma, good haemostasis, closed suction drainage of dead space and no haematoma, which is a culture medium.

Recognising and managing it. Increasing wound pain (if sensation is present), erythema, swelling, warmth, purulent discharge and wound breakdown are the signs; fever and tachycardia are late. Open the wound to drain it, take deep tissue cultures, give intravenous antibiotics guided by culture, return to theatre for debridement if the infection is deep, and consider residual osteomyelitis.

Long-term foot care. Custom therapeutic footwear with depth and cushioning, podiatry every 3 months for the high-risk patient, daily self-inspection with a mirror for the soles, moisturising and treatment of fungal infection, and nail care by the podiatrist. The team around the patient is the endocrinologist for glycaemic control, the vascular surgeon for revascularisation, the podiatrist for footwear and callus, the orthotist for bracing and prosthetics, the wound-care nurse, the physiotherapist for gait and strengthening and the orthopaedic surgeon for the surgical complications.

What decides whether an ulcer heals. Vascular status is the most critical factor: an ischaemic ulcer will not heal without revascularisation. Glycaemic control, depth, infection, offloading adherence and nutrition follow.

Healing rates. A superficial uninfected ulcer heals in 80-90% of cases by 12 weeks; a deep ulcer without osteomyelitis in 60-70%; an ulcer with osteomyelitis in 40-60% with antibiotics and offloading; and an ischaemic ulcer without revascularisation in under 30%.

Amputation. Healing rate, mobility and 5-year survival by level:

After a major amputation. Five-year mortality is 50-70%, worse than colorectal, breast or prostate cancer, reflecting a severe systemic disease burden; the main causes of death are cardiovascular disease, renal failure and sepsis. Re-amputation to a higher level occurs in 10-15% within the first year, and the contralateral amputation risk is 50% at 5 years. Aggressive cardiovascular risk modification is essential, and counselling should include the realistic prognosis: amputation is not a foot problem.

Charcot. With total contact casting the acute inflammation resolves in 3-6 months typically, though some feet progress to chronic deformity despite casting, recurrent ulceration runs at 20-30% and function depends on the final deformity; afterwards many need a CROW walker or similar for life, some manage custom footwear on a stable braceable foot, and some achieve regular shoe wear. Exostectomy heals the ulcer in 75-85%, the prominence recurs in 15-20% and instability is untouched. Arthrodesis fuses in 70-80%, a higher nonunion rate than in non-diabetics; with a successful fusion the ulcer heals in 80-90%, complications (infection, hardware failure, nonunion) affect 30-50%, and limb salvage is 85-90% at 2 years.

Glycaemic control and progression. What intensive control does, and the two things it does not do.