Peripheral neuropathy — diabetic feet, neuropathic pain and the painful acute pitfall

Diagnosis: diabetic distal symmetric (length-dependent) sensorimotor polyneuropathy complicated by a neuropathic foot ulcer. The classic picture — longstanding diabetes, glove-and-stocking sensory disturbance, absent ankle reflexes, loss of protective sensation on monofilament testing, and a painless plantar ulcer under a metatarsal head — is diabetic peripheral neuropathy (DPN), the commonest cause of polyneuropathy worldwide.^[1][2]

Assessment — pattern first, cause second. Confirm a distal symmetric, slowly progressive course. Examine for large-fibre loss (vibration at the hallux with a 128-Hz tuning fork, proprioception, positive Romberg), small-fibre loss (pinprick and temperature), motor signs (distal weakness/wasting) and autonomic signs (orthostatic BP drop, gastroparesis). Inspect both feet: calluses, ulcers (under metatarsal heads), deformity, pulses, and temperature (to exclude Charcot neuroarthropathy — a warm, swollen, erythematous foot).^[3]

Investigations — confirm the cause and the pattern, exclude mimics.

• Confirm diabetes and control: HbA1c (already elevated at 78 mmol/mol), fasting glucose.
• Exclude other treatable causes: vitamin B12 (± methylmalonic acid; remember metformin depletes B12), FBC and MCV (macrocytosis), U&E (uraemia), TSH, LFTs, lipid profile; serum protein electrophoresis with immunofixation and ANA/ANCA only if the pattern is atypical.^[3]
• Nerve conduction studies (NCS) with needle EMG: confirm an axonal, length-dependent pattern — reduced sensory and motor amplitudes with only mildly slowed conduction velocities. (Markedly slowed velocity, conduction block and temporal dispersion would instead point to a demyelinating process such as CIDP.)^[1]
• The ulcer: probe-to-bone, swab/deep tissue culture, plain radiograph or MRI for osteomyelitis; assess arterial supply (palpable pulses here, but consider ABI if in doubt).^[2]

Management — five strands.^[1][2]

1. Treat the underlying cause (the only disease-modifying step). Optimise glycaemic control (tighter control slows DPN, especially in type 1; address diet, oral agents, insulin), plus multifactorial risk reduction (BP, lipids, smoking cessation). Glycaemic control slows but does not reverse established DPN.
2. The neuropathic foot ulcer — a diabetic-foot emergency. Offload the foot (total contact cast or removable offloading boot), sharp debridement of callus and non-viable tissue, topical wound care, broad-spectrum antibiotics if there is surrounding cellulitis or deep infection, urgent podiatry and diabetic-foot/vascular referral, and daily inspection. Pulses are palpable here (predominantly neuropathic), but reassess perfusion and arrange vascular input if ischaemia coexists.
3. Neuropathic pain. Start ONE first-line agent and titrate: pregabalin (150 mg/day, titrate to 300 to 600 mg/day) or gabapentin (titrate to 1800 to 3600 mg/day), or duloxetine (30 to 60 mg once daily, particularly recommended for DPN by ADA and NICE), or amitriptyline (10 to 75 mg nocte). Combine classes on partial response. Topical lidocaine 5% patches or capsaicin for localised pain. Avoid opioids for chronic neuropathic pain — ineffective and addictive.^[2]
4. Foot-care education and prevention — the single most effective intervention to prevent amputation. Daily foot inspection, never walk barefoot, well-fitting footwear, regular podiatry, moisturise (not between toes), and seek urgent help for any blister or injury.
5. Multidisciplinary support: physiotherapy, dietetics, diabetes nurse, pain team, psychological support.