Diabetic neuropathy Flashcards
What is the definition of diabetic neuropathy?
Involvement of cranial, peripheral, and autonomic nerves may be found in patients with diabetes and termed diabetic neuropathy; this usually suggests a diffuse, predominantly sensory peripheral neuropathy. The effects on nerve function can be both acute or chronic as well as being transient or permanent.
What are the 4 most common presentations of diabetic neuropathy?
- Altered sensation (both pain and ↑ sensitivity to normal sensation).
- Neuropathic ulcers, usually on the feet.
- Erectile dysfunction (with autonomic neuropathy).
- Charcot arthropathy.
What is the pathophysiology of diabetic neuropathy?
Diabetic neuropathy is one of the microvascular complications of diabetes. Pathologically, distal axonal loss occurs with focal demyelination and attempts at nerve regeneration. The vasa nervorum often shows basement membrane thickening, endothelial cell changes, and some occlusion of its lumen. This results in slowing of nerve conduction velocities or a complete loss of nerve function. Both metabolic and vascular changes have been implicated in its aetiology.
Is peripheral sensorimotor neuropathy usually gradual or sudden?
Usually insidious onset with numbness or paraesthesiae, often found on screening rather than as a presenting problem.
Give 6 differentials other than diabetic neuropathy for peripheral neuropathy?
- Uraemia.
- Vitamin B12 deficiency.
- Infections (e.g. HIV and leprosy).
- Toxins (e.g. alcohol, lead, mercury).
- Drugs (chemotherapeutic agents).
- Malignancy.
Give 6 categories of drugs which can be used for painful peripheral neuropathy. Give an example for each. Which of these two drugs have actually been approved in this use?
Only two (duloxetine and pregabalin) have been formally approved by the EMA and FDA for the treatment of painful DN.
- Tricyclic antidepressants (TCAs):
- Amitriptyline 25–75mg/day.
- Imipramine 25–75mg/day.
- Serotonin noradrenaline reuptake inhibitors (SNRIs):
- Duloxetine 60–120mg/day.
- Anticonvulsants:
- Gabapentin 300–3,600mg/day.
- Pregabalin 300–600mg/day.
- Opiates:
- Tramadol 200–400mg/day.
- Oxycodone 20–80mg/day.
- Morphine sulphate SR 20–80mg/day.
- Capsaicin cream (0.075%)—applied sparingly 3–4 times per day.
- IV lidocaine (for refractory painful neuropathy)—5mg/kg, given IV over 1h with ECG monitoring.
What is the commonest presentation of autonomic neuropathy?
Erectile dysfunction
Name 5 features of autonomic neuropathy
- Erectile dysfunction.
- Postural hypotension—giving dizziness and syncope in up to 12%.
- Resting tachycardia or fixed heart rate/loss of sinus arrhythmia—in up to 20%.
- Gustatory sweating—sweating after tasting food.
- Delayed gastric emptying, nausea/vomiting, abdominal fullness.
- Constipation/diarrhoea.
- Urinary retention/overflow incontinence.
- Anhidrosis—absent sweating on the feet is especially problematic, as it increases the risk of ulceration.
- Abnormal pupillary reflexes.
Give 5 features of a diabetic foot.
- Warm.
- Dry skin.
- Palpable foot pulses.
- No discomfort with ulcer.
- Callus present.
Give 6 features of an ischaemic foot
- Cold/cool.
- Atrophic/often hairless.
- No palpable foot pulses
- More often tender/painful.
- Claudication/rest pain.
- Skin blanches on elevation and reddens on dependency.
Give 9 risk factors for development of diabetic foot ulcer development
- Peripheral neuropathy (seen in up to 80% of diabetic patients with foot ulcers) reduces awareness of pain and trauma caused by footwear and foreign bodies in shoes. Look for reduced sensation on 10g monofilament and reduced vibration perception thresholds (e.g. reduced sensation to a 128Hz tuning fork for <10s or >25V with a biosthesiometer).
- Autonomic neuropathy, leading to anhidrosis, can dry out the skin and cause it to crack, so allowing a portal of entry for infection. These feet are often warm and dry, with distended veins.
- Motor neuropathy can result in altered foot muscle tone, wasting of small muscles, raising of the medial longitudinal arch, and clawing of the toes. This puts more pressure through the metatarsal heads and heels, predisposing to callus and ulcer formation. Electrophysiology can help examine this but is not in widespread routine use.
- Peripheral vascular disease (seen in up to 10% of patients) and microvascular circulatory disease lead to local ischaemia, ↑ the potential for ulcer formation and delaying wound healing. Always examine peripheral pulses, and consider Doppler studies if abnormal. An ankle:brachial artery ratio of >1.1 suggests arterial disease (the ratio of the BP in the ankle and the arm measured while at rest).
- Duration of diabetes is an independent risk factor, as is ↑ age. Remember type 2 diabetes may be present and undiagnosed for some time.
- The presence of other microvascular complications, such as nephropathy and retinopathy, is also a risk factor for foot ulcer development.
- Previous ulceration is an important risk factor, and anyone with previous problems needs very careful monitoring/follow-up.
- Lack of diabetes monitoring and lack of previous examinations of the feet are also recognized risk factors.
- Mechanical, chemical, or thermal trauma/injury is often the predisposing factor, and any profession or pastime that increases the risk of these is a risk factor.
What is the general management of diabetic foot ulcers?
- Optimize diabetic control.
- Reduction of oedema is important to aid healing.
- Regular debridement of callus and dead tissue/skin is important for both neuropathic and ischaemic ulcers.
- Infection control. Infection may be localized, but any evidence of deeper infection or sinus formation raises the possibility of osteomyelitis. Systemic symptoms of an infection may be minimal as may pain/tenderness in the foot itself, so be suspicious of more severe infection than you can see. The organisms may be ordinary skin commensals given a port of entry, but send swabs for culture and think of Staphylococcus aureus or streptococci as likely organisms.
- If a sinus is present, probe it, and, if down to bone, assume there is osteomyelitis. Culture anything you get out. Plain radiographs may show bone erosion or destruction with osteomyelitis; radioisotope scans using technetium can show ↑ uptake in both infection and Charcot arthropathy. The use of MRI scanning can be useful to differentiate in this situation.
- If infection is present, use antibiotics according to local microbiology guidelines and culture results. Commonly: ‘triple therapy’ with flucloxacillin (500mg qds), ampicillin/amoxicillin (500mg tds), and metronidazole (200mg tds); or co-amoxiclav (amoxicillin/clavulanic acid, 250/125mg tds) or ciprofloxacin (500–750mg bd) and clindamycin (300–450mg bd). IV treatment initially if the infection is severe, and, for the deeper infections, several months of therapy may be needed. For osteomyelitis, again follow local guidelines, but agents, such as ciprofloxacin or sodium fusidate which have better bone penetration, can be used, again for several months. Linezolid is also a useful therapy as a second- or third-line agent, but care with hepatic and renal impairment, and the need to monitor for potential thrombocytopenia, anaemia, or pancytopenia may limit its use.
- In some patients, this approach fails to control osteomyelitis adequately, and resection/amputation is required, so regular surgical liaison is imperative.
- Reducing trauma and pressure relief in neuropathic ulcers. Padded socks can reduce shear stress and trauma. Suitable shoes and insoles can help to relieve pressure to allow healing to occur as long as unnecessary walking is minimized. If this is not enough, a pneumatic boot/Aircast boot or a total contact cast may be needed. These allow the patient to be mobile but take the weight away from the ulcerated area or foot and put through to the calf instead. The involvement of both podiatrists and orthotists is essential.
- Revascularization. Always consider coexistent vascular disease. Vascular bypass grafting/reconstruction or angioplasty can give excellent results, with a 70–95% limb salvage rate often quoted. The improved blood supply will also help healing of existing ulcers and may negate the need for amputation or allow the area requiring resection to be minimized. If vascular intervention is unsuccessful or not possible, then amputation is required, preferably as a below-knee procedure to give a better mobilization potential post-operatively.
What is the pathogenesis of Charcot foot?
It is suggested that blood flow increases due to sympathetic nerve loss. This causes osteoclast activity and bone turnover to increase, so making the bones of the foot more susceptible to damage. Even minor trauma can, therefore, result in destructive changes in this susceptible bone.
What are the most common sites for Charcot foot?
The most likely site is the tarsal–metatarsal region or the metatarsophalangeal joints.
What are the two classic deformities in Charcot foot?
Eventually, in the untreated patient, two classic deformities are seen:
- A ‘rocker bottom’ deformity due to displacement and subluxation of the tarsus downwards.
- Medial convexity due to displacement of the talonavicular joint or tarsometatarsal dislocation.
