Diagnosis and Treatment

As noted above, the diagnosis of all the diabetic neuropathies is always one of exclusion of other nondiabetic causes. It is important to exclude non-

Table 5. Management of the stages of neuropathy Stage

Referral No clinical neuropathy Education to reduce

Objectives

Key elements

As required risk of progression;

Education; glycaemic

control; annual assessment

maintenance of near- normoglycaemia

Clinical neuropathy Management of symptoms; prevention of foot ulceration

Acute/chronic painful

Stable glycaemic control;

Diabetologist/neurologist

symptomatic treatment (simple analgesics or tricyclic drugs or carbamazepine). Consider referral of acute sensory neuropathy

Painless/loss of sensation

Education, especially foot

Diabetologist/neurologist

care; glycaemic control according to needs

Other types of diabetic

Diabetologist/neurologist neuropathy

Early referral

Late complications Prevention of new/ Emergency referral if lesions Diabetologist/neurologist/ recurrent lesions and

chiropodist/podiatrist/ amputation

present; otherwise referral

within 4 weeks

diabetes specialist nurse/ diabetes foot clinic if available

From Boulton et al. [1998], with permission of J. Wiley & Sons.

diabetic neurological disease which may be responsible for up to 5% of neuropathy in diabetic individuals. These include malignant disease, HIV, meta-

bolic conditions including vitamin B 12 deficiency, hypothyroidism, drug therapy, exposure to toxins and alcoholic polyneuropathy. Atypical features that might alert the clinician to the possibility of a nondiabetic neuropathy would include rapid progression, foot drop, back or neck pain, family history, weight loss and asymmetrical clinical features.

The management of the different stages of peripheral sensory neuropathy is summarized in table 5. Of all the treatments, tight and stable glycaemic

control is probably the only one that might provide symptomatic relief as

Table 6. Drugs for symptomatic (painful) neuropathy Class

Comments Tricyclic drugs

Drug

Dose/day

Imipramine

Troublesome Amitriptyline

25–150 mg

25–150 mg H dosage

AEs limit Desipramine

25–150 mg

Anticonvulsants Carbamazepine

CNS AEs Gabapentin

200–800 mg

900–3,600 mg

Centrally acting Tramadol

CNS AEs Other therapy

50–400 mg

Topical capsaicin

Up to 4¶daily

(0.075% cream)

topically

Acupunctue Opsite

AEs>Adverse events; CNS>central nervous system. These agents are used, if required, in addition to stable glycaemic control.

well as slowing the relentless progression that typifies the natural history of neuropathy. It is likely that unstable blood glucose control induces neuropathic pain, so stability rather than the actual level of glycaemic control is most important in pain relief.

A large number of drugs have been reported to be useful in the relief of neuropathic pain: these are summarized in table 6. Until we have a greater experience with some of the newer therapies, the tricyclic drugs remain the first-line medications for painful neuropathic symptoms: they have been proven to be effective in several randomized controlled trials. Thus the order of listing of drugs in table 6 is normally the order in which these drugs would be used. The newer agents such as Gabapentin and Tramadol (table 6) are promising and already have proven efficacy in randomized controlled trials.

The limitations of all the drugs listed in table 6 relate to adverse effects which tend to be dose related and predictable. Other therapies such as capsaicin,

acupuncture and Opsite may be useful in some cases. Capsaicin is a topical application and tends to be more helpful in localized pain. Acupuncture has been shown to be efficacious in several uncontrolled studies, with reported efficacy in up to 70% of treated cases. As this is without side effects, it is a useful therapy for diabetic neuropathy. Opsite is a transparent dressing which has reported efficacy in an uncontrolled study: it is reported to work through the gate control mechanism of pain.

None of the above listed agents has any affect on the natural history of diabetic sensory-motor neuropathy which, as noted above, is one of slow

progression. A number of agents are under investigation that might slow or halt progression in diabetic neuropathy and these include the antioxidant

a -lipoic acid, a number of aldose reductase inhibitors, and essential fatty acids such as c-linolenic acid. Finally, all patients with diabetic sensory peripheral neuropathy must be considered as being at risk of insensitive foot ulceration and should receive education on foot care and if necessary a podiatry referral. These patients require more frequent follow-up, always paying particular attention to foot inspection to reinforce the educational message of the need for regular foot care.

Diagnosis and Treatment