Diabetic Peripheral Neuropathy.

  • The presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after exclusion of other causes.

 ETIOLOGY/ PATHOGENESIS

  • Described in patients with primary (types 1 and 2) and secondary diabetes of diverse causes, suggesting a common etiologic mechanism based on chronic hyperglycemia. The contribution of hyperglycemia has received strong support from the Diabetes Control and Complications Trial (DCCT). Pathologically, numerous changes have been demonstrated in both myelinated and unmyelinated fibers.
  • An estimated 10-65% of patients with diabetes have some form of peripheral neuropathy. Neuropathy is estimated to be present in 7.5% of patients at the time of diabetes diagnosis. One half of patients have distal symmetric polyneuropathy, and one fourth have compression or entrapment neuropathies (mainly carpal tnnel syndrome).
  • Patients with untreated or inadequately treated diabetes have higher morbidity and complication rates related to neuropathy than patients with tightly controlled diabetes. Repetitive trauma to affected areas may cause skin breakdown, progressive ulceration, and infection. Amputations and death may result.
  • Male patients with diabetes usually have a higher incidence of diabetic neuropathy than female patients.
  • Diabetic neuropathy can occur at any age but is more common with increasing severity and duration of diabetes.
  • Symptomatic presentation is most common in patients older than 50 years.

 PERTINENT HISTORICAL FINDINGS/ CLINICAL SYMPTOMS

  • Sensory symptoms: feelings of numbness or deadness, which patients may describe as being akin to wearing gloves or socks. Loss of balance, especially with the eyes closed, and painless injuries due to loss of sensation are common, burning, prickling pain, tingling, electric shock–like feelings, aching, tightness, or hypersensitivity to touch.
  • Motor problems may include distal, proximal, or more focal weakness.
  • In the upper extremities, distal motor symptoms include impaired fine hand coordination and difficulty with tasks such as opening jars or turning keys. Foot slapping and toe scuffing or frequent tripping may be early symptoms of foot weakness.
  • Symptoms of proximal limb weakness include difficulty climbing up and down stairs, difficulty getting up from a seated or supine position, falls due to the knees giving way, and difficulty raising the arms above the shoulders.
  • Autonomic symptoms: dry skin due to lack of sweating or excessive sweating in defined areas, pupillary (poor dark adaptation, sensitivity to bright lights), cardiovascular (postural lightheadedness, fainting), urinary (urgency, incontinence, dribbling), gastrointestinal (diarrhea, constipation, nausea, or vomiting), and sexual (erectile impotence and ejaculatory failure in men, loss of ability to reach sexual climax in women).

 PERTINENT PHYSICAL EXAM FINDINGS

  • Wasting of muscle is a prominent feature of many sensorimotor or motor neuropathies
  • Atrophy frequently occurs in muscles of dorsiflexion, such as the tibialis anterior, and in intrinsic hand muscles, such as the first dorsal interosseus.
  • Fasciculations, which appear as small twitches of the muscle, are sometimes present, particularly in axonal neuropathies.
  • Weakness is often most pronounced in foot dorsiflexion and eversion and in the intrinsic hand muscles.
  • In the lower extremities, weakness usually progresses to the muscles of plantar flexion before more proximal muscles become involved.
  • Sensory loss is usually in a stocking-glove distribution in both large and small fiber neuropathy. Cold, erythematous, or bluish discolored feet suggest loss of small fiber function.
  • Large fiber sensory loss, or “sensory ataxia,” in the upper extremities can often be detected by an inability of the patient to locate the thumb accurately with the opposite index finger while the eyes are closed or by the presence of a characteristic irregular tremor (pseudoathetosis) of the fingers.
  • The sensory examination should include vibration, position, and light touch, as well as pain and temperature. It is important to determine the degree and extent of sensory loss, in addition to the pattern of deficits (symmetrical or asymmetrical; distal or generalized; focal, multifocal, or diffuse).
  • On gait testing, subtle weakness in the feet can be detected by an inability of the patient to heel walk. Sensory ataxia can be appreciated by a wide-based gait or inability to tandem walk

 DIFFERENTIAL DIAGNOSIS

  • Amyloid polyneuropathy
  • Spinal cord tumors
  • Vitamin B-12 deficiency

 DIAGNOSTIC EVALUATIONS

  • Basic studies are suggested to exclude other common causes of neuropathy: Complete blood cell count, complete metabolic panel (electrolytes and liver function panel), vitamin B-12 and folate levels, thyroid-stimulating hormone and thyroxine, erythrocyte sedimentation rate, serum protein electrophoresis with immunofixation electrophoresis.
  • Other studies that can be ordered depending on the patient’s history and examination findings: Antinuclear antibody, Rheumatoid factor, Paraneoplastic antibodies
  • Imaging Studies: MRI of the cervical, thoracic, and/or lumbar regions may help to exclude another cause for symptoms mimicking diabetic neuropathy.
  • Quantitative sensory testing can assess and quantify vibratory, thermal, or painful sensory function in patients with peripheral neuropathies or other sensory disorders. Although the stimulus is an objective physical event, the response represents a subjective report and requires cooperation from the patient; as a result, this test by itself cannot diagnose sensory neuropathies or sensory loss.
  • Electromyography (EMG) and nerve conduction studies can determine whether a neuropathy is primarily demyelinating or axonal and can confirm whether the process is symmetrical or asymmetrical.
  • Nerve biopsy is occasionally indicated to address specific questions, such as whether vasculitis, tumor, or another infiltrative or metabolic disorder is present. Biopsy of sural nerves is performed just above the ankle.

MEDICAL MANAGEMENT

  • Stable glycemic control is most important for slowing the progression of neuropathy.
  • Tricyclic antidepressants, gabapentin, pregabalin, topical lidocaine, and duloxetine.
  • Other medications: carbamazepine, oxcarbazepine, phenytoin, lamotrigine, and opioids may also be used.
  • Topical therapy: capsaicin or lidocaine patches may be useful in some patients, especially those with more localized pain.

SURGICAL MANAGEMENT (when applicable)

  • Not applicable

EMERGENCY MANAGEMENT (when applicable)

  • Not applicable

PATIENT EDUCATION/ MAINTENANCE – PREVENTION

  • Educate patients on the importance of glycemic control and impact on disease and progression.
  • Any patient with diabetic peripheral neuropathy is at risk for foot ulceration. Provide education on foot care. If necessary, a podiatry referral should be provided.
  • Patients with diabetic peripheral neuropathy require more frequent follow-up, with particular attention to foot inspection to reinforce the need for regular self-care.

slide019 Peripheral-Neuropathy

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