NEUROPATHY
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Commonest complication associated with diabetes.
Diabetic neuropathy is a demonstrable disorder, either subclinical or clinically evident, that occurs in diabetes without other obvious cause.
Poor glycemic control, increasing age of the patient, increasing duration of diabetes, presence of cardiovascular disease, hypertension, dyslipidemias and a positive smoking history are associated with an increasing prevalence of diabetic nerve disease.
Most commonly distal sensory nerves are affected, but motor nerves and the autonomic nervous system are also often involved.
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| SCREENING |
Careful History.
Questions related to the sensory (tingling, numbness, anaesthesia, parasthesias, inco-ordination), motor (wasting, weakness, nocturnal muscle cramps) and autonomic (gastrointestinal and bladder symptoms, sexual dysfunction, postural light-headedness) nervous systems, etc.
Tests for Peripheral Sensation.
Check for touch, pain (pinprick) and vibration thresholds (calibrated tuning fork).
Motor Involvement.
Check for muscle weakness and wasting.
Reflexes
Cardiovascular Autonomic Tests;
Including tests for postural hypotension and R-R interval variation on deep breathing, if possible.
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| Clinical Presentations. |
Diabetic neuropathy has a varied clinical presentation.
Two of presentations associated with significantly morbidity are :
Distal Symmetrical Sensorimotor Polyneuropathy; and
Cardiovascular autonomic neuropathy.
Distal Symmetrical Sensorimotor Polyneuropathy
Commonest form of diabetic neuropathy;
Manifests in three stages, early, symptomatic and severe;
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| Stages : |
Early: Usually asymptomatic, but sensory loss may be detectable; neurophysiological abnormalites are demonstrable.
Symptomatic: Manifested by sensory loss, often with frank numbness and accompanied by paraesthesias, most commonly tingling or a sensation of pinprick; may also be accompanied by pain which in some cases may be severe enough to present as "burning feet" syndrome;
Severe: Is usually associated with motor involvement and accompanied by disabling symptoms; high potential for ulceration which may lead to infection, necrosis, gangrene and loss of limb.
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| Cardiovascular Autonomic Neuropathy |
Possibly, a leading cause of sudden death.
Diabetics with cardiovascular autonomic neuropathy should have a screen for its presence and severity before undergoing general anaesthesia, since such patients have an increased mortality risk from such anaesthesia.
Parasympathetic damage (failure of heart rate, or R-R interval or ECG, to increase in response to posture and breathing manouvres) occurs early.
Followed later by sympathetic damage (marked fall of blood pressure with posture or failure to increase with exercise).
Screening for the presence of cardiovascular autonomic neuropathy can be done by testing for heart rate control (changes in R-R intervals) in response to deep breathing (paced respiration), or after standing from the lying position and/or circulatory response to the Valsalva manouvre.
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| MANAGEMENT OF DIABETIC NEUROPATHY |
Somatic Neuropathy
Improved glycemic control may significantly improves symptoms if the patient presents early.
Although many drugs have been tried, no drug shown to be specific for treating diabetic neuropathy.
Topical application of Caspian (0.025-0.075% strength) may improves superficial pain or discomfort.
Severe pain may require the use of carbamazepine, or antidepressants. GABA-penetene may be of help.
Burning feet syndrome is difficult to manage; usually seen in patients who have been prescribed a severe calories and nutrient restricted diet, or have significant weight loss, and possibly managed with relatively large OHA, especially metformin, doses; often associated with efforts for rapid glycemic control, with episodes of hypoglycemia; relief often possible with high calorie diet, insulin therapy in small doses and weight gain; antidepressants and non steroidal anti-inflammatory agents help in the interim.
Muscle pain may be improved by stretching exercise, skeletal muscle relaxants, and use of non steroid anti-inflammatory agents.
Physiotherapy for improvement in gait disturbance due to pain and muscle imbalance.
Deformities caused by muscle imbalance (claw toes, hammer toes etc.) must be adequately managed.
The most important aspect of management of diabetic somatic neuropathy must be the prevention of foot complications.
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| Autonomic neuropathy |
Good glycemic control may prevent the onset and progression of autonomic neuropathy.
Mild symptomatic postural hypotension (>11-20mm Hg) may respond to elastic stockings; more severe postural hypotension (>30mm Hg) may require fludrocortisone; but any decision to use this drug must be made judiciously, especially if the patient has hypertension; in mild cases without any symptoms, no active therapy may be necessary.
Gastroparesis responds to prokinetics such as cisapride.
Diarrhea and constipation may improve with bulk forming agents and/or antispasmodics; some patients may require gut antibiotics.
Troublesome sweating may be helped by anticholinergics, but this is rarely required; there is no therapy for bizarre sweating patterns.
Patients with bladder dysfunction and urinary retention should be taught to void every 3-4 hours using manual suprapubic pressure; long term antibiotics may be required in patients with recurrent urinary tract infections.
Erectile dysfunction merits special attention; other causes such as associated drug therapy, hormonal disturbances must be ruled out. CUMRI, intra-urethral injections, vacuum devices and penile implants are are treatment modalities which can be offered; sildanefil citrate ( Viagra), if used judiciously, may be of significant help in some patients.
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| REFERRAL to a specialist is recommended when |
There is markedly diminished sensation in the legs.
Isolated mononeuropathies.
Severe muscle wasting.
Severe nocturnal foot pain or paraesthesias.
Neuropathic ulcers and jpoint deformities.
Signs and symptoms of significant autonomic involvement, especialy of the cardiovascular system.
Erectile dysfuntion.
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