Autonomic Dysreflexia

Autonomic dysreflexia is a potentially lethal complication of a spinal cord injury that affects people with injuries at or above the thoracic level (usually T6 or above). The condition is manifest by severe headache (caused by an abrupt elevation of blood pressure), hypertension, profuse sweating, and activation of other autonomic reflexes. Symptoms come from overactivity of the autonomic (involuntary) nervous system cells in the spinal cord because of the blocked nerve impulses from the brain that normally keep these cells under restraint. The most frequent triggers of autonomic dysreflexia are an impacted bowel or an overfull bladder. The overactive sympathetic nerve and its branches cause a narrowing of the blood vessels, which, in turn, dramatically elevates blood pressure. Death from seizures, stroke, and abnormal heart beat rhythm can ensue if autonomic dysreflexia is not urgently treated.

Because autonomic dysreflexia is most often set off by bladder distention or bowel impaction, many individuals with spinal cord injuries have learned means of self-care to avoid emergency treatment by sitting upright to check urinary drainage or empty their bowel. An array of nonpharmacological and pharmacological agents are also available for emergency medical treatment (PVA, 2001).

Pressure Ulcers

Pressure ulcers are a highly frequent and serious complication of a spinal cord injury that affect physical, psychological, and social functioning. Ulcers are lesions caused by unrelieved pressure (if the force is perpendicular) or shear (if the force is tangential) to the tissue surface. The constant pressure can also interfere with the pressure in the capillaries and can therefore affect the exchange and elimination of nutrients and metabolites. Prolonged circulatory interference ultimately leads to cell death. In severe cases, individuals can develop a severe internal infection (septic shock), which can lead to organ failure. Stage I lesions are marked by discoloration and changes in tissue consistency on the skin surface, whereas the most serious lesions, stage IV lesions, are marked by extensive tissue necrosis and damage to muscle, bone, or supporting structures. About 32 percent of individuals with spinal cord injuries admitted to specialized care centers have been reported to develop pressure ulcers during the acute care stage, and at 2 years of follow-up the prevalence of pressure ulcers was 8.9 percent (Yarkony and Heinemann, 1995). The Consortium for Spinal Cord Medicine’s clinical practice guideline advocates a range of prevention strategies, including the avoidance of prolonged positional immobilization, use of support devices on beds and wheelchairs, and dietary changes. Treat-

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