It occurs in 20% to 70% of patients, 1 month to 1 year after spinal cord injury.
Cord injury is usually above the T6 level, with dysreflexia unlikely to occur after an injury below the T10 level. Life-threatening hypertension is provoked by a noxious stimulus below the level of spinal cord injury; in about 85% of patients, the stimulus is a urologic disorder, such as bladder distention or urinary tract infection. In up to 85% of cases, the cause is bladder distension, often due to a blocked bladder catheter. Bowel distension and fecal impaction are the second most common precipitants; they account for 13 to 19 % of cases.
Visceral or cutaneous stimulation below the level of spinal cord injury provokes reflex sympathetic activity, resulting in diffuse vasoconstriction and an increase in blood pressure (BP). Normally, the increase in BP would stimulate parasympathetic compensation with vasodilation and correction of BP. However, if the spinal cord is injured, the parasympathetic response cannot travel below the spinal cord lesion, and continued vasoconstriction then leads to continued injurious hypertension. With a lesion below T10, the splanchnic vascular bed innervation remains intact, allowing compensatory parasympathetic dilation in this region. Provocative stimuli include distention of a hollow viscus (eg, bowel or bladder), pressure ulcers, urinary tract infection, fractures, medical or surgical procedures, and even sexual intercourse.
Symptoms of autonomic dysreflexia are variable, intermittent. and usually sudden in onset. They include headache, nausea and vomiting, problems with vision, nasal congestion, and feelings of anxiety and doom. Profuse sweating, flushing, and piloerection occur above the level of spinal cord injury; vasoconstriction with dry, pale skin occurs below the level of injury.
Hypertension may result in hypertensive crisis, with pulmonary edema, intracranial hemorrhage, seizures, retinal detachment, myocardial infarction, and death.
Autonomic dysreflexia should be suspected in a patient with a spinal cord injury above the level of T6, severe hypertension, and increased sympathetic activity, especially if provoked by distention of a hollow viscus.
Clinicians should suspect autonomic dysreflexia if patients have a T6 or higher spinal cord lesion and report headache. In such patients, BP should be measured immediately and corrected as needed. Any stimulus that causes pain or discomfort (eg, pressure sores, ingrown toenails) in a patient without spinal cord injury may result in autonomic dysreflexia in patients with spinal cord injury. A thorough medical evaluation may be required.
Treatment of autonomic dysreflexia requires close monitoring of vital signs. Provocative stimuli should be corrected and/or removed. Severe hypertension is immediately treated with rapid-acting drugs such as nitrates, hydralazine, labetalol, or nifedipine.
Pregnant women may require expert obstetric care.
Chemodenervation of the bladder using onabotulinumtoxinA has been shown to help prevent autonomic dysreflexia when used appropriately (ie, when all other measures to prevent it have been ineffective).
Intravesical lidocaine before changing a bladder catheter may reduce the frequency of episodes of bladder distention.
Autonomic dysreflexia occurs after a spinal cord injury and can result in life-threatening hypertension.
Symptoms include headache, nausea and vomiting, problems with vision, nasal congestion, and feelings of anxiety and doom, with profuse sweating, flushing, and piloerection above the level of spinal cord injury and vasoconstriction with dry, pale skin below the level of injury.
Suspect autonomic dysreflexia in patients with a spinal cord injury above the level of T6, severe hypertension, and increased sympathetic activity, especially if provoked by distention of a hollow viscus (often caused by a blocked bladder catheter).
Correct the cause if possible, and treat severe hypertension with rapid-acting drugs.