Autonomic dysreflexia

Medical condition

Autonomic dysreflexia (AD) is a potentially fatal medical emergency classically characterized by uncontrolled hypertension and cardiac arrhythmia. AD occurs most often in individuals with spinal cord injuries with lesions at or above the T6 spinal cord level, although it has been reported in patients with lesions as low as T10. Guillain–Barré syndrome may also cause autonomic dysreflexia. The most common causes include bladder or bowel over distension from urinary retention and fecal compaction, pressure sores, extreme temperatures, fractures, undetected painful stimuli (such as a pebble in a shoe), sexual activity, and extreme spinal cord pain. The noxious stimuli activates a sympathetic surge that transmits through intact peripheral nerves, resulting in systemic vasoconstriction below the level of the spinal cord lesion. The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system to inhibit the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion and is insufficient to reduce elevated blood pressure. while other inciting causes must be investigated for the symptoms to resolve.

Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical problems like soft tissue pressure injuries or hemorrhoids. Long term therapy may include alpha blockers or calcium channel blockers. Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction, or cerebral hemorrhage. Additional organs that may be affected include the kidneys and retinas of the eyes. There are many possible triggers of AD, though the most common causative factor is bladder distention. Other causes include urinary tract infection, urinary retention, blocked catheters, constipation, hemorrhoids or fissures, skin damage, fractures, and sexual intercourse. Not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli, e. g. broken bones, may not result in AD, and may in fact even go unnoticed. In the absence of clear triggering factors, episodes of AD that are recurrent can be important signs that there is an undetected underlying pathology in a patient that has not yet been elucidated.

Supraspinal vasomotor neurons send projections to the intermediolateral cell column, which is composed of sympathetic preganglionic neurons (SPN) through the T1 L2 segments. Autonomic dysreflexia differs from autonomic instability, the various modest cardiac and neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension, and ambient temperature intolerance. Because of this, elevated blood pressures in patients with baseline hypotension may not be recognized unless compared with their baseline levels. Diagnosis of AD may be differentiated by additional symptoms in addition to hypertension, including sweating, spasms, erythema (more likely in upper extremities), headaches, and blurred vision. Older patients with very incomplete spinal cord injuries and systolic hypertension without symptoms may be experiencing essential hypertension, not autonomic dysreflexia.

Initial management of AD includes measuring and monitoring blood pressures and sitting the patient upright to attempt to lower blood pressure as well as searching for and correcting the triggering stimuli. Tight clothing and stockings should be removed. Catheterization of the bladder should be performed as well as evaluation for possible urinary tract infection (UTI). Relief of a blocked urinary catheter tube may resolve the problem, and indwelling catheters should be checked for obstruction. A rectal examination can be performed to clear the rectum of any possible stool impaction. If the noxious precipitating trigger cannot be identified, prompt pharmacologic treatment may be needed to decrease elevating intracranial pressure until further studies can identify the cause. Drug treatment includes the rapidly acting vasodilators, including sublingual or topical nitrates or oral hydralazine or clonidine. Ganglionic blockers are also used to control sympathetic nervous system outflow.

Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be quite severe. The cause of autonomic dysreflexia itself can be life threatening, and must also be completely investigated and treated appropriately to prevent unnecessary morbidity and mortality.