Autonomic dysreflexia

Autonomic dysreflexia
Other names	Autonomic hyperreflexia[1]
Specialty	Neurology

Autonomic dysreflexia (AD) is a potentially fatal medical emergency classically characterized by uncontrolled hypertension and cardiac arrhythmia.^[2][3][4] 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.^[5] Guillain–Barré syndrome may also cause autonomic dysreflexia.^[1]

The uncontrolled hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache; however, severe symptoms may result in potentially life-threatening complications including seizure, intracranial bleed (stroke), myocardial infarction, and retinal detachment.^[2]

AD is triggered by either noxious or non-noxious stimuli, resulting in sympathetic stimulation and hyperactivity.^[6] The most common causes include bladder or bowel over-distension from urinary retention and fecal compaction,^[7] 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.^[8] 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.^[8] This results in bradycardia, tachycardia, vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while there is piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow.^[8] Bradycardia is a common symptom though some patients may experience tachycardia instead.

Autonomic dysreflexia should be treated immediately by removing or correcting the noxious stimuli. This involves sitting the patient upright, removing any constrictive clothing (including abdominal binders and support stockings), rechecking blood pressure frequently, and then checking for and removing the inciting issue, which may require urinary catheterization or bowel disimpaction.^[2][4] If systolic blood pressure remains elevated (over 150 mm Hg) after initial steps, fast-acting short-duration antihypertensives are considered,^[9] while other inciting causes must be investigated for the symptoms to resolve.^[2]

Prevention of AD involves educating the patient, family and caregivers of the precipitating cause, if known, and how to avoid it, as well as other triggers.^[4] Since bladder and bowel are common causes, routine bladder and bowel programs and urological follow-up for cystoscopy/urodynamic studies may help reduce the frequency and severity of attacks.^[2]