Autonomic dysreflexia

Autonomic dysreflexia (AD) is a life-threatening medical emergency characterized by hypertension and cardiac arrhythmias. This condition is sometimes referred to as autonomic hyperreflexia. Most cases of AD occur in individuals with spinal cord injuries. Lesions at or above the T6 spinal cord level are more frequently reported, although there are reports of AD in patients with lesions as low as T10. Guillain–Barré syndrome may also cause autonomic dysreflexia.

Hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache. Severe symptoms may result in life-threatening complications including seizure, intracranial bleeds (stroke), myocardial infarction, and retinal detachment.

Both noxious and non-noxious stimuli can trigger AD. The result is stimulation and hyperactivity of the sympathetic nervous system. The noxious stimuli activate a sympathetic surge that travels 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. This surge originates 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 to reduce elevated blood pressure. This can result in bradycardia, tachycardia, vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion. Piloerection and pale, cool skin occur below the lesion due to the prevailing sympathetic outflow.

The most common causes include bladder or bowel over-distension from urinary retention and fecal compaction. Other causes include pressure sores, extreme temperatures, fractures, undetected painful stimuli (such as a pebble in a shoe), sexual activity, and extreme spinal cord pain.

Treating AD immediately involves removing or correcting the noxious stimuli. This entails sitting the patient upright, removing any constrictive clothing (including abdominal binders and support stockings), and rechecking blood pressure often. The inciting issue may require urinary catheterization or bowel disimpaction. If systolic blood pressure remains elevated (over 150 mm Hg) after these steps, fast-acting short-duration antihypertensives are considered, while other inciting causes must be investigated for the symptoms to resolve.

Educating the patient, family, and caregivers about the avoidance of triggers and the cause, if known, is important in the prevention of AD. Since bladder and bowel are common causes, routine bladder and bowel programs and urological follow-up may help reduce the frequency and severity of attacks. These follow-ups may include cystoscopy/urodynamic studies.

Prognosis of AD is generally good and mortality is rare, given that the trigger is identified and managed.

This condition is distinct and usually episodic. An elevation of 20 mm Hg over baseline systolic blood pressure, with a potential source below the neurological level of injury, meets the current definition of dysreflexia.