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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. AD is estimated to occur in 20 to 70 percent of patients with injuries above T6. The severity and frequency of AD attacks varies with the severity of the SCI.

The uncontrolled hypertension in AD may be asymptomatic or 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.

AD is triggered by noxious stimuli below the level of the spinal cord injury, resulting in sympathetic stimulation and hyperactivity. The most common causes include bladder or bowel over-distension from urinary retention and fecal compaction, pressure sores, extreme temperatures, bone fractures, and undetected painful stimuli (such as a pebble in a shoe). Sexual activity can also be a trigger. The noxious stimuli activates a sympathetic response that transmits through intact peripheral nerves, resulting in systemic vasoconstriction below the level of the spinal cord lesion. The resulting hypertension activates the baroreceptors, leading to a compensatory 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. This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while there is piloerection and pale, cool skin below the lesion due to the prevailing sympathetic outflow. 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), and performing urinary catheterization or bowel disimpaction. If systolic blood pressure remains elevated after initial steps, vasodilating medication may be necessary in order to prevent complications of severe hypertension.

Prevention of AD involves educating the patient, family, and their caregivers on recognizing and avoiding precipitating causes or triggers. Since bladder and bowel distension 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.

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Signs and symptoms

This condition is distinct and usually episodic. Common presenting symptoms include headache, diaphoresis, and increased blood pressure. Patients may also experience facial erythema, goosebumps, nasal stuffiness, a "feeling of doom" or apprehension, and blurred vision. The first episode of autonomic dysreflexia may occur weeks to years after spinal cord injury takes place, but most people at risk develop their first episode within the first year after injury.

Complications

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.^{[citation needed]}

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.

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Causes

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.

Diagnosis

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Diagnosis of AD is made by measuring an increase in systolic blood pressure greater than 20 to 30mmHg. The associated symptoms vary from life-threatening to asymptomatic. 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. Older patients with very incomplete spinal cord injuries and systolic hypertension without symptoms may be experiencing essential hypertension, not autonomic dysreflexia.

Treatment

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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 can also used to control sympathetic nervous system outflow. Epidural anesthesia has been demonstrated to be effective in reducing AD in women in labor, though there is less evidence for its use in reducing AD during general surgical procedures.

Prognosis

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

Attacks can be prevented by recognizing and avoiding triggering stimuli. Because bladder distension is a common trigger of AD, botulinum toxin used to treat bladder dysfunction in SCI may be effective in reducing attacks. Prophylactic use of nifedipine, prazosin, and terazosin has also been reported to prevent attacks. Topical analgesics such as lidocaine and bupivacaine are also commonly used to reduce episodes of AD triggered by bowel and bladder management, though their effectiveness in reducing AD remains inconclusive.

The Consortium for Spinal Cord Medicine has developed evidence-based clinical practice guidelines for the management of autonomic dysreflexia in adults, children, and pregnant women. There is also a consumer version of this guideline.