Autonomic dysreflexia

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.[5] 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.[10]

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.[12]

There are many possible triggers of AD, though the most common causative factor is bladder distention.[13] 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.[14][15]

Supraspinal vasomotor neurons send projections to the intermediolateral cell column, which is composed of sympathetic preganglionic neurons (SPN) through the T1-L2 segments.[7] The supraspinal neurons act on the SPN and its tonic firing, modulating its action on the peripheral sympathetic chain ganglia and the adrenal medulla.[7] The sympathetic ganglia act directly on the blood vessels they innervate throughout the body, controlling vessel diameter and resistance, while the adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine.[7] In a patient with a spinal cord lesion, the descending autonomic pathways that are responsible for the supraspinal communication with the SPN are interrupted, resulting in decreased sympathetic outflow below the level of the injury.[7] In this circumstance, the SPN is controlled only by spinal influences.[7] After a spinal injury, the decreased sympathetic outflow causes reduced blood pressure and sympathetic reflex.[7] Eventually, synaptic reorganization and plasticity of SPN develops into an overly sensitive state, which results in abnormal reflex activation of SPN due to afferent stimuli, such as bowel or bladder distension.[7] Reflex activation then results in systemic vasoconstriction below the spinal cord disruption. This peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system which inhibits the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion.[8] This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, contrasted with piloerection, paleness, and cool skin below the lesion due to the prevailing sympathetic outflow.[8] This issue is much more prominent for lesions at or above the T6 level because the splanchnic nerves emerge from the T5 level and below.

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.[16] 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.[17]

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.[18][9] 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.[19]

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.[16]

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.[11] 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.[20]