AUTONOMIC DYSREFLEXIA HYPERREFLEXIA

Autonomic Dysreflexia
Patients with spinal cord injuries at or above the T6 level are at risk for developing autonomic dysreflexia (also called autonomic hyperreflexia). This reflex is initiated by a noxious stimulus from below the level of the patient's spinal cord lesion. Intact sensory neurons below the level of the lesion transmit a message up the spinothalamic tract and posterior columns, where interconnections stimulate the intermediolateral gray matter neurons, producing sympathetic outflow from spinal cord levels between T6 and L2, releasing norepinephrine, -hydroxylase, and dopamine. This sympathetic reflex is relatively unopposed because the normal inhibitory impulses that would prevent it originate above T6 and are blocked at the level of injury.

The sympathetic response produces a rise in blood pressure, vasoconstriction, skin pallor, and piloerection below the level of the lesion. Intact carotid and aortic arch baroreceptors detect the hypertension, producing increased parasympathetic activity in the vagus nerve causing bradycardia and, above the level of the lesion, profuse sweating, vasodilation, and skin flushing.

Common signs and symptoms of autonomic dysreflexia are a pounding headache, nasal congestion, a feeling of apprehension or anxiety, visual changes, and most significant, a marked increase in systolic and diastolic blood pressure above baseline. Patients with spinal cord injury at or above the T6 level often have lower baseline systolic blood pressures, in the 90- to 110-mm Hg range. Therefore, blood pressure elevations of 20 to 40 mm Hg or systolic pressures of 130 to 150 mm Hg are significant. Acute elevation in blood pressure is the most worrisome and potentially life-threatening manifestation of this syndrome.

A variety of stimuli can produce an acute episode of autonomic dysreflexia. The most common causes usually involve the urinary system: bladder distention, urinary tract infection, and kidney stones. The second most common reasons involve the colon: fecal impaction or bowel distention. However, any noxious stimulus below the level of injury can lead to autonomic dysreflexia, including peptic ulcers, appendicitis, and gallstones, fractures, deep venous thrombosis (DVT), pressure ulcers, ingrown toenails, tight-fitting clothing, sunburns, blisters, heterotopic ossification, sexual intercourse, pregnancy, and labor and delivery.

Treatment begins with monitoring and controlling the patient's blood pressure. If possible, the patient should sit up to lower blood pressure. All constrictive clothing items should be loosened. If the systolic blood pressure is above 150 mm Hg, an antihypertensive agent with a rapid onset and short duration should be used. Nitroprusside and nitrates are the most commonly used agents. More aggressive treatment should be undertaken if these agents do not adequately correct the elevated blood pressure.

After assessment of the blood pressure, the bladder should be checked for distention and infection. If the patient does not already have a urinary catheter, one should be placed. The stimulus of catheterization may add to the autonomic reflex, and lidocaine jelly should be used in the urethra prior to catheter insertion if it is readily available, but its lack should not delay the placement of the catheter. If the patient already has an indwelling urinary or suprapubic catheter, it should be checked for obstruction and proper placement. The bladder can be gently irrigated through the catheter with body-temperature normal saline solution to check for obstruction and improper placement. Urine should be sent for urinalysis and culture.

If symptoms persist, the physician should suspect fecal impaction. Prior to the rectal examination, the patient's blood pressure should be managed, and the anal opening should be anesthetized with lidocaine jelly placed into the rectum for 5 min before beginning the examination. The patient's blood pressure should be monitored to ensure that the hypertension is not aggravated during this procedure, since rectal examination can exacerbate autonomic dysreflexia. If the blood pressure increases, stop the examination, instill more anesthetic agent, and wait additional time. If the bladder or bowel does not appear to be the cause of the patient's symptoms, a search for other causes should be undertaken.

Following relief of an acute episode, patients should be monitored for at least 2 h after resolution to ensure that there is no recurrence. Patients with bladder distention do not routinely require discharge with an indwelling urinary catheter. It is best to discuss that option with the patient's physician. If the patient responds poorly or the cause has not been identified, the patient may be admitted for more aggressive pharmacologic control of blood pressure and a more thorough investigation of the cause.