What manifestation is expected when a person with a spinal cord injury develops autonomic dysreflexia?

Hypertension is the cardinal manifestation of autonomic dysreflexia and is the most life-threatening aspect of this condition. Autonomic dysreflexia occurs in individuals with spinal cord injury at or above the T6 level. A noxious stimulus below the level of injury — most commonly a distended bladder or bowel — triggers a massive, unmodulated sympathetic discharge below the level of injury, causing intense vasoconstriction and a dramatic rise in blood pressure, sometimes exceeding 200/100 mmHg. Because the injury prevents normal descending inhibition, compensatory baroreceptor responses above the injury level produce parasympathetic effects such as bradycardia, flushing, and diaphoresis above the lesion level — but cannot adequately counteract the systemic hypertension. Tachycardia is incorrect; the reflex baroreceptor response actually causes bradycardia as the body attempts to compensate for the hypertension above the level of injury. Chest pain may occasionally be reported but is not a hallmark manifestation. Hyperkalemia is a separate concern in renal failure or crush injuries and is not a feature of autonomic dysreflexia. Nurses must recognize and treat this emergency immediately by sitting the patient upright, removing the triggering stimulus, and monitoring blood pressure.