A patient with a spinal cord injury presented to our clinic with signs and symptoms that our staff did not recognize. It was later determined to be autonomic dysreflexia. What is important to know about autonomic dysreflexia?-GE, GA
Julianne Mercado, RN; Amanda Ruiz, RN; and Bridget Parsh, EdD, RN, CNS respond- Autonomic dysreflexia (AD), also known as autonomic hyperreflexia, is a potentially life-threatening acute syndrome that occurs in 20% to 70% of patients with spinal cord injury (SCI) at or above the level of T6.1,2 Unfortunately, knowledge of AD is low among healthcare professionals.3
Uninhibited or exaggerated sympathetic responses to noxious stimuli below the level of the SCI result in diffuse vasoconstriction and hypertension. A compensatory parasympathetic response causes bradycardia and vasodilation above the level of the SCI, but it is insufficient to decrease the BP.
In most cases, urologic issues such as urinary tract infection, distended bladder, or a blocked indwelling urinary catheter can be the trigger for AD.1 Other stimuli that can cause AD include constipation, fecal impaction, gastric ulcers, hemorrhoids, pressure injuries, ingrown toenails, and burn injuries.1,4 Additional triggers include tight clothing, sexual activity, menstrual cramps, ovarian cysts, or bone fractures.5 Wrinkled sheets can also trigger a patient who lays on them. Patients with AD may be unaware of these stimuli due to either absent or reduced sensation below the level of injury.5
Clinical manifestations
A severe, debilitating headache is usually the initial presenting symptom of AD along with a rise in BP.5 The headache can be unilateral, bilateral, or generalized with radiation to the neck.6 The elevated BP can range from asymptomatic hypertension to hypertensive crisis. Most patients with an SCI at T6 and above have a systolic BP (SBP) between 90 and 110 mm Hg. Therefore, healthcare providers might not interpret an increase of over 20-40 mm Hg in BP as a sign of AD unless compared with baseline levels.6
Other signs and symptoms of AD include diaphoresis, flushing, nasal congestion, piloerection, bradycardia, nausea, vomiting, blurred vision, and anxiety.1,2,7
Severe signs may include cardiac dysrhythmias such as atrial fibrillation, and SBP levels above 300 mm Hg which may lead to cerebral hemorrhage, seizures, and death.6
Management
The priority intervention is to identify and remove any noxious stimuli.2 Monitor vital signs, especially BP, and immediately place the patient in high Fowler's position with legs dangling to help lower BP. Remove any tight or restrictive clothing.7 BP should be measured at least every 5 minutes; consider arterial line placement.7
The current standard of care is to identify and eliminate the inciting factors, when possible, before pharmacologic approaches are considered. Patients with significant hypertension may require pharmacotherapy such as nitrates, calcium channel blockers, I.V. hydralazine, or I.V. labetalol.7
Nursing considerations
When caring for patients at risk for AD, obtain a history of any previous AD episodes, monitor vital signs, and assess for any signs and symptoms of AD especially if there is a known trigger.1
The goal of AD management is prevention and early identification. Strict adherence to bowel, bladder, and skin care can help prevent AD episodes.6 Ensure the patient and family understand the signs and symptoms and treatment of AD. Teach self-management techniques so that signs and symptoms can be alleviated promptly, possibly without the need for medical intervention.7
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