• Autonomic hyperreflexia (AH) is a syndrome characterized by profound and imbalanced reflex sympathetic discharge occurring in patients with spinal cord injury (SCI) at or above the T6 level.
  • Inciting stimulus ranges from innocuous to noxious.
  • Unchecked sympathetic discharge occurs below the level of injury in response to a stimulus also below the level of injury.
  • Compensatory hemodynamic responses occur above the level of injury.
  • Also known as "autonomic dysreflexia"
• Patients with SCI commonly present to the operating room for urologic and other lower extremity procedures (e.g., decubitus ulcers) that can elicit AH.

Any stimulation below the level of SCI. Most commonly:

• Bladder distension
• Bowel distension
• Surgery
• Pressure sores
• Urinary tract infection (UTI)
• Cholelithiasis
• Sexual intercourse

• AH can be seen after the initial spinal shock phase of SCI, when autonomic reflexes return.
• Injury at or above the T6 level is above major splanchnic sympathetic outflow (T6 to L2).
• Sensory input below the level of injury is transmitted via peripheral nerves to the spinothalamic tract and posterior columns of the spinal cord, and activates sympathetic neurons.
• However, normal, descending inhibitory outflow is blocked at the level of injury; this leads to unopposed and abnormal sympathetic discharge and elevated blood pressure (due to unopposed vasoconstriction).
• Brainstem and carotid baroreceptor reflexes above the level of injury attempt to compensate for the elevation in blood pressure (below the level of injury) by increasing parasympathetic discharge to the heart via the vagus nerve; this leads to bradycardia and compensatory vasodilation above the level of injury.

• Despite the possible loss of sensation, anesthesia for procedures below the level of SCI is advisable to prevent AH.
  • General anesthesia and spinal anesthesia are preferred methods.
  • Epidural anesthesia may also be beneficial, but to a lesser extent due to reduced block density and sacral nerve sparing.
• Be prepared to treat manifestations of AH (e.g., with short-acting and direct-acting antihypertensives).

Headache, blurred vision, nasal congestion, chest pain, anxiety

• Prophylactic efforts include the removal of inciting stimulus:
  • Bladder catheterization, fecal disimpaction, etc.
• Sitting patient up from the supine position, legs down

No specific routine medications

• Decubitus ulcers
• Contractures and deconditioning
• Frequent UTIs
• Pulmonary impairment

• Acute episodes of AH should trigger a search for, and removal of, inciting stimulus, and/or postponement of nonemergent surgical interventions.
• Emergent surgical intervention during an AH episode should be performed under spinal or general anesthesia.

None

Following an episode of AH, monitor blood pressure and heart rate in a monitored setting for at least 2 hours.

• If the patient had an intraoperative episode of AH, antihypertensives should be continued, as appropriate
• If myocardial ischemia is suspected:
  • Electrocardiogram
  • Troponin levels
  • Opioids, nitrates, oxygen, vasopressors, as needed
  • Cardiology consultation

Profound sympathetic discharge can result in (2):

• Cardiac ischemia
• Cerebral edema
• Cerebral hemorrhage
• Renal failure
• Ophthalmic/retinal disease
• Pulmonary edema

• Spinal Shock
• Autonomic Nervous System

337.3 Autonomic dysreflexia

G90.4 Autonomic dysreflexia

John F. Bebawy , MD

Antoun Koht , MD