Autonomic Hyperreflexia

Patients with a spinal cord injury at T7 or higher are at risk for autonomic hyperreflexia. Normally, the reflexic response to cutaneous, visceral (bladder), and proprioceptive stimuli are to some extent attenuated by descending, inhibitory impulses. However, in patients with SCI, these impulses may be curtailed, leading to uninhibited spinal cord reflexes and consequent vascular instability – initially a substanial increase BP above the level of the lesion, followed by an overzealous vagal response, with bradycardia, heart block, vasodilation, and flushing all possible.

Autonomic Hyperreflexia

• Anatomy: Spinal cord injury T7 or above
• Stimulus: Cutaneous, visceral (bladder), proprioceptive, below the level of the lesion
• Etiology: Spinal reflex which is normally inhibited by descending feedback
• Result: hypertension followed by overzealous vagal response (brady, heart block, vasodilation)

Updated definition 2020:

Autonomic dysreflexia, or hyperreflexia, is an exaggerated sympathetic response to a stimulus, usually noxious such as a distended viscous, below the level of a Spinal Cord Injury (SCI). This can occur in patients with a SCI above the level of T6. The exaggerated response causes diffuse vasoconstriction below the lesion and possible vasodilation above the level.

Symptoms often include:

• Sudden Hypertension; SBP often >200
• Dysrhythmias: bradycardia, heart block, sinus arrest and tachycardias
• Flushing above the level
• Headache
• Nasal Congestion
• Acute Left Heart Failure
• Myocardial Infarction
• Intracranial Hemorrhage
• Seizures

Treatment includes:

• Stop or remove the inciting event
• Deepen the Anesthetic is able
• Position the Head-Up
• Administer 100% oxygen
• Treat Hypertension with a vasodilator – beta-blockers could exacerbate bradycardia
• Treat Arrhythmias as appropriate
• Monitor for ST changes concerning for MI
• Consider placing an arterial catheter for monitoring blood pressure