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Autonomic Hyperreflexia (AHR)

Anesthesia Implications

Anesthesia Implications

Treatment of AHR

  • Notify the surgeon and remove the stimulus
  • Deepen the anesthetic by increasing the MAC of the inhaled agent, administer opioids, and/or administer an epidural bolus
  • administer direct-acting vasodilators (these may need to be continued into the postoperative period)
    • Sodium Nitroprusside Infusion (0.5 - 5.0 mcg/kg/min)
    • Labetalol (5 - 10 mg IV)
    • Phentolamine (2 - 5 mg IV)
  • Treat bradycardia (Atropine 1.0 mg IV or Robinul 0.2 - 0.4 mg IV)
Brady, Tachy, Arrhythmia, Arrest - If it is a true case of AHR, bradycardia will be seen first, followed by tachycardia with possible V-fib and cardiac arrest. Symptoms of extreme hypertension can precipitate seizures, intracranial hemorrhage, and/or myocardial infarction. Drugs to Avoid - succinylcholine, atracurium, meperidine, and ketamine - succinylcholine can lead to hyperkalemia, atracurium and meperidine have a seizure-inducing metabolite, and ketamine increases ICP and thereby heightens the risk for intracranial hemorrhage. Don't rely on history - Paraplegics and quadriplegics may experience AHR without a previous history of it - so be mindful of the signs/symptoms. Any surgery below the SCI - ANY surgery resulting in cutaneous or visceral stimulation below the level of spinal cord injuries (SCI) may result in AHR (eg. Cystoscopy, Extracorporeal shock wave lithotripsy, etc.) ANY noxious stimulation below the SCI - may result in AHR (eg. Bladder distention, bowel distention, uterine contractions, etc). Keep pain under tight control Extubate deep - Consider deep extubation unless contraindicated

Pathophysiology

This condition is acquired and occurs in 85% of patients with SCIs above T5-T8. It occurs as a result of disruption of normal autonomic nervous system (ANS) regulation. This is much more common in patients with complete transections of the spinal cord. AHR is a massive sympathetic discharge that is the result of stimulus BELOW the level of injury. Afferent impulses are obstructed at the level of the SCI. As a result, the ANS responds by increasing sympathetic outflow. This causes vasoconstriction and hypertension BELOW the level of the SCI. Hypertension initiates the baroreceptor reflex which causes bradycardia. The ANS responds to the baroreceptor reflex by efferent parasympathetic outflow, which causes vasodilation ABOVE the level of injury. AHR is the result of stimulus BELOW the level of injury. The ANS responds by a massive sympathetic discharge that causes vasoconstriction and hypertension. Hypertension initiates the baroreceptor reflex, which causes bradycardia. The ANS then compensates as a response to the baroreceptor reflex . This compensation is parasympathetic outflow, which because of the injury, only results in compensatory vasodilation ABOVE the level of injury. As a result, you have compensation above the level of injury, and uncompensated hypertension BELOW the level of injury. In summary, the symptoms are: Bradycardia, hypertension, dysrhythmias, cutaneous flushing/vasodilation and sweating ABOVE the SCI, blurred vision, headache, and nasal stuffiness.

Reference

Chu and Fuller. Manual of clinical anesthesiology. 2012.
Hemmings. Pharmacology and Physiology for Anesthesia. 1st Edition. 2012.
Jaffe. Anesthesiologist’s manual of surgical procedures. 15th edition. 2014.