Autonomic dysreflexia

Autonomic dysreflexia

Other names	Mass reflex
Anesthetic relevance	Critical
Anesthetic management	Consider neuraxial or MAC If GA, run deep
Specialty	Neurology, Cardiology
Signs and symptoms	Hypertension Headache Diaphoresis Bradycardia or tachycardia
Diagnosis	Most common with lesions above T6. Has been described in lesions as low as T10
Treatment	Rapidly titratable vasodilators Deepen anesthesia
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Autonomic dysreflexia is potentially life threatening sympathetic hyperactivity which can emerge following spinal cord injury, and involves dysregulation of the autonomic nervous system leading to a disorganized response to noxious stimulus below the level of the spinal cord injury.

Anesthetic implications

Preoperative optimization

Preoperative history is essential in alerting the anesthesiologist to the possibility of intraoperative AD. Key information includes the spinal cord injury history (timing, degree of injury and importantly the level), prior history of autonomic dysreflexia and associated triggers (if known).

The planned procedure also significantly impacts the likelihood of intraoperative AD. Stimulus above the injury level are less likely to provoke autonomic dysreflexia while injuries below are higher risk.

Intraoperative management

An anesthetic plan can include general or neuraxial techniques for patients at risk.

If general anesthesia is chosen, patients should be kept at a sufficiently deep level of anesthesia to prevent dysreflexia. Fast acting agents that can quickly be titrated are preferred such as Propofol and the insoluble volatile anesthetics.

Neuraxial anesthesia may be used, especially a spinal which can effectively prevent the development of autonomic dysfunction. However, limitations include difficulty determining the level of spinal block. Epidural anesthesia is less effective than spinal anesthesia for patients with SCI but can be considered.

For patients with no sensation at the surgical site and with injury below T6, MAC is an acceptable option.

Signs and symptoms

Sympathetic hyperreactivity below the lesion presents with vasoconstriction (pale, dry skin), systemic hypertension and associated headache. Parasympathetic hyperreactivity above the lesion presents with vasodilation, flushing, piloerection, miosis, nausea, and vomiting. Awake patients may also endorse lightheadedness, anxiety, and sensation of doom.

Vital sign changes consistent with AD include severe hypertension and bradycardia. Hypertension can evolve to end organ dysfunction including pulmonary edema, left ventricular dysfunction, intracranial hemorrhage, seizures or even death. Bradycardia may also range from asymptomatic to sinus arrest.