|Other names||Mass reflex|
Consider neuraxial or MAC
|Signs and symptoms||
Most common with lesions above T6. Has been described in lesions as low as T10
Rapidly titratable vasodilators Deepen anesthesia
Autonomic dysreflexia is potentially life threatening sympathetic hyperactivity in patients with spinal cord injury which can emerge in response to noxious or non-noxious stimulation below the level of injury. Autonomic dysreflexia typically occurs in patients with lesions at or above T6, but has been reported in injuries as low as T10.
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.
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. 
Goal is to maintain mean arterial pressure within 20 to 25 percent of patient's baseline.
Minimize potential triggers of AD such as post op bladder distention
Related surgical procedures
Most common surgical stimulus includes distention of hollow viscus, most commonly urinary bladder distention.
Impairment of autonomic regulation due to high spinal cord injury leads to sympathetic over-reactivity. Likely, there are synaptic changes post spinal cord injury (e.g. reduced gliosis) which may contribute to impaired regulation. The result is an uninhibited sympathetic response to stimuli causing hypertension due to splanchnic and peripheral vasoconstriction. Uninjured spinal cord above the level of injury counters with a parasympathetic response which is unable to adequately regulate blood pressure but does result in a response in heart rate (i.e. bradycardia).
Injuries below the level of T6 generally do not result in autonomic dysreflexia due to intact innervation/regulation of the splanchnic circulation.
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.
Of note, it is important to note patient's baseline resting blood pressure which may be lower in the setting of spinal cord injury (to assess for relative hypertension). This is important in early identification of AD.
Management of hypertension
- Deepen level of anesthesia, consider Mac-BAR
- If epidural, re-dose
- Fast-acting titratable agents:
- Nitroprusside infusion (0.2 to 10 mcg/kg/minute)or nitroglycerin infusion (5 mcg/minute to 200 to 500 mcg/minute)
- Nicardipine 0.2 to 0.5 mg IV bolus with nicardipine infusion (2.5 to 15 mg/hour)
- Consider labetalol, however bradycardia usually contraindicates beta blockade
Management of bradycardia:
- Atropine or glycopyrrolate
Stop causative stimulus – Communication with surgical team to pause surgery with the goal of limiting continued noxious stimulus while hemodynamics are addressed
AD usually develops within the first year after spinal cord injury. It has been reported in anywhere between 20-70% of patients with injury above the level of T6.
- Vallès, M.; Benito, J.; Portell, E.; Vidal, J. (2005). "Cerebral hemorrhage due to autonomic dysreflexia in a spinal cord injury patient". Spinal Cord. 43 (12): 738–740. doi:10.1038/sj.sc.3101780. ISSN 1362-4393. PMID 16010281.
- Mathews, Letha (May 2021). "Anesthesia for adults with chronic spinal cord injury". www.uptodate.com. Retrieved 2021-06-18.
- Bycroft, J.; Shergill, I. S.; Chung, E. a. L.; Choong, E. a. L.; Arya, N.; Shah, P. J. R. (2005-04). "Autonomic dysreflexia: a medical emergency". Postgraduate Medical Journal. 81 (954): 232–235. doi:10.1136/pgmj.2004.024463. ISSN 0032-5473. PMC 1743257. PMID 15811886. Check date values in:
- Helkowski, Wendy M.; Ditunno, John F.; Boninger, Michael (2003). "Autonomic dysreflexia: incidence in persons with neurologically complete and incomplete tetraplegia". The Journal of Spinal Cord Medicine. 26 (3): 244–247. doi:10.1080/10790268.2003.11753691. ISSN 1079-0268. PMID 14997966.