Clinics in Medical Education

In Situ Simulation for Less Common but Critical Conditions.
Featured: Autonomic Dysreflexia (AD)

Nadav Levy, MD, Lior Levy, MD, Adil Al-Karim Manji, MD, Peva Gbagornah, MD, Dario Winterton, MD, Shireen Saeed, MD

Published October 1, 2024 | Clinics in Medical Education 

Issue 3 | Volume 1 | September 2024

One of our recent Thursday in situ simulation scenarios focused on a critical but preventable complication of spinal cord injury (SCI) — autonomic dysreflexia (AD), also known as autonomic hyperreflexia. The patient in the scenario is a young, otherwise healthy male with a T4 SCI resulting from a car accident a few years ago. He has a neurogenic bladder with clots and is scheduled for a cystoscopy with continuous irrigation. Due to his lack of sensation below T4, the attending anesthesiologist opted
for MAC (Monitored Anesthesia Care) sedation. The case was then handed over to a resident, and the urologist began the procedure.

Suddenly, the patient’s blood pressure surged to 220/110, and his heart rate dropped into the 40s—classic signs of an AD crisis. This is a perfect example of a preventable AD episode. Our residents promptly instructed the surgeon to stop the stimulus, administered nicardipine (0.2-0.5 mg IV bolus, followed by an infusion of 2.5-15 mg/hr if needed), and halted the sedation to assess neurological function. The team then proceeded with general anesthesia using an endotracheal tube (ETT), taking care to avoid succinylcholine, which is contraindicated in SCI patients after 48 hours post-injury.

Autonomic dysreflexia occurs in up to 85% of patients with SCI above the T6 level. It is characterized by an exaggerated sympathetic response to stimuli below the injury site, most commonly a distended viscus (e.g., bladder, intestines, or cervix). Sensory input travels through intact peripheral nerves and triggers a massive sympathetic surge, causing vasoconstriction—especially in the splanchnic vasculature—leading to severe hypertension. Baroreceptors in the neck signal the brain, but due to the SCI, parasympathetic inhibitory impulses cannot travel below the injury. The result is a mismatch: parasympathetic overflow above the lesion (reactive bradycardia, flushing, headache, sweating) and unopposed sympathetic tone below the lesion (hypertension, dysrhythmia, goosebumps, cold, pale skin). Severe cases of AD can lead to life-threatening conditions such as myocardial ischemia, sinus arrest, intracranial hemorrhage, and seizures.

Key Management Steps for Autonomic Dysreflexia:

  • Stop the stimulus immediately.
  • Position the patient with the head elevated.
  • Treat hypertension with vasodilators like nicardipine, nitroglycerin, or nitroprusside for severe cases.
  • Deepen anesthesia to prevent further episodes.

Preventing AD is key. Although SCI patients may not feel pain, sensory input from the viscera must be suppressed to avoid AD crises. Neuraxial anesthesia is often the preferred option for urologic procedures. If this is not possible, a deep general anesthetic is required—MAC sedation is insufficient.

During our post-simulation debrief, we discussed another high-risk patient population: pregnant women with SCI. AD can occur due to distention of a hollow viscus, including the uterus. AD is most likely to arise during labor, particularly during cervical exams, the use of constrictive clothing or devices, fundal massages, and uterine contractions. In addition to severe maternal hypertension and cardiac arrhythmias, uteroplacental vasoconstriction can result in fetal hypoxia and bradycardia. It is critical to distinguish AD-induced hypertension from preeclampsia. While AD-associated hypertension typically improves between contractions, proteinuria is not expected in AD but may be present in preeclampsia. However, a new headache combined with severe hypertension may point towards preeclampsia.

Figure 1

Features of AD, adapted from Spinal Cord Injury Zone

For pregnant SCI patients, an early anesthesia consultation is recommended, along with the involvement of a multidisciplinary team. Even though these patients may not feel pain below the T6 level, neuraxial anesthesia can prevent AD and be lifesaving for both mother and baby. Early epidural administration by an experienced provider is recommended, despite potential technical difficulties due to the SCI. Neuraxial anesthesia can also be used postpartum. While vaginal delivery with forceps or vacuum assistance is possible if AD is well-controlled, cesarean delivery is the preferred option
for around 68-69% of these patients. When appropriate, spinal anesthesia is better at controlling AD compared to epidurals, which may not provide adequate sacral coverage or may be patchy due to spinal deformities.

In cases of severe hypertension in labor, treatment options include sublingual or IV nitroglycerin, or nicardipine. However, caution is advised as these drugs can reduce uterine tone, increasing the risk of hemorrhage. Nitroprusside should only be used as a last resort due to the risk of fetal cyanide toxicity. For less acute hypertension, hydralazine, labetalol, or oral nifedipine are appropriate options.

Conclusion

AD is a life-threatening condition that anesthesiologists must understand, prevent, and treat—especially in SCI patients. By recognizing the signs, stopping the stimulus, and providing appropriate anesthesia, we can significantly reduce the risk of this dangerous complication.

REFERENCES

1.  Allen KJ, Leslie SW. Autonomic Dysreflexia. [Updated 2023 May 30]. In: StatPearls [Internet].

2.  Balik V, Šulla I. Autonomic Dysreflexia following Spinal Cord Injury. Asian J Neurosurg. PMID: 36120615

3.  Soh SH, Lee G, Joo MC. Autonomic dysreflexia during
pregnancy in a woman with spinal cord injury: a case report. PMID: 31187679