LAUSR

To JNA Readers: Autonomic dysreflexia (AD) is a potentially devastating complication of spinal cord injury (SCI) above level T6, typically developing several months after injury and triggered by noxious stimulation below the level of injury.1–3 We present a case, in which severe hypertension, refractory to initial treatment, developed in a sedated patient who had sustained a recent SCI. A 59-year-old obese male (body mass index=37) with a long-standing history of hypertension, diabetes mellitus type 2, and drug-eluting stent placement 11 months previously, presented for cervical laminectomy and fusion from C2-C7 with neuromonitoring. He was quadriplegic after being struck as a pedestrian 17 days previously and sustaining a C4-C5 injury. No surgery followed the injury, and during the hospitalization, there were no reported episodes of hemodynamic instability. After placement of standard ASA monitors, a dexmedetomidine infusion at 0.7mcg/kg/h was started. Blood pressure was at 130/70 and pulse rate at 70bpm. Labetalol 10mg was given. Lidocaine 2% was injected to the puncture placement site before arterial cannulation. As soon as the radial artery was pierced, the blood pressure increased to 200/80 and pulse rate increased to 140bpm. The patient verbally denied pain or discomfort. Over the next 30 minutes, nitroglycerin boluses of 80, 80, 120, and 100mg were administered intravenously with little to no effect. Midazolam 2mg was added and a remifentanil infusion at 0.3mg/kg/min was commenced. Propofol 260mg and fentanyl 150mg were given in divided doses. The blood pressure remained elevated. Endotracheal intubation was accomplished by fiberoptic bronchoscopy. Sevoflurane 2% was initiated following endotracheal intubation. The blood pressure remained around 200/80 for 90 minutes before finally decreasing to 140/60. During positioning from supine to prone, the blood pressure again increased to 190/80 despite infusions of nitroglycerin, propofol, and remifentanil with repeated boluses of fentanyl and nitroglycerin. Sevoflurane was continued. Incision was made without additional hemodynamic instability. Four hours later, the blood pressure decreased suddenly to 80/50 requiring phenylephrine boluses with immediate response. Surgery was completed after 5 hours and the patient was transported to the surgical intensive care unit intubated, in stable condition. The postoperative course in the surgical intensive care unit was unremarkable, and the patient was extubated within 24 hours. No further episodes of AD or other hemodynamic instabilities were documented. During postoperative visits, we educated the patient and his family on the signs and symptoms of AD as well as alerting his other health care providers of the hypertensive episodes. AD is defined as episodic hypertension with blood pressure increases >20mm Hg above baseline. The complication is seen in up to 90% of patients with SCI, and develops some weeks or months after injury. Common triggers include noxious and non-noxious stimulation below the level of the injury, usually bladder or hollow organ distension. Preventive measures include avoidance of triggers, provision of adequate sedation, analgesia, or anesthesia before any stimulation. Treatments include nonpharmacologic measures, such as reverse Trendelenberg position, loosening constrictive devices, and reducing the stimuli, as well as pharmacologic agents, such as nifedipine, nitrates, and captopril, and all antihypertensive agents with rapid onset and short duration of action. Our case underscores the complexities of AD and its varied expression. Not only did the complication occur very soon after SCI but a severe hypertensive response developed despite considerable local anesthesia and sedation and proved very difficult to control for several hours. All health care workers should be aware that any patient with SCI is at risk of developing AD at any time, and be prepared to prevent or treat it. The likelihood of AD developing should also be discussed with patients and their families preoperatively.