Cardiovascular Dysfunction Due to Sympathetic Hypoactivity After Complete Cervical Spinal Cord Injury A Case Report and Literature Review

Spinal cord injury (SCI) is one of the most devastating of all traumatic events; it may cause permanent dysfunction in several organ systems and lead to motor and sensory impairment. Cardiovascular dysfunction has been recognized to be the leading cause of morbidity and mortality in the acute and chronic stages following SCI. Although cardiovascular dysfunction causes the deaths of many SCI patients, most clinicians are unfamiliar with the phenomenon. The purpose of reporting our case is to remind clinicians to consider the possibility of cardiovascular dysfunction in patients with complete SCI. The patient signed informed consent for publication of this case report and any accompanying image. The ethical approval of this study was waived by the ethics committee of the Chonbuk National University Hospital, Jeonju, Korea, because this study was a case report and the number of patients was <3. A 63-year-old man was transferred to our emergency room after a fall. He complained of weakness and numbness of the lower extremity. Radiologic evaluation revealed C7/T1 unilateral facet dislocation with spinal cord contusion. On neurologic examination, the patient exhibited a paraplegic state below the T4 dermatome because of complete SCI. His vital signs were stable, but respiration was shallow. We performed intraoperative manual reduction and anterior interbody fusion. On the second postoperative day, the patient experienced sudden cardiac arrest after he was shifted from a supine to a semilateral position. Upon position change, heart rate was decreased <40 beats/min and blood pressure could not be checked. We immediately started cardiac massage and administered atropine 0.5 mg and epinephrine 1 mg, and the patient was successfully resuscitated. Cardiac arrest recurred when we performed endotracheal suction or changed patient's position. Echocardiographic and Holter monitoring findings demonstrated normal heart function and sinus bradycardia, and there was no evidence of pulmonary thromboembolism. We concluded that cardiac arrest was induced by sympathetic hypoactivity following complete SCI. Two months later, this phenomenon had resolved, and 4 months after presentation, he was discharged reliant on a home ventilator. Through this report, we emphasize that a thorough understanding of cardiovascular dysfunction following SCI is important for establishing a diagnosis and optimizing clinical outcomes.