Unique Considerations for the Spinal Cord Injured Patient Undergoing Cardiac Surgery Utilizing Cardiopulmonary Bypass

Abstract

A 37-year-old male with mitral valve regurgitation presented for mitral valve replacement. He has been a C5 quadriplegic for 13 years. The patient had been discharged 2 months before to this admission after a complicated hospital course for Staphylococcus aureus infection of the left hip. His course was complicated by adult respiratory distress syndrome (ARDS) requiring prolonged intubation, acute renal failure (ARF) requiring dialysis, 10-day coma, and bacterial endocarditis now requiring mitral valve replacement. After initial stabilization with antibiotics and gradual improvement of the multiorgan system failure, the patient presented for valve replacement and worsening congestive heart failure (CHF). Para- and quadriplegic patients rarely undergo cardiac surgery requiring cardiopulmonary bypass (CPB). The explanation for this low incidence of heart surgery in this patient population ranges from physiologic changes from the spinal cord injury to their relatively short life span. Therefore, there is no vast knowledge of how these patients with spinal cord injury will physiologically respond to CPB. Chronic paraplegia presents unique anesthetic and perfusion challenges. General anesthesia for a patient with prolonged spinal cord damage can be difficult because of dysreflexia, muscle wasting, and potassium changes with depolarizing muscle relaxants. For the perfusionist, chronic paraplegia also accentuates hemodynamic responses to nonpulsatile flow with low peripheral vascular resistance common and difficult to treat. Dramatic increases in circulating catecholamine levels are a secondary result of the initiation of CPB that can cause a hypo- and hypertensive state. Depending on the level of spinal cord injury, one might expect acute hypo- or hypertension with the various phases of open-heart surgery and CPB. A viscous circle may occur because the hypertensive state is exaggerated because of inhibitory signals not passed below the spinal cord lesion and, therefore, the vasoconstrictive reflex continues unabated. The attack usually occurs abruptly and can lead to cerebrovascular hemorrhage and death if not controlled. Fortunately, we found this patient did not develop mass autonomic dysreflexia and was not difficult to wean from CPB. The problems associated with spinal cord injury present potential complications to this patient population. Numerous triggering mechanisms may lead to a variety of clinical complications. Consideration of a response/treatment management plan for potential problems must be exercised by the surgical team.