Abstract
Vasoplegia syndrome (VS) is seen in cardiac surgery post-cardiopulmonary bypass (CPB) and defined by increasing requirements for more than one vasoactive agent to which the patient's response is reduced. It is also associated with normal or high cardiac output (CO). Prolonged CPB time is the second commonest precipitating factor. Here, we describe a young adult, with good right ventricular (RV) and left ventricular (LV) function, who previously was a renal transplant recipient with a functioning kidney who developed VS and shock after CPB to replace the mitral and aortic valves. During the first two hours of CPB, his mean arterial blood pressure (MAP) was never lower than 50 mmHg. His brain regional cerebral oxygen saturation (rSO(2)) remained above baseline, and his body temperature was kept at 33 degrees C. Urine output was constant at 40 ml/hr. He came off CPB requiring two inotropes and two vasoconstrictors. Even so, his systolic blood pressure was low, and his pulse pressure narrows. He was then started on methylene blue which improved his MAP. On arrival to the intensive care unit (ICU), he immediately required continuous veno-veno haemodialysis (CVVHD) and developed acute liver failure. At 16 hours, he showed a clinically fair neurological recovery. Forty-eight hours post-surgery, he suffered multiorgan failure and developed an intractable arrhythmia and died. The unusual components were as follows: he was normally responsive to phenylephrine during CPB; despite normal rSO(2) and a clinically neurological recovery, he suffered multiorgan failure; and his serial high-sensitivity (HS) troponin I levels never fell below 500,000 pg/ml (normal <14 pg/ml).