In Situ Split Liver Transplantation using a Donor with a Recent History of HELLP Syndrome

Abstract

HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count) is a complication of pregnancy characterized by microvascular endothelial cell damage and intravascular platelet activation leading to periportal necrosis and intrahepatic hemorrhage, subcapsular hematoma formation and hepatic rupture (1, 2). Although the liver is a primary target, most patients recover without permanent liver injury and the leading cause of death is cerebral hemorrhage. This leads to some such patients being considered as organ donors (3). We report a 42-year-old woman who developed HELLP syndrome at 32-weeks gestation and underwent Cesarean section at 36-weeks. She recovered well and the liver tests normalized; however, on day 14 postpartum she suffered a subarachnoid hemorrhage and became brain dead. At the time of organ procurement, the liver appeared macroscopically normal, she was hemodynamically stable with minimal inotropes and the liver tests were entirely normal (total Bilirubin 8 μmol/L, AST 16 U/L, ALT 14 U/L, ALP 80U/L). Donor weight was 60Kg. An in situ split was performed and the segment 2/3 graft transplanted into a 1year old with biliary atresia. Ischemic time was 11 hr. The recipient INR and AST peaked at 3.3 and 1360 U/L respectively on postoperative day (POD) 2. A biopsy at that time demonstrated diffuse hepatic swelling with numerous apoptotic and degenerate hepatocytes. The tests normalized by POD 7 and the recipient remains well 2 years later. The right lobe was shipped to another center and transplanted into a 64 year old, 65 Kg male with Hepatitis B cirrhosis and a 5 cm hepatocellular carcinoma previously treated with intra-arterial radioactive I131. The graft to recipient weight ratio was 0.8 and ischemic time was 8.45 hr. The patient developed severe early graft dysfunction with a peak INR of 5.3 on POD 2, encephalopathy and renal failure requiring dialysis. He remained cholestatic and suffered from chest infection requiring re-intuabation. Early Doppler ultrasounds showed a normal arterial signal (RI 0.7) but the day 11 the RI fell to 0.22 and an angiogram the following day demonstrated hepatic artery thrombosis. The recipient died of sepsis on POD 39. Many centers have been reluctant to transplant livers from donors with HELLP syndrome because preservation injury may exacerbate the condition (4). Recently a few successful cases have been reported, in which the livers appeared normal macroscopically and biopsy revealed only minimal hepatocellular necrosis or steatosis (5–7). In our case the donor liver appeared normal at organ procurement and fulfilled our criteria for splitting. Because of this no biopsy was done but in retrospect a biopsy may have been helpful (5, 6). Despite fulfilling splitting criteria, both grafts developed moderate to severe early graft dysfunction. The right lobe recipient developed multiple complications including delayed hepatic artery thrombosis and died of sepsis. Small-for-size syndrome may have contributed to the poor outcome in this case. Nevertheless this experience suggests that the liver from a donor with HELLP syndrome, even after apparent full recovery, may be more vulnerable to preservation injury and should be regarded as ‘marginal' and not ideally suitable for splitting. Motohiko Yasutomi John McCall Stephen Munn New Zealand Liver Transplant Unit Auckland City Hospital Auckland, New Zealand Meindert Sosef Michael Crawford Australian National Liver Transplant Unit Royal Prince Alfred Hospital New South Wales, Australia