The abdomen was opened through a midline incision. The bleeding was found to be emanating from a ragged laceration on the anterior aspect of the right lobe of the liver which was fully accessible without the need for mobilisation of the liver (figure 2). Coagulopathy prevented haemostasis OSI-906 concentration by electro-cautery or using topical agents and thus haemostasis was secured by packing the liver with gauze swabs placed above and around the liver in a routine manner. A hysterotomy and removal of a non-viable fetus was also performed. The abdomen was closed with interrupted PDS sutures to the fascia and clips to the skin

without undue difficulty. A second-look laparotomy was performed at 48 hours at which stage the swabs were removed and a liver biopsy taken with a Tru-cut biopsy needle. There was no evidence

of abdominal compartment syndrome at any stage. Figure 2 Intraoperative finding of a large liver haematoma overlying the infero-lateral border of the liver. Her post operative course was check details eventful in that she developed multi-organ failure requiring a two week stay in the intensive care unit with renal replacement therapy, mechanical ventilation and vasopressor support. Fortunately, she made a prompt recovery and was discharged home on day 20. She was counselled against attempting to get pregnant again in view of the risk of recurrence of the HELLP syndrome. Hepatic biopsy revealed massive hepatic necrosis explaining see more the patients liver failure (figure 3). Figure 3 Hepatic biopsy showing patchy ballooning of surviving hepatocytes in Zone 1 and coagulative necrosis. Discussion With only 200 cases

of hepatic rupture documented in the global literature, it is not surprising that few doctors have experience in dealing with this condition [1]. Aetiology In the Tennessee Classification System, diagnostic criteria for HELLP are haemolysis with increased LDH (> 600 U/L), AST (≥ 70 U/L), and platelets < 100 × 109/L. The pathophysiology of this condition is complex and poorly understood. The origin of pre-eclampsia/HELLP can be attributed to defective trophoblastic invasion. As a consequence of this trophoblastic dysfunction, a desirable high flow, low resistance circuit for adequate placental function fails to develop. It appears that the fundamental component of this situation is abnormal placental cyclo-oxygense activity. COX 1 activity remains the same in the placenta however, COX 2 expression is decreased [2]. The net result of this is preferential production of thromboxane, a potent vasoconstrictor and mediator of platelet aggregation over prostacyclin. As a consequence of this vasoconstrictive stimulus, and increased afterload on the heart secondary to uteroplacental dysfunction, mean arterial pressure increases. Hypertension, in addition to thromboxane causes endothelial dysfunction in the maternal vasculature particularly in the organs with highest blood flow (liver, kidneys, brain).