Although effective antiviral therapies have been made available for neonatal herpes simplex virus (HSV) disease, recent data demonstrate that no progress has been made in decreasing the interval between onset of HSV symptoms and initiation of antiviral therapy [4]. We report a case of fatal neonatal HSV 2 infection presenting with fulminant hepatic failure despite an uneventful medical history concerning maternal HSV 2 infection and caesarean section before rupture of the membranes for suspected maternal appendicitis. Neonatal HSV 2 infection via maternal viraemia must be taken into the differential diagnosis of acute liver failure in newborns despite an unremarkable medical history concerning HSV 2 infection. To improve outcome, early antiviral treatment is warranted in these infants. A male Afro-American infant was delivered at 37 weeks of gestation by caesarean section, weighing 2.65 kg and subsequently breast-fed. Caesarean section was performed prior to rupture of membranes for suspected maternal acute appendicitis. There was no history of maternal primary herpetic genital lesions. Post partum, the mother continued to have fever for 3 days. Histopathological examination of the appendix, however, did not show any signs of acute inflammation. The family history was uneventful, except for portal vein thrombosis of unknown origin in the father. The mother and the infant were discharged home on day 3, but the neonate was readmitted to a community hospital on day 10 because of hyperpyrexia (39.4 C), poor feeding and umbilical cord bleeding. Due to the development of generalised bleeding, the infant was thereafter transferred to our hospital for suspected sepsis. On admission, the infant was in a collapsed state with multiple haematomas. No oral or vesicular lesions were noted. The grossly enlarged liver was of increased consistency. The patient required ventilation and inotropic support. He was treated with broad-spectrum antibiotics. Initial investigations showed the white blood cell count was 3700/ll with neutropenia (29% neutrophils), thrombocytopenia 18000/ll and anaemia (haemoglobin 9.5 g/dl; reticulocyte count 13 &), and profound coagulopathy compatible with disseminated intravascular coagulation (PTZ 6%; thrombin time 76 s; activated PTT >140 s, fibrinogen <20 mg/dl; d-dimers 6.45 mg/l). Liver function test results showed the following serum concentrations: cholinesterase 2.43 kU/l, total bilirubin 7.6 mg/dl, conjugated bilirubin 1.83 mg/ dl, albumin 24 g/l, glutamic pyruvic transaminase 2232 U/l, glutamate dehydrogenase 3469 U/l, gammaglutamyltransferase 261 U/l, lactate dehydrogenase 13340 U/l, and ammonia 350 lg/dl. The C-reactive protein was 17.5 mg/l and procalcitonin 2.2 ng/ml. On admission, the blood glucose concentration was 94 mg/ dl; no glucosuria was noted. The patient had severe lactic acidosis (lactate 11.2 mmol/l). Serum ferritin was excessively elevated (124840 ng/ml) with a serum iron of 471 lg/dl. HSV 1 (PCR was available within 24 h), hepatitis A, B, and C virus, Epstein-Barr virus, human immunodeficiency virus 1 and 2, enterovirus, and cytomegalovirus infections were excluded using virological or serological methods. On ultrasonography, portal vein thrombosis was suspected in this infant. Despite intensive supportive care consisting of substitution of platelets, fresh frozen plasma, prothrombin complex concentrate, and the administration of sodium benzoate, carnitine, and N-acetylcysteine, the clinical course was aggravated by renal failure which required haemodialysis. The patient was proposed for liver transplantation but died on day 5 after admission to our hospital secondary to multiple organ failure. Pathological analysis of the liver S. Meyer (&) AE A. Baghai AE G. Loffler AE L. Gortner AE S. Gottschling Department of Neonatology and Paediatric Intensive Care Medicine, University Children’s Hospital of the Saarland, Kirrbergerstrasse, 66421 Homburg, Germany E-mail: sascha.meyer@uniklinik-saarland.de Tel.: +49-6841-1628374 Fax: +49-6841-1628363