CASE REPORT Budd–Chiari syndrome, ascites and shunt malfunction due to hyperosmolar hypernatremia in operated pediatric craniopharyngiomas: a red herring Sunil V. Furtado & P. K. Dash & K. Reddy & A. S. Hegde Received: 3 December 2007 / Published online: 19 March 2008 # Springer-Verlag 2008 Abstract Introduction Postoperative management of sellar and suprasellar lesions in children involves regular evaluation of fluid, electrolyte, and neuroendocrine parameters. On discharge, maintenance of water homeostasis is difficult especially among those with access to only basic primary health care. Complications of a chronic hypernatremic state can lead to severe morbidity and mortality. Cases The authors present two cases of craniopharyngioma who developed inferior vena cava thrombosis, Budd–Chiari syndrome, and shunt malfunction postoperatively. Factors which predispose to a hypercoagulable state are evaluated along with measures undertaken to identify and treat the cause of ascites and shunt malfunction. Discussion The role of hypernatremia, serum hyperosmo- lality, and Vasopressin analogs in the pathology are discussed along with imaging and treatment. Keywords Craniopharyngioma . Budd–Chiari syndrome . Hydrocephalus . Ascites Introduction Sellar and suprasellar lesions account for 20–30% of pediatric brain tumors [8].The postoperative period in patients operated for these tumors is marked by fluid, electrolyte and hormonal imbalance, growth, behavioral and cognitive changes [14]. Consequently, many children have decreased motor activity. Because the hemostatic system is mature in older children, only a hereditary deficiency of an innate anticoagulant or an underlying systemic disease can make them prone to venous thrombosis [12]. Case report Case 1 A 4-year-old boy underwent subtotal excision of a craniopharyngioma in November 2003. He underwent further excision of the lesion with Ommaya reservoir placement and a ventriculoperitoneal shunt in August 2005. He presented in December 2005 with oliguria and abdominal distension (abdominal girth, 52 cm). Protein level in the ascitic fluid was high (Table 2). An ultrasonogram (USG) and computed tomogram (CT) scan of the abdomen revealed an enlarged liver with normal spleen, massive ascites, and a thrombus in the intrahepatic segment of inferior vena cava (IVC; Fig. 1). Magnetic resonance venogram (MRV) and an IVC angiogram showed intrahepatic IVC thrombosis, 8 cm in length and involving 70% of the lumen. The area was dilated with 12×4-mm Meditech balloon (Boston Scientific Corporation, Waterdown, MA, USA). A resultant residual stenosis of 30% was achieved. The child was again symptomatic in February 2006 with ascites, headache, and vomiting. On examination, he was dull and apathetic. The IVC segment had rethrombosed, with 80% occlusion of lumen. A self expandable 14×60-mm Childs Nerv Syst (2008) 24:1051–1055 DOI 10.1007/s00381-008-0629-1 S. V. Furtado (*) : A. S. Hegde Department of Neurosurgery, Sri Satya Sai Institute of Higher Medical Sciences, EPIP Area, Whitefield, Bangalore 560066, India e-mail: sunilvf@gmail.com P. K. Dash Department of Cardiology, Sri Satya Sai Institute of Higher Medical Sciences, Bangalore, India K. Reddy Department of Radiology, Sri Satya Sai Institute of Higher Medical Sciences, Bangalore, India