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ABDOMINAL PARACENTESIS RESTORING VENTRICULOPERITONEAL (VP) SHUNT FUNCTION IN AN OBTUNDED PATIENT
N Ahmed, P Wong
McGill University, Division of Gastroenterology, Montreal Quebec
INTRODUCTION: Distal VP shunt obstruction can be caused by cerebrospinal fluid (CSF) infection, abdominal pathology (such as bowel obstruction, perforation, and pancolitis) or improper abdominal shunt placement. We describe a case of distal shunt obstruction secondary to malignant ascites.
Case: A 48 year old male was admitted to the ICU with increasing headaches and confusion. Three years previously he underwent a lobectomy and chemotherapy for adenocarcinoma of the lung. Approximately 3 months prior to the present admission he developed headaches and confusion. A head CT scan revealed hydrocephalus. An MRI demonstrated nodular enhancement of his meninges suggestive of widespread leptomeningeal metastases. A VP shunt was placed with resolution of his hydrocephalus. Cytology from his CSF was negative.
Approximately 1 month prior to his present admission, routine blood work demonstrated a cholestatic liver enzyme pattern with ALP 192 and GGT 601, but normal bilirubin. Abdominal ultrasonography was normal. Over three weeks the patient noted increasing abdominal girth and the development of headaches and confusion. He presented to the hospital and was transferred to the neurosurgery service; a CT scan demonstrated significant acute hydrocephalus of lateral and third ventricles. The patient’s intra-abdominal pressures were markedly elevated (measured by urinary bladder pressures). Physical examination demonstrated the presence of significant ascites, which had not been present on the ultrasound. The GI service was consulted, and it was agreed that an abdominal paracentesis was warranted to urgently decompress and potentially restore VP shunt function. Two litres were removed and the patient regained consciousness with rapid return of baseline neurological function. Ascitic fluid studies demonstrated a SAAG of only 6, suggesting a non-portal hypertensive etiology, with a significant neutrophilia of 620, consistent with peritonitis. He was started on empiric ceftriaxone, and an abdominal CT scan demonstrated intense peritoneal reaction consistent with carcinomatosis. The peritoneal fluid samples were sent for cytology, but were lost. However, the CSF sample from the VP shunt demonstrated adenocarcinoma consistent with his lung pathology. Unfortunately, despite maximal medical therapy, the patient continued to decline and he expired.
CONCLUSION: This case report highlights the possibility that significant ascites (in this case, malignant) can produce increased intra-abdominal pressures and VP shunt dysfunction. Restoration of normal intra-abdominal pressures returned the patient to an awake and alert neurological status.