Infectious Diseases in Clinical Practice:
Department of Medical Gastroenterology, Stanley Medical College Hospital, Chennai, India.
Address correspondence and reprint requests to Joye Varghese, MD, Department of Medical Gastroenterology, Stanley Medical College Hospital, Royapuram, Chennai 600 001, India. E-mail: email@example.com.
A 19-year-old boy with tuberculous meningitis had a ventriculoperitoneal (VP) shunt in August 2005 for an obstructed hydrocephalus. He discontinued antituberculous treatment (ATT). One year later, he presented again with features of intracranial hypertension. The shunt had occluded and was replaced. Antituberculous treatment was restarted. On the fourth postoperative day, the patient developed painless progressive asymmetrical distension of the lower abdomen. Now, on examination, he was afebrile. There was no focal neurological deficit. Abdomen examination showed a localized cystic mass occupying the lower abdomen, pelvis, and either flanks. Shifting dullness and fluid thrill could not be elicited.
Hematologic and biochemical investigations were noncontributory. Chest radiograph was normal. Sonogram of the abdomen revealed 1 large encysted collection with coarse internal echoes occupying almost the entire abdomen and stretching anterior to the great vessels and a smaller second pseudocyst anterior to the left kidney. Computed tomogram confirmed a nonenhancing noncalcified large hypodense cystic lesion measuring 20.3 × 9.6 cm (Hounsfield unit was 15) within the peritoneal cavity extending from the second lumbar vertebra to the pelvis with thin septations (Fig. 1).
The straw-colored cystic fluid on aspiration had a protein content of 4.5 g/dL with several lymphocytes. Culture was negative for microorganisms and acid-fast bacillus. Patient is symptomatically better with ATT and is on follow-up.
Ventriculoperitoneal shunt is a recommended treatment protocol for obstructed hydrocephalus with an intention to divert the excess cerebrospinal fluid (CSF) from the ventricular system to the peritoneal cavity. Physiologically, after shunt procedure, there is minimal or no fluid accumulation within the peritoneal cavity. However, complications are common.1-3 These are CSF loculation and cyst formation resulting in pseudocyst in subphrenic or peritoneal omental cyst, formation of an intractable CSF ascites, bowel obstruction secondary to adhesions, perforation of a bowel resulting in a CSF-enteric fistula, displacement and migration of the shunt, and dissemination of infection or malignancy particularly in drainage for brain tumor. Our patient presented with loculated infected cysts within the peritoneal cavity.
The very first case of an intra-abdominal collection of CSF (pseudocyst) after a VP shunt was reported by Harsh4 in 1954. The overall prevalence of this complication in subsequent series has varied from less than 1% to 4.5%.5,6 The pseudocyst may be the resultant reaction of the intraperitoneal structures to either the catheter or the CSF. High protein content of CSF, shunt infection, subclinical peritonitis, and previous laparotomy are the incriminated factors involved in the pathogenesis of peritoneal pseudocyst.7 Clinically, patients present with nausea, vomiting, abdominal pain, and/or localized distension; shifting dullness is absent, and skiagram of the abdomen reveals displacement of the bowel gas.8
Treatment is surgical: removal and replacement of the obstructed catheter in a different quadrant with or without excision of the pseudocyst wall3 or diversion of CSF into the atrium or pleural cavity and later incorporation of the catheter into the peritoneal cavity.1 Laparoscopic excision of the pseudocyst and repositioning of the catheter into the peritoneal cavity reduces intraperitoneal adhesions and visually confirms the patency of the VP shunt.9-11 Infected cysts require additional antibiotics. Our patient is responding to ATT with regression of the pseudocyst.
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