According to our review of relevant literature a

According to our review of relevant literature, a large CSF pseudocyst in the anterior extraperitoneal space has not been reported. We investigated the cause of the notch signaling and dislocation of the distal end of the VP shunt catheter. One case report describes a subcutaneous fat pad that slid down in the standing position, dragging the catheter out of the peritoneal cavity. In our case, the distal end of the catheter was exceedingly short, and thus the catheter easily migrated from the peritoneal cavity. Vigorous flexion–extension movement of the head may act as a windlass, facilitating upward movement of the peritoneal catheter. However, dislocation of the VP shunt usually causes it to lose function. In our case, the function of the VP shunt was patent and the large CSF pseudocyst appeared to develop under the relatively lower pressure of the anterior extraperitoneal space, compared with the intracranial pressure, and the CSF dissected the extraperitoneal fascia. Therefore, the large pseudocyst developed gradually.
Introduction Spontaneous biliary perforation is a rare surgical condition in children. It was first reported in 1932 by Dijkstra. Based on a literature review, fewer than 200 cases have been reported in the medical literature. This condition typically presents in infants aged 1–12 weeks and is extremely rare in late infancy and childhood. The cause is idiopathic. Trauma and Choledochal cyst are two differential diagnoses that are ruled out in a child presenting with spontaneous biliary perforation. Preoperative diagnosis and management of the condition is difficult. Early and limited surgical intervention to achieve adequate external biliary drainage produces optimal results. Herein, we report a rare case of a 7-year-old boy with spontaneous biliary perforation and discuss the dilemma in its management.
Case report Laparotomy showed bilious ascites (∼200 mL, mostly in the Morrison\'s pouch) with mucus flakes over the gallbladder and in the Calot\'s triangle (Fig. 1). A perforation was observed in the CBD, immediately inferior to its junction with the cystic duct (Fig. 1). The patient underwent cholecystectomy, thorough abdominal lavage, and external biliary drainage with a T-tube after flushing of the bile duct. The rest of the abdominal viscera were normal. The patient was administered third generation cephalosporin in the postoperative period. On the 7th postoperative day, the patient developed central abdominal pain, distension and episodes of vomiting that were initially managed conservatively. There was a recurrence of obstructive symptoms on the 16th postoperative day, which necessitated a second exploratory laparotomy. Numerous interloop small bowel adhesions were revealed. Adhesiolysis was performed. The postoperative period was uneventful. The T-tube was clamped intermittently, beginning 3 weeks after the first surgery. T-tube cholangiogram was performed at 4 weeks and revealed normal intra- and extrahepatic biliary system (normal calibre biliary system), the absence of an anomalous pancreaticobiliary duct junction (APBDJ), no filling defects, free flow into the duodenum and no extravasation of dye. The T-tube was subsequently removed. Eventual recovery was favorable and liver function tests remained normal at the 3-year follow-up.
Discussion Spontaneous perforation of the nondilated biliary apparatus is extremely rare, especially after age 4 years. Peak incidence is reported in the first year of life. In our case, the patient was age 7 years, which is an extreme rarity. The etiology of spontaneous biliary perforation remains elusive. The presumed obstruction causing the perforation was due to biliary sludge, inspissated bile, stones, or stenosis of the ampulla of vater with increased ductal pressure in 25% of cases. In addition APBDJ has been postulated to contribute to the etiology. APBDJ is also an etiological factor for the origin of choledochal cyst. The disease may be associated with sepsis and incompatibility of the ABO blood group in neonates. Congenital weakness of the bile duct, the presence of a diverticulum, pancreatitis, viral infection of the bile duct, tuberculosis, and necrotizing enterocolitis are other proposed risk factors.