Sclerosing encapsulating peritonitis in a child secondary to peritoneal dialysis

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Abstract

Sclerosing encapsulating peritonitis, or “abdominal cocoon,” is a rare but serious complication of continuous ambulatory peritoneal dialysis. It is characterized by the diffuse appearance of marked sclerotic thickening of the peritoneal membrane resulting in intestinal obstruction.

A 14-year-old adolescent boy with a history of end-stage renal failure on continuous ambulatory peritoneal dialysis presented with symptoms of acute intestinal obstruction. A computed tomography scan of the abdomen revealed distended small bowel loops clustered and displaced to the right upper quadrant. The overlying peritoneum was markedly thickened and calcified. Laparotomy confirmed the diagnosis of sclerosing encapsulating peritonitis and the patient was treated with excision of the fibrocollagenous membrane. Postoperatively, he had prolonged ileus requiring parenteral nutritional support and peritoneal dialysis was restarted on postoperative day 10.

A high degree of cognizance is needed to facilitate diagnosis and treatment of this uncommon and potentially life-threatening condition.

Section snippets

Case report

A 14-year-old Chinese adolescent boy with a history of end-stage renal failure on CAPD presented with right-sided abdominal distension, abdominal pain, vomiting, and absolute constipation of 2 days' duration. He had been diagnosed with end-stage renal failure secondary to acute tubular necrosis as a result of a bout of severe gastroenteritis in infancy. Peritoneal dialysis using hypertonic dextrose was commenced 10 years ago and used almost continuously, interrupted by 6 episodes of bacterial

Discussion

The etiology of SEP is poorly understood but is believed to be multifactorial. Although seen most frequently as a complication of CAPD, this condition is not specific to CAPD. Other causes implicated include drug therapy (particularly β-blockers), sarcoidosis, systemic lupus erythematosus, abdominal tuberculosis, gastrointestinal malignancy, protein S deficiency, and luteinized ovarian thecomas [4], [5], [6], [7]. Regardless of the predisposing causes, the most plausible pathophysiological

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