Sclerosing Peritonitis After Kidney Transplantation: A Not-So-Silky Cocoon

Abstract

A 55-year-old woman with end-stage renal disease secondary to systemic lupus erythematosus had undergone two renal transplants over a 15-year period. Of note, her renal replacement between the two transplants was via peritoneal dialysis for a 5-year period while she awaited a deceased donor kidney. Her past medical history was also significant for hypertension, hyperlipidemia, anemia, and depression. Following her second successful kidney transplant, she had persistent nausea and vomiting, which she considered similar to her preoperative state and not disruptive to her daily activities. She was admitted to a community hospital several months following the transplant complaining of worsening vomiting over 3 weeks. She also experienced early satiety, belching, epigastric fullness, crampy abdominal pain and daily watery stools, and she had lost 30 lb over the preceding months. At the time of admission, her creatinine was elevated at 2.2 mg/dl, but corrected to 1.3 mg/dl with hydration. A computed tomography (CT) scan demonstrated edema of the bowel wall and a pelvic fluid collection. Upper endoscopy revealed mild duodenitis, gastritis, and an atonic and dilated stomach. She was transferred to Stanford University Medical Center with the preliminary diagnosis of gastroparesis. On our exam, she had a firm, mildly distended, but nontender abdomen. Total parenteral nutrition (TPN) was initiated. A gastric emptying study was attempted, but could not be completed due to vomiting. Repeat CT scan showed a large fluid collection in the abdomen and pelvis with a thick enhancing wall (Figs. 1, 2). There was also dilation of the duodenum and stomach with an abrupt transition at the proximal jejunum consistent with mechanical obstruction due to sclerosing peritonitis (Fig. 3). The interventional radiology team placed a drain in the abdomen and 1 l of sterile serosanguineous fluid was extracted. A nasogastric tube was placed for bowel decompression. Repeat endoscopy did not demonstrate any obstruction at the proximal jejunum, but did reveal reflux esophagitis. An upper GI series with small bowel followthrough then revealed high-grade obstruction at the level of the proximal jejunum (Fig. 4). Given the high-grade obstruction and her failure to improve with nonoperative management, she underwent exploratory laparotomy. At surgery, she was found to have thickened peritoneum encasing all of her small bowel. The entire small bowel contents were compressed into a tight ball or ‘‘abdominal cocoon.’’ She also had complete interloop adhesions. One loop of very proximal jejunum in the left upper quadrant appeared particularly kinked, near the site of obstruction that had been observed on the upper GI series. Extensive lysis of adhesions was performed during a 5-h operation. She did not undergo any bowel resection, but from the lysis of adhesions alone, it appeared that 25% of the small intestine had been deserosalized because it was not possible to effectively peal loops of bowel from one another. All of the serosa on the outer surface of the cocoon E. H. Morrow (&) Department of Surgery, Stanford University Medical Center, Palo Alto, CA, USA e-mail: emorrow@stanford.edu