A 62-years-old man had hepatocellular carcinoma (HCC) on top of chronic HCV. The patient previously underwent esophageal variceal ligation. The patient was on warfarin treatment for portal and superior mesenteric vein thrombosis. At the time of admission, he had massive ascites and the Child-Pugh classification was B. The patient underwent LDLT and splenectomy in December 2010. A left lobe was used as a graft harvested from his brother. After LT, the patient was readmitted several times to our clinic due to cholangitis secondary to anastomotic biliary strictures and was managed by percutaneous transhepatic biliary drainage (PTBD) and balloon dilatation. Eight months after transplant, he returned with a complaint of nausea, vomiting, and abdominal distension. The laboratory values were: white blood cells (WBCs) 6.7×10⁹/L, hemoglobin (Hb) 10 g/dl, platelet count (PLT) 348,000/µl, aspartate transferase (AST) 39 IU/L, alanine transferase (ALT) 32 IU/L, gama-glutamyl-transferase (GGT) 295 IU/L, alkaline phosphatase (ALP) 1,094 IU/L, total bilirubin (T.bil) 0.7 mg/dl, creatinine (Cr) 1.5 mg/dl, and C-reactive protein (CRP) 2.6 mg/dl. An abdominal computed tomography (CT) scan revealed remarkable ascites, thickening of the peritoneum, fibrous membranes surrounding the small intestine leading to paralytic ileus, and eventually mechanical intestinal obstruction (Fig. 1). The CT scan findings were consistent with SEP. On laparotomy, we found the small intestine encapsulated by a fibrous membrane. We removed the fibrous membrane, and subsequently, total adhesiolysis and enteroclysis were performed (Fig. 2A, B). The postoperative course was uneventful, and the patient was discharged.

A 54-years-old man suffered from chronic HCV infection and was a chronic carrier of Human T-Cell Lymphotropic Virus (HTLV). At the time of admission, a huge HCC was detected in the right liver lobe that was complicated with portal vein thrombosis (PVT), and lung metastases during his surveillance in 2007. After receiving two cycles of interferon/5-fluorouracil (IFN/5FU) therapy by hepatic artery infusion, the tumor shrank and follow-up chest CT images had been negative since then. Right hepatectomy was performed. In 2008, the patient underwent splenectomy to increase platelets count. In August 2014, the patient underwent LDLT for end-stage of liver disease secondary to liver cirrhosis and the Child-Pugh classification was B. Right lobe liver graft was used. The postoperative course was uneventful and the patient was discharged. On the 59th postoperative day, the patient developed fever and abdominal pain. Further examination revealed hepatic artery pseudoaneurysm and intraabdominal fluid collection. Coiling embolization and fluid collection drainage were performed. Enterococcus was detected in the sampled drained fluid. In July 2015, the patient had repeated ileus episodes. Abdominal CT scan revealed small intestinal loops encased by a fibrous sheath with secondary ileus (Fig. 3). The laboratory values were: WBC 7.7×10⁹/L, Hb 11.5 g/dl, PLT 337,000/µl, AST 21 IU/L, ALT 16 IU/L, ALP 397 IU/L, GGT 56 IU/L, T.Bil 0.4 mg/dl, D.Bil 0.1 mg/dl, albumin 2.7 g/dl, Cr 0.9 mg/dl, and CRP 0.2 mg/dl. The patient did not respond to conservative treatment, and could not tolerate oral feeding, so we decided to perform surgery. An exploratory laparotomy revealed extensive membranous adhesions in the abdominal cavity. The entire small intestine was wrapped around with the fibrous membrane, consistent with intra-abdominal cocoon (Fig. 4). Subsequently, the fibrous peel was removed and adhesiolysis was performed. The patient's postoperative course was uneventful and he was discharged thereafter.

A 63-years-old man suffered from ESLD secondary to HCV cirrhosis. The patient underwent LDLT in July 2002. Previously, the patient had received interferon and ribavirin treatment for HCV recurrence. Five years after transplant, the patient developed refractory ascites due to PVT, and warfarin administration was started. The patient had suffered from hepatic encephalopathy (HE) in November 2015 and spontaneous bacterial peritonitis (SBP) in February 2016, respectively. The patient developed portal hypertension and chronic liver disease. The liver function was poor, and he was on the waiting list for cadaveric liver transplantation. The Child-Pugh classification was C. Due to deterioration in condition; he was admitted to the intensive care unit (ICU) in October 2016. He had HE, and his laboratory values were: WBC 4.3×10⁹/L, Hb 9 g/dl, PLT 63,000/µl, AST 19 IU/L, ALT 16 IU/L, GGT 26 IU/L, ALP 360 IU/L, T.bil 1.5 mg/dl, CRP 0.7 mg/dl, Cr 1.5 mg/dl, and PT/INR 1.9. Blood ammonia level was 193 µg/dl. An abdominal CT revealed ascites, splenomegaly, and PVT with collateral veins. The CT scan also showed the presence of a fibrous sheath around the intestine with intestinal dilatation (Fig. 5). According to these findings, a diagnosis of the abdominal cocoon was made. We considered doing a surgical intervention but the liver function and clinical condition of the patient worsened and unfortunately, we lost the patient.

A 60-year-old man had ESLD due to liver cirrhosis secondary to chronic HCV. He underwent LDLT in July 2003. Ten years after LT, a relapsing HCV episode was treated with interferon administration. Recurrent episodes of cholangitis due to biliary stricture, with hepaticojejunostomy, carried out. In 2014, the patient was diagnosed with diabetes mellitus, coronary artery disease, and chronic kidney disease. Subsequently, he underwent coronary artery stenting and peritoneal dialysis. In December 2016, the patient experienced abdominal pain, nausea, and vomiting. Abdominal CT revealed ascites, small bowel dilatation, and peritoneal wall inflammation consistent with sclerosing peritonitis (Fig. 6A). The patient was admitted to our clinic, and conservative therapy was started (oral intake was stopped, a nasogastric tube was placed for decompression, and intravenous fluid was given). At the time of admission, his laboratory values were: WBC 4.5×10⁹/L, Hb 8.6 g/dl, PLT 86,000 /µl, AST 45 IU/L, ALT 39 IU/L, GGT 210 IU/L, T.bil 1.0 mg/dl, D.bil 0.7 mg/dl, albumin 2.7 g/dl, PT/INR 1.05, Cr 5.95 mg/dl, and CRP 0.5 mg/dl. Despite conservative treatment, no improvement in the patients' conditions was observed. Repeated abdominal CT showed that contrast material did not pass through the colon, and the ileus continued (Fig. 6B). Surgery was decided and laparotomy was performed. At laparotomy, we found dense, thick fibrotic peel wrapping loops of small bowel (Fig. 7). After the excision of the peel, an edematous appearance of the affected ileal loops was found and multiple serosal injuries occurred during dissection. Around 30 cm of the affected ileal segment was resected and end-to-end anastomosis was performed. The patient developed fever and abdominal pain on the 8th postoperative day, and on further examination, an anastomotic leakage was detected. The patient was reoperated, and ileostomy and abdominal washing were performed. The postoperative course was uneventful, and the patient was discharged. After 3 months, the patient was readmitted and the stoma was closed.