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Splenic peliosis: case report A 43-year-old man developed splenic peliosis during immunosuppressive treatment with hydrocortisone, mycophenolate mofetil, prednisolone and tacrolimus [not all routes and dosages stated; time to reaction onset not stated]. The man underwent deceased donor liver transplantation for cryptogenic decompensated chronic liver disease in 2018. Initially, he received immunosuppression with IV hydrocortisone 100mg and oral tacrolimus. It was followed by a direct taper to 20mg of prednisolone from postoperative day 2 [initial dose not stated]. Later, the dose of tacrolimus was gradually increased to maintain trough levels between 7 and 10. On post-operative day 4, he started receiving mycophenolate mofetil. On postoperative day 5, he had high drain output and prerenal acute kidney injury. Therefore, dose of tacrolimus was reduced and he received unspecified albumin and crystalloids. He developed a sudden onset shortness of breath on postoperative day 13. He also developed acute abdominal distension and pain in the left hypochondrium, which exacerbated by movement. On physical examination, he was apyrexial and exhibited tachycardia and hypotension. Abdominal examination showed tenderness in the left hypochondrium. He was shifted to the emergency care unit and volume resuscitated. An urgent triphasic CT of the abdomen demonstrated a large hematoma in the perisplenic region arising from the upper pole of the spleen with active extravasation of the intravascular contrast from the upper pole of the spleen into the perisplenic haematoma. The spleen revealed a few lacerations extending through the splenic parenchyma and few areas of focal hypoattenuation. The hematoma extended along the left paracolic gutter into his pelvis with high‑density ascites. Thus, the man was taken to the operation theater for re‑exploration. He underwent splenectomy with evacuation of the intra‑abdominal clot. The splenic haematoma weighed 1.28kg. From within his peritoneal cavity, 2000mL of free blood was evacuated. Macroscopically, the spleen was ruptured at its upper pole with active bleeding. Histopathology showed the areas of blood‑filled lakes in the parafollicular region of the splenic red pulp. These blood‑filled vascular spaces did not have any endothelial or epithelial lining. All these findings were consistent with peliosis of the spleen. The ruptured area of the spleen demonstrated neutrophilic infiltration and congestion of the red pulp. He showed spontaneous recovery post splenectomy. Within 48 hours, he was shifted back to the ward and was discharged after 5 days. He was treated with aspirin after a week in view of thrombocytosis. At 6 month follow‑up, he is asymptomatic. Later, it was confirmed that his splenic peliosis was complicated by spontaneous splenic rupture, and it was associated with immunosuppression caused by hydrocortisone, mycophenolate mofetil, prednisolone and tacrolimus. Sonavane A, et al. Splenic peliosis and spontaneous splenic rupture: A rare compli