Portal, Mesenteric, and Splenic Vein Thrombosis Following a Splenectomy for Myeloid Metaplasia

Postsplenectomy portal, mesenteric, or splenic vein thrombosis is a rare, but often fatal, complication which may be related to thrombocytosis, abnormal platelet function, and stasis in the splenic vein remnant. In the recent literature, there have been reports concerning portal and mesenteric venous thrombosis complicating splenectomy for hematologic disoders. Many thrombosis have occurred following splenectomy for myeloid metaplasia and have been associated with postsplenectomy thrombocytosis. The vast majority of patients with idiopathic myelofibrosis remain incurable, and current management is directed towards alleviating the symtoms and improving the quality of life. The splenectomy for myeloid metaplasia is palliative and carries a significant morbidity, and mortality. Under these circumstances, repeated assessment of indications, morbidity and duration of patient survival is of importance to physi cians and surgeons participating in the management of myeloid metaplasia. Because of the significant incidence and high mortality of postsplenectoimy thrombosis in myeloid metaplasia, the prophylactic use of anticoagulant agents and antiplatelet drugs and long-term maintenance therapy are necessary. At the time of the splenectomy, an attempt should be made to ligate the splenic vein as close as possible to its junction with the idiopathic myelofibrosis. A small bowel resection is indicated if focal, persistent paralytic ileus of mecanical obstruction occurs.

Portal, Mesenteric, and Splenic Vein Thrombosis Following a Splenectomy for Myeloid Metaplasia

Postsplenectomy portal, mesenteric, or splenic vein thrombosis is a rare, but often fatal, complication which may be related to thrombocytosis, abnormal platelet function, and stasis in the splenic vein remnant. In the recent literature, there have been reports concerning portal and mesenteric venous thrombosis complicating splenectomy for hematologic disoders. Many thrombosis have occurred following splenectomy for myeloid metaplasia and have been associated with postsplenectomy thrombocytosis. The vast majority of patients with idiopathic myelofibrosis remain incurable, and current management is directed towards alleviating the symtoms and improving the quality of life. The splenectomy for myeloid metaplasia is palliative and carries a significant morbidity, and mortality. Under these circumstances, repeated assessment of indications, morbidity and duration of patient survival is of importance to physi cians and surgeons participating in the management of myeloid metaplasia. Because of the significant incidence and high mortality of postsplenectoimy thrombosis in myeloid metaplasia, the prophylactic use of anticoagulant agents and antiplatelet drugs and long-term maintenance therapy are necessary. At the time of the splenectomy, an attempt should be made to ligate the splenic vein as close as possible to its junction with the idiopathic myelofibrosis. A small bowel resection is indicated if focal, persistent paralytic ileus of mecanical obstruction occurs.

Clinicopathological study of adrenal tumors / 대한비뇨기과학회지

From September 1980 to November 1989, eight patients with adrenal tumors had been admitted to our Department of Urology, Chonbuk National University hospital. Nine tumors consisted of 5 adrenal adenomas, 2 pheochromocytomas. a neuroblasloma and adrenocortical cancer. A clinicopathological study was made and the results were obtained as follows : 1. The 8 patients in these series included 2 men and 6 women. Age was ranged from 12 years to 47 years at the lime of presentation (average ; 27.5 years). 2. Four tumors occurred in the right adrenal gland and 5 in the left including a case of bilateral pheochromocytoma. 3. In nonfunctioning tumor (a case of adrenal denoma), the main clinical manifestations were localizing symptoms and signs such as abdominal pain, palpable mass and nonspecific laboratory findings. The others were functioning tumors (2 cases of Cushing`s syndrome due to adrenal adenoma and adrenocortical carcinoma, 2 cases of primary aldosteronism due to drenal demoma, a case of neuroblastoma and 2 cases of pheochromocytoma). There were unique generalized symptoms, signs and laboratory findings due to overproduction of hormones by the tumors 4. Nine adrenalectomies in 8 patients were performed. The weight of resected adrenal mass was 330gm in nonfunctioning adrenal adenoma, 190gm in adrenocortical carcinoma, 5.2gm in Cushing`s syndrome due to derenal adenoma, 2.5gm and 3.2gm in aldosteronism due to adrenal adenoma, 960gm in neurobladstoma, and 85gm, 20gm and 75gm in phepchromocytoma. 5. Results of hormonal assays which were checked 2 days and 2 weeks postoperatively returned to almost normal levels 6. Final characreristic of adrenal tumors could be made mostly by clinical diagnostic procedures, but some of underlying diseases should be differentiated by pathologic confirmation.