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Gastric necrosis and perforation as a complication of splenectomy. Case report and related references.

Abstract
Necrosis of the stomach after isolated splenectomy with the formation of gastrocutaneous fistula is a rare event that occurs in less than 1% of splenectomies. It is more frequent when the removal of the spleen is done because of hematological diseases. Its mortality index can reach 60% and its pathogenesis is controversial, as it may be attributed both to direct trauma of the gastric wall and to ischemic phenomena. Although the stomach may exhibit exuberant arterial blood irrigation, anatomical variations can cause a predisposition towards the appearance of potentially ischemic areas, especially after ligation of the short gastric vessels around the major curvature of the stomach. Once this is diagnosed in the immediate postoperative period, it becomes imperative to reoperate. The surgical procedure will depend on the conditions of the peritoneal cavity and patient's clinic status. The objective of this study was to report on the case of a patient submitted to splenectomy because of closed abdominal traumatism, who then presented peritonitis and percutaneous gastric fistula in the post-operative period. During the second operation, perforations were identified in anterior gastric wall where there had been signs of vascular stress. The lesion was sutured after revival of its borders, and the patient had good evolution. Prompt diagnosis and immediate treatment of this unusual complication are needed to reduce its high mortality rate.
AuthorsC A Martinez, J Waisberg, R T Palma, S H Bromberg, M A Castro, P A Santos
JournalArquivos de gastroenterologia (Arq Gastroenterol) 2000 Oct-Dec Vol. 37 Issue 4 Pg. 227-30 ISSN: 0004-2803 [Print] Brazil
PMID11460603 (Publication Type: Case Reports, Journal Article)
Topics
  • Adolescent
  • Female
  • Gastric Fistula (etiology)
  • Humans
  • Necrosis
  • Peritonitis (etiology)
  • Reoperation
  • Splenectomy (adverse effects)
  • Stomach (pathology)
  • Stomach Rupture (etiology)

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