Pyun Dae Keun, Kim Kyung Jo, Ye Byong Duk, Byeon Jeong Sik, Myung Seung Jae, Yang Suk Kyun, Kim Jin Ho, Yoon Sang Nam
Department of Internal Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
Korean J Gastroenterol. 2009 Sep;54(3):180-5. doi: 10.4166/kjg.2009.54.3.180.
Several forms of colonic complications are rarely observed during the clinical course of acute pancreatitis, and potentially fatal in some cases. Colonic lesions associated with acute pancreatitis can be divided into several groups from a pathogenic point of view. Possible pathogenesis includes: 1) spread of pancreatic enzymes through the retroperitoneum to mesocolon, causing pericolitis, 2) external inflammatory compression by mesocolic mass secondary to necrosis of fatty tissue, and 3) hypotension due to shock, and thrombosis of mesenteric arteries. These might lead to colonic infarction, fistula formation, perforation, and obstruction during follow-up. We report two cases of colonic obstruction following acute pancreatitis with possible different mechanisms and review Korean cases. One patient developed colonic obstruction due to severe necrotizing pancreatitis, possibly as a result of pericolitis, and the other developed stenosis as a result of ischemic colitis induced by acute pancreatitis.
在急性胰腺炎的临床过程中，几种形式的结肠并发症很少见，但在某些情况下可能致命。从发病机制的角度来看，与急性胰腺炎相关的结肠病变可分为几组。可能的发病机制包括：1）胰腺酶通过腹膜后扩散至结肠系膜，引起结肠周炎；2）脂肪组织坏死继发的结肠系膜肿块造成外部炎性压迫；3）休克导致的低血压和肠系膜动脉血栓形成。这些情况可能导致随访期间出现结肠梗死、瘘管形成、穿孔和梗阻。我们报告两例急性胰腺炎后结肠梗阻的病例，其机制可能不同，并回顾韩国的相关病例。一例患者因严重坏死性胰腺炎导致结肠梗阻，可能是结肠周炎的结果，另一例患者则因急性胰腺炎诱发的缺血性结肠炎导致狭窄。
