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Pathogenic mechanisms of intestinal pneumatosis and portal venous gas: should patients with these conditions be operated immediately?

We aimed to histologically observe portal venous gas (PVG)-causing intestinal pneumatosis (IP) and evaluate pathogenic mechanisms and therapeutic strategies, including decisions on whether emergency surgery should be performed. Autopsy was performed in two cases of nonocclusive mesenteric ischemia (...

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Detalles Bibliográficos
Autores principales: Mitsuyoshi, Akira, Hamada, Shinshichi, Tachibana, Tsuyoshi, Momono, Teppei, Aoyama, Hiroki, Kondo, Yuhei, Inoguchi, Kenta, Yokoyama, Daiju, Nakau, Masayuki, Suzaki, Sato, Okabe, Hiroshi, Yanagibashi, Ken
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4607681/
https://www.ncbi.nlm.nih.gov/pubmed/26943428
http://dx.doi.org/10.1186/s40792-015-0104-7
Descripción
Sumario:We aimed to histologically observe portal venous gas (PVG)-causing intestinal pneumatosis (IP) and evaluate pathogenic mechanisms and therapeutic strategies, including decisions on whether emergency surgery should be performed. Autopsy was performed in two cases of nonocclusive mesenteric ischemia (NOMI). We directly histologically observed the pathogenic mechanisms of IP caused by gas-producing bacteria and IP considered to be caused by mechanical damage to the intestinal mucosa. IP can be classified hypothetically into the following types according to pathogenesis: (1) infection, (2) rupture (damage) of the intestinal mucosa + increased intestinal intraluminal pressure, and (3) mixed type. In cases of IP caused by gas-producing bacteria or IP associated with intestinal wall damage extending beyond the mucosa to the deep muscular layer, emergency surgery should be considered. However, it is highly possible that patients who test negative for infection with gas-producing bacteria whose intestinal wall damage remains only in the mucosa can be conservatively treated.