Abstract
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.
Highlights
For a long time, portal venous gas (PVG) has been considered to be a sign of poor prognosis in abdominal diseases [1, 2]
PVG-causing intestinal pneumatosis (IP) can be broadly classified into IP caused by intestinal wall infection with gas-producing bacteria and IP caused by mechanical rupture of the intestinal mucosal wall [4, 5], no report has clearly described the actual processes of the conditions by using histological findings
We report a summary of the pathogenic mechanisms and primary diseases, as well as therapeutic strategies and prognosis, in these two cases, along with a brief literature review
Summary
Portal venous gas (PVG) has been considered to be a sign of poor prognosis in abdominal diseases [1, 2]. When PVG is caused by intestinal necrosis due to ischemia, the mortality rate is high even after emergency laparotomy with intestinal resection [1, 3]. PVG-causing intestinal pneumatosis (IP) can be broadly classified into IP caused by intestinal wall infection with gas-producing bacteria and IP caused by mechanical rupture of the intestinal mucosal wall [4, 5], no report has clearly described the actual processes of the conditions by using histological findings. We report a summary of the pathogenic mechanisms and primary diseases, as well as therapeutic strategies and prognosis, in these two cases, along with a brief literature review
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