Pneumatosis intestinalis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
There are two theories on pathogenesis of pneumatois intestinalis. Mechanical theory suggests that gas dissects into the bowel wall from either the intestinal lumen or the lungs via the mediastinum due to some mechanism causing increased pressure. Bacterial theory proposes that gas-forming bacilli enter the submucosa through mucosal rents or increased mucosal permeability and produce gas within the bowel wall. | There are two theories on pathogenesis of pneumatois intestinalis. Mechanical theory suggests that gas dissects into the [[bowel]] wall from either the intestinal lumen or the [[lungs]] via the [[mediastinum]] due to some mechanism causing increased pressure. Bacterial theory proposes that gas-forming [[bacilli]] enter the submucosa through mucosal rents or increased mucosal permeability and produce gas within the bowel wall. | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 07:28, 11 April 2013
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Pneumatosis Intestinalis Microchapters |
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Differentiating Pneumatosis Intestinalis from other Conditions |
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Diagnosis |
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Overview
There are two theories on pathogenesis of pneumatois intestinalis. Mechanical theory suggests that gas dissects into the bowel wall from either the intestinal lumen or the lungs via the mediastinum due to some mechanism causing increased pressure. Bacterial theory proposes that gas-forming bacilli enter the submucosa through mucosal rents or increased mucosal permeability and produce gas within the bowel wall.