Pneumatosis Intestinalis

Jonathan Levi Streeter, MD - Case Coordinator
John Dewolfe Mackenzie, MD - Radiology Discussion
Bharti Khurana, MD - Additional Contributor to Rad
Miguel N Rivera, MD - Pathology Discussion
Pablo R Ros, MD, MPH - Attending Radiologist

November 25, 2002

Presentation

Imaging Findings

There is a loop of bowel with non-dependent gas (possibly intramural), as well as several small foci of gas, probably in small mesenteric veins. The bowel wall is not discernable in multiple locations. The bowel is somewhat, though not markedly, distended. Bowel ischemia (reversible) or infarct (transmural; irreversible) is likely, given the gas within the vessels and the non-dependent gas in the bowel wall.

Following admission, the patient's status deteriorated rapidly. He was found to have Staphylococcus aureus sepsis. The patient expired, and an autopsy was performed.

Diagnosis

Discussion

The first gross image, taken during the autopsy, illustrates the marked difference between necrotic and normal loops of bowel (purple versus pink-tan in color). A photograph of the mucosal surface of the necrotic bowel shows numerous air bubbles which have lifted the mucosa away from the muscularis. Microscopically, most of the tissue is bright pink and nuclear staining is absent. These features are characteristic of necrosis. The muscularis and mucosa are separated by gas bubbles.

The diagnosis was pneumatosis intestinalis involving the jejunum. Both the SMA and IMA were patent and no evidence of perforation or peritonitis was found. One possible scenario is that sepsis led to profound bowel hypoperfusion and subsequent infarct.

Radiology Discussion

Pneumatosis intestinalis can be defined as gas within the subserosal and/or submucosal layers of the bowel. The finding of pneumatosis suggests either an underlying chronic disorder or an acute, life-threatening process. Chronic processes associated with pneumatosis include pulmonary disease (e.g., COPD, artificial ventilation), inflammatory bowel disease, connective tissue disease (e.g., scleroderma, SLE), and Whipple disease. Acute processes include ischemia caused by necrotizing enterocolitis, mesenteric vascular disease, colonic obstruction (air dissecting distally), trauma (e.g., sigmoidoscopy, biopsy, barium enema, postsurgical anastomosis), infection (e.g., primary infection, parasites, perforated jejunal diverticula), or inflammation. Pneumatosis intestinalis associated with ischemia has a high mortality rate of approximately 50-75% of cases. Therefore, it is important to understand the clinical history (and any indications of ischemia) when pneumatosis is seen.

Bowel wall thickening and dilation, with or without pneumatosis, are warning signs for ischemia and infarct. Infarct occurs with transmural necrosis. This can occur quickly, so that there is no time for submucosal edema to manifest as wall thickening. Therefore, dilatation without wall thickening should immediately suggest infarct, which paralyses the bowel.

It is not certain how the gas becomes trapped within the bowel wall. One hypothesis suggests that gas-forming bacteria invade the wall. Another suggests that the gas is produced by the fermentation of carbohydrates in the bowel wall. For cases associated with COPD and other benign entities, one hypothesis is that blebs burst and the gas interpolates into the bowel wall. The trapped gas may be visible as "bubbles" or as "bands". The bubble appearance is generally considered to be early stage; with air bubbles trapped in the submucosa, the condition is potentially reversible. The band appearance manifests in transmural infarction, in which the gas is able to expand under the serosal surface.

References

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