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Our interest in the subject of pneumatosis intestinalis and, in particular , its etiology, was stimulated by the occurrence of 3 cases in our hospital within one month. The common feature in these cases was severe pulmonary disease in exacerbation and lack of gastrointestinal complaints or demonstrable gastrointestinal involvement prior to the onset of th e pneumatosis. This suggested that pneumatosis intestinalis in a significant number of cases might occur as a result of air in the lung becoming interstitial from alveolar rupture, subsequently passing to the mediastinum and thence to the retroperitoneal area, and then dissecting along the vascular supply of the viscera. This seemed the more probable in that the distribution of the pneumatosis in our cases seemed to follow the pattern of vascular supply. Our experimental work has been directed toward proving or disproving this concept.

Very soon after we started laboratory investigation, impetus to our study was given by a report by Doub and Shea (1) of 16 cases of pneumatosis intestinalis, of which 15 were associated with asthma and 1 with pulmonary fibrosis. A majority of their cases occurred in the left colon, while our small series involved predominantly the right and transverse colon.


Probably the key paper on this subject is that of Macklin (2), published in 1939. This excellent treatise does not even mention “pneumatosis intestinalis” but does report the experimental production of “emphysema” of the mediastinum, neck, axilla, and pericardium, pneumothorax, and air in the retroperitoneal space as a result of alveolar ectasia and rupture. We are concerned with the latter and propose to show that the presence of retroperitoneal air is at least a potential for pneumatosis intestinalis. Macklin clearly demonstrated that air from alveolar rupture dissects along pulmonary vessels to the lung root and mediastinum and then takes divergent routes, as mentioned above.

Koss (3) summarized the literature on pneumatosis intestinalis up to 1952, including 213 reported cases. Fifty-eight per cent were explained on the mechanical basis of duodenal or pyloric obstruction (perforation assumed). A few other cases were attributed to sigmoidoscopy or biopsy of the sigmoid, or appendiceal disease. This left approximately 40 per cent in the “primary” category, i.e., etiology unknown.

Theories of the etiology of pneumatosis intestinalis have basically been of three types: mechanical, neoplastic, and bacterial. Only the mechanical theory has been supported by documented proof. Multiple articles, reporting 1 to 7 cases and reviewing the literature, lean toward the mechanical theory, when they lean at all. It is interesting to note that the report of 7 cases by Mujahed and Evans (4) included 5 with pulmonary disease.

Methods of Investigation

The dog, the pig, and the unembalmed cadaver were used for our experimental investigations.

Article History

Published in print: May 1961