Benign Pneumatosis Intestinalis: A Case Report and Review of the Literature

Testing for C difficile was negative. An abdominal radiograph was obtained and revealed no bowel obstruction but, alarmingly, showed extensive intramural bowel gas, suggestive of PI (Figure 1). His leukocyte count, serum bicarbonate, and serum lactate levels remained within normal limits. A CT with contrast of the abdomen and pelvis demonstrated no vascular obstruction but confirmed the presence of diffuse intramural gas in his stomach and proximal small bowel, as well as the presence of mesenteric and portal venous gas (Figures 2 and 3). Although his abdominal examination had not changed and did not suggest peritonitis, general surgery was consulted to discuss the need for surgical intervention. Given his overall clinical stability and high surgical risk due to his many comorbidities, surgery recommended a conservative approach.

Through the following hospital days, his enteral nutrition was held and serial abdominal examinations were performed without change. Serial laboratory studies, including serum lactate and leukocyte count, remained reassuringly within normal limits. His urine culture eventually revealed multidrugresistant Pseudomonas aeruginosa . Antimicrobial therapy was narrowed to piperacillintazobactam for a complete course. Enteral nutrition was gradually reintroduced at a low rate, ultimately reaching goal rate with return of bowel function by hospital day 9. Despite extensive workup, the etiology of his transient enteral nutrition intolerance remained uncertain, though an adverse effect of antibiotic therapy was thought possible. Follow-up abdominal radiographs demonstrated interval improvement of PI. He was discharged back to his skilled nursing facility on hospital day 11 without incident.

Discussion

PI is an incompletely understood condition seen in multiple diseases. Patients may present with highly variable symptoms, often more attributable to the underlying disease causing the PI than the presence of PI, as patients may be entirely asymptomatic. When symptoms are attributed to PI, those most reported are abdominal pain, bloody stools, and diarrhea. ¹ It is often detected on abdominal plain films. Alternative methods of diagnosis include ultrasonography, barium enema, and endoscopy although the last method has been known to occasionally lead to bowel perforation. ^2-6 The most sensitive method of detection is CT, which also provides additional information about abdominal pathology and may identify the underlying process responsible for the PI. ⁷

While not fully understood, much information about PI and its pathogenesis is known. Understanding the mechanisms of PI is vital to direct the clinician’s evaluation of the patient for reversible conditions that may cause PI. Early descriptions of PI in the literature documented an association with pyloric stenosis, leading to the theory that gas from the intestinal lumen is driven into the submucosal space during episodes of forceful vomiting with increased intraluminal pressure. ⁸ As PI was subsequently described in multiple other disease states not typically associated with increased intraluminal pressure such as inflammatory bowel disease, GI malignancy, cryptosporidiosis and CMV infection, additional theories about the pathogenesis of PI have arisen. ^9-24 There is now experimental data to support multiple mechanisms of intramural gas accumulation. It has become accepted that PI represents a common pathway shared across various pathologic states and results from multifactorial mechanisms of gas entry into the intestinal wall. ^25-29