1918 A Case of Recurrent Pneumatosis Intestinalis and Portal Venous Gas

Abstract

INTRODUCTION: Mesenteric ischemia (MI) is caused by inadequate blood flow through the mesenteric vessels resulting in ischemic bowel. The most serious cases cause gangrenous bowel, leading to pneumatosis intestinalis (PI) and portal venous gas (PVG), often an ominous sign. CASE DESCRIPTION/METHODS: This is a case of a 63-year-old male who presented to the hospital with hematemesis and severe anemia. After massive transfusion, an EGD revealed actively bleeding gastric ulcers, requiring serial EGDs for successful control of bleeding. A CT revealed gastric distention with thickening of the duodenum and bilateral femoral vein opacities, later confirmed as deep vein thromboses. An IVC filter was subsequently placed, as he was not a candidate for anticoagulation. The patient was subsequently discharged on oral pantoprazole. Of note, there was no history of NSAID use or evidence of H. pylori. Repeat EGD 2 months later noted mild gastritis, but no ulcers were seen. A screening colonoscopy at the time noted only diverticulosis. He was continued on pantoprazole. 3 months later he presented to the hospital with acute onset nausea, vomiting, and diarrhea. A CT revealed PI at the gastric fundus, as well as PVG. An infectious work-up was negative, lactate was normal, and his symptoms resolved quickly. A subsequent repeat CT noted resolution of the PVG and reduction in PI. He represented to the hospital 1 month later again with nausea, vomiting, and diarrhea. A CT noted small bowel dilatation with air fluid levels, PI at the esophagus, stomach, and jejunum, and significant PVG. The initial lactate level was mildly elevated and his symptoms resolved quickly after bowel decompression. A subsequent CTA noted a significant reduction in PVG without evidence of vascular occlusion. A follow up EGD showed diffuse subepithelial hemorrhages without any evidence of recurrent ulcers. A subsequent CTE noted a thrombus above the IVC filter and an evolving hepatic infarction. He was asymptomatic at the time, however, he was admitted to the hospital for anticoagulation. He has since remained on warfarin without any recurrence of symptoms, PI, or PVG. A follow-up CTA showed a full resolution of venous thromboses. DISCUSSION: Previous case reports have described the development of PI and PVG secondary to underlying MI. This case highlights an example of MI secondary to an increase in the resistance of mesenteric blood flow due to venous thromboses. When investigating IP and PVG, underlying venous thromboses should always be considered.