Presentation
24hours abdominal pain, lactate 5 ?ischemic bowel
Patient Data
Arterial and portal venous phase contrast enhanced exam of abdomen and pelvis.
Extensive portal venous gas, superior mesenteric venous gas, and small bowel pneumatosis.
Gas also within the splenic artery, common hepatic artery, and likely left gastric artery.
No free intraperitoneal gas.
Large volume gas within the urinary bladder.
Filling defect in the left distal superior mesenteric artery in keeping with thrombus.
Multiple distended small bowel loops, with poorly enhancing small bowel wall.
Gastric distension, with extensive gas within the vessels of the stomach.
Small volume gallstones in a thin-walled gallbladder.
Multiple foci of hypoattenuation in the renal cortices bilaterally in keeping with multiple small infarcts.
Inferior vena cava is collapsed, suggesting shocked status.
Hyper enhancement of right adrenal in keeping with hypoperfusion complex.
Poor enhancement of the spleen suggesting infarction. Poor enhancement at the head of the pancreas, may represent an area of infarction.
Likely gas in antidependent position in the right atrium and right ventricle.
Impression of thin filling defect in left ventricle posteriorly.
Small locules of gas within the left atrium.
Small bilateral pleural effusions.
Bilateral ground-glass change and patchy consolidation.
Degenerative changes of the imaged spine particularly at lumbar sacral junction. No concerning bony abnormality.
Opinion:
Appearances of a moribund status.
Extensive small bowel infarction with pneumatosis, portal venous gas, and further gas in branches of the celiac axis as described.
Gas within bladder.
Multiple renal infarcts, infarcted spleen, possible head of pancreas infarct. Upstream embolic source suspected, possible mural thrombus along left ventricle wall.
Case Discussion
A dramatic case of small bowel infarction with extensive portal venous gas and even arterial gas and gas within the bladder.
The renal infarcts may be due to upstream embolic source (there was a history of atrial fibrillation) alternatively the profound shock may have lead to hypoperfusion leading to infarction.
The splenic infarct may be due to gas within the splenic artery obstructing arterial flow, or be due to upstream source or profound shock.
It is unclear how the gas came to be within the bladder and arterial system, one hypothesis being that the gas produced by the infarction dissolved within the blood and condensed back in to gas in the arterial system, and dissolved through the capillary bed in to bladder lumen.
The patient sadly did not survive.