Aortoenteric fistula

Last revised by Khalid Alhusseiny on 3 Feb 2024

Aortoenteric fistulas are pathologic communications between the aorta (or aortoiliac tree) and the gastrointestinal tract and represent an uncommon cause of catastrophic gastrointestinal hemorrhage.

Aortic fistulas may be considered primary (associated with a complicated abdominal aortic aneurysm) or secondary (associated with graft repair). 

The annual incidence of primary aortoenteric fistulas is thought to be around 0.007 per million while that of secondary aortoenteric fistulas is about ~1% (range 0.6-2%) 1.

The incidence of secondary aortoenteric fistulas is found to be higher in patients following open aortic repair compared to patients with endovascular stent placement.

  • classically, aortoenteric fistula may initially present with minor "herald" gastrointestinal hemorrhage, followed by a later catastrophic life-threatening gastrointestinal hemorrhage

  • primary aortoenteric fistula may present with recurrent septicemia with enteric pathogens

A primary aortoenteric fistula forms when a large abdominal aortic aneurysm or a penetrating aortic ulcer 1 closely abuts bowel loops, usually the 3rd or 4th parts of the duodenum. Similarly, in the chest, when a large thoracic aortic aneurysm compresses the esophagus. Due to long-standing pressure, the aneurysm slowly erodes into the bowel or esophageal wall. These are most commonly due to infected mycotic aneurysms.

Secondary aortoenteric fistulas are seen as a complication of aortic reconstructive surgery with or without the placement of an aortic stent-graft. Secondary fistulas that result from perigraft infection may occur between 2 weeks and 10 years after surgery. 

Direct signs include:

  • ectopic gas adjacent to or within the aorta

  • presence of vascular contrast within the gastrointestinal tract

Indirect signs include:

  • bowel/esophageal wall thickening overlying an aneurysm

  • disruption of the aortic fat cover

  • retroperitoneal/mediastinal hematoma or hematoma within the bowel wall or lumen

  • increased perigraft soft tissue

  • pseudoaneurysm formation

  • disruption of aneurysmal wrap

  • increased soft tissue between the graft and aneurysmal wrap

The only curative treatment is surgery. Without prompt surgical intervention, mortality approaches 100%. Operative mortality itself is as high as 50%.

On imaging, consider:

First described by Sir Astley Cooper (1768-1841), a British surgeon in the early 19th century 6.

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