Vascular Malformations and Arteriovenous Fistulas of the Gastrointestinal Tract

Thomas E. Brothers

The vast majority of vascular malformations and arteriovenous fistulas of the gastrointestinal tract never come to the attention of peripheral vascular surgeons. These lesions most typically consist of angiodysplasias of the colon or stomach that are quite ably managed endoscopically or with direct resection by the gastroenterologist or gastrointestinal surgeon. However, there exist a number of primary and secondary vascular malformations and arteriovenous fistulas for which the knowledge and expertise of a vascular specialist are warranted.

Arteriovenous Fistulas

Arteriovenous fistulas, which rarely appear as primary but more commonly occur as secondary lesions, are usually considered according to their location, because location significantly affects the therapeutic approach. Most such fistulas do not directly involve the hollow gastrointestinal viscera but rather the neighboring solid organs.

Arteriovenous fistulas of the liver can occur in association with blunt or penetrating abdominal trauma, and most penetrating trauma is iatrogenic. Arteriovenous fistulas of the liver are mostly arterioportal and occur after 5% of percutaneous liver biopsies and 4% of percutaneous transhepatic cholangiographic procedures. Such fistulas also arise in association with hepatocellular carcinoma, localized rupture of hepatic artery aneurysms, hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu syndrome), hepatic abscess, bilary atresia, type IV Ehlers–Danlos syndrome, or following radiofrequency ablation of hepatic malignancies. These fistulas often lead to abdominal pain, diarrhea, and gastrointestinal bleeding, which is believed to be related to hyperemia of the mucosa. Congenital arterioportal fistulas are rarely described, but when detected in children they may be associated with failure to thrive.

Arterialization of the portal venous system ensues, leading to the development of the typical signs of presinusoidal portal hypertension of esophageal varices, ascites, and splenomegaly, although it usually takes a few years for this to occur. On the other hand, although infrequently reported in conjunction with hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu syndrome), high-output congestive heart failure is typically avoided owing to the effective resistance of the hepatic portal bed to higher levels of flow.

Physical examination of someone suffering from an arterioportal arteriovenous fistula often leads to detection of an abdominal bruit or thrill in the right upper quadrant in up to one third of such patients. Doppler ultrasound reveals abnormal portal venous flow, and computed tomography (CT) scanning with intravascular contrast can reveal early filling of the portal vein during the arterial phase with transient, wedge-shaped areas detected in the periphery. Findings of magnetic resonance imaging are similar to those of CT.

Splenic arteriovenous fistulas represent the second most common visceral abdominal fistulas and can occur spontaneously or after trauma, most particularly operative trauma. The classic source of splenic arteriovenous fistulas is mass ligation of the splenic pedicle during splenectomy, especially when suture ligation is employed. Similarly, penetrating trauma with simultaneous arterial and venous injury can result in arteriovenous fistula formation. Increasingly, such penetrating trauma may be iatrogenic when percutaneous placement of drains or tissue biopsy injures both structures. Rupture of a splenic arterial aneurysm into the adjacent vein can forestall intraabdominal catastrophe and immediate hemodynamic collapse, but it can result in secondary portal hypertension with its attendant morbidity. Similarly, the development of a pseudocyst with erosion into splenic arterial and venous vessels can create a pseudoaneurysm that can lead to fistula. Naturally, the pancreaticoduodenal vessels are also at risk of this occurrence, depending upon the location of the pseudocyst. The third most frequently described type of arterioportal fistulas involves the superior mesenteric artery, but these are decidedly uncommon.

A number of options exist for treatment of gastrointestinal arteriovenous fistulas, and the array of endovascular options continues to expand. Isolated arteriovenous fistulas within a hollow visceral structure may be most simply cured by operative resection with reconstitution of continuity.

Many small iatrogenic fistulas of the solid abdominal visceral organs close spontaneously, especially those in the periphery of the liver. These may be followed by ultrasound for a month or more to confirm closure of the fistula. If the fistula is large (>4 mm), the fistula fails to close, or there is evidence of portal hypertension, then intervention appears warranted.

Extrahepatic arterioportal fistulas rarely close spontaneously, so all of these should be treated when discovered. If the arteriovenous connection flows directly into a large vein that can be sacrificed, then obliteration with thrombin and gel foam, tufted steel coils, isobutyl cyanoacrylate, or an endosclerosant such as alcohol, is reasonable to consider. Coils may be less likely to embolize distally than gel foam particles with larger fistulas, although a combination of the two may be employed. Although most lesions may be managed with embolization therapy, use of a covered stent as an adjunct or primarily can also lead to prompt closure of the fistula without open operation. If there is a single large, direct connection with a vein that is vital and cannot be compromised, then blanketing of the feeding artery with a covered stent has demonstrated great success.

If the artery is too small to permit use of the commercially available covered stents, deployment of a self-expanding stent coupled with placement of coils across the stent may be entertained.

In the unique situation of the spleen, which has the benefit of secondary perfusion from the short gastric arteries, total occlusion of the splenic artery with coils, detachable balloons, and/or gel foam appears to be the preferred alternative. Rarely in the endovascular era is open operative ligation of the splenic or proper hepatic artery necessary, and the excellent outcomes for endovascular intervention appear to be quite durable. Splenectomy proves to be even more rarely required. However, should this be necessary, a hybrid approach with embolization of the splenic artery prior to splenectomy represents a strategy to reduce operative blood loss. If localized to a limited segment of the liver, anatomic liver resection may be employed with caution. In the case of extensive involvement of the majority of the liver parenchyma, liver transplantation has been successful.

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