Small bowel arteriovenous malformation

1 day of abdominal pain and bloody stool and normal vital signs. Colonoscopy revealed large volume blood. Upper endoscopy was negative. The patient had sudden onset diaphoresis and lightheadedness with acute haemoglobin drop 5.4 points. Angiography revealed arteriovenous malformation and 2 feeding arteries were coiled with haemoglobin stabilisation and discharge.

CT abdomen/pelvis revealed jejunal mural enhancement with early draining vein and no intraluminal bleeding (Figures 3 and 4). Emergency angiography revealed a tangled mass of arteries arising from the jejunal wall with early venous drainage consistent with an arteriovenous malformation (Figures 5 and 6).

Angiodysplasia, a gastrointestinal arteriovenous malformation (AVM), is a dilation of submucosal and mucosal vessels thought to be acquired by chronic, intermittent strain on the bowel wall.

Small bowel AVMs are less common but represent up to 75% of “obscure” GI bleeding (OGIB), or bleeding that persists or recurs after negative endoscopy and contrast radiographs [1]. AVMs might present earlier in patients with congenital disorders such as hereditary haemorrhagic telangiectasia (HHT), Ehlers-Danlos, CREST syndrome, Henoch Schonlein Purpura and Klippel-Trenaunay-Weber syndrome [2]. Because upper endoscopy is often insufficient to visualise beyond the duodenum, other methods such as capsule endoscopy (CE), deep small bowel enteroscopy, computed tomographic angiography/enterography (CTA/CTE) are often required.

The approach to OGIB should be directed by patient haemodynamic stability and risk factors. In haemodynamically stable patients, early CE following second look endoscopy has largely replaced radiographic imaging as the initial study [3]. Alternatives for patients in whom CE is contraindicated (e.g. small bowel obstruction) include CTE and CTA [4]. There is evidence that CTE is more sensitive than CE in OGIB [5]. CTA increases the diagnostic yield when used with CE but its role in OGIB is not well defined [6]. Haemodynamically unstable patients with overt bleeding more often proceed directly to angiography following initial resuscitation, with or without imaging localisation. Angiodysplasia characteristically appears as 5-10 mm, flat, cherry-red lesions with arborizing, ectatic vasculature on endoscopic evaluation. Characteristically on CTA, enhancement is brightest during the enteric phase, fading on the delayed phase and undetectable on the arterial phase. Early antimesenteric vein filling indicates some degree of arteriovenous shunting [6].

Approximately 90% of bleeding caused by angiodysplasia spontaneously cease [7]. Treatment options for symptomatic angiodysplasia include endoscopic interventions and angiographic therapy (e.g., embolisation, intra-arterial vasopressin) with surgical options reserved for severe, refractory cases. Approximately one-third of patients with angiodysplasia will experience rebleeding 22 months after haemostasis [8]. The risk rebleeding is even greater with small bowel angiodysplasia [8]. Medical management has not been shown to be effective in the long-term but supportive therapy (e.g. iron, transfusion) might be warranted [4].

Angiodysplasia is the most common cause of OGIB. The role of CT/CTE is not well-defined in diagnostic algorithms but might offer advantages over capsule endoscopy, particularly in acute bleeds where clinical suspicion is high.