ECR 2018 / C-2499
Complications of vascular impingement in the median arcuate ligament syndrome
Congress: ECR 2018
Poster No.: C-2499
Type: Educational Exhibit
Keywords: Obstruction / Occlusion, Hemorrhage, Aneurysms, Embolisation, Complications, Arterial access, Ultrasound-Colour Doppler, Percutaneous, CT-Angiography, Vascular, Arteries / Aorta, Abdomen
Authors: S. Accogli, V. Napoli, M. Gabelloni, R. Cioni, D. Caramella; Pisa/IT
DOI:10.1594/ecr2018/C-2499

Background

 MAL is a fibrous arch bridging the diaphragmatic crura on either side of the aortic hiatus, normally passing over the aorta at the level of L1, superior to the coeliac artery origin. In 10-24% of cases, it is low-lying and might cross over the proximal portion of CA, causing extrinsic compression of the vessel1 (Fig. 1) .

 Most patients are asymptomatic. However, some of them may develop symptoms of MALS or Dunbar syndrome, typically non-specific, such as post-prandial abdominal pain, weight loss, nausea, and vomiting2. Postulated cause of mesenteric angina associated with MALS includes an insufficient blood supply to gastrointestinal organs due to an haemodynamically significant compression of blood flow,  even if the majority also develop a rich collateralization between the CA and superior mesenteric artery (SMA) which should prevent visceral ischemia. It is believed that also collaterals are a source of pain because they can generate a form of vascular steal syndrome where they shunt blood away from the SMA to the smaller vessels distal to the stenosis in the CA. Even a direct compression of coeliac ganglia is postulated for the causing pain in MALS3,4 (Fig. 2).

 Although MALS is often considered a benign anatomical occurrence, severe compression with haemodynamic significance is seen in 1% of the population and complications of this anatomical variation are described, such as dilatation of the PD collateral pathways with subsequent formation of a visceral arteries aneurysms (VAAs) and bleeding2,3,5,6 (Fig. 3). 

 VAAs are a rare but potentially lethal form of vascular disease because, overall, it is estimated that 15–22% of them rupture2,5. Pancreaticoduodenal artery (PDA) aneurysms are particularly uncommon, account for only 2% of all splanchnic arterial aneurysms7, and are reported to be associated with many causative factors, including trauma, pancreatitis, infection, and congenital anomalies. CA stenosis or occlusion due to intraluminal pathology accounts for about 50-60% of all PDA aneurysm8; PD arcade aneurysms due to chronic compression by the MAL are seldom described in the literature and are limited to isolated case reports due to their rare occurrence9. In general, the risk of rupture of PDA aneurysms is uncertain as the number of cases is too small to determine a reliable statistical evaluation. Rupture is however well described and carries a range of 17-29% mortality rate in different studies, depending on their location and associated comorbidities of the affected patient5,8

 The treatment protocol for PDA aneurysms is still unclear and not unique, depending on the presence of a ruptured or unruptured aneurysm, and on the patient's haemodynamic stability and associated morbidities8,10

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