- Open Access
Gastroduodenal artery aneurysm, diagnosis, clinical presentation and management: a concise review
© Habib et al.; licensee BioMed Central Ltd. 2013
- Received: 30 March 2012
- Accepted: 25 March 2013
- Published: 16 April 2013
Gastroduodenal artery (GDA) aneurysms are rare but a potentially fatal condition if rupture occurs. They represent about 1.5% of all visceral artery (VAA) aneurysms and are divided into true and pseudoaneurysms depending on the etiologic factors underlying their development. Atherosclerosis and pancreatitis are the two most common risk factors. Making the diagnosis can be complex and often requires the use of Computed Tomography and angiography. The later adds the advantage of being a therapeutic option to prevent or stop bleeding. If this fails, surgery is still regarded as the standard for accomplishing a definite treatment.
- Celiac Artery
- Gastroduodenal Artery
- Gastric Outlet Obstruction
- Pancreaticoduodenal Artery
Visceral artery aneurysms (VAA) are infrequent conditions characterized by a wide range of clinical presentations and various clinical outcomes. Depending on the mechanism of formation and etiologic factors, they can be divided into true aneurysms or pseudoaneurysms. True aneurysms are the results of vessel wall abnormalities while pseudoaneurysms occur after vascular injuries or erosions such as in trauma or inflammation , (i.e. pancreatitis, autoimmune disorders, vascular intervention, laparoscopic cholecystectomy and hepatic transplantation .
They have been reported in almost all the visceral arteries  but are most commonly seen in the splenic artery (46%), followed by the renal artery (22%), the hepatic artery (16.2%) and the pancreaticoduodenal artery (1.3%) . Those involving the gastroduodenal artery comprise only 1.5% of all reported VAA  and most of them are pseudoaneurysms due to their high occurrence rates in the setting of pancreatitis. Thus, true aneurysms in the pancreaticoduodeal and gastroduodenal arteries are extremely rare and represent only 3.5% of all VAA . In a review of the English literature over a 25 year period from 1970 to 1995, pancreatitis was found to be the most common associated condition with gastroduodenal artery aneurysm accounting for 47% of all cases followed by ethanol abuse (25%), peptic ulcer disease (17%) and cholecystectomy (3%) [5, 7, 8]. Other reported causes include congenital abnormalities (such as Marfan syndrome and Ehlers- Danlos syndrome ), liver cirrhosis , other vascular abnormalities such as fibro-muscular dysplasia, polyarteritis nodosa and predisposing events such trauma and septic emboli .
The pathogenesis of GDA aneurysms is not fully understood. Trauma, hypertension and atherosclerosis have been cited as potential risk factors for true aneurysms . The pathophysiologic changes that underlay the development of true gastroduodenal artery aneurysms comprise mainly atherosclerosis of the celiac artery with subsequent stenosis but also rarely congenital absence of the celiac axis . These two circumstances can be distinguished by the morphology of the collaterals that develop. The collateral vessels that form early on have usually parallel walls, are of uniform caliber and are limited to one or two vessels. In contrary, arteriosclerotic collaterals are more abundant, dilated and tortuous and hence more prone to aneursymal formation within the vessel’s wall. This occurs regardless of the location of the stenosis .
The pancreaticoduodenal artery is the main collateral pathway between the celiac axis and the superior mesenteric artery. Increased blood flow in the pancreaticoduodenal artery, as compensation for celiac artery stenosis, may cause a pancreaticoduodenal artery aneurysm . The same theory suggests that occlusion or stenosis of the superior mesenteric artery or celiac axis could be an etiologic factor predisposing to the formation of a gastroduodenal artery aneurysm [13, 15, 16].
As for pseudoaneurysms, inflammation with the most common cause being pancreatitis, results in vascular wall destruction that is mediated by pancreatic proteolytic enzymes leading to pseudoaneurysm formation .
Common presenting symptoms of GDA
1. Rupture (hematemesis, melena, shock)
2. Abdominal pain
3. Gastric outlet obstruction
4. Compressive symptoms (nausea, vomiting)
5. Hemobilia/ Hemosuccus pancreaticus
6. Pulsatile abdominal mass/ Bruit
Prior to the era of sophisticated imaging modalities the majority of cases of GDA aneurysms were undiagnosed until rupture occurred. Currently with the various imaging studies available, an increasingly larger number of cases are being incidentally detected in asymptomatic patients.
Doppler US may reveal turbulent arterial blood flow within or adjacent to a pseudocyst which is also suspicious for an aneurysm.
Plain X-ray of the abdomen is a rarely helpful study but may show shell-like calcifications in an atherosclerotic aneurysm .
New modalities such as Contrast-enhanced 3-dimensional magnetic resonance angiography or multi-detector row computed tomography have been reported to be as effective as visceral angiography in the diagnosis of abdominal vascular lesions [31, 32]. Other diagnostic studies are available including Pulse Doppler US, color Doppler US, endoscopic ultrasound and magnetic resonance imaging [33–35] but are less frequently used.
Endovascular options include embolization of the aneurysms or stent graft deployment [41, 42] (Figure 3). Some anatomical conditions are required though for technical feasibility of these procedures (saccular aneurysm with a narrow neck, fusiform aneurysm with adequate collateral flow, aneurysm of a vessel supplying an organ that has multiple arterial sources) [41, 43].
Even though this less aggressive option plays an important role in high risk surgical candidates, it has its potential complications such as visceral ischemia resulting in sacrifice of the involved visceral vessel, end-organ thrombosis, and late-term vessel recanalization. Transcatheter embolization is the most popular endovascular intervention performed despite the potential risk of visceral ischemia and organ infarction . Other complications include coil/stent migration [45, 46], intra-procedural aneurysm dissection, or rupture , embolisms, access artery pseudoaneurysms and contrast-induced nephropathy. In contrast, surgical interventions have their own share of complications such as paralytic ileus, wound infection, massive bleeding, or acute pancreatitis . These complications have a significantly higher rate of occurrence in patients with previous abdominal surgery where adhesions are present, making the endovascular approach the preferred treatment option in those patients .
Despite the fact that endovascular treatments do not represent a standard option and require both a specific training and a learning curve, the development of new technologies, such as the multilayer stent, could offer a new alternative to VAA treatment, particularly in high-risk patients .
In conclusion, physicians might only encounter GDA aneurysms as an incidental finding on CT scans. In unfortunate patients, rupture might occur and lead to a fatal outcome if an emergent intervention is not made. Depending on the patient’s condition, the decision to proceed with angiography or surgery should be taken without any delay to prevent the worst outcome.
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