Asian Cardiovasc Thorac Ann 2008;16:68-72
© 2008 Asia Publishing EXchange Ltd
Endovascular Treatment of Gastroduodenal Artery Aneurysm
Weng Wah Roland Chong, MBBS,
Seck Guan Tan, FRCS,
Maung Myint Austin Htoo, FRCR1
Department of General Surgery
1 Department of Radiology Singapore General Hospital Singapore
For reprint information contact: Weng Wah Roland Chong, MBBS Tel: 65 6321 4051 Fax: 65 6220 9323 Email: malathione{at}yahoo.com, Department of General Surgery, Singapore General Hospital, Outram Road, 169608 Singapore.
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ABSTRACT
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Gastroduodenal artery aneurysms are rare. Common causes include blunt trauma, pancreatitis, infection, autoimmune disorders, vascular intervention and surgery. We report 2 patients with gastroduodenal artery aneurysms, the first being an idiopathic true aneurysm and the next, a pseudoaneurysm resulting from pancreatitis. Diagnoses were made by computed tomography scans with successful embolization of both patients. Treatment of gastroduodenal artery aneurysms includes surgery, endovascular techniques or observation. Embolization is a feasible option for gastroduodenal artery aneurysms and pseudoaneurysms.
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INTRODUCTION
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True peripancreatic aneurysms involving the gastroduodenal and pancreaticoduodenal arteries are extremely rare, accounting for only 3.5% of more than 3,000 splanchnic aneurysms reported in the literature since 1960.1 We report 2 patients, 1 with a gastroduodenal artery (GDA) aneurysm, and the other with a gastroduodenal artery pseudoaneurysm.
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CASE REPORTS
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CASE 1
A 55-year-old male hepatitis B carrier, on routine ultrasound surveillance, was found to have gallstones and a 4.7 cm aneurysm in the mid-abdomen area. On examination, a small epigastric pulsatile mass was found. A computed tomographic (CT) angiogram of the abdomen showed a 5.4 cm x 4.8 cm enhancing mass inferior to the liver which represented an aneurysm of the gastroduodenal artery (Figure 1A
). No contrast leakage or surrounding inflammatory changes were seen. Embolization of the gastroduodenal artery was performed in view of its large size.
On angiography, a large 5.4 cm x 4.8 cm aneurysm was seen arising from the descending portion of the gastroduodenal artery (Figure 1B) The inflow segment was readily visualized but the outflow segment could not be identified. There was also a small lesion seen within the inferior portion of the atrophic right hepatic lobe which could have been a hepatic pseudoaneurysm. The inflow segment of the gastroduodenal artery aneurysm was embolized with five 14 cm x 0.4 cm Nester Platinum Embolization Coils (Cook Medical Inc., Bloomington, IL, USA) (Figure 1C). The procedure was uneventful. The patient was re-admitted a month later for embolization of the presumed hepatic pseudoaneurysm. The repeat angiography showed that the highly vascular hepatic lesion was more likely to be a hemangioma than a pseudoaneurysm. The gastroduodenal artery aneurysm had completely thrombosed. At follow-up, a magnetic resonance imaging scan was done to further assess the hepatic hemangioma and to assess for stability. This showed interval stability of the hypervascular nodule. At follow-up, the embolized aneurysm of the GDA remained stable in size and there was no enhancement (Figure 1D).
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Figure 1B. Pre-embolization angiography showing absence of outflow vessel. GDA = gastroduodenal artery.
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Figure 1C. Post-embolization angiography showing successful embolization of the gastroduodenal artery aneurysm.
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Figure 1D. Post gadolinium T1 weighted magnetic resonance imaging scan of the abdomen showing stability of the gastroduodenal artery aneurysm.
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CASE 2
A 46-year-old male alcoholic was admitted for relapsing pancreatitis. Computed tomographic scan of his abdomen showed a well-defined, 7.4 cm soft tissue focus located between the gall bladder, second part of the duodenum, and pancreatic head (Figure 2A) Following administration of contrast, pooling of contrast medium within the right part of the mass persisted into the portal venous phase but was not evident in the delayed phase. This suggested a pseudoaneurysm arising from the gastroduodenal artery. The patient passed a large amount of fresh melenic stools and became hypotensive. His hemoglobin level fell from 10.3 to 6.5 g·dL–1. Esophago-gastro-duodenoscopy was performed, which was normal. A triple vessel angiogram was done which showed that the patient was bleeding from his gastroduodenal artery pseudoaneurysm. Embolization was performed to stop the bleeding (Figures 2B and 2C). Post-procedural hepatic and superior mesenteric artery angiograms showed satisfactory embolization with no further opacification of the pseudoaneurysm. The impression then was that the gastroduodenal artery pseudoaneurysm was eroding into the small bowel resulting in melena. However, the patient had another episode of fresh melena and a check angiography was performed the next day. The coils within the gastroduodenal artery were noted with no active bleeding or filling of the gastroduodenal artery pseudoaneurysm. There was late and faint filling of part of the gastroduodenal artery via small collaterals on injection of contrast into the superior mesenteric artery.
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Figure 2C. Post-embolization angiogram showing complete obliteration of the gastroduodenal artery pseudoaneurysm.
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Three days later, a computed tomographic angiogram was done showing the embolization coils in the gastroduodenal, right gastroepiploic, and superior pancreatico-duodenal arteries. The gastroduodenal artery pseudoaneurysm was completely thrombosed with a decrease in size, from 7.4 cm to 5.7 cm (Figure 2D).
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Figure 2D. Computed tomography abdomen showing the gastroduodenal artery pseudoaneurysm completely thrombosed.
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DISCUSSION
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Visceral artery aneurysms (VAA) can be true aneurysms or pseudoaneurysms. Pseudoaneurysms result from a variety of mechanisms. Common causes of pseudoaneurysms include blunt trauma of the upper abdomen, pancreatitis, infection, autoimmune disorders, vascular intervention and surgery. The incidence of pseudoaneurysms in patients with severe acute pancreatitis is up to 10%.2 Activation and release of pancreatic enzymes causes the rupture of membrana elastica interna of the splanchnic vessels, followed by segmental thrombosis of the vessel. Thrombosis of the vasa vasorum causes ischemia of the arterial wall with resultant necrosis. Massive bleeding occurs if the weakened vessel wall suddenly ruptures. A pseudoaneurysm develops when the rupture is contained and the hematoma is surrounded by a reactive fibrous capsule. Gastroduodenal artery aneurysms are extremely rare, comprising only 1.5% of all reported peripheral aneurysms.2 Reports of GDA aneurysms and pseudoaneuryms are very few. As such, we reviewed a series of reports on VAAs to investigate their pathology.
Patients with VAA are often asymptomatic (72%).3 Such patients are incidentally picked up on abdominal ultrasound, CT or angiography for other reasons. In other intances, the presentation may range from a palpable epigastric mass, pain or signs of gastrointestinal bleeding and anemia as in our 2nd case. Computed tomography with intravenous contrast material provides optimal visualization of these vascular abnormalities. The demonstration of a homogeneously enhancing structure within or adjacent to a pseudocyst or contiguous with a vascular structure in a case of pancreatitis is highly suggestive of an associated pseudoaneurysm.4 Angiography serves an important role for both diagnostic and therapeutic purposes as shown in our cases. These aneurysms are important because of the risk of rupture and subsequent mortality. A recent review suggests that 35% of GDA aneurysms are ruptured at presentation, carrying a mortality of 21%.5 Also, as the risk of rupture is unrelated to size, any GDA aneurysm should be considered for definitive treatment once diagnosis is made. Visceral artery aneurysms can be treated by revascularization, ligation or endovascular techniques depending on clinical presentation, hemodynamic status and location. Transarterial catheter angioembolization is an option that is much less invasive than surgery but patient selection for suitability for embolization is of utmost importance.
Three recent studies have reviewed between 31 to 65 VAA to compare the mortality and morbidity of surgical versus endovascular treatment.6–8 The first showed that VAA could be treated by ligation in most cases or by embolization if the hemodynamic status of the patient allows.6 As a result of the risk of rupture, endovascular or open repair is warranted for VAA and has a favorable prognosis. In unruptured cases, the morbidity rate associated with surgical treatment was 12%. The morbidity rate associated with endovascular treatment was 18% including cholecystitis and bile duct stenosis. The VAA recanalization rate following embolization was 9%. In the ruptured group, treatment was mainly ligation with resection of ischemic viscera in few cases. Other options included bypass and embolization. The mortality rate was 20% for the ruptured group. The morbidity rate associated with surgical treatment was 46% including bile duct stenosis, ischemic cholecystitis, duodenal fistula, pancreatic fistula, bile tract fistula and colonic ischemia. It is thus important to follow-up on embolized patients as recanalization requiring repeat interventions has been documented in short-term follow-up.
The second retrospective study reviewed 31 VAA in 28 patients.7 In the surgical group the perioperative mortality rate was 3.6%. The perioperative morbidity rate was 7.1% (one case of respiratory distress manifested in the immediate postoperative period and one urgent case of bilious fistula). In the endovascular group none of the patients died; the perioperative morbidity rate was 14.3% (one case of hepatic artery thrombosis after failure of gastroduodenal artery aneurysm embolization). Failure of the procedure was 42.9% (3 cases of aneurysm recanalization). The authors, in this study, believed that an aggressive surgical approach was justified, even in the case of asymptomatic VAA. This is because of the low morbidity and mortality rates. They also propose that endovascular treatment should be reserved for selected cases.
The last study reviewed 65 patients with VAA.8 Management consisted of 18 (27.7%) endovascular interventions, 9 (13.9%) open surgical repairs, and 38 (58.5%) observations. The initial technical success rate of the endovascular procedures was 94.4%. However, 22.2% of the patients had major endovascular procedure-related complications: one late recurrence requiring open surgical repair, two large symptomatic splenic infarcts and one episode of severe pancreatitis. These four patients had distal splenic artery aneurysms at or adjacent to the splenic hilum. There were no endovascular procedure-related deaths. Reasons for performing open surgical repair included 3 splenic artery aneurysms ruptures diagnosed at laparotomy and complex anatomy not amenable to endovascular intervention (6 patients). One surgical patient had a postoperative small bowel obstruction treated nonoperatively; and there was one perioperative death in a patient operated on emergently for rupture. Endovascular management of visceral artery aneurysms is a reasonable alternative to open surgical repair in carefully selected patients. Individual anatomic considerations play an important role in determining the best treatment strategy if intervention is warranted. However, 4 of 11 (36.4%) patients with distal splenic artery aneurysms treated with endovascular embolization developed major complications. Based on the authors’ experience, traditional surgical treatment of splenic artery aneurysms with repair or ligation and concomitant splenectomy when necessary may be preferred in these cases.
Thus, vessel anatomy, location, etiology of disease and the patient’s underlying condition must be taken into account in the decision to embark on endovascular or surgical therapy. For those unsuitable for embolization, a surgical bypass or ligation would be more appropriate. In cases of intraperitoneal rupture with hypotension, open surgery is the management of choice. In cases of erosion into the surrounding bowel structure, endoscopic techniques to identify and stop the source of bleed can be attempted initially as in our 2nd case. In the event of failure, either endovascular or surgical techniques would be the management method of choice. Our patients had gastroduodenal artery aneurysms. The 2nd patient presented with erosion into the gastrointestinal tract with melena and hypotension. We decided to proceed with the endovascular technique after stabilization of the patient.
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CONCLUSION
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Visceral artery aneurysms is an uncommon condition. Rupture is a significant and common initial presentation and timely intervention is appropriate. An endovascular approach with embolization of the aneurysm is a feasible, minimally invasive option in an elective setting and some incidences of erosion. Patient selection is of utmost importance. We present 2 cases of GDA aneurysm with different presentations and etiologies. Both were managed successfully with endovascular techniques.
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REFERENCES
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ABSTRACT
INTRODUCTION
