Endovascular Treatment of Hepatic, Gastroduodenal, Pancreaticoduodenal, and Splenic Artery Aneurysms

Historical Background

Hepatic artery aneurysms are the second most common type of visceral aneurysms after those of the splenic artery. In 1809 Wilson first described a hepatic artery aneurysm as the “size and shape of a heart involving the left hepatic artery,” and in 1903 Kehr reported the first successful ligation of a hepatic artery aneurysm. Hepatic artery aneurysms comprise 20% of visceral artery aneurysms, and although still not well defined, the natural history of the hepatic artery aneurysm typically results in enlargement, rupture, and life-threatening hemorrhage. The optimal management of hepatic artery aneurysms remains controversial, and the risk-benefit ratio of treating asymptomatic cases is difficult to assess.

True aneurysms involving the gastroduodenal artery (GDA) or the pancreaticoduodenal artery (PDA) are extremely rare, accounting for only 3.5% of all visceral artery aneurysms (PDA = 2%, GDA = 1.5%). The first PDA aneurysm was reported by Ferguson in 1895, and fewer than 100 cases have been reported in the literature. These types of aneurysms are primarily caused by arterial injury during surgery on surrounding organs, autoimmune disease, or pancreatic inflammation. GDA aneurysms are significant because of their high associated risks of rupture and death.

First reported by Beaussier in 1770, splenic artery aneurysm (SAA) is the most commonly reported visceral aneurysm, accounting for up to 60% of such lesions. The vast majority are smaller than 2 cm and are saccular, and more than 80% are located in the midsplenic or distal splenic artery. SAAs are found in women four times more frequently than in men, and the reported risk of rupture ranges from 3.0% to 9.6%. Approximately 70% of SSAs are true aneurysms and occur at the bifurcation within the splenic hilum. Most frequently asymptomatic, these aneurysms are usually identified as an incidental finding. A curvilinear or signet ring-shaped calcification may be observed in the left upper quadrant of an abdominal radiographic examination. Symptomatic patients present with left upper quadrant or epigastric pain that radiates to the left shoulder. Rupture of the aneurysm, which may manifest as hypovolemic shock, occurs in less than 2% of patients.

Common causes for SAAs include atherosclerosis, portal hypertension, and pancreatitis, which may cause pseudoaneurysms. Less common etiologies include idiopathic dissection, septic emboli, essential hypertension, polyarteritis nodosa, and systemic lupus erythematosus. Pseudoaneurysms of the splenic artery are most often caused by chronic pancreatitis or trauma. The incidence of SAAs is higher in multiparous women with, on average, 4.5 pregnancies and in patients with splenomegaly or those who have undergone orthotopic liver transplantation.

Indications

Most authors have recommended repair of hepatic artery aneurysms, whether symptomatic or not, because of the associated risk of rupture and death. Intervention is indicated for all nonatherosclerotic aneurysms and for multiple hepatic aneurysms because of the higher incidence of eventual symptoms and rupture. For asymptomatic atherosclerotic hepatic artery aneurysms, which are 2 to 5 cm in diameter, treatment options are more controversial in patients with marginal health. Intervention should be reserved for those aneurysms that enlarge or become symptomatic.

The literature includes only case reports and small case series. A definitive study evaluating the natural history of both GDA and PDA aneurysms or the preferred method for treatment has not been conducted. The risk of rupture of GDAs and PDAs is unrelated to size, and any aneurysm should be considered for definitive treatment.

Treatment for an SAA is recommended for any symptomatic patient, as well as for asymptomatic pregnant women, women of childbearing age who may subsequently become pregnant, patients who may undergo liver transplantation, and those who present with a pseudoaneurysm associated with an inflammatory process. Patients with aneurysms larger than 2 to 2.5 cm should be considered for treatment. With the advent of endovascular techniques, percutaneous transcatheter embolization or stent-graft placement has become a preferred option.

Preoperative Preparation

• Nothing should be taken by mouth after midnight except regular medications. If the patient is diabetic, half the insulin dose should be given and sulfonylureas should be held.

• Coumadin should be discontinued, and heparin bridge therapy should be used as appropriate. Enteric-coated acetylsalicylic acid (aspirin) may be taken the day of the procedure.

• In the presence of renal insufficiency (serum creatinine > 1.5 mg/dL), normal saline should be administered to prevent contrast nephropathy. Alternatively, dextrose with sodium bicarbonate (150 mEq/L) should be infused at 3 mL/kg for 1 hour before contrast load and 1 mL/kg/hr for 6 hours after contrast load. Six doses of N -acetylcysteine (600 or 1200 mg) should be administered twice daily beginning 12 hours preoperatively.

• In the presence of a contrast allergy, oral prednisone (50 mg) should be prescribed 13, 7, and 1 hour before contrast load and both ranitidine (50 mg intravenously), and diphenhydramine (50 mg intravenously) should be administered 1 hour before contrast load.

Pitfalls and Danger Points

• Arterial injury, including dissection, rupture, and pseudoaneurysm

• Occlusion of the main vessel while attempting to preserve it

• Loss of access during the procedure, including force buildup with recoil resulting in the stent system inadvertently displacing the guide catheter

• Access angle to the celiac axis that may require a change in primary access from femoral to brachial artery, or vice versa

• Organ infarction because of occlusion of the main splenic or proper hepatic arteries without sufficient collateral vessels or in the presence of liver disease

• Errant coil and stent deployment

• Stent-graft foreshortening with type I or II endoleak

Endovascular Strategy

Two strategies are available for the endovascular treatment of visceral aneurysms. The first entails excluding the aneurysm and its donor artery and relying on collateral arterial pathways to reconstitute blood supply to the spleen or liver. The second involves excluding the aneurysm while maintaining arterial flow through the donor artery. The first strategy requires embolization, and the second requires stent-graft placement with or without coil embolization of collateral branches to prevent backbleeding (type II endoleak).

Rarely, upper celiac, hepatic, splenic, gastroduodenal, or pancreaticoduodenal aneurysms are inaccessible using transcatheter techniques. In these instances direct percutaneous puncture of the aneurysm can be performed, embolizing the aneurysm with coils or by thrombin injection. Another alternative is to perform a “hybrid procedure” that involves a laparotomy, dissection, and surgical cutdown for isolation of vessels that lead directly to the aneurysm for access combined with cannulation and transcatheter techniques for management of the aneurysm.

Endovascular Technique