SPLANCHNIC ARTERY ANEURYSMS
Splanchnic artery aneurysms are historically cited as rare and mainly asymptomatic. In the past, most
were syphilitic or mycotic, while contemporary visceral aneurysms are largely true aneurysms caused
by atherosclerosis or medial degeneration.83 True aneurysms are defined by the involvement of all three
arterial wall layers (intima, media, and adventitia) while false aneurysms, or pseudoaneurysms,
represent a collection of extravasating blood outside of the artery that remains confined next to the
vessel by surrounding tissue. The incidence of splanchnic artery aneurysms is estimated at 0.1% to 2%
and autopsy series suggest a prevalence that may approach 10%.84,85 A minority of aneurysms present
with life-threatening rupture and while historic-associated mortality rates approached 25% to 70%;
more contemporary series suggest mortality rates of 15%, possibly reflecting improvements in
perioperative management and the increasing use of endovascular techniques.86 Most splanchnic
aneurysms are asymptomatic however, and diagnosed as incidental findings by cross-sectional
imaging.87 False aneurysms may carry a higher rate of rupture in comparison to true aneurysms (76%
vs. 3% in once series).88
The natural history of these aneurysms remains elusive in light of their rarity and anecdotal, mainly
institutional and retrospective, evidence to date. Indications for intervention remain conservative,
especially as no significant difference has been identified between the diameters of ruptured and
nonruptured aneurysms.88 Additionally, aneurysm calcification and intraluminal thrombus are not
associated with rupture risk. Treatment is recommended for symptoms and size >2 cm or aneurysm
diameter three times greater than the respective normal artery. Patients with splanchnic aneurysms
generally have 10-year survival rates >80% and open surgical treatment provides excellent, durable
long-term results with low perioperative mortality and morbidity following elective surgery.86,89,90
While surgical repair has remained the mainstay of treatment, minimally invasive endovascular
techniques continue to evolve and are increasingly applied for both elective treatment and that of
rupture. Endovascular intervention with local anesthesia offers excellent technical success, negligible
morbidity and mortality in elective cases, and brief hospital stays.86,88,90–94 Transcatheter embolization
of visceral artery aneurysms offers additional advantages that include precise aneurysm localization,
assessment of collateral flow, and negate the need for certain (i.e., intrahepatic) difficult arterial
exposures.83 Notably, embolization has become the standard of care for splanchnic artery
pseudoaneurysm.92,95 Additionally, endovascular therapy may offer decreased postoperative morbidity
and mortality rates in cases of rupture when compared to open surgery (2.7% to 7% vs. 24% to 29%,
respectively).86,91
6 Distribution of splanchnic artery aneurysms is as follows: Splenic artery (60%) > hepatic arteries
(20%) > superior mesenteric artery (SMA) (5.5%) > celiac artery (4%) and gastric and gastroepiploic
arteries (4%) > ileocolic arteries (3%) > pancreaticoduodenal arteries (2%) > GDA (1.5%) > IMA
(<1%).84,87 Most patients present in the sixth decade of life.87,88 Symptomatic patients will present with
abdominal pain and frank hemorrhagic shock with rupture. Rupture may be intra-abdominal, although
erosion into a gastrointestinal lumen may result in sporadic gastrointestinal bleeding (i.e., herald bleed)
and erosion into adjacent mesenteric veins results in arteriovenous fistulae. The asymptomatic patient
inconsistently reveals a bruit on auscultation and rarely a palpable mass on examination. Each
splanchnic aneurysm warrants individual consideration.
Splenic Artery Aneurysm
Splenic artery aneurysms account for 60% of all splanchnic artery aneurysms and are the third most
common intra-abdominal arterial aneurysm. Their prevalence in the general population is very low
approximating 0.16% to 0.8%.96 These aneurysms occur two to four times more frequently in women
than men and are associated with multiparity.83,87,90,96,97 Hormonal and local hemodynamic events
likely contribute to the evolution of splenic aneurysms. An etiologic classification system has previously
been proposed by Stanley and Fry that implicates arterial dysplasia, portal hypertension, local
inflammation, and hormonal and hemodynamic events in the pathogenesis of these aneurysms.96
Hypertension is a common comorbidity affecting 50% to 60% of patients with splenic aneurysm, and up
to 20% of patients will demonstrate concurrent aneurysms affecting alternate arterial beds.94,95,98
Additional etiologic risk factors for true aneurysms may include dissection, septic emboli, polyarteritis
nodosa, systemic lupus erythematosus, and connective tissue disorders like Ehlers–Danlos syndrome,
while splenic pseudoaneurysms are typically attributed to chronic pancreatitis and trauma.87 Splenic
aneurysms most often arise at branch points off the mid- and distal main splenic artery. Tortuosity of
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the main splenic artery is common (Fig. 91-15). The majority (80%) of splenic aneurysms are solitary
and saccular, although 90% of patients with portal hypertension will demonstrate multiple splenic
aneurysms. Those aneurysms measuring >5 cm are often described as “giant lesions” and appear to be
more common in older males.99
Splenic aneurysms typically rupture into the lesser sac with limited self-containment. Later
hemorrhage into the peritoneal cavity results in cardiovascular collapse and the so-called “double
rupture.” The incidence of splenic aneurysm rupture approximates 2% to 5% and is not associated with
calcification, blood pressure, or age.84,87,95,96 Increased levels of aneurysmal peripheral calcification are
associated with smaller aneurysm size at the time of diagnosis, but appear to have no impact on
aneurysm growth.95 Growth rates among surveyed aneurysms (out to 3.1 years) have been calculated as
0.2 mm/yr.95 Rupture-associated mortality is dramatically increased in the peripartum patient (68% to
75% vs. 25%), and associated fetal mortality approaches 100%.96,98,100 Rupture in this setting occurs
most commonly during the last trimester.83 While historically a strong association between pregnancy
and splenic aneurysm rupture was reported, a contemporary series reporting on >67,000 consecutive
live births over 5 years identified no cases of splenic artery aneurysm rupture.98 There is no apparent
role for routine screening for splenic aneurysm in the pregnant patient.101 Rupture risk is increased two
fold by liver transplantation, the mortality following which is 50%.102,103
Figure 91-15. (A) CT angiogram and (B) splenic arteriogram revealing a tortuous splenic artery with two large aneurysms affecting
the main splenic artery; the distal aneurysm (arrow) has extensive calcification and mural thrombus.
Indications for treatment include rupture, symptoms, size >2.0 to 2.5 cm and any size asymptomatic
aneurysm at the time of liver transplantation or in women of childbearing age.87,95,104,105 Historically,
the open surgical treatment of splenic artery aneurysms included aneurysm resection or splenectomy.
Recognizing the immunologic benefits of splenic preservation, arterial ligation, and aneurysm excision
is preferred when possible; however, those patients with multiple and perihilar aneurysms may still
require splenectomy. Laparoscopic and robotic techniques at ligation, aneurysm resection and
splenectomy have become common-place offering negligible risk of open conversion, need for
reoperation and mortality.106–108 Splenic vaccinations and education regarding the need for booster
vaccinations at regular 5-year intervals should be provided. Perioperative morbidity and mortality are
estimated as 9% to 25% and 1% to 5%, respectively, across series.95,96,109–111
More recently, endovascular therapy has been utilized with increasing frequency for both elective and
ruptured cases boasting decreased early morbidity, mortality, and hospital length of stay. While only
2% of all splenic aneurysms were managed with endovascular therapies in 1999, this proportion
increased to 70% between the years 2010 and 2013.111 Embolization with coils, gelfoam, glue,
thrombin, and vascular plugs has been advocated for saccular aneurysms with narrow necks (Fig. 91-
16). Larger vessels with complex wide-neck aneurysms may be better approached with covered stents or
stent-assisted coil embolization.112 Technical success for endovascular treatment is 93% to 98%, limited
primarily by vessel tortuosity that may be overcome with newer, steerable catheters.95,111,113,114
Conversion to open surgery is rarely necessary (<2%) to accomplish successful aneurysm exclusion.111
Postembolization syndrome (PES) complicates 10% to 30% of cases across series and may include left
upper quadrant pain, fever, ileus, platelet dysfunction, leukocytosis, and pancreatitis following
embolization with and without radiographic evidence of splenic infarction.95,111,114,115 Up to 21% of
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patients will demonstrate major splenic infarct and may require reintervention for splenic abscess by
way of percutaneous drainage or splenectomy.95,113 Portal hypertension appears to increase
dramatically the risk of major splenic infarction.113 With late follow-up, endovascular repair is
associated with an average regression in aneurysm size of 1.5 mm/yr.95 Late complications may arise at
an average rate of 3.7% per year, and there is a 3.2% rate of reintervention per year following
endovascular repair.111
Figure 91-16. (A) Celiac arteriogram of a 78-year-old woman with a 4-cm splenic artery aneurysm; (B) Splenic arteriogram
demonstrating a catheter in the proximal splenic artery. Vascular occlusion devices (arrows) have been positioned in the main
splenic artery outflow (distal to the aneurysm) and inflow (proximal to the aneurysm) with multiple vascular coils embedded
within the aneurysm sac.
Patients with splenic aneurysms have long-term survival rates that approach 90% at 10 years
following aneurysm-directed treatments; cause of death is typically unrelated to aneurysm.95 The most
recent meta-analysis of splenic aneurysm therapies identifies significantly greater technical success
balanced with greater 30-day mortality following open repair in comparison to significantly higher rates
of acute minor complications, late complications, and reinterventions following endovascular repair.111
Moreover, a recent decision analysis investigating the cost-effectiveness of open repair, conservative
management, and endovascular repair for splenic aneurysm identified endovascular therapy as the most
cost-effective treatment independent of gender and risk profile of the patient.116
Figure 91-17. Reformatted CT angiogram demonstrating a bilobed and calcified hepatic artery aneurysm.
Hepatic Artery Aneurysm
Hepatic artery aneurysms (Fig. 91-17) account for 20% of all splanchnic artery aneurysms, affecting
men twice as often as women.83,84,117 These aneurysms are mainly solitary and while small hepatic
artery aneurysms (<2 cm) are typically fusiform, larger aneurysms will more often appear saccular.117
The vast majority of these aneurysms are extrahepatic with the common hepatic artery and right hepatic
artery most often affected; 20% to 30% of hepatic aneurysms however, are intrahepatic.84,97,117 Hepatic
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artery pseudoaneurysms are increasingly frequent and account for approximately 50% of hepatic artery
aneurysms.87,97 Pseudoaneurysms may result from diagnostic and therapeutic interventions that require
liver penetration (e.g., biliary stents), liver transplantation, and trauma; their incidence appears to be
increasing secondary to the more frequent and regular use of CT imaging following blunt liver trauma
and hepatobiliary intervention.88,97 True aneurysms present most often during the sixth decade of life
and proposed etiologic mechanisms include mainly atherosclerosis and acquired medial degeneration.
Polyarteritis nodosa, cystic medial necrosis, portal hypertension, infection, arterial fibrodysplasia,
neurofibromatosis, and other arteriopathies are less commonly implicated.87,117
As with most splanchnic artery aneurysms, hepatic artery aneurysms rarely cause symptoms.
Symptomatic patients will most commonly describe right upper quadrant or epigastric abdominal pain
that may radiate to the back, while those patients with rapidly expanding aneurysms may describe
abdominal complaints that mimic pancreatitis. Large aneurysms may erode into the stomach or
duodenum resulting in gastrointestinal hemorrhage or they may obstruct the biliary tract resulting in
biliary colic, hemobilia, and obstructive jaundice.87 Additional physical examination findings like a
palpable pulsatile mass and bruit are uncommon. Diagnosis is often made incidentally by cross-sectional
CT/MRI, ultrasound or arteriography performed for a nonvascular indication.
Rupture appears to complicate a minority of hepatic artery aneurysms (20% to 30%) and results in an
equal distribution of hemorrhage into the peritoneum and the biliary tract.84,87 Rupture into the biliary
tract results in hematobilia, hematemesis, and cholangitis; rarely is there melena and chronic anemia.
Rupture-related mortality approximates 35% to 40%.117 The relationship of rupture risk to aneurysm
size remains unclear and a small series of 22 patients with a mean hepatic artery diameter of 2.3 cm
(range 1.5 to 5 cm) were followed for a mean of 68.4 months without complication.87,117 The presence
of multiple aneurysms and nonatherosclerotic etiology are proposed risk factors for rupture.117 While
historically treatment was recommended for all asymptomatic aneurysms >2 cm in size, some authors
have proposed elective intervention for all and any-size nonatherosclerotic aneurysms and for those
patients with multiple hepatic artery aneurysms while reserving a more conservative approach for those
atherosclerotic hepatic artery aneurysms measuring 2 to 5 cm in size.117
Open reconstruction is favored for aneurysms of the common hepatic artery by way of
aneurysmectomy or exclusion. Often revascularization is not required in light of extensive foregut
collaterals from the GDA and right gastric artery that preserve hepatic perfusion. When necessary,
options for reconstruction may include primary or patch angioplastic closure of the common hepatic
artery, aortorenal bypass, and splenohepatic bypass. Proper hepatic artery aneurysms may be treated by
aneurysmectomy requiring reconstruction using a saphenous vein interposition graft or simple
aneurysmorrhaphy. Distal or intraparenchymal lesions may require resection of the involved liver
parenchyma.89 Elective open surgical repair is associated with approximately 30% morbidity and
negligible mortality.90,92,117 Additional options include transcatheter embolization, which may be an
especially useful adjunct for intrahepatic arterial aneurysms obviating the need for hepatic lobectomy,
and stent graft exclusion for high-risk patients.83,87,90,92,94,118 Technical and clinical success rates with
transcatheter embolization approach 100% and 79%, respectively and offers efficient control of
hemorrhage, shorter hospital length of stay and lower transfusion requirements in cases of rupture
specifically.119 Transient success and recanalization is well described however, mandating thoughtful
postembolization surveillance.
Superior Mesenteric Artery Aneurysm
Superior artery aneurysms account for up to 7% to 14% of all splanchnic aneurysms, depending on the
series.84,86,88,90,91 These aneurysms affect men more frequently than women in their sixth decade of life
and are mainly solitary.84,120,121 SMA aneurysms may result from infection (i.e., nonhemolytic
streptococci in bacterial endocarditis), dissection (Fig. 91-18), medial degeneration, atherosclerosis,
FMD, vasculitis, connective tissue disorder, and trauma.84,88 Additionally, false aneurysms may occur in
the setting of pancreatitis and complicated peptic ulcer disease.120 Concomitant hypertension is
common, affecting >20% of patients with SMA aneurysm, as are associated aortic and
peripheral/splanchnic aneurysms.90,94,121,122
While most patients with SMA aneurysm are asymptomatic, abdominal pain is the most common
symptom followed by nausea, emesis, GI bleeding, and fever in cases of mycotic aneurysm.120–122
Clinical examination may reveal a pulsatile mass in up to one-third of patients. Diagnosis is most
commonly established by CT imaging, although these aneurysms can be appreciated by ultrasound,
MRI, and angiography. Complications may include AMI resulting from thromboembolism and rupture.
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Rupture risk has historically been considered rare and while rupture-associated mortality has historically
approached 50%, more contemporary series cite 30-day mortality rates as low as 12.5% to 38%.84,91,121
No comorbidities or aneurysm characteristics have been found to predict rupture risk.121
Figure 91-18. (A) CT angiogram and (B) intraoperative photo of a large 3.6-cm asymptomatic SMA aneurysm associated with
extensive thoracoabdominal aortic and SMA dissection. The aneurysm was repaired by way of an SMA interposition bypass graft
using nonreversed great saphenous vein; additionally the proximal SMA dissection flap was sharply fenestrated.
Surgical management of SMA aneurysm most often requires aneurysm excision (or exclusion) with
revascularization, most often by way of aortomesenteric bypass.90 Both autologous and prosthetic
conduits have been described. Autologous conduit is favored in cases of mycotic aneurysm and frank
contamination complicating intestinal ischemia while reinforced prosthetic conduit resists
compression/kinking and future dilation.94 Aneurysmorrhaphy and simple ligation of inflow and
outflow vessels (in those patients with appropriate collateralization) have also been described with
success.84,94,120 Contemporary elective surgical results boast negligible morbidity and mortality.94
Endovascular SMA aneurysm exclusion with a stent graft and embolization have been described and
increasingly employed for patients with severe cardiopulmonary disease; these therapies remain limited
by thromboembolic risks to the collateral circulation, endoleak, and limited long-term followup.90,121–125 Aneurysms with a small neck distal to the SMA origin may be conducive to transcatheter
embolization provided angiographic determination of collateral flow is determined as adequate.121
Celiac Artery Aneurysm
Celiac artery aneurysms account for approximately 4% of all splanchnic aneurysms affecting men more
frequently than women in their sixth decade of life.126,127 The incidence in the general population is
unknown. Historically celiac artery aneurysms were primarily associated with infection like syphilis or
tuberculosis and primarily diagnosed postmortem.126 Contemporary etiologic risk factors include
primarily atherosclerosis, developmental risk factors such as common celiacomesenteric trunk, arterial
dysplasia with medial degeneration, collagen vascular disorder, trauma, and dissection.126,127
Concomitant hypertension (20%), aortic aneurysm (18% to 40%), and alternate splanchnic aneurysms
(38%) are common in patients with celiac artery aneurysm.126,127
As with most splanchnic artery aneurysms, celiac artery aneurysms rarely cause symptoms.127
Symptoms may include abdominal pain, primarily epigastric in location with radiation to the back.126
Less common associated symptoms may include nausea, emesis, dysphagia, anorexia, weight loss, and
GI bleeding. Abdominal mass and bruit may be appreciated on physical examination. Diagnosis is most
commonly established by CT imaging, although these aneurysms can be appreciated by ultrasound,
MRI, and angiography.127 Historically, rupture complicated approximately 70% of celiac artery
aneurysms, resulting in near-certain mortality.126 More contemporary estimates suggest rupture rates of
13% with associated 50% mortality.126 Hypertension, aneurysm calcification, presence of thrombus,
gender, and aneurysm etiology do not appear to influence risk of rupture, which has been described in
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