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Visceral Aneurysms
JordanTasse, BulentArslan, andUlkuCenkTurba
Pathophysiology
Visceral artery aneurysms (VAAs) occur in 0.01–0.2% of
the population [1]. They can either be visceral artery true
aneurysms (VATAs) or visceral artery pseudoaneurysms
(VAPAs), i.e., “false aneurysms.” Both types are clinically
signicant, and patients can present with life-threatening
bleeding after rupture. Visceral artery aneurysms present
with rupture 22% of the time and death in 8% [1]. Detection
has increased due to widespread usage of cross-sectional
imaging such as CT and MRI. Historically, splenic artery
aneurysms have been the most frequent visceral artery aneurysms. The number of hepatic artery aneurysms has
increased during the past two decades, likely due to the
increased numbers of percutaneous liver and biliary procedures and liver transplantation [1].
Visceral Artery True Aneurysms (VATAs)
VATAs occur due to vessel wall degeneration with a defect
in the arterial media, loss of the elastic bers, and decreased
smooth muscle volume. Atherosclerosis, bromuscular
dysplasia, congenital syndromes, and collagen disorders
are all precursors to VAAs. The most common VATAs is the
splenic artery followed by the pancreaticoduodenal arcade.
The risk of rupture is low in aneurysms less than 2cm in
diameter. During pregnancy, however, the risk of rupture
for splenic aneurysms of all sizes increases signicantly.
Pancreaticoduodenal aneurysms occur most frequently due
to an altered ow state secondary to median arcuate ligament
J. Tasse · B. Arslan · U. C. Turba (*)
Rush University Medical Center, Department of Radiology,
Division of Interventional Radiology, Chicago, IL, USA
e-mail: Jordan_c_tasse@rush.edu; Bulent_arslan@rush.edu;
ulku_c_turba@rush.edu
25
compression of the celiac artery or atherosclerotic occlusion. Increased retrograde pressure within the pancreaticoduodenal arcades leads to aneurysm formation in the
absence of bowel or pancreatic abnormalities.
Key Point
The most common VATA is the splenic artery followed
by the pancreaticoduodenal arcade. The most common
site for VAPAs is the hepatic artery.
Visceral Artery Pseudoaneurysm (VAPA)
Visceral artery pseudoaneurysms occur most commonly
due to chronic inammation caused by conditions such as
pancreatitis, infection or vasculitis, blunt, or penetrating
trauma or iatrogenic etiologies such as surgery or percutaneous procedures. The most common site for VAPAs is the
hepatic artery.
Clinical Indication
VATA
The rarity of these aneurysms precludes large studies to
quantify rupture risk with size; thus most size thresholds for
interventions are based on retrospective series or consensus
of experts. Generally, aneurysms are treated when greater
than 2–3cm in diameter [2]. Factors such as clinical symptoms, contained rupture, rapid growth, pregnancy, or anticoagulation use should prompt intervention [3]. With current
techniques and tools, the risk of procedural complications
may be outweighed by risks of surveillance of aneurysms
approaching treatment threshold sizes.
© Springer International Publishing AG, part of Springer Nature 2018
N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_25
285
286
J. Tasse et al.
VAPA
All visceral artery pseudoaneurysms should be treated,
regardless of size, due to their high-risk of rupture [4]. Most
patients with VAPA will have a history of recent surgery, percutaneous or endoscopic procedures, inammation, or infection. These can usually be differentiated from VATA by
clinical presentation and imaging characteristics. Crosssectional imaging will commonly show an otherwise normal
artery with a focal aneurysm and possible surrounding
inammation or fat stranding, indicating a partial or complete rupture. VAPAs typically do not have a sharp surrounding margin, while VATAs do; VAPAs are usually surrounded
by hematoma or fat stranding. Most VAPAs can and should
be treated by interventional techniques [5].
Conventional Therapy
Management of VAAs depends on a multitude of factors,
including size and location of the aneurysm, clinical status of
the patient, and the arterial anatomy associated with the
aneurysm. Medical management of these patients includes
blood pressure control to minimize the risk of aneurysm
growth. Serial imaging at 6-month or yearly intervals can be
considered depending on comorbidities and risk for aneurysm growth and/or rupture.
Surgical management for visceral artery aneurysms has
historically been the standard of therapy. However, with
advancements in minimally invasive techniques, interventional management has surpassed surgery as the preferred
method. Today, nearly all VATAs and VAPAs can be managed
using endovascular techniques in centers with experienced
interventional radiologists. That said, open surgical repair and
reconstruction remain important in patients who may be
hemodynamically unstable or have complex aneurysms such
as one arising at the branch point of the main renal artery [6].
Surgical management involves ligation or excision of an
aneurysm, which can be performed open, laparoscopic, or
using robotic techniques. This can be performed with or
without vascular reconstruction, depending on the status of
collaterals. When necessary, end-organ resection (splenectomy, bowel, etc.) is performed. Open surgical repair in a
hostile anatomic environment, such as in the setting of pancreatitis, sepsis, or multiple previous surgeries, can be technically challenging and is associated with high rates of
morbidity and mortality.
Interventional Therapy
Pre-procedure CT or MR angiography imaging is essential for
diagnosis and procedural planning to determine the aneurysm
location, size, and type and the most suitable intervention.
Favorable characteristics for catheter-based therapy include
saccular aneurysms with a narrow neck, aneurysms with collateral ow, and those involving vessels that are not the only
source of blood supply to that organ [7].
Interventional techniques for treating VAAs include:
1. Embolization of inow (front door) and outow (back
door) branches +/− packing of the aneurysm
2. Stent-graft placement +/− packing of the aneurysm to
preserve parent vessel ow
3. Percutaneous embolization
Interventional treatment is best for aneurysms involving
the parenchymal branches of the hepatic, splenic, renal, or
pancreaticoduodenal arteries [8]. VAPAs should be treated
with proximal and distal embolization of the inow and outow arteries. Although VATAs can also be treated with this
method, often coil packing and preservation of the native
arterial circulation is preferred. Fusiform aneurysms involving bifurcations require endovascular exclusion with the
placement of coils in the inow and outow arteries to obtain
complete occlusion. In these cases, perfusion of the end
organ can be at least partly maintained by collateral ow.
A variety of embolization agents can be used for manage-
ment of VAAs, depending on patient’s clinical status and aneurysm size, type, and location. These include coils and vascular
plugs, particles, microspheres, EVOH, cyanoacrylate glues,
Gelfoam, stent grafts, or uncovered stents in combination with
other embolic agents or rarely thrombin injection.
The How To
1. Arterial access can be obtained through the femoral
or radial approach in order to reach the vessel of
interest (refer to Chap. 8 for more information).
2. Angiogram of the parent vessel (celiac, SMA or
IMA) is performed to delineate the vessel course
and characterize the aneurysms.
3. A catheter, wire, and microcatheter are used to
reach or pass through the aneurysm so that embolics or stent grafts can be delivered. Several techniques exist for treatment of the aneurysmal sac:
(a) Embolization of artery proximal and distal to
the aneurysm sac
This is a commonly used method for both VATAs
and VA PAs and can be easily accomplished with
coils and vascular plugs. Permanent embolic agents
are necessary with this technique to prevent recanalization of the arterial supply to the aneurysm sac.
critical with this technique prior to embolization of
proximal embolization can “close the door” for
further embolization if it becomes necessary.
25.1a)
(continued)
E
s
25 Visceral Aneurysms
287
(b) Exclusion of aneurysm sac with stent graft
25.1b)
This is the preferred method of aneurysm exclusion for both VATAs and VA PA s when distal perfusion to an organ is necessary (e.g., a proximal SMA
25.2). Stent grafts
are most appropriate in larger, more proximal arteries, ones without branch points and non-mycotic
aneurysms. While endografts have been successfully used in mycotic aortic aneurysms, this should
not be the primary approach for visceral aneurysms
when other endovascular options exist due to the
risk of graft infection.
(c) Pa cking aneurysm sac with coils
25.1c)
Packing of saccular aneurysms may allow preser-
rysms. Dense packing is mandatory to assure initial
thrombosis and prevent the recognized risk of coil
25.3).
(d) Packing aneurysm sac with coils after uncov-
ered stent placement
25.1d)
This is another method for preserving parent
aneurysm and a microcatheter advanced through
the stent interstices to pack the aneurysm around
the stent.
(e) Pe rcutaneous embolization
25.1e)
The approach is used for aneurysms that may be
relatively inaccessible by endovascular means. The
aneurysm is directly punctured using CT, ultrasound,
aneurysm until thrombosis of the sac is achieved.
percutaneous needle access into deep visceral arter-
Inflow Outflow
A
B
-
C
Microcatheter
D
Fig. 25.1 Illustration of the various visceral artery endovascular treat-
ment options. (a) Embolization of the artery proximal and distal to the
aneurysm sac. (b) Exclusion of the aneurysm sac with a stent graft. (c)
Packing of the aneurysm sac with coils. (d) Packing of the aneurysm
sac with coils after uncovered stent placement. (e) Percutaneous
embolization
A
Embolic material
Covered stent
Embolic material
Uncovered stent
Percutaneou
needle
thrombin injection, and risk of distal embolization of
thrombus into nontarget territories. If an aneurysm
Splenic Artery Aneurysms
has a short or wide neck, a balloon-assisted approach
can be pursued. The risk of thrombin in these unusual
cases is unintended dissemination into nontarget
areas such as other bowel branches risking infarc-
Approximately 60–80% of all VAAs involve the splenic
artery [8]. These are more frequent in women, pregnancy,
and portal hypertension. During pregnancy, the high-ow
state and estrogen and progesterone receptors in the arte-
at the aneurysm neck to prevent leakage of the percutaneously injected materials.
rial wall may lead to rapid growth or higher rupture risk.
Splenic pseudoaneurysms can occur and are most commonly associated with pancreatitis or direct trauma. Most
aneurysms are small, saccular, asymptomatic, and located
in the mid to distal third of the splenic artery [8]. These
often occur at branch points near the splenic hilum.
Multiple aneurysms are more common in patients with
portal hypertension.
288
J. Tasse et al.
Fig. 25.2 A 57-year-old male with 3.1cm splenic artery aneurysm (arrow) (a) incidentally discovered on CT imaging. (b) Celiac arteriography
demonstrated a splenic aneurysm (arrow). (c) Splenic aneurysm excluded with a covered stent (arrowheads)
Percutaneous intervention has become the mainstay of
treatment due to its high technical success rates and low morbidity [6, 9]. Exclusion of splenic aneurysms can be accomplished via three main techniques:
dysplasia, or aortic pathologies such as dissection; pseudoaneurysms can occur following partial nephrectomy or percutaneous intervention. Renal artery true aneurysms most
frequently occur in the renal hilum at branch points, and
pseudoaneurysms occur distally following biopsies or surgi-
1. Stent-graft placement across the aneurysm neck. This
may be the preferred option, when possible, because it
maintains perfusion to the spleen, preventing possible
infarction. This frequently cannot be accomplished due to
the tortuosity of the splenic artery.
2. Filling the sac with coils or other embolic agents (see
cal intervention. More proximal aneurysms can often be
managed with stent-graft deployment or aneurysm sac
embolization. However, for distal aneurysms, embolization
techniques will often involve at least some degree of
infarction; attempts should be made to minimize this to preserve renal function.
Fig.25.1c).
3. Exclusion of the sac via embolization of proximal and
distal branches. Both sides of an aneurysm must be embo-
Hepatic Artery Aneurysms
lized as collateral ow to the sac can occur in a retrograde
fashion via pancreatic and short gastric arterial branches.
Hepatic artery aneurysms are the second most common
VAA, accounting for approximately 20% [8] of cases.
Approximately 50% are VAPAs occurring secondary to prior
Renal Artery Aneurysms
surgery, liver transplantation, or percutaneous intervention
[7]; therefore, most intrahepatic aneurysms are pseudoaneuRenal artery aneurysms can present as true aneurysms secondary to atherosclerosis, vasculitis such as bromuscular
rysms. When ruptured, hepatic artery aneurysms can present
with hemobilia, intraperitoneal hemorrhage, or subcapsular
25 Visceral Aneurysms
289
Fig. 25.3 A 67-year-old female presenting with hematochezia. (a)
Mesenteric angiography demonstrated pseudoaneurysm (arrow) arising from the inferior mesenteric artery. (b) Vasa recta angiography
through a microcatheter shows the pseudoaneurysm (arrow) in detail.
bleeding. Approximately 80% of patients with hepatic artery
aneurysms present with aneurysmal rupture [10].
Embolization of both inow and outow arteries is essential
because of the extensive arterial collateral supply and risk of
retrograde reperfusion. Hepatic ischemia is rare due to the
portal vein supply of the liver. Stent grafts have played a role
in treating hepatic artery aneurysms as well (Fig.25.4).
(c) Postembolization angiography shows exclusion of the pseudoaneu-
rysm via selective coil embolization (arrowheads). Preservation of sur-
rounding bowel supply is evident
Gastroduodenal Artery (GDA) andPancreatic
andPancreaticoduodenal Artery (PDA)
Aneurysms
GDA, pancreatic, and PDA pseudoaneurysms most com-
monly occur secondary to inammation caused by
pancreatitis; peptic disease; pancreatic, bowel, or liver sur-
290
J. Tasse et al.
Fig. 25.4 A 65-year-old male presenting with hemobilia and gastroin-
testinal hemorrhage after a percutaneous liver biopsy. (a) Selective
hepatic arteriography demonstrates relatively large pseudoaneurysm
(arrowheads). (b) Angiogram demonstrates the pseudoaneurysm arises
gery; or endoscopic procedures, e.g., sphincterotomy
(Fig.25.5). VAPAs usually present after rupture with epigastric abdominal pain and/or gastrointestinal bleeding. They
can almost always be treated with transcatheter embolization. However, due to the rich collateral network of this vascular bed, it is critical to identify and embolize the distal and
proximal arteries adjacent to an aneurysm. Failure to do so
will often result in repeat hemorrhage.
True aneurysms may also occur in this territory and
account for approximately 6% of visceral artery aneurysms,
most commonly from the GDA (Fig.25.6) [10]. The etiology of aneurysm formation is often an altered ow state
caused by celiac, superior mesenteric artery, or inferior
mesenteric artery stenosis or occlusion. It may be prudent
from the proximal right hepatic artery (arrowheads). (c) Following
endovascular treatment, angiographic images demonstrating exclusion
of the large right hepatic pseudoaneurysm successfully treated with
covered stent placement (arrows)
to address these stenoses to prevent future aneurysm formation via surgical release of the median arcuate ligament and
rarely stents.
Celiac Artery Aneurysms
Celiac artery aneurysms account for only 4% of VAAs [7].
These are most frequently true aneurysms secondary to atherosclerosis or median arcuate ligament compression.
These can accompany aortic aneurysms in 20% of cases or
other VAAs in 40% [8]. Endovascular management can be
challenging, as they often occur at branch points of the
celiac artery. Options include aneurysm sac coiling, uncov-
25 Visceral Aneurysms
291
ered (bare) stent placement with coiling through the struts,
or intentional embolization of the left gastric and splenic
arteries to allow stent-graft placement into the hepatic
artery (see Fig.25.1c, d). Surgical resection (aneurysmectomy) or aorto-celiac bypass grafting is an option.
Superior andInferior Mesenteric Artery
Aneurysms (SMA andIMA)
Aneurysms of the superior and inferior mesenteric arteries
are rare. The SMA accounts for approximately 5% and the
IMA 1% of all visceral artery aneurysms [10, 11]. When
present, they usually occur within the rst 5cm of the artery
origin. Preferred treatment in these locations would be
options that allow distal blood ow such as a stent grafting or
coiling the aneurysmal sac with or without bare stent in the
artery.
Complications
Complications following endovascular management of visceral artery aneurysms are rare.
Splenic Aneurysm
Splenic Infarction
Distal embolization of the splenic artery increases the
likelihood of ischemia and infarction. Proximal splenic
artery occlusion rarely results in signicant splenic ischemia due to collateral vasculature including the left gastric, dorsal pancreatic, and gastroepiploic arteries.
Nontarget embolization can also lead to infarction. Partial
splenic infarction can typically be managed with supportive care and antibiotics. Complete splenic infarction may
require splenectomy.
Fig. 25.5 A 71-year-old woman with high-grade stenosis at the celiac
artery origin and inferior pancreaticoduodenal artery aneurysm
(Courtesy of Westley Smith, MD)
Pancreatitis
Pancreatitis is a rare complication but may result from occlusion of the short or dorsal pancreatic branches during splenic
artery embolization.
Fig. 25.6 An 82-year-old female presents with acute rupture of GDA
pseudoaneurysm. (a) GDA pseudoaneurysm rupture (arrowheads)
resulting in extravasation into the duodenum. (b) GDA angiography
after embolization with coils (arrowheads) and a microvascular plug
shows no residual aneurysm lling or extravasation
292
J. Tasse et al.
Renal Aneurysm
The renal arteries do not collateralize within the kidney.
Therefore, complete embolization of a branch containing an
aneurysm will result in infarction of that portion of the renal
parenchyma. This may be acceptable in peripheral interrenal
aneurysms; however, larger and more proximal aneurysms
must be treated with approaches that preserve parent vessel
ow to the downstream kidney (see Fig.25.1b–d).
Hepatic Aneurysm
Hepatic Ischemia, Infarction, or Abscess
Occlusion of the common, proper, or lobar hepatic artery
will typically cause an increase in liver function tests.
Depending on underlying liver function, this will typically
be transient, normalizing after days to weeks. This is due to
the predominant perfusion of the liver via the portal venous
circulation. If there is portal venous compromise, infarction
and subsequent abscess can occur.
Cholecystitis
Ischemic cholecystitis is rare; however, it can occur during
hepatic aneurysm embolization if occlusion of the cystic
artery occurs.
GDA andMesenteric Aneurysms
Stomach andSmall or Large Bowel Ischemia or Infarction
Due to the rich collateral supply, this complication is rare.
However, care must be taken when embolizing distal
branches of the superior or inferior mesenteric artery. At the
vasa recta level, there may be few collateral branches such
that bowel ischemia or infarction becomes a greater risk.
Patients with prior bowel of gastric surgery, such as a
Whipple procedure, may have reduced collateralization,
increasing potential risk for ischemia after embolization.
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Renal Artery Stenosis
AndreUacker andAlanH.Matsumoto
26
Pathophysiology
Renal artery stenosis (RAS) is the anatomic narrowing of
one or more of the arteries to the kidney(s). Once RAS
begins to impair blood ow and perfusion to the kidney(s),
a cascade of physiologic effects occurs. The renal medullary
juxtaglomerular apparatus releases renin in response to a
decrease in renal capillary perfusion pressure. Renin is an
enzyme that converts angiotensinogen to angiotensin I,
which is then converted to angiotensin II by angiotensinconverting enzyme in the lungs. Angiotensin II stimulates
the release of aldosterone, which leads to sodium and water
retention and potassium wasting. Angiotensin II also causes
peripheral vasoconstriction, activation of the sympathetic
nervous system, and vascular remodeling. The physiological effects that result from diminished perfusion to the
kidney(s) lead to so-called renovascular hypertension
(RVH) [1–4].
In the presence of RAS, the intrarenal autoregulatory
pathways will also try to maintain intrarenal perfusion and
delivery of blood and oxygen to supply the high energy
demands of the renal medulla. With RAS, inammation, oxidative stress, and microvascular injury can result and lead to
the generation of reactive oxygen species and intrarenal
brosis. Ultimately, chronic kidney injury and a decrease in
the glomerular ltration rate (GFR) can be sequelae of
chronic renal ischemia. The interactions between the inammatory, intrarenal, intracellular, and regenerative autoregulatory mechanisms and the physiologic responses to a decrease
in perfusion to the kidney(s) are very complex and not fully
explained by the Goldblatt RAS model alone [1–3].
A. Uacker · A. H. Matsumoto (*)
University of Virginia Health System, Department of Radiology
and Medical Imaging, Charlottesville, VA, USA
e-mail: au2b@virginia.edu; ahm4d@virginia.edu
Key Point
Goldblatt renal artery stenosis model:
Constriction of the renal artery leads to decreased
renal perfusion which causes the release of renin and
the renin-angiotensin-aldosterone cascade activation,
leading to hypertension.
In addition, there are believed to be two stages of RVH:
acute and chronic. In the acute phase of RVH, the patient
has an increase in intravascular volume due to water retention and signicant peripheral vasoconstriction, both
factors contributing to the hypertension. Relief of the
hemodynamic stenosis results in spontaneous diuresis and
peripheral vasodilation. In the more chronic stage of RVH,
the hypertension is less volume dependent, and there has
been a recalibration of the renin-angiotensin-aldosterone
axis so that the elimination of the stenosis may not have
as dramatic a physiologic effect on intravascular volume
and peripheral vasodilation. What controls when a patient
transitionsfrom an acute to chronic phase of RVH is not
known. Similarly, what triggers the stimulation of intrarenal inammatory processes with chronic ischemia is not
totally understood [3, 5].
There are many examples of patients with severe RAS
found at autopsy who were known to have normal blood
pressure and renal function. In addition, the autonomic nervous system (ANS) may have a role in the genesis of hypertension [6]. The interplay between the ANS and RAS is
unclear at this time. Therefore, rather than trying to account
for the complex pathophysiology and ANS nuances and
interactions that occur with RAS, this chapter will focus on a
practical clinical approach to the management of patients
with signicant RAS and RVH. However, the reader should
be aware that RAS is a contributing factor for hypertension
in less than 2% of patients with hypertension.
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