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Aneurysms of splanchnic and visceral arteries
1. Aneurysms of Splanchnic and
visceral arteries
Dr Rutvij Shah
DNB SS trainee
Vascular surgery
Sir Ganga Ram Hospital
2. Definition
Rare but Lethal
First described - > 200 years ago
De Bakey et al (1953) - first successful treatment of
SMA aneurysm.
First large case series - 1980s.
INTRODUCTION
3. 1/3 of splanchnic artery aneurysm - aortic, renal, iliac,
lower extremity, or cerebral artery aneurysm.
Incidence in general adult population - 0.1% to 2%
10% in the elderly
Saccular vs fusiform - No established significance
pertaining to differences in etiology or rupture risk
EPIDEMIOLOGY
4. Spleenic AA - 60%
Hepatic AA - 20%
SMA A - 5.5%
Celiac AA - 4%
Gastric AA - 4%
Jejunal, ileal,
and colic AA - 3%
Pancreaticoduodenal AA - 2%
Gastroduodenal AA - 1.5%
IMAA - <1%
5. True splanchnic aneurysms
Atherosclerosis (m/c)
medial degeneration
collagen vascular diseases
fibromuscular dysplasia.
Specific for SAA
Multi-parity
portal hypertension
Post-transplant status
Pseudoaneurysms
infectious or inflammatory conditions - vasculitis
surgery or other iatrogenic intervention
trauma
ETIOLOGY
6. Multiple splanchnic aneurysms
systemic arteritis
endocarditis with septic emboli
connective tissue disorders
excessive acetaminophen use.
Von Recklinghausen’s disease
Ehlers-Danlos’ syndrome type IV
Periarteritis Nodosa
Bechets disease
7. Aneurysm rupture - devastating clinical scenario -
perioperative mortality rates - 20% to 70%
22% present as clinical emergencies
SAAs - relatively low rupture rate (< 2%) in cases not
associated with pregnancy.
“Double rupture” - 25%
SAAs in pregnant women - Maternal mortality - 75% in the
setting of ruptured SAAs, with a concomitant fetal
mortality of 95%.
> 50% - rupture during pregnancy, 2/3rd - in 3rd trimester.
Risk of rupture?
8. Rates or risk factors of rupture for less prevalent
splanchnic artery aneurysms – unknown
Reported rates
60% to 80% for HAAs,
38% for SMAAs,
7% for CAAs,
68% for PDAAs,
56% for GDAAs, and
90% for gastroepiploic artery aneurysms
SAA, CAA and SMA – relatively lower rupture rates
9. Open surgery / Laparoscopic surgery
Minimally invasive management - coil or glue embolization
or covered stents or thrombin injection
Incorporation of two modalities in a staged procedure
approach
A recent review of 27 case series over the last 20 years –
No consensus about precise indications
Nor the best type of surgical treatment
• Depends on - both patient and aneurysm characteristics.
Age, gender, and presence of comorbidities
Size of the aneurysm, anatomic location, and collateral
circulation
TREATMENT - PRINCIPLES
10. Patient evaluation
H/o trauma, pancreatitis, infectious and/or inflammatory
process to ascertain etiology and risk of rupture.
Past surgical intervention / hepatobiliary instrumentation /
current pregnancy status / risk factors associated with
atherosclerosis
Previous imaging - any growth aneurysm
A cardiac workup
Patients undergoing SAA embolization or ligation - risk for
splenic loss - Pneumococcal vaccine
All pseudoaneurysms - increased growth rate and
propensity to rupture - treated, irrespective of size or
location
ELECTIVE REPAIR
11. Ruptured aneurysms - true surgical emergency
Often the preoperative diagnosis - ruptured abdominal aortic
aneurysm
Resuscitate - exploratory laparotomy - Ligation of a splanchnic
aneurysm with or without vascular reconstruction.
Ruptured SAA usually - concomitant splenectomy.
Ruptured SMAAs and CAAs - Reconstruction necessary
Proximal HAAs, PDAs, and GAAs - Vascular reconstruction is rarely
needed in emergent treatment – extensive collateralization
Mesenteric arterial aneurysms - any small bowel affected by ischemia
may require resection.
Endovascular management of ruptured splanchnic artery aneurysms -
reported as a feasible option, but should only be used in selective
stable cases.
EMERGENT TREATMENT
12. For SAA
< 2 cm and asymptomatic – observe with serial imaging
Except - women - pregnant or childbearing age
No consensus regarding other Splanchnic AA
OBSERVENT MANAGEMENT
13. Standard of care
Aneurysmectomy and bypass grafting
Aneurysmectomy and end-to-end anastomosis
Aneurysmorrhaphy with arterial reconstruction
Ligation.
Frank rupture and hemodynamic collapse - Ligation without
reconstruction
Vein grafts used preferentially
Esp -in suspected infection or bowel ischemia
Laparoscopic treatment - effective alternative
esp in elective setting
in aneurysms located in the distal Splenic artery
Laparoscopy - not for rupture and pregnant females
OPEN SURGERY
14. Advantages –
Direct visualization of end organs
Concomitant diseases processes (e.g., pancreatic
pseudocysts or abscesses)
Determining the need for arterial reconstruction (eg - if
intestinal viability is compromised)
Mitigates the need for closer follow-up and serial
imaging required after endovascular therapies.
15. Multiple options –
Coils and glue
Particle or gelfoam injection
Covered stents and flow-diverting stents
Injection of thrombin or ethyl alcohol
Cleveland Clinic reported results of the endovascular treatment
of 48 patients - 20 aneurysms and 28 pseudoaneurysms
Mayo Clinic reported - 185 splanchnic artery aneurysms over 10
years
ENDOVASCULAR REPAIR
16. Advantages
Shorter hospital stay,
Local anesthesia
Patients with comorbidities/ intra-abdominal malignancy or
previous surgery
Drawbacks
Risk of access-related injury
Contrast toxicity
End-organ embolization
Relatively higher rate of failure compared with open surgery
Prolonged post-embolization imaging surveillance
17. Access – Femoral/Brachial
Anticoagulation
A 5F, 6F, or 7F long sheath - to accommodate vascular
devices.
Sheath must be well placed into the proximal artery
proximal to the aneurysm
Principles
18. Cyanoacrylate glue
The rate of glue polymerization – usage of ethiodized oil
dilution
1: 1 oil-to-glue - to embolize a vessel with high rates of
blood flow
2 :1 or 3 : 1 - when the blood flow rates are slower or the
catheter tip cannot be closely approximated to the
desired site of polymerization.
3F microcatheter system
EMBOLIZATION
19. Fibered or non fibered coil
Pushable and detachable
Fibered coils - superior
Inconel (Ni-Chr superalloy) or platinum
The coils ranging from 0.014- to 0.052-
inch sizes are available
20% oversize - is recommended
First distally to the sac and then
proximally to the sac.
For aneurysms supplied by terminal
branches - sac can be directly injected
or coiled
COIL EMBOLIZATION
Nester Fibered
coil by cook
20. In selected cases
Advantage - preserving prograde blood flow
Limited by relatively large and rigid delivery devices - Not
ideal for navigating secondary and tertiary visceral branches.
Risk of occluding flow into side branches of the target vessel.
Oversizing of the endograft should be avoided.
Proven safe in several major visceral branches, with an
excellent success rate and safety profile
Follow-up imaging is not limited by artifacts from radiopaque
coils or glue - allows for accurate documentation and
surveillance
COVERED STENTS
21. Specially designed multilayered stents
Reduce flow velocity in the aneurysm
sac - promoting thrombosis and
maintaining flow within the main artery
The FDSs originally - intracranial
aneurysms
A study of FDS - 19 splanchnic artery
aneurysms - reported encouraging
results of freedom from rupture,
patency of the stents, aneurysm
thrombosis, sac shrinkage, and low
morbidity and mortality.
FLOW DIVERTING STENTS
23. Most common - 60%
Incidence - 0.78%, (incidental, on NCCT/MR)
F:M - 4 : 1
Younger age compared with splanchnic aneurysms
SAAs associated with symptoms and/or rupture - average 3
cm
Saccular morphology
Location - mid or distal splenic A
“Giant” SAAs (> 10 cm) - more often in men.
EPIDEMIOLOGY
25. Most - incidental
Xray abdomen- Circular calcified shadows or “signet rings” seen in
the left upper quadrant
CT/MRI
Some patients - vague abdominal pain or even an abdominal bruit
Giant SAAs - mass effect on the adjacent viscera
Hemosuccus pancreaticus
Rupture - Hemodynamic collapse with acute left-sided abdominal
pain - “double rupture”
Pseudoaneurysms - rupture into adjacent structures
Gastrointestinal tract
Pancreatic duct
Splenic vein
Pancreatic pseudocysts.
CLINICAL PRESENTATION
26. Indications
All symptomatic and ruptured SAA
Orthotropic liver transplantation or portal hypertension
Asymptomatic pregnant or childbearing age females
Pseudoaneurysm
If none of above - Consensus in the literature - > 2 cm -
dependent on confounding factors like age or medical
condition (Serial observation – safe and viable option)
TREATMENT
27. • Lakin et al reviewed the Cleveland Clinic - 128 SAAs - 15 years
Average growth rate - 0.2 mm/year
No rupture
A large review by Mayo Clinic - 217 patients with SAAs.
168 – non-operative management for 75 months
The mean size in non-operative group - 2.1 cm
10% - noted to have growth averaging 0.06 cm/year
No rupture
3 of the original 168 patients - intervention - for aneurysm
growth
28. Options –
Ligation with arterial
reconstruction
Proximal and distal ligation of the
aneurysm
Complete resection with
splenectomy
Approach – Left subcostal /
midline
Principles - Mobilization of the
spleno-colic ligament –
mobilization of the splenic
flexure - aneurysm sac identified
OPEN SURGERY
29. Splenectomy
Not needed - short gastric vessels adequately perfuse
Preferred for lesions adjacent to the splenic hilum or
involving the intra splenic branches
30. All options – reported by laparoscopic intervention
with long-term results of high survival and low
complication rate
In Mayo Clinic series - 49 patients treated surgically
39 - elective surgery
Operative mortality - 20% in ruptured group and 5.1% in
elective group
No reported aneurysm recurrence over a mean follow-
up of 70 months.
31. Coil embolization / cyanoacrylate glue or a combination
A Cleveland Clinic series - 49 SAAs treated with
endovascular intervention
Coil embolization - 45 cases ( 11 - glue used adjunctively)
Technical success rate – 96%
Complications - Access site hematoma requiring operative
drainage, and two brachial artery access site injuries
Post-embolization syndrome (PES) - five patients.
ENDOVASCULAR
32. Covered stent repair - ideal for exclusion of aneurysm
with preservation of the splenic artery
The use of covered stents - limited to proximal
lesions, and their use has not been as widespread as
endovascular ablation
34. Second most common location - 20%
First described by Wilson in 1809
First successful ligation reported in 1903
Incidence - less than 0.4%
HAA incidence on the rise - increasing use of hepatobiliary
instrumentation and manipulation
Some recent series - HAAs - most frequently reported
aneurysms
Concomitant aneurysms of other splanchnic vasculature –
1/3rd of HAAs
EPIDEMIOLOGY
36. Most HAAs – Atherosclerotic
In a Mayo Clinic series of 36 true HAAs
Most commonly associated comorbidity – hypertension
Other etiologies –
Arterial dysplasia
Trauma
PAN
Biliary diseases
Percutaneous and endoscopic procedures
Mycotic etiology - frequently in patients with a history of
endocarditis - decreased with the widespread antibiotics
ETIOLOGY
37. The age of presentation - 60 years (if trauma etiologies excluded)
Majority of HAAs – asymptomatic - incidentally
HAAs – 25% chance of rupture
Symptoms –
Abdominal discomfort and back pain
Rupture into the bile ducts - Quincke’s triad – hemo-bilia, jaundice, and
right upper quadrant pain
Erosion into the stomach - rare - upper and lower gastrointestinal
bleeding
No studies correlating HAA size with likelihood of rupture
CLINICAL PRESENTATION
38. True and false HAAs
The Cleveland Clinic found –
Pseudoaneurysms - likely to be symptomatic versus true aneurysms
Pseudoaneurysms - required urgent intervention
Most of the splanchnic pseudoaneurysms - presented with
gastrointestinal bleeding or hemobilia - 92% required urgent
intervention
All splanchnic pseudoaneurysms – treated (regardless of size)
Association of HA pseudoaneurysm after liver transplantation.
Incidence - 0.3% to 2%
Present with intra-abdominal or gastrointestinal bleeding within 2
months after transplantation
39. Indications
Symptomatic aneurysm
Pseudoaneurysm
Aneurysms more than 2 cm in size
Multiple HAAs
Patients with PAN or other inflammatory condition
Observant treatment - patients with significant
comorbidities or life expectancy of less than 2 years
TREATMENT
40. Approach - Right subcostal incision/Midline
laparotomy
Principles – Identification of gastro-hepatic
omentum – Hepatic artery
The liver and gall bladder - examined and
palpated - bile stones, signs of infection, or
occult malignancy.
Examination of visceral vasculature - any
concomitant splanchnic artery aneurysm
TREATMENT – OPEN SURGERY
41. Open surgical repair of HAAs depends on -
anatomic location, collateral flow, condition
of the liver, and medical status of patient
Techniques –
Excision
Ligation with or without bypass
If needed - hepatic resection
Common HAAs - simple ligation -
gastroduodenal artery - sufficient collateral
flow
HAAs distal to GDA -arterial reconstruction
42. If Hepatic artery ligated - increase in oxygen content of
the portal vein blood through splanchnic arteriovenous
shunting - hence never performed in cirrhosis or
compromised liver function.
Proper or right hepatic artery ligation - gall bladder is at
risk for necrosis - cholecystectomy should be performed
simultaneously
Aneurysms located within
the parenchyma
Resection
Ligation
Embolization.
43. Options – Embolization/covered stents
Adv vs Disadv of both
Endovascular intervention (coil embolization) - safe
and effective method of repair
ENDOVASCULAR TREATMENT
46. 5.5%
M=F
Average age - 50 years
Incidence - 1 in 12,000 to 1 in 19,000
Almost exclusively along the first 5 cm of the artery
MC etiology – infection(60%) (bacterial endocarditis)
Size and orientation of its base in relation to the aorta
Other conditions - atherosclerosis, connective tissue
disease, pancreatitis, and trauma
EPIDEMIOLOGY + ETIOLOGY
47. Incidental discovery
Non ruptured (70-90%) SMAAs are more likely to
cause symptoms
Vague colicky pain
Intestinal angina
Nausea/Vomiting/Weight loss
GI bleeding
Signs of bowel ischemia
SMAAs - rupture rate -38% to 50%
CLINICAL PRESENTATION
48. High risk for rupture and associated mortality – Always repair
Observational management – small, non-infected SMAAs in
patients with significant comorbidities
Progressing symptoms and enlarging aneurysms - endovascular
stent placement
Bowel ischemia or failed endo luminal intervention - open
surgical management
SMAAs can be treated surgically
Aneurysmectomy with arterial reconstruction
Simple ligation- rare
TREATMENT
49. SMAAs - predilection for mycotic or
inflammatory etiology - contraindication
for PTFE or Dacron
Approach - midline approach or
retroperitoneal approach
Maddox maneuver - left-sided medial
visceral rotation
Confirm the presence or absence of
aberrant right hepatic artery branch
Preferred - Aneurysmectomy with arterial
reconstruction
SMAA surgical repair - relatively high
mortality of - 15%
50. INDICATIONS
High-risk candidates
Hostile abdomen
OPTIONS
Coil embolization
Stent grafts
Long-term outcomes – not available
Reported complications - fractured stents and
embolization of stent fragments
ENDOVASCULAR
52. 4%
True prevalence based on autopsy review - 1 in 8000
Concomitantly with
Other splanchnic artery aneurysms - 40%
Abdominal aortic aneurysms - 20%
Majority - Atherosclerosis
Infectious etiology - 20%
Iatrogenic intervention
Spontaneous isolated dissections (younger age group)
Median arcuate ligament syndrome
M>F
Average age - 56 years
Reported association with anomalous origins of the right and left
hepatic arteries, a common celiaco-mesenteric trunk, and other
anomalous mesenteric vasculature
EPIDEMIOLOGY + ETIOLOGY
53. Unlike SAAs, most CAAs - symptomatic at presentation
Vague colicky abdominal pain
Intestinal angina
Signs and symptoms of bowel ischemia
Can present with rupture (earlier studies)
10% to 20% cases
Mortality of 50%
Acute abdominal pain
Hemorrhagic shock are frequently encountered in cases of rupture
Double rupture
No established aneurysm characteristic or patient comorbidities that
may predict rupture risk - Size at presentation, aneurysm etiology,
and aneurysm calcification
CLINICAL PRESENTATION
54. Mayo Clinic series
Endovascular intervention - appropriate option for
high risk patients
Endovascular intervention - Used with increasing
success
Coil or glue embolization
Percutaneous thrombin or ethanol injection
Stent-grafting
TREATMENT
55. Surgical options
Simple ligation
Aneurysmectomy with or without arterial reconstruction
Arterial reconstruction depends on - aneurysm location and
the adequacy of mesenteric collateralization
Ligation alone - reported with good results - avoided in
patients with liver disease
Approach – midline trans-peritoneal abdominal approach
Post op - Intestinal viability should be monitored
OPEN SURGERY
57. Less than 4%
Most common - Atherosclerosis (30%)
Trauma in 25%
Infection in 15%
Comorbid conditions - peptic ulcer disease, vasculitis,
and pancreatitis
Sixth or seventh decade of life
Majority - along the left or right gastric artery
GA : GEA aneurysms - 1:10
ETIOLOGY
58. >90% of reported GEAAs - ruptured
Epigastric pain
Hemo-peritoneum – peritonitis
Hemorrhagic shock
Peritonitis - laparotomy - diagnosis
Can present with symptoms other than rupture
Incidental diagnosis – increased with advanced
imaging
CLINICAL PRESENTATION
59. Mortality rates of ruptured
GAAs and GEAAs - 70%
REPAIR
Emergent or ruptured cases - Open laparotomy
Options - Aneurysmectomy or exclusion
Depending on the location, simultaneous revascularization
to maintain arterial inflow is required
Endovascular approach - coil embolization - accepted
form of treatment
Isolation of the aneurysm neck vs proximal and distal
embolization vs proximal embolization alone
TREATMENT
61. 2% and 1.5%
Roughly 100 cases of PDAAs are described in the literature -
most - single case reports
Pseudo-aneurysms - associated with pancreatic pathology,
celiac occlusion or stenosis, abdominal trauma, iatrogenic
injury
M : F - 4 :1
Average age - sixth decade
True aneurysms - likely caused by increased blood flow
through the pancreatic arcades secondary to celiac
occlusive disease or median arcuate ligament syndrome
ETIOLOGY
62. Majority of patients have clinical findings
Rupture > Symptomatic > Incidental
Symptoms - Gastrointestinal bleeding, hypotension,
emesis, diarrhea
Rupture –
65% - into gastrointestinal or biliary tract
35% - into the retroperitoneal space
In one series, 75% of PDAAs presented as ruptured,
with 50% mortality
CLINICAL PRESENTATION
63. Patients with rupture - mortality rates - 30% to 40%, even with
intervention
General consensus - Treatment of these lesions, regardless of size
In addition to ligation of the aneurysm, a partial pancreatectomy
or pancreaticoduodenectomy may need to be performed
Endovascular techniques - excellent option - Coil embolization
Promising success rates
Percutaneous transabdominal thrombin injection - also described
TREATMENT
65. Rare
Most reported lesions are small (<1cm)
Etiologies - poorly defined
Inflammation and infection - one third of cases
PAN and the development of multiple IMAAs.
Collagen vascular disease and autoimmune disorders
M:F - 5:1
There is also an association with inferior mesenteric
branch aneurysm formation and stenosis or occlusion of
the SMA and celiac trunk
EPIDEMIOLOGY AND ETIOLOGY
66. Usually symptomatic and often ruptured
Rupture - mortality - 20%
Diagnosis is often made at the time of laparotomy.
CLINICAL PRESENTATION
67. Any lesion encountered should be treated
Open surgical treatment - ligation of the aneurysm
with arterial reconstruction
Endovascular treatment
Treatment results - favorable with few reported
technical failures
TREATMENT
68. Rare
Meta-analysis of English and French literature - 176 patients
with 198 visceral venous aneurysms
Location - main portal vein, junction of the superior
mesenteric and splenic veins, hepatic hilum
Complications - thrombosis, adjacent organ compression,
and rupture
Treatment - Open aneurysmorrhaphy or aneurysmectomy
is indicated for symptomatic/complicated cases
Role for endovascular intervention remains undefined
VISCERAL VEIN
ANEURYSM