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Aneurysms of Splanchnic and
visceral arteries
Dr Rutvij Shah
DNB SS trainee
Vascular surgery
Sir Ganga Ram Hospital
 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
 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
 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%
 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
 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
 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?
 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
 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
 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
 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
 For SAA
 < 2 cm and asymptomatic – observe with serial imaging
 Except - women - pregnant or childbearing age
 No consensus regarding other Splanchnic AA
OBSERVENT MANAGEMENT
 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
 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.
 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
 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
 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
 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
 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
 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
 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
SPLENIC ARTERY ANEURYSM
 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
 Most SAAs –
 Atherosclerosis (m/c)
 Arterial fibrodysplasia
 Arteritis
 Multiparity
 Studies
 Portal hypertension
 Studies
 Pseudoaneurysm
 blunt trauma, infection, and pancreatitis
 Rare co-related diseases –
 Hematologic and non hematologic neoplasms
 Amyloidosis
 Rheumatologic diseases.
ETIOLOGY
 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
 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
• 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
 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
 Splenectomy
 Not needed - short gastric vessels adequately perfuse
 Preferred for lesions adjacent to the splenic hilum or
involving the intra splenic branches
 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.
 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
 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
HEPATIC ARTERY ANEURYSM
 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
 75% to 80% -
extrahepatic vasculature 4% 5%
28%
63%
 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
 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
 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
 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
 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
 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
 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.
 Options – Embolization/covered stents
 Adv vs Disadv of both
 Endovascular intervention (coil embolization) - safe
and effective method of repair
ENDOVASCULAR TREATMENT
HAA
PSEUDO
TRUE
EXTRA
ENDOVASCULAR
INTRA
OPEN
SMA ANEURYSM
 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
 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
 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
 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%
 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
CELIAC ARTERY ANEURYSM
 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
 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
 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
 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
GASTRIC AND GASTRO-EPIPLOIC
ARTERY ANEURYSM
 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
 >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
 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
PANCREATICO-DUODENAL and
GASTRO-DUODENAL ARTERY
ANEURYSMS
 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
 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
 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
Inferior Mesenteric, Jejunal, Ileal, and
Colic Artery Aneurysms
 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
 Usually symptomatic and often ruptured
 Rupture - mortality - 20%
 Diagnosis is often made at the time of laparotomy.
CLINICAL PRESENTATION
 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
 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
THANK YOU

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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
  • 24.  Most SAAs –  Atherosclerosis (m/c)  Arterial fibrodysplasia  Arteritis  Multiparity  Studies  Portal hypertension  Studies  Pseudoaneurysm  blunt trauma, infection, and pancreatitis  Rare co-related diseases –  Hematologic and non hematologic neoplasms  Amyloidosis  Rheumatologic diseases. ETIOLOGY
  • 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
  • 35.  75% to 80% - extrahepatic vasculature 4% 5% 28% 63%
  • 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
  • 64. Inferior Mesenteric, Jejunal, Ileal, and Colic Artery Aneurysms
  • 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