Visceral aneurysm Diagnosis and Interventions M.NEDEVSKA
History 1953 De Bakey and Cooley
Visceral aneurysm � VAAs –rare, reported incidence of 0.01 to 0.2% on routine autopsies. � Clinically important � Potentially lethal � 22% present as clinical emergencies � 8% result in death. Visceral artery aneurysm: risk factor analysis and therapeutic opinion. Huang YK, Hsieh HC, Tsai FC, Chang SH, Lu MS, Ko PJ Eur J Vasc Endovasc Surg. 2007 Mar; 33(3):293-301.
Visceral aneurysm � Most аsymptomatic. � Found incidentally on imaging. � Increasingly diagnosed- cross sectional imaging, aging population. � 1/3 of patients – concomitant aneurysms. � Etiology, pathogenesis and natural history is not well known. � True and False aneurysm. � High mortality rate with rupture.
Visceral Aneurysm � Splenic artery 60 % � Hepatic artery 20% � Superior mesenteric artery (SMA) 5,5% � Celiac artery 4% � Gastric and gastroepiploic artery 4% � Gastroduodenal and pancreatic branches 3% � Inferior mesenteric artery (IMA) less than 1%.
Etiology True VAA False VAA Pseudo aneurysm � Atherosclerosis � Spontaneous dissection � Fibromuscular dysplasia � Infection of adjacent organs � Hereditary disease : � Inflammation � Collagen vascular disorders � Abdominal trauma � Hemorrhagic telangiectasia � Iatrogenic arterial trauma
Visceral artery pseudoaneurysm Clinical features Imaging features � History of arterial trauma � Focal arterial disruption � Biliary tract manipulation � Otherwise normal artery � Intraabdominal or retroperitoneal � Irregular aneurysmal wall inflammation � Presence of perivascular inflammation � Malignancy
Clinical presentation � Silent clinical presentation, incidental findings. � Epigastric or postprandial pain and weight loss - compression of adjacent structures, thrombosis with or without distal embolization with clinical signs of mesenteric ischemia or solid organ infarction. � Pain due to complications - at the time of rupture or impending rupture - life threatening hemorrhage. VAA rupture intraperitoneal, retroperitoneal and GI bleeding, bleeding into adjacent organs
Risk of rupture � Patient characteristics � Aneurysm diameter � VAA localization � Aneurysm etiology and morphology - true or false � Underlying disease – congenital defects, atherosclerosis. � Mycotic/inflammatory aneurysm � Rate of growth
Diagnosis � US examinations � CTA is generally the preferred imaging method - allows for accurate diagnosis, anatomical characterization, and interventional planning � MRA may be a reasonable alternative.
Diagnosis � Diagnosis confirmation � Analysis of vessel tortuosity � Celiac trunc stenosis � Aneurysm morphology- size, shape, diameter of involved artery before and after the aneurysm, size of the neck (sacciform), length (fusiform) � Number of afferent and efferent branches � Locoregional anatomy – collateral vessels, anatomical variants, aneurysm in other locations. � Determining procedural approach
Clinical management – to treat or not � Treatment � Watchful waiting � No evidence based data � Individual treatment decisions – clinicians experience and technical facilities � VAA > 2sm. � Selection of treatment modality- clinical symptoms, location and co-morbidities.
Specific patients group European Journal of Vascular and Endovascular Surgery 2017 53, 460-510DOI:(10.1016/j.ejvs.2017.01.010)
What kind of treatment? Endovascular treatment Open or laparoscopic surgery � Implantation of a covered stent � Resection and end to end anastomosis � Embolization with coils or glue � Reimplantation � Arterial stenting � Graft interposition � Inflow and outflow occlusion of the � Simple ligation involved vessel � Organ resection if necessary. � Flow diverting stents � Percutaneous thrombin injection.
What kind of treatment? Open or laparoscopic surgery Endovascular treatment � Excluding the aneurysm completely with � Greater benefit in cases with VAA rupture minimal compromise of the collateral circulation � Early failure rate � Higher perioperative morbidity � Late reperfusion rate � Complex procedures in rupture – results in a higher physiological insult.
Endovascular treatment � Aneurysms with a narrow neck � Aneurysms with adequate collateral flow � Aneurysms of vessels that are not the only source of blood supply to that organ � Inflow and outflow vessels to and from the aneurysm can be accessed and occluded by a catheter-based system � End organ perfusion can be preserved by collateral flow or stent graft therapy Mortality rates after elective treatment of VAAs is estimated to be 5%
Pretreatment decisions Preservation or occlusion of the involved vessel � region of perfusion � presence of collateral pathways Careful individualized evaluation is necessary to determine the need for arterial patency European Journal of Vascular and Endovascular Surgery 2017 53, 460-510DOI:(10.1016/j.ejvs.2017.01.010)
Pancreatico- duodenal artery aneurysms � Around 2 % of all splanchnic aneurysms � The risk of rupture is independent of the aneurysmal size � Hemodynamic alterations in blood flow du to celiac trunk stenosis � The pathogenesis behind CT stenosis may be intrinsic in nature ( caused by atherosclerosis or dysplasia) or extrinsic (caused by median arcuate ligament compression) � High flow rate or kinetics of turbulent blood in the smallest branches of SMA � Increased shear stress on the intima, altered biochemical profile, development of erosion, increased permeability � These changes reflect deeply into the media layer, responsible for the integrity and elasticity of vessel � Media becomes dysfunctional, resulting in aneurysm formation
Management � The presence of PDA – life threatening � Clinical presentation with GI bleeding � No correlation between size and the rate of rupture � High mortality rate 50-75% � No treatment guidelines � Once detected – must be treated
Splenic artery anatomy � One of the major branches of celiac axis � It courses along the superior aspect of the body, and the tail of the pancreas � The artery is commonly tortious � It divides into separate branches that provide a segmental blood supply to the spleen � Common aneurysmal location – in the middle or distal third, near the bifurcation � SAAs are usually saccular as opposed to fusiform.
Splenic artery aneurysm � SAA represent 60% to 70% of patients diagnosed with VAAs. � Etiology - atherosclerosis, portal hypertension, and connective tissue disorders, necrotizing vasculitis. � Pregnancy – in multiparous women. Multiple factors - increased blood flow, estrogen and progesterone induced medial degeneration, elevated levels of elastin during pregnancy � Splenic pseudoaneurysms - trauma (blunt, penetrating or iatrogenic during instrumentalisation) or inflammation. Occur in up to 21% of patients diagnosed with chronic pancreatitis.
Follow up � Underlying disease � Chosen therapeutic method: � Open repair- not require routine imaging surveillance � Endovascular therapy early CT or MR to confirm successful aneurysm occlusion or thrombosis repeated imaging - risk of late recurrence European Journal of Vascular and Endovascular Surgery 2017 53, 460-510DOI:(10.1016/j.ejvs.2017.01.010)
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