Visceral aneurysm Diagnosis and Interventions M.NEDEVSKA History - - PowerPoint PPT Presentation

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 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 Atherosclerosis Spontaneous dissection Fibromuscular dysplasia Hereditary disease : Collagen vascular disorders Hemorrhagic telangiectasia False VAA Pseudo aneurysm Infection of adjacent organs Inflammation Abdominal trauma Iatrogenic arterial trauma

Visceral artery pseudoaneurysm

Clinical features

History of arterial trauma Biliary tract manipulation Intraabdominal or retroperitoneal inflammation Malignancy

Imaging features

Focal arterial disruption

Otherwise normal artery Irregular aneurysmal wall Presence of perivascular inflammation

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.

European Journal of Vascular and Endovascular Surgery 2017 53, 460-510DOI:(10.1016/j.ejvs.2017.01.010)

Specific patients group

What kind of treatment?

Open or laparoscopic surgery

Resection and end to end anastomosis Reimplantation Graft interposition Simple ligation Organ resection if necessary.

Endovascular treatment

Implantation of a covered stent Embolization with coils or glue Arterial stenting Inflow and outflow occlusion of the involved vessel Flow diverting stents Percutaneous thrombin injection.

What kind of treatment?

Open or laparoscopic surgery

Excluding the aneurysm completely with minimal compromise of the collateral circulation Higher perioperative morbidity Complex procedures in rupture – results in a higher physiological insult.

Endovascular treatment

Greater benefit in cases with VAA rupture Early failure rate Late reperfusion rate

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

European Journal of Vascular and Endovascular Surgery 2017 53, 460-510DOI:(10.1016/j.ejvs.2017.01.010)

Careful individualized evaluation is necessary to determine the need for arterial patency

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)