BC Vascular Day. Contents. November 3, Abdominal Aortic Aneurysm 2 3. Peripheral Arterial Disease 4 6. Deep Venous Thrombosis 7 8

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BC Vascular Day Contents Abdominal Aortic Aneurysm 2 3 November 3, 2018 Peripheral Arterial Disease 4 6 Deep Venous Thrombosis 7 8

Abdominal Aortic Aneurysm Conservative Management Risk factor modification Smoking cessation, controlling hypertension and dyslipidemia * Medical optimization for the purpose of minimizing future surgical risk Surgical Management Definition Focal dilatation of abdominal aorta to 50% or greater than native diameter. Can be infrarenal, juxtarenal or pararenal. Risk Factors Open repair Endovascular aneurysm repair (EVAR) Smoking Advanced age, male, Caucasian Hypercholesterolemia, hypertension Personal or family history of aneurysm Connective tissue disorders Infections inflammatory (Diabetes appears protective) Presentation Asymptomatic screening or incidental Symptomatic Abdominal/back/flank pain Embolism Rupture contained vs. free Indications for Repair Diameter greater than 5.5cm (male), 5cm (female) * Because rupture risk increases with size, it is sensible to delay surgery in patients at higher surgical risk and reassess growth * Rapidly expanding > 1cm per year * Symptomatic pain, embolism, rupture Overview of EVAR deployment (Gore Sim) 1. Arterial access through percutaneous puncture or surgical exposure of both groins to introduce sheaths 2. Wire access into aneurysm sac 3. Aortogram performed to evaluate location of renal arteries 4. Introduction of main body of stent graft, deployment below renal arteries 5. Wire cannulation of contralateral limb 6. Angiogram to determine location of contralateral internal iliac artery origin 7. Deployment of contralateral stent graft 8. Angiogram to determine origin of ipsilateral side internal iliac artery 9. Deployment of ipsilateral extension 10. Ballooning of sealing zones and areas of graft overlap 11. Completion angiogram to determine patency of renal arteries and presence of endoleaks

Abdominal Aortic Aneurysm Complications Endoleak, delayed rupture Stent migration Limb thrombosis For these reasons, lifetime surveillance is required for EVAR What is an Endoleak? Persistent blood flow into the aneurysm sac after EVAR repair. Found in up to 30-40% of patients intraoperatively Seen in 20-40% of EVARs during follow up Management Type I and III: Requires treatment If found in OR must be fixed Type II: Serial imaging, consider treatment for expanding aneurysm sac * Endovascular vs. open options for type II Transarterial vs. translumbar Type IV: Rare in modern endograft devices Type V: Controversial Graft Types Different companies offer different grafts with varying indications for use, each with advantages Type Ia: failure to obtain proximal seal (ie. aneurysm remains untreated) Type Ib: failure to obtain distal seal Type II: persistent flow due to backbleeding of branch arteries (IMA, lumbar arteries) Type IIIa: separation of graft components Type IIIb: defect within graft material Type IV: porosity of graft material (rare in modern devices) Type V: endotension, or endoleak NYD

Peripheral Arterial Disease Introduction Insufficient blood supply to the extremities Most commonly as a result of atherosclerosis Risk factors o Smoking o Diabetes o Dyslipidemia o Hypertension o Age o Renal insufficiency Disease can be divided into inflow (aortoiliac) and outflow (infrainguinal) distribution Acute peripheral arterial occlusions can occur with or without a background of arterial disease Diagnosis Can be evaluated clinically by ABI, or with non-invasive or invasive imaging ABI Interpretation >1.4 Calcified vessels 0.9-1.4 Normal 0.7-0.9 Mild / asymptomatic 0.4-0.7 Moderate / claudication <0.4 Severe / rest pain, wound Non-invasive imaging duplex ultrasound, CT angiogram, MR angiogram Invasive imaging catheter-directed angiogram Distinguishing between claudication and critical limb ischemia is crucial

Peripheral Arterial Disease Management Conservative management o Antiplatelets o Control of hypertension, dyslipidemia, diabetes o Exercise generation of new collaterals vs. improved utilization of existing circulation o Smoking cessation o COMPASS trial: combining ASA and low-dose rivaroxaban decreases MI, stroke, and amputation rates at cost of increase in non-critical bleeding Hemostemix: trial of stem cell therapy Indications for surgery o Critical limb ischemia or severely disabling claudication o Angioplasty, endarterectomy, bypass surgery Key features can distinguish between vascular and neurogenic claudication o Characterization of pain Vascular consistent cramping Neurogenic inconsistent sharp, shooting, electric shocklike o Aggravating maneuvers Vascular pain does not begin until exercise Neurogenic pain begins as soon as patient stands up o Palliating maneuvers Vascular pain relief can be obtained while patient is still standing Neurogenic pain must be relieved by change of position (eg. sitting down or leaning forward) A note about ABI: normal ABI values do not exclude arterial disease, especially in diabetics Angioplasty and stenting Clinical Pearl Endarterectomy Bypass

Peripheral Arterial Disease Endovascular vs. Surgery Indications for Angioplasty vs. Stenting There are anatomical criteria (TASC II) that guide the choice for whether endovascular vs. open surgery is preferred In general, shorter and isolated lesions can be treated with balloons and stents, while complex lesions have better durability if repaired surgically This is balanced with patient surgical risk Below the inguinal ligament, a traditional approach is to address every lesion with angioplasty alone first; if a residual stenosis remains after treatment, a stent is placed Balloon-expandable stents are more accurate to deploy Self-expanding stents can conform to arteries that are more tortuous and dynamic (external iliac, femoropopliteal) Stents are not benign, and can fracture or undergo restenosis over time; this can make subsequent surgical revascularization more difficult Newer drug-coated balloons and drugeluting stents (eg. Boston Scientific Ranger) have paclitaxel as an active ingredient to delay restenosis

Deep Venous Thrombosis Risk Factors Stasis o Surgery, hospitalization o Anatomical abnormalities e.g. May-Thurner syndrome Vessel injury o Trauma o Previous DVT o Venous catheterization Hypercoagulability o Malignancy o Cancer therapy o Estrogen therapy (OCP or HRT) o Thrombophilia Presentation Asymptomatic Calf pain or tenderness Swelling with pitting edema Erythema Superficial vein dilatation Cyanosis and gangrene in severe cases Diagnosis Well's criteria for pretest probability High risk patients require imaging o Duplex ultrasound is test of choice, but can miss proximal DVTs o If highly suspicious of DVT in setting of negative U/S should repeat U/S in 1 week or proceed to CT venogram or MR venogram o Ultrasound findings of DVT include reduced compressibility, lack of flow, and absence of flow augmentation with distal compression o Acute DVTs tend to be free-floating and partially compressible o Chronic DVTs often have collaterals and recanalization, and tend to be adherent

Deep Venous Thrombosis Treatment Based on proximal vs. distal location and provoked or not Distal DVTs (confined to the femoral vein and below) are typically managed medically with 3 months of anticoagulation, potentially longer if the thrombus is provoked or recurrent Proximal DVTs (extending proximally into the iliac vein or beyond), if in the acute phase, may be treated with catheter-directed thrombolysis; more on this below In patients for whom anticoagulation is contraindicated, IVC filters may be placed To date there have been two randomized trials (CaVENT, ATTRACT) that showed contradictory results regarding the prevention of PTS by catheterdirected thrombolysis There are endovascular and surgical options for chronic venous insufficiency Non-operative management is based on lifestyle modification and use of compression stockings (Bauerfeind) Post-Thrombotic Syndrome Venous thrombosis causes venous hypertension, which over time causes valve reflux and outflow obstruction This can cause pain, heaviness, edema, and hyperpigmentation (ie. same symptoms of chronic venous insufficiency), and is referred to as postthrombotic syndrome (PTS) Treatment of iliofemoral DVTs with catheter-directed or surgical techniques to re-establish venous circulation can prevent PTS