Acute Arterial and Graft Occlusion

January 31, 2013

Pathophysiology of Ischemia

Progressive depletion of high-energy substrate from lack of oxygen delivery

Conversion to anaerobic metabolism The rate of metabolism allows for different

consequences depending on duration of ischemia for a particular organ/tissue Heart/Brain – Maximally extract oxygen

Increase in oxygen demand is met by increase in blood flow

Kidney/Skeletal Muscle – Do not maximally extract oxygen

Increase in oxygen demand met by greater tissue extraction of oxygen

Skeletal Muscle

Tolerant of Ischemia Slow resting metabolic rate Glycogen stores High-energy phosphate bonds (creatine

phosphate) Ability to function by anaerobic glycolysis

Measurement of contractile function better predictor of ischemic injury than time

Cellular Response to Ischemia

Maintenance of Cellular Function Use of ATP stores Anaerobic glycolysis Use of energy stores (creatine) ATP metabolized to ADP and AMP

Failure to Maintain Transmembrane Gradients

Cell Membrane CompromisedNet Cellular Calcium Influx

Duration of

Ischemia

Reperfusion Injury

Catabolism of adenine nucelotides

and accumulation of hypoxanthine

Reintroduction of Oxygen

Proteolytic conversion of xanthine

dehydrogenase to xanthine oxidase

Production of Superoxide Radicals

+ +

Pathophysiology of Reperfusion Injury

Upregulation of hypoxia-inducible factor (HIF-1) and vascular endothelial growth factor (VEGF) Increased endothelial cell permeability

Tissue edema Macromolecule extravasation Compartment HTN

Pathophysiology of Reperfusion Injury

“No-Reflow” Phenomenon Prevents nutrient delivery despite restored blood flow Prolongs ischemic injury Mechanism of injury

Progressive microcirculatory obstruction• Leukocyte adhesion to venules (**Theoretical)• Leukocyte extravasation (**Theoretical)

Endothelial swelling Studies have shown injury due to macromolecular

leakage and tissue edema and not leukocyte-capillary plugging

Role of leukocyte is uncertain

Pathophysiology of Reperfusion Injury

Changes in vasomotor tone and responsiveness Due to reduction in nitric oxide (NO) levels from

ischemia Administration of arginine increases

accumulation of NO Decreases superoxide production Increases smooth muscle relaxation

Pathophysiology of Reperfusion Injury

Release of cytokines cause profound affect on hemodynamics and remote organs (ie. ALI) TNFα, IL-1β, TXA, LKT

Myonephropathic-metabolic syndrome Similar to effects from a crush-type injury Release of acidic blood into systemic circulation

causing metabolic acidosis Hyperkalemia Myoglobinuria > ARF

Etiology of Acute Arterial Occlusion

EmbolismThrombosisTraumaOutflow Venous OcclusionLow-Flow States

Embolism

Few collateral vessels to the affected bed causing severe symptoms

Lodges at vessel bifurcation LE>UE

Causes Cardiac

Myocardial Infarction - MCC• Dyskinetic heart serves as reservoir of stagnant blood and thrombus

formation Rheumatic Disease Prosthetic Valves Atrial Myxomas Endocarditis

Paradoxical Embolus – DVT with PFO Aneurysms Atherosclerotic Plaque

Thrombosis

Atherosclerosis SFA at adductor canal

Arterial enlargement from atheroma is blunted Intimal lipid deposition with disruption

Macrophages, matrix metalloproteinases

Low-Flow States Associated with concomitant intimal disease

Hypercoagulable States HITT** Malignancy

Chemotherapy (may aggravate process)

Trauma

Penetrating Direct vessel injury Indirect injury

Missile emboli Proximity

• High-velocity missiles with intimal disruption of adjacent artery

Blunt Intimal flap Spasm Suprocondylar fracture of humerus

Brachial artery injury Distal femur fracture or posterior knee dislocation

Popliteal injury Iatrogenic

Percutaneous endovascular techniques Medical devices Arterial line insertion

Allen test to document integrity of palmar arch External compression

Tourniquet or cast application Drug Administration

Drug toxicity Drug microembolization

Outflow Venous Occlusion

Compartment Syndrome Following revascularization procedures

Increased compartment pressures can impede venous outflow leading to restriction of arterial inflow

Venous Thrombosis (rare) > Phlegmasia

Low-Flow States

Shock Cardiogenic Hypovolemic

Exacerbated by vasoactive drugs

Vascular Graft Failure

Mechanisms Same processes discussed previously Infection should not be overlooked

Pseudomonas and Salmonella

Autogenous Graft Failure

Early Failure Graft Defect

Prior superficial phlebitis Technical Error

Harvest injury• Aggressive handling• Graft distention

External Compression Twisting or Kinking

Residual AVF (in situ grafts) Edema more likely than failure

Inadequate Valve Lysis (in situ or non-reversed grafts) Presence of conduit stenosis

Autogenous Graft Failure

Late Failure Intimal Hyperplasia

Can affect proximal or distal anastomosis Aneurysmal dilatation

Thrombosis or distal embolization

Prosthetic Graft Failure

Stenoses External compression Twisting or kinking during implantation

Increasing frequency from EVAR

Progression of distal diseaseInfectionHypercoagulable State

Clinical Manifestations

Acute Arterial Occlusion Severity

Level and Severity of Obstruction Collateral Circulation

• Concomitant arterial occlusive disease History

Embolic Phenomenon – no history of claudication or prior vascular reconstruction

Physical Examination Comparison to contralateral extremity “Five Ps”

• Pain MCC complaint

• Pallor Waxy appearance replaced by mottling and vasodilatation with stagnant

circulation Nonblanching area represents gangrene

• Paresthesia• Paralysis

Proprioception and light touch lost first• Pulselessness

Occlusion proximal one joint proximal to ischemic manifestations

Clinical Manifestations

Vascular Graft Occlusion Usually determined by operative indication Progression of primary disease more likely to present with limb-

threatening ischemia Graft-related causes present similar to original presentation Initial limb-threatened patients with failure present with

claudication Most do not require intervention with conservative management

The failing graft Present with diminished pulses, recurrent symptoms, failure to heal

areas of tissue loss, or without symptoms• Duplex scanning

No sensitive cutoff velocities >45cm/sec have good long-term patency

Initial Evaluation

Acute Arterial Occlusion Exclusion of MI Stabilization of hemodynamics History

No claudication or prior vascular reconstruction Prior embolic event Atrial fibrillation Thrombotic occlusions less likely to have severe symptoms or

transition zones Arteriography versus revascularization

Meniscus sign or multiple filling defects suggestive of embolus Location of occlusion Propagation of clot can cause difficulty

Initial Evaluation

Vascular Graft Occlusion Presentation may influence urgency Disabling claudication or limb-threatening

ischemia indicate intervention Thrombolysis to identify cause of failure

Treatment Goals

Limb salvageMethod determined by degree of ischemia

and relative/absolute contraindications

Treatment

ThrombolysisOperative Management

Embolectomy Bypass Graft Thrombectomy Bypass Graft Revision or Replacement Fasciotomy Delayed Embolectomy

Nonoperative Management

Thrombolysis

Advantages Avoidance of surgical morbidity Determination of etiology

Disadvantages Time

Delaying revascularization and increasing tissue loss May require additional operative intervention

Risk of Bleeding from Lytic Agents Technique

Ability to traverse thrombus Monitoring of fibrinogen levels

>100mg/dL associated with increased bleeding Agents

Retelplase, t-PA, urokinase Additional use of glycoprotein IIb/IIIa inhibitors for platelet inhibition

• RELAX trial – prospective study comparing reteplase to reteplase-abciximab combination

• No difference in efficacy or safety• Decreased rate of distal embolic events with combination drugs

Thrombolysis

Embolectomy

Historically Direct exposure of arterial segment Passage of suction catheters or rigid

instruments to remove clot 1963 – Introduction of Fogarty catheter

Femoral Embolectomy

Vertical groin incision Exposure of CFA, SFA, PFA Longitudinal arteriotomy for disease

Patch angioplasty to prevent narrowing No. 4 Fogarty catheter

Insertion to 25cm Saline inflation while maintaining

traction Directing course of catheter

90% into peroneal Bending tip Over-the-wire technique with

fluoroscopy Palpation of distal artery

Assessing flow Inflow easily determined Presence of backbleeding unreliable Arteriography

Residual thrombus Repassage of catheter Distal exploraton Infusion of fibrinolytic agents

Popliteal Embolectomy

Indicated with infrapopliteal embolism

Technique Infrageniculate incision

Access to tibial branches Cannulation of individual

tibial branches Exposure of tibio-peroneal

trunk Longitudinal arteriotomy

Permits visualization of origin of ATA

Patch closure No. 3 Fogarty catheter

Aortic Embolectomy

Bilateral transfemoral approachSimultaneous passage of No. 5 or No. 6

Fogarty catheters Prevent spillage of thrombus to contralateral

sideFailure to establish inflow

Fem-fem bypass Transperitoneal exploration

Visceral embolization

Bypass Graft Thrombectomy

Similar principles of Fogarty catheter embolectomy Special care taken not to overinflate balloon

Intimal disruption or tear in fibrotic segments of vein grafts Infrainguinal Prosthetic Grafts

Exposure of distal anastomosis Assessment of outflow system Most common site of intimal hyperplasia Closure with patch angioplasty May need extension of graft or replacement

Infrainguinal Vein Grafts Best for early failures or presence of hypercoagulable state Poor long-term results for late failures

Progression of proximal or distal disease Graftotomy difficult to repair due to fibrosis and thickening of graft

Bypass Graft Revision

Identification of cause of failure Stenotic lesion in midportion of vein graft

Short (<5cm) – Balloon angioplasty Longer, multiple lesions – require patch angioplasty or

interposition graft replacement

Residual AV fistula treated with ligation Residual valve treated with patch angioplasty Anastomotic lesions treated with patch

angioplasty

Fasciotomy

Compartment Pressure Normal – Zero Tissue perfusion is impaired at 20

mm Hg Flow significantly decreased

within 30 mm Hg of DBP Compartment Syndrome is Clinical

Diagnosis Tense muscle group Pain on passive motion Numbness of nerve distribution

Semiclosed Fasciotomies Used for Prophylaxis or Mild Cases

Open Fasciotomy Single incision – creation of skin

flaps Two incision Fibulectomy

Injury to peroneal neurovascular bundle is common

Nonoperative Management

High-Dose Heparinization Selects patients with viable extremities for

elective revascularization Bolus 20K U, followed by infusion of 2-4K U/h 67% limb salvage, 7.5% mortality (Blaisdell)

Complications

Recurrent EmbolizationRethrombosisArterial Injuries from Balloon CatheterMyonephropathic Metabolic Syndrome

Recurrent Embolization

Incidence of 6-45%Long-term anticoagulation

Started immediately following initial surgery 9% vs 31% without anticoagulation

Rethrombosis

Etiology Residual Thrombus Untreated Proximal Thrombus Inadequate Anticoagulation

Prompt Re-exploration Thrombetomized or revised grafts may need

new graft

Anticoagulation

Injury from Balloon Catheter

Intimal Hyperplasia Delayed

Perforation Compartment Syndrome Pseudoaneurysm AVF

Results of Therapy

Acute Arterial Occlusion 85-95% limb salvage 10-15% mortality Atherosclerosis negatively influences outcome

Vascular Graft Occlusion 50% 5 year salvage rate (all-comers)

Highest patency with autogenous graft replacement 85% patency for vein patch angioplasty 0% patency (3 years) replacement with prosthetic graft

Frequent follow-up for surveillance of graft

Neonatal Aortic Thrombosis

Related to Catheter Use Clinical Manifestations

Variable presentation depending on affected artery HTN - Renal Proximal HTN (similar to coarctation) – Aorta LE Ischemia - Aorta

Treatment Treatment determined by clot burden Surgical thrombectomy, thrombolysis, anticoagulation,

supportive care