1. Acute Arterial and Graft
Occlusion
January 31, 2013

2. 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

3. 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

4. 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 Compromised
Net Cellular Calcium Influx
DurationofIschemia

5. 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
+ +

6. 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

7. 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

8. 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

9. 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

10. Etiology of Acute Arterial Occlusion
Embolism
Thrombosis
Trauma
Outflow Venous Occlusion
Low-Flow States

11. 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

12. 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)

13. 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

14. 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

15. Low-Flow States
Shock
 Cardiogenic
 Hypovolemic
Exacerbated by vasoactive drugs

16. Vascular Graft Failure
Mechanisms
 Same processes discussed previously
 Infection should not be overlooked
 Pseudomonas and Salmonella

17. 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

18. Autogenous Graft Failure
Late Failure
 Intimal Hyperplasia
 Can affect proximal or distal anastomosis
 Aneurysmal dilatation
 Thrombosis or distal embolization

19. Prosthetic Graft Failure
Stenoses
 External compression
 Twisting or kinking during implantation
 Increasing frequency from EVAR
Progression of distal disease
Infection
Hypercoagulable State

20. 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

21. 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

22. 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

23. Initial Evaluation
Vascular Graft Occlusion
 Presentation may influence urgency
 Disabling claudication or limb-threatening
ischemia indicate intervention
 Thrombolysis to identify cause of failure

24. Treatment Goals
Limb salvage
Method determined by degree of ischemia
and relative/absolute contraindications

25. Treatment
Thrombolysis
Operative Management
 Embolectomy
 Bypass Graft Thrombectomy
 Bypass Graft Revision or Replacement
 Fasciotomy
 Delayed Embolectomy
Nonoperative Management

26. 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

27. Thrombolysis

28. Embolectomy
Historically
 Direct exposure of arterial segment
 Passage of suction catheters or rigid
instruments to remove clot
 1963 – Introduction of Fogarty catheter

29. 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

30. 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

31. Aortic Embolectomy
Bilateral transfemoral approach
Simultaneous passage of No. 5 or No. 6
Fogarty catheters
 Prevent spillage of thrombus to contralateral
side
Failure to establish inflow
 Fem-fem bypass
 Transperitoneal exploration
 Visceral embolization

32. 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

33. 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

34. 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

35. 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)

36. Complications
Recurrent Embolization
Rethrombosis
Arterial Injuries from Balloon Catheter
Myonephropathic Metabolic Syndrome

37. Recurrent Embolization
Incidence of 6-45%
Long-term anticoagulation
 Started immediately following initial surgery
 9% vs 31% without anticoagulation

38. Rethrombosis
Etiology
 Residual Thrombus
 Untreated Proximal Thrombus
 Inadequate Anticoagulation
Prompt Re-exploration
 Thrombetomized or revised grafts may need
new graft
Anticoagulation

39. Injury from Balloon Catheter
Intimal Hyperplasia
 Delayed
Perforation
 Compartment Syndrome
 Pseudoaneurysm
 AVF

40. 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

41. 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