Acute Arterial and Graft
Occlusion
January 31, 2013
Pathophysiology of Ischemia
 Progressive depletion of high-energy substrate
from lack of oxygen delivery
 Conversion to ...
Skeletal Muscle
Tolerant of Ischemia
 Slow resting metabolic rate
 Glycogen stores
 High-energy phosphate bonds (creat...
Cellular Response to Ischemia
Maintenance of Cellular Function
 Use of ATP stores
 Anaerobic glycolysis
 Use of energy...
Reperfusion Injury
Catabolism of
adenine nucelotides
and
accumulation of
hypoxanthine
Reintroduction of
Oxygen
Proteolytic...
Pathophysiology of Reperfusion Injury
Upregulation of hypoxia-inducible factor
(HIF-1) and vascular endothelial growth
fa...
Pathophysiology of Reperfusion Injury
 “No-Reflow” Phenomenon
 Prevents nutrient delivery despite restored blood flow
 ...
Pathophysiology of Reperfusion Injury
Changes in vasomotor tone and
responsiveness
 Due to reduction in nitric oxide (NO...
Pathophysiology of Reperfusion Injury
Release of cytokines cause profound
affect on hemodynamics and remote
organs (ie. A...
Etiology of Acute Arterial Occlusion
Embolism
Thrombosis
Trauma
Outflow Venous Occlusion
Low-Flow States
Embolism
 Few collateral vessels to the affected bed causing
severe symptoms
 Lodges at vessel bifurcation
 LE>UE
 Cau...
Thrombosis
 Atherosclerosis
 SFA at adductor canal
 Arterial enlargement from atheroma is blunted
 Intimal lipid depos...
Trauma
 Penetrating
 Direct vessel injury
 Indirect injury
 Missile emboli
 Proximity
• High-velocity missiles with i...
Outflow Venous Occlusion
Compartment Syndrome
 Following revascularization procedures
 Increased compartment pressures ...
Low-Flow States
Shock
 Cardiogenic
 Hypovolemic
Exacerbated by vasoactive drugs
Vascular Graft Failure
Mechanisms
 Same processes discussed previously
 Infection should not be overlooked
 Pseudomona...
Autogenous Graft Failure
 Early Failure
 Graft Defect
 Prior superficial phlebitis
 Technical Error
 Harvest injury
•...
Autogenous Graft Failure
Late Failure
 Intimal Hyperplasia
 Can affect proximal or distal anastomosis
 Aneurysmal dila...
Prosthetic Graft Failure
Stenoses
 External compression
 Twisting or kinking during implantation
 Increasing frequency...
Clinical Manifestations
 Acute Arterial Occlusion
 Severity
 Level and Severity of Obstruction
 Collateral Circulation...
Clinical Manifestations
 Vascular Graft Occlusion
 Usually determined by operative indication
 Progression of primary d...
Initial Evaluation
 Acute Arterial Occlusion
 Exclusion of MI
 Stabilization of hemodynamics
 History
 No claudicatio...
Initial Evaluation
Vascular Graft Occlusion
 Presentation may influence urgency
 Disabling claudication or limb-threate...
Treatment Goals
Limb salvage
Method determined by degree of ischemia
and relative/absolute contraindications
Treatment
Thrombolysis
Operative Management
 Embolectomy
 Bypass Graft Thrombectomy
 Bypass Graft Revision or Replace...
Thrombolysis
 Advantages
 Avoidance of surgical morbidity
 Determination of etiology
 Disadvantages
 Time
 Delaying ...
Thrombolysis
Embolectomy
Historically
 Direct exposure of arterial segment
 Passage of suction catheters or rigid
instruments to rem...
Femoral Embolectomy
 Vertical groin incision
 Exposure of CFA, SFA, PFA
 Longitudinal arteriotomy for disease
 Patch a...
Popliteal Embolectomy
 Indicated with
infrapopliteal embolism
 Technique
 Infrageniculate incision
 Access to tibial b...
Aortic Embolectomy
Bilateral transfemoral approach
Simultaneous passage of No. 5 or No. 6
Fogarty catheters
 Prevent sp...
Bypass Graft Thrombectomy
 Similar principles of Fogarty catheter embolectomy
 Special care taken not to overinflate bal...
Bypass Graft Revision
 Identification of cause of failure
 Stenotic lesion in midportion of vein graft
 Short (<5cm) – ...
Fasciotomy
 Compartment Pressure
 Normal – Zero
 Tissue perfusion is impaired at 20
mm Hg
 Flow significantly decrease...
Nonoperative Management
High-Dose Heparinization
 Selects patients with viable extremities for
elective revascularizatio...
Complications
Recurrent Embolization
Rethrombosis
Arterial Injuries from Balloon Catheter
Myonephropathic Metabolic Sy...
Recurrent Embolization
Incidence of 6-45%
Long-term anticoagulation
 Started immediately following initial surgery
 9%...
Rethrombosis
Etiology
 Residual Thrombus
 Untreated Proximal Thrombus
 Inadequate Anticoagulation
Prompt Re-explorati...
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 influe...
Neonatal Aortic Thrombosis
 Related to Catheter Use
 Clinical Manifestations
 Variable presentation depending on affect...
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Moore Chapter: Acute Arterial and Graft Occlusion

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Moore Chapter: Acute Arterial and Graft Occlusion

  1. 1. Acute Arterial and Graft Occlusion January 31, 2013
  2. 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. 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. 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. 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. 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. 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. 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. 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. 10. Etiology of Acute Arterial Occlusion Embolism Thrombosis Trauma Outflow Venous Occlusion Low-Flow States
  11. 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. 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. 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. 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. 15. Low-Flow States Shock  Cardiogenic  Hypovolemic Exacerbated by vasoactive drugs
  16. 16. Vascular Graft Failure Mechanisms  Same processes discussed previously  Infection should not be overlooked  Pseudomonas and Salmonella
  17. 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. 18. Autogenous Graft Failure Late Failure  Intimal Hyperplasia  Can affect proximal or distal anastomosis  Aneurysmal dilatation  Thrombosis or distal embolization
  19. 19. Prosthetic Graft Failure Stenoses  External compression  Twisting or kinking during implantation  Increasing frequency from EVAR Progression of distal disease Infection Hypercoagulable State
  20. 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. 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. 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. 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. 24. Treatment Goals Limb salvage Method determined by degree of ischemia and relative/absolute contraindications
  25. 25. Treatment Thrombolysis Operative Management  Embolectomy  Bypass Graft Thrombectomy  Bypass Graft Revision or Replacement  Fasciotomy  Delayed Embolectomy Nonoperative Management
  26. 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. 27. Thrombolysis
  28. 28. Embolectomy Historically  Direct exposure of arterial segment  Passage of suction catheters or rigid instruments to remove clot  1963 – Introduction of Fogarty catheter
  29. 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. 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. 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. 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. 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. 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. 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. 36. Complications Recurrent Embolization Rethrombosis Arterial Injuries from Balloon Catheter Myonephropathic Metabolic Syndrome
  37. 37. Recurrent Embolization Incidence of 6-45% Long-term anticoagulation  Started immediately following initial surgery  9% vs 31% without anticoagulation
  38. 38. Rethrombosis Etiology  Residual Thrombus  Untreated Proximal Thrombus  Inadequate Anticoagulation Prompt Re-exploration  Thrombetomized or revised grafts may need new graft Anticoagulation
  39. 39. Injury from Balloon Catheter Intimal Hyperplasia  Delayed Perforation  Compartment Syndrome  Pseudoaneurysm  AVF
  40. 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. 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

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