Venous Thromboembolism

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  • 1. Venous Thromboembolism in Intensive Care Medicine Kenneth E. Wood, DO Professor of Medicine and Anesthesiology Director of Critical Care Medicine and Respiratory Care The Trauma and Life Support Center University of Wisconsin Hospital and Clinics
  • 2. Venous Thromboembolism in ICU
    • Pathophysiology of Thrombosis
    • Prophylaxis and DVT
    • Pathophysiology of Pulmonary Embolism
    • Pulmonary Embolism Diagnostics
    • Pulmonary Embolism Therapeutics
  • 3. ICU Venous Thromboembolism Overview Diagnostics Therapeutics Secondary Development Virchows Triad Risk Factors Prophylaxis Cardiac Echo Spiral CT Doppler US D-dimer Angiogram Warfarin UF Heparin LMWH Lepirudin Argatroban Thrombolytics
    • Hypercoaguable (25%)
    • Stasis
    • Vessel Damage
    Primary Presentation Respiratory Failure Hemodynamic Instability
  • 4. Venous Thromboembolism in ICU Pathophysiology of Thrombosis
  • 5. Venous Thromboembolism
    • “ The detachment of larger or smaller fragments from the end of the softening thrombus are carried along by the current of blood and driven in remote vessels. This gives rise to the very frequent process upon which I have bestowed the name EMBOLIA.”
    Vessel Injury Stasis Hyper-coagulability Virchow 1846 Acquired Inherited
  • 6. Virchows Triad
    • Hypercoagulable
    • Stasis
    • Vessel Damage
  • 7. Intensivists General Paradigm Pipes Stuff Flow
  • 8. Hematology 101 for Intensivists = Biologically Active Conduit Clot Bleed Stuff Pipe Flow Stuff Coagulation fibrinolysis
  • 9. Hematology 101 for Intensivists = Biologically Active Conduit Bleed Stuff Pipe Flow (stasis) Stuff Coagulation fibrinolysis Clot
  • 10. Pathogenesis of Venous Thromboembolism Thrombogenic Stimuli
    • Endothelial Damage
      • Exposure of tissue factor/subendothelial matrix
      • Hypoxia  receptors for leukocytes
      • Activation by inflammatory cytokines (IL-1, TNF)
      • Express tissue factor
      • Internalize thrombomodulin
      • Release PAI-1
    • Activation of Coagulation
      • Inflammation (IL-1, TNF)
        • Monocytes  tissue factor and tethered leukocytes
        • Internalize thrombomodulin (  Protein C activation)
        • Shedding endothelial protein C receptor
      • Coagulation cascade activation
    Adapted from Wertz Lung Biology Health Disease 2003 Clot Bleed
  • 11. Pathogenesis of Venous Thromboembolism Thrombogenic Stimuli
    • Blood Flow (Stasis)
      • Systemic
        • Immobilization pools blood in calve venous sinuses
        • Increased blood viscosity
      • Local
        • Hypoxia of valve cusps produces tissue factor and activates coagulation
        • Accumulation of clotting factors in venous sinuses of calf or valve cusp pockets
    Adapted from Wertz Lung Biology Health Disease 2003 Clot Bleed
  • 12. ICU Venous Thromboembolism Adopted from Dalen CHEST 2002; 122:1440-56 X X X Catheter X X Sepsis X Burns X Stroke X MI/CHF X X X Trauma X X X Major Surgery Vessel Stasis Hypercoag ICU Risk Factors
  • 13. Venous Thromboembolism in ICU Prophylaxis and DVT
  • 14. Importance of DVT Prophylaxis
    • Acute DVT/PE prevention
    • Valvular Damage
    • Symptomatic proximal DVT can be an extension of distal DVT that was previously asymptomatic
    • Significant number of fatal PE’s NOT preceded by symptomatic DVT
    • Most preventable cause of hospital associated death in medical patients  PE
    Recurrence Post-phlebitic syndrome DVT PE
  • 15. Asymptomatic DVT ICU Admit 6.3% Fraisse Am J Resp CCM 2000; 161:1109-14 MICU-Resp fail/vent 19% Goldberg Am J Resp CCM 1996; 153:A94 MICU-Resp fail/vent 10.7% Schonhster Respiration 1998; 65:173-7 Respiratory ICU 7.5% Harris J Vas Surg 1997; 26:734-9 Surgical ICU % DVT Patient Population
  • 16. Prospective Eval DVT Critically Ill Non-Prophylaxed 28% 85 Venogram Vent COPD Fraisse 2000 31% 390 US Medical Kapoor 1999 32% 104 US Medical Hirsch 1995 29% 60 Fib LS General Cade 1982 13% 23 Fib LS Respiratory Moser 1981 % DVT # Screen Control Study
  • 17. Natural History of DVT 132 Surgical patients no prophylaxis 56% No PE (5) 44% PE (4) 42% Calf only (17) 23% propagation Popliteal/femoral (9) 35% Calf with spontaneous lysis (14) 30% DVT (40) 70% No DVT (92) Kakkar Lancet 1969; 6:230-32
  • 18. Incidence of VTE Major Trauma Without Prophylaxis
    • 50% face chest abdomen
    • 54% major head injury
    • 62% spinal injury
    • 69% lower extremity ortho
    • 61% pelvic fractures
    • 80% femoral fractures
    • 77% tibial fractures
    Incidence Geerts NEJM 1994; 331:1601-1606
    • Lower leg DVT 58%, proximal DVT 18%
    • Vast majority clinically not apparent
  • 19. DVT Prophylaxis Trials in Critically Ill Geerts J Crit Care 2002; 17:95-104 15% Nadroparin 28% Placebo Fraisse 00 11% UF Heparin 31% Placebo Kapoor 99 13% UF Heparin 29% Placebo Cade 82 % DVT Treatment % DVT Control Study
  • 20. Femoral Catheter Associated DVT 11% US Med/Surg Jogut 00 9% Femoral 26% Tibial Venogram Med/Surg Durbec 97 7% Femoral 17% Tibial Venogram Med/Surg Durbec 97 25% US Med/Surg Trottier 95 14% US Trauma 8.5 Fr Meredith 93 % DVT Screen Population Study
  • 21. Pulmonary Embolism in Patients with Upper Extremity Catheter DVT
    • 86 consecutive patients catheter DVT
    • 15% high probability (PE) V/Q scan (13/86)
    • 31% PE patients symptomatic (4/13)
    • 15% PE patient mortality (2/13) despite full anticoagulation
    •  DVT polyvinyl chloride or polyethylene
    Monreal Throm Haemost 1994; 72:548-50
  • 22. Autopsy Studies PE Critically Ill Geerts J Crit Care 2002; 17:95-104 PE Autopsy Fatal Present ICU Setting Study 12% 27% Med/Surg Neuhaus 1978 0% 20% Respiratory Moser 1981 1% 10% Surgical Cullin 1986 3% 8% Surgical Willemsen 2000 2% 7% Medical Blosser 1998 -- 23% Medical Pingleton 1981
  • 23. VTE Prophylaxis Pharmacologic Unfractionated heparin Low molecular weight heparin Vit K Antagonists Mechanical Graduated Compression Stockings Intermittent Pneumatic Compression Devices IVC filters
  • 24. Thromboembolism Risk Surgical Patients  Prophylaxis Geerts CHEST 2004;126(3)Supplement: 338S-400S Surgery with multiple risk factors (age > 40 yr, cancer, prior VTE) Hip or knee arthroplasty, HFS Major trauma, SCI 0.2-5% 4-10% 10-20% 40-80% Highest Risk Surgery >60, 94 40-60 with additional risk factors (prior VTE, cancer, hypercoagulability) 0.4-1.0% 2-4% 4-8% 20-40% High Risk Minor surgery risk factors Surgery 40-60 no risk factors 0.1-0.4% 1-2% 2-4% 10-20 % Moderate Risk Minor Surgery < 40 no risk factors <0.01% 0.2% 0.4% 2% Low Risk Fatal Clinical Proximal Calf PE, % DVT, %
  • 25. Collins NEJM 1988; 318:1162-73 0 30 40 50 60 70 20 10 C ontrol Heparin Screening DVT Fatal PE Percentage 60.5 20.3 1.9 0.6 Relative risk reduction 67% Relative risk reduction 68%
  • 26. Trauma and Venous Thromboembolism
    • Patients recovering from major trauma have highest risk for developing VTE amongst all hospitalized patients (Geerts NEJM 1994; 331:1601-06)
    • Without prophylaxis, multisystem or major trauma have a DVT risk exceeding 50% (Kudsk Am J Surg 1989; 158:515-19)
    • PE is the third leading cause of death in trauma patients that survive beyond the first day (Acosta J Am Coll Surg 1998; 186:528-33)
  • 27. Significant Risk Factors and Odds Ratios for Venous Thromboembolism Developed From the National Trauma Data Bank Knudson Ann Surg 2004; 240:490-98 Odds Ratio (95% CI) Risk Factor (Number at Risk) 4.32 (3.91 – 4.77) *Major surgical procedure (n=73,974) 1.95 (1.62 – 2.34) Shock on admission (BP<90 mm Hg) (n=18,510) 7.93 (5.83 – 10.78) *Venous injury (n=1450) 10.62 (9.32 – 12.11) *Ventilator days > 3 (n=13,037) 2.59 (2.31 – 2.90) *Head injury (AIS score  3) (n=52,197) 3.39 (2.41 – 4.77) Spinal cord injury with paralysis (n=2852) 3.16 (2.85 – 3.51) *Lower extremity fracture (n=63,508) 2.93 (2.01 – 4.27) Pelvic fracture (n=2707) 2.29 (2.07 – 2.55) *Age  40y (n=178,851)
  • 28. Knudson Ann Surg 2004; 240:490-498 INJURED PATIENT
    • High Risk Factors
    • (Odds ratio for VTE = 2 – 3)
      • Age  40
      • Pelvic fx
      • Lower extremity fx
      • Shock
      • Spinal cord injury
      • Head Injury (AIS  3)
    • Very High Risk Factors
    • (Odds ratio for VTE = 4 - 10)
      • Major operative procedure
      • Venous injury
      • Ventilator days > 3
      • 2 or more high risk factors
    Does the patient have contraindication for Heparin? Does the patient have contraindication for Heparin? Yes No Yes No Mechanical Compression LMWH* * Prophylactic dose LMWH* and Mechanical Compression Mechanical Compression and serial CFDI OR Temporary IVC filter
  • 29. Critical Care Patient
    • Mechanical Prophylaxis
      • Graduated compression stockings (GCS)
      • Intermittent pneumatic compression devices (IPC)
    • Delayed prophylaxis until high risk bleeding abates
    • Screen for proximal DVT with Doppler US in high risk patients
    • Low dose unfractionated heparin (LDUH)
    • Low molecular weight heparin (LMWH)
    • Combination of LMWH and mechanical prophylaxis for high risk patients
    Assess Bleeding Risk High Low Adapted from Geerts CHEST 2003; 124(6)S:357S-363S
  • 30. Critical Care Patient Adapted from Geerts CHEST 2003; 124(6)S:357S-363S Prophylaxis Recommendation Thrombosis Risk Bleeding Risk GCS or IPC  LMWH when bleeding risk subsides High High GCS or IPC  LDUH when bleeding risk subsides Moderate High
    • LMWH
        • Dalteparin
        • Enoxaparin
    High Low LDH 5000 units SC bid Moderate Low
  • 31. Anti-Xa Activity After Enoxaparin 40 mg SQ 1.0 Time (hours) Anti Xa activity (U/ml) 0 3 6 9 12 0 0.2 0.4 0.6 0.8 Ward (Group 2), n=13 ICU patients (Group 1), n=16 Priglinger CCM 2003; 31:1405-09
  • 32. Vena Caval Filters
    • 5 filter types-all equal efficacy
    • Pulmonary embolism 2.6%-3.8%
    • Deep Venous Thrombosis 6%-32%
    • Insertion site thrombosis 23%-36%
    • Inferior caval thrombosis 3.6%-11.2%
    • Postphlebitic syndrome 14%-41%
    Streiff Blood 2000; 95:3669-77
  • 33. Venous Thromboembolism in ICU Pathophysiology of Pulmonary Embolism
  • 34.  
  • 35. Major Pulmonary Embolism mPAP - LVEDP PVR = CO Pulmonary Artery Pressure Q = Flow = Cardiac Output Incremental Resistance Mean Closing Pressure P 2 - P 1 Q = R mPAP - LVEDP CO = PVR
  • 36. Major Pulmonary Embolism Pulmonary Artery Pressure Q = Flow = Cardiac Output Effect of Pulmonary Embolism Mean Closing Pressure Incremental Resistance
  • 37.  
  • 38. Venous Thromboembolism in ICU Pulmonary Embolism Diagnostics
  • 39. Massive Pulmonary Embolism Diagnostics Angio Helical CT MRI Angio Echo
    • History
    • Physical
    • CXR
    • ABG
    • EKG
  • 40. Risk Stratification In Pulmonary Embolism Data from MAPPET – Kasper JACC 1997; 30:1165-1171 High Risk Low Risk Predictions History/Physical Diagnostic Studies
    • EKG
    • CXR
    • ABG
    • Troponin
    • BNP
    • Echo
    Confirmatory Studies
    • V/Q
    • CT Angio
    • Angio
    Clinical State Mortality Normal BP and RV 0-1% Normal BP RV dysfunction 8.1% Hypotension without hypoperfusion 15% Shock 25% Cardiac Arrest 65%
  • 41.  
  • 42. EKG Manifestations
    • Normal EKG
        • UPET 14% (6% massive and 23% submassive)
        • PIOPED 30%
    • Rhythm disturbances rare
        • Atrial fibrillation/flutter 0-5%
        • Blocks or ventricular dysrhythmias non existent
        • PEA cardiac arrest
    • Electrocardiographic Cor Pulmonale
        • Right axis, RBBB, S I Q III T III
        • Related to embolism size
    • Non-specific ST-T segment changes
        • UPET 42%
        • PIOPED 49%
  • 43.  
  • 44. Chest X-Ray (CXR)
    • UPET
        • Normal CXR 34%
        • Parenchymal abnormalities 67%
            • Elevated hemidiaphragm 46%
            • Consolidation 39%
            • Pleural effusion 30%
            • Atelectasis 28%
        • Vascular abnormalities 37%
            • Diminished vascularity 22%
            • Prominent central PA 86%
    • PIOPED
        • Normal 16%
        • Atelectasis/parenchymal abnormality 68%
        • Pleural effusion 48%-blunting 86%
  • 45. Arterial Blood Gas (ABG)
    • Hypoxia not uniform
        • PaO 2  80
            • 12% UPET
            • 19% PIOPED
    • Normal A-a gradient does NOT exclude PE
        • PIOPED (PaO 2 >80,PaCO 2 >35)
            • 38% without cardiopulmonary disease
            • 14% with cardiopulmonary disease
  • 46. D-Dimer
    • Elevated in clinical conditions where fibrin cross links are cleaved by plasmin
    • High sensitivity and negative predictive value
    • Low specificity
    • ELISA
        • Accurate quantitative measurement
        • Expensive and labor intensive
    • Semi-quantitative latex assay
        • Faster and less expensive
        • Unacceptably low sensitivity
  • 47. Estimating Pre-test Probability of PE
    • Implicit (empiric)
        • Uses clinician knowledge and experience
        • Frequent disagreement
        • Experience level influences assessment
        • Estimates trend towards middle few low or high probability groups
        • Inaccurate low risk assessment
    • Explicit Criteria
        • Scoring systems
        • Prediction rules
        • Clinical decision rules
  • 48. Canadian Score for Pre-test Probability Wells Throm Haemost 2000; 83:416-420. Creating the Score 1.0 Malignancy (on treatment, treated in thep past 6 mo, or palliative 1.0 Hemoptysis 1.5 Previous DVT/PE 1.5 Immobilization or surgery in the previous 4 wk 1.5 Heart rate >100 beats/min 3.0 An alternative diagnosis is less likely than PE 3.0 Suspected DVT Points Criteria High 7 66.7 >6 points Moderate 53 20.5 3-6 points Low 40 3.6 0-2 points Interpretation of Risk Patients with this Score, % Mean Probability of PE, % Score Range Interpretation of the Score
  • 49. Geneva Score for Assessment of Pretest Probability for Pulmonary Embolism
    • Age 60-79 years
    • Age > 79 years
    • Prior DVT/PE
    • Recent surgery
    • Heart rate > 100 beats/min
    • PaCO 2 , mmHg
    • <36
    • 36-39
    • PaO 2 , mmHg
    • <49
    • 49-60
    • >60-71
    • >71-82
    • Chest radiograph
    • Platelike atelectasis
    • Elevation of hemidiaphragm
    Creating the score Points Interpretation of the score Criteria 0-4 points 5-8 points 9-12 points 10 38 81 49 44 6 Low Moderate High Score range Mean probability of PE, % Patients with this score, % Interpretation of risk 1 2 2 3 1 2 1 4 3 2 1 1 1 Wicki Arch Int Med 2001; 161:92-97
  • 50. Clinical Gestalt vs Prediction Rules “ Clinical gestalt of experienced clinicians and prediction rules used by physicians of varying experience have shown similar accuracy in discriminating among patients who have a low, moderate or high pretest probability of PE” Chandilal JAMA 2003; 290:2849-2858 Prediction Rules Clinical Gestalt 38% - 98% 46% - 91% High 16% - 46% 26% - 47% Moderate 3% - 28% 8% - 19% Low Rate Pulmonary Embolism Rate Pulmonary Embolism Pretest Prob
  • 51. Diagnostic Approach to Pulmonary Embolism High Clinical Probability CT Angio Positive CT Diagnosis confirmed Negative CT Duplex Ultrasound Positive Negative Diagnosis Confirmed Pulmonary Angiography Positive Negative Diagnosis Excluded Diagnosis Confirmed Fedullo NEJM 2003; 349:1247-56
  • 52. Diagnostic Strategies for Excluding Pulmonary Embolism with Upper 95% Confidence Limit of 3% or less and 3 month risk Marieke Ann Int Med 2003; 138:941-951 0.2 (0.8) Normal D-dimer low clinical probability 0.0 (1.8) Normal D-dimer 0.6 (1.2) Normal lung scan, normal legs 0.9 (2.3) Normal lung scan 0.8 (2.1) Normal pulmonary angiogram 3-month Risk for VTE complications (upper 95% CL) Diagnostic Strategy Initial Evaluation
  • 53. Clinical Validity of a Negative CT Scan in Suspected Pulmonary Embolism
    • Overall negative likelihood ratio of VTE after negative chest CT Scan -> 0.07 (CI 0.05 – 0.11)
    • Overall negative predictive value -> 99.1% (CI 98.7% - 99.5%)
    • Negative likelihood ratio of VTE after a negative single slice spiral CT scan -> 0.08 (CI 0.05 – 0.13)
    • Negative likelihood ratio of VTE after negative multidetector-row CT scan -> 0.15 (CI 0.05 – 0.43)
    • Overall negative likelihood ratio of mortality attributable to PE -> 0.01 (CI 0.01 – 0.02)
    • Overall negative predictive value 99.4% (CI 98.7% - 99.9%)
    “ Clinical validity of using a CT Scan to rule out PE is similar to that reported for angiography” Quiroz JAMA 2005; 293:2012-2017
  • 54. BNP and Troponins Complementary Biomarkers for Risk Stratification Future Directions? Hemodynamically Stable PE
            • And
    •  Stretch  Ischemia
    •  RV Dysfxn  RV damage
    •  BNP < 50  TnT > 0.01 detects
    • detects low risk high risk
    BNP Troponin Both Elevated Both Normal Low risk Heparin Floor Outpatient High risk Echocardiogram Heparin Medical or Surgical Embolectomy vs
  • 55. Major Pulmonary Embolism Echo Findings
    • Right sided thrombi
    • Correlation with obstruction
    • RV dilatation/hypokinesis
    • Pul Art Dilatation
    •  LV size;  RV/LV ratio
    • Tricuspid regurgitation
    • Abnormal/paradoxical septum
    • Loss of inspiratory collapse IVC
    • AM I
    • Tamponade
    • Aortic dissection
    • Valvular disease
    Pulmonary Embolism Alternative Diagnosis
  • 56. Major Pulmonary Embolism Transthoracic Echo Transesophageal Echo RV Dilatation PE bilateral PE 50%-90% central/proximal
    • TEE sensitivity 80-97% specificity 84%-100%
    • Comparable sensitivity to spiral CT attributed to TEE ability to visualize proximal extending mobile portions of distally impacted emboli
    • Low sensitivity beyond proximal
    Pruszczyk Chest 1997; 112:722-28 Wittlich J Am Soc Echo 1992; 5:515-24
  • 57. Venous Thromboembolism in ICU Pulmonary Embolism Therapeutics
  • 58. Massive Pulmonary Embolism Therapeutics Heparin Thrombolytics Embolectomy Vena Caval filters Standard Bolus Catheter Surgical
  • 59.  
  • 60. ACCP Therapeutic Recommendations
    • High suspicion PE- anticoagulate eval period
    • Non-massive PE- LMWH over UFH
    • Non-massive PE- initial LMWH/UFH for at least 5 days
    • Renal failure- IV UFH over LMWH
    • UFH- aPTT prolongation plasma heparin level 0.3 to 0.7
    • Inability to achieve therapeutic aPTT-measure anti-Xa
    • Initiate VKA on day 1 and discontinue heparin when INR is stable and greater than 2.0
    CHEST 2004; 126(3):401S-428S
  • 61. ACCP Recommendations Long Term
    • Transient reversible risk- VKA 3 months
    • First idiopathic PE- VKA 3-6 months (consider indefinite treatment)
    • PE and Cancer- LMWH 3 to 6 months
    • Antiphosopholipid antibodies or two or more thrombophilic conditions- 12 months
    • First episode with deficiency of protein C, protein S, prothrombin 20210 gene mutation, homocysteinemia or high factor VIII levels- 6-12 months
    • Two or more episodes-indefinite treatment
    • INR target 2.5 (range 2.0 to 3.0)
    • PE and cancer-LMWH for 3-6 months
    CHEST 2004; 126(3):401S-428S
  • 62. Major Pulmonary Embolism Potential Benefits of Thrombolytic Therapy
    • Eliminate venous thrombi  decrease recurrent PE
    • Prevent chronic vascular obstruction and pulmonary HPT
    • Reduction of morbidity and mortality
    Rapid Clot Lysis Enhance pulmonary perfusion Early hemodynamic improvement Improve gas exchange
  • 63. Thrombolytic Therapy-Randomized Trials Heparin Lysis 3.4% 3.4% 2.9% 2.2% 256 Konstantinides 2002 0% 0% -- 100% 8 Sanchez 1995 0% 0% 9% 4% 101 Goldhaber 1993 0% 3% 0% 0% 58 Levine 1990 -- 11% -- 0% 13 PIOPED 1990 0% 0% 0% 0% 30 Marini 1988 -- 0% -- 9% 20 Ly 1978 -- 0% -- 8% 30 Tibbutt 1974 15% 9% 19% 7% 160 UPET 1970 Recurrent Mortality Recurrent Mortality # Study
  • 64. Major Pulmonary Embolism Thrombolytic Therapy “Facts”
    • Heparin better than placebo
    • Barritt Lancet 1961; 1:729
    • 12 hr Urokinase=24 hr Urokinase  24 Streptokinase  heparin
    • UPET II JAMA 1974; 229:1606-13
    • 2 hr TPA>12/24 hr Urokinase
    • Goldhaber Lancet 1988; 2:293-98; Meyer J Am Coll Cardiol 1992; 19:239-45
    • 2 hr TPA=2 hr short infusion Urokinase
    • Goldhaber J Am Coll Cardiol 1992; 20:24-30
    • IV= Intrapulmonary TPA
    • Verstraete Cir 1988; 77:353-60
    • Bolus TPA=2 hr TPA
    • Levine CHEST 1990; 98:1473-79; Goldhaber CHEST 1994; 106:718-24;
    • Sors CHEST 1994; 106:712-17
    • 2 hr TPA>12 hr Streptokinase
    • Meneveau Eur Heart J 1997;18:1141-48
    • 2 hr TPA=2 hr Streptokinase
    • Meneveau J Am Coll Cardiol 1998; 31:1057-63
  • 65. Major Pulmonary Embolism Complications of Thrombolytic Therapy
    • Major hemorrhage (12%)
      • TPA 13.7%
      • UK 10.2%
      • SK 8.8%
    • Intra-cranial hemorrhage (1.2%)
      • Fatal in 50%
      • SK-none reported
      • UK 1.3%
      • TPA 1.6%
      • Elevated diastolic BP as risk
    • Fatal
    • Intra-cranial
    • Requiring transfusion/surgery
    Arcasoy CHEST 1999; 115:1695-1707
  • 66. Major Pulmonary Embolism
    • Diagnostic confirmatory studies can delay definitive treatment and contribute to mortality; angio 14%-67%
    • Cardiopulmonary bypass > venous inflow occlusion
    • Mortality decreasing but variable (16% - 46%)
        • 1960’s 57% 1990’s 26%
        • Highest mortality with cardiac arrest (60%)
    • Catheter fragmentation an option if no arrest
    Surgical or Catheter Embolectomy
  • 67. Heparin Induced Thrombocytopenia Hypercoagulable Paradox
    • Thrombosis risk  degree of thrombocytopenia
        • Mild thrombocytopenia 50%
        • Severe thrombocytopenia 90%
    • Isolated “HIT”  50% thrombosis post dx/stop heparin
    Warkentin Heparin Induced Thrombocytopenia 2001 Venous
    • Aortic or iliofemoral thrombosis acute limb ischemia infarct (5-10%)
    • Acute thrombotic stroke (3-5%)
    • Myocardial infarction (3-5%)
    Arterial
    • DVT 50%
    • PE (25%)
    • Cerebral vein thrombosis
    • Adrenal hemorrhagic infarct
  • 68. Venous Thromboprophylaxis in the Critically Ill
    • Venous thromboembolism is common in critically ill patients
    • Modifiable risk factors are limited in ICU
    • DVT prophylaxis is essential
    • PE risk stratification is crucial to define optimal Tx
    Summary