Pulmonary embolism2006


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Pulmonary embolism2006

  2. 2. PE refers to obstruction of the pulmonary arteryor one of its branches by material (eg, thrombus,tumor, air, or fat ) that originated elsewhere inthe bodyDEFINITIONS
  3. 3. PE Epidemiology Pathophysiology Prevention/Risk factors Screening Diagnosis Treatment
  4. 4. PE Epidemiology Five million cases of venous thrombosis each year 10% of these will have a PE 10% will die Correct diagnosis is made in only 10-30% of cases Up to 60% of autopsies will show some evidence of pastPE
  5. 5. PE Epidemiology 90-95% of pulmonary emboli originate in the deepvenous system of the lower extremities Other rare locations include Uterine and prostatic veins Upper extremities Renal veins Right side of the heart
  6. 6. Risk Factors CHF Malignancy Obesity Estrogen/OCP Pregnancy (esp postpartum) Lower ext injury Coagulopathy Venous Stasis Prior DVT Age > 70 Prolonged Bed Rest Surgery requiring > 30minutes generalanesthesia Orthopedic Surgery
  7. 7. Virchow’s Triad Rudolf Virchow postulated more than a century agothat a triad of factors predisposed to venousthrombosis Local trauma to the vessel wall Hypercoagulability Stasis of blood flow It is now felt that pts who suffer a PE have anunderlying predisposition that remains silent until aacquired stressor occurs
  8. 8. Venous Stasis Accumlation of activated procoagulants. Immobilization Inadequate cardiac pump. Promotes thrombus formation.
  9. 9. Vessel Wall Injury Acute or chronic injury to vessel endothelium. Leads to activation of platelets and clotting cascade. Promotes thrombus formation.
  10. 10. Vessel Injury
  11. 11. Platelet Adhesion
  12. 12. Aggregation
  13. 13. Alternations in Coagulation Increase in procoagulant factors. By trauma to vascular wall or extravascular tissues. Releases tissue thromboplastin and phospholipid. Leads to formation of prothrombin activator. Prothrombin  Thrombin
  14. 14. Alterations in Coagulation Decrease in anticoagulant factors. Thrombomodulin Antithrombin III Heparin Alpha2-Marcoglobulin Plasmin Leads to hypercoagulable state by formation ofthrombin.
  15. 15. Thrombosis Formation Platelet nidus at site of injury. Growth by aggregation of platelets and fibrin. Activation of clotting cascade. Larger growth to a red fibrin thrombus. Thrombus fractures and embolizes to other areas ofthe body.
  16. 16. Predisposing Factors or Diseases forDevelopment of PTE Hypercoagulable state Nephrotic syndrome Immobilization Amyloidosis Early DIC Hyperadrenocorticism Capillary fragility Activation of clotting cascade.
  17. 17. Predisposing Factors or Diseases forDevelopment of PTE Hypercoagulable state Capillary fragility Diabetes Mellitus Immune–mediated hemolyitc anemia Sepsis Hyperadrenocorticism Activation of clotting cascade.
  18. 18.  Factor V Leiden mutation Protein C deficiency Protein S deficiency Antithrombin deficiency Prothrombin gene mutation A20210 Anticardiolipin antibodies Lupus anticoagulant Hyperhomocystinemia
  19. 19. Predisposing Factors or Diseases forDevelopment of PTE Hypercoagulable state Capillary fragility Activation of clotting cascade. Sepsis Pneumonia/pyothorax Heartworm disease Surgery Bacterial endocarditis Neoplasia
  20. 20. Factor V Leiden Most frequent inherited predisposition tohypercoagulability Resistance to activated Protein C Single point mutation (Factor V Leiden) Single nucleotide substitution of glutamine for arginine Frequency is about 3% in healthy American male .
  21. 21. PE When venous emboli become dislodged from their siteof origin, they embolize to the pulmonary arterialcirculation or, paradoxically to the arterial circulationthrough a patent foramen ovale About 50% of pts with pelvic or proximal leg deepvenous thrombosis have PE Isolated calf or upper extremity venous thrombosis posea lower risk for PE
  22. 22. Pathophysiology Increased pulmonary vascular resistance Impaired gas exchange Alveolar hyperventilation Increased airway resistance Decreased pulmonary compliance
  23. 23. Consequences of PTE Respiratory. Increased alveolar dead space. Hyperventilation. Hypoxemia. Ventilation/perfusion inequality. Intrapulmonary shunts.
  24. 24. Normal Alveolus
  25. 25. Increased Alveolar Dead Space
  26. 26. HypoxemiaResults from ventilation-perfusioninequality, physiologic shunting andincreased dead space.
  27. 27. Intrapulmonary Shunts Blood that has not been to areas of ventilated lung andenters systemic circulation without gas exchangetaking place. Poorly oxygenated blood enters the arterial systemlowering the PaO2. Not responsive to oxygen therapy.
  28. 28. Ventilation/Perfusion Inequality V/Q inequality occurs when distribution of blood isaltered to the alveoli. O2 increase in the alveoli and CO2 decreases.
  29. 29. Hemodynamic Changes Increase in pulmonary vascular resistance. Increased afterload to the right heart. Can lead to circulatory collapse and shock.
  30. 30. Right Ventricular Dysfunction Progressive right heart failure is the usual immediatecause of death from PE As pulmonary vascular resistance increases, rightventricular wall tension rises and perpetuates furtherright ventricle dilation and dysfunction Interventricular septum bulges into and compressesthe normal left ventricle
  31. 31. Clinical Syndromes Pts with massive PE present with systemic arterialhypotension and evidence of peripheral thrombosis Pts with moderate PE will have right ventricularhypokinesis on echocardiogram but normal systemicarterial pressure Pts with small to moderate PE have both normal rightheart function and normal systemic arterial pressure
  32. 32. Well’s CriteriaClinical Signs and Symptoms of DVT?(Calf tenderness, swelling >3cm, errythema, pittingedema affected leg only)+3PE Is #1 Diagnosis, or Equally Likely +3Heart Rate > 100 +1.5Immobilization at least 3 days, or Surgery in thePrevious 4 weeks+1.5Previous, objectively diagnosed PE or DVT? +1.5Hemoptysis +1Malignancy w/ Rx within 6 mo, or palliative? +1>6: High Risk2 to 6: Moderate Risk2 or less: LowAdapted with permission from Wells PS, Anderson DR, Rodger M, Ginsberg JS, Kearon C, Gent M, et al. Derivation of a simpleclinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED d-dimer.Thromb Haemost 2000;83:416-20.
  33. 33. Diagnosis H&P Always ask about prior DVT, or PE Family History of thromboembolism Dyspnea is the most frequent symptom of PE Tachypnea is the most frequent physical finding Dyspnea, syncope, hypotension, or cyanosis suggest amassive PE Pleuritic CP, cough, or hemoptysis
  34. 34. Signs of P.E. Tachypnea Rales Tachycardia Hypoxia S4 Accentuated pulmonic component of S2 Fever: T <102 F
  35. 35. Signs in Massive P.E. “Massive PE”: hemodynamic instability with SBP <90or a drop in baseline SBP by >/=40mmHg for morethen 30 min Signs as before PLUS: Acute right heart failure Elevated J.V.P. Right-sided S3 Parasternal lift
  36. 36. P.E. & Leg Symptoms Most patients with P.E. do not have leg symptoms attime of diagnosis Patients with leg symptoms may have asymptomaticP.E.
  37. 37. Differential Diagnosis USA, MI Pneumonia CHF Asthma Costochondritis, Rib Fx, Pneumothorax PE can coexist with other illnesses!!
  38. 38. Physical Signs & SymptomsDyspnea 73%Pleuritc Pain 66%Cough 43%Leg Swelling 33%Leg Pain 30%Hemoptysis 15%Palpitations 12%Wheezing 10%Angina-Like pain 5%
  39. 39. Diagnosis Serum Studies D-dimer Elevated in more than 90% of pts with PE Reflects breakdown of plasmin and endogenous thrombolysis Not specific: Can also be elevated in MI, sepsis, or almost anysystemic illness Negative predictive value ABG-contrary to classic teaching, arterial blood gaseslack diagnostic utility for PE
  40. 40. Diagnosis CXR Usually reveals a non specific abnormality. 14% normal Classic abnormalities include: Westermark’s Sign - focal oligemia Hampton’s Hump - wedge shaped density Enlarged Right Descending Pulmonary Artery (Palla’s sign)
  41. 41. Chest X-ray Eponyms of PE Westermarks sign A dilation of the pulmonary vessels proximal to theembolism along with collapse of distal vessels,sometimes with a sharp cutoff. Hampton’s Hump A triangular or rounded pleural-based infiltrate with theapex toward the hilum, usually located adjacent to thehilum.43
  42. 42. PEHamptonsHump
  43. 43. PEWestermark’s Sign
  44. 44. Radiographic Eponyms- Hampton’s Hump, Westermark’s Sign46Westermark’sSignHampton’s Hump
  45. 45. PE whichappears likea mass.
  46. 46. PE with effusionand elevated diaphragm
  47. 47. How About This???Westermarks Sign: an abrupt tapering of a vessel caused bypulmonary thromboembolic obstruction.This CXR shows enlargement of the left hilum accompanied by leftlung hyperlucency, indicating oligemia (Westermarks sign).
  48. 48. What’s This???Hampton’s Hump
  49. 49. Lab & Radiologic Findings in P.E. ABG BNP Cardiac Enzymes: Troponin D-dimer EKG CXR Ultrasound V/Q Scan Angiography
  50. 50. Lab Findings in P.E.(ABG) ABG: Hypoxemia Hypocapnia (low CO2) Respiratory Alkalosis Massive PE: hypercapnia, mix resp and metabolicacidosis (inc lactic acid) Patients with RA pulse ox readings <95% are atincreased risk of in-hospital complications, resp failure,cardiogenic shock, death
  51. 51. Lab Findings in P.E. (BNP) BNP (beta natruretic peptide) Insensitive test Patient’s with PE have higher levels than pts without,but not ALL patients with PE have high BNP Good prognostic value measure: if BNP >90associated with adverse clinical outcomes (death, CPR,mechanical vent, pressure support, thrombolysis,embolectomy)
  52. 52. Lab Findings in P.E. (Troponin) Troponin High in 30-50% of pts with mod to large PE Prognostic value if combined pro-NT BNP Trop I >0.07 + NT-proBNP >600 = high 40 day mortality
  53. 53. Lab Findings in P.E.(D-dimer) D-dimer: Degredation product of fibrin >500 is abnormal Sensitivity: High, 95% of PE pts will be positive Specificity: Low Negative Predictive Value: Excellent
  54. 54. Lab Findings in P.E. (cont’d) EKG 2 Most Common finding on EKG: Nonspecific ST-segment and T-wave changes Sinus Tachycardia Historical abnormality suggestive of PE S1Q3T3 Right ventricular strain New incomplete RBBB
  55. 55. S1Q3T3!!!
  56. 56. RADRight Atrial Enlargement
  57. 57. Venous Ultrasonography Relies on loss of vein compressibility as the primarycriterion About 1/3 of pts will have no imaging evidence ofDVT Clot may have already embolized Clot present in the pelvic veins (U/S usually inadequate) Workup for PE should continue even if dopplers (-)in a pt in which you have a high clinical suspicion
  58. 58. V/Q Scan Historically, the principal imaging test for thediagnosis of PE A perfusion defect indicates absent or decreasedblood flow Ventilation scan obtained with radiolabeled gases A high probability scan is defined as two or moresegmental perfusion defects in presence of nlventilation scan
  59. 59. V/Q Scan Useful if the results are normal or near normal, or ifthere is a high probability for PE As many as 40% of pts with high clinical suspicion forPE and low probability scans have a PE on angiogram
  60. 60. High Probability V/Q Scan
  61. 61. Pulmonary Angiogram Most specific test available for diagnosis of PE Can detect emboli as small as 1-2 mm Most useful when the clinical likelihood of PE differssubstantially from the lung scan result or when thelung scan is intermediate probability
  62. 62. Pulmonary Angiogram
  63. 63. PE on pulmonary angiogram
  64. 64. Echocardiogram Useful for rapid triage of pts Assess right and left ventricular function Diagnostic of PE if hemodynamics by echo are consitentwith clinical
  65. 65. Spiral CT Scan Identifies proximal PE (which are the ones usuallyhemodynamically important) Not as accurate with peripheral PE
  66. 66. CT revealing pulmonary infarct
  67. 67. CT revealing emboli in pulmonary artery.
  68. 68. DiagnosisSpiral CT/ MultisliceAscending AortaLt PulmonaryArteryMain PulmonaryArteryRt PulmonaryArteryDescendingAortaThrombus
  69. 69. Bilateral PE
  70. 70. SPIRAL CT SCANCriteria for PE extension: obstruction index according to the scoring systemof Qanadli∑ (n · d)n = number of segmentalbranchesd = obstruction degree(1 if partial 2 if complete)
  71. 71. 2-slice CT19922 x 2.7 mm25 sec4-slice CT19984 x 1 mm25 sec64-slice200464 x 0.625 mm4 sec16-slice CT200216 x 0.75 mm10 secPE at MDCT
  72. 72. DiagnosisMRI MR Angiogram Very good to visualize the blood flow. Almost similar to invasive angiogram
  73. 73. Clinical probability assessmentLow or intermediate High (≈ 30%)Diagnosis of PE in stable patientsD-dimerNormal ElevatedPE excluded (≈30%)Multi-detector CTPositive for PE No PETreat
  74. 74. EchocardiographyRVD present No RVDDiagnosis of PE in un-stable patientsTreat & stabilizeMultidetector CTSearch for alternativediagnosis
  75. 75. Treatment Begin treatment with either unfractionatedheparin or LMWH, then switch to warfarin(Prevents additional thrombus formation and permits endogenousfibrinolytic mechanisms to lyse clot that has already been formed,Does NOT directly dissolve thrombus that already exists) Warfarin for atleast 3 months, INR 2-3
  76. 76. Treatment Pain Relief Supplemental Oxygen Dobutamine for pts with right heart failure andcardiogenic shock Volume loading is not advised because increased rightventricular dilation can lead to further reductions inleft ventricular outflow
  77. 77. Anticoagulation Start during resuscitation phase itself If suspicion high, start emperic anticoagulation Evaluate patient for absolute contraindication(i.e.: active bleeding)
  78. 78. Anticoagulation (cont’d) HEPARIN: Lovenox: if hemodynamically stable, no renal function 1mg/kg BID OR 1.5mg/kg QDay Heparin gtt: if hypotension, renal failure 80units/kg bolus then 18units/kg infusion Goal PTT1.5 to 2.5 times the upper limit of normal COUMADIN: Start once acute anticoagulation achieved Start with 5mg PO qday OR 10mg PO q day If start with 10mg then achieve therapeutic INR 1.4 days sooner Complications and morbidity no different in 5mg or 10mg start Goal INR 2 to 3
  79. 79. Duration of Anticoagulation for DVT orPE*Event Duration Strength ofRecommendationFirst Time event ofReversible cause(surgery/trauma)At least 3 mos AFirst episode ofidiopathic VTEAt least 6 mos ARecurrent idiopathicVTE or continuing riskfactor (e.g.,thrombophilia, cancer)At least 12 mos BSymptomatic isolatedcalf-vein thrombosis6 to 12 weeks A*From American College of Chest Physicians
  80. 80. Thrombolysis Considered once P.E. diagnosed If chosen, hold anticoagulation duringthrombolysis infusion, then resumed Associated with higher incidence of majorhemorrhage Indications: persistent hypotension, severehypoxemia, large perfusion defecs, rightventricular dysfunction, free floating rightventricular thrombus, paten foramen ovale Activase or streptokinase
  81. 81. IVC Filter Indication: Absolute contraindication to anticoagulation (i.e.active bleeding) Recurrent PE during adequate anticoagulation Complication of anticoagulation (severe bleeding) Also: Pts with poor cardiopulmonary reserve Recurrent P.E. will be fatal Patient’s who have had embolectomy Prophylaxis against P.E. in select patients(malignancy)
  82. 82. Embolectomy Surgical or catheter Indication: Those who present severe enough to warrantthrombolysis In those where thrombolysis is contraindicated or fails
  83. 83. Recommendations Heparin therapy should be continued for at least fivedays. Oral anticoagulation should be overlapped withheparin therapy for four to five days. Heparin and warfarin therapy can be initiatedsimultaneously, with heparin therapy discontinuedon day five or six if the INR has been therapeutic fortwo consecutive days. Longer periods of initial heparin therapy may beconsidered in the case of massive pulmonaryembolism or iliofemoral thrombosis.
  84. 84. Recommendations Therapy of acute deep vein thrombosis orpulmonary embolism should be initiated with IVheparin …
  85. 85. Recommendations Heparin therapy should be continued for at least fivedays. Oral anticoagulation should be overlapped withheparin therapy for four to five days. Heparin and warfarin therapy can be initiatedsimultaneously, with heparin therapy discontinuedon day five or six if the INR has been therapeutic fortwo consecutive days. Longer periods of initial heparin therapy may beconsidered in the case of massive pulmonaryembolism or iliofemoral thrombosis.
  86. 86. Recommendations LMW heparin may be used in place ofunfractionated heparin. Dosing requirements are individualized for eachproduct.
  87. 87. RecommendationsDuration of therapy First thromboembolic event in the context of areversible risk factor-- treated for three to six months Idiopathic first thromboembolic event-- AT LEAST full six months of treatment-- further therapy at discretion of clinician Recurrent venous thrombosis or a continuing riskfactor -- treated indefinitely.
  88. 88. Recommendations IVC filter placement is recommended when-- anticoagulation is contraindicated-- recurrent thromboembolism despite adequateanticoagulation-- chronic recurrent embolism with pulmonaryhypertension-- high-risk of recurrent embolization-- conjunction with the performance of pulmonaryembolectomy or endarterectomy
  89. 89. TreatmentIVC filter With filter 5% risk ofrecurrent pulmonaryembolus, especially after 6mos. complication of leg swellingcan occur. anticoagulation is continuedif possible.
  90. 90. Conclusion PE is often a misdiagnosed clinical disorder. Rapid identification and appropriate treatment mayoften prevent unnecessary morbidity and mortality.