Pulmonary embolism@ghanem@.2013

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PowerPoint presentation about pulmonary embolism -- Teaching at Zagazig university cardiology department ,
Egypt in 2013 by Islam Ghanem , assistant lecturer of cardiology

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Pulmonary embolism@ghanem@.2013

  1. 1. Islam Ghanem MSC Cardiology 2013
  2. 2. 3
  3. 3. Definition Introduction Pathophysiology Clinical Features Investigations Treatment Pulmonary embolism in pregnancy Prognosis Home Message
  4. 4. Pulmonary Embolus is a fragment of the thrombus that breaks off and travels in the blood until it lodges at the pulmonary vasculature. Exogenous or endogenous material (usually a venous thrombus) travelling to lungs (via the venous circulation)
  5. 5.  Acute PE is a relatively common cardiovascular emergency.  High mortality rate if left untreated  Clinical presentation is highly variable and non- specific  Diagnosis requires appropriate and accurate imaging  Prompt diagnosis and treatment can reduce mortality from 30% to 2-8%
  6. 6.  Highest incidence in hospitalized patients  Autopsy reports suggest it is commonly “missed” diagnosed  A Common disorder and potentially deadly  The incidence of PE in USA is 500,000 per year  50,000 individuals die from PE each year in USA
  7. 7.  90-95% of pulmonary emboli originate in the deep venous system of the lower extremities  Other rare locations include  Uterine and prostatic veins  Upper extremities  Renal veins  Right side of the heart
  8. 8. Rudolph Virchow, 1858  Triad:  Hypercoagulability  Stasis to flow  Vessel injury Rudolf Virchow postulated more than a century ago that a triad of factors predisposed to venous thrombosis
  9. 9. Know something about a great scientist who gave us a lot in VTE-------Rudolph Virchow
  10. 10.  Born in Pomerania 1821  graduated in medicine 1843  presented work on thrombosis 1845 but could not get it published  founded own journal
  11. 11. This is the first page of the original manuscript, which consists of this narrative introduction entitled “Wichtigste Arbeiten” followed by the chronological outline. Ackerknecht in his biography of Virchow called the manuscript a curriculum vitae. The form of the manuscript however is more akin to a simple autobiographical piece of work. Virchow used one single sheet of 81/2” by 11” paper that was folded in half with the “Most Important
  12. 12.  Appointed Professor of Pathology in Wurzburg  Described leukaemia, pulmonary embolism and much more  1856 appointed Professor of Pathology in Berlin despite government opposition
  13. 13.  1858 published ‘Cellular Pathology’ one of the most influential medical books ever written  Died aged 81 after fracturing his hip jumping from a moving tram
  14. 14. Hypercoagulability Malignancy Nonmalignant thrombophilia Pregnancy Postpartum status (<4wk) Estrogen/ OCP’s Genetic mutations (Factor V Leiden, Protein C & S deficiency, Prothrombin mutations, anti-thrombin III deficiency, antiphospholipid syndrome) Mutation of Factor V Leiden rendering factor V resistant to inactivation by activated protein C is the most common congenital coagulopathy
  15. 15. Venous Statis Bedrest > 24 hr Recent cast or external fixator Long-distance travel or prolong automobile travel Venous Injury Recent surgery requiring endotracheal intubation Recent trauma (especially the lower extremities and pelvis)
  16. 16.  Modifiable : Obesity Metabolic syndrome Cigarette smoking Hypertension Abnormal lipid profile High consumption of red meat and low consumption of fish, fruits, and vegetables
  17. 17.  Non Modifiable : Advancing age Arterial disease, including carotid and coronary disease Personal or family history of venous thromboembolism Recent surgery, trauma, or immobility, including stroke Congestive heart failure (So in AHF , prophylaxis is indicated) Chronic obstructive pulmonary disease Acute infection Air pollution Long-haul air travel Pregnancy, oral contraceptive pills, or postmenopausal hormone replacement therapy Pacemaker, implantable cardiac defibrillator leads, or indwelling central venous catheter
  18. 18.  The risk of fatal PE in this setting is less than 1 in 1 million.  Activation of the coagulation system during air travel.  For each 2-hour increase in travel duration, there appears to be an 18% higher risk of VTE.
  19. 19.  Increased pulmonary vascular resistance  Impaired gas exchange  Alveolar hyperventilation  Increased airway resistance  Decreased pulmonary compliance
  20. 20.  More than 50% of the vascular bed has to be occluded before PAP becomes substantially elevated  When obstruction approaches 75%, the RV must generate systolic pressure in excess of 50mmHg to preserve pulmonary circulation  The normal RV is unable to accomplish this acutely and eventually fails
  21. 21. Symptoms in Patients with Angio Proven PTE SymptomPercent Dyspnea84 Chest Pain, pleuritic74 Anxiety59 Cough53 Hemoptysis30 Sweating27 Chest Pain, nonpleuritic14 Syncope13
  22. 22. Symptoms in Patients with Angio Proven PTE SymptomPercent Dyspnea84 Chest Pain, pleuritic74 Anxiety59 Cough53 Hemoptysis30 Sweating27 Chest Pain, nonpleuritic14 Syncope13
  23. 23. Signs with Angiographically Proven PE SignPercent Tachypnea > 20/min92 Rales58 Accentuated S253 Tachycardia >100/min44 Fever > 37.843 Diaphoresis36 S3 or S4 gallop34 Thrombophebitis32 Lower extremity edema24
  24. 24. Signs with Angiographically Proven PE SignPercent Tachypnea > 20/min92 Rales58 Accentuated S253 Tachycardia >100/min44 Fever > 37.843 Diaphoresis36 S3 or S4 gallop34 Thrombophebitis32 Lower extremity edema24
  25. 25.  Hypotension + elevated JVP + distant H.S or clear back  In Pulmonary embolism RV infarction Pericardial tamponade Tension pneumothorax
  26. 26.  Imaging Studies  CXR  V/Q Scans  Spiral Chest CT  Pulmonary Angiography  Echocardiograpy  Laboratory Analysis  CBC, ESR, Hgb/Hct,  D-Dimer  ABG’s  Ancillary Testing  EKG  Pulse Oximetry
  27. 27. Chest X-Ray Myth: “We have to do a chest x-ray so we can find Hampton’s hump or a Westermark sign.” Reality: Most chest x-rays in patients with PE are nonspecific and insensitive Normal CXR in setting of severe respiratory distress Think of Pulmonary embolism
  28. 28. Hampton’s Hump – consists of a pleura based shallow wedge-shaped consolidation in the lung periphery with the base against the pleural surface.
  29. 29. 36
  30. 30. Peripheralright pulmonary embolus Hampton ’s Hump causing elevated hemi- diaphragm
  31. 31. Westermark sign – Dilatation of pulmonary vessels proximal to embolism along with collapse of distal vessels, often with a sharp cut off. Pruning)
  32. 32. Westermark’s Sign Hampton’s Hump
  33. 33. - Palla’s sign: dilated descending right The vessel often tapers rapidly after the enlarged portion pulmonary artery.
  34. 34. o A common modality to image the lung and its use still stems. o Relatively noninvasive and sadly most often non diagnostic o In many centers remains the initial test of choice o Preferred test in pregnant patients o 50 mrem vs 800mrem (with spiral CT) o Less radiation exposure to the mother, but more to the foetus
  35. 35. Only three indications to obtain a lung scan exist: (1) renal insufficiency, (2) anaphylaxis to intravenous contrast agent that cannot be suppressed with high-dose corticosteroids (3) pregnancy (lower radiation exposure to the mother). High probability scan: If 2 or more segmental perfusion defects with normal ventilation
  36. 36. Technique
  37. 37.  Major advantage of Spiral CT is speed:  Often the patient can hold their breath for the entire study, reducing motion artifacts.  Allows for more optimal use of intravenous contrast enhancement.  Spiral CT is quicker than the equivalent conventional CT permitting the use of higher resolution acquisitions in the same study time.  Contraindicated in cases of renal disease.  Sensitive for PE in the proximal pulmonary arteries, but less so in the distal segments.
  38. 38.  Quickly becoming the test of choice for initial evaluation of a suspected PE.  CT unlikely to miss any lesion.  CT has better sensitivity, specificity and can be used directly to screen for PE.  CT can be used to follow up “non diagnostic V/Q scans.
  39. 39. Chest computed tomography scanning demonstrating extensive embolization of the pulmonary arteries.
  40. 40.  Size, location, and extent of thrombus Other diagnoses that may coexist with PE or explain PE symptoms:  Pneumonia Atelectasis Pericardial effusion Pneumothorax Left ventricular enlargement Pulmonary artery enlargement, suggestive of pulmonary hypertension  Age of thrombus: acute, subacute, chronic  Location of thrombus: pulmonary arteries, pelvic veins, deep leg veins, upper extremity veins  Right ventricular enlargement  Contour of the interventricular septum: whether it bulges toward the left ventricle, thus indicating right ventricular pressure overload  Incidental masses or nodules in lung
  41. 41. Spiral CT
  42. 42. Before After
  43. 43.  Gadolinium-enhanced magnetic resonance angiography (MRA) is far less sensitive than CT for the detection of PE.  However, unlike chest CT or catheter-based pulmonary angiography, MRA does not require ionizing radiation or injection of iodinated contrast agent.  In addition, magnetic resonance pulmonary angiography can assess right ventricular size and function.  Three-dimensional MRA can be carried out during a single breath-hold and may provide high resolution from the main pulmonary artery through the segmental pulmonary artery branches.
  44. 44. MRA with contrast
  45. 45. MRA Real Time
  46. 46.  Gold Standard.  Positive angiogram provides 100% certainty that an obstruction exists in the pulmonary artery.  Negative angiogram provides > 90% certainty in the exclusion of PE.  However, pulmonary angiography is required when interventions are planned, such as suction catheter embolectomy, mechanical clot fragmentation, or catheter-directed thrombolysis.  “Court of Last Resort”
  47. 47. Left-sided pulmonary angiogram showing extensive filling defects within the left pulmonary artery and its branches.
  48. 48. 65
  49. 49.  This modality generally has limited accuracy in the diagnosis.  The overall sensitivity and specificity for diagnosis of central and peripheral pulmonary embolism by ECHO is 59% and 77%.  It may allow diagnosis of other conditions that may be confused with pulmonary embolism.  Used after diagnosis of PE to stratify the risk of the patient which may aid in treatment.  Used for follow up of residual pulmonary hypertension 2 weeks after the acute event (CTEPH).
  50. 50.  RV enlargement or hypokinesis especially free wall hypokinesis,with sparing of the apex (the McConnell sign) The most specific sign  Interventricular septal flattening and paradoxical motion toward the LV, resulting in a “D-shaped” LV in cross section.  Tricuspid regurgitation, reduced RV systolic function(TAPSE 16mm)  Direct visualization of the thrombus in the pulmonary arteries or RV or RA (In transit PE)  Dilated IVC , lost normal respiratory collapse
  51. 51. Before After
  52. 52. Present the 2 videos in the folder
  53. 53.  No validated clinical decision rules  No consensus in evidence for diagnostic imaging algorithm  Balance risk of radiation vs. risk of missed fatal diagnosis or unnecessary anticoagulation  MDCT delivers higher radiation dose to mother but lower dose to fetus than V/Q scanning  Consider low-dose CT-PA or reduced-dose lung scintigraphy
  54. 54.  Plain chest radiograph – Usually normal and non- specific signs.  Radionuclide ventilation-perfusion lung scan – Excellent negative predictive value.  CT Angiography of the pulmonary arteries – Quickly becoming method of choice.  Pulmonary angiography – Gold standard but invasive.
  55. 55. WBC  Poor sensitivity and nonspecific  Can be as high as 20,000 in some patients Hgb/Hct  PTE does not alter count but if extreme, consider polycythemia, a known risk factor ESR  Don’t get one, terrible test in regard to any predictive value
  56. 56.  Fibrin split product ( reflect plasmin’s breakdown Of fibrin Endogenous but ineffective Fibrinolysis)  Quantitative test have 80-85% sensitivity, and 93-100% negative predictive value  High negative predictive value in non hospitalized patients  False Positives: Pregnant Patients Post-partum < 1 week Malignancy Surgery within 1 week Advanced age > 80 years Sepsis Hemmorrhage CVA AMI Collagen Vascular Diseases Hepatic Impairment
  57. 57. D-dimer Qualitative  Bed side RBC agglutination test  “SimpliRED D-dimer”  Quantitative  Enzyme linked immunosorbent asssay “Dimertest”  Positive assay is > 500ng/ml  VIDAS D-dimer, 2nd generation ELISA test
  58. 58.  ABG has a limited role.  It usually reveal hypoxemia, hypocapnia and respiratory alkalosis.
  59. 59.  The electrocardiogram (ECG) helps exclude acute myocardial infarction.  T wave inversion in leads V1 to V4 has the greatest accuracy for identification of right ventricular dysfunction in patients with acute PE.  Electrocardiographic manifestations of right-sided heart strain ,which is an ominous prognostic finding.
  60. 60.  Sinus tachycardia:8-73%  P Pulmonale : 6-33%  Rightward axis shift : 3-66%  Inverted T-waves in >/= right chest leads: 50%  S1Q3T3 pattern: 11-50% (S1-60%, Q3-53% ,T3-20%)  Clockwise rotation:10-56%  RBBB (complete/incomplete): 6-67%  AF or A flutter: 0-35%  No ECG changes: 20-24%
  61. 61. S1 Q3 T3 Pattern
  62. 62. Rt. Bundle Branch Block
  63. 63. Rt. Ventricular Strain
  64. 64.  BNP & NT- Pro BNP  cTroponin T & I  H-FABP (Heart type)  Growth differentiation factor -15
  65. 65.  Conclusion: Elevated troponin levels were associated with a high risk of (early) death resulting from pulmonary embolism (OR, 9.44; 95% CI, 4.14 to 21.49)  These findings identify troponin as a promising tool for rapid risk stratification of patients with pulmonary embolism.
  66. 66.  Typically greater in patients with PE.  Sensitivity of 60% and specificity of 62%.  At a threshold of 500 pg/mL, the sensitivity of pro- BNP for predicting adverse events was 95%, and the specificity was 57%.
  67. 67. Principle - Veins are normally compressible; Presence of DVT renders veins non-compressible 50% of patients with PE have positive ultrasound (95% of PE are due to leg DVT)
  68. 68. Oxygen saturation Nonspecific, but suspect PE if there is a sudden, otherwise unexplained decrement D-dimer An excellent “rule-out” test if normal, especially if accompanied by non–high clinical probability Electrocardiography May suggest an alternative diagnosis, such as myocardial infarction or pericarditis Lung scanning Usually provides ambiguous result; used in lieu of chest CT for patients with anaphylaxis to contrast agent, renal insufficiency, or pregnancy Chest CT The most accurate diagnostic imaging test for PE ; beware if CT result and clinical likelihood probability are discordant Pulmonary angiography Invasive, costly, uncomfortable; used primarily when local catheter intervention is planned Echocardiography Best used as a prognostic test in patients with established PE rather than as a diagnostic test ; many patients with large PE will have normal echocardiograms Venous ultrasonography Excellent for diagnosis of acute symptomatic proximal DVT; a normal study does not rule out PE because a recent leg DVT may have embolized completely; calf vein imaging is operator dependent Magnetic resonance Reliable only for imaging of proximal segmental pulmonary arteries; requires gadolinium but does not require iodinated contrast agent
  69. 69.  No consensus on who to test  Increased likelihood if:  Age <50 years without immediate identifiable risk factors (idiopathic or unprovoked)  Family history  Recurrent clots  If clot is in an unusual site (portal, hepatic, mesenteric, cerebral)  Unprovoked upper extremity clot (no catheter, no surgeries)  Patients with warfarin-induced skin necrosis (they may have protein C deficiency)
  70. 70.  Protein C or S deficiency  Factor V leiden deficiency  Anti-thrombin III deficiency  Prothrombin gene mutation  Antiphospholipid antibody  High Homocysteine The most common cause of congenital hyper- coagulability is protein C resistance due to factor V Leiden mutation
  71. 71.  Pneumothorax  Myocardial ischemia  Pericarditis  Asthma  Pneumonia  MI with cardiogenic shock  Cardiac tamponade  Aortic dissection
  72. 72.  Pre test probability  Risk stratification
  73. 73.  Pre test probability  Risk stratification
  74. 74.  Definition: “The probability of the target disorder (PE) before a diagnostic test result is known”.  Used to decide how to proceed with diagnostic testing and final disposition
  75. 75. SCORE POINTS DVT symptoms or signs 3 An alternative diagnosis is less likely than PE 3 Heart rate >100/min 1.5 Immobilization or surgery within 4 weeks 1.5 Prior DVT or PE 1.5 Hemoptysis 1 Malignancy (on treatment, treated in the past 6 months, palliative) 1 >4 score points = high probability ≤4 score points = non–high probability
  76. 76. DVT symptoms or signs 1 An alternative diagnosis is less likely than PE 1 Heart rate >100/min 1 Immobilization or surgery within 4 weeks 1 Prior DVT or PE 1 Hemoptysis 1 Cancer treated within 6 months or metastatic 1 >1 score point = high probability ≤1 score point = non–high probability
  77. 77.  Pre test probability  Risk stratification
  78. 78.  Massive  Submassive  Low-Risk PE  Pulmonary infarction syndrome
  79. 79.  Acute PE with sustained hypotension (systolic blood pressure 90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as  Arrhythmia  Hypovolemia  Sepsis  Left ventricular (LV) dysfunction  Pulselessness  Persistent profound bradycardia (heart rate 40 bpm with signs or symptoms of shock)
  80. 80.  Acute PE without systemic hypotension (systolic blood pressure 90mm Hg) but with either RV dysfunction or myocardial necrosis  RV dysfunction means the presence of at least 1 of the following  RV dilation (apical 4-chamber RV diameter divided by LV diameter 0.9) or RV systolic dysfunction on echocardiography  RV dilation (4-chamber RV diameter divided by LV diameter 0.9) on CT  Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)  Elevation of BNP (90 pg/mL)  Elevation of N-terminal pro-BNP (500 pg/mL)  myocardial necrosis means the presence of at least 1 of the following  Elevation of troponin or H-FABP
  81. 81.  Acute PE and the absence of the clinical markers of adverse prognosis that define massive or submassive PE
  82. 82.  Caused by a tiny peripheral pulmonary embolism  Pleuritic chest pain, often not responsive to narcotics  Low-grade fever  Leukocytosis  Pleural rub  Occasional scant hemoptysis
  83. 83. Goals:  Prevent death from a current embolic event  Reduce the likelihood of recurrent embolic events  Minimize the long-term morbidity of the event
  84. 84.  Oxygen inhalation up to ventillatory support  Anticoagulation  Inferior vena cava filter  Additional options for massive PE  Thrombolytic agent  Catheter embolectomy  Surgical embolectomy  Haemodynamic support - inotropes
  85. 85.  Begin treatment with either unfractionated heparin or LMWH, then switch to warfarin (Prevents additional thrombus formation and permits endogenous fibrinolytic mechanisms to lyse clot that has already been formed, Does NOT directly dissolve thrombus that already exists)  It is important that a patient should be anticoagulated with heparin before initiating warfarin therapy  Target INR is 2 – 3
  86. 86.  80 units/kg bolus (minimum, 5000 units; maximum, 10,000 units) followed by a continuous infusion of 18 units/kg/h maximum 1000 units/h)  aPTT monitoring is required
  87. 87.  Subcutaneous UFH: aPTT monitoring  15,000 units or 17,500 units every 12 h (initial dose for patients weighing 50–70 kg and >70 kg, respectively)  Subcutaneous UFH: no aPTT monitoring  330 units/kg bolus then 250 units/kg every 12 h
  88. 88.  Anticoagulant pentasaccharide that specifically inhibits activated factor X  By selectively binding to antithrombin, fondaparinux potentiates (about 300 times) the neutralization of factor Xa by antithrombin  Fondaparinux does not cross-react with heparin- induced antibodies  FDA has approved fondaparinux for initial treatment of acute PE and acute DVT as a bridge to oral anticoagulation with warfarin
  89. 89. 127 Important drug interactions with warfarin Drugs that decrease warfarin requirement Drugs that increase warfarin requirement Phenylbutazone Barbiturates Metronidazole Carbamazepine Trimethoprim-sulfamethoxazole Rifampin Amiodarone Penicillin Second- and third-generation cephalosporins Griseofulvin Clofibrate Cholestyramine Erythromycin Anabolic steroids Thyroxine
  90. 90. 128 Dosage and monitoring of anticoagulant therapy After initiating heparin therapy, repeat APTT every 6 h for first 24 h and then every 24 h when therapeutic APTT is achieved Warfarin 5 mg/d can be started on day 1 of therapy; there is no benefit from higher starting doses Platelet count should be monitored at least every 3 d during initial heparin therapy Therapeutic APTT should correspond to plasma heparin level of 0.2–0.4 IU/mL Heparin is usually continued for 5–7 d Heparin can be stopped after 4–5 d of warfarin therapy when INR is in 2.0– 3.0 range
  91. 91.  Promise immediate onset of action and administration in fixed doses without routine laboratory coagulation monitoring  These drugs have few drug-drug or drug-food interactions, making them more “user friendly”  Dabigatran is a direct thrombin inhibitor  Rivaroxaban is a factor Xa inhibitor  Both are approved in Canada and Europe for VTE prevention after knee or hip arthroplasty
  92. 92.  Thrombolysis  1. Hemodynamically compromised by PE – definitie indication  2. Right ventricular dysfunction (strain) detected by echocardiography (better), positive troponin.
  93. 93.  Massive or major PE: Thrombolytic therapy is indicated  Submassive (non-massive) PE: Thrombolytic therapy may be indicated in the presence of RV dysfunction
  94. 94.  At present, the alteplase regimen in which 100 mg is administered intravenously over two hours is the most rapidly administered protocol that is currently approved for use in the United States
  95. 95. These should be particularly scrutinized if lytic therapy is considered
  96. 96.  Intravenous route -- primary method of delivery  Rapid infusion -- Shorter regimens may not only prove efficacious but also reduce the risk of hemorrhagic complications  Catheter-directed therapy -- for massive PE, may induce major bleeding
  97. 97.  Potential benefits include  More rapid resolution of symptoms (eg, dyspnea, chest pain, and psychological distress)  Stabilization of respiratory and cardiovascular function without need for mechanical ventilation or vasopressor support  Reduction of RV damage  Improved exercise tolerance  Prevention of PE recurrence  Increased probability of survival
  98. 98.  Potential harm includes  Disabling or fatal hemorrhage including intracerebral hemorrhage  Increased risk of minor hemorrhage, resulting in prolongation of hospitalization and need for blood product replacement
  99. 99.  Performed as an alternative to thrombolysis  When there are contraindications  When emergency surgical thrombectomy is unavailable or contraindicated  Hybrid therapy that includes both catheter-based clot fragmentation and local thrombolysis is an emerging strategy  Goals of catheter-based therapy include  Rapidly reducing pulmonary artery pressure, RV strain, and pulmonary vascular resistance (PVR)  Increasing systemic perfusion  Facilitating RV recovery
  100. 100.  3 general categories of percutaneous intervention  Aspiration thrombectomy  Thrombus fragmentation  Rheolytic thrombectomy
  101. 101.  The Greenfield embolectomy catheter  Balloon angioplasty and stents  Pigtail rotational catheter  Amplatz thrombectomy device (ATD)  Hydrodynamic thrombectomy catheter devices  Aspirex pulmonary embolism thrombectomy catheter
  102. 102.  When contraindications preclude thrombolysis  Surgical excision of a right atrial thrombus  Rescue patients whose condition is refractory to thrombolysis  Older case series suggest a mortality rate between 20% and 30%  In a more recent study, 47 patients underwent surgical embolectomy in a 4-year period, with a 96% survival rate
  103. 103.  PREPIC Trial randomized 400 patients with proximal DVT at high risk for PE  IVC filters significantly reduced the incidence of recurrent PE at 12 days (1.1% versus 4.8%, P0.03) and at 8 years (6.2% versus 15.1%, P0.008)  IVC filters were associated with an increased incidence of recurrent DVT at 2 years (20.8% versus 11.6%, P0.02) (act as a nidus)
  104. 104. Adapted from Becker et al.)
  105. 105. Early complications Device malposition (1.3%) Pneumothorax(0.02%), Hematoma (0.6%) Air embolism (0.2%) Inadvertent carotid artery puncture (0.04%) Arteriovenous fistula (0.02%) Recurrent DVT (21%) IVC thrombosis (2% to 10%), IVC penetration (0.3%) Filter migration (0.3%) Late complications
  106. 106. Mechanical:  Leg elevation  Graded compression stocking  Early ambulation  Pneumatic compression boot
  107. 107. Pharmacological:  Un-fractionated heparin (UFH): given every 8 hours SC  Low-molecular weight heparin: Enoxaparin 30- 40mg SC every 24 hours  Fondaparinux: 2.5mg SC every 24 hours  Desirudin: A recombinant direct thrombin inhibitor. Dose: 15mg SC every 12 hours  Rivaroxaban: A novel oral anti-Xa agent. Dose: 10mg every 24 hours
  108. 108. Inferior vena cava (IVC) filter:  Considered as secondary prophylaxis or secondary prevention against PE but not DVT.  IVC filter is indicated in patients with high risk of recurrence when other methods are contra- indicated (Class IIb, LOE B).  The routine use of IVC filters is not recommended (Class III, LOE B).
  109. 109.  Unfractionated heparin 5000 units SC bid or tid or  Enoxaparin 40 mg SC qd or  Dalteparin 2500 or 5000 units SC qd
  110. 110.  Unfractionated heparin 5000 units SC bid or  Enoxaparin 40 mg SC qd and  Graduated compression stockings or intermittent pneumatic compression  Consider surveillance lower extremity ultrasonography
  111. 111.  Oncologic surgery Enoxaparin 40 mg SC qd  Thoracic surgery Unfractionated heparin 5000 units SC tid and Graduated compression stockings or intermittent pneumatic compression
  112. 112.  Septic embolism- drug addicts, catheters & pacemaker wires, septic thrombophlebitis  Intravascular foreign bodies- broken catheters, guidewires,vena cava filters  Fat embolism- trauma  Venous air embolism  Amniotic fluid embolism- occur in 1/8000 – 1/80,000, high maternal & fetal mortality  Talc embolism
  113. 113.  No validated clinical decision rules  No consensus in evidence for diagnostic imaging algorithm  Balance risk of radiation vs. risk of missed fatal diagnosis or unnecessary anticoagulation  MDCT delivers higher radiation dose to mother but lower dose to fetus than V/Q scanning  Consider low-dose CT-PA or reduced-dose lung scintigraphy
  114. 114.  V/Q scan should be the first imaging modality  Thrombolysis carries high bleeding risk, but should be used in critical cases  Anticoagulation: Heparin should be used in the 1st-12th w., after 36th w., but warfarin should be used in 13th-36th w.  Anicoagulation should extend to 3 months after delivery
  115. 115.  Hemodynamic instability  Right ventricular hypokinesis on echocardiogram  Right ventricular enlargement on echocardiogram or chest CT scan  Right ventricular strain on electrocardiogram  Elevated cardiac biomarkers
  116. 116.  Pulmonary Emboli remain a potentially deadly and common event which may present in various ways  Don't’ be fooled if your patient lacks the “classic” signs and symptoms!  Consider PE in any patient with an unexplainable cause of dyspnea, pleuritic chest pain, or findings of tachycardia, tachpnea, or hypoxemia  2nd Generation Qualitative D-Dimers have NPV of 93-99%  Heparin remains the mainstay of therapy with the initiation of Warfarin to follow  Simplified Algorithm: ( Pretest probability, D-Dimer, +/- CT angio), then risk stratification and treatment)
  117. 117. THANKYOU

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