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Update on Pulmonary Embolism
- 1. Dr. Muhanad Majeed EmergencyPhysician Burjeel Emergency Medicine Seminar Pulmonary Thrombo-embolism Management in Emergency Department
- 3. Objectives Pretest Probabilityin PE Clinical prediction rules D-dimer sensitivity Excluding PE in Primary care setup
- 4. Definition PE results froma clot that formed hours, days, or weeks earlier in the deep veins that dislodges, travels through the venous system, traverses the right ventricle, and lodges in the pulmonary vasculature.
- 5. Primary Causes Threeprimary influences predispose a patient to thrombus formation; these form the so- called Virchow triad, which consists of the following Endothelial injury Stasis or turbulence of blood flow Blood hypercoagulability
- 6. Pathophysiology of Pulmonary VascularOcclusion • Rest dyspnea seems to be the clinical manifestation of distorted and irregular blood flow within the lung, referred to as ventilation-perfusion inequality. • venous admixture: A lodged clot can redistribute blood flow to areas of the lung with already high perfusion relative to ventilation and as such cause more blue blood to pass through the lung without being fully oxygenated
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- 8. Venous Thromboembolic RiskFactors Inherited predisposing factors include the following: • Increased coagulation factor activity/function Activated protein C resistance Factor V Leiden mutation Prothrombin gene mutation Elevated factor VIII levels • Defects of coagulation factor inhibitors Antithrombin Protein C Protein S • Defects in fibrinolysis • Hyperhomocysteinemia • Altered platelet function
- 9. Venous Thromboembolic RiskFactors Acquired predisposing factors include the following: Advancing age (particularly > 60 years) Previous episode of venous thromboembolism Obesity Malignancy Surgery Trauma Hormone replacement therapy Pregnancy Heparin-induced thrombocytopenia Autoimmune associated hypercoagulability (ie, lupus anticoagulant)
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- 11. Prehospital Care stabilizationof the patient’s airway, breathing, and circulation If present, chest pain should be treated Caution should be used before treating patients with possible PE with vasodilating agents (such as nitroglycerin), as patients with PE may be preload dependent. hypotension may be treated with normal saline bolus infusion
- 12. History, Physical Examination,And Risk Stratification Risk stratification is key to the emergency medicine approach to diagnosing PE. Factors from the history and physical examination are used to determine how likely the diagnosis of PE is in an individual patient Clinical gestalt The first study describing the use of clinical gestalt in predicting PE is the original PIOPED (Prospective Investigation Of Pulmonary Embolism Diagnosis) study
- 13. Risk stratification Clinical gestalt •It is the implicit, unstructured estimate of the pretest probability of disease and is based on the clinician’s education, clinical experience, and, ultimately, overall • The first study describing the use of clinical gestalt in predicting PE is the original PIOPED (Prospective Investigation Of Pulmonary Embolism Diagnosis) study
- 14. Risk stratification Wells score Themost commonly used method to predict clinical probability, the Wells score, is a clinical prediction rule, whose use is complicated by multiple versions being available Although the Wells score is the most studied, it continues to be criticized for the lack of true objectivity. Most notably, the “an alternative diagnosis is less likely than PE” criterion is weighted heavily and, alone, can move someone from “no risk” to “moderate risk.”
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- 17. Risk stratification Simplified RevisedGeneva Score
- 18. Risk stratification Simplified RevisedGeneva Score Low risk: ≤ 2 points; high risk: ≥ 3 points.
- 19. Risk stratification Pulmonary EmbolismRule-Out Criteria (PERC) The PERC rule was developed by Kline et al with the specific objective of identifying patients who have more than trivial risk of PE but can be safely discharged without any ancillary testing. The PERC rule requires that the clinician already have a clinical impression of risk for PE < 15% (“very low risk”). It then asks a series of 8 yes/no questions If the answer to all 8 questions is “no,” then the risk of having a PE is considered to be minimal.
- 20. Risk stratification Pulmonary EmbolismRule-Out Criteria (PERC) 1. Is the patient > 49 years of age? 2. Is the pulse rate > 99 beats per minute? 3. Is the pulse oximetry reading < 95% while the patient breathes room air? 4. Is there a present history of hemoptysis? 5. Is the patient receiving exogenous estrogen? 6. Does the patient have a prior diagnosis of venous thromboembolism? 7. Has the patient had recent surgery or trauma requiring endotracheal intubation or hospitalization in the previous 4 weeks? 8. Does the patient have unilateral leg swelling (visual observation of asymmetry of the calves)?
- 21. Risk stratification Sensitivity AndSpecificity Of Clinical Gestalt, Wells Score, And Revised Geneva Score
- 25. Diagnostic Studies • Chestradiography (chest x-ray) • Electrocardiogram (ECG) • Arterial blood gas analysis • Quantitative D-dimer • Computerized tomographic pulmonary angiography (CTPA) of the chest • Ventilation/perfusion (V/Q) lung scan • Cardiac echocardiography • Venous compression ultrasonography
- 26. Chest X-ray • ChestX ray – most common finding with a PE is a normal x-ray • But they are useful as X-rays help to rule out pneumonia and pneumothorax as causes of dyspnoea etc • Possible signs indicating a PE are as follows
- 27. Chest X-ray Hamptons Hump •Not always seen • Wedged shaped pleural based lesion • PE in one area (Bottom arrow) and everywhere else is infarct • Causes pleurisy, irritation
- 28. Westermark Sign • Onthis X-ray PE is in Left lung • Increase in blood flow to right side. • Minimal blood flow seen to Left lung • So the side that looks clearer is the side with reduced blood flow, therefore the clot
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- 30. ECG • A normalECG can be seen in 30% of patients with PE. • The classic S1Q3T3 has a sensitivity and specificity of 54% and 62%, respectively, and was found to occur in only 20% of patients with angiographically proven PE. • Sinus tachycardia was found in only 36% . • T-wave inversion in the precordial leads V1 thru V4 may also be a sign of acute or chronic right ventricular strain, particularly acute pulmonary embolism, 19% in non-massive pulmonary embolism and in 85% in massive pulmonary embolism, and is the most sensitive and specific electrocardiographic finding in massive pulmonary embolism.
- 31. ECG S1Q3T3 Lead I Exaggerated Swave Lead III Exaggerated Q wave T Wave inversion Not specific to PE, but gets you to possibly think of the diagnosis Can be seen in any cor-pulmonale syndrome where pulmonary artery systolic pressure is elevated
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- 33. Sinus tachycardia, withan S1Q3T3 pattern noted by the circles and anterior-inferior T-wave inversions noted by the triangles. Electrocardiogram Of Patient With Massive Pulmonary Embolism
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- 35. D-dimer D-dimer testing isof clinical use when there is a suspicion of • deep venous thrombosis (DVT) • pulmonary embolism (PE) • disseminated intravascular coagulation (DIC). • It is under investigation in the diagnosis of aortic dissection.
- 36. D-dimer • For avery high score, or pretest probability, a D-dimer will make little difference and anticoagulant therapy will be initiated regardless of test results, and additional testing for DVT or pulmonary embolism may be performed. • For a moderate or low score, or pretest probability: • A negative D-dimer test will virtually rule out thromboembolism: the degree to which the D-dimer reduces the probability of thrombotic disease is dependent on the test properties of the specific test used in the clinical setting: most available D-dimer tests with a negative result will reduce the probability of thromboembolic disease to less than 1% if the pretest probability is less than 15-20%. • If the D-dimer reads high, then further testing (ultrasound of the leg veins or lung scintigraphy or CT scanning) is required to confirm the presence of thrombus. Anticoagulant therapy may be started at this point or withheld until further tests confirm the diagnosis, depending on the clinical situation.
- 37. D-dimer • Age-Adjusted D-DimerCutoff Levels to Rule Out Pulmonary Embolism The ADJUST-PE Study
- 38. D-dimer • Age adjustmentof the D-dimer cut-off value increases the specificity for the exclusion of venous thromboembolism in higher age groups without overly affecting sensitivity. Thus, the proportion of elderly patients, in whom a thromboembolic event can be ruled out, increases
- 39. PE in PrimaryCare • Qualitative point-of-care (POC) D-dimer • Quantitative laboratory-based D-dimer Combined with the Wells PE rule, both tests are safe to use in excluding PE. The quantitative test seemed to be safer than the POC test, albeit not statistically significant. The specificity of the POC test was higher, resulting in more patients in whom PE could be excluded. Journal of Thrombosis and Haemostasis
- 40. Computerized Tomographic Pulmonary Angiography CTPA has become the primary radiologic study ordered for the evaluation of PE52,53 and is the overwhelming choice among both emergency clinicians The use of CTPA for the visualization of the pulmonary vasculature and the evaluation of PE was first described in 1992 by Remy-Jardin Studies evaluating multidetector CT are fewer, but, as expected, they show improved accuracy, with sensitivities between 83% and 100% and specificities between 89% and 98%.
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- 45. Tomographic scan showinginfarcted left lung, large clot in right main pulmonary artery
- 46. CTPA Limitations Adrawback to the use of CTPA is the exposure to radiation and iodinated intravenous contrast material. A CTPA subjects the patient to an average effective radiation dose of 15 mSv (ranges between 2 and 20 mSv), which is equivalent to approximately 150 2-view chest x-rays There are 2 primary adverse reactions to iodinated intravenous contrast media: 1. development of anaphylaxis or other immediate systemic allergic reaction. 2. contrast-induced nephropathy. Therefore, a history of allergy to intravenous contrast iodine and a history of renal insufficiency may make V/Q scan the better choice.
- 47. Ultrasound • Non-invasive • Looksat lower limbs • Doppler USS looks at vein for flow and compressibilty to see if clot present
- 48. USS Results • If+ve for DVT and patient has respiratory distress symptoms you can rule in a PE, since the DVTs can embolise easily and enter the lungs causing respiratory problems • If -ve for DVT, unsure whether there is a PE or not, as a clot from other part of body may have embolised the lung, or a whole DVT may have travelled to the lung • So a –ve result does not give a thorough answer, whilst a +ve result may rule it in
- 49. ECHO • Sometimes beneficial •The right ventricle pumps blood to lungs • If clot is present the pressure at site of clot increases and so does the pressure in the right ventricle
- 50. ECHO • The severityof this Pulmonary Artery Pressure (PAP) and the severity of the clot, is found by looking at the tricuspid valve and noting how much regurge occurs (Tricuspid jet) • If tricuspid jet is high then PAP differential between RA and RV is great and the clot burden is large • All these tests may help in the possible diagnosis of a PE, but are not definitive tests
- 51. VQ Scan • Nuclearmedicine scan • Looks at perfusion and ventilation • In pneumonia for example, you would get decreased perfusion and decreased ventilation due to the purulent material present this is a “Matched Deficit” • In a PE there is decreased perfusion of the lung in the area but ventilation remains the same this is an “Unmatched Deficit” • Does Not affect patient in renal failure • Impaired view if patient has pneumonia etc
- 52. VQ Scan • Thepatients ventilation is assessed by them breathing in Xenon • For perfusion the patient is injected with Technigas (Tc99mMAA) • Use Gamma Camera (a glorified Geiger counter) to measure the nuclear material
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- 54. Probability of PE •Normal - Full ventilation and perfusion seen • Low Probability for PE – (<20%) • Intermediate probability for PE- V and P in same area (Matched deficit) (20-80%) • High Probability for PE – Normal V and P (Un-Matched deficit) (>80%)
- 55. Gold Standard • PulmonaryAngiogram – Most accurate test, but not always best for patient (most invasive) • Catheter inserted into right side of the heart, dye is injected directly into pulmonary artery, observed under fluoroscopy • Dangerous, • mortality rate, especially in patients with PE
- 56. Management approach Empirical anticoagulation Supportivetherapies • Respiratory support • Intravenous fluids • Vasopressors • Bed rest Initial anticoagulation Thrombolytic therapy Surgical intervention Venous filters Long-term (extended) anticoagulation
- 57. Anticoagulation • In patientswith confirmed PE, anticoagulation should continue for at least 3 months. • dabigatran, rivaroxaban, apixaban, or edoxaban, are recommended over vitamin K antagonist (VKA) therapy (usually warfarin) • VKA is in turn recommended over low-molecular weight heparin (LMWH) • Fondaparinux is generally reserved for patients with heparin- induced thrombocytopenia (HIT) BMJ Best Practice Last updated Sep 12, 2016
- 58. IVC Filter • Ifanticoagulation treatment contraindicated IVC Filter If clot travels it gets caught in IVC Filter
- 59. IVC Filter • Itis possible for blood clot to be caught and develop in IVC filter • Cochrane Collaboration recommends IVC for 1. Recurrent PE despite use of anticoagulation, or in absolute contra-indication to anticoagulation 2. Proximal DVT with massive pulmonary thrombosis – next one could kill patient 3. Trauma Patient – needing operation
- 60. Prevention • Bilateral LowerExtremity Sequential Compression Devices TEDs and Flowtrons When the legs are squeezed the veins release a factor which thins the blood stopping clot formation, the rhythmic motion copies that of leg movement • Thromboprophylaxis Dalteparin
- 61. Genetic Blood Tests •25-50% of patients with VTE have an inherited disorder • There are genetic causes of metabolism which may be tested for - Factor V Leiden – causes increased clotting as variant cannot be inactivated by Factor Protein C (5% of popn and 20% of pts with thrombus) - Factor Protein C Deficiency – results in normal cleaving of Factor Va and Factor VIIIa - 20210 (prothrombin) Mutation – 2-3 times risk of clot formation - MTHMFR affects regulation of homocysteine - Lupus anticoagulant- prothrombotic agent which can cause inappropriate clotting - Anti phospholipid antibody – confused autoimmune response If any of these are positive and patient has a clot then may need treatment for longer
- 63. Summary The decisionto discharge a patient who presents with chest pain as the primary complaint should be made only after careful consideration of potential consequences. Evaluation and decision (with reasoning) must be well documented. Patients with Chest Pain Are at Risk—Use Both Liberal Consultation and Liberal Admission Policies It is better to sound foolish than be unsafe
- 64. References American Collegeof Chest Physicians evidence-based clinical practice guidelines. Chest. 2012 Feb;141(2 Suppl):e419S- 94S.Cayley, W.E. Diagnosing the cause of chest pain. (2005). American Family Physician, Vol 72 (10), 2012-21. Diagnostic approach to chest pain in adults. (2014). UpToDate. Differential diagnosis of chest pain in adults. (2014). UpToDate. Evaluation of chest pain in the emergency department. (2014). UpToDate.
- 65. Pearl Great EKG PracticeSite http://ecg.bidmc.harvard.edu/maven/mavenmain.asp
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