![TREATMENT
Immediate full anticoagulation is mandatory for all patients suspected of having a
pulmonary embolism.
In the acute setting, parenteral anticoagulation is recommended :
Anticoagulation medications include:
Unfractionated Heparin [UFH] IV / SC
Low-molecular weight heparin [LMWH] (eg.enoxaparin [clexane] IV/SC
Fondaparinux SC
The American College of Chest Physicans (ACCP) recommends LMWH or
Fondaparinux over IV UFH and over SC UFH
However LMWH or Fondaparinux are retained in patients with renal impairment and have impaired
absorption in obese patients.](https://image.slidesharecdn.com/pe-170911130444/75/pulmonary-embolism-32-2048.jpg?cb=1668028704)
![ORAL ANTICOAGULANTS
Vitamin K Antagonist [VKA] eg.Warfarin
Factor Xa inhibitor (eg. Apixaban [eliquis], Rivaroxaban
[xarelto])
DirectThrombin Inhibitors (eg Dabigatran)](https://image.slidesharecdn.com/pe-170911130444/75/pulmonary-embolism-34-2048.jpg?cb=1668028704)
Pulmonary Embolism
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A BRIEF CASE ALONG WITH GENERAL overview of pulmonary embolism
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Pulmonary Embolism
- 1. A CASE OF PULMONARY EMBOLISM June 9, 2016
- 2. CASE HISTORY PL Age 41 Female PC- SOB Known to have Hypertension but have been off meds for quite a while. Had a sudden episode of palpitations then sat down and felt severe SOB associated with pre-syncopal episode, diaphoresis and dizziness. No history of orthopnea, PND or leg swelling
- 3. She denies any cough, wheeze but admits a low grade chest pain worsened by inspiration. She had travelled abroad 1-2 weeks ago No history of trauma, personal history of malignancy, recent surgery or any prior history of DVT She presented to her private practitioner who then referred her to this intuition. Past Medical History: nil prior medical admissions
- 4. Past Surgical History: LSCS Feb 2015 (pre-eclampsia) Drug History: nil, no h/o hormonal contraceptive usage Nil known drug allergies Family History: breast ca (aunt) Nil known family history of thrombophilia Social History: Does not smoke nor drink alcohol
- 5. EXAMINATION O/E Middle aged morbidly obese female in mild respiratory distress MM= pink + moist, anicteric, afebrile, acyanotic Vitals BP 170/104 P 110 RR 28 T 96.3 F SpO2 90% RS : Trachea central , air entry equal bilaterally, nil creps, nil rhonchi appreciated. CVS- Pulses synchronous and regular. JVP not appreciated Heart sounds 1 & 2 heard, nil other sounds, nil murmurs Mild pitting oedema bilaterally
- 6. Abd: Obese soft, non-tender nil organomegally CNS: unremarkable, oriented in time, place and person. Nil gross deficits MSK: nil calf tenderness, nil warmth or erythema
- 7. ASSESSMENT Pre Syncope R/O Pulmonary embolism Hypertension Morbid Obesity
- 8. PLAN Admit to ward Serial ECG , CXR Bedside Echocardiogram Supplemental oxygen therapy Bed rest Tropinin I x2 CT Chest Heparin 14,000 SC tds
- 9. ECG
- 13. LABORATORY/ INVESTIGATIVE RESULTS Hb 13.4 PCV 0.41 WBC 10.8 Plt 115 Na 137 K 4.1 Cl 100 CO2 20 BUN 2.5 Creat 49 CPK 240 CKMB 25 LDH 398 Bed side ECHOCARDIOGRAM – Right Ventricular dilatation CXR- Lung fields clear. Boot-shaped heart – Probable Cardiomegaly
- 14. ADMISSION-DAY 1 Assessment: Acute SOB R/O Acute Coronary Syndrome R/O Decompensated Heart Failure R/O Pulmonary Embolism Uncontrolled Hypertension Morbid Obesity Plan:Troponin I Cholesterol Profile Repeat Ck/Ck-MB
- 15. HDL 1.8 LDL 3.0 CHOL 4.7 TRI 0.6 CPK 229 CK-MB 70 TROPONIN I 1 TROPONIN I 2 206.2 233.0
- 16. DAY 2 S- nil complaints O/E RS- chest clinically clear CVS- S1 S2 nil Murmurs A- SOB Pulmonary Embolism Hypertension Morbid Obesity P – For CT Pulmonary Angiogram Continue Heparin anticoagulation PT, PTT, INR VITALS BP 135/87 HR 94 RR 23 Temp 98.4 SOB R/O Pulmonary Embolism Hypertension Morbid Obesity
- 17. DAY 3 S- nil complaints O/E RS- chest clinically clear CVS- S1 S2 nil Murmurs P – For CT Pulmonary Angiogram VITALS BP 132/84 HR 98 RR 22 Temp 98 SOB R/O Pulmonary Embolism Hypertension Morbid Obesity
- 19. DAY 4 S- nil complaints O/E RS- chest clinically clear CVS- S1 S2 nil Murmurs Abd – unremarkable CNS- unremarkable A- Stable Plan – For (Rx) Pradaxa 150mg PO bd Continue Management VITALS BP 130/80 HR 95 RR 20 Temp 98 Pulmonary Embolism Hypertension Morbid Obesity
- 20. DAY 5 S- nil complaints O/E RS- chest clinically clear CVS- S1 S2 nil Murmurs Abd – unremarkable CNS- unremarkable A- Stable Plan – For HOME Pradaxa 150mg PO bd MOPD X 1/12 VITALS BP 133/97 HR 98 RR 20 Temp 97.7 Pulmonary Embolism Hypertension Morbid Obesity
- 21. PRADAXA (DABIGATRAN) Dabigitran is an oral direct thrombin inhibitor It can be easily started following at least 5 days of heparin (LMWH) in the case of a DVT/PE. It has its own reversal drug , Praxbind that can be used in a life- threatening bleed Patients with mild to moderate renal impairment can be treated with Pradaxa however, it is contraindicated in those with severe renal impairment (CrCL <30mL/min).
- 22. PRADAXA It does not need routine clinical monitoring, when used for either short- or long-term treatment. Currently approved for: Treatment of DVT/PE Prevention of recurrent DVT/PE Stroke prevention in non valvular Atrial Fibrillation VTE post surgery
- 23. QUESTIONS?
- 25. Pulmonary embolism is not a disease of itself, but is a complication of venous thrombosis. Pulmonary emboli usually arise from thrombi that originate in the deep venous system of the lower extremities. Pulmonary embolism is potentially lethal and most patients succumb to the event within the first few hours of the event.
- 26. RISK FACTORS
- 28. SIGNS AND SYMPTOMS TYPICAL Shortness of Breath Chest pain (pleuritic) Coughing Palpitations/Tachycardia Hypoxia Tachypnea ATYPICAL Seizures Syncope Abdominal pain Fever Wheezing Decreasing level of consciousness New onset of atrial fibrillation Hemoptysis Flank pain Delirium (in elderly patients)
- 29. INVESTIGATIONS D-Dimer ECG - classic S1Q3T3 pattern, most common finding sinus tachycardia, RBBB, atrial fibrillation, non specificT-wave changes and non specific ST segment changes CXR – non specific generally may show pleural effusion, atelectasis and consolidation ABG- might show significant hypoxia, however it can be normal Cardiac Biomarkers (Troponins and Brain Natriuretic Peptide)
- 30. Echocardiography – might show RV dilatation ,TR, septal flattening, left diastolic ventricular impairment due to septal displacement, pulmonary artery hypertension etc CT-PA -The standard imaging modality Ventilation-Perfusion Scanning – 2nd line less costly, helpful in patients with renal insufficiency, contrast allergy, obesity or in pregnancy. Pulmonary Angiography - infrequently used now since the advent of CT-PA, invasive and costly Magnetic Resonance Angiography- an alternative for patients with contrast allergy and renal impairment
- 31. ANTICOAGULATION
- 32. TREATMENT Immediate full anticoagulation is mandatory for all patients suspected of having a pulmonary embolism. In the acute setting, parenteral anticoagulation is recommended : Anticoagulation medications include: Unfractionated Heparin [UFH] IV / SC Low-molecular weight heparin [LMWH] (eg.enoxaparin [clexane] IV/SC Fondaparinux SC The American College of Chest Physicans (ACCP) recommends LMWH or Fondaparinux over IV UFH and over SC UFH However LMWH or Fondaparinux are retained in patients with renal impairment and have impaired absorption in obese patients.
- 34. ORAL ANTICOAGULANTS Vitamin K Antagonist [VKA] eg.Warfarin Factor Xa inhibitor (eg. Apixaban [eliquis], Rivaroxaban [xarelto]) DirectThrombin Inhibitors (eg Dabigatran)
- 36. TREATMENT Thrombolytic therapy is indicated in patients who have hypotension (systolic BP <90mm Hg) who do not have a high bleeding risk. Thrombolytic agents include: Alteplase Reteplase Urokinase Streptokinase Surgical Methods Placement of vena cava filters Catheter embolectomy
- 37. ADDITIONAL ACCP GUIDELINES Patients with PE provoked by surgery, anticoagulation is recommended for 3months Patients with PE by a non surgical factor, anticoagulation is recommended for at least three months. After three months, they should be evaluated for further therapy. Extended therapy is recommended for patients with recurrent PE and active cancer. For patients with PE and no cancer who are not treated with dabigatran, rivaroxaban, apixaban, or edoxaban, we suggestVKA therapy over low-molecular weight heparin (LMWH).
- 38. SUMMARY Pulmonary embolism is as a result of venous thrombosis. Treatment is initiated on suspicion before confirmation as it has lethal consequences. Anticoagulation is the mainstay of management
- 39. REFERENCES Bartholomew, J. R., MD. (2012, December).VenousThromboembolism (Deep VenousThrombosis & Pulmonary Embolism). Retrieved May 31, 2016, from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/car diology/venous-thromboembolism/ Antithrombotic Therapy ForVte Disease: Chest Guideline And Expert Panel Report Kearon C, Akl EA, Ornelas J, et al.Chest. 2016;149(2):315- 352.doi:10.1016/j.chest.2015.11.026.http://journal.publications.chestnet.org/articl e.aspx?articleid=2479255 Updated Guidelines on Outpatient Anticoagulation. (2013, April 15). Retrieved June 08, 2016, from http://www.aafp.org/afp/2013/0415/p556.html#sec-3 Ouellette, D. R., MD. (2015, October 9). Pulmonary Embolism. Retrieved June 05, 2016, from http://emedicine.medscape.com/article/300901-overview
- 40. THANKYOU
Notas del editor
- Relatively well until the morning of presentation while walking from her bedroom she had a sudden onset episode of palpitation. She sat down then had SOB , this being described as so severe that she felt like she was going to pass out , had diaphoresis
- The Wells score or Wells criteria can refer to one of two clinical prediction rules in clinical medicine DVT probability scoring for diagnosing deep vein thrombosis Pulmonary embolism probability scoring for diagnosing pulmonary embolism
- Two doses 150mg BD & 110mg BD ( patients at risk for bleeding,patients >80, on verapamil,
- How do I switch my patients to Pradaxa from warfarin? To switch to Pradaxa from warfarin, or any other vitamin K antagonist (VKA), treatment with the VKA and start the patient on Pradaxa once their INR falls to <2.0.1 For your DVT/PE patients, Pradaxa can be easily started following at least 5 days of heparin (LMWH).1 Give Pradaxa 0–2 hours prior to the time at which the dose of LMWH would have been due.1 How do I switch my patients from Pradaxa to a parenteral anticoagulant? For patients being treated for primary prevention of venous thromboembolism (pVTEp), it is recommended to wait 24 hours after the last dose of Pradaxa before switching to a parenteral anticoagulant.1 For patients with non-valvular atrial fibrillation (NVAF) being treated for stroke prevention, it is recommended to wait 12 hours after the last dose of Pradaxa before switching to a parenteral anticoagulant.1 How do I switch my patients to Pradaxa from a parental anticoagulant? When switching a patient to Pradaxa from an injectable anticoagulant, give Pradaxa 0–2 hours prior to the time the next dose of injectable anticoagulant would have been due.1 For your DVT/PE patients, Pradaxa can be easily started following at least 5 days of heparin (LMWH).1 Give Pradaxa 0–2 hours prior to the time at which the dose of LMWH would have been due.1
- http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/venous-thromboembolism/
- D-Dimer Testing for PE Patients with a low pretest probability score for PE and negative D-dimer have a high negative predictive value similar to that observed in patients with DVT. However, the patient who has an intermediate to high pretest probability score with a negative D-dimer requires further diagnostic testing to exclude PE.28 Electrocardiography The major utility of electrocardiography (ECG) in the diagnosis of PE is to rule out other major diagnoses, such as acute myocardial infarction (MI). The most specific finding on ECG is the classic S1Q3T3 pattern, but the most common findings consist of nonspecific ST-segment and T-wave changes. Other commonly reported but nonspecific findings include sinus tachycardia, atrial fibrillation, and right bundle-branch block.29 Chest Radiography Chest radiography may also be more helpful in establishing other diagnoses. The most common findings are nonspecific and include pleural effusion, atelectasis, and consolidation. Arterial Blood Gas Determination Pulmonary embolism can result in significant hypoxia, and in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study, only 26% of patients with angiographically proven PE had a PaO2 greater than 80 mmHg.30 Therefore, a normal PaO2 cannot rule out PE; however, hypoxia in the absence of cardiopulmonary disease should raise suspicion for this diagnosis. In patients with cardiopulmonary collapse, a normal PaO2 suggests an alternative diagnosis. Similarly, an elevated alveolar-arterial gradient is suggestive but not specific for the diagnosis of an acute PE. Therefore if the alveolar-arterial gradient is normal, an acute PE cannot be excluded.31 Biomarkers (Troponins and Brain Natriuretic peptide) Elevated levels of cardiac troponins correlate with echocardiographic findings of RV pressure overload in patients with acute PE and overall mortality. In-hospital complications are more frequent in these patients compared to patients with normal levels.38 Brain natriuretic peptide (BNP) elevation in the absence of renal dysfunction is also a marker of RV dysfunction in patients with PE and has been shown to predict adverse outcome in patients with acute PE.39 Causes of troponin elevation other than MI include the following: Myocarditis Pericarditis Cardiac contusion/trauma Aortic dissection Endocarditis Cardiac surgery Pulmonary embolism Stroke (ischemic or hemorrhagic) Cardiopulmonary resuscitation (CPR) Defibrillation Chronic severe heart failure Cardiac arrhythmias (tachyarrhythmias, bradyarrhythmias, heart blocks) Sepsis
- Echocardiography (Transthoracic and Transesophageal) More than 50% of hemodynamically stable patients with PE do not have evidence of RV dysfunction on transthoracic echocardiography (TTE).40 Patients with hemodynamic collapse, however, generally suffer severe RV dysfunction, and TTE or transesophageal echocardiography (TEE) can provide rapid bedside assessment in these critically ill patients who are at increased risk for death. Echocardiography findings include RV dilatation, RV hypokinesis, tricuspid regurgitation, septal flattening, paradoxical septal motion, diastolic left ventricular impairment resulting from septal displacement, pulmonary artery hypertension, lack of inspiratory collapse of the inferior vena cava, and occasionally direct visualization of the thrombus. In patients with large PE, it has been observed that despite moderate or severe RV free-wall hypokinesis there is relative sparing of the apex. This finding is referred to as McConnell's sign and has a specificity of 94% and a positive predictive value of 71% for acute PE.41 McConnell's sign may be useful in discriminating RV dysfunction resulting from PE from that of other causes. Computed Tomographic Pulmonary Angiography Because of its wide availability and ability to visualize thrombus directly, computed tomographic pulmonary angiography (CTPA) imaging has become the standard imaging technique for diagnosing PE. Although initially considered useful only for evaluating central PE and not thought to be the equal to ventilation perfusion (V/Q) scanning, the sensitivity and specificity of newer CTPA scans with multiple slices has increased greatly for diagnosing smaller peripheral or subsegmental PEs. In a study by Anderson and colleagues, patients were randomly assigned to undergo either PTCA or V/Q scanning. The results suggested that CTPA was more sensitive than V/Q scans.32 CTPA also allows direct imaging of the inferior vena cava and the pelvic and leg veins, and can identify other pathologies that can mimic acute PE. The major disadvantages of CTPA are radiation exposure, higher cost, and the possibility of contrast-induced nephrotoxicity. In a meta-analysis of 23 studies involving 4,657 patients with suspected PE who had a normal CTPA, only 1.4% developed VTE and 0.51% developed fatal PE by 3 months.33 These rates are similar to those seen in studies of patients with suspected PE who had normal pulmonary angiograms.34 CTPA can also identify right ventricle enlargement (defined as a ratio of right ventricle diameter to left ventricle diameter >0.9), which has been shown to predict adverse clinical events. This procedure may be an alternative to echocardiography for diagnosing RV enlargement.35 Ventilation-Perfusion Scanning Ventilation-perfusion scanning is now considered a second-line imaging method for the diagnosis of PE. It is helpful in patients who have normal chest radiography or who are unable to undergo CTPA (patients with renal insufficiency, contrast allergy, obesity, or pregnancy). A normal perfusion scan rules out the diagnosis of PE, whereas a high-probability scan along with a high degree of clinical suspicion is diagnostic. Unfortunately, nondiagnostic lung scans (intermediate or low probability) are the most common, and in the PIOPED study they occurred in 72% of patients, thereby limiting the usefulness of this modality.36 It must also be noted that in PIOPED, patients with a high or intermediate clinical suspicion for PE but a low-probability scan had a 40% and 16% rate of PE diagnosed by pulmonary angiography, respectively.36 Hence, it is currently advised that patients with a high or intermediate clinical suspicion for PE but a low-probability V/Q scan have additional tests to confirm or exclude the diagnosis. More recently, PIOPED II, using a different classification system (present or absent) reported that 21% of studies were nondiagnostic leading the authors to suggest that the lung scan may be making a revival.37 Pulmonary Angiography Pulmonary angiography remains the reference standard diagnostic test for PE, but it has been used infrequently since the advent of CTPA. It is invasive, costly, and associated with nephrotoxicity due to contrast exposure; however, in experienced centers, associated morbidity and mortality are low. An intraluminal filling defect or an abrupt cutoff of a pulmonary artery is considered diagnostic. Magnetic Resonance Angiography Magnetic resonance angiography (MRA) may be an alternative to CTPA for the diagnosis of PE in patients who have contrast allergy or for whom avoidance of radiation exposure is desired. Reports of sensitivity and specificity are varied but compared to CTPA, MRA has been reported to be both less sensitive and less specific and limited by interobserver variability
- http://www.aafp.org/afp/2013/0415/p556.html Natural anticoagulants Antithrombin III Protein C & S Tissue factor Plasminogen Inhibitor Thrombomodulin
- UFH binds to the enzyme inhibitor antithrombin III (AT), activated AT then inactivates thrombin and other proteases involved in blood clotting LMWH binds to anti-thrombin, creates a conformational change. This change accelerates its inhibition of activated factor X in conversion of prothrombin to thrombin. LMWH VS UFH Less frequent subcutaneous dosing than for heparin for postoperative prophylaxis of venous thromboembolism. Once or twice daily subcutaneous injection for treatment of venous thromboembolism and in unstable angina instead of intravenous infusion of high dose heparin. No need for monitoring of the APTT coagulation parameter as required for high dose heparin.[15] Possibly a smaller risk of bleeding. Smaller risk of osteoporosis in long-term use. Smaller risk of heparin-induced thrombocytopenia, a potential side effect of heparin. LMWH--- once daily administration is preferred than twice daily Fondaparinux–Factor 10a inhibitor. Unlike direct factor Xa inhibitors, it mediates its effects indirectly through antithrombin III, but unlike heparin, it is selective for factor Xa It also potentiates Anti-thrombin III (about 300 times) the innate neutralization of Factor Xa . One potential advantage of fondaparinux over LMWH or unfractionated heparin is that the risk for heparin-induced thrombocytopenia (HIT) is substantially lower. Local considerations such as cost, availability and familiarity dictate the choice In patients where thrombolytic therapy is considered or planned, IV UFH is preferred
- The oral anticoagulants available in the UK are warfarin, acenocoumarol, phenindione, dabigatran etexilate, rivaroxaban and apixaban.[1] Warfarin continues to be the most widely used oral anticoagulant but the use of the newer oral anticoagulants (dabigatran etexilate, rivaroxaban and apixaban) is increasing. Warfarin antagonises vitamin K (needed for the synthesis of clotting factors) and takes 2-3 days to exert its full effect. In some situations heparin needs to be given for immediate anticoagulation, whilst waiting for the INR to get into the required range. Dabigatran etexilate, rivaroxaban and apixaban are relatively newer oral anticoagulants. Dabigatran etexilate is a direct thrombin inhibitor, whilst rivaroxaban and apixaban inhibit activated factor Xa. Dabigatran etexilate, rivaroxaban and apixaban do not require monitoring of the INR. Contraindicated in pregnancy As it is teratogenic Studies have not yet been done on the use of the other agents
- http://www.aafp.org/afp/2013/0415/p556.html#sec-3
- Cathether embolectomy is : -required if they failed thrombolysis -Contraindications to thrombolysis -Patients in shock
- http://journal.publications.chestnet.org/article.aspx?preview=true&articleid=2479255 More studies are being done to on the newer anticoagulants.