Presentation on theme: "Pulmonary Embolism: Saving your Patient, your Rand and making sense of the “clot” ! Dr Sa’ad Lahri Emergency Medicine Registrar Dr Sa’ad Lahri Emergency."— Presentation transcript:
Pulmonary Embolism: Saving your Patient, your Rand and making sense of the “clot” ! Dr Sa’ad Lahri Emergency Medicine Registrar Dr Sa’ad Lahri Emergency Medicine Registrar
Outline and Objectives Clinical Presentation Lab Tests and the ECG in PE Risk Stratification PE in Pregnancy Do you understand your Imaging? Treatment Protective documentation Take Home Points
Background More than 600,000 cases / yr and 60,000 – 100,000 deaths / yr 70% diagnosed at autopsy 25 - 35% = Mortality if untreated 2 - 8% = Mortality if treated Detecting it makes a difference It kills you We miss it It’s common Carson, NEJM, 92 Background
Is the Presentation “boring?” Movie … Is the clinical presentation “boring” ?
Classic teaching: Dyspnoea,tachycardic, tachypnoeic, and has pleuritic pain Clinical Presentation
Acute PE - Spectrum that ranges from: Clinically unimportant Clinically unimportant / incidentalHaemoptysis Minor emboli ± infarction Pleuritic pain Pulmonary signs Large pulmonary emboli Dyspnoea Ischaemic pain Massive emboli Collapse / Cardiac
Symptoms Signs Dyspnoea 73% Pleuritic pain 66% Cough 37% Leg Swelling 28% Leg Pain 26% Haemoptysis 13% RR>20 70% Rales 51% Tachycardia 30% Loud P2 23% Temp>38.5 C 7% Wheezes 5% Clinical Presentation Stein, Chest 1991 & Miniati Am J Resp CC 1999
Symptoms Signs Dyspnoea 73% vs 59% Pleuritic pain 66%vs 43% Cough 37% vs 25% Leg Swelling 28% Leg Pain 26% Haemoptysis 13% vs 7% RR>20 70% vs 68% Rales 51% Tachycardia 30%vs 23% Loud P2 23% Temp>38.5 7%vs 17% Wheezes 5% Clinical Presentation Stein, Chest 1991 & Miniati Am J Resp CC 1999
Dyspneoa, Tachypneoa, or Pleuritic CP – the Triggers! History and Physical Exam –Ask about recent travel, surgery, or leg swelling –O2 Sat & Respiratory Rate - Measure yourself –Examine and even measure the extremities (> 3cm asymmetry 10 cm below tibial tuberosity) Don’t make an alternate diagnosis by misinterpreting non-specific findings –(ex. Partially reproducible pain => Costochondritis) Signs/Symptoms Pearls
Acute Medical Illness CHF/COAD - not recognised / similar presentation Obesity - under recognised Risk factors for PE
Risk Factors - Pearls Risk Factors increase your suspicion However 20% of patients with PE have no known Risk Factors Therefore Lack of Risk Factors by no means excludes PE Risk factor Pearls
Clinical Gestalt Clinical Algorithms – Wells/ Wicki/ Kline/ Miniati Hard to remember … memorise?? Do not agree on any single finding that is predictive of PE Risk Stratification
Clinical Gestalt Using D – Dimer in low risk Clinical Gestalt + Clinical decicion rule Excellent outcomes
Runyon et al., Acad EM, 2005 The unstructured clinical estimate of low pretest probability for PE compares favorably with the Canadian score and the Charlotte rule. Interobserver agreement for the unstructured estimate is moderate. Clinical Gestalt: Works Just as well
Clinical Algorithms We Don’t Remember Them!!!!! Runyon et al., Acad EM, 2007 Half of all clinicians reporting familiarity with the rules use them in more than 50% of applicable cases. Spontaneous recall of the specific elements of the rules was low to moderate.
Gestalt appears equivalent to Algorithms Algorithms may be beneficial for trainees Algorithms may be beneficial for institutional uniformity Risk Stratification Pearls
SpPin: with high Specificity, a Positive result tends to rule in SnNout: with high Sensitivity, a Negative result tends to rule out Some Essential Stats
Quantitative D Dimer (Elisa) High sensitivity (>96%) Low specificity (AMI, pneumonia, dissection, sepsis) High negative predictive value (99%) D Dimer and PE +>0.5mg/l, -ve <0.25mg/l
D Dimers continued… NHLS have D Dimer Latex reagent (agglutination assay) Latex kits demonstrate inadequate sensitivity to reliably exclude PE in multiple studies (pooled sensitivity=70% and specificity=76% Positive samples … semi Quantitative method Private Labs?
Combing Clinical Probability & D-Dimer ðChristopher Study 1 (n = 3,306) ð Christopher Study 1 (n = 3,306) ð Dichotomized Wells score ≤ 4 ð Dichotomized Wells score ≤ 4 ð D-Dimer ≤ 500 ng/ml ð D-Dimer ≤ 500 ng/ml ð Negative predictive value > 99.5% ð Useful in excluding PE in outpatients ð Safe to withhold treatment ð Safe to withhold treatment 1. Van Belle A, et al. Effectiveness of Managing Suspected Pulmonary Embolism Using an Algorithm Combining Clinical Probability, D-Dimer Testing, and Computed Tomography. JAMA 2006;295(2):172-179 D Dimer and PE
Combing Clinical Probability & D-Dimer ðPatients with high probability 1 (n = 1,722) ð Patients with high probability 1 (n = 1,722) ð Dichotomized Wells score > 4 ð Dichotomized Wells score > 4 ð D-Dimer ≤ 500 ng/ml ð D-Dimer ≤ 500 ng/ml ð VTE confirmed in 9.3% ! ð VTE confirmed in 9.3% ! ð VTE in 1.1% with low probability ð VTE in 1.1% with low probability (p<0.001) (p<0.001) 1. Gibson NS, et al. The Importance of the Clinical Probability Assessment in Interpreting a Normal D-Dimer in Patients with Suspected Pulmonary Embolism. Chest 2008;134:789-793 D Dimer and PE
Conclusion on D-Dimers IF your patient has low pretest probability for venous thromboembolic disease, and… IF you use an ELISA, rapid ELISA, turbidimetric, or erythrocyte agglutination D-dimer test…
Conclusion on D-Dimers …THEN you can drive your false negative rate to below 2% and safely rule out pulmonary embolism
Conclusion on D-Dimers IF pretest probability is high, then NO D-dimer can safely rule out VTE D-dimer is NOT a “screening test.” It is a diagnostic test to “Rule out” in appropriate patients
Modified Wells score 1 (“dichotomised”) 1. Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients’ probability of pulmonary embolism: increasing the model’s utility with the SimpliRED D-dimer. Thromb Haemost. 2000;83:416-420. Score ≤ 4 PE “unlikely” > 4 PE “likely”
8138 – suspected PE 2/3 Low suspicion 20% low suspicion and met PERC rule Sensitivity 97.4% Specificity 21.9% PERC rule takes a low probability subgroup of patients and makes the risk even lower The combination of gestalt estimate of low suspicion for PE and PERC reduces the probability of VTE to below 2% PERC Rule Kline et al J Thromb Haemost 2008; 6: 772–80.
B-type natriuretic peptide Cardiac troponin elevated in congestive heart failure/Pulm Hypt negative predictive value for an uneventful outcome of 99%. not sensitive as a diagnostic tool significantly associated with RV dysfunction on ECHO &complicated in hospital course and mortality Cardiac Biomarkers and PE Those with positive BNP and troponin testing should be considered for ECHO assessment of RV function
Utility of CXR? Clinical Bottom Line Alone little value in diagnosis Value is in ruling out other causes or as part of a risk stratification strategy http://www.bestbets.org/bets/bet.php?id=611 Hampton’s Hump
T-wave inversions, especially in right precordial leads (V1-V3) + inferior leads S 1Q3T3 pattern in acute cor pulmonale (12%). Right axis deviation, transient right bundle branch block (RBBB), Arrhythmias (sinus tachycardia, atrial flutter, atrial fibrillation, atrial tachycardia, and atrial premature contractions) Normal The most common abnormalities are nonspecific ST segment-T wave changes with sinus tachycardia, unfortunately, these findings are extremely nonspecific ECG in Pulmonary Embolism Poor sensitivity Cannot be used alone!
Classic “SIQ3T3 pattern” Mistakenly considered pathognomonic for acute PE by many clinicians Seen less frequently--15% to 25% of patients ultimately diagnosed with PE will have this pattern Panos R J, Barish RA, Depriest WW, et al: The Electrocardiographic manifestations of pulmonary embolism. J Emerg Med 1988; 6:301-7 ECG in Pulmonary Embolism
PE often causes ECG changes that resemble cardiac ischemia Don’t just “rule out MI” when the ECG appears to show cardiac ischemia ECG in Pulmonary Embolism
ABG? The PO2 on arterial blood gases analysis (ABG) has a zero or even negative predictive value in a typical population of patients in whom PE is suspected clinically Other diseases that may masquerade as PE (eg, [COPD, pneumonia, CHF) affect oxygen exchange > PE High incidence of PE and a lower incidence of other respiratory ailments (eg, postoperative orthopedic patients with sudden onset of shortness of breath), a low PO2 has a strongly positive predictive value for PE. Use it in conjunction with other tests
Advantages Disadvantages Low complication rate Moderate radiation exposure Can be used in renal dysfunction Far away Majority non diagnostic – add testing Major abn on CXR – (collapse/P effusions) indeterminate scan Ventilation Perfusion Scanning
V/Q Scan High Probablity PE Diagnosed Normal Excludes PE Low/ Intermediate Debate! Low risk and low probability D/C Intermediate and D Dimer neg ? No or additional/CTPA +u/s N Engl J Med 2008;358:1037-52.
Preferable to V/Q in patients with prexisting lung disease Specificity (93-99%) Sensitivity (85%) Combined with CTV – Sensitivity (90%) Other causes of chest pain imaged/found CTV using dye from CTPA image venous system Renal dysfunction/contrast allergies … Problem Radiation dosing high … !!! CTPA N Engl J Med 2008;358:1037-52.
Rapid and accurate – PE instability Exclude other causes of hypotension and raised JVP Can be performed in resus room and guide thromobolytic therapy for unstable patient Echocardiography
Low-dose oral contraceptives/HRT risk increases PE risk increased all trimesters D Dimers ? Consider use/ Levels increased Do ultrasound of lower limbs If CT scanning use lead shielding Thromboytic therapy not withheld Life threatening PE Long term anticoagulation : LMWH Warfarin Teratogen Pulmonary Embolism & Pregnancy
LMWH Need to monitor in patients with Weight 150kg Pregnant Renal Impairment Measure level of activity against factor Xa Treatment: Anticoagulation N Engl J Med 2008;358:1037-52.
Not thrombolytic – fibrinolytic system to x unopposed Decrease thromboembolic burden LMWH vs unfractionated heparin LMWH = Un Heparin tx PE Greater bioavailablity Ease admin, no monitoring of INR … Lower risk of HIT Treatment: Anticoagulation
Thrombolytic therapy- Background Faster clot lysis May reverse RV failure Decrease risk recurrence Risk: Major haemorrhage 1.8-6.3% ICH : 1.2 % Treatment
Fibrinolytic Therapy in PE Cardic Arrest? Clear Benefit- Risk Ratio NO Absolute contraindications Prolonged CPR not CI
Clear benefit in Cardiac Arrest and haemodynamically unstable due to PE No benefit in stable patients with normal RV function Stable but RV dysfunction on echo – “may improve mortality” … jury is still out… Current evidence not there Hypoxaemia? Subgroup worse prognosis, may necessitate need for thrombolysis Fibrinolytic Therapy in PE Loebinger et al, QJ med 2004;97:361-364
Tenecteplase, may have higher efficacy than alteplase due to its bolus dosing, longer half- life, higher fibrin specificity, and more rapid fibrinolytic capacity In cardiac arrest suspected to be caused by PE, the immediate use of a 50-mg alteplase bolus “may be lifesaving” Streptokinase (250,000 U bolus, followed by 100,000 U/h for 24 hours) approved by FDA [Ann Emerg Med. 2003;41:257-270.] Fibrinolytic Therapy in PE
You cannot work everyone up! Defensible practice : Low risk+CDR Negative D Dimer PE Ruled out Protective Documentation
Neat, thorough and legible Risk factors Chest pain… think ACS, PE, Dissection Leg Exam ??? Homan’s Clinical Gestalt Clinical Decision rule (write PERC negative) Let them know you are thinking!!! Protective Documentation
PE - considered in patients who have cardiopulmonary disease who present with an apparent worsening of chest pain or dyspneoa, or change in baseline Assign a risk –Gestalt –Clinical algorithm Pulmonary Embolism can cause ECG changes that simulate ACS Take Home Points
Spiral Ct Scan- well established as primary imaging modality Thrombolysis - Haemodynamically unstable and cardiac arrest Document Clearly Take Home Points