pulmonary embolism: saving your patient, your rand and making sense of the “clot” !

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Pulmonary Embolism: Saving your Patient, your Rand and making sense of the “clot” ! Dr Sa’ad Lahri Emergency Medicine Registrar

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Pulmonary Embolism: Saving your Patient, your Rand and making sense of the “clot” !. 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 - PowerPoint PPT Presentation

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Pulmonary Embolism

Pulmonary Embolism:

Saving your Patient, your Rand and making sense of the clot !

Dr Saad LahriEmergency Medicine Registrar

In this presentation hoping to give you some insights into PE and hopefully make you more comfortable in the mx thereby helping you in title1Outline and ObjectivesClinical PresentationLab Tests and the ECG in PERisk StratificationPE in PregnancyDo you understand your Imaging?TreatmentProtective documentationTake Home Points

Focus on things that tend to bother us such as risk stratification those Dimers, rest of slide as is2BackgroundMore than 600,000 cases / yrand 60,000 100,000 deaths / yr70% diagnosed at autopsy25 - 35% = Mortality if untreated2 - 8% = Mortality if treatedDetecting it makes a differenceIt kills youWe miss itIts commonCarson, NEJM, 92Background

N Engl J Med 2008;358:1037-52

Figure 1. Pathophysiology of Pulmonary Embolism.Pulmonary embolism usually originates from the deep veins of the legs, most commonly the calf veins. These venous thrombi originatepredominantly in venous valve pockets and at other sites of presumed venous stasis (inset, bottom). If a clot propagates to the kneevein or above, or if it originates above the knee, the risk of embolism increases. Thromboemboli travel through the right side of the heartto reach the lungs. LA denotes left atrium, LV left ventricle, RA right atrium, and RV right ventricle.5

Pathophysiology

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 / incidental

Haemoptysis Minor emboli infarction Pleuritic pain Pulmonary signs

Large pulmonary emboliDyspnoea

Ischaemic pain Massive emboliCollapse /Cardiac

Symptoms SignsDyspnoea 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 PresentationStein, Chest 1991 & Miniati Am J Resp CC 1999

Symptoms SignsDyspnoea 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 PresentationStein, Chest 1991 & Miniati Am J Resp CC 1999

Dyspneoa, Tachypneoa, or Pleuritic CP the Triggers!

History and Physical ExamAsk about recent travel, surgery, or leg swellingO2 Sat & Respiratory Rate - Measure yourselfExamine and even measure the extremities(> 3cm asymmetry 10 cm below tibial tuberosity)

Dont make an alternate diagnosis by misinterpreting non-specific findings (ex. Partially reproducible pain => Costochondritis)Signs/Symptoms Pearls

Risk factors for PE

This you will get from articles and textbooks what do you notice long and blurred not something that typically suit EPs13Acute Medical Illness

CHF/COAD - not recognised / similar presentation

Obesity - under recognised

Risk factors for PE

Risk Factors - PearlsRisk Factors increase your suspicion

However 20% of patients with PE have no known Risk Factors

Therefore Lack of Risk Factors by no means excludes PERisk 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

Runyon et al., Acad EM, 2005The 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 Dont Remember Them!!!!!Runyon et al., Acad EM, 2007Half 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 uniformityRisk Stratification Pearls

SpPin: with high Specificity, a Positive result tends to rule in

SnNout: with high Sensitivity, a Negative result tends to rule outSome Essential Stats

D Dimer and PE

Fibrin degradation products (FDPs) are formed whenever fibrin is broken down by enzymes (e.g., plasmin). Determining FDPs is not considered useful, as this does not indicate whether the fibrin is part of a blood clot (or being generated as part of inflammation).D-dimers are unique in that they are the breakdown products of a fibrin mesh that has been stabilized by Factor XIII.

22Quantitative 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 99.5% Useful in excluding PE in outpatients 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

Patients with high probability1 (n = 1,722) Dichotomized Wells score > 4 D-Dimer 500 ng/ml VTE confirmed in 9.3% ! VTE in 1.1% with low probability (p 4 PE likely

PE?Clinical Probability: Wells Score 4> 4D-DimerImaging, e.g. CTPA 0.5> 0.5Pulmonary Embolism excluded

Diagnostic Pathway

328138 suspected PE2/3 Low suspicion20% low suspicion and met PERC ruleSensitivity 97.4% Specificity 21.9%PERC rule takes a low probability subgroup of patients and makes the risk even lowerThe combination of gestalt estimate of low suspicion for PE and PERC reduces the probability of VTE to below 2%PERC RuleKline et al J Thromb Haemost 2008; 6: 77280. < 2%

PERC Rule

simple and validate. What we do any way . Giving us permission to say super low risk testing not gonna help us34B-type natriuretic peptideCardiac troponinelevated in congestive heart failure/Pulm Hyptnegative predictive value for an uneventful outcome of 99%.not sensitive as a diagnostic toolsignificantly associated with RV dysfunction on ECHO &complicated in hospital course and mortalityCardiac Biomarkers and PEThose with positive BNP and troponin testingshould be considered for ECHO assessment of RV function

Utility of CXR?Clinical Bottom LineAlone little value in diagnosis Value is in ruling out other causes or as part of a risk stratification strategyhttp://www.bestbets.org/bets/bet.php?id=611

HamptonsHump

A rare late finding of pulmonary infarction is the Hampton hump, a triangular or rounded pleural-based infiltrate with theapex pointed toward the hilum, frequently located adjacent to the diaphragmWestermark sign (ie, a dilatation of the pulmonary vessels proximal to an embolism along withcollapse of distal vessels, sometimes with a sharp cutoff).36Atelectasis and/or pulmonary parenchymal abnormalities were most common, 79 of 117 (68 percent)

cardiac enlargement (27% ), normal (24% ), pleural effusion (23% ), elevated hemidiaphragm (20% ), pulmonary artery enlargement (19% ), atelectasis (18% ), and parenchymal pulmonary infiltrates (17%)CXR in Pulmonary Embolism

Stein PD - Chest - 01-SEP-1991; 100(3): 598-603

Chest - Volume 118, Issue 1 (July 2000)

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) NormalThe most common abnormalities are nonspecific ST segment-T wave changes with sinus tachycardia, unfortunately, these findings are extremely nonspecificECG in Pulmonary EmbolismPoor sensitivity

Cannot be used alone!

38 Classic SIQ3T3 patternMistakenly considered pathognomonic for acute PE by many cliniciansSeen 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; 6:301-7ECG in Pulmonary Embolism

ECG in Pulmonary Embolism

T-wave inversions, especially in right precordial leads (V1-V3) + inferior leads Marriott and others: combination of T-wave inversions in right precordial andinferior leads is highly specific for acute pulmonary hyptertension, pulmonaryembolism40T wave Inversions in anteroseptal and inferior leads

Highly specific for PE (99%)

Kosuge (Am J Cardiology 2007)ECG in Pulmonary Embolism

Chest Pain Tunnel Vision

Is of the diagnostic pitfalls that we fall into every day ! It is always ACS?42PE often causes ECG changes that resemble cardiac ischemiaDont just rule out MI when the ECG appears to show cardiac ischemiaECG 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 clinicallyOther diseases that may masquerade as PE (eg, [COPD, pneumonia, CHF) affect oxygen exchange > PEHigh 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

Imaging studies

AdvantagesDisadvantagesLow complication rateModerate radiation exposureCan be used in renal dysfunction Far awayMajority non diagnostic add testingMajor abn on CXR (collapse/P effusions) indeterminate scan

Ventilation Perfusion Scanning

V/Q ScanHigh ProbablityPE DiagnosedNormalExcludes PELow/IntermediateDebate!Low risk and low probabilityD/CIntermediate and D Dimer neg ? No or additional/CTPA +u/sN Engl J Med 2008;358:1037-52.

Preferable to V/Q in patients with prexisting lung diseaseSpecificity (93-99%) Sensitivity (85%)Combined with CTV Sensitivity (90%)Other causes of chest pain imaged/foundCTV using dye from CTPA image venous systemRenal dysfunction/contrast allergies ProblemRadiation dosing high !!! CTPAN 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 patientEchocardiography

N Engl J Med 2008;358:1037-52.

Low-dose oral contraceptives/HRT risk increasesPE risk increased all trimestersD Dimers ? Consider use/ Levels increased Do ultrasound of lower limbsIf CT scanning use lead shieldingThromboytic therapy not withheld Life threatening PELong term anticoagulation : LMWH Warfarin Teratogen Pulmonary Embolism & Pregnancy

Management: Adjuvant therapyN Engl J Med 2008;358:1037-52.

LMWHNeed to monitor in patients withWeight 150kgPregnantRenal ImpairmentMeasure level of activity against factor Xa Treatment: AnticoagulationN Engl J Med 2008;358:1037-52.

Not thrombolytic fibrinolytic system to x unopposedDecrease thromboembolic burdenLMWH vs unfractionated heparin

LMWH = Un Heparin tx PEGreater bioavailablityEase admin, no monitoring of INR Lower risk of HIT Treatment: Anticoagulation

Thrombolytic therapy- BackgroundFaster clot lysisMay reverse RV failureDecrease risk recurrenceRisk: Major haemorrhage 1.8-6.3%ICH : 1.2 % Treatment

Fibrinolytic Therapy in PE

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 thrombolysisFibrinolytic Therapy in PELoebinger et al, QJ med 2004;97:361-364

Fibrinolytic Therapy in PE

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

Protective Documentation

Neat, thorough and legibleRisk factorsChest pain think ACS, PE, DissectionLeg Exam ??? HomansClinical GestaltClinical Decision rule (write PERC negative)Let them know you are thinking!!!Protective Documentation

?

62PE - considered in patients who have cardiopulmonary disease who present with an apparent worsening of chest pain or dyspneoa, or change in baseline

Assign a riskGestaltClinical 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

Email:[email protected]!

Thank you for your attention, its been a pleasure. please dont forget to reg for the conference www.emssa2009.co.za65