Pulmonary Embolism

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Pulmonary Thromboembolism Pulmonary Thromboembolism (PTE)(PTE)

Jamil A. Alarafi, D.O.

An Elusive Diagnosis

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GoalsGoals Understand the historical context of pulmonary emboli

Comprehend the pathophysiology and know some common risk factors

Be aware of the clinical features of PE and have a basic understanding of various diagnostic test

Gain a therapeutic approach to the treatment of PE and discuss a simplified method in the work-up of PE

Attempt to dispel a few “myths”about pulmonary emboli

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PerspectivePerspective

A Common disorder and potentially deadly

650,000 cases occurring annually

Highest incidence in hospitalized patients

Autopsy reports suggest it is commonly “missed” diagnosed

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PerspectivePerspective

Presentation is often “atypical”

Signs and symptoms are frequently vague and nonspecific and rarely “classic”

Untreated mortality rate of 20% - 30%, plummets to 5% with timely intervention

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Historical ContextHistorical Context

Pre-1930’s

Heparin

Eugine Robin article

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Historical ContextHistorical Context

PIOPED (Prospective Investigation of Pulmonary Embolism Diagnosis)

The Electronic Era, 2000 and Beyond…

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So What Do We Do ???So What Do We Do ???

Confusing for Emergency Physician

Do we under diagnose/over diagnose?

Why don’t we have a standardized method of work up after all these years?

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PathophysiologyPathophysiology

Rudolph Virchow, 1858

Triad: Hypercoagulability Stasis to flow Vessel injury

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Risk FactorsRisk Factors

HypercoagulabilityMalignancyNonmalignant thrombophilia

PregnancyPostpartum status (<4wk)Estrogen/ OCP’s Genetic mutations (Factor V Leiden, Protein C & S deficiency, Factor

VIII, Prothrombin mutations, anti-thrombin III deficiency)

Venous StatisBedrest > 24 hr Recent cast or external fixatorLong-distance travel or prolong automobile travel

Venous InjuryRecent surgery requiring endotracheal intubationRecent trauma (especially the lower extremities and pelvis)

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Clinical PresentationClinical Presentation The Classic Triad: (Hemoptysis, Dyspnea, Pleuritic

Pain)

Not very common! Occurs in less than 20% of patients with documented PE

Three Clinical Presentations

– Pulmonary Infarction– Submassive Embolism– Massive Embolism

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Mythology of PEMythology of PE

Myth

– “Patients with pulmonary embolism are short of breath and have chest pain!”

Reality: You can forget about making the diagnosis on

clinical grounds, but wait…don’t plan on completely ruling it out either!

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Clinical Features Clinical Features

Symptoms in Patients with Angio Proven PTE

Symptom Percent

Dyspnea 84Chest Pain, pleuritic 74Anxiety 59Cough 53Hemoptysis 30Sweating 27Chest Pain, nonpleuritic 14Syncope 13

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Clinical Features Clinical Features

Signs with Angiographically Proven PE

Sign Percent

Tachypnea > 20/min 92Rales 58Accentuated S2 53Tachycardia >100/min 44Fever > 37.8 43Diaphoresis 36S3 or S4 gallop 34

Thrombophebitis 32Lower extremity edema 24

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Who do we work up?Who do we work up?- - Pretest ProbabilityPretest Probability

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

“Gestalt”– This is really what it boils down to!

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Diagnostic TestDiagnostic Test 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

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Diagnostic TestingDiagnostic Testing- CXR’s- CXR’s

Chest X-Ray Myth:

“You have to do a chest x-ray so you can find Hampton’s hump or a Westermark sign.”

Reality:

Most chest x-rays in patients with PE are nonspecific and insensitive

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Diagnostic Testing Diagnostic Testing -- CXR’s CXR’s

Chest radiograph findings in patient with pulmonary embolism

Result PercentCardiomegaly 27%Normal study 24%Atelectasis 23% Elevated Hemidiaphragm 20%Pulmonary Artery Enlargement 19%Pleural Effusion 18%Parenchymal Pulmonary Infiltrate 17%

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Chest X-ray Eponyms of PEChest X-ray Eponyms of PE Westermark's sign

– A dilation of the pulmonary vessels proximal to the embolism along with collapse of distal vessels, sometimes with a sharp cutoff.

Hampton’s Hump

– A triangular or rounded pleural-based infiltrate with the apex toward the hilum, usually located adjacent to the hilum.

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Radiographic EponymsRadiographic Eponyms- Hampton’s Hump, Westermark’s Sign - Hampton’s Hump, Westermark’s Sign

Westermark’s Sign

Hampton’s Hump

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Diagnostic TestingDiagnostic Testing – EKG’s– EKG’s

EKG

– Most Common Findings:

Tachycardia or nonspecific ST/T-wave changes

– Acute cor pulmonale or right strain patterns

Tall peaked T-waves in lead II (P pulmonale) Right axis deviation RBBB S1-Q3-T3 (occurs in only 20% of PE patients)

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Diagnostic TestingDiagnostic Testing - - Pulse OximetryPulse Oximetry

The Pulse Oximetry Myth:

– “ You must do a pulse oximetry reading, since patients with pulmonary embolism are hypoxemic!”

Reality:

– Most patients with a PE have a normal pulse oximetry, and most patients with an abnormal pulse oximetry will not have a PE.

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Diagnostic Testing Diagnostic Testing - ABG’s- ABG’s

The ABG/ A-a Gradient myth:

– “You must do an arterial blood gas and calculate the alveolar-arterial gradient. Normal A-a gradient virtually rules out PE”.

Reality:

– The A-a gradient is a better measure of gas exchange than the pO2, but it is nonspecific and insensitive in ruling out PE.

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Diagnostic TestingDiagnostic Testing

Echocardiography

– Consider in every patient with a documented pulmonary embolism

EKG maybe helpful in demonstrating right heart strain

– Early fibrinolysis can reduce mortality 50%!

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Ancillary TestAncillary Test 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

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D-dimer TestD-dimer Test Fibrin split product

Circulating half-life of 4-6 hours

Quantitative test have 80-85% sensitivity, and 93-100% negative predictive value

False Positives:

Pregnant Patients Post-partum < 1 weekMalignancy Surgery within 1 weekAdvanced age > 80 years SepsisHemmorrhage CVAAMI Collagen Vascular

DiseasesHepatic Impairment

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Diagnostic TestingDiagnostic Testing

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

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Ventilation/Perfusion ScanVentilation/Perfusion Scan- “V/Q Scan”- “V/Q Scan”

A common modality to image the lung and its use still stems from the PIOPED study.

Relatively noninvasive and sadly most often nondiagnostic

In many centers remains the initial test of choice

Preferred test in pregnant patients 50 mrem vs 800mrem (with spiral CT)

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V/Q ScanV/Q Scan Technique

Interpretation

– Normal – Low probability/”nondiagnostic” (most common)– High Probability

Simplified approached to the interpretation of results:

High probability Treat for PENormal Scan If low pre-test, your doneEverything else Purse another study (CT, Angio)

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Spiral (Helical) Chest CTSpiral (Helical) Chest CT Advantages

– Noninvasive and Rapid– Alternative Diagnosis

Disadvantages

– Costly ($600 - 900/scan)– Risk to patients with borderline renal function– Hard to detect subsegmental pulmonary emboli

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Pulmonary AngiographyPulmonary Angiography

“Gold Standard”– Performed in an Interventional Cath Lab

Positive result is a “cutoff” of flow or intraluminal filling defect

“Court of Last Resort”

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Treatment: Treatment:

Goals: Prevent death from a current embolic event

Reduce the likelihood of recurrent embolic events

Minimize the long-term morbidity of the event

Dr. Batizy explaining the CT results

Patient replies: “Uh-huh, when do I get to eat!”

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TreatmentTreatment

Anticoagulants– Heparin

Provides immediate thrombin inhibition, which prevents thrombus extension

Does not dissolve existing clot

Will not work in patients with antithrombin III def.– In this case use hirudins

Few absolute contraindications

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TreatmentTreatment

Anticoagulants– Heparin

Available as Unfractionated or LMW Heparin

– FDA approved dosing:

• Unfractionated: 80 units/kg bolus, 18 units/kg/hr

• LMWH: 1 mg/kg Q 12 or 1.5mg/kg Q D

LMWH (Lovenox) prefered in pregnant patients

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TreatmentTreatment

Anticoagulants– Warfarin (Coumadin)

Interferes with the action of Vit-K dependent factors: II, VII, IX, and X, as well as protein C & S

Causes temporary hypercoagulable state in first 5 days of treatment

– Important a patient is anticoagulated with heparin before initiating warfarin therapy

Target INR is 2.5 – 3.0

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TreatmentTreatment

Fibrinolytic Therapy (Alteplase)– Indications:

Documented PE with:– Persistent hypotension

– Syncope with persistent hemodynamic compromise

– Significant hypoxemia

– +/- patient with acute right heart strain

Approved Altivase regimen is 100mg as a continuous IV infusion.

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TreatmentTreatment

Embolectomy– Prefininolytic therapy this was only therapy

for massive PE

– Carries a 40% operative mortality

– Alternative is Transvenous Catheter Embolectomy

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A Simplified AlgorithmA Simplified Algorithm

Pre-test probabilityD-dimer (VIDAS-DD) CT angiography

Low Pre-test, D-dimer (-), patient had < 1.7% 90 day PE occurrence in a Mayo Clinic Study

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Special CircumstancesSpecial Circumstances

Morbid Obesity

Pregnancy V/Q has considerable less radiation

– 50 mrem vs. 800 mrem Almost all will have positive D-Dimer Heparin safe in pregnancy

Witnessed Cardiac Arrest Standard ACLS, if known PE, the lytics.

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ConclusionConclusionSummary PointsSummary Points

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 disposition)

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The End!The End!

Questions????

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1. Which of the following is not a part of virchows triad?

a) Hypercoagulability

b) Stasis to flow

c) Vessel injury

d) History of previous DVT

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2. Which of the following is the propper treatment of fat emboli?

a) Platelets

b) High dose steroids

c) Heparin

d) cryoprecipitate

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3. The Classic Triad of patients presenting to the ED with PE includes all of the following except:

a) Hemoptysisb) Dyspneac) + Homans’ signd) Pleuritic Pain

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4. What is the most common symptom in a patient with Angio Proven PTE?

a) Dyspneab) Chest Pain, pleuriticc) Anxietyd) Cough

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5. What is the most common ecg finding in patients with PE?

a) Right axis deviation

b) RBBB

c) S1-Q3-T3

d) Tall peaked T-waves in lead II (P pulmonale)

e) Sinus tachycardia

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AnswersAnswers

1. D2. B3. C4. A 5. E