Pulmonary Embolism
Pulmonary Embolism
Pulmonary Embolism
An Elusive Diagnosis
Goals
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 mythsabout pulmonary emboli
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Perspective
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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Perspective
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
Historical Context
Pre-1930s
Heparin
Historical Context
So What Do We Do ???
Confusing
Do we under diagnose/over diagnose? Why dont we have a standardized method of work up after all these years?
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Pathophysiology
Rudolph Virchow, 1858
Triad:
Risk Factors
Hypercoagulability
Malignancy Nonmalignant thrombophilia
Pregnancy Postpartum status (<4wk) Estrogen/ OCPs Genetic mutations (Factor V Leiden, Protein C & S deficiency, Factor VIII, Prothrombin mutations, anti-thrombin III deficiency)
Venous Statis
Bedrest > 24 hr Recent cast or external fixator Long-distance travel or prolong automobile travel
Venous Injury
Recent surgery requiring endotracheal intubation Recent trauma (especially the lower extremities and pelvis)
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Clinical Presentation
Not very common! Occurs in less than 20% of patients with documented PE
Mythology 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 waitdont plan on completely ruling it out either!
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Clinical Features
Symptoms in Patients with Angio Proven PTE
Symptom
Dyspnea Chest Pain, pleuritic Anxiety Cough Hemoptysis Sweating Chest Pain, nonpleuritic Syncope
Percent
84 74 59 53 30 27 14 13
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Clinical Features
Signs with Angiographically Proven PE
Sign Tachypnea > 20/min Rales Accentuated S2 Tachycardia >100/min Fever > 37.8 Diaphoresis S3 or S4 gallop Thrombophebitis Lower extremity edema Percent 92 58 53 44 43 36 34 32 24
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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 Test
Imaging Studies CXR V/Q Scans Spiral Chest CT Pulmonary Angiography Echocardiograpy Laboratory Analysis
CBC, ESR, Hgb/Hct, D-Dimer ABGs
Ancillary Testing
EKG Pulse Oximetry
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Diagnostic Testing
- CXRs
Chest X-Ray Myth: You have to do a chest x-ray so you can find Hamptons hump or a Westermark sign. Reality: Most chest x-rays in patients with PE are nonspecific and insensitive
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Diagnostic Testing
- CXRs
Chest radiograph findings in patient with pulmonary embolism
Result Cardiomegaly Normal study Atelectasis Elevated Hemidiaphragm Pulmonary Artery Enlargement Pleural Effusion Parenchymal Pulmonary Infiltrate Percent 27% 24% 23% 20% 19% 18% 17%
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Westermark's sign
A dilation of the pulmonary vessels proximal to the embolism along with collapse of distal vessels, sometimes with a sharp cutoff.
Hamptons 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 Eponyms
- Hamptons Hump, Westermarks Sign
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Diagnostic Testing
EKGs
EKG
Most Common Findings:
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 Testing
- Pulse Oximetry
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
- ABGs
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 Testing
Echocardiography
Consider in every patient with a documented pulmonary embolism
Ancillary Test
WBC
Poor sensitivity and nonspecific
Hgb/Hct
PTE does not alter count but if extreme, consider polycythemia, a known risk factor
ESR
Dont get one, terrible test in regard to any predictive value
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D-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 Malignancy Advanced age > 80 years Hemmorrhage AMI Hepatic Impairment Post-partum < 1 week Surgery within 1 week Sepsis CVA Collagen Vascular Diseases
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Diagnostic Testing
D-dimer
Qualitative
Quantitative
Enzyme linked immunosorbent asssay Dimertest Positive assay is > 500ng/ml VIDAS D-dimer, 2nd generation ELISA test
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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
V/Q Scan
Technique
Interpretation
Normal Low probability/nondiagnostic (most common) High Probability
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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 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:
Goals:
Prevent death from a current embolic event Reduce the likelihood of recurrent embolic events Minimize the long-term morbidity of the event
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Treatment
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
Treatment
Anticoagulants
Heparin
Treatment
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
Treatment
Documented PE with:
Persistent hypotension Syncope with persistent hemodynamic compromise Significant hypoxemia +/- patient with acute right heart strain
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Treatment
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 Algorithm
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Special Circumstances
Conclusion
Summary 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!
Questions????
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2.
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3.
The Classic Triad of patients presenting to the ED with PE includes all of the following except:
Hemoptysis Dyspnea + Homans sign Pleuritic Pain
a) b) c) d)
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4.
What is the most common symptom in a patient with Angio Proven PTE?
Dyspnea Chest Pain, pleuritic Anxiety Cough
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a) b) c) d)
5.
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Answers
1. 2. 3. 4. 5.
D B C A E
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