Pulmonary Thromboembolism (PTE)

An Elusive Diagnosis

Jamil A. Alarafi, D.O.

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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

Eugine Robin article

Historical Context

PIOPED (Prospective Investigation of Pulmonary Embolism Diagnosis)

The Electronic Era, 2000 and Beyond

So What Do We Do ???
 Confusing

for Emergency Physician

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:
  

Hypercoagulability Stasis to flow Vessel injury

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


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 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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Who do we work up?

- Pretest 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 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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Chest X-ray Eponyms of PE X

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

Westermarks Sign Hamptons Hump

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Diagnostic Testing
EKGs


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 Testing
- Pulse 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
- ABGs


The ABG/ A-a Gradient myth:

You must do an arterial blood gas and calculate the alveolararterial 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 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 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
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


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 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 Scan


Technique

Interpretation
Normal Low probability/nondiagnostic (most common) High Probability

Simplified approached to the interpretation of results:

High probability Normal Scan Everything else Treat for PE If low pre-test, your done Purse another study (CT, Angio)

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Spiral (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 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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Dr. Batizy explaining the CT results

Treatment:

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

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

Few absolute contraindications

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Treatment


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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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

Target INR is 2.5 3.0

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Treatment


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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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


Pre-test probability  D-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 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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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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1. Which of the following is not a part of virchows triad?

a) b) c) d)

Hypercoagulability Stasis to flow Vessel injury History of previous DVT

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2.

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

a) b) c) d) Platelets High dose steroids Heparin cryoprecipitate

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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.

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

a) b) c) d) e) Right axis deviation RBBB S1-Q3-T3 Tall peaked T-waves in lead II (P pulmonale) Sinus tachycardia

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Answers
1. 2. 3. 4. 5.

D B C A E

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