Pulmonary Embolism

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Introduction

 

 

The Case of...

a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.

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Causes and Risk Factors

thrombus from deep veins in legs or pelvis

Air

amniotic fluid

fat

foreign bodies

parasites

septic emboli

tumour

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Pathophysiology

Once a clot dislodges from site of origin, it travels through the circulation until it becomes trapped in a pulmonary artery. The affected lung segment develops an increased ventilation/perfusion (V/Q) ratio, increasing dead space and leading to inefficient gas exchange.

Pulmonary infarction is rate due to collateral circulation and bronchial arteries.

PE can cause acute cor pulmonale.

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Signs and Symptoms

Pulmonary embolism often presents with acute shortness of breath accompanied by chest pain, hemoptysis, severe hypoxemia, and circulatory collapse due to shock.

Often, however, signs and symptoms are much more subtle, with mildly increased dyspnea on exertion and atypical chest pain the only symptoms.

Physical exam may reveal sounds ranging from isolated crackles to diffuse wheezing. Pleural effusions may be present.

 

PERC rule

 

  • history
  • physical exam

History

sudden onset shortness

recent history of surgery or trauma

signs or symptoms of DVT

immobility

hypercoagulability

medications: oral contraceptives

Physical Exam

 

General appearance: degree of respiratory distress or fever

increased pulmonic component of 2nd heart sound

Assess for DVT.

Identify pleural rubs, wheezes, crackles, or signs of pneumothorax.

Hypotension, tachycardia, tachypnea, fever

 

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Investigations

  • lab investigations
  • diagnostic imaging

Lab Investigations

A D-dimer should be done only if low probability.

 

Arterial blood gases may show acidemia, hypoxemia, and hypercapnia, but even sublte changes such as mild alkalosis may be present (why?) Elevated LDH can result from tissue infarction, but is neither sensitive nor specific.

 

D-dimer is sensitive (95-97%) but not specific (45%). It is useful in people with low pre-test probability.

If there is a high probability, not as useful, except to exclude PE.

Degradation product of cross-linked fibrin

Other factors, such as troponin, can help with prognosis, though not diagnosis

 

 

Thrombophilia workup

FVL

Protein C and Protein S (though do not measure if on warfarin)

antithrombin III

prothrombin gene mutation

APLA, ACl-A, LAC

Diagnostic Imaging

CT or VQ scan should be done if risk is low but D-dimer is high

CT/VQ should be first-line if risk is high

 

 

ECG is abnormal in 70%.

  • sinus tachycardia and arrhythmia/flutter
  • RAD, RVH
  • most specific sign is S1Q3T3 - S in I, Q and inverted T in III

 

Chest X-ray

Chest X-ray can often show pulmonary infarction, though most cases are normal and its main role is to exclude other causes. A wedge-shaped area is strongly suggestive. Chest X ray is often normal but can show atelectasis, isolated infiltrates, or small pleural effusion.

Abrupt cutoff of pulmonary vessels or enlarged central pulmonary arteries may also be present (Westermark's sign).

 

CT

CT angiography (spiral CT) is useful for PE. Use contrast material, excuding those at risk of nephrotoxicity. Sensitive for main, lobar, and segmental arteries, but not subsegmental. Can also help identifty differential diagnoses. More specific than VQ scan.

 

 

Ventilation-Perfusion Scan

V/Q scan. is a nuclear test. More sensitive, but less specific than spiral CT. Nucleotide injection peripherally and assess for areas of low perfusion. Step 2: Radionuclides inhaled, and lung fields assessed.

Tests reveals

  • low
  • intermediate
  • high probability (~80% of PE)

If underlying lung disease, like COPD, makes tests less diagnostic.

Negative predictive value of 91%.

With low probability V/Q and low clinical probability: 4% cahnce of PE

 

CT angiography

CT pulmonary angiography (CT PA): dye injected just as they enter the CT. If patients have poor kidney function, or are allergic to dye, will not work.

Capable of evaluating to 5th order pulmonary arterial branch, to 2-3 mm or even smaller.

Findings include:

  • central intra-arterial filling defect
  • complete occlusion of pulmonary artery

With a high-quality CTPA, a negative result will safely rule out PE.

However, it is invasive, requires contrast, and is not readily available.

 

U/S

Doppler compression ultrasound of legs is the most effective bedside test.

 

 

Echocardiography

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Differential Diagnosis

Differential diagnosis of PE includes:

Simplified Wells Clincial Model

 

 

V/Q scan compares lung ventilation with lung perfusion using radiolabeled tracer gas. Spiral CT and angiography can be used with certainty though attendant risks.

Doppler ultrasounds of the legs can be used to identify sites of thrombosis.

 

PERC rule (PE rule-out criteria)

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Treatments

 

PE is treated with supportive measures to sustain life. Mechanical removal of clots is difficult and dangerous, and medical treatments are used to dissolve existing clots and prevent future events.

 

Acute Management

Unfractionated/low-molecular-weight heparin is started acutely for a minimum of 5 days. Initiate oral anticagulants such as warfarin on day 1. Heparin can be stopped once INR >2.0 for 24h. Patients can be treated as outpatients.

 

Thrombolytics can be used to existing clots. Indications:

 

Long-Term Treatment

Coumadin/warfarin s

Reasonable to do a thorough history and physical exam to examine for risk factors

 

Inferior vena cava filters

There are risks and benefits to these.

 

Prevention

Ambulation

Compression stockings

heparin and warfarin

 

 

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Consequences and Course

 

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The Patient

 

 

 

 

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Health Care Team

 

 

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Community Involvement

 

 

 

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Resources and References

 

 

 

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Topic Development

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