Pulmonary Embolism

 

Causes and Risk Factors

PE is a complication principally affecting people with underlying disorders, such as cardiovascular disease or cancer. Immobilized patients are at much higher risk. PE is the sole or a major contributing factor in 10% of acute adult deaths in hospitals.

 

Over 95% of pulmonary emboli originate from deep vein thromboses, and its risk factors accordingly mirror those of thrombosis. These include:

 

Massive PE: main pulmonary arteries. Can have hypotension, presyncope, or syncope, with SOB.

 

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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.

 

  • history
  • physical exam
  • ECG
  • diagnostic imaging
  • lab investigations
  • differential diagnosis

History

sudden onset

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

Assess for DVT.

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

Hypotension, tachycardia, tachypnea, fever

 

ECG

S1Q3T3

Diagnostic Imaging

 

Chest X-ray can often show pulmonary infarction. Most cases are normal. 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.

 

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.

 

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.

 

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

 

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

 

Echocardiography

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

 

Lab Investigations

 

Arterial blood gases

 

D-dimer is sensitive but not specific. 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

 

 

Thrombophilia workup

FVL

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

antithrombin III

prothrombin gene mutation

APLA, ACl-A, LAC

 

Differential Diagnosis

Differential diagnosis of PE includes:

 

 

 

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Diagnosis

 

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.

 

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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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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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 heparin or 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

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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References