Pulmonary Embolism

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Introduction

Pulmonary embolism (PE) is an obstruction of the pulmonary vasculature following the lodging of a substance there. This can represent a life-threatening event, whereby oxygenation of blood is reduced. PE is a common and serious cause of chest pain.

 

Most PE result from deep vein thrombosis (DVT) or blot clot in the leg. They normally start in the calf and then travel proximally to involve the popliteal, femoral, and iliac veins. However, there are other causes of PE as well, as described below.

 

 

 

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

  • cancer
  • immobilization
  • surgery
  • previous VTE
  • smoker
  • oral contraception
  • APLA
  • pregnancy

other causes

  • air
  • amniotic fluid
  • fat (from fracture of long bone)
  • foreign bodies
  • parasites
  • septic emboli
  • tumour

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Pathophysiology

Once a clot or other embolus dislodges from its 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 rare 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 dramatic pain and shortness of breath, with clear evidence on physical exam of abnormality. Often, however, signs and symptoms are much more subtle, with mildly increased dyspnea on exertion and atypical chest pain the only symptoms.

 

  • history
  • physical exam
  • clinical decision tools

History

Symptoms of the PE itself include:

  • sudden onset shortness of breath
  • chest pain that may be pleuritic
  • hemoptysis

 

Risk factors for DVT include:

  • stasis: immobilization, obesity, CHF, chronic venous insufficiency
  • endothelial damage: post-operative, trauma
  • hypercoagulability: smoking, oral contraception, cancer, pregnancy, post-partum, nephrotic syndrome, coaglulopathy, family history, prior DVT

signs or symptoms of DVT

immobility

hypercoagulability

medications: oral contraceptives

Physical Exam

Vital signs

  • severe hypoxemia
  • hypotension
  • tachycardia
  • tachypnea
  • fever

Respiratory exam findings can vary:

  • isolated crackles
  • diffuse wheeze
  • pleural rubs
  • pleural effusion
  • pneumothorax
  • respiratory distress

Cardiovascular exam

  • increased pulmonic component of 2nd heart sound

evidence of DVT may be present:

  • leg pain
  • swelling
  • erythema
  • dilated peripheral veins

Clinical Decision Tools

 

Simplified Wells Clincial Model

item

  • previous history of DVT
  • HR >100
  • recent immobility or surgery
  • clinical signs of DVT
  • alternate diagnosis less likely
  • hemoptysis
  • cancer

score

  • 1.5
  • 1.5
  • 1.5
  • 3
  • 3
  • 1
  • 1

low probability: 0-2; moderate 2-6, high >6

 

 

PERC rule (PE rule-out criteria)

  • age <50
  • pulse rate <100 bpm
  • oxygen saturation >94%
  • no hemoptysis
  • no unilateral leg swelling
  • no recent major surgery or trauma
  • etc
  • etc

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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 subtle changes such as mild alkalosis may be present.

 

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

ECG is abnormal in 70%, revealing:

  • sinus tachycardia and arrhythmia/flutter
  • most specific sign is S1Q3T3 - S in I, Q waves and inverted T in III
  • right axis deviation or a right bundle branch block may be present

 

Chest X-ray

Chest X ray is often normal but can show atelectasis, isolated infiltrates, or small pleural effusion.

Westermark's sign: abrupt cutoff of pulmonary vessels or enlarged central pulmonary arteries.

Hampton's hump: wedge-shaped infarction (usually a later sign).

 

 

CT pulmonary angiography (CT PA)

CTPA involves dye that is injected just as the patient enters the CT scanner. It is sensitive for occlusions in the main, lobar, and segmental arteries, but not subsegmental arteries. While it is not as sensitive than VQ scans (described below), it is more specific. CTPA can also be used to evaluate differential diagnoses in situations of chest pain or dyspnea.

 

If patients have poor kidney function, or are allergic to dye, this test is not an option.

Positive findings include:

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

 

 

Ventilation-Perfusion (VQ) Scan

V/Q scan is a nuclear test that compares lung ventilation with lung perfusion using radiolabeled tracer gas. It is 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

 

 

Ultrasound

Doppler compression ultrasound of legs is the most effective bedside test to assess for DVT.

 

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Differential Diagnosis

Differential diagnosis of PE includes:

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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 also be used to existing clots. Indications:

 

Long-Term Treatment

Coumadin/warfarin should be provided for at least 6 months, and perhaps longer, if history and physical exam suggest ongoing risk.

 

 

Inferior vena cava filters

There are risks and benefits to these; they are only used if there is a contraindication to anticoagulation.

 

 

Prevention

Ambulation

Compression stockings

heparin and warfarin

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Consequences and Course

PE can be life-threatening.

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Resources and References

 

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Topic Development

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reviewers:

 

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