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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.
a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.
thrombus
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other causes
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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.
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.
Symptoms of the PE itself include:
Risk factors for DVT include:
signs or symptoms of DVT
immobility
hypercoagulability
medications: oral contraceptives
Vital signs
Respiratory exam findings can vary:
Cardiovascular exam
evidence of DVT may be present:
Simplified Wells Clincial Model
item
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score
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low probability: 0-2; moderate 2-6, high >6
PERC rule (PE rule-out criteria)
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
FVL
Protein C and Protein S (though do not measure if on warfarin)
antithrombin III
prothrombin gene mutation
APLA, ACl-A, LAC
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:
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:
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
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.
Differential diagnosis of PE includes:
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.
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:
Coumadin/warfarin should be provided for at least 6 months, and perhaps longer, if history and physical exam suggest ongoing risk.
There are risks and benefits to these; they are only used if there is a contraindication to anticoagulation.
Ambulation
Compression stockings
heparin and warfarin
PE can be life-threatening.
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