A pulmonary embolism results from the migration of venous thrombi from the systemic veins to pulmonary arterial system, resulting in varying degrees of obstruction of pulmonary arterial blood flow.
The incidence of pulmonary emboli in the United States exceeds 500,000 per year, with a mortality approaching 10%. If not diagnosed or if improperly treated, the mortality rate can reach 30%.
Common Sources:
Up to 90% of pulmonary emboli originate from the deep venous system of the legs. The upper extremities can also be a source of venous thrombi. Usually related to trauma, congenital fibromuscular bands, or the use of central venous catheters, 12% of all upper extremity thrombi result in pulmonary emboli. In addition, blood clot formation in the pelvic veins may cause either septic or bland pulmonary emboli, especially in the setting of complicated obstetric procedures or gynecologic surgery.
Other causes of pulmonary arterial obstructive emboli include air introduced during intravenous injections, hemodialysis, or the placement of central venous catheters; amniotic fluid secondary to vigorous uterine contractions; fat as a result of multiple long bone fractures; parasites; tumor cells; or injected foreign material (talc, mercury).
Risk Factors:
Three basic risk factors, known collectively as Virchow’s triad, are associated with thrombus formation and subsequent pulmonary emboli:
Diagnosis:
In the setting of an acute pulmonary embolism, the arterial blood gas measurement classically reveals a low PCO2, low PO2, and a widened alveolar-arterial oxygen gradient. However, many other disorders cause similar abnormal arterial blood gas results and 10% to 15% of patients with proven pulmonary emboli maintain a normal alveolar-arterial oxygen gradient.
The chest radiograph findings of pulmonary emboli are nonspecific. Typically, infiltrates, atelectasis, effusions, or any combination of these are encountered. It is not usual for the chest radiograph to be normal. A peripheral wedge-shaped infiltrate, sometimes referred to as a Hampton’s hump, occurs when the embolism is associated with infarction, and occasionally decreased pulmonary vascular markings are noted (Westermark’s sign), indicative of decreased blood flow to a section of the lung.
The electrocardiogram is helpful in ruling out ischemic heart disease. In patients with pulmonary emboli, the electrocardiogram usually demonstrates sinus tachycardia or is normal. Only in the presence of massive embolization is a right axis deviation and an S1, Q3, T3 pattern seen.
These test results help narrow the differential diagnosis. The chest radiograph findings rule out a pneumothorax, and a true bacterial pneumonia is less likely in light of the normal sputum findings. The lack of ischemia on the electrocardiogram makes a primary cardiac abnormality unlikely. With the presentation of shortness of breath, a widened alveolar-arterial oxygen gradient, and chest radiograph findings consistent with an infarction, a pulmonary embolism is now the most likely diagnosis.
CT angiography is indicated and if positive shows filling defects in large- and medium-sized pulmonary arteries. Ventilation/perfusion scans are now reserved for patients who cannot tolerate a dye load due to renal insufficiency or have a known iodine allergy. Measurement of the serum D-dimer, a fibrin degradation product that demonstrates a level below 500 µg/L, excludes the diagnosis of pulmonary embolism. Pulmonary angiography is rarely indicated.
If the CT angiogram is inconclusive and the suspicion still high Doppler venous studies of the lower extremities, if positive, may substantiate the need for anticoagulation.
In the setting of an acute pulmonary embolism, the arterial blood gas measurement classically reveals a low PCO2, low PO2, and a widened alveolar-arterial oxygen gradient. However, many other disorders cause similar abnormal arterial blood gas results and 10% to 15% of patients with proven pulmonary emboli maintain a normal alveolar-arterial oxygen gradient.
The chest radiograph findings of pulmonary emboli are nonspecific. Typically, infiltrates, atelectasis, effusions, or any combination of these are encountered. It is not usual for the chest radiograph to be normal. A peripheral wedge-shaped infiltrate, sometimes referred to as a Hampton’s hump, occurs when the embolism is associated with infarction, and occasionally decreased pulmonary vascular markings are noted (Westermark’s sign), indicative of decreased blood flow to a section of the lung.
The electrocardiogram is helpful in ruling out ischemic heart disease. In patients with pulmonary emboli, the electrocardiogram usually demonstrates sinus tachycardia or is normal. Only in the presence of massive embolization is a right axis deviation and an S1, Q3, T3 pattern seen.
These test results help narrow the differential diagnosis. The chest radiograph findings rule out a pneumothorax, and a true bacterial pneumonia is less likely in light of the normal sputum findings. The lack of ischemia on the electrocardiogram makes a primary cardiac abnormality unlikely. With the presentation of shortness of breath, a widened alveolar-arterial oxygen gradient, and chest radiograph findings consistent with an infarction, a pulmonary embolism is now the most likely diagnosis.
CT angiography is indicated and if positive shows filling defects in large- and medium-sized pulmonary arteries. Ventilation/perfusion scans are now reserved for patients who cannot tolerate a dye load due to renal insufficiency or have a known iodine allergy. Measurement of the serum D-dimer, a fibrin degradation product that demonstrates a level below 500 µg/L, excludes the diagnosis of pulmonary embolism. Pulmonary angiography is rarely indicated.
If the CT angiogram is inconclusive and the suspicion still high Doppler venous studies of the lower extremities, if positive, may substantiate the need for anticoagulation.
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