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Approximately 600,000 patients per year are diagnosed with pulmonary embolism (PE).1 By far, most pulmonary emboli are thromboembolic in nature, although other causes, such as air, fat, amniotic fluid, tumor, and septic emboli, do occur.

The risk factors for thromboembolic PE mirror those for deep venous thrombosis (DVT) and include recent surgery, malignancy, confinement to a hospital or nursing home, confinement to a bed (“bed rest”), immobility, oral contraceptives or hormone replacement therapy, and paresis of an extremity.2 The mortality rate is high. In a large observational study of 2,388 hospitalized patients that evaluated cause of death, it was found that approximately 10% of all deaths were due to PE.3 With prompt diagnosis and treatment, mortality can be significantly impacted and the incidence of long-term complications such as chronic thromboembolic pulmonary hypertension and cor pulmonale can be reduced.

The clinical diagnosis of PE can be very challenging. The classic findings—or triad—of dyspnea, pleuritic chest pain, and tachycardia can be found in up to 95% of patients with confirmed PE. However, they are very nonspecific and could be indicative of any number of disorders. Furthermore, the first two, being symptoms, are difficult or impossible to evaluate in patients who are intubated and/or sedated, such as many ICU patients. Still, PE should be considered in any patient with any of these signs or symptoms.

Dyspnea is the most common symptom related to PE and is caused by a ventilation–perfusion (V/Q) mismatch. Chest pain is the second most common symptom, although up to one third of patients with PE deny chest pain or complain only of a vague chest discomfort. Hemoptysis secondary to PE is due to pulmonary infarction and is an uncommon and late finding. When present, it should significantly raise clinical suspicion. Fever is also rare but, if present, is usually “low grade” (<102°F), and appears more commonly when hemoptysis is present. Tachycardia is due to the cardiopulmonary stress created by the PE, but lacks sensitivity. Approximately 50% of all patients ultimately diagnosed with PE never demonstrated a persistent heart rate above 100 beats/min.3 Furthermore, patients on chronic β-blocker therapy will likely not develop a tachycardic response. Other clinical findings include diaphoresis, anxiety, cough, rales, murmur, syncope, cyanosis, and altered mental status. Cardiac arrest occurs in approximately 2% of patients suffering an acute PE, with pulseless electrical activity the initial rhythm in 60% of patients and asystole in 33%.4

Patients presenting with any of the above clinical findings along with unilateral arm or leg swelling have a significant risk for both DVT and PE; yet the finding of a single swollen limb is often overlooked. In the previously mentioned study, of the 2,388 autopsies performed, 83% of the patients with confirmed PE had evidence of DVT in their lower extremities but only 19% of them had reported symptoms of DVT prior to death.2

The clinical presentation of PE can be very nonspecific and the consequences of misdiagnosis can be dire. Therefore, clinicians should have a low threshold for ordering diagnostic testing. Because the diagnosis of PE is often elusive, a large body of current research focuses on ...

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