Epidemiology

The annual incidence of diagnosed pulmonary embolism (PE) is approximately 1.5 new cases per 1000 persons and is relatively similar among western populations.¹ Dyspnea and chest discomfort are the most typical symptoms of PE, and these chief complaints are responsible for between 9 and 10 million annual patient visits to U.S. emergency departments (EDs).² Physicians evaluate large numbers of patients for PE because the symptoms can be vague and severity may range from asymptomatic to shock and subsequent cardiac arrest.³

The widespread availability of D-dimer and computed tomography (CT) testing for PE, as well as medical-legal concerns of missing the diagnosis, continues to result in dramatic increases in testing relative to the last decade. In some settings it is not uncommon for 1% to 3% of all adult ED patients to undergo some testing for PE. Physicians have become aware that patients without what was previously thought to be “classic” risk factors (hypercoagulability, trauma, and immobility) may still have PE. In addition, the aging demographics of the U.S. population will continue to drive the need to evaluate for PE in the ED because increased age is a strong independent risk factor for PE. To deal with these challenges, the practicing physician has three aims:

Pathophysiology

PE is part of the continuum of venous thromboembolism (VTE), which most often starts with deep vein thrombosis (DVT) in the leg. Patients with DVT often have concurrent PE when evaluated with imaging tests, and many patients with PE have concurrent DVT. Treatment is similar for both. Risk factors for VTE include the triad described by Virchow: injury, venous stasis, and hypercoagulability. These conditions are most commonly thought of as occurring at the level of the venous endothelium, but it is helpful to also think of them as occurring at the level of the patient. For instance, overall injury to the patient (trauma), stasis of the patient (immobility), and hypercoagulability of the patient (malignancy and known thrombophilic conditions) all result in elevated risk. Table 70.1 lists several risk factors for VTE. Understanding risk factors is critical to recognizing the potential for PE to exist.

Table 70.1 Risk Factors for Pulmonary Embolism

An embolus in the pulmonary vasculature may result in a large bilateral central clot with severe obstruction of flow (so-called saddle embolism), a medium clot in the lobar or segmental branches, or a small clot in the peripheral vasculature. Embolism involving the pulmonary vasculature activates the process of local inflammation and thereby leads to vasoconstriction and some degree of pulmonary hypertension with resultant symptoms of dyspnea and possibly chest pain.

Presenting Signs and Symptoms

Dyspnea and chest pain are the most common findings in patients with PE. Brief, resolved chest pain in the absence of any shortness of breath or any respiratory signs or symptoms is not a typical manifestation. Other symptoms that can be associated with PE include syncope, cough, flank pain, abdominal pain, and even fever (Box 70.1). The severity of symptoms in a given patient is a function of two factors: the baseline cardiopulmonary status of the patient and the size of the clot⁴ (Fig. 70.1). This is why large clots are occasionally tolerated fairly well in young patients with no cardiopulmonary disease whereas a much smaller clot burden may result in hypotension, hypoxemia, and deterioration in patients with preexisting cardiopulmonary disease. Older patients often have a worse clinical course and outcome with PE, largely as a consequence of having worse cardiopulmonary status at baseline rather than simply being elderly.

Fig. 70.1 The degree of severity of symptoms in a given patient is a function of two factors: (1) the baseline cardiopulmonary status of the patient and (2) the size of the clot. PE, pulmonary embolism; R, right.

(Adapted from Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism. Chest 2002;121:877-905.)

Shock may be a primary sign of PE. Patients may not be able to provide a history of symptoms or risk factors for PE and may not be sufficiently stable to allow imaging outside the ED, yet consideration of empiric treatment of PE with anticoagulation may be warranted. A rapid bedside evaluation to search for clues to non-PE diagnoses can be done promptly and is described in Figure 70.2. A potential pitfall is to attribute shock to a primary cardiac etiology despite an electrocardiogram (ECG) with no significant ischemic changes and no significant dysrhythmia and a chest radiograph with no evidence of pulmonary vascular congestion or cardiomegaly. If patients can be stabilized, imaging with CT should be done. If not, emergency bedside echocardiography to look for signs of massive PE (right ventricular dilation and hypokinesis, septal shift to the left, tricuspid regurgitation) should be done as an alternative means of heightening certainty of the diagnosis of PE.

Fig. 70.2 Stepwise approach to undifferentiated shock with consideration of pulmonary embolism (PE) as a possible cause.

CXR, Chest x-ray; ECG, electrocardiogram; GI, gastrointestinal.

The other end of the spectrum is the diagnosis of PE in patients with relatively mild symptoms. Despite the fact that patients may have PE with normal oxygen saturation, no known risk factors, and no pulmonary symptoms, this combination is uncommon. Strict attention to details such as oxygen saturation after walking, physician-obtained respiratory rate, examination of the legs, and serial assessment may help either reassure physicians that patients have such a low probability of PE that testing is unwarranted or provide evidence to justify an evaluation for PE.

Differential Diagnosis and Medical Decision Making

Because of the vague yet common nature of dyspnea and chest pain, the differential diagnosis is broad. However, a targeted diagnostic approach should be used rather than a “chest pain work-up” in an attempt to test for every diagnosis possible without regard to the pretest probability or negative consequences of overtesting. This is particularly important for PE because tests are not 100% sensitive or specific and the consequences of a false-positive diagnosis may include 6 months of oral anticoagulation with high direct and indirect costs to the patient and society. This is especially true in young patients with limitations in activity, as well as in older patients at risk for falls, medication interaction, and bleeding. Table 70.2 lists potential alternative diagnoses in ED patients evaluated for PE and clues to assist in rapid decision making. It is not surprising that many of these conditions are common entities such as pneumonia, bronchitis, asthma, musculoskeletal pain, gastroesophageal reflux or spasm, and anxiety or panic attack. Many of the most threatening alternative diagnoses can initially be evaluated with a chest radiograph, an ECG, bedside cardiac ultrasound, and cardiac enzyme testing during the first hour in the ED.

Table 70.2 Other Diagnoses That Should Be Considered Along with Pulmonary Embolism

It is most helpful to think of PE as a continuum of cardiopulmonary stress as shown in Figure 70.1. Even in normotensive patients, in-hospital or 30-day mortality in those with diagnosed PE is approximately 8% to 13%.^5–9 This mortality in PE patients without shock is greater than that for acute myocardial infarction.¹⁰ When early signs of right heart dysfunction occur, mortality begins to curve upward. This is followed by compensated shock, which may initially respond to intravenous fluid. Later, as left-sided filling is decreased because of septal shift into the left ventricle, as well as decreased filling of the left atrium, overt shock is present and mortality is in excess of 30%. If untreated, cardiac arrest ensues, with pulseless electrical activity being the most likely first rhythm.^11,12

Diagnostic Testing

Pretest probability is the probability that the physician believes to be present before any test results are obtained. It is typically calculated by either a scoring system or the physician’s own “gestalt” estimation. Despite the fact that debate exists over the relative accuracy of using gestalt versus a structured means of assessing pretest probability, the American College of Emergency Physicians practice guideline of 2003 recommended pretest probability assessment in patients being evaluated for PE.¹³

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