Chapter 113

Pulmonary Embolism

Nena Tucker

Definition and Epidemiology

Pulmonary embolism (PE) is the blockage of one or more of the pulmonary arteries or their branches by a thrombus or other embolic material that dislodges and enters the pulmonary circulation.¹^,² Emboli may be caused by thrombi, fat, or other foreign material such as parasites. The most common cause of PE is a thrombus or blood clot that has formed in the pelvis or legs.¹ The focus of this chapter is pulmonary emboli caused by thrombi.

The true incidence of PE is unknown; more than half of all PEs go undiagnosed.³ Estimates of PE incidence range from 300,000 to 600,000 people affected each year. It is the third most common cause of cardiovascular death, with approximately 100,000 to 200,000 deaths in the United States each year.⁴ Of patients with acute PE, 8% to 10% die within the first hour.¹ Many occurrences go undiagnosed and are not identified until autopsy. It is estimated that as many as one in three cases are not identified.² A review of clinical studies from 1939 to 2000 found the prevalence of PE diagnosed at the time of autopsy to range from 9% to 55%.³

Pathophysiology

PE is not a disease, but a complication of an underlying issue. Most frequently, the PE is the result of a thrombus that has entered pulmonary circulation.¹ Several factors contribute to susceptibility to thrombus formation, including stasis, vascular damage, and hypercoagulability.³ Deep venous thrombosis (DVT) poses the greatest risk for PE; the thrombus develops most commonly in the lower extremities and pelvis.¹ The deep vein thrombus dislodges from the originating vessel, travels through the venous system, enters the lung via the right ventricle, and partially or completely occludes one or more of the pulmonary arteries or its branches or one or more of the pulmonary arteries or its branches.¹ The resulting hemodynamic response is dependent on the size of the embolism, cardiopulmonary reserve, and other neurohumoral effects.² It is estimated that 10% of emboli will cause pulmonary infarction.¹

Immediate emergency department referral or physician consultation is indicated for all patients with suspected PE. A through, timely evaluation is warranted; the patient’s condition may deteriorate rapidly, and long-term consequences may develop.

Clinical Presentation

The clinical presentation is nonspecific and varies greatly, making the diagnosis of PE difficult. A key piece of the clinical picture is the patient’s history. Those with a recent history of surgery, trauma, long bone fracture, travel, period of immobility, malignancy, stroke, paralysis, heart failure, smoking, central venous instrumentation, pregnancy or postpartum status, estrogen therapy, or a history of previous PE are at risk for PE.² The clinical assessment, inclusive of history, is not diagnostic but instead should prompt the provider to include PE in the differential diagnosis.

The classic presentation includes dyspnea, tachypnea, pleuritic chest pain, and calf or thigh pain and swelling.³ Studies suggest that tachypnea is the most sensitive clinical sign.² Other symptoms include hemoptysis, orthopnea, tachycardia, jugular venous distention, and abnormal lung sounds.³ Complaints of calf or thigh leg pain and swelling are not indicative of PE, but suggestive of DVT. Atypical presentations may include complaints of nonspecific malaise, weakness, dizziness, syncope, and extremity discomfort.²

Physical Examination

The physical findings vary greatly and reflect the nature of the PE.² The occult PE may be fatal because it is not routinely suspected or diagnosed; however, it may be benign because healthy lung tissue can filter out small emboli. An embolus of any size can produce cardiopulmonary signs depending on the effected area, including acute respiratory distress, tachycardia, hypotension, abnormal heart sounds, jugular vein distention, hypoxemia, tachypnea, cyanosis, and abnormal lung sounds.¹^,⁵ A thorough, accurate physical examination is important because abnormal physical examination findings are subsequently used as part of clinical prediction tools.¹

Diagnostics

An appropriate diagnostic workup varies and is patient and symptom specific. The combination of patient presentation, history, and physical examination findings should be used to guide diagnostic testing. A PE clinical prediction model can also be used to determine the risk of PE and suggest diagnostic tests. The Wells score, revised Geneva score, and pulmonary embolism rule-out criteria (PERC) score are three clinical decision rules that have been validated and can be used to determine the need for imaging.³

Laboratory tests are nonspecific to PE and are used primarily to detect the cardiopulmonary effects of PE as well as to exclude other differential diagnoses.¹^,²^,⁵ Arterial blood gases (ABGs) are used to evaluate oxygenation and the need for supplemental oxygenation or advanced ventilation.³ Elevated troponin and brain natriuretic peptide (BNP) levels result in microinfarction and myocardial stretch. They are predictive of PE complications and mortality.⁶ D-dimer is the product of the degradation of cross-linked fibrin.⁷ This is an important measurement in the patient whose PE is caused by a thrombus, wherein the concentration increases in the presence of acute DVT.⁵ Serum D-dimer assays have good negative predictive value and sensitivity but have poor positive predictive value and specificity, making them a useful tool for excluding but not confirming the diagnosis of PE.⁸ D-dimer is not useful in the postoperative, trauma, hospitalized, or critically ill patient because of the coagulation and fibrolysis that occur as a result of the disease process.⁴

The electrocardiogram (ECG) is an integral part of PE evaluation. A ECG cannot diagnose PE but may demonstrate myocardial infarction, atrial fibrillation, and right ventricular dysfunction.³ It is important to remember the ECG is neither sensitive nor specific and does not identify the cause of the ECG abnormality.

Abnormalities seen on the chest x-ray film may include pleural effusion, diaphragmatic elevation, Hampton hump, Westermark sign, or atelectasis but are not specific to PE.²^,³ The most widely used imaging modality for PE diagnosis has been the ventilation/perfusion () scan.⁵^,⁶ A scan measures both the ability of air to enter the lungs and the perfusion to the lungs. A defect in perfusion coupled with abnormal ventilation can suggest a low, intermediate, or high probability of PE. CT angiography has largely replaced the scan and is the gold standard for PE diagnosis because of its rapid result and ability to directly visualize PE.⁴ CT angiography is more invasive, expensive, and contraindicated in clinical scenarios in which contrast cannot be used.³ Spiral chest computed tomography (CT) with intravenous (IV) contrast is commonly used because of its availability and noninvasive nature. Owing to the high levels of radiation and contrast that may be involved in PE imaging, clinical decision tools were designed to provide providers with a diagnostic strategy and mitigate patient exposure and risk.