Acute Pulmonary Embolism

Etiology

Pulmonary embolism (PE) refers to blood clot(s) within the pulmonary arterial system, usually caused by migration of deep vein thrombosis (DVT) from the lower extremities. Rarely, emboli are from other sources, such as the iliac veins, renal veins, inferior vena cava, right heart chambers, or upper extremity veins. More recently, there are speculations of PE developing de novo. Risk factors for PE are the same as those for DVT, including immobilization, trauma, surgery, active malignancy, prior history of venous thromboembolism (VTE), pregnancy, use of oral contraceptives, indwelling catheters, and hereditary hypercoagulable states, such as deficiency of protein C or S.

Prevalence and Epidemiology

The reported incidence for PE ranges from 29 to 78 per 100,000 person-years. The incidence rates increase with age. An increase in the incidence rate from 2001 to 2009 has been observed, thought to reflect, at least in part, increased use of multidetector computed tomography (MDCT) and improved image resolution. In a recent study, 54% of all PE in oncologic patients and 19% of all PE in non-oncologic patients are diagnosed incidentally on CT performed for purposes other than to look for PE, such as for cancer restaging or evaluation of pleural effusions or pneumonia. The recurrence rate of PE is 15 to 29 per 100,000 person-years.

PE is the third most common cause of cardiovascular death after myocardial ischemia and stroke, with an untreated mortality of 30%. The mortality rate is lower with treatment, although it is estimated that in one-quarter of patients experiencing PE, the initial clinical presentation is sudden death. Predictors of poor survival after PE include syncope and systemic hypotension.

Clinical Presentation

The clinical manifestations of acute PE depend on several factors that individually or in combination influence the effect of vascular occlusion on the lung parenchyma: the presence or absence of associated cardiopulmonary disease; the size, number, and location of emboli; the presence of multiple embolic episodes and the time interval between them; and the rate of thrombus organization and lysis, whether spontaneously or with therapy. The most common symptoms are dyspnea, tachypnea, and pleuritic chest pain. A sudden onset of these symptoms in the absence of underlying respiratory disease is highly suggestive of acute PE. On the contrary, the clinical diagnosis of acute PE is difficult in patients with chronic respiratory diseases, and this situation is exemplified by patients with chronic obstructive pulmonary disease (COPD), in whom acute PE may mimic COPD exacerbation.

The clinical probability assessment, an important component of strategies for optimal diagnosis of acute PE based on noninvasive tests, is therefore much more helpful in patients devoid of underlying cardiopulmonary disease than in patients with COPD. Various clinical probability assessment scores have been validated—the Wells score, the Geneva score (recently revised), and the Pisa score. The use of a combination of clinical probability scores and serum D-dimer test, which has a very high negative predictive value for VTE, has been shown to be effective in reducing the use and improving the positive yield of computed tomography pulmonary angiography (CTPA) and is recommended by the American College of Physicians' Best Practice Advice in the evaluation of patients with suspected acute PE. Both the American College of Radiology Appropriateness Criteria and American Thoracic Society and American College of Chest Physicians Choosing Wisely campaign stated that CTPA should not be performed in patients with a low clinical probability and negative result of a highly sensitive D-dimer assay.

Pathology

The potential consequences of acute PE are hemorrhage or, less commonly, infarction within the lung parenchyma; acute pulmonary hypertension; and right ventricular dysfunction. The last is sometimes responsible for left ventricular failure because of impairment of left ventricular preload and decreased coronary arterial perfusion.

In most cases PEs are degraded through the effects of fibrinolysis. Less commonly, they may break down into small fragments that embolize to the peripheral arterial branches. Delayed recanalization can also be seen with creation of multiple small vascular channels within the endoluminal clot.

The effect of thromboemboli in individual patients is influenced by the degree of obstruction of the pulmonary circulation, the presence and extent of underlying lung abnormalities, and the status of the patient's fibrinolytic system.

Manifestations of the Disease

Radiography

The chest radiograph has an important role in excluding other diagnoses that can mimic the clinical picture of acute PE, such as a pneumothorax or pneumonia. The chest radiograph, however, is both insensitive and nonspecific in the diagnosis of acute PE.

The radiographic manifestations of acute PE include a spectrum of abnormalities ranging from a normal chest radiograph to a series of focal changes reflecting the pleural or parenchymal consequences of acute pulmonary vascular obstruction.

Radiographic Features Observed in the Absence of Infarction or Hemorrhage

Peripheral oligemia caused by obstruction of the pulmonary artery or vasoconstriction of distal hypoxic lung result in peripheral hyperlucency, referred to as the Westermark sign ( Fig. 50.1 ).

Dilatation of a major pulmonary artery (Fleischner sign; see Fig. 50.1 ) is identified more easily in the right hilum and can be seen in conjunction with a truncated appearance of the enlarged vessel, reflecting the arterial amputation. These findings are seen only in patients with massive acute PE.

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