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Commentary |
1 Both authors: Department of Radiology, University of Washington Medical Center, Seattle, Box 357115, 1959 NE Pacific St., Seattle, WA 98195.
Received March 14, 2008; accepted after revision March 17, 2008.
Address correspondence to S. N. J. Pipavath
(snjp{at}u.washington.edu).
Keywords: acute pulmonary thromboembolism • CT pulmonary angiography • Hampton's hump
Acute pulmonary thrombo embolism is the third most common cause of cardiovascular death. Accurate diagnosis of this condition is essential to minimize mortality and treatment-related morbidity. Over many decades, new diagnostic methods and treatments have been explored. The classic articles by Hampton and Castleman [1] in 1940 and by Goodman et al. [2] in 1995 nicely bracket the advances in imaging of pulmonary thromboembolism over more than five decades.
The celebrated article by Hampton and Castleman [1] in 1940 described the radiographic appearance of pulmonary embolism and pulmonary infarction. Hampton's hump, the peripheral, wedge-shaped consolidation with its base against the pleural surface and with a rounded central margin, is now a well-known sign of pulmonary infarction. This article has enjoyed widespread popularity, reflecting the excellent radiologic–pathologic correlation from postmortem examinations. The de scriptions were subsequently confirmed by other imaging techniques and are still valid today. Other signs of infarction besides Hampton's hump include peripheral consolidation without air bronchogram [3]; the melting sign of resolving infarct [4]; aseptic cavitation [5]; and, recently, consolidation containing air lucencies (distinct from air bronchograms) [6]. Infarction caused by acute pulmonary thromboembolism is less common than might be expected because the bronchial artery can maintain perfusion to the lung when pulmonary arterial perfusion is blocked by pulmonary thromboembolism [7–9].
Diagnosing acute pulmonary thromboembolism is more important than diagnosing pulmonary infarction in a patient with acute chest symptoms. Although a chest radiograph is almost always obtained, the radiographic features of acute pulmonary thromboembolism are insensitive and nonspecific. The Westermark sign—oligemia of the lung beyond the occluded vessel—did not live up to early enthusiasm [10]. Similarly, elevation of the ipsilateral hemidiaphragm, enlargement of the proximal pulmonary artery, atelectasis, and pleural effusion are all nonspecific. The most common radiographic findings in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study were atelectasis and patchy pulmonary opacity [11]. However, the prevalence of these findings in patients who did not have pulmonary thromboembolism was not significantly different.
Radionuclide imaging (scintigraphy) became the mainstay of noninvasive imaging but had limitations. A normal ventilation–perfusion scan reliably excluded acute pulmonary thromboembolism, and a high-prob ability scan made this diagnosis with reasonable accuracy. However, a substantial proportion of ventilation–perfusion studies were nondiagnostic [12].
Over the years, the introduction of newer, safer, and quicker investigations has led to a progressive decrease in mortality from acute pulmonary thromboembolism [13]. In the early 1990s, the value of CT in the diagnosis of central pulmonary thromboembolism was documented by Remy-Jardin et al. [14]. CT was 90% sensitive and 96% specific for detection of central and lobar pulmonary thromboembolism, but segmental and subsegmental pulmonary thromboembolism was not assessed.
In 1995, Goodman et al. [2] significantly advanced the field by comparing helical CT angiography (CTA) with pulmonary angiography in patients with unresolved suspicion for pulmonary thromboembolism and addressing the issue of segmental and subsegmental pulmonary thromboembolism. They reported 86% sensitivity, 92% specificity, and a likelihood ratio of 10.7 for CTA in the detection of pulmonary thromboembolism in the central pulmonary arteries (including segmental branches). When the sub segmental branches were included, specificity remained high (89%), but sensitivity dropped to 63% and the likelihood ratio to 5.7. Subsequent studies showed higher sensitivity and better interobserver agreement for CTA than for scintigraphy [15].
In 1996, CTA was still poor in detecting subsegmental pulmonary thromboembolism but was nonetheless considered valuable because of the limited clinical significance of isolated subsegmental emboli [16]. Occurrence of an isolated subsegmental pul monary thromboembolism was con sidered a risk for future acute pulmonary thromboembolism. In a study of patients with isolated subsegmental pulmonary thromboembolism, those who did not receive anticoagulation therapy had no evidence of recurrent pulmonary thromboembolism at 3-month follow-up; most patients with inconclusive findings on CTA were not given anticoagulants but did not suffer adverse outcomes [17].
The difficulty in diagnosing subsegmental pulmonary thromboembolism kept CTA from replacing conventional angiography as the reference standard until the introduction of MDCT, which has better ability to detect subsegmental pulmonary thromboembolism. In 2005, a meta-analysis comparing single-detector CT with 4-MDCT concluded that with newer scanners, the sensitivity and specificity of CTA had improved [18]. The introduction of 64-MDCT led to further reduction in the rate of nondiagnostic studies, improved visualization of pulmonary artery branches to the sixth order, and an increased rate of detection of segmental and subsegmental pulmonary thromboembolism [19, 20].
In 2006, the multicenter PIOPED II study found that the sensitivity of CTA was 83% and the specificity was 96% in diagnosis of acute pulmonary thromboembolism [21]. Positive predictive values were 96% with a concordantly high or low probability on clinical assessment, 92% with an intermediate probability on clinical assessment, and nondiagnostic if clinical probability was discordant. The sensitivity of CTA and CT venography combined (CTA–CTV) was 90% and specificity was 95%. CTA–CTV was also nondiagnostic when clinical probability was discordant.
Enlargement of the right ventricle, straightening of the interventricular septum, and reflux of contrast material into the hepatic inferior vena cava (IVC) or hepatic veins at CT may indicate right ventricular dysfunction, an independent predictor of mortality within 30 days [22, 23]. In the future, CT may obviate the use of transthoracic echocardiography to assess right ventricular function in acute pulmonary thromboembolism.
CT has now mostly replaced scintigraphy as the noninvasive test of choice for suspected pulmonary thromboembolism [24]. Often when pulmonary thromboembolism is not found, CT provides a different specific diagnosis, such as pneumonia or cancer. Thus, CT often provides a complete evaluation when a patient presents with acute chest symptoms.
Enthusiasm for CTA as the mainstay of imaging for suspected pulmonary thromboembolism must be tempered by consideration of radiation dose. Increases in cancer rates have been projected on the basis of increasing exposure of patients to medical x-rays [25]. Thus, it is important that clinicians devise diagnostic algorithms that balance effectiveness against radiation risk. For the future, CT protocols that decrease dose while maintaining image quality [26] and advances in MR angiography [27] warrant attention.
The imaging of acute pulmonary thromboembolism has come a long way. Hampton and Castleman [1] in 1940 and Goodman et al. [2] in 1995 have provided important milestones on this journey.
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S. N. J. Pipavath and J. D. Godwin Reply Am. J. Roentgenol., June 1, 2009; 192(6): W343 - W343. [Full Text] [PDF]
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