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 Table of Contents  
Year : 2020  |  Volume : 4  |  Issue : 1  |  Page : 29-32

Role of Chest X-ray for the Detection of Pulmonary Thromboembolism: A Critical Evaluation

1 Department of Cardiovascular Radiology and Endovascular Interventions, All India Institute of Medical Sciences, New Delhi, India
2 Department of Radiodiagnosis and Imaging, Fortis Escorts Heart Institute, New Delhi, India
3 Formerly Junior Resident at National Heart Institute, Community Centre East of Kailash, New Delhi, India
4 Department of Cardiology, Fortis Escorts Heart Institute, New Delhi, India

Date of Submission23-Aug-2019
Date of Acceptance21-Nov-2019
Date of Web Publication11-Apr-2020

Correspondence Address:
Dr. Poonam Khurana
Fortis Escorts Heart Institute, Okhla Road, New Delhi - 110 025
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jiae.jiae_44_19

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Pulmonary thromboembolism is a common prevalent problem leading to various kinds of morbidities and can be the potential cause of deaths directly or indirectly in approximately onethird of the cases. Early diagnosis accompanied by early treatment has shown to reduce the morbidity. Due to variable clinical presentation and non-specific symptoms, early diagnosis can be challenging at times. Suspecting this entity on plain radiograph can play important role in early detection and use of subsequent image modalities, i.e. CT angiography and/or echocardiography to establish the diagnosis, leading to improved outcomes. This review highlights the role of chest X ray and CT in diagnosis of pulmonary thromboembolism.

Keywords: Chest X-ray, computed tomography scan, echocardiography, pulmonary thromboembolism

How to cite this article:
Khurana R, Khurana P, Kumar P, Shrivastava D, Shrivastava S. Role of Chest X-ray for the Detection of Pulmonary Thromboembolism: A Critical Evaluation. J Indian Acad Echocardiogr Cardiovasc Imaging 2020;4:29-32

How to cite this URL:
Khurana R, Khurana P, Kumar P, Shrivastava D, Shrivastava S. Role of Chest X-ray for the Detection of Pulmonary Thromboembolism: A Critical Evaluation. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2020 [cited 2020 Sep 21];4:29-32. Available from: http://www.jiaecho.org/text.asp?2020/4/1/29/282206

  Introduction Top

Pulmonary thromboembolism (PTE) is a form of venous thromboembolism, which leads to obstruction of a pulmonary artery by a thrombus. PTE is a common prevalent problem as the estimated annual incidence of clinically detected PTE is around 23–69 patients per 100,000/year in various studies.[1],[2]

It can be the potential cause of deaths directly or indirectly in one-third of the cases, in addition to causing various kinds of morbidity. Early diagnosis accompanied by early treatment with anticoagulants has shown to drastically slash down the morbidity. However, early diagnosis is challenging at times as clinical presentation of PTE is variable and often nonspecific.

To suspect PTE on chest radiographs in the hands of experienced radiologist and physicians can play an important role in early detection. Subsequently, other imaging modalities can be employed either to establish or to rule out PTE. Accordingly, the outcome of the morbidity and mortality due to PTE can be improved and can be proved a game changer for this entity.

  Clinical Presentation Top

PTE may be undetected as it may remain clinically silent or the nonspecific clinical signs and symptoms did not arouse suspicion of PTE. Mostly, the patients present with pleuritic chest pain, tachypnea, and dyspnea.[3] Known to be pathognomonic of PTE, the classic triad of sudden chest pain, shortness of breath, and hemoptysis is seen in less number of the cases. Various other symptoms and signs include cough, syncope, tachycardia, fever, and signs of deep venous thrombosis. Some patients may also present with cardiac arrest.

Several risk factors have been attributed which may predispose to the development of PTE, such as increasing age, previous venous thromboembolic disease, instrumentation (e.g., indwelling intravenous catheters), neoplasm, immobilization, surgery, hypercoagulable state, and hormonal treatment including oral contraceptives, and pregnancy.[4] However, in some cases, the underlying cause remains even unknown.

The disease entities PTE and deep vein thrombosis are considered two sides of the same coin. In more than 90% of the cases, the thrombus originates from the deep veins of the legs or pelvis. A part of the thrombus breaks off and is transported by the blood flow through the right side of the heart into the pulmonary arteries. Emboli may lodge either at the bifurcation of branching pulmonary arteries or in the peripheral small pulmonary branches. A few may be situated at the bifurcation of the main pulmonary artery which is referred to as saddle thrombus. During pathogenesis, the thrombus is normally either lysed by the patient's fibrinolytic system or becomes organized with recanalization. The outcome of the sequelae, to which each of these processes occurs, depends to some extent on the patient's fibrinolytic system, the amount of thrombus deposited on the embolus, and the degree of organization of the embolic material itself. In cases of repeated thromboembolism without lysis of the embolic material, arterial hypertension has been observed as an outcome.

  Diagnosis of Pulmonary Embolism Top

As already stated above, the clinical presentation of PTE can be varied and non specific. There are no reliable bedside tests available to diagnose PTE. Chest X-ray, electrocardiogram (ECG), and measurement of arterial pO2 form the baseline investigation.

ECG and measurement of arterial pO2 are not diagnostic for pulmonary embolism (PE) and are more useful in suggesting other causes for the patient's symptoms, e.g. myocardial infarction. A D-dimer blood test has a very high negative predictive value. However, the negative predictive value is not 100%, meaning that a negative test cannot exclude PE. The D-dimer test generally is performed in combination with a clinical probability estimate, usually a clinical prediction rule. Several clinical prediction rules, such as the Wells and Geneva rules, have been developed, of which the original and the simplified Wells rule are the best evaluated and most frequently used. The D-dimer test is nonspecific as there are many causes of activation of the thrombolytic system, such as inflammation, pregnancy, recent operation, neoplastic disease, and increasing age. Consequently, this test is of limited value in hospitalized patients.

  Imaging Findings Top

Plain chest radiography

Chest X-ray may be normal (up to 40% of patients with PTE) or show nonspecific findings, even in extensive PE. The chest X-ray is performed not to diagnose PE but to exclude other causes of the symptoms, such as pneumonia, pleuritis, or pneumothorax. Although they are infrequently present, yet nonspecific, there are several signs related to PE, which can be picked up by experienced radiologists. These findings can serve as pointers to the differential diagnosis of PTE, which can further be probed to establish or rule out PTE [Figure 1] and [Figure 2].
Figure 1: Chest X-ray frontal projection showing haziness in left lower zone, costophrenic angle (white arrow), and in right cardiophrenic angle (white arrowhead)

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Figure 2: (a) Chest X-ray anteroposterior projection showing hazy left base and costophrenic angle, (b) computed tomography pulmonary angiogram showing hypodense filling defect (white arrow) in the left descending pulmonary artery s/o thrombus

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Hampton's hump refers to a sign on plain radiograph

This is a pleural-based, wedge-shaped opacity with the apex of the triangle pointing toward the occluding vessel/hilum. It is typically not seen in the first 24 h after the PE and represents a parenchymal infarction. It may take 3–5 weeks up to months to resolve, and a band-like opacity due to scarring or focal pleural thickening may remain. The opacity may not always be triangular as the infarction may be surrounded by hemorrhage. If the infarcted area becomes secondarily infected, cavitation may occur. The latter may also be caused by septic emboli. These opacities may not only be seen in case of infarction but can also be the result of only edema and hemorrhage. The latter are usually found in the lower lobes, from 12 h to several days after the thromboembolic event, and show relatively rapid resolution (up to 7–10 days).

Westermark sign

It is defined by a hyperlucent area with decreased vascularity due to oligemia of the involved part of the lung. Although this finding is not specific for PE, PE should be strongly suspected, especially if newly found.

“Knuckle” or “sausage” sign

It describes as a dilatation of a central pulmonary artery due to occlusion by the embolus with collapse or constriction of the distal arteries, resulting in an abrupt tapering of these arteries.

Other secondary findings that may be present are plate-like atelectasis (hemorrhagic), pleural effusion, and an elevation of the diaphragm, either due to pleuritic pain or as a result of decreased pulmonary compliance. If PE is severe, the signs of right ventricular failure may be encountered, such as dilatation of the right heart, the superior vena cava, and the azygos vein.

  Computed Tomography Pulmonary Angiography Top

Computed tomography (CT) pulmonary angiography is now considered the preferred method of diagnostic imaging in patients with a clinical risk score indicative of PE because it provides a high-resolution image and is accurate and less invasive compared with pulmonary angiography, which was earlier considered as the “gold standard” test.

  Diagnostic Criteria for Pulmonary Embolism Top

For each lung, the main, lobar, segmental, and subsegmental arteries are examined for PE. Both acute and chronic PE cause intraluminal filling defects that should have a sharp interface with the intravascular contrast material [Figure 3].
Figure 3: Computed tomography pulmonary angiogram. (a) Hypodense filling defects in upper lobar pulmonary artery (white open arrow) and in segmental branches (white arrowhead) suggesting of pulmonary thromboemboli. (b) Hypodense filling defects in segmental branches of bilateral lower lobes with wedge-shaped parenchymal opacity in left lower lobe

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Acute pulmonary embolism

The diagnostic criteria for acute PE include the following:a

  • Arterial occlusion with failure to enhance the entire lumen due to a large filling defect
  • A partial filling defect surrounded by contrast material, producing the “polo mint” sign on images acquired perpendicular to the long axis of a vessel and the “railway track” sign on longitudinal images of the vessel [Figure 4] and [Figure 5].
Figure 4: Computed tomography pulmonary angiogram: Hypodense filling defect in the right descending pulmonary artery giving “railway-track” sign) suggesting of acute pulmonary thromboembolism

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Figure 5: Computed tomography pulmonary angiogram: Hypodense filling defect in the right descending pulmonary artery surrounded by contrast material producing the “polo mint” sign

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Peripheral wedge-shaped areas of hyperattenuation that may represent infarcts, along with linear bands, have been demonstrated to be statistically significant ancillary findings associated with acute PE.[5] Early detection of acute right ventricular failure allows implementation of the most appropriate therapeutic strategy. Dilated right atrium and ventricle with mobile thrombus may be seen on echocardiography [Figure 6] and [Figure 7] along with monitoring of right ventricular strain or failure. However, some morphologic abnormalities that suggest right ventricular failure can be quantified with CT pulmonary angiography. These CT findings include (a) right ventricular dilatation (in which the right ventricular cavity is wider than the left ventricular cavity in the short axis with or without contrast material reflux into the hepatic veins); (b) deviation of the interventricular septum toward the left ventricle, or (c) a PE index >60%.[6],[7]
Figure 6: Two-dimensional echocardiography – Thrombus traversing right atrium into right ventricle (arrow)

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Figure 7: Two-dimensional echocardiography – Large thrombus in the right atrium (arrow)

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CT pulmonary angiography can help identify diseases that have symptoms similar to those of acute PE. The more common diseases that can be detected with CT include pericarditis, which may manifest as pericardial thickening or fluid; acute myocardial infarction, which may manifest as a filling defect within a coronary artery or as a perfusion defect of the myocardium; and aortic dissection. Esophagitis and, rarely, esophageal rupture may also be identified, as well as pneumonia, lung cancer, and pleural disease, including pneumothorax and pleuritis. Chest wall abnormalities such as rib fractures and metastatic deposits may also mimic PE.

Chronic pulmonary embolism

The diagnostic criteria for chronic PE include (a) complete occlusion of a vessel that is smaller than adjacent patent vessels, (b) a peripheral, crescent-shaped intraluminal defect that forms obtuse angles with the vessel wall, (c) contrast material flowing through thickened, often smaller arteries due to recanalization, (d) a web or flap within a contrast material–filled artery, and (e) secondary signs, including extensive bronchial or other systemic collateral vessels an accompanying mosaic perfusion pattern or calcification within eccentric vessel thickening.

Ancillary findings in chronic PE may include CT changes caused by pulmonary arterial hypertension: a pulmonary artery diameter >33 mm and pericardial fluid.[8],[9]

A V/Q scan is another established diagnostic test. As compared to CT pulmonary angiography, it exposes patients to significantly lower levels of radiation. Hence, it is preferred in pregnant and young patients or those with severe renal impairment. A V/Q scan indicating a high probability of PE provides sufficient evidence for the initiation of treatment, but a low probability scan does not rule out PE, necessitating the need for further diagnostic tests.

  Conclusion Top

Precisely speaking, the diagnosis of PTE is made on CT where the findings obtained are pathognomonic. India being a developing country where the availability of a good-quality CT scanner may be confined to urban areas, however majority of people dwells in rural areas. The findings obtained on chest X-ray are nonspecific in nature and several entities may be considered as a part of differential diagnosis of thromboembolism. The joint efforts made by the clinicians along with good-quality chest X-rays may raise the sensitivity of the test to a certain degree and then can provide an indication for option for an echocardiogram and/or quick CT examination, which provide vital clues for early diagnosis and early intervention. A couple number of lives can be saved.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Anderson FA Jr., Wheeler HB, Goldberg RJ, Hosmer DW, Patwardhan NA, Jovanovic B, et al. A population-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism. The Worcester DVT Study. Arch Intern Med 1991;151:933-8.  Back to cited text no. 1
Silverstein MD, Heit JA, Mohr DN, Petterson TM, O'Fallon WM, Melton LJ 3rd. Trends in the incidence of deep vein thrombosis and pulmonary embolism: A 25-year population-based study. Arch Intern Med 1998;158:585-93.  Back to cited text no. 2
Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, et al. Clinical characteristics of patients with acute pulmonary embolism: Data from PIOPED II. Am J Med 2007;120:871-9.  Back to cited text no. 3
Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P, et al. Guidelines on the diagnosis and management of acute pulmonary embolism: The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J 2008;29:2276-315.  Back to cited text no. 4
Coche EE, Müller NL, Kim KI, Wiggs BR, Mayo JR. Acute pulmonary embolism: Ancillary findings at spiral CT. Radiology 1998;207:753-8.  Back to cited text no. 5
Contractor S, Maldjian PD, Sharma VK, Gor DM. Role of helical CT in detecting right ventricular dysfunction secondary to acute pulmonary embolism. J Comput Assist Tomogr 2002;26:587-91.  Back to cited text no. 6
Wu AS, Pezzullo JA, Cronan JJ, Hou DD, Mayo-Smith WW. CT pulmonary angiography: Quantification of pulmonary embolus as a predictor of patient outcome-initial experience. Radiology 2004;230:831-5.  Back to cited text no. 7
Edwards PD, Bull RK, Coulden R. CT measurement of main pulmonary artery diameter. Br J Radiol 1998;71:1018-20.  Back to cited text no. 8
Baque-Juston MC, Wells AU, Hansell DM. Pericardial thickening or effusion in patients with pulmonary artery hypertension: A CT study. AJR Am J Roentgenol 1999;172:361-4.  Back to cited text no. 9


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]


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