The role of computed tomography in the diagnosis of acute and chronic pulmonary embolism

Abstract

Pulmonary embolism (PE) is a potentially life threatening condition requiring adequate diagnosis and treatment. Computed tomography pulmonary angiography (CTPA) is excellent for including and excluding PE, therefore CT is the first-choice diagnostic imaging technique in patients suspected of having acute PE. Due to its wide availability and low invasiveness, CTPA tends to be overused. Correct implementation of clinical decision rules in diagnostic workup for PE improves adequate use of CT. Also, CT adds prognostic value by evaluating right ventricular (RV) function. CT-assessed RV dysfunction and to lesser extent central emboli location predicts PE-related mortality in normotensive and hypotensive patients, while PE embolic obstruction index has limited prognostic value. Simple RV/left ventricular (LV) diameter ratio measures >1.0 already predict risk for adverse outcome, whereas ratios <1.0 can safely exclude adverse outcome. Consequently, assessing the RV/LV diameter ratio may help identify patients who are potential candidates for treatment at home instead of treatment in the hospital. A minority of patients develop chronic thromboembolic pulmonary hypertension (CTEPH) following acute PE, which is a life-threatening condition that can be diagnosed by CT. In proximal CTEPH, involving the more central pulmonary arteries, thrombectomy usually results in good outcome in terms of both functional status and long-term survival rate. CT is becoming the imaging method of choice for diagnosing CTEPH as it can identify patients who may benefit from thrombectomy. New CT developments such as distensibility measurements and dual-energy or subtraction techniques may further refine diagnosis and prognosis for improved patient care.

Figure 1

a, b. A 82-year-old man presenting with hypoxemia, hypotension, sinus tachycardia and ECG-changes suggesting right ventricular strain. Multidetector CT (a) shows a saddle embolism, with signs of right ventricular dysfunction with high RV/LV diameter ratio of 2.8 (arrows in b; arrow in the LV cavity is partly overlying the papillary muscle). The patient was treated with thrombolysis which resolved the pulmonary embolism (b), however, the patient finally died of ventilation-associated pneumonia and septic shock.

Figure 2

Pathophysiology of hemodynamic instability due to pulmonary embolism, development of CTEPH, and its cardiovascular and pulmonary parenchymal changes. Predisposing factors may cause DVT that can dislodge and cause pulmonary embolism. Pulmonary embolism can cause RV failure directly or indirectly after inadequate lysis of emboli and development of CTEPH. Right lower box shows morphologic changes that may be observed on CT. DVT, deep vein thrombosis; PE, pulmonary embolism; RV, right ventricular; LV, left ventricular; IVS, interventricular septal; CTEPH, chronic thromboembolic pulmonary hypertension; BNP, brain natriuretic peptide; NT-proBNP, aminoterminal-probrain natriuretic peptide; NO, nitric oxide; RA, right atrial; GGO, ground glass opacity.

Figure 3

a–c. CTPA and HRCT reconstruction in CTEPH and mosaic perfusion. A 53-year-old man with CTEPH who presented with persistent dyspnea and dyspnea on exertion lasting several months, known with a history of adequately treated acute PE six years before. Blood analysis was unremarkable except elevated NT-proBNP (1212 ng/mL), echocardiography showed severe RV and right atrial dilatation with moderate tricuspid insufficiency and an estimated pulmonary artery pressure of 62 mmHg. Right-sided catheter measurements showed a pulmonary vascular resistance of 781 dyne·s/cm⁵ and a mean pulmonary artery pressure at rest of 46 mmHg. CTPA with high resolution reconstructions in lung setting (a) shows mosaic perfusion with hyperperfused pulmonary areas of high attenuation associated with larger vessels, and areas of hypoperfusion with low attenuation that contain smaller vessels. In soft tissue setting (b), the diameter ratio of the main pulmonary artery to the aorta is >1, indicative for pulmonary hypertension. Also note the wall-adherent thrombus and atherosclerotic calcification of the main pulmonary arteries, as signs of pulmonary hypertension. There is intraluminal web in the segmental artery to the left upper lobe. Dilated RV and flattening of the ventricular septum indicate RV dysfunction (c). Figure is published with patient’s permission and courtesy of Dr. I. Bahce and Dr. A. Boonstra, Department of Pulmonary Diseases at the VU University Medical Center Amsterdam, the Netherlands.