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Analysis of perfusion defects by causes other than acute pulmonary thromboembolism on contrast-enhanced dual-energy CT in consecutive 537 patients. | LitMetric

Analysis of perfusion defects by causes other than acute pulmonary thromboembolism on contrast-enhanced dual-energy CT in consecutive 537 patients.

Eur J Radiol

Department of Radiology and Research Institute of Radiology, University of Ulsan College of Medicine, Asan Medical Center, 388-1, Poongnap-dong, Songpa-gu, Seoul 138-736, Republic of Korea.

Published: April 2012

Objective: To assess causes, incidence and patterns of perfusion defects (PDs) on dual-energy perfusion CT angiography (DECTA) in clinically suspected acute pulmonary thromboembolisms (PTE).

Materials And Methods: Consecutive 537 patients who underwent DECTA for suspicion of PTE were retrospectively reviewed. After excluding patients with possible PTE or unsatisfactory perfusion map quality, 299 patients with 1697 lobes were included. The DECTA (Somatom Definition, Siemens) was performed at 140kV and 80kV. Color-coded perfusion images were obtained with a lung PBV application of the workstation software (Syngo Dual Energy). The presence, incidence, three patterns of PDs (wedge-shaped, heterogeneous, and regionally homogeneous), pulmonary diseases, and the matchedness between the PD and the disease extent were studied.

Results: 315 of 1697 lobes (18.6%) in 156 of 299 patients (81.3%) showed PDs. Among them, 51 (3%), 257 (15.1%), and 7 (0.4%) lobes had PDs due to vascular, nonvascular, and unidentifiable causes, respectively. Vascular causes include: pulmonary arterial (PA) hypertension (0.7%), extrinsic occlusion of PA by fibrosis (0.6%), PA hypoplasia (0.6%), vasculitis (0.5%), cancer mass compressing PA, venous occlusion, AVM, and pulmonary angiosarcoma. Most of PDs were wedge-shaped and well-matched. Nonvascular causes include: mosaic attenuation (4.1%), emphysema (3.2%), interstitial fibrosis (1.6%), bronchitis (1.4%), GGO (1.2%), cellular bronchiolitis (1%), bronchiectasis, airway obstruction, compensaroty lung hyperinflation, air trapping, cor-pulmonale, bronchopneumonia, physiologic decreased ventilation, and segmental bronchial atresia. Most of PDs showed heterogeneous pattern and were not matched.

Conclusions: Various vascular and nonvascular diseases cause PDs on DECTA. Each disease shows different pattern of PD depending on pathophysiology and physiologic compensation.

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Source
http://dx.doi.org/10.1016/j.ejrad.2012.01.026DOI Listing

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