OBJECTIVES: The aims of the study were to investigate the computed tomography (CT) features and clinical course of septic pulmonary embolism (SPE) caused by Klebsiella pneumoniae liver abscess (KPLA) and to explore the possible mechanism underlying the spread of infection. METHODS: Twenty-one patients with KPLA-induced SPE admitted to our hospital between January 2010 and May 2015 were evaluated. According to the presence or absence of extrapulmonary metastatic infection (EMI), they were divided into EMI and non-EMI groups and clinical and CT features of the 2 groups were compared. Hepatic vein thrombophlebitis was evaluated on liver CT images. Chest CT features included nodules, wedge-shaped lesions, ground-glass opacity, consolidation, cavitation, feeding vessel sign, pleural effusion, and lymphadenopathy. RESULTS: All the vessels within the so-called feeding vessel sign were confirmed as pulmonary veins by multiplanar reconstruction, so we used an alternative name draining vessel sign (DVS) instead. Peripheral nodules, DVS, and consolidation were the main CT features of KPLA-induced SPE. Peripheral nodules and DVS were more frequently seen in the EMI group than in the non-EMI group (P = 0.019 and 0.008, respectively). Five of 8 patients with hepatic vein thrombophlebitis had lung consolidation, whereas only 3 of 13 patients without hepatic vein thrombophlebitis had lung consolidation, although the difference was not significant (P = 0.09). CONCLUSIONS: Multiple pulmonary nodules and DVS were associated with EMI. Hepatic and pulmonary vein invasion are possible causes underlying the metastatic spread of infection.
OBJECTIVES: The aims of the study were to investigate the computed tomography (CT) features and clinical course of septic pulmonary embolism (SPE) caused by Klebsiella pneumoniae liver abscess (KPLA) and to explore the possible mechanism underlying the spread of infection. METHODS: Twenty-one patients with KPLA-induced SPE admitted to our hospital between January 2010 and May 2015 were evaluated. According to the presence or absence of extrapulmonary metastatic infection (EMI), they were divided into EMI and non-EMI groups and clinical and CT features of the 2 groups were compared. Hepatic vein thrombophlebitis was evaluated on liver CT images. Chest CT features included nodules, wedge-shaped lesions, ground-glass opacity, consolidation, cavitation, feeding vessel sign, pleural effusion, and lymphadenopathy. RESULTS: All the vessels within the so-called feeding vessel sign were confirmed as pulmonary veins by multiplanar reconstruction, so we used an alternative name draining vessel sign (DVS) instead. Peripheral nodules, DVS, and consolidation were the main CT features of KPLA-induced SPE. Peripheral nodules and DVS were more frequently seen in the EMI group than in the non-EMI group (P = 0.019 and 0.008, respectively). Five of 8 patients with hepatic vein thrombophlebitis had lung consolidation, whereas only 3 of 13 patients without hepatic vein thrombophlebitis had lung consolidation, although the difference was not significant (P = 0.09). CONCLUSIONS:Multiple pulmonary nodules and DVS were associated with EMI. Hepatic and pulmonary vein invasion are possible causes underlying the metastatic spread of infection.