PMC9721361_01
Changes in pulmonary embolism of CT pulmonary arteriography before and after percutaneous catheter-directed therapy. (A) Multiple filling defects in bilateral pulmonary artery trunks and their branches (white arrow) before CDT. (B) Thrombus eliminated 1 month after CDT and anticoagulation.
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F1
A pulmonary embolism was suspected, and a subsequent CTPA confirmed a massive PE with bilateral pulmonary emboli (Figure 1A). A CTPA showed that the PE had completely dissolved (Figure 1B) a month later.
Changes in the pulmonary arteriography before and after CDT. (A) Pulmonary angiogram showing a mass filling defect in the distal end of bilateral pulmonary artery trunks and branches of the left lower lobes and poor perfusion before CDT. (B) Pulmonary angiogram showing the reduced defect of the thrombus in bilateral pulmonary artery trunks and improved perfusion after CDT. Pulmonary artery pressure before and after were 44/29 mmHg and 45/20 mmHg, respectively.
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F2
She then underwent a pulmonary angiogram with percutaneous mechanical thrombus removal and thrombectomy, an inferior vena cava angiogram, and filter placement (Figure 2).
Cerebral MRI contrast of ischemic hypoxic encephalopathy. T2WI and T2-FLAIR show extensive gyral swelling and hyperintensity in basal ganglia bilaterally. DWI demonstrates bilateral symmetrical diffusion restriction throughout the cortex of both cerebral hemispheres, particularly involving the perirolandic and occipital cortices. (A) T1WI, (B) T2WI, (C) DWI, (D) T2-FLAIR. MRI, magnetic resonance imaging; T1WI, T1-weighted imaging; T2WI, T2-weighted imaging; DWI, diffusion-weighted imaging; FLAIR, fluid-attenuated inversion recovery.
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F3
Brain magnetic resonance imaging (MRI) with contrast demonstrated ischemic hypoxic encephalopathy, in which global hypoxic brain injury caused diffused edema with pronounced diffusion restriction of the perirolandic and occipital cortices (Figure 3).