<p><strong>Background</strong> MRI performed at 3.0 T offers greater signal-to-noise ratio and better spatial resolution than does MRI performed at 1.5 T; however, for fetal MRI, there are concerns about the potential for greater radiofrequency energy administered to the fetus at 3.0-T MRI. <strong>Purpose</strong> To compare the specific absorption rate (SAR) and specific energy dose (SED) of fetal MRI at 1.5 and 3.0 T. <strong>Materials and Methods</strong> In this retrospective study, all fetal MRI examinations performed with 1.5- and 3.0-T scanners at one institution between July 2012 and October 2016 were evaluated. Two-dimensional (2D) and three-dimensional (3D) steady-state free precession (SSFP), single-shot fast spin-echo, 2D and 3D T1-weighted spoiled gradient-echo (SPGR), and echo-planar imaging sequences were performed. SAR, SED, accumulated SED, and acquisition time were retrieved from the Digital Imaging and Communications in Medicine header. Data are presented as mean ± standard deviation. Two one-sided tests with equivalence bounds of 0.5 (Cohen effect size) were performed, with statistical equivalence considered at &lt; .05. <strong>Results</strong> A total of 2952 pregnant women were evaluated. Mean maternal age was 30 years ± 6 (age range, 12-49 years), mean gestational age was 24 weeks ± 6 (range, 17-40 weeks). A total of 3247 fetal MRI scans were included, with 2784 (86%) obtained at 1.5 T and 463 (14%) obtained at 3.0 T. In total, 93 764 sequences were performed, with 81 535 (87%) performed at 1.5 T and 12 229 (13%) performed at 3.0 T. When comparing 1.5- with 3.0-T MRI sequences, mean SAR (1.09 W/kg ± 0.69 vs 1.14 W/kg ± 0.61), mean SED (33 J/kg ± 27 vs 38 J/kg ± 26), and mean accumulated SED (965 J/kg ± 408 vs 996 J/kg ± 366, &lt; .001) were equivalent. <strong>Conclusion</strong> Fetal 1.5- and 3.0-T MRI examinations were found to have equivalent energy metrics in most cases. The 3.0-T sequences, such as two-dimensional T1-weighted spoiled gradient-echo and three-dimensional steady-state free precession, may require modification to keep the energy delivered to the patient as low as possible. © RSNA, 2020</p>

<p><strong>BACKGROUND: </strong>Children with Noonan syndrome are known to have increased risk for lymphatic disorders, the extent and nature of which are poorly understood.</p>

<p><strong>OBJECTIVE: </strong>Our objective was to describe the imaging findings of the central lymphatic abnormalities in children with Noonan syndrome who underwent central lymphatic imaging.</p>

<p><strong>MATERIALS AND METHODS: </strong>We conducted a single-center retrospective review of all children with a confirmed history of Noonan syndrome who presented for lymphatic imaging over a 5-year period. Imaging evaluation was performed on unenhanced T2-weighted (T2-W) imaging, dynamic-contrast MR lymphangiography or conventional lymphangiography. Two readers evaluated the imaging in consensus for the distribution of fluid on T2-W imaging and for lymphatic flow of intranodal contrast agent and thoracic duct abnormalities on dynamic-contrast MR lymphangiography and conventional lymphangiography. We performed a chart review for clinical history and outcomes.</p>

<p><strong>RESULTS: </strong>We identified a total of 10 children, all but one of whom had congenital heart disease. Presenting symptoms included chylothorax (n=9) and ascites (n=1). Nine had T2-W imaging, seven had dynamic-contrast MR lymphangiography, and seven had conventional lymphangiography. All with T2-W imaging had pleural effusions. On both dynamic-contrast MR lymphangiography and conventional lymphangiography, perfusion to the lung was seen (n=6), with intercostal flow also seen on dynamic-contrast MR lymphangiography (n=6). The thoracic duct was not present in three children and the central thoracic duct was not present in three. A double thoracic duct was seen in two children.</p>

<p><strong>CONCLUSION: </strong>Children with Noonan syndrome and clinical evidence of lymphatic dysfunction have central lymphatic abnormalities characterized by retrograde intercostal flow, pulmonary lymphatic perfusion, and thoracic duct abnormalities.</p>