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      Neonatal Thyroid Function After Administration of IV Iodinated Contrast Agent to 21 Pregnant Patients

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          Abstract

          The objective of our study was to document neonatal thyroid function after in utero exposure to nonionic iodinated contrast material to determine the potential risk of subsequent neonatal hypothyroidism.

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          The use of iodinated and gadolinium contrast media during pregnancy and lactation.

          The use of iodinated or gadolinium-based contrast media in pregnant or lactating women often causes concerns in the radiology department because of the principle of not exposing a fetus or neonate to any drugs. Because of the uncertainty about the use of contrast media during pregnancy and lactation, the Contrast Media Safety Committee of the European Society of Urogenital Radiology decided to review the literature and draw up guidelines. An extensive literature search was carried out and summarized in a report. Based on the limited information available, simple guidelines have been drawn up. The report and guidelines were discussed at the 11th European Symposium on Urogenital Radiology in Santiago de Compostela, Spain. Mutagenic and teratogenic effects have not been described after administration of gadolinium or iodinated contrast media. Free iodide in radiographic contrast medium given to the mother has the potential to depress fetal/neonatal thyroid function. Neonatal thyroid function should be checked during the 1st week if iodinated contrast media have been given during pregnancy. No effect on the fetus has been seen after gadolinium contrast media. Only tiny amounts of iodinated or gadolinium-based contrast medium given to a lactating mother reach the milk, and only a minute proportion entering the baby's gut is absorbed. The very small potential risk associated with absorption of contrast medium may be considered insufficient to warrant stopping breast-feeding for 24 h following either iodinated or gadolinium contrast agents.
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            Increasing utilization of computed tomography in the adult emergency department, 2000-2005.

            This study aims to characterize changes in computed tomography (CT) utilization in the adult emergency department (ED) over a 5-year period. CT scans ordered on adult ED patients from July 2000 to July 2005 were analyzed in five groups: head, cervical spine, chest, abdomen, and miscellaneous. ED patient volume and triage acuity scores were determined. Triage acuity scores are used to determine the severity of a patient's illness or injury and the need for immediate evaluation and treatment. There were 46,553 CT scans performed on 27,625 adult patients in the ED during the study period. During this same period, 194,622 adult patients were evaluated in the ED. From 2000 to 2005, the adult emergency department patient volume increased by 13% while triage acuity remained stable. During this same period, head CT increased by 51%, cervical spine CT by 463%, chest CT by 226%, abdominal CT by 72%, and miscellaneous CT by 132%. Although increases were generally greater for patients over age 40, the increase in those less than 40 years was also substantial. Of the 4,320 individual patients who underwent chest CT, 83 (2%) had chest CT on three or more separate ED visits. Of 10,960 patients undergoing abdominal CT, 406 (4%) had abdominal CT on three or more separate ED visits. ED CT utilization has increased at a rate far exceeding the growth in ED patient volume. This presumably reflects the improved utility of CT in diagnosing serious pathology, its increased availability, and a desire on the part of physicians for diagnostic certainty. Whether this increase in utilization results in improved patient outcomes is at present unclear and deserves additional study.
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              The potential repercussions of maternal, fetal, and neonatal hypothyroxinemia on the progeny.

              The adequate functioning of both the maternal and fetal thyroid glands play an important role to ensure that the fetal neuropsycho-intellectual development progresses normally. Three sets of clinical disorders are considered, that may eventually lead to impaired brain development. Firstly, in infants with a defect of glandular ontogenesis (congenital hypothyroidism), the participation of maternal thyroid hormones to the fetal circulating thyroxine environment is normal and, therefore, risk of brain damage results exclusively from the insufficient hormone production by the abnormal fetal thyroid gland. Secondly, when it is only the maternal thyroid gland that is functionally deficient (autoimmune hypothyroidism), the severity and temporal occurrence of maternal underfunction will both drive the resulting consequences for impaired fetal neuronal development. Clinical situations of this type may obviously take place already during early gestation (in women with known but untreated hypothyroidism) or appear only during later gestational stages (in women who have AITD and remain euthyroid during the first half of gestation). Lastly, in conditions with iodine deficiency, both maternal and fetal thyroid functions are affected and, therefore, it is primarily the degree and precocity of the maternal hypothyroxinemia due to iodine deficiency during pregnancy that will drive the potential repercussions for fetal neurological development. In the present review, we summarize available data and develop our present concepts concerning the complex feto-maternal thyroid relationships and the potential impacts of thyroid function abnormalities on the ideal development of the offspring.
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                Author and article information

                Journal
                American Journal of Roentgenology
                American Journal of Roentgenology
                American Roentgen Ray Society
                0361-803X
                1546-3141
                July 2008
                July 2008
                : 191
                : 1
                : 268-271
                Article
                10.2214/AJR.07.3336
                18562757
                97ce3bf6-8282-4e9f-8e16-0c6289aff7cb
                © 2008
                History

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