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21/95. Foetal warfarin syndrome--a complex airway problem. Case report and review of the literature.

    Premature cartilaginous calcification and nasal hypoplasia following first trimester exposure to warfarin are known as the Foetal warfarin syndrome (FWS). There are over 40 cases reported in the literature, many of which describe breathing and feeding difficulties in the first few months of life. We report a case where a child had had difficulties breathing and feeding in the first months of life. These had been attributed to nasal hypoplasia. After proper ENT assessment the child benefitted from adenoidectomy. ENT surgeons should be aware of the syndrome as more women of child bearing age are taking warfarin following cardiac surgery and treatment of thromboembolic disease. ENT surgeons may be asked to review these children who often present with airway and feeding problems which have been attributed to nasal hypoplasia.
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22/95. radiotherapy for glioma during pregnancy: fetal dose estimates, risk assessment and clinical management.

    Cancer in pregnancy is relatively uncommon, but constitutes a major problem. We report the measurement of scatter dose to the fetus and the estimated fetal risk from that exposure in an illustrative case of a patient, 20 weeks pregnant, with a grade 3 anaplastic astrocytoma. A clinical decision was made to withhold radiotherapy, if possible, until after delivery. Sequential magnetic resonance imaging (MRI) showed no progression during the pregnancy. In the event, she was managed conservatively until the successful completion of her pregnancy. In case radiotherapy was required, an estimation of the fetal risk was made. Phantom measurements were undertaken to assess the likely fetal dose. Film badges were used to estimate the scattered radiation energy. Measurements were made on a Varian 600C at 6 MV and Asea Brown Boveri (ABB) accelerator at 8 and 16 MV. Doses were measured at 30, 45 and 60 cm from the isocentre; the fetus was assumed to lie at about 60 cm and not closer than 45 cm from the isocentre. Estimated doses to the position of the fetus were lowest with the 6 MV Varian accelerator. Using this machine without additional abdominal shielding, the estimated dose on the surface at 45 cm from the tumour volume was 2.2 cGy for a tumour dose of 54 Gy; using the ABB accelerator, the dose varied between 49-59 cGy. The energy of scattered radiation was in the range 208-688 keV, so that additional shielding would be practical to further reduce the fetal dose. The risk of cancer up to the age of 15 years attributable to radiation is 1 in 1700 per cGy, of which half will be fatal (i.e. 1 in 3300 per cGy). A dose of 2.2 cGy adds a risk of fatal cancer by the age 15 years of only 1 in 1500. Because the addition of shielding might halve the fetal dose, this risk should be reduced to 1 in 3000. For comparison, the overall UK risk of cancer up to the age 15 years is 1 in 650. In conclusion, careful choice of linear accelerator for the treatment of a pregnant woman and the use of additional shielding is valuable, as this can dramatically affect fetal dose.
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23/95. Differential cerebral and neuropsychological consequences in dizygotic twins with prenatal alcohol exposure.

    AIM: To relate structural and functional findings in one adolescent dizygotic twin pair with prenatal alcohol exposure. METHOD: Neuropsychological and volumetric magnetic resonance studies were carried out on a 13-year-old preterm dizygotic twin pair with prenatal alcohol exposure. RESULTS: Neuropsychological and brain structural findings differed between the twins. The child with the more affected phenotype had large-scale cognitive deficits and presented significant atrophy in several brain structures. Both subjects had white matter volume reductions relative to the whole cerebral volume. CONCLUSION: The neuropsychological and neuroimaging data reflect long-term consequences of prenatal alcohol exposure.
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ranking = 7
keywords = exposure
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24/95. ergotamine as a possible cause of Mobius sequence: additional clinical observation.

    A case of Mobius sequence after exposure to ergotamine during early development is reported. Vascular disruption is one of the theories explaining the pathogenesis of Mobius sequence. ergotamine can cause vasospasm and a prolonged and marked increase in uterine tone. This is the second report suggesting a relation between maternal ingestion of ergotamine in early pregnancy and subsequent Mobius sequence in a child.
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25/95. Aplasia cutis congenita after methimazole exposure in utero.

    We describe a patient who was exposed to the antithyroid drug methimazole during the first 6 weeks of gestation and was born prematurely with scalp and skull defects associated with facial asymmetry. A review of the literature seems to support the hypothesis that methimazole is a potential teratogen. Although the risk of birth defects is low with clinically applied doses of the drug, it cannot be regarded as safe and should therefore be avoided in the treatment of pregnant women.
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ranking = 4
keywords = exposure
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26/95. Severe adverse effects in a newborn with two defective CYP2D6 alleles after exposure to paroxetine during late pregnancy.

    paroxetine, like other SSRIs, is reported not to increase the number of malformations in infants exposed to these drugs in utero. However, late pregnancy exposure to SSRIs sometimes leads to perinatal complications resembling the symptoms seen in serotonergic overstimulation. We report here a case of third trimester paroxetine exposure with adverse birth outcome in a newborn. The clinical symptoms in the infant included severe tremor and rigidity as well as loose stools during the first 4 days of life. plasma paroxetine concentrations in infant plasma were quite low after birth, but she was genotyped to be a poor metabolizer of CYP2D6, the enzyme catalyzing the metabolism of paroxetine. In accordance with an earlier report, we suggest that even low plasma concentrations of paroxetine may be related to perinatal complications in infants exposed to paroxetine during late pregnancy and that the poor metabolizer genotype of CYP2D6 may be a risk factor for these complications.
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27/95. Fetal toxic effects of angiotensin ii receptor antagonists: case report and follow-up after birth.

    OBJECTIVE: To report a child born with renal impairment following severe anhydramnios due to maternal exposure to an angiotensin ii receptor type 1 (AT1) antagonist, valsartan, and hydrochlorothiazide during the first 28 weeks of pregnancy. CASE SUMMARY: A hypertensive woman treated with valsartan 80 mg/day, hydrochlorothiazide 12.5 mg/day, prazosin 10 mg/day, lysine acetylsalicylate 100 mg/day, and levothyroxine 250 microg/day became pregnant. At 28 weeks' gestational age, severe anhydramnios associated with high beta2-microglobulin levels in the fetal blood cord was observed. Upon discontinuation of valsartan, fetal renal prognosis improved. In this case, using the Naranjo probability scale, the renal insufficiency of the child was probably related to valsartan. At the age of 2.5 years, the child presented with only mild chronic renal insufficiency. growth parameters were within the normal range, and there was no evidence of developmental delay. DISCUSSION: Exposure to AT1 antagonists during the second part of pregnancy can lead to abnormalities similar to those observed after exposure to angiotensin-converting enzyme inhibitors, that is, reduced fetal kidney perfusion that may result in oligoamnios and neonatal renal insufficiency. Fourteen previous reports of maternal exposure to AT1 antagonists during this period have been published. In 6 cases, fetal or neonatal death occurred; in 2 cases, pregnancy was terminated because of complete anhydramnios or fetal abnormalities; in 1 case, renal insufficiency persisted at 8 months of age; in 2 cases, kidney function was fairly normal at birth; and in 4 cases, including the one described here, neonatal renal failure improved in the first year of life. CONCLUSIONS: AT1 antagonists should be avoided throughout pregnancy. If these agents are prescribed accidentally to a pregnant woman, monitoring of amniotic fluid volume and beta2-microglobulin fetal blood levels after discontinuation of the AT1 antagonist can provide critical data for advising parents on pregnancy and fetal outcome.
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ranking = 3
keywords = exposure
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28/95. Fetal warfarin syndrome.

    Fetal warfarin syndrome (FWS) or warfarin (coumadin) embryopathy is a rare condition as a result of fetal exposure to maternal ingestion of warfarin during pregnancy. A male infant, whose mother was treated with the anticoagulant (warfarin) because of a mechanical heart valve replacement after rheumatic heart disease, presented with signs of warfarin embryopathy. The facial dysmorphism included hypoplasia of nasal bridge, laryngomalacia, pectus carinatum, congenital heart defects (atrial septal defect and patent ductus arteriosus), ventriculomegaly, stippled epiphyses, telebrachydactyly, and growth retardation. The pathogenesis and management of FWS are discussed.
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ranking = 1
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29/95. Neonatal toxicity and transient neurodevelopmental deficits following prenatal exposure to lithium: Another clinical report and a review of the literature.

    I report the case of an infant girl who was exposed to lithium during gestation and her follow-up at the age of 1 year. She presented with transient neurodevelopmental deficits including lethargy, hypotonia, and poor oral feeding ability in the neonatal period. She required supportive treatment and made gradual improvement in neurologic functioning. On examination at the age of 1 year, physical findings and psychomotor development were normal. The English literature from 1978 to 2004 is reviewed. A total of 30 patients who were exposed to lithium during gestation with adequate clinical description were identified. A significant number of these babies presented with neurodevelopmental deficits and depressed neurological status including hypotonia, respiratory distress syndrome, cyanosis, lethargy, and weak suck and Moro reflexes in the neonatal period. The majority of these abnormalities resolved and most babies made full recovery. Other abnormalities were structural as well as functional involvement of the cardiovascular system, macrosomia, prematurity, jaundice, diabetes insipidus, and involvement of the thyroid gland. While the use of lithium during pregnancy does not appear to significantly increase the risk of congenital anomalies, it is frequently associated with perinatal complications and reversible neonatal toxicity. Suggested guidelines for appropriate monitoring of infants and breast-feeding of exposed babies are presented. In addition, prenatal surveillance of women with bipolar disorders who are being treated with lithium is briefly discussed.
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ranking = 4
keywords = exposure
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30/95. The neurodevelopmental consequences of prenatal alcohol exposure.

    During pregnancy, ingestion of alcohol, a known teratogen, can cause harm to the fetus. Prenatal alcohol exposure is one of the leading causes of birth defects, developmental disorders, and mental retardation in children. The fetal central nervous system is particularly vulnerable to alcohol; this vulnerability contributes to many of the long-term disabilities and disorders seen in individuals with prenatal alcohol exposure. Diagnoses associated with prenatal alcohol exposure include fetal alcohol syndrome (FAS), partial fetal alcohol syndrome, fetal alcohol effects, alcohol-related neurodevelopmental disorder, and alcohol-related birth defects. Once diagnosed, early intervention improves the long-term outcome of affected children. Without documentation of maternal alcohol use, a diagnosis, and consequently treatment, is often difficult to attain. It is imperative that nurses, physicians, and other healthcare providers become comfortable with obtaining a history of, and providing anticipatory guidance and counseling about, alcohol use.
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ranking = 7
keywords = exposure
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