Cases reported "Fetal Growth Retardation"

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1/9. Longitudinal observation of deterioration of Doppler parameters, computerized cardiotocogram and clinical course in a fetus with growth restriction.

    We report on a fetus with intrauterine growth restriction detected at 27 weeks' gestation, who was longitudinally followed up until delivery by cesarean section 33 days later (31 5 weeks) due to severe decelerations in CTG. Longitudinal Doppler assessment of the umbilical artery (UA), the middle cerebral artery (MCA) and the main branch of the right pulmonary artery (RPA), the ductus venosus (DV) and the left coronary artery was compared to clinical course and computerized CTG. At first presentation (day--33) increased resistance in both the UA and uterine arteries with bilateral notches was found. Absent enddiastolic flow (AED) in the UA was found at day--19 and reverse flow (RED) at day--11. The MCA showed a decreased pulsatility first at day--19 and again at day--11 together with RED in the UA. The RPA initially (day--33) showed increased PI which returned to normal values at day--19 but increased again at day--1, when the DV showed RED and the coronary arteries became visible. The DV was normal until day--11, then its PI began to increase together with occurence of RED in the UA, but reverse flow in the DV occurred only on the eve (day--1) of severe decelerations in CTG. Short-term variability in computerized CTG was stable at 6 to 7 ms, except for an intermediate drop to 4 ms at day--10. Maternal hypertension was found at day--19 and mild preeclampsia developed at day--12. A reduction of fetal movements was noticed at day--5. This report shows that at 29 weeks gestation despite detection of AED resp. RED in the UA a prolongation of pregnancy for 19 resp. 11 days is possible. In addition to abnormal CTG, late signs of fetal deterioration are reverse flow in the DV and visibility of the coronary arteries. The role of increased resistance in the main branches of the pulmonary arteries should be examined in the future.
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2/9. Atypical variable decelerations and intrauterine growth restriction.

    Variable decelerations of the fetal heart rate are the most common changes noted during continuous fetal monitoring. In general, they are presumed to represent a normal response to fetal baroceptor stimulation. When atypical features are present, other considerations are warranted.
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3/9. sjogren's syndrome diagnosed in pregnancy: a case report.

    BACKGROUND: As in most other autoimmune diseases, sjogren's syndrome is seen predominantly in women. Since the peak age is around the late reproductive and early postmenopausal period, the obstetric aspect has not been well studied. CASE: A 28-years-old woman, pregnant for 22 weeks and 5 days, was admitted with worsening general status, skin lesions, arthralgias, and oral and ocular symptoms typical of sjogren's syndrome. She underwent hemodialysis for renal insufficiency. To prevent autoantibody formation, progression of the disease, therapy with methyl prednisolone, 100 mg/d intravenously; cyclophosphamide, 500 mg/month in a single intravenous application; hemodialysis 3 times a week; and plasmapheresis 7 times was instituted. An 1,100-g, male infant at 27 weeks and 5 days was delivered by cesarean section because of premature preterm rupture of membranes and severe late decelerations on cardiotocography. The infant was discharged from the neonatal intensive care unit after 30 days, weighing 1,800 g. Postnatal echocardiographic examination of the infant revealed neither cardiac malformations nor arrhythmias. CONCLUSION: Since the presence of autoantibodies against SS-A and SS-B are reported to accompany congenital heart block, the primary goal of therapy should be preventing this untoward effect of the disease. Close monitoring during pregnancy is mandatory to detect preeclampsia, intrauterine growth retardation and preterm labor.
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4/9. The significance of cardiotocographic monitoring in pregnancy complicated by intrauterine growth retardation and prematurity.

    Intrauterine growth retardation is a condition of chronic fetal compromise. The most accurate method of fetal assessment in this condition is by serial cardiotocography. In pregnancy associated with intrauterine growth retardation, abnormal cardiotocography with spontaneous decelerations may be an indicator of imminent fetal death in utero. Delivery should be effected immediately if the fetus is at a gestation where viability is probable.
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5/9. Manifestations of pseudoxanthoma elasticum during pregnancy: a case report and review of the literature.

    A 30-year-old white woman with pseudoxanthoma elasticum (PXE) was followed throughout her pregnancy with several fetal ultrasonographic examinations and other diagnostic studies; these showed normal development up to the 26th wk and then a marked deceleration of fetal growth. The ultrasonographic appearance of the placenta was abnormal at all times probably related to the microscopic changes. The baby, born at 36 wk, showed severe intrauterine growth retardation as a probable consequence of the abnormal placenta detected by ultrasound and corroborated at birth. The cotyledons were small and more numerous than normal. One third of the placenta was hypoplastic or atrophic, with focal calcification in septa, stroma, villi, and decidua, and increased deposition of fibrin around villi. The most striking change was the increased number of septa and the abnormal elastic tissue.
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6/9. Changes in blood velocities of fetal circulation in association with fetal heart rate abnormalities: effect of sublingual administration of nifedipine.

    nifedipine has been used to treat hypertension in pregnancy, and does not influence fetal or uteroplacental circulations in patients with preeclampsia. A 29-year-old multi-gravid woman presented at 32 weeks' gestation with significant elevation of her blood pressure. After sublingual administration of nifedipine, the blood pressure decreased from 208/122 to 136/96 mm Hg at 30 minutes. In her growth-retarded fetus with abnormal flow velocity waveforms, pulsatility index values for middle cerebral artery and umbilical artery did not change; however, peak systolic velocities, end-diastolic velocities, and time-averaged mean peak velocities for these arteries became significantly elevated. Simultaneously, severe variable decelerations and late decelerations occurred. The adverse effect of nifedipine on fetal circulation might occur in a growth-retarded fetus with abnormal flow velocity waveforms.
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7/9. Fetal circulatory system in growth-retarded fetus with late decelerations and oligohydramnios.

    We present 4 cases of growth-retarded fetuses with fetal heart rate late decelerations and oligohydramnios. Doppler ultrasound revealed significantly decreased pulsatility index (PI) values of the middle cerebral artery; however, the PI values of the renal artery, femoral artery and umbilical artery were within normal ranges in all fetuses. Relative redistributions in the fetal circulatory system were shown with fetal hypoxemia without acidosis.
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8/9. Twenty-day cerebral and umbilical Doppler monitoring on a growth retarded and hypoxic fetus.

    In one growth retarded and hypoxic fetus, the cerebral and umbilical hemodynamic changes were assessed (by Doppler), daily over 20 days. The fetal brain was investigated by magnetic resonance imaging (MRI) close to the delivery, and because the fetus died at delivery we performed an anatomical study of the fetal brain. The evolution of the fetal hemodynamics (day by day) was interpreted according to the MRI findings and the clinical findings. During the period of observation (under sustained hypoxia) the fetal deterioration was characterized by: (a) the progressive development of the oligohydramnios (190d), (b) the disappearance of the vascular reactivity (eight successive cerebral resistance index (RI) constant at 194d), (c) the occurrence of fetal heart rate decelerations (199d), and finally (d) the increase of the cerebral vascular resistances with reduction of the brain perfusion (204d). The anatomical study of the brain showed a periventricular congestion however the histology revealed hypoxic lesions like gliosis and a marked vasodilation of the anterior and middle cerebral arteries. Finally in addition to single Doppler measurements performed 1 week before delivery (for prediction of fetal outcome), one can suggest to use the 'loss of fluctuation of the cerebral RI' to identify the beginning of the period of very high risk for the fetus. Such hypothesis may have to be confirmed on a larger number of pathological pregnancies.
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9/9. Spontaneous motility in preterm, small-for-gestational age infants. II. Qualitative aspects.

    In order to document in detail the developmental course of qualitative aspects of early spontaneous motility in intrauterine growth-retarded infants, sequential videotape recordings were made in 19 preterm infants with a birth weight below the 5th percentile. The quality of general movements (GMs) was studied longitudinally during the preterm and postterm period until approximately 20 weeks corrected age, using Prechtl's method of quality assessment. An abnormal quality of GMs was present in 15 out of 19 infants. Compared to a low-risk group, consisting of appropriate-for-gestational age preterm infants, the proportion of infants with normal findings on brain scans who had an abnormal quality of GMs was high. The presence of 'abrupt chaotic' GMs was related to late fetal heart-rate decelerations and ischaemic alterations of the placenta. The quality of GMs normalized before or during the third month postterm in most infants with abnormal GMs. In four infants, the GMs did not normalize during the study period. The quality of fidgety movements was, in particular, a marker for neurological outcome at 24 months. This study demonstrates that intrauterine growth retardation may cause prolonged, but in most cases transient brain dysfunction; the qualitative assessment of GMs may help to identify infants at increased risk for neurodevelopmental abnormalities.
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