Cases reported "Fetal Diseases"

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1/18. Severe nonimmune hydrops fetalis and congenital corneal opacification secondary to human parvovirus B19 infection. A case report.

    BACKGROUND: In parvovirus infections in animals, congenital anomalies are seen, but the teratogenic potential in humans seems fairly low. CASE: A fetus with hydrops, ascites and pleural effusion was seen at a prenatal ultrasound examination. Fetal cordocentesis was performed, and fetal blood was positive for parvovirus antibodies. Intravascular fetal blood transfusion was given at 21 and 23 weeks of gestation. At 39 weeks labor started spontaneously, and a 2,960-g, female infant was delivered. The newborn had bilateral opacification of the cornea. CONCLUSION: In this case a combination of fetal parvovirus B19 infection and congenital corneal opacification was seen. This case also demonstrates that blood transfusions in hydropic fetuses may reverse the hydrops and prevent intrauterine death.
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2/18. Multiple cystic and focal encephalomalacia in infancy and childhood with brain stem damage.

    Two cases are described in which damage to the brain stem was associated with extensive necrosis of the cerebral hemisphere. In the first case--a monochorionic twin--there was clear evidence that injury of an ischaemic or hypoxic type had occurred during fetal life and some evidence that an inadequate share of the placental circulation was an important aetiological factor. In the second case death occurred 4 yr after an asphyxial episode at birth. The lesions in the hemispheres and brain stem were extensive, although less than in the first example. The lesions are discussed in the context of our knowledge of the anatomy and physiology of the developing nervous system. Although they cannot as yet be fitted into the concepts of "critical periods" and "vulnerable periods" of development, this is perhaps because observations on human cases are scanty in comparison with the extensive animal studies which have been reported. The lesions are contrasted and compared with those seen in animals.
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3/18. Brain macrophages and microglia in human fetal hydrocephalus.

    Whereas several studies have addressed the activation of microglia (the resident mononuclear phagocytes of the brain) and macrophages within the nervous system in experimental animal models of congenital and induced hydrocephalus, little is known of their state of activation or regional distribution in human fetal hydrocephalus. This investigation aimed to address such questions. Ten human fetal cases [20-36 gestational weeks (GW) at postmortem] previously diagnosed with hydrocephalus on ultrasound examination in utero, and 10 non-hydrocephalic controls (22-38 GW at postmortem) were assessed immufcnohistochemically with antibodies directed against MHC class II and CD68 antigens, and lectin histochemistry with lycopersicon esculentum (tomato lectin). Adjacent sections were also immunoreacted with an antiserum to laminin to detect cerebral blood vessels. Eight out of the 10 hydrocephalus cases showed numerous CD68 and tomato lectin-positive macrophages located at focal regions along the ependymal lining of the lateral ventricles (particularly within the occipital horn). However, only five of these cases demonstrated MHC class II positive macrophages associated with the ventricular lining. Microglial reactivity within periventricular regions could also be identified using the lectin in four cases, two of which were also immunoreactive with CD68 (but not with MHC class II). By comparison, in control cases five out of 10 fetal brains (aged between 20 and 24 GW) showed few or no ependymal or supraependymal macrophages. One case at 28 GW, and cases at 32 and 38 GW (two of which were diagnosed with intrauterine hypoxic-ischemia) did, however, show some MHC class II (CD68 negative) cells located at the ependymal surface. Nevertheless, these were not as numerous or intensely immunoreactive as in the hydrocephalus cases. microglia interspersed throughout the intermediate zone and circumscribing the basal ganglia were within normal confines in all cases examined. Hydrocephalic cases additionally showed focal regions of hypovascularization or alterations in the structure and orientation of capillaries within periventricular areas, compared to controls. The macrophage response detected at the ependymal lining of the ventricles and within the periventricular area in hydrocephalus may be related both to the severity of hydrocephalus and the age of the fetus.
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4/18. Congenital oculomotor nerve synkinesis associated with fetal retinoid syndrome.

    INTRODUCTION: isotretinoin (RA), used for the treatment of cystic acne, is a powerful teratogen, causing craniofacial dysmorphisms and neural tube defects. We present two patients with RA embryopathy and oculomotor nerve synkinesis. methods: Retrospective review of patient records. RESULTS: Two patients presented with third nerve synkinesis and fetal RA exposure. Both had marked elevation of the upper eyelids on adduction such that the lid fissures alternately opened and closed on gaze from side to side. Both patients showed typical dysmorphisms of RA embryopathy. The first patient had complete agenesis of the cerebellar vermix and died at 2 years. The second patient had restricted extraocular muscles in one eye and was exotropic and hypotropic. DISCUSSION: Both patients demonstrated simultaneous innervation of the medial rectus and levator palpebrae muscles causing coincident lid elevation in adduction. This evidence of oculomotor nerve synkinesis is consistent with animal studies showing abnormalities in the formation of cranial nerve ganglia following fetal RA exposure. CONCLUSION: RA is a powerful teratogen. These patients provide additional clinical evidence of its influence on neural migration during early development.
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5/18. Foetal kidney maldevelopment in maternal use of angiotensin ii type I receptor antagonists.

    We report renal lesions observed in a foetus exposed throughout pregnancy to angiotensin ii type I (AT 1) receptor antagonists. The mother suffered from essential hypertension and was treated with Cozaar (losartan 50 mg). autopsy examination of the foetus revealed severe renal lesions, including tubular dysgenesis, hypertrophy of the endothelial and medial cells lining the arterial and arteriolar walls, hyperplasia of the juxtaglomerular apparatus and poorly developed vasa recta. Similar lesions have already been observed in foetuses of women treated with angiotensin-converting enzyme antagonists and also in foetuses and neonates of animals undergoing experimental blockade of the renin-angiotensin system. The purpose of this report is to describe structural lesions observed in the kidneys, and, particularly, vascular lesions. Our results suggest that the use of AT 1 receptor antagonists during pregnancy may have a severe deleterious effect on kidney development in the foetus.
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6/18. Brain hemorrhages in cocaine-exposed human fetuses.

    Autopsies of 4 fetuses exposed to maternal cocaine are reported. Brain examination revealed hemorrhages in 3 of the fetuses involving the germinal matrix. The hemorrhages resembled subependymal germinal matrix hemorrhages seen as postnatal complications in premature infants with idiopathic respiratory distress syndrome. One of the placentas had sonographic evidence of abruption which could not be confirmed pathologically. The findings are discussed in light of reports of neurobehavioral deficits and other congenital anomalies in children and animals exposed to cocaine in utero. Speculations about the pathophysiologic events leading to these findings are made.
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7/18. Fetal globoid cell leukodystrophy.

    The early lesions of globoid cell leukodystrophy in a 110-g, 18-week-old fetus were characterized in relation to fetal myelination, and comparisons made to the animal models of this disease. Uninucleated and binucleated periodic acid-Schiff-positive cells were present in the spinal cord but not in ventral roots within regions at very early stages of myelination. These cells stained with the lectin ricinus communis agglutinin, which preferentially binds to beta-D-galactosyl residues as found in stored metabolites of globoid cell leukodystrophy. Ultrastructural examination of the spinal cord revealed typical tubular spicular cytoplasmic inclusions in cells corresponding to the periodic acid-Schiff-positive cells. The degree and distribution of myelin tubules and myelination glia was similar to that in weight- and size-matched control fetuses. These results indicate that the first appearance of inclusion-bearing cells is closely associated with the onset of myelination in the central nervous system, apparently earlier in the stage of myelination than occurs in the central nervous system of the mouse model. Characteristic tubular inclusions are also present in renal epithelium in animal models but have not been seen in the human kidney. We have since identified noncharacteristic crystalline inclusions in the kidney of this human fetus.
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8/18. Hepatic disease associated with intrauterine parvovirus B19 infection in a newborn premature infant.

    A hydropic premature infant with intrauterine growth retardation died at 4 days of age and was found at necropsy to have advanced liver disease. Clinical and serologic findings in mother and infant were consistent with recent parvovirus B19 infection. parvovirus can cause fetal liver disease in animals, and some instances of congenital hepatic dysfunction in man may be due to intrauterine parvovirus B19 infection.
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9/18. The effect of embryonic and fetal exposure to x-ray, microwaves, and ultrasound: counseling the pregnant and nonpregnant patient about these risks.

    The term radiation evokes emotional responses both from lay persons and from professionals. Many spokespersons are unfamiliar with radiation biology or the quantitative nature of the risks. Frequently, microwave, ultrasound, and ionizing radiation risks are confused. Although it is impossible to prove no risk for any environmental hazard, it appears that exposure to microwave radiation below the maximal permissible levels present no measurable risk to the embryo. Ultrasound exposure from diagnostic ultrasonographic-imaging equipment also is quite innocuous. It is true that continued surveillance and research into potential risks of these low-level exposures should continue; however, at present ultrasound not only improves obstetric care, but also reduces the necessity of diagnostic x-ray procedures. In the field of ionizing radiation, we have a better comprehension of the biologic effects and the quantitative maximum risks than for any other environmental hazard. Although the animal and human data support the conclusion that no increases in the incidence of gross congenital malformations, IUGR, or abortion will occur with exposures less than 5 rad, that does not mean that there are definitely no risks to the embryo exposed to lower doses of radiation. Whether there exists a linear or exponential dose-response relationship or a threshold exposure for genetic, carcinogenic, cell-depleting, and life-shortening effects has not been determined. In establishing maximum permissible levels for the embryo at low exposures, refer to tables 4, 5, 6, 8, and 9. It is obvious that the risks of 1-rad (.10Gy) or 5-rad (.05Gy) acute exposure are far below the spontaneous risks of the developing embryo because 15% of human embryos abort, 2.7% to 3.0% of human embryos have major malformations, 4% have intrauterine growth retardation, and 8% to 10% have early- or late-stage onset genetic disease. The maximal risk attributed to a 1-rad exposure, approximately 0.003%, is thousands of times smaller than the spontaneous risks of malformations, abortion, or genetic disease. Thus, the present maximal permissible occupational exposures of 0.5 rem for pregnant women (see Table 10) and 5 rem for medical exposure, are extremely conservative. Medically indicated diagnostic roentgenograms are appropriate for pregnant women, and there is no medical justification for terminating a pregnancy in women exposed to 5 rad or less because of a radiation exposure.(ABSTRACT TRUNCATED AT 400 WORDS)
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10/18. Early experience with open fetal surgery for congenital hydronephrosis.

    The fetus with severe bilateral hydronephrosis and associated oligohydramnios in the second trimester is doomed at birth by ongoing pulmonary and renal damage. Since decompression with percutaneously placed catheters anesthetic, surgical, and tocolytic techniques for open fetal anesthetic, surgical, and tocolytic techniques for open fetal urinary tract decompression in animals, and have now applied those techniques to a small group of five patients. One had bilateral ureterostomies and the subsequent four had marsupialization of the bladder. All pregnancies proceeded to cesarean delivery at 32 to 35 weeks' gestation. There was no long-term maternal morbidity, and two mothers have since experienced normal pregnancies. Three fetuses had return of normal amniotic fluid dynamics, and all three had adequate pulmonary function at birth, suggesting that fatal pulmonary hypoplasia associated with early severe oligohydramnios had been reversed. Two neonates died at birth with pulmonary hypoplasia. One had no amniotic fluid even after decompression, and the other had some amniotic fluid after decompression but a tiny chest cavity due to the long period of severe oligohydramnios before decompression. Of the three surviving infants, one had normal renal function when she died of unrelated causes at 9 months of age. One has normal renal function at 23 months and the third had failing renal function at 2 1/2 years and has grown and developed normally, but will require renal transplantation. We have now developed selection criteria that would exclude from treatment the two fetuses who died of pulmonary hypoplasia and the one who developed renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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