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Few studies of the histopathological features of the placenta in cases of fetal death are available. We will describe the placental findings from 24 midtrimester spontaneous abortions and 54 stillborn infants of more than 28 weeks' gestation. In almost 100% of midtrimester abortions and in 48% of the placentas from stillborn infants of more than 28 weeks' gestation, chorioamnionitis, deciduitis, and/or villitis were present. Because of this very high percentage of lesions, which suggests an infectious causation, it is mandatory that studies be performed that might identify pathogens. One third of the stillborn infants of more than 28 weeks' gestation were associated with maternal complications (diabetes, preeclampsia, and urinary tract infection), in addition to placental fetal vasculopathy, ischemia, infarcts, and chorangiosis (villous capillary hyperplasia). We emphasize the use of the placenta for the recognition of maternal diabetes.
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PMID:Pathological features of the placenta in fetal death. 94 56

Pregnancy is marked by a state of hypomagnesemia. The serum magnesium level shows no gestational dependence (mean, 1.79 +/- 0.44 mg/dl) until 33 weeks, at which point it continuously declines. Serum magnesium is not depressed further with the onset of labor at term. Patients in preterm labor have a significantly depressed serum magnesium level (mean, 1.60 +/- 0.46 mg/dl; 21 to 33 weeks; p less than 0.0005). This level was not dependent on whether the etiology for the preterm labor was premature rupture of the membranes (PROM), twin gestation, abruption, placenta previa with bleeding, or chorioamnionitis. With PROM, the serum magnesium level was not depressed prior to the initiation of preterm labor. However, observation of hypomagnesemia for this and other etiologies just prior to the initiation of preterm labor were not available. Possible mechanisms by which hypomagnesemia induces uterine irritability are explored, including inhibition of adenyl cyclase with resultant increase in cytoplasmic calcium levels. Patients with diabetes mellitus appeared to have slightly reduced serum magnesium levels, but the results were not statistically significant. Magnesium levels in patients with preeclampsia were not significantly different from controls. Hypomagnesemia (magnesium 1.4 mg/dl or less) may be a marker for true preterm labor.
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PMID:Serum magnesium levels in pregnancy and preterm labor. 200 37

Pregnancies that produced 56,857 children were analyzed to evaluate the relationship of the mothers' relative pregravid body weight to pregnancy outcome. Perinatal mortality rates progressively increased from 37 of 1000 in offspring of thin subjects to 121 of 1000 in the offspring of obese subjects (p less than 0.001). Nearly half of this mortality increase was due to preterm deliveries, particularly before 31 wk of gestation. More than half of the increase in preterm births was caused by acute chorioamnionitis. Other factors that made major contributions to the overall mortality increase were rises in the frequencies of older gravidas (ages 35-50 y), gravidas who had diabetes mellitus, children who had major congenital malformations, and dizygous twins.
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PMID:Maternal body weight and pregnancy outcome. 237 93

We report six cases of chronic intervillositis, an infrequently recognized placental lesion that is characterized by a prominent mononuclear inflammatory cell infiltrate in the intervillous space and that is associated with poor fetal outcome. In all six placentas, the inflammatory infiltrate was essentially limited to the intervillous space: chronic villitis was present focally only in one and absent in the other five. Additional placental histopathologic findings included increased villous fibrinoid material in all six, infarcts in two, atherosis in decidual vessels in two, and acute chorioamnionitis in two. Results of immunohistochemical staining confirmed the predominantly histiocytic nature of the intervillous infiltrate. Two mothers had a history of severe preeclampsia, one had elevated blood pressure at the time of delivery, two had a history of substance abuse, two had a history of systemic lupus erythematosus treated with prednisone, and one of these last two also had diabetes. Five of the six pregnancies resulted in perinatal death. One fetus was nonviable, one was anencephalic, one died in utero, and two died of complications of prematurity shortly after birth; one of the premature infants was small for gestational age. The mononuclear nature of the inflammatory cell infiltrate and its association with increased villous fibrinoid material and atherosis suggests an immunological origin, although the possibility that this lesion may have an infectious cause cannot be excluded.
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PMID:Chronic intervillositis of the placenta. 821 26

We sought to identify the significance of recurrent stillbirth and to determine the contributory etiologic factors for this phenomenon. Data were analyzed and retrospective chart review conducted for all stillbirths occurring during a 13-year period. Subjects were divided into two groups: those for whom the current stillbirth was the first and those who had had a previous stillbirth. The study included 48,479 consecutive multiparous women, of whom 403 had delivered stillborn infants (8.31/1,000 live births). For 34 of these subjects, this represented a recurrent stillbirth (84.36/1,000 live births). The recurrent-stillbirth group had a 10.15-fold higher risk for stillbirth. Additionally, this group had a twofold higher incidence of diabetes and hypertensive disease than did those women experiencing their first stillbirths; furthermore, the gestational age and birth weight of the stillborn infants were significantly lower in the recurrent-stillbirth group (P < .0004 and < .007, respectively). Such factors as socioeconomic class, chorioamnionitis and erythroblastosis fetalis, traditionally cited as contributing to repeated fetal loss, were not significant. Although recurrent stillbirth remains an unsolved problem, improving health care to specific groups within high-risk populations may reduce fetal loss.
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PMID:Recurrent stillbirth. Significance and characteristics. 827 86

A retrospective case-control study of necrotizing enterocolitis (NEC) affecting infants weighing > 2,000 g at birth was performed to determine those factors which could contribute to the development of NEC. Twenty-four infants met the criteria of definite NEC. For each case the next 2 healthy newborns were matched as controls. When compared with the control group, NEC infants had a significantly higher frequency of prolonged rupture of membranes, chorioamnionitis, Apgar score < 7 at 1 and 5 min, respiratory problems, congenital heart disease, hypoglycemia, and exchange transfusions. Only 3 infants with NEC were healthy newborns with an unremarkable perinatal course before NEC. There were no differences in the frequency of preeclampsia, maternal diabetes, maternal drug abuse, meconium-stained amniotic fluid and polycythemia. These results indicate that most of these more mature infants have a predisposing factor before developing NEC.
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PMID:Necrotizing enterocolitis in full-term or near-term infants: risk factors. 916 50

Preterm labor, cervical cerclage (especially when performed as an emergency procedure), and diabetes mellitus are all associated with an increased risk of chorioamnionitis. It might be expected that the combination of all 3 could lead to especially severe infection. We report such a case. A woman with a history of two spontaneous midtrimester abortions had had cervical cerclage performed at 13 weeks. She was referred at 24 weeks' gestation with preterm labor, and the cervix was found to be dilated. An emergency repeat cerclage was performed. The following day, ultrasonography revealed the presence of intra-amniotic gas. Infection was confirmed by the presence of a purulent cervical discharge, a neutrophilia with a left shift, and an elevated C-reactive protein level. The cervical stitch was removed and labor induced. The infant was liveborn, but succumbed to the complications of prematurity and sepsis. E. coli was isolated. In her subsequent pregnancy, severe gestational diabetes was diagnosed and following pregnancy, permanent diabetes mellitus was confirmed. The combination of infection, diabetes, and intact membranes may lead to a particularly severe form of chorioamnionitis, with the production of gas within the amniotic cavity. Infection should be excluded before emergency cervical cerclage, especially in the woman with diabetes mellitus.
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PMID:Emphysematous chorioamnionitis diagnosed by ultrasonography. 925 46

Aside from recognized overgrowth syndromes, instances of visceromegaly are not uncommon at perinatal autopsy. The database of the University of Michigan Teratology Unit was screened for individual viscera exceeding the 90th centile for body and brain weight standards. The data were stratified for several maternal (hypertension, diabetes, obesity), gestational (chorioamnionitis, oligohydramnios, amniorrhaea, polyhydramnios), and fetal (body wall defect, cardiac malformation, renal malformation, diaphragmatic hernia, nonimmune hydrops, twin transfusion syndrome) characteristics and tested for statistically significant excessive numbers of heavy organs. The most striking associations were heavy adrenal glands and liver with chorioamnionitis, heavy heart with polyhydramnios and in the twin transfusion syndrome, and heavy heart and liver with nonimmune hydrops. Excessive brain weight for body weight had a number of correlations, each most likely reflecting growth restriction with sparing of brain growth.
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PMID:Correlates of prenatal visceromegaly. 978 3

Lymphocytic inflammation of the fetal membranes is unusual and has been termed chronic chorioamnionitis. We report the clinicopathologic and immunohistochemical findings in 31 placentas with chronic chorioamnionitis. The most common histopathologic association was chronic villitis of unknown etiology, which was identified in 22 (71%) of the 31 placentas. The severity of the chronic villitis did not correlate with the severity of chronic chorioamnionitis. Additional placental findings included chronic intervillositis in two, fetal vessel thrombosis in five, hemorrhagic endovasculitis in four, decidual chronic vasculitis in three, and atherosis in one. Maternal history included pregnancy-induced hypertension in six and diabetes in one. Twelve infants were preterm, and five had intrauterine growth retardation. There was no neonatal sepsis or death. Immunohistochemical staining in areas of chronic chorioamnionitis showed CD3+ and CD8+ cells present in moderate numbers, and CD4+ cells in smaller numbers. CD20+ and CD56+ cells were rare or absent. Chronic chorioamnionitis is commonly associated with chronic villitis of unknown etiology, shares similar clinical associations, and may have a related cause, possibly immunologic.
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PMID:Chronic chorioamnionitis: a clinicopathologic and immunohistochemical study. 986 33

Streptococcus agalactiae strains or group B streptococci (GBS) are the leading cause of bacterial pneumoniae, sepsis and meningitis in neonates. GBS is also a major cause of bacteriemia in pregnant women. Colonization of the human rectovaginal tract with GBS is a risk factor associated with chorioamnionitis and transmission of the infection to the infant. Neonatal exposure to high concentrations of GBS, mainly during vaginal delivery, leads to colonisation of the lung airways and subsequent onset of severe diseases like pneumonia, sepsis and menigitis. GBS is present in the genitourinary tract of 10% to 40% of pregnant women, about 50% of the newborns of these mothers will be colonised during delivery and of these neonates, 1% to 2% present a severe invasive disease. The early-onset disease, appear in the neonates within 7 days of life and more than 90% occur within the first day of life. Fatal infection is associated commonly with fulminat and overwhelming early-onset disease. Maternal-intrapartum chemoprophylaxis is able to prevent the transmission of GBS to the newborn and to reduce the frequency and the severity of early onset disease. In many countries, in particular in US, several recommendations have been proposed to prevent the perinatal GBS infection. In this paper some recommendations to prevent GBS disease of the newborn, performed in collaboration with Italian Society of Perinatal Medicine, are presented. The most important problem in the prevention programme is the identification of the cases to treat, since it is not possible to give antibiotics to all the women. We combine two strategies for the identification of the women to be treated, one risk based and the other screening based. Intra-partum administration of ampicillin or penicillin is recommended for the women with one or more risk-factors (labour < 37 weeks of gestation, duration of ruptured membranes > = 18 hours, intrapartum temperature > = 38 degrees C, previous infant with invasive GBS disease, diabetes) and for women with collect vaginal and rectal swab for GBS culture at 36-38 weeks' gestation, positive for GBS. No treatment is required for the babies of women intrapartum treated or with negative culture performed near term. Treatment with ampicillin is necessary, only in the new-borns of women with incomplete or unknown results or not done cultures and in those born from mothers with positive cultures, but not intrapartum treated. Collection of swabs for GBS is recommended before antibiotic administration. If the culture is negative, we suggest to stop the antibiotic therapy, otherwise the treatment must be continuated for 5-7 days. In conclusion, a written protocol for prevention of GBS infection in new-born must be adopted in every delivery centre and one possible protocol is proposed in this paper.
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PMID:[Prevention of perinatal infection caused by group B beta-hemolytic streptococcus]. 1140 19


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