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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neonatal outcomes of 30 pregnancies that were complicated by premature and prolonged rupture of the membranes that had started in the second trimester of pregnancy, were reviewed. The neonatal mortality was 11 (36%), the main cause of death being pulmonary hypoplasia. Two infants died of sepsis, but these were the only proved episodes of maternal or fetal infection. Of the survivors, 27% developed compressive limb abnormalities, all of which responded to passive physiotherapy. Pulmonary hypoplasia was significantly associated with earlier onset of rupture of the membranes, and the absence of fetal breathing movements. Compressive limb abnormalities were significantly associated with longer periods of oligohydramnios. We conclude that premature rupture of the membranes, even with onset in the second trimester, may be associated with a favourable outcome and this may be predicted by the persistence of fetal breathing movements. We therefore, recommend expectant management of such pregnancies, but suggest elective delivery at 34 weeks to limit fetal exposure to uterine compression and minimise the risks of prematurity.
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PMID:Neonatal outcome after prolonged rupture of the membranes starting in the second trimester. 319 69

A retrospective study was carried out on 72 liveborn babies in whom perinatal infection was suspected. Twenty-nine of the 72 neonates were effectively infected. Analysis of intrapartum FHR recordings showed that tachycardia (base line FHR above 160 beats/min) during labor, occurred more often among infected babies (P less than 0.001). When fetal tachycardia is associated with meconium stained amniotic fluid (MSAF), the relative risk of fetal infection is 51 times as great as in babies without MSAF. Fetal tachycardia is not related to maternal fever nor to prematurity. It is not a sign of limited placental or amniotic fluid infection, but implies infection of the fetus itself. Since most infected babies displayed infectious diarrhea immediately at birth, it is suggested that MSAF may eventually be due to antenatal intestinal infection and intrauterine emission of infected stools. Although great caution is advocated for the management of labor in the presence of fetal tachycardia, MSAF should not be always regarded as a sign of acute fetal distress when antenatal infection of the fetus is suspected.
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PMID:Fetal tachycardia and meconium staining: a sign of fetal infection. 613 5

Preterm premature rupture of the membranes (PPROM) is diagnosed when rupture of the amniotic membranes occurs prior to the completion of the 36th week of gestation. PPROM accounts for 25% of all cases of premature rupture of the membranes and is responsible for 30%-40% of all preterm deliveries. In mothers diagnosed with PPROM without evidence of infection, active labor, or fetal compromise, the current standard of care is expectant management. The goal of expectant management is the prolongation of the pregnancy to increase fetal gestational age thus potentially decreasing the effects of prematurity. Expectant management consists of ongoing observation for signs and symptoms of infection, active labor, and/or nonreassuring fetal status. This article provides clinical nursing guidelines for the mother diagnosed with PPROM who is managed expectantly. Eight targeted areas for nursing assessment and intervention are described: preterm labor, side effects of tocolytic therapy, maternal/fetal infection, fetal compromise, side effects of extended bed rest, maternal stress, educational needs, and routine prenatal care.
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PMID:Nursing care of the patient with preterm premature rupture of membranes. 1512 69

Periventricular leukomalacia (PVL), the major lesion underlying cerebral palsy in survivors of prematurity, is characterized by focal periventricular necrosis and diffuse gliosis of immature cerebral white matter. Causal roles have been ascribed to hypoxiaischemia and maternal-fetal infection, leading to cytokine responses, inflammation, and oligodendrocyte cell death. Because interferon-gamma (IFN-gamma) is directly toxic to immature oligodendrocytes, we tested the hypothesis that it is expressed in PVL (N = 13) compared to age-adjusted controls (N = 31) using immunocytochemistry. In PVL, IFN-gamma immunopositive macrophages were clustered in necrotic foci, and IFN-gamma immunopositive reactive astrocytes were present throughout the surrounding white matter (WM). The difference in the number of IFN-gamma immunopositive glial cells/high power field (IFN-gamma score, Grades 0-3) between PVL cases (age-adjusted mean 2.59+/-0.25) and controls (age-adjusted mean 1.39+/-0.16) was significant (p<0.001). In the gliotic WM, the IFN-gamma score correlated with markers for lipid peroxidation, but not nitrative stress. A subset of premyelinating (04+) oligodendrocytes expressed IFN-gamma receptors in PVL and control cases, indicating that these cells are vulnerable to IFN-gamma toxicity via receptor-mediated interactions. In PVL, IFN-gamma produced by macrophages and reactive astrocytes may play a role in cytokine-induced toxicity to premyelinating oligodendrocytes as part of a cytokine response stimulated by ischemia and/or infection.
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PMID:Interferon-gamma expression in periventricular leukomalacia in the human brain. 1577 42

The authors examined 273 newborns weighing less than 1500 g. Their birth weight was very low (1001-1500 g) in 179 but extremely low (< 1000 g) in 94 newborns. Neurological damage was proved in 101 cases (36.99%). The probable reasons for intra- (peri-) ventricular and cerebral hemorrhages in these newborns were the following: respiratory distress syndrome (in 11 cases or 10.89%), mother-fetal infection (in 16 cases or 15.84%), and combination of asphyxia and infection (in 10 cases or 9.9%). The severe degree of prematurity (and immaturity) remained the only causative factor in the rest 64 premature newborns (63.37% of the cases). The results from the distribution of the neurological lesions according to the gestational age were also considered. Usage of monofactorial regression models detected statistically significant differences between asphyxia, infection and brain damage in the newborns of different gestational age.
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PMID:[Intranatal asphyxia, prematurity and congenital infection--their role for brain damage in very low birth weight newborns]. 1551 66

Periventricular leukomalacia (PVL) is the major substrate of cerebral palsy in survivors of prematurity. Its pathogenesis is complex and likely involves ischemia/reperfusion in the critically ill premature infant, with impaired regulation of cerebral blood flow, as well as inflammatory mechanisms associated with maternal and/or fetal infection. During the peak period of vulnerability for PVL, developing oligodendrocytes (OLs) predominate in the white matter. We hypothesize that free radical injury to the developing OLs underlies, in part, the pathogenesis of PVL and the hypomyelination seen in long-term survivors. In human PVL, free radical injury is supported by evidence of oxidative and nitrative stress with markers to lipid peroxidation and nitrotyrosine, respectively. Evidence in normal human cerebral white matter suggests an underlying vulnerability of the premature infant to free radical injury resulting from a developmental mismatch of antioxidant enzymes (AOE) and subsequent imbalance in oxidant metabolism. In vitro studies using rodent OLs suggest that maturational susceptibility to reactive oxygen species is dependent, not only on levels of individual AOE, but also on specific interactions between these enzymes. Rodent in vitro data further suggest 2 mechanisms of nitric oxide damage: one involving the direct effect of nitric oxide on OL mitochondrial integrity and function, and the other involving an activation of microglia and subsequent release of reactive nitrogen species. The latter mechanism, while important in rodent studies, remains to be determined in the pathogenesis of human PVL. These observations together expand our knowledge of the role that free radical injury plays in the pathogenesis of PVL, and may contribute to the eventual development of therapeutic strategies to alleviate the burden of oxidative and nitrative injury in the premature infant at risk for PVL.
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PMID:Oxidative and nitrative injury in periventricular leukomalacia: a review. 1619 89

Perinatal brain injury in survivors of premature birth has a unique and unexplained predilection for periventricular cerebral white matter. Periventricular white-matter injury (PWMI) is now the most common cause of brain injury in preterm infants and the leading cause of chronic neurological morbidity. The spectrum of chronic PWMI includes focal cystic necrotic lesions (periventricular leukomalacia; PVL) and diffuses myelination disturbances. Recent neuroimaging studies support that the incidence of PVL is declining, whereas focal or diffuse noncystic injury is emerging as the predominant lesion. Factors that predispose to PVL during prematurity include hypoxia, ischemia, and maternal-fetal infection. In a significant number of infants, PWMI appears to be initiated by perturbations in cerebral blood flow that reflect anatomic and physiological immaturity of the vasculature. Ischemic cerebral white matter is susceptible to pronounced free radical-mediated injury that particularly targets immature stages of the oligodendrocyte lineage. Emerging experimental data supports that pronounced ischemia in the periventricular white matter is necessary, but not sufficient to generate PWMI. The developmental predilection for PWMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible oligodendrocyte progenitors. Injury to oligodendrocyte progenitors may contribute to the pathogenesis of PWMI by disrupting the maturation of myelin-forming oligodendrocytes. Chemical mediators that may contribute to white-matter injury include reactive oxygen species glutamate, cytokines, and adenosine. As our understanding of the pathogenesis of PWMI improves, it is anticipated that new strategies for directly preventing brain injury in premature infants will develop.
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PMID:Perinatal white matter injury: the changing spectrum of pathology and emerging insights into pathogenetic mechanisms. 1680 10

Early premature rapture of the membranes (PROM) during pregnancy is associated with a high risk of perinatal morbidity and mortality. Early PROM impairs lung structures and function through 3 mechanisms : 1) oligo-hydramnios ; 2) fetal inflammatory syndrome ; and 3) prematurity. Thus, the related causes of respiratory failure at birth after PROM are: hyaline membrane disease, persistent pulmonary hypertension induced by impaired endothelial function and/or lung hypoplasia, materno-fetal infection, and bronchopulmonary dysplasia resulting at least in part from the fetal inflammatory syndrome. Severity of the respiratory morbidity is largely unpredictable. Even if gestational age at PROM is considered as a prognostic factor, survival without morbidity exist after PROM as early as 18 weeks GA. Better knowledge of the pathophysiology improved the outcome of the preterm infants born after early PROM. Optimal management of the respiratory failure including minimizing barotrauma is required to prevent from bronchopulmonary dysplasia.
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PMID:[Consequences of premature rupture of the membranes in the perinatal lung]. 1793 57

Congenital syphilis is still a cause of perinatal morbidity and mortality. Untreated maternal infection leads to adverse pregnancy outcomes, including early fetal loss, stillbirth, prematurity, low birth weight, neonatal and infant death, and congenital disease among newborns. Clinical manifestations of congenital syphilis are influenced by gestational age, stage of maternal syphilis, maternal treatment, and immunological response of the fetus. It has been traditionally classified in early congenital syphilis and late congenital syphilis. Diagnosis of maternal infection is based on clinical findings, serological tests, and direct identification of treponemes in clinical specimens. Adequate treatment of maternal infection is effective for preventing maternal transmission to the fetus and for treating fetal infection. Prenatal diagnosis of congenital syphilis includes noninvasive and invasive diagnosis. Serological screening during pregnancy and during preconception period should be performed to reduce the incidence of congenital syphilis.
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PMID:Syphilis Infection during pregnancy: fetal risks and clinical management. 2282 47

Injury to the preterm brain has a particular predilection for cerebral white matter. White matter injury (WMI) is the most common cause of brain injury in preterm infants and a major cause of chronic neurological morbidity including cerebral palsy. Factors that predispose to WMI include cerebral oxygenation disturbances and maternal-fetal infection. During the acute phase of WMI, pronounced oxidative damage occurs that targets late oligodendrocyte progenitors (pre-OLs). The developmental predilection for WMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible pre-OLs that are vulnerable to a variety of chemical mediators including reactive oxygen species, glutamate, cytokines, and adenosine. During the chronic phase of WMI, the white matter displays abberant regeneration and repair responses. Early OL progenitors respond to WMI with a rapid robust proliferative response that results in a several fold regeneration of pre-OLs that fail to terminally differentiate along their normal developmental time course. Pre-OL maturation arrest appears to be related in part to inhibitory factors that derive from reactive astrocytes in chronic lesions. Recent high field magnetic resonance imaging (MRI) data support that three distinct forms of chronic WMI exist, each of which displays unique MRI and histopathological features. These findings suggest the possibility that therapies directed at myelin regeneration and repair could be initiated early after WMI and monitored over time. These new mechanisms of acute and chronic WMI provide access to a variety of new strategies to prevent or promote repair of WMI in premature infants.
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PMID:Pathophysiology of glia in perinatal white matter injury. 2468 30


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