Risk Factor For Neonatal Morbidity Research Articles

150 Incidence of and Risk Factors for Neonatal Morbidity After Active Perinatal Care: Extremely Preterm Infants Study in Sweden (Express)

Aims: To determine the incidence of neonatal morbidity in extremely preterm infants and to identify associated risk factors. Methods: Population based study of infants born before 27 gestational weeks and admitted for neonatal intensive care in Sweden during 2004-2007. Results: Of 638 admitted infants, 141 died. Among these, life support was withdrawn in 55 infants because of anticipation of poor long-term outcome. Of 497 surviving infants, 10% developed severe intraventricular haemorrhage (IVH), 5.7% cystic periventricular leucomalacia (cPVL), 41% septicaemia and 5.8% necrotising enterocolitis (NEC); 61% had patent ductus arteriosus (PDA) and 34% developed retinopathy of prematurity (ROP) stage ≥ 3. Eighty-five per cent needed mechanical ventilation and 25% developed severe bronchopulmonary dysplasia (BPD). Forty-seven per cent survived to one year of age without any severe IVH, cPVL, severe ROP, severe BPD or NEC. Tocolysis increased and prolonged mechanical ventilation decreased the chances of survival without these morbidities. Maternal smoking and higher gestational duration were associated with lower risk of severe ROP, whereas PDA and poor growth increased this risk. Conclusions: Half of the infants surviving extremely preterm birth suffered from severe neonatal morbidities. Studies on how to reduce these morbidities and on the long-term health of survivors are warranted.

Incidence of and risk factors for neonatal morbidity after active perinatal care: extremely preterm infants study in Sweden (EXPRESS)

The aim of this study was to determine the incidence of neonatal morbidity in extremely preterm infants and to identify associated risk factors. Population based study of infants born before 27 gestational weeks and admitted for neonatal intensive care in Sweden during 2004-2007. Of 638 admitted infants, 141 died. Among these, life support was withdrawn in 55 infants because of anticipation of poor long-term outcome. Of 497 surviving infants, 10% developed severe intraventricular haemorrhage (IVH), 5.7% cystic periventricular leucomalacia (cPVL), 41% septicaemia and 5.8% necrotizing enterocolitis (NEC); 61% had patent ductus arteriosus (PDA) and 34% developed retinopathy of prematurity (ROP) stage > or =3. Eighty-five per cent needed mechanical ventilation and 25% developed severe bronchopulmonary dysplasia (BPD). Forty-seven per cent survived to one year of age without any severe IVH, cPVL, severe ROP, severe BPD or NEC. Tocolysis increased and prolonged mechanical ventilation decreased the chances of survival without these morbidities. Maternal smoking and higher gestational duration were associated with lower risk of severe ROP, whereas PDA and poor growth increased this risk. Half of the infants surviving extremely preterm birth suffered from severe neonatal morbidities. Studies on how to reduce these morbidities and on the long-term health of survivors are warranted.

Aldosterone levels are inversely correlated to superoxide dismutase acitivity in the low birth weight newborn

Low birth weight (LBW), is a risk factor for neonatal morbidity, mortality, and increased risk for cardiovascular (CV) disease. Epidemiological and experimental studies report increased aldosterone levels and oxidative stress as contributors to CV risk. Thus, the purpose of this study was to determine whether alterations in plasma aldosterone and activity of superoxide dismutase (SOD), an antioxidant, are associated to LBW. In a rodent model of pre‐term LBW induced by placental insufficiency Aldosterone levels were increased in LBW offspring (48±13 vs. 8±1 pg/ml/g, P<0.05; LBW vs. NBW, respectively). In a cohort of 39 newborn delivered at the University of Mississippi, pre‐term and term LBW newborns show increased aldosterone levels (354 ±110 vs. 197±11 pg/ml/k P<0.05; LBW vs. NBW, respectively); and reduced SOD activity (2±0.3 vs. 10±1 U/ml/k, P<0.05; LBW vs. NBW, respectively). A negative correlation was observed between aldosterone and birth weight in the animal model of LBW (Spearman r −0.9 P<0.05); and in human LBW newborns (Spearman r −0.4 P < 0.05). A negative correlation was observed between aldosterone levels and SOD activity in human LBW newborns (Spearman r −0.4 P < 0.05); and a positive correlation between SOD activity and birth weight (Spearman r −0.9 P < 0.05). Thus, studies from human and an animal model suggest parallel findings related to increased aldosterone and oxidative stress in LBW.

A Method on Assessing Complication-Base Risk Factors for Neonatal Morbidity: Application for Pattani Hospital Delivery

We investigated risk factors for neonatal morbidity based on a database of 19,268 singleton maternal deliveries atPattani Hospital during the period from 1 October 1996 to 30 September 2005 inclusive. This database includesdemographics of the mother and delivery outcomes including birth weight, one- and five-minute Apgar scores, and atmost one complication selected from a list of 62 by the deliverer. In our study the neonatal risk associated with acomplication was defined by averaging the results given by 11 obstetricians who independently scored eachcomplication on a scale from 0 to 9 (highest risk to baby). Using logistic regression to adjust for demographic andpregnancy-history factors, we found risk that Muslim women have higher neonatal morbidity risks, particularly thoseassociated with severe pregnancy-induced hypertension, eclampsia and thick mecomium stain.

Mitochondrial DNA variant A4917G, smoking and spontaneous preterm birth

Spontaneous preterm birth (PTB; <37 weeks gestation) is a major risk factor for neonatal morbidity and mortality. The exact cause of PTB is unknown but oxidative stress may play an important role. Genetic studies have recently begun to elucidate the role of genetic variation in PTB but these studies have overlooked the mitochondrial genome/gene(s) as a plausible PTB candidate. In the present study, we sought to document association between nonsynonymous mitochondrial DNA (mtDNA) variants A4917G, G10398A and T4216C and PTB. We performed a case (PTB; <36 weeks gestation)-control (normal term) analysis of these mtDNA markers and examined their potential interaction with smoking in PTB. A sample of 422 pregnant Caucasian women (220 preterm and 202 terms) was examined for association. Haplogroup T marker A4917G was identified as a possible candidate for association with PTB after adjusting for smoking (OR=1.99 [95% CI 0.93–4.24]) as was T4216C (OR=1.63 [95% CI 0.93–2.83]). No significant multi-locus interactions or interactions with other environmental variables were observed. Our data, although preliminary, support the hypothesis that mitochondrial genome polymorphisms may play a significant role in PTB through an interaction with smoking.

Preterm premature rupture of membranes is not an independent risk factor for neonatal morbidity

To evaluate the risk factors for development of neonatal morbidity in cases of preterm premature rupture of membranes (PPROM). The study population consisted of 2326 singleton preterm births occurring between 1994 and 1997 at Soroka University Medical Center. The neonatal morbidity included respiratory distress syndrome, intraventricular hemorrhage (grade III-IV), necrotizing enterocolitis, periventricular leukomalacia, bronchopulmonary dysplasia, neonatal pneumonia and sepsis. A cross-sectional study was designed to compare neonatal morbidity between two groups: the study group consisted of patients with PPROM (n = 376) and the comparison group of patients without PPROM (n = 1950). The prevalence of the neonatal morbidity associated with PPROM was 13.0% (49/376). There was no statistically significant difference in neonatal morbidity rates between the PPROM group and the group with intact membranes in any of the birth-weight groups (Mantel-Haenszel weighted odds ratio 1.20; 95% CI 0.80-1.20), or gestational-age groups (Mantel-Haenszel weighted odds ratio 1.03; 95% CI 0.79-1.55). There was no statistically significant difference in neonatal morbidity between patients with PPROM and those with intact membranes according to clinical chorioamnionitis. Congenital anomalies did not influence the neonatal morbidity when comparing patients with and without PPROM (44.4% vs. 32.8%, respectively; p = 0.23). PPROM was not an independent risk factor for neonatal morbidity in preterm births. Neonatal morbidity was affected mainly by prematurity itself, rather than by the occurrence of PPROM.

Preterm premature rupture of membranes is not an independent risk factor for neonatal morbidity

Preterm premature rupture of membranes is not an independent risk factor for neonatal morbidity

Congenital anomalies are an independent risk factor for neonatal morbidity and perinatal mortality in preterm birth

Objective: To determine whether congenital anomalies are associated with a high rate of neonatal morbidity in preterm birth. Study design: 312 singletons (22–36 wk) with congenital anomalies that were delivered preterm were compared with a random sample of 936 preterm singleton without congenital anomalies. Data was obtained using the computerized birth discharge records. Statistical analysis included univariate and multivariate logistic regression analyses. Results: Three thousand five hundred and seventy-eight (3578) women with preterm births met the inclusion criteria (singleton with prenatal care). The prevalence of congenital anomalies in the study population was 8.7% (312/3578). Gestational age at delivery was significantly lower in the congenital anomaly group compared with the control (32.0±3.7 SD vs. 34.4±2.7 SD; p<0.001). The following pregnancy complications were higher in the group with congenital anomalies than in those without anomalies: severe pregnancy induced hypertension (PIH), hydramnions, oligohydramnion, intrauterine growth restriction (IUGR), fetal distress, cesarean section, malpresentation and mal position, abruption placenta, meconium stained amniotic fluid, 1 min Apgar score (<2), 5 min Apgar score (<7). Perinatal mortality rates in 28–32 wk and 33–36 wk were significantly higher in the group with congenital anomalies than in the control group. Neonatal morbidity data (necrotizing enterocolitis, respiratory distress syndrome, bronchopulmonary dysplasia, intraventricular hemorrhage, and sepsis) was available for 909 neonates (239 with congenital anomalies and 670 without congenital anomalies). After adjusting for gestational age, the presence of congenital anomalies remained strongly associated with neonatal morbidity (having one or more of the above mentioned conditions) (adjusted OR: 5.3, 95% CI 3.4–9.2). When adjusting for other confounding variables, congenital anomalies were strongly associated with neonatal morbidity (OR: 6.44, 95% CI 3.94–10.51), and perinatal mortality (OR: 3.08, 95% CI 2.04–4.65). In terms of attributable fraction in our population of preterm births, the proportion of neonatal morbidity and the proportion of perinatal mortality attributable to congenital malformation is 32% and 15%, respectively. Conclusion: Congenital anomalies in preterm birth are associated with a higher rate of pregnancy complications and are an independent risk factor for neonatal morbidity and perinatal mortality.

Zur Vorhersagbarkeit einer schweren intrapartalen Azidose (NapH &lt; 7,00) bei reifen Neugeborenen und deren Auswirkungen auf die frühkindliche Entwicklung

Fragestellung: Die peripartale Asphyxie bzw. schwere Azidose gilt als bedeutender Risikofaktor neonataler Morbidität und späterer neurologischer Schäden. Trotzdem sind wichtige Fragestellungen im Zusammenhang mit dem Krankheitsbild bisher relativ wenig und nur an kleinen Kollektiven untersucht. In der vorliegenden Arbeit wird deshalb folgenden Fragen nachgegangen: 1. Gibt es Schwangerschaftsrisiken, deren Beobachtung das Auftreten einer schweren fetalen Azidose unter der Geburt relativ wahrscheinlich macht? 2. Lassen sich prädiktive Faktoren für das Auftreten neurologischer Auffälligkeiten im Alter von 18 Monaten bei Kindern mit schwerer Azidose unter der Geburt nachweisen?

Can group B streptococci cause symptomatic vaginitis?

Background Maternal cervicovaginal colonization with Lancefield group B streptococci (GBS) is an important risk factor for neonatal morbidity and mortality. About 15% of women are carriers of GBS. Usually, they are asymptomatic. Cases We describe two patients with symptomatic vaginitis for which no apparent cause was found. Both patients were heavily colonized with GBS. After antibiotic treatment, both became asymptomatic and culture negative, but after recolonization with GBS, symptoms resumed. This phenomenon was repeatedly observed. After emergence of resistance to antibiotics, local application of chlorhexidine appeared to be the only useful treatment. Conclusion We hypothesize that GBS-vaginitis may be a possible disease entity. Although at present it is not clear why some patients become symptomatic, we speculate that the immunologic response is somehow selectively hampered in such patients. Infect. Dis. Obstet. Gynecol. 7:206–209, 1999. © 1999 Wiley-Liss, Inc.

Can Group B Streptococci Cause Symptomatic Vaginitis?

Background Maternal cervicovaginal colonization with Lancefield group B streptococci (GBS) is an important risk factor for neonatal morbidity and mortality. About 15% of women are carriers of GBS. Usually, they are asymptomatic. Cases We describe two patients with symptomatic vaginitis for which no apparent cause was found. Both patients were heavily colonized with GBS. After antibiotic treatment, both became asymptomatic and culture negative, but after recolonization with GBS, symptoms resumed. This phenomenon was repeatedly observed. After emergence of resistance to antibiotics, local application of chlorhexidine appeared to be the only useful treatment. Conclusion We hypothesize that GBS-vaginitis may be a possible disease entity. Although at present it is not clear why some patients become symptomatic, we speculate that the immunologic response is somehow selectively hampered in such patients. Infect. Dis. Obstet. Gynecol. 7:206–209, 1999. © 1999 Wiley-Liss, Inc.

THROMBOPOIETIN (TPO) SIGNIFICANTLY INCREASES NEONATAL (NB) RAT MYELOPOIESIS AND THROMBOPOIESIS: THE ADDITION OF RHG-CSF IS ADDITIVE RELATIVE TO MYELOPOIESIS BUT ABROGATES THE EFFECT OF TPO ON PLATELET PRODUCTION

Immaturities in NB hematopoiesis include defects in both myelopoiesis and thrombopoiesis. 25% of babies admitted to the NICU experience thrombocytopenia(Castle et al, J Peds 108:1986), and it is a risk factor for neonatal morbidity and mortality (Andrews et al, J Peds 110:1987). TPO and rhG-CSF have been shown to be potent stimulators of thrombopoiesis and myelopoiesis, respectively. (Blood 86:(10), 1995) The present study investigates the effects of TPO alone and in combination with rhG-CSF in modulating NB rat hematopoiesis. NB Sprague Dawley rats (24-36 hrs, n=16/tx) were given SC TPO (10 μg/kg, (provided by Genentech), rhG-CSF (100μg/kg) (provided by Amgen), TPO + rhG-CSF (same doses) or PBS/HSA × 14 days. CBC and PLT were obtained on alternate days from d 0-20. Random animals (n=3/tx) were sacrificed on d 14 for bone marrow CFU-GM, MEG and proliferation studies. TPO alone or + rhG-CSF had no effect on HCT or RBC. However, significant increases in ANC (/mm3) were seen with TPO alone vs PBS/HSA beginning on d 2 (1386 ± 101.3 vs 1057.0 ± 68.6, p< 0.05), d 8 (1032.8 ± 96.3 vs 509.0 ± 62.7, p< 0.05), d 14 (1490.4 ± 233.6 vs 835.2 ± 72.3, p< 0.05). A significant increase in ANC (/mm3)was also seen with TPO + rhG-CSF vs rhG-CSF alone beginning on d 4 (2486.0 ± 256.1 vs 1714.4 ± 342.8, p< 0.01), d 8 (2207.2 ± 218.2 vs 1476.0 ± 179.1, p< 0.001), d 14(2124.0 ± 150.2 vs 1175.2 ± 169.2, p< 0.01). Significant increases in PLT (K/mm3) were seen with TPO alone d 4-18 with no effect seen with rhG-CSF alone. However, a significant abrogation of PLT was seen with TPO + rhG-CSF vs TPO alone beginning on d 8 (1674.4 ± 235.5 vs 2188 ± 148.1, p < 0.05), d 14 (2466.0 ± 330.8 vs 2980.8± 100.9, p < 0.05). Significant increases were seen in CFU-Meg and GM with TPO alone & TPO+ rhG-CSF vs C (colonies/2×105c) (MEG: 23.3 ± 1.0, 20.33 ± 3.8 vs 6.0 ± 1.0, p< 0.05) (GM: 144.0 ± 4.51, 106.7 ± 15.4 vs 84.3 ± 6.5, p< 0.01). Megakaryocyte proliferation was increased in TPO alone & TPO + rhG-CSF vs PBS/HSA (%C) (250.1 ± 44.3 & 246.8±21.1 vs 100, p< 0.05). These data suggests that TPO induces myeloid and megakaryocytic progenitor cells, and increases neutrophil and platelet production in the NB rat. However, the addition of rhG-CSF abrogates the TPO effect on platelet production. Further studies are required to determine the clinical implications of the combination of TPO + rhG-CSF in the treatment of neonatal thrombocytopenia and neutropenia.

α1-PROTEINASE INHIBITOR PHENOTYPES IN PRETERM NEWBORNS

α- proteinase inhibitor (α1 PI) phenotypes were determined by isoelectric focusing in polyacrylamide gel in 305 preterm newborns and 109 their mothers, special attention being paid to the presence of Z allele responsible for deficiency of this protein. The newborns were divided in four groups according to anthropometric data: 1) appropriate for gestational age (AGA), 2) small for birth weight (SBW), 3) small for birth length (SBL), and 4) small for gestational age (SGA). Prevalence of Z allele (2,95%) in the total group of preterm newborns did not differ significantly from its prevalence in population study (1,7396). Z allele was more prevalent (5,4596) in preterm newborns with infections, birth defects (5,88%) and with combination of these pathological conditions (6,14%). Especially high prevalence (15%) of Z allele was encountered in SBW newborns with infections. We suggest that prematurity and α1PI deficiency (phenotypes PI MZ and PI ZZ) are high risk factors for neonatal morbidity.

Vaginal colonization with Group B beta-hemolytic streptococcus as a risk factor for post-cesarean section febrile morbidity

Vaginal colonization of mothers with Group 8 beta-hemolytic streptococcus (GBS) has been recognized as a risk factor for neonatal morbidity. The relationship of G8S colonization to risks for the mother who undergoes cesarean section has not been defined. In this study, we found that, among patients who underwent cesarean section, the 19% of them who were colonized with GBS had a higher incidence of standard fever (66.6% vs. 30.5%), clinical diagnosis of endomyometritis (61.1% vs. 12.5%); and use of antibiotics (61.1% vs. 26.3%) in relationship to a significantly increased frequency of premature rupture of the membranes (50.0% vs. 14.8%). Reasons for the association between vaginal colonization and increased morbidity are discussed.