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PubMed1995

High prevalence of muscular ventricular septal defect in neonates.

OBJECTIVES: This study sought to use echocardiography to evaluate the prevalence of muscular ventricular septal defect in neonates. BACKGROUND: Ventricular septal defect is usually asymptomatic and closes spontaneously. An increase in its prevalence has been noted recently. One reason is the improved detection of small defects, especially with the increased used of echocardiography. Therefore, one would expect a higher prevalence in neonates on the basis of echocardiographic screening. METHODS: Color Doppler echocardiography was performed in 1,053 consecutive neonates 6 to 170 h old at Western Galilee Hospital, Israel. Data on the neonates, parents and family were obtained to analyze the influencing factors. The identified patients were followed up for 1 to 10 months or until ventricular septal defect closure. RESULTS: Muscular ventricular septal defect was found in 56 (25 male, 31 female) of the 1,053 neonates, a prevalence of 53.2/1,000 live births. All neonates were asymptomatic. Six had a systolic murmur. Electrocardiographic findings were normal in 44 (97.8%) of 45 neonates followed up, and left ventricular hypertrophy occurred in 1 (2.2%). By echocardiography, 50 ventricular septal defects (89.3%) were single and 6 (10.7%) were multiple. The defects (range 1 to 5 mm in diameter, mean [+/- SD] 2.3 +/- 0.8) occurred anywhere along the muscular septum; 43 (76.8%) were detectable only on color Doppler imaging. The left atrium and left ventricle were mildly dilated. Of 45 neonates who were followed up for 6 to 10 months or until closure of the defects, 40 (88.9%) had defects that closed spontaneously. The risk of ventricular septal defect was not significantly associated with gestational age, birth weight, birth order, maternal age, diabetes, smoking, exposure to drugs or infection, paternal age, familial congenital heart disease, religion or consanguinity. CONCLUSIONS: There is a prevalence of muscular ventricular septal defect in neonates of 53.2/1,000 live births. The patients were asymptomatic, and 88.9% had defects that closed spontaneously within 1 to 10 months. These defects may be caused by environmental factors. In many cases, muscular ventricular septal defect may also result from delayed physiologic development.

Echocardiography, Doppler, Color↗
PubMed1991

Membrane-bound hemoglobin as a marker of oxidative injury in adult and neonatal red blood cells.

A comparative study of the effect of hydrogen peroxide on adult and neonatal red blood cell (RBC) membrane protein composition has been carried out. The results indicate that (a) the native neonatal RBC membranes contain higher levels of membrane-bound hemoglobin (MBHb) than the adult RBC membranes. (b) The content of MBHb increases when RBCs are incubated with increasing concentrations of hydrogen peroxide (H2O2), more so in neonatal than in adult RBCs; however, neonatal RBC membrane proteins are less susceptible to H2O2 oxidation than adult ones. This could be attributed to the fact that Hb F, which is more susceptible to oxidation than Hb A, adds to the reduction potential of neonatal RBC (in which it is present in large amounts) and partially protects neonatal membrane proteins against oxidant stress compared to Hb A in adult RBC. (c) In both neonatal and adult RBCs, Spectrin 1 is relatively more susceptible to oxidant stress than spectrin 2, and spectrins in adult RBC are more labile for peroxidation than the spectrins in neonatal RBC. (d) Based on electrophoretic studies with and without reduction of membranes with mercaptoethanol, we have classified two types of MBHb: Type I is adsorbed to membrane by noncovalent interactions and Type II MBHb is chemically crosslinked to membrane components by disulfide bridges; the content of both these types increases when RBCs are incubated with increasing concentrations of H2O2. (e) Band 6 protein is present in higher amounts in neonatal than in adult RBC membranes. (f) Since the total content of MBHb increases linearly with the level of oxidant stress, we suggest that it could be used as a marker for oxygen radical-induced injury to tissues.

Adult↗
PubMedDate not supplied

Diazepam and caffeine administration during the first week of life: changes in neonatal and adolescent behavior.

The male offspring of hooded Lister rats were fostered at birth into 23 experimental litters. One pup in each litter was allocated to each of the following treatment groups: vehicle control; caffeine (15 or 30 mg/kg); diazepam (10 mg/kg, alone or plus caffeine 15 or 30 mg/kg). Pups were given daily injections on neonatal days 1-7 and were observed for 15 min following each injection. Diazepam significantly increased paddling and forward walking, particularly on days 5 and 7; caffeine also increased these behaviors, but less markedly. Diazepam increased the incidence of clonic jerks, particularly on day 7 and increased the spontaneous loss of righting reflex. The pups were then left undisturbed until weaning at day 21 and testing from days 35-42. There were no lasting effects of the neonatal treatments in two tests of anxiety, or in passive avoidance performance. Rats that had been treated neonatally with diazepam had significantly lower motor activity scores and reared less in the holeboard than did controls, and neonatal treatment with caffeine also resulted in lower motor activity scores. Neonatal treatment with caffeine made rats more aggressive (increased kicking and pushing) when they were intruding into another rat's territory. Neonatal treatment with diazepam increased aggression in resident rats, and this was counteracted by neonatal treatment with caffeine. Neonatal caffeine treatment enhanced rats' unconditioned preference for the black chamber in a black-white preference test and neonatal diazepam treatment reduced it.

Aggression↗
PubMed2006

Part 1: a matter of size: evaluating the growth-restricted neonate.

The relative size of a neonate impacts many aspects of prenatal and postnatal surveillance and care. The designations of appropriate for gestational age, small-for-gestational age, intrauterine growth restriction, and large-for-gestational age are systematic categorizations used to assess and monitor growth throughout pregnancy and delivery. Each abnormal growth descriptor aids in anticipating neonatal needs after birth because each has the potential for complications related to feeding, glucose utilization, short- and long-term growth, and development. Maternal risk factors that impact the neonate's size-related can have immediate implications in the delivery room as well as significant effects postnatally. Caring for neonates at risk for size complications requires knowledge based on prenatal and postnatal complications. Neonates must be carefully measured and plotted on growth charts to confirm a visual assessment of size. Each growth complication requires individual attention to detail and careful planning to maximize adequate postnatal growth and nutrition. Size matters when it comes to the health and welfare of neonates. Anticipatory guidance can improve outcomes in the neonate at risk for failure to thrive from size complications at birth. Part 1 of this article provides an overview of the size classifications and a discussion of clinical factors that are associated with or contribute to small-for-gestational age births. Once the neonate's size for gestational age is calculated, a focused physical assessment is described along with nursing care and prognostic implications. Part 2 will focus on the physical assessment, nursing care, prognosis, and complications associated with large-for-gestational-age neonates.

Anthropometry↗
PubMed2004

Intrauterine growth restriction increases morbidity and mortality among premature neonates.

OBJECTIVE: Intrauterine growth restriction (IUGR) is an important reason for premature delivery and has been reported to be associated with increased mortality, but in some studies paradoxically, improved morbidities. Data on neonatal outcomes for infants with IUGR at each viable gestational age at birth from large numbers of deliveries are lacking. More particularly, data on perinatal outcome related to an antenatal diagnosis of IUGR compared with a neonatal diagnosis are particularly deficient. Therefore, by using a large contemporary database, we evaluated the outcomes of neonates with IUGR and the gestational age-specific associations between growth restriction, morbidity, and mortality. STUDY DESIGN: With the use of a database formed from a computer-assisted tool that generates clinical progress notes and discharge summaries on neonatal intensive care unit (NICU) admissions, we reviewed data on neonates discharged from 124 NICUs between January 1, 1997, and December 31, 2001. We evaluated singleton, inborn neonates who delivered between 23 and 34 weeks, excluding major congenital anomalies. We compared 3 measures of IUGR: antenatally diagnosed IUGR; a birth weight below the 10th percentile (small for gestational age [SGA]), and newborn infants with either or both of these diagnoses against a control group of gestational age-matched infants meeting none of these criteria whose birth weights were no greater than the 90th percentile. RESULTS: Our sample included 29,916 prematurely born neonates; 1,451 (4.8%) with IUGR, 2,936 (9.8%) who were SGA, and 3,708 (12.3%) had at least 1 of these 2 markers. There were 22,798 (76%) normally grown control neonates. Within each gestational age group from 25 to 32 weeks, each marker of IUGR was associated with increased mortality, necrotizing enterocolitis, need for respiratory support at 28 days of age, and retinopathy of the premature. When corrected for gestational age, exposure to antenatal steroids, gender, and mode of delivery, these associations remained significant. CONCLUSION: IUGR remains a serious problem that is associated with increased morbidity and mortality among prematurely born neonates, regardless of the definition used or whether the diagnosis is made antenatally or after birth. These results are important for obstetric counseling and decision making and for the anticipation and treatment of premature newborn infants.

Female↗
PubMed2005

Neonates with aortic coarctation and cardiogenic shock: presentation and outcomes.

BACKGROUND: Some neonates with coarctation of the aorta (COA) present with cardiogenic shock and secondary end-organ injury. The management of this subgroup imposes unique challenges. We review our perioperative strategy and outcomes for neonates with COA who presented with cardiogenic shock. METHODS: Neonates (younger than 30 days) with isolated COA or COA with aortic arch hypoplasia were identified. Retrospective review was performed to identify and characterize patients who presented with cardiogenic shock, defined as impaired left ventricular (LV) or right ventricular (RV) systolic function, or both, respiratory failure requiring tracheal intubation, and metabolic acidosis. RESULTS: Thirteen neonates presented in cardiogenic shock and underwent surgical repair. No patients required catheter or surgical reintervention for recoarctation. There were no deaths at a mean follow-up of 54 months. Group I neonates (isolated COA, n = 7) underwent end-to-end anastomosis through left thoracotomy. The mean age and pH at presentation were 9 (+/-1.1) days and 7.07 (+/-0.21), respectively. The mean preoperative and postoperative LV myocardial performance indices (MPI) were 0.81 (+/-0.22) and 0.37 (+/-0.16), respectively (p = 0.002). Group II neonates (COA with arch hypoplasia +/- ventricular septal defect, n = 6) underwent aortic arch advancement and ventricular septal defect closure through median sternotomy. The mean time from diagnosis to surgery in group II was 5.5 (+/-1.9) days versus 2.4 (+/-1.5) days in group 1 (p = 0.01). The mean age and pH at presentation were 11.8 (+/-9.3) days and 7.02 (+/-0.21), respectively. The mean preoperative and postoperative LV MPI were 0.46 (+/-0.13) and 0.35 (+/-0.11), respectively (p = 0.02). The total hospital length of stay in group II patients was 18 (+/-6.23) days versus 11.3 (+/-5. 7) days in group I (p = 0.04). CONCLUSIONS: Timely intervention with a strategy individualized to the patient anatomy can be performed with excellent outcomes in neonates with COA and cardiogenic shock. Neonates with isolated COA had worse preoperative LV MPI, which reflects more significant global left ventricular systolic dysfunction in this subgroup. The elapsed time from diagnosis to surgery was decreased in neonates with isolated COA.

Aortic Coarctation↗
PubMed2005

Studies in hemolysis in glucose-6-phosphate dehydrogenase-deficient African American neonates.

BACKGROUND: The role of hemolysis in the mechanism and prediction of hyperbilirubinemia was contrasted between glucose-6-phosphate dehydrogenase (G-6-PD)-deficient and -normal African American neonates. METHODS: Corrected end tidal carbon monoxide (ETCOc) values from the subset of male neonates born to non-smoking African American mothers, drawn from a previously published study, were analyzed. The relationship between ETCOc and bilirubin values, the latter represented as percentiles on the hour of life specific bilirubin nomogram, was determined. Hyperbilirubinemia was defined as any bilirubin value > or =95th percentile for hour of life. RESULTS: 18.6% of 59 G-6-PD-deficient neonates developed hyperbilirubinemia, compared with 7.5% of 362 controls (relative risk 2.50, 95% confidence interval 1.31 to 4.76). As reported, ETCOc values (median, interquartile range) were significantly higher among G-6-PD-deficient neonates than controls (2.4 [2.0-2.9] vs. 2.1 [1.7-2.5] ppm, p<0.001. However, higher ETCOc values were limited to those G-6-PD-deficient neonates with lower bilirubin percentiles: among those whose bilirubin value did not exceed the 95th percentile ETCOc was 2.30 [2.00-2.85] vs. 2.00 [1.70-2.40] ppm in controls, p=0.001. In contrast, among the hyperbilirubinemic neonates ETCOc values were similar between G-6-PD-deficient neonates and controls: 2.7 [2.03-3.33] vs. 2.6 [2.33-3.45] ppm, p=0.9. In the G-6-PD-deficient neonates ETCOc > or =75th percentile contributed no additional predictive value for hyperbilirubinemia (likelihood ratio 1.8). CONCLUSIONS: G-6-PD-deficient African American neonates have increased hemolysis and increased rate of hyperbilirubinemia, but the hemolysis is neither a predominant factor in the pathogenesis of hyperbilirubinemia nor is it predictive of hyperbilirubinemia, over and above the already increased risk conferred by G-6-PD deficiency.

Black People↗
PubMed2005

Glucose-6-phosphate dehydrogenase activity in term and near-term, male African American neonates.

BACKGROUND: We determined values for glucose-6-phosphate dehydrogenase (G-6-PD) activity in African American neonates. METHODS: G-6-PD activity was measured on umbilical cord blood from term and near-term healthy, male neonates. Neonates were stratified according to the number of neonates for each numerical unit of G-6-PD activity. Corrected end tidal carbon monoxide (ETCOc), a non-invasive index of hemolysis, was performed on each neonate. At least one predischarge transcutaneous bilirubin determination was performed. RESULTS: Five hundred neonates were studied. Two subpopulations were apparent, with no overlap between the subgroups. Mean value for the 64 (12.8%) infants with the lower values (G-6-PD deficient) was 2.7+/-1.1 U/g Hb, range 0.4-6.6 U/g Hb, while that for the 436 neonates with the higher values (G-6-PD normal) was 21.8+/-2.9 U/g Hb, range 14.5-33.8 U/g Hb. No significant differences in activity were noted between those neonates <37 weeks gestational age and those >37 weeks. Enzyme activity in the lower range in both groups was not related to the development of hyperbilirubinemia. G-6-PD enzyme activity did not correlate with ETCOc values either for the entire cohort or for the individual subsets. CONCLUSIONS: G-6-PD-deficient neonates formed a separate subgroup from those with normal enzyme activity. The data supplied should facilitate interpretation of G-6-PD test results.

Black or African American↗
PubMed2005

Early life host-bacteria relations and development: long-term individual differences in neuroimmune function following neonatal endotoxin challenge.

Neonatal animals have a proportionately greater risk, relative to the adult animal, of developing a bacterial infection. Research has revealed that such infections can influence biological processes long after the actual infection has been resolved. Indeed, studies examining the long-term alterations induced by early-life infection, simulated using endotoxin, have indicated that some aspects of the systemic inflammatory response in the adult animal are susceptible to modification. Available evidence suggests that altered inflammatory activities observed in the neonatally endotoxin challenged adult may be the result of potentiated hypothalamic pituitary adrenal (HPA) activity, specifically increased corticosterone production. Few studies, however, have examined whether altered corticosterone production is actually associated with changes in systemic inflammation in the neonatally endotoxin challenged adult animal. The aim, therefore, of the current study was to simultaneously examine the relationship between altered inflammatory activities and corticosterone production in the neonatally endotoxin challenged adult rat. Our findings demonstrate no significant differences exist between adults neonatally treated with saline or endotoxin in terms of their production of corticosterone following endotoxin challenge. While not appearing to influence the production of corticosterone neonatal endotoxin challenge did result in a marked attenuation in the adult's febrile response following endotoxin challenge. Interestingly, circulating levels of IL-1beta and TNF-alpha were found to be equivalent in neonatal treatment groups following endotoxin administration in adulthood, indicating that the reduction in fever was unlikely to be the result of altered pro-inflammatory cytokine production. Further, no differences were found between neonatal treatment groups in net food consumption, water consumption or weight loss following endotoxin challenge in adulthood. Collectively, these findings demonstrate that neonatal endotoxin challenge does not affect a blanket down regulation of inflammatory processes but rather appears to induce highly specific alterations in the adult male Fischer-344 rat.

Age Factors↗
PubMed1996

Neonatal complications in newborns with an umbilical artery pH < 7.00.

OBJECTIVE: Our purpose was to determine the significance of an umbilical artery pH < 7.00 in relation to neonatal morbidity and mortality. STUDY DESIGN: Between 1986 and 1993 acid-base assessment of the umbilical artery was performed routinely in 10,699 deliveries. In a retrospective cohort study 84 nonanomalous neonates with an umbilical artery pH < 7.00 were individually matched with 84 neonates with an umbilical artery pH > 7.24. Matched variables included year of delivery, gender, parity, maternal age, delivery mode, fetal presentation, gestational age, and birth weight. Differences in morbidity between the two groups during the neonatal period (until 28 days after delivery) were investigated. RESULTS: Neonates with an umbilical artery pH < 7.00 versus > 7.24 showed significant differences in the following: neonatal condition directly post partum; neurologic, respiratory, cardiovascular, and gastrointestinal complications; and neonatal intensive care unit admissions. No significance was found in renal dysfunction and mortality rate. The proportion of premature infants (< 37 weeks) was 17% in both groups. In the acidotic group a 1-minute Apgar score < or = 3 and a 5-minute Apgar score < 7 was predictive for neonatal complications. CONCLUSIONS: Severe intrapartum asphyxia, quantified by an umbilical artery pH < 7.00, poses a threat to the neonate's health.

Acidosis↗
PubMed2002

Reversal of sex differences in morphine analgesia elicited from the ventrolateral periaqueductal gray in rats by neonatal hormone manipulations.

Male rats display significantly greater analgesic responses than female rats following systemic, ventricular and intracerebral morphine administration into either the ventrolateral periaqueductal gray (vlPAG) or the rostral ventromedial medulla, and following beta-endorphin administration into the vlPAG. Although adult gonadectomy severely reduces nonopioid forms of swim stress-induced analgesia, the marked sex differences in morphine analgesia were minimally affected by either male or female adult gonadectomy. Since very little is known about neonatal effects of gonadal hormones upon sex differences in morphine analgesia elicited from the vlPAG, the present study evaluated the effects of neonatal (within 1 day of birth) castration in male rat pups relative to sham-operated controls, and systemic androgenization with testosterone propionate in female rat pups relative to vehicle-injected controls upon baseline nociceptive thresholds and morphine analgesia elicited from the vlPAG in rats tested as adults. Significant sex differences in morphine analgesia elicited from the vlPAG were observed with adult males receiving neonatal sham surgeries displaying significantly greater morphine analgesia on two nociceptive measures than adult females tested during the estrous phase and receiving neonatal vehicle injections. Neonatal gonadectomy essentially reversed the pattern of sex difference effects upon morphine analgesia elicited from the vlPAG. Neonatally-castrated male rats tested in adulthood displayed dramatic reductions in morphine analgesia elicited from the vlPAG on both the tail-flick (approximately 15-fold rightward shift) and jump (6-fold rightward shift) tests relative to sham-operated males, and essentially mirrored those of vehicle-treated females. Conversely, neonatally-androgenized female rats tested in adulthood displayed dramatic increases in morphine analgesia elicited from the vlPAG on the tail-flick (5-fold leftward shift) and jump (12-fold leftward shift) tests relative to vehicle-treated females, and approximated those observed in sham-operated males. The potent differences between neonatally-castrated and sham-operated male rats and between neonatally-androgenized and vehicle-treated female rats suggest a possible 'organizational' role of gonadal hormones in mediating sex differences in morphine analgesia elicited from the vlPAG.

Analgesics, Opioid↗
PubMed1996

Differences in isoproterenol stimulation of Ca2+ current of rat ventricular myocytes in neonatal compared to adult.

The developmental changes in the isoproterenol stimulation of the L-type calcium current (ICa(L)) were studied in freshly isolated neonatal (3-5-day-old) and adult (2-3-month-old) rat ventricular myocytes using whole-cell voltage clamp (at room temperature). ICa(L) was measured as the peak inward current at a test potential of +10 mV (or +20 mV) by applying a 300 ms pulse from a holding potential of -40 mV. The pipette solution was Cs(+)-rich and Ca(2+)-free. The external solution was Na(+)-free and K(+)-free. Isoproterenol stimulated ICa(L) in a dose-dependent manner. The concentrations of isoproterenol for half-maximal effect were 6.8 nM in neonatal and 13.3 nM in adult. The maximal stimulation of ICa(L) was 147 +/- 14% in neonatal and 97 +/- 7% in adult. The steady-state inactivation curves were not affected by isoproterenol, whereas the steady-state activation curve was shifted to the left in both neonatal and adult. Forskolin (10 microM) increased ICa(L) by 105 +/- 10% in neonatal and 90 +/- 12% in adult. After stimulating ICa(L) by forskolin, the addition of isoproterenol produced a further increase of ICa(L) by 99 +/- 27% in neonatal, but only by 19 +/- 3% in adult. The presence of an inhibitor of cAMP-dependent protein kinase in the pipette did not affect this marked difference between neonatal (87 +/- 23%) and adult (11 +/- 8%). We conclude that, in rat ventricular myocytes, (1) stimulation of ICa(L) by the beta-adrenoceptor agonist, isoproterenol, is already fully developed in the neonatal stage and actually decreases during development; (2) there is evidence for a cAMP-independent stimulation of Ca2+ channels by isoproterenol, and this is greater in neonatal than in adult. We believe that the cAMP-independent pathway is the direct pathway mediated by Gs alpha protein.

Adrenergic beta-Agonists↗
PubMed1981

Interferon induction of natural killer cytotoxicity in human neonates.

Low natural killer cytotoxicity has been associated with serious herpes simplex virus infections. Neonates' mononuclear cells had significantly lower NKC to HSV infected (P less than 0.001) and uninfected (P less than 0.005) target cells than did adults' MC. Under appropriate conditions, both neonates' MC to NKC was increased by exogenous human leukocyte interferon. Although neonates' and adults' MC had a similar sensitivity to interferon, there was a significant (P = 0.05) lack of consistency in neonates' MC response. Twenty-three percent (4/17) of neonates' MC samples did not respond with increased NKC in the presence of interferon, unlike adults' MC, all of which demonstrated increased NKC. Neonates' MC did not suppress adults' MC-NKC. These data demonstrate the efficacy of interferon as an NKC stimulator in the neonate, but indicate a heterogeneous response of neonatal cells. We are encouraged with the prospect of clinical trials of interferon to treat severe viral infections in neonates. We urge the inclusion of immune surveillance in these trials.

Adult↗
PubMed1998

Neonatal nucleated red blood cell and lymphocyte counts in fetal brain injury.

OBJECTIVE: To determine whether neonatal lymphocyte or nucleated red blood cell (RBC) counts can be used to date fetal neurologic injury. METHODS: Singleton, term infants with hypoxic-ischemic encephalopathy, permanent neurologic impairment, and sufficient laboratory data were divided into two groups: infants with preadmission injury, manifested by a nonreactive fetal heart rate (FHR) pattern from admission until delivery; and infants with acute injury, manifested by a normal FHR pattern followed by a sudden prolonged FHR deceleration. Lymphocyte and nucleated RBC values were compared with published high normal counts for normal neonates: 8000 lymphocytes/mm3 and 2000 nucleated RBCs/mm3. RESULTS: The study population consisted of 101 neonates. In the first hours of life, lymphocyte counts were elevated among injured newborns, and then the counts rapidly normalized. Brain-injured neonates were 25 times more likely to have a lymphocyte count greater than 8000 than were normal neonates (54 [62%] of 87 versus 6 [7%] of 84; odds ratio 25.5; 95% confidence interval 8.8, 80.1; P < .001). The mean lymphocyte count tended to be higher in the preadmission-injury group than in the acute-injury group. In comparison, nucleated RBC values were not correlated as strongly with neonatal hours of life; nucleated RBC counts tended to be higher and persist longer among neonates with preadmission injury than among those with acute injury. CONCLUSION: Compared with normal levels, both lymphocyte and nucleated RBC counts were elevated among neonates with fetal asphyxial injury. Both counts appear to be more elevated and to remain elevated longer in newborns with preadmission injury than in infants with acute injury. However, the rapid normalization of lymphocyte counts in these injured neonates limits the clinical usefulness of these counts after the first several hours of life.

Brain Injuries↗
PubMed1999

Maternal magnesium sulfate and the development of neonatal periventricular leucomalacia and intraventricular hemorrhage.

OBJECTIVE: Neonatal periventricular leucomalacia and intraventricular hemorrhage are strong correlates of cerebral palsy. Our objective was to evaluate the effect of maternal magnesium sulfate exposure on the incidence and severity of periventricular leucomalacia and intraventricular hemorrhage in preterm neonates. METHODS: Nine hundred eighteen consecutive inborn neonates with birth weights from 500 to 1750 g were divided primarily into two groups on the basis of maternal exposure to magnesium sulfate. The groups were divided secondarily into two clinical groups, a physician-initiated group, which consisted of neonates delivered for maternal or fetal indications, and a preterm delivery group, which included neonates delivered as a result of preterm labor or preterm premature rupture of membranes. These clinical groups were stratified further into magnesium sulfate-exposed and -unexposed subgroups. Neonatal neurosonograms were performed on days 3 and 7 of life and described as normal or abnormal. Abnormal sonograms included any periventricular leucomalacia or intraventricular hemorrhage. Severe lesions included periventricular leucomalacia, periventricular leucomalacia with intraventricular hemorrhage, or grades 3 or 4 intraventricular hemorrhage. The magnesium sulfate groups and the clinical groups with their magnesium sulfate strata were compared for the incidence and severity of abnormal sonograms. They also were compared for maternal and neonatal characteristics. RESULTS: Maternal magnesium sulfate exposure was not associated with reduction in the incidence of abnormal sonograms when compared with the unexposed group (27% compared with 33%, P = .06). However, fewer severe lesions were observed in the exposed group (14% compared with 21%, P = .004). When clinical groups were examined, magnesium sulfate was not associated with a decrease in abnormal sonograms (adjusted odds ratio [OR] 1.09, 95% confidence interval [CI] 0.78, 1.52, P = .40) or severe lesions (adjusted OR 1.11, 95% CI 0.73, 1.68, P = .42). Logistic regression analyses of magnesium sulfate exposure within clinical groups controlling for the confounding effects of maternal and neonatal characteristics revealed no protective effect of magnesium sulfate exposure on the incidence of abnormal sonograms (adjusted OR 1.01, 95% CI 0.70, 1.44, P = .97) or severe lesions (adjusted OR 1.01, 95% CI 0.70, 1.74, P = .69). Within clinical groups, the preterm delivery group exhibited an increased risk for abnormal sonograms (adjusted OR 1.63, 95% CI 1.01, 2.67, P = .05) and severe lesions (adjusted OR 9.79, 95% CI 3.27, 29.29, P = .001) when compared with the physician-initiated delivery group, independent of maternal magnesium sulfate exposure. CONCLUSION: Maternal magnesium sulfate exposure had no protective effect on the incidence or severity of periventricular leucomalacia and intraventricular hemorrhage in preterm neonates. The prevalence of these lesions was correlated better with the clinical group of origin and indication for its use.

Anticonvulsants↗
PubMedDate not supplied

Local understandings of vulnerability and protection during the neonatal period in Sylhet District, Bangladesh: a qualitative study.

BACKGROUND: Understanding of local knowledge and practices relating to the newborn period, as locally defined, is needed in the development of interventions to reduce neonatal mortality. We describe the organisation of the neonatal period in Sylhet District, Bangladesh, the perceived threats to the well-being of neonates, and the ways in which families seek to protect them. METHODS: We did 39 in-depth, unstructured, qualitative interviews with mothers, fathers, and grandmothers of neonates, and traditional birth attendants. Data on neonatal knowledge and practices were also obtained from a household survey of 6050 women who had recently given birth. FINDINGS: Interviewees defined the neonatal period as the first 40 days of life (chollish din). Confinement of the mother and baby is most strongly observed before the noai ceremony on day 7 or 9, and involves restriction of movement outside the home, sleeping where the birth took place rather than in the mother's bedroom, and sleeping on a mat on the floor. Newborns are seen as vulnerable to cold air, cold food or drinks (either directly or indirectly through the mother), and to malevolent spirits or evil eye. Bathing, skin care, confinement, and dietary practices all aim to reduce exposure to cold, but some of these practices might increase the risk of hypothermia. INTERPRETATION: Although fatalism and cultural acceptance of high mortality have been cited as reasons for high levels of neonatal mortality, Sylheti families seek to protect newborns in several ways. These actions reflect a set of assumptions about the newborn period that differ from those of neonatal health specialists, and have implications for the design of interventions for neonatal care.

Bangladesh↗
PubMed2000

Effects of neonatal rat Borna disease virus (BDV) infection on the postnatal development of the brain monoaminergic systems.

Effects of neonatal Borna disease virus infection (BDV) on the postnatal development of brain monoaminergic systems in rats were studied. Tissue content of norepinephrine (NE), dopamine (DA) and its metabolite, 3,4-dihydroxyphenol acetic acid (DOPAC), and serotonin (5-HT) and its metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA) were assayed by means of HPLC-EC in frontal cortex, cerebellum, hippocampus, hypothalamus and striatum of neonatally BDV-infected and sham-inoculated male Lewis rats of 8, 14, 21, 60 and 90 days of age. Both NE and 5-HT concentrations were significantly affected by neonatal BDV infection. The cortical and cerebellar levels of NE and 5-HT were significantly greater in BDV-infected rats than control animals at postnatal days (PND) 60 and 90. Tissue content of NE in hippocampus was unaffected. In hippocampus, neonatally BDV-infected rats had lower 5-HT levels at PND 8 and significantly elevated levels at PND 21 and onwards. Neither striatal levels of 5-HT nor hypothalamic levels of 5-HT and NE were affected by neonatal BDV infection, suggesting that the monoamine systems in the prenatally maturing brain regions are less sensitive to effects of neonatal viral infection. 5-HIAA/5-HT ratio was not altered in BDV-infected rats indicating no changes in the 5-HT turnover in the brain regions damaged by the virus. Neither DA nor DOPAC/DA ratio was affected by neonatal BDV infection in any of the brain regions examined. The present data demonstrate significant and specific alterations in monoaminergic systems in neonatally BDV-infected rats. This pattern of changes is consistent with the previously reported behavioral abnormalities resulting from neonatal BDV infection.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Neonatal dopamine-rich grafts and 6-OHDA lesions independently provide partial protection from the adult nigrostriatal lesion syndrome.

Previous studies have shown that neonatally dopamine-depleted rats are subsensitive to dopamine antagonists and do not respond to homeostatic imbalances as adults. This suggests that these animals maintain themselves independent of the dopamine system. If this is so, they should be insensitive to treatment with adult 6-hydroxydopamine (6-OHDA) lesions. Other experiments have shown that dopamine-rich grafts in the neonatal brain will provide some protection from the severe ingestive deficits induced by bilateral 6-OHDA lesions in adulthood. Three groups of animals received either nigra grafts into the intact neonatal brain, neonatal 6-OHDA lesions, or both neonatal 6-OHDA lesions and nigra grafts. A fourth group served as sham-operated controls. Methylamphetamine and haloperidol challenges showed that the neonatally lesioned animals regulated locomotor activity, eating and drinking independent of the dopamine system. Remarkably, however, 80% of these nevertheless showed the full syndrome of aphagia, adipsia and akinesia in response to adult lesions. The grafts into intact group showed enhanced survival in that 36% of the rats were able to maintain themselves following the adult lesion. The graft into neonatally lesioned rats restored their activational response to pharmacological challenges but did not provide any additional protection from the adult lesion. This suggests that different mechanisms underlie the protection against adult nigrostriatal lesions provided by neonatal grafts and neonatal lesions.

Animals↗