The results of intensive care therapy for neonates: I. Overall neonatal mortality rates. II. Neonatal mortality rates and long-term prognosis for low birth weight neonates.
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The following recommendations of the Neonatal Hemostasis Subcommittee of the Scientific and Standardization Committee of the ISTH for the management of neonatal immune thrombocytopenia were prepared by the working party on neonatal immune thrombocytopenia. Evaluation, diagnosis, and treatment of the mother and neonate with alloimmune and autoimmune thrombocytopenia are discussed and current recommendations provided. This document is likely to require frequent future revision(s).
Neonatal anthropometry, including timed skinfold measurements, was performed on 55 products of selected pregnancies. These skinfold measurements were compared with published standards of measurements obtained by similar techniques. Values outside the 3rd percentile to 97th percentile range were overlaid on the birth weight/menstrual age relationship of these subjects. Seven of 10 subjects with the lowest midtriceps skinfolds weighed more than 2500 g at birth (2 more than 3500 g) and 2 of 4 with the largest midtriceps skinfold had birth weights less than 4000 g. This comparison emphasizes the imprecision of birth weight as a measure of quality of fetal growth. Since skinfold thickness measurement is cumbersome for clinical use, other neonatal measures that may be more readily available to the clinician were examined for correlation with skinfolds. Simple birth weight/crown-heel length ratio was found to have the closest relationship of the parameters examined. Although estimated fetal weight was found to be the ultrasonography-derived parameter best correlated with skinfold thickness, ultrasonography discriminated poorly between babies with normal and low skinfolds. Low skinfold thickness predicted thermal vulnerability in the nursery better than did birth weight.
As an extension of an earlier study showing that manometry can identify preterm newborns at risk for feeding intolerance, the authors investigated whether abnormalities of intestinal motor activity underlie the feeding intolerance seen in asphyxiated newborns. Low-compliance perfusion manometry was recorded within the first postnatal week in 25 term neonates admitted consecutively for respiratory diseases. Eleven of these neonates were identified to have experienced birth asphyxia because three concurrent features were present: 1-minute Apgar score of less than 2; 5-minute Apgar score of less than 4; and recurrent seizures within the first 48 postnatal hours. The remaining 14 neonates, who did not have any of these three characteristics, were considered to be nonasphyxiated control neonates. Motor activity differed in nonasphyxiated and asphyxiated neonates during fasting and feeding. During fasting, asphyxiated neonates had less migrating activity than nonasphyxiated neonates. In addition, episodes of motor quiescence and clustered phasic activity were less well organized in asphyxiated neonates. Both groups of neonates displayed a change in motor activity in response to a feeding infusion; however, the response was initiated significantly sooner in asphyxiated than in control neonates. All of the 11 asphyxiated neonates were intolerant of enteral feedings during the first poststudy week, but no control neonate was feeding intolerant. Six of the asphyxiated neonates were reevaluated 1 to 2 weeks later. During this latter study, motor activity in these asphyxiated neonates was similar to that of nonasphyxiated neonates; 5 of 6 of these neonates subsequently tolerated enteral feedings. It is speculated that changes in motor activity underlie the feeding intolerance that asphyxiated neonates typically exhibit.(ABSTRACT TRUNCATED AT 250 WORDS)
Numerous surveys at the national and regional level have demonstrated that large inequalities in infant health status exist in Southern Africa. Few studies have assessed infant mortality at the intra-urban scale of geographic analysis. Comparisons between infant mortality rates from different areas are made even more meaningful if the data are divided into two primary categories based on period-of-death; these being the neonatal and post-neonatal components. This study presents the results of a survey undertaken in Metropolitan Cape Town (population 1.6 million) during 1982. The aim was to determine the spatial variation of neonatal and post-neonatal mortality at the suburb (or community) level within the city. Overall, a total of 36,789 live births and 928 infant deaths were recorded; 53.4% in the neonatal period and 46.6% in the post-neonatal period. The mean infant mortality rate was 25.2 per 1000 live births; the neonatal mortality rate and post-neonatal mortality rate being 13.5/1000 and 11.7/1000, respectively. A marked range in death rates was evident for both components. For the neonatal category it was 0.0-49.9/1000 and 0.0-40.0/1000 for the post-neonatal period. The generally low post-neonatal mortality rate among the 69 suburbs studied has made the neonatal component the dominant contributor to the infant mortality rate. However, in the lowest socio-economic areas the post-neonatal mortality rate was responsible for over 60% of infant deaths.(ABSTRACT TRUNCATED AT 250 WORDS)
The relationship between gestational age, neonatal size and neonatal death is complex. To date, most authors have used birth weight as a proxy for neonatal size and have neglected to examine head circumference and crown heel length. In addition, they have assumed the size and gestational age were linearly related to neonatal death. In this study we use nonparametric multiple logistic regression to examine the relationship between gestational age, neonatal size and neonatal death. On its own, gestational age was nonlinearly associated with neonatal death. This nonlinearity disappeared with the addition of birth weight, crown heel length and head circumference. Birth weight, head circumference and crown heel length all had significant nonlinear associations with neonatal death in univariate analysis. With all factors in the model, birth weight and head circumference were nonlinearly associated with neonatal death and crown heel length was linearly associated with neonatal death. The complex relations between gestational age, neonatal size and neonatal death were explored with greater ease with nonparametric logistic regression.
Neonatal host defense simulates a clinical state of immunodeficiency that predisposes the preterm and term newborn to overwhelming bacterial sepsis. There are various immunologic components that are deficient in the newborn and new methods to enhance their function. Defects in both the quantitative and qualitative aspects of the neonatal phagocyte contribute substantially to the immaturity of neonates' immune systems. The neonate lacks an adequate number of granulocyte bone marrow progenitor cells, and has a decreased neutrophil storage pool and an increased tendency to peripheral neutropenia during neonatal sepsis. Additionally, the neonatal granulocyte demonstrates altered physiologic function compared with that found in the adult with respect to chemotaxis, phagocytosis, oxidative metabolism, and bacterial killing. Some recent clinical studies have suggested the benefit of using adult neutrophil transfusions as adjuvant treatment during neonatal bacterial sepsis, yet other studies have found the use of polymorphonuclear neutrophil leukocyte transfusions to be inconclusive. Reduced circulating immunoglobulins and impaired production of specific antibody have also led to recent trials in the use of prophylactic intravenous immunoglobulin in preterm infants predisposed to sepsis. Recently, hematopoietic colony-stimulating factors have been demonstrated to improve in vitro neonatal neutrophil physiologic activity. Future therapy of neonatal sepsis will depend on new nontoxic methods for enhancing neonatal host defense.
Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is frequently associated with neonatal hyperbilirubinemia, and sometimes kernicterus, often in the absence of any identifiable trigger or hematological evidence of hemolysis. The aim of this study was to compare the incidence and severity of, and the effect of phototherapy on, jaundice in G 6-PD-deficient vs G-6-PD-normal neonates in the Sephardic-Jewish community. Healthy term newborns, born to mothers of families stemming from geographic areas known to be "at risk" for G-6-PD deficiency, were screened for the condition and surveyed for hyperbilirubinemia. Seventy-five G-6-PD-deficient neonates formed the study group, while 266 neonates with normal levels of the enzyme formed the control group. Neonates with any other identifiable cause for jaundice were excluded. Phototherapy was commenced when the serum bilirubin levels reached 16 mg/dL (274 mumol/L) or more, and it was discontinued at 12 mg/dL (205 mumol/L) or less. Hyperbilirubinemia developed in 27 (36%) of the deficient neonates (serum total bilirubin greater than 13.9 mg/dL [238 mumol/L]), compared with 50 (18.8%) of control neonates (P = .002), while 20 (26.7%) of the study group required phototherapy, compared with 31 (11.7%) of control neonates (P = .002). Two neonates in the study group required exchange transfusion (serum bilirubin greater than 20 mg/dL [342 mumol/L]), vs 0 in the control group (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)
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A prospective case-control study was carried out in 118 severely small-for-gestational age (SGA) infants and in 118 control infants born during 1985 in the catchment area of the University Central Hospital of Turku to investigate the neonatal complication rate in SGA infants during modern obstetric and neonatal care. All SGA infants had a birth weight below the 2.5th percentile in our fetal growth curve and the control infants were matched for gestational age and mode of delivery. Neonatal complications were found in 42% of SGA neonates compared to 18% of control infants. Hypoglycemia, polycythemia and abnormal neurologic symptoms were more frequently found in SGA neonates than in control neonates. Asphyxia was found in 16% of SGA infants and in 8.5% of control infants. A five-fold risk for hypoglycemia and a eight-fold risk for abnormal neonatal neurologic signs in SGA infants were found. SGA boys had more often asphyxia (22% versus 12%) and hypoglycemia (25% versus 5%) than SGA girls. The antenatal diagnosis of SGA infant was made in 35 cases (30%). Of these diagnosed infants 14 were delivered by cesarean section (39%), while the cesarean section rate in all SGA infants was 27%. Although antenatal diagnosis of poor intrauterine growth did not decrease the neonatal complication rate, the antenatal diagnosis resulted in more active intervention during delivery. The SGA infants still run an increased risk for complications during delivery and neonatal period and need special attention.
To determine whether multiple doses of bovine surfactant would improve neonatal mortality in very premature neonates, we conducted two multicenter controlled trials under identical protocols; the results were combined for analysis. Four hundred and thirty neonates born between 23 and 29 weeks gestation and weighing 600 to 1250 g at birth were assigned randomly at birth to receive either 100 mg of phospholipids/kg of Survanta, a modified bovine surfactant (n = 210), or a sham air placebo (n = 220) within 15 minutes of birth. Neonates who developed respiratory distress syndrome and required mechanical ventilation with at least 30% oxygen could be given up to three more doses in the first 48 hours after birth. Dosing was performed by investigators not involved in the clinical care of the neonates; nursery staff were kept blinded as to the treatment assignment. Cause of death was determined by a panel of three independent, board-certified neonatologists after blindly reviewing case report forms and autopsy reports. Fewer Survanta-treated neonates died of any cause (11.4% vs 18.8%, P = .031), died of respiratory distress syndrome (1.9% vs 15.6%, P less than .001), and either died or developed bronchopulmonary dysplasia due to respiratory distress syndrome (39.5% vs 49.1%, P = .044). The incidence of respiratory distress syndrome was also lower in Survanta-treated neonates (28.0% vs 56.9%, P less than .001), and the Survanta-treated neonates' oxygenation and ventilatory status were improved significantly at 72 hours. Survanta-treated neonates were also at lowered risk of developing pulmonary interstitial emphysema (23.3% vs 36.9%, P = .002) and other forms of pulmonary air leaks (9.6% vs 20.8%, P .002).(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: To describe 10 infants with benign neonatal sleep myoclonus. DESIGN: Patient series, representing the experience of one pediatric neurologist. SETTING: Referral-based Pediatric Neurology Service at a Children's Hospital. PATIENTS: Sequential sample of 10 neonates referred for assessment of seizures and found to have benign neonatal sleep myoclonus. Neonates who did not have the events of concern during electroencephalography or in whom electroencephalography was not done were excluded even if the clinical features suggested the entity. RESULTS: Our patients met the criteria for the diagnosis. The myoclonus often increased with gentle restraint. The amplitude and duration of events mimicked convulsive status epilepticus and serial seizures in four neonates. In two of them the myoclonus worsened in spite of anticonvulsant therapy, decreasing substantially when such treatment was stopped. CONCLUSION: Benign neonatal sleep myoclonus, an entity characterized by (1) neonatal onset, (2) myoclonic jerks only during sleep, (3) abrupt and consistent cessation with arousal, (4) absence of concomitant electrographic changes suggestive of seizures, and (5) good outcome must be included in the differential diagnosis of neonatal seizures.
In a study of neonatal malaria at the University of Benin Teaching Hospital, we documented the features of six neonates in an effort to highlight that the manifestations of malaria in the newborn cannot be readily distinguished from those of neonatal sepsis. Maternal peripartum fever, an important identifiable risk factor for neonatal sepsis, also featured prominently in the mothers of these babies. These mothers ingested pyrimethamine weekly in the course of their pregnancy. All six neonates were critically ill. Their cultures of blood, CSF and urine for bacterial pathogens yielded no growth and they were unresponsive to conventional antibiotics. The diagnosis of malaria should be considered, in spite of regular maternal ingestion of antimalarial prophylaxis with pyrimethamine, in critically ill neonates in malarious areas. All six neonates responded satisfactorily to oral doses of chloroquine. We therefore suggest that a blood film for malaria parasites be included in screening for neonatal sepsis as part of the initial work-up.
Investigations concerning carnitine metabolism and possible requirements for exogenous carnitine in human preterm neonates are limited by ethical considerations. The neonatal piglet is a potential animal model for these investigations. Tissue carnitine concentrations were determined in fetuses from cross-bred domestic gilts at stages of gestation corresponding to those of neonates found in neonatal intensive care units. Fetal piglet plasma and red blood cell carnitine levels decreased from approximately 90 d to term. Skeletal muscle carnitine increased from 60 d to term. Temporal changes in fetal carnitine concentrations in plasma, red blood cells and skeletal muscle throughout gestation are similar to the pattern reported by our laboratory for the human neonate. Cardiac muscle carnitine increased earlier than skeletal muscle but also continued to increase to term. Carnitine concentrations in fetal liver, kidney and intestine were maximal at 90 d and decreased until term. Similarities in physiology, metabolism and profiles of tissue carnitine concentration between the newborn piglet and the human neonate indicate that the neonatal piglet is an appropriate animal model for investigations concerning neonatal carnitine metabolism.
The concentrations of serum retinol-binding protein (RBP), prealbumin (PA) and vitamin A of Indonesian neonates were compared with those of Japanese neonates. The mean serum concentrations of both PA and vitamin A did not differ significantly in Indonesian and Japanese neonates. Indonesian neonates had significantly higher serum RBP (2.75 +/- 0.87 mg/dl, mean +/- SD) than Japanese neonates (1.65 +/- 0.55 mg/dl, p less than 0.01). The molar ratio of vitamin A:RBP in Indonesian infants was significantly lower than in Japanese infants (p less than 0.02), and this in turn is indicative of increased concentrations of retinol-free RBP in the plasma of Indonesian neonates. The results suggest that RBP metabolism in Indonesian neonates differs from that in Japanese neonates.
The neonatal period is a time of transition between pituitary-independent fetal growth and the pituitary-dependent growth seen in older mammals. To evaluate pituitary-dependent neonatal growth, Wistar rats were hypophysectomized (Hx) on postnatal day 6. Nineteen days post-Hx, body weight and tail length were inhibited 48% and 34%, respectively, compared with sham-Hx controls. Organ weights determined on days 10, 15, 20, 25, and 30 revealed three patterns of pituitary-dependence: 1) pituitary-independent growth in the brain and lung; 2) moderate pituitary-dependent growth in the heart, liver, kidney, and intestine; and 3) marked pituitary-dependent growth in the adrenals, spleen, and testes. Both serum insulin-like growth factor (IGF)-I and -II levels fell significantly in Hx pups by 54 h after Hx (P = 0.0005), and Northern analysis on day 15 showed a significant decrease in liver messenger RNA (mRNA) for IGF-II. Analysis of the major IGF binding proteins (BPs) was performed by Western ligand blots. Hx performed on day 6 resulted in a linear decrease in the amount of the 22k BP from day 10 to day 30. In contrast, the major neonatal BP (IGFBP-2, a 29.5k molecule) showed a biphasic response to neonatal Hx. On postnatal day 10, 4 days after Hx, a significant decrease in IGFBP-2 occurred, which persisted through day 15; by postnatal day 20 and continuing through postnatal day 30, the amount of IGFBP-2 in the serum dramatically increased. The 40 to 50k fraction of IGFBP-3 first appeared in significant quantities by postnatal day 20, and after Hx dropped to 10% of sham-control values. Similarly, Northern analysis on day 15 demonstrated a significant decrease in liver, but not brain, mRNA for IGFBP-2 after Hx, whereas on postnatal day 25, liver mRNA for IGFBP-2 was increased in Hx pups compared with sham controls. We conclude that the pituitary gland exerts significant but selective effects on neonatal growth, with the notable exception of brain growth. Serum levels of both IGF-I and IGF-II, as well as their BPs, are pituitary dependent in the neonatal period. Pituitary-dependent neonatal growth thus appears to be mediated by IGF and modulated by IGF-binding proteins. On the other hand, that portion of the persistent growth in the neonatal Hx rat that is independent of the pituitary-IGF axis may be a good model for investigation of fetal growth.
To determine if outcomes of low birth weight neonates with respiratory distress syndrome can be improved by the administration of multiple doses of bovine surfactant, we conducted two identical multicenter, controlled trials, and the results were combined for analysis. Seven hundred and ninety-eight neonates weighing 600 to 1750 g at birth who had developed respiratory distress syndrome within 6 hours of birth were assigned randomly to receive either 100 mg of phospholipid/kg of Survanta, a modified bovine surfactant (n = 402), or a sham dosing procedure (n = 396). Neonates whose respiratory distress persisted could be given up to three more doses, with all doses to be given in the first 48 hours after birth. Dosing was performed by investigators not involved in the clinical care of the neonates; nursery staff were kept blinded as to the treatment assignment. Fewer Survanta-treated neonates died of any cause (18.4% vs 27.3%, P = .002), died of respiratory distress syndrome (9.0% vs 20.3%, P less than .001), and either died or developed bronchopulmonary dysplasia due to respiratory distress syndrome (51.2% vs 64.6%, P less than .001). Neonates who received Survanta also had greater improvement in their oxygenation and ventilatory status from baseline to 72 hours than did control neonates. Survanta-treated neonates were at lowered risk for developing pulmonary interstitial emphysema (18.6% vs 39.3%, P less than .001) and other pulmonary air leaks (11.5% vs 25.9%, P less than .001). We conclude that multiple doses of Survanta given after diagnosis of respiratory distress syndrome reduce mortality and morbidity.
To evaluate the effect of the type of delivery, gestational age, maternal dexamethasone treatment, and neonatal complications on the serum cortisol levels in early infancy, a total of 92 neonates were investigated with 611 cortisol determinations (specific radioimmunoassay after Lipidex chromatography). Umbilical cord blood samples were taken immediately after delivery and capillary blood samples from the infant's heel 30--60 minutes after delivery and at 8:00 AM and PM on the second, fourth, and sixth days of life. Umbilical cord cortisol concentration after elective cesarean section was lower than after emergency cesarean section or after normal vaginal delivery, while neonatal cortisol values did not show any correlation with the type of delivery. Prematurity did not affect neonatal cortisol levels. In postterm infants the activation of cortisol production was retarded to some degree. After maternal dexamethasone therapy, neonatal cortisol concentration decreased 30--60 minutes after delivery, but from the second day on it was at the same level as in infants without maternal therapy. Respiratory distress syndrome, especially in fatal cases, caused an elevation in neonatal cortisol levels, while hyperbilirubinemia did not have an effect on plasma cortisol concentrations of the neonates.