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 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The National Neonatal Perinatal Database (NNPD) network is a collaborative group of leading neonatal units in India involved in the prospective collection of morbidity and mortality data on uniform protocols. The present article reports the morbidity and mortality profile of outborn neonates in the year 2000. Ten centers provided data on outborn neonates. The data were analysed at the nodal center using Epi-Info statistical software version 6 and Excel 97. A total of 3831 neonates were admitted at the participating institutions. A majority of them (87.2 per cent) were delivered in nursing homes and small hospitals. Most of the admissions (68.7 per cent) were male. Nearly half of them (48.7 per cent) were low birthweight and one-third (32.1 per cent) were preterm. Overall mortality was 16.4 per cent, while 7.5 per cent left hospitals against medical advice. Nearly half of all neonatal deaths occurred within the first 48 h following admission. Common primary causes of deaths (n = 630) included: infections (36.0 per cent), prematurity related conditions (26.5 per cent), perinatal hypoxia (10.0 per cent), and malformations (7.8 per cent). Systemic infections (28.4 per cent), hyperbilirubinemia (27.9 per cent), seizures (11.7 per cent), hypoglycemia (11.5 per cent), hypoxic ischemic encephalopathy (8.3 per cent), anemia (8.9 per cent), and hypocalcemia (8.6 per cent) were common morbidities observed. Of systemic infections, 39.2 per cent were culture positive and 51.4 per cent were early onset (< 72 h). Sick babies were managed with antibiotics (75 per cent), oxygen administration (45.3 per cent), phototherapy (34.9 per cent), and assisted ventilation (16.3 per cent). In conclusion, the present study describes the morbidity and mortality profile of a large multicentric cohort of outborn neonates from a developing country.
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PMID:Morbidity and mortality among outborn neonates at 10 tertiary care institutions in India during the year 2000. 1523 94

The etiologic profile and possible predictors of etiology in children with spastic quadriplegia were assessed in a consecutive cohort of children with this motor impairment. Medical records from a single pediatric neurology practice over a 14-year interval were retrospectively and systematically reviewed. Variables comprised possible demographic, prenatal, perinatal, and postnatal risk factors. Of the 99 patients included in the study, 39 were premature (<37 weeks gestation). The overall etiologic yield was 83%. The top three diagnoses were hypoxic-ischemic perinatal asphyxia (33%), periventricular leukomalacia (15%), and central nervous system infections (11%). In premature children, the most common diagnoses were periventricular leukomalacia (33%), perinatal asphyxia (26%), and central nervous system infections (15%). In term-born children, the most frequent diagnoses were perinatal asphyxia (37%), metabolic disease (12%), and structural malformation or infection (9% each). Factors predicting the identification of an etiology included male sex (P = 0.05), low birth weight (P = 0.003), prematurity (P = 0.01), perinatal complications (P = 0.002), and neonatal encephalopathy (P = 0.006). The etiologic yield in patients with spastic quadriplegia was 83%, with differing underlying etiologies depending on gestational age. These results should help guide physicians in investigating possible underlying etiologies in patients with spastic quadriplegia.
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PMID:Etiologic profile of spastic quadriplegia in children. 1835 17

It has been asserted that hypoxic-ischemic encephalopathy (HIE) with cerebral swelling in the absence of marked trauma may be responsible for subural hemorrhage in the young. As this may have considerable implications in determining both the mechanism of death and the degree of force required to cause injury in certain cases of inflicted head injury in infancy, clarification is required. A retrospective study of 82 fetuses, infants, and toddlers with proven HIE and no trauma was undertaken from forensic institutes in Australia, the United Kingdom, Germany, Denmark, and the United States. The age range was 35 weeks gestation to 3 years, with a male to female ratio of 2:1. All cases had histologically confirmed HIE. Causes of the hypoxic episodes were temporarily resuscitated sudden infant death syndrome with delayed death (N = 30), drowning (N = 12), accidental asphyxia (N = 10), intrauterine/delivery asphyxia (N = 8), congenital disease (N = 6), aspiration of food/gastric contents (N = 4), inflicted asphyxia (N = 3), epilepsy (N = 1), dehydration (N = 1), drug toxicity (N = 1), complications of prematurity (N = 1), and complications of anesthesia (N = 1). The initiating event was not determined in 4 instances. In no case was there macroscopic evidence of subdural hemorrhage. In this study no support could be given to the hypothesis that HIE in the young in the absence of trauma causes subdural hemorrhage.
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PMID:Lack of evidence for a causal relationship between hypoxic-ischemic encephalopathy and subdural hemorrhage in fetal life, infancy, and early childhood. 1800 Nov 63

Hypoxia-ischemia is relatively common in human infants. Hypoxia-ischemia can occur as a result of complications associated with prematurity or birth, frequently leading to altered brain development and cognitive and behavioral deficits that persist throughout life. Despite the relative frequency of neonatal hypoxic-ischemic encephalopathy, the immature brain sustains relatively less damage than an adult who experiences a similar crisis of oxygen and nutrient deprivation. Therefore, factors may be present that protect the developing brain. During late gestation, the infant brain encounters high levels of the steroid hormone 17beta-estradiol. This observation, combined with evidence supporting 17beta-estradiol as a neuroprotective agent, led us to hypothesize that increasing the basal level of 17beta-estradiol would reduce the amount of hypoxia-ischemia induced injury to the neonatal brain. To test that hypothesis we administered 17beta-estradiol using either a repeated dosing paradigm or a single dose paradigm to immature male and female rats. Here we show that the repeated dosing paradigm (three doses of 17beta-estradiol) provided approximately 70% protection of the hippocampus, basal ganglia, and amygdala. By contrast, a single administration of 17beta-estradiol 24 h prior to hypoxia-ischemia conferred little protection. The only exception was the pyramidal layer of the female hippocampus, which was modestly protected (16% reduction in damage). The protection afforded by the multiple administrations of 17beta-estradiol was similar for females and males, with the only exception being the male amygdala, which displayed less damage than the female amgydala. We conclude that 17beta-estradiol acts as a potent neuroprotective agent against hypoxia-ischemia induced damage to the developing brain, and that pretreating infants at risk for hypoxic-ischemic injury may be advisable.
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PMID:17beta-estradiol protects the neonatal brain from hypoxia-ischemia. 1795 Feb 81

Attention-deficit/hyperactivity disorder is a neurobiological syndrome with an estimated prevalence among children and adolescents of 5%. It is a highly heritable disorder, but acquired factors in etiology are sometimes uncovered that may be amenable to preventive measures or specific therapy. Early reports have described symptoms similar to attention-deficit/hyperactivity disorder that followed brain trauma or viral encephalitis, and recent MRI studies have demonstrated brain volumetric changes that may be involved in the pathophysiology of the syndrome. The American Psychiatric Association's Diagnostic Statistical Manual, introduced in 1968, emphasizes symptomatic criteria in diagnosis. Here, an overview of environmental factors in the etiology of attention-deficit/hyperactivity disorder is presented to encourage more emphasis and research on organic causal factors, preventive intervention, and specific therapies. An organic theory and the genetic and biochemical basis of attention-deficit/hyperactivity disorder are briefly reviewed, and an etiologic classification is suggested. Environmental factors are prenatal, perinatal, and postnatal in origin. Pregnancy- and birth-related risk factors include maternal smoking and alcohol ingestion, prematurity, hypoxic-ischemic encephalopathy, and thyroid deficiency. Childhood illnesses associated with attention-deficit/hyperactivity disorder include virus infections, meningitis, encephalitis, head injury, epilepsy, toxins, and drugs. More controversial factors discussed are diet-related sensitivities and iron deficiency. Early prenatal recognition, prevention, and treatment of environmental etiologies of attention-deficit/hyperactivity disorder may reduce physician reliance on symptomatic modification with medication, a frequent reason for parental concern.
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PMID:Etiologic classification of attention-deficit/hyperactivity disorder. 1824 8

Early stroke in the premature infant has rarely been described. Presented here are the cases of 23 infants, born between 23 and 35 weeks gestational age, with focal arterial ischemic stroke occurring before 44 weeks gestational age. Ten (43%) were male. Five children (22%) were half of a twin pair; no co-twin died. The most commonly affected territory was the middle cerebral artery territory. Three children with extreme prematurity (< or =26 weeks) had cerebellar infarcts. Twelve children had unilateral or bilateral intraventricular hemorrhages (grade 3 or higher in 8 of the 12). Twelve children had white matter injury: periventricular leukomalacia, hypoxic-ischemic encephalopathy, or both. Most children had multiple comorbidities, and the median neonatal intensive care unit stay was 63 days (range, 14-365). One child died in the neonatal intensive care unit (age 123 days). All 22 survivors were left with disabilities. Seventeen (77%) had cerebral palsy, 10 (45%) had epilepsy, and 17 (77%) had cognitive impairment. Arterial ischemic stroke appears to add to the neurologic disabilities commonly associated with prematurity.
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PMID:Very early arterial ischemic stroke in premature infants. 1841 Aug 48

Although apnea is common in premature babies, there is a paucity of information concerning the pathophysiologic basis of these episodes and their relationship to other perinatal conditions such as hyperbilirubinemia. Unconjugated hyperbilirubinemia in premature infants, even in moderately high levels, may cause encephalopathy affecting brainstem functions and has been linked to increased incidence of apnea in these infants. Thus, there is a need to clarify mechanisms by which bilirubin may alter respiratory control and induce apnea of prematurity. In this study, bilirubin or placebo was infused i.v. in 9-d-old rat pups (n = 36). Serum hyperbilirubinemia peaked in the first hours after bilirubin infusion. Twenty-four hours after bilirubin infusion, respiration was recorded by plethysmography at rest and under hypercapnic and hypoxic conditions. In treated pups, minute ventilation in room air was significantly reduced, hyperventilatory response to CO2 was blunted, and hypoxic ventilatory depression was increased, compared with placebo-injected rat pups. Brainstem bilirubin deposition and immunoreactivity to bilirubin was detected in the brainstem on histologic analysis. We speculate that high serum bilirubin levels may cause prolonged inhibition of brainstem autonomic function and that this could underlie the exacerbation of apnea noted in premature babies who have experienced jaundice.
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PMID:Hyperbilirubinemia diminishes respiratory drive in a rat pup model. 1845 54

Prematurity remains a public health problem with a considerable psychosocial impact. Premature infants are discharged home more fragile and more precociously than infants born at term. Post-discharge nutrition and growth of the preterm infants should be carefully followed because of specific needs of these infants. Infections and cardiorespiratory abnormalities are more frequent in ex-premature infants. Some cerebral lesions may be shown by brain imaging suggesting future sequelae. However, estimation of their real consequences remains imperfect and long term prognosis contains many uncertainties. Cerebral palsy seems to be less severe nowadays, but all current gravity is due to disabilities which express later: hearing disorders, visual impairments, alterations of eye-hand coordination skills, attention deficit disorders, psychological troubles and school difficulties. Multidisciplinary consultations are designed for these children because early screening and adapted care can improve long term prognosis. All this underlines the importance of prolonged follow-up program after discharge for premature infants and others who presented worse suffer from hypoxic/ischemic encephalopathy.
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PMID:[Care and follow-up of premature infants after discharge]. 1857 75

Neonatal hypoxic-ischemic encephalopathy, prematurity, sepsis-meningitis, and serious forms of complex congenital heart disease requiring infant heart surgery are just a few examples of disorders that share high mortality and morbidity rates. Newborn heart surgery represents a period of planned and deliberate ischemia-reperfusion injury, which is obliged to occur to cure or palliate complex forms of congenital heart disease. Advances in cardiothoracic surgical and anesthetic techniques, including cardiopulmonary bypass and deep hypothermic circulatory arrest, have substantially decreased mortality, expanding the horizon to address functional neurologic and cardiac outcomes in long-term survivors. Interest in the functional status of survivors now stretches beyond the newborn period to childhood, adolescence, and adulthood.
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PMID:Neuroprotection in infant heart surgery. 1902 42

While the number of survivors of term hypoxic-ischemic encephalopathy (HIE) is lower than the number of survivors of extreme prematurity, the proportion of neonates with long-term sequelae is higher. All neonates with Sarnat stages 2 (moderate) and 3 (severe) should be enrolled in follow-up programs. The present paper discusses the clinical and imaging diagnostic criteria for HIE, which are essential to decisions about follow-up. Prognostic indicators are also summarized. The recommendations for follow-up and intervention are based on the clinical condition of the baby at the time of discharge from intensive care, including an assessment of feeding, vision, hearing and whether seizures continue to be present. Early assessments (at four to eight months) focus on head growth, general health and motor neurodevelopment. Assessments at 12 to 24 months focus on cognitive skills and language development. Preschool assessments are also strongly recommended to provide for the identification of children requiring early education programs. Knowledge of long-term outcome and its secular changes enhance prognostication, and the evaluation of new preventive and therapeutic approaches.
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PMID:Follow-up of the term infant after hypoxic-ischemic encephalopathy. 1903 Feb 89


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