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 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study describes the results of examination of blood cultures from infants born in a community with a high prevalence of fatal amniotic fluid infection. The incidence of first-week neonatal septicaemia was 5.5 per 1000 births. Septicaemia was detected in 38% within 12 hours and 75.6% within 72 hours of birth. The aetiological pattern of the septicaemia was similar to that of fatal amniotic fluid infections. The increase in mortality from septicaemia occurred in infants born after 34 weeks of gestation. Nearly 80% of the infections apparently occurred through intact membranes. Respiratory distress with or without radiological evidence of pneumonia was the only manifestation of septicaemia in most infants under four days of age. Low Apgar scores and multiple apnoeic episodes were more common in infants with septicaemia than in those without septicaemia. Neonatal jaundice with serum bilirubin in excess of 11 mg/dl was more common in septicaemic infants and indicated poor prognosis. Meningitis associated with septicaemia occurred in 3.8% and in all these infants the diagnosis of septicaemia was delayed beyond 72 hours. The results suggest that early recognition and treatment of antenatal bacterial infections may prevent mortality and morbidity from complications of septicaemia such as neonatal apnoea, meningitis and bilirubin encephalopathy.
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PMID:Consequences of amniotic fluid infections: early neonatal septicaemia. 26 66

Neonatal jaundice is a major clinical problem globally, especially in the Asian and south-east Asian regions. There is no universal definition of hyperbilirubinaemia, and comparisons of management and control of hyperbilirubinaemia in infants at different centres are difficult. G6PD deficiency, ABO incompatibility, low birth weight and sepsis are the common causes of neonatal jaundice, but there is a group of babies whose cause of neonatal jaundice has yet to be found. Genetic factors may be responsible for ethnic differences in the ability to eliminate bilirubin, while unidentified environmental factors may also play a role in the prevalence of neonatal jaundice. As a result of a surveillance programme for neonatal jaundice in Singapore, involving health education of doctors, nurses and the lay public, screening of the newborn and the early treatment of jaundice, we have not seen a single case of kernicterus in Singapore for more than 10 years.
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PMID:Neonatal jaundice in Asia. 159 89

Jaundice among Nigerian preterm infants under special care was studied to determine the incidence of clinical jaundice, the predisposing factors and outcome among those with significant hyperbilirubinaemia (SBR greater than or equal to 10mg/dl). The incidence of jaundice among 292 preterm infants over an 18-month period was 71.2%. The male: female ratio was 1:1.04. Of the 74 infants with serum bilirubin 10mg/dl or more, prematurity alone was the identified cause in 44 (59.5%), Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and septicaemia were the only additional factors in 13 (17.6%) and 7 (9.5%) respectively, while multiple aetiological factors (prematurity, septicaemia and G-6-PD deficiency) were identified in six (8.1%) of the babies. Septicaemia was associated with higher mean bilirubin levels and the highest mortality. The two kernicteric infants in the study had septicaemia. Thus, the single most important cause of jaundice was prematurity. G-6-PD deficiency alone did not appear to increase the incidence and severity of hyperbilirubinaemia in this study. Septicaemia should be suspected and promptly treated in order to reduce mortality and risk of kernicterus among preterm infants with hyperbilirubinaemia.
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PMID:Neonatal jaundice among Nigerian preterm infants. 208 1

Clinical features of bilirubin encephalopathy vary depending on the age of the infant and the degree of hyperbilirubinemia. In term infants with hyperbilirubinemia, three distinct clinical phases are apparent in the first weeks of life, and long-term consequences include extrapyramidal disturbances (particularly athetosis), hearing loss, gaze abnormalities (particularly limitation of upward gaze), and, in a minority, intellectual deficits. In term infants with moderate hyperbilirubinemia, minor delay in motor development during the first year has been demonstrated, but with longer follow-up this delay is not apparent. Associated conditions such as sepsis, anoxia, and acidosis may increase the likelihood of neurotoxicity of bilirubin in these infants. The clinical consequences of moderate hyperbilirubinemia in premature infants are unclear. No acute clinical syndrome is recognizable during the first weeks. The results of follow-up studies are variable. Hearing loss is the commonest consequence. Follow-up through age 2 years in one large study suggests that static encephalopathy may be a sequel. Longer follow-up is needed to understand the clinical consequences of moderate hyperbilirubinemia in this important group of infants.
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PMID:Clinical features of bilirubin encephalopathy. 219 35

To focus attention on the problem of infant mortality in Lebanon, data were compiled on infant mortality from 1978 to 1986 at the American University of Beirut Medical Center. Causes of death are analyzed for 602 males and 398 females. 54.9% deaths occurred at 1 month of age and 77.4% died within the 1st year. Autopsies were performed on .7%. 37.7% of all neonatal deaths were due to neonatal diseases such as hyaline membrane disease, asphyxia neonatorum, immaturity, necrotizing enterocolitis, hemorrhage, hemolysis, meconium aspiration, and kernicterus. Better prenatal care would reduce this group, or the administration of corticosteroids to the mother 24-48 hours prior to delivery, as well as rapid resuscitation at birth and prevention of the 5 curses: hypoxemia, hypoglycemia, hypothermia, hypotension, and acidosis. Although unavailable in Lebanon, administration of surfactants through an endotracheal tube would also help. Infections constitute 25.1% of deaths; many are preventable through adequate public health measures and strict personal hygiene, i.e., diseases such as sepsis, pneumonia, meningitis, gastroenteritis, hepatitis, encephalitis, and 1-2 cases of the following: diphtheria, measles, peritonitis, tetanus, tuberculosis, cytomegalis inclusion, herpes, parathyphoid, pertussis, poliomyelitis, and shigellosis. Congenital diseases were 21.6%. In utero diagnosis could prevent some diseases and in utero treatment is possible for hydrocephalus and hydronephrosis. Screening programs postnatally could lead to treatment. 5.9% were malignancies such as leukemia, lymphoma, brain tumors, histocytosis, Wilm's tumor, Ewing sarcoma, and Hodgkin's disease. Early diagnosis is critical if mortality is to be reduced in this group, but medical advances are still needed. 2.9% are miscellaneous diseases such as poisoning, rheumatic diseases, marasmus, Reye's syndrome, nephrosis, rickets, and epilepsy. Most of these diseases are preventable, except for rheumatic inflammation of the heart. Recommended necessary steps to reduce infant mortality are: prenatal care, diagnosis and screening, intrauterine surgery; resuscitation and intensive care centers with modern equipment and trained personnel; national vaccination and screening programs; adequate public health measures and hygiene; parental education; and well-equipped hospitals to serve all regardless of income level.
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PMID:Pediatric mortality: an avoidable tragedy. 251 28

Four hundred and thirty three exchange transfusions (ET) for neonatal hyperbilirubinemia in 225 full term (Group I) and 110 premature/low birth weight (Group II) babies were analyzed. A total of 78.5% cases required one, 15.22% two, 4.8% three and 1.5% four ET. In Group I ABO HDN (35.94%), Rh HDN (10.7%), septicemia (8.9%), and G-6-PD deficiency (6.2%) were the major causes. Nearly 20% had multiple factors and in 9.3% no cause was identified. In multifactorial cases 13.3% had septicemia, 17.3% ABO HDN and 6.2% Rh HDN in various combinations. Common causes in Group II babies were septicemia (20.9%), ABO HDN (19.07%), Rh HDN (6.4%) and G-6-PD deficiency (5.4%). Nearly 8% had multifactorial etiology while 30.9% were idiopathic. Complications occurred in 20.4% Group I and 41.8% in Group II babies during ET. Procedure related mortality was 3.2/100 ET which declined to 0.9/100 ET when high risk babies were excluded. Overall mortality in babies subjected to ET was 10.6/100 ET. Cardiorespiratory arrest during procedure (30.4%), septicemia (26.1%) and kernicterus (19.6%) were the leading causes of death. Anemia (23.5% Group I and 50.9% Group II babies) and clinical septicemia (14.2% Group I and 16.4% Group II babies) were major delayed complications.
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PMID:Exchange transfusion in neonatal hyperbilirubinemia. 263 Apr 76

An analysis of the causes of death in the neonatal nursery of the Port Moresby General Hospital in Papua New Guinea from 1982-1985 is presented, and conclusions were enumerated. The nursery has beds for 24 babies, subdivided into intensive care, infection and growing areas. Dormitory space for 12 mothers is available, and breast feeding is encouraged, whether by sucking, cup or tube: no bottle feeding is done. Up to 9 sisters staff the unit. A total of 2948 infants were admitted, including 831 cesarean births. 343 deaths occurred. 80 deaths were previable babies less than 1000 g. The neonatal mortality was 10/1000. The most common causes of death were septicemia or meningitis (24%), perinatal asphyxia (20%), respiratory distress syndrome (15%), congenital abnormalities (12%), meconium aspiration 7%, apnea of prematurity (7%). Other causes included pneumonia, hypothermia, intrauterine infection syndrome, cerebral hemorrhage and kernicterus. Note that hypothermia can occur in tiny babies, even in the tropics. Both respiratory distress and jaundice appear to be rare in melanesians compared to caucasians. Infections were due to tetanus, E. coli, S. aureus a Strep. faecalis, rather than the Group B hemolytic Strep. more often seen in the West. It was concluded that several inexpensive measures can be put in place to markedly enhance survival: train birth attendants to prevent perinatal asphyxia; maintain body temperature by available means; feed adequately, using expressed breast milk if necessary; maintain oxygenation properly using simple equipment such as a nasal catheter or perspex head box; prevent infection by scrupulous hand washing, cord care and overall cleanliness; manage neonatal jaundice.
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PMID:Neonatal care in perspective: results of neonatal care at Port Moresby. 347 16

The purpose of this work was to review the literature about the newborn neurological pathology and to compare it with our results starting from the observation of 650 children who born at the Clinical Hospital of Porto Alegre from September 1979 to June 1980. Out of these, 100 presented with neonatal neurological pathology. These newborn were studied as to the age of the mother at the birth time, Apgar rate, weight and cephalic perimeter at the birth time, probable etiologies, and clinical picture and evolution. These newborn were compared to control groups and the results were discussed on the grounds of literature. Out of 100 newborn with neurological pathology, 65% presented with pathological neurological examination and 35% with normal neurological examination. The 65 newborn with pathological neurological examination had hypotonia, decreased deep tendon reflexes, decreased or absence of superficial reflexes in 40 cases. Hyperactivity, hypertonia and tremors were observed in 25 cases. Coma was present in 6 of these newborn with apathy and hypotonia. Seizures were present in 41 cases. EEG was performed in 29 of these 41 cases in the first five days of life. The EEG was normal in 15 (51.7%) newborn and it was pathologic in 14 (48.3%) newborn. The 100 newborn had the following diagnosis: 37 birth anoxia, 13 hemorrhages, 24 meningitis, 14 metabolic seizures, 4 sepsis, 1 kernicterus, 2 chromosomopathies, 3 malformation, 1 cerebral palsy, and 1 congenital rubeola. Out of the 37 newborn with birth anoxia, 20 (54.1%) had a good evolution, 7 (18.9%) had sequela and 10 (27.0%) died. Out of 13 newborn with hemorrhages 2 (15.4%) had a good evolution, 5 (38.5%) had sequela, and 6 (46.1%) died. Out of 24 newborn with meningitis, 18 (75.0%) had a good evolution, 5 (20.8%) had sequela, and 1 (4.2%) died. Out of 58 newborn with a good evolution, 30 had normal newborn neurological exam, and 28 had transient alterations. Out of 23 newborn who presented with sequela later on, only 5 had normal newborn neurological exam. All the 19 who died, had pathological newborn neurological exam.
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PMID:[Neurological pathology in the newborn infant]. 653 54

Yellow staining of central nervous system (CNS) nuclei occurs in the brains of some neonates, despite low levels of serum bilirubin. Two conditions appear to be important in the evolution of this form of kernicterus: prematurity and asphyxia. In a seven year retrospective study of a large neonatal autopsy population, 102 cases had kernicterus as indicated by selective macroscopic yellow staining and microscopic damage within specific CNS nuclei. Neuropathological study disclosed minor variations and numerous similarities in the manifestations of kernicterus in the asphyctic premature neonate with low levels of serum bilirubin, as compared to kernicterus in the full-term neonate with high levels of serum bilirubin. Acidosis, hypoxia, hyperoxia, hypothermia and sepsis have been considered significant risk factors, but recent comparative clinical studies have not defined predictive indices. Analysis of this disorder is difficult because of the concurrence of other complications of asphyxia and its pathological correlates in premature infants. Diagnostic difficulties are also compounded by variations in the definitions of kernicterus as used by different investigators.
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PMID:The neuropathology of kernicterus in the premature neonate: diagnostic problems. 669 27

Reserve albumin concentration (the concentration of albumin available for binding of unconjugated bilirubin) was determined in 95 sera from 76 subjects by dialysis with 14C-monoacetyl diamino diphenyl sulfone (MADDS). An index, I of bilirubin toxicity in the plasma was calculated for each subject, based on the bilirubin and reserve albumin concentrations, the affinity of bilirubin for serum albumin, and the pH-dependent solubility of bilirubin in the plasma. The values of reserve albumin and of I varied significantly with gestational age, clinical condition (whether sick or well), and serum bilirubin level. The value of reserve albumin was decreased and I was increased in association with clinical factors (e.g., hyperbilirubinemia, hypoxia, acidosis, or sepsis) recognized as increasing the risk for bilirubin encephalopathy. The lowest values of reserve albumin and the highest values of I were found in the least mature and sickest infants.
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PMID:Reserve albumin and bilirubin toxicity index in infant serum. 688 Jul 30


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