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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-five infants participated in a double-blind study of indomethacin therapy for the closure of patent ductus arteriosus. Seventeen infants died. There was no significant difference in autopsy findings between the groups with respect to pneumonia, disseminated intravascular coagulopathy, necrotizing enterocolitis, sepsis, intraventricular hemorrhage, hydrocephalus, kernicterus, brain softening, and renal damage. For those infants who survived and returned for follow-up at approximately 1 year of age, there was no significant difference between the control (n = 17) and indomethacin (n = 13) groups with respect to physical growth, Bayley scores, respiratory infection, abnormal eye ground, neurological defects, and abnormal EEG. Four in the control group (24%) and three in the indomethacin group (23%) had moderate to severe neurological defects and/or scored less than 80 on the Bayley Mental Development Index or Psychomotor Development Index. It appeared that indomethacin therapy did not have a long-term adverse effect on premature infants.
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PMID:Intravenous indomethacin therapy in premature infants with patent ductus arteriosus. Causes of death and one-year follow-up. 711 4

Unbound bilirubin, bilirubin binding capacity, and bilirubin binding affinity were determined by the horseradish peroxidase method at the time of maximum hyperbilirubinemia and/or before exchange transfusions in 13 preterm infants who later died and had autopsies performed. Five of the 13 infants had kernicterus at autopsy. There were no significant differences in weight, gestational age, highest indirect bilirubin level, albumin concentration, severity of acidosis, use of assisted ventilation, sepsis, or other major clinical complications between the five infants with kernicterus and the eight infants without kernicterus. Compared with the eight nonkernicteric infants, the five kernicteric infants had significantly higher unbound bilirubin concentrations (13 +/- vs 27 +/- 9 nmoles/liter, respectively, P less than .05) and significantly lower bilirubin binding capacity and affinity. The data suggest an association between low bilirubin binding capacity and affinity, increased unbound bilirubin, and kernicterus in preterm infants with severe clinical complications.
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PMID:Unbound bilirubin and kernicterus in low-birth-weight infants. 720 Feb 29

Hyperbilirubinemia in the newborn results not only in visible yellow discoloration of the skin but, in high concentration, may cause bilirubin encephalopathy. Such damage to the central nervous system may be subtle and not apparent for several years, as with visual-motor perceptive defects; or it may cause severe neurologic damage (Kernicterus)--even death. Sick and immature infants are the most vulnerable to bilirubin toxicity. Although this condition affects nearly half of all newborns to some degree, only about 10% require treatment. Two methods of treatment are really effective in correcting hyperbilirubinemia, exchange blood transfusions, and/or phototherapy with light radiation in the blue part of the visible spectrum. If the rate of production of bilirubin is excessive or an infant's capacity to conjugate and excrete the pigment is deficient, bilirubin will accumulate in plasma, and will be taken up by other lipid-containing tissues, collagen, and (unless firmly bound to albumin) brain tissue. Many factors combine to raise plasma levels of bilirubin to toxic levels; for example, acidosis, sepsis, hypoxia, hemolysis, hypoalbuminemia, and certain competitive albumin binders. Bilirubin is photolabile in vivo, and if the whole body is irradiated with visible light in the absorption band (450-490 nm) of bilirubin, the pigment will undergo photocatabolism. Under phototherapy bilirubin undergoes photoisomerization at the meso double-bond to conformations less lipophyllic. It is now known that the major photo products of bilirubin IX-alpha are an unresolved mixture of its E, Z and Z, E isomers, easily excreted by the liver. Thus, phototherapy will reduce the accumulation of bilirubin in skin and other tissues and in circulating plasma.
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PMID:Molecular basis of hyperbilirubinemia and phototherapy. 725 51

A total population of 29,395 neonates cared for in the six-year period from 1971 to 1976 was reviewed for evidence of autopsy-proven kernicterus. A total of 327 neonates died and 232 were autopsied. The only cases of kernicterus occurred in four near-term infants with antemortem proven sepsis. All four of these infants weighed more than 2,200 gm and were delivered after gestations of either 36 or 37 weeks. These cases of kernicterus occurred during a period when more aggressive management of hyperbilirubinemia in low-birth-weight infants had apparently eliminated immaturity as a predisposing factor in the development of kernicterus, uncovering bacterial infection as the major remaining etiologic co-factor.
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PMID:The association of kernicterus with bacterial infection in the newborn. 735 31

Free bilirubin concentration, bilirubin-binding capacity, and bilirubin-binding affinity were determined by peroxidase oxidation in 66 newborn infants. Twelve healthy term infants whose unconjugated bilirubin concentration was 15.8 +/- 3.7 mg/dl (mean +/- SD) had a binding capacity of 31.9 +/- 3.7 mg/dl (bilirubin: albumin molar ratio = 0.89 +/- 0.07) and Ka = 28 +/- 11 x 10(7)/M. Twelve term infants with clinical complications of asphyxia, acidosis, respiratory distress, or sepsis, and 17 preterm infants with no complications had lower serum albumin concentrations and slightly reduced binding capacity and affinity compared to the healthy term infants. Free bilirubin concentrations were similar in these three groups, averaging 8 to 9 nmol/l in each group. Twenty-five preterm infants with complications had significantly higher free bilirubin (19 +/- 11 nmol/l), lower binding capacity, and lower binding affinity than any of the other three groups (P less than 0.01 for all comparisons). Five of the 25 sick preterm infants had kernicterus at autopsy. These five infants were similar to the other 20 in birth weight, gestational age, serum bilirubin, and serum albumin level, but had significantly higher free bilirubin and significantly lower binding capacity and affinity. The data suggest that serious neonatal illness is associated with a marked reduction in bilirubin-binding capacity and affinity and an increased risk of kernicterus in preterm infants. The mechanism by which neonatal morbidity decreases bilirubin binding is not known.
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PMID:Free bilirubin concentrations and bilirubin-binding affinity in term and preterm infants. 735 54

In recent years kernicterus at autopsy has been observed in sick premature infants in the absence of markedly elevated levels of serum bilirubin. Potentiating factors have been suggested to explain kernicterus in such a setting. In order to establish which factors are associated with increased risk for kernicterus in these small babies, this retrospective matched control study was undertaken. Thirty-two infants with kernicterus at autopsy were matched for gestational age, birth weight, length of survival, and year of birth to 32 control infants without kernicterus. Multiple historical, clinical, and laboratory factors were compared, including therapy, sepsis, hypothermia, asphyxia as reflected by Apgar score, hematocrit, acidosis, hypercarbia, hypoxia, hypoglycemia, and hyperbilirubinemia. No statistically significant differences between the kernicteric and nonkernicteric infants were demonstrated for any of these factors, including peak total serum bilirubin levels. Multivariant analysis also failed to determine a group of factors associated with increased risk for kernicterus. It was not possible to separate those infants with and without kernicterus at autopsy on the basis of the clinical factors evaluated.
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PMID:Lack of identifiable risk factors for kernicterus. 743 34

Severe neonatal hyperbilirubinemia can occur without apparent reason in term healthy breast-fed infants and some develop kernicterus. The aim of our study was to assess the incidence of severe hyperbilirubinemia in term healthy newborns discharged from the hospital. From January 1 through December 31, 1994, 6705 infants were delivered at Bikur-Cholim and Misgav-Ladach Community Hospitals. All 1448 newborns discharged with a serum bilirubin level > 10.0 mg/dL were instructed to return to the hospital within 3 days for follow-up, as well as bilirubin determination. Twenty-one newborns with a bilirubin level > 18.0 mg/dL were identified and readmitted at mean +/- standard deviation (SD) 5.5 +/- 1.8 (range, 5 to 10 days of life). This represents 1.7% of the 1220 infants who returned for follow-up examination. Mean +/- SD serum bilirubin levels at readmission were 19.6 +/- 2.5 mg/dL. All but one of the infants were breast-fed. No cases of ABO incompatibility were found and two newborns were glucose-6-phosphate dehydrogenase (G6PD)-deficient. Sepsis work-up and direct Coomb's tests were negative in all cases. None had hemolysis or were found to have any cause for hyperbilirubinemia other than breast-feeding. Phototherapy was provided in all but two cases, and an exchange transfusion was performed in one case. Three additional infants, with bilirubin levels < 10 mg/dL at discharge, were readmitted due to hyperbilirubinemia. One was diagnosed with neonatal hepatitis. We conclude that, based on our study population, 0.36% of term infants may subsequently develop severe neonatal hyperbilirubinemia in the first postnatal week.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hospital readmission due to neonatal hyperbilirubinemia. 756 38

Of the 587 neonates born in ABUTH, Zaria, Nigeria and successfully followed up, 99 were clinically jaundiced (16.9%). Of these, only 38 (38%) had significant hyperbilirubinaemia (serum bilirubin above 170 umol/L). During the same period, 279 neonates were admitted through Emergency Paediatric Unit (EPU) of whom 70 (25%) were jaundiced and 64 (95%) of them had serum bilirubin above 170 umol/L. Jaundice was more severe and the incidence of kernicterus higher in babies born outside the hospital than in those born in hospital and periodically followed up. The incidence of kernicterus was 20.3% and 2.6% respectively. The pattern of aetiological factors was similar in the two groups of jaundiced neonates. Septicaemia (50%) and G6PD deficiency (40%) were the major aetiological factors. Exposure to traditional herbal medications, oxytocin induced/augmented labour, cephalhaematoma and tribal incidences did not play statistically significant roles. Jaundice due to Rh-incompatibility was not encountered. Results of this double prospective study were compared with the previous findings in this and other centres in Nigeria.
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PMID:Neonatal jaundice in Zaria, Nigeria--a second prospective study. 762 27

Forty-two children who sustained a serum bilirubin (SBR) level above 339 mumol/L as newborn infants were assessed at our Growth and Development Clinic to determine presence of sequelae. Only one child (2.3%) had mild sensorineural deafness and one child (2.3%) performed below age-matched standards on psychological testing. As the SBR level rose the psychological scores were lower. Three infants had sepsis associated with the hyperbilirubinaemia. Two (maximum SBR levels of 371 and 366 mumol/L) children were normal (General Cognitive Index (GCI) 117 and 119, respectively) and one child (maximum SBR level 556 mumol/L) was borderline abnormal (GCI 74) on psychological testing; he also suffered from Rhesus erythroblastosis. Premature infants recorded a mean GCI of 109.9 (+/- 33.4) and for term infants mean GCI was 110.3 (+/- 17.3; NS); however, the youngest premature infant was 32 weeks' gestation. When maximum SBR level was correlated with GCI and Motor Index (MI) the only significant correlation (r = -0.7445; P = 0.03) occurred in infants with Rhesus erythroblastosis and GCI. Since exchange transfusion has a mortality of between 0.3 and 5.3% and an associated morbidity incidence of 5.2% we suggest that the standard indication for its use (SBR level of 342 mumol/L) should only apply to infants with Rhesus erythroblastosis. The actual SBR level which places a newborn infant at significant risk of bilirubin encephalopathy, where the cause of jaundice is other than Rhesus erythroblastosis, cannot be determined by this study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Perhaps vigintiphobia should only apply to infants with Rhesus erythroblastosis. 794 48

To investigate the possible role of sepsis with endotoxemia in kernicterus, we studied the effect of endotoxin on accumulation of bilirubin and albumin in rat brain. Male Sprague-Dawley rats were given Escherichia coli endotoxin i.v. After 150 min 10 microCi 125I-bovine serum albumin was given intravenously, followed by a 1-hour bilirubin infusion. Brain bilirubin was significantly higher in the endotoxin group than in the controls (1.34 +/- 0.47 vs. 0.83 +/- 0.31 microgram/g, p < 0.05). However, the difference between the ratios of brain bilirubin to total serum bilirubin at the time of sacrifice were not significant. Total and unbound bilirubin values were significantly higher in the endotoxin-treated group at 165 min. Endotoxemia increased the net accumulation of bilirubin in rat brain, but this increase was probably secondary to an increase in total and unbound bilirubin, rather than an increase in the transfer per se of bilirubin across the blood-brain barrier.
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PMID:Endotoxemia and brain bilirubin in the rat. 832 97


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