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At least 19 recordsLinked to original sources
PubMed1975

The use of critical levels of birth weight and "free bilirubin" as an approach for prevention of kernicterus.

Free bilirubin (FB) and total bilirubin (TB) were determined in 154 samples of blood taken from 112 jaundiced newborns: 51 prematures without hemolysis (19 of these with RDS); 26 full terms presenting ABO incompatibility; 35 newborns (both prematures and full terms) presenting rhesus incompatibility. Kernicterus was observed in seven cases and only three occurred in the TB group above 20 mg/100 ml; 57 cases had FB equal to or above 0.1 mg/100 ml and all kernicterus fell into this category. In the other 55 cases in which FB was less than 0.1 mg/100 ml no kernicterus was observed. In the group of healthy full-term newborns presenting ABO incompatibility, 15 had FB above or equal to 0.1 mg/100 ml ranging between 0.1 and 0.4 mg/100 ml; however no kernicterus was observed during the neonatal period. On the contrary, in the group of prematures a little more than half of the cases had a FB ranging from 0.1 to 0.4 mg/100 ml whereas four macroscopic kernicterus cases were observed. The difference between the two groups compels us to consider other factors than those acting on the albumin-bilirubin binding especially those acting on the blood-brain barrier and on the fixation of the pigment by the neurons. A second series of 605 consecutive autopsies, on a period of 10 years, on prematures excluding light-for-dates and cases of hemolysis, evaluates the distribution of 40 kernicterus as a function of birth weight. On this second series kernicterus appears with maximal frequency for birth weight between 1,000 and 1,250 g, with a nonnegligible frequency at 1,500 to 2,000 g and was absent between 2,000 and 2,500 g. 13 kernicterus were observed for a peak TB below 12 mg/100 ml. These results seem to justify a systematic determination of FB in the premature weighing less than 2,000 g from the 24th hour of life whether he has jaundice or not.

ABO Blood-Group System↗
PubMed1987

[Critical study of erythrocyte bilirubin and predictive factors of kernicterus in premature low birth weight infants].

Among 217 premature neonates with birth-weights less than or equal to 1,500 g who died, in whom post mortem examination was carried out during the years 1978-1984, 11 cases of kernicterus (5%) were found. A comparative study was undertaken between these 11 children and 42 children of the same population matched for birth-weight, gestational age and life duration. The following clinical and biological perinatal data were found more frequently in the kernicterus group: meningitis (3/11 vs 0/42), p less than 0.01), hyperchloronatremic dehydration (3/11 vs 1/42, p less than 0.05) and hypoglycemia either severe (less than 0.83 mumol/l) (5/11 vs 3/42, p less than 0.01) or prolonged (less than 1.66 mumol/l for at least 36 hrs) (3/11 vs 0/42, p less than 0.01). The mean value of total bilirubin highest levels was 261 +/- 76 mumol/l in cases with kernicterus and 266 +/- 58 mumol/l in the control group (NS). In a case with kernicterus the total bilirubin level was 149 mumol/l (87 mg/l). Erythrocyte bilirubin was repeatedly assayed in 16 children, 4 of which were found to have kernicterus. There was no significant difference in the mean maximum peak of erythrocyte bilirubin between the 2 groups (kernicterus group: 17.8 +/- 3.4 mumol/l in the 4 cases with kernicterus. Finally, hypoglycemia, respiratory and/or metabolic acidosis were found associated with the highest erythrocyte bilirubin level, or during the 24 preceding hours in children with kernicterus only.

Acidosis↗
PubMed1992

Kernicterus in preterm newborns: past, present, and future.

This historical overview of kernicterus in prematurity, from the 1950s to the present, provides a unique perspective on this clinical conundrum. Three separate periods of pediatric history are detailed in relationship to our understanding of kernicterus in the preterm newborn: (1) the pre-intensive care era (1950 to 1965); (2) the low bilirubin kernicterus era (1965 to 1982); and (3) the 1980s. Each period demonstrates selected insights regarding kernicterus in prematurity, and together with recent reports suggest that premature newborns are now at extremely low risk of developing kernicterus when managed using current standards of care. However, the current conservative empiric guidelines for preventing kernicterus are questioned, and it is suggested that additional study is needed to clarify this issue in the 1990s.

Bilirubin↗
PubMed1984

The neuropathology of kernicterus in the premature neonate: diagnostic problems.

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.

Asphyxia Neonatorum↗
PubMed1991

Risk factors associated with kernicterus in the newborn infant: importance of benzyl alcohol exposure.

The prevalence of kernicterus in our neonatal intensive care unit (NICU) decreased from more than 2/1000 live births in 1980 to none in 1984. To clarify predictors of kernicterus, we examined the medical records of infants born during that time who died between 2 and 28 days of age. Infants were divided into three groups: those with kernicterus, all born before June 10, 1982 (n = 29); contemporaneous controls (n = 28); and infants born after June 10, 1982 (n = 32). Benzyl alcohol was not used after June 10, 1982. Kernicteric infants were more likely than contemporaneous controls to have seizures (p less than 0.001). Indices of pulmonary disease, arterial partial pressure of carbon dioxide and end-expiratory pressure on the ventilator were higher after 1982. However, exposure to benzyl alcohol was not different in kernicteric infants and contemporaneous controls, suggesting that benzyl alcohol exposure was not the explanation for the decrease in the prevalence of kernicterus in our NICU.

Analysis of Variance↗
PubMed1984

Value and limitations of bilirubin binding capacity in predicting the development of kernicterus.

The serum bilirubin (SBR) and the bilirubin binding capacity (BBC) were determined on hospital admission in 181 consecutive neonates with neonatal jaundice. Twenty-three babies were less than 2500 g and two were of birth weight less than 2000 g. Fifteen babies were preterm. There were eight cases of kernicterus. Although the serum bilirubin was generally higher in infants with a BBC less than 34 mumol/l, there was no correlation between the bilirubin binding capacity and the presence of kernicterus (r = 0.28, P greater than 0.05). However, when both the serum bilirubin and the bilirubin binding capacity were used, a low value of BBC less than 34 mumol/l increased the risk of kernicterus. Higher values of BBC, on the other hand, did not mean that there was less risk of kernicterus, other factors being equal. This, while the bilirubin binding capacity may provide an additional source of information, its limitations should always be borne in mind.

Bilirubin↗
PubMed1992

Determination of serum unbound bilirubin for prediction of kernicterus in low birthweight infants.

Serum unbound bilirubin concentrations (UBC) and serum total bilirubin concentrations (TBC) were measured serially in 138 low birthweight (LBW) infants treated with phototherapy for non-hemolytic hyperbilirubinemia. We attempted to assign the suitable critical UBC levels for predicting bilirubin encephalopathy into two different birthweight groups: a very low birthweight (VLBW) group (birthweight < 1,500 g) and an LBW group (birthweight between 1,500 g and 2,499 g). Twelve infants were diagnosed as 'at risk' for kernicterus, of whom 11 had signs of acute bilirubin encephalopathy and received exchange transfusion. One VLBW infant had neurological sequelae at a 3 year follow-up, although exchange transfusion was not carried out because of low TBC. Sensitivity and specificity for predicting kernicterus were calculated at different UBC levels between 0.6 microgram/dl and 1.5 micrograms/dl and TBC levels between 8 mg/dl and 26 mg/dl. The receiver-operating characteristic (ROC) curves plotted for UBC as a predictor of kernicterus were clearly shifted up and to the left compared with the curves for TBC in the VLBW and LBW groups. Thus, the UBC measurement may well provide a more rational basis for evaluating the risk of kernicterus in LBW infants. The optimal cut-off points were derived from these curves. In the VLBW group, the sensitivity was 100% and the specificity was 96% for a UBC of 0.8 microgram/dl, and 80% and 64% for a TBC of 11 mg/dl. In the LBW group, the sensitivity was 100% and the specificity was 98% for a UBC of 1.0 microgram/dl and 71% and 78% for a TBC of 16 mg/dl.(ABSTRACT TRUNCATED AT 250 WORDS)

Bilirubin↗
PubMed1989

Relationship of benzyl alcohol to kernicterus, intraventricular hemorrhage, and mortality in preterm infants.

Intraventricular hemorrhage and death in preterm neonates has been associated with the use of fluid containing benzyl alcohol, a bacteriostatic agent, to flush intravascular catheters. The hospital and autopsy records of infants admitted to a nursery during the last 18 months that benzyl alcohol was in use (218 patients) were reviewed and compared with those of infants admitted in the first 18 months after benzyl alcohol was withdrawn (232 patients). The volume of flush solution administered to each patient was estimated. Exposure to benzyl alcohol was significantly associated with the development of kernicterus (P less than .005), and intraventricular hemorrhage (P less than .000,000,5). Kernicterus did not develop in any patient after benzyl alcohol was withdrawn. Many patients with kernicterus or intraventricular hemorrhages received small daily volumes of fluid containing benzyl alcohol. Withdrawal of benzyl alcohol from clinical use had no demonstrable effect on mortality. Medications intended for neonatal use should not contain benzyl alcohol. Our data indicate that patients not exposed to benzyl alcohol have a greatly reduced risk of kernicterus. If this finding is confirmed by other investigators, present indications for exchange transfusions in preterm infants with moderate elevations of serum bilirubin should be reconsidered.

Benzyl Alcohol↗
PubMed1979

Auditory brain stem responses of kernicterus infants.

Auditory brainstem evoked responses (ABRs) and behavioral audiometry in 25 infants with kernicterus were studied to determine the level of the lesion causing their hearing disorders. ABR thresholds, peak latencies of wave I and V, and interwave latency of wave V-I were measured; behavioral audiometric thresholds were determined through conditioned orientation reflex audiometry (COR). Eighty-eight per cent of infants with kernicterus who showed ABR threshold elevation with respect to age-matched normals, were found to show ABR abnormalities associated with peripheral hearing loss, and 84% of these were found to have COR threshold elevation. The ABR abnormalities were threshold elevation of wave V, prolonged latency of wave I and V, and the absence of ABRs. However, no brainstem lesion pattern was found in our cases. Our results suggested that at least some lesions which produce hearing disorders in kernicterus occur in the cochlea or auditory nerve.

Adolescent↗
PubMed1987

Neonatal bilirubin toxicity. A review of kernicterus and the implications of drug-induced bilirubin displacement.

Kernicterus, the primary manifestation of neonatal bilirubin toxicity, remains an important complication of unconjugated hyperbilirubinaemia despite advances made with phototherapy and exchange transfusions. It results from the penetration of bilirubin into neuronal tissues of the CNS with subsequent damage to the mitochondrion. A number of factors may modify or potentiate bilirubin toxicity, including drugs administered to the infant. The importance of drug-bilirubin interactions in the pathogenesis of kernicterus was first realised quite inadvertently in the 1950s, and the potential risk for significant drug-bilirubin interactions has since become an important consideration in neonatal drug therapy. All drugs intended for use in newborn infants should be evaluated for their capacity to displace bilirubin. A number of techniques have been developed which have facilitated investigation of the mechanisms mediating the bilirubin-displacing effects of drugs and the pharmacokinetics of drug-bilirubin interactions. Further, the clinical risk for inducing kernicterus has been investigated for many of the drugs to which neonates may be exposed by direct administration, transplacentally, or through breast milk. This review summarises the available knowledge concerning the physicochemical properties and toxicities of bilirubin, reviews the methodologies used in evaluating drug-bilirubin interactions, and focuses on the mechanisms, pharmacokinetics and clinical significance of the bilirubin displacing effects of antibiotics, anticonvulsants, diuretics, and other important drug classes used in the treatment of neonates.

Bilirubin↗
PubMed1992

[Clinical study on the prevention of kernicterus caused by hereditary glucose-6-phosphate dehydrogenase deficiency].

A combined preventive scheme was conducted in four hospitals in Guangzhou to lower the rate of kernicterus and mental retardation caused by related neonatal jaundice due to G6PD deficiency. Observation was focused on 330 G6PD deficient infants, and the effects were measured according to the incidence of hyperbilirubinemia and kernicterus. The results, as compared to those of a retrospective study, showed that the incidence of hyperbilirubinemia was significantly decreased (51.4% to 21.2%), and neither kernicterus nor mental retardation infant was found in this series (12.5% in the control group). The authors conclude that this combined scheme is extremely effective and can be used in any large population area in which there is a high gene frequency of G6PD deficiency.

Female↗
PubMed1986

Kernicterus in an adult.

A 43-year-old woman was initially seen because of icterus. Clinical investigations revealed severe hepatic damage probably due to non-A, non-B hepatitis. She was treated with extracorporeal charcoal-column perfusion but died two weeks later in a hepatic coma. At autopsy, the brain showed kernicterus with typical discoloration of the hippocampus, the subthalamic nuclei, and the cerebellar dentate nuclei. Kernicterus in an adult is very rare. In this case, extracorporeal charcoal-column perfusion treatment led repeatedly to severe depletion of fibrinogen, with extensive hemorrhages. Overload of the already reduced hepatic glucuronyl-transferase capacity resulted in high serum levels of unconjugated bilirubin, an apparent prerequisite for the development of bilirubin encephalopathy.

Adult↗
PubMed1985

Kernicterus in term infants.

Kernicterus is a frequent occurrence in Chinese term infants. In a previous study, the mean level of serum bilirubin of 152 kernicteric infants was 35.4 mg/dl (605.3 mumol/l) and the range was 22.3-50 mg/dl. More recently, three further term infants developed kernicterus and one exhibited bilirubin level of only 23.3 mg/dl. Features of haemolysis were lacking in 56.8% of these infants. Evidence of brain damage occurred in 26.5% in a former series and in 5.5% of the more recent study of those infants who developed bilirubinaemia exceeding 20 mg/dl. Such a high risk favours the present practice of exchange transfusion for rising bilirubin beyond 20 mg/dl (342 mumol/l) in Chinese term infants.

ABO Blood-Group System↗
PubMed1990

Deposition of bilirubin acid in the central nervous system--a hypothesis for the development of kernicterus.

On the basis of the concentration of unconjugated bilirubin and available albumin for the binding of bilirubin it is possible to calculate the level of unbound bilirubin in a serum sample. The solubility of bilirubin can further be calculated when the pH is known. In cases of threatened kernicterus the free bilirubin concentration in serum samples from newborn infants surpasses the solubility by a factor close to one hundred. It is hypothesized that deposition of bilirubin in tissues takes place as an ongoing event, the deposited pigment being eliminated by bilirubin oxidase in healthy infants. Kernicterus results when the rate of deposition becomes overwhelming as a result of high bilirubin concentration, low albumin reserve, low pH, after administration of a displacing drug, or if the bilirubin oxidase system has been compromised by preceding birth asphyxia or other forms of central nervous system injury.

Adolescent↗
PubMed1990

Assessing the risk of kernicterus using nuclear magnetic resonance.

Kernicterus is the end result of injury to the central nervous system by bilirubin and other factors. Serum bilirubin levels alone are poor predictors of kernicterus especially in sick preterm infants. We need a rapid noninvasive indicator of neurotoxicity and impending cell injury. Bilirubin first seems to affect neuronal conduction before energy metabolism is impaired. Unchecked, this may lead to failure of ATP synthesis, resulting in the breakdown of all active intracellular processes. It is now possible to measure energy metabolism in vivo and noninvasively by surface coil 31P NMR spectroscopy. Recent animal studies demonstrate perturbations in energy metabolism when hyperbilirubinemia is associated with an open BBB. Perhaps the further developments in NMR spectroscopy and imaging will permit regional assessment of impending or actual bilirubin neurotoxicity and allow us to identify those infants in need of immediate treatment.

Adenosine Triphosphate↗
PubMed1986

Patterns of bilirubin staining in nonhemolytic kernicterus.

Patterns of bilirubin staining were studied in nine infants with kernicterus related to nonhemolytic hyperbilirubinemia, all weighing less than 1200 g, and nine matched controls. Three staining patterns were disclosed: a localized pattern in the central nervous system of kernicteric infants, with only the thalamus staining significantly often; staining, in extraneural tissues (adrenal, myocardial, renal, and colonic mucosa) only in kernicteric infants, despite similar bilirubin levels in both groups; and yellow staining of the alveolar hyaline membranes as a function of survival duration in both groups. Bilirubin staining of tissue is apparently a generalized phenomenon, most recognized in the central nervous system as kernicterus. Failure to maintain the impermeability of the cell membrane coupled with regional differences in blood flow would best explain bilirubin distribution. In contrast, the degree of bilirubin staining of alveolar hyaline membranes is time related in kernicteric and control infants.

Bilirubin↗
PubMed1988

Controversial topics in kernicterus.

The physiology of the blood-brain barrier and its disruption by a variety of pathophysiologic processes in the development of experimental and clinical kernicterus are reviewed. The use of currently available methods for measuring free and bound bilirubin in developing strategies for the prevention of kernicterus and more subtle sequelae of hyperbilirubinemia also are presented.

Bilirubin↗
PubMed1978

The supranuclear disturbances of gaze in kernicterus.

Five patients with kernicterus and ocular motility disturbances are reported. All of the patients showed some defect in vertical gaze but not always upgaze. The most severely affected patient exhibited slowness of horizontal saccades in addition to a total vertical gaze palsy. In general, the severity of the ocular motility disturbance paralleled the severity of hearing loss. It is suggested that damage to the periaqueductal area accounts for disturbances in vertical gaze and the infrequent horizontal saccadic disturbances results from interruption of the descending centrifugal fibers. It is emphasized that kernicterus must be included in the differential diagnosis of any supranuclear vertical gaze disturbance.

Athetosis↗