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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↗
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↗
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↗
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↗
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↗
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↗
PubMedDate not supplied

[Kernicterus. Anatomo clinical correlation in 64 newborn infants].

The case histories and autopsy reports of 64 neonates who died from kernicterus were reviewed. The most outstanding findings were: high incidence of kernicterus with serum indirect bilirubin less than 15 mg.; different clinical picture of the premature in comparison with term neonate; predisposing factors such as respiratory distress and intrauterine malnutrition were often associated in the premature. Preventive, educational and therapeutic measures were discussed at the end.

Autopsy↗
PubMed1979

The pathochemistry of kernicterus.

The stoichiometry of bilirubin--albumin interaction has been analyzed and quantitated in several recent studies, confirming that albumin binding of bilirubin obeys the law of mass action [4, 5, 14, 16, 26, 36, 43, 46, 61, 65, 73, 92, 111]. These studies provide a basis for interpreting bilirubin transport, cell uptake and toxicity from physicochemical and pharmacologic perspectives [35, 42, 58, 59]. In this report, we propose a model of the pathogenesis of kernicterus which views serum albumin and tissue as competing with each other for binding the miscible bilirubin pool. Evidence is presented to show that bilirubin normally binds reversibly to cellular membranes and certain soluble enzymes just as it does to albumin; the unbound bilirubin concentration is the driving force for both albumin and tissue binding. We propose that albumin binding is determined by the concentration of free bilirubin anion (which is essentially unaffected by physiologic pH changes), and that tissue binding is mainly determined by the concentration of free bilirubin acid (which is greatly influenced by pH). When bilirubin--tissue complexes are formed, essential cell functions may be inhibited, producing cellular acidosis, irreversible intracellular aggregation of bilirubin, and cell death. In developing this argument, we will sequentially discuss relevant features of bilirubin chemistry, the binding of bilirubin to albumin, the formation of bilirubin--tissue complexes, bilirubin toxicity, alternative viewpoints of bilirubin transport, and, finally, the implications of this model to the clinical management of jaundiced infants. It should be emphasized that this paper is an attempt to analyze bilirubin transport and toxicity using basic chemical principles; it is an extension of previously published proposals [17, 77], and will undoubtedly require further modification as additional experimental data becomes available.

Bilirubin↗
PubMed1979

Is kernicterus due to inhibition of brain hexose-monophosphate shunt activity by bilirubin?

Degradation of biogenic amines in the central nervous system is accomplished by the monoamine oxidase system. The by-products of this reaction, hydrogen peroxide and amino aldehydes, are toxic to neurones. Detoxification of these by-products is normally mediated by generation of NADPH via the hexosemonophosphate (HMP) shunt. It is proposed that inhibition of the HMP shunt by unconjugated bilirubin leads to the toxic accumulation of hydrogen peroxide and aldehydes.

Bilirubin↗
PubMed1977

Prevention of kernicterus, based on recent progress in bilirubin chemistry.

A review is presented of recent progress in bilirubin chemistry, its binding to albumin, displacement by drugs, and the mechanism of phototherapy. Quantitative formulations of the effect of albumin dosage, of varying pH, and of fatty acids result in a diagram which may be tried as an aid to indications for therapy.

Albumins↗
PubMed1975

Bilirubin interaction with ganglioside: possible mechanism in kernicterus.

Reaction of bilirubin with increasing amounts of ganglioside purified from neonatal brain significantly alters the spectral absorption of bilirubin in proportion to the quantity of ganglioside added. Increments in absorbance occur at 353 nm with a prompt but transient increase at 486 nm. A decrease in absorbance occurs which is most marked at 447 nm. When gangliosides are added to bilirubin (9.1 mug/ml or 0.016 muM/ml), the decrease in absorbance is essentially linear up to the highest concentration of purified ganglioside tested (182 mug/ml or 0.097 muM/ml), which represents a molar ratio of 6.1:1. The asymptotic nature of the bilirubin-ganglioside reaction as measured by the decrease in absorbance with time suggests a stoichiometric relationship between the two substances. An isosbestic point was demonstrated at 405 nm. Observations reported here suggest bilirubin reaction with ganglioside is at least a two-step process.

Bilirubin↗
PubMed1992

Management of neonatal hyperbilirubinaemia and prevention of kernicterus.

Hyperbilirubinaemia remains one of the most common and more important pathological conditions in the newborn. The possibility that the so-called physiological or developmental hyperbilirubinaemia, with relatively low levels of serum bilirubin, could be responsible for bilirubin encephalopathy in the small premature infant is of great concern to the neonatologist; premature newborns are prone to developing hyperbilirubinaemia. Current methodologies for suppressing severe neonatal jaundice include: (a) attempts to stimulate liver conjugating enzymes using drugs such as phenobarbital; (b) attempts to degrade bilirubin with phototherapy; and (c) exchange transfusion. It is too soon to consider tin-protoporphyrin as a drug for the prevention and treatment of neonatal hyperbilirubinaemia. However, if it can be shown that tin-protoporphyrin can serve as a safe and less costly alternate treatment, a considerable improvement in the management of neonatal jaundice would be achieved.

Bilirubin↗