Kernicterus in a Full Term Infant

PEDIATRICS ◽  
1994 ◽  
Vol 93 (6) ◽  
pp. 1003-1006
Author(s):  
Anna A. Penn ◽  
Dieter R. Enzmann ◽  
Jin S. Hahn ◽  
David K. Stevenson

Neonatal jaundice can represent a benign physiologic process or be the harbinger of serious illness with associated severe neurotoxicity. The neurological manifestations of kernicterus, a condition resulting from the deposition of unconjugated bilirubin in the central nervous system, are rarely seen in modern neonatal care, but jaundice, which reflects elevated serum bilirubin levels, is one of the most common findings in the neonatal period.1 More than half of all term infants will develop some neonatal jaundice and at least 6% will have a serum bilirubin concentration above 12.9 mg/dL.2 The appropriate treatment of hyperbilirubinemia is currently a topic of much debate in pediatrics, particularly treatment of full term infants without risk factors for hemolytic disease.3,4

PEDIATRICS ◽  
1982 ◽  
Vol 70 (3) ◽  
pp. 464-467 ◽  
Author(s):  
M. Jeffrey Maisels ◽  
Sarah Conrad

A total of 292 transcutaneous bilirubin (TcB) measurements were performed in 157 white full-term infants: 157 were obtained from the forehead and 135 from the midsternum. TcB measurements correlated well with serum bilirubin determinations (r = .93, P < .0001). The sensitivity of the test was 100% and the specificity 97%. It was possible to establish guidelines for the TcB measurement which identified all infants whose serum bilirubin concentrations exceeded 12.9 mg/100 ml (221 µmoles/liter) with no false-negative and only five false-positive determinations (3%). The positive predictive value for the TcB measurements was 58%. This implies that, in our population, an infant with a TcB index ≥24 has a 58% chance of having a serum bilirubin concentration >12.9 mg/100 ml. The negative predictive value was 100%. Thus, a negative test will correctly predict the absence of hyperbilirubinemia in all cases. As these measurements were obtained prospectively in a well-baby population with a prevalence of hyperbilirubinemia (>12.9 mg/100 ml) of 4.5%, the positive predictive value should be applicable to other similar populations and will, in fact, increase in populations with a higher prevalence of hyperbilirubinemia. TcB measurements can be recommended for the identification of significant neonatal jaundice in full-term infants. It is important to recognize, however, that because of potential variations in TcB meters as well as serum bilirubin measurements in different laboratories, each institution should establish its own criteria for the use of this instrument.


PEDIATRICS ◽  
1983 ◽  
Vol 71 (3) ◽  
pp. 457-459
Author(s):  
M. JEFFREY MAISELS ◽  
CHERYL LEE

The transcutaneous bilirubin meter has been shown to be a useful screening device for the identification of significant neonatal jaundice in full-term infants.1-3 Investigators have, nevertheless, emphasized the necessity for each institution to establish the relationship between the transcutaneous bilirubin index, as measured with a particular instrument, and the serum bilirubin determination obtained from the institution's laboratory. 3 This is important, because of the known variation between laboratories in the measurement of serum bilirubin concentration4 and because no information has been published regarding the potential variation in the response of different transcutaneous bilirubin meters.


1994 ◽  
Vol 15 (11) ◽  
pp. 422-432
Author(s):  
Lawrence M. Gartner

Jaundice in the newborn has presented a diagnostic challenge to clinicians for millennia. Because virtually every newborn infant has an elevated serum bilirubin in comparison with the normal adult and more than 50% are visibly jaundiced during the first week of life, the physician's first challenge is to differentiate pathology from variations within the normal range. Today, clinicians are faced with critical therapeutic decisions as well; treatment should be instituted only when benefit will accrue. During the past several years, clinical experts and scholars have reconsidered the risks and possible benefits of bilirubin in the newborn, have altered indications for diagnostic procedures, and have suggested new criteria for therapy. In addition, the relationship between breastfeeding and neonatal jaundice has been clarified. These major new concepts have changed the management of jaundice in the newborn significantly, particularly in the healthy term infant. This review examines these new concepts, places them in a clinical perspective, and provides guidelines for management based on a synthesis of expert opinions and the recently published practice guidelines of the American Academy of Pediatrics. 1 Definitions The term neonatal jaundice designates all situations in the newborn infant in which the serum bilirubin is sufficiently elevated to cause at least minimally visible yellowing of the skin, ocular sclerae, or both.


PEDIATRICS ◽  
1984 ◽  
Vol 73 (4) ◽  
pp. 520-525 ◽  
Author(s):  
Lucy M. Osborn ◽  
Michael I. Reiff ◽  
Roger Bolus

Hyperbilirubinemia is the most common problem experienced by the full-term infant in the immediate neonatal period. The development of jaundice was prospectively investigated in 866 newborns. Significant correlations were found between the serum bilirubin level and the method of birth, perinatal complications, blood group incompatibilities, birth weight, and method of feeding. Breast-feeding was highly related to the development of exaggerated jaundice. The most common occurrence of jaundice requiring phototherapy was in breast-feeding infants in whom no cause for the jaundice could be determined. Study findings were most compatible with a theory of relative caloric deprivation as an explanation of the increased incidence of hyperbilirubinemia found in breast-fed newborns.


PEDIATRICS ◽  
1979 ◽  
Vol 63 (5) ◽  
pp. 812-815
Author(s):  
Edward R. Chaplin ◽  
Gary W. Goldstein ◽  
David Norman

During the first days of life intracranial hemorrhage is a frequent cause of convulsions in the full-term infant.1,2 If spinal fluid is bloody and there is no evidence of asphyxia, infection, or acute metabolic disease, then a presumptive diagnosis of primary subarachnoid hemorrhage is often made.1-3 These infants appear remarkably well in the interictal period, and their outcome is usually good.1,2 Since pathologic confirmation is not available, it has been assumed that bleeding occurs directly into the subarachnoid space and not as an extension of a subdural, intraventricular, or intracerebellar hemorrhage.1,3-5 During a 13-month period at our institution, only four full-term infants had seizures and bloody spinal fluid.


PEDIATRICS ◽  
1951 ◽  
Vol 8 (3) ◽  
pp. 431-434
Author(s):  
HEYWORTH N. SANFORD ◽  
J. HAROLD ROOT ◽  
R. H. GRAHAM

Chairman Sanford: Dr. Herman N. Bundesen, Commissioner of Health of Chicago, organized 12 years ago the "Chicago Premature Plan." This consists in registering all premature infants with the City Health Department within a few hours after birth. The premature infant who is born at home, or in a hospital that does not have adequate premature care, is transported in an oxygenated incubator ambulance to a hospital which specializes in such care. From 1936 to 1947 premature infant deaths in Chicago have been lowered 6½%. The full term infant death rate during the same period has been lowered about 3%. Inasmuch as the premature death rate has been lowered about double that of the full term infant rate, we believe this procedure has been the cause of reduction. In 1936 there were 47,000 live births in Chicago. In 1947 there were 82,000, or an increase of 80%. In this number the full term infants increased from 45% to 60%, whereas the premature infants increased from 2000 to over 5000, or about 140% increase of premature infants born in Chicago during the last 10 years. This adds a considerable increase to the number of infants for our available premature infants beds. Where formerly we planned 5 premature births to each 100 full term births, we now find that prematures have increased to 8 per 100 full term infants. Causes of prematurity are multiple births, toxemia, heart disease, syphilis, tuberculosis, infections, accidents, premature separation of the placenta and abnormalities of the reproduction tract. It is generally understood that there is a tendency for more premature births among the Negro race than the white race.


PEDIATRICS ◽  
1950 ◽  
Vol 5 (2) ◽  
pp. 184-192
Author(s):  
HERBERT C. MILLER

An analysis of the significant causes of death in 4117 consecutive births was made; there were 66 fetal deaths and 85 neonatal deaths. A significant cause of death was determined in 51 fetuses and 56 live-born infants. Eighty-five per cent of the live-born infants who weighed over 1000 gm. at birth and had postmortem examinations had causes of death which were considered to be significant. Almost half of the live-born premature infants with birth weights between 1000 and 2500 gm. were considered to have had more than one significant cause of death. The so-called significant causes of death among live-born infants differed from those determined for fetuses dying before birth. Among the former, pathologic conditions in the infants were determined four times more frequently than in those dying before birth and, in the latter, maternal complications of pregnancy and labor were diagnosed as significant causes of death five times more frequently than in infants dying in the neonatal period. Hyaline-like material in the lung was considered to be the most frequent significant cause of death in live-born premature infants; congenital malformation and anoxia resulting from complications of labor were the most frequently determined significant causes of death in live-born full term infants. No differences were found in the significant causes of death in premature and full term fetuses. Anoxia resulting from accidental and unexpected interruption of the blood flow in the placenta and umbilical cord and from dystocia was the most frequently determined significant cause of death in both groups. A plea has been made for the adoption by obstetricians, pathologists and pediatricians of a formal uniform plan of classifying the causes of fetal and neonatal death which would divest current efforts to determine the cause of death of as much vague terminology and arbitrary opinion as possible.


PEDIATRICS ◽  
1968 ◽  
Vol 41 (3) ◽  
pp. 574-587 ◽  
Author(s):  
D. W. Thibeault ◽  
E. Poblete ◽  
P. A. M. Auld

Twenty-six premature and five full-term infants, ranging in birth weight from 860 to 4,040 gm and in age from 3 hours to 98 days, were the subjects of this study. Measurements of thoracic gas volume and determination of alveolar-arterial oxygen gradient and arterial-alveolar carbon dioxide gradient were performed. All infants showed a decrease in thoracic gas volume in the first days of life. The initial high thoracic gas volume is thought to be due to trapped gas. The ability to trap gas was demonstrated in a number of infants. In the full-term infant the decrease in thoracic gas volume is associated with improvement in lung function. In the premature infants the decrease in lung volume is associated with a persistently elevated alveolar-arterial oxygen gradient and in an inequality of perfusion and ventilation, as evidenced by the large arterial-alveolar carbon dioxide gradient. In a small group of infants increase in functional residual capacity produced by negative pressure around the chest resulted in a decrease in the carbon dioxide and oxygen gradients, indicating that the infant's lung volume is less than optimum. These observations characterize in physiological terms some of the respiratory difficulties in small premature infants.


1982 ◽  
Vol 28 (2) ◽  
pp. 317-322 ◽  
Author(s):  
R Jedeikin ◽  
S K Makela ◽  
A T Shennan ◽  
R D Rowe ◽  
G Ellis

Abstract Isoenzymes of creatine kinase (ATP:creatine phosphotransferase; EC 2.7.3.2; CK) were measured by electrophoresis in serum from cord blood and skin-puncture blood taken from 45 healthy full-term infants during the first three postnatal days. Mean total CK activities (in U/L at 30 degrees C) were 185 in cord samples, 536 in samples taken between 5--8 h postnatally, 494 between 24--33 h, and 288 in the 72-100 h samples. Values for all three isoenzymes increased to a peak over this period, with the highest values generally being found in the samples taken 5--33 h after birth; the subsequent decline was most rapid for CK-BB. Serum CK isoenzymes in cord samples and those taken at 72--100 h in the 11 babies delivered by cesarian section did not differ significantly from those of babies delivered vaginally. However the postnatal increases in total CK, CK-MM, and CK-MB (but not in CK-BB) were significantly greater in those patients born by vaginal delivery. The reasons for the increases in CK isoenzymes after birth are not clear, but our results and reported studies on the ontogeny of CK suggest that CK-MB cannot be regarded as a "cardiac-specific" isoenzyme in the neonatal period.


Author(s):  
M Andrew ◽  
B A Paes ◽  
R A Milner ◽  
P J Powers ◽  
M Johnston ◽  
...  

A cohort study was performed to determine the postnatal development of the coagulation system in the “healthy” premature infant. Mothers were approached for consent and a total of 132 premature infants were entered into the study. The group consisted of 64 infants with gestational ages of 34-36 weeks (prem 1) and 68 infants whose gestational age was 33 weeks or less (prem 2). Demographic information and a 2 ml blood sample were obtained on days 1, 5, 30, 90, and 180. Plasma was fractionated and stored at −70°C for batch assaying of the following tests: screening tests, PT, APTT; factor assays (biologic (B)); fibrinogen, II, V, VII, VIII:C, IX, X, XI, XII, prekallikrein, high molecular weight kininogen, XIII (immunologic (I)); inhibitors (I), antithrombin III, aα2-antiplasmin, α2-macroglobulin, α-anti-trypsin, Cl esterase inhibitor, protein C, protein S, and the fibrinolytic system (B); plasminogen. We have previously reported an identical study for 118 full term infants. The large number of premature and full term infants studied at varying time points allowed us to determine the following: 1) coagulation tests vary with the gestational age and postnatal age of the infant; 2) each factor has a unique postnatal pattern of maturation; 3) near adult values are achieved by 6 months of age; 4) premature infants have a more rapid postnatal development of the coagulation system compared to the full term infant; and 5) the range of reference values for two age groups of premature infants has been established for each of the assays. These reference values will provide a basis for future investigation of specific hemorrhagic and thrombotic problems in the newborn infant.


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