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Biomedical subjects

R T Hall

Publications and source records attributed to R T Hall.

At least 73 records · Page 4Linked to original sources
PubMed1981

Etiologic factors in rickets of very low-birth-weight infants.

The incidence of rickets was found to be 32% (39/125) in a retrospective review of consecutive survivors of very low birth weight in whom serial radiographic and biochemical data were obtained. A higher proportion of these infants were black, had a greater initial weight loss, and had a longer hospitalization; there was a prevalence of births in the spring. Soy formula, supplemented with calcium and vitamin D but not phosphorus, was used predominantly in both groups; cumulative calcium, phosphorus, vitamin D, and caloric intakes were the same. We believe that the etiology of rickets in VLBW infants is multifactorial; however, nutritional deficiency is of central importance. Soy isolate formula, as well as human milk and many other commercially available formulas, do not provide sufficient calcium and phosphorus to keep pace with rates of intrauterine accretion. Supplementation with calcium, phosphorus, and vitamin D, beginning as soon as possible after birth, is indicated.

Black People↗
PubMed1980

Glucose disappearance in infants of diabetic mothers. III. Relationship of spontaneous glucose disappearance to glucose tolerance, neonatal hypoglycemia and lowest blood glucose.

Spontaneous glucose disappearance in the first 90 min of life and glucose disappearance following an intravenous injection of 1 g/kg dextrose were measured in 23 infants of insulin-dependent diabetic mothers. Spontaneous disappearance was log-linear in 12/23 infants, providing for calculation of an endogenous Kt which correlated significantly (P < 0.01) with the exogenous Kt determined after the dextrose injection, r = 0.74. Hypoglycemia < 20 mg/dl occurred in 4/23 infants, and was identified during the spontaneous glucose disappearance (3 infants) and/or predicted by an endogenous Kt greater than or equal to 3.0%/min (2 infants). There was also a significant inverse correlation (P < 0.01) of the lowest blood glucose obtained within the first 24 h of life with the endogenous Kt, r = 0.61. There was no correlation of the endogenous or exogenous Kt, lowest blood glucose or hypoglycemia with White's classification of the maternal diabetes, diabetic control during pregnancy, the maternal blood glucose at delivery or the cord blood glucose. These data indicate that determination of spontaneous glucose disappearance within the first 90 min of life is useful in identifying infants of diabetic mothers with hypoglycemia or those who will subsequently develop hypoglycemia.

Blood Glucose↗
PubMed1980

Cerebrospinal fluid lactate dehydrogenase in infants with perinatal asphyxia.

Cerebrospinal fluid (CSF) lactate dehydrogenase was determined in 19 control infants without asphyxia (Group I), 24 infants with perinatal asphyxia (Group II), and 26 asphyxiated infants with seizures (Group III). Mean birthweights, gestational ages, CSF glucose, protein and red blood cells, and the ages at which the lumbar punctures were performed were not significantly different among the three groups. Mean CSF lactate dehydrogenase was significantly higher in Group III than in Groups I and II. Isoenzyme patterns indicated that the origin of the CSF lactate dehydrogenase was neuronal tissue, or a plasma transudate from increased permeability of the blood-brain barrier. There were 10 deaths due to anoxic encephalopathy in Group III, but none in Groups I or II. Follow-up of survivors at 10 to 30 months of age revealed neurological sequelae in three infants in Group I, two in Group II and five in Group III. Mean CSF lactate dehydrogenase in those with sequelae had not been significantly different from that of normal survivors; however, the mean was significantly higher in infants who died with anoxic encephalopathy compared with normal infants. These data indicate that CSF lactate dehydrogenase is significantly elevated in infants with fatal anoxic brain damage, and suggest that determinations may be of prognostic value in non-fatal cerebral hypoxia.

Asphyxia Neonatorum↗
PubMed1979

Tracheal agenesis.

Tracheal agenesis is a rare cause of respiratory distress in the neonatal period. Temporary survival depends on ventilation through the esophagus. Thirty-eight case reports of tracheal agenesis (including one from this institution) have appeared in the literature. In this paper, we present the case reports of our 2 patients and review the literature. Tracheal agenesis is associated with a wide variety of congenital anomalies, the most frequent being ventricular septal defect. A new classification encompassing seven types of tracheal agenesis is described.

Abnormalities, Multiple↗
PubMed1979

Urine culture in the evaluation of suspected neonatal sepsis.

Clinical records of patients in a neonatal intensive care unit were reviewed to determine the efficacy of obtaining a urine culture in the detection of neonatal sepsis. During a 12-month period, 188 sets of concomitant blood and urine cultures were obtained in infants less than 72 hours of age (early onset group) and 189 sets of cultures in infants over 72 hours of age (late onset group). Blood cultures were positive in nine instances in the early onset group and 11 instances in the late onset group. All but one blood culture in each group was accompanied by a negative urine culture. Urine cultures alone were positive in two instances in the early onset group and 13 instances in the late onset group (P less than 0.05). Symptoms did not differentiate infants with bacteremia from infants with bacteruria. Culture of the urine was shown to be necessary for the detection of a significant number of late onset infections. Urine culture in the early onset age group had a significantly lower yield, and the risk of suprapubic bladder tap in this group may not be justified.

Bacterial Infections↗
PubMed1979

Strain specificity of opsonins for group B streptococci types II and III.

Strains of types II and III group B streptococci do not appear to be uniformly susceptible to opsonization by antibody-containing human sera, as studied using both a chemiluminescence and a radiolabeled bacterial uptake technique. We could not demonstrate a correlation of serum-sensitive or resistant strains with capsular antigen quantities, although serum absorption studies with whole organisms and HCl, trichloroacetic acid, and saline extracts indicated that the antibody to type-specific capsular polysaccharide is important in opsonizing both serum-resistant and serum-sensitive strains. Since trypsin treatment produced significantly enhanced opsonization of serum-resistant and serum-sensitive strains, proteins present on some group B streptococci may be important antiphagocytic factors.

Antibodies, Bacterial↗
PubMed1979

Neonatal cellular and humoral immunity to group B streptococci.

The mechanisms of host resistance to group B streptococci have not been defined precisely. In the studies reported here we have assessed the contributions of both humoral and cellular factors in protection against strains of this group. With assays of specific opsonic activity based upon the production of polymorphonuclear leukocyte chemiluminescence and radiolabeled bacterial uptake, we have demonstrated that specific heat-stable antibody and the classic complement pathway are major factors in opsonization of these organisms. In the absence of specific antibody, fresh serum resulted in markedly reduced bacterial uptake indicating, at best, a minor role for the alternative complement pathway. Additional studies have indicated that strain-specific antiphagocytic factors as well as type-specific ones may play a role in the virulence of these organisms. Neonates who developed group B streptococcal sepsis usually lacked opsonic activity in their infecting strain. In addition, polymorphonuclear leukocytes from normal term and stressed neonates showed impaired metabolic activation as measured in the chemiluminescence assay following exposure to opsonized group B streptococci. These results suggest that neonates who develop group B streptococcal disease may have defects in both the humoral and cellular aspects of their acute inflammatory response which may contribute to the high mortality observed in this most fulminant of bacterial infections.

Antibody Formation↗
PubMed1979

Morbidity and mortality of advanced gestational age: post-term or postmature.

A 6-year retrospective review of 53 post-term infants admitted to a neonatal intensive care unit (NICU) was undertaken to determine whether morbidity and mortality related to uteroplacental insufficiency were confined to infants with the postmaturity syndrome. Objective identification of infants with significant intrauterine growth retardation (IUGR) was done using the ponderal index (PI). All neonatal deaths occurred in large, appropriately grown infants and were associated with anoxic encephalopathy. Morbidity was equally distributed between normally grown and malnourished infants. Developmental outcome was similar in the 2 groups of infants. Neonatal complications and sequelae occurred in the absence of recognizable fetal malnutrition. Therefore, the post-term infant should be considered at risk, even if normally grown.

Asphyxia Neonatorum↗
PubMed1978

Blood-transfusion in group-B streptococcal sepsis.

Transfusion of fresh whole blood was evaluated as a means of supplying opsonins and lessening the high mortality of group-B streptococcal sepsis in neonates. Pre-transfusion and post-transfusion sera from 22 infants were examined for the presence of opsonins against group-B organisms. Opsonic activity rose only when donor blood containing heat-stable antibody was administered in high volume (greater than 40% of blood-volume). 9 of 9 infants transfused with blood containing antibody to their infecting strain survived septic episodes. 3 of 6 who received blood lacking antibody to their infecting strain died.

Antibodies, Bacterial↗