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Biomedical subjects

J A Low

Publications and source records attributed to J A Low.

At least 91 records · Page 5Linked to original sources
PubMed1978

Intrauterine growth retardation: a preliminary report of long-term morbidity.

This is a preliminary report of a prospective follow-up study of 88 intrauterine growth-retarded (IUGR) babies and a control group of 97 babies with weights appropriate for gestational age. The characteristic clinical features of IUGR pregnancies were observed in the obstetric patients of the IUGR group. The babies of the IUGR group have a phase of accelerated growth during the 3 months following delivery although they continue to be smaller than the babies of the control group at 12 months of age. No major neurologic abnormalities have been noted in the IUGR babies although behavioral differences were observed during the neonatal period and at 12 months of age. There were lower mental and physical development indices at 12 months of age which were due to the IUGR babies of lowest birth weight and those with a low maternal urinary estrogen index.

Asphyxia Neonatorum↗
PubMed1977

Intrapartum fetal asphyxia: clinical characteristics, diagnosis, and significance in relation to pattern of development.

The clinical and fetal heart rates and acid-base characteristics and their sequelae have been reviewed in 587 patients. The relevant clinical factors in the asphyxia group were the preterm fetus, the intrauterine growth retarded fetus, maternal toxemia, and midforceps delivery. The duration of the developing metabolic acidosis in the asphyxia group ranged from terminal to the last two hours of labor. Marked patterns of total decelerations and moderate and marked patterns of late decelerations are of predictive value in the diagnosis of intrapartum fetal asphyxia with a trend to an increased incidence in the longer duration categories, between four and two hours prior to delivery, and a significant increase in all categories during the last two hours of labor. The significance of intrapartum fetal asphyxia to the newborn infant is evident from the low Apgar scores, increased incidence of moderate and severe respiratory distress syndrome, and central nervous system complications in the asphixia group in relation to the normal group.

Acid-Base Equilibrium↗
PubMed1977

Urethral behavior during the involuntary detrusor contraction.

The bladder-urethral pressure records of 77 patients with involuntary detrusor contractions have been reviewed to described the behavior of the urethra in relation to the involuntary detrusor contraction. The involuntary detrusor contraction is preceded by a fall of urethral pressure in a manner similar to that observed with normal voiding. Parasympathetic blockade will completely or partially prevent the detrusor contraction with a limited effect upon the urethral pressure fall. The meschanism proposed is an interruption of synpathetic effect in the urethra and bladder with parasympathetic stimulation of the detrusor as in normal voiding. The stimulus of this mechanism in the involuntary detrusor contraction is not known; however, a wide range of possibilities should be considered.

Humans↗
PubMed1977

Intrapartum fetal heart rate profiles with and without fetal asphyxia.

Fetal heart rate profiles for periods up to 12 hours prior to delivery have been reviewed in 515 patients with a fetus at risk. Mechanisms other than fetal asphyxia will cause fetal heart rate decelerations, and fetal asphyxia may in some instances develop in the absence of total or late decelerations. However, an increasing incidence of total decelerations and late decelerations and particularly a marked pattern of total decelerations and late decelerations are of value in the prediction of fetal asphyxia. Fetal heart rate deceleration patterns can predict the probability of fetal asphyxia at the time of initial intervention, while a progression of fetal heart rate deceleration patterns in the individual fetus can be of assistance in the subsequent scheduling of serial acid-base assessments during labor.

Asphyxia↗
PubMed1976

Fetal heart deceleration patterns in relation to asphyxia and weight-gestational age percentile of the fetus.

The relation between fetal heart rate deceleration patterns and fetal asphyxia and the weight-gestational age percentile characteristics of the fetus has been reviewed from data obtained from 533 patients monitored during the intrapartum period. There is a significant relation between the frequency of total and late decelerations and fetal asphyxia, again confirming this as a useful criterion in the identification of fetal asphyxia. There is a significant relation between decreasing weight-gestational age percentile of the fetus and increasing frequency of total and late decelerations, identifying this fetal characteristic as another variable which will influence fetal heart rate deceleration patterns. The appreciation of the effect of this variable is useful in the interpretation of the fetal heart rate record during the intrapartum period.

Birth Weight↗
PubMed1975

The acid-base and biochemical characteristics of intrapartum fetal asphyxia.

The maternal and fetal acid-base, lactate, and pyruvate characteristics during the course of labor and at delivery were studied in 124 patients delivered of an infant with evidence of metabolic acidosis at delivery. This metabolic acidosis is principally caused by hyperlactatemia resulting from the tissue oxygen debt accompanying fetal asphyxia. Hypoxemia was one mechanism contributing to this fetal asphyxia and tissue oxygen debt. This evidence of fetal asphyxia developed during the last half and principally during the last two hours of the intrapartum period. Acid-base assessment of fetal blood with identification of a metabolic acidosis will provide an accurate objective diagnosis of intrapartum fetal asphyxia.

Acid-Base Equilibrium↗
PubMed1975

Clinical characteristics of pregnancies complicated by intrapartum fetal asphyxia.

The clinical characteristics of 124 pregnancies complicated by intrapartum fetal asphyxia have been reviewed. The evidence of fetal asphyxia tends to appear earlier in patients with maternal medical and obstetric complications than in those with labor complications. Evidence of clinical fetal distress was present in 36 per cent and was not related to the severity of the asphyxia. Low Apgar scores occurred in 40 per cent of infants with moderate asphyxia and in 80 per cent of infants with severe asphyxia at delivery. In the newborn infants, clinical evidence of cerebral abnormality was observed in 3 per cent, and evidence of the respiratory distress syndrome was seen in 3 per cent of the study group.

Acidosis↗
PubMed1975

The incidence of fetal asphyxia in six hundred high-risk monitored pregnancies.

Six hundred high-risk monitored obstetric patients were reviewed for evidence of fetal asphyxia at delivery. The over-all incidence was 20 per cent, i.e., 8 times the incidence in a normal obstetric population. Highly significant indicators of risk for asphyxia were severe toxemia (79 per cent), prematurity with further medical or obstetric complications (36 per cent), and clinical fetal distress, particularly meconium staining with fetal heart rate abnormality (33 per cent). All obstetric, medical, or gestational complications in this review were associated with an increased risk for fetal asphyxia when compared to that in a normal obstetric population.

Asphyxia Neonatorum↗
PubMed1971

Classification of perinatal mortality.

A classification based upon pathophysiological mechanisms has been applied to perinatal mortality. The approximate relevance of each group was: fetal insufficiency 40%, respiratory failure 30%, developmental abnormality 20%, and the specific mechanisms 10%. Secondary subclassification of each category according to the maturity of the gestation emphasizes the importance of prematurity in the total perinatal mortality (66%) and the relevance of each pathophysiological mechanism in each phase of maturity. The principal mechanism in the mature group is fetal insufficiency and in the premature group, particularly between 20 and 28 weeks, it is neonatal respiratory failure. Perinatal death due to developmental abnormalities occurs most frequently in the mature infant and due to specific mechanisms in the premature infant, particularly between 29 and 36 weeks. It is suggested that greater emphasis should be placed on perinatal mortality rather than the separate consideration of stillbirth and neonatal mortality.

Congenital Abnormalities↗