Search

Experimentally modified breathing pattern in human subjects, by varying the inspired gas mixture or administering different neuromodulators, has been studied extensively in the past, yet unmodified breathing has not. Moreover, most data refer to infants during sleep and adults during wakefulness. We studied the baseline breathing pattern of preterm infants [n = 10; GA 30 (27-34) wk (median, range)]; term infants [n = 10; GA 40 (39-41) wk)], and adult subjects [n = 10; age 31 (17-48) y)] during quiet sleep. A flow-through system was used to measure ventilation. We found: (i) instantaneous ventilation was 0.273 ± 0.006, 0.200 ± 0.003, and 0.135 ± 0.002 L · min[sup -1] · kg[sup -1] in preterm, term infants, and adult subjects; the coefficients of variation were 39%, 25%, and 14% (p < 0.01). The greater coefficient of variation in neonates compared to adults related to increased variability in Vt (39% and 25% in preterm and term infants vs 14% in adults; p < 0.01) and f (39% and 22% vs 9%; p < 0.01). The major determinant of frequency in preterm infants was Te (81% variability), Ti varying less (25% variability); (ii) V[sub T]/Ti decreased and Ti/Ttot increased with age; (iii) the higher breath-to-breath variability in preterm infants was associated with larger changes in alveolar PCO[sub 2] and a larger variability in O[sub 2] saturation than later in life. We conclude: (i) the high breath-to-breath variability in frequency in preterm infants closely relates to variation in Te; (ii) decreased effective inspiratory timing (Ti/Ttot) in preterm infants compared with adults likely reflects their high pulmonary impedance; and (iii) greater breath-to-breath variability in ventilation in neonates with large variations in alveolar PCO[sub 2] and O[sub 2] saturation remains when compared with values in the sleeping adult. We speculate that high variability in Te early in life represents an effort to maintain lung volume through increased post-inspiratory diaphragmatic activity and increased upper airway resistance in an attempt to avoid collapse due to poor chest wall recoil. [ABSTRACT FROM AUTHOR]

Background: The perinatal-neonatal course of very-low-birth-weight (VLBW) infants might affect their childhood growth. We evaluated the effect of parental anthropometry and perinatal and neonatal morbidity of VLBW neonates on their childhood growth., Methods: We obtained parental anthropometry, height and weight at age 6-10.5 years of 334 children born as VLBW infants. Parental, perinatal and neonatal data of these children were tested for association with childhood anthropometry., Results: (1) Maternal and paternal weight standard deviation score (SDS) and discharge weight (DW) SDS were associated with childhood weight SDS (R(2)= 0.111, p < 0.00001); (2) Maternal and paternal height SDS, corrected gestational age (GA) at discharge, maternal assisted reproduction and SGA status were associated with childhood height SDS (R(2)= 0.208, p < 0.00001); (3) paternal weight SDS, DW SDS and surfactant therapy were associated with childhood body mass index (BMI) SDS (R(2)= 0.096, p < 0.00001). 31.1% of VLBW infants had DW SDS < -1.88, and are to be considered small for gestational age ('SGA'). One quarter of these infants did not catch up by age 6-10.5 years., Conclusion: Childhood anthropometry of VLBW infants depends on parental anthropometry, postnatal respiratory morbidity and growth parameters at birth and at discharge. Almost one-third of VLBW premature infants had growth restriction at discharge from neonatal intensive care unit (NICU), a quarter of whom did not catch up by age 6-10.5 years.

Over the last two decades, drug and alcohol abuse by pregnant women has spread to epidemic proportions. Maternal drug abuse has neurobehavioral and somatic effects which may be long-lasting and devastating to the offspring. Opiates, such as heroin and pain killers that contain a narcotic component, are widely abused today. A prominent manifestation of fetal exposure to these drugs is the neonatal withdrawal syndrome, which typically includes wakefulness, jitteriness and other symptoms of cerebral irritability. These, in turn, may interrupt early mother-infant interaction, affecting the infant's long-term emotional and cognitive development. Fetal cocaine exposure may cause neonatal cerebral irritability, changes in habituation responses, reduced head circumference, poor mental development and long-lasting impairment of the brain. Benzodiazepines can cause fetal dysmorphism (including microcephaly), neurological and behavioral impairments and neonatal withdrawal symptoms. Maternal use of amphetamines may cause neonatal dysphoria and agitation, as well as long-term lassitude and drowsiness that may result in poor feeding. Fetal exposure to alcohol may cause neonatal withdrawal symptoms, maladaptive behavior in childhood and the fetal alcohol syndrome (including microcephaly). Maternal alcohol consumption is also a common cause of mental retardation. Fetal exposure to marijuana may delay maturation of the visual system and impair memory and verbal performance at 2 years of age. The inevitable conclusion is that society must seek ways not only to treat, but also to prevent this epidemic. To this end, a key factor would be to identify potential drug abusing mothers before they reach the stage of prenatal care and educate them regarding the fatal consequences of drug abuse.