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It is not known how immaturity and disease influence postnatal thyroid function in infants <30 wk of gestational age. We performed serial measurements of plasma thyroxine (T4), free T4 (FT4), triiodothyronine (T3), reverse T3 (rT3), TSH, and T4-binding globulin (TBG) in 100 infants of <30 wk of gestation, during the first 8 postnatal weeks, to investigate the influences of disease and gestational age on the time course of thyroid hormones. One hundred infants were divided twice into two groups: 1) in a group of 25-28 and of 28-30 wk of gestation; and 2) in a sick and a healthy group, with similar gestational ages. The time course of T4, FT4, T3, TSH, and TBG, but not rT3 differed significantly (p < 0.005) between the gestational age groups. T4 and FT4 decreased to levels below the cord blood value with a deeper FT4 nadir on d 7 in the youngest group. Disease decreased T4, FT4, T3, TSH, and TBG concentrations especially during the 1st wk after birth (p < 0.005). However, the FT4 nadir on d 7 was similar in sick and healthy infants. After 3 wk, T4, FT4, T3, and TBG were higher in the sick group compared with the healthy group. rT3 levels were not increased in sick infants. We conclude that the extent of the FT4 decrease after birth in infants of <30 wk gestation is mainly influenced by gestational age and probably reflects a transient depletion of thyroidal hormone reserves. rT3 cannot be used as a marker of nonthyroidal illness in very preterm infants.

Both being born with a raised U/C ratio and an acceleration of VEP latencies are negatively associated with cognitive outcome at 5 years of age. Fetal brain-sparing, although a seemingly beneficial adaptive mechanism for intact neurologic survival, is, however, later associated with a poorer cognitive outcome.

A total of 12.6% of young adults who were born very preterm and/or with a very low birth weight had moderate or severe problems in cognitive or neurosensory functioning. Compared with the general Dutch population, twice as many young adults who were born very preterm and/or with a very low birth weight were poorly educated, and 3 times as many were neither employed nor in school at age 19.

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Objective To determine the influence of intrauterine growth retardation of preterm infants on mortality and cognitive development.Design A nationwide study cohort of very preterm and/or small for gestational age infants (< 32 weeks and/or < 1500 g) born alive in 1983 in the Netherlands. Assessment on neuromotor and cognitive development at five years, and a parental questionnaire on school performance at nine years. Cognitive outcome is defined as handicap for mental and speech-language development, and need for special education.Sample 134 small for gestational age infants (< 10th centile) and 410 appropriate for gestational age infants (between 25th and 75th centile) of all infants between 25 and 32 weeks of gestational age were identified; infants with congenital malformations and not of Caucasian race were excluded.Main outcome measures Neonatal mortality, in-hospital and five years mortality; Cognitive outcome at five years; School performance at nine years. ResultsThe mortality risk for small for gestational age compared with appropriate for gestational age infants was significantly higher, after adjustment for gestational age, sex, multiple pregnancy and mode of delivery (OR 2-56,95% CI I *26-5.26). Small for gestational age infants showed more often gross motor and minor neurological dysfunction, but less cerebral palsy than appropriate for gestational age infants. Cognitive outcome at five years in small for gestational age infants was significantly worse than appropriate for gestational age infants stratified for mode of delivery OR 2.44 (95% CI 1.05-5-55). At nine years of age significantly more small for gestational age infants (1 6.4%) needed special education than appropriate for gestational age infants (1 1.9%). ConclusionIntrauterine growth retardation increases the risk of mortality and of cognitive disorders.

The use of ACV in pregnancy is not yet recommended for two main reasons : its safety has not been established and the,lack of studies on pharmacokinetics. In this paper, we have.reviewed data concerning nine pregnant women who was iven ACV in the perinatal period. Route of administration ani doses were as following : orally (0) 350 mg/8 hours (5), lntravenousl (IV) 5-10 mg/kg/8 hours ( 4 ) . Plasm? trough (T) and eak (P) fevels of ACV was deteroinated by radio~mmuno assay. At girth, plasma ACV levels were achieved in the mother and her offspring. P and T after IV were effective to inhiblt viral replication (17-41 pmol/l 1 22-1 36 umol/l) and hi her than in vitro ID 50 for Herpes'vi;adea'viruses (0.1-4 pmoY/l) ; whereas T and P ranged from 0.32 to 0, 59 pmol/l and from 1.79 to 3.78 pmol/l after 10 doses given orally. Furthermore steady state plasma level was not achieved even after 10 doses 0. The maternal foetal ratio of ACV level was approximately 1. No side effects were noted in newborns. Conclnsion : If this drug is felt,to be used in a pregnant.voman, IV administration seems to be advisable regarding it's efficacy. 0 administration requires more data about recommended dosage. Transplacental passa e of ACV occurs. Plasma ACV levels in the mother reflect probagly foetal ACV level. Fifteen very low birth weight I1tLBY1 children, nine appropriate for qeitati;i;al age in6A. aean birth weight 1302tIb4 g, gestational age 30t_1.5 neeksl, and six jrall for gestaticaa! aqe ISSR, aean birth neigih I:b3t117 g, qestatlonal age 35.35.5 weeks), xere studied at the age of 7-12 years, and coapared to trentysix age-, sex-, and height-latched healthy children, who were born at term (lean birth weight 3?2b+ib7 51. !lox of :Ce YLRY rhildren had developed chronic broncopullonary disease, The hab~tua! !ere1 of physical act~vity was not different in the YLBY and control Grcup. Pulronary function tests and progresirre exercise tests on treadlill were perforled. Forced v!tal caoacity, forced expiraiory ?oliiae at one second and forced expiratory flow between 251 and 751 of vital capaclty were in tb: norral range for all the subjects. No difference; were founo in aaxiwda oxyeen con'.um~tion (YO2 aaxl, anaerobic threshold IATI and #axiral heart rate between :he ASR !'lo2 lax - Lidoca~rcis either a convulsant or an anticonvulwnt drug, according to the plasmatic levels. W e used its anticonvulwnt effect in scizures of various etiology. Lidocairtinfusion (L.I.) was efficient in 19/29 full term (FT) and in 10/13 prcmaturc babies (PT) with seizures (confirmed by EEG) resisting to Phenobarbital and Diazepam therapy. L.1. was given at decreasing dosage (4 mg/kg/h, day 1; 3 mg/kg/h, day 2; 2 mg/kg/h,day 3; 1 mg/kg/h,day 4). After L.I. beginning : -seizures were controlled within 30 min. in 23 cases, aftcr 3 to 13 hours in 4 cases; -background EEG changed in some casts, immediatly or after a delay (up to 24 hours) into a very discontinuous pattern. In 2 cases L.I. alone did not control seizures, but an additional bolus (2 mg/Kg) was efficient ...

Besides being one of the mechanisms responsible for ventilator-induced lung injury, atelectasis also seems to aggravate the course of experimental pneumonia. In this study, we examined the effect of reducing the degree of atelectasis by natural modified surfactant and/or open lung ventilation on bacterial growth and translocation in a piglet model of Group B streptococcal pneumonia. After creating surfactant deficiency by whole lung lavage, intratracheal instillation of bacteria induced severe pneumonia with bacterial translocation into the blood stream, resulting in a mortality rate of almost 80%. Treatment with 300 mg/kg of exogenous surfactant before instillation of streptococci attenuated both bacterial growth and translocation and prevented clinical deterioration. This goal was also achieved by reversing atelectasis in lavaged animals via open lung ventilation. Combining both exogenous surfactant and open lung ventilation prevented bacterial translocation completely, comparable to Group B streptococci instillation into healthy animals. We conclude that exogenous surfactant and open lung ventilation attenuate bacterial growth and translocation in experimental pneumonia and that this attenuation is at least in part mediated by a reduction in atelectasis. These findings suggest that minimizing alveolar collapse by exogenous surfactant and open lung ventilation may reduce the risk of pneumonia and subsequent sepsis in ventilated patients.