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Anesthesia for cesarean section--VII. Early effects on neonatal renal function of enflurane anesthesia for cesarean section.

Fourteen women undergoing elective cesarean section were anesthetized with enflurane for induction and maintenance of anesthesia. Blood enflurane and serum inorganic fluoride levels were studied in the mothers at delivery and in the neonates at delivery and in the early neonatal period. Also neonatal urinary excretion of inorganic fluoride was determined. Renal function of the neonates was tested with a sodium load at the age of 1 day. Enflurane showed the expected distribution between mothers and neonates. The enflurane level of the neonates declined rapidly after delivery. Serum inorganic fluoride level increased significantly in the mothers from start of anesthesia until delivery. The neonatal level was lower and did not reach the level of neonates in areas with a high natural fluoride content in drinking water. The level of inorganic fluoride in urine was higher than the corresponding serum level, indicating an inorganic fluoride concentrating effect of the neonatal kidney. The difference between urinary excretion and serum content of inorganic fluoride showed neonatal metabolism of enflurane. The urinary sodium excretion did not differ from that of infants delivered without halogenated inhalation agents given to the mothers.

Anesthesia, Inhalation↗

Serum transferrin receptor levels in the evaluation of iron deficiency in the neonate.

Iron deficiency anemia (IDA) is a major global problem. Early onset of iron deficiency in developing countries makes it imperative to identify iron deficiency in neonates. Most conventional laboratory parameters of iron status fail to distinguish neonates with iron deficient erythropoiesis. Serum transferrin receptor (STFR) levels are a recent sensitive measure of iron deficiency and the present study was carried out to evaluate the usefulness of cord serum transferrin receptors in identifying iron deficient erythropoiesis in neonates. A complete hemogram, red cell indices, iron profile: serum iron (SI), percent transferrin saturation (TS%) and serum ferritin (SF) was carried out in 100 full-term neonates and their mothers at parturition. Cord and maternal STFR levels were estimated using a sensitive enzyme-linked immunosorbent assay (ELISA) technique. Anemic women had a significantly lower SI, their TS% and high STFR levels suggesting that iron deficiency was responsible for the anemia. In the neonates of iron deficient mothers, cord SI, TS% and cord ferritin were not significantly different from those of neonates born to non-anemic mothers. Cord STFR level correlated well with hemoglobin (Hb) and laboratory parameters of iron status, and its level was significantly higher in neonates born to anemic mothers than in those born to non-anemic mothers. It was the only laboratory parameter to differentiate between neonates born to anemic and non-anemic mothers. Therefore, STFR is a sensitive index of iron status in neonates and identifies neonates with iron deficient erythropoiesis.

Adolescent↗

Clinical and echocardiographic evaluation of neonates with heart murmurs.

In this study, 116 neonates (58M, 58F), aged 12h to 14d, with heart murmurs were examined by echocardiography: 26 were preterm and 90 full-term neonates. The clinical diagnosis was classified into definite heart disease, possible heart disease and innocent murmur. The final diagnosis was based on echocardiography and, in some cases, cardiac catheterization or surgery. The results showed that 97 (84%) neonates had heart diseases; 19 (16%) had a normal heart, including 7 with tricuspid regurgitation and 9 with physiological peripheral pulmonic stenosis. Out of 88 neonates with clinically definite heart disease, the final diagnosis was changed to normal heart in 9 (10%) cases and the lesion-specific diagnosis was changed in 9 (10%) neonates. In four cases, the clinical diagnosis of ventricular septal defect or pulmonary stenosis was changed to double-outlet right ventricle, single ventricle, hypoplastic left heart syndrome or tetralogy of Fallot. The clinical diagnosis was correct in 77-85% for varying simple lesions. In 5 of 21 neonates with clinically possible heart disease, the diagnosis was changed to normal heart. In one of six neonates with clinically innocent murmurs, the diagnosis was changed to small muscular ventricular septal defect. We concluded that 84% of heart murmurs in neonates were due to heart diseases and only 16% were innocent murmurs. Although clinical evaluation could determine the presence or absence of heart disease in most neonates, the lesion-specific diagnosis was not quite satisfactory. Echocardiography is necessary for neonates with a clinically diagnosed heart disease or possible heart diseases, and may be unnecessary for those with innocent murmurs diagnosed by paediatricians.

Diagnosis, Differential↗

Prothrombotic factors in neonates with cerebral thrombosis and intraventricular hemorrhage.

AIM: To investigate whether the factor V Leiden mutation (FVL), the prothrombin gene G20210A variant or the methylenetetrahydrofolate reductase (MTHFR) C677T genotype are risk factors for central nervous system (CNS) thrombosis or intraventricular hemorrhage (IVH) in neonates. METHODS: Thirteen full-term infants with cerebral infarct documented with magnetic resonance imaging were assessed with the whole spectrum of assays for thrombophilia including the three DNA-based prothrombotic factors. The frequency of congenital defects was compared with that observed in 38 healthy full-term infants. The genetic defects were also assessed in 55 premature neonates, gestational age <32 wk, 17 of whom developed IVH, grade II-IV. The remaining 38 premature neonates without IVH were used as controls. RESULTS: In the CNS thrombosis group: a prothrombotic factor was detected in 53% of patients and an underlying disease or a triggering event in 61.5%. The frequency of FVL in thrombosed neonates was higher (23%) than in the group of healthy full-term infants (10.5%), although it did not reach statistical significance. IVH developed in 30.9% of premature neonates. Apart from several maternal or neonatal risk factors for IVH, FII G20210A was found in a considerably higher prevalence in the cohort of neonates with IVH (12%) than in those without (2%), although the difference was not statistically significant. CONCLUSION: The pathogenesis of cerebral thrombosis or IVH in neonates is multifactorial. Along with underlying diseases or triggering events, congenital prothrombotic factors (FVL or FII G20210A) showed a trend towards a higher frequency in full-term infants with CNS thrombosis or premature neonates with IVH than in controls. However, their contribution to neonatal cerebral thrombosis or IVH remains to be determined.

Birth Weight↗

Increased sensitization of the myofilaments in rat neonatal portal vein: a potential mechanism.

The contractile regulation of neonatal smooth muscle was studied in rat neonatal portal vein. Strips of beta-escin-permeabilized portal vein from 3- to 5-day-old rats and 5- to 6-week-old rats were mounted on a 'bubble chamber' in calcium solutions buffered with 10 mM EGTA. Although the overall tension development was lower in neonatal muscle as expected, the calcium sensitivity of the neonatal permeabilized portal vein was significantly higher than in developed portal vein. Endothelin-1-induced sensitization of the myofilaments was investigated. Endothelin-1 produced an increase in tension of permeabilized neonatal portal vein in a calcium solution buffered with 10 mM EGTA. This sensitization was proportionally higher in neonatal than in developed smooth muscle, despite similar initial submaximal calcium contractions. GTP gamma S-induced calcium sensitization was also proportionally higher in neonatal permeabilized strips than in fully developed smooth muscle. These changes may be due to alterations in the intracellular signalling pathways which mediate calcium sensitization in smooth muscle. As some endothelin-1-mediated responses are known to occur via activation of the heterotrimeric GTP-binding protein, Gq, the levels of protein expression of Gq alpha were studied. In membrane preparations from neonatal rat portal vein the expression of Gq alpha was significantly higher than in portal vein membrane preparations loaded with equal protein from 5- to 6-week-old rats. In conclusion, agonist-induced sensitization of the myofilaments was higher in neonatal rat portal vein than in fully developed portal vein. This difference is the result of changes in intracellular signalling and may be partly produced by the greater expression of Gq alpha observed in neonatal portal vein.

Actin Cytoskeleton↗

Functional capacities of tactile afferent fibres in neonatal kittens.

1. Responses were recorded from individual tactile afferent fibres isolated by microdissection from the median nerve of pentobarbitone-anaesthetized neonatal kittens (1-5 days post-natal age). Experiments were also conducted on adult cats to permit precise comparisons between neonatal and adult fibres.2. Neonatal fibres with receptive fields on the glabrous skin of the foot pads were classified into two broad groups, a slowly adapting class (40%) which responded throughout a 1 sec period of steady indentation and a rapidly adapting or dynamically sensitive class comprising 60% of units. Fibres in these two groups had overlapping conduction velocities in the range 4.3 to 7.5 m/sec and were believed to be the developing Group II afferents of the adult.3. Neonatal slowly adapting fibres qualitatively resembled their adult counter-parts. They displayed graded stimulus-response relations which, over the steepest segment of the curves, had mean slopes of 15.7 impulses/100 mum of indentation. Plateau levels of response were often reached at amplitudes of skin indentation of < 0.5-0.7 mm.4. Dynamically sensitive fibres with receptive fields on the glabrous skin were studied using sinusoidal cutaneous vibration which in the adult enables them to be divided into two distinct classes. However, in the neonate, they formed a continuum whether criteria of sensitivity or responsiveness were used.5. In response to vibration neonatal fibres differed from adult ones according to the following quantitative indices: (i) sensitivity as measured by both absolute thresholds and thresholds for a 1: 1 pattern of response, both of which were higher in the neonate than in the adult at all frequencies > 50 Hz and differed by an order of magnitude at frequencies >/= 200 Hz; (ii) responsiveness based on the mean impulse rate evoked at a fixed amplitude of cutaneous vibration; (iii) band width of vibratory sensitivity which in the neonate was confined to approximately 5-300 Hz whereas in the two classes of adult units it covered the range 5-800 Hz; (iv) capacity for coding information about vibration frequency. Impulse activity of neonatal fibres was less tightly phase-locked to the vibratory stimulus and showed a poorer reflection of the periodic nature of the vibratory stimulus than impulse patterns of adult units.6. The results reveal that tactile receptors and afferent fibres in the neonate are functionally immature. Their restricted coding capacities suggest that peripheral tactile sensory mechanisms impose limits on the ability of the new-born animal to derive information about its tactile environment.

Animals↗

Neonatal programming of the rat neuroimmune response: stimulus specific changes elicited by bacterial and viral mimetics.

Recently, it has been shown that the neonatal immune environment can have significant programming effects on the adult neuroimmune response. A single neonatal immune challenge with the bacterial mimetic lipopolysaccharide (LPS) can alter the neuroendocrine, neurochemical and febrile responses to a subsequent, homotypic (LPS) immune challenge as adults. As the programming effects of viral stimuli during this neonatal period are unknown, we tested whether the viral mimetic polyinosinic-polycytidylic acid (PolyIC), administered on postnatal day 14 (P14) would alter the adult neuroimmune responses to a subsequent PolyIC challenge. Our results show that animals treated neonatally with PolyIC had significantly attenuated febrile responses to an adult PolyIC challenge, which coincided with a heightened corticosteroid response. When the corticosteroid receptor blocker RU486 was administered prior to the adult PolyIC challenge, animals treated neonatally with PolyIC no longer displayed attenuated febrile responses. Similar responses to an adult LPS challenge have been seen in animals that were exposed neonatally to LPS, indicating that both neonatal immune stimuli elicit highly similar programming effects on the adult neuroimmune responses. However, we find that neither neonatal PolyIC nor neonatal LPS challenges led to an alteration in the adult febrile or corticosteroid responses to a heterotypic adult immune challenge, indicating that the programming effects of the neonatal immune environment are stimulus specific, and do not alter the adult responses to other immune stimuli.

Age Factors↗

Timing of birth and infant and early neonatal mortality in Sweden 1973-95: longitudinal birth register study.

OBJECTIVE: To assess the impact of time of birth on infant mortality and early neonatal mortality in full term and preterm births. DESIGN: Analysis of data from the Swedish birth register, 1973-95. PARTICIPANTS: 2 102 324 spontaneous live births of infants without congenital malformation. OUTCOME MEASUREMENTS: Absolute and relative risk of infant mortality, early neonatal mortality, and early neonatal mortality related to asphyxia. RESULTS: Infant mortality, early neonatal mortality, and early neonatal mortality related to asphyxia were higher in infants who were born during the night (9 pm to 9 am) compared with those born during the day for 1973-9, 1980-9, and 1990-5. The difference was more dramatic for preterm infants. The largest difference was observed during 1990-5, when there was a 30% increase in early neonatal mortality (relative risk 1.31, 95% confidence interval 1.10 to 1.57) and a 70% increase in early neonatal mortality related to asphyxia (1.70, 1.22 to 2.38) in preterm infants born during the night compared with rates for preterm infants born during the day. A detailed analysis over 24 hours revealed two "high risk" periods: between 5 pm and 1 am and around 9 am. CONCLUSIONS: Infants born during the night have a greater risk of infant and early neonatal mortality and early neonatal mortality related to asphyxia than those born during the day. There has been no improvement over the past two decades. The problem is more serious for preterm births and was even worse in the 1990s. Shift changes and the hours immediately after such changes are high risk periods for neonatal care.

Asphyxia Neonatorum↗

Unilateral neonatal cerebral infarction in full term infants.

AIMS: To determine the prevalence of unilateral neonatal cerebral infarction in infants born at 32 weeks gestation and above; to describe the clinical course, imaging results, and outcome of neonatal cerebral infarction; and to investigate possible aetiology. METHODS: Twelve cases of unilateral neonatal cerebral infarction were identified from neonatal unit records for the years 1987-93. Each case was matched with two controls. RESULTS: All cases of neonatal cerebral infarction occurred in full term infants. The prevalence was around 1 in 4000, and neonatal cerebral infarction was found in 12% of infants presenting with neonatal seizures. Cerebral ultrasound scans failed to demonstrate lesions seen by computed tomography in nine of 12 cases. Cases were more likely than controls to require assisted ventilation for resuscitation at birth (OR 7.0, 95% confidence interval 1.04-53.5), but Apgar scores at 5 minutes were no different. One infant with neonatal cerebral infarction developed a hemiparesis, the other 11 had normal motor development when assessed at 11-60 (median 33) months. None had overt cognitive deficits or persisting seizure disorder. CONCLUSIONS: Neonatal cerebral infarction is a relatively common cause of neonatal seizures, but the aetiology remains unclear. Parents need to be made aware of possible neurological sequelae, but most cases in this series had a normal outcome.

Cerebral Infarction↗

Neonatal lenticulostriate vasculopathy: further characterisation.

BACKGROUND: Lenticulostriate vasculopathy (LSV) is sometimes detected on routine brain ultrasonography in neonates, and is often associated with various perinatal and neonatal abnormalities. However, most reports on LSV are retrospective with no controls. OBJECTIVES: To compare the perinatal and neonatal clinical characteristics of neonates with LSV with matched controls and to summarise all published reports of LSV. DESIGN: A prospective study that summarises the clinical, laboratory, and neurosonographic data of neonates with LSV. METHODS: Of 1184 neonates admitted to the neonatal intensive care unit (NICU) during a three year period, 857 had a routine head ultrasound examination. Twenty one had LSV, and were compared with 42 matched controls with regard to gestational, perinatal, neonatal, laboratory, and neurosonographic characteristics. RESULTS: LSV was detected in 21 of the 857 (2.45%) neonates. It was bilateral in 10 of the 21 cases and located in the thalamus (n = 14) and basal ganglia (n = 7). Infants with LSV were not significantly different from matched controls in most tested variables. However, compared with the control group, the LSV group included significantly more multiple births and more disturbances in amniotic fluid volume, but less meconial amniotic fluid. In addition, the patients with LSV required fewer blood transfusions and less phototherapy. CONCLUSIONS: Except for more multiple births, neonates with LSV did not display more adverse findings than their matched controls.

Basal Ganglia Cerebrovascular Disease↗

Impaired cerebrovascular autoregulation after hypoxic-ischemic injury in extremely low-birth-weight neonates: detection with power and pulsed wave Doppler US.

PURPOSE: To evaluate regional cerebral blood flow with power and pulsed wave Doppler ultrasound (US) in extremely low-birth-weight neonates with periventricular leukomalacia (PVL), germinal matrix hemorrhage (GMH), or both. MATERIALS AND METHODS: The lenticulostriate arteries of 17 preterm neonates (birth weight < or = 1,100 g) were assessed daily with Doppler US during the first 5-6 days of life. The mean arterial pressure and bilateral peak velocity, resistive index, coronal vascular cross-sectional area, and product of the peak velocity and vascular cross-sectional area were measured. RESULTS: Five neonates developed PVL, GMH, or both; results of follow-up examinations in 11 patients were normal. One neonate with severe intrauterine growth retardation and renal tubular acidosis was excluded. Neonates with PVL, GMH, or both showed significantly greater mean values and more variable values of vascular cross-sectional area and product of peak velocity and cross-sectional area than neonates without PVL or GMH (P < .025). Mean resistive index was significantly lower in neonates with PVL, GMH, or both than in neonates without (P < .01). There were no significant differences between mean arterial pressure in neonates with and those without PVL, GMH, or both. CONCLUSION: By enabling the detection of autoregulatory fluctuations in cerebral blood flow associated with hypoxic-ischemic injury, power and pulsed wave Doppler US may enable identification of preterm neonates who are at risk of developing PVL, GMH, or both during the 1st week of life.

Blood Flow Velocity↗

Plasma and urine elastase alpha-1-proteinase inhibitor levels in neonatal urinary tract infection.

OBJECTIVE: To examine whether plasma or urine elastase alpha(1)-proteinase inhibitor (E-alpha(1)-PI) levels could be used as a diagnostic marker of urinary tract infection (UTI) in neonates. SUBJECTS AND METHODS: Plasma and urine E-alpha(1)-PI levels were measured by immunoassay in 23 neonates with UTI at the time of admission and 72 h after the onset of treatment and in 10 'normal' neonates (i.e. with trivial problems). Additionally E-alpha(1)-PI plasma levels were measured in 15 neonates with septicemia. RESULTS: E-alpha(1)-PI plasma levels did not differ between normal neonates and those with UTI. Urine E-alpha(1)-PI levels were significantly higher in neonates with UTI on admission compared to normal neonates. A significant decrease in urine E-alpha(1)-PI levels was noticed 72 h after the onset of treatment in all but 2 neonates in whom infection persisted. In this study, we have found that the urine E-alpha(1)-PI concentration at a cutoff level of 48 microg/l had a sensitivity of 83%, a specificity of 90%, a positive predictive value of 95% and a negative predictive value of 69% for the diagnosis of neonatal UTI. CONCLUSION: Elevated levels of E-alpha(1)-PI in urine seem to be a useful tool for the diagnosis of UTI in neonates (even in those that have already been started on antibiotics) and possibly a valuable marker for early recognition of treatment failure.

Bacteremia↗

Neonatal imprinting and regulation of estrogen receptor alpha and beta mRNA expression by estrogen in the pituitary and hypothalamus of the male rat.

In male rodents, complete reproductive function is critically dependent on adequate estrogen action at different levels of the hypothalamic-pituitary-testicular axis. However, administration of high doses of estrogen during the critical period of neonatal differentiation results in multiple defects in the reproductive axis that disrupt male fertility, the molecular mechanism(s) behind such a phenotype remaining poorly characterized. The aim of this study was twofold: (1) to characterize the effects of neonatal estrogenization upon the pattern of estrogen receptors ERalpha and ERbeta mRNA expression in the pituitary and hypothalamus of the male rat, and (2) to evaluate the ability of estrogen to acutely regulate pituitary and hypothalamic ERalpha and ERbeta mRNA expression in the male rat. To achieve the first goal, groups of male rats were treated on the first day of life with estradiol benzoate (EB; 500 microg/rat), and pituitary and hypothalamic expression of ERalpha and ERbeta mRNA levels were assayed by semiquantitative RT-PCR at different ages from the neonatal period until adulthood (days 1-75 of life). In addition, the mechanism(s) of altered pituitary expression of ERalpha and ERbeta messages in neonatally estrogenized rats was explored by comparison of the effects of neonatal treatment with estrogen or a potent gonadotropin-releasing hormone (GnRH) antagonist. For the second goal, the acute effects of a single dose of EB (12.5-25 microg/rat) on hypothalamic and pituitary ERalpha and ERbeta mRNA expression were assessed in prepubertal and adult male rats. Neonatal estrogenization permanently decreased pituitary ERalpha and ERbeta mRNA expression levels respective to control values at all ages studied. This pattern of response was similar to the short-term effects of neonatal blockade of endogenous GnRH actions. In contrast, neonatal exposure to estrogen transiently increased the hypothalamic expression levels of ERalpha and ERbeta messages. This effect was detected in neonatal (5-day-old), infantile (15-day-old) and prepubertal (30-day-old) rats, and it disappeared at puberty. In addition, estrogen was able to acutely regulate mRNA expression levels of its cognate receptor subtypes in the pituitary and hypothalamus of intact male rats. In adult (75-day-old) males, EB administration (25 microg/rat) induced a significant time-dependent decrease in pituitary ERalpha and ERbeta mRNA levels. In contrast hypothalamic expression of ERalpha and ERbeta messages was increased after acute exposure to EB (12.5 microg/rat) in prepubertal males (30 days old); yet differences in the time course of the response to estrogen were noticed between targets. In conclusion, our data indicate that estrogen is able to neonatally imprint and acutely regulate mRNA expression levels of ERalpha and ERbeta in the pituitary and hypothalamus of the male rat. Regulation of pituitary and hypothalamic ERalpha and ERbeta gene expression by the cognate ligand represents a novel mechanism whereby estrogen modulates its own biological actions upon different levels of the male reproductive axis throughout the life span.

Animals↗

Plasma transforming growth factor beta1 levels in thrombocytopenic and nonthrombocytopenic neonates.

In this study, we determined the plasma TGF-beta1 levels in healthy and thrombocytopenic and nonthrombocytopenic neonates who had perinatal risk factors and examined the association between plasma TGF-beta1 levels and platelet counts in these newborns to investigate the role of TGF-beta1 in the pathogenesis of neonatal thrombocytopenia. Three groups were defined in this prospective study: group 1, thrombocytopenic neonates (n=22) who had perinatal risk factors; group 2, nonthrombocytopenic neonates who had similar perinatal risk factors for thrombocytopenia (n=20); group 3, healthy and nonthrombocytopenic neonates without any risk factors (n=20). Plasma TGF-beta1 levels were measured with ELISA. Plasma TGF-beta1 levels of the thrombocytopenic neonates were significantly lower than those of healthy nonthrombocytopenic neonates but did not differ significantly from nonthrombocytopenic neonates who had similar perinatal risk factors for thrombocytopenia. There was a significant positive correlation between plasma TGF-beta1 levels and platelet counts. Further studies are needed to determine the cause of low plasma TGF-beta1 levels in thrombocytopenic neonates and to investigate the role of plasma TGF-beta1 levels in the pathogenesis of neonatal thrombocytopenia.

Case-Control Studies↗

Continuous insulin infusion in hyperglycaemic extremely-low- birth-weight neonates.

BACKGROUND: The inability of the newborn to inhibit gluconeogenesis in response to a glucose infusion leading to insulin resistance has been postulated as an important cause of hyperglycaemia observed in premature infants. AIM: The aim of this study was to determine the efficiency and rate of response to continuous insulin infusion in improving glucose tolerance in hyperglycaemic extremely-low-birth-weight (ELBW) neonates (< or =1,000 g) compared to neonates with birth weight >1,000 g (LBW). METHODS: We included in the study 115 consecutive neonates in the neonatal intensive care unit who developed hyperglycaemia from January 2000 to December 2001. A standard protocol for the use of exogenous insulin infusions was commenced for all hyperglycaemic neonates. The efficiency of continuous insulin infusion was compared in two groups of infants: ELBW < or =1,000 g compared with neonates with birth weight >1,000 g (LBW). RESULTS: The duration (hours) of insulin infusion required to normalise blood glucose level was significantly longer in the ELBW group compared to LBW group (p < 0.0001). Average insulin infusion (units/kg/h) required to maintain normoglycaemia was also significantly higher in the ELBW group (p < 0.0001). No significant difference was found in the mean amount of intravenous dextrose tolerated, mean postnatal age (hours) at which infusions were initiated and the average blood glucose recorded. ELBW infants were more likely to receive steroid administration, have surgery, higher CRIB scores and sepsis. CONCLUSION: Continuous insulin infusion was relatively safe and effective in the treatment of persistent hyperglycaemia in premature neonates. No serious adverse side effects of insulin therapy were noted. With the current protocol for use of exogenous insulin infusion at our unit, the response to treatment was significantly slower in the ELBW neonates. The dose of insulin infusion required to maintain normoglycaemia was also higher in this group of neonates. There may be a need for different treatment schedules for this subgroup of neonates so that normalisation of blood glucose can be achieved earlier.

Blood Glucose↗

Iodine saturation of Roma neonates in prague is not at an optimum level.

AIM: The purpose of our study was to determine urinary iodine as an indicator of iodine supplementation in Roma (Gypsy) neonates compared to majority population neonates. METHODS: The groups studied were formed by 30 full-term Roma neonates and 151 majority population neonates. Iodine was determined from samples of urine collected on the 4th day after delivery, after alkaline ashing, using the Sandell-Kolthoff method. RESULTS: The median of urinary iodine in Roma neonates was 92.15 microg/l urine and in neonates from majority population mothers it was 109.20 microg/l urine. The mean of urinary iodine in Roma neonates was 114.55 microg/l urine (SD 71.68 microg/l) and in neonates from majority population mothers it was 141.86 microg/l urine (SD 87.42 microg/l). The difference was not statistically significant. Majority population mothers more frequently consumed nutrition supplements containing iodine as well as fish. CONCLUSIONS: Compared to older data, supplementation of neonates with iodine is higher. However, it does not reach optimum levels. The urinary iodine median in Roma neonates lies in the mild iodine deficiency band.

Adult↗

Effect of neonatal cerebrospinal fluid on monocyte chemotaxis.

We have reported in our previous study that macrophages constitute 58% of the total number of white cells in noninfected neonatal cerebrospinal fluid (CSF). CSF macrophages are probably derived from blood monocytes. To explain their predominance, we compared the chemotactic response of monocytes from cord and adult blood to neonatal (NCSF) and non-neonatal spinal fluids (NNCSF). Zymosan-activated serum (ZAS) was used as a positive control. Significance was accepted as p less than or equal to 0.05. We observed that both random migratory (RM) activity and chemotactic responses (CM) of cord monocytes to neonatal CSF and ZAS were greater than those of monocytes obtained from adult blood, resulting in a significant increase in the chemotactic differential (CD). Chemotactic responses of neonatal monocytes were significantly greater in the presence of neonatal CSF as compared to CSF from older children as indicated by CD. The CD of neonatal monocytes to neonatal CSF was greater than that of neonatal neutrophils. These findings are consistent with the presence of specific monocyte chemotaxins in noninfected neonatal CSF.

Adolescent↗

Detection of transposition of the great arteries in fetuses reduces neonatal morbidity and mortality.

BACKGROUND: Transposition of the great arteries (TGA) is a life-threatening malformation in neonates, but it is amenable to complete repair. Prenatal detection, diagnosis, and early management may modify neonatal mortality and mortality. METHODS AND RESULTS: Preoperative and postoperative morbidity and mortality were compared in 68 neonates with prenatal diagnosis and in 250 neonates with a postnatal diagnosis of TGA over a period of 10 years. The delay between birth and admission was 2+/-2.8 hours in the prenatal group and 73+/-210 hours in the neonatal group (P<0.01). Clinical condition at arrival, including metabolic acidosis and multiorgan failure, was worse in the neonatal group (P<0.01). Once in the pediatric cardiology unit, the management was identical in the 2 groups (atrioseptostomy, PGE1 infusion, operation date). Preoperative mortality was 15 of 250 (6%; 95% CI, 3% to 9%) in the neonatal group and 0 of 68 in the prenatal group (P<0.05). Postoperative morbidity was not different (25 of 235 versus 6 of 68), but hospital stay was longer in the neonatal group (30+/-17 versus 24+/-11 days, P<0.01). In addition, postoperative mortality was significantly higher in the neonatal group (20 of 235 versus 0 of 68, P<0.01); however, the known risk factors for operative mortality were identical in the 2 groups. CONCLUSIONS: Prenatal diagnosis reduces mortality and morbidity in TGA. Prenatal detection of this cardiac defect must be increased to improve early neonatal management. In utero transfer of fetuses with prenatal diagnosis of TGA in an appropriate unit is mandatory.

Humans↗