Weight change in the term baby in the first 2 weeks of life.

BACKGROUND: Midwives once used serial weighing to highlight lactation problems, but this is now discouraged for the fear of undermining maternal confidence. AIM: To explore weight changes in healthy newborn term babies, to gain information to aid interpretation of such measurements and to construct a centile chart for those exclusively breastfed during the first 2 weeks. METHOD: Two hundred ninety-nine mothers weighed their baby daily using the same electronic scales. In 46 cases, three or more consecutive measurements were omitted leaving 253 series to evaluate, of which 111 were exclusively breastfed. RESULTS: Breastfed babies lost a mean 6.4% of birthweight (95% CI: 5.5-7.3%) before starting to gain, and 54% took more than 8 days to regain birthweight. Artificially fed babies lost less (3.7%, 95% CI: 2.7-4.7%), but 39% had not regained their birthweight by 8 days. Once birthweight was regained, average gain was about 1% of birthweight per day in both breast- and artificially-fed babies. Measurements less than 5 days apart predicted average weight gain poorly. CONCLUSIONS: Feeding problems should be considered if weight is not increasing by 6 days, but some healthy babies take 17 days to regain their birthweight.

Variability of four limb blood pressure in normal neonates.

AIMS: To assess the variation in blood pressure (BP) between limbs in normal neonates. To assess whether comparison of arm and leg BP in neonates is reproducible enough to allow the difference to raise suspicion of coarctation of the aorta. METHODS: Infants recruited from the postnatal wards and the postnatal murmur clinic underwent echocardiography and BP measurement in each limb using a Dinamap Compact T 482210. The method of BP measurement was guided by a telephone survey of 40 UK neonatal units. RESULTS: Forty healthy neonates underwent echocardiography and all had a normal aortic arch. BP was measured in 39. In three, BP in the arms was 20 mm Hg higher than in the legs. This gave a specificity of comparison of the upper and lower limb BPs of 92 (36/39) or a false positive rate of 8% (3/39). The standard deviation in BPs was 15.7 mm Hg between arms, 14.5 mm Hg between legs, and 11 mm Hg when the nearest arm and leg were compared. CONCLUSIONS: With current measurement techniques, normal neonates may have a wide variation in BP between limbs. A difference of 20 mm Hg in isolation is more likely to be due to random variability in measurement than to coarctation of the aorta. If coarctation of the aorta is suspected, it can only be excluded or confirmed by echocardiography.

Routine pulse oximetry in the asymptomatic newborn.

OBJECTIVE: To assess the effect of routine measurement of postductal oxygen saturation as an adjunct to routine clinical examination in the asymptomatic newborn. DESIGN AND SETTING: Prospective study in a district general hospital. PATIENTS: All 6166 infants inborn between 1 April 1999 and 31 March 2001. INTERVENTION: Oxygen saturation was measured over two minutes, after the age of 2 hours and before discharge, in one foot of all babies not admitted directly to the neonatal unit. Babies with fractional (as opposed to functional) oxygen saturation (SaO(2)) below 95% were examined by the midwife. If this examination was abnormal or if normal but further measurements were below 95%, an echocardiogram was performed. All babies with cardiac malformations diagnosed by 1 year of age were identified from databases maintained at the regional cardiology referral unit and the regional congenital malformation survey. RESULTS: Measurements were made in 98% of eligible babies. A fractional SaO(2) less than 95% was found in 5% but persisted in only 1%. Structural cardiac malformations were found in 50 (8.1/1000), 26 of whom had isolated ventricular septal defects. Of the remaining 24 with other cardiac malformations, attention was first drawn to six by low SaO(2), and four more, first noticed for other reasons, also had low SaO(2). Low SaO(2) also first drew attention to 13 other babies ill for other reasons. CONCLUSION: Newborn babies with important cardiac malformations are often asymptomatic initially and the yield from clinical examination is poor. Measuring postductal saturation routinely in newborn babies before discharge is easy and can alert staff to ill babies.

Undiagnosed cardiomyopathy in a neonate: significance of low oxygen saturation during anaesthesia.

A case study is described of a 7-day-old full term baby with bilateral congenital cataracts who underwent surgical removal of both cataracts 2 days apart. Problems with oxygen saturation during and after the first anaesthetic prompted further investigation that revealed a non-obstructive hypertrophic cardiomyopathy. The significance and possible causes of low oxygen saturation in a previously healthy neonate during anaesthesia are discussed. The likely diagnosis of Sengers syndrome, and the evaluation of asymptomatic babies with cardiac pathology are discussed.

IL-8 and neutrophil elastase levels in the respiratory tract of infants with RSV bronchiolitis.

The aim of this study was to determine whether interleukin (IL)-8 is released within the upper respiratory tract of infants during respiratory syncytial virus (RSV) bronchiolitis and whether the large number of polymorphonuclear neutrophils (PMNs) present in the respiratory tract of these infants are contributing to the inflammation through release of inflammatory mediators. Twenty-seven infants with acute bronchiolitis were recruited during one winter epidemic and 20 infant control subjects were recruited from a cohort participating in a community-based vaccine study. Samples of airways fluid were obtained using nasal lavage. The lavage fluid was spun to remove the cells, and the supernatant was stored at -70 degrees C. The supernatants were subsequently assayed for the presence of IL-8, total human neutrophil elastase (HNE) and neutrophil elastase activity. In the children with bronchiolitis compared with control infants, elevated levels of IL-8 (median (range) 1.53 (0-153) versus 0 (0-5.6) ng x mL(-1)) HNE (136 (32-694) versus 14 (0-516) ng x mL(-1)) and elastase activity (4 (1-220) versus 1 (0-339) mU x mL(-1)) were found. These results indicate that interleukin-8 is released in the upper respiratory tract in response to respiratory syncytial virus infection and suggest that polymorphonuclear neutrophil products are playing an important role in the inflammatory response to respiratory syncytial virus infection in infants with acute bronchiolitis. This contrasts with the predominantly eosinophilic response evident in atopic upper and lower respiratory tract disease.

Effect of nimodipine on systemic, renal, and cerebral haemodynamics after a mild hypoxic-ischaemic insult in newborn piglets.

Because many Ca2+ channel blocking agents are known to cause adverse systemic effects, in this study we tested the haemodynamic side effects of nimodipine with and without a mild hypoxic-ischaemic (HI) insult in a newborn piglet model. Fifteen min after completing a brief period of asphyxia we gave i.v. nimodipine as 5 micrograms kg-1 bolus followed by 0.1 microgram kg-1 min-1 continuous infusion for 105 min in six piglets, while the same treatment was repeated in five animals without preceding HI insult. At third group of six served as sham operated controls. In the HI insult group by 105 min of nimodipine infusion the mean BP dropped by 30% and the cardiac output dropped by 23% of respective baseline. In this group, the renal blood flow dropped between 65% and 77% of baseline and regional cerebral blood flow dropped between 28% and 55% of respective baseline by 45 min and 105 min of nimodipine fashion. In the group with no prior HI insult, 105 min of nimodipine infusion caused no significant changes in these variables. Despite nimodipine infusion, HI insult caused a significant increase in the mean brain water content compared to the two control groups: 89 +/- 3.2% compared to 82.7 +/- 0.5% in the nimodipine control group, and 83.7 +/- 1.7% in the sham group (P < 0.0001). We conclude that while nimodipine therapy without prior asphyxial insult does not cause significant adverse haemodynamic effects, its infusion after even a mild HI insult could cause reduction in renal blood flow and moderate reduction in regional cerebral blood flow, BP, and cardiac output, suggesting a differential effect. A 15 min lag between HI insult and nimodipine therapy may be too long to prevent cerebral oedema.

Antenatal diagnosis of congenital heart disease and Down's syndrome: the potential effect on the practice of paediatric cardiology.

OBJECTIVE: To predict the effect of antenatal ultrasound screening for congenital heart disease and maternal serum screening of Down's syndrome on the practice of paediatric cardiology and paediatric cardiac surgery. DESIGN: A retrospective and prospective ascertainment of all congenital heart disease diagnosed in infancy in 1985-1991. SETTING: One English health region. PATIENTS: All congenital heart disease diagnosed in infancy by echocardiography, cardiac catheterisation, surgery, or necropsy was classified as "complex", "significant", or "minor" and as "detectable" or "not detectable" on a routine antenatal ultrasound scan. RESULTS: 1347 infants had congenital heart disease which was "complex" in 13%, "significant" in 55%, and "minor" in 32%. 15% of cases were "detectable" on routine antenatal ultrasound. Assuming 20% detection and termination of 67% of affected pregnancies, liveborn congenital heart disease would be reduced by 2%, infant mortality from congenital heart disease by 5%, and paediatric cardiac surgical activity by 3%. Maternal screening for Down's syndrome, assuming 75% uptake, 60% detection, and termination of all affected pregnancies, would reduce liveborn cases of Down's syndrome by 45%, liveborn cases of congenital heart disease by 3.5%, and cardiac surgery by 2.6%. CONCLUSIONS: Screening for congenital heart disease using the four chamber view in routine obstetric examinations and maternal serum screening for Down's syndrome is likely to have only a small effect on the requirements for paediatric cardiology services and paediatric cardiac surgery.

Presentation of obstructive left heart malformations in infancy.

This study documents the presentation of acutely life threatening congenital heart disease in infancy in order to assess the performance of screening examinations soon after birth and at 6 weeks of age. All cases of obstructive left heart malformations presenting in infancy in one health region from 1987-91 were analysed retrospectively. Altogether, 120 infants presented with either hypoplastic left heart syndrome, interruption of the aortic arch, coarctation of the aorta, or aortic valve stenosis. Twelve became symptomatic or died within 24 hours. Thirty four had an abnormal neonatal examination, eight of whom were referred. Six more became symptomatic before discharge. Ninety four babies went home, 51 developed heart failure before 6 weeks, and another seven died without diagnosis. Twenty five of 36 (69%) reaching 6 weeks without diagnosis had a second examination which was abnormal in 17. Two babies died undiagnosed after 6 weeks and the other 18 presented at up to 11 months of age. The neonatal and 6 week examinations perform poorly as screening tests for congenital heart disease. A normal neonatal examination does not exclude life threatening congenital heart disease.

Death in infancy from unrecognised congenital heart disease.

This study was undertaken to identify all congenital heart disease in infancy, including deaths before diagnosis, to provide a truer picture of the spectrum of congenital heart disease and to assess the 'treatability' of those dying before diagnosis. All births, infant deaths, and surviving babies with congenital heart disease in one health region in 1985-90 were identified and were classified as 'complex', 'significant', or 'minor'. Of the 1074 infants diagnosed in infancy, 185 died and 56 of these (30%) died undiagnosed. Severe non-cardiac malformations were present in 29 of the 56 while 27 were otherwise normal. Cardiovascular abnormalities in the latter group were complex in 13/27 and significant in 14/27. Identification of undiagnosed cardiovascular anomalies will improve epidemiological evaluation of congenital heart disease and, more importantly, earlier recognition of treatable abnormalities may reduce mortality.

Cardiovascular effects of carbon dioxide in ventilated preterm infants.

Sick preterm infants may, under certain conditions, demonstrate blood pressure passive cerebral blood flow in response to changes in arterial carbon dioxide tension. Blood pressure in turn depends on cardiac output and peripheral resistance. A Doppler technique for assessing cardiac output compared favourably in terms of reproducibility to a thermodilution technique in a group of infants undergoing cardiac catheterization for congenital heart disease. Doppler was subsequently used to monitor changes in cardiac output following an increase in arterial carbon dioxide tension of 1 kPa in 25 ventilated preterm infants. Blood pressure increased significantly (p = 0.006). However, heart rate did not change significantly (p = 0.16) and, in addition, both stroke and minute volume decreased (p = 0.023, p = 0.02, respectively). This suggests that accompanying changes in components of peripheral resistance exert important effects on blood pressure in the preterm neonate in response to changes in arterial carbon dioxide tension.

Morphine metabolism in acutely ill preterm newborn infants.

To examine the manner in which morphine is metabolized in acutely ill premature infants, we measured the levels of morphine, morphine-3- and -6-glucuronides, and codeine in timed urine specimens and paired plasma specimens at 4 hours and 24 hours after a single dose of morphine in 16 preterm infants (less than 32 weeks of gestational age). A large amount of unmetabolized morphine was found in the urine in 13 (81.2%) of the 16 infants at 4 hours; in 12 of them, morphine was excreted even at 24 hours. Urinary morphine levels varied greatly; the coefficient of variation was 130% at 4 hours and 118% at 24 hours. Codeine was not found in any of the infants. In 10 (62.5%) of the 16 infants, at least one metabolite was found in either plasma or urine. Plasma and urinary levels of morphine conjugates also varied greatly among these 10 infants (coefficient of variation: 109% to 317%). All six infants (37.5%) who had no metabolites excreted large amounts of unmetabolized morphine in the urine for up to 24 hours. Birth weight, gestational age, postnatal age, systemic blood pressure, and other clinical or physiologic variables did not differ significantly between the 10 infants who had morphine conjugates and the six who did not. We conclude that (1) nearly two thirds of acutely ill preterm infants born at less than 32 weeks of gestational age conjugate morphine; (2) irrespective of their ability to produce morphine conjugates, preterm infants excrete large amounts of morphine unmetabolized, as late as 24 hours after a single dose; (3) morphine handling patterns are highly variable among premature infants, and no obvious factors account for the variability; and (4) such variability in morphine handling in general, and the production of the highly potent morphine-6-glucuronide in particular, could explain the variance in morphine pharmacokinetic measures and in the clinical responses to morphine during the newborn period.