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Revised UK neonatal screening guidelines recommend that a second blood sample for assay of thyroid stimulating hormone (TSH) be taken when preterm infants reach a postmenstrual age of 36 weeks.To examine the results of a regional screening programme to see whether a rise in TSH concentration was observed in some preterm infants between the first sample taken around 5 days after delivery and the second sample taken at around 36 weeks.Whole-blood TSH concentrations in preterm infants born over a 2-year period (April 2005 to March 2007) were assessed, and the number of infants in whom there was a fall or rise to values below or above the local screening threshold (6 mU/l) was determined.Baseline TSH samples were obtained from 2238 preterm infants (median gestational age 32 weeks, range 21-35) with second samples obtained from 2039 (median gestational 32 weeks, range 23-35). In 19 infants, TSH concentrations fell from above to below the screening threshold, and in five infants values rose from below the screening threshold to 6-10 mU/l. However, TSH concentrations fell to6 mU/l on a further blood spot in four of these infants, and the remaining infant had a serum TSH of 6.8 mU/l. Three infants had raised TSH concentrations on both occasions with unequivocal hypothyroidism (serum TSH80 mU/l). The initial TSH concentration in one of these infants was 6-10 mU/l.No infant with a normal TSH concentration on first sampling had a TSH concentration that rose above 10 mU/l on second sampling, and no infants with a normal TSH concentration on first screening are receiving long-term thyroxine treatment. This study suggests that a second sample may not be necessary with a screening threshold of 6 mU/l.

Hypoglycaemia has long been recognised as a feature of the failure of metabolic adaptation in infants who are small for gestational age (SGA). This study examined the process of metabolic adaptation by measuring, longitudinally, the concentrations of metabolic fuels and substrates in 33 SGA infants in the first postnatal week, and relating these to cross sectional data in 218 infants of appropriate weight for gestational age (AGA). SGA term infants had higher mean blood lactate concentrations than AGA term infants at delivery (2.98 v 2.10 mmol/l) and in the first few postnatal hours (3.05 v 1.91 mmol/l). Subsequently, although there were no differences in blood glucose concentrations, SGA term infants had lower mean ketone body concentrations (for example day 2: 0.07 v 0.41 mmol/l), and failed to mount a ketogenic response to low blood glucose concentrations. At birth, SGA preterm infants had lower mean blood glucose concentrations than AGA preterm infants (3.17 v 4.16 mmol/l), but there were few postnatal metabolic differences between the two groups. Mean blood glucose concentrations did not differ between AGA and SGA preterm infants. For variables that differed between the groups, multiple regression analysis suggested that both the degree and asymmetry of growth retardation were related to the severity of the metabolic abnormalities. These data suggest that, although there are early metabolic differences between SGA and AGA infants, it is possible that current clinical management is effective in preventing subsequent hypoglycaemia. This is important because of the failure of SGA infants to mount a ketogenic response.

Neonatal hypoglycaemia is a common clinical problem and the traditional treatment for the condition is intravenous glucose administration. The glycaemic effects of two additional treatments were investigated, in a randomised trial, in 23 neonates who were receiving intravenous glucose as treatment for hypoglycaemia. Eleven infants received an intravenous bolus dose of glucagon (200 micrograms/kg) and 12 infants received intragastric medium chain triglyceride (MCT) (5 ml/kg). Blood concentrations of glucose and intermediary metabolites were measured before and one hour after treatment, and, using stable isotope infusion, glucose production rates were calculated. After glucagon, there was a mean rise in blood glucose concentration of 1.6 mmol/l and in the glucose production rate of 2.6 mg/kg/min. After MCT, there was a small mean rise in blood glucose concentration of 0.4 mmol/l, but the effect of MCT on glucose production rate was variable. Intravenous bolus glucagon administration exerted a glycaemic effect which was associated with an increase in glucose production rate. The use of glucagon, as an alternative treatment to intravenous glucose, should be investigated further.

Little is known of the ability of hypoglycaemic infants who are small for gestational age (SGA) to mount the coordinated hormonal and metabolic counterregulatory response that is seen in healthy older subjects during glycopenia. This response was studied in 22 SGA infants (birth weight < 10th centile) by measuring the blood concentrations of glucose, intermediary metabolites, and glucoregulatory hormones. Plasma non-esterified fatty acid and blood ketone body concentrations were low, even when blood glucose concentrations were low. Plasma insulin and glucagon varied widely (< 1.0-53.1 mU/l and 16.6-87.1 pmol/l, respectively). Concentrations of noradrenaline and glucagon were raised, but cortisol and adrenaline were lower than those found in hypoglycaemic adults. There was no relationship between the concentration of any hormone and blood glucose concentration. We postulate that hypoglycaemia and the failure to mobilise alternative fuels in some SGA infants is secondary both to a poorly coordinated counterregulatory hormone response and to a peripheral insensitivity to the actions of the hormones. Those infants, who fail to mount a counterregulatory response, should be identified by accurate and reliable blood glucose monitoring, and an adequate exogenous supply of energy, either enteral or parenteral, should be ensured.

Some neonates, such as those who are preterm or small for dates, become hypoglycaemic or hyperglycaemic. These disorders represent a failure of neonatal metabolic adaptation, but the underlying mechanisms are unclear. Data from studies of hypoglycaemic and hyperglycaemic infants were reviewed in the light of new data from studies of healthy neonates. Data from 28 neonates, who had disordered blood glucose homoeostasis, were analysed to determine the interrelationships between circulating concentrations of glucose, intermediary metabolites, glucagon and insulin, and glucose production rates. Blood glucose concentrations ranged from 2.5 to 26.1 mmol/l, and glucose production rates from 0 to 19.2 mg/kg/min. Blood glucose concentrations were positively related to intravenous glucose infusion rates and to glucose production rates. A negative relationship existed between plasma glucagon and blood glucose concentrations, but there was a wide variation in plasma insulin levels at all blood glucose concentrations. No relationship between either plasma insulin or glucagon concentration and glucose production rate was shown. It is concluded that in neonates with disordered blood glucose homoeostasis, blood glucose concentration is influenced by the rate of administration of glucose, with less precise internal control mechanisms than older subjects. This emphasises the importance of blood glucose monitoring and careful prescribing of exogenous glucose by clinicians caring for such infants.

A pilot scheme of appraisal and career counselling for senior house officers (SHOs) in the Northern region has been undertaken. There were two sets of guidelines for the conduct of these interviews, one was a list of topics and the other a modification of the Manchester rating scale. All appraisal interviews were evaluated separately by the participating SHOs and consultants. There was strong concordance between these evaluations irrespective of the format chosen. Almost all participants considered that the interviews were useful, resulted in a fair assessment of performance, and fulfilled the stated aims of the scheme.

OBJECTIVE: To investigate the diurnal occurrence of Sudden Infant Death Syndrome (SIDS) and interaction with established risk factors in the infant sleeping environment. METHODS: A 3 year population-based case-control study, in five English Health Regions. Parentally defined day-time or night-time deaths of 325 SIDS infants and reference sleep of 1300 age-matched controls. RESULTS: The majority of SIDS deaths (83%) occurred during night-time sleep, although this was often after midnight and at least four SIDS deaths occurred during every hour of the day. The length of time from last observed alive until the discovery of death ranged from

Aims: To determine the combined effects of sudden infant death syndrome (SIDS) risk factors in the sleeping environment for infants who were “small at birth” (pre-term (

Could mediation help? The UK readership of Archives will remember October 2004 for Charlotte Wyatt1,2 and Luke Winston-Jones.3,4 Charlotte was severely disabled following complications of extreme prematurity, and Luke with trisomy 18. In each case the clinical teams believed that active, life prolonging medical interventions would not be in the best interests of the baby. The cases were brought to the civil courts because fundamental and irreconcilable differences between the families and the clinical teams came to an impasse, leaving the respective hospitals with no alternative but to seek a judicial ruling on the management of each child. Observers from other units will either feel that they have been there too, or dread the time that they may find themselves in similar situations. We should reflect constructively on these cases and be thankful that they remain rare. Most of the time, even in the most difficult situations, we are able to work alongside parents, …

An infant of 31 weeks' gestation presented with refractory neonatal hypoglycaemia secondary to islet cell dysregulation. Treatment was started with somatostatin analogue and his glycaemic control improved initially. Tolerance developed, however, in that the dose required to maintain control increased by a factor of 40. The infant subsequently underwent pancreatectomy. It is safe to use somatostatin analogue in a preterm infant, but tolerance to the drug rapidly develops.

The protocol suggested by the Kennedy report is good, but will it work? T here is now another “Kennedy report” for paediatricians to consider.1 This time the chair was Baroness Helena Kennedy QC, the working group was set up by the royal colleges of Paediatrics and Child Health and of Pathology, and the subject was the investigation of sudden unexpected deaths in infants (SUDI). The report recommends a systematic and evidence based protocol for the history, examination, investigation, autopsy, death scene investigation, and subsequent multiprofessional meeting in relation to each death.1 It also recommends that this should be compulsory, although it doesn't say how that might be enforced. But will it have the desired effect? The background is several recent high profile cases in the United Kingdom of mothers accused of killing their infants: the quashing of the convictions of Sally Clarke and Angela Cannings; the acquittal of Trupti Patel; and cases such as that of Maxine Robinson, who originally protested her innocence of the deaths of the two children she was …

Helpful, harmful, or don’t we know? (see pages1106 and 1111) The publication in the Lancet of the European Concerted Action on sudden infant death syndrome (SIDS) (ECAS study)1 resulted in front page headlines such as “Don’t sleep with your baby” ( Daily Telegraph : D Derbyshire, Science Correspondent, 16 January 2004). Yet the ECAS study said nothing new about bed-sharing and cot death: both the CESDI study (Confidential Enquiry into Stillbirth and Death in Infancy),2 data from New Zealand,3 and work from Ireland4 have superficially come to similar conclusions. Is the quality of evidence such that paediatricians, midwives, and health visitors should reasonably dissuade mothers from bed-sharing or co-sleeping, or is there more to it than that? First, we must question the validity of extrapolating health messages from case controlled data sets. Bradford-Hill suggested robust criteria (temporal relationship, specificity, biological plausibility, coherence; others would add dose response) for inferring causality from associative data when prospective randomised trials are impossible.5 It took some time before these criteria were satisfied to such an extent that the successful “back to sleep” campaign could be accepted as public policy. That success should not seduce us into accepting a lower standard of evidence of causality for some “new” hypothetical risk factor. Arguably, now that we have good reason to promote supine sleeping, an appropriate thermal environment, and the avoidance of cigarette smoke, the benefit of any further message on reducing the risk of SIDS is likely to be marginal at best. Second, there is a general lack of understanding about the heterogeneity of bed-sharing in particular, and infant sleep environments in general, in the data collection and analyses of case control studies. These …

Bladder Exstrophies and Epispadias Complex: Prevalence, Associated Anomalies, Prenatal Diagnosis and Survival in the North of England

The glucoregulatory role of insulin in adult subjects is undisputed. However, less is known about the secretion of insulin and its actions in the neonatal period, either for healthy subjects, or for those at risk of disordered blood glucose homoeostasis. The relationships between blood glucose and plasma immunoreactive insulin concentrations were therefore examined in 52 healthy children (aged 1 month-10 years), 67 appropriate birth weight for gestational age (AGA) term infants, and 39 AGA preterm neonates. In children and AGA neonates, plasma immunoreactive insulin concentration was positively related to blood glucose concentration. However, although both groups of neonates had significantly lower blood glucose concentrations than children, plasma immunoreactive insulin concentrations were significantly higher in both term and preterm neonates, when compared with children. The variation in plasma immunoreactive insulin concentrations was greater for neonates than for children. These data suggest, that compared with older subjects, plasma immunoreactive insulin concentrations are high in newborn babies and that neonatal pancreatic insulin secretion is less closely linked to circulating blood glucose concentrations. There are important implications for the interpretation of studies in hypoglycaemic and hyperglycaemic neonates.

The increased risk of hypoglycaemia for infants who are small for gestational age (SGA) is well known, and further information regarding metabolic adaptation can be gained by examining the profiles of glucose and other metabolic fuels in such infants. Not all SGA infants experience hypoglycaemia, however, and the ability to identify, antenatally, those at most risk would be helpful for obstetric and neonatal management. This study investigated metabolic differences between two groups of SGA infants who had antenatal umbilical artery Doppler studies. Fourteen had end diastolic velocities (EDV) present and 11 had absent EDV. The absent EDV group had significantly lower non-esterified fatty acid (NEFA) concentrations at birth, and lower blood glucose and NEFA concentrations in the first six hours after birth. After the first day, few metabolic differences were found between the two groups. Antenatal Doppler studies may identify those SGA infants who fail to achieve neonatal metabolic adaptation and are most at risk of early neonatal hypoglycaemia.

There have been few comprehensive accounts of the relationships between glucose and other metabolic fuels during the first postnatal week, especially in the context of modern feeding practises. A cross sectional study was performed of 156 term infants and 62 preterm infants to establish the normal ranges and interrelationships of blood glucose and intermediary metabolites in the first postnatal week, and to compare these with those of 52 older children. Blood glucose concentrations varied more for preterm than for term infants (1.5-12.2 mmol/l v 1.5-6.2 mmol/l), and preterm infants had low ketone body concentrations, even at low blood glucose concentrations. Breast feeding of term infants and enteral feeding of preterm infants appeared to enhance ketogenic ability. Term infants had lower prefeed blood glucose concentrations than children but, like children, appeared to be capable of producing ketone bodies. This study demonstrates that neonatal blood glucose concentrations should be considered in the context of availability of other metabolic fuels, and that the preterm infant has a limited ability to mobilise alternative fuels.

Doctors and members of ethics committees need guidance that is underpinned by sound evidence on parental attitudes to research In recent years, the journal has carried several papers on parental consent (assent) for participation of their babies in clinical trials.1,2 This is important because Archives is read by many of those who organise neonatal research projects. The approach to parents is often fraught with ethical dilemmas. Clinicians and members of ethics committees alike need guidance that is underpinned by sound research evidence on parental attitudes and beliefs about participating in research, rather than well meant assumptions about how parents might feel. Readers of the Journal of Medical Ethics would find little of direct use when confronted by the clinical realities and research questions of neonatal care—although this journal once published a neonatal study on the variability of ethics committee views. Rather, it is to specialist or …

Top of pageAbstract A study was designed to test the hypothesis that the lymphopenia caused by surgical stress in children may arise through selective depletion of one or more lymphocyte subsets. Blood samples from 18 children were taken pre- and post-operatively and 6, 12, 24 and 48 hours after surgery. Lymphocyte subsets were identified and counted using monoclonal antibodies and indirect immunofluorescence. By 6 hours post-operatively, the mean total lymphocyte count had fallen by 2.04×10/1 (p

Top of pageAbstract In order to test the hypothesis that the metabolic response to surgery in childhood would vary both with age and severity, 46 children aged 1 month to 10 years undergoing a variety of operations under a standard anaesthetic were studied. Blood samples were drawn pre- and post-operatively and 6, 12, 24 and 48 hours after surgery. Blood concentrations of glucose and 7 other metabolic fuels were measured by micro enzymatic assays and serum insulin by radioimnunoassay. Severity of surgery was scored using the Oxford surgical stress scale (SSS). Surgery caused significant increases in the concentrations of lactate, pyruvate and ketone bodies which vrere related to SSS (tau=0.34 (p