Who is blaming the baby?

Sudden unexplained collapse within the first 12 h of life is a rare but recognised event. Over a 2-year period, five infants, previously assessed as healthy, were found collapsed in our maternity unit in the care of their primiparous mothers. Two were found prone on their mother's chest, and two were in their mother's bed. The outcomes were poor, with four neonatal deaths and one death at 18 months. The rate of sudden unexplained neonatal collapse was 0.4 per 1000 live births. No cause for collapse was identified despite extensive investigations, which included postmortem in all the neonatal deaths. One infant, however, showed widespread antenatal brain damage at postmortem. It is postulated that some infants with an underlying vulnerability may maladapt to extrauterine life following an hypoxic stressor possibly caused by positional airway obstruction.

Blood pressure in children aged 4-8 years: comparison of Omron HEM 711 and sphygmomanometer blood pressure measurements.

OBJECTIVE: To collect normal data on blood pressure (BP) in healthy children aged 4-8 and to compare measurements of BP made in the same subjects with a sphygmomanometer and a portable automated oscillometric BP monitor (Omron HEM 711 with child cuff). METHODS: Cross-sectional observational study of 764 children. BP measurements were made at school, using both a sphygmomanometer and an Omron HEM 711. Immediately after the BP measurement children were asked to state which device they preferred (if any). RESULTS: Children had no preference for whether the sphygmomanometer or the Omron was used. Bland-Altman plots showed a lack of consistency between the two methods of BP measurement. With systolic BP there was a trend for the Omron to underestimate when low and overestimate when high. CONCLUSIONS: Children were equally distributed in their preference for BP device. There was a wide variation between the two methods of BP measurement, which suggests that comparison of automated BP measurements with normative data obtained by sphygmomanometer is not valid.

Cortisol and growth hormone responses to spontaneous hypoglycaemia in infants and children.

AIMS: To evaluate responses of cortisol and growth hormone (GH) to spontaneous hypoglycaemia in infants and children. METHODS: Retrospective review of laboratory and clinical data in paediatric patients investigated for suspected hypoglycaemia over a five year period. Thirty patients (16 aged <3 months) had hypoglycaemia confirmed by laboratory analysis (glucose <2.5 mmol/l) and were compared with 26 patients (11 aged <3 months) with glucose > or =2.5 mmol/l. RESULTS: The commonest causes of hypoglycaemia were transient hyperinsulinism in infants <3 months and intercurrent infection in those >6 months of age. In both hypo- and non-hypoglycaemic patients, cortisol was positively (r(s) +0.66 and +0.68) and GH inversely (r(s) -0.65 and -0.75) correlated with age. Hypo- and non-hypoglycaemic infants <3 months had median cortisol concentrations of 205 and 116 nmol/l respectively compared with 1370 and 736 nmol/l in hypo- and non-hypoglycaemic children >6 months. Conversely, median GH was 46.5 and 51.2 mU/l in hypo- and non-hypoglycaemic infants compared with 14.3 and 12.1 mU/l in older hypo- and non-hypoglycaemic patients. Older non-hypoglycaemic patients with glucose levels below the glycaemic thresholds established for cortisol and GH secretion in adults had higher cortisol and GH concentrations than patients whose glucose levels exceeded these thresholds. CONCLUSIONS: Cortisol and GH responses to spontaneous hypoglycaemia in children are highly age dependent. Young infants mount a poor cortisol response compared with older infants and children. Children older than 6 months may have glycaemic thresholds for cortisol and GH similar to those established for adults.

Plasma cortisol, cortisone and urinary glucocorticoid metabolites in preterm infants.

OBJECTIVE AND METHODS: In the fetal circulation, there is a low cortisol:cortisone (F:E) ratio ( approximately 0.3) suggesting high activity of 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2). The circulating F:E ratio rises after birth in term infants, but little is known about infants born prematurely. Our hypothesis was that the low fetal plasma F:E ratio would persist in infants born prematurely, due to persistently high tissue 11betaHSD2 activity. To test this hypothesis, a longitudinal observational study of plasma F, E levels and urinary F and E metabolites was performed in 22 preterm infants of 24-31 weeks gestation. RESULTS: Median plasma F was 234-380 nmol l(-1), median 124-177 nmol l(-1) from 1 to 14 days age. Plasma F fell with increasing postnatal and postconceptional age. The F:E ratio was 3 in the first week of life, and thereafter was 1-2, falling with postnatal age. Urinary glucocorticoid metabolites were low in quantity ( approximately 48-120 microg kg(-1) day(-1)), consisted of E metabolites until term, and did not reflect the plasma F:E ratio. CONCLUSIONS: The fetal plasma F:E ratio did not persist in these preterm infants, due to tenfold higher levels of F. The F:E ratios were similar to those reported in term infants. These data suggest that the low F:E ratio in utero is due to low fetal production of cortisol, and effective placental inactivation of maternal F by 11betaHSD2.

Adrenal function in preterm infants: ACTH may not be the sole regulator of the fetal zone.

The fetal zone of the adrenal gland is known to persist after preterm birth, but there is uncertainty as to how long adrenal fetal zone steroid production continues and how it is regulated. The purpose of this study was to test two hypotheses. First, that the urinary excretion of 3beta-OH-5-ene steroids persists until term, and then declines, as it does in full-term infants. Second, that the persistence of the fetal zone is due to continuing ACTH stimulation. A longitudinal observational study was undertaken in 22 preterm infants of 24-31-wk gestation. Sequential measurements were made of urinary 3beta-OH-5-ene steroids (fetal zone steroid metabolites), plasma dehydroepiandrosterone sulfate (DHEAS), and ACTH. Excretion of urinary 3beta-OH-5-ene steroids was 1500-2000 microg kg(-1) d(-1), persisting until term, and declining abruptly at approximately 42 wk postconceptional age (PCA), to levels comparable to term infants at the same PCA. Median plasma ACTH levels rose from <7.6 pg mL(-1) at 25-wk PCA to 34.5 pg mL(-1) at 46-wk PCA. Urinary 3beta-OH-5-ene steroids were highest when ACTH levels were lowest, and were declining when ACTH was rising. In four infants given dexamethasone, urinary excretion of 3beta-OH-5-ene steroids and plasma DHEAS were not suppressed fully, when plasma ACTH and cortisol, and urinary cortisol metabolites were. These data suggest that ACTH is not the sole regulator of the adrenal fetal zone steroid synthesis and that involution of the fetal zone is related to gestation rather than birth.

Activity of the adrenal fetal zone in preterm infants continues to term.

In term babies, steroids from the fetal zone of the adrenal gland decline in the blood and urine in the first few weeks after birth. In infants born prematurely, fetal zone steroids (3 beta-OH-5ene steroids) persist but it is not known for how long. The present study set out to address this by examining changes in the synthesis and metabolism of adrenal steroids with postconceptional age, using serial measurements of steroid metabolites in the urine. 21 preterm infants, median gestation 29 weeks (range 24-31 weeks) and median birth weight 933g were examined. 3 beta-OH-5ene steroids represented around 90% of the total steroids excreted until 2 weeks past term, falling to 55% by 12 weeks after term. 3 beta-OH-5ene steroids were excreted in the urine at levels of 1500-2000 micrograms kg-1 d-1, until 3-4 weeks past term, after which these urinary fetal zone steroid metabolites declined, falling to 500 micrograms kg-1 d-1 six weeks past term. We conclude that activity of the adrenal fetal zone in preterm infants continues to term, after which it diminishes. This suggests that it is gestation that determines fetal zone activity rather than birth.

Mannan-binding protein in human umbilical cord blood.

Mannan binding protein (MBP) may be important for host defence particularly in infancy. MBP concentration was measured in 237 umbilical cord blood samples from singleton pregnancies and compared to those of 352 blood donors. Both data sets yielded a bimodal frequency distribution, consisting of a log-normal peak and a long tail of lower values. The range (0-23 U/ml) and median (7.2 U/ml) of cord blood values were significantly lower than those of blood donors (range 0-43 U/ml; median 8.3 U/ml). MBP was also measured in the cord blood samples of 8 pairs of twin siblings. Discordant values in two pairs of twins suggest that cord blood MBP is derived from the fetoplacental unit and not from the maternal circulation by transplacental passage.

Virilisation of female preterm infants.

Two cases of hypertrophy of the clitoris in premature girls are reported; this was associated with persistently high concentrations of adrenal fetal zone androgens.