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Arch Dis Child. 2007 June; 92(6): 474–475.
PMCID: PMC2066171

Avoiding hypernatraemic dehydration in healthy term infants

Short abstract

Perspective on the paper by van Dommelen et al (see page 490)

Hypernatraemic dehydration arises when there is a disproportionate deficit of body water relative to body sodium. Although the serum sodium concentration is elevated, whole body sodium content may be reduced, unchanged or increased. When the condition occurs in an otherwise healthy full term, breast‐fed baby the cause is poor milk intake. In this situation there is loss of body sodium but a greater deficit in body water.

Hypernatraemic dehydration may have serious adverse consequences. At the most severe end of the spectrum these include cerebral oedema, convulsions, venous sinus thrombosis, intracranial haemorrhage, disseminated intravascular coagulation, renal failure, permanent brain injury and death. Infants admitted to hospital usually undergo extensive investigation and rehydration with intravenous fluids and formula. This has led to concern about how best to detect the condition, particularly in newborns in the community as biochemical testing would require referral to hospital. In this issue, a group of Dutch researchers describe the construction of a reference chart for relative postnatal weight change and propose the use of this chart by midwives assessing babies at home.1 They conclude that beyond the first postnatal week, the guideline or “rule‐of‐thumb” that weight loss in excess of 10% of birth weight is abnormal is a reasonable trigger for referral to hospital. However, they argue that relative weight loss in the first week exceeding

−2.5 SDS is preferable because the 10% rule would result in a greater number of referrals. They recommend the use of a chart for relative weight change as a screening tool. Is this a reasonable approach to dealing with the problem of hypernatraemic dehydration?

Let us consider this from two perspectives: the utility of the approach as a guideline and the utility as a screening tool.

Guidelines promote consistency in clinical practice. At best they are strongly evidence based and describe management proven to be beneficial to outcome. If evidence is lacking, consistency in practice is still considered desirable because at the very least outcomes can be surveyed objectively without confounding by random variations in practice. The guideline proposed by van Dommelen et al is that midwives should refer babies assessed in the community to hospital if relative weight change between postnatal days 3 and 6 exceeds −2.5 SDS and thereafter 10% of birth weight. They found that this approach had a sensitivity (the test is positive if the condition is present) of 85.5% and a specificity (the test is negative if the condition is absent) of 99.4%. Thus accuracy (sensitivity plus specificity) was 184.9. The authors argue that for screening purposes specificity should be high to reduce the number of referrals to hospital. However, should the principal purpose of the guideline be to reduce unnecessary referrals or to correctly identify at‐risk infants? If the latter, the focus should be upon optimising sensitivity. Referral based upon the time‐honoured 10% postnatal weight loss was found to have a sensitivity of 90.4% and specificity of 98.3%. Accuracy was thus greater, namely 188.7. This argues against the former approach being considered superior. The argument becomes stronger when the simplicity of the 10% guideline is set against the complexity of constructing population based relative weight change reference charts and instructing heath care professionals in their use. Of course as a guideline neither approach is adequately evidence based because the true rate of hypernatraemic dehydration is not known, nor has it been established that early detection through systematic screening – as opposed to detection through clinical presentation – improves outcome.

There are other considerations. Hypernatraemia can occur without excessive weight loss (van Dommelen et al report eight cases out of 83) and excessive weight loss can occur without hypernatraemia. The magnitude of postnatal weight loss is dependent upon the relative contributions of dehydration and starvation, superimposed upon normal physiological postnatal loss of extracellular fluid. In preterm babies born below 32 weeks' gestation, 10% of the total body water present at birth is lost during normal postnatal adaptation.2 In these babies the median time to postnatal weight loss of 6% is 2–3 days,3 which is closely comparable to the mean time to 6% weight loss at 3 days reported in healthy term babies by van Dommelen et al. Total body water content increases with decreasing gestation and therefore physiological weight loss will be proportionally greater the more immature the baby, regardless of the contribution of starvation and loss of body solids, in keeping with van Dommelen et al's observation of an inverse relationship between birth weight and relative weight change. In clothed term babies insensible water loss is low and of the order of less than 12 ml/kg/day4 but will rise with tachypnoea, radiant heat sources and a low humidity environment. Urinary concentrating ability is initially low, only improving with postnatal age as the tonicity of the renal medullary interstitium increases. Inadequate milk intake results in progressive depletion of whole body sodium. In term babies with hypernatraemic dehydration, it is possible that this is compounded by dehydration induced natriuresis, a defence mechanism in mammalian species which serves to buffer dehydration induced hyperosmolarity.5,6 There is evidence that dehydration induced natriuresis is mediated by osmoreceptor stimulated oxytocin release7 and occurs even in the sodium restricted state. The high urinary sodium concentration in babies with hypernatraemic dehydration should not be interpreted as evidence of sodium excess,8 even when considered in conjunction with a high concentration of sodium in breast milk. Breast milk sodium is initially high but declines to less than 20 mmol/l as lactation is established and volumes increase. Continuing high breast milk sodium concentrations are indicative of lactation failure.9

Although a guideline based upon an unambiguous cut‐off value has the undoubted attraction of simplicity, postnatal weight loss might be predicted to be, and indeed is, variable. The case is well made that weighing alone is unlikely to prevent the problem.10 I suggest that a more appropriate focus for a guideline concerned with the detection of lactation failure is the baby and the mother. Is the baby well on examination, and neither fractious nor lethargic? Does the baby latch on and suck well? Is the mother well and not overly tired? Is her milk in? Surely this should be the first step of a management algorithm and not, as van Dommelen et al suggest, the last? If mother and baby are well, it would not be unreasonable to review the situation the following day even though weight loss appears excessive. Concerns about the baby warrant referral, regardless of weight loss, as should progressive weight loss or inadequate weight gain. Concerns about the mother and adequacy of lactation equally warrant intervention. But here we enter into dangerous territory. Hypernatraemic dehydration is a consequence of a failure in breast feeding. Lactation failure if managed well is more often than not temporary. However, a mother who is sleep‐deprived, exhausted and anxious, will not lactate well nor in these circumstances will insistence upon exclusive breast feeding help, regardless of whether this is self‐imposed or imposed by professional advice. Regrettably it has become difficult to suggest that there are situations where a continued insistence on exclusive breast feeding is counterproductive. The Baby Friendly Initiative aimed to reverse the tragic worldwide decline in breast feeding that occurred in the 20th century, but the requirements of the initiative should not be interpreted to the detriment of the infant. A baby with hypernatraemic dehydration is at serious clinical risk and, as admission to hospital reduces the chances of a mother continuing to breast feed successfully, of being denied the benefits of human milk. Perhaps it is time to acknowledge that in order to safeguard both babies and breastfeeding, this is a situation that calls for a less uncompromising and more common sense approach.

I am sceptical about guidelines that simplify management but have a poor evidence base. In these circumstances I suggest that a better foundation for a guideline is that it should provide a check list of the relevant physiological principles upon which to make a clinical evaluation. Let us train people to make sound clinical assessments and let us empower them to support a breast feeding mother in any way appropriate, even if that means providing a rare bottle of formula to provide respite for her and to avoid hypernatraemic dehydration in her baby.

Acknowledgements

I am grateful to Dr Gary Hartnoll for helpful discussion of this perspective.

Footnotes

Competing interests: The author has received research funding in the past 5 years from Action Medical Research, The Bailey Thomas Charitable Fund, The Hospital Infection Society, the Institute of Obstetrics and Gynaecology Trust, London Specialised Commissioners, March of Dimes, Numico Research, Portland Hospital, the Wellcome Trust and Westminster Children's Research Fund. She is chief investigator for planned and current trials involving newborn feeding.

References

1. van Dommelen P, van Wouwe J P, Breuning‐Boers J M. et al Reference chart for relative weight change to detect hypernatraemia dehydration. Arch Dis Child 2007. 92490–494.494 [PMC free article] [PubMed]
2. Tang W, Ridout D, Modi N. The influence of respiratory distress syndrome on body composition after preterm birth. Arch Dis Child 1997. 77F28–F31.F31
3. Hartnoll G, Bétrémieux P, Modi N. Randomised controlled trial of postnatal sodium supplementation on body composition in 25–30 week gestation infants. Arch Dis Child Fetal Neonatal Ed 2000. 82F24–F28.F28 [PMC free article] [PubMed]
4. Hammarlund K, Sedin G. Transepidermal water loss in newborn infants. III. Relation to gestational age. Acta Paediatr Scand 1979. 68795–801.801 [PubMed]
5. Andersen L J, Andersen J L, Pump B. et al Natriuresis induced by mild hypernatremia in humans. Am J Physiol Regul Integr Comp Physiol 2002. 282R1754–R1761.R1761 [PubMed]
6. McKinley M J, Evered M D, Mathai M L. Renal sodium excretion in dehydrated and rehydrated adrenalectomized sheep maintained with aldosterone. Am J Physiol Regul Integr Comp Physiol 2000. 279R17–R24.R24 [PubMed]
7. Huang W, Lee S L, Arnason S S. et al Dehydration natriuresis in male rats is mediated by oxytocin. Am J Physiol 1996. 270R427–R433.R433 [PubMed]
8. Karthikeyan G, Modi N. Neonatal hypernatremia due to high breast milk sodium? Indian Pediatr 2003. 4072–73.73 [PubMed]
9. Morton J A. The clinical usefulness of breast milk sodium in the assessment of lactogenesis. Pediatrics 1994. 93802–806.806 [PubMed]
10. Harding D, Moxham J, Cairns P. Weighing alone will not prevent hypernatraemic dehydration. Arch Dis Child Fetal Neonatal Ed 2003. 88F349

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