We were concerned by the recent paper from
Bajpai et al.(1) in which the authors advocated cessation
of breast feeding. We question the conclusions the authors draw in
attempting to link the high infant urinary sodium concentration to
the high sodium concentration in their mother’s expressed breast
milk.
Neville et al.(2) have shown that breast
milk sodium is high during the colostrum phase of lactation. It
then declines rapidly as the milk volume increases to
approximately 300 mL and then levels out with breast milk volumes
above 500 mL. Morton(3) evaluated the clinical usefulness of
breast milk sodium in the assessment of lactogenesis in 130
nursing mothers. Breast milk sodium was initially measured between
the 3rd and 8th postpartum day. Mothers in whom breast milk sodium
was normal ( £16mmol/L)
were followed up at 1 month and those in whom breast milk sodium
was elevated were provided with breast feeding support. Repeated
estimations of breast milk sodium were performed until this
dropped to £16 mmol/L. 95.4% of mothers with a normal initial breast milk sodium
concentration were breastfeeding successfully at 1 month whereas
only 55% of those with a high breast milk sodium concentration
were successful despite the intervention. The longer the sodium
concentration remained elevated, the lower the success rate. The
highest breast milk sodium seen in this study was 134 mmol/L on
the eighth day.
Dehydration induced natriuresis is a defence
mechanism in mammalian species which serves to buffer the
hyperosmolarity and increased sodium concentration occurring with
dehydration(4). There is evidence that this dehydration induced
natriuresis is a physiological response that occurs even in the
sodium restricted state and it appears to be mediated by
osmoreceptor stimulated oxytocin release(5).
In the light of the above evidence, we consider
that both the key messages of the article by Bajpai et al.
are flawed. An elevated breast milk sodium concentration is a
reflection of failed lactogenesis and not the cause of
hypernatremia seen in these babies. Given that the total volume of
milk ingested by these infants would undoubtedly have been
severely reduced, the actual sodium intake not be greatly elevated
and would be well within the excretory capacity of a term infant.
The elevated urinary sodium concentration is a compensatory
defence mechanism to maintain serum osmolality and not a result of
hypernatremia.
Simple calculations will show that these
neonates are sodium depleted inn addition to being water depleted.
The water deficit is proportionally greater than the sodium
deficit and it is this that results in the hypernatremia. We
estimate that the approximate whole body sodium deficit of cases
I, II and III were 67, 54 and 75 mmol respectively, Bajpai et
al.(1) do not state what fluid was used during rehydration and
we wonder if the seizures noted in case I might have resulted from
the inappropriate use of salf-free or salt-poor fluid.
We were pleased to note that two of the three neonates
described in this article went on to establish breast feeding
satisfactorily. We wish to emphasise that this condition relates
to breast-feeding failure. It should not be attributed to human
milk and/or its composition and cessation of beast-feeding should
not be advocated.
1. Bajpai A,
Aggarwal R, Deorari AK, Paul VK. Neonatal hypernatremia due to
high breast milk sodium. Indian Pediatr 2002; 39: 193-196.
2. Neville MC,
Keller R, Seacat J, Lutes V, Neifert M, Casey C et al.
Studies in human lactation: milk volume in lactating women
during the onset of lactation and full lactation. Am J Clin Nutr
1988; 48: 1375-1386.
3. Morton JA. The
clinical usefulness of breast milk sodium in the assessment of
lactogenesis. Pediatrics 1994; 93: 802-806.
4. McKinley MJ,
Evered MD, Mathai ML. Renal sodium excretion in dehydrated and
rehydrated adrenalectomized sheep maintained with aldosterone.
Am J Physiol Regul Integr Comp Physiol 2000; 279: R17-24.
5. Huang W, Lee SL, Arnason SS,
Sjoquist M. Dehydration natriuresis in male rats is mediated by
oxytocin. Am J Physiol 1996; 270: R427-433.
