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Letters

Hyponatraemia can be caused by standard fluid regimens

BMJ 2000; 320 doi: https://doi.org/10.1136/bmj.320.7239.943 (Published 01 April 2000) Cite this as: BMJ 2000;320:943
  1. Andrew Durward, consultant in paediatric intensive care,
  2. Shane M Tibby, consultant in paediatric intensive care,
  3. Ian A Murdoch, consultant in paediatric intensive care
  1. Guy's Hospital, London SE1 9RT

    EDITOR—The article by Bhalla et al highlighted the dangers from giving excessive hypotonic fluids to children at home.1 The striking omission from their article is that most perpetrators of this are members of the medical community. Hypotonic intravenous fluid continues to be given to hospitalised children on the basis of dogma laid down some 40 years ago, but which survives unchallenged today, even in the light of current understanding of the mechanisms of antidiuretic hormone secretion in acute illness.2

    During acute illness, a number of physiological stimuli such as fever, pain, nausea, and stress are associated with the non-osmotic release of antidiuretic hormone, thereby limiting the renal excretion of water free of electrolytes.3 4 The source of electrolyte free water in these circumstances is often not recognised because standard maintenance fluids (4% dextrose with 0.18% saline) are calculated to provide the correct water and salt requirements for healthy children, rather than the correct tonicity for sick children. Under these conditions, treatment with even “normal quantities” of hypotonic fluid will result in the net accumulation of electrolyte free water when antidiuretic hormone acts, and hence hyponatraemia will occur.

    When a simple calculation based on a tonicity balance is used, as advocated by Halperin and Goldstein, a “standard” fluid maintenance regimen of 100 ml/kg/day of 4% dextrose and 0.18% saline would result in the accumulation of about 50 ml/kg/day of electrolyte free water (generously assuming that half the water intake is excreted renally or as insensible losses in an acutely ill child when antidiuretic hormone acts). This represents a gain of about 8% in electrolyte free water relative to the total body water (600 ml/kg total body water+50 ml/kg electrolyte free water) which would proportionally drop the serum sodium concentration from 140 mmol/l to 129 mmol/l (8% of 140) after 24 hours.

    The key to avoiding hyponatraemia in this scenario lies in maintaining the tonicity balance—that is, matching what the patient is putting out in terms of both volume and electrolyte content. We hope that the adoption of this simple principle by clinicians will reduce the incidence of hyponatraemia acquired in hospital and its associated complications.

    References

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