Elsevier

The Lancet

Volume 362, Issue 9392, 18 October 2003, Pages 1320-1323
The Lancet

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Intravenous fluids for seriously ill children: time to reconsider

https://doi.org/10.1016/S0140-6736(03)14577-1Get rights and content

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Impaired free-water excretion during severe infections

Antidiuresis during fever and sepsis has been known for over a century, especially in pneumonia and meningitis. Hippocrates' description of pneumonia included scanty and high-coloured urine. In a rhesus monkey model of pneumococcal sepsis, urine volume and free-water clearance decreased to 25% and 17% of baseline values, respectively, during the first 9 h of infection.9 When 0·45% saline, equal to 105% of urine output in controls, was intravenously infused into septic monkeys, their bodyweight

Hyponatraemia in severe infections

Hyponatraemia arises in between 20% and 45% of children with meningitis,11, 12 pneumonia,13 encephalitis,14 septicaemia,15 cerebral malaria,16, 17 and somewhat less often in those with bronchiolitis.10 The patho-physiological basis is not fully understood, but many factors could be active in the same patient (table 1). Dilution of extracellular fluid because of impaired free-water excretion and increased urinary sodium losses seem to be the main mechanisms. Other mechanisms, including shifts of

Antidiuretic hormone

High concentrations of antidiuretic hormone are seen in many acute febrile illnesses,22 and are traditionally described as inappropriate. When applied generally, this term indicates our incomplete understanding of the potency of different stimuli to antidiuretic hormone release and suppression (table 1). Hypovolaemia might be a more potent stimulus for secretion of antidiuretic hormone than hypo-osmolarity is to its suppression. In a retrospective study of 300 children with meningitis,

Adverse effects of hyponatraemia

In the peripheral circulation, sodium moves freely throughout the extracellular fluid; the hydrostatic pressure gradient and oncotic pressure (predominantly made up of plasma proteins) are responsible for preventing the movement of water out of the vasculature. Cerebral circulation is different. Endothelial tight junctions prevent free movement of sodium across the intact blood-brain barrier, and therefore effective osmolarity is the major determinant of water movement into the brain

Potential pitfalls

Use of an isotonic, rather than hypotonic, solution does not mean that progressive hyponatraemia would not take place, but that it is much less likely. Although use of high-sodium-containing solutions in children with meningitis in the first 24 h was not associated with development of hypernatraemia,6 during the later phases of illness there is a theoretical risk of hypernatraemia if isotonic saline is used. Diuresis and low urine osmolarity is a feature of the convalescent phase of childhood

Possible solution

We postulate that 0·9% saline (with 5% dextrose) at less than standard maintenance volumes results in a lower frequency of hyponatraemia, seizures, and adverse neurological events than do hypotonic solutions (0·18%-0·3% saline), in acutely unwell children with brain injury of any type (meningitis, encephalitis, cerebral malaria, febrile seizures); serum sodium less than 138 mmol/L;30 or severe infection associated with greatly impaired free-water excretion.

Ideal testing of this hypothesis would

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      This might be explained by the empiricism of historical recommendations published roughly 60 years ago, favoring dextrose 5% in water (D5W) with low amounts of sodium (e.g., a quarter [NS/4] or half [NS/2] of normal saline [NS]) [1]. Furthermore, the syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) often occurs in several diseases currently seen in children (e.g., acute gastroenteritis, viral bronchiolitis, encephalitis, meningitis; Table 1), which impairs the excretion of free water and favors the occurrence of hypotonic hyponatremia [2]. In the 2000s, two American pediatric nephrologists reported a series of children with severe hypotonic fluid-induced severe hyponatremia leading to severe neurological sequelae and death [3,4].

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