Prevention of hospital-acquired hyponatraemia: individualised fluid therapy

Abstract

Background: Large amounts of fluids are daily prescribed to hospitalised patients across different medical specialities. Unfortunately, inappropriate fluid administration commonly causes iatrogenic hyponatraemia with associated increase in morbidity and mortality.

Methods/results: Fundamental for prevention of hospital-acquired hyponatraemia is an understanding of what determines plasma sodium concentration (P-[Na(+) ]) in the individual patient. P-[Na(+) ] is determined by balances of water and cations according to Edelman. This paper discusses the mechanisms influencing water and cation balances. In the hospitalised patient, non-osmotic antidiuretic hormone secretion is frequent and results in a reduced renal electrolyte-free water clearance (EFWC). This condition puts the patient at risk of hyponatraemia upon infusion of fluids that are hypotonic such as 5% glucose, Darrow-glucose, NaKglucose and 0.45% NaCl in 5% glucose. It is suggested that individualised fluid therapy includes the following: Firstly, bolus therapy with Ringer-acetate/Ringer-lactate/0.9% NaCl in the hypovolaemic patient to minimise the risk of fluid under-/overload. Secondly, P-[Na(+) ] should be monitored together with the balances influencing P-[Na(+) ]. This may include EFWC in patients at additional risk of hyponatraemia. In patients with potentially reduced intracranial compliance (e.g. meningitis, intracranial bleeding, cerebral contusion and brain oedema), even a small decrease in P-[Na(+) ] induced by slightly hypotonic fluids like Ringer-acetate/Ringer-lactate can increase the intracranial pressure dramatically. Consequently, 0.9 % NaCl is recommended as first-line fluid for such patients.

Conclusions: The occurrence of hospital-acquired hyponatraemia may be reduced by prescribing fluids, type and amount, with the same dedication as shown for other drugs.