Prevention of hospital-acquired hyponatraemia: individualised fluid therapy.

Abstract

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