• Ewout J Hoorn, Michiel G H Betjes, Joachim Weigel, and Robert Zietse.
• Erasmus Medical Center, Dialysis Unit, Room Bd 391, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. ejhoorn@gmail.com
• Nephrol. Dial. Transplant. 2008 May 1;23(5):1562-8.

BackgroundOur objective was to study the risk factors and mechanisms of hypernatraemia in critically ill patients, a common and potentially serious problem.MethodsIn 2005, all patients admitted to the medical, surgical or neurological intensive care unit (ICU) of a university hospital were reviewed. A 1:2 matched case-control study was performed, defining cases as patients who developed a serum sodium >/=150 mmol/l in the ICU.ResultsOne hundred and thirty cases with ICU-acquired hypernatraemia (141 +/- 3 to 156 +/- 6 mmol/l) were compared to 260 controls. Sepsis (9% versus 2%), hypokalaemia (53% versus 34%), renal dysfunction (53% versus 13%), hypoalbuminaemia (91% versus 55%), the use of mannitol (10% versus 1%) and use of sodium bicarbonate (23% versus 0.4%) were more common in cases (P < 0.05 for all) and were independently associated with hypernatraemia. During the development of hypernatraemia, fluid balance was negative in 80 cases (-31 +/- 2 ml/kg/day), but positive in 50 cases (72 +/- 3 ml/kg/day). Cases with a positive fluid balance received more sodium plus potassium (148 +/- 2 versus 133 +/- 3 mmol/l, P < 0.001). On average, cases were polyuric (40 +/- 5 ml/kg). Mortality was higher in cases (48% versus 10%, P < 0.001), for which hypernatraemia was an independent predictor (odds ratio 4.3, 95% confidence interval 2.5 to 7.2).ConclusionsHypernatraemia seems to develop in the ICU because various factors promote renal water loss, which is then corrected with too little water or overcorrected with relatively hypertonic fluids. Therapy should therefore rely on adding electrolyte-free water and/or creating a negative sodium balance. Adjustments in intravenous fluid regimens may prevent hypernatraemia.

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