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NDT Advance Access originally published online on September 2, 2005
Nephrology Dialysis Transplantation 2006 21(1):70-76; doi:10.1093/ndt/gfi082
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


Original Articles: Clinical Nephrology

Development of severe hyponatraemia in hospitalized patients: treatment-related risk factors and inadequate management

Ewout J. Hoorn1, Jan Lindemans2 and Robert Zietse1

Departments of 1 Internal Medicine and 2 Clinical Chemistry, Erasmus Medical Center, Rotterdam, The Netherlands

Correspondence and offprint requests to: Robert Zietse, MD, Dr Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. Email: r.zietse{at}erasmusmc.nl

Background. Although hyponatraemia [plasma sodium (PNa) <136 mmol/l] frequently develops in hospital, risk factors for hospital-acquired hyponatraemia remain unclear.

Methods. Patients who presented with severe hyponatraemia (PNa ≤ 125 mmol/l) were compared with patients with hospital-acquired severe hyponatraemia in a 3 month hospital-wide cohort study.

Results. Thirty-eight patients had severe hyponatraemia on admission (PNa 121±4 mmol/l), whereas 36 patients had hospital-acquired severe hyponatraemia (PNa 133±5 -> 122±4 mmol/l). In hospital-acquired hyponatraemia, treatment started significantly later (1.0±2.6 vs 9.8±10.6 days, P<0.001) and the duration of hospitalization was longer (18.2±11.5 vs 30.7±23.4 days, P = 0.01). The correction of PNa in hospital-acquired hyponatraemia was slower after both 24 h (6±4 vs 4±4 mmol/l, P = 0.009) and 48 h (10±6 mmol/l vs 6±5 mmol/l, P = 0.001) of treatment. Nineteen patients (26%) from both groups were not treated for hyponatraemia and this was associated with a higher mortality rate (seven out of 19 vs seven out of 55, P = 0.04). Factors that contributed to hospital-acquired hyponatraemia included: thiazide diuretics (none out of 38 vs eight out of 36, P = 0.002), drugs stimulating antidiuretic hormone (two out of 38 vs eight out of 36, P = 0.04), surgery (none out of 38 vs 10 out of 36, P<0.001) and hypotonic intravenous fluids (one out of 38 vs eight out of 36, P = 0.01). Symptomatic hyponatraemia was present in 27 patients (36%), and 14 patients died (19%).

Conclusions. The development of severe hyponatraemia in hospitalized patients was associated with treatment-related factors and inadequate management. Early recognition of risk factors and expedited therapy may make hospital-acquired severe hyponatraemia more preventable.

Keywords: antidiuretic hormone; hypotonic intravenous fluids; post-operative hyponatraemia; syndrome of inappropriate antidiuretic hormone secretion; thiazide diuretics; water–sodium balance


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