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QJM Advance Access originally published online on June 13, 2005
QJM 2005 98(7):529-540; doi:10.1093/qjmed/hci081
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© The Author 2005. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Commentary

Diagnostic approach to a patient with hyponatraemia: traditional versus physiology-based options

E.J. Hoorn1, M.L. Halperin2 and R. Zietse1

From the 1Department of Internal Medicine, Erasmus Medical Center, Erasmus University Rotterdam, Rotterdam, The Netherlands, and 2Division of Nephrology, St. Michael's Hospital, University of Toronto, Toronto, Canada

Address correspondence to Dr R. Zietse, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. email: r.zietse{at}erasmusmc.nl

The usual diagnostic approach to a patient with hyponatraemia is based on the clinical assessment of the extracellular fluid (ECF) volume, and laboratory parameters such as plasma osmolality, urine osmolality and/or urine sodium concentration. Several clinical diagnostic algorithms (CDA) applying these diagnostic parameters are available to the clinician. However, the accuracy and utility of these CDAs has never been tested. Therefore, we performed a survey in which 46 physicians were asked to apply all existing, unique CDAs for hyponatraemia to four selected cases of hyponatraemia. The results of this survey showed that, on average, the CDAs enabled only 10% of physicians to reach a correct diagnosis. Several weaknesses were identified in the CDAs, including a failure to consider acute hyponatraemia, the belief that a modest degree of ECF contraction can be detected by physical examination supported by routine laboratory data, and a tendency to diagnose the syndrome of inappropriate secretion of antidiuretic hormone prior to excluding other causes of hyponatraemia. We conclude that the typical architecture of CDAs for hyponatraemia represents a hierarchical order of isolated clinical and/or laboratory parameters, and that they do not take into account the pathophysiological context, the mechanism by which hyponatraemia developed and the clinical dangers of hyponatraemia. These restrictions are important for physicians confronted with hyponatraemic patients and may require them to choose different approaches. We therefore conclude this review with the presentation of a more physiology-based approach to hyponatraemia, which seeks to overcome some of the limitations of the existing CDAs.


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