Hyponatraemia for the Clinical Endocrinologist

Rebecca M. Reynolds; Jonathan R. Seckl


Clin Endocrinol. 2005;63(4):366-374. 

In This Article


Hyponatraemia is the most frequent electrolyte disorder seen in hospital practice and is by no means rare in community patients. Mild hyponatraemia (plasma sodium 130–135 mmol/l) is found in as many as 15–30% of hospitalized patients or in the institutionalized elderly,[1] although the clinical significance of this finding is usually uncertain. More severe hyponatraemia (plasma Na+ <130 mmol/l) is seen in 14% of inpatients and often reflects more serious underlying disease. Hyponatraemia is often asymptomatic when mild or when it develops slowly, but severe hyponatraemia (plasma sodium <120 mmol/l), particularly if of rapid onset, is associated with substantial morbidity and can be life-threatening.[2] Hospital patients with hyponatraemia have a substantial additional mortality,[3] although how much this reflects the electrolyte disturbance per se, as opposed to the severity of the underlying condition(s), remains uncertain. Hyponatraemia is also an important predictor of mortality in heart failure[4] and cirrhosis,[5] although again this is likely to reflect the severity of the primary underlying disorder and its treatments. Unfortunately, hyponatraemia is often iatrogenic. There are several excellent detailed reviews of the physiology of sodium homeostasis, thirst and vasopressin action, as well as the pathogenic mechanisms causing hyponatraemia.[6–10] Here we concentrate only upon the essential pathophysiology (below).

Moderate to severe hyponatraemia bears a substantial associated morbidity and mortality.[3] Thus, making a timely and accurate diagnosis and instituting appropriate therapy is crucial. Indeed, many texts teach that diagnosing the cause of hyponatraemia is key to guiding appropriate therapy. Certainly, correct management is critical as overly rapid correction of sodium may lead to severe neurological morbidity and mortality, while inadequate or inappropriate therapy has its own hazards. However, because distinguishing the cause(s) underlying an individual case of hyponatraemia is usually difficult and frequently unfeasible in clinical practice, and because there is an almost complete lack of prospective randomized controlled trial (RCT) evidence for commonly employed therapies, we concentrate on the empirically based pragmatic management of the hyponatraemic patient. We also highlight some recent advances of therapeutic promise in this complex but important area.


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