Hypernatraemia

Published on 01/03/2015 by admin

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Last modified 01/03/2015

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10

Hypernatraemia

Hypernatraemia is an increase in the serum sodium concentration above the reference interval of 133–146 mmol/L. Just as hyponatraemia develops because of sodium loss or water retention, so hypernatraemia develops either because of water loss or sodium gain.

Water loss

Pure water loss may arise from decreased intake or excessive loss. Severe hypernatraemia due to poor intake is most often seen in elderly patients, either because they have stopped eating and drinking voluntarily, or because they are unable to get something to drink, e.g. the unconscious patient after a stroke. The failure of intake to match the ongoing insensible water loss is the cause of the hypernatraemia. Less commonly there is failure of AVP secretion or action, resulting in water loss and hypernatraemia. This is called diabetes insipidus; it is described as central if it results from failure of AVP secretion, or nephrogenic if the renal tubules do not respond to AVP.

Water and sodium loss can result in hypernatraemia if the water loss exceeds the sodium loss. This can happen in osmotic diuresis, as seen in the patient with poorly controlled diabetes mellitus, or due to excessive sweating or diarrhoea, especially in children. However, loss of body fluids because of vomiting or diarrhoea usually results in hyponatraemia (see pp. 16–17).

Sodium gain

Hypernatraemia due to sodium gain (often referred to generically as ‘salt poisoning’ even where there is no suggestion of malicious or self-induced harm) is much less common than water loss. It is easily missed precisely because it may not be suspected. It can occur in several clinical contexts, each very different. Firstly, sodium bicarbonate is sometimes given to correct life-threatening acidosis. However, it is not always appreciated that the sodium concentration in 8.4% sodium bicarbonate is 1000 mmol/L. A less concentrated solution (1.26%) is available and is preferred. Secondly, near-drowning in salt-water may result in the ingestion of significant amounts of brine, the sodium concentration of which is once again vastly in excess of physiological. Thirdly, infants are susceptible to hypernatraemia if given high-sodium feeds either accidentally or on purpose. For example, the administration of one tablespoon of NaCl to a newborn can raise the plasma sodium by as much as 70 mmol/L.

The pathophysiological parallel to the administration of sodium is the rare condition of primary hyperaldosteronism (Conn’s syndrome), where there is excessive aldosterone secretion and consequent sodium retention by the renal tubules. Similar findings may be made in the patient with Cushing’s syndrome, where there is excess cortisol production. Cortisol has weak mineralocorticoid activity. However, in both these conditions the serum sodium concentration rarely rises above 150 mmol/L. The mechanisms of hypernatraemia are summarized in Figure 10.1.

Clinical features

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