Hyponatraemia is defined as a serum sodium concentration below the reference interval of 133–146 mmol/ L. It is the electrolyte abnormality most frequently encountered in clinical biochemistry.
Development of hyponatraemia
The serum concentration of sodium is simply a ratio, of sodium (in millimoles) to water (in litres), and hyponatraemia can arise either because of loss of sodium ions or retention of water.
- Loss of sodium. Sodium is the main extracellular cation and plays a critical role in the maintenance of blood volume and pressure, by osmotically regulating the passive movement of water. Thus when significant sodium depletion occurs, water is lost with it, giving rise to the characteristic clinical signs associated with ECF compartment depletion. Primary sodium depletion should always be actively considered if only to be excluded; failure to do so can have fatal consequences.
- Water retention. Retention of water in the body compartments dilutes the constituents of the extracellular space including sodium, causing hyponatraemia. Water retention occurs much more frequently than sodium loss, and where there is no evidence of fluid loss from history or examination, water retention as the mechanism becomes a near certainty.
Water retention
The causes of hyponatraemia due to water retention are shown in Figure 8.1
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| Fig 8.1 The causes of hyponatraemia. |
Water retention usually results from impaired water excretion and rarely from increased intake (compulsive water drinking). Most patients who are hyponatraemic due to water retention have the so-called syndrome of inappro- priate antidiuresis (SIAD). The SIAD is encountered in many conditions, e.g. infection, malignancy, chest disease, and trauma (including surgery); it can also be drug-induced. SIAD results from the inappropriate secretion of AVP. Whereas in health the AVP concentra- tion fluctuates between 0 and 5 pmol/ L due to changes in osmolality, in SIAD huge (non-osmotic) increases (up to 500 pmol/ L) can be seen. Powerful non- osmotic stimuli include hypovolaemia and/or hypotension, nausea and vomit- ing, hypoglycaemia, and pain. The frequency with which SIAD occurs in clinical practice mirrors the widespread prevalence of these stimuli. It should be stressed that the increase in AVP secretion induced by, say, hypovolaemia is an entirely appropriate mechanism to try to restore blood volume to normal. The term ‘inappropriate’ in SIAD is used specifically to indicate that the secretion of AVP is inappropriate for the serum osmolality.
AVP has other effects in the body aside from regulating renal water han- dling (Table 8.1).
Sodium loss
The causes of hyponatraemia due to sodium loss are shown in Figure 8.1. Sodium depletion effectively occurs only when there is pathological sodium loss, either from the gastrointestinal tract or in urine. Gastrointestrinal losses (Table 8.2) commonly include those from vomiting and diarrhoea; in patients
with fistulae due to bowel disease, losses may be severe. Urinary loss may result from mineralocorticoid deficiency (espe- cially aldosterone) or from drugs that antagonize aldosterone, e.g. spironolactone.
Initially in all of the above situations, sodium loss is accompanied by water loss and the serum sodium concentra- tion remains normal. As sodium and water loss continue, the reduction in ECF and blood volume stimulates AVP secretion non-osmotically, overriding the osmotic control mechanism. The increase in AVP secretion causes water retention and thus patients become hyponatraemic. Another reason why sodium-losing patients may become hyponatraemic is because a deficit of isotonic sodium-containing fluid is replaced only by water.
As indicated above, when significant sodium depletion occurs water is lost with it, giving rise to the clinical signs characteristic of ECF and blood volume depletion. In the context of hyponatraemia these findings are diagnostic of sodium depletion; the clinical findings are evidence of fluid (water) depletion, whilst the hyponatraemia indicates that the ratio of sodium to water is reduced.
Sodium depletion – a word of caution Not all patients with sodium depletion are hyponatraemic. Patients with sodium loss due to an osmotic diuresis may
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| Fig 8.2 Water tank models showing that reduced ECF volume may be associated with reduced, increased or normal serum [Na+]. |
become hypernatraemic if more water than sodium is lost. Life-threatening sodium depletion can also be present with a normal serum sodium concentra- tion. In short, the serum sodium concentration does not of itself provide any information about the presence or severity of sodium depletion (Fig 8.2). The history and clinical examination are much more useful in this regard.
Pseudohyponatraemia
Hyponatraemia is sometimes reported in patients with severe hyperproteinaemia or hyperlipidaemia. In such patients, the increased amounts of protein or lipoprotein occupy more of the plasma volume than usual, and the water less (Fig 8.3). Sodium and the other electrolytes are distributed in the water fraction only, and these patients have a normal sodium concentration in their plasma water. However, many of the methods used in analytical instruments measure the sodium concentration in the total plasma volume, and take no account of a water fraction that occupies less of the total plasma volume than usual. An artefactually low sodium result may thus be obtained in these circumstances. Such pseudohyponatraemia should be suspected if there is a discrepancy between the degree of apparent hyponatraemia and the symptoms that one might
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| Fig 8.3 Pseudohyponatraemia |
expect due to the low sodium concentration (see pp. 18–19), e.g. a patient with a sodium concentration of 110 mmol/ L who is completely asymptomatic. The serum osmolality is unaffected by any changes in the fraction of the total plasma volume occupied by proteins or lipids, since they are not dissolved in the water fraction and, therefore, do not make any contribution to the osmolal- ity. A normal serum osmolality in a patient with severe hyponatraemia is, thus, strongly suggestive of pseudohy- ponatraemia. This can be assessed formally by calculating the osmolal gap, the difference between the measured osmolality and the calculated osmolality
Clinical note
Oedema is not just a consequence of secondary hyperaldosteronism. In some situations, the factors that cause the expansion of the ECF compartment (such as inflammation or restricted venous return) are localized.
Hyponatraemia: pathophysiology
- Hyponatraemia because of water retention is the commonest biochemical disturbance encountered in clinical practice. In many patients the non-osmotic regulation of AVP overrides the osmotic regulatory mechanism and this results in water retention, which is a non-specific feature of illness.
- Hyponatraemia may occur in the patient with gastrointestinal or renal fluid losses that have caused sodium depletion. The low sodium concentration in serum occurs because water retention is stimulated by increased AVP secretion.
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