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Diagnosis and treatment of hyponatraemia

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Hyponatraemia is the most common electrolyte abnormality encountered by physicians in the hospital setting. It is associated with increased mortality and length of hospital stay. However, the basis of the relationship of hyponatraemia with clinical outcome is not clear. Doubt remains as to whether the relationship is causal. It may reflect the association of two independent variables both of which are linked with disease severity.

Serum sodium concentration is regulated through integrated neuro-humeral mechanisms that overlap with those regulating circulating volume. A mechanistic approach to the classification of hyponatraemia can support a framework for investigation and differential diagnosis based on urine osmolality and urine sodium concentration. Such a framework is more reliable than those based on the clinical assessment of volume status.

In the emergency setting, the initial management of hyponatraemia is cause-independent. In other clinical contexts, a cause-specific approach is recommended. Over-rapid correction of serum sodium risks precipitating osmotic demyelination syndrome. Avoiding over-rapid correction is critical in any approach to patient care.

Sodium is the major circulating cation and thus a key determinant of overall plasma osmolality. Serum sodium concentration is maintained within a tight physiological range over time, despite wide variation in both sodium and water intake. Hyponatraemia (serum sodium concentration <135 mmols/L) is the most common electrolyte disturbance in clinical practice. All clinicians should be aware of the scope and scale of the problem.

Section snippets

Epidemiology

Hyponatraemia is a clinical feature in 15–42% of non-selected emergency admissions to secondary care. Importantly, it is associated with increased length of hospital stay and morbidity in patients presenting with a range of conditions [1]. Moreover, it has prognostic significance. Hyponatraemia is a predictive indicator of outcome in malignancy and an independent predictor of all-cause in-patient mortality [2], [3]. However, the relationship between serum sodium concentration and clinical

Presentation of hyponatraemia: the clinical picture

The symptoms and signs of hyponatraemia cover a broad range from coma and seizures, to normal or near-normal function [10] (Table 1). Of course it is common for hyponatraemia to be only one feature of the overall clinical presentation, which is often dominated by the major underlying precipitant (e.g. sepsis, intra-cranial haemorrhage). Given this context, the symptoms and signs attributable to the electrolyte disturbance may be either not apparent, or non-specific. This has practical

The physiology of body water homeostasis

Serum sodium concentration reflects both sodium and water content of the aqueous phase of the circulation. Sodium balance, water balance and circulating volume are regulated in parallel through integrated neurohumoral processes that have key roles in the development and maintenance of hyponatraemia.

Sodium balance is regulated chiefly though the Renin-Angiotensin-Aldosterone system (RAS), natriuretic peptides and sympathetic nervous system working to modify renal sodium loss. Activation of the

Investigation and differential diagnosis of hyponatraemia

Identifying the mechanism(s) underlying presentation with hyponatraemia can be challenging. Several factors contribute to this challenge. Multiple comorbidities are common in patients presenting with hyponatraemia; and concurrent medication is a common confounder. As a consequence, hyponatraemia is often multifactorial. Moreover the clinical situation may be dynamic; and key supportive information may not be available when it's needed most.

As effective circulating volume status is a key driver

Treatment of hyponatraemia

Hyponatraemia can be life threatening. However, because of the capacity of the CNS to adapt to osmolar stress, long standing hyponatraemia can be tolerated very well, even when it is profound. Indeed correction of hyponatraemia to which the brain has adapted can produce significant changes in volume of neurones and supporting cells, triggering osmotic demyelination syndrome (ODS). This is a rare but life-threatening complication of over-rapid correction of hyponatraemia. The treatment of

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