Diagnosis and management of hyponatraemia in hospitalised patients

Abstract

Hyponatraemia is a commonly encountered electrolyte abnormality in hospitalised patients and is associated with significant morbidity and mortality. The fact that most cases of hyponatraemia are the result of water imbalance rather than sodium imbalance underscores the role of antidiuretic hormone (ADH) in the pathophysiology. Hyponatraemia can be classified according to the measured plasma osmolality as isotonic, hypertonic or hypotonic. Hyponatraemia with a normal plasma osmolality usually indicates pseudohyponatraemia, while hyponatraemia because of a high plasma osmolality is typically caused by hyperglycaemia. After excluding isotonic and hypertonic causes, hypotonic hyponatraemia is further classified according to the volume status of the patient as hypovolaemic, hypervolaemic or euvolaemic. Hypovolaemic hyponatraemia is accompanied by extracellular fluid (ECF) volume deficit, while hypervolaemic hyponatraemia manifests with ECF volume expansion. The syndrome of inappropriate ADH (SIADH) should be suspected in any patient with euvolaemic hyponatraemia with a urine osmolality above 100 mOsm/kg and urine sodium concentration above 40 mEq/l. In the management of any hyponatraemia regardless of the patient's volume status, it is advised to restrict free water and hypotonic fluid intake. Hypertonic saline and vasopressin antagonists can be used to correct symptomatic hyponatraemia. The rate of correction is dependent upon the duration, degree of hyponatraemia and the presence or absence of symptoms. Symptomatic acute hyponatraemia (< 48 h) is a medical emergency requiring rapid correction to prevent the worsening of brain oedema. In asymptomatic patients with chronic hyponatraemia (> 48 h or unknown duration), fluid restriction and close monitoring alone are sufficient, while a slow correction by 0.5 mEq/l/h may be attempted in symptomatic patients. Excessive rapid correction should be avoided in both acute and chronic hyponatraemia, because it can lead to irreversible neurological complications including central osmotic demyelination.