Hyponatremia is one of the most frequently encountered electrolyte abnormalities in clinical practice and is associated with significant morbidity and mortality. Among its various forms, hyperglycaemia-induced hyponatremia represents a unique and often reversible subtype characterized by a reduction in measured serum sodium concentration in the presence of elevated plasma glucose levels. This phenomenon is primarily driven by osmotic shifts of water from the intracellular to the extracellular compartment, resulting in dilutional hyponatremia rather than a true deficit of total body sodium. Hyperglycaemia itself is a frequently observed biochemical abnormality and may be detected incidentally during routine laboratory testing in asymptomatic individuals. It can also occur in situations that place increased demand on pancreatic β-cells, such as pregnancy, severe illness, or treatment with medications like corticosteroids, a condition commonly referred to as stress hyperglycaemia. In some cases, however, patients present with acute metabolic emergencies caused by uncontrolled hyperglycaemia, including diabetic ketoacidosis, which requires prompt medical intervention. Understanding the relationship between hyperglycaemia and hyponatremia is clinically important, as the reduction in serum sodium in these cases primarily reflects osmotic fluid shifts rather than actual sodium depletion. Consequently, management should focus on correcting the underlying hyperglycaemia, which typically leads to normalization of serum sodium levels. Recognizing this mechanism helps clinicians avoid unnecessary sodium replacement and guides appropriate treatment strategies for patients with diabetes presenting with electrolyte abnormalities.
Asharaf et al. (Thu,) studied this question.