ABSTRACT
Clinical presentation The cells of the CNS are very intolerant of the volume changes described above and this leads to clinical signs including obtundation, head pressing, seizures, ataxia, tremors, blindness and coma. In addition, signs of volume depletion are often present in hypernatraemia secondary to hypotonic fluid losses, while signs of hypervolaemia (e.g. pulmonary oedema) may be present in cases of net solute gain. Clinical signs typically develop if the sodium concentration alters at a rate of >1 mmol/l/ hour (>1 mEq/l/hour) or if the absolute sodium concentration exceeds 180 mmol/l (180 mEq/l). If sodium concentrations alter slowly, the brain adapts by producing idiogenic osmoles such as taurine, sorbitol and inositol. These molecules increase intracellular osmolality, buffering cell volume against the increased extracellular sodium concentration. Rapid correction of chronic hypernatraemia (>0.5-1 mmol/l/hour [>0.5-1 mEq/l/ hour]) can lead to osmotic gradient reversal, inducing water to move into cells and causing cell swelling, cerebral oedema and clinical signs of intracranial hypertension.
