Low plasma bicarbonate level in hyponatremia related to adrenocorticotropin deficiency.

Patients with hyponatremia related to adrenocorticotropic deficiency are not easily distinguished by routine laboratory studies from patients with nonendocrine inappropriate secretion of antidiuretic hormone (SIADH). We wanted to investigate whether, in the routine biological analysis of such patients, some parameters could help to better identify this subgroup of hyponatremic patients. The biochemical profiles of 13 consecutive patients with hyponatremia related to ACTH deficiency were analyzed and compared with 30 consecutive patients with classical SIADH.

Azotemia (48 h) decreases the risk of brain damage in rats after correction of chronic hyponatremia.

Brain myelinolysis complicates excessive correction of chronic hyponatremia in man. Myelinolysis appear in rats for correction levels deltaSNa) > 20 mEq/l/24 h. We previously showed in rats that when chronic hyponatremia was corrected with urea, the incidence and the severity of brain lesions were significantly reduced compared to hypertonic saline.

Lack of major hypoxia and significant brain damage in rats despite dramatic hyponatremic encephalopathy.

Brain myelinolysis could complicate the excessive correction of chronic hyponatremia. Recently it was suggested that hypoxia rather than correction of hyponatremia would be responsible for myelinolysis. We analyzed the incidence and the severity of potentially associated hypoxia and its consequences on survival and on the development of brain damage in rats in which major hyponatremic encephalopathy had developed after either pure acute hyponatremia (serum sodium concentration: -40 mEq/L/3 hr, group I, n = 8) or acute hyponatremia (serum sodium concentration: -30 mEq/L/3 hr, group II, n = 12) superimposed on chronic hyponatremia of 3 days' duration (serum sodium concentration: 113 mEq/L).

Reinduction of hyponatremia improves survival in rats with myelinolysis-related neurologic symptoms.

Brain myelinolysis occurs after excessive correction (delta SNa > 20 mEq/1/24 hours) of chronic hyponatremia. However, we showed recently that the mechanisms leading to brain myelinolysis remain reversible. Indeed, reinduction of the hyponatremia by water administration despite 12 hours of sustained excessive correction could prevent the development of demyelination in rats still asymptomatic at that time.

Brain myelinolysis following hypernatremia in rats.

Brain myelinolysis could develop after excessive correction (delta SNa > 20-25 mEq/1/24 hour [h]) of chronic hyponatremia; however, this neurological event is not recognized as a complication of hypernatremia when arising from a normonatremic baseline. Previous animal studies were unable to reproduce these brain lesions in hypernatremia after acute increase of serum sodium to moderately hypernatremic levels. We hypothesize that to produce brain dehydration and myelinolysis from normonatremic baseline requires a more important osmotic gradient than when starting from hyponatremic state.