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). Our study revealed the following: (1) Despite dramatic hyponatremic encephalopathy (convulsions, coma), hypoxia (PO2 < 70 mm Hg) was present, but the PO2 was not decreased below 40 mm Hg. All of these rats died rapidly if they remained hyponatremic. (2) In the animals rescued by NaCl, the incidence of brain myelinolysis was low (10%), whatever the duration (pure acute or chronic plus acute) of the hyponatremia and despite the combination of hypoxia with major hyponatremic encephalopathy. (3) When acute hyponatremia is superimposed on a chronic preexisting hyponatremic state, the acute component of serum sodium concentration decrease could be rapidly corrected (serum sodium concentration: +35 mEq/L/21 hr) without fear of permanent brain damage. Our results suggest that even in the presence of dramatic hyponatremic encephalopathy and associated hypoxia, neuropathologic sequelae are uncommon. Brain lesions related to post-anoxic encephalopathy probably develop only after respiratory arrest occurs.