The development of acute hyponatraemia can have profound neurological consequences. After creation of an osmotic gradient between the intravascular compartment and the intracellular compartment, water must somehow gain access to the brain tissue. This appears to be mediated, at least partially, by aquaporin 4, based on evidence from mouse knockout models. Those mice deficient in AQP4 had significantly less brain oedema compared to wild-type animals after the induction of acute hyponatraemia.
In very acute situations the brain does not have enough time to implement its adaptive response mechanisms (which involve loss of intracellular solutes and osmolytes), and so acute cellular oedema can occur. It is in this situation that acute neurological sequelae are more common.
What if a patient presents to the ED post-generalized seizure, and the labs come back with a serum sodium of 130mmol/L? Could this seizure be ascribed to hyponatraemia? It actually could - one potential explanation is that the patient may have a pre-existing brain lesion that is more susceptible to osmotic changes. The second potential mechanism lies with the downstream effects of the seizure itself. Following the seizure, skeletal muscle cells can take on substantial amounts of water. This in turn may result in a ‘rise’ in the serum sodium concentration, by up to 10-15mmol/L in some estimates (from one of Dr M. Halperin’s acid-base textbooks). Definitely something to keep in mind.
2 comments:
The explanation that I remember for the muscle uptake of water (causing acute elevation of Na) is that during seizure there is massive, sudden conversion of ATP to ADP and inorganic phosphate, the latter causing sudden increase in osmolarity and water shift into the muscle. However I do not recall a reference for it and would be interested in hearing of the reference or of any other possible mechanisms for this phenomenon.
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