Cerebral hyponatremia: salt wasting syndrome vs SIADH

The story of neurological hyponatremia is probably as interesting as the management is complicated. While early reports (where side effects of therapy cannot have played a role) clearly depicted salt wasting, the discovery of SIADH left the salt wasting syndrome forgotten until rediscovered in the 80ies, not the least by Wijdicks, who then saw it everywhere.

Start out with any patient on your neurocritical ward, say a subarachnoid hemorrhage patient, who develops hyponatremia. Before you think, grab all data you can get, such as

  • history (fluid balance, speed of development, drugs, …)
  • examination (hypovolemia vs. eu- or hypervolemia)
  • osmolality, Na, K, Cl, uric acid, urea/BUN, creatinine, TSH, (cortisol level if in doubt)
  • urine osmo, Na, K, Cl, uric acid, urea/BUN, creatinine

Then open your favorite textbook, review article or any proper neurocritical care reference (such as those below) to arrive at a categorical diagnosis. Most of the time, it will be diuretic-induced, but in your Neuro patient it could also be neurological hyponatremia, meaning

  • we don’t know where it comes from,
  • it has to do with the patient’s disease (rather than our treatment) and
  • it looks like SIADH, but could also be CSWS.

The problem is that both diagnoses might be unstable over time (what looks like SIADH today, can waste salt tomorrow) and that the volume status is the arbiter between them, while clinical assessment of volume status is difficult at best – we all know how bad CVP is for deciding the volume status and all other physical signs fare even worse. And how do you judge the volume status of your septic right heart failed hypalbuminic swollen post-SAH patient?

In these difficult cases  I recommend  to just give some saline, say 500-1000 cc. Then give the patient some time (say 1 hour) and remeasure sodium – if it is not worse, your strategy was fine. Otherwise try the management of SIADH (which includes vaptans nowadays). By the way – fludrocortisone can be helpful in either case.

Of course, you have to remember the 0,5 mmol/h maximum rule – if Na rises more quickly, counter that with D5.

With this strategy I am not as tough as Sterns his in his block-diuresis-and-fill-up-the-sodium-slowly approach, as recently studied in this series (which has not been tried in Neuro patients).

References