The NDT paper on clinical practice guidelines suggests some
interesting changes in diagnosis and treatment in hyponatremia. In the series of posts , we shall highlight
the major findings of their report.
Pathophysiology update:
1.
Once the hyponatremia has been deemed hypotonic
– the first test recommended is urine osmolarity and the break down after that
is interesting. If urine
osm<100Mosm/kg, primary polydipsia and water intoxication is considered a
likely potential. If urine osm>100,
we go into our usual categories and then order a urine Na. If urine Na <30, low effective arterial
volume is deemed and volume exam will determine next cause( from volume loss to
CHF). If urine Na>30, one either has
kidney disease or diuretic use and or if ECF is reduced could be renal salt
wasting or cerebral salt wasting. But if normal ECF- then SIAD.
2.
A nice table on page 21 discusses the much
debated SIADH vs cerebral salt wasting.
While uric acid in the serum is same in both, it’s the BUN that is
usually low in SIADH. Urine volume is
much higher in cerebral salt wasting.
And patients are usually orthostatic in the later. CVP is also low in
the later.
For full details click here
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