Episode 57: Hyponatremia with Paul Adams Critical Care Scenarios

We tackle the knotty dilemma of diagnosing and treating hyponatremia, with Dr. Paul Adams, a dual-trained nephrologist and intensivist at the University of Kentucky.







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Takeaway lessons









* Start by asking whether the hyponatremia needs to be corrected emergently, as well as its cause. Instability means correct it emergently, and instability usually manifests as seizure.







* While hyponatremia is often categorized by volume status, volume status is a tricky determination with ample gray area and room for overlap. It’s more useful to approach hyponatremia by asking whether ADH is active or not.







* If urine osm is >300, ADH is definitely present to some extent.







* The hypovolemic and/or low solute patient will be fixed with crystalloid, although they are at risk of overcorrection. Overcorrection almost always occurs due to autodiuresis, not from exogenously administered salt.







* A high urine sodium implies lack of sodium reabsorption by the kidneys, more consistent with diuresis (thiazides) or ATN (failure of absorptive mechanisms). Low urine sodium is a broader differential, e.g. most of the appropriate-ADH hyponatremias.







* While there is overlap between hypovolemia (often acute) and low solute intake (often more subacute/chronic), they are distinct syndromes. They can be differentiated by the urine osm: both urine sodiums will be low, but urine osm will be low only in the low solute patient (because they simply aren’t taking osms in). The hypovolemic is at greater risk of overcorrection as well.







* It’s often impossible to determine how acute hyponatremia is, so generally assume chronic and correct slowly.







* Overcorrection from acute hypovolemia will be mediated by dilute polyuria, so a good monitoring strategy may be to simply send serial urine osms, particularly if polyuria occurs. Have a low threshold to clamp them with DDAVP if it occurs.







* When risk for osmotic demyelination is highest (risks: longer duration of hyponatremia, low solute intakes like malnourishment and alcoholism, and lower sodium), consider prophylactically clamping with DDAVP.







* Use small boluses (100 ml) over about ten minutes to correct hyponatremia-induced seizures and repeat as needed until seizures stop. Trend labs but don’t stop until symptoms resolve, or you correct by 5 mEq. Most cases of true hyponatremia-induced seizure or severe encephalopathy will require around 500 ml total. Other concentrations could probably be used but are subject to logistical issues and are really just manipulating the amount of diluent volume.







* Theoretically, inducing hyponatremia in neurologic patients could create the same risk as rapidly correcting hyponatremia, but data is limited and from a bedside perspective, this doesn’t generally seem to cause demyelination.







* For SIADH, a loop diuretic can be useful, but the mainstay is fluid restriction. The right amount of restriction depends on free water clearance; a cirrhotic who only produces 500 ml of free water a day should theoretically be restricted below this intake (which is not easy).







* Vaptans have a limited role outside specific use-cases like bridging to transplant (although not for liver – they may cause hepatotoxicity).







* Confusing pictures (eg SIADH vs hypovolemia vs CSW) can be clarified by a sodium challenge – bolus a liter of normal saline and se...