Pseudohyponatremia

Measured osmolality is the discriminator - Send a measured serum osmolality alongside the sodium and compare it to the calculated value. Normal osmolality (280 to 300 mOsm/kg) with a low reported sodium is pseudohyponatremia; below 280 mOsm/kg the hyponatremia is real and needs a real workup. A wide gap between measured and calculated osmolality means a confounder is present.

Hyperosmolar hyponatremia is a different animal - A sodium that is low because of hyperglycemia, mannitol, radiographic contrast, or glycine irrigant is truly low: the osmotically active solute has pulled water out of cells. An osmolality above 295 mOsm/kg points here, not to a lab artifact, and that sodium will move as you treat the solute. Do not file it under pseudohyponatremia.

The harm is in treating the number - Hypertonic saline or fluid restriction aimed at a sodium that was never low drives a genuine hypernatremia, with muscle twitching, lethargy, seizures, and death at the extreme. If the osmolality is normal, the sodium does not need correcting.

Overcorrection is the other hazard - Where a true chronic hyponatremia does coexist, correcting it too fast risks central pontine myelinolysis. Most sources hold correction to no more than 10 mEq/L in 24 hours, or about 1 mEq/L every 2 hours, with frequent serum sodium checks.

Look at the tube - A grossly lipemic, hyperviscous, or discolored sample points at severe hypertriglyceridemia. Some cholesterol fractions are soluble in blood and change neither viscosity nor color, so a normal-looking sample does not rule it out.

Who to suspect it in - Hyperlipidemia, plasma cell dyscrasias including monoclonal gammopathy, multiple myeloma, and amyloidosis, malignancy, cryoglobulinemia, chronic hepatitis C, HIV, and any patient receiving exogenous immunoglobulin. Prevalence is unclear, but it clusters in patients who already carry one of these on the problem list.

Confirm with direct ion-selective electrode when it changes the plan - Direct ISE potentiometry does not dilute the sample and reports the true sodium. Most cases do not need it. Reserve it for when the diagnosis is genuinely uncertain, when several confounders coexist, or when confirmation would materially change management.

Exclude true hyponatremia before you accept the artifact - Fatigue, muscle cramps, altered mentation, headache, and seizure are symptoms of real hyponatremia and should be absent. A documented artifact does not exclude a coexisting sodium disorder that the lab error is masking; a patient can have both.

Reconcile the medication list - Diuretics, SSRIs, carbamazepine, and desmopressin all disturb sodium homeostasis. A full medication reconciliation belongs in the same visit as the osmolality, so a drug cause is not mistaken for a lab artifact.

Perioperative posture - Pseudohyponatremia by itself is not associated with increased morbidity or mortality and is not a reason to delay a case. What drives the anesthetic is the disorder that produced the artifact - myeloma with its renal impairment and fracture risk, or the chronic infection behind the paraproteinemia - plus confirming the sodium is genuinely normal before anyone reaches for hypertonic saline.

Pseudohyponatremia is a laboratory artifact, not a sodium problem: a reported serum sodium below 135 mEq/L with a normal serum osmolality of 280 to 300 mOsm/kg. Plasma is roughly 93% water and 7% solute, and sodium is dissolved almost entirely in the water phase. Indirect ion-selective electrode and flame photometry methods dilute the sample and apply a fixed correction factor of 0.93 for that ratio.

When severe hypertriglyceridemia or a heavy protein load displaces plasma water, the solid-to-water ratio shifts unpredictably and the reported sodium falls, while the sodium the patient's cells actually see is normal. True hyponatremia carries a low serum osmolality below 280 mOsm/kg; a normal osmolality is the tell.