TOC  |  Lytes  


A. With depleted extracellular fluid (ECF) volume

  1. Renal losses: a. Diuretics. b. Adrenal insufficiency. c. Salt losing nephropathy. d. Renal tubular acidosis with bicarbonaturia (proximal type)  e. Osmotic diuresis (glucose, mannitol, urea)
  2. Extra renal losses: a. Vomiting or diarrhea.   b. "3rd" spacing: burns, pancreatitis, traumatized muscle, etc.

B. With normal or slilght excess ECF volume

  1. Hypothyroidism
  2. Pain, emotion, drugs
  3. Glucocorticoid deficiency
  4. Syndrome of Inappropriate ADH Screation (SIADH)

C. Profound excess ECF volume (edema)

D. Artifactual

  1. Laboratory error.
  2. Hyperglycemia - the correction factor of 2.4 meq/L decrease in [Na] per 100 mg/cL increase in [glucose] is a better overall estimate of this association than the usual correction factor of 1.6.    (Am J Med April 1999;106:399 - Teresa Hillier, etc.)
  3. Hypertriglyceridemia, hyperproteinemia                                                     

Correct the underlying cause if possible.
Reduce free water intake in normal or modest excess ECF pts.
Demeclocycline 600-1,200 mg/d if needed.
Hypertonic 3-5% saline at a rate sufficient to raise the serum Na concentration by 2 meq/l/hr for a final concentration of 125-130 meq/l in symptomatic or markedly hyponatremic pts.

Conivaptan (Vaprisol)
Loading dose 20 mg IV over 30 min, then continuous infusion 20 mg over 24 hours for 1-4 days. Titrate to desired serum sodium.  Max dose 40 mg/day as continuous infusion.
- for euvolemic or hypervolemic hyponatremia.  (8-2007)

Chronic Hyponatremic Encephalopathy in Postmenopausal Women
JAMA June 23, 1999;281:2299 - J.Carlos Ayus, Allen I. Arieff
Chronic symptomatic hyponatremia in postmenopausal women can be associated with major morbidity and mortality. Therapy with IV sodium chloride was associated with significantly better outcomes than fluid restriction.

Editorial: -James P. Knochel, MD
There has been an ongoing controversy regarding the treatment of chronic hyponatremia. The initial reports suggesting that overzealous treatment of hyponatremia with hypertonic saline may cause central pontine myelinolysis or osmotic demyelination in the brain provoked a voluminous literature that continues to be just as lively now as it was at the time the first reports were published.   Today, most clinicians who deal with electrolyte disorders appear to agree that acute symptomatic hyponatremia, or more precisely, acute water intoxication, imposes the risk of cerebral edema, uncal herniation, and death. In these patients, when hyponatremia is of recent onset, immediate administration of hypertonic saline in a quantity calculated to increase serum sodium levels by approximately 10 mmol/L may be lifesaving. However, total correction or overcorrection may result in irreversible damage to the brain.