Hyponatremia
                                ============

þ Decide if:

 - hypovolemic:
   diuretics
   mineralocorticoid deficiency
   salt-losing nephropathy (e.g., medullary cystic disease.)
   TREAT WITH NS until euvolemic

 - euvolemic:
   diuretics
   glucocorticoid deficiency
   hypothyroidism (decreased cardiac output)
   pain, psychosis, physiologic stress (surgery, anaesthesia)
   drugs (lots): potentiate ADH effect or cause release
   SIADH: euvolemic, but no obvious cause for increased ADH
      þ CNS disturbances (e.g., trauma causing SIADH then central DI; tumor;
        Gullian Barre)
      þ Lung CA (esp oat cell): paraneoplastic effect from tumor ADH
      þ Non-malignant lung processes: via afferent nervous stimulation

 - hypervolemic:
   nephrosis
   cirrhosis
   CHF ("congestivosis," "cardiosis")

þ Osmotic stimulus for ADH release:  hypertonicity
þ Nonosmotic stimuli for ADH release:  hypoperfusion; must be more than 10% loss
   of volume to see this happen.

þ Central Pontine Myelinolysis (CPM):  from hypertonic saline.

þ in acute hyponatremia, brain water is high, but in chronic, brain water is
  only slightly increased (probably due to intracellular K loss and amino acid
  polymerization).  Hypertonic saline is probably OK in acute symptomatic
  hyponatremia, therefore, but not if chronic and asymptomatic.

þ Rate of correction:  never more than 1 mEq/hr.;
  studies show that at .4 mEq/hr., no CPM; at .6 mEq/hr, some CPM; at 1 mEq and
  above, much more CPM.  If acutely symptomatic, can give Lasix, too.

þ Maximal correction:  don't overcorrect (much more CPM)
                               (per Dr. Nasca, 1991 Sierras Emergency Care Conf)