Thanks to Joe for presenting the case of a young man with no known medical history who presented with acute onset of generalized weakness, found to have symptomatic hyponatremia to 120 resulting from psychogenic polydipsia!

Clinical Pearls

• Hyponatremia is largely a problem of too much free water (sometimes compounded by too little solute) and defined as a Na <135
• Pick a systematic approach to solving the underlying diagnosis for any patient with hyponatremia (see below for one possible outline).
• The term “pseudohyponatremia” refers to the presence of substances that interfere with laboratory measurement of sodium concentration in the blood, specifically high triglycerides and paraproteins.
  • Hyperglycemia does NOT fall into this category because glucose is osmotically active and pulls water into the intravascular space, resulting in a dilutional and true hyponatremia.
• Chronic hyponatremia (>72 hours) must be corrected slowly to avoid osmotic demyelinating syndrome (ODS).  Acute hyponatremia (<48 hours) can be corrected more rapidly.  That said, we rarely have a Na value within 48 hours prior to patient presentation to determine acuity.  As a result, and given the neurologic risks, most patients are treated as if they have chronic hyponatremia.
• ADH leads to increased uric acid excretion through the kidneys so low serum uric acid levels have been associated with SIADH.  But this test is not very specific.
• Osmolarity of normal saline is 308 compared to human serum which is normally 280-295.  In a hyponatremic patient, NS infusion becomes a relatively hypertonic (rather than isotonic) solution!

For more detailed information, refer to this prior post and this review article.