Hyponatremia

1. Approach to hyponatremia:

a) First must determine the plasma osmolarity to rule of pseudohyponatremia or hyperosmolar hyponatremia (typically due to glucose).

b) Vast majority of cases are a hypoosmolar state, due to water retention in kidneys in response to ADH.

c) Key is to determine why ADH is being released.

 

2. ADH physiology:

a) ADH is released by the posteroir pituitary, and acts on the V2 receptors in the collecting tubule, resulting in fusion of aquaporins with the luminal membrane and absorption of water.

b) The major stimuli to ADH release are increased osmolality and volume depletion.

c) Osmoreceptors in the brain are exquisitely sensitive, and maintain serum osmolality between 280-290 msom/kg.

d) Carotid sinus baroreceptors sense a decrease in effective circulating volume as a decrease in the stretch of the receptors.

d) The ADH response to baroreceptors is less sensitive than that of the osmoreceptors, but once MAP drops, the ADH response is robust.

e) Hyponatremia occurs in hypovolemia because the body prioritizes plasma volume over a normal osmolality.

 

3. States of elevated ADH:

a) ADH release leads to water absorption, and will thus increase urine osmolality.

b) Once it is concluded that ADH is being released, the next step is to assess volume status (orthostatics, JVP).

c) ADH release in response to low effective circulating volume (urine sodium and FENa typically low):

      - Hypovolemia

      - Heart failure: decreased CO --> decreased MAP --> decreased carotid baroreceptor stretch --> ADH release

      - Cirrhosis: decreased SVR --> decreased MAP --> decreased carotid baroreceptor stretch --> ADH release

d) "Inappropriate" ADH release in response to normal effective circulating volume (urine sodium typically elevated)

      - Causes: CNS pathology, paraneoplastic, drugs, pain, lung pathology

e) Hormonal:

      - Hypothyroidism (decreased CO, decreased GFR --> reduced delivery of water to collecting tubule).

      - Adrenal insufficiency (CRH stimulates ADH release)

 

4. States of suppressed ADH:

a) Kidney disease (nephrotic syndrome): kidney unable to dilute urine

b) Primary polydipsia: diluting capacity of kidney overwhelmed

      - Minimum urine concentration if 50 msom/kg

      - Normal diet results in excretion of 500 mosm/day

      - If water intake exceeds 10L, hyponatremia will result

c) Low solute intake:

      - Minimum urine concentration if 50 msom/kg

      - With poor dietary intake, excretion can decrease to 200 mosm/day

      - Water intake above solute excretion/50 (e.g. 4L in above case) results in hyponatremia

 

5. Management of hyponatremia:

a) Key is to determine rapidity of development, as well as presence of neurologic symptoms, as this dictates rate of correction.

b) If pt is symptomatic, there is concern for brain edema, and thus goal is to correct Na by 4-6 meq/L rapidly over 2 hours with hypertonic saline.

c) If pt asymptomatic, rate of correction should be 0.5 meq/L/hr.

d) Choice and rate of fluids:

      - First, determine sodium deficit: TBW x (goal sodium - current sodium)

      - Calculate volume of fluid based on sodium content (NS: 154 meq/L, 3% hypertonic saline: 513 meq/L)

      - Calculate rate based upon how quickly you want goal sodium to be reached

 

6. Complications of treatment of hyponatremia:

a) Feared complication is osmotic demyelination, which results from overly rapid correction.

b) In acute hyponatremia, cerebral edema results, so goal is rapid correction to reduce swelling.

c) In chronic hyponatremia, brain adapts by decreasing the production of osmolytes, thus brain size remains stable --> rapid correction will lead to shrinking of brain size and demyelination.

d) To prevent this, Na should be monitored closely, and if the rate of increase is too rapid, free water or DDAVP given.

 

 

 

• Most commonly Hypotonic (hypo-osmolar); serum osms <285
• Hyperosmolar: hyperglycemia (ie. DKA, this is real hyponatremia, it is just that the Na corrects when you correct the hyperglycemia, as the serum osmolarity normalizes), osmotic diuretics (mannitol)
• Iso-osmolar (pseudohyponatremia): hypertriglyceridemia, hyperparaproteinemia due to lab artifact (not commonly applicable anymore as lab testing is more sophisticated)
• You generally do NOT need to check serum osms (generally it is hypotonic hyponatremia, unless DKA etc.)
• Clinical evaluation:
  • Hypovolemic (diarrhea, vomiting, strenuous exercise)
  • Euvolemic (SIADH, adrenal insuff, hypothyroid) or
  • Hypervolemic (CHF, cirrhosis, nephritic synd).
  • **remember that hypovolemic and hypervolemic hyponatremia are both states of low effective circulating volume

Urine studies:

· urine Osms—high in all 3 (except primary/psychogenic polydipsia), due to increased ADH

· urine Na—low in hyper and hypovolemia (increased aldosterone), but high in SIADH and primary polydipsia (aldosterone is appropriately suppressed). ** diuretics can falsely elevate UNa.

 

Great review of hyponatremia in NEJM: http://content.nejm.org.laneproxy.stanford.edu/cgi/content/full/342/21/1581

 

(Christopher Woo MD, 7/9/10)

(Victoria Kelly MD, 10/12/10)