-Send serum osmolality!
-determine fluid status: hypo-, eu-, or hypervolemic
-if asymptomatic, fluid restriction. Don’t give fluids!
-max rate of correction = 8 mEq/h
-Goal: <10-12 mEq total increase in 24h
Hypovolemic hyponatremia mechanism = decreased arterial perfusion of kidneys -> ADH secretion -> reabsorption of free water
–fix the underlying problem: volume replete
Hypervolemic hyponatremia (CHF, cirrhosis) mechanism = depleted intravascular volume despite excess extravascular volume = decreased effective arterial perfusion of kidneys -> ADH secretion -> reabsorption of free water
-SIADH – inappropriate excess ADH secretion
-psychogenic (excess free water intake), beer potomonia + “tea and toast syndrome” (inadequate solute intake)
-bolus NS if shock/hypoperfusion
-replace total body water (TBW) deficit
1. Treat Neurologic Emergencies Related to Hyponatremia
In the event of a seizure, coma or suspected cerebral herniation as a result of hyponatremia, IV 3% hypertonic saline should be administered as soon as possible according to the following guide:
- Administer 3% hypertonic saline 100-150cc IV over 5-10min
- If the patient does not improve clinically after the first bolus, repeat a second bolus of hypertonic saline.
- Stop all fluids after the second bolus of hypertonic saline to avoid raising the serum sodium any further
What if hypertonic saline is not readily available? –> Administer one ampule of Sodium Bicarbonate IV over 5min.
Ringer’s lactate has a sodium concentration of 128mmol/L which will be more isotonic to the hyponatremic patient. Although never shown in clinical studies, administering Ringer’s lactate will likely result is a slower rise in serum serum sodium than Normal Saline, and therefore have a lower risk of potentiating osmotic demyelination syndrome. Ringer’s lactate is therefore recommended by our experts as the fluid of choice for resuscitation of the hypovolemic/hyponatremic patient.
Practical Approach to the Differential Diagnosis of Hyponatremia
- Look at chief complaint: look for conditions which can increase output or decrease intake such as vomiting and diarrhea, pain or altered level of awareness
- Review Medication List: look for those that cause SIADH, especially thiazide diuretics and SSRIs; patients who have been on chronic steroids may have adrenal insufficiency
- Evaluate PMHx: Look for history of end organ failure (CHF, liver failure and renal failure) or cancers (a cause of SIADH)
- Lab work: glucose (hyperglycemia), potassium (hyperkalemia may suggest adrenal insufficiency), TSH (hypothyroidism)
Note: if by history the hyponatremia is acute, it is safe to correct it quickly. The patients who are at risk of central pontine demyelinolysis are those whose hyponatremia is chronic.
Other lytes concepts:
-replete low ionized Ca after PRBC transfusions (contains citrate)
-alkylosis (ex: primary hyperventilation) causes more Ca from its ionized state to be bound to albumin (may develop signs of hypoCa)
-severe hypocalcemia -> cardiovascular collapse (loss of contractility/inotropy)
-hypocalcemia -> QTc prolongation -> torsades
-CaCl2 = 3x more ions than Ca-gluconate
-beware of further increasing serum bicarb for a pt that is hypoventilating (ex CHF exacerbation) – will worsen compensatory respiratory acidosis (hypercarbia). This is why MICU gives acetazolamide to CHF pts on BIPAP
-Dialysis dysequilibrium syndrome (dizziness during dialysis) – due to the rather rapid removal of BUN, which has an osmotic effect
—–serum osmolality = 2x(Na) + glucose/18 + BUN/2.8
0.9% NS = 154 mEq Na
0.45% NS = 77 mEq
plasmalyte = 140 mEq
LR = 128 mEq
D5W = 0 mEq
3% hypertonic saline = 513 mEq (3 / 0.9 = 3.33 x 154mEq)