Hypernatremia

Hypernatremia management

1. Hypernatremia [Na]> 150 mEq /L

2. Extracellular-Fluid and Intracellular-Fluid Compartments under Normal Conditions and during States of Hypernatremia.

3. Effects of Hypernatremia on the Brain and Adaptive Responses.

4. Clinical Signs of Hypernatremic States Related to Serum Osmolality Osmolality ( mOsm /kg) Manifestations 350–375 Restlessness, irritability 375–400 Tremulousness, ataxia 400–430 Hyperreflexia , twitching, spasticity >430 Seizures and death

5. Causes of Hypernatremia * Likely or important ED diagnostic considerations. Inadequate water intake *     Inability to obtain or swallow water    Impaired thirst drive    Increased insensible loss Excessive sodium    Iatrogenic sodium administration      Sodium bicarbonate      Hypertonic saline    Accidental/deliberate ingestion of large quantities of sodium      Substitution of salt for sugar in infant formula or tube feedings      Salt water ingestion or drowning    Mineralocorticoid or glucocorticoid excess *      Primary aldosteronism      Cushing syndrome      Ectopic ACTH production    Peritoneal dialysis      Loss of water in excess of sodium GI loss *      Vomiting, diarrhea, intestinal fistula    Renal loss       Central diabetes insipidus      Impaired renal concentrating ability      Osmotic diuresis (multiple causes) *         Hypercalcemia         Decreased protein intake         Prolonged, excessive water intake         Sickle cell disease         Multiple myeloma         Amyloidosis         Sarcoidosis         Sjögren syndrome         Nephrogenic diabetes insipidus         Congenital    Drugs/medications      Alcohol, lithium, phenytoin, propoxyphene, sulfonylureas, amphotericin, colchicine    Skin loss      Burns, sweating Essential hypernatremia

6. Most hypernatremia encountered in the ED is related to severe volume loss. In otherwise healthy patients, hypovolemia leads to conservation of free water by the kidneys that results in low urine output (<20 mL/h) with high osmolality (usually >1000 mOsm/kg water).

7. Diabetes Insipidus Diabetes insipidus is characterized by the failure of central or peripheral ADH response. Urine osmolality is low (200 to 300 mOsm/kg, with urinary [Na+] of 60 to 100 mEq/kg)

8. Treatment The cornerstone of treatment is volume repletion. Volume should be replaced first with NS or lactated Ringer's solution. Some practitioners inappropriately fear using NS solution from concern that an [Na + ] of 154 mEq/L exceeds normal serum [Na + ]. However, in most hypernatremic states, there is a total body [Na + ] deficit, and the use of NS allows a more gradual decrease in serum [Na + ]. Once perfusion has been established, the solution should be converted to 0.45% saline or another hypotonic solution until the urine output is at least 0.5 mL/kg/h. The reduction in [Na + ] should not exceed 10~15 mEq/L per day.

9. Calculation of Free Water Deficit Replacement Volume = TBW deficit × 1 / (1 － X) X = [Na + ] of resuscitation fluid / [Na + ] of isotonic saline

10. 70 公斤的成人，抽血發現 [Na + ] 160 mEq /L 計算式： TBW deficit = 0.6 ×70× [160/140 － 1]= 6 L 若使用 0.45NaCl 做為輸液 Replacement volume = 6 × 1/ (1 － ½ )=12 L 水分缺損要在 48 小時 補足 點滴速度大約每小時要 250 mL

11. Reference Fluids and Electrolytes, Tintinalli‘s Emergency Medicine 2010: 117-121 Hypernatremia , NEJM 2000; 342:1493-1499 Hyponatremia , NEJM 2000; 342:1581-158 Hypertonic and hypotonic Conditions, The ICU Book 2007: 595-602