Treatment of Symptomatic Hyponatremia

Treatment of Symptomatic Hyponatremia

• Goal is to achieve a safe serum sodium concentration (120-125 mEq/L) to avoid adverse neurologic outcomes in symptomatic patients.
• Increase serum sodium by 0.75-1 mEq/L/hour to a concentration of 120 mEq/L, but not more than 10-12 mEq/L in 24 hours.
• In severe symptoms, serum sodium can be increased by up to 2 mEq/L/hour for a short time, as long as the maximum change of 10-12 mEq/L in 24 hours is not exceeded.
• Infusion rate of 3% hypertonic saline is generally 1-2 mL/kg/hour for severe symptoms.

Complications of Hypertonic Saline

• Osmotic demyelination syndrome (includes central myelinolysis) can occur with rapid correction of hyponatremia.
• Hypokalemia can occur with large volumes of hypertonic saline.
• Hyperchloremic acidosis can result from the administration of chloride salts.
• Hypernatremia can occur due to fluid overload from initial volume expansion.
• Phlebitis if administered in a peripheral vein.
• Coagulopathy caused by platelet dysfunction.

Correcting Hypokalemia

• Hypokalemia will cause a reduction in serum sodium because Na+ enters cells to account for the reduction in IC K+ to maintain cellular electroneutrality.
• Administration of K+ will help correct hyponatremia.
• Use caution when giving K+ to prevent rapid correction of serum sodium.

Hypernatremia and Hyperosmolar States

• Hyperosmolality with serum sodium greater than 145 mEq/L.
• The osmotic gradient associated with hypernatremia causes water movement out of cells and into the EC space.
• Symptoms are related primarily to the dehydration of brain cells.

Causes of Hypernatremia

• Loss of water because of fever, burns, infection, renal loss (e.g., diabetes insipidus), gastrointestinal (GI) loss.
• Retention of Na+ because of the administration of hypertonic saline or any form of Na+.
• Certain neurologic injuries receive hypertonic saline to target a higher sodium goal.

Prevention of Hypernatremia

• Plasma osmolality is maintained at 275-290 mOsm/kg, despite changes in water and Na+ intake.
• Hypernatremia is prevented first by the release of ADH, causing water reabsorption.
• Hypernatremia is also prevented by thirst.

Symptoms of Hypernatremia

• Lethargy, weakness, and irritability.
• Twitching, seizures, coma, and death if serum sodium is greater than 158 mEq/L.
• Cerebral dehydration can cause cerebral vein rupture with subsequent intracerebral or subarachnoid hemorrhage.

Treatment of Hypernatremia

• Rapid correction of chronic hypernatremia can result in cerebral edema, seizure, permanent neurologic damage, and death.
• Serum sodium should be reduced slowly by no more than 0.5 mEq/L/hour or 12 mEq/L/day.
• Treat hypernatremia by replacing water deficit slowly over several days to prevent overly rapid correction of serum sodium.

Disorders of K+

• Normal plasma potassium concentrations are 3.5-5 mEq/L.
• K+ balance is maintained between the IC and EC compartments by several factors, including β2-adrenergic stimulation and insulin.
• Plasma potassium concentration directly correlates with movement of K+ in and out of cells because of passive shifts based on the concentration gradient across the cell membrane.

Hypokalemia

• Causes of hypokalemia include reduced intake, renal loss, gastrointestinal loss, diuretic-induced depletion, and increased IC shift.
• Muscle weakness or paralysis is caused by changes in neuromuscular conduction; it typically occurs when plasma potassium exceeds 8 mEq/L.

Treatment of Hyperkalemia

• Patients with asymptomatic hyperkalemia can be treated with a cation exchange resin (e.g., sodium polystyrene sulfonate) alone.
• Urgent and immediate treatment is required for patients with severe muscle weakness, ECG changes, or plasma potassium greater than 6.5 mEq/L.
• Calcium gluconate can be administered intravenously to patients with symptomatic hyperkalemia to prevent hyperkalemia-induced arrhythmias, even if patients demonstrate normocalcemia.