HyperNa+ & hyperK+

Dear Goh,

Hypernatremia:

Definition:
- Serum sodium > 145 mEq/L (> 145 mmol/L)

- Increased thirst and water intake is the first defense against hypernatremia.(An intact thirst mechanism usually prevents hypernatremia. Rarely, excessive sodium intake may cause hypernatremia)

- Urine osmolality helps differentiate renal from nonrenal water loss.

Treatment (Type of fluid for replacement):

1) Hypernatremia with hypovolemia

– Severe hypovolemia: give 0.9% saline (osmolality 308 mosm/kg) to restore volume deficit and treat hyperosmolality, followed by 0.45% saline to replace any remaining free water deficit

– Milder hypovolemia: give 0.45% saline and 5% dextrose in water

2) Hypernatremia with euvolemia

– Encourage water drinking or give 5% dextrose and water to cause excretion of excess sodium in urine

– If GFR is decreased, give diuretics to increase urinary sodium excretion; however, diuretics may impair renal concentrating ability, increasing quantity of water that needs to be replaced

3) Hypernatremia with hypervolemia

– Give 5% dextrose in water to reduce hyperosmolality, though this will expand vascular volume

– Administer loop diuretic (eg, furosemide, 0.5–1.0 mg/kg) intravenously to remove excess sodium

– In severe renal injury, consider hemodialysis


Hyperkalemia:

Definition:

- Serum potassium > 5.0 mEq/L ( > 5.0 mmol/L)

- Hyperkalemia may develop in patients taking angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), and potassium-sparing diuretics, or their combination, even with no or only mild kidney dysfunction

- The ECG may show peaked T waves, widened QRS and biphasic QRS–T complexes, or may be normal despite life-threatening hyperkalemia

Causes:

1) Spurious

– Leakage from erythrocytes, marked thrombocytosis or leukocytosis

– Repeated fist clenching during phlebotomy

– Specimen from arm with K+ infusion

2) Decreased excretion

– Kidney disease, acute and chronic

– Renal secretory defects, eg, interstitial nephritis, sickle cell disease

– Hyporeninemic hypoaldosteronism (type IV renal tubular acidosis), eg, diabetic nephropathy, heparin, AIDS; adrenal insufficiency

– Drugs that inhibit K+ excretion (spironolactone, triamterene, eplerenone, ACE inhibitors, trimethoprim, nonsteroidal anti-inflammatory drugs)

3) Potassium shift from within the cell

– Burns, rhabdomyolysis, hemolysis, severe infection, internal bleeding, vigorous exercise

– Metabolic acidosis

– Hypertonicity (solvent drag)

– Insulin deficiency

– Hyperkalemic periodic paralysis

– Drugs: digitalis toxicity, -adrenergic antagonists, succinylcholine, arginine

4) Excessive intake of K+

– Ingestion or iatrogenic

Treatment:
(Treatment consists of withholding exogenous potassium, identifying the cause, reviewing the patient’s medications and dietary potassium intake, and correcting the hyperkalemia.)

1) Intravenous bicarbonate,(50 mEq IV over 5 minutes, raises urinary and blood pH. Onset of action within minutes. Only likely to be efficacious if underlying acidosis present.)

2) Calcium (Calcium chloride or calcium gluconate - these are cardioprotective only & don't lower calcium levels. One ampule of calcium chloride has approximately 3 times more calcium than calcium gluconate. Onset of action is < 5 min. Doses should be titrated with constant monitoring of ECG changes during administration; repeat dose if ECG changes do not normalize within 3-5 min.), and

3) Insulin given together with 50% dextrose may be appropriate. (Insulin temporarily shift K+ into cells; Glucose prevents hypoglycaemia.)

Avoid calcium if digoxin toxicity is suspected. Magnesium sulfate (2 g over 5 min) may be used alternatively in the face of digoxin-toxic cardiac arrhythmias. Check out this table for better understanding.

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