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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