Electrolyte Imbalances
Physical examination: 1. anorexia 2. nausea and vomiting 3. constipation 4. fatigue 5. diminished reflexes 6. lethargy 7. Decreased level of consciousness 8. Confusion 9. Personality change 10. Cardiac dysrhythmias 11. Possible flank pain from renal calculi 12. Hypercalcemia caused by shift of calcium from bone: pathological fractures 13. Signs of digoxin toxicity at normal digoxin levels
Hypercalcemia
High serum potassium level
Hyperkalemia
Laboratory findings: 1. Serum K+ level greater than 5 mmol/L 2. Possible ECG abnormalities
Hyperkalemia
Physical examination: 1. Bilateral muscle weakness in quadriceps 2. Transient abdominal cramps and diarrhea 3. Cardiac dysrhythmias 4. Cardiac arrest
Hyperkalemia
High serum magnesium level
Hypermagnesemia
Laboratory findings: 1. Serum Mg2+ level greater than 1.25 mmol/L 2. Possible ECG abnormalities
Hypermagnesemia
Physical examination: 1. Lethargy 2. Hypoactive deep tendon flexes 3. Bradycardia 4. Hypotension 5. Acute elevation in magnesium levels: flushing, sensation of warmth 6. Severe hypermagnesemia: flaccid muscle paralysis 7. Decreased rate and depth of respirations 8. Cardiac dysrhythmias 9. Cardiac arrest
Hypermagnesemia
Laboratory findings: 1. Total serum Calcium less than 2.1 mmol/L 2. Ionized Calcium level less than 1.1 mmol/L 3. Possible ECG abnormalities
Hypocalcemia
Low serum calcium level
Hypocalcemia
Physical examination: 1. Positive Chvostek's sign (contraction of facial muscles when facial nerve is tapped) 2. Positive Trousseau's sign (carpal spasm with hypoxia), 3. Numbness and tingling of fingers and circumoral (around mouth) region 4. Hyperactive reflexes 5. Muscle twitching and cramping 6. Tetany 6. Seizures 7. Laryngospasm 8. Cardiac dysrhythmias
Hypocalcemia
Laboratory findings: 1. Serum K+ level less than 3.5 mmol/L 2. Possible ECG abnormalities
Hypokalemia
Low serum potassium (K+) level
Hypokalemia
Physical examination: 1. Bilateral muscle weakness that begins in the quadriceps and may ascend to respiratory muscles 2. Abdominal distention 3. Decreased bowel sounds 4. Constipation 5. Cardiac dys rhythmias 6. Signs of digoxin toxicity at normal digoxin levels
Hypokalemia
Laboratory findings: Serum Mg2+ level less than 0.75 mmol/L
Hypomagnesemia
Low serum magnesium level
Hypomagnesemia
Physical examination: 1. Positive Chvostek's and Trousseau's signs 2. Hyperactive deep tendon reflexes 3. Insomnia 4. Muscle cramps and tetany 5. Seizures 6. Cardiac dysrhythmias 7. Signs of digoxin toxicity at normal digoxin levels
Hypomagnesemia
Milk-alkali syndrome
Increased calcium intake and absorption (hypercalcemia)
1. Steatorrhea 2. Chronic diarrhea
Increased calcium output (hypocalcemia)
High serum calcium level
Hypercalcemia
Adrenal insufficiency
Decreased K+ & Mg 2+ output (hyperkalemia, hypermagnesemia)
Excessive use of potassium-free IV solutions
Decreased K+ intake and absorption (hypokalemia)
Acute or chronic oliguria (e.g. ECV deficit, end-stage renal disease)
Decreased K+ output (hyperkalemia)
Adrenal insufficiency
Decreased K+ output (hyperkalemia)
Use of potassium-sparing diuretics
Decreased K+ output (hyperkalemia)
1. Malnutrition 2. Chronic alcoholism 3. Chronic diarrhea, laxative misuse 4. Steatorrhea (e.g. pancreatitis)
Decreased Mg2+ intake and absorption (hypomagnesemia)
1. Calcium-deficient diet 2. Vitamin D deficiency (includes end-stage renal disease) 3. Chronic diarrhea, laxative misuse 4. Steatorrhea (e.g. pancreatitis)
Decreased calcium intake and absorption (hypocalcemia)
Use of thiazide diuretics
Decreased calcium output (hypercalcemia)
1. End-stage renal disease 2. Adrenal insufficiency
Decreased magnesium output (hypermagnesemia)
Laboratory findings: 1. Total serum calcium greater than 2.6 mmol/L 2. Serum ionized calcium greater than 1.3 mmol/L 3. Possible ECG abnormalities
Hypercalcemia
Aldosterone excess
Increased K+ & Mg2+ output (hypokalemia & hypomagnesemia)
Excessive ingestion of K+ salt substitutes
Increased K+ intake and absorption (hyperkalemia)
Iatrogenic administration of large amounts of IV potassium
Increased K+ intake and absorption (hyperkalemia)
Rapid infusion of stored blood
Increased K+ intake and absorption (hyperkalemia)
Acute or chronic diarrhea, vomiting, or other GI losses
Increased K+ output (hypokalemia)
Glucocorticoid therapy
Increased K+ output (hypokalemia)
Polyuria
Increased K+ output (hypokalemia)
Use of potassium-wasting diuretics
Increased K+ output (hypokalemia)
1. Excessive use of magnesium-containing laxatives and antacids 2. Parenteral overload of magnesium
Increased Mg2+ intake and absorption (hypermagnesemia)
1. Aldosterone excess 2. Use of thiazide or loop diuretics 3. Steatorrhea, chronic diarrhea or other GI losses
Increased Mg2+ output (hypomagnesemia)
1. Prolonged immobilization 2. Hyperparathyroidism 3. Bone tumors 4. Nonosseous cancers that secrete bone-resorbing factors
Shift if calcium from bone into ECF (hypercalcemia)
Rapid administration of citrated blood
Shift of Mg2+ into inactive form (hypomagnesemia)
1. Hypoparathyroidism 2. Rapid administration of citrated blood 3. Hypoalbuminemia 4. Alkalosis 5. Hyperphosphatemia (includes end-stage renal disease)
Shift of calcium from ECF into bone or inactive form (hypocalcemia)