How should I evaluate and treat electrolyte disturbances including hyponatremia, hypernatremia, hypo‑ and hyperkalemia, hypo‑ and hypercalcemia, and hypo‑ and hypermagnesemia?

Systematic Approach to Electrolyte Disturbances

Initial Assessment Framework

Begin by obtaining a basic metabolic panel, magnesium level, and ECG in all patients with suspected electrolyte abnormalities. 1 The ECG is critical because life-threatening arrhythmias can occur before symptoms develop, particularly with potassium and calcium disorders. 1

Key Clinical Context to Establish

• Medication review: Loop diuretics, thiazides, ACE inhibitors, ARBs, aldosterone antagonists, NSAIDs, digoxin, and corticosteroids are the most common culprits 1, 2
• Volume status: Assess for hypovolemia (orthostatic hypotension, decreased skin turgor, dry mucous membranes) versus hypervolemia (peripheral edema, pulmonary crackles, elevated JVP) 3
• Renal function: eGFR <45 mL/min dramatically increases risk of both hypokalemia and hyperkalemia complications 1, 4
• Cardiac disease: Heart failure, coronary disease, or arrhythmia history makes electrolyte disturbances far more dangerous 1, 2
• GI losses: Vomiting, diarrhea, high-output ostomy, or fistulas cause massive potassium and magnesium depletion 1

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Hyponatremia (Na <135 mEq/L)

Severity Classification and Immediate Actions

Severe symptomatic hyponatremia (Na <120 mEq/L with seizures, altered mental status, or coma) requires immediate hypertonic saline 3% at 1-2 mL/kg/hour to raise sodium by 4-6 mEq/L in the first 4-6 hours. 3 The maximum correction rate is 10-12 mEq/L in 24 hours to prevent osmotic demyelination syndrome. 3

Diagnostic Algorithm

1. Assess volume status clinically (not just by labs) 3
2. Measure serum osmolality and urine osmolality simultaneously 3
3. Measure urine sodium concentration 3

• Hypovolemic hyponatremia: Urine Na <20 mEq/L suggests extrarenal losses (vomiting, diarrhea); urine Na >20 mEq/L suggests renal losses (diuretics, salt-wasting nephropathy) 3
• Euvolemic hyponatremia: Consider SIADH (urine osmolality >100 mOsm/kg with inappropriately concentrated urine), hypothyroidism, or adrenal insufficiency 3
• Hypervolemic hyponatremia: Heart failure, cirrhosis, or nephrotic syndrome with total body sodium excess but relative water excess 3, 2

Treatment by Etiology

• Diuretic-induced: Stop the diuretic temporarily if Na <125 mEq/L; this is the most common cause in hospitalized patients 3, 5
• SIADH: Fluid restriction to 800-1000 mL/day is first-line; consider tolvaptan for refractory cases 6
• Hypovolemic: Replace volume with isotonic saline (0.9% NaCl) 3

Critical Pitfall

Check for concurrent hypokalemia and hypomagnesemia in all hyponatremic patients—these occur in 15-17% of cases and must be corrected simultaneously. 5 Hypomagnesemia makes hypokalemia refractory to treatment. 7, 5

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Hypernatremia (Na >145 mEq/L)

Immediate Management

Hypernatremia represents free water deficit and requires gradual correction over 48-72 hours to prevent cerebral edema. 3 Reduce sodium by no more than 10-15 mEq/L per 24 hours. 3

Calculate Free Water Deficit

Free water deficit (L) = 0.6 × body weight (kg) × [(current Na / 140) - 1] 3

Replace half the deficit in the first 24 hours with hypotonic fluids (0.45% saline or D5W), then the remainder over the next 24-48 hours. 3

Etiology-Specific Considerations

• Diabetes insipidus: Urine osmolality <300 mOsm/kg despite hypernatremia; central DI requires desmopressin 6
• Inadequate water intake: Common in elderly, debilitated, or intubated patients 3
• Osmotic diuresis: Hyperglycemia, mannitol, or high-protein tube feeds 3

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Hypokalemia (K <3.5 mEq/L)

Severity-Based Treatment Algorithm

Mild hypokalemia (3.0-3.5 mEq/L) without cardiac disease can be managed with oral potassium chloride 20-40 mEq/day divided into 2-3 doses. 1

Moderate hypokalemia (2.5-2.9 mEq/L) requires prompt correction with oral potassium chloride 40-60 mEq/day because of significant cardiac arrhythmia risk, especially in patients with heart disease or on digoxin. 1 ECG changes (ST depression, T wave flattening, prominent U waves) indicate urgent treatment need. 1

Severe hypokalemia (K ≤2.5 mEq/L) requires IV potassium replacement with continuous cardiac monitoring due to extreme risk of ventricular fibrillation and cardiac arrest. 1 Administer potassium chloride at ≤10 mEq/hour via peripheral line (maximum concentration 40 mEq/L) or up to 20 mEq/hour via central line. 1

Mandatory Pre-Treatment Step

Check and correct magnesium FIRST—hypomagnesemia occurs in 42% of hypokalemic patients and makes hypokalemia completely refractory to correction. 7, 1 Target magnesium >0.6 mmol/L (>1.5 mg/dL). 1 Use organic magnesium salts (aspartate, citrate, lactate) rather than oxide for superior bioavailability. 1

Medication Adjustments

For persistent diuretic-induced hypokalemia, adding a potassium-sparing diuretic (spironolactone 25-100 mg daily, amiloride 5-10 mg daily, or triamterene 50-100 mg daily) is more effective than chronic oral potassium supplements. 1 This provides stable levels without peaks and troughs. 1

Stop or reduce potassium-wasting diuretics if K <3.0 mEq/L. 1 The combination of loop diuretics and thiazides causes massive renal potassium losses. 1

Patients on ACE inhibitors or ARBs alone or with aldosterone antagonists frequently do not require routine potassium supplementation, and such supplementation may be deleterious because these medications reduce renal potassium losses. 1

Monitoring Protocol

• Check potassium and renal function within 3 days and again at 7 days after starting supplementation 1
• Continue monitoring every 1-2 weeks until values stabilize, then at 3 months, then every 6 months 1
• More frequent monitoring needed if patient has renal impairment (eGFR <45 mL/min), heart failure, diabetes, or is on medications affecting potassium 1

Critical Contraindications

Never give potassium supplements to patients with:

• eGFR <30 mL/min without specialist consultation 1
• Baseline potassium >5.0 mEq/L 1
• Concurrent use of potassium-sparing diuretics 1
• Triple combination of ACE inhibitor + ARB + aldosterone antagonist 1

Avoid NSAIDs entirely during potassium replacement—they cause acute renal failure and severe hyperkalemia when combined with potassium therapy. 1

Special Populations

In diabetic ketoacidosis, add 20-30 mEq/L potassium (2/3 KCl and 1/3 KPO4) to IV fluids once K+ falls below 5.5 mEq/L with adequate urine output. 1 If K+ <3.3 mEq/L, delay insulin therapy until potassium is restored to prevent life-threatening arrhythmias. 1

In heart failure patients, maintain potassium strictly between 4.0-5.0 mEq/L—both hypokalemia and hyperkalemia increase mortality risk in this population. 1, 2 Consider aldosterone antagonists for mortality benefit while preventing hypokalemia. 1

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Hyperkalemia (K >5.0 mEq/L)

Emergency Management by Severity

Severe hyperkalemia (K >6.5 mEq/L) or any ECG changes (peaked T waves, prolonged PR, widened QRS) require immediate treatment in this sequence: 4

1. Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes to stabilize cardiac membranes (onset 1-3 minutes, duration 30-60 minutes) 4
2. Insulin 10 units IV with dextrose 50% (D50W) 50 mL to shift potassium intracellularly (onset 30-60 minutes, lowers K by 0.5-1.2 mEq/L) 4
3. Albuterol 10-20 mg nebulized over 10 minutes (onset 30-60 minutes, lowers K by 0.5-1.0 mEq/L) 4
4. Sodium bicarbonate 50 mEq IV over 5 minutes if severe metabolic acidosis present 4

Recheck potassium within 1-2 hours after insulin/glucose administration, then every 2-4 hours during acute treatment phase. 4

Potassium Removal Strategies

For moderate hyperkalemia (5.5-6.5 mEq/L) not on maximal RAAS inhibitor therapy, initiate a potassium-lowering agent such as patiromer or sodium zirconium cyclosilicate. 4 These newer binders are superior to sodium polystyrene sulfonate (Kayexalate), which has serious GI adverse effects including bowel necrosis. 1

For K >6.5 mEq/L, discontinue or reduce RAAS inhibitors immediately and initiate a potassium-lowering agent as soon as K levels >5.0 mEq/L. 4

Urgent hemodialysis is indicated for:

• Severe hyperkalemia refractory to medical therapy 4
• eGFR <15 mL/min with K >6.0 mEq/L 8
• Uremic symptoms (encephalopathy, pericarditis, severe acidosis) 8

Medication Review

Immediately review and discontinue or dose-adjust medications that worsen hyperkalemia: 8

• ACE inhibitors and ARBs 4, 8
• Aldosterone antagonists (spironolactone, eplerenone) 4
• NSAIDs and COX-2 inhibitors 4, 8
• Potassium-sparing diuretics (amiloride, triamterene) 4
• Trimethoprim, pentamidine, heparin, β-blockers, calcineurin inhibitors 4

Chronic Hyperkalemia Management

For patients with stage 4-5 CKD and recurrent hyperkalemia, implement dietary potassium restriction and use newer potassium binders (patiromer or sodium zirconium cyclosilicate) to maintain serum potassium 4.0-5.0 mEq/L while continuing cardioprotective RAAS inhibitor therapy. 4

Limit foods rich in bioavailable potassium (especially processed foods), avoid salt substitutes containing potassium, and avoid herbal supplements that raise K+ (alfalfa, dandelion, horsetail, nettle). 1

Monitoring in High-Risk Patients

Check potassium within 7-10 days after starting or increasing RAAS inhibitors in patients with CKD, diabetes, or heart failure. 4 The risk of hyperkalemia increases progressively as GFR decreases, particularly when GFR falls below 15 mL/min/1.73 m². 4

Patients with chronic kidney disease and/or chronic heart failure who receive RAAS inhibitors have highest risk of recurrent hyperkalemia if they have: 4

• Initial moderate to severe hyperkalemia (≥5.6 mEq/L) 4
• Low GFR (<45 mL/min/1.73 m²) 4
• Diabetes 4
• Use of spironolactone 4

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Hypocalcemia (Corrected Ca <8.5 mg/dL)

Correction Formula

Always correct calcium for albumin: Corrected Ca = measured Ca + 0.8 × (4.0 - albumin) 3

Acute Symptomatic Hypocalcemia

Severe symptomatic hypocalcemia (tetany, seizures, laryngospasm, prolonged QT) requires immediate IV calcium gluconate 1-2 grams (10-20 mL of 10% solution) over 10-20 minutes, followed by continuous infusion of 0.5-2 mg/kg/hour elemental calcium. 3

Etiology-Specific Treatment

• Hypoparathyroidism: Requires oral calcium carbonate 1-2 grams elemental calcium TID plus calcitriol 0.25-0.5 mcg BID 3
• Vitamin D deficiency: Ergocalciferol 50,000 IU weekly for 8 weeks, then maintenance 3
• Hypomagnesemia-induced: Correct magnesium first—hypocalcemia will not respond until magnesium is normalized 3, 7
• Hyperphosphatemia-induced (CKD): Phosphate binders plus calcitriol 3, 4

Monitoring

Check ionized calcium, magnesium, phosphate, PTH, and vitamin D levels to determine etiology. 3 Recheck calcium 24-48 hours after initiating therapy. 3

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Hypercalcemia (Ca >10.5 mg/dL)

Immediate Management

Severe hypercalcemia (Ca >14 mg/dL or symptomatic) requires aggressive IV hydration with 0.9% saline at 200-300 mL/hour to restore euvolemia, followed by loop diuretics (furosemide 20-40 mg IV) to promote calciuresis. 3, 6

Calcitonin 4 IU/kg IM/SC every 12 hours provides rapid but temporary reduction (onset 4-6 hours, lowers Ca by 1-2 mg/dL). 3

Bisphosphonates (zoledronic acid 4 mg IV or pamidronate 60-90 mg IV) provide sustained reduction but take 2-4 days to work. 3

Etiology-Specific Considerations

• Primary hyperparathyroidism: Most common outpatient cause; requires parathyroidectomy for definitive treatment 6
• Malignancy-associated: Second most common cause; treat underlying cancer 3
• Thyrotoxicosis: Treat hyperthyroidism with beta-blockers and antithyroid drugs 6
• Vitamin D intoxication: Stop all vitamin D and calcium supplements; may require glucocorticoids 6
• Adrenal insufficiency: Glucocorticoid replacement normalizes calcium 6

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Hypomagnesemia (Mg <1.5 mg/dL)

Clinical Significance

Hypomagnesemia occurs in 15% of hospitalized patients and is found in 42% of hypokalemic patients, 29% of hypophosphatemic patients, and 22% of hypocalcemic patients. 7 It causes refractory hypokalemia and hypocalcemia that will not correct until magnesium is normalized. 7, 1

Treatment

Severe symptomatic hypomagnesemia (seizures, arrhythmias, tetany) requires IV magnesium sulfate 1-2 grams over 15-30 minutes, followed by continuous infusion. 1 For cardiac arrest with hypomagnesemia, give 1-2 grams IV push. 1

Asymptomatic or mild hypomagnesemia can be treated with oral magnesium supplementation 200-400 mg elemental magnesium daily, divided into 2-3 doses. 1 Use organic magnesium salts (aspartate, citrate, lactate) rather than oxide for superior bioavailability. 1

Common Causes

• Diuretic therapy (loop and thiazides) 1, 2
• Proton pump inhibitors 7
• Alcohol use disorder 7
• Diarrhea or malabsorption 7
• Diabetic ketoacidosis 7

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Hypermagnesemia (Mg >2.5 mg/dL)

Management

Severe hypermagnesemia (Mg >4 mg/dL) with cardiac or neuromuscular manifestations requires immediate IV calcium gluconate 1-2 grams to antagonize effects, plus aggressive IV hydration and loop diuretics to promote renal excretion. 3

Hemodialysis is indicated for severe hypermagnesemia with renal failure. 3

Prevention

Avoid magnesium-containing antacids and laxatives in patients with eGFR <30 mL/min. 1 Magnesium supplements should be avoided in patients with creatinine clearance <20 mg/dL. 1

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Key Monitoring Principles Across All Electrolyte Disorders

Frequency of monitoring should be based on: 4

• Severity of initial abnormality 4
• Presence of cardiac disease or arrhythmias 4
• Renal function status (eGFR) 4
• Concurrent medications affecting electrolyte homeostasis 4
• History of recurrent electrolyte abnormalities 4

In patients with CKD, heart failure, or diabetes on RAAS inhibitors, check electrolytes within 2-3 days and again at 7 days after any medication change, then monthly for 3 months, then every 3-6 months. 1, 4

Electrolyte disturbances frequently cluster—when you find one abnormality, actively look for others. 7, 5 Hyponatremia, hypokalemia, hypomagnesemia, and hypophosphatemia commonly coexist, especially in patients on diuretics or with heart failure. 5, 2