How should abnormal serum sodium and potassium levels be managed, including treatment for hyponatremia, hypernatremia, hypokalemia, and hyperkalemia?

Management of Sodium and Potassium Disorders

Hyperkalemia Management

For life-threatening hyperkalemia (K+ ≥6.5 mEq/L or any ECG changes), immediately administer IV calcium gluconate 10% (15-30 mL over 2-5 minutes) to stabilize cardiac membranes, followed by insulin 10 units IV with 25g dextrose and nebulized albuterol 10-20 mg to shift potassium intracellularly, then use loop diuretics or hemodialysis for definitive removal. 1, 2

Severity Classification

• Mild: K+ 5.0-5.5 mEq/L 1, 2
• Moderate: K+ 5.5-6.0 mEq/L (or 6.0-6.4 mEq/L per some guidelines) 1, 2
• Severe: K+ >6.0 mEq/L (or ≥6.5 mEq/L) 1, 2

Emergency Treatment Algorithm

Step 1: Cardiac Membrane Stabilization (if ECG changes present)

• Administer calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 1, 2
• Alternative: calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred via central line due to tissue injury risk) 1, 2
• Onset: 1-3 minutes; duration: 30-60 minutes 1
• Repeat dose if no ECG improvement within 5-10 minutes 1
• Critical caveat: Calcium does NOT lower potassium—it only temporarily protects the heart 1, 2

Step 2: Intracellular Potassium Shift (administer all simultaneously)

• Insulin-glucose: 10 units regular insulin IV + 25g dextrose (50 mL D50W) 1, 2

  • Lowers K+ by 0.5-1.2 mEq/L within 30-60 minutes 1
  • Duration: 4-6 hours 1
  • Never give insulin without glucose—hypoglycemia can be fatal 1

• Nebulized albuterol: 10-20 mg in 4 mL over 10-15 minutes 1, 2

  • Lowers K+ by 0.5-1.0 mEq/L within 30 minutes 1
  • Duration: 2-4 hours 1
  • Can repeat every 2 hours if needed 1

• Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 1, 2

  • Onset: 30-60 minutes 1
  • Do NOT use without documented acidosis—it is ineffective and wastes time 1

Step 3: Definitive Potassium Removal

• Loop diuretics: Furosemide 40-80 mg IV if eGFR >30 mL/min and adequate urine output 1, 2
• Hemodialysis: Most reliable method for severe hyperkalemia 1, 2
  • Absolute indications: K+ >6.5 mEq/L unresponsive to medical therapy, oliguria/anuria, ESRD, ongoing K+ release (tumor lysis, rhabdomyolysis), eGFR <15 mL/min, persistent ECG changes 1
  • In hemodynamically unstable patients, use CRRT over intermittent hemodialysis 1

Step 4: Potassium Binders (for subacute/chronic management)

• Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily 1, 2

  • Onset: ~1 hour (suitable for urgent scenarios) 1

• Patiromer (Veltassa): 8.4g once daily with food, titrated up to 25.2g daily 1, 2

  • Onset: ~7 hours (for subacute/chronic control) 1
  • Must be separated from other oral medications by ≥3 hours 1

• Avoid sodium polystyrene sulfonate (Kayexalate): Risk of bowel necrosis, colonic ischemia, limited efficacy 1, 2

Medication Management During Acute Episode

Hold immediately when K+ >6.5 mEq/L: 1

• RAAS inhibitors (ACE-I, ARBs, mineralocorticoid receptor antagonists)
• NSAIDs
• Potassium-sparing diuretics
• Trimethoprim-containing agents
• Heparin
• Beta-blockers
• Potassium supplements and salt substitutes

After acute resolution:

• Restart RAAS inhibitors at lower dose once K+ <5.0 mEq/L 1
• Initiate potassium binder (SZC or patiromer) to enable continuation of life-saving RAAS therapy 1, 2

Monitoring Protocol

Acute phase:

• Recheck K+ 1-2 hours after insulin/glucose or beta-agonist therapy 1
• Continue K+ checks every 2-4 hours until stable 1
• Obtain repeat ECG to confirm resolution of cardiac changes 1

Post-acute phase:

• Check K+ within 1 week after initiating/escalating RAAS inhibitors 1
• Reassess 7-10 days after starting potassium binder 1
• Individualize monitoring frequency based on eGFR, heart failure, diabetes, or prior hyperkalemia 1

Critical Pitfalls to Avoid

• Never delay calcium if ECG changes present—do not wait for repeat labs 1
• Never give insulin without glucose 1
• Calcium, insulin, and beta-agonists are temporizing only—they do NOT remove K+ from the body 1
• Never use sodium bicarbonate without documented metabolic acidosis 1
• Never permanently discontinue RAAS inhibitors—use K+ binders instead 1, 2

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Hypokalemia Management

For severe hypokalemia (K+ <2.5 mEq/L) or moderate hypokalemia with ECG changes/cardiac symptoms, administer IV potassium chloride at maximum concentration of 40 mEq/L via peripheral line (or 60 mEq/L via central line) at maximum rate of 10-20 mEq/hour with continuous cardiac monitoring. 3, 2

Severity Classification

• Mild: K+ 3.0-3.5 mEq/L 3, 2
• Moderate: K+ 2.5-2.9 mEq/L 3, 2
• Severe: K+ <2.5 mEq/L 3, 2

Treatment Algorithm

Step 1: Check and Correct Magnesium FIRST

• Hypomagnesemia is the most common reason for refractory hypokalemia 3
• Target magnesium >0.6 mmol/L (>1.5 mg/dL) 3
• Use organic magnesium salts (aspartate, citrate, lactate) rather than oxide/hydroxide for superior bioavailability 3

Step 2: Determine Route of Replacement

Indications for IV replacement: 3, 2

• Severe hypokalemia (K+ ≤2.5 mEq/L)
• ECG abnormalities (ST depression, T wave flattening, prominent U waves)
• Active cardiac arrhythmias
• Severe neuromuscular symptoms
• Non-functioning GI tract
• Cardiac disease or digoxin therapy with K+ <4.0 mEq/L

IV Replacement Protocol:

• Standard concentration: ≤40 mEq/L via peripheral line; ≤60 mEq/L via central line 3, 2
• Maximum rate: 10-20 mEq/hour 3, 2
• Preferred formulation: 2/3 KCl + 1/3 KPO4 to address concurrent phosphate depletion 3
• Continuous cardiac monitoring required for severe hypokalemia 3, 2
• Recheck K+ within 1-2 hours after IV administration 3

Oral Replacement (for mild-moderate hypokalemia without severe symptoms):

• Mild hypokalemia: 20-60 mEq/day in divided doses 3, 2
• Moderate hypokalemia: 40-80 mEq/day in divided doses 3, 2
• Divide doses into 2-3 separate administrations to prevent GI intolerance and rapid fluctuations 3

Step 3: Address Underlying Cause

Stop or reduce potassium-wasting diuretics if K+ <3.0 mEq/L 3

For persistent diuretic-induced hypokalemia, add potassium-sparing diuretic (superior to chronic oral supplements): 3

• Spironolactone: 25-100 mg daily (first-line) 3
• Amiloride: 5-10 mg daily 3
• Triamterene: 50-100 mg daily 3

Contraindications to potassium-sparing diuretics: 3

• eGFR <45 mL/min
• Baseline K+ >5.0 mEq/L
• Concurrent ACE-I/ARB use without close monitoring

Target Potassium Levels

• All patients (especially cardiac disease or digoxin use): 4.0-5.0 mEq/L 3, 2
• Both hypokalemia and hyperkalemia increase mortality risk in heart failure patients 3

Monitoring Protocol

Initial monitoring:

• Check K+ and renal function within 3-7 days after starting supplementation 3
• Continue monitoring every 1-2 weeks until values stabilize 3
• Then check at 3 months, then every 6 months 3

When adding potassium-sparing diuretics:

• Monitor every 5-7 days until K+ stabilizes 3
• If K+ >5.5 mEq/L, halve the dose and recheck in 1-2 weeks 3
• If K+ >6.0 mEq/L, discontinue immediately 3

High-risk patients requiring more frequent monitoring: 3

• Renal impairment (creatinine >1.6 mg/dL or eGFR <45 mL/min)
• Heart failure
• Diabetes
• Concurrent medications affecting K+ (RAAS inhibitors, aldosterone antagonists)

Special Considerations

Patients on ACE-I/ARBs:

• Routine K+ supplementation may be unnecessary and potentially harmful 3
• These medications reduce renal K+ losses 3
• If supplementation needed, start at lower doses (10-20 mEq daily) and monitor closely 3

Diabetic ketoacidosis:

• Add 20-30 mEq/L K+ to IV fluids once K+ <5.5 mEq/L with adequate urine output 3
• Use 2/3 KCl + 1/3 KPO4 3
• Delay insulin if K+ <3.3 mEq/L to prevent life-threatening arrhythmias 3

Critical Pitfalls to Avoid

• Never supplement K+ without checking and correcting magnesium first—most common reason for treatment failure 3
• Never combine K+ supplements with K+-sparing diuretics without intensive monitoring 3
• Never use NSAIDs during K+ replacement—they worsen renal function and increase hyperkalemia risk 3
• Verify eGFR >30 mL/min before initiating K+ supplementation 3

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Hyponatremia Management

For severely symptomatic hyponatremia (Na+ <125 mEq/L with seizures, coma, or cardiorespiratory distress), immediately administer 3% hypertonic saline 100 mL IV bolus over 10 minutes, repeat up to 3 times until symptoms improve, targeting 4-6 mEq/L increase in first 1-2 hours but no more than 10 mEq/L in 24 hours to avoid osmotic demyelination syndrome. 4, 5

Severity Classification

• Mild: Na+ 130-134 mEq/L 4
• Moderate: Na+ 125-129 mEq/L 4
• Severe: Na+ <125 mEq/L 4

Clinical Presentation

• Mild symptoms: Nausea, vomiting, weakness, headache, mild neurocognitive deficits 4
• Severe symptoms: Delirium, confusion, impaired consciousness, ataxia, seizures, brain herniation, death 4
• Chronic mild hyponatremia: Cognitive impairment, gait disturbances, increased falls/fractures, osteoporosis 5

Emergency Treatment (Severely Symptomatic Hyponatremia)

Indications for emergency treatment: 4, 5

• Na+ <125 mEq/L with severe symptoms (somnolence, obtundation, coma, seizures, cardiorespiratory distress)

Treatment protocol:

• 3% hypertonic saline: 100 mL IV bolus over 10 minutes 4, 5
• Repeat up to 3 times until symptoms improve 4, 5
• Target: Increase Na+ by 4-6 mEq/L within 1-2 hours 4, 5
• Correction limit: No more than 10 mEq/L in first 24 hours 4, 5
• Use calculators to guide fluid replacement to avoid overly rapid correction 4

Critical warning: Overly rapid correction of chronic hyponatremia can cause osmotic demyelination syndrome (parkinsonism, quadriparesis, death) 5

Non-Emergency Treatment (Based on Volume Status)

Step 1: Categorize by fluid volume status 4, 5

Hypovolemic Hyponatremia:

• Treatment: Normal saline (0.9% NaCl) infusions 6, 4
• Mechanism: Results from overzealous diuretic therapy, prolonged negative sodium balance, marked loss of extracellular fluid 6
• Requires: Expansion of plasma volume and cessation of diuretics 6

Euvolemic Hyponatremia (including SIADH):

• First-line: Fluid restriction (1-1.5 L/day for severe hyponatremia Na+ <125 mEq/L) 6, 4
• Alternative options: 4, 5
  • Salt tablets
  • Urea (poor palatability, gastric intolerance)
  • Vaptans (V2 receptor antagonists: tolvaptan, satavaptan, lixivaptan)
    • Benefit: Increase solute-free water excretion, improve Na+ in 45-82% of cases 6
    • Risks: Overly rapid correction, increased thirst 5
    • Safety established only for short-term use (1 week to 1 month) 6

Hypervolemic Hyponatremia (heart failure, cirrhosis):

• Primary treatment: Manage underlying cause 4
• Adjunct: Fluid restriction 4
• Mechanism: Non-osmotic hypersecretion of vasopressin, enhanced proximal nephron Na+ reabsorption, impaired free water clearance 6
• Note: Fluid restriction rarely improves Na+ because restriction to <1 L/day is not tolerated 6

Special Considerations

Cirrhosis with ascites:

• Hyponatremia associated with: Higher prevalence of refractory ascites, hepatic encephalopathy, SBP, HRS, mortality 6
• Chronic asymptomatic hyponatremia: Seldom needs treatment 6
• Temporarily discontinue diuretics if Na+ <125 mmol/L 6

Vaptans in cirrhosis:

• Short-term use: Effective in improving Na+ 6
• Long-term use: Despite improving Na+, satavaptan increased gastrointestinal bleeding and did not improve survival 6
• Insufficient evidence for routine IV albumin outside LVP setting 6

Monitoring and Correction Rates

Acute hyponatremia (<48 hours):

• Correction rate: 1 mmol/L/hour increase 7

Chronic hyponatremia (>48 hours):

• Maximum correction rate: 0.5 mmol/L/hour or less 7
• High risk of osmotic demyelination if corrected too rapidly 7

General correction limits:

• First hour: 5 mmol/L (for severely symptomatic) 6
• First 24 hours: No more than 8-10 mmol/L per day 6, 4, 5

Common Causes to Identify

• Certain medications 4
• Excessive alcohol consumption 4
• Very low-salt diets 4
• Excessive free water intake during exercise 4
• Diuretic therapy 6

Key Principles

• Identify the cause if possible, but do not delay treatment 4
• Sodium restriction (not fluid restriction) results in weight loss as fluid passively follows sodium 6
• Hyponatremia is associated with increased mortality even when mild 5

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Hypernatremia Management

For severe hypernatremia with symptoms or requiring IV fluids, administer hypotonic fluid replacement (0.45% saline or D5W) at a rate that corrects Na+ by no more than 10-12 mEq/L per 24 hours to avoid cerebral edema, while simultaneously addressing the underlying cause (dehydration, diabetes insipidus, impaired thirst mechanism). 4

Clinical Presentation

• Mild hypernatremia: Often caused by dehydration from impaired thirst mechanism or lack of access to water 4
• Severe hypernatremia: Accompanied by circulatory failure, muscular asthenia, disorientation, convulsions, coma, cerebral symptoms 8

Treatment Approach

Step 1: Address underlying etiology 4

• Dehydration (impaired thirst, lack of water access)
• Diabetes insipidus (lack of antidiuretic hormone due to intracranial metastasis or other causes) 8
• Water loss from vomiting, diarrhea, renal insufficiency 8

Step 2: Correct fluid deficit 4

For severe hypernatremia, symptomatic patients, or those requiring IV fluids:

• Use hypotonic fluid replacement (0.45% saline or D5W) 4
• Correction rate: No more than 10-12 mEq/L per 24 hours 4
• Rationale: Avoid cerebral edema from overly rapid correction 4

For mild hypernatremia:

• Oral water replacement if patient can tolerate 4
• Address access to water if impaired 4

Monitoring

• Carefully conduct fluid replacement after complete diagnosis of severity 8
• Monitor for cerebral edema during correction 4

Critical Considerations

• Hypernatremia is less common than hyponatremia 4
• Requires careful fluid management to avoid complications 4, 8