How do I manage hyperkalemia (elevated potassium levels), hypokalemia (low potassium levels), hypernatremia (elevated sodium levels), and hyponatremia (low sodium levels) in a patient's chart?

Management of Electrolyte Disorders: Hyperkalemia, Hypokalemia, Hypernatremia, and Hyponatremia

Hyperkalemia Management

For hyperkalemia, immediately assess severity and ECG changes, then follow a three-step approach: stabilize cardiac membranes with IV calcium, shift potassium into cells with insulin/glucose and albuterol, and eliminate potassium with diuretics or binders—while maintaining RAAS inhibitors whenever possible using newer potassium binders rather than discontinuing life-saving medications. 1

Severity Classification and Initial Assessment

• Mild hyperkalemia: K+ 5.0-5.5 mEq/L 2
• Moderate hyperkalemia: K+ 5.5-6.0 mEq/L (European Society of Cardiology) or 5.6-5.9 mEq/L (Mayo Clinic) 2
• Severe hyperkalemia: K+ >6.0 mEq/L (European Society) or >5.9 mEq/L (Mayo Clinic) 2
• Life-threatening: K+ ≥6.5 mEq/L or any ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) 1

Step 1: Cardiac Membrane Stabilization (Immediate - Within 2-5 Minutes)

• Administer calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes 1
• Alternative: calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 1
• Calcium chloride provides more rapid increase in ionized calcium and is preferred in critically ill patients 1
• Use central line when possible as extravasation through peripheral IV causes severe tissue injury 1
• Monitor heart rate during infusion; stop if symptomatic bradycardia occurs 1
• Effect begins within minutes but lasts only 30-60 minutes 2
• Critical point: Calcium does NOT lower potassium—it only protects against arrhythmias 1

Step 2: Shift Potassium Into Cells (Effect Within 15-30 Minutes)

• Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL D50W) over 15-30 minutes 1, 3

• Onset: 15-30 minutes; duration: 4-6 hours 2, 3

• Monitor glucose hourly for 4-6 hours and potassium every 2-4 hours 3

• Risk factors for hypoglycemia: low baseline glucose, no diabetes history, female sex, renal dysfunction, lower body weight 3

• Nebulized albuterol: 10-20 mg over 15 minutes 1

• Can reduce K+ by 0.5-1.0 mEq/L 1

• Onset: 15-30 minutes; duration: 4-6 hours 1

• Sodium bicarbonate: 50 mEq IV over 5 minutes 1

• Most effective when concurrent metabolic acidosis present 2, 1

Critical warning: These measures provide only temporary benefit (1-4 hours) and do NOT increase potassium excretion—rebound hyperkalemia occurs after 2 hours 2, 3

Step 3: Eliminate Potassium From Body (Definitive Treatment)

For Acute Management:

• Loop diuretics: Furosemide 40-80 mg IV 1

• Only effective with adequate renal function 1

• Traditional cation exchange resin: Sodium polystyrene sulfonate (Kayexalate) 15-50 g orally or rectally with sorbitol 1

• Warning: Cases of fatal GI injury reported with SPS 2

• Onset variable; takes several hours 2

For Chronic/Recurrent Hyperkalemia (Preferred Approach):

Newer potassium binders are safer and allow continuation of RAAS inhibitors:

• Patiromer (Veltassa):

  • Starting dose: 8.4 g once daily orally 2
  • Titrate up to 16.8 g or 25.2 g daily as needed 2
  • Onset: 7 hours 2
  • Separate from other oral medications by 3+ hours 2
  • Exchanges calcium for K+ in colon 2
  • Monitor for hypomagnesemia and rare hypercalcemia 2

• Sodium zirconium cyclosilicate (ZS-9/Lokelma):

  • Correction phase: 10 g three times daily for 48 hours 2
  • Maintenance: 5 g every other day to 15 g daily 2
  • Onset: 1 hour (fastest acting) 2
  • Highly selective for K+ 2
  • Contains 400 mg sodium per 5g dose 2
  • Monitor for mild-moderate edema 2

• Hemodialysis: Most effective for severe hyperkalemia, especially with renal failure 1

Management Based on RAAS Inhibitor Therapy

The European Society of Cardiology provides clear thresholds for RAAS inhibitor management:

K+ 4.5-5.0 mEq/L:

• If not on maximum-tolerated guideline-recommended RAAS inhibitor dose: initiate/up-titrate therapy and closely monitor K+ 2
• Start K+-lowering therapy if K+ increases to >5.0 mEq/L 2

K+ >5.0 to 6.5 mEq/L:

• If on maximum-tolerated RAAS inhibitor dose: initiate K+-lowering therapy (patiromer or SZC) and continue RAAS inhibitor 2, 1
• If not on maximum dose: start RAAS inhibitor when K+ <5.0 mEq/L; closely monitor and maintain K+-lowering therapy 2

K+ >6.5 mEq/L:

• Discontinue or reduce RAAS inhibitor therapy 2, 1
• K+-lowering therapy may be started as soon as K+ >5.0 mEq/L 2
• Closely monitor serum K+ 2

Medication Review for Hyperkalemia

Identify and address contributing medications: 2

• Potassium-sparing diuretics (spironolactone, triamterene, amiloride)
• Beta-blockers
• NSAIDs
• Sacubitril/valsartan
• RAAS inhibitors (ACE inhibitors, ARBs, MRAs)
• Direct renin inhibitors (aliskiren)
• Calcineurin inhibitors (cyclosporine, tacrolimus)
• Trimethoprim-sulfamethoxazole
• Heparin

Key principle: Up to 73% of patients with advanced CKD and 40% with chronic heart failure develop hyperkalemia 2. Rather than discontinuing life-saving RAAS inhibitors, use newer K+ binders to maintain therapy 2, 1.

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Hypokalemia Management

For hypokalemia, determine severity and symptoms, then replace potassium targeting 4.0-5.0 mEq/L using oral supplementation for mild cases and IV replacement only for severe/symptomatic cases, while addressing underlying causes and considering potassium-sparing diuretics for diuretic-induced hypokalemia.

Severity Classification

• Mild hypokalemia: K+ 3.0-3.5 mEq/L 4
• Moderate hypokalemia: K+ 2.5-2.9 mEq/L 4
• Severe hypokalemia: K+ <2.5 mEq/L 4

Target range: 4.0-5.0 mEq/L for all patients, especially those with heart disease or on digoxin 4

Mild Hypokalemia (K+ 3.0-3.5 mEq/L)

• Often asymptomatic but correction recommended to prevent cardiac complications 4
• ECG changes typically absent but may show T wave flattening 4
• Oral potassium chloride 20-60 mEq/day 4
• Dietary advice to increase potassium-rich foods may be sufficient for milder cases 4
• Recheck K+ and renal function within 1-2 weeks after initiation or dose adjustment 4

Moderate Hypokalemia (K+ 2.5-2.9 mEq/L)

• Requires prompt correction due to increased arrhythmia risk 4
• ECG changes: ST depression, T wave flattening, prominent U waves 4
• Oral potassium chloride 40-80 mEq/day in divided doses 4
• For patients on diuretics with persistent hypokalemia despite supplementation: add potassium-sparing diuretics 4
  • Spironolactone 25-100 mg daily 4
  • Amiloride 5-10 mg daily in 1-2 divided doses 4
  • Triamterene 50-100 mg daily in 1-2 divided doses 4
• Check serum K+ and creatinine 5-7 days after initiating potassium-sparing diuretic 4
• Continue monitoring every 5-7 days until values stabilize 4

Severe Hypokalemia (K+ <2.5 mEq/L or Symptomatic)

This is a medical emergency requiring IV replacement with cardiac monitoring:

• Establish large-bore IV access 4
• Cardiac monitoring essential due to risk of ventricular fibrillation and asystole 4
• IV potassium replacement protocol: 5, 6
  • Maximum concentration: 40 mEq/L in peripheral line; up to 60 mEq/L in central line
  • Maximum rate: 10-20 mEq/hour (rates >20 mEq/hour only in extreme circumstances with continuous cardiac monitoring)
  • Recheck serum K+ within 1-2 hours after IV correction 4
• Correct concurrent hypomagnesemia as it makes hypokalemia resistant to correction 4

Special Clinical Scenarios

Diabetic Ketoacidosis:

• Add 20-30 mEq potassium (2/3 KCl and 1/3 KPO4) to each liter IV fluid once K+ <5.5 mEq/L and adequate urine output established 4
• If K+ <3.3 mEq/L: delay insulin therapy until potassium restored to prevent life-threatening arrhythmias 4

Patients on Loop or Thiazide Diuretics:

• Check serum K+ and renal function within 3 days and again at 1 week after initiation 4
• Monitor at least monthly for first 3 months, then every 3 months 4
• Potassium-sparing diuretics more effective than oral supplements for persistent diuretic-induced hypokalemia 4
• Avoid potassium-sparing diuretics if GFR <45 mL/min 4

Patients on RAAS Inhibitors:

• In patients taking ACE inhibitors or ARBs alone or with aldosterone antagonists, routine potassium supplementation may be unnecessary and potentially harmful 4
• When initiating aldosterone antagonists, reduce or discontinue potassium supplements to avoid hyperkalemia 4

Critical Medications to Avoid or Adjust in Hypokalemia

Medications requiring extreme caution or temporary hold:

• Digoxin: Question orders in severe hypokalemia—can cause life-threatening arrhythmias 4
• Risk factors for digoxin toxicity: hypokalemia, hypomagnesemia, hypercalcemia, CKD, hypoxia, acidosis 4
• Thiazide and loop diuretics: Can further deplete potassium; use with caution until corrected 4
• Most antiarrhythmic agents: Should be avoided as they exert cardiodepressant and proarrhythmic effects in hypokalemia 4
• Only amiodarone and dofetilide have not been shown to adversely affect survival 4

During active KCl replacement:

• Temporarily discontinue aldosterone antagonists and potassium-sparing diuretics to avoid overcorrection 4
• Consider dose reduction of ACE inhibitors/ARBs as combination increases hyperkalemia risk 4

Monitoring Protocol

• Early phase (2-7 days): Check K+ before each additional dose if needed; otherwise recheck at 3-7 days 4
• Maintenance: Monitor at 1-2 weeks after dose adjustment, at 3 months, then every 6 months 4
• Always correct hypomagnesemia concurrently 4

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Hypernatremia Management

For hypernatremia, determine volume status (hypovolemic, euvolemic, or hypervolemic), then correct slowly at no more than 0.4 mmol/L/h (10 mmol/L per 24 hours) using hypotonic fluids for severe cases or addressing underlying cause for mild cases, with faster correction only if hypernatremia developed acutely.

Severity Classification

• Mild hypernatremia: Na+ 146-149 mEq/L 7
• Moderate hypernatremia: Na+ 150-159 mEq/L 7
• Severe/threatening hypernatremia: Na+ ≥160 mEq/L 7

Clinical Presentation

• Symptoms: vomiting, cerebral seizures, somnolence, coma 8
• Often caused by dehydration from impaired thirst mechanism or lack of water access 9

Classification by Volume Status and Pathogenesis

Hypovolemic Hypernatremia (Most Common):

• Renal losses: diuretics, osmotic diuresis, post-obstructive diuresis
• Extrarenal losses: GI losses (vomiting, diarrhea), skin losses (burns, excessive sweating)
• Treatment: Isotonic saline (0.9% NaCl) initially to restore volume 8
• Once hemodynamically stable, switch to hypotonic fluids 9

Euvolemic Hypernatremia:

• Diabetes insipidus (central or nephrogenic):
  • Central DI: traumatic, vascular, or infectious causes 7
  • Nephrogenic DI: lithium, hypokalemia 7
• Treatment: Address underlying cause and replace free water deficit 9, 7

Hypervolemic Hypernatremia:

• Acute: Excessive sodium intake (hypertonic NaCl, NaHCO3 solutions) 7
• Chronic: Primary hyperaldosteronism 7
• Treatment: Address underlying cause, consider diuretics 7

Correction Rate: Critical Safety Consideration

The rate of correction depends on acuity of development:

Acute Hypernatremia (Developed Over Hours):

• Rapid correction improves prognosis by preventing cellular dehydration 7
• Can correct more quickly than chronic hypernatremia 7

Chronic Hypernatremia (Developed Over Days):

• Maximum correction rate: 0.4 mmol/L/h (approximately 10 mmol/L per 24 hours) 7
• Slower correction prevents cerebral edema 7
• Brain cells adapt to chronic hypernatremia by accumulating organic osmolytes; rapid correction causes water influx and cerebral edema 10

Treatment Approach

Mild Hypernatremia (Na+ 146-149 mEq/L):

• Often caused by dehydration 9
• Increase oral water intake if patient can drink 9
• Address underlying cause 9

Moderate to Severe Hypernatremia (Na+ ≥150 mEq/L):

Step 1: Calculate free water deficit:

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

Step 2: Choose appropriate fluid:

• Hypotonic fluids required when sodium severely elevated, patient symptomatic, or IV fluids needed 9
• Options: 0.45% NaCl, 5% dextrose in water (D5W), or 0.2% NaCl 9
• For hypovolemic patients: start with isotonic saline until hemodynamically stable 8

Step 3: Monitor closely:

• Check serum sodium every 2-4 hours initially 7
• Adjust fluid rate to maintain correction rate ≤10 mmol/L per 24 hours for chronic hypernatremia 7
• Use calculators to guide fluid replacement to avoid overly rapid correction 9

Initial Laboratory Diagnostics

• Serum electrolytes 8
• Serum glucose 8
• Serum and urine osmolarity 8
• Urine sodium 8
• Assess volume status clinically 8

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Hyponatremia Management

For hyponatremia, classify by volume status (hypovolemic, euvolemic, or hypervolemic) and symptom severity, then treat severely symptomatic cases with hypertonic saline boluses to increase sodium by 4-6 mEq/L within 1-2 hours (but <10 mEq/L in 24 hours), while managing mild cases by treating underlying cause and restricting free water.

Severity Classification

• Mild hyponatremia: Na+ 130-134 mEq/L 10, 9
• Moderate hyponatremia: Na+ 125-129 mEq/L 10, 9
• Severe hyponatremia: Na+ <125 mEq/L 10, 9

Symptom Classification (More Important Than Absolute Sodium Level)

Mild Symptoms:

• Nausea, vomiting, weakness, headache, mild neurocognitive deficits 9
• Chronic mild hyponatremia associated with cognitive impairment, gait disturbances, increased falls and fractures 10

Severe Symptoms (Medical Emergency):

• Delirium, confusion, impaired consciousness, ataxia, seizures, coma 9
• Somnolence, obtundation, cardiorespiratory distress 10
• Requires immediate treatment with hypertonic saline 10

Classification by Volume Status

Hypovolemic Hyponatremia:

• Treatment: Isotonic saline (0.9% NaCl) infusions 9, 8
• Restore volume first 9

Euvolemic Hyponatremia:

• Most commonly SIADH (syndrome of inappropriate antidiuresis) 10
• Other causes: medications (neurotropic drugs), excessive free water intake during exercise 8
• Treatment options:
  • Free water restriction (first-line) 9
  • Salt tablets 9
  • Urea (effective but poor palatability, gastric intolerance) 10
  • Vaptans (IV or oral; risk of overly rapid correction and increased thirst) 10, 9

Hypervolemic Hyponatremia:

• Underlying causes: heart failure, cirrhosis 10, 9
• Treatment: Manage underlying condition and restrict free water 9
• Vaptans can be effective in heart failure patients 10

Treatment of Severely Symptomatic Hyponatremia (Medical Emergency)

US and European guidelines recommend:

• 3% hypertonic saline bolus to increase serum sodium by 4-6 mEq/L within 1-2 hours 10
• Maximum correction limit: 10 mEq/L within first 24 hours 10
• Goal: reverse hyponatremic encephalopathy 10

Critical warning: Overly rapid correction of chronic hyponatremia causes osmotic demyelination syndrome (ODS), a rare but severe neurological condition resulting in parkinsonism, quadriparesis, or death 10

Correction rate limits to prevent ODS:

• <10 mmol/L increase within first 24 hours 8
• <18 mmol/L increase within first 48 hours 8

Practical Treatment Algorithm

Step 1: Assess Symptom Severity

• Severely symptomatic (seizures, coma, somnolence, obtundation, cardiorespiratory distress): Immediate hypertonic saline 10
• Mildly symptomatic or asymptomatic: Treat based on volume status 9

Step 2: Determine Volume Status

• Hypovolemic: Isotonic saline 9, 8
• Euvolemic: Free water restriction, consider vaptans or urea for SIADH 10, 9
• Hypervolemic: Treat underlying cause (heart failure, cirrhosis), restrict free water 9

Step 3: Monitor Closely

• Check serum sodium every 2-4 hours during active correction 10
• Use calculators to guide fluid replacement to avoid overly rapid correction 9
• Adjust treatment if correction rate exceeds limits 10

Step 4: Identify and Treat Underlying Cause

• Common causes: medications (diuretics, SSRIs, carbamazepine), excessive alcohol, very low-salt diets, excessive free water intake during exercise 9
• Treatment should not be delayed while diagnosis pursued in severely symptomatic patients 9

Initial Laboratory Diagnostics

• Serum electrolytes 8
• Serum glucose 8
• Serum and urine osmolarity 8
• Urine sodium 8
• Clinical volume status assessment 8

Common Pitfalls

• Failing to recognize severely symptomatic hyponatremia as medical emergency 10
• Correcting chronic hyponatremia too rapidly (>10 mEq/L in 24 hours) causing osmotic demyelination 10, 8
• Not monitoring sodium levels frequently enough during correction 10
• Treating based solely on sodium level rather than symptom severity 10, 9