Neonatal Hyperkalemia

Neonatal Electrolyte Disorders Introduction Definition & Epidemiology Pathophysiology & Etiology Diagnosis & Clinical Features Management Complications & Prevention

Neonatal Hyperkalemia

Neonatal hyperkalemia is defined as serum potassium level >5.5 mEq/L in term infants and >6.0 mEq/L in preterm infants. Non-oliguric hyperkalemia of prematurity (NOHP) is a distinct entity occurring in extremely premature infants.

Key Points

• Critical threshold: Severe hyperkalemia >7.0 mEq/L
• Higher risk in extremely low birth weight infants
• Life-threatening cardiac complications
• Requires immediate recognition and treatment
• Common in acute kidney injury

Definition & Epidemiology

Classification

• Term infants:
  • Mild: 5.6-6.0 mEq/L
  • Moderate: 6.1-7.0 mEq/L
  • Severe: >7.0 mEq/L
• Preterm infants:
  • Mild: 6.1-6.5 mEq/L
  • Moderate: 6.6-7.5 mEq/L
  • Severe: >7.5 mEq/L

Epidemiology

• Prevalence:
  • 30-40% in extremely low birth weight infants
  • 10-15% in very low birth weight infants
  • 5-10% in term infants
• Risk Factors:
  • Extreme prematurity (<28 weeks)
  • Birth weight <1000g
  • Acute kidney injury
  • Perinatal asphyxia
  • Sepsis
  • Major surgery

Pathophysiology & Etiology

Mechanisms

• Non-oliguric hyperkalemia of prematurity:
  • Immature Na+/K+-ATPase function
  • Shift from intracellular to extracellular space
  • Limited renal K+ excretion
• Other mechanisms:
  • Decreased K+ excretion:
    • Acute kidney injury
    • Oliguria/anuria
    • Medications affecting K+ excretion
  • Increased K+ load:
    • Hemolysis
    • Tissue breakdown
    • Excessive K+ supplementation

Common Causes

• Primary disorders:
  • NOHP in extremely premature infants
  • Congenital adrenal hyperplasia
  • Pseudohypoaldosteronism
• Secondary disorders:
  • Acute kidney injury
  • Birth asphyxia
  • Sepsis
  • Major tissue trauma
  • Massive transfusion

Diagnosis & Clinical Features

Clinical Manifestations

• Cardiac manifestations:
  • Bradycardia
  • Arrhythmias
  • Cardiac arrest
• Neuromuscular:
  • Muscle weakness
  • Hypotonia
  • Respiratory compromise
• ECG Changes (progressive):
  • Peaked T waves
  • Shortened QT interval
  • Prolonged PR interval
  • Widened QRS complex
  • Loss of P waves
  • Sine wave pattern

Diagnostic Workup

• Laboratory evaluation:
  • Serial serum K+ levels
  • Complete metabolic panel
  • Blood gases
  • Calcium levels
  • Creatinine kinase
  • Complete blood count
• Cardiac assessment:
  • Continuous ECG monitoring
  • 12-lead ECG
  • Frequent vital signs

Management

Emergency Management

• Cardiac stabilization:
  • Calcium gluconate 10%: 0.5-1.0 mL/kg IV over 5-10 minutes
  • Repeat based on ECG changes
• Cellular shift interventions:
  • Insulin and glucose:
    • Regular insulin: 0.1 units/kg/hour
    • Glucose: 0.5 g/kg/hour
    • Monitor blood glucose q30min
  • Sodium bicarbonate:
    • 1-2 mEq/kg over 10-20 minutes
    • Only if metabolic acidosis present
  • Beta-2 agonists:
    • Albuterol nebulization
    • Consider in stable patients

Definitive Management

• K+ elimination:
  • Loop diuretics if adequate renal function
  • Ion exchange resins:
    • Sodium polystyrene sulfonate
    • Patiromer (newer agent)
  • Dialysis indications:
    • Refractory hyperkalemia
    • Severe acidosis
    • Oliguria/anuria

Preventive Measures

• Regular monitoring in high-risk infants
• Careful K+ supplementation
• Appropriate storage of packed RBCs
• Prevention of tissue breakdown

Complications & Prevention

Complications

• Immediate:
  • Life-threatening arrhythmias
  • Cardiac arrest
  • Respiratory failure
• Treatment-related:
  • Hypoglycemia from insulin therapy
  • Hypocalcemia
  • Volume overload
  • Rebound hyperkalemia

Monitoring

• Clinical monitoring:
  • Continuous cardiac monitoring
  • Frequent vital signs
  • Neurological status
  • Urine output
• Laboratory monitoring:
  • Serial K+ levels (q2-4h initially)
  • Blood glucose during insulin therapy
  • Calcium levels
  • Acid-base status

Prevention Strategies

• Risk identification:
  • Early recognition of high-risk infants
  • Regular monitoring
  • Prevention of triggering factors
• Prophylactic measures:
  • Careful K+ supplementation
  • Prevention of tissue breakdown
  • Appropriate blood product management

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