Overview
Definition:
Neonatal hyperkalemia is defined as a serum potassium concentration greater than 6.5 mEq/L in a neonate
It is a potentially life-threatening condition characterized by cardiac arrhythmias and neuromuscular dysfunction.
Epidemiology:
Hyperkalemia is a common electrolyte abnormality in critically ill neonates, with reported incidence rates varying from 1-10% in NICU populations
It is more prevalent in premature infants, infants with congenital anomalies, and those with renal insufficiency.
Clinical Significance:
Severe hyperkalemia can lead to life-threatening cardiac arrhythmias, including bradycardia, ventricular fibrillation, and asystole, which are leading causes of mortality in neonates
Prompt recognition and management are crucial for preventing cardiovascular collapse and improving outcomes.
Causes In Neonates
Prematurity And Renal Immaturity:
Immature renal function in preterm neonates leads to reduced potassium excretion.
Increased Potassium Intake:
Administration of potassium-containing intravenous fluids, incorrect formula preparation, or blood transfusions (especially stored blood).
Decreased Potassium Excretion:
Renal failure (oliguria/anuria), congenital adrenal hyperplasia, drugs affecting potassium excretion (e.g., ACE inhibitors, spironolactone), and certain metabolic disorders.
Cellular Shift Of Potassium:
Metabolic acidosis, tissue damage (hemolysis, rhabdomyolysis), and certain drugs (e.g., succinylcholine).
Ecg Changes
Early Changes:
Peaked T waves: Typically the earliest sign, appearing as narrow, tall, tented T waves, especially in precordial leads
Hyperacute T waves can occur in severe hyperkalemia.
Progressive Changes:
Prolongation of PR interval: Indicating impaired AV nodal conduction
Widening of QRS complex: Reflecting impaired ventricular conduction, which can lead to bundle branch blocks or complete heart block.
Severe Changes:
Flattening of P waves: As hyperkalemia worsens, atrial conduction is impaired.
Terminal Changes:
Sine wave pattern: A smooth, undulating waveform that merges the QRS and T waves, preceding ventricular fibrillation or asystole
This is a grave sign.
Diagnostic Approach
History Taking:
Detailed history of maternal conditions (e.g., diabetes), gestational age, delivery complications, fluid and medication administration (especially potassium-containing fluids, blood products), presence of oliguria or anuria, and any signs of tissue injury or acidosis.
Physical Examination:
Assess vital signs (heart rate, blood pressure), observe for signs of respiratory distress, assess hydration status, check for edema, and perform a thorough abdominal examination for distension or signs of bowel issues
Auscultate heart sounds for murmurs or arrhythmias.
Laboratory Investigations:
Serum electrolytes (potassium, sodium, chloride, bicarbonate), blood urea nitrogen (BUN), creatinine, blood gas analysis (pH, pCO2, HCO3) to assess for acidosis, glucose levels, and complete blood count
Consider lactate levels if tissue hypoxia is suspected.
Interpretation Of Ecg:
Serial ECG monitoring is crucial
Identify the characteristic changes: peaked T waves, prolonged PR, widened QRS, flattened P waves, and sine wave pattern
Note the correlation between serum potassium levels and ECG severity.
Management
Stabilization Of Cardiac Membrane:
Calcium chloride (10% solution) IV infusion: 100-200 mg/kg over 5-10 minutes
Repeat if ECG changes persist or worsen
This directly antagonizes the effects of potassium on the cardiac muscle, but does not lower serum potassium.
Shift Of Potassium Intracellularly:
Insulin and glucose infusion: Regular insulin 0.1 unit/kg IV bolus followed by 0.1 unit/kg/hr infusion with concurrent glucose infusion (e.g., 10% dextrose at 2-4 ml/kg/hr) to prevent hypoglycemia
Aim to increase glucose to 150-200 mg/dL
Beta-agonists (e.g., albuterol nebulization): 0.1-0.2 mg/kg (max 5 mg) of albuterol in 3-5 ml normal saline via nebulizer
Sodium bicarbonate IV: 1-2 mEq/kg over 5-10 minutes, especially if severe metabolic acidosis is present.
Removal Of Potassium From Body:
Diuretics: Furosemide (Lasix) 1-2 mg/kg IV if renal function is adequate and the patient is not volume overloaded
Cation-exchange resins (e.g., sodium polystyrene sulfonate - Kayexalate): Oral or rectal administration, binds potassium in the GI tract
Use with caution due to potential for bowel necrosis, especially in neonates with ileus.
Supportive Care And Monitoring:
Continuous ECG monitoring
Strict fluid balance and input/output charting
Management of underlying cause (e.g., treating sepsis, correcting acidosis)
Discontinue potassium-containing fluids
Dialysis: Hemodialysis or peritoneal dialysis may be necessary for severe, refractory hyperkalemia or if renal failure is significant.
Key Points
Exam Focus:
Recognize ECG changes of hyperkalemia in neonates (peaked T waves, widening QRS)
Understand the tiered approach to management: membrane stabilization, intracellular shift, and potassium removal.
Clinical Pearls:
Always check serum potassium and ECG in any neonate with unexplained bradycardia, arrhythmia, or oliguria
Rapid correction of acidosis can unmask hypokalemia, but uncorrected acidosis contributes to hyperkalemia.
Common Mistakes:
Over-reliance on only one treatment modality
Failure to monitor ECG continuously
Delaying aggressive treatment in the face of significant ECG changes
Inadequate management of underlying causes like acidosis or renal failure.