What are the possible causes of elevated serum potassium in a 2‑month‑old infant?

Causes of Elevated Potassium in a 2-Month-Old Infant

In a 2-month-old baby, elevated potassium is most commonly caused by pseudohyperkalemia from hemolysis during blood draw, followed by true hyperkalemia from renal immaturity, acute kidney injury, or hemolysis from underlying disease.

Immediate Assessment: Rule Out Pseudohyperkalemia First

The single most important first step is to determine whether the hyperkalemia is real or artifactual, as pseudohyperkalemia accounts for the vast majority of elevated potassium results in healthy infants.

• In pediatric emergency department patients with hemolyzed samples showing hyperkalemia, 98% had normal potassium on repeat testing, meaning only 2% had true hyperkalemia 1
• Pseudohyperkalemia occurs when red blood cells rupture during or after blood collection, releasing intracellular potassium into the serum 1
• If the sample is hemolyzed and the infant has normal blood urea nitrogen and creatinine, repeat sampling is generally unnecessary unless clinical suspicion exists for true hyperkalemia 1
• Obtain a repeat sample using careful venipuncture technique (not heel stick) if the initial result is concerning and the sample quality is poor 1

True Hyperkalemia: Age-Specific Definitions

Use gestational age-corrected thresholds to avoid overdiagnosis:

• In term infants (≥37 weeks gestation): hyperkalemia is defined as potassium ≥6.0 mmol/L 2
• In preterm infants (<37 weeks gestation): hyperkalemia is defined as potassium >6.5 mmol/L 2
• These higher thresholds in preterm infants reflect physiologic differences in potassium handling during early postnatal adaptation 2

Common Causes of True Hyperkalemia in 2-Month-Old Infants

1. Non-Oliguric Hyperkalemia (Most Common in Preterm Infants)

• Non-oliguric hyperkalemia occurs in up to 50% of extremely low birth weight infants in the first week of life, though it can persist beyond this period 3
• This condition develops even without potassium intake and with normal urine output 4
• Mechanism: Transcellular shift of potassium from intracellular to extracellular space due to immature cellular Na-K-ATPase pump function 3
• Risk factors include: lack of antenatal corticosteroids, systemic acidosis, birth asphyxia, massive hematomas, hemolysis, and catabolic state 4
• Urine potassium is typically >20 mmol/L, indicating the kidneys are attempting to excrete potassium 4
• This form usually resolves spontaneously as renal function matures and diuresis begins 3

2. Oliguric Hyperkalemia from Acute Kidney Injury

• Acute kidney injury was identified in 43.6% of neonates with true hyperkalemia in a large 10-year study 2
• Characterized by oliguria (urine output <0.5 mL/kg/hour) and urine potassium <20 mmol/L 4
• Common causes in term infants: perinatal asphyxia, hypoxic-ischemic encephalopathy, sepsis 2
• Common causes in preterm infants: hypoxia, intraventricular hemorrhage, necrotizing enterocolitis 2
• Serum creatinine and urea are typically elevated 5

3. Hemolytic Anemia

• Massive hemolysis releases large amounts of intracellular potassium into the bloodstream 6
• Associated findings: low hemoglobin, elevated bilirubin, reticulocytosis, elevated lactate dehydrogenase 6
• Causes include: ABO/Rh incompatibility, G6PD deficiency, hereditary spherocytosis, sepsis-induced hemolysis 6
• A case report documented potassium of 9.8 mmol/L in a newborn with hemolytic anemia from placental abruption 6

4. Metabolic Acidosis

• Acidosis causes hydrogen ions to move into cells in exchange for potassium moving out, raising serum potassium 5
• Base excess significantly decreased in hyperkalemic preterm infants compared to normokalemic controls 5
• Common causes at 2 months: sepsis, dehydration from diarrhea, inborn errors of metabolism, renal tubular acidosis 5

5. Catabolic State and Tissue Breakdown

• Elevated creatine phosphokinase and decreased calorie intake were significantly associated with hyperkalemia in preterm infants 5
• Tissue breakdown from any cause (trauma, surgery, infection) releases intracellular potassium 5
• Inadequate calorie intake prevents anabolic processes that would drive potassium back into cells 5

6. Congenital Adrenal Hyperplasia (Salt-Wasting Form)

• Congenital adrenal hyperplasia was identified as one of the most common causes of hyperkalemia in term neonates 2
• Classic presentation: hyperkalemia, hyponatremia, hypoglycemia, and shock between 1-4 weeks of age (but can present later) 2
• Aldosterone deficiency causes renal sodium wasting and potassium retention 2
• This is a life-threatening emergency requiring immediate hydrocortisone and fludrocortisone 2

7. Sepsis and Systemic Infection

• Early-onset sepsis (including fungal sepsis) was confirmed in hyperkalemic neonates 6
• Inflammatory markers (CRP, leukocytosis) are typically elevated 6
• Sepsis causes hyperkalemia through multiple mechanisms: tissue breakdown, acidosis, acute kidney injury, and hemolysis 6

8. Excessive Potassium Intake (Iatrogenic)

• Inadvertent excessive potassium intake during parenteral nutrition can cause hyperkalemia 4
• In parenterally fed infants, serum electrolytes should be monitored daily for the first days of treatment 4
• Potassium supplementation should be deferred in extremely low birth weight infants during the oliguric phase 4

Clinical Manifestations Requiring Urgent Intervention

Hyperkalemia becomes immediately life-threatening when cardiac manifestations appear:

• Cardiac arrhythmias (most dangerous): peaked T waves, widened QRS, sine wave pattern, ventricular tachycardia, cardiac arrest 6, 5
• Five of 19 hyperkalemic preterm infants developed arrhythmias, with one death from cardiac arrest 5
• Severe hyperkalemia (>7 mmol/L) requires prompt intervention regardless of symptoms 4
• Neuromuscular symptoms: muscle weakness, hypotonia, depressed reflexes (less common in neonates) 7

Diagnostic Workup for True Hyperkalemia

Obtain the following tests simultaneously to identify the underlying cause:

• Repeat potassium measurement (non-hemolyzed sample) to confirm 1
• Complete blood count with differential (assess for hemolysis, infection) 6
• Comprehensive metabolic panel: sodium, calcium, glucose, creatinine, blood urea nitrogen 5
• Venous blood gas (assess for acidosis) 5
• Urinalysis and urine electrolytes (sodium, potassium, creatinine) 4
• Creatine phosphokinase (assess for tissue breakdown) 5
• If hyponatremia present: 17-hydroxyprogesterone, cortisol, aldosterone, renin (rule out congenital adrenal hyperplasia) 2
• Blood and urine cultures if sepsis suspected 6

Management Priorities

Treatment depends on severity and presence of ECG changes:

Severe Hyperkalemia (K >7 mmol/L) or ECG Changes

• Immediate cardiac stabilization: Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (or 0.5-1 mL/kg in infants) to protect the heart 6
• Shift potassium intracellularly: Insulin 0.1 units/kg IV with glucose 0.5 g/kg (D10W 5 mL/kg) over 30-60 minutes 6
• Remove potassium from the body: Sorbisterit enema (sodium polystyrene sulfonate) or exchange transfusion in extreme cases 6
• Continuous cardiac monitoring is mandatory 6

Moderate Hyperkalemia Without ECG Changes

• Identify and treat underlying cause (sepsis, dehydration, adrenal insufficiency) 2
• Avoid potassium intake in parenteral nutrition until levels normalize 4
• Ensure adequate urine output and renal function 4
• Monitor potassium levels every 4-6 hours until stable 4

Common Pitfalls to Avoid

• Do not treat pseudohyperkalemia: Repeating the sample with proper technique avoids unnecessary interventions 1
• Do not use adult potassium thresholds: Preterm infants tolerate higher potassium levels physiologically 2
• Do not overlook congenital adrenal hyperplasia: This diagnosis is easily missed but rapidly fatal if untreated 2
• Do not add potassium to IV fluids in the first 24-48 hours in extremely preterm infants: They are at high risk for non-oliguric hyperkalemia 4
• Do not assume oliguria means renal failure: Non-oliguric hyperkalemia is more common in preterm infants and has a different mechanism 4
• Do not delay exchange transfusion in severe cases: When hyperkalemia causes hemodynamic instability and ECG changes, exchange transfusion may be life-saving 6