Increased potassium intake. From excessive amount in IV fluids, excessive oral supplementation (as in excess KCL supplementation in a bronchopulmonary dysplasia/chronic lung disease infant), or medications containing potassium. Potassium supplements usually are not necessary on the first day of life and often are not necessary until day 3, with the typical requirement of 1–2 mEq/kg/d. This is rare cause because the kidneys usually excrete any excess potassium.
Pathologic hemolysis of RBCs. May be secondary to intraventricular hemorrhage, use of a hypotonic glucose solution (<4.7% dextrose), sepsis (most commonly, Pseudomonas), intravascular hemolysis, cephalohematoma, bleeding, asphyxia, or Rh incompatibility.
Tissue necrosis and breakdown. In certain disease states, such as necrotizing enterocolitis (NEC), tissue necrosis can occur and hyperkalemia may result. Trauma and severe hypothermia can cause rhabdomyolysis.
Renal failure/insufficiency. Impaired kidney function can lead to hyperkalemia. Oliguria can cause decreased potassium clearance and hyperkalemia.
Immaturity-related nonoliguric hyperkalemia (NOHK). Occurs in up to 50% of extremely low birthweight infants and is defined as a potassium level >6.5 mEq/L in the absence of acute renal failure/acute kidney injury or a serum potassium ≥7 mEq/L during the first 72 hours of life with urinary output ≥1 mL/kg/h. This occurs without potassium intake or oliguria. It can result from a shift of potassium from intracellular to extracellular space, immature renal tubular and glomerular functions, and a decreased response to aldosterone. Hyperkalemia is often associated with hyperglycemia as a result of insulin resistance and intracellular energy failure (“hyperglycemia-hyperkalemia syndrome”).
Metabolic acidosis. Causes potassium to move out of cells, resulting in hyperkalemia. For every 0.1-unit decrease in pH, the serum potassium increases ∽0.3–1.3 mEq/L. Respiratory acidosis rarely causes significant hyperkalemia.
Dehydration. Causes hyperkalemia. Volume depletion and congestive heart failure can cause renal hypoperfusion and therefore hyperkalemia.
Medications containing potassium. May elevate the serum potassium level. Digoxin therapy can lead to hyperkalemia secondary to redistribution of potassium. K+-sparing diuretics cause decreased potassium losses. Both propranolol and phenylephrine are associated with hyperkalemia. High glucose load can lead to hyperkalemia secondary to increases in plasma osmolality. Other medications, including tromethamine, indomethacin, angiotensin-converting enzyme inhibitors, β-blockers, heparin, trimethoprim, captopril, and nonsteroidal anti-inflammatory drugs are associated with hyperkalemia.
Adrenal insufficiency. Seen in congenital adrenal hyperplasia and bilateral adrenal hemorrhage. In salt-losing congenital adrenal hyperplasia, infants have low serum sodium, chloride, and glucose; elevated levels of potassium; and hypotension. In bilateral adrenal hemorrhage, anemia, thrombocytopenia, and jaundice are seen, and bilateral adrenal masses are palpable. Renal tubular hyperkalemia/hyperkalemic distal renal tubular acidosis type IV occurs secondary to hypoaldosteronism. Infants present with metabolic acidosis and hyperkalemia. It is seen in adrenal disorders (hypoaldosteronism, congenital adrenal hyperplasia) and obstructive uropathy, reduced renal mass, renal reflux, urinary tract infection, and pseudohypoaldosteronism.
Decreased insulin levels. Associated with hyperkalemia. Insulin drives potassium into cells; insulin deficiency can cause hyperkalemia.
Transfusion-induced hyperkalemia. Irradiation accelerates the leakage of potassium out of stored RBCs, which can induce the risk of transfusion-induced arrhythmias from hyperkalemia. Washing of irradiated RBCs reduces potassium and lactate loads. Exchange transfusion can also be a cause.
Hyperosmolality. Caused by inappropriately diluted formula/hyperosmolar amino acid solution/glucose infusions.