Potassium is a positively charged electrolyte that plays a fundamental role in regulating cellular function, particularly in nerve impulse transmission and muscle contraction. The body maintains a precise balance of potassium, with the majority stored inside the cells and only a small fraction circulating in the bloodstream. When the serum potassium concentration rises significantly above the normal range—typically defined as above 6.0 to 6.5 mmol/L in newborns—the condition is termed hyperkalemia. This electrolyte imbalance in neonates can disrupt the electrical stability of the heart muscle.
Hyperkalemia Unique to Premature Infants
The most frequently observed cause of high potassium in the neonatal intensive care unit (NICU) is Non-Oliguric Hyperkalemia of Prematurity (NOHP). This condition is seen almost exclusively in extremely premature infants, particularly those born before 28 weeks of gestation or with very low birth weight (VLBW) below 1500 grams. NOHP develops early, typically peaking within the first 24 to 72 hours of life, and is characterized by elevated potassium despite the infant producing a normal amount of urine.
The primary mechanism for NOHP involves a functional immaturity of the cell membranes and the renal system. Preterm infants often have a reduced ability to shift potassium from the bloodstream back into the cells, a process normally managed by the sodium-potassium pump (Na+/K+-ATPase). This temporary insufficiency leads to potassium accumulating in the extracellular fluid. Furthermore, the immature kidneys are not yet capable of adequately excreting the potassium load, even when urine output is preserved.
This transient form of hyperkalemia is considered a functional rather than a pathological issue, meaning it arises from the developmental stage of the organs, not from a primary disease. The condition is often self-limiting, resolving as the infant matures and the kidneys begin to function more effectively. Despite its transient nature, NOHP poses a risk for cardiac arrhythmias, requiring close monitoring of electrolyte balance during the initial days.
Impaired Kidney Function and Excretion
A second major category of hyperkalemia causes centers on a failure of the kidneys to eliminate potassium from the body. The kidneys are normally responsible for excreting about 90% of the body’s potassium, making any impairment a direct cause of accumulation. Acute kidney injury (AKI) is common in newborns who have experienced significant distress, such as severe birth asphyxia or prolonged episodes of low oxygen, which can damage renal tissue.
Chronic kidney disease or congenital anomalies of the renal system can also result in inadequate potassium excretion. When kidney function is compromised, toxins and waste products, including potassium, build up in the blood. This failure of elimination is distinct from the functional immaturity seen in NOHP, representing a true structural or pathological defect.
Specific endocrine disorders further contribute to impaired excretion by interfering with the hormones that regulate renal potassium handling. Congenital Adrenal Hyperplasia (CAH), for example, can lead to a deficiency in the hormone aldosterone, which signals the kidneys to excrete potassium. Without this hormonal instruction, the kidneys retain potassium, causing high serum levels alongside low sodium levels.
Cellular Release and External Factors
Some cases of high potassium occur not because of an inability to excrete it, but because a massive amount is suddenly released from the body’s cells or introduced from an external source. Potassium is the main ion inside cells, so widespread cell damage causes it to spill rapidly into the bloodstream. Conditions involving significant tissue breakdown or necrosis, such as severe birth trauma, massive internal bleeding like an intraventricular hemorrhage, or extensive injury from oxygen deprivation, lead to this type of release.
A process called hemolysis, the rapid breakdown of red blood cells, is another source of sudden potassium release because red blood cells contain a high concentration of the electrolyte. Hemolysis can occur due to incompatible blood transfusions or certain blood disorders, overwhelming the body’s capacity to manage the influx. Metabolic acidosis, a condition where the body’s pH drops, causes a transcellular shift, forcing potassium out of the cells and into the circulation in exchange for hydrogen ions.
The introduction of excessive potassium from outside the body, known as iatrogenic hyperkalemia, represents an entirely different mechanism. This can happen if an infant receives intravenous (IV) fluids or total parenteral nutrition (TPN) with an inappropriately high concentration of potassium. Similarly, blood transfusions, especially if the blood is not fresh, can contain potassium that has leaked from the stored red blood cells, resulting in a sudden external potassium load.
Recognizing and Confirming High Potassium Levels
Identifying hyperkalemia in a newborn can be challenging because the initial symptoms are often subtle and non-specific. Affected infants may present with lethargy, poor feeding, or an overall appearance of being unwell. The most concerning signs relate to the heart, as high potassium levels interfere with the heart’s electrical system, potentially leading to slow heart rate or cardiac arrest.
The definitive diagnosis relies on a blood test to measure the serum potassium level. Because blood samples taken from a heel prick can sometimes rupture red blood cells and create a falsely elevated reading (pseudohyperkalemia), a high result must be confirmed with a non-hemolyzed sample drawn from a vein or artery. Once hyperkalemia is suspected or confirmed, an electrocardiogram (EKG or ECG) is immediately performed to assess the danger to the heart.
Specific changes on the EKG, such as tall, narrow, and “peaked” T waves or a widening of the QRS complex, indicate that the high potassium is actively affecting the heart muscle. Monitoring these electrical changes is the most reliable indicator of severity and urgency for intervention. The presence of these cardiac signs necessitates immediate attention, even if the infant appears outwardly stable.