Potassium homeostatsis is a crucial aspect of the fluid and electrolyte balance in extremely low birth weight (ELBW) infants. These neonates often experience hyperkalemia during the first few days of life(1). There is scant literature concerning life threatening cardiac arrhythmias due to hyperkalemia in extremely premature newborn infants(2). We report an ELBW neonate who developed ventricular tachycardia following hyperkalemia.

Baby girl R was born at 28 weeks gestation following preterm labour, with no perinatal asphyxia. She weighed 1000 grams at birth. She was ventilated for hyaline membrane disease. The clinical course was complicated by pulmonary air leaks, hypotension, metabolic acidosis and sclerema, but all these complications settled by the third day of life. The cranial ultrasound was normal.

The baby had normal serum potassium for the first 3 days of life, being 3.7 mEq/L, 5.1 mEq/L and 5.6 mEq/L respectively. The corresponding creatinine values were 0.5 mg/dL, 0.6 mg/dL and 0.8 mg/dL. However, on day 4, the serum potassium was reported to be 9.6 mEq/L. The corresponding serum sodium was 143 mEq/L, blood urea was 40 mg/dL and serum creatinine was 0.7 mg/dL. The arterial blood gases showed pH 7.32, bicarbonate 18 mEq/L and base excess-6.

She developed an irregularity of the cardiac rhythm and a recurrence of hypotension. The ECG showed evidence of ventricular tachycardia. The baby was administered an intravenous calcium gluconate bolus, sodium bicarbonate and dextrose insulin infusions as per the standard management protocol for hyperkalemia. The ventricular tachycardia however persisted. The baby was given an intravenous bolus (1mg/kg) of lignocaine (XylocardTM) followed by a maintenance infusion at 40 mcg/kg/min. This resulted in a return to normal sinus rhythm. There was no evidence of WPW syndrome and aberrant conduction on the ECG after recovery. Xylocard was omitted after 8 hours of infusion. The baby had no recurrence of ventricular tachycardia. On day 5, the serum potassium was 5.4 mEq/L, and it remained in the normal range thereafter.

A search for the secondary causes of hyperkalemia did not yield any contributory result. The initial sickness of the child had settled by day 3. Septic screen and blood culture, done to rule out a fresh episode of sepsis, were negative. The urine output, urine examination and ultrasound examination of the kidneys and adrenals were all normal. Major hemolysis was ruled out as the hemoglobin did not drop significantly (19.4 g/dL on day 1 to 17.1 g/dL on day 4), reticulocyte count was 2.3%, the plasma and urine hemoglobin were negative and erythrocyte morphology was normal. There was no soft tissue injury. No potassium had been adminsitered in the intravenous fluids during this period, because of high normal values of serum potassium on days 2 and 3. She was not receiving any drugs in the form of potassium salts. Her external genitalia were normal. Hence she was diagnosed to have severe hyperkalemia due to prematurity, and hyperkalemia induced ventricular tachycardia.

A week later she acquired a fresh nosocomial septicemia and expired.

Hyperkalemia (serum potassium level >6 mEq/L) occurs in approximately 30% of all newborns born weighing less than 1000 g(3), even in the absence of renal failure, due to reasons that are peculiar to this gestational age group. This non-oliguric hyperkalemia usually presents within the first 72 hours of life and is the result of immature distal tubular function and a state of relative hypoaldosteronism with a compromized ability to excrete potassium(3). It may also be due, in part, to a shift of potassium from the intracellular space to extracellular space associated with a decrease in Na+-K+-ATPase activity(4). In sick newborn infants with renal dysfunction, hyperkalemia may occur, particularly when combined with metabolic acidosis and a hypercatabolkic state(5). Rarer causes of hyperkalemia include hypoadrenal crises, massive hemolysis, tissue damage or excessive administration of potassium as drugs or intra-venous fluids.

In our patient, hyperkalemia can be attributed to the immaturity of the renal tubules and the Na+-K+-ATPase in absence of these causes. The baby presented with hyperkalemia on the fourth day of life, unlike previous reports that describe the onset of non-oliguric hyperkalemia within the first three days.

Hyperkalemia produces a sequence of ECG changes that may lead to life threatening cardiac arrhythmias, if left untreated. In neonates, serum potassium values greater than 6.7 mEq/L have been shown to be associated with ECG changes(3). In one study, 8 of 18 infants weighing less than 1000 grams developed non-oliguric hyperkalemia (serum potassium > 6.8 mEq/L) during the first 3 days of life. All infants with hyperkalemia had electrographic changes, cardiac dysrhythmias or both(3). In another study, 5 of 43 consecutive infants born at less than 28 weeks gestation, with plasma potassium greater than 7 mEq/L, developed cardiac arrhythmias and 4 died of this complication(6).

We are reporting this case to highlight the fact that ELBW babies may develop severe hyperkalemia and life-threatening arrhythmias, solely due to the immaturity of their physiology. The electrolyte disturbances may not be strictly limited to the first 72 hours of life. Serum electrolytes should be regularly monitored in such babies. Prompt treatment may be life saving.

Daljit Singh,
Sourabh Dutta,
Anil Narnag,
Division of Neonatology,
Department of Pediatrics,
PGIMER, Chandigarh 160 012, India.

1. Kilbride HW, Cater G, Warady BA. Early onset hyperkalemia in extremely low birth weight infants. J Perinatol 1988; 8: 211-214.

2. Maclaine Pont J, Hack WW, Sobotka-Plojhar M, Ekkelkamp S. Two newborn infants with severe arrhythmia caused by hyperkalemia. Tijdschr Kindergeneeskd 1987; 55: 28-32.

3. Gruskay J, Costarino AT, Polin RA, Baumgart S. Nonoliguric hyperkalemia in the premature infant weighing less than 1000 grams. J Pediatr 1988; 113: 381-286.

4. Stefano JL, Norman Me, Morales MC, Goplerud JM, Mishra OP, Delivoria-Papadopoulos M. Decreased erythrocyte Na+-K+-ATPase activity associated with cellular potassium loss in extremely low birth weight infants with nonoliguric hyperkalemia. J Pediatr 1993; 122: 276-284.

5. Fukuda Y, Kojima T, Ono A, Matsuzaki S, Iwase S, Kobayashi Y. Factors causing hyperkalemia in premature infants. Am J Perinatol 1989; 6: 76-79.

6. Leslie GI, Carman G, Arnold JD. Early neonatal hyperkalaemia in the extremely premature newborn infant. J Pediatr Child Health 1990; 26: 58-61.