Baby of SV was one of twins conceived by in vitro fertilization, delivered at 27 to 28 weeks gestation by Caesarean section following onset of preterm labor. The pregnancy was complicated by gestational diabetes mellitus well controlled with low doses of insulin. The male infant weighed 830g at birth. The infant had mild respiratory distress, that was treated with minimal supplemental oxygen for two days. Apnea of prematurity was treated with aminophylline. Antibiotics were started and stopped in 5 days, following negative sepsis screen. Feeds of expressed breastmilk by nasogastric tube were started on day 4 and gradually advanced. During this time, IV fluids were given to administer 4 to 6 mEq/kg/day of sodium and 2 to 3 mEq/kg/day of potassium. Electrolytes were normal in the first week. On the 9th day of life, the infant developed feeding intolerance with abdominal distenion and bilious NG aspirate. Complete blood counts, C-reactive protein were within normal limits. Serum electrolytes showed serum No of 125 mEq/l, and serum K of 3.1 mEq/l. The baby was hemodynamically stable with SpO2 96% in room air. Urine output was about 3 to 5 cc/kg/hour. X-ray showed dilated bowel loops. Pending cultures, antibiotics were restarted. Sodium and potassium supplementation were given.

At Birth

Although sepsis screen was negative, the baby continued to have large volumes of nasogastric bilious aspirate for 3 days which was replaced with Ringer Lactate. Serum potassium varied from 1.9 - 4 mEq/l over the next 3 weeks. Hypokalemia persisted even after decrease in nasogastric aspirate. Potassium supplements were given
at 4 to 6 mEq/kg/day, initially parenterally and then orally.

ECG was continuously monitored. Serum sodium normalized in 2 weeks. The baby had intermittent hypoglycemia that necessitated administration of glucose at 8 to 10 mg/kg/min. Blood urea, serum bicarbonate, magnesium, calcium and creatinine were repeatedly within normal limits. Sepsis screen was negative. With supplementation of potassium, the ileus gradually resolved and the baby tolerated feeds. The baby was discharged on potassium supplements, which was stopped a week after discharge. The baby is now thriving well.

At Discharge

Hypokalemia results in paralytic ileus and feeding intolerance. However, the etiology of hypokalemia in a baby who received normal maintenance requirements of potassium, and who did not have vomiting, diarrhea, alkalosis or diuretic therapy is unclear. A combination of loss of K-rich gastric fluid, possible increase in beta adrenergic activity due to hypoglycemia, increased insulin sensitivity and renal tubular immaturity resulting in mild acidosis, polyuria and salt wasting, could have contributed to the hypokalemia. Serum electrolytes should be monitored and dyselectrolytemia treated carefully in extreme preterm infants. Dyselectrolytemia, primarily due to renal tubular immaturity, can result in feed intolerance or failure to thrive. A high index of suspicion is needed. Also, one needs to remember that all ileus in the NICU is not sepsis!

Dr Deepa Hariharan MBBS, A.B
(Paeds/Neo) (USA),FAAP
Dr Ezhilarasan md(Paeds),DM(Neo)
-Neonatologists, GG Hospital.