Severe Cow’s Milk Allergy Presenting With Life-Threatening Metabolic Acidosis in an Extremely Preterm Infant: A Case Report

TL;DR

An extremely preterm infant developed life-threatening metabolic acidosis due to cow's milk allergy, which improved dramatically after switching to a special formula.

Contribution

Highlights severe cow's milk allergy as a rare but critical cause of metabolic acidosis in extremely preterm infants.

Findings

Switching to an amino acid-based formula resolved life-threatening metabolic acidosis in a preterm infant.

The infant showed rapid clinical improvement and significant weight gain after dietary change.

Cow's milk allergy should be considered in preterm infants with unexplained metabolic acidosis and feeding intolerance.

Abstract

Cow's milk allergy (CMA) is a common food allergy in infancy, but its diagnosis in preterm infants remains challenging due to nonspecific symptoms that often mimic complications of prematurity. Early recognition is crucial to prevent significant morbidity in this vulnerable population. We present a case of a male infant born at 27 weeks and four days of gestation with a birth weight of 960 grams. His clinical course was complicated by persistent feeding intolerance, respiratory symptoms, severe metabolic acidosis, and profound growth failure despite multiple interventions for suspected sepsis and necrotizing enterocolitis. On day 45 of life, he developed life-threatening metabolic acidosis (pH: 6.815, bicarbonate: 3.9 mmol/L, base excess: -30.4 mmol/L) with borderline hyperammonemia, initially raising suspicion for an inborn error of metabolism, which was ruled out by normal tandem mass spectrometry.

The infant was initially fed exclusively with expressed breast milk (EBM) from birth. The mother had a normal diet including dairy products throughout the breastfeeding period, providing indirect exposure to cow's milk proteins through breast milk. On day 52 of life, a diagnosis of CMA was considered due to recurrent severe abdominal symptoms and failure to respond to conventional treatments. The infant was switched from EBM to an extensively hydrolyzed, amino acid-based formula (Neocate). Following the dietary change, there was a rapid and dramatic clinical improvement. The metabolic acidosis resolved, feeding intolerance decreased, and the infant demonstrated excellent weight gain (260 grams in eight days). He was successfully discharged home on day 96 of life with a discharge weight of 1.785 kg. This case highlights that severe CMA can present with life-threatening metabolic acidosis in extremely preterm infants, emphasizing the need for high clinical suspicion and early consideration of dietary elimination as both diagnostic and therapeutic intervention. Healthcare providers should consider CMA earlier in the differential diagnosis when standard treatments for common neonatal complications fail to provide adequate clinical improvement.

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