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Severe Cow's Milk Allergy Presenting With Life-Threatening Metabolic Acidosis in an Extremely Preterm Infant: A Case
Nasser Al Shafouri1, Mahmoud Khalid1, Ahmed Al Muqarshi1
1Pediatrics and Neonatology, Ibri Hospital, Ibri, OMN.
Insights
Cow's milk allergy (CMA) in preterm infants can mimic serious conditions, causing severe metabolic acidosis. Early diagnosis and dietary changes, such as switching to amino acid-based formula, are crucial for recovery.
Area of Science:
- Neonatology
- Pediatric Allergy
- Gastroenterology
Background:
- Cow's milk allergy (CMA) is a frequent cause of infant allergy.
- Diagnosis in preterm infants is challenging due to nonspecific symptoms resembling prematurity complications.
- Early recognition of CMA is vital to prevent severe morbidity in vulnerable preterm infants.
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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