Case Presentation: A 20-day-old female former full-term, appropriate for gestational age infant presented to the pediatrician’s office for her first checkup. She was born via uncomplicated vaginal delivery following a normal pregnancy and had normal newborn screening results. She was exclusively breastfed. She was found to be 27% below birth weight and was therefore urgently admitted to the hospital where initial labs showed metabolic acidosis, acute kidney injury, and hyperchloremia. The initial exam revealed an extremely malnourished, pale infant with yellow sclera and a sunken anterior fontanelle. She was noted to be alert without focal neurologic deficits. Capillary refill time was 2-3 seconds. Her exam was also remarkable for a protruding thoracic cage and xiphoid process. Lactation, speech therapy, and nutrition were consulted and weights were obtained pre- and post-breastfeeding, which showed minimal transfer of breastmilk. Per family preference, the patient was then started on a combination of breastfeeding and bottle-feeding expressed breastmilk.By hospital day 3, the patient’s weight trajectory improved and she began gaining approximately 40 grams per day. While her hyperchloremia and metabolic acidosis resolved, the patient developed hypophosphatemia. Potassium levels were difficult to assess due to hemolysis. Additionally, the patient developed significant hypercalcemia (peak 12.4 mg/dL) of unclear etiology. Further evaluation demonstrated normal levels of 25 OH vitamin D (36 ng/mL) and 1,25 dihydroxy vitamin D (71 pg/mL), an appropriately suppressed parathyroid hormone level (1 pg/mL) and no skin findings to support a diagnosis of subcutaneous fat necrosis. Labs did not support a diagnosis of adrenal insufficiency and urinary calcium was elevated. Her hypercalcemia persisted for 7 days along with hypophosphatemia. Given continued electrolyte derangements and symptoms of irritability and poor appetite, sodium phosphate supplementation was given, with abrupt resolution of hypercalcemia and hypophosphatemia the following day. The patient was discharged on hospital day 11 having gained 0.56 kg (9% below birth weight). Electrolytes remained normal after discharge.
Discussion: Refeeding syndrome is characterized by electrolyte changes that follow nutritional supplementation in malnourished patients. Hypophosphatemia, the most well-described disturbance, occurs when insulin drives phosphate intracellularly in patients who already have low phosphate stores due to malnutrition. Hypercalcemia, which occurred in our patient, is not a hallmark feature of refeeding syndrome. In fact, reports of hypercalcemia in refeeding syndrome are limited to low birth weight, very low birth weight, and extremely low birth weight infants receiving parenteral nutrition. Thus, this is the first case we are aware of in which refeeding syndrome caused hypercalcemia in a full-term, normal birthweight infant receiving breastmilk. Interestingly, the PTH-independent hypercalcemia seen in this case appears to have been driven by hypophosphatemia due to refeeding syndrome, which was rapidly reversible when the hypophosphatemia was treated.
Conclusions: This case emphasizes the importance of clinician awareness of refeeding syndrome and the novel point that neonates may experience hypercalcemia in addition to more classic refeeding syndrome findings. It also highlights that refeeding syndrome can occur in full-term, birthweight infants if there is profound weight loss after birth.