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Background Blood sodium and ketone are parameters of dehydration and fasting, respectively. Little is known, however, about the postnatal changes in these parameters in healthy, term, exclusively breast‐fed neonates. Methods Capillary blood sodium, β‐hydroxybutyrate (β‐OHB), and glucose levels in 628 samples obtained from 392 healthy, term, exclusively breast‐fed neonates during the first 12–143 h of life were examined. Results Blood sodium and β‐OHB gradually increased and reached a peak at 48–59 h of life (mean blood sodium, 142.3 ± 2.8 mEq/L; mean blood sodium increase, 3.3 mEq/L; mean β‐OHB, 1.16 ± 0.46 mmol/L; mean β‐OHB increase, 0.65 mmol/L), and then gradually decreased and reached a nadir at 120–143 h of life. Blood glucose gradually decreased and reached a nadir at 48–59 h of life (mean, 62.4 ± 12.2 mg/dL; mean decrease, 4.7 mg/dL), and then gradually increased and peaked at 120–143 h of life. These changes were synchronized with changes in weight‐loss percentage. Conclusions The postnatal changes in blood sodium, ketone, and glucose levels during the first 12–143 h of life are described in healthy, term, exclusively breast‐fed neonates. The parameters seemed to be associated with the sufficiency of the breast‐milk supply. These results can serve as normal reference values for healthy, term, exclusively breast‐fed neonates during the early postnatal period.

Herein we describe the case of a 1-month-old boy with acute viral myocarditis, who presented with two kinds of paroxysmal supraventricular tachycardia, and who was cured after medical treatment. He was brought to the emergency room with poor feeding due to fever. On the third day of hospitalization, a narrow QRS tachycardia (180-200 beats/min) was detected. Echocardiography showed a high echoic area at the atrial septum around the atrioventricular node. The patient was clinically diagnosed with acute myocarditis. The narrow QRS tachycardia was diagnosed as incessant junctional ectopic tachycardia. The patient was treated with propranolol and landiolol. The frequency of the tachycardia decreased, but a different narrow QRS tachycardia was detected on the 15th day of hospitalization on electrocardiogram (220 beats/min), which was ascribed to atrioventricular nodal re-entrant tachycardia. Atenolol was effective for the tachycardia. At 2 years follow up, cardiac function was normal and tachycardia had not recurred.

Background Severe neonatal hypoglycemia may cause irreversible neurological sequelae. Although blood glucose (BG) screening in term neonates without risk factors for hypoglycemia (non‐risk neonates) is not recommended in the current guidelines, severe hypoglycemia can occur in such neonates. To evaluate the necessity of BG screening in non‐risk neonates, it is important to determine the accurate incidence of severe hypoglycemia in those neonates. Methods We conducted a 10 year survey of all normal‐weight term neonates diagnosed with severe neonatal hypoglycemia who were treated at secondary‐ and tertiary‐level neonatal centers in Toyama Prefecture, Japan, between January 2011 and December 2020. Results During the study period, 11 cases of severe neonatal hypoglycemia (six of which occurred in non‐risk neonates) were identified. The overall incidence of severe hypoglycemia was 1 in 5,827 normal‐weight term births, and the incidence in non‐risk neonates was 1 in 10 682 normal‐weight term births. All of the cases in non‐risk neonates were diagnosed as hyperinsulinemic hypoglycemia. Conclusions This is the first population‐based study to have identified the actual incidence of severe pathological neonatal hypoglycemia in non‐risk neonates. The incidence was not low compared with those of the newborn screening disorders, justifying the necessity of BG screening even in non‐risk neonates.

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