ECG was a safe and reliable method for showing HR, and was used to determine the initiation and the effectiveness of resuscitation in the delivery room.

No abstract

Background: Neonatal hypoglycemia is a common and treatable risk factor for neurological impairment. Real-time continuous glucose monitoring (RT-CGM) can show glucose concentration in real time. Using an RT-CGM alarm, physicians can be alerted and intervene in hypoglycemia. No reports, however, have evaluated the reliability of RT-CGM at low glucose levels in infants. This study therefore investigated the difference between blood glucose (BG) and RT-CGM sensor data at low glucose levels and assessed the optimum method of using a hypoglycemic alarm in infants. Methods: We enrolled infants whose glycemic management was difficult. We calculated the mean absolute difference (MAD) and mean absolute relative difference (MARD) between BG and RT-CGM sensor data. We compared the MAD and MARD between the low BG fluctuation and high BG fluctuation groups. Results: We used RT-CGM for 12 patients (29 times) and investigated 448 pairs of BG and RT-CGM sensor data. The MAD between these pairs was 9.3 AE 8.9 mg/dL, and the MARD was 11.5%. The MAD at low glucose was 7.7 AE 6.0 mg/dL, and the MARD was 16.2%. The MAD and MARD were 6.8 AE 5.4 mg/dL and 7.8% in the low fluctuation group and 10.1 AE 9.5 mg/dL and 12.7% in the high fluctuation group, respectively. Conclusions: The difference between BG and RT-CGM sensor data changes with the degree of fluctuation in BG. When physicians set the hypoglycemic alarm, consideration of this difference and a change in the alarm setting according to the degree of fluctuation in BG may be useful.

We report our experience with a preterm infant with severe hemolytic jaundice who required exchange transfusion just after birth. The patient was negative for alloimmune hemolysis as a result of maternal-fetal blood type incompatibility, and tests for inherited defects in erythrocyte metabolism, membrane function, and hemoglobin synthesis were normal. We also performed a bone marrow examination, but could not identify the cause of hemolysis. The patient had several other complications, including porencephaly, epilepsy, elevated serum levels of creatine kinase, and persistent microscopic hematuria. Later, we detected a genetic mutation in COL4A1, which was recently found to be associated with hemolytic anemia. We therefore believe that all of the patient's clinical features, including hemolytic anemia, were due to the mutation in COL4A1. Genetic testing for COL4A1 mutations is recommended in neonates who exhibit hemolytic disease of unknown etiology, especially when other complications compatible with COL4A1-related disorders are present.