Diabetic ketoacidosis is the most common acute complication in children and adolescents with type 1 diabetes, and contributes significantly to morbidity, mortality, and healthcare burden. This review aims to explore the multifaceted aspects of severe diabetic ketoacidosis in pediatric age, including its epidemiology, pathogenesis, risk factors, complications and emphasizing advances in prevention strategies. Incidence rates vary due to influences from geographic, socioeconomic, cultural and demographic factors. Pathogenesis is linked to insulin deficiency and an excess of counter-regulatory hormones, which disrupt glucose, protein, and lipid metabolism, causing hyperglycemia, ketosis, acidosis, dehydration, and electrolyte imbalances. According to the International Society for Pediatric and Adolescent Diabetes guidelines, severe diabetic ketoacidosis is characterized by a pH < 7.1 or bicarbonate < 5 mmol/L. This condition can lead to a wide range of life-threatening complications, including cerebral edema that represents the leading cause of death. Several prevention strategies, including awareness campaigns, early diagnosis of diabetes, regular monitoring and management, effective insulin therapy, education, access to healthcare and technological assistance, may contribute to reduce the risk of severe diabetic ketoacidosis episodes in children and adolescents.

Background and Objectives: Automated insulin delivery (AID) systems represent a major advancement in type 1 diabetes (T1D) management, particularly in pediatric populations. However, real-world evidence comparing their effectiveness to conventional multiple daily injection (MDI) therapy in youth remains limited. This study aimed to evaluate the impact of transitioning from MDI therapy to AID systems on glycemic control in children and adolescents with T1D, and to explore potential differences based on baseline HbA1c levels and device type. Materials and Methods: In this single-center, retrospective observational study, 76 children and adolescents with T1D were evaluated before and after switching from MDI to either the Medtronic MiniMed™ 780G or Tandem t:slim X2™ Control-IQ system. Glycemic control was assessed using continuous glucose monitoring (CGM)-derived metrics at three time points: the last 15 days of MDI therapy (T0), 15 days after (T1), and 6 months after (T2) AID initiation. Statistical comparisons were conducted across time points and between subgroups stratified by baseline HbA1c and AID system. Results: Significant improvements in glycemic control were observed as early as 15 days after AID initiation, with sustained benefits at 6 months. Time in range (TIR) increased from 62.0% at baseline to 76.7% at 15 days and 75.8% at 6 months, and time in tight range (TITR) from 39.8% to 53.9% at T1 and 52.1% at T2 (both p < 0.001). Improvements were more pronounced in participants with higher baseline HbA1c (+16.9% for TITR and +22.3% for TIR). No significant differences in glycemic outcomes were observed between device groups, although algorithm-driven differences in insulin delivery patterns were noted. Total daily insulin dose and BMI increased significantly over time (p < 0.001 and p = 0.008, respectively). Conclusions: AID therapy leads to rapid and sustained improvements in glycemic control among youth with T1D, particularly in those with suboptimal baseline control. These benefits highlight the clinical value of AID systems, while also emphasizing the need for monitoring potential metabolic impacts.