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Published on: June 11, 2012
Severe Diabetic Ketoacidosis With Extreme Acidemia and Preserved Consciousness: Intensive Care Management Guided by
Orazio Stefano Giovanni Filippelli1, Daniela Procopio1, Anna Maria Giglio1
1Anesthesia and Critical Care, Azienda Ospedaliero Universitaria 'Renato Dulbecco' di Catanzaro, Catanzaro, ITA.
Insights
Severe diabetic ketoacidosis (DKA) in adolescents can be managed non-invasively. This case shows that careful monitoring and gradual correction, without bicarbonate or intubation, successfully treated extreme acidemia in a cooperative patient.
Area of Science:
- Pediatric Endocrinology
- Critical Care Medicine
- Metabolic Disorders
Background:
- Diabetic ketoacidosis (DKA) is a serious complication of type 1 diabetes, especially in children and adolescents.
- Aggressive interventions like bicarbonate and mechanical ventilation are common but not always evidence-based.
- Severe acidemia in DKA can present with preserved consciousness and hemodynamic stability.
Abstract:
Diabetic ketoacidosis (DKA) is a severe and potentially life-threatening metabolic emergency, frequently observed in pediatric and adolescent patients, often representing the initial manifestation of type 1 diabetes mellitus. The presence of extreme acidemia commonly prompts aggressive interventions, including bicarbonate administration and invasive ventilatory support, although such approaches are not always supported by current evidence or the overall clinical context. We report the case of a 16-year-old female presenting with severe DKA (pH 6.8-7.0), who was alert, oriented, and cooperative, with marked Kussmaul respiration and preserved hemodynamic stability. Lactate levels remained consistently within the normal range, effectively excluding significant systemic hypoperfusion and supporting the interpretation of a "pure" ketoacidotic state. Management included initial fluid resuscitation, followed by transfer to the intensive care unit for close monitoring and controlled metabolic correction. Continuous intravenous insulin infusion, dynamic potassium supplementation, and the timely introduction of 5% dextrose during the phase of glycemic reduction were implemented. Neither bicarbonate therapy nor endotracheal intubation was performed. Serial arterial blood gas analyses demonstrated a progressive and coherent correction of metabolic acidosis, with closure of the anion gap within approximately 24 hours. The high-frequency monitoring strategy, including hourly glucose measurements and arterial blood gas analysis every two hours, allowed precise titration of therapy and minimized the risk of rapid osmotic shifts. This case highlights the potential dissociation between biochemical severity and clinical presentation in DKA, emphasizing the critical role of physiological compensation. Although management was consistent with current guidelines, the combination of extreme acidemia with preserved consciousness and successful non-invasive management remains clinically uncommon and relevant. It supports a physiology-guided approach based on gradual correction and careful monitoring, rather than rapid normalization of laboratory values, thereby avoiding unnecessary and potentially harmful invasive interventions.
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