Peer-reviewed article
When diabetic ketoacidosis becomes a neurological emergency: cerebral edema in a child with new-onset type 1 diabetes mellitus - a case report and narrative review.
Mateusz Okonek, Anna Paczkowska, Kinga Drzewińska, Patrycja Rozwadowska-Kunecka, Anna Wołoszyn-Durkiewicz et al. ·
Summary
Written by AI, not yet AICS's view · claude-haiku-4-5-20251001This is a medical case report and literature review describing one child who developed cerebral edema as a complication of diabetic ketoacidosis from newly diagnosed type 1 diabetes. The report documents the clinical presentation, diagnosis, and treatment of this rare neurological emergency. While it highlights the importance of early glucose screening in children with nonspecific symptoms, it is a single clinical case rather than a study of child well-being outcomes or interventions.
Key points
Limitations
This document is a single case report with a narrative review, not a study evaluating interventions or measuring child well-being outcomes at population level. It cannot tell us about the prevalence, risk factors, or effectiveness of prevention or treatment strategies for diabetic ketoacidosis in children.
Abstract
BACKGROUND: Diabetic ketoacidosis (DKA) is a life-threatening complication of type 1 diabetes mellitus (T1D), potentially leading to severe outcomes, including cerebral edema (CE). The case describes an eight-year-old child with previously undiagnosed T1D complicated by DKA, and subsequent development of CE. It is followed by a short literature review including other pediatric cases of clinically overt CE. CASE PRESENTATION: A boy was admitted to the outpatient clinic with a several-day history of vomiting, abdominal pain and headache, leading to a presumptive diagnosis of gastrointestinal infection. The following day, the patient's condition deteriorated. Despite a positive family history of T1D (the patient's father), his blood glucose level was measured for the first time by the emergency medical service (25.6 mmol/L (460 mg/dL)). Further evaluation revealed DKA secondary to previously undiagnosed T1D. On admission, the boy was in severe general condition. Severe DKA was confirmed (pH 6.88), and appropriate treatment was implemented, resulting in temporary clinical stabilization. However, on the second day of hospitalization, the patient's condition deteriorated again. He was somnolent, with fluctuating consciousness and nuchal rigidity. An increase in intracranial pressure (ICP) was suspected. Optic nerve ultrasonography revealed increased optic nerve sheath diameters, also suggestive of raised ICP. Anti-edema therapy with mannitol was initiated based on clinical suspicion, resulting in clinical improvement. Dexamethasone and furosemide were administered as adjunctive therapy. Subsequent CT findings supported the diagnosis of CE. The patient was discharged after 10 days in good general condition. CONCLUSIONS: DKA can be a diagnostic challenge for clinicians due to its nonspecific symptoms. Early signs suggesting this condition should not be underestimated, and bedside blood glucose should be measured early in children presenting with unexplained vomiting, weight loss, tachypnea, dehydration or altered consciousness. Close monitoring for complications is critical during treatment, especially for CE, one of the most serious and potentially life-threatening consequences of DKA.