SEVERE DIABETIC KETOACIDOSIS AND SYSTEMIC INFLAMMATORY RESPONSE IN CRITICALLY ILL PATIENTS

Abstract

INTRODUCTION: Severe diabetic ketoacidosis is a potentially fatal metabolic emergency characterized by marked hyperglycemia, metabolic acidosis, and excessive ketone body production, frequently associated with acute decompensations of diabetes mellitus. In critically ill patients, this condition can be aggravated by the activation of the systemic inflammatory response, which contributes to organ dysfunction, hemodynamic instability, and increased morbidity and mortality. The interaction between metabolic disorders and systemic inflammation represents a relevant clinical challenge in the context of intensive care units, demanding early interventions and evidence-based intensive management. OBJECTIVE: To describe severe diabetic ketoacidosis and the systemic inflammatory response in critically ill patients, highlighting their clinical and prognostic implications. METHODOLOGY: This is an integrative literature review. The search was conducted in the SciELO, LILACS, and PubMed databases, using controlled descriptors from DeCS/MeSH: “Diabetic Ketoacidosis”, “Intensive Care Unit”, and “Systemic Inflammatory Response Syndrome”, combined using Boolean operators. Articles published between 2020 and 2025, available in full text, in Portuguese, English, or Spanish, addressing clinical, pathophysiological, and therapeutic aspects of severe diabetic ketoacidosis in critically ill patients were included. Duplicate studies, editorials, letters to the editor, conference abstracts, and publications unrelated to the topic were excluded. RESULTS AND DISCUSSION: Sixteen articles were analyzed. Studies have shown that severe diabetic ketoacidosis is associated with significant activation of inflammatory mediators, such as pro-inflammatory cytokines and markers of oxidative stress, contributing to endothelial dysfunction, microcirculatory alterations, and progression to multiple organ failure. The intensity of the inflammatory response has been observed to correlate with longer ICU stays, increased need for ventilatory support, and worse clinical outcomes, especially in patients with comorbidities and associated infections. The findings indicate that the systemic inflammatory response plays a central role in the severity and progression of diabetic ketoacidosis in critically ill patients, amplifying the impact of metabolic alterations and hindering clinical stabilization. Early identification of inflammation, coupled with rigorous control of hyperglycemia, correction of electrolyte disturbances, and intensive care management, is essential to reduce complications. However, challenges persist related to clinical variability, differential diagnosis with sepsis, and the need for integrated protocols that address the inflammatory component. CONCLUSION: It is concluded that severe diabetic ketoacidosis associated with systemic inflammatory response constitutes a highly complex clinical picture in critically ill patients, negatively impacting prognosis. Early recognition of this interaction and the adoption of integrated therapeutic strategies are fundamental to improving outcomes, reducing complications, and enhancing intensive care.