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Emergency Medicine19 papers

Hyperglycemic disorder

Last edited: 4/14/2026

Overview

Hyperglycemic emergencies encompass diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS), characterized by severe hyperglycemia leading to significant metabolic derangements and potential organ dysfunction 16.

Diagnosis

  • Key Criteria: Hyperglycemia (typically >600 mg/dL), presence of ketoacidosis (ketonuria/ketonemia) in DKA, hyperosmolality in HHS 16.
  • Recommended Tests: Blood glucose, serum electrolytes (including corrected sodium), arterial blood gas, serum osmolality, renal function tests, and urine ketones 13.
  • Grading: Severity often assessed by degree of hyperglycemia, acidosis, and osmolality levels 16.
  • Management

  • First-Line Treatments:
  • - Insulin Therapy: Continuous intravenous insulin infusion for DKA and HHS 16. - Fluid Resuscitation: Initial bolus followed by maintenance fluids, tailored to degree of dehydration 63.
  • Adjunctive Treatments:
  • - Electrolyte Correction: Monitor and correct electrolyte imbalances, particularly potassium and sodium 13. - Monitoring: Frequent monitoring of glucose, electrolytes, and renal function to prevent complications 13.

    Special Populations

  • Pediatrics: Younger age correlates with higher risk of neurologic dysfunction during transport; careful monitoring of pH and corrected sodium is crucial 4.
  • Elderly: Specific considerations for fluid management and comorbid conditions affecting treatment response are essential but not detailed in provided abstracts.
  • Comorbidities: Acute kidney injury (AKI) common; chloride load does not significantly impact recovery from AKI 3.
  • Key Recommendations

  • Gradually reduce serum glucose levels to minimize cerebral edema risk, aiming for an average hourly correction rate ≤75 mg/dL 1 (Evidence: Moderate).
  • Tailor fluid resuscitation based on degree of dehydration, avoiding inadequate fluid administration in HHS 6 (Evidence: Expert opinion).
  • Closely monitor electrolytes, particularly sodium and potassium, during insulin therapy to prevent complications 13 (Evidence: Moderate).
  • In pediatric hyperglycemic emergencies, prioritize monitoring for neurologic dysfunction, especially in younger patients 4 (Evidence: Moderate).
  • References

    1 Ibarra F, Hung F, Balakrishnan L, DeLaere C, Falkenstein B. Optimal Glucose Reduction in Diabetic Emergencies (OG-RIDE). The Annals of pharmacotherapy 2026. link 2 Iwamoto Y, Kimura T, Shimoda M, Morimoto Y, Dan K, Iwamoto H et al.. A clinical model for highly accurate prediction of blood glucose depression after continuous intravenous insulin therapy in hyperglycemic emergencies, a multicenter retrospective cohort study. Journal of diabetes investigation 2025. link 3 Takahashi K, Uenishi N, Sanui M, Uchino S, Yonezawa N, Takei T et al.. High versus low chloride load in adult hyperglycemic emergencies with acute kidney injury: a multicenter retrospective cohort study. Internal and emergency medicine 2024. link 4 Scollay G, Cantor Z, Fraser DD, MacDonald R, McGahern C, Reddy D et al.. Investigating the Risk Factors Associated With Acute Neurologic Dysfunction in Pediatric Hyperglycemic Emergencies on Transport. Pediatric emergency care 2024. link 5 Owolabi FA, Kolawole BA, Ikem RT, Soyoye DO. Hyperglycaemic Emergencies are Associated with Increased Pro-inflammatory Cytokine (Interleukin-6) and Cortisol. West African journal of medicine 2021. link 6 Nambam B, Menefee E, Gungor N, Mcvie R. Severe complications after initial management of hyperglycemic hyperosmolar syndrome and diabetic ketoacidosis with a standard diabetic ketoacidosis protocol. Journal of pediatric endocrinology & metabolism : JPEM 2017. link 7 Bagdure D, Rewers A, Campagna E, Sills MR. Epidemiology of hyperglycemic hyperosmolar syndrome in children hospitalized in USA. Pediatric diabetes 2013. link 8 Martin G, Jaros PP, Besse G, Keller R. The hyperglycemic neuropeptide of the terrestrial isopod, Porcellio dilatatus. II. Immunocytochemical demonstration in neurosecretory structures of the nervous system. General and comparative endocrinology 1984. link90104-7) 9 . Medical staff conference. Hyperosmolar non-ketotic diabetes. California medicine 1967. link

    Original source

    1. [1]
      Optimal Glucose Reduction in Diabetic Emergencies (OG-RIDE).Ibarra F, Hung F, Balakrishnan L, DeLaere C, Falkenstein B The Annals of pharmacotherapy (2026)
    2. [2]
    3. [3]
      High versus low chloride load in adult hyperglycemic emergencies with acute kidney injury: a multicenter retrospective cohort study.Takahashi K, Uenishi N, Sanui M, Uchino S, Yonezawa N, Takei T et al. Internal and emergency medicine (2024)
    4. [4]
      Investigating the Risk Factors Associated With Acute Neurologic Dysfunction in Pediatric Hyperglycemic Emergencies on Transport.Scollay G, Cantor Z, Fraser DD, MacDonald R, McGahern C, Reddy D et al. Pediatric emergency care (2024)
    5. [5]
      Hyperglycaemic Emergencies are Associated with Increased Pro-inflammatory Cytokine (Interleukin-6) and Cortisol.Owolabi FA, Kolawole BA, Ikem RT, Soyoye DO West African journal of medicine (2021)
    6. [6]
    7. [7]
      Epidemiology of hyperglycemic hyperosmolar syndrome in children hospitalized in USA.Bagdure D, Rewers A, Campagna E, Sills MR Pediatric diabetes (2013)
    8. [8]
    9. [9]

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