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Managing Diabetic Emergencies

October 8th, 2025

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Diabetes is a major public health concern with increasing global and national prevalence. In the United States alone, more than 38 million people have diabetes, and more than 97 million have prediabetes. This epidemic translates to a high frequency of emergency department visits because of both acute and chronic diabetic complications. Among the most critical are diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic syndrome (HHS), euglycemic diabetic ketoacidosis (EDKA), and severe hypoglycemia — all of which can be life-threatening if not rapidly identified and treated.

Epidemiology and Risk Factors

Globally, more than 537 million adults have diabetes, a figure projected to rise to 783 million by 2045. In the United States, diabetes is the eighth leading cause of death. Alarmingly, type 2 diabetes (DM2) has increased by 95% in individuals younger than 20 years of age between 2001 and 2017, particularly among Black, Hispanic, and American Indian youth. DKA is more prevalent in younger individuals and those with Type 1 diabetes (DM1), while HHS is more common in older adults with DM2. Ethnic and socioeconomic disparities are evident, with higher rates of severe hyperglycemic emergencies and worse glycemic control among minority and low-income populations.

Etiology and Pathophysiology

DKA and HHS

Both DKA and HHS share common triggers, such as infection and missed insulin doses. DKA is characterized by absolute or relative insulin deficiency, leading to hyperglycemia, ketonemia, and metabolic acidosis. HHS involves profound hyperglycemia and hyperosmolality but lacks significant ketosis due to partial insulin activity. Fluid shifts, osmotic diuresis, and electrolyte imbalances are central to both.

EDKA

EDKA presents similarly to DKA but without significant hyperglycemia (glucose < 250 mg/dL). Common triggers include sodium-glucose cotransporter 2 (SGLT-2) use, pregnancy, and fasting. The pathophysiology revolves around carbohydrate deficit and ongoing ketogenesis despite normal glucose levels.

Hypoglycemia

Hypoglycemia, defined as glucose < 70 mg/dL (or < 54 mg/dL for clinically significant events), often arises from insulin or sulfonylurea therapy, especially in older adults or those with renal/hepatic impairment. Counterregulatory failure over time in diabetic patients leads to impaired autonomic responses, heightening risk.

Clinical Features

DKA

Patients may present with nausea, vomiting, abdominal pain, dehydration, fruity breath, and Kussmaul respirations. Neurologic symptoms and hypotension may indicate severity. DKA typically develops within hours to days.

HHS

This condition progresses over days to weeks, with signs including profound dehydration, polyuria, polydipsia, and neurologic deficits (confusion, seizures). Abdominal pain is uncommon, and osmolality > 320 mOsm/kg is typical.

EDKA

Symptoms mimic DKA but with normal glucose levels, making diagnosis challenging. Clinicians must maintain high suspicion in patients on SGLT-2 inhibitors, pregnant women, or those fasting.

Hypoglycemia

Symptoms are neuroglycopenic (e.g., confusion, seizures) or autonomic (e.g., palpitations, diaphoresis). Whipple’s triad — symptoms, low glucose (< 70 mg/dL), and resolution after glucose correction — confirms diagnosis.

Diagnosis

Laboratory and Imaging

Key diagnostics include point-of-care glucose, serum ketones (especially beta-hydroxybutyrate), venous/arterial blood gas for pH, serum bicarbonate, and comprehensive metabolic panels. End-tidal carbon dioxide is a rapid proxy for acidosis in DKA. HHS features hyperglycemia > 600 mg/dL and elevated serum osmolality, while EDKA presents with acidosis and ketonemia without marked hyperglycemia. Hypoglycemia is diagnosed via fingerstick or serum glucose.

Management

DKA and EDKA

Initial management includes:

  • Fluid resuscitation: normal saline or balanced solutions, transitioning to dextrose-containing fluids once glucose < 250 mg/dL.

  • Electrolyte correction, especially potassium.

  • Insulin therapy: continuous intravenous insulin (0.1 units/kg/hour), adjusted based on glucose and acidosis resolution.

  • Addressing triggers, including infection and medication errors.

EDKA management is similar but requires early glucose-containing fluids due to normoglycemia. SGLT-2 inhibitors should be discontinued.

HHS

Treatment emphasizes slow correction of glucose and osmolality to avoid cerebral edema:

  • Gradual fluid replacement over 48 hours.

  • Insulin initiation may be delayed until after initial fluid resuscitation.

  • Monitoring for sodium/osmolality changes is critical.

Hypoglycemia

  • Mild cases: Oral glucose.

  • Severe/altered patients: intravenous dextrose (D50), intramuscular glucagon, or glucagon nasal spray.

  • Recurrent/severe cases (e.g., sulfonylurea-induced): octreotide administration.

Disposition

Many patients with DKA, HHS, or EDKA require hospital admission, often to the intensive care unit. Mild DKA may be managed with subcutaneous insulin protocols. Hypoglycemia patients may be discharged if symptoms resolve and no high-risk features are present.

Conclusion

Diabetic emergencies demand rapid recognition and tailored treatment strategies. While DKA and HHS share many therapeutic principles, key distinctions—especially in fluid and insulin management — are vital. EDKA and hypoglycemia require nuanced evaluation. Preventative strategies, education, and early identification remain central to reducing morbidity and mortality.

For more information about identifying and managing diabetic emergencies, click here.