Diabetic Emergencies: A Comprehensive Review for Critical Care Practitioners

Dr Neeraj Manikath , claude.ai

Abstract

Diabetic emergencies remain a significant cause of morbidity and mortality in critical care settings, requiring prompt recognition and targeted management. This comprehensive review examines the pathophysiology, diagnosis, and management of diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state (HHS), and hypoglycemic emergencies, with emphasis on special populations and emerging clinical scenarios. We present evidence-based management strategies alongside practical clinical pearls for postgraduate trainees in critical care medicine.

Keywords: Diabetic ketoacidosis, hyperosmolar hyperglycemic state, hypoglycemia, critical care, emergency medicine

Introduction

Diabetic emergencies encompass a spectrum of life-threatening conditions that require immediate recognition and intervention. Despite advances in diabetes management, these emergencies continue to present significant challenges in critical care settings, with mortality rates ranging from 1-10% for DKA and up to 20% for HHS¹. The increasing prevalence of diabetes mellitus, coupled with the introduction of novel antidiabetic medications, has created new clinical scenarios that demand updated management approaches.

This review provides a comprehensive analysis of diabetic emergencies, emphasizing practical management strategies for critical care practitioners, including specific considerations for complex patient populations and emerging clinical patterns.

Diabetic Ketoacidosis (DKA)

Pathophysiology

DKA results from absolute or relative insulin deficiency combined with counter-regulatory hormone excess (glucagon, cortisol, catecholamines, growth hormone)². The cascade involves:

Hyperglycemia: Due to increased hepatic glucose production and decreased peripheral glucose utilization
Ketogenesis: Free fatty acid oxidation produces ketone bodies (β-hydroxybutyrate, acetoacetate)
Metabolic acidosis: Ketoacids overwhelm buffering capacity
Dehydration: Osmotic diuresis leads to profound fluid losses

Diagnostic Criteria

The American Diabetes Association defines DKA by the triad³:

Hyperglycemia (>250 mg/dL or >13.9 mmol/L)
Ketonemia (β-hydroxybutyrate >3.0 mmol/L) or ketonuria
Metabolic acidosis (pH <7.30, bicarbonate <15 mEq/L)

Clinical Pearl: Always measure ketones directly. Urine ketones may remain positive for 24-48 hours after resolution of DKA, while serum β-hydroxybutyrate provides real-time assessment of ketosis.

Management Protocol

Initial Assessment and Resuscitation

ABC assessment with particular attention to Kussmaul respirations
Fluid resuscitation:
- Normal saline 15-20 mL/kg/hr for first hour
- Subsequent rate based on hemodynamic status and corrected sodium
Electrolyte monitoring: Potassium, phosphate, magnesium

Insulin Therapy

Standard Protocol:

Loading dose: 0.1 units/kg IV bolus (optional)
Continuous infusion: 0.1 units/kg/hr
Target glucose decline: 50-75 mg/dL/hr

Clinical Hack: If glucose drops faster than ketones clear, reduce insulin to 0.05 units/kg/hr and add dextrose to IV fluids. The goal is ketone clearance, not just glucose normalization.

Electrolyte Management

Potassium: Target 4.0-5.0 mEq/L
Phosphate: Replace if <1.0 mg/dL
Magnesium: Often depleted, replace empirically

Special Considerations

Euglycemic DKA

An increasingly recognized phenomenon, particularly with SGLT2 inhibitor use⁴:

Glucose may be <250 mg/dL
Maintain high index of suspicion in patients on canagliflozin, dapagliflozin, empagliflozin
Ketone monitoring becomes crucial for diagnosis and monitoring

Oyster: A patient on SGLT2 inhibitors presenting with nausea, vomiting, and abdominal pain may have euglycemic DKA even with normal glucose levels. Always check ketones.

Cerebral Edema Prevention

Avoid excessive fluid resuscitation (>4L in first 4 hours)
Gradual correction of hyperglycemia and hyperosmolality
Consider mannitol if neurological deterioration occurs

Clinical Pearl: Cerebral edema risk is highest in children and young adults, particularly with severe DKA (pH <7.1, glucose >500 mg/dL).

Hyperosmolar Hyperglycemic State (HHS)

Pathophysiology

HHS represents severe dehydration with marked hyperglycemia but minimal ketosis⁵. Key features include:

Preserved endogenous insulin preventing significant ketogenesis
Extreme hyperglycemia (often >600 mg/dL)
Severe dehydration with hyperosmolality
Neurological complications due to cellular dehydration

Diagnostic Criteria

Glucose >600 mg/dL (>33.3 mmol/L)
Effective osmolality >320 mOsm/kg
pH >7.30
Bicarbonate >15 mEq/L
Minimal ketonemia

Formula for Effective Osmolality: 2[Na⁺] + glucose/18 + BUN/2.8

Management Strategy

Fluid Management

More conservative approach compared to DKA:

Hour 1: Normal saline 15-20 mL/kg
Hours 2-12: Adjust based on corrected sodium and hemodynamic status
Goal: 50% fluid deficit correction in first 12-24 hours

Insulin Protocol

Lower initial rate: 0.05-0.1 units/kg/hr
Target glucose decline: 50-70 mg/dL/hr
Add dextrose when glucose reaches 300 mg/dL

HHS in Malnutrition: Special Considerations

Malnourished patients with HHS require modified management⁶:

Gentle Rehydration Protocol

Risk: Cerebral edema due to rapid osmolality changes
Strategy:
- Initial rate: 250-500 mL/hr normal saline
- Monitor neurological status closely
- Consider smaller volume boluses (10 mL/kg)

Reduced Insulin Dosing

Initial rate: 0.05 units/kg/hr (half the standard dose)
Rationale: Enhanced insulin sensitivity in malnourished states
Monitoring: More frequent glucose checks (every 1-2 hours)

Clinical Hack: In malnourished patients with HHS, think "slow and steady." Aggressive correction can cause more harm than the initial hyperglycemia.

Nutritional Assessment

Albumin and prealbumin levels
Thiamine supplementation (100-200 mg daily)
Multivitamin replacement
Early nutrition consultation

Oyster: Don't mistake malnutrition-associated diabetes for Type 1 DM. These patients may have significant insulin resistance initially but become very insulin-sensitive as nutritional status improves.

Hypoglycemic Emergencies

Definition and Classification

Severe hypoglycemia: Glucose <54 mg/dL (<3.0 mmol/L) with neuroglycopenic symptoms requiring assistance⁷.

Emergency Management

Conscious Patients

Oral glucose: 15-20g (3-4 glucose tablets)
Alternative: 150-200 mL fruit juice
Recheck glucose in 15 minutes

Unconscious Patients

IV dextrose: 25g (50 mL of 50% dextrose) IV push
Alternative: Glucagon 1mg IM/SC
Continuous glucose infusion if recurrent

Clinical Pearl: After IV dextrose, always start continuous dextrose infusion (D10W at 100 mL/hr) to prevent rebound hypoglycemia, especially with long-acting insulin or sulfonylurea overdose.

Special Populations

Sulfonylurea-Induced Hypoglycemia

Prolonged duration: Up to 24-72 hours
Management: Continuous glucose infusion + octreotide
Octreotide dose: 50-100 μg SC q8h

Alcohol-Related Hypoglycemia

Mechanism: Inhibition of gluconeogenesis
High-risk: Malnourished, fasting patients
Treatment: Dextrose + thiamine (prevent Wernicke encephalopathy)

Monitoring and Complications

Laboratory Monitoring Framework

Initial Assessment (Every 1-2 hours):

Glucose, electrolytes, arterial blood gas
Ketones (β-hydroxybutyrate preferred)
Creatinine, BUN

Stabilization Phase (Every 4-6 hours):

Basic metabolic panel
Magnesium, phosphate
Ketones until <1.0 mmol/L

Common Complications

Hypokalemia

Incidence: >90% of DKA patients
Mechanism: Insulin-mediated cellular shift
Management: Aggressive replacement (20-40 mEq/hr if K⁺ <3.5)

Hypophosphatemia

Clinical significance: Respiratory muscle weakness
Replacement: K-Phos 20-30 mmol IV over 6 hours

Cerebral Edema

Risk factors: Age <20 years, severe DKA, rapid correction
Signs: Headache, altered mental status, bradycardia
Treatment: Mannitol 0.25-1.0 g/kg IV

Emerging Concepts and Future Directions

SGLT2 Inhibitors and Diabetic Emergencies

The widespread use of SGLT2 inhibitors has introduced new clinical scenarios:

Euglycemic DKA Risk Factors:

Recent surgery or illness
Reduced food intake
Dehydration
Alcohol consumption

Management Pearls:

Discontinue SGLT2 inhibitors 3 days before surgery
Patient education on sick day management
Low threshold for ketone testing

Technology Integration

Continuous Glucose Monitoring (CGM)

ICU applications: Trending data valuable despite accuracy limitations
Alarm fatigue: Balance between safety and practicality
Calibration: Still requires fingerstick confirmation for treatment decisions

Precision Medicine Approaches

Genetic Considerations:

MODY subtypes: May present as DKA but require different long-term management
Pharmacogenomics: CYP2C9 variants affect sulfonylurea metabolism

Practical Clinical Pearls and Hacks

Assessment Pearls

"The 3 Ps Rule": Polyuria, polydipsia, polyphagia - but in DKA, patients often can't tolerate oral intake
Corrected sodium formula: Na⁺ + 2.4 × (glucose - 100)/100
Anion gap pearls: May be normal in DKA if severe dehydration or hyperchloremia present

Management Hacks

"Two-bag system": Prepare both saline and dextrose bags early to avoid delays
"Ketone-guided therapy": Ketone clearance is more important than glucose normalization
"Potassium first rule": Never start insulin if K⁺ <3.3 mEq/L

Communication Pearls

Family education: DKA is preventable with proper sick day management
Transition planning: Overlap IV insulin with SC insulin by 1-2 hours
Discharge criteria: Eating, tolerating oral intake, ketones <1.0 mmol/L

Oysters (Diagnostic Pitfalls)

The "Normal" Glucose DKA

Scenario: Patient with vomiting, dehydration, but glucose 180 mg/dL
Reality: SGLT2 inhibitor-associated euglycemic DKA
Action: Always check ketones in symptomatic diabetics

The "Improving" Patient Who Deteriorates

Scenario: DKA patient initially improving, then becomes confused
Reality: Cerebral edema from too-rapid correction
Action: Slow down fluid resuscitation, consider mannitol

The "Insulin Resistant" HHS

Scenario: HHS requiring massive insulin doses
Reality: Concurrent illness (sepsis, MI) or medication interference
Action: Address underlying precipitants, consider stress-dose steroids

The "Recurrent" DKA

Scenario: Multiple DKA admissions in young patient
Reality: Insulin omission, eating disorder, or psychosocial factors
Action: Multidisciplinary approach including mental health evaluation

Quality Improvement and Protocols

Standardized Order Sets

Implementing standardized protocols reduces errors and improves outcomes:

DKA Protocol Checklist:

[ ] IV access and initial labs
[ ] Ketone measurement
[ ] Insulin infusion calculation
[ ] Potassium replacement plan
[ ] Fluid resuscitation protocol
[ ] Monitoring frequency defined

Outcome Metrics

Length of stay (target <3 days for uncomplicated DKA)
Time to ketone clearance (target <12 hours)
Hypoglycemia episodes (target <10%)
Readmission rates (target <15% at 30 days)

Conclusion

Diabetic emergencies require systematic, evidence-based approaches with attention to individual patient factors and emerging clinical scenarios. The increasing use of SGLT2 inhibitors has introduced new presentations such as euglycemic DKA, while special populations like malnourished patients require modified management strategies. Success in managing these complex cases depends on understanding pathophysiology, implementing standardized protocols, and maintaining awareness of potential complications.

Critical care practitioners must remain vigilant for atypical presentations, prioritize ketone monitoring alongside glucose management, and tailor therapy to individual patient characteristics. The integration of technology, precision medicine approaches, and multidisciplinary care models will continue to evolve our management of diabetic emergencies.

Future research should focus on personalized treatment algorithms, optimal monitoring strategies in the era of continuous glucose monitoring, and prevention strategies for high-risk populations. By combining evidence-based medicine with practical clinical experience, we can continue to improve outcomes for patients experiencing diabetic emergencies.

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Conflicts of Interest: The authors declare no conflicts of interest.

Funding: No specific funding was received for this work.

Sunday, August 17, 2025