Diabetic Ketoacidosis (DKA): Comprehensive ICU Guide

1. DIAGNOSIS

Biochemical Triad (Goldman-Cecil)

1. Hyperglycemia - glucose may range from near-normal to >1000 mg/dL (though glucose level does not tightly correlate with severity)
2. Ketonemia/Ketonuria - urinary ketones 2+ or serum β-hydroxybutyrate ≥3.0 mmol/L
3. Acidosis - arterial or venous pH <7.3, serum bicarbonate <18 mmol/L

Key point on ketone testing: Nitroprusside-based tests (urine dipstick, Acetest) detect only acetoacetate, NOT β-hydroxybutyrate. Since β-hydroxybutyrate is synthesized 3x faster and predominates in DKA, these tests underestimate true ketosis. Preferred test: quantitative serum β-hydroxybutyrate (normally >3 mmol/L in DKA). Paradoxically, as treatment begins, β-HB converts to acetoacetate, making nitroprusside tests appear to worsen even as the patient improves. - Harrison's 22e, Tintinalli's EM

Severity Classification (Harrison's 22e)

ICU Admission Criteria / Severity Markers

• Fluid losses 5-10 L and electrolyte losses requiring large-volume resuscitation
• Severe acidosis (pH <7.0)
• Altered mental status or coma
• Hemodynamic instability (hypotension, tachycardia)
• Associated comorbidities (cardiac disease, renal failure)

Laboratory Workup

• Bedside glucose, venous blood gas (VBG), serum electrolytes, BUN/creatinine
• Serum β-hydroxybutyrate (preferred over urine ketones)
• Anion gap = Na - (Cl + HCO₃) [normal 8-12 mEq/L; elevated in DKA]
• Phosphate, magnesium, calcium
• CBC, urinalysis, ECG (for hyperkalemia, rule out MI as precipitant)
• Corrected Na: add 1.6 mEq/L for every 100 mg/dL glucose >100 (some use 2.4 at glucose >400)
• A normal measured Na in DKA indicates more profound water deficit

2. FLUID THERAPY - Which Fluid to Choose?

Initial Resuscitation: 0.9% Normal Saline

• Rate: 2-4 liters in the first 2-4 hours in DKA (slower in HHS if cardiac or renal comorbidity)
• If corrected serum sodium is high (hypernatremia), can switch to 0.45% NaCl once volume is restored

The Saline vs. Balanced Crystalloid Debate

• Prolong the apparent acidosis after DKA resolves
• Cause volume overload
• Mimic persistent DKA on labs

Practical Approach

• Phase 1 (0-1 h): 0.9% NS at 500-1000 mL/h for volume resuscitation
• Phase 2 (after volume restored): Switch to 0.45% NS or balanced crystalloid (LR/Plasma-Lyte) at 250-500 mL/h
• Phase 3 (when glucose reaches ~200-250 mg/dL): Add dextrose 5% to prevent hypoglycemia while continuing insulin to clear ketones

Dextrose Addition

3. INSULIN THERAPY

• Do NOT start insulin if K⁺ <3.3 mEq/L - replete potassium first (20-40 mEq/h IV) until ≥3.5 mEq/L
• IV regular insulin: 0.1 units/kg/h continuous infusion (standard ICU approach)
• Alternatively, SC short-acting insulin analogues for uncomplicated cases
• Target glucose decline: 50-100 mg/dL per hour
• As acidosis resolves, reduce infusion to 0.02-0.1 units/kg/h
• Transition to SC long-acting insulin when patient resumes eating

Subcutaneous vs IV Insulin

4. POTASSIUM MANAGEMENT

• Monitor K⁺ every 2 hours during initial treatment
• Goal: maintain serum K⁺ between 4-5 mEq/L
• Rate via peripheral IV: max 10 mEq/h; via central line: max 20 mEq/h
• Continuous cardiac monitoring mandatory for severe hypokalemia

5. ROLE OF SODIUM BICARBONATE

Current Consensus: Generally NOT Recommended

Theoretical Disadvantages of Bicarbonate in DKA

• Worsening hypokalemia (drives K⁺ into cells)
• Paradoxical CNS acidosis (CO₂ crosses BBB faster than HCO₃⁻)
• Impaired oxyhemoglobin dissociation (left shift)
• Worsening intracellular acidosis
• Hypertonicity and sodium overload
• Delayed recovery from ketosis
• Possible precipitation of cerebral edema (especially in children)
• Elevation of lactate levels

When to Consider Bicarbonate - pH Thresholds

• Decreased cardiac contractility and peripheral vasodilation
• Life-threatening hyperkalemia
• Severe coma with pH <6.9
• Elderly with cardiovascular instability

6. ROLE OF DIALYSIS IN DKA

Indications for Emergent Dialysis in DKA Context (Rosen's EM)

1. Coexisting acute kidney injury / renal failure with:
   • Severe metabolic acidosis refractory to standard therapy
   • Volume overload precluding adequate fluid resuscitation
   • Hypocalcemia preventing safe bicarbonate administration
   • Hyperkalemia unresponsive to medical management
2. Severe electrolyte/acid-base disturbances in patients with pre-existing CKD/ESRD who cannot clear ketoacids renally
3. Hyperkalemia - if severe and life-threatening, hemodialysis is preferred over peritoneal dialysis due to higher clearance rates

When Standard DKA Treatment Cannot Work

• ESRD on dialysis - already has impaired ketoacid clearance; will need dialysis as part of DKA management
• Severe AKI - oliguria prevents the urinary excretion of ketoacids and electrolytes that is part of DKA resolution
• Volume overload - prevents adequate saline resuscitation

Key Point

7. OTHER ELECTROLYTES

Phosphate

• Not routinely replaced (no proven benefit, risk of hypocalcemia with aggressive K₂PO₄ use)
• Replace if severe hypophosphatemia develops during therapy

Magnesium

• Hypomagnesemia may develop during DKA therapy - supplement if severe

8. DKA RESOLUTION CRITERIA

• Glucose <200 mg/dL
• Serum bicarbonate ≥15 mEq/L
• Venous pH >7.3 (anion gap normalization)

Summary Table