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Diabetic Ketoacidosis (DKA) - Complete Clinical Guide

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1. DEFINITION & OVERVIEW

• Hyperglycemia ("D" - diabetes/elevated glucose)
• Ketosis ("K" - urinary ketones ≥2+ or β-hydroxybutyrate ≥3.0 mmol/L)
• Metabolic Acidosis ("A" - arterial or venous pH < 7.3)

• Goldman-Cecil Medicine, p. 2484

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2. PATHOPHYSIOLOGY

A. Lipolysis Pathway (left column)

• Insulin deficiency → increased lipolysis and triglyceride breakdown
• Elevated free fatty acids (FFA) flood the liver
• Liver converts FFA to ketone bodies (β-hydroxybutyrate, acetoacetate, acetone)
• Ketone bodies accumulate → ketonuria → decreased alkali reserve → Acidosis

B. Hyperglycemia Pathway (center)

• Decreased glucose uptake by peripheral cells
• Glycosuria → osmotic diuresis → massive loss of water, Na⁺, K⁺, Mg²⁺, Ca²⁺, PO₄³⁻
• Cellular dehydration → volume depletion → impaired renal function (worsens acidosis)

C. Proteolysis Pathway (right column)

• Muscle breakdown releases amino acids to liver
• Liver uses amino acids for gluconeogenesis → more hyperglycemia → more osmotic diuresis

• Rosen's Emergency Medicine, p. 2540-2543

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3. PRECIPITATING FACTORS

Key point: ~25% of all DKA episodes occur in patients with previously undiagnosed diabetes.

• Goldman-Cecil Medicine, p. 2483; Rosen's Emergency Medicine, p. 2543

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4. SIGNS & SYMPTOMS

History / Symptoms

Physical Examination Findings

Remember: Fever is NOT a feature of DKA itself. Its presence strongly suggests an infectious precipitant.

• Rosen's Emergency Medicine, p. 2541; Goldman-Cecil Medicine, p. 2484

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5. DIAGNOSTIC CRITERIA

ADA Classification of DKA Severity

The Three Fundamental Features (Goldman-Cecil Criteria)

1. Hyperglycemia OR history of diabetes
2. Urinary ketones ≥ 2+ OR β-hydroxybutyrate ≥ 3.0 mmol/L
3. Arterial or venous pH < 7.3, serum HCO₃⁻ < 18 mEq/L

Typical Lab Values in DKA vs HHS

• Rosen's Emergency Medicine, p. 2543; Goldman-Cecil Medicine, p. 2484

Important Electrolyte Nuances

• Potassium: May appear normal or even HIGH initially (due to acidosis driving K⁺ extracellularly), but total body K⁺ is always depleted. Will drop precipitously once insulin is given.
• Sodium: Measured sodium is falsely LOW due to osmotic dilution; corrected Na = measured Na + 1.6 × [(glucose - 100) / 100]
• WBC: Elevated even without infection (due to metabolic acidosis itself); not reliable for diagnosing infection
• Anion Gap: AG = Na⁺ - (Cl⁻ + HCO₃⁻); normal 8-12 mEq/L; in DKA typically elevated

Acid-Base Analysis Tools

• Winter's formula: Expected PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2 → confirms appropriate respiratory compensation
• Delta gap: (Delta AG - Delta HCO₃⁻) > +6 = coexisting metabolic alkalosis; < -6 = coexisting hyperchloremic acidosis

Note on Euglycemic DKA

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6. MANAGEMENT

Step-by-step approach: Fluids → Electrolytes → Insulin → Treat Precipitant

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A. FLUID REPLACEMENT

• Adults typically have a 3-5 L fluid deficit
• If in hypovolemic shock: 0.9% NS bolus as fast as possible (adults); or 20 mL/kg boluses in children until systolic BP ≥ 80 mmHg
• Standard initial rate: 1 L/hr of 0.9% NS or Lactated Ringer's (LR) for first 1-2 hours
• After initial resuscitation: Switch to 0.45% NS at 250-500 mL/hr
• When glucose drops to ≤ 250-300 mg/dL: Switch IV fluid to D5W/0.45% NS to prevent hypoglycemia while continuing insulin to clear ketones

Avoid overhydration - risk of pulmonary edema and cerebral edema (especially in children)

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B. INSULIN THERAPY

• Do NOT start insulin until potassium is confirmed ≥ 3.5 mEq/L (risk of fatal hypokalemia)
• Dose: 0.1 units/kg/hr Regular insulin IV (no bolus needed in most guidelines)
• Continue insulin infusion until DKA resolution criteria are met
• Do NOT stop insulin when glucose normalizes - continue until ketoacidosis is cleared
• Switch to subcutaneous insulin 1-2 hours before stopping IV infusion (to prevent rebound)

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C. POTASSIUM REPLACEMENT

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D. PHOSPHATE REPLACEMENT

• Total body phosphate depleted due to osmotic diuresis
• Routine replacement not clearly beneficial; consider if serum PO₄ < 1.0 mg/dL, respiratory distress, hemolytic anemia, or cardiac dysfunction

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E. MAGNESIUM REPLACEMENT

• Common in DKA; can worsen hypokalemia and hypocalcemia, cause cardiac dysrhythmia
• Dose: 1-3 g MgSO₄ IV if deficient

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F. SODIUM BICARBONATE - NOT routinely recommended

• Previously used for pH < 7.0, but research shows worse outcomes with bicarbonate:
  • Worsens hypokalemia
  • Delays clearance of ketosis
  • Paradoxical CSF acidosis (CO₂ crosses blood-brain barrier more freely than HCO₃⁻)
  • Exacerbates cerebral edema
• Exception: May use in imminent cardiac arrest; pre-intubation in severely acidemic patients (to prevent cardiovascular collapse)

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G. TREATING THE PRECIPITANT

• Cultures, antibiotics if infection suspected
• ECG, troponin if ACS suspected
• Do not dismiss abdominal pain as DKA-related in adults

H. MONITORING (Flow Sheet)

• Vital signs, urine output
• Blood glucose
• Serum K⁺, Na⁺, Cl⁻, HCO₃⁻, pH
• Insulin infusion rate
• Fluid intake/output balance

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I. INTUBATION NOTE

• Avoid intubation in DKA when possible - patients have tremendous respiratory drive compensating for acidosis; matching that minute ventilation on a ventilator is very challenging
• If intubation required (comatose, vomiting): maintain hyperventilation on vent; use pre-intubation bicarbonate bolus to prevent cardiovascular collapse from acute pH drop

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7. CRITERIA FOR DKA RESOLUTION (Recovery Monitoring)

Critical Note: Glucose normalizes BEFORE ketoacidosis resolves. Never stop insulin early just because glucose is normal. Always add dextrose to IV fluids instead and continue insulin until all three criteria above are met.

β-Hydroxybutyrate as Recovery Marker

Transition to Subcutaneous Insulin

• Patient must be able to tolerate oral fluids before switching
• Overlap IV insulin with subcutaneous injection by 1-2 hours before stopping the infusion
• Choose subcutaneous insulin regimen based on whether patient has known vs new-onset diabetes

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8. COMPLICATIONS OF DKA

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9. DIFFERENTIAL DIAGNOSIS

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10. SPECIAL POPULATIONS

Pregnancy

• DKA can occur at lower blood glucose levels (as low as 200 mg/dL)
• Higher risk due to insulin resistance of pregnancy
• All pregnant DKA patients: admit to ICU + consult endocrinologist + high-risk obstetrician

Children

• ~50% present with abdominal pain (usually resolves with treatment)
• Cerebral edema far more common in young children (< 5 years)
• Outpatient management possible only if: initial pH ≥ 7.35, HCO₃⁻ ≥ 20 mEq/L, tolerating oral fluids, symptoms resolving, no precipitant requiring hospitalization

New-Onset Diabetes

• 25% of all DKA; need diabetes education, supplies training, insulin titration planning

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11. PROGNOSIS & PREVENTION

• Treated DKA mortality: ~4-5% overall; primary causes of death are infection, arterial thrombosis, and shock
• Mortality is higher in: extremes of age, severe precipitating illness, delayed presentation

Prevention (Sick-Day Rules)

• Frequent blood glucose monitoring during illness
• Never omit insulin during illness even if not eating
• Check urine/serum ketones when glucose > 250
• Drink small frequent carbohydrate-containing fluids
• Early medical contact if unable to manage at home
• Hospital admission after DKA: see diabetes educator before discharge
• Goldman-Cecil Medicine, p. 2485; Rosen's Emergency Medicine, p. 2541-2545

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QUICK REFERENCE SUMMARY

DKA TRIAD:  Glucose >250 + Ketones + pH <7.3 / HCO₃⁻ <18

MANAGEMENT SEQUENCE:
  1. IV Fluids → 0.9% NS 1L/hr (shock: bolus 20mL/kg)
  2. Check K⁺ → if <3.5, replace FIRST before insulin
  3. Insulin → 0.1 units/kg/hr Regular IV
  4. When glucose <250-300 → Add D5W to prevent hypoglycemia
  5. Replace K⁺, Mg²⁺, PO₄ as needed
  6. Find and treat precipitant
  7. Monitor q1-2h: glucose, pH, HCO₃⁻, electrolytes

RESOLUTION CRITERIA (all three):
  ✓ Glucose <250
  ✓ pH ≥7.30
  ✓ HCO₃⁻ ≥18 mEq/L