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Treatment of Diabetic Ketoacidosis (DKA)

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Diagnostic Workup First

• Serum glucose, electrolytes, BUN/creatinine, serum ketones (beta-hydroxybutyrate preferred)
• ABG (or VBG)
• CBC with differential
• Urinalysis, urine/blood cultures if infection suspected
• ECG (to detect hyperkalemia changes or MI as precipitant)
• Chest X-ray if indicated

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1. Fluid Resuscitation

• Aim for positive fluid balance over 12-24 hours
• Correct no faster than 3 mOsm/kg/h to reduce risk of osmotic encephalopathy
• In pediatric DKA: 20 mL/kg NS in the first hour
• Monitor BP and urine output to guide rate adjustments

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2. Insulin

• Do NOT start insulin until potassium is ≥ 3.5 mEq/L (risk of fatal hypokalemia otherwise)
• Initial bolus: 0.1 units/kg regular insulin IV
• Continuous infusion: 0.1 units/kg/h regular insulin IV
  • Standard preparation: 100 units regular insulin in 100 mL 0.9% saline (1 unit/mL)
• Target glucose reduction: 50-75 mg/dL/h (avoid >100 mg/dL/h to prevent osmotic encephalopathy)
• When glucose reaches <250 mg/dL: add dextrose and reduce insulin to 0.05 units/kg/h
• Continue insulin until: HCO3 >15 mEq/L, anion gap closed, and clinical improvement
• Before stopping infusion: give subcutaneous basal insulin 2 hours prior to discontinuing IV insulin to prevent rebound ketosis
• Two-bag approach (separate dextrose bag + saline bag) allows independent titration and has been shown to shorten treatment duration

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3. Potassium

• Add at 10-20 mEq/h to fluids
• Place on telemetry due to risk of arrhythmias from K+ shifts

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4. Bicarbonate

• pH < 6.9
• HCO3 < 5 mEq/L
• Hemodynamic instability / shock / coma
• Severe hyperkalemia with cardiac/respiratory dysfunction

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5. Phosphate and Magnesium

• Phosphate: not routinely replaced; may give K-Phos IV if patient is not eating or levels critically low
• Magnesium: correct with 1-2 g MgSO4 IV; give 10-20 mEq MgSO4 IV for ventricular arrhythmias

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6. Treat the Precipitant

• Infection (most common) - start empiric broad-spectrum antibiotics for sepsis or documented infection. Note: DKA itself does not cause fever, so fever means infection.
• Missed/insufficient insulin doses
• New-onset diabetes
• Myocardial infarction
• Medications (steroids, SGLT2 inhibitors)
• Pancreatitis, surgery, trauma

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Monitoring During Treatment

• Serum sodium should rise as hyperglycemia corrects; if it doesn't, suspect overhydration with free water
• Anion gap closure is a less reliable endpoint than serum bicarbonate normalization (hyperchloremia from NS can close the gap before true resolution)
• Beta-hydroxybutyrate normalization is the gold standard for resolution

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Resolution Criteria (all three must be met)

1. Blood glucose < 200-250 mg/dL
2. HCO3 ≥ 15 mEq/L
3. Anion gap closed (< 12 mEq/L)

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Complications to Watch For

• Cerebral edema - most feared, especially in children; caused by too-rapid osmotic shifts
• Hypokalemia - from insulin therapy; potentially fatal arrhythmias
• Hypoglycemia - from excess insulin without dextrose
• Lactic acidosis - suspect if persistent anion gap despite treatment; manage with volume, control sepsis
• Arterial thrombosis (stroke, MI, limb ischemia) - increased frequency in DKA; anticoagulate only for specific thrombotic events
• Acute lung injury - rare

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Special Considerations

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Diabetic Ketoacidosis (DKA) - Complete Overview

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Definition

1. Hyperglycemia (or history of diabetes)
2. Ketonemia/ketonuria - urinary ketones ≥ 2+ or serum beta-hydroxybutyrate ≥ 3.0 mmol/L
3. Metabolic acidosis - arterial or venous pH < 7.3 (bicarbonate < 15 mEq/L)

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Pathophysiology

Insulin deficiency
        |
        ├── Liver: ↑ glycogenolysis + ↑ gluconeogenesis → HYPERGLYCEMIA
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        ├── Adipose: Hormone-sensitive lipase activated → ↑ free fatty acids
        |       └── FFAs → liver → Acetoacetate + β-hydroxybutyrate + Acetone
        |                                    → KETONEMIA / KETONURIA
        |                                    → Elevated anion gap metabolic ACIDOSIS
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        └── Kidney: Osmotic diuresis from hyperglycemia
                    → Loss of H₂O, Na, K, Mg, Ca, PO₄
                    → Dehydration + electrolyte depletion

• Total-body potassium is depleted despite often normal or high serum K+ at presentation (acidosis shifts K+ extracellularly)
• Serum sodium may be factitiously low - add 2.4 mEq/L per every 100 mg/dL glucose above 100
• Serum creatinine may be factitiously elevated (nitroprusside assay interference)
• Leukocytosis is common from stress and hemoconcentration; WBC >25,000 or bands >10,000 suggests infection

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Precipitating Causes

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Clinical Features

• Polyuria, polydipsia, polyphagia
• Nausea, vomiting, abdominal pain (can mimic acute abdomen)
• Weakness, fatigue
• Altered mental status / coma (correlates with hyperosmolality)

• Kussmaul breathing - deep, rapid respirations (respiratory compensation for metabolic acidosis)
• Fruity/acetone breath (acetone)
• Dehydration: dry mucous membranes, decreased skin turgor, sunken eyes
• Tachycardia, hypotension (severe cases)
• Hypothermia (DKA itself does not cause fever - fever suggests infection)

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Diagnostic Criteria (ADA Severity Classification)

• Serum glucose, electrolytes (with anion gap), BUN/Cr
• Beta-hydroxybutyrate (preferred over urine ketones)
• Venous blood gas (venous pH ~0.03 lower than arterial; avoids arterial puncture)
• CBC, urinalysis, blood cultures
• ECG (r/o MI as precipitant; assess for K+ changes)
• CXR if respiratory symptoms

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Treatment

1. Fluids

• Initial: 1 L 0.9% NS bolus, then 500-1000 mL/h
• After volume restored: Switch to 0.45% NS at 150-500 mL/h (use 0.9% if hyponatremic)
• When glucose <250 mg/dL: Add D5W (to prevent hypoglycemia while continuing insulin)
• Fluid deficit ~3-5 L (7-9% body weight); correct over 12-24 hours
• Fluids alone lower glucose ~18% by improving renal perfusion
• Two-bag approach (separate dextrose + saline bags) allows independent titration and shortens treatment duration

2. Insulin

⚠️ Do NOT start insulin if K+ < 3.3 mEq/L - correct potassium first

• Bolus: 0.1 units/kg regular insulin IV
• Infusion: 0.1 units/kg/h (standard: 100 units in 100 mL NS)
• Target glucose drop: 50-75 mg/dL/h (never >100 mg/dL/h - cerebral edema risk)
• When glucose reaches <250 mg/dL: reduce to 0.05 units/kg/h + start dextrose
• Before stopping infusion: give SC basal insulin 2 hours prior to prevent rebound ketosis
• Continue until: glucose <200-250, HCO₃ ≥15, anion gap closed

3. Potassium

• Monitor on telemetry continuously

4. Bicarbonate

• pH < 6.9
• HCO₃ < 5 mEq/L
• Severe shock/coma, or severe hyperkalemia with cardiac dysfunction

5. Phosphate & Magnesium

• Phosphate: not routine; replace if severely low or patient not eating (use K-Phos)
• Magnesium: 1-2 g MgSO₄ IV; 10-20 mEq for ventricular arrhythmias

6. Treat the Precipitant

• Start antibiotics empirically for suspected/confirmed infection
• Manage MI, pancreatitis, etc.

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Monitoring

• Serum Na should rise as glucose falls - if not, suspect over-hydration
• Hyperchloremia from large-volume NS can close the anion gap before true DKA resolution - use serum bicarbonate normalization as the primary endpoint
• A falsely positive/worsening nitroprusside ketone test can occur as therapy converts beta-hydroxybutyrate to acetoacetate

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Resolution Criteria (all three required)

1. Glucose < 200-250 mg/dL
2. HCO₃ ≥ 15 mEq/L
3. Anion gap closed (< 12 mEq/L)

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Complications

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DKA vs. HHS (Hyperosmolar Hyperglycemic State)

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