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Diabetic Ketoacidosis (DKA)

What is DKA?

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Pathophysiology

Insulin Deficiency
        |
   ┌────┴────────────────┐
   ↓                     ↓
LIVER                 ADIPOSE TISSUE
Gluconeogenesis ↑     Lipolysis ↑ (hormone-sensitive lipase activated)
Glycogenolysis ↑      Free Fatty Acids (FFA) ↑
        |                     |
        ↓                     ↓
   HYPERGLYCEMIA         FFAs → Liver → Ketone bodies
   (glucose >250)        (β-hydroxybutyrate, acetoacetate, acetone)
        |                     |
        ↓                     ↓
  Osmotic Diuresis       KETOACIDOSIS (pH <7.3)
  → Dehydration                |
  → Electrolyte loss    Kussmaul breathing (compensatory)
        |
   Hemoconcentration → further ↑ glucose

• β-hydroxybutyrate is the dominant ketone in DKA, but it does NOT react with nitroprusside strips - this can cause falsely low urine ketone readings
• Muscles release amino acids → liver converts them to glucose (gluconeogenesis)
• Osmotic diuresis causes loss of water, Na⁺, K⁺, Mg²⁺, Ca²⁺, PO₄³⁻

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Precipitating Causes ("The 6 I's" + extras)

• Infections (most common trigger - ~40%)
• Inadequate insulin / non-adherence
• Initial presentation of new-onset Type 1 DM
• Ischemia (Acute Coronary Syndrome, stroke, PE)

• Acute pancreatitis, mesenteric thrombosis
• Cushing syndrome, thyrotoxicosis, acromegaly
• Drugs: Corticosteroids, SGLT-2 inhibitors (can cause euglycemic DKA!), clozapine, olanzapine, cocaine, sympathomimetics, thiazide diuretics
• Alcohol intoxication, severe burns

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Clinical Features

• Polyuria, polydipsia, polyphagia
• Nausea, vomiting, anorexia
• Weakness, lethargy, weight loss
• Abdominal pain - ~50% of patients (especially children; in adults, suspect a real abdominal cause triggering DKA)
• Visual blurring

• Kussmaul breathing - deep, rapid respirations (respiratory compensation for metabolic acidosis)
• Fruity/acetone breath (from acetone)
• Tachycardia, hypotension (orthostatic or frank)
• Dry skin and mucous membranes (dehydration)
• Depressed sensorium - ranges from drowsiness to coma (correlates with hyperosmolality)
• Fever suggests infection as the precipitant (DKA itself rarely causes fever)

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Diagnosis - Lab Findings

DKA vs. HHS - Key Differences

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Differential Diagnosis

• Methanol / Metformin (lactic acidosis)
• Uremia
• Diabetic ketoacidosis / starvation ketoacidosis
• Propylene glycol
• Isoniazid / Iron
• Lactic acidosis (sepsis!)
• Ethylene glycol
• Salicylates

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Management - DRIP Approach

D - Diagnosis & monitoring | R - Rehydration | I - Insulin | P - Potassium (electrolytes)

Step 1 - Initial workup

• Serum glucose, ABG/VBG, electrolytes (BMP), BUN/Cr
• β-hydroxybutyrate (blood ketones)
• CBC with differential, UA, blood cultures if infection suspected
• ECG (rule out ACS; look for K⁺ changes)
• Chest X-ray

Step 2 - Rehydration (FIRST and MOST IMPORTANT step)

• Adults: 1-2 L of Normal Saline (0.9% NaCl) IV over 1-3 hours
• Children: 20 mL/kg NS in the first hour
• Once glucose drops to ≤300 mg/dL → switch to D5W / 0.45% NaCl to prevent hypoglycemia while continuing insulin to close the anion gap

Step 3 - Potassium Replacement (BEFORE insulin if K⁺ < 3.3)

• If K⁺ < 3.3 mEq/L → HOLD insulin, replete K⁺ first (20-40 mEq/hr IV)
• If K⁺ 3.3-5.5 mEq/L → add 20-40 mEq KCl per liter of IV fluid
• If K⁺ > 5.5 mEq/L → hold K⁺, monitor closely
• Reason: insulin drives K⁺ into cells - if you give insulin with low K⁺, you can cause fatal hypokalemia and cardiac arrest!

Step 4 - Insulin

• Regular insulin 0.1 units/kg/hour IV infusion (standard)
• Target: blood glucose decrease of 50-70 mg/dL/hour
• Some protocols use a 0.1 units/kg IV bolus first, then 0.1 units/kg/hr
• Do NOT stop insulin until the anion gap closes (even if glucose is normal)
• Do NOT give insulin if K⁺ < 3.3 mEq/L

Step 5 - Bicarbonate?

• Generally NOT recommended unless pH <6.9
• Risks of bicarb: paradoxical CNS acidosis, hypokalemia, alkalosis overshoot
• IV fluids + insulin will correct acidosis naturally

Step 6 - Phosphate?

• Generally not necessary to replenish unless severely low (<1 mg/dL) with symptoms

Step 7 - Find and treat the precipitant

• Antibiotics for infection, treat ACS, review medications (stop SGLT-2i)

Monitoring - Meticulous flowsheets every 1-2 hours:

• Vital signs, urine output
• Serum glucose, K⁺, Cl⁻, HCO₃⁻, pH
• Insulin infused

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Resolution Criteria (When to stop IV insulin)

1. Blood glucose <200 mg/dL
2. Bicarbonate ≥15 mEq/L
3. pH >7.3
4. Anion gap closed (≤12)

• Overlap subcutaneous insulin for 2 hours before stopping IV insulin infusion
• Transition to eating and subcutaneous insulin regimen

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Complications of DKA and Its Treatment

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Prognosis

• DKA mortality: ~4% (despite aggressive treatment)
• HHS mortality: up to 20%
• Mortality is higher at extremes of age, with severe precipitants, and in comorbid patients

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Prevention / Patient Education ("Sick Day Rules")

• Never stop insulin when sick - you need MORE, not less
• Frequent blood glucose monitoring when unwell
• Check urine/blood ketones when glucose >250
• Small, frequent carbohydrate-containing fluids (prevents starvation ketosis on top of DKA)
• Seek medical attention early if ketones rising or not tolerating fluids

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High-Yield Summary Table

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