Summary

Diabetic Ketoacidosis (DKA) is a life-threatening acute complication of diabetes (usually Type 1) characterized by the triad of Hyperglycemia, Ketosis, and Metabolic Acidosis. It is a state of uncontrolled catabolism (body eating itself) caused by absolute or relative insulin deficiency. It is a major medical emergency. Mortality is low (<1%) in expert centers but remains significant in the elderly or where diagnosis is delayed.

Diagnostic Criteria (Joint British Diabetes Societies)

1. Hyperglycemia: Blood Glucose >11 mmol/L (or known diabetes).
2. Ketosis: Blood Ketones >3.0 mmol/L (or Urine ketones ++).
3. Acidosis: pH <7.3 (or Bicarbonate <15 mmol/L).

Note: Euglycemic DKA (Normal glucose DKA) can occur with SGLT2 inhibitors.

Pathophysiology (The Biochemical Storm)

DKA is fundamentally a state of Insulin Deficiency combined with Stress Hormone Excess (Glucagon, Cortisol, Adrenaline, Growth Hormone).

1. Hyperglycemia (The Sugar Trap)

• Without insulin, peripheral tissues (muscle, fat) cannot utilize glucose (GLUT4 transporters remain closed).
• The liver perceives "starvation" and ramps up Gluconeogenesis (making new sugar) and Glycogenolysis.
• Result: Massive hyperglycemia (>20-30 mmol/L).
• Consequence: Osmotic Diuresis. Glucose spills into urine, dragging water and electrolytes with it. Result = 5-8 Litre fluid deficit.

2. Ketogenesis (The Acid Factory)

• Lipolysis: Without insulin to inhibit it, Hormone Sensitive Lipase (HSL) goes wild, breaking down triglycerides into Free Fatty Acids (FFA).
• Beta-Oxidation: FFAs flood the liver mitochondria.
• The Bottleneck: The Krebs cycle is overwhelmed. Acetyl-CoA accumulates.
• Ketone Bodies: Acetyl-CoA is shunted to produce:
  1. Acetoacetate
  2. Beta-hydroxybutyrate (B-OHB) (The main ketone measured in blood).
  3. Acetone (Volatile, causes pear-drop breath).

3. Acidosis (The Buffer Failure)

• Ketone bodies are strong acids.
• They dissociate, releasing H+ ions.
• Bicarbonate Buffering: Serum bicarbonate (HCO3-) binds the H+ to neutralize it. bicarbonate levels crater (<15, then <10, then <5).
• Anion Gap: The measured cations don't change much, but unmeasured anions (ketones) rise. Result = High Anion Gap Metabolic Acidosis (HAGMA).

Image: Ketogenesis Pathway

1. Infection (Pneumonia, UTI) - Most common.
2. Insulin omission (Missed doses, pump failure, eating disorder).
3. Infarction (MI, Stroke).
4. Intercurrent illness.
5. Initial presentation of T1DM.

History Taking

• Polyuria / Polydipsia: Excessive thirst and urination.
• Abdominal Pain: Common in DKA (often mimics acute abdomen/appendicitis in children - resolves with treatment).
• Vomiting: Worsens dehydration.
• Weight loss: Recent history.

Physical Examination

• Kussmaul Respiration: Deep, sighing breathing (blowing off CO2 to compensate for acidosis).
• Pear Drop Symptoms: Acetone smell on breath.
• Dehydration: Dry mucous membranes, tachycardia, hypotension.
• Confusion: Reduced GCS correlates with severity of acidosis/osmolality.

Principles: Restore Volume, Clear Ketones, Correct Electrolytes.

Principles: Restore Volume, Clear Ketones, Correct Electrolytes.

Image: DKA Management Protocol

Step 1: Fluid Resuscitation (The Priority)

• Rationale: Patients are 5-8 Litres depleted.
• Initial Bolus: 500ml-1000ml 0.9% Saline over 15 mins if SBP <90mmHg.
• Maintenance:
  • 1L over 1 hour.
  • 1L over 2 hours.
  • 1L over 4 hours.
• Fluid Choice: 0.9% Saline is standard. Hartmann's/Plasma-Lyte is acceptable (and may prevent hyperchloremic acidosis).

CRITICAL DIFFERENCES: Children are NOT little adults. The risk of Cerebral Edema is significantly higher (0.5-1%). Mortality from cerebral edema is 20-25%.

Physiological Differences

• ratio of Brain-to-Skull size is tighter.
• Faster metabolic rate.
• More susceptible to rapid fluid shifts.

BSPED (British Society for Paediatric Endocrinology and Diabetes) Rules

1. Fluid Calculation:
   • Do NOT use "1L stat".
   • Calculate deficit (usually 5-10%).
   • Replace deficit over 48 hours (slowly!), not 24 hours.
   • Subtract limit of initial bolus from the total deficit.
2. Insulin Delay:
   • Start fluids 1 hour before starting insulin.
   • Why? Letting glucose drop slightly with just fluids reduces the osmotic shift when insulin is started.
3. Neurological Obs: Hourly. Watch for headache, bradycardia, hypertension (Cushing's Triad).

Treatment of Cerebral Edema in Kids

• Hypertonic Saline (3%): 3-5ml/kg over 10-15 mins.
• Mannitol: 0.5-1g/kg.
• Position: Head up 30 degrees.
• Fluid: Restrict by 1/3.

They are distinct but overlapping entities.

Mixed Presentation

• Some patients present with BOTH (Hyperosmolar DKA).
• Treat as DKA but use cautious fluids (like HHS).

1. "The Glucose is Normal but they are still Acidotic"

• Cause: You have fixed the hyperglycemia but not the ketosis.
• Action: This is why we add 10% Dextrose. You must CONTINUE INSULIN to clear the ketones. Do not stop insulin just because glucose is 5.0.

2. "The pH is Normal but Bicarbonate is low"

• Cause: Hyperchloremic Acidosis. Large volume of 0.9% Saline (rich in Chloride) causes a non-anion gap metabolic acidosis.
• Action: Check the Ketones. If Ketones are <0.6, the DKA is resolved. The low bicarb is just from the saline. You can stop the protocol and switch to subcut insulin.

3. "The Potassium is 3.4"

• Action: STOP THE INSULIN PUMP. Hang a bag of K+ immediately. Restart insulin only when K > 3.5.
• Why: Insulin drives K+ into cells faster than you can infuse it. Arrhythmia risk is extreme.

Step 2: Potassium Replacement (The Killer)

• The Trap: Initial K+ looks high/normal (due to acidosis shifting K+ out of cells).
• The Drop: As soon as you start insulin, K+ rushes back into cells. Serum levels crash.
• The Rule:
  • K+ > 5.5: Give no K+.
  • K+ 3.5 - 5.5: Add 40mmol KCl per litre.
  • K+ < 3.5: HOLD INSULIN. Give K+ only. Starting insulin here causes fatal arrhythmia.

Image: Potassium Shift

Step 3: Insulin (The Ketone Clearer)

• Fixed Rate Intravenous Insulin Infusion (FRIII).
• Dose: 0.1 units/kg/hour (e.g., 70kg = 7 units/hr).
• Goal: Suppress Ketogenesis.
• Basal Insulin: CONTINUE the patient's long-acting insulin (Lantus/Levemir). This prevents rebound hyperglycemia when the infusion stops.

Step 4: Glucose (The Fuel)

• When Blood Glucose drops <14 mmol/L.
• Start 10% Dextrose: Run at 125ml/hr alongside the saline.
• Why?: We need to keep giving insulin to clear the ketones. If we don't give sugar, the patient will hypo. The dextrose allows us to continue the insulin safely.

Stop the protocol when:

1. pH > 7.3
2. Ketones < 0.6 mmol/L
3. Patient eating and drinking.

Action: Switch to subcut insulin. Calculate basal dose. Give subcut insulin 30 mins before stopping the IV (overlap).

• The Drug: "Flozins" (Dapagliflozin, Empagliflozin).
• The Mechanism: They cause glycosuria (sugar peed out). Glucose looks normal (<11), so insulin is held. But ketogenesis continues.
• The Trap: Patient feels awful, vomiting. Doctor checks BM -> 6.0 -> "Not DKA".
• The Fix: ALWAYS CHECK KETONES in an unwell diabetic, regardless of glucose.

1. The "Golden" Rules

• K+ < 3.5: HOLD INSULIN.
• Basal Insulin: DO NOT STOP IT.
• Euglycemic DKA: Check ketones even if glucose is normal.

2. Viva Questions

• Q: Why do we use Fixed Rate Insulin?
  • A: We need a steady substrate to switch off hepatic ketogenesis. Variable rates are for glucose control (sliding scale), fixed rates are for ketone suppression.
• Q: What is the cause of death in children?
  • A: Cerebral Edema.
• Q: What is the cause of death in adults?
  • A: Hypokalemia (Arrhythmia) or underlying cause (Sepsis/MI).

3. Patient Explanation (The "Acid Blood")

"Because you had no insulin, your body thought it was starving. It started melting down your fat for energy. This creates toxic acid waste (ketones). We need to wash the acid out with fluids and switch off the fat-burning with insulin."

Key Guidelines

Evidence-Based Recommendations