Diabetic ketoacidosis is characterized by hyperglycemia, ketosis, and metabolic acidosis. It is caused by insulin deficiency in type 1 diabetics who stop taking insulin or due to other precipitants like infection, drugs, or surgery. This leads to increased gluconeogenesis and lipolysis resulting in high blood sugar, fatty acids, and ketone bodies causing acidosis. Treatment involves intravenous fluids, insulin administration, monitoring blood sugar and electrolytes, and bicarbonate replacement if the pH is low.

1. Diabetic ketoacidosis
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2. Diabetic ketoacidosis
• hyperglycemia (blood sugar >250 mg/dL)
• ketosis (plasma ketone ++↑)
• metabolic acidosis (increased anion gap)
(pH<7.3)

3. Precipitants
• Insulin deficiency (type 1 DM erroneously stop
insulin)
• Iaotrogenesis (gulcocorticoid)
• Infection
• Infarction
• Drugs (cocain)
• Surgery
• Trauma

4. Pathophysiology
• relative or absolute insulin deficiency +
glucagon, catecholamine, cortisol, GH excess
• Gluconeogenesis, glycogenolysis ↑
• Glycolysis ↓
• GLUT4 ↓ → glucose uptake into fat, muscle ↓
• Lipolysis ↑, FFA ↑, TG ↑, vLDL ↑, ketone body ↑

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6. Clinical features
• develop over 24 hr

7. Treatment
1. 1-3hr → 2-3L of 0.9% saline
2. When hemodynamic stable and adequate urine
output → 0.45% saline 150-300 mL/hr
3. Short acting insulin (0.1U/kg) (IV or IM) +
circulating insulin (0.1U/kg/hr)
4. Blood sugar 200/250 mg/dL → 5% glucose in
0.45% saline 100-200 mL/hr
5. If acidosis resolve → 0.05-0.1U/kg/hr insulin
6. If K+<3.3 mEq/L → repletion of K+: 20-40/40-80
mEq/L in IV fluid
7. If pH<7.0 → repletion of bicarbonate

9. Reference
• Harrison’s 19th edition
• uptodate