Diabetic Ketoacidosis is an acute, life-threatening complication of diabetes mellitus characterized by hyperglycemia , ketonemia , and metabolic acidosis . It results from absolute or relative insulin deficiency and increased counter-regulatory hormones (glucagon, cortisol, catecholamines, growth hormone), leading to increased lipolysis, ketogenesis, and gluconeogenesis.
Etiology & Risk Factors
Common precipitating events include:
- Infection (most common): pneumonia, urinary tract infection
- Insulin omission or non-compliance
- New-onset Type 1 Diabetes Mellitus (DKA is the presenting symptom in ~25% of cases)
- Myocardial infarction, stroke, trauma
- Pancreatitis
- Medications : corticosteroids, thiazides, sympathomimetics
- Substance use : alcohol, cocaine
- Surgery or other major physiological stressors
Occurs in:
- Type 1 Diabetes Mellitus (most common)
- Type 2 DM with severe insulin deficiency (e.g., during stress or illness)
Diagnostic Criteria (ADA)
- Hyperglycemia : Blood glucose > 250 mg/dL
- Ketosis : Positive serum or urine ketones
- Metabolic Acidosis :
- Arterial pH < 7.3
- Serum bicarbonate < 15 mEq/L
- Anion gap metabolic acidosis (AG >12)
Note: Severity of DKA is not directly proportional to the level of hyperglycemia.
Clinical Features
Symptoms:
- Polyuria, polydipsia
- Nausea, vomiting
- Abdominal pain
- Generalized weakness and fatigue
- Altered mental status (lethargy → stupor → coma)
- Symptoms of underlying illness (e.g., fever, cough)
Signs:
- Dehydration (dry mucosa, hypotension, tachycardia)
- Kussmaul respiration (deep, labored breathing)
- Fruity (acetone) breath odor
- Abdominal tenderness
- Hypothermia (especially in children)
- Signs of infection or other precipitating causes
Management of DKA
1. Fluid Resuscitation
- Start with 0.9% Normal Saline (NS) :
- 15–20 mL/kg/hr for the first 1–2 hours
- Then adjust to 250–500 mL/hr
- Switch to 0.45% NS if corrected Na⁺ is normal/high
- When glucose < 200–250 mg/dL , switch to D5½NS to prevent hypoglycemia
Corrected Sodium = Measured Na⁺ + [1.6 x (Glucose - 100)/100]
2. Insulin Therapy
- Initial IV bolus : 0.1 unit/kg regular insulin (optional)
- Then continuous IV infusion : 0.1 unit/kg/hr
→ Goal: reduce glucose by 50–70 mg/dL/hr
Do not start insulin if serum K⁺ <3.3 mEq/L → risk of severe hypokalemia
3. Potassium Replacement
Before insulin, check potassium!
- K⁺ >5.3 → no replacement, monitor q2h
- K⁺ 3.3–5.3 → add 20–30 mEq KCl per liter of fluid
- K⁺ <3.3 → hold insulin, replete potassium first
4. Bicarbonate Therapy (Controversial)
- Only if pH <6.9 or in severe hyperkalemia with ECG changes
- Dose: 50–100 mEq sodium bicarbonate over 2 hours
5. Phosphate Replacement
- If phosphate <1 mg/dL or patient has cardiac/muscular dysfunction
- Add 20–30 mEq potassium phosphate to IV fluids
Transition to Subcutaneous Insulin
- Once patient is eating, hydrated, and anion gap is closed :
- Give SC basal insulin + meal bolus 2 hours before stopping IV insulin
- If insulin-naive: initiate 0.5–0.8 U/kg/day , divided into basal and prandial components
- Add correctional/“sliding scale” insulin with meals
Complications of DKA
- Cerebral edema (esp. in children/adolescents)
- Presents with headache, confusion, bradycardia, respiratory arrest
- Treat with IV mannitol or hypertonic saline
- Hypophosphatemia
- Hypoglycemia , hypokalemia
- Myocardial infarction
- Thromboembolism (DVT/PE)
- Cardiac arrhythmias
Pitfalls & Key Considerations
- Dilutional hyponatremia due to hyperglycemia
- Falsely elevated creatinine from ketones (interfering with assays)
- Triglycerides may cause pseudohyponatremia or affect glucose reading
- Monitor:
- Blood glucose hourly
- BMP every 2–4 hours
- Anion gap and acid-base status
High-Yield Pearls
- DKA is not always hyperglycemic (>250 mg/dL); euglycemic DKA can occur (especially in pregnancy or with SGLT2 inhibitors).
- Treat potassium before insulin if K⁺ is low.
- Anion gap closure is the best indicator of DKA resolution.
- Cerebral edema in DKA is a medical emergency—watch for sudden neurological changes after treatment initiation.