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Diabetic Ketoacidosis (DKA) - Treatment
Overview
DKA is an acute, life-threatening complication of diabetes characterized by hyperglycemia, ketosis, and metabolic acidosis. Management ideally takes place in an ICU. The three pillars of treatment are: fluid replacement, insulin administration, and potassium repletion.
Treatment Algorithm
Algorithm 11.3 - Mulholland and Greenfield's Surgery
1. Initial Workup
Before starting treatment, confirm the diagnosis and identify the precipitant:
- Serum glucose, electrolytes, ketones, arterial blood gas
- CBC with differential, urinalysis, chest X-ray, ECG
- Beta-hydroxybutyrate levels (more reliable than urine ketones)
- Look for precipitants: infection, missed insulin, MI, pancreatitis, new-onset T1DM
Diagnostic criteria:
- Blood glucose >250 mg/dL
- pH <7.3
- Serum bicarbonate <18 mEq/L
- Anion gap >10-12
- Ketonemia/ketonuria
2. IV Fluids
The first priority is restoring circulating volume and then replacing total-body water deficit (usually 7-9% of body weight).
| Phase | Fluid | Rate |
|---|
| Immediate bolus | 0.9% NS | 1 L (children: 20 mL/kg) over 1-3 hours |
| Volume repletion | 0.9% NS | 500-1000 mL/h (if cardiac and renal function normal) |
| After initial repletion | 0.45% NS (or 0.9% NS if hyponatremic) | 150-500 mL/h |
| When glucose ≤300 mg/dL | Switch to D5W/0.45% NS | Continue until ketoacidosis resolves |
- Adjust rate based on BP and urine output
- Avoid correcting osmolality faster than 3 mOsm/kg/h
- Aim for positive fluid balance over 12-24 hours
- Serum sodium should rise as hyperglycemia corrects - if it doesn't, suspect overhydration
3. Insulin
Do NOT start insulin if K+ < 3.3-3.5 mEq/L - correct potassium first.
- Bolus: 0.1 units/kg IV regular insulin
- Infusion: 0.1 units/kg/h IV (regular insulin 100 units in 100 mL 0.9% NS at 10 mL/h = 10 units/h)
- Target glucose fall: 50-75 mg/dL/h (do not exceed 100 mg/dL/h - risk of osmotic encephalopathy)
When glucose reaches <250 mg/dL:
- Add dextrose (D5W) to prevent hypoglycemia while continuing insulin
- Consider the "two-bag approach" - separate dextrose infusion + reduced insulin at 0.05 units/kg/h (allows independent titration; shown to shorten treatment duration)
- Subcutaneous (SQ) approach for mild-moderate DKA: 0.3 units/kg rapid-acting insulin SQ, check glucose q2h
Stopping the insulin drip:
- Continue infusion until HCO3- >15 mEq/L, anion gap closed, and clinical improvement
- Give SC basal insulin 2 hours before stopping the IV infusion to prevent rebound ketosis
4. Potassium
DKA causes total-body potassium depletion (3-10 mEq/kg), even if serum K+ appears normal or high at presentation (due to transcellular shifts from insulin deficiency and acidosis). Insulin drives K+ into cells, causing serum K+ to fall during treatment.
| Serum K+ | Action |
|---|
| < 3.3-3.5 mEq/L | Replace K+ BEFORE starting insulin; 20 mEq KCl/hr |
| 3.5-5.3 mEq/L | Add 20-40 mEq KCl to each liter of IV fluid |
| > 5.3 mEq/L | No potassium yet; monitor BMP every 4 hours until stable |
- Check ECG for hyper/hypokalemia changes
- Potassium phosphate (KPhos) is preferred if co-existing hypophosphatemia
5. Bicarbonate
Not routinely recommended. Administer only in selected situations:
- pH <6.9, or HCO3- <5 mEq/L
- Shock or coma
- Severe cardiac or respiratory dysfunction
- Severe hyperkalemia
Dose: 50-100 mEq NaHCO3 in 1 L 0.45% NS over 30-60 min. Always add 10 mEq KCl to avoid hypokalemia. Follow arterial pH.
6. Phosphate & Magnesium
- Phosphate: Not routinely replaced, but potassium phosphate (KPhos) IV may be given in non-eating patients or if hypophosphatemia is significant
- Magnesium: 10-20 mEq MgSO4 IV if ventricular arrhythmias or documented deficiency
7. Monitoring
| Parameter | Frequency |
|---|
| Blood glucose | Every hour |
| Electrolytes, HCO3-, anion gap | Every 2-4 hours |
| Arterial blood gas | As needed (more frequently if severely acidotic) |
| Vital signs + urine output | Continuous |
| Fluid balance | Running total |
| Beta-hydroxybutyrate | Serial measurements helpful |
Telemetry is recommended given electrolyte instability.
8. Treat the Precipitant
Always search for and correct the underlying cause:
- Infections (most common) - start IV antibiotics promptly for documented/suspected infections; DKA itself causes leukocytosis, so fever is a meaningful sign
- Missed insulin doses
- New-onset Type 1 DM
- Myocardial infarction, stroke
- Drugs (steroids, SGLT2 inhibitors - euglycemic DKA)
- Pancreatitis (use lipase, not amylase, for diagnosis - amylase can be elevated in DKA)
9. Resolution Criteria (to stop insulin drip)
- Serum HCO3- >15 mEq/L (most reliable index of metabolic recovery)
- Anion gap closed (note: hyperchloremia from NS may close gap before true resolution - rely on HCO3-)
- Blood glucose <200-250 mg/dL
- Clinical improvement
10. Admit / Disposition
- ICU preferred for moderate-severe DKA
- Telemetry unit acceptable for stable patients
- Outpatient treatment may be considered in children only if: initial pH ≥7.35, HCO3- ≥20 mEq/L, tolerating oral fluids, symptoms resolved, reliable caregiver, no underlying precipitant
Recent Guideline Update (2024)
A 2024 consensus report on hyperglycemic crises (reviewed in
Cleveland Clinic J Med 2025) has updated management recommendations, including guidance on SGLT2 inhibitor-associated euglycemic DKA. This should be considered when patients present with DKA but relatively normal glucose levels.
Sources:
- The Washington Manual of Medical Therapeutics, pp. 890-891
- Rosen's Emergency Medicine, Box 115.1
- Mulholland and Greenfield's Surgery, Algorithm 11.3
- Goldman-Cecil Medicine