Immediate Treatment of Type 1 Diabetes with Diabetic Ketoacidosis
Begin aggressive fluid resuscitation with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour, followed by continuous intravenous regular insulin infusion at 0.1 units/kg/hour once hypokalemia is excluded, while simultaneously monitoring and replacing electrolytes—particularly potassium—every 2-4 hours until DKA resolves. 1, 2, 3
Initial Assessment and Diagnostic Workup
Upon presentation, immediately obtain the following laboratory studies to confirm DKA and guide treatment 1, 3:
- Arterial blood gases (pH <7.3 confirms DKA) 3
- Plasma glucose (typically >250 mg/dL, though euglycemic DKA can occur) 3
- Serum electrolytes with calculated anion gap (anion gap >12 mEq/L) 3
- Serum ketones (β-hydroxybutyrate preferred over nitroprusside method) 3
- Complete blood count with differential 1, 3
- Urinalysis and urine ketones 1, 3
- Blood urea nitrogen, creatinine, and osmolality 1, 3
- Electrocardiogram (to assess for cardiac complications and potassium abnormalities) 1, 3
If infection is suspected as a precipitating factor, obtain bacterial cultures of urine, blood, and throat, and initiate appropriate antibiotics 2, 3. Chest X-ray should be obtained if clinically indicated 2.
Fluid Resuscitation Protocol
First Hour
Start with isotonic saline (0.9% NaCl) at 15-20 mL/kg body weight/hour (approximately 1-1.5 L in the average adult) 1, 3. This initial aggressive fluid replacement is critical for restoring circulatory volume and tissue perfusion 4.
Subsequent Fluid Management
After the first hour, adjust fluid choice based on hydration status, corrected serum sodium, and urine output 1, 3. The corrected sodium should be calculated by adding 1.6 mEq/L for every 100 mg/dL of glucose above 100 mg/dL 1.
Critical timing consideration: When plasma glucose reaches 250 mg/dL, switch to 5-10% dextrose with 0.45-0.75% NaCl to prevent hypoglycemia while continuing insulin therapy until ketoacidosis resolves 1, 3. This is a common pitfall—many clinicians mistakenly stop insulin when glucose normalizes, but insulin must continue until acidosis resolves (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L) 3, 4.
Total fluid replacement should correct estimated deficits within 24 hours, with osmolality changes not exceeding 3 mOsm/kg/h to minimize cerebral edema risk 1.
Insulin Therapy
Critical Pre-Insulin Check
Do NOT start insulin if serum potassium is <3.3 mEq/L 3. This is a potentially fatal error. Despite often presenting with normal or elevated potassium, all DKA patients have total body potassium depletion, and insulin will drive potassium intracellularly, potentially causing life-threatening cardiac arrhythmias 3. If K+ <3.3 mEq/L, aggressively replace potassium first until levels reach ≥3.3 mEq/L 3.
Insulin Dosing
Once hypokalemia is excluded, start continuous intravenous regular insulin infusion at 0.1 units/kg/hour (5-7 units/hour in most adults) 1, 2, 3. An initial IV bolus of 0.1 units/kg may be given, though this is optional 2.
Expected glucose decline: 50-75 mg/dL per hour 1, 3. If plasma glucose does not fall by at least 50 mg/dL in the first hour, verify adequate hydration status, then double the insulin infusion rate every hour until achieving steady glucose decline 1, 3.
Alternative for Mild-Moderate Uncomplicated DKA
For patients with mild to moderate uncomplicated DKA who are alert and hemodynamically stable, subcutaneous rapid-acting insulin analogs combined with aggressive fluid management are equally effective and may be safer and more cost-effective than IV insulin 1, 3. However, continuous IV insulin remains the standard of care for critically ill or mentally obtunded patients 1, 3.
Electrolyte Management
Potassium Replacement (Critical)
Potassium management is one of the most important aspects of DKA treatment, as inadequate monitoring and replacement is a leading cause of mortality 3.
Potassium replacement algorithm 3:
- If K+ <3.3 mEq/L: Hold insulin, give aggressive potassium replacement until ≥3.3 mEq/L
- If K+ 3.3-5.5 mEq/L: Add 20-30 mEq potassium per liter of IV fluid (use 2/3 KCl and 1/3 KPO₄) once adequate urine output confirmed 1, 3
- If K+ >5.5 mEq/L: Withhold potassium initially but monitor closely every 2 hours, as levels will drop rapidly with insulin therapy 3
Target serum potassium: 4-5 mEq/L throughout treatment 3.
Bicarbonate (Generally NOT Recommended)
Do not administer bicarbonate for DKA patients with pH >6.9-7.0 1, 3. Multiple studies demonstrate no difference in resolution of acidosis or time to discharge with bicarbonate use, and it may worsen ketosis, hypokalemia, and increase cerebral edema risk 1, 3.
Phosphate
Include phosphate in potassium replacement (1/3 as KPO₄) to prevent potential complications of severe hypophosphatemia 1, 3.
Monitoring During Treatment
Draw blood every 2-4 hours to measure 1, 3, 4:
- Serum electrolytes (especially potassium)
- Glucose
- Blood urea nitrogen and creatinine
- Venous pH (typically 0.03 units lower than arterial pH, adequate for monitoring) 3
- Anion gap
- Osmolality
Check blood glucose every 1-2 hours initially 1, 2.
Monitor β-hydroxybutyrate levels if available, as this is the preferred method for tracking ketone resolution (nitroprusside method only measures acetoacetate and acetone, not the predominant ketone) 3.
DKA Resolution Criteria
DKA is resolved when ALL of the following are met 3, 4:
- Glucose <200 mg/dL
- Serum bicarbonate ≥18 mEq/L
- Venous pH >7.3
- Anion gap ≤12 mEq/L
Target glucose between 150-200 mg/dL until these resolution parameters are achieved 3.
Transition to Subcutaneous Insulin
Once DKA is resolved and the patient can eat, transition to a multiple-dose subcutaneous insulin regimen using short/rapid-acting and intermediate/long-acting insulin 1, 2, 4.
Critical transition protocol: Administer basal insulin (glargine or detemir) 2-4 hours BEFORE stopping the IV insulin infusion 1, 2, 3. This is the most common error leading to DKA recurrence—never stop IV insulin without prior basal insulin administration 2.
Identifying and Treating Precipitating Factors
Successful DKA management requires identifying and treating the underlying cause 3, 4. Common precipitants include:
- Infection (most common: urinary tract infection, pneumonia) 5
- Insulin omission or inadequate dosing 1, 3
- Myocardial infarction 1, 3
- Cerebrovascular accident 3
- Pancreatitis 1, 3
- Trauma or surgery 3, 5
- Medications (particularly SGLT2 inhibitors, which should be discontinued 3-4 days before any surgery) 1, 3
Special Considerations and Common Pitfalls
Euglycemic DKA
Be aware that DKA can occur with glucose <250 mg/dL, particularly in patients on SGLT2 inhibitors or ketogenic diets 6. In these cases, start dextrose-containing fluids earlier while continuing insulin therapy 6.
Cerebral Edema Risk
While rare in adults, cerebral edema is more common in children and adolescents 1, 7. Avoid overly rapid correction of osmolality (should not exceed 3 mOsm/kg/h) 1.
Thromboprophylaxis
DKA creates a hypercoagulable state 4. Consider standard hospital thromboprophylaxis protocols (such as enoxaparin) after initial fluid resuscitation, particularly in critically ill patients 4.
Mixed DKA/HHS
Approximately one-third of patients present with mixed features of DKA and hyperosmolar hyperglycemic state 8. These patients require the same three-pronged approach (fluids, insulin, electrolytes) but may need more aggressive fluid resuscitation 8.