Emergency Management Protocol for Adult Diabetic Ketoacidosis

Immediate Initial Assessment and Resuscitation

Begin aggressive isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in the first hour) immediately upon suspicion of DKA to restore intravascular volume and renal perfusion. 1, 2

Diagnostic Laboratory Panel (Stat)

Draw blood immediately for: plasma glucose, arterial or venous pH, serum electrolytes with calculated anion gap, β-hydroxybutyrate (preferred ketone test), BUN, creatinine, serum osmolality, urinalysis with ketones, complete blood count with differential, and electrocardiogram 1, 2
Use direct blood β-hydroxybutyrate measurement—not nitroprusside-based urine or serum tests—because nitroprusside methods only detect acetoacetate and acetone, completely missing β-hydroxybutyrate, the predominant ketone body in DKA 1, 3
Obtain bacterial cultures (blood, urine, throat) if infection is suspected, as infection is the most common precipitating factor 1, 2

Diagnostic Criteria for DKA

Blood glucose >250 mg/dL 1, 3
Arterial pH <7.3 (or venous pH <7.27, since venous pH is typically 0.03 units lower than arterial) 1, 3
Serum bicarbonate <15 mEq/L 1, 3
Moderate-to-large ketonemia or ketonuria 1, 3
Anion gap >12 mEq/L (calculated as [Na⁺] - [Cl⁻ + HCO₃⁻]) 1, 3

Severity Classification

Mild DKA: pH 7.25-7.30, bicarbonate 15-18 mEq/L, alert mental status 3
Moderate DKA: pH 7.00-7.24, bicarbonate 10-15 mEq/L, drowsy/lethargic 3
Severe DKA: pH <7.00, bicarbonate <10 mEq/L, stupor or coma—requires ICU-level monitoring 3

Fluid Resuscitation Protocol

First Hour

Administer isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour regardless of corrected sodium level 1, 2
The typical total body water deficit in DKA is 6-9 L; plan to replace this over 24 hours 1, 2

After the First Hour

Calculate corrected serum sodium: add 1.6 mEq/L for each 100 mg/dL glucose above 100 mg/dL 1, 2
If corrected sodium is normal or elevated: switch to 0.45% NaCl at 4-14 mL/kg/hour 1, 2
If corrected sodium is low: continue 0.9% NaCl at 4-14 mL/kg/hour 1, 2

When Glucose Falls to 250 mg/dL

Change IV fluid to 5% dextrose with 0.45-0.75% NaCl while maintaining the same insulin infusion rate to prevent hypoglycemia and ensure complete ketone clearance 1, 2
Never stop insulin when glucose normalizes—ketoacidosis resolves more slowly than hyperglycemia, and premature insulin cessation causes recurrent DKA 1, 2

Special Monitoring

Monitor closely for fluid overload in patients with cardiac or renal compromise 1, 2
Limit the change in serum osmolality to ≤3 mOsm/kg/hour to reduce cerebral edema risk 1, 2

Potassium Management (Class A Evidence)

Total body potassium depletion is universal in DKA (approximately 3-5 mEq/kg) even when initial serum potassium appears normal or elevated, because acidosis, insulin deficiency, and hyperosmolality shift potassium extracellularly. 1, 2

Potassium Algorithm (Check BEFORE Starting Insulin)

If K⁺ <3.3 mEq/L:

This is an absolute contraindication to insulin therapy (Class A evidence) 1, 2
Hold insulin completely and aggressively replace potassium at 20-40 mEq/hour until K⁺ ≥3.3 mEq/L 1, 2
Obtain electrocardiogram to assess for cardiac effects of hypokalemia 2
Confirm adequate urine output (≥0.5 mL/kg/hour) before aggressive repletion 1, 2
Initiating insulin when K⁺ <3.3 mEq/L can precipitate fatal cardiac arrhythmias, cardiac arrest, and respiratory muscle weakness 1, 2

If K⁺ 3.3-5.5 mEq/L:

Insulin may be started safely 1, 2
Add 20-30 mEq/L potassium to each liter of IV fluid once adequate urine output is confirmed 1, 2
Use a mixture of approximately 2/3 potassium chloride (or potassium acetate) and 1/3 potassium phosphate 1, 2
Target serum potassium of 4.0-5.0 mEq/L throughout treatment 1, 2

If K⁺ >5.5 mEq/L:

Start insulin immediately without delay 1, 2
Withhold potassium supplementation initially 1, 2
Monitor potassium every 2-4 hours as levels will decline rapidly with insulin therapy 1, 2
Begin adding 20-30 mEq/L potassium to IV fluids once K⁺ falls below 5.5 mEq/L 1, 2

Insulin Therapy Protocol

Standard IV Insulin Regimen (Moderate-to-Severe DKA or Critically Ill Patients)

Continuous intravenous regular insulin infusion at 0.1 units/kg/hour is the standard of care for moderate-to-severe DKA or critically ill and mentally obtunded patients. 1, 2

Verify serum potassium ≥3.3 mEq/L before initiating insulin 1, 2
Optional: Give IV bolus of 0.1-0.15 units/kg regular insulin 1, 2
Start continuous IV infusion of regular insulin at 0.1 units/kg/hour 1, 2
Prepare insulin solution: add 100 units regular insulin to 100 mL 0.9% NaCl (concentration 1 unit/mL) 2
Prime infusion tubing with 20 mL of prepared solution before patient connection 2

Insulin Titration

Target glucose decline of 50-75 mg/dL per hour 1, 2
If glucose does not fall by at least 50 mg/dL in the first hour despite adequate hydration, double the insulin infusion rate each subsequent hour until a steady decline is achieved 1, 2
When glucose reaches 250 mg/dL, add dextrose to IV fluids while continuing insulin infusion at the same rate 1, 2

Alternative Subcutaneous Regimen (Mild-to-Moderate Uncomplicated DKA Only)

For hemodynamically stable, alert patients with mild-moderate uncomplicated DKA, subcutaneous rapid-acting insulin analogs (0.1-0.2 units/kg every 1-2 hours) combined with aggressive fluid management are equally effective, safer, and more cost-effective than IV insulin 1, 2
This approach requires adequate fluid replacement, frequent point-of-care glucose monitoring, treatment of concurrent infections, and appropriate follow-up 1, 2
Continuous IV insulin remains the standard for critically ill and mentally obtunded patients 1, 2

Monitoring During Treatment

Frequency

Check blood glucose every 1-2 hours during active insulin infusion 1, 2
Draw blood every 2-4 hours for: serum electrolytes (especially potassium), glucose, BUN, creatinine, calculated osmolality, venous pH, bicarbonate, anion gap, and β-hydroxybutyrate 1, 2

What to Monitor

Use venous pH for ongoing monitoring—it is typically 0.03 units lower than arterial pH and eliminates the need for repeated arterial blood gases 1, 3
Monitor β-hydroxybutyrate levels (when available) as the most accurate marker of ketone clearance 1, 2
Monitor serum potassium closely as insulin drives potassium intracellularly, causing rapid declines 1, 2

Bicarbonate Administration

Bicarbonate is NOT recommended for DKA patients with pH >6.9-7.0 (Class A evidence). 1, 2

Multiple studies show no difference in resolution of acidosis or time to discharge with bicarbonate use 1, 2
Bicarbonate may worsen ketosis, cause hypokalemia, and increase cerebral edema risk 1, 2
Consider bicarbonate only if pH <6.9: administer 100 mmol sodium bicarbonate diluted in 400 mL sterile water, infused at 200 mL/hour 2

Resolution Criteria

DKA is considered resolved when ALL of the following are achieved simultaneously: 1, 2

Glucose <200 mg/dL 1, 2
Serum bicarbonate ≥18 mEq/L 1, 2
Venous pH >7.3 1, 2
Anion gap ≤12 mEq/L 1, 2
Continue insulin infusion until all resolution criteria are met, regardless of glucose level 1, 2
Ketonemia resolves more slowly than hyperglycemia; premature insulin discontinuation is the most common cause of recurrent DKA 1, 2

Transition to Subcutaneous Insulin

Administer basal insulin (intermediate or long-acting such as glargine, detemir, or NPH) 2-4 hours BEFORE stopping the IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia. 1, 2

Transition Protocol

Continue IV insulin infusion for an additional 1-2 hours after the basal subcutaneous dose to ensure adequate absorption 1, 2
Calculate basal insulin dose: use approximately 50% of the total 24-hour IV insulin amount as a single daily dose of long-acting insulin 2
Divide the remaining 50% of the 24-hour IV insulin dose equally among three daily meals as rapid-acting insulin 2

When Patient Can Eat

Start a multiple-dose insulin schedule using a combination of short/rapid-acting and intermediate/long-acting insulin 1, 2
For newly diagnosed patients, start total daily insulin dose of approximately 0.5-1.0 units/kg/day 1, 2

If Patient Remains NPO After DKA Resolution

Continue IV insulin and fluid replacement, supplementing with subcutaneous regular insulin as needed 1, 2

Identification and Treatment of Precipitating Causes

Identifying and treating the underlying precipitating cause is crucial for successful DKA treatment. 1, 2

Common Precipitants to Investigate

Infection (most common): pneumonia, urinary tract infection, sepsis—obtain cultures and start appropriate antibiotics promptly 1, 2
Insulin omission or inadequacy: nonadherence, pump failure, inadequate dosing 1, 2
Myocardial infarction: obtain troponin and ECG; DKA can both precipitate and mask MI 1, 2
Cerebrovascular accident (stroke): assess for focal neurological deficits 1, 2
Pancreatitis: check lipase and amylase 1, 2
SGLT2 inhibitor use: discontinue immediately and do not restart until 3-4 days after metabolic stability 1, 2
Glucocorticoid therapy: can precipitate hyperglycemia and DKA 1, 2
Pregnancy: pregnant individuals may present with euglycemic DKA 1, 2

Special Considerations: Euglycemic DKA

Euglycemic DKA is defined by blood glucose <200-250 mg/dL together with arterial pH <7.3, serum bicarbonate <15-18 mEq/L, anion gap >12 mEq/L, and ketonemia or ketonuria. 1

SGLT2 Inhibitors (Leading Cause)

SGLT2 inhibitors are the leading contemporary cause of euglycemic DKA 1
Stop SGLT2 inhibitor immediately when DKA is suspected 1
Do not restart until 3-4 days after metabolic stability is achieved 1
Incidence: 0.6-4.9 events per 1,000 patient-years in type 2 diabetes, with relative risk of 2.46 versus placebo 1

Management Modifications for Euglycemic DKA

Initiate dextrose-containing IV fluids (5% dextrose with 0.45-0.75% NaCl) simultaneously with insulin infusion from the outset to prevent hypoglycemia while allowing insulin-mediated ketone clearance 1, 2
Provide 150-200 g of carbohydrate per day to suppress ongoing ketogenesis 1, 2
If oral intake is tolerated, administer liquid carbohydrate sources (juice, broth, sports drinks) in small, frequent portions 1, 2

Critical Pitfalls to Avoid

Starting insulin before correcting severe hypokalemia (K⁺ <3.3 mEq/L) can cause life-threatening arrhythmias and cardiac arrest 1, 2
Stopping insulin when glucose falls to 250 mg/dL without adding dextrose leads to recurrent ketoacidosis 1, 2
Discontinuing IV insulin without prior administration of basal subcutaneous insulin (2-4 hours earlier) is the most common cause of DKA recurrence 1, 2
Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA 1, 2
Overly rapid correction of serum osmolality (>3 mOsm/kg/hour) increases the risk of cerebral edema 1, 2
Relying on nitroprusside-based ketone tests (urine or serum) misses β-hydroxybutyrate and delays appropriate treatment 1, 2
Using bicarbonate for pH >6.9-7.0 provides no benefit and may worsen outcomes 1, 2

Discharge Planning

Identify outpatient diabetes care provider before discharge 1, 2
Educate patient on recognition, prevention, and management of DKA 1, 2
Provide instruction on glucose monitoring, insulin administration, and sick-day management 1, 2
Ensure appropriate insulin regimen is prescribed with attention to medication access and affordability 1, 2
Schedule follow-up appointment prior to discharge 1, 2
For patients on SGLT2 inhibitors: educate to check urine or blood ketones during illness even if glucose is normal, avoid prolonged fasting and very-low-carbohydrate diets, and discontinue SGLT2 inhibitor during any acute illness 1

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