What are the symptoms and treatment for a young to middle-aged adult with a history of diabetes, possibly type 1, presenting to the emergency room (ER) with suspected diabetic ketoacidosis (DKA)?

Diabetic Ketoacidosis: Emergency Department Recognition and Management

Clinical Presentation and Diagnostic Criteria

DKA presents with a triad of hyperglycemia (>250 mg/dL), metabolic acidosis (pH <7.3, bicarbonate <15 mEq/L), and ketonemia/ketonuria, though you must recognize that euglycemic DKA can occur, particularly in patients on SGLT2 inhibitors. 1, 2

Key Symptoms to Assess

Early symptoms develop gradually over hours to days and include: 3, 4

• Polyuria, polydipsia, and dehydration 4
• Nausea, vomiting, and abdominal pain 5
• Generalized weakness and malaise 2
• Fruity (acetone) breath odor 3
• Kussmaul respirations (deep, labored breathing) 2

Late/severe symptoms indicating critical illness: 3

• Altered mental status ranging from drowsiness to confusion to coma 3
• Flushed face and dry mucous membranes 3
• Tachycardia and hypotension (indicating severe volume depletion) 6

Critical Pitfall: SGLT2 Inhibitors

Always ask about SGLT2 inhibitor use—these medications can cause euglycemic DKA where glucose may be only mildly elevated (150-250 mg/dL) despite severe ketoacidosis, creating a dangerous diagnostic trap. 6, 2 Discontinue these medications immediately and do not restart until 3-4 days after metabolic stability. 6, 1

Immediate Laboratory Evaluation

Order the following stat labs on every suspected DKA patient: 7, 6

• Plasma glucose, serum ketones (β-hydroxybutyrate preferred), and basic metabolic panel with calculated anion gap 7, 1
• Venous or arterial blood gas (venous pH typically 0.03 units lower than arterial) 1
• Complete blood count with differential 7
• Urinalysis with urine ketones 7
• Electrocardiogram (to assess for MI as precipitant and potassium effects) 7, 5
• Blood urea nitrogen, creatinine, and osmolality 7

If infection is suspected (the most common DKA precipitant), obtain bacterial cultures of blood, urine, and throat, plus chest X-ray if respiratory symptoms present. 7, 5

Initial Resuscitation Protocol

Fluid Therapy: First Priority

Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 liters in average adult) for the first hour to restore intravascular volume and tissue perfusion. 7, 6, 1 This aggressive initial fluid resuscitation is critical and improves insulin sensitivity. 1

After the first hour, adjust fluid rate based on hydration status, electrolyte levels, and urine output. 1 When glucose falls to 200-250 mg/dL, switch to 5% dextrose with 0.45-0.75% saline while continuing insulin infusion to prevent hypoglycemia and ensure complete ketoacidosis resolution. 6, 1

Potassium Management: The Life-Threatening Priority

This is where most errors occur—total body potassium depletion averages 3-5 mEq/kg despite initial serum levels, and insulin will unmask this by driving potassium intracellularly. 1

Follow this algorithm strictly: 7, 6, 1

• If K+ <3.3 mEq/L: DO NOT START INSULIN—this is an absolute contraindication due to risk of fatal cardiac arrhythmias. 7, 6 Continue isotonic saline, confirm adequate urine output, then aggressively replace potassium with 20-40 mEq/L in IV fluids until K+ ≥3.3 mEq/L. 7, 6

• If K+ 3.3-5.5 mEq/L: Add 20-30 mEq/L potassium to IV fluids (use 2/3 KCl and 1/3 KPO₄) once adequate urine output confirmed, then start insulin. 7, 1

• If K+ >5.5 mEq/L: Withhold potassium initially but monitor closely every 2-4 hours, as levels will drop rapidly with insulin therapy. 1

Target serum potassium of 4-5 mEq/L throughout treatment. 1

Insulin Therapy Protocol

For Moderate-to-Severe DKA or Critically Ill Patients

Once K+ ≥3.3 mEq/L, give IV bolus of 0.1 units/kg regular insulin, followed by continuous infusion at 0.1 units/kg/hour. 7, 6, 1 Some evidence suggests the bolus may be omitted in adults without compromising outcomes, but the continuous infusion rate remains standard. 5

Target glucose decline of 50-75 mg/dL per hour. 7, 6 If glucose doesn't fall by 50 mg/dL in the first hour, verify adequate hydration, then double the insulin infusion rate hourly until achieving steady decline. 7, 1

Critical point: Continue insulin infusion until DKA resolves (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L) regardless of glucose levels—do not stop insulin just because glucose normalizes. 1 This is when you add dextrose to IV fluids. 1

Alternative for Mild-to-Moderate Uncomplicated DKA

For hemodynamically stable, alert patients with mild-moderate DKA, subcutaneous rapid-acting insulin analogs (0.15 units/kg every 2-3 hours) combined with aggressive fluid management are equally effective, safer, and more cost-effective than IV insulin. 6, 1 This requires adequate fluid replacement, frequent glucose monitoring, and treatment of concurrent infections. 1

Monitoring Requirements

Check every 2-4 hours during active treatment: 7, 6, 1

• Blood glucose (can check more frequently) 7
• Serum electrolytes, particularly potassium 7, 1
• Venous pH and anion gap 7, 1
• Blood urea nitrogen, creatinine, and osmolality 7

β-hydroxybutyrate measurement in blood is preferred over urine ketones, as nitroprusside methods only detect acetoacetate and acetone, not the predominant ketone β-hydroxybutyrate. 1

DKA Resolution Criteria

All four criteria must be met simultaneously: 7, 6, 1

• Glucose <200 mg/dL 1
• Serum bicarbonate ≥18 mEq/L 1
• Venous pH >7.3 1
• Anion gap ≤12 mEq/L 1

Transition to Subcutaneous Insulin

This is the second most common error: Administer basal insulin (glargine or detemir) 2-4 hours BEFORE stopping IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia. 7, 6, 1 Never stop IV insulin without prior basal insulin administration—this causes immediate DKA recurrence. 7, 1

Once patient can eat, start multiple-dose regimen with combination of rapid-acting and long-acting insulin. 7, 1 Estimate total daily requirement at 0.3-0.4 units/kg/day, with half as basal and half as prandial coverage. 6

Bicarbonate: Generally NOT Recommended

Do not give bicarbonate for pH >6.9-7.0—multiple studies show no benefit in resolution time or outcomes, and it may worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 1 Reserve bicarbonate only for pH <6.9-7.0 if used at all. 1

Identifying and Treating Precipitating Factors

Search aggressively for the trigger—infection is most common (40-60% of cases), but also consider: 7, 6, 5

• Medication noncompliance or insulin omission 5
• Myocardial infarction (can both precipitate and be masked by DKA) 1, 5
• Cerebrovascular accident/stroke 1, 2
• Acute pancreatitis 1
• Sepsis or necrotizing soft tissue infection (look for pain out of proportion, bullae, crepitus) 5
• New-onset diabetes (20-30% of DKA cases) 8

Administer appropriate antibiotics if infection confirmed, and obtain chest X-ray if respiratory symptoms present. 7, 6

Special Populations and Complications

Cerebral edema occurs more commonly in children and adolescents than adults and is one of the most dire complications—monitor closely for altered mental status, headache, or neurological deterioration. 1

Hypoglycemia from insulin therapy can present with sweating, tremor, confusion, seizures, or loss of consciousness—always have dextrose immediately available. 3