A 17-year-old male with polyuria, polydipsia, polyphagia, weight loss, abdominal pain, drowsiness, dehydration, tachypnea, tachycardia, random glucose 25 mmol/L, arterial pH 7.10, bicarbonate 10 mmol/L (anion‑gap metabolic acidosis) after receiving 0.9% saline—what is the most appropriate next step: intravenous insulin infusion, intravenous ceftriaxone, intravenous potassium chloride, or intravenous sodium bicarbonate?

Management of Diabetic Ketoacidosis in a 17-Year-Old

Initiate intravenous insulin therapy immediately (Option B). This patient presents with diabetic ketoacidosis (DKA) requiring urgent insulin treatment to correct the life-threatening metabolic derangement.

Clinical Presentation Confirms DKA

This patient meets all diagnostic criteria for DKA:

• Hyperglycemia: Random glucose 25 mmol/L (450 mg/dL) 1
• Metabolic acidosis: pH 7.10 (normal 7.36-7.45) and bicarbonate 10 mmol/L (normal 21-28) 1
• Anion gap acidosis: Calculated anion gap = 130 - (96 + 10) = 24 mEq/L (>12 indicates DKA) 1
• Classic symptoms: Polyuria, polydipsia, polyphagia, weight loss, abdominal pain, and drowsiness 1

The severity classification is severe DKA based on pH <7.00-7.24 and bicarbonate <10-15 mEq/L 1.

Why Insulin is the Immediate Priority

After initial fluid resuscitation with 0.9% saline (already initiated), insulin therapy is the definitive next step to correct the underlying metabolic derangement 1. The American Diabetes Association guidelines explicitly state that in individuals with ketoacidosis, "treatment with subcutaneous or intravenous insulin should be initiated to rapidly correct the hyperglycemia and the metabolic derangement" 1.

Insulin Administration Protocol:

• Intravenous regular insulin is preferred for DKA management 1
• Start with continuous IV insulin infusion after confirming potassium >3.3 mEq/L 1
• This patient's potassium is 4.4 mEq/L, which is safe for insulin initiation 1

Why Other Options Are Incorrect

Option C (Potassium Chloride) - Premature

• Current potassium is 4.4 mEq/L (normal range) 1
• Potassium supplementation becomes necessary during insulin therapy, not before 1
• Insulin drives potassium intracellularly, causing hypokalemia during treatment 1
• Add 20-30 mEq/L potassium to IV fluids once insulin is started and renal function is confirmed 1

Option D (Sodium Bicarbonate) - Not Indicated

• Bicarbonate is NOT routinely recommended in DKA, even with severe acidosis 1
• Guidelines do not support bicarbonate use unless pH <6.9 or life-threatening hyperkalemia exists 1
• This patient's pH of 7.10, while low, does not meet criteria for bicarbonate therapy 1
• Insulin therapy will correct the acidosis by stopping ketone production 1

Option A (Ceftriaxone) - Addresses Wrong Priority

• While infection is a common DKA precipitant, there are no clear signs of infection here 1
• Temperature is normal (37.2°C), and leukocytosis (WBC 14) is common in DKA itself 1
• Antibiotics can be considered after metabolic stabilization if infection is confirmed 1
• The immediate life-threat is the metabolic acidosis, not potential infection 1

Critical Management Sequence

1. Continue IV fluid resuscitation (0.9% saline at 15-20 mL/kg/hr already started) 1
2. Start IV insulin infusion immediately (regular insulin, typically 0.1 units/kg/hr) 1
3. Add potassium to IV fluids (20-30 mEq/L) once insulin is started 1
4. Monitor glucose hourly and switch to dextrose-containing fluids when glucose reaches 250 mg/dL (13.9 mmol/L) 1
5. Once acidosis resolves (pH >7.3, bicarbonate >15), initiate metformin and transition to subcutaneous insulin 1

Common Pitfalls to Avoid

• Never delay insulin waiting for potassium supplementation if K+ >3.3 mEq/L 1
• Avoid bicarbonate unless pH <6.9—it can worsen intracellular acidosis and cause paradoxical CNS acidosis 1
• Don't stop insulin when glucose normalizes—continue insulin with dextrose-containing fluids until ketoacidosis resolves 1
• Monitor for cerebral edema in adolescents, especially with rapid fluid administration (though more common in younger children) 1