Diabetic Ketoacidosis
This 11-year-old child most likely has diabetic ketoacidosis (DKA), making option A the correct answer. The clinical presentation of vomiting, lethargy, fruity breath odor (acetone), mild hypotension, hyperglycemia (8.9 mmol/L = 160 mg/dL), and hyponatremia following a recent upper respiratory infection represents the classic triad of DKA: hyperglycemia, metabolic acidosis, and ketosis 1, 2.
Why This is DKA and Not the Other Options
The fruity breath odor is pathognomonic for ketoacidosis and results from acetone production during fat breakdown when insulin deficiency prevents glucose utilization 3. This single finding, combined with the clinical context, essentially confirms DKA 2, 3.
Key Distinguishing Features:
Option B (Uncontrolled Hyperglycemia): The blood glucose of 8.9 mmol/L (160 mg/dL) is actually relatively modest for simple hyperglycemia without ketoacidosis. DKA can occur with blood glucose levels even lower than this, particularly in the era of euglycemic DKA 2. The fruity breath and systemic symptoms indicate ketoacidosis, not just hyperglycemia alone 1, 2.
Option C (Hyponatremia): While hyponatremia (124 mmol/L) is present, it is a consequence of DKA, not the primary diagnosis. The hyponatremia results from osmotic shifts due to hyperglycemia and volume depletion from vomiting and osmotic diuresis 4. Hyponatremia alone would not explain the fruity breath or the constellation of symptoms 4.
Option D (Hyperosmolar state): Hyperosmolar hyperglycemic state typically occurs in type 2 diabetes with much higher glucose levels (often >600 mg/dL), minimal ketosis, and no fruity breath odor 2, 5. This patient's presentation with ketotic breath excludes this diagnosis 2.
Clinical Pathophysiology in This Case
The preceding upper respiratory infection served as the metabolic stressor that triggered counter-regulatory hormone release (cortisol, catecholamines, glucagon), which increased insulin resistance and precipitated DKA in a child with likely undiagnosed type 1 diabetes 4, 6. Infections are among the most common precipitating factors for DKA, particularly in children 2, 5, 7.
The DKA Cascade:
- Absolute insulin deficiency → impaired glucose utilization → hepatic ketone production from free fatty acids 3
- Ketoacidosis → stimulation of chemoreceptors → Kussmaul respirations (though not explicitly mentioned here) 3
- Osmotic diuresis from glucosuria → hypovolemia → hypotension 3
- Vomiting and decreased oral intake → worsening dehydration and electrolyte losses 2, 5
Critical Diagnostic Confirmation Needed
Immediately check blood or urine ketones to confirm DKA, as this is the definitive diagnostic step 1, 8. The American Diabetes Association recommends that ketones >2 mmol/L with blood glucose >270 mg/dL (15 mmol/L) requires emergency assessment 8. However, given this child's clinical presentation with fruity breath, ketones are almost certainly elevated even with the relatively modest glucose level 2.
Additional urgent laboratory evaluation should include 2, 5:
- Venous or arterial blood gas (pH <7.3 and bicarbonate <18 mEq/L confirm DKA)
- Complete metabolic panel with anion gap calculation (anion gap >10 mEq/L)
- Serum electrolytes including potassium (critical for management)
- Blood urea nitrogen and creatinine (assess renal function and dehydration)
Immediate Management Priorities
This child requires hospital admission for intravenous fluid resuscitation and insulin therapy 1, 2, 5. The American Diabetes Association recommends 1:
- Fluid resuscitation: Restore perfusion and correct dehydration 7
- Insulin therapy: Continuous IV insulin infusion to stop ketogenesis 2, 5
- Electrolyte replacement: Particularly potassium monitoring and replacement once urine output is established 2, 7
- Close monitoring: Hourly vital signs, neurologic status, and capillary glucose; electrolytes every 2-4 hours 1
Critical Pitfall to Avoid
Cerebral edema is the most common cause of death in pediatric DKA, particularly in children under age 5 and those presenting with new-onset diabetes 7. Risk factors include overhydration, rapid osmolar shifts, and hypoxia 7. Monitor neurologic status closely and have mannitol immediately available 7. The lethargy described in this patient warrants particular vigilance for deteriorating mental status 5, 7.