In a child with a known fatty‑acid‑oxidation disorder who develops fatigue and hypoglycemia during a viral illness, what is the most effective intervention to prevent metabolic decompensation in future illness episodes?

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Management of Fatty Acid Oxidation Defects During Acute Illness

Continuous glucose infusion (Option A) is the most effective measure to prevent metabolic decompensation in children with fatty acid oxidation defects during illness episodes. 1

Pathophysiology and Rationale

Children with fatty acid oxidation defects cannot properly metabolize fatty acids for energy, placing them at high risk for hypoketotic hypoglycemia, hepatic dysfunction, cardiomyopathy, rhabdomyolysis, and Reye-like syndrome during viral illnesses, vomiting, or fasting. 2, 1, 3, 4 These patients are unable to convert fatty acids into energy substrates, resulting in decreased ATP and glucose availability for high-energy-requiring organs. 4

Evidence-Based Acute Management Protocol

The American Association for the Study of Liver Diseases recommends intravenous glucose infusion of at least 10 mg/kg/min to maintain serum glucose above 100 mg/dL during a crisis as first-line therapy. 2, 1

Specific Implementation Steps:

  • Initiate IV glucose at ≥10 mg/kg/min immediately when illness begins to prevent metabolic crisis 1
  • Maintain serum glucose >100 mg/dL throughout the illness to ensure adequate energy supply and prevent lipolysis 2, 1
  • Continue glucose infusion until the child can tolerate adequate oral carbohydrate intake 5, 6

Why Other Options Are Incorrect

Option B (Fasting to promote ketone production) is absolutely contraindicated. These patients have hypoketotic hypoglycemia—they cannot produce adequate ketones from fatty acid oxidation. 3, 4 Fasting would precipitate severe metabolic decompensation and potentially death. 1, 5

Option C (High-fat diet) is contraindicated during acute illness. Long-chain fatty acid oxidation defects specifically require fat restriction (10% of total energy from long-chain triglycerides), not increased fat intake. 6 During illness, these patients need glucose, not fat, as their primary fuel source. 1, 6

Option D (Protein restriction) has no role in fatty acid oxidation defects. Unlike urea cycle disorders or organic acidemias, protein restriction is not indicated in FAODs. 5, 6

Critical Pitfalls to Avoid

  • Never allow elective fasting for procedures without IV glucose support, as prolonged fasting can precipitate metabolic crisis 1
  • Do not delay glucose administration during acute illness—early aggressive treatment with IV glucose can reverse symptoms and prevent progression to fulminant liver failure 2, 1
  • Do not rely on dietary management alone during acute illness—intravenous glucose is required regardless of oral intake attempts 1, 6
  • Avoid the misconception that these patients need ketones—they have hypoketotic hypoglycemia and cannot generate adequate ketones 3, 4

Long-Term Preventive Measures

Between illness episodes, management includes avoiding fasting, maintaining frequent carbohydrate-rich meals, and in long-chain defects, restricting long-chain triglycerides while supplementing medium-chain triglycerides. 5, 6 However, during acute illness, continuous IV glucose supersedes all other interventions. 1

Prognosis with Appropriate Management

Prompt glucose intervention can reverse symptoms, including those associated with acute liver failure, and preclude the need for liver transplantation. 2, 1 The maximum rate of dextrose administration without producing glycosuria is 0.5 g/kg/hour, with about 95% retained when infused at 0.8 g/kg/hour. 7

References

Guideline

Management of Fatty Acid Oxidation Defects During Illness

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Clinical manifestations and management of fatty acid oxidation disorders.

Reviews in endocrine & metabolic disorders, 2020

Research

Fatty acid oxidation disorders.

Annals of translational medicine, 2018

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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