What is the primary source of fuel in critical illness or acute injury?

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Primary Source of Fuel in Critical Illness or Acute Injury

The primary source of fuel in critical illness or acute injury is skeletal muscle, which is broken down to provide amino acids for gluconeogenesis and to support the body's increased metabolic demands during the stress response. 1

Metabolic Response in Critical Illness

Critical illness and acute injury trigger a complex metabolic response characterized by distinct phases:

  1. Acute Early Phase (ICU day 1-2):

    • Characterized by insulin resistance and accelerated glucose production
    • Often called "stress diabetes" or "diabetes of injury"
    • Lower energy expenditure compared to pre-injury
    • Endogenous glucose production is enhanced 2, 1
  2. Acute Late Phase (ICU day 3-7):

    • Continued catabolic state with breakdown of tissue
    • Altered pathways of energy production
    • Sustained protein catabolism 2, 1
  3. Recovery Phase (after ICU day 7):

    • Anabolic recovery phase when resynthesis of lost tissue can occur
    • Body becomes more metabolically able to process delivered nutrients 2, 1

Fuel Sources and Their Roles

  • Skeletal Muscle (Primary Source):

    • Broken down to provide amino acids for:
      • Gluconeogenesis
      • Acute phase protein synthesis
      • Wound healing
      • Immune function 1
    • This catabolic response explains the significant muscle wasting observed in critically ill patients
  • Liver:

    • Plays a crucial role in glucose metabolism
    • Increases glucose production through upregulation of both gluconeogenesis and glycogenolysis
    • Requires amino acids from skeletal muscle breakdown to produce glucose
    • Not the primary fuel source itself, but a key processor of fuel 1, 3
  • Fat:

    • Lipid metabolism is increased as fatty acids are used as a fuel source
    • This is secondary to skeletal muscle breakdown in importance 1
  • Amino Acids:

    • Function as substrates rather than primary fuel sources
    • Mobilized from skeletal muscle to support gluconeogenesis and protein synthesis 1, 4

Clinical Implications

  • Hyperglycemia is common due to insulin resistance and accelerated glucose production 5, 6
  • High insulin infusion rates are needed to normalize glucose concentrations in traumatized patients 5
  • Normalization of glucose is primarily achieved by reducing endogenous glucose production rather than increasing glucose disposal 5
  • Recent evidence suggests that aggressive early nutrition may not improve outcomes and could potentially cause harm in some patients 2
  • Less than 100% of energy expenditure should be targeted in the early phase due to endogenous glucose production 2

Nutritional Considerations

  • Higher protein requirements (1.2-2 g/kg/day) are recommended to minimize muscle loss 1
  • Energy provision should be equal or lower than measured energy expenditure during the acute phase 2, 1
  • Careful monitoring of glucose levels is essential due to the common occurrence of insulin resistance 5, 6

Common Pitfalls

  • Overfeeding in the early phase of critical illness may be harmful as endogenous production is already enhanced 2
  • Underestimating protein requirements can lead to excessive muscle catabolism 1
  • Failure to recognize that normalization of glucose requires reduction of endogenous glucose production rather than increasing glucose disposal 5

References

Guideline

Critical Illness and Acute Injury: Metabolic Response and Nutritional Support

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Endogenous Glucose Production in Critical Illness.

Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition, 2021

Research

Metabolic response to critical illness and injury.

AACN clinical issues in critical care nursing, 1994

Research

Alterations in fuel metabolism in critical illness: hyperglycaemia.

Best practice & research. Clinical endocrinology & metabolism, 2001

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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