What provides the main energy source during critical illness or acute injury?

Adipose Tissue is the Main Energy Source During Critical Illness/Acute Injury

During critical illness or acute injury, adipose tissue (fat) is the main energy source for the body. 1 This metabolic adaptation is crucial for survival and reflects the body's shift in substrate utilization during stress states.

Metabolic Changes During Critical Illness

Energy Substrate Utilization

• Critical illness triggers a complex metabolic response characterized by:
  • Insulin resistance and hyperglycemia 1
  • Altered substrate metabolism with increased reliance on fat oxidation
  • Decreased glucose oxidation despite hyperglycemia
  • Mobilization of energy stores to fuel the stress response

Evidence for Fat as Primary Energy Source

• The most recent evidence demonstrates that critically ill patients with acute kidney injury oxidize:
  • Much fewer carbohydrates (only 56.7% of expected)
  • Much more lipids (150.7% of expected) 1
• This finding has been consistently replicated in multiple studies 1

Metabolic Phases of Critical Illness

1. Acute early phase (ICU day 1-2):

   • Initial "ebb" phase with endogenous glucose production
   • Mobilization of fat stores begins
   • Hormonal changes prioritize delivery of energy substrates to vital tissues 1

2. Acute late phase (ICU day 3-7):

   • "Flow" or catabolic phase with increased fat utilization
   • Breakdown of tissue to provide substrates for survival 1

3. Recovery phase (after ICU day 7):

   • Anabolic recovery with resynthesis of lost tissue
   • Gradual normalization of metabolism 1

Why Fat is the Primary Energy Source

1. Metabolic Efficiency:

   • Fat provides 9 kcal/g versus 4 kcal/g for carbohydrates and proteins
   • Large energy reserves in adipose tissue even in lean individuals

2. Glucose Conservation:

   • Critical illness creates a state where glucose is preferentially directed to:
     • Brain (obligate glucose consumer)
     • Wound healing
     • Immune cell function
   • Fat oxidation spares glucose for these essential functions

3. Insulin Resistance:

   • Critical illness induces insulin resistance
   • This metabolic adaptation limits glucose utilization by peripheral tissues
   • Promotes fat mobilization and oxidation 1

Clinical Implications

• Nutritional Support:

  • Standard EN and PN formulations may contain excessive carbohydrates for critically ill patients 1
  • Consider increasing lipid intake and reducing carbohydrate provision based on actual substrate utilization 1

• Glucose Management:

  • Hyperglycemia is common and should be monitored
  • Target blood glucose of 90-150 mg/dl (5-8 mM) 1
  • Avoid both hyperglycemia and hypoglycemia

• Energy Requirements:

  • During acute phase, energy intake should be equal to or lower than measured energy expenditure
  • In recovery phase, energy intake can be increased 1

Common Pitfalls

1. Overfeeding with Carbohydrates:

   • Can exacerbate hyperglycemia
   • Increases lipogenesis and fat deposition
   • May cause liver steatosis and enhanced production of VLDL triglycerides 1
   • Increases CO2 production and minute ventilation 1

2. Ignoring Additional Energy Sources:

   • For patients on kidney replacement therapy, remember to account for energy from:
     • Citrate (3 kcal/g)
     • Lactate (3.62 kcal/g)
     • Glucose in dialysis/hemofiltration solutions 1

3. Focusing Only on Glucose Control:

   • While glucose management is important, understanding the primary role of fat metabolism is crucial for optimal nutritional support

In conclusion, while all energy sources (carbohydrates, proteins, and fats) are utilized during critical illness, adipose tissue serves as the main energy source, with the body showing a preference for fat oxidation over carbohydrate utilization during these stress states.