Classically described as three distinct phases:

Timing: < 24 hours

 

Characterized by reconstruction of the body’s normal tissue perfusion and efforts to protect homeostasis. In this phase, there is a decrease in total body energy and urinary nitrogen excretion.

 

 

  • Initial period of shock:
    • ↓ cardiac output
    • Hypotension may occur
    • Lactic acid accumulates
  • Acute inflammatory response occurs at the site of injury:
    • Release of cytokineso
    • Systemic vasodilatation follows
  • The body tries to preserve volume:
    • Hypercoagulable state to reduce bleeding
    • Activation of RAA system
    • ↑ ADH secretion
    • ↑ sodium retention and ↓ urine output
  • Neuro-Endocrine changes:
    • ↑ Activation of sympathetic nervous system
    • ↑ catecholamines
    • ↑ glucagon and ↓ insulin
    • Mildly ↑ glucose
  • Period of ↓ metabolism:
    • ↓ BMR
    • ↓ temperature
    • Substrate is mobilised but not utilised

Timing: 2-8 days

 

Characterized by catabolism and volume replacement to provide a compensating response to the initial trauma. Response is directed to the supply of energy and protein substrates to repair damaged tissues and protect critical organ functions. While necessary for survival in the short term, it can become damaging for the body when the response is severe or long-lasting.

 

  • Period of hypermetabolism
    • ↑ cardiac output
    • ↑ O2 consumption
    • Normal / high body temp
  • Changes driven by:
    • ↑ catecholamines
    • ↑ Counterregulatory hormones
    • ↑ cytokines
  • Ongoing fluid & sodium retention to replenish volume:
    • The third spacing of fluid occurs
  • Widespread metabolic changes
    • Carbohydrate metabolism
      • ↑ Glycogenolysis
      • ↑ Gluconeogenesis
      • Insulin resistance of tissues•
      • Hyperglycaemia
    • Fat metabolism
      • ↑ Lipolysis
      • Free fatty acids used as energy substrate by tissues (except brain)
      • Some conversion of free fatty acids to ketones in liver (used by brain)
      • Glycerol converted to glucose in the liver
    • Protein metabolism
      • ↑ Skeletal muscle breakdown
      • Amino acids converted to glucose in liver
      • Shift toward production of acute-phase proteins
      • Increased nitrogen excretion (negative nitrogen balance)

Timing: 3-14 days

Characterized by the restoration of body weight, skeletal muscle mass and fat stores. Occurs following the period of catabolism, when the release of pro-inflammatory mediators has subsided, and is often associated with clinical improvement in patients such as increased appetite and mobility. 

 

  • Timing of transition depends on injury severity:
    • 3–8 days after uncomplicated elective surgery
    • Several weeks after severe trauma and sepsis
  • Mediated by catabolic hormones:
    • ↑ insulin
    • ↑ growth hormone
    • ↑ androgens
  • Metabolic changes include:
    • Gradual restoration of body protein and fat stores
    • Transition to normal positive nitrogen balance
  • Clinically coincides with
    • ↑ diuresis
    • ↑ appetite
    • ↑ mobility
  • Can last for several months after serious injury