What is "Metabolic Response to Injury"?

The 11 Sections in Your PDF

1. Introduction & Homeostasis

• The body normally keeps a stable internal environment (homeostasis). Injury disrupts it.
• The response has two phases: a catabolic (breakdown) phase, then an anabolic (rebuilding) phase.

2. The Magnitude of the Response

• Figure 1.1 explained: Two graphs showing that more severe injury = higher metabolic rate + more urinary nitrogen loss (= more muscle breakdown). Major trauma peaks at 130–135% of normal metabolic rate. Starvation alone actually LOWERS the metabolic rate.

3. Tissue Damage & Inflammation

• Damaged cells release DAMPs (danger signals). Immune cells detect them via Toll-like receptors.
• This activates inflammasomes → caspases → cytokines (IL-1, IL-6, TNF-alpha, IL-8).
• Unchecked, this becomes SIRS → MODS (organ failure, 25% mortality).

4. The Neuroendocrine Response

• Figure 1.2 explained: A pathway diagram showing injury → nerve signals → hypothalamus → pituitary → cortisol + adrenaline + glucagon. Simultaneously, immune cytokines rise and insulin/IGF-1/testosterone/T3 all fall.
• The result is an emergency fuel mobilisation system.

5. Metabolic Changes After Surgery & Trauma

• Catabolic phase (0–48 hours): low BP, low temperature, high blood sugar, lactic acid.
• Flow phase (days–weeks): hypermetabolism, fever, muscle wasting, fluid leakage into tissues.
• The whole response is driven by IL-1, IL-6, and TNF-alpha.

6. Managing the Catabolic Stress Response

• Figure 1.3 explained: An arrow diagram showing that the body deliberately transfers amino acids (especially glutamine and alanine) FROM muscle/fat/skin TO the liver, immune system, and wound. Muscle wasting is intentional — it is the body funding its repair programme.

7. Hypermetabolism & Muscle Wasting

• Trauma patients burn 15–25% more energy than normal.
• Figure 1.4 explained: A circular molecular diagram of the ubiquitin-proteasome system — the "shredder" that breaks muscle proteins into amino acids in steps: cut (caspases/calpains) → tag with ubiquitin (E1/E2/E3 enzymes + ATP) → feed into 26S proteasome → release amino acids. In severe sepsis, this destroys up to 500 g of muscle per day.

8. Liver Changes & Insulin Resistance

• The liver switches from making albumin to making CRP, fibrinogen, and complement proteins.
• Insulin resistance develops (like Type 2 diabetes) — cells ignore insulin, blood sugar stays high.

9. Body Composition Changes

• Figure 1.5 explained: A stacked bar showing that a 70 kg man has ~13 kg fat, ~12 kg protein, ~42 L water, ~3 kg minerals. The protein (muscle) reserve is what gets raided during catabolism.
• Figure 1.6 explained: Three curves showing different weight trajectories: sepsis patients gain fluid weight first then crash; surgical patients lose weight then recover; starvation patients steadily lose weight.

10. Avoidable Factors

• Figure 1.7 explained: A flowchart showing that pain, hypothermia, immobility, starvation, bleeding, and low blood pressure all amplify the catabolic response by activating the sympathetic system and cytokine cascade simultaneously. Fix these = better survival.

11. Enhanced Recovery After Surgery (ERAS)

• Figure 1.8 explained: Two recovery curves showing that ERAS (minimal access surgery + epidural pain control + early feeding + early mobilisation) produces a much shallower dip in functional capacity and recovery in days instead of weeks. Hospital stay reduced by 30–50%.