Acute Inflammation & Injury Management – Key Vocabulary

Sequence After Cell Injury

  • Trauma → cell injury (reversible) ± cell death.
  • Dead/damaged cells release chemical mediators (e.g. cytokines, lysosomal contents).
  • Mediators initiate inflammation → simultaneous vascular & cellular responses.

Vascular Response

  • Immediate vasoconstriction (limits bleeding).
  • Vasodilation of arterioles/venules.
  • ↑ Permeability of endothelium.
  • ↑ Blood flow → ↑ hydrostatic pressure → fluid (transudate) escapes.
  • Loss of fluid → ↑ blood viscosity (stasis) → slowed flow.
  • With ongoing permeability + stasis, protein & cells leak (exudate).
  • Leukocyte adhesion to endothelium readies cellular phase.

Cellular Response

  • Chemotaxis: inflammatory cells follow chemical gradient.
  • Early infiltrate: neutrophils → later macrophages.
  • Other arrivals: red blood cells, plasma proteins, fibroblasts.
  • Neutrophils/macrophages:
    • Phagocytosis of debris/pathogens.
    • Release enzymes, MMPs\text{MMPs}, ROS, further cytokines.
  • Fibroblasts begin extracellular-matrix repair.

Cardinal Signs of Acute Inflammation

  • Heat & Redness: vasodilation + ↑ blood flow.
  • Swelling: transudate → exudate accumulation in tissue.
  • Pain: cytokines, ROS, MMPs ↑ nociceptor sensitivity + pressure from swelling.
  • Loss of function: combination of pain, swelling, protective inhibition.

PEACE & LOVE (Updated Acute Injury Care)

• P – Protect: short rest limits excessive vasodilation/swelling, prevents further cell death.
• E – Elevate: gravity ↑ venous & lymphatic return → ↓ transudate/exudate.
• A – Avoid anti-inflammatories: early (< 48!–!72  h48!–!72\;\text{h}) NSAIDs blunt necessary inflammatory phase.
• C – Compression: external pressure counteracts vascular leakage, aids lymph drainage.
• E – Education: explain normalcy of inflammation/pain → lowers fear & pain amplification.
• L – Load (after acute phase): graded stress stimulates tissue remodelling & restores function.
• O – Optimism: positive expectations ↓ pain perception, supports recovery.
• V – Vascularisation: light aerobic activity promotes blood supply, nutrient delivery.
• E – Exercise: progressive, functional movements consolidate vascularisation, collagen alignment & full function.

Anti-Inflammatory Medication: Key Points

  • NSAIDs inhibit COX\text{COX} enzymes → ↓ prostaglandins, cytokines.
  • Pros: ↓ pain & swelling → earlier daily function.
  • Cons: If taken in first 48!–!72  h48!–!72\;\text{h} may delay healing (less inflammatory stimulus for repair).
  • Use case-by-case: elite tissue healing vs everyday comfort; monitor GI risks with prolonged use.
  • Simple analgesics (e.g. paracetamol) preferable in early phase for pain control without dampening inflammation.

Innate vs Acquired Responses (Trauma vs COVID)

  • Local mechanical injury: primarily innate, localised (vascular + neutrophil/macrophage) changes at site.
  • Viral infection (e.g. COVID): systemic release of mediators; strong acquired arm—
    • T cells (cytotoxic) target infected cells.
    • B cells produce antibodies → neutralise virus.
  • Cytokine output becomes widespread (“cytokine storm”) → generalised fever, myalgia rather than focal redness/swelling.

Quick Numerical Reminders

  • Vessel–cell distance ≈ 50  μm50\;\mu\text{m} (cells always near capillaries).
  • Early NSAID avoidance window: 48!–!72  h48!–!72\;\text{h} after injury.