Acute Inflammation Demystified | 5 Cardinal Signs

Definition: Acute Inflammation

Localized, short-term immune response triggered by tissue injury or infection. (Not a synonym for infection)

Cardinal Sign	Description	Mediators
Rubor (Redness)	Vasoactive mediators → arteriolar smooth muscle relaxation → ↑ blood flow	Prostaglandins, bradykinin, histamine, NO
Dolor (Pain)	Due to stimulation of free nerve ending	Bradykinin, PGE2
Calor (Heat)	Vasodilation → Increased blood flow → Warmth	Prostaglandins, bradykinin, histamine, NO
Tumor (Swelling)	Damage to endothelium → separation of endothelial junction → ↑ vascular permeability → leakage of exudate from postcapillary venule	Histamine, Leukotrienes, Serotonin
Functio Laesa	Loss of function or impaired function in the affected area	–

Cardinal Signs of Inflammation

Event	Description
1. Vasoconstriction of arterioles	Brief vasoconstriction due to neurogenic reflex
2. Vasodilation of arterioles	Histamine and other vasodilators relax vascular smooth muscle, leading to increased blood flow
3. Increased permeability of venules	Histamine and other mediators cause endothelial cell contraction, resulting in endothelial gaps and increased vascular permeability
4. Swelling of tissue (tumor, edema)	Transudate (fluid low in proteins and cells) moves into interstitial tissue due to increased hydrostatic pressure
5. Reduced blood flow	Outflow of fluid into interstitial tissue exceeds lymphatic drainage capacity, leading to reduced blood flow

Fluid exudation
- endothelial injury
- ↑ post-capillary venule permeability
- vasodilation
Leukocyte activation
- emigration
- chemotaxis (bacterial products, complement, chemokines)
- phagocytosis
- killing
Potential outcomes
- restoration of normal structure
- granulation tissue
  - highly vascularized and fibrotic
- abscess
  - fibrosis surrounding pus
- fistula
  - abnormal communication
- fibrosis/scarring
collagen deposition resulting in altered structure and function

	Acute Inflammation	Chronic Inflammation
Pathogenesis	Microbial pathogens, trauma, burns	Persistent AI, foreign bodies, autoimmune disease, certain types of infection (eg TB, Leprosy)
Primary Cells Involved	Neutrophils	Monocytes/macrophages (Key cells), B and T lymphocytes, plasma cells, fibroblasts
Primary Mediators	Histamine (Key mediator), prostaglandins, leukotrienes	Cytokines (e.g., IL-1), growth factors
Necrosis	Present	Less prominent
Scar Tissue	Absent	Present
Onset	Immediate	Delayed
Duration	Few days	Weeks, months, years
Outcome	Complete resolution, progression to chronic inflammation, abscess formation	Scar tissue formation, disability, amyloidosis
Main Immunoglobulin	IgM	IgG
SPE Effect	Mild hypoalbuminemia	Polyclonal gammopathy; greater degree of hypoalbuminemia
Peripheral Blood	Neutrophilic leukocytosis	Monocytosis

AI, Acute inflammation; SPE, serum protein electrophoresis; TB, tuberculosis.

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