1. Acute Inflammation
By
Dr Mohammad Manzoor Mashwani

2. Definition
• It is a rapid host response that serves to deliver
leukocytes and plasma proteins, such as
antibodies, to sites of infection or tissue injury.
• Minutes- Hours- Days
• Less than 48 hours.

3. Time course
Acute inflammation: Less than 48 hours
Chronic inflammation: Greater than 48 hours
(weeks, months, years)
Cell type
Acute inflammation: Neutrophils
Chronic inflammation: Mononuclear cells
(Macrophages, Lymphocytes, Plasma cells).

4. ACUTE INFLAMMATION
LOCAL MANIFESTATIONS
• Heat
• Redness
• Swelling
• Pain
• Loss of function
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5. Pathogenesis: Three main processes occur at the site
of inflammation, due to the release of chemical
mediators :
1.Increased blood flow (redness and warmth).
2.Increased vascular permeability (swelling, pain & loss
of function).
3.Leukocytic Infiltration.

6. Cardinal Signs of Inflammation
Redness : Hyperaemia.
Warm : Hyperaemia.
Pain : Nerve, Chemical
mediators.
Swelling : Exudation
Loss of Function: Pain

9. MechanismInflammation
1. Vaso dilatation
2. Exudation - Edema
3. Emigration of cells
4. Chemotaxis

10. Major components of Ac.
Inflammation
• It has three major components:
1. Alterations in vascular caliber that lead to an
increase in blood flow
2. Structural changes in the microvasculature that
permit plasma proteins and leukocytes to leave
the circulation.
3. Emigration of the leukocytes from the
microcirculation, their accumulation in the
focus of injury, and their activation to eliminate
the offending agent.
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11. Increased Vascular Permeability
(Vascular Leakage)
• A hallmark of acute inflammation causing edema.
• Contraction of endothelial cells resulting in increased
interendothelial spaces is elicited by chemical mediators.
• It is immediate transient response usually short-lived (15–30
minutes).
• In some mild injuries e.g burns, x or ultraviolet radiation, certain
bacterial toxins, occurs after a delay of 2 to 12 hours lasting for
several hours or days, mild endothelial damage.
• Late-appearing sunburn is an example of this type of leakage.
• Increased transport of fluids and proteins, called transcytosis,
through the endothelial cell.
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12. 12

13. ACUTE INFLAMMATION
SYSTEMIC MANIFESTATIONS
• Fever
• Chills
• Myalgia
• Malaise
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14. ACUTE INFLAMMATION
LABORATORY MANIFESTATIONS
1. Leukocytosis
2. Increased ESR
3. Elevated serum acute phase proteins
(C-reactive protein, fibrinogen, etc)
1. Hypercoagulability
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15. STIMULI
for acute inflammation
1. INFECTIOUS
2. PHYSICAL
3. CHEMICAL
4. Tissue Necrosis
5. Foreign Bodies (FBs)
6. Immune “responses”, or “complexes”

16. ACUTE INFLAMMATION
• VASCULAR EVENTS
• CELLULAR EVENTS
• “MEDIATORS”

17. :Lymphatics in inflammation
Lymphatics are responsible for draining edema.
Edema: An excess of fluid in the interstitial tissue
or serous cavities; either a transudate or an
exudate

18. EXUDATION
• AN EXUDATE: A filtrate of blood plasma.
 Extravascular fluid
 High protein concentration
 Contains cellular debris &
 High specific gravity.
• Its presence implies an increase in the normal
permeability of small blood vessels in an area of
injury and, therefore, an inflammatory reaction.18

19. TRANSUDATE:
 A fluid with low protein content
 Little or no cellular material &
 Low specific gravity.
 It is an ultrafiltrate of plasma, resulting from
osmotic or hydrostatic imbalance across the vessel
wall without an increase in vascular permeability.
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21. PUS
Neutrophils + Dead cells + Microbes
 A purulent (infectious) inflammatory
exudate.
 Rich in leukocytes.
 Mostly neutrophils
 Debris of dead cells &
 In many cases microbes.
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22. Leukocyte exudation
 Divided into 4 steps
1. Margination, rolling, and adhesion to endothelium
2. Diapedesis (trans-migration across the endothelium)
3. Migration toward a chemotactic stimuli from the
source of tissue injury.
4. Phagocytosis

24. PHAGOCYTOSIS
• RECOGNITION
• ENGULFMENT
• KILLING
(DEGRADATION/DIG
ESTION)

25. Inflammation Outcome
Fibrosis/Scar
Resolution
Acute Chronic
Injury Inflammation Inflammation
Abscess Fungus
Virus
Cancers
Ulcer .T.B. etc
Fistula Sinus

26. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 12 May 2005 10:21 PM)
© 2005 Elsevier

27. Factors affecting outcome of acute
inflammation
1. Severity of tissue damage
2. Capacity of cells to divide
3. Type of agent causing damage
4. The responsiveness of the host
5. Site involved
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28. Morphologic PATTERNS
of Acute INFLAMMATION
• Serous (watery)
• Fibrinous (hemorrhagic, rich
in FIBRIN)
• Suppurative (PUS)
• Ulcerative

29. BLISTER, “Watery”, i.e., SEROUS

30. PUS
=
PURULENT
ABSCESS
=
POCKET
OF
PUS

31. Ulcerative
• Necrotic and eroded epithelial surface
• Underlying acute and chronic inflammation
• Trauma, toxins, vascular insufficiency

32. Summary
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