1. Inflammatory Process

2. Inflammation What is Inflammation
A vascular and cellular response to trauma. Its purpose is to initiate the healing of the injured tissue
The body’s attempt to dispose of micro-organisms, foreign material and dying tissues so that tissue repair can occur
An inflammatory response may result from external or internal factors (infection)
Protects to the body by localizing and removing the injuring agent

3. Signs of Swelling Redness (Rubor) Swelling (Tumor) Pain (Bolar)
Warmth (Calor)
Loss ROM

4. Signs of Inflammation (Cardinal Signs)
Redness (Rubor):
Caused by blood vessel dilation (the arterioles)
Chemical mediators promote the vessel dilation (contained in the capillary walls or endothelium resulting in immediate response)
Histamine
Seritonin
Bradykinins
Prostaglandins
Note: a 1x increase in arteriole diameter yields a 4x increase in blood flow

5. Signs of Inflammation Cont.
Swelling (tumor)
Edema fluid varies with the stage of inflammation
initially vessel permeability is only slightly altered and no cells or protein escapes and the fluid is mainly water and dissolved electrolytes (transudate): like synovial fluid
As capillary permeability increases and plasma proteins escape the extravascular fluid becomes cloudy and more viscous. This is called exudate (contains a large amount of leukocytes (called pus)

6. Causes of Edema/Swelling-
bleeding from torn vessels
cell death due to anoxia, allows fluid leakage (permeability increases)
increased proteins raise extracellular osmotic pressure, drawing fluids from the capillaries
Chemicals alter cell permeability to proteins and fluid
Gravity may increase swelling (Capillary filtration pressures)

7. This is what we try to do as therapists through modality use
Edema/Swelling
To cease hemorrhage/swelling/edema
Must reverse the condition
pressure gradient
vessel repair
This is what we try to do as therapists through modality use

8. Signs of Inflammation Cont.
Pain (bolar)
Results from irritation of nerve ending by physical or chemical factors
Physical trauma may irritate pain receptors
Chemical mediators release when cell damage occurs sensitize pain receptors
Trauma may result in cell anoxia because of interference with blood flow due to capillary damage

9. Signs of Inflammation Cont.
Warmth (calor)
The result of chemical activity and increased blood flow in the injured area.
Loss of Function
May occur due to pain causing reflex guarding or muscle spasm, spasm decreases metabolic activity and constricts blood flow which causes more pain due to ischemia; thus the pain cycle

10. Phases of the Inflammatory Process
Phase I: Acute Phase
inflammatory response: lasts 2-4 days but is complete in 2 weeks
Phase 2: Tissue Formation (Proliferation)
Subacute phase, Tissue rebuilding approximately 2-3 weeks
This does not include chronic inflammation
Phase 3: Remodeling Phase
Adapt to original tissue
Continues for up to 1 year post injury

11. Phase I: The Inflammatory Process
Early Phase
Insult occurs - may be internal (infection) or external (trauma)
Vasoconstriction to decrease blood flow (first 10 minutes)
Vasodilatation
Late Phase
Tissue Repair
Regeneration

12. Phase I: Acute Inflammation

13. Inflammatory Phases
Chart Designates Percent of phase over time

14. Phase I: Early Phase Inflammation - Vasodilatation
Chemical mediators are released:
histamine, bradykinis, serotonin, prostaglandin's - increase vascular permeability released from mast cells and blood platelets into traumatized tissue.
As fluid filtrates through “gaps in the extravascular spaces this is calls exudation.

15. Phase I: Vasodilatation Cont.
The accumulation of excess fluid is called edema (Swelling)
Vascular permeability due to action of the histamine is short-lived, lasting less than 1 hour

16. Phase I: Early Phase Inflam. - Lymphatic channels are blocked
Local lymphatic channels are blocked by fibrin plugs formed during coagulation. Obstruction of the local lymphatic channels prevents drainage of fluid from the injured site, thus localizing the inflammatory reaction.

17. Phase I: Early Phase Inflammation - Margination
When trauma occurs the endothelial wall is disrupted exposing collagen fibers creating a “stickiness”
WBC’s concentrate in the injury site to rid the body of foreign substances and dead (necrotic) tissue

18. Phase I: Margination Cont.
As circulation slows, leukocytes migrate and adhere to the walls of post-capillary venuels (for approx 1 hour)
The leukocytes pass through the walls of the vessels (diapedesis) and travel to the site of injury (Chemotaxis)

19. Phase I: Early Phase Inflammation - Phagocytosis
Body’s cellular defense to remove toxic material via lymphatic system
Phagocytosis: a process when leukocytes capture and digest foreign matter and dead tissue
1st line of defense: neutrophiles(in most abundance from 1-3 days) - phagocytic activity reaches maximum effectiveness within 7-12 hours

20. Phase I: Phagocytosis Cont.
2nd line of defense: monocytes (which convert into large cells called macrophages) and lymphoctes consume large amounts of bacteria and cellular debris. Monocytes are critical in the initiation of tissue repair because the attract fibroblasts
Bacteria
Macrophage

21. Phagocytosis Cont.
Pus is the end result - it contains leukocytes, dead tissue and phagogenic material
Prolonged puss accumulation can prevent fibroplasia which begins the wound healing
Fibrobalsts are connective tissue responsible for collagen synthesis
Ligaments, joint capsule, tendon
Osteoblasts: responsible for bone synthesis
Fibropblast
Macrophages

22. Phase I: Late Phase Blood Clotting
Ruptured vessels release Enzyme (Factor X)
Factor X reacts with prothrombin (free floating in blood)
Thrombin then stimulates fibrogen into its individual form fibrin
Fibrin grouped together to form “lattice” around injured area
Fibrin lattice contracts to remove plasma and compress platelets forming a “patch”

23. Phase I: Late Phase Blood Clotting
Factor X
Prothrombin
Fibrin Forms Seal
Thrombin
Fibrin Mesh
Fibrogen and Thrombin Meet
Fibrin Monomer

24. Phase II: Regeneration:
The replacement of destroyed cells by reproducing healthy cells adjacent to the wound (humans capacity to regenerate tissue is limited and further affected by age and nutritional state).

25. Phase II: Stages of Regeneration:
Stage starts with periphery
Re-eptheliaization is proliferation of peripheral epithelial tissue which then migrates to the wound until the area is covered.
Capillarization (Capillary buds proliferate and connect forming new capillaries which gives the red, granular appearance to the scar (granular tissue)

26. Phase II: Stages of Regeneration: Cont.
Fibroplasia occurs due to fibroblasts which arises from undifferentiated mesenchymal cells and migrate into the area along fibrin strands and begin to synthesize scar tissue. Scar tissue is CT and mostly collagen and mucopolysaccharides. Fibroblasts secrete both, contributing tensile strength to the repair. Scar tissue very inelastic compared to surrounding tissue.

27. Phase II: Stages of Regeneration: Cont.
Vascularization - occurs with the proliferation of collagen synthesis
Formation of blood vessels (angiogensis)

28. Phase II: Collagen Synthesis:
Occurs within 12 hours of injury to 6 weeks (average 3 weeks)
Type I: collagen: associate with muscular tissue (larger and stronger fibers)
Type III collage: smaller fibers, less cross linking and highly disorganized (ligamentous, tendinous)
Type III with time is replaced by Type I collagen

29. Phase II: Collagen Synthesis Cont.
Tissue Healing Times
Muscle : approximately 3 weeks
Tendon: 4-6 weeks
Extent of the tissue damage and vascularity will aid in determining healing time
Age may also be a factor in healing

30. Phase II: Stages of Regeneration: Cont.
Wound Contraction:
Wound contraction begins to occur in CT as the myobroblasts (actin-rich fibroblasts) contract. Myofibroblasts move toward the center of the wound, helping reduce the size of the area to be covered.
Outside-in

31. Phase III: Maturation/Remodeling Phase
Purpose of this phase
Strengthen the repaired tissue
Firoblasts, myofobrpb;asts & Macrophages reduced to preinjury state
Type I fibrin continues to be replaced by type III

32. Phase III: Maturation/Remodeling Phase (day 9 onward)
Blends in with the repair phase, original collagen fibers were randomly oriented. During remodeling, the fibers become more organized, parallel to the wound surface which provides greater tensile strength
The type of tissue involved will determine the duration and extent of remodeling activity

33. Phase III: Maturation/Remodeling Phase Cont.
Strengthening of scar tissue continues from 3 months to 1 year, but fully mature scar in only 70% as strong as intact tissue.
Motion will influence the structure and functional capacity of scar tissue (controlled stress increases functional capacity, allows healing and reduces adhesion formation).

34. Chronic Inflammation Inflammation which continues past 1 month
Marked by a loss of function
Fibroblast activity continues forming granuloma

35. Chronic Inflammation Complications
Granuloma: large mass of weaker scar tissue (usually due to large inflammation and activity without regard to healing time)
Retardation of muscle fiber: with excessive granuloma fibroblasts cannot reach damaged tissue
Adhesions/contractures in tissue
Keloid/hypotrophic scars

36. Abnormal scarring:
Hypertophic scar or keloid scar. Biological difference not well understood, but clinically hypertrophic scar is contained within the boundaries of the original wound while a keloid scar extends beyond the borders of the original wound.

37. Summary

38. THE BIG QUESTIONS! When do we use cold? When do we use heat?
When do we use medications?
When do we use Electrical modalities?

39. Treatment Planning: Phase I - Inflammation

40. Treatment Planning: Proliferation Phase

41. Treatment Planning: Maturation Phase