The document summarizes the inflammatory process in three phases: Phase I is the acute phase lasting 1-2 weeks involving vascular responses, swelling, pain, heat, and loss of function due to chemical mediators. Phagocytosis occurs as leukocytes remove dead tissue. Phase II is the tissue formation phase lasting 2-3 weeks involving regeneration, collagen synthesis, wound contraction, and vascularization. Phase III is the remodeling phase lasting up to 1 year involving collagen remodeling and scar maturation to adapt to original tissue. Treatment planning focuses on controlling inflammation, encouraging repair, and functional rehabilitation.

1. THE INFLAMMATORY
PROCESS
NCM 104 – LECTURE
CLASS 2015

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 microorganisms, 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

5. 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

6. 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)

7. 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)

8. Edema/Swelling
• To cease hemorrhage/swelling/edema
• Must reverse the condition
• pressure gradient
• vessel repair

9. 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

10. 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/spasm cycle

11. Phases of the Inflammatory Process
• Phase I: Acute Phase ( 2 subphases)
• Early (Acute): inflammatory response: lasts 2-4 days
• Late (Sub-Acute): continue inflammatory phase
which is usually complete in 2 weeks
• Phase 2: Tissue Formation (Proliferation)
• 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

12. 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

13. Phase I -Early Phase: Acute Inflammation
In ju ry
O n s et
C h em ic al M ed iators R eleas ed (C h em otaxis )
C u as es V as od ilation
In c reas es B lood , P las m a, P rotien s , P h ag oc ytic m aterial
P rotien s are In c reas ed at In ju ry S ite
In c reas e in p rotien s c au s es os m otic relation s h ip with p las m a
H 2 O flows from h ig h er p rotien s c on ten t (in ju ry)
to in ters tial flu id c au s in g ed em a/s wellin g
S wellin g /ed em a are d ec reas ed b y lym p h atic s ys tem

14. Inflammatory Phases
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
Phase III
Phase II
Phase I Late
Phase I Early
Day 1 Day 2 Day 3 Day10 Day 30 Day 90
Chart Designates Percent of phase over time

15. 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 called exudation.

16. Phase I- Early Phase:
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

17. 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.

18. Phase I- Late Phase: 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 days

19. Phase I- Late Phase:
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

20. Phase I- Late Phase
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
• Fibroblasts are connective tissue
responsible for collagen synthesis
• Ligaments, joint capsule, tendon
• Osteoblasts: responsible for bone
synthesis
Fibroblast
Macrophages

21. 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

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

23. 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”

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

25. 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).

26. 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)

27. 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.

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

29. 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

30. 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

31. 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

32. Phase III: Maturation/Remodeling
Phase
• Purpose of this phase
• Strengthen the repaired tissue
• Firoblasts, myofobrpblasts &
Macrophages reduced to pre-injury
state
• Type III fibrin continues to be replaced
by Type I

33. 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

34. 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).

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

36. 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

37. 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.

38. Injury R esp onse
W ond H ealing
Summary
P hase I:
A cute P hase
P hase II:
Tissue R ep air
P hase III:
M aturation P hase
Inflam m ation
A p p roxim ate Tim e Tab le
7-10 days
(A cute p hase 3 days)
R esolution
M inor to no cell death
R ep lacem ent of Typ e III
collag en w ith Typ e I
C ollag en
G ranulation
F ib rob lasts lay dow n collag en
C ap illarization
R eg eneration
S car tissue form ed
C ap ilarization
O ccurs for up to
1 year
C hm eical M ediators R elease
V asodialation
Lym p hatic C hannels b locked
O sm otic P ressure
R esult edem a/sw elling
P hag ocytosis
M arg ination
A p p roxim ate tim e tab le 2-3 w eeks

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

40. Treatment Planning for Phases of Tissue
Healing
P hase I
P hase II T issue
H ealing
P hase III:
M aturation
C ontrol A ctive
E ncourage
E ncourage
Inflam . L im it
R epair/
T issue
scope of O rig.
R eplacem ent R em odeling and
Injury
D am aged T issue A lignm ent w ith
F unc. S tresses.

41. Treatment Planning:
P h ase I
Im m o b ilizatio n
C o ld M o d alities
P u lsed U ltraso u n d
C o m p ressio n
E lev atio n
E -S tim
P h ase II T issu e
H ealin g
C o n trast B ath s
C o m p ressio n
D ev ices
E -S tim
P u lsed /
C o n tin u o u s U S
T ractio n
M assag e
B io feed b ack
H eat M o d alities
P h ase III:
M atu ratio n
H eat M o d alitie s
C o n tin u o u s U S
E -S tim
M assag e

42. Treatment Planning: Maturation Phase
Phase I
Cryokinetics
Isometics
Controlled ROM
(CPM)
Proprioception
CV conditioning
Phase II Tissue
Healing
Manual Therapy
Passive ROM
Active ROM
Progressive
Resistance Ex
Functional Ex
Cv Exercise
Phase III:
Maturation
Overload
Resistance Ex
Proprioception Ex
Activity Specific
Functional Ex
Cv Exercise

43. END OF TOPIC - A

44. INFECTION

45. Review of Physiology
• Resistance
A. Non-specific Resistance
- Body surface barriers
- Anti Microbial Secretions
- Internal Anti Microbial agents
- Phagocytosis part of the reticoendothelial
system
a. phagocytes
- Microphages
- Macrophages

46. • B. Specific Resistance
- lymphatic system
- lymph vessels
- lymph nodes
- lymph
- spleen

47. Specific Resistance (cont)
• Antigen
A. B-lymphocytes
B. T – Lymphocytes
C. Memory Cells

48. • Antibody
1. IgG
2. IgA
3. IgM
4. IgD
5. IgE

49. • Antigen – antibody reactions
a. Agglutination
b. Cytolysis
c. Opsonization
d. Neutralization (viral)
e. Neutralization (toxin)
f. Precipitation

50. Chain of Infection
Susceptible host
Portal of Entry
Etiologic Agent (microorganism)
Reservoir
Method of transmission from reservoir to (Source)
susceptible host
Portal of exit

51. Pathogens
• Bacteria
– Aerobic
– Anaerobic
• Viruses
- intracellular parasite capable of reproducing outside of a living cell.
• Mycoplasma
– similar to bacteria and have no cell wall
– resistant to antibiotics that inhibit cell wall synthesis
• Rickettsiae & Chlamydia
- rigid cell wall; with some feature of both bacteria and viruses.
– Chlamydia- transmitted by direct contact
– Rickettsiae- infect cells of arthropods and are transmitted by these vectors.
• Fungi
- self-limited, affecting the skin and subcutaneous tissue.
• Parasites

52. Reservoir
-where the pathogen lives and multiplies
– Endogenous
– Exogenous
• Mode of Transmission
– Direct contact
– Indirect contact
• Vector
– Droplet or airborne transmission

53. Host Factors
• Factors that enable a host to resist infections:
• Physical barriers
• Hostile environment created by stomach acid
secretions, urine & vaginal secretions.
• Antimicrobial factors e.g. saliva, tears
• Respiratory defenses
• Specific and nonspecific immune responses to
pathogenic invasion.
• Age
• Nutrition

54. Portal of Entry
• Respiratory Tract
• GI Tract
• Genitourinary Tract
• Skin and mucous membrane
• Bloodstream

55. Stages of Infectious Process
• Incubation period
– period begins with active replication but with no symptoms
• Prodromal stage
– Symptoms first appear
• Acute phase
– proliferation and dissemination of pathogens
• Convalescent stage
- containment of infection and pathogens are eliminated
• Resolution
– total elimination of pathogens without residual manifestation
Nosocomial infection
– Infection acquired in a health care setting.
– Typically manifest after 48 hrs.
– UTI most common type

56. FACTORS AFFECTING RISK
OF INFECTION
•
•
•
•
•
•
•
AGE
HEREDITY
LEVEL OF STRESS
NUTRITIONAL STATUS
CURRENT MEDICAL THERAPY
PRE-EXISTING DISEASE
IMMUNIZATION STATUS

57. Standard precautions
•
•
•
•
Blood
All body fluids, secretions, excretions,
Non-intact skin
Mucous membranes
• Essential elements:
• Use barrier protection
• Prevent inadvertent percutaneous exposure, dispose of
needles
• Immediate and thorough hand washing

58. Infection Control and Prevention

59. Infection Control in In-Patient Health Care
Agencies
•
•
•
•
Hand Hygiene
Patient Placement
Protective Equipment
Proper disposal of Soiled Equipment

60. Infection Control In Community – Based
Setting
•
•
•
•
Sanitation
Proper Disposal of Waste
Food Preparation
Report CD Occurrence