Transcript Inflammatory Process

Inflammatory Process
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
Signs of Swelling
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Redness (Rubor)
Swelling (Tumor)
Pain (Bolar)
Warmth (Calor)
Loss ROM
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)
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Histamine
Seritonin
Bradykinins
Prostaglandins
Note: a 1x increase in arteriole diameter yields a 4x
increase in blood flow
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)
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)
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
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
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
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
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
Phase I: Acute Inflammation
Injury
Onset
Chemical Mediators Released (Chemotaxis)
Cuases Vasodilation
Increases Blood, Plasma, Protiens, Phagocytic material
Protiens are Increased at Injury Site
Increase in protiens causes osmotic relationship with plasma
H2O flows from higher protiens content (injury)
to interstial fluid causing edema/swelling
Swelling/edema are decreased by lymphatic system
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
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.
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
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.
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
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)
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
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
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
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”
Phase I: Late Phase Blood
Clotting
Factor X
Prothrombin
Fibrin Forms
Seal
Thrombin
Fibrin
Mesh
Fibrin Monomer
Fibrogen and
Thrombin Meet
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).
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)
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.
Phase II: Stages of Regeneration:
Cont.
• Vascularization - occurs with the
proliferation of collagen synthesis
– Formation of blood vessels (angiogensis)
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
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
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
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
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
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).
Chronic Inflammation
• Inflammation which continues past 1 month
– Marked by a loss of function
– Fibroblast activity continues forming
granuloma
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
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.
Summary
Injury Response
Wond Healing
Phase I:
Acute Phase
Phase II:
Tissue Repair
Phase III:
Maturation Phase
Inflammation
Approximate Time Table
7-10 days
(Acute phase 3 days)
Resolution
Minor to no cell death
Replacement of Type III
collagen with Type I
Collagen
Granulation
Fibroblasts lay down collagen
Capillarization
Vasodialation
Regeneration
Scar tissue formed
Capilarization
Occurs for up to
1 year
Lymphatic Channels blocked
Approximate time table 2-3 weeks
Chmeical Mediators Release
Osmotic Pressure
Result edema/swelling
Phagocytosis
Margination
THE BIG QUESTIONS!
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When do we use cold?
When do we use heat?
When do we use medications?
When do we use Electrical modalities?
Treatment Planning: Phase I Inflammation
Phase I
Phase II Tissue
Healing
Phase III:
Maturation
Control Active
Encourage
Encourage
Inflam. Limit
Repair/
Tissue
scope of Orig. Replacement Remodeling and
Injury
Damaged Tissue Alignment with
Func. Stresses.
Treatment Planning: Proliferation
Phase
Phase I
Immobilization
Cold Modalities
Pulsed Ultrasound
Compression
Elevation
E-Stim
Phase II Tissue
Healing
Contrast Baths
Compression
Devices
E-Stim
Pulsed/
Continuous US
Traction
Massage
Biofeedback
Heat Modalities
Phase III:
Maturation
Heat Modalities
Continuous US
E-Stim
Massage
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