Inflammatory Process

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Inflammatory Process
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Inflammation

• What is Inflammation
• A vascular and cellular response to trauma. Its
  purpose is to initiate the healing of the injured
  tissue
• The bodys 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

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Signs of Swelling

• Redness (Rubor)
• Swelling (Tumor)
• Pain (Bolar)
• Warmth (Calor)
• Loss ROM

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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

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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)

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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)

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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

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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

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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

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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

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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

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Phase I Acute Inflammation
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Inflammatory Phases
Chart Designates Percent of phase over time
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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.

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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

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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.

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Phase I Early Phase Inflammation - Margination

• When trauma occurs the endothelial wall is
  disrupted exposing collagen fibers creating a
  stickiness
• WBCs concentrate in the injury site to rid the
  body of foreign substances and dead (necrotic)
  tissue

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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)

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Phase I Early Phase Inflammation - Phagocytosis

• Bodys 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

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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
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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
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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

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

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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)

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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.

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Phase II Stages of Regeneration Cont.

• Vascularization - occurs with the proliferation
  of collagen synthesis
• Formation of blood vessels (angiogensis)

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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

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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

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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

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Phase III Maturation/Remodeling Phase

• Purpose of this phase
• Strengthen the repaired tissue
• Firoblasts, myofobrpbasts Macrophages reduced
  to preinjury state
• Type I fibrin continues to be replaced by type III

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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

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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).

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Chronic Inflammation

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

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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

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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.

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Summary
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THE BIG QUESTIONS!

• When do we use cold?
• When do we use heat?
• When do we use medications?
• When do we use Electrical modalities?

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Treatment Planning Phase I - Inflammation
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Treatment Planning Proliferation Phase
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Treatment Planning Maturation Phase