Inflammatory Process

KIN 195

Inflammation

What is InflammationA 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

Signs of Swelling

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)HistamineSeritoninBradykininsProstaglandinsNote: 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

inflammationinitially 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 vesselscell death due to anoxia, allows fluid leakage

(permeability increases)increased proteins raise extracellular osmotic

pressure, drawing fluids from the capillariesChemicals alter cell permeability to proteins

and fluidGravity may increase swelling (Capillary

filtration pressures)

Edema/Swelling

To cease hemorrhage/swelling/edemaMust reverse the condition

pressure gradientvessel 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 factorsPhysical trauma may irritate pain receptorsChemical mediators release when cell damage

occurs sensitize pain receptorsTrauma 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/spasm cycle

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 weeksPhase 2: Tissue Formation (Proliferation)

Tissue rebuilding approximately 2-3 weeksThis does not include chronic inflammation

Phase 3: Remodeling PhaseAdapt 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 PhaseTissue Repair Regeneration

Phase I -Early Phase: Acute Inflammation

C h em ica l M ed ia to rs R e leased (C h em otaxis )C u ases V asod ila tion

In c reases B lood , P lasm a, P ro tien s , P h ag ocytic m ate ria l

P ro tien s a re In c reased a t In ju ry S iteIn c rease in p ro tien s cau ses osm otic re la tion sh ip w ith p lasm a

H 2 O flow s from h ig h er p ro tien s con ten t (in ju ry)to in te rs tia l flu id cau s in g ed em a/sw e llin g

S w e llin g /ed em a are d ec reased b y lym p h atic sys tem

In ju ryO n se t

Inflammatory Phases

0%10%20%30%40%50%60%70%80%90%

100%

Day 1 Day 2 Day 3 Day10 Day 30 Day 90

Phase IIIPhase IIPhase I LatePhase I Early

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 called exudation.

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

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- 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 tissue1st line of defense: neutrophiles (in most

abundance from 1-3 days) - phagocytic activity reaches maximum effectiveness within 7-12 days

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

Macrophage

Bacteria

Phase I- Late Phase Phagocytosis Cont.

Pus is the end result - it contains leukocytes, dead tissue and phagogenic materialProlonged puss accumulation can prevent

fibroplasia which begins the wound healing

Fibroblasts are connective tissue responsible for collagen synthesisLigaments, joint capsule, tendon

Osteoblasts: responsible for bone synthesis

Fibroblast Macrophages

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- 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)

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 fibrinFibrin grouped together to form “lattice”

around injured areaFibrin lattice contracts to remove plasma and

compress platelets forming a “patch”

Phase I: Late Phase Blood Clotting

Factor X

Prothrombin

Thrombin

Fibrogen and Thrombin Meet

Fibrin Monomer

Fibrin Mesh

Fibrin Forms Seal

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 peripheryRe-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 synthesisFormation 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 TimesMuscle : approximately 3 weeks Tendon: 4-6 weeksExtent of the tissue damage and vascularity will

aid in determining healing timeAge 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 PhasePurpose of this phase

Strengthen the repaired tissueFiroblasts, myofobrpblasts & Macrophages

reduced to pre-injury stateType III fibrin continues to be replaced by

Type I

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 functionFibroblast activity continues forming

granuloma

Chronic Inflammation

ComplicationsGranuloma: 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 tissueKeloid/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

O sm otic P ressureR esult edem a/sw elling

Lym phatic C hannels b locked

Vasodia lation

C hm eical M ediators R elease

M arg ination

Phagocytos is

Inflam m ationApp rox im ate T im e Tab le

7-10 days(Acute phase 3 days)

Phase I:Acute P hase

App rox im ate tim e tab le 2-3 w eeks

R eg enerationScar tissue form ed

C ap ilarization

G ranulationF ib rob lasts lay dow n collagen

R esolutionM inor to no ce ll death

Phase II:T issue R epair

O ccurs for up to1 year

C ap illarization

R ep lacem ent of Type IIIco llagen w ith Type I

C ollagen

Phase III:M aturation P hase

In jury R esponseW ond H ealing

THE BIG QUESTIONS!

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

Treatment Planning for Phases of Tissue Healing

Phase I Phase II Tissue Healing

Phase III: Maturation

Control Active Inflam. Limit scope of Orig.

Injury

Encourage Repair/

Replacement Damaged Tissue

Encourage Tissue

Remodeling and Alignment with Func. Stresses.

Treatment Planning:

Phase I Phase II Tissue Healing

Phase III: Maturation

Immobilization Cold Modalities

Pulsed Ultrasound Compression

Elevation E-Stim

Contrast Baths Compression Devices E-Stim Pulsed/ Continuous US Traction Massage Biofeedback Heat Modalities

Heat Modalities Continuous US

E-Stim Massage

Treatment Planning: Maturation Phase

Phase I Phase II Tissue Healing

Phase III: Maturation

Cryokinetics Isometics Controlled ROM (CPM) Proprioception CV conditioning

Manual Therapy Passive ROM Active ROM Progressive Resistance Ex Functional Ex Cv Exercise

Overload Resistance Ex

Proprioception Ex Activity Specific

Functional Ex Cv Exercise