THE INJURY RESPONSE PROCESSTHE INJURY RESPONSE PROCESS

EXSS 380: Therapeutic ModalitiesHoffman

STRESSES PLACED ON THE CELLSTRESSES PLACED ON THE CELL

– Body/Cells respond to stress in one of three ways:• Adapt• Becomes injured, but recovers• Dies

The General Adaptation The General Adaptation Syndrome:Syndrome:

• Mechanism for coping with stress• Stages

– ALARM-• “fight or flight response”

– RESISTANCE• -plateau in adaptation (physical fitness)

– EXHAUSTION• -body can’t tolerate stress /system failure

TISSUE TYPES TISSUE TYPES

• Different abilities to regenerate and transmit or absorb various forms of energy.

• Epithelial Tissues: lines the: skin, gut, blood vessels, heart….

• NOTES– Stratum corneum: outer epidermal layer of

nonliving cells– Most modalities must pass through to affect

target tissues.– Transdermal: medications pass through SC via

holes in hair follicles & sweat glands.

TISSUE TYPES cont.TISSUE TYPES cont.• Adipose: fat tissue

– High water content– May hinder modality delivery

• Connective: support structure cells– Collagen

• 11 types• Non elastic

– Elastin

• Muscular: contractile tissues• Nervous: CNS-cells not replaced, PNS-may

regenerate– Not often treated directly with modalities

PreviewPreview

• Injury Process• Phases of Healing

THE INJURY PROCESSTHE INJURY PROCESSFig. 1-2Fig. 1-2

• Primary Response– Tissue injury resulting from traumatic force

• Irreversible

• Secondary Response– Primary injury causes cell death (necrosis),

decreased O2 supply to area– Further cell death

• Figure 1-2 Cycle must be controlled so healing occurs.

Details on Primary Details on Primary ResponseResponse

• 1ST 3-4 DAYS 7 Initial response to trauma• First 10min. vasoconstriction

– Prevents local blood loss

• Vasodilation after 10min., h blood volume to area

• h capillary permeability to fluids and proteins• EXUDATE formed in tissues

– Protein-rich fluid with high concentration of cells

• Prostaglandin (PGE1) increase vascular permeability

• Prostaglandin (PGE2) attracts leukocytes to area– WBC’s that act as scavengers

• Fluids/proteins leak into interstitial space through capillaries and deposit leukocytes to remove dead material (swelling)

• Venous & lymphatic flow blocked-further increased blood flow

• Chemical mediators control inflammation.

Figure 1-2Figure 1-2

PHASES OF HEALINGPHASES OF HEALING

• Inflammatory Phase: – Attempt to isolate and localize trauma

• Proliferation Phase:– Preparation to rebuild damaged tissue

• Remodeling (Maturation) Phase:– Collagen/fibroblasts align and attempt

to replicate original structure/function

OUTLINEOUTLINE

• Healing Phases– Inflammation

• Levels– Circulation and Cellular

• Phases– ACUTE, SUBACUTE, CHRONIC

– Proliferation• Regeneration vs Replacement• Revascularation• Wound contraction• Remodeling

– Maturation

ACUTE INFLAMMATORY ACUTE INFLAMMATORY RESPONSE (Table 1-8)RESPONSE (Table 1-8)

• INFLAMMATION: essential to healing process– Natural, physiological reaction to injury

which mobilizes the body’s defense systems.

• Purpose: control effects of injury and restore tissue homeostasis.

• Triggered by chemical irritation, heat, mechanical trauma, or bacteria.

• Hemodynamic (blood flow) and cellular changes.• 3 Phases: Acute (initial reaction), Sub-acute (2-

4wks), Chronic (>1month.)

CARDINAL SIGNS OF CARDINAL SIGNS OF INFLAMMATIONINFLAMMATION

• HEAT: blood flow, metabolic rate• REDNESS: histamine release• SWELLING:

– Inflammatory agents into area, blocked venous return

• PAIN:– Chemical irritants released (bradykinin,

histamine, prostaglandins, etc.).– Mechanical & chemical pressure on nerve

receptors• LOSS OF FUNCTION:

– Primary tissue damage,muscle guarding…

HEMORRHAGE & EDEMAHEMORRHAGE & EDEMA

• HEMORRHAGE: – Vessel rupture,

vascular permeability– Gradient: pressure in

vessel > external pressure

– Ecchymosis: skin bruising, subcutaneous hemorrhage

– Hematoma: hemorrhage to deep tissue

• EDEMA: buildup of interstitial fluid due to pressure imbalance or obstructed lymphatic & venous return.Depends on:– Severity of injury– Changes in vascular

permeability– Amount of primary &

secondary hemorrhage– Presence of chemical

mediators

EDEMA CONT.EDEMA CONT.• Formation & removal dependent on:

– Vascular hydrostatic pressure: capillary to tissues– Plasma osmotic pressure: tissues to capillaries– Limb hydrostatic pressure: dependent on limb

position

• Normal: vascular = plasma pressure• Injury: capillary permeability, hydrostatic pressure

forces material out.– Edema exacerbates inflammatory process

• Prevents blood & O2 into area• Inhibits venous & lymphatic return by clogging

pathway• Necrosis, pain, ROM

• GOAL: reduce edema through venous & lymphatic return.

VENOUS & LYMPHATIC RETURNVENOUS & LYMPHATIC RETURN

• Thoracic duct: connects lymphatic system to venous

• Venous flow not affected by blood pressure

• Muscle contraction – vessel diameter, blood forced through 1-way valve, valve closes (Fig. 1-5)

• Gravity, passive motion, E-stim., massage all venous flow.

PROLIFERATION PHASEPROLIFERATION PHASE 72HRS.72HRS.3WKS3WKS..

• Growth of new tissue, permanently replaces exudate produced during inflammatory phase.

• Regeneration vs. replacement (Table 1-1)• Replacement: different cell than original

– Skin cells regenerate, muscle cells replace with fibrous scar tissue

– Uncontrolled causes function

PROLIFERATION PHASE:PROLIFERATION PHASE:

• Soft-tissue repair: proliferation of granulation tissue– Fibroblast formation– Collagen synthesis– Tissue remodeling– Tissue alignment

• ATP regulates rate & quality of healing– Provides energy to restore cell-membrane

properties

• Fibroblasts, platelets & macrophages contribute.

PROLIFERATION PHASE:PROLIFERATION PHASE:

• Contraction: wound pulled together forming a “scar”– Weak collagen, vulnerable to tensile forces

• Remodeling: develops more organized matrix in newly developed scar tissue.– External stress dictates alignment--Early ROM

good.– 5-11 days after injury, weak collagen replaced by

stronger, tensile strength.– Scar never as functional as tissue it replaces.

• Inelastic, more similar to ligament & tendon than muscle.

MATURATION PHASEMATURATION PHASE

• Final phase of injury response process—”clean-up”.– May last 1 year or more.

• Decreased vascularity, capillaries, water content.– Fading redness of scar, normalizing skin color,

texture.

• Macrophages, fibroblasts, myofibroblasts reduced to preinjury state.

• Type I collagen increases, tensile strength increases.

• GOAL:– Insure adequate tissue tensile strength by

placing increased stresses on replaced tissue.

THERAPEUTIC MODALITIESTHERAPEUTIC MODALITIES

• THERAPEUTIC MODALITY:• The application of thermal, mechanical,

electrical, or chemical stress to the body for the purpose of healing it from injury.

• Balance between protection from further injury and returning to normal function.