THE INJURY RESPONSE PROCESS EXSS 380: Therapeutic Modalities Hoffman

STRESSES PLACED ON THE CELL –Body/Cells respond to stress in one of three ways: Adapt Becomes injured, but recovers Dies

The General Adaptation 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 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. 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

Preview Injury Process Phases of Healing

THE INJURY PROCESS Fig. 1-2 Primary Response –Tissue injury resulting from traumatic force Irreversible Secondary Response –Primary injury causes cell death (necrosis), decreased O 2 supply to area –Further cell death Figure 1-2 Cycle must be controlled so healing occurs.

Details on Primary Response 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 1-2

PHASES 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

OUTLINE Healing Phases –Inflammation Levels –Circulation and Cellular Phases –ACUTE, SUBACUTE, CHRONIC –Proliferation Regeneration vs Replacement Revascularation Wound contraction Remodeling –Maturation

ACUTE INFLAMMATORY 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 INFLAMMATION 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 & 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. 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 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 PHASE 72HRS.  3WKS. PROLIFERATION PHASE 72HRS.  3WKS. 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: 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: 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 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 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.