Modalities Midterm

Power points from Intro-Compression

inflammatory stage (time)

around 1- 6 days

proliferative stage (time)

around 3 - 20 days

maturation stage (time)

around 9 - 2 years

inflammatory stage

• prepares the wound for healing (but can become excessive causing damage and scarring)

• sequelae depends on:

  • type of tissue and site of injury

  • local metabolic status

  • type of injury: acute and chronic

• signs: heat, redness, swelling, pain, and loss of function

• 4 stages:

  • vascular response

  • hemostatic response

  • cellular response

  • immune response

inflammatory vascular response

• capillaries, post capillary venules, lymphatic vessels may bleed with trauma

• initial vasoconstriction of damaged vessels (5-10 minutes)

  • mediated by NE

• followed by vasodilation by nearby uninjured vessels (up to 1 hr post)

  • increased capillary permeability

    • vasoactive chemicals:

      • histamine, hageman factor, bradykinin, protaglandins

histamine

causes vasodilation and attracts leukocytes

hageman factor

causes coagulation and increased vascular permeability

bradykinin

causes increased permeability and pain

prostaglandins

causes fevers, increased vascular permeability, and sensitivity of pain receptors

inflammatory hemostatic response

• controls blood loss from damaged vessels

• platelets: create a CLOT to limit bleeding by:

  • BINDING to exposed collagen

  • RELEASING:

    • fibrin- stim clotting and plug the vessel

    • PDGF- attracts fibroblasts, macrophages, monocytes, neutrophils

  • SUPPORTS the wound during this stage

inflammatory cellular response

• leukocytes (WBC) are delivered to area by plasma-within hrs to:

  • clear the area of debris and microorganisms

    • neutrophils and eosinophils

  • prepare area for tissue repair

    • basophils: release histamine and contribute to increased vascular permeability

    • macrophages: phagocytosis and produce enzymes that facilitate removal of necrotic tissue and bacteria

neutrophils

attack FIRST

• spray pathogen and release anti-microbials

• 1st 24 hrs

• clear bacteria and debris by phagocytosis

monocytes

attack SECOND

• macrophage engulfs pathogen

• 24-48 hrs post

• produce chemicals, collagen enzymes, ingest microorganisms, help remove dead tissue and bacteria

lymphocytes

attack THIRD

• coat pathogen with markers for immune response

• supply antibodies to mediate immune response

  • B cells, T cells, natural killer (NK) cells

basophils

• release histamine-increase vascular permeability

eosinophils

• combat parasitic infections, inflammatory cells, contribute to phagocytosis

plasma

carries antobodies, nutrients, coagulation factors, removes waste

RBC

erythrocytes: O2/CO2 exchange

WBC

leukocytes: inflammatory/immune responses

• granulocytes

• eutrophils, basophils, eosinophils

• monosytes

• lymphocytes

platelets

thrombocytes: blood clotting along with coagulation factors

inflammatory immune response

• pathogen in immune system—>

  • neutrophils: attack first

  • macrophages try to eat pathogen

  • complement system:

    • classical

    • alternative

  • T cells: help macrophages destroy pathogen or can destroy infected cell

  • not successful and pathogen invades cell—> NK cell will infected cell

proliferative stage

• rebuilds damaged structures

• strengthens the wound—> collagen production

• involves both:

  • epithelial cells: mucous and membranous linings and skin epidermis

  • connective tissue: fibroblasts, ground substance, and fibrous strands: provide structure

• breakdown fibrin clot allows formation of granulation tissue —> development of new scar

epithelialization

• proliferative stage

  • re-establishment of epidermis (early in superficial, late in deep)

  • provides a barrier against fluid/electrolyte loss and infection

    • cover wound

    • uninjured epithelial cells reproduce and migrate over wound

      • pulls epidermis over the wound

epithelialization/collagen production

• fibroblasts make collagen (in CT)

• formation of new granulation tissue

  • new capillaries, fibroblasts, and myofibroblasts

  • granulation tissue gradually replaces fibrin clot

• fibroblasts initially make type III

• day 12: type I starts to replace type III

wound contraction

• proliferative stage

  • pulls edges of injured area together—> smaller scar formation

• starts by day 5, peaks in 2 wks

• myofibroblasts are primarily reponsible

• longitudinal wounds with edges close tg heal quicky

• circular heal more slowly

• types

  • primary union: use sutures

  • indirect union: natural healing

  • delayed primary intention: sutures applied later

neovascularization

• angiogenesis+ growth of new blood vessels

  • new vacular network

  • anastomosis to pre-existing vessel

  • coupling vessels in injured area

• new cappilaries are weak

  • excessive motion can cause hemorrhaging

  • early motion should be controlled

maturation phase

• can start as esrly as day 9

  • modifies scar tissue into its mature form

  • longest healing process

• scar becomes whiter as vascularization decreases and scar matures

• collagen 3 lysed by enzymes while collagen 1 synthesized to replace it

  • type1: bone, skin, tendon; predominant in mature scars

  • type2: predominant collagen in cartilage

  • type3: initial collagen in wounds, GI tract, uterus, blood vessels

• collagen I synthesis > collagen 3 lysis= hypertrophic scarring (raised scar) or keloids develop

• synthesis of type 1 needs O2, lysis does not

  • use pressure dressings to limit BF

theories of collagen formation

• induction:

  • new collagen automatically mimics the structure of tissue it’s replacing

• tension:

  • internal and external stresses, on injured area, during the maturation phase, determine final collagen structure

    • mm tension, joint mvmt, ST loading and unloading, fascial gliding, temp changes, mobilization

acute inflammation

response <2 weeks

subacute inflammation

>4 weeks

chronic inflammation

months to years

• simultaneous progression of inflammation, tissue destruction, and healing

• results from:

  • repeated injury or interruption of healing process

  • immune response to foreign material or autoimmune disease

local factor affecting healing

• type, size and location of injury

• infection—> affects collagen metabolism

• vascular supply

• external forces—> physical agents

• mvmt—> early mvmt

systemic factors affecting healing

• age (younger is better)

• disease

• medications

• nutrition

cartilage (healing)

• limited healing ability to lack of lymphatics, blood vessels, nerves

• isolated injury—> no clot formed; no neutrophils or macrophages recruited

• this + subchondral bone injured—> subchondral bone vascular network allows formation of fibrin clot

  • inflammatory process leads to formation of granulation tissue

tendons (healing)

• inflammatory and proliferative phases are similar to other tissues

• maturation unique because repaired ___ is very close to original structure (almost regenerated)

ligaments (healing)

• capsular and extracapsular—> usually able to respond to injury with the repair process

• intracapsular:

  • does not respond as well

  • difference due to: synovial environment, limited neovascularization, limited fibroblast migration from surrounding tissue

skeletal muscle (healing)

• injured by contusion, strain, disease

• mm cells cant regenerate but satellite cells may proliferate and differentiate in some cases to form new mm cells after the death of adult mm fibers

bone

• specialized tissue

• can heal itself with the sam tissue as original

• healing classified as: primary (ORIF) and secondary (natural)

• 4 phases

  • (impaction)

  • (induction)

  • inflammation

  • soft callus

  • hard callus

  • bone remodeling

    • begins with fx clinically and radiologically healed

    • ends when healed fibrous bone (weak) is converted to lamellar bone (strong)

      • medullary canal patency is restored

inflammatory phase (modalities)

• reduce circulation, pain, enzyme activity rate, control motion, promote progress to next phase

• cold

• compression

• laser (low-dose—> blue)

• US (pulsed)

proliferative phase (modalities)

• increasing circulation, enzyme activity rate, collagen deposition, promote progress to next phase

• heat

• US (continuous)

• laser (moderate dose)

• mechanical-CPM

maturation phase (modalities)

• modulating the balance of collagen deposition/resoprtion

• improve alignment of new collagen fibers

• heat (superficial and deep)

• cold (post ex)

• mechanical (US, CPM, compression)

• hydro (WP)

• laser (moderate to high dose)