Chapter 10 tissue response to injury
1 / 68

Chapter 10: Tissue Response to Injury - PowerPoint PPT Presentation

  • Uploaded on

Chapter 10: Tissue Response to Injury. Inflammatory Response. Acute Inflammation Short onset and duration Change in hemodynamics, production of exudate, granular leukocytes Chronic Inflammation Long onset and duration Presence of non-granular leukocytes and extensive scar tissue.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about ' Chapter 10: Tissue Response to Injury' - juana

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
Chapter 10 tissue response to injury

Chapter 10:Tissue Response to Injury

Inflammatory response
Inflammatory Response

  • Acute Inflammation

    • Short onset and duration

    • Change in hemodynamics, production of exudate, granular leukocytes

  • Chronic Inflammation

    • Long onset and duration

    • Presence of non-granular leukocytes and extensive scar tissue

Cardinal signs of inflammation
Cardinal Signs of Inflammation

  • Rubor (redness)

  • Tumor (swelling)

  • Color (heat)

  • Dolor (pain)

  • Functio laesa (loss of function)

Phases of the inflammatory response
Phases of the Inflammatory Response

(3 separate phases)

  • 1. Acute phase

  • 2. Repair phase

  • 3. Remodeling phase

Phase i acute phase
Phase I: Acute Phase

  • Initial reaction to an injury occurring 3 hours to 4 days following injury

  • Goal

    • Protect

    • Localize

    • Decrease injurious agents

    • Prepare for healing and repair

  • Caused by trauma, chemical agents, thermal extremes, pathogenic organisms

  • First hour death

    • Vasoconstriction and coagulation occur to seal blood vessels and chemical mediators are released

    • Immediately followed by vasodilation or blood vessel

  • Second hour

    • Vasodilation decreases blood flow, increased blood viscosity resulting in edema (swelling)

  • Second hour (continued) death

    • Exudate increases (high concentration of RBC’s) due to increased vessel permeability

    • Permeability changes generally occur in capillary and venules

    • Margination occurs causing leukocytes to fill the area and line endothelial walls

    • Through diapedesis and chemotaxis leukocytes move to injured area

  • Cellular response death

    • Mast cells (connective tissue cells) and leukocytes (basophils, monocytes, neutrophils) enter area

    • Mast cells with heparin and histamine serve as first line of defense

    • Basophils provide anticoagulant

    • Neutrophils and monocytes are responsible for small and large particles undergoing phagocytosis - ingestion of debris and bacteria

  • Cellular mediation death

    • Histamine provided by platelets, mast cells and basophils to enhance permeability and arterial dilation

    • Serotonin provides for vasoconstriction

    • Bradykinin is a plasma protease that enhance permeability and causes pain.

    • Heparin is provided by mast cells and basophils to prevent coagulation

    • Leukotrienes and prostaglandins are located in cell membranes and develop through the arachadonic acid cascade

    • Leukotrienes alter permeability

    • Prostaglandin add and inhibit inflammation

  • Complimentary systems death

    • Enzymatic proteins that destroy bacteria and other cells through their impact on cell lysis

  • Bleeding and exudate

    • Amount dependent on damage

    • Initial stage: thromboplastin is formed

    • Second stage: Prothrombin is converted to thrombin due to interaction with thromboplastin

    • Third stage: thrombin changes from soluble fibrinogen to insoluble fibrin coagulating into a network localizing the injury

Phase ii repair phase
Phase II: Repair Phase death

  • Phase will extent from 48 hours to 6 weeks following cleaning of fibrin clot, erythrocytes, and debris

  • Repaired through 3 phases

    • Resolution (little tissue damage and normal restoration)

    • Restoration (if resolution is delayed)

    • Regeneration (replacement of tissue by same tissue)

  • Scar formation death

    • Less viable than normal tissue, may compromise healing

    • Firm, inelastic mass devoid of capillary circulation

    • Develops from exudate with high protein and debris levels resulting in granulation tissue

    • Invaded by fibroblasts and and collagen forming a dense scar and while normally requiring 3-14 weeks may require 6 months to contract

  • Primary healing (healing by first intention) death

    • Closely approximated edges with little granulation tissue production

  • Secondary healing (heal by secondary intention)

    • Gapping, tissue loss, and development of extensive granulation tissue

    • Common in external lacerations and internal musculoskeletal injuries

  • Regeneration death

    • Related to health, nutrition and tissue type

    • Dependent on levels of:

      • debris (phagocytosis)

      • endothelial production (hypoxia and macrophages stimulate capillary buds)

      • production of fibroblasts (revascularization allows for enhanced fibroblast activity and collagen production which is tied to Vitamin C, lactic acid, and oxygen

Phase iii remodeling
Phase III: Remodeling death

  • Overlaps repair and regeneration

  • First 3-6 weeks involves laying down of collagen and strengthening of fibers

  • 3 months to 2 years allowed for enhanced scar tissue strength

  • Balance must be maintained between synthesis and lysis

  • Take into consideration forces applied and immobilization/mobilization time frames relative to tissue and healing time

Chronic inflammation
Chronic Inflammation death

  • Result of failed acute inflammation resolution within one month termed subacute inflammation

  • Inflammation lasting months/years termed chronic

    • Results from repeated microtrauma and overuse

    • Proliferation of connective tissue and tissue degeneration

Characteristics of chronic inflammation
Characteristics of Chronic Inflammation death

  • Proliferation of connective tissue and tissue degeneration

  • Presence of lymphocytes, plasma cell, macrophages(monocytes) in contrast to neutrophils (during acute conditions)

  • Major chemicals include

    • Kinins (bradykinin) - responsible for vasodilation, permeability and pain

    • Prostaglandin - responsible for vasodilation but can be inhibited with aspirin and NSAID’s

Factors that impede healing

Extent of injury death



Poor Vascular Supply

Separation of Tissue

Muscle Spasm



Keloids and Hypertrophic Scars


Humidity, Climate, Oxygen Tension

Health, Age, and Nutrition

Factors That Impede Healing

Soft tissue healing
Soft Tissue Healing death

  • Cell structure/function

    • All organisms composed of cells

    • Properties of soft tissue derived from structure and function of cells

    • Cells consist of nucleus surrounded by cytoplasm and encapsulated by phospholipid cell membrane

    • Nucleus contains chromosomes (DNA)

    • Functional elements of cells (organelles) include mitochondria, ribosomes, endoplasmic reticulum, Golgi apparatus & centrioles

Tissues of the body
Tissues of the Body death

  • Bone - not classified as soft tissue

  • 4 types of soft tissue

    • Epithelial tissue

      • Skin, vessel & organ linings

    • Connective tissue

      • Tendons, ligaments, cartilage, fat, blood, and bone

    • Muscle tissue

      • Skeletal, smooth, cardiac muscle

    • Nerve tissue

      • Brain, spinal cord & nerves

Soft tissue adaptations
Soft Tissue Adaptations death

  • Metaplasia - transformation of tissue from one type to another that is not normal for that tissue

  • Dysplasia - abnormal development of tissue

  • Hyperplasia- excessive proliferation of normal cells in normal tissue arrangement

  • Atrophy- a decrease in the size of tissue due to cell death and re-absorption or decreased cell proliferation

  • Hypertrophy - an increase in the size of tissue without necessarily changing the number of cells

Cartilage healing
Cartilage Healing death

  • Limited capacity to heal

  • Little or no direct blood supply

  • Chrondrocyte and matrix disruption result in variable healing

  • Articular cartilage that fails to clot and has no perichondrium heals very slowly

  • If area involves subchondral bone (enhanced blood supply) granulation tissue is present and healing proceeds normally

Ligament healing
Ligament Healing death

  • Follows similar healing course as vascular tissue

  • Proper care will result in acute, repair, and remodeling phases in same time required by other vascular tissue

  • Repair phase will involve random laying down of collagen which, as scar forms, will mature and realign in reaction to joint stresses and strain

  • Full healing may require 12 months

Skeletal muscle healing
Skeletal Muscle Healing death

  • Skeletal muscle cannot undergo mitotic activity to replace injured cells

  • New myofibril regeneration is minimal

  • Healing and repair follow the same course as other soft tissues developing tensile strength (Wolff’s Law)

Nerve healing
Nerve Healing death

  • Cannot regenerate after injury

  • Regeneration can take place within a nerve fiber

  • Proximity of injury to nerve cell makes regeneration more difficult

  • For regeneration, optimal environment is required

  • Rate of healing occurs at 3-4 mm per day

  • Injured central nervous system nerves do not heal as well as peripheral nerves

Modifying soft tissue healing
Modifying Soft-Tissue Healing death

  • Varying issues exist for all soft tissues relative to healing (cartilage, muscle, nerves)

  • Blood supply and nutrients is necessary for all healing

  • Healing in older athletes or those with poor diets may take longer

  • Certain organic disorders (blood conditions) may slow or inhibit the healing process

Management concepts
Management Concepts death

  • Drug utilization

    • Anitprostaglandin agents used to combat inflammation

    • Non-steroidal anti-inflammatory agents (NSAID’s)

    • Medications will work to decrease vasodilatation and capillary permeability

  • Therapeutic Modalities death

    • Thermal agents are utilized

      • Heat stimulates acute inflammation (but works as a depressant in chronic conditions)

      • Cold is utilized as an inhibitor

    • Electrical modalities

      • Treatment of inflammation

      • Ultrasound, microwave, electrical stimulation (includes transcutaneous electrical muscle stimulation and electrical muscle stimulation

  • Therapeutic Exercise death

    • Major aim involves pain free movement, full strength power, and full extensibility of associated muscles

    • Immobilization, while sometimes necessary, can have a negative impact on an injury

      • Adverse biochemical changes can occur in collagen

    • Early mobilization (that is controlled) may enhance healing

Fracture healing
Fracture Healing death

  • Potential serious bone fractures are part of athletics

  • Time is necessary for proper bone union to occur and is often out of the control of a physician

  • Conservative treatment will be necessary for adequate healing to occur

  • Bone undergoes constant remodeling through osteocyte activity

  • Osteocytes cellular component of bone

    • Osteoblasts are responsible for bone formation while osteoclasts resorb bone

  • Cambium (periosteum)

    • A fibrous covering involved in bone healing

    • Vascular and very dense

  • Inner cambium

    • less vascular and more cellular.

    • Provides attachments for muscle, ligaments and tendons

Acute fracture of bone
Acute Fracture of Bone activity

  • Follows same three phases of soft tissue healing

  • Less complex process

  • Acute fractures have 5 stages

    • Hematoma formation

    • Cellular proliferation

    • Callus formation

    • Ossification

    • Remodeling

Hematoma formation
Hematoma Formation activity

  • Trauma to the periosteum and surrounding soft tissue occurs due to the initial bone trauma

  • During the first 48 hours a hematoma within the medullary cavity and the surrounding tissue develops

  • Blood supply is disrupted by clotting vessels and cellular debris

  • Dead bone results in an inflammatory response (vasodilation, exudate cell migration)

Cellular formation
Cellular Formation activity

  • Granulation forms constructing fibrous union between fractured ends

  • Capillary buds allow endosteal cells influx from cambium layer

  • Cells evolve from fibrous callus to cartilage, to woven bone

  • High oxygen tension = fibrous tissue

  • Low oxygen tension = cartilage tissue

  • Bone growth will occur with optimal oxygen tension and compression

Callus formation
Callus Formation activity

  • Soft callus is a random network of woven bone

  • Osteoblasts fill the internal and external calluses to immobilize the site

  • Calluses are formed by bone fragments that bridge the fracture gap

  • The internal callus creates a rigid immobilization early

Ossification months

  • Adequate immobilization and compression will result in new Haversian systems developing

  • Haversian canals allow for the laying down of primary bone

  • Ossification is complete when bone has been laid down and the excess callus has been resorbed by osteoclasts.

Remodeling months

  • Occurs following callus resorption and trabecular bone is laid along lines of stress

  • Bioelectric stimulation plays a major role in completing the remodeling process

    • Osteoblasts are attracted to the electronegative (concave/compression) side

    • Osteoclasts are attracted to the electropositive (convex/tension) side

  • The process is complete when the original shape is achieved or the structure can withstand imposed stresses

Acute fracture management
Acute Fracture Management months

  • Must be appropriately immobilized, until X-rays reveal the presence of a hard callus

  • Fractures can limit participation for weeks or months

  • A clinician must be certain that the following areas do not interfere with healing

    • Poor blood supply

    • Poor immobilization

    • Infection

  • Poor blood supply months

    • Bone may die and union/healing will not occur (avascular necrosis)

    • Common sites include:

      • Head of femur, navicular of the wrist, talus, and isolated bone fragments

    • Relatively rare in healthy, young athletes except in navicular of the wrist

  • Poor immobilization

    • Result of poor casting allowing for motion between bone parts

    • May prevent proper union or result in bony deformity

  • Infection months

    • May interfere with normal healing, particularly with compound fractures

    • Severe streptococcal and staphylococcal infections

    • Modern antibiotics has reduced the risk of infections

    • Closed fractures are not immune to infections within the body or blood

  • If soft tissue alters bone positioning, surgery may be required to ensure proper union

Healing of stress fractures
Healing of Stress Fractures months

  • Result of cyclic forces, axial compression or tension from muscle pulling

  • Electrical potential of bone changes relative to stress (compression, tension, or torsional)

  • Constant stress axially or through muscle activity can impact bone resorption, leading to microfracture

  • If osteoclastic activity is not in balance with oesteoblastic activity bone becomes more susceptible to fractures

  • To treat stress fractures a balance between osteoblast and osteoclast activity must be restored

  • Early recognition is necessary to prevent complete cortical fractures

  • Decreased activity and elimination of factors causing excess stress will be necessary to allow for appropriate bone remodeling

Pain oesteoblastic activity bone becomes more susceptible to fractures

  • Major indicator of injury

  • Pain is individual and subjective

  • Factors involved in pain

    • Anatomical structures

    • Physiological reactions

    • Psychological, social, cultural and cognitive factors

Nociception oesteoblastic activity bone becomes more susceptible to fractures

  • Pain receptors -free nerve endings sensitive to extreme mechanical, thermal and chemical energy

  • Located in meninges, periosteum, skin, teeth, and some organs

  • Pain information transmitted to spinal cord via myelinated C fibers and A delta fibers

  • Nociceptor stimulation results in release of substance P

  • Signal travels along afferent nerves to the spinal cord oesteoblastic activity bone becomes more susceptible to fractures

    • A delta fiber (fast) transmit information to the thalamus concerning location of pain and perception of pain being sharp, bright or stabbing

    • C fibers (slower conduction velocity) deal with diffused, dull, aching and unpleasant pain

    • C fibers signal also passed to limbic cortex providing emotional component to pain

  • Nociceptive stimuli is at or close to an intensity which would result in tissue injury

Endogenous analgesics
Endogenous Analgesics oesteoblastic activity bone becomes more susceptible to fractures

  • Nervous system is electrochemical in nature

  • Chemicals called neurotransmitters are released by presynaptic cell

  • Two types mediate pain

    • Endorphins

    • Seretonin

  • Neurotransmitters release stimulated by noxious stimuli- resulting in activation of pain inhibition transmission

  • Stimulation of periaqueductal gray matter (PGA) and raphe nucleus of pons and medulla cause analgesia

  • Analgesia is the result of opioids release

    • Morphine like substance manufactured in the PGA and CNS

    • Endorphins and enkephalins

  • Other pain modulators

    • Norepinephrine (noradrenergic

    • Seretonin also will serve as neuromodulator

Pain categories
Pain Categories nucleus of pons and medulla cause analgesia

  • Pain sources

  • Fast versus slow pain

  • Acute versus chronic

  • Projected or referred pain

  • Pain sources nucleus of pons and medulla cause analgesia

    • Cutaneous, deep somatic, visceral and psychogenic

    • Cutaneous pain is sharp, bright and burning with fast and slow onset

    • Deep somatic pain originates in tendons, muscles, joints, periosteum and blood vessels

    • Visceral pain begins in organs and is diffused at first and may become localized

    • Psychogenic pain is felt by the individual but is emotional rather than physical

  • Fast versus Slow Pain nucleus of pons and medulla cause analgesia

    • Fast pain localized and carried through A-delta axons

    • Slow pain is perceived as aching, throbbing, or burning (transmitted through C fibers)

  • Acute versus Chronic Pain

    • Acute pain is less than six months in duration

    • Chronic pain last longer than six months

    • Chronic pain classified by IASP as pain continuing beyond normal healing time

  • Projected (Referred) Pain nucleus of pons and medulla cause analgesia

    • Pain which occurs away from actual site of injury/irritation

    • Unique to each individual and case

    • May elicit motor and/or sensory response

    • A-alpha fibers are sensitive to pressure and can produce paresthesia

    • Three types of referred pain include: myofascial, sclerotomic, and dermatomic

  • Myofascial Pain nucleus of pons and medulla cause analgesia

    • Trigger points or small hyperirritable areas within muscle resulting in bombardment of CNS

    • Acute and chronic pain can be associated with myofascial points

    • Often described as fibrositis, myositis, myalgia, myofasciitis and muscular strain

    • Two types of trigger points (active and latent)

    • Active points cause obvious complaint

    • Latent points are dormant potentially causing loss of ROM

  • Trigger points do not follow patterns nucleus of pons and medulla cause analgesia

  • Trigger point area referred to as reference zone which may or may not be proximal to the point of irritation

  • Sclerotomic and dermatomic pain

    • Deep pain with slow or fast characteristics

    • May originate from sclerotomic, myotomic or dermatomic nerve irritation/injury

    • Sclerotomic pain transmitted by C fibers causing deep aching and poorly localized pain

    • Can be projected to multiple areas of brain causing depression, anxiety, fear or anger

    • Gate Theory nucleus of pons and medulla cause analgesia

      • Area in dorsal horn of spinal cord causes inhibition of pain impulses ascending to cortex

      • T-cells will transmit signals to brain

      • Substantia gelatinosa functions as gate determining if stimulus sent to T-cells

      • Pain stimuli exceeding threshold results in pain perception

      • Stimulation of large fast nerves can block signal of small pain fiber input

      • Rationale for TENS, accupressure/puncture, thermal agents and chemical skin irritants

    Central biasing theory
    Central Biasing Theory nucleus of pons and medulla cause analgesia

    Release of b endorphins
    Release of nucleus of pons and medulla cause analgesiaB-Endorphins

    Variation of pain sensitivity
    Variation of Pain Sensitivity nucleus of pons and medulla cause analgesia

    • Hyperesthesia, paresthia or analgesia

    • Pain modulation

      • Mixture of physical and psychological factors

      • Pain management is a challenge to treat

      • Generally acute pain management in athletic training setting

    • Pain assessment nucleus of pons and medulla cause analgesia

      • Self report is the best reflection of pain and discomfort

      • Assessment techniques include:

        • visual analog scales (0-10, marked no pain to severe pain)

        • verbal descriptor scales (marked none, slight, moderate, and severe)

    • Pain Treatment

      • Must break pain-spasm-hypoxia-pain cycle through treatment

      • Agents used; heat/cold, electrical stimulation-induced analgesia, pharmacological agents

    • Heat/Cold nucleus of pons and medulla cause analgesia

      • Heat increases circulation, blood vessel dilation, reduces nociception and ischemia caused by muscle spasm

      • Cold applied for vasoconstriction and prevention of extravasation of blood into tissue

      • Pain reduced through decrease in swelling and spasm

    • Induced analgesia

      • Utilize electrical modalities to reduce pain

      • TENS and acupuncture commonly used to target Gate Theory

    • Pharmacological Agents nucleus of pons and medulla cause analgesia

      • Oral, injectable medications

      • Commonly analgesics and anti-inflammatory agents

    Psychological aspects of pain
    Psychological Aspects of Pain nucleus of pons and medulla cause analgesia

    • Pain can be subjective and psychological

    • Pain thresholds vary per individual

    • Pain is often worse at night due to solitude and absence of external distractions

    • Personality differences can also have an impact

    • A number of theories relative to pain exist and it physiological and psychological components

    • Athlete, through conditioning are often able to endure pain and block sensations of minor injuries