1. Chapter 10: Tissue Response to Injury
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The Healing Process
Essential for athletic trainer to possess in depth knowledge of healing process
Understand phases
Time frames physiological changes associated with each phase
Must create a conducive environment for healing
Healing is a continuum
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Figure 10-1
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4. Cardinal Signs of Inflammation
Rubor (redness)
Tumor (swelling)
Color (heat)
Dolor (pain)
Functio laesa (loss of function)
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5. Phases of the Inflammatory Response
(3 separate phases)
1. Inflammatory response phase
2. Fibroblastic repair phase
3. Maturation and remodeling phase
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6. Phase I: Inflammatory Response Phase
Healing begins immediately
Injury results in altered metabolism and liberation of various materials
Initial reaction by leukocytes and phagocytic cells
Goal
Protect
Localize
Decrease injurious agents
Prepare for healing and repair
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Chemical Mediators
Derived from invading organisms, damaged tissue, plasma enzyme systems and white blood cells (WBC’s)
Histamine (from mast cells)
Causes vasodilatation and changes cell permeability owing to swelling
Leukotrienes & prostaglandins
Impact margination (adherence along cell walls)
Increase permeability locally for fluid and protein passage (diapedesis)
Facilitates exudate formation and neutrophil entrance to injured site
Cytokines
Regulate leukocyte and phagocytic activity
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Vascular Response
Vasoconstriction and coagulation occur to seal blood vessels and chemical mediators are released
Presses endothelial lining together to produce local anemia
Followed by vasodilation of blood vessel 5-10 minutes later
Initially increases blood flow (transitory)
Vasodilation decreases blood flow, increased blood viscosity resulting in edema (swelling)
WBC’s able to adhere to walls
Initial effusion of blood and plasma lasts hours
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Figure 10-3
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Clot Formation
Platelets adhere to exposed collagen leading to formation of plug (clot)
Clots obstruct lymphatic fluid drainage and aid in localizing injury
Requires conversion of fibrinogen to fibrin
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
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Figure 10-2
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Chronic Inflammation
Occurs when acute inflammatory response does not eliminate injuring agent
Tissue not restored to normal physiologic state
Involves replacement of leukocytes with macrophages, lymphocytes and plasma cells
As inflammation persists necrosis and fibrosis prolong healing process
Granulation and fibrotic tissue continue to develop within highly vascular and loose connective tissue.
Cause for shift from acute to chronic is unknown
Typically associated with overuse, overload, cumulative microtrauma
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13. Phase II: Fibroblastic Repair Phase
Scar formation through 3 phases
Resolution (little tissue damage and normal restoration)
Restoration (if resolution is delayed)
Regeneration (replacement of tissue by same tissue)
Referred to as fibroplasia
Complaints of pain and tenderness gradually subside during this period
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Figure 10-2
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Scar formation
Capillary buds form
Formation of delicate connective tissue (granulation tissue)
Consists of fibroblasts  extracellular matrix
Develop collagen, Elastin, ground substance, proteoglycans, glycosaminoglycans
With proliferation of collagen scar tensile strength increases
# of fibroblasts gradually diminishes
Types of collagen
16 types; body is 80-90% Types I, II, & III
Normal sequence = minimal scarring
Persistent inflammation = extended fibroplasia
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16. Phase III: Maturation & Remodeling
Long-term process
Realignment of collagen relative to applied tensile forces
Continued breakdown and synthesis of collagen = increased strength
Tissue will gradually assume normal appearance
May require several years to complete
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Figure 10-2
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Role of Progressive Mobilization
Initially must maintain some immobilization in order to allow for initial healing
As healing moves into repair phase controlled activity should be added
Work towards regaining normal flexibility and strength
Protective bracing should also be incorporated
During remodeling aggressive ROM and strength exercises should be incorporated
Facilitates remodeling and realignment
Must be aware of pain and other clinical signs – may be too much too soon
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19. Factors That Impede Healing
Extent of injury
Edema
Hemorrhage
Poor Vascular Supply
Separation of Tissue
Muscle Spasm
Atrophy
Corticosteroids
Keloids and Hypertrophic Scars
Infection
Humidity, Climate, Oxygen Tension
Health, Age, and Nutrition
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Soft Tissue Healing
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
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Figure 10-4
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Tissues of the Body
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
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23. Soft Tissue Adaptations
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
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Cartilage Healing
Limited capacity to heal
Little or no direct blood supply
Chondrocyte 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
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Ligament Healing
Follows similar healing course as other vascular tissues
Proper care will result in acute, repair, and remodeling phases in same time required by other vascular tissues
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
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Factors affecting healing
Surgically repaired ligaments tend to be stronger due to decreased scar formation
With intra-articular tears synovial fluid will dilute hematoma and prevent clotting and spontaneous healing
Exercised ligaments are stronger
Exercise vs. Immobilization
Muscles must be strengthened to reinforce the joint
Increased tension will increase joint stability
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27. Skeletal Muscle Healing
Initial bleeding followed by proliferation of ground substance and fibroblast
Myoblastic cells form = regeneration of new myofibrils
Collagen will mature and orient along lines of tension
Healing could last 6-8 weeks depending on muscle injured
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Tendon Healing
Requires dense fibrous union of separated ends
Abundance of collagen is required for good tensile strength
Too much = fibrosis – may interfere with gliding
Initially injured tendon will adhere to surrounding tissues (week 2)
Week 3 – tendon will gradually separate
Tissue not strong enough until weeks 4-5
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Nerve Healing
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
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30. Modifying Soft-Tissue Healing
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 patients or those with poor diets may take longer
Certain organic disorders (blood conditions) may slow or inhibit the healing process
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Management Concepts
Drug utilization
Anti-prostaglandin agents used to combat inflammation
Non-steroidal anti-inflammatory agents (NSAID’s)
Medications will work to decrease vasodilatation and capillary permeability
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Therapeutic Modalities
Thermal agents are utilized
Heat facilitates acute inflammation
Cold is utilized to slow inflammatory process
Electrical modalities
Treatment of inflammation
Ultrasound, microwave, electrical stimulation (includes transcutaneous electrical muscle stimulation and electrical muscle stimulation)
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Therapeutic Exercise
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
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Bone Healing
Follows same three phases of soft tissue healing
Less complex process
Acute fractures have 5 stages
Hematoma formation
Cellular proliferation
Callus formation
Ossification
Remodeling
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Figure 10-6
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Hematoma Formation
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
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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
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Hard callus becomes more well-formed as osteoblasts lay down cancellous bone, replacing cartilage
With crystallization of callus remodeling begins
Less than ideal immobilization produces a cartilaginous union instead of a bony union
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Ossification is complete when bone has been laid down and the excess callus has been resorbed by osteoclasts
Bone continually adapts to applied stresses
Balance between osteoblast and osteoclast activity
Time required is dependent on various factors
Severity and site of fracture
Age and extent of trauma
Time will range from 3-8 weeks
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40. Acute Fracture Management
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
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Poor blood supply
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
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Infection
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
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43. Healing of Stress Fractures
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
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If osteoclastic activity is not in balance with osteoblastic 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
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Pain
Major indicator of injury
Pain is individual and subjective
Factors involved in pain
Anatomical structures
Physiological reactions
Psychological, social, cultural and cognitive factors
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Pain Categories
Pain sources
Fast versus slow pain
Acute versus chronic
Projected or referred pain
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Pain sources
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
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Fast versus Slow Pain
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 International Association for the Study of Pain (IASP) as pain continuing beyond normal healing time
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Referred Pain
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
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Myofascial Pain
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, myofascitis and muscular strain
Active points cause obvious complaint
Trigger points do not follow patterns
Trigger point area referred to as reference zone which may or may not be proximal to the point of irritation
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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
Autonomic changes may result (vasomotor control, BP and sweating
Dermatomic pain (irritation of A-delta fibers) is sharp and localized
Projects to the thalamus and cortex directly
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Nociception
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 (first-order afferent fibers)
Nociceptor stimulation results in release of substance P
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Second order afferent fibers
Sensory message from dorsal horn to brain (nociceptive specific)
Receive input from A- beta, delta and C-fibers
Overlapping receptive field
Nociceptive-specific second order afferents receive input only from A-delta and C-fibers
All of these neurons synapse with third order neurons
Transmit information to brain centers via ascending spinal tracts
Information is integrated, interpreted and acted upon
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54. Facilitators and Inhibitors of Synaptic Transmission
Nervous system is electrochemical in nature
Chemicals called neurotransmitters are released by pre-synaptic cell to transmit message
Two types mediate pain
Endorphins
Serotonin
Neurotransmitters release stimulated by noxious stimuli- resulting in activation of pain inhibition transmission
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55. Mechanisms of Pain Control
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Gate Theory
Sensory information from cutaneous receptors enters A-Beta afferents to dorsal horn of spinal cord
Pain simultaneously travels along A-delta and c-fibers
Sensory information overrides pain information, closing gate
Pain message never received
Gate control occurs at the level of the spinal cord
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Gate Control Theory
Figure 10-7
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58. Descending Pathway Pain Control
Figure 10-8
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Central Biasing
Stimulation of descending pathways used to inhibit A-delta and C-fiber pain transmission
Involves release of enkephalin and norepinephrine release in dorsal horn blocking and inhibiting synaptic transmission
Release of B-endorphins
Noxious stimuli can trigger endorphin release
Stimulation of pain sensory fibers required
Causes release from hypothalamus
Strong analgesic effects
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60. Release of β -Endorphins
Figure 10-9
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Pain assessment
Self report is the best reflection of pain and discomfort
Utilize multi- and uni-dimensional questionnaires
Assessment techniques include:
Visual analog scales (0-10, marked no pain to severe pain)
Pain charts
McGill Pain questionnaire
Activity pain indicator profiles
Numeric rating scale
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Treating Pain
Modalities
Must have clear rationale for use
Used to relieve pain and control other signs and symptoms of injury/surgery
Must use in conjunction with exercise
Induced analgesia
Introduce thermal agents for pain control
Utilize electrical modalities to reduce pain
TENS, superficial heat/cold, massage used to target Gate Theory
Acupuncture, electrical stimulation, deep massage used to stimulate endorphin release
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Pharmacological Agents
Oral, injectable medications
Commonly analgesics and anti-inflammatory agents
Important to work with referring physician or pharmacist to ensure patient is taking appropriate medications
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64. Psychological Aspects of Pain
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
Physiological and psychological components
Patients, through conditioning, are often able to endure pain and block sensations of minor injuries
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