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Tissue Response to Injury
Inflammatory Response• Acute Inflammation– Short onset and duration– Production of exudate, leukocytes
• Chronic Inflammation– Long onset and duration– Presence of extensive scar tissue
Cardinal Signs of Inflammation
• Rubor (redness)• Tumor (swelling)• Color (heat)• Dolor (pain)• Functio laesa (loss of function)
Phases of the Inflammatory Response
(3 separate phases)
• 1. Acute phase• 2. Repair phase• 3. Remodeling phase
Phase I: Acute Phase• Initial reaction to an injury occurring 3 hours to
2 days following injury• Goal– Protect– Localize– Decrease injurious agents– Prepare for healing and repair
• Caused by trauma, chemical agents, thermal extremes, pathogenic organisms
• External and internal injury result in tissue death and cell death
• Decreased oxygen to area increases cell death
• Rest, ice, compression & elevation are critical to limiting cell death
• First hour– 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)– Exudate increases (high concentration of
RBC’s) due to increased vessel permeability– Permeability changes generally occur in
capillary and venules
• Cellular response– 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
Phase II: Repair Phase• 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– 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)– 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– 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• 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
• 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
• 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• 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
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
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
Cartilage Healing• 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• 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 cannot undergo mitotic activity to replace injured cells
• New myofibril regeneration is minimal• Healing and repair follow the same
course as other soft tissues.
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
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 athletes or those with poor
diets may take longer• Certain organic disorders (blood conditions)
may slow or inhibit the healing process
Management Concepts
• 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– 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– 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
• 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• Follows same three phases of soft tissue healing• Less complex process• Acute fractures have 5 stages– Hematoma formation– Cellular proliferation– Callus formation– Ossification– Remodeling
Callus Formation
• 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
• Hard callus formation occurs after 3-4 weeks and lasts 3-4 months
• Hard callus is a gradual connection of bone filaments to the woven bone
• Less than ideal immobilization produces a cartilagenous union instead of a bony union
Ossification
• Ossification is complete when bone has been laid down and the excess callus has been resorbed by osteoclasts.
Remodeling• Occurs following callus resorption and
trabecular bone is laid along lines of stress• Bioelectric stimulation plays a major role
in completing the remodeling process• The process is complete when the original
shape is achieved or the structure can withstand imposed stresses
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
• 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
• 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
• Gate Theory– 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
• Pain assessment– 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– 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
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 and it
physiological and psychological components• Athlete, through conditioning are often able to endure
pain and block sensations of minor injuries