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Tissue Response to Injury

Tissue healing

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Page 1: Tissue healing

Tissue Response to Injury

Page 2: Tissue healing

Inflammatory Response• Acute Inflammation– Short onset and duration– Production of exudate, leukocytes

• Chronic Inflammation– Long onset and duration– Presence of extensive scar tissue

Page 3: Tissue healing

Cardinal Signs of Inflammation

• Rubor (redness)• Tumor (swelling)• Color (heat)• Dolor (pain)• Functio laesa (loss of function)

Page 4: Tissue healing

Phases of the Inflammatory Response

(3 separate phases)

• 1. Acute phase• 2. Repair phase• 3. Remodeling phase

Page 5: Tissue healing

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

Page 6: Tissue healing

• 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

Page 7: Tissue healing

• 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)

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• Second hour (continued)– Exudate increases (high concentration of

RBC’s) due to increased vessel permeability– Permeability changes generally occur in

capillary and venules

Page 9: Tissue healing

• 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

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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)

Page 11: Tissue healing

• 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

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• 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

Page 13: Tissue healing

• 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

Page 14: Tissue healing

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

Page 15: Tissue healing

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

Page 16: Tissue healing

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

Page 17: Tissue healing

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

Page 18: Tissue healing

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

Page 19: Tissue healing

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

Page 20: Tissue healing

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

Page 21: Tissue healing

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

Page 22: Tissue healing

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.

Page 23: Tissue healing

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

Page 24: Tissue healing

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

Page 25: Tissue healing

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

Page 26: Tissue healing

• 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

Page 27: Tissue healing

• 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

Page 28: Tissue 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

Page 29: Tissue healing

• 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

Page 30: Tissue healing

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

Page 31: Tissue healing
Page 32: Tissue healing

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

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• 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

Page 34: Tissue healing

Ossification

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

Page 35: Tissue healing

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

Page 36: Tissue healing

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

Page 37: Tissue healing

• 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

Page 38: Tissue healing

• 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

Page 39: Tissue healing

• 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

Page 40: Tissue healing

• 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

Page 41: Tissue healing

• 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

Page 42: Tissue healing

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