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Chapter 10:
Tissue Response to
Injury
© 2011 McGraw-Hill Higher Education. All rights reserved.
The Healing Process
Essential for athletic trainer to possess in
depth knowledge of healing process
 Three Phases:

1. Inflammatory Response
2. Fibroblastic Repair Phase
3. Maturation- Remodeling Phase
Healing is a continuum
 Can not speed up the process but one can
impede it

© 2011 McGraw-Hill Higher Education. All rights reserved.
Figure 10-1
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Inflammatory Response
Phase
Once tissue is injured- the process of
healing begins immediately
 Cardinal Signs of Inflammation (caused
by damged tissue)

Rubor (redness)
 Tumor (swelling)
 Color (heat)
 Dolor (pain)
 Functio laesa (loss of function)

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Phase I: Inflammatory
Response Phase
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)
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QUESTION
What are the 5 cardinal signs of
inflammation?
 What are the goals during the
inflammatory phase?

Vascular Response
Vasoconstriction (decrease in diameter of
blood vessel) and coagulation occur to seal
blood vessels and chemical mediators are
released
 Followed by vasodilation (increase in
diameter of blood vessel) 5-10 minutes
later

 Initially
increases blood flow (transitory)
 Swelling
 WBC’s able to adhere to walls
 Initial effusion of blood and plasma lasts 24-36
hours
© 2011 McGraw-Hill Higher Education. All rights reserved.
Figure 10-3
© 2011 McGraw-Hill Higher Education. All rights reserved.
QUESTION

What happens to the vascular system
during the Inflammatory Phase?
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
Figure 10-2
© 2011 McGraw-Hill Higher Education. All rights reserved.
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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SCENARIO- INFLAMMATORY
Phase II: Fibroblastic Repair
Phase
Scar formation (begins within the first few
days and last as long as 4- 6 weeks)
 Patient has complaints of pain and
tenderness gradually subside during
this period

Persistent inflammation = extended
fibroplasia
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Figure 10-2
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Phase III: Maturation &
Remodeling
Long-term process, may require several
years to complete
 Realignment of collagen relative to applied
tensile forces
 Continued breakdown and synthesis of
collagen = increased strength
 Tissue will gradually assume normal
appearance

© 2011 McGraw-Hill Higher Education. All rights reserved.
Figure 10-2
© 2011 McGraw-Hill Higher Education. All rights reserved.
Role of Progressive Mobilization
Initially must maintain some immobilization
in order to allow for initial healing during
Inflammation Phase
 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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Factors That Impede Healing





Extent of injury:

macrotears (acute) vs microtears
(chronic)

Edema (swelling)
Hemorrhage
(bleeding)

Poor Vascular
Supply
Separation of
Tissue (smooth vs jagged

edge)


Muscle Spasm
Atrophy

Corticosteroids
Keloids and
Hypertrophic
Scars
Infection
Humidity, Climate,
Oxygen Tension
Health, Age, and
Nutrition
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SCENARIO- MATURATIONREMODELING PHASE
Tissues of the Body
Bone - not classified as soft tissue
 4 types of soft tissue

1. Epithelial tissue
 Skin,
vessel & organ linings
2. Connective tissue
 Tendons,
ligaments, cartilage, fat, blood, and
bone
3. Muscle tissue
 Skeletal,
smooth, cardiac muscle
4. Nerve tissue
 Brain,
spinal cord & nerves
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Cartilage Healing
Limited capacity to heal
 Little or no direct blood supply
 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
Factors affecting ligament healing
Surgically repaired ligaments tend to be
stronger due to decreased scar formation
 With intra-articular tears (inside the joint
capsule) synovial fluid prevents 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
since ligament is more lax
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Skeletal Muscle Healing
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
Nerve Healing
Nerve cell 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

© 2011 McGraw-Hill Higher Education. All rights reserved.
Modifying Soft-Tissue
Healing
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

© 2011 McGraw-Hill Higher Education. All rights reserved.
Management Concepts

Drug utilization
Non-steroidal anti-inflammatory agents
(NSAID’s)
 Medications will work to decrease
vasodilatation and capillary permeability
 Concerns may interfere with Inflammatory
Phase

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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)
© 2011 McGraw-Hill Higher Education. All rights reserved.

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
© 2011 McGraw-Hill Higher Education. All rights reserved.
PART II
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

© 2011 McGraw-Hill Higher Education. All rights reserved.
Figure 10-6 A: Blood vessels broken, forms a hematoma B:
Blood vessels grow into the fracture, soft callus C:
Fibrocartilage becomes ossified forms a bony cartilage D:
Osteoclasts remove excess tissue
© 2011 McGraw-Hill Higher Education. All rights reserved.
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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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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Acute Fracture Management
Must be appropriately immobilized, until Xrays 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

© 2011 McGraw-Hill Higher Education. All rights reserved.

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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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
 Management: Decreased activity and
elimination of factors causing excess
stress will be necessary to allow for
appropriate bone remodeling

To treat stress fractures a balance
between osteoblast and osteoclast activity
must be restored
 Early recognition is necessary to prevent
complete cortical fractures

© 2011 McGraw-Hill Higher Education. All rights reserved.
What are the 4 Conditions that
may interfere with fracture
healing?
Poor Blood Supply
 Poor Immobilization
 Infection
 Soft Tissues between severed ends of
bone

Pain
Major indicator of injury
 Pain is individual and subjective
 ATC needs to have balance between pain
and progression
 Factors involved in pain

Anatomical structures
 Physiological reactions
 Psychological, social, cultural and cognitive
factors

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Scenario- Fracture Healing
Pain Categories
Pain sources
 Fast versus slow pain
 Acute versus chronic
 Projected or referred pain

© 2011 McGraw-Hill Higher Education. All rights reserved.

Pain sources
Cutaneous pain: is sharp, bright and
burning with fast and slow onset
(lacerations, burns, bumps)
 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
(appendix)
 Psychogenic pain: is felt by the individual
but is emotional rather than physical

© 2011 McGraw-Hill Higher Education. All rights reserved.
What are the 4 Pain Sources?
Cutaneous
 Deep somatic
 Visceral
 Pyschogenic


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

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
 Active points cause obvious complaint
 Trigger points do not follow patterns

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Nociception: Pain receptors
Pain receptors -free nerve endings
sensitive to extreme mechanical,
thermal and chemical energy
 Located in meninges, periosteum, skin,
teeth, and some organs
 Afferent nerve fibers: transmit nerve
fibers towards the spinal cord
 Efferent nerve fibers: transmit nerve
fibers from the spinal cord to the
periphery

© 2011 McGraw-Hill Higher Education. All rights reserved.
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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Mechanisms of Pain
Control:
Three Models or Theories
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1. Gate Theory
Sensory information from cutaneous
receptors enters the 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

 Example:
When you bump your head you rub
it . Why?
© 2011 McGraw-Hill Higher Education. All rights reserved.
Gate
Control
Theory
Figure 10-7
© 2011 McGraw-Hill Higher Education. All rights reserved.
Descending
Pathway Pain
Control
Figure 10-8
© 2011 McGraw-Hill Higher Education. All rights reserved.
2. Central Biasing (Descending
pathway)
Stimulation of descending pathways used
to inhibit pain transmission
 Involves release of enkephalin and
norepinephrine release in dorsal horn
blocking and inhibiting synaptic
transmission

 The
pain from the cut on your hand eventually
subsides or reduces to a lower intensity.
 If you consciously distract yourself, you don't
think about the pain and it bothers you less.
 People given placebos for pain control often
report that the pain ceases or diminishes.
© 2011 McGraw-Hill Higher Education. All rights reserved.
Release of
β -Endorphins
Figure 10-9
© 2011 McGraw-Hill Higher Education. All rights reserved.
3. Release of B-endorphins
•
•
•
•
•
Noxious stimuli can trigger endorphin
release
Stimulation of pain sensory fibers required
Causes release from hypothalamus
Strong analgesic effects
IE: acupuncture, acupressure, runner’s
high
Pain assessment: subjective
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: Location and scale
 McGill Pain questionnaire: 78 words may take
20 minutes
 Activity pain indicator profiles: housework,
running
 Numeric rating scale: Verbal
© 2011 McGraw-Hill Higher Education. All rights reserved.
Visual Analog Scale
Pain chart. Use the following instructions: “Please use all of the figures to show me exactly where all
your pains are, and where they radiate to. Shade or draw with blue marker. Only the athlete is to
fill out this sheet. Please be as precise and detailed as possible. Use yellow marker for numbness
and tingling. Use red marker for burning or hot areas, and green marker for cramping. Please
remember: blue = pain, yellow = numbness and tingling, red = burning or hot areas, green =
cramping.” Used with permission from Melzack R: Pain measurement and assessment, New York,
1983, Raven Press.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.

Pharmacological Agents
Oral, injectable medications
 Commonly analgesics and antiinflammatory agents
 Important to work with referring physician
or pharmacist to ensure patient is taking
appropriate medications

© 2011 McGraw-Hill Higher Education. All rights reserved.
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
Patients, through conditioning, are often able to
endure pain and block sensations of minor
injuries
© 2011 McGraw-Hill Higher Education. All rights reserved.