Transcript HM 100: Prevention & Care Tissue Response to Injury

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
– Understand phases
– Time frames physiological changes
associated with each phase
• Must create a conducive environment
for healing
• Healing is a continuum
© 2011 McGraw-Hill Higher Education. All rights reserved.
Figure 10-1
© 2011 McGraw-Hill Higher Education. All rights reserved.
Cardinal Signs of
Inflammation
•
•
•
•
•
Rubor (redness)
Tumor (swelling)
Color (heat)
Dolor (pain)
Functio laesa (loss of function)
© 2011 McGraw-Hill Higher Education. All rights reserved.
Phases of the Inflammatory
Response
(3 separate phases)
1. Inflammatory response phase
2. Fibroblastic repair phase
3. Maturation and remodeling phase
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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 510 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 24-36
hours
© 2011 McGraw-Hill Higher Education. All rights reserved.
Figure 10-3
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
Figure 10-2
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 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
– 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
Figure 10-4
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
• 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
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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.
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
© 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
Pain
• Major indicator of injury
• Pain is individual and subjective
• Factors involved in pain
– Anatomical structures
– Physiological reactions
– Psychological, social, cultural and cognitive
factors
© 2011 McGraw-Hill Higher Education. All rights reserved.
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, 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• Fast versus Slow Pain
– Fast pain localized and carried through Adelta 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
Mechanisms of Pain Control
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 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.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
Release of
β -Endorphins
Figure 10-9
© 2011 McGraw-Hill Higher Education. All rights reserved.
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.
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
• 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
© 2011 McGraw-Hill Higher Education. All rights reserved.