Chapter 2: Understanding &
Managing the Healing Process
Through Rehabilitation
Understanding the Healing
Process
• Programs must be
based on healing
process framework
• Phases
– Inflammatory
– Fibroblastic-repair
– Maturationremodeling
– No definitive
beginning or end
The Primary Injury
• Described as either chronic or acute
• Macrotraumatic injuries
– Result of acute trauma
– Produce immediate pain and disability
– Fractures, dislocations, sprains, strains
• Macrotraumatic injuries
– Overuse injuries, resulting from repetitive
overload, incorrect mechanics
– Tendinitis, tenosynovitis bursitis
• Secondary injury
– Inflammatory or secondary hypoxic injury
Inflammatory Response
Phase I
• Injury results in altered cellular metabolism and
chemical mediators
• Macroscopic characteristics
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Swelling
Tenderness
Redness
Increased temperature
• Initial response is critical in healing process
– An injury must cause the “Inflammatory
Response”
• Vascular Reaction
– Involves vascular spasm, formation of clot and fibrous
tissue growth
– Vasoconstriction occurs 5-10 minutes following injury
– Causes anemia followed by hyperemia due to dilation
– Ultimately a slowing of blood flow occurs progressing
to stasis and stagnation
– Initial response lasts 24-48 hours
• Chemical Mediators
– Histamine
• Vasodilation and
increased cell
permeability
– Leukotaxin
• Margination
• Increased
permeability
– Necrosin
• Phagocytic activity
• Swelling is directly
related to extent of
vessel damage
• Clot Formation
– Disrupted vessel walls expose collagen within
endothelium walls
– Platlets adhere to vascular wall in conjunction
with leukocytes forming a plug
– Plug obstructs local lymphatic fluid drainage
– Results in localization of the injury
– Precipitated by fibrinogen  fibrin conversion
• Cascade of events involving thromboplastin,
prothrombin, and thrombin
– Clot formation begins 12 hours after injury
and is complete within 48 hours
– Clot vs. Scab
• Chronic inflammation
– Occurs when acute inflammation does not eliminate
injuring agents and restore normal physiological state
– Leukocytes are replaced with macrophages,
lymphocytes and plasma cells
– Specific mechanism is unknown
• Overuse and overload related
– No specific time frame in which acute becomes
chronic inflammation
– Resistant to physical and pharmacological agents
– Introduction of non-steroidal anti-inflammatory drugs
(NSAID’s) some research indicates impedance of
healing
Fibroblastic-Repair
Phase II
• Fibroplasia
– Active scar formation
– May last 4-6 weeks
– Signs and symptoms
will subside
– Endothelial capillary
buds develop
allowing for aerobic
healing
– Increased blood flow
for nutrient delivery
• Fibroblastic-Repair (continued)
– Granulation tissue develops with breakdown of fibrin
clot
– Granulation tissue composed of fibroblasts, collagen
and capillaries
– Fibroblasts synthesize extracellular matrix containing
collagen and elastin
• Proteoglycans
• Glycosaminoglycans
• Fluid
– Collagen is deposited randomly at day 6 or 7
• Results in increased scar tensile strength
– Persistent inflammatory response promotes extended
fibroplasia, resulting in increased scarring
Maturation-Remodeling
Phase III
• Realignment of collagen
• Continued breakdown and
synthesis of collagen
• Increased stress and strain
results in increased collagen
realignment
• Nonvascular, contracted,
strong, firm scar present after
3 weeks
• Maturation may require
several years to complete
Role of Progressive Controlled
Mobility
• Wolff’s Law
– Bone and soft tissue will respond to physical
demands placed upon them
– Remodeling and realignment
• Initial immobilization is necessary – what happens
to: ligaments, tendons, bone?
• Controlled mobilization enhances
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Scar formation
Revascularization
Muscle regeneration and fiber reorientation
Tensile properties
• Controlled activity allows for gradual return to
normal levels of function
Factors that Impede Healing
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Extent of Injury
Edema
Hemorrhage
Poor Vascular Supply
Separation of tissue
Muscle spasm
Atrophy
• Corticosteroids
• Keloids and
hypertrophic scars
• Infection
• Humidity, climate, and
oxygen tension
• Health, age, and
nutrition
Pathophysiology of Injury to
Various Tissues
• Epithelial Tissue
– Covers internal and external surfaces
• Skin, outer layer of organs, inner lining of blood vessels,
glands
– Purposes:
• to protect and form structure for other tissues
• Function in absorption and secretion
– Relies on diffusion for fluid, oxygen, waste and
nutrient transport
– Injuries
• Abrasions, lacerations, punctures, avulsions
• Infection, inflammation or disease
• Connective Tissue
– Functions
• Provides body framework, fill space, stores fat
• Helps repair tissue, produces blood cells, protects
against infection
– Cell types
• Defined by extracellular matrix (fibers, ground
substance)
• Macrophages, mast cells, fibroblasts
– Collagen
• Strong, flexible inelastic structure that holds connective
tissue together
• Enables tissue to resist mechanical deformation –
oriented in direction of tensile stress
• Mechanical properties
– Elasticity, viscoelasticity, plasticity
• Physical properties
– Force-relaxation, creep response, hysteresis
• Types of Connective Tissue
– Fibrous
• Dense – tendon, aponeurosis, fascia, ligaments, joint
capsule
• Loose – adipose
– Cartilage
• Rigid connective tissue composed of chondrocytes
within a collagen, elastin, ground substance matrix
• Poor blood supply slows healing
• Hyaline, fibrocartilage and elastic
– Reticular connective tissue
• Composed of collagen and supports structural walls of
organs
– Elastic connective tissue
• Composed of elastic fibers and found in blood vessels,
airways and hollow organs
• Bone
– Consists of living
cells and mineral
deposits
– Cancellous – spongy
bone
– Cortical bone – solid
– Rich blood supply
– Functions to provide
support, movement
and protection
• Blood
– Compose of various cells suspended in fluid
intracellular matrix (plasma)
– Plasma contains red blood cells, white blood cells
and platelets
– Essential for nutrition, cleansing, and physiology
of the body
Ligament Sprains
• Sprains involve
damage to a
ligament
• Ligaments
– Inelastic band of
tissue
– Provides joint
stability, controls
bone position during
joint motion,
provides
proprioceptive input
• Grades of Ligament Sprains
– Grade I - some pain, minimal loss of function, no
abnormal motion, and mild point tenderness
– Grade II - pain, moderate loss of function, swelling,
and instability
– Grade III - extremely painful, inevitable loss of
function, severe instability and swelling, and may
also represent subluxation
Ligament Healing
• Follows same course of repair events as with
other vascular tissues
– Ligaments sprained extra-articularly result in bleeding
in the subcutaneous space
– Intra-articular ligament sprains result in bleeding
within the capsule
– Vascular proliferation, fibroblastic activity and clot
formation occur during the initial 6 weeks of recovery
– Collagen and ground substance work to bridge torn
ends of ligaments via scarring
– Scar maturation will gradually occur and collagen
tensile strength will increase
Factors Affecting Ligament
Healing
• Surgically repaired extra-articular ligaments
– Heal with less scarring
– Stronger than un-repaired ligaments
• Non-surgically repaired ligaments
– Heal via fibrous scarring resulting in ligament lengthening
and increased joint instability
• Intra-articular ligament damage
– Results in synovial fluid presence, diluting hematoma,
disrupting clot and healing
• Ligament healing and immobilization
• Muscle strength training can enhance joint stability
Fractures of Bone
• Acute bone fractures - partial or complete disruption
that can be either closed or open (through skin);
serious musculoskeletal condition
• Risk of infection is increased with open fractures
• Type of fractures include:
– greenstick, impacted, longitudinal, oblique, serrated,
spiral, transverse, comminuted, blowout, and avulsion
A: Greenstick
E: Comminuted
B: Transverse
F: Impacted
C: Oblique
G: Avulsion
D: Spiral
• Stress fractures- no specific cause but with a
number of possible causes
– Overload due to muscle contraction
– Altered stress distribution due to muscle fatigue, changes
in surface
– Rhythmic repetitive stress vibrations
• Signs and symptoms
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Focal tenderness and pain
Pain with activity
Pain becomes constant and more intense,
Does not show up on X-ray until osteoblastic activity
begins callus formation
• Treatment
– Removal from activity for at least 14 days
– Does not usually require casting unless normal fracture
occurs
Bone Healing
• Significantly different from soft tissue healing
• Additional functional elements associated with
healing
– Torsion
– Bending
– Compression
• Trauma results in disruption of blood vessels,
periosteal damage and clot formation
• Fibrous collagen network is constructed after ~1
week -serves as framework for chondroblasts
• Cartilage begins to infiltrate callus
• Osteoblasts begin to proliferate, forming
cancellous and trabeculae
• Callus crystallizes – remodeling begins
• Osteoclasts appear to resorb bone fragments
and clean debris
• Bone transition during remodeling
– Fibrous cartilage  fibrous bone  lamellar bone
• Osteoblasts and osteoclasts respond to stresses
placed on bone
• Immobilization is required for 3-8 weeks
– Dependent on bone, severity, location, patient age
Cartilage Damage
• Osteoarthritis
– Arthritis is an inflammatory condition with secondary
destruction
– Arthrosis – degenerative process with cartilage
destruction, bone remodeling and secondary
inflammation
• Cartilage fibrillates
– Release of fibers and ground substance into joint
– Often occurs in peripheral cartilage
– Fibrillation – degenerative process associated with
poor nutrition and disuse
– Can extend to stressed areas and increase
proportionally to stress applied
• Osteophytosis
– Attempt at increasing surface area to decrease
contact force
• Chondromalacia
– Non-progressive cartilage transformation with areas
of irregularity and softening
– Begins in non-weight bearing areas and progresses
to areas of stress
• Use patterns, external force application, altered
joint mechanics (laxity or trauma related) can
serve as predisposing factors
• Injuries conducive to osteoarthritic changes
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Dislocations and subluxations
Osteochondritis dissecans
Recurrent synovial effusion and hemarthrosis
Ligament damage resulting in altered mechanics and
cartilage damage
– Additional factors
• Loss of ROM, strength, power
• Altered mechanics
Cartilage Healing
• Limited healing capacity
• Variable healing depending on damage to
cartilage and or subchondral bone
• Articular cartilage fails to undergo clot formation
or cellular response
– Defective region remains defective
• When subchondral bone is involved the
inflammatory process proceeds as normal
Injuries to Musculotendinous
Structures
• Skeletal muscle exhibits
4 traits
– Elasticity
– Extensibility
– Irritability
– Contractility
• Muscle size and
architecture often
contribute to type and
magnitude of motion
(gross vs. fine, powerful
vs. coordinated)
Muscle Strains
• Strains occur when the
musculotendinous unit is:
– Overstretched
– Forced to contract against
too great a resistance
• Damage occurs
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Muscle
Tendon
Musculotendinous junction
Tendon-bone interface
Muscle Strain Classifications
• Grade I :
– some fibers have been stretched or actually torn
resulting in tenderness and pain on active ROM,
movement painful but full range present
• Grade II:
– number of fibers have been torn and active
contraction is painful, usually a depression or divot is
palpable, some swelling and discoloration result
• Grade III:
– Complete rupture of muscle or musculotendinous
junction, significant impairment, with initially a great
deal of pain that diminishes due to nerve damage
Muscle Healing
• Similar healing to other soft tissues
• Hemorrhaging and edema lead to phagocytosis
• Fibroblasts and ground substance produce a
gel-like matrix leading to fibrosis and scarring
• Myoblastic cell infiltrate the region promoting
myofibril regeneration
• Collagen undergoes maturation – with active
contractions being critical to apply tensile stress
• Lengthy recovery for each grade
• Patience is a must
Tendinitis
• Term used to describe multiple pathological
tendon conditions
– Inflammation of tendon, with no involvement of
paratenon
• Paratenonitis
– Inflammation of tendon outer layer
– Friction injury
• Tendinosis
– Degenerative tendon changes with no clinical or
histological signs of inflammation
• Chronic Tendinitis
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Tendon degeneration
Loss of normal collagen and cellularity
No inflammatory cellular response
Signs and symptoms
• Pain with movement
• Swelling
• Crepitus
– Key treatment = rest
– Additional treatment options
• NSAID’s and modalities
• Alternative activities
Tenosynovitis
• Due to friction and decreased space for sliding
synovial sheaths are necessary in tendons
• Overuse results in inflammation and
development of sticky adhesions within the
sheath
• Signs and symptoms
– Similar to tendinitis
– Movement may be more limited with tenosynovitis
– Treatment is the same as if the athletic trainer were
treating tendinitis
Tenosynovitis
Tendon Healing
• Large amounts of collagen are required for
adequate healing
• However, collagen synthesis can become excessive
resulting in fibrosis and interfering with tendon
sliding action
• Scar tissue will gradually elongate allowing for
appropriate tendon motion
• If a synovial sheath surrounds an injured tendon the
injury could be devastating
• Typical tendon healing may require 4-5 weeks
before strong contractions can be imparted on
tendon
Injury to Nerve Tissue
• Generally involve
contusion or
inflammation
• More severe injuries
involve crushing or
severing
– Causes life-long
disability
– Paraplegia or
quadriplegia
• Peripheral nerves can regenerate if injury does
not impact cell body
– Slower regeneration with proximity to cell body
• Regeneration requires an optimal environment
– Degenerative changes occur
– Increased metabolism and protein production for
regeneration
– While cell body contains genetic material necessary
to maintain axon is does not transmit to distal
segments of axon
– Schwann cells
• If cut contacts Schwann cells re-innervation of distal
segments is more likely
– New axon buds will develop on the proximal axon
– One sprout will form new axon
– Contact with Schwann cells will allow for Schwann
cell proliferation = new myelin
• Regeneration is slow
– Occurs at a rate of 3-4 mm per day
– Can be obstructed by scar formation
• CNS nerves regenerate poorly due to lack of
connective tissue support
Additional Musculoskeletal
Injuries
• Dislocations and Subluxations
– Dislocations present with total disunion of bone
apposition between articular surfaces- requiring
manual or surgical realignment
– High level of incidence in fingers and shoulder
– Subluxations are partial dislocations causing
incomplete separation of two bones
– Reduction should not occur without and X-ray
(necessary to rule out fractures)
– Inappropriate reduction may complicate the injury
– Return to play is largely governed by the degree of
soft tissue injury
Bursitis
• Result of excessive movement or trauma to
bursa
• Causes irritation, inflammation and increased
synovial fluid production
– May continue to become inflamed with repeat
irritation with increasingly more pain
• Commonly impacted bursa
– Pre-patellar
– Olecranon
– Subacromial
Muscle Soreness
• Overexertion in strenuous exercise resulting in
muscular pain
• Two types of soreness
– Acute-onset muscle soreness
• accompanies fatigue, muscle pain experienced immediately
after exercise
– Delayed-onset muscle soreness (DOMS)
• pain that occurs 24-48 hours following activity that gradually
subsides
• Caused by slight microtrauma to muscle or connective tissue
structures
• Prevention and treatment
– Gradual build-up of intensity
– Some form of stretching
Contusions
• Result of sudden blow to body
• Can be both deep and superficial
• Hematoma results from blood and lymph flow into
surrounding tissue
– Localization of extravasated blood into clot,
encapsulated by connective tissue
– Speed of healing dependent on the extent of damage
• If muscle damage occurs ROM will be impacted
• Incidents of repeated blows may result in myositis
ossificans development
– Prevention = rest and protection
– Allow for calcium re-absorption
Managing the Healing Process
Through Rehabilitation
• Pre-Surgical Phase
– Involves only those athletes requiring surgery
– If surgery can be delayed, exercise may help to
improve outcome
– Maintaining or increasing strength, ROM,
cardiorespiratory fitness, neuromuscular control may
enhance the athlete’s ability to perform rehabilitation
after surgery
Phase I: Acute Injury Phase
• Initial swelling management and pain control are
crucial
– PRICE
– If the athletic trainer is too aggressive during the first
48 hour the inflammatory process may not have time
to accomplish what it needs to
• Immobilization for 24-48 hours is a must
• By days 3-4 the athlete should be engaged in some
mobility exercises and should be encouraged to
gradually bear weight if it is a lower extremity injury
• Use of NSAID’s
Phase 2: Repair Phase
• As the inflammatory process has subsided and
pain decreases with passive ROM exercises
should be added
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Increase cardiorespiratory fitness
Restore full ROM
Restore or increase strength
Re-establish neuromuscular control
• Continued modality use for pain modulation and
swelling control
– Cryotherapy
– Electrical stimulation
Phase 3: Remodeling Phase
• Longest phase with the ultimate goal being
return to play
– Continued collagen realignment
– Pain continues to decrease with activity
• Regain sports-specific skills
– Dynamic functional activities
– Sports-directed strengthening activities
– Plyometric strengthening
• Functional testing
– Determine specific skill weakness
• Heating modalities
– Ultrasound, diathermy
– Increase circulation in deeper tissue
• Manual therapy
– Massage
– Reduce guarding, spasm, pain
• Enhanced and lymphatic flow will deliver
essential nutrients and increase
breakdown/removal of waste, respectively
Using Medication to Effect the
Healing Process
• Used primarily for pain modulation
• Non-steroidal anti-inflammatory drugs (NSAID’s)
– Aspirin, acetaminophen, ibuprofen, naproxen sodium,
ketoprofen
• Aspirin
– Aspirin interferes with pain signal transmission from
thalamus
– Tissue damage results in release of arachidonic acid
from phospholipid walls
• Results in production of prostaglandins, thromboxane,
prostacyclin
• Mediate inflammatory response
– Effects
• NSAID’s block pain and inflammation by inhibiting
prostaglandin synthesis
• Modulate lysosomal membrane destruction
(enzymes)
• Aspirin (only NSAID) that irreversibly inhibits
cyclooxygenase (other NSAID’s = reversible)
• Alters sympathetic outflow of hypothalamus for
fever reduction
– Side effects
• Gastric distress, heartburn, nausea, tinnitus,
headache, diarrhea
– Cautions
• Impairs clotting, irreversible inhibition of
cyclooxygenase
• Prolonged bleed risk
• Ibuprofen
– Analgesic and antipyretic effects
– Similar side effects
• No impact on platelet aggregation
– Dose of 400mg serves as analgesic and antiinflammatory agent
• Acetaminophen
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Analgesic and antipyretic effects
Limited anti-inflammatory capabilities
Used to somatic pain and fever reduction
No gastric irritation or bleeding
No impact on clotting factors
• NSAID’s
– Anti-inflammatory, analgesic and antipyretic agents
– Should not be used if suffer from aspirin allergy triad
– Use cautiously if athlete is exposed to dehydration
• Inhibits prostaglandin synthesis, compromising elaboration of
prostaglandins in kidney
– Ischemia within kidneys occurs
– Fewer side effects and longer lasting than aspirin
– May require liver function monitoring
– While medications can be effective, irritating agent
causing inflammation must also be eliminated
• Oral muscle relaxants
– Reduce spasm and guarding
– Facilitate rehabilitation programs
– No evidence of superiority over analgesics or
sedatives
• Many analgesics and anti-inflammatory products
are available over the counter (OTC)
– Combination of products
– Chronic aspirin, phenacetin or acetaminophen use
can result in papillary necrosis or analgesicassociated nephropathy
– Caffeine dependence
Sports Medicine Approach to the
Healing Process
• Assist/manipulate the natural process of the body
while doing no harm
• Primary goals
– Have a positive influence on inflammation and repair
process
– Expedite recovery of function
• ROM, strength, cardiorespiratory fitness, neuromuscular control
– Minimize early effects of inflammatory process
• Pain, spasm, edema accumulation, decreased motion
– Prevent recurrence of injury
• Resist future periods of tissue overload through strengthening