2022 Wound_Healing_OTs

WOUND HEALING

Before beginning this module, make sure that you have read the
associate chapter in your textbook, Physical Agent Modalities: Theory and
Application for the Occupational Therapist, by Alfred Bracciano.

Biology of Wound Healing
Learning Objectives

The astute clinician with a working knowledge of wound healing is able
to design and implement successful interventions using their understanding of
scar biology. By the end of this module, you will be able to:

• classify types of soft tissue injuries;
• address the three phases of tissue repair, namely inflammation,

proliferation, and maturation;
• discuss the cellular processes occurring in each phase;
• describe complications that interfere with normal healing; and
• review appropriate intervention methods based on research findings.

Soft Tissue Injury Classifications

Injury to soft tissues below the skin is dependent upon:
✓ the nature of the causative factor
✓ the location (either superficial or deep)
✓ the material properties of the tissue

Soft Tissue Injury Classifications
✓ Muscle Injury

• contusions
-ecchymosis
-swelling and formation of hard-feeling mass
-hematoma

• cramps
• muscle spasms
• inflammation

-myositis
-fasciitis

Muscle contusions, or bruises, result from compression and vary in
severity and depth. Ecchymosis, or tissue discoloration, is present if there is
hemorrhage of blood vessels and lymph flow into the damaged area. This can
result in swelling and formation of a hard-feeling mass that is composed of
blood and dead tissue. A hematoma may result, which can restrict joint
motion and even lead to nerve compression. This injury can be rated
according to the extent of impairment in joint range-of-motion: “Grade 1”
refers to little or no range-of-motion loss, whereas “Grade 3” indicates a
severe loss of range-of-motion.

Muscle can also be injured in such a way as to cause painful, involuntary
muscle contractions, such as cramps or spasms. A cramp is a painful, clonic-
type muscle pain with alternating contraction and relaxation cycles. A muscle
spasm is involuntary contraction of short duration that is often a reflex action
caused either biochemically or by a blow to a muscle or nerve.

Inflammation can affect muscle connective tissue, as in myositis, or the
sheaths of fascia surrounding the muscle, as in fasciitis.

Soft Tissue Injury Classifications
✓ Muscle and Tendon Strains, Ligament Sprains

Muscle and tendon strains and ligament sprains are common types of injuries
treated in occupational therapy. In severe injuries, the muscle portion will
usually rupture first because tendons are twice as strong as the muscles to
which they attach. Tendons develop tears when they are stretched
approximately 5 to 8% beyond their normal length.

✓ A first-degree sprain or strain results in pain, some micro-tearing of collagen
fibers, and usually no readily observable tissue destruction.

✓ A second-degree sprain or strain results in more severe pain, extensive
rupturing of tissue, and detectable joint instability and muscle weakness.

✓ A third-degree sprain or strain results in severe pain, loss of tissue continuity,
decreased range-of-motion, and complete joint instability.

Other common related soft tissue pain conditions can be caused by
inflammation of a tendon, referred to as tendonitis, or a tendon sheath,
referred to as tenosynovitis. These conditions can be either acute or chronic
and cause pain and swelling with tendon movement. Less common
conditions include myositis ossificans, an accumulation of mineral deposits in
the muscle; calcific tendonitis, mineral deposits in a tendon; and bursitis, an
irritation of the bursae surrounding some joints.

Soft Tissue Injury Classifications

Skin is the most frequently injured tissue of the body. We often experience
scratches, bruising, and mild burns to the skin that are healed by epidermal
regeneration. Nature has provided us with a means of survival, not
comparable to the regeneration process of which some animals are capable,
but that is a primary means of repair for all vertebrates.
Special cells in our bodies respond to injury by forming a collagenous glue. This
“body glue” is called granulation scar tissue. Maintenance of our well-being
depends on our body's ready ability to sense a disruption to the skin or
underlying structure, alert the appropriate cells to action, and oversee the
sequence of repair without complications.

Scar Characteristics

How is it possible for the body's repair system to duplicate the original form
and function of the injured tissue with only one type of glue? Our bodies are
largely composed of several different types of collagen. Mature scar tissue is
formed from type-I collagen; however, the greatest contribution to the healing
process is its ability to imitate the structure of other collagen types.

Scar Characteristics

The scar formed in dense tissue "senses" the need for strength and
attempts to mimic the surrounding tissue structure. Likewise, a scar filling a
defect in loose, flexible tissue will change in its last phase of healing to
reproduce, as much as possible, those physical characteristics. Thus, in
response to certain internal and external influences, scar does differentiate to
become quasi-specific to the surrounding tissue.

Normal Wound-Healing Phases

No matter where or how an individual is injured, the body can sense
this and signals for initiation of a well-orchestrated repair sequence. Once this
sequence is begun, it continues through its phases until the wound is covered
with scar. If one were to stop the scar-forming process, wound healing would
stop as well.

The body's response to any injury is immediate, whether it is traumatic
in origin or surgically induced. The wound progresses through three phases to
complete its repair cycle: 1) the inflammation phase, 2) the proliferation
phase, and 3) the maturation phase. The inflammation phase prepares the
injured tissue for healing, the proliferation phase rebuilds the structure, and
the maturation phase remodels the scar to approximate the surrounding
tissue. Timetables for the beginning and end of each phase are not exact and
serve only as general guides. Furthermore, not only do different tissues heal
at different rates, the same wound can exhibit some areas of rapid healing
and other areas that heal more slowly.

So when is the healing process finished? This is a critical question to
answer in order to define when someone might be able to return to work, be
ready for additional surgical procedures, or be ready for a permanent
impairment rating. Using your knowledge of scar biology, the phases of
wound healing, and objective appraisal procedures, you will be able to make
sound decisions for patient care.

Inflammation Phase

Inflammation is a normal and essential prerequisite to healing and is the
natural result of changes in vascular flow occurring in response to the initial
injury. Many specialized cells involved in this phase of the wound healing
process are delivered through the blood.

At the time of injury, blood vessels are damaged or cut, and they begin
to pour blood into the wound. This initial flow will flush out the wound and
clear the area of debris. The blood will eventually coagulate and seal off the
injured blood vessels and lymphatic channels. Ultimately it provides a
temporary closure to the wound. The fibrin plugs that clot the wound also
form inside lymphatic vessels. Lymphatic flow is blocked to further seal off the
wound and to prevent the spread of infection. These channels remain closed
and will not open until later in the healing process.

Inflammation Phase

Very shortly after injury, non-injured blood vessels dilate in response to
histamine being released by injured tissues. A combination of blood exudate
and serous transudate creates a reddened, hot, swollen, painful environment
in the vicinity of the damaged tissue and wound. The inflammatory edema fills
all spaces within the wound, surrounding all damaged or repaired structures,
thereby binding them all together as a one-wound-structure.

Some swelling in a wound is necessary to trigger the inflammatory
process. However, if too little inflammation occurs the healing response is
slow; if too much inflammation occurs, excessive scar is produced. This
inflammatory fluid, initiated by blood, is high in fibrinogen. Fibrinogen
coagulates in the wound and in the surrounding fluid-filled tissues. This
coagulated gel begins to mature into dense scar tissue. At this point, excessive
swelling must be avoided.

Inflammation Phase

• Treatment: PRICE protocol
-Position
-Rest
-Ice
-Compression
-Elevation

Using an intervention plan that incorporates the principles of
positioning, rest, ice, compression, and elevation (PRICE), swelling or edema
can be reduced. All traumatic or acquired wounds, to include controlled
surgical procedures, require edema care.
• Joints respond to swelling by assuming positions of comfort.
• Muscles facilitate actions that draw the joint into the "comfortable" position
and neurologically inhibit antagonistic muscles.

Interventions of hand injuries in this phase need to provide good
support and position the hand correctly through the use of bulky dressings
and splints. Active exercise may be disadvantageous during this phase until
the edema is reduced, thus removing the inhibitory effect of distended
sensory receptors.

For healing to begin, two things must occur: 1) the wound must be
decontaminated by phagocytosis, and 2) a new blood supply must become
available.

Inflammation Phase

The main purpose of phagocytosis is to rid the wound of infection. All
wounds, even those created under sterile conditions such as surgery, are
contaminated. Certain circumstances can open the system to infection: the
type of bacteria present, presence of foreign debris, necrotic tissue,
inadequate oxygen supply, malnutrition, certain vitamin deficiencies, radiated
tissues, and immuno-suppressed conditions. Fortunately, our bodies have a
system to prevent minor contamination from developing into a major
infection. Chemical changes in the wound induce and attract white blood cells
to slip through the enlarged capillary pores and migrate to the site of injury.
Administration of anti-inflammatory steroids at this stage of healing can act to
inhibit the amount and mobility of white blood cells. The first white blood
cells to reach the wound are polymorphonuclear leukocytes. These short-lived
cells begin the process of phagocytosis by fixing to bacteria, extending their
membrane around them, then dissolving and digesting these invaders. In a
few days, macrophages begin to dominate the area and remain until
inflammation is resolved.



Inflammation Phase

The macrophage has two important functions in wound repair. First, it
continues the important job of phagocytosis. As a scavenger cell, the
macrophage not only attacks and engulfs bacteria but also disposes of
necrotic tissue in the wound. As macrophages ingest microorganisms, they
also excrete ascorbic acid, hydrogen peroxide, and lactic acid as byproducts of
phagocytosis. Hydrogen peroxide aids in controlling anaerobic microbial
growth and is believed to be the substance that signals the extent of damage.
Build-up of ascorbic acid and lactic acid signals the need for more
macrophages.

Inflammation Phase

The more macrophages present in the wound tissue, the more
byproducts produced. The biophysical response to a larger number of
macrophages is a greater and more prolonged inflammatory phase.
Chronically active macrophages create a chronically inflamed wound.
Clinically, we can potentially influence this process by assisting the
macrophage in its work. The use of low-dosage, pulsed ultrasound
significantly decreases infection. Ultrasound is capable of disintegrating
macrophages; their debris may then signal more phagocytic cells to the
treated area. Removal of all foreign materials, debridement of necrotic tissue,
evacuation of hematomas, use of antibiotics, use of wet-to-dry dressings as a
form of microdebridement, and, if necessary, frequent whirlpool cleaning, will
result in a clean wound bed that is ready for healing. Once a clean wound bed
exists, the inflammatory phase desists.

Inflammation Phase

In its second function, the macrophage is often referred to as the
"director cell" of repair because of its influence on scar production. The
macrophage "directs" the future course of repair by chemically triggering the
number of fibroblastic repair cells activated. The macrophage has been
described as a key factor in regulating events in the inflammatory period. Its
presence is vital as a phagocytic agent and appraiser of damage, and its role in
recruiting fibroblasts is significantly related to the final amount of scar
produced.

Inflammation Phase: Neovascularization

The inflammatory response so far has proceeded without any new
regrowth of blood vessels. However, healing will not continue unless new,
functional blood vessels are present to supply oxygen and nourishment to the
injured tissue. Once again, the macrophage signals vascular regeneration to
begin. Patent vessels in the wound periphery develop small buds or sprouts
that grow into the wound area. The capillary sprouts, when first formed, lack
full thickness, which renders them delicate and easily disrupted.
Immobilization is essential during this phase to permit vascular regrowth and
to prevent new breakdown. These capillary outgrowths will eventually come
in contact with and join other arteriolar or venular buds to form a capillary
loop.

The color of scar is an excellent prognostic guide as to the potential for
further changes in scar characteristics. The new circulatory loops filling the
wound create a highly pink to reddish color. The young wound will remain
redder in contrast to the normal adjacent tissues throughout healing because
of this inundation of capillary loops. Areas that remain gray in appearance or
that have a positive delayed blanch test following pressure indicate
inadequate circulation. As the wound approaches final maturity, a signal
reaches the scar tissue and causes the majority of loops to cease functioning
and retract. Therefore, a fully matured scar appears whiter than adjacent
tissue.

Phase I Intervention

Studies have concluded that early motion in the inflammation phase
following surgery resulted in increased edema, wound breakdown, and
infection.

• Early motion protocols should commence at the completion of this
phase, and not before.

• Heat application during this phase will cause increased bleeding from
these fragile vessels and is therefore contraindicated.
As this phase comes to a close, fibrinolysin in blood vessels is produced

to dissolve clots. The lymphatic channels also reopen to assist in reducing the
wound edema.

Reviewing the complex, interrelated dynamics that have occurred in this
first phase would lead one to believe that weeks must be necessary for
completion. In normal conditions, all these events happen within the first four
days after injury; however, complications, major injuries, and secondary
trauma elsewhere in the body can prolong the inflammatory period.

Phase I Intervention

• minimize all factors that can prevent or prolong inflammation
• assist role of macrophages
• antibiotics
• debridement
• wound cleaning
• PRICE regimen

Our main directive is to minimize all factors that can prevent or prolong
inflammation. Treatment is directed toward assisting the role of the
macrophage through the use of antibiotics, debridement, wound cleaning,
PRICE regimen, and proper positioning.

Proliferation Phase

With the inflammatory phase completed, rebuilding can commence.
Although many different cells are involved in the inflammatory phase, fewer
types of cells operate in the proliferation phase, which typically lasts about
three weeks. The purpose of this phase is to resurface and impart strength to
the wound. Three processes occur simultaneously in the proliferation phase
to achieve wound closure: 1) epithelialization, 2) wound contraction, and 3)
collagen production.

There is a priority of nature inherent in healing. Factors critical to survival,
such as phagocytosis, blood flow, and surface covering, occur early in healing.
The body "knows" invading organisms are from the outside environment.
Providing even a one- cell layer of its own covering will reduce the chances for
infection. A protective barrier will further aid healing by preventing loss of
fluid from the wound. Within hours after injury, undamaged epithelial cells at
the wound margin begin to reproduce. If the wound bed is viable and has a
good blood supply available, then migration of these new cells begins, with
those from the periphery moving in and those from appendages moving out.
These migratory cells remain attached to their parent cells; therefore, their
movement causes a "pull" on the normal skin around the wound edge. The
advancing edge of the epithelium seeks out moist, oxygen-rich tissue.
Dressings that are kept moist and not permitted to dry out will facilitate this
migration; if allowed to dry, the dressings will adhere to this thin skin, and
removal will result in microdebridement of the healing tissue. Additionally, if
the necrotic tissue or the wound is too extensive or oxygen availability is poor,
epithelial migration cannot proceed. Likewise, if sufficient capillary circulation
is not available to maintain epithelial integrity, wound dehiscence can occur.

Factors interfering with epithelial migration

• excess necrotic tissue
• large wounds
• poor oxygen availability
• insufficient capillary circulation

Proliferation Phase
• Epithelialization

When epithelial cells from one direction meet similar migratory cells, contact
inhibition causes cessation of movement. Should the epithelial edge meet
eschar, foreign material, sutures, or blood clots, it will dive downward to
maintain contact with the vascular loop network in the wound. The epithelial
margin must release lytic enzymes, which act to cleave the attachments of
nonviable tissue from the viable wound bed. As it gradually undermines, the
eschar loosens and detaches from the wound. A red, highly vascular wound
with a thin, almost transparent covering is now visible. It is believed that the
scab forms a temporary barrier for the wound and should not be disturbed
until epithelialization is complete. Although clean, approximated wounds are
clinically resurfaced within 48 hours, larger, open wounds require a longer
period. Several weeks are required for this thin covering to become
multilayered and to differentiate into the various strata of normal epidermis.

Epithelialization, then, can be facilitated by maintaining moist dressings,
protecting the wound from minor repetitive trauma, avoiding chemical
irritants or infection, debriding the wound, and possibly applying topical
oxygen therapy.

Proliferation Phase
• Wound Contraction

There is another force at work aimed at closing the wound. Unlike
epithelialization, which closes the wound surface, contraction is a process that
actually pulls the entire wound together, in essence shrinking the defect.
Fibroblasts originate from mesenchymal cells located in loose tissue around
blood vessels and fat. In response to chemical influences generated by the
injury, fibroblasts are transformed into myofibroblasts that contain the
contractile properties of smooth muscle cells and that exhibit a migratory
ability. The myofibroblasts attach to the skin margins and pull the entire
epidermal layer inward. These unusual cells have been identified in other
conditions associated with contraction processes, such as Dupuytren's
contracture, tenosynovitis, and hypertrophic scars, and in fibrous capsules
formed around implants. The "picture-frame" theory identifies the wound
margin beneath the skin as the location of myofibroblast action. Contractile
fibroblasts convene near the
wound perimeter, forming a
"picture-frame" that will
move inward, decreasing the
size of the wound. Although
contractile forces start out
equal in all wounds, the
shape of the picture frame
predicts the resultant speed
of contraction: linear
wounds contract rapidly,
square or rectangular
wounds contract at a moderate pace, and circular wounds contract slowly.
Approximated and sutured wounds minimize the need for contraction forces,
but not all wounds can be closed primarily.

Wound contraction begins about four days post-injury. If the wound is not
closed by 14 to 21 days post-injury, contraction stops because of the restraint
of the surrounding stretched tissue.

Successful contraction results in a smaller wound to be repaired by scar
formation. Minimizing the area to be healed is truly beneficial in certain
tissues with fixed, deep structures covered by mobile, loose skin, such as on
the abdomen or forearm area. Wound contraction, however, may be harmful
in the hand. The close interplay of multiple joints, muscles, tendons, and
sheaths all joined by fascial connections requires every millimeter of skin and
tissue length. Because permitting an open wound on the hand to heal by
uncontrolled contraction results in deformities, the goal should be inhibition of
wound contraction. If contraction occurs, the centripetal force will pull all
structures toward the wound. Joint contractures, as sometimes seen in full-
thickness hand burns, are often the result of uncontrolled wound contraction.

Studies have shown that contraction is diminished through the use of skin
grafts. The thickness of the graft correlates with the degree to which
contraction is suppressed.

• Split-thickness grafts diminish contraction of the wound bed by 31%;
• full-thickness grafts diminish contraction by 55%.
• The early combined use of full-thickness grafts with splinting inhibits

contraction by 77%.
Rudolph points out that grafts must be applied early, in the inflammatory phase
before contraction is initiated. If the myofibroblasts are already mobilized and
functioning, then excision of the wound margins prior to graft application is
necessary to prevent contraction from occurring beneath the graft.

Proliferation Phase
• Collagen Production

The climax of wound healing occurs with collagen production. If this
event does not occur, the wound will not heal. Migratory fibroblasts are now
present throughout the wound. These myofibroblasts follow the fibrin
meshwork created earlier in the wound fluid milieu. Because the wound fluid
bathed all injured structures, the myofibroblast has access to all depths of the
wound. Once in place, the myofibroblast transforms back to a fibroblast and
is stimulated to synthesize and secrete collagen. Adequate supplies of oxygen,
ascorbic acid, and other cofactors such as zinc, iron, and copper are needed to
create the proper environment for fibroplasia. Having its metabolic needs met
for nutrients, the fibroblast produces a triple-helical molecule called a
tropocollagen molecule.

Tropocollagen molecules form collagen fibrils. These fibrils, or filaments, lay
disorganized in the wound, still in a gelatinous state. The amount of collagen
filaments formed does not build strength. Wound durability, or tensile
strength, is dependent on the microscopic welding that must occur within each
filament and from one filament to another. These sites of bonding are called
cross-links. Initially, weak electrostatic forces aid in attracting and holding the
fibrils together. These ionic charges, together with early hydrogen bonds,
keep the molecule weakly stable. Salt water application, vibration, heat, and
enzymes can easily denature and separate the chains. With further
maturation into tropocollagen, the chains move at specific sites to permit
stronger cross-links to form. Intermolecular bonds form between
tropocollagen molecules and are the major force holding tropocollagen
filaments together, thus imparting tensile strength to the wound. The number
of intermolecular bonds formed will enhance the strength of the filament.
Bone tissue has the highest ratio of intermolecular bonds, and this dense
connective tissue can be considered highly cross-linked.

At the end of this three-week time frame, the wound has the greatest
mass of collagen assembled, but the tensile strength is roughly only 15% of
normal. A bulky, rough, tender, red scar is visible and palpable. The
formation of cross-links in this phase allows the wound to tolerate early,
controlled motion without fear of disruption. Wound progress is bi-directional
at this time; under optimal healing circumstances, they proceed to the next
phase, but complications can cause a recurrence of inflammation. Edema,
infection, and rough handling can cause the wound to become re-inflamed.
Mobilization aimed at breaking scar will create a new wound, ultimately with
further scar formation.
A secondarily inflamed wound results in collagen deposition in addition to that
already present. The quantity of scar produced at this time is an indication of
final outcome.

Maturation Phase

Successful wound healing requires more than closing the wound with
sufficient tensile strength. The ultimate goal is the return of function.
Remodeling requires the scar to change to fit the tissue. For example,
repaired ligaments must have firm, intransigent scar formed with a parallel
weave in order to resist deforming joint forces during stretching activities, yet
the scar fibers must pleat with relaxation when tension is removed. Just
millimeters away, however, the scar formed between ligaments and bone or
moving parts must have a random orientation of scar fibers, with thin and
lengthy adhesions to permit motion between parts. Wound repair is optimal
when this remodeling of scar tissue occurs and less than optimal when it does
not occur. Several factors assist in the maturation and final physical
characteristics of the scar. The process of scar remodeling is responsible for
the final aggregation, orientation, and arrangement of collagen fibers.
Remodeling is influenced by both synthesis-lysis balance and fiber orientation.

Maturation Phase
• Synthesis-Lysis Balance

In healthy adults, tissues are continuously breaking down old collagen
and replacing it with new collagen in a balanced fashion. With normal
wounds, collagen synthesis and lysis are in balance with each other, even
though both are higher than pre- injury rates. Inflammation from injury
results in a hormonal stimulation of the enzyme collagenase that destroys the
bonds between collagen, which in turn results in the bonds becoming soluble
and being absorbed as waste byproducts. Collagen turnover is accelerated as
old fibrous tissue is removed and new fibrous tissue is formed. This
continuous breaking down and rebuilding of bonds between collagen explains
why an injured hand immobilized throughout all three phases of wound repair
can have multiple contractures in injured as well as non-injured soft tissue
structures. A fundamental underlying principle of hand management is to
keep all non-injured structures normal throughout the repair process. If joints
and tissues can lose mobility quickly, they can also regain it quickly with
proper management.

As long as the scar exhibits a rosier
appearance than normal, remodeling is
underway. Despite the fact that collagen
synthesis continues at a high rate, no
further increase in scar mass usually
occurs. This process of collagen
dissolution and replacement continues
until the remodeling phase ends at six
months to a year post- injury, depending
on the extent of the injury. The high
collagen turnover in this phase can be
either beneficial or detrimental.

What happens when the synthesis-lysis relationship falls out of balance?
Hypertrophic scar and keloids both involve normal synthesis but have an

inhibition of lysis following wounding. The difference between hypertrophic
scar and keloids is based on boundaries. Hypertrophic scars will not exceed
the boundaries of the scar limits and will become raised tissue. Keloids will
result in synthesis of tissue that exceeds the boundaries of the scar. We can
restore the balance in hypertrophic scarring by applying pressure to the scar.
Prolonged, constant pressure creates an ischemic condition where blood flow,
and therefore oxygen, is decreased in the wound tissue.
With less oxygen, synthesis is curtailed while lysis is unaffected. Tissue
balance is achieved when scar bulk is flattened to approximate normal tissue.
This pressure treatment must be continued until remodeling is complete and
all collagen turnover returns to a normal level.

HYPERTROPHIC SCAR KELOID SCAR

Maturation Phase
• Collagen Fiber Orientation

o How does a change in scar orientation change tissue function?

During the lengthy period of maturation, remodeling involves collagen
turnover that results in the early, randomly-deposited scar tissue being
rearranged in both linear and lateral orientations. This orientation will
approximate the tissues that surround it. Whereas the original wound resulted
in one scar filled with one tissue, now it is to be replaced to provide a function,
such as tendons, muscles, and skin. How does a change in scar orientation
change tissue function? Scar is non-elastic. However, scar that forms with
redundant folds will permit mobility of the structures to which it is affixed.
The physical weave pattern of collagen fibers is largely responsible for the final
functional behavior of the wound. What forces are at play to direct this
collagen realignment? Two theories are offered to explain these forces.

Maturation Phase
• Induction Theory

The induction theory hypothesizes that scar attempts to mimic the
characteristics of the surrounding tissue it is healing. The tissue structure
defines the collagen weave. Thus, dense tissues create dense, highly cross-
linked scar; pliable tissues create a loose, coiled, less cross-linked scar. Scar
can adapt through the remodeling forces of synthesis and lysis as previously
discussed. Dense tissues seem to have preference or greater influence when
multiple tissue types are found in close proximity. Using principles inherent in
the induction theory, the surgeon attempts to design the repair field by
separating dense and soft tissues. Tendon repairs left immobile over bone
fractures will ultimately resolve into bony adhesions encasing the non-gliding
tendon. When repair sites cannot be separated by manual positioning,
sequencing of repair, or interposition of fat and other tissues, then early
controlled movement protocols are beneficial.

Loose Connective Tissue Fibrous (Dense) Tissue

Maturation Phase
• Tension Theory

The tension theory states that permanent elongation of scar can be
achieved through a low-load, long-duration application of stress during the
appropriate healing phase. The stresses referred to in the tension theory are
the internal and external forces affecting the wound area during the
remodeling phase. Muscle tension, joint movement, passive gliding of fascial
planes, soft tissue loading and unloading, splinting, temperature changes, and
mobilization are all examples of forces acting on the collagen array.

Clinical studies have demonstrated that the application of appropriate
tension causes an increase in tensile strength during healing. Dynamic splints,
serial casting, positional heat and stretching techniques, functional electrical
stimulation, and selective hand activities are
examples of methods used to achieve the
low-load, long-duration stress necessary to
change scar configuration. Conversely,
immobilization and stress deprivation have
been shown to cause loss of tensile strength
and normal collagen array in skin, fascia,
tendon, ligament, cartilage, capsule, and
bone. The recovery curves for tissue
experimentally immobilized for two to four
weeks reveal that reversibility requires months to complete and often is never
fully successful.

Phase III Intervention

Scar Management:

Purpose: to alter the physical and mechanical properties of scar tissue thus

altering scar maturation; to promote tissue strength and gliding by preventing

adhesions.

Scar massage During the proliferative stage massage has a beneficial

role in collagen synthesis, as it prevents adhesions and

helps in collagen synthesis; this mechanical stress when

applied to the intermolecular bonds, helps in realigning

collagen.

Splinting Splinting can be used at all stages of wound healing, to

immobilize at the earlier stages and with the aid of

passive or active stretches to modify collagen alignment.

Static and dynamic splinting can alter the viscoelastic

properties of tissues thus it can elongate and stretch

tissues over time.

Silicon gel Silicone gel through sheeting and elastomers are said to

have a hydrating effect on the scar. It helps to soften and

elongate a scar by increasing the pressure, temperature

and in turn blood flow to the scar.

Ultrasound therapy The known effect of ultrasound is to promote healing in

the inflammatory and proliferative stages. It stimulated

the synthesis of growth factor that in turn increase the

strength and elasticity of the collagen fibers formed.

Laser Laser inhibits collagen and improves keloid and

hypertrophic scarring. It improves pruritus but has no

effect on the cosmoses of the scar.

Pressure Therapy When used for edema management and cosmoses in case

of keloid and hypertrophic scars. These garments inhibit

collagen synthesis in a remodeling scare through a

mechanism that is unknown. Pressure therapy can reduce

the scar height and erythema when applied for 23 hours

per day for 12 hours. This should be applied at 20 to 30

mmHg and replaced every 2 to 3 months. This reduce

abnormal pigmentation and accelerates scar maturation

Source: Physiopedia (https://www.physio-pedia.com/Scar_Management)

Remodeling Factors

The goal during the maturation phase is to influence scar formation by
applying controlled stress as the scar matures. Controlling the amount and
location of scar begins with inspection of the wound, planned surgical
procedures, and rational postoperative therapeutic care. Postoperative
therapeutic care usually involves controlled-motion protocols. The type of
controlled motion depends upon the type of tissue to be repaired as well as
the type of stress that the tissue requires for its functional integrity. Tendon
and ligament repairs are held immobile throughout the inflammatory phase;
controlled motion is begun during the proliferation phase. Controlled motion
involves splinting that allows for restrictive motion in such a way as not to
disrupt the repair process or stimulate re-inflammation. It will allow stress
forces throughout the soft tissue and wound bed. Ultimately, a dense, parallel
union of scar tissue to surrounding tissue is the preferred outcome.

Summary

In summation, knowledge of wound healing and repair is essential for
clinicians to design and implement intervention programs that are based on
scar biology. Understanding the sequence of repair; knowing the stages at
which the repair process can be stopped, enhanced, or modified; and having a
repertoire of modalities that influence the development of scar tissue permits
flexibility in management as the wound progresses. Through this knowledge
adverse reactions and complications can be recognized, dealt with, or avoided
altogether.

Course Development Team