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

3. Wound Healing: At the end of this module, you will:
3.a. classify types of soft tissue injuries
3.b. address the three phases of repair (inflammation, proliferation, and maturation)
3.c. discuss the cellular processes occurring in each phase
3.d. review appropriate intervention methods based on research findings
3.e. describe complications that interfere with normal healing.

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

• soft tissue injury dependent upon:

- nature of causative factor
- location

• superficial
• deep

- material properties of tissue

Injury to soft tissues below the skin is dependent upon the nature of the causative
factor, the location (either superficial or deep), and 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

• first-degree sprain/strain
-no readily observable tissue destruction

• second-degree sprain/strain
-detectable joint instability and muscle weakness

• third-degree sprain/strain
-severe pain
-loss of tissue continuity
-decreased ROM
-complete joint instability

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.

Soft Tissue Injury Classifications

• common soft tissue pain conditions
-tendonitis, tenosynovitis

• conditions can be acute or chronic
• tendon movement causes pain and swelling
• less common soft tissue pain conditions

-myositis ossificans
-calcific tendonitis
-bursitis

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 most frequently injured tissue

- scratches, bruising, and mild burns

healed by epidermal regeneration
formation of granulation scar tissue

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

• body senses injuries and signals repair sequence to begin
• wound progresses through three phases:

1. inflammation phase
2. proliferation phase
3. maturation phase

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

• normal and essential prerequisite to healing
• initial blood flow

- flushes
- coagulates
- closes off wound

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

• too little inflammation = healing response is slow
• too much inflammation = excessive scar is produced

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

• avoid positions of comfort at this stage
• curtail active exercise

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

Phagocytosis

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

Macrophage

• scavenger cells

- attack and engulf bacteria
- dispose of necrotic tissue in wounds

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

Macrophage

clinical interventions

- low-dosage, pulsed ultrasound
- debridement of necrotic tissue
- evacuation of hematomas
- antibiotics
- wet-to-dry dressings
- whirlpool cleaning

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

Macrophage

• director cells

- chemically trigger number of fibroblastic repair cells activated
- significantly related to final amount of scar produced

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

• Healing will not proceed without a supply of oxygen and nourishment to the injured tissue.
• Immobilization is essential to permit vascular regrowth and to prevent new breakdown.

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.

Inflammation Phase

Neovascularization

• color of scar is an excellent prognostic guide

- pink to reddish
- gray or delayed blanch
- lighter/whiter than adjacent tissue

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

• early motion protocols should commence ONLY at completion of this phase
• heat application is also contraindicated
• fibrinolysin dissolves clots, lymphatic channels reopen to assist in reducing edema
• inflammatory phase can be prolonged by:

- complications
- major injuries
- secondary trauma

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
• proper positioning

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

• three weeks approximate duration
• wounds are resurfaced and strengthened
• three processes occur simultaneously

1. epithelialization
2. wound contraction
3. collagen production

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.

Proliferation Phase

Epithelialization

• critical survival factors occur early on
• protective barrier reduces risk of infection,

prevents loss of fluid from wound

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

• contact inhibition causes cessation of epithelial cell migration
• epithelial edge continues to advance under eschar, foreign

material, sutures, or blood clots
• scab forms a temporary barrier and should not be disturbed
• thin covering becomes multilayered and differentiates into the

various strata of normal epidermis over several weeks

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.

Proliferation Phase

Epithelialization

• facilitated by

- maintaining moist dressings
- protecting wound from minor repetitive trauma
- avoiding chemical irritants or infection
- debriding wound
- applying topical oxygen therapy

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

• myofibroblasts pull epidermal layers inward
• "picture-frame" theory

- location of myofibroblast action identified as
wound margin beneath skin
- shape of wound predicts contraction speed

• linear wounds contract rapidly
• square/rectangular wounds contract moderately
• circular wounds contract slowly

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.

Proliferation Phase

Wound Contraction

• begins about four days post-injury; restrained by
surrounding stretched tissue 14-21 days post- injury

• successful contraction creates smaller wound for scar
formation

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.

Proliferation Phase

Wound Contraction

• skin graft thickness = degree to which contraction is suppressed

- split-thickness grafts = 31% reduction
- full-thickness grafts = 55% reduction
- early full-thickness grafts combined with splinting = 77% reduction

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.

Proliferation Phase

Collagen Production

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.

Proliferation Phase

Collagen Production

• early, controlled motion is tolerated
• complications can cause wound to become re- inflamed
• mobilization to break scar will create further scar formation
• quantity of scar produced at this time indicative of final outcome

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

- wound closure
- sufficient tensile strength
- return of function

• scar remodeling is responsible for final
aggregation, orientation, and arrangement of
collagen fibers

- synthesis-lysis balance
- fiber orientation

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

• normal wounds

- synthesis and lysis remain in balance
- higher rates than pre-injury

• no additional scar tissue is usually formed
• high rate of collagen turnover can be either

beneficial or detrimental

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.

Maturation Phase

Synthesis-Lysis Balance
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

• 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

• scar mimics surrounding tissue it is healing

- dense tissues = dense, highly cross-linked scar
- pliable tissues = loose, coiled, less cross-linked scar

• dense tissues have priority over other tissue types in close proximity
• early controlled movement is beneficial when design of repair field is not possible

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.

Maturation Phase

Tension Theory

• low-load, long-duration stress application results in permanent elongation of scar
• internal and external stresses

- muscle tension
- joint movement
- fascial gliding
- soft tissue loading and unloading
- splinting
- temperature changes
- mobilization

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.

Maturation Phase

Tension Theory

• intervention approaches

- dynamic splints
- serial casting
- positional heat and stretch
- functional electrical stimulation
- selective hand activities

• immobilization can require months to reverse and is often unsuccessful

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

• scar formation influenced by application of
controlled stress as scar matures

• amount and location of scar

- wound inspection
- planned surgical procedures
- postoperative therapy

• preferred outcome is dense, parallel union of
scar tissue to surrounding tissue

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

• Knowledge of wound healing and repair based on
scar biology

- understanding sequence of repairs
- knowing stages at which the repair process can be
stopped, enhanced, or modified
- having a repertoire of modalities that influence
development of scar tissue

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