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Thomas Test

Thomas Test (or as it called Hugh

Owen Thomas well leg raising test)
Table of Contents [ ➖ ]
is used to measure the flexibility of
Soft Tissue Injury Classification the hip flexor muscles.

Primary Soft Tissue Injury:

Secondary Soft Tissue Injury:

Shoulder SLAP Lesion
Soft Tissue Healing

Tissue Healing Stages SLAP Lesion is the abbreviation of

Superior Labrum from Anterior to
1. Coagulation and Inflammation Stage:
Posterior tears in the shoulder joint
2. Migratory and Proliferative Stage:
labrum.
3. Remodeling Stage:

Factors Affecting Wound Healing

Durkan Test For Carpal Tunnel
Intrinsic (Local) Factors:

Systemic Factors: Syndrome

Extrinsic Factors:
Durkan Test or as it called the
References carpal compression test is used to
test for Carpal Tunnel Syndrome
where the median nerve is
compressed in the carpal tunnel.
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Soft tissue injury of all types is extremely common in the general population.

Studies have shown that there is a linear relationship between soft tissue injury
Brachial Plexus Anatomy

and aging, with fewer than 10% of individuals younger than 34 years being The brachial plexus Anatomy is a
affected, in contrast to 32–49% of those older than 75 being affected. complicated network of nerves
arises from the anterior rami of the
Whether a stress proves to be beneficial or detrimental to a tissue is very much cervical spine roots of (C5 - C6 -
C7 - C8 - T1).…
dependent on the physiologic capacity of the tissue to accept load.

The physiologic capacity of the tissue is dependent on a number of factors,

Ankle Anatomy
among them:
The ankle anatomy is a complex
hinged synovial joint that is formed
Private by three bones: the tibia, the fibula
Internet and the talus bone.
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Health of the tissue: Healthy tissues are able to resist changes in their shape.

Any tissue weakened by disease or trauma may not be able to adequately resist SNAC and SLAC of the wrist

the application of force.

SLAC of the wrist is a disorder
resulting from altered stress around
Age: Increasing age reduces the capacity of the tissues to cope with stress
an unstable scaphoid, while SNAC
loading. results from a scaphoid fracture
non-union.
Proteoglycan and collagen content of the tissue: Both increasing age and

exposure to trauma can result in unfavorable alterations in the proteoglycan and

Maudsley Test
collagen content of the tissue.
Maudsley Test (or tennis
Ability of the tissue to undergo adaptive change: All musculoskeletal tissue elbow test) is used for lateral
epicondylitis of the elbow joint, also
has the capacity to adapt to change. This capacity to change is determined
known as ”Tennis Elbow”.
primarily by the viscoelastic property of the tissue.

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The speed at which the adaptive change occurs: This is dependent on the

type and severity of the insult to the tissue. Insults of low force and longer

duration may provide the tissue an opportunity to adapt. In contrast, insults of a

higher force and shorter duration are less likely to provide the tissue time to

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The distinction between sudden and repetitive stress is important: vivo Indonesia Open

An acute stress (loading) occurs when a single force is large enough to

cause injury on biological tissues; the causative force is termed

macrotrauma.

A repetitive stress (loading) occurs when a single force itself is

insufficient to cause injury on biological tissues. However, when repeated or

chronic stress over a period of time causes an injury, the injury is called a

chronic injury, and the causative mechanism is termed microtrauma.

Etiologic factors for microtraumatic soft tissue injury are of two basic types:

Intrinsic factors: are physical characteristics that predispose an individual to

microtrauma injuries and include muscle imbalances, leg length discrepancies,

and anatomical anomalies.

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Extrinsic factors: which are the most common cause of microtrauma injuries, are

related to the external conditions under which the activity is performed. These

include training errors, type of terrain, environmental temperature, and incorrect

use of equipment.

Soft Tissue Injury Classification

Soft Tissue Injury can be classified as primary or secondary Tissue Injury.

Primary Soft Tissue Injury:

Primary or macrotraumatic injuries can be self-inflicted, caused by another

individual or entity, or caused by the environment. These injuries include

fractures and dislocations, which are outside the scope of practice for a physical

therapist, and subluxations, sprains, and strains, which make up the majority of

conditions seen in the physical therapy clinic. For the purposes on the

intervention, primary injuries are generally classified into acute, subacute, or

chronic.

Acute: This type of Soft Tissue Injury is usually caused by macrotrauma and

indicates the early phase of injury and healing, which typically lasts approximately

7–10 days.

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Subacute: This phase occurs after the acute phase and typically lasts from 5–10

days after the acute phase has ended.

Chronic: This type of injury can have several definitions. On the one hand it may

indicate the final stage of tissue healing that occurs 26–34 days after injury. On

the other hand the term may be applied to an injury that lasts longer than normal

and does not appear to be improving due to a persistent inflammatory state.

The persistent inflammatory state results in an accumulation of repetitive scar

adhesions, degenerative changes, and other harmful effects referred to as

subclinical adaptations.

Secondary Soft Tissue Injury:

Secondary or microtraumatic injuries are essentially the inflammatory response

that occurs with the primary injury. Microtraumatic injuries include tendinitis,

tenosynovitis, and bursitis.

Soft Tissue Injury types

Soft Tissue Healing

Fortunately, the majority of Soft Tissue Injury heal without complication in a

predictable series of events.

The most important factor regulating the regional time line of healing is sufficient

blood flow.

Complications such as infection, compromised circulation, and neuropathy have

an adverse effect on the healing process and can cause great physical and

psychological stress to the involved patients and their families.

Soft Tissue Injury Healing

Tissue Healing Stages

After microtrauma, macrotrauma, or disease, the body attempts to heal itself

through a predictable series of overlapping events that include coagulation and

inflammation (acute), which begins shortly after the initial injury; a migratory and

proliferative process (subacute), which begins within days and includes the

major processes of healing; and a remodeling process (chronic), which may last

for up to a year depending on the tissue type and is responsible for scar tissue

formation and the development of new tissue.

Whereas simplification of the complex events of healing into separate categories

may facilitate understanding of the phenomenon, in reality these events occur as

an amalgamation of different reactions, both spatially and temporally.

Soft Tissue Healing Stages

1. Coagulation and Inflammation Stage:

A soft tissue injury triggers a process that represents the body’s immediate

reaction to trauma. The reaction that occurs immediately after a soft tissue injury

includes a series of repair and defensive events. Following an injury to the

tissues, the cellular and plasma components of blood and lymph enter the

wound. Capillary blood flow is disrupted, causing hypoxia to the area. The blood

congeals and, through several steps, a clot is formed. This initial period of

vasoconstriction, which lasts 5–10 minutes, prompts a period of vasodilation, and

the extravasation of blood constituents.

Extravasated blood contains platelets, which secrete substances that form a clot

to prevent bleeding and infection, clean dead tissue and nourish white cells.

These substances include macrophages and fibroblasts. Coagulation and platelet

release results in the excretion of platelet-derived growth factor (PDGF), platelet

factor transforming growth factor-alpha (TGF-a), and transforming growth factor-

beta (TGF-b).

The main functions of a cell-rich tissue exudate are to provide cells capable of

producing the components and biological mediators necessary for the directed

reconstruction of damaged tissue while diluting microbial toxins and removing

contaminants present in the wound. Inflammation is mediated by chemotactic

substances, including anaphylatoxins that attract neutrophils and monocytes.

Neutrophils: Neutrophils are white blood cells of the polymorphonuclear (PMN)

leukocyte subgroup (the others being eosinophils, and basophils) that are filled

with granules of toxic chemicals (phagocytes) that enable them to bind to

microorganisms, internalize them, and kill them.

Monocytes: Monocytes are white blood cells of the mononuclear leukocyte

subgroup (the other being lymphocytes). The monocytes migrate into tissues

and develop into macrophages, providing immunological defenses against many

infectious organisms. Macrophages serve to orchestrate a long term response to

injured cells subsequent to the acute response.

Neutrophils & Monocytes

The white blood cells of the inflammatory stage serve to clean the wound debris

of foreign substances, increase vascular permeability, and promote fibroblast

activity. Other cell participants include local immune accessory cells, such as

endothelial cells, mast cells, and tissue fibroblasts. The PMN leukocytes, through

their characteristic “respiratory burst” activity, produce superoxide anion radical,

which is well known to be critical for defense against bacteria and other

pathogens. Superoxide is rapidly converted to a membrane permeable form,

hydrogen peroxide (H2O2), by superoxide dismutase activity or even

spontaneously.

Release of H2O2 may promote formation of other oxidants that are more stable

(longer half-life) including hypochlorous acid, chloramines, and aldehydes. The

phagocytic cells that initiate the innate immune response produce a set of

proinflammatory cytokines (e.g., TNF-a, IL-1, and IL-6) in the form of a cascade

that amplifies the local inflammatory response, influences the adaptive immune

response, and serves to signal the CNS of an inflammatory response.

The extent and severity of this inflammatory response depend on the size and

the type of the injury, the tissue involved, and the vascularity of that tissue.

Local vasodilation is promoted by biologically active products of the

complement and kinin cascades:

The complement cascade involves 20 or more proteins that circulate

throughout the blood in an inactive form. After soft tissue injury, activation

of the complement cascade produces a variety of proteins with activities

essential to healing.

The kinin cascade is responsible for the transformation of the inactive

enzyme kallikrein, which is present in both blood and tissue, to its active

form, bradykinin. Bradykinin also contributes to the production of tissue

exudate through the promotion of vasodilation and increased vessel-wall

permeability.

Because of the variety of vascular and other physiological responses

occurring, this stage of soft tissue healing is characterized by:

1. swelling,

2. redness,

3. heat,

4. impairment or loss of function.

The edema is due to an increase in the permeability of the venules, plasma

proteins, and leukocytes, which leak into the site of injury, resulting in edema.

New stroma, often called granulation tissue, begins to invade the wound space

approximately 4 days after injury. The complete removal of the wound debris

marks the end of the inflammatory process.

Clinically, this stage is characterized by pain at rest or with active motion, or

when specific stress is applied to the injured structure. The pain, if severe

enough, can result in muscle guarding and a loss of function.

Two key types of inflammation are recognized: the normal acute inflammatory

response and an abnormal, chronic, or

persistent inflammatory response.

Common causes for a persistent chronic inflammatory response include:

1. infectious agents,

2. persistent viruses,

3. hypertrophic scarring,

4. poor blood supply,

5. edema,

6. repetitive mechanical trauma,

7. excessive tension at the wound site,

8. hypersensitivity reactions.

The monocyte-predominant infiltration, angiogenesis, and fibrous change are the

most characteristic morphologic features of chronic inflammation. This

perpetuation of inflammation involves the binding of neutrophilic

myeloperoxidase to the macrophage mannose receptor.

2. Migratory and Proliferative Stage:

The second stage of soft tissue healing, characterized by migration and

proliferation, usually occurs from the time of the initial injury and overlaps the

inflammation phase. This stage is responsible for the development of wound

tensile strength.

Characteristic changes include:

1. capillary growth

2. granulation tissue formation,

3. fibroblast proliferation with collagen synthesis,

4. increased macrophage and mast cell activity.

After the wound base is free of necrotic tissue, the body begins to work to close

the wound.

The connective tissue in healing wounds is composed primarily of:

1. collagen, types I and III,

2. cells,

3. vessels,

4. a matrix that contains glycoproteins and proteoglycans.

Proliferation of collagen results from the actions of the fibroblasts that have been

attracted to the area and stimulated to multiply by growth factors, such as PDGF,

TGF-b, fibroblast growth factor (FGF), epidermal growth factor, and insulin-like

growth factor-1, and tissue factors such as fibronectin. This proliferation

produces first fibrinogen and then fibrin, which eventually becomes organized

into a honeycomb matrix and walls off the injured site.

The wound matrix functions as a glue to hold the wound edges together, giving

it some mechanical protection while also preventing the spread of infection.

However, the wound matrix has a low tensile strength and is vulnerable to

breakdown until the provisional extracellular matrix (ECM) is replaced with a

collagenous matrix. The collagenous matrix facilitates angiogenesis by providing

time and protection to new and friable vessels. Angiogenesis occurs in response

to the hypoxic state created by tissue damage as well as to factors released from

cells during injury.

The process of neovascularization during this phase provides a granular

appearance to the wound as a result of the formation of loops of capillaries and

migration of macrophages, fibroblasts, and endothelial cells into the wound

matrix.

Once an abundant collagen matrix has been deposited in the wound, the

fibroblasts stop producing collagen, and the fibroblast-rich granulation tissue is

replaced by a relatively acellular scar, marking the end of this stage.

This fibrous tissue repair process occurs gradually and can last anywhere from 5

to 15 days to approximately 10 weeks, depending on the type of tissue and the

extent of damage. Upon progressing to this stage, the active effusion and local

erythema of the inflammation stage are no longer present clinically. However,

residual effusion may still be present at this time and resist resorption.

3. Remodeling Stage:

An optimal wound environment lessens the duration of the inflammatory and

proliferative phases and protects fragile tissue from breakdown during early

remodeling. The remodeling phase involves a conversion of the initial healing

tissue to scar tissue. This lengthy phase of contraction, tissue remodeling, and

increasing tensile strength in the wound can last for up to 1 year.

Fibroblasts are responsible for the synthesis, deposition, and remodeling of the

ECM. Following the deposition of granulation tissue, some fibroblasts are

transformed into myofibroblasts, which congregate at the wound margins and

start pulling the edges inward, reducing the size of the wound.

Increases in collagen types I and III and other aspects of the remodeling process

are responsible for wound contraction and visible scar formation. Epithelial cells

migrate from the wound edges and continue to migrate until similar cells from the

opposite side are met. This contracted tissue, or scar tissue, is functionally

inferior to original tissue and is a barrier to diffused oxygen and nutrients.

Eventually, the new epidermis becomes toughened by the production of the

protein keratin. The visible scar changes color from red or purple that blanches

with slight pressure to non-blanchable white as the scar matures.

Imbalances in collagen synthesis and degradation during this phase of healing

may result in hypertrophic scarring or keloid formation with superficial wounds.

If the healing tissues are kept immobile, the fibrous repair is weak and there are

no forces influencing the collagen if left untreated, the scar formed is less than