The Healing ProcessGuidelines for Choosing the Proper Modality
How do you know what to use, and how do you know when to use it?◦ Theoretical knowledge◦ Practical experience
*You can’t follow the same recipe for every patient; avoid “cookie cutter” treatment plans
Choosing the Proper Modality
Modalities should be an adjunct to TEs◦ ROM and strengthening TEs are the desired end
goal Rehab protocols and progressions must be
based primarily on the physiologic responses of the tissues to injury and on an understanding of how various tissues heal
What does this mean?◦ The therapist must understand the healing
process in order to choose the proper modality at the proper time
Modalities in a POC
Decisions on how and when modalities may be best used relies upon:◦ Recognition of signs and symptoms◦ Awareness of the time frames associated with the
various phases of the healing process Important to note that the healing process
is a continuum◦ 3 phases are identified◦ Phases of the healing process overlap and have
no true definitive beginning or end points
Modalities in a POC
1. Inflammatory response phase 2. Fibroblastic-repair phase (granulation) 3. Maturation-remodeling phase
(contraction)
Phases of Healing
Leukocyte – white blood cell; scavengers and infection fighters Phagocyte – a cell that engulfs and absorbs waste material, harmful
microorganisms, or other foreign bodies in the bloodstream and tissues Phagocytosis – the process by which certain cells (leukocytes and
phagocytes) engulf and destroy microorganisms and cellular debris Exudate – fluid with a high protein and cellular debris content that has
escaped vessels and been deposited in tissues , usually as a result of inflammation
Anemia – reduction of blood components Hyperemia – excess of blood in a part Chemical mediators – (histamine, leucotaxin, necrosin) chemicals that
limit the amount of exudate and swelling following injury Secondary hypoxic injury – Disruption of blood flow to the injury site
and surrounding uninjured tissue that causes hypoxia and can lead to further tissue damage
Phase I – Inflammatory Response - Vocabulary
Once a tissue is injured, the process of healing begins immediately
Destruction of tissue = injury to cells◦ Cellular injury results in the release of materials
(fluid, other cells, wastes) that initiate the inflammatory response
◦ Characterized by redness, swelling, tenderness, and increased temperature
Phase I - Inflammatory Response
Inflammation is a process where leukocytes, other phagocytes, and exudate are delivered to the injured tissue◦ Protective reaction◦ Serves to localize or dispose of injury by-products
(blood, damaged cells) through phagocytosis Sets the stage for repair of damaged tissue
Phase I – Inflammatory Response
The immediate response to damage is constriction of the walls of the vessels (spasm)◦ Lasts 5-10 minutes◦ Presses the inner walls of the vessels together to
cause local anemia This is followed by rapid hyperemia as the
spasm reverses into dilation of the vessels◦ Eventually the flow slows and stagnates
The initial movement of exudate into the tissues usually lasts 24-36 hours (Swelling)
Phase I – Inflammatory Response
Swelling – Good or bad? Good
◦ The exudate brings cells to the injured area that help to eliminate dead cells, tissue, etc.
◦ It also helps to “splint” the area to limit movement Bad
◦ Painful; ROM limitations; spasm; limits blood flow◦ Can cause secondary hypoxic injury
The disruption of blood flow to the injured and surrounding healthy tissue causes hypoxia
Hypoxia (lack of oxygen) causes pain, spasm, and further tissue damage
Phase I – Inflammatory Response
Chemical mediators limit the amount of exudate and swelling
Histamine, leucotaxin, and necrosin◦ Histamine – causes vasodilation and increased cell
permeability◦ Leucotaxin – assists fluid and WBC to move
through cell walls to form exudate◦ Necrosin – responsible for phagocytic activity
*Chemical mediators allow for just enough exudate formation and delivery, but not too much*
Phase I – Inflammatory Response
Platelets do not normally adhere to vessel walls◦ Good thing, or we would form clots within blood
vessels all the time! Disruption of vessel walls allows platelets and
leukocytes to adhere to the damaged spot◦ This forms a plug to block lymph drainage and localize
the injury response Lastly the damaged cells release a protein that
helps to form a fibrin clot that shuts off blood supply to the injured area◦ Clot formation begins around 12 hours after injury and
is completed by 48 hours
Phase I – Inflammatory Response
This combination of factors walls the injured area off during this stage
The leukocytes phagocytize most of the debris toward the end of the phase, which sets the stage for the fibroblastic phase
The initial inflammatory response phase lasts for approximately 2 to 4 days following injury
Phase I – Inflammatory Response
Collagen – the major protein of the white fibers of connective tissue, cartilage, and bone; “the glue that holds the body together”
Fibroblast – an immature, fiber-producing cell
Fibroplasia – period of scar formation Granulation tissue – delicate connective
tissue consisting of fibroblasts, collagen, and capillaries
Phase II – Fibroblastic-Repair - Vocabulary
Fibroplasia begins within the first few hours following injury and may last for as long as 4 to 6 weeks
Production and regeneration of tissues leads to scar formation and repair of injured tissue◦ During this period many of the s/s associated with
the inflammatory response subside Patients typically still report some tenderness and pain
with certain stressful movements As scar formation progresses, tenderness and pain
gradually subside
Phase II – Fibroblastic-Repair
Inflammation causes a lack of oxygen to the injured area (hypoxia)
The body responds by growing new capillaries to deliver oxygenated blood◦ Along with increased blood and oxygen delivery
comes nutrients essential for tissue regeneration in the injured area
The fibrin clot begins to break down as new capillaries grow
Phase II – Fibroblastic-Repair
The delivery of the nutrients, plus the breakdown of the fibrin clot, causes formation of granulation tissue◦ Fills in the gaps during the healing process
The fibroblasts in the granulation tissue begin to (perform magic to) form the immature scar tissue
On day 6 or 7 they also begin depositing collagen fibers throughout the scar tissue◦ Collagen fibers increase tensile strength of the scar◦ As tensile strength increases, the number of fibroblasts
decreases to signal the beginning of the next phase of healing
Phase II – Fibroblastic Repair
The is a long-term process Features realignment or remodeling of the
collagen fibers that make up the scar tissue according to the tensile forces to which the scar in subjected◦ Ongoing process of breakdown and synthesis of
collagen that causes an increase in tensile strength of the scar
Phase III – Maturation-Remodeling
With increased stress and strain the collagen fibers realign in a position of maximum efficiency parallel to the lines of tension◦ The tissue gradually assumes a normal appearance
and function◦ Rarely as strong as uninjured tissue
Usually by the end of approximately 3 weeks a firm, strong, contracted, nonvascular scar exists
The maturation phase of healing may require several years to be totally complete
Phase III – Maturation-Remodeling
Factors That Impede Healing Extent of the injury
◦ Determines extent and length of the inflammatory response Microtears
Involve only minor damage Most often associated with
overuse Macrotears
Involve significantly greater destruction of soft tissue
Result in clinical symptoms and functional alterations
Generally caused by acute trauma
Edema◦ Increases pressure caused by swelling slows the
healing process via: Separation of tissues Inhibiting neuromuscular control Impeding nutrient delivery in the injured part
This is why edema control is so important during initial first aid
Factors That Impede Healing
Hemorrhage◦ Even the smallest amount of damage to the
capillaries causes bleeding◦ Produces the same negative effects as edema
The presence of bleeding produces additional tissue damage and thus makes the injury worse
Factors That Impede Healing
Poor vascular supply◦ Tissues that have a poor blood supply heal poorly
and slowly◦ Related to:
Lack of nutrient delivery Failure in delivery of phagocytic cells and fibroblasts
necessary for formation of scar tissue
Factors That Impede Healing
Separation of tissue◦ Physical separation of the edges of the wound
A wound with smooth edges and good approximation will usually heal with minimal scarring
A wound with jagged, separated edges must heal by filling in the gaps with granulation tissue, resulting in excessive scarring
Factors That Impede Healing
Muscle spasm◦ Spasms cause pull on both ends of the wound,
separating the ends and disallowing approximation
◦ Spasms can cause swelling and lack of blood flow
Factors That Impede Healing
Atrophy◦ Wasting away of muscle tissue begins
immediately with injury◦ Strengthening and early movement of the injured
structure minimizes atrophy
Factors That Impede Healing
Corticosteroids◦ Use of corticosteroids in early stages of healing
can inhibit fibroplasia, capillary formation, and collagen synthesis
Factors That Impede Healing
Keloids and hypertrophic scars◦ Keloids occur when the rate of collagen
production exceeds the rate of collagen breakdown during the maturation phase
◦ Leads to hypertrophy of scars
Factors That Impede Healing
Infection◦ The presence of bacteria in the wound can delay
healing◦ Often causes excessive granulation tissue and
large scars
Factors That Impede Healing
Humidity, climate, oxygen tension◦ Humidity increases the process of forming
epithelium A moist wound promotes the migration of the
necrotic tissue to the surface where it is shed◦ Oxygen tension relates to optimal oxygen
saturation and maximal tensile strength development
Factors That Impede Healing
Health, age, and nutrition◦ Elastic qualities of skin decrease with age◦ Degenerative diseases also affect wound healing◦ Nutrition greatly affects wound healing
Vitamins C (scurvy), K (clotting), and A & E (collagen synthesis)
Zinc (enzyme systems) Amino acids (cell walls)
Factor That Impede Healing
No matter how old an injury is, it should be classified according to the signs and symptoms (acute vs. chronic)
If the classic s/s of inflammation are present, treat injury as if it is in the inflammatory response phase◦ S/S of active inflammation present = acute injury◦ S/S are no longer present = chronic injury
Injury Management Using Modalities
Based upon this definition of acute and chronic, the rehab progression following injury will be based upon 4 phases:◦ 1. Initial acute◦ 2. Inflammatory response◦ 3. Fibroblastic-repair◦ 4. Maturation-remodeling
The phases overlap, and time frames vary between patients
Injury Management Using Modalities
Modality use should be directed toward limiting swelling and reducing pain◦ Cryotherapy (+ elevation)◦ Compression (+ elevation)◦ Electrical stimulation◦ Ultrasound◦ Laser
(Rest – 48-72 hours)
Initial Acute Injury Phase
Cryotherapy – reduce swelling and pain◦ Ice bags, cold packs, ice massages◦ Not cold baths or cold whirlpools
Most important function is to produce analgesia
Should be used with elevation
Initial Acute Injury Phase
Compression (+ elevation)◦ Intermittent compression (pumping action)
Compression + cold = better Compression + cold + elevation = best
Initial Acute Injury Phase
Electrical stimulation◦ Used to address pain in this phase◦ Avoid intensities that cause muscle contraction as
it may increase clotting time
Initial Acute Injury Phase
Ultrasound◦ Can be used to facilitate healing when used
immediately after injury through the 1st 48 hours◦ Lower intensities produce nonthermal effects that
alter cell membrane permeability to ions that aide in healing
Initial Acute Injury Phase
Low-power laser◦ Effective in pain modulation◦ Low power is used so as not to cause tissue death
Initial Acute Injury Phase
Begins as early as day 1 and may last as long as day 6 post injury
Goals similar to initial acute injury phase Cryotherapy
◦ Important to not switch to heat modalities too early
◦ May use contrast baths with longer cold to hot ratio
Compression, e-stim, l-p laser
Inflammatory Response Phase
After initial acute injury phase, the patient should work on AROM and PROM
Exercise progression determined by injury’s response to exercise
If s/s of inflammation increase with exercise, reduce intensity
Aggressive rehab is desirable, but will always be limited by the healing process
Inflammatory Response Phase
As early as day 4 post-injury and may last a few weeks◦ Swelling has usually stopped ◦ Tenderness remains with touch and ROM
exercises Modalities include:
◦ Cryotherapy => Thermotherapy◦ Compression◦ E-stim◦ Low-power laser◦ ROM and strengthening exercises
Fibroblastic-Repair Phase
Treatments may switch from cold to heat◦ Use swelling as an indicator
Thermotherapy increases circulation to an area to promote healing and reduce pain◦ Includes moist hot packs, paraffin, fluidotherapy,
and warm whirlpool
Fibroblastic-Repair Phase
Intermittent compression – facilitates removal of by-products from area
E-stim – now used to elicit muscle contraction for a muscle pumping action to aid in lymphatic flow and to reduce pain
Low-power laser to reduce pain
Fibroblastic-Repair Phase
May last several years Main goal is to return to activity The collagen fibers must be realigned
according to tensile stresses and strains placed upon them
Most to all modalities are typically safe to use in this phase
Massage is particularly effective in this phase to assist in scar remodeling
Maturation-Remodeling Phase
Thermotherapy◦ Deep heating most beneficial
Ultrasound, shortwave and microwave diathermy Increased blood and lymphatic flow
◦ Superficial heating less effective, though helpful for pain and flexibility
E-stim◦ Pain modulation◦ Muscle contractions for increasing ROM and strength
Low-powered laser◦ Pain modulation
Maturation-Remodeling Phase
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