the healing process

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)


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


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*


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


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


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


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


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


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


Atrophy◦ Wasting away of muscle tissue begins

immediately with injury◦ Strengthening and early movement of the injured

structure minimizes atrophy


Corticosteroids◦ Use of corticosteroids in early stages of healing

can inhibit fibroplasia, capillary formation, and collagen synthesis


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


Infection◦ The presence of bacteria in the wound can delay

healing◦ Often causes excessive granulation tissue and

large scars


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


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


Compression (+ elevation)◦ Intermittent compression (pumping action)

Compression + cold = better Compression + cold + elevation = best


Electrical stimulation◦ Used to address pain in this phase◦ Avoid intensities that cause muscle contraction as

it may increase clotting time


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


Low-power laser◦ Effective in pain modulation◦ Low power is used so as not to cause tissue death


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


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


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

the healing process

Documents

process of healing

injury byproducts blood

healing processimportant

healing processguidelines

tissue damage phase

injury site

damaged cells

inflammatory response