Guidelines 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

 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

 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

 1. Inflammatory response phase  2. Fibroblastic-repair phase (granulation)  3. Maturation-remodeling phase (contraction)

 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

 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

 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

 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 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

 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

 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

 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

 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

 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

 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

 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)

 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

 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

 Modality use should be directed toward limiting swelling and reducing pain ◦ Cryotherapy (+ elevation) ◦ Compression (+ elevation) ◦ Electrical stimulation ◦ Ultrasound ◦ Laser  (Rest – hours)

 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 1 st 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

 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

 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

 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

 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