In response to Dr. SandellPosted by Elyse B on 6/18/04 at 07:40 (153366)
I took the libery of doing some research, let me know what you think:
What is mobilization?
Mobilization is a hands-on manual therapy designed to restore joint movement, power, and range of motion. The therapist gently coaxes joint motion by passive movement within or to the limit of a joint's normal range of motion. The therapist's movement of the joint is very precise and is limited by the amount of joint play, which may be less than 1/8th of an inch.
The overall goal of mobilization is to restore normal joint function including the surrounding soft tissue (e.g. muscle, ligaments, fascia). Physical Therapists, Osteopaths, and Chiropractors perform mobilization.
What part of the spine is treated?
In the spine, any of the facet joints and/or the costovertebral articulations (thoracic spine and ribs) may become stiff causing joint dysfunction. When a joint is unable to move freely, a cycle of muscle spasm, pain, and fatigue may begin.
What causes joint dysfunction?
Joint dysfunction can be caused by poor posture, trauma, spinal disease, or congenital problems. Left untreated, joint dysfunction can affect the surrounding soft tissue and may lead to a loss of strength and flexibility.
Are other treatments involved in mobilization?
Myofascial release, or soft tissue mobilization, is a therapy used to release tension stored in the fascia. Fascia are sheets of fibrous tissue that encase and support muscles separating them into groups and layers. Fascia also covers joints capsules and ligaments. Following trauma, the fascia and muscles may shorten restricting joint movement and blood flow. The techniques used in myofascial release break up fascial adhesions and relaxes muscle tension helping to normalize physical motion within the joint capsule.
Rehabilitation of Soft Tissue Injuries in the 1990s
The days of prolonged immobilization are a part of the past for the treatment of soft tissue injuries. The increased attention toward sports medicine throughout the late 1970s and 1980s has led to research and many clinical studies that will outline the course of rehabilitation throughout the years to come. A review of the current literature on acute soft tissue injuries classifies different types of soft tissue lesions as well various phases of healing.1 Current literature redefines the aims and objectives of rehabilitation pointing out the many benefits of the use of modalities, early mobilization, and the importance of a full rehabilitation program.
Over the past two decades, soft tissue injuries have hit the spotlight. Almost all traumatic injuries, automobile accidents, athletic or other injuries result in some degree of soft tissue damage. It's now recognized that many soft tissue injuries result in a degree of permanent impairment and leave their host with some permanent pain, restrictions, and loss of function.2 To combat the debilitating (aftermath) of soft tissue injury, new technology and rehabilitation protocols have been developed.
Etiology of Soft Tissue Injuries, Direct and Indirect Trauma
Many soft tissue injuries come from direct trauma such as being struck by a moving object or a fall; other injuries may be classified as indirect trauma and result from overloading or chronic overuse, thus giving us the classification of direct and indirect etiology.3 Indirect can be further divided into three sub-classes: acute -- which occurs from sudden overloading as seen in many lifting injuries; chronic or overuse -- which are often seen in many assembly line or factory workers who must perform repetitive movements hundreds of times daily; acute on chronic -- occurs when a chronic conditions hits an acute phase. This third sub-class is also very common in the work environment where the same job is performed day in and day out. By first defining the etiology of a condition, we are on the proper course toward treatment and the prevention of further injury.
Phases of Healing -- Phase I
The current literature describes three main phases of soft tissue healing. An initial reaction phase which lasts up to 72 hours post-injury.4 This phase is also referred to as the acute inflammation phase.3 The reaction phase displays with the classic signs of inflammation with pain, swelling, redness and warmth. In the cases of indirect etiology, these classic signs may not be readily visible but are proceeding at the microscopic level.5
The long-used application of cryotherapy (ice) is still supported by numerous studies as very effective treatment in this initial phase.6,7,8,9 Cryotherapy slows the inflammatory process as well as provides an analgesic effect. Ultrasound may also be used to decrease swelling in this inflammatory phase, but must be used for short periods to prevent hyperemia.10 Transcutaneous nerve stimulation (TNS) and electric muscle stimulation (EMS) have also been shown to be effective.
The use of continuous passive motion (CPM) has been shown to clear hemoarthrosis (blood present in the synovial joints post-trauma) during the initial reaction phase. In the 24 hours following trauma, the synovial fluid in joints treated with CPM displayed less blood than immobilized joints. At 48 hours the joints treated by CPM demonstrated the synovial fluid was clear where as the immobilized joint remained grossly bloody.11
The use of manipulation can also be employed in the reaction phase and is suggested in the areas of fixation that have resulted from the injury. This will expedite the removal of hemoarthrosis, reduce spasms, edema and pain as well as reduce nerve root irritation when present.12 Cyriax states, 'When free mobility was encouraged from the onset, the fibers in the scar were arranged lengthwise as in a normal ligament. Gentle passive movements do not detach fibrils from their proper formation at the healing breach, but prevent their continued adherence at abnormal sites.'13
In the initial reaction phase, the use of CPM and manipulations (which are both mobilization techniques) must be used in a controlled protective manner to prevent any further damage to the healing ligaments.11
The initial reaction phase can be treated effectively using classic cryotherapy, specific modalities, as well as a controlled program of CPM and manipulations.
Phase of Healing -- Phases II and III
The second stage of healing, the repair phase, may last from 48 up to 6 weeks. This phase is characterized by the production and laying down of new collagen.4 During this phase, the collagen is not fully oriented in the direction of tensile strength.5
The third phase, the remodeling phase, which lasts from 3 weeks to 12 months or more, is the phase in which the collagen is remodeled and along with with phase II determines the functional capabilities of the soft tissue after the healing process is completed.14 True rehabilitation must focus on maintaining these functional capabilities. Oakes3 describes the aims of rehabilitation as regaining pain-free movement with full strength, power and range of motion, thus describing the functional capabilities of the soft tissue.
To regain the functional capabilities, stresses of function must be put on the healing tissue. As described by Roy:15 'If a limb is completely immobilized during the recovery process, the tissues may emerge fully healed but poorly adapted functionally with little chance for change, particularly if the immobilization has been prolonged.' Mobilization techniques must take place throughout the repair and remodeling phases to insure proper tissue adaptation. Several benefits of mobilization have been defined which include increased strength3,16 and flexibility of healed tissue, less scar formation and adhesions,14 increased cartilage nutrition,17 and lesser incidence of recurrence of injury.18
Rehabilitation protocol following soft tissue injury must include mobilization techniques to insure good functional adaptation. A program combining manipulations, the use of modalities, mobilization technique, and a strengthening program will insure optimal rehabilitation.
Manipulations and modalities should be used during all three phases of healing to limit fixations, control pain and spasms as well as maintain neurologic integrity. Mobilization should be carried out within the limits of pain on the patient, starting with controlled passive motion. Controlled passive motion should be employed until a maximum range of motion is reached. At this point, active assistive motion should be employed. As the injury heals and the tissue adapts, the patient can be graduated to active resistive motion. Active resistive motion should be followed by a strengthening program of kinetic resistive exercise. This will insure a return to maximum strength for the patient. Keep in mind all rehabilitation should be performed within the patient's limits of pain and periodic re-evaluation and testing such as muscle testing and surface EMG should be performed to evaluate the patient's progress. Also remember that the final remodeling phase can last over a year post injury; rehabilitation should be directed accordingly.
By following this rehabilitation protocol and progression, a return to maximum functional capabilities can be insured, returning the patient to maximum pain free range of motion and strength.
Rehabilitation in the 1990's focuses on regaining function. After all, function does determine what we can do with our lives.
J. Scott Brown, D.C.
Soft Tissue Injuries
SOFT TISSUE INJURIES
Defined as an injury to muscle tissue, tendons, ligaments, fascia, and innervating nerve supply. It is common for soft tissue injuries to be coupled with joint pain, offering a worsening of pain upon initial movements (waking, sit to stand) or lessen with mild activity
History may reveal the following:
~ Blunt trauma
~ Rapid deceleration or acceleration (Such as injuries sustained in a motor vehicle accident)
~ Overstretching a tissue beyond its normal anatomical limits (Such as with over exertion or sports injuries)
~ Range of motion-restricted due to pain- sensation of 'pulling'
~ Motor and sensory- possible decrease in sensory perception
~ Orthopedic testing- may not be positive for adjacent joints
~ Palpation-may elicit warmth and throbbing sensation. Edema and myospasm evident.
Treatment may include:
~ Cryotherapy (acute stages)
~ Interferential muscle stimulation
~ Hot fomentation
~ Manual therapies including deep friction massage and joint mobilization
~ Passive and active stretching
~ Gentle, progressive resistance exercises both in office and at home
Due to the fact that there are three phases of soft tissue healing there are specific treatment objectives for each.
• Acute Phase- reduce inflammation, edema, and pain with physical therapy modalities
• Remodeling Phase- Scar tissue must be mobilized and tissue elasticity must be restored through manual techniques and passive and active stretching
• Rehabilitative Phase- It is important to strengthen all tissues in and around injured region. Education may be necessary for long-term prevention in the areas of posture, lifting techniques, and maintenance of exercise and overall health.
Physical therapy may be necessary to break the pain/myospasm cycle and to restore tissue to a normal pain free function. Additionally, there may be a need for gradual, supervised return to daily activity to avoid relapses.
Adverse affects of untreated injury could include:
Chronic pain or functional limitations due to:
~ Tissue shortening
~ Range of motion restrictions
~ Joint degeneration
~ Accumulation of adhesions along muscular fibers
Immobilization or Early Mobilization After an Acute Soft-Tissue Injury?
Pekka Kannus, MD, PhD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 28 - NO. 3 - MARCH 2000
In Brief: Experimental and clinical studies demonstrate that early, controlled mobilization is superior to immobilization for primary treatment of acute musculoskeletal soft-tissue injuries and postoperative management. Optimal treatment and rehabilitation follow four steps that address response to trauma. First is treating the damaged area with PRICES: protection, rest, ice, compression, elevation, and support. Second, during the first 1 to 3 weeks after the injury, immobilization of the injured tissue areas allows healing without extensive scarring. Third, when soft-tissue regeneration begins, controlled mobilization and stretching of muscle and tendons stimulate healing. Fourth, at 6 to 8 weeks postinjury, the rehabilitative goal is full return to preinjury level of activity.
Acute soft-tissue injuries such as muscle-tendon strains, ligament sprains, and ligament or tendon ruptures occur frequently in sports and exercise. Without correct diagnosis and proper treatment, they may result in long-term breaks in training and competition. Far too often, injuries become chronic and end careers of competitive athletes or force recreational athletes to abandon their favorite activity. For these reasons, an increased focus has been on finding ways to ensure optimal healing. In this regard, the question has centered on immobilization or early mobilization in treatment.
Soft-Tissue Response to Trauma
Musculoskeletal soft tissue responds to trauma in three phases: the acute inflammatory phase (0 to 7 days), the proliferative phase (about 7 to 21 days), and the maturation and remodeling phase (21 days and thereafter; table 1). (1)
TABLE 1. Phases of Healing After an Acute Soft-Tissue Injury
Phase Approximate Days After Injury
Maturation and remodeling >21
Acute inflammatory phase. In this phase, ischemia, metabolic disturbance, and cell membrane damage lead to inflammation, which, in turn, is characterized by infiltration of inflammatory cells, tissue edema, fibrin exudation, capillary wall thickening, capillary occlusions, and plasma leakage. Clinically, inflammation manifests as swelling, erythema, increased temperature, pain, and loss of function. The process is time dependent and mediated by vascular, cellular, and chemical events culminating in tissue repair and sometimes scar (adhesion) formation.
Proliferative phase. These changes include fibrin clotting and a proliferation of fibroblasts, synovial cells, and capillaries. The inflammatory cells eliminate the damaged tissue fragments by phagocytosis, and fibroblasts extensively and markedly elevate production of collagen (initially, the weaker, type 3 collagen, later type 1) and other extracellular matrix components.
Maturation and remodeling phase. In this phase, the proteoglycan-water content of the healing tissue decreases and type 1 collagen fibers start to assume a normal orientation. Approximately 6 to 8 weeks postinjury, the new collagen fibers can withstand near-normal stress, although final maturation of tendon and ligament tissue may take as long as 6 to 12 months.
Injury and Four-Step Treatment
After an injury, the ideal treatment and rehabilitation program should include four steps.
PRICES. Immediately after injury, the damaged area should be treated with PRICES: protection, rest, ice (cold), compression, elevation, and support (table 2) (1,2). The aim is to minimize hemorrhage, swelling, inflammation, cellular metabolism, and pain, and to provide optimal conditions for healing (2). Since prolonged inflammation may lead to excessive scarring, early, effective treatment seeks to prevent it. On the other hand, one must remember that inflammation is not only the body's response to insult, but also the initial step in healing.
TABLE 2. Basic Treatment Plan for Acute Musculoskeletal Injury ('PRICES' Mnemonic)
P = Protection from further damage
R = Rest to avoid prolonging irritation
I = Ice (cold) for controlling pain, bleeding, and edema
C = Compression for support and controlling swelling
E = Elevation for decreasing bleeding and edema
S = Support for stabilizing the injured part
Immobilization and protection. The second step is immobilization and protection of the injured tissue area during the first 1 to 3 weeks. In the early phase of healing, immobilization allows undisturbed fibroblast invasion of the injured area that leads to unrestricted cell proliferation and collagen fiber production. Premature and intensive mobilization at this time leads to enhanced type 3 collagen production and weaker tissue than that produced during an optimal immobilization period (2). Protection (such as with a cast or brace) prevents secondary injuries and early distension and lengthening of injured collagenous structures such as a torn anterior cruciate ligament (ACL) (3).
Maturation. About 3 weeks after injury, collagen maturation and final scar tissue formation begins (1,2,4). In this phase, injured soft tissues need controlled mobilization. Less injured portions of the tissue or joint, however, can be mobilized earlier, sometimes even during the proliferative phase. Prolonged immobilization, though, must be avoided to prevent atrophy of cartilage, bone, muscle, tendons, and ligaments (5-12). Controlled muscle stretching and joint movement enhance new collagen fiber orientation parallel to the stress lines of the normal collagen fibers; these activities also serve to prevent tissue atrophy from immobilization. Treatment can be supported with physical therapy to improve local circulation and proprioception, inhibit pain, and strengthen muscle-tendon units.
Resumption of activity. Approximately 6 to 8 weeks after the injury, new collagen fibers can withstand near-normal stress, and the goal for rehabilitation is rapid and full recovery to activity. If the previous steps were followed, protection is no longer needed, and each component of the damaged soft tissue is ready for a progressive mobilization and rehabilitation program (2).
Soft-Tissue Healing: Experimental Studies
The current literature on experimental acute soft-tissue injury speaks strongly for the use of early, controlled mobilization rather than immobilization for optimal healing.
Knee joint. Studies by Woo and colleagues (reviewed in Woo and Hildebrand ) have shown that an experimentally induced tear of the medial collateral ligament (MCL) in animals heals much better with early, controlled mobilization than with immobilization. Early mobilization influenced healing even more than did surgical repair performed on the rupture. Exercise had an adverse effect on ligament healing and knee stability only when the animals' joints had been rendered unstable by transection of both the ACL and the MCL. These results probably reflect the poor regeneration potential of the ACL after rupture or transection (3,13).
Muscle. Much of the experimental data about the effects of early mobilization versus immobilization on muscle injury repair have come from studies in Tampere and Turku, Finland, and have been reviewed in Järvinen and Lehto (2). In experimentally injured rat gastrocnemius muscle, fiber regeneration is often inhibited by dense scar-tissue formation. Immobilization immediately after injury limits the size of the connective tissue area formed within the injury site. Penetration of muscle fibers into the connective tissue is prominent, but their orientation is complex and fibers are not parallel to the uninjured muscle fibers. In addition, immobilization for longer than 1 week resulted in marked atrophy of the injured gastrocnemius. Mobilization instituted immediately after injury resulted in dense scar formation and interfered with muscle regeneration.
In the rat model, the best results were achieved when mobilization was started after 3 to 5 days of immobilization. In the gastrocnemius, muscle fiber penetration through the immature connective tissue appeared optimal, and orientation of regenerated muscle fibers aligned with the uninjured muscle fibers. The gain in strength and capacity for energy absorption has been similar and as good as that of muscles treated by early immediate mobilization alone (2).
Tendons. Using a rat model, Enwemeka et al (14) demonstrated a significant increase in Achilles tendon strength after repair and early mobilization compared with repair and immobilization. In divided, unrepaired rat Achilles tendons, Murrell et al (15,16) obtained similar results. Gelberman at al (17) reported that mobilization of an animal extremity enhanced the orientation and organization of tendon collagen. Thus, after the inflammatory phase, a controlled stretching and strengthening of the regenerating, repaired tendon is likely to increase the final tensile properties of the tendon. However, suspicion remains that even with optimal therapy after repair, the collagen fibers in the tendon may be deficient in content, quality, and orientation (10). If so, this deficiency may present increased risk of inflammatory reaction, tendon degeneration, and tendon reruptures during later activities.
Soft-Tissue Healing: Clinical Trials
Early controlled mobilization. Controlled clinical trials of acute soft-tissue injuries support the results of experimental studies and have shown that early controlled mobilization is superior to immobilization, not only in primary treatment, but also in postoperative management. The superiority of early controlled mobilization has been especially clear in terms of quicker recovery and return to full activity without jeopardizing the subjective or objective long-term outcome. Evidence has been systematic and convincing for many injuries (table 3): acute ankle ligament rupture (18-20); after surgery for ankle ligament rupture (21); after surgery for chronic ankle ligament instability (22); knee ligament injury (6,23); articular cartilage injury (24); minimally displaced distal radius fracture (25); and complete Achilles tendon rupture (26-28). In addition, in many other injuries such as elbow or shoulder dislocation and many nondisplaced fractures, early mobilization yielded good results, although not all studies used a control group (10,29).
TABLE 3. Soft-Tissue Injuries That Have Been Shown to Have Better Outcomes With Early Mobilization Than With Immobilization
Acute ankle ligament tears
Postsurgery acute or chronic ankle ligament tears
Knee ligament injuries
Complete Achilles tendon ruptures
Randomized studies. The importance of results from prospective, randomized trials cannot be overemphasized; they may dramatically change our thinking and conventional treatment protocols. For example, 2-year results from a prospective, randomized study (27) from Hannover, Germany, (conservative functional treatment alone vs surgery plus similar functional treatment) support the use of early functional rehabilitation alone in complete Achilles tear. This finding is supported by an experimental observation in rats that surgical repair of a surgically divided Achilles tendon did not improve the outcome obtained by functional treatment (free-cage activity) alone (30).
Other examples come from investigations of patellar dislocation: Two randomized studies (31,32) from Finland indicate that after a 2-year follow-up, conservative treatment of acute patellar dislocation gives results at least as good as surgical treatment followed by similar conservative treatment. Comparable observations have been made in acute, complete rupture of the ankle ligaments: Early controlled mobilization alone gives results at least as good as surgery plus early controlled mobilization (18,21,33).
Avoiding atrophy. Obviously, the best method for preventing immobilization atrophy is usage. Complete immobilization should be minimal and often is not needed at all. During the last 10 to 15 years, many postoperative protocols, especially those involving knee and ankle ligament injuries, have undergone a major change from long, complete immobilization to early, controlled mobilization using elastic or other bandages, rehabilitative braces, continuous passive devices, or a combination immediately after the trauma. Also, active joint motion and weight bearing is allowed earlier than before, and training during immobilization is becoming more and more effective (10). Even modern fracture treatment has considerably reduced the degree and duration of cast immobilization (10,25).
Early mobilization. Early mobilization is the best method to avoid joint contracture and its harmful consequences on articular cartilage. The technique also serves to maintain and return joint proprioception, which, in turn, may be important in preventing reinjury and in hastening recovery to full fitness. In addition, Frank et al (34) have suggested that joint motion may help reduce postinjury and postoperative pain, swelling, and thromboembolic complications.
The efficacy of early motion in preventing immobilization atrophy depends on how well it controls pain, inflammation, and swelling. Inflammation and pain result in voluntary inhibition of muscle activity across the affected joint. Spencer et al (35) have even reported that pain is not required to cause muscle inhibition; swelling alone is sufficient (so-called reflex inhibition). Therefore, primary treatment should control all three factors using early controlled motion in combination with other treatment modalities such as cold, anti-inflammatory analgesics, and transcutaneous neural stimulation.
Rehabilitation programs. For each joint and each type of injury, rehabilitation programs must be individualized, taking into account the injured structures that should be protected from premature and intensive mobilization, as well as the uninjured structures that should be mobilized as soon as possible. To prevent muscle dysfunction when immobilization must be used, diverse stimuli are needed throughout the entire period; these include strength, power, and endurance exercises. The modern operational principle in the treatment of acute soft-tissue injuries and during immobilization is that 'within the limits of pain, everything that is not explicitly forbidden is allowed.' (10) This, of course, requires good cooperation between the patient and the attending physician and physical therapist.
Controlled experimental and clinical trials have yielded convincing evidence that early, controlled mobilization is superior to immobilization for musculoskeletal soft-tissue injuries. This holds true not only in primary treatment of acute injuries, but also in their postoperative management. The superiority of early controlled mobilization is especially apparent in terms of producing quicker recovery and return to full activity, without jeopardizing the long-term rehabilitative outcome. Therefore, the technique can be recommended as the method of choice for acute soft-tissue injury.
MEDICO LEGAL NEWS
ALAN M. IMMERMAN, D.C.
DECEMBER 10, 1998
ACUTE SOFT TISSUE INJURIES: DO THEY HEAL PARTIALLY OR COMPLETELY?
As described by Kellett, there are three stages in the healing of soft tissue (referring to ligament and tendon):
1. Acute Inflammatory Phase: Marked by swelling, redness, warmth and pain, the acute inflammatory phase lasts about 72 hours. During this period of time, the body minimizes blood loss by activating the blood coagulation system; dilates (widens) the blood vessels so that healing elements may be more quickly delivered to the damaged tissues; and removes debris which results from the damage to soft tissue cells.
2. Repair Phase: This phase lasts from 48 hours to 6 weeks. Early in the repair phase the body finishes the job of cleansing the entire area of the soft tissue injury. Next the body synthesizes new fibers (collagen) to replace the damaged fibers. The new collagen is not, however, fully orientated in the direction of tensile strength.
3. Remodeling Phase: This phase lasts from 3 weeks to 12 months or more. During this phase, the body remodels the newly synthesized collagen in order to increase the functional capabilities of the tendon or ligament to withstand the stresses imposed on it. (Kellett, 1986)
It is important to note that normal ligaments are composed of type I collagen whereas damaged and healed ligaments contain a large proportion of type III collagen. Type III collagen is considered an 'immature' form of collagen because it is deficient in the number of cross-linkages between and within the collagen subunits. Experiments which have studied ligament healing in rabbits have found that 40 weeks after injury the collagen is still deficient in content and quality. (Kellett, 1986) The cross-linkages are of critical importance in determining the strength of the newly synthesized collagen. (Loitz and Frank, 1993)
What do other authors say about the final extent of healing? Woo and Buckwalter in 1987 stated: 'It became apparent that most injuries to the Musculoskeletal soft tissues do not result in repair that restores normal tissue structure and function and that the long-term results vary. Unlike bone, regeneration of normal tissue and complete restoration of normal function rarely occurs in the musculoskeletal soft tissues.' (Woo and Buckwalter, 1987)
In 1993, Loitz and Frank stated: 'Cellular changes indicative of scar maturation are present by 12 months and continue to approach normality for up to 30 months, but to date, no study has documented an end to scar remodeling and a return of the ligament to ‘normal.'' (Loitz and Frank, 1993)
The only reasonable conclusion that can be drawn from the existing research and literature is that acute soft tissue injuries never heal completely. Normal ligament and tendon is replaced by an inferior type of tissue.
Tissue Response to Injury
THE INFLAMMATORY REPSONSE
Phase 1; Acute phase
- Loss of function
- Cellular death continues after initial injury because of the following;
o Lack of oxygen caused by disruption of circulation
o Digestive enzymes of the engulfing phagocytes that spill over to kill normal cells
- Vascular response
o First hour; Vasoconstriction; Decrease in the diameter of a blood vessel
o Second hour; Vasodilation; Increase in the diameter of a blood vessel.
§ Exudate; Fluid with a high protein content and containing cellular debris that comes from blood vessels
and accumulates in the area of the injury
§ Permeable; Permitting the passage of a substance through a vessel wall
§ The vadodilator theory of autoregulation suggests that metabolic byproducts increase blood flow by
causing vasodilation in localized area
- Cellular response
o Mast cells; Connective tissue cells contain heparin (blood anticoagulant) and histamine
o Leukocytes; Consist of two types – granulocytes (e.g., basophils and neutrophils) and agranulocytes
(e.g., monocytes and lymphocytes)
o Phagocytosis; Process of ingesting microorganisms, other cells, or foreign particles, commonly performed
by monocytes (white blood cells)
o Macrophages engulf large quantities of bacteria
o Diapedesis is the process by which leukocytes squeeze through pores in the capillary wall
- Chemical mediators
o Histamine (Released by mast cells and platelets); Increased capillary permeability
o Serotonin (Released by mast cells and platelets)
- Complement system
o Leukocyte chemotaxis
- Bleeding and exudate
o Blood coagulation; Thromboplastin + Calcium = Prothrombin = Thrombin = Fibrinogen
= Insoluble fibrin clot (+ Vitamin K)
Phase 2; Repair Phase (Fibroplasis phase); Scar formation
- Tissue repairs;
o By resolution
o By granulation tissue
o By regeneration
- Tissue repair depends on
o Elimination of debris
o Regeneration of endothelial cells
o Production of fibroblasts
- Fibroblasts become active during regeneration phase of the inflammatory response to begin building collagen
Phase 3; Remodeling phase (up to 1 ~2 years)
- Remodeling depends on the amount and type of scar tissue present
- Synthesis; Process of forming or building up
- Lysis; Process of breaking down
- Chronic inflammation can stem from repeated acute microtraumas and overuse.
Tissue Response to injury
Acute inflammation has a short onset and a short duration. It consists of hemodynamic changes, production of an exudate, and the presence of granular leukocytes. Chronic inflammation has a long onset and a long duration. It displays a presence of nongranular leukocytes and a more extensive formation of scar tissue.
Acute inflammation: vascular and cellular events
- 5 cardinal signs of inflammation (4) originally by Roman physician Celsius in 1st Century AD; Galen, a Greek physician added functio laesa in the second century.
- serve as reminder to athlete of injury and to prevent the athlete from exceeding safe limits and reinjuring area
- redness (rubor)
- swelling (tumor)
- heat (calor)
- pain (dolor)
- loss of function (functio laesa)
Three phases: acute, reactive, or substrate inflammatory phase; the repair and regeneration phase; and the remodeling phase.
Phase I: Acute phase
The acute phase of inflammation is the initial reaction of body tissue to an irritant or injury and is characteristic of the first 3 or 4 days after injury. Acute inflammation is the fundamental reaction designed to protect, localize, and rid the body of some injurious agent in preparation for healing and repair. The main causes of inflammation are trauma, chemical agents, thermal extremes, and pathogenic organisms.
First hour. At the time of trauma, before the usual signs of inflammation appear, a transitory vasoconstriction occurs, causing decreased blood flow. At the moment of vasoconstriction, coagulation begins to seal broken blood vessels, followed by the activation of chemical influences. Vasoconstriction is replaced by dilation of venules, arterioles, and capillaries in the immediate area of the injury.
Second hour. Vasodilation brings with it a slowing of blood flow, increased blood viscosity, and stasis, which leads to swelling (edema). With dilation also comes exudation of plasma and concentration of red blood cells (hemoconcentration). Much of the plasma exudate results from fluid seepage through the intact vessel lining, which becomes more permeable, and from higher pressure within the vessel. Permeability is relatively transient in mild injuries, lasting only a few minutes, with restoration to a pre-injury state in 15 to 30 minutes. In slightly more severe situations there may be a delayed response with a late onset of permeability. In such cases, permeability may not appear for hours and then appears with some additional irritation and a display of rapid swelling lasting for an extended period.
A redistribution of leukocytes occurs within the intact vessels, caused in part by a slowing of circulation. These leukocytes move from the center of the blood flow to become concentrated and then line up and adhere to the endothelial walls. This process is known as margination, or pavementing, and occurs mainly in venules. The leukocytes pass through the wall of the blood vessel by ameboid action, known as diapedesis, and are directed to the injury site by chemotaxis (a chemical attraction to the injury). It should be noted that ameboid motion is a slow process, taking about 6 hours. With an injury there is also an increase in lymph flow because of a high interstitial tissue pressure.
In phase I of acute inflammation, mast cells and leukocytes are in abundance. Mast cells are connective tissue cells that contain heparin (a blood anticoagulant) and histamine. Basophils, monocytes, and neutrophils are the major leukocytes. Basophils leukocytes are believed to bring anticoagulant substances to tissues that are inflamed and are present during both acute and chronic inflammatory healing phases. The neutrophils representing about 60% to 70% of the leukocytes arrive at the injury site before the larger monocytes. They immigrate from the bloodstream. Neutrophils emigrate from the bloodstream through diapedesis and phagocytosis to ingest smaller debris than do monocytes. Phagocytosis is the process of ingesting material such as bacteria, dead cells, and other debris associated with disease, infection, or injury. Opsonin is a protein substance in the blood serum that coats microorganisms and other cells, making them more amenable to phagocytosis. The phagocyte commonly accomplishes this process by projecting cytoplasmic pseudopods, which engulf the object and ingest the particle through enzymes. When the neutrophils disintegrates, it gives off enzymes called lysozomes, which digest engulfed material. These enzymes act as irritants and continue the inflammatory process. Neutrophils also have chemotactic properties, attracting other leukocytes to the injured area. The monocyte, which is a nongranular leukocyte, arrives on the scene into large macrophages that have the ability to ingest large particles of bacteria or cellular debris.
Chemical mediators for the inflammatory process are stored and given off by various cells. Histamine, the first chemical to appear in inflammation, is given off by blood platelets, basophils leukocytes, and mast cells. It is a major producer of arterial dilation, venule, and capillary permeability. Serotonin is a powerful vasoconstrictor found in platelets and mast cells. With an increase in blood there is an increase in local metabolism. Permeability is produced by the contraction of the endothelial cells of the capillary wall, producing a gap between cells. Gaps allow plasma to leak proteins, platelets, and leukocytes. Plasma proteases, with their ability to produce polypeptides, act as chemical mediators. A major plasma protease in inflammation is bradykinin, which increases permeability and causes pain.
Heparin is also given off by mast cells and basophils and temporarily prevents blood coagulation. In addition, in the early stages of acute injury, prostaglandins and leukotrienes are produced. Both of these substances stem from arachidoic acid; however, prostaglandins are produced in almost all body tissues. They are stored in the cell membranes phospholipids. Leukotrienes alter capillary permeability and, it is believed, play a significant role, along with prostaglandin, in all aspects of the inflammatory process. Prostaglandins apparently encourage, as well as inhibit, inflammation depending on the conditions that are prevalent at the time.
Inflammation response Mediators
vasoconstriction serotonin from platelets and mast cells
vasodilation histamine from platelets, basophils, and mast cells
prostaglandin from arachidonic acid
leukotrienes from arachidonic acid
bradykinin from body fluids
margination and pavementing loss of micro-circulation, increase in blood viscosity
emigration of leukocytes leukocytes pass through capillary walls (diapedesis)
chemotaxis leukocytes attract other leukocytes
phagocytosis leukocytes, debris, complement, opsonization
Bleeding and exudate
The extent of fluid in the injured area is highly dependent on the extent of damaged vessels and the permeability of the intact vessel. Blood coagulates in three stages. In the initial stage thromboplastin is formed. In the second stage prothrombin is converted into thrombin under the influence of thromboplastin with calcium. In the third stage, thrombin changes from soluble fibrinogen into soluble fibrin. The plasma exudate then coagulates into a network of fibrin and localizes the injured area.
Phase II: Repair phase
The term repair is synonymous with healing, whereas regeneration refers to restoration of destroyed or lost tissue. Healing, which extends from the inflammatory phase (48 to 72 hours to approximately 6 weeks), occurs when the area has become clean through the removal of cellular debris, erythrocytes, and the fibrin clot. Tissue repair is accomplished through three processes: by resolution, in which there is little tissue damage and normal restoration; by the formation of granulation tissue, occurring if resolution is delayed, and by regeneration the replacement of tissue by the same tissue. The formation of scar tissue after trauma is a common occurrence; however, because scar tissue is less viable than normal tissue, the less scarring the better. When mature, scar tissue represents tissue that is firm, fibrous, inelastic, and devoid of capillary circulation. The type of scar tissue known as adhesion can complicate the recovery of joint or organ disabilities. Healing by scar tissue begins with an exudate, a fluid with a large content of protein and cellular debris that collects in the area of the injury site. From the exudate, a highly vascular mass develops known as granulation tissue. Infiltrating this mass is a proliferation of immature connective tissue (fibroblasts) and endothelial cells. Gradually the collagen protein substance, stemming from fibroblasts, forms a dense, fibrous scar. Collagenous fibers have the capacity to contract approximately 3 to 14 weeks after an injury and even as long as 6 months afterward in more severe cases.
During this stage, two types of healing occur. Primary healing, healing by first intention, takes place in an injury that has even and closely opposed edges, such as a cut or incision. With this type of injury, if the edges are held in very close approximation, a minimum of granulation tissue is produced. Secondary healing, healing by secondary intention, results when there is a gaping lesion and large tissue loss leading to replacement by scar tissue. External wounds such as lacerations and internal musculoskeletal injuries commonly heal by secondary intention.
Phase III: Remodeling Phase
Remodeling of the traumatized area overlaps that of repair and regeneration. Normally in acute injuries the first 3 to 6 weeks are characterized by increased production of scar tissue and increased strength fibers. Strength of scar tissue continues to increase from 3 months to 2 years after injury. Ligamentous tissue takes as long a 1 year to become completely remodeled. To avoid a rigid, non-yielding scar, there must be a physiological balance between synthesis and lysis. There is simultaneous synthesis of collagen by fibroblasts and lysis by collagenase enzymes. The tensile strength of collagen apparently is specific to the mechanical forces imposed during the remodeling phase. Forces applied to the ligament during rehabilitative exercise will develop strength specifically in the direction that force is applied. If too early or excessive strain is placed on the injury, the healing process is extended. For proper healing of muscles and tendons, there must be careful consideration to mobilize the site. Early mobilization can assist in producing a more viable injury site; on the other hand, too long a period of immobilization can delay healing. The ideal of collagen remodeling is to have the healed area contain a preponderance of mature collagenous fibers that have a number of cross-linkages. As stated, collagen content and quality may be deficient for months after injury.
If acute inflammation reaction fails to be resolves in 1 month, it is termed a sub-acute inflammation. If it lasts for months or even years, the condition is termed chronic. Major chemicals found during chronic inflammation are the kinins (especially bradykinin), which also cause vasodilation, increased permeability, and pain. Prostaglandin, also seen in chronic conditions, causes vasodilation. Prostaglandin can be inhibited by aspirin.
Soft tissue healing
All tissues of the body can be defined as soft tissue except for bone. The human body has four types of soft tissue: epithelial tissue, which consists of the skin and the lining of vessels and many organs; connective tissue, which consists of tendons, ligaments, cartilage, fat, blood vessels, and bone; muscle, which can be skeletal, cardia, or visceral and nervous tissue, which consists of the brain, spinal cord, and nerves.
Articular cartilage has limited capacity to heal. Cartilage has little or no direct blood supply. When chondrocytes are destroyed and the matrix is disrupted, healing is variable. Articular cartilage that fails to clot and as no perichondrium heals and repairs slowly. On the other hand, if the affected area includes the subchondral bone, which has a greater blood supply, granulation tissue is formed and the healing process proceeds normally.
Ligament healing follows the same course of healing as other vascular tissue. If proper immediate and follow-up management is done, a sprained ligament will undergo the acute, repair, and remodeling phases in approximately the same time period as other vascular tissues.
During the repair phase, collagen fibers realign in reaction to joint stress and strains. Full ligament healing with scar maturation may take as long as twelve months.
Skeletal muscle healing
Skeletal muscles cannot undergo the mitotic activity required to replace cells that have been injured. In other words, regeneration of new myofibers is minimal. Skeletal muscle healing and repair follow the same process as other soft tissue developing tensile strength according the Wolffs law.
Wolffs law states that after injury both bone and soft tissue will respond to the physical demands placed on them, causing them to remodel or realign along lines of tensile force. Therefore it is critical that injured structures be exposed to progressively increasing loads throughout the rehabilitation process.
Because of the nature of nerve cells, they cannot regenerate after they have died. Regeneration can take place within a nerve fiber. The closer the injury is to the nerve cell, the more difficult regeneration becomes.
For nerve regeneration to occur, an optimal environment must be present. If peripheral nerve regeneration occurs, it is at a rate of only 3 to 4 mm per day. Injured nerves within the central nervous system do not regenerate as well as peripheral nerves do.
Modifying Soft-Tissue healing
The healing process is unique in each athlete. Age and general nutrition can play a role in healing. The older athlete may be more delayed in healing than younger athletes are. The injuries of an athlete with poor nutritional status may heal more slowly than normal. Athletes with certain organic disorders may heal slowly. For example, blood conditions such as anemia and diabetes often inhibit the healing process.
1. Drugs to treat the inflammation. There is a current trend toward the use of antiprostaglandin medications, or nonsteroidal anti-inflammatory drugs (NSAIDs). The intent of this practice is to decrease vasodilation and capillary permeability.
2. Therapeutic modalities. Both cold and heat are used for different conditions. In general, heat stimulates acute inflammation and cold acts as an inhibitor. Conversely, in chronic conditions, heat may severe as a depressant. A number of electrical modalities are used for the treatment of inflammation stemming from sports injuries.
3. Therapeutic exercise. A major aim of soft-tissue rehabilitation through exercise is pain-free movement, full-strength power, and full extensibility of associated muscles. The ligamentous tissue, if related to the injury, should become pain free and have full tensile strength and full range of motion. The dynamic joint stabilizers should regain full strength and power. Immobilization of a part after injury or surgery is not always good for all injuries. When a part is immobilized over an extended period of time, adverse biochemical changes occur in collagenous tissue. Early mobilization used in exercise rehabilitation that is highly controlled may enhance the healing process.
The osteoblast is the cellular component of bone and forms its matrix; the osteocyte both forms and destroys bone, and osteoclasts destroy and resorb bone. The constant ongoing remodeling of bone is caused by osteocytes; osteoclasts are related mainly to pathological responses. Osteoclasts come from the cambium layer of the periosteum, which is the fibrous covering of the bone, and are involved in bone healing. The inner cambium layer, in contrast to the highly vascular and dense external layer, is more cellular and less vascular. It serves as a foundation for blood vessels and provides a place for attaching muscles, tendons, and ligaments.
Acute fracture healing
Acute fracture healing follows the same three phases that soft tissue does but is more complex. In general acute fracture healing has five stages: hematoma formation, cellular proliferation, callus formation, ossification, and remodeling.
Acute inflammation usually lasts approximately four days. When a bone fractures, there is trauma to the periosteum and surrounding soft tissue. With hemorrhaging, a hematoma accumulates in the medullary canal and surrounding soft tissue in the first 48 to 72 hours. The exposed ends of vascular channels become occluded with clotted blood accompanied by dying of the osteocytes, disrupting the intact blood supply. The dead bone and related soft tissue begin to elicit a typical inflammatory reaction, including vasodilation, plasma exudates, and inflammatory cells.
The hematoma in a bony fracture, like in a soft-tissue injury, begins its organization in granulation tissue and gradually builds a fibrous junction between the fractured ends. At this time the environment is acid, but it will slowly change to neutral or slightly alkaline. A major influx of capillary buds that carry endosteal cells from the bones cambium layer occurs. These cells first produce a fibrous callus, then cartilage, and finally a woven bone. When there is an environment of high oxygen tension, fibrous tissue predominates, whereas when oxygen tension is low, cartilage develops. Bone will develop at the fracture site when oxygen tension and compression are in the proper amounts.
The soft callus, in general, is an unorganized network of woven bone formed at the ends of the broken bone that is later absorbed and replaced by bone. At the soft-callus stage, both internal and external calluses are produced that bring an influx of osteoblasts that begin to immobilize the fracture site. The internal and external calluses are formed by bone fragments that grow to bridge the fracture gap. The internal callus grows rapidly to create a rigid immobilization. Beginning in the three to four weeks, and lasting three to four months, the hard callus forms. Hard callus is depicted by a gradual connecting of bone filament to the woven bone at the fractured ends. Less than satisfactory immobilization produces a cartilaginous rather than bony union.
With adequate immobilization and compression, the bone ends become crossed with a new haversian system that will eventually lead to the laying down of primary bone. The ossification stage is the completion of the laying down bone. The fracture has been bridged and firmly united. Excess has been resorbed by osteoclasts.
Remodeling occurs after the callus has been resorbed and trabecular bone is laid down along the lines of stress. Complete remodeling may take many years. The influence of biochemical stimulation (piezoelectric effect) is the basis for development of new trabecular bone to be laid down at a point of greatest stress. This influence is predicted on the fact that bone is electropositive on its convex side and electronegative on its concave side. The convex considered the tension side, whereas the concave is the compression side. Significantly, osteoclasts are drawn to a positive electrical charge and osteoblasts to a negative electrical charge. Remodeling is considered complete when a fractured bone has been restored to its former shape or has developed a shape that can withstand imposed stresses.
Management of Acute Fractures
1. If there is poor blood supply to the fractured area and one of the parts of the broken bone is not properly supplied by the blood, that part will die and union or healing of the fracture will not take place. This condition is known as avascular necrosis and often occurs in the head of the femur, the navicular of the wrist, the talus of the ankle, and isolated bone fragments.
2. Poor immobilization of the fracture site, resulting from poor casting by the physician and permitting motion between the bone parts, may not only prevent proper union but may also, in the event that union does transpire, cause deformity to develop.
3. Infection can materially interfere with the normal healing process, particularly in the case of a compound fracture, which offers an ideal situation for development of a severe streptococcal or staphylococcal infection.
Pain receptors, known as nociceptors, or free nerve endings, are sensitive to extreme mechanical, thermal, and chemical energy. They are commonly found in meninges, periosteum, skin, teeth, and some organs.
A nociceptive neuron transmits pain information to the spinal cord via the unmyelinated C fibers and the myelinated A-delta fibers. The smaller C fibers carry the impulses at a rate of 0.5 to 2.0 m per second and larger A-delta fibers at a rate of 5 to 30 m per second. When a nociceptor is stimulated there is release of a neuropeptide (substance P) that initiates an electrical impulse along the afferent fiber toward the spinal cord. The faster A-delta afferent fiber impulse moves up the spinal cord at a moderately rapid speed to the thalamus, which gives a precise location of the acute pain, which is perceived as being bright, sharp, or stabbing. In contrast the slower-conducting smaller unmyelinated C fibers are concerned with pain that is diffused, dull, aching, and unpleasant. It also terminates in the thalamus, with projections to the limbic cortex that provide an emotional aspect to this pain. Nociceptive stimuli are at close to an intensity that produces tissue damage.
The nervous system is powered electromechanically. Chemicals released by a presynaptic cell cross a synapse, stimulating or inhibiting a postsynaptic cell. This is called a neurotransmitter. Two types of chemical neurotransmitters that mediate pain are the endorphins and serotonin. They are generated by noxious stimuli, which activate inhibition of pain transmission.
Stimulation of the periaqueductal gray area (PGA) of the midbrain and the raphe nucleus in the pons and medulla causes analgesia. Analgesia is produced by the stimulation of opiods, morphine-like substances manufactured in the PGA and many other areas of the central nervous system. These endogenous opoid peptides are known as endorphins and enkephalins.
Noradrenergic neurons stimulating norepinephrine can also inhibit pain transmission. Serotonin has also been identified as a neuromodulator.
1. Fast or slow fast pain is localized and carried through A-delta axons located in the skin. Slow pain is perceived as aching, throbbing, or burning. It is conducted through the C-fibers.
2. Acute or chronic acute pain is less than 6 months. Chronic pain has a duration longer than 6 months.
3. Projected (referred) pain. Such pain occurring away from actual sire of irritation. Example Kehrs sign indicates an involved spleen.
Common to musculoskeletal injuries is the cyclic condition of pain-spasm-hypoxia-pain. Disrupting this cycle can occur trough a variety of means such as heat or cold, electrical stimulation-induced analgesia, or selected pharmacological approaches.
The gate theory and TENS
The gate theory, as developed by Melzack and Wall, sets forth the idea that the spinal cord is organized in such a way that pain or other sensations may be experienced. An area located in the dorsal horn causes inhibition of the pain impulses ascending to the cortex for perception. The area, or gate, within the dorsal horn is composed of T cells and substantia gelatinosa. T cells apparently are neurons that organize stimulus input and transmit the stimulus to the brain. The substantia gelatinosa functions as a gate-control system. It determines the stimulus input sent to the T cells from peripheral nerves. If the stimulus from a noxious material exceeds a certain threshold, pain is experienced. Apparently the smaller and slower nerve fibers carry pain impulses, and larger and faster nerve fibers carry other sensations. Impulses from the faster fibers arriving at the gate first inhibit pain impulses. In other words, stimulation of large, rapidly conducting fibers can selectively close the gate against the smaller pain fiber input. This concept explains why acupuncture, acupressure, cold, heat, and chemical skin irritation can provide some relief against pain. It also provides a rationale for the current success of TENS.