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Physical Medicine & Rehabilitation 6of6(2)

Physical Medicine & Rehabilitation 6of6(2)

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3/4/2010

Define the following Soft Tissue Injuries
• • • • • • • • Sprain Strain Bursitis Tendinitis Rupture Fibromyositis Fibrositis Myosistis

Physical Medicine & Rehabilitation Lecture Series 6/6

Sprain
• An injury involving the stretching or tearing of a ligament (tissue that connects bone to bone) or a joint

Sprain
• A severely damaged ligament or joint capsule can cause instability in a joint.

capsule (connective tissue secreting
synovial fluid), which help provide joint stability.

Sprain
• Symptoms may include
– Pain – Inflammation – inability to move a limb (arm, leg, foot)

Types of ligament injury
• Partial
– a. part of the ligament may be torn while the rest are undamaged – b. & c. part of the ligament attachment may have been torn away from its insertion with or without a bone fragment

• Sprains occur when a joint is forced beyond its normal range of motion, such as turning or rolling your ankle.

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Types of ligament injury
• Complete
– a. ligament is totally torn and the ends separated from each other – b. the entire ligament attachment is detached from the bone – c. the fragment of bone to which the ligament is attached has been torn away from the rest of the bone

Grading of Sprains
• Grade I – disruption of few fibers • Grade II
– Minor - disruption of less than half of fibers – Major – disruption of more than 50% of fibers

• Grade III – disruption of all the fibers

Treatment
• • • • Apply cold modalities Support the joint with elastic bandages Encourage rest and unloading Elevate the limb

Rehabilitation
• Healing ligament takes 6 weeks • Early joint mobilization is desirable • For unstable joints, bracing will be used at 3 to 6 weeks • Early protected motion exercises is implemented

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Strain
• Are injuries that involve the stretching or tearing of a musculo-tendinous (muscle and tendon) structure. • An acute (instant or recent) strain of the musculo-tendinous structure occurs at the junction where the muscle is becoming a tendon. These strains take place when a muscle is stretched and suddenly contracts, as with running or jumping.

Strain
• This type of injury is frequently seen in runners who strain their hamstrings. Many times the injury will occur suddenly while the runner is in full stride.

Strain
• Symptoms for an acute muscle strain
– Pain – muscle spasm – loss of strength – limited range of motion

Epidemiology
• 10-30% of all sport injuries • Muscles may be damaged by direct trauma (impact) or by indirect trauma (overloading) • Ruptures – can be partial or total and may be subdivided into distraction and compression ruptures • Hematomas – either inter or intramuscular types

Bursitis
• Bursa – small fluid filled sacs whose function is to distribute stress and reduce friction • Conditions which affect bursae are inflammatory (bursitis) or caused by impact with subsequent bleeding (haemobursa)

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Frictional Bursitis
• Occurs in athletes who carry out repetitive movements. • Mechanical irritation stimulates inflammation which in turn causes fluid to be secreted into the bursa with resultant swelling and tenderness

Chemical bursitis
• Caused by substances formed as a result of inflammatory or degenerative conditions of tendons • Associated with calcium deposits from the tendon draining into the bursa (calcific bursitis)

Septic bursitis
• Caused by bacteria entering a bursa from the bloodstream or from the outside environment through damaged skin

Haemobursa
• Usually caused by direct trauma • It may also be caused indirectly by tendon rupture or bleeding within a joint

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Treatment
• The treatment of trochanteric bursitis usually begins with simple measures and moves to more serious treatments if simple measures fail. • The vast majority of patients with trochanteric bursitis will never require surgery.

Treatment
• • • • Conservative Injection Surgery Rehabilitation

Tendinitis
• Inflammation of the tendon and its sheath (peritendinitis, tenovaginitis) • An inflammatory reaction in a tendon and its sheath may be initiated by repetitive one-sided movements or by chronic mechanical irritation

Symptoms
• Tendinitis produces the following symptoms near a joint that is aggravated by movement:
– Pain – Tenderness – Stiffness – – – – –

Symptoms
• Tendinitis in various locations in your body produces these specific types of pain:
Tennis elbow Achilles tendinitis Adductor tendinitis Patellar tendinitis Biceps tendinitis

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Symptoms
• If the sheath of tissue that surrounds the tendon becomes scarred and narrowed, it may cause the tendon to lock in one position, such as in the condition called trigger finger. • The pain of tendinitis is usually worse with activities that use the muscle that is attached to the involved tendon.

Treatment
• The goals of tendinitis treatment are to relieve your pain and reduce inflammation. • Often, simple home treatment — which includes rest, ice and over-thecounter pain relievers — is all that you need.

Treatment
– Injected steroids. – Strengthening exercises. People with tendinitis and tendonosis may also benefit from a program of specific exercise designed to strengthen the force-absorbing capability of the muscle-tendon unit.

Treatment
– Surgery. When a tendon is torn, you may need a reconstructive operation to clean inflamed tissue out of the tendon sheath or to relieve pressure on the tendon by removing bone

Fibromyositis
• Fibromyalgia is a chronic disorder characterized by pain throughout much of the body. The pain may begin gradually or have a sudden onset. • The exact cause of this disorder is unknown.

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· Fatigue. · Irritable bowel syndrome. · Sleep disorders. · Chronic headaches. · Jaw pain. · Cognitive or memory impairment. · Muscle pain morning stiffness. · Painful menstruation. · Numbness and tingling in the extremities. · Dizziness or light headedness. · Skin and chemical sensitivities.

Symptoms
• • • • Muscle spasms Fatigue Muscle tissue stiffness Non- restorative (unrefreshing) sleep.

Symptoms
• Pain: The most prominent symptom of fibromyalgia is pain. Unlike arthritis, the discomfort is not in the joints but in the muscles and ligaments. The tenderness is worse in the mornings and has been described as flulike, burning, throbbing, aching, or stabbing. • Fatigue: Another frequent complaint associated with fibromyalgia is fatigue. The severity of the fatigue can range from mild to incapacitating. No amount of sleep at night or rest during the day is helpful.

Symptoms
• Fibrofog: Another common symptom is a mental haziness some people call fibrofog. This refers to the inability to concentrate, memory loss, and depression that occurs with fibromyalgia. • Other symptoms associated with fibromyalgia are headaches, nervousness, numbness, dizziness, and intestinal disturbances.

Diagnosis
• According to the American College of Rheumatology, before the diagnosis of fibromyalgia can be made, the muscle pain must be present for longer than 3 months. • Pain must occur at specific sites on the body called tender points. There are 18 of these sensitive spots. Most are located on the neck and back.

Treatment
• Although there is no cure for fibromyalgia, home treatment can relieve some of the symptoms. • The most important therapy for muscle pain is regular, low-impact exercise. Keeping muscles conditioned and healthy by exercising 3 times a week decreases the amount of discomfort.

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Treatment
• Heat applied to sore muscles • Stretching exercises • Massage

Myosistis
• A rare disease in which the immune system chronically inflames the body’s own healthy muscle tissue. No one knows what triggers the immune system’s attack. • Persistent inflammation progressively weakens the muscles. • Myositis can take several forms, usually develops slowly over time and can range in severity from mild to debilitating or worse.

Symptoms
• Weakness and pain in the muscles of the hips and shoulders is often a first sign of myositis. • Myositis can affect the muscles in the front of the neck and throat, making it hard to speak or swallow (dysphagia). • When it affects the lungs or chest muscles, you may have trouble breathing.

Diagnosis
• Physical exam will probably include one or more blood tests to look for autoantibodies and muscle enzymes such as creatine kinase (CK). • Other specialized tests such as an electromyogram (EMG), which measures the electrical pattern of the muscles.

Forms of myositis
• • • • Polymyositis (PM) Dermatomyositis (DM) Inclusion Body Myositis (IBM) Juvenile Myositis (JM)

Polymyositis (PM)
• PM inflames and weakens muscles in many parts of the body, especially those closest to the trunk (proximal). Dysphagia is common, as is fatigue and pain in the joints and muscles.

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Dermatomyositis (DM)
• DM inflammation damages both muscle fibers and skin. Like PM, you develop muscle weakness, pain and fatigue. In addition, you have a distinctive patchy, reddish rash on the eyelids, cheeks, bridge of the nose, back or upper chest, elbows, knees and knuckles. In some cases, you may develop hardened bumps under the skin.

Inclusion Body Myositis (IBM)
• Symptoms of IBM typically begin after age 50 with very gradual weakening of muscles throughout the body. You may develop dysphagia, weak wrists or fingers and atrophy of the forearms and/or thigh muscles. Unlike other forms of myositis, IBM occurs more often in men than in women and, unfortunately, there are no effective treatments known for IBM.

Juvenile Myositis (JM)
• Although some children develop juvenile forms of PM and IBM, children usually get juvenile DM with symptoms of muscle weakness, skin rash and dysphagia.

Treatment
• Medications: Corticosteroids (i.e., prednisone) and other drugs that suppress the immune system (immunosuppresants) may slow down the attack on healthy tissue and improve skin rash. • Exercise: After drug treatment takes effect, a program of regular stretching exercises prescribed by your doctor can help maintain range of motion in weakened arms and legs. Physical therapy may also help prevent permanent muscle shortening. • Rest: Getting enough rest is an important component of managing myositis.

Wound Healing
• The past decade has seen an explosive growth of wound healing research that promises to facilitate clinical wound repair.

TISSUE INJURY AND TYPES OF HEALING
• Primary intention • Secondary intention • Third intention

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Primary intention
• Primary or first intention healing occurs in closed wounds in which the edges are approximated, such as a clean skin incision closed with sutures. The incisional defect reepithelializes rapidly, and matrix deposition seals the defect.

Secondary intention
• Healing occurs when the wound edges are not apposed, such as an open punch skin biopsy wound, a deep burn, and an infected wound left open to granulate. Granulation tissue fills the wound, and the wound contracts and reepithelializes.

Third intention
• Also called delayed primary healing • Healing occurs when an open wound is secondarily closed several days after injury. Such a wound is initially left open because of gross contamination.

Common Features of Wound Helaing
• The formation of granulation tissue to fill the wound space, and resurfacing with epithelium, serosa, mucosa, endothelium, or mesothelium. • • • • •

Repair Process
Inflammation Granulation Epithelialization Fibroplasia Contraction

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Inflammation
• Inflammation is the first stage of wound healing. • After tissue injury, vessels immediately constrict, thromboplastic tissue products are exposed, and the coagulation and complement cascades are initiated.

Inflammation
• At least three types of storage organelles
– (1) alpha granules contain growth factors such as plateletderived growth factor (PDGF), transforming growth factorbeta (TGF-b), and insulin-like growth factor-1 (IGF-1), as well as adhesive glycoproteins such as fibronectin, fibrinogen, thrombospondin, and von Willebrand's factor; – (2) dense bodies store vasoactive amines such as serotonin, which increase microvascular permeability; and – (3) lysosomes contain hydrolases and proteases.

Inflammation
• Monocytes infiltrate later at the wound site and differentiate into macrophages that are crucial in the orchestration of tissue repair. • Most wound macrophages are converted monocytes that are recruited from the circulation, but some are tissue macrophages that can proliferate locally. • Macrophages continue to consume tissue and bacterial debris but, more important, secrete a plethora of growth factors

Granulation
• Granulation tissue is characterized by its beefy-red appearance, a consequence of endothelial cell division and migration to form a rich bed of new capillary networks (angiogenesis) at the wound site. • Granulation is most prominent in wounds healing by second intention.

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Granulation
• The initial provisional wound matrix is composed of fibrin, fibronectin, and the glycosaminoglycan (GAG) hyaluronic acid.

Epithelialization
• Within minutes after injury, morphologic changes in keratinocytes at the wound margin are evident. In skin wounds, the epidermis thickens, and marginal basal cells enlarge and migrate over the wound defect. • Keratinocytes lay down laminin and Type IV collagen as part of their basement membrane.

Epithelialization
• Cell adhesion glycoproteins such as fibronectin, vitronectin, and tenascin provide a railroad track to facilitate epithelial cell migration over the wound matrix. • Subsequent epithelial thickening and keratinization produce fibrotic reactions, cysts, and/or sterile abscesses centered on the suture.

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Fibroplasia
• Scar is defined morphologically as the lack of tissue organization compared with surrounding normal tissue architecture. • The initially dense capillary network and fibroblast infiltrate regress until relatively few capillaries and fibroblasts remain. • Wounds become stronger with time. • The tensile strength of a skin wound increases rapidly from 1 to 6 weeks after wounding

Fibroplasia
• Tensile strength increases at a slower pace and has been documented to increase up to 1 year after wounding in animal studies. • The overall tensile strength of various wounded tissue varies (by 3 weeks % to normal healing)
– – – – skin obtains 30% fascia about 20%, intestine 65%, urinary bladder 95%.

• At best, the tensile strength of wounded skin reaches only about 80% that of unwounded skin.

Contraction
• The destruction of soft tissue and its eventual repair involve the migration of a number of different cell types into the wound site, forming a new connective tissue matrix. • The myofibroblast is a mesenchymal cell with functional and structural characteristics in common with fibroblasts and smooth muscle cells.

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Myofibroblast
• This specialized cell is a classic feature of contracting wounds and is also observed in abundance in fibrocontractive diseases such as fibromatoses, hepatic cirrhosis, renal and pulmonary fibrosis, Dupuytren's contracture, and neoplasia-induced desmoplastic reactions.

Contraction
• Having formed abundant collagen fibers, the fibroblasts transform either into fibrocytes or myofibroblasts, the latter has contractile properties. Consequently the collagen fibers tighten.

Scar Contracture
• Scar contracture occurring over a joint, restricting joint movement; esophageal stricture after caustic ingestion; and common bile duct stricture after injury.

Scar Contracture
• In contrast to wound contraction is scar contracture, in which the contractile process follows completed wound closure. • Scar contracture can be detrimental because established fibrotic tissue undergoes a reduction in surface area that can disrupt the mechanical function of neighboring tissue or structures.

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Scar Contracture
• A contracture scar is a permanent tightening of skin that may affect the underlying muscles and tendons that limit mobility and possible damage or degeneration of the nerves. • Contractures develop when normal elastic connective tissues are replaced with inelastic fibrous tissue. This makes the tissues resistant to stretching and prevents normal movement of the affected area.

Growth Factors
• Growth factors play a prominent role in the regulation of wound healing. • These polypeptides are released by a variety of activated cells at the wound site, and they can stimulate or inhibit cell proliferation, movement, and biosynthetic activity. • They can act as autocrine (produced by the cell to act on itself) or paracrine (produced by one cell type to act on another in the local area) factors.

Growth Factors
• Growth factors also chemoattract new cells to the wound. Myriad growth factors can be present in wounds. Many growth factors have overlapping functions, and their various biologic effects are only beginning to be understood.

EGF and KGF
• Epithelization is stimmulated by epidermal growth factor and keratinocyte growth factor • EGF is released by keratinocytes to act in an autocrine manner, whereas KGF is released by fibroblasts to act in a paracrine manner to stimulate keratinocyte division and differentiation. • EGF is the same protein as urogastrone, a peptide found in human urine that inhibits gastric acid secretion.

Many other growth factors affect wound repair
• For example, IGF-1 stimulates collagen synthesis by fibroblasts and functions synergistically with PDGF and bFGF to facilitate fibroblast proliferation. • Interferon-gamma has been shown to downregulate collagen synthesis. • The various interleukins mediate inflammatory cell functions at the wound site.

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TGF-b
• The topical application of TGF-b accelerates normal healing. • The name TGF-b is derived from the observation that normal cells exposed to TGF-b while grown in soft agar proliferate as though they had been virally transformed. • The mammalian TGF-b family consists of three known isoforms—b1, b2, and b3—that are closely related both structurally and functionally.

TGF-b
• TGF-b is released from platelets and macrophages in the wound. In addition, TGF-b is released from fibroblasts and acts in an autocrine manner to further stimulate its own synthesis and secretion. • TGF-b stimulates the deposition of collagen and other matrix components by fibroblasts, inhibits collagenase, blocks plasminogen inhibitor, enhances angiogenesis, and is chemotactic for fibroblasts, monocytes, and macrophages.

PDGF
• Is released from platelet alpha granules immediately after injury. PDGF attracts neutrophils, macrophages, and fibroblasts to the wound and serves as a powerful mitogen. • Macrophages, endothelial cells, and fibroblasts also synthesize and secrete PDGF. • PDGF stimulates fibroblasts to synthesize new extracellular matrix, predominantly noncollagenous components such as GAGs and adhesion proteins.

PDGF
• PDGF also increases the amount of fibroblastsecreted collagenase, indicating a role for this cytokine in tissue remodeling.

aFGF and bFGF
• Angiogenesis is stimulated by acidic and basic fibroblast growth factors • Angiogenesis is the formation of new blood vessels by directed endothelial cell migration and growth. This widespread process occurs in development, cancer, and wound healing.

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MATRIX FORMATION AND REMODELING
• Collagen • Proteoglycans • Adhesion Glycoproteins and Integrins

Collagen
• Collagen is the principal component of the extracellular matrix (25% of total body protein), and a scar is loosely defined as an abnormal, disorganized collection of collagen following wound repair.

Type*
I II III IV V VI

Molecular Formula
[a(I)]2a(I) [a(II)]3 [a(III)]3 [a(IV)]2a(IV) [a(V)]2a(V)

Tissue Distribution
All connective tissues except cartilage and basement membranes; accounts for 90% of body collagen Cartilage, vitreous humor, intervertebral disc Skin, blood vessel, internal organs Basement membrane Essentially all tissues

[a(VI),a(VI),a(VI)] Essentially all tissues

*Collagen Type VI is composed of three types of alpha chain, Types I and IV are composed of two types of alpha chain, and Types II and III are composed of only one type of alpha chain. Most collagens contain three alpha chains interacting in a helical structure. Only 6 types of collagen are shown, but more than 12 types have been described to date.

Collagen
• Fibroblasts exposed to hypoxia or high lactate concentrations, conditions found in the wound microenvironment, increase their rate of collagen synthesis when oxygen levels are increased. • Hypoxia causes accumulation of Lactate • increases collagen gene transcription • Increases prolyl hydroxylase activity.

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Proteoglycans
• Alterations in the synthesis of proteoglycans (PGs) and their constituent GAGs correlate with the cell proliferation, migration, and collagen synthesis that accompany adult wound healing.

Adhesion Glycoproteins and Integrins
• As cells become mobile during wound repair. • Specific interactions occur between them and the extracellular matrix that allow cells to detach and migrate. • The matrix provides the scaffolding for cell attachment and migration through various glycoprotein components

Glycoprotein Components
• • • • • • fibronectin tenascin laminin fibrinogen thrombospondin vitronectin

Integrins
• Cell-surface adhesion receptors • Integrins provide a bond among a cell's cytoskeleton, its surrounding extracellular matrix, and adjacent cells. • Cell motility direction may be determined by the relative integrin-ligand binding affinities of the various adhesion glycoproteins bound to a particular cell.

Fibronectin
• Fibronectins are prominent matrix molecules involved in wound contraction, cell migration, collagen matrix deposition, and re-epithelialization. • Fibronectin is one of the first proteins to be laid down in a wound and forms part of the preliminary matrix. • Fibronectin acts as the scaffold for cell migration and collagen deposition.

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Fibronectin
• Fibronectin is produced by fibroblasts, epithelial cells, and macrophages, and it can bind a wide variety of molecules involved in wound healing, including collagens, actin, fibrin, HA, heparin, fibronectin itself, and cell-surface receptors on fibroblasts. • Granulation tissue fibroblasts are coated with a layer of fibronectin matrix, and myofibroblasts are covered with fibronectin, which forms part of the fibronexus attachment that effects wound contraction.

CLINICAL FACTORS THAT AFFECT WOUND HEALING
• • • • Nutrition Oxygen, Anemia, and Perfusion Diabetes Mellitus and Obesity Corticosteroids, Chemotherapy, and Radiation Therapy • Infection

Nutrition
• Protein depletion impairs wound healing if recent weight loss exceeds 15% to 25% of body weight.
– Vitamin C is necessary for hydroxylation of proline and lysine residues. Without hydroxyproline, newly synthesized collagen is not transported out of cells. Without hydroxylysine, collagen fibrils are not cross-linked.

Nutrition
– Vitamin A (retinoic acid) requirements increase during injury. Severely injured patients require supplemental vitamin A to maintain normal serum levels. Vitamin A also partially reverses the impaired healing in chronically steroid-treated patients. – Vitamin B 6 (pyridoxine) deficiency impairs collagen cross-linking. Vitamin B 1 (thiamine) and vitamin B 2 (riboflavin) deficiencies cause syndromes associated with poor wound repair.

Nutrition
• Deficiencies of trace metals such as zinc and copper have been implicated in poor wound repair, since these divalent cations are cofactors in many important enzymatic reactions. • Zinc deficiency is associated with poor epithelialization and chronic, nonhealing wounds.

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Oxygen, Anemia, and Perfusion
• Oxygen is required for successful inflammation, angiogenesis, epithelialization, and matrix deposition. • Conversely, increased oxygen delivery at the wound improves healing. • Anemia in a normovolemic patient is not detrimental to wound repair as long as the hematocrit is greater than 15%, because oxygen content in blood does not affect wound collagen synthesis

Oxygen, Anemia, and Perfusion
• Tissue perfusion is the ultimate determinant of wound oxygenation and nutrition.

Diabetes Mellitus and Obesity
• Wound healing is impaired in diabetic patients by unknown mechanisms. • Healing is enhanced if glucose levels are well controlled. • Obesity interferes with repair independently of diabetes. • Obese patients with diabetes have impaired wound healing regardless of the degree of glucose control and insulin therapy.

Corticosteroids, Chemotherapy, and Radiation Therapy
• Use of pharmacologic steroids impairs healing, especially when given in the first 3 days after wounding. • Steroids reduce wound inflammation, epithelialization, and collagen synthesis. • Both radiation and chemotherapeutic agents have their greatest effects on dividing cells. The division of endothelial cells, fibroblasts, and keratinocytes is impaired in irradiated tissue, which slows wound healing

Corticosteroids, Chemotherapy, and Radiation Therapy
• Irradiated tissue usually has some degree of residual endothelial cell injury and endarteritis, which causes atrophy, fibrosis, and poor tissue repair. • Chemotherapeutic agents are not administered until at least 5 to 7 days postoperatively to prevent impairment of the initial healing events.

Infection
• Wound contamination by bacteria causes clinical wound infection and delays healing if more than 10 5 organisms per mg. tissue are present.

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FIN

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