Physical Medicine & Rehabilitation 6of6(2)

8/14/2019 Physical Medicine & Rehabilitation 6of6(2)

http://slidepdf.com/reader/full/physical-medicine-rehabilitation-6of62 1/21

3/4/20

Soft Tissue Injuries

Physical Medicine & Rehabilitation

Lecture Series 6/6

Define the following

• Sprain

• Strain

• Bursitis

• Tendinitis

• Rupture

• Fibromyositis

• Fibrositis

• Myosistis

Sprain

• An injury involving the stretching or

tearing of a ligament (tissue that

connects bone to bone) or a jointcapsule (connective tissue secreting

synovial fluid), which help provide jointstability.

Sprain

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

Sprain

• Symptoms may include

– Pain

– Inflammation

– inability to move a limb (arm, leg, foot)

• Sprains occur when a joint is forcedbeyond its normal range of motion, such

as turning or rolling your ankle.

Types of ligament injury

• Partial

– a. part of the ligament may be torn while therest are undamaged

– b. & c. part of the ligament attachment mayhave been torn away from its insertion with orwithout a bone fragment



3/4/20

Types of ligament injury

• Complete

– a. ligament is totally torn and the endsseparated from each other

– b. the entire ligament attachment is detachedfrom the bone

– c. the fragment of bone to which the ligamentis attached has been torn away from the restof 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 at3 to 6 weeks

• Early protected motion exercises isimplemented



3/4/20

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 atendon. These strains take place when a muscleis stretched and suddenly contracts, as withrunning or jumping.

Strain

• This type of injury is frequently seen inrunners who strain their hamstrings. Manytimes the injury will occur suddenly whilethe 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 besubdivided into distraction and compressionruptures

• Hematomas – either inter or intramuscular types

Bursitis

• Bursa – small fluid filled sacs whose

function is to distribute stress and reducefriction

• Conditions which affect bursae areinflammatory (bursitis) or caused byimpact with subsequent bleeding

(haemobursa)



3/4/20

Frictional Bursitis

• Occurs in athletes who carry out repetitivemovements.

• Mechanical irritation stimulates

inflammation which in turn causes fluid tobe secreted into the bursa with resultantswelling and tenderness

Chemical bursitis

• Caused by substances formed as a resultof inflammatory or degenerativeconditions of tendons

• Associated with calcium deposits from thetendon draining into the bursa (calcificbursitis)

Septic bursitis

• Caused by bacteria entering a bursa from

the bloodstream or from the outsideenvironment through damaged skin

Haemobursa

• Usually caused by direct trauma

• It may also be caused indirectly by tendonrupture or bleeding within a joint



3/4/20

Treatment

• The treatment of trochanteric bursitisusually begins with simple measures and

moves to more serious treatments if simple measures fail.

• The vast majority of patients withtrochanteric bursitis will never requiresurgery.

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 repetitiveone-sided movements or by chronicmechanical irritation

Symptoms

• Tendinitis produces the following symptoms neara joint that is aggravated by movement: – Pain

– Tenderness

– Stiffness

Symptoms

• Tendinitis in various locations in your bodyproduces these specific types of pain: – Tennis elbow

– Achilles tendinitis

– Adductor tendinitis

– Patellar tendinitis

– Biceps tendinitis



3/4/20

Symptoms

• If the sheath of tissue that surrounds the tendonbecomes scarred and narrowed, it may cause

the tendon to lock in one position, such as in thecondition called trigger finger.

• The pain of tendinitis is usually worse withactivities that use the muscle that is attached tothe involved tendon.

Treatment

• The goals of tendinitis treatment areto relieve your pain and reduceinflammation.

• Often, simple home treatment —which includes rest, ice and over-the-counter pain relievers — is all that

you need.

Treatment

– Injected steroids.

– Strengthening exercises. People with tendinitisand tendonosis may also benefit from aprogram of specific exercise designed tostrengthen the force-absorbing capability of the muscle-tendon unit.

Treatment

– Surgery. When a tendon is torn, you mayneed a reconstructive operation to cleaninflamed tissue out of the tendon sheath or torelieve 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 orhave a sudden onset.

• The exact cause of this disorder isunknown.



3/4/20

· 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 ispain. Unlike arthritis, the discomfort is not in the jointsbut in the muscles and ligaments. The tenderness isworse in the mornings and has been described as flulike,burning, throbbing, aching, or stabbing.

• Fatigue: Another frequent complaint associated withfibromyalgia is fatigue. The severity of the fatigue canrange from mild to incapacitating. No amount of sleep atnight or rest during the day is helpful.

Symptoms

• Fibrofog: Another common symptom is a mentalhaziness some people call fibrofog. This refers to theinability to concentrate, memory loss, and depressionthat occurs with fibromyalgia.

• Other symptoms associated with fibromyalgia areheadaches, nervousness, numbness, dizziness, andintestinal disturbances.

Diagnosis

• According to the American College of Rheumatology, before the diagnosis of fibromyalgia can be made, the muscle pain mustbe present for longer than 3 months.

• Pain must occur at specific sites on the bodycalled tender points. There are 18 of thesesensitive spots. Most are located on the neck and back.

Treatment

• Although there is no cure for fibromyalgia, hometreatment can relieve some of the symptoms.

• The most important therapy for muscle pain isregular, low-impact exercise. Keeping musclesconditioned and healthy by exercising 3 times aweek decreases the amount of discomfort.



3/4/20

Treatment

• Heat applied to sore muscles

• Stretching exercises

• Massage

Myosistis

• A rare disease in which the immune systemchronically inflames the body’s own healthy

muscle tissue. No one knows what triggers theimmune system’s attack.

• Persistent inflammation progressively weakensthe muscles.

• Myositis can take several forms, usually developsslowly over time and can range in severity frommild to debilitating or worse.

Symptoms

• Weakness and pain in the muscles of the hipsand 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 orswallow (dysphagia).

• When it affects the lungs or chest muscles, youmay have trouble breathing.

Diagnosis

• Physical exam will probably include one ormore blood tests to look forautoantibodies and muscle enzymes suchas creatine kinase (CK).

• Other specialized tests such as anelectromyogram (EMG), which measuresthe 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 inmany parts of the body, especially thoseclosest to the trunk (proximal). Dysphagiais common, as is fatigue and pain in the joints and muscles.



3/4/20

Dermatomyositis (DM)

• DM inflammation damages both musclefibers and skin. Like PM, you develop

muscle weakness, pain and fatigue. Inaddition, you have a distinctive patchy,reddish rash on the eyelids, cheeks, bridgeof the nose, back or upper chest, elbows,knees and knuckles. In some cases, youmay develop hardened bumps under theskin.

Inclusion Body Myositis (IBM)

• Symptoms of IBM typically begin after age 50with very gradual weakening of muscles

throughout the body. You may developdysphagia, weak wrists or fingers and atrophy of the forearms and/or thigh muscles. Unlike otherforms of myositis, IBM occurs more often in menthan in women and, unfortunately, there are noeffective treatments known for IBM.

Juvenile Myositis (JM)

• Although some children develop juvenileforms of PM and IBM, children usually get juvenile DM with symptoms of muscleweakness, skin rash and dysphagia.

Treatment

• Medications: Corticosteroids (i.e., prednisone) andother drugs that suppress the immune system(immunosuppresants) may slow down the attack onhealthy tissue and improve skin rash.

• Exercise: After drug treatment takes effect, a programof regular stretching exercises prescribed by your doctorcan help maintain range of motion in weakened armsand legs. Physical therapy may also help preventpermanent 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



3/4/20

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 re-

epithelializes 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 re-

epithelializes.

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



3/4/20

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 platelet-

derived growth factor (PDGF), transforming growth factor-beta (TGF-b), and insulin-like growth factor-1 (IGF-1), aswell as adhesive glycoproteins such as fibronectin,fibrinogen, thrombospondin, and von Willebrand's factor;

– (2) dense bodies store vasoactive amines such asserotonin, 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 theorchestration of tissue repair.

• Most wound macrophages are converted monocytesthat are recruited from the circulation, but some aretissue macrophages that can proliferate locally.

• Macrophages continue to consume tissue andbacterial debris but, more important, secrete aplethora 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.



3/4/20

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.



3/4/20

Fibroplasia

• Scar is defined morphologically as the lack of tissueorganization compared with surrounding normal

tissue architecture.• The initially dense capillary network and fibroblast

infiltrate regress until relatively few capillaries andfibroblasts remain.

• Wounds become stronger with time.

• The tensile strength of a skin wound increasesrapidly from 1 to 6 weeks after wounding

Fibroplasia

• Tensile strength increases at a slower pace and hasbeen documented to increase up to 1 year afterwounding in animal studies.

• The overall tensile strength of various woundedtissue 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 reachesonly 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.







3/4/20

TGF-b

• The topical application of TGF-b accelerates normal

healing.

• The name TGF-b is derived from the observation thatnormal 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 tofurther 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 immediatelyafter injury. PDGF attracts neutrophils, macrophages,and fibroblasts to the wound and serves as apowerful mitogen.

• Macrophages, endothelial cells, and fibroblasts alsosynthesize and secrete PDGF.

• PDGF stimulates fibroblasts to synthesize newextracellular matrix, predominantly noncollagenouscomponents such as GAGs and adhesion proteins.

PDGF

• PDGF also increases the amount of fibroblast-

secreted 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.





3/4/20

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 todetach and migrate.

• The matrix provides the scaffolding for cellattachment and migration through variousglycoprotein components

Glycoprotein Components

• fibronectin

• tenascin

• laminin

• fibrinogen

• thrombospondin

• vitronectin

Integrins

• Cell-surface adhesion receptors

• Integrins provide a bond among a cell'scytoskeleton, its surrounding extracellularmatrix, and adjacent cells.

• Cell motility direction may be determined bythe relative integrin-ligand binding affinities of the various adhesion glycoproteins bound to aparticular 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.



3/4/20

Fibronectin

• Fibronectin is produced by fibroblasts, epithelialcells, 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 onfibroblasts.

• Granulation tissue fibroblasts are coated with a layerof fibronectin matrix, and myofibroblasts are coveredwith fibronectin, which forms part of the fibronexusattachment 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 prolineand lysine residues. Without hydroxyproline,newly synthesized collagen is not transported outof cells. Without hydroxylysine, collagen fibrils arenot cross-linked.

Nutrition

– Vitamin A (retinoic acid) requirements increase

during injury. Severely injured patients requiresupplemental vitamin A to maintain normal serumlevels. Vitamin A also partially reverses theimpaired healing in chronically steroid-treatedpatients.

– Vitamin B 6 (pyridoxine) deficiency impairscollagen cross-linking. Vitamin B 1 (thiamine) andvitamin B 2 (riboflavin) deficiencies causesyndromes 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.



3/4/20

2

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 detrimentalto wound repair as long as the hematocrit is greaterthan 15%, because oxygen content in blood does notaffect 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 byunknown mechanisms.

• Healing is enhanced if glucose levels are wellcontrolled.

• Obesity interferes with repair independently of diabetes.

• Obese patients with diabetes have impaired woundhealing regardless of the degree of glucose controland insulin therapy.

Corticosteroids, Chemotherapy, and

Radiation Therapy

• Use of pharmacologic steroids impairs healing,especially when given in the first 3 days afterwounding.

• Steroids reduce wound inflammation,epithelialization, and collagen synthesis.

• Both radiation and chemotherapeutic agents havetheir greatest effects on dividing cells. The division of endothelial cells, fibroblasts, and keratinocytes isimpaired 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.



3/4/20

FIN

Documents

Physical Medicine & Rehabilitation 6of6(2)