Orthopaedic Nursing

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    Different injuries of the musculoskeletalsystem its management and care

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    ARTICULAR DISOR DERS

    y Osteoarthritisy R heumatoid arthritisy Gouty arthritis

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    Rheumatoid Arthritisy Chronic, systemic, inflammatory

    disease of the synovium/synovial membrane

    y W ith remission and exacerbationy Commonly affecting the smaller

    synovial joints

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    P athophysiology y A utoimmune response leukocytes

    infiltration of synovium stage 1: synovitis

    accumulation of inflammatory exudates joint effusion joint capsule thickens withconnective tissue stage 2: p annusformation erosion of articular cartilageand subchondral bones stage 3: fibrousankylosis stage 4: bony ankylosis

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    S igns and S ym p tomsy B ilateral/symmetrical involvement y F every Inflammatory response (pain, swelling,

    heat, redness)y E arly morning stiffness (15-30 mins)y Limited ROMy M uscle fatiguey A nemia and Leukocytosis

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    Laboratory/Diagnostic Testsy Increased A lkaline P hosphatase,

    Erythrocyte Sedimentation R ate (E SR ), c-reactive protein

    y M oderate anemia and leukocytosisy X-ray findings ( soft tissue swelling, joint

    space narrowing, cartilage erosion)y A rthrogramy A rthroscopy

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    Rheumatoid arthritis y Pannus formation

    secondary tosynovitis

    y Thickening of thejoint capsule

    y Knobby wrist andknuckels

    y Ulnar drifty Z-hand deformityy Swan neck and

    buotonniere

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    M anagementy

    S ym p tomaticy R elief of pain

    y A nalgesics, R est, Ice/Hot packs, A ssistivedevices

    y NSAI Ds or corticosteroidsy P revent deformity

    y P rovide support to joint at all times, provide

    passive or active ROM exercisesy Surgery

    y S ynovectomy, A rthrodesis, A rthroplasty, A rthrotomy, Osteotomy

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    O steoarthritisy Chronic, nonsystemic, non-

    inflammatory disease characterized by d egeneration and loss of articularcartilage in synovial joints

    y Idiopathic and slowly progresssive

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    Osteoarthritisy Chronic, nonsystemic,

    and noninflammatory

    form of arthritisy Commonly affecting weight-bearing joints of the body

    y

    Cartilage degenerationsecondary to aging,obesity or wear and tearof the joint

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    y P atho p hysiology y

    O besity, wear & tear of jt., agingdegeneration of articular cartilagethinning of the cartilage destruction of cartilage exposure of underlying bonefriction develops bone spurs/ bony overgrowth formed deformity fatigue

    immobility y S ame management as with RA (symptomatic)

    y R elief of painy P revent deformity y Surgery

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    Gouty A rthritisy S ystemic and inflammatory disorder of the

    diarthrodial joint secondary to h yperuricemiay Exessive accumulation of serum uric acidy M ay be hereditary due to abnormal purine

    metabolismy Characterized with recurring acute attacks and

    intervals of freedom from painy Causes crippling, deforming arthritis, nephritis,

    renal calculi, cardiovascular lesions

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    y Commonly affecting d istal jointsy P

    rimarily in men 40 y/o and

    abovey Stages of Gouty A symptomatic hyperuricemia

    y Elevated serumuric acid level but produce nosymptoms

    y A cute gouty arthritisy P odagray M ay subsidee quickly or last for days/weeks

    y Intercritical gouty 2nd attack may occur within 2 mos-10 yrs

    y Chronic tophaceous gouty Skin may ulcerate and release a chalky, white

    exudate or pus

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    Gouty arthritisy Common sites of

    tophus: ear lobe, wrist,and fingers

    y Skin may ulceratey Tophus

    characterized ascheesy, chalky, whiteand pasty appearance

    y Secondary tohyperuricemia

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    Gouty arthritisy Chronic

    tophaceous goutstagey Tophus/tophi

    formationy Deposits of

    monosodiumurate crystals

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    M anagementy A ntigout medications ( Colchicine, A llopurinol,

    P robenecid)y NSAI DS to control inflammationy Bed rest, affected extremity may be immobilized

    in a pillow; bed cradley Ice pack y Gradual weight reductiony A dequate hydration (3 L/day)y Diet: High CHO , alcohol restriction, low purine

    (avoid organ meats, yeasts, fish, mushrooms,poultry products, shellfish, asparagus, spinach)

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    M usculoskeletal Traumasy SP RAI Ny

    STRAI Ny F RACTUR Ey DISLOCATIO Ny CO NTUSIO N

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    SP RAI N V S. STRAI Ny A sprain is a stretching or tearing of ligaments, the tough,

    fibrous bands of tissue that connect bones to one anotherat a joint.

    y

    A strain is a stretching or tearing of muscle tissue,commonly called a pulled muscle.y A nything that places sudden or unaccustomed stress on --

    or chronic overuse of -- joints or muscles may cause asprain or strain.

    y Falls, lifting heavy objects, and the exertion of anunfamiliar sport are common culprits.

    y Being overweight, inactive, or in poor physical condition boosts the likelihood of injury. Improperly warming upand not stretching muscles before intense physicalactivity can also result in injury.

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    Ankle Sp rain* M ay be due to suddentwisting/ankleinversion* M ost common:Talofibular ligament

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    ST RAIN*

    Tendinitis/ elbow strain

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    F RACTUR Ey SALT ER -H ARRRIS CLASSI F ICATIO N

    W hen I explain bone structure to my patients, I tellthem to think of the bone like an Oreo cookie.

    You have the top cookie (metaphysis), the bottomcookie (epiphysis), and the creamy middle (growthplate). Salter Harris fractures can occur to either thetop or bottom part of the bones, or both.

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    SALT ER -H ARRIS CLASSI F ICATIO N

    y S alter Harris T y p e I Fracturesy T ype I growth plate fractures involve a fracture

    through the growth plate. Imagine taking the oreocookie and seperating the top and bottom halves.This type of fracture may not be visible on an X-ray,and usually doesn't cause any growth problems.

    y

    Treatment usually consists of immobilization for aperiod of time, 4-6 weeks.

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    y

    T y p e II Fracturesy This is the most common type of Salter Harris

    fracture. A type II fracture involves a break in the bone through the metaphysis and extending into the

    growth plate.y So, in the O reo example, imagine breaking off part of

    the top cookie.y T ype II fractures usually do not cause growth

    problems, and are treated with immobilization. I t isimportant that the fracture be aligned correctly inorder to heal properly.

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    y T y p e III Fractures

    y T ype three fractures extend through the epiphysisinto the growth plate. This type of fracture is morelikely to cause growth problems because of theinvolvement of the epiphysis and the disruption of the growth plate.

    y They may also require surgical intervention in orderto re-align the bones for optimal recovery.

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    T y p e IV Fractures

    y This Salter Harris F racture extends through both themetaphysis and the epiphysis.

    y Imagine breking your Oreo cookie in two.y Long term disability and growth problems are

    common with this type of fracture because of thedisurption of both the metaphysis and epiphysis.

    y Surgical intervention is common in order to re-alignthe bones correctly.

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    DISLOCATIO N

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    CO NGEN ITAL BONE D ISOR DERSy Congenital Hip Dislocation/ Developmental Hip

    Dysplasiay

    Clubfoot/ Talipes Equinovarusy Osteogenesis Imperfecta

    y ACQUIR ED DE F ECTy Coxa plana/ Legg-calve-perthes disease

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    Congenital Hip Dislocationy A .k.a. hip dysplasiay Displacement of

    femoral head from theacetabulum

    y M ay be secondary to breech delivery orabnormal release of maternal hormonesduring the 3 rdtrimester

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    Special testsy Ortolanis test

    y Barlows testy Telescoping

    y

    Galleaziy Trendelenburg

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    MA N A GEM EN T

    1. R eduction2. Immobilization3. R ehabilitation

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    CLU BF

    OOT

    Combinations:1. Tali p es equinovarus2. Talipes equinovalgus

    3.Talipes calcaneovalgus4.Talipes calcaneovarus

    y A genetic malformation in which the foot is twistedout of its normal position

    y Variations:y Talipes equinusy Talipes calcaneusy

    Talipes varusy Talipes valgus

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    M anagementinclude:

    Careful footmanipulation

    Serial casting

    Surgicaloperation

    Use of Dennis Brownesplint

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    Osteogenesis imperfectay Congenital

    brittle-bonediseasey M ay be

    secondary togenetic defecty Blue sclera

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    Osteogenesis Imperfectay Hyperextensibility

    of ligamentsy Secondary to

    aberration of

    p rocollagen

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    Osteogenesis Imperfecta

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    C oxa planay A lso known as Legg- Calve-

    P erthes diseasey F lattening of femoral head

    secondary to avascularnecrosis

    y Self-limiting commonamong boys

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    S igns & S ym p tomsy K nee pain (may be the only symptom, initially)y P ersistent thigh or groin painy A trophy (wasting) of muscles in the upper thighy Slight shortening of the leg, or legs of unequal

    lengthy Hip stiffness restricting movement in the hipy Difficulty walking, walking with a limp (which is

    often painless)y Limited range of motion

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    T reatmenty The aim of treatment is to protect the bone and jointfrom further stress and injury while the healingprocess takes place.

    y Bedrest or crutches may be needed during the initialphase.

    y A brace, cast, or splint to immobilize the hipsposition may be used while bone regrowth takes

    place.y Surgery may be performed to keep the hip in its

    socket.

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    Stages of

    LCPD

    y A vascularnecrosis

    y R evascularizationy R eparativey

    R egenerative

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    SP IN AL DISOR DER y Herniated Nucleus P ulposus/ R uptured

    Intervertebral disk y Scoliosisy Lordosis

    y K yphosisy P otts disease

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    Herniated nucleus

    pulposusy Slipped discy May be secondary to

    fall or improper

    back mechanicsy Displacement of the

    nucleus pulposusfrom annulusfibrosus(intervertebraldiscs)may causecompression ofspinal nerves

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    Herniated

    NucleusP ul p osus

    *L5- S1** Sciatica ( radiating

    p ain from low back tothe buttocks andp osterior thigh)aggravated by coughing valsalvamaneuver andsneezing***P ro p er back mechanics

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    Scoliosis

    y Lateral

    curvature of thespine withrotation

    y Curvature ismeasured throughCobb method

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    ClassificationI . A ccording to etiology

    y Idiopathicy

    Structuraly Nonstructural/postural

    II . Severity III . Convexity y M ild * dextroscoliosis y M oderate * levoscoliosis ( L)y Severe

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    LOR DOSIS vs. K Y P HOSISy S wayback deformity Humpback deformity y Cervical, lumbar Thoracic spiney P

    regnancy, obesity TB, compressionlarge abdominal tumor spine fx,osteoporosisy Excessive pelvic angle, >40 degrees, canP rotruded abdomen/buttocks cause pulmonary

    and G I dysfunctiony P ostural exercises

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    P athophysiology of

    metabolic bone disorders

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    P redisposing factors toM etabolic bone conditions

    y Inadequate exposure to sunlighty

    Hypothyroidism, hyperparathyroidismy Osteopenia

    y Steatorrheay Very low fat diet

    y Strict vegetarianismy Chronic renal failure

    y Liver disease

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    OST EOP OROSISy porous bonesy Characterized with greater bone resorption than

    formation; low Bone M ass Density y M odifiable risk factors Non-modifiable risk factor

    y A lcohol consumption * age, sex, race, long termy Calcium low glucocorticoid usey Corticosteroid usey Estrogen low y Smokingy Sedentary lifestyle

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    Sympt o matic

    management:H igh Calcium dietPostural exercisesPrevent complications

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    R ickets and Osteomalaciay S oftening of bones

    among children and

    adults, res p ectively y Secondary to vit. D

    deficiency y P igeon-chesty Genu varumy W eak and brittle bones

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    y Encourage highcalcium diet

    y Vit. D supplementy P revent

    complicationsy Exercisesy Use of assistive

    devices, bracesy Surgery to correct

    deformities

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    Osteitis Deformansy A .k.a. P agets diseasey Characterized with

    excessive osteoclasticactivity

    y Honeycombedappearance of bones seenon X-ray

    y Expanded skull, barrel-chest, wider hips, genu

    varum are the commondeformities

    y IM calcitonin may be indicated

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    P OTT S DIS E ASEy caused by M ycobacterium tuberculosis .y P otts caries , Davi d' s d isease , and

    extrapulmonary TB, is a medical condition of thespine.

    y A .k.a. tuberculous spondylitis (one of the oldestdemonstrated diseases of humankind, having

    been documented in spinal remains from theIron A ge and in ancient mummies from Egypt

    and P eru)y In 1779, P ercivall P ott, for whom P ott disease is

    named, presented the classic description of spinal tuberculosis

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    P athophysiology Direct / metastatic infection

    A ccumulation of tubercle bacilli in the spine

    Inflammatory response

    P us/ A bscess develops

    Liquefaction of the spine

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    Destruction of vertebral bodies

    Collapse of vertebral bones

    K yphosis/ Gibbus deformity

    Narrowing of spinal canal

    Compression of spinal nerves/ SC

    P otts paraplegia

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    Signs and symptomsy back pain, night sweats, fever, weight loss,

    and anorexiay may also develop a spinal mass, which

    results in tingling, numbness, or a generalfeeling of weakness in the leg muscles

    y K yphosis/gibbus deformity y walking in an upright and stiff position due

    to painy P araplegia in the late stage

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    P athophysiology y P ott disease is usually secondary to an extraspinal

    source of infection. The basic lesion involved in P ottdisease is a combination of osteomyelitis andarthritis that usually involves more than one

    vertebra. The anterior aspect of the vertebral body adjacent to the subchondral plate is area usually affected.

    y Tuberculosis may spread from that area to adjacentintervertebral disks. In adults, disk disease issecondary to the spread of infection from the

    vertebral body. In children, because the disk is vascularized, it can be a primary site. 3

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    y P otts disease is caused when the vertebrae becomesoft and collapse as the result of caries or osteitis.

    y T ypically, this is caused by mycobacteriumtuberculosis .

    y A s a result, a person with P ott's disease oftendevelops kyphosis , which results in a hunchback.This is often referred to as P otts curvature/gibbus

    y In some cases, a person with P ott's disease may alsodevelop paralysis, referred to as P otts paraplegia ,

    when the spinal nerves become affected by thecurvature.

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    y OT HE R SI GNS A ND S Y M P TOMSy A person with P ott's disease may experience

    additional complications as a result of thecurvature.

    y F or example, an infection can more easily spread from the paravertebral tissue, whichcan cause abscesses to occur.

    y R egardless of the complications that may occur, P ott's disease is typically slow spreadingand can last for several months or years.

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    y MA N A GEM EN Ty prevention is possible through proper control

    (the best method is reduce or eliminate thespread of tuberculosis)

    y P ott's disease may be treated through a variety of options:

    y He or she may utilize analgesics or antituberculousdrugs to get the infection under control. ( RI P ES)

    y I t may also be necessary to immobilize the area of thespine affected by the disease, or the person may needto undergo surgery in order to drain any abscesses thatmay have formed or to stabilize the spine.

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    y In addition, testing for tuberculosis is animportant preventative measure, as those

    who are positive for purifie d proteind erivative (PP D) can take medication toprevent tuberculosis from forming.

    y A tuberculin skin test is t h e most commonmet h od used to screen for tuberculosis,

    y though blood tests , bone scans, bone biopsies, and radiographs may also be usedto confirm the disease.

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    OST EOM YELITISy inflammation an d d estruction of bone cause d by

    bacteria, mycobacteria, or fungi.y Common symptoms are localize d bone pain an d

    ten d erness wit h constitutional symptoms (in acuteosteomyelitis) or wit h out constitutional symptoms(in c h ronic osteomyelitis).

    y M ost common cause is the Staphylococcus aureus;affecting primarily long bones

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    Etiology y Contiguous spread (from infected tissue or aninfected prosthetic joint)

    y Bloodborne organisms (hematogenousosteomyelitis)

    y Open wounds (from contaminated open fractures or bone surgery)

    y

    Trauma, ischemia, and foreign bodies predispose toosteomyelitis.y Osteomyelitis may form under deep decubitus ulcers.

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    P athophysiology Direct/ M etastatic infection

    A ccumulation of microorganism

    Inflammatory response

    P us/ A bscess formation

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    Cutting off of blood supply

    Lack of blood supply to the area

    Necrosis

    Septic shock

    Death

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    Signs and symptomsy acute osteomyelitis of peripheral bones:

    y weight loss, fatigue, fever, and localized warmth,swelling, erythema, and tenderness.

    y vertebral osteomyelitisy localized back pain and tenderness with paravertebral

    muscle spasm that is unresponsive to conservativetreatment. P atients are usually afebrile.

    y

    chronic osteomyelitisy intermittent (months to many years) bone pain,

    tenderness, and draining sinuses.

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    D iagnosisy ESR or C-reactive proteiny X-rays, MRI , or radioisotopic bone scanningy Culture of bone, abscess, or both

    T reatmenty A ntibiotics; meticulous wound & skin carey Surgery if abscess, constitutional symptoms,

    potential spinal instability, or much necrotic boney A ntibiotics are selected to cover both gram-positive

    and gram-negative organisms until culture resultsand sensitivities are available.

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    T hi si nt r ao

    per ati v e

    phot o

    s

    how san

    AH O

    l esi on

    w it hi n

    t he

    ti bi a.

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    AM P UTATIO Ny W hat is am p utation?y W hen performing an amputation, a surgeon

    removes a limb, or p art of a limb , that is nolonger useful to you and is causing you great pain, orthreatens your health because of extensive infection.

    y P hysicians as well as patients consider amputation alast resort .

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    CAUS ESy (P ERI P HE RAL ART ERIAL DIS E ASE) P A D is the

    leading cause of amputation in people age 50 andolder, and accounts for up to 90 percent of amputations overall.

    y traumatic injury, such as a car accident or a severe burn, can also destroy blood vessels and cause tissuedeath.

    y cancerous tumor

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    NURSI NG INTER VENTIO NSy Discuss

    y R ehab.program and use of prosthesisy Upper extremity exercise such as push up in bedy Crutch walkingy

    A mputation dressingy P hantom limb sensation as normal occurence

    y O bserve stump dressing for signs of hemorrhage andmark outside of dressing so rate of bleeding can be

    assessedy K eep torniquet readily available at bedsidey P revent edema

    y R aise extremity with pillow for first 24 hrs.

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    LEVEL S O F A M PUT A T IO N

    1. B elow K nee A mputation2 . A bove K nee A mputation3 . B elow Elbow A mputation4 . A bove Elbow A mputation

    5. Disarticulation-through the jt.

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    B MD test

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    P ersonundergoing a

    bone scan on

    the skull.

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    An example of shoulder

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    arthroscopy. Thesurgeon looks at a videoscreen which isconnected to a camerathat is inserted into thebody, together withworking instruments.

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    L eft knee aspi r ati o nusing the medial

    pa r apatella r app ro ach.

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