Reey8t.b. Osteomyelitis

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    Chronic Osteomyelitis

    Factors responsible for chronicity Local factors: Cavity, Sequestrum, Sinus,

    Foreign body, Degree of bone necrosis General:Nutritional status of the involved

    tissues, vascular disease, DM, low immunity

    Organism:Virulence Treatment:Appropriateness and compliance

    Risk factors:Penetrating trauma, prosthesis,

    Animal bite

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    Chronic Osteomyelitis

    Types

    A complication of acute Osteomyelitis

    Post traumatic

    Post operative

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    Chronic Osteomyelitis

    Clinical picture

    Continuous or intermittent suppuration and

    sinus formation with acute exacerbations.

    Pain, fever, redness, and tenderness

    during acute exacerbations.

    Discharging sinus with +ve/-ve culture.

    Pathological fracture.

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    Chronic Osteomyelitis

    Investigation

    Lab tests/ culture

    Plain X-ray:

    Bone rarefaction surrounded by the densesclerosis, sequestration and cavity formation

    Sinogram

    Bone scan & gallium scan

    To detect chronic multifocal osteomyelitis

    CT Scan & MRI

    Biopsy

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    Chronic Osteomyelitis

    Complications

    Recurrence & Recurrence& Recurrence

    Pathological fractures

    Growth disturbance

    Amyloid disease Epidermoid carcinoma of the fistula

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    CHRONIC OSTEOMYELITIS Sequel of acute/open fracture/opt.

    C/F: pain, discharging sinus, scars

    Xray- bone resorption, sequestra,

    CT/MRI: extent of bone loss, oedema,hidden abscess

    Lab-raised ESR pus-cs

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    TREATMENTAntibiotics.

    Local treatment.

    Operations.

    After care.

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    TUBERCULOSIS A surgeon could

    gain experience in

    the management ofTB. Of bone and

    joint only if hechoose to work in

    econmically lessdeveloped countries.(edit, Br.Med.J>1968)

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    T.B. OSTEOMYELITIS 1/3 population infected.

    Over 80,000 people in Nepal have TB.

    22,000 develop Pul. TB every year.

    Total 50,000.

    10,000 die of TB. LEADING CAUSE OF DEATH.

    1 3% skeletal TB

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    TB Cause by Mycobacterium tuberculosis,

    occasionally by M.bovis/africanum.

    Also known as tubercle bacilli as theyproduce lesion tubercles.

    Acid fast bacilli.

    Transmission

    airborne droplets. Risk- extent of exposure to droplets and

    susceptibility to infection.

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    TB Primary infection

    Exposure to tubercle bacilli

    Lungs

    multiplication of bacilli in terminalalveoli (Ghon focus) lymphatic drain itto hilar lymph nodes (PRIMARYCOMPLEX) BLOOD SPREAD.

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    TB C/F:Cough >3wks.,sputum production,

    weight loss, monoarticular.

    Respiratory

    haemoptysis, chest pain,breathlesness.

    Constitutional:fever/night sweat ,

    tiredness , loss of appetite. Physical sign: non specific,muscle

    wasting, loss of ROM

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    TB 3 days sputum.

    Ziehl-Neelsen stain.

    X-ray: cavitation, infilteration,lymphadenopathy.

    Full blood count:Relative lymphocytosis,^ESR,Anemia.

    Serology. Lymphnode biopsy.

    CT/ MRI

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    BONE TUBERCULOSIS Spread from primary complex to any

    bone/joints.

    Can effect any bone but the weightbearing bones are more likely to beaffected.

    Spine

    commonest, hip, knee , foot.

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    STAGES OF ARTICULAR TB 1 SYNOVITIS. 2 EARLY ARTHRITIS.

    3 ADVANCED ARTHRITIS.

    4 ADV.ART. PATHOLOGICAL DISLOCATION /SUBLUXATION.

    5 AFTER MATH TERMINAL OF GROSS ARTHRITIS.

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    STAGES C/F XRAY PROGNOSIS

    1 synovitis ROM>75% SOFT TISSUE SWELLING,OSTEOPOROSIS

    NEAR NORMAL

    2 earlyarthritis

    ROM50-75% JT.SPACE DIMINITION ANDMARGINAL EROSION

    RESTORATIONUPTO 75%

    3 Adv.arthritis

    ROM >75%ALL

    DIRECTION

    DESTRUCTION OF JT.SURFACE

    ANKYLOSIS

    4Adv. Arthpath/disln

    DO DISORGANISE JT.DIS/SUB.LOCATION

    ANKYLOSIS

    5

    Aftermath

    GROSS

    DEFORMITY

    DEFORMED JT. , OA ANKYLOSIS

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    TB - TYPES Caseous exudative-

    more destruction,

    exudation & abscessformation.Symptoms moremarked.

    Onset is lessinsidious.

    Granular type lessdestructive. Abscess

    formation rare. Drylesion.adults

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    TUBERCULOSIS

    Spine is the mostcommon site of skeletal

    TB

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    TUBERCULOSIS

    Pathology Blood borne - settles

    in vertebral body

    anteriorly usually more bone

    destruction, moresequestra, larger

    abscess, gaseouspus than pyogenicOM

    intervertebral discspreserved until late

    disease

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    TB SPINE -Classification 1- pre-destructive

    2- early destructive.

    3- mild angular kyphos.

    4- moderate angular kyphos.

    5- severe kyphos (humpback)

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    STAGES

    1 & 2 Predestructive

    straightening of

    curvatures , spasmof perivertebralmuscles, MRI-marrow oedema.

    Early destructive Diminished disk

    space and paradiscalerosion.MRI-marrowoedema and breakof osseous

    margin.CT-marginalerosion /cavitaion

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    STAGE 3,4&5 Body

    destruction with Kyphos

    Mild 2-3 vertebra Kyphosis

    10-30*

    moderate >3 body 30-60*

    severe >3 body >60*

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    TB SPINE

    D/DAGE- anomalies.

    Infection.

    Tumour.

    Traumma.

    Osteoporosis ,Osteochondrosis. Spondylolisthesis.

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    TB SPINE C/F:Back pain of variable duration, fever and

    weight loss.

    O/E: local tenderness, spasm, mild kyphosis-late Gibbus, cold abscess and paraparesis.

    DIAGNOSIS: XRAY-erosion of the anterioredges of the superior and inferior boarders of

    adjacent vertebral bodies with narrowing ofdisc space.

    USG :paravertebral abscess.

    Biopsy/ CT scan

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    TB HIP C/F: pain/limping, irritable hip child. Gradual

    loss of range of movement, flexion deformity,

    wasting of thigh muscles. Xray: both hip to compare.Early changes

    rarefaction of the bone and widening of thejoint space, later destruction of the joint.

    Synovial bioposy.

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    TB KNEE / ANKLE.

    C/F: pain and synovial swelling, musclewasting., contracture, draining sinuses.

    X-ray.

    Synovial biopsy.

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    PRINCIPLES OF

    MANAGEMENT OF TB General.

    Rest, mobilization & brace.

    Abscess, effusion & sinuses.

    Antitubercular drugs.

    surgery

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    TB PROBLEMS Diagnosis.

    Treatment .

    Anti tuberculous drugs.

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    Tuberculous lesion Resolve completely.

    Complete healing with varying degree of

    deformity / loss of function. Lesion may be complete walled off and the

    caseous tissue may calcified.

    Persist as a low grade ch.fibromatous

    granulating & caseating lesion. Infection may spread.

    Damage growth centre with shortening.

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    CONCLUSION Slow progressive course of clinical symptoms

    and radiological signs of tuberculosis creates

    difficulty in early diagnosis. Anti tuberculous treatment is effective but the

    functional outcome depends on earlydiagnosis before the development of

    radiological evidence of joint destruction. Always keep TB in D?Diagnosis

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    Thank you for not sleepingNow you can ask your questions

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