Osteomyelitis Kuliah

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    Agianto, S.Kep., Ns., MNS

    Adult Nursing Department

    School of Nursing UNLAM

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    Nelaton (1834): coined osteomyelitis

    The root words osteon (bone) and myelo

    (marrow) are combined with i t is

    (inflammation) to define the clinical state

    in which bone is infected with

    microorganisms.

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    Common clinical problemDefined as a progressive infection of the

    bone that results in inflammatory

    destruction of the bone, bone necrosisand new bone formation

    Classification by pathogenesis and

    chronicity

    Early diagnosis is difficult

    Delay in diagnosis leads to decreased

    cure rates and increased rates of

    complication and morbidity

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    The term acute osteomyelitis is

    used clinically to signify a

    newly recognized bone

    infection. Patients usually

    present within several days to

    one weekafter the onset of

    symptoms. In addition to local

    signs of inflammation and

    infection, patients have signs

    of systemic illness

    The relapse of a previously treated or

    untreated infection is considered a

    sign of chronic disease. Clinical signs

    persisting for more than 10 days

    correlate roughly with the development

    of necrotic bone and chronic

    osteomyelitis. The clinical pattern may

    evolve over months or even years and

    is characterized by lowgrade

    inflammation; the presence of pus,

    microorganisms,and sequestra ; a

    compromised soft-tissue envelope;and

    sometimes a fistula.

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    Sequestrum :

    is a devitalized avascularsegment of bone, surrounded, by pus

    /infected granulation tissue and is more

    dense than surrounding bone .Because ofavascularity , sequestrum does not decalcify ,

    is more radio opaque and heavy , so sinks in

    water

    Its outer surface is usually jagged / irregular

    due to erosive process by proteolytic

    enzymes in granulation tissue

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    .)

    I nvolucrum :

    is derived from the word volvere

    i.e. to wrap .It is the result of reactive

    new bone formed by periosteal

    reaction , in an attempt to wall off the

    infection by forming a thick tense wall

    It is jagged on its inner surface

    but smooth on its outer surface

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    .)

    Cloacae :

    are single or multiple openings in

    involucrum and are caused by rupture

    of periosteum due to pus undertension .

    Exudates , sequestra are extruded

    through the cloacae on the surface

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    According to the duration of the disease acute

    chronic

    On the basis of the pathogenesishematogenous

    secondary to a contiguous focus of infection

    associated with peripheral vascular disease

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    Acute Osteo Sub-Acute Osteo Chronic Osteo

    Begins with marrow

    edema, cellular infiltration

    and vascular engorgement

    May progress to necrosis

    and abscess formation

    Spread within the

    intramedullary cavityextension through cortex

    by Havers and Volkmans

    canalssubperiosteal

    spaceperiosteum

    soft tissues

    Rupture of joint space

    septic arthritis

    Occurs in abnormal bone

    or after inadequate

    antibiotics

    Localized pyogenic

    process

    Commonly appears as a

    well-defined osteolyticmetaphyseal lesion

    (Brodies abscess) with a

    sclerotic margin that fades

    peripherally (fuzzy

    sclerotic margin)

    S. aureus is most common

    pathogen

    Occurs after inadequate tx or in

    pts with altered immunity

    Distinguishing feature is

    necrotic bone surrounded by

    granulation tissue

    Interruption of blood supply

    necrosisdevitalized bonefragments (sequestra)

    A thick sheath of new periosteal

    bone can develop around the

    sequestra (involucrum)

    Fistula tract formation

    Sharp interface between normal

    and diseased marrow

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    Age (adult v. child)Site (foot, vertebra, long bone)

    Source (trauma/surgery, hematogenous, or

    contiguous spread/cellulitis,)Presence or absence of foreign body (hardware)

    Acute vs. chronic

    SeverityComorbidity (e.g., diabetic, sickle cell)

    Organism

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    PATHOPHYSIOLOGY

    Hematogenous Osteomyelitis

    Contiguous-Focus Osteomyelitis

    Peripheral Vascular Disease-associated

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    PATHOPHYSIOLOGY

    Microorganisms enter bone (Phagocytosis).

    Phagocyte contains the infection

    Release enzymes

    Lyse bone

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    PATHOPHYSIOLOGY

    Bacteria escape host defenses by:

    Adhering tightly to damage bone

    Persisting in osteoblasts

    Protective polysaccharide-rich biofilm

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    PATHOPHYSIOLOGYPus spreads into vascular channels

    Raising intraosseous pressure

    Impairing blood flow

    Chronic ischemic necrosis

    Separation of large devascularized fragment

    New bone formation

    (involucrum)

    (Sequestra)

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    PATHOLOGY

    Acute Infiltration of PMNs

    Congested or thrombosed vessels

    Chronic Necrotic boneAbsence of living osteocyteMononuclear cells predominate

    Granulation & fibrous tissue

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    Hematogenous

    Osteomyelitis

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    HEMATOGENOUS OSTEPMYELITIS

    Rapidly growing bone

    Children:Long bone, Femur, Tibia, Humerus

    Older patients: Vertebral bone

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    HEMATOGENOUS OSTEOMYELITIS

    Neonate & infant < 1 year old

    Septic arthritis is common.

    Growth deformities is common.

    Soft tissue involvement is common.

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    HEMATOGENOUS OSTEOMYELITIS

    Children: 116 years old

    Most frequent in the metaphysis of long bone.

    Slugging blood flow through asinusoidal venous system.

    Deficiency of phagocytic cells.

    Poor collateral circulation

    Susceptibility of this region to trauma.

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    HEMATOGENOUS OSTEOMYELITIS

    Children: 116 years old

    History of antecedent trauma in 30%

    Involucrum

    Sequestration

    Associated septic arthritis

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    HEMATOGENOUS OSTEOMYELITIS

    Adult

    Less common

    Spread infection to joint space.

    Vertebral Osteomyelitis is common> 50y

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    HEMATOGENOUS OSTEOMYELITIS

    Special considerationSickle cell disease

    Injection drug users (IDUs)HemodialysisHIV/AIDS

    ImmunosuppressionProsthetic orthopedic device

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    HEMATOGENOUS OSTEOMYELITIS

    Microbiologic featuresStaphylococci Aureus, EpidermidisStreptococci Group A & B

    Haemophilus influenzaeGram-negative enteric bacilliAnaerobes

    PolymicrobialMycobacterialFungi

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    HEMATOGENOUS OSTEOMYELITIS

    Clinical manifestationClassic presentation: Sudden onsetUsually presentation: Slow, insidious

    High fever, Night sweatsFatigue, Anorexia, Weight loss

    Restriction of movementLocal edema, Erythema, & Tenderrness

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    HEMATOGENOUS OSTEOMYELITIS

    Differentials

    CellulitisGas gangreneNeoplasmAseptic bone infection

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    Clenched fist

    osteomyelitis

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    HEMATOGENOUS OSTEOMYELITIS

    Diagnosis & work-upLab study:

    WBC May be elevated, Usually normal

    C-Reactive Protein (CRP)Erythrocyte Sedimentation Rate(Usually is elevated at presentation

    Falls with successful therapy)

    Blood culture

    ( Acute osteomyelitis + ve > 50% )

    {

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    HEMATOGENOUS OSTEOMYELITIS

    Diagnosis & work-up

    ImagingRadiology:NormalSoft tissue swellingPeriosteal elevation

    Lytic changeSclerotic changew

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    HEMATOGENOUS OSTEOMYELITIS

    Diagnosis & work-upImaging

    MRI:Early detectionSuperior to plan X ray & CT Scan &

    radionuclide bone scan in slectedanatomic location.Sensitivity 90100%

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    HEMATOGENOUS OSTEOMYELITIS

    Diagnosis & work-up

    ImagingRadionuclide bone scan:

    A 3-phase bone scan ( Technetium 99m )

    Positive as early as 24 h afteronset of symptoms.

    False positive Tumor, osteonecrosis

    Artheritis, Cellulitis,

    Abscess

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    HEMATOGENOUS OSTEOMYELITIS

    Diagnosis & work-up

    ImagingCTScan:

    Useful in evaluation of Spinal, pelvic,Sternum, Calcaneus

    Provides exellent images of bone corteIs used for biopsy localization

    Os + gaz in diabetic foot

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    Septic arthritis

    Of

    Right hip

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    HEMATOGENOUS OSTEOMYELITIS

    Diagnosis & work-upUltrasonography

    Simple & inexpensive

    Demonstration anomaly 12 days after onset

    Soft tissue abscess, Fluid collection, &Periosteal elevation

    It allows for aspiration

    It doesnt allow for evaluation of bone cortex.

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    HEMATOGENOUS OSTEOMYELITIS

    Diagnosis & work-upNeddle Aspiration or Open biopsy:

    From: Soft tissue collection

    Subperiosteal abscessIntraosseos lesions

    For: SmearCulturePathology

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    TREATMENTInitial treatment shoud be aggressive.

    Inadequate therapy Chronic disease

    Antibiotic use:

    Surgery

    ParenteralHigh dosesGood penetration in boneFull course

    Empiric therapy

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    TREATMENT

    Empiric Initial TherapyNeonate S.aureus PRP +Infant

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    TREATMENTMonitoring Therapeutic Response

    1.Symptoms & Signs

    2.ESR & CRP

    3.Radiography

    4.Serial Bone Scan?

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    TREATMENT

    Indication for Surgery

    Diagnostic

    Hip joint involvementNeurologic complicationPoor or no response to IV therapy

    Sequestration

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    S U R G I C A L M A N A G E M E N T

    General principles of surgical therapy include

    1.To remove dead , devitalized and infected bone

    2.To obliterate any dead space left after

    debridement

    3.To obtain soft tissue coverage of exposed bone

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    PROGNOSIS

    Is related to:Causative organisms

    Duration of symptoms & sign

    Patient age

    Duration of antibiotic therapy

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    COMPLICATION

    Bone abscessBacteremia

    FractureLoosing of the prosthetic implant

    Overlying soft-tissue cellulitisDraining soft-tissue tract

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    Septic Osteomyelitis

    Osteomyelitis Scar

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    Osteomyelitis Deformity of the Forearm

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    Plain radiograph of the tibia

    and fibula in a 14 y/o patient

    demonstrating a pathologic

    fracture of the proximalfibula with periosteal

    reaction and erosion of the

    cortical bone secondary to

    subacute osteomyelitis

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    CONTIGUOUS-FOCUSOSTEOMYELITIS

    Contiguous focus Osteomyelitis

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    Contiguous-focus Osteomyelitis

    Clinical setting:

    Postoperative infection

    Contamination of bone

    Contiguous soft tissue infection

    Puncture wounds

    Contiguous focus Osteomyelitis

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    Contiguous-focus Osteomyelitis

    Microbiologic featuresStaphylococci Aureus, Epidermidis

    Gram-negative bacteria

    Anaerobic infection

    Unusual organismsClostridia, Nocardia

    Contiguous focus Osteomyelitis

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    Contiguous-focus Osteomyelitis

    DiagnosisLeukocyte countBlood culture (infrequently positive)

    ESR & CRPRadiologic evaluation

    Technetium bone scanOpen bone biopsy

    Culture of wound & draining sinuses??

    Contiguous focus Osteomyelitis

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    Contiguous-focus Osteomyelitis

    Treatment

    Surgery is essential.

    Antibiotics SpecificDuration

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    ASSOCIATED WITHPERIPHERAL VASCULAR DISEASE

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    Clinical Features

    erythema and drainage

    either no pain (if there is advanced neuropathy) or excruciating pain

    (if the destruction of bone has been acute).

    patients are afebrile,

    present with an ulcer without evidence of surrounding inflammation.

    The ulcer size (> 2 cm2) and depth (> 3 mm) are predictive of the

    likelihood of bone involvement. If bone can be felt with a sterile blunt

    probe, the likelihood of osteomyelitis is high.

    a high ESR, especially if it is over 70 mm/hour, is helpful in making

    the diagnosis of osteomyelitis

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    Found almost exclusively in the feet in

    patients with a long history of diabetes

    mellitus and peripheral neuropathy.

    Bone involvement usually occurs after an

    extension of soft tissue infection involving a

    plantar ulcer.

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    ETIOLOGY

    Most infections are polymicrobialS. aureus remains the most common

    pathogen

    others include Enterococcus faecalis,group B streptococci, Enterobacteriaceae,

    anaerobic bacteria (especially peptococci,

    peptostreptococci, and Bacteroides

    species), and P. aeruginosa

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    Vertebral

    Osteomyelitis

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    Risk factors: Male

    Age > 50

    IVDU

    Etiology

    Virtually always hematogenous

    Lumbar more common then cervical

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    Localized pain and tenderness

    Diagnosis often missed ordelayed

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    Plain films

    MRI best

    CT-guided needle biopsy

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    Staph Aureus in about 50%

    Other organisms:

    Gram negative aerobes

    Streptococcus sp.

    Tuberculosis

    Pseudomonas and candida in

    IVDU

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    6 to 12 weeks IV antibiotics if medicaltreatment alone

    Surgical treatment indicated if

    abscess

    cord compression

    failure of medical treatment

    Can follow CRP for reoccurrence or

    failure of treatment response

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    Modality of choice for initial evaluation

    Advantages Inexpensive

    Exclude other conditions

    May help guide further work-up

    DisadvantagesOften normal for the first 10 to 21 days of

    infectionSensitivity: 43-75%

    Specificity: 75-83%

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    Earliest finding deep softtissue swelling

    Active infection for 1-2 weeks bone destruction and periostealreaction

    Localized osteoporosisPathologic fracture

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    Assessment11 functional of Gordon,

    Intans Screening Diagnoses Assessment

    (ISDA)

    Nursing Diagnoses (NDx)NANDA-I2012-2014

    Nursing OutcomesNOC (2008)

    Nursing InterventionNIC (2008) Implementation

    Evaluation

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    Deficient diversional activity r/t prolonged

    immobilization, hospitalization.

    Fear, parental r/t concern regarding

    possible growth plate damage caused byinfection, concern that infection may

    become chronic.

    Ineffective health maintenance r/tcontinued immobility at home, possible

    extensive casts, continued antibiotic

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    Hyperthermia r/t infectious process

    Impaired physical mobility r/t imposed immobility

    as a result of infected area.

    Acute pain r/t inflammation in affected extremity. Risk for constipation: risk factor: immobility

    Risk for infection: risk factor: inadequate primary

    and secondary defenses

    Risk for impaired skin integrity: risk factor:irritation from splint or cast

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    Definition: decreased stimulation from (or

    interest or engagement in) recreational or

    leisure activities.

    Defining characteristics: Clients statements regarding boredom (e.g., wish

    there was something to do, to read, etc.); usual

    hobbies cannot be undertaken in hospital

    Related factors (r/t): environmental lack of

    diversional activity

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    NOC Suggested outcomes

    Leisure participation as evidence by the following

    indicators: expresses satisfaction with leisureactivities/feels relaxed from leisure activities/enjoys

    leisure activities.

    Play participation

    Social involvement

    Client outcomes

    Client will (specify time frame):

    Engage in personally satisfying diversional activities.

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    NIC Suggested NIC interventions

    Recreation therapy

    Self-responsibility facilitation Ng intervention & rationales (activities)

    Example for recreation therapy: assist the client to

    identify meaningful recreational activities; provide safe

    recreational equipment.

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