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Osteomyelitis

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  • 1. OSTEOMYELITIS
    ACUTE OSSTEOMYELITIS
    CHRONIC OSTEOMYELITIS
  • 2. OSTEOMYELITIS
    DEFINITION : inflammation of the bone
    Osteo= bone, myelitis= inflammation of the marrow
    Bone becomes infected either through
    haematogenous spread of organisms, or,
    secondary to a contiguous focus of infection. (invasion from a skin puncture, operation or open fracture)
    Contiguous-focus osteomyelitis:
    bone infection with relatively normal vascularity and
    bone infection with generalized vascular insufficiency (eg: diabetic foot)
    Acute or chronic.
  • 3. Anatomy of the bone
  • 4. EPIDEMIOLOGY
    Osteomyelitis affects about 2 in 10,000 people.
    In childrenlong bones
    In adults vertebrae, feet, and the pelvis
    Risk factors are
     recent trauma
     diabetes
     Hemodialysis
    IV drug abuse
     People who had splenectomy.
  • 5. SOURCES OF INFECTIONS
    INFECTION OF ADJACENT JOINT/SOFT TISSUEEXTENSION TO THE BONE
    PENETRATING WOUND, OPEN FRACTURE, SURGERY TRAUMATIC AND IATROGHENIC IMPLANTATION
    SKIN ABRASION, BOIL, SEPTIC TOOTH HEMATOGENOUS SPREAD OF ORGANISMIMPLANTED AT BONE
  • 6. ACUTE HEMATOGENOUS OMPATHOGENESIS
    Bloodstream is invaded, perhaps from minor skin abrasion or boil or in the newborn from an infected umbilical cord
    In adults  source of infection – arterial line or dirty needle and syringe
  • 7. MICROBIAL INVASION
    Organism usually settles in the metaphysis possibly because of –
     highly vascular
     hairpin arrangement of capillaries slows down the rate of blood flow (sluggish blood flow)
     has relatively fewer phagocytic cells than the physis or diaphysis
     thin cortex
  • 8. Foci of osteomyelitis
    Epiphysis
    Terminal branches of metaphyseal artery form loops at growth plate and enter irregular afferent venous sinusoid. Blood flow slowed and turbulent, predispose to bacterial seeding plus, lining cell have little/no phagocytic action made it favourable for bacteria.
    Looped capillary
    Venous sinusoid
    Metaphyseal artery
  • 9. MICROBIAL INVASION
    1)TRIGGER ACUTE INFLAMMATION
    • Vascular congestion
    • 10. Fluid exudation
    • 11. PMN leukocyte infiltration
    INCREASE INTRAOSSEOUS PRESSURE
    intense pain and obstruction of blood flow
  • 12. 2)SUPPURATION(2ND DAY)
    Pus appears in the medulla and spread along Volkmann’s canals and elevate periosteum to forms a sub-periosteal abscess then spread along shaft
    • The pus can spread from here back into the bone, into an adjacent joint or into the soft tissues.
    Growth plate
    periosteum
    In infants, infxn often extends into epiphysis and thence into the joint. In older children the physis is a barrier to direct spread but where metaphysis is partly intracapsular (e.g. hip, shoulder, or elbow) pus may discharge through periosteum into the joint.
  • 13. 3)NECROSIS (END OF WEEK)
    Rising intraosseouspressure, vascular stasis, infective thrombosis and periostealstripping compromise the blood supply to the bone resulting in bone death and formation of a sequestrum.
    sequestrum
    4)NEW BONE FORMATION
    At 10-14 days new bone forms from the deep layer of the stripped periosteum. With time, new bone thickens to form involucrum enclosing infected tissue and sequestra.
    involucrum
    Medullary cavity
  • 14. 5)RESOLUTION
    if infection is controlled and intraosseous pressure released, the bone will heal
    If infection persist, pus may discharge through perforation in involucrum and track by sinus to the skin surface. The condition is now established as a chronic osteomyelitis
  • 15. Over 90% of acute osteomyelitis cases are caused by Staphylococcus aureusbut Streptococcus pyogenesandHaemophilusinfluenzaemay also cause acute infection of the bone although infection with Haemophilusinflenzae is rare following the widespread use of the Hib vaccine.
    Pseudomonas aeruginosais often isolated from intravenous drug abusers with vertebral osteomyelitis.
    Aetiological agents
  • 16. ACUTE HEMATOGENOUS OM
  • 17. CLINICAL FEATURES
    In child, presented with
    • pain, malaise and fever
    • 18. H/o preceding skin lesion, injury, sore throat
    • 19. Limb is held still
    • 20. Restricted joint movement
    • 21. Local redness, swelling, warmth and edema- presence of pus
  • 22. In infant,
    • Fails to thrive, drowsy and irritable
    • 23. h/o birth difficulties or umbilical artery cathetherization
    • 24. Metaphyseal tenderness and resistance to joint movement
    • 25. Look for other sites – multiple infections
  • In adult, commonest site of hematogenous spread is spine – backache, mild fever
  • 26. INVESTIGATION
    BLOOD
    FBC – leucocytosis
    ESR AND CRP – elevated
    (CRP is a measurement of the acute phase response and is especially useful in monitoring the course of treatment of acute osteomyelitis because it normalizes much sooner than the ESR.)
    Blood C&S
    ASPIRATION AND BIOPSY
     aspiration of pus from subperiosteal abscess or the adjacent joint  send for bacteriological examination and sensitivity to antibiotics
  • 27.
  • 28. IMAGING
    1)Plain Radiograph or tomography (changes may lag by 10-14 days)
    Early changes
    soft tissue swelling, blurring of fat plane and periosteal reaction
    Intermediate changes
    bone destruction (ill defined lytic lesion)
    Cloaca
    Osteopenia
    Late Changes
    Sequestrum formation
    Involucrum and bony sclerosis
  • 29.
  • 30. 2. Nuclear medicine
    Bone scan – can be confirmed earlier (48 hours)
    Technitium 99m-labeled phosphonate
    Galium 67-labeled citrate
    Indium-labeled leucocyte
    Increased uptake of tracer in bone scans and white cell scans.
    High sensitivity but other processes such as arthritis and soft tissue infection can appear similar. (lower specificity)
  • 31. Acute Osteomyelitis
    Bone scan
    Radiograph of knee
    Increased uptake of radiopharmaceutical in the right femur just above the knee joint.
    Plain film reveals a large lytic area
  • 32. Acute Osteomyelitis
    Bone Scan of the foot
    Bone scans, both anterior (A) and lateral (B), showing the accumulation of radioactive tracer at the right ankle (arrow).
    This focal accumulation is characteristic of osteomyelitis.
  • 33. 3. Magnetic Resonance Imaging (MR)
    Demonstrate OM as early as isotope scanning
    High sensitivity but other processes such as fractures and tumors can be similar in appearance.
    Excellent for demonstrating associated soft tissue infection
    4.Computed Tomography
    Demostrate change in subacute and chronic OM
    Sequestra
    Cloacae
    Periostitis
    Soft tissue masses
  • 34. 5. Culture of fluoroscopically or CT guided aspirate
    Confirm infection
    Determine which organism is causing the infection
    When the organism is isolated, then treat the patient with the single appropriate antibiotic.
    Lesion must first be visible with some form of imaging
    Failure to grow an organism is common, especially if patient has been treated with antibiotics
    A positive culture gives a definitive diagnosis and identifies organism and sensitivities
  • 35. Complications
    Chronic OM
    Bone abscess (pocket of pus)
    Bone necrosis (bone death)
    Spread of infection to the
     joint-septic arthritis
    other bones – metastatic osteomyelitis
    Inflammation of soft tissue (cellulitis)
    Growth disturbance  if physis is damaged- leads to shortening, deformity
    Sepsis
  • 36. TREATMENT
    PRINCIPLES OF TREATMENT
    • Provide analgesia and general supportive measures
    • 37. To rest the affected part
    • 38. To initiate antibiotic treatment
    • 39. To undertake surgical eradication of pus and necrotic tissue
  • 1)ANTIBIOTICS
    • Initially the choice of antibiotics based on examination and best guess at the most likely pathogen
    • 40. More appropriate drug can be subtitued once organism is identify
    Older children and previously fits adult
    • Probably have staphylococcal infection
    • 41. Antibiotic
    -intravenous flucloxacillinand fusidic acid ( may be changed once results of sensitivity are known)
    -continued until there is clinical and laboratory evidence of improvement (usually for 1-2 weeks)
    - followed by oral antibiotic for another 2-3 weeks
  • 42. Children under 4 years old
    • High incidence of haemophilus infection
    • 43. Antibiotic: third generation cephalosporin
    2)ANALGESICS- paracetamol
    3) SPLINTAGE
     Complete bed rest is essential.
    Splint could be used but should not conceal affected area.
  • 44. 4)DRAINAGE
    • If antibiotics given early, drainage may not be necessary
    • 45. If subperiosteal abscess can be detected, or if pyrexia and local tenderness persists >24 hr after tretment with adequate antibiotics, the pus should be let out.
    • 46. About 30% of patient with confirmed OM are likely to need an operation
    5)FOLLOW UP
    Once infection subsided, movement are encouraged
    to look for recurrence of infection