Osteomyelitis

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Osteomyelitis

  1. 1. Osteomyelitis Dr.punita adajania 1
  2. 2.  NELATON (1834) : coined osteomyelitis  The root words osteon (bone) and myelo (marrow) are combined with itis (inflammation) to define the clinical state in which bone is infected with microorganisms. 2
  3. 3. Defination of Osteomyelitis Osteomyelitis is defined as an acute or chronic inflammatory process of bone, bone marrow and its structure secondary to infection with micro organisms. 3
  4. 4. CLASSIFICATION  Duration , Mechanism & Host response.  Duration - Acute / Subacute / Chronic  Mechanism - Heamatogenous(Blood) - Exogenous (open fractures)  Host response - Pyogenic / Granulomatous 4
  5. 5.  Duration of infection Acute ( <2 WEEKS) 2. Subacute (2-3 WEEKS) 3. Chronic ( >3 WEEKS) 1. 5
  6. 6. ACUTE OSTEOMYELITIS  Age : Infancy and childhood.  Sex : Males predominate 4:1  Location : Metaphysis of long bone.  Cause: Poor nutrition, unhygienic surroundings. 6
  7. 7. Etiological Agents  Infants < 1 year – Group B streptococci Staph aureus E.coli  1- 16 years – S. aureus , S. pyogens , H. Influenza  > 16 years – S.aureus , S.epidermidis , Gram –ve bacteria 7
  8. 8. Pathogenesis Introduction of bacteria from :  Outside through a wound or continuity from a neighboring soft tissue infection  Hematogenous spread from a pre existing focus (most common route of infection) 8
  9. 9. PATHOLOGY OF ACUTE OSTEOMYELITIS  Staph. aureus is the commonest causative organism.  Others: strepto and pneumococci 9
  10. 10. MICRO ORGANISMS REACH BONE VIA BLOOD CIRCULATION BACTERIA GET LODGED IN THE METAPHYSIS 10
  11. 11. HOST BONE INITIATES AN INFLAMMATORY REACTION LEADS TO BONE DESTRUCTION AND PRODUCTION OF INFLAMMATORY EXUDATE (PUS) AFTER SUFFICIENT PUS FORMATION,IT SPREADS INTO DIFFERENT DIRECTIONS(MEDULLARY CAVITY, CORTEX) 11
  12. 12. CLINICAL FEATURES  Fever (High Grade)  Child refuses to use limb (pseudoparalysis)  Local redness , swelling , warmth , oedema  Newborn – failure to thrive , drowsy , irritable. 12
  13. 13. Laboratory Tests  Elevations in the peripheral white blood cell count (WBC)  Erythrocyte sedimentation rate (ESR) is elevated.  The C-reactive protein level usually is elevated.  Blood culture is positive in most of the cases. 13
  14. 14.  X-RAYS: Earliest sign to appear is periosteal new bone deposition at metaphysis.(7-10 days)  BONE SCAN  Aspiration of bone using thick needle: for pus removal 14
  15. 15. 15
  16. 16. Differential Diagnosis  Acute septic arthritis(tenderness and swelling at joint rather than at metaphysis)  Acute rheumatic arthritis( features same as septic arthritis but blood levels helps in diagnosis)  Scurvy(mimics O.M, but absence of pain, tenderness and fever points towards scurvy)  Acute poliomyelitis(presence of fever and muscle tenderness but bones are not tender) 16
  17. 17. Management of acute osteomyelitis.
  18. 18.  Bone abscess  Septic Arthritis  Septicemia  Fracture  Growth arrest  Overlying soft-tissue cellulitis  Chronic infection 18
  19. 19. Chronic Osteomyelitis  Definition: “ A severe, persistent and incapacitating infection of bone and bone marrow ” Term used for chronic pyogenic osteomyelitis. 19
  20. 20. 3 types:  Chronic osteomyelitis secondary to acute osteomyelitis  Garre’s osteomyelitis  Brodie’s abscess 20
  21. 21. Aetiological Agents Usual organisms (with time there is always a mixed infection)  Staph.aureus(commonest)  Staph.pyogenes  E.coli  Pseudomonas  Staph.epidermidis (commonest in surgical implant) 21
  22. 22. Clinical Features Pain Pyrexia Redness Tenderness Discharging sinus (seropurulent discharge to thick pus) Lower end of femur(commonest site) a) b) c) d) e) 22
  23. 23. Pathogenesis Inadequate treatment of acute OM /Foreign implant / Open fracture Inflammatory process continues with time together with persistent infection by Staphylococcus aureus Persistent infection in the bone leads to increase in intramedullary pressure due to inflammatory exudates (pus) stripping the periosteum 23
  24. 24. Pathogenesis (Contd.) Vascular thrombosis Bone necrosis (Sequestrum formation) New bone formation occur (Involucrum) Multiple openings appear in this involucrum, through which exudates & debris from the sequestrum pass via the sinuses (Sinus formation) 24
  25. 25. Radiographic Findings 1)    X-ray examination Thickening and irregularity of the cortex Patchy sclerosis (honey combed appearance) Sequestrum seen. Appears denser than the surrounding normal bone. 2) CT scan & MRI - Show the extent of bone destruction, reactive oedema, hidden abscess and sequestra 25
  26. 26.  BLOOD: ESR may be slightly elevated. Total blood counts are increased.  Pus culture 26
  27. 27. Treatment - Antibiotics - Chronic infection is seldom eradicated by antibiotics alone. - Antibiotic (IV route) is given for 10 days prior to surgery. - Bactericidal drugs are important to: a) Stop the spread of infection to healthy bone b) Control acute flares - After the major debridement surgery, antibiotic is continued for another 6 weeks (min) but usually >3months. [treat until inflammatory parameters (ESR) are normal] - Antibiotics used in treating chronic osteomyelitis (Fusidic acid, Clindamycin, Cefazolin) 27
  28. 28. Surgical Treatmentsequestrum.  SEQUESTRECTOMY: Removal of A window is made in the overlying involucrum and the sequestrum is removed.  SAUCERIZATION: Bone cavity is converted into a “saucer” by removing its wall. Allows free drainage of the infected material. 28
  29. 29.  CURETTAGE: The wall of the cavity, lined by infected granulation tissue is curetted until the underlying normal-looking bone is seen.  EXCISION OF AN INFECTED BONE: Excision of the infected bone segment without compromising the functions of the limb, and building up the gap by transporting a segment of the bone from adjacent part. 29
  30. 30.  AMPUTATION: Very rarely done. Preferred in case of long standing discharging sinus ( especially when the sinus undergoes a malignant change).  In many cases, combination of these procedures are also performed.  After surgery, wound is closed over a “continuous irrigation system”. 30
  31. 31. Complications 1) Pathological Fracture - This occurs in the bone weakened by chronic osteomyelitis 2) Deformity – In children the focus of osteomyelitis destroys part of the epiphysis growth plate. 3) Shortening/ lengthening Destruction of growth plate arrest growth. Stimulation of growth plate due to hyperemia. 31
  32. 32.  The type of rehabilitation for osteomyelitis depends on PHYSIOTHERAPY of the infected bone and the underlying cause MANAGEMENT the location of infection.  Splinting or cast immobilization: This may be necessary to immobilize the affected bone and nearby joints in order to avoid further trauma and to help the area heal adequately.  Splinting and cast immobilization are frequently done in children, although motion of joints after initial control is important to prevent stiffness and atrophy. 32
  33. 33.  Rehabilitation is aimed at restoring normal range of motion, flexibility, strength, and endurance.  The goal of rehabilitation for progressive osteomyelitis is to maintain function and enhance mobility.  Active range of motion initially helps maintain flexibility and strength and relieves the musculoskeletal pain associated with muscular weakness, paralysis, and immobility. 33
  34. 34.  As the therapy progresses, passive range of motion exercises are preferable to avoid overexertion or possible damage to the muscles.  In the event of muscle weakness to the legs, balance exercises may be utilized.  As strength continues to progress, endurance becomes a focus in the individual's rehabilitation program for osteomyelitis. 34
  35. 35.  Aerobic exercises that increase cardiovascular fitness are recommended.  The American Heart Association recommends 30 to 60 minutes of aerobic activity 3 or 4 times a week. 35
  36. 36. 36

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