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bone diseases.pptx

5 de Mar de 2023
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bone diseases.pptx

  1. Objectives At the end of this lecture we should be able to: Define acute OM. Describe the natural history of the evolution of acute OM. Describe the clinical and radiographic features of acute OM. Define differential diagnosis of acute OM. Outline Complications of acute OM. Describe principles of management of children with acute OM.
  2. Osteomyelitis is a pyogenic infection of the bone and bone marrow. Age: 50% of cases occur in preschool-aged children. Disease of childhood ; but can occur in adults.
  3. Classification of osteomyelitis A. Duration- ❖ acute (less than 2 weeks) ❖ subacute ( 2-6 weeks( ❖ chronic (>6 weeks) B. Mechanism ❖ Exogenous ❖ hematogenous.
  4. The organisms bone by: Blood can reach the stream (haematogenous). From without (an infected open fracture). Direct spread (osteomyelitis tibia from an overlying chronic ulcer of the leg). From neighboring focus of infection such as Mastoiditis from middle ear infection.
  5. Open fracture of tibia. This is a potential direct source of bacterial contamination. Osteomyelitis is common in open fractures. Right leg chronic osteomyelitis in a 70-year- old diabetic man. He has had this wound for 15 years. Skin biopsy was negative for malignancy.
  6. Gram +ve Staphylococcus aureus [70-90 %] Community-associated methicillin-resistant S. aureus has also become an increasing problem . Streptococci pyogen Pneumococci. Gram –ve Haemophilus influenzae(50% < 4 y) E .coli Pseudomonas auroginosa, Proteus mirabilis. Organism: Salmonella is a common pathogen in patients with sickle-cell anemia. Immunocompromised children are prone to infection with a variety of fungi and bacteria.
  7. The organism usually reaches the blood stream from a septic focus (tonsillitis, furuncles and skin boils, chest infection). tonsillitis boil furuncles
  8. General: lower vitality; convalescence from fevers; e.g. measles. Local : trauma Sex: Male-to-female : 2:1 . Why? Factors related to increased incidence in males may include increased trauma due to risk-taking behavior or other physical activities that predispose to bone injury.
  9. Diaphysis metaphysise E.P Epiphysis E.P Epiphysis metaphysise
  10. Metaphysis of long bones (tibia, femur; humerus) The commonest sites are the lower end of femur and the upper end of the tibia. Site
  11. Vascular arrangement : Blood flow slows down in large sinusoidal veins. Vulnerable to minor trauma, as (site of attachment of ligaments). Lack of active phagocytosis in metaphysis ; as compared to diaphysis. Poor collateral circulation Anatomy of long bone and distribution of blood supply.
  12. Bacteria pass through nutrient vessels to the metaphyses where they lodge and proliferate Metaphyseal inflammation → Exudation ↑ intraosseous pressure Vascular stasis Thrombosis Bone necrosis &bone resorption. Physeal plate acts as barrier to epiphyseal extension of infection because it is avascular. Sometimes infection can extend into the adjacent joint E.P
  13. Acute inflammatory reaction :↑ intraosseous pressure → Intense pain Obstruction of blood flow Interavascular thrombosis. Local changes
  14. Suppuration: pus forms rapidly which spread → subperiosteal abscess.
  15. .Acute O.M with an abscess in the medulla
  16. Bone destruction & New bone formation Sequestration (necrosis, bone death). New bone formation (involucrum).
  17. Organisms once localized in bone→ Bacteria proliferate and induce inflammatory reaction and cause cell death. → Bone undergoes necrosis within first 48 hours → Bacteria and inflammation spread within the shaft of the bone and may percolate throughout the haversian systems and reach the periosteum→ Subperiosteal abscess→ Segmental bone necrosis sequestrum (dead piece of bone) → Rupture of periosteum leads to an abscess in the surrounding soft tissue and the formation of draining sinus. Subperiosteal abscess. Involucrum
  18. The diagnosis of osteomyelitis is based primarily on the clinical findings, with data from the initial history, physical examination and laboratory tests.
  19. Child or infants with a history of mild trauma followed in 1-3 days by rapid onset of fever Bone pain General malaise Child refuses to use the affected limb (Guarding ). High temperatures, rapid pulse and toxemia. Inability to support weight and asymmetric movement of extremities are often early signs in newborns and young infants.
  20. Sudden onset High fever, Night sweats Fatigue, Anorexia, Weight loss Restriction of movement Local edema, Erythema, & Tenderrness Sharp local tenderness to palpation and particularly to percussion over the site of the lesion Such signs as hyperaemia of the skin and fluctuation in the region of the lesion are very late signs and are evidence of neglected osteomyelitis
  21. Painful focal swelling (+hotness & redness). Localized Focal point (finger tip ) tenderness over the affected bone (sever tenderness). Later, edema,warmth, and redness. Draining sinus and bone deformity are both rare in acute disease. When present, these symptoms suggest subacute or chronic infection. Adjoining joint movement is restricted due to joint involvement or associated soft tissue inflammation. Physical Examination
  22. Blood sample: culture & sensitivity. Blood cultures are positive in up to 50% of children with acute OM. CBC:PMN leucocytosis. High ESR. High C-reactive protein ..
  23. Aspiration is the “key” to the diagnosis Don’t wait for imaging Subperiosteal aspiration Aspiration of subperiosteal abcess.
  24. Plain X-ray: Normal in first 3 weeks. Later, rarified bone & periosteal reaction. Plain X-ray usually only show soft tissue swelling and loss of normally visible tissue planes Plain X-ray can be useful in detecting bone tumors, fractures, and healing fractures. Osteopenia, lytic lesions, and periosteal changes are late radiographic signs, but their absence does not exclude a diagnosis of acute osteomyelitis.
  25. A lucent moth eaten appearance Periosteal new bone formation Radiology: ❑Normal in first 3 weeks. ❑Soft tissue swelling ❑Periosteal elevation ❑Lytic change ❑Sclerotic change
  26. Soft tissue swelling can be seen by 1- 3 days after infection. Destructive bone changes don't occur on plain film until 10-14 days after infection starts. Initially see a lucent moth eaten appearance to bone. There is extension of infection through the metaphyseal cortex leading to periosteal new bone formation which if untreated may completely encircle the bone becoming an involucrum which can envelope the non viable infected bone which is called a sequestrum. plain film
  27. Enhanced uptake of the radioisotope, demonstrates ↑osteoblastic activity of the infected bone and distinguishes osteomyelitis from deep cellulitis. It has a false-negative rate (20%), particularly in the first few days of illness. Fractures, bone tumors, and surgery also cause enhanced technetium uptake Three-phase technetium radionuclide bone scanning
  28. Bone scan :increase uptake in area of OM A bone scan is usually positive 24 hours after infection and demonstrates a well defined focus of tracer activity 1 - 2 hours post injection that is correlated with radiotracer in same area on dynamic scans.
  29. MRI can be extremely helpful in unclear situations MRI: to differinate between pus and blood. This test is increasingly used to define bone involvement in patients with a negative bone scan. Changes in bone marrow caused by inflammation result in an area of low signal intensity within bright fatty marrow. These abnormalities need to be correlated with the clinical picture before a diagnosis is made, as they are not specific for osteomyelitis. MRI
  30. :MRI • Early detection • Superior to plan X ray & CT Scan & radionuclide bone scan in slected anatomic location. • Sensitivity 90 – 100%
  31. An ultrasound examination can detect fluid collections (e.g., an abscess) and surface abnormalities of bone (e.g., periostitis). CT scan can reveal small areas of osteolysis in cortical bone.
  32. 1.Rheumatic arthritis 2.Septic arthritis. 3.Cellulitis. 4.Subcutaneous abscess 5.Sickle-cell crisis
  33. 6. Ewing’s sarcoma. 7. Neuroblastoma . 8. Osteosarcoma. 9. Fractures 10. In newborns and infants in whom osteomyelitis may present as a pseudoparalysis, also consider nervous system disease (eg, polio), cerebral hemorrhage, trauma, scurvy, and child abuse.
  34. Septic arthritis. Chronic OM. Metastatic infection in other bones, serous cavities,brain and lung Pyameia. Pathological fracture. Squamous cell carcinoma in a sinus tract (A rare, long- term complication ).
  35. The inflammatory exudate may develop considerable pressure and penetrate the cortex causing sinus tracts through the cortical bone into the soft tissues and through the skin Squamous cell carcinoma in a sinus tract (A rare, long-term complication ). Sinus
  36. 1. Bed rest. 2. Fluids for dehydration 3. Analgesics, antipyretics. 4. Splint for the limb for comfort. 5. Antibiotics : Broad spectrum. Adequate dose regimen. Bactericidal ; Antistaph. Injection A sufficiently prolonged antibiotic course are essential [6 weeks in adults and at least 4 weeks in children].
  37. 1. Drainage of subperiosteal abscess. 2. Bone drilling: To relieve increased intraosseous pressure and evacuate pus; if sever pain and local tenderness persists hours of antibiotic after 24 effective treatment.
  38. An acute osteomyelitis becomes chronic due to : Improper drainage of pus in the acute stage. Undrained cavity in the bone Formation of sequestrum. Presence of foreign bodies .
  39. ❖May follow acute OM ❖May start De Novo: ❑following operation ❑following open fractures
  40. Pathology: one of Bone cavity. Sequestrum (dead bone). Sinuses. Cavities Cloacae Involucrum Histological picture is chronic inflammation Organisms: are usually mixed infection. mostly staph. Aureus E. Coli . Strep Pyogen, Proteus.
  41. Sequestrum
  42. Chronic osteomyelitis is characterized by a protracted course with remissions and exacerbations. The fistulae may close during a remission. In exacerbation, body temperature increases, tenderness and toxicosis intensify. Pus is again discharged from the fistulae, sometimes in abundance
  43. Sinogram
  44. Right leg chronic osteomyelitis in a 70-year-old diabetic man. He has had this wound for 15 years. Skin biopsy was negative for malignancy. Cortical defect and intramedullary sequestrum.
  45. Sequestrectomy & saucerisation Excision of sinus tract. Sequestrectomy & saucerisation
  46. Treatment of chronic osteomyelitis in adults is sometimes compared to treating entities such as giant cell tumors, in that a radical resection of the infected bone is the first step, followed by efforts at reconstruction.
  47. The treatment of chronic osteomyelitis in children is somewhat easier in that the child's periosteum is capable of bone regeneration. The basic principle is the same, of eradicating the avascular bone, and providing a means for the limb to regenerate a replacement.
  48. Antibiotic (Gentamycin) impregnated collagen sheet (Septocol sheet) to assist in local control of infection, Papineau's open bone grafting technique.
  49. Pathological Fr. Amyloid disease in long continued chronic OM with persistent discharging pus. Retardation of growth of bone due to affection of epiphyseal plate.
  50. It is a special form of chronic OM. There is a localized abscess within the bone near the metaphysis Arises insidiously without history of acute attack. X-ray: circular or oval cavity surrounded with a zone of sclerosis. Treatment: De-roofing of the cavity & evacuation of pus. Brodie’s Abscess
  51. MRI
  52. Non-suppurative type of OM affecting the shafts of long bones. No abscesses. No sinuses. Diffuse thickening of bone with encroachment of the medullary canal. X-ray: increased bone density and cortical thickening . Treatment: Gutter to release tension inside the bone.
  53. BoneScan Tec- bone scan in sclerosing OM
  54. Septic arthritis (bacterial, suppurative, purulent, or infectious arthritis ) is inflammation of a synovial membrane with purulent effusion into the joint capsule, usually due to bacterial infection.
  55. 1. Haematogenous ❖ ❖ ❖ 2. Acute OM (interarticular metaphysis) 3. Direct invasion Pnetrating wound Intra-articular inj Arthroscopy
  56. Organisms: Staph. Aureus, Streptococci Haemophilus or influenza; E.coli. Pathology: Infection starts in the synovial membrane (synovitis) then articular cartilage is destroyed. Subchondral marrow spaces are filled with pus.
  57. temperature, Toxemia, inability to walk. Deformity, sever pain & tenderness. Limitation of motion and muscle spasm. Leucocytosis . ESR. Aspiration: pus (pus cells and culture & sensitivity).
  58. An infant with septic arthritis of the left hip. The child holds his hip rigidly in the classic position of flexion, abduction, and external rotation, a position that maximizes capsular volume. The patient is relatively comfortable as long as the hip joint remains immobile in this position. The joint is further subluxated
  59. Bacteria Enzymes Destroy cartilage Irreversible joint damage White cells Enzymes Septic Arthritis
  60. Plain radiography - Anteroposterior and lateral views Findings are often normal. Radiography may be helpful when considering hip involvement in young children. Look for soft tissue swelling around the joint, widening of the joint space, and displacement of tissue planes. In later stages of progression, look for bony erosions and joint space narrowing. Ultrasonography is very sensitive in: detecting joint effusions generated by septic arthritis. defining the extent of septic arthritis Needle guided aspiration. Differentiating septic arthritis from other conditions (eg, soft tissue abscesses, tenosynovitis) in which treatment may differ. Imaging Studies
  61. 3 weeks after presentation, Lt. hip is dislocated, and new periosteal bone formation is noted (an associated osteomyelitis of Lt. femur).
  62. May be the initial best diagnostic and therapeutic procedure in the vast majority of cases May allow thorough decompression of joint Can be repeated serially to achieve relief of symptoms, decrease joint effusion, and clear bacteria and synovial WBCs. Poor choice in joints with loculations Diagnostic Procedures
  63. Rest Fluids. Splint Systemic antibiotics. Arthrotomy (drainage).
  64. Bone destruction. Chronic septic arthritis. Pathological dislocation Growth disturbance due to destruction of the epiphysis.
  65. ❑Complete recovery ❑Partial loss of the articular cartilage ❑Fibrous or bony ankylosis
  66. 1. Acute osteomyelitis 2. Trauma 3. Irritable joint 4. Hemophilia 5. Rheumatic fever 6. Gout 7. Gaucher disease
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