1. Bone infection Dr. Sami Abdalla

2. Definition An inflammation of the bone caused by an infective organism, leading to inflammatory destruction of bone, necrosis and new bone formation.

3. Classification Based on :  Duration and type of symptoms.  According to the mechanism.  Host response.

4. Risk factors Systemic : – Malnutrition. – Sickle cell anaemia. – Diabetes. – Immuno-suppressive conditions. Local: – Trauma. – Foreign body. – contiguous infection.

6. Acute haematogenous osteomyelitis.

7. Causal organism: – Staph. aureus 80% – Strept., Pneumococcus, H. infleunzae (<2yrs), – Pseudomonas  heroin addicts. – Salmonella  sickle cell anaemia.

8. Sources fo infection Minor skin abrasion, boil, septic tooth. Infected umbilical cord. Urethral catheterization.

9. Pathogenesis The organism usually settle in the metaphysis of : – Proximal tibia. – Proximal and distal femur. – Proximal end of the humerus.

10. Acute inflammatory reaction: – Increase intra-osseous pressure. – Obstruction to the blood flow. – Intravascular thrombosis.

11. Suppuration: – Pus forms within the bone in the 2 nd and 3 rd day. – Through volkman’s canal  subperiosteal abscess forms.

12. Bone necrosis: – By the end of the first week. – Due to infective thrombosis Periosteal stripping. Bacterial toxin. Leucocyte enzymes.

13. New bone formation; – By the end of the 2 nd week.

14. Resolution:

16. Clinical features Constitutional symptoms. Severe pain. Tenderness, Lymphadenopathy. In adult  backache and mild fever.

17. Investigation Blood culture  +ive in 50%. Blood test. Culure aspirate. Ulrasoud. M.R.I. Radiography. Bone scan.

18. Differential diagnosis Cellulitis. Strep. Necrotizing myositis. Acute suppurative arthritis, Acute rheumatism. Sickle cell crisisl Gaucher’s disease.

20. Treatment Supportive treatment. Splintage Antibiotic therapy – Best guess. – Gm stain. – Culture and sensitivity.

21. Surgical treatment; – Unresponsiveness within 36 hrs of starting treatment. – Signs of deep pus.

22. Complication Septicaemia.( rare). Metastatic infection ( infants) Suppurative arthrits. Altered bone growth. Chronic osteomyelitis.

24. Subacute haematogenous osteomyelitis.

25. Differ from AHO in severity of symptoms and signs. Common in distal femur, proximal and distal tibia. Staph. Aureus and epidermis are the predomint organisms.

26. Clinical picture The patient is usually a child or adolescent. Pain for severa weeks or even months. Mild constitutional symptoms. Limping and slight swelling. Muscle wasting and local tenderness.

27. This indolent course is due to – increase host resistance. – Lower bacterial virulence. – Antibiotic administration.

28. Investigation TWB normal. ESR 50% Blood culture  usually are not +ive. Culture of bone aspirate or biopsy 60%. X-ray.

29. Treatment Conservative : – For typical lesions. – Antibiotics for 6/52.

30. Biopsy and curretage; – For aggressive lesion. – If the diagnosis is in doubt.

31. THANK YOU

32. Post-traumatic osteomyelitis

33. Most common cause in adults. Common organisms – Staph.aureus. – Gm –ive coliform. – An aerobic organisms,

34. Clinical picture Constitutional symptoms. Sero-purulent discharge. Delayed union. Leucocytosis and increase in ESR

35. Treatment Prophylaxis. – Cleaning and debridement of open # – Provision of drainage by leaving the wound open. – Immobilization of the # – Antibiotics.

36. Pyogenic wound infection; – Regular wound dressing. – Debridement. – External fixation for unstable fracture. – If these failed: The management is essentially that of chronic osteomyelitis.

37. Chronic osteomyelitis Used to be due to acute haematogenous osteomyelitis, but nowadays it more frequently follows an open fracture or operation. The usual organisms (mixed infection) are staph.aureus, E.coli, strept.pyogenes, proteus and pseudomonos.

38. Chronic osteomyelitis Pathology: – The disease may take one 2 forms: 1.Pus + sequestrum surrounded by vascular tissue beyond which is an area of sclerosis. Sequestra act as substrates for bacterial adhesions, ensuring persistence till they are removed or discharged through a draining sinus

39. Chronic osteomyelitis – Two factors are responsible for the chronicity of the disease : 1.presence of dead infected bone 2.the intra-osseous cavity can’t be obliterated because of the rigid walls and as a result, the body’s normal defense mechanisms and antibiotics are unable to reach all the bacteria in the bone

40. Chronic osteomyelitis 2.Brodie’s abscess: – This form is closely contained creating chronic abscess within the bone (pus or jelly-like granulation tissue) surrounded by sclerotic bone. This may be a sequel to pyogenic septicemia from which the pt has recovered but stayed dormant for years or may be found in a pt which is known to have had osteomyelitis affecting a bone other than in which Brodie’s abscess is discovered

41. Chronic osteomyelitis Clinical Features: It may remain quiescent for months or years with acute and subacute attacks (flares) i.e. – recurring pain local Transitory effusion – Pyrexia and tenderness – Discharging sinus (seropurulent) – In long standing cases, tissues may be puckered in where a scar or sinus is attached

42. Chronic osteomyelitis Investigations: – ↑ESR & TWBCs during acute flares – ↑ASO titre – C&S

43. Chronic osteomyelitis – Radiography is diagnostic: The classical picture of bone resorption (as patchy loss of density or frank excavation) with thickening and sclerosis of the surrounding bone. However there is marked variations (no more than localized trabeculation, or an area of osteoporosis, or periosteal thickening)

44. Chronic osteomyelitis Bone scan: increased activity CT and MRI: – extent of bone destruction – Reactive edema – Hidden abscesses and sequestra

45. Chronic osteomyelitis Treatment: 1.Antibiotics Exacerbations are treated by immobilization and antibiotics but only to recur again It is also used to stop spread of infection to healthy bone 2.Local treatment: Sinus: dressing Abscess: drainage

46. Chronic osteomyelitis 3.Operation: Waiting policy. The objective is removal of dead bone and elimination of dead space Under antibiotic cover, all infected soft tissue and all dead bone must be excised Dead material can be identified by pre-op injection of sulphan blue or probing a sinus or by radiograph Access to the bone is usually through a previous scar

47. Chronic osteomyelitis Double-lumen tubes are laid in the resulting cavity and the tissues are closed with the tubes emerging through separate stab wounds. an appropriate antibiotic solution is instilled 4-hourrly and cleared shortly before the next procedure by low pressure suction. Cavity injection and drainage should be cont. until the effluent is sterile (usually 3-4 weeks). The tubes are then gradually withdrawn as the cavity diminishes in size. Gentamicin –impregnated beads

48. Chronic osteomyelitis Driange tube (double lumen tube)

49. Chronic osteomyelitis Dead space is obliterated by packing the cavity with cancellous bone chips or local muscle flap. Amyloid disease is taken into consideration when copious amount of pus has persisted for years Amputation: if exacerbations are frequent and prolonged. Brodie’s abscess should be treated by evacuation and curettage of the cavity under antibiotic cover. If the cavity is of moderate size, packing with cancellous bone chips is used.

50. Chronic osteomyelitis Aftercare : Success is difficult. prognosis should always be guarded The watchword is cautious optimism and after all, probable cure is better than no cure.

51. Chronic osteomyelitis

52. Definition Inflammation of a synovial membrane with purulent effusion into the joint capsule, often due to bacterial infection

53. Synonyms Bacterial, suppurative, purulent or infectious arthritis, gonococcal or nongonococcal

54. A Big Problem Despite advances in diagnostic studies, powerful antibiotics, and early drainage, significant joint destruction commonly occurs Why ? – Lack of clinical suspicion – Delay in definitive diagnostic needle aspiration – Failure to adequately drain the joint

55. Frequency 2-10 cases per 100,000 in the general population 30-70 cases per 100,000 in patients with immunological disorders or deficiencies, and joint replacements Gonococcal: women 3x > men

56. Etiology Staph aureus Streptococci In all age groups, 80% due to gram-positive aerobes, 20% due to gram-negative anaerobes Neonates and infants < 6mos S aureus and gram- negative anaerobes – Incidence of H. influenzae has decreased due to the vaccine

57. Pathophysiology Adults – Knee 40-50 % – Hip 20-25 % – Infants and young children Hip 95 %

58. Infection Sources Trauma: direct Hematogenous: IV drug injection Osteomyelitis adjacent to joint capsule Soft tissue infections: cellulitis, abscess, bursitis, tenosynovitis

59. Clinical Presentation: “red, hot, painful joint” Fever Erythema Edema Heat Pain Markedly decreased passive and active ROM

60. Age Related Presentation Young sexually active pts: + fever, tenosynovitis, migratory polyarthralgia and dermatitis ( papular rash over trunk and distal extremity extensor surfaces that may turn hemorrhagic ) = Suspect N gonorrheae IVDU = Pseudomonas Infants and young children = difficult

61. Pediatric Presentation Fever, decreased appetite and irritability without obvious joint involvement is common Differentiation from transient synovitis important: 4 independent variables – History of fever – Non-weight-bearing – ESR > 40mm/h – WBC > 12,000/uL

62. Diagnosis Needle aspiration, open drainage and lavage (arthroscopically or arthrotomy) Contraindications to arthrocentesis: 1. avoid aspirating from an area that has overlying soft tissue infection 2. Bleeding disorders 3. Anticoagulation therapy

63. Lab Studies CBC with diff: leukocytosis and left shift ESR: monitor treatment CRP: monitor treatment Blood cultures: may be + in 50% S aureus Urethral, cervical, pharyngeal and rectal swabs: N gonorrheae Synovial fluid analysis: Gram stain, culture, cell count, and crystal analysis

64. Treatment Supportive. Splintage. Drainage of pus. Antibiotics. physiotherapy.