1. ACUTE AND CHRONIC OSTEOMYELITIS
PRESENTER DR KARANU JOSEPH
MODERATOR PROFESSOR ATINGA

2. DEFINITION
Inflammation of the bone caused by an infecting organism

3. HISTORY
In the early 1900’s about 20% of patients with osteomyelitis died and patients who survived had significant morbidity.

4. Introduction-
Oldest known evidence of osteomyelitis fractured spine of dimetrodon permian reptile million years ago
Hippocrates BC infection after fracture
Nelaton credited with introducing the term osteomyelitis in 1844

5. Introduction
The key to successful management is early diagnosis and appropriate surgical and antimicrobial treatment.
A multi disciplinary approach is required, involving an orthopaedic surgeon, an infectious disease specialist, and a plastic surgeon in complex cases with significant soft tissue loss.

6. Classification The duration - acute, subacute and chronic
Mechanism of infection – exogenous or hematogenous
The type of host response to the infection- pyogenic or non pyogenic

7. Acute hematogenous osteomyelitis
Most common type of bone infection, usually seen in children
Decrease in incidence, could be due to higher standard of living and improved hygiene.
Bimodal distribution- younger than 2 years, and 8-12 years
More common in males

8. Acute hematogenous osteomyelitis- causes
Caused by a bacteraemia
Bacteriological seeding of bone generally is associated with other factors such as localized trauma, chronic illness, malnutrition or an inadequate immune system.

9. Acute hematogenous osteomyelitis pathophysiology
In children the infection generally involves the metaphyses of rapidly growing long bones
Bacterial seeding leads to an inflammatory reaction which can cause local ischaemic necrosis of bone and subsequent abscess formation

10. Acute hematogenous osteomyelitis pathophysiology
As the abscess enlarges, intramedullary pressure increases causing cortical ischaemia, which may allow purulent material to escape through the cortex into the subperoisteal space.

12. Acute hematogenous osteomyelitis pathophysiology
A subperisoteal abscess then develops
If left untreated this process eventually results in extensive sequetra formation and chronic osteomyelitis

13. Acute hematogenous osteomyelitis pathophysiology
In children younger than 2 years, blood vessels cross the physis, thus epiphysis may be involved
Limb shortening or angular deformity may occur

14. Acute hematogenous osteomyelitis pathophysiology
Joint may be involved in some cases- hip joint most common, especially for intraarticular physes- proximal humerus,radial neck, distal fibula
Metaphysis has relatively fewer phagocytic cells than the physis or diaphysis, hence more infection here

15. Acute hematogenous osteomyelitis pathophysiology
In children older than 2 years the physis effectively acts as a barrier to the spread of a metaphyseal abscess
Metaphyseal cortex thicker, hence diaphysis more at risk
After physes are closed acute hematogenous osteomyelitis is much less common

16. Acute hematogenous osteomyelitis pathophysiology
After the physes are closed, infection can extend directly from the metaphysis into the epiphysis and involve the joint
Septic arthritis resulting from acute hematogenous osteomyelitis generally is seen only in infants and adults.

17. Acute hematogenous osteomyelitis microbial pattern
Staphylococcus aureus most common in older children and adults
Gram negative bacteria- increasing trend- vertebral
Pseudomonas most common in intravenous drug abusers
Salmonella in sicke cell
Fungal infections in chronically ill patients on long term intravenous therapy.

18. Acute hematogenous osteomyelitis microbial pattern
Infants- staph aureus most common but group B streptococcus and gram negative coliforms
Prematures staph aureus andgram negative organisms
Hemophilus influenzae primarily in children 6 months to 4 years old, incidence decreased dramatically by immunizations

19. Acute hematogenous osteomyelitis microbial pattern
Ngetich, 2002 found that of children presenting with haematogenous osteomyelitis in Kenyatta national hospital the commonest isolated organism was staphylococcus aureus accounting for 29 (60.4%)of the cases, 15 (60%) of these were MRSA strains

20. Acute hematogenous osteomyelitis diagnosis
History and physical examination
Fever and malaise
Pain and local tenderness
Sweliing
Compartment syndrome in children

21. Acute hematogenous osteomyelitis diagnosis
Laboratory tests
White blood cell count
Erythrocyte sedimentation rate
C-reactive protein
checked very 2- 3 days post treatment initiation
Aspiration for suspected abscess

22. Acute hematogenous osteomyelitis diagnosis
Plain radiographs
Technetium-99m bone scan +/- MRI

23. Radiographs Soft tissue swelling Periosteal reaction Bony destruction
(10-12 days)

24. Bone scan
Can confirm
diagnosis
24-48 hrs after
onset

25. Acute hematogenous osteomyelitis Treatment
Surgery and antibiotic treatment are complementary, in some cases antibiotics alone may cure the disease.
Choice of antibiotics is based on the highest bacteriocidal activity, the least toxicity and the lowest cost

26. Acute hematogenous osteomyelitis Treatment
Nade’s 5 principles of treatment
An appropriate antibiotic is effective before pus formation
Antibiotics do not sterilize avascular tissues or abscesses and such areas require surgical removal

27. Acute hematogenous osteomyelitis Treatment- nades principles
If such removal is effective, antibiotics should prevent their reformation and primary wound closure should be safe
Surgery should not damage already ischaemic bone and soft tissue
Antibiotics should be continued after surgery

28. Acute hematogenous osteomyelitis Treatment
The two main indications for surgery in acute hematogenous osteomyelitis are:
The presence of an abscess requiring drainage
Failure of the patient to improve despite appropriate intravenous antibiotic treatment

29. Acute hematogenous osteomyelitis Treatment- surgery
The objective of surgery is to drain any abscess cavity and remove all non viable or necrotic tissue
Subperiosteal abscess in an infant-several small holes drilled through the cortex into the medullary canal
If intramedullary pus is found, a small window of bone is removed
Skin is closed loosely over drains and the limb splinted

30. Acute hematogenous osteomyelitis Treatment
Generally a 6 week course of intravenous antibiotics is given
Orthopedic and infectious disease followup is continued for at least 1 year

31. SUBACUTE HEMATOGENOUS OSTEOMYELITIS
More insidious onset and lacks severity of symptoms
Indolent course hence diagnosis delayed for more than two weeks.

32. SUBACUTE HEMATOGENOUS OSTEOMYELITIS CLINICAL FEATURES
The indolent course of subacute osteomyelitis is due to:
increased host resistance
decreased bacterial virulence
administration of antibiotics before the onset of symptoms
Systemic signs and symptoms are minimal
Temperature is only mildly elevated
Mild to moderate pain

33. SUBACUTE HEMATOGENOUS OSTEOMYELITIS INVESTIGATIONS
White blood cell counts are generally normal
ESR is elevated in only 50% of patients
Blood cultures are usually negative
Plain radiographs and bone scans generally are positive

34. SUBACUTE HEMATOGENOUS OSTEOMYELITIS INVESTIGATIONS
S. Aureus and Staphylococcus epidermidis are the predominant organisms identified in subacute osteomyelitis

35. SUBACUTE HEMATOGENOUS OSTEOMYELITIS BRODIE ABSCESS
Localized form of subacute osteomyelitis occuring most commonly in the long bones of the lower extremeties
Intermittent pain of long duration is most times the presenting compliant, along with tenderness over the affected area

36. Brodie abscess

37. SUBACUTE HEMATOGENOUS OSTEOMYELITIS BRODIE ABSCESS
On plain radiographs appears as a lytic lesion with a rim of sclerotic bone
S aureus is cultured in 50% of patients and in 20% the culture is negative
The condition requires open biopsy with curetage to make the diagnosis
The wound should be closed loosely over a drain

38. SUBACUTE HEMATOGENOUS OSTEOMYELITIS Gledhill classification

39. SUBACUTE HEMATOGENOUS OSTEOMYELITIS TREATMENT
Biopsy and curettage followed by treatment with appropriate antibiotics for all lesions that seem to be aggressive
For lesions that seem to be a simple abscess in the epiphysis or metaphysis biopsy is not recommended- IV antibiotics for 48 hrs followed by a 6 week course of oral antibiotics

40. CHRONIC OSTEOMYELITIS
Hallmark is infected dead bone within a compromised soft tissue envelope
The infected foci within the bone are surrounded by sclerotic, relatively avascular bone covered by a thickened periosteum and scarred muscle and subcutaneous tissue

41. com
Sinus track cultures usually do not corelate with cultures obtained at bone biopsy

42. COM in KNH
2008-= 108
2009 = 79
2010-= 99
2011-= 79
2012= 53

43. Classification of COM

44. Anatomical classification

45. Classification of COM

46. Diagnosis COM
Based on
Clinical
laboratory and
imaging studies

47. Clinical evaluation COM
Skin and soft tissue integrity
Tenderness
Bone stability
Neurovascular status of limb
Presence of sinus

48. Laboratory COM Erythrocyte sedimentation rate C reactive protein
WBC count only elevated in 35%
Biopsy for histological and microbiological evaluation
Staphyloccocus species
Anaerobes and gram negative bacilli

49. Organisms in COM
Girasi, 1981 found that the commonest organisms found at the orthopaedic unit at Kenyatta national hospital, then in kabete was staphylococcus aureus which was resistant to penicillin and ampicillin

50. Imaging studies in COM Plain X rays Cortical destruction
Periosteal reaction
Sequestra
Sinography

51. Sinography

52. Imaging -
Isotopic bone scanning more useful in acute than in chronic osteomyelitis
Gallium scans increased uptake in areas where leucocytes and bacteria accumulate. Normal scan excludes osteomyelitis

53. COM Imaging CT Scan Identifying sequestra
Definition of cortical bone and surrounding soft tissues

54. COM Imaging MRI Shows margins of bone and soft tissue oedema
Evaluate recurrence of infection after 1 year
Rim sign- well defined rim of high signal intensity surrounding the focus of active disease
Sinus tracks and cellulitis

55. Treatment of COM Surgical treatment mainstay Sequestrectomy
Resection of scarred and infected bone and soft tissue
Radical debridement
Resection margins >5mm

56. Surgical treatment of COM
Adequate debridement leaves a dead space that needs to be managed to avoid recurrence, or bony instability
Skin grafts,
Muscle and myocutaneous flaps
Free bone transfer
Papineau technique
Hyperbaric oxygen therapy
Vacuum dressing

57. Treatment of COM Antibiotic duration is controversial
6 week is the traditional duration
1 week IV, 6 weeks of oral therapy
Antibiotic polymethyl methacrylate (PMMA) beads as a temporary filler of dead space
Biodegradable antibiotic delivery system

58. Resection or excision for COM
Resection of a segment of affected bone may be necessary to control infection
With techniques of bone and soft tissue transport, massive resections can be performed and reconstructed without significant disability.

59. Resection or excision for COM

60. Amputation for osteomyelitis
Amputation indications include
Arterial insufficiency
Major nerve paralysis
Non functional limb-stiffness, contracture
Malignant change
Prevalence of maliganacy arising from COM reported as 0.2 to 1.6% of cases.
Most are squamous cell carcinoma, also reticulum cell carcinoma,fibrosarcoma

61. Sclerosing osteomyelitis of garre’
Bone is thickened and distended, but abscesses and sequestra are absent.
Cause unknown
Thought to caused by a low grade, possibly anaerobic bacterium

62. Sclerosing osteomyelitis of garre’

63. References
Canale Terry and Beaty James (2007) Campbell’s Operative Orthopaedics, Philadelphia, Mosby
Ben Mbonye-Girasi (1981) Mode of Presentation and End results of Management of Haematogenous Osteomyelitis at the Orthopaedic Unit Kenyatta National Hospital over a Five Year Period. Nairobi : unpublished masters in medicine project, School of Medicine, University of Nairobi
Issac K Ngetich (2002) A Study of Haematogenous Osteomyelitis in Children in Kenyatta National Hospital Kenya. Nairobi : unpublished masters in medicine project, School of Medicine, University of Nairobi
Lewis R P, Sutter V L and Finegold S M (1978) Bone Infections Involving Anaerobic Bacteria. Baltimore pub med PMID