power point

1. AETIOLOGY,PATHOLOGY AND
MANAGEMENT OF OSTEOMYELITIS
SANUSI A.A
DEPT OF ORTHOPAEDICS AND TRAUMA
JUTH

2. OUTLINE
• Introduction
– Definition
– Statement of surgical importance
– Epidemiology
– Relevant physiologic anatomy
– Classification
• Aetiology
– Microbiology
– Susceptibility/predisposition
• Pathogenesis

3. OUTLINE
• Pathology
– Inflammation
– Suppuration
– Necrosis
– New bone formation
– Resolution /chronicity
• Management
– Diagnosis
• History
• Symptoms
• Physical examination
• Investigations
– Treatment

4. OUTLINE
• Complications
• Peculiarities
• Conclusion
• References

5. INTRODUCTION
• Definition
– Osteomyelitis is an inflammation of bone and
marrow caused by an infecting organism
• Statement of surgical importance
– It is one of the most difficult and challenging
problems encountered in orthopaedics
– It can frustrate the best effort of orthopaedic
surgeons

6. INTRODUCTION
• Epidemiology
– Worldwide, childhood acute haematogenous
osteomyelitis is commoner
– Changing trends in the developed world
– Incidence
• <3/100,000 in Europe
• 8 cases per 100,000 children/year by POSNA
– Much higher among less affluent populations
– Male: female 2:1
– Commonly affects the long bones
– Lower limbs > upper limbs

7. INTRODUCTION
• Relevant physiologic anatomy
– Penetration of physeal cartilage by metaphyseal
vessels in the first 6-9 months of life
– Nutrient arterial system
• Hairpin bend
• Reduced oxygen tension
• Decreased phagocytic and reticuloendethelial function
– Rapid growth at metaphyseal region

8. Schematic representation of the blood supply to a long bone

9. Microcirculation of the metaphysis predisposes it to sludging and
infection

10. INTRODUCTION- CLASSIFICATION
• The duration
– Acute
– Sub-acute
– Chronic
• Mechanism of infection
– Exogenous
– Haematogenous
• The type of infecting organism
– Pyogenic
– Non pyogenic

11. AETIOLOGY
• Microbiology
– Acute osteomyelitis
• Neonate and infants
– Group B streptococcus, Staphylococcus aureus
Escherichia coli
• Older children
– Staph aureus
– Streptococcus pyogens
– Haemophilus influenzae
– Kingella kingae
• Adults
– Staphylococcus epidermidis
– S. aureus
– Pseudomonas aeruginosa
– E. coli

12. AETIOLOGY
• Microbiology
– Acute osteomyelitis
• Sickle cell patients
– Staph aureus
– Salmonella spp
• Immunocompromised/iv drug users
– Staph aureus
– H. influenzae

13. AETIOLOGY
• Microbiology
– Chronic osteomyelitis
• Usually polymicrobial
• Common organism
– Staphylococcus aureus
– Escherichia coli
– Streptococcus pyogenes
– Proteus mirabilis
– Pseudomonas aeruginosa
– Staphylococcus epidermidis ( in the presence of
implant)

14. AETIOLOGY
• Susceptibility/predisposition
– Local factors
• Trauma
• Old scar
• Poor circulation
• Chronic bone or joint diseases
• Presence of foreign bodies
– Systemic factors
• Malnutrition
• Co-morbidities
• Steroid/ immunosuppression
• Very young and very old

15. PATHOGENESIS
• Route of infection
– Haematogenous
• Suppurative infections e.g. abscess, boil, OM
• Endocarditis
• URTI
• UTI
• Drug addicts
– Direct contamination
• Trauma
– Penetrating wounds
– Contamination of compound fracture
• Surgery

16. PATHOGENESIS
• Route of infection
– Direct spread from contiguous focus of infection
• Dental abscess
• Acute purulent frontal sinusitis
• Deep pressure sore
• Infection usually starts in the vascular
metaphysis of a long bone
• Epiphyseal involvement can occur in children
<2years

17. PATHOGENESIS
Source of Infection
Metaphysis
Bacterial colonization
Blood stream
Venous stasis

18. PATHOLOGY
• The pathological picture depends on;
– the patient’s age,
– the site of infection,
– the virulence of the organism and the
– host response
• However, the classical picture is seen in children
2-6years of age
• Involves growing bone
• Particularly the metaphyses of the long bone
(distal femur, proximal tibia, distal humerus ,
distal radius)

19. PATHOLOGY
• In infants, infection frequently spreads to the
epiphysis and from there to the adjacent joint
• Acute osteomyelitis in adults usually follows an
open injury, an operation or spread from a
contiguous focus of infection
• True haematogenous osteomyelitis is uncommon
in adults and when occurs usually affect one of
the vertebrae

20. PATHOLOGY
• The pathologic process involves
– Inflammation
– Suppuration
– Necrosis
– New bone formation
– Resolution/ Chronicity

21. PATHOLOGY
• Inflammation
– The earliest change in the metaphysis
– First 24 hours
– Vascular congestion
– Polymorphonuclear leukocyte infiltration
– Exudation
– 2-3 day if not treated with antibiotic
– Intraosseus pressure  intense pain
 intravascular
thrombosis  ischemia

22. PATHOLOGY
• Suppuration
– 4-5 days
– Pus formation
– Pus spreads via Volkmann canals
• Children – subperiosteal abscess, Epiphysis, joint
• Adult- medullary cavity
• soft tissue
– In vertebrae it spreads via end plates and disc to
adjacent vertebral bodies

23. Spread of pus in haematogenous osteomyelitis

24. PATHOLOGY
• Necrosis
– Bone death by the end of a week
– Bone destruction
• Toxin
• Ischemia
– Epiphyseal plate injury
– Sequestrum formation
• small  removed by macrophage, osteoclast
• large  remained

25. PATHOLOGY
• New bone formation
– By the end of 2nd week
(10 – 14 days)
– Involucrum (new bone formation from deep layer of
periosteum ) surround infected tissue.
– If infection persist- pus discharge through sinus to
skin surface Chronic osteomyelitis

26. PATHOLOGY
• Resolution
– Pathologic process is halted
• Infection controlled early
• Intraosseous pressure released
– Increased bone density
– Normal anatomy may be reconstituted or bone is left
permanently deformed

27. PATHOLOGY
• Chronicity
– The hallmark- infected dead bone within a
compromised soft tissue envelope
– Dead or devitalized bone- sequestrum- is
surrounded by a cavity containing pus
– Pathology in COM include
• Sequestrum formation
• Involucrum
• Cloaca
• Multiple sinuses
• Soft tissue fibrosis

28. PATHOLOGY
• Chronicity
– The chronicity is favoured by formation of a biofilm
• Formation of conditioning film
• Bacterial adhesion
• Bacterial aggregation
• Biofilm maturation/mutation
• Detachment/dispersion

29. MANAGEMENT OF ACUTE OSTEOMYELITIS
• History
• Presentation is influenced by the age of the patient
• Infants
– High index of suspicion
» Birth difficulties
» Umbilical artery catheterization
» site of infection
– Refusal of feeds
– Failure to thrive
– Fever

30. MANAGEMENT OF ACUTE OSTEOMYELITIS
• History
• Children
– Pain in the affected limb
– Fever
– Swelling
– Malaise
– Refusal to use the limb
– Not allowing the limb to be touched
– History of septic focus
» Infection of toe
» Ear discharge
» Sore throat
» Boil

31. MANAGEMENT OF ACUTE OSTEOMYELITIS
• History
• Adults
– Pain
– Fever
– Malaise
– Swelling
– History of prior surgical intervention

32. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Physical examination
• General signs
– Toxic
– Dehydration
– Palor
– Pyrexia
– Tachycardia
– Features of shock
– Systemic features may be mild in very elderly and
immunocompromised

33. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Physical examination
– Local signs
• Limb held still
• Tenderness
• Restricted joint movement
• Swelling
• Multiple sites
• Lymphadenopathy
• Local signs- late signs

34. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Investigations
– Radiological
• Plain x-ray
– Features usually manifest after 2 weeks
– Feature of soft tissue swelling
– Patchy rarefaction of the metaphysis
– Faint extra cortical outline- new bone formation
– Periosteal thickening
– Combination of regional osteoporosis with a localized
area of reduced density

35. Radiographic features of acute osteomyelitis

36. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Investigations
– Radiological
• Uss
– Detection of subcutaneous/subperiosteal fluid
collection
• Raddionuclide scanning
– Detects signs of inflammation as early as 24-48hrs
– Highly sensitive but has relatively low specificity

37. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Investigations
– Radiological
• MRI
–Involvement of axial skeleton
–Bone marrow inflammation
–Differentiate between soft tissue infection and
osteomyelitis
–Extremely sensitive but low specificity

38. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Investigations
– Laboratory
• Blood culture
–3 different samples
–2hrs apart or at the height of fever
• Culture and sensitivity of available aspirate
• FBC + diff
• C- reactive protein
• ESR

39. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Differential diagnosis
– Cellulitis
– Septic arthritis
– Pyomyositis
– Rheumatic fever
– Sickle cell bone crisis
– Malignant tumour

40. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Treatment
– Acute osteomyelitis is an orthopaedic emergency
– Principles of treatment
• Supportive treatment
• Splintage
• Antibiotic therapy
• Surgical drainage

41. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Treatment
– Supportive treatment
• Analgesics
• Antipyretics
• Rehydration
• Correction of anaemia if present
• Nutritional support

42. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Treatment
– Splintage of the affected limb
• For comfort
• Prevents joint stiffness
• Reduces risk of pathological fracture
• Can be done through;
–Cast splintage
–Continuous traction

43. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Treatment
– Antibiotic therapy
• Principles
– Appropriate drug
– Appropriate dosage
– Appropriate route
– Appropriate time to stop
– Appropriate adjunctive measures
• Preferably investigation samples should be taken before
commencing antibiotic
• Empirical therapy is started pending results of culture and
sensitivity
• I/V antibiotics is given until patient is clinically better
(usually about 2 weeks) then oral for further 4 weeks

44. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Treatment
– Antibiotic therapy
• Neonates and infants
– Flucloxacillin + 3rd generation cephalosporin, or
– Flucloxacillin + benzypenicillin + gentamicin
• Children and adults
– Flucloxacillin + fusidic acid or benzylpenicillin
– 3rd generation cephalosporin can be used in cases of
allergy to penicillin
• Elderly
– Flucloxacillin + 2nd or 3rd generation cephalosporin

45. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Treatment
– Antibiotic therapy
• Sickle cell disease patients
– Fluoroquinolones or 3rd generation cephalosporin
• IV drug users and immunocompromised
– Fluoroquinolones or 3rd generation cephalosporin

46. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Treatment
– Surgical intervention
• Indication
– Abscess formation
– Failure to respond to IV antibiotics after 48hrs
– Debridement of infected tissues
• Aim of surgery
– Drain abscess cavity
– Remove all non viable/necrotic tissues

47. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Treatment
– Surgical intervention
• Methods
– Open drainage
– Drilling
– Opening small bone window
• Post operative
– Splintage of the affected limb
– Post op antibiotics
– Follow up for at least one year

48. MANAGEMENT OF ACUTE OSTEOMYELITIS
• Treatment
– Inflammatory phase
• Antibiotics
– Suppurative phase
• Core decompression
– Bone destruction phase
• Debridement ± incision and drainage

49. COMPLICATIONS OF ACUTE OSTEOMYELITIS
• Septic arthritis
• Septicaemia
• Pathologic fracture
• Chronic osteomyelitis

50. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• History
• May arise as a result of inappropriately treated acute
osteomyelitis
• Following trauma
• Characterized by recurrent episodes of acute
exacerbations
• Presentation
– Pain (recurrent)
– Sinus discharge – continuous or recurrent
– Swelling of the affected limb with or without
deformity

51. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Physical examination
• Multiple discharging sinuses
• Hyper-pigmentation of surrounding skin
• Skin excoriation may be present
• Puckering and adherence of soft tissue to the underlying
bone
• Bone deformity or non union in post traumatic
• Limb shortening if growing epiphysis is affected

52. Chronic osteomyelitis in a child

53. Chronic osteomyelitis in an adult

54. Osteomyelitis following fracture

55. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Investigations
– Radiological
• Plain x-ray
– Sequestra- indicating areas of necrotic bone surrounded by a
dense involucrum
– A sizeable length of the diaphysis may be devitalized and
encased in a thick involucrum
– There may be pathological fracture
• A sinogram may help to localize the site of infection
• CT and MRI
– Useful in planning operative treatment:
– Will show
» the extent of bone destruction
» reactive oedema
» hidden abscesses and sequestra

56. Radiographic features of chronic osteomyelitis

57. Radiographic features of chronic osteomyelitis

58. A sinogram

59. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Investigations
– Laboratory
• Culture and sensitivity of specimen from discharging
sinus
• FBC + diff
• C- reactive protein
• ESR may be high during acute flares
• Biopsy specimen for histology and microbiological
studies

60. CLASSIFICATION OF COM
• Cierny and Mader Staging System for Chronic
Osteomyelitis

61. Anatomic classification of COM

62. CLASSIFICATION OF COM
Cierny and Mader Staging System for Chronic

63. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Difficult to eradicate completely
– Multifaceted approach
– Goal- Eradication of the infection by achieving a
viable and vascular environment
– Principles
• Antibiotic therapy
• Treatment of co morbidities
• Surgical debridement
• Dead space management
• Soft tissue care

64. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Antibiotic therapy
• To suppress the infection and prevent its spread to healthy
bone
• To control acute flares
• Choice- microbiological studies
• Must be able to penetrate sclerotic bone
• Should be non toxic with long term use

65. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Antibiotic therapy
• Common antibiotics
– Clindamycin
– Fusidic acid
– Cephalosporins
– Fluoroquinolones
– Rifampicin
– Vancomycin in MRSA
• Administered for 4-6 weeks before considering surgical
intervention

66. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Treatment of co morbidities
• Optimization of blood sugar in diabetic patients
• Cessation of smoking
• Treatment of liver or renal malfunction
• Nutritional rehabilitation
• Correction of anaemia

67. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Surgical debridement
• A waiting policy/period
• Indication
– Intractable wound
– Failure of antibiotic treatment
– Clear evidence of sequestrum
– Infected and/or non united fracture
– Presence of foreign implant

68. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Surgical debridement
• Surgery is done when
– Acute flare has subsided
– Living bone can be distinguished from dead bone
– Mature Involucrum
• All the sinus tracts are injected with methylene blue 24
hours before surgery
• Sinus tracts are excised and laid open up to the cloaca
• Involves sequestrectomy and resection of scared and
infected soft tissues

69. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Management of dead space
• Antibiotics impregnated beads
– 2 staged procedure
– 1 staged procedure
• Papineau technique
– Radical excision of all the infected tissue
– Cancellous autogenous bone grafting mixed with
antibiotics and fibrin sealant
– Wound coverage by skin grafting and other techniques
• Archdeacon and Messerschmitt modification of the
Papineau technique

70. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Management of dead space
• Closed suction drains- Lautenbach technique
– Radical debridement
– Closed irrigation and suction drainage with antibiotic
solution
• Local muscle flap and skin grafting
• Microvascular transfer of muscle, myocutaneous, osseous,
and osteocutaneous flaps
• The use of bone transport (Ilizarov technique)

71. Lautenbach drainage system

72. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Soft tissue cover
• Small defects- split thickness skin grafts
• larger wounds -local musculocutaneous flaps, or free
vascularized flaps

73. MANAGEMENT OF CHRONIC OSTEOMYELITIS
• Treatment
– Adjunctive therapy
• Hyperbaric oxygen
• Use of growth factors
– Bone morphogenic proteins (BMP)
– Plasma rich peoteins (PRP)
• Physical energy modalities
– Pulsed electromagnetic field (PEMF)
– Ultrasound

74. COMPLICATION OF CHRONIC OSTEOMYELITIS
• Pathologic fracture
• Acute exacerbation of chronic disease
• Deformity
• Growth disturbance
• Amyloidosis
• Epithelioma/malignant transformation

75. PECULIARITIES
• Poor socio-economic conditions
• Late presentation

76. CONCLUSIONS
• The key to successful management is early
diagnosis, appropriate antimicrobial and surgical
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

77. REFERENCES
• Louis Solomon et al; Infections, in Apley’s System
of Orthopaedics and Fractures, 9th ed. 2010; 2:
29-41
• John Ebenezer; Osteomyelitis, in Textbook of
Orthopaedics, 5th ed. 2010; 38:540-550
• O. Popoola; Acute and chronic infections of bone
and joints, in Principles and Practice of Surgery
in the Tropics including Pathology, 5th ed. 2015;
54:1136-1140

78. REFERENCES
• Gregory D. Dabov; Osteomyelitis, in Campbell’s
operative orthopaedics, 12th ed. Vol. I, 2013;
21:725-747
• S. C. Goel; Pyogenic haematogenous
osteomyelitis, in Textbook of orthopaedics and
trauma, 2nd ed. Vol. I, 2008; 27:249-267
• Martin McNally et al; infections of the bone and
joints, in Bailey and Love’s Short Practice of
Surgery, 26th ed. 2013; 40: 541-549