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BONE INFECTIONS

OSTEOMYELITIS
Infection of bone and bone marrow caused by direct inoculation or by blood borne organisms.
Acute hematogenous osteomyelitis Acute osteomyelitis Chronic osteomyelitis Subacute osteomyelitis Sclerosing Osteomyelitis Multifocal Osteomyelitis Osteomyelitis with unusual organisms

BONE INFECTIONS
OSTEOMYELITIS Acute hematogenous osteomyelitis

BONE INFECTIONS
OSTEOMYELITIS Acute hematogenous osteomyelitis

BONE INFECTIONS
OSTEOMYELITIS Acute hematogenous osteomyelitis

BONE INFECTIONS
OSTEOMYELITIS Acute hematogenous osteomyelitis

BONE INFECTIONS
OSTEOMYELITIS
Acute hematogenous osteomyelitis Pathology 1. Inflammation 2. Suppuration 3. Necrosis 4. New bone formation 5. Resolution

BONE INFECTIONS
OSTEOMYELITIS Acute hematogenous osteomyelitis Pathology 1. Inflammation Acute inflammatory reaction with vascular congestion Rise in intra-osseous pressure causing intense pain 2. Suppuration At 2-3 days pus forms within the bone and forces its way down the haversian canals, surface, adjacent joint or into the soft tissues Vertebral infection can spread through the end plate, disc and into the next vertebral body

BONE INFECTIONS
OSTEOMYELITIS Acute hematogenous osteomyelitis 3. Necrosis At 7 days, rising pressure, vascular stasis, infective thrombosis and periosteal stripping compromise the blood supply resulting in a sequestrum 4. New bone formation At 10-14 days this forms from the deep surface of the stripped periosteum forming the involucrum 5. Resolution With release of the pressure and appropriate antibiotics healing can occur. There may be permanent deformity

BONE INFECTIONS
ACUTE HEMATOGENOUS OSTEOMYELITIS Clinical features: Children (invariably) Pain, malaise, fever Limp or not weight bearing Infants Failure to thrive, drowsiness, irritable Adults The commonest site is the thoracolumbar spine (Batson's venous complex from the pelvis) Other bones involved especially in DM, IVDA, immunosuppressed

BONE INFECTIONS
ACUTE HEMATOGENOUS OSTEOMYELITIS Examination:

Local erythema Swelling and tenderness indicates that the pus has broken through the periosteum

BONE INFECTIONS
ACUTE HEMATOGENOUS OSTEOMYELITIS Investigations: FBC incr. WCC Differential shows incr. neutrophils ESR may be normal within the first 48 hours but rises rapidly and may exceed 100mm/hr CRP raised Blood cultures Positive in 50% of cases ASO titres raised in 50% Antibodies to acid cell wall of S.aureus sensitivity 82% in acute osteomyelitis

BONE INFECTIONS
ACUTE HEMATOGENOUS OSTEOMYELITIS Radiographic studies: Normal in the first 10 days Soft tissue swelling - 2-3 days adjacent to the metaphysis, with displaced fat planes Demineralization - 10-14 days, at the site of the infection New bone formation at the surface 10-14 days

BONE INFECTIONS
ACUTE HEMATOGENOUS OSTEOMYELITIS Bone scan 99mTechnetium Positive before any x-ray changes (24-48hrs of infection) 67Gallium Uptake related to the local accumulation of PMN 111Indium Reported specificity 86% and sensitivity 83% and accuracy 83% MRI Intra and extra osseous changes will be detected early but are not diagnostic

BONE INFECTIONS
ACUTE HEMATOGENOUS OSTEOMYELITIS Aspiration and biopsy This will yield a positive culture in 80% of cases

Pathogens S. Aureus in 60-90% of cases H. influenza (Hib) makes up 20% of cases under 4yrs

BONE INFECTIONS
MANAGEMENT Acute hematogenous osteomyelitis Antibiotic Infant < 1yr Grp B Streptococcus, S.aureus, H.influenza, E.coli Children 1-16 yr & No underlying disease S.aureus, Strep.pyogenes, H.influenza Sickle cell S.aureus, Salmonella Adults S.aureus, E.coli, Serratia marcescens, Pseudomonas aeruginosa

BONE INFECTIONS
OSTEOMYELITIS Acute hematogenous osteomyelitis

Minimum duration of treatment is 6 weeks 20% failure of treatment if antibiotics given for only 3 weeks Blood levels should be 8 times the minimum bactericidal level

Surgery

If clinical abscess formed or not settling within 48hrs of antibiotics. Incision and drainage of the affected area Drilling of bone is not recommended but any soft areas of bone can be probed Skin closed over a drain

BONE INFECTIONS
SUBACUTE OSTEOMYELITIS Patient presents with a painful limp, systemically well and may have no signs of local infection There may be signs of a subperiosteal collection, synovitis or pus within a joint X-rays show a well-established lesion in the bone Femur and tibia are by far the most common sites Blood tests WCC and ESR may be raised but in 50% cases tests are normal

BONE INFECTIONS
SUBACUTE OSTEOMYELITIS

Brodie's Abscess Commonly occur in the metaphyses of tubular bones but can also occur in flat bones, vertebral body and the diaphysis They are usually manifestations of subacute osteomyelitis

BONE INFECTIONS
CHRONIC OSTEOMYELITIS Etiology 1. Inadequately treated acute osteomyelitis 2. Haematogenous spread 3. Iatrogenic 4. Penetrating trauma 5. Open fractures 6. Contiguous focus infection, secondary to a breakdown in the overlying soft tissue e.g. vascular/neuropathic ulcer, DM 7. The adjacent soft tissues are always involved except in Brodies abscess

BONE INFECTIONS
CHRONIC OSTEOMYELITIS Causative organism

If secondary to acute osteomyelitis the organism is almost always S.aureus Following trauma S.aureus is most common but it may be polymicrobial Gram ve organisms are now isolated from ~50% of patients with osteomyelitis Animal bites pasturella multocida Human bites eikenella corrodens

BONE INFECTIONS
Treatment Principles Surgical debridement and bony stabilisation Control of dead space Soft tissue cover Antibiotics Surgical debridement Aim is to remove all dead and infected tissue and bone Send samples for Microscopy Culture Histology (0.5% will develop SCC, Marjolins ulcer)

BONE INFECTIONS
GARRS CHRONIC SCLEROSING OSTEOMYELITIS

Children and young adults, average age 16 years No necrosis or pus present Intense periosteal proliferation leading to bone formation Aetiology unclear but may be due to anaerobic organisms Local pain and tenderness in shaft of long bones Difficult to distinguish from primary osteogenic sarcoma No satisfactory treatment and antibiotic therapy does not affect course Recurrent for years then gradually subsides

BONE INFECTIONS
SEPTIC ARTHRITIS

In children septic arthritis can occur at any age 50% of cases occur in children under 5years and 30% of cases occur in children under 2years Hip most commonly affected in infants, and knee in older children 10% of cases will have more than 1 joint affected

BONE INFECTIONS
SEPTIC ARTHRITIS Route of spread Haematogenous Spread from metaphyseal osteomyelitis where the metaphysis is intra-articular Spread from contiguous soft tissue infection Direct inoculation

BONE INFECTIONS
SEPTIC ARTHRITIS

BONE INFECTIONS
SEPTIC ARTHRITIS Causative organism Under 2 years S.aureus, E.coli, Group B Strep, Haemophilus

2-16 years S.aureus, Strep. Pyogenes, Streptococci (C,G), Haemophilus 16-30 yearsover S.aureus, Strep. Pyogenes, N.gonorrhoea 30 years S.aureus, Streptococci (A,B,C,G,pneumon)

BONE INFECTIONS
SEPTIC ARTHRITIS Investigations FBC, ESR, CRP USS for detection of hip effusion XR may show subluxation or dislocation Diagnostic aspiration Send sample for Gram stain and microscopy Septic arthritis strongly suspected if the WCC is >50,000mm-3 with 90% PMN, even if the cultures are negative Culture

BONE INFECTIONS
SEPTIC ARTHRITIS Treatment IV antibiotics broad spectrum aimed at best guess first then adjusted according to microbiology results Length of treatment (minimum) IV 2 weeks Oral child 2-4 weeks Adult 4-6 weeks

BONE INFECTIONS
TREATMENT Surgical drainage Hips should always be drained surgically Best approach anterolateral Arthroscopic washout acceptable in the knee but open drainage may be required Complications Despite alarming XR changes there is a favorable outcome in many children AVN Coxa vara