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Paediatric Orthopaedic Infections

Paediatric Orthopaedic Infections. Chris Dowding March 18 2013 CHEO Monday Rounds. Outline. Osteomyelitis Septic Arthritis CRMO. Osteomyelitis. Classification. Duration of Symptoms: Acute Osteomyelitis Subacute Osteomyelitis Chronic Osteomyelitis Mechanism of Infection: Exogeneous

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Paediatric Orthopaedic Infections

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  1. Paediatric Orthopaedic Infections Chris Dowding March 18 2013 CHEO Monday Rounds

  2. Outline • Osteomyelitis • Septic Arthritis • CRMO

  3. Osteomyelitis

  4. Classification • Duration of Symptoms: • Acute Osteomyelitis • Subacute Osteomyelitis • Chronic Osteomyelitis • Mechanism of Infection: • Exogeneous • open fractures • surgery (iatrogenic) • contiguous spread from infected local tissue • Hematogeneous

  5. Acute vs Chronic Osteomyelitis • Chronic • simultaneous presence of microorganisms and necrotic bone • Persistent infection lasting more than six weeks should be considered chronic

  6. Diagnosis • More common on boys • <1 year, 3-10 years • History: • PMHx: • Immunization record • Meds • Smoking • Pain, fever, drainage • Baseline Function • Duration and recurrence of symptoms • Trauma • Often present with history of trauma • Surgical history, Hardware

  7. Diagnosis • PE: • Integrity of the skin and soft tissue • Determine areas of tenderness • Assess bone stability • LLD • Allignment • Neurovascular status of the limb. • Labs: • ESR and CRP usually elevated • WBC usually normal

  8. Inflammatory Markers • ESR: • Peaks within 3 to 5 days of an infection • The value slowly returns to normal within 3 weeks following effective treatment • CRP: • In the presence of an inciting infection, CRP levels increase 1000-fold within 6 hours of onset and reach peak within 36 to 50 hours • Because of short half life of CRP (24-48 hours) and constant clearance rate, rapid resolution to normal commonly occurs within 7 days following effective treatment in uncomplicated cases. • Good negative predictor for lack of infection (87%)

  9. Challenges in Diagnostic Imaging • Radiographic changes delayed in acute osteomyelitis • Post traumatic changes • Bone altered by previous infections, or bone regeneration • Presence of metallic implants • Differentiating neuropathic bony changes

  10. Conventional Radiographs

  11. Conventional Radiographs

  12. Bone scintigraphy has been suggested to be a sensitive technique to screen for bone alterations caused by chronic osteomyelitis. Poor specificity • MRI is very sensitive for detecting bone alterations in the absence of metalic implants, but lacks specificity • PET has the highest accuracy for confirming or excluding the diagnosis of chronic osteomyelitis. • Leukocyte scintigraphy can be used with satisfactory diagnostic accuracy for detecting chronic osteomyelitis in the peripheral skeleton.

  13. Acute Hematogenous Osteomyelitis

  14. Acute Hematogenous Osteomyelitis • Most common in children • Bimodal distribution, generally affecting children younger than 2 years and children 8 to 12 years old • Predisposing factor: • localized trauma • chronic illness • Malnutrition • inadequate immune system

  15. Pathogenesis in Children • Generally involves the metaphysis • Inflammatory reaction can cause local ischemic necrosis of bone and subsequent abscess formation • As the abscess enlarges, intramedullary pressure increases causing cortical ischemia, which may allow purulent material to escape through the cortex into the subperiostealspace • If left untreated, this process eventually results in extensive sequestra formation and chronic osteomyelitis.

  16. Diagnosis • Pain and local tenderness are common findings • In infantsclinicalfindings may be minimal • Fever and malaise may or may not be present in the early stages of the disease • WBC count often is normal • ESR and CRP level usually are elevated

  17. Pathogenesis in Children • In children younger than 2 years, some blood vessels cross the physis and may allow the spread of infection into the epiphysis • Physis acts as a barrier that prevents the direct spread of a metaphyseal abscess into the epiphysis.

  18. Diagnosis • Standard radiographs generally are negative, but may show soft-tissue swelling • Skeletal changes, such as periosteal reaction or bony destruction, generally are not seen on plain films until 10 to 12 days into the infection • Bone scan or MRI • The causative organism can be identified in approximately 50% of patients through blood cultures • Bone aspiration • CT guided biopsy

  19. Septic Arthritis in setting of Acute OM • Generally seen only in infants and adults. • The physis acts as a barrier to spread • In children younger than 2 years • the common blood supply of the metaphysis and epiphysis crosses the physis and can allow spread of a metaphyseal abscess into the epiphysis and eventually into the joint • Skeletal maturity: • After the physes are closed, infection can extend directly from the metaphysis into the epiphysis and involve the joint Epiphyseal Separation

  20. Microbiology • Staphylococcus aureus • is the most common infecting organism found in older children • Pseudomonas • is the most common infecting organism found in intravenous drug abusers with osteomyelitis. • Fungal osteomyelitis • is seen increasingly in chronically ill patients receiving long-term intravenous therapy or parenteral nutrition • Salmonellaosteomyelitis • has long been associated with SC hemoglobinopathies. • This infection tends to be diaphyseal rather than metaphyseal Sickle Cell patient

  21. Treatment • Empiric antibiotics following local culture and blood culture • F/U cultures and sensitivities • The CRP should be checked every 2 to 3 days after the initiation of antibiotic therapy • If no appreciable clinical response to antibiotic treatment is noted within 24 to 48 hours, occult abscesses must be sought, and surgical drainage should be considered • Surgical indications: • the presence of an abscess requiring drainage • failure of the patient to improve despite appropriate intravenous antibiotic treatment.

  22. SubacuteHematogenous Osteomyelitis

  23. Clinical Presentation: • Symptoms usually of >2 weeks duration • Insidious onset and lacks the severity of symptoms • Systemic signs and symptoms are minimal • Mild-to-moderate pain is one of the only consistent signs suggesting the diagnosis • WBC generally normal • ESR elevated in 50% of patients • Blood cultures are usually negative • Bone aspirate or biopsy: • Pathogen identified in only 60% of the time • Radiographs and bone scans usually positive

  24. Pathogenesis • Is thought to be the result of increased host resistance along with decreased bacterial virulence • S. aureus and Staphylococcus epidermidis are the predominant organisms identified in subacute osteomyelitis

  25. Classification: • Type 1: • central metaphyseallesion; • Type 2: • eccentric metaphyseal lesion with cortical erosion • Type 3: • diaphysealcortical lesion • Type 4: • diaphyseallesion with periosteal new bone formation, but without definite bony lesion • Type 5: • primary subacute epiphyseal osteomyelitis • Type 6: • subacuteosteomyelitis crossing physis to involve metaphysis and epiphysis.

  26. Characteristics • Most common type in the pediatric population is the metaphyseal lesion • Second most common type is the epiphyseal lesion (Type V) • Despite crossing the physis, subacute osteomyelitis rarely causes permanent growth alteration

  27. Brodie Abscess • Generally appears as a lytic lesion with a rim of sclerotic bone • Before physeal closure, the metaphysis is most often affected. • S. aureus is cultured in 50% of patients; in 20%, the culture is negative

  28. Benign radiologic features associated with subacute OM • Lesions surrounded by sclerosis • Lesions crossing the growth plate • Lesions with serpentine shape or multiple cavities • Lesions in the epiphysis • A hole in bone with no surrounding destruction.

  29. All articles in the English literature on paediatric osteomyelitis were searched using MEDLINE, CINAHL, EMBASE, Google Scholar, the Cochrane Library and reference lists. A total of 1854 papers were identified, 132 of which were examined in detail. All aspects of osteomyelitis were investigated in order to formulate recommendations.

  30. Clinical Presentation

  31. Summary of imaging for osteomyelitis

  32. The causative organisms in paediatric osteomyelitis

  33. Non hematogeneous Osteomyelitis

  34. Acute Non hematogeneous OM • Etiology: • Open fracture • Microbial contamination after surgical management of a closed fracture • Contiguous spread from infected local tissue

  35. Challenges to Eradication of infection • Suboptimal condition of the local environment • Necrotic bone • Presence of devitalized tissues • Biofilm • Hardware • Presence of an unstable fracture • Soft-tissue envelope • Patient factors

  36. Microbiology • Staphylococcus aureus: • 65-70% of patients • Pseudomonas aeruginosa: • 2nd most common • 20-37% of patients • Osteomyelitis is often polymicrobial • 32-79% of patients • Immunocompromised patients: • Consider Atypical mycobacteris or fungi

  37. Treatment Principles • Surgical debridement • Necrotic bone • Devitalized tissue • Hardware: • Remove or Retain? • Local antibiotics • Systemic Antibiotics • Subsequent surgeries: • Soft tissue coverage

  38. Chronic Osteomyelitis

  39. Pathogenesis of Chronic OM • Sequestrum: • Compromised blood supply secondary to infection leads to bony necrosis • Resorption and revascularization is limited and ineffective, and the sequestrum (infected dead bone) is secluded from antibiotics and host defense mechanisms • Involucrum: • Reactive new bone is formed in an effort to contain the infection

  40. Principles of operative management • Débridement, • Skeletal stabilization • Administration of systemic and local antibiotics • Soft-tissue coverage • Management of un-united fractures and existing bone defects. • Multidisciplinary care: • Orthopaedics • Plastics • Infectious disease • Wound care • Physiotherapy • Home care

  41. Medical Management • Systemic Antibiotics • Infectious disease consult • PICC line • Based on culture and sensitivity results • Generally given for 4 to 6 weeks • Optimize host factors • Glycemic control • Nutrition • Smoking cessation • Hyperbaric Oxygen therapy

  42. Septic Arthritis • Most often hematogenous • Vs direct innoculation • Vs transepiphyseal spread from metaphyseal OM • 4:100000 children • Boys > girls • Causative agent • Staph. Aureus • Strep pyogenes • Strep pneumo • HIB used to be very common, still important in areas without vaccination • Frequency highest in young children

  43. Septic Arthritis • Presentation • Warmth • Swelling • Tenderness • Decreased ROM • Refusal to weight bear or use limb • Limp • pseudoparalysis • Usually hip or knee • Larger joints more common than small • One or more joints • If more, thinkg gonococci or meningococci • Presence of fever unreliable marker • 70% of cases • May have concurrent osteomyelitis

  44. Septic Arthritis • Hip • Neonates will have flexed, externally rotated limb

  45. Septic Arthritis

  46. Septic Arthritis • Work-up • Blood work • CBC • ESR • CRP • Most useful to follow response to treatment • Blood culture • Positive in 40-50% • Aspirate • Cell count • < 50 less likely but still possible • >50 more likely • > 100 very likely • Gram stain • Often no organisms seem • Culture • Only positive 70% • +/- general anesthesia • Depends on age and joint

  47. Septic Arthritis • X-ray • Not useful for acute setting • > 10 days • Ostepenia • Loss of jt space • Soft tissue swelling • Ultrasound • Can detect effusion • Ultrasound guided tap • MRI if diagnosis unclear or OM suspected • No real gold standard

  48. Septic Arthritis • DDX • Most important is transient synovitis • Reactive inflammation due to other infection • Differentiation • Fever • Inability to WB • ESR > 40 • WBC > 12 • CRP is good negative predictor • If less than 1.0 then 87% not septic arthritis • If > 2 and fever > 38 than strong predictor

  49. Treatment • Closed needle aspiration vs. arthroscopy and drainage • No good evidence • Experience of surgeon

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