management of acute osteomyelitis (1).pptx

management principles of acute osteomyelitis

1. MANAGEMENT OF ACUTE OSTEOMYELITIS DR UDOGU PRINCEWILL MEDICAL OFFICER, ORTHOPEDIC SURGERY UNIT ASOKORO GENERAL HOSPITAL

2. Introduction Aetiology Pathogenesis Management Long term management Follow up care Prevention Conclusion References OUTLINE

3. 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 INTRODUCTION

4. EPIDERMIOLOGY Worldwide , childhood acute haematogenous osteomyelitis is commoner Incidence <3/100,000 in Europe 43-200/ 100,000 children in Africa Accounts for at least 1% of cases in most hospitals in Nigeria Much higher among less affluent populations Male: female 2:1 Commonly affects the long bones, femur and tibia most commonly affected long bones Lower limbs > upper limbs INTRODUCTION

5. RELEVANT PHYSIOLOGIC ANATOMY Penetration of physeal cartilage by the epiphseal and metaphyseal vessels starts in the first 6-9 months of life In children, the epiphyseal arteries are crucial for longitudinal bone growth while the metaphyseal arteries support bone growth and remodelling in the metaphysis where the growth plate is located. Nutrient arterial system contribute 50-70% of blood supply to adult long bones INTRODUCTION

6. This refers to a high pressure vascular network within long bones that supplies blood to the inner portion of the bone, including the marow cavity and bone cortex . It is critical for bone health, growth and repair. The nutrient arterial system involves the Main arteries , Intramedullary branches , The Haversian and Volkmann canals and the Periosteal artery system The nutrient arteries are generally derived from an adjacent major systemic artery. A nutrient artery enters a bone through its nutrient foramen, which leads into a nutrient canal, and once the vessel reaches the medullary cavity, it divides into ascending and descending medullary branches forming the central arteries. NUTRIENT ARTERIAL SYSTEM

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

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

9. Based on duration Acute (2-4 weeks) Sub-acute Chronic (>4 weeks) Based on Mechanism of infection Exogenous- trauma, surgery, foreign bodies i.e implants, prosthetics Haematogenous (via systemic circulation )- otitis media, thrombophlebitis , abscess, infective endocarditis Based on Type of infecting organism Pyogenic ( bacterial) Non pyogenic (fungal, viral or non infectious) INTRODUCTION CLASSIFICATION OF OSTEOMYELITIS

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

11. Microbiology Sickle cell patients Staph aureus Salmonella spp Immunocompromised /iv drug users Staph aureus H. influenzae AETIOLOGY

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

13. PREDISPOSING FACTORS Local factors Trauma Old scar Poor circulation Chronic bone or joint diseases ( compromising blood supply, weakens immune system, pre existing inflammation eg osteoarthritis, rheumatoid arthritis, malignancies, sickle cell disease, peripheral vascular disease) Presence of foreign bodies- implants, prosthesis Systemic factors Malnutrition Co-morbidities (diabetes mellitus , hypertension, dyslipidemias ) Steroids/ immunosupression Very young and very old AETIOLOGY

14. ROUTES OF INFECTION Haematogenous Suppurative infections Infective Endocarditis URTI ( otitis , pneumonia) UTI Drug addicts ( Iv drug administration) Direct contamination Trauma Penetrating wounds Contamination of compound fracture Surgery PATHOGENESIS

15. 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 PATHOGENESIS

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

17. 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) PATHOGENESIS

18. The pathologic process involves Inflammation Suppuration Necrosis New bone formation Resolution/ Chronicity PATHOGENESIS

19. Inflammation The earliest change in the metaphysis First 24 hours Vascular congestion within venous sinusoids Polymorphonuclear leukocyte ( neutrophils ) infiltration Exudation (fluids, proteins an blood cells leak into surrounding tissue) By 2-3 day if not treated with antibiotics  Intraosseus pressure  intense pain  intravascular thrombosis  ischemia PATHOGENESIS

20. Suppuration 4-5 days Pus formation (purulent exudates) Pus spreads via Volkmann canals Children – subperiosteal abscess, Epiphysis, joint space Adult- localised to the medullary cavity soft tissue In vertebrae it spreads via end plates and discs to adjacent vertebral bodies PATHOGENESIS

21. Spread of pus in haematogenous osteomyelitis

22. Necrosis Bone death by the end of a week Bone destruction Toxins I schemia Epiphyseal plate injury Sequestrum formation small  removed by macrophage, osteoclast large  remained PATHOGENESIS

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

24. 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 PATHOGENESIS

25. 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 PATHOGENESIS

26. Early intervention in acute osteomyelitis is crucial to prevent long term complications and to improve outcomes the importance of early intervention in acute osteomyelitis includes Prevention of permanent bone damage - if untreated or indequately treated, significant bone damage, including bone loss and necrosis Preventing complications- chronic osteomyelitis , septic arthritis, soft tissue infections, pathological fractures Reducing risk of systemic infections Improving patient outcomes - better prognosis, improvement of qualityof life of patients, minimize duration of illness, reduce the risk of long term sequelae Minimize treatment needs - reduce the need for extensive surgical intervention and prolonged antibiotic courses IMPORTANCE OF EARLY INTERVENTION

27. CLINICAL ASSESSMENT HISTORY Presentation is influenced by the age of the patient Infants High index of suspicion Birth difficulties (prolonged labor, instrumental delivery, obstructed labor) Umbilical artery catheterization Refusal of feeds Failure to thrive Fever MANAGEMENT OF ACUTE OSTEOMYELITIS

28. 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 Ear discharge ( Otitis ) Sore throat Abscess MANAGEMENT OF ACUTE OSTEOMYELITIS

29. History Adults Pain in affected limb Fever Malaise Swelling around affected limb History of prior surgical intervention MANAGEMENT OF ACUTE OSTEOMYELITIS

30. Physical examination General signs Dehydration Palor Pyrexia Tachycardia Features of shock ( low blood pressure, rapid and weak pulse, rapid and shallow breathing, pale and clammy skin) Systemic features may be mild in very elderly and immunocompromised MANAGEMENT OF ACUTE OSTEOMYELITIS

31. Local signs- usually late signs Limb held still Limb Tenderness Restricted joint movement Swelling Multiple sites Lymphadenopathy ( axillary , epitrochlear , inguinal, femoral, popliteal lymph node enlargement) MANAGEMENT OF ACUTE OSTEOMYELITIS

32. Investigations Imaging studies incude the following- Plain X ray Ultrasound scan Mri Ct scans Radioisotope studies (Radionuclide scanning) Plain x-ray (AP/Lat) Features usually manifest after 2 weeks Feature of soft tissue swelling Patchy rarefaction of the metaphysis (areas of reduced bone density within the metaphysis ) Faint extra cortical outline- new bone formation ( involucum ) Periosteal thickening Combination of regional osteoporosis with a localized area of reduced density MANAGEMENT OF ACUTE OSTEOMYELITIS

33. Radiographic features of acute osteomyelitis

34. Ultrasound scan Detection of subcutaneous/ subperiosteal fluid collection Hypoechoic widening of periosteal space Flaccid periosteum Radionuclide scanning (bone scintigraphy )- uses radioactive tracers injected into the bloodstream and taken up by bone. The distribution of this tracer is then projected through images to show areas of increased bone activity which could be a sign of an ongoing infection. Detects signs of inflammation as early as 24-48hrs Focal hyperperfusion , focal hyperemia and focally increased bone uptake of radioactive tracer Highly sensitive but has relatively low specificity MANAGEMENT OF ACUTE OSTEOMYELITIS

35. Ultrasound scan features of acute osteomyelitis

36. Bone scintigraphy features of acute osteomyelitis

37. Radiological MRI (Magnetic Resonance Imaging) Indicated for involvement of axial skeleton Shows Bone marrow inflammation Differentiates between soft tissue infection and osteomyelitis Extremely sensitive but low specificity CT SCAN (Computed tomography scan) Useful in detecting subtle changes in bone marrow which may be missed on plain radiographs For assessing the extent of bone and soft tissue involvement Key features include soft tissue swelling, periosteal reaction, cortical irregularty /destruction, bone marrow changes, soft tissue edema, abscess formation MANAGEMENT OF ACUTE OSTEOMYELITIS

38. Laboratory Investigations Laboratory investigations are generally non specific for osteomyelitis and should not be used alone for diagnosis Blood culture - positive blood cultures significant in diagnosis 3 different samples 2hrs apart or at the height of fever Microscopy, Culture and sensitivity (MCS) of available aspirate Bone Biopsy - if blood cultures are negative and imaging suggests osteomyelitis , a bone biopsy can help confirm the diagnosis and identify the causative organism. FBC + differentials – leukocytosis >11,000 cells/ ul (norm 4500-11000 cells/ ul ), Neutrophilia >7,700 cells/ ul ( norm 2500-7000 cells/ ul ) Anaemia MANAGEMENT OF ACUTE OSTEOMYELITIS

39. INFLAMMATORY MARKERS (CRP, ESR) C- reactive protein ( crp >10mg/dl) norm-0-10mg/dl ESR (males >15mm/hr, females >20mm/hr) A persistently normal CRP and ESR can help rule out acute osteomyelitis OTHERS Genotype - haemoglobinopathies ( hbss , thalassemia ) Serology - rvst , hbsag , hcv Blood glucose assessment- ( fbs (norm- 3.9mmol/l-5.6mmol/l), hba1c (norm- 4%- 5.6%))

40. E/U/CR - chronic kidney disease, patients undergoing haemodialysis at increased risk of developing osteomyelitis . Many antibiotics used in treatment of osteomyelitis can be nephrotoxic like aminoglycosides ( gentamicin ) and fluoroquinolones ( levofloxacin ) Urea (norm-2.5-7.8 mmol /l), creatinine ( norm- 62-106umol/l ) LFT Evaluates the livers ability to handle the demands of fighting off infection and support the treatment process Elevated ALP (Alkaline phosphatase , norm-40-129u/l ) -indicates bone damage

41. Elevated ALT ( Alanine transaminase , norm-7-55 u/l) and Elevated AST ( Aspartate Transaminase , norm- 8-48u/l) indicate liver inflammation or damage Elevated bilirubin (norm-0.1-1.2mg/dl) indicatesobstruction of bile flow or liver dysfunction Reduced serum albumin) (norm-3.5-5.5g/dl ) can indicate liver disease or malnutrition Lfts can also detect hepatotoxicity from certain drugs used to treat osteomyelitis like cephalosporins and penicillins .

42. Cellulitis Septic arthritis Pyomyositis Rheumatoid arthritis Sickle cell bone crisis Malignant tumour DIFFERENTIAL DIAGNOSIS

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

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

45. Supportive treatment Analgesics- NSAIDS like ibuprofen, diclofenac OR opioid analgesics like pentazocine Antipyretics- paracetamol , diclofenac , ibuprofen Rehydration- iv fluids Correction of anaemia if present Nutritional support- to boost immune system MANAGEMENT OF ACUTE OSTEOMYELITIS

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

47. 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 MANAGEMENT OF ACUTE OSTEOMYELITIS

48. 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 MANAGEMENT OF ACUTE OSTEOMYELITIS

49. Antibiotic therapy Neonates and infants Flucloxacillin + 3 rd generation cephalosporin ( ceftriazone ) Flucloxacillin + benzypenicillin + gentamicin Children and adults Flucloxacillin + fusidic acid or benzylpenicillin 3 rd generation cephalosporin can be used in cases of allergy to penicillin Ceftriazone + metronidazole + clindamycin Elderly Flucloxacillin + 2 nd or 3 rd generation cephalosporin Ceftriazone + metronidazole + Clindamycin MANAGEMENT OF ACUTE OSTEOMYELITIS

50. Antibiotic therapy Sickle cell disease patients Fluoroquinolones ( levofloxacin ) or 3 rd generation cephalosporin IV drug users and immunocompromised Fluoroquinolones ( Levofloxacin ) or 3 rd generation cephalosporin MANAGEMENT OF ACUTE OSTEOMYELITIS

51. Antibiotic therapy usually determined by likely pathogen Often requires initial broad spectrum coverage followed by targeted therapy based on culture and sensitivity results Initial emperical therapy - 3 rd generation cephalosporins + vancomycin / linezolid (gram + ve and grm – ve coverage) Staphylococcus aureus including MRSA - vancomycin or linezolid Gram negative organisms ( eg pseudomonas )- Clindamycin , meronidazole , cefepime , ceftazidime or other broad spectrum gram – ve antibiotics Streptococcus and enterococcus -penicillin G, clindamycin , vancomycin SELECTION OF ANTIBIOTICS BASED ON LIKELY PATHOGENS

52. The typical duration of treatmet for acute osteomyelitis is 4-6 weeks often administered intravenous initially and then transitioned to oral antibiotics Treatment may be shorter for children with acute osteomyelitis (2-3 weeks) but longer courses (8+ weeks ) may be necessary for patients with certain risk factors or chronic osteomyelitis DURATION OF TREATMENT

53. Treatment Surgical intervention Indications 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 MANAGEMENT OF ACUTE OSTEOMYELITIS

54. Surgical intervention Methods Open drainage ( Incision and drainage) Drilling Opening small bone window Post operative Splintage of the affected limb Post op antibiotics Follow up for at least one year MANAGEMENT OF ACUTE OSTEOMYELITIS

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

56. Regular follow up and monitoring- regular clinic assessment, repeat imaging if necessary, adjusting treatment based on response Monitoring for complications Monitoring for recurrence of infection Functional recovery- recovery of affected limb or joint to normal function Rehabilitation and physical therapy- rehabilitation back into the society and daily activities LONG TERM MANAGEMENT

57. It is crucial to minimize the risk of infection especially in individuals with increased vulnerability. These includes- Proper wound care Proper hand hygeine Proper management of medical conditions that weakens the immune system Additionally, seeking prompt medical attention for any concerning symptoms or infections is essential PREVENTION

58. The key to successful management is early diagnosis, appropriate antimicrobial administration and surgical intervention when necesssary A multi disciplinary approach is required, involving an orthopaedic surgeon, an infectious disease specialist, and a plastic surgeon in complex cases CONCLUSIONS

59. Louis Solomon et al; Infections, in Apley’s System of Orthopaedics and Fractures, 9 th ed. 2010; 2: 29-41 John Ebenezer; Osteomyelitis, in Textbook of Orthopaedics, 5 th 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, 5 th ed. 2015; 54:1136-1140 REFERENCES

60. Gregory D. Dabov ; Osteomyelitis, in Campbell’s operative orthopaedics, 12 th ed. Vol. I, 2013; 21:725-747 S. C. Goel ; Pyogenic haematogenous osteomyelitis, in Textbook of orthopaedics and trauma, 2 nd 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, 26 th ed. 2013; 40: 541-549 REFERENCES

61. THANK YOU