Acute osteomyelitis-1.pptx by Marian Afful-Eshun

Acute osteomyelitis, presented by Marian Afful-Eshun, surgical resident cape coast teaching hospital, Ghana

1. ACUTE OSTEOMYELITIS PRESENTED BY MARIAN AFFUL-ESHUN 1

2. Outline of presentation Introduction History Epidemiology Relevant anatomy Classification Risk factors Microbiology Pathophysiology Biofilm formation in osteomyelitis Principles of management Differential Diagnosis Prognosis Complications conclusion 2

3. INTRODUCTION Definition: it is an inflammatory condition of the bone and bone marrow, usually caused by infection, leading to progressive bone destruction, necrosis and new bone formation. The term osteomyelitis was coined by a French surgeon Auguste Nelaton in 1844. Derived from the Greek words: Osteon: Bone Myelos : marrow Itis: inflammation 3

4. introduction It remains a challenging condition in orthopaedic practice due to difficulty in diagnosis, complex surgical and medical management, high recurrence rate and the cost burden of management. Effective management requires a multidisciplinary approach 4

5. HISTORY The oldest known evidence of osteomyelitis is from a Permian reptile's fractured spine, which lived 250–291 million years ago. In 460–370 BC, Hippocrates recognized that bone fractures could lead to infection. In 1773, William Bromfield published his observations of " abcessus in medulla", which referred to infected fatty tissues within the bone's inner cavity. In 1844, Auguste Nélaton coined the term "osteomyelitis" to describe a bone infection. 5

6. history Pre-antibiotic era : Treatment for osteomyelitis was surgical and included debridement, saucerization, and wound packing . Adjunctive tpies : Adjunct therapies included irrigation with Dakin's solution, maggot therapy, and instillation of bacteriophage cocktails into the surgical space In the 1940s, the introduction of penicillin improved the mortality rate for staphylococcal osteomyelitis from around 30% to 10%. Early 20 th Century: The clinical differentiation between acute and chronic osteomyelitis began to emerge. . 6

7. EPIDEMIOLOGY Globally an estimation of 2-5 cases per 10,000 persons occur annually. Accounts for approximately 20% of all bone infections in orthopaedic practice. The burden is higher in low income and developing countries due to poor hygiene, high rates of trauma and open fractures which are poorly managed, poor access to health. In high income countries they are mostly post traumatic, post surgical or prosthetic related. 7

8. Children between 5-15yrs are commonly affected by acute hematogenous osteomyelitis( metaphyses of long bones being the most afftected ) In adults its mostly post traumatic or contigious spread from soft tissue infections( eg diabetic foot ulcers, vascular ulcers etc ), prosthetic joints. Males are most commonly affected (2:1) Recurrence rate of 10-30% in chronic osteomyelitis treatment 8

9. EPIDEMIOLOGY- CCTH 179 cases of osteomyelitis was recoreded between 2020-2024, with 122(68.2%) cases being males and 57cases (31.8%). M:F ratio 2:1 Age group(years) Cases 0-9 39 10-19 54 20-29 21 30-39 20 40-49 14 50-59 13 60-69 14 70-79 3 80-89 1 9

10. Epidemiology- CCTH Commonly affected bones Bone Cases Tibia 22 Femur 21 Humerus 7 Foot 6 Radius 5 vertebra 1 unspecified 117 10

11. RELEVANT ANATOMY 11

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15. Classification of acute osteomyelitis WALDVOGEL CLASSIFICATION OF OSTEOMYELITIS(1970) The duration - acute, subacute and chronic Route of infection – hematogenous , contigious , direct inoculation Vascular insufficiency-diabetes mellitus, peripheral vascular disease, venous/arterial ulcers 15

16. Routes of infection Hematogenous spread: most common in children, bacteria seed into bone via the blood stream especially at the metaphyseal region of long bones in children Contiguous spread: usually from adjacent soft tissue infection, ulcers or trauma. Commonly seen diabetic foot ulcers, pressure sores and chronic wounds Direct inoculation: open fractures, penetrating injuries, post operative infections( orif , implants, prosthesis) 16

17. Cierny mader classification of osteomyelitis Anatomical type TYPE CHARACTERISTICS I Medullary osteomyelitis II Superficial osteomyelitis III Localised osteomyelitis IV Diffuse osteomyelitis Physiological class A Good immune system and delivery BL Compromised locally BS Compromised systemically C Treatment worse than disease, not surgical candidate 17

18. Factors affecting physiological class systemic local Malnutrition Renal or hepatic failure Diabetes mellitus Chronic hypoxia Immunosuppression Extremes of age Immunodefeciency Tobacco abuse Alcohol abuse malignanacy Chronic lymphedema Venous stastis Major vessel compromise Arteritis Extensive scarring Radiation fibrosis Small vessel disease neuropathy 18

19. Anatomical classification 19

20. Predisposing factors systemic local Diabetes mellitus Open fractures Peripheral vascular disease Prosthetic implants Sickle cell disease Chronic ulcers Iv drug use Peripheral neuropathy Immunosuppression(HIV, steroid use, chemotherapy) malnutrition 20

21. MICROBIOLOGY PATIENT POPULATION IMPLICATED ORGANISMS Neonates and infants <4months S. aureus, Group B streptoccocsus , E.coli 4mon- 4yrs S.aureus , Kingella Kingae , Group A streptoccus , E.coli >4yrs- adolescents S. aureus, Group A streptococcus, H. Influenzae , E.coli Adults S. aureus, E.coli, streptococcus spp Atypical Presentations Sexually active Niesseria gonorrhoeae Sickle cell anaemia Salmonella spp IV drug users Pseudomonas Parenteral nutrition, immunosuppression Fungal: aspergillus, candida Diabetic foot/vascular ulcers polymicrobial (s. aureus, s. epidermidis, pseudomonas, E. coli, proteus , anaerobes) Prosthetic joint infections s. aureus, s. epidermidis, gram negative bacilli Mycobacterium osteomyelitis mycobacterium tuberculosis, commonly affects the vertebrae( potts disease) 21

22. Natural History of Untreated Acute Haem . OSM Inflammation ( within 24hrs ) Bacterial seeding → an acute inflammatory reaction in the bone medulla + vascular congestion (transudation )  endosteal vessels occlusion(onset of ischaemia ) & inflammation of bone tissue The intraosseous /intramedullary pressure rises steeply (because of rigid bone lamellae) causing constant and intense pain; worsening bone ischaemia , intravascular thrombosis, septic embolisation & PMN infiltration Suppuration ( between 48 & 72hrs) Pus forms within the medullary cavity, pressure increases within the medullary cavity due to the compact nature of the bone. It pushes along the Volkmann canals and Harvesian canal → subperiosteal abscess with longitudinal or circumferential periosteal stripping. Systemic responses set in Pathogenesis: 22

23. Pathogenesis 23

24. Pathogenesis 3. Late suppuration - Pus break through the periosteum and erode into surrounding soft tissue This usually occurs at naturally weak anatomical sites such a muscle attachments, where the periosteum is thin and also along fascial planes forming soft tissue abscesses. Pus may also track back into the bone through the volkmans canal Pus may also track into adjacent joints leading septic arthritis 24

25. Pathogenesis Bone necrosis ( by 7days ) Due to: - Ischaemia (from stasis, thrombosis & periosteal stripping) - Bacterial toxins - Leucocytic enzymes - Osteoclastic activity Dead bone ( sequestrum ) of varying sizes are formed depending on amount of periosteum stripped. 25

26. Pathogenesis 5. Reactive new bone formation, involucrum ; by day 14 New bone forms on viable surfaces in the bone diaphysis and from the deep layers of the stripped periosteum . Less commonly seen in adult patients 6. Resolution/ chronicity Bone debris may be phagocytosed by macrophages and osteoclasts.. If there is poor infection control and persistence of sequestrum , it progresses to chronic osteomyelitis 26

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28. Pathogenesis Acute Hematogenous OSM The pathological picture varies depending on the patient’s age, the site of infection, the virulence of the pathogen and the host response. In infants Infection can reach the epiphysis through transphyseal vessels. Spread to adjacent joints common. In adults Spine is most frequently involved, then flat bones, less common in long bones. Growth-plate-barrier not present in long bones( Adults lack physis ). Metaphyseal vessels anastomose with epiphyseal vessels. Joint involvement is more common. Also periosteum not as tough as in children. Pus easily breaks through. No extensive tracking/stripping. 28

29. 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 29

30. 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. 30

31. Pathogenesis: Trueta staging of Acute Haem . OSM Three stages were described by Trueta & Morgan in 1954 for early mgt of the disease. Stage 1 ‘Boil’ in bone. Severe and constant pain around lesion & point of max. tenderness on exams. No redness or swelling or heat or fluctuation. Stage 2 Pus in medullary & subperiosteal space. Symptoms & signs more marked. Fever, malaise, general aches & pains appear. Stage 3 Pus in soft tissues. Acute local signs( rubor et tumor, calorie etc.) now present. 31

32. Stages of Biofilm formation in osteomyelitis Initial attachment: reversible binding by weak forces Irreversible adhesion: strong binding via adhesions Microcolony formation(early biofilm growth) Biofilm maturation Dispersion ( detachement / seeding ) 32

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34. Principles of management Multidisciplinary approach ( orthopaedic , plastic, infectious disease, microbiology, physiotherapy) Goals of management Eradicate infection Preserve or maximize function Prevent progression to chronic osteomyelitis Prevent recurrence 34

35. History Physical examination Investigations: imaging, laboratory, biopsy Treatment Rehabilitation 35

36. history Clinical presentation Acute phase Presenting complaint: localized bone pain(abrupt onset, becomes worse over days), swelling, erythema and reduced function or mobility of the limb . Risk factors: hx recent of systemic illness, hx of trauma, open fractures, DM, iv drug use, chronic ulcers, prosthetic implants, sexual partners Systemic symptoms: fever, chills, malaise, irritability, poor feeding, dizziness, palpitations, easy fatiguability , chronic cough, contact with persons with chronic cough, weight loss, night sweats 36

37. Physical examination General examination: signs of chronic illness(wasting, anemia), fever, tachycardia . Systemic examination Status localis : Inspection: swelling, erythema, shiny skin Palpation: differential warmth, localized tenderness, Range of motion: painful, restricted in adjacent joints Neurovascular examination: assess distal pulses, crt , nerve involvement( esp if surgery/ trauma related) 37

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39. Investigations: Lab studies Leukocyte count (WBC) Erythrocyte sedimentation rate (ESR) C-reactive protein Liver function test( Albumin) Blood cultures Microbiology. (gold-standard is bone culture) Histopathology 39

40. Investigation: Imaging Role of imaging in management of osteomyelitis Confirm diagnosis when clinical suspicion exists Define extent of disease: bone, soft tissue and joint involvement Guide management: surgical planning, biopsy site selection Monitor response to therapy and detect recurrence 40

41. Imaging modalities in osteomyelitis Modality Earliest detection sensitivity specificity findings strengths limitations X-ray (First line) 7-14 days Low (43-75%) Moderate (75-83%) >7-14days: soft tissue swelling, loss of fat planes, periosteal reaction, lytic areas, cortical destruction Chronic: sequestrum , invoulucrum , cloaca, sinus tract Cheap, readily available Poor early detection, limited soft tissue detail Ultra- sound Early Soft tissue stage Variable (50-80%) variable Subperiosteal abscess collection Joint effusion in adjacent septic arthritis Guides aspiration/ biopsy Cannot assess intramedullary or cortical bone involvement 41

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45. Imaging modalities in osteomyelitis Modality Earliest detection sensitivity specificity findings strengths limitations CT scan Days -weeks Moderate (65-85%) High (85-95%) Cortical disruption, abscesses and sinus tracts, mineralized sequestrum , involurum Better cortical bone detail Useful in surgical planning Radiation exposure Less sensitive for marrow/soft tissue changes MRI Gold standard for early detection 24-48hrs High (>90%) High (>80%) T1 shows low marrow signal T2/STIR shows high marrow signal hence detecting abscesses and soft tissue oedema Post contrast: rim enhancing abscess Able to detect marrow/soft tissue involvement Costly Contindicated in implants and pacemakers 45

46. CT image of osteomyelitis in an 11 yr old 46

47. MRI images 47

48. Imaging modalities in osteomyelitis Modality Earliest detection sensitivity specificity strengths limitations Bone scintigraphy 2-3 days8 High (2-100 %) Low (25-50%) Early detection, Whole body scan for multifocal lesions Poor specificity (tumor, trauma, arthritis) PET scan 2-3 days Very high >95% Very high >95% Excellent in chronic OM, PJI Multifocal dx Expensive Not readily available Labelled leukocyte scan 2-3 days High 80-90% High 80-90% More specific Limited availability Labor intensive 48

49. Treatment of acute osteomyelitis Antibiotic therapy is the main stay of treatment. Empirical antibiotics are started until culture and sensitivity results are ready based on blood culture or bone aspirate culture results Samples for culture and sensitivity should be taken before antibiotics are initiated Duration of therapy: IV antibiotics for 2 weeks Oral antibiotics 4 weeks 49

50. Empirical antibiotics Risk group/risk factor Likely pathogens Empiric antibiotic of choice Neonates (<1month) S. aureus, Group B strep, Gram negative bacilli(E. Coli) Oxacillin or naficillin + cefotaxime Children( 1-18months) S. Aureus(MSSA/MRSA) Streptococcus spp Cloxacillin /cefazolin add vancomycin if MRSA is prevalent Adults ( with no other risk factors) S. Aureus(MRSA<MSSA) Naficillin / oxacillin / cefazolin (MSSA) Vancomycin(MRSA risk) Sickle cell disease S. aureus, salmonella spp Ceftriazone or fluoroquinolone(ciprofloxacin) +/- vancomycin IV drug users MRSA, pseudomonas aeruginosa Vancomycin+/- ceftazidime /piperacillin tazobactam.pol Post traumatic/post surgical Polymicrobial ( gram positive,gram negative, anaerobes) Vancomycin + pipercillin-tazobactam / carbapenem Immunocompromised/ DM Polymicrobial , including MRSA and gram negatives Vancomycin+cefepime /piperacillin- tazobactam 50

51. Supportive treatment 1. pain control: NSAIDS, paracetamol, opiods 2. immobilization: splints, braces or traction to reduc pain and prevent fracture 3. nutritional support: high protein and high calorie diet promotes healing, correct vit D and calcium deficiency if present, iron, vit c and zinc supplementation in chronic disease or anaemia 4.Hydration and electrolyte balance 5.management of comorbidities: screen and manage SCD, immunodeficiency, malnutrition, optimize glycemic control in DM 6. physiotherapy and Rehabilitation: prevent joint stiffness and muscle wasting. Gradual return of function once acute infection resolves 51

52. Indications for surgery in acute osteomyelitus Abscess formation: subperiosteal , intramedullary or soft tissue abscesses. Imminent complications: impending pathological fractire , compartment syndrome, neurovascular compromise. Diagnostic uncertainty: biopsy is done to confirm diagnosis and obtain samples for culture and sensitivity 52

53. Surgical procedures in acute osteomyelitis Drainage of abscesses: soft tissue or subperiosteal abscess vacuation relieves pressure and reduces bacterial load Cortical window and intramedullary drainage: small cortical window drilled to decompress intramedullary pus Debridement: removal of necrotic soft tissue and bone if already formed, prevents progression to chronic osteomyelitis Biopsy/culture: bone biopsy for histopathology and culture and sensitivity Skeletal stabilization: if the bone is weak and there is risk of pathological fracture, external fixation or a splint can be applied to stabilize the bone 53

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55. Prognosis With early diagnosis + appropriate antibiotics, most patients achieve complete recovery; prognosis worsens with delayed treatment and complications. Favorable prognostic factors: Prompt initiation of antibiotics Localized infection without abscess or necrosis Good immune status and absence of comorbiditis 55

56. 2. Poor prognostic factors Delayed diagnosis and treatment(>2weeks) Presence off sequestrum or extensive bone necrosis Immunocompromised state: HIV, malignanacy Comorbidities: SCD, DM, malnutrition Infections with resistant organisms Complications: pathological fractures, joint involvement, growth plate involvement, sepsis, progression to chronicity 56

57. Differential diagnosis Acute febrile illness: malaria, URTI, Septic arthritis Cellulitis Pyomyositis Ewing sacorma Osteosarcoma Stress fractures/ traumatic bone injury Bone infarction in SCD patients 57

58. Complications of acute osteomyelitis 1. local complications Abscess formation Sequestrum formation: nidus for chronic osteomyelitis Pathological fractures due to weakened bone Growth disturbances: when the physeal plate is affected this could lead to limb length discrepancy and angular deformities. 2. Functional complications: a. chronic pain and joint stiffness b. Muscle wasting c. Loss of function or disability in severe case 58

59. 3. systemic complications sepsis/septic shock Bacteremia which can lead to secondary infections such as septic arthritis, pneumonia etc. 59

60. Conclusion Early diagnosis and treatment is critical to prevent progression to chronicity and complications Prompt iv antibiotics remain the cornerstone of treatment Surgical decompression and debridement is indicated when abscess, necrosis or poor response to antibiotics occurs Supportive care must be given and comorbidities managed appropriately Prognosis is good with timely management 60

61. References Apleys system of orthopaedics Ortho bullets AO surgery reference BAJA 61

62. Thank You 62