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BONE AND JOINT INFECTIONS นพ. ยอดปิ ติ ตั้งตรงจิตร กลุ่มงานศัลยกรรมกระดูก โรงพยาบาลแพร่ 3 ตุลาคม 2555 1 SEPTIC ARTHRITIS 2 Septic Arthritis • Epidemiology ~2 to 10/100,000 in general population ~30-40/100,000 in RA ~40-68/100,000 in joint prostheses • 2 age peaks : < 5 years , > 64 years 3 • knee 40-50% • hip 20-25% • Shoulders, ankles, elbows 10-15% • wrist 10% • in infants and very young children, hip is the most common joint infection. 4 Definition • Acute - < 14days • Subacute – 2-6 wks • Chronic - > 6wks • Monoarthritis – 1 joint • Oligoarthritis – 2-3 joints • Polyarhritis - > 4 joints 5 Acute Monoarthritis Crystal-induced synovitis Septic arthtitis Acute traumatic and hemorrhagic arthritis Acute presentation of systemic rheumatic diseases eg.RA, SNSA Other rheumatic disorders – Adult still’s disease 6 Microorganisms • Bacteria - the most important – Neisseria – Non-neisseria • Viruses • Fungi • Parasites 7 Gram-Positive Cocci Streptococci • S. pyogenes (beta-hemolyticus group A) • S. pneumoniae • Group B and G hemolytic Streptococci. Staphylococci • Staph. aureus • Staphylococcus epidermidis 8 Gram Negative Organism Neisseria • Neisseria gonorrhoeae – septic or reactive forms of arthritis, • N. meningitidis, 9 Gram Negative Organism Non- Neisseria • Haemophilus influenzae • Gram-negative rods – Enterobacteriaceae • • • • • • • • E. coli Shigella Salmonella Yersinia Klebsiella pneumoniae. Proteus mirabilis Pasteurellaceae ( Pasteurella multocida) Campylobacter jejuni 10 • Viruses – – – – HIV parvovirus B19 herpes viruses adenoviruses • Anaerobes – – – – – Clostridium Eubacterium Propionibacterium Bacteroides Fusobacterium Others • • • • Mycobacterium Nocardia. Spirochetes Borrelia burgdorferi ( Lyme disease) • Chlamydias • Mycoplasmas and Ureaplasma. • Fungi, Parasites 11 Bacterial isolation Organism Percentage of cases Staphylococcus aureus 40–50 Staphylococcus edidermis 10–15 Streptococcal species 20 Gram-negative bacteria 15 S. pneumoniae 2 H. influenzae 2 Anaerobes 5 12 Microbiology 13 14 Clinical features • Acute bacterial infection – – – – – – Fever 60%-80% (< 39°c ) Monarticular : inv. 90% Limited ROM Swelling (seen synovial effusion) Most common : knee > hip Refusal walk ,limping, Irritability, failure to thrive, asymmetry of limb position 15 Clinical Features • Systemic symptoms - neonatal period – High fever – sepsis • local signs – children, adult – – – – Pain Swelling Erythema and warm Limitation of movement 16 17 18 19 • Predisposing factors. 1) prosthetic joint. 2) age> 60 yrs. 3) present underlying jt. disease( RA, much less for OA ). 4) co morbidity( malignancy, DM, alcoholism, cirrhosis, hemophilia) 5) use of immunosuppressive drug. 6) skin infection. 20 Predisposing Factors Abnormal joint RA Crystal induced synovitis Prosthetic joint Severe OA Severe Charcot’s joint Severe hemarthrosis Intrarticular injection Abnormal host Chronic systemic disease - DM ,SLE, CRF, liver disease HIV IVDU Chronic steroid therapy Malignancy Old age New born 21 Risk factors for the development of joint sepsis • • • • • • • • rheumatoid arthritis (RA) or osteoarthritis prosthetic joints low socioeconomic status intravenous drug abuse alcoholism diabetes previous intra-articular corticosteroid injection cutaneous ulcers 22 Differential diagnosis 23 Pathogenesis • Mechanism – Hematogenous route. • Skin, oral cavity, respiratory tract, urinary or intestinal tract infections, or endocarditis. – Dissemination from metaphysis or epiphysis. – Vicinity of the joint – Iatrogenic or penetrating trauma 24 Source of infection 25 Hematogenous spread Systemic bacteremia Invade synovial cartilaginous junction Synovial infected Increase inflammatory cell Destruction of the articular cartilage Joint dislocation, subluxation, osteomyelitis 26 1. Hematogenous route. 4. Vicinity of the joint 2,3 Dissemination from bone 5. Iatrogenic or penetrating trauma 27 Bacteria Synovium Inflammation Synovial cell proliferation Leukocytes migration Blood flow Erythema Exudation Swelling Tenderness Irreversible destruction Enzymes Destruction Pannus 28 Investigations • • • • • CBC,ESR,CRP Blood culture Synovium fluid Plain radiographs ( 2-3 weeks or more) Scintigraphy – 99mTc phosphate (three-phase bone scan) – 99mTc nanocolloid scanning – Indium 111-labeled leukocytes • Computed tomography (CT) • Magnetic resonance imaging (MRI) 29 Laboratory • CBC - often normal. - predominance of segmented neutrophil. • ESR ( erytrocyte sedimentation rate) - elevation, but not specific for infections. - present for less than 48 hr, return to normal ~3 weeks. 30 level CRP xx ESR 3-5days 24 48 72 time Subside 31 Laboratory • CRP ( C- reactive protein). - elevation. - inc. within 6 hr, return to normal 1 week after treatment began. - better way to follow the response to ATB. • Blood culture - positive~ 50%-70%. 32 Laboratory • Synovial fluid analysis - should be aspirated immidiately if there is suspicious. - recommended: crystals examination. 33 Diagnosis Joint aspiration disease WBC % PMN normal <200 <25 traumatic <5,000+rbc <25 Toxic synovitis 5,000-15,000 <25 Acute rheumatic 10,000-15,000 50 JRA 15,000-80,000 75 Septic arthritis >80,000 >75 34 Synovial fluid Percent Method Gram positive Gram negative N. gonorrhea Gram strain 80 50 25 Synovial C/S 80-90 60-70 40 35 36 Streptococci 37 Neisseria gonorrhoeae 38 Radiologic Evaluation Initial plain x-ray baseline assessment exclude osteomyelitis Definitive changes usually take a number of weeks Rapidity depends on virulence of organism 39 Radiologic Evaluation Earliest : joint effusion with displacement of fat pad During first week – periarticular osteoporosis Within 7-14 days - joint space narrowing & erosions >20days: bone destruction 40 41 Radiologic Evaluation periarticular osteoporosis 42 Radiologic Evaluation joint space narrowing & erosions 43 Radiologic Evaluation CT / MRI Difficulty to evaluate clinically Complex anatomical structure ( hip, shoulder, SC jt, SI jt ) Early bony erosions, soft tissue extension Bone scan Axial joints infections sensitivity Cannot differentiate septic from aseptic Jt. 44 Laboratory • CT scan – good definition of contiguous bone lesions and ability to guide needle aspiration • MRI – better defines soft tissue (distended joint space and extension to periarticular structures) 45 Laboratory • Radionuclide - physiologic picture. - reflect inflammatory change/ reaction of bone to infection. - 3 most common use 1) Technitium 99m phosphate. 2) gallium 67 citrate. 3) indium 111-labled leukocytes. 46 Bone scan 47 Polyarticular Septic Arthritis 15% 50% RA systemic illness/IVDU Most common S.aureus Group G streptococcus H.influenza S. Pneumoniae Polymicrobial 30% died!! 49 Treatment Principle in the management of acute septic arthritic (Nade ) 1. Joint must be adequately drained 2. Antibiotic must be given to diminish the systemic effects of sepsis 3. Joint must be rested in a stable position 50 Treatment. 1. synovial analysis and blood cultures before IV antibiotic treatment 2. rapid administration of IV antibiotics IV oxacillin in combination with IV ceftriaxone, cefotaxime, or ceftizoxime. 3. drainage of the septic joint 4. evaluation 5. Arthroscopic drainage or arthrotomy 51 Treatment & Outcome ATB should be started as soon as ATB selected on the basis of gram stain and clinical picture Adjust ATB on the basis of sensitivity, toxicity and cost Most iv ATB at least 2 weeks ,followed by 1-2 weeks of oral ATB 52 53 Organism ATB of choice Alternative S. Aureus MRSA Cloxacillin Vancomycin Cefazilin,clindamycin Streptococcus Group A non group A pneumococci Penicillin PG + aminoglycoside Penicillin Cefazolin Cefazolin + aminoglycoside vancomycin N. Gonorrhea 3rd cephalosporin Ciplofloxacin, olfloxacin H. Influenza Amox. + calvulanate 3rd cephalosporin, Ciplofloxacin Enterobacteria 3rd cephalosporin Imipenem Ps. Aeruginosa Antipseudomonas Imipenem Anaerobe Metronidazole, doxycycline Clindamycin 54 Treatment • 1) 2) 3) Recommendation for arthrotomy/ arthroscope Hip joint. Immunocompromised host Joint that are difficult to access: sacroiliac, sternoclavicular jt. 4) Difficult to completely drain: shoulder, wrist. 5) Close needle aspiration> 7 days. 6) P.aeruginosa or gram negative bacteria. 55 Treatment • Recommendation for arthrotomy/ arthroscope 7) Sepsis 8) Extension into soft tissue or secondary osteomyelytis 9) Fungal infection 10) Prosthetic or FB 11) Unresponse to ATB 12) Superimpose on joint disease - RA 56 Closed needle aspiration should be the initial Rx of choice Serial synovial fluid c/s & wbc count Acute,suppurative phase : sling/splint/cast should be used to maintain the joint in optimal position : muscle-tightening exercises 57 Poor prognosis factors – – – – – – – – – – Immunodeficiency RA prematurity osteomyelitis, hip prosthetic infections + blood cultures, symptoms >1 week, >4 joints, + cultures after aspiration after 7 days of abx tx 58 Complication – arthritis stiffness – Dislocation or subluxation – AVN – local growth distrubance – Osteomyelitis – postinfection synovitis 59 Postinfectious arthritis recurrent inflammatory when begin ambulate, but sterile effusion DDx - incompletely treated infection NSAIDs 60 Outcome Results of Rx 10-15% mortality 25-50% chronic joint damage & disability Poor outcome Persist/ Recurrent infection Marked decrease ROM/ankylosis Persistent pain 61 Factors associated to poor outcome Duration of infection Virulense of bacteria The infected joints Host defences Age of patient Comorbidity Effective therapy 62 OSTEOMYELIS 63 Osteomyelitis • Inflammation of the bone by organism. – single portion. – surrounding regions ; marrow , cortex & periosteum 64 Classification 1. 2. 3. 4. Acute , subacute , chronic Exogenous , hematogenous Pyogenic , nonpyogenic Neonate , children , adult 65 Source of infection • Blood circulation : – infection in Oral, Throat, Ear, Gastrointestinal tract, Urinary tract, Skin and soft tissue • Trauma (30-50%) – หกล้ม กระแทก – Minor trauma Caution : in infant < 18 month มักเกิด septic arthritis ร่ วมกับ Osteomyelitis 66 Acute Hematogenous Osteomyelitis • Most common usually seen in children. • Infection involve the metaphyses of rapidly growing long bones 67 Natural history and Pathogenesis of Acute hematogenous osteomyelitis • Almost at “metaphysis” – lower extremities > upper extremities 5 เท่า โดย เฉพาะที่ distal femur และ proximal tibia – metaphysis (no phagocytosis cell) ≠ diaphysis (diaphysis = reticuloendothelial tissue + phagocytosis cells) 68 Why organism seeding the metaphyses ? • nutrient capillaries form sharp loops to establishment of infection • metaphysis has relatively fewer phagocytetic cell than the physis or diaphysis. 69 Pathogenesis Source of Infection Blood stream Metaphysis Venous stasis Bacterial colonization 70 Inflammation: acute osteomyelitis • First 24 hours • Vascular congestion • Polymorphonuclear leukocyte infiltration • Exudation 71 Inflammation: acute osteomyelitis • 2-3 day No treat with antibiotic • Intraosseus pressure intense pain intravascular thrombosis ischemia เด็กจะร้ องปวดมาก 72 Suppuration 4-5 days Pus formation Subperiosteal abscess via Volkmann canals Pus spreading epiphysis joint medullary cavity soft tissue 73 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 74 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 75 Primary osteomyelitis 76 Primary osteomyelitis 77 • Children < 2 yr. blood vessel cross the physis & spread infection into epiphysis. • Children > 2 yr. , the physis effectively barrier to spread. 78 • In adult , after the physes closed , acute osteomyelitis is less common ; ; infection extend directly metaphysis to epiphysis to joint & hematogenous seeding in compromised host 79 • Spread to joint in children < 2 yr. , most commonly is hip joint . ( proximal humerous , radius neck , distal fibular are intraarticular , can lead to septic arthritis. ) 80 Diagnosis • History , Physical exam. • Clinical : fever , malaise , fatigue , irritability , pain , local tenderness , swelling , restriction of movement 81 82 • Investigation : X- Ray , WBC , ESR , CRP , Bone scan , MRI , Blood culture , Bone aspiration for gram strain , culture & sensitivities. 83 X-ray soft tissue swelling , periosteal reaction , bony destruction , 10–12 day after onset. WBC often normal ESR elevated CRP elevated 84 • Bone scan can confirm diagnosis 24-48 hr. after onset. • MRI show early inflamation changes in bone marrow and soft tissue 85 Treatment acute osteomyelitis • Sequestered abscesses drainage. • Simple inflammation without abscess ; antibiotic based on Gram strain • Gram strain not found ; empirical antibiotics for most likely organism. • CRP every 2-3 days 86 Two main indications for surgery • abscess requiring drainage. • failure iv antibiotic treatment. ( no clinical response 24-48 hr. ) 87 Nade proposed five principles for treatment 1. appropriate antibiotic will be effective before pus formation. 2. avascular tissues or abscesss require surgical remove. 3. if such removal is effective , antibiotics should prevent their reformation & primary wound closure should be safe. 88 4. surgery should not further damage already ischemic bone & soft tissue. 5. antibiotics should be continuous after surgery. 89 Organism Patient Type Neonate Propable Organism Grp. B Strep , S. aureus , Gram-neg. rod (H. influenza) Infants & children S. aureus Sickle cell disease S. aureus , Sallmonella 90 Antibiotic • Appropriate ; infection type , organisms , sensitivity , host , antibiotic • Iv 4 – 6 wk. , switch iv 1 wk. + oral 6 wk. 91 Subacute osteomyelitis • insidious onset & lacks the severity of symptom • diagnosis delayed for more than 2 wks. • systemic signs & symptoms are minimal. • WBC normal • ESR elevation ( 50% ) • blood culture ; usually negative. 92 • bone aspirate or biopsy ; 60% pathogen identified • x-ray & bone scan ; positive. • course ; increased host resistance , decreased bacterial virulence , antibiotic before the onset of symptom. • differentiation lesion from a primary bone tumor. 93 Classification of subacute osteomyelitis 94 Differential Type I Langerhans’cell histiocytosis , Brodie abscess II Eosinophilic granuloma , Osteogenic sarcoma III Osteoid osteoma IV Ewing sarcoma V Chondroblastoma VI Tuberculosis ; osteogenic sarcoma 95 Treatment subacute osteomyelitis • Ross & Cole recommended biopsy & currettage aggressive lesions and antibiotics. • biopsy not recommended in simple abscess lesion 96 Chronic osteomyelitis • Systemic symptom subside ; bone contain purulant material , infection tissue • Intermittant acute exacerbation ; respond antibiotic & rest • Multiple organism ; culture & biopsy 97 98 Cierny & Mader Staging System for Chronic Osteomyelitis Anatomical type I II III IV Physiological class A host B host C host Medullary Superficial Localized Diffuse Normal Compromised Prohibitive 99 100 Diagnosis • • • • • Gold standard ; biopsy , microbiological PE. skin , soft tissue , neurovascular ESR & CRP ; elevation WBC ; normal X-ray ; cortical destruction , periosteal reaction • Bone scan • MRI 101 Treatment • Sequestrectomy , resection scar & infection bone • Antibiotics 6 wk. ( 1 wk. for iv , 6 wk. for oral form) • Reconstruction of bone & soft tissue ( bone graft , bone transfer , myoplasty , flap ) 102 103 Fracture management •Active infection ; sequestrectomy , debridement , antibiotics ( > 6 m.) & immobilization •Active infection without involucrum ; debridement , bone graft , antibiotics & immobilization •Inactive infection & no involucrum ; immobilization & bone graft. 104 Amputation for osteomyelitis • malignant change • arterial insufficiency , major nerve paralysis , joint stiffness 105 106