Septic Arthritis-Osteomyelitis 2022 Past Paper PDF
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Marmara Üniversitesi
Doç.Dr. Evrim Şirin
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This document contains information about septic arthritis and osteomyelitis. It covers topics such as causes, diagnosis, treatment, and classification. Written by Evrim Şirin, from Marmara Üniversitesi.
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OSTEOMYELITIS Doç.Dr. Evrim Şirin Marmara Üniversitesi Tıp Fakültesi Ortopedi ve Travmatoloji AD. Osteomyelitis Osteomyelitis is infection of the bone. Infection is more common in the long bones and vertebras of the body, but it can affect any bone in the body Etiology S. Aureus Etiology Age Grou p...
OSTEOMYELITIS Doç.Dr. Evrim Şirin Marmara Üniversitesi Tıp Fakültesi Ortopedi ve Travmatoloji AD. Osteomyelitis Osteomyelitis is infection of the bone. Infection is more common in the long bones and vertebras of the body, but it can affect any bone in the body Etiology S. Aureus Etiology Age Grou p Patient Characteristics Causative Agent Neonatal (Birth to 8th wk) S. aureus, group B streptococcus, Escherichia coli, Infantile (2 to 18mo) S. aureus, Kingella kingae, Streptococcus pneumoniae, Klebsiella species Neisseria meningitidis, Haemophilus influenzae type b Early Childhood (18mo to 3 yr) S. aureus, K. kingae, S. pneumoniae, N. meningitidis, H. Childhood (3 to 12 yr) S. aureus, GABHS Adolescent (12 to 18 yr) S. aureus, GABHS, Neisseria gonorrhoeae influenzae type b Adult Risk Facto r Sickle Cell Disease Salmonella species, S. aureus, S. pneumoniae Foot puncture wound Pseudomonas aeruginosa, S. aureus HIV S. aureus, Streptococcus species, Salmonella species, Nocardia asteroides…. Chronic Granulomatous Disease Aspergillus species, Staphylococcus species, Burkhol deria cepacia, Nocardiaspecies, Mycobacterium species Classification According to: – Duration of symptoms Acute Subacute (Brodie 1836, Billroth 1881) Chronic Chronic recurrent multifocal (CRMO)* – Mechanism of infection (Waldvogel, 1971) Hematogenous (Children and elderly) Direct inoculation (Open wounds, open Fx, iatrogenicoperations) Contiguous focus of infection (vascular insufficiency, diabetes) Classification CIERNY & MADER 4 factors affecting outcome; Host Site Degree of necrosis Degree of impairment Anatomic Classification (Cierny-Mader) I: II: III: IV: Classification Break-Down 1. Medullary Endosteal nidus, min soft tissue involvement, ? Sinus tract 2. Superficial Surface of bone, usu 2° to soft tissue defect 3. Localized Localized sequestra, usu sinus tract, Usually stable s/p excision 4. Diffuse Permeative process, combination of I/II/III, Usu Unstable s/p excision Acute Hematogenous Osteomyelitis Most common bone infection (mostly children) Male > Female (in all age groups) S. Aureus; most common agent Hematogeneous spread most commonly affects the metaphyseal region of long bones the question is from here Subacute Osteomyelitis (Described by Brodie 1836, “subacute” Term Billroth 1881) - Less common than acute hematogeneous OM Age ~ 7,5y S. aureus is the most common Diagnosis is difficult to establish insidious onset mild symptoms Normal or slightly elevated laboratory values Subacute Osteomyelitis Chronic Osteomyelitis Inappropriately treated acute osteomyelitis Immunosuppressed patients (diabetic, iv drug abusers) Skin & soft tissue involvement may lead to squamous cell ca (particularly on the sinus tract) Pathophysiology Poorly defined – Direct inoculation – Hematogenous spread – Local invasion Pathophysiology Infection – Starts in metaphysis – Spread via Volkman’s canal (Haversian system) – Cortical breakdown – Subperiosteal pus – Spread to soft tissues – (occasionally) spread to epiphysis and joint Pathophysiology Gaps in endothelium metaphyseal vessel Bacteria pass Adhere to Type 1 collagen Increase pressure in bone/ decrease blood flow Bone infarction / Dead Diagnosis Pain – Neonate pseudoparalysis – Failure to use limb Fever Lethargy Anorexia Swelling (neonates / older kids) Diagnosis Blood work – – – – CBC ESR CRP Blood Culture Diagnosis WBC increased 30-40% Left Shift 65% ESR increased 91%……….24-36 hrs CRP increased 97%…………4-6 hrs Diagnosis Blood Culture – (+) in 30-60% of patients – Decreased with antibiotic Diagnosis Pus aspiration - occasionally helpful in superficial bones (tibia) Radiology Plain X-rays - Soft tissue swelling in 48hrs - Periosteal reaction in 5-7days - Osteolysis in 10-15 days (need > 50% bone loss) Radiology MRI – Sensitivity 83-100% – Specificity 75-100% - Marrow and soft tissue involvement Radiology T1-weighted images – Best for acute infection – Gadolinium helps – Changes similar to Infarct Bruise Tumor Post surgical Sympathetic edema !!! Radiology CT – Cortical destruction – Sequestrum Treatment Combination of surgery and medical treatment – Surgery to improve local environment – Remove infected devitalized bone – Decompress abscess cavity Treatment Surgery indicated in; – – – – – Subperiosteal abscess Soft Tissue abscess Bone Abscess Bone infart (sequestrum) Failure of clinical response to antibiotic – Associated septic arthritis Treatment Treatment Antibiotic treatment (usually cephalosporins) – Parenteral / oral combinations – Often empirical – Serum level more important than route Follow WBC, ESR, CRP SEPTIC ARTHRITIS suppurative infection of the synovia and synovial fluid caused by various microorganisms SYNOVIAL JOINT SEPTIC ARTHRITIS Septic arthritis can be seen in all age groups – children and older adults ar more prone, particularly if predisposing factors exist - Abnormal joint; trauma, hemophilia, osteoarthritis, RA - Immunosupression (cancer, DM, alcoholism, uremia etc ) ETIOLOGICAL AGENT CAN DIFFER DUE TO AGE AND PREDISPOSING FACTORS Clinical Factor AGE Neonatal Etiological Agent S. aureus 2 y S. aureus Young adult Adult Neisseria gonorrhoeae S. aureus (50%), streptokok, Gr(-) basil Structural abnormalities Aspiration, injection Replacement arthroplasty Early infection S. epidermidis Late infection Gr(+) kok, anaerobes Medical conditions i.v. drug use Trauma Rheumatoid arthritis SLE, Sickle cell anemia Hemophilia Immunsupression S. aureus Gr(-) basil, anaeroplar, S. aureus Atypical Gr(-) bacils (e.g., Pseudomonas spp.) S. aureus Salmonella spp. S. aureus (50%), streptokok, Gr(-) basil S. aureus, Mycobacterium spp., fungi SEPTIC ARTHRITIS STAPHYLOCOCCUS AUREUS Most common microorganism in all age groups CLINICAL FINDINGS SYSTEMIC SIGNS – fever, nausea, lethargy, anorexia, etc. LOCAL INFLAMMATION SIGNS – – – – – SWELLING ERYTHEMA PAIN TENDERNESS DECREASED JOINT MOTION patenit persents with cardinal signs of infalmamtion CLINICAL FINDINGS ACUTE PRESENTATION – Acute: pyogenic infection (S.Aureus) – Chronic: non-pyogenic (Mycobacterium Tbc, Brusella, fungal inf.) USUALLY MONOARTICULAR (90%) – Knee and hip are most commonly involved joints Polyarticular involvement (10%) – Viral etiology (parvovirus, rubella virus, hepatitis B, C, and A viruses, cytomegalovirus, and HIV ) – Rheumatoid arthritis – DM – Steroid – SLE CLINICAL FINDINGS More acute presentation than osteomyelitis what are the acute persentaion of spetic artherits ? – Pseudoparalysis in newborn – No motion at the involved joint Antalgic gait/inability to walk in older child ROUTES OF SPREAD HEMATOGENEOUS ROUTE DIRECT ROUTE from adjacent osteomyelitis focus (particularly important in infants) DIRECT INOCULATION by aspiration, arthrotomy DIRECT ROUTE Metaphyseal osteomyelitis can spread to epiphysis and joint space by transepiphyseal vessels PATHOGENESIS - introduction of bacteria/bacterial products into joint space - PMNL infiltration by chemotaxis - inflamatory cells produce proteolytic NZs and cytokines synovial membrane proliferation, neovascularization, bone and cartilage damage PATHOGENESIS acute infection becomes chronic after 3 weeks CARTILAGE DESTRUCTION STARTS SIGNIFICANTLY BETWEEN 4-6 DAYS AND COMPLETE IN 4. WEEK ? !!!! subluxation or dislocation of the joint can be observed during the course of the disease what is the sign of septic srtherits ? DIAGNOSIS PHYSICAL EXAMINATION ASPIRATION OF JOINT FLUID – Culture, Gram-staining – Cell count (WBC >50.000, 80% PMNL), biochemistry (glucosis↓, protein↑) – Antigen, PCR (Borrelia burgdorferi, Neisseria gonorrhoeae) BLOOD CULTURE, CBC, BIOCHEMISTRY, ESR-CRP IMAGING (X-ray, BT, MRI) BONE SCAN DIAGNOSIS Fever Refusal to bear weight ESR >> 40 WBC count >>> 12000 Increased CRP >>> 5 ¾ of predictors (%73-93) Septic arthritis (Bakterial, fungal, micobacterial) Hemoragic Arthritis (Hemophilia, trauma) Test Noninflamatory arthritis (OA) İnflamatory arthritis (Gut arthritis, RA, SLE) Color Yellow Yellow-white Yellow-green Red-brownish Appearance Clear Turbid Turbid Turbid Viscosity High Low Low Low Mucin, clot formation Good İmpaired İmpaired İmpaired WBC (cell/µL) 200-2.000 2.000-100.000 10.000-100.000 >500 PMNL (%) 50 >75 >25 Glucose ~ serum < serum < serum ~ serum Culture negative negative positive negative the onlytype of artherits with positive culture is septic`/ DIAGNOSIS JOINT FLUID Osteoarthritis R.A. Gut Septic Arthritis Trauma IMAGING / X-ray IN ACUTE STAGE – widening of the joint space – subluxation / dislocation LONG-TERM CHANGES – narrowing of the joint space – marginal and central bone and cartilage erosion – peri-articular osteoporosis – ankylosis CT is more sensitive in detecting early bone and cartilage destruction IMAGING / X-ray SUBLUXATION / DISLOCATION IMAGING / X-ray bone and cartilage (femoral head) destruction dislocation of the hip joint IMAGING / CT bone and cartilage (femoral head) destruction dislocation of the hip joint IMAGING / X-ray LONG-TERM CHANGES (narrowing of the joint space, cartilage erosion, peri-articular osteoporosis, ankylosis) IMAGING / MRI Synovial hypertrophy Perisynovial edema Joint effusion Abnormal signal in bone marrow (associated osteomyelitis) – MRI findings can be detected in first 24 hours – MRI sensitivity 100% spesifity 77% IMAGING / MRI Synovial hypertrophy IMAGING / MRI Perisynovial edema IMAGING / MRI Contrast enhancement around synovia Joint effusion DIFFERENTIAL DIAGNOSIS Gout Pseudogout ARF Acute juvenile arthritis RA Reactive arthritis Viral arthritis (hepatitis B, mumps, measles, parvovirus B19...) Transient Synovitis! (most commmon cause of acute hip pain between 3-10 years of age) Fungal arthritis Tuberculosis arthritis Osteomyelitis Cellulitis Hemarthrosis Periarticular syndromes (bursitis, tendinitis) Ruptured Baker cyst DVT PVNS TREATMENT SURGICAL DRAINAGE (arthroscopic or open, multiple aspirations) ANTIBIOTIC TREATMENT – AMPIRIC TX – SPECIFIC TX (due to culture results) STABILIZATION OF THE JOINT SURGICAL TREATMENT OPEN DRAINAGE BY POSTEROLATERAL APPROACH SURGICAL TREATMENT OPEN DRENAGE BY POSTEROMEDIAL APPROACH SURGICAL TREATMENT ARTHROSCOPIC DRAINAGE (irrigation by saline, RL) - knee - elbow - shoulder - ankle AMPIRIC ANTIBIOTIC TX – Neonatal: (S. Aureus, Enterobac., Group B streptococci) Nafcillin and cefotaxime or gentamicin – < 5 y.o: (S. Aureus, Haemophilus influenzae, Streptococci) Nafcillin or cefuroxime – > 5 y.o: (S. Aureus, Streptococcus species) Nafcillin – Adult: (Neisseria gonorrhoeae, S. Aureus) Ceftriaxone or cefotaxime – Adult (postoperative, implant infection): (S. Epidermidis, S. Aureus, Streptococcus species) Vancomycin and ceftazidime or aztreonam TREATMENT Stabilization of the involved joint (by splint) Isometric muscle and active ROM exercises by regression of the infection PROGNOSIS Differs due to the virulence of the pathogen – Gonococcal infections: good response to tx – S. Aureus and Gr (-) bacillus: worse response to tx Duration of infection TIMING AND ADEQUACY OF TREATMENT Associated joint diseases THANK YOU