Beth L. Jonas, M.D. University of North Carolina Chapel Hill

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Presentation transcript:

Beth L. Jonas, M.D. University of North Carolina Chapel Hill INFECTIOUS ARTHRITIS Beth L. Jonas, M.D. University of North Carolina Chapel Hill

Acute Monoarthritis Differential Diagnosis Infection Crystal-induced Hemarthrosis Tumor Intra-articular derangement Systemic rheumatic condition

ACUTE MONOARTHRITIS IS SEPTIC UNTIL PROVEN OTHERWISE !!

Risk Factors for Septic Arthritis Previous arthritis Trauma Diabetes Mellitus Immunosupression Bacteremia Sickle cell anemia Prosthetic joint

Pathogenesis of Septic Arthritis Bacteria enter joint and deposit in synovial lining. Hematogenous spread or local invasion Acute inflammatory response Rapid entry into synovial fluid No basement membrane

Septic arthritis Clinical presentation Acute monoarthritis Cardinal signs of inflammation Rubror, tumor, calor, dolor +/- Fever +/- Leukocytosis Atypical presentations are not uncommon

Septic Arthritis Joints Involved

Polyarticular Septic Arthritis More likely to be over 60 years Average of 4 joints Knee, elbow, shoulder and hip predominate High prevalence of RA Often without fever and leukocytosis Blood cultures + 75% Synovial fluid culture + 90% Staph and Strep most common POOR PROGNOSIS 32%mortality (compared to 4% with monoarticular disease)

Synovial fluid analysis is essential in the diagnosis of infectious arthritis

Synovial Fluid Analysis in Septic Arthritis Cell count: >50,000 wbcs/mm3 Differential: >75% PMNs Glucose: Low Gram stain : relatively insensitive test Culture: postive Always use a wide bore needle when you suspect infection, as pus may be very viscous and difficult to aspirate

Up-to-Date 2004

When to order special cultures History of TB exposure Trauma Animal bite Live in or travel to endemic sites for Fungi or Borrelia Immunocompromised host Unresponsive to conventional therapy

Special Populations Prosthetic joints Patients on TNF inhibitors Sickle cell anemia HIV disease Transplant setting

IV Drug users Multiple risk factors for septic arthritis Unusual sites Soft tissue infections, transient bacteremias, other comorbidities- hepatitis, endocarditis,HIV Unusual sites Fibrocartilagenous joints- SC, costochondral, symphysis Unusual organisms S. aureus still most common Gram negative infections next most common Pseudomonas, Serratia, Enterobacter sp. Candida

Management Joint aspiration Antibiotic therapy Surgical intervention Daily or more frequently as needed. Antibiotic therapy Based on gram stain/culture and clinical factors Duration is variable and depends on organism and host factors Surgical intervention Only necessary if pt is not responding after 48 hrs of appropriate therapy

Empiric Therapy for Septic Arthritis You must cover Staph and Strep Oxacillin Vanco if PCN-allergic or if concern for MRSA If infection is hospital acquired or prosthetic joint- cover gram negatives 3rd generation cephalosporin Empiric coverage for GC is recommended because of the high prevalence rate

Septic arthritis Radiographs Minimal diagnostic utility Document any existing joint damage Evaluate for possible osteomyelitis

Septic hip-early disease Late disease

Prosthetic joint infections Stage I within 3 months of surgery Usually transmitted at the time of surgery Staph and other gram positives most common Pain, wound drainage, erythema, induration Stage II 3-24 months Stage III >2 years post-surgery Usually caused by hematogenous spread to abnormal joint surfaces Joint pain predominates

Prosthetic joint infections Synovial fluid analysis May require biopsy If cultures are positive Remove prosthesis Treat with parenteral antibiotic until sterile Usually 6 weeks + Reoperate Revision is at high risk for recurrent infection

Lyme Arthritis Caused by infection with the spirochete Borrelia Burgdorferi Early stage disease Localized - Erythema chronicum migrans, fever, arthralgia and myalgia, sore throat, Disseminated- disseminated skin lesions, facial palsy, meningitis, radiculoneuropathy, and rarely heart block Early disease may remit spontaneously 50% of untreated cases develop late features Late Arthritis is a manifestation of late disease-months or years after exposure Intermittent migratory asymmetric mono- or oligo-arthritis 10% develop chronic large joint inflammatory arthritis

Lyme Arthritis Diagnosis EM rash in endemic area Screening ELISA Adequate for treatment Screening ELISA Confirmatory Western Blot IgM Western Blot – high false positive rates Most useful in the first 4 weeks of disease IgG Western Blot– high specificity Most useful in disseminated or late stage disease

Lyme Arthritis Treatment Early localized Doxy 100 mg po BID or Amox 500 TID (kids) for 2-4 weeks Early disseminated or late disease Oral or parenteral abx depending on the severity of the disease Neuro or cardiac disease usually treated with IV ceftriaxone 2 g daily for 3-4 weeks. Lyme arthritis may be treated with oral abx for 4 weeks.

Disseminated gonococcal infection Occurs in 1-3% on patients infected with GC Most patients have arthritis or arthralgia as a principal manifestation Common cause of acute non-traumatic mono- or oligo-arthritis in the healthy host

Gonococcal arthritis Host factors Women > men Recent menstruation Pregnancy or immediate postpartum state Complement deficiency (C5-C9) SLE

Gonococcal arthritis Presentation Tenosynovitis, rash, polyarthralgia Wrist, finger, ankle, toe Painless pustules or vesicles*** Fever and malaise Synovial cultures usually negative—urethral and cervical cultures may be helpful Purulent arthritis Knee, wrist, or ankle most common Synovial cultures usually positive These two presentations may overlap

Gonococcal arthritis Other considerations Consider screening/treating for chlamydia HIV testing Syphillis testing Screen sexual partners

Gonococcal arthritis Ceftriaxone 1gm IV or IM q24 hours Spectinomycin 2 gm IV or IM q12 hours for ceph allergic patients May use fluoroquinolones if susceptible *CDC guidelines recommend treating for at least 7 days. Patients with purulent arthritis may need a longer duration of therapy.

Parvovirus B19 Arthritis Small non-enveloped DNA virus Erythrovirus genus Replicates only in erythrocyte precursors Transmission Respiratory, parenteral, vertical 25-68% of infections are asymptomatic

Erythema Infectiosum “5th disease” 10% of children and 50% of adults have joint symptoms

Parvovirus B19 Arthritis Begins about 2 weeks after infection Symmetrical involvement of the small joints of the hands and wrists and the knees Usually resolves in about a month without joint damage 20% may have persistent disease**

Parvovirus B19 Clinical features may mimic an early autoimmune disease High prevalence of autoantibodies RF, ANA, ACA, ANCA, anti-ds DNA May persist for some time after infection is cleared Has been implicated in the pathogenesis in both RA and SLE

Diagnosis and Therapy Parvovirus B19 IgM + PCR can be used Parvovirus B19 IgG indicates past infection. highly prevalent in the general population since asymptomatic infxn is very common. PCR can be used Immuncompromised people may not mount an antibody response Therapy is supportive NSAIDs Steroids are rarely necessary

Tuberculous arthritis History of exposure is helpful PPD may be negative Synovial fluid stain usually negative Culture may take 6-8 weeks to grow Best yield is probably synovial biopsy

Tuberculous synovitis

Acute Rheumatic Fever JONES CRITERIA Evidence of preceding strep infxn plus 2 major criteria or 1 major and 2 minor MAJOR Carditis Migratory polyarthritis Syndenham chorea Erythema marginatum Subcutaneous nodules MINOR Fever Arthralgia previous rheumatic fever or rheumatic heart disease

Take Home Points Acute monoarthritis is septic until proven otherwise Synovial fluid analysis must be performed Choose appropriate empiric abx Consider unusual pathogens in the setting of immunocompromise Serial synovial fluid analyses should be performed to document clearance of infection Consult ortho if not improving with aggressive percutaneous drainage and abx