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Septic arthritis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]

Synonyms and keywords: Bacterial arthritides, bacterial arthritis, infectious arthritides, infectious arthritis, septic arthritides, suppurative arthritides, suppurative arthritis, non-gonococcal bacterial arthritis, gonococcal arthritis

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayesha A. Khan, MD[2] Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [3]

Overview

Septic arthritis is the one of the most serious medical emergency of a patient present with one or more hot and swollen joints.[1] It is the most rapidly destructive joint disease.[2] It is most common in patients with longstanding rheumatoid arthritis and it is a an important consideration in adults presenting with monoarticular arthritis in 80 to 90% of patients. It can involve any joint, but most commonly involves knee > hip > shoulder > ankle.[3] Other joints such as sacroiliac joint, sternoclacicular or costoclavicular joints may be involved in patient with history of intravenous drug abuse (IVDA), penetrating trauma, animal or human bites and local steroid injections. Septic arthritis is joint inflammation secondary to an infectious etiology, usually bacterial, but occasionally fungal, mycobacterial, viral, or other uncommon pathogens. Septic arthritis is usually monoarticular involving one large joint such as the hip or knee; however, polyarticular septic arthritis involving multiple or smaller joints may also occur. Though uncommon, septic arthritis is an orthopedic emergency that can cause significant joint damage leading to increased morbidity and mortality.

Historical Perspective

  • First case of septic arthritis described in literature by Walter Whitehead in 1902, as “The open method of treating exceptional cases of septic arthritis of the knee”.[4]
  • An experimental and clinical Study on arthritis deformans described by Nathan PW in 1917.[5]
  • Surgical management of septic arthritis by By Captain W. Rankin in 1917.[6]

Classification

Septic arthritis broadly classified based on the etiology as gonococcal or non-gonococcal arthritis and based on the clinical presentation it is classified as mono articular septic arthritis or poly articular septic arthritis.[7][8]

Pathophysiology

Septic arthritis most commonly develop as a result of hematogenous spreading of bacteria into the synovial membrane, that induces inflammatory reactions. Eventually, release of cytokines and activation of both host humoral and immunological response along with bacterial virulence factors cumulatively damages articular surface and cartilage.[9][10]

Causes

Septic arthritis caused by bacteria or tiny disease-causing microorganisms that spread through the bloodstream to a synovium. It may also occur when the joint is directly infected with a microorganism from an injury or during surgery. The most common sites for this type of infection are the knee and hip. Most cases of acute septic arthritis are caused by bacteria such as staphylococcus or streptococcus. Chronic septic arthritis (which is less common) is caused by organisms such as Mycobacterium tuberculosis and Candida albicans.

Differential Diagnosis

Patient present with septic arthritis should be differentiate from other causes of acute monoarticular arthritis.

Differential diagnosis of acute monoarticular arthritis
Infectious Crystal induced Hemorrhagic Systemic rheumatological

disorders

Intra-articular derangement

Epidemiology and Demographics

  • Incidence of septic arthritis approximately varies between 2 to 10 cases per 100,000 per year in the general population.[11]
  • Incidence of septic arthritis in patients with history of rheumatoid arthritis and patients with joint prostheses is ~30–70 cases per 100,000 per year.[12]
  • Incidence of septic arthritis in patients with joint prostheses is 40-68 cases per 100,000 per year.
  • The case-fatality rate of septic arthritis is estimated to be 10-25%.[13]
  • Even after survival from septic arthritis, 25-50% of the patients suffer from irreversible loss of joint function.[14][15]

Risk Factors

Most common risk factors that predisposes septic arthritis are rheumatoid arthritis, prosthetic joint or joint replacement and skin infections. Other common risk factors includes:

Natural History, Complications & Prognosis

Septic arthritis commonly present with either mono articular involvement associate with tenosynovitis and dermatitis (gonococcal) or polyarticular involvement (non gonococcal).[13] It is more common in patients in extreme age groups with pre existing joint disorders such as rheumatoid arthritis or predisposing factors such as skin infection.[16] Prompt diagnosis. rapid initiation of treatment, early physical therapy and mobilization are crucial for the outcome of septic arthritis. Complications of septic arthritis mainly depends on the pre existing joint disease and treatment of current infection. Common complications include Joint degeneration (~ 40%) bacteremia (5-20%) osteomyelitis and growth retardation (in children)[17] Prognosis of septic arthritis depends on various factors such host immune response, pre existing joint disease, presence of risk factors, virulence of the pathogen and the duration between onset of symptoms and diagnosis.[18]

Diagnosis

Patients with history of chronic joint disease and concurrent septic arthritis can be misdiagnosed as acute flareup of underlying chronic disease which often delays the treatment for septic arthritis. So, patients with acute flare of one or two new inflamed joints with underlying chronic joint diseases or with another connective tissue disease, it should be assumed that the joint is septic until proven otherwise, should always rule out concurrent septic arthritis with appropriate diagnostic studies.[2] In patients with acute effusion of unknown etiology, might have concurrent crystal-induced arthritis and septic arthritis. So, the synovial fluid should always be cultured and examined for crystals in the evaluation of an acute effusion.[19]

History and Symptoms

Septic arthritis commonly present with joint pain (knee> hip>shoulder>ankle) associate with fever, malaise and local joint symptoms such as swelling, erythema and decreased range of motion at the level of joint. In children, hip is commonly affected. Abrupt onset of a single hot, swollen, and painful joint indicate non gonococcal arthritis.[13] It can involve any joint, but most commonly knee is the site of infection in 50% of cases of adults and elderly patients. Hip infection is the most common site in children.[11] Disseminated gonococcal infection(DGI) often present initially with migratory polyarthralgias, tenosynovitis, dermatitis, and fever. Less commonly, patients with DGI will present with purulent joint effusion, most often of the knee or wrist.[20] Often present with inflamed and tender tendons of the wrist, ankles, and small joints.

Physical Examination

  • Swelling of the joint that involved
  • Decreased range of motion such as pseudo paralysis
  • Patient hold the hip in flexed and externally rotated position if SA involving hip.
  • If child, unwillingness to bear weight on the affected joint (antalgic gait)

Diagnostic Evaluation

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hot, swollen joint suspecting septic arthritis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Joint aspiration
send synovial fluid for Gram stain, culture and cell count
 
 
 
 
 
 
 
 
 
 
 
If dry tap:
Do image guided joint apiration with ultrasound or CT
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Inflammatory/Purulent joint fluid
Presence of PMN 50,000-150,000 cells and mostly neutrophils
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Non-inflammatory fluid/Crystals
Suspect non bacterial arthritis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Gram positive cocci
Start empiric Vancomycin or Nafcicillin
 
 
 
 
 
Gram negative bacilli
Start empiric 3rd generation cephalosporins + aminoglycosides
 
 
 
 
 
Negative Gram stain
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Follow-up with synovial fluid culture results
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
If culture positive
❑ Treat for septic arthritis
❑ Change antibiotics according to the culture results
❑ Joint drainage
 
 
 
 
 
If culture negative
❑ Assess for true or false positivity of Gram stain
❑ Assess for clinical response
 
 
Immunocompromised
start empiric Vancomycin and 3rd generation cephalosporins
 
 
 
 
 
Immunocompetent
start empiric vancomycin
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Wait for culture results
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
If culture positive,
❑ Treat for septic arthritis
❑ Change antibiotics according to the culture results
❑ Joint drainage
 
 
 
 
 
 
 
 
If culture negative
Confirmed non bacterial arthritis and look for alternative diagnosis
 
 
 
 
 
 
 
 
 
 

Imaging Studies

X-ray

X-ray of the joint with septic arthritis are usually normal in the first few days of infection as there is no joint destruction seen usually or may show a preexisting joint disease such as rheumatoid arthritis or osteoarthritis. So, the initial x-ray may be useful to determine pre-existing conditions, such as osteoarthritis or simultaneous osteomyelitis, or may be useful as a baseline image in monitoring the treatment response. However, in the late stages of septic arthritis, X-ray film may show: swelling of the joint capsule and soft tissue around the joint, fat pad displacement, and joint space widening due to localized edema and effusion.[21]

CT

Computerised tomography is used to diagnose ambiguous cases of septic arthritis to differentiate it from other causes of acute arthritis or to determine the extent of bone and soft tissue infections. But, it is less sensitive in the early stages of the disease. In the late stages of septic arthritis, CT shows: visualization of joint effusion, soft tissue swelling, para-articular abscesses, joint space widening due to localized edema, bone erosions, foci of osteitis, and scleroses.[22][7]

MRI

The role of MRI in the diagnosis of septic arthritis has been increasing in recent years in an effort to detect this entity earlier.[23] Findings are usually evident within 24 hours following the onset of infection and include: synovial enhancement, perisynovial edema and joint effusion. Signal abnormalities in the bone marrow can indicate a concomitant osteomyelitis.[24] The sensitivity and specificity of MRI for the detection of septic arthritis has been reported to be 100% and 77% respectively.

Treatment

Medical Therapy

Acute nongonococcal septic arthritis is a medical emergency which causes severe joint destruction and may increase both morbidity and mortality. So prompt diagnosis and treatment with antibiotic therapy and prompt drainage which reduces long-term complications. Vancomycin is recommended as either empirical therapy for patients with Gram-positive cocci on a synovial fluid Gram stain or as a component of regimen for those with a negative Gram stain if methicillin-resistant Staphylococcus aureus (MRSA) is prevalent. If Gram-negative bacilli are observed, an anti-pseudomonal Cephalosporin (e.g., Ceftazidime, Cefepime) should be administered. Carbapenems should be considered in conditions such as colonization or infection by extended-spectrum β-lactamase–producing pathogens. The optimal duration of therapy for septic arthritis remains uncertain. A minimum 3- to 4 week course is suggested for septic arthritis caused by S. aureus or Gram-negative bacteria. The use of Corticosteroids or intraarticular antibiotics is not advisable.[25][26]

Surgical Therapy

Successful treatment of septic arthritis include both anti microbial therapy and removal of intra-articular pus with surgical management. Surgical or arthroscopic management will increase the risk of infections when compared to diagnostic athroscopic procedures without further procedures. Infection rate depends on the type of procedure (open procedures ~17% and arthroscopic procedures 1~1%), duration of the procedure and prior joint disease.[27] Surgical management options include:

  • Closed needle aspiration
  • Open drainage
  • Tidal irrigation
  • Arthroscopy
  • Arthrotomy

Primary Prevention

Prevention of septic arthritis is possible by intensive treatment of risk factors such as old age patients having rheumatoid arthritis, diabetes mellitus, joint prostheses or joint surgery and skin infection.[12]

References

  1. Mathews CJ, Weston VC, Jones A, Field M, Coakley G (2010). “Bacterial septic arthritis in adults”. Lancet. 375 (9717): 846–55. doi:10.1016/S0140-6736(09)61595-6. PMID 20206778.
  2. 2.0 2.1 Goldenberg DL (1998) Septic arthritis. Lancet 351 (9097):197-202. DOI:10.1016/S0140-6736(97)09522-6 PMID: 9449882
  3. Barton LL, Dunkle LM, Habib FH (1987) Septic arthritis in childhood. A 13-year review. Am J Dis Child 141 (8):898-900. PMID: 3498362
  4. Whitehead W (1902) Observations ON THE “OPEN METHOD” OF TREATING EXCEPTIONAL CASES OF SEPTIC ARTHRITIS OF THE KNEE. Br Med J 1 (2164):1523-4. PMID: 20760321
  5. Nathan PW (1917) Arthritis Deformans as an infectious Disease : An experimental and Clinical Study from the Carnegie Laboratory (University and Bellevue Medical College) and the Montefiore Home and Hospital for Chronic Diseases. J Med Res 36 (2):187-224.11. PMID: 19972362
  6. Rankin W (1917) ON THE TREATMENT OF CERTAIN SELECTED CASES OF SEPTIC ARTHRITIS OF THE KNEE. Br Med J 2 (2957):287-9. PMID: 20768715
  7. 7.0 7.1 Shirtliff ME, Mader JT (2002) Acute septic arthritis. Clin Microbiol Rev 15 (4):527-44. PMID: 12364368
  8. Dubost JJ, Fis I, Denis P, Lopitaux R, Soubrier M, Ristori JM et al. (1993) Polyarticular septic arthritis. Medicine (Baltimore) 72 (5):296-310. PMID: 8412643
  9. Klein RS (1988) Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection. Clin Geriatr Med 4 (2):375-94. PMID: 3288326
  10. Atcheson SG, Ward JR (1978) Acute hematogenous osteomyelitis progressing to septic synovitis and eventual pyarthrosis. The vascular pathway. Arthritis Rheum 21 (8):968-71. PMID: 737020
  11. 11.0 11.1 Morgan DS, Fisher D, Merianos A, Currie BJ (1996) An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect 117 (3):423-8. PMID: 8972665
  12. 12.0 12.1 Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA (1995) Risk factors for septic arthritis in patients with joint disease. A prospective study. Arthritis Rheum 38 (12):1819-25. PMID: 8849354
  13. 13.0 13.1 13.2 Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
  14. Kaandorp CJ, Krijnen P, Moens HJ, Habbema JD, van Schaardenburg D (1997) The outcome of bacterial arthritis: a prospective community-based study. Arthritis Rheum 40 (5):884-92. <884::AID-ART15>3.0.CO;2-6 DOI:10.1002/1529-0131(199705)40:5<884::AID-ART15>3.0.CO;2-6 PMID: 9153550
  15. Bengtson S, Knutson K (1991) The infected knee arthroplasty. A 6-year follow-up of 357 cases. Acta Orthop Scand 62 (4):301-11. PMID: 1882666
  16. Esterhai JL, Gelb I (1991) Adult septic arthritis. Orthop Clin North Am 22 (3):503-14. PMID: 1852426
  17. Nelson JD, Koontz WC (1966) Septic arthritis in infants and children: a review of 117 cases. Pediatrics 38 (6):966-71. PMID: 5297142
  18. Goldenberg DL, Cohen AS (1976) Acute infectious arthritis. A review of patients with nongonococcal joint infections (with emphasis on therapy and prognosis). Am J Med 60 (3):369-77. PMID: 769545
  19. Ilahi OA, Swarna U, Hamill RJ, Young EJ, Tullos HS (1996). “Concomitant crystal and septic arthritis”. Orthopedics. 19 (7): 613–7. PMID 8823821.
  20. O’Brien JP, Goldenberg DL, Rice PA (1983) Disseminated gonococcal infection: a prospective analysis of 49 patients and a review of pathophysiology and immune mechanisms. Medicine (Baltimore) 62 (6):395-406. PMID: 6415361
  21. Jaramillo D, Treves ST, Kasser JR, Harper M, Sundel R, Laor T (1995) Osteomyelitis and septic arthritis in children: appropriate use of imaging to guide treatment. AJR Am J Roentgenol 165 (2):399-403. DOI:10.2214/ajr.165.2.7618566 PMID: 7618566
  22. Seltzer SE (1984) Value of computed tomography in planning medical and surgical treatment of chronic osteomyelitis. J Comput Assist Tomogr 8 (3):482-7. PMID: 6725696
  23. Modic MT, Pflanze W, Feiglin DH, Belhobek G (1986) Magnetic resonance imaging of musculoskeletal infections. Radiol Clin North Am 24 (2):247-58. PMID: 3714999
  24. Tehranzadeh J, Wang F, Mesgarzadeh M (1992) Magnetic resonance imaging of osteomyelitis. Crit Rev Diagn Imaging 33 (6):495-534. PMID: 1476623
  25. Mathews, Catherine J.; Weston, Vivienne C.; Jones, Adrian; Field, Max; Coakley, Gerald (2010-03-06). “Bacterial septic arthritis in adults”. Lancet. 375 (9717): 846–855. doi:10.1016/S0140-6736(09)61595-6. ISSN 1474-547X. PMID 20206778.
  26. Sharff KA, Richards EP, Townes JM (2013) Clinical management of septic arthritis. Curr Rheumatol Rep 15 (6):332. DOI:10.1007/s11926-013-0332-4 PMID: 23591823
  27. Armstrong RW, Bolding F, Joseph R (1992) Septic arthritis following arthroscopy: clinical syndromes and analysis of risk factors. Arthroscopy 8 (2):213-23. PMID: 1637435


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Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]

Overview

Septic arthritis is a most rapidly destructive joint disease most common in patients with longstanding rheumatoid arthritis, osteomyelitis, or chronic skin infections. The first case of septic arthritis described in literature by Walter Whitehead in 1902, as “The open method of treating exceptional cases of septic arthritis of the knee” and the cultural techniques of blood and synovial fluid to diagnose septic arthritis described by Robert N. Nye in 1924.[1][2]

Historical Perspective

  • First case of septic arthritis described in literature by Walter Whitehead in 1902, as “The open method of treating exceptional cases of septic arthritis of the knee”.[2]
  • An experimental and clinical Study on arthritis deformans described by Nathan PW in 1917.[3]
  • Surgical management of septic arthritis by By Captain W. Rankin in 1917.[4]
  • A. Mackenzie Forbes, described first case of septic arthritis in infant in 1923.[5]
  • Streptococci as the cause of septic arthritis is first described in 1924.[6]
  • Cultural techniques of blood and synovial fluid to diagnose septic arthritis described by Robert N. Nye in 1924.[1]

References

Template:WH Template:WS

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]

Overview

Septic arthritis broadly classified based on the etiology and based on the clinical presentation.

Classification

Classification Based on the Etiology

Septic arthritis can be classified into 2 types based on the etiology:[1]

Classification Based on the Presentation

Septic arthritis can be classified into 2 types based on the involvement of number of joints involved during presentation:[2]

  • Mono articular septic arthritis (MASA)
    • Most common type of presentation
  • Poly articular septic arthritis (PASA)

References

  1. Shirtliff ME, Mader JT (2002) Acute septic arthritis. Clin Microbiol Rev 15 (4):527-44. PMID: 12364368
  2. Dubost JJ, Fis I, Denis P, Lopitaux R, Soubrier M, Ristori JM et al. (1993) Polyarticular septic arthritis. Medicine (Baltimore) 72 (5):296-310. PMID: 8412643


Template:WikiDoc Sources

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]

Overview

Septic arthritis most commonly develop as a result of hematogenous spreading of bacteria into the synovial membrane, that induces inflammatory reactions. Eventually, release of cytokines and activation of both host humoral and immunological response along with bacterial virulence factors damages articular surface and cartilage.[1][2]

Pathophysiology

Bacterial colonization and adherence into the synovium
Mechanism of transmission Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[1] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.

Determinants of hematognous seeding:[1]

Risk factors: Diabetes mellitus, HIV, immunosuppressants, intravenous drug abuse, osteoarthritis, prosthetic joint and rheumatoid arthritis.[3][4][5]

Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties.[2][6][5]

Risk factors: Previous history of intra-articular injection, prosthetic joint: early and delayed, recent joint surgery.[3]

Contiguous spread: Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection.

Risk factors: Skin infection, cutaneous ulcers.[3][4]

Role of bacterial products in pathogenesis Bacterial attachment protein receptors termed as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) that attach host joint extracellular matrix proteins such as collagen, laminin, elastin etc. and promote colonization and initiate the infectious process.[7][8] The role of bacterial products is activation of host immune response and deteriorate the tissue destruction.[9]
Escape mechanism developed by pathogen Adherence of pathogen to fibronectin on host tissue with its fibronectin receptors[10]

Internalization of pathogen by host mechanisms such as pseudopod formation or through receptor-mediated endocytosis via clathrin-coated pits[11]

After internalization pathogen into the host cells such as osteoblasts, it survives intracellularly and induces apoptosis in the other cells through the activation of host immune response[12]

Host immune response Due to rapid proliferation of bacteria predesposes to activation of host acute inflammatory response

Synovial cells releases host inflammatory cytokines such as IL-1 and IL-6 into the synovium[13]

Activation of acute phase reactants by Interleukins[14]

Acute phase reactants bind to pathogen and promote opsonization and phagocytosis and activates complement system[15]

Phagocytosis of pathogen by macrophages, synovial cells and neutrophils with the release of inflammatory cytokines such as tumor necrosis factor, IL-6 and nitric oxide.[16]

Humoral immunity and adaptive immunity also activates by superantigens of pathogens and promote clearance of pathogen by releasing Interferon-gamma, IL-4, IL-10 that reduces the host mortality and joint destruction.[17][18]
Joint destruction As long as the immune system is able to remove the pathogen from synovium quickly, host is able to protect the joint. If immune system is weak or it is unable to clear the pathogen quickly, there is a potent activation of immune system that causes the joint destruction.
Potent activation of immune system and release of cytokines and oxygen free radicals[19]

Activation and release of

Metalloproteinases, Lysosomal enzymes and proteolytic enzymes from lysosomes, neutrophils and other inflammatory cells[20]

Further damage of joint by bacterial toxins[21]

Infectious process and inflammatory response lead to joint effusion[22][23][24]

Increased intra-articular pressure

Mechanical obstruction to the joint blood supply

Further destruction of bone and cartilage

References

  1. 1.0 1.1 1.2 Klein RS (1988) Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection. Clin Geriatr Med 4 (2):375-94. PMID: 3288326
  2. 2.0 2.1 Atcheson SG, Ward JR (1978) Acute hematogenous osteomyelitis progressing to septic synovitis and eventual pyarthrosis. The vascular pathway. Arthritis Rheum 21 (8):968-71. PMID: 737020
  3. 3.0 3.1 3.2 Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA (1995) Risk factors for septic arthritis in patients with joint disease. A prospective study. Arthritis Rheum 38 (12):1819-25. PMID: 8849354
  4. 4.0 4.1 Weston VC, Jones AC, Bradbury N, Fawthrop F, Doherty M (1999) Clinical features and outcome of septic arthritis in a single UK Health District 1982-1991. Ann Rheum Dis 58 (4):214-9. PMID: 10364899
  5. 5.0 5.1 Le Dantec L, Maury F, Flipo RM, Laskri S, Cortet B, Duquesnoy B et al. (1996) Peripheral pyogenic arthritis. A study of one hundred seventy-nine cases. Rev Rhum Engl Ed 63 (2):103-10. PMID: 8689280
  6. Gray RG, Tenenbaum J, Gottlieb NL (1981) Local corticosteroid injection treatment in rheumatic disorders. Semin Arthritis Rheum 10 (4):231-54. PMID: 6787706
  7. Herrmann M, Vaudaux PE, Pittet D, Auckenthaler R, Lew PD, Schumacher-Perdreau F et al. (1988) Fibronectin, fibrinogen, and laminin act as mediators of adherence of clinical staphylococcal isolates to foreign material. J Infect Dis 158 (4):693-701. PMID: 3171224
  8. Rydén C, Tung HS, Nikolaev V, Engström A, Oldberg A (1997) Staphylococcus aureus causing osteomyelitis binds to a nonapeptide sequence in bone sialoprotein. Biochem J 327 ( Pt 3) ():825-9. PMID: 9581562
  9. Yacoub A, Lindahl P, Rubin K, Wendel M, Heinegård D, Rydén C (1994) Purification of a bone sialoprotein-binding protein from Staphylococcus aureus. Eur J Biochem 222 (3):919-25. PMID: 8026501
  10. Lammers A, Nuijten PJ, Smith HE (1999) The fibronectin binding proteins of Staphylococcus aureus are required for adhesion to and invasion of bovine mammary gland cells. FEMS Microbiol Lett 180 (1):103-9. PMID: 10547450
  11. Essawi T, Na’was T, Hawwari A, Wadi S, Doudin A, Fattom AI (1998) Molecular, antibiogram and serological typing of Staphylococcus aureus isolates recovered from Al-Makased Hospital in East Jerusalem. Trop Med Int Health 3 (7):576-83. PMID: 9705193
  12. Ram S, Mackinnon FG, Gulati S, McQuillen DP, Vogel U, Frosch M et al. (1999) The contrasting mechanisms of serum resistance of Neisseria gonorrhoeae and group B Neisseria meningitidis. Mol Immunol 36 (13-14):915-28. PMID: 10698346
  13. Koch B, Lemmermeier P, Gause A, v Wilmowsky H, Heisel J, Pfreundschuh M (1996) Demonstration of interleukin-1beta and interleukin-6 in cells of synovial fluids by flow cytometry. Eur J Med Res 1 (5):244-8. PMID: 9374445
  14. Osiri M, Ruxrungtham K, Nookhai S, Ohmoto Y, Deesomchok U (1998) IL-1beta, IL-6 and TNF-alpha in synovial fluid of patients with non-gonococcal septic arthritis. Asian Pac J Allergy Immunol 16 (4):155-60. PMID: 10219896
  15. Verdrengh M, Tarkowski A (1998) Granulocyte-macrophage colony-stimulating factor in Staphylococcus aureus-induced arthritis. Infect Immun 66 (2):853-5. PMID: 9453655
  16. Sakiniene E, Bremell T, Tarkowski A (1997) Inhibition of nitric oxide synthase (NOS) aggravates Staphylococcus aureus septicaemia and septic arthritis. Clin Exp Immunol 110 (3):370-7. PMID: 9409638
  17. Hultgren O, Kopf M, Tarkowski A (1999) Outcome of Staphylococcus aureus-triggered sepsis and arthritis in IL-4-deficient mice depends on the genetic background of the host. Eur J Immunol 29 (8):2400-5. PMID: 10458752
  18. Puliti M, von Hunolstein C, Bistoni F, Mosci P, Orefici G, Tissi L (2000) Influence of interferon-gamma administration on the severity of experimental group B streptococcal arthritis. Arthritis Rheum 43 (12):2678-86. <2678::AID-ANR7>3.0.CO;2-A DOI:10.1002/1529-0131(200012)43:12<2678::AID-ANR7>3.0.CO;2-A PMID: 11145025
  19. Roy S, Bhawan J (1975) Ultrastructure of articular cartilage in pyogenic arthritis. Arch Pathol 99 (1):44-7. PMID: 1111494
  20. Riegels-Nielsen P, Frimodt-Møller N, Sørensen M, Jensen JS (1989) Antibiotic treatment insufficient for established septic arthritis. Staphylococcus aureus experiments in rabbits. Acta Orthop Scand 60 (1):113-5. PMID: 2929280
  21. Smith RL, Schurman DJ, Kajiyama G, Mell M, Gilkerson E (1987) The effect of antibiotics on the destruction of cartilage in experimental infectious arthritis. J Bone Joint Surg Am 69 (7):1063-8. PMID: 3654698
  22. Mitchell M, Howard B, Haller J, Sartoris DJ, Resnick D (1988) Septic arthritis. Radiol Clin North Am 26 (6):1295-313. PMID: 3051098
  23. Nelson JD, Koontz WC (1966) Septic arthritis in infants and children: a review of 117 cases. Pediatrics 38 (6):966-71. PMID: 5297142
  24. Knights EM (1982) Infectious arthritis. J Foot Surg 21 (3):229-33. PMID: 6749955

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]

Overview

Septic arthritis develops when bacteria or tiny disease-causing microorganisms that spread through the bloodstream to a synovium. It may also occur when the joint is directly infected with a microorganism from an injury or during surgery.[1] The most common etiological agent of all nongonococcal causes of septic arthritis in the United States is Staphylococcus aureus.[2] The most common sites for this type of infection are the knee and hip. Most cases of acute septic arthritis are caused by bacteria such as staphylococcus or streptococcus. Chronic septic arthritis (which is less common) is caused by organisms such as Mycobacterium tuberculosis and Candida albicans.Gram-negative bacilli account for 10 to 20% of septic arthritis causes.[2] ~10% of patients with nongonococcal septic arthritis are due to polymicrobial cause of infections. Anaerobes are also can cause septic arthritis in few cases.

Causes

Gram-negative bacilli account for 10 to 20% of septic arthritis causes.[2] ~10% of patients with nongonococcal septic arthritis are due to polymicrobial cause of infections. Anaerobes are also can cause septic arthritis in few cases. Most common cause of septic arthritis in children age < 2 years are Haemophilus influenzae (in immunized children), Staph. aureus, group A Streptococcal infections and Kingella kingae.[3] The source of infection in most of the cases (~50%) often from the skin, lungs or bladder.

Common Causes

Common microorganisms causing septic arthritis includes:[4][5][6][4][7][4][8]

Less Common Causes


Microorganism or other infectious disease Associated risk factors Key clinical clues
Staphylococcus aureus
Streptococcus pyogenes

Streptococcal pneumonia

  • Healthy adults with spleenic dysfunction
Groups B Streptococcal infection
  • Healthy adults with spleenic dysfunction
Neisseria gonorrhoeae
Gram-negative bacilli
Haemophilus influenzae
  • Unimmunized children[14]
Anaerobes
Mycobacterium spp.
  • Recent history of travel to endemic areas
  • Immunocompromised patients
  • Recent history of travel to endemic areas (e.g. India, South Africa, Mexico etc.)
  • Incidious onset of monoarthritis
Fungal infection such as
Mycoplasma hominis
  • Recent history of urinary tract procedure
Viral arthritis
HIV infection
  • History of multiple sexual partners
  • History of IVDA
Lyme disease
  • History of recent visit to endemic Lyme area
Reactive arthritis
  • Recent gastrointestinal/ genitourinary infection
Endocarditis

References

  1. Dubost JJ, Fis I, Denis P, Lopitaux R, Soubrier M, Ristori JM et al. (1993) Polyarticular septic arthritis. Medicine (Baltimore) 72 (5):296-310. PMID: 8412643
  2. 2.0 2.1 2.2 2.3 Deesomchok U, Tumrasvin T (1990) Clinical study of culture-proven cases of non-gonococcal arthritis. J Med Assoc Thai 73 (11):615-23. PMID: 2283490
  3. Yagupsky P, Bar-Ziv Y, Howard CB, Dagan R (1995) Epidemiology, etiology, and clinical features of septic arthritis in children younger than 24 months. Arch Pediatr Adolesc Med 149 (5):537-40. PMID: 7735407
  4. 4.0 4.1 4.2 O’Callaghan C, Axford JS (2004). Medicine (2nd ed. ed.). Oxford: Blackwell Science. ISBN 0-632-05162-0.
  5. Bowerman SG, Green NE, Mencio GA (1997) Decline of bone and joint infections attributable to haemophilus influenzae type b. Clin Orthop Relat Res (341):128-33. PMID: 9269165
  6. Peltola H, Kallio MJ, Unkila-Kallio L (1998) Reduced incidence of septic arthritis in children by Haemophilus influenzae type-b vaccination. Implications for treatment. J Bone Joint Surg Br 80 (3):471-3. PMID: 9619939
  7. Topics in Infectious Diseases Newsletter, August 2001, Pseudomonas aeruginosa.
  8. Kaandorp CJ, Dinant HJ, van de Laar MA, Moens HJ, Prins AP, Dijkmans BA (1997) Incidence and sources of native and prosthetic joint infection: a community based prospective survey. Ann Rheum Dis 56 (8):470-5. PMID: 9306869
  9. Goldenberg DL, Cohen AS (1976) Acute infectious arthritis. A review of patients with nongonococcal joint infections (with emphasis on therapy and prognosis). Am J Med 60 (3):369-77. PMID: 769545
  10. 10.0 10.1 Le Dantec L, Maury F, Flipo RM, Laskri S, Cortet B, Duquesnoy B et al. (1996) Peripheral pyogenic arthritis. A study of one hundred seventy-nine cases. Rev Rhum Engl Ed 63 (2):103-10. PMID: 8689280
  11. Vassilopoulos D, Chalasani P, Jurado RL, Workowski K, Agudelo CA (1997) Musculoskeletal infections in patients with human immunodeficiency virus infection. Medicine (Baltimore) 76 (4):284-94. PMID: 9279334
  12. Morgan DS, Fisher D, Merianos A, Currie BJ (1996) An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect 117 (3):423-8. PMID: 8972665
  13. Schattner A, Vosti KL (1998) Bacterial arthritis due to beta-hemolytic streptococci of serogroups A, B, C, F, and G. Analysis of 23 cases and a review of the literature. Medicine (Baltimore) 77 (2):122-39. PMID: 9556703
  14. De Jonghe M, Glaesener G (1995) [Type B Haemophilus influenzae infections. Experience at the Pediatric Hospital of Luxembourg.] Bull Soc Sci Med Grand Duche Luxemb 132 (2):17-20. PMID: 7497542
  15. Luttrell LM, Kanj SS, Corey GR, Lins RE, Spinner RJ, Mallon WJ et al. (1994) Mycoplasma hominis septic arthritis: two case reports and review. Clin Infect Dis 19 (6):1067-70. PMID: 7888535


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Differentiating Septic Arthritis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]

Overview

Septic arthritis should be differentiate from other causes of monoarticular arthritis such as other infectious arthritis, inflammatory arthritis, non inflammatory arthritis, hemorrhagic arthritis and intra articular derangement that causes acute arthritis. Most cases of acute septic arthritis are caused by bacteria such as staphylococcus or streptococcus and it should be differentiated from other causes of arthritis as prompt diagnosis and rapid initiation of treatment is required to limit the complications.

Differential Diagnosis

Differentiating gonococcal arthritis from non-gonococcal arthritis
Characteristic Gonococcal arthritis Non gonococcal arthritis
Patient profile
  • Mostly sexually active young adult
  • Female > male
Initial presentation
  • Single hot, swollen and painful joint
  • Polyarthralgia is very rare
Polyarticular involvement
  • Common (~40–70% of patients)
  • Usually involves 2-3 joints
  • Rare (~10–20% of patients).
  • Mostly monoarticular involvement (>85%)
Recovery of bacteria
  • Positive blood culture <10%
  • Positive synovial fluid culture <50%
  • Positive blood culture 50%
  • Positive synovial fluid culture >90%
Response to antibiotics
  • Within a few days outcome excellent
  • Takes weeks
  • Joint drainage must be adequate
  • Outcome often poor


Infectious Differential for Bacterial Arthritis

Microorganism or other infectious disease Associated risk factors Key clinical clues
Staphylococcus aureus
Streptococcus pyogenes

Streptococcal pneumonia

  • Healthy adults with spleenic dysfunction
Groups B Streptococcal infection
  • Healthy adults with spleenic dysfunction
Neisseria gonorrhoeae
Gram-negative bacilli
Haemophilus influenzae
  • Unimmunized children[7]
Anaerobes
Mycobacterium spp.
  • Recent history of travel to endemic areas
  • Immunocompromised patients
  • Recent history of travel to endemic areas (e.g. India, South Africa, Mexico etc.)
  • Incidious onset of monoarthritis
Fungal infection such as
Mycoplasma hominis
  • Recent history of urinary tract procedure
Viral arthritis
HIV infection
  • History of multiple sexual partners
  • History of IVDA
Lyme disease
  • History of recent visit to endemic Lyme area
Reactive arthritis
  • Recent gastrointestinal/ genitourinary infection
Endocarditis

Differentiatial Diagnsosis for Acute Arthritis

Septic arthritis should be differentiated from other causes of acute arthritis:[9][10][11][12][13]

Type of

Arthritis

Color Transparency Viscosity Volume

(in ml)

WBC count

(per mm3)

PMN

cellcount (%)

Gram stain Gram Culture polymerase chain reaction

(PCR) test

Crystals
Normal Clear Transparent High/thick < 3.5 < 200 < 25 Negative Negative Negative Negative
Gonococcal arthritis Yellow Cloudy-opaque Low Often >3.5 34,000 to 68,000 > 75 Variable (< 50 percent) Positive (25 to 70 percent) Positive (> 75 percent) Negative
Non-gonococcal arthritis Yellowish-green Opaque Very low Often >3.5 > 50,000 (> 100,000 is

more specific)

> 75 Positive (60 to

80 percent)

Positive (> 90 percent) Negative
Inflammatory:

crystalline arthritis

(e.g.Gout, Pseudogout)

Yellow Cloudy Low/thin Often >3.5 2,000 to 100,000 > 50 Negative Negative Negative Positive
Inflammatory:

non-crystalline arthritis

(e.g. Rheumatoid arthritis, reactive arthritis)

Yellow Cloudy Low/thin Often >3.5 2,000 to 100,000 > 50 Negative Negative Negative Negative
Noninflammatory arthritis

(e.g. Osteoarthritis)

Straw Translucent High/thick Often >3.5 200 to 2,000 < 25 Negative Negative Negative Negative
Hemorrhagic Red Bloody Variable Usually >3.5 Variable 50-75 Negative Negative Negative Negative
Lyme arthritis Yellow Cloudy Low Often >3.5 3,000 to 100,000

(mean: 25,000)

> 50 Negative Negative Positive (85 percent) Negative

Microorganism Involved Based on The Clinical History and Symptoms

Clinical history Joints involved Most likely microorganism
Intravenous drug use[14][6] Involvement of axial joints

(e.g. sternoclavicular or sacroiliac joint)

Pseudomonas aeruginosa

Staphylococcus aureus

Sexual activity Tenosynovial involvement in hands, wrists, or ankles Neisseria gonorrhoeae
Terminal complement deficiency[14] Tenosynovial involvement in hands, wrists, or ankles Neisseria gonorrhoeae
Dog or cat bite Small joints involvement Capnocytophaga species

Pasteurella multocida

Ingestion of unpasteurized dairy products[14] Monoarticular involvement, in specific sacroiliac joint Brucella sps
Nail through shoe Foot Pseudomonas aeruginosa
Soil exposure/gardening Monoarticular involvement: knee, hand, or wrist Nocardia sps

Sporothrix schenckii

Soil or dust exposure containing decomposed wood

(north-central and southern United States)[15]

Monoarticular: knee, ankle, or elbow Blastomyces dermatitidis
Southwestern United States, Central and South America

(primary respiratory illness)

Knee Coccidioides immitis
Cleaning fish tank[14][16] Small joints involvement (e.g. fingers, wrists) Mycobacterium marinum

Septic arthritis must be differentiated from other causes of rash and arthritis[17][18][19]

Disease Findings
Nongonococcal septic arthritis
  • Presents with an acute onset of joint swelling and pain (usually monoarticular)
  • Culture of joint fluid reveals organisms
Acute rheumatic fever
  • Presents with polyarthritis and rash (rare presentation) in young adults. Microbiologic or serologic evidence of a recent streptococcal infection confirm the diagnosis.
  • Poststreptococcal arthritis have a rapid response to salicylates or other antiinflammatory drugs.
Syphilis
  • Presents with acute secondary syphilis usually presents with generalized, pustular lesions at the palms and soles with generalized lymphadenopathy
  • Rapid plasma reagin (RPR), Venereal Disease Research Laboratory (VDRL) and Fluorescent treponemal antibody absorption (FTA-ABS) tests confirm the presence of the causative agent.
Reactive arthritis (Reiter syndrome)
  • Musculoskeletal manifestation include arthritis, tenosynovitis, dactylitis, and low back pain.
  • Extraarticular manifestation include conjunctivitis, urethritis, and genital and oral lesions.
  • Reactive arthritis is a clinical diagnosis based upon the pattern of findings and there is no definitive diagnostic test
Hepatitis B virus (HBV) infection
  • Presents with fever, chills, polyarthritis, tenosynovitis, and urticarial rash
  • Synovial fluid analysis usually shows noninflammatory fluid
  • Elevated serum aminotransaminases and evidence of acute HBV infection on serologic testing confirm the presence of the HBV.
Herpes simplex virus (HSV)
  • Genital and extragenital lesions can mimic the skin lesions that occur in disseminated gonococcal infection
  • Viral culture, polymerase chain reaction (PCR), and direct fluorescence antibody confirm the presence of the causative agent.
HIV infection
  • Present with generalized rash with mucus membrane involvement, fever, chills, and arthralgia. Joint effusions are uncommon
Gout and other crystal-induced arthritis
  • Presents with acute monoarthritis with fever and chills
  • Synovial fluid analysis confirm the diagnosis.
Lyme disease
  • Present with erythema chronicum migrans rash and monoarthritis as a later presentation.
  • Clinical characteristics of the rash and and serologic testing confirm the diagnosis.

References

  1. Goldenberg DL, Cohen AS (1976) Acute infectious arthritis. A review of patients with nongonococcal joint infections (with emphasis on therapy and prognosis). Am J Med 60 (3):369-77. PMID: 769545
  2. 2.0 2.1 Le Dantec L, Maury F, Flipo RM, Laskri S, Cortet B, Duquesnoy B et al. (1996) Peripheral pyogenic arthritis. A study of one hundred seventy-nine cases. Rev Rhum Engl Ed 63 (2):103-10. PMID: 8689280
  3. Vassilopoulos D, Chalasani P, Jurado RL, Workowski K, Agudelo CA (1997) Musculoskeletal infections in patients with human immunodeficiency virus infection. Medicine (Baltimore) 76 (4):284-94. PMID: 9279334
  4. Morgan DS, Fisher D, Merianos A, Currie BJ (1996) An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect 117 (3):423-8. PMID: 8972665
  5. Schattner A, Vosti KL (1998) Bacterial arthritis due to beta-hemolytic streptococci of serogroups A, B, C, F, and G. Analysis of 23 cases and a review of the literature. Medicine (Baltimore) 77 (2):122-39. PMID: 9556703
  6. 6.0 6.1 Deesomchok U, Tumrasvin T (1990) Clinical study of culture-proven cases of non-gonococcal arthritis. J Med Assoc Thai 73 (11):615-23. PMID: 2283490
  7. De Jonghe M, Glaesener G (1995) [Type B Haemophilus influenzae infections. Experience at the Pediatric Hospital of Luxembourg.] Bull Soc Sci Med Grand Duche Luxemb 132 (2):17-20. PMID: 7497542
  8. Luttrell LM, Kanj SS, Corey GR, Lins RE, Spinner RJ, Mallon WJ et al. (1994) Mycoplasma hominis septic arthritis: two case reports and review. Clin Infect Dis 19 (6):1067-70. PMID: 7888535
  9. Goldenberg DL (1995) Bacterial arthritis. Curr Opin Rheumatol 7 (4):310-4. PMID: 7547108
  10. Shmerling RH, Delbanco TL, Tosteson AN, Trentham DE (1990) Synovial fluid tests. What should be ordered? JAMA 264 (8):1009-14. PMID: 2198352
  11. Mathews CJ, Kingsley G, Field M, Jones A, Weston VC, Phillips M et al. (2008) Management of septic arthritis: a systematic review. Postgrad Med J 84 (991):265-70. DOI:10.1136/ard.2006.058909 PMID: 18508984
  12. Jalava J, Skurnik M, Toivanen A, Toivanen P, Eerola E (2001) Bacterial PCR in the diagnosis of joint infection. Ann Rheum Dis 60 (3):287-9. PMID: 11171695
  13. Liebling MR, Arkfeld DG, Michelini GA, Nishio MJ, Eng BJ, Jin T et al. (1994) Identification of Neisseria gonorrhoeae in synovial fluid using the polymerase chain reaction. Arthritis Rheum 37 (5):702-9. PMID: 8185697
  14. 14.0 14.1 14.2 14.3 Margaretten ME, Kohlwes J, Moore D, Bent S (2007) Does this adult patient have septic arthritis? JAMA 297 (13):1478-88. DOI:10.1001/jama.297.13.1478 PMID: 17405973
  15. Horowitz DL, Katzap E, Horowitz S, Barilla-LaBarca ML (2011). “Approach to septic arthritis”. Am Fam Physician. 84 (6): 653–60. PMID 21916390.
  16. Gardam M, Lim S (2005). “Mycobacterial osteomyelitis and arthritis”. Infect Dis Clin North Am. 19 (4): 819–30. doi:10.1016/j.idc.2005.07.008. PMID 16297734.
  17. Rompalo AM, Hook EW, Roberts PL, Ramsey PG, Handsfield HH, Holmes KK (1987). “The acute arthritis-dermatitis syndrome. The changing importance of Neisseria gonorrhoeae and Neisseria meningitidis”. Arch Intern Med. 147 (2): 281–3. PMID 3101626.
  18. Rice PA (2005). “Gonococcal arthritis (disseminated gonococcal infection)”. Infect Dis Clin North Am. 19 (4): 853–61. doi:10.1016/j.idc.2005.07.003. PMID 16297736.
  19. Bleich AT, Sheffield JS, Wendel GD, Sigman A, Cunningham FG (2012). “Disseminated gonococcal infection in women”. Obstet Gynecol. 119 (3): 597–602. doi:10.1097/AOG.0b013e318244eda9. PMID 22353959.

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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]Shivani Chaparala M.B.B.S [3]

Overview

Septic arthritis is an orthopaedic emergency with potential high morbidity and mortality.Septic arthritis is also becoming increasingly common among people who are immunosuppressed and elderly persons. Of people with septic arthritis, 45% are older than 65 years. These groups are more likely to have various comorbidities. 56% of patients with septic arthritis are male.

Epidemiology

Incidence

  • Worldwide, the incidence of septic arthritis ranges from a low of 2 per 100,000 persons/ year to a high of 10 per 100,000 persons/ year[1]
  • Worldwide, the Incidence of septic arthritis in patients with history of rheumatoid arthritis and patients with joint prostheses ranges from a low of 30 per 100,000 persons/ year to a high of 70 per 100,000 persons/ year.[2]
  • Worldwide, the Incidence of septic arthritis in patients with joint prostheses ranges from a low of 40 per 100,000 persons/ year to a high of 68 per 100,000 persons/ year.

Case Fatality rate

  • The case-fatality rate of septic arthritis is estimated to be 10-25%.[3]
  • Even after survival from septic arthritis, 25-50% of the patients suffer from irreversible loss of joint function.[4][5]

Demographics

Age

  • Gonococcal arthritis is more common in reproductive age group.
  • Non gonococcal arthritis is more common in extreme age groups such as age >80 years or children <2 years.[6]

Gender

  • In comparison to male, female have a four-fold increased risk of predisposition to gonococcal arthritis due to the asymptomatic nature of gonorrheal infection in women.
  • Poly-articular septic arthritis (PASA) is more common in men when compared to women.[6]

References

  1. Morgan DS, Fisher D, Merianos A, Currie BJ (1996) An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect 117 (3):423-8. PMID: 8972665
  2. Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA (1995) Risk factors for septic arthritis in patients with joint disease. A prospective study. Arthritis Rheum 38 (12):1819-25. PMID: 8849354
  3. Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
  4. Kaandorp CJ, Krijnen P, Moens HJ, Habbema JD, van Schaardenburg D (1997) The outcome of bacterial arthritis: a prospective community-based study. Arthritis Rheum 40 (5):884-92. <884::AID-ART15>3.0.CO;2-6 DOI:10.1002/1529-0131(199705)40:5<884::AID-ART15>3.0.CO;2-6 PMID: 9153550
  5. Bengtson S, Knutson K (1991) The infected knee arthroplasty. A 6-year follow-up of 357 cases. Acta Orthop Scand 62 (4):301-11. PMID: 1882666
  6. 6.0 6.1 Dubost JJ, Fis I, Denis P, Lopitaux R, Soubrier M, Ristori JM et al. (1993) Polyarticular septic arthritis. Medicine (Baltimore) 72 (5):296-310. PMID: 8412643

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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]

Overview

Common risk factors that predisposes septic arthritis include rheumatoid arthritis, prosthetic joint or joint replacement and skin infections. Other risk factors may include recent history of bacteremia, cirrhosis,chronic kidney disease,hypogammaglobulinemia,systemic lupus erythematosis, gout, psuedogout, and charcot’s arthropathy.

Risk Factors

Common Risk Factors

Most common risk factors that predisposes septic arthritis are rheumatoid arthritis, prosthetic joint or joint replacement and skin infections.[1][2][3][4]

Other common risk factors that predispose septic arthritis are as follows:[5][4][6][7][8]

Type of risk factor Examples
Host phagocytic defects
Impaired host defense mechanisms
Direct penetration
  • Intravenous drug use
  • Puncture wonds
  • Intra articular steroid injection
Joint damage
Other risk factors

Micrbiological Clue Based on Risk factors

Type of risk factor Examples
Rheumatoid arthritis Staphylococcus aureus[12][13][8][14][4]
Immunocompromised patients Staphylococcus aureus, Streptococci, Enteric gram-negative bacilli, Listeria monocytogenes
Recent joint surgery Staphylococcus aureus
Intravenous drug use Staphylococcus aureus, Pseudomonas aeruginosa
Diabetes mellitus Staphylococcus aureus, Streptococcus agalactiae
Sexually active young adults

Menstruating females

Neisseria gonorrhea
Elderly adults Staphylococcus aureus, streptococci, Gram-negative bacilli
Post-aspiration or injection Staphylococcus aureus
Trauma Gram-negative bacilli, anaerobes, Staphylococcus aureus
Animal bite (e.g.Cat or dog) Pasteurella multocida, Capnocytophaga spp, Anaerobes
Human bite Eikenella corrodens, Viridans streptococci, Anaerobes
Rat bite Streptobacillus moniliformis
Neonates and children age < 4 years Kingella kingae, Gram-negative bacilli
Unvaccinated children Haemophilus influenza
Systemic lupus erythematosus Salmonella
Sickle cell anemia Salmonella
Hemophilia Staphylococcus aureus, streptococci, Gram-negative bacilli
Ingestion of unpasteurized dairy products Brucella spp

References

  1. Esterhai JL, Gelb I (1991) Adult septic arthritis. Orthop Clin North Am 22 (3):503-14. PMID: 1852426
  2. Dubost JJ, Fis I, Soubrier M, Lopitaux R, Ristori JM, Bussière JL et al. (1994) [Septic arthritis in rheumatoid polyarthritis. 24 cases and review of the literature.] Rev Rhum Ed Fr 61 (3):153-65. PMID: 7920511
  3. Gristina AG, Giridhar G, Gabriel BL, Naylor PT, Myrvik QN (1993) Cell biology and molecular mechanisms in artificial device infections. Int J Artif Organs 16 (11):755-63. PMID: 8150521
  4. 4.0 4.1 4.2 4.3 Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA (1995) Risk factors for septic arthritis in patients with joint disease. A prospective study. Arthritis Rheum 38 (12):1819-25. PMID: 8849354
  5. Dickie AS (1986) Current concepts in the management of infections in bones and joints. Drugs 32 (5):458-75. PMID: 3792229
  6. Morgan DS, Fisher D, Merianos A, Currie BJ (1996) An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect 117 (3):423-8. PMID: 8972665
  7. Rozadilla A, Nolla JM, Mateo L, del Blanco J, Valverde J, Roig D (1992) [Septic arthritis induced by pyogenic germs in patients without parenteral drug addiction. Analysis of 44 cases.] Med Clin (Barc) 98 (14):527-30. PMID: 1602850
  8. 8.0 8.1 Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
  9. Lagaay AM, van Asperen IA, Hijmans W (1992) The prevalence of morbidity in the oldest old, aged 85 and over: a population-based survey in Leiden, The Netherlands. Arch Gerontol Geriatr 15 (2):115-31. PMID: 15374369
  10. Lurie DP, Musil G (1983) Staphylococcal septic arthritis presenting as acute flare of pseudogout: clinical, pathological and arthroscopic findings with a review of the literature. J Rheumatol 10 (3):503-6. PMID: 6887177
  11. Rubinow A, Spark EC, Canoso JJ (1980) Septic arthritis in a Charcot joint. Clin Orthop Relat Res (147):203-6. PMID: 6989540
  12. Goldenberg DL (1998) Septic arthritis. Lancet 351 (9097):197-202. DOI:10.1016/S0140-6736(97)09522-6 PMID: 9449882
  13. Frazee BW, Fee C, Lambert L (2009) How common is MRSA in adult septic arthritis? Ann Emerg Med 54 (5):695-700. DOI:10.1016/j.annemergmed.2009.06.511 PMID: 19665261
  14. Mathews CJ, Coakley G (2008) Septic arthritis: current diagnostic and therapeutic algorithm. Curr Opin Rheumatol 20 (4):457-62. DOI:10.1097/BOR.0b013e3283036975 PMID: 18525361


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Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]

Overview

Septic arthritis can lead to the development of bacteremia and sepsis.Prompt diagnosis, rapid initiation of treatment, early physical therapy and mobilization are crucial for the outcome of septic arthritis.Prognosis of septic arthritis depends on various factors such host immune response, pre-existing joint disease, presence of risk factors, virulence of the pathogen and the duration between onset of symptoms and diagnosis.Poly-articluar septic arthritis in particular, carries a poor prognosis because of bacteremia and sepsis which is associated with increased mortality.Close attention has to be paid to identify and rule out common and chronic joint disorder such as rheumatoid arthritis co-existing with septic arthritis.

Natural History

Septic arthritis commonly presents with either mono-articular involvement associated with tenosynovitis and dermatitis (gonococcal) or polyarticular involvement (non gonococcal).[1] It is most commonly observed in patients of extreme age groups with pre existing joint disorders such as rheumatoid arthritis or predisposing conditions such as skin infection.[2] Prompt diagnosis, rapid initiation of treatment, early physical therapy and mobilization are crucial for the outcome of septic arthritis. Diagnostic delay is an important contributer for the poor outcome of septic arthritis, which carries a 30–50% case-fatality rate.[3] If septic arthritis involving multiple joints, case fatality rate will be >50%.[4]

Complications

Complications of septic arthritis mainly depends on the pre existing joint disease and treatment of current infection. Major complications of septic arthritis includes:[5][6][7][8][9][10]

Common Complications

In children: As the growth plate is in very close to epiphysis, direct extension of a joint infection to the growth plate can lead to reduced bone growth in children.[11][12]

Less Common Complications

Prognosis

Prognosis of septic arthritis depends on various factors such host immune response, pre existing joint disease, presence of risk factors, virulence of the pathogen and the duration between onset of symptoms and diagnosis.[13][1][14]

Indicators of poor prognosis:

  • Delayed beginning of antibiotic therapy, especially 7 days after initial presentation
  • Unable to sterilize synovium with in 6 days of antimicrobial therapy
  • Septic arthritis due to virulent organism that produces super antigens (e.g. Staph. aureus, Gram -ve bacilli)
  • Late mobilization and absence of physical therapy

References

  1. 1.0 1.1 Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
  2. Esterhai JL, Gelb I (1991) Adult septic arthritis. Orthop Clin North Am 22 (3):503-14. PMID: 1852426
  3. Goldenberg DL (1998) Septic arthritis. Lancet 351 (9097):197-202. DOI:10.1016/S0140-6736(97)09522-6 PMID: 9449882
  4. Gupta MN, Sturrock RD, Field M (2001). “A prospective 2-year study of 75 patients with adult-onset septic arthritis”. Rheumatology (Oxford). 40 (1): 24–30. PMID 11157138.
  5. Andersen K, Bennedbaek FN, Hansen BL (1994) [Septic arthritis.] Ugeskr Laeger 156 (26):3871-5. PMID: 8059468
  6. Dubost JJ, Fis I, Denis P, Lopitaux R, Soubrier M, Ristori JM et al. (1993) Polyarticular septic arthritis. Medicine (Baltimore) 72 (5):296-310. PMID: 8412643
  7. Kaandorp CJ, Dinant HJ, van de Laar MA, Moens HJ, Prins AP, Dijkmans BA (1997) Incidence and sources of native and prosthetic joint infection: a community based prospective survey. Ann Rheum Dis 56 (8):470-5. PMID: 9306869
  8. Kaandorp CJ, Krijnen P, Moens HJ, Habbema JD, van Schaardenburg D (1997) The outcome of bacterial arthritis: a prospective community-based study. Arthritis Rheum 40 (5):884-92. <884::AID-ART15>3.0.CO;2-6 DOI:10.1002/1529-0131(199705)40:5<884::AID-ART15>3.0.CO;2-6 PMID: 9153550
  9. Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA (1995) Risk factors for septic arthritis in patients with joint disease. A prospective study. Arthritis Rheum 38 (12):1819-25. PMID: 8849354
  10. Klein RS (1988) Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection. Clin Geriatr Med 4 (2):375-94. PMID: 3288326
  11. Knights EM (1982) Infectious arthritis. J Foot Surg 21 (3):229-33. PMID: 6749955
  12. Nelson JD, Koontz WC (1966) Septic arthritis in infants and children: a review of 117 cases. Pediatrics 38 (6):966-71. PMID: 5297142
  13. Goldenberg DL, Cohen AS (1976) Acute infectious arthritis. A review of patients with nongonococcal joint infections (with emphasis on therapy and prognosis). Am J Med 60 (3):369-77. PMID: 769545
  14. Goldenberg DL, Brandt KD, Cohen AS, Cathcart ES (1975) Treatment of septic arthritis: comparison of needle aspiration and surgery as initial modes of joint drainage. Arthritis Rheum 18 (1):83-90. PMID: 1115748


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Diagnosis

Diagnosis

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Treatment

Treatment

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