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:
- Age >80 years
- Recent history of bacteremia
- Intravenous substance abuse
- Corticosteroid therapy
- Cytotoxic chemotherapy
- Diabetes mellitus
- Alcoholism
- Leukemia
- Granulomatous diseases
- Hypogammaglobulinemia
- Cirrhosis
- Chronic kidney disease
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
- ↑ 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.
- ↑ 2.0 2.1 Goldenberg DL (1998) Septic arthritis. Lancet 351 (9097):197-202. DOI:10.1016/S0140-6736(97)09522-6 PMID: 9449882
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 7.0 7.1 Shirtliff ME, Mader JT (2002) Acute septic arthritis. Clin Microbiol Rev 15 (4):527-44. PMID: 12364368
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 11.0 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
- ↑ 12.0 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
- ↑ 13.0 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
- ↑ 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
- ↑ 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
- ↑ Esterhai JL, Gelb I (1991) Adult septic arthritis. Orthop Clin North Am 22 (3):503-14. PMID: 1852426
- ↑ Nelson JD, Koontz WC (1966) Septic arthritis in infants and children: a review of 117 cases. Pediatrics 38 (6):966-71. PMID: 5297142
- ↑ 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
- ↑ Ilahi OA, Swarna U, Hamill RJ, Young EJ, Tullos HS (1996). “Concomitant crystal and septic arthritis”. Orthopedics. 19 (7): 613–7. PMID 8823821.
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ Tehranzadeh J, Wang F, Mesgarzadeh M (1992) Magnetic resonance imaging of osteomyelitis. Crit Rev Diagn Imaging 33 (6):495-534. PMID: 1476623
- ↑ 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.
- ↑ 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
- ↑ 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
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
- ↑ 1.0 1.1 Nye RN, Waxelbaum EA (1930) STREPTOCOCCI IN INFECTIOUS (ATROPHIC) ARTHRITIS AND RHEUMATIC FEVER. J Exp Med 52 (6):885-94. PMID: 19869811
- ↑ 2.0 2.1 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
- ↑ 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
- ↑ 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
- ↑ Forbes AM (1923) A Case of Septic Arthritis in an Infant. Can Med Assoc J 13 (2):118. PMID: 20314617
- ↑ Cecil RI (1930) Bacteriological Studies on Rheumatic Fever and Infectious Arthritis. Trans Am Climatol Clin Assoc 46 ():36-7. PMID: 21408998
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]
- Gonococcal septic arthritis
- Non-gonococcal septic arthritis
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)
- Less common presentation (~15% of total septic arthritis cases)
- Commonly caused by staphylococcus aureus and other non gonococcal infections such as streptococci and gram negative bacteria.
References
- ↑ Shirtliff ME, Mader JT (2002) Acute septic arthritis. Clin Microbiol Rev 15 (4):527-44. PMID: 12364368
- ↑ 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
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 ⬇ | |
References
- ↑ 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
- ↑ 2.0 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
- ↑ 3.0 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
- ↑ 4.0 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
- ↑ 5.0 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
- ↑ Gray RG, Tenenbaum J, Gottlieb NL (1981) Local corticosteroid injection treatment in rheumatic disorders. Semin Arthritis Rheum 10 (4):231-54. PMID: 6787706
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ Verdrengh M, Tarkowski A (1998) Granulocyte-macrophage colony-stimulating factor in Staphylococcus aureus-induced arthritis. Infect Immun 66 (2):853-5. PMID: 9453655
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ Roy S, Bhawan J (1975) Ultrastructure of articular cartilage in pyogenic arthritis. Arch Pathol 99 (1):44-7. PMID: 1111494
- ↑ 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
- ↑ 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
- ↑ Mitchell M, Howard B, Haller J, Sartoris DJ, Resnick D (1988) Septic arthritis. Radiol Clin North Am 26 (6):1295-313. PMID: 3051098
- ↑ Nelson JD, Koontz WC (1966) Septic arthritis in infants and children: a review of 117 cases. Pediatrics 38 (6):966-71. PMID: 5297142
- ↑ Knights EM (1982) Infectious arthritis. J Foot Surg 21 (3):229-33. PMID: 6749955
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]
- Staphylococcus aureus
- Streptococcal pyogenous
- Streptococcal agalectae
- Streptococcal pneumonia
- Neisseria gonorrhoeae
- Escherichia coli
- Staphylococcus epidermidis
- Haemophilus influenzae
- Pseudomonas aeruginosa
- Salmonella
Less Common Causes
- Peptostreptococcus
- Bacteroides fragilis
- Fusobacterium species
- Borrelia burgdorferi
- Brucella
- Mycobacterium tuberculosis
- Mycoplasma hominis
- Fungal infection such as
| Microorganism or other infectious disease | Associated risk factors | Key clinical clues |
|---|---|---|
| Staphylococcus aureus |
| |
| Streptococcus pyogenes |
|
|
| Groups B Streptococcal infection |
|
|
| Neisseria gonorrhoeae |
|
|
| Gram-negative bacilli |
|
|
| Haemophilus influenzae |
|
|
| Anaerobes |
|
|
| Mycobacterium spp. |
|
|
| Fungal infection such as |
| |
| Mycoplasma hominis |
|
|
| Viral arthritis | ||
| HIV infection |
|
|
| Lyme disease |
|
|
| Reactive arthritis |
|
|
| Endocarditis |
|
References
- ↑ 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
- ↑ 2.0 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
- ↑ 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
- ↑ 4.0 4.1 4.2 O’Callaghan C, Axford JS (2004). Medicine (2nd ed. ed.). Oxford: Blackwell Science. ISBN 0-632-05162-0.
- ↑ 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
- ↑ 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
- ↑ Topics in Infectious Diseases Newsletter, August 2001, Pseudomonas aeruginosa.
- ↑ 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
- ↑ 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
- ↑ 10.0 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
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
| Characteristic | Gonococcal arthritis | Non gonococcal arthritis |
|---|---|---|
| Patient profile |
|
|
| Initial presentation |
|
|
| Polyarticular involvement |
|
|
| Recovery of bacteria |
|
|
| Response to antibiotics |
|
|
Infectious Differential for Bacterial Arthritis
| Microorganism or other infectious disease | Associated risk factors | Key clinical clues |
|---|---|---|
| Staphylococcus aureus |
| |
| Streptococcus pyogenes |
|
|
| Groups B Streptococcal infection |
|
|
| Neisseria gonorrhoeae |
|
|
| Gram-negative bacilli |
|
|
| Haemophilus influenzae |
|
|
| Anaerobes |
|
|
| Mycobacterium spp. |
|
|
| Fungal infection such as |
| |
| Mycoplasma hominis |
|
|
| Viral arthritis | ||
| HIV infection |
|
|
| Lyme disease |
|
|
| Reactive arthritis |
|
|
| 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 |
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 |
| 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 |
| 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 |
| 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 |
|
| Acute rheumatic fever |
|
| Syphilis |
|
| Reactive arthritis (Reiter syndrome) |
|
| Hepatitis B virus (HBV) infection |
|
| Herpes simplex virus (HSV) |
|
| HIV infection |
|
| Gout and other crystal-induced arthritis |
|
| Lyme disease |
|
References
- ↑ 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
- ↑ 2.0 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 6.0 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
- ↑ 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
- ↑ 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
- ↑ Goldenberg DL (1995) Bacterial arthritis. Curr Opin Rheumatol 7 (4):310-4. PMID: 7547108
- ↑ Shmerling RH, Delbanco TL, Tosteson AN, Trentham DE (1990) Synovial fluid tests. What should be ordered? JAMA 264 (8):1009-14. PMID: 2198352
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 14.0 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
- ↑ Horowitz DL, Katzap E, Horowitz S, Barilla-LaBarca ML (2011). “Approach to septic arthritis”. Am Fam Physician. 84 (6): 653–60. PMID 21916390.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
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
- ↑ 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
- ↑ 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
- ↑ Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
- ↑ 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
- ↑ 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
- ↑ 6.0 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
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 |
| |
| Joint damage |
| |
| Other risk factors | ||
Micrbiological Clue Based on Risk factors
References
- ↑ Esterhai JL, Gelb I (1991) Adult septic arthritis. Orthop Clin North Am 22 (3):503-14. PMID: 1852426
- ↑ 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
- ↑ 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
- ↑ 4.0 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
- ↑ Dickie AS (1986) Current concepts in the management of infections in bones and joints. Drugs 32 (5):458-75. PMID: 3792229
- ↑ 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
- ↑ 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
- ↑ 8.0 8.1 Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
- ↑ 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
- ↑ 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
- ↑ Rubinow A, Spark EC, Canoso JJ (1980) Septic arthritis in a Charcot joint. Clin Orthop Relat Res (147):203-6. PMID: 6989540
- ↑ Goldenberg DL (1998) Septic arthritis. Lancet 351 (9097):197-202. DOI:10.1016/S0140-6736(97)09522-6 PMID: 9449882
- ↑ 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
- ↑ 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
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
- Joint degeneration (arthritis): common with non gonococcal arthritis (~ 40%)
- Bacteremia (5-20%)
- Osteomyelitis
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:
- Elderly patient (age > 80 yrs)
- Pre existing medical conditions such as diabetes mellitus or pre existing joint diseases such as rheumatoid arthritis or prosthetic joint
- Presentation with poly articular involvement which increases the risk of bacteremia
- 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
- ↑ 1.0 1.1 Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
- ↑ Esterhai JL, Gelb I (1991) Adult septic arthritis. Orthop Clin North Am 22 (3):503-14. PMID: 1852426
- ↑ Goldenberg DL (1998) Septic arthritis. Lancet 351 (9097):197-202. DOI:10.1016/S0140-6736(97)09522-6 PMID: 9449882
- ↑ 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.
- ↑ Andersen K, Bennedbaek FN, Hansen BL (1994) [Septic arthritis.] Ugeskr Laeger 156 (26):3871-5. PMID: 8059468
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ Knights EM (1982) Infectious arthritis. J Foot Surg 21 (3):229-33. PMID: 6749955
- ↑ Nelson JD, Koontz WC (1966) Septic arthritis in infants and children: a review of 117 cases. Pediatrics 38 (6):966-71. PMID: 5297142
- ↑ 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
- ↑ 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
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | X Ray | CT | MRI | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgical Therapy | Primary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Related Chapters
Related Chapters
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