Septic arthritis overview
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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]
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.
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 which damages articular surface and cartilage along with bacterial virulence factors.[9][10]
Causes
Septic arthritis develops when bacteria or other tiny disease-causing organisms (microorganisms) spread through the bloodstream to a joint. 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
Diagnosis
Patients with history of chronic disease with 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]
History and Symptoms
Septic arthritis commonly present with joint common (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.[11] 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.[12] Disseminated gonococcal infection(DGI) often present initially with migratory polyarthralgias, tenosynovitis, dermatitis, and fever and less commonly, <50% of patients with DGI will present with purulent joint effusion, most often of the knee or wrist.[13] 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 neutrphils | 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 varncomycin | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
CT
CT is more sensitive than plain films for the detection of early bone destruction and effusion.
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. 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. The sensitivity and specificity of MRI for the detection of septic arthritis has been reported to be 100% and 77% respectively.
Treatment
Medical Therapy
Therapy is usually with intravenous antibiotics, analgesia and washout/aspiration of the joint to dryness.
Primary Prevention
Preventive (prophylactic) antibiotics may be helpful for people at high risk.
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
- ↑ 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
- ↑ Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
- ↑ 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
- ↑ 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