Sandbox:septic arthritis: Difference between revisions
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== Causes == | == Causes == | ||
The most common etiological agent of all nongonococcal causes of septic arthritis in the United States is Staphylococcus aureus.<ref name="pmid2283490">Deesomchok U, Tumrasvin T (1990) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=2283490 Clinical study of culture-proven cases of non-gonococcal arthritis.] ''J Med Assoc Thai'' 73 (11):615-23. PMID: [https://pubmed.gov/2283490 2283490]</ref> | The most common etiological agent of all nongonococcal causes of septic arthritis in the United States is Staphylococcus aureus.<ref name="pmid2283490">Deesomchok U, Tumrasvin T (1990) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=2283490 Clinical study of culture-proven cases of non-gonococcal arthritis.] ''J Med Assoc Thai'' 73 (11):615-23. PMID: [https://pubmed.gov/2283490 2283490]</ref> | ||
Gram-negative bacilli account for 10 to 20% of septic arthritis causes.<ref name="pmid2283490">Deesomchok U, Tumrasvin T (1990) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=2283490 Clinical study of culture-proven cases of non-gonococcal arthritis.] ''J Med Assoc Thai'' 73 (11):615-23. PMID: [https://pubmed.gov/2283490 2283490]</ref> | |||
== Pathophysiology == | == Pathophysiology == | ||
Revision as of 20:22, 9 January 2017
Overview
Septic arthritis is a very much important consideration in adults presenting with acute monoarticular arthritis.
Defintion
Historical perspective
Causes
The most common etiological agent of all nongonococcal causes of septic arthritis in the United States is Staphylococcus aureus.[1] Gram-negative bacilli account for 10 to 20% of septic arthritis causes.[1]
Pathophysiology
Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[2]
Direct inoculation: Direct inoculation of microorganisms may occur during joint surgery, particularly in association with knee and hip arthroplasties.
Contiguous spread: Bone infection can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection. This kind of spread is more common in children as the small capillaries can cross the epiphyseal growth plate and permit extension of infection into the epiphysis and joint space.[3][4]
Risk Factors
- Recent history of joint aspiration or local corticosteroid joint injection.[5][2]
- History of Rhematoid arthritis[6]
- History of diabetes mellitus[7]
References
- ↑ 1.0 1.1 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
- ↑ 2.0 2.1 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
- ↑ 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
- ↑ Buckholz JM (1987) The surgical management of osteomyelitis: with special reference to a surgical classification. J Foot Surg 26 (1 Suppl):S17-24. PMID: 3559051
- ↑ Hunter JA, Blyth TH (1999) A risk-benefit assessment of intra-articular corticosteroids in rheumatic disorders. Drug Saf 21 (5):353-65. PMID: 10554051
- ↑ 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
- ↑ 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