Septic Arthritis

Septic arthritis is a medical and surgical emergency that can lead to rapid destruction of the joint and irreversible loss of function. It is caused by invasion of the microorganisms into the synovial space. Bacteria are the most common cause of joint of infection although other pathogens such as viruses, fungi and mycobacteria may also be responsible.

Bacteria enter the joint through several mechanisms including direct inoculation, penetrating trauma, surgical incision including arthroscopy, spread from a contiguous focus of soft tissue infection or hematogenous seeding from a distant focus. Hematogenous seeding is the most common route. Negative prognostic factors include older age, delay in onset of treatment, pre-existing arthritis, immunosuppressive therapy, resistant organisms and multiple joint involvements. Septic arthritis results in loss of function in 25% to 50% of patients despite appropriate therapy. Table 1 lists the microbiology of bacterial arthritis in relationship to patient’s age.

Zeller V, et al. Continuous Clindamycin Infusion, an Innovative Approach to Treating Bone and Joint Infections. Antimicrobial Agents and Chemotherapy. 2010;54(1):88-92.

RISK FACTORS

Degenerative joint disease, rheumatoid arthritis, and corticosteroid therapy are the most common predisposing conditions. Total joint arthroplasties are susceptible to intraoperative or hematogenous seeding which can result in subsequent prosthetic infection. While patients infected with HIV demonstrate a higher prevalence of septic arthritis or osteomyelitis than does the general population this may be due to intravenous drug abuse and multiple transfusions in this patient population (25).

NON GONOCOCCAL BACTERIAL SEPTIC ARTHRITIS

In adults non gonococcal acute septic arthritis occurs with an incidence of 0.034% to 0.13%. One to two percent of patients with total joint arthroplasty may develop septic complications. 90% of cases are mono-articular with knee being involved in 50% of these cases. Staphylococcus aureus and streptococci remain the predominant organism although certain other unusual organisms may be seen in specific clinical settings (Table 2). In addition, certain microorganisms may be associated with reactive arthritis (Table 3). Several unusual organisms such as Kingella spp., A. actinomycetemcomitans, M. catarrhalis and P. multocida have been implicated in osteoarticular infections.

PATHOPHYSIOLOGY

Bacterial invasion of the highly vascular synovium results in bacterial trapping and multiplication in the subsynovium. The host responds with acute inflammatory reaction and phagocytosis by the polymorphonuclear leucocytes. Toxins and enzymes are released by bacterial and stimulated T-cells leading to destruction of the articular cartilage. Revascularization, synovial proliferation and granulation tissue develop. Synovial fluid white blood cell count can exceed over 50,000/mm3 and increased intracavitary of pressure from accumulation of the purulent fluid resulting in necrosis of the synovium and cartilage. Pro-inflammatory cytokines such as interluken-1 and tumor necrosis factor α also contribute to joint injury.

(Printable Version of Causes of Septic Arthritis)

CLINICAL PRESENTATION

Clinical signs and symptoms may be variable and imprecise. The key to diagnosis is thorough clinical history, physical examination along with laboratory studies of the synovial joint fluid from the affected joint. Pain and limited motion of the involved joint is present in more than 80% of the patients. Fever is seen in 60% to 80% of the patients unless masked by the use of anti-inflammatory agents and steroids.

Joint Distribution: Knee is the most commonly involved joint. 45% to 50% of the septic arthritis in adults involves the knee. Other large joints include hip 15%, ankle 9%, elbow 8%, wrist 6% and shoulder 5%. Polyarticular disease is seen in 10% to 20% of cases. It is usually asymmetric and involves an average of four joints. Major risk factors are steroid therapy, rheumatoid arthritis, lupus and diabetes mellitus.

LABORATORY DIAGNOSIS

The laboratory abnormalities suggestive septic arthritis includes peripheral leucocytosis, elevated sedimentation rate and C-reactive protein. The synovial fluid cell count greater than 50,000/mm3 with more than 75% polymorphonuclear leucocytes is a commonly used threshold for empiric therapy. Blood cultures are likely to be positive in non gonococcal bacterial arthritis. A presumptive diagnosis of septic arthritis may be made with positive blood culture and a negative synovial fluid culture in an appropriate clinical setting.

The definitive diagnosis of bacterial arthritis requires identification of bacteria from synovial fluid obtained through athrocentesis. This procedure should be performed in all patients with inflammatory arthritis in whom septic arthritis is suspected. Synovial WBC count >25000/μL, percentage of polymorphonuclear cells ≥ 90% and LDH> 250 U/L provide the high sensitivity in diagnosing septic arthritis (sensitivity: 88%, 92% and 100%, respectively) (17, Table 7).

Microscopic examination of the synovial fluid may eliminate crystal-induced inflammatory arthritis. Gram stain of the fluid is highly specific but not sensitive and may vary based upon the pathogen (Table 7). Culture of the synovial fluid is essential and the yield for positive culture may be maximized with inoculation into blood culture medium rather than plating on solid media. Direct inoculation of synovial fluid into blood culture medium bottles may improve the recovery of pathogens (12, 31).

Polymerase chain reaction (PCR) can be used in microbiological confirmation of septic arthritis. The problem of false-positive results needs to be addressed by more refined techniques which may replace the current methods of diagnosis.

(Printable Version of Clinical Presentation and Diagnosis of Septic Arthritis)

MANAGEMENT

Treatment comprises of three facets: appropriate antibiotic therapy to eradicate the infection, decompression of the joint with evacuation of infected and inflammatory exudate and restoration of stability and function of the joint.

Antimicrobial Agent Therapy

Septic arthritis is frequently a medical and surgical emergency. It is important to withhold antibiotics until operative cultures are obtained, especially if the clinical course is atypical or subacute. After obtaining appropriate cultures of blood and synovial fluid, empiric antibiotic therapy should be started immediately.

Gram stains are important to review. If positive, antibiotic therapy can be more readily targeted toward a specific pathogen. If negative, empiric therapy should almost always include therapy against S. aureus (Table 4). Age is an important consideration for coverage against H. influenza and N. gonorrhoeae (Table 1). The three variables of antimicrobial therapy are selection, route and duration of treatment (Tables 4-5).

Adjunctive Therapy

Joint decompression may be accomplished by several methods and often debated between medical and surgical specialists. However, there are no randomized controlled studies comparing different forms of drainage. In the order of invasiveness, cost and effectiveness in the drainage procedure, the methods include needle aspiration, tidal irrigation, arthroscopy and arthrotomy as outlined in Table 6. If the joint is easily accessible and if the infected material be easily removed, patients may be treated at the bed side with repeated aspirations. Tidal irrigation can also be performed at the bed side and is reported as effective as arthroscopy. Arthroscopic lavage is being used increasingly in the management of septic arthritis including hips. Surgeons tend to prefer open drainage which allows rapid decompression, complete removal of accumulated debris including polymorphonuclear byproducts and bacterial toxins. In addition, this procedure allows for lysis of adhesions, removal of thick exudate, clot and fibrin. Arthrotomy is often recommended in cases where joint needs to be decompressed urgently. The role of synovectomy in acute septic arthritis is unclear. It is an essential part of persistent or chronic infection.

Rehabilitation of the joint begins at the time of diagnosis. Initially the joint should be immobilized in a position of function. Active and passive range of motion should begin as soon as the acute symptoms subside or soon after the drains are removed and the drain-sites are sealed.

(Printable Version of Management for Septic Arthritis)

Zeller V, et al. Continuous Clindamycin Infusion, an Innovative Approach to Treating Bone and Joint Infections. Antimicrobial Agents and Chemotherapy. 2010;54(1):88-92.

READING LIST

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12. Hughes JG, Vetter EA, Patel R, Schleck CD, Harmsen S, Turgeant LT, Cockerill FR 3rd. Culture with BACTEC Peds Plus/F bottle compared with conventional methods for detection of bacteria in synovial fluid. J Clin Microbiol. 2001 Dec;39(12):4468-71. [PubMed]

13. Kocher MS, Mandiga R, Murphy JM, Goldmann D, Harper M, Sundel R, Ecklund K, Kasser JR. A Clinical Practice guideline for Treatment of Septic Arthritis in Children. J Bone Joint Surg Am 2003;85-A(6):994-999. [PubMed]

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15. Lentino JR. Prosthetic joint infections. Clin Inf Dis 2003;36:1157-1161. [PubMed]

16. Mader JT, Shirtliff ME, Bergquist S, Calhoun JH. Bone and Joint Infections in the Elderly. Drugs Aging 2000;16:67-80. [PubMed]

17. Margaretten ME. Does This Adult Patient Have Septic Arthritis? JAMA 2007; 297:1478-1488. [PubMed]

18. Mariani BD, Tuan RS. Advances in the diagnosis of infection in prosthetic joint implant. Molecular Med Today 1998;4:207-213. [PubMed]

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26. Shmerling R. Synovial Fluid Tests JAMA 1990;264:1009-1014. [PubMed]

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Table 1 Microbiology of Bacterial Septic Arthritis Related to Age of Patient.

Adapted from Gorbach SL et al (Eds), Infectious Diseases, 2^nd Edition, 1998

Table 2. Septic Arthritis Complicating a Clinical Setting

Table 3. Microorganisms Associated with Reactive Arthritis

Adapted from Hughes and Keat (11)

Table 4. Empiric Antibiotic Therapy of Suspected Septic Arthritis

MRSA = methicillin-resistant Staphylococcus aureus

Table 5. Antibiotic Therapy for Specific Pathogens

TMP/Sulfa=Trimethrorim/Sulfamethoxazol

Table 6. Comparison of Drainage Procedures in Septic Arthritis

Table 7. Test Characteristics of Synovial Fluid Studies

Modified from  32 and 17

    a) Sensitivity/Specificity (%) for septic arthritis  (Data taken from 32)

      >10,000                  40/99

      > 50,000                 70/92

      > 25,000                 88/71

   b) Highly sensitive (Sensitivity/Specificity  92/78 (%)) for septic arthritis

   c) Glucose concentration may give spurious results unless obtained after prolonged fasting, and differences between joint and blood samples

        may not be significant unless >50 mg/dL.  Joint tap should be performed, preferably after the patient has been fasting for >4 hrs, and a

        blood glucose determination should be performed simultaneously.

   d) Serum/synovial fluid glucose ratio of less than 0.5 or 0.75, synovial fluid glucose level of less than 1.5mmol/mL, or both Sen/Spe  64/85(%) 

       for septic arthritis

   e) Highly sensitive (Sensitivity/Specificity  100/51 (%)) for septic arthritis.

       Gas liquid chromatography assay is superior to enzymatic analysis of LDH

   f) Gram stain: highly specific, low sensitive (Sensitivity/Specificity 50-70/100(%)).

       Gram-negative diplococci for gonococcal arthritis are demonstrated in only 10-25%

       Culture                               Sensitivity           Specificity

        Non-gonococcal                75-95                      >90

        Gonococcal                         10-50                     >90

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