Septic Arthritis

Authors: Nalini Rao, M.D., FACP, FSHEA,  Bruce H. Ziran, M.D.

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.


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).


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. actinomycetemcomitansM. catarrhalis and P. multocida have been implicated in osteoarticular infections.

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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.


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.

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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) (17Table 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 (1231).

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.

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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.

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

Organism Children (6 mo. to 5 yrs.) Young adult Adult Elderly
Staphylococcus aureus 10% - 20% 15% - 20% 60% - 70% 45% - 65%
Streptococci 5% - 10% 1% - 5% 15% - 20% 10% - 15%
Gram-negative bacteria 1% - 5% Rare 10% - 15% 15% - 35%
Haemophilus influenzae 30% - 50% 1% - 5% 1% - 5% Rare
Neisseria gonorrhoeae 1% - 5% 60% - 80% 1% - 5% Rare

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

Table 2.   Septic Arthritis Complicating a Clinical Setting

Clinical Setting

Risk Factors


Frequency of Pathogen

Special Points

Rheumatoid Arthritis


Disabling arthritis

Skin lesions

Infected rheumatoid nodule

TNF suppression therapy

Staphylococcus aureus

Streptococcus pyogenes


M. catarrhalis,

Listeria –with

TNF suppression




Patient education

Early diagnosis

Surgical debridement and antibiotics

Special caution with TNF suppression therapy

Advanced Age

Diabetes mellitus, Urinary tract infection Biliary tract    infection, Diverticulitis

Staphylococcus aureus

Gram negatives bacilli



Poor outcome if treatment started after 7 days of symptoms


Bacterial Endocarditis

Septic immobilization Reactive immune arthritis

Intravenous drug use


Staphylococcus aureus

Streptococcus pyogenes

Pseudomonas aeruginosa




Adverse affects of antibiotics


4- 6 weeks

Prosthetic Joints

Dental procedures



DM, hemophilia, UTISkin Infection, Previous Joint infection

Joint replacement < 2 yrs

Staphylococcus species

Streptococcus species

Gram negative bacilli




Antibiotic prophylaxis indicated

Immunosuppression, AIDS and Stem cell transplantation


Decreased humoral and cell mediated immunity





Atypical mycobacteria



and unusual organisms

Whipple’s Disease


Tropheryma whippelii




Decreased humoral immunity





Microinfracts in intestinal wall.


Staphylococcus aureus


Osteomyelitis more common than septic arthritis

Human and Animal Bites

 Inoculation of indigenous mouth flora

Pasteurella multocida,

Eikenella corrodensStreptobacillus moniliformis


Septic arthritis

in proximity to site of injury.

Knuckle osteo with clenched fist injury.

Intravenous drug use



Staphylococcus aureus

Pseudomonas aeruginosa

Candida species




Seen in sacroiliac, strenocostal and strenclavicular clavicular joints

Plant Thorns

Puncture wound

Foreign body

Pantoea agglomerans,Sporotrichosis,

Atypical mycobacteria,Nocardia,

Clostridium sordellii,actinomycosis


Image joint for foreign body

Resident in endemic area with known or suspected tick exposure


Borrelia burgdorferi



Exposure to aquatic environment


M. marinum


Small joints of hand

Positive Tuberculin skin test.  Resident in endemic area


M. tuberculosis



Axial skeleton and large joint

Table 3. Microorganisms Associated with Reactive Arthritis

Chlamydia trachomatis

Shigella flexneri

Salmonella enteriditis

Salmonella typhimurium

Yersinia enterocolitica

Yersinia pseudotuberculosis

Campylobacter jejuni

Adapted from Hughes and Keat (11)

Table 4. Empiric Antibiotic Therapy of Suspected Septic Arthritis

Gram stain of synovial fluid

Antibiotic therapy

Gram-positive cocci


     No risk factors for MRSA

Cefazolin 2 g IV q 8 h

     MRSA risk factors or β-lactam allergy

Vancomycin 1 g IV q 12 h

Gram negative cocci (presumptive Neisseria sp)

Ceftriaxone 1 g IV q 24 h

Gram-negative rods

Cefepime 2 g IV q 8 h, or


4.5 g IV q 6 h

No organisms on gram stain


Previously healthy, low MRSA risk

Cefazolin 2 g IV q 8 h

MRSA risks present

Vancomycin 1 g IV q 12 h plus cefepime, 2 g IV

 q 8 h, or

Piperacillin/tazobactam 4.5 g IV q 6 h

MRSA = methicillin-resistant Staphylococcus aureus

Table 5.   Antibiotic Therapy for Specific Pathogens


Antimicrobial agent



Streptococcus species

Penicillin or ampicillin

Clindamycin or first-generation cephalosporin


3 – 4 weeks

Methicillin-sensitiveStaph. aureus

Nafcillin or first-generation cephalosporin


3 – 4 weeks or longer

Methicillin-resistant Staph. aureus



Quinupristin/Dalfopristin Linezolid

3 – 4 weeks or longer

N. gonorrheae


Fluoroquinolone  IV

2 – 3 weeks

Gram-negative bacilli other than Pseudomonas aeruginosa

Third-generation cephalosporins

Extended spectrum penicillin, Fluoroquinolone, TMP/Sulfa

3 – 4 weeks

Pseudomonas aeruginosa

Pipercillin plus aminoglycosides

Cefepime plus aminoglycosides Ciprofloxacin,Levofloxacin

3 – 4 weeks or longer


Table 6. Comparison of Drainage Procedures in Septic Arthritis

Factors Aspiration Tidal irrigation Arthroscopy Arthrotomy




Operating room

Operating room






Joint accessibility

All joints (rpt aspirations limited to large, superficial joints

Limited to large, superficial joints

Limited to

Large joints

All joints

Drainage accessibility





Adhesion lysis















Recovery time





Cost Inexpensive Inexpensive Expensive Expensive

Table 7.  Test Characteristics of Synovial Fluid Studies

    Septic arthritis   Acute inflammatory   Non-inflammatory   Normal

Turbid yellow

Turbid yellow

Clear, straw

Clear, colorless

Fibrin clot





  WBCs count      (/μL)   Septic Arthritisa Gonococal Arthritis

TB  Arthritis

Acute Gouty        Arthritis Rheumatic Fever Rheumatoid Arthritis   <5000   <200
Range    15600- 21,300  1500-10,800  2500-10,500  750-45,000  300-98,000  300-75,000
Average  65400  14000  23500  13500  17800  15500
PMN (%) Range    ≥90 b  2-96  29-96  48-94  8-98  5-96   <25   <25
Average  95  64  67  83  46  65

Blood- synovial glucose difference


Low glucosed     

Range    40-122  0-97  0-108    0-41    0-88



Average  71  25  57  12  6  31
LDH (U/L)   >250e   >100  <250  <250
Gram stein/ Culture   Positivef  Negative  Negative  Negative
Crystals  Negative  Monosodium urate (gout), Calcium pyrophosphate (pseudogout), Hydroxyappatite  Negative  Negative

   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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