Septic Arthritis/Infection native joints

OVERVIEW: What every practitioner needs to know

Are you sure your patient has infectious arthritis? What should you expect to find?

  • The symptoms, signs and presentation of septic arthritis are dependent upon:

    The class or type of pathogen (bacterial, fungal, mycobacterial, or viral)

    Location of the afflicted joint

    Underlying illnesses and immune function of the infected individual.

  • In general, septic arthritis is characterized by its presentation as either acute or chronic.

    Acute infectious arthritis, also called bacterial, pyogenic, septic or suppurative arthritis is predominately caused by bacterial pathogens

    Chronic infectious arthritis is most often due to fungal and mycobacterial pathogens (see discussion in Mycobacterial and Fungal joint Infection below).

    Viral infections may also be associated with arthritis either due to direct infection of the joint or sterile inflammation related to systemic infection and its immune response.

  • Acute non-gonococcal bacterial arthritis almost always presents with some combination of pain, swelling, or loss of function of one or more joints.

    A single large joint is most often afflicted

    Multiple joints may be infected in 10-20% of patients

    The knee is involved in a little over 50% of cases

    Other sites of large joint infection in adults include the hip, shoulder, wrist and ankle

    In children the hip is most commonly infected

    Symptoms may arise over a few hours but usually steadily increase over a few days

    In a systematic review:

    Joint pain and swelling at presentation was noted in 85 and 78 percent of patients respectively

    Fever and malaise is noted by many patients, high fever, rigors, shaking chills and night sweats are uncommon

    In persons who are immunocompromised, elderly or with significant comorbid illness, the presentation of acute bacterial arthritis may be less obvious with fewer joint symptoms and less fever.

    Active bacterial joint infection in patients with rheumatoid arthritis may manifest only as an subtle increase in preexisting joint inflammation or dysfunction.

    Systemic and articular steroids will also mask symptoms of acute joint infection.

  • The presentation of gonococcal arthritis is usually that of disseminated gonococcal infection (DGI) and may be similar to monoarticular or oligoarticular arthritis as outlined above.

    More commonly, the presentation is one of a syndrome of:

    Tenosynovitis – involves the fingers, hands and wrists more often than the joints of the distal lower limb

    Dermatitis – solitary scattered, painless, nonpruritic lesions of the limbs (including the palms and soles), appears with the onset of tenosynovitis, and often self resolves after 4-5 days

    Polyarthralgia without overt manifestations of suppurative joint infection.

    Disseminated gonococcal infection often presents concurrently with or immediately follows menstruation in females

    Fever and chills are reported by most patients

    Mono/oligoarticular gonococcal arthritis may occasionally follow the classic tenosynovitis syndrome of DGI or present without this prodrome

    Joint symptoms may be severe and predominate in either presentation

    Symptoms of mucosal gonorrhea of the urethra, uterine cervix, throat or rectum are usually absent but occasionally may predate or coexist with DGI or gonococcal arthritis.

  • The physical findings of acute bacterial arthritis are that of acute inflammation, including:

    Joint tenderness



    Limited/painful active or passive range of motion

    Increased skin temperature and redness is often noted when compared to the non-afflicted joint

    Fever may or may not be present on presentation

    Physical signs of infection may be subtle or absent in joints that have recently been injected with intraarticular steroids or previously afflicted with chronic joint disease such as rheumatoid arthritis

  • Exam findings in a patient with disseminated gonococcal infection will often show:

    The characteristic swelling, tenderness, erythema and painful movement of tenosynovitis

    Careful inspection should be made for the characteristic discrete, nontender macular, papular and pustular lesions often on the distal extremities:

    Older lesions may have central necrosis

    Lesions are seen on presentation in 60-70% of patients

    Usually no obvious evidence of purulent urethritis or cervicitis on genital examination

  • Some authors suggest that in 50% of patients a careful history and physical examination will suggest a primary site or origin for the pathogen causing acute or chronic septic arthritis.

How did the patient develop infectious native joint arthritis? What was the primary source from which the infection spread?

  • Acute bacterial septic arthritis of native joints is usually acquired hematogenously during clinically evident or occult bacteremia.

    Bacteremia may be community- or hospital-acquired and may predate the onset of acute septic arthritis by days, weeks or sometimes months.

    Nosocomial cases may involve primary bacteremia due to:


    Intravenous catheter infections

    Secondary bacteremia complicating focal infection

    Community-acquired cases may be secondary to bacteremia associated with:


    Intravenous drug use

    Long-term intravenous catheters

    Focal infections including pneumonia

    Occult bacteremia can arise from skin lesions or disease, even if overt skin infection is absent

    Potential sources of bacteremia as a source for a septic joint should be explored in the history and physical exam, and with ancillary tests and imaging if indicated

  • Other routes of joint infection that should be considered include:

    Contiguous spread from infected periarticular tissues or bone

    Percutaneous puncture from sharp foreign bodies

    Trauma or human/animal bites

    Surgery, arthrotomy or arthroscopic

    Aspiration or injection

  • Septic arthritis is a rare complication of arthroscopic reconstructive surgery occurring in less than 1% of patients in most studies.

  • Direct joint inoculation of potential pathogens rarely occurs during a single joint aspiration or injection, but may involve:

    Unusual bacterial, or fungal pathogens

    Occur in clusters or outbreaks caused by distribution or compounding of contaminated medication, particularly corticosteroids.

  • The source of disseminated gonococcal infection (DGI) is usually the uterine cervix or urethra. Throat and rectal origin has also been described.

    The vast majority of patients with DGI or gonococcal arthritis are sexually active and a detailed sexual history should be obtained.

    Dissemination from the uterine cervix is greatly enhanced during menstruation, pregnancy, and in the immediate post-partum state.

  • The origin of chronic articular infection is dependent on the specific pathogen and its natural history of infection.

    Joint introduction of these pathogens is mostly due to hematogenous dissemination

    Other routes exist, similar to those noted above

    Dimorphic, environmental fungi, Cryptococcus neoformans, and Mycobacterium tuberculosis will usually have a primary respiratory source.

Which individuals are of greater risk of developing septic arthritis?

  • The most important underlying risk factor predisposing an individual for septic arthritis is a pre-existing arthritis particularly that due to inflammatory arthritides, especially rheumatoid arthritis.

  • Other causes of arthritis, including:

    Crystalline arthropathies (gout and pseudogout)

    Osteoarthritis, also increase this risk but not to the degree of rheumatoid arthritis

    Host immunodeficiency due to chemotherapy and drugs commonly used in inflammatory arthritides including penicillamine, sulfasalazine and prednisone, but not methotrexate, also predisposes to joint infection.

    Anti-tumor necrosis factor agents also increases this risk

    Opportunistic and intracellular pathogens are more prevalent in these immunocompromised patients

    Human immunodeficiency virus infection likely only marginally increases the risk of infectious arthritis, if at all

  • The most important predisposing factors and their relative risks, and positive/negative likelihood ratios are listed in Table I below. It should be noted that a combination of risk factors in one patient carries a synergistic, not additive, risk.

Table I.
Risk Factor RelativeRisk PositiveLikelihood Ratio NegativeLikelihood Ratio
Recent Joint Surgery 8.4 6.9 0.78
Rheumatoid Arthritis 5.4 2.5 0.45
Hip or knee prosthesis 4.1 3.1 0 73
Age > 80 years 4.1 3.5 0.86
Skin infection 3.6 2.8 0.76
Diabetes mellitus 2.8 2.7 0.93
Hip or knee prosthesis ANDSkin Infection 18 15.0 0.77
Beware: there are other diseases that can mimic bacterial infectious arthritis of native joints:
  • The differential diagnosis of bacterial suppurative arthritis includes several sterile inflammatory arthritides as well as joint infections due to nonbacterial pathogens. The former include:

    Crystalline joint disease



    Rheumatoid arthritis (RA)

    Reactive arthritis (Reiter’s syndrome)

    Still’s disease

    Rheumatic fever

  • By far the most difficult entity to differentiate from pyogenic arthritis is acute attacks of the crystalline joint diseases.

    Like septic arthritis, gout and pseudogout usually cause acute monoarticular inflammatory arthritis that may involve the large joints of the lower and upper extremities

    Often associated with fever and leukocytosis

    Clinical factors suggesting gout over pyogenic arthritis are:

    Involvement of stereotypical joints such at the 1st metatarsal

    Prior similar attacks in a patient with an established diagnosis

    Although unusual, some patients will have concomitant gout and bacterial joint infection

    In such cases, the knee is most often involved followed by the ankle, shoulder, and wrist.

    Most of these patients are known to have well established tophaceous gout

    Even if a diagnosis of gout or pseudogout seems likely and synovial fluid analysis shows characteristic crystals, fluid Gram-stain and culture should still be performed in order to rule out simultaneous infection.

    Concomitant pseudogout, gout and septic arthritis has been reported

  • Rheumatoid arthritis (RA) typically presents with symmetric polyarticular arthritis, especially of smaller joints, and in such cases pyogenic arthritis is unlikely.

    Atypical cases may occur where a single or small number of large joints may present asymmetrically in acute fashion, mimicking septic arthritis.

    Bacterial infection of a joint previously afflicted with RA is not uncommon and the symptoms and signs may be masked by pre-existing inflammation or immunosuppressive drugs.

  • Reactive arthritis (formerly Reiter’s syndrome) can present with mono- or oligoarthritis usually of the feet and lower extremities.

    May occur spontaneously

    Often follows a recent gastrointestinal or genitourinary tract infection

    Many persons with reactive arthritis will have associated tenosynovitis/enthesitis, urethritis, and occasionally skin and mucous membrane lesions (keratoderma blennorrhagica), the presentation can closely resemble that of disseminated gonococcal infection (DGI).

  • Hemarthrosis due to trauma or intraarticular injury can mimic septic arthritis of the knee and a history of trauma or injury is fairly easy to illicit.

    For the rare case of septic arthritis following blunt, nonpenetrating joint trauma, an aspiration with culture is usually required to establish the diagnosis.

What laboratory studies should you order and what should you expect to find?

  • Routine laboratory evaluation of patients with acute nongonococcal bacterial arthritis will show:

    An elevated peripheral white blood cell (WBC) count (90% of cases)

    Elevated erythrocyte sedimentation rate (ESR) (95% of cases), and C-reactive protein (CRP) (77% of cases).

    Many times the results are only modestly elevated and if abnormal do not markedly increase the pretest likelihood of bacterial septic arthritis due to their very low specificity.

  • Serum procalcitonin (PCT), an acute phase reactant that increases rapidly in persons with bacterial infection, is more sensitive and specific than ESR and CRP.

    Generally PCT is not elevated in sterile inflammatory conditions or viral infections

    Evaluated in a meta-analysis of 583 patients with fever and orthopedic symptoms in order to assess its predictive values for osteomyelitis and septic arthritis.

    For those patients with septic arthritis the sensitivity and specificity were found to be 65% and 88%, and the positive and negative likelihood ratio (+LR, -LR) were 5.25 (95 % CI: 2.5 – 10.95), and 0.40 (95 % CI: 0.16 – 1.02), respectively.

    Using a lower test cut-off of 0.2-0.3ng/ml modestly improves the test performance

    An elevated PCT might help suggest bacterial septic arthritis in a patient with an acutely inflamed joint, but that it is not useful for ruling it out. Unfortunately, the later performance measure is the most important.

  • In patients with gonococcal arthritis or DGI mild leukocytosis or ESR elevations are noted in only about half of patients.

  • Other laboratory tests such as serum electrolytes, BUN, creatinine and liver associated enzymes should be performed to assess comorbidity and as a baseline prior to monitoring for adverse affects of therapy.

What studies should be ordered and what should I expect to find?

Synovial fluid analysis
  • As outlined below in “Initial Approach to the Patient” synovial fluid analysis is critical for the evaluation of a patient suspected to have septic arthritis. Synovial fluid is obtained through arthrocentesis of one or more affected joints at the time of initial patient presentation, and before the administration of any empiric antibiotics. Joint fluid should be visually assessed for clarity, color and viscosity. Laboratory analysis should include:

    Leukocyte count and differential

    Crystal evaluation under polarized light

    Gram stain and bacterial culture

    In subacute or chronic cases fungal and mycobacterial stains and culture

  • Synovial fluid tests that are not useful due to low specificity and sensitivity are glucose, protein, lactate dehydrogenase, lactic acid/lactate, and bacterial capsular antigens.

  • Polymerase chain reaction tests are not widely available or validated for synovial fluid.

  • The expected findings of analysis of synovial fluid from patients with selected causes of painful, stiff, and/or swollen joints are listed in Table II.

  • The most important synovial fluid parameter to assess is the white blood cell (WBC) count and differential. The fluid WBC count is typically over 50,000 cells/mm3 in cases of bacterial septic arthritis and the higher the count, the higher the likelihood of this diagnosis. Unfortunately, lower counts are occasionally encountered and do not rule out septic arthritis. Table III illustrates the sensitivity, specificity and likelihood ratios of the synovial fluid WBC count and differential compiled from 5 studies for the diagnosis of septic arthritis.

  • Similar to nongonococcal septic arthritis, the synovial fluid findings of gonococcal arthritis are that of a WBC count between 50,000 and 100,000. Patients with DGI associated with joint infection will often exhibit lower synovial fluid neutrophil counts.

Table II.
Parameter Normal Noninflammatory Inflammatory Septic
Clarity Transparent Transparent Translucent Opaque
Color Clear/straw Straw/yellow Yellow to milky Milky yellow to grey/green
Viscosity High High Low Low
WBC/mm3 <200 <2000 5000 to 75,000 15,000 to >100,000
PMN cells (%) <25 <25 50 to 75 > 75

WBC = White Blood Cell, PMN = polymorphonuclear

Table III.
WBC/mm3 Sensitivity Specificity PositiveLikelihood Ratio NegativeLikelihood Ratio
> 100,000 29 99 28.0 0.71
> 50,000 62 92 7.7 0.42
> 25,000 77 73 2.9 0.32
PMNs > 90% 73 79 3.4 0.34
Table IV.
Organism Preferred antibiotic Dosea Alternative antibiotic
Gram-positive cocci Vancomycin 30mg/kg (ABW) IV daily,divided every 8-12 hrsb Daptomycinc orlinezolidc
Gram-negative coccid Ceftriaxone 1g every 24 hrs See footnote e
Gram-negative rods CeftazidimefCefepimef 2g IV every 8 hrs2g IV every 12 hrs Piperacillin-tazobactam4.5g every 6 hrsf orCarbapenemg orAztreonam 2g every 8 hrsf,h orFluoroquinoloneh,i
Gram-stain negative Vancomycin PLUSCeftazidime or Cefepime dose as above Daptomycin or linezolidc PLUSpiperacillin-tazobactam, or carbapenemg, oraztreonamh or fluoroquinoloneh,i(see dosages above)

All indicated dosages are IV for persons with normal renal function

Therapeutic monitoring should be performed to achieve trough levels of 15-20mg/L. Do not exceed 3gms/day

For patients with vancomycin intolerance or allergy daptomycin 6mg/kg q 24 hours, or linezolid 600mg IV or PO q 12 hours are recommended

Equivacal Gram-negative morphology should be considered as Gram-negative rods

Gram-negative cocci with epidemiology or history suggested of gonococcus should be initially treated with the antimicrobial choice suggested by the current Centers for Disease Control STD guidelines. Current evidence and the CDC guidelines do not suggest a suitable antimicrobial drug for alternative therapy for patients with a history of Stevens-Johnson syndrome or severe IgE mediated beta-lactam allergies such as anaphylaxis. Possible choices pending joint fluid and mucosal site culture results include spectinomycin (not available in the US), gentamicin, tobramycin, ciprofloxacin or azithromycin 500mg daily

For patients with risk factors for antimicrobial resistant Gram-negative pathogens (significant health-care exposure, immunosuppression or history of extended-spectrum beta-lactamase colonization or infection), a carbapenem is preferred first-line over beta-lactam antimicrobials including aztreonam

Doripenem 500mg q 8 hrs, imipenem 500mg q 6 hrs, or meropenem 1gm q 8 hrs

For patients with a history of Stevens-Johnson syndrome or severe IgE mediated beta-lactam allergies such as anaphylaxis

Ciprofloxacin 400mg IV every 8 hrs or 750mg PO every 12 hrs, OR levofloxacin 750mg IV or PO every 24 hrs

ABW: Actual Body Weight; hrs = hours

Results that confirm the diagnosis of septic arthritis.

  • The diagnosis of septic arthritis can be microbiologically confirmed by culturing the causative organism from synovial fluid, or in the setting of probable septic arthritis from the blood. Blood cultures are positive in 50-70% of patients with nongonococcal pyogenic arthritis and should be ordered in patients when the diagnosis is suspected, even if they are not febrile at the time of presentation.

  • Depending on the fastidiousness of the pathogen, synovial fluid culture in patients with nongonococcal septic arthritis will yield bacterial growth in as much as 80-90% of the time. Traditional teaching is that the yield for more fastidious pathogens may be increased by directly inoculating synovial fluid into bottles of blood culture media at the bedside. However, a study of a direct comparison of culture methods including BACTEC® blood culture bottles, lysis centrifugation, and conventional agar plate culture failed to show a difference in yields. Synovial fluid gram stain, while rapid and easy to perform, is positive in 50% or less of cases in which the culture is eventually positive.

  • The yield of both blood and synovial fluid culture decreases steadily after antimicrobial therapy has been initiated. Thus, it is important to obtain these cultures prior to starting antimicrobials unless the patient is in septic shock or the cultures cannot be obtained promptly.

  • Gonococcal arthritis:

    For patients with frank suppurative gonococcal arthritis, joint culture will yield the organism in approximately 50% of patients but fluid gram stains will show intra- and extracellular Gram-negative cocci in only 25% of those proven to have the diagnosis.

    The yield in DGI is less, N. gonorrhoeae growing in culture only 20-30% of the time

    The yield of blood cultures for the diagnosis of DGI is low (<30%)

    Gram stain and culture of skin lesions are rarely diagnostic

    For patients in which gonococcal arthritis or DGI is suggested by epidemiologic factors and/or the clinical presentation, mucosal sites should be cultured in addition to performing nucleic acid amplification (NAAT) tests on swabs and freshly voided morning urine. Sites should include the urethra, uterine cervix, oropharynx, and rectum.

    Cultures of the uterine cervix and urethra are positive in 50-90% of women and 50-70% of men respectively. Yields of cultures from the oropharynx and rectum are lower.

    While positive NAAT tests of mucosal sites alone might strongly suggest the diagnosis of gonococcal arthritis or DGI, it is extremely important that culture also be performed in order to provide an opportunity for N. gonorrhoeae antimicrobial sensitivities to be performed. Because of the multiple drug resistances of N. gonorrhoeae, knowing the organisms drug sensitivities greatly assists in the choice of an oral step down therapy.

What imaging studies will be helpful in making or excluding the diagnosis of septic arthritis?

  • Radiographs should be obtained in all patients of joints that are painful, swollen, and/or with reduced range of motion. While they seldom add additional information to support or exclude the diagnosis of a joint infection, they will occasionally demonstrate associated osteomyelitis or osseous joint destruction, especially in more advanced cases.

    The usual radiographic findings in septic arthritis are nonspecific and include:

    Periarticular swelling

    Fat pad edema

    (and/or) Effusion

    They are also useful for the identification of metallic foreign bodies and as a baseline for later assessment of progressive infection or its sequelae.

  • Computed tomography (CT) and magnetic resonance imaging (MRI) are more useful than plain film radiographs for:

    The assessment of joint effusions

    Erosive bone changes

    Periarticular extension of infection

  • MRI is the most sensitive and specific but also the most expensive and cannot be used with some metal joint implants.

    MRI is better than CT for identification of associated soft tissue infection such as abscess or fistula, and osteomyelitis of contiguous bone.

    Both modalities are particularly helpful in assessing for deep joint infection where pain may be the only presenting symptom and physical findings are absent (see Deep Joint Infection below).

    CT guidance is sometimes required for aspirating deep joints such as the sacroiliac or pubic symphysis.

  • Scintography, including three or four phase bone scanning using technetium is sensitive, but not specific for septic arthritis and seldom yields additional information. It is occasionally useful for screening for joint infection in patients with nonspecific symptoms of pain.

What consult service or services would be helpful for making the diagnosis and assisting with treatment?

  • Many cases of septic arthritis can be diagnosed and managed by primary care physicians with initial specialty consultation from an orthopedic surgeon. Orthopedic surgery consultation is often required for assistance with joint drainage and debridement (see section on Treatment below).

  • Orthopedic or rheumatologic consultation may be helpful for obtaining synovial fluid for analysis, particularly for joints that are more difficult to aspirate.

  • Infectious diseases consultation is often helpful for diagnosis in cases that are not straight forward, or for assistance with antimicrobial choice, especially for patients with negative cultures, antibiotic allergies, or for those who are not responding to therapy as expected.

  • All cases of suspected or confirmed gonococcal infection should be reported to the local public health agency.

What should be the initial approach to the patient?

  • The diagnosis of acute bacterial arthritis is considered a rheumatologic emergency and should be suspected in any patient with acute mono- or polyarticular arthritis.

    The pretest probability of septic arthritis should be assessed based on the patient’s demographics, clinical history, preexisting comorbidity and joint disease (if any), physical exam and initial laboratory results (see “Which individuals are of greater risk of developing septic arthritis? and the section on synovial fluid analysis above).

    The most useful parameters for assessing this probability are:

    The patient’s demographic risk factors

    The synovial fluid white blood cell count (WBC) and differential (see tables I, II and III).

  • Joint aspiration should be performed on any and all affected joints as soon as the diagnosis of septic arthritis is entertained.

    Aspiration should be performed through skin that is not visibly involved by infection.

    Synovial fluid should be sent for cell count and leukocyte differential, gram stain, bacterial culture, and crystal analysis.

  • Blood cultures should be obtained

  • If present, wound cultures should also be sent.

  • All cultures should be sent prior to antimicrobial therapy unless the patient shows signs of severe sepsis and joint aspiration must be delayed.

  • Plain film joint radiographs should be performed. CT or MRI imaging should be considered for patients where there is concern for soft tissue or osseous extension of infection, or for those with prolonged or atypical joint symptoms or signs.

  • Bacterial joint infection will often progress rapidly resulting in joint destruction and subsequent morbidity and disability.

    Therapy should not be delayed while waiting for definitive culture results.

    If the pretest likelihood of septic arthritis is high based on the above findings, appropriate therapy including joint drainage and debridement, and intravenous antimicrobials should be initiated.

    Orthopedic consultation should be obtained for most patients.

  • Due to the relatively high prevalence of bacterial infection and gout, patients with a positive synovial fluid crystal examination from nonstereotypical joints should have antimicrobial therapy initiated. Such treatment should be continued until synovial fluid bacterial cultures are negative after 72 hours of incubation.

  • For patients with suspected gonococcal arthritis or disseminated gonorrhea infection, direct nucleic acid amplification tests and gonococcal culture on chocolate and Thayer-Martin media should be performed on urethral, cervical, throat, and rectal swabs.

  • For patients with subacute or chronic presentations synovial fluid cultures should also be sent for mycobacterial and fungal smear and culture.

If you feel the patient has native joint bacterial arthritis, what therapies should you initiate immediately?

  • Therapy of acute bacterial septic arthritis should be approached like that of abscesses and other closed space infections. In order to limit long-term sequelae and joint damage proper management requires urgent:

    Surgical joint drainage and/or debridement.

    Empiric antimicrobial drugs, in most cases given intravenously (see Anti-infective Agents Below).

  • Adequate joint drainage is recommended for all patients with acute septic arthritis and can be accomplished by:

    Daily closed needle aspiration until the amount of aspirated purulent synovial fluid is minimal

    Surgical intervention via arthroscopy

    Surgical intervention via arthrotomy (open joint surgery)

  • The approach to joint drainage depends upon the joint involved, and the severity of infection. Unfortunately, there are no randomized clinical trials comparing the three modalities in adults and there is some controversy as to which method is best.

  • Repeated needle aspiration is less invasive and can be considered for accessible, native peripheral joints. Synovial fluid analysis should be performed on each aspiration for a cell count, WBC differential, gram stain and culture to help assess the response to therapy.

  • A surgical approach is preferred for patients with poor prognostic factors such as:

    Underlying diseases: rheumatoid arthritis, diabetes, immunosuppression

    Severe sepsis

    A long duration of symptoms

    A poor response to repeated needle drainage

    Surgical approaches allow for better visualization for debridement, and more adequate lavage and irrigation of the joint

    Athroscopy is often preferred over arthrotomy for infections of the knee, shoulder and wrist, and may need to be repeated for more severe infections.

    Hip or sternoclavicular infections in the adult might require arthrotomy for better joint exposure

  • Patients with purulent gonococcal arthritis should also be managed with drainage and antibiotics, although disseminated gonorrhea infection without frank suppurative arthritis can usually be managed with antibiotics alone.

1. Anti-infective agents

If I am not sure what pathogen is causing the infection what anti-infective should I order?
  • Anti-infective therapy should be initiated as soon as acute bacterial septic arthritis is suspected. Delays in therapy increase the risk for further articular destruction and long-term joint dysfunction and disability.

    There are no randomized controlled trials that have evaluated choice of empiric or directed therapy for this infection and thus there is minimal high quality evidence to assist with therapeutic decision making.

    A limited meta-analysis of antibiotic selection for bone and joint infections, as well as clinical experience, suggest that antibiotic efficacy is equivalent among agents as long as the antimicrobial spectrum and pharmacodynamics are adequate for the causative pathogen.

  • Initial antimicrobials should be directed by synovial fluid gram stain, which is positive approximately 50% of the time. Except possibly for the highly bioavailable fluoroquinolones or linezolid, initial therapy should be given intravenously (See “What is the anti-infective therapy for bacterial joint infections when a pathogen and anti-infective susceptibility are identified?”).

    For cases with a negative gram stain, empiric therapy should be chosen based on the most likely pathogens (see “What Pathogens are Responsible for Acute Septic Arthritis”). In this case, both Staphylococcus aureus (beta-lactam sensitive and resistant) and Gram-negative pathogens have a high enough pre-test probability to be the causative bacterium that antibiotic coverage should include this wide spectrum of organisms.

    The inclusion Gram-negative therapy is especially important for patients with history of injection drug use, indwelling catheters, advanced age, history of trauma, or immunodeficiency. See Table VI for suggested empiric antimicrobial therapies.

  • Infections due to direct joint penetration by an animal or human bite should be treated with ampicillin-sulbactam 3gms intravenously every 6 hours. In those patients who have a prompt clinical response and joint debridement, intravenous therapy can be converted to oral amoxicillin-clavulanate after approximately 7 days of intravenous therapy. For patients allergic to penicillin alternatives include clindamycin plus ciprofloxacin, or moxifloxacin.

  • Suspected DGI should be treated with ceftriaxone 1gm IV every 24 hours.

Table VI.
Organism Duration of Therapy(weeks) Comments
Staphylococcus aureus (MSSA and MRSA) 4 For patients with bacteremia evaluation for endocarditis is recommended. For complicated bacteremia or endocarditis, 6 weeks of therapy is suggested.
Group B streptococcus 4 Many of these patients have significant comorbidity, advanced age or immunosuppression.
Streptococcus pneumoniae and other streptococci 2
Enteric Gram-negative bacilli 2-4 4 weeks recommended for those with significant comorbidity, advanced age or immunosuppression. Oral fluoroquinolone antibiotics can be used for susceptible isolates in patients tolerating food and liquids by mouth.
Pseudomonas aeruginosa 4 Oral fluoroquinolone antibiotics can be used for susceptible isolates in patients tolerating food and liquids by mouth.
Neisseria gonorrheae 2 1 week of therapy for disseminated gonorrhea without suppurative arthritis.
Culture negative 4
Table VII.
Clinical or Epidemiologic Feature Etiologic Agent
Rheumatoid arthritis Staphylococcus aureus
Intravenous drug use S. aureus or Pseudomonas aeruginosa
Diabetes or malignancy S. aureus, Group B Streptococcus
Immunocompromised hosts S. aureus, Group B Streptococcus, enteric gram-negative bacilli, Listeria monocytogenes
Fibrocartilaginous joints (e.g pubic symphysis, sternoclavicular or sternomanubrial) S. aureus, P. aeruginosa
Residents or travelers to Southeast Asia Burkholderia pseudomallei (Melioidosis), Streptococcus suis
Table VIII.
Organism % of total isolates
Staphylococcus aureus 46
Staphylococci, coagulase negative 4
Streptococci 22
S. pyogenes 8
S. pneumoniae 7
Steptococcus agalactiae (Group B) 3
Other streptococci 5
Escherichia coli 4
Pseudomonas aeruginosa 2
Salmonella spp. 1
Other Gram-negative bacilli 5
Hemophilus influenzae 5
Neisseria gonorrhoeae 3
Neisseria meningitidis 1
Polymicrobial 1
Miscellaneous including anaerobes 6

What is the anti-infective therapy for bacterial joint infections when a pathogen and anti-infective susceptibility are identified?

  • Empiric antimicrobial therapy should be de-escalated or narrowed based on the results of culture of synovial fluid, blood and for gonococcal infections, mucosal sites. Suggestions for definitive therapy are listed in Table V for the more common pathogens causing native joint septic arthritis.

  • Fluoroquinolones penetrate joints and bone tissues well and are highly bioavailable. Thus, for patients with a functioning gastrointestinal tract and Gram-negative septic arthritis due to organisms susceptible to ciprofloxacin or levofloxacin these antibiotics can be given in the oral rather than IV route.

  • Linezolid is also highly bioavailable and the oral route is preferred for those with a functioning gut.

  • For patients with a high pre-test probability of bacterial septic arthritis and negative cultures who are responding to empiric therapy, the initially administered antimicrobials should be continued to complete a full treatment course.

Table V.
Organism Preferred antibiotic Dosea Alternative antibiotic
Methicillin susceptibleStaphylococcus aureus Nafcillin or oxacillinCefazolinCephalothin 2gms IV every 4 hrs2gms IV every 8 hrs2gms IV every 6 hrs Ceftriaxone 2gms IV every 24 hrsbVancomycin 30mg/kg (ABW) IV daily, divided every 8-12 hrsc,dClindamycin 600mgs IV every 6-8 hrsb
Methicillin resistantStaphylococcus aureus Vancomycin 30mg/kg (ABW) IV daily,divided every 8-12 hrsc Daptomycine orlinezolide
Streptococci includingGroup B Streptococcus andPCN susceptible S. pneumoniae (MIC<4) PCNAmpicillin 12-18 mil. units/d IV (divided Q4H)2gms IV every 4-6 hrs Vancomycin 30mg/kg (ABW) IV daily, divided every 8-12 hrsc,d
PCN resistant S. pneumoniae (MIC<4)f CeftriaxoneCefotaxime 2gms IV every 24 hrs2gms IV every 8 hrs Vancomycin 30mg/kg (ABW) IV daily, divided every 8-12 hrsc,d
Enteric gram-negative bacilli (non-ESBL)f CeftriaxoneCefotaximeFluoroquinoloneg 2gms IV every 24 hrs2gms IV every 8 hrssee footnote g Cefepime 2g IV every 12 hrsCeftazadime 2g IV every 8 hrsCarbapenemhAztreonam 2g IV every 8 hrsi
Enteric gram-negative bacilli (ESBL)f FluoroquinolonegCarbapenemh see footnote gsee footnote h Based on susceptibility testing
Pseudomonas aeruginosaf,j FluoroquinolonegCefepimeCeftazadime see footnote g2g IV every 12 hrs2g IV every 8 hrs Carbapenemh
Neisseria gonorrhoeae Ceftriaxone 1g IV every 24 hours see footnote k

All indicated dosages are IV for persons with normal renal function

These antibiotics been used with similar outcomes to the preferred beta-lactam antibiotics but data is limited in for this indication in adults and this alternative remains controversial

Therapeutic monitoring should be performed to achieve trough levels of 15-20mg/L. Do not exceed 3gms/day

For patients with beta-lactam and vancomycin intolerance or allergy, clindamycin, daptomycin 6mg/kg q 24 hours, or linezolid 600mg IV or PO q 12 hours may be used

For patients with vancomycin intolerance or allergy, daptomycin 6mg/kg q 24 hours, or linezolid 600mg IV or PO q 12 hours are recommended

The organism should be tested for and sensitive to the suggested antibiotic

Ciprofloxacin 400mg IV every 8hrs or 750mg PO every 12 hrs, OR levofloxacin 750mg IV or PO every 24 hrs

Doripenem 500mg every 8 hrs, ertapenem 1gm every 24 hrs, imipenem 500mg every 6 hrs, or meropenem 1gm every 8 hrs. Ertapenem dosing is more convenient than the other carbapenems

For patients with isolates not susceptible to fluoroquinolones and a history of Stevens-Johnson syndrome or severe IgE mediated beta-lactam allergies such as anaphylaxis

For P. aeruginosa, some experts recommend the addition of a gentamicin or tobramicin 5mg/kg IV every 24 hours

Should be based on culture sensitivities if available. Every attempt should be made to culture the organism from synovial fluid, cervix, urethra, pharynx and rectum prior to initiating empiric antibiotics in order the increase the probability of obtaining the organism for susceptibility testing. For susceptible isolates fluoroquinolones, and cefixime can be used (the later as step down therapy after a clinical response). For patients highly allergic to cephalosporin antibiotics with isolates resistant to fluoroquinolones, possible choices include spectinomycin (not available in the US), gentamicin, tobramycin, and azithromycin 500mg daily.

ABW = Actual Body Weight; ESBL = extended spectrum beta-lactamase producer; hrs = hours; PCN = penicillin

What is the recommended duration of therapy for native joint bacterial septic arthritis

  • The duration of therapy for bacterial septic arthritis has not been studied in controlled trials and should consider the causative pathogen and host comorbidity and immune function. Parenteral antibiotics are traditionally given for 2-4 weeks, although if fluoroquinolones or linezolid are used, intravenous therapy can be converted to oral early in the treatment course.

  • Recent retrospective evidence suggests that for patients who have undergone thorough joint drainage or debridement and exhibit a prompt response to therapy, a shorter course of 7-14 days of parenteral therapy may be just as efficacious as longer treatment courses. In this single center study:

    7 days of intravenous therapy was found to be equivalent to 8-21 days

    14 days of parenteral antibiotics had the same outcome as 15-28 days

    Factors significant in predicting a relapse of infection were:

    Gram-negative infection

    Lack of surgical drainage

    An immunocompromised host

    It was concluded that further prospective studies should confirm these finding before they can be taken as recommendations for short course of treatment in septic arthritis.

  • Suggested durations of therapy for selected pathogens are listed in Table VI.

2. Are there other therapeutic modalities for septic arthritis?
  • The use of oral or adjunctive oral steroids has been studied in children. A positive outcome was associated with:

    Shorter duration of fever, pain and local inflammatory signs

    Decreased residual joint dysfunction

    The data supporting the adjunctive use of steroids is quite limited and there are no studies in adults

  • Due to concerns of immunosuppression and reduced antibiotic efficacy there currently is no role for intra-articular or systemic corticosteroids in the therapy of bacterial septic arthritis.

  • For patients with septic arthritis who are already on immunosuppressive drugs for treatment of an underlying disease these agents should be held or reduced in dosage if possible.

What should you tell the family about the patient’s prognosis?

  • The complications or sequelae of bacterial septic arthritis are predominately that of:

    Chronic pain and decreased joint function and mobility due to cartilage destruction and subchondral bone loss.

    These complications can occur in up to 30-50% of patients.

    There is often acceleration of prior joint destruction in patients with underlying chronic arthritis.

    joint inflammation and destruction may continue after the articular space and synovium are rendered sterile with antimicrobial therapy.

    Unfortunately the prognosis of native joint bacterial arthritis has not improved much over the last few decades despite advances in surgical techniques, antimicrobial agents and hospital care.

  • As compared to community-acquired bone and joint infections, those that are health-care associated are more likely to result in:


    Longer length of hospital stay

    Greater financial cost

    Morbidity due to methicillin-resistant Staphylococcal aureus infections may be greater than that due to methicillin susceptible isolates.

  • Other factors which influence functional outcomes include:

    Prior underlying joint health


    The virulence of the causative pathogen

    Promptness of antimicrobial therapy

    S. aureus polyarticular arthritis in patients with underlying rheumatoid arthritis has a very poor prognosis

  • Rarely, bacterial septic arthritis may necessitate arthrodesis, prosthetic joint implantation or amputation.

  • Mortality due to bacterial arthritis in adults vary between 7% and 15% and may be as high as 30% in those with significant comorbidity, advanced age, or coexisting bacteremia and sepsis.

  • The usual hospital length of stay for septic arthritis can be expected to be 5-10 days.

What if the patient is not responding to expected therapy?

  • Patients should start to improve after joint drainage or debridement and 48-72 hours of antimicrobial therapy. Slower responses may be seen in patients with underlying immunosuppression, diabetes, advanced age, rheumatoid arthritis, and S. aureus, or P. aeruginosa as causative pathogens. For patients who are not improving by 72-96 hours, further investigation for potential causes should be performed.

  • The reasons for a lack of therapeutic response in patients with septic arthritis include:

    Inadequate joint debridement or drainage

    Resistant bacterial pathogen

    Non-bacterial pathogen such as mycobacteria or fungi

    Foreign body or prosthesis

    Concomitant or adjacent soft tissue or bone abscess requiring drainage

    Joint inflammatory condition other than infection (i.e. gout)

  • For those patients not responding as expected to therapy:

    The joint should be imaged with computerized tomography or magnetic resonance imaging

    Re-aspirated for synovial fluid analysis, Gram stain and culture. Stains and cultures should also be performed for mycobacterial and fungal pathogens.

    If the patient has not already undergone joint drainage by arthroscopic or open surgical approach, a referral should be made for this procedure.

    For those patients in whom surgical joint drainage was performed at presentation a repeat procedure should be considered.

  • For patients with negative blood and joint cultures who were initially treated with vancomycin the addition of Gram-negative coverage should be considered as outlined in Table 5.

  • If not already involved, Infectious diseases and/or rheumatology consultation should be requested.

How do you contract native joint septic arthritis and how frequent is it?

Epidemiology and incidence
  • The yearly incidence of native joint septic arthritis in the general population ranges between 2 and 10 cases per 100,000 individuals and is rising due to the increasing number of persons with significant risk factors (see below) .

    For patients with rheumatoid arthritis the incidence is much higher, approaching 70 cases per 100,000 person-years.

    In patients presenting with one or more acutely painful joints the proportion due to bacterial joint infection is 8 to 27% depending on the studied population.

  • Bacterial septic arthritis is an uncommon complication of orthopedic therapeutic procedures. In one retrospective review the incidence was 11 per 100,000 procedures involving arthrotomy, arthroscopy or arthrocentesis.

    Joint infection follows

    Arthroscopy of the knee in 0.04 to 0.4% of cases

    Arthroscopic or reconstructive surgery in 0.14 to 1.7 % of cases

  • Patient-related predisposing risk factors for septic arthritis include:

    Joint disease due to rheumatoid or crystal induced arthritis

    Osteoarthritis or Charcot’s arthropathy

    Advanced age

    Chronic systemic disease such as diabetes, malignancy or renal, liver, sickle cell or collagen vascular disease

    Immunosuppression (not due to human immunodeficiency virus)

    Intravenous drug use

  • The most important patient factor is rheumatoid arthritis.

Origins and causes of joint infection
  • Bacterial native joint septic arthritis is acquired through a hematogenous, direct contiguous, or traumatic inoculation of the joint. After joint inoculation, local and bacterial factors facilitate bacterial adherence and infection.

  • Hematogenous septic arthritis

    Bacterial native joint arthritis is most often acquired during overt or occult hematogenous spread of bacteria from a distant source. After a careful investigation, the source may be apparent in some patients, and is often found to be skin disease or a lesion that may or may not exhibit signs of infection. Many patients, however, will not have a source of infection identified. In septic arthritis due to S. pneumoniae, the organism is thought to be hematogenously spread from the respiratory tract, although a fair number of patients will not have evidence of concurrent or prior pneumonia. In intravenous drug users and patients with indwelling intravenous catheters or undergoing dialysis, bacteria are introduced directly into the intravascular bloodstream.

    Hematogenous seeding of joint synovium is facilitated by its extreme vascularity and lack of a limiting basement membrane. Abnormal joint architecture due to prior injury or underlying arthritis greatly increases the risk of hematogenous infection. The major pathogens seen in septic arthritis of hematogenous origin include S. aureus (methicillin susceptible and resistant), S. pneumoniae, enteric Gram-negative bacilli, Pseudomonas aeruginosa, Group B Streptococcus and Neisseria gonorrheae. Staphylococcus aureus and P. aeruginosa are not uncommon causes of bacterial arthritis in intravenous drug users.

    Bacterial arthritis may complicate endocarditis, especially when caused by S. aureus.

  • Septic arthritis due to direct inoculation

    Bacteria can be directly introduced into the joint by trauma, percutaneous puncture (needle, thorn or nail), surgery, or intra-articular injection. One common traumatic source is an animal or human bite which often involves the small joints of the hand. Pasteurella multocida is characteristically isolated from animal bites and Eikenella corrodens from human bites, in addition to staphylococci, viridans streptococci, and anaerobes. Organisms typically associated with plant material such as Bacillus cereus, Pantoea agglomerans and Nocardia spp. may be inoculated during trauma or implantation of a thorn.

    Staphylococcus aureus (MSSA and MRSA) are the most common pathogens associated with arthroscopic or open joint surgery. Rarely, bacterial or fungal pathogens may be introduced with joint aspiration or corticosteroid injection. Regional and nationwide outbreaks of septic arthritis due to unusual molds have been associated with joint injection of contaminated corticosteroids obtained from compounding pharmacies.

  • Contiguous focus septic arthritis often involves S. aureus or enteric Gram-negative organisms and arises from adjacent osteomyelitis or infected soft tissue. Septic arthritis of the small joints of the foot are often due to contiguous ulcerations and soft tissue infection in diabetic patients.

  • Septic arthritis is occasionally acquired from direct contact with animals. These zoonotic joint infections are rare in the United States and if encountered, are usually in travelers or residents from endemic areas. Brucella spp.can be a cause of septic arthritis due to contact with infected ungulate animals or unpasteurized dairy products. Streptococcus suis has been reported to cause septic arthritis in people exposed to pigs in China and Southeast Asia.

What pathogens are responsible for this disease?

Bacteria usually cause acute septic arthritis with the exception of Borrelia burgdorferi, the causative agent of Lyme Disease. When involving prosthetic joints, such bacteria do not cause chronic infection.

Mycobacterial joint infection
  • Mycobacterium tuberculosis (TB) is a cause of chronic septic arthritis and tuberculous bone and joint infection accounts for 1-3% of all TB cases. TB arthritis is more commonly seen in the developing world and is quite rare in the United States. Risk factors for TB arthritis include older age, female sex, lower socioeconomic status, incarceration, origination from a region with high TB endemnicity, debilitating illness, and immunosuppression including HIV infection.

  • Joint TB follows symptomatic or occult pulmonary TB and is usually monoarticular. Infection may be latent for months or years and typically involves the knee, hip and ankle. Symptomatic pulmonary TB is absent in 50% of cases and these patients generally do not report fever. Tubercular chronic arthritis is indistinguishable from other causes of chronic arthritis. Physical exam of a patient with mycobacterial chronic infectious arthritis will usually show joint swelling, as well as painful reduced range of motion. Skin erythema is usually absent. In advanced cases a sinus tract from the joint may be present.

  • Diagnosis requires synovial fluid analysis and in many cases synovial biopsy. If present, fluid from draining sinus tracts may be stained and cultured for mycobacteria. Synovial fluid usually shows between 10,000 and 20,000 leukocytes/mms. Mycobacterial stains of synovial fluid are usually negative and culture will confirm the diagnosis in 80% of cases. If still suspected in culture negative cases, synovial biopsy will often yield the organism on stain or culture and show the characteristic granulomatous inflammation on pathologic examination. Susceptibility tests should be performed on all culture isolates to assess for drug resistance.

  • Therapy is with isoniazid, rifampin, ethambutol, and pyrazinamide as suggested by the Centers for Disease Control and Prevention.

  • Other nontuberculous mycobacteria rarely cause septic arthritis. These include Mycobacterium avium-intracellulare, M. kansasii, and M. marinum.

Fungal joint infection
  • Fungal pathogens that are encountered in septic arthritis include: Candida spp, Cryptococcus neoformans, Blastomyces dermatitidis, Coccidioides spp., Sporothrix schenckii, Aspergillus spp, Scedosporium spp, and Fusarium. Candida, Cryptococcus, Aspergillus and other mold joint infections are more often seen in immunocompromised hosts, while the dimorphic fungi such as Blastomyces, Coccidioides and Sporothrix are more commonly encountered in healthy hosts.

  • Candida arthritis is increasing in frequency due to the rising number of at risk hosts. Risk factors for Candida infection include loss of skin integrity, malnutrition, malignancy, intravenous drug use, hyperalimentation, central intravenous lines, and immunosuppression including corticosteroids. Infection is monoarticular and the knee is most commonly involved. Joint inflammation may be readily apparent, or in some cases, indolent with minimal symptoms. Synovial fluid analysis is similar to bacterial septic arthritis and bacterial and fungal culture yields Candida in most cases.

  • Recommended therapy of Candida arthritis is fluconazole 400 mg daily for at least 6 weeks or a lipid formulation of amphotericin B (3-5 mg/kg daily) for at least 2 weeks followed by fluconazole to complete the course of therapy. Fluconazole may be given orally rather than IV and echinocandins can be used as an alternative agent. Therapeutic joint drainage is often required similar to bacterial arthritis.

  • Cryptococcal native joint arthritis is uncommon, even in patients with disseminated infection. Therapy is usually with fluconazole for 6-12 months and joint drainage is usually not required.

Viral arthritis is often acute, occurs together with other symptoms and signs of systemic viral illness, and is self resolving. Viral causes of infectious arthritis are:

  • Parvovirus B19

  • Rubella (wild-type or immunization strain)

  • Acute hepatitis B

  • Hepatitis C

  • Human T cell leukemia virus-1 (HTLV-1)

  • Human immunodeficiency virus (HIV)

  • Chikungunya fever

  • Other alpha viruses

Helminths and filiariae rarely can cause infectious arthritis.

How do these pathogens cause native joint septic arthritis?

  • Bacterial joint infection is dependent on bacterial adherence and subsequent proliferation of organisms on the synovial membrane with generation of a host inflammatory response. Bacterial infection rapidly spreads to the synovial fluid as does inflammatory cells and mediators. Bacterial adherence is facilitated by low shear conditions of synovial fluid and host-derived extracellular matrix proteins such as fibronectin, collagen, laminin, elastin and hyaluronic acid.

  • Host-derived inflammatory mediators play an important role in both an effective immune response to infection but also in progressive joint destruction including cartilage degradation and subchondral bone loss. Such mediators include leukocyte derived proteases, interleukin 1, 6, and 10, and tumor necrosis factor-alpha. In addition, the inflammatory response increases intra-articular pressure hampering capillary blood flow which contributes to synovial membrane necrosis and cartilage destruction. Intra-articular cartilage destruction may be seen in as little as 3 days and synovial proliferation in 7 days.

  • Bacterial factors that are important in joint inflammation are best known for S. aureus and include surface adhesions called “microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) and fibrinogen binding adhesion (FbsA). Bacterial pili, DNA and other specific toxins are also likely important bacterial virulence factors.

  • Gonococcal strains with the ability to disseminate, including to joints, are serum resistant and express protein 1A, an outer membrane protein. Interestingly most of the strains that disseminate beyond the urethral mucosa are susceptible to penicillin and other commonly used antibiotics.

What are the other clinical manifestations of deep joint infection?

  • Infection of deep joints such as the sacroiliac and pubic symphysis are often insidious and difficult to diagnosis. They usually present with pain, often without systemic evidence of inflammation such as fever. Pain will often be exacerbated by ambulation or direct pressure over the joint. Peripheral white blood cell (WBC) counts may be normal. Erythrocyte sedimentation rates (ESR) and C-reactive protein (CRP) tests are frequently, but not always, elevated.

  • Computed tomography (CT) and magnetic resonance imaging (MRI) are helpful in making the diagnosis of deep joint septic arthritis. CT is also useful for assisting in joint aspiration for Gram stain and culture to microbiologically confirm the diagnosis.

  • Septic arthritis of these joints often involves contiguous osteomyelitis and therefore therapy based on culture and sensitivity is usually continued for at least 6 weeks. For patients with negative cultures, infection of the sacroiliac and pubic symphysis should be empirically treated with antimicrobials directed against Staphylococcus aureus and Gram-negative pathogens including Pseudomonas aeruginosa. See Table V above.

What other additional laboratory tests are promising for the diagnosis of septic arthritis?

  • Identification of bacterial DNA in synovial fluid by polymerase chain reaction (PCR) testing shows promise for improving the sensitivity and accuracy of the diagnosis of septic arthritis. Broad-range real-time PCR using a 16 S RNA gene target was shown to have a sensitivity and specificity as high as 95% and 97% respectively, although other studies with similar approaches but different methodologies yielded more modest results. While PCR testing is promising, the test is not readily available and the results need to be replicated in large prospective studies of patients with painful, swollen joints to determine its performance characteristics.

WHAT’S THE EVIDENCE for specific management and treatment recommendations?

Brennan, MB, Hsu, JL. “Septic Arthritis in the Native Joint”. Curr Infect Dis Rep. vol. 14. 2012. pp. 558-65. (A thorough and recent review covering the important aspects of septic arthritis.)

Calabrese, LH, Naides, SJ. “Viral arthritis”. Infect Dis Clin North Am. vol. 19. 2005. pp. 963-80. (A good, comprehensive review of viral arthritis.)

Clerc, O, Prod’hom, G, Greub, G. “Native septic arthritis: a review of 10 years of experience and lessons from empirical antibiotic therapy”. J Antimicrob Chemother. vol. 66. 2011. pp. 1168-73. (An important discussion of antimicrobial therapy for septic arthritis.)

Coakley, G, Mathews, C, Field, M. “BSR & BHPR, BOA, RCGP and BSAC guidelines for management of the hot swollen joint in adults”. Rheumatology (Oxford). vol. 45. 2006. pp. 1039-41. (Succinct guidelines for the diagnosis and management of septic arthritis in adults. Antimicrobial therapy suggestions include antibiotics only available in the European Union. These guidelines were reviewed by the societies in 2012 and found to be relevant and not in need of updating.)

Cuellar, ML, Silveira, LH, Espinoza, LR. “Fungal Arthritis”. Ann Rheum Dis. vol. 51. 1992. pp. 690-97. (Although a bit dated, a review of the topic.)

Fangtham, M, Baer, AN. “Methicillin-resistant Staphylococcus aureus septic arthritis in adults: case report and review of the literature”. Semin Arthritis Rheum. vol. 41. 2012. pp. 604-10. (This case report and review illustrates the increasing role of MRSA in septic arthritis.)

Goldenberg, DL. “Septic arthritis”. Lancet. vol. 351. 1998. pp. 197-202. (An authoritative and accurate review of the subject.)

Gupta, MN, Sturrock, RD, Field, M. “Prospective comparative study of patients with culture proven and high suspicion of adult onset septic arthritis”. Ann Rheum Dis. vol. 62. 2003. pp. 327-31. (Outlines the epidemiology and risk factors for septic arthritis.)

Kaandorp, CJ, van Schaardenburg, D, Krijnen, P. “Risk factors for septic arthritis in patients with joint disease. A prospective study”. Arthritis Rheum. vol. 38. 1995. pp. 1819-25. (A descriptive study of the risk factors for septic arthritis, particularly in patients with rheumatoid arthritis.)

Kohli, R, Hadley, S. “Fungal arthritis and osteomyelitis”. Infect Dis Clin Norht Am. vol. 19. 2005. pp. 831-51. (A good review of the topic.)

Li, SF, Cassidy, C, Change, C. “Diagnostic utility of laboratory tests in septic arthritis”. Emerg Med J. vol. 24. 2007. pp. 75-77. (Useful for considering the use of laboratory tests in bacterial arthritis.)

Margaretten, ME, Kohlwes, J, Moore, D. “Does this adult patient have septic arthritis?”. JAMA. vol. 297. 2007. (An excellent report on the predictive values for symptoms, signs and laboratory tests for the diagnosis of bacterial septic arthritis. The ensuing discussion provides clarity and assistance for this difficult to diagnose infection.)

Mathews, CJ, Weston, VC, Jones, A. “Bacterial septic arthritis in adults”. Lancet. vol. 375. 2010. pp. L846-55. (An excellent review of the subject.)

Mathews, CJ, Coakley, G. “Septic arthritis: current diagnostic and therapeutic algorithm”. Curr Opin Rhematol. vol. 20. 2008. pp. 457-62.

Ross, JJ, Saltzman, CL, Carling, P. “Pneumocococcal septic arthritis: review of 190 cases”. Clin Infect Dis. vol. 36. 2003. pp. 319-27. (A comprehensive review of the causative bacterial pathogens in 2302 compiled cases of septic arthritis.)

Stengel, D, Bauwns, K, Schouli, J. “Systematic review and meta-analysis of antibiotic therapy for bone and joint infections”. Lancet Infect Dis.. vol. 1. 2001. pp. 175-88. (Makes a compelling case for the lack of superiority of any one therapy for septic arthritis.)

DRG CODES and expected length of stay
  • 550 if there is not a complication or comorbidity

  • 549 if there is complication or comorbidity

  • 548 if there is major complication or comorbidity

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