REVIEW
Peripheral Bacterial Septic Arthritis
Review of Diagnosis and Management
Ahmed S. Hassan, MD,* Allison Rao, MD,† Augustine M. Manadan, MD,‡ and Joel A. Block, MD§
Abstract: Septic arthritis refers to an infection in a joint due to a bacterial,
mycobacterial, or fungal cause. Joint infections are a serious cause of mor-
bidity and mortality and constitute a true musculoskeletal emergency. The
estimated incidence of septic arthritis in the general population is between
2 and 6 cases per 100,000 people per year. The most common presentation
is an acute monoarthritis. Identification of organisms in the synovial fluid
is the criterion standard for diagnosis. Synovial fluid aspiration should be
performed prior to initiating antibiotics. While no diagnostic cutoff exists
for synovial fluid white blood cell count, increasing leukocytosis is associ-
ated with a higher likelihood of an infectious cause of arthritis, and patients
commonly present with values greater than 50,000/μL. The cornerstones of
treating septic bacterial arthritis are adequate drainage and antimicrobials.
Joint drainage is always recommended in septic arthritis; however, no clear
guidelines or strong evidence exist to guide the preferred method of drain-
age. Options for joint drainage include daily needle aspiration, arthroscopy,
or open surgical drainage via arthrotomy.
Key Words: arthrocentesis, arthroscopic drainage, bacterial arthritis,
joint infections, management of septic arthritis, rheumatologic
emergencies, septic arthritis
(J Clin Rheumatol 2017;00: 00–00)
S eptic, infectious, pyogenic, suppurative, or purulent arthritis
refers to an infection in a joint due to a bacterial, mycobacterial,
or fungal cause. Joint infections are a serious cause of morbidity
and mortality and constitute a true musculoskeletal emergency
where a substantial difference in outcomes depends on a timely di-
agnosis and early institution of treatment. Several challenges in
the management of bacterial septic arthritis include selection of
appropriate antimicrobials and selection of appropriate joint fluid
drainage method. In this narrative review, we focus on the epide-
miology, mechanism, pathogenesis, clinical signs, diagnosis, and
treatment of native joint bacterial septic arthritis.
EPIDEMIOLOGY
The estimated incidence of septic arthritis in the general pop-
ulation is between 2 and 6 cases per 100,000 people per year.1,2
The incidence is higher in populations predisposed to septic arthri-
tis, such as among patients with rheumatoid arthritis (RA), where
the incidence has been estimated to be up to 70 per 100,000 people
per year.3 A prior systematic review of 14 studies and 6242 patients
identified several risk factors for septic arthritis; these included dia-
betes mellitus (DM), RA, the presence of a prosthetic joint, recent
From the *Cook County Health & Hospital Systems; †Midwest Orthopedics
Rush University Medical Center; ‡Division of Rheumatology, Rush Uni-
versity Medical Center; §Division of, Rush University, Chicago, IL.
The authors declare no conflict of interest.
Correspondence: Ahmed S. Hassan MD, Cook County Health & Hospital
Systems, 1900 W Polk, Suite 740 Chicago, IL 60612.
E‐mail: ahassan@cookcountyhhs.org.
Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.
ISSN: 1076-1608
DOI: 10.1097/RHU.0000000000000588
JCR: Journal of Clinical Rheumatology • Volume 00, Number 00, Month 2017
Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
joint surgery, intravenous (IV)–drug abuse, skin infections, and
prior intra-articular corticosteroid injection.4
MICROBIOLOGY
The most common organism identified in septic arthritis in
adults is Staphylococcus aureus, responsible for an estimated 37%
to 56% of cases5,6 with methicillin-resistant S. aureus (MRSA) in-
creasingly common. Several risk factors were proposed to identify
patients at a higher risk of MRSA infections such as those with
IV-drug use, human immunodeficiency virus infection, or DM.
The most well-documented at-risk group is patients recently admit-
ted to a hospital within 1 year.7 The next most common causative or-
ganisms are groups A and B streptococci, which are especially
prevalent among the elderly and among those with chronic diseases
such as DM or cirrhosis.8 Gram-negative organisms are less com-
mon. The 2 most frequently observed gram-negative organisms are
Neisseria gonorrhoeae and Neisseria meningitidis.5 Gram-negative
enteric organisms are generally limited to patients who are immuno-
compromised or who are IV-drug abusers and include Escherichia
coli, Proteus mirabilis and Klebsiella.9 In approximately 20% to
50% of cases of septic arthritis, no causative organisms are identi-
fied; this is often due to antibiotic treatment prior to arthrocentesis10
(Tables 1 and 2).
MECHANISM
The synovium is highly vascularized and lacks a protective
basement membrane; thus, the most common route of bacterial
entry is via hematogenous spread.16–18 Joints with preexisting
damage, such as in RA or osteoarthritis, are especially prone to
septic arthritis.19 Similarly, there are suggestions of elevated risk
in other forms of arthritis, such as gout and pseudogout.20
Rare means of joint infection include direct inoculation after
trauma or surgery disrupting the integrity of the joint capsule. Sep-
tic arthritis only rarely occurs following intra-articular corticoste-
roid injections or arthrocentesis, with an estimated risk of less
than 1 in 1000.21 Upon introduction to the joint space, microorgan-
isms precipitate an acute inflammatory reaction that may progress
to involve the surrounding bone. Destruction is due to inflammatory
cytokines and proteases.22 Bacterial toxins may also be destructive;
for example, staphylococcal enterotoxins and superantigens produced
in staphylococcal toxic shock syndrome have been shown to damage
cartilage in animal models, and this effect may be ameliorated by
prevaccination with recombinant staphylococcal enterotoxin.23 Mi-
crobial surface components such as adhesins that mediate staphylo-
coccal adherence to intra-articular proteins (e.g., elastin, laminin,
fibronectin), so-called microbial surface components recognizing ad-
hesive matrix molecules, have also been shown to influence the abil-
ity of certain S. aureus strains to cause septic arthritis.24
CLINICAL PRESENTATION
The most common presentation of septic arthritis is an acutely
swollen, warm, and painful single joint with a limited range of mo-
tion4,25; fever is present in approximately only 40% to 60% of pa-
tients,26,27 especially among the elderly who usually may not
www.jclinrheum.com 1
Hassan et al. JCR: Journal of Clinical Rheumatology • Volume 00, Number 00, Month 2017

of several rheumatologic conditions such as RA. However, bio-

TABLE 1. Most Common Organisms Known to Cause Septic
Arthritis4–8
S. aureus Mycobacterium tuberculosis
Streptococcus pyogenes E. coli
S. pneumoniae P. mirabilis
Haemophilus influenzae P. aeruginosa
N. gonorrhoeae Klebsiella pneumoniae
N. meningitidis Salmonella species
Kingella kingae Multiple species of microorganisms
Fungi
present with fever.4 Fever is usually low-grade, but up to 40% of
patients can present with high-grade fever.22 There are insufficient
data to correlate specific causative pathogens with a higher inci-
dence of fever.
In more than 50% of adult cases, the knee is the site of the in-
fection, followed by the shoulders, wrists, hips, and ankles, whereas
the hip is the most commonly affected joint in children.20,28 Less
commonly affected joints such as the sacroiliac (SI) joint and sym-
physis pubis can have unique presentations. Septic arthritis of the
SI joint can present with buttocks pain, gait changes, and fever.29
Infection of the symphysis pubis can occur with pelvic malignan-
cies and in female patients who have undergone urinary inconti-
nence surgeries or in IV-drug abusers and can present with fever,
suprapubic pain, and an antalgic gait.30
Septic arthritis is usually monoarticular, but is oligoarticular in
approximately 10% to 20% of cases, typically in patients with over-
whelming sepsis, multiple systemic comorbid conditions, or RA.31,32
The increased risk of septic arthritis in patients with RA has
been attributed to several factors including the preexisting joint
damage, as well as immune suppression from medications com-
monly used to treat RA such as the biological agents.32 Further re-
search is needed to identify if the hypervascularity seen in the
synovium of RA patients plays a role in predisposing them to sep-
tic arthritis via hematogenous spreading.
Biologic Agents and Septic Arthritis Risk
Biologic drugs targeting tumor necrosis factor and interleukin
1, among others, are increasingly being used in the management
logic agents have also been associated with a 2-fold increased risk
of septic arthritis, with the highest risk being in the months follow-
ing the initiation of treatment. Notably, some patients who re-
ceived tumor necrosis factor α inhibitors had septic arthritis
caused by organisms that rarely cause the disease, including Sal-
monella, Listeria, and Pseudomonas aeruginosa.28,32
DIAGNOSIS
Identification of organisms in the synovial fluid is the crite-
rion standard for diagnosis. Synovial fluid aspiration should be
performed prior to initiating antibiotics, and the analysis should
include a white blood cell (WBC) count with differential, Gram
stain, culture, and examination for crystals under polarized mi-
croscopy.28 A Gram stain can provide immediate information
and is often positive in bacterial arthritis, with a sensitivity be-
tween 29% and 50%.4,33,34 In addition, synovial fluid WBC count
tends to be highly elevated. Although no definitive cutoff value
exists, a culture-proven diagnosis of septic arthritis was made in
approximately only 5% of patients with a synovial fluid WBC
count of less than 50,000/μL, 47% of patients with values greater
than 50,000 but less than 100,000/μL, and 77% of patients with a
synovial fluid WBC count exceeding 100,000/μL.1,6,35,36
While the results are typically available after the synovial
fluid WBC and Gram stain, synovial fluid cultures are extremely
sensitive in nongonococcal bacterial arthritis and are positive in
the majority of cases.26 Their sensitivity can be compromised in
patients who have received antibiotic treatment prior to obtaining
cultures and can also be falsely negative in infections caused by
less common organisms such as Mycoplasma.36 Studies have
demonstrated conflicting results when attempting to improve the
yield of the synovial fluid culture by inoculation of blood culture
bottles at the bedside compared with the traditionally used agar
plate cultures, with 1 study showing a third of specimens obtained
prior to initiating antibiotics yielding positive culture results in
blood culture bottles while being negative on conventional solid
media.37 Another report challenged this claim, however, in a study
involving 90 patients with acute joint effusions where no statisti-
cally significant differences were found in the rates of isolating
bacteria with either method.38 Advances in the diagnosis of less
common organisms such as Yersinia and Chlamydia species as

TABLE 2. Differential Diagnoses for Septic Arthritis

Differential Diagnosis Notes

Crystal arthritis11,12
• Can present in a very similar fashion and can coexist with bacterial arthritis
• Diagnosis is made by microscopic visualization of monosodium urate or calcium
pyrophosphate crystals in gout and pseudogout, respectively
• Other clues: tophi and first metatarsophalangeal joint involvement in gouty arthritis and
radiographs showing chondrocalcinosis in pseudogout
• The presence of crystals in the synovial fluid does not definitively exclude
bacterial arthritis
Reactive arthritis13 • May report a recent gastrointestinal or genitourinary tract infection and may report
other symptoms such as skin lesions, enthesitis, dactylitis, or ocular inflammation
Rheumatoid arthritis4,14 • Typically present with chronic symmetrical polyarthritis; however, they can still present
with an acute monoarthritis with elevated synovial fluid WBC counts
• If an RA patient with good disease control acutely presents with an inflamed joint,
then septic arthritis should be considered
Lyme disease15 • Infections with B. burgdorferi causing Lyme disease generally develop many weeks
after a visit to an endemic area and after the acute picture of fever with a characteristic rash
• Measurement of serum Borrelia immunoglobulin G levels and synovial fluid
analysis with PCR can be helpful in distinguishing the 2 conditions

2 www.jclinrheum.com © 2017 Wolters Kluwer Health, Inc. All rights reserved.

Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
JCR: Journal of Clinical Rheumatology • Volume 00, Number 00, Month 2017
well as N. gonorrhoeae and Borrelia burgdorferi have been made
using synovial polymerase chain reaction (PCR).26
Other clues to the diagnosis include a low synovial fluid glu-
cose level and elevated protein or lactic acid levels; however, those
laboratory values are nonspecific and can be found in all forms of
inflammatory arthritis. Elevated inflammatory markers, such eryth-
rocyte sedimentation rate and C-reactive protein, and an elevated
serum WBC count are nonspecific on their own for the diagnosis
of septic arthritis. However, elevated inflammatory markers and leu-
kocytosis, along with a clinical history suggestive of septic arthritis
and an elevated synovial WBC count greater than 50,000/μL, can
increase the overall sensitivity close to 100%.39,40 Measuring
C-reactive protein levels in the synovial fluid offers no added sensi-
tivity compared with measuring it in the serum, and the 2 laboratory
values generally strongly correlate.41
The first imaging modality of an infected joint should be a
radiograph and should be compared with a baseline image if avail-
able and later to a follow-up image in cases of nonresponse to
treatment. Characteristics of an acutely inflamed joint include
joint space widening, periarticular fat pad displacement, loss of
the white cortical line over extended and continuous segments,
and, occasionally, erosive changes.42 Other imaging modalities are
more sensitive and specific than plain radiographs for detecting in-
flammation or effusions especially early in the disease process and
include ultrasonography, computed tomography, magnetic reso-
nance imaging, and scintigraphy. Advanced imaging methods can
be especially useful for examining the SI and hip joints where in-
flammatory changes may be difficult to identify on a plain radio-
graph.43 Ultrasonography is a safe and easily conducted bedside
imaging modality to assist in the identification of joint effusions
and can be used to guide arthrocentesis. It is especially helpful in
hip arthrocentesis, a procedure otherwise traditionally performed
under fluoroscopic guidance.44–46
Gonococcal Arthritis and Disseminated
Gonococcal Infection
The typical presentation of gonococcal arthritis or dissemi-
nated gonococcal infection (DGI) is in a young (usually <40 years
old), sexually active patient presenting with fever, polyarthralgia,
tenosynovitis, and painless skin lesions, which can progress to
persistent oligoarthritis or monoarthritis. At this stage, it may be
difficult to distinguish DGI from typical pyogenic arthritis.47–49
It is important to note that N. gonorrhoeae cannot be reliably cul-
tured from routine culture media. Synovial fluid Gram stains have
a very low sensitivity in DGI being positive in less than 10% of
cases, and synovial fluid cultures are commonly negative.50 Pa-
tients suspected to have DGI should have pharyngeal, urogenital,
and rectal cultures sent for N. gonorrhoeae because most of pa-
tients with DGI will have evidence of infection in those sites even
without symptoms.50 Synovial fluid cultures on Thayer-Martin
medium or nucleic acid amplification testing of the synovial fluid
to identify N. gonorrhoeae are both diagnostic of DGI, the latter
being the preferred test.51,52 Synovial fluid testing with PCR to de-
tect gonococcal DNA has also been used with a reported sensitiv-
ity of approximately 78% in patients with DGI.53
Tuberculous Arthritis
The presentation of a patient with monoarthritis or oligoarthritis
refractory to treatment and with repeatedly negative synovial fluid
cultures should raise suspicion for tuberculous arthritis, especially
if the patient is from a tuberculosis endemic area. The most com-
monly affected joints are the hips and knee; however, tuberculous
arthritis may be found in any joint.54 Synovial fluid analysis is
generally nonspecific, and cultures are frequently negative for
© 2017 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Review of Diagnosis and Management
tuberculosis, but may be confounded by colonizing organisms
(bacteria or fungi) that are not the true causative organisms.55,56
Synovial biopsies with culture are more sensitive and should be
obtained whenever clinical suspicion is high.57
Brucellosis
Despite its relatively low incidence in North America, bru-
cellosis is one of the most common zoonotic infections worldwide
and one with significant human and animal morbidity.58 Caused
by Brucella species (Brucella melitensis, Brucella suis, and Bru-
cella abortus), the infection is transmitted by human contact with
bodily fluids from infected animals or food products.59,60 The typ-
ical presentation of acute brucellosis is a patient with a history of ex-
posure to animal products presenting with fever, night sweats,
weight loss, myalgias, and arthralgias.61 The most common focal
presentation of brucellosis is osteoarticular involvement, usually af-
fecting the SI, hip, or knee joints.62–64 The diagnosis is made by
positive blood and synovial fluid cultures and/or enzyme-linked im-
munosorbent assay testing for Brucella species.65,66 Synovial fluid
analysis is generally nonspecific for diagnosing brucellosis.67
Lyme Disease
Infections with B. burgdorferi causing Lyme disease gener-
ally develops many weeks to months after a visit to an endemic
area and after the acute picture of fever with a characteristic rash.
Lyme arthritis presents with either an intermittent or persistent
monoarthritis of the knee or, less commonly, an asymmetric
oligoarthritis. Measurement of serum Borrelia immunoglobulin
G levels and synovial fluid analysis with PCR can also be helpful
in distinguishing Lyme disease from septic arthritis.14
DIFFERENTIAL DIAGNOSIS
The chief differential diagnoses for bacterial arthritis are other
causes of acute mono or oligoarthritis and include acute crystal ar-
thropathies (gout and pseudogout), reactive arthritis, RA, and Lyme
disease (Table 2).
Crystal arthritis is usually the first diagnosis to consider be-
cause it can present in a very similar fashion and can coexist with
bacterial arthritis. The diagnosis can be made by polarizing micro-
scopic visualization of monosodium urate or calcium pyrophos-
phate crystals in gout and pseudogout, respectively. Other clues
include the presence of tophi and first metatarsophalangeal joint
involvement in gouty arthritis and knee radiographs showing
chondrocalcinosis in pseudogout.11,12,68 It is critical to remember
that neither the presence of crystals in the synovial fluid nor the
absence of a positive synovial fluid Gram stain can definitively ex-
clude bacterial arthritis.
Patients with reactive arthritis may report a recent gastrointes-
tinal or genitourinary tract infection and may report other symptoms
such as skin lesions, enthesitis, dactylitis, or ocular inflammation.69
Patients with RA typically present with chronic polyarthritis that is
symmetrical and not associated with fever or leukocytosis; however,
they can still present with an acute monoarthritis with elevated sy-
novial fluid WBC counts. It should be noted that if an RA patient
with good disease control acutely presents with an inflamed joint,
then septic arthritis should be considered. The 2 conditions can still
overlap, and RA is a risk factor for bacterial arthritis as previously
discussed.4,13 Lyme disease is another important differential diag-
nosis as discussed previously.14
MANAGEMENT
The cornerstones of treatment include adequate drainage
and antimicrobials (Figure). The initial choice of antibiotics is
www.jclinrheum.com 3
Hassan et al. JCR: Journal of Clinical Rheumatology • Volume 00, Number 00, Month 2017

FIGURE. Suggested management algorithm of nongonococcal bacterial peripheral native joint septic arthritis. *Synovial WBC count
elevated (usually >50,000/μL), blood culture positive, Gram stain–positive, and/or synovial culture–positive. **Patient characteristics that
may affect selection of drainage type include joint size/accessibility, comorbidities, and inability to tolerate anesthesia. ***Exact frequency
of serial joint aspiration has not been studied but typically is performed daily until synovial fluid WBC count approaches normal, fluid stops
accumulating, and cultures sterilize. Consideration for more frequent aspiration during the first 24 to 36 hours is reasonable if fluid
reaccumulates quickly.

generally based on epidemiological factors, as well as the age, risk
factors, and clinical presentation in addition to Gram stain results.
No randomized controlled trials to date have compared different
antibiotic regimens for the treatment of bacterial arthritis, nor is
there strong evidence to guide the duration of treatment.6,15 Sim-
ilarly, there is no evidence to recommend joint immobilization, but
weight bearing is generally discouraged until after the resolution of
the acute inflammation.22 Further research is needed to determine
the ideal time to fully restart daily activities or start physical therapy.
Antibiotic Therapy
Vancomycin is generally the initial antibiotic used in the
United States. If the patient is immunocompromised or an
IV-drug abuser, vancomycin plus a third-generation cephalosporin
such as ceftriaxone, cefotaxime, or ceftazidime should be given.
The initial antibiotic regimen should be tailored to Gram stain,
culture, and susceptibility results.44 If the clinical picture is sug-
gestive of disseminated gonococcal or meningococcal infections,
IV ceftriaxone provides adequate coverage.13 If P. aeruginosa is
suspected, then a third-generation cephalosporin plus gentamicin
should be given.13,70 The use of intra-articular antibiotics is not
advised because it adds no therapeutic benefit and exposes the pa-
tient to the potential of an inflammatory response to intra-
articular antibiotics.36
There have been no controlled trials so far to identify the op-
timal duration of antibiotic treatment in septic arthritis. Intrave-
nously administered antibiotics are typically administered for
14 days followed by a similar-duration course of oral antibiotics;
however, some organisms that are commonly difficult to treat such
as P. aeruginosa may need 4 to 6 weeks of parenteral therapy.
There is insufficient evidence in favor of the use of systemic
corticosteroids along with antibiotics in septic arthritis in adult pa-
tients; however, studies in the pediatric population did suggest a
possible benefit. A double-blind, randomized, placebo-controlled trial
of dexamethasone for 4 days in the management of hematogenous
septic arthritis in 100 children significantly shortened the duration
of symptoms in the acute phase, as well as the residual joint dysfunc-
tion at the end of therapy and at 12 months of follow-up.71 A theoret-
ical benefit can also be conceived as most damage inflicted upon
infected joints is a result of the host's own inflammatory response
as opposed to direct damage caused by the organisms.33
Synovial Fluid Drainage
Septic arthritis, like any other form of a closed infection,
needs drainage in conjunction with antibiotics. However, as there
have not been randomized controlled trials in adults comparing
drainage methods, namely, daily needle aspiration, arthroscopic
drainage, or open surgical drainage via arthrotomy, the choice has

4 www.jclinrheum.com © 2017 Wolters Kluwer Health, Inc. All rights reserved.

Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
JCR: Journal of Clinical Rheumatology • Volume 00, Number 00, Month 2017 Review of Diagnosis and Management

TABLE 3. Summary Points

(1) Septic arthritis can be caused by a variety of microorganism including S. aureus, streptococcal species, N. gonorrhoeae, Gram-negative rods,
Brucella fungal organisms (sporotrichosis, blastomycoses), and Mycobacterium tuberculosis.
(2) Methods of joint infection include hematogenous dissemination, contiguous spread (adjacent osteomyelitis, cellulitis), or direct inoculation
(prosthesis, arthrocentesis, penetrating trauma).
(3) Joint drainage in addition to appropriate antibiotics is usually needed for successful treatment of typical pyogenic septic arthritis.
(4) There exists controversy about the preferred method of drainage. Orthopedic surgeons prefer arthroscopic lavage, and rheumatologists
prefer daily needle arthrocenteses.
(5) Inability to completely drain joint (inaccessibility, viscous fluid, or loculations) would favor arthroscopic lavage over daily needle
arthrocentesis.
(6) Neisseria gonorrhoeae septic arthritis may not always require extensive joint drainage.
(7) Patients with features to suggest disseminated N. gonorrhoeae should have multiple cultures (synovial, urethral, cervical, rectal, and
pharyngeal) submitted on Thayer-Martin media or DNA PCR analysis.
(8) Patients with N. gonorrhoeae septic arthritis should be offered screening for other sexually transmitted diseases (syphilis serology,
chlamydia cultures, and human immunodeficiency virus screening).
(9) Crystal arthritis can coexist with septic arthritis.
(10) Crystal arthritis can cause synovial cell counts higher than 50,000–100,000/μL (pseudoseptic arthritis).
(11) Synovial cell counts less than 50,000/μL do not exclude septic arthritis.
(12) Gram stain and preliminary cultures may be negative in septic arthritis. Prior antibiotics may affect microbiologic yield.
(13) Tuberculosis septic arthritis often requires synovial biopsy for diagnosis.
(14) Plain radiographs of involved joint may appear normal on presentation. Ultrasonography is helpful in the diagnosis of effusions and hip
joint arthrocentesis. Effusions and soft tissue extension are better visualized by computed tomography scan.
(15) Septic arthritis can involve axial joints such as sternoclavicular joint and SI joint.
(16) Risk factors for septic arthritis include DM, RA, IVDA, and immunosuppression.
(17) Septic arthritis after therapeutic intra-articular joint injection is extremely rare.
(18) Septic arthritis is a potentially life-threatening infection that can be complicated by fasciitis, osteomyelitis, secondary hematogenous
dissemination, and permanent articular damage.
(19) Brucella is a zoonosis (goats and sheep) often transmitted via unpasteurized milk or cheese or by inhalation. Brucella can infect a variety
of organs including bone and SI joints.
(20) Initial empiric antibiotic regimen in the United States is vancomycin and possibly a third-generation cephalosporin but is then tailored
based on Gram stain, culture, and sensitivity.
(21) Neisseria gonorrhoeae septic arthritis is usually treated with IV ceftriaxone followed by oral cefixime.
IVDA, intravenous drug abuse.

generally been guided by retrospective studies and often depends
on the extent and duration of the infection, site of the effected joint,
and procedural availability. One study found that patients hospital-
ized in the orthopedic unit were more likely to be treated with sur-
gical intervention compared with patients hospitalized in the
medical unit with no statistically significant difference in treatment
failure rates between the 2 groups.72
Studies performed to date were all retrospective and with a
small sample size, making it difficult to establish evidence-based rec-
ommendations for either strategy. For instance, a retrospective study
over an 8-year period of patients with nongonococcal septic arthritis
seemed to show better outcomes with daily needle aspiration com-
pared with surgical treatment (67% vs. 42% achieved good clinical
outcomes defined as complete recovery and no secondary ankylo-
sis, osteomyelitis, or flexion deformities).73 However, because this
was a retrospective study, it is likely that there were significant dif-
ferences in the overall health of patients treated surgically compared
with those treated conservatively. Randomized controlled trials
comparing daily needle aspiration, arthroscopy, and arthrotomy in
various joints are needed to outline a standardized approach that
provides the best outcomes.
Daily Needle Arthrocentesis
Daily needle arthrocentesis, usually performed with an 18-
gauge needle, has many advantages. It can be performed safely
at the bedside; it can be performed in patients who are poor surgi-
cal candidates and allows for daily measure of clinical response
through synovial WBC counts and cultures. The main disadvan-
tages are inability to debride and reach loculated effusions. Also,
some joints such as hips are inaccessible. Some clinical clues that
suggest success of daily needle arthrocentesis include improvement
of joint pain and swelling, resolution of fever and systemic leukocy-
tosis, and improvement of synovial fluid WBC count. If daily-need
arthrocentesis is utilized, then repeated analyses of the synovial
fluid WBC count are recommended to document improvement
and, more significantly, synovial fluid sterility.74
Arthroscopic Drainage
Benefits of surgical drainage include the ability to remove
nonviable tissue, obtain biopsies after debridement, and evaluate for
a potential synovectomy. These benefits may be more pronounced
in infections of the knees, wrist, and shoulders, where arthroscopy
provides better visualization and easier access to irrigation.75–77
Arthroscopic and open arthrotomy can both be used as treat-
ment options for management of an acute bacterial septic joint.
Arthroscopic treatment is primarily used in treatment of the knee,
shoulder, or hip joint involvement, given the ease of use and avail-
able equipment.78–81 Arthroscopic treatment may also be used in
acutely detected infection; a delayed diagnosis may warrant a
more extensive open approach for thorough examination.82 With
either open or arthroscopic treatment, the surgeon's preferred ap-
proach can be used. After entry into the joint, multiple tissue sam-
ples are sent for microbiologic analysis including aerobic and

© 2017 Wolters Kluwer Health, Inc. All rights reserved. www.jclinrheum.com 5

Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Hassan et al. JCR: Journal of Clinical Rheumatology • Volume 00, Number 00, Month 2017
anaerobic culture. If using an arthroscopic technique, a motorized
shaver is used to debride fibrinous or inflamed synovial tissue. A
minimum of 6 L, with up to 20 L for arthroscopic treatment, is
used for irrigation.83 The wound is often closed over a closed suc-
tion drain. All aspects of the involved joint must be visualized and
explored to ensure complete debridement and irrigation. Range of
motion and weight bearing are sometimes held for a brief period
postoperatively to support wound healing.
Delayed treatment can have devastating local consequences
including bone and cartilage destruction, osteonecrosis, second-
ary arthritis, and potentially ankylosis. In addition, multiple surgi-
cal debridements may be necessary, with evidence showing that
only 62% of septic joints may be effectively managed with a sin-
gle surgical debridement.81,84 Risk factors for a failed single sur-
gical treatment include RA, diabetes, a synovial fluid of more
than 85,000/μL, involvement of a large joint, delayed diagnosis,
and an infection with S. aureus.81
Outcomes
Poor joint outcomes in bacterial arthritis range from mild de-
terioration of joint function to the need for arthrodesis, prosthetic
surgery, or amputation. Outcomes seem to vary widely, depending
on several factors pertaining to the causative organism, as well as the
host. Factors that predicted poor outcomes identified in retrospective
studies include older patient age, DM, renal and liver diseases,
preexisting joint disease, and infection with MRSA.73,85 Studies
reporting outcomes in infections caused by S. aureus in adult patients
showed poor joint outcomes in up to 50% of cases compared with
only 5% in infections caused by Streptococcus pneumoniae.2,16,36
SUMMARY
Septic arthritis is a musculoskeletal emergency and a cause
of significant morbidity and mortality. Staphylococcus aureus is
the most common infectious organism and is typically transmitted
hematogenously. Patients typically present with a monoarthritis,
sometimes with systemic symptoms such as low-grade fever.
The knee is the most commonly affected joint and is involved in
approximately 50% of the cases. A definitive diagnosis is made
by a positive synovial fluid culture in the face of a consistent clin-
ical presentation. Although no diagnostic cutoff exists for synovial
fluid WBC, increasing leukocytosis is associated with a higher
likelihood of an infectious cause of arthritis, and patients com-
monly present with values greater than 50,000/μL. Synovial fluid
Gram stains, although helpful, are not always positive in septic ar-
thritis, and a negative Gram stain should not be used to exclude a
septic arthritis. The cornerstones of treating septic bacterial arthritis
are adequate drainage and antimicrobials. Joint drainage is always
recommended in septic arthritis; however, no clear guidelines or
strong evidence exists to guide the preferred method of drainage.
Options for joint drainage include daily needle aspiration, arthros-
copy, or open surgical drainage via arthrotomy. Outcomes depend
on the causative organism, patient age and risk factors, and timely
management (Table 3).
REFERENCES
1. Mathews CJ, Weston VC, Jones A, et al. Bacterial septic arthritis in adults.
Lancet. 2010;375:846–855.
2. Weston VC, Jones AC, Bradbury N, et al. Clinical features and outcome
of septic arthritis in a single UK Health District 1982–1991. Ann Rheum
Dis. 1999;58:214–219.
3. Favero M, Schiavon F, Riato L, et al. Rheumatoid arthritis is the major
risk factor for septic arthritis in rheumatological settings. Autoimmun Rev.
2008;8:59–61.
6 www.jclinrheum.com
Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
4. Margaretten ME, Kohlwes J, Moore D, et al. Does this adult patient have
septic arthritis? JAMA. 2007;297:1478.
5. Sharp JT, Lidsky MD, Duffy J, et al. Infectious arthritis. Arch Intern Med.
1979;139:1125–1130.
6. Mathews CJ, Coakley G. Septic arthritis: current diagnostic and therapeutic
algorithm. Curr Opin Rheumatol. 2008;20:457.
7. Furuno JP, McGregor JC, Harris AD, et al. Identifying groups at high risk
for carriage of antibiotic-resistant bacteria. Arch Intern Med. 2006;166:
580–585.
8. Goldenberg DL. Septic arthritis. Lancet. 1998;351:197–202.
9. Goldenberg DL, Brandt KD, Cathcart ES, et al. Acute arthritis caused by
gram-negative bacilli: a clinical characterization. Medicine (Baltimore).
1974;53:197–208.
10. Nade S. Septic arthritis. Best Pract Res Clin Rheumatol. 2003;17:183–200.
11. Wallace SL, Robinson H, Masi AT, et al. Preliminary criteria for the
classification of the acute arthritis of primary gout. Arthritis Rheum. 1977;
20:895.
12. Epstein JH, Zimmermann B 3rd, Ho G Jr. Polyarticular septic arthritis.
J Rheumatol. 1986;13:1105–1107.
13. Allison DC, Holtom PD, Patzakis MJ, et al. Microbiology of bone and joint
infections in injecting drug abusers. Clin Orthop Relat Res. 2010;468:
2107–2112.
14. Guidelines for laboratory evaluation in the diagnosis of Lyme disease.
American College of Physicians. Ann Intern Med. 1997;127:1106–1108.
15. Mathews CJ, Kingsley G, Field M, et al. Management of septic arthritis:
a systematic review. Ann Rheum Dis. 2007;66:440–445.
16. Ross JJ, Saltzman CL, Carling P, et al. Pneumococcal septic arthritis:
review of 190 cases. Clin Infect Dis. 2003;36:319–327.
17. Cooper C, Cawley MI. Bacterial arthritis in an English health district: a
10 year review. Ann Rheum Dis. 1986;45:458–463.
18. McCarthy DJ. Joint sepsis: a chance for cure. JAMA. 1982;247:835.
19. Kaandorp CJ, Krijnen P, Moens HJ, et al. The outcome of bacterial arthritis:
a prospective community-based study. Arthritis Rheum. 1997;40:884.
20. Goldenberg DL. Septic arthritis and other infections of rheumatologic
significance. Rheum Dis Clin North Am. 1991;17:149.
21. von Essen R, Savolainen HA. Bacterial infection following intra-articular
injection. A brief review. Scand J Rheumatol. 1989;18:7–1.
22. Smith JW, Chalupa P, Shabaz HM. Infectious arthritis: clinical features,
laboratory findings and treatment. Clin Microbiol Infect. 2006;12:309–314.
23. Frank G, Mahoney HM, Eppes SC. Musculoskeletal infections in children.
Pediatr Clin North Am. 2005;52:1083–1106. ix.
24. Nilsson IM, Verdrengh M, Ulrich RG, et al. Protection against
Staphylococcus aureus sepsis by vaccination with recombinant
staphylococcal enterotoxin A devoid of superantigenicity. J Infect Dis.
1999;180:1370.
25. Nilsson IM, Lee JC, Bremell T, et al. The role of staphylococcal
polysaccharide microcapsule expression in septicemia and septic arthritis.
Infect Immun. 1997;65:4216–4221.
26. Pioro MH, Mandell BF. Septic arthritis. Rheum Dis Clin North Am. 1997;
23:239–258.
27. Goldenberg DL, Cohen AS. Acute infectious arthritis: a review of patients
with nongonococcal joint infections (with emphasis on therapy and
prognosis). Am J Med. 1976;60:369–377.
28. Tarkowski A. Infection and musculoskeletal conditions: infectious arthritis.
Best Pract Res Clin Rheumatol. 2006;20:1029–1044.
29. Mancarella L, De Santis M, Magarelli N, et al. Septic sacroiliitis: an
uncommon septic arthritis. Clin Exp Rheumatol. 2009;27:1004–1008.
30. Ross JJ, Hu LT. Septic arthritis of the pubic symphysis: review of 100 cases.
Medicine (Baltimore). 2003;82:340.
© 2017 Wolters Kluwer Health, Inc. All rights reserved.
JCR: Journal of Clinical Rheumatology • Volume 00, Number 00, Month 2017
31. Dubost JJ, Fis I, Denis P, et al. Polyarticular septic arthritis. Medicine
(Baltimore). 1993;72:296–310.
32. Galloway JB, Hyrich KL, Mercer LK, et al. Risk of septic arthritis in
patients with rheumatoid arthritis and the effect of anti-TNF therapy: results
from the British Society for Rheumatology Biologics Register. Ann Rheum
Dis. 2011;70:1810–1814.
33. Klinger HM, Baums MH, Freche S, et al. Septic arthritis of the shoulder
joint: an analysis of management and outcome. Acta Orthop Belg. 2010;76:
598–603.
34. Faraj AA, Omonbude OD, Godwin P. Gram staining in the diagnosis of
acute septic arthritis. Acta Orthop Belg. 2002;68:388–391.
35. Goldenberg DL, Reed JI. Bacterial arthritis. N Engl J Med. 1985;312:764.
36. Maneiro JR, Souto A, Cervantes EC, et al. Predictors of treatment failure
and mortality in native septic arthritis. Clin Rheumatol. 2015;34:
1961–1967.
37. von Essen R, Holtta A. Improved method of isolating bacteria from joint
fluids by the use of blood culture bottles. Ann Rheum Dis. 1986;45:
454–457.
38. Kortekangas P, Aro HT, Lehtonen OP. Synovial fluid culture and blood
culture in acute arthritis. A multi-case report of 90 patients. Scand J
Rheumatol. 1995;24:44–47.
39. Li SF, Cassidy C, Chang C, et al. Diagnostic utility of laboratory tests in
septic arthritis. Emerg Med J. 2007;24:75–77.
40. Hariharan P, Kabrhel C. Sensitivity of erythrocyte sedimentation rate and
C-reactive protein for the exclusion of septic arthritis in emergency
department patients. J Emerg Med. 2011;40:428.
41. Tetreault MW, Wetters NG, Moric M, et al. Is synovial C-reactive protein a
useful marker for periprosthetic joint infection? Clin Orthop Relat Res.
2014;472:3997.
42. Brower AC. Septic arthritis. Radiol Clin North Am. 1996;34:293–309.
43. Zimmermann B 3rd, Mikolich DJ, Lally EV. Septic sacroiliitis. Semin
Arthritis Rheum. 1996;26:592.
44. Shmerling RH. Synovial fluid analysis: a critical reappraisal. Rheum Dis
Clin North Am. 1994;20:503–512.
45. Laine JC, Denning JR, Riccio AI, et al. The use of ultrasound in the
management of septic arthritis of the hip. J Pediatr Orthop B. 2015;24:
95–98.
46. Freeman K, Dewitz A, Baker WE. Ultrasound-guided hip arthrocentesis in
the ED. Am J Emerg Med. 2007;25:80–86.
47. Coutlakis PJ, Roberts WN, Wise CM. Another look at synovial fluid
leukocytosis and infection. J Clin Rheumatol. 2002;8:67–71.
48. Rompalo AM, Hook EW 3rd, Roberts PL, et al. The acute
arthritis-dermatitis syndrome. The changing importance of Neisseria
gonorrhoeae and Neisseria meningitidis. Arch Intern Med. 1987;147:
281–283.
49. O'Brien JP, Goldenberg DL, Rice PA. Disseminated gonococcal infection: a
prospective analysis of 49 patients and a review of pathophysiology and
immune mechanisms. Medicine (Baltimore). 1983;62:395.
50. McCutchan HJ, Fisher RC. Synovial leukocytosis in infectious arthritis.
Clin Orthop Relat Res. 1990;257:226–230.
51. Rice PA. Gonococcal arthritis (disseminated gonococcal infection). Infect
Dis Clin North Am. 2005;19:853–861.
52. Centers for Disease Control and Prevention. Recommendations for the
laboratory-based detection of Chlamydia trachomatis and Neisseria
gonorrhoeae—2014. MMWR Recomm Rep. 2014;63:1–19.
53. Liebling MR, Arkfeld DG, Michelini GA, et al. Identification of Neisseria
gonorrhoeae in synovial fluid using the polymerase chain reaction.
Arthritis Rheum. 1994;37:702.
54. Hodgson SP, Ormerod LP. Ten-year experience of bone and joint
tuberculosis in Blackburn 1978–1987. J R Coll Surg Edinb. 1990;35:
259–262.
© 2017 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Review of Diagnosis and Management
55. Kim SJ, Postigo R, Koo S, et al. Total hip replacement for patients with
active tuberculosis of the hip: a systematic review and pooled analysis.
Bone Joint J. 2013;95-B:578.
56. Lewinsohn DM, Leonard MK, LoBue PA, et al. Official American
Thoracic Society/Infectious Diseases Society of America/Centers for
Disease Control and Prevention clinical practice guidelines: diagnosis of
tuberculosis in adults and children. Clin Infect Dis. 2017;64:e1–e33.
57. Allali F, Mahfoud-Filali S, Hajjaj-Hassouni N. Lymphocytic joint fluid
in tuberculous arthritis. A review of 30 cases. Joint Bone Spine. 2005;
72:319.
58. Merino P, Candel FJ, Gestoso I, et al. Microbiological diagnosis of spinal
tuberculosis. Int Orthop. 2012;36:233–238.
59. Colmenero JD, Reguera JM, Martos F, et al. Complications associated
with Brucella melitensis infection: a study of 530 cases. Medicine
(Baltimore). 1996;75:195–211.
60. Mantur BG, Amarnath SK, Shinde RS. Review of clinical and
laboratory features of human brucellosis. Indian J Med Microbiol.
2007;25:188–202.
61. Young EJ. An overview of human brucellosis. Clin Infect Dis. 1995;21:
283–289.
62. Pappas G, Akritidis N, Bosilkovski M, et al. Brucellosis. N Engl J Med.
2005;352:2325.
63. Bosilkovski M, Krteva L, Caparoska S, et al. Osteoarticular involvement
in brucellosis: study of 196 cases in the Republic of Macedonia.
Croat Med J. 2004;45:727–733.
64. Geyik MF, Gür A, Nas K, et al. Musculoskeletal involvement of
brucellosis in different age groups: a study of 195 cases. Swiss
Med Wkly. 2002;132:98–105.
65. Hashemi SH, Keramat F, Ranjbar M, et al. Osteoarticular complications
of brucellosis in Hamedan, an endemic area in the west of Iran. Int
J Infect Dis. 2007;11:496.
66. Mantecón Mde L, Gutiérrez MP, Zarzosa Mdel P, et al. Influence of
brucellosis history on serological diagnosis and evolution of patients
with acute brucellosis. J Infect. 2008;57:397.
67. Al Dahouk S, Tomaso H, Nöckler K, et al. Laboratory-based diagnosis of
brucellosis—a review of the literature. Part II: serological tests for
brucellosis. Clin Lab. 2003;49:577–589.
68. Chen LX, Schumacher HR. Current trends in crystal identification.
Curr Opin Rheumatol. 2006;18:171.
69. Sieper J, Rudwaleit M, Braun J, et al. Diagnosing reactive arthritis:
role of clinical setting in the value of serologic and microbiologic assays.
Arthritis Rheum. 2002;46:319–327.
70. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the
Infectious Diseases Society of America for the treatment of
methicillin-resistant Staphylococcus aureus infections in adults and
children. Clin Infect Dis. 2011;52:e18.
71. Odio CM, Ramirez T, Arias G, et al. Double blind, randomized,
placebo-controlled study of dexamethasone therapy for hematogenous
septic arthritis in children. Pediatr Infect Dis J. 2003;22:883–888.
72. Lim SY, Pannikath D, Nugent K. A retrospective study of septic arthritis
in a tertiary hospital in West Texas with high rates of methicillin-resistant
Staphylococcus aureus infection. Rheumatol Int. 2015;35:1251–1256.
73. Goldenberg D, Brandt KD, Cohen AS, et al. Treatment of septic arthritis:
comparison of needle aspiration and surgery as initial modes of joint
drainage. Arthritis Rheum. 1975;18:83–90.
74. Nusem I, Jabur MK, Playford EG. Arthroscopic treatment of septic
arthritis of the hip. Arthroscopy. 2006;22:902. e1.
75. Manadan AM, Block JA. Daily needle aspiration versus surgical lavage
for the treatment of bacterial septic arthritis in adults. Am J Ther. 2004;
11:412–415.
www.jclinrheum.com 7
Hassan et al. JCR: Journal of Clinical Rheumatology • Volume 00, Number 00, Month 2017

76. Thiery JA. Arthroscopic drainage in septic arthritides of the knee: a
multicenter study. Arthroscopy. 1989;5:65–69.
77. Stutz G, Kuster MS, Kleinstück F, et al. Arthroscopic management of septic
arthritis: stages of infection and results. Knee Surg Sports Traumatol
Arthrosc. 2000;8:270–274.
78. Bosilkovski M, Dimzova M, Grozdanovski K. Natural history of
brucellosis in an endemic region in different time periods. Acta Clin Croat.
2009;48:41–46.
79. Darren de SA, Cargnelli S, Catapano M, et al. Efficacy of hip arthroscopy
for the management of septic arthritis: a systematic review. Arthroscopy.
2015;31:1358–1370.
80. Wirtz D, Marth M, Miltner O, et al. Septic arthritis of the knee in adults:
treatment by arthroscopy or arthrotomy. Int Orthop. 2001;25:239–241.
81. Jeon IH, Choi CH, Seo JS, et al. Arthroscopic management of septic
arthritis of the shoulder joint. J Bone Joint Surg Am. 2006;88:1802–1806.
82. Chen C, Lin H, Hung S, et al. Surgical treatment for septic arthritis of the
knee joint in elderly patients: a 10-year retrospective clinical study.
Orthopedics. 2013;36:e434–e443.
83. Balabaud L, Gaudias J, Boeri C, et al. Results of treatment of septic knee
arthritis: a retrospective series of 40 cases. Knee Surg Sports Traumatol
Arthrosc. 2007;15:387–392.
84. Hunter JG, Gross JM, Dahl JD, et al. Risk factors for failure of a single
surgical debridement in adults with acute septic arthritis. J Bone Joint
Surg Am. 2015;97:558–564.
85. Deng GM, Tarkowski A. The features of arthritis induced by CpG motifs
in bacterial DNA. Arthritis Rheum. 2000;43:356.

8 www.jclinrheum.com © 2017 Wolters Kluwer Health, Inc. All rights reserved.

Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.