Septic Arthritis 

Updated: Sep 16, 2021
Author: John L Brusch, MD, FACP; Chief Editor: Michael Stuart Bronze, MD 

Overview

Background

Septic arthritis (SA), also known as infectious arthritis, represents an invasion of a joint space by a wide range of microorganisms, most commonly bacteria. Various viruses, mycobacteria, and fungi are also causative. Because of their rapidly destructive nature, the current discussion will focus primarily on the bacterial septic arthritides. Even when expeditiously and appropriately treated, these pathogens characteristically result in significant rates of morbidity and mortality.

Reactive arthritis represents a sterile inflammatory process that is triggered by an extra-articular infection.

Approximately 20,000 cases of septic arthritis occur in the United States each year (7.8 cases per 100,000 person-years), with a similar incidence occurring in Europe.[1]  The incidence of arthritis due to disseminated gonococcal infection is 2.8 cases per 100,000 person-years. Because of the increasing use of prosthetic joints, infection associated with these devices has become the most challenging type of SA encountered by most clinicians.[2] The incidence of prosthetic joint infection (PJI) among all prosthesis recipients ranges from 2% to 10%. These figures may be falsely low because surveillance is limited to the operative hospital, which may lead to underestimation of the rate of PJIs.[3]

Patients who have undergone treatment for infection of a native joint are at an increased risk for PJI after a total joint arthroplasty of that particular joint.[4]

Septic arthritis is increasingly common among persons older than 65 years, among immunosuppressed individuals, and among those with various  comorbiditiees such as diabetes. Fifty-six percent of patients with septic arthritis are male.

Gonococcal and nongonococcal bacterial/suppurative arthritis

Bacterial SA is commonly described as either gonococcal or nongonococcal.[1, 2, 5, 6, 7, 8]  Neisseria gonorrhoeae remains the most common pathogen (75% of cases) among younger sexually active individuals.[9, 10, 11] The increased incidence of S aureus parallels the rise of prosthetic joint implantation, intravenous drug abuse (IVDA), and the use of immunosuppressive agents. This pathogen causes 80% of infected joints affected by rheumatoid arthritis.

Streptococcal species, such as Streptococcus viridans, S pneumoniae,[12, 13] and group B streptococci[14] account for 20% of cases. Aerobic gram-negative rods are involved in 20-25% of cases. Most of these infections occur among very young and very old,[15]  patients with diabetes, immunosuppressed individuals, and people who use intravenous drugs.[16, 17]

Infection of the cartilaginous joints (sternoclavicular, sacroiliac, and pubic joints) with Pseudomonas aeruginosa or Serratia species occurs almost exclusively among people who abuse intravenous drugs. Individuals with leukemia are susceptible to Aeromonas infections.[18]

Polymicrobial joint infections (5-10% of cases) and infection with anaerobic organisms (5% of cases) are usually a consequence of trauma or abdominal infection. Individuals with multiple pathogens have a higher rate of previous native and prosthetic joint infections. The most common pathogens were coagulase-negative Staphylococcus (CoNS), MSSA, and enterococci.[4]

The organism that causes Lyme disease, Borrelia burgdorferi, commonly produces a septic arthritis picture.[17]  In some, the signs and symptoms of the acute infection persist despite successful eradication of the pathogen. This is due to ongoing inflammatory response that continues the synovial inflammation, vascular damage, and autoimmune processes that interfere with appropriate tissue repair.

Brucella may cause septic arthritis in areas where cattle are not vaccinated. The organism of Whipple disease, Mycoplasma species, and Ureaplasma species infrequently involve septic joints.[2]

A wide variety of viruses (eg, human immunodeficiency virus [HIV], lymphocytic choriomeningitis virus, hepatitis B virus, rubella virus), mycobacteria, fungi (eg, Histoplasma species, Sporothrix schenckii, Coccidioides immitis, Blastomyces species), and other pathogens produce nonsuppurative joint infections.[18]

Types of prosthetic joint infections

 There are 3 major categories of PJIs: those that develop within 3 months of implantation; those that appear within 3-24 months of implantation; and those that occur later than 24 months. Most cases of early prosthetic joint infection are caused by S aureus. The 3- to 24-month group are usually caused by coagulase-negative S aureus (CoNS) or gram-negative aerobes, both of which are acquired in the operating room. Late cases of prosthetic joint infection are secondary to hematogenous spread from a variety infectious foci.[19, 20]

Reactive arthritis represents a sterile inflammatory process that is triggered by a variety of extra articular infections.[21]

See also Pediatric Septic Arthritis, Pediatric Septic Arthritis Surgery, and Septic Arthritis Surgery.

Etiology and Pathophysiology

Organisms may invade the joint by direct inoculation, by contiguous spread from infected periarticular tissue, or via the bloodstream (the most common route).[8]

The normal joint has several protective components. Healthy synovial cells possess significant phagocytic activity, and synovial fluid normally has significant bactericidal activity. Rheumatoid arthritis and systemic lupus erythematosus hamper the defensive functions of synovial fluid and decrease chemotaxis and phagocytic function of polymorphonuclear leukocytes. Patients with deficiencies of the terminal components of complement are susceptible to neisserial bacteremia and joint infections.

Pathogenic invasion

Previously damaged joints, especially those damaged by rheumatoid arthritis, are the most susceptible to infection. The synovial membranes of these joints exhibit neovascularization and increased adhesion factors; both conditions increase the chance of bacteremia, resulting in joint infection. Some microorganisms have properties that promote their tropism to the synovium. S aureus readily binds to articular sialoprotein, fibronectin collagen, elastin, hyaluronic acid, and prosthetic material via specific tissue adhesion factors (microbial surface components recognizing adhesive matrix molecules [MSCRAMMs]). In adults, the arteriolar anastomosis between the epiphysis and the synovium permits the spread of osteomyelitis into the joint space.

The major consequence of bacterial invasion is damage to articular cartilage. This may be due to the particular organism's pathologic properties, such as the chondrocyte proteases of S aureus, as well as to the host's polymorphonuclear leukocytes response. The cells stimulate synthesis of cytokines and other inflammatory products, resulting in the hydrolysis of essential collagen and proteoglycans. Infection with N gonorrhoeae induces a relatively mild influx of white blood cells (WBCs) into the joint, explaining, in part, the minimal joint destruction observed with infection with this organism relative to destruction associated with S aureus infection.

As the destructive process continues, pannus formation begins, and cartilage erosion occurs at the lateral margins of the joint. Large effusions, which can occur in infections of the hip joint, impair the blood supply and result in aseptic necrosis of bone. These destructive processes are well advanced as early as 3 days into the course of untreated infection.

Viral infections may cause direct invasion (rubella) or production of antigen/antibody complexes. Such immunologic mechanisms occur in infections with hepatitis B, parvovirus B19, and lymphocytic choriomeningitis viruses.

Reactive/postexposure process

Reactive, or postexposure, arthritis is observed more commonly in patients with human lymphocyte antigen B27 (HLA-B27) histocompatibility antigens. Although various infections can cause reactive arthritis, gastrointestinal processes are by far the most common. Gastrointestinal pathogens associated with reactive arthritis include the following[21] :

  • Salmonella enteritidis

  • Salmonella typhimurium

  • Yersinia enterocolitica

  • Campylobacter jejuni

  • Clostridium difficile

  • Shigella sonnei

  • Entamoeba histolytica

  • Cryptosporidium

Genitourinary infections, especially those due to Chlamydia trachomatis, are the second most common cause of reactive arthritis. The arthritis of Lyme disease usually results from immunologic mechanisms, with a minority of cases due to direct invasion by an organism. A reactive/postexposure process may occur months after the gastrointestinal or genitourinary process has resolved.

COVID-19 infection has been increasingly implicated as a cause of reactive arthritis especially among patients with rheumatoid arthritis.[1, 22]

Local infection

 PJIs may be a consequence of local infection, such as intraoperative contamination (60-80% of cases), or of bacteremias (20-40% of cases).[2] The bacteremias may be spontaneous (ie, gingival disease) or secondary to various manipulations. Delayed wound healing is a major factor behind early prosthetic joint infection. Until the fascia has healed, the usual tissue barriers to infection of the implant are not present. Eventually, the implanted hardware becomes less susceptible to infection by hematogenous spread, because a pseudocapsule develops around it.

The biofilm of coagulase-negative S aureus (CoNS) protects the pathogen from the host's defenses, as well as from various antibiotics. Polymethylmethacrylate cement inhibits WBC and complement function.

Overall, the most common organisms of prosthetic joint infections are CoNS (22% of cases) and S aureus (22% of cases). Enteric gram-negative organisms account for 25% of isolates.[20] Streptococci, including S viridans, enterococci, and the beta-hemolytic streptococci, cause 21% of cases. Anaerobes are isolated from 10% of patients.

Other distinctive host and/or situation-pathogen associations have been described, including Pasteurella multocida, Capnocytophaga species (dog and cat bites), Eikenella corrodens, anaerobes (especially Fusobacterium nucleatum and streptococcal species [human bites]), Aeromonas hydrophila (myelogenous leukemia), P aeruginosa, Serratia species, Candida species (particularly common in persons who abuse intravenous drugs), Mycobacterium marinum (water exposure), S schenckii (gardening), and S pneumoniae (sickle cell anemia).

Unlike their causative role in sickle cell osteomyelitis, Salmonella species are not associated with the septic arthritis of sickle cell anemia. Ten to 30% of patients with brucellosis have lumbosacral spine involvement.

Prognosis

The primary morbidity of septic arthritis is significant dysfunction of the joint, even if treated properly. Fifty percent of adults with septic arthritis have significant sequelae of decreased range of motion or chronic pain after infection.[1] Thirty percent of cases of reactive arthritis may become chronic. Complications include dysfunctional joints, osteomyelitis, and sepsis.

Predictors of poor outcome in suppurative arthritis include the following[23] :

  • Age older than 60 years
  • Infection of the hip or shoulder joints
  • Underlying rheumatoid arthritis
  • Positive findings on synovial fluid cultures after 7 days of appropriate therapy
  • Delay of 7 days or longer in instituting therapy

The mortality rate depends primarily on the causative organism. N gonorrhoeae septic arthritis carries an extremely low mortality rate, whereas that of S aureus can approach 50%.[22]  S aureus is the most common cause of septic arthritis in all age groups. Among those aged 15-50 years, N gonorrhea runs a close second, especially among those who are sexually active.

 

Presentation

History

Because joint infections are uncommon, be especially attentive to features of the patient's history that may indicate an infectious process instead of a primary rheumatologic or orthopedic process.[2, 7, 8, 19, 20, 23, 24, 25]

Pay attention to the following symptoms:

  • Acuteness of onset of the joint pain

  • Whether the pain is superimposed on chronic pain

  • Previous history of joint disease or trauma, whether accidental or iatrogenic (eg, infection complicates 0.4% of arthrocenteses)

  • Whether the process is monoarticular or polyarticular and which joints are involved

  • The presence of extra-articular symptoms

  • Whether the patient has had vascular invasion due to catheterizations or intravenous drug abuse

Obtain a history regarding the possible presence of sexually transmitted diseases (STDs) or exposure to ticks (Lyme disease). The increase of group B streptococcal joint infections is associated with the increased prevalence of diabetes and increasing life expectancy.

Numerous conditions that adversely affect the host's defenses (eg, liver disease, diabetes mellitus, lymphoma, solid tumors, complement deficiencies [C7, C8], immunosuppressive drugs, hypogammaglobulinemia) are increasingly observed in patients with septic arthritis. Determine the possible contribution of these diseases to the clinical presentation.

The most important historical feature is the existence of underlying joint disease, especially rheumatoid arthritis. In addition, the possibility of recent injury to the joint or penetrating or blunt trauma must be explored. Ask the patient about needle aspiration of the joint or injections of corticosteroids into the joint. Elicit a history of diarrheal disease.

Symptoms

Patients with an infected joint typically present with the triad of fever (40-60% of cases), pain (75% of cases), and impaired range of motion. These symptoms may evolve over a few days to a few weeks. Fever is usually low-grade (< 102°F), with rigors present in only 20% of cases. Spiking fevers and chills are much more common with crystalline arthritis.

Lyme disease

Months after infection onset, 60% of patients with untreated Lyme disease develop swelling and pain, chiefly affecting the large joints. Usually, Lyme disease affects 1-2 joints at a time, with the knee involved most commonly. The distinguishing pattern is attacks extending from a few weeks to months and separated by periods of complete remission. The rate of recurrence lessens by about 15% per year. A small percentage of individuals develop chronic arthritis (ie, inflammation of a joint lasting ≥ 1 y). This type of relapsing course almost always precedes the chronic stage of Lyme arthritis.

Prosthetic joint infection

Compared with patients with infections of native joints, most patients with PJI exhibit a prolonged low-grade course with gradually increasing pain. However, with gram-negative infections, especially with enteric organisms, PJI may be far more acute in onset.

Usually, no significant fever or swelling occurs (delayed prosthetic joint infection). However, individuals with early prosthetic joint infection present with an acute illness characterized by high-grade fever, focal swelling, and redness. Cellulitis and draining sinus tracts often develop.

Because late prosthetic joint infection is usually secondary to bacteremia, the clinical picture is often dominated by the source of the bloodstream infection.

The nature of the invading organism, the type of tissue infected, and the route of infection determine presentation. Thus, a high index of suspicion is needed for identification of bacteremic and delayed prosthetic joint infection. Because of its many pathogenic mechanisms, S aureus is usually associated with a fulminant course, as opposed to the indolent course of coagulase-negative S aureus (CoNS) that dominates delayed prosthetic joint infection. Relatively devitalized tissues (eg, wound hematomas) are conducive to rapid bacterial replication and a more acute course. Bacteremic spread allows infection with fewer organisms and leads to a more muted course.

Reactive and tuberculous arthritides

Reactive arthritis usually begins several weeks after the underlying infection has resolved.[21] Few concurrent systemic symptoms occur.

Symptoms of tuberculous arthritis are quite indolent; the diagnosis may be delayed for several years. Usually, the purified protein derivative (PPD) results are negative, and no signs, past or present, of pulmonary tuberculous exist.

Viral septic arthritis

Table 1, below, provides a summary of the clinical features of arthritis caused by various viral organisms.

Table 1. Clinical Features of Viral Disease–Associated Arthritis (Open Table in a new window)

Virus

Clinical Features of Viral Disease–Associated Arthritis

Parvovirus B19

Occurs in adult women with erythema infectiosum, often an itchy rash

Hepatitis A

Muscle aches and rash in 10% of cases

Hepatitis B

Onset in the preicteric phase; usually resolves as jaundice develops; chronic arthritis possible in patients with chronic hepatitis B infection

Hepatitis C

History similar to hepatitis B joint infection; usually associated with cryoglobulinemia

Rubella (natural infection and vaccine related)

Onset is possible before, during, or after the appearance of the rash; usually resolves in a few weeks; may recur and, more commonly, may persist

Human immunodeficiency virus [HIV] (2 types occur, both with noninflammatory, sterile joint fluid)

Develops over several days, and severe knee or ankle pain is characteristic; excellent response to nonsteroidal anti-inflammatory agents (NSAIDS)

Sudden onset of severe pain in the shoulders and elbows, closely resembling an acute gouty attack; Opiates often necessary to control pain

Mumps

Occurs in adult men 2 weeks after the presentation of parotitis

Physical Examination

The most commonly involved joint in septic arthritis is the knee (50% of cases), followed by the hip (20%), shoulder (8%), ankle (7%), and wrists (7%). The elbow, interphalangeal, sternoclavicular, and sacroiliac joints each make up 1-4% of cases.

A thorough inspection of all joints for signs of erythema, swelling (90% of cases), warmth, and tenderness is essential for diagnosing infection. Infected joints usually exhibit an obvious effusion, which is associated with marked limitation of both active and passive ranges of motion (ROMs). Frequently, these findings are apparent but may be diminished or poorly localized in cases of infection of the spine, hip, and shoulder joints.[18]

Signs and symptoms of infection may be muted in people who are elderly, patients who are immunocompromised (especially those with rheumatoid arthritis), and those who inject drugs.

Pattern of joint involvement

Nongonococcal bacterial/suppurative arthritis

The pattern of joint involvement is an extremely important diagnostic feature. Of cases of nongonococcal suppurative arthritis, 85-90% are monoarticular. If the disease affects more than one joint, S aureus is most commonly implicated. Polyarticular arthritis is usually observed in gonococcal disease, various viral infections, Lyme disease, reactive arthritis, and various noninfectious processes.

Group B streptococci most commonly infect the sacroiliac and sternoclavicular joints.

Gonococcal bacterial/suppurative arthritis

Gonococcal musculoskeletal involvement may present in 1 of 2 ways, as described below.[2, 7, 8, 26]

Fever, arthralgias of multiple joints, and multiple skin lesions (dermatitis-arthritis syndrome) characterize disease that develops soon after the gonococcus disseminates from the cervix, urethra, or pharynx. Usually, this disease exhibits no clinical direct joint findings, but the process is one of tenosynovitis of asymmetric distribution. Typically, hand joints are involved most often, as well as those of the knee, wrist, ankle, and elbow. Skin lesions are multiple but seldom number more than 12, whereas lesions associated with meningococcemia may number more than 100. The lesions evolve over a few days from papular to pustular or vesicular to necrotic. This course may recur for several months. Findings on cultures of blood and mucosal surfaces are often positive; findings on cultures of joint fluid are usually negative. Sixty percent of disseminated gonococcal infections are of this type.

Monoarticular arthritis without associated systemic symptoms, tenosynovitis, or skin lesions characterizes gonococcal disease that begins later after gonococcal dissemination than does dermatitis arthritis syndrome.[25] Dermatitis-arthritis syndrome may or may not precede this phase. In a joint infected by the Lyme organism, swelling may be disproportionate to the level of pain. Baker cysts are a frequent feature of this type of infectious arthritis. Because the pain of an infected hip joint may not be localized directly and swelling of the joint is inconspicuous, perform specific maneuvers, such as the Fabere maneuver. Infection of the sacroiliac joint often presents as buttock, hip, or anterior thigh pain. Direct pressure usually elicits tenderness in the joint. Alternatively, hyperextension of the hip and leg while the patient is lying down (ie, Gaenslen maneuver) elicits pain in a suppurative sacroiliac joint.

Septic bursitis most commonly involves the olecranon and prepatellar bursae. Swelling and pain are present. However, an infected bursa does not limit the range of motion of the underlying joint the way an actual joint infection does.[27]

Prosthetic joint infections

Physical findings are usually minimal in an infection of the prosthetic joint, and swelling is usually slight. The most distinctive finding is a draining sinus presumed to originate in the underlying infected prosthetic joint.

Reactive, viral, and tuberculous arthritides

Most cases of reactive arthritis involve a few large joints in an asymmetric fashion, whereas viral arthritis usually exhibits symmetric involvement of the smaller joints, especially the hands, with a concurrent rash. The joints of tuberculous arthritis can appear to be boggy on palpation.[28]

 

DDx

Diagnostic Considerations

When evaluating a patient with suspected septic arthritis, also consider conditions such as primary rheumatologic disorders (eg, vasculitis, crystalline arthritides), drug-induced arthritis, and reactive arthritis (eg, postinfectious diarrhea syndrome, postmeningococcal and postgonococcal arthritis, arthritis of intrinsic bowel disease).[2]

In early disseminated gonococcal infection, an early tenosynovitis predominates without actual joint invasion such as occurs in the later variety of disseminated gonococcal infection. A viral syndrome usually produces polyarticular arthritis. Pustular lesions are consistent (as is almost any type of skin lesion) with staphylococcal bacteremia. Whenever vesicles are present, one needs to strongly consider staphylococcal infection.

Unlike salmonella osteomyelitis, the frequency of salmonella septic arthritis is not greatly increased in patients with sickle cell anemia. However, when septic arthritis does occur, Salmonella is more commonly identified.

Staphylococcus aureus remains the most common infectious agent in people who abuse intravenous drugs. However, a high rate of infections with gram-negative organisms, especially Pseudomonas aeruginosa and Serratia species, occurs in cases of septic arthritis. A higher rate of fungal and anaerobic infections has been documented. Unusual locations, such as the sternoclavicular joint, have more frequently been encountered.

The syndromic approach to the dDiagnosis of SA

The priority of the clinician is to recognize SA and to initiate appropriate therapy as soon as possible, so as to minimize the morbidity and mortality of the infection. With the proliferation of imaging studies and serological testing, along with the increase of immunosuppressed patients and IVDA , the practitioner is more and more challenged to avoid basing a diagnosis solely on test result and/or Imaging studies. These findings must be validated with a compatible history/symptoms and physical examination. A disease represents a grouping of signs (physical findings, test results, imaging studies) and symptoms that together characterize a particular syndrome or disease. Such a diagnostic approach is termed syndromic analysis (Syn Ana).

The following are the 5 steps of syndromic analysis:

1) Identify the primary organ system involved.

2) Determine whether the process is acute, subacute, or chronic in nature.

3) On the basis of history, physical examination, and nonspecific laboratory tests and imaging studies, compile a provisional list of the most likely diagnoses. 

4) Factor in any history of relevant diseases and/or medication that would effect the clinical presentation, physical findings, and results of laboratory tests and imaging studies.

5) Arrive at the correct diagnosis and its etiology by utilizing appropriate specific laboratory tests, cultures, imaging studies, and biopsy results  to rule out the other preliminary diagnoses.

 

 

 

 

 

 

 

 

Workup

Approach Considerations

An approach to rapid evaluation of an acutely inflamed joint is to screen the synovial fluid for crystals via polarizing microscopy and for organisms via Gram stain (63-96% sensitive). If crystals are present and the Gram stain findings are negative, treatment for crystal-associated arthritis should be initiated. However, an exception to this would be the presence of significant risk factors for infection (eg, the focus of infection lies somewhere that could lead to bacteremia, such as pneumonia or pyelonephritis). Therapeutic decisions cannot be delayed until results of the synovial fluid culture are available.

The Musculoskeletal Infection Society (MSIS) has updated its criteria for diagnosing joint infection on the basis of culture results, synovial fluid studies, and inflammatory markers.[29]

If no crystals are detected within the joint fluid, treat the patient for presumed infection even if the Gram stain findings are negative. The Gram stain has variable sensitivity for detection of bacteria in synovial fluid. Always send the fluid for culture, regardless of the result of the screening evaluation. A joint damaged by gout or pseudogout is prone infection. Culture of synovial tissue may be necessary to detect mycobacteria or fungi.

If the patient's condition does not improve significantly after 5 days, the joint must be reaspirated and examined. Most septic joints have a white blood cell (WBC) count that exceeds 50,000/μL, with more than 75% polymorphonuclear leukocytes. However, various sterile inflammatory processes may exhibit the same cellular profile.

Other considerations

The fluid of an infected bursa closely resembles that of a bacterial joint infection.[19]

An elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) is useful in following the patient's response to therapy, as well as in detecting an acute process in chronically affected joints. Serum procalcitonin may be a more useful biomarker of joint infection than C-reactive protein or white blood cell (WBC) counts.[30]

Measurement of serum uric acid levels cannot be used to establish or negate the diagnosis of uric acid arthropathy. Values may range widely during an acute attack.

Appropriate serologic tests for the diagnosis of various vasculitides or rheumatologic disorders are often indicated.[31]

Obtaining a biopsy of the synovium may be necessary to diagnose one of the many causes (ie, mycobacterial, fungal) of granulomatous synovitis. Examining the synovium histologically often establishes a diagnosis of fungal or mycobacterial joint infections.

Joint Fluid Analysis and Culture

Always perform joint aspiration under the most sterile conditions possible to prevent the introduction of infection.[32]

Normal joint fluid is clear and colorless and produces a stringlike structure when ejected from a syringe, indicating normal viscosity. Infected joint fluid is typically yellow-green due to elevated levels of nucleated cells, and the cell count is usually markedly elevated, demonstrating a predominance of polymorphonuclear leukocytes. An evaluation of the synovial fluid (ie, via leukocyte count, appearance on Gram stain, polarizing microscopy examination, culture) is the most rewarding approach in assessing a potentially infected joint. Additional stains and/or cultures should be obtained depending on the differential diagnosis considered.[26, 32, 33, 34] Alterations in the glucose and protein concentration of the synovial fluid are nonspecific; these should not be measured routinely.

Culture of the synovial fluid or of synovial tissue itself is the only definitive method of diagnosing septic arthritis. Culture results in patients with nongonococcal septic arthritis are almost always positive, unless the patient has received antibiotics before the joint aspiration. Cultures of the joint fluid in gonococcal infections yield positive results in only about 25% of cases. If this diagnosis is suspected, the organism can be cultured from other sites, such as the cervix, urethra, or throat. The effectiveness of standard culture techniques is much more limited in patients with PJI, probably owing to the high rate of antibiotic preadministration prior to arthrocentesis or surgery. If the patient is clinically stable, stop the administration of antibiotics for 2 weeks before obtaining cultures and hold for 14 days.

A minimum of 3 and preferably 6 periprosthetic tissue samples should be obtained. Ultrasonication of removed prosthetic material increases the return of cultures, especially in patients who had recently received antibiotics. This technique also helps retrieve organisms that reside in the biofilms that coat the prosthetic material.[23, 35]

Lyme disease

Findings from examination of the synovial fluid in Lyme arthritis are similar to those found in infection caused by any other type of bacterium. Positive serology results (ie, antibody measurements, Western blot, polymerase chain reaction [PCR] for Lyme disease) do not establish the diagnosis of Lyme arthritis. A positive result on any of these tests simply indicates that the patient has encountered B burgdorferi; a positive result does not necessarily establish a connection between the patient's musculoskeletal symptoms and Lyme disease.[17]

Silver stains can be used to detect organisms in 5% of cases of Lyme arthritis.

Prosthetic joint infection

Evaluation of a possibly infected prosthetic joint is similar to that of a natural joint.[2, 28, 29]  The presence of leukocytes in the aspirated fluid is variable. Because many of the potential pathogens are also classic contaminating organisms (eg, coagulase-negative S aureus [CoNS], Propionibacterium species, Corynebacterium species), repeat aspirates are often required to confirm the diagnosis. The use of multiple types of media with prolonged incubation times may increase both the sensitivity and specificity of the culture in prosthetic joint infection. The sensitivity of periprosthetic-tissue culture ranges from 65% to 94%.[27]  Material from fistulous tracts is associated with a high rate of contamination and is probably best avoided.

Reactive and tuberculous arthritides

The synovial fluid of reactive arthritis demonstrates few signs of inflammation. PCR may reveal the DNA of the purported causative organism.

The synovial fluid of a joint infected with Mycobacterium tuberculosis shows marked leukocytosis. Although findings on acid-fast stains are usually negative, culture results are positive in 80% of cases. Culture results of synovial biopsies are positive in 94% of specimens.

Blood and Other Cultures

Obtain at least 2 sets of blood cultures to rule out a bacteremic origin of the septic joint.

In the setting of possible gonococcal infection, obtaining cultures from the patient's rectum, cervix, urethra, and pharynx and from any skin lesions is most helpful. Immediate plating of the joint fluid directly onto appropriate media and/or rapid delivery of the specimen to the laboratory for appropriate plating and culturing are of benefit in improving the relatively low yield.[36]

Polymerase Chain Reaction

Polymerase chain reaction (PCR) holds promise for detection of bacterial DNA in joint fluid and synovial tissue.[30] PCR has led to diagnosis of infective arthritis due to Yersinia species, B burgdorferi, Chlamydia species, N gonorrhoeae, and Ureaplasma species. However, caveats concerning this approach are raised, because it cannot be used to distinguish between live and dead organisms and it is susceptible to contamination. PCR techniques hold promise in detecting pathogens in patients who have recently received antibiotics. Unfortunately, many patients receive empirically administered antibiotics before the collection of synovial fluid.

Radiologic Studies

At times, imaging studies may be required to determine the significance of a given culture.

Radiography and ultrasonography

Plain radiography is of limited value in evaluating a joint for infection[22] ; periarticular soft-tissue swelling is the most common finding. This imaging modality is most useful in ruling out underlying osteomyelitis or periarticular osteomyelitis caused by the joint infection itself.

In addition, plain radiography can reveal the linear deposition of calcium pyrophosphate. The radiographic findings of reactive arthritis are usually limited to those of soft-tissue swelling. Periarticular osteoporosis may be detected.

A 30-year-old man who was taking steroids presenteA 30-year-old man who was taking steroids presented with a joint effusion and knee pain. Anteroposterior view of the knee demonstrates patchy demineralization of the tibia and femur and joint-space narrowing. This was caused by tuberculoid infection of the joint.
Septic arthritis. Anteroposterior view of the shouSeptic arthritis. Anteroposterior view of the shoulder demonstrates subchondral erosions and sclerosis in the humeral head. These are relatively late findings of septic arthritis. Periosteal reaction due to coincident osteomyelitis is present adjacent to the surgical neck of the humerus.
During the progression of infectious arthritis of During the progression of infectious arthritis of the hip, this image was obtained early in the disease and shows only concentric joint-space loss.

Ultrasonography may be used to diagnose effusions in chronically distorted joints (secondary to trauma or rheumatoid arthritis). It is an underutilized technique.[37]    

CT scanning, MRI, and radionuclide scanning

Computed tomography (CT) scanning and magnetic resonance imaging (MRI) are more sensitive for distinguishing osteomyelitis, periarticular abscesses, and joint effusions. The information gained usually does not justify the increased cost; however, these tests are most helpful in patients with sacroiliac or sternoclavicular joint infection to rule out extension into the mediastinum or pelvis. MRI is preferred because of its greater ability to image soft tissue.

Radionuclide scans (ie, technetium-99m [99m Tc], gallium-67 [67 Ga], indium-111 [111 In] leukocyte scans) are used to nonspecifically localize areas of inflammation. They cannot be used to distinguish infectious from sterile processes. However, radionuclide scans may be of use in diagnosing septic arthritis in relatively sequestered areas, such as the hip and sacroiliac joints.

Imaging in prosthetic joint infection

In prosthetic joint infection [PJI], plain radiography can reveal new subperiosteal bone growth and transcortical sinus tracts.[2, 38] These findings are specific for infection. Arthrography can demonstrate loosening of the prosthesis and abscesses. Nuclear scans of all types are of limited diagnostic use in patients with prosthetic joint infection, and MRIs are limited by the type of implanted material (this diagnostic modality can safely image only titanium or tantalum devices). Fludeoxyglucose-positron emission tomography (FDG-PET) scans may hold some promise in diagnosing lower-extremity prosthetic joint infections. However, this approach cannot differentiate aseptic loosening from infection. Sensitivity and specificity were 87% and 82%, respectively.[33, 38]  CT scans are useful in ascertaining the state of the surrounding soft tissue.[39]

 

Treatment

Approach Considerations

Medical management of infectious arthritis focuses on adequate and timely drainage of the infected synovial fluid; administration of appropriate antibiotic(s); and debridement of any associated osteomyelitis or soft tissue infection with immobilization of the joint to control pain. The major challenges are duration of oral and intervenous anabiotic administration, especially in the setting of PJI.

Acute PJI (< 3 wk in duration) can be cured medically if it is of the early type or secondary to hematogenous spread without any evidence of periarticular soft-tissue involvement or joint instability.[9]  However, it is imperative to monitor therapy by repeat ultrasounds or other imaging studies of the joint, as well as inflammatory markers such as CRP.

Overall, the mean length of hospitalization for septic arthritis is 11.5 days. However, outpatient antibiotic therapy in stable patients can significantly reduce hospital stays.[40]

Consultations

In general, obtain a consultation with an orthopedic surgeon or rheumatologist. If the initial treatment response is poor or the etiology of the synovitis remains unknown, consult with an infectious disease specialist.

Antibiotic Therapy

In native joint infections, antibiotics usually are administered parenterally for at least 2 weeks. As a rule, the SA of disseminated gonnorhea responds to 2 weeks of intravenous antibiotic.[36]  However, each case must be evaluated independently. The medical dogma that infection with either methicillin-resistant S aureus (MRSA) or methicillin-susceptible S aureus (MSSA) requires at least 4 full weeks of intravenous has recently been challenged. In a randomized controlled study of 1,054 patients(OVIVA trial), 61% had hardware-associated infections, 38% infected with S aureus and 27% infected with CONS. In the OVIVA trial, standard intravenous antibiotic therapy was begun within 7 days of surgery  and administered for at least 6 weeks. In the other arm of the study, patients received oral antibiotic therapy. Both groups of patients could receive follow-up oral antibiotics. At the end of one year, there did not seem to be a  significant dfference in the rate of failure between both groups. Standard treatment failed in 14.6 % of the IV group and 13.2% of the oral group.[40] The oral agents were generally quinolones or penicillins. Intravenous agents were usually the glycopeptides and cephalosporins. In both groups, therapy was 'tweaked " to meet the therapeutic challenges of each subject. More data are emerging to support shortened antibiotic courses for septic arthritis of native joints.[41]

 The DATIPO study compared the efficacy of 6 weeks versus 12 weeks of antibiotic therapy in patients with PJI who had undergone appropriate  surgical procedures to eradicate associated osteomyelitis and soft issue infection or joint replacement by I or 2 stage procedure. The medium duration of IV antibiotic administration was 9 days for both groups. The failure rate to eradicate joint infection was 18.1% for the 6-week group and 9.4 % for the 12 week group.[42]  The biggest risk for failure was among those who underwent one simple debridement without removal of the prosthetic material.

In summary, the study emphasized the importance of removal of the implant. Optimal duration of therapy needs to balance the increased risk for side effects related to prolonged eposure to these agents against treatment failure.

Caveats to this shortened course of IV antibiotic therapy include the presence of extensive periarticular osteomyelitis, leukopenia, or other immunosuppressive states. In patients with blood cultures that are positive for S aureus, it is imperative to exclude underlying valvular infection. Measuring the response of various inflammatory markers must be strongly considered to augment the clinical response to antibiotic treatment.

Antibiotic selection

Initial antibiotic choices must be empirical, based on the sensitivity pattern of the pathogens of the community. Consider the rise of resistance among potential bacteria when choosing an initial antibiotic regimen. If local incidence of MRSA is high (in particular, marked increase in the resistance of the pneumococcus), prescribe alternate antibiotics initially. Because many isolates of group B streptococci have become tolerant of penicillin, use a combination of penicillin and gentamicin or a later-generation cephalosporin. MRSA is becoming established outside of the hospital setting. Enterobacteriaceae and P aeruginosa are becoming more resistant to multiple antibiotics. Knowing the resistance patterns in the community, as well as in the hospital, is most important.

Preferably, the antibiotic should be bactericidal with some effect against the slow-growing organisms that are protected within a biofilm (eg, coagulase-negative S aureus [CoNS]). Rifampin fulfills these requirements; however, this agent should never be used alone because of the rapid development of bacterial resistance to the drug.

If, after 5 days of therapy, the joint shows some degree of improvement, consider an empirical trial of an anti-inflammatory agent for increased symptomatic relief. If the joint fails to respond after 5 days of appropriate antibiotic therapy (eg, presence of clinically significant fever, continued synovial purulence, persistently positive findings on culture), reassess the therapeutic approach, as follows:

  • Reculture the fluid and reexamine for crystals
  • Perform appropriate serologies for diagnosis of Lyme disease; if these are positive, treat per guidelines
  • If fungal or mycobacterial infection is possible, consider obtaining a synovial biopsy
  • Consider the possibility of reactive arthritis; nonsteroidal inflammatory agents (NSAIDs) are the primary therapeutic agents for reactive arthritis
  • Perform imaging studies, either radiographs or magnetic resonance imaging (MRI), to rule out periarticular osteomyelitis.

Antibiotics have a role in suppressing associated chronic osteomyelitis and chronically infected prosthetic material that cannot be removed for various reasons.

The use of fluoroquinolones for an extended period should be considered when the removal of an infected prosthesis is not possible. Cure rates as high as 62% have been documented in relatively small series. Generally, such prolonged therapy is seen as suppressive and not curative.[24]

Joint Immobilization and Physical Therapy

Usually, immobilization of the infected joint to control pain is not necessary after the first few days. If the patient's condition responds adequately after 5 days of treatment, begin gentle mobilization of the infected joint. Most patients require aggressive physical therapy to allow maximum postinfection functioning of the joint.

Initial physical therapy consists of maintaining the joint in its functional position and providing passive range-of-motion exercises. The joint should bear no weight until the clinical signs and symptoms of synovitis have resolved. Aggressive physical therapy is often required to achieve maximum therapy benefit.

Synovial Fluid Drainage

The choice of the type of drainage, whether percutaneous or surgical, has not been resolved completely.[9, 31, 43] In general, use a needle aspirate initially, repeating joint taps frequently enough to prevent significant reaccumulation of fluid. Aspirating the joint 2-3 times a day may be necessary during the first few days. If such drainage is required past this point, surgical drainage should be initiated.

Purulent gonococcal arthritis requires frequent joint drainage. However, the joints of patients with disseminated gonococcemia characterized by the triad of tenosynovitis, dermatitis, and polyarthralgia rarely require surgical drainage.[44]

Surgical drainage is indicated when one or more of the following occur:

  • The appropriate choice of antibiotic and vigorous percutaneous drainage fails to clear the infection after 5-7 days
  • The infected joints are difficult to aspirate (eg, hip)
  • Adjacent soft tissue is infected

Routine arthroscopic lavage is rarely indicated. However, drainage through the arthroscope is replacing open surgical drainage. With arthroscopic drainage, the operator can visualize the interior of the joint and can drain pus, debride, and lyse adhesions.

Surgical Intervention in Prosthetic Joint Infection

Debridement and retention of the prosthesis  can be considered in patients who develop prosthetic joint infection within 30 days of implantation or who present within 3 weeks of the development of symptoms if the prosthesis appears to be well fixed and is without a sinus tract.[23]  Otherwise, removal of all of the prosthetic material is mandatory.

First, remove the prosthesis and follow with an appropriate antibiotic. Then, place the new joint, impregnating the methylmethacrylate cement with an anti-infective agent (ie, gentamicin, tobramycin). Antibiotic diffusion into the surrounding tissues is the goal. The success rate for this approach is approximately 95% for both hip and knee joints.

An intermediate method is to exchange the new joint for the infected joint in a 1-stage surgical procedure with concomitant antibiotic therapy. This method, with concurrent use of antibiotic cement, may be successful in 70-90% of cases. What is unclear is the total duration of post procedural antibiotic therapy. A recent study compared the effectiveness of 6 weeks versus 12 weeks of total of anabiotic therapy.[40]  Forty-one persent underwent debridement alone; 37% underwent a 1 stage exchange; and 22% received a 2 stage exchange of the implants.

Thirty-eight percent of S aureus infections received 6 weeks of antibiotic therapy, whereas 30% received 12 weeks of antibiotics. Thirty percent of CoNS received 6 weeks and 35% received 12 weeks of antimicrobials. Both received 9 days of parenteral antmicrobials. The fluoroquinolones and rifampin were the most frequently employed.

The design of this study is problematic in that there was a wide variety of surgical interventions employed as well as specific antibiotic regimens. Even the 12-week course is generally shorter than that usuallyfollowed in the United States. It is consistent with recent studies.[41]  The response to antibiotic therapy needs to be monitored by follow-up exams and appropriate imaging studies and measurement of inflammatory markers.

Medical Care

Strictly adhere to sterile procedures whenever the joint space is invaded (eg, in aspiration or arthroscopic procedures).

Antibiotic prophylaxis with an antistaphylococcal antibiotic has been demonstrated to reduce wound infections in joint replacement surgery. Polymethylmethacrylate cement impregnated with antibiotics may decrease perioperative infections.

Using antibiotic prophylaxis on the same theoretic basis as that for cardiac valvular disease has been advocated. Whenever a sustained bacteremia may be encountered, be aware of the possibility of joint involvement, especially for prosthetic joints. Consideration should be given to more prolonged treatment of the bacteremia to cover the possibility of very early joint infection (secondary prophylaxis). The implanted hardware most likely is at greatest risk of bacteremia infection within a few months of placement. The risk probably decreases as a pseudocapsule evolves. During this time, prophylaxis is probably most beneficial. The results of a recent well-designed study support the recommendation that all joint replacement patients require antibiotic prophylaxis prior to dental procedures.[45]  The author will continue to provide such prophylaxis.

Treat any infection promptly to lessen the chance of bloodstream invasion. In addition, decreasing the incidence of underlying infections best prevents reactive arthritis.

Patient education

Instruct patients with a prosthetic joint in place to recognize early signs of joint infection and, more importantly, to recognize bacterial infections in other parts of their bodies to prevent associated bacteremias.

For patient education information, see Arthritis Center as well as Knee Pain and Ticks.

Complications

The risk of repeat arthroplasty performed for septic arthritis is 6 times that when it is performed for other indications. Patients with septic arthritis who underwent arthroplasty also exhibited a significantly increased mortality rate over the 15 years following the procedure.[46, 47]

For various reasons, joint infection may fail to respond to combined surgical and antibiotic therapy.[46] In such cases, an orally administered suppressive antibiotic therapy usually is administered. The increasing prevalence of resistant organisms among these individuals is eliminating this option; subcutaneous injection of beta-lactam drugs provides another option.[47]

Consultations

An infectious diseases consultation is recommended for any native joint infection and should be considered mandatory for any prosthetic joint. 

 

Medication

Medication Summary

The empiric choice of antibiotic therapy is based on results of the Gram stain, the clinical picture, and the medical background of the patient. When the Gram stain fails to reveal any microorganisms (40-50% of cases), the individual's age and sexual activity become the major determinants to differentiate gonococcal from nongonococcal arthritis. When there is no evidence supporting any extra-articular infection, antibiotics must cover S aureus, streptococcal species, and gonococci (in patients who are sexually active). Synovial fluid examination may be helpful in approximately 50%  of cases. Because of the significant adverse consequences of inadequate therapy, the author empirically covers for the presence of MSSA, MRSA, CoNS, N gonnorhea, and gram-negative aerobes. A typical combination would be ceftriaxone and vancomycin. In the presence of implanted material, rifampin should be added because of its unique ability to penetrate the biofilms of infected prosthetic devices.[48, 49, 50]  

Evidence exists that earlier initiation of an appropriate antibiotic regimen produces better functional results. Generally, treatment is administered intravenously for 3-4 weeks. The major exception to this is gonococcal infection, for which total therapy is approximately 2 weeks with an eventual switch to oral therapy.

No indication exists for direct installation of antibiotics into the joint cavity. Such a practice may increase the inflammatory surge that can add to permanent joint damage.

The following section presents antibiotics frequentllly used by the author.[51]

Refer to the sections on empiric and organism-specific therapy of native and prosthetic septic arthritis for more detailed discussion of antibiotic choices in as well as dosing strategies.

Xxxxx

Ciprofloxacin (Cipro)

Ciprofloxacin is an alternative antibiotic to ceftriaxone to treat N gonorrhoeae and gram-negative enteric rods.

Linezolid (Zyvox)

Linezolid is an alternative antibiotic that is used in patients allergic to vancomycin and for the treatment of vancomycin-resistant enterococci.

Oxacillin

Oxacillin  and. Nafcillin are bactericidal semisynthetic penicillin that inhibit cell wall synthesis. Useful against methicillin-sensitive S aureus (MSSA).Nafcilli has the advantage innot requiring adjustment in renal failure andydoes not lead to lleukopeniae thrombocytopenia with prolonged usage.

Dalbavancin (Dalvance)

The prolonged half-life (360 hours) allows weekly dosing of dalbavancin. In addition, its effectiveness against gram-positive cocci, including biofilm producers, makes it a very desirable agent for the outpatient treatment of native and prosthetic joint infections.

Rifampin

Rifampin is used in combination with other drugs. It inhibits RNA synthesis in bacteria by binding to the beta subunit of DNA-dependent RNA polymerase, which, in turn, blocks RNA transcription.Rifampin's antimicobial spectrum is wide rangingIt's ability to penetrate the biofilm that forms on prosthetic material is unique. Because  many pathogens rapidly develop resistance to it ,1or2 appropriate  antibiotics should be started 2 days  before  and continued  throughout the course of rifampin

Lipopeptide

Cephalosporins, 3rd Generation

Cefixime (Suprax)

Cefixime is a third-generation oral cephalosporin with broad activity against gram-negative bacteria. By binding to one or more of the penicillin-binding proteins, this agent arrests bacterial cell wall synthesis and inhibits bacterial growth.

Oral cefixime is used as a follow-up to intravenous (IV) ceftriaxone to treat N gonorrhoeae.

Ceftriaxone

Cephalosporin withlong half life effective against essentially all of the gram-negative and Enteric organismsinvolved in SA

Oxazolidinones

Linezolid

 Linezolid is  effective against many positive pathogens including MSSA MRSA ,VSE,VRE. Serum levels essentially equal whether given either by oral or intervenous administration.Dosing  does not need to be adjusted  according  to renal function .Side effects  include potential severe hepatotoxicity . After two weeks of administration ,the risk of severe leukopenia and thrombocytopenia and various types of neuropathy markedly increase.

Glycopeptides

Vancomycin (Vancocin)

Vancomycin is an anti-infective agent used against MSSA, MRSA ,methicillin-resistant CoNS, and ampicillin-resistant enterococci  and in patients allergic to penicillin.It is key to insure that therapeutic serum levels have been acheived(trough level 5-12mcg/ml). In the face of fluctuating renal function, this may be an impossible task. Switching to linezolid  is advisable.

Lipopeptides

Daptomycin (Cubicin)

 

 Prior vancomycin administration may induce resistance to this medication.

Concurrent use of nafcillin or ampicillin may potentiate its bacteriacidal effect 

Dosing may range from 4mg/kg -12mg/kg per 24 hr

.

 

Questions & Answers

Overview

What is septic arthritis?

What is the incidence of septic arthritis?

Which groups are at highest risk for septic arthritis?

What are the most common causes of septic arthritis?

What is the prevalence of septic arthritis caused by streptococcal species?

What is the role of polymicrobial joint infections (PJI) in the etiology of septic arthritis?

What are the types of prosthetic joint infection (PJI)?

What is the pathogenesis of septic arthritis?

Why are previously damaged joints more susceptible to septic arthritis?

What is the pathophysiology of joint destruction in septic arthritis?

What is the role of viral infections in the pathogenesis of septic arthritis?

Which GI pathogens associated with reactive arthritis?

Which infections cause of reactive arthritis?

How do prosthetic joint infections (PJIs) lead to septic arthritis?

What is the role of coagulase-negative S aureus (CoNS) in the etiology of septic arthritis?

Which prosthetic joint infections (PJIs) cause septic arthritis?

What are situation-pathogen associations for septic arthritis?

What are the morbidities of septic arthritis?

Which factors are predictors of poor outcome in septic arthritis?

What is the mortality rate for septic arthritis?

Presentation

What should be the focus of history in suspected septic arthritis?

What are the signs and symptoms of septic arthritis?

Which conditions in a patient’s history increase the likelihood of septic arthritis?

What are possible comorbidities of septic arthritis?

What is the most important historical feature in septic arthritis?

What is the typical presentation of septic arthritis?

What is the presentation of Lyme disease-caused septic arthritis?

What is the presentation of prosthetic joint infection (PJI) septic arthritis?

What are the signs and symptoms of reactive arthritis?

What are the symptoms of tuberculous septic arthritis?

What are the clinical features of viral septic arthritis?

What is the most commonly involved joint in septic arthritis?

What physical findings suggest septic arthritis?

In which patients can signs and symptoms of septic arthritis be muted?

What is the significance of the pattern of joint involvement in the diagnosis of septic arthritis?

Which joints are most commonly infected in GBS septic arthritis?

What is the presentation of gonococcal musculoskeletal involvement in patients with septic arthritis?

What are the physical findings of septic arthritis caused by prosthetic joint infections (PJIs)?

How are reactive, viral, and tuberculous arthritis differentiated?

DDX

Which conditions should be considered in the differential diagnoses of septic arthritis?

What is characteristic of early disseminated gonococcal infection?

What is the frequency of salmonella septic arthritis in patients with sickle cell anemia?

What is the most common cause of septic arthritis among IV drug users?

Workup

When is reaspiration indicated in the evaluation of septic arthritis?

What is the initial screening method for septic arthritis?

What is the role of microscopy in screening for septic arthritis?

Which lab tests may be useful in the evaluation of septic arthritis?

What is the role of joint aspiration in the diagnosis of septic arthritis?

What is the role of synovial fluid culture in the diagnosis of septic arthritis?

Which synovial fluid findings are characteristic of Lyme septic arthritis?

How are prosthetic joint infections (PJIs) evaluated for septic arthritis?

Which synovial fluid findings suggest reactive arthritis?

Which synovial fluid findings suggest tuberculous septic arthritis?

What is the role of blood cultures in the diagnosis of septic arthritis?

What is the role of PCR in the diagnosis of septic arthritis?

What imaging findings suggest prosthetic joint infection septic arthritis?

What is the role of imaging studies in the diagnosis of septic arthritis?

What is the role of radiography in the diagnosis of septic arthritis?

How is ultrasonography used to diagnose septic arthritis?

How are CT scanning and MRI used to diagnose septic arthritis?

What is the role of radionuclide scanning in the diagnosis of septic arthritis?

Treatment

What is the focus of medical management of septic arthritis?

When is a medical cure for acute prosthetic joint infection (PJI) septic arthritis most likely?

What is the typical length of inpatient treatment for septic arthritis?

What specialist consultations are indicated for the treatment of septic arthritis?

What are the treatment options for native joint infections of septic arthritis?

What is the role of dalbavancin in the treatment of septic arthritis?

How is gonococcal arthritis treated?

What is the basis for antibiotic selection in the treatment of septic arthritis?

What are the treatment options for septic arthritis if antibiotic therapy fails?

What is the role of antibiotics in the management of septic arthritis?

What is the role of fluoroquinolones in the treatment of septic arthritis?

What is the role of joint immobilization in the treatment of septic arthritis?

What is included in physical therapy for septic arthritis?

How is synovial fluid drainage performed in the treatment of septic arthritis?

What is the role of surgical drainage for gonococcal-infected joints in patients with septic arthritis?

When is surgical drainage indicated for treatment of septic arthritis?

What is the role of arthroscopic lavage in the treatment of septic arthritis?

What is the role of debridement in treatment of septic arthritis?

How is debridement and retention of prosthesis performed in patients with septic arthritis?

What is the intermediate method for debridement and retention of prosthesis in septic arthritis?

How can infections of joint replacements be prevented?

What information about septic arthritis should patients receive?

Medications

How are medications selected for the treatment of septic arthritis?

Which medications in the drug class Xxxxx are used in the treatment of Septic Arthritis?