Septic arthritis is infection and inflammation of a joint caused by bacterial, fungal, or viral invasion of the synovium. Bacterial septic arthritis involves a single joint in 90% of cases. The knee is the most commonly involved joint, followed by the hip, shoulder, ankle, and wrist. Patients with septic arthritis typi- cally have acute swelling and warmth around the joint, effusion, tenderness to palpation, and extreme pain with minimal range of motion.
Bacteria can reach a joint in four ways: (1) from the blood, that is, via hematogenous seeding during bacteremia;(2) from the out- side environment through direct inoculation of organisms following penetrating trauma, joint aspiration, or surgery;(3) from the localized spread of a nearby soft-tissue infection, such as cellulitis or bursitis; or (4) from spread of a bone infection near the joint (periarticular osteomyelitis).1 Hematogenous seeding is the most common cause of infectious arthritis.
Septic arthritis is rare in the normal adult population; fewer than 5% of cases of acute arthritis have an infectious cause. Bacterial septic arthritis is more common in infants, the elderly, and patients with impaired immunity. Risk factors include a history of rheumatoid arthritis (RA) or intravenous drug use. Patients with RA are more likely to have multiple joint involvement. Intravenous drug users often have infections in atypical joints, such as the sternoclavicular, sacroiliac, and manubriosternal joints.2,3
Information about patient age, medical history, and risk factors must be obtained because these factors not only identify the potential for infection but also the possible infecting organism. With this information, the physician can initiate empiric antibiotic treatment once the diagnosis is established but before identification of a specific bacterium. Staphylococcus aureus is the most common cause of all joint infections; therefore, empiric antibiotics must cover it, even if there is a specific bacteria associated with a particular demographic. For example, pa- tients with a history of illicit drug use are known to have an increased risk of Pseudomonal infection, but even among these patients staphylococcal infection is common as well. Thus, empiric treatment of infection in these patients must cover that organism as well.
Hematogenous septic arthritis occurs when bacteria are able to seed the joint after escaping from the synovial capillaries, which do not have a basement membrane. In normal joints, host defense mechanisms are able to destroy these bacteria; however, when these mechanisms are compromised, the organ- isms can survive and cause infection.
While open trauma to a joint is an obvious risk factor for infection, closed trauma is also a risk factor for reasons that are not entirely clear. Possible explanations include a reactive hyperemia increasing exposure to bacteria, disruption of the local anatomy allowing bacteria easier access to the joint and interfering with defense mechanisms, and formation of a hematoma providing an ideal culture medium for bacterial growth.1
Many bacteria can bind to articular cartilage. S aureus has an increased ability to bind to articular cartilage compared with other bacteria, which may explain why it is the most common pathogen in bacterial septic arthritis.1 Within hours after entering the synovium, bacteria induce a neutrophilic in- filtration of the synovium. Cartilage destruction begins within 48 hours as a result of the release of proteases and cytokines from inflammatory cells and increased intra- articular pressure (Fig. 1).
While neutrophils are one of the primary host defenses against joint infection, they also are a major cause of joint destruction in septic arthritis.
The cytokine interleukin-1 (IL-1), released by macrophages and tissue monocytes in response to bacteria, plays an important role in the destruction of cartilage. Exposure of the joint surface to IL-1 leads to proteogly- can release, increased secretion of collagenase, release of metalloproteases, activation of latent collagenases, and inhibition of glycosaminoglycan synthesis.1
If the septic process is terminated early, the proteoglycan losses can be reversed and normal function restored. If too much matrix is lost, the chondrocytes are exposed to increased mechanical stress and die, which leads to further matrix loss. The remaining chondrocytes are exposed to more stress and are more apt to die, perpetuating a vicious cycle that can lead to complete joint destruction.4
In adults, S aureus accounts for 60% of the cases of bacterial septic arthritis.5 Other common organisms include streptococci and gram-negative organisms. Although S aureus is still the most common infectious organism in patients who are intravenous drug users, gram-negative infections, especially Pseudomonal infections, can also be transmitted via intravenous drug use. 2
S aureus is a pathogen that may be found in all children, but when infection occurs, several other organisms need to be considered, based on the age of the patient. In infants from birth to 6 weeks of age, the most likely pathogens are group A and group B streptococci, Streptococcus pneumoniae, and Escherichia coli.6 Neisseria gonorrheae infection acquired via maternal transmission at birth also needs to be considered in this age group.
In children younger than 5 years, an in- creasing number of cases of septic arthritis are caused by Kingella kingae. This organism is thought to colonize the nasopharynx and then spread to the joints via invasion of the bloodstream. Haemophilus influenzae type B (HIB) was a common pathogen in children of this age in the past; however, with the advent of widespread vaccination, HIB infection has become extremely rare. S pneumoniae is also an important organism in this age group.5
In children older than 5 years, S aureus, group A streptococci, and S pneumoniae are the most common pathogens. As children get older, the incidence of staphylococcal infections increases, and the incidence of streptococcal infections decreases.
Disseminated gonococcal infection, classically associated with a syndrome of fever, chills, rash, and migratory arthritis of the large joints, always precedes gonococcal septic arthritis, nor- mally involving a single joint. Although gonococcal septic arthritis is always preceded by systemic gonococcal infection, this stage may go unnoticed in up to 30% of patients.7 Gono- coccal infection is the most common type of infectious arthritis in healthy adults. It generally affects patients younger than 40 years, and women are two to three times more likely to be affected than men.
A typical medical history for septic arthritis would be an 80-year-old female nursing home resident being treated with cortico steroids and methotrexate for RA. She has had increasingly worse knee pain for the past 2 days, with perhaps a history of minor trauma. Upon presentation, her temperature is 100.3°F, and she has a large warm effusion on her knee that is diffusely tender to palpation. She also has extreme pain with minimal range of motion. Although she was able to walk 3 days ago, she now finds weight bear- ing painful. Her skin appears normal, al- though cellulitis, a skin infection, is certainly common in such patients.
Radiographs of the knee joint typically show soft-tissue swelling and periarticular osteopenia consistent with long-term RA. In this setting, there is no particular need for special imaging studies. When hip infection is suspected, ultrasound or MRI may be need- ed because these studies can detect an effu- sion with great sensitivity.
When evaluating a patient for infection, it is helpful to obtain a white blood cell count, erythrocyte sedimentation rate, and C-reactive protein level. The essential laboratory test, how- ever, is the analysis of fluid obtained from joint aspiration. This fluid must be examined microscopically (Gram stain) and then sent to the laboratory for a white blood cell count and culture. Aspirates with more than 50,000 white blood cells per milliliter are thought to represent infection. Some patients with inflammatory arthritis but no infection may have more than 50,000 white blood cells per milliliter, whereas some patients with infection and immune suppression (which limits white cell production) may have less. The best criterion to use depends on the utility (value) of each possible outcome.
The differential diagnosis of septic arthritis depends on the clinical scenario. Conditions to consider include inflammatory arthritis, reactive arthritis (a noninfectious joint inflammation following infection else- where in the body), trauma, superficial infection or abscess near but not in the joint, and collagen vascular disorders.
Treatment and Prevention
The goals of treatment include sterilization of the joint, removal of inflammatory cells and their enzymes, elimination of the destructive synovial pannus, and restoration of function.1 Prompt administration of antibiotics and drain- age of the involved joint can prevent cartilage destruction, minimizing the risk of secondary arthritis, joint instability, deformity, and loss of function. Empiric antibiotics should be started as soon as cultures of the blood and synovial fluid are obtained (ie, before interpretation).
The initial choice of antibiotic should be based on the morphology of organisms visualized on Gram stain, if any, and the likely pathogens based on the patient’s age and risk factors. Antibiotics should be given intravenously to achieve rapid peak serum concentrations. Direct injection of the joint with antibiotics is not advised because it can cause a chemical synovitis.
In order to limit cartilage destruction and decrease intra-articular pressure, early drainage of pus and necrotic material is required. Three methods are available: (1) repeated needle aspiration, often at the bedside; (2) arthroscopic lavage; and (3) arthrotomy (open surgery). For easily accessible joints, such as the knee, repeated needle aspirations can be used; however, patient dis- comfort and the difficulty draining thick collections of pus often make arthroscopy a better choice. For less accessible joints, such as the hip, arthrotomy is the best means for irrigation and débridement. Following arthrotomy, the joint should be closed over suction drainage, which can be removed after several days as the volume of drainage de- creases and the patient’s condition improves. If repeated aspirations are attempted and systemic antibiotics are administered, failure to improve within 48 hours is an indication for surgical drainage.
Postoperatively, the joint should be splint- ed in the functional position with assisted range-of-motion exercises initiated once the inflammatory response has decreased. Pro- longed immobilization should be avoided because it promotes the formation of adhesions, atrophy, and contractures. For joints in the lower extremity, weight bearing should be protected until the inflammation has subsided and range of motion and strength are al- most normal.3
Gonococcal septic arthritis is unique in that surgical drainage may not be needed, even with large effusions. This form of septic arthritis is less destructive and rarely requires surgical decompression. Instead, intravenous ceftriaxone and aspiration may be sufficient. Once there is clear improvement, oral antibiotics can be given for a total of 14 days.