Septic Arthritis

Septic arthritis refers to an active joint infection, usually bacterial in origin. It is not common in companion animals, but when it occurs, it can be devastating for the joint. Treatment and outcome depend on the source, organism involved, and duration of infection.

Etiology

Septic arthritis occurs from exogenous inoculation or hematogenous spread of bacteria to the joint. Penetrating injuries, surgical procedures, and intra-articular injections are common exogenous sources. Hematogenous infection occurs when bacteria from distant sites, such as the respiratory tract, oral cavity, umbilicus, genitourinary tract, or heart, localize in the joint [1]. Preexisting disease or conditions causing immunosuppression predispose to joint infection [2,3]. Young animals are often affected, although no breed or age predilection exists [4].

Escherichia coli, Staphylococcus, Streptococcus, and Pasteurella species are commonly isolated from septic joints, with staphylococcal infections being most prevalent [5,6]. Borrelia burgdorferi, bacterial L-forms, Mycoplasma spumans, Mycobacterium tuberculosis, fungi, protozoa, and rickettsial organisms have also been implicated [2].

Pathophysiology

Once exposed to bacteria, a cascade of events initiates the potentially destructive process within the joint environment. Bacterial infiltration results in synovial tissue edema, activation of the immune system, and initiation of the inflammatory cascade. Inflammation of the synovium, capillary rupture, and necrosis promote extravasation of fibrin, clotting factors, polymorphonuclear leukocytes, and proteinaceous fluid into the joint [7]. Intraarticular pressure increases, potentially leading to ischemia, subluxation, or avascular necrosis of intra-articular structures. Lysosomal enzymes and enzyme by-products released during activation of the inflammatory cascade degrade cartilage, disrupt synovial fluid dynamics, and impair cartilage nutrition [7]. Granulation tissue formed as a result of inflammation can penetrate and undermine the cartilage, causing further joint destruction [8]. As the process progresses and cartilage is destroyed, subchondral bone can also become involved [8]. Destruction of articular cartilage and degenerative joint changes combined with thickening and scarring of periarticular tissues leads to restricted joint mobility, and in severe cases, loss of joint function. Early therapeutic intervention is imperative to minimize destructive joint changes [8,9].

Diagnosis

Isolation of bacteria from the joint in question is necessary for definitive diagnosis of septic arthritis, but this is not always possible and degree of suspicion plays a role. Attempt at bacterial isolation is made by aseptic arthrocentesis followed by cytologic evaluation and culture of the synovial fluid. Abnormal cytologic findings consistent with septic arthritis include increased numbers of white blood cells (40,000/μL or greater, mostly neutrophils that may or may not be degenerate), loss of fluid viscosity, presence of intracellular bacteria, and increased fluid turbidity (Table 92-1) [5,6,10]. Direct plating of synovial fluid for culture is not ideal because this leads to frequent negative results [11,12]. Culture of the synovium has been clinically shown to be more beneficial than culture of synovial fluid alone [5,13], but reports are conflicting in that experimental tests have not shown the same [11]. Submission of synovial fluid on a culture swab has the potential to inhibit some organisms, resulting in decreased yield [14], although reasonable success can be achieved using the technique [11]. To facilitate bacterial growth, synovial fluid should immediately be placed in blood culture media at a 1:9 ratio. The synovial fluid-culture media combination is incubated for 24 hours at 37°C (98.6°F) before being plated for identification of organisms [11].

Other diagnostics depend on the suspected type of infection. In all cases a complete blood count, chemistry panel, and urinalysis should be performed to evaluate the animal as a whole and to look for systemic disease, although yield might be low. In cases of aspergillosis, fungal hyphae might be seen and can be cultured from synovial fluid [15]. Special stains such as India ink, periodic acid-Schiff, and silver nitrate stains, or treatment of preparations with 10% potassium hydroxide can improve visualization of fungal organisms [16,17]. Synovial fluid from cats with calicivirus infection can be normal or can have elevated cell counts with a predominance of mononuclear cells; virus isolation is possible from synovial fluid and tissues of affected joints [18]. Polymerase chain reaction with DNA isolation can be useful in some cases of septic arthritis in which definitive diagnosis is difficult, such as mycobacterial infections [19]. The source of infection should be isolated in cases of hematogenous seeding of the joint with bacteria.

Early radiographic changes associated with septic arthritis include joint effusion and soft-tissue swelling. With progression of disease, bone lysis, joint surface irregularity, bone sclerosis, ankylosis, and subluxation can be seen [20]. Nuclear scintigraphy provides earlier diagnostic information than does conventional radiography. Positive joints do not specifically indicate infection [21-23]; however, newer scintigraphic agents have the potential to differentiate infection from other forms of inflammation [24]. Advanced imaging through computed tomography or magnetic resonance imaging might also be beneficial in the diagnosis of joint infection [20,25].

Clinical Findings

In animals suffering from septic arthritis, the affected joint is usually swollen and painful. Only one joint is typically involved. The joint might be warm to the touch and the animal is often severely lame or unable to bear weight. Systemic signs such as malaise, inappetence, and fever are variable in cases of exogenous disease, but with hematogenous infection, they are more likely to be present [13]. In addition to fever, anorexia, depression, and oral ulcerations, cats affected with calicivirus can exhibit acute swelling and pain of the distal joints and may be reluctant to move [18,26].

Treatment

Therapy is directed at minimizing cartilage destruction and eradicating the infection. Antimicrobials are administered after synovial fluid for cytologic evaluation, culture, and susceptibility testing has been obtained. Intravenous administration of a broad spectrum, bactericidal antimicrobial is indicated initially, but a favorable initial response permits a change to oral antimicrobial administration within the first 3 to 5 days of therapy. Long-term antimicrobial administration is based on culture and bacterial susceptibility testing. If culture results are negative, antimicrobial therapy is continued based on positive clinical response to treatment. Antimicrobials should be continued for a minimum of 4 weeks or at least 2 weeks beyond the resolution of clinical signs.

Final antibiotic choice is based on culture and antimicrobial susceptibility testing. If empiric antibiotic administration is necessary, care should be taken in antibiotic selection because antimicrobial resistance of commonly isolated organisms is constantly changing. Staphylococci, in one report, showed 18% resistance to first-generation cephalosporins [27]. Clinical response to treatment should always be monitored. Common first-line defense antimicrobials would include first-generation cephalosporins and penicillins supplemented with ß-lactamase inhibitors because Staphylococci are most commonly isolated from joint infections [27]. Tetracycline is recommended for those animals with infectious arthritis secondary to Borrelia, rickettsial infections, Mycoplasma, and bacterial L-forms [2,13].

Antibiotic penetration into joint cavities and efficacy against the causative organism is necessary for resolution of infection. Synovial fluid and serum antibiotic kinetics are similar, with synovial fluid concentrations gradually increasing as serum concentrations rise [28,29]. Final synovial fluid concentration depends on the molecular size of the antibiotic and inflammation-dependent changes in synovial membrane permeability [28,29]. Synovial fluid antibiotic concentrations decrease as joint inflammation resolves, but therapeutic antibiotic concentrations within the joint likely remain [12,30]. Following equilibration, antibiotic concentration within the joint is the same or higher after systemic administration when compared with intra-articular injection, so systemic therapy alone is typically sufficient [31]. Furthermore, intra-articular injection of antibiotics can cause chemical synovitis with worsening of the pathologic process and should be avoided [32,33].

Medical management consisting of appropriate antimicrobial therapy, passive range of motion exercises, and pain management can result in resolution of infection and return to function if the animal is treated aggressively and early in the course of disease [34]. However, joint lavage is essential to remove cellular and enzymatic constituents in some cases. In young animals, decompression can be especially important to reduce pressure within the joint and preserve epiphyseal vascularity [7]. Needle aspiration and lavage alone do not adequately remove deleterious materials from the joint, but can provide some benefit if surgical lavage is not an option [34]. Arthrotomy or arthroscopy with surgical debridement and copious lavage of the affected joint is indicated for postoperative joint infections, septic joints untreated for 72 hours or more, joints that have not responded to 72 hours of appropriate medical management, or joint infection secondary to penetrating wounds. [9,34] At the time of surgery, the joint is explored, cultured, debrided of necrotic debris, and lavaged with large volumes of an isotonic solution. Joints with healthy appearing tissues after debridement and lavage are closed primarily at the time of surgery. If the tissue appears unhealthy, open-joint management or ingress-egress systems may need to be utilized.

An ingress-egress flushing system allows for continued joint lavage during the postoperative period and is considered for animals with severe infections and extensive tissue damage. However, intra-articular drainage systems can be difficult to maintain. Open-joint management is an effective alternative. Open joints and lavage systems should be managed aseptically and the drains removed or the joint closed when drainage is minimal and less purulent to decrease the chance of nosocomial infection. Open joints should be kept moist until they are closed. Cytologic evaluation of exudate can be helpful in deciding when to remove the drain or close the joint.

Fluid therapy and nutritional supplementation should be instituted as needed. The inciting cause in cases of hematogenous seeding of the joint with bacteria must be found and treated appropriately. Pain medication is imperative to facilitate joint mobility and patient comfort. It is also important to maintain joint mobility through passive range of motion activity, yet limit heavy weight-bearing to prevent undue stress on the already weakened articular cartilage. Swimming or underwater treadmill activity would be beneficial because joint stress is reduced through these activities. In severe cases that have not responded to antibiotic therapy or surgery and in cases with irreversible, severe joint damage or stiffness, amputation is a feasible alternative. For some joints, arthrodesis is indicated if the infection, but not the severe destructive changes within the joint, can be eliminated.

Prognosis

Prognosis is variable and depends on the degree of cartilage destruction and duration of disease. Arthritis is expected following joint infection, but the severity and resulting disability are difficult to predict. Up to 50% of people suffer permanent joint dysfunction and 75% have residual disabilities after treatment of septic arthritis [35,36]. Many animals recover with minimal deficits, but others suffer permanent joint dysfunction [6,34]. Furthermore, some animals will have a residual lameness secondary to a continued immune response to lingering microbial antigens within the joint, even though the infection has been eradicated [37]. These animals might respond to corticosteroid therapy, but treatment should only be initiated after repeated negative joint cultures [2]. Calicivirus infection in kittens is usually self-limiting, but can be associated with a 25% mortality rate in adults cats [18,26].

In summary, septic arthritis can lead to severe joint destruction and debilitation if not treated aggressively and early in the course of the disease. Parenteral antibiotic therapy followed by long-term oral antibiotic administration is imperative. Surgical intervention is necessary in some instances to decompress the joint, debride devitalized tissue, and lavage. Arthritis is expected after joint infection, but early treatment can minimize joint destruction.