Septic Arthritis Flashcards
Background
Septic arthritis, also known as infectious arthritis, may represent a direct invasion of joint space by various microorganisms, most commonly caused by bacteria. However, viruses, mycobacteria, and fungi have been implicated. Reactive arthritis is a sterile inflammatory process that may result from an extra-articular infectious process. Bacteria are the most significant pathogens in septic arthritis because of their rapidly destructive nature. For this reason, the current discussion concentrates on the bacterial septic arthritides. Failure to recognize and to appropriately treat septic arthritis results in significant rates of morbidity and may even lead to death.
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. 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 common and challenging type of septic arthritis encountered by most clinicians. 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.
Septic arthritis is also becoming increasingly common among people who are immunosuppressed and elderly persons. Of people with septic arthritis, 45% are older than 65 years; these groups are more likely to have various comorbid disease states. Fifty-six percent of patients with septic arthritis are male.
Gonococcal and nongonococcal bacterial/suppurative arthritis
Septic arthritis due to bacterial infections is commonly classified as either gonococcal or nongonococcal.
Overall, although Neisseria gonorrhoeae remains the most common pathogen (75% of cases) among younger sexually active individuals,
Staphylococcus aureus infection is the cause of the vast majority of cases of acute bacterial arthritis in adults and in children older than 2 years. The increased incidence of this pathogen parallels the increase in presence of prosthetic joints and in the use of immunosuppressive agents. This pathogen is the cause in 80% of infected joints affected by rheumatoid arthritis.
Streptococcal species, such as Streptococcus viridans, S pneumoniae, and group B streptococci, account for 20% of cases. Aerobic gram-negative rods are involved in 20-25% of cases. Most of these infections occur in people who are very young, who are very old, [who are diabetic, who are immunosuppressed, and who abuse intravenous drugs.
Infection of the sternoclavicular and sacroiliac joints with Pseudomonas aeruginosa or Serratia species occurs almost exclusively in persons who abuse intravenous drugs. Persons with leukemia are predisposed to Aeromonas infections.
Polymicrobial joint infections (5-10% of cases) and infection with anaerobic organisms (5% of cases) are usually a consequence of trauma or abdominal infection. The organism of Lyme disease (ie, Borrelia burgdorferi), a large 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 may produce nonsuppurative joint infection.
Types of prosthetic joint infections
Three major types of prosthetic joint infections exist:
(1) those that occur early, within 3 months of implantation
(2) those that are delayed, within 3-24 months of implantation; and
(3) those that occur later than 24 months following the implantation.
Most cases of early prosthetic joint infection are caused by S aureus, whereas delayed infections are due to coagulase-negative S aureus (CoNS) and gram-negative aerobes. Both of these types are acquired in the operating room.
Late cases of prosthetic joint infection are secondary to hematogenous spread from various infectious foci.
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).
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 a joint infection. Some microorganisms have properties that promote their tropism to the synovium. S aureus readily binds to articular sialoprotein, fibronectin collage, 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: 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.
Local infection
Prosthetic joint infections (PJIs) may be a consequence of local infection, such as intraoperative contamination (60-80% of cases), or of bacteremias (20-40% of cases). 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 the 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. [17] 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 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. 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:
- 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%. 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.
Septic Arthritis Clinical Presentation
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.
Pay attention to the following symptoms:
1. Acuteness of onset of the joint pain
2. Whether the pain is superimposed on chronic pain
3. Previous history of joint disease or trauma, whether accidental or iatrogenic (eg, infection complicates 0.4% of arthrocenteses)
4. Whether the process is monoarticular or polyarticular and which joints are involved
The presence of extra-articular symptoms
5. Whether the patient has had vascular invasion due to catheterizations or intravenous drug abuse
Obtain a thorough 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 of Septic Arthritis
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 prosthetic joint infection (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.
Physical Examination
Septic Arthritis
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.
Signs and symptoms of infection may be muted in people who are elderly, who are immunocompromised (especially those with rheumatoid arthritis), and who abuse intravenous 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.
Work-Up
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.
If microscopy demonstrates no crystals, 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 to be infected. 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.
