Kevin D. Kerin
Infectious Arthritis
A septic joint is a medical emergency.
Definition and Epidemiology
Inflammation of a joint is called arthritis and is an observable finding, whereas pain in a joint is called arthralgia and is a subjective description. One important type of arthritis is infectious arthritis, considered to be a medical emergency. Infectious arthritis can be caused by a large number of organisms, including bacteria, fungi, viruses, and filariae. The term septic arthritis is most commonly used to describe arthritis caused by a bacterial pathogen. An infectious cause of joint inflammation needs to be considered even when a noninfectious type of inflammatory arthritis (rheumatoid arthritis, gout) has been previously diagnosed. Bacterial and viral arthritides usually manifest acutely with systemic and articular symptoms. In contrast, Lyme disease and mycobacterial, fungal, filarial, and some bacterial arthritides (Neisseria gonorrhoeae, Neisseria meningitidis) may be subacute or chronic and relatively indolent. Infectious arthritis is seen in all age groups, although the highest incidence is in children and the elderly.
Pathophysiology
Synovial joints such as the knee and hip are particularly vulnerable to infection. Abnormal synovial joints, such as those previously damaged by other traumatic, inflammatory, or degenerative processes, are especially susceptible to infection. One explanation is that synovial tissue is highly vascularized, lacks a basement membrane, and is thus susceptible to the hematogenous spread of infectious organisms from a locus of infection.1 Other avenues of infection of the joint space include extension of infection from osteomyelitis or adjacent soft tissue infection and direct inoculation from penetration of a foreign body. A joint infection is a medical emergency and can be a rapid, severely destructive process. Once a bacterial infection is established in a joint space, a complex cascade of events follows: changes in synovial tissue; migration of acute and chronic inflammatory cells to the joint space; release of inflammatory cytokines, proteases, and collagenases; changes in intra-articular fluid volume and pressure; and chondrocyte changes.2
Staphylococcus aureus is the most common cause of acute bacterial arthritis across all age groups.2 Its affinity for joints can be explained in part by the structure of the microbe, which elaborates certain surface and secreted proteins that may facilitate colonization of tissue. This organism also has receptors for glycoproteins found in joints and has frequent access by hematogenous seeding from minor wounds and abrasions because of its presence as normal skin flora. Streptococci are also considered to be normal skin flora, and are second only to S. aureus as causative agents of infectious arthritis. N. gonorrhoeae is the most common cause of infectious arthritis from a sexually transmitted bacterium and is most frequently seen in sexually active adults younger than 30 years.3 This is not unexpected, given the ease with which N. gonorrhoeae invades the bloodstream during menses or parturition and after acute urethritis. Gram-negative bacilli cause approximately 10% of cases of septic arthritis, often in older adults and neonates, and are associated with a better outcome than gram-positive infections.4 In a community-based study of septic arthritis in native joints, older age and limited range of motion were predictors for gram-positive cocci as the cause, whereas diabetes mellitus with end-organ damage and malignant change were predictors for gram-negative bacteria.4 Anaerobes are an uncommon cause of infectious arthritis and are associated with human bites, intra-abdominal abscesses, and periarticular decubitus ulcers.5 Alphavirus infection, after initial febrile illness, may progress to cause a polyarticular inflammatory arthritis that bears similarity to seronegative rheumatoid arthritis. Chikungunya viral arthritis (transmitted by mosquito) is an example of an alphavirus and appeared in the United States in 2014.6,7
Clinical Presentation
Septic arthritis usually manifests with the acute onset of a painful, red, swollen joint that is warm to the touch. An important historical point that helps distinguish septic arthritis from sterile inflammation is that the affected joint is painful at rest as well as with motion and weight bearing. The rapid accumulation of fluid volume and rise in intra-articular pressure are prime contributors to rest pain. The affected joint will be held in a position that allows maximum intra-articular volume. The pain of arthritis from other causes usually is relieved with rest. Fever in a patient with septic arthritis is usually present but may be low grade or absent (especially in older adults); rigors caused by bacteremia may also be present. Fever and rigors have low sensitivity and specificity in the diagnosis of septic arthritis because these findings may also be seen in acute crystal-induced arthritis. Any joint may be involved in infectious arthritis, yet the knee and hip are the most commonly affected. Septic arthritis in an unusual location, such as the sternoclavicular or sacroiliac joint, should raise the suspicion of injection drug use.8 The sudden onset of monoarticular arthritis is the usual presentation of nongonococcal arthritis, although a polyarticular presentation is not unusual. A polyarticular septic arthritis is sometimes seen with streptococcal or staphylococcal infections but usually affects only two or three joints (pauciarticular).
Infectious arthritis occurs more commonly in patients with an impaired immune system and in those with preexisting joint abnormalities, such as rheumatoid arthritis, gout, osteoarthritis, or a prosthetic joint. It is important to consider infection as a cause of an acute monoarticular or pauciarticular flare, even in those with an established diagnosis of a chronic rheumatologic condition. The fever and joint inflammation are less striking in gonococcal arthritis, which is characterized by a migrating polyarticular course.9 Human immunodeficiency virus (HIV) infection with the associated immunosuppression is a special situation in which septic arthritis is uncommon; however, when it is seen, it may be a result of atypical organisms, such as Mycobacterium tuberculosis, Sporothrix schenckii, and Candida albicans, in addition to more common organisms such as S. aureus and N. gonorrhoeae.10
Physical Examination
The manifestations of inflammation were vividly described by Celsus in the first century AD as rubor, tumor, calor, and dolor (redness, swelling, heat, and pain). The inflamed joint is erythematous, warm to the touch, swollen, and painful, with passive and active range of motion. Synovial effusion is usually present, although it is less obvious in certain joints, such as the hip and shoulder. A large effusion creates an asymmetry in size with loss of anatomic landmarks. A smaller effusion in the knee may be detected by a “bulge sign” (the examiner presses on the medial aspect of the knee to displace fluid toward the suprapatellar region and then looks for a small bulge in this area after applying pressure on the opposite side of the knee) or patellar ballottement (see Fig. 173-8) (the examiner taps on the patella while applying pressure to the suprapatellar area to try to elicit a “click,” signifying synovial fluid beneath the patella).
Decreased range of motion, muscle spasm, and apprehension to joint examination are prominent features of the examination. The proximal lymph node may be enlarged and tender, indicative of proximal lymphangitic spread of infection. An original source of infection, such as an abscess, cellulitis, gonococcal urethritis, pneumonia, urinary tract infection, or endocarditis, should be sought. Distinct clinical presentations are seen in special situations, which are discussed in the following sections.
Gonococcal Arthritis
Disseminated gonococcal infection (see Chapter 153) is the most common cause of septic arthritis in sexually active adolescents and young adults.11 There appear to be two distinct clinical presentations. One has been called the arthritis-dermatitis syndrome and reflects a bacteremic stage; the other is a localized septic arthritis.11 The classic triad of clinical findings in disseminated infection is dermatitis, tenosynovitis, and a migratory polyarthritis. The first group is distinguished by tenosynovitis and dermatitis. Skin lesions are present in countable numbers and multiple stages; these lesions are most often maculopapular but are sometimes necrotic, pustular, or vesicular. The lesions are painless and nonpruritic and typically spare the face and scalp. The lesions resolve in several days without scarring.12 An asymmetric migratory polyarthralgia that affects knees, elbows, wrists, ankles, metacarpophalangeal joints, and associated tendon sheaths is the presentation more common than actual polyarthritis. Synovial fluid cell counts are lower than those commonly seen in bacterial arthritis, and the synovial fluid culture is often negative. The blood culture may be positive. Only 25% of patients have genitourinary symptoms of gonorrhea.3
The more focal septic arthritis seen in the second group may occur after a migratory polyarthritis, tenosynovitis, or dermatitis, with the arthritis now settled in one or two joints. The synovial fluid is more purulent, and the culture is more likely to be positive. Blood cultures are typically negative. Taken as a group, cultures of the pharynx, cervix, urethra, and rectum are positive in up to 80% of patients if specimens are obtained early on selective media (e.g., Thayer-Martin).3 Synovial fluid culture specimens should be plated directly onto chocolate agar.
There may be clinical uncertainty about the diagnosis, especially in the context of a wide range of synovial fluid leukocyte counts and negative blood cultures. In this situation, ceftriaxone, 1 g/day intravenously for 24 hours, can be a valid diagnostic and appropriate therapeutic strategy.
Prosthetic Joint Infection
Millions of people have prosthetic joints, and it is estimated that approximately 4 million knee or hip arthroplasties will be performed annually by the year 2030.13 Although the rates of infection after hip or knee arthroplasty have declined significantly to approximately 1%,14 the large number of current and projected prosthetic joints makes this a relatively common problem. It is a serious, potentially devastating problem and is associated with major disability and cost. In most cases, in patients not considered to be too frail or poor surgical candidates, the prosthetic joint needs to be removed, and the patient will require up to 6 weeks of intravenous antibiotics (with or without an antibiotic-impregnated cement spacer), followed by reimplantation of a new prosthetic joint once infection has been eradicated.15 Biofilms, complex microbial communities formed by bacteria causing prosthetic joint infections, contribute to antibiotic resistance.16 Coagulase-negative staphylococci are common in this clinical setting and produce an indolent course. Hematogenous seeding at the bone-cement interface with S. aureus or group A streptococci may manifest more acutely with sepsis or toxic shock, which is characteristic of these more virulent organisms.16
Infections in older patients with underlying disease may include gram-negative bacilli (15% to 20%) and anaerobes (7%).17
One way to classify prosthetic joint infections is by the amount of time elapsed since joint surgery: early (within 3 months), delayed (3 to 24 months), and late (>24 months). Early and delayed infections have their origin at the time of prosthetic placement, whereas late infections are caused by hematogenous seeding of bacteria. Infection in a prosthetic joint is often difficult to diagnose, and clinical manifestations may vary by the timing of the infection in relation to the surgery. As a rule, most patients have joint pain with or without radiographic evidence of loosening of the prosthesis. A minority of patients have fever, joint swelling, or sinus track drainage. It may be difficult to differentiate a delayed-onset infection of a prosthetic joint from a noninfectious inflammation, such as a reaction to components of the prosthetic joint or a mechanical problem with the hardware (e.g., loosening, dislocation, hemarthrosis, and malposition).18 A helpful observation is that mechanical problems are painful during motion, weight bearing, and pivoting but are comfortable while at rest. Constant joint pain suggests an infection.
Laboratory tests such as acute-phase reactants (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]) and leukocyte count are not especially helpful because a number of inflammatory conditions can cause elevated levels in any of these tests, and normal values do not rule out infection. Plain radiographs may be helpful, especially if serial studies are available for comparison. Classic radiographic findings of infection include lucencies along the bone-cement interface, migration of the prosthesis, and periosteal reactions. These findings are not present in acute or early infections and are difficult to differentiate from mechanical complications in those with delayed-onset infections. A technetium bone scan may take up to 1 year to become normal after surgery19 because of bone remodeling, yet a normal bone scan provides strong evidence against an infected prosthetic joint if the timing is right. Other radiologic techniques, such as sequential bone and gallium scanning or combined leukocyte-marrow scintigraphy, have shown greater accuracy in the diagnosis of a prosthetic joint infection, but are costly, time-consuming, and not widely available. Ultimately, the diagnosis of a prosthetic joint infection relies on aggressive attempts to isolate an organism by obtaining joint fluid or tissue.
The recommendations to patients with prosthetic joints about antibiotic prophylaxis for dental procedures are debated and confusing, with conflicting recommendations over the years. Currently, the American Academy of Orthopaedic Surgeons recommends that clinicians consider antibiotic prophylaxis for essentially all patients with prosthetic joints before dental procedures.20 A case-control study concluded, however, that dental procedures are not risk factors for infection of knee or hip prosthetic joints.21
Lyme Disease
The clinical manifestations of Lyme disease can be separated into early localized disease (1 to 30 days), early disseminated disease (days to 10 months), and late disease (months to years) on the basis of the elapsed time from tick exposure to symptoms (see Chapter 234). Only 30% of patients with Lyme disease recall a tick bite, but in the setting of known tick exposure, 80% of patients with early, localized Lyme disease experience arthralgias or migratory arthritis.22 During this stage, the characteristic rash (erythema chronicum migrans) appears with an expanding red border and central clearing, occasionally creating the classic bull’s eye appearance. Fever, headache, myalgias, arthralgias, and lymphadenopathy may be more noticeable than the skin lesions, which are usually painless.
The manifestations of early, disseminated Lyme disease include multiple systemic features: cardiac problems (pericarditis, atrioventricular nodal heart block, and myopathy), neurologic problems, and musculoskeletal problems (migratory polyarthralgias or polyarthritis) in 50%.22 More prolonged attacks of true arthritis develop in a few joints. In late Lyme disease, about 60% of patients have a migratory polyarthritis and 10% of patients develop a chronic arthritis that settles in one or two large joints, usually the knees.23
In Lyme disease, the causative spirochete, Borrelia burgdorferi, is difficult to culture from synovial fluid, but sensitive methods of antigen detection, such as enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR), can reveal its presence. Having a high index of suspicion in the right clinical setting is essential to establishing the diagnosis. In the wrong clinical setting (without sufficiently high pretest probability), serologic tests for Lyme disease are misleading because of the high false-positive rate; therefore, such tests should not be ordered indiscriminantly.22 All patients with true arthritis attributed to early, disseminated, or late Lyme disease should have a positive response on the Lyme ELISA, subsequently confirmed by Western blot.
The outcome is better if diagnosis and treatment are rendered early in this form of infectious arthritis. Medical therapy fails in approximately 50% of patients with late Lyme disease arthritis; progressive joint destruction may then merit synovectomy or total joint arthroplasty.23
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