Adult Reconstruction, 1st Edition

Section II - Knee

Part B - Evaluation and Treatment of Knee Disorders

20

Septic Arthritis

  1. Wade Shrader

David J. Jacofsky

Acute bacterial infection of a joint, known as acute septic arthritis, is a serious, and can be a life-threatening, infection. Septic arthritis occurs primarily through three mechanisms: (a) direct inoculation through an open wound or penetrating object (including surgery); (b) spread from adjacent infected tissue, such as a soft tissue infection or local osteomyelitis; or (c) hematogenous seeding from bacteremia. Even with appropriate, aggressive intervention and treatment, septic arthritis can cause substantial morbidity, and a delay in diagnosis or treatment can make the consequences even more serious.

Septic arthritis most commonly affects small children and the geriatric population. Patients with any immune system compromise are especially at risk, including those patients with diabetes, rheumatoid arthritis, malnutrition, and chronic renal or liver failure. Patients using intravenous drugs and those with chronic indwelling intravenous catheters are at higher risk. Vascular insufficiency may increase the risk of infection by compromising host immune defenses and also can impair the treatment of infection by decreasing delivery of antimicrobial agents to infected tissues.

Pathogenesis

The incidence of septic arthritis in the general population has been estimated to be 2 cases per 100,000, although the incidence is much higher in immunocompromised populations. In patients with rheumatoid arthritis, the incidence has been estimated to be between 30 and 70 cases per 100,000. The most commonly affected joint is the knee.

The most common source of infection is hematogenous spread. Joints are at risk for hematogenous seeding because of the lack of basement membranes in the synovial tissues. Thus, bacteria that are present in the blood vessels have relatively easy access to the joint space without the barrier of the basement membrane.

The most common infectious agent in adult septic arthritis is Neisseria gonorrhea. This infection often occurs in sexually active young adults, is typically polyarticular, and may be associated with a papular rash. Gonococcal septic arthritis can be successfully treated with antibiotics and is the only type of joint infection that does not require surgical debridement.

The most common cause of nongonococcal septic arthritis in adults is from Staphylococcus aureus. Patients typically have monoarticular involvement, and bacteria are usually spread hematogenously. The hip and knee are the most common joints involved, although infections of the shoulder, elbow, wrist, and ankle also may be seen. Methicillin-resistant strains of staphylococcus (MRSA) are becoming more prevalent, with three out of four positive S. aureus cultures being methicillin-resistant in some centers.

Other infectious agents may be responsible for septic arthritis, depending on the patient population and the environment. Streptococci,Salmonella, and Pseudomonas are all frequently encountered organisms.

Diagnosis

The clinician must maintain a high level of suspicion for septic arthritis because of the serious consequences of a missed diagnosis. Patients typically present with a swollen, red, painful joint. They often will not be able to bear weight on the affected lower extremity and will complain of decreased joint motion secondary to pain. Fevers and chills are sometimes present. Often, however, all of these complaints are not present, and the severity of the symptoms can be quite variable. A thorough history should be elicited, specifically considering any recent infections, immune compromise, social history, travel history (to exclude tick bites), and a complete sexual history. Musculoskeletal infections caused by mycobacterial or fungal organisms do not typically present with the acute, dramatic inflammatory response seen in bacterial infections. The diagnosis in these cases often is made based on a high index of suspicion of the health care provider.

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Physical Exam

The physical exam should focus on determining if any signs of infection are present. Vital signs, including temperature, should be obtained. The joint should be examined for effusion, erythema, and tenderness to palpation. The most specific sign of septic arthritis is pain with passive range of motion, which should be determined in any physical exam of the extremities. In the knee, septic arthritis may be differentiated from septic prepatellar bursitis by determining if pain with range of motion is seen only in deeper flexion (bursitis) or can be elicited at near full extension as well.

Radiographic Features

Plain radiographs are recommended for most musculoskeletal complaints of the extremities. Plain films should be scrutinized to determine if there are any fractures, dislocations, or other pathologic bony processes that might explain the patient's symptoms. Plain radiographs may not always be helpful in the diagnosis of septic arthritis, although in more chronic cases erosive changes can be seen. Soft tissue swelling, loss of soft tissue planes, or effusions may be the only findings on radiographs of patients with septic arthritis. Chronic or neglected infections can progress to adjacent osteomyelitis, which often can be detected on plain radiographs.

Magnetic resonance imaging (MRI) can be helpful in some circumstances. MRI views will definitely show effusion and fluid collections that may be infectious. MRI also may demonstrate other reasons for joint swelling, such as ligament rupture or meniscal tear. Nuclear imaging with technetium bone scan or indium-tagged white blood cell scan also can be used, but often are not necessary to confirm the diagnosis.

Laboratory Workup

Screening laboratory values should be obtained in all patients, both to assist in the diagnosis of the septic arthritis and to follow the indices after treatment. A complete white blood count with differential, erythrocyte sedimentation rate (ESR), and C-reactive protein should be obtained if infection is suspected, although inflammatory disorders alone can lead to false-positive results.

The gold standard in diagnosis of septic arthritis remains arthrocentesis (joint fluid aspiration). The joint should be aspirated with a large-bore needle, and this should be done before empiric antibiotic treatment is begun. Fluoroscopy can be used to aid in the aspiration, if necessary for some joints (e.g., hip). The fluid should immediately be sent for Gram stain, cell count, culture, and crystal analysis. Cultures from superficial sites such as draining fistulas should be avoided, as the organisms colonizing these sites may not be the same as the deeper infecting organism. Joint fluid cultures are positive in about 85% of nongonococcal septic arthritis, but only in about 25% of cases in which gonococcus is the infecting agent.

A joint fluid aspirate analysis that shows a nucleated white blood cell count >100,000/mm3 is indicative of septic arthritis, and counts between 50,000/mm3 and 100,000/mm3 are inflammatory but not necessarily infectious. The white blood cell differential count also provides valuable information to aid in the diagnosis. A differential count with an unusually high proportion of polymorphonuclear cells (>90%) is also highly suggestive of septic arthritis, whereas <50% neutrophils is unlikely to be an acute infection.

Joint fluid analysis must be performed in a timely, urgent fashion to allow treatment that will prevent the systemic spread of infection and preserve the health of the articular cartilage. Intra-articular lysosomal enzyme release, including metalloproteases and collagenases, can digest glycosaminoglycans and cause articular cartilage cell death. The release of these enzymes is mediated by cytokines such as interleukin-1 (IL-1). Cartilage softening and fissuring can be seen secondary to glycosaminoglycan depletion within 7 days from the onset of infection. Laboratory investigations in animal models have shown that joint debridement and lavage decrease the rate and magnitude of collagen breakdown, probably through the removal of leukocytes and associated destructive enzymes.

Treatment

The three classic principles in management of the acute septic joint are as follows: (a) thorough joint drainage and synovial debridement, (b) appropriate antibiotic therapy, and (c) joint rest in a stable position. All three of these treatment principles are crucial in the successful treatment of septic arthritis.

There are three techniques to drain a septic joint: (a) open drainage, lavage, and debridement; (b) arthroscopic drainage, lavage, and debridement; and (c) serial aspirations, lavage, and drainage. Controversy remains over which method is the most appropriate way to treat a septic joint. The gold standard remains an open arthrotomy, which allows for adequate drainage and lavage and provides the opportunity for a thorough synovial debridement, a factor that many surgeons feel is key to successful treatment. Experienced arthroscopists argue that they can provide equally efficacious drainage and lavage through the arthroscope. Proponents of arthroscopic debridement also argue that they can actually perform a more thorough synovial debridement by using posterior portals to allow for debridement of the posterior compartment of the knee. Although its indications and use are limited, serial aspirations and lavage also can be successful in treating the native septic joint, particularly if the infection is <72 hours old and the patient is not immunocompromised. It is critical, however, that if the patient does not show significant improvement within 24 to 48 hours with repeated aspirations, surgical irrigation and debridement should be performed. In general, closed suction drainage for 24 to 48 hours after operation is recommended.

The initial antibiotic should be chosen based on the patient risk factors, patient history and clinical signs, and the initial Gram stain. Culture results should dictate change to the most appropriate antibiotic, based on sensitivity data.

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Typically, intravenous antibiotics are continued for 4 to 6 weeks. When nonviable tissue is encountered in the joint and when a clinical response to treatment is not seen, a “second-look” surgery and repeat debridement may be indicated.

The joint should be kept immobilized for the first 48 to 72 hours of treatment. However, once clinical improvement is noted, the patient should begin rehabilitation, including range-of-motion and strengthening exercises. Some surgeons advocate the use of continuous passive motion (CPM) devices to minimize the possibility of forming postinfectious intra-articular adhesions. Dynamic splints, passive motion exercises, and joint manipulations are used as needed but are rarely necessary.

After the septic arthritis has been successfully treated, the joint involved may develop arthritis, or suffer from decreased loss of motion. Any subsequent surgical treatment aimed at that joint (for example: capsular release, osteotomy, arthroplasty) must take into account the possibility of residual infection.

Suggested Readings

Canale ST, ed. Campbell's Operative Orthopedics. 9th ed. St. Louis, MO: Mosby—Year Book; 1998.

Dubost JJ, Soubrier M, Sauvezie B. Pyogenic arthritis in adults. Joint Bone Spine. 2000; 67(1):11-21.

Kohli R, Hadley S. Fungal arthritis and osteomyelitis. Infect Dis Clin North Am. 2005; 19:831-851.

Koval KJ, ed. Orthopedic Knowledge Update 7, Home Study Syllabus. Rosemont, IL: American Academy of Orthopedic Surgeons; 2006.

Leirisalo-Repo M. Early arthritis and infection. Curr Opin Rheumatol. 2005; 17(4):433-439.

Morrissy RT, Weinstein SL. Lovell and Winter's Pediatric Orthopedics. 4th ed. Philadelphia: Lippincott-Raven Publishers; 1996.

Perry CR. Septic arthritis. Am J Orthop. 1999; 28:168-178.

Rice PA. Gonococcal arthritis (disseminated gonococcal infection). Infect Dis Clin North Am. 2005; 19:853-861.

Ross JJ. Septic arthritis. Infect Dis Clin North Am. 2005; 19:799-817.

Smith JW, Chalupa P, Shabaz Hasan M. Infectious arthritis: clinical features, laboratory findings and treatment. Clin Microbiol Infect. 2006; 12(4):309-314.

Zimmermann B III, Mikolich DJ, Ho G Jr. Septic bursitis. Sem Arth Rheum. 1995; 24:391-410.



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