Infection of the synovial sheaths that surround a tendon is known as te-nosynovitis. The flexor muscle-associated tendons and tendon sheaths of the hand are most commonly involved (flexor tenosynovitis). Penetrating trauma is the most common inciting event and infection then can travel rapidly from the digit to ulnar and radial bursae. Acute infection is most commonly attributable to S aureus and other skin-associated flora, such as streptococci, although the nature of the traumatic injury may impact the associated microbiology (ie, organisms associated with mammal bites, gardening, or fish handling) . Nontraumatic causes of tenosynovitis are classically associated with disseminated gonococcal infection (DGI). In DGI, one or several tendons may be involved (extensor more often than flexor), usually targeting the ankles, toes, wrists, and fingers . Chronic infectious flexor tenosynovitis is caused primarily by fungi and mycobacteria.
Patients who have acute flexor tenosynovitis present with erythematous fusiform swelling of an involved finger, which is held in a semiflexed position. Tenderness over the length of the tendon sheath and pain with extension of the finger also are typical . Classically, patients who have DGI have fever, rash, tenosynovitis, and an asymmetric polyarthritis. The rash initially is macular, papular, or petechial before progressing to a pustular stage that can become hemorrhagic and necrotic. The lesions characteristically are few in number (ie, < 20-30) and are distributed periarticularly over distal extremities.
Patients in whom there is clinical suspicion of flexor tenosynovitis should be evaluated by a hand surgeon and receive empiric antibiotics. The nature of the exposure and the underlying status of the host dictate the antimicrobial selection. Infection in an immunocompetent host resulting from a simple puncture would require at least Gram-positive skin flora coverage against staphylococci and streptococci. Pet bite-associated infectious tenosynovitis dictates expanded coverage to include Gram-negative organisms, such as Pasteurella and anaerobes. Imaging of the involved area, particularly with MRI, may be helpful in identifying the presence of gas, bone infection, foreign body, or fluid, and the extent of infection, but a definitive diagnosis requires evaluation of fluid from within the tendon sheath. Although some patients who present within 48 hours of developing trauma-associated flexor tenosynovitis can be treated with intravenous antibiotics and splinting alone, effective surgical drainage coupled with pathogen-directed therapy established by microbiologic evaluation of drainage material typically is required. DGI-associated tenosynovitis can be diagnosed with blood cultures. In addition, the organism may be detected in mucosal sites, such as the rectum, oropharynx, cervix, and urethra, and in the synovial fluid (when arthritis is present). Initial therapy with ceftriaxone intramuscularly or intravenously and hospitalization are recommended for patients who have DGI. Unless the diagnosis is excluded, treatment of concomitant chla-mydial infection also should be administered. Intravenous therapy can be switched to oral antibiotics, such as cefixime, 24 to 48 hours after improvement begins to complete at least one week of treatment .
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