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Infectious tenosynovitis

Infectious tenosynovitis
Literature review current through: Jan 2024.
This topic last updated: Sep 15, 2022.

INTRODUCTION — Tenosynovitis refers to inflammation of a tendon and its synovial sheath; this condition occurs most frequently in the hand and wrist but can occur in any part of the extremities where a tendon glides within a synovial-lined fibro-osseous sheath.

Issues related to infectious tenosynovitis will be reviewed here.

ANATOMY — The anatomic arrangement of tendons, their sheaths, and the adjacent bursae (figure 1) has important implications for the clinical manifestations and management of tenosynovitis. (See "Finger and thumb anatomy".)

Extensor and flexor tendon sheaths have two surfaces: an inner visceral layer (visceral paratenon) adherent to the tendon and an outer parietal layer (parietal paratenon) abutting adjacent structures such as adjacent muscles and retinacular structures. Normally, the visceral and parietal layers abut one another. In the setting of tenosynovitis, the potential space between these two layers may fill with inflammatory or purulent fluid.

The visceral and parietal layers of most tendons coalesce at the proximal and distal ends to produce a closed tendon sheath compartment. The thumb flexor sheath is contiguous with the radial bursa, and the small finger flexor sheath is contiguous with the ulnar bursa; these two bursae extend proximally into the carpal tunnel. The radial and ulnar bursae communicate at the wrist in 50 to 80 percent of patients [1,2]. Therefore, infection in the thumb tendon sheath can spread to the small finger sheath via the ulnar bursa (or vice versa), creating a "horseshoe abscess."

Additionally, infectious tenosynovitis may spread via adjacent anatomic spaces, including the thenar and midpalmar spaces and the space of Parona (a potential space overlying the superficial fascia of the pronator quadratus muscle). Spread of infection may occur if parietal sheath integrity is compromised due to increased pressure associated with fluid accumulation; for example [3,4]:

Infectious tenosynovitis involving the extensor tendons on the dorsum of the hand can spread to the volar surface of the hand via bursae.

Infectious tenosynovitis involving the tendon sheaths of the wrist can spread to adjacent bursae and tendon sheaths surrounding the ulna and radius.

Infectious tenosynovitis of the small finger flexor tendon sheaths can spread into the carpal tunnel, producing symptoms similar to carpal tunnel syndrome. (See "Carpal tunnel syndrome: Clinical manifestations and diagnosis".)

Infectious tenosynovitis of the small finger flexor tendon sheaths can spread to the flexor sheath of the thumb via direct communication between the ulnar and radial bursae or via the space of Parona in the volar wrist [5].

Spread of infection from tendon sheaths to surrounding soft tissue can cause compartment syndrome and tissue necrosis.

The flexor retinaculum in the wrist and hand acts as a pulley system to facilitate movement and optimize the biomechanical efficiency of the flexor apparatus [6]. These anatomic compartments are relatively isolated environments, which may potentiate persistent and/or worsening infection.

In contrast, most extensor tendons lack an extensive retinacular system, so well-localized infection of extensor tendons is rare. For these reasons, extensor tenosynovitis may be difficult to distinguish from a simple soft tissue infection.

MECHANISMS AND MICROBIOLOGY — Tenosynovitis associated with bacterial infection develops via one of three mechanisms:

Trauma with direct inoculation (eg, laceration, puncture, or bite or after surgery)

Contiguous spread from infected adjacent soft tissues

Hematogenous spread

The microbiology of these entities is discussed in the following sections.

Tenosynovitis due to chikungunya virus has also been described [7]. (See 'Clinical manifestations' below.)

In immunosuppressed patients, tendon sheath infections may be due to common organisms (such as staphylococci and streptococci) or unusual pathogens (such as Cryptococcus spp and Histoplasma capsulatum) [8].

Trauma and contiguous spread — Most cases of infectious tenosynovitis present as acute infection via trauma with direct inoculation. In such cases, the most common pathogens are skin flora (eg, gram-positive cocci such as Staphylococcus aureus and streptococci) [4]. Lacerations and bites are commonly associated with polymicrobial infection, including gram-negative organisms. Tenosynovitis in the setting of diabetes is more likely to be polymicrobial and to include gram-negative bacilli [9]. Infectious tenosynovitis can also be a complication of surgical procedures such as trigger finger releases [10].

Types of trauma with specific associated pathogens include:

Cat and dog bites – Cat and dog bites are relatively common causes of infectious tenosynovitis. These infections are frequently polymicrobial. S. aureus and Pasteurella multocida are important pathogens, either alone or together. (See "Animal bites (dogs, cats, and other mammals): Evaluation and management".)

Puncture wounds – Puncture wounds due to thorns or woody plants may result in fungal tenosynovitis [11]. (See "Mycology, pathogenesis, and epidemiology of Fusarium infection" and "Clinical features and diagnosis of sporotrichosis".)

Intravenous drug use – Intravenous drug use can lead to infectious tenosynovitis, with or without abscess. Such infections are caused by skin or mouth flora, including Eikenella spp [12]. (See "Human bites: Evaluation and management".)

Water exposure (fresh or salt water) – Wounds associated with exposure to fresh or salt water can result in tenosynovitis due to Mycobacterium marinum. Other nontuberculous mycobacteria species have also been associated with infectious tenosynovitis [13,14]. (See "Soft tissue infections following water exposure".)

Subacute presentations (eg, delay between exposure or injury and the appearance of clinical findings) can occur in the setting of infection due to nontuberculous mycobacteria and fungi such as Sporothrix. Such presentations are more likely to occur in patients with impaired immune systems [15]. (See "Clinical features and diagnosis of sporotrichosis" and "Bone and joint tuberculosis".)

Hematogenous infection — Pathogens associated with tenosynovitis due to hematogenous spread include Neisseria gonorrhoeae and mycobacteria.

N. gonorrhoeae should be suspected in sexually active patients with the triad of tenosynovitis, vesiculopustular skin lesions, and polyarthralgia without polyarthritis, even if microbiological studies are negative (picture 1). Rarely, Neisseria meningitidis can cause a tenosynovitis similar in appearance to that caused by gonococci [16]. (See "Disseminated gonococcal infection".)

Tuberculous tenosynovitis may manifest as rubbery masses overlying tendon sheaths that enlarge gradually [17,18]. These lesions may be only moderately tender and lack typical findings of infection such as warmth and redness. Such findings may progress to tendon destruction and rupture before a diagnosis is established. (See "Bone and joint tuberculosis".)

CLINICAL MANIFESTATIONS — Most cases of infectious tenosynovitis involve the upper extremities; occasionally, infectious tenosynovitis occurs in the lower extremity, in which case patients may develop the inability to bear weight [19,20]. Infectious flexor tenosynovitis is more common than infectious extensor tenosynovitis.

Flexor tenosynovitis — The cardinal signs of infectious flexor tenosynovitis (called Kanavel signs) are [21,22]:

Tenderness along the course of the flexor sheath

Symmetric or fusiform enlargement of the affected digit

Finger slightly flexed at rest

Pain along the tendon with passive extension

The Kanavel signs have high sensitivity (91 to 97 percent) but low specificity (51 to 69 percent) for flexor tenosynovitis [23]. In one study including 75 patients with upper extremity infectious flexor tenosynovitis, the earliest finding was pain with passive extension [22]. Tenderness along the tendon sheath was a late sign; this finding suggests a more proximal extension of the infection. In another series including 16 patients with flexor tenosynovitis of the hand, fusiform swelling and pain with passive extension were the most common findings (100 percent and 75 percent, respectively) [24].

Severe tenderness following a bite or puncture wound should raise the possibility of tenosynovitis regardless of whether the above findings are observed. Rarely, small puncture injuries can be overlooked because they are minor or because they did not occur in temporal proximity to onset of symptoms [24].

Fever may or may not be present; in one study including 75 patients with infectious flexor tenosynovitis, only 17 percent had fever [22].

Infections involving flexor tendons progress in the following stages [25]:

Stage 1 – Distention of the inflamed tendon sheath with exudative fluid

Stage 2 – Distention of the inflamed tendon sheath with purulent fluid

Stage 3 – Septic necrosis and destruction of the tendon sheath and surrounding retinacular structures

The time frame for these stages varies depending on the pathogen. As examples, infection due to S. aureus or group A Streptococcus is typically acute (presentation within days); infection due to Pasteurella spp or M. marinum may be subacute (presentation within days to weeks).

The stage of infection is important for determining the approach to treatment. In general, during the first two stages, the tendon sheath remains viable. (See 'Anatomy' above and 'Role of surgery' below.)

Extensor tenosynovitis — Infections involving extensor tendon sheaths are unusual; when they do occur, the wrist and the ankle (in the region of the extensor retinaculum) are the most common sites. Given the limited extent of the extensor retinacular structures, patients with extensor tenosynovial infections often lack the typical findings seen in infectious flexor tenosynovitis. Thus, delays in diagnosis or misdiagnosis as an uncomplicated soft tissue infection may occur [26]. (See 'Anatomy' above.)

Complications — Complications include subcutaneous purulence (due to rupture of tendon sheath) and cutaneous signs of ischemia including skin necrosis. Less commonly, these infections may be associated with underlying osteomyelitis or progress to necrotizing fasciitis. These findings have important prognostic implications. (See 'Prognosis' below.)

DIAGNOSIS — Infectious flexor tenosynovitis should be suspected in patients with tenderness along the course of the flexor sheath, symmetric enlargement of the affected digit, slightly flexed finger at rest, and pain along the tendon with passive extension. Fever may or may not be present. The diagnosis should be considered carefully for patients with worsening symptoms, particularly with a history of local skin compromise such as from a bite, open injury, or recent surgery.

Infectious extensor tenosynovitis should be suspected in patients with findings resembling soft tissue infection involving the wrist or ankle that do not improve clinically with appropriate antimicrobial therapy and/or if findings are more focal than in typical cellulitis.

The diagnosis of infectious tenosynovitis is established by tendon sheath aspiration and/or biopsy. Specimens should be submitted for culture (including bacteria, mycobacteria, and fungal culture) and histopathologic examination.

Blood cultures should be obtained for patients with suspected tenosynovitis and systemic symptoms or signs (eg, fever, chills, hypotension).

Plain radiographs are usually normal in patients with infectious tenosynovitis; in some cases, asymmetric soft tissue shadowing may reflect swelling. Plain radiographs are useful to rule out bony involvement or the presence of a foreign body.

Chronic tenosynovitis may be associated with destructive radiographic changes consistent with osteomyelitis. Early signs of necrotizing fasciitis may include evidence of gas within the soft tissues. However, an open wound or puncture injury can introduce air into the soft tissue planes, creating a similar radiographic appearance. (See "Approach to imaging modalities in the setting of suspected nonvertebral osteomyelitis" and "Necrotizing soft tissue infections".)

Other imaging modalities (including magnetic resonance imaging, computed tomography, or ultrasound) may be useful to define the anatomic extent of infection, guide surgical planning, and evaluate for associated osteomyelitis or other conditions [27,28]. (See "Musculoskeletal ultrasonography: Clinical applications" and "Musculoskeletal ultrasonography: Nomenclature, technical considerations, and basic principles of use".)

DIFFERENTIAL DIAGNOSIS — A variety of conditions can mimic infectious tenosynovitis. These include:

Gout – Clinical manifestations of gout include erythema, warmth, swelling, and pain at the site of an involved joint [29]. The diagnosis of gout is established by visualization of uric acid crystals in aspirated joint fluid. (See "Clinical manifestations and diagnosis of gout".)

Herpes zoster – Herpes zoster can mimic infectious tenosynovitis when cutaneous lesions occur over a tendon sheath [30]. Clinical manifestations of herpes zoster include pain accompanied by presence of erythematous papules, which evolve into vesicles. The diagnosis of herpes zoster is usually established clinically but can be confirmed by viral culture, immunofluorescence, or polymerase chain reaction. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster".)

Psoriatic arthritis – Psoriatic arthritis may present as a symmetric polyarthritis, an asymmetric oligoarthritis, arthritis of the distal interphalangeal joints, as a destructive arthritis, or as a spondyloarthritis. The diagnosis of psoriatic arthritis may be made in patients with psoriasis and inflammatory arthritis in a typical pattern. (See "Clinical manifestations and diagnosis of psoriatic arthritis".)

Rheumatoid arthritis (RA) – Clinical manifestations of RA include joint pain, stiffness, and swelling. Typically, the metacarpophalangeal and proximal interphalangeal joints of the fingers and the interphalangeal joints of the thumbs are involved. The diagnosis of RA may be made in the setting of arthritis involving three or more joints, positive rheumatoid factor and/or anti-citrullinated peptide/protein antibody, and elevated inflammatory markers. Inflammatory tenosynovitis may be a manifestation of RA in some cases. (See "Clinical manifestations of rheumatoid arthritis".)

Pseudogout – Pseudogout is characterized by self-limited acute or subacute attacks of arthritis involving one or several extremity joints (monoarthritis and pauci[oligo]-arthritis, respectively). The diagnosis is established by visualization of calcium pyrophosphate crystals in aspirated joint fluid. (See "Clinical manifestations and diagnosis of calcium pyrophosphate crystal deposition (CPPD) disease".)

de Quervain stenosing tenosynovitis – de Quervain tendinopathy affects the abductor pollicis longus and extensor pollicis brevis tendons at the point where they pass through a fibro-osseous tunnel (the first dorsal compartment) at the styloid process of the radius. The diagnosis is based on history and physical examination. (See "de Quervain tendinopathy".)

Trigger finger – Trigger finger is caused by a disparity in the size of the flexor tendons and the surrounding retinacular pulley system; the flexor tendon catches when it attempts to glide through a relatively stenotic sheath, resulting in an inability to smoothly flex or extend the finger. The diagnosis is based on history and physical examination. (See "Trigger finger (stenosing flexor tenosynovitis)".)

Trauma – Local reaction following traumatic injury or arthropod bite may resemble clinical manifestations of infectious tenosynovitis. These are distinguished based on clinical history.

Soft tissue infection – Soft tissue infection manifests with skin erythema, edema, and warmth. The diagnosis is usually based upon clinical manifestations. Infectious extensor tenosynovitis should be suspected in patients with findings resembling soft tissue infection involving the wrist and ankle that do not improve clinically with appropriate antimicrobial therapy.

TREATMENT — Treatment of infectious tenosynovitis consists of inpatient administration of intravenous antibiotic therapy; in some cases, surgical intervention is also warranted.

Antibiotic therapy — Empiric antibiotic therapy should be guided by the mechanism of injury; subsequently, antibiotic therapy should be tailored to microbiology and susceptibility data when available.

For empiric treatment of tenosynovitis (mechanism unknown or attributable to trauma), a reasonable regimen consists of vancomycin (table 1) and a third-generation cephalosporin such as ceftriaxone (1 to 2 g IV every 24 hours).

For empiric treatment of tenosynovitis associated with known water exposure, a reasonable empiric regimen consists of vancomycin (table 1) and an agent with activity against Pseudomonas aeruginosa such as ceftazidime (2 g IV every 8 hours). (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of skin and soft tissue infections" and "Soft tissue infections following water exposure" and "Pseudomonas aeruginosa skin and soft tissue infections".)

For empiric treatment of tenosynovitis associated with bite wounds, the approach depends on the source of the bite; this is discussed separately. (See "Animal bites (dogs, cats, and other mammals): Evaluation and management" and "Human bites: Evaluation and management".)

Treatment of tenosynovitis associated with hematogenous spread depends on the nature of the systemic infection. (See "Clinical approach to Staphylococcus aureus bacteremia in adults" and "Disseminated gonococcal infection".)

The optimal duration of antibiotic therapy is uncertain; for uncomplicated bacterial infection with no associated bacteremia, 7 to 14 days of therapy is reasonable. Antibiotic therapy may be completed with oral therapy in some cases; the decision to switch from IV to oral therapy is made based on individual circumstances. Factors to consider include the microbiology, antibiotic susceptibility data, and patient comorbidities.

Patients with involvement of adjacent structures may require a longer duration of therapy (for example, bony involvement warrants four to six weeks of therapy). (See "Nonvertebral osteomyelitis in adults: Treatment".)

Role of surgery — Patients presenting with early signs and symptoms of tenosynovitis (local inflammation, mild pain that does not limit full passive motion of the involved tendon compartment) may be observed closely on antibiotic therapy for signs of progression [31]. Such patients warrant elevation of the involved limb, protective splinting, restricted activity, and anti-inflammatory therapy.

Surgery is warranted in patients with early tenosynovitis that does not improve within a few days of empiric antimicrobial therapy and in patients with established tenosynovitis (based on clinical manifestations). The surgical approach is guided by the stage of infection [22] (see 'Flexor tenosynovitis' above):

Patients with stage 1 infection failing to improve with empiric medical management should undergo tendon sheath irrigation and drainage, with or without debridement.

Patients with stage 2 or stage 3 infection should undergo surgical debridement of the tendon sheaths and surrounding necrotic tissue.

Drainage of tendon sheaths can be accomplished via catheter irrigation or open washout [32-35]. Outcome comparisons for these treatment methods are difficult as indications are guided typically by clinical severity. In severe cases, serial debridement may be required, particularly if an abscess is found during the initial evaluation [36,37]. Tissue cultures and biopsy at the time of surgical drainage/debridement can assist with the diagnostic evaluation and help guide treatment.

The above approach is based on small case series and clinical experience; there are no rigorous trials evaluating the approach to surgical management of tenosynovitis [22].

Other indications for surgical intervention include associated bursal involvement, bony involvement, or presence of compartment syndrome. (See "Nonvertebral osteomyelitis in adults: Treatment" and "Acute compartment syndrome of the extremities".)

PROGNOSIS — Early administration of antimicrobial therapy, prompt irrigation, and debridement (if necessary) are associated with better functional outcomes [33].

In one study including 120 patients with infectious tenosynovitis, poor prognostic factors included advanced infection at presentation, infection due to Streptococcus pyogenes, and delayed surgical debridement [37]. In another study including 75 patients with infectious tenosynovitis, poor prognostic factors included subcutaneous purulence, digital ischemia, polymicrobial infection and presence of diabetes mellitus, peripheral vascular disease, or renal failure [22]. Patients who presented with stage 3 infection had the worst prognosis (amputation rate 59 percent).

Long-term complications of pyogenic tenosynovitis include finger stiffness and tendon sheath adhesions, boutonniere deformity, and tendon necrosis [33].

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Tenosynovitis (The Basics)")

SUMMARY AND RECOMMENDATIONS

Tenosynovitis refers to inflammation of a tendon and its synovial sheath; this condition occurs most frequently in the hand and wrist. The anatomic arrangement of tendons, their sheaths, and the adjacent bursae has important implications for the clinical manifestations and management of tenosynovitis (figure 1). (See 'Introduction' above and 'Anatomy' above.)

Mechanisms for development of tenosynovitis due to bacterial infection include trauma due to direct inoculation (most common), contiguous spread from infected adjacent soft tissues, and hematogenous spread. (See 'Mechanisms and microbiology' above.)

Infectious flexor tenosynovitis should be suspected in patients with tenderness along the course of the flexor sheath, symmetric enlargement of the affected digit, slightly flexed finger at rest, and pain along the tendon with passive extension. Infections involving flexor tendons progress in the following stages (see 'Flexor tenosynovitis' above):

Stage 1 – Distention of the inflamed tendon sheath with exudative fluid

Stage 2 – Distention of the inflamed tendon sheath with purulent fluid

Stage 3 – Septic necrosis and destruction of the tendon sheath and surrounding retinacular structures

Since most extensor tendons lack an extensive retinacular system, well-localized infection of extensor tendons is rare. Therefore, extensor tenosynovitis may be difficult to distinguish from a simple soft tissue infection. (See 'Extensor tenosynovitis' above.)

The diagnosis of infectious tenosynovitis is established by tendon sheath aspiration and/or biopsy. Specimens should be submitted for culture and histopathological examination. Blood cultures should be obtained for patients with systemic symptoms or signs. (See 'Diagnosis' above.)

Plain radiographs are usually normal in patients with infectious tenosynovitis; they are useful to rule out bony involvement or presence of foreign body. Other imaging modalities (including magnetic resonance imaging, computed tomography, or ultrasound) may be useful to define the anatomic extent of infection, guide surgical planning, and evaluate for other conditions. (See 'Diagnosis' above.)

Treatment of infectious tenosynovitis consists of inpatient administration of intravenous antibiotic therapy; in some cases, surgical intervention is also warranted. For empiric treatment of tenosynovitis (mechanism unknown or attributable to trauma), we administer vancomycin and a third-generation cephalosporin such as ceftriaxone. Subsequently, antibiotic therapy should be tailored to microbiology and susceptibility data when available. (See 'Antibiotic therapy' above.)

Patients presenting with early signs and symptoms of tenosynovitis (local inflammation, mild pain that does not limit full passive motion of the involved tendon compartment) may be observed closely on antibiotic therapy for signs of progression. Such patients warrant elevation of the involved limb, protective splinting, restricted activity, and anti-inflammatory therapy. (See 'Role of surgery' above.)

In the setting of established infectious tenosynovitis, the surgical approach is guided by the stage of infection. For patients with stage 1 infection, we perform tendon sheath irrigation with or without debridement. For patients with stage 2 or state 3 infection, we perform surgical debridement of the tendon sheaths and surrounding necrotic tissue. Surgical specimens should be sent for cultures and biopsy to assist in establishing a diagnosis and to guide treatment. (See 'Role of surgery' above.)

Other indications for surgical intervention include associated bursal involvement, bony involvement, or presence of compartment syndrome. (See 'Role of surgery' above.)

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