Updated: Jan 17, 2023
  • Author: Christopher S Crowe, MD; Chief Editor: Harris Gellman, MD  more...
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Practice Essentials

Tenosynovitis is a broadly defined as inflammation of a tendon and its respective synovial sheath. This inflammation can derive from a great number of distinct processes, including idiopathic, infectious, and inflammatory causes.

The most common form of tenosynovitis is referred to as idiopathic or stenosing tenosynovitis and includes such processes as trigger finger, trigger thumb, and de Quervain tenosynovitis.  Although many patients with these conditions will attribute their symptoms to overuse, most cases start without a change in activity level, and classification as an overuse injury is likely incorrect. Similarly, although the term tenosynovitis suggests inflammation via the "-itis" suffix, the actual histopathologic findings are noninflammatory and include fibrocartilaginous metaplasia of the retinacular pulley with narrowing of the fibro-osseous canal.

Digit swelling in the case of trigger finger is usually nonapparent or minimal, but there is a palpable nodular enlargement of the flexor tendon near the A1 pulley and often reproducible catching or "triggering." This condition is typically characterized by insidious onset and gradual progression, with intermittent catching or locking of the digit and/or pain with activity. Treatment often involves corticosteroid injection, which can be curative in a majority of a patients. Alternatives can involve braces or orthoses or surgical release of the A1 pulley. 

In contrast to idiopathic tenosynovitis, infectious and inflammatory tenosynovitis will be characterized by prominent symptoms and signs of inflammation. The digit is often enlarged as a result of swelling, with associated hyperemia, altered posture, and limited motion.

The acute infectious etiology of pyogenic flexor tenosynovitis (PFT) is a closed-space infection of the flexor tendon sheath, which represents a surgical emergency. Untreated PFT may rapidly destroy the gliding mechanism, cause adhesion formation, and potentially give rise to necrosis of the tendon and its fibro-osseous sheath. Given the potentially severe disruption of hand function resulting from loss of a functional flexor tendon, rapid identification and treatment of PFT are critical to preventing poor outcome. Chronic infectious flexor tenosynovitis can be caused by atypical microorganisms such as gonococci and mycobacteria (eg, Mycobacterium tuberculosis or M avium complex).

Noninfectious inflammatory tenosynovitis of the digital flexor tendons and other tendons of the hand may be due to crystalline deposition (eg, gout or calcium pyrophosphate disease [CPPD; pseudogout]), inflammatory arthropathy (eg, rheumatoid arthritis [RA]), or reactions to penetrating wounds from sharp objects (eg, rose thorns or sea urchin spines). Each case must be individually assessed, and management must be directed at addressing the specific underlying etiology.

Below is a brief overview regarding the diagnosis and management of tenosynovitis of the hand, which will be covered in greater depth in subsequent sections.

Signs and symptoms

Pyogenic flexor tenosynovitis

Most patients with PFT will present with complaints of pain, redness, and swelling of the affected digit over the period of hours to days. A thorough history may reveal an antecedent palmar-side puncture wound or laceration. Infection may also begin in the adjacent soft tissues and subesequently spread to the sheath and its contents. Instances of hematogenous spread are quite rare, and gonococcal infection should be considered when suspected. Physical examination of the affected digit may reveal some or all of Kanavel's four cardinal signs of flexor tendon sheath infection, [1, 2]  which are as follows:

  • Finger held in slight flexion
  • Uniform swelling of the digit
  • Tenderness along the flexor tendon sheath
  • Pain with passive extension of the digit

Clinical features of gonococcal tenosynovitis will typically include Kanavel's signs but will usually be preceded by a disseminated gonococcal infection with the following characteristics:

  • Fevers, chills, arthralgias
  • Hemorrhagic macules or papules on the extremities or trunk
  • Septic arthritis (which, along with tenosynovitis, may exist in isolation without the preceding bacteremia symptomatology)

Noninfectious inflammatory tenosynovitis

Inflammatory tenosynovitis not caused by an infection has the following characteristics:

  • Usually is secondary to an underlying disease process (eg, RA or gout)
  • Generally has an indolent presentation but progresses if treatment is not initiated
  • Swelling is the most common initial finding
  • Hallmark is a difference in active vs passive flexion
  • As the tissue expands and impingement occurs, pain and restricted motion ensue

Delayed presentations can have the appearance of PFT with Kanavel signs or may involve tendon rupture if the patient delays seeking treatment long enough.

See Clinical Presentation for more detail.



If infection is suspected, culture of the suppurative synovial fluid is recommended before definitive antimicrobial treatment is initiated. The sheath space should be accessed away from any cellulitic-appearing skin. These cultures should include the following samples:

  • Aerobic
  • Anaerobic
  • Fungal
  • Acid-fast bacilli (AFB)
  • Atypical AFB

Diagnostic arthrocentesis is indicated if joint effusion is present with tenosynovitis. Most patients with disseminated gonococcal infection will have concommitant septic arthritis.

Hematologic studies

  • Complete blood count (CBC)
  • C-reactive Protein (CRP) and erythrocyte sedimentation rate (ESR)
  • Rheumatoid factor (RF) if RA is a consideration


Synovial biopsy for histopathologic examination is helpful in diagnosing granulomatous changes observed in Mycobacterium infections and in cases of chronic inflammatory processes.


Obtain standard anteroposterior (AP) and lateral radiographs to determine bony irregularity (arthritis, tophi, etc), osteomyelitis, or presence of a foreign body. [3]

See Workup for more detail.


Nonsurgical management of PFT has been proposed in early mild cases. Prompt medical management of acute nonsuppurative PFT may render surgical intervention unnecessary. However, this must be carefully considered, in that extensive purulence in the tendon sheath can result in extensive adhesions, loss of both diffusion and perfusion of nutrition to the tendon, necrosis, and amputation. Nonoperative treatment for PFT includes the following:

  • Broad-spectrum intravenous (IV) antibiosis 
  • Elevation and soft-tissue splinting in the position of safety
  • Rehabilitation consisting of range-of-motion (ROM) exercises and edema control once infection is under control

The indication for surgical drainage arises when patients present outside the window of early management or with progressive signs and symptoms. Surgical exploration of the flexor tendon sheath can be performed with limited incisions and will allow the surgeon to directly inspect the tendon and its sheath. Thus, when any concern exists, a drainage procedure should be performed.

Nonoperative management is the primary treatment for idiopathic and inflammatory flexor tenosynovitis. Therapy also includes the following:

  • Icing and elevation of the affected area
  • Administration of a nonsteroidal anti-inflammatory drug (NSAID) if tolerated by the patient
  • Consideration of a short course of oral steroids
  • Administration of flexor tendon sheath or carpal tunnel corticosteroid injections to decrease pain and the inflammatory response
  • Splinting - If used, splinting should be limited in area to a pain-free ROM
  • Rehabilitation - Slow rehabilitation prevents reinitiation of the inflammatory phase

Surgical management of noninfectious inflammatory tenosynovitis may be pursued in functionally limiting and progressive cases. Managment in this context is dependent on the underlying disease process.

See Treatment and Medication for more detail.

For patient education information, see the Infections Center, as well as Tendinitis and Rheumatoid Arthritis.



Infectious tenosynovitis

Pyogenic flexor tenosynovitis (PFT) is one of many closed-space infections of the hand, and an understanding of the relevant anatomy is key for adequate treatment. The flexor sheaths of the index, middle, and ring fingers extend from the metacarpal neck at the level of the first anular (A1) pulley proximally to the flexor digitorum profundus (FDP) insertion on the distal phalanx distally.

The small finger and thumb sheaths are unique in that their sheaths are often continuous with the ulnar and radial bursae in the palm (see the image below). Symptoms may be initially be less severe in these digits because infection can decompress into the respective bursa. Infections of either the small finger or the thumb are at risk for communicating proximally in the potential space beneath the FDP tendons and above the pronator quadratus muscle. This area is known as the Parona space, and infection within it may cause symptoms of median neuropathy.

Flexor tendon sheaths and radial and ulnar bursae. Flexor tendon sheaths and radial and ulnar bursae.

Although in theory the initial process is relegated to the closed space of the tendon sheath, infection may migrate into the fascial spaces of the hand, adjacent osseous structures, and synovial joint spaces, or it may erode through the layers of the skin and exit superficially as a draining wound.

The tendon sheath is made up of an inner visceral layer that is continuous at its most distal and most proximal extents with an outer parietal layer. The visceral layer is in close approximation to the flexor tendon. The parietal layer is reinforced by a series of five anular pulleys (A1-5) and three cruciform pulleys (C1-3). The A2 and A4 pulleys are critical for flexor tendon function, and transection should be avoided during surgical manipulation of the infected sheath (see the image below). Synovial fluid fills the space between these two layers. 

Location of anular and cruciform pulleys. Location of anular and cruciform pulleys.

The tendon and synovial sheath recieve two distinct sources of nutrient support. The first is via direct blood supply from the vincula, and the second is from diffusion through the synovial fluid. Given the relative paucity of bloodflow to these tissues, bacteria may proliferate unchecked once inoculated into this space. As pus accumulates within a flexor tendon sheath, an increase in compartmental pressure can further limit the intrasynovial blood supply and cause necrosis and subsequent rupture of the tendon. In one study, eight of 14 patients with flexor tendon sheath infections had hand tendon sheath pressure in excess of 30 mg Hg. [4]  

PFT has classically been described as occurring in three distinct stages, according to a system known as the Michon classification [5] : (see Table 1 below):

Table 1. Michon Classification of Infectious Flexor Tenosynovitis (Open Table in a new window)

Stage I Early inflammation of the tendon sheath and accumulation of exudative fluid
Stage II Continued inflammation of the tendon sheath and distention with purulent fluid
Stage III Necrosis of the tendon and tendon sheath, possible tendon rupture

Idiopathic or stenosing tenosynovitis

The most common form of tenosynovitis is secondary to narrowing of the tendon's retinacular sheath and consequent entrapment of the tendon. As tendons cross the joints of the wrist and digits, they pass under a series of tight fibro-osseous sheaths. The purpose of these retinacular structures is to approximate the tendon closely with the underlying bone in order to optimize force and motion distally for muscle activation.

High forces at the pulley cause microtrauma to the tendon and sheath. Consequent narrowing of the retinacular space causes impingement on the tendon, resulting in further tendon edema that affects gliding and occasionally leads to painful triggering or locking. In the case of trigger finger and trigger thumb, the flexor tendon sheath is constricted at the A1 pulley, but constriction has also been infrequently found at other anular pulleys. [6] A similar process takes place at the first dorsal compartment (see the image below) in de Quervain tenosynovitis.

First dorsal compartment of wrist includes tendon First dorsal compartment of wrist includes tendon sheath that encloses abductor pollicis longus and extensor pollicis brevis tendons at lateral border of anatomic snuffbox.

Histopathologic analysis will demonstrate profound thickening secondary fibrocartilaginous metaplasia of the retinacular pulley and nodular swelling of the corresponding tendon. [7, 8]  In patients without a history of inflammatory disorders, the tendon and sheath do not show generalized inflammatory changes, [9]  despite being amenable to corticosteroid injection. The root cause of the entrapment in primary types (ie, those not due to an underlying disorder) is disputed. However, risk factors for the development of tendon entrapment syndromes are well established and are discussed in greater detail in following sections.

Inflammatory tenosynovitis

Rheumatoid arthritis

Inflammatory tenosynovitis is quite common in patients with rheumatoid arthritis (RA) and may even precede symptoms related to the joint spaces. Proliferation of the synovial-lined tendon sheaths occurs in a similar manner to the intra-articular involvement of the disease process. Early proliferation of the synovium causes classic swelling in the digit. As inflammatory tissue builds up, the synovial lining of the tendon sheath thickens and may cause entrapment of the tendon as it glides through the narrow sheath. This process may progress to involve the tendon itself, weakening it and predisposing to rupture. Attritional changes secondary to development of bony spicules and osteophytes may also contribute to rupture.

Crystalline deposition

Precipitation of crystalline material within the tendon sheath results in a tenosynovitis that is often difficult to differentiate from that caused by infectious processes. Gout is one of the more common crystalline deposition disorders. It represents a dysfunction of urate metabolism, and overproduction of uric acid may cause buildup of monosodium urate crystals in the peripheral tissues. Attempted phagocytosis of this material by immune cells results in a severe inflammatory response characterized by pain, swelling, and erythema of the digit.

A similar process is seen in pseudogout (calcium pyrophosphate disease [CPPD]), in which calcium pyrophosphate dihydrate accumulates and may also cause an acute inflammatory response. Calcific tendinitis is characterized by the accumulation of calcium salts within the synovial sheaths in a manner resembling calcium deposition into the joint spaces of the hip, knee, elbow, and shoulder. The cause of calcium deposition has not been identified but is known not to be related to hypercalcemia.

Accumulation of beta-microglobulin is known as amyloidosis. This can be secondary to known enzymatic dysfunction but is more commonly associated with accumulation secondary to hemodialysis.



Infectious tenosynovitis

In cases of infectious tenosynovitis—specifically, PFT—an organism is most commonly introduced directly into the tendon sheaths through a palmar-side puncture wound, bite, or laceration, often occurring a day or days prior to presentation. Local spread from an adjacent soft-tissue infection (eg, felon, paronychia, or abscess) may also occur. Hematogenous spread as a result of bacteremia is rare but does occur in cases of gonococcal tenosynovitis.

Infectious tenosynovitis results from an infectious agent using the nutrient-rich synovium as a growth medium and multiplying within the closed space of the flexor tendon sheath. Natural immune response mechanisms cause swelling and migration of inflammatory cells and mediators. The septic process and this inflammatory reaction within the tendon sheath quickly interfere with the gliding mechanism, leading to adhesions and scarring. If this is left untreated, consequences include tendon necrosis, disruption of the tendon sheath, and digital contracture. [10, 4]

Predisposing factors for PFT include diabetes mellitus, IV drug abuse, and arteriosclerosis obliterans.

Identification of the causative organism not only influences antibiotic selection but also provides prognostic value, in that polymicrobial infections generally have a worse prognosis. [11]  The following is a list of potential causative agents:

  • Staphylococcus aureus - Most commonly isolated bacteria, associated with ~80% of infections
  • Streptococcus species - Second most commonly isolated bacteria [12]
  • Pasteurella multocida - High index of suspicion if the infection develops within 24 hours after a cat bite
  • Eikenella corrodens - Higher incidence with human bite wounds ( Staphylococcus and Streptococcus species still most common causes)
  • Anaerobes ( Bacteroides and Fusobacterium species most common)
  • Haemophilus species
  • Capnocytophaga canimorsus - Infrequently isolated after dog bites
  • Mycobacterium tuberculosis and other Mycobacterium species - Suspected in chronic, more indolent infections [13, 14, 15]
  • Clostridium difficile - Case report following antibiotic treatment for ear infection in a child [16]
  • Pseudomonas aeruginosa
  • Listeria monocytogenes
  • Vibrio vulnificus - Present in marine environments
  • Fungus (eg, Cryptococcus species and  Histoplasma capsulatum) - Consider atypical pathogens in immunocompromised individuals [17]
  • Virus - Case report involving Chikungunya virus–related rheumatism [18]

Infectious flexor tenosynovitis most often occurs after a preceding puncture injury; it rarely occurs from hematogenous spread. Gonococcal infection with Neisseria gonorrhoeae affords one example of tenosynovitis occurring via bacteremia. It originates as a mucosal infection of the genital tract, rectum, or pharynx. Dissemination occurs in ~1-3% of patients with mucosal infection, and about two thirds of patients with disseminated infection develop tenosynovitis. Along with septic arthritis, gonococcal tenosynovitis may occur in isolation without symptoms consistent with dissemination. [19]  Although it more commonly affects the flexor tendons of the hand, involvement of the extensor tendons has been reported. [20]

Idiopathic or stenosing tenosynovitis

Symptoms of idiopathic or stenosing tenosynovitis (eg, trigger finger or de Quervain tenosynovitis) result from a mismatch in diameter between the tendon and its retinacular sheath. Narrowing of the retinacular space causes impingment on the tendon prevening normal tendon gliding. Although this form of tenosynovitis is often referred to as an overuse syndrome, many patients report no change in activity preceding the onset of symptoms; thus, it is frequently idiopathic. Multiple studies have been unable to find associations between certain occupations and trigger digits. The exact mechanism by which narrowing of the sheath occurs is not entirely understood but is most certainly multifactorial. [21]

Inflammatory tenosynovitis

The term inflammatory tenosynovitis, in this context, refers to a noninfectious inflammatory process within the space of the tendon sheath. This can be secondary to autoimmune disorders (eg, RA and psoriatic arthritis) or crystalline deposition disorders (eg, gout, CPPD [pseudogout], and amyloidosis). Local inflammation involving the tendon and tendon sheath will often produce a profound swelling with resulting pain, stiffness, and contracture.

RA is characterized by inflammation of synovial tissue with erosion of the small joints. Similar proliferation of inflammatory tissue within the tendon sheath (also synovium-lined) may lead to a progressive tenosynovitis. Involvement of the tendon sheath has been argued to be a hallmark feature of the disease and is symptomatically present in a majority of patients, [22]  with an even greater number having subclinical evidence of tenosynovitis on magnetic resonance imaging (MRI). [23, 24, 25]

Gout, another form of inflammatory tenosynovitis, is due to crystalline deposition secondary to a defect of uric acid metabolism. Overproduction of uric acid leads to deposition of monosodium urate in the peripheral tissues. Phagocytosis of this foreign material and lysomal release lead to a profound inflammatory response. Classically, the small joints of the hand and feet are involved, though tenosynovitis is a described extra-articular manifestation of the disease. [26, 27]  

CPPD (pseudogout) clinically resembles gout, though it is thought to be due to excessive production of pyrophosphate in the cartilage. Precipitation of calcium pyrophosphate crystals in the tendon-sheath complex may also rarely result in a tenosynovitis. [28, 29]

Amyloidosis [30] and calcific tendinitis [31] are two other forms of crystalline deposition–related tenosynovitis.



The incidence and prevalence of tenosynovitis are closely to the underlying pathologic process and are of little use to the clinician without subdivision. Below are epidemiologic considerations for the various forms of tenosynovitis.

Infectious tenosynovitis

Infectious tenosynovitis has been reported to account for 2.5-9.4% of all hand infections. The possibility of concomitant infection is much higher when there evidence to suggest inoculation of the tendon sheath. Infectious tenosynovitis via hematogenous spread is limited to isolated case reports, usually as part of a disseminated gonoccocal infection (DGI). DGI more commonly results in septic arthritis, affecting approximately 40% of cases. There are isolated reports of septic arthritis and tenosynovitis occurring without evidence of prior dissemination. [19, 20]   

Idiopathic or stenosing tenosynovitis

Trigger finger is a common hand condition, with a reported prevalence of 2% in the general population. [32]  This frequency increases by fivefold or more in individuals with diabetes mellitus. [33]  The incidence of trigger digits has a bimodal distribution, with a peak in childhood and a second peak in middle age. In adults, there is a female predilection, and the ring finger is the digit most commonly affected. [9, 34]  De Quervain tenosynovitis is historically reported in lactating mothers. One large population study determined the incidence to be 0.94 per 1000 person-years. [35]  Female sex, age greater than 40 years, and black race were all found to be risk factors for development.

Inflammatory tenosynovitis

Involvement of the tendon sheath is a common feature of rheumatoid hand disease. Gray et al found that approximately 55% of patients with RA reported symptoms of tenosynovitis, affecting an average of 3.1 tendons. [36]  Prior reports of tendon involvement probably underrepresented the true incidence, and as many as 87% of patients have radiographic evidence of tenosynovitis on MRI. [23, 24, 25]

Although psoriasis is uncommon, the prevalence of psoriatic arthritis among those with psoriasis is between 6% and 41%. Tenosynovitis has been postulated as a transition between psoriasis and psoriatic arthritis. [37]  

True tendon involvement in crystalline deposition disorders is rare. Development of tophi and osteophytes may cause irritation of tendons and affect proper gliding.



Infectious tenosynovitis

Cases of PFT in healthy patients that present early have a favorable prognosis. Patients with fulminant infection, those with chronic infection, and those with impaired immune status are at increased risk for long-term complications and impairment.

The most common complication in PFT is digit stiffness secondary to adhesions. If loss of functional motion persists, tenolysis is considered after a period of rehabilitative hand therapy. One study showed improvement between the 6-week postoperative evaluation and 3-month follow-up. The second major complication is soft-tissue necrosis, which is more commonly seen in patients with delayed presentation or in those with diabetes. For either of these reasons, amputation may be pursued either at the time of the initial infection of if the digit has become nonfunctional, stiff, and painful.

An intial study of outcomes by Maloon et al [38] found that the following were associated with poor outcome:

  • Presence of diabetes mellitus
  • Late presentation
  • Association with a human bite

Pang et al later conducted a review of 75 patients with PFT and found that the risk of amputation was related to the following [11] :

  • Age greater than 43 years
  • Presence of diabetes mellitus, renal failure, or peripheral vascular disease
  • Ischemic changes at the time of presentation
  • Subcutaneous purulence
  • Polymicrobial infections

Prognosis in this study was closely related to the presence of digitial ischemia. [11] Without ischemic changes, amputation was rare. Total active range of motion (ROM) was 72% vs 80%, depending on the presence of subcutaneous purulence. Those with both subcutaneous purulence and ischemic change underwent amputation in 59% of cases and recovered only 49% of their total active ROM.