Updated: Jan 06, 2021
Author: Christopher S Crowe, MD; Chief Editor: Harris Gellman, MD 


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. 




General considerations

The history and examination will guide the differential diagnosis of tenosynovitis. Acute pathologies (eg, pyogenic flexor tenosynovitis [PFT] and gout) will often be seen in the emergency department (ED). More indolent or progressive pathologies will often be seen in the clinic. Regardless of setting, a thorough history should be gathered as part of any hand evaluation.

Handedness, occupation, vocations, and functional status should all be ascertained during the patient interview. When infectious etiologies are under consideration, the past medical history should focus on the presence of diabetes mellitus, immunosuppression, peripheral vascular disease, renal disease, smoking status, and injection drug use. When inflammatory tenosynovitis is being considered, determine if the patient has a prior diagnosis, presence of arthritis, or other sites of tendinitis. The onset of symptoms should be estimated as accurately as possible.

Infectious tenosynovitis

Patients may describe antecedent trauma in the form of a puncture wound, laceration, or bite, though no obvious injury may be reported. Often, patients will describe progressive pain, swelling, stiffness, and erythema along the affected finger. Fever was infrequent (17%) in one large study, and no patients had signs of systemic infection.[11]  

Gonococcal flexor tenosynovitis most commonly affects sexually active teenagers and young adults. It is more common in women, especially during pregnancy or after menstruation, when systemic dissemination of gonorrhea is more likely to occur. Features of gonococcal tenosynovitis include the following:

  • The interval from sexual exposure to onset of symptoms of dissemination can range from 1 day to several weeks
  • Vaginal or penile discharges are usually absent
  • Fever, chills, malaise, and polyarthralgias are common
  • The most commonly affected sites are the dorsum of the wrist, hand, and ankle

Idiopathic or stenosing tenosynovitis

Patients with early development of trigger digits may describe a painless clicking with passive digit motion that generally improves throughout the day. With disease progression, patients may describe painful catching or locking of the digit into flexion. This may or may not require passive extension with the contralateral hand to "unlock" the affected digit. This phenomenon is related to the powerful flexor's ability to overcome a stenotic sheath (and the extensor's inability to generate the necessary force to unlock the digit). In severe delayed cases, prolonged locking of the digit can lead to secondary contractures. 

The primary symptom of de Quervain tenosynovitis is pain along the thumb radial wrist that often radiates proximally and is typically gradual in onset. Pain is usually worse with power grip and weightbearing with the wrist in the neutral position. Swelling may be noted adjacent to the radial styloid. Crepitus and frank triggering are rarely reported. Classically, de Quervain tendinitis may afflict new mothers who are repeatedly lifting newborns and infants.

Inflammatory tenosynovitis

The presentation of inflammatory tenosynovitis is typically more indolent and progressive fashion than that of infectious tenosynovitis. However, it may sometimes mimic that of an infection, which may be further complicated if the patient has no prior diagnosis (eg, gout or rheumatoid arthritis [RA]). Reported symptoms are similar to those of other types of tenosynovitis and include digital stiffness, swelling, and, in some instances, frank triggering. When an acute inflammatory response is present, the digit may be erythematous. Gout can be severe enough in some cases to cause malaise or even low-grade fever. 

Physical Examination

Infectious tenosynovitis

Patients with PFT can present at any time after a penetrating injury. Initial inspection may reveal an erythematous, swollen digit. The patient may guard the hand because of exquisite tenderness and may be resistant to demonstrating active motion. Kanavel signs are observed with varying frequency and include the following:

  • Semiflexed digit at rest
  • Uniform swelling of the entire digit
  • Tenderness along the flexor tendon sheath
  • Exquisite pain along the volar surface of the digit with passive extension

The presence of these signs and their routine use to confirm a diagnosis of flexor tenosynovitis has been a topic of debate. Whereas uniform swellling is a sensitive finding,[11] other infectious and inflammatory processes also cause diffuse swelling; therefore, this finding may not differentiate cellulitis or dorsal finger abscesses from PFT.[39] ​ Some authors believe pain with passive extension to be the most reproducible sign[40] ; others have not found this to be the case.

More recent study has shown that these signs have considerable sensitivity but lack specificity on an individual basis.[39] Furthermore, these signs may be entirely absent in cases of early presentation, chronic infection, immunocompromise, or recent antibiotic administration.

One critical misunderstanding has to do with so-called fusiform swelling. The term fusiform refers to a spindle-shaped enlargement that is often seen in patients with rheumatoid tenosynovitis.[39] Kanavel never used this term to describe the swelling encountered in PFT, instead describing it as uniform.[39] This point becomes clinically relevant insofar as it may provide the clinician with a subtle feature that can differentiate between causes of tenosynovitis.

Additional clinical features of gonococcal tenosynovitis include the following:

  • Fever is common
  • Dermatitis is also common (occurring in approximately two thirds of disseminated gonococcal tenosynovitis cases); it is characterized by hemorrhagic macules or papules on the distal extremities or trunk

Idiopathic or stenosing tenosynovitis

Trigger digits are often confirmed by replicating the describe locking of the affected finger. If popping or locking cannot be demonstrated on active or passive flexion of the digit, then the examination becomes slightly more nuanced. A nodule, representing focal swelling of the tendon proximal to the A1 pulley, may be palpated in the palm. 

Patients with de Quervain tenosynovitis will typically have swelling at the first dorsal comparment. Palpation of the retinaculum is painful. Two eponymous tests have been described to aid with diagnosis and will generate characteristic pain at the first dorsal compartment[41] :

  • The Finkelstein maneuver is performed by having the patient passively deviate the wrist ulnarly; the thumb is then grasped by the examiner and flexed into the palm
  • The Eichoff maneuver (see the image below) is performed by having the patient close the fist around a flexed thumb; the wrist is then passively deviated ulnarly by the examiner
Eichoff test is performed by having patient make f Eichoff test is performed by having patient make fist with thumb inside fingers. Clinician then applies ulnar deviation of wrist to reproduce presenting symptoms of dorsolateral wrist pain.

One study using asymptomatic volunteers found the Eichoff maneuver to generate more false positives.[42]  

Inflammatory tenosynovitis

As mentioned previously, inflammatory flexor tenosynovitis usually is the result of an identifiable underlying disease process. Findings similar to those found in PFT may eventually present. In inflammatory flexor tenosynovitis, swelling is the most common initial finding. The hallmark of this condition is a difference in active, as opposed to passive, flexion. As the tissue expands and impingement occurs, pain and restricted motion ensue. Delayed presentations can have the appearance of fulminant flexor tenosynovitis with all Kanavel signs or may involve tendon rupture if the patient delays seeking treatment long enough.

Patients with RA will most frequently have involvement of the small joints (eg, metacarpophalangeal [MCP], proximal interphalangeal [PIP], or metatarsophalangeal [MTP] joints). It may be difficult to distinguish articular findings from tenosynovitis. Rheumatoid nodules may be present in 25% of those with RA, fewer in the first year of their disease progression. Tenosynovitis may frequently involve the extensor tendons. 



Diagnostic Considerations

The primary diagnostic consideration is differentiating between infectious and noninfectious causes of tenosynovitis. Below are other conditions whose presentations may overlap with that of pyogenic flexor tenosynovitis (PFT).

Differential Diagnoses



Approach Considerations

Pyogenic flexor tenosynovitis (PFT) represents an orthopedic emergency; tenosynovitis from other causes can undergo a less urgent workup. All patients with suspected flexor tenosynovitis should be transferred to a center capable of specialty evaluation and should be evaluated upon presentation to the emergency department (ED). For patients whose presentations are unclear or who are thought to have early infection, judicious use of nonsurgical management can be initiated and repeat evaluation performed in 6-12 hours.

Laboratory Studies

A complete blood count (CBC) with differential is appropriate when there is concern for systemic illness. Characteristics include the following:

  • White blood cell (WBC) count is generally within the normal range for isolated hand infections, though it may be elevated in the presence of progessive infection or systemic involvement
  • WBC count is generally not elevated in nonsuppurative conditions and in immunocompromised patients
  • Left shift is frequently observed in acute processes

The erythrocyte sedimentation rate (ESR) and the C-reactive protein (CRP) level are nonspecific inflammatory markers that may be obtained and followed to determine response to treatment. These will also frequently be normal in closed-space infections of the hand.

Creatinine will provide information about renal function, which may have an impact on antibiotic selection.

Coagulation studies are needed in anticoagulated patients or in patients with a known or suspected bleeding diathesis. In severe infections where systemic sepsis is a concern, disseminated intravascular coagulation (DIC), though quite rare, must be ruled out.

Rheumatoid factor (RF) should be tested for if rheumatoid arthritis (RA) is a consideration.

If the patient is febrile or has any degree of vital instability, blood cultures should be drawn and sent before antibiotic therapy is initiated.

Gonococcal cultures of the urethra or cervix, rectum, and pharynx are appropriate if gonococcal tenosynovitis is suspected. One of these cultures is positive in approximately 80% of patients. In addition, transiently elevated liver function studies (LFTs) have been described with disseminated gonococcal infection.

Imaging Studies

Standard anteroposterior and lateral radiographs should be obtained to rule out bony involvement (eg, osteomyelitis, arthritis, or unrecognized trauma) or a foreign body.[43]

Magnetic resonance imaging (MRI) has proved accurate in assisting in the diagnosis of tenosynovitis.[44] It is expensive and generally unnecessary, in that the diagnosis is usually clinically evident.

Aspiration and Evaluation of Joint Fluid

Aspiration of synovial fluid will allow microbiologic and histopathologic analysis of the fluid. Culture and gram stain should ideally be obtained before the initiation of definitive antibiotic therapy and typically includes aerobic, anaerobic, fungal, acid-fast bacilli (AFB), and atypical AFB samples. Histopathologic analysis of synovial fluid may show nonbirefringent crystals (gout) or birefringent crystals (calcium pyrophosphate disease [CPPD; pseudogout]).

Diagnostic arthrocentesis is indicated when joint effusion is present with tenosynovitis because most patients with disseminated gonococcal infection have coexistent septic arthritis. (Most gonococcal arthritis is monoarticular; ~25% of cases are polyarticular.) Characteristics of the aspirated fluid can include the following:

  • Sterile fluid is common with gonococcal arthritis; cultures are negative in 50% of patients
  • Joint fluid glucose is usually normal.
  • WBC counts are usually below 50,000/μL
  • A Gram stain is positive in only 25% of patients

Histologic Findings

Histopathologic examination of synovial biopsy specimens is helpful in diagnosing granulomatous changes observed in Mycobacterium infections and in cases of chronic processes.

Synovial biopsy may reveal acute or chronic inflammatory changes. These histologic findings help to confirm a diagnosis of inflammatory arthropathy.[45] Gram stains may reveal bacteria. A higher index of suspicion should be present for chronic infections or atypical presentations.



Approach Considerations

Nonoperative management

Naturally, treatment for tenosynovitis will depend entirely on the etiology of inflammation. Nonoperative management is frequently pursued for nonsuppurative flexor tenosynovitis, but surgical intervention may be indicated for chronic conditions. 

Infectious flexor tenosynovitis, however, remains an orthopedic emergency, and there is a very narrow indication for trialing nonoperative management. Accordingly, many surgeons recommend early operative drainage in all cases. Nevertheless, the current literature demonstrates that medical treatment can be pursued for early, uncomplicated infections. Prompt improvement of symptoms and physical findings must follow within the ensuing 12 hours; otherwise, surgical intervention is necessary.

Surgical management

In instances of delayed presentation or progressive infection, prompt operative exploration and irrigation of the tendon sheath are warranted. Several approaches to access the flexor tendon sheath have been described. In general, these either provide wide exposure of the sheath or attempt to access the space via minimally invasive incisions distally and proximally. For Michon stage I (accumulation of exudative fluid in tendon sheath) and stage II (purulent fluid, granulomatous synovium) flexor tenosynovitis, either approach can be used. Strong evidence and widespread agreement support wide exposure of Michon stage III infections (necrosis of the tendon, pulleys, or tendon sheath).

Dailiana et al, in a retrospective study of 41 patients with purulent flexor tenosynovitis, found that the best functional outcome associated with this condition resulted from early diagnosis, drainage through small incisions, and continuous postoperative irrigation; worse outcomes resulted in cases of delayed treatment and infections with specific pathogens.[46]  Staphylococcus aureus was detected in most cases. Some surgeons still advocate radical tenosynovectomy for Mycobacterium infections, whereas others prefer partial tenosynovectomy with a multiple antibiotic regimen and close observation.

Pharmacologic and Noninvasive Therapy

Infectious tenosynovitis

Prompt medical management of acute infectious flexor tenosynovitis (ie, pyogenic flexor tenosynovitis [PFT]) may preclude the need for immediate surgical intervention. Nonoperative treatment for infectious flexor tenosynovitis includes the following:

  • If possible, aspiration of synovial fluid from the flexor sheath for gram stain and culture through noncellulitic skin
  • Broad-spectrum intravenous (IV) antibiotics initially, culture-directed narrowing with resolution of infection
  • Elevation of the affected hand
  • Splinting in “position of safety”
  • Rehabilitation, inlcuding digital range-of-motion (ROM) exercises and edema control, once infection is under control

If the diagnosis is equivocal, consultation with a hand specialist (eg, from plastic surgery or orthopedic surgery) and the use of elevation and broad-spectrum antibiotics that include staphylococcal coverage, streptococcal coverage, or both are necessary. Addition of anaerobic coverage is warranted if anaerobic infection is likely (eg, in cases of bite injury). Empiric antibiotics for penetrating trauma and infection should be guided by hospital antibiograms.

For immunocompromised or diabetic patients, early surgical intervention is warranted. If medical treatment alone is attempted, then inpatient observation for at least 48 hours is indicated. Surgical drainage is necessary if no obvious improvement has occurred within 12-24 hours.

Gonococcal tenosynovitis

The patient should be admitted to the hospital with IV or intramuscular (IM) antibiotics (eg, ceftriaxone or spectinomycin). Surgical drainage may be indicated if antibiotic therapy does not significantly improve the patient’s condition within 48 hours.

Idiopathic or stenosing tenosynovitis

The mainstay of therapy for tenosynovitis caused by stenosing conditions is cessation of the insult through modification of activity. 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 utilized, splinting should be limited in area to a pain-free ROM
  • Rehabilitation - Slow rehabilitation prevents reinitiation of the inflammatory phase

Caution must be exercised with corticosteroid injections, because they are detrimental if done directly into the tendon or ligament. Multiple injections also can weaken the tendon and lead to rupture in patients with diabetes or inflammatory arthritis (eg, rheumatoid arthritis [RA]). Therefore, corticosteroid injections should be used with particular care in patients with these conditions. Also, the use of injectable or oral steroids is contraindicated if infectious flexor tenosynovitis has not been completely ruled out.

De Quervain tenosynovitis

For patients with minimal symptoms rest, NSAIDs, and a thumb spica wrist splint should be prescribed.[47]

Peritendinous lidocaine-corticosteroid injection is considered by many to be the initial treatment of choice for de Quervain tenosynovitis. One review of the literature showed corticosteroid treatment to have a cure rate of greater than 80% and concluded that corticosteroid injection is safe.[48] Surgical therapy is an option if conservative management fails.[49]

A study examined injections of triamcinolone for de Quervain tenosynovitis and found an 89% efficacy rate for the drug.[50] In this report, patients could receive a maximum of three injections 2 weeks apart. A favorable result was measured by a questionnaire indicating no disruption in daily life.

One retrospective review concluded that in patients with more than minimal symptoms in de Quervain tenosynovitis, steroids are superior to NSAIDs and splinting.[51]

Trigger digits

Peritendinous lidocaine-corticosteroid injection is the initial treatment of choice for trigger finger.[52] In a randomized trial, patients with this condition who were treated with corticosteroid injection showed a greater reduction in pain severity and frequency of triggering than did patients treated with placebo. The short-term effects were maintained during a 12-month follow-up phase.[53]

In a double-blind randomized controlled study from Taiwan that compared ultrasound-guided injection of hyaluronic acid with steroid injection in 36 patients with trigger finger (39 digits), Liu et al found that the former treatment yielded promising results for the treatment of this condition, though optimal regimens remained to be defined.[54]

Treatment also includes activity modification (ie, avoidance of activities that cause triggering) and NSAIDs. Splinting is another treatment modality that has been studied. This is appropriate for patients who do not want to have a steroid injection.

Surgical tendon release should be considered if injection fails. Surgical release for trigger finger has success rates higher than 90%.

Inflammatory flexor tenosynovitis

Nonoperative management is the primary treatment for inflammatory tenosynovitis. In patients refractory to at least 3-6 months of good medical management or in patients with tendon ruptures, flexor tenosynovectomy should be performed.

Treatment for rheumatoid inflammatory flexor tenosynovitis includes ice, NSAIDs, rest, splinting, hydroxychloroquine, gold, penicillamine, and methotrexate. Persistent cases may require oral steroid treatment. For acute flares of flexor tenosynovitis in patients with RA, corticosteroid injections may provide prompt relief. Injections should be limited so as to avoid tendon rupture.[55]

Drainage, Irrigation, and Tenosynovectomy

Infectious tenosynovitis

Several drainage techniques can be used in PFT. The choice of method is based on the extent of the infection. The Michon classification scheme can be a helpful guide in surgical intervention (see Table 2 below).

Table 2. Treatment of Infectious Tenosynovitis According to Michon Stage (Open Table in a new window)

Infection Stage

Characteristic Findings



Increased fluid in sheath, mainly serous exudate

Catheter irrigation


Purulent fluid, granulomatous synovium

Minimal invasive drainage ± indwelling catheter irrigation


Necrosis of tendon, pulleys, or tendon sheath

Extensive open débridement and possible amputation

Most current recommendations for stage I and stage II infections advocate proximal and distal incisions for adequate drainage and irrigation.

The proximal incision is made over the A1 pulley. If the radial or ulnar bursa is the suggested point of tenosynovitis, the incision should be made just proximal to the transverse carpal ligament. In the digit, either a standard Brunner incision or a midaxial incision may be utilized.

The distal incision is made over the region of the A5 pulley. If the midaxial approach is taken, the incision should be dorsal to the neurovascular bundle. A Brunner incision allows better initial exposure but may complicate closure or coverage if skin necrosis ensues and is more likely to interfere with therapy postoperatively.

A 16-gauge polyethylene catheter or a 3.5- to 5-French feeding tube then is inserted into the tendon sheath through the proximal incision. The sheath is copiously irrigated with a minimum of 500 mL of normal saline. Excessive fluid extravasation into the digit must be avoided because it can result in necrosis of the digit.

The catheter can be loosely sewn in or simply removed after irrigation. A small drain is placed in the distal incision, and the wounds are left open. A splint is applied, the hand is elevated, and the appropriate empiric antibiotic coverage is started while the clinician awaits culture results.

Some clinicians prefer the continuous irrigation technique over a period of 24-48 hours. The catheter is sewn in place, and a small drain is secured at the distal incision site. Either continuous irrigation with sterile saline at a rate of 25 mL/hr or intermittent irrigation every 2-4 hours with 25-50 mL of sterile saline may be performed; the two techniques are equally effective.[56, 57, 58]

Indications for open tendon sheath débridement include the following:

  • Stage III infections
  • Chronic infections
  • Infections caused by atypical mycobacteria

To expose the tendon sheath, a volar zigzag Brunner incision or a longitudinal midaxial incision is made. The midaxial incision is preferred because of postoperative coverage concerns. The thumb and small fingers are approached from the radial side; the other digits are approached from the ulnar side. The incision begins distally at the level of the A5 pulley, or just distal to the distal flexion crease, and is extended proximally to the web space. The incision is kept dorsal to the neurovascular bundle.

For extensive infections, the sheath may be opened at all of the cruciform pulleys with preservation of the anular pulleys, especially the A2 and A4 pulleys. If the small finger or thumb is involved and there is evidence of proximal involvement, an additional incision, proximal to the transverse carpal ligament, is made to ensure adequate drainage of the radial and ulnar bursae.

The sheath is copiously irrigated, and the wounds are left open with drains in place. Empiric antibiotics are started. The hand is dressed and splinted, and the wounds are reevaluated after 48 hours. If the infection has abated, the drains are removed and postoperative therapy is initiated. If the infection is not controlled, repeat irrigation and débridement are necessary.

For Mycobacterium infection, extensive tenosynovectomy may be necessary, depending on the chronicity of infection.

Idiopathic or stenosing tenosynovitis

Release of the A1 pulley may be performed in cases not amenable to steroid injection. Percutaneous approaches have been described, though these place the neurovascular bundle at risk in that the bundle cannot be directly visualized during transection of the pulley. In an open approach, a small incision is made at the metacarpophalangeal (MCP) crease palmarly. Dissection proceeds down to the level of the A1 pulley. Neurovascular bundles are retracted away if encountered, and the A1 pulley is completely sectioned. The digit should be passively and actively flexed to ensure full release.

Inflammatory tenosynovitis

For inflammatory tenosynovitis, extensive volar Brunner incisions are typically used to perform a tenosynovectomy. The diseased tenosynovium is excised, while the anular pulleys are carefully preserved.

Postoperative Care

Infectious tenosynovitis

In the case of PFT, remove the dressing, splint, and drains, and inspect the wounds approximately 24-48 hours after surgery. Initiate active and passive ROM exercises, as well as soapy soaks or whirlpool treatments. Usually, a removable splint is fabricated and elevation is continued.

For persistent infection, repeat operative débridement may be required. IV antibiotics should continue for an additional 48-72 hours; the length of IV antibiotic treatment is determined by the culture and sensitivity results and by specific patient factors. The switch from IV to oral antibiotics should be based not only on culture results but also on the clinical examination and patient progress. Oral antibiotics should be continued for 5-14 days, depending on the following:

  • Intraoperative findings
  • Comorbidities
  • Organism isolated
  • Response to therapy

Generally, the wounds should be left open so they can heal promptly by secondary intention. Delayed primary closure is not needed.

Inflammatory tenosynovitis

During the postoperative course of tenosynovectomy performed for inflammatory tenosynovitis, remove the patient’s bandage, splint, and drain (if used) at 24-48 hours post surgery. At that time, an intrinsic plus resting splint is fabricated. Wounds are fully closed at the time of the index procedure. Sutures can be removed 7-14 days postoperatively, depending on the condition of the rheumatoid skin.


Consultations and referrals may include the following:

  • Primary care or hand specialty outpatient referral for follow-up care of de Quervain tenosynovitis and trigger finger
  • Emergency medical or hand specialty consultation for suspected gonococcal tenosynovitis for hospital admission and IV antibiotics
  • Emergency hand specialty consultation for nongonococcal infectious tenosynovitis for hospital admission, IV antibiotics, and possible surgical drainage

Long-Term Monitoring

For infectious tenosynovitis, provide follow-up 72 hours after IV antibiotics have been stopped to ensure that the oral regimen is adequate and that no relapse of infection has occurred. Follow-up should continue until the infection has resolved, the wounds are closed, and full motion has returned. Monitor the patient until pain-free motion and strength have been maximized.

For inflammatory tenosynovitis, hand therapy is started at 24-48 hours after the procedure and should consist of gentle active ROM exercises, along with swelling and pain modalities. Near-full active ROM can be achieved by around 3 weeks, after which time cautious strengthening can be added. However, it is not uncommon for progress to be slow, resulting in a rehabilitation course lasting 3-4 months.



Medication Summary

The goals of tenosynovitis therapy are to reduce pain and eradicate infection. Initial treatment for suspected infectious FT may include IV antibiotics if the patient presents very early.

In inflammatory tenosynovitis resulting from an entrapment, NSAIDs can be administered if tolerated by the patient. Flexor tendon sheath or carpal tunnel corticosteroid injections can be administered to decrease pain and the inflammatory response. However, corticosteroid injections should be used with caution, as they are detrimental if injected directly into the tendon or ligament. Multiple injections also can weaken the tendon and lead to rupture in patients with diabetes or inflammatory arthritis.

Pharmacologic treatment for rheumatoid inflammatory tenosynovitis includes NSAIDs, hydroxychloroquine, gold, penicillamine, and methotrexate. Persistent cases may require oral steroid treatment. For acute flares of FT in patients with rheumatoid arthritis, corticosteroid injections may provide prompt relief.

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

Class Summary

NSAIDs are most commonly used for the relief of mild to moderate pain. Although the effects of NSAIDs in pain treatment tend to be patient specific, ibuprofen usually is the drug of choice (DOC) for initial therapy. Other options include fenoprofen, flurbiprofen, mefenamic acid, ketoprofen, indomethacin, and piroxicam. NSAIDs are primarily used for de Quervain and volar flexor tenosynovitis.

Ibuprofen (Motrin, Advil, NeoProfen)

This agent inhibits inflammatory reactions and pain, probably by decreasing the activity of the enzyme cyclooxygenase (COX), in this way inhibiting prostaglandin synthesis. Ibuprofen is usually the DOC for the treatment of mild to moderate pain if no contraindications exist.

Naproxen (Anaprox, Naprelan, Naprosyn, Aleve)

Naproxen is used for the relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing the activity of the enzyme COX.


Ketoprofen inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis. Smaller initial dosages are particularly indicated in elderly patients and in those with renal or liver dysfunction. Doses higher than 75 mg do not improve the therapeutic response and may be associated with a higher incidence of adverse effects.


Meclofenamate inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis. Compared with other NSAIDs, it is associated with a higher incidence of diarrhea.

Mefenamic acid (Ponstel)

Mefenamic acid inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis. Compared with other NSAIDs, it is associated with a higher incidence of diarrhea.


Flurbiprofen may inhibit cyclooxygenase, thereby inhibiting prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.

Fenoprofen (Nalfon)

Fenoprofen decreases the formation of prostaglandin precursors by inhibiting cyclooxygenase 1 and 2 enzymes. It may also inhibit neutrophil aggregation/activation, inhibit chemotaxis, alter lymphocyte activity, and decrease proinflammatory cytokine levels.


Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Ceftriaxone (Rocephin)

Ceftriaxone is a third-generation cephalosporin that has a broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. By binding to 1 or more of the penicillin-binding proteins, it arrests bacterial cell wall synthesis and inhibits bacterial growth. Ceftriaxone is used because of an increasing prevalence of penicillinase-producing N gonorrhoeae.

Ciprofloxacin (Cipro)

This is a bactericidal antibiotic that inhibits bacterial DNA synthesis and (consequently) growth by inhibiting DNA-gyrase in susceptible organisms. The duration of treatment depends on the severity of the infection.

Ampicillin and sulbactam (Unasyn)

This drug combination uses a beta-lactamase inhibitor with ampicillin; it covers skin, enteric flora, and anaerobes. Ampicillin/sulbactam is used for the treatment of nongonococcal infectious tenosynovitis. Its coverage includes Staphylococcus and Streptococcus species, as well as anaerobes.


Cefazolin is a first-generation, semisynthetic cephalosporin that, by binding to 1 or more of the penicillin-binding proteins, arrests bacterial cell wall synthesis and inhibits bacterial growth. It is active primarily against skin flora, including Staphylococcus aureus. It is typically used alone for skin and skin-structure coverage. Cefazolin is administered for the treatment of suspected staphylococcal and/or streptococcal tenosynovitis (anaerobes not suspected).


Class Summary

These agents have anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids have profound and varied metabolic effects. In addition, these drugs modify the body's immune response to diverse stimuli.

Dexamethasone acetate (Baycadron)

This agent decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reducing capillary permeability. Dosage varies with the degree of inflammation and the size of the affected area.

Methylprednisolone acetate (Depo-Medrol, Medrol, Solu-Medrol, A-Methapred)

Methylprednisolone acetate decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Dosage varies with the degree of inflammation and the size of the affected area.

Hydrocortisone acetate (Solu-Cortef, Cortef, A-Hydrocort)

Hydrocortisone acetate decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Dosage varies with the degree of inflammation and the size of the affected area.


Questions & Answers


What is tenosynovitis?

What are the signs and symptoms of pyogenic flexor tenosynovitis (PFT)?

What are the signs and symptoms of noninfectious inflammatory tenosynovitis?

How is tenosynovitis diagnosed?

How is pyogenic flexor tenosynovitis (PFT) treated?

How are idiopathic and inflammatory flexor tenosynovitis treated?

What is the pathophysiology of pyogenic flexor tenosynovitis (PFT)?

What is the pathophysiology of idiopathic or stenosing tenosynovitis?

What is the pathophysiology of rheumatoid arthritis-related tenosynovitis?

What is the role of crystalline deposition in the pathophysiology of tenosynovitis?

What causes infectious tenosynovitis?

What causes idiopathic or stenosing tenosynovitis?

What causes inflammatory tenosynovitis?

What is the prevalence of tenosynovitis?

What is the prevalence of infectious tenosynovitis?

What is the prevalence of idiopathic or stenosing tenosynovitis?

What is the prevalence of inflammatory tenosynovitis?

What is the prognosis for infectious tenosynovitis?


Which clinical history findings are characteristic of tenosynovitis?

Which clinical history findings are characteristic of infectious tenosynovitis?

Which clinical history findings are characteristic of idiopathic or stenosing tenosynovitis?

Which clinical history findings are characteristic of inflammatory tenosynovitis?

Which physical exam findings are characteristic of infectious tenosynovitis?

Which physical exam findings are characteristic of idiopathic or stenosing tenosynovitis?

Which physical exam findings are characteristic of inflammatory tenosynovitis?


Which conditions are included in the differential diagnoses of tenosynovitis?

What are the differential diagnoses for Tenosynovitis?


What is the initial approach in the emergency department in cases of suspected tenosynovitis?

What is the role of lab tests in the workup of tenosynovitis?

What is the role of imaging studies in the workup of tenosynovitis?

What is the role of synovial fluid aspiration in the workup of tenosynovitis?

What is the role of arthrocentesis in the workup of tenosynovitis?

Which histologic findings are characteristic of tenosynovitis?


What are the nonoperative treatment options for tenosynovitis?

What is the role of surgery in the treatment of tenosynovitis?

How is infectious tenosynovitis treated?

What are the nonsurgical treatments for idiopathic or stenosing tenosynovitis?

How is De Quervain tenosynovitis treated?

How are trigger digits treated?

What are the nonsurgical treatments for inflammatory flexor tenosynovitis?

What are the surgical treatments for infectious tenosynovitis?

What are the surgical treatments for idiopathic or stenosing tenosynovitis?

What are the surgical treatments for inflammatory tenosynovitis?

What is included in the postoperative care following surgical treatment of infectious tenosynovitis?

What is included in the postoperative care following surgical treatment of inflammatory tenosynovitis?

Which specialist consultations are beneficial to patients with tenosynovitis?

What is included in the long-term monitoring of patients with infectious tenosynovitis?

What is included in the long-term monitoring of patients with inflammatory tenosynovitis?


What is role of medications in the treatment of tenosynovitis?

Which medications in the drug class Corticosteroids are used in the treatment of Tenosynovitis?

Which medications in the drug class Antibiotics are used in the treatment of Tenosynovitis?

Which medications in the drug class Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are used in the treatment of Tenosynovitis?