Tenosynovitis 

Updated: Aug 27, 2018
Author: Mark R Foster, MD, PhD, FACS; Chief Editor: Harris Gellman, MD 

Overview

Practice Essentials

Tenosynovitis is inflammation of a tendon and its sheath (see the image below). Most acute cases of flexor tenosynovitis (FT)—which involves disruption of normal flexor tendon function in the hand—result from infection. However, FT also can develop secondary to acute or chronic inflammation from a noninfectious cause, such as diabetes, overuse, or arthritis.

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

Cases of infectious FT that present early and have no comorbidities have a good prognosis, but patients with fulminant infection, chronic infection, or an impaired immune status have increased risk of long-term complications and impairment.

Signs and symptoms

Infectious tenosynovitis

Patients with infectious FT can present at any time following a penetrating injury, with complaints of pain, redness, and fever. Physical examination reveals Kanavel signs of flexor tendon sheath infection, which are as follows:

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

Clinical features of gonococcal tenosynovitis include the following:

  • Erythema, tenderness to palpation, and painful range of motion (ROM) of the involved tendon(s)
  • Fever - A common sign
  • Dermatitis - Also a common sign; it occurs in approximately two thirds of disseminated gonococcal infections; it is characterized by hemorrhagic macules or papules on the distal extremities or trunk

Inflammatory flexor tenosynovitis

  • Usually the result of an underlying disease process
  • Presentation is indolent but progressive if therapy is not initiated
  • Similar findings to those found in infectious FT eventually present
  • Swelling is the most common initial finding
  • Hallmark is a difference in active, versus passive, flexion
  • As the tissue expands and impingement occurs, pain and restricted motion ensue

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

See Clinical Presentation for more detail.

Diagnosis

If infection is suggested, culture of the suppurative synovial fluid is mandatory prior to beginning definitive antimicrobial treatment. 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, because most patients with disseminated gonococcal infection have coexistent septic arthritis.

Hematologic studies

  • Complete blood count (CBC)
  • Erythrocyte sedimentation rate (ESR)
  • Rheumatoid factor - If rheumatoid arthritis is a consideration

Biopsy

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

Imaging

Obtain standard anteroposterior and lateral radiographs to rule out bony involvement or a foreign body.[1]

See Workup for more detail.

Management

Infectious flexor tenosynovitis

Prompt medical management of acute nonsuppurative flexor tenosynovitis (FT) may preclude the need for surgical intervention. Nonoperative treatment for infectious FT includes the following:

  • IV antibiotics - May be included in initial treatment if the patient presents very early with suspected infectious FT
  • Elevation - Initially, until infection is under control
  • Splinting - In "safe position"
  • Rehabilitation - ROM exercises and edema control, initiated once FT is under control

Inflammatory flexor tenosynovitis

Nonoperative management is the primary treatment for inflammatory FT. The mainstay of therapy for FT caused by overuse syndromes is cessation of the insult by 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 used, splinting should be limited in area to a pain-free ROM
  • Rehabilitation - Slow rehabilitation prevents reinitiation of the inflammatory phase

Treatment for rheumatoid inflammatory FT includes ice, NSAIDs, rest, splinting, hydroxychloroquine, gold, penicillamine, and methotrexate.

Drainage

The indication for surgical drainage includes history and physical examination consistent with acute or chronic FT. In certain circumstances when acute FT presents within the first 24 hours of infection development, medical management may initially be used. Prompt improvement of symptoms and physical findings must follow within the ensuing 12 hours; otherwise, surgical intervention is necessary.

See Treatment and Medication for more detail.

Background

Tenosynovitis is inflammation of a tendon and its sheath. Most acute cases of flexor tenosynovitis (FT), which involves disruption of normal flexor tendon function in the hand, are the result of infection. However, FT also can develop secondary to acute or chronic inflammation from a noninfectious cause, such as diabetes, overuse, or arthritis. (See Pathophysiology and Etiology.)

Much of the original work on infectious FT was done by Kanavel. Septic FT is diagnosed if a patient presents with the four Kanavel signs, as follows (see Presentation and Workup):

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

Septic FT has the ability to rapidly destroy a finger's functional capacity and is considered an orthopedic emergency. (See Prognosis, Treatment, and Medication.)

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

Pathophysiology

Infectious flexor tenosynovitis

Infection can be introduced directly into the tendon sheaths through a skin wound (most often) or via hematogenous spread, as occurs with gonococcal tenosynovitis.

Infectious FT is a closed-space infection. Sheaths of the index, middle, and ring fingers run from the metacarpal neck at the level of the first annular (A1) pulley proximally to the insertion of the flexor digitorum profundus distally. The small finger and thumb sheaths are continuous with the ulnar and radial bursae in the palm, respectively (see the image below). Because the radial and ulnar bursae are contiguous, infections in either the small finger or the thumb are at risk of communicating and potentially progressing to the carpal tunnel.

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

Infection in any of the fingers may spread proximally into the wrist and forearm (Parona space). The initial infection also may move into the fascial spaces within the hand, adjacent osseous structures, or synovial joint spaces, or it may erode through the layers of the skin and exit superficially.

The tendon sheath is made up of an inner visceral layer and an outer parietal layer. Between the two layers is the synovial space, which is filled with synovial fluid. The visceral layer is in close approximation to the flexor tendon. The parietal layer is reinforced by a series of five annular pulleys (A1-5) and three cruciform pulleys (C1-3). The A2 and A4 pulleys are critical for flexor tendon function and should be avoided during surgical manipulation of the infected sheath. (See the image below.)

Location of annular and cruciform pulleys on the v Location of annular and cruciform pulleys on the volar finger.

With the accumulation of pus in flexor tendon sheath infections, pressure can increase within the closed-space compounds of the flexor tendon sheath, thus inhibiting the inflammatory response. In one study, eight of 14 patients with flexor tendon sheath infections had hand tendon sheath pressure in excess of 30 mg Hg. The increased pressure also inhibits blood flow and adds to the destructive process. Tendon ischemia increases the likelihood of tendon necrosis and rupture.

Flexor tendons of the fingers receive their nutrient supply from a combination of direct vascular sources and diffusion from synovial fluid. An avascular segment of the flexor digitorum superficialis has been found at the proximal phalangeal level. The flexor digitorum superficialis has two distinct vascular supplies, and three have been identified for the flexor digitorum profundus. As a result, the profundus has two avascular segments, which are located over the proximal and middle phalangeal regions.

Inflammatory flexor tenosynovitis

Inflammatory FT occurs through a process different from the one that produces infectious FT, though it can lead to similar complications. In inflammatory FT, proliferation of fibrous tissue occurs until there is impingement or constriction of the tendon and surrounding structures. The flexor tendons and the flexor retinaculum can create a tourniquet effect, producing distal swelling and pain. Nodularity of the tendons can lead to crepitus and sometimes frank triggering as the tendon becomes impinged adjacent to a thickened segment of the tendon sheath.[2, 3]

Overuse

Overuse syndromes go through predictive stages that can lead to FT. Overuse is defined as repetitive microtrauma that is sufficient to overwhelm the ability of the tissue to adapt. Pathologic stages of overuse include inflammation, proliferation, and, finally, maturation. They proceed as follows:

  • Inflammatory stage - Starts immediately following injury, with release of chemotactic and vasoactive substances; the resulting inflammatory cells create pain, swelling, erythema, and warmth; this stage can last from 48 hours to 2 weeks unless further injury occurs
  • Proliferative stage - Lasts up to 2 weeks and is characterized by the production of collagen and ground substances; the tendon is extremely vulnerable to injury during this period
  • Maturation stage - Lasts up to 12 weeks, during which time the healing phases are completed; unrestricted activity should be avoided until this stage is complete; if the inflammatory response is reinitiated at this time, fibrosis can result from repeated or continued release of inflammatory substances

Tendon rupture

Several causes of tendon rupture in rheumatoid arthritis (RA) exist. An attrition rupture may occur after the tendon has passed over roughened bony surfaces or has been eroded by chronic synovitis. The tendon also may be weakened by direct invasion of the rheumatoid tenosynovium or by ischemic necrosis secondary to surrounding pressures and diminished vascular supply.

Etiology

Noninfectious causes

Noninfectious causes of tenosynovitis include the following:

  • Diabetes mellitus [4, 5, 6]
  • RA [7]
  • Crystalline deposition
  • Overuse syndromes [8, 9]
  • Amyloidosis
  • Ochronosis
  • Psoriatic arthritis
  • Systemic lupus erythematosus
  • Sarcoidosis

Overuse injury

Overuse syndromes cause cumulative microtrauma to the tendon and tendon sheath. The protective inflammatory process paradoxically leads to tenosynovitis.[8, 9, 2, 3, 10]

In de Quervain tenosynovitis, overuse leads to thickening of the extensor retinaculum of the first dorsal compartment and narrowing of the fibro-osseous canal.

In volar flexor tenosynovitis (ie, trigger finger), overuse is thought to be the most common cause, but multiple etiologies have been identified. The triggering phenomenon is thought to be caused by hypertrophy of the first annular pulley.

Nongonococcal infectious tenosynovitis

Predisposing factors include diabetes mellitus, intravenous (IV) drug abuse, debility, and arteriosclerosis obliterans.

The primary inciting event of infectious FT usually is penetrating trauma, such as a bite wound.[11, 12] Hematogenous spread may occur. Infecting organisms include the following:

  • Staphylococcus aureus and Streptococcus species - The most common etiologic agents, but infection is frequently mixed (aerobic and anaerobic) [13]
  • 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 cause)
  • Anaerobes - Bacteroides and Fusobacterium species most common
  • Haemophilus species
  • Capnocytophaga canimorsus - Can infrequently be isolated after dog bites
  • Miscellaneous gram-negative organisms
  • Mycobacterium tuberculosis
  • Other Mycobacterium species
  • Clostridium difficile - Case reported following antibiotic treatment for ear infection in a child [14]
  • Pseudomonas aeruginosa
  • Listeria monocytogenes
  • Vibrio vulnificus - Stings from marine life

Mycobacterium

Several Mycobacterium species have been cultured following animal contacts or simple lacerations/puncture wounds, including the following:

  • M terrae
  • M marinum
  • M intracellulare
  • M avium
  • M kansasii
  • M asiatica
  • M bovis
  • M malmoense

Infection with Mycobacterium species may be suspected in chronic, more indolent infections. Late or missed diagnosis can lead to disastrous outcomes.[15, 16, 17]

Gonococcal tenosynovitis

Gonococcal infection from Neisseria gonorrhoeae originates as a mucosal infection of the genital tract, rectum, or pharynx. Dissemination occurs in approximately 1-3% of patients with mucosal infection. Approximately two thirds of patients with disseminated gonococcal infection develop tenosynovitis.

Pyogenic flexor tenosynovitis

Pyogenic FT results from an infectious agent multiplying in the closed space of the flexor tendon sheath and culture-rich synovial fluid medium. 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. The ultimate consequences are tendon necrosis, disruption of the tendon sheath, and digital contracture.[18, 19]

Epidemiology

Infectious flexor tenosynovitis

No data exist regarding the incidence of infectious FT. With penetrating injuries, the possibility of concomitant infection is very high when there is inoculation of the tendon sheath. Infectious FT via hematogenous spread is limited to isolated case reports.

Inflammatory flexor tenosynovitis

The incidence of inflammatory FT is well documented, as follows:

  • Diabetes - One third of all cases of hand and finger FT are associated with diabetes mellitus
  • RA - An estimated 64-95% of patients with RA develop hand or wrist FT

Prognosis

Cases of infectious FT that present early and have no comorbidities have a good prognosis. Patients that present with fulminant infection, those with chronic infection, and those with impaired immune status have increased risk of long-term complications and impairment.

The most common complication in FT is loss of range of motion (ROM) secondary to adhesions. If loss of functional motion persists, tenolysis is considered at 4 months post surgery. 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 patients with inflammatory FT, flexor tendon rupture is a potential complication.

Pyogenic flexor tenosynovitis

Pang et al conducted a review of 75 patients with pyogenic FT and found that the following risk factors were associated with poorer outcomes[20] :

  • Age over 45 years
  • Presence of diabetes mellitus, renal failure, or peripheral vascular disease
  • Ischemic changes at the time of presentation
  • Subcutaneous purulence
  • Polymicrobial infection at the time of surgery

Tenosynovitis and rheumatoid arthritis

Eshed et al found that FT that is diagnosed by magnetic resonance imaging (MRI) is a strong predictor of early RA (sensitivity = 60%, specificity = 73%). The investigators also found that an even stronger predictor of RA is the combination of FT on MRI and a positive serum anti-cyclic citrullinated peptide or positive rheumatoid factor.[21]

Another study, by Navalho et al, indicated that MRI offers a better means than Doppler ultrasonography does of predicting the development of RA through the identification of tenosynovitis and carpal joint synovitis. The study involved 45 patients with untreated recent-onset polyarthritis. The hands and wrists of these patients were imaged using 3T MRI and Doppler ultrasonography, and 12 months later the patients were evaluated to determine whether or not their polyarthritis had progressed to fulfill the criteria for RA.[22]

The investigators found that 30 patients met the criteria for RA at follow-up and that 12 months earlier, 3T MRI had identified FT in 86.7% of these patients and also identified carpal joint synovitis in exactly the same percentage of this group. Doppler ultrasonography found FT and carpal joint synovitis in, respectively, 50% and 63.3% of the patients with RA.[22]

Using multivariate logistic regression analysis, the investigators found MRI identification of FT and carpal joint synovitis in early polyarthritis to be a powerful predictive tool in assessing a patient's chance of progressing to RA.[22]

Tenosynovitis and diabetes

Kameyama et al found evidence that among patients with stenosing FT, those with diabetes have a higher prevalence of multiple joint involvement than do those without diabetes.[23]

 

Presentation

History

Gonococcal tenosynovitis

This type of tenosynovitis most commonly affects teenagers and young adults; it is more common in women, especially during pregnancy or after menstruation, when 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

Nongonococcal infectious tenosynovitis

Features of this form of tenosynovitis include the following:

  • Dry, cracked skin or a puncture wound, laceration, bite, or high-pressure injection injury (eg, paint, grease gun) may be present
  • Frequently, no obvious portal of injury is present
  • Pain and swelling occur along the affected tendon; flexor hand tendons are most commonly involved

Inflammatory tenosynovitis

De Quervain tenosynovitis

Patients have a history of repetitive pinching motion of the thumb and fingers (eg, assembly line work, driving in screws, weeding). Pain in the radial aspect of the wrist becomes worse with activity and better with rest. Onset of pain is typically gradual in nature, with no history of acute trauma. This condition is most common in middle-aged women. The affected area is shown in the image below.

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

Volar flexor tenosynovitis

The features of this condition (also known as trigger finger) include the following:

  • Most commonly affects the thumb or ring finger
  • Most common in middle-aged women
  • More common in patients with diabetes

Locking of the involved finger in flexion is followed by sudden release (hence the name trigger finger); hand pain radiates to fingers. In more severe cases, the finger may require passive manipulation to regain extension.

Physical Examination

Infectious tenosynovitis

Patients with infectious flexor tenosynovitis (FT) can present at any time after a penetrating injury, with complaints of pain, redness, and fever. Physical examination reveals Kanavel signs of flexor tendon sheath infection, which are as follows:

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

However, Kanavel signs may be absent in patients with the following:

  • Recently administered antibiotics
  • Early manifestations of the condition
  • Immunocompromised state
  • Chronic infections

Additionally, patients with immunocompromising conditions may present with a rather innocuous injury, such as a small puncture wound from a foreign body. Presenting symptoms may be vague in certain indolent infectious states.

Gonococcal tenosynovitis

Clinical features include the following:

  • Erythema, tenderness to palpation, and painful range of motion (ROM) of the involved tendon(s) are present
  • Fever is common
  • Dermatitis is also common (occurs in approximately two thirds of disseminated gonococcal); it is characterized by hemorrhagic macules or papules on the distal extremities or trunk

Inflammatory flexor tenosynovitis

Inflammatory FT usually is the result of an underlying disease process. Presentation is indolent but progressive if therapy is not initiated. Similar findings to those found in infectious FT eventually present. In inflammatory FT, swelling is the most common initial finding. The hallmark of inflammatory FT is a difference in active, versus passive, flexion. As the tissue expands and impingement occurs, pain and restricted motion ensue. Delayed presentations can have the appearance of fulminant FT with all Kanavel signs or may involve tendon rupture if the patient delays seeking treatment long enough.

Volar flexor tenosynovitis

Clinical features of this condition (also known as trigger finger) include the following:

  • Tenderness is present at the proximal end of the tendon sheath, in the distal palm (just proximal to the metacarpal head)
  • Palpable tendon thickening and nodularity may be present
  • Crepitation and catching of the tendon may be appreciated when the finger is flexed

De Quervain tenosynovitis

Clinical features include the following:

  • Pain occurs on palpation along the radial aspect of the wrist
  • Pain occurs with passive ROM of the thumb
  • Pain occurs with ulnar deviation of the wrist with the thumb cupped in a closed fist; this is termed the Finkelstein test (see the image below)
The Finkelstein test is performed by having the pa The Finkelstein test is performed by having the patient make a fist with the thumb inside the fingers. The clinician then applies ulnar deviation of the wrist to reproduce the presenting symptoms of dorsolateral wrist pain.
 

DDx

Diagnostic Considerations

In addition to the conditions listed in the differential diagnosis, other problems to be considered include the following:

  • Inflammatory (nonsuppurative) FT
  • Herpetic whitlow
  • Pyarthrosis
  • Gout
  • Pseudogout
  • Dactylitis
  • Phalanx fracture
  • Arthritis
  • Sesamoiditis and angiolipoma - Both found in case reports masquerading as FT
  • Hand infections
  • Hand injury, high pressure
  • Hand injury, soft tissue
  • Knee injury, soft tissue
  • Reactive arthritis
  • Rheumatic fever
  • Osteoarthritis
  • Subcutaneous abscess

Differential Diagnoses

 

Workup

Laboratory Studies

A complete blood count (CBC) with differential is appropriate if an infectious etiology is suspected. Characteristics include the following:

  • The white blood cell (WBC) count may be elevated in the presence of proximal infection or systemic involvement
  • It is not elevated in nonsuppurative conditions and often is not elevated in immunocompromised patients
  • A left shift is frequently present in acute processes

Determination of the erythrocyte sedimentation rate (ESR) is appropriate if an infectious etiology is suspected in tenosynovitis, though the ESR is nonspecific for the disorder. Characteristics include the following:

  • The ESR typically is elevated in acute or chronic infections and may serve as a marker to follow resolution of an infection
  • The ESR may be elevated in cases of inflammatory flexor tenosynovitis (FT) as well
  • The ESR is not elevated in nonsuppurative conditions

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

Test for rheumatoid factor if rheumatoid arthritis is a consideration.

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

Obtain standard anteroposterior and lateral radiographs to rule out bony involvement or a foreign body.[1]

Magnetic resonance imaging (MRI) has proven accurate in assisting in the diagnosis of tenosynovitis[24] ; however, it is expensive and generally unnecessary, in that the diagnosis is usually clinically evident.

Aspiration and Evaluation of Joint Fluid

If infection is suggested, culture of the suppurative synovial fluid is mandatory before definitive antimicrobial treatment is initiated. These cultures should include aerobic, anaerobic, fungal, acid-fast bacilli (AFB), and atypical AFB samples. In nonsuppurative conditions, synovial fluid may show nonbirefringent crystals (gout) or birefringent crystals (calcium pyrophosphate disease [CPPD], or 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; approximately 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.
  • White blood cell (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. Gram stains may reveal bacteria. A higher index of suspicion should be present for chronic infections or atypical presentations. These histologic findings help to confirm a diagnosis of inflammatory arthropathy.[25]

 

Treatment

Approach Considerations

Nonsuppurative flexor tenosynovitis (FT) frequently is treated nonoperatively, but in chronic conditions, surgical intervention may be necessary. If the patient's overall medical condition may preclude the aggressive treatment of nonsuppurative FT, rely on medical management.

Infectious FT remains an orthopedic emergency. Many advocate early surgical therapy for all cases. The literature clearly shows, however, that medical treatment can be used initially for early, uncomplicated infections, but timing is controversial.

Some authors have used single-incision irrigation and drainage. For stage I (increased fluid in tendon sheath, mainly a serous exudate) and stage II (purulent fluid, granulomatous synovium) infections, the authors advise proximal and distal incisions, with sterile saline intraoperative irrigation in conjunction with empiric intravenous (IV) antibiotics. The authors prefer repeat surgical irrigation and débridement rather than postoperative indwelling catheter irrigation.

Strong evidence and agreement exist for open treatment of stage III (necrosis of the tendon, pulleys, or tendon sheath) infections. Some physicians still advocate radical tenosynovectomy for Mycobacterium infections, while others adhere to partial tenosynovectomy with a multiple antibiotic regimen and close observation. The devastating potential complication of infectious FT warrants prompt aggressive treatment.

Dailiana et al, in a retrospective study of 41 patients with purulent FT, 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. Staphylococcus aureus was detected in most cases.[26]

The indication for surgical drainage includes history and physical examination consistent with acute or chronic FT. In certain circumstances when acute FT presents within the first 24 hours of infection development, medical management may initially be used. Prompt improvement of symptoms and physical findings must follow within the ensuing 12 hours; otherwise, surgical intervention is necessary.

Pharmacologic and Noninvasive Therapy

Infectious flexor tenosynovitis

Prompt medical management of acute nonsuppurative FT may preclude the need for surgical intervention. Nonoperative treatment for infectious FT includes the following:

  • IV antibiotics - May be included in initial treatment if the patient presents very early with suspected infectious FT
  • Elevation - Initially, until infection is under control
  • Splinting - In “safe position”
  • Rehabilitation - Digital range-of-motion (ROM) exercises and edema control, initiated once FT is under control

Empiric antibiotics for penetrating trauma include the following:

  • Otherwise healthy individuals - Cefazolin 1-2 g IV every 6-8 hours; if penicillin-allergic, clindamycin 600 mg IV every 8 hours or erythromycin 500-1000 mg IV every 6 hours
  • Immunocompromised individuals - Ampicillin-sulbactam 1.5-3 gm IV every 6 hours, OR cefoxitin 2 g IV every 6-8 hours; if penicillin-allergic, clindamycin 600 mg IV every 8 hours PLUS levofloxacin 500 mg IV once daily (for adults) OR clindamycin plus trimethoprim-sulfamethoxazole (TMP-SMZ) (for children)
  • Bite wound - Same as in immunocompromised individual

For patients who are immunocompromised or have diabetes, 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

Admit the patient 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.

Nongonococcal infectious tenosynovitis

If the diagnosis is equivocal, consultation with a hand specialist (eg, plastic surgery or orthopedics) and the use of elevation and broad-spectrum antibiotics that include staphylococcal coverage, streptococcal coverage, or both are necessary. Add anaerobic coverage if anaerobic infection is likely (ie, with cat or human bites). If the diagnosis of tenosynovitis is definite, refer the patient to a hand specialist for urgent surgical incision and drainage.

Inflammatory flexor tenosynovitis

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

Overuse syndromes

The mainstay of therapy for FT caused by overuse syndromes is cessation of the insult by 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

Use caution with corticosteroid injections, 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. Therefore, corticosteroid injections should be used judiciously, especially in patients with diabetes or rheumatoid arthritis. Also, the use of injectable or oral steroids is contraindicated if infectious FT has not been completely ruled out.

De Quervain tenosynovitis

Prescribe rest, NSAIDs, and a thumb spica wrist splint for patients with minimal symptoms.[27]

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.[28] (Surgical therapy is an option if conservative management fails.)[29]

A study examined injections of triamcinolone for de Quervain tenosynovitis and found an 89% efficacy rate for the drug.[30] 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.[31]

Volar flexor tenosynovitis

Peritendinous lidocaine-corticosteroid injection is the treatment of choice for volar FT (ie, trigger finger).[32] 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.[33]

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 the former treatment yielded promising results for the treatment of this condition, though optimal regimens remained to be defined.[34]

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.

Consider surgical tendon release if injection fails. Surgical release for trigger finger has success rates higher than 90%.

Rheumatoid arthritis

Treatment for rheumatoid inflammatory FT includes ice, NSAIDs, rest, splinting, 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. Limit injections to avoid tendon rupture.[35]

Drainage, Irrigation, and Tenosynovectomy

Infectious flexor tenosynovitis

Several drainage techniques can be used in infectious FT. 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 1 below).

Table 1. Michon Classification Scheme (Open Table in a new window)

Infection Stage

Characteristic Findings

Treatment

Stage I

Increased fluid in sheath, mainly a serous exudate

Catheter irrigation

Stage II

Purulent fluid, granulomatous synovium

Minimal invasive drainage +/- indwelling catheter irrigation

Stage III

Necrosis of the 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, make the incision 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 utilizing the midaxial approach, the incision should be dorsal to the neurovascular bundle. A Brunner incision allows better initial exposure but may complicate closure/coverage if skin necrosis ensues and is more likely to interfere with therapy postoperatively.

A 16-gauge polyethylene catheter or a 3.5-5 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. Avoid excessive fluid extravasation into the digit 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 is equally effective.[36, 37, 38]

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 annular 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 species infection, extensive tenosynovectomy may be necessary, depending on the chronicity of infection.

Inflammatory flexor tenosynovitis

For inflammatory FT, extensive volar Brunner incisions are used. The diseased tenosynovium is excised, while the annular pulleys are carefully preserved.

Postoperative Care

Infectious flexor tenosynovitis

In the case of infectious FT, approximately 48 hours after surgery, remove the dressing, splint, and drains, and inspect the wounds. Initiate active and passive ROM exercises, as well as 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 flexor tenosynovitis

During the postoperative course of tenosynovectomy due to inflammatory FT, 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

Consultations and referrals may include the following:

  • Primary care or hand specialty outpatient referral for follow-up care of de Quervain tenosynovitis and volar flexor tenosynovitis
  • 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 FT, 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 FT, 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

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 FT resulting from an overuse syndrome, 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 FT 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

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

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

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.

Antibiotics

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

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).

Corticosteroids

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

Overview

What is tenosynovitis?

What are the signs and symptoms of infectious tenosynovitis?

What are the signs and symptoms of gonococcal tenosynovitis?

What is inflammatory flexor tenosynovitis?

How is tenosynovitis diagnosed?

Which hematologic studies are performed in the evaluation of tenosynovitis?

What is the role of biopsy in the evaluation of tenosynovitis?

What is the role of imaging in the evaluation of tenosynovitis?

What is included in the nonoperative treatment of infectious flexor tenosynovitis?

What is included in the nonoperative treatment of inflammatory flexor tenosynovitis?

What is the role of surgical drainage in the treatment of tenosynovitis?

What is tenosynovitis?

What is the pathophysiology of infectious flexor tenosynovitis?

What is the pathophysiology of inflammatory flexor tenosynovitis?

What are the pathologic stages of overuse in inflammatory flexor tenosynovitis?

What is the role of tendon rupture in the pathogenesis of tenosynovitis?

What are noninfectious causes of tenosynovitis?

How does overuse injury cause tenosynovitis?

What causes nongonococcal infectious tenosynovitis?

Which Mycobacterium species cause nongonococcal infectious tenosynovitis?

What causes gonococcal tenosynovitis?

What causes pyogenic flexor tenosynovitis?

What is the incidence of infectious flexor tenosynovitis?

What is the incidence of inflammatory flexor tenosynovitis?

What is the prognosis of infectious flexor tenosynovitis?

What is the prognosis of pyogenic flexor tenosynovitis?

What is the etiologic role tenosynovitis in rheumatoid arthritis?

What is the prognosis of tenosynovitis with comorbid diabetes?

Presentation

Which history is characteristic of gonococcal tenosynovitis?

Which history is characteristic of nongonococcal infectious tenosynovitis?

What history is characteristic of inflammatory tenosynovitis?

Which history is characteristic of volar flexor tenosynovitis?

Which physical findings suggest infectious tenosynovitis?

Which physical findings suggest gonococcal tenosynovitis?

Which physical findings suggest inflammatory flexor tenosynovitis?

Which physical findings suggest volar flexor tenosynovitis?

Which physical findings suggest de Quervain tenosynovitis?

DDX

Which conditions should be included in the differential diagnosis of tenosynovitis?

What are the differential diagnoses for Tenosynovitis?

Workup

Which findings on complete blood count (CBC) suggest infectious flexor tenosynovitis?

Which erythrocyte sedimentation rate (ESR) findings suggest infectious flexor tenosynovitis?

Which lab studies are performed for the evaluation of tenosynovitis?

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

What is the role of aspiration and evaluation of joint fluid in the evaluation of tenosynovitis?

Which histologic findings are characteristic of tenosynovitis?

Treatment

What are the treatment options for tenosynovitis?

What is included in nonoperative treatment of infectious flexor tenosynovitis?

What is the role of empiric antibiotics in the treatment of infectious flexor tenosynovitis?

What are the treatment options for gonococcal tenosynovitis?

What are treatment options for nongonococcal infectious tenosynovitis?

What are treatment options for inflammatory flexor tenosynovitis?

What is included in the treatment of inflammatory flexor tenosynovitis due to overuse syndrome?

What are treatment options for de Quervain tenosynovitis?

What are treatment options for volar flexor tenosynovitis?

What are treatment options for rheumatoid inflammatory flexor tenosynovitis?

What is the Michon Classification Scheme for infectious flexor tenosynovitis?

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

What are the indications for open tendon sheath débridement for infectious flexor tenosynovitis?

What are techniques for open tendon sheath débridement of infectious flexor tenosynovitis?

What surgical techniques can be used in the treatment of inflammatory flexor tenosynovitis?

What is included in postoperative care for infectious flexor tenosynovitis?

What is included in postoperative care for inflammatory flexor tenosynovitis?

Which specialist consultations are beneficial in the treatment of tenosynovitis?

What is included in long-term monitoring of tenosynovitis?

Medications

Which medications are used 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?