Infectious and Inflammatory Flexor Tenosynovitis 

Flexor tenosynovitis (FT) is a pathophysiologic state causing disruption of normal flexor tendon function in the hand. A variety of etiologies are responsible for this process. Most acute cases of FT are the result of infection. However, FT also can be secondary to acute or chronic inflammation as a result of diabetes, overuse, or arthritis.

Much of the original work on infectious FT was done by Kanavel. If a patient presents with the 4 Kanavel signs, septic FT is diagnosed. The 4 Kanavel signs are (1) finger held in slight flexion, (2) fusiform swelling, (3) tenderness along the flexor tendon sheath, and (4) pain with passive extension of the digit. The process has the ability to rapidly destroy a finger's functional capacity and is considered an orthopedic emergency.

Recent studies

Eshed et al found that flexor tenosynovitis that is diagnosed by MRI is a strong predictor of early rheumatoid arthritis (sensitivity = 60%, specificity = 73%) and that an even stronger predictor of rheumatoid arthritis is the combination of flexor tenosynovitis on MRI with a positive serum anti-cyclic citrullinated peptide (CCP) or positive rheumatoid factor (sensitivity = 79%, specificity = 73%).^[1]

According to Kameyama et al, limited joint mobility in patients with diabetes is closely related to stenosing flexor tenosynovitis. The authors studied 302 patients with diabetes and compared them with 235 patients without diabetes to determine involvement of multiple digits. Patient study findings showed that diabetic patients had a significantly higher prevalence of multiple digit involvement than patients without diabetes (p < 0.0001).^[2]

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. Staphylococcus aureus was detected in most cases.^[3]

Crediting the surgeons who first described the techniques for irrigation and debridement of the flexor sheath is difficult. Dickson-Wright suggested postoperative sheath irrigation in 1943. Closed continuous irrigation and debridement techniques were championed by Besser,^[4] Carter et al,^[5] and Nevaiser^[6] as early as the 1960s.

Tenosynovectomy for inflammatory flexor tenosynovitis was supported by the work of Howard,^[7] Straub and Wilson,^[8] Potter and Kuhns,^[9] Kessler and Vainio,^[10] and Nalebuff and Potter,^[11] and later by work by Nalebuff and Patel,^[12] Milendur and Nalebuff,^[13] and Brown and Brown.^[14]

Pyogenic flexor tenosynovitis (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.^{[15, 16]}

Inflammatory FT usually is the result of rheumatoid arthritis (or other inflammatory and degenerative arthropathies), diabetes, overuse, or connective tissue disease. With diabetes, a proliferation of fibrous tissue in the tendon sheath causes constriction of the sheath. Overuse syndromes cause cumulative microtrauma to the tendon and tendon sheath. The protective inflammatory process paradoxically leads to tenosynovitis. A common example of overuse injury is stenosing flexor tenosynovitis (ie, Trigger Finger).^{[17, 18, 19, 20, 21]}

Frequency

No data exist regarding the incidence of flexor tenosynovitis (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.

The incidence of inflammatory FT is well documented. An estimated 64-95% of patients with rheumatoid arthritis develop hand or wrist FT. Furthermore, one third of hand and finger FT cases are associated with diabetes mellitus.

The primary inciting event of infectious flexor tenosynovitis (FT) usually is penetrating trauma. Most infections are caused by native skin flora, including both Staphylococcus and Streptococcus species.^[22] The most common organism that causes infectious FT is Staphylococcus aureus. Other causes include the following:

• Bite wounds^{[23, 24]}
• 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
• Hematogenous spread
• Mycobacterium tuberculosis
• Neisseria gonorrhoeae^{[25, 26]}
• Clostridium difficile –Case reported following antibiotic administration for ear infection in a child^[27]
• Miscellaneous
• Pseudomonas aeruginosa
• Listeria monocytogenes
• Vibrio vulnificus (stings from marine life)
• Mycobacterium species: Several, including Mycobacterium terrae, Mycobacterium marinum, Mycobacterium intracellulare, Mycobacterium avium, Mycobacterium kansasii, Mycobacterium asiatica, Mycobacterium bovis, and Mycobacterium malmoense, have been cultured following animal contacts or simple lacerations/puncture wounds. Infection with Mycobacterium species may be suspected in chronic more indolent infections. Late or missed diagnosis can lead to disastrous outcomes.^{[28, 29, 30]}

Other noninfectious causes include diabetes mellitus,^{[31, 32, 33]} rheumatoid arthritis,^[34] crystalline deposition, overuse syndromes,^{[17, 18]} amyloidosis, ochronosis, psoriatic arthritis, systemic lupus erythematosus, and sarcoidosis.

Infectious flexor tenosynovitis (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. Because the radial and ulnar bursae are contiguous, infections in either the small finger or thumb are at risk of communicating and potentially progressing to the carpal tunnel.

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 2 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 5 annular pulleys (A1-5) and 3 cruciform pulleys (C1-3), as seen in the image below. The A2 and A4 pulleys are critical for flexor tendon function and should be avoided during surgical manipulation of the infected sheath.

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, 8 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 2 distinct vascular supplies, and 3 have been identified for the flexor digitorum profundus. As a result, the profundus has 2 avascular segments, which are located over the proximal and middle phalangeal regions.

Inflammatory FT is a different process that may lead to similar potential complications. Proliferation continues 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.^{[19, 20]}

Overuse syndromes go through predictive stages that can lead to flexor tenosynovitis. 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.

• The 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.
• The 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.
• The 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.

Patients with rheumatoid arthritis may present with tendon rupture. Several causes of tendon rupture in rheumatoid arthritis 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.

Patients with infectious flexor tenosynovitis (FT) present at any time following a penetrating injury with complaints of pain, redness, and fever. Physical examination reveals Kanaval signs of flexor tendon sheath infection, which are (1) finger held in slight flexion, (2) fusiform swelling, (3) tenderness along the flexor tendon sheath, and (4) pain with passive extension of the digit. However, Kanaval 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 rather innocuous injury, such as a small puncture wound from a foreign body. Presenting symptoms may be vague in certain indolent infectious states.

The differential diagnosis of flexor tenosynovitis includes the following:

• Inflammatory (nonsuppurative) flexor tenosynovitis
• Herpetic whitlow
• Pyarthrosis
• Gout
• Dactylitis
• Phalanx fracture
• Arthritis
• Sesamoiditis and angiolipoma (both found in case reports masquerading as 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.

The indication for surgical drainage includes history and physical examination consistent with acute or chronic flexor tenosynovitis. In certain circumstances when acute flexor tenosynovitis 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.

Nonsuppurative flexor tenosynovitis frequently is treated nonoperatively, but in chronic conditions, surgical intervention may be necessary.

Much of the anatomy of the flexor tendon sheaths is discussed in the Pathophysiology section.^[35] The location of the flexor tendon sheaths and the aforementioned radial and ulnar bursae can be seen in the first image below. The annular pulley is shown in the second image below.

The patient's overall medical condition may preclude the aggressive treatment of nonsuppurative flexor tenosynovitis. If this is the case, rely upon medical management.