You are in: eMedicine Specialties > Orthopedic Surgery > HAND AND UPPER EXTREMITY Infectious and Inflammatory Flexor TenosynovitisArticle Last Updated: Apr 19, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Randle L Likes, DO, Consulting Staff, Department of Emergency Medicine, Gateway Medical Center Randle L Likes is a member of the following medical societies: American College of Emergency Physicians and American Medical Association Coauthor(s): Sean D Ghidella, MD, Chief of Orthopedic Service, Consulting Surgeon, Department of Orthopedic Surgery, Madigan Army Medical Center Editors: Peter M Murray, MD, Associate Professor of Orthopedic Surgery, Mayo Clinic College of Medicine; Director of Education, Mayo Foundation for Medical Education and Research, Jacksonville; Consultant, Department of Orthopedic Surgery, Mayo Clinic, Jacksonville; Consulting Staff, Nemours Children's Clinic and Wolfson's Children's Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Thomas R Hunt III, MD, John D Sherrill Professor and Director of Orthopaedic Surgery, Surgeon in Chief of UAB Highlands Hospital, Director of Hand and Upper Extremity Fellowship, University of Alabama at Birmingham; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Harris Gellman, MD, Consulting Surgeon, Broward Hand Center, Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami School of Medicine Author and Editor Disclosure Synonyms and related keywords: acute flexor tenosynovitis, flexor tendon sheath infection, flexor tenosynovitis, pyogenic flexor tenosynovitis, suppurative flexor tenosynovitis, septic flexor tenosynovitis INTRODUCTIONSection 2 of 12
  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. History of the ProcedureCrediting 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,1 Carter et al,2 and Nevaiser3 as early as the 1960s. Tenosynovectomy for inflammatory FT was supported by the work of Howard (1955), Straub and Wilson (1956), Potter and Kuhns (1958), Kessler and Vainio (1966), and Nalebuff and Potter (1968), and later by work by Nalebuff and Patel,4 Milendur and Nalebuff,5 and Brown and Brown.6 ProblemPyogenic 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.7, 8 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).9, 10, 11, 12, 13 FrequencyNo data exist regarding the incidence of flexor tenosynovitis. 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. EtiologyThe primary inciting event of infectious FT usually is penetrating trauma. Most infections are caused by native skin flora, including both Staphylococcus and Streptococcus species.14 The most common organism that causes infectious FT is Staphylococcus aureus. Other causes include the following:
Other noninfectious causes include diabetes mellitus,23, 24, 25 rheumatoid arthritis,26 crystalline deposition, overuse syndromes,9, 10 amyloidosis, ochronosis, psoriatic arthritis, systemic lupus erythematosus, and sarcoidosis. PathophysiologyInfectious 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) (see Image 1). 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.11, 12 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.
ClinicalPatients 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 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:
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 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. INDICATIONSSection 3 of 12
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. RELEVANT ANATOMYSection 4 of 12
Much of the anatomy of the flexor tendon sheaths is discussed in the Pathophysiology section.27 The location of the flexor tendon sheaths and the aforementioned radial and ulnar bursae can be seen in Image 2. The annular pulley is shown in Image 1. CONTRAINDICATIONSSection 5 of 12
The patient's overall medical condition may preclude the aggressive treatment of nonsuppurative flexor tenosynovitis. If this is the case, rely upon medical management. WORKUPSection 6 of 12
Lab Studies
Imaging Studies
Other Tests
Diagnostic Procedures
Histologic FindingsSynovial 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 confirm diagnosis of inflammatory arthropathy. TREATMENTSection 7 of 12
Medical therapyPrompt medical management of acute nonsuppurative flexor tenosynovitis may preclude the need for surgical intervention.
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 is indicated. Surgical drainage is necessary if no obvious improvement has occurred within 12-24 hours. 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. The mainstay of therapy for FT caused by overuse syndromes is ceasing the insult by modifying activity. Ice and elevate the affected area, and administer a nonsteroidal anti-inflammatory drug (NSAID) if tolerated by the patient. Consider a short course of oral steroids. Flexor tendon sheath or carpal tunnel corticosteroid injections can decrease pain and the inflammatory response. If splinting is utilized, it should limit the area to pain-free ROM. 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 are used judiciously, especially in patients with diabetes and those with rheumatoid arthritis. Also, use of injectable or oral steroids is contraindicated if infectious FT has not been completely ruled out. Treatment for rheumatoid inflammatory FT includes ice, NSAIDs, rest, splinting, hydroxychloroquine, gold, penicillamine, and methotrexate. Persisting cases may require oral steroid treatment. For acute flares of FT patients with rheumatoid arthritis, corticosteroid injections may provide prompt relief. Limit injections to avoid tendon rupture. Preoperative detailsSeveral surgical approaches can be used to drain infectious FT. The method used is based upon the extent of the infection. The Michon classification scheme can be a helpful guide. Michon Classification Scheme
Most current recommendations for stage I and stage II infections advocate proximal and distal incisions for adequate drainage and irrigation. Intraoperative detailsInfectious flexor tenosynovitis 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 No. 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 awaiting culture results. (See Medical therapy.) Some 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. Continuous irrigation with sterile saline at 25 mL/hr or intermittent irrigation every 2-4 hours with 25-50 mL of sterile saline are equally effective.28, 29, 30 Indications for open tendon sheath debridement include stage III infections, chronic infections, or 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 while preserving 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 debridement are necessary. For Mycobacterium species infection, extensive tenosynovectomy may be necessary depending on the chronicity of infection. Inflammatory flexor tenosynovitis For inflammatory FT infection, extensive volar Brunner incisions are used. The diseased tenosynovium is excised while carefully preserving the annular pulleys. Postoperative detailsIn 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 persisting infection, repeat operative debridement may be required. Intravenous antibiotics should continue for an additional 48-72 hours. Length of IV antibiotic treatment is determined by the culture and sensitivity results and specific patient factors. The switch from IV to oral antibiotics should be based not only on the culture results but also on the clinical examination and patient progress. Oral antibiotics should be continued for 5-14 days, depending on the following:
Generally the wounds should be left open so they can heal promptly by secondary intention. Delayed primary closure is not needed. During the postoperative course of tenosynovectomy due to inflammatory FT, remove bandage, splint, and drain (if used) at 24-48 hours postsurgery. 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. Follow-upFor 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; then, cautious strengthening can be added. However, it is not uncommon for progress to be slow, resulting in a rehabilitation course lasting 3-4 months. For excellent patient education resources, visit eMedicine's Hand, Wrist, Elbow, and Shoulder Center, Arthritis Center, and Infections Center. Also, see eMedicine's patient education articles Tendinitis and Rheumatoid Arthritis. COMPLICATIONSSection 8 of 12
The most common complication is loss of ROM secondary to adhesions. If loss of functional motion persists, tenolysis is considered at 4 months postsurgery. 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 inflammatory FT, flexor tendon rupture is a potential complication. OUTCOME AND PROGNOSISSection 9 of 12
Cases of infectious FT that present early and have no comorbidities have a good prognosis. Patients that present with fulminant infection, those with chronic infections, and those with impaired immune status all have increased risk of long-term complications and impairment. FUTURE AND CONTROVERSIESSection 10 of 12
Infectious FT remains an orthopedic emergency. Many advocate early surgical therapy for all cases. The literature clearly shows 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 and II infections, the authors advise proximal and distal incisions with sterile saline intraoperative irrigation in conjunction with empiric IV antibiotics. The authors prefer repeat surgical irrigation and debridements rather than postoperative indwelling catheter irrigation. Strong evidence and agreement exist for open treatment of stage III 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 flexor tenosynovitis warrants prompt aggressive treatment. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Infectious and Inflammatory Flexor Tenosynovitis excerpt Article Last Updated: Apr 19, 2008 | ||||||||||||||||||||||||||
