For patients with suspected flexor tenosynovitis, the mainstay of diagnosis is a thorough history and physical examination. The examination is guided by evaluating the patient for Kanavel’s four cardinal signs. Empiric antibiotics should be started immediately on diagnosis covering skin flora and gram-negative bacteria. Typically, surgery is required. Appropriate exposure is required for adequate treatment and incisions should be tailored to preserve areas of skin compromised from draining sinuses and abscess pressure. Diabetes mellitus and peripheral vascular disease place patients at higher risk of poor outcomes including stiffness and amputation; early administration of antibiotics is the intervention that correlates most closely with good outcomes.
Key points
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Physical examination, including evaluation of Kanavel’s four cardinal signs, is the primary mode of diagnosis for flexor tenosynovitis (FTS).
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The mainstay treatment of FTS is the same as any other abscess: surgical debridement and irrigation, followed by IV antibiotics; occasionally early identified cases may be treated with IV antibiotics alone.
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Multiple approaches have been described for debridement and irrigation (eg, closed sheath irrigation, open midaxial incision); the surgeon must use judgment to balance adequate debridement and the size, location, and morbidity of incisions.
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Postoperative irrigation on the ward is not supported by evidence and the benefits rarely merit the increased burden for nurses and discomfort to patients.
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Diabetes mellitus and peripheral vascular disease place patients at higher risk of poor outcomes including stiffness and amputation; early administration of antibiotics is the intervention that most correlates with good outcomes.
Introduction
The potential diagnosis of flexor tenosynovitis (FTS) tends to provoke anxiety in primary evaluators and surgeons given the difficulty of diagnosis and treatment. The unique anatomy and function of the hand make prompt and appropriate surgical or nonsurgical treatment imperative. The surgical treatment of FTS is considered an essential skill for graduating orthopedic surgery residents. Postoperative rehabilitation must not be overlooked as a key component of functional recovery. This article demystifies FTS and provides the latest evidence available for diagnosis and treatment.
Introduction
The potential diagnosis of flexor tenosynovitis (FTS) tends to provoke anxiety in primary evaluators and surgeons given the difficulty of diagnosis and treatment. The unique anatomy and function of the hand make prompt and appropriate surgical or nonsurgical treatment imperative. The surgical treatment of FTS is considered an essential skill for graduating orthopedic surgery residents. Postoperative rehabilitation must not be overlooked as a key component of functional recovery. This article demystifies FTS and provides the latest evidence available for diagnosis and treatment.
Historical perspective
The seminal work of Kanavel describing the aggressive surgical treatment of pyogenic FTS dramatically improved the natural history of this infection, including the sequelae of finger stiffness, tendon necrosis and rupture, hand dysfunction, systemic infection, and even death. The introduction of antibiotics further revolutionized management such that the mainstay of FTS treatment today is intravenous (IV) antibiotics coupled with surgical debridement and irrigation; occasionally, cases identified early may even be treated by IV antibiotics alone. More recent advances include efforts to decrease the morbidity of surgical access while adequately debriding the closed space of the flexor sheaths.
Anatomy
The flexor tendon sheath provides nutrition and an optimal gliding and restraining interface to the extrinsic tendons to the digits. The sheath is formed of two layers, as a “double-walled ‘tube’” : the visceral layer, which is synonymous with the epitenon, and the parietal layer, which is confluent with the fibrous pulley system. In the normal hand, these two layers coalesce to form a sealed synovial space. In the index, middle, and ring fingers, the sheath extends 1 to 3 mm proximal to the palmar aponeurosis pulley at the level of the metacarpal necks. The small finger sheath is confluent with the ulnar bursa in a significant portion of hands (80% in earlier texts and 30% in more recent studies ) and Parona space in the forearm. The sheaths of the fingers end proximal to the distal interphalangeal joint. The thumb sheath extends from 2 cm proximal to the radial styloid to just distal to the interphalangeal joint.
Multiple communicating patterns between the flexor sheaths, the ulnar and radial bursae, and Parona space have been identified ; furthermore, septic sheaths may develop abnormal connections given increased synovial pressure and tissue degradation. During the initial evaluation and serial examinations, the surgeon must keep in mind that an infection starting in one digit may spread to the hand, forearm, and other digits. An infection involving the radial and ulnar flexor sheaths is thus termed a “horseshoe” abscess.
Once bacteria are inoculated into the space between the visceral and parietal layers, the synovial fluid that normally provides nutrition to the tendon becomes a medium for bacterial growth. Sheath interconnections in the palm and with Parona space in the forearm allow for spread, and the closed nature of the sheath limits the host’s ability to combat the infection.
The confined space within the dermis of the digits has been compared with the fascia of muscle compartments, where increased pressure within the digit (or compartment) can limit perfusion and delivery of antibiotics and the host’s innate immune system. In 14 digits taken to surgery for FTS, Schnall and colleagues found all patients had increased subcutaneous pressures compared with contralateral control digits, with an average pressure of 33 mm Hg (range, 20–73). Eight of the patients had pressures greater than 30 mm Hg, fitting an older definition of compartment syndrome.
If surgery is required, an understanding of pertinent hand anatomy is paramount. Extra care must be taken because the edematous hand and digits may have displaced neurovascular structures that are under greater tension than usual. With Kaplan cardinal line drawn from “the apex of the interdigital fold between the thumb and the index finger to the hook of the hamate,” the superficial palmar arch is found 18 ± 4 mm distal to the intersection of Kaplan cardinal line and a line extending from the ulnar border of the middle finger.
Common digital arteries branch from the superficial arch and course distally until branching into proper digital arteries. At the level of finger web spaces, the proper digital arteries and veins flank the flexor tendons sheath. The arterial supply to the thumb is typically via the princeps pollicis (80%), a branch of the radial artery or deep palmar arch, or a branch of the superficial palmar arch (20%).
Branches of the median and ulnar nerves typically pass between the superficial and deep transverse metacarpal ligaments, after which the nerve courses on the palmar aspect of the digital artery. In the thumb, the radial digital nerve crosses over the flexor pollicis longus tendon 0.9 ± 2.3 mm proximal to a line extending along the radial border of the index finger.
The pulley systems of the fingers and thumb have been extensively studied and should be understood to perform safe and adequate debridement and irrigation. In addition to five annular pulleys, the index, middle, ring, and small fingers also have three cruciate pulleys; the palmar aponeurosis also has some pulley function ( Table 1 ). The thumb has 4 well-described variations of pulleys ( Table 2 ).
| Pulley Name | Pulley Location |
|---|---|
| PA | Metacarpal neck |
| A1 | MP joint |
| A2 | Proximal half of proximal phalanx |
| C1 | Distal half of distal proximal phalanx |
| A3 | PIP joint |
| C2 | Proximal quarter of middle phalanx |
| A4 | Middle quarter of middle phalanx |
| C3 | Distal quarter of middle phalanx |
| A5 | Distal most aspect of middle phalanx |
| Pulley Name | Pulley Location |
|---|---|
| A1 | MP joint |
| Av | Variable, proximal half of proximal phalanx |
| Type I | Absent |
| Type II | Transverse |
| Type III | Oblique |
| Type IV | Confluent with A1 |
| Oblique | Third quartile of proximal phalanx |
| A2 | Distal quartile of proximal phalanx |
Microbiology
Most cultures from FTS identify skin flora, specifically Staphylococcus and Streptococcus . In a recent large series with 71 consecutive patients, Staphylococcus and Streptococcus accounted for 70% of FTS infections, including 13% methicillin-resistant Staphylococcus aureus (MRSA). No growth was found in 18%, and the remaining 11% were caused by gram-negative organisms, Mycobacterium , and Cryptococcus . Table 3 shows the culture results from representative studies from 1975 to 2012.
| Microbes | Pollen, 1974 | Neviaser, 1978 | Maloon et al, 1990 | Juliano & Eglseder 1991 | Schnall et al, 1996 | Pang et al, 2007 | Dailiana et al, 2008 | Bishop et al, 2013 | Nikkhah, 2012 | Average a | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Staphylococcus | 11 | 36.7% | 12 | 60.0% | 26 | 56.5% | 5 | 17.9% | 2 | 14.3% | 32 | 42.7% | 9 | 22.0% | 27 | 38.0% | 4 | 25.0% | 34.8% |
| MRSA | — | — | — | — | — | — | — | — | — | — | — | — | 10 | 24.4% | 9 | 12.7% | 1 | 6.3% | 14.4% |
| Streptococcus | 5 | 16.7% | — | — | 7 | 15.2% | 1 | 3.6% | 1 | 7.1% | 11 | 14.7% | 2 | 4.9% | 14 | 19.7% | 3 | 18.8% | 12.6% |
| Gram negatives | — | — | 4 | 20.0% | 3 | 6.5% | 2 | 7.1% | — | — | 18 | 24.0% | 4 | 9.8% | 5 | 7.0% | 1 | 6.3% | 11.5% |
| Polymicrobial | 1 | 3.3% | — | — | — | — | — | — | 7 | 50.0% | — | — | 3 | 7.3% | — | — | 0 | — | 20.2% |
| No growth | 13 | 43.3% | 4 | 20.0% | 10 | 21.7% | 19 | 67.9% | 4 | 28.6% | 17 | 22.7% | 13 | 31.7% | 13 | 18.3% | 6 | 37.5% | 32.4% |
| Total number of cases | 30 | — | 20 | — | 46 | — | 28 | — | 14 | — | 75 | — | 41 | — | 71 | — | 16 | — | — |
a Average percentages do not add to 100% given categorization of data and exclusion of rare and atypical organisms.
Atypical organisms should also be considered, especially for patients with diabetes mellitus or who are immunocompromised. Although less frequent, MRSA-induced FTS has shown a higher rate of complications including tissue necrosis, long-term stiffness, and amputation. Mycobacterium species should be considered in cases of indolent infections. Mycobacterium marinum should be suspected when a penetrating injury happens in a marine setting. Mycobacterium tuberculosis and Candida may be seen in immunocompromised hosts. Neisseria gonorrhea should be considered in sexually active patients, especially those without history of a puncture wound near the flexor sheath.
Patient presentation
History
Certain aspects of the history should be emphasized when evaluating a patient with suspected FTS, specifically the details regarding the inciting injury and the patient’s immune status. Patients typically present 2 to 5 days following an injury, often after failing a course of outpatient antibiotics. Although hematogenous spread may seed the flexor sheath in rare cases, most are caused by a penetrating injury.
Patients should be asked about associated symptoms including fever, chills, anorexia, and malaise. Additionally, the evaluator must ask about the proximal extent of pain and swelling in the upper extremity, and other sites of pain ( Box 1 ).
Injury factors
Was there a penetrating injury?
For example, knife, needle, thorn, animal bite
If no injury, then other sources of infection?
For example, Neisseria gonorrhea , Clostridium difficile
When was the injury?
What treatments have been tried?
For example, oral antibiotics, splinting
Patient factors
Handedness, occupation
Immunocompromise
For example, diabetes mellitus, human immunodeficiency virus, needle drug user
Drug allergies, specifically antibiotics
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