Pyogenic flexor tenosynovitis, or suppurative flexor tenosynovitis, is a closed-space bacterial hand infection of the digital flexor tendon sheath that can cause considerable morbidity. The majority of these infections follow traumatic penetrating injuries; therefore, skin flora, including Staphylococcus aureus, are the most common infecting organisms1. Kanavel classified this condition among the grave infections of the hand, describing the classic cardinal signs of flexor sheath infections, including pain with passive extension of the digit, symmetric digital swelling (sausage digit), tenderness along the flexor sheath, and a semiflexed resting posture of the involved digit1. A high (38%) rate of complications, including stiffness, persistent infection, boutonniere deformity, and amputation, has been reported2. Several risk factors have been associated with poor outcomes following the treatment of pyogenic flexor tenosynovitis, including an age of more than forty-three years, the presence of diabetes mellitus, peripheral vascular disease, renal failure, the presence of subcutaneous purulence, digital ischemia, polymicrobial infection3, methicillin-resistant Staphylococcus aureus infection, and delay in diagnosis4. Nonoperative treatment with intravenous antibiotics may be possible if the infection is detected and treated early (e.g., within twenty-four to forty-eight hours)1. Surgical drainage with or without tendon sheath irrigation is the essential mode of treatment of pyogenic flexor tenosynovitis, especially in patients with failed nonoperative treatment or with obvious purulence.
In this study, Draeger and coauthors, citing reports of the effectiveness of corticosteroids or local antibiotics for the treatment of other closed-space infections (septic arthritis, septic bursitis, infectious nephritis, and bacterial meningitis), created a novel chicken pyogenic flexor tenosynovitis model. To date, there are no known reports on the effectiveness of local corticosteroids or local antibiotics for the treatment of pyogenic flexor tenosynovitis. In this study, the authors hypothesized that adjunctive treatment with the injection of corticosteroids into the flexor tendon sheath would be as effective, or more effective, than antibiotics and surgical drainage alone for the treatment of pyogenic flexor tenosynovitis. The hypothetical mechanism of action of corticosteroids is to decrease inflammatory cell recruitment, which may be involved in the production of flexor tendon adhesions. In addition, the authors hypothesized that a dose of locally administered antibiotics followed by systemic antibiotics would be more effective for the treatment of pyogenic flexor tenosynovitis than would systemic antibiotics alone. They concluded that, at the end of the study period (twenty-eight days), two of three groups of chickens that were treated with locally administered corticosteroids and the group that was treated with intrasynovial antibiotics alone (without surgery) regained significantly more active flexion than did the chickens that were treated with systemic antibiotics and surgical drainage. Their pooled data revealed that the steroid-treated groups regained significantly more active flexion at all post-treatment time points.
This well-controlled study does have several limitations, which may make this study less comparable with clinical practice. The pyogenic flexor tenosynovitis infections produced in this study were from a single infecting organism with a known antibiotic sensitivity. Clinically, pyogenic flexor tenosynovitis is produced either by an unidentified bacterium or by multiple bacteria with unknown antibiotic sensitivities. The use of corticosteroids in the presence of antibiotic-resistant bacteria or with an inappropriate antibiotic regimen may be dangerous. In addition, all experimental treatment groups (surgical drainage, corticosteroid injection, local antibiotics, and systemic antibiotics) were treated within twenty-four hours after bacterial inoculation. Clinically, patients with pyogenic flexor tenosynovitis frequently are treated more than twenty-four hours after the onset of infection.
Other study limitations noted by the authors, mainly related to the fact that this was an animal model, include the method of tendon sheath irrigation (a single one-time injection of 10 mL of sterile saline solution into the tendon sheath instead of larger amounts of saline solution or the use of continuous or serial irrigations with an indwelling catheter) and the use of intramuscular antibiotics instead of intravenous antibiotics. The accuracy of measuring active flexion in a chicken digit may be limited, and there is no ability to determine if there is any pain associated with the loss of digital motion.
Corticosteroids have long been used for the treatment of tendinopathy (trigger finger, lateral epicondylitis, Achilles tendinopathy, rotator cuff tendinopathy). The obvious question that this study raises is the direct effect of corticosteroids on an infected flexor tendon. Studies on animal models have shown that intratendinous corticosteroids may or may not5 adversely affect the biomechanical properties of tendons. Corticosteroids can inhibit the formation of adhesions, granulation, and connective tissue; can reduce tendon mass; and can decrease biomechanical integrity and the amount of load that can be taken before failure5. The biomechanical effects of peritendinous corticosteroid on human tendons are unknown. However, tendon ruptures after steroid injections have been reported5. As this study was limited to twenty-eight days, the possibility of detecting tendon ruptures associated with the steroid injections is restricted.
The authors are to be congratulated for raising interesting questions that challenge the effectiveness of the currently accepted forms of treatment for pyogenic flexor tenosynovitis. The authors are in turn challenged to perform the necessary clinical trials that will be needed to provide the impetus for us to change our clinical practice.