Pyogenic flexor tenosynovitis (PFT) is a closed-space infection of the digital tendon sheaths of the hand, which can lead to a compartment syndrome-like presentation (1). Despite PFT accounting for 2.5% to 9.4% of all hand infections, it is often misdiagnosed leading to high rates of morbidity (1,2). In 1905, Kanavel identified four cardinal signs of PFT:
- uniform, symmetric digit swelling,
- digit is held in partial flexion at rest,
- excessive tenderness along the entire flexor tendon sheath, and
- pain along the tendon sheath with passive digit extension.
Despite how long ago these findings were established, they remain relevant and are the standard diagnostic criteria (3). The most reliable of these physical examination findings are tenderness along the flexor tendon sheath and pain with passive extension. Jardin et al. (4) and Hyatt and Bragg (5) noted that only 22% to 56% of patients whom they suspected to have PFT demonstrated all four cardinal symptoms. Adjunctive laboratory studies, such as white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP), are not specific enough to diagnose PFT and may be late findings, thus decreasing their clinical utility (5). Radiographs are used to rule out bone trauma or foreign bodies. Magnetic resonance imaging is rarely used, and there are no current studies evaluating its usefulness in diagnosing PFT (5). Ultrasonography did prove useful in diagnosing PFT in one prospective study, allowing for early diagnosis of this emergent situation and potentially providing a tool for serial monitoring (4). In current practice, most clinicians do not use imaging modalities, and if they have a high index of suspicion, they proceed directly to surgical treatment (4). This report demonstrates the role of ultrasonography in diagnosing PFT in a young male and its ability to monitor a patient's recovery via outpatient management without the need for a surgical debridement.
The patient was a previously healthy 32-year-old solider who presented to a sports medicine clinic with complaints of a 2-d history of progressive swelling, tenderness, and pain along the palmar aspect of his left small finger. He was a self-reported avid weightlifter, but denied any trauma, cuts, or scrapes to that finger. His medical and surgical history were noncontributory to include a negative review of systems for rheumatologic conditions or a family history of rheumatologic conditions.
Upon physical examination, he was in no acute distress, and his vital signs were stable. Inspection of his small finger demonstrated swelling at the metacarpophalangeal (MCP) joint with the finger held in slight flexion, warmth, but no erythema. He was tender to palpation along the entire palmar aspect of his finger. Passive flexion and extension exacerbated his pain. He actively flexed his finger albeit with significant pain. His flexor digitorum profundus and flexor digitorum superficialis were both clinically intact. Point-of-care (POC) ultrasonography performed on his finger was indicative of soft tissue edema, peritendinous fluid, and cobble stoning consistent with cellulitis (Fig. 1). The patient was subsequently diagnosed with PFT because of his warm, painful edematous finger and ultrasound findings consistent with a soft tissue infection.
Because of the severity of PFT if untreated, the patient was directed to the Emergency Department for consultation with an on-call orthopedic surgeon. Laboratory evaluation in the emergency department revealed a WBC of 7.2 (normal [nl], 3.4–9.6) with normal differential, ESR of 8 (nl, 0–22), and CRP of 0.058 (nl < 3.0). The evaluating orthopedist concurred with the diagnosis of PFT after correlating the clinical examination with the ultrasound report. He agreed that laboratory values lack utility in diagnosing PFT, and other diagnostic tools, such as ultrasonography, are more useful in these circumstances. The patient was discharged home with cephalexin and naproxen, as well as close follow-up.
The patient was called 24 h later and reported no worsening of his condition. At 48 h, he stated the pain had decreased. At his appointment 72 h later, he continued endorsing decreased pain and now decreased swelling. A repeat ultrasound was performed, which demonstrated a decrease in fluid within the tendon sheath (Fig. 2). At 96 h, other than mild tenderness of the small finger, his physical examination was symmetric as compared contralaterally. Ultrasound showed continued improvement with mild soft tissue edema, and the flexor tendons were moving freely (Fig. 3). The patient finished the 10-d course of cephalexin and was instructed to use padded lifting gloves. At his 2-month follow-up, he had complete resolution of his pain, but required naproxen and finger massage to limit swelling and stiffness, respectively. At his 1-year follow-up, he had complete resolution of all symptoms.
We do understand that a definitive diagnosis of PFT cannot be made in our case because tissue cultures were not obtained. The patient wished to pursue a nonsurgical option if possible. We were confident in our diagnosis based on the presence of three of four Kanavel's signs and the ultrasound findings. This patient's ultrasound findings were consistent with the findings in the Jardin et al. (4) study, which confirmed PFT with tissue positive cultures.
Other conditions were considered in the differential, such as stenosing tenosynovitis in trigger finger and seropositive arthropathies. Stage 1 trigger finger can present with palmar MCP joint tenderness, but this is often preceded by a clicking or locking sensation and an inability to fully extend the affected finger, which this patient did not demonstrate (6). The patient also did not display any systemic symptoms; therefore, inflammatory arthropathies were low on the differential.
PFT is an orthopedic emergency and should be suspected if Kanavel's cardinal symptoms are present. If diagnosis is delayed, the patient is at increased risk of tendon necrosis, adhesion formation, amputation, and spread of infection to the radial/ulnar bursa or the Parona space (3). Previously, the difficulty with diagnosis is that it was largely clinical, but multiple studies have demonstrated that ultrasound can be used to confidently diagnosis PFT (4,5,7,8). Jardin et al. (4) reported on 57 patients that ultrasonography has a sensitivity of 94.4%, specificity of 74.4%, a positive predictive value of 63%, and a negative predictive value of 96.7% using surgical exploration as a reference. Therefore, the major utility of ultrasonography is in ruling out PFT. Hmamouchi et al. (8) made a similar conclusion while studying ultrasound use in detecting early arthritis, determining that it is very sensitive at detecting early inflammation. Jardin et al. (4) and Padrez et al. (9) both identified characteristic ultrasonographic findings of PFT from their respective studies:
- hypoechogenic peritendinous effusion with no signal on color Doppler, and
- thickened synovial sheath that is hypoechoic and hyperemic on color Doppler in the acute inflammatory phase.
This case report differs from other studies in that we utilized ultrasonography as an objective treatment monitoring device versus solely for diagnostic purposes. The use of ultrasound aided in early diagnosis of PFT and allowed for nonoperative treatment of our patient, as well as serial monitoring.
Historically, the mainstay of treatment involves surgical intervention, including either open debridement with irrigation or percutaneous catheter irrigation. There have been no statistically different outcomes with either treatment, but open debridement has been associated with higher rates of complications (10). While surgical treatment with PFT is the current standard therapy, it must be performed judiciously due to potential complications including postoperative stiffness, intraoperative damage to pedicles, and wound healing defects (4).
Since surgical therapy is not completely benign in nature, we explored antibiotic therapy as a monotherapy. Although antibiotic use has been increasing, there is a lack of uniformity and minimal literature supporting the use of antibiotics as monotherapy (2). Current literature suggests that nonoperative management of PFT may be appropriate if a patient presents within 48 h of development of symptoms and the chosen antibiotics cover both Staphylococcus and Streptococcus species at a minimum to include consideration for methicillin-resistant Staphylococcus aureus (MRSA) (10). Antibiotic use was appropriate in our otherwise healthy patient because of his early presentation and ability to have daily follow-up to inquire about his subjective improvement and objective improvement as evidenced on ultrasonography.
In this case report, we demonstrated that PFT can be successfully detected and monitored using ultrasound in conjunction with a clinical examination. The ability of the ultrasonographer to interpret the effectiveness of antibiotic monotherapy allowed us to treat this patient without surgical intervention or having to obtain invasive tissue culture for diagnosis. We believe that serial monitoring with ultrasonography should be systematically studied. The use of ultrasound does have its limitations including access and ability to interpret the findings. This can be overcome with resourcing, education, and training. We believe that the utility of POC ultrasonography is only beginning to be realized and recommend more studies and guidelines on its proper implementation.
The authors declare no conflict of interest and do not have any financial disclosures.
The views expressed are solely those of the authors and do not reflect the official policy or position of the US Army, US Navy, US Air Force, the Department of Defense, or the US Government.
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