Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy of the upper limb. Although many cases are idiopathic, structural or inflammatory pathology of the flexor tendon sheath can result in secondary median nerve compression. Diabetes mellitus predisposes to such changes due to chronic connective tissue alterations, but secondary CTS arising solely from noninfective flexor tenosynovitis remains uncommon. A 49-year-old woman with recently diagnosed type 2 diabetes presented with a 2-month history of progressive right-wrist pain, paresthesia, and volar swelling. Magnetic resonance imaging revealed marked tenosynovitis of the finger flexors with palmar bowing of the flexor retinaculum and associated median nerve edema, whereas nerve conduction studies confirmed compressive neuropathy. Conservative therapy failed, and open carpal tunnel release was performed, yielding immediate symptom relief and improved hand function at 6-week follow-up. Secondary CTS due to chronic flexor tenosynovitis should be suspected in diabetic patients with refractory symptoms. Early multimodal evaluation and timely decompression may prevent irreversible neuropathy.

Trigger finger is commonly attributed to thickening of the A1 pulley or flexor tendons. Although calcific tendinitis is well recognized in regions such as the shoulder, calcification within the A1 pulley itself is extremely rare and seldom reported as a primary cause of triggering. We describe a 43-year-old woman who presented with painful triggering of the right little finger, accompanied by morning stiffness, snapping, and focal tenderness with warmth over the volar metacarpophalangeal (MCP) joint. Radiographs and high-resolution ultrasonography revealed a calcific deposit in the superficial layer of the A1 pulley, with surrounding hypervascularity on Doppler imaging. The patient underwent three sessions of ultrasound-guided prolotherapy in conjunction with physiotherapy and night splinting, which led to complete resolution of pain, stiffness, and triggering. This case identifies A1 pulley calcification as a rare but distinct etiology of trigger finger and highlights the diagnostic utility of ultrasonography in detecting this lesion. Moreover, it demonstrates that ultrasound-guided prolotherapy can provide an effective, minimally invasive alternative to surgical release, particularly when standard conservative management fails. Ultrasound-guided prolotherapy was selected as the primary intervention, instead of corticosteroid injection (CI), given its potential to promote tissue repair and resorption of calcific deposits, which are less effectively addressed by corticosteroids whose effect is primarily anti-inflammatory. Symptom improvement was observed after each biweekly session, with complete resolution achieved four weeks after the initial intervention. In addition to pain reduction documented by the Visual Analog Scale (VAS), the patient experienced the elimination of morning stiffness and snapping and restoration of full finger range of motion (ROM) following the final prolotherapy session.

Background: Trigger finger occurs primarily at the A1 pulley. However, triggering of the flexor tendon can also occur at the A2 pulley. The full release of the A2 pulley should be avoided because it may cause bowstringing and flexion weakness. To reduce the incidence of postoperative complications, we have performed a complete release of the A1 pulley via a volar approach and a complete release of the A2 pulley at the radial edge via a radial mid-lateral approach. This study aimed to investigate the outcome of our procedure. Methods: Seventeen fingers underwent A2 pulley release at the radial edge via a mid-lateral approach after complete release of the A1 pulley via a volar approach. The mean age of patients was 68 years. Regarding the Quinnell classification, 15 fingers were grade IV, 1 finger was grade II with triggering at the A2 pulley level and 1 finger was grade I with a ganglion on the A1 pulley. Results: The mean extension loss of the PIP joint was 23° preoperatively and 2° at the final examination, and the respective mean tip-palmar distances were 19 mm and 3 mm. No symptoms or signs suggested the bowstring of the flexor tendon during the observation period (mean: 99 weeks; range: 19-180 weeks). Conclusions: Our procedure is preferable for managing the tenosynovitis at the A1 and A2 pulleys. The release of the A2 pulley at the radial edge via a radial mid-lateral approach yielded a favourable result without bowstringing. Level of Evidence: Level IV (Therapeutic).

Nontuberculous mycobacteria (NTM) are uncommon causes of cutaneous and musculoskeletal infections. Here, we present an immunocompromised patient with persistent swelling in the left hand, wrist, and distal forearm. MRI findings revealed flexor tenosynovitis with synovial hypertrophy of the left hand and wrist and loculated fluid containing rice bodies along the distal flexor digitorum muscles in the volar aspect of the left wrist. The patient underwent flexor tenosynovectomy, and histological examination of the excised tenosynovium and mass revealed noncaseating granulomas. Mycobacterium intracellulare was identified in microbiological cultures. Antimycobacterial therapy was administered postoperatively to manage the infection. This report underscores the significance of maintaining a high index of suspicion for NTM infection when assessing chronic hand swelling, particularly in individuals with compromised immune systems.

Pyogenic or suppurative flexor tenosynovitis (PFT) is a severe bacterial infection within the closed space of the digital flexor tendon sheaths.[1][2] PFT accounts for 2.5 to 9.5% of hand infections that can cause necrosis of the tendons and devitalization of fingers.[3] This infection alters the gliding mechanism and creates adhesions within the flexor tendon sheath, resulting in marked loss of finger movements. PFT can result from bloodstream infection but is more commonly caused by penetrating finger injuries involving the flexor tendon sheath. Allen B. Kanavel, in 1912, described three cardinal signs for pyogenic flexor tenosynovitis: flexor sheath tenderness, flexed position of the affected digit, and painful digital extension. Later, a fourth sign, fusiform swelling of the digit, was added to the four cardinal signs.[4]  The detection of the four Kanavel signs on physical assessment has high sensitivity (91.4 to 97.1%) to diagnose pyogenic flexor tenosynovitis.[5] A timely diagnosis and prompt treatment are of paramount importance to limit the severe complications associated with this condition.  Anatomy of Flexor Tendon Sheaths The knowledge of the anatomy of hand flexor tendon sheaths is crucial for better understanding and management of PFT.  Each flexor tendon sheath comprises two layers; an inner visceral layer and an outer parietal layer. The visceral layer closely covers the flexor tendon forming the epitenon.[6] The outer parietal layer is conjoined with five annular and three cruciform pulleys. There is space filled with synovium between the flexor sheath parietal and visceral layers, which provides nutrition to the tendons within the sheath. Flexor tendons receive their vascular supply from the surrounding digital arteries via the vincular system.[7]  As the PFT develops, pus accumulates within the flexor sheath synovial space, causing high pressures up to 30 mm Hg within the flexor sheath closed space.[8] This high-pressure interferes with vascular supply to the flexor tendon, resulting in tendon scarring and rupture.  The flexor tendon sheaths for the index, middle, ring, and little fingers terminate at the level of flexor digitorum superficialis tendon insertion in the distal phalanx.  In the thumb, the flexor tendon sheath ends at the level of flexor pollicis longus tendon insertion. Proximally, the flexor sheaths of the index, middle, and ring fingers extend to the A1 pulley at the level of the neck of the metacarpal bone. The sheath of the flexor pollicis longus tendon communicates with the radial bursa proximally. The little finger flexor sheath communicates with the ulnar bursa in about 80 % of the population.[9] The radial and ulnar bursa are connected in 80% of the population, explaining how a little finger or thumb infection can cause the horseshoe abscess.[10]

Tenosynovitis with rice bodies is a rare presentation, diagnosable by MRI. Surgical excision is the preferred treatment for tendon sheath masses containing rice bodies. The etiology was Mycobacterium tuberculosis in our case, highlighting the need to consider extrapulmonary TB in atypical presentations, ensuring effective treatment.