StatPearls: Pyogenic Flexor TenosynovitisStatPearls. StatPearls Publishing: Treasure Island (FL).BOOK
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]
