Pyogenic Flexor Tenosynovitis

Excerpt

Pyogenic or suppurative flexor tenosynovitis (PFT) is a severe bacterial infection within the closed space of the digital flexor tendon sheaths. PFT accounts for 2.5% to 9.5% of hand infections and can cause necrosis of the tendons and devitalization of fingers. 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 generally caused by penetrating finger injuries involving the flexor tendon sheath. In 1912, Allen B. Kanavel described 3 cardinal signs of pyogenic flexor tenosynovitis: flexor sheath tenderness, flexed position of the affected digit, and painful passive digital extension. Later, a fourth sign, fusiform swelling of the digit, was also added to become the 4 cardinal signs.

The detection of the 4 Kanavel signs on physical assessment has high sensitivity (91.4%-7.1%) to diagnose pyogenic flexor tenosynovitis. A timely diagnosis and prompt treatment are paramount 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 a better understanding and management of PFT. It has 2 parts: the inner synovial and the outer fibrous. Each flexor tendon sheath comprises 2 layers: an inner visceral and an outer parietal. The visceral layer closely covers the flexor tendon, forming the epitenon. The outer parietal layer is conjoined with 5 annular and 3 cruciform pulleys. Space filled with synovium between the flexor sheath parietal and visceral layers provides nutrition to the tendons within the sheath. Flexor tendons receive their vascular supply from the surrounding digital arteries via the vincular system. However, the vascular supply to the tendon sheaths is precarious, making the closed space an ideal breeding ground for infectious organisms.

As the PFT develops, pus accumulates within the flexor sheath synovial space, causing high pressures of up to 30 mm Hg within the flexor sheath closed space. This high pressure further interferes with vascular supply to the flexor tendon, resulting in scarring and rupture.

The flexor tendon sheaths for the index, middle, ring, and little fingers terminate at the level of the flexor digitorum profundus tendon insertion into the distal phalanx. The flexor tendon sheath ends at the flexor pollicis longus tendon insertion level in the thumb. 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. The radial and ulnar bursa are connected in 80% of people in the space of Parona, a potential space between the digital flexor tendons and the pronator quadratus in the volar distal forearm. This anatomic space allows a little finger or thumb infection to cause a horseshoe abscess.