Hermena Shady, Tiwari Vivek
Ninewells Hospital , Dundee, Scotland
Apollo Sage Hospital, Bhopal, India
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. 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.
化脓性屈指肌腱腱鞘炎（PFT）是指在手指屈肌腱鞘的封闭间隙内发生的严重细菌感染。PFT占手部感染的2.5%至9.5%，可导致肌腱坏死和手指失活。这种感染会改变滑动机制，并在屈肌腱鞘内形成粘连，导致手指活动明显受限。PFT可由血流感染引起，但通常是由涉及屈肌腱鞘的手指穿透伤所致。1912年，艾伦·B·卡纳韦尔描述了化脓性屈指肌腱腱鞘炎的3个主要体征：屈肌鞘压痛、患指屈曲位以及被动伸指疼痛。后来，又增加了第4个体征，即手指梭形肿胀，从而形成了4个主要体征。体格检查中发现这4个卡纳韦尔体征对诊断化脓性屈指肌腱腱鞘炎具有较高的敏感性（91.4% - 7.1%）。及时诊断和迅速治疗对于限制与该病症相关的严重并发症至关重要。了解手部屈肌腱鞘的解剖结构对于更好地理解和处理PFT至关重要。它分为两部分：内层滑膜和外层纤维膜。每个屈肌腱鞘由两层组成：内层脏层和外层壁层。脏层紧密覆盖屈肌腱，形成腱外膜。外层壁层与5个环形滑车和3个十字形滑车相连。屈肌腱鞘壁层和脏层之间充满滑膜的间隙为鞘内的肌腱提供营养。屈肌腱通过腱纽系统从周围的指动脉获得血供。然而，肌腱鞘的血供不稳定，使得这个封闭间隙成为感染性生物体的理想滋生地。随着PFT的发展，脓液积聚在屈肌鞘滑膜间隙内，导致屈肌鞘封闭间隙内压力高达30 mmHg。这种高压进一步干扰屈肌腱的血供，导致瘢痕形成和断裂。示指、中指、环指和小指的屈肌腱鞘在指深屈肌腱插入远节指骨的水平处终止。拇指的屈肌腱鞘在拇长屈肌腱插入水平处结束。近端，示指、中指和环指的屈肌鞘延伸至掌骨颈部水平的A1滑车。拇长屈肌腱鞘近端与桡侧滑液囊相通。在大约80%的人群中，小指屈肌鞘与尺侧滑液囊相通。在掌侧前臂远端，指屈肌腱和旋前方肌之间的潜在间隙——帕罗娜间隙中，80%的人桡侧和尺侧滑液囊相互连通。这个解剖间隙使得小指或拇指感染可导致马蹄形脓肿。
