Etiopathogenesis

Acute noninfectious tenosynovitis is a traumatic synovitis/capsulitis of the sheath lining. As for joints, a traumatic synovitis/capsulitis can be caused by accumulative low-grade trauma associated with normal exercise, acute trauma associated with direct impact force (e.g., overreach), or an abnormal force outside the normal range of movement of the fetlock region (e.g., hyperextension). Synovitis/capsulitis is more frequently secondary to damage to the internal or supporting structures of the DFTS, such as disruption of the visceral or parietal synovial layers, tearing of the vincula, tearing of the sheath wall with herniation or synoviocele formation, central or marginal damage to the flexor tendons, tearing of the manica flexoria, and spraining of the PAL or proximal digital annular ligament. Each of these complicating conditions is likely to result in continuous irritation of the sheath and cause chronic tenosynovitis. Chronic tenosynovitis may be associated with villonodular thickening of the sheath lining, especially in the proximal recess; adhesion formation between the visceral and parietal synovial lining; and fibrosis with reduced elasticity of the DFTS capsule. When these conditions are present, a self-perpetuating cycle occurs of improvement with rest, followed by repeated inflammation with exercise. This results in increased inflammation and lameness, further fibrosis, and eventually thickening of the PAL and stenosis of the fetlock canal (see the following discussion of PAL syndrome). Complex tenosynovitis has been defined as tenosynovitis with thickening of the PAL, synovial distention, and adhesions or synovial masses, or both (Figure 74-2).¹² Windgalls, especially those occurring bilaterally in the hindlimbs, are another form of low-grade chronic tenosynovitis. Although lameness is not usually a feature of windgalls, the synovial effusion is still likely to reflect the presence of low-grade chronic synovitis of the DFTS, caused by the continuous stress of use-induced overloading.

Fig. 74-2 Stage 3 tenosynovitis of the digital flexor tendon sheath with adhesions and synovial mass formation (arrow).

Diagnosis

Acute tenosynovitis is characterized by a sudden onset of mild to severe lameness, accompanied by DFTS distention that can be palpated in the proximolateral and proximomedial pouches of the sheath and in the palmarodistal recess between both branches of the SDFT. The palmar or plantar region of the fetlock has increased skin temperature, and forced flexion of the fetlock is painful and exacerbates lameness. Chronic tenosynovitis produces similar signs, except for the signs of acute inflammation, although repeat injury may cause these signs to be superimposed on an established tenosynovitis. Disproportionate distention and pain in different regions of the DFTS can reflect the site of the primary pathology; pain on palpation of the proximal aspect of the DFTS is present when there is tearing of the digital flexor tendons in this location.

Ultrasonographic examination is essential for identifying any primary pathology responsible for the tenosynovitis, such as adhesions and complicating injuries of the digital flexor tendons (see Figure 69-8, A), the intersesamoidean ligament, or annular ligaments, and to document the staging of the condition.¹³ DFTS effusion may also accompany injury to the intrathecal part of the SDFT associated with a classic bowed tendon (see Chapter 69). However, intrathecal tendon injuries occur more commonly as focal core lesions in the DDFT (see Chapter 70) or as longitudinal tears of the SDFT, DDFT, or manica flexoria. DDFT tears usually involve the lateral or medial borders of the tendon in the forelimb; hence oblique ultrasonographic views can sometimes identify defects on these borders, although they are easily missed. Oblique images are also required to image the abaxial margins of the SDFT. Manica flexoria tears are more frequently seen in hindlimb tenosynovitis and are also easily missed using transverse ultrasonographic images because the tears are usually incomplete and located at the site of attachment of the manica flexoria to the SDFT. Recently, we have found that a midline longitudinal scan immediately proximal to the PSBs provides the best image for identifying instability and/or thickening of the manica flexoria that accompanies tears (Figure 74-3). However, negative ultrasonographic findings do not preclude a tear in the manica flexoria.

Fig. 74-3 Longitudinal ultrasonographic images from the midline immediately proximal to the metatarsophalangeal joint (distal to the left). The left limb has a normal manica flexoria (arrow). In the right hindlimb, the manica flexoria is displaced from the dorsal surface of the deep digital flexor tendon and is thickened (arrow).

Ultrasonographically, tenosynovitis has three progressive stages.¹⁴ Symmetrical distention of the DFTS without evidence of synovial proliferation represents stage 1, or the effusive stage of synovitis. More pronounced, often asymmetrical distention of the proximal pouch, which feels firm on palpation and is accompanied by synovial proliferation, is stage 2. In stage 3 synovitis, extensive synovial proliferation occurs with or without adhesion formation in the sheath. Adhesions are manifest as echogenic material between the tendon and wall of the DFTS and can be more easily seen when fluid from marked distention provides negative contrast. Care must be taken to avoid undue pressure on the ultrasound transducer, which will obliterate this fluid from the field of view. However, the presence of adhesions can be easily overestimated with ultrasonography.

Treatment