Ultrasonography of the Fetlock
1AZURVET Referral Veterinary Centre, Cagnes sur Mer, France
2The Royal Veterinary College, North Mymms, Hatfield, UK
The Fetlock Joint
Preparation and Scanning Technique
High-frequency (7.5–16 MHz) linear array transducers provide optimal information in this area, although a micro-convex probe may be useful to image the distal aspect of the proximal sesamoid bones. A standoff pad may be used to improve probe-to-skin contact and structure alignment. However, with copious amounts of coupling gel, placing the probe directly on the skin provides finer control of the pressure exerted on the skin and underlying structures. Excessive pressure may cause pain, alter the shape of structures examined, and displace an effusion, which may thus be overlooked.
Images obtained in a longitudinal (parasagittal) plane, i.e. in a direction perpendicular to the joint space, are easier to interpret, although both longitudinal and transverse planes should be used in combination (Figure 2.1). The joint is examined with the horse weightbearing. Examination starts on the dorsal aspect, then both abaxial aspects are assessed, including the collateral ligaments, abaxial aspect of the sesamoid bones, and the palmar/plantar joint pouch. The intersesamoidean ligament is assessed from a palmar approach through the flexor tendons and proximal scutum (fibrocartilage covering the palmar aspect of the sesamoid bones). The limb is eventually picked up and flexed to evaluate the distal metacarpal/metatarsal joint surfaces.
Ultrasonographic Anatomy of the Normal Fetlock Joint
The ultrasonographic anatomy of the fetlock has been described by Denoix (see Recommended Reading at the end of the chapter). The fetlock is grossly similar in the thoracic and pelvic limbs. “Metacarpus” and “palmar” will therefore be used for both “metatarsus” and “metacarpus”, and both “palmar” and “plantar” in the following text.
The structures at the dorsal aspect of the joint are schematically reviewed in Figure 2.2. The distal metacarpus forms a smooth, cylindrical surface, horizontally oriented and separated into two condyles (lateral and medial) by the sagittal ridge. The latter is perfectly round and smooth in longitudinal section and triangular in cross-section (Figure 2.3). The cartilage is anechogenic and regular in thickness. It is thickest over the sagittal ridge (usually 1–1.2 mm) and thinner over the condyles, typically less than 0.7 mm. The mineralized part of the cartilage and underlying subchondral bone cannot be differentiated; they form a smooth, hyperechogenic interface, producing shadowing and reverberation.
Proximal to the condyles and sagittal ridge, the cartilage is interrupted and there is often a small step between the edge of the cartilage and bare bone proximal to it. In this location, bone is actually covered by synovium up to the proximal insertion of the joint capsule. This area may be variable in shape, slightly irregular or concave (Figure 2.4).
The dorsoproximal edge of the proximal phalanx (P1) is rounded and smooth and its proximal articular surface is not visible (Figure 2.3). The dorsomedial and dorsolateral eminences of P1 are slightly convex, the medial one being slightly more prominent. In normal joints, the capsule and synovium are tightly applied against the bone surfaces. With severe effusion, the capsule may be displaced away from the bone surfaces.
The joint capsule on the dorsal aspect of the joint is thick, fibrous (isoechogenic to the extensor tendons), and elastic (Figures 2.2 and 2.3). It inserts proximally on the metacarpus 3–4 cm proximal to the edge of the condyles and distally on the dorsoproximal aspect of P1, approximately 2 cm distal to the proximal edge. There the capsule adheres to the common/long digital extensor tendon. The lateral digital extensor tendon blends broadly into the fibrous capsule.
Dorsally the synovial membrane forms a transverse ridge, triangular in longitudinal section, which fills the space between the metacarpal condyles and P1. Proximally, the membrane reflects back to form a thin, flat, and transversely oriented fold or pad, normally not visible unless there is marked thickening and/or effusion. No fluid is normally visible.
The thin (2–4 mm) common (or long) digital extensor tendon (CDET) is separated from the joint capsule by a small subtendinous bursa. The latter is virtual and rarely visible in normal horses (Figure 2.3).
Abaxially (laterally and medially), the medial (MCL) and lateral (LCL) collateral ligaments are mere focal thickening of the joint capsule (Figure 2.5). Their borders are therefore difficult to differentiate from the rest of the fibrous capsule in cross-sections. In longitudinal (frontal) planes, parallel striation similar to that of tendons is clearly identified. Each ligament is made out of two separated branches: a long, superficial part and a shorter, deep part. The superficial branch extends from the metacarpal epicondyle down to the abaxial border of P1, 2 cm distal to the joint space. The deep branch originates dorsodistal to the epicondyle, crosses in a distopalmar direction under the superficial branch and inserts on the edge of P1, close to the joint space. The collateral ligaments are therefore X-shaped and each branch must be examined separately. The transversely oriented collateral ligaments of the proximal sesamoid bones blend into the deep branches of the collateral ligament.
The palmar aspect of the joint is largely hidden by the proximal sesamoid bones (Figure 2.6). The sagittal ridge of the distal metacarpus is visible from the palmar aspect of the limb between them, through the transversely oriented intersesamoidean ligament and hypoechogenic proximal scutum.
The palmar recess of the fetlock joint is a large synovial pouch located between the metacarpus, the apex of the sesamoid bones, the branches of the suspensory ligament, and the distal extremity (“button”) of the splint bones (second and fourth metacarpal bones). In normal horses, it is mostly filled by synovial folds and contains little fluid. It can however fill up with a moderate amount of fluid in clinically normal horses.
Ultrasonographic Abnormalities of the Fetlock
Synovitis refers to inflammation of the synovial lining of the joint. It is a feature of most joint diseases but may occur as a primary entity, particularly in sports and race horses. It should not be mistaken for a non-inflammatory joint effusion (“cold effusion”) where abnormal amounts of anechogenic fluid are present without any thickening of the synovium.
Acute synovitis is characterized by mild to severe thickening of the synovial layer of the capsule (this layer is not normally visible) because of edema, vascular hyperemia, and distension of the synovial pouches by joint fluid (Figure 2.7). The inflammation is most obvious dorsoproximally. The dorsal fold (“synovial pad”) is displaced away from the articular surface, and becomes hypoechogenic, mildly thickened, and clubbed (Figure 2.8). The palmar pouch contains large synovial villi that rapidly become hypertrophied and fill up the pouch within a matter of days. These form dense, amorphous, and highly vascularized masses.
The fluid is normally anechogenic. In early, acute stages, mildly echogenic, “cellular” and grainy fluid may be present (Figure 2.9). This is typical of hemarthrosis, although this appearance is very similar to that of septic exudate. Bleeding probably occurs through trauma and tearing of the capsule and synovium. The fluid rapidly becomes anechogenic unless recurrent bleeding or sepsis is present, although fibrin clots and pannus may remain adhering to cartilage for several days to weeks (Figure 2.10).
Chronic synovitis may develop as a complication of nearly any fetlock joint pathology that has been left untreated for too long or has not responded to treatment. The echogenicity of the synovial membrane increases, mostly because of a cellular infiltrate and secondary fibroplasia. It becomes more homogeneous and isoechogenic relative to the fibrous capsule. Fibrosis and retraction lead to rounding of the synovial pads and ridges (Figure 2.11).
Assessment of the synovial fold on the dorsal aspect of the joint is usually used as a reference point to confirm chronic inflammatory changes. There currently is a lack of quantitative data regarding what tissue thickness should be regarded as abnormal. Denoix suggests that thickening of the dorsoproximal synovial fold over 2 mm in thickness is a sign of inflammation while other authors use a cut-off thickness of 4 mm. (See Recommended Reading for further information.)
In the palmar pouch, hypertrophic villi may be clubbed or rounded or form localized, dense masses, which can eventually undergo fibrocartilaginous metaplasia or even become mineralized (thus producing hyperechoic acoustic shadowing artifacts).
Synovial hypertrophy and hyperplasia can form space-occupying lesions (Figure 2.12). Initially referred to as villonodular synovitis, they are most frequently recognized in the dorsal proximal pouch, where a pressure-induced, smooth, and rounded defect is often observed on the dorsodistal aspect of the metacarpus on radiographs as on ultrasound images. Similar hyperplastic masses are also common in the palmar pouch. This condition is purely inflammatory in horses and should therefore be referred to as chronic hypertrophic synovitis. In-between stages, spanning from mild proliferation to very large mass formation, are encountered.
Enthesophytes, characterized by an irregular capsule-to-bone interface and the presence of hyperechogenic spurs at the capsule insertions, often occur at the collateral ligament insertions and at the capsule and extensor tendon attachments on the dorsoproximal aspect of P1.
Traumatic Cartilage/Subchondral Bone Injury
Traumatic arthritis of the fetlock can include bone contusion and various degrees of bone surface damage (subchondral bone or cartilage injuries, fragmentation etc.). Although radiography, using specific oblique views, can show the presence of fragmentation or defects, radiographs are often non-diagnostic. Scintigraphy and magnetic resonance imaging (MRI) are the most sensitive techniques to confirm such lesions. Ultrasonography will often confirm the presence of subchondral bone defects or cartilage erosions (Figure 2.13). Lesions located on the palmar part of the metacarpal condyles are hidden from view by the sesamoid bones. Large lesions may, however, be identified with the joint fully flexed. Proximal P1 subchondral injuries are not amenable to ultrasonographic diagnosis. Further investigations may be indicated if there is ultrasonographic evidence of severe synovitis without specific lesions identified on either radiography or ultrasonography.
Fetlock OA is extremely common. Radiographic signs are often subtle and occur late in the disease process, at a stage where cartilage damage has become irreversible. Ultrasonography provides much earlier signs of joint disease and permits identification of very subtle lesions or new bone production.
Typically the earliest signs of OA include mild to severe synovitis and subtle cartilage changes, with focal or diffuse irregularity and discrete hyperechogenic foci. Thinning is most obvious on the sagittal ridge (although care should be taken not to misinterpret the incidental irregularity frequently seen at the dorsoproximal end of this ridge). Erosions may be visible on the distal aspect of the metacarpal condyles (Figure 2.14). In severe cases, there may be barely any visible cartilage left, the capsule coming into contact with the subchondral bone. Focal defects may result from contact (“kissing”) lesions induced by osteochondral fragments (Figure 2.15). High-frequency probes (12–18 MHz) may be required to provide details of cartilage integrity.
Osteophytes are bony proliferations at the ends of the subchondral bone plate, where the synovial membrane replaces cartilage. True osteophytes form irregular to spiky, hyperechogenic interfaces that protrude into the joint (Figure 2.16). They are typically in alignment with the joint surface. They are most commonly encountered at the dorsoproximal border of P1, along the proximo-abaxial edges of P1 and the disto-abaxial edges of the metacarpal condyles, along the dorsoproximal margin of the cartilage-covered condyles and at the apex of the sesamoid bones. There may also be marked irregularity of the proximal extremity of the sagittal ridge.
Enthesophytes are bony new bone productions within the insertion of capsules, ligaments, or tendons. They may secondary to chronic inflammation, OA, primary capsulitis, or collateral desmitis. They are encountered within the dorso-abaxial insertion of the capsule, and at the collateral ligament attachments on P1 and the metacarpus.
Chronic hypertrophic synovial hyperplasia is usually present in OA, although repeat intra-articular medication with steroid drugs may prevent chronic inflammatory changes, especially in young racehorses, making the diagnosis more difficult to confirm on ultrasound examination.
Osteochondrosis and Cyst-Like Lesions
Subtle erosions or defects in the subchondral bone outline are more readily identified ultrasonographically than radiographically. The extent of the lesion in both longitudinal and transverse planes can be accurately established. Associated soft tissue inflammatory changes, cartilage thinning, and adhesions can also be detected. Depending on the stage of the lesion, it may be difficult to differentiate osteochondrosis from osseous cyst-like lesions, subchondral bone trauma, and erosions secondary to OA.
Osteochondrosis (OC) is common in the fetlock. The most common site is the dorsal aspect of the sagittal ridge where it can span from mild, usually clinically silent flattening of the ridge, to various degrees of subchondral bone defects (Figure 2.17). Lesions may also occur immediately lateral and/or medial to the sagittal ridge dorsoproximally. The thickness and echogenicity of the cartilage are both increased in OC, although thinning of the cartilage will eventually occur as a result of fragmentation and fibrillation of the damaged cartilage, and secondary OA. Cartilage dissection (osteochondrosis dissecans or OCD) may be identified by the formation of an interface between the cartilage and bone defect in some cases (Figure 2.18). Hyperechogenic areas of mineralization may be seen within affected cartilage and loose cartilage or osteochondral fragments (“joint mice”) may be identified within the joint space (Figure 2.19).