05/09/2023
Deep Digital Flexor Tendon (DDFT)
Brian S. Burks, DVM
Diplomate, ABVP
Board Certified in Equine Practice
The Deep digital flexor muscle originates at the elbow from the medial humeral epicondyle, radius and ulna and inserts underneath the distal phalanx, or coffin bone. It serves to flex the distal phalanx.
The deep digital flexor tendon arises as three muscle bellies from its origin on the medial humeral epicondyle and ulna, fusing to form a common tendon just above the carpus on the caudal aspect of the limb. The muscle continues distally along the back of the radius, giving rise to the DDF tendon just above the carpus. The single tendon passes distally, enclosed in the carpal sheath, through the carpal canal. In the mid-metacarpal region, the tendon is enforced by the distal accessory ligament (inferior check ligament). At the metacarpophalangeal (fetlock) joint, the DDFT passes over the sesamoid groove. In the middle of the proximal phalanx, or long pastern bone, the DDFT runs between the branches of the SDFT and over the distal sesamoid (navicular) bone to insert on the underside of the distal phalanx.
The navicular bursa is a synovial sac between the DDFT and the distal sesamoid (navicular) bone. It extends beyond the borders of the distal sesamoid bone proximally, distally and laterally. The distal parts of the superficial and deep digital flexor tendons are supported by three annular ligaments:
Palmar annular ligament
Proximal digital annular ligament
Distal digital annular ligament
There are several disorders associated with excessive tension of the DDFT, including clubbed feet, navicular bursitis, and laminitis. Two primary forces of the DDFT affect structures within the foot: pressure on the navicular bone and a downward or rotational pull on the coffin bone.
The cause of excessive DDFT tension is often unknown. Factors implicated include developmental orthopedic disease (DOD), eating habits (i.e., standing with one limb forward and the other back), pain higher up in the affected limb(s), the horse being “right-” versus “left-handed” (or vice-versa), genetics, and rate of growth. Despite the actual cause(s), the consequences of increased DDF tension are consistent.
It is typical for one thoracic limb to demonstrate more tension than the other. This causes the feet to be different- one limb more contracted than the other.
A clubbed foot is when the heel has grown long, causing the hoof-pastern axis to a more forward position, where the angle of the foot is steeper than the angle of the pastern. Due to the insertion of the DDFT on the coffin bone, increased tension will pull or rotate the bone downward, creating a steep hoof angle with high, contracted heels and a broken forward HPA. This results in misarticulation of the coffin joint and osteoarthritis. A foot is not considered to be clubbed until the distal limb axis is broken forward.
Rotation of the third phalanx can result in separation of the sensitive and insensitive tissue along the laminar interface of the hoof. This delamination occurs slowly and is not associated with laminitis. Dishing of the dorsal hoof wall confirms that separation has occurred. This separation can allow ubiquitous fungi and bacteria to enter the damaged tissue, leading to white line disease. Elimination of the open space eliminates the infection.
The navicular bone serves as a fulcrum to change the direction of the DDFT as it travels inside the foot. Increased tension of the DDFT causes more pressure on the navicular bursa and bone. This is a cause of navicular disease.
Laminitis is the result of both biomechanical and metabolic processes within the laminae. Increased tension of the DDFT causes distraction forces on the laminae, leading to separation of the sensitive and insensitive laminae and therefore rotation of the coffin bone within the hoof capsule.
As these conditions are the result of excessive DDFT tension, treatment includes techniques to lessen the tension. Decreased DDFT tension reduces the pressure on the navicular bone and less rotational pull on the distal phalanx. This tension can be reduced by lengthening the tendon or shortening the distance between the origin and insertion of the tendon.
Younger horses may benefit from stretching the DDFT and/or limiting growth rate of the bones. Trimming the heel lower will increase tension on the tendon but may help to stretch the tendon. This should not be done if the horse is lame or the horse is older, as this will likely negatively affect the condition. Also in young horses, decreasing the energy intake will slow growth and allow the slower growing tendon to lengthen in response to bone growth; bone grows faster than tendon, causing increased tension. Contraction of the DDFT is associated with elevated carbohydrate levels and mineral imbalances, especially calcium, phosphorus, and copper/zinc.
Foals and weanlings may benefit from intravenous oxytetracycline to treat tendon contraction. Adult horses may benefit from treatment, but the results are less profound. The high dose required has the potential to cause renal toxicity, gastrointestinal distress, though these effects are not common in my experience. It must be diluted in normal saline and given slowly via IV catheter. Its purported mechanism is to chelate calcium, but serum calcium does not decrease significantly. This treatment modality is often combined with other treatment strategies.
The inferior check ligament originates from the palmar carpal ligament and inserts on the deep digital flexor tendon in the mid metacarpal region. It functions to ‘check’ the DDFT and prevent overstretching in normal horses. The distal accessory ligament transmits loads to the distal portion of the tendon during movement; it transmits more force to the tendon than the DDF muscle, and the load is much less after desmotomy of the check ligament. It has also been shown that the DDF musculotendinous unit lengthens following desmotomy. If excessive DDF tendon tension persists by the time the horse reaches 8-10 months of age, then surgical intervention in the form of distal accessory (check) desmotomy is often elected. The procedure is also used in older horses with navicular disease and laminitis.
If excessive tension persists after ICLD, the DDF tendon can be transected in horses with laminitis. This eliminates tension across the navicular bone and the pull on the distal phalanx. Since an intact DDF tendon is required for sound movement, this procedure is considered only for salvage, and return to performance is not expected.
After 18-24 months or age, the DDF tendon has lost most of its pliability, and is generally not willing to “stretch” easily. In older horses, therefore, treatment strategies are usually directed at shortening the distance between the origin and insertion of the tendon. This is typically accomplished through corrective shoeing.
There are several ways that corrective shoeing can alleviate DDFT tension. Allowing the heel to grow and shortening the toe, along with the use of wedge pads. Elevation of the heels results in “dropping” of the fetlock and tension is transferred to the suspensory ligament. Too much heel elevation causes misarticulation of the coffin joint, crushing of the heels, and excessive strain on the suspensory ligament.
Facilitation of breakover is also important; the break-over point should be moved back, which shortens the stride length. There is less foot extension and thus less tension on the DDFT. Break-over is moved back by trimming the toe and/or rolling the toe.
The origin of DDFT tension is not always known and can be challenging to treat. There are several treatment strategies that may be employed to alleviate the tension. No treatment is considered a permanent fix.
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