CHAPTER 127 Deep Digital Flexor Tendon Injuries in the Foot
Although it has long been suspected that injury to the digital portion of the deep digital flexor tendon (DDFT) is a potential cause of lameness originating in the foot, practitioners’ inability to use diagnostic imaging techniques to assess soft tissues inside the hoof has limited antemortem diagnosis of this condition. Consequently, previous reports consist of reviews of cases that were diagnosed postmortem. Since the advent of magnetic resonance imaging (MRI) and, to a lesser extent, computed tomography (CT), it has become clear that tendonitis of the DDFT is the most common soft tissue injury causing lameness in the equine foot. Tendonitis of the digital portion of the DDFT may occur alone, in conjunction with navicular bone pathology, or as one component of a complex of a multiple soft tissue injuries in the foot.
The DDFT broadens distally into a fanlike expansion that occupies the entire space between the medial and lateral palmar processes of the distal phalanx. It inserts on the axial margins of both palmar processes as well as on the palmar border (facies flexoria) of the central part of the distal phalanx. Within the digit, the DDFT has an important role in providing palmar stability to the distal interphalangeal (coffin) joint. Tension in the DDFT results in compression of the dorsal articular surface of the navicular bone against the palmar aspects of the middle and distal phalanges. The DDFT has a dorsal fibrocartilaginous pad that supports pressure of the distal transverse ridge of the middle scutum during weight bearing. During the first half of the weight-bearing phase (dampening part) of the stride, the DDFT is also in contact with the distal palmar aspect of the navicular bone. During the second half (propulsion part) of the weight-bearing phase of the stride, however, the DDFT bends around the transverse ridge of the middle scutum and comes into full contact with the palmar surface of the navicular bone. At this time, active extensor muscle contraction and DDF tendon elasticity result in extension of the coffin joint, and the DDFT is under maximum tension and therefore most susceptible to injury. During maximum extension of the coffin joint at the end of the propulsion phase, the pull on the DDFT creates a shear force between the DDFT and the navicular apparatus, including the impar ligament. At the beginning of the swing phase of the stride, the tension in the DDFT induces flexion of the interphalangeal joints.
Limited information is available concerning the pathophysiology of digital DDFT injuries. Primary DDF tendonitis may be the result of repetitive overload stress or acute traumatic tearing. Predisposition to injury may increase as degenerative aging changes affect the DDFT or overload stress results in progressive increase in proteoglycans in the tendon matrix. Possible risk factors for DDFT injury include hoof conformation, angle of the distal phalanx, the horse’s athletic discipline, and previous palmar digital neurectomy. Theoretical modeling has indicated that for every 1-degree decrease in the palmar angle of the distal phalanx, the force affected by the DDFT on the navicular bone increases by 4%. However, a recent clinical study did not reveal any difference in the palmar angle of the distal phalanx of horses with or without DDFT tendonitis in the digit.
Horses used for jumping have a significantly higher risk of injuring the digital portion of the DDFT than those that are used for other sporting endeavors. Additionally, it would seem that risk increases proportionally with the height and intensity of jumping, further supporting the theory of overload injury taking place during maximum extension of the coffin joint.
Horses that have undergone palmar digital neurectomy are at significant risk of catastrophic deterioration in existing DDFT pathology, even when changes were only subtle at the time of surgery, because of the continued overloading of this compromised support structure. Recurrence of lameness after palmar digital neurectomy for treatment of “navicular syndrome” is frequently a result of proximal extension of a DDFT lesion into a region of the DDFT that is no longer desensitized by the neurectomy.
Recent pathologic surveys revealed four types of lesions in the digital portion of the DDFT: core lesions, sagittal plane splits, insertional lesions (enthesopathy), and dorsal border lesions. Core lesions (Figure 127-1) are characterized by gross fiber disruption in the center of usually only one lobe. Core lesions most frequently span the upper extent of the T-ligament into the proximal recess of the navicular bursa but can extend a variable distance proximodistally and occasionally cause a continuous core defect from the insertion to the level of the distal aspect of the proximal phalanx.
Figure 127-1 Cross section of the deep digital flexor tendon (DDFT) at the level of the proximal border of the navicular bursa in a 12-year-old Warmblood show jumper that became acutely lame in the right forelimb following a jumping class 4 weeks previously. Notice the large core lesion in the enlarged medial lobe of the DDFT (arrow) that contains degenerated matrix and torn tendon fibers.
Sagittal plane splits (Figure 127-2) develop mostly in the navicular bursal portion of the DDFT, at the level of the flexor surface of the navicular bone, and can extend proximodistally. The depth of a sagittal plane split may vary from superficial, extending no more than 20% through the thickness the affected lobe, to deep, extending from the dorsal surface to the palmar surface of the DDFT.
Figure 127-2 Dorsal surface of the left front deep digital flexor tendon (DDFT) at the level of the navicular bone of a 7-year-old Warmblood gelding with chronic bilateral foot lameness. Notice the full-thickness sagittal plane split in the lateral lobe of the DDFT that extends from the insertion of the DDFT to the proximal reflection of the navicular bursa (forceps). The horse had a similar lesion in the opposite forelimb.
Insertional lesions (Figure 127-3) are limited to the distal 10 to 20 mm of the DDFT near its insertion on the distal phalanx. They consist of small core lesions, sagittal plane splits, or osseous changes at the insertion site. Core lesions and sagittal plane splits can be encountered in this location as a distal continuation of more proximal lesions or may occur in isolation. Osseous changes of enthesopathy include focal cortical bone loss, cyst formation, entheseous new bone production, and sclerosis.
Figure 127-3 Palmar view of the right forelimb distal phalanx and transected insertion of the DDFT of a 9-year-old Thoroughbred riding horse with intermittent right forelimb lameness that was occasionally severe after exercise but improved quickly with stall rest. A small core lesion can be seen near the dorsal surface of the lateral lobe, characterized by a tissue defect surrounded by pale fibrous scar tissue (arrow).
Lesions of the dorsal border of the DDFT (Figure 127-4) are found primarily in the navicular bursa and consist of superficial fibrillations or diffuse lesions communicating with the dorsal margin of the DDFT. Dorsal DDFT erosions and abrasions consist of longitudinal strips of superficial fiber damage extending the length of the navicular bursa. Although other DDFT lesions frequently develop without abnormalities of the navicular bone, lesions of the dorsal border are invariably accompanied by degenerative changes of the palmar surface of the navicular bone. Not infrequently, fibrillated tendon fibers adhere to exposed areas of the flexor cortex.
Figure 127-4 Dorsal surface of the digital portion of the left front deep digital flexor tendon (DDFT) of a 10-year-old dressage horse with chronic intermittent bilateral forelimb lameness. Notice the vertical fibrillations with fiber loss on the dorsal surface of both lobes of the DDFT (arrows) within the navicular bursa. A small granuloma of torn superficial tendon fibers is evident at the proximal attachment of synovial membrane of the navicular bursa to the lateral lobe of the DDFT (forceps). Similar lesions in the contralateral DDFT and fibrocartilage erosions on the palmar surface of both navicular bones were seen in the opposite limb.
Any of the described lesion types may be seen alone or in combination with others. Generalized diffuse tendonitis has been described associated with MRI, but pathologic descriptions of this entity are lacking at present.
There are generally no visual or palpable abnormalities that indicate injury of the digital portion of the DDFT as the cause of lameness. Occasionally distension of the digital synovial sheath is seen in horses with a lesion that extends proximally to the level of the sheath. Even more rarely a focal, painful, firm soft tissue swelling can be appreciated on the palmar aspect of the DDFT in the distal aspect of the pastern.
Flexion and extension tests of the digit yield variable results but are not specific for digital tendonitis. Surprisingly, elevation of the heel by 15 to 20 degrees by application of a wooden wedge frequently results in marked exacerbation of lameness.