CHAPTER 123 Chronic Laminitis
Chronic laminitis is defined by mechanical collapse of the lamellae and displacement of the distal phalanx within the hoof capsule. It can occur as a direct sequel to acute laminitis, that is, within the first 72 hours of onset of clinical signs, or as a sequel to subacute laminitis, by definition, the phase following the acute disease but without mechanical collapse of the lamellae. In simplistic terms, the acute phase is the phase of injury, and the subacute and chronic phases are phases of tissue repair. The chronologic divide between acute and subacute laminitis is obviously arbitrary because the disease process is a continuum in which the injurious processes gradually yield to restorative processes. The fundamental difference between the pathogenesis of subacute laminitis and that of chronic laminitis is the difference in the repair processes caused by displacement of the distal phalanx. This inevitably has consequences for treatment and prognosis.
Separation of the lamellae is a consequence of the severity of the original pathologic processes of inflammation, ischemia, and thrombosis in the face of the mechanical stresses superimposed on the lamellae. Lamellar separation at any point around the circumference of the distal phalanx is therefore a balance between the severity of the underlying disease processes and the magnitude of lamellar stresses (i.e., disease without lamellar stress or lamellar stress without disease), and no separation occurs (the possible exception being prolonged excessive weight bearing by one limb). The way in which the distal phalanx displaces is related to the distribution of lamellar separation around the circumference of the distal phalanx and is therefore related to the distribution of the disease and stresses. Little is known about the distribution of the disease processes.
The greatest stress imposed on the lamellae is weight bearing. Superimposed on weight bearing stress is the stress caused by the moment about the distal interphalangeal joint, wherein tension in the deep digital flexor tendon (DDFT) is opposed by tension in the dorsal lamellae. Movement of the horse alters the magnitude and position of the ground reaction force and the tension in the DDFT and, therefore, the magnitude and distribution of lamellar stresses. As a horse lifts one foot off the ground, the load on the contralateral limb is doubled. Also, as a horse moves, stress is concentrated in the dorsal hoof wall at breakover. Relatively uniform lamellar loss predisposes to distal displacement (sinking) of the entire distal phalanx within the hoof capsule. In contrast, relatively greater lamellar disruption at the toe or either quarter will cause the distal phalanx to displace asymmetrically within the hoof capsule. When this loss is greatest dorsally, the result is dorsal capsular and phalangeal rotation. Capsular rotation refers to deviation of the parietal surface of the distal phalanx with respect to the hoof capsule. Phalangeal rotation refers to rotation of the distal phalanx with respect to the axis of the proximal phalanges (i.e., distal interphalangeal joint flexion). In an acutely rotated horse, both occur simultaneously. When one quarter is affected more than the other, the distal phalanx displaces unilaterally (sinks medially or laterally, perhaps more appropriately described as medial or lateral capsular rotation), a far less frequent scenario than dorsal capsular rotation. In reality it is unlikely that lamellar injury is confined to any one area around the perimeter of the foot, so most horses display a combination effect.
Immediately following mechanical failure of the dorsal lamellae and rotation of the distal phalanx, the dorsal hoof wall is still straight and of normal thickness, and the space created by the separation is filled with hemorrhage and inflamed and necrotic tissue. The result of the repair process is that the space is variably filled with hyperplastic and hyperkeratinized epidermis. The lamellae exhibit varying degrees of dysplasia, widening, fusion, shortening, or loss of primary or secondary lamellae. This results in a loss of surface area between the epidermal and dermal lamellae and consequent decreased strength of attachment.
Concurrent with lamellar repair is continued hoof growth and development of the characteristic distortion of the dorsal wall. The severity of the distortion of the hoof wall varies with changes in thickness and divergence from the parietal surface of the distal phalanx. The change in thickness of the hoof wall appears to be related to a change in the conformation of the coronary groove so that it is wider and shallower. There are several potential causes for the redirection of the dorsal hoof wall away from the distal phalanx: the differential growth rate between the hoof at the heels and toe, the composition of the repair tissue between the hoof capsule and the distal phalanx, pressure on the distal surface of the wall causing continued distraction from the distal phalanx, and redirection of the dermal papillae of the coronary band.
At the onset of chronic laminitis, the eventual degree of hoof capsule distortion is unpredictable. In most horses new wall growth advances from the coronary band approximately parallel to the parietal surface of the distal phalanx, at least until it has reached the junction of the proximal and middle thirds of the hoof wall. At this juncture the proximal and distal portions of the hoof wall form two distinct angles with the ground that are separated at the margin between hoof wall formed before the onset of laminitis and that formed subsequently. As the new hoof wall grows through the middle third of the dorsal hoof wall, a varying amount of deviation away from the parietal surface of the distal phalanx occurs. In other horses the newly formed hoof wall diverges from the parietal surface of the distal phalanx at the coronary band.
Displacement of the distal phalanx within the hoof capsule also causes the normal arch of the sole to drop. As the new dorsal hoof wall grows out and reaches the ground surface, the white line becomes wider, reflecting the increased space between the stratum medium of the hoof wall and the parietal dermis.
Complications during rehabilitation from chronic laminitis are common and include infection, perforation of the sole, contraction of the hoof, and contracture of the flexor apparatus. The combination of a cavity filled with hemorrhage or necrotic tissue and damage to the structural integrity of the white line sole is an invitation to infection. Most frequently the infection involves the nonkeratinized layers of the epidermis and the dermis. The resulting accumulation of exudate causes pain and further separation of the hoof capsule from the underlying soft tissues. Drainage may occur at the coronary band, through the white line, or through the sole, and separation of the hoof capsule may be extensive. If the wall is sufficiently unstable, movement of the wall of the hoof capsule against the underlying soft tissues may cause severe chafing and loss of germinal epithelium. If sufficient damage occurs, infection spreads to the distal phalanx. Contraction of the hoof capsule may be secondary to the pain or may result from certain shoeing practices used in the treatment of the disease, namely placement of the nails in the palmar half of the foot and elevating the heels. Contraction of the flexor apparatus is also likely a sequel to chronic pain.
The exact causes of pain in chronically laminitic horses are undetermined but are likely to be related to continued ischemia, inflammation, and trauma to the dorsal lamellae and ischemia or inflammation associated with bruising of the soft tissues of the sole immediately distal to the solar margin of the distal phalanx. Pain is also associated with foci of infection causing increased subsolar or intramural pressure. Additionally, contraction of the hoof may cause pain localized to the palmar aspect of the foot.
The diagnosis of chronic laminitis is seldom a challenge because the gait and appearance of the foot are characteristic of the disease, and radiographs usually remove all doubt. Occasionally, nerve blocks are necessary to localize the pain to the foot in mildly affected horses and should be interpreted in conjunction with the results of hoof tester application and radiographic findings.
Horses with chronic laminitis have several possible clinical manifestations: (1) as the continuation of acute laminitis, (2) as a recurrence of past chronic laminitis, or (3) with an unknown history because the acute phase was never observed or the horse was purchased without knowledge of the disease.
Full evaluation of the history, the horse, and the digits are all important in determining the prognosis and treatment. The severity of the initial acute phase is the best indicator of the extent of the original damage and hence a major factor in the prognosis. The duration of the disease since the acute phase gives some indication as to how much the lamellar repair process may have stabilized the distal phalanx within the hoof capsule. How lame the horse is, including how willing it is to walk, how stiffly it walks, how willing it is to lift a foot, and how much it lies down do not correlate as well with the prognosis as they do in acute laminitis, and they do not necessarily correlate with the clinical appearance of the foot or the radiographic changes. How the animal preferentially places its foot may indicate the distribution of lamellar injury; for example, a horse that preferentially bears weight on its heels reduces the tension in the dorsal lamellae and the compression of the sole beneath the dorsal margin of the distal phalanx. Similarly, a horse that is landing on one side of its foot may be protecting the contralateral wall or sole. Additionally, the way a horse moves is an adjunct to determining the type of shoe to use and its placement. Observation of the hoof wall, sole, and white line, along with the response to palpation of the coronary band, provides clinical indicators of the pathology that has occurred within the digit, including capsular distortion, displacement of the distal phalanx, the presence of infection, and secondary contraction of the hoof or flexor apparatus.
From the perspective of diagnosis, the radiographic features of chronic laminitis are well documented. To assist in the prognosis and treatment, several observations are valuable. High-quality lateral, dorsopalmar, and dorsopalmar oblique projections are necessary. The exposure must include good images of the hoof capsule. Radio-opaque markers are invaluable to determine the position of the distal phalanx in relation to surface landmarks. For the lateral radiograph, a linear marker should be placed on the midsagittal dorsal hoof wall, starting at the coronary band and extending distally, and a point marker should be placed at the true apex of the frog. Additionally, for the dorsopalmar radiograph, linear markers may be placed on the medial and lateral walls of the hoof capsule. Finally a linear marker should be embedded in the surface of the radiography block.
The lateral radiograph should be examined to determine the thickness of the dorsal hoof wall, the degree of capsular rotation, the angle between the solar surface of the distal phalanx and the ground, and the distance between the dorsal margin of the distal phalanx and the ground. The dorsopalmar view is most useful to determine whether there is mediolateral rotation of the distal phalanx within the hoof capsule or mediolateral imbalance. The location of gas pockets is determined by correlating the findings of the lateral and dorsopalmar radiographs. The margin of the distal phalanx is evaluated for pedal osteitis, sequestra, and margin fractures on the oblique dorsopalmar view.
Positive-contrast venography of the foot may indicate the presence of filling defects in the digital vasculature that signify a poor prognosis—namely, defects in filling of the lamellar vessels, the circumflex area, and the terminal arch. It is important that the venogram is performed with a good tourniquet and the contrast medium infused while the foot is unloaded to prevent artifactual filling defects.
The eventual outcome of the treatment for horses with chronic laminitis can be divided into functional and morphologic outcomes. The functional outcome is most likely to dictate whether the horse can return to athletic activities, can regain only pasture soundness, or must be euthanized. The morphologic outcome is more likely to determine the degree to which continued and potentially lifelong corrective measures are necessary. While there is fair correlation between the functional and morphologic outcomes, some horses with seemingly modest morphologic changes are euthanized, whereas others are performing more strenuous athletic activity than the morphologic appearance would lead one to expect.
At the onset of chronic laminitis, the eventual outcome is hard to predict, but the most important indicator for survival remains the severity of the initial insult to the lamellae. The appearance of the initial radiographs does not necessarily correlate with either the functional or the morphologic outcome. However, the thickness of the sole and the angle between the solar surface of the distal phalanx and the ground are fair indicators of the difficulty of treatment of horses with dorsal phalangeal rotation, and both are more useful than the degree of capsular rotation in successfully predicting the rehabilitation of the horse. The thickness of the soft tissues dorsal to the parietal surface of the distal phalanx is suggestive of the prognosis in horses with distal displacement of the distal phalanx inasmuch as it indicates the severity of the original injury. In horses with capsular rotation, the eventual morphologic outcome only becomes apparent as the new dorsal hoof grows down through the middle third of the wall.
The desired outcome of treatment of horses with laminitis is freedom from pain and feet with normal appearance and function. Obviously there are major limitations that interfere with achieving these ideals. The treatment of chronic laminitis is multifaceted and includes providing supportive care of the feet, medical therapy, surgical intervention, and nutritional management. In contrast to treating horses with acute laminitis, in which medical therapy frequently assumes priority, supportive therapy is the most important element for success in treating horses with chronic laminitis.
It is not possible to directly reattach the mechanically separated lamellae. Rather, the return of mechanical function of the wall is a gradual process that could take as long as 9 months without complications. Supportive therapy maintains an environment that enhances natural healing and the efficacy of other therapy. In horses with chronic laminitis, this is rest and hoof care. Absolute stall rest in acute and in the early stages of chronic laminitis is imperative because movement is associated with increased stress within the damaged lamellae. Later on, rest must be balanced against the need to restore normal function of the hoof capsule, which comes with repeated expansion and contraction as the animal moves.
The mainstay of hoof care is therapeutic shoeing. In considering hoof care in horses with chronic laminitis, there are three goals of therapy: to stabilize the distal phalanx within the hoof capsule, control pain, and encourage new hoof growth that will assume the most normal relationship possible to the distal phalanx. It is necessary to stabilize the foot so that there is no further injury to the remaining lamellar attachments or to the new lamellar attachments being formed. It is desirable to control the horse’s pain for humane reasons as well as to restore some degree of function to spare the other limbs from excessive weight bearing. Encouraging the foot to return to normal form, both in appearance and anatomically, is the surest way to optimize future function.
Stabilizing the distal phalanx within the hoof capsule deserves special attention. Attempting to stabilize the distal phalanx within the hoof capsule is important in preventing further rotation or displacement, promoting healing, and decreasing pain. Therefore, understanding how the stability of the distal phalanx within the hoof capsule affects the convalescence of a chronically laminitic horse is crucial to effective treatment. Unfortunately, there is no direct measure of phalangeal stability except the obvious progression of displacement as determined by radiographs. It is assumed that the distal phalanx is least stable immediately after displacement and that it becomes more stable with time as the tissues repair unless there is another acute episode of the disease. The best indication available that the distal phalanx is more stable is that the horse is more comfortable because increased stability decreases tissue trauma. It is important to differentiate between the temporary stability that can be produced by supportive hoof care and the more permanent kind of stability obtained with tissue repair; the former is immediately reversed if the supportive care is discontinued.
To achieve each of these goals, several principles or objectives must be followed. These objectives cannot be completely separated by goal, as the goals are at least in part interdependent; that is, a given objective may partially satisfy more than one goal. For example, increasing stability helps decrease pain because instability is in part the cause of pain. Although instability and pain in the foot are both of immediate concern when treating laminitis, restoring the normal relationship between the distal phalanx and the hoof capsule is initially a secondary consideration; the latter becomes more important as instability and pain are controlled and the new hoof wall grows out.
Stabilizing the hoof capsule requires decreasing the stress on the most damaged lamellae. Therefore, the objectives are to reduce the load on the most severely affected wall, transfer load to the less severely affected wall, transfer load to the ground surface of the foot, and decrease the moment about the distal interphalangeal joint as necessary. Pain caused by lamellar stress and injury is in part controlled by increasing stability within the foot. Pain associated with subsolar ischemia, trauma, and bruising is limited by shoeing to prevent direct pressure on the ground surface of the foot immediately distal to the margin of the distal phalanx. The most important principle in limiting the residual capsular rotation as the hoof initially grows out is to eliminate load on the distal dorsal wall. Later, if there is concavity to the dorsal hoof wall, more direct intervention may be needed. A limited, though steadily increasing, number of tools are available to the veterinarian and farrier to apply these principles, but the permutations in which they may be applied is far greater.
The starting point of supportive therapy varies greatly with clinical severity, pattern of distal phalangeal displacement, and prior duration of the disease. As such, each horse must be treated as an individual. Therefore, no one technique applied systematically in the same manner is going to be satisfactory. This does not mean maintaining a battery of techniques for specific situations but rather understanding how flexible application of different techniques can satisfy different circumstances. Above all, focus should be maintained on principles and not methods.