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EQUINE LAMINITIS
In the spring of 2006, the world watched in dismay as Barbaro, a promising young Thoroughbred racehorse, shattered his right hind leg at the start of the Preakness Stakes at the Pimlico Race Course in Maryland. After surgery Barbaro developed laminitis, first in his left hindfoot and later in both front feet. This disease ultimately contributed to the loss of the 2006 Kentucky Derby champion because of the chronic pain and the poor prognosis for any reasonable quality of life. The silver lining in this sad tale is that more research and new information is being generated and now helping in the prevention and treatment of laminitis than ever before.
Laminitis Explained
Laminitis is a common and potentially devastating foot problem that affects all members of the equine family: horses, ponies, donkeys mules, and wild equids. The disease process involves a breakdown of the bond between the hoof wall and the distal phalanx, commonly called the coffin bone, pedal bone, or simply P3.
Figure 1a
Figure 1b
The distal phalanx in the horse is equivalent to the bone at the top of the middle finger (Fig. 1a-drawing and 1b- radiograph). It is completely encased in the hoof, a keratinized, modified nail-like structure. As with the human fingernail, the hoof wall is firmly attached to the coffin bone by a strong dermal-epidermal bond.
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This hoof wall-coffin bone bond is the only thing that prevents the horse's body weight (approximately 500 kg, or 1100 lb, in a horse of Barbaro's size) from forcing the coffin bone through the bottom of the hoof. This bond must be strong enough to withstand the forces sustained by the hoof at a gallop, yet dynamic enough to allow the hoof wall to grow uninterrupted as it is worn at the ground surface.
In order to maximize the strength of this bond, the dermal-epidermal interface is extensively folded into several hundred lamellae (Figure 2). (Note: These folds are often referred to as laminae, although anatomically they are more correctly termed lamellae). The term laminitis is based on the word lamina.) The surface of each lamella is folded into many smaller secondary lamellae, which further increases the surface area and thus the strength of the hoof wall-coffin bone bond.
Figure 2
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Just like the skin, the dermal and epidermal cells of the hoof are separate, yet bonded together by a thin layer of extracellular matrix material called the basement membrane. This structure is a critical component of the hoof wall-coffin bone bond, and its destruction and subsequent failure is one of the fundamental events in the development of laminitis.
Because the lamellae comprises living cells and the material they produce, the hoof wall-coffin bone bond is susceptible to interruptions in its nutrient supply and to biochemical breakdown. A wide variety of insults can cause or contribute to the development of laminitis in horses (see Table 1). Regardless of their other local or systemic effects, each compromises the hoof wall-coffin bone bond through one or more of the following mechanisms:
Destruction of the basement membrane by specific protein-degrading enzymes called matrix metalloproteinases (MMP-2, MMP-9, and MMP-14). Interference with glucose utilization by the epidermal cells, which results in detachment of the cells from their basement membrane. Interruption of the blood supply (ischemia-reperfusion injury) within the lamellar dermis.
Factors Implicated in the Development of Laminitis
Primary Causes
Carbohydrate overload-excessive dietary intake of soluable sugars and starches, such as grains and high-fructan grasses. Severe intestinal disease: Surgical colic or enterocolitis. Sepsis: severe bacterial toxemia such as pleuroneumonia, septic metritis secondary to retained placenta in postfoaling mares, septic peritonitis. Exposure to black walnit (Juglans nigra) heartwood as wood shavings used for bedding.
Contributing Factors
Excess circulating glucocorticoid; Equine Cushing's Disease or corticosteroid administration. Metabolic syndrome: typically associated with obesity. Ingestion of ergot alkaloids, such as are found in endophyte-infested fescue grass or hay. Inactivity (often coupled with obesity). Unaccustomed strenuous exercise. Excessive concussion on the feet from exercise on a hard surface: "road founder." Stress: high-stress occupation or environment, long-distance transporting, hospitalization. Poor hoof conformation or improper trimming or shoeing. History of laminitis: previous damage to the digital vasculature or the lamellar dermis.
Table 1
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Figure 3
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Whatever the mechanism(s), if the hoof wall coffin bone bond is sufficiently compromised, the hoof wall and distal phalanx separate and displace under the variety of forces including the horse's body weight, the pull of the deep digital flexor tendon where it attaches to the coffin bone, and stress on the front of the hoof wall from contact with the ground surface during each step. Commonly, the bond is most severely compromised at the front of the foot, so the coffin bone rotates downward within the hoof capsule, forcing the tip of the bone down onto the dermis of the sole and compromising the vasculature (blood vessels) in that area (Fig. 3/Rotation). Less commonly, but more destructive, the entire coffin bone separates and drops or "sinks" (Fig 4/Sinking) within the hoof capsule, causing severe pain and extensive vascular injury.
Figure 4
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The dermis of the hoof wall and sole has an abundant supply of sensory nerve endings, so severe laminitis is a very painful condition. In fact, it is the extreme and unmanageable pain experienced by horses with severe laminitis that most prompts humane destruction in these cases. Other sequelae of severe laminitis tipping the scale in favor of humane destruction and worsens the prognosis for a good recovery include:
Extensive destruction of the blood supply within the hoof. Chronic bacterial infection within the hoof due to poor blood flow. Bone destruction at the tip of the coffin bone from abnormal mechanical loading, loss of blood supply, and/or bacterial infection.
Laminitis varies greatly in severity from mild, where it may not be noticed by the horse owner and only evident by subtle changes in hoof growth or in radiographic (x-ray) changes of the coffin bone, to death and loss of the entire hoof capsule.
Most cases fall somewhere in between. Prevention is far better than treatment with laminitis cases as even mild damage can result in long term problems.
Diagnosis and Treatment
A clinical diagnosis of laminitis is based on clinical signs and radiographic findings. Laminitis is a painful condition, so the most consistent sign is lameness. Other signs vary with the severity of the damage and whether the laminitis episode is acute (hours or days old) or chronic (lasting more than a week). An increase in pulse pressure in the arteries that supply the affected foot referred to as "bounding digital pulse," is a common finding, although not specific for laminitis.
Radiographic changes also vary with the severity and chronicity of the condition. They range from vague changes within the lamellar dermis such as widening of the lamellar zone, change of radiographic density indicating fluid accumulation, to marked displacement of the coffin bone and, later, destruction of the bone (Figure 5).
Figure 5
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Figure 6
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Contrast venography, in which a radiopaque liquid is used to outline the individual blood vessels within the hoof, is a valuable addition to regular radiography, because it reveals areas of reduced or absent blood flow (Figure 6).
Treatment requires appropriate medical and/or surgical management of the underlying cause, intensive anti-inflammatory and pain therapy, and focused hoof care. In severely affected horses, meticulous nursing care is also essential, as these horses may spend a major part of their time lying down, a state that is not conducive to good health in any horse. Horses are not designed to stand on three (or fewer) legs nor lie down for long periods. Severe and chronic lameness can have devastating consequences in the horse.
Figure 7
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Hoof care primarily involves trimming the hoof and using deep bedding, sole pads, boots, or shoes to restore normal biomechanical alignment of the coffin bone relative to the rest of the digit and to the ground surface. This strategy helps normalize forces on the remaining hoof wall-coffin bone bond and blood flow through the hoof, and therefore improves the rate and quality of recovery. A recent study showed that using glue-on shoes improves the outcome in horses with laminitis, presumably because it allows the veterinarian and farrier (blacksmith) to fine-tune the mechanics of the hoof (Figure 7).
Recent and Ongoing Research
Laminitis is one of the most studied diseases of horses. Even so, there is still much we do not fully understand. Consequently, prevention and treatment of laminitis remain the challenge.
The period during which we have the greatest potential to influence outcome is the developmental stage - before the horse starts showing signs of foot pain. Once the horse shows signs of laminitis, the destructive process is well under way. During this stage of the disease in at-risk horses, cryotherapy (cold therapy) has been shown to be protective to the foot and a means of prevention (Figure 8).
Figure 8
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With naturally occurring grain overload (carbohydrate/CHO)-induced laminitis, there is a period of approximately 40 h between ingestion of the carbohydrate and the onset of foot pain. This lag period is called the developmental, prodromal, or preclinical phase of laminitis. With other causes of laminitis, there is also a lag period, although its duration varies with the specific event. For example, it may be as short as 4 h with black walnut-induced laminitis, or as long as several weeks with excessive weightbearing load referred to as contralateral limb laminitis.
A recent investigation using gene chip technology, DNA microarrays that use DNA sequence information to monitor expression levels of the corresponding genes on a chip, provided a fascinating and unprecedented glimpse into the developmental stage of CHO-induced laminitis (Figure 9). The study showed that over 150 specific genes were upregulated within the lamellar dermis in the first 24-32 h after carbohydrate overload (this is, well before the horses showed signs of foot pain). Genes coding for the production of proinflammatory biochemical or cellular processes and those involved in protein degradation or turnover predominated. Interestingly, several regulatory or anti-inflammatory genes were also upregulated.
Figure 9
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Based on this research, it would appear that, at least in the case of CHO-induced laminitis, inflammation is a primary event, rather than a secondary one, because at the time point evaluated the structural changes characteristic of laminitis, including separation of the dermal-epidermal bond, are not yet under way. This research is exciting because it suggests that targeted anti-inflammatory therapy, applied during this preclinical phase in at-risk individuals, may stop the progression of the biochemical and cellular events that ultimately lead to destruction of the hoof wall-phalangeal bond.
Further research is needed, including identification of the specific trigger(s) that can incite the upregulation of these genes. In all likelihood with the CHO model, gut-derived factors are involved. It is well established that carbohydrate/grain overload in horses causes significant changes in the pH and bacterial population of the hindgut (cecum and colon), generates vasoactive amines (substances that, if absorbed, could affect blood flow in the feet), and increases the permeability of the bowel lining. Whether the trigger is a bacterial fraction or a product that reaches the feet via the bloodstream, or whether it is an aggressive systemic response to the transgression of microbial products across the compromised gut barrier, or both, remains to be determined.
We also need to apply these findings and techniques to other naturally occurring causes of laminitis. If different mechanisms or genes prove to be involved, then different preventive and therapeutic strategies are needed.
Adapted from: Orsini, James A. Equine Laminitis in McGraw-Hill Yearbook of Science and Technology 2008, 114-118.
When to Seek Referral
ACVS board-certified veterinary surgeons in equine practice have been trained in the management of orthopedic diseases in horses, including laminitis. Most ACVS board-certified veterinary surgeons in equine practice are affiliated with referral hospitals equipped with state-of-the-art diagnostic and treatment methods.
—James A. Orsini, DVM
Diplomate ACVS
Posted 1/11/2006
Revised 9/17/2010 by Dr. Orsini
Reviewed by Drs. Schwartz and Bowman
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