Laminitis occurrs in all limbs, but most commonly affects the forelimbs bilaterally and is usually more severe in the front feet.
The disease, which can occur subacutely, acutely or chronically, is the result of transient oxidative stress leading to pedal ischemia and coagulopathy, causing separation of the laminae within the hoof, with eventual separation from the underlying bone and rotation of the pedal bone which may eventually perforate the sole.
Once thought to be an autoimmune disease, it is no known to occur as a result of underlying metabolic disorders. The nutrition and health of horses is closely tied to their gastrointestinal microflora. Gut bacteria break down plant structural carbohydrates and produce volatile fatty acids, which are a major source of energy for horses. Bacterial communities are also essential for maintaining gut homeostasis and have been hypothesized to contribute to various diseases including laminitis.
Excess nonstructural carbohydrates (i.e., starches, fructans, or simple sugars) that are not digested in the foregut enter the cecum and colon, where bacterial fermentation produces byproducts including lactic acid and gas, which can cause colic. The same initiators can also lead to the development of laminitis, which often occurs subsequent to overconsumption of grain or after feeding on lush pasture rich with nonstructural carbohydrates.
Laminitis can develop in the forefeet, all four feet, or occasionally only in the hindfeet. Biomechanical laminitis can be seen in a single foot, usually as a complication of a severe lameness or orthopedic disease in the contralateral limb.
The most common causes of laminitis are ingestion of excess carbohydrate (grain overload), grazing of lush pastures (especially in ponies), and excess exercise and concussion in an unfit horse. It also may develop secondary to postparturient metritis, endotoxemia, hyperinsulinaemia, use of corticosteroids, colic and enteritis.
The risk is higher in ponies and in horses that are overweight and unfit. Incidence of the acute and subacute forms is higher whenever there is a flush of new grass.
The role of endotoxemia in the development of laminitis remains unclear. Although systemic inflammation is a risk factor for laminitis in hospitalized horses, experimental endotoxin administration fails to induce the disease.
In chronic cases, the corona of the pedal bone may penetrate the sole just in front of the frog. The prognosis in severe cases is poor because the changes become irreversible, and secondary infection is common. In subacute and chronic cases, the rotation of the pedal bone occurs relatively slowly. The sole tends to become convex and thicken, and the hoof alters shape to accommodate the new position.
Clinically affected horses present with depression, anorexia, fever and a reluctance to walk. When forced, there is a markedly slow, crouching, short-striding gait. Each foot, once lifted, is set down as quickly as possible.
Usually, heat is apparent in the whole hoof, especially near the coronary band. An exaggerated and bounding pulse can be palpated and may be visible in the digital arteries. Pain can cause muscular trembling, and a fairly uniform tenderness can be detected when pressure is applied to the feet. The pedal bone may rotate during or after the acute stage if efficacious treatment is not given rapidly. Radiographic evidence of rotation can be present as early as the third day.
Subacute cases may exhibit any or all of the above clinical signs but to a lesser degree. Often, there is only a mild change in stance, with reluctance to walk and some increased sensitivity to concussion on the soles of the affected feet. There may be no demonstrable heat in the coronary band or increase in digital pulse. The acute and subacute forms of laminitis tend to recur at varying intervals and may develop into the chronic form. The most common clinical signs are increased digital pulses, difficulty turning and a short, stilted gait at walk.
Chronic laminitis is characterized by changes in the shape of the hoof and usually follows one or more attacks of the acute form. Bands of irregular horn growth (laminitic rings) may be seen in the hoof, close at the toe and diverging at the heel. The hoof itself becomes narrow and elongated, with the wall almost vertical at the heel and horizontal at the toe.
As the condition progresses, the sole becomes thickened and either flattened or somewhat convex in outline. The gait is similar to that already described, and when standing, the body weight is continually shifted from one foot to the other. Radiography reveals rotation and some osteoporosis of the pedal bone. The corona of the bone is forced downward and presses on the horny sole. In severe cases, it may penetrate the sole just in front of the point of the frog.
In acute and severe laminitis, diagnosis is based on the history (eg, grain overload) and posture of the horse, increased temperature of the hooves, a hard pulse in the digital arteries, and reluctance to move. Mild cases with no visible hoof deformity can be identified via radiography of the affected feet, which show a lack of parallelism on the lateral projection between the hoof wall and cranial face of the third phalanx. Divergence of ≥11° indicates a guarded to unfavorable prognosis for return to performance.
A differential diagnosis of stiff-gaited stance would include colic.
Acute laminitis constitutes a medical emergency because pedal rotation can occur rapidly. Despite prompt therapy, the prognosis is guarded until recovery is complete and it is evident that the hoof architecture is not altered. In acute laminitis, especially in cases of grain overload, mineral oil is indicated; 1 gal. (4 L), PO, acts as a laxative and tends to prevent absorption of toxic material from the GI tract. Purgation should not be done in the acute phase because most horses tend to be dehydrated.
Traditionally, cold packs or ice packs applied to the affected feet have been advocated, but recent evidence suggests that hot packs used early in the course of the disease may be more beneficial. Antihistamines are of doubtful value during acute lameness, but isoxsuprine hydrochloride paste, a peripheral vasodilating agent, may be of value. Heparin (40 u/kg, tid for 3 days) has been used because of the suspected accompanying coagulopathy and thromboembolism; however, heparin therapy in horses has been associated with RBC clumping which, in a dehydrated animal, could aggravate dynamics of local blood flow in the feet.
Flunixin meglumine and phenylbutazone are the preferred anti-inflammatory agents, and meclofenamic acid also has been of value; however, all three may be toxic. These NSAID should be used according to label instructions and, if used in combination, the dosage of each should be reduced accordingly.
Phenoxybenzamine hydrochloride has been used in severe and acute cases of laminitis. However, it may cause depression and should be avoided in horses in shock.
Heart-bar shoes have been used in acute cases in an attempt to diffuse sole pressure and avoid pedal rotation. Because an improperly fitted heart-bar shoe aggravates the pain, correct fitting is essential.
Administration of corticosteroids is contraindicated because serious cellular catabolism and inhibition of the immune responses often result in muscular wasting and worsening of the laminitis. Because gram-negative endotoxins due to carbohydrate overload have been implicated in laminitis, it is especially important to preserve the normal immune responses during treatment.
Digital nerve blocks in the early stages of the disease permit the horse to be walked, which increases the arterial blood flow through the terminal arch. However, nerve blocking and walking are contraindicated once pedal rotation has begun. Because of its value in hoof keratinization, methionine has been used at dosages of 10 mg/lb (22 mg/kg), daily for 1 week followed by 5 mg/lb for the second week and 2.5 mg/lb for the third.
Treatment of chronic laminitis has consisted of attempting to restore the normal alignment of the rotated coffin bone and encouraging frog pressure by lowering the heels, removing excess toe, and protecting the dropped sole. This requires corrective hoof trimming and the use of full leather pads or a heart-bar shoe. Acrylic compounds are useful in conjunction with proper trimming to build up the toe and to protect the sole. The hoof should be trimmed and the shoe reset at 4- to 6-week intervals. This approach can be successful in selected cases but is expensive, labor intensive, and prolonged.
Resection of the separated hoof wall may also be indicated and has been used in acute and chronic cases, particularly those with seedy toe or infection. This surgical procedure carries risk and should follow consultation between the veterinarian and farrier.
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