A Practical Approach To Treating Laminitis

Stephen E. O'Grady, DVM, MRCVS

Laminitis is among the most devastating and crippling diseases that affect horses. This disease often accompanies or follows a primary disease process that affects another body system, such as the gastrointestinal, respiratory, reproductive or musculoskeletal system. Many different forms of therapy have been proposed over the last twenty years, yet no one treatment appears to be consistently effective. The primary disease process can lead to a pathologic response within the foot, resulting in decreased capillary perfusion, ischemia and necrosis of the laminae. Common disease processes and other factors contributing to laminitis include colic, enteritis, pleuritis, retained placenta, grain overload, exhaustion, corticosteroid administration and exposure to black walnut shavings. In addition, vascular disruptions in the foot are occasionally caused by direct hoof trauma, such as excessive concussion or subsolar bruising from improper trimming.

Laminitis can be classified as uncomplicated or complicated, depending on the horse's response to therapy1. Most cases of laminitis are uncomplicated. In these cases, the horse responds favorably regardless of the therapy. The remainder of laminitis cases are complicated-the patient fails to respond to prompt, aggressive medical treatment. These horses have a guarded prognosis. The cause of the laminitis often determines whether the case is complicated or uncomplicated. The severity of the initial damage to the laminae is the most important factor affecting the outcome of the case.

Pathogenesis
Recent research findings have increased our understanding of the physiologic response within the foot during laminitis, but a single agent has not been identified as the specific mediator for triggering laminitis. The blood flow to the dorsal laminae primarily moves in a palmar to dorsal and distal to proximal direction. This flow against gravity probably predisposes the dorsal laminae to ischemia. In addition, the arteriovenous anastomoses, which are under adrenergic neuronal control, will open, shunting blood away from the capillaries and increasing blood flow to the foot. The increase in blood flow accounts for the elevation in digital pulse pressure and heat during the early phases of laminitis.

Alterations in capillary perfusion may also be attributed to venoconstriction caused by an unknown vasoactive mediator, which acts to increase precapillary and particularly postcapillary resistance. Increases in capillary bed vascular resistance allow fluid afflux from the vasculature into the interstitial tissue of the laminae. Increases in interstitial pressure further impede capillary blood flow and lead to ischemia4. Ischemia, impeded capillary blood flow, and increases in interstitial pressure contribute to the development of microthrombosis.

Dr. Chris Pollitt's latest work suggests the activation of a lammelar enzyme ("MMP-2") may be responsible for the separation in the secondary lamina.

These mechanisms (shunting of blood away from the laminar capillaries, digital venoconstriction and toxic effects on the lamina), which may be interrelated, lead to ischemia of the secondary laminae, which results in laminitis. If the disease process is allowed to continue, laminar necrosis will ensue and disrupt the laminar bond between the hoof wall and the distal phalanx, leading to a mechanical change within the hoof capsule. The downward load through the bony column of the affected limb, coupled with the distractive force of the deep digital flexor tendon on the palmer aspect of the distal phalanx, results in rotation, or distal displacement, of the distal phalanx.

Radiographic Evaluation
Radiographic evaluation should be an integral part of the management of a laminitis case. In order to detect subtle changes within the hoof capsule, high-quality radiographs must be obtained. A uniform technique should be used for the initial and subsequent radiographs. Because variations in technique affect subsequent interpretation of radiographs (specifically the distance and angle measurements), it is essential to standardize the radiographic procedure in order to detect small changes that may occur between examinations.

For a lateromedial radiograph, I prefer using a 3-in thick wooden positioning block with a wire embedded longitudinally in the top.Another wire is taped vertically to the dorsal surface of the hoof wall. These wires allow accurate measurements to be determined within the hoof capsule. A consistent focal spot-to-film distance will eliminate one source of film exposure variability, and a line level placed on top of the machine will maintain a level primary beam. The primary beam is centered midway between the toe and heel, 2 to 3 cm above the bottom of the foot.

One of the earliest radiographic signs of developing laminitis is an increased distance between the dorsal cortex of the distal phalanx and the hoof wall. Tis distance should be less than 18 mm in the normal horse. An increase in this distance indicates laminar swelling and early laminar degeneration.

Another early radiographic indication of laminitis is a change in the position of the coronary band. On a lateral radiograph of a normal foot, the coronary band is positioned over the hoof wall. With the laminitic changes, a soft tissue depression appears on the radiograph at the usual site of the coronary band7. Ventral rotation of the tip of the distal phalanx away from the hoof wall and distal displacement of the extensor process with respect to the coronary groove can also be seen radiographically in laminitic horses.

The phases of laminitis and corresponding treatment Laminitis can be arbitrarily divided into three phases: developmental, acute and chronic. Specific therapy can be directed toward each phase.

The developmental phase The developmental phase begins when the horse is affected by one of the primary disease processes or factors previously discussed and ends when clinical signs of lameness appear. Treatment during the developmental phase attempts to prevent clinical laminitis. During this phase of the disease, there are few clinical signs other than an increased digital pulse and warm hooves. The radiographic signs are usually normal during this phase. Treatment is therefore based upon the probability that laminitis will occur.

Therapy during the developmental phase is directed toward eliminating the inciting cause and increasing blood flow to the secondary laminae. Using some form of foot support to protect the laminae should be considered.

Removal of the inciting cause may entail dietary changes or the administration of mineral oil, antibiotics, intravenous fluids or hyperimmune anti-endotoxin serum. Anti endotoxin serum has been successful in preventing the onset of laminitis when administered at the same time carbohydrate overload is induced in experimental horses9.

Vasodilation of the secondary laminae may be accomplished with the use of alpha-adrenergic antagonists such as acepromazine and phenoxybenzamine for three to five days, unless signs of the acute phase appear. In my experience, acepromazine appears to be effective at a dosage of 0.06 mg/kg intramuscularly, three times daily. Phenoxybenzamine provides prolonged action, but is not readily available. When this drug is administered intravenously at a dosage of 0.66 mg/kg, diluted in sterile saline solution, vasodilatation will last 12 to 24 hours. (If hypovolemia and shock are present, it is imperative that these conditions be treated appropriately [e.g. isotonic intravenous fluid administration] before vasodilator therapy is initiated.)

Heparin (40 to 70 units/kg given subcutaneously b.i.d.) has been effective in preventing laminitis when administered during the initial stages of the disease5. Aspirin (5 to 10 mg/kg every other day) can be administered for its antiplatelet effect. Flunixin meglumine may be beneficial when used at the anti-endotoxin dose of 0.25 mg/kg given intravenously four times a day.

The acute phase The acute phase of laminitis begins just after the onset of clinical signs of lameness. These may include a marked digital pulse, warm hooves, a painful response to a hoof tester examination, the characteristic laminitic stance and lameness, which is classified using the Obel grading system.

With Obel grade 1 lameness, the horse constantly shifts its weight from one leg to the other. Lameness is not noticed at a walk. But at a trot, the horse's gait is stiff and stilted. Obel grade 2 lameness is characterized by a stiff, stilted gait at both a walk and a trot. A front foot may be lifted of the ground without difficulty. With Obel grade 3 lameness, the horse exhibits a markedly stiff, stilted gait; is reluctant to move; and resists attempts to lift a front foot. When Obel grade 4 lameness is present, the horse refuses to move unless forced and spends much of its time recumbent.

Lameness in the acute stage is due to pain and inflammation from ischemia of the secondary laminae. The severity of the lameness relates to the severity of the damage to the laminae. The acute phase lasts 48 hours or until movement of the distal phalanx occurs10.

Therapy (medication and foot care) during the acute phase is directed toward relieving pain and preventing rotation of the distal phalanx.

Drug therapy Since systemic hypertension and peripheral vasoconstriction are coincident with the pain, it is important to begin or continue vasodilator therapy in the acute phase. In addition, anti-inflammatory therapy is important in decreasing laminar edema, easing pain, and therefore indirectly aids circulation. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most effective drugs for treatment of acute laminitis. Phenylbutazone and flunixin meglumine are most commonly used.

Phenylbutazone may be the most effective of the NSAIDs for the treatment of acute laminitis. The initial dose is 4.4 mg/kg given orally or intravenously twice a day. After the pain has lessened and other clinical signs have improved, the horse is then maintained on 3 g of phenylbutazone divided into two daily doses to reduce the possibility of gastrointestinal or renal damage. Flunixin meglumine can be administered at a dose of 1.1 mg/kg orally or intravenously, twice a day for three to five days. Dimethyl sulfoxide (DMSO) is another potent anti-inflammatory agent that can be administered once or twice daily for three days. DMSO (1 g/kg diluted in 3 liters of saline) administered by nasogastric tube may reduce edema in the laminae. It may also be helpful in reducing laminar inflammation because of its activity as an oxygen or hydroxyl radical scavenger. The use of 2 percent nitroglycerine patches placed on the palmar or plantar aspect of the pastern to dilate the digital vessels have been described. The benefit of these patches has not been proven. Gloves must be worn during the application of the nitroglycerine ointment, as it is a potent vasodilator in humans as well, and can be absorbed through the skin. Because of the implications for contamination of the person applying the drug, liability issues may make it unwise to dispense nitroglycerine for owner use. The use of aspirin is initiated or continued at the dose of 5 to 10 mg/kg every other day.

Foot Care The horse must be confined to a stall. Methods of foot care at this stage are aimed at supporting and protecting the compromised laminae. Shoes are never used at this stage. Removing excess toe length (beveling the hoof wall at the toe back to the white line) will decrease the bending force or lever arm exerted on the laminae. Foot support should utilize all of the structures in the caudal part of the foot, but secondary support can also be helpful in the solar area. Sand has always been a readily available, inexpensive and often-effective form of foot support. It provides even support over the entire ground surface of the foot and allows the animal to angle his toes down into the sand, changing the angle of the fetlock and decreasing the tension on the deep digital flexor tendon.

Recently, the use of 3-in industrial styrofoam has become popular as a form of foot support. (See" how to" apply foot support) It is easy to apply, very forgiving and provides good support. The emphasis of the weight bearing is placed on the structures of the heels, which allows support to be placed under the sole. Another easy method of foot support is to use a 4o wedge pad. Draw the outline of the foot on a wedge pad, extending to the bulbs of the heels. Cut the wedge pad following the outline. Fill the bottom of the foot with dental impression material and place the pad on the foot using a few small nails or tape. This method provides the best heel elevation.

A third method of foot support is to use 3-M Custom Support Foam®. The roll of foam is folded in layers the width of the bottom of the foot, ending up with more folds in the heel area. The foam is then placed in water and the horse is then made to stand on it so that it forms a contour to the bottom of the foot. After it dries, it is trimmed around the perimeter and taped to the bottom of the foot.

All of the above methods are easy to apply, provide firm but forgiving support and allow easy removal to examine the bottom of the foot. All three methods can be used to provide mild heel elevation, which is important in that it reduces one of the distractive forces caused by the deep flexor tendon.

The horse should remain on one of the above forms of support until it becomes comfortable and medication is reduced or eliminated. Only at this point should shoes be applied. The use of foot support allows medical therapy to be more effective in relieving pain and increasing capillary perfusion.

The chronic phase The chronic phase of laminitis begins when rotation of the distal phalanx occurs. Therapy at this stage depends on the severity of the damage to the laminae within the digit. Therapeutic shoeing to re-establish correct alignment of the distal phalanx and hoof capsule and to establish appropriate support of the skeletal column is imperative. If the damage to the laminae is extensive and the patient is unresponsive to therapeutic trimming and shoeing, a deep digital flexor tenotomy can be performed.

Conclusion Currently, there is no single treatment that can be recommended for all cases of laminitis. The severity of the laminar damage cannot be predicted in the initial phases of the disease. If the ischemic insult is severe enough, no systemic treatment or foot therapy will prevent rotation of the distal phalanx. I believe systemic treatment instituted before the appearance of clinical signs of laminitis to be the best hope for preventing severe laminar damage. Successful therapy of laminitis requires teamwork between the owner, veterinarian and farrier. When this group is willing to spend the time and effort, treatment of these cases can be rewarding. However, without their joint dedication, treatment is frustrating and usually ends with euthanasia of the horse.

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