Laminitis is among the most devastating and crippling diseases that affect horses. This disease often accompanies or follows a primary disease process far removed from the foot, such as a process involving the gastrointestinal, respiratory, reproductive or musculoskeletal system. Many different forms of therapy, both medical and mechanical, have been proposed over the last twenty years, yet no one treatment has been consistently effective.1 Treatment regimens for acute and chronic laminitis remain empiric and are based on the past experience of the attending veterinarian. It is the extent and severity of the lamellar pathology that influences the outcome of the case, not the treatment regimen itself, although inappropriate treatment certainly can negatively affect the outcome.
Laminitis can be defined as idiopathic inflammation or ischemia of the submural structures of the foot.2 Laminitis can be divided into developmental, acute, and chronic stages. If treatment during the acute stage of laminitis does not lead to full recovery, the disease will progress to the point where there is clinical and radiographic evidence of displacement of the distal phalanx (P3) within the hoof capsule. Stated another way, there is a failure of the attachment between P3 and the inner hoof wall. 3
Recent research findings have increased our understanding of the pathologic response that occurs within the foot during laminitis, yet the mechanism or trigger that initiates this response remains elusive. Working hypotheses vary between an ischemic insult to the laminae and enzymatic degradation of the basement membrane that lies between the epidermal and dermal laminae. A theory has been proposed based on in vitro studies that decreased glucose metabolism may precipitate laminitis. 4 Hoof lamellar explants kept in tissue culture medium consume glucose and the laminae will readily separate if glucose is absent from the tissue medium.
The significance of the metabolic stress that accompanies acute disease processes such as gastrointestinal diseases; metritis and grain overload is that glucose consumption in many peripheral tissues is reduced 5. Two anatomical features of the equine foot may contribute to the pathogenesis of laminitis: (1) The blood flow to the dorsal laminae primarily moves in a palmar to dorsal and distal to proximal direction. This flow against gravity may predispose the dorsal laminae to ischemia. (2) The arteriovenous anastomoses in the digital vasculature, which are under adrenergic neuronal control, open during developmental laminitis, shunting blood away from the capillaries within the laminae and increasing blood flow to the foot, which accounts for the heat observed during this stage.
Laminitis can result from a variety of systemic disease processes. The most common site of initial pathology is the gastrointestinal tract. Grain overload, ingestion of lush pasture in the spring, the acute abdomen, colitis and diarrhea may each precipitate laminitis. Other causes include pleuritis, retained placenta, Potomac Horse Fever, exhaustion, rhabdomyolysis and exposure to black walnut shavings. Vascular disruptions in the foot that occur with direct hoof trauma, such as excessive concussion on a hard surface, subsolar bruising from improper trimming and bearing excessive weight on one foot following injury to the contralateral limb also may induce laminitis. Pituitary dysfunction (e.g. equine Cushing's disease) is often complicated by so-called "refractory" laminitis. Although not proven scientifically, it is the clinical impression of many practitioners that administration of corticosteroids, when coupled with another factor(s) such as the concurrent administration of other medications, being overweight, unfitness, change in diet or environment and the stress of travel, has the potential to induce laminitis. 6
Radiographic evaluation should form an integral part of the management of a laminitis case. In order to detect subtle changes within the hoof capsule, high-quality radiographs with good soft tissue detail must be obtained. Variations in technique affect subsequent interpretation of radiographs (specifically the distance and angle measurements), so it is essential to standardize the radiographic procedure in order to detect small changes that may occur initially and between examinations. Magnification factors must be taken into account so accurate measurements can be made from the radiographs. To appreciate bone position, the radiographs should be taken with the horse bearing weight on both feet, and both feet placed on wooden blocks of equal height.
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 on the length of the dorsal surface of the hoof wall. A radiopaque marker such as a thumbtack can be placed near the apex of the frog. 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.
THE PHASES OF LAMINITIS AND CORRESPONDING TREATMENT
The Developmental Phase
The developmental phase of laminitis begins when the horse is affected by one of the primary diseases previously discussed and ends when clinical signs of lameness appear. It can be as short as 12-24 hrs with black walnut toxicity, or as long as 40-50 hrs with carbohydrate overload. During this phase, the feet may remain asymptomatic or there may be a mild increase in digital pulse pressure and warm hooves. Treatment is therefore based upon the probability that laminitis will occur. Therapy directed toward eliminating the inciting cause may include dietary changes, administration of mineral oil or activated charcoal via nasogastric tube, antibiotics, and intravenous fluids. Gastrointestinal diseases, septic metritis and retained placenta are associated with endotoxin release, so hyperimmune anti-endotoxin serum may be beneficial. Anti endotoxin serum has been successful in preventing the onset of laminitis when administered at the same time carbohydrate overload is induced in experimental horses7. Flunixin meglumine may be helpful; a dosage of 0.25 mg/kg intravenously t.i.d. is commonly used.
Attempts at increasing blood flow to the secondary laminae during this stage have been recommended. Acepromazine (an alpha-adrenergic antagonist) has been used at a dose of 0.02 to 0.06 mg/kg intramuscularly t.i.d.8 As this drug has hypotensive properties, hydration should be closely monitored. Using some form of foot support to protect the laminae should be considered. Placing the horse in deep bedding such as sawdust or standing the horse in sand are two easy methods to provide support. Another easy method is to leave the shoes in place and fill the solar surface inside the confines of the shoe with a rubber dental impression material.
The Acute Phase
The acute phase of laminitis begins with the onset of clinical foot pain and lameness. It lasts until the horse either recovers or shows clinical and radiographic evidence of displacement of P3. Signs include markedly increased digital pulse pressure, warm hooves, a pain response to hoof testers in the sole dorsal to the apex of the frog, the characteristic laminitic stance and lameness. Many horses show all the symptoms of acute laminitis but have mild lameness. When treated aggressively, they respond within 24 hours and appear to make a full recovery. These cases should be confined to a stall and observed for an additional 10 days. The severity of the lameness relates to the severity and extent of the damage to the laminae.
Radiographs should be taken at the initial examination. They will serve as a baseline for subsequent radiographs, reveal if any previous displacement of P3 exists and provide a means to measure the distance between the dorsal hoof wall and the dorsal cortex of the distal phalanx. This distance should be less than 18 mm in the normal horse.9 An increase in this distance indicates laminar swelling and early laminar degeneration. Serial radiographs in the acute stage are used to monitor rotation or distal displacement of P3 (sinking). Early radiographic evidence of distal displacement of P3 always carries a grave prognosis irrespective of the treatment.
Aggressive treatment of the causative disease should continue during the acute stage. The foot pain of acute laminitis is attributed to lamellar degeneration. With the inflammation, hemorrhage and edema that coincide with lamellar degeneration, logic questions whether adequate drug distribution is possible through this swollen laminar tissue that is encased in a rigid hoof capsule. Using nonsteroidal anti-inflammatory drug (NSAIDs) to treat acute laminitis is well accepted among clinicians. Phenylbutazone appears to be the most effective NSAID for pain relief in horses with acute laminitis; it is given at an initial dose of 4 grams per 1000-lb horse and is immediately decreased to 1 to 1.5 grams b.i.d. This lower dose is used to keep the horse comfortable but not relieve pain to the extent the horse moves around excessively and won't lie down. The increased perfusion to the foot that occurs in the acute phase of laminitis makes the use of vasodilator agents controversial; they should be used at the discretion of the attending clinician. 8 The use of 2 % nitroglycerine patches placed on the palmar / plantar aspect of the pastern to dilate the digital vessels has been described. The benefit of these patches has not been proven and along with vasodilator drugs, their indication is questionable. Furthermore, it is this author's opinion that this type of drug creates a liability issue for the clinician because of the potential hazardous effects on human health.
Dimethyl sulfoxide (DMSO) is used for its free radical scavenging and anti-inflammatory properties. Although its efficacy has not been proven in treating laminitis, favorable clinical impressions promote its continued use. DMSO (1 g/kg diluted in 3 liters of saline) is administered by nasogastric tube once or twice daily for 3 days.
Methods of foot care during the acute stage are aimed at removing the biomechanical forces placed on the compromised laminae and supporting the foot in an attempt to counteract the weight of the horse. The mechanical principles include aiding breakover, heel elevation to decrease the distractive forces of the deep digital flexor tendon (DDFT) and support for the palmar/plantar section of the foot.
The horse should be confined to a stall to prevent further trauma to the already weakened laminae. As shoes concentrate the weight bearing surface around the periphery of the foot, they should be removed. This can be accomplished in an atraumatic fashion by using a nail puller and removing each nail individually. To remove the stresses placed on the laminae at breakover, a line is drawn across the solar surface of the foot approximately ? inch dorsal to the apex of the frog. The hoof wall and sole are beveled at a 90 degree angle dorsal to this line using a rasp. This effectively decreases the bending force or lever arm exerted on the dorsal laminae. It also moves the breakover point back. Heel elevation and support can be applied in one of three ways. (1) Sand is a readily available, inexpensive and often-effective form of foot support. It provides even support over the entire solar surface of the foot, and it allows the animal to angle its toes down into the sand, thus raising the heels and changing the angle of the fetlock. (2) The use of 3-inch high-density industrial Styrofoam has gained popularity as a form of foot support. When applied to the foot, the weight of the horse crushes the Styrofoam, forming a resilient mold in the bottom of the foot. It is easy to apply, is very forgiving, and it provides heel elevation and good ground support. Additional heel elevation can easily be fabricated. Once the horse has crushed the original piece of Styrofoam, this piece is cut in half and the palmar half is retained and used as a heel insert. Another full sized piece of Styrofoam is applied underneath it. (3) The third method utilizes a commercially available combination of two 5-degree wedge pads that are riveted together, along with an attached cuff so they can be taped to the foot.
These wedges are combined with a resilient silastic material placed in the bottom of the foot for support. This method is used on horses that have underrun heels, a broken hoof-pastern axis or radiographically show a negative heel angle (the solar margin of P3 is lower at the heels than at the toe on the lateral radiograph). To apply this method, fill the bottom of the foot with dental impression material, hold the foot up until the impression material sets, place the foot in the wedges and tape in place. This method provides the best heel elevation. All of the above support methods are easy to apply, provide firm but forgiving support and allow easy removal to examine the bottom of the foot. They also provide uniform support to the frog, sole and bars in the palmar/plantar two-thirds of the foot. This is accomplished without causing local ischemia and pressure necrosis which may occur if treatment is reliant on frog support alone.
There are only anecdotal reports of the benefits of hot or cold foot soaks during the acute stage; therefore the author elects to use neither in order to prevent the hoof capsule from becoming saturated and soft.
The Chronic Phase
The acute phase merges into the chronic phase when there are clinical and radiographic signs of displacement of P3. Treatment at this stage is strictly mechanical as medical therapy, other than analgesia, is of limited value. The mechanical change that most commonly defines chronic laminitis is rotation, or distal displacement of the tip of P3. The separation of the laminae that results in rotation explains the instability of P3 and is a source of pain. Rotation concentrates pressure at the toe region of P3, rather than weight being more evenly distributed over the entire solar surface of P3. Focal pressure on the solar corium beneath the tip of P3 causes chronic pain, ischemia of the solar corium, and decreased sole growth, which can only be ameliorated by reorienting P3 to a more normal position in relation to the ground surface.
Therapeutic trimming and shoeing has long been the mainstay of therapy for chronic laminitis. However, the author prefers to continue the supportive therapy begun in the acute stage until the horse is comfortable, on minimal medication, and there has been no further radiographic deterioration for at least 10 days before the application of shoes is considered. The objective of corrective trimming of the hoof capsule is to realign P3 to its proper position in relation to the ground while maintaining an appropriate hoof-pastern axis. However, loss of sole depth due to P3 displacement, stage and severity of the disease, individual foot conformation, prolapse of the sole, and limited available hoof wall (e.g. underrun heels) may preclude realignment through trimming alone. Hence, trimming is usually accompanied by therapeutic shoeing of some form.
Radiographs during this stage are used not only to assess the alignment of P3 with the hoof capsule, but also for guidance when trimming. It is useful to classify displacement of P3 as capsular rotation or phalangeal rotation. Capsular rotation describes divergence of the hoof capsule from the dorsal surface of P3, regardless of the position of P3 in relation to the other phalanges. Phalangeal rotation describes displacement of P3 in relation to the long axis of the first and second phalanges, which indicates flexion of the DIP joint. In cases with significant phalangeal rotation, a surgical release procedure may be indicated to facilitate reorientation of P3. Depending on the severity and chronicity of the condition, surgical release may involve tenotomy of the deep digital flexor tendon or desmotomy of the inferior check ligament.
In chronic laminitis, it appears to make little difference what shoeing system is used as long as one adheres to the principles of unloading the damaged laminae and reestablishing weight bearing on the solar surface of P3. The author uses glue-on shoe technology to manage chronic laminitis cases. Clinical experience has shown glue-on shoes to be a relatively simple and atraumatic method for effectively realigning P3 in horses with chronic laminitis. Using radiographic guidance, the shoe is bonded to the foot in a manner that reorients P3 relative to the ground surface. In so doing, weight bearing is normalized over the solar surface of P3 and compression of the solar corium is relieved, which reduces pain and promotes sole growth10.
Surgical intervention in the form of a deep digital flexor tenotomy is indicated for horses that show progressive rotation of P3 despite aggressive medical and mechanical foot therapy. This surgery should also be considered on horses where P3 is about to penetrate the sole or has already penetrated the sole. Deep digital flexor tenotomy can and should be used to correct flexure deformities that often occur secondary to chronic laminitis. Tenotomy allows realignment of P3 using therapeutic shoeing.
Currently, there is no single treatment that can be recommended for all cases of laminitis.1 The author relies on the judicious use of NSAIDs and mechanical principles to reverse the forces at play on the compromised laminae. The severity of the laminar damage cannot be predicted in the initial phases of the disease. If the laminar insult is severe enough, no medical or mechanical treatment will prevent rotation or distal displacement of P3. 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.
1. Moyer W, et al. (2000), Chronic laminitis: Considerations for the owner and prevention of misunderstandings, in Proceedings 46th Annu Conv Am Assoc Equine Practnr; 59-61.
2. Hood DM. (1999), Laminitis in the horse. Vet Clin North Am Equine Practice; 15:287-293, 437-463.
3. Pollitt CC. (1999), Equine laminitis: a revised pathophysiology. In Proceedings. 45th Annu Conv Am Assoc Equine Practnr; 189-192.
4. Pass MA, Pollitt S, Pollitt CC. (1998), Decreased glucose metabolism causes separation of hoof lamellae in vetro: a trigger for laminitis? Equine vet. J Suppl., 26:133-138
5. Pollitt CC. (1991), The role of arteriovenous anastomoses in the pathophysiology of equine laminitis. . in Proceedings. 37th Annu Conv Am Assoc Equine Practnr; 711-719.
6. Eustace RA, Redden R. (1990), Iatrogenic laminitis (letter). Veterinary Record, 126:586.
7. Allen D. (1998), Acute laminitis, in Current techniques in equine surgery and lameness, N White and J Moore, ed. Philadelphia, PA, W B Saunders, 115: 544-547.
8. Braumbaugh GW, Lopez HS, Sepulveda ML. (1999), The Pharmacologic basis for the treatment of developmental and acute laminitis. Vet Clin North Am Equine Practice, 15:345-351.
9 Linford, R.L., O'Brien, T.R, Trout, D.R. (1993) Qualitative and morphometric radiographic findings in the distal phalanx and soft tissues of sound thoroughbred racehorses. Am. J. vet. Res. 54, 38-51.
10. O'Grady SE, Watson E (1999), How to glue-on therapeutic shoes. In Proceedings. 45th Annu Conv Am Assoc Equine Practnr; 115-119..