THE MERCK VETERINARY MANUAL
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Laminitis in Horses

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Equine laminitis is a crippling disease in which there is a failure of attachment of the epidermal laminae connected to the hoof wall from the dermal laminae attached to the distal phalanx. As the laminae are responsible for suspending the distal phalanx within the hoof wall, laminar failure in combination with the downward forces of the weight of the horse and distracting forces such as the tension from the deep digital flexor tendon commonly results in a catastrophic displacement of the distal phalanx resulting in severe lameness. Laminitis affects all breeds of horses.

There are 3 main disease states thought to be associated with laminitis: 1) diseases associated with sepsis or endotoxemia, 2) equine metabolic syndrome (pasture-associated laminitis, see Equine Metabolic Syndrome), and 3) supporting limb laminitis. The pathogenesis of laminitis is still controversial and most likely varies widely between these 3 primary causes. A fourth, less common cause is ingestion of shavings (sometimes inadvertently used for bedding) from black walnut heartwood. The most common causes of sepsis or endotoxemia-related laminitis are diseases associated with gram-negative bacterial (or polymicrobial) sepsis and include ingestion of excess carbohydrate (grain overload), postparturient metritis (retained fetal membranes), colic (anterior enteritis, large colon volvulus), and enterocolitis. Laminitis secondary to equine metabolic syndrome most commonly occurs in overweight horses and ponies, and is commonly exacerbated when grazing lush pastures. Supporting limb laminitis can occur any time the animal places excessive weight on one limb for an extended period of time due to inability to use the other limb (eg, postoperative orthopedic procedures, radial nerve paralysis).

The basic cause of laminar failure in laminitis is a failure of attachment of the laminar basal epithelial cells (LBEC) of the epidermal laminae to the underlying dermal laminae. Although the cause of this failure was thought to be primarily due to breakdown of the matrix molecules in the basement membrane and dermis (to which the LBEC attach) by matrix metalloproteases, it now appears that the LBEC may also be losing attachment due to dysregulation of the hemidesmosomes, the adhesion molecules on the LBEC that attach the cells to the underlying matrix molecules. Marked increases of inflammatory mediators and enzymes (eg, proinflammatory cytokines, cyclooxygenase-2) occur in the laminae in the early stages of laminitis and may injure the LBEC. Hypoxia and ischemia due to aberrant vascular flow is also likely to play a role in LBEC dysfunction.

The pathophysiology behind laminitis associated with equine metabolic syndrome is not as well researched but is proposed to occur due to a similar inflammatory state as that associated with insulin resistance in obese humans with metabolic syndrome and that leads to vascular injury. The pathogenesis of supporting limb laminitis is not known.

Following loss of integrity of the laminar attachments, the distal phalanx can undergo 3 types of displacement depending on the forces placed on the foot and the pattern of laminar injury. Distal displacement of the entire phalanx (usually termed “sinking”) occurs when there is circumferential loss of laminar attachments, most commonly observed in severe cases of sepsis or endotoxemia but also observed in equine metabolic syndrome. Palmar rotation of the distal margin of the distal phalanx (usually termed “rotation”) is the most common displacement observed, and most likely occurs due to primary loss of the dorsal laminar attachments with some integrity maintaining in the quarters. Rarely, unilateral distal displacement of the distal phalanx occurs, most commonly to the medial side; this displacement can only be visualized on an anterior-posterior radiograph of the foot. In laminitis related to sepsis and equine metabolic syndrome, the forelimbs are most commonly affected, although the hindlimbs can also be affected in severe cases. In supporting limb laminitis, either a front or rear foot is affected depending on which opposite limb has the weight-bearing problem.

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Classically, laminitis is considered acute, subacute, or chronic. Acute cases are of short duration (usually <3 days) and have not undergone displacement of the distal phalanx. Subacute cases have continued >3 days, but still have no distal phalangeal displacement. Chronic laminitis cases have distal phalanx displacement regardless of the duration of the disease. Early in laminitis, the horse is depressed and anorectic and stands reluctantly. Resistance to any exercise is marked, and the normal stance is altered in attempts to relieve the weight borne by the affected feet. If only the forelimbs are affected, the horse will stand with the forelimbs placed far forward (to decrease the weight on the front digits); the hindlimbs also are placed more forward in order to support more of the weight. If forced to walk, the horse shows a slow, crouching, short-striding gait. If all 4 limbs are affected, the animal will appear “camped out” with the forelimbs placed more forward than usual, and the hindlimbs placed more caudally than usual. Each foot, once lifted, is set down as quickly as possible.

The entire hoof wall may be warm in the acute stage. 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. There is commonly an increased pulse rate (60–120/min) and respiratory rate (80–100/min). In exceptionally severe cases, for which the prognosis is unfavorable, a blood-stained exudate may seep from the coronary bands. Radiographic evidence of displacement of the distal phalanx can be present as early as the third day after the onset of disease in horses with sepsis or endotoxemia. However, a recent MRI study has shown that, in the acute case, the animal may have normal-appearing distal phalanx radiographs, despite destruction of the entire dorsal laminar attachment that is visible on MRI.

Subacute cases, commonly observed in horses with equine metabolic syndrome, 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.

During and immediately following displacement of the distal phalanx, the horse is usually extremely lame and may spend a great deal of time recumbent. In severe cases, the foot may prolapse through the sole cranial to the frog, or the coronary band may separate; both occurrences gravely affect the prognosis. Longterm cases of chronic laminitis are characterized by changes in the shape of the hoof and usually follow 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 distal phalanx. 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 usually straightforward and 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. Abaxial sesamoid nerve blocks of the forelimb digits in the very lame horse allow assessment of possible involvement of the hind feet (by walking the animal a few steps) and enable full assessment of the soles of both feet (for solar prolapse, etc). These nerve blocks also make it possible to obtain good quality lateral and anterior-posterior radiographs of the foot. Lidocaine should be used for the nerve block as it will only last a short time, ie, not long enough for the animal to move excessively and further damage the laminae. Gross observation and distinct measurements from the radiographs allow determination of whether distal displacement, rotation, both distal displacement and rotation, or unilateral sinking has occurred.

Acute laminitis constitutes a medical emergency because phalangeal displacement 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. Most animals should be administered NSAID, with flunixin meglumine being the drug of choice if the horse is still systemically ill (ie, enterocolitis). Phenylbutazone is usually used in the early chronic stage when the horse is lame but does not have signs of systemic disease. Close attention to the potential toxicities of NSAID therapy, particularly with phenylbutazone, is required. Because phenylbutazone accumulates in the tissue (unlike flunixin or most other NSAID), it is best to skip a day every 5–7 days to “clear the system” (flunixin can be administered that day). NSAID should be used according to label instructions and, if used in combination, the dosage of each should be reduced accordingly. Another recent option for treatment of chronic laminitis is the COX-2-selective NSAID firocoxib, which is available in a formulation for horses and is safer than flunixin or phenylbutazone in horses at risk of renal or GI complications. Other options for analgesia include detomidine, butorphanol, morphine, or a constant-rate infusion of a “cocktail” of sedatives and analgesics.

For treatment of possible ongoing ischemia, acepromazine is the only drug found to effectively increase digital blood flow, but only for a short period of time. Acepromazine has the added benefit of providing some sedation to stressed horses with laminitis. In a horse at risk or in the early stages of laminitis, cooling of the foot by placing it directly in ice water has recently been popularized again by several experimental studies demonstrating a beneficial effect.

During the first 2–3 wk, it is important to remove standard shoes, as shoes place the majority of stress on the hoof wall and therefore the laminae. The feet should be padded with a soft, resilient substance such as a 1- to 2-in. thick piece of closed-cell foam cut to the diameter of the foot. Pads can also be made from the different putties available to the farrier to provide sole support. Decreasing padding (or beveling the pad) in the region dorsal to the apex of the frog decreases the stress on the dorsal laminae. Styrofoam insulation (2 in. thick) can be used in small equids but usually provides minimal support in larger animals. Other shoes (eg, Redden Ultimate and Steward clog) that can be applied without severe concussion are available for application to the foot in the first few weeks.

Shoeing horses with laminitis is usually not a good option until ~3 wk after the onset of laminitis, when the laminar structure may be stabilizing. The type of shoeing depends on the type of displacement. In a horse with distal phalangeal rotation, an attempt is made to begin realigning the palmar surface of the distal phalanx to the sole, while not allowing excessive forces on the laminae. The breakover of the shoe is moved as far caudally as possible, and some of the caudal hoof (from the frog apex caudally) is removed to allow realignment to the sole. This may have to be performed in combination with raising of the heel (with wedge pads, etc), which still allows alignment of the distal phalanx to the solar surface while avoiding excessive changes in relation to the ground surface, thus preventing excessive tension on the deep digital flexor tendon and the dorsal laminae. It is usually appropriate to place some type of resilient putty on the solar surface to provide support to the distal phalanx. Multiple types of shoes can be used, including heart bar shoes, egg bar shoes, and natural balance shoes. Steward clogs are an option for treating horses with distal displacement of the distal phalanx; these allow the animal to maximize comfort in multiple directions (and therefore minimize laminar stress).

Surgical options include deep digital flexor tenotomy, to neutralize the pull of the deep digital flexor tendon, and dorsal hoof wall resections. Deep digital flexor tenotomy is most commonly performed in cases of chronic rotation that do not respond to the above shoeing techniques; it should always be accompanied by aggressive derotation via rasping of the caudal foot. The farrier and veterinarian must address subluxation of the coffin joint subsequent to surgery in the majority of cases (usually by applying adequate heel wedging to neutralize the subluxation). Generally, only a partial hoof wall resection is performed (usually on the distal hoof wall) due to the severe digital instability caused by removing the entire dorsal wall.

Last full review/revision March 2012 by Stephen B. Adams, DVM, MS, DACVS; Joerg A. Auer, DrMedVet, Dr h c, MS, DACVS, DECVS; James K. Belknap, DVM, PhD, DACVS; Jane C. Boswell, MA, VetMB, CertVA, CertES (Orth), DECVS, MRCVS; Peter Clegg, MA, Vet MB, PhD, CertEO, DECVS, MRCVS; Andrew L. Crawford, BVetMed, CertES (Orth), MRCVS; Jean-Marie Denoix, DVM, PhD, Agregé; Marcus J. Head, BVetMed, MRCVS; C. Wayne McIlwraith, BVSc, PhD, DSc, FRCVS, DACVS, DACVSMR; James Schumacher, DVM, MS, DACVS, MRCVS; John Schumacher, DVM, MS, DACVIM; Roger K. W. Smith, MA, VetMB, PhD, DEO, DECVS, MRCVS; Chris Whitton, BVSc, FACVSc, PhD

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