Laminitis - Horse

Introduction

Laminits is a common and debilitating condition of horses cause by separation of the laminae of the hoof. It can be acute or chronic and can result in the horse being put down. To revise the anatomy of the hoof see Equine Phalanges - Anatomy & Physiology

Aetiology

Laminitis is an acute degeneration of the sensitive primary and secondary Laminae. The cause for this is unknown.

Epidemiology

Although the cause for laminitis is not fully understood, several risk factors have been recognised:

• Obesity
• Access to lush pastures - particularly in the early morning when high levels of fructans are present in the grass
• Grain overload (Ingestion of large quantities of soluble carbohydrates)
• Retained Placenta, colic, diarrhoea and any other systemic illness causing endotoxaemia
• Animals having little exercise
• Pituitary Pars Intermedia Dysfunction / Equine Cushing's
• Equine Metabolic Syndrome
• Trauma/excessive work on hard surfaces
• Increased weight bearing on one limb
• Pony breeds
• Lameness in the contralateral limb

Pathogenesis

Severe pedal bone rotation with penetration into the hoof sole (Wikimedia Commons)

The separation of the sensitive laminae (originated from the third phalanx/pedal bone) from the laminae lining the inside surface of the hoof. This allows the pedal bone to rotate within the hoof capsule and come to rest on the sole. This causes the sole to be pushed downwards and at the toe the pedal bone mat penetrate the sole. Rotation occurs due to torque from the deep digital flexor tendon. Also due to the weight of the animal the pedal bone can sink (displace ventrally). The bone may rotate, sink or both. Serum accumulates in the space between the laminae and can breakdown the white line.

Mechanism of Separation of the Laminae

The mechanism is unknown but theories are:

(1) Ischaemia and necrosis. Ischaemia may be caused by vasoconsriction, arterio-venous shunts, interstitial oedema or a mixture of all three mechanisms.

(2) Inflammation and then degeneration of the sensitive laminae

(3) Enzymatic digestion of laminae by Matrix Metalloproteins (MMPs)

(4) Abnormalities in the hoof metabolism or corticosteriods (Endogenous cortisol or iatrogenic) which results in increased glucocorticoid activity.

Subsequent to separation of the laminae a pain-hypertension-vasoconstiction cycle will occur in acute cases. Pain causes the release of vasoconstictors such as catecholamines, angiotensin II, and vasopressin. This vasoconstriction then causes a reduced blood flow to the foot and systemic hypertension.

Clinical Signs

Acute Disease

Acute disease develops rapidly and most commonly occurs in the front feet. In the early stages of disease or if the case is mild the horse presents as reluctant to move, with frequently shifting of weight between the affected feet and a characteristic stilted gait.

In more severe cases the horse normally presents with a characteristic posture in which the horse appears to be leaning back on its heels. In this posture the feet are placed normally but the head is low, the back arched as the horse attempts to relieve the pressure on the toe, particularly in the fore-feet. The horse may also be unwilling to move or pick up its feet and can potentially collapse if it is forced to do so. Signs of pain such as anxiety, sweating, increased heart and respiration rate are frequently seen. In the most severe cases there may be serum like exudate at the coronary band and the hoof may become detached and shed. Although this does indicate a bleak prognosis, with good and dedicated owners, vets and farriers who are prepared for the time and cost of treatment the horse can survive sloughing of the hoof and go back to normal work.

Chronic Disease

In chronic cases separation of the laminae and sinking and/or rotation of the pedal bone will have occurred. The sole drops and the hoof wall spreads which results in marked transverse ridges on the hoof. Also the angle of the hoof as viewed laterally decreases. Degeneration of the white line may allow for infection to enter, potentially resulting in sepsis of the pedal bone. It is common for the animal to become lame with exercise and have repeated bouts of mild laminitis. Often there is a recognised underlying cause such as Cushings disease in chronic laminitis cases.

Diagnosis

Diagnosis should be based on clinical signs and patient history. Pain may be present on palpation around the coronet and the horse may display a marked withdrawal in response to hoof testers. Increased height and strength of pulse in the palmer digital artery If the pedal bone has sunk a concavity may be palpable at the junction of the coronet, and in very severe cases the pedal bone may be visible through the sole of the hoof. Definitive diagnosis is achieved using radiography.

Radiography

Radiograph of the laminitic foot (Wikimedia Commons)

Radiographs should be taken of front feet or all feet if all legs are affected. A metal strip should be placed on the dorsal wall of the hoof and the sole should be maked with a similar metal strip or a pin can be used. They the angle of the pedal bone in relation to the hoof can then be analysed and the radiograph should be shown to the farrier who is working with you on the case for corrective farriery. Radiographs are essential for prognosis. There may be no radiographic changes if the case is acute or mild. However, radiographs in more severe cases radiographs may show:

• Rotation of the pedal bone as a tilting of the distal aspect towards the sole
• Sinking of the pedal bone (which is the main indicator of prognosis).

Serum build up may be evident as a radiolucent line between the dorsal hoof wall and the pedal bone.

You should measure:

• Distance between the top of the hoof wall the top of the extensor process of pedal bone
• Distance between dorsal hoof wall and dorsal cortex of pedal bone

REPEATS FOR FARRIER

Prognosis

Several factors effect the prognosis in laminitis cases. The pursuit of treatment and the likelihood of its success is very dependant of financial and emotional commitment of the owners. Larger and heavier animals carry a poorer prognosis, as do animals with a greater number of affected feet. Clinical signs help guide prognosis but there are big differences between the signs displayed by stoical and relatively wimpy horses, and it is considered better to use response to treatment in the individual horse as a guide. The Obel grading system was developed (in 1948) to help grade prognosis, with lower grade horses having a better prognosis:

GRADE 0. There is no lameness at walk or straight trot on a hard surface

GRADE 1. At rest, the horse alternately lifts its feet, but no lameness is observable at walk. There is a short stilted gait at straight trot on a hard surface and when turned at walk

GRADE 2. The horse does not move freely at walk and has a ‘stiff’ gait. At trot on a hard surface, the animal has a short stilted gait, and it turns with great difficulty. A foot can be lifted off the ground without great difficulty

GRADE 3. The horse is reluctant to move at walk on any surface. It is difficult to lift a limb and the animal might be virtually non-weightbearing on the affected limb

GRADE 4. The horse will not move without coercion. It is particularly reluctant to move from a soft to a hard surface and it is almost impossible to lift a limb

GRADE 5. The horse is mostly recumbent and will not stand for more than a few minutes

Radiography is the main tool required for prognostics. It is generally recognised that the worse the rotation of the pedal bone the less chance of returning to athletic function. However there should not be too much emphasis placed on pedal bone rotation when considering the prognosis. The fast rate of rotation is suggestive of further structure collapse - repeat radiographs are useful when assessing this.

The level of sinking of the pedal bone is the main prognostic indicator, with distal movement of the pedal bone suggesting a poor prognosis.

Differential Diagnosis

Symptoms of the following diseases can be similar but there is no pain in the feet:

• Equine Rhabdomyolysis Syndrome
• Tetanus
• Colic
• Spinal Ataxia

Treatment

Acute laminitis is an emergency. Box rest is an important part of treatment and return to work should be very gradual.

Aims:

• Removing inciting cause
• Relieve pain and reduce inflammation
• Dilate blood vessels in the foot
• Prevent microthrombi formation
• Prevent rotation or sinking of the pedal bone
• Promote hoof growth

Analgesics, mainly NSAIDs (Phenylbutazone) are the main treatment. It may also help break the theorised pain-hypertension-vasoconstriction cycle. Other available NSAIDs are Flunixin Meglumine, Ketoprofen and Dimethyl Sulfoxide. Vasodilators and anticoagulants are also optional add on drugs, depending on the case.

Mechanical support is important and may provide some pain relief and help prevent rotation or sinking of the pedal bone. It can be done with polystyrene or other packing materials or keeping the animal on soft, deep bedding. Elevating the heel with a wedge or wedge shoe may be useful to take off some of the strain on the deep digital flexor tendon and help to reduce rotation. The farrier will be able to help with the use of egg bar, heart bar and plastic shoes.

Treatment should be monitored physically and radiographically.

References

Rendle, D (2006) Equine laminitis 2. Management and Prognosis in the Chronic Stage In Practice 2006 28: 526-536

Obel, N. (1948) Studies on the histopathology of acute laminitis Almquisst and Wiksells Boktryckeri ab Uppsala