Treatment

Whilst resting the horses in rocky, rough hill country may produce a harder foot, it seldom corrects the original defect – indeed it may sometimes cause serious break-back of the wall. Thin-soled horses benefit from polypropylene pads or a thin 2–3 mm layer of acrylic filler applied over the whole solar surface. Chrome-treated leather has also been glued with contact adhesive to the soles under the shoes. Glue-on plastic shoes help considerably by avoiding the need for any nails at all but they are not as durable and the methacrylate adhesive often loses its strength if allowed to get wet for long periods. Acrylic hoof support bandages applied around the wall before shoeing assist some horses and can be used to provide extra hoof strength. Daily supplementation with biotin and methionine may improve the quality of the hoof structure but it is not usually curative on its own.

Treatment

There is no effective medical option and therapy is limited to placement of well-seated shoes and avoidance of hard or rough going. Polypropylene or leather anti-concussion pads can be applied to help cushion foot impact.

Profile

An idiopathic defect in cornification of the coronary band which affects all four hooves more or less simultaneously and equally. Mature horses of draught breeds seem most susceptible and most cases are reported to be affected from a young age; the signs may not be severe and may easily be overlooked in the growing horse.

Key points: Coronary band (dysplasia) dystrophy

1. A sporadic rare disorder of the coronary band largely restricted to heavy draught breeds. Possibly therefore some genetic aspect.

2. Proliferative, scaling condition of the coronary band only; the pastern skin is usually unaffected. Possibly some consequent alterations in the hoof quality, particularly with loss of periople and a rough, crumbly hoof wall quality.

3. Diagnosis is made by eliminating other causes of coronary band disease and inflammation.

4. Treatment is difficult. Restoration of normal keratinocyte function may be possible with retinoids.

5. The prognosis for resolution is poor – ongoing management and hoof difficulties are almost inevitable. Some horses cope well for many years.

Clinical signs

Onset is usually insidious and often the first sign of a problem is the poor hoof wall quality. All four coronary bands show progressive proliferation and hyperkeratotic changes with extensive scaling and have a greasy feel. There are usually obvious hoof wall changes in severe or prolonged cases (Fig. 17.1).

Figure 17.1 This middle-aged part Irish Draught gelding had a long history of poor hoof quality (A) and showed the typical signs of coronary band dystrophy on all four feet. Note the scaling and thickening of the coronary band (B) and the generally poor hoof wall quality with flaking and horizontal lines of abnormal horn growth. Secondary inflammatory changes may be found at the coronet or over the heels (C).

There is no pain or pruritus unless secondary infection develops.

Open lesions are often present with cracks and fissures which can bleed or ooze serum (Fig. 17.2). The ergot and chestnut are seldom affected similarly.

Figure 17.2 Coronary band dystrophy.

Differential diagnosis

Diagnostic confirmation

Treatment

Only palliative measures are possible; removal of excessive horn and application of emollient creams to affected tissues at coronet. Topical retinoids such as tazarotene may usefully but temporarily restore normal keratinocyte function. Systemic or topical corticosteroids have no material effect.

Mild counterirritants applied to the coronet may be helpful in encouraging healthy coronary tissues but equally may make the condition worse. Dietary supplementation with evening primrose oil, biotin and methionine may be useful.

The owner must be apprised of the chronic nature of the disease. Regular attention to the feet and early intervention if secondary infection develops are important in the long and short term.

Profile

These are characterized by fissures in the hoof capsule. Coronary band injuries are a common cause of clinically significant secondary cracks and horn defects. Wall, toe and quarter cracks have a defect which is parallel to the laminae, while transverse cracks are at right angles to the laminae. Most cracks of the former type are superficial and due to prolonged desiccation or to trauma/defects of the coronary band. Deep cracks may extend into the sensitive laminae (Fig. 17.3).

Figure 17.3 Deep toe crack extending from solar margin to coronary band and down to sensitive tissue.

Toe and quarter cracks

These are mostly due to neglect from allowing the hoof to dry out, or improper dressing to reduce ‘winging’ of the quarters and heels. They may also arise from sudden turns on rough ground or injuries to the coronary band (Fig. 17.4).

Figure 17.4 Quarter crack extending from solar margin to coronary band.

Transverse cracks

Coronary band injuries or infections spreading up the white line from sole abscesses are usually responsible for these. They only become serious if they are extensive and when they have nearly grown out at the solar margin (Fig. 17.5).

Figure 17.5 Transverse crack.

An interesting condition occurs where there is repeated localized bulla formation usually at the dorsal aspect of the coronary band. The condition is pain-free and unexplained. It results in a localized hoof wall deficit that grows down some way before another focus develops. The syndrome is not usually recognized except by farriers (Fig. 17.6).

Figure 17.6 This Warmblood gelding had a regular focal blistering of the dorsal coronary band without obvious pain or discomfort. The consequent horn defect gradually grew down the hoof (A) but other episodes occurred at irregular intervals. (B) Note the rather poor quality hoof more proximal to the hoof wall defect (arrow) indicating that the primary condition actually caused more extensive damage. The syndrome has not been investigated fully.

Sole cracks

These are caused by a combination of excessive drying of the sole and standing on rocks or other hard objects in paddock/grazing horses (Fig. 17.7). They are not commonly observed in shod horses.

Figure 17.7 Sole crack (arrows).

Heel cracks

Cracks in the wall of the heel usually have two fairly distinct causes: (a) coronet injury leading to a persistent defect in the coronary band and so to a wall deficit; (b) bearing-surface injuries which seem to occur more frequently from poor heel support. This is encountered where the angle of the heel becomes more and more acute, leading to tearing of the laminae (Fig. 17.8).

Figure 17.8 Heel crack due to poor hoof conformation and lack of corrective farriery. The true extent may be visible only after careful dressing.

Clinical features

Superficial cracks are not often associated with lameness. Deep cracks with pressure on the sensitive laminae may cause lameness. Haemorrhage or purulent discharging sinuses and foci with movement of the wall have serious implications. Working the horse may cause bleeding from the area and, in paddock/grazing horses, pus is often associated with neglected hoof injuries.

Heel cracks are often painful and contact with the ground is too far forward compared with the horn at the coronary band. The cracks are often deep and easily bleed and/or become infected.

Diagnostic confirmation

Treatment

The first objective is to address the underlying cause. Brittle horn and weak horn have both been improved by prolonged feeding of gelatin at 30 g per day or by continuous feeding of biotin at 15–20 mg per day. Foot balance and regular farriery are very important at any stage in the development of a crack. It is important to ensure that the crack is not a secondary manifestation of a seedy toe area.

Profile

Wire cuts or overreaching injuries are very common and are probably the commonest traumatic injury to the hoof and coronary band (Fig. 17.9). Horses paw at fences, hook the heel over wire, and either pull back or saw the leg sideways, often causing extensive damage to the skin, lateral cartilage, tendons and coronary band (Fig. 17.10).

Figure 17.9 This severe wire wound is typical of those injuries that involve the heels and the coronet. In this case the large flap incorporated the coronary band (A). In spite of the gross displacement and almost certain vascular compromise (B) it healed very well within 4 weeks following repair using delayed primary healing under a rigid half-limb limb cast. There was a persistent defect in the coronary band which created more problems for the farrier than the horse. The prognosis for such injuries is remarkably good except of course if they involve synovial or neurovascular structures or when the injury is poorly managed. Rapid attention is vital to the prognosis.

Figure 17.10 Extensive wire injuries involving the hoof, coronary band and deeper tissues of the foot and the pastern and fetlock.

All injuries that physically damage or disrupt the continuity of the corium result in persistent hoof growth abnormalities (Fig. 17.11). In many cases the horse will manage provided that appropriate foot care is given. Complications involving synovial structures, tendons or neurovascular tissues carry a much worse prognosis and in all cases of acute trauma these aspects must be investigated fully.

Figure 17.11 A permanent hoof defect as a result of a coronary band injury.

Clinical signs

Injuries involving the coronary band or abnormality of the coronary band caused by previous injury are usually very obvious. Acute injuries must be assessed carefully to establish extent of damage to vascular and nervous supply to foot and damage to heel tissues and lateral cartilage.

Secondary defects in horn growth are very variable and depend largely on the extent of treatment applied at the acute stage. Cracks in the hoof wall commencing at the coronary band defect and extending distally are common outcomes.

Instability of the two sides of the resulting defect/crack may cause repeated lameness and even bleeding from the site. Secondary infection is common and can be very painful.

Diagnostic confirmation

Treatment

Very careful assessment of the wound is essential: most are heavily contaminated and/or infected. Prompt, careful debridement using a scalpel (not scissors) of all dead or compromised or contaminated tissues is an essential first step. Hydrosurgical debridement is a useful technique for these injuries because it debrides very efficiently without removing any attached/viable tissue (Knottenbelt 2007).

It is very rare that wounds of this type can be sutured at the time of injury and most attempts to do so result in failure or worse. The choice should be made between allowing the wound to heal by delayed union or using a delayed primary union technique. The choice will depend on the facilities available and the type of injury but the value of rigid limb casting cannot be overstated.

Initially the debrided and cleaned wound should be irrigated carefully and packed with a hydrogel wound dressing material and a cavity absorbent dressing should be inserted into any defect to minimize dead space and to remove wound exudate. This dressing should be replaced at 48-hour intervals (or more frequently if exudate is excessive or patently infected) until granulation tissue is obvious and the wound bed is healthy. At this point (usually 2–5 days) the wound can often be closed surgically following scrupulous debridement.

Application of rigid limb casts over a suitable dressing is a rewarding procedure which has been made simpler and safer by synthetic polypropylene or polyurethane resin bandage casting materials. These are light, strong and easy to apply but the cast should always be applied (and removed) strictly according to the manufacturer’s instructions. Cast management is vitally important. Unless complications develop, the cast can be left for 3–4 weeks. In the event of any complication (pain is often the earliest evidence of something going wrong) it must be removed immediately and if necessary replaced. Casts should be used until healing is well advanced. Early removal of support can lead to the wound splitting open over the original wound site.