Virginia Therapeutic Farriery

Flexural deformities of the distal interphalangeal joint (clubfeet)

Reprinted with permission from Equine Veterinary Education (EVE). Original published in Equine Veterinary Education Vol 27 April 2012.

S. E. O'Grady
Northern Virginia Equine, Marshall, Virginia, USA.

Keywords: horse; flexural deformity; clubfoot; farriery; inferior check ligament desmotomy

Summary

A true clubfoot results from a flexural deformity of the distalinterphalangeal joint that is characterised by a shorteningof the deep digital flexor tendon musculotendinous unit.Flexural deformities are a problem not only in foals but arealso responsible for the clubfoot conformation seen inmature horses. Treatment is most successful when thecause is investigated and therapy initiated as early aspossible, and when the biomechanical properties of thefoot are thoroughly understood. Flexural deformities in foalsand mature horses are addressed through appropriatefarriery, often combined with surgery.

Introduction

Despite the recent advances in breeding, nutrition andfarm management, flexural deformities are still areasonably common occurrence. A flexure deformity canbe defined as a shortening of the musculotendinous unitof the deep digital flexor tendon (DDFT) that results inhyperflexion of a given anatomic region of the limb(Adams 2000; Greet 2000; Hunt 2000, 2011; Greet andCurtis 2003). Flexural deformities have been traditionallyreferred to as 'contracted tendons'; however, theprimary defect appears to be a shortening of themusculotendinous unit rather than a shortening ofjust the tendon portion; making 'flexural deformity' thepreferred descriptive term (Kidd and Barr 2002).Shortening of the musculotendinous unit produces astructure of insufficient length to allow normal alignmentof the distal phalanx (P3) relative to the middle phalanxand results in variable clinical signs ranging from anupright hoof angle to a clubfoot. The focus of this paper isto define and recommend therapy for flexural deformitiesinvolving the DDFT and the distal interphalangeal joint(DIPJ). The emphasis is on the forelimb unless otherwise stated in the text. The paper is divided into flexuraldeformities of foals and flexural deformities of maturehorses. Severe flexural deformities of foals and maturehorses are commonly referred to as clubfeet.

Fig 1: The structures involved in a flexural deformity of the DIPJ. Note the close association between the AL-DDFT (red line) and the DDFT (green line).
Fig 2: Grade 4 clubfoot. Note the broken forward hoof-pastern axis, fullness of the coronet, the disparity between hoof wall growth at the toe and the heel, the concavity in the dorsal hoof wall and the poor hoof wall consistency at the ground surface of the capsule.

Anatomy review

In the antebrachium, the muscle bellies of the DDFT liedirectly on the caudal aspect of the radius and arecovered by the muscle bellies of the superficial digitalflexor tendon (SDFT) and the flexors of the carpus. Thedeep digital flexor muscle consists of 3 muscle bellies(the humeral head, the inconsistent radial head andthe ulna head), which form a common tendon proximalto the carpus. This tendon, along with the SDFT, passesthrough the carpal canal and continues down thepalmar aspect of the third metacarpal bone. Below thefetlock, at the level of the middle phalanx, the DDFTperforates the tendon of the SDFT, continues distallyand inserts on the flexor surface of the distal phalanx(P3). A strong tendinous band known as the accessoryligament of the DDFT (AL-DDFT) originates from thedeep palmar carpal ligament and fuses with the DDFTat the middle of the metacarpus (Fig 1). The design andfunction of the anatomical structures is such that anyprolonged shortening of the musculotendinous unitaffects the position of the DIPJ. The palmar surface ofthe distal phalanx is pulled palmarly by this shortenedmusculotendinous unit, placing the DIPJ in a flexedposition. The alignment of the bone within the hoofcapsule remains constant while the hoof capsule is pulledwith the distal phalanx. The flexed position of the DIPJcombined with the altered load on the foot leads to arapid distortion of the hoof capsule and thus the clubfootconformation. It can also be noted from the anatomy thattransecting the AL-DDFT, when necessary, lengthens themusculotendinous unit either functionally or by allowingrelaxation of the proximal muscle belly associated with the DDFT.

Classification of flexural deformities (clubfeet)

Flexural deformities have been classified as type 1where the hoof-ground angle is ≤90° and type 2 wherethe hoof-ground angle is >90° (Adams 2000). A recentmethod of classifying flexural deformities using a gradingsystem (Grade 1-4) has been proposed (Redden 2003).Regardless of the method, it would appear beneficial toclassify the severity of the flexural deformity to devise anappropriate treatment plan and monitor the response toa given therapy. A grading system would also enhancerecord keeping as well as improve communicationbetween the veterinarian, farrier and owner with regard to treatment strategies. A Grade 1 clubfoot has a hoofangle 3-5° greater than the contralateral foot anda characteristic fullness present at the coronet. Thehoof-pastern axis generally remains aligned. A Grade 2clubfoot has a hoof angle 5-8° greater than thecontralateral foot, the angle of the hoof-pastern axis issteep and slightly broken forward, growth rings are wider atthe heel than at the toe, and the heel may not touch theground when excess hoof wall is trimmed from the heel. AGrade 3 clubfoot has a broken-forward hoof-pastern axis,often a concavity in the dorsal aspect of the hoof wall, andthe growth rings at the heels are twice as wide as those atthe toe. A Grade 4 clubfoot has a hoof angle of ≥80°, amarked concavity in the dorsal aspect of the hoof wall, asevere broken-forward hoof-pastern axis, and the coronaryband from the toe to the heel has lost all slope and ishorizontal with the ground (Fig 2). For simplicity, the authoruses a grading system based on the severity or degree offlexion noted in the DIPJ on the lateral radiographicprojection to classify flexural deformities.

Flexural deformities in young horses

Flexural deformities in foals can be divided into congenitalor acquired deformities. As such, congenital deformitiesare noted at birth, and acquired deformities generallyoccur during the first 6 months of life as the foal grows anddevelops.

Congenital flexure deformities

Congenital flexural deformities are present at birth,may involve a combination of joints (e.g. carpus,metacarpophalangeal and DIP joints) and arecharacterised by abnormal flexion of these joints and theirinability to extend. Proposed aetiologies of congenitalflexural deformities include malpositioning of the fetus in utero, nutritional mismanagement of the mare duringgestation, teratogens in various forages ingested by themare and maternal exposure to influenza virus, or thedeformities could be genetic in origin (Kidd and Barr 2002;Hunt 2011). The affected foal tends to walk on the toeof the hoof capsule, is unable to place the heel on theground and assumes a so-called 'ballerina' stance.Treatment of foals with a congenital flexural deformityvaries with the severity of the deformity. A mild to moderateflexural deformity in which the foal can readily stand, nurseand ambulate is generally self-limiting and resolves withouttreatment. Brief intervals of exercise once or twice daily in asmall paddock on firm footing for the first few days of lifemay be all that is necessary for the deformity to resolve. Ifthe condition is severe or has not improved by the third daypost foaling, i.v. administration of oxytetracycline (2-3 g)repeated every other day if necessary is frequentlybeneficial (Madison et al. 1994). A variety of bandagingtechniques and splints are used, along with physicaltherapy, to 'stretch' the involved area to hasten recovery.Foals with severe congenital flexural deformities usually donot have just one isolated structure or joint that isresponsible for the deformity, therefore, in the author'sopinion, the use of a toe extension is not indicated.

Acquired flexural deformities

Acquired flexural deformities generally develop when thefoal is aged 2-6 months and generally involves the DIPJinitially. The aetiology of this deformity is unknown, butspeculated causes include genetic predisposition, impropernutrition (i.e. overfeeding, excessive carbohydrate [energy]intake, unbalanced minerals in the diet) and excessiveexercise. A recent study looked at grazing patterns in a smallnumber of foals and showed that foals with long legs andshort necks had a tendency to graze with the same limbprotracted (van Heel et al 2006). Fifty percent of the foalsdeveloped uneven feet with a higher heel on the protractedlimb, leading researchers to feel there may be a possiblecorrelation between conformational traits and an acquiredflexural deformity. It is the current author's opinion that alarge contributing factor to this syndrome is contraction ofthe muscular portion of the musculotendinous unit causedby a response to pain, the source of which could be physealdysplasia or trauma from foals exercising on hard ground.Discomfort may follow aggressive hoof trimming whereexcessive sole is removed, rendering the immature structureswithin the hoof capsule void of protection and susceptibleto trauma and bruising. Any discomfort or pain in the footor lower portion of the limb coupled with reducedweightbearing on the affected limb appears to initiatethe flexor withdrawal reflex, which seems to cause the flexormuscles proximal to the tendon to contract, leading toan altered position of the DIPJ. This shortening of themusculotendinous unit shifts weightbearing to the dorsal halfof the foot causing a decrease in sole depth and bruising ofthe sole, reduced growth of the dorsal aspect of the hoof wall, and excessive hoof wall growth at the heel tocompensate for the shortening of the musculotendinousunit. As the flexural deformity may be secondary to pain inthese cases, it is essential that the source of pain should becarefully evaluated by physical examination and bylocalisation using regional analgesia and diagnostic imagingtechniques.

A genetic component must also be considered foracquired flexure deformities, as some mares consistentlyproduce foals that develop a flexural deformity in thesame limb as the dam or grand dam in which a similardeformity is present. The genetic component of the flexuraldeformity may be the ultimate determinant of the severityof the deformity. A genetic component should alsobe considered in the aetiology of acquired flexuraldeformities, although there is no scientific evidence for thisat present. Some mares appear to consistently producefoals that develop flexural deformities, sometimes in thesame leg as was affected in their dam or grand dam.

Mild acquired flexural deformities

Clinical signs

The initial clinical sign of a flexural deformity may beabnormal wear of the hoof at the toe, which is oftendiscovered by the farrier during routine hoof care. Closerinvestigation may reveal that the dorsal hoof wall angle isincreased and that after the heels of the hoof capsulehave been trimmed to a normal length, the heels may nolonger contact the ground. A prominent coronary bandmay or may not be present at this stage. Most foalsaffected to this degree have a mildly broken-forwardhoof-pastern axis. Increased palpable digital pulse, heat inthe affected foot, and signs of pain when a hoof tester isapplied to the dorsal aspect of the toe are not uncommonclinical findings. These findings are generally the result oftrauma or excessive weightbearing on the toe.

Fig 3: A mild flexural deformity before (a) and after trimming (b). Note the change in breakover created under the dorsal hoof in b).

Treatment

Conservative treatment, such as correcting thenutritional status of the foal (i.e. weaning the foal to avoidpossible excessive nutrition from the mare), restrictingexercise to reduce trauma, judiciously administering anonsteroidal anti-inflammatory drug (NSAID) to relievepain, administering oxytetracycline to facilitate musclerelaxation, and carefully trimming the hoof is, in theauthor's opinion, a good starting point. NSAIDs shouldbe administered short-term and should be used judiciouslyin foals due to the potential side effects, such asgastroduodenal irritation and nephrotoxicity. For analgesia,the author will administer firocoxib (0.1 mg/kg bwt q. 24 h) orflunixin meglumine (1.1 mg/kg bwt q. 24 h) combined with agastric protectant. Hoof trimming begins with lowering theheels from the middle of the foot palmarly until the hoof wallat the heels and the frog are on the same plane. The bars should be thinned or removed, and the heels adjacent tothe sulci should be angled to 45° to promote spreading.Breakover is moved palmarly by creating a mild bevel,with a rasp that begins just dorsal to the apex of the frogand extends to the perimeter of the dorsal aspect of thehoof wall (Fig 3). If improvement is noted, this trimmingregime is best performed at 2 week intervals. If the toe isconstantly being bruised or undergoing abscessation, ahoof composite (Equilox or Vettec) can be applied to thedorsal aspect of the sole and the distal dorsal aspect ofthe hoof wall to form a toe 'cap' to provide protection.The acrylic composite-impregnated fibreglass or urethanecomposite used to form the toe cap covers the solarsurface of the foot to the apex of the frog, protecting thatarea from further damage. A bevel toward the toe can becreated is the composite with a rasp or Dremel tool tofacilitate breakover. If there is adequate integrity of thedorsal hoof wall, the author believes that application of atoe extension is unwarranted. The above treatment can betemporary, appears to work best when initiated at the firstsign of foot deformity before a marked flexural deformityis noted and, if possible, following elimination of incitingcauses.

Severe acquired flexural deformities (clubfeet)

Fig 4: Severe flexural deformity. Note the prominent coronet, the steep angle of the dorsal hoof wall, the load being placed on the toe and the heels of the hoof capsule off the ground.

Clinical signs

A mild acquired flexural deformity may progress in severitydespite conservative treatment, or a severe acquiredflexural deformity may be acute in onset.Asevere acquiredflexural deformity is characterised by a foot with a hoofangle >60°, a prominent fullness at the coronary band, abroken-forward pastern axis, disparity in the length of theheel relative to the toe of the hoof, and heels that fail tocontact the ground (Fig 4). If the cause of the deformity isallowed to persist, the foot eventually assumes a boxy,tubular shape due to the overgrowth of the heels toaccommodate the lack of ground contact and approachthe length of the toe. Increased stress on the toe willeventually cause a concavity along the dorsal surface ofthe hoof wall. Stress exerted on the sole-wall junction in thetoe area will cause it to widen allowing separations to occur.

The diagnosis is straightforward and based on thecharacteristic foot and limb conformation. Radiographsshould be used to confirm the diagnosis and assesschanges in the joint. The author will administer mildsedation (half the recommended dose of xylazine[0.33-0.44 mg/kg bwt i.v.] combined with butorphanol[0.022-0.066 mg/kg bwt] i.v.) and place each of the foal'sfeet on separate wooden blocks of equal height, whichallows normal loading of both forefeet. Lateral-to-medialand weightbearing (horizontal) dorsopalmar views of bothforefeet should be obtained. The degree of flexion of theDIPJ, the angle of the dorsal hoof wall and abnormalities atthe margin of the distal phalanx should be observed(Fig 5). Interestingly, in all the cases where the author hasobtained weightbearing (horizontal) dorsopalmar views, the width or thickness of the distal phalanx of the affectedfoot appears to be increased (Fig 6). This finding maypossibly be due to radiographic projection with thechange of angle of the distal phalanx to the horizontal butthe author has also noted the change in width in foalswithout a flexural deformity. The significance of this findingis speculative but certainly adds credence to the geneticfactor in the aetiology and the susceptibility of certainindividuals to acquire a flexural deformity.

Fig 5: Radiographic view of the RF foot shows a broken forward hoof-pastern axis when compared to the LF foot, which shows normal alignment of the digit.
Fig 6: Thickness of the distal phalanx may appear greater in the limb with the flexural deformity on the weightbearing dorsopalmar radiographic view.

Treatment

When a severe flexural deformity is present and confirmedduring radiographic examination of the feet, conservativetreatment and hoof trimming alone are generally oflittle benefit. Elevating the heels has been advocated,after trimming the foot, to reduce tension in the DDFT andto promote weightbearing on the entire solar surface ofthe hoof. Although elevating the heels improves thehoof-pastern axis and makes the foal more comfortableinitially, the author has not been able to subsequentlylower the heel or to remove the wedge and establish anormal hoof angle with the heel on the ground. Once amarked flexural deformity of the DIPJ and distortion ofthe hoof capsule are present or occurring, the authorrecommends transection of the AL-DDFT combined withthe appropriate farriery.

Fig 7: Illustration of the lateral side of the foot shows the placement of a reverse wedge after the foot has been trimmed. Illustration of the ground surface of the foot shows the composite wedge reinforced with an aluminium plate.

Desmotomy of the AL-DDFT

The author has been consistently successful in treatingfoals with severe flexural deformities with desmotomy ofthe AL-DDFT combined with the appropriate farriery. Theauthor no longer uses a toe extension at the time ofsurgery, but applies an acrylic composite beneath thedorsal aspect of the toe to create a reverse wedge. Thewedge affords protection for the toe region, appears toredistribute the load to the palmar aspect of the foot,increases the stresses on the DDFT, and restores theconcavity to the sole. The author has found it beneficialto do both procedures at the same time while the foalis anaesthetised. The foal is placed under generalanaesthesia and the surgery is performed in a routinemanner as described elsewhere (Fackelman et al. 1983;Wagner et al. 1985; White 1995; Kidd and Barr 2002; Auer2006). The farriery can be performed before or after thesurgery. The heels are lowered from the point of the frogpalmarly, until the sole adjoining the hoof wall (sole plane)at the heels becomes solid. Any concavity in the dorsalaspect of the hoof wall is removed with a rasp. The groundsurface of the foot dorsal to the frog and the perimeterof the dorsal hoof wall are prepared for a compositeusing a rasp or Dremel tool. Deep hoof wall separationsin the sole-wall junction at the toe are explored and filledwith clay, if necessary, to prevent infection beneath the composite. Foals undergoing this procedure are usuallyaged 3-5 months, and so, because of their size and weight,reinforcing the composite with fibreglass is necessary. Asmall section of fibreglass is separated into strands andmixed with the composite. The composite is applied to thesolar surface of the foot beginning at the apex of the frogand extending to the perimeter of the hoof wall where athin lip is formed. The composite is moulded into a wedgestarting at 0° at the apex of the frog and extending to 2-3°at the toe (Stone and Merritt 2009) (Fig 7). If desired, apiece of 3 mm aluminium plate can be cut out in theshape of the dorsal aspect of the sole. Multiple holesare drilled in the plate and it is gently placed into thecomposite. The aluminium is pushed down so that thecomposite material extrudes through the holes andthe aluminium plate is then covered with additionalcomposite. This additional reinforcement allows the olderfoals to be walked daily or turned out in a small paddockwithout the composite wearing out.

Aftercare

The surgical aftercare is at the discretion of the attendingclinician. Controlled exercise in the form of daily walkingor turn-out in a small paddock is essential. There is thepotential for pain with the initiation of exercise, requiringclose monitoring of the foal and exercise should beincreased sequentially. The foal is trimmed at roughly2 week intervals, based on the amount of hoof growthwith the objective of establishing normal hoof capsule conformation. The composite wedge is removed onemonth after the surgery. At subsequent trimmings, the heelsare lowered as necessary and hoof wall at the toe istrimmed from the outer dorsal aspect of the hoof walluntil the desired conformation is attained. No sole dorsal tothe frog is removed. When the desired conformation isreached, the foot is trimmed in a routine manner on amonthly basis. It is important to emphasise that when thehoof capsule returns to an acceptable conformation, onlythat portion of the sole that is shedding should be removedto avoid any discomfort in the dorsal solar area that canresult in the horse re-developing, to some degree, theoriginal deformity.

Fig 8: Typical appearance of a clubfoot in a mature horse. Note the broken forward hoof-pastern axis, the concavity in the dorsal hoof wall, the disparity in hoof wall growth between the toe and the heel and the poor hoof wall consistency distally.

Flexural deformities in the mature horse

Clubfeet

There is minimal information in the veterinary literatureregarding the management of a mature horse with aclubfoot. An upright conformation of the foot associatedwith a flexural deformity of the DIPJ is defined as a clubfoot(O'Grady 2011) (Fig 8). A flexural deformity is generallydiagnosed and treated while the horse is immature butoften a mild flexural deformity is ignored or the foal istreated inappropriately. When the horse enters training,the existing flexural deformity may become exacerbatedby the type and amount of exercise, inadequatefarrier care, such as inappropriate or infrequent trimmingand shoeing, or some type of underlying disease. Whena clubfoot conformation is acquired in the maturehorse, it is almost invariably secondary to an underlyingcause or disease, such as: an injury that results in anonweightbearing lameness; excessive trimming of the toeresulting in solar pain; chronic, low-grade laminitis; or chronic heel pain. Furthermore, flexural deformities havebeen reported as a cause of decreased athleticperformance and chronic, low-grade lameness in themature horse (Balch et al. 1995; Turner and Stork 1998). Thealtered biomechanics of the foot result in an increasedload (i.e. weightbearing) being placed on the dorsalsection of the foot leading to decreased sole growth, solebruising, a shortened stride on the affected limb, andvarious degrees of lameness and poor performance. Themajority of horses with a clubfoot maintain soundness, yetthe clubfoot conformation and the altered load on thefoot may be responsible for poor performance.

The hoof capsule distortion

To apply the appropriate farriery, understanding theproposed mechanism leading to the clubfootconformation is helpful. When a flexural deformity ispresent, the musculotendinous unit is shortened, thedegree of which is dependent on the amount of flexion inthe DIPJ. This causes a disparity of hoof wall growth, withmore growth at the heel than at the toe to compensate forthe decreased length of the soft tissue structures. The froggenerally recedes due to the excessive hoof wall growth atthe heels so that the energy of impact is assumed entirelyby the hoof wall, bypassing the soft tissue structuresin the palmar foot and transferring the load directly ontothe bones of the digit through the laminar interface. Theflexural deformity, combined with the excess hoof wallgrowth at the heels, places the DIPJ in flexion and distalphalanx in an abnormal alignment relative to the digit,promoting toe-first landing, and excessive load is assumedby the dorsal section of the joint and the dorsal sectionof the foot. Hoof abnormalities associated with clubfootconformation are thin flat soles, poor hoof wall consistency(especially at the toe), toe cracks, hoof wall separationand 'white line disease' (O'Grady and Poupard 2003).Injuries associated with a high hoof angle are thoughtto include inflammation of the DIPJ due to abnormalloading of the joint, sole bruising and increased strain onthe suspensory ligaments of the navicular bone (Turner1992).

Fig 9: Radiograph showing a moderate flexural deformity involving the DIPJ in a horse with a clubfoot. Note the ideal soft tissue parameters of the hoof capsule that can be assessed on this radiograph.

Radiology

Good quality radiographs, consisting of lateral to medialand weightbearing (horizontal) dorsopalmar views, arenecessary for the clinician and farrier to evaluate andtreat a horse with a clubfoot. Good soft-tissue detailallows the distortion of the hoof capsule to be accessed. Alateral to medial radiographic examination reveals theweightbearing properties of the foot, the position of thedistal phalanx within the hoof capsule, solar depth, lengthof the heels, the osseous integrity of the perimeter of thedistal phalanx, and the severity of the flexural deformity ofthe DIPJ. The degree of flexion indicates the amount of shortening of the musculotendinous unit. The radiographsare used to diagnose any pathology present, determinetreatment options and can be used as a template forfarriery (Fig 9).

Therapeutic farriery

Therapeutic farriery forms the mainstay of treatment forclubfeet. Farriery should be based on principles rather thana particular method, and the principles remain the sameregardless of the severity of the flexural deformity (O'Grady2009). The principles are to achieve normal alignmentbetween the proximal, middle and distal phalanges, andthus normal orientation and loading of the distal phalanxrelative to the ground. Trimming and shoeing is aimed atremoving weightbearing from the toe and dorsal aspectof the distal phalanx and re-establishing weightbearing tothe entire solar surface of the distal phalanx and thecorresponding hoof wall. Historically, farriers have beentaught to trim (lower) the heels to correct the distortedhoof capsule and promote weightbearing in the heelarea, but this type of trimming comes with a price. As theseverity of the flexural deformity increases, so too does theshortening of the musculotendinous unit; therefore,lowering the heels directly increases the tension within themusculotendinous unit, and these stresses may lead toirresolvable tearing of the dorsal lamellae and widening ofthe sole-wall junction similar to that seen in the chroniclaminitic hoof (Floyd 2007). The increased forces placed onthe DDFT also promote hoof capsule distortion andabnormal loading.

Fig 10: Wedge pad can be placed under the toe of a horse with a clubfoot that will test the response when tension is exerted on the DDFT. The farrier can then determine the amount of hoof wall that can be safely removed from the heels of the hoof capsule.
Fig 11: Moderate clubfoot. Following the appropriate trim, the horse is shod with a wide web aluminium shoe with heel elevation and breakover created palmarly in the shoe.

Farriery

Distinguishing between a foot with steep hoof angleand a true clubfoot is important. High hoof angleswithout phalangeal misalignment or with mild phalangealmisalignment can generally be improved by graduallylowering the heels in a tapered fashion from the apex ofthe frog to the heels. This increases the ground surfaceof the foot and attempts to re-establish weightbearing onthe entire solar surface of the foot. Breakover is movedpalmarly at the same time to compensate for anyincreased tension in the DDFT created by lowering theheels. If improvement is noted, trimming should berepeated at 4 week intervals.

Farriery to correct a high hoof angle accompanied bya flexural deformity becomes more of a challenge. Again,the object of farriery is to load the heels, compensate forthe shortening of the DDFT and improve the hoof-pasternaxis. To accomplish these objectives, farriery is directedat lowering the heels, but the amount to remove can bedifficult to determine. In mild to moderate clubfeet, anestimate of how much heel to remove can be made byplacing the thick end of a 2° or 3° wedge pad under thetoe of the foot and allowing the horse to stand on it(Fig 10). If the horse does not resent the tension it places onthe DDFT, this test allows the farrier to safely trim the hoofwall at the heels in a tapered fashion starting at the widestpart of the foot using the thickness of the degree pad as aguide. The toe is shortened by trimming the outer surfaceof the dorsal hoof wall with a rasp. The trimmed foot is fittedwith a shoe that has the breakover forged or ground into itstarting just dorsal to the apex of the frog and taperingtoward the toe to further decrease the stresses on theDDFT.

With the more advanced cases of clubfeet, the heelsshould still be lowered to load the heels and unload thetoe, but the addition of heel elevation following thetrim is necessary to compensate for the shortening ofthe musculotendinous unit. The amount of heel elevation needed can be demonstrated following the trim byplacing the trimmed foot on the ground 15-20 cm palmarto the contralateral limb. A space will generally appearbetween the heels of the foot and the ground. The authoruses a wedge shoe or places a degree pad or a bar wedgebetween the heels of the foot and the shoe to compensatefor the shortening of the muscle-tendon unit (Fig 11). Thismethod allows the heels to be weightbearing but at thesame time decreases the stresses on the musculotendinousunit. Creating breakover in the shoe to further relieve stressin the DDFT, as described above, is essential.

Farriery combined with surgery

In selected cases, horses with a severe flexural deformity orhorses that have not responded to appropriate farriery andremain lame may benefit from a distal check ligamentdesmotomy (Turner 1992; Floyd 2007; O'Grady 2011). Thisrelease procedure, along with therapeutic farriery, allowsrealignment of the distal phalanx within the remainder ofthe digit and readily allows the accompanying distortionof the hoof capsule to be improved. The author believesthat if this surgery is being contemplated, it should beperformed early in the horse's athletic career, beforethere is a significant hoof capsule distortion and beforeradiographic changes involving the DIPJ and/or themargin of the distal phalanx become evident.

In the mature horse, the surgery can be performedunder general anaesthesia or with standing sedation/local or regional analgesia. In the standing horse, the heelshould be elevated by taping a 12° wedge to the footto decrease tension in the inferior check ligament/DDFTcomplex allowing the check ligament to be easilyidentified, separated and transected away from thecutaneous incision. The client should be forewarned thatthe surgery involves an extended recovery period, anda blemish or fibrous thickening at the surgery site isinevitable due to the mature nature of the tissue. Cautionis advised when performing the farriery that accompanies the surgery because the soft tissue structures withinthe hoof capsule and the digit have adapted/accommodated for the distortion of the hoof capsule.The author will trim the hoof in moderation and,according to information obtained from the radiographs,then apply two or three 2° wedge pads using either ashoe or a cuff. After surgery, the horse is walked daily, anda degree pad is removed every 7-10 days dependingon the comfort of the horse. After 3 weeks, the horse isallowed turnout in a small paddock for an additional 3weeks and then turnout in a larger area for 3-6 monthsbefore exercise is resumed. The cosmetic appearanceof the limb is maximised by keeping the limb bandagedfor the first 6 weeks. In a limited number of cases thatthe author has managed or consulted on, the benefitsreturning the horse to soundness have far outweighedthe rehabilitation process being labour intensive (S.E.O'Grady, unpublished data). The author has not realisedany benefit in applying a toe extension to the shoe in themature horse following surgery. Many mature horses witha clubfoot frequently have damage to the dorsal laminasimilar to that found in horses with laminitis, and, therefore,toe extensions may markedly exacerbate detrimentalmechanical forces on the lamellae.

Conclusion

The clubfoot can be a significant cause of equine lamenessand a challenge to the veterinarian and farrier. The clinicianmust recognise and understand the altered mechanics thatare placed on the osseous structures within the hoof and onthe hoof capsule that accompany a flexural deformityinvolving the DIPJ. This understanding allows the clinicianto apply the appropriate treatment and appreciatesubsequent improvement. Additionally, it is essential to lookbeyond the deformed foot to identify and remove, ifpossible, any underlying cause(s). As with most disorders,early recognition and intervention significantly increasethe chances for a successful outcome. This is especially truewhen dealing with the young horse. Thorough physicalexamination, high quality radiographic imaging, familiaritywith composite materials, and surgical competence are allessential to properly treat horses presented with a widerange of clubfoot abnormalities. Owners and trainers mustbe informed regarding the severity of any individual horse'sflexural deformity, the treatment options, the expectedoutcome, and the aftercare. Knowledge, skill, andinteraction between the veterinarian and farrier arenecessary for a successful outcome when treating a horsewith a flexural deformity, regardless of whether treatment islimited to farriery or combined with surgery.

Acknowledgements

The author would like to thank Drs Jim Schumacher andLiberty Getman for their invaluable help in critiquing thismanuscript.

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