Podiatry Proceedings
From Our Practice to Yours 2019
11th Annual NEAEP Symposium
Table of Contents
Shoeing For Sport Horse Injuries: My Point Of View Pg 3 What’s Going on Back There? A Unique Look at The Back Of The Hoof Pg 7 Trimming the Hoof Capsule to Improve Foot Structure & its Function Pg 17 Navicular Syndrome: Questions Needing To Be Asked Pg 32 Maybe It’s a Nerve Pg 44 New Developments In Our Understanding Of What Causes Different Forms Of Laminitis Pg 49
Hoof Capsule Trimming to Improve the Internal Foot of Navicular Syndrome Affected Horses Pg 54
Evidence-Based Approaches to Treatment and Prevention of Laminitis Pg 66 Trimming Practices Can Encourage Decline In Overall Foot Health Pg 69 A Practical Approach to a Therapeutic Shoeing Prescription Pg 72
Power Point Presentations for this program can be found online at www.theneaep.com/members-only . The password to access this section is: “neaep2019”
2 www.theneaep.com Shoeing For Sport Horse Injuries: My Point Of View
Professor Roger K.W. Smith MA VetMB PhD FHEA DEO ECVDI LAAssoc. DipECVSMR DipECVS FRCVS Dept. of Clinical Sciences and Services, The Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, Herts. AL9 7TA. U.K. E-mail: [email protected]
Synopsis ‘No foot no horse’ is a well-known statement that sums up the importance of the fore (and hind) foot in equine lameness and performance. This presentation will focus on what this presenter considers the most important biomechanical principles in his practice of treating foot-related injuries in sports horses.
Introduction Corrective farriery is rarely completely effective without other concurrent treatments although individual horses vary in their response to therapeutic shoeing, and so can be remarkably effective in some. There is considerable variation on what is advised for corrective farriery with a wide array of therapeutic shoes available to the practitioner and many of these shoes work best for the person who first invented them. It is therefore important to work with the farrier to achieve the desired result. If the aim is to change (improve) the foot balance, it can often take at least 2-3 rounds of trimming and shoeing before a beneficial effect on the foot balance can be achieved. Consideration should be given to sound biomechanical principles and use repeat radiography to assess whether the correction of foot balance is being achieved.
Roles for therapeutic shoeing - For managing foot problems – o Navicular disease – correction of dorsopalmar foot balance o Solar/distal phalanx bruising – thin soles - For protecting tendons and ligaments - For managing fractures
Managing foot problems This requires the following approach: a) Accurate diagnosis. Achieving this will necessitate localizing the lameness to the foot and then undertaking diagnostic imaging to identify the pathology. Radiography may be sufficient (eg for advanced navicular disease and fractures of the distal phalanx and navicular bone) but will often require more advanced imaging, such as MRI, to identify more subtle causes of lameness, including soft tissue pathology of the foot. Ultrasonography can be used through the three ultrasound ‘windows’ (dorsal coronary band; between the heels, and transcuneal) but there are still considerable limitations to this imaging modality compared to MRI. b) Assessment of foot balance Assessment of foot balance should be done both visually and radiographically. Visual appraisal should be from all directions (dorsal, lateral, palmar/plantar, and solar)
3 www.theneaep.com and should be interpreted in the light of the conformation of the rest of the limb. Foot pastern axis (FPA) assess the relationship between the pastern and the foot conformation and is usually only assessible visually because the foot is usually raised on a block for lateromedial radiography which can distort the FPA. Visual appraisal is thus still important to perform first and will inform the interpretation of radiographic foot balance. Mediolateral hoof balance is, in this author’s opinion, a less important parameter than dorsopalmar foot balance. This is because it is strongly influenced by the conformation of the rest of the limb (carpal and fetlock valgus/varus; base narrow versus base wide stance) and by the dynamic aspects of foot placement (landing lateral versus medial) which makes simple recommendations for changing fraught with the risk of exacerbating the problem. In contrast, dorsopalmar foot balance is less influenced by upper limb conformation has a strong influence on the loading of the navicular bone and deep digital flexor tendon1,2. Navicular disease is believed to be the consequence of aberrant remodeling associated with mechanical overload which is exacerbated by the positive feedback loop that occurs when the horse has pain in the heels that induces increased tension in the DDFT in the first half of the stance phase3. The most important parameter for unloading the DDFT and navicular bone is the solar angle of the distal phalanx – for every one degree increase in the downward angulation of the distal phalanx there is a 4% reduction in the peak force exerted by the DDFT on the navicular bone2,4,5. The other dorsopalmar foot balance parameters assessed include the position of the centre of rotation of the distal interphalangeal joint which should be within the middle third of the weight bearing surface of the foot, and the height (length) and angle of the dorsal wall and heels. In addition, the thickness of the sole has strong implications with respect to solar (and distal phalangeal) bruising and corrective farriery (see below).
Shoeing for specific foot conditions 1) Navicular disease and DDFT pathology – trimming and shoeing to correct dorsopalmar foot balance This is achieved by preserving the heels while trimming the sole at the toe to improve the downward angulation of the distal phalanx within the hoof capsule. This is only possible when there is a thick enough sole with which to achieve this alteration in angle. If the case of thin soles, artificial elevation of the heels is achieved with wedges or a graduated shoe. This has the same effect in unloading the DDFT but tends to unload the heels which can encourage heel collapse and so should only be used temporarily. The branches of the shoe should be extended as far caudally as possible (to centre the centre of rotation of the distal interphalangeal joint), the toe shortened (dumped), and a shoe with a rolled toe fitted to ease break-over. Suitable shoes would be wide-webbed seated out shoes, natural balanced shoes or egg-bar shoes.
2) Solar/distal phalangeal bruising This injury is most commonly associated with thin soles and shoeing strategies aim to protect the sole through the use of protective soft materials that cover the sole to a greater or less extent. Rim pads offer some protection but leave a large part of the sole open. A wide array of modern packing materials can be used to cover the sole, usually with a pad
4 www.theneaep.com that covers the entire sole. This provides excellent protection of the sole but they can, in themselves, causes solar bruising if too firm. Simple ‘corns’ (bruising of the medial heel; often caused by delayed trimming of overlong foot and reshoeing) can been treated with a short period of time unshod and foot trimming or with a shoe with the end of the medial branch of the shoe seated out on the ground surface of the shoe.
3) Sheared heels Instability of the heels results in one heel being pushed proximally compared to the other. A simple bar shoe, with trimming of the heels of the ‘higher’ heel can be effective at matching heel height and restoring stability.
Protecting tendons and ligaments Traditionally egg-bar shoes or shoes with good palmar extension have been advised to ‘protect’ the suspensory ligament (and distal sesamoidean ligaments) although the former has been associated with increased strains in the suspensory ligament5. More recently, shoes with increased width at the toe compared to the heels (see figure 1) have been suggested as being effective in soft ground to increase the load in the DDFT (by the heels sinking in more than the toe) and thereby reduce the loading in the suspensory ligament (and superficial digital flexor tendon) via the extra support provided to the fetlock by the increased tension in the DDFT. However, studies to try and show this effect have been somewhat variable5,6. Nevertheless the biomechanical principle appears plausible and this author uses this approach in hindlimbs but not forelimbs because of the worry of initiating overload of the navicular region. Asymmetric branches of the shoes have also been advised to protect the injured collateral ligament with a wider branch on the side of the injury when the horse is exercising on soft ground (see figure 1). The wider branch does not sink in as far which has the effect of tilting the foot to reduce strain in the injured collateral ligament. Again, this biomechanical principle seems sound and this author advises these shoes when a horse with a diagnosis of asymmetric desmitis of the collateral ligaments of the distal interphalangeal joint returns to work after the initial period of rest to allow the ligament to heal. The deep digital flexor tendon and soft tissues of the navicular region can also be unloaded by raising the heels, either with trimming, wedges or a graduated shoe (see above).
Managing fractures of the distal phalanx (and navicular bone and sidebone) In order to minimise movement at the fracture site, prevention of hoof expansion under weight-bearing load is minimised by using a bar shoe with multiple quarter clips. A rim shoe is more difficult to fit effectively and so supplementing the bar shoe with casting tape around the hoof capsule only should offer better immobilisation, although a large retrospective study did not identify any relationship of hoof immobilisation to outcome7.
5 www.theneaep.com Figure legend
Figure 1 – Examples of shoes for protecting loading of the suspensory ligament (left) and collateral ligament of the distal interphalangeal joint (right).
References 1. Wilson AM, McGuigan MP, Fouracre L, et al: The force and contact stress on the navicular bone during trot locomotion in sound horses and horses with navicular disease. Equine Vet J 33:159-165, 2001. 2. Eliashar E, McGuigan MP, Wilson AM: Relationship of foot conformation and force applied to the navicular bone of sound horses at the trot. Equine Vet J 36:431-435, 2004. 3. McGuigan MP, Wilson AM: The effect of bilateral palmar digital nerve analgesia on the compressive force experienced by the navicular bone in horses with navicular disease. Equine Vet J 33:166-171, 2001. 4. Lochner FK, Milne DW, Mills EJ, et al: In vivo and in vitro measurement of tendon strain in the horse. Am J Vet Res 41:1929-1937, 1980. 5. Riemersma DJ, van den Bogert AJ, Jansen MO, et al: Influence of shoeing on ground reaction forces and tendon strains in the forelimbs of ponies. Equine Vet J 28:126-132, 1996. 6. Lawson SE, Chateau H, Pourcelot P, et al: Effect of toe and heel elevation on calculated tendon strains in the horse and the influence of the proximal interphalangeal joint. J Anat 210:583- 591, 2007. 7. Rijkenhuizen AB, de Graaf K, Hak A, et al: Management and outcome of fractures of the distal phalanx: a retrospective study of 285 horses with a long term outcome in 223 cases. Vet J 192:176-182, 2012.
6 www.theneaep.com What’s Going On Back There? A Unique Look At The Back Of The Hoof By Paige Poss Eventually, every hoof care professional will face hooves that do not respond as intended to the care given to them. In these cases, digital radiographs or MRIs can be incredibly helpful. However, a deep understanding of anatomy (and experience gained from hoof and limb dissections) can also really help hoof care professionals deal with complicated and bizarre cases. There are two approaches to studying anatomy. The first is to learn the terminology, which enables a base for clear communication between professionals. The second is to learn the spatial relationship of the structures, which deepens the understanding of the mechanics of the hoof. The dissections and images presented in this paper fall into the second category. Hundreds of dissections and thousands of images have led to many interesting observations in how the capsule and soft tissues interact in the palmar aspect of the hoof.
The Caudal Hoof The constitution and placement of the structures in the back half of the hoof are fundamental to the functionality of the overall hoof capsule. This region of the hoof is designed to absorb concussive forces but does not hold up well when under constant compression as this type of force generally leads to distortion of the hoof capsule. The external structures in the palmar aspect of the hoof share a dynamic relationship to the tissues that lie beneath them. The internal soft structures provide a basic form or framework that the walls, frog, heels, bars and sole follow. Both the internal and external components function and change as a unit and failure of any one part will affect all others. The back half of the hoof is comprised exclusively of flexible structures. The most rigid structure in this region of the foot is the hoof wall, but as it is connected to the lateral cartilages in this region, it is still able to easily flex. Changes in the external structures of the caudal hoof can offer clues to the forces being applied. By learning to recognize the relationship between the internal and external structures we can gain greater insight into the distortions occurring inside the hoof. This can help practitioners determine if they are improving the health of the hoof, merely managing a problem, or actually causing harm.
A fitting visualization of this is the construction of a paper mache project using a balloon as the base. In this analogy, the balloon represents the internal structures of the hoof which are the framework that determine the shape of the outer shell. Without undue outside pressure, the two structures will equally support each other. If the paper shell gets distorted by some kind of
7 www.theneaep.com outside pressure it will impact the shape of the balloon. Likewise, if the balloon loses its form (via air leaking out), then the external structure will be weakened. While it is easy to see the changes occurring to the shell around the balloon, it is hard to tell how the internal structures are changed. Due to the diversity of the internal structures of the hoof, changes there are obviously much more complex than in the balloon analogy, but just as difficult to see. In the neonate, the hoof, coffin bone, and cartilages are symmetrical and the hoof capsule forms around the perfect structures beneath. Once the foal is born, the ground and movement quickly force changes to this ideal state and it does not take long for asymmetries and distortions to appear. The material presented here is a culmination of many simple observations. Each led to the next, and as a whole, they deepened my understanding of how the heel region works as a unit.
Tubule angles A pattern to note is the relationship between the wall tubules and the underlying laminae: the angles of both directly correspond to one another. There may not always be a perfect correlation between the laminae and wall tubules, but the pattern appears to be consistent and trustworthy. It is a way to relate the external hoof to the internal structures. Trusting this correlation helps to clarify the next layer of detail involving the collateral cartilages. (Figure 1)
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Just as with the paper mache shell, the shape and orientation of the cartilage directly determines the shape of the capsule in the back of the foot. (Figures 2 & 3) Figure 2
Figure 3
9 www.theneaep.com The heels, bars, and frog also follow the shape of the collateral cartilages and digital cushion. Knowing that the angle of the laminae and tubules mirror each other, we can assume heel shape is a reflection of the cartilage beneath it. (Figure 4) The collateral cartilages also determine the shape of the heel bulb. However, heel bulb morphology varies tremendously. Low and negative palmar angled hooves frequently appear to have elongated soft tissues verses a rounder appearance in the more upright hooves. (Figure 5) Figure 4
10 www.theneaep.com Figure 5
Palmar angle appears to play a part in heel morphology and may be a reflection of the level of compression and load on the soft tissues comprising the back of the hoof.
If the angle of the tubules matches the angle of the lateral cartilage, are we helping the tubules to stand up straighter by trimming them shorter? Or are we changing the angle by loading the cartilage differently? Looking for changes to tubule angles and shape of the heel bulb has helped me assess my own work.
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Digital Cushion Think again about the paper mache analogy. A balloon filled to capacity will be a more supportive base for the paper shell than a loosely filled balloon. Likewise, collateral cartilages that are supported by a strong, healthy digital cushion will be less likely to distort. Without proper support, cartilages will collapse inward and the heels will contract, or the heel bulbs will elongate and the heels will appear to under-run. (Figures 6 & 7) Figure 6
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Figure 7
True Heel There is an anatomical point on the lateral cartilage where the bar and wall laminae converge with the solar papillae. This is referred to as the anatomical heel or “true heel.” All of the tissues caudal to this point are either cartilage or digital cushion and are vulnerable to distortion. (Figures 8 & 9)
13 www.theneaep.com Figure 8
Figure 9
14 www.theneaep.com Hundreds of dissections led to some concern regarding the term “under-run heels.” There appears to be only slight changes in the location of the anatomical heel. It seems to be a relatively stationary point, with very little anatomical evidence that it moves toward the toe. In fact, it appears that the collateral cartilages distort caudally and pitch back, causing the heel bulb to look like it elongates. Or the opposite can occur, and the heels appear to be moving back when actually, the heel angle and bulbs are rotating forward as in the case of club feet. ( Fig. 10) Figure 10
It is common and considered appropriate to trim the heels back or to add a wedge to support the structures in the back of the foot. There may be a point where the load is brought too far back and ends up being detrimental and undermining the benefits. In extreme cases, the heel bulb itself becomes weight bearing. It appears this improper loading increases detrimental changes of the cartilages and they pitch further back. The backwards rotation of the heels would appear as a worsening of the ‘under-run’ heel.
Conclusion: The palmar aspect of the hoof is designed to disperse concussion, so it is built around flexible structures. This built-in ability to distort is how the hoof deals so effectively in its shock absorbing role. However, this also makes it more prone to pathology. Our role as hoof care providers is to ensure the appropriate balance is maintained in all the structures so that the hoof neither under-distorts and becomes too rigid, nor over-distorts and becomes too soft, as both will lead to concussive damage to the skeleton.
15 www.theneaep.com Tracking changes to the heel tubule angles and paying attention to the general heel bulb shape are two trusty landmarks to help professionals determine if the hooves are improving or deteriorating. Use this information to monitor if your favorite protocol is working and make adjustments if necessary.
Fig. 1: The growth patterns of the tubules of the hoof wall align with the underlying laminae. Fig.2: The shape of the capsule mirrors the underlying structures. Fig.3: (image on left) Here P2 has been removed and the palmar process of the coffin bone has been highlighted in blue. (image on right) This is the internal aspect of the lateral cartilage Fig. 4: An upright dissected foot (top) and a low-heeled dissected foot (bottom). The green lines represent the tubule angle of the hoof wall Fig. 5: Dissection of three feet with different heel bulb morphologies. Fig. 6: Palmar angle appears to play a part in heel morphology Fig. 7: The digital cushion is an integral component of the hoof Fig. 8: The blue circles marking the true heels. Fig. 9: The blue arrow marks the area where the lamellar and solar coria converge – the anatomical or “true heel”. Fig. 10: Is it pivoting from the true heel?
16 www.theneaep.com Trimming The Hoof Capsule To Improve Foot Structure And Its Function
Robert M. Bowker, VMD, PhD Professor Emeritus of Anatomy Michigan State University East Lansing, Michigan 48824 & Corona Vista Equine Center, LLC 4711 Martin Road Charlotte, Michigan 48813
The importance of understanding the biology of the equine hoof and foot is critical to having a healthy and sound horse during any athletic performance. Many clinicians, farriers, trimmers and the like have lectured on the horse’s foot in terms of its anatomy and physiology under both normal and pathological conditions, discussing its biomechanical and kinematic actions and responses during these conditions and those during “normal” stance and movement. Today while this lecture cannot cover all aspects of the foot during these short lecture time periods, several references below may aid people in obtaining more information in examining and understanding many of these aspects and how people have addressed their functioning in the past (1-6). With this trimming lecture I wish to present some of my own findings on how the distal phalanx changes due to our trimming practices as well as how we can trim to improve the overall health of the foot and return the horse to a sound condition for the owner. These ideas have arisen from detailed dissections and study of the distal limb from literally thousands of horses, both live and cadaveric specimens of more than thirty years. Several general points I wish to make even before we get started are as follows:
1. The foot is very adaptable and is constantly changing internally depending upon how the foot is trimmed. Its conformation is merely “a point in time” and not a permanent or fixed anatomical structured form.
2. Every time you touch the foot for trimming, rasping, shoeing, etc., you will change the foot internally -both the anatomy and physiology- as it will adapt and respond to your procedure (s) regardless how minimalist it may be. This change can be in a positive direction or a negative direction!
3. Certain parts of the foot -the palmar foot- contain special cellular elements capable of responding to hostile insults allowing the foot to recover and heal itself if given a chance to recover (i.e., rehab).
These three points are important to appreciate in understanding how and why the foot should be trimmed to address the concept of a healthy foot. It is my belief that many, if not most of the common foot conditions, are a result of our everyday trimming practices; any trimming will alter the loading and physical forces impinging upon the hoof and foot and then the foot will respond to these new loading forces and adapt to change the
17 www.theneaep.com anatomy of the foot (both bone and soft tissues). The epitome of the bad trimming practices in facilitating foot issues is navicular syndrome- our trimming practices promote or facilitate this condition! Most of the horses that I deal with have varying degrees of chronic foot lameness issues (usually grade 3 lameness or more with radiographic changes of structures within the digit and foot (distal phalanx and navicular bone), especially as they relate to navicular syndrome and laminitis. Our overall goal is to begin to allow the foot to heal so the owner can enjoy their horse when it is being ridden, i.e., get their horse back! As most anyone knows who has worked with the horse’s foot under both” normal” and pathological conditions, understanding the foot can be and usually is a very humbling journey. However, in my experience one learns the most about the anatomy, physiology and biology of the foot when the presented case is a difficult one, even if the outcome is not always positive. As you will learn very quickly the foot – especially the enclosed internal structures- is a very adaptable organ and usually will respond positively if it is “given a chance”!
This paper is not intended to be a comprehensive review of previous veterinary, farriery or trimming practices of the equine foot, but we would like to present several anatomical findings that many people often do not associate them with being “causal factors” of many if not most problems in dealing with the horse’s foot. Many of these findings are present in most examined feet, but they have not yet reached to the level of being noticed by the owner, i.e., pain? However, when a horse becomes sore or lame, one or more of these areas will potentially have more “damage” to that one area than other horses.
In this brief presentation a few conditions affecting various internal anatomical structures will be described that I have found to be very widespread within the general horse population. However, in sound horses these same conditions may not have reached the level being noticed by the horse (i.e., favoring or exhibiting lameness) or the owner (i.e., not being sufficiently observant to detect subtle behavioral or movement change in their horse). These conditions are very common and to varying degrees present in many if not most horse; but they can be corrected!
The long toed-underrun heel condition: This condition is a very common finding in most feet of horses wherever I have traveled (United States and Canada, Australia and New Zeeland, United Kingdom and Northern Europe to name a few countries) and it is mainly caused by our trimming practices: not trimming inside of the white line “periodically”. Most horses have long toes and varying degrees of having underrun heels. A wide range of the outward appearances in the form of the feet exists with this condition with some feet having minor, or barely noticeable, external changes, while others have significant changes in the external hoof. However, the internal damage could be extensive and widespread in both types of feet. On the other hand, it is rare that I see a “short-toed” healthy foot. Unfortunately, the biomechanical effects upon the foot’s tissues initiated with the gradual onset of this condition is constantly changing and these changes facilitate the deterioration of these tissues. Below are four common changes observed in the foot when the toe becomes longer, and the heels underrun: (a.) atrophy of the frog and a decrease in its functional abilities to support the horse and dissipate energy. (b) the caudal migration of the central sulcus and its frog stay and loss of functioning of the
18 www.theneaep.com palmar foot. This caudal migration can further lead to sheared heels. Although the frog stay usually is not assigned any significant function in most all veterinary textbooks, it is critical for the overall health and function of the foot. (NOTE: it’s primary role, in my opinion, is not to pump blood out of the foot.) The frog with the central sulcus should just make “light contact” with the ground surface (no pressure) with a wide shallow concavity and be closed caudally (palmarly). This conformation is commonly seen in the younger horse (i.e., 2-4-year-old horses, or less), but infrequently in older horses. When in this position the frog is functioning well: its purpose is to anchor the fascial bands allowing them to support the horse and dissipate energy (see below).When the frog migrates caudally the frog stay begins to be oriented towards the digital bones and becomes smaller internally. The fascial bundles collapse in the palmar foot. (c.) the toe of the distal phalanx begins to elongate (bone creep) through periosteal elevation dorsally and subsequent proliferation of bone under the periosteum. No increase in bone width under these conditions. (d.) The bone creep results in the entire distal phalanx to undergo remodeling as the bone grows forward in order to support the bony column and the dorsal cortex. These changes may be occurring nearly continuously if we do not trim inside of the white line. With continuous remodeling, eventually the distal phalanx will not be able to support the horse’s weight, resulting in catastrophic events during certain diseases- i.e., crushed toes in laminitis.
This condition can be corrected through beveling the wall around the solar surface of the foot as well as bringing the heels back gradually (greater solar loading) (Figure 1A-1C). The common saying below may be useful when treating this condition as most horse owners want “quick fixes”!
Good, Better, Best, Never let it rest, 'Til your good gets better and your better gets best!
St. Jerome
You can always improve the condition of the foot if you work at it frequently by rasping a little bit to permit it to adapt internally. By removing a small amount of hoof frequently, you will permit the internal foot tissues to adapt and respond without making the horse sorer than when you started. Usually for best results the veterinarian and farrier/or trimmer should try to engage the owner to help a need to shorten the toe from the solar surface by rasping inside of the white line by removing a ”little” bit of sole at the toe through the white line 2-4 times per week (1-2 swipes at most). This will bring the breakover back significantly without removing much hoof wall. Other husbandry practices (diet, overweight, metabolic state, etc.) need to be incorporated into this rehabbing protocol. Rasping from the traditional dorsal surface of the hoof will NOT be successful as you must remove so much hoof wall to have the same effect as removing a little bit from the solar surface! (NOTE: More than 100 years ago both veterinarians and farriers were on the same page as they both believed that when trimming and/or shoeing the horse “one should not touch the sole and frog under any conditions, even thrush”.)
19 www.theneaep.com (Not sure about the thrush idea, but hopefully you get my point.) Common sense and patience go a long way in successfully curing this condition (See Diagram (Figure 1 and Details will be discussed at lecture).
2. Maintain hoof balance: Many of our husbandry practices in trimming or shoeing of the foot have resulted in more horses having a longer toe and underrun heels than we would like to have. Often horses with these feet will eventually have clinical problems of periodic lameness. More recently farriers and trimmers have set a goal of 50:50 ratio of the distance from center of rotation of the second phalanx (perpendicular line to ground) to the toe and from this point to the heels. This distance has been suggested as helpful for a healthy foot; however, in most feet (long toes-underrun heels) the ratio approaches a 60:40 ratio to the toe and to the heels respectively, if you measure these distances (Figure 2). The hoof should be trimmed to change the internal structure of the foot. By trimming the hoof capsule to shorten the toe, and to promote caudal heel migration, this ratio of 50:50 can be gradually achieved; however, this ratio can be improved further to approach 40:60 ratio as the internal foot adapts and responds. Under these conditions the caudal frog and heels will become more robust and enlarge as the central sulcus returns to the solar surface of the foot. Simultaneously, the foot structures within the cuneate frog and digital cushion can structurally improve internally. Under these three different ratios of 60:40, 50:50, and 40:60, the internal structures of the foot will change from a negative direction at a 60:40 ratio and a more positive direction of 40:60 ratio (figure 3A-D). The foot is always changing whether you are aware of it or not.
A second part of hoof balance is having the foot balanced medially to laterally and vice versa. Often this shape of the foot is easy to say rather than to obtain this balance as the hoof walls are not symmetrical from the front and caudal aspects as one side may be more sloping- usually the lateral side- while the other side is more upright or steeper. More often than not, the steeper side is the medial aspect of the hoof all. Steep and flared shapes of the hoof wall are very common, and most hoof care professions have a personal preference for trying to correct this unbalanced foot (represent improper or unbalanced trimming) (1-6). Unfortunately, this imbalance alters the physical forces impinging and passing through the foot’s tissues, including both the distal phalangeal and second phalangeal bones. The hoof and foot will now try to compensate for these different loading and supporting forces upon the foot. As a result, the anatomy of the bones and the distal interphalangeal joint within the foot will change in response to these biomechanical forces. (i.e. Many have referred to the mechanisms of these loading changes as Wolff’s Law).
With regards to the distal phalanx, the bone on the flared side of the distal phalanx will be significant less dense than on the steep side of the bone from the same foot. This side of the foot is the same side of the foot where pedal osteitis occurs usually along this flared side of the bone. This work was done in nine nearly symmetrical feet on feet from horses aged 5-9 years of age. In nine specimens’ sections (1 cm tissue blocks were obtained from the dorsal cortex at the midline and on both sides of the midline beginning at the distal margin and sampling proximally.) Five blocks were obtained in each of these three strips along the dorsal cortex and examined statistically. To make matters worse, the
20 www.theneaep.com anatomy of the distal interphalangeal (DIP), or coffin, joint is not a symmetrical joint front to back, but an eccentric one; this is due in part to the enlarged tubercles on the palmar side of the second phalanx when compared to the dorsal side (Figure 4A). This joint eccentricity becomes important when the toe becomes excessively long as a “broken back” condition becomes visible, creating greater compressive pressures along the articular cartilages between the second phalanx and the navicular bone and the navicular bone and the distal phalanx (7-10). In addition, greater and even excessive tensile forces are placed upon the impar ligament. As a result of the creation of the “steep and flared” sides of the distal phalanx, the tubercles of the middle phalanx will adapt to this medial- lateral imbalance and become misshapened (Figure 4B). The tubercle becomes shaped like an “ice cream cone”: one side has a great circumference of the distal tubercle (P2) (usually the flared side of the distal phalanx) while the other steeper side of the same bone has a smaller circumference. During dorsiflexion of the DIP joint, the greater circumference creates greater tensile forces in the ipsilateral impar ligament at its attachment onto the navicular bone. The navicular bone will respond and create an outgrowth of bone along the flexor cortex of the navicular, which usually can be seen on a navicular radiographic shot through the coronet. Such a scenario may eventually result in a chip fraction on the navicular bone on this flared side of the foot bone (Figure 4C). This chip fracture is believed to create pain as chip fractures are often diagnosed as being a part of NS (4). Simultaneously, greater movement (up and down; proximal and distal) of the navicular bone occurs as the insertion attachment sites exhibit greater bone loss and enlargement of their pores.
Introduction to anatomy of the palmar foot
Before we can begin to understand these changes and how we can begin to explain their potential pathogenic processes related to the clinical signs associated with NS, we need to briefly orient you into the basic anatomy of (1) the palmar foot and (2) other more widespread pathologies associated with NS affected horses. Early anatomists described the tissues of the frog and DC as being a “modified subcutaneous tissue” (10,11). While these descriptions were more than 100 years ago, our present understanding of fascia and connective tissues is more advanced and these tissues are more complex, but also interesting in terms of rehabilitation of both humans and animals alike (12). From anatomical dissections and microscopic and histological examinations of the forelimb palmar foot for more than thirty years, I have come to believe that it is truly different than what I was taught and learned in veterinary school!!!!! The following observations, while from numerous horses, are part of a detailed study that is near its completion phase: it is from more than 20 horses under 7 years of age, including various breeds of both domestic and feral horses from different areas of the world. While the internal structures of the cuneate frog and the proximal part of the DC were observed to be remarkably consistent in terms of their overall organization of their many tissues, small variations were present, which may have been influenced by sensory input stimulation to the foot (Bowker, 2018). Many studies have examined the frog and described their contents of having dense regular and irregular connective tissues, adipocytes, and elastic fibers with scant vasculature (11,12). The very early anatomists also mentioned ligamentous cords passing through the palmar foot from the proximal digit to the frog (11), but unfortunately no further studies were performed to reveal their basic anatomy and
21 www.theneaep.com functions. All descriptions to date have indicated no or very little organized structure of these palmar foot tissues from the earliest in the late 1800’s to more recent studies (10, 11). However, we have observed that there is “logic to the madness of how the tissues of the frog and DC are organized”!! The fiber bundles passing through the frog are more like fascial sheets and bundles rather than ligaments as the former appears to be capable of transforming itself into active tissue elements that communicate with other systems via “neural-like” mechanisms and can adapt and respond the other stimuli; ligaments do not seem to be able to react to stresses in this manner (13). These fascial sheets and bands were not organized randomly, but their origins and insertions were concentrated in a few specific sites, even though there was some variation between specimens. We believe these subtle differences in the patterns are due to the foot’s reaction to external (sensory) influences during movements and foot-ground contacts. The fascial sheets formed three distinct patterns, based upon their architectures and upon their associations with an extensive microvasculature within each region of the palmar foot. The fascial and vascular relationships suggested further that each enclosed larger area (or compartment) within the frog and DC has potentially differences and purposes in their functions. In Figure 5 is a drawing from a thin (3-4 mm thick) sagittal section through the equine foot serves to orient the reader as to the structural organization within the palmar foot and the differences in the patterns of the fascial orientation. Compartment 1: The first and smallest compartment was immediately ventral to and positioned against the convex surface of the DDFT; they formed 3 to 9 parallel sheets originating from the distal most attachments of the DDFT and distal phalanx and inserted mainly on the lateral carilages. The insertions of these sheets in compartment 1 were widespread throughout the foot and proximal digit: (1) the lateral cartilages (chondropulvinale ligaments) and (2) the fibrous pad at pastern joint in association with the ligament of the Ergot, and proximal digit. The distal annular ligament (DAL) of the digit was the largest and most variable fascial sheet in this compartment 1. It functions more than just a band holding the DDFT in place, i.e., retinaculum, by seems to purposefully enhance the functioning of the entire digit. These fasciae of compartment 1 formed a “hammock” supporting the bony column during loading. Compartment 2: The second and largest compartment was ventral to the first one and occupied most of the cuneate frog. This compartment was created by the fascial sheets originating from the distal phalanx and inserting within the hypodermal layer throughout the cuneate frog and onto the frog stay. The sheets straddled and enclosed several major arterial branches, including solar branches from the circumflex artery, palmar branches of the distal phalangeal arteries and branches of the distal navicular arteries. Compartment 3: The third, and most caudal, compartment was formed between and including the lateral cartilages occupying much of digital cushion. This third compartment appeared to be structurally and functionally unique in comparison to the first two compartments as it appears to serve an alternative role in the creation of the negative pressures recorded within the foot and in supporting the load of the horse through this flexible skeleton of the frog and DC. The digital cushion that you have all palpated in anatomy laboratories and perhaps on live horses resembles a yellow “marshmallow- like” masse (tela subcutanea tori) on each side of the foot. The rest of the DC tissues consist of (1) fascial cords arising from the frog stay to pass to the bony digit, (2) large veins-capacitance veins collecting return blood from the caudal foot with fewer microvessels, (3) fascial sheets that insert upon the lateral cartilage, (4) the tela subcutanea tori -yellow “marshmallows” and
22 www.theneaep.com myxoid cells (13). The organization of these fascia were different than in the first two compartments as this third compartment did not appear to form smaller chambers with small vessels among the collagen bundles as were evident in compartment 2. Vascular pattern through the cuneate frog: In foot sections cut is different planes the vasculature to this central portion of the foot was extensive as viewed with several different anatomical methods including India ink filling of microvessels and clearing of tissues (Spalteholzte technique), confocal microscopy and immunohistochemistry. At least five different, but significant, arterial sources were identified from the India ink filled sections to directly contribute to vasculature of the frog. These vascular networks received arterial blood both directly and indirectly from the medial and lateral palmar digital arteries. Most of the vessels within the cuneate frog are 4-5 to 25 microns in diameter with virtually all of them having a layer of smooth muscle., indicating they are not capillaries (no smooth muscle). (NOTE: healthy red blood cells can easily fold themselves and conform to smaller shapes and sizes in order to negotiate through the smallest of passageways in the body.) These microvessels form an extensive interconnecting system of arterioarterial anastomoses passing to the large frog tubules and the vasculature passing between the fascial sheets of frog ventral to DDFT. The physiology of these vessels follows that of Poiseuille’s Law (Resistance to flow is inversely related to the radius raised to the fourth power). They are primarily a network of unique resistance vessels that are design to provide support of the bony column and dissipate energy simultaneously. They are “swizzle sticks” – very small tubes we use to stir our coffee cups in the morning- which ensure a mechanism to support the bony column and reduce the vibration energies of the foot. Large vessels greater than this diameter have less of a role is energy dissipation. The specific introduction to this novel organization of the equine palmar foot is because the three compartments and contents are all pathologically damaged early in the disease processes of NS before progressing to detectable pathology involving the NB (i.e., changes in the NB and the opposing surface of the DDFT. In NS affected horses the compartmental fascial sheets forming compartments 1, 2 and 3 are severely compromised structurally and functionally as the fascial sheets become edematous and fractured with a reduction to disappearance of nuclei in collagen fibers with smaller chambers being destroyed. The microvessels are often affected by being in an extreme vasoconstriction state. The microvasculature (and most likely the neural fibers) is also damaged as vessels are affected (1) physiologically as they are often in different specimens in a severe state of constriction, and (2) pathologically as many may disappear sometimes fewer immunostained vessels are labeled. These changes we believe are all due mainly to our husbandry practices, and, as a result, makes NS a man-made condition!
1. Denoix J. 1999. Functional anatomy of the equine interphalangeal joints, in Proceedings. Am Assoc Equine Pract. 45: 174–177. 2.
23 www.theneaep.com 2. Johnston C, Back W. 2006. Hoof ground interaction: when biomechanical stimuli challenge the tissues of the distal limb. Equine Vet J. 38:634–641. 3. Eliashar E. 2007. An evidence-based assessment of the biomechanical effects of the common shoeing and farriery techniques. Vet Clin N Am Equine 23:425–442. 4. Dyson, SJ. 2003. Navicular Disease and other soft tissue causes of palmar foot pain. In: Lameness in the Horse, MW Ross and SJ Dyson, WB Saunders, Philadelphia, pp.286-299. 5. Parks, A.H. 2012. Aspects of Functional Anatomy of the distal Limb. AAEP Proceedings. 58:132-137. 6. O’Grady, S.E. 2009. Guidelines for Trimming the Equine Foot: A Review. AAEP Proceedings. Vol. 55. 7. Bowker, R.M. 2003. Contrasting structural morphologies of “good” and “bad” footed horses. 49th Amer. Assoc. Eq. Pract. 49: 186-209. 8. Bowker, RM. 2012. The Concept of The Good Foot: Its Evolution and Significance in A Clinical Setting. In: Care and Rehabilitation of the equine foot. Ed. Pete Ramey, pp. 1-33. 9. Bowker, RM, Atkinson, PJ, Atkinson, TS, Haut, RC.2001. Effect of contact stress in bones of the distal interphalangeal joint on microscopic changes in articular cartilage and ligaments. Am J Vet Res. 62:414-424.
10. Bowker, R.M., K.K. Van Wulfen, S.E. Springer and K.E. Linder. 1998. Functional anatomy of the cartilage, the distal phalanx and digital cushion in the equine foot and hemodynamic flow hypothesis of energy dissipation. Amer. J. Vet. Res. 59:961-968.
11. Sisson, S. Common Integument. In: Sisson and Grossman’s The Anatomy of the Domestic Animals, Robert Getty. 5th Ed, W.B.Saunders Co., Philadelphia, 1975, pp. 728-735. 12. Nickel, R, Schummer, A, Seiferfle, E, et al. Digital joints of horse. In: The Locomotor System of the Domestic Mammals, Springer-Verlag, New York. 1986, pp197-201. 13. Stecco, C. Functional Atlas of the Human Fascial System, Churchhill Livingstone Elsevier, Philadelphia 2015, pp. 1-102. 13. Egerbacher, M, Helmreich, M, Probst, et al. 2005. Digital Cushions in Horses Comprise Coarse Connective Tissue, Myxoid Tissue, and Cartilage but Only Little Unilocular Fat Tissue Anat. Histol. Embryol. 34, 112–116.
24 www.theneaep.com 1. Figure 1: 1A: Schematic diagram showing a side view of foot. Normally we trim at the outer edge of white line (red oval)- if mark a Sharpie pen line around inner hoof wall at outer white line, and then remove much of hoof wall at 45 degrees from Sharpie line, you will be left the black Sharpie line, white line, sole and the frog. Need to bring heels back as well -can rasp to a level flush with the frog through a level of the central sulcus. Coronet should be straight line angled downward in caudal direction. Any downward curve at the heels means that central sulcus is usually not on the ground. This may take several trimming periods as the heels must become straighter. DO NOT TOUCH THE FROG. If you shoe the foot you usually will have wall edge flat around foot; the breakover will be at the front edge of the foot (red circle). If bevel the foot around foot the breakover will be at the red oval- considerably shorter foot without removing much of foot.
Figure 1B: Schematic diagram to show how to bring foot back under the horse WITHOUT making him sorer. You should probably do this is several steps over a period of 3-5 days to a week or so. Initially place the rasp flat on the sole and rasp forward until you get to the front edge of the white line and then have sharper angle to rasp much of hoof wall off between 10-2 o’clock. Best to remove a little bit frequently rather than do same amount at one time. THE INTERNAL FOOT HAS TO CHANGE TO BE SUCCESSFUL. Often the horse owner begins to have second thoughts if horse becomes sore, so “common sense” hat needs to be operational! The second or third and subsequent ones start with the rasp flat on the sole (red line and the red arrows) and then gradually get more aggressive as you can go into white line and pass through the white line (remove more of it externally than closer to the solar surface). ON THE SOLE YOU WILL BE REMOVING ONLY A FRACTION OF A MILLIMETER OF SOLE THICKNESS ) FEW SWIPES?). NEED TO BRING HEELS BACK AS WELL -IF ALREADY HAVE LOW HEELS, NEED TO MAKE TOE SHORTER WITH MORE AGRRESIVE BEVEL AT THE TOE AND LESS AT HEELS; MAY TAKE SEVERAL TRIMMING INTERVALS. THE HEELS WILL BEGIN TO BECOME ELEVATED. If you take photographs and have small mm ruler in pictures, you will be able to show the owner the changes as they occur fast- with a few days (in 3-4 days you should see observable changes with ruler as a measurement
25 www.theneaep.com guide! If you do not your trimming is not totally “correct”-i.e., have seen people bevel or round the heels off a little, hoping that would ease the foot with better ground contact. If you use ruler, you will see that the heels will stop migrating caudally and straighter, but they will return to migrating forward again!!)
26 www.theneaep.com 2. Figure 2: Sagittal section of 3 YO racing QH foot. If you drop a perpendicular line from center of rotation of P2 to the ground and measure to the tip of hoof wall, you will see that the toe is considerably longer (>60%) than that distance from the center of rotation to the heels.
3. Figure 3A-D. 3A: Photograph of LF foot showing lame horse with long toe and underrun heels. Observed the caudal curvature of the coronet indicting that the central sulcus is not on the ground but has migrated caudally towards the fetlock joint.
27 www.theneaep.com 3B: Photograph showing solar view of same foot: notice the long toe with crena at the tip; always means that toes are too long. The frog has atrophied as it is long and narrow with central sulcus open at caudal end- this means that the frog stay is undergoing changes -getting smaller and beginning to point toward digit. The heel bulbs are atrophied as well. Observe where the hoof makes contact with the ground. If have photographs with rulers in them, you will be able to follow positive changes in foot.
3C: Photograph of solar view approximately one year after started trimming this NS affected horse. Observe that frog enlarging, central sulcus moving forward and foot coming back to engulf frog (Half of pictures have ruler present.) Horse sound has been sound for 5-6 months, ridden with boots. Notice that breakover is on sole between at color transition mark seen around front of sole.
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3D: Lateral photograph of same horse; notice where breakover is and horse walking preferentially on solar surface. Observe that coronet is curved caudally so heels can still move backward to get central sulcus forward and on ground.
Figure 4A and 4B: 4A: Photographs showing distal interphalangeal joint with large palmar distal tubercle forming an eccentric joint. The pin is in the proximal ligament of the collateral sesamoidean ligament attaching to the NB. The distal tubercle is larger than the dorsal one of P2.
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4B: Photograph showing distal end of P2 with larger tubercle (usually) on steep side of foot (right) with more flared side of foot (left). This asymmetry usually appears between 2-3 years of age and is variable in its extend as appears to be related to trimming/shoeing practices, i.e., mediolateral balance.
4C: Photograph showing palmar view of NB-P3 relationship with chip fracture on flare side (left) side of foot. The flared side (left) on sole is also wider than on the right side. Observe where the impar ligament inserts onto P3 that the pores are larger than normal (should be pinpoint), indicating greater up and down movement and pulling on impar ligaments due to less support in frog.
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5. Figure 5: Schematic drawing of fascial sheets passing through frog and digital cushion. Compartment is ventral to DDFT and insert on lateral cartilage while largest compartment 2 contains blood vessels and is ventral to compartment 1. Compartment 3 contain vertical fascial cords between frog stay and digit.
31 www.theneaep.com Navicular Syndrome: Questions needing to be asked: Other Observed Pathologies? Other Treatments? Can a Horse Begin to Achieve Long Term Soundness? Robert M. Bowker, VMD, PhD Professor Emeritus of Anatomy Michigan State University & Corona Vista Equine Center 4711 Martin Road Charlotte, Michigan 48813
The Horse’s Foot: Gateway to Long Term Soundness
While we all realize that the horse’s foot is the primary organ used for navigating through its environment, it is also one of the main avenues of obtaining sensory information about the physical features of its environment during movement and stance. As the horse moves, ground surface features are detected by a wealth of various “neural sensors” that are distributed throughout the foot and lower leg and this information is transmitted up the leg to the back, hind limbs and the rest of the body and especially the nervous system. While we have previously assumed that this “nervous activity” becomes incorporated into the body’s activities for the control and mediation of different reflexes during posture or movements, we are slowly learning though that these same neural sensors can have profound effects on other body tissues, including the vasculature, fascia, other nerves and receptors, and brain(1). The motor nerves exiting the spinal cord control the proximal musculature of the horse’s limbs, providing a coordination of the flexor and extensor muscles to create smooth movements. During these same muscular contractions the sensory receptors within the muscles and associated ligaments, tendons, and fascia will also be activated by these movements to produce sensory information to be utilized in body regions: (1) the generated sensory information will affect muscles and fascia in other limbs and axial spinal cord, and (2) the activated sensory nerves are known to release various other neurotransmitters into these tissues, thereby, acting in a secondary parallel efferent or “motor” system upon these same muscles and other bodily tissues. Thus, these same movements can generate other and more widespread effects within the same limb, and in other tissues in other body areas, including fascia which can adapt and become functionally stronger. These sensory- motor feed-back mechanisms within the different tissues provide an effective method for the proximal limbs and axial skeleton to detect changes occurring elsewhere in the body thereby enabling fascial connections to adapt and respond to the developed tensions in these connective tissues. These changes may provide initial insights of how these bodily tissues can detect, change and adapt to protect themselves. How the neural systems interact with the musculature and how they interact with the fascial systems to form parallel and responsive systems during movements will remain critical to long term soundness and overall health of our horses. So we can begin to appreciate the importance of trimming the foot to ensure the foot’s effect on other areas of the horse’s body are beneficial, supportive and hopefully not cause harm.
32 www.theneaep.com Several factors needed for long term soundness: The term soundness is usually used to describe the horse of having no detectable lameness at least in the lameness scale adopted by the American Association of Equine Practitioners. Most veterinarians, farriers and trimmers usually employ this scale (0-5) to describe most lameness cases in the horse. However, from our long-term perspective, and in the present discussion of the foot, the term soundness only refers to the absence of any lameness condition and does not infer nor imply the overall state (s) of how healthy the tissues are within the horse’s foot; in its simplest case, it only means that we cannot see any evidence of lameness. We have long hypothesized that tissues within the horse’s foot can respond to various stimuli and can adapt positively to strengthen these tissues in the palmar foot. These tissues through adaptation can be sufficiently robust and healthy to prevent or “resist” the development of clinical signs and anatomical or pathological findings that are related to navicular disease or syndrome. Navicular disease or syndrome has been our long-term research interests in understanding the horse’s foot and this lameness condition. We believe that our research is beginning to show that palmar foot appears to be a critical component in the overall health of the foot; conversely in navicular syndrome (NS) affected horses, these tissues are distinctly different through long term deterioration and show widespread pathology in the foot tissues due, in part, to our poor husbandry practices. Basically, the healthier footed tissues will have beneficial changes through better husbandry practices throughout the horse’s limbs and upper body. Conversely, in NS affected horses, the deterioration of the foot’s tissues can begin to occur at a young age and will potentially have negative (or less positive) effects on the development of tissues of the more proximal limbs and upper body tissues. We believe that if one knows what is inside the foot in terms of its anatomy and how it functions and how these tissues adapt and respond positively through better husbandry (hoof and footcare), then one will also become aware that the foot has far-reaching and widespread effects upon other areas of the body and that these same body areas will in return have reciprocal effects upon the foot tissues through good to better husbandry practices, i.e., feet and teeth affect each other. However, even in horses that have very “good” and healthy foot tissues, they can become unsound via traumatic injury and abscessations, etc.; we all can appreciate the occasional (hopefully) miscue when an accident occurs! So, we are not saying that a “good footed” horse cannot become unsound or exhibit some lameness condition. This example though differentiates the conditions and tissues of the foot under different states of soundness as being healthy versus unhealthy, from our perspective as related to NS. When focusing upon the foot some of the factors or potential factors are listed below that may contribute to our goals for our horses to have long term soundness: 1. Short toes 2. Healthy (untrimmed) frog 3. Dense coffin bone 4. High vascularity to frog & solar dermis 5. Thick lateral cartilages and fascial sheets w/i frog
33 www.theneaep.com These factors or goals are what I hope to achieve when I begin to help a horse; other hoof care professionals may have additional goals that they strive to obtain when in trimming/rehabbing the foot. However, these other goals are difficult to describe in isolation; as I have mentioned already this week everything you do will affect the foot- when you begin to make changes in one area of the foot you will also cause adaptive changes in other areas. In addition, when the foot begins to go “bad” through “a lack of attention to details” on our husbandry practices, it seems that many if not everything begins to go bad, not only the internal tissues but also the external hoof wall!! What I mean is when we begin to appreciate the “long toe” in a front foot, we already have numerous things “out of whack”, including atrophic frog, increased stresses in the navicular apparatus (both bones and ligaments), a loss of bone mineral density in the distal phalanx, as well as alteration of blood flow through the foot. You could call it the “domino effect”, tipping over of one domino chip causes many other domino chips to fall over or things to go wrong in the foot! While it is difficult to describe “healthy” tissues, an alternate method of describing these goals to achieve soundness is by describing the opposite condition as these conditions are well known by many horse people as being unhealthy and usually they have already contributed to lameness when they are realized. Several factors listed below can be primary contributors to an unsound, or lame, horse: 1. Long toes (and under run heels) 2. Atrophic frog 3. Peripheral loading 4. Disruption/destruction of vascularity-frog, dermis 5. Deterioration of the palmer foot More information is known about these latter factors contributing to foot problems as they are well known by most hoof care professionals and veterinarians as being associated with several equine foot diseases. However, each does not just show up one day, but they have usually been slowly developing due to a variety of reasons over a long time period. While each one will be described briefly in their roles as contributing to a bad or unsound foot, they are rarely seen in isolation by themselves as they are usually common to feet of horses both sound and unsound. 1. Long toes (and under run heels): We have already briefly mentioned this problem. These two aspects of the foot are very commonly observed in the US and around the world, including Australia, New Zeeland and Sweden where I travel mostly, as most horses have one or both conditions. Generally, the toe angles are commonly reported to be between 45-55 degrees, or something similar. However, the longer the toe becomes, the dorsal wall has a more sloping angle (smaller angle in degrees), often being less than 50 degrees, usually closer to 44-45 degrees. The heels are often parallel the angle of the dorsal wall, but with long toes, often the heels are lying flat on the ground! This condition in the foot is due to the continued growth of the hoof wall and the forward movement of the sole. Usually two obvious causes are possibilities: (a) the reluctance of the owner to have the foot trimmed frequently enough or the hoof care professional not trimming inside of the white line. This long toe (both the dorsal wall and the sole) creates greater biomechanical stresses on the coffin and navicular bones, flexor tendon and
34 www.theneaep.com associated navicular ligaments and has been discussed by others (2-4); we have already addressed different aspects of these changes. But there are additional changes, often unseen, occurring. The distance from the frog apex to the breakover has been measured to be between 2.5 to 3.8 cm; this wide range in the distance between the toe and the frog apex will include horses with long toes, unfortunately (3,4). Further, it has often been reported that the center of the rotation (CR) of the coffin joint should be in the mid-portion of the foot, thereby, forming an isosceles triangle (two equal sides of triangle) between the toe and the heels (3,4). Thus, from a perpendicular line from the CR to the ground surface, the distance between this point to the toe and this point to the heels the heels are equal. This concept of equidistance from this CR perpendicular line to the toe and heels was pointed out to me several years ago at a meeting of hoof care professionals as being a sign of a healthy or well-trimmed foot. This concept can easily be appreciated in lateral radiographs and sagittally sectioned feet: when a perpendicular line from the CR intersects the midpoint of the foot, a 50:50 ratio occurs between the front to the midpoint and then to back of the foot. Figure 1 of a sagittal foot section is a typical example of a long toed underrun heel foot. When measured from the CR to the toe and to the heels, many if not most feet observed in the US will have this relationship of nearly 60% to 40%. This means that nearly 60% of the foot is in front of the perpendicular line from the CR, while 40% of the foot is behind this line. In these feet the frog will be atrophied, and the digital cushion will be underdeveloped internally. Feet such as these will have greater biomechanical stresses upon the navicular apparatus than those feet that have the 50:50 ratio between the heels to the CR and the CR line to the toe. In trimming the foot to encourage the palmar foot to develop, the toes must be beveled to make the toe become shorter to encourage the palmar foot to enlarge. As this happens you will notice that the coronet becomes straight throughout its entirety from the toe to the heel bulbs (lateral perspective- the angle of the coronet to the ground is not that critical in my opinion except to have the foot with a slightly downward sloping angle). When this happens, the central sulcus is on the ground flat and its caudal aspect closed – but not between the heel bulbs. In horses diagnosed as a NS affected horse with radiographic changes being evident, feet of these horses usually have a 60:40 ratio on lateral radiographs, the coronet is curved caudally, and the central sulcus is half-way to the fetlock joint as the palmar foot is underdeveloped! After several (varying between 6-15 months) months of rehabbing these horses, the ratio of the front to back parts of the foot can approach a 40:60 relationship, which means that the palmar foot is much larger than the front part of the foot (Figure 2). The central sulcus and coronet become healthier as described. We believe that this 40:60 ratio is a goal to attempt to achieve when trimming for a healthy foot. In addition, the negative changes we have already discussed with regards to the tidemarks, ligamentous deterioration changes and the decrease in bone mineral density usually does not happen with this conformation, i.e., 40% to 60% ratio. 2. Atrophic frog: The atrophic frog is a very common finding on many if not most adult horses. Usually the frog is thin from the apex to the central sulcus and the heels of the foot are contracted (2-4). In the above situation just mentioned (long toes and under run heels), the frogs are very much underdeveloped; however, many hoof care professionals assume that this type of frog is acceptable, because it is observed often in the horses regardless of their state of soundness. The atrophic frog can become a sheared heel in these patients if the central sulcus
35 www.theneaep.com appears to migrate caudally. This condition can easily be corrected with proper trimming, shortening the toes from the solar side and bringing the heels back frequently! 3. Peripheral loading: Peripheral loading of the foot usually means that the hoof wall is the primary loading structure as opposed to other parts of the foot. When a shoe is applied to the hoof wall the wall assumes 80-100% of the weight applied to the loading surface of the foot, while in the unshod condition more of the load is supported by the solar structures. Obviously, an unshod hoof that extends well beyond the solar surface will carry more of the horse’s weight than if the wall were at a level similar to that of the sole. Using finite element model of a cross- section of the front portion of the foot, loads applied to the hoof wall will result in bone being lost in the distal third of the coffin bone, while being deposited more proximally in the bone where the loading forces enter the hoof wall. In addition, though, such loading of the foot will change the supporting architecture of the inner wall, including the dermis and both cortical and trabecular bone of the distal phalanx. These findings are demonstrated through histology and measurements of the cortical bone thicknesses which show significantly less bone in the distal and lateral portions of the coffin bone. On radiographs consistent findings along the dorsal cortex can be observed with the proximal cortical bone being thicker than the distal cortical bone supporting this notion bone loss distally. These observations we believe are early indications of an “unhealthy” or “less than healthy” bone structure of the distal phalanx as it can become an early victim during a bout of laminitis as the distal phalanx cannot support the horse’s weight of the horse, resulting in its destruction when loaded, i.e., crushed bone at the toe. When the loading is preferentially on the solar surface of the foot, and not exclusively on the wall, bone is not lost using this same experimental method. The dorsal and ventral cortex of the coffin bones can be observed to be thicker than the bone tissue in peripherally loaded feet. One other aspect of this thinning the dorsal cortex is the forward migration or elongation of the distal bone due to not trimming inside of the white line, i.e., bone creep (Bowker, R.M. 2018) Usually these distal phalangeal changes – bone creep and bone loss distally are components of bone remodeling processes-will occur simultaneously. 4. Disruption of vascularity-frog, dermis: When the foot loses its ability to support itself fully and to dissipate energy, the impact vibration energies begin to overwhelm the mechanisms of “energy absorption”. These changes can be seen in a gradual loss of the vasculature and of the “gel pad” (a mixture of proteoglycans, collagen fibers, and vessels in healthy feet) (Figure 3), located ventral to the distal phalanx, commonly seen in many horses (Bowker, 2018). These changes are typical of horses (both affected by NS and chronic laminitis) suffering from “winter laminitis” when the feet are not able to thermoregulate sufficiently. As a result, the foot’s tissues begin to undergo dissolution, resulting the inability of the foot to provide enough support for itself, as well as proper thermoregulation. The deleterious changes become progressive and will lead to clinical signs associated with unsoundness. 5. Deterioration of the palmar foot: Deterioration of the palmar foot indicates that thinner lateral cartilages are present as the result of being damaged, and the fascial sheets of the frog and digital cushion have undergone fracturing and deterioration (5-7). In previous works we had shown that the palmar foot can undergo changes that are either beneficial or detrimental to the overall health of the foot (5). In NS affected horses the lateral cartilages were significantly
36 www.theneaep.com thinner than that of other horses. While we hypothesized that these NS affected horses did not have an opportunity to develop a healthier foot, we have realized that these structures in the younger horse were initially reasonably robust but through “the lack of proper husbandry”, they have already begun to deteriorate without any opportunity to recover or rebuild these tissues. These observations suggest that concussive forces and impact vibrations are overwhelming the energy absorption mechanisms in many horses, not only quantitatively with each foot fall but also temporally throughout all four seasons. Both seem to promote NS. Newer thoughts regarding Navicular Syndrome- 2019: With this gradual loss of soundness in the horse there is also a gradual emergence of lameness issues with one common on affecting the forelimb bilaterally. This condition has been called navicular disease or navicular syndrome. This lameness disease remains a scourge among horse owners as it occurs often and frequently at an early age when the horse is beginning to achieve its peak performance level. This disease is defined as a deteriorating or degenerative disease of the podotrochlear apparatus, which includes the navicular bone and its supporting ligaments as well as the adjacent deep digital flexor tendon (DDFT) (2). This affliction has been called by several different terms over the past 200 years, but the distinct localization of the affected tissues associated with the navicular apparatus has remained the same since its earliest descriptions. Unfortunately, the overall prognosis of NS generally lacks optimism, even with many of the current treatment regimes, as usually the pathological changes of the disease and the associated lameness condition progress to a more severe and chronic state, preventing the continued successful performance of the horse. The pathogenesis of NS has been discussed many times with two major ideas being accepted as most likely, and perhaps related, causes of the chronic lameness disease: (1) circulatory issues and (2) excessive mechanical forces (2-4). (1) Circulatory issues: While most researchers believe that some sort of ischemic process or disturbance involving the navicular bone and its ligaments, the specific sites of vascular damage are only just now being examined (2). (2) High mechanical loading: The increased mechanical loading of the palmar foot or increased mechanical pressure of the DDFT against the navicular bone are believed to the causes for the structural changes in the NB (2). While other ideas have been mentioned they have received lukewarm support by most investigations. Each of these two former ideas has some value in their theories of the pathogenic processes. However, neither one can fully explain the pathogenic findings that have been described clinically nor the negative results in experimental studies of partial to complete occlusion of the digital arteries. While previous studies focused on the podotrochlear apparatus as the initial or primary site for the pathogenesis for NS, we believe that the podotrochlear apparatus represents only a terminal or “tip of the iceberg”, site rather than the initial site where the pathological injuries begin to occur. The “tip of the iceberg” refers to our way of thinking about NS in that research has focused upon damage only being related to the podotrochlear region and to adjacent tissues (the suspensory ligaments, NB and DDFT) and its tissue elements primarily the vasculature. More than 200 hundred years ago damage to the NB and DDFT were seen to be associated with this specific site during necropsies, resulting in its identification, but this time period was prior radiographic or microscopic examinations were present in most veterinary colleges. However, regarding the “iceberg tip”, the Titanic, and NS comparisons, it was the ice below the ocean surface that did the
37 www.theneaep.com major damage to the seaworthiness of the ship, causing the demise of this unsinkable ship!! We believe that the damage to this area and tissues represents the terminal end stage(s) of the actual disease rather than the initial sites of pathology within the foot. Our laboratory has discovered early, but significant, damage occurring to other foot tissues besides the navicular apparatus prior to the appearance of any clinical signs of lameness. This damage within the cuneate frog and overlying digital cushion and their microvasculature can be seen in horses as young as three-year- old racehorses and in other horses, even 5-8 years prior to the onset of clinical signs of lameness suffering from NS signs. The damage to these tissues becomes progressively worse with continued work as their demise reduces the support of the distal limb and the inability to dissipate the impact vibrational energies during movements. This initially damaged area results in the breakdown of the protection provided by the cuneate frog and microvasculature of the podotrochlear apparatus during loading of the distal limb. Such a breakdown in the foot’s protection as a support cushion of the podotrochlear apparatus and the dissipation of the impact energies through this central foot zone results in progressively greater vibrational energies negatively affecting the mechanical impact zone upon the NB, DDFT and surrounding ligaments of the podotrochlear apparatus. This hypothesized pathogenic mechanism produces significant initial damage at a more distant site in the cuneate frog and once this site is destroyed and the protective mechanisms removed, there is continuous and progressive damage to the NB and the DDFT through loading of these tissues through the bony column (6-9). Before we can begin to understand our observations and how we believe we can begin to explain the potential pathogenic processes related to the clinical signs associated with NS, we need to briefly present our findings on (1) the palmar foot and (2) other more widespread pathologies associated with NS affected horses. In a current study of the anatomical dissections and histological examinations of the forelimb palmar foot of more than 20 horses under 7 years of age, the internal structures of the cuneate frog part of the DC and the proximal part of the DC were observed to be remarkably consistent in terms of their overall organization of the fascial or ligamentous cords and sheets coursing through the palmar foot. These fiber bundles were not organized randomly nor were their origins and insertions restricted to only a few specific sites, suggesting that the external environment may have had sensorial input to their formation and organization. The fascial sheets formed three distinct patterns, based upon their architectures and upon their associations with an extensive microvasculature within each region of the palmar foot. The fascial and vascular relationships differed in each compartment, suggesting that each enclosed larger area (or compartment) has potentially differences and purposes in their functions. In Figure 4 is shows macroscopically all compartments as seen grossly in a thin (3-4 mm thick) sagittal section through the equine foot (healthy foot) serves to orient the reader as to the structural organization of the frog and digital cushion within the palmar foot and their differences. Compartment 1: The first and smallest compartment was immediately ventral to the convex surface of the DDFT and was formed by 3 to 9 parallel sheets originating from the distal most attachments of the DDFT. The insertions of these sheets in compartment one were widespread throughout the foot and proximal digit: (1) to the lateral cartilages (chondropulvinale ligaments). (2) to the fibrous pad at pastern joint in association with the ligament of the Ergot, and (3) to other fascial and myofascial expansions in the proximal digit. (4) The distal annular ligament (DAL) of the digit formed highly variable structure at different insertions, indicating that it must have more function than merely a fibrous retinaculum, similar to that of humans (13).
38 www.theneaep.com Compartment 2: The second and largest compartment was ventral to the first one and occupied most of the cuneate frog. This compartment was created by the fascial sheets associated arising from the distal phalanx and inserting within the hypodermal layer throughout the cuneate frog and adjacent to the frog stay. Smaller zones, or chambers, within this compartment 2 varied with the relative number of fascial sheets. The sheets straddled and enclosed several major arterial branches, including solar branches from the circumflex artery, palmar branches of the distal phalangeal arteries and branches of the distal navicular arteries (11,12). Compartment 3: The third, and most caudal, compartment was formed between, but including the lateral cartilages, and occupying much of digital cushion. This third compartment appeared to be structurally and functionally unique in comparison to the first two compartments as appears to serve an alternative role in the creation of the negative pressures recorded within the foot, as well as providing structural support within the palmar foot. The fascial sheets did not appear to form smaller chambers with small vessels among the collagen bundles as were evident in compartment 2 with most microvessels being within the lateral cartilages. However, the tela subcutanea tori is the soft fluctuant mass most think of when they palpate the DC of the horse. Each side of compartment 3 has a small mass, being about the size of a marshmallow, that contains fascia, milieu of hyaluronic acid and myxoid cell clusters (Bowker, R.M., 2019). Vascular pattern through the cuneate frog: In foot sections cut is different planes the vasculature to this central portion of the foot was extensive as viewed with several different anatomical methods including India ink filling of microvessels and clearing of tissues (Spalteholtz technique), confocal microscopy and immunohistochemistry. At least five different, but significant, arterial sources were identified from the India ink filled sections to directly contribute to vasculature of the frog. These vascular networks received arterial blood both directly and indirectly from the medial and lateral palmar digital arteries (11,12). In NS affected horses the compartmental fascial sheets forming compartments 1 -3 are severely damaged as the small walled chambers are destroyed. The microvasculature is also damaged as vessels are affected (1) physiologically as they are often in a severe state of constriction through the presumptive impact vibrations, and (2) pathologically as many to most disappear. These changes are due mainly to our husbandry practices, and as a result, this means that NS is a man- made condition! Our view of NS, which differs from most people, is that it is an entire foot problem, rather than a problem (s) specifically affecting or related to the podotrochlear apparatus. Our view is that, as most areas of the foot are subjected to the environmental stresses, these tissues within the foot will adapt and remodel on a cellular level to these stresses either positively or negatively. Within the foot the frog and digital cushion are specially designed and best suited to adapt and respond to these environmental stresses: (1) they have components for dissipating energy and for providing support, but also (2) tissue elements for recuperating and rebuilding the tissues in this area of the foot. The components of energy dissipation and support have been the main focus of our lecture series in dealing with the fascial sheets and bundles of the three compartments within the frog and digital cushion. However, embedded within the fascia, microvasculature and the internal milieu of hyaluronic acid within this region are myxoid cells. These cells can facilitate
39 www.theneaep.com the regrowth and /or regeneration of many of the fascial and vascular tissues within this region of the frog and digital cushion (Bowker, RM. 2018). The myxoidal cells are associated with the growth and regeneration of several connective tissues, including adipose, fibrous and fibrocartilage (13). However, these myxoidal cells are not present in the dermis of the dorsal hoof wall nor are they present within the dermis ventral to the distal phalangeal bone (Bowker, RM. 2018). As a result, it is important to realize that these myxoidal cells within the frog and digital cushion are potentially capable, and are best suited, of providing these palmar foot tissues with an opportunity to recover from many, or perhaps most, damaging insults. Thus far, the trimming protocol, like what we have described in these lectures, may be one important ingredient in a recipe for promoting “the best possible environment” the frog and digital cushion to heal and recover during rehabilitation! On the other hand, the dermal tissues associated with the dorsal hoof wall and that located ventral to the distal phalanx may only have similar “normal and general healing” properties and capabilities of dermal tissues located elsewhere in the body, which may be through the formation of scar tissue. These two possibilities for the horse’s foot do provide a “ray of hope” in helping these horses recover from NS and needs further research study.
1. Dyson, SJ. 2003. Navicular Disease and other soft tissue causes of palmar foot pain. In: Lameness in the Horse, MW Ross and SJ Dyson, WB Saunders, Philadelphia, pp.286-299. 2. Parks, A.H. 2012. Aspects of Functional Anatomy of the distal Limb. AAEP Proceedings. 58:132-137. 3. O’Grady, S.E. 2009. Guidelines for Trimming the Equine Foot: A Review. Vol. 55. 4. Bowker, R.M., K.K. Van Wulfen, S.E. Springer and K.E. Linder. 1998. Functional anatomy of the cartilage, the distal phalanx and digital cushion in the equine foot and hemodynamic flow hypothesis of energy dissipation. Amer. J. Vet. Res. 59:961-968. 5. Bowker, R.M. 2003. Contrasting structural morphologies of “good” and “bad” footed horses. 49th Amer. Assoc. Eq. Pract. 49: 186-209. 6. Bowker, RM. The Concept of The Good Foot: Its Evolution and Significance in A Clinical Setting. In: Care and Rehabilitation of the equine foot. Ed. Pete Ramey, 2012, pp. 1-33.
7. Bowker, RM, Atkinson, PJ, Atkinson, TS, Haut, RC Effect of contact stress in bones of the distal interphalangeal joint on microscopic changes in articular cartilage and ligaments. Am J Vet Res. 2001; 62:414-424.
8. Van Wulfen, KK and Bowker, RM. 2002. Microanatomic characteristics of the insertion of the distal sesamoidean impar ligament and the deep digital flexor tendon on the distal phalanx in healthy feet obtained from horses. Amer. J. Vet. Res. 63:215-221.
9. Van Wulfen, KK and Bowker, RM. 2002. Evaluation of tachykinins and their receptors to determine the sensory innervation in the dorsal hoof wall and insertion of the distal sesamoidean
40 www.theneaep.com impar ligament and deep digital flexor tendon on the distal phalanx in healthy feet of horses. Amer. J. Vet. Res. 63:222-228.
10. Sisson, S. Common Integument. In: Sisson and Grossman’s The Anatomy of the Domestic Animals, Robert Getty. 5th Ed, W.B.Saunders Co., Philadelphia, 1975, pp. 728-735. 11. Nickel, R, Schummer, A, Seiferfle, E, et al. Digital joints of horses, In: The Locomotor System of the Domestic Mammals, Springer-Verlag, New York. 1986, pp197-201. 12.Egerbacher, M, Helmreich, M, Probst, et al. 2005. Digital Cushions in Horses Comprise Coarse Connective Tissue, Myxoid Tissue, and Cartilage but Only Little Unilocular Fat Tissue Anat. Histol. Embryol. 34, 112–116. 13. Stecco, C. Functional Atlas of the Human Fascial System, Churchill Livingstone Elsevier, Philadelphia 2015, pp. 1-102. Figure Legends: Figure 1: Sagittal section from 3YO racing QH, showing the long toe and the approximate ratio of 60:40 with more of the foot in front of a perpendicular line from P2.
Figure 2: Solar view of NS affected that has been trimmed as described in the first lecture. The frog is wider than when first started rehabbing foot. The horse is now sound and active again.
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Figure 3: Gel pad present in dermis ventral to coffin bone in healthy feet. The pad is created by boiling feet for 10-12 hours and carefully removing bones with hoof. You are left with a “cooked mixture” of proteoglycans, fibrous tissue and vessels. In healthy foot this gel pad is 4-5 mm thick AFTER everything has been precipitated and “cooked”. In NS and laminitic horse this same structure is less than 1 mm thick (i.e., thin a sheet of paper) with scant proteins and only fibrous tissue and vascular remnants.
Figure 4: Section of foot showing 3 compartments in healthy foot. Compare to NS affected horses in previous lectures.
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43 www.theneaep.com Maybe It’s a Nerve By Paige Poss
The dissection images included in this photographic lecture have had a significant impact on my understanding as a hoof care professional.
This lecture is a photo documentary showing how primary nerves descend through the soft tissue structures of the caudal aspect of the hoof. Viewing or understanding the structural aspect gives rise to questions about current approaches in hoof care to address caudal foot pain in every facet and discipline.
This unique view will demonstrate why horses occasionally have adverse reactions to certain approaches of trimming or implementation of differing hoof care packages.
Introduction: Caudal foot pain is a well-known and widespread problem within the horse industry. Often, horses that present with lameness caused by apparent pain in the caudal aspect of the hoof undergo a wide array of tests and treatment options – in many cases with no clear improvement or positive outcome. To navigate the potential causes of that pain and the different therapeutic strategies, it is important to look within the palmar part of the foot. For me, it has proven helpful to explore the anatomical structures through dissections.
The dissection described here represents the most detailed and exhaustive description of key neural structures within the hoof capsule reported to date. The images are clear and carefully presented so that the viewer, with more insight, can draw their own conclusions. Further dissections of hooves would shed light on the impact of nerve placement. One specimen cannot answer if the nerve placement is common or normal.
Here, dissection of a lower limb cadaver of the front reveals critical anatomical information that provides insight into potential sources of observable anomalies or pain. There is no specific history on this specimen, but I am confident that is likely from a Thoroughbred. Based on my experience, the shoeing application and level of hoof care suggest it was possibly from a working Fox Hunter or 3-Day eventer. Horses of this description are common from the source of this specimen.
By tracking the proper palmar digital nerve as it descends through the soft tissue structures of the caudal aspect of the hoof, it reveals many interesting details.
The palmar digital nerve, as well as the rest of the neurovascular bundle, descends medially and laterally down the distal limb and into the hoof capsule. This dissection carefully follows the bundle and documents the spatial placement of each structure. At the peak of the lateral cartilage, the proper palmar digital vein splits superficially into the coronal vein and superficial ungular plexus. The proper palmar digital nerve and artery descends beneath the proximal attachment of the digital cushion and the peak of the lateral cartilage. (Figure 1). This observation is consistent with many previous dissections and suggests a possibility that this placement is significant. Could this lead to the occasional case of nerve impingement in this region of the foot? At this time there is no data to support this, and is purely conjecture given the organization and structure of neural tissue in the hoof capsule. However, let’s consider what occurs functionally for these tissues.
Changing the load to the soft tissues in the caudal aspect of the hoof causes the proximal edge of the collateral cartilages to lift and expand. It is easy to manipulate the limb in dissected hooves and explore
44 www.theneaep.com this phenomenon. If expansion is easily accomplished in this area of the cartilages, could a contraction or restriction occur when there is improper load? Could the proximal edge of the lateral cartilage curl inward and down if the frog and digital cushion descend downward? Would this possibly cause pain?
Following the nerve as it descends behind the peak of the lateral cartilage, it clearly branches. (Figure 2). In this specimen, the bifurcation aligns with the bottom edge of the coronary groove near the end of the palmar process.
Using the scalpel to make a sagittal cut of the cartilage, we can track the palmar digital nerve as it branches further within the ungular cartilage. In Figure 2 you can see a main branch of the nerve, while Figure 3 shows it branching within the cartilage.
Close observation revealed tendrils of nerve embedded within the body of the ungular cartilage (Figure 3). This was an unexpected detail and could possibly explain some cases of mysterious caudal heel pain. Common imaging methods would probably not uncover this level of detail and so it is not be surprising that as a source of pain, this would be difficult to diagnose (and treat).
Following the nerve deeper into the hoof, there was yet another branch of the nerve behind the distal edge of the cartilage. (Figure 4). This nerve branch/process was tucked into a groove created by cartilage and the deep digital flexor tendon and was thinly covered with solar or bar lamellar coria (data not shown).
It is clearly visible that the ramus is passing between the deep digital flexor tendon and the digital cushion. This segment of nerve seems particularly vulnerable to the morphology of the bar. Placing the dissected hoof into the hoof capsule emphasizes the location of the exposed nerve and its’ relationship to the internal aspect of the bar commissure (Figure 5). Would increasing pressure to this region of the foot result in pain? Could this explain why therapeutic packing, pads, or a variety of caudal support applications cause horses to sometimes complain?
These preliminary anatomical observations offer a plethora of follow up questions regarding diffuse caudal foot pain in horses and the therapeutic approaches for these conditions. For example, with different therapeutic hoof care packages in mind:
• Would excess pressure on the cartilages or concussive forces cause pain? • Would the volume and consistency of the digital cushion help alleviate excess pressure on the collateral cartilages? • Could there be a link with the integrity of the internal bar tissues, involving unspecified heel pain? • Could supporting the back of the hoof by adding pressure to the frog with packing, pads or various shoes or hoof protection help further relieve pressure and/or pain?
Clearly, more analysis is needed to answer questions about the relevance of digital cushion volume and consistency in conjunction with caudal foot pain. Does the condition of the digital cushion and collateral cartilages make them key or even supporting factors for specific treatment plans? Based on this, and many other dissections, while the architecture and innervation of the hoof may vary individually, it seems clear that factors impacting these structures could result in non-specific lameness.
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Figure 1: A general overview of the dissected caudal portion of the foot.
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Figure 2: The palmar digital nerve branches behind the lateral cartilage.
Figure 3: Unaltered photograph of the nerve and its tendrils (left panel). Altered image of the same nerve bundle enhanced to clarify the location of the tendrils connected to the cartilage (right panel).
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Figure. 4: Caudal part of the dissected foot with the digital cushion removed
Figure 5: Replacing the dissected foot into the hoof capsule emphasizes the location of the exposed nerve in the hoof capsule.
48 www.theneaep.com New developments in our understanding of what causes different forms of laminitis
Andrew van Eps BVSc PhD DACVIM University of Pennsylvania, School of Veterinary Medicine, New Bolton Center Kennett Square, PA, 19382
We use the term laminitis to describe the clinical and pathological consequences of disturbances in the attachment between inner hoof wall and distal phalanx that is normally provided by the digital lamellae. Importantly, the lamellae normally act to suspend the bone within the hoof capsule and it is the largely unrecoverable loss of this suspensory function that leads to the lameness, dysfunction and morphological derangements characteristic of chronic laminitis. Pathologic alterations in the lamellae can be mild and insidious, with slow and progressive lengthening of lamellae due to stretch and cellular proliferation (as in many cases of endocrine- associated laminitis) or may be characterized by rapid loss of tissue mechanical integrity due to widespread cellular adhesion and cytoskeletal failure (more common in sepsis-associated and supporting limb laminitis). Once the suspensory function of the lamellae is lost, the pain, morphological derangement and progression of digital pathology are largely consequences of novel mechanical forces now acting between the distal phalanx, sole and ground surface, together with the proliferative and dysplastic response of the lamellar epidermis to injury. These chronic processes are common regardless of the inciting cause. Over the last decade however, researchers have recognized that there are key differences (and some similarities) in the initial events that lead to laminitis depending on the inciting cause. A focus on these early events is leading to a better understanding of why laminitis occurs in different clinical situations and is helping to identify therapeutic targets.
Are there common pathways to lamellar dysfunction? In all 3 types of laminitis (sepsis-associated, supporting-limb laminitis [SLL] and endocrinopathic laminitis), the lamellar epithelial cell is central to the events that lead to lamellar failure. In each case lamellar failure is caused by a combination of: 1. Loss of the normal cell shape (stretching) of the lamellar epithelial cells and 2. Failure of epithelial cell adhesions (both between cells, and to the dermis via the basement membrane). Endocrinopathic laminitis is dominated by cell stretch with less evidence of adhesion loss, whereas sepsis-associated laminitis and SLL is dominated by adhesion loss. Cell stretching/loss of shape is caused by disruption of the cytoskeleton, and adhesion loss is due to disruption of hemidesmosome/desmosome dynamics. These events could occur as a result of either aberrant cellular signaling or a lack of cellular energy to maintain the dynamic cytoskeletal components and adhesions. The unique environment of the lamellar epithelium means that the cells are normally subjected to profound mechanical stresses and therefore even minor events affecting regulation of the cytoskeleton and/or adhesion complexes could rapidly escalate and cause loss of mechanical integrity. Disruption of energy supply as a cause of epithelial cell adhesion loss/stretch could occur as a result of perfusion failure (ischemia) or could be associated with more subtle tissue energy dysregulation/imbalances. Traditionally ischemia was hypothesized to play a central role in all types of laminitis, however to date there is only evidence for ischemia playing a role in SLL.
49 www.theneaep.com There is preliminary evidence of subtle oxidative energy failure in sepsis-associated laminitis (see below) and lamellar energy balance has not yet been evaluated during endocrinopathic laminitis development. Since maintenance of epithelial cell cytoskeleton and adhesion complexes involves dynamic processes, aberrant cellular signaling may be involved in disrupting the normal balance and triggering laminitis. There is evidence emerging (from the Belknap laboratory at OSU in particular) that lamellar signaling in models of all 3 types of laminitis converge at the level of the mTOR signaling pathway, which plays a central role in cellular growth and homeostasis. The mTOR signaling pathway regulates epithelial-mesenchymal transition (EMT) which is important is many disease processes and dysfunction of mTOR signaling is implicated in an increasing number of conditions including cancer and diabetes. Since cytoskeletal rearrangement and cell adhesion dissolution are initial events EMT (and laminitis), aberrant mTOR signaling may be responsible for lamellar structural failure by causing disruption of these same cellular processes in lamellar epithelial. Furthermore, the role of mTORC1 as a metabolic sensor and regulator of cellular energy metabolism may be critical in laminitis pathophysiology, underlined by preliminary data demonstrating perturbations of energy metabolism in models of the SRL and SLL forms of laminitis.
Sepsis-associated laminitis Laminitis occurs as a consequence of a range of conditions in horses where systemic inflammation is a feature; particularly when this inflammation is driven by bacteria or bacterial products liberated into the bloodstream (sepsis). Gram negative sepsis and endotoxaemia accompany metritis, pneumonia and colitis/enteritis in horses and these conditions are most often complicated by the development of acute laminitis. Experimental alimentary carbohydrate overload models traditionally used to study laminitis feature clinical signs that are characteristic of sepsis and studies have confirmed the presence of endotoxin in the blood and a systemic inflammatory response with these models. It is not surprising that endotoxin, usually of gastrointestinal origin, is an important trigger of sepsis in horses considering their exquisite sensitivity to it, but interestingly investigators have not been able to induce laminitis with experimental infusion of endotoxin alone. Nevertheless, the presence of clinical signs of endotoxaemia/sepsis is an established risk factor for the development of laminitis in hospitalised horses. Sepsis is a malignant systemic inflammatory process triggered by bacteria and their products (including endotoxin) in the blood with a resultant cascade of haemodynamic alterations, coagulopathy and metabolic alterations. In most species including humans, the development of organ failure (“multiple organ dysfunction syndrome” [MODS]), most commonly affecting the lungs, liver and kidneys, has a major effect on survival in cases of sepsis/SIRS. Laminitis appears to be a form of end organ dysfunction/failure that is ultimately most important in terms of recovery for the adult horse with sepsis. The pathophysiology of organ dysfunction in sepsis (and sepsis associated laminitis) is still poorly understood. Efforts to determine the mechanisms that lead to sepsis-associated laminitis have mirrored those in human MODS research, with the investigation of circulatory derangements, local inflammatory processes, apoptosis and non- ischaemic derangement of cellular energy metabolism receiving the most attention. Although there is some evidence of microvascular dysfunction in MODS and laminitis there is no evidence of true ischaemia. The central role of inflammation in the pathogenesis of acute laminitis has been highlighted experimentally, with endothelial activation, cytokine and chemokine upregulation, and leukocyte emigration into the lamellar tissue occurring early during the
50 www.theneaep.com development of experimentally induced laminitis. There is little evidence that apoptosis or oxidative damage play a primary role in laminitis development. Since the lamellae have a unique mechanical role, the lamellar basal epithelial cell adhesions and the integrity of the extracellular matrix have received special research attention, however recent evidence suggests that enzymatic degradation of extracellular matrix components by e.g. matrix metalloproteinase (MMP) enzymes appear to play only a secondary role. There is evidence of non-ischaemic energy failure (mitochondrial dysfunction) in models of human sepsis that is thought to play a role in MODS, but there is debate over whether this may represent a downregulation of cellular metabolic pathways that is actually protective in tissues during sepsis. Similar disruption of energy metabolism in sepsis-induced laminitis has not been definitively documented in the early developmental period, however preliminary results from a study in the author’s laboratory suggest that there is dysregulation/failure of oxidative energy metabolism in the late developmental/early acute phase of experimentally-induced sepsis-associated laminitis: this may contribute to the failure of lamellar epidermal basal cells to maintain their critical intercellular and cell-matrix adhesions. Although insulin dysregulation may be a feature of sepsis in horses, it is clear from experimental models that laminitis develops in the absence of clinically significant hyperinsulinaemia. There is evidence that mTORC1 growth factor signaling is upregulated in experimental sepsis-associated laminitis – in this case through IL6 activation. These pathways are consistently blocked by hypothermia experimentally, which also ameliorates the laminitis lesion.
Endocrinopathic laminitis Endocrinopathic laminitis encompasses laminitis associated with obesity, insulin dysregulation, pasture-associated laminitis, equine metabolic syndrome (EMS), pituitary pars intermedia dysfunction (PPID) or glucocorticoid administration. This type of laminitis appears to be the most common worldwide. Recent research has shown that prolonged hyperinsulinaemia can induce laminitis in healthy ponies and horses. In contrast to sepsis-associated laminitis, lamellar inflammation does not appear to be a major feature and evidence of systemic or gastrointestinal inflammation is not apparent in models or natural disease. The histological changes seen in the lamellae are dominated by epithelial cell stretch rather than adhesion failure, and as the pathology progresses there is increased mitotic activity and cellular proliferation. Current evidence suggests that overstimulation of the growth factor receptor IGF-1R by excess insulin is responsible for triggering a proliferative response in lamellar epidermal cells which involves disruption of normal cell adhesions. Interestingly, excessive activity of the same growth factor receptor, IGF1R, is a major cause of epithelial-mesenchymal transition (EMT) in epithelial cancers and this is mediated through mTORC1. It is therefore likely that the cytoskeletal and adhesion dysregulation of endocrinopathic laminitis is due to mTORC1 activation occurring though activation of IGF1R by excessive insulin. The contribution of cellular energy failure through interference with perfusion, glucose uptake or metabolic pathways has not been specifically studied to date but appears unlikely on current evidence. The concentrations of insulin in blood (and therefore tissue) vary widely in naturally occurring endocrinopathies and peak in association with soluble carbohydrate ingestion in particular. Episodes of hypersinulinemia in natural cases are also much less profound and more transient compared to those achieved in the protocol of insulin infusion used to induce laminitis experimentally. Transient hyperinsulinemic insults in natural cases are likely to contribute to the insidious and sometimes subclinical disease course of laminitis in many endocrinopathic cases.
51 www.theneaep.com More severe and profound hyperinsulinemia upon exposure to carbohydrate-rich pasture for instance can still result in more severe acute laminitis in prone horses through these mechanisms.
Supporting-limb laminitis Supporting limb laminitis (SLL) remains a primary limiting factor to long-term treatment success in horses with painful limb conditions including fractures. The clinical onset of SLL is unpredictable and once clinically apparent it tends to be rapidly progressive. The incidence has been estimated at approximately 10-15% of horses that present for painful limb problems (or require limb casts) in North American studies, with bodyweight and duration of casting identified as risk factors. Although the overall incidence in the general population appears to be low, the impact of SLL lies in the fact that treatment of complicated orthopedic conditions is often avoided in favor of euthanasia due to the risk of SLL, even if the primary injury could be managed effectively. Furthermore, severe lameness in the primary injured limb may mask the clinical signs (lameness) of SLL: subclinical laminitis pathology in the contralateral limb is perhaps not uncommon and it is difficult to determine how this may ultimately affect recovery and return to athletic activity in horses that are treated successfully for their primary condition. Mechanical and vascular mechanisms have been considered as potential contributors to the pathophysiology of SLL, but there is very little published evidence.
Mechanical factors It is well accepted that in the standing horse, the body mass is divided between the fore and hind limbs approximately in a 60:40 ratio; therefore a single forelimb is subjected to vertical ground reaction forces equivalent to approximately 0.3 x bwt in a square stance. Peak ground reaction forces on a single limb increase to be equivalent to greater than 0.5 x bwt at the walk, 1.2 x bwt at the trot, and up to 3 x bwt at the gallop and therefore it seems unlikely that compensatory load redistribution in the standing horse could exceed the mechanical tensile strength of the lamellae. However, consistent increases in load (even if modest) could potentially trigger lamellar epidermal remodelling: there is existing evidence that such remodelling occurs in response to mechanical stresses associated with normal locomotion and this has important implications for the pathophysiology of SLL.
Perfusion and energy balance There is growing evidence that cyclic limb loading is critical for normal lamellar perfusion and that perfusion deficits and negative energy balance contribute to the development of SLL. Maintenance of lamellar epithelial adhesions required to withstand immense mechanical stress is an energy consuming process; therefore glucose consumption by the digit is relatively high and uptake is non-insulin dependent (GLUT-1 transporter mediated) in the lamellae. There is no means for local glycogen storage therefore uptake must be matched by constant delivery via the blood. Despite this, the normal lamellar dermis (responsible for nutrient and oxygen delivery to the lamellar epithelial cells) is relatively poorly perfused and is relatively hypoxic. Glucose deprivation in vitro causes disruption of lamellar epithelial adhesion and cytoskeletal dynamics and loss of lamellar structural integrity. Imaging studies have shown that limb load affects digital perfusion and microdialysis studies demonstrate that lamellar perfusion and energy balance are dependent on limb load cycling (weight shifting/walking). A recent study using a preferential weight-bearing model demonstrated increases in lamellar hypoxia-inducible factor
52 www.theneaep.com 1α (HIF-1α) concentration in the supporting limb lamellae in the absence of changes in inflammatory signaling, supporting a role for ischemia in the development of supporting limb laminitis and studies using this model are ongoing.
Other factors The contribution of other factors such as systemic inflammation and endocrine dysregulation (implicated in other forms of laminitis) to the development of SLL remains unclear; however, many SLL cases in clinical practice are complicated by infection and presumably suffer at least transient periods of ID during treatment for their primary injury and this warrants further study.
What is the way forward? Recent research is helping to clarify the relationship between limb loading patterns, lamellar perfusion/energy balance and signaling events at the level of the lamellar epithelial cell that lead to laminitis. Simple monitoring techniques focused on tracking limb load cycling in patients with painful limb conditions, coupled with powerful new methods of monitoring perfusion and metabolic function within the foot (microdialysis, PET scanning) will guide interventions in horses at risk of SLL. These interventions may be simple physical therapy strategies such as controlled walking/static limb load cycling, or may be focused on partial and intermittent limb load relief.
53 www.theneaep.com Hoof Capsule Trimming To Improve The Internal Foot Of Navicular Syndrome Affected Horses
Robert M. Bowker, VMD, PhD Professor Emeritus of Anatomy Michigan State University East Lansing, Michigan 48824 & Corona Vista Equine Center, LLC 4711 Martin Road Charlotte, Michigan 48813
Navicular Syndrome (NS) affecting a beloved horse has been the scourge of any horse owner, as well as veterinarians, farriers and trimmers alike for the past 100 plus years as the devastating effects of chronic lameness in these performing horses has been overwhelming and taken its toll! Clinically, this chronic shifting forelimb lameness condition usually includes shorter forefoot strides with off and on lameness along with positive hoof tester responses when pressure is applied across the frog and hoof wall. Usually the horse becomes significantly better with desensitization of the palmar digital nerves and/or of the coffin joint and navicular bursa (1). Radiographic changes affecting the navicular bone with lucent areas along the distal edge and medullary cavity of the bone being present, as well as other changes in the proximal and distal suspensory ligament changes of the navicular bone, are also prominent. This wide range of antemortem changes are often consistent among horses and have been usually been confirmed at necropsy. While the actual causes of NS and the biomechanical theories are still open to some speculation, generally we have focused our attention on the pressure of the DDFT against the navicular bone (1). With that in mind we have usually followed this diagnosis with the routine treatment of raising the heels with some form of pad between the foot and shoe.
What is the usual or perhaps a more classical description of pathology associated with NS? Generally, most of the previously published reports have dealt with the more advanced findings in the NB, DDFT and associated suspensory ligaments of the NB. On a sagittal cut through the center of the foot, there are several pathological findings that support making such a diagnosis (Figure 1). These findings include the adhesion between the flexor cortex of the NB and the DDFT and fibrillation changes along the interior surface of the DDFT, etc. In the radiographs there are also detectable bony changes along the flexor cortex of NB consistent with the clinical history and diagnosis. Often the radiographic changes along the NB are used for a more definitive diagnosis of NS (1). However, there are both radiographic and histological changes at the DSIL insertion site on the facies flexoria of the distal phalanx (2). Many of these changes associated with the NB have been described or alluded to previously as they were among the initially described changes (1-3). What else do we see when we look at these radiographs? Anything beyond the NB? Question: if we see certain changes that are constantly present on the radiographs or during necropsy of NS affected horses or in many horses that are sufficiently lame in palmar foot to euthanize but without radiographic changes, could they also be a part of this same disease process we call NS? How effective is the localization of the painful sites that we use with routine nerve blocks on the distal limb? Are there other findings beyond the navicular apparatus that may indicate a more widespread effects of this disease process? One
54 www.theneaep.com area may include the external surface of the DDFT of many NS affected horses: one can often see some irregularities in the surface features, which represent changes in the integrity of the tissues (Figure 1). If this area was a site of painful sensation, a palmar digital nerve block at the coronet or at the distal digit may desensitize this region, but one could not be certain of the specific regional localization. In higher power photographs of “normal” horses one can see that the DDFT has many of the small India ink filled vessels penetrating through the thickness of the DDFT except at the fibrocartilage (Figure 2A). (Proximal and distal to the fibrocartilage one can see many of the microvessels penetrations (Figure 2B), which are mainly for nutritional purposes as well maintenance of the tendon’s integrity. If we compare the macroscopic sections of the fresh sagittal cuts of a NS affected horses and the sections prepared with the Spalteholtz technique following India ink perfusion (Figure 2B, 2C), we can see that much of the tendinopathy overlaps with the distribution of the small microvasculature (Figure 1).
Another change associated with the navicular apparatus in NS that has been overlooked has been the anatomy and its changes associated with the distal sesamoidean impar ligament (DSIL) (2). The DSIL inserts on the facies flexoria of the distal phalanx and on the distal edge of the navicular bone. This proximal and distal suspensory apparatus of the NB are important for changing the direction of the DDFT forces as it subtends the NB to insert on the distal phalanx. While it is important to be aware of biomechanical loading of the limb and the direction of the forces (5-9), how the foot is trimmed determines the extent of the generated forces on these structures. In biomechanical experiments (9) (Figure 3, graph), using cadaveric specimens pressure sensitive film was placed between the corresponding joints between the middle phalanx and the navicular bone and the navicular bone and the distal phalanx (Figure 4, top panel for orientation). A small load (approximately 1330 N for 200 msec- approximating the normal loading of limb) was applied to the limb to simulate loading of limb in straight digital bone alignment, normal stance with slight angle of pastern joints, and in dorsiflexed position (broken back pastern axis). Significant loading stresses between the navicular bone and distal phalanx and navicular bone and middle phalanx were present as seen in the graph (9) (Figure 3). There were also significantly greater biomechanical stresses, i.e., greater compressive and shearing forces, generated within the articular cartilages of all four joint surfaces (between the middle phalanx and NB, and between the NB and P3), when the limb was in a broken back pastern axis position (9) (Figure 5 A). Histologically, these changes were observed in the articular cartilage of these same bones. In Figure 5A the tissue sections were staining with safranin O stain for showing the relative extent of the red proteoglycans in articular cartilage of a young horse (left panel). Red coloration shows the extent of the articular cartilage (red color) over lying the calcified bone (blue) of the NB. On the right panel through the articular cartilage, the non- calcified articular cartilage has much proteoglycans while the part of the articular cartilage directly overlying the bone has calcium (Ca) in it as it fuses with the blue bone (Right side of panel). Tidemarks (t) are thought to be produced within the articular cartilage when significant shearing forces occur, i.e., two joint surfaces slide over each other as opposed to “normal” compression (9). Increased tidemark staining was present between these two joints, but not between the middle and distal phalanges, indicating high shearing stresses between these two joints. In Figure 5B the three panels two navicular affected horse show varying degrees of proteoglycan loss in the articular cartilage (i.e., loss of red coloration) and a gradual increase in tidemarks (tidemark duplication) (right two panels). Also notice that more and more red stain (proteoglycans) is lost from cartilage. The middle panel from NS affected horse had up to 12-18 tidemarks (middle panel) while in the right panel multiple tidemarks were present in this NS
55 www.theneaep.com affected horse and were considerably more numerous than a sound horse. This “tidemark duplication” occurs when the joint cartilage is NOT able to withstand the applied forces and to support the loads applied the bones. As a result, the joint cartilage is replaced by calcium deposits, to “strengthen itself”, but the cartilage gradually loses its ability to support and dissipate impact energies, i.e., loss of proteoglycans and thus water in the cartilage. The joints where this happens in humans become severely arthritic and painful joints when 4-5 tidemarks are found on histology (9). With the broken back pastern axis and its association with long toes and under run heels in horses, the articular cartilage of these joints undergoes significant degeneration with the loss of proteoglycans. In NS affected horses, greater tidemark duplication was evident in those horses diagnosed with NS than other horses between the ages of 2-31 years of ages (2, 9). It has been a consistent finding in NS affected horses as compared to other horses between the age of 2 -31 years of age (9). However, while it is known that severely, painful arthritic joints are associated with high tidemark numbers in people, in horses we do not know as when the coffin joint is injected with local anesthetic, the anesthetic would desensitize everything exposed to the joint surfaces as well as surrounding coffin joint tissues, and then gradually defuse to other synovial cavities.
Similarly, at the insertions of the DSIL into the P3 bone, there are changes in the insertions of the DSIL and DDFT (Figure 4, middle and bottom panels). We have observed considerable degeneration of the DSIL and the dorsal half of the DDFT in horses affected with NS (2, 9-11). In a group of horses, greater proteoglycan staining of the collagen cells was indicative of high stresses at the DSIL insertion and extensive bone remodeling in P3 with the formation of large bony pores at the insertion sites of DSIL and DDFT on the facies flexoria of the distal phalanx. The enlarged pores are due to greater instability and movement of the navicular apparatus as well as bone loss in the distal phalanx at that site (2). These microscopic changes are due to the eccentric joint and the long toe creating the broken back pastern axis (See first lecture photograph). All changes associated with the NB, DDFT and the DSIL are common observations in horses diagnosed with NS.
In retrospective evaluations these above changes can be identified as being evident much earlier in the clinical history than we initially thought. In detailed macroscopic examinations and supported by histological findings, other foot tissues, including the cuneate frog, lateral cartilages and distal phalanx can been seen to have degenerative changes much earlier than those that become evident in the navicular apparatus with radiological methods. We believe that these other changes represent early, but progressive, evidence of “navicular pathology” that would eventually engulf the navicular apparatus. With better understanding of these early pathologic changes in foot tissues, initiating rehabilitating methods earlier in the foot may improve much of its internal structures and reverse the tissue deterioration so often reported in this disease. See the figures below showing pathology in other areas besides the podotrochlear apparatus (Figures 6- 8):
By removing a small amount of hoof frequently (See diagram in the first lecture), you will permit the internal foot tissues to adapt and respond without making the horse sorer than when you started. Usually for best results the veterinarian and farrier/or trimmer should try to engage the owner to help a need to shorten the toe from the solar surface by rasping inside of the white line by removing a ”little” bit of sole at the toe through the white line 2-4 times per week (1-2 swipes at most). Other husbandry practices (diet, overweight, metabolic state, etc.) needs to be
56 www.theneaep.com incorporated into this rehabbing protocol. Rasping from the traditional dorsal surface of the hoof will NOT be successful! (NOTE: More than 100 years ago both veterinarians and farriers were on the same page as they both believed that when trimming and/or shoeing the horse “one should not touch the sole and frog under any conditions, even thrush”.) Common sense and patience go a long way in successfully curing this condition (See Diagram and Details in the first lecture).
1. Dyson, SJ. 2003. Navicular Disease and other soft tissue causes of palmar foot pain. In: Lameness in the Horse, MW Ross and SJ Dyson, WB Saunders, Philadelphia, pp.286-299.
2. Bowker, RM. 2003. Contrasting structural morphologies of “good” and “bad” footed horses. 49th Amer. Assoc. Eq. Pract. 49: 186-209.
3. Rijkenhuizen,A, Nemeth, F., Dik, K, et al. 1989. The arterial supply of the navicular bone in adult horses with navicular disease. Eq Vet J. 418.
4. Denoix J. 1999. Functional anatomy of the equine interphalangeal joints, in Proceedings. Am Assoc Equine Pract. 45: 174–177. 2. 5. Johnston, C, Back, W. 2006. Hoof ground interaction: when biomechanical stimuli challenge the tissues of the distal limb. Equine Vet J. 38:634–641. 6. Eliashar E. 2007. An evidence-based assessment of the biomechanical effects of the common shoeing and farriery techniques. Vet Clin N Am Equine 23:425–442. 7. Parks, A.H. 2012. Aspects of Functional Anatomy of the distal Limb. AAEP Proceedings. 58:132-137. 8. O’Grady, S.E. 2009. Guidelines for Trimming the Equine Foot: A Review. AAEP Proceedings. Vol. 55. 9. Bowker, RM, Atkinson,PJ, Atkinson, TS, Haut, RC Effect of contact stress in bones of the distal interphalangeal joint on microscopic changes in articular cartilage and ligaments. Am J Vet Res. 2001; 62:414-424
10. Van Wulfen, KK and Bowker, RM. 2002. Microanatomic characteristics of the insertion of the distal sesamoidean impar ligament and the deep digital flexor tendon on the distal phalanx in healthy feet obtained from horses. Amer. J. Vet. Res. 63:215-221.
11. Van Wulfen, KK and Bowker, RM. 2002. Evaluation of tachykinins and their receptors to determine the sensory innervation in the dorsal hoof wall and insertion of the distal sesamoidean impar ligament and deep digital flexor tendon on the distal phalanx in healthy feet of horses. Amer. J. Vet. Res. 63:222-228.
57 www.theneaep.com Figure Legend: Figure 1: Sagittal section through the foot showing commonly reported pathology associated with NS. The navicular bone has adhesions between the it and the DDFT as well as tendon pathology on the surface associated with the flexor cortex of the NB and its ventral surface of DDFT. The DSIL has degenerative changes with microscopic finding associated with increased proteoglycan staining. However, degenerative (pathological) changes occur throughout the horse’s foot. Most reports do not mention these degenerative changes associated with the fascial sheets coursing through the frog, edema collection along the hypodermis of the frog. The degenerative changes include reduction and loss of tenocyte nuclei, collagen degeneration etc. visible in most of these cases.
58 www.theneaep.com Figure legend 2: 2A: In feet perfused with India ink and then the tissue was cleared to visualize the vasculature, the India ink filled vessels can be seen along the superficial surface of the DDFT. In figure 2B the filled vessels form an extensive penetration zone along the DDFT except at the fibrocartilage plate in the DDFT. In Figure 2C, compare pathological zone of the NS affected horse (2C) with the India ink filled vasculature seen in 2A and in 2B. These two areas overlap showing where the pathology is located and where the microvessels are located.
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Figure Legend 3: Graph showing stresses between (1) middle phalanx and NB and the NB and distal phalanx when in broken back position (0 degrees), normal stance (15 degrees) and straight digit (30 degrees). Stresses are highest during broken back position between the P2-navicular bone and P3 and the navicular bone (left side of graph). No increased stresses were evident between P2-P3 as there were not an increase in tidemarks.
60 www.theneaep.com Figure Legend 4: Sections showing the anatomy in sagittal section of impar ligament and DDFT (Top) along with NB and distal phalanx (Top panel). Middle section: In histological section is the interface between the P3 bone (upper left) and the impar ligament inserting into the bone (DSIL) (lower right) of normal horse. The transition between the calcified bone and the non- calcified DSIL is called a tidemark (light blue line) and marks the zone of biomechanical stress in ligaments. With the impar ligament inserting into bone, it becomes biomechanically stressed with high loading forces and movements of NB; this biomechanical stress causes many collagen fibrocytes of the ligament to produce more proteoglycans to strengthen itself. This produced proteoglycan stains a red color when the tissues are prepared histologically. When ligament has “normal” degree of activity in terms of some stress, the DSIL fibrocytes may or may not be activated to produce more “strength producing proteins” within the ligament (no stained cells), or they may have a few stained cells with safranin O for proteoglycan (slight increase in cellular staining). In this section “normal” horses had no or a few stained cells for proteoglycans, meaning that little morphological changes were evident in the ligament or in the adjacent bone at the insertion site onto P3. These normal horses included active racehorses (i.e., died at the track), pleasure horses, and older (20-26 years), but active, horses. In more than 30 cases of the “normal” horses, the staining ranged from no staining to slight staining of fibrocytes in impar ligament. All stained cells were present along the insertion, but they all were within 1 mm of coffin bone. In bottom two sections (A and B) of two NS affected horses, intense proteoglycan staining was observed throughout the much of the length of the impar ligament (> 5-9 mm) between the coffin bone insertion and the origin attachment on the NB, indicating highly stressed collagen fibers biomechanically. In addition, when the DSIL is biomechanically stressed with increased proteoglycan production, the insertion side becomes very porous which become larger in size and bone loss becomes significant such that NS affected horses have a third less bone in the coffin bone than other horses.
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Figure 5: 5A: Safranin O stain of the navicular bone and distal phalanx showing proteoglycan staining and tidemarks. In the left panel from “normal” horse the red proteoglycan staining of the cartilage (no calcium). In the right panel a higher power view showing the red staining of the articular cartilage, tidemark (t) and the calcified (Ca) part of cartilage next to the bone.
62 www.theneaep.com Figure 5B: Sections show NS affected horses with loss of proteoglycan (less red stain) and progressive increase in tidemarks. See text for details.
Figure 6: Lame horse (15-16 YO) shod with heart bar shoe. While NB is not as yet involved pathologically, the compartments 1-3 show degenerative signs with fractures of fascial sheets, disruption of hypodermal layer along frog epidermis (hemorrhage, thinning hypodermal layer, fracture of fascia), irregularities in external surface of DDFT ( edematous, degeneration of Distal annular lig of digit), and vascular changes in front of frog. No changes are evident in DSIL.
63 www.theneaep.com Figure 7: Teenage horse shod in egg bar shoes was clinically lame and showing fracturing of fascial sheets, edema and disruption of hypodermal layer, all three compartments fascia severely compromised; NB has thinning of flexor cortex; no adhesion or damage to DDFT opposite flexor cortex. Vasculature passing through DDFT insertion disrupted (edema, hemorrhage), thickened DAL of Digit proximally to its attachment to SDFT. Radiographs negative on navicular bone.
Figure 8: 13 YO QH clinically lame with NS; All 3 compartments compromised with fascia ruptured, DAL of digit thickened and edematous to proximal attachment of SDFT. Small erosion on flexor cortex (Not evident radiographically, insurance case), hypodermis disrupted, edematous, fascial sheets thickened (positive adaptation), but rupture sheets, vasculature ventral to DDFT damaged.
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Figure 9: 20 YO Morgan sound; Thinning flexor cortex, thinning in couple places of hypodermis. Fascial bands intact as well as vasculature through DDFT. Impar ligament and NB- not remarkable, few enlarged vessels prior to entering lateral cartilage (no apparent pathological changes). Figure 9A: Higher power showing more clearly individual compartments 1-3 and the relative intactness of the fascial sheets. The NB and the distal annular ligament of the digit is not remarkable although the DAL of digit is adapted to become functionally as it inserts on the superficial digital flexor tendon.
65 www.theneaep.com Evidence-based Approaches To Treatment And Prevention Of Laminitis Andrew van Eps BVSc PhD DACVIM University of Pennsylvania, School of Veterinary Medicine, New Bolton Center Kennett Square, PA, 19382
Laminitis pathology is largely irreversible, therefore efforts should be focused on prevention and early intervention in acute cases. We now recognize that there are important differences in the mechanisms that lead to laminitis depending on the inciting cause: sepsis-associated, endocrinopathic or supporting limb laminitis, with the preventative/therapeutic strategies and priorities being different for each.
Sepsis-associated laminitis Conditions associated with a high risk of laminitis development include colitis, enteritis, complicated gastrointestinal obstructions, metritis, pneumonia and alimentary carbohydrate overload. Therapeutic efforts to control the primary disease including intravenous fluids for circulatory support, binding of circulating endotoxin (polymixin B and hyperimmune plasma), and NSAIDs to control downstream inflammation are reasonable treatment strategies particularly in cases of gut-derived sepsis. Prophylactic continuous cooling of the feet has been demonstrated in several experimental studies and one clinical study of naturally occurring colitis to be protective. Any horse that is at immediate risk of developing acute laminitis is an appropriate candidate for the application of digital hypothermia and there is experimental evidence of a therapeutic effect even in the acute sepsis-associated laminitis. Continuous cooling of all four feet until after the abatement of clinical signs/clinical laboratory evidence of sepsis is generally recommended, which may be several days in some cases. Based on experimental data, digital hypothermia should be aimed at achieving hoof wall surface temperatures that are (at least) consistently below 10˚C, and it appears that cooling from the mid-cannon region distally (including the hoof and sole) is required to effectively cool incoming arterial blood as well as prevent heat transfer from the environment to the lamellae via the hoof itself.
Endocrinopathic laminitis The key to prevention of endocrinopathic laminitis is early identification of horses at risk. Testing for evidence of insulin dysregulation (including insulin resistance as well as the propensity for post-prandial hyperinsulinemia) using insulin testing pre and post oral sugar challenge is the most effective way to identify horses and ponies at risk of laminitis development early. Management to reduce the laminitis risk in these cases can then include a combination of dietary control, pasture access management, weight loss and exercise, which can dramatically reduce the risk of laminitis development or progression. Cases that have a profound
66 www.theneaep.com hyperinsulinemic response to oral sugar ingestion may benefit from medications such as metformin that blunt this insulin response. Since the systemic effects of metformin on insulin sensitivity appear inconsistent, the use of targeted administration (prior to meal/turnout) appears most effective and rational in order to reduce postprandial hyperinsulinemia in these cases. Testing for pituitary pars intermedia dysfunction (PPID) in appropriately aged horses (at least >5 years) can help to identify this condition before the development of irreversible laminitis pathology. It is important to recognize that although laminitis may be the only important clinical manifestation of PPID in some horses, the recognition of clinical signs of laminitis (lameness) often only occurs after the development of irreversible laminitis pathology, which can be insidious and gradual. When treating PPID with pergolide, dosage adjustment guided by frequent monitoring of ACTH is required for adequate control and these cases may benefit from additional medication to help control insulin dysregulation. It is impossible to adequately control chronic laminitis in cases where there is inadequate control of an underlying endocrinopathy.
Supporting-limb laminitis It appears that cyclic loading and unloading of the feet plays an essential role in maintaining normal lamellar microvascular perfusion. The key to SLL prevention is therefore likely to be the development of strategies to monitor and then regulate limb load cycling frequency in the supporting limb of patients at-risk. Monitoring should include some form of serial assessment of limb load cycling activity: a method that can detect both walking steps as well as more subtle weight shifting events requires development and validation. In horses at risk, regular encouragement to walk may be beneficial; however, there is insufficient data to support specific recommendations at this stage, and the logistics of this intervention may depend on the nature and severity of the primary condition. Strategies to reduce load on the supporting limb may include partial (and preferably dynamic) sling support. Careful attention to analgesia for the primary condition will help to normalise limb weight distribution and cycling frequency, however medications with a sedative effect may be best avoided. Although sedation may help to encourage recumbency, it also reduces voluntary exercise and limb load cycling in stabled patients and therefore may be contraindicated in these cases.
Management of acute laminitis Common treatment principles for acute laminitis regardless of the inciting cause include 1. Aggressive treatment of the underlying condition (including insulin dysregulation) 2. Minimization of further lamellar damage 3. Provision of analgesia 4. Monitoring of progression Strategies to minimize ongoing lamellar damage include: 1. Anti-inflammatory therapy
67 www.theneaep.com 2. Confinement and restriction of locomotor activity 3. Mechanical foot support 4. Digital hypothermia The influence of mechanical distraction on outcome cannot be overemphasized in acute cases. Restriction of ambulation is paramount and horses should be confined to a stall and encouraged to lie down by providing deep comfortable bedding. Tranquillizers and sedatives may encourage recumbency and reduce voluntary ambulation in horses with acute laminitis. Further minimization of distractive forces can be achieved by redistribution of load from the hoof wall onto the frog/caudal sole and facilitation of breakover using conservative trimming, orthotic support material and/or bedding material (e.g. sand). Continuous digital hypothermia is the only therapy that has been demonstrated to alter the progression of the acute laminitis lesion. There is also new evidence demonstrating a preventative effect in the hyperinsulinemic clamp model of endocrinopathic laminitis. This provides rationale for the use of hypothermia as a first aid measure in cases of endocrinopathic laminitis as well as sepsis-associated laminitis.
68 www.theneaep.com Trimming Practices Can Encourage Decline In Overall Foot Health Robert M. Bowker, VMD, PhD Professor Emeritus of Anatomy Michigan State University East Lansing, Michigan 48824 & Corona Vista Equine Center, LLC 4711 Martin Road Charlotte, Michigan 48813
Different trimming practices of the hoof capsule vary considerably from one hoof professional to another, but usually they prefer the hoof wall to be rasped near the external surface of the white line or near the mid to outer thickness of the hoof wall surface. Such trimming or shoeing practices will affect the frog and the sole internally to promote the gradual decline of the entire foot’s internal structures. (NOTE: I changed the wording of the previous sentence just before press time from “may” to “will” as it is paramount that we change our thinking processes about trimming and shoeing and our husbandry practices!) Such practices usually result in the more obvious external changes of the foot (elongation of the toe and under run heels), and an under development or atrophy of the frog. However, the internal foot structures will also undergo some major renovation with ALL tissues responding to these hoof wall changes- an elongation of the foot at the toe and underrunning of the tissues. However, these internal changes are much more drastic and catastrophic to the functioning of the foot as opposed to the mere change in shape of the hoof wall. For example, while the front portion of the distal phalanx migrates forward, the vasculature also migrates forward as does the supporting architecture of the front part of the bone, as well as of the remainder of the entire coffin bone. With regards to the vasculature, some same volume of blood previously passing to the foot must now supply a greater tissue area of the front part of the foot, but at a greater distance, which usually will result in less than beneficial advantages. The architecture of the entire distal phalanx must also change to support the biomechanical changes that the foot is undergoing. The basic structure and internal architecture of the entire foot becomes modified through this “lack of attention to details” in the trimming and hoof care of the foot! In the first talk I only mentioned several changes but did not go into any detail as we focused on several other aspects of this and other conformational topics. Now I wish to demonstrate what happens and why I believe that the development of the long toe is one issue that marks the rapid decline of the foot. Several obvious changes occur when the toe is not kept sufficiently short: (a.) frog atrophy with caudal migration of the central sulcus and frog stay, (b.) the toe of the bony distal phalanx begins to migrate forward as the tip of the distal phalanx elongates (bone creep). No increase in bone width under these conditions. (c.) This toe creep encourages the entire distal phalanx to undergo an extensive remodeling process as everything will move forward within the bone. Distal phalangeal bone creep:
69 www.theneaep.com At the toe as the hoof wall grows longer and longer, the movement of the hoof wall at the toe will “pull” the periosteum from the bone; this elevation permits changes to promote a subsequent proliferation of bone under the periosteum. On radiographs this elevation is commonly seen as “slipper toe” or bone proliferation at the toe. This new bone proliferation will extend a small distance proximally depending upon the elevation distance along the distal phalanx. Over a period of several months (4-6 months) this new bone growth of a few millimeters appears to become a permanent part of the tip of the distal phalanx as the “slipper toe” appears to disappear. However, the “slipper toe” becomes incorporated into the new growth at the coffin bone. Evidence supporting this conclusion is based on measuring the distance from the semilunar line to the tip of P3 young 3-year-old QH and comparing this distance to the same distance in older Quarter Horses. In the 35 3-year- old QH, this measurement had a mean distance of 31.9 +/- 2.4 mm, while in older QH up to nearly 20 years old with the same sized foot (N=10 to date; the widths were superimposable), there was a progressive increase, but variable, distance in the older QH, extending up to 48 mm, but the distance was always greater than in these 3 Y0 QH. This difference in measurement ranged between 1-2 mm up to 15-16 mm differences in this group of specimens. In Sweden we are observing the same findings in 2-5-year-old Standardbreds as they had a similar distance between the semilunar line and the P3 tip when they were 2-3 years of age. This distance increased by approximately 3-7 mm as the horses got older between 3 years and 5 years of age (age range (2-5 years) of the 18 distal phalangeal bones examined). Other features of the distal phalanx also migrated forward, including the depression for the attachment of the collateral ligament of the DIP joint (Note: examine figures). In addition, various measurements obtained to date are consistent with this idea that the distal phalanx undergoes extensive remodeling due to the trimming practices resulting in the toe becoming elongated. In these young specimens the site of loading of the middle phalanx onto the navicular bone and distal phalanx also shifts a few mm forward while the widest part of the distal phalanx migrates from the ends of the palmar processes to the level of the depression of the collateral ligament (the exact measurements are in process of being completed). We hypothesize that this elongation of the coffin bones between the semilunar line and the P3 tip is due to not trimming inside of the white line periodically on the hoof wall to maintain a shorter toe. In Standardbreds in Sweden we hypothesize further that this elongation may occur sooner than in the QH as a common trimming practice with Standardbreds is to promote elongation early to minimize the gait changes during races. Further study and examination of the bones are still in progress. Previous works (1,2) have indicated that the differences in bone architecture is related to the individual horse’s innate conformation and is stationary. These initial observations suggest otherwise that the internal tissues are very dynamic and continuously changing due to loading patterns, husbandry practices, etc. Such a possibility suggests that may need to re-evaluate our husbandry practices. 1. Sisson, S. Common Integument. In: Sisson and Grossman’s The Anatomy of the Domestic Animals, Robert Getty. 5th Ed, W.B.Saunders Co., Philadelphia, 1975, pp. 728-735. 2. Nickel, R, Schummer, A, Seiferfle, E, et al. Digital joints of horses, In: The Locomotor System of the Domestic Mammals, Springer-Verlag, New York. 1986, pp197-201.
70 www.theneaep.com Figure 1: Figure of two distal phalanges of 3 YO QH (left) and 15 YO QH (right). Observe that the angle of the dorsal cortex is steeper in the left coffin bone as opposed to the older bone- there is a 9-degree difference between these two bones. Other observed differences in the younger bones (3 YO) in comparison to the older bones (4-22 YO) were a progressive forward migration of the depression of the collateral ligaments of the coffin joint attach, the changes in bone remodeling around the vascular foramina and the palmar processes and degree of porosity of the distal phalanx.
71 www.theneaep.com A Practical Approach to a Therapeutic Shoeing Prescription By Stuart Muir NZCEF, CJF, DIPWCF, APF Resident Farrier at Rood and Riddle Equine Hospital, Lexington, Kentuck The simple act of shoeing a horse can be a very straightforward process when the horse is sound and performing well. Unfortunately, when lameness enters the equation, shoeing prescriptions can escalate quickly. Identification of pathology or diseases can make a shoeing prescription challenging. Diagnostics in relation to Farriery can streamline the process of getting horses to return to their particular discipline faster. Ensuring that the shoeing prescription doesn’t contradict itself is an important aspect of more pathology based, complex shoeing. Complex cases can encourage Farriers to think out side the box, and it may also make certain traditional approaches either not feasible, or sustainable over time. It can be important to break the shoeing process down into logical steps to ensure the shoeing is well thought out, and therefore functional. Limb conformation can greatly affect the forces that are dissipated onto the distal limb. It can be useful to approach each limb as an individual case to maximize both the horses and Farriers chances of success. The loading affects of limb conformation, can often be seen when hoof care providers start interpreting the hoof capsule health, contour, and shape. Hoof capsules that are showing signs of being over loaded in certain areas can be a normal response from proximal limb alignment. Horses that have deviations in the bone column will direct greater forces, caused through static and dynamic loading to different quadrants of the hoof capsule, than a horse with more ideal conformation. The ground reaction force in relation to dissipating weight from locomotion can often be indicated by hoof capsule health, function and form. Deviations in limb conformation can often be undesirable, and the affect on internal structure needs to be appreciated. Gait assessment prior to shoeing can offer the practitioners valuable insight to any current lameness, and help to identify how the horse is travelling in relation to limb alignment. Static and dynamic assessments of conformation coupled with external examination can help the provider to assess the effectiveness of the horses current hoof care prescription. External forces can be the cause of heel distortions, or other distortions that create compression or leverage within the hoof capsule. These may also affect the function of the shock-absorbing structures in the foot. Often, if the horse has pathology or hoof distortion, the origin of lameness may manifest in relation to loading force. Externally, this can be seen in terms of quarter cracks, flares, and a steeper vertical wall structure. Vertical deviation of structure is generally an indication of the quadrant of the hoof capsule that is dissipating the most significant amount of load.
72 www.theneaep.com Heel structure, which is in a distorted position, can be one of the first indications that the hoof capsule is not managing load adequately. When the hoof capsule is migrating dorsally, the hoof care provider could consider the use of artificial break-over principles like rocker toes or shoes that have mechanics already artificially manufactured into them. Differing geographical locations will present different distortions to the hoof care provider. Humidity and high saturation levels can leave a horses wall structure more pliable under load, in contrast, dry desert like condition may leave a hoof capsule in a dry contracted state. This element of the shoeing equation is a consideration for the sport horse that may travel thousands of miles during the show season. Often being pragmatic in your approach to hoof- care can allow the farrier to offset some of these changes with an alteration in trimming style or shoe selection. A thorough examination of the external structures can help identify any areas of soreness or inflammation in the distal limb prior to shoeing. Taking the time to make a full evaluation of the structure and health can pay dividends when lameness is identified. Hoof testers can be used to manually palpate areas of interest. This simple approach can be used to evaluate how pliable the structures are, and also assess how much hoof mass the horse has. Horses with shallow vertical depth of foot can be difficult to trim. Depending on the approach, sole and wall integrity can be lost through excessive rasping in an effort to bring the toe back into a “normal” parameter. Hoof mass is a key component of a healthy hoof capsule. While the concept of hoof capsule balance is widely known in professional circles, ensuring the horse has enough hoof mass is just as important. The horses ability to dissipate energy before it transfers to the coffin bone is one of the most basic functions of the hoof capsule. In cases where a horse is suffering from a lack of sole mass, often the solar corium can be affected to the point where it isn’t capable of excreting the horn needed to recuperate. Using a pragmatic approach to hoof care can be one of the quickest routes to rehabilitation when hoof health has been challenged. The use of graduated shoes, or wedging of the hoof capsule, can over time be detrimental to the overall health of the foot without correct caudel support. When hoof care providers offer the horse instant palmar angle relief through wedging, the caudal region of the foot can be put under further stress with centre of pressure changes. Heel position and wall health is an important element to consider when putting together a shoeing prescription. When a horses hoof capsule is showing signs of being overloaded, the hoof care provider might consider that the internal structures that lay in close proximity are also compromised. Within a physiological range, compression and stimulation can be normal and very healthy. Stimulation of structures through compression is a part of the developmental process in equine limbs. However, when the forces exceed the structures capability, failure can
73 www.theneaep.com happen. The functionality of the internal structures ability to generate new healthy growth can often be the determining factor in the horses ability to recover from distortion-based lameness. Managing internal pathology can be as challenging as managing external hoof capsule distortion. Managing pathology can be a dynamic situation as pathology can be progressive in nature. Depending on the lameness, forces applied to the hoof capsule through shoeing may change with the movement of the centre of pressure. This is often seen when altering the hoof capsule angle with the use of graduated or wedge shoes. Elevating the hoof capsule higher off the ground can ultimately challenge the central aspect of the foot. Disengagement of the central aspect of the foot can overload the peripheral structures further. Ideally the trimmed frog would mirror the sensitive frog shape and form. For horses that are showing signs of the solar region being overloaded, shoe selection can benefit the horse greatly. Stock dimension can reduce the strain from proximal related force or load alone. The void created by the dimension of stock coupled with the disengagement of the frog can also cease the stimulation of the structures that lay proximal to that particular region. Reducing the amount of distance between the foot and ground surface can help engage the caudel and central structures of the hoof capsule. Traditionally, the hoof capsules solar region was thought to be unable to take any significant weight caused through load bearing. Historically, solar support was generally offered through bar shoes and plastic or leather pads. While this may be true for chronically thin-soled horses, other foot types can do well with the assistance of load sharing solar support. Horses that have poor wall and sole quality may need the added benefit of incorporating other structures into a load sharing capacity. Solar support comes in numerous options and can be used in varying ways. The introduction of modern materials in the Farrier market can offer numerous approaches to aid the central aspect of the hoof capsule. A shoeing prescription can be vastly enhanced with the introduction of passive topical treatments. The management of external diseases of the hoof capsule can be important to the overall health of the hoof. Depending on environment and location of the horse, topical solutions and shoeing can play a pivotal role in successful management. Identification of the infection and tissue affected is an important element to consider. The effectiveness of passive treatment on dermal and epidermal structures can vary. Caustic burning may be possible with many over the counter products. If the hoof care provider is in doubt about the effectiveness of certain products, veterinary intervention is most likely necessary. Having a systematic approach for evaluating a horse for shoeing can be one of the fastest routes to the reintroduction of equine soundness. It may be important to re-evaluate the shoeing periodically and make any changes that are indicated through hoof capsule distortion or progressive pathological change.
74 www.theneaep.com Identifying limb conformation and hoof health, prior to shoeing, can offer the practitioners a great deal of information. This coupled with veterinary diagnostics and equine sports medicine can enable equine athletes the fastest route to high-level performance.
References:
1. Morrison, S. (2013). The Thoroughbred Racehorse Foot: Evaluation and Management of Common Problems. Lexington KY: Rood and Riddle Equine Hospital. 2. Ramey, P. (2011). Care and Rehabilitation of the Equine Foot, Georgia: Hoof Rehabilitation Publishing LLC. 3. Morrison, S. Understanding Ground Impact and Heel Pain 4. Duckett, D. (2008). The External Reference Points of the Equine Hoof. The American Association of Equine Practitioners, 54th Annual Convention. San Diego, California: Presentation. 5. Redden, R.F. (2006) When and How to Use the Full Rocker Motion Shoe. 6. Bowker, R. (2003). Contrasting Structural Morphologies of “Good” and “Bad” Footed Horses. East Lansing, MI: Department of Pathology and Diagnostic Investigation, Michigan State University. 7. Curtis, S. (2002). Corrective Farriery: A textbook of remedial horseshoeing Volume I. Newmarket, Suffolk, UK: R&W Communications. 8. Curtis, S. (2006). Corrective Farriery: A textbook of remedial horseshoeing Volume II. Newmarket, Suffolk, UK: R&W Communications. 9. Hickman, J and Humphrey, M. (1988). Hickmans Farriery: Second Edition. London, Great Britain: J.A. Allen & Co. Ltd. 10. Butler, Dr. D and Butler, J. (2004). The Principles of Horseshoeing (P3). LaPorte, Colorado: Doug Butler Enterprises, Inc. 11. Colhan, P. Leach and D. Muir, G. (1991). Centre of Pressure Location of the Hoof with and without Hoof Wedges. Gainesville, FL: Department of Large Animal Services, University of Florida.
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