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Graduate Theses and Dissertations Graduate College

2009

biomechanical considerations in equine laminitis


Jennifer Anne Cerfogli
Iowa State University

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Biomechanical considerations in equine laminitis

by

Jennifer Anne Cerfogli

A thesis submitted to the graduate faculty

in partial fulfillment of the requirements for the degree of

MASTER OF SCIENCE

Major: Veterinary Clinical Science

Program of Study Committee:


Scott R. McClure, Major Professor
Brett A. Sponseller
Tim R. Derrick

Iowa State University

Ames, Iowa

2009

Copyright © Jennifer Anne Cerfogli, 2009. All rights reserved.


ii

Dedication

To my father, William G. Schleining, who taught me the importance of setting goals and to

my husband, Frank, who has journeyed with me


iii

TABLE OF CONTENTS

LIST OF FIGURES iv

ACKNOWLEDGEMENTS v

CHAPTER 1. GENERAL INTRODUCTION 1


Thesis Organization 1
Introduction to Normal Biomechanical Function of the Equine Foot 2
General Overview of Laminitis 5
Biomechanical Implications of Laminitis 8
Overall Goal 10
References 11

CHAPTER 2. REVIEW OF LITERATURE 18


Current Therapies for Laminitis Prevention 18
Current Treatments for Clinical Laminitis 20
References 26

CHAPTER 3. THE CENTER OF PRESSURE AND LOAD DISTRIBUTION IN THE


FOREFEET OF HORSES 33
Abstract 33
Introduction 34
Materials and Methods 37
Results 40
Discussion 41
References 45

CHAPTER 4. GENERAL CONCLUSION 56


General Discussion 56
Direction of Future Studies 56
References 57
iv

LIST OF FIGURES

Figure 1-1. Normal biomechanical forces of the equine foot 4


Figure 2-1. Foam pads immediately following placement 51
Figure 2-2. Standardized coordinate system 51
Figure 2-3. Graph of total surface contact area over time 52
Figure 2-4. Graph of total contact pressure over time 53
Figure 2-5. Graph of peak contact pressure over time 54
Figure 2-6. Graph of the least squares means of the center of pressure over time 55
v

ACKNOWLEDGEMENTS

There are many people who deserve recognition for their role in the development of

my career thus far. I feel extremely fortunate to have been mentored in the art of surgery by

two extraordinary surgeons, Drs. Eric Reinertson and D. Scott Taylor. Dr. Reinertson’s

influence began when I was a veterinary student and there began my love of surgery. As a

surgical resident under Dr. Reinertson, his patient direction, love of teaching, and endless

enthusiasm for surgery inspired me to continue my career in academia in hopes of making a

difference. Dr. Taylor’s drive for success in every case and dedication to service inspired me

to pursue surgery as a specialty. He is an extremely talented businessman and I learned

much from him not only in the skill of managing surgical cases, but in the skill of managing

people.

I also wish to thank the members of my program of study committee. When I first

approached Dr. Scott McClure about pursing graduate school, I had a 3 month old daughter

and a husband deploying overseas with the Army. Not once did he say, “I don’t think you

can do this.” His support and commitment to seeing me through my program through

sometimes difficult circumstances is a testament to his vision of the development of the

clinical researcher. I extend my gratitude to Dr. Brett Sponseller who has served as a role

model. He has made me a better veterinarian and faculty member through his mentorship

and invaluable advice. And to Dr. Tim Derrick who made me realize that I do, in fact, like

physics. His enthusiasm for understanding human limb movement in health and disease is

contagious. He served as an advocate for my interest in applying biomechanical principles to

horses and for that I am grateful.


1

CHAPTER 1. GENERAL INTRODUCTION

Thesis Organization

This thesis offers a contemporary review of the biomechanics involved in the disease

of equine laminitis with respect to the methods of prevention and treatment. It starts with an

introduction of the anatomy of the equine foot and how that anatomy serves a biomechanical

purpose. The forces acting on a normal equine foot are presented with respect to different

periods of the stance phase. The reaction of the internal structures of the foot to impact

shocks and weightbearing is also outlined. Using the most current data, a generalized

overview of laminitis follows. While each theory is briefly explained, it is beyond the scope

of this thesis to compare and contrast the many different proposed etiologies for the

pathophysiologic origin of laminitis. However, regardless of the inciting pathophysiologic

mechanism, there is agreement that laminitis has four distinct phases which are covered in

detail. Known risk factors for laminitis and identified epidemiologic trends as well as

economic impact are presented. Chapter one concludes with a look at laminitis from a

biomechanical perspective and how the biomechanical consequences may affect prognosis.

Chapter two is a compilation of the scientific literature specifically relating to the

biomechanical effects of current methods of laminitis prevention and treatment. Chapter

three is organized as a scientific journal manuscript and outlines a study evaluating the center

of pressure and load distribution in a population of normal horses utilizing a common, but

unsubstantiated, treatment for acute laminitis. This chapter is intended for publication and

will be submitted to the Journal of the American Veterinary Medical Association. Chapter

four concludes the thesis and provides a summary of our current understanding of the
2

biomechanics of laminitis, treatment and prevention options, and direction for future studies

utilizing information gained from the study described in chapter three.

Introduction to the Normal Biomechanical Function of the Equine Foot

The biomechanical function of the equine foot is to accept loads from the ground and

musculoskeletal system and effectively absorb, transmit, and disperse those loads amongst

the soft tissues and bones of the distal limb.1 Anatomically, the foot is composed of the hoof,

the skin between the bulbs of the heel, and all structures within. This includes the distal

interphalangeal joint, the third phalanx, the laminae, the terminal deep digital flexor tendon,

the navicular bone and its associated structures (bursa and ligaments), the collateral

cartilages, the digital cushion, the sole, the frog, and an extensive network of arteries and

veins arising from the palmar (or plantar) digital artery and vein.2,3 At a gallop, a single

forelimb can sustain substantial vertical loads up to 1.7 times the horse’s body weight. This

can be upwards of 9000 N.4 Because of the extreme loads placed on the equine digit, the

individual components of the foot would certainly fail if exposed to these loads alone. This

makes one acutely aware of the importance of all structures in the foot working in concert to

absorb and dissipate these loads. Here, special attention is given to the laminae.

The laminae are villi-like structures that functionally attach the hoof capsule to the

third phalanx. There are approximately 600 primary sensitive, or dermal, laminae originating

from the laminar corium which is contiguous with the periosteum covering the parietal

surface of the third phalanx. These interdigitate with the insensitive, or horny, laminae of the

stratum internum, the deepest layer of the hoof wall. Each of these primary laminae contains
3

approximately 100 secondary laminae increasing the functional surface area and overall

strength of the laminar junction.3,5,6

In the normal horse, loads encountered at the ground/hoof interface are transmitted

through the hoof wall, to the laminae, the third phalanx, and finally to the bony column of the

leg.7 Additionally, when the foot experiences higher loads, such as when the horse is

cantering or galloping, the frog contacts the ground assisting in load dissipation. The wedge

shape of the frog allows loads to be transferred to the bars and caudal hoof wall. This is then

transmitted to the sole and digital cushion.3 In an in vitro study examining the attenuation of

impact shocks, it was determined that the bones and interphalangeal joints were responsible

for a reduction of shock amplitude, but the laminar structures and hoof wall attenuated the

frequency similar to a low pass filter.8 In contrast, an in vitro study found that 67% of impact

vibration damping occurred at the interface between the hoof wall and the distal phalanx, i.e.

the laminae.9 This finding was supported by an in vivo study performed by Gustas et al that

concluded vertical and horizontal impact-related shocks were mostly absorbed by structures

within the foot and distal limb and were negligible by the time the shocks reached the

metacarpophalangeal joint.10 This establishes the importance of the laminae and structures of

the distal limb in shock attenuation and load transmission.

The forces acting on a normal static foot at mid-stance are outlined in Figure 1-1.

The main force is directed vertically and represents the support function of the limb. This is

broken down into the force exerted on the ground by the weight of the horse countered by the

ground reaction force directed upward. Also included is the tensile force exerted by the

laminae on the hoof wall, tensile force of the deep digital flexor muscle via the insertion of

the deep digital flexor tendon on the solar surface of the third phalanx, and the tensile force
4

exerted by the common (or long) digital extensor tendon on the extensor process of the third

phalanx.3 These relationships are important when calculating joint moments and tendon

forces using the method of inverse dynamics.11 When the foot is in static equilibrium, such

as the instantaneous moment when the ground reaction force is greatest, the force of the deep

digital flexor muscle on the third phalanx can be calculated by multiplying the moment arm

created by the ground reaction force and the center of rotation of the distal interphalangeal

joint by the magnitude of the ground reaction force.11

A
D

Figure 1-1. Biomechanical forces of the equine digit. The weight of the horse (A) is

countered by ground reaction force (B). Other forces include the tensile forces of the deep

digital flexor tendon (C), the laminae (D), and the common(or long) digital extensor tendon

(E). Arrows are for illustrative purposes only and are not scaled according to magnitude.

Illustration courtesy of Dr. Stephanie S. Caston.


5

For the purposes of biomechanical analysis, gait is divided into two phases, stance

and swing.2 The stance phase of gait is defined as the time period when the foot is in contact

with the ground. This is further separated into three segments correlating to the movement of

the hoof with respect to the surface. The first of these segments, impact or “heel strike”,

occurs when there is a rapid decrease in acceleration (deceleration) corresponding to a high

rate of loading. This lasts approximately the first 30 msec of stance.2 The second, and

longest, phase is support where the entire foot contacts the ground and the load is high. The

final segment is breakover which begins when the heel leaves the ground and ends at the

point of toe lift-off as the flexing moment about the distal interphalangeal joint exceeds the

extending moment.2,12,13 While this phase comprises only 5% of the total stance phase,

breakover is constantly manipulated by farriers and veterinarians in an effort to elicit a

biomechanical advantage for both athletic function and in disease treatment.14

During the stance phase, the third phalanx undergoes controlled displacement within

the hoof capsule.6 During impact, the third phalanx displaces toward the sole and away from

the wall in response to being loaded. As the foot progresses through the support phase and

enters breakover, the sole reaches maximal compression and then acts as a fulcrum for the

third phalanx. Consequently, the distal aspect of the third phalanx is displaced toward the

wall and the proximal aspect of the bone continues to displace toward the sole due to the

compliance of the digital cushion.6

General Overview of Laminitis

Laminitis, termed “founder” in its chronic form, is defined as inflammation within the

laminar structures.15 The disease can be crippling, excruciatingly painful, life-threatening,


6

and often ends the athletic career of the horses it affects.16 Multiple etiologies for laminitis

have been proposed. Current research is concentrated on three main pathways, one involving

a vascular/hemodynamic mechanism, one a toxic/metabolic/enzymatic mechanism, and

finally, a traumatic/mechanical process.17 It is believed that the onset of laminitis is likely

multi-factorial, and therefore, it is difficult to identify a single inciting mechanism of action.

Many in vitro experiments have provided potential pathways in the development of laminitis

but they are difficult to corroborate in vivo.17 While the exact etiology of laminitis remains

elusive, the stages of laminitis can be classified into four phases. These include

developmental, acute, subacute, and chronic.15

The developmental stage of laminitis is the stage which precedes clinical detection. It

is estimated the duration of this stage ranges from 24 to 60 hours making the window for

intervention very small.15 The next stage is acute laminitis and covers the period from the

onset of clinical signs to evidence of rotation and/or distal displacement (“sinking”) of the

third phalanx. If mechanical failure of the foot does not occur, the acute phase is considered

over by 72 hours after the onset of clinical signs and is followed by the subacute phase.15

The subacute phase is defined as the time required by the foot to completely heal from the

inflammatory insult without experiencing digital collapse. The length of this stage is

variable, but can last several months during which time the laminar structures are

considerably weaker than their normal state.15 The final stage is the chronic stage which is

initiated by digital collapse. Digital collapse is identified by rotation and/or vertical digital

displacement of the third phalanx.15

Laminitis usually occurs in the front feet which is logical given that horses bear

approximately 60% of their weight on their front limbs.18, 19, 20 However, laminitis of all four
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feet is not uncommon, nor is laminitis of a single digit when it assumes the responsibility of

weightbearing subsequent to an injury or lameness of the opposing limb.18,21

While the exact etiology of laminitis evades us, risk factors for laminitis have been

identified. Horses aged 5-7 and 13-31 years, of the female gender, and of a breed other than

Quarter Horse or Thoroughbred are more likely to develop acute laminitis. For chronic

laminitis, horses were at a greater risk if they were between the ages of 10-14 years or 15-38

years, were a female, and were a breed other than Thoroughbred, with ponies being 9.1 times

more likely to develop chronic laminitis than Thoroughbreds.22 Conversely, in an

epidemiological study there were no associations between age, breed, sex, or weight and

development of acute laminitis.23 However, when chronic laminitis was examined females

and older horses were more commonly affected. An early study linked testosterone and an

increased risk of laminitis with geldings having fewer incidences of laminitis versus their

intact male counterparts. That study also concluded that ponies were 4.3 times more likely to

develop laminitis than all other equine species.24 For horses with unilateral lameness that

developed laminitis of a contralateral limb, duration of lameness, but not weight, was found

to be a significant risk factor. Additionally, horses that developed contralateral limb

laminitis were more likely to be euthanized than their matched controls.21 In horses

diagnosed with duodenitis/proximal jejunitis at a university hospital, those weighing more

than 550kg and horses having hemorrhagic gastric reflux at the time of presentation were

twice as likely to develop laminitis.25 Additional predisposing factors include other

gastrointestinal diseases,23,26endotoxemia and sepsis,18,27 nutritional derangements (grain

overload and “grass founder”),18,28 retained placenta,18,28 direct digital trauma,28 obesity18,

and endocrinopathies.18,29
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Economically, laminitis has a substantial impact and has afflicted the equine

population for centuries.30 The cost of lameness (including laminitis) in 1998 was estimated

at $678 million with 110 days of lost use per lameness event.31 More recent data indicates

that in 2007, nearly 200,000 horses were diagnosed with laminitis in the United States.32,33

According to the United States Department of Agriculture’s National Animal Health

Monitoring Service, 13% of all horse facilities in the United States reported a case of

laminitis on their premise within the previous 12 months.33 Given these economic

consequences and the lack of an identified etiology despite the efforts of prominent

researchers, the need for continued investigation is clear. This is supported by the United

States Department of Agriculture’s priority funding of laminitis research and the inception of

a laminitis fund named in honor of the 2006 Kentucky Derby winner, Barbaro, at the

University of Pennsylvania’s New Bolton Center after he succumbed to laminitis in 2007.

Biomechanical Implications of Laminitis

In the acute phase of laminitis, the laminae undergo microscopic changes that alter

their biomechanical function. The initial histopathological change observed following

lameness detection is vascular endothelial cell swelling followed by erythrocyte congestion

and occlusion of capillaries by 8 hours.34 Leukocyte migration to the perivascular tissues

follows and initiates the movement of inflammatory cells into the epidermal tissues. By 24

hours, microvascular thrombi and marked edema have occurred with hemorrhage appearing

in the primary dermal laminae by 72 hours.35 Cellular response to the ischemic injury results

in cell edema, vacuolization, nuclear swelling and pyknosis.35 This causes a distortion of the

laminae defined as an initial thinning and lengthening of the laminae followed by reduction,
9

flattening, and detachment of the basement membrane.36 The basement membrane is critical

for laminar attachment37and the loss of its integrity leads to destabilization of the foot

resulting in mechanical breakdown.38 In another etiologic theory of laminitis, matrix

metalloproeinases (MMP’s) are responsible for basement membrane pathology.39

During stance, the laminae withstand both tensile and shear forces.6 When loss of

laminar attachment occurs, the third phalanx effectively moves independent of the hoof

capsule and the main force acting on the bone is the tensile force of the deep digital flexor

tendon.40 When the dorsal laminae are predominantly damaged to the point that they are no

longer able to counter the force of the deep digital flexor tendon, rotational displacement

about the distal interphalangeal joint occurs.6 In a study of ponies with naturally occurring

chronic laminitis and 6º-13º of phalangeal rotation, the force exerted by the deep digital

flexor tendon was significantly less than that of control ponies as calculated by the method of

inverse dynamics. The force from the deep digital flexor tendon did not reach normal levels

until the end of stance phase.41 However, when damage has occurred to the laminae

circumferentially, shear forces resulting from weightbearing cause the third phalanx to

displace vertically. In these situations much of the responsibility for stabilizing the third

phalanx shifts to the sole and is seen as an increase in the compressive force applied by the

displaced third phalanx.6 Clinically, this can be seen as a flat, or even convex, sole. In severe

cases, the tip of the third phalanx will prolapse through the sole.35 A study of the laminar

junction collected from two groups of horses with chronic laminitis, “treatable” and “non-

treatable”, were compared to that of normal horses. In the “treatable” classification, the

strength of the laminar junction was 60% of normal values. However in the horses classified
10

as “non-treatable”, those that had been refractory to treatment for six months, the strength of

the laminar junction was only 42% of normal.42

The prognosis is generally poor for horses that experience rotational displacement

and grave for those that have distal displacement of the third phalanx.18,35,43 In one study,

horses with less than 5.5º of rotation returned to athletic performance, but those with more

than 11.5 º of rotation did not.44 Conversely, a subsequent study revealed that radiographic

assessment of rotation did not correlate with outcome and that the degree of lameness was a

more accurate predictor of outcome.45 While the exact origin of pain in laminitis is not

understood, it can be reasonably concluded that the degree of pain is likely proportional to

the severity of laminar damage.18,43 Another predictor of outcome may be the manner and

speed in which the animal responds to treatment. Because of the many factors involved in

case progression (i.e. how long the patient has been experiencing laminitis prior to treatment,

how many and which treatments have been attempted, etc.) a solid time frame in which

recovery is expected cannot be given. Each case must be handled individually. However,

cases refractory to treatment will generally have a worse outcome.18

Overall Goal

Given the plethora of often conflicting empirical information regarding the treatment

of laminitis, together with a lack of understanding of the cellular mechanisms that cause

laminitis and the realization that there may be many different pathways resulting in the

disease that work alone or in concert with one another, one objective of this masters program

was to become educated in the current understanding of the disease process. However, the

overall goal was to identify areas where biomechanical assessment is lacking that
11

consequently provide an opportunity for research and contribution of scientific evidence

leading to the successful treatment of the disease.

References

1. Hood D.M., Jacobson A.C. The principles of equine hoof wall conformation. In:

Proceedings of The Hoof Project. Eds. Hood D.M., Wagner I.P, Jacobson A.C. College

Station: Texas A&M University, 1997;2-20.

2. Johnston C., Back W. Hoof ground interaction: when biomechanical stimuli challenge the

tissues of the distal limb. Equine Vet J 2006;38:634-641.

3. Kainer R.A. Clinical Anatomy of the Equine Foot. Vet Clin North Am Equine Pract

1989;5:1-27.

4. Roland E.S., Hull M.L., Stover S.M. Design and demonstration of a dynamometric

horseshoe for measuring ground reaction loads of horses during racing conditions. J Biomech

2005;38:2102-2112.

5. Dyce K.M., Sack W.O., Wensing C.J.G. The forelimb in the horse. In: Textbook of

Veterinary Anatomy. 2nd ed. Dyce K.M., Sack W.O., Wensing C.J.G. eds. W.B. Saunders

Company. Philadelphia, Pennsylvania. 1996:595-600.


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6. Hood D.M. The mechanisms and consequences of structural failure of the foot. Vet Clin

North Am Equine Pract 1999;15:437-461.

7. Olivier A., Wannenburg J., Gottschalk R.D., van der Linde M.J., Groeneveld H.T. The

effect of frog pressure and downward vertical load on hoof wall weight-bearing and third

phalanx displacement in the horse – an in vitro study. J S Afr Vet Assoc. 2001;72:217-227.

8. Lanovaz J.L., Clayton H.M., Watson L.G. In vitro attenuation of impact shock in equine

digits. Equine Vet J Suppl. 1998;26:96-102.

9. Willeman M.A., Jacobs M.W.H., Schamhardt H.C. In vitro transmission and attenuation of

impact vibrations in the distal forelimb. Equine Vet J Suppl. 1999;30:245-248.

10. Gustas P., Johnston C., Roepstorff L., Drevemo S. In vivo transmission of impact shock

waves in the distal forelimb of the horse. Equine Vet J Suppl. 2001;33:11-15.

11. Buchner H.H.F. Distal limb internal dynamics: Joint moments, tendon forces, and lessons

for orthopedic shoeing, in Proceedings. 51st Annu Conv Am Assoc Equine Practnr.

2005;51:134-140.

12. van Heel M.C.V., Moleman M., Barneveld A., van Weeren P.R., Back W. Changes in

location of centre of pressure and hoof-unrollment pattern in relation to an 8-week shoeing

interval in the horse. Equine Vet J. 2005;37:536-540.


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13. Eliashar E., McGuigan M.P., Wilson A.M. Relationship of foot conformation and force

applied to the navicular bone of sound horses at the trot. Equine Vet J. 2004;36:431-435.

14. Ramey D. Evidence-based clinical question – Do rolled or squared toes affect rate of

breakover in horses? Eq Vet Educ 2007;19:447-448.

15. Hood D.M. Laminitis in the horse. Vet Clin North Am Equine Pract 1999;15:287-294.

16. Eades SC, Holm AMS, Moore RM. A review of the pathophysiology and treatment of

acute laminitis: Pathophysiologic and therapeutic implications of endothelin-1, in

Proceedings 48th Annu Conv Am Assoc Equine Practnr 2002;48:353-361.

17. Moore RM, Eades SC, Stokes AM. Evidence for vascular and enzymatic events in the

pathophysiology of acute laminitis: which pathway is responsible for initiation of this process

in horses? Equine Vet J 2004;36:204-209.

18. Baxter G.M. Acute laminitis. Vet Clin North Am Equine Pract. 1994;3:627-642.

19. Hood D.M., Hunter J.F., Beltz W.D., Taylor B.E., Beckham A.S., Pierce J.R. Digital

loading in the normal standing horse. In: Proceedings of The Hoof Project. Eds. Hood D.M.,

Wagner I.P, Jacobson A.C. College Station: Texas A&M University, 1997;36-43.
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20. Hood DM, Taylor D, Wagner IP. Effects of ground surface deformability, trimming, and

shoeing on quasistatic hoof loading patterns in horses. Am Journ Vet Res 2001;62:895-900.

21. Peloso J.G., Cohen N.D., Walker M.A., Watkins J.P., Gayle J.M., Moyer W. Case-

control study of risk factors for the development of laminitis in the contralateral limb in

equidae with unilateral lameness. J Am Vet Med Assoc 1996;209:1746-1749.

22. Alford P., Geller S., Richrdson B., Slater M., Honnas C., Foreman J., Robinson J.,

Messer M., Roberts M., Goble D., Hood D., Chaffin M. A mulitcenter, matched case-control

study of risk factors for equine laminitis. Prev Vet Med. 2001;49:209-222.

23. Slater M.R., Hood D.M., Carter G.K. Descriptive epidemiological study of equine

laminitis. Equine Vet J. 1995;27:364-367.

24. Dorn C.R., Garner H.E., Coffman J.R., Hahn A.W., Tritschler L.G. Castration and other

factors affecting the risk of equine laminitis. Cornell Vet. 1975;65:57-64.

25. Cohen N.D., Parson E.M., Seahorn T.L., Carter G.K. Prevalence and factors associated

with development of laminitis in horses with duodenitis/proximal jejunitis: 33 cases (1985-

1991). J Am Vet Med Assoc. 1994;204:250-254.

26. Divers T.J. Prevention and treatment of thrombosis, phlebitis, and laminitis in horses with

gastrointestinal diseases. Vet Clin North Am Equine Pract. 2003;19:779-790.


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27. Baxter G.M. Equine laminitis caused by distal displacement of the distal phalanx: 12

cases (1976-1985). J Am Vet Med Assoc. 1986;189:326-329.

28. Hood D.M. The pathophysiology of developmental and acute laminitis. Vet Clin North

Am Equine Pract. 1999;15:321-343.

29. Johnson P.J. The equine metabolic syndrome peripheral cushing’s sydrome. Vet Clin

North Am Equine Pract. 2002;18:271-293.

30. Wagner I.P., Heymering H. Historical perspectives on laminitis. Vet Clin North Am

Equine Pract. 1999;15:295-309.

31. United States Department of Agriculture 2000. Lameness and Laminitis in U.S. Horses.

USDA:APHIS:VS, CEAH, National Animal Health Monitoring System. Fort Collins, CO

#N318.0400.

32. The Economic Impact of the Horse Industry on the United States. American Horse

Council, 2007

33. Kane AJ, Traub-Dargatz J, Losinger WC, Barber LP. The occurrence and causes of

lameness and laminitis in the U.S. horse population, in Proceedings. 46st Annu Conv Am

Assoc of Equine Practnr 2000;46:277-280.


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34. Hood D.M., Grosenbaugh D.A., Mostafa M.B., Morgan S.J., Thomas B.C. The role of

vascular mechanisms in the development of acute equine laminitis. J Vet Intern Med.

1993;7:228-233.

35. Stokes A.M., Eades S.C., Moore R.M. Pathophysiology and treatment of acute laminitis.

In: Equine Internal Medicine, 2nd Edition. eds. Reed S.M., Bayly W.M., Sellon D.C.

Saunders, St. Louis, Missouri 2004:522-531.

36. Obel N. Studies of the histopathology of acute laminitis. (Thesis) Vet Stockholm

50:1948.

37. Pollitt C.C. The basement membrane at the equine hoof dermal epidermal junction.

Equine Vet J. 1994;26:399-407.

38. Pollitt C.C. Basement membrane pathology: a feature of acute equine laminitis. Equine

Vet J. 1996:28;38-46.

39. Kyaw-Tanner M.T., Wattle O., van Eps A.W., Pollitt C.C. Equine laminitis: membrane

type matrix metalloproteinase-1 (MMP-14) is involved in acute phase onset. Equine Vet J.

2008;40:482-487.
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40. Coffman J.R., Johnson J.H., Finocchio E.J., Guffy M.M. Biomechanics of pedal rotation

in equine laminitis. J Am Vet Med Assoc. 1970;156:219-221.

41. McGuigan M.P., Walsh T.C., Pardoe C.H., Day P.S., Wilson A.M. Deep digital flexor

tendon force and digital mechanics in normal ponies and ponies with rotation of the distal

phalanx as a sequel to laminitis. Equine Vet J. 2005;37:161-165.

42. Burt N.W., Baker S.J., Wagner I.P., Hogan H.A., Hood D.W. Digital instability as a

potential prognostic indicator in horses with chronic laminitis. In: Proceedings of The Hoof

Project. eds. Hood D.M., Wagner I.P, Jacobson A.C. College Station: Texas A&M

University, 1997;105-115.

43. Swanson T.D. Clinical presentation, diagnosis, and prognosis of acute laminitis. Vet Clin

North Am Equine Pract. 1999:15;311-319.

44. Stick J.A., Jann H.W., Scott E.A., Robinson N.E. Pedal bone rotation as a prognostic sign

in laminitis of horses. J Am Vet Med Assoc. 1982;180:251-253.

45. Hunt R.J. A retrospective evaluation of laminitis in horses. Equine Vet J. 1993;25:61-64.
18

CHAPTER 2. REVIEW OF LITERATURE RELEVANT TO


PREVENTION AND TREATMENT

Current Therapies for Laminitis Prevention

The best manner in which to treat laminitis is to prevent it altogether. While this

statement seems logical, without an accurate etiology, prevention has proven to be very

difficult. Further compounding this fact is the understanding that a lone etiology likely is not

adequate to describe all situations of laminitis. At this time, prevention is mainly directed at

addressing known predisposing factors with the hope that it will prevent laminitis from

occurring. Prevention with respect to the biomechanics of some of the most common

predisposing factors will be addressed. Many of these preventative measures are also used in

the treatment of acute and chronic laminitis and further exploration of the biomechanical

benefits of these treatments will be addressed in the following section on laminitis treatment.

Support limb laminitis occurs in a limb that has assumed the majority of

weightbearing when its opposing limb has an injury or other painful or neurologic condition

precluding normal weightbearing. In this situation, clinical signs usually appear between 2

and 5 weeks following a shift in weightbearing.1 It has been shown that the weight placed on

a single forelimb increases from 28% to 54% of body weight during unilateral weightbearing.

This change in weightbearing causes a significant decrease in total blood flow to the foot.2

Measures should be taken to prevent contralateral laminitis because if treatment is delayed

until clinical signs develop, the result can be catastrophic.1,3 The best method of prevention

in this case is to address the inciting cause of the lameness to encourage normal
19

weightbearing of the ipsilateral limb. This is important because it has been shown that the

most important risk factor in the development of support limb laminitis is the length of

increased weightbearing by the contralateral limb.4 Biomechanically, prevention of support

limb laminitis usually occurs in the form of measures to encourage weight loss, recruit the

sole and frog to assume weightbearing responsibility, and decrease the moment arm about the

distal interphalangeal joint (move the center of pressure palmarly).1 Means by which to do

this include application of frog support, encouraging the horse to lie down, beveling or

rolling the toe, placing the horse in soft sand, and temporary use of a full body sling.1,5

For laminitis secondary to systemic disease (namely colitis, enteritis, endotoxemia,

metritis, and generalized sepsis), prevention mainly lies in treatment and correction of the

underlying disease while applying supportive treatment to the feet. Usually attention is paid

to all four feet rather than just the forelimbs as whatever constitutes the triggering mechanism

is likely carried to the feet by the bloodstream making it plausible that all four feet will be

affected.6 Recently, the use of distal limb cryotherapy has returned promising results in the

prevention of acute laminitis when used in the developmental stage.7 The mechanism by

which cryotherapy is effective is not fully known, but it is hypothesized that its success can

be attributed to one or both of the following: potent vasoconstriction causing the prevention

of systemic trigger factors from reaching the foot and/or the induction of a hypometabolic

state within the laminar cells making them more resistant to the effect of trigger factors.7,8

Mechanical support to the foot includes recruiting the sole and frog to assist with

weightbearing and decreasing the pull of the deep digital flexor tendon on the third phalanx

by a number of different methods that will be discussed in the treatment section. Other

pharmacologic therapies outside the scope of this thesis include anti-endotoxic, low-dose
20

administration of flunixin meglumine and polymixin B, non-steroidal anti-inflammatory

therapy, vasodilator administration (i.e. acepromazine and nitroglycerin), anticoagulant

therapy, administration of oxygen free radical scavengers (DMSO), and hemorrheologic

agents (Pentoxifylline), supportive fluid therapy, and other amino acid

supplementation.9,10,11,12

Current Treatment of Laminitis

Many of the therapies introduced in the section on prevention are also applicable to

treatment after clinical signs have developed. While noting that pharmacologic intervention

is very important, the main focus here will be placed on the biomechanical effects of

different treatment regimens and the scientific evidence of their efficacy.

As outlined previously, the main goals of laminitis treatment are to remove the

inciting cause, minimize pain and suffering, prevent or minimize permanent damage to the

laminae, and prevent or reduce the amount of mechanical collapse. Various pharmacologic,

biomechanical, and surgical mechanisms are used to achieve these goals.3,12 Addressing the

inciting cause usually involves medical support and management, is dependent on the

predisposing factor, and will not be covered here. The minimization of pain and suffering

also has a pharmacologic basis, but efforts to manage the biomechanical deficiencies of

laminitis usually have an effect on the patient’s comfort level as well.

Attempts to minimize permanent damage to the laminae come in many forms. It is

generally accepted that recruiting the sole and/or frog to disperse the load placed on the

dorsal hoof wall is desirable. The importance of this practice is emphasized by a study in

which the load exerted on the front limbs of horses experiencing acute laminitis was not
21

different than that experienced prior to induction of laminitis via carbohydrate overload.

Load was not different until after phalangeal displacement had occurred.13 However, the

mechanism by which this is accomplished is not as straightforward. There is much anecdotal

evidence to support the use of different methods, but scientific proof of efficacy for many

treatments is lacking. External methods of frog support are believed to add stability and

support to the third phalanx by decreasing pressure normally placed on the wall and laminae.

This may thereby decrease pain and, in theory, prevent rotational displacement of the third

phalanx. Caution should be advised because too much rigid support may be

counterproductive, further compromising blood flow to the sole via compression.12 There are

numerous methods of applying external frog support described in the literature. One is the

temporary application of roll gauze to the frog with tape. While certain texts advocate its

placement over the entire frog,12,14 others recommend placing it only on the caudal third of

the frog3 and the gauze characteristics are not addressed (porosity, size of roll, duration of

placement, etc.). A commercial frog support, the Lily Pad®, is available for use as an

emergency aid and is marketed as being able to “offer the painful foot a resilient cushion

support as well as protection, slight heel elevation and the benefit of slightly reduced

breakover.”15 However, no scientific data is available to substantiate these claims. A study

on the effect of Lily Pads® on the level of pain in horses with naturally occurring chronic

laminitis concluded that their application did not decrease pain level. Additionally, horses

were more comfortable following removal of the pad.16 The use of Styrofoam® placed on

the bottom of the foot is another method used to provide frog, and in addition, sole support.

Commercial foam pads are marketed as part of the Equine Digital Support System (EDSS) or

can easily be made by cutting out supports from a sheet of industrial insulation sheeting.
22

Many authors reference the use of Styrofoam® in the developmental and acute stages of

laminitis, but consistency among application methods is lacking.14,17,18 Additionally, while

each author explains the purported benefits of Styrofoam®, no scientific evidence is

presented.

More expensive, aggressive support in the form of special shoeing provides an

additional option for sole and/or frog support. One of the more familiar shoes for treatment

of laminitis is the heart bar shoe and it is available in adjustable and non-adjustable forms.19

The construction of the heart bar shoe includes a triangle-shaped plate forged onto the caudal

aspect of the shoe that connects the heels and extends over the dimensions of the frog. It has

followings of both loyal fans and devoted enemies likely due to the fact that the shoe in one

person’s hands appears to be successful, while in another it is disastrous.19,20,21 When used

improperly, the heart bar shoe can cause further damage to the frog and digital cushion,

compromising healthy structures and increasing patient discomfort.19 Biomechanically, the

heart bar is believed to decrease the strain on the laminar structures by providing additional

weightbearing surface area to the foot, decrease the pressure placed on the solar plexus by the

third phalanx thereby aiding digital perfusion, and prevent rotational displacement of the

third phalanx.12 While there are several references for construction and application of a heart

bar shoe,14,22,23 little scientific evidence is available to document the biomechanical benefit of

such. One study reviewed the ability of the heart bar to reduce the amount of pain in

chronically affected laminitic horses. It concluded that after 7 days, there was no

improvement in the level of pain following placement of a heart bar shoe.24 On the other

hand, when scintigraphy was used to assess digital perfusion, a significant increase in dorsal

laminar perfusion was seen 12 weeks after application of a heart bar-egg bar shoe.25
23

Additionally, horses were significantly less lame by 6 weeks following shoe placement. A

notable drawback of that paper, however, is the lack of a control group, and it cannot be

concluded that these horses progressed any differently than horses who did not have heart

bar-egg bar shoes.25 No other concrete evidence to substantiate the biomechanical claims of

the benefits of the heart bar shoe are published.

A reverse shoe with an adjustable frog support plate was evaluated in vitro using

normal cadaver limbs. Pressure applied to the frog just less than that causing patient

discomfort as assessed prior to euthanasia significantly decreased total hoof wall

weightbearing and caused palmar movement of the third phalanx up to loads of 1300N.26

Other methods of support utilizing various shoeing techniques include filling the shoe with a

range of commercial epoxy formulations to recruit weight bearing from the sole and

frog.18,23,27 However, the only study examining the benefits of a filler used a polyurethane-

filled standard keg shoe applied to normal horses. The pressure exerted on the sole was not

significantly different from a shoe without polyurethane until the horse was exposed to a

deformable surface.27 This study has implications for the use of fillers in laminitic horses as it

emphasizes the importance of the surface the horse is housed on during recovery and

rehabilitation.

Another avenue used to minimize damage to the dorsal laminae includes the

manipulation of breakover. It is a common belief that decreasing breakover, or decreasing

the amount of time from heel-off to toe-off, provides a biomechanical advantage by

decreasing the strain on the dorsal laminae through manipulation of the moment about the

distal interphalangeal joint. There are many ways by which farriers and clinicians attempt to

do this. One of these methods is by “rolling the toe”. This is easily accomplished by using a
24

hoof rasp to decrease the amount of toe contacting the ground or by placing a shoe with a roll

at the toe (i.e. a “rolled toe” or “rocker toe” shoe). Many times this is done concurrently with

squaring the toe. However, several studies have refuted the claim that squaring or rolling the

toe actually decreases breakover. The first of these compared characteristics of breakover in

horses shod with rocker toe, rolled toe, and square toe shoes with standard steel shoes. No

difference in breakover was detected.28 In a similar study comparing rocker toe shoes with

standard shoes in non-lame horses using both motion capture and force platform data, no

difference was found in the length of breakover.29 While yet another study was in agreement

with the duration of breakover being unchanged, a rolled toe shoe improved the

characteristics of the unrollment pattern and decreased the peak loading of the distal limb

during breakover leading to the conclusion that a rolled toe was, in fact, favorable.30 An

evidence-based article addressing the question of whether or not rolled or squared toes

affected the rate of breakover concluded that there was no scientific evidence to support the

claim of improved breakover.31 Shoes with a squared toe, such as the Natural Balance shoe,

also have self-purported claims of improving breakover.32 However, despite decreasing the

moment arm when compared to toe-clip shoes, both Natural Balance and quarter-clip shoes

failed to improve the peak moment about the distal interphalangeal joint countering the claim

of the ability of those shoes to ease breakover.33

Raising the heels is another reported method of protecting the damaged dorsal

laminae from mechanical collapse, and is advocated by many authors.3,5,14,34,35 This is

believed to decrease the stress on the laminae by decreasing the tensile stress placed on the

third phalanx by the deep digital flexor tendon.34 An 18º heel wedge was reportedly

successful in the majority of 29 cases in which it had been used on the basis of improvement
25

in the level of the horse’s comfort, but no biomechanical assessment was included.34 In a

study utilizing a computer generated, model-based system based on kinematic and computed

tomography data, peak strain in the deep digital flexor tendon was significantly decreased

with a 6º heel elevation. A toe elevation resulted in a significant increase in peak strain of

the deep digital flexor tendon.36 Other publications have documented an increase in the

flexion angle of the distal interphalangeal joint with heel elevation and subsequently

concluded a likely decrease in the strain of the deep digital flexor tendon, but no direct

measurements of strain occurred.29,37,38 Another study using a finite element model of the

equine hoof under a simulated 5º heel wedge resulted in decreased stresses within the hoof

capsule.39 Finally, use of a hoof cast incorporating a 15-20º heel wedge was found to

decrease strain by 59% on the dorsal hoof wall, but increase strain on the lateral hoof wall by

34%, using rosette strain gauges instrumented on cadaver specimens.35

Surgical techniques have been employed as a salvage effort in severe cases of

laminitis to prevent further rotational displacement of the third phalanx.40,41,42 This

effectively removes the stress applied by the deep digital flexor tendon by performing a deep

digital flexor tenotomy at mid-metacarpus or at the level of the pastern. Tenotomy of the

accessory ligament of the deep digital flexor tendon has also been documented as an

alternative to transection of the deep digital flexor tendon, but is not recommended due to the

fact that it actually increases the peak load of the deep digital flexor tendon at certain stance

times.43 The procedure of deep digital flexor tenotomy is usually reserved as a “last ditch”

effort to prevent further rotational displacement of the third phalanx and is reserved for cases

which are either refractory to other treatments or display a rapid progression of rotation.12

While the biomechanical effects have not been specifically studied, it is reasonable to expect
26

that by removing the pull of the deep digital flexor tendon, the stress placed on the damaged

laminae is decreased. In one retrospective study following the procedure mid-pastern, 85%

of horses returned to comfort in the follow up period.41 Similarly, a study of 35 cases showed

that 77% of horses subjected to a tenotomy at the mid-metacarpus survived greater than 6

months, and 59% were still alive after 2 years. Obel grade lameness, degree of third

phalangeal rotation, and horse body weight had no effect on outcome.40 Conversely, another

study found that while pain relief followed the surgical procedure in the short term, only 30%

of horses were alive at 6 months following surgery and that it may not alter outcome.42

References

1. Baxter G.M., Morrison S. Complications of unilateral weight bearing. Vet Clin North Am

Equine Pract. 2009:24;621-642.

2. Baker S.J., Steinheimer D., Burt N.W., Hood D.M. The effect of weight bearing on equine

digital blood flow.

3. Baxter G.M. Acute laminitis. Vet Clin North Am Equine Pract. 1994;3:627-642.

4. Peloso J.G., Cohen N.D., Walker M.A., Watkins J.P., Gayle J.M., Moyer W. Case-control

study of risk factors for the development of laminitis in the contralateral limb in equidae with

unilateral lameness. J Am Vet Med Assoc 1996;209:1746-1749.


27

5. Parks A., O’Grady S.E. Chronic laminitis: current treatment strategies. Vet Clin North Am

Equine Pract. 2003;19:393-416.

6. Pollitt C.C. Laminitis in perspective. In: Equine Laminitis. ed. Pollitt C.C., Rural

Industries Research and Development Corporation: Barton, Australia, 2001:24-35.

7. van Eps A.W., Walters L.J., Baldwin G.I., McGarry M., Pollitt C.C. Distal limb

cryotherapy for the prevention of acute laminitis. Clin tech equine pract. 2004;3:64-70.

8. van Eps A.W., Pollitt C.C. Equine laminitis: cryotherapy reduces the severity of the acute

lesion. Equine Vet J. 2004;36:255-260.

9. Brumbaugh G.W., Lopez H.S., Sepulveda M.L.H. The pharmacologic basis for the

treatment of developmental and acute laminitis. Vet Clin North Am Equine Pract.

1999;15:345-363.

10. Divers T.J. Prevention and treatment of thrombosis, phlebitis, and laminitis in horses with

gastrointestinal diseases. Vet Clin North Am Equine Pract. 2003;19:779-790.

11. Cohen N.D., Parson E.M., Seahorn T.L., Carter G.K. Prevalence and factors associated

with development of laminitis in horses with duodenitis/proximal jejunitis: 33 cases (1985-

1991). J Am Vet Med Assoc. 1994;204:250-254.


28

12. Goetz T.E. The treatment of laminitis in horses. Vet Clin North Am Equine Pract.

1989;5:73-108.

13. Hood D.M., Wagner I.P., Taylor D.D., Brumbaugh G.W., Chaffin M.K. Voluntary limb-

load distribution in horses with acute and chronic laminitis. Am J Vet Res. 2001;62:1393-

1398.

14. O’Grady S. Foot Care. In: Concise Guide to Laminitis in the Horse. ed. D.W. Ramey.

Trafalgar Square Publishing. North Pomfret, Virginia. 2003:65-76.

15. Nanric, Inc. website. Available at www.nanricstore.com/servlet/the-90/LILY-

PADS/Detail. accessed 20 June, 2009.

16. Hood D.M., Beckham A.S., Chaffin M.K., Hunter J.F., Matthews N.S., Moyer W., Slater

M.R. Comparison of lily pads and corrective trimming on expressed pain in horses with

chronic laminitis. In: Proceedings of The Hoof Project. Eds. Hood D.M., Wagner I.P,

Jacobson A.C. College Station: Texas A&M University, 1997;83-90.

17. Stokes A.M., Eades S.C., Moore R.M. Pathophysiology and treatment of acute laminitis.

In: Equine Internal Medicine, 2nd Edition. eds. Reed S.M., Bayly W.M., Sellon D.C.

Saunders, St. Louis, Missouri 2004:522-531.


29

18. Parks A.H., Balch O.K., Collier M.A. Treatment of acute laminitis – supportive therapy.

Vet Clin North Am Equine Pract. 1999;15:363-374.

19. Goetz T.E. Anatomic, hoof, and shoeing consideration for the treatment of laminitis in

horses. J Am Vet Med Assoc. 1987;190:1323-1332.

20. Eustace R.A., Caldwell M.N. Treatment of solar prolapse using the heart bar shoe and

dorsal hoof wall resection technique. Equine Vet J. 1989;21:370-372.

21. Moyer W., Redden R.R. Chronic and severe laminitis: a critique of therapy with heart bar

shoes and hoof wall resection. Equine Vet J. 1989;21:317-318.

22. Eustace R.A., Caldwell M.N. The construction of the heart bar shoe and the technique of

dorsal wall resection. Equine Vet J. 1989;21:367-369.

23. Pollitt C.C. Therapeutic Shoeing. In: Equine Laminitis. ed. Pollitt C.C., Rural Industries

Research and Development Corporation: Barton, Australia, 2001:79-93.

24. Taylor D., Hood D.M., Wagner I.P. Short-term effect of therapeutic shoeing on severity

of lameness in horses with chronic laminitis. Am J Vet Res. 2002;63:1629-1633.


30

25. Ritmeester A.M., Blevins W.E., Ferguson D.W., Adams S.B. Digital perfusion, evaluated

scintigraphically, and hoof wall growth in horses with chronic laminitis treated with egg bar-

heart bar shoeing and coronary band grooving. Equine Vet J Suppl. 1998;26:111-118.

26. Olivier A., Wannenburg J., Gottschalk R.D., van der Linde M.J., Groeneveld H.T. The

effect of frog pressure and downward vertical load on hoof wall weight-bearing and third

phalanx displacement in the horse – an in vitro study. J S Afr Vet Assoc. 2001;72:217-227.

27. van Heel MCV, Back W. Ground surface and poly-urethane (PU) filling alter the

pressure distribution pattern in square standing horses. Pferdeheikunde 2006;22:592-596.

28. Clayton H.M., Sigafoos R., Curle R.D. Effect of three shoe types on the duration of

breakover in sound trotting horses. J Equine Vet Sci. 1991;11:129-132.

29. Willemen M.A., Savelberg H.H.C.M., Jacobs M.W.H., Barneveld A. Biomechanical

effects of rocker-toed shoes in sound horses. Vet Q Suppl. 1996;18:S75-S78.

30. van Heel M.C.V., Weeren P.R., Back W. Shoeing sound warmblood horses with a rolled

toe optimizes hoof-unrollment and lowers peak loading during breakover. Equine Vet J.

2006;38:258-262.

31. Ramey D. Evidence-based clinical question – Do rolled or squared toes affect rate of

breakover in horses? Eq Vet Educ 2007;19:447-448.


31

32. Natural Balance Hoof Care website. Available at

www.hopeforsoundness.com/index.html. Accessed 20 June 2009.

33. Eliashar E., McGuigan M.P., Rogers K.A., Wilson A.M. A comparison of three

horseshoeing styles on the kinetics of breakover in sound horses. Equine Vet J. 2002;34:184-

190.

34. Redden R.F. 18º elevation of the heel as an aid to treating acute and chronic laminitis in

the equine. In: Proceedings. 38th Annu Conv Am Assoc of Equine Practnr 1992;38:375-379.

35. Hansen N., Buchner H.H., Haller J., Windischbauer G. Evaluation using hoof wall strain

gauges of a therapeutic shoe and a hoof cast with a heel wedge as potential supportive

therapy for horses with laminitis. Vet Surg. 2005;34:630-636.

36. Lawson S.E.M., Chateau H., Pourcelot P., Denoix J.M., Crevier-Denoix N. Effect of toe

and heel elevation on calculated tendon strains in the horse and the influence of the proximal

interphalangeal joint. J Anat. 2007;210:583-591.

37. Crevier-Denoix N., Roosen C., Dardillat C., Pourcelot P., Jerbi H., Sanaa M., Denoix

J.M. Effects of heel and toe elevation upon the digital joint angles in the standing horse.

Equine Vet J Suppl. 2001;33:74-78.


32

38. Chateau H., Degueurce C., Denoix J.M. Effects of egg-bar shoes on the 3-dimensional

kinematics of the distal forelimb in horses walking on a sand track. Equine Vet J Suppl.

2006;36:377-382.

39. Hinterhofer C., Stanek C., Haider H. The effect of flat horseshoes, raised heels and

lowered heels on the biomechanics of the equine hoof assessed by finite element analysis

(FEA). J Vet Med 2000;47:73-82.

40. Eastman T.G., Honnas C.M., Hague B.A., Moyer W., Dieter von der Rosen H. Deep

digital flexor tenotomy as a treatment for chronic laminitis in horses: 35 cases (1998-1997). J

Am Vet Med Assoc. 1999;214:517-519.

41. Allen Jr. D., White II N.A., Foerner J.F., Gordon B.J. Surgical management of chronic

laminitis in horses: 13 cases (1983-1985). J Am Vet Med Assoc. 1986;189:1604-1606.

42. Hunt R.J., Allen D., Baxter G.M., Jackman B.R., Parks A.H. Mid-metacarpal deep digital

flexor tenotomy in the management of refractory laminitis in horses. Vet Surg 1991;20:15-20.

43. Buchner H.H.F., Savelberg H.H.C.M., Becker C.K. Load redistribution after desmotomy

of the accessory ligament of the deep digital flexor tendon in adult horses. Vet Q Suppl.

1996;18:S70-S74.
33

CHAPTER 3. THE CENTER OF PRESSURE AND LOAD


DISTRIBUTION IN THE FOREFEET OF NORMAL HORSES

To be submitted to the Journal of the American Veterinary Medical Association

Jennifer A. Schleining, DVM; Scott R. McClure, DVM, PhD; Timothy R. Derrick,

PhD; Chong Wang, PhD

From the Departments of Veterinary Clinical Sciences (Schleining, McClure),

Kinesiology (Derrick), Veterinary Diagnostic and Production Animal Medicine (Wang), and

Statistics (Wang), Iowa State University, Ames, IA 50011

Abstract

Objective – To evaluate the ability of pads created from industrial foam insulation sheeting

to redistribute loads placed on normal weight bearing structures of the foot and shift the

location of the center of pressure palmarly. The overall goal was to assess the ability of foam

pads to decrease the load on the laminar structures with the long-term goal of providing an

evidence-based approach to treatment of acute laminitis.

Design - Self-controlled study with repeated measurements

Animals – 25 sound mature horses

Procedures – Both right and left forefeet from each horse were included in the study. Center

of pressure data and solar load distribution patterns were recorded during a five second trial

using a commercial pressure measurement system prior to placement of foam sole support.

These measurements were repeated at 0, 6, 12, 24, and 48 hours after placement. Total
34

contact surface area, contact pressure, peak contact pressure, and center of force positions

were then compared using a linear mixed model with repeated measurements.

Results – Total contact surface area was increased significantly at all time points while

contact pressure and peak contact pressure were significantly decreased at all time points

following application of foam sole supports. Immediately following application of sole

support, the position of the center of pressure was significantly moved anteriorly. However,

for the remaining time periods, there was a trend of palmar movement of the center of

pressure and by 48 hours the center of pressure was significantly positioned more palmarly

than prior to application of the foam supports.

Conclusions and Clinical Relevance - The results of this study support the use of foam sole

supports as an effective, economical, and immediate treatment for acute laminitis.

Introduction

In the normal horse, sensitive lamina on the dorsal surface of the third phalanx

interdigitate with the insensitive lamina on the deep surface of the hoof wall effectively

attaching the third phalanx (coffin bone) to the hoof capsule.1 Laminitis has afflicted the

equine population for centuries and continues to be a significant contributor to equine

morbidity.2 In a recent study, 13% of all equine facilities in the United States reported a case

of laminitis on their premise within the previous 12 months.3,4 The American Horse Council

reports that nearly 200,000 animals per year are affected with laminitis.5 The disease can be

crippling, life-threatening, elicit signs of severe pain, and often ends the athletic career of

affected horses.6 Although difficult to accurately quantify, the ramifications of lameness and
35

laminitis on the horse industry are substantial. The economic cost of lameness in 1998 was

estimated at $678 million with 110 days of lost use per lameness event.7

Multiple etiologies for laminitis have been proposed and can be categorized into three

mechanistic processes: 1) Those involving a vascular/hemodynamic mechanism; 2) a

toxic/metabolic/enzymatic mechanism, and 3) a traumatic/mechanical process.8 It is believed

that the onset of laminitis is likely multi-factorial, and therefore, it is difficult to identify a

single mechanism of action. Many in vitro experiments have provided insight to potential

pathways for the development of laminitis but they are difficult to confirm in vivo.8 While the

exact etiology of laminitis remains elusive, the stages of laminitis can be classified into four

phases. These include developmental, acute, subacute, and chronic.2

Treatment is dependant on the phase of laminitis. Acute laminitis should be

considered an emergency as the opportunity for possible successful intervention is relatively

short at 72 hours.2,9 Early recognition and institution of treatment may potentially prevent or

minimize displacement of the coffin bone and change the course of the disease.9 Horses with

radiographic signs of displacement of the third phalanx have a guarded prognosis for return

to athletic soundness and even survival.6 There is considerable controversy regarding the

best way to approach and treat laminitis in the acute phase.10 Many treatments have been

proposed and are generally based on empirical evidence, clinician/farrier preference, and past

successes. Often one treatment is attempted, and when that treatment fails to elicit an

improvement, another is tried. Treatment of acute laminitis can be a frustrating obstacle for

owners, farriers, and veterinarians alike. It is not possible to predict which cases will have

catastrophic outcomes and which ones will improve with little intervention.11 At this time,
36

the goals of treatment of acute laminitis are mainly supportive – relieve pain, halt or slow

progression of the disease, and enhance recovery.12

Recent interest in utilizing an evidence-based approach to medicine highlights the

need for high-quality studies to substantiate these treatments.13 Current treatments for

laminitis include stall confinement, shoe removal, bedding the horse in sand or deep

shavings, application of a supportive synthetic material to the sole to redistribute weight

bearing over a larger surface, beveling the toe to decrease breakover, hoof wall resection,

hoof wall grooving, and a number of different methods to elevate the heel.12 Additionally,

administration of nitroglycerin with or without an endothelin receptor antagonist,14,15

therapeutic shoes and hoof casts9,16, frog supports17, vasodilator (i.e. Isoxsuprine and

acepromazine) therapy18,19, and prolonged limb cryotherapy20,21have been utilized. Non-

steroidal anti-inflammatory medications, hemorrheologic agents (i.e. Pentoxifylline) and

dimethylsulfoxide (DMSO) have also been advocated.19,22

This study evaluates the effect of the application of industrial foam insulation

sheeting (“blue foam”) to the sole of the foot. The popular belief is that the support offered

by the foam redistributes the weight of the horse from mainly being borne by the hoof wall to

include the entire bottom of the foot.10,17 This would then decrease primary weight bearing

on the hoof wall and laminar structures and redistribute weight to the sole and frog. In

addition, it may provide support to the digital cushion and tissues between the coffin bone

and the sole. To this effect, prevention of laminar separation may be possible.

The purpose of this study was to evaluate the ability of foam sole supports to increase

the weight bearing surface area of the foot, decrease contact pressure, move the center of

pressure palmarly thereby decreasing the load exerted by the deep digital flexor tendon, and
37

validate its use as an effective means of minimizing load on the laminar structures with the

long-term goal of providing an evidence-based approach to treatment of acute laminitis of the

foot. We hypothesized that the weight bearing surface area in the forefeet of horses would be

increased, the contact pressure decreased, and the center of pressure would be moved

palmarly with placement of commercial blue foam.

Materials and Methods

Twenty five healthy, mature horses (mean age 11 years, range 3-25; mean weight

493kg, range 311-667) were used in this study. There were 10 Quarter Horses, 3 Paints, 2

Thoroughbreds, 2 Arabians, 2 Appaloosas, 2 Friesian crossbreds, 1 Haflinger, 1 Morgan, 1

Thoroughbred crossbred, and 1 Arabian crossbred. Each horse was required to have a history

of regular foot care, currently be barefoot, and have had no previous history of laminitis.

Prior to inclusion in the study each horse was determined to be healthy based on a normal

physical examination including attitude, rectal temperature, pulse rate, respiratory rate, and

digital pulses and be free of lameness. Physical inspection of each foot was used to identify

and exclude horses with divergent growth rings, prolapsed soles, and defects at the coronary

band. Radiographs were obtained of each front foot to confirm absence of previous laminitis

(i.e. displacement of the third phalanx, third phalanx remodeling, etc.). Horses were housed

in individual stalls with wood shaving bedding over rubber mats, allowed free access to

water, and fed a grass/alfalfa mix hay twice daily. Daily monitoring of general attitude, feed

intake, water intake, urination and defecation was performed. This study was approved by

Iowa State University’s Institutional Animal Care and Use Committee.

Study Design
38

Due to the need for equal weightbearing on both front feet during each condition of

the study it was necessary to employ a block design. Each front limb of all horses was

subjected to two test conditions and served as its own control. In the first (control) condition

each forefoot was thoroughly cleaned with a hoof pick and wire brush and positioned on a

high-resolution pressure mata on a smooth, level, concrete surface. Each horse was allowed

time to stand calmly and evenly. Care was taken to ensure each horse was standing squarely.

Center of pressure data and solar load distribution patterns were then recorded during a five

second trial at a sampling frequency of 100 Hz. If the horse moved during the sampling

time, that trial was terminated and a new trial initiated. Following data collection of the

control condition, a foam sole support was placed on each front foot initiating the treatment

condition. The horse was then allowed to briefly bear weight on each foam support prior to

positioning each foot again on the pressure mat for data collection at time 0. The horse was

returned to its stall and data collection repeated at time points 6, 12, 24, and 48 hours.

Calibration of the pressure mat occurred prior to data collection at each time period.

Sole Supports

Each foot was placed on a section of 3.8cm (1.5 inch) thick industrial foam closed

cell insulation sheetingb to obtain an outline of the hoof. The foot was then removed and the

foam cut to match the perimeter of the hoof. A foot bandage to secure the foam to the sole

was created from approximately 35cm strips of duct tape placed perpendicularly to each

other until it was roughly 1.5 times the diameter of the foam cutout. The foam cutout was

then placed on the center of the duct tape and positioned in contact with the sole of the foot.

The duct tape was then folded proximally to provide adherence to the hoof wall securing the

foam. Wraps of tape circumferentially around the hoof wall were then used to further secure
39

the duct tape. A layer of elastic tapec was used proximally to prevent shavings from

interfering with the duct tape. (Figure 1) If the horse did not bear weight squarely on the

foam support as determined by visual inspection, (i.e. the support slipped during initial

weight bearing) a new foam cutout was created and replaced.

Solar Load Distribution and Center of Pressure Measurements

A high-resolution commercial pressure measuring system connected to a computer

was used to record pressure distribution patterns for each foot.a The thin-film (0.18mm)

tactile pressure mat sensor is composed of 8448 evenly distributed individual pressure

sensing elements arranged in rows and columns across the sensor surface with a spatial

resolution of 3.9 sensing elements per cm2. The dimension of each sensing element is 0.508

cm x 0.508 cm with each element separated by 0.508 cm. A custom software packaged

calculated the total contact surface area, total contact pressure, and peak contact pressure for

each frame of data. Center of pressure was output as x and y coordinates on the pressure mat

grid. A consistent coordinate system was created with the horizontal x-axis defined by a line

connecting the heels. This was done for the purpose of standardizing the center of pressure

location allowing for accurate comparison. The axis origin was located at the medial heel of

the right foot and lateral heel of the left foot. From the data obtained, the initial x and y

coordinates for the center of pressure were determined by the investigators (JAS and TRD)

and converted to the standard coordinate system (x’ and y’) using the following formulas.

The Greek symbol α denotes the calculated angle of rotation. (Figure 2)

x’ = xcosα + y sinα

y’ = -xsinα + ycosα
40

Center of pressure was defined as the mathematical location of the point of action of the

ground reaction force on the foot. The standardized y coordinate was used as the response in

statistical analysis. Contact pressure was defined as the total pressure encountered by the

loaded sensing elements. Peak contact pressure was defined as the pressure of the single

sensing element experiencing the largest amount of load. Total contact surface area was

defined as the surface area of all loaded sensing elements.

Statistical Analysis

For each response, data were analyzed using a linear mixed model with repeated

measurements. Treatment and Time (nested within Treatment) were considered as fixed

effects, while Horse and its interactions with the fixed effects were considered as random

effects. Foot was the subject of repeated measurements. Three structures were considered for

the covariance matrix of the repeated measurements from the same subject: variance

components, compound symmetry and unstructured. Akaike's information criterion (AIC)

was used as a goodness-of-fit statistic for model selection: The covariance structure with the

smallest AIC was chosen for the report. Analysis was performed using the MIXED

procedure in SAS software.e F-tests with Kenward and Roger adjustment to degrees of

freedom were applied for significance of the fixed effects. If a fixed effect was found to be

signficant, post-hoc Tukey's t-tests were applied for pairwise comparisons between group

means. Statistical significance was set at a level of 0.05.

Results

The foam sole supports were well tolerated by all horses and all supports remained in

place during the study interval. For total surface contact area, contact pressure, and center of

pressure location, the unstructured covariance matrix structure gave the best fit to data. For
41

peak contact pressure, a variance component covariance structure gave the best fit. For total

surface contact area, both Treatment and Time were found to be significant. Using Tukey’s

adjustment for multiple comparisons, all pairwise differences between time periods (control,

0, 6, 12, 24, 48) were significant. (Figure 2) For contact pressure, both Treatment and Time

were found to be significant. Using Tukey’s adjustment for multiple comparisons,

differences between the control time and all other times were significant and differences

between time 0 and all other times were significant. (Figure 3) For peak contact pressure

both Treatment and Time were found to be significant. Using Tukey’s adjustment for

multiple comparisons, differences between the control time and all other times (0, 6, 12, 24,

and 48) were significant and differences between time 0 and all other times (6, 12, 24, 48)

were significant. (Figure 4) For center of pressure location Time was found to be significant.

At times 0 and 6, the center of pressure was significantly shifted anteriorly from the control

location with a subsequent trend of palmar movement after time 0. By 48 hours a significant

shift of center of pressure in the palmar direction from the control location was

detected.(Figure 5)

Discussion

The results of this study indicate the use of foam sole support increases the weight

bearing surface contact area, decreases total contact pressure, decreases peak contact

pressure, and shifts the center of pressure to the palmar aspect of the foot for at least 48

hours. Recruitment of a larger surface area on the sole of the foot reduces the weight bearing

demand on the hoof wall and laminae. While the importance of recruiting the sole and frog

to distribute the load placed on the foot during episodes of developmental and acute laminitis

is recognized by the majority of practitioners and farriers, the means by which to do so are
42

not as straightforward. This is supported by the myriad of home-made and commercially

available products with varying degrees of evidence that weight bearing is

altered.16,23,24,25,26,27,28 Foam supports have been advocated by many practicing veterinarians

and farriers, but scientific evidence for its use has previously been unavailable.10,12,19,29

Our study shows that total surface contact area is significantly increased up to 48

hours after placement of foam sole supports. However, it is important to note that while

there was still a significant increase in surface area at 48 hours over the control condition,

after time 0 there was a significant decrease in surface area at each time point compared to

the previous time point likely due the conformability of the closed-cell industrial foam.

Twelve hours after sole support placement 10 of 50 (20%) feet already had dimensions of

varying size that were devoid of any weight bearing in the areas of the sole and frog that had

previously borne weight. At 24 hours, 23 of 50 (46%) showed similar characteristics and by

48 hours this number increased to 42 of 50 (84%). By the end of the study 16 of the 50 foam

sole supports (32%) were worn through exposing the toe of the foot. The authors recognize

that this study was performed in normal ambulatory horses, some of whom spent

considerable time walking about their stalls, and this may have been a contributory factor in

foam wear. Yet, if practitioners are faced with an acutely laminitic horse that is reluctant to

lay down and spends most of its time standing, the results of this study would be expected to

apply.

In a study evaluating the effect of a polyurethane filled standard steel shoe on

pressure distribution in normal feet, there was no difference in pressure distribution pattern or

mean pressure between horses with standard shoes and those with polyurethane filled shoes

when horses were on a non-deformable, concrete surface. Significance was found in both of
43

these variables, however, when horses stood on a deformable surface.27 Our horses were

housed on concrete floors covered with rubber mats and wood shavings which may have had

an effect on how the foam was compressed. The shavings could allow for further

compression of the foam against the concave sole and frog. Consequently, when the horse is

removed from the shavings, the concavity remains. During data collection the horses stood

on the pressure mat on a level concrete surface without shavings between the mat and the

foot. This could explain the areas devoid of weightbearing observed at 12, 24, and 48 hours.

As the weight of the horse molded the foam to the contours of the foot, the contact

pressure steadily and significantly decreased until 6 hours after application. Since pressure is

a measurement of force over area this result was not unexpected. However, after 6 hours,

there was no further significant decrease in contact pressure. Likewise, the peak contact

pressure decreased significantly following application of the supports and remained

significantly decreased from the control condition throughout the study. But when compared

to the peak pressure immediately following foam placement (Time 0), the peak pressures at

the remaining time periods were significantly increased.

In the front feet, the center of pressure at mid-stance is usually located in the cranial

medial quarter of the foot.30,31,32 However, center of pressure (also termed ‘center of force’)

is dependent on leg and foot conformation, the manner in which the horse is standing over its

body mass, position of the foot in the stance phase, and shoeing and trimming

methods.27,30,32,33,34,35 For these reasons, special care was taken to ensure horses were

standing squarely and comfortably before recording any data. A palmar shift in the center of

pressure decreases the moment arm acting at the distal interphalangeal joint, thereby

decreasing the stress on the third phalanx from the deep digital flexor tendon.36 This is an
44

important concept in the acute phase of laminitis where minimizing the pull of the deep

digital flexor tendon may be desirable.37 The significant anterior movement of the center of

pressure at the time of foam placement was not expected. The center of pressure did not

return to the control location until between 12 and 24 hours and was not significantly shifted

palmarly until 48 hours after wear. It is not likely that the foam cutout was physically

weaker at the toe as it is uniformly constructed and the anterior movement was not isolated to

just a few horses. It could be explained as a reaction to an unfamiliar weight bearing surface

and exposure to a new situation by the horses as a change in their stance. The clinical

significance of this finding, however, would indicate that it would be desirable to maintain a

foam support for at least 48 hours to benefit from a palmar shift in center of pressure.

The method of treatment of acute laminitis is a controversial topic. Even consensus

on the appropriate use of foam supports is not established. Some practitioners advocate the

use of two layers of foam rather than one. Some replace the support altogether at 24 hours.

Agreement on the appropriate thickness of the foam is not recognized. According to our

data, foam supports provide a significant increase in weightbearing surface area and a

significant decrease in contact pressure for 48 hours and a significant palmar movement of

the center of pressure between 24 and 48 hours. While recognizing the use of normal horses

as being a limitation of this study, the scientific evidence presented here suggests the use of

foam sole supports as described holds promise in the treatment of early laminitis. Using the

results of this study, further investigation into this economical and effective treatment can

continue. Additionally, further studies of this treatment in a population of acutely laminitic

horses are indicated.


45

a. Matscan HR MatTM 7101E, Tekscan, Inc., South Boston, Massachusetts

b. Styrofoam®, Dow Chemical Company, Midland, Michigan

c. Elasticon, Johnson & Johnson Co., Skillman, New Jersey

d. HR Mat Research v. 6.3, Tekscan, Inc., South Boston, Massachusetts

e. Version 9.1.3 Service Pack 4, SAS System for Windows, SAS Institute Inc., Cary, North

Carolina

References

1. Dyce KM, Sack WO, Wensing CJG. Textbook of Veterinary Anatomy, Second Edition.

WB Saunders Company: Pennsylvania, 1996. pp.595-600.

2. Hood DM. Laminitis in the horse. Vet Clin North Am Equine Pract. 1999;15:287-294.

3. Wagner IP and Heymering H. Historical perspectives on laminitis. Vet Clin North Am

Equine Pract. 1999;15:295-309.

4. Kane AJ, Traub-Dargatz J, Losinger WC, Barber LP. The occurrence and causes of

lameness and laminitis in the U.S. horse population, in Proceedings. 46st Annu Conv Am

Assoc of Equine Practnr 2000;46:277-280.

5. The Economic Impact of the Horse Industry on the United States. American Horse

Council, 2007
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6. Eades SC, Holm AMS, Moore RM. A review of the pathophysiology and treatment of

acute laminitis: Pathophysiologic and therapeutic implications of endothelin-1, in

Proceedings 48th Annu Conv Am Assoc Equine Practnr 2002;48:353-361.

7. United States Department of Agriculture 2000. Lameness and Laminitis in U.S. Horses.

USDA:APHIS:VS, CEAH, National Animal Health Monitoring System. Fort Collins, CO

#N318.0400.

8. Moore RM, Eades SC, Stokes AM. Evidence for vascular and enzymatic events in the

pathophysiology of acute laminitis: which pathway is responsible for initiation of this process

in horses? Equine Vet J 2004;36:204-209.

9. Redden RF. Shoeing the laminitic horse, in Proceedings. 43rd Annu Conv Am Assoc

Equine Practnr 1997;43:356-359.

10. O’Grady, S. Foot Care. in Concise Guide to Laminitis in the Horse. Ed. David W.

Ramey, Trafalgar Square Publishing: Vermont, 2003. pp. 65-76.

11. Swanson TD. Clinical presentation, diagnosis, and prognosis of acute laminitis. Vet Clin

North Am Equine Pract. 1999;15:311-319.

12. Parks AH, Balch OK, Collier MA. Treatment of acute laminitis: supportive therapy. Vet

Clin North Am Equine Pract. 1999;15:363-374.


47

13. Brown DC. Outcomes based medicine in veterinary surgery: Getting hard measure of

subjective outcomes. Vet Surg 2007;36:289-292.

14. Gilhooly MH, Eades SC, Stokes AM, Moore RM. Effects of topical nitroglycerine

patches and ointment on digital venous plasma nitric oxide concentrations and digital blood

flow in healthy conscious horses. Vet Surg 2005;36:604-609.

15. Eades SC, Stokes AM, Moore RM. Effects of an endothelin receptor antagonist and

nitroglycerin on digital vascular function in horses during the prodromal stages of

carbohydrate overload-induced laminitis. Am Journ Vet Res 2006;67:1204-1211.

16. Hansen N, Buchner F, Haller J, Windischbauer G. Evaluation using hoof wall strain

gauges of a therapeutic shoe and a hoof cast with a heel wedge as potential supportive

therapy for horses with laminitis. Vet Surg 2005;34:630-636.

17. Pollitt CC. Therapeutic Shoeing. in Equine Laminitis. Ed. Chris Pollitt, Rural Industries

Research and Development Corporation: Barton, Australia, 2001. pp.79-93.

18. Erkert RS and Macallister CG. Isoxsuprine hydrochloride in the horse: a review. J vet

Pharmacol Therap 2002;25:81-87.


48

19. Stokes AM, Eades SC, Moore RM. Pathophysiology and treatment of acute laminitis.

In:Reed S, Bayly W, Sellon D, 2nd ed. Equine Internal Medicine. St. Louis, MO: Elsevier

2004;522-531.

20. Pollitt CC and Van Eps AW. Prolonged, continuous distal limb cryotherapy in the horse.

Equine Vet J 2004 36(3):216-220.

21. Van Eps AW, Pollitt CC. Equine laminitis: cryotherapy reduces the severity of the acute

lesion. Equine Vet J 2004 36(3):255-260.

22. Brumbaugh GW, Lopez HS, Sepulveda MLH. The pharmacologic basis for the treatment

of developmental and acute laminitis. Vet Clin North Am Equine Pract. 1999 Aug;15(2):345-

362.

23. Goetz TE. Anatomic, hoof, and shoeing considerations for the treatment of laminitis in

horses. J Am Vet Med Assoc1987;190:1323-1332.

24. Olivier A, Wannenburg J, Gottschalk RD, et al. The effect of frog pressure and

downward vertical load on hoof wall weight-bearing and third phalanx displacement in the

horse – An in vitro study. J S Afr Vet Assoc 2001;72:217-227.

25. Goetz TE. The treatment of laminitis in horses. Vet Clin North Am Equine Pract

1989;5:73-108.
49

26. Eustace RA, Caldwell MN. Treatment of solar prolapse using the heart bar shoe and

dorsal hoof wall resection technique. Equine Vet J 1989;21:370-372.

27. van Heel MCV, Back W. Ground surface and poly-urethane (PU) filling alter the

pressure distribution pattern in square standing horses. Pferdeheikunde 2006;22:592-596.

28. Baxter GM. Acute laminitis. Vet Clin North Am Equine Pract 1994;10:627-642.

29. Divers TJ. Prevention and treatment of thrombosis, phlebitis, and laminitis in horses with

gastrointestinal diseases. Vet Clin North Am Equine Pract 2003;19:779-790.

30. Hood DM, Taylor D, Wagner IP. Effects of ground surface deformability, trimming, and

shoeing on quasistatic hoof loading patterns in horses. Am Journ Vet Res 2001;62:895-900.

31. Hood DM and Jacobson AC. The principles of equine hoof wall conformation. In: Hood

DM, Wagner IP, Jacobson AC eds. Proceedings of The Hoof Project. College Station: Texas

A&M University, 1997;2-20.

32. van Heel MCV, Barneveld A, van Weeren PR et al. Dynamic pressure measurements for

the detailed study of hoof balance: The effect of trimming. Equine Vet J 2004:36:778-782.
50

33. Wilson AM, Seelig TJ, Shield RA, et al. The effect of foot imbalance on point of force

application in the horse. Equine Vet J. 1998;30:540-545.

34. van Heel MCV, Moleman M, Barneved A, et al. Changes in location of centre of

pressure and hoof-unrollment pattern in relation to an 8-week shoeing interval in the horse.

Equine Vet J 2005;37:536-540.

35. Roepstorff L, Johnston C, and Drevemo S. The effect of shoeing on kinetics and

kinematics during the stance phase. Equine Vet J Suppl 1999;30:279-285.

36. Buchner HHF. Distal limb internal dynamics: joint moments, tendon forces, and lessons

for orthopedic shoeing in Proceedings. 51st Annu Conv Am Assoc of Equine Practnr

2005;51:134-140.

37. Hood DM. The mechanisms and consequences of structural failure of the foot. Vet Clin

North Am Equine Pract 1999;15:437-461.


51

Figure 2-1. Foam pads immediately following placement. Each horse was allowed time to

stand calmly and evenly. Care was taken to ensure each horse was standing squarely and

looking straight ahead during data collection.

y’

α
x’

Figure 2-2. A consistent coordinate system was created with the horizontal x-axis defined by

a line connecting the heels. This was done for the purpose of standardizing the center of

pressure location allowing for accurate comparison. The axis origin was located at the

medial heel of the right foot and lateral heel of the left foot. From the data obtained, the

initial x and y coordinates for the center of pressure were determined by the investigators

(JAS and TRD) and converted to the standard coordinate system (x’ and y’). α denotes the

calculated angle of rotation.


52

b
c
d
e
f

Figure 2-3. Mean ± SD of total surface contact area over time. Significant differences

between all time periods were detected. a-fDifferent letters indicate a significant (p<0.05)

difference between time points.


53

c c
c c

Figure 2-4. Mean ± SD total contact pressure over time. A significant difference between the

control time and all other times and a significant difference between time 0 and all other
a-c
times were detected. Different letters indicate a significant (p<0.05) difference between

time points.
54

c
c
c
c

Figure 2-5. Mean ± SD of peak contact pressure over time. Significant differences between

the control time and all other times and significant differences between time 0 and all other
a-c
times were detected. Different letters indicate a significant (p<0.05) difference between

time points.
55

b b,c
a,c,d

a a,e
e

Figure 2-6. Mean ± SD of the least squares means of the position of the center of pressure on

the dorsal-palmar axis of the foot over time. Significant differences between the control

condition and time 0 and between control and 48 hours were detected. a-eTime points not

having a common letter are significantly (p<0.05) different.


56

CHAPTER 4. General Conclusion

General Discussion

There is a general paucity in the scientific evidence for many current treatments for

laminitis. Our documentation of the benefit of foam sole supports fills only a small void, but

provides an important stepping stone for further assessment of approaches to treatment. We

know that a major factor in phalangeal displacement begins with disruption of the basement

membrane of the laminae.1 Pharmacologic intervention will likely take precedence in

preventing displacement at this level. Before that can occur, however, a distinct etiologic

mechanism must be identified. In the meantime, a biomechanical approach to treatment and

prevention will be important. It is conceivable that more than one approach may be more

beneficial than one alone. Raising the heels to decrease load from the deep digital flexor

tendon while providing solar support appears promising.2 Additionally, recruiting the sole

and/or frog to bear weight and decrease load on the hoof wall and laminae seems rational in

the short developmental and acute phases.

Direction of Future Studies

Our study assessing a foam sole support requires validation in clinical cases and is the

next logical step in continuation of the work presented. Specific questions that need to be

addressed include how to best minimize the force of the deep digital flexor tendon on the

third phalanx and how to best manage the foot to achieve less force on the laminae while still
57

providing an owner with a reasonable outcome. While the obvious need for identification of

the pathologic mechanism responsible for laminitis is inherent, biomechanical assessment of

current treatment strategies is equally important. Providing scientific evidence to both

support and refute laminitis treatments serves to unite practitioners and farriers with the

ultimate goal of benefiting the horse. Future studies should focus on improving our

understanding of the biomechanical consequences of laminitis, so accurate assessment of

treatment can follow. Additionally, research should identify the effect of different treatment

mechanisms on the forces acting on the laminar junction. Development of strain gauges that

can be inserted through the hoof wall in a minimally-invasive manner to accurately detect

strain at the laminar junction could provide important information about the effect of

different treatment mechanisms. The potential of finite element modeling in predicting loads

under simulated conditions lends promise as an alternative to inducing laminitis in normal

horses. However, current models of the horse foot will require refinement before being able

to use them accurately.3,4

References

1. Pollitt C.C. Basement membrane pathology: a feature of acute equine laminitis. Equine Vet

J. 1996:28;38-46.

2. Hansen N., Buchner H.H., Haller J., Windischbauer G. Evaluation using hoof wall strain

gauges of a therapeutic shoe and a hoof cast with a heel wedge as potential supportive

therapy for horses with laminitis. Vet Surg. 2005;34:630-636.


58

3. Thomason J.J., McClinchey H.L., Jofriet J.C. Analysis of strain and stress in the equine

hoof capsule using finite element methods: comparison with principal strains recorded in

vivo. Equine Vet J. 2002;34:719-725.

4. Hinterhofer C., Stanek C., Haider H. Finite element analysis (FEA) as a model to predict

effects of farriery on the equine hoof. Equine Vet J Suppl. 2001;33:58-62.

Related Interests