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Pathogenesis of Supporting Limb Laminitis: Four Questions

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Abstract

Despite how far we’ve come with laminitis research, there are still some gaps in our understanding of this destructive disease. Supporting limb laminitis (SLL) is a veritable dark corner when it comes to our goal of fully elucidating the pathogenesis and thus the prevention of all forms and presentations of laminitis. We do know that SLL occurs in the foot of the contralateral or supporting limb in horses with a severe, unilateral lameness that persists for more than a couple of weeks. So, clearly mechanical load or overload is a primary factor in its pathogenesis. But why? The equine hoof wall has been said to be “overengineered,” given that during normal locomotion the stratum medium experiences only one-tenth of the compressive force required to cause its structural failure. The highly adapted dermal-epidermal connection which anchors the hoof wall to the distal phalanx—now termed the suspensory apparatus of the distal phalanx, or SADP—may be similarly described. The surface area of the SADP in the average-size hoof is calculated to be about 0.8 m sq, which is about 8.6 ft sq. At the gallop, the hoof wall and the SADP withstand compressive and distractive forces of up to 3 times the horse’s body weight without sustaining any apparent damage. So, why does the mere act of standing around cause the SADP to fail? And why does it fail in only some horses with severe, unilateral lameness (reportedly less than 20% of at-risk horses)? Why does it typically not appear until weeks or months after the injury or infection which caused the primary lameness? And why don’t we see it as commonly in foals and yearlings as in adults? If we can answer just these four questions, then we will have a much better understanding of both the pathogenesis of this devastating complication and its prevention.
Pathogenesis of Supporting Limb Laminitis
Four Questions
Christine King, BVSc, MANZCVS, MVetClinStud
August, 2020
Despite how far we’ve come with laminitis research, there are still some gaps in our
understanding of this destructive disease. Supporting limb laminitis (SLL) is a veritable dark
corner when it comes to our goal of fully elucidating the pathogenesis and thus the prevention of
all forms and presentations of laminitis. We do know that SLL occurs in the foot of the
contralateral or supporting limb in horses with a severe, unilateral lameness that persists for more
than a couple of weeks (Peloso et al. 1996; Redden 2004; Baxter and Morrison 2009; van Eps et
al. 2010; Virgin et al. 2011). So, clearly mechanical load or overload is a primary factor in its
pathogenesis.
But why? The equine hoof wall has been said to be “overengineered,” given that during
normal locomotion the stratum medium experiences only one-tenth of the compressive force
required to cause its structural failure (Pollitt 2010). The highly adapted dermal-epidermal
connection which anchors the hoof wall to the distal phalanx—now termed the suspensory
apparatus of the distal phalanx, or SADP—may be similarly described. The surface area of the
SADP in the average-size hoof is calculated to be about 0.8 m2 (Leach and Oliphant 1983),
which is about 8.6 ft2. At the gallop, the hoof wall and the SADP withstand compressive and
distractive forces of up to 3 times the horse’s body weight without sustaining any apparent
damage (van Eps et al. 2010).
So, why does the mere act of standing around cause the SADP to fail? And why does it fail in
only some horses with severe, unilateral lameness (reportedly less than 20% of at-risk horses)?
Why does it typically not appear until weeks or months after the injury or infection which caused
the primary lameness? And why don’t we see it as commonly in foals and yearlings as in adults?
If we can answer just these four questions, then we will have a much better understanding of
both the pathogenesis of this devastating complication and its prevention.
Why does the SADP fail at rest?
This is the one question for which we have a good answer, based on available data. We don’t
have an experimental model for SLL as we do for laminitis induced by carbohydrate overload,
black walnut extract, or hyperinsulinaemia—and understandably so. Nevertheless, we have a
sound experimental basis for drawing the following conclusions about why the SADP fails at rest
in these horses. The mechanism, which involves the combination of chronic weight-bearing load
and arterial occlusion, has recently been explained and illustrated in detail (van Eps et al. 2010),
so just a brief review should suffice here.
Arterial occlusion under load
We’ve known for some time that, when the foot is fully loaded, vascular filling in the
lamellar dermis is substantially decreased or even absent in angiographic studies (Redden 2004;
van Eps et al. 2010). But recently, computer-generated models using computed tomography of
the distal limb under load have revealed some further, and even surprising, insights into this
phenomenon: occlusion of the palmar/plantar digital arteries occurs at various levels, including
sites proximal to the coronary band, depending on the intensity of load (van Eps et al. 2010).
Under conditions of moderate load, the arteries are occluded at the abaxial margins of the
distal sesamoid (navicular) bone and at the proximal aspect of the second phalanx (P2), so blood
flow is occluded particularly to the quarters and heels. Blood flow to other regions of the foot is
relatively unchanged, as the dorsal branches of the palmar/plantar digital arteries are
unobstructed and arterial anastomoses are plentiful within the digital vasculature (van Eps et al.
2010; Pollitt 2010).
Under conditions of heavy load, such that the fetlock sinks within its suspensory apparatus,
the arteries are occluded at or near the base of the proximal sesamoid bones—proximal to dorsal
branching of the digital arteries in the pastern region— so blood flow to the entire foot is
occluded; there is no filling of any artery below the coronary band. The vertical load required to
cause this extent of occlusion in cadaver limbs was less than the weight of the horse’s
forequarters (van Eps et al. 2010).
Role of the deep flexor
It has been proposed that the deep digital flexor tendon (DDFT) causes occlusion of the
vessels in the dorsal lamellar dermis via its pull on the distal or third phalanx (P3) and thus on
the SADP (Redden 2004). In support of that theory, Redden reported a SLL incidence of only
2.3% (2 of 85 horses) with the pre-emptive use of his 18-degree heel wedge and toe cuff system
(Redden 2004). However, the aforementioned models of limb loading clearly show that arterial
occlusion does indeed involve the DDFT, but it occurs both more proximally and more directly
than previously thought. Arterial occlusion occurs prior to the entry of the digital arteries into the
solar foramina of P3—and even proximal to the coronary band—and these locations closely
approximate the points at which the DDFT lies against a bony fulcrum (van Eps et al. 2010;
Davies and Philip 2007).
As the limb is loaded, the tendon is flattened against the navicular bone and the proximal
palmar/plantar processes of P2, or perhaps its associated scutum, and with heavy loads against
the proximal sesamoid bones; as a consequence, the adjacent vessels are compressed. It is likely
that other connective tissues of the digit contribute to this occlusive effect, as the digit is
ensheathed in circumferential and interconnecting layers of relatively inelastic fascia, including
the palmar and digital annular ligaments (Davies and Philip 2007). This small point assumes
greater importance later in the discussion.
Persistence of load
Evidently, these are normal mechanisms which prevent arterial backflow in the absence of
valves and in the presence of hydraulic pressures within the hoof that greatly exceed systolic
blood pressures during peak load (van Eps et al. 2010). However, they clearly are designed to be
intermittent and interspersed with regular, repeated intervals of unloading during which
antegrade arterial flow is restored. No studies have yet been published which demonstrate
changes in arterial blood flow in the supporting feet of horses with severe, unilateral lameness,
but Redden showed using retrograde venography how the simple act of lifting and holding up
one of the horse’s forefeet effectively impedes vascular filling in the loaded foot (Redden 2004).
In a noninvasive study of pedal haemodynamics using near infrared spectroscopy, Hinkley et al.
(1995) showed that either manual occlusion of the palmar digital arteries or lifting and holding
up the contralateral limb for 1 minute caused changes in the dorsal hoof wall recordings that
were consistent with ischemia and reperfusion responses documented in human studies.
Ordinarily, this normal occlusive load effect lasts less than a minute and evidently has no
adverse effects on tissue metabolism within the foot. However, this apparent efficiency can make
for a great deal of trouble when the system that is designed for nearly constant movement
suddenly finds itself at enforced rest and the limb under fairly constant load beyond its normal
share. (Body weight distribution in normal horses is estimated to be 25–30% of total body weight
in each forelimb and 20–25% in each hindlimb [extrapolated from Hood et al. 2001].) Under
such circumstances, ischemic necrosis and/or ischemia-reperfusion injury may result in
degradation of the basement membrane (BM), which is a critical element of the SADP (Pollitt
2010), and thus failure of the SADP under even resting loads.
Glucose deprivation
A related element very likely is an interruption in glucose supply to the basal epidermal cells
of the SADP—living, respiring cells on the far side of the BM which depend on delivery of
glucose and oxygen across the BM from the dermal capillaries. Furthermore, the
hemidesmosomes which anchor the cells to the BM are formed and maintained by glucose-
consuming reactions (Pollitt 2010). In short, a fairly constant supply of glucose to the SADP is
essential to its structural integrity. Concurrent with vascular occlusion would be an interruption
in the supply of both oxygen and glucose to these cells. Pollitt and his group have demonstrated
the great reliance on glucose availability by the epidermal cells of the SADP and how readily the
dermal and epidermal lamellae may be separated under conditions of glucose deprivation (Wattle
and Pollitt 2004).
That’s all well and good, but why does the SADP fail in only some of the horses at risk for
this complication?
Why does the SADP fail in only some at-risk horses?
We don’t yet have any broad epidemiological studies which show the overall incidence or risk
for SLL in horses with severe, unilateral lameness, but from what we can gather, the current
incidence is between 10% and 20% of horses at risk. In two studies published in the mid-1980s,
the incidence of SLL in Thoroughbreds was 37% for those with traumatic disruption of the
suspensory apparatus of the fetlock (Bowman et al. 1984) and 44% for those with staphylococcal
cellulitis of a limb (Markel et al. 1986). However, more recent studies, involving various breeds
and presenting complaints, showed an incidence of between 11% and 16% (Hand et al. 2001;
Levine and Richardson 2007; Fjordbakk et al. 2008; Virgin et al. 2011).
Lame limb loading
Of all the reasons one may posit for why only some of the horses at risk develop SLL—
individual variations in the severity of injury/lameness in the primary limb, in pain
perception/response, in medical/surgical management, etc.—most boil down to the individual
horse’s ability or willingness to take at least some load on the lame limb, thereby allowing the
horse to periodically relieve the weight-bearing contralateral or supporting limb and thus restore
blood flow through the loaded foot.
Hoof shape and horn quality
Redden observed that the risk for SLL in any given horse is also related to the health of that
horse’s hoof. Of particular note, horses with the long-toe, low-heel hoof conformation are
considered to be at increased risk, as are those with poor quality horn (Redden 2004). In other
words, the relative risk is related to the ability of the hoof-skeleton complex to resist failure
under load. But does the combination of constant load (and its vascular consequences) and poor
hoof quality or shape adequately answer why so few—evidently only 1 or 2 out of 10— horses at
risk develop SLL?
Movement
Put another way, might these various data and observations also be painting a picture of
movement, even slight but frequent movement, being protective against SLL? Redden (2004)
observed that the horses who are willing to bear even a little weight on the injured limb and
move about the stall are less likely to develop SLL than are those who stand around all day with
the supporting limb fully loaded. He also noted in a venographic study of a normal horse how
simply getting the horse to flex the carpus a few degrees on the fully loaded limb restored
vascular filling in the foot (Redden 2004). In other words, the horse needn’t lift the foot to
restore vascular filling; simply changing a joint angle by a few degrees was enough.
Hinkley et al. (1995) inadvertently noticed a similar thing. In what was no more than an
admission of technical difficulties, we may find something illuminating: “movement artefacts”
sometimes interfered with the spectroscopy recordings in healthy, unsedated ponies, and light
sedation was required to record smooth patterns of change over the course of the 1-minute data
collection period. Even at rest, movement is a characteristic of normal horses. Healthy horses
have been observed to shift their weight from one forefoot to the other an average of 125 + 55
times/hour, or 1–5 times per minute (Baxter and Morrison 2009; van Eps et al. 2010). In fact, it
has been suggested that the structure and dynamics of circulation in the equine digit indicate that
continuous movement is a requirement for healthy circulation in the distal limb (Baxter and
Morrison 2009).
Other risk factors
Other potential risk factors have been examined in the few epidemiological studies we have,
but none helps answer the question of why only certain horses develop SLL. In a case-control
study of risk factors for the development of SLL, Peloso et al. (1996) found no significant effects
of age, breed, gender, body weight, lame limb (fore- vs. hindlimb), presenting complaint (i.e.
type or location of lesion causing the primary lameness), duration of anaesthesia, whether a cast
was applied to the lame limb, number of days on antibiotics or nonsteroidal anti-inflammatory
drugs (NSAIDs), number of antibiotics or NSAIDs given, or systemic status at admission (rectal
temperature, heart rate, and findings on bloodwork).
In a more recent study confined to the incidence of SLL in horses treated with a cast (half
limb, full limb, or transfixion pin), Virgin et al. (2011) likewise reported no significant
associations with breed, presenting condition (fracture vs. other reason), limb affected (fore- vs.
hindlimb), or the horse’s ability to bear weight on the injured limb at admission. They did report
a significant effect of body weight (p=0.05); however, the effect was small (odds ratio of 1.01),
and only 18 kg separated the mean body weights for the horses that did develop SLL (507 kg)
and those that did not (489 kg).
Although it seems logical that the heavier the horse, the greater the risk, the data do not
support a clear or strong association. Perhaps they would, were we to be able to tease out a
correlation between hoof size relative to body weight and risk for SLL. Turner reported an
association between foot lameness and small hoof size (circumference of the proximal hoof wall)
in relation to body weight (Turner 1992). But obesity and teacup-footed Quarter Horses aside,
hoof size and body size/weight should be fairly well matched in most horses, such that the larger
the horse, the larger the foot (Stachurska et al. 2011)—and, one would expect, the larger the
surface area for loading in the supporting foot.
Systemic changes, such as metabolic or endocrinopathic alterations and systemic
inflammatory response syndrome, occurring in injured or sick horses have also been proposed as
at least contributory factors for SLL (van Eps et al 2010). However, as plausible as they may be,
we cannot yet say whether any of them help us answer the question of why only some—in fact,
relatively few—of the horses at risk develop SLL. Furthermore, if systemic changes are
significantly in play, then we should expect to see SLL more commonly in hospitalised horses
and see laminitis in the other feet as well. Occasionally that happens, but typically SLL is a
localised disease process (Baxter and Morrison 2009). And still to be explained is the time lag
between primary lameness and SLL.
Why does SLL typically not appear until weeks or months after injury/infection?
Peloso et al. (1996) reported that the median interval between admission for a severe, unilateral
lameness and onset of SLL was 40 days; the range was 17 days to 134 days (4.8 months). Those
data fit with other reports (Zamos and Parks 1992; Toppin and Lori 2006; Virgin et al. 2001) and
with our clinical experience. Over 20 years ago, a colleague and I reported on a case of SLL in a
Standardbred stallion that developed 6 months after severe, comminuted fracture of the third
metacarpus and both splint bones (Orsini and Nunamaker 1988). Of more recent memory,
Barbaro developed SLL almost 2 months after the racing injury that caused his breakdown
during the Preakness Stakes.
Why this time lag, when in carbohydrate overload, black walnut extract, and
hyperinsulinaemic models of laminitis clinical signs are evident within 24–48 hours of insult,
and biochemical and histopathological changes are observable in the lamellar dermis within 12–
24 hours after insult? Given that necrosis occurs within hours following ischemic insult or
ischemia-reperfusion injury, and that at-risk horses typically are most lame at admission and in
the first few days or weeks after medical or surgical treatment of the primary condition, one
would expect to see signs of SLL within those first few days if it is simply a matter of load-
induced ischaemia. If there is also a pain or stress component, such as an effect of elevated levels
of adrenaline, cortisol, or other vasoactive substances on digital blood flow, then that, too, should
be most in play at the time of admission and in the first few days or weeks of treatment.
Competing pains...
A common explanation given for this lag is that signs of SLL are not noticed until the pain in
the laminitic supporting limb exceeds that in the primarily injured/infected limb (Redden 2004;
Baxter and Morrison 2009; van Eps et al. 2010). In other words, the horse was too sore on the
injured limb to show signs of pain in the laminitic supporting limb any earlier. However, given
how painful acute laminitis typically appears to be, and that most veterinarians managing horses
with severe, unilateral lameness are fully aware of the risk and the dangers of SLL and monitor
the supporting limb closely, it is doubtful that the development of SLL is being missed in most
cases.
Or cumulative damage?
A more plausible explanation is that there is repeated microdamage in the supporting foot
that is cumulative; when it reaches “critical mass,” the SADP fails. Were arterial occlusion to be
complete, global (i.e. involving the entire foot), and sustained, then we could expect the SADP to
fail within hours or, at most, a day or two after the commencement of full, occlusive loading. But
were it to be incomplete, regional, and/or intermittent, then we could expect the SADP to fail
only after a time, or not at all.
As mentioned earlier, Hinkley et al. (1995) noted that, in unsedated ponies, “major
movement artefacts” altered the haemodynamic pattern in the dorsal hoof wall. The pattern was
interpreted to mean that full arterial occlusion to the foot was not achieved either by manual
compression of the palmar digital arteries or by lifting and holding up the opposite leg, so arterial
collaterals sustained the oxyhaemoglobin concentration in the lamellar dermis. From this, we
may conclude that arterial compromise in the supporting foot may indeed be incomplete,
regional, and/or intermittent, which supports the theory of repeated and cumulative
microdamage—which helps explain both the lag and the variable length of the developmental
period in horses with SLL. In further support of this concept of cumulative microdamage, the
duration of lameness is consistently correlated with the risk for SLL: the longer the horse is
severely lame on the primary limb, the greater the risk for SLL (Peloso et al. 1996; Baxter and
Morrison 2009; Virgin et al. 2011).
Individual threshold and circumstances
There evidently is both a threshold and a set of factors that are unique to each horse or foot,
because not only the timing but the pattern of failure is inconsistent among horses with SLL. In
some cases, the failure is sudden and complete, and is manifested as circumferential detachment
with symmetrical “sinking” or distal displacement of P3 within the hoof capsule; there may also
be detachment of the proximal hoof wall from the coronary band (Peloso et al. 1996; Baxter and
Morrison 2009; van Eps et al. 2010). In other cases, the failure is regional, and perhaps more
gradual, and results in dorsal detachment with rotation of P3 and/or in lateral or medial
detachment with sinking of P3 on that side of the foot (Baxter and Morrison 2009; van Eps et al.
2010).
Delayed hoof wall growth?
Ischaemic delay or defect of hoof wall growth may be another contributor to the time lag.
The primary regions of epidermal cell proliferation in the hoof wall include the coronary
papillae, the germinal layer in between papillae, and the proximal lamellae deep to this area
(Pollitt 2010). Just as in the lamellar region of the hoof wall proper, the BM is a central figure in
the dermal-epidermal connection in these coronary regions and in orderly hoof wall growth
(Pollitt 2010). Furthermore, arteriovenous anastomoses are just as plentiful around the base of
the coronary papillae as they are in the lamellar dermis (Pollitt 2010). Given what we now know
about limb loading and digital blood flow, persistent loading of the supporting foot may impede
blood flow to these germinal centres and slow their growth or otherwise compromise their
structural integrity, rendering them just as vulnerable to load-induced ischaemia as the lamellar
region. In support of this theory, separation or dislocation of the hoof wall from the coronary
band is often a feature of SLL (van Eps et al. 2010).
The perfect storm
If we consider SLL to be a “perfect storm” of contributing factors, with the set of
circumstances unique to each case yet with some common threads, then we are closer to
understanding the pathogenesis of this destructive event, and hopefully to its prevention.
Although, one question remains. It may be the most intriguing of all and the most difficult to
answer from available data; but in its answer may lie a crucial piece of the puzzle.
Why don’t we see SLL as commonly in foals and yearlings?
It is very uncommon to see SLL in horses under 2 years of age. Instead, what we most often see
in the supporting limbs of foals and yearlings with severe, unilateral lameness are angular limb
deformities or flexor tendon laxity (Embertson et al. 1986; Hance et al. 1992; Zamos and Parks
1992; Baxter and Morrison 2009). In other words, the system is breaking down proximal to the
hoof. Granted, the physeal cartilage is a particularly vulnerable point for load-induced damage.
However, even as the physis is being compromised, the young horse is still bearing more than
the normal amount of body weight on its supporting limb, yet it does not develop SLL.
Evidently, the pattern of load distribution in the supporting limb, and probably in the entire body,
of the young horse is somehow protective against SLL.
Body weight?
One might be tempted to assume that the reason we so seldom see SLL in foals and yearlings
is because they are smaller and lighter than adult horses of the same breed. However, not only is
there not a strong association between body weight and SLL in older horses, but this assumption
fails to account for the fact that the feet of foals and yearlings are immature and thus potentially
more vulnerable than those of adults. Bidwell and Bowker (2006) showed that, at birth, the
primary epidermal lamellae of the hoof wall are homogeneous and symmetrically distributed
around the circumference of the hoof. Thereafter, considerable changes occur in the number and
regional density of the lamellae during the first year of the foal’s life, and these changes are
taken to reflect a response to load.
When one considers that, at any age after birth, the hoof mass, the surface area of the SADP,
and the digital vasculature must keep pace with the increases in body weight associated with
growth—weight increases that, at times, may outstrip the pace of the musculoskeletal system as a
whole to accommodate them—then we might expect to see SLL more commonly in the first year
or two of life. Yet seldom do we see SLL in this age group. Why is that, and might we be able to
make use of the mechanism(s) to reduce the risk of SLL in older horses?
Of all the differences we might name between foals and adults, three stand out in relation to
SLL risk: (1) foals lie down more, (2) foals move more, (3) and the foal’s musculoskeletal
system is far more flexible and accommodating than that of an adult.
Foals lie down more
There can be no doubt that static or persistent vertical load is a primary factor in the
development of SLL, nor that reduction in this load is protective against SLL. In their case-
control study of SLL, Peloso et al. (1996) observed that the duration of lameness was short (<18
days) in all but 3 of the control horses with severe, unilateral lameness. Those 3 horses were
severely lame for 3–8 months, but all 3 horses spent several hours per day recumbent. However,
recumbency as a preventive strategy for SLL in adult horses presents some obvious challenges
and drawbacks. The same goes for suspending the horse in a sling or water for prolonged periods
of time.
Foals move more
The other two characteristics of foals are more easily co-opted for use in the adult patient.
We have already explored the importance of movement—of the intermittent, repeated relieving
of full limb loading—for healthy digital blood flow. This factor cannot be overstated. It does
seem to be one of the distinguishing features of those horses at risk that do not develop SLL.
How to get at-risk horses to move more begins with appropriate treatment of the primary
lameness and adequate pain management so that the horse is both able and willing to bear even a
little weight on the lame limb without compromising its repair. Treatment of the primary
lameness is beyond the scope of this discussion. Pain management for the orthopaedic patient
has recently been reviewed (Goodrich 2009). In brief, perioperative analgesia, whether
preoperative, intraoperative, or both, can reduce the amount of analgesia needed postoperatively
and avoid the wind-up phenomenon that is characterised by persistent pain, hypersensitivity, and
allodynia. Furthermore, uncontrolled pain stimulates the synthesis and release of substance P and
calcitonin gene-related peptide (Goodrich 2009), both of which have a vasodilatory effect on the
arteriovenous anastomoses of the equine foot (Molyneux et al. 1994).
By the same token, Pollitt (2010) raised an interesting point about analgesia potentially
damping the protective sensory neural signals from the fully loaded foot which prompt the horse
to periodically unload the foot. Clearly, there is a middle ground with effective pain management
in horses at risk for SLL, wherein pain is still present to a sufficient degree that it exercises its
appropriate protective role, but not to the degree that it inhibits mobility and compromises the
regulation of blood flow in the foot.
As for how to encourage at-risk horses to move more within the restrictions of their primary
condition and its treatment (e.g. internal fixation of a fracture), the observations of Redden
(2004) and Hinkley et al. (1995) indicate that small movements can be enough to restore blood
flow through the digital circulation. The foot need not be raised in order to alter the distribution
of load through the limb—i.e. through the various myofascial structures which support the
limb—and thus relieve the occlusive effect of full load on the digit. Foals seem to make these
small, constant movements naturally; in fact, they are in perpetual motion when standing. In an
adult horse at risk for SLL, it may be necessary for the nursing staff or a physical therapist to
manually encourage the horse to do likewise if the horse is not performing enough self-directed
movement to protect its weighted foot.
Foals are more flexible
Foals are more loose and limber than adults. Put another way, a characteristic of maturity is a
relative stiffening of the musculoskeletal system. Part of that stiffening is an increase in muscle
mass with growth and use, and part is the repetition of patterns or habits of movement and the
structural and neuromuscular adaptations that go along with them. And then there is the
stiffening that develops in response to injury.
The relative flexibility of the foal’s musculoskeletal system allows for more variable
distribution of body weight away from the lame limb and even from the supporting limb into the
uninjured fore- or hindquarters. In addition, the relative flexibility of the foal’s limb allows for
more variable pathways for transmission of the body’s weight down through the supporting limb
to the foot. On the downside, this feature likely contributes to angular limb deformities or flexor
laxity in the immature supporting limb. But on the upside, it appears to protect the immature foot
from SLL.
Somewhat in support of this “stiffness” theory, Virgin et al. (2011) reported that the
incidence of SLL was higher with the use of full-limb and transfixion pin casts than with half-
limb casts. The more extensive casts would reduce flexibility and accommodation in the lame
limb much more than would a shorter cast, although obviously the type of cast used was related
to the location and severity of the condition being treated. However, in that study and in the one
by Peloso et al. (1996), the type of presenting condition was not significantly associated with the
risk for SLL.
Baxter and Morrison (2009) advised attaching a flat pad and wooden block to the underside
of the supporting foot when a cast or splint is used on the lame limb which functionally
lengthens that limb and tips the horse’s weight onto the supporting limb. The pad and block
raises the supporting foot about 2 inches and helps to distribute load more evenly between the
two limbs. This simple strategy may also help reduce the inevitable stiffness of chronic load in
the otherwise functionally shorter supporting limb, which would make it easier for the horse to
move.
Raising the heels on the supporting foot has been shown to reduce the incidence of SLL
(Redden 2004). In addition to improving blood flow in the foot, it likely alters load through the
various fascial structures of the lower limb in a beneficial way. However, Baxter and Morrison
(2009) warned that not all horses are comfortable with heel elevation, and in some horses
extreme heel wedging (more than about 10 degrees) overloads the heels and quarters and can
cause damage in the supporting foot.
Physical therapy that is aimed at relieving tension and stiffness throughout the entire
musculoskeletal system may open up alternate paths for weight transfer similar to those of the
foal that would enable the horse to move more readily and periodically relieve load in the
supporting limb more easily. Even before the horse may safely leave the stall without
compromising repair of the primary condition, stationary weight-shifting exercises can be
performed in the stall. Using his or her own weight against the horse’s body, the therapist shifts a
little of the horse’s weight from the supporting limb onto the uninjured fore- or hindquarters and
slowly repeats the exercise in a slow, rocking motion. As soon as the primary condition allows,
the horse can also be encouraged to move with hand-walking or small pen turnout as appropriate.
The freer the system becomes, the more comfortable the horse becomes and the more willing to
perform small self-directed movements throughout the day that, theoretically, should spare the
supporting foot from SLL.
Final Thoughts
The pathogenesis of supporting limb laminitis clearly involves load-induced ischaemia.
However, clinical experience and the limited study findings we have thus far both indicate that
this mechanism, while correct, is incomplete. Various other factors are at play, the presence and
relative importance of which appear to be highly individualised. It is my fervent hope that, armed
with this greater awareness of the factors that may be involved in any given horse, we can reduce
the incidence of SLL to nearly zero, one horse at a time.
Author’s note: This article was written by me (Christine M. King) on commission in 2012 and published
under another person’s name. This article is some of my best work to date, yet it is credited to someone
else—an act of intellectual dishonesty, the ramifications of which I did not appreciate at the time. This
article is entirely my own original work, exactly as I submitted it. I retain the copyright.
References
Baxter, G.M. and Morrison, S. (2009) Complications of unilateral weight bearing. Vet. Clin.
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The study was conducted to find out the most reliable parameter of the hoof size in relation to the horse body size, exemplified in mares. The mares of four breeds belonging to different origin types were examined: Purebred Arabian, half bred Anglo-Arabian, primitive Polish Konik and Polish Cold-Blood, 77 mares in total. The mares were four to 13 years old, classified into three age groups. Three body measurements were taken: height at withers, chest circumference and cannon circumference. The boniness index (cannon circumference to height at withers ratio) was also defined. After trimming, three left fore hoof measurements were taken: toe length, solar length and hoof width. Total length and width were calculated as a hoof solar size measure. On the basis of the parameters obtained, nine fore hoof to body dimension ratios were defined. To evaluate the results, least squares means analysis was used and correlation coefficients between body parameters (1), between hoof parameters (2), as well as between body and hoof parameters (3) were identified. The results show the hoof to body dimension ratios grow according to the increasing cannon circumference to height at withers ratio. The hoof width to chest circumference ratio was found to be a useful parameter of the hoof size. The means (%) obtained (5.93±0.10, 6.41±0.08, 6.56±0.11 and 7.26±0.09 in Purebred Arabian, Anglo-Arabian, Polish Konik and Polish Cold-Blood horses, respectively) are suggested as standards to which individual ratios in mares of similar breeds may be compared judging the horse's conformation. The age hardly affected the hoof solar size to height at withers ratio in mares four to nine years old.
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