Clinical Diagnosis of Foot and Leg

La me nes s i n C at t l e
Jan K. Shearer, DVM, MSa, Sarel R. Van Amstel, BVSc, M MED VET
b
,
Bruce W. Brodersen, DVM, MS, PhDc,*

KEYWORDS
 Bovine lameness  Cattle lameness  Lameness diagnosis  Locomotor diseases
 Record keeping

KEY POINTS
 Posture and locomotion are important observations for assessment of foot and leg health
in cattle.
 A lameness evaluation should always start with a thorough examination of the foot.
 The diagnosis of foot and claw (hoof) lesions may be determined by considering the
visual appearance of the lesions, foot, or claw zone affected.
 Advances in computer hardware and software have facilitated the capture of lameness
and foot care information on-farm.
 Upper leg lameness presents diagnostic challenges that begin with obtaining a history of
clinical signs and previous treatment, and proceeds with careful observation of posture
and gait, palpation of joints, muscles, tendons and bones; manipulation of the limb to
assess areas of pain, and other diagnostic procedures.

Incidence of clinical lameness exceeds that of most other diseases in many herds.
Detection remains a challenge because cows are good at disguising discomfort. Eval-
uating posture and gait can help to identify the subtle signs of lameness so intervention
can occur before the disorder has progressed. Once a cow is identified as lame, the next
steps are to conduct a thorough examination to determine its source (ie, foot, claw,
upper leg, or elsewhere) and apply an appropriate treatment. In many herds, it all

The authors have nothing to disclose regarding any relationship with a commercial company
that has a direct financial interest in the subject matter or materials discussed in their article
or with a company making a competing product.
a
Dairy Production Medicine, Lameness, Animal Welfare, Department of Veterinary Diagnostic
and Production Animal Medicine, College of Veterinary Medicine, 2436 Lloyd Vet Med Center,
Iowa State University, Ames, IA 50011, USA; b Department of Large Animal Clinical Sciences,
College of Veterinary Medicine, The University of Tennessee, 2407 River Drive, Knoxville, TN
37996, USA; c Veterinary Diagnostic Center, School of Veterinary Medicine and Biomedical
Sciences, University of Nebraska-Lincoln, 1900 North 42nd Street, Lincoln, NE 68506-0907, USA
* Corresponding author.
E-mail address: [email protected]

Vet Clin Food Anim 28 (2012) 535–556

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536 Shearer et al

ends with treatment. Contrasted to dairy cattle, in which the histories of the environment,
handling, and diets of the animals are often known, feedlot cattle often come from
several, often unknown, sources. In those situations, with little knowledge of prior
handling, environment, and rations, feedlot personnel are often working in a black box
when trying to evaluate factors involved in cases of lameness.
Owners or managers may be aware of an increase in overall herd lameness. Until
they know about the occurrence of specific disorders (eg, sole ulcers, white line
disease, or digital dermatitis) and rates of these conditions, it may be hard to identify
underlying causes and develop a rational management strategy to address them. The
collection and maintenance of records are time consuming and represent a significant
cost of doing business. In the United States, compatibility with farm record-keeping
systems such as the Dairy Herd Improvement Association or other systems is an
important objective. This permits data on lameness to be incorporated into the farm’s
database on animals so that as summary reports (on individual cows or on the herd)
are retrieved, other pertinent information (eg, milk production, reproductive status,
etc) can be reviewed. In this article, the authors discuss the next step, which is to
capture this information for better management of individual cows and herd lameness.

CLINICAL DIAGNOSIS OF FOOT LAMENESS

Most lameness in dairy cattle is associated with disorders of the foot. Observation
indicates that nearly 90% of lameness involves the foot. In conditions that affect the
foot, nearly 90% involve the rear feet and most (70%–90%) affect the lateral claw.
Although nutrition is frequently cited as an underlying cause, the distribution of disor-
ders to the outer claw of the rear foot suggests something different. When a cow
develops laminitis, the vascular insult is not limited to the outer claw. All claws are
affected. Result research indicates that lameness is complicated by metabolic
factors,1–4 such as housing and management conditions5 that require prolonged
standing on hard-flooring surfaces and natural weight-bearing forces that contribute
to mechanical overloading of claws as a result of horn overgrowth.6 Therefore, lame-
ness occurs most commonly in the medial claw of front feet and the lateral claw of
back feet. Posture and gait abnormalities may offer some suggestions regarding the
cause of claw lesions. A specific diagnosis requires a careful examination of the foot.
Beyond the underlying metabolic and physical factors associated with claw disor-
ders are infectious disorders of the foot skin and sometimes deeper tissues. These
bear a close relationship to housing and environmental conditions that result in the
contamination of feet with organic matter and moisture. Diagnosis of these conditions
is generally made through the visual observation of lesions.

OBSERVATION FOR DETECTION OF POSTURAL ABNORMALITIES

Much can be learned from just observing an animal and its posture quietly from
a distance. Cows with pain in a foot or feet will naturally attempt to reduce weight
bearing in the affected foot or feet. In Fig. 1, a cow stands with its front legs crossed
because of bilateral sole ulcers in the medial claws. Because more weight is normally
borne on the medial claws, crossing the front legs will eliminate or at least reduce
weight bearing on the medial claws and thus reduce some of the discomfort. A lesion
in the outer claw of the front foot will cause the cow to stand with a base-wide posture
of the front legs. Shifting of weight from one side to the other is also indicative of foot
discomfort and may provide a clue regarding which foot is involved. Lameness is most
often associated with a lesion in the outer claw in the rear legs. In these situations, the
cow will stand with the foot or feet abducted or, as viewed from the rear, with feet in
 Clinical Diagnosis of Foot and Leg Lameness 537

Fig. 1. Standing with front legs crossed as a consequence of bilateral sole ulcers in the
medial claws.

a “cow-hocked” posture. By rotating the claws outward, the cow is able to displace
more weight to the inner claws.

REAR VIEW OF HINDLIMB POSTURE (LEG SCORE SYSTEM)

This system, based on the work of Toussaint Raven,6 is used to make a determination
of a cow’s or herd’s need for trimming. Research has demonstrated a correlation
between hindlimb posture as seen from the rear and overgrowth of the claws. In non-
lame cows that are not experiencing overgrowth of the lateral claws, the back legs are
straight and parallel. As the outer claw of the rear leg becomes overgrown, particularly
at the heel and sole, the cow becomes progressively more cow-hocked (by rotating
her feet outward) in an attempt to displace more weight on the inner claw.
Leg score is determined by the angle of the spine in relation to the interdigital space
created by the outward rotation of the feet. It is graded as 1, normal (no deviation); 2,
17 to 24 deviation, and 3, greater than 24 deviation. Recommendations for the
application of the leg score system are as follows: whole herd trimming is indicated
if (1) less than 40% of the herd attains a score of 1, (2) more than 20% of cows attain
a score of 3, or (3) more than 50% of cows attain a score of 2 or 3.
Other postural abnormalities associated with lameness include lowering of the head
and arching of the spine, shoulders, and hips. Sometimes animals will lean to one side
or the other, attempting to reduce weight bearing on the foot coincident with problem.
A cow with laminitis will stand in a “camped under” (Fig. 2) posture whereby she will
hold both the front and rear legs beneath her. Cows with heel lesions stand on their
toes, which causes the toe to wear more and become shorter. Cows with toe lesions
place more weight on the heels, which results in overgrowth and extension of the toe.
Hyperextension of the fetlock joint with concomitant relaxation of the flexor tendons
may occur in chronic cases. These conformational changes (long heels or long toes)
of the claw horn capsule often require correction during trimming.

OBSERVATION FOR ABNORMALITIES OF GAIT

The most useful of observations for determination of lameness is gait assessment. It is

necessary to know what constitutes normal gait and what to look for when trying to
discern if a cow is lame. Because cows are naturally inclined to disguise discomfort
early, lameness can be difficult to detect.
538 Shearer et al

Fig. 2. Cow with acute laminitis displaying the typical “camped under” posture.

Gait characteristics are altered by conditions that make the surfaces of floors more
or less slippery. On wet, manure-covered concrete floors, cows will alter their gait by
slow walking speeds, changing limb angles and reducing the length of their step, in an
effort to increase stability.7–9 Hardness of the flooring surface will also affect detection
of gait abnormalities. With an earthen surface traction that is more forgiving, signs of
discomfort may be less exaggerated and harder to detect. Gait assessment should be
performed on dry, firm flooring surface.

LOCOMOTION SCORING

Primary characteristics to assess when evaluating locomotion include walking speed

(lame cows walk slower), stride length (lame cows take shorter strides), tracking (does
the back foot come down where the front foot leaves the ground?), weight bearing
(does the cow avoid putting weight on the leg?), posture of the spine (lame cows
tend to arch their back or spine), and head bob (does the head bob up and down
as the cow walks?) (Fig. 3).10–12
Locomotion scoring can be used to assess lameness in individual cows or as a tool
to assess foot health on a herd basis. When used on individual cows, the purpose of
lameness scoring is to identify lame cows for timely intervention, thereby limiting pain
and discomfort for the cow and economic losses to the owner. Locomotion scoring on
a herd basis provides a quick overview of the herd’s lameness status.

Fig. 3. Lame cow with arched back and head lowered.

 Clinical Diagnosis of Foot and Leg Lameness 539

One of the more prevalent locomotion scoring systems is that devised by Sprecher
and colleagues,13 which is based on the observation of spinal posture of cows while
standing and walking. Although Sprecher and colleagues used the system to assess
the effects of lameness on reproductive performance, in recent years the system has
gained popularity as a tool for the early detection of lameness disorders in individual
cows and for assessing herd foot health. Observations require that animals be
observed while standing and walking on a flat surface that provides sound footing.
Scores range from 1 to 5 with 1 indicating normal (ie, a cow that stands and walks
with a flat back and gait is normal); 2 indicates mildly lame (ie, a cow that stands
with a flat back but arches the back when walking has a normal gait); 3 indicates
moderately lame (ie, a cow that has an arched back while standing and walking has
a gait described as short strides in 1 legs); 4 indicates (ie, a cow that has an arched
back while standing and walking and favors 1 limbs); and 5 indicates severely lame
(ie, a cow has an arched back while standing and walking and refuses to place or has
great difficulty placing weight on 1 limbs).

EXAMINATION OF THE FOOT

A thorough examination of the foot is important whether cattle are simply presented
for routine preventative trimming or when observed as lame and presented for further
examination and treatment. When early claw lesions are detected during the course of
preventative trimming, they can be corrected at that time, preventing the possibility of
the lesion progressing to a more serious condition.
Once the cow is properly restrained and the foot is secured, it should be cleaned
with soap and water. Inspect the foot, particularly the interdigital skin and heel bulbs,
for lesions, swelling, or evidence of foreign bodies. Focus on the claws and proceed
with the 3-step functional trimming procedure described by Toussaint Raven.6
Correction of claw horn overgrowth, early lesions, and the reestablishment of the
claw capsule to its normal proportions should be part of every examination. Removal
of superficial layers of horn over the white line regions of the sole and the typical site
for sole ulcers helps to uncover evidence of separation, hemorrhages, or granulation
tissue that might be indicative of claw lesions.
Hoof testers (Fig. 4) are used in cases of lameness when the lesions are not obvious.
The authors’ diagnostics require knowledge of whether there is pain in the claw.14,15
The tester should be applied with firm, consistent pressure to areas where one would

Fig. 4. Hoof tester in use to assess pain in the sole.

540 Shearer et al

expect to find a lesion: the apical region of the toe, along the white line, and over the
typical site for sole ulcers. It may be applied to the dorsal and abaxial wall to test for
lesions underlying the wall or to detect deeper problems such as a fracture of the third
phalanx (P3). It can also be used on the sole to assess sole thickness.16,17 Extreme
flexibility of the sole suggests that the sole is too thin and unlikely to support the
cow’s weight on a firm flooring surface such as concrete.10,17–20
Hoof testing can yield conflicting results as to the specific area affected (ie, foot or
upper leg). Intravenous regional anesthesia can be a very useful diagnostic procedure
to isolate the site of the lesion. The technique consists of placing a tourniquet above
the dewclaw (Fig. 5) and administering approximately 20 mL of 2% lidocaine intrave-
nously in either the medial, lateral, or dorsal digital veins. A 19-gauge butterfly catheter
with a 12-inch extension tube is ideal for conducting this procedure. The needle is
inserted rapidly to its hub and slowly withdrawn until the needle enters the vein and
blood is flowing freely through the catheter. The lidocaine is injected slowly to avoid
damage to the vein. When intravenous regional anesthesia is used for diagnostic
purposes the tourniquet should be left in place for approximately 5 minutes to assure
uniform distribution of the lidocaine to target tissues. The tourniquet is removed and
the animal is released for gait observation. Using this technique, cows that leave
the trim chute and walk away with less observable lameness are likely to have
a problem in the foot. Those that show no improvement probably have a lesion in
the upper leg.14

DIAGNOSIS BY VISUAL APPEARANCE, LOCATION, AND CLAW ZONE AFFECTED

Veterinarians and trimmers alike tend to refer to claw lesions as abscesses or sole
abscesses. In fact, most are either an ulcer, white line disease, or a traumatic lesion
of the sole. Foreign bodies are also common causes of traumatic sole lesions, and
there are many of these, including sharp stones, wire, nails, teeth, and various other
types of materials. The point is that reference to a claw lesion as an abscess or
a sole abscess is useless information from a management standpoint. Knowing that
the claw lesion one observes is an ulcer, white line disease, or a solar puncture,
regardless of whether it has abscessed, offers the most usable information. Much

Fig. 5. Intravenous regional anesthesia using a 19-gauge butterfly catheter and 20 mL of 2%

lidocaine.
 Clinical Diagnosis of Foot and Leg Lameness 541

of the foot work and trimming are done on farms by farm employees or foot trimmers.
Some have a good understanding of proper terms and names for foot conditions and
some who do not. In such cases, one may choose to rely more on the location of the
lesion as identified by means of the claw zone affected.18,21
Foot and claw conditions are diagnosed by visual appearance, taking into consid-
eration the location and the claw zone affected. An ulcer is defined as a full-thickness
defect of the epidermis (horn) that exposes the underlying corium. Ulcers that occur in
the apex of the toe (zone 5) are termed toe ulcers, those occurring at the heel–sole
junction are sole ulcers (zone 4), and those occurring in the heel are heel ulcers
(zone 6) (Fig. 6). Lesions occurring in zone 1, 2, or 3 that correspond to the areas of
the white line are termed white line disease. Beyond ulcers and white line disease,
one may observe traumatic lesions of the sole and/or foreign bodies in zones 1
through 6 of the weight-bearing surface. Lesions occurring in zone 0 are likely to be
interdigital dermatitis, interdigital fibroma, foot rot, or digital dermatitis, and in zone
10, lesions are most often associated with digital dermatitis. If cases of heel erosion
are recorded using a system such as this, they might be noted as lesions occurring
in zone 6.18
Diagnostic details of an individual animal’s lameness disorder are useful for the
proper management of its specific condition; the database necessary for effective
problem solving on a herd basis often requires little more than a simple enumeration
of these events to be meaningful. Large herds tend to be less interested in detailed
information on individuals and more interested in summary statistics that might signal
errors in the areas of cow comfort, feeding, and management. Specific lesion details
(ie, severity, chronicity, size, etc) regarding a toe lesion in zone 5 may offer ideas for
treatment, time to recheck, a prognosis, or possible need for culling of an animal.
No matter how detailed this information is, it does not offer much in answering the
question of the predominant cause of lameness for a particular herd. Knowing, for
example, that 20% of the last 150 cows presented to the trimmer for treatment in
the past 100 days had a lesion in zone 5 provides valuable information as to a possible
cause and where one might want to focus more attention for greater definition of the
problem. Consider the following data set from a large dairy in South Georgia where
record keeping relies almost exclusively on identification of the claw zone affected
by a group of well-trained on-farm trimmers.

Fig. 6. Claw zone diagram from Greenough and Weaver.

542 Shearer et al

Lameness was studied in a large dairy in the southeastern United States.22 Data
collected included records for 4915 cows, of which 1861 had at least one recorded
lameness event:
 20% were thin-sole toe ulcers recorded as lesions occurring in zones 1 and 2 as
a result of a separation of the sole from the white line
 16% were sole ulcers in zone 4
 13% were thin soles, which includes zones 1 through 6
 10% were caused by white line disease in zone 3
 8% were heel ulcers in zone 6
 6% were leg injuries
 4% were injuries that caused upper leg lameness
 2% were toe ulcers associated with laminitis and rotation of P3 in zone 5
 20% were other conditions including digital dermatitis, corkscrew claw, and
foot rot
Annual incidence risk for lameness was determined to be 49.1% and lameness
rates for all lesions were highest during the summer months. In addition to these
descriptive statistics for this herd, researchers were able to determine that as parity
increased, so did incidence rates for thin soles, sole ulcers, white line disease, heel
ulcers, and injuries. Heel, sole, and toe ulcers all occurred with greater frequency
during mid-lactation. Analysis of these data clearly demonstrated that the lameness
problem experienced in this herd was primarily the result of thin soles and thin-sole
toe ulcers, which accounted for 33% of recorded lesions. Thin soles also predispose
to thin-sole toe ulcers and a higher incidence of sole ulcers, white line disease, and
heel ulcers. The recommendation to this dairy based on these data was to apply
rubber flooring to travel lanes, holding areas, and eventually barns as needed to
reduce the rate of claw horn wear.

PROBLEMS WITH INFORMATION ON LAMENESS IN DAIRY RECORDS

The greatest deficiency in the recording of health information has been in the area of
foot care. This is especially interesting as lameness has been cited as the single most
costly clinical disease of dairy cattle. Only in recent time have record-keeping systems
such as Dairy Comp 305 and Dairy Herd Improvement Association records started to
work on better ways to capture lameness information. It is important to point out that
the deficiency is not the result of a failure of trimmers to collect the information. The
problem lies with the inability to efficiently transfer this information to herd records,
where it can be analyzed and interpreted.21
A second problem with lameness data is that they lack uniformity. Trimmers
throughout the country use different terms in their descriptions of foot conditions. In
some cases, the problem is related to language barriers; in others, the person collecting
the information is unfamiliar with the proper terms for the various lameness conditions.
Some dairymen do not understand the information even if proper terms are used. They
need help interpreting the information to make necessary management changes. As
described previously, all too frequently, claw conditions such as ulcers and white line
disease are collectively referred to as sole abscesses or laminitis. So, the information
may be available, it may be difficult to interpret because the terms used are not specific,
or, in the worst case scenario, the information may be erroneous or unknown.21
If record keeping of lameness disorders is to become a routine management prac-
tice on dairy farms, the mechanism for collection of the information must be simple,
convenient, and sufficiently comprehensive to yield information of value in decision
 Clinical Diagnosis of Foot and Leg Lameness 543

making. This information will be of greatest interest to those who are managing lame-
ness conditions in individual cows. For others, information on lameness disorders will
be of more value as a herd monitoring and management tool. There are newer tech-
nologies that combine software and specific computer hardware with the capability
for accomplishing the needs of both. It is beyond the scope of this article to completely
describe these technologies.
The original concept of recording lesions by means of the use of claw zones was
introduced by Greenough and Weaver in 1992. The American Association of Bovine
Practitioners offered a reporting scheme that incorporated the use of a lesion code
along with claw zone to record lameness conditions in 2004.23 There did not seem
to be widespread use of this reporting scheme, in part because most trimming and
foot care is conducted by trimmers and not by veterinarians. A study by Cramer
and colleagues,24 in 2008, demonstrated almost perfect agreement among trimmers
who were taught to use a modified version of this record-keeping system. These
results were corroborated by observations from the study described earlier of the
thin-sole herd in the southeastern United States. Commercial applications of this
system using computer touch-screen technology have been developed in the United
States (Hoof Supervisor, Supervisor Systems, Wisconsin). Additionally, a system
developed in Austria by Dr Johann Kofler and colleagues uses a similar system to
record and analyze foot lesion data.25 Hoof Supervisor has gained widespread accep-
tance in North America (S. Martin, personal communication, 2011).

THE ALBERTA DAIRY HOOF HEALTH PROJECT AND HOOF SUPERVISOR

Beyond the need for information to better understand lameness in individual herds is
the need to understand lameness from a regional, state, province, and national
perspective. This affords the opportunity for herd-to-herd, region-to-region, etc,
comparisons. The best example of this is the Alberta Dairy Hoof Health Project (S.
Martin, personal communication, 2011). As of August 20, 2011, 147 Alberta herds
and 69 herds from British Columbia had contributed trimming records and DHI data
to The Alberta Dairy Hoof Health Project’s hoof health database, including records
for 35,229 individual cows. In Alberta, 48.6% of these cows had one or more of the
14 claw lesions documented by hoof trimmers in this project; in British Columbia,
57.5% of cows trimmed had one or more of these lesions. The top 5 of these lesions
from the Alberta Hoof Health Project are listed in Table 1.

Table 1
Summary data on selected conditions from the Alberta Dairy Hoof Health Project

Alberta British Columbia

Participating farms 147 69
Total distinct cows 27,092 8137
Cows with lesions 13,174 48.6% 4679 57.5%
Digital dermatitis 8164 44.9% 2581 40.3%
Sole ulcer 2999 16.5% 821 12.8%
White line lesion 2559 14.1% 846 13.2%
Sole hemorrhage 1103 6.1% 490 7.6%
Toe ulcer 888 4.9% 335 5.2%

Preliminary results point to a high prevalence of digital dermatitis and claw horn disruption
(S. Martin, personal communication, 2011).
544 Shearer et al

Digital dermatitis was by far the most common lesion observed, accounting for 48%
of all lesions recorded. Next in order of decreasing prevalence were sole ulcer, white
line lesion, sole hemorrhage, and toe ulcer. Combined, these 4 lesions accounted for
41.8% of all lesions recorded. All data were collected by trimmers using Hoof Super-
visor, which forwards the information from the herds to a central source for summari-
zation of the data from both provinces. The long-term objectives of this project are to
determine the most common causes of lameness and the specific areas of hoof health
that need further research (S. Martin, personal communication, 2011).

SPECIFIC DISORDERS OF FEET

Deep Digital Sepsis Conditions
There are at least 3 clinical entities that may be observed: (1) avulsion of the deep
digital flexor tendon and retroarticular space abscess formation, (2) infection of the
distal interphalangeal joint (DIP), and (3) heel abscess (Fig. 7).10–12,14,26
Avulsion of the deep digital flexor tendon occurs after osteitis and a pathologic frac-
ture of the flexor tuberosity of P3. This is most commonly observed as a secondary
complication of a chronic sole ulcer. The lesion begins as an ascending infection
that extends upward through the corium and digital cushion and into the flexor tuber-
osity of P3.10,11,14,26 Other structures that may be involved include the navicular bursa,
deep flexor tendon sheath, and surrounding tissues. Abscess formation in the retroar-
ticular space located between the second phalanx and the deep flexor tendon is
a common sequela. These changes often occur without involvement of the DIP.
Infection of the DIP occurs via 3 primary routes: an ascending infection through the
sole or white line may extend to the joint either (1) proximal to the navicular bone via
the palmar/plantar pouch of the DIP joint that is located adjacent to the retroarticular
space; (2) via breakdown of the ligamentous attachment between the ligamentous

Fig. 7. Infection of the DIP.

 Clinical Diagnosis of Foot and Leg Lameness 545

attachment of the distal part of the navicular bone and P3, or (3) via the extension of
infection from the interdigital skin (foot rot) through the axial joint capsule or dorsal
pouch of the DIP joint capsule.10,11,14,26
Heel abscesses occur most commonly via the extension of a white line disease
abscess (zone 3) or a heel abscess (zone 6). These are often simple to treat as they
often localize in the fibroelastic pad of the heel retinaculum.

Diagnosis of Deep Digital Sepsis Conditions

Foot rot usually presents as a generalized swelling of the foot that extends to or above
the dew claws. In most cases, this swelling is accompanied by a painful necrotic lesion
in the interdigital skin and severe lameness. Although the conditions just described
may be similar in appearance, they are often unilateral in their occurrence. Careful
examination is important for determination of the most likely underlying cause.
Start by cleaning the foot and interdigital skin with soap, water, and a brush.
Examine the foot, claws, interdigital area, and heel bulbs for areas of swelling, injury,
or other abnormality. Assuming all is normal, using a hoof knife, or preferably an angle
grinder with a coarse grinding disk, clean the soles of each claw by removal of a super-
ficial layer of horn that will permit examination of the white line for evidence of sepa-
ration. Also, examine the skin horn junction both axially and abaxially for evidence of
loose horn. If such areas are found, use the hook of the hoof knife to explore the extent
to which the horn is undermined. Remove all loose horn until reaching the point at
which the horn is reattached to the underlying corium.
In the case of retroarticular space abscesses, it is not uncommon to find a chronic
sole ulcer adjacent to the swollen heel (Fig. 8). In most cases, one can find a draining
tract that with pressure on the heel will exude purulent material. This tract should be
gently probed with a teat cannula or other probing device to determine the extent
and location of the abscess capsule. Once the probe is inserted to the full extent of
the tract/abscess, it can be left in place to serve as a guide for surgical correction
of the problem. Gentle probing of draining purulent tracts is a useful diagnostic proce-
dure for determination of the primary location of abscess capsules. In most cases,
there will be evidence of avulsion of the deep flexor tendon, which causes the toe
of the affected claw to rotate upward.

Fig. 8. Retroarticular space abscess. Intravenous regional anesthesia is being applied for
surgical correction.
546 Shearer et al

Septic arthritis of the DIP is characterized by a prominent swelling of the coronet

that extends upward to the fetlock. This condition is sometimes accompanied by a dis-
charging tract on the craniolateral aspect of the coronet that is considered by many to
be near pathognomic for septic arthritis of the distal interphalangeal joint. As with ret-
roarticular space abscesses, animals with septic DIP joints exhibit severe lameness
that is difficult to alleviate even with a foot block applied to the healthy unaffected
claw.10,11,14,26

Fractures of the Claw Capsule and P3

Traumatic fractures of the claw capsule are not uncommon and may occur in a multi-
tude of ways. Sometimes they are accompanied by fracture of P3. These may be
caused by slatted flooring in trailers and barns, rails or side boards in a gate or fence,
or other structural obstruction that results in the claw becoming wedged or stuck and
subsequently dislodged by a rapid twisting, sideward, or other movement of the foot
and lower leg. Extent of the damage and corrective measures begin with intravenous
regional anesthesia and close inspection of the claw for fractures of P3 that may
require removal of the fractured portion of the bone and other permanently damaged
tissues.
Traumatically induced fractures of P3 may also occur without visible evidence of
trauma to the claw horn capsule. Animals that exhibit severe pain in a claw but with
no indication of white line disease, puncture of the sole, or other lesion present a signif-
icant diagnostic challenge that often requires a radiograph for confirmation of the frac-
ture. Diagnostic anesthesia of the foot to determine if pain is in fact coming primarily
from the foot or upper leg is also useful.
Another cause of fracture of the P3 that may not be accompanied by external
evidence on the claw capsule is that related to pathophysiologic factors. These are
sometimes detected radiographically or they may be found during the process of
corrective trimming of toe lesions. Removal of necrotic foul-smelling horn and purulent
material in the toe of the claw sometimes leads to the isolation of a sequestrum that is
actually the apex of P3. Often, removal of the sequestrum and associated necrotic
tissue is sufficient to provide long-term relief.10,11,14

Septic Tenosynovitis
Swelling associated with a complicated claw lesion (septic DIP joint or retroarticular
space abscess) that extends well above the fetlock is highly suggestive of septic teno-
synovitis. Diagnosis may be confirmed by aspirating fluid from the sheath with a needle
and syringe. Sepsis of the tendon and tendon sheath is indicated by a total white cell
count of more than 25,000/mL and a total protein of more than 4.5 g/dL. Ultrasonog-
raphy of the tendons that demonstrates the presence of floating echogenic particles
in the compartments of the flexor tendon sheath may also be used to confirm tenosyn-
ovitis. A 7.5-MHz probe is preferred by these authors for making this assessment.10,14

Injuries/Conditions Involving Loss of the Claw Capsule (Also Known as “Degloving”

Injuries)
Degloving-type lesions most often occur as a consequence of injuries whereby an
animal’s foot may become stuck or wedged between 2 objects and, when finally
removed, results in loss of the claw horn capsule. These are diagnosed by simple
observation that demonstrates complete or partial loss of the horn shell. These usually
involve 1 claw, but on occasion both claws may be involved. Although these lesions
may seem catastrophic, depending on the severity of the damage to the underlying
corium tissues, most will heal uneventfully if the animal is offered appropriate care.11
 Clinical Diagnosis of Foot and Leg Lameness 547

Emphasis in managing these conditions is to clean the lesions and remove loose
horn or any foreign material that may be lodged in or impinging on the exposed corium
tissues. If only 1 claw is affected, apply a foot block to the healthy unaffected claw to
relieve weight bearing on the damaged claw. Application of a nonirritating topical
medication beneath a loose bandage should be applied to protect delicate corium
tissues. If both claws are affected, the animal should be restricted from movement
on hard flooring surfaces and housed in a well-bedded area.
Laminitis
Laminitis manifests as clinical disease with rapid onset of acute pain and lameness
(see Fig. 2). This occurs as the result of metabolic acidosis shortly after alimentary
overload of readily fermentable carbohydrates. With carbohydrate overload, there is
systemic release of vasoactive substances that reduce blood flow in the hoof and
thus an interruption in production of hoof wall and sole by germinal epithelial cells.27
Clinical signs of lameness can be seen as soon as 24 to 33 hours after carbohydrate
overload.28 Histologic lesions of laminitis can be detected as soon as 48 hours after
carbohydrate overload. Laminitis can have differing degrees of severity. The most
severely affected cases are manifested by breakdown of the suspensory tissue that
holds P3 suspended in the hoof. This breakdown leads to separation of the hoof
wall from the corium and rotation of the P3 in the hoof. After separation of the corium
from the hoof wall, there is abnormal hoof growth resulting in the classic presentation
of overgrown hooves that curl upward. In cases of laminitis, there can be interruption
in production of hoof wall and sole by germinal epithelial cells. This is manifested by
the presence of horizontal bands in the hoof wall and, in some cases, clefts in the
sole (Fig. 9).
Papillomatous Digital Dermatitis (Hairy Heel Warts)
Papillomatous digital dermatitis (PPD) has been long recognized as a cause of lame-
ness in cattle.29 Beginning as a mild superficial dermatitis, PPD progresses to a prolif-
erative and erosive lesion (Fig. 10). This lesion is characterized by marked dermal
thickening, as a result of proliferation of granulation tissue, marked hyperkeratosis,
and growth of papillomatous projections of epidermis.30 These proliferative lesions
are heavily colonized by spirochetes that extend into the stratum spinosum. Previ-
ously, Treponema phagedenis–like spirochetes were isolated from cases of PPD,31
and recently, PPD has been experimentally reproduced by cultures of mixed

Fig. 9. Cleft in sole as a result of prior episode of laminitis. Note separation of distal phalanx
from hoof wall (arrow). (Courtesy of Bruce Brodersen, DVM, PhD, Lincoln, NE.)
548 Shearer et al

Fig. 10. Heel of feedlot steer with papillomatous digital dermatitis. (Courtesy of Alan R.
Doster, DVM, PhD, Lincoln, NE.)

treponemes grown from tissues derived from natural cases of PPD.32 Treatment has
been successful with topical application of various antibiotics.33

SPECIFIC DISORDERS OF LEGS

Approach to Diagnosis of Upper Leg Lameness in Cattle
When dealing with upper leg lameness, the first step is to obtain a history in terms of
the duration, severity, onset of clinical signs, and any previous treatment. This infor-
mation is useful for making a reasonable prognosis and for deciding on possible
follow-up treatment approaches.
Examination begins with an observation of the animal from a distance while
standing and walking. This is followed by hands-on examination techniques that, for
the upper leg, include palpation during standing and walking and manipulation of
the leg with the animal in lateral recumbency (ie, lying on its side). In some cases, it
may be difficult to distinguish upper from lower leg problems. As described previously,
this can be done by placing a tourniquet at the level of the fetlock joint followed by
intravenous injection of 20 mL of 2% lidocaine into a vein below the tourniquet.
Remove the tourniquet after 5 minutes or so and immediately allow the animal to
walk. In cases of upper leg problems, the lameness will persist.19

Front Legs (Summary of Causes and Diagnostic Approach)

Inability to advance or difficulty in advancing the leg may be associated with supra-
scapular or radial nerve injury or bicipital bursitis (Table 2).34 In addition, the leg
may be held in semiflexion with the elbow dropped in the case of damage to the radial
nerve at the level of the brachial plexus.10 The radial nerve innervates the extensor
muscles of the carpus and foot and serves to provide sensory innervation to the lateral
skin of the forelimb from the elbow to the carpus.35
Lesions involving the eighth cervical and first thoracic vertebrae result in paralysis
that prevents an animal from extending its elbow, carpus, and fetlock to bear weight.
The elbow is dropped, the carpus and fetlock are in partial flexion, and the limb is
dragged, causing abrasion to the dorsal surface of the foot.35 In the absence of frac-
tures and obvious muscle damage, difficulty advancing the limb and an inability to
extend the elbow, carpus, and fetlock to bear weight, in combination with an absence
of skin sensation on the lateral and dorsal surface of the lower limb, confirm radial
nerve paralysis.36
 Clinical Diagnosis of Foot and Leg Lameness 549

Table 2
Common causes and diagnostic approach for front upper leg lameness

Cause Diagnostic Clinical Signs and Procedures

Suprascapular nerve Atrophy of supraspinatus and infraspinatus
Inability to extend shoulder and abduct the limb
Lower limb reflexes
Sensation intact
Proximal radial nerve Elbow: dropped
Inability to extend elbow and lower leg and advanced the leg
Leg in flexed position/loss of skin sensation lateral and dorsal
on lower limb
Distal radial nerve Elbow: normal position
Inability to extend lower leg/leg in flexed position
Loss of skin sensation lateral and dorsal on lower limb
Bicipital bursitis Decrease flexion of elbow
Shortened stride/increased fluid in bursa on ultrasound
Carpal and fetlock Walks on toes and knuckles forward
flexor deformity Walks on dorsum of foot
(contracted tendons) Unable to straighten the leg or bear weight
Unable to rise
Superficial and deep flexor contracture/tendons of flexor carpi
radialis and ulnaris tight on palpation
Septic arthritis Joint swollen, hot, painful
Joint effusion on palpation, ultrasound
Joint fluid has high white blood cell count and protein
Predominant neutrophil population
Degenerate/bacteria sometimes

Clinical signs of suprascapular nerve injury include stumbling, inability to support

weight in severe cases, inability to support and extend the shoulder, a shorten stride,
and abduction of the leg. Reflexes and sensation in the lower limb remain normal if
only the nerve is affected. Atrophy of the supraspinatus and infraspinatus muscles
may become visible as early as 5 to 7 days post injury.34 With bicipital bursitis, the
brachial biceps muscle and its bursa can be visualized ultrasonographically in a trans-
verse plane in the cranial shoulder region. In cases of bursitis, there is an increase in
the amount of fluid in the bursa.37
In calves, contracture of the flexors (ie, clinically referred to as “contracted
tendons”) may cause flexion of both the carpus and fetlock.38 In such cases, the leg
usually cannot be straightened, and the flexor carpi ulnaris and flexor carpi radialis
can be felt as tight bands at the back of the knee in addition to the superficial and
deep digital flexors.38 Semiflexion of the knee can also be caused by abnormal confor-
mation or metabolic bone disease. Depending on the level of contracture of the
flexors, only the fetlock may be in various degrees of flexion. In milder cases, the
animal may be able to walk on its toes and knuckle forward during weight bearing.
In more severe cases, the animal bears weight on the dorsum of the foot.38 The super-
ficial and deep flexor tendons and the suspensory ligament of the proximal sesamoid
feel tight on palpation.38
The carpus is one of the common joints affected in cases of septic arthritis in
calves.37 The joint is warm and often painful, and there is a palpable effusion in the
joint. Use of ultrasound over the longitudinal plane of the dorsal surface of the joint
will facilitate arthrocentesis. Individual joint recesses that can be visualized include
550 Shearer et al

the radiocarpal, intercarpal, and carpometacarpal joints. In the absence of ultrasound,

joint fluid can usually be obtained from the radiocarpal pouch with the carpus in slight
flexion.37 A high white cell count in the presence of degenerate neutrophils confirms
septic arthritis. Bacteria may not always be visible on the slide. In chronic cases,
the joint looks and feels thicker and has reduced range of motion. In such cases,
chronic degenerative changes will be visible radiographically,39 and may be initially
detected over the cranial surfaces of the proximal carpal row. The radiocarpal joint
space will be widened, and subchondral bone destruction along with new bone forma-
tion may be observed simultaneously.39

Back Legs (Summary of Causes and Diagnostic Approach)

Knuckling at the fetlock may indicate lesions of the spine, sciatic, peroneal, or tibial
nerves; dropping of the hock during standing but more so during walking often indicates
gastrocnemius rupture; overextension of the hock is associated with peroneal nerve
damage, peroneus tersius rupture, upper fixation of the patella, flexor tendon con-
tracture, straight hocks (post hocks), and advanced degenerative joint disease10,39;
intermittent spastic contracture of both legs with flexion of the hock is caused by spas-
modic syndrome, whereas spastic contracture of one or both hind legs with overexten-
sion of the hock is caused by spastic paresis40; and asymmetry of the pelvis may be
caused by hip dislocation or other lesions involving the pelvis (Table 3).

Table 3
Common causes and diagnostic approach for back upper leg lameness

Cause Diagnostic Clinical Signs and Procedures

Hip joint dislocation–dorsal Cow up or down/asymmetry in hips
Crepitation over hip area/leg shorter and hock higher than
opposite leg
Radiographs
Hip dislocation–caudoventral Cow down
Femoral head in obturator foramen
Radiographs
Anterior cruciate rupture Increased laxity in stifle
Audible noise during movement
Joint effusion
Medial collateral ligament Increased joint space medially
rupture Instability of medial meniscus
Upward patella fixation Limb locked in extension
Exaggerated motion during flexion
Peroneus tersius rupture Overextended hock

Tibia and metatarsus can be extended to 180
Swelling cranial on tibia
Peroneal neuropathy Overextended hock
Knuckling of fetlock
Decreased skin sensation on dorsal surface of metatarsus
and fetlock
Tibial neuropathy Dropped hock
Knuckling of fetlock
Loss of skin sensation palmar aspect of lower limb
Partial sciatic neuropathy Bilateral dropped hocks
Knuckling of fetlocks
 Clinical Diagnosis of Foot and Leg Lameness 551

Instability within the stifle joint associated with cranial cruciate rupture is often seen
when the animal is walking and may be accompanied by an audible sound (click). This
is caused by sliding of the femoral condyles over the tibial plateau.39 The animal tends
to stand with the fetlock slightly flexed and the heel raised. Weight bearing is primarily
on the tip of the toe. In cases of medial collateral ligament instability, the leg is held in
an abducted position to relieve weight bearing on the medial side of the stifle and
weight is placed on the medial claw when walking.39 Upward fixation of the patella
will cause the limb to “lock” when in full extension, resulting in a stringhalt-type exag-
gerated motion during flexion. The animal may have a normal gait in between steps.
Rarely, the leg may become locked in extension.10,39
With superficial flexor tendon contracture, the proximal interphalangeal joint may
become subluxated, resulting in knuckling of the joint.38 The animal may walk and
stand on its toe and the leg may seem to be shorter than the opposite side. With
gastrocnemius rupture, the hock is dropped and partially flexed and moves farther
down when walking. The fetlock may knuckle during locomotion.10 Tibial nerve paral-
ysis also results in a dropped hock and slight knuckling of the fetlock. The hock
remains dropped while the animal is walking but does not sink during weight bearing
compared with rupture of the gastrocnemius muscle.10
Obturator nerve paralysis primarily affects the adductor muscles of the inner thigh of
the rear legs. Affected animals have a wide base stance and may seem ataxic, and
they are predisposed to splaying their back legs.10 Cows with damage to the peroneal
nerve will stand with the foot knuckled over onto the dorsum of the pastern and fetlock
joint. At the same time, the hock joint will seem to be overextended. In mild cases, the
fetlock tends to knuckle over intermittently when the cow walks.10 General indicators
of an upper leg lameness problem include joint or soft tissue swelling.

DISORDERS INVOLVING SPECIFIC JOINTS OF THE REAR LEG

Hip Joint
Slight abduction of the back leg with outward rotation of the toe is often associated
with lesions in the stifle or hip.39 Crepitation (crackling or grating) may be felt while
rocking the animal sideways with one or both hands on the greater trochanter. Crep-
itation, however, is not a reliable sign of the presence of lesions within the hip joint.39
What sometimes feels like crepitation may turn out to be a normal joint, and crepitation
originating from the stifle may be interpreted as coming from the hip.
Specific problems may include rupture of the round ligament in the hip joint, hip
dislocation; pelvic fractures; fractures of the head of the femur, slipped capital femoral
epiphysis, or severe coxitis.39 The relative position of the greater trochanter to the
tuber coxae and the tuber ischia should be determined and should form a triangle
with the ventral point representing the greater trochanter t.41 This triangle is lost
with craniodorsal luxation with the greater trochanter being placed in-line with the
tuber coxae and tuber ischia.41 With caudoventral dislocation, the trochanter major
may not be palpable.41 A rectal examination should be performed to determine the
presence of crepitation while moving the animal from side to side or of hard bony
protrusions, which may indicate the presence of a pelvic fracture.
More frequently, the animal will be down particularly with fractures or caudoventral
hip dislocation. Examination should be carried out with the animal in lateral recum-
bency. With craniodorsal displacement, the leg may seem shortened and the hock
higher than the opposite hock.39 Abduction and adduction and rotation of the leg
by an assistant while both hands of the examiner are cupped over the greater
trochanter may elicit crepitation. Manipulation is more painful with caudoventral
552 Shearer et al

dislocation and the animal resists flexion of the leg. It is possible to palpate the femoral
head in the obturator foramen in the case of caudoventral dislocation.39
Ultrasound-guided arthrocentesis can be carried out in cases in which an increase
in joint fluid can be visualized. Ultrasound is carried out in a longitudinal-oblique plane
with the transducer placed parallel to the long axis of the femoral neck and moving it
craniodorsally to where a line drawn between the 2 tuber coxae intersects the longi-
tudinal axis of the vertebral column.37 Radiographs are useful in establishing the cause
of the lameness. The animal should be anesthetized and placed in dorsal recumbency.
The size of the musculature will to a large extent determine the detail visible in the
radiograph.39

Stifle Joint
Severity of lameness can vary depending on structures involved such as the cranial
cruciate ligament, menisci, or the collateral ligaments in addition to the time after onset
of the problem. Examination in the standing animal involves palpation of the joint for
fluid effusion and stability. Demonstration of instability of the joint can be done in
the following ways: the examiner stands behind the animal and reach around the
leg with both hands. Lock the fingers over the tibial crest while leaning into the back
of the thigh. The leg is stabilized against that of the examiner while the tibia is pulled
back. Alternatively, the examiner may stand in front of the affected leg and try to
demonstrate laxity by pushing on the tibial crest.41 The foot has to be stabilized during
this procedure. Distention of the joint capsule can cause swelling between the patellar
ligaments despite the presence of the fat pad. In addition, there are extensions of the
joint capsule between the quadriceps femoris muscle and the femur and distally
around the tendons of the peroneus tertius and the long digital extensor muscle.39,41
To distinguish between trauma and sepsis of the joint, arthrocentesis is a useful
diagnostic tool. Total cell count in nonseptic cases is normally less than 1000 cells/
mL, and the polymorphonuclear cells are less than 10% of the total.39 The following
should be considered with arthrocentesis of the stifle. There is communication
between the femoropatellar and medial femorotibial joint cavities. These compart-
ments do not always communicate with the lateral femerotibial space. To enter this
compartment, a needle is introduced behind the lateral patellar ligament and directed
caudally. To enter the femeropatellar and the femorotibial compartments, the needle is
inserted between the medial and middle patellar ligaments and directed slightly down-
ward and toward the medial lip of the trochlea.39,41 Use of ultrasound will confirm the
presence of increased joint fluid and facilitate collection.37
With medial collateral ligament damage, the medial meniscus becomes detached
and the joint capsule stretched, resulting in more laxity on the medial side of the joint.
The limb is usually kept in an abducted position and more weight is placed on the
medial claw. If the leg is pulled outward, an increase in the joint space on the medial
side can be palpated and excessive movement of the medial meniscus can be demon-
strated by palpation between the medial collateral ligament and the medial patellar
ligament.37
Overly straight hocks may lead to degenerative joint disease in the stifle, resulting in
lameness. There may be some joint enlargement and crepitation on movement of the
joint. Radiographic changes in chronic cases will confirm the presence of chronic
degenerative changes such as thickening of the joint capsule, epiphyseal deformity,
and osteophyte formation at the joint margins.37
Lateral luxation of the patella may follow femoral nerve injury or could be congenital.
Femoral nerve injury may occur after forced traction during birth. The calf is unable to
support weight on the leg and the hock and stifle are flexed while walking. The patella
 Clinical Diagnosis of Foot and Leg Lameness 553

may be luxated or can easily be moved out of the groove. Progressive atrophy of the
quadriceps occurs, which gives the leg a hollowed-out appearance over the lower
femur.15,37 With upward fixation of the patella, it is important to understand that palpa-
tion of the stifle may not reveal any obvious abnormalities.10 However, the medial
patellar ligament may feel abnormally tight.
Diagnostic radiographs of the stifle can be difficult to obtain in adult cattle because
of the thickness of the structures that need to be penetrated. The anteroposterior view
is unrewarding. Positioning of the cassette in standing animal may be difficult, and for
that reason lateral recumbency with the leg in extension may be a better choice.39

Hock Joint
Rupture of the peroneus muscle results in overextension of the hock because this
muscle group is the primary flexors of this joint. In cattle, rupture occasionally occurs
in the mid belly or at the junction of the proximal or distal tendon. If the limb is manually
lifted and extended caudally, the tibia and metatarsus are in a straight line while the
stifle joint remains at 90 . Damage usually results in a painful swelling over the cranial
shaft of the tibia.10
Peroneal neuropathy may result in loss of skin sensation on the dorsal aspect of the
lower limb and overextension of the leg. The peroneal nerve passes superficially over the
lateral aspect of the rear leg where it is vulnerable to external trauma. It is often damaged
in cows that suffer milk fever or downer cow syndrome as a result of the cow’s body
weight that puts pressure on the nerve where it crosses over the bone. The hock joint
will seem to be overextended in cows with damage to this nerve. In mild cases, the
fetlock tends to knuckle over intermittently when the cow walks.10 In severe cases,
cows will experience a decreased sensation on the dorsal aspect of the fetlock. The
prognosis for cows affected with peroneal nerve damage depends on the severity of
the nerve injury. Recovery may take days to months depending on severity.10,36
Overflexion of the hock is seen with gastrocnemius rupture. There is swelling at site
of rupture. The gastrocnemius muscle originates from caudal femoral surface and
inserts on point of hock. Rupture can occur in 3 places: in the muscle belly, the
muscle–tendon junction, which is the most common site to rupture or the insertion
of the tendon on the tuber calcis. Diagnosis is based on the typical clinical signs,
tendon laxity, and swelling with edema at the rupture site.10 Differentials may include
calcanean bursitis, luxation of superficial flexor tendon, or tarsal fracture. With
complete rupture, the animal is down and unable to rise. The ability to fold the affected
leg completely on itself is diagnostic for complete rupture.15
The tibial nerve innervates the palmar/plantar aspect of the skin of the lower limb,
which may show partial or complete loss of sensation in cases of tibial neuropathy.
Partial sciatic nerve injury following calving or trauma to the spine is usually bilateral.
The cow walks with short stilted steps while both the hocks and fetlocks remain in
semiflexion. The spine should be palpated and a rectal examination performed to
investigate the possibility of a fracture.
Swelling of the hock joint is usually associated with peritarsal bursitis, septic arthritis
of the hock joint, or swelling caused by degenerative joint disease, which may or may
not be associated with post hocks.10,39 Peritarsal bursitis is a chronic cellulitis
involving the lateral aspect of the hock joints. It is usually bilateral. Lameness is usually
absent except in cases that cause mechanical impairment of the joint or in cases of
severe abscessation or septic arthritis. In such cases, the animal may become
severely lame with a discharging tract over the lateral aspect of the joint. The swollen
joint may feel warm, fluctuant, and painful to touch or manipulation. Needle aspirate
will confirm the presence of an exudate.
554 Shearer et al

A peritarsal abscess should be distinguished from a septic joint. This can be done
with the use of ultrasound. The tibiotarsal pouch communicates with the proximal
intertarsal compartment but not the distal intertarsal and tarsometatarsal compart-
ments. An abscess will show as a walled-off cavity outside the joint filled with fluid
with a cellular appearance.37
In cases of chronic degenerative joint disease, the joint swelling will be hard and less
painful compared with acute or subacute septic tarsitis. The needle is inserted on the
dorsal surface medial to the extensor tendons and at the level of articulation between
the tibia and proximal tarsal bones.10 Degenerative changes within the joint may also
be associated with chronic infections such as those caused by Mycoplasma sp.
Chronic bone changes within the joint can be shown radiographically.

Fetlock Joint
Instability (flexion during weight bearing or knuckling) of the fetlock can result from
spinal injury caused by trauma such as getting caught under the sides of the free stall
or spinal lymphosarcoma. Damage to the sciatic nerve (particularly the peroneal
branch of the sciatic) will result in knuckling of the fetlock joint. Conditions of the
back of the foot such as sole ulcer or severe digital dermatitis may also cause knuck-
ling as a result of redistribution of weight toward the toe.41 The foot should always be
examined for the presence of lesions that may cause the animal to knuckle.
Peroneal nerve paralysis is a common secondary complication with milk fever,
downer cow syndrome, or other conditions that may cause a cow to remain down
for an extended period of time. In severe cases, cows will experience a decreased
sensation on the dorsal surface of the fetlock. Overextension of the fetlock may occur
following flexor tendon rupture or rupture of the suspensory ligaments of the proximal
sesamoid. The fetlock is overextended to the point that the animal bears weight on the
plantar/palmar aspect of the foot. There may be a visible swelling above the dew
claws, and the presence of an effusion in the tendon sheath or core lesions in the flexor
tendons may be visible on ultrasound.37

SUMMARY

The causes of lameness in cattle are multifactorial and involve a combination of

housing, management, and environmental factors and a variety of infectious agents.
There can be white line disease with white line separation, laminitis, and ascending
infection into the hoof, leading to tenosynovitis. Arriving at a cause can often require
concerted efforts during an extended period of time. A diagnosis of lameness is often
based mainly on clinical observations. A detailed record of those observations over
time and among several animals within a herd can provide valuable information toward
solving lameness problems. Advances in computer hardware and software help facil-
itate more detailed collection of data and analysis of that data.

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