Locomotor disorders

Chapter 7 Locomotor disorders

Lower limb and digit


In dairy cattle, approximately 80% of all lameness originates in the foot, most often in one of the hind feet, arising in the lateral hind claw in the majority of cases. In addition to significant welfare implications, lameness is a major cause of economic loss, as affected animals lose weight rapidly, yields fall and, in protracted cases, fertility is affected. There is also increased culling, and considerable sums of money are spent on treatment and preventive hoof trimming. The severe pain associated with lameness (7.1) is seen as an arched back, front legs forward and apart to take increased weight, and head lowered to bring the center of gravity forward and away from the painful left hind limb. Although accurate figures are not available, lameness in beef cattle has a lower incidence and less economic importance. Many etiological factors are involved, including excessive standing, especially on hard, unyielding tracks and surfaces; rough handling when moving cattle; feet kept continually wet in corrosive slurry; reduced horn growth at calving; and high-concentrate/low-fiber feeds leading to acidosis. All of these factors can precipitate laminitis/coriosis, the consequences of which are abnormal horn growth and hoof wear, softening of the sole horn, dropping of the distal phalanx within the hoof, and a weakening and widening of the white line, all of which predispose to digital lameness.

This chapter illustrates the common foot lesions in cattle, namely white line abscess, sole ulcer, interdigital necrobacillosis, interdigital skin hyperplasia, and digital dermatitis. Complications of these primary conditions may produce deeper digital infections, often involving the navicular bursa and, eventually, the pedal (distal interphalangeal) joint. Flexor tendon rupture or coronary band abscessation may result. The final section deals with laminitis/coriosis. Digital lesions due to systemic disease, e.g., foot-and-mouth (12.7) are described in the relevant chapters. The zones of the foot, as defined by the International Ruminant Lameness Symposium, are shown in 7.2, and this nomenclature will be used in the following sections.

Disorders of the sole and axial wall

White line disorders

Clinical features

early cases of white line disease are seen as a yellow discoloration (caused by serum) or reddening (caused by hemorrhage) of the white line cement. 7.3 illustrates white line hemorrhage in zone 2 in the right (lateral) claw, hemorrhage at the sole ulcer site (zone 4 left claw), and areas of yellow discoloration in both claws. In more advanced cases (7.4) a fissure develops in the defective white line allowing the penetration of stones and other debris, which then act as a wedge, producing further white line separation. Infection reaching the corium may track either across the sole, or proximally along the laminae, as in 7.5, to discharge at the coronary band. The abaxial white line of the hind lateral claw is most frequently involved, especially zone 3 toward the heel, as it represents a mechanical stress line between the rigid hoof wall and the movement of the flexible heel during locomotion.

A variety of white line abscesses are seen, depending on both the initial site of penetration of the infection and on the direction of spread. On the left claw of 7.6 light-grayish pus is exuding from the point of entry of infection at the white line near the toe. Pus has tracked under the sole horn, leading to separation of the horn from the underlying corium. Lameness was pronounced. In 7.7 the under-run sole has been removed to expose new sole horn, developing as a layer of creamy-white tissue (A) in the center of the sole and against the edge of the trimmed horn. The hemorrhagic area (B) at the white line is the original point of entry of infection. Progressively deeper penetration of infection occurs in untreated cases. In 7.8, another sole view, the corium has been eroded to expose the tip of the pedal bone (A). This resulted in severe lameness, although the cow eventually made a full recovery. In 7.9 a white line lesion had tracked from the sole dorsally along the laminar corium, then the papillary corium to discharge at the coronary band. Removal of the under-run hoof wall revealed a brown necrotic line. This has permitted drainage. A wooden block has been glued onto the sound claw to rest the affected digit. Although this cow walked soundly within 3 weeks, more than 12 months elapsed before sufficient horn had grown down from the coronet fully to repair the damaged hoof.

Sole overgrowth

Sole ulcers (“Rusterholz”)

Clinical features

in the digit in 7.12 (a plantar view) the wall has been worn down to the level of the sole or lower, and a wedge of sole horn (A) is growing from the axial aspect of the right (lateral) claw towards the left claw. This wedge becomes a major weightbearing surface and transmits excess weight to the sole corium, causing hemorrhage, bruising, and eventually defective horn formation. Note also the heel erosion (B). Another cow (7.14) shows that when such a sole wedge is pared away, a discrete area of sole hemorrhage is revealed in the right (lateral) claw. Note the reddening of the white line in the same claw, indicative of coriosis/laminitis, and also that both claws are overgrown. Further paring and removal of the hemorrhagic horn (7.15) revealed under-run horn and necrosis characteristic of a sole ulcer. Some sole ulcers (7.16) develop a large, protruding mass of granulation tissue. The longitudinal section of another case (7.17) illustrates a mild, chronic ulcer in its characteristic site beneath the flexor tuberosity at the sole–heel junction. The sole horn has been perforated (A) and inflammatory changes have tracked up towards the insertion of the deep flexor tendon. The heel horn is slightly under-run (B) and there is laminitic hemorrhage (coriosis) at the toe (C). Sole ulcers are typically found on the lateral claws of hind feet and, less frequently, on the medial claws of front feet. Often the lateral digits of both hind feet are involved to a different extent. More extensive damage to the corium means ulcers heal more slowly than a white line abscess or an under-run sole (7.7).

Heel ulcers

Toe ulcers

Clinical features

they may present as larger areas of hemorrhage in zone 5 (7.20) or more commonly simply as a softening of the sole, as in 7.21. Note how the hoof wall has been worn away at the toe, and the presence of early subsolar hemorrhage in 7.21. Frequently seen when heifers and young bulls are introduced into a dairy herd without prior acclimatization to concrete, they appear to be related to trauma and excessive wear. Both front and hind feet may be affected. Excess sole wear is becoming a major problem in some herds, and has led to a suggestion that the frequency, or the extent, of hoof trimming should be reduced.

Toe necrosis (osteomyelitis of distal phalanx)

Clinical features

the condition occurs in both dairy cows and in feedlot cattle, and may be associated with excess wear leading to thinning of the horn at the toe. Dairy cows walk with the affected foot forward to relieve pain in the toe, and this typically leads to overgrowth of horn, seen on the medial toe of the right hind foot of 7.22. Note the predisposing poor hygiene underfoot. In another cleaned foot in 7.23 much of the under-run sole and wall at the toe has largely been removed to reveal a black necrotic area tracking up under the dorsal wall. The lesion invariably has a pronounced putrid smell, rarely present in other hoof disorders. The necrotic tip of the pedal bone may be palpated. In a cross-section of another digit (7.24) the apex of the pedal bone has clearly been eroded at A, dry fecal debris is impacted into the residual cavity at the toe, and gray areas of necrotic pedal bone are visible.

Vertical fissure (vertical sandcrack)

Clinical features

vertical fissures occur as a result of damage to the superficial periople and underlying coronary band, e.g., following hot, dry weather, or damage to the coronary band from trauma or a digital dermatitis infection. Both claws of the overgrown left forefoot in 7.29 are affected, although the major fissure appears only on the medial claw. Note its irregular course and its origin at the coronary band (A). Note also the section (B), which is slightly loose due to an oblique crack at (C). In 7.30 an extensive, wide, vertical horn crack is shown, in which the laminae are very liable to become exposed, resulting in severe lameness, even though little pus may be present. Another beef cow presented as acutely lame, and extensive paring of a vertical fissure in the front foot eventually led to the release of pus (7.31) and resolution of the lameness. In advanced cases (7.32), where granulation tissue protrudes from the fissure, it is highly probable that an inflamed corium has produced a proliferative osteitis of the extensor process of the pedal bone, and the expanded bone will no longer fit inside the confined space of the hoof.

Horizontal fissure (horizontal sandcrack)

Corkscrew claw

Clinical features

the lateral claw of the front or the hind feet can be affected by this partially heritable growth defect. The overgrown lateral toe in 7.34 deviates upward, and in the same digit, the abaxial wall curls under the sole (7.35), inevitably altering the weightbearing surfaces. The axial sole overgrowth (A) consequently becomes a major weightbearing surface and lameness can result from sole ulcers and/or pedal bone compression (see also 7.11). In the pedal bone specimen in 7.36, osteolysis secondary to corkscrew claw compression is seen near the toe, at A. The left pedal bone and the cavitation are normal. 7.35 also shows early bilateral heel erosion (see also 7.67), and cavitation of the sole of the medial claw due to impaction by debris.

Complications of digital hoof disorders

Superficial under-running of the corium is easily treated by removal of separated horn and allowing regrowth of new hoof. Infection of deeper tissues leads to additional clinical signs especially swelling around the coronary band of the affected digit, and usually a more severe and protracted lameness. A range of conditions may be seen including abscesses at the coronary band or the heel, rupture of the deep flexor tendon, and deeper sepsis.

Rupture of the deep flexor tendon

Clinical features

complications from severe white line abscess, sole ulcer, or, as in 7.41, retroarticular heel abscess can lead to infection and the subsequent rupture of the deep flexor tendon. In 7.41 the coronary band is severely distorted, the heel is swollen, and the toe deviates upward (plantigrade), leading to continual overgrowth and lack of wear of the affected claw. A longitudinal section of a septic digit (7.42) reveals the site of an ulcer that perforated the sole horn (A), and the point of rupture of the deep flexor tendon (B). Note the horn overgrowth at the toe. At this stage the joint is not affected and recovery is possible with prompt treatment.

Septic pedal arthritis (distal interphalangeal sepsis)

Clinical features

pedal arthritis typically results from a severe or neglected white line abscess, sole ulcer or interdigital necrobacillosis infection and produces severe, often non-weightbearing, lameness. Note the marked unilateral enlargement of the left heel in 7.43, with inflammation tracking up toward the fetlock and causing distortion of the claw. The navicular bursa and pedal joint are also infected, producing a septic pedal arthritis. Gross enlargement can result in lifting of digital sole and heel horn, especially at the heel and toward the interdigital space. The Hereford cow in 7.44 had been lame for 8 weeks. The affected lateral claw is grossly enlarged and inflamed, there is swelling of the coronet and separation of horn at the coronary band (A), and granulation tissue protrudes into the interdigital space at the point where pus discharges from the infected joint. Despite a less severe degree of swelling in the more chronic case in 7.45, the hoof on the affected lateral claw is being avulsed by pressure and necrosis from a septic coronitis.

Long-standing digital infections may lead to an osteitis and a proliferation of new bone, as in 7.46, which is a boiled-out specimen of a chronically infected sole ulcer in a Holstein cow. A deep cavity was present at the ulcer site, with extensive new bone proliferation in the navicular bone, digital cushion, and coronary areas. When P1, P2, and P3 became ankylosed, the severity of lameness decreased. In 7.47, which is a sagittal section following digital amputation, necrosis in the navicular bone has extended to cause severe sepsis in the distal joint. Infection at the coronary band (B) has produced swelling above the coronet.

Disorders of the digital skin and heels

Whereas hoof disorders arise from the corium and are largely managemental in origin, diseases of the interdigital skin have a large infectious component.

Interdigital necrobacillosis (phlegmona interdigitalis, “foul”, “footrot”)

Clinical features

early cases have an obvious lameness and show a symmetrical, bilateral, hyperemic swelling of the heel bulbs that may extend to the accessory digits. At this stage, the interdigital skin is swollen but intact, and the claws appear to be pushed apart when the animal stands. After 24–48 hours the interdigital skin splits (7.48) (some sloughed epidermis has been removed), and in later cases the dermis is exposed (7.49). More extensive exposure of the dermis is often seen (7.50), with development of granulation tissue. A foul-smelling, caseous exudate may be present (7.51). 7.52 is a dorsal view of a neglected case after cleansing, with sloughed necrotic debris in the interdigital space. The depth of the necrotic process has caused proliferation of granulation tissue. Early separation of the axial wall of the left claw (A) and swelling of the coronet suggest early inflammatory changes in the pedal joint. The horizontal groove (B) distal to the coronary band indicates that the problem has existed for about 1 month.

A peracute form of interdigital necrobacillosis exists known as “super foul” (7.53), where severe necrosis extends from the interdigital cleft onto the heel skin. The dermal necrosis is savage in onset and there may be joint involvement within 48 hours of initial clinical signs. The same causative organisms are involved, although the antibiotic sensitivity pattern may differ. Prompt and aggressive therapy is vital.

Interdigital skin hyperplasia (fibroma, “corn”)

Jul 8, 2016 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Locomotor disorders
Premium Wordpress Themes by UFO Themes