Sole ulcer (Rusterholz) — where it comes from and how to treat it

Every trimmer sees sole ulcers weekly, and almost everyone misreads where they come from. An ulcer does not start on the sole. It starts underneath it, and by the time you see anything at the crush the damage is already weeks or months old.

This article draws on two papers: van Amstel and Shearer's review in the Journal of Veterinary Internal Medicine, and the cross-sectional study by Bicalho and colleagues at Cornell in the Journal of Dairy Science. Full references at the end.

What a sole ulcer actually is

The first accurate description came from Rusterholtz in 1920, which is where the common name has hung on for over a century. Scientifically it is pododermatitis circumscripta, and the definition is short: a full-thickness break in the epidermis.

Clinically it appears in three forms, and the distinction matters because each implies something different:

• Pododermatitis circumscripta haemorrhagica — haemorrhage of the corium, horn still intact
• Pododermatitis circumscripta perforata — perforation of the corium through a full-thickness break
• Pododermatitis circumscripta complicata (or purulenta profunda) — once trauma, granulation tissue and ascending infection join in

Where to look

The most common site — the "typical" one — is the junction of the sole and the heel. Less often the apex of the toe, less often the heel itself. Overwhelmingly it is the lateral claw of a hind limb, frequently bilateral, with a high rate of recurrence.

That is not chance. Weight distribution in the hind limbs loads the outer claw more heavily, which accelerates horn growth, particularly at the heel.

What happens inside the claw

The pedal bone does not rest on the sole. It hangs inside the horn capsule, on the laminar corium and on bundles of collagen fibres running from the bone to the basal layer of the epidermis.

In cattle this suspensory apparatus is far weaker than in the horse: the laminar corium is less extensive and there are no secondary laminae. A cow cannot carry as much load on the claw wall as a horse can, so the weight has to be displaced onto the sole and the heel.

When the suspensory apparatus fails, the bone sinks. The flexor tubercle begins to compress the digital cushion and the solar corium. Compression brings ischaemia, congestion, oedema and thrombosis in the microcirculation — and a compromised blood supply means abnormal keratogenesis. The horn produced from that point on is defective.

That is the whole mechanism. An ulcer is not an infection that got in from outside; it is mechanical injury inflicted from within.

The digital cushion: why it decides the outcome

The digital cushion is three parallel, fat-filled cylinders beneath the pedal bone. All three together in one claw come to roughly 5.7 mL. They have one job: absorbing shock.

This is where Bicalho and colleagues come in — 501 lactating Holsteins, digital cushion thickness measured by ultrasound at the typical ulcer site. The results speak plainly:

Cushion thickness turned out to be a strong predictor of lameness: cows in the upper quartile had an adjusted lameness prevalence 15 percentage points lower than those in the lower quartile.

Body condition translates directly into cushioning

The relationship with body condition score is linear and unmistakable:

A cow losing condition is literally losing the padding under her pedal bone. In animals with a claw lesion the cushion was thinner (0.88 cm) than in animals without one (0.95 cm).

One hundred and twenty days after calving

The single most useful number in the study: digital cushion thickness falls steadily from calving and reaches its low point around day 120 of lactation.

That is the window in which the claw has the least protection it will ever have. If you are scheduling preventive trimming, that date deserves more weight than calendar convenience.

Two routes to the same ulcer

van Amstel and Shearer describe two ways the suspensory apparatus weakens, both ending in the same place.

The non-inflammatory route is the hormonal and biochemical shift around calving. Hydrocortisone and prolactin reduce protein synthesis in claw tissue. High concentrations of a 52-kDa protease were found in heifers after calving but not in maiden heifers. That explains why sole haemorrhages appear en masse two to four months after calving: in one study 94% of primiparous and 66% of multiparous cows had them at trimming.

The inflammatory route involves vascular change and activation of matrix metalloproteinases, classically attributed to subclinical laminitis. The authors point out, though, that in cattle the changes affect a different part of the corium than in the horse, and suggest a more accurate term: coriosis.

A third route: overgrowth of the outer claw

Sinking needs neither hormones nor inflammation. Overgrowth of the outer claw on a hind limb is enough on its own.

The cow tries to compensate by shifting weight onto the inner claw. To do that she rotates her feet outward and her hocks inward, becoming progressively more cow-hocked. But that posture moves weight onto the inner part of the heel and sole of the lateral claw, where a thick ledge of horn builds up at the interdigital space.

This is exactly the problem that proper functional trimming solves — steps 1 to 3 of the Dutch Method.

Catching it early

The early sign is sole haemorrhage, with one catch: it only becomes visible weeks or months after the injury itself. When you see it, you are looking at something that happened a long time ago.

The cow may stand with her hind feet placed well behind her, or visibly cow-hocked, shifting weight onto the medial claws. In a mature lesion the horn around the ulcer is loose and undermined; pare it away and the corium protrudes through the defect.

Treatment: the block matters more than anything else

The single most important element of treatment is relieving the affected claw by gluing a block to the sound one. That is what provides pain relief and what makes healing possible. Everything else is an addition.

For the block to work it has to go on properly:

• Pare the sound claw flat, so the weight-bearing surface is perpendicular to the long axis of the limb
• The block must support the heel
• Clear the adhesive from between the block and the heel — heel horn is soft, and a hard cured edge damages it
• Take it off in time: left on longer than about two months, or applied badly, a block becomes a cause of lameness in its own right

In an early lesion with no break in the horn, simply lowering the heel of the affected claw can transfer enough weight for healing to take place.

What not to do

This is the most practical part of both papers and it is worth knowing by heart.

Do not open an early haemorrhagic lesion. It can feel soft under pressure and it is tempting to cut into it. Cutting creates a full-thickness defect and exposes the corium — it turns an early lesion into an ulcer.

Do not cut holes in the sole. Deep defects trap manure and retard healing. Instead, create a gentle slope in the horn around the ulcer, taking care not to damage the corium.

Do not use caustic agents on granulation tissue. They are contraindicated: they impede healing by interfering with cell growth from the edges of the ulcer. Excess granulation tissue is removed surgically, down to the level of the surrounding trimmed and sloped horn.

Be careful with copper sulphate on the lesion itself. It penetrates horn extensively and can make it brittle. This is not an argument against footbaths — it is an argument against treating copper as a dressing for an ulcer.

A bandage does not replace a block. In the studies cited, bandaging did not improve healing rates compared with leaving the lesion open with a block fitted.

When it stops being a job for the trimmer

A complicated ulcer looks different and needs a vet. The warning signs: severe lameness, reluctance to move, lying down most of the time, marked weight loss, no response to conventional treatment, unilateral swelling of the digit around the heel extending toward the coronary band, a draining tract, an overextended toe.

Behind that is usually necrotising osteomyelitis of the flexor tubercle, a pathological fracture and avulsion of the deep flexor tendon. No block will fix it.

Healing takes longer than you think

Serial biopsies give a timeline worth knowing before you write a treatment off as ineffective:

• Day 9 — regeneration and epithelialisation begin, new blood vessels form in the corium
• Day 14 — the ulcer is covered by a layer of soft cornified epithelium, though the structure is not yet organised
• Day 19 — cornification well advanced, maturation of the epidermis nearly complete
• Day 50 — a fully differentiated cornified epidermis, though small areas of dyskeratosis can persist

Fifty days. A check-up at two weeks is not assessing a cure — it is assessing whether the process started at all.

What this means for your records

Sole ulcers recur, and they recur in the same place on the same claw. An ulcer in one lactation raises the risk in the next. If your record says only "sole ulcer, left hind", you have thrown away precisely the detail that carries prognostic weight.

The practical minimum worth recording:

• The exact zone, not just the limb — a recurrence in the same zone is a different story from a new lesion elsewhere
• Which claw, medial or lateral
• Whether a block went on and when, so it comes off on time rather than after three months
• Days in milk, because the cushion is thinnest around day 120
• Body condition, because that is what predicts the cushioning

Cownt records the zone of the lesion and the clinical claw side, counts blocks and wraps separately for each claw, and the portal surfaces recurrences of the same lesion in the same place. That is not an accessory to trimming — it is the only way to answer, a year later, whether this cow is actually getting better.

References

• van Amstel, S. R., & Shearer, J. K. (2006). Review of Pododermatitis Circumscripta (Ulceration of the Sole) in Dairy Cows. Journal of Veterinary Internal Medicine, 20(4), 805–811.
• Bicalho, R. C., Machado, V. S., & Caixeta, L. S. (2009). Lameness in dairy cattle: A debilitating disease or a disease of debilitated cattle? A cross-sectional study of lameness prevalence and thickness of the digital cushion. Journal of Dairy Science, 92(7), 3175–3184. doi:10.3168/jds.2008-1827
• ICAR Claw Health Atlas — the international standard for classifying claw disorders.