Indepth Equine Podiatry Symposium Notes Written and presented January 2009 by R.F. (Ric) Redden, DVM
This disease is caused by bacteria and fungus involving the stratum medium (the white zone) of the wall. Anatomists many years ago named the terminal laminae the "white line" which was a terrible misrepresentation and has caused much confusion. The terminal laminae are yellow to brown in color, never white, but lie on the inner border of the white zone, the non-pigmented portion of the hoof wall. There have been numerous fungi and bacteria cultured from horn defects and it appears geographic location is a determining factor.
Fungi are opportunists looking for a place to grow. It is my opinion that a scar, defect or structural weakness is present prior to all fungi invasion of the horn. Treating a large number of white line disease cases over the last 30 years, I have found that 100% of all unilateral cases involve the club foot or high heel foot. Many times it is only a grade one to two club, which is seldom recognized as a club foot. But looking at the subtle differences in the two feet visually and radiographically reveals typical club foot characteristics. Examining the history on several cases revealed that the majority had an abscess break at the coronary band as weanlings or yearlings due to typical excessive toe wear found in club feet. Those that toe in will normally have a white line disease lesion along the anterior-lateral quarter. Those that toe out tend to have a white line disease lesion along the anterior/medial quarter.
A clinical exam can be conclusive, especially in the advanced stage. The solar surface will be void of horn wall in the area of involvement. The sole migrates forward, pushing the terminal laminae forward and proximal. The only way the defect can be observed is by lifting the sole. Tapping on the wall can create a hollow sound. Radiographs clearly reveal the defect, but radiographic interpretation can be deceptive.
Radiographic lesions characteristic of white line disease are similar but strikingly different from those found with laminitis. Both frequently encountered syndromes can have significant capsular rotation, a greater than normal palmar angle, very thin soles and a lucent submural lesion. Stark differences in shape and precise correlation of the lucent zone clearly distinguish white line disease from laminitis. White line disease involves the horn side of the horn-lamellar (HL) zone while laminitis involves the lamellar side. Bacteria and fungi invade the soft, non-pigmented (white zone) portion of the horn wall at the ground surface, apparently along small fissure lines, disrupted areas of horn or along existing scar tissue caused by previous toe cracks or abscesses that have migrated up the wall. The invading organism quickly destroys the integrity of inner horn wall and creates an irregular shaped air density lesion that is routinely evident at the ground surface and has irregular borders that are often superimposed over bone.
Close examination often reveals dirt, sand and debris in the confines of the air space. The debris enters the void via the small opening formed by the sole that has grown forward. Lucent lesions due to laminitis and bone displacement occupy space that is created at the junction of horn and laminae as the coffin bone is pulled away from the lamellar horn attachment. The shape of the lucent zone is relative to the direction of bone displacement. Pure sinkers routinely start with extreme swelling of the L side of the HL zone before sinking. The lucent zone has a very uniform border that closely reveals the path the bone has taken. Cases that rotate or have a combination of rotation and sinking also leave a lucent trail that describes the path of displacement. The proximal limits of the lesion have a rounded border at the distal end never extends to the ground surface, but it is confined to the limit of the inner sole even when penetration has occurred.
The clinical signs of white line disease can also be very similar to laminitis as both can have an elevated pulse, extreme heat, a dropped sole (centered on the foot or off to one side) and are very sensitive to hoof testers.
The history remains one of the most significant parts of any examination, especially concerning syndromes with similar clinical signs. Most white line disease cases are often diagnosed when very significant damage has occurred, causing large air pockets and often extensive bone displacement. The typical case is a sport or speed horse that develops acute lameness following a race. Radiographs reveal tremendous damage in a horse that has just raced very successfully. This is the key. Laminitis cases do not present in this fashion. They are always lame several days to weeks before lucent lesions are radiographically demonstrable.
Farriers often detect the presence of white line disease when shoeing the sound athlete. The wall may sound hollow when subjected to the action of the nipper, rasp or hammer. Close examination reveals a small slit at the toe in which a large shoeing nail or screw driver can easily be inserted.
Example 1: The athlete that is suddenly lame.
These cases are a bit more straight forward than the one that has a large defect but is currently sound. Acute pain is apparently caused by direct trauma to the sole and bone due to the loss of horn support, which allows sagging of the bone, significant compromise to the vascular supply and excessive pressure of bone against sole corium. Venograms closely reveal the compressive nature of the focal displacement.
Treating the syndrome is much like the toe crack case. Significantly reducing DDF pull will immediately unload the internal load of bone against sole corium and aid prevention of further mechanical horn tearing along the upper margin of the defects. The decision to remove the horn is dependant on several factors. First, it is important to consider the immediate and long term goals of the client. As a rule the cases with extensive loss of horn integrity and acute lameness need to be immediately taken out of training. All undermined horn wall should be removed, the exposed horn thoroughly debrided and a rocker rail shoe applied in a fashion that creates a zero PA between the wings of PIII and the foot side of the shoe and a self-adjusting PA of 15-20 degree with the ground. Recovery can take several months and I do not put horses back in training until the lesion has completely grown out, the medial-lateral balance is once again acceptable and the sole depth is measured at 15-18mm. Systemic, anti-fungal medications can be helpful but used alone do not offer favorable results.
Example 2: The sound horse with significant white line disease lesions.
These cases present a totally different picture than the previous example. Farriers and vets frequently put themselves in a precarious position when making the decision to remove the wall and clean up the larger defects that are found with a routine check up, shoeing or even following a pre-purchase exam. Before removing the wall it is imperative that the responsible party is fully informed of the significance of the lesion, treatment options and the risk of continued training if the lesion is ignored. This very important conversation is always based over past experience with the disease and becomes a judgment call for all concerned. Rule of thumb that helps me predict the client’s interest is the health of the foot.
If the lesion only extends up to the level of the apex of PIII, I clean up from the bottom, pack the defect with oakum, apply a rocker action shoe and treat daily with a topical antifungal agent. The horse stays in full work and I monitor the defect radiographically at every reset session.
When the lucent zone extends only 5-10mm above the apex and the hoof wall and sole are reasonably strong and healthy I will treat basically the same. A small hole is drilled in the outer wall at the most proximal limit of the defect. White, chalky material is removed from the bottom with a very small curette and the areas are packed with oakum and treated daily with antifungal agents. The horse is taken out of full training. Strenuous exercise is put on hold and the lesion is monitored closely for the following 6-8 weeks for signs of advancing or migration up the wall. Preferably the horse is shod with a high mechanical shoe that promotes accelerated horn and sole growth and is compatible with breed specific conditioning exercise.
When the lesion is half way up the face of PIII I recommend the horse be taken completely out of training to achieve a more successful outcome. When the client elects to go against my recommendation but requests that I try to patch the foot up for one more race or event I offer to do so but with a written note describing the risk involved and the fact that the client is fully accepting the responsibility of the risks. There are clients who can defy all common sense laws of Mother Nature and get a few more starts or shows out of a horse that should not be in training. Catastrophic injuries and fatal consequences for horse and rider have occurred as a result of such thinking. As professionals we are responsible for good advice and concern for not only the health of the foot, but for the rider as well.
Soundness and the ability to race and show successfully is not always an indication of good health. This disease clearly points that out.