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2002 - 15th Annual Bluegrass Laminitis Symposium Notes

Classifying Laminitic Damage: How Using a Simple Scale Can Help All Concerned Understand and Project the Aggressiveness Needed, the Length, Cost and Future Outcome For What Lies Ahead

Written and presented January 2002 by R.F. (Ric) Redden, DVM

Laminitis is one of the most complex disease syndromes facing the veterinarian and farrier. The disease is extremely complex and not well understood. And to compound the problem, the foot is actually a very poorly understood piece of the equine anatomy. The last couple decades have certainly changed the concept of "no foot - no horse" with the modern day horseman and professional. Advanced technology, current research and numerous articles concerning the foot have also fostered new concepts and ultimately a whole new mindset.

Laminitis has traveled the same road. There have been tremendous advancements and increased knowledge about the syndrome; but unfortunately, even with all that is offered today in the prevention and treatment of the disease, little effort has been spent on classifying the degree of damage.

I learned many years ago that seldom, if ever, do two horses have the same degree of damage. Likewise, feet are rarely affected the same on each horse even when the same mechanics and therapeutic regime are used. Several factors seem to influence the overall assessment as well as the progress rate and overall outcome. Just simply designing a detailed plan that adequately reverses the forces at play is all but a shot in the dark without first assessing the damage and identifying the precise areas compromised. Being able to grossly and radiographically assess the overall health of the digit requires a good working knowledge of the vast range of norm for all major breeds of horses. Training your eye to recognize the norm is quite simple if a rigid, methodical x-ray protocol is used for all radiographic exams. Picking lesions from x-rays that just might be the problem has inherent risk that often lead to misdiagnosis. Putting too much focus on the "abnormal" lesion can easily overshadow the benefit of observing the whole picture.

The first mission in treating the foot is to develop an eye for foot characteristics. Become familiar with all sizes and shapes of feet that are breed specific. See them and feel them in three dimensions. The farrier has a tremendous advantage over the veterinarian from this perspective simply because they handle literally hundreds and thousands of feet annually. They soon develop the feel for what they normally see and begin to see what they normally feel.

Conversely, most farriers do not have the knowledge and experience to interpret radiographic information. The result is that they often fail to manipulate the digit to gain maximum mechanical advantage for addressing hot spots, creating an optimal healing environment and reperfusing the digit.

Veterinarians on the other hand have the academics, but only a few have the opportunity and time to develop a sense of feel for the normal foot. Therefore, it becomes difficult to relate radiographic lesions to the hoof capsule. Veterinarians and farriers who want to be podiatrists must learn to fully assess the foot internally as well as grossly. Without a working range of normal, subtle changes in soft-tissue parameters, as well as bone lesions, are meaningless.

Mark Twain once advised that a riverboat pilot must learn more than is allowed for one man to know. Furthermore, he noted that to be a good riverboat pilot, one must learn everything he knows in another fashion every 24 hours. Watching for tree snags in an attempt to avoid sinking demanded unprecedented alertness on the part of all steamboat pilots. This holds true for the podiatrist, as every case is a challenge that demands a constant search for perfection.

Lets assume that the range of norm is not an issue at this point, and we can go on to discover the slight variance of "normal" that are a reflection of the degree of damage to a given foot. Overall hoof conformation now plays a major factor. For example, Standardbreds, Morgans and some Arabs have a tremendous horn capsule. They have thick, heavy walls and dense, concave soles with lots of mass. Typical feet may have the following characteristics:

  • Hoof Angle 53-56 degrees
  • Heel Tubule Angle 45-50 degrees
  • Sole Depth 20mm with a 10 mm cup
  • Palmar Angle positive 3-5 degrees
  • Digital Breakover 23mm

Picture this foot. Draw it. Look for it. Memorize it. This is a strong, healthy foot given that all other intricate pieces of anatomy are normal. This foot can withstand a very significant insult to the laminae and still retain a normal foot given some sort of adequate treatment and a few months to heal.

Let's look at another totally different type foot. This is a Thoroughbred weighing 1,000 pounds, race fit with the following characteristics:

  • Sole Depth 1mm or less with no cup
  • Palmar Angle negative 2 degrees
  • Hoof Angle 40-45 degrees
  • Heel Tubule Angle 15 - 20 degrees heel tubule angle
  • CE 15 mm below the coronary groove

This particular case also experienced a chronic toe crack, as well as a few migrating abscesses, when he was young. He has paper-thin walls that have been backed up into the white zone at the toe. This horse has a flat tire on a good day. Give him a little dose of laminitis and you have a total disaster.

Determining the degree of damage to each respective foot is where a grading scale comes into play. My scale is very arbitrary, and I do not use it to come up with a specific number. Instead, I determine a range of damage based on several observable factors. It is nearly impossible to successfully treat a large range of damage without first determining how much damage is present and what you have to work with.

Previous pathology or extensive stress on a foot also reduces the overall resistance of the digit. This makes it a high-risk case. In my book, Understanding Laminitis, I have the following basic scale:

The 1 – 1000 scale could just as easily be 1 – 10 or 1 – 100, the significance of the 1000 scale is it emphasizes the large range of damage that can be found between, breeds, individuals and even feet on the same horse. The scale is there to develop a new mindset about how we talk about this complex disease syndrome. Having a much better feeling for the degree of damage, chronicity of the same and the sequence of cascading event that plague most all significant insult cases offers tremendous advantages for the veterinarian – farrier team that others are not afforded. When your working protocol is designed to attack the high scale cases then you have a plan. The failure to consider the large range of damage has brought bloodshed among farrier and veterinarians as they attempt to argue mute points concerning two totally different problems. If we are to speak about the success of a particular mechanical treatment we must not only identify the start model but also the degree of damage and specific areas of most damage.

Zones of Concern
The proverbial degree of rotation can be used as a perimeter indicator so long as we don’t get too carried away. I seldom if ever attempt to measure the degree of capsular rotation as it is a bit meaningless and quite arbitrary. There are not many feet with perfectly straight walls from the coronary ground to toe and none with a straight faced coffin bone. Draw your lines wherever you like, it doesn’t matter, you can easily see if there is 5 – 10 or 15 degrees, being more specific is a waste of time as it is not the damage along the anterior face of PIII that creates the major problem. For many years we have been taught that rasping the rotation away is a helpful adjunct to treatment. I don’t believe it and find no validity in removing the angle of capsular rotation. This is erroneously considered derotation and has no bearing on the outcome of the case other than to weaken the anterior arch of horn. But for the sake of describing perimeter variations we will use the broad brackets of 5 – 10 – 15 degrees as a means to describe rotation in the active rotating cases (not chronic, long term cases).

Sinking
We must be careful describing degree of sinking. Degree of sinking is relative compared to what? The distance between the top of the horn wall and top of extensor process varies greatly among horses. I find only the strong, upright foot to consistently have the extensor process quite close to the same plane as the top of the horn wall. Weaker, flatter feet with numerous types of pathology can be as much as 20 mm. below the horn wall and survive as quite sound animals. Therefore unless the extensor process is at the level of the horn wall on the first radiographic examination the significance of it being lower may have little validity if it has been there for some time. Regardless, marking the hoof wall with radiopaste points starting at the hard horn of the coronary band produces a very distinct marker for tracking the descending coffin bone, especially sinkers. I look for no sinking, 5 mm, 10 mm, 15 mm, and 20mm; this is actual movement from the start point not a one time assessment without prior knowledge of the norm for that individual.

Sole depth is measured straight beneath PIII to the top surface of the shoe or ground marker on the barefoot horse; be as accurate as possible within one millimeter when possible. Make certain the primary beam is centered close to the palmar surface of PIII in order to accurately measure sole depth and palmar angle. It is the sole beneath the wing that is measured not a sagittal cut. Performance Thoroughbreds and Quarter Horses often are found with less than 10 mm. of sole, not that they are sound but they often remain competitive. They can go to 3 – 5 mm. and seem to survive it where a horse with 15 to 20 mm. compressed to 3 to 4 mm.is in serious jeopardy. Laminitic Warmbloods with 20 – 2 5 mm. of sole compressed to 15 mm. are seriously compromised and soon develop to high scale damage, therefore the start point is once again part of the assessment. Considering the sole depth with extensor process measurement can be helpful with comparative film when there is little sole, less than ten degrees and no change at the top, I call this the Belotta syndrome. The foot has been rasped off, sole thinned since the last film was made. The palmar distance looks like a sinker but the perimeter at the top has not changed. This is a very significant finding on a bilaterally lame horse that look very laminitic, e.g., can’t walk, and front feet out front, throbbing pulse, painful to testers or even thumb pressure, horn – lamellar zone normal, extensor process 5 – 10 below horn wall, 5 - mm. of sole – guess what? No foot, simply trimmed inside the comfort zone. Put them on thin soles then try to cup it out on barefoot horses and you have a sore baby that can take weeks to heal.

Palmar Angle is measured by drawing a line along the wings of the palmar surface (not the toe area of the apex) as it relates to the ground surface. We also speak of it as it relates to the heel zone of the shoe. Several factors influence palmar angles:
Club feet naturally have a much higher palmar angle than the opposite which can have a negative angle or caudal rotation. Ponies, mules and many others with very upright feet have a strong palmar angle (15 – 20 degrees). The angle changes constantly with horn growth and routine trimming and shoeing. Farriers that are conscious of the angle and how they can influence it have a tremendous advantage over their colleagues. Range of normal will vary somewhat even among light breeds. Light breeds with healthy, strong feet normally have between 3- 5 degrees in front and slightly higher behind. Many Mustangs will be flat (zero), most domestic horses that are zero have crushed their heels and have folded the heal tubules forward.

Significant lamellar damage often precipitates rotation of PIII around its axis apparently due to the action lever of the toe resisting the normal pull of the deep flexor tendon. As the digit rotates around PIII the palmar angle increases. The palmar angle increases as rotation occurs, very chronic cases may have 15 to 20 degrees palmar angle and 30 to 40 degrees capsular rotation. Measuring capsular angle of rotation once noticeable, distorted horn growth has occurred is questionable as it is a reflection of horn and lamellar pathology, not rotation around the articulation. Race horses with a 5 degree negative palmar angle must actually rotate 5 degrees just to be horizontal. Without baseline film at the onset these very significant finding may be overlooked. The palmar angle is by far one of the most valuable perimeters for the podiatrist as it offers direct insight to the force of the deep digital flexor and many options that can significantly influence these forces. Having said that, let’s describe a high scale case of laminitis, right front grade 2 club foot, horn – lamellar zone 18/22 mm, 60 degrees hoof angle, less than 10 degrees capsular rotation, 15 degrees palmar angle, 2 mm. of sole depth sagging below the shoe and grade 2 bone disease, a venogram would finalize this assessment. The opposite foot has a hoof angle of 50 degrees, heel tubule angle less than 20 degrees (underun), less than 5 degrees capsular rotation, less than 5 degrees palmar angle, horn – lamellar zone 17/17 mm. (15/15 mm. norm), digital breakover 50 mm., extensor process less than 15 mm. If this is the first film how do we determine what is new and what is old damage? If this is the first few days of the syndrome we could be in big trouble. The club foot has significant bone damage characteristics of chronic apex loading; some of the rotational forces could be associated with the club which is quite normal. The opaque zones will help determine this if you can see it. Ten degrees is too much displacement though for a mid scale club, possibly though a few recurrent abscesses have thickened the horn – lamellar zone. How do we know where he is in the syndrome? Subsequent comparative film, coupled with clinical signs is helpful but may require 3 – 10 days to pick up any subtle changes. Secondly, digital venogram is extremely helpful when trying to determine how old a displacement lesion may be. Acute lamellar tears have a very characteristic pattern, old scars do also, remodeled circumflex vessels appear totally different from acute prolapsed vessels. I encourage any podiatrist to learn this technique, use normal animals to gain confidence, competence and a basic range of normal.

Lucent areas: Sub wall and sub solar; where are they and how extensive do they seem to be? Especially the lucent lines that run the entire length of the sole and most of the wall, draining tracks – where are they and how extensive? What is the color of the exudate and how much draining is present on a daily basis. Gas density lesions can be in many areas of the digit, all these for a very specific reason. A first glance it is easy to assume that all lesions found in a specific location have the same etiology but closer examination reveals stark differences in shape and precise location. Pertinent facts concerning the history also become important as they often help describe the nature and longevity of the lesion. The sub wall lucent zones that can appear several days to weeks following a significant bout of laminitis occurs just within the stratum medium along the ectodermal lamellar layer. This air dense zone is thought to be nitrous oxide seen as the result of lamellar disruption. The characteristic shape has a smooth linear side, small radius at the most proximal end and a slightly larger radius at the distal end that stops adruptly at the inner sole margin. Even with penetrated coffin bones this zone stops at the inner sole margin. Often there is a lucent line that runs from the distal end of the lucency to the apex of PIII. This area decides the path of travel for the descending coffin bone. The lamellar lucent zone is quite different from that found with advanced white line disease. White line disease is the result of bacterial and fungal invasion of the stratus medium, the non-pigmented (white) zone of the wall. Therefore, the name is quite descriptive as it basically involves only the white zone of the hoof capsule. Anatomist years ago gave the terminal laminae a misleading name when they called it the white line. Possibly the color has changed over the past centuries but presently it is never white but yellow to tan in color in all horses. The striated lines are the end of the ectodermal lamellar junction of sole and wall. As the innermost horn wall deteriorates the terminal laminae are bent forward by the sole as the counter face of the wall is absent. The terminal laminae are most visible in the white line case as the sole has migrated at the outer margin of the wall. This is the first clue that pathology has occurred. There is little or no wall and no terminal laminae along the toe which is quite a different picture for laminitis. The terminal laminae become stretched and distorted as the effects of rotation disfigures the delicate network. The air dense zone that occurs with white line disease starts at the ground surface, small but demonstrable it can be seen at ground contact. The sides of the lesion are very irregular in shape and the apex of the lesion is often pointed with several distinct fingerlike projections. The prior lateral views often reveal a lucent zone that appears to extend into the bone but it actually is only superimposed over the bone which can be confirmed with other tangent views. Most all significant cases of white line disease will have capsular rotation, many times measuring 30 to 40 degrees. The inexperienced eye that is looking for rotation and air density beneath the wall will often be mislead by the similarities of the lamellar lesions. The stark difference are therefore of utmost importance. A closer look often reveals dirt, small stones and sand within the horn wall that has entered along the deficit at the ground surface. The weight of the horse closes this flap when loaded creating a one way ball valve effect. Once the very vulnerable ectodermal laminae become severely compressed by this space occupying, foreign body the horse shows signs of pain, other anatomical areas are compromised with extensive displacement that can occur in same planes that also create a painful response. Regardless most of all cases remain quite sound well after radiographic lesions are quite well established, a totally different picture is found with laminitis. Sub solar lucency occurs for several reasons; those found with laminitis are often due to extensive bruising and/or sepsis of the sole corium. These areas are often trapped with the sole layer as new horn is laid down at the inner face. It is often thought that many sub sole lucencies are abscesses and must be opened. The contrary is often more true. Abscesses that are the result of trauma can be seen in several areas of the sole long after the fact. Invading these areas on a horse that is quickly recovering from a bout of lameness can take weeks to months to heal. Therefore great consideration must be given to the exact location, distinct characteristics, longevity and clinical findings of each case.

Coronary band separation
This is another important zone to classify. With experience you will soon be able to put it in the right perspective. Ongoing, hot, swollen, painful, draining coronary bands, are super high scale, can be slough time. Also the moist more subtle separations that have a slight serosanguineous drainage are potentially lethal also. The dry separation looks scary but seldom causes a problem. Small suppurative ruptures seldom create a serious threat, I do not rate them but take note of where and how frequent they appear and should go into your data bank as an aid to prepare a treatment design.

Venograms
This procedure is technique sensitive but offers a world of information concerning the degree of damage and how it relates to the overall prognosis. The scope of this paper does not offer time to dwell on the large range of norm or large range of damage but I will list the unique characteristics that spell big trouble. I strongly suggest that you develop the skills for the technique using normal feet for several reasons; time is of essence, the bet film are taken within 30 to 45 seconds following injection to the dye. I like to take 4 to 6 views in this time frame. The contrast rapidly leaks into the interstitial tissue reducing the accuracy of interpretation. It is best to become familiar with several normal contrast patterns before attempting to read pathological changes. The most common error is tourniquet leak which will create a stark loss pattern and false negative data.
Listed below are examples of contrast patterns that hold significant data and can be used as prognostic indicators. Note: it is vital that you obtain full digital perfusion before attempting to read the venogram.
  1. Stark loss of contrast to the entire digit, this is a dead foot with no where to go.
  2. Total loss of contrast along coronary groove, anterior face, circumflex and terminal arch; extremely grave prognosis.
  3. Stark loss of contrast along coronary groove and/or medial or lateral cartilage and laminae due to medial listing or sinking. A very difficult case to say the least, long term aggressive therapy, best hope is for a yard ornament, pasture companion, broodmare (E.T), this is a tough, expensive venture. 
  4. Moderate to good perfusion along coronary crest and lamellar terminal arch. Prolapsed circumflex vessels and heavy loss of contrast along medial quarter due to medial listing. Reasonably good prognosis for future brood stock, still requires six to eight months recovery.

Due to the many variables found between breeds, conformation, environmental influences and overall foot management programs, I encourage you to become competent with the procedure and develop a working knowledge of normal feet before attempting to use the venogram to make life and death decisions. Failure to fill the digit due to leakage can produce a tree top pattern, the vessels in the heel zone are very distinct and more sparse than normal and taper out much like tree limbs. This pattern can be very misleading to the novice eye.

Using a meaningful grading system also helps me be more focused on many separate aspects of the syndrome that I otherwise may overlook. As the case proceeds I constantly look for areas of improvement and also stay cognoscente of the areas that are deteriorating, often as one foot gains ground the other will lose ground.

Full evaluation of the case on the initial visit is very important as the career, life and death decisions must be made which can be devastating news to clients. I feel as veterinarians, we have a tremendous responsibility to offer viable options to our clients concerning any and all life threatening syndromes. To have a list of meaningful options we must first assess the damage taking into consideration all the points mentioned above. Once we have accurately defined the degree of damage we must use our personal expertise and knowledge of the subject to offer options. The big question; how do we do that when we have had little or no good experience treating this devastating disease process? There are numerous veterinarians and farriers that have a good handle on this syndrome, use them, learn from them and call for help if needed. Study the film, history and evidence presented, we must realize that the career or life of this patient is left in our hands, are we qualified to take that responsibility? If not, we must become competent or refer them to those that are. Twenty-seven years have passed since I received the outstanding student award in equine medicine and surgery and I feel as though I am finally qualified to treat acute and chronic laminitis. The road to this goal set many years ago has been long, treacherous and humbling. Every single case, every foot has it’s unique characteristics, damage and response to therapy.

A basic question that clients often ask; how bad is the damage? I often answer compared to what? Then I proceed to determine the damage compared to a normal foot, compatible with the breed and other particulars of the case. The expense of fully evaluating a laminitic case can be very significant and must be discussed before proceeding. Yes, we can pull out an array of suggested treatments and just go for it without a clue what to expect. Many cases have the potential of being high risk, will hold there own, appear to be doing just fine for six to eight weeks. Apparently the foot has a tremendous reserve not offered to any other part of the body. It can withstand long periods of circulatory compromise or collapse with little or no apparent ill effects. This alone is the big killer, as most all mid to high scale cases will appear quite content and maybe only slightly lame on a very minimum dose of Bute for several weeks, then suddenly they are extremely painful. Films taken at this stage often reveal serious PIII displacement. I must caution, using only the attitude and visual assessment of the animal to determine degree of damage is potentially lethal. I encourage all podiatry focused farriers and veterinarians to become dedicated to learning all they know in a different fashion every 24 hours. Learning is contagious and raises the enthusiasm levels of all concerned. Compromise the circulation to any other part of the body to the same degree that the feet suffer and it would be obvious that the horse was in trouble. The foot is quite different and looking at its amazing function it doesn’t surprise me. The highly specialized cells that form the durable digit apparently also have the ability to function for an extended period of time under very adverse conditions with significant loss of circulation. Take good film every five to six days, track your progress or regression before the horse tells you that the foot is going south.