How To Treat High Scale Laminitis With Wall Ablation And Transcortical Cast
Updated: Apr 20, 2020
2003 - 16th Annual Bluegrass Laminitis Symposium Notes
Written and presented January 2003 by R.F. (Ric) Redden, DVM
Laminitis remains one of the horse industry’s biggest killers. Insurance companies recognize colic just ahead of laminitis, therefore it is a very important subject. Unfortunately there are no consistent guidelines to help clinicians and farriers successfully deal with laminitis. In my book, Understanding Laminitis, I have a very simple scale that helps group the cases according to degrees of damage to the vascular supply, soft tissue and bone. The scale in reality is quite complex requiring in-depth knowledge of the subject and good clinical experience. Most veterinarians and farriers see less than six cases a year and may never see a high-scale case. The low to low mid-scale cases fortunately make up the majority of cases across the board. These cases are responsive to a multitude of mechanical devices that include shoes, trim techniques and often professional neglect (simply doing nothing). Mother Nature often smiles on these cases and most recover with little or no life threatening damage. The lower scale cases offer a false sense of security to those responsible for treatment and when no effort is made to clearly define the degree of damage, disaster strikes when the higher scale cases are treated in the same manner.
Let's take a quick look at a high scale case. A typical history of the cases I see during foaling season; mare foals, very difficult dystocia. The foal is usually very large, has to be pulled or possibly requires fetatomy to deliver. Heavily stressed, the mare has acute laminitis within hours of delivery. Most cases very painful, grade 5/5, glued to the ground in front and treading water with the hind feet which spells big trouble with this history. Placing her in Modified Ultimates or in Styrofoam doesn't alter her clinical picture as one normally finds with the lower scale cases. The mare continues to fall apart as the day proceeds, heavy breathing, very anxious eye, unwilling to move, eat or drink. Coronary bands are changing rapidly; a very distinct ledge can be felt around the entire coronary crown. Taking radiographs can be a task due to the pain response, blocking the feet just for the sake of taking film is not recommended as more damage quickly ensues when the feet are blocked. Without prior base lines the first set of film may be difficult to accurately interpret. Large Thoroughbred broodmares with some age will often have 20-22mm HL (horn - lamellar) zones and frequently are found with chronic capsular rotation, especially those with poor quality feet. Flat or dropped soles, full thickness toe cracks, typical dish are common findings on some of the world’'s best mares. Nevertheless the radiographic damage may be seen only as lamellar swelling which can be up to 25mm or not demonstrable at this stage. I have seen a handful of cases that went through the massive lamellar slough so quickly that little or no swelling was seen radiographically, they are rare cases. Most cases will show very distinct thickening of the laminae within hours of a significant bout of laminitis. Very disciplined, methodical, repeatable, soft tissue films are necessary to see these early changes. Rotation remains a popular radiographic sign but be keenly attuned to what is happening at the HL (horn - lamellar) zone as it is by far the most useful information. Films made only a few hours later can clearly show an increase in horn - lamellar zone, decrease in sole depth and an increase in C.E. (coronary band - extensor process). Palmar angles may be unchanged. All these subtle but measurable signs indicate massive lamellar dysfunction has occurred and the boney column is descending. Heavy, strong hoof capsules with 25mm of sole certainly have a better reserve than the previously described case, but this case can be very deceptive as rotation may not be seen at all.
A venogram is the only way that I can accurately assess the degree of damage at this or any other stage for that matter. The procedure is quite easy, requires very little equipment, but is a timely exercise that must flow along quickly in order to produce quality film. All film must be made within 45 seconds following injection of the dye. I strongly advise everyone to practice the technique on normal horses before attempting a severe laminitic case. Film interpretation must be relative to what is normal. A large range of normal exists as well as a large range of pathology. Making life or death decisions based on little or no experience is high risk and often spells disaster. I cannot stress enough the importance of technique and interpretation. The venogram on most of the mares above will have stark loss of contrast along the anterior face of PIII, stark loss along the circumflex zone and often little or no contrast in the terminal arch. The coronary plexus will appear as a crown well above the hoof, the heel area is most often well perfused. Caution: Tourniquet failure is one of the biggest problems I see with many of the venograms I read. The typical under perfused pattern may appear as described above, but the vessels in the heel region appear as an upside down tree, the vessels taper to finer points much like tree limbs. Avoid misinterpreting the artifacts found with poor technique as it may decide the fate of your patient. When the venogram describes a foot that is basically depleted of the vital blood supply, the primary emergency goal is to restore adequate blood supply to the digit before irreversible damage has occurred.
I have used my partial decompression technique to include lower wall resection, upper wall resection and internal decompression technique (deep flexor tenotomy) followed by realigning the palmar surface of PIII, all with a reasonable degree of success. Looking back over literally hundreds of cases, some that pulled through, many that made it but were left crippled and others that simply slipped away from me regardless of my efforts has been humbling. I have often asked myself, what were the determining factors that seperated these cases? Venograms during all stages of the syndrome on a large number of cases has convinced me it was the degree of vascular damage,the speed that it occurred and the time lapse or chronicity of the comressive forces. Full Wall Ablation: The fall of 2000 I removed the entire hoof capsule from a nice filly that was draining sersosanguineous fluid from the top of the right front coronary band. I placed her in a transcortical cast to protect the healing digit offering her immediate clinical relief and bought her enough time to cornify the laminae and grow 10-15mm of sole before the pins were removed. She grew a very nice horn capsule, sole and frog and was very happy for several months, but unfortunately the coffin bone had large areas of irreversible vascular damage and the new horn was formed around the partially dead bone with a pseudo laminae attachment. The persistent decaying effect on the bone and less than favorable horn attachment finally resulted in the decision to euthanize this very nice prospective broodmare. Seeing this opportunity to help others I realized the technique had promise but I had to move much quicker in order to minimize permanent damage to the coffin bone. Since this case I have removed the entire hoof capsule on 13 feet, 8 horses;
1 case euthanized due to lack of a favorable response.
1 case responded well and appeared to be on the mend. It developed a septic coffin joint and was eu