To use all functions of this page, please activate cookies in your browser.
With an accout for my.bionity.com you can always see everything at a glance – and you can configure your own website and individual newsletter.
- My watch list
- My saved searches
- My saved topics
- My newsletter
Laminitis is a disease of the digital laminae of the foot in a horse and the foot in cattle. The digital laminae is responsible for suspension of the axial skeleton of the animal within the hoof and dissipates concussive forces during locomotion. The laminae is comprised of two interdigitating layers, the epidermal laminae attached to the hoof wall and the dermal laminae attached to the bone. Laminitis results from a compromise of this interaction, the mechanism of which remains unclear and is currently the subject of much research. Laminitis literally means inflammation of the laminae, and while it remains controversial whether this is the primary mechanism of disease, evidence of inflammation occurs very early in some instances of the disease.Loftus JP, Black SJ, Pettigrew A, Abrahamsen EJ, Belknap JK (2007). "Early laminar events involving endothelial activation in horses with black walnut- induced laminitis". Am. J. Vet. Res. 68 (11): 1205–11. doi:10.2460/ajvr.68.11.1205. PMID 17975975.
Coffin bone rotation
Rotation and sinking are two possible consequences of a single severe laminitic episode or of repeated episodes and refer to varying degrees of separation of dermal and epidermal laminae, with resulting anatomical changes in the position of the coffin bone. This result is also commonly called "founder", from the nautical term "to sink". Informally, particularly in the United States, "founder" has come to mean any chronic changes in the structure of the foot that can be linked to laminitis. In some texts, the term "founder" is even used synonymously with laminitis, though such usage is technically incorrect. Put simply, not all horses that experience laminitis will founder but all horses that founder will first experience laminitis.
Rotation occurs when the damage to the laminae is less severe and it will show up mainly in the toe area of the foot. One possible reason for this is the pull of the tendon attached to the coffin bone, the deep flexor tendon, literally pulling the dorsal face of the coffin bone away from the inside of the hoofwall. It is also theorized that the body weight of the animal contributes to rotation of the coffin bone. Rotation results in an obvious misalignment between PII (the short pastern bone) and PIII (the coffin bone). In some cases, the rotation may also result in the tip of PIII penetrating the sole and becoming exposed externally.
Sinking is less common and much more severe. It results when there is a significant failure of the interdigitation between the sensitive and insensitive laminae around the entire perimeter of the hoof. In extreme cases this event allows the entire bony column, often described by its most distal bone, the third phalanx (a.k.a. PIII, P3, coffin bone, pedal bone, distal phalanx) to sink within the bottom of the hoof capsule.
Depending upon the severity at the onset of the pathology, there may be no movement of the coffin bone, rotation only, sinking only or a combination of both rotation and sinking, to varying extents. It is generally agreed that a severe "sinker" warrants the gravest prognosis and may, depending upon many factors, including the quality of after care, age of the horse, diet and nutrition, skill, knowledge and ability of the attending veterinarian and farrier(s), lead to euthanasia of the patient.
Progress of the condition, diagnosis, and treatment
In laminitis cases, a clear distinction must be made between the acute situation, starting at the onset of a laminitis attack and a chronic situation. A chronic situation can be either stable or unstable. The difference between acute, chronic, stable and unstable is of vital importance, when choosing a treatment protocol.
Laminitis can be mechanical or systemic, unilateral (on one foot) or bilateral (on two feet) or may also occur in all four feet.
Systemic laminitis follows from some metabolic disturbance within the horse, from a multitude of possible causes, and results in the partial dysfunction of the epidermal and dermal laminae, which attach the distal phalanx to the hoof wall. With this dysfunction, the deep digital flexor tendon (which attaches to the semi-lunar crest of the distal phalanx and serves to flex the foot) is able to pull the bone away from the wall, instead of flexing the foot. When the coffin bone is pulled away from the hoofwall, the remaining laminae will tear. This may lead to abscesses, within the hoof capsule, that can be severe and very painful. Also, a laminar wedge may form, between the front of the hoof wall and the pedal bone. This laminar wedge may, in some cases, prevent the proper re-attachment (interdigitation) of the laminae. Under certain conditions and only after consultation with an experienced veterinarian and farrier team, a dorsal hoof wall resection, to remove this laminar wedge, may be undertaken.
Systemic laminitis is usually bilateral and is most common in the front feet, although it sometimes affects the hind feet.
Mechanical laminitis or "mechanical founder" does not start with laminitis or rotation of the distal phalanx. Instead, the wall is pulled away from the bone or lost, as a result of external influences. Mechanical founder can occur when a horse habitually paws, is ridden or driven on hard surfaces or loses laminar function, due to injury or pathologies affecting the wall.
Mechanical founder can be either unilateral or bilateral and can affect both front and hind feet.
It is important to note that, once the distal phalanx rotates, it is essential to de-rotate and re-establish proper spatial orientation of p3 within the hoof capsule, to ensure the best long-term prospects for the horse. With correct trimming and, as necessary, the application of orthotics, one can effect this re-orientation. This attempt at re-orientation may be less than one hundred per cent effective, however.
Successful treatment for any type of founder must necessarily involve stabilization of the bony column by some means. Stabilization can take many forms but most include trimming the hoof to facilitate "break over" and trimming the heels to ensure frog pressure. While some horses stabilize if left barefooted, some veterinarians believe that the most successful methods of treating founder involve positive stabilisation of the distal phalanx, by mechanical means, e.g., shoes, pads, polymeric support, etc.
Steps taken to stabilize the bony column gain maximum effect when combined with steps that will reduce the pulling force of the flexor tendon attached to the coffin bone, the deep flexor tendon.
Predisposing factors for laminitis
Many cases of laminitis are caused by more than one factor and are rather due to a combination of causes.
One of the more common causes. Current theory states that if a horse is given grain in excess or eats grass that is under stress and has accumulated excess non-structural carbohydrates (NSC, i.e. sugars, starch or fructan), it may be unable to digest all of the carbohydrate in the foregut. The excess then moves on to the hindgut and ferments in the cecum. The presence of this fermenting carbohydrate in the cecum causes proliferation of lactic acid bacteria and an increase in acidity. This process kills beneficial bacteria, which ferment fiber. The endotoxins and exotoxins may then be absorbed into the bloodstream, due to increased gut permeability, caused by irritation of the gut lining by increased acidity. The endotoxaemia results in impaired circulation, particularly in the feet. This results in laminitis.
Laminitis can also be caused by insulin resistance in the horse (See also Equine Metabolic Syndrome, below. Insulin resistant horses tend to become obese very easily and, even when starved down, may have abnormal fat deposits in the neck, shoulders, loin, above the eyes and around the tail head, even when the rest of the body appears to be in normal condition. The mechanism by which laminitis associated with insulin resistance occurs is not understood but may be triggered by sugar and starch in the diet of susceptible individuals. Ponies and breeds that evolved in relatively harsh environments, with only sparse grass, tend to be more insulin resistant, possibly as a survival mechanism. Insulin resistant animals may become laminitic from only very small amounts of grain or "high sugar" grass. Slow adaptation to pasture is not effective, as it is with laminitis caused by microbial population upsets. Insulin resistant horses with laminitis should be removed from all green grass and be fed only hay that is tested for Non Structural Carbohydrates (sugar, starch and fructan) and found to be below 11% NSC on a dry matter basis. Soaking hay underwater may remove excess carbohydrates and should be part of a first-aid treatment for any horse with laminitis associated with obesity or abnormal fat deposits. This can have the effect of depleting the hay of soluble minerals and vitamins, however, so care with dietary balance is important.
Nitrogen compound overload
Herbivores are equipped to deal with a normal level of potentially-toxic non-protein nitrogen (NPN) compounds in their forage. If, for any reason, there is rapid upward fluctuation in levels of these compounds, for instance in lush spring growth on artificially fertilized lowland pasture, the natural metabolic processes can become overloaded, resulting in liver disturbance and toxic imbalance. For this reason, many avoid using artificial nitrogen fertilizer on horse pasture. If clover is allowed to dominate the pasture, this may also allow excess nitrogen to accumulate in forage, under stressful conditions such as frost or drought. Many weeds eaten by horses are nitrate accumulators. Direct ingestion of nitrate fertilizer material can also trigger laminitis, via a similar mechanism.
Whenever possible, avoid working horses on hard ground. This includes concrete or gravel roads. An indoor or outdoor arena should be periodically dragged with a rake, to loosen the soil and to prevent it from hardening. Hard surfaces increase the concussion upon the horse's feet. The greater and more prolonged the concussion, the more likely it is that the horse will contract laminitis.
When releasing horses back into a pasture, after being kept inside (typically during the transition from winter stabling to spring outdoor keeping), it is important to re-introduce them gradually. Feed horses before turning them out and limit the amount of time outside (45 minutes to an hour at first, gradually increasing the amount of time) and decrease the amount fed to them beforehand, as the season progresses. If a horse consumes too much lush pasture, after a diet of dry hay, the excess carbohydrate of grass can be a shock to its digestive system. If the horse is fed beforehand, it will not eat as much fresh grass when turned out and will be less likely to founder. It is also true that ponies are much more susceptible to this form of laminitis than are larger horses.
Some cases of laminitis have occurred after ingestion of frosted grass. The exact mechanism for this has not been explained but sudden imbalance of the normal bowel flora can be surmised, leading to endotoxin production.
Freezing or overheating of the feet
Cases of laminitis have been observed following an equine standing in extreme conditions of cold, especially if there is a depth of snow. Laminitis has also followed prolonged heating such as may be experienced from prolonged contact with extremely hot soil or from incorrectly-applied hot-shoeing. In either case, it is possible to understand how the circulation of the feet may become adversely affected.
Cold exposure however has been shown to have a protective effect when horses are experimentally exposed to CHO overload. Feet placed in ice slurries were less likely to experience laminitis than "un-iced" feet.
Infections, particularly where caused by bacteria, can cause release of endotoxins into the blood stream, which may trigger laminitis. A retained placenta in a mare (see below) is a notorious cause of laminitis and founder.
Lameness causes a horse to favor the injured leg, resulting in uneven weight distribution. This results in more stress on the healthy legs and can result in laminitis.
A notable case where this may have been the cause is that of the 2006 Kentucky Derby winner Barbaro who sustained a racing injury to the right hind leg in 2006, and soon after succumed to laminitis in the left.
Cushing's disease is common in older horses and ponies and causes an increased predisposition to laminitis.
Peripheral Cushing's disease
Peripheral Cushing's disease (or more properly, Equine Metabolic Syndrome) is an area of much new research and is increasingly believed to have a major role in laminitis. It involves many factors such as cortisol metabolism and insulin resistance. It has some similarities to type II diabetes in humans (see also insulin resistance, described above). In this syndrome, peripheral adipocytes (fat cells) synthesise adipokines which are analogous to cortisol, resulting in Cushings-like symptoms.
It is common practice, in horse-breeding establishments, to check by careful inspection that the entire placenta has been passed, after the birth of a foal. It is known that mares that retain the afterbirth can founder, whether through toxicity or bacterial fever or both.
Anecdotally there have been reports of laminitis following the administration of drugs, especially in the case of corticosteroids. The reaction however may be an expression of idiosyncrasy in a particular patient as many horses receive high dose glucocorticoid into their joints without showing any evidence of clinical laminitis.
No evidence exists to show the mechanism by which glucocorticoids may trigger laminitis in the horse nor is there any research definitely proving a causal link between the two.
Exposure to agrichemicals
Even horses not considered to be susceptible to laminitis can become laminitic when exposed to certain agrichemicals. The most commonly-experienced examples are herbicide and synthesized nitrate fertilizer.
Cellular and Molecular Biology of Laminitis
At present, three primary hypotheses exist for the mechanism of laminar failure. The first is classical inflammation, which includes infiltration of potentially destructive white blood cells. The second is ischemia-reperfusion injury. Researchers have observed both decreased and increased blood flow to the laminae. As ischemia-reperfusion injury reconciles both observations, it has received much attention in past years. Finally, metabolic derangements that lead to impaired cell function and proteolytic enzyme activation has been proposed to be the primary mechanism for development of laminitis.
Signs of laminitis
The sooner the diagnosis is made the faster the treatment and the recovery process can begin. Diagnosing Laminitis is the main problem since the general problem often starts somewhere else in the horses body.
Complications of laminitis
Separation of the hoof wall
The destruction of the sensitive laminae results in the hoof wall becoming separated from the rest of the hoof. Pus may leak out at the white line or at the coronary band.
Rotation of the third phalanx
The third phalanx, also known as the coffin bone, rotates downward. Normally, the front of the third phalanx should be parallel to the hoof wall and its lower surface should be roughly parallel to the ground surface but, in laminitis, a combination of forces (e.g., the tension of the deep digital flexor tendon and the weight of the horse) allows the coffin bone to rotate. The degree of rotation may be determined by severity of the initial attack or by how soon laminitis is detected and how soon actions are taken to treat the horse.
Penetration of the third phalanx through the sole
If rotation of the third phalanx continues, its tip can eventually penetrate the sole of the foot. Penetration of the sole is not fatal; many horses have been returned to service by aggressive treatment by a veterinarian and farrier, but the treatment is time-consuming, difficult and expensive.
There is no cure for a laminitic episode and many go undetected. However, there is one known treatment that involved applying the NOLAN HOOF PLATE. The Nolan Hoof Plate is a band of perforated sheet metal that is wrapped partially around a horse’s hoof. It is applied to the hoof along with a horseshoe. The Nolan Hoof Plate and the horse shoe together form an inflexible exoskeleton cage for the bony foot which keeps the hoof walls immobilized, and enhances blood flow in the circumflex artery (proven through research by research farrier Michael Savoldi and observed with Thermo graphic cameras). The enhanced blood flow occurs because the bars of the foot, when experiencing improved range of motion, together with a stabilized hoof wall, better support the coffin bone. Since the hoof wall is constrained against outward flexing when weighted, pressure on the circumflex artery is relieved, allowing a greater volume of blood to pass through the foot. Since the coffin bone is prevented from descending and tearing the laminae, pain is relieved and the horse walks normally in the short term. In the long term, it enables accelerated healing and stimulates hoof growth in length and wall thickness. Research farrier Michael Savoldi suggests that this exoskeleton cage acts as an orthotic and helps restore the hoof arch.
During the first three to four weeks as the deteriorating interior foot condition slows and reverses, there is not much visible change to the hoof, Thereafter, the entire hoof grows with unusual speed as a result of the enhanced blood flow. All of this healing takes time, which is why the recommended treatment period is 18-20 weeks. This works for most horses.
The enhanced blood flow has shown advantages in improving the health of the hoof. X-rays have shown that, during this extended treatment period with the Nolan Hoof Plate, the hoof capsule rotates back measurably and “re-aligns” with the boney structure of the foot, returning the horse to a sound condition.
A horse can live with laminitis for many years, and although a single episode of laminitis predisposes to further epidodes, with good management and prompt treatment, it is by no means the catastrophe sometimes supposed: most horses suffering an acute episode without pedal bone displacement make a complete functional recovery. Rest and corrective shoeing, can help improve a horse's condition. Common treatments involve pedal bone (PIII) support (either with commercially manufactured pads, or styrofoam blacks bandaged onto the feet), analgesics (usually phenylbutazone - "bute" - or suxibuzone - a related drug with fewer gastric side effects), and a vasodilator to improve laminar blood flow. Systemic acepromazine is commonly used for this purpose, as a powerful peripheral vasodilator with the fringe benefit of mild sedation which reduces the horse/pony's movements and thus reduces concussion on the hooves. Nitroglycerine may also be applied topically to increase blood flow. With modern treatment, most laminitics will be able to bear a rider or completely recover, if the laminitis was not severe or complicated (e.g. by Equine Metabolic Syndrome or Cushing's disease). Even in these cases, a clinical cure can normally be achieved. Endotoxic laminitis (e.g. after foaling) tends to be more difficult to treat. Successful treatment requires a competent farrier and veterinarian and success is not guaranteed. Alternative therapies such as herbal and homeopathic medicine may aid recovery but require expert veterinary input.
The barefoot movement
Laminitis and founder should be seen as two separate maladies.
Laminitis (itis=Inflammation of the laminae) as it stands has only one treatment that has been scientifically tested and that is cryotherapy. Dr. Chris Pollitt has shown that the proteins that trigger breakdown of the laminae fillae do not chemically react with the tissue if it is too cold. Road founder and mechanical founder both irritate the Laminae by physical stress not inflammation though it could be argued that the laminae is inflamed, the cause is external.
Founder is the repositioning of the hoof bones and hoof capsule, this is based on mechanical forces and the quality of the tissue holding things in place.
Since the beginning of this millennia the barefoot methodology has been proven as a suitable treatment for foundered horses. You only have to search the web for case studies and documents on the recovery of horse's. In the past many farrier’s have dabbled with barefoot when all else failed, with some rare but good success. Now rather than being a last ditched effort, barefoot trimming with the right people is the best front line tool for healing horses. It is through the work of people like Pete Ramey and others who have studied the natural hoof that we understand what works and why. In the wild, horses do suffer from laminitis but due to quality of hoof form this does not lead to founder as the foot is functioning correctly.
In the domestic horse with a properly trimmed hoof the risk of founder is almost non existent. Horse's have been diagnosed by Veterinarians with Obel Grade 4 laminitis, the only treatment was phenylbutazone Bute to help with circulation issues and cold water. The horse is usually sound again within 7 days and being ridden on the roads within 14 Days, and these are endocrine system compromised horses (Cushings or Insulin Resistance) and so would be high risk. The most interesting factor is that the hoof wall shows no ring that is usually connected to founder, so bad laminitis if managed correctly does not lead to founder.
Once you have a medically diagnosed disruption of the hoof capsule (Founder), barefoot trimming will gain the fastest recovery to a normal healthy horse. Though this is complicated by horses that have previously been shod or trimmed badly, as on top of the founder you have to deal with weak walls, thin soles and hoof contraction. Luckily with modern technology we now have clip on hoof boots (Old Mac, Epic), that do not do the damage of nail on shoes or screw on plates. These boots allow a horse to walk normally while their hoof is healing. This is all done much faster and stronger than with a nail on or glue on solution. Veterinarian Dr. Tomas Teskey noted that if the hoof heals with an artificial support IE: hoof putty or screw on plates the tissue heals to function within the support structure. The hoof only receives enough stimulation to heal as if the support is always going to be there. The same as when breaking a bone requires the cast to be removed within 4-6 weeks to start true healing. Dr. Teskey discovered the hoof needs a second 6 month healing process if the hoof was artificially supported for more than a few weeks. With hoof boots the padding system can be changed daily to accommodate the changing needs of the hoof.
The advantage barefoot has over a shod or glued on approach is that the hoof can be trimmed to speed up healing and minimise pressures within the wall, this will reverse any perceived rotation and allow the new hoof capsule to grow in tightly to the bone. With barefoot trimming you can see a distinct change in the angulations of the hoof wall growing down from the coronet within 4 weeks. Unfortunately nail on shoes or screw on plates which unless removed on a weekly basis tend to cause the hoof wall to stretch forward and delay healing.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Laminitis". A list of authors is available in Wikipedia.|