The digital laminae are responsible for suspension of the axial skeleton of the animal within the hoof and dissipate concussive forces during locomotion. There are about 600 pairs of interleaved laminae: the epidermal laminae attached to the hoof wall and the dermal laminae attached to the coffin 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.
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.
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.
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.
Rotation and sinking of the coffin bone (in horses) 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 digital flexor tendon, literally pulling the dorsal face of the coffin bone away from the inside of the hoofwall. There are also ligaments attaching the collateral cartilages to the digit, primarily in the palmar portion of the foot, possibly contributing to a difference in support from front to back. 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. Coffin bones pierce the bottom of the hoof (near the frog).
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.
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.
Laminitis has multiple causes, some of which commonly co-occur. These causes can be grouped into broad categories.
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.
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 (or any legume) 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.
Laminitis can sometimes develop after a serious case of colic, due to the release of endotoxins into the blood stream. You may want to look into an article referring to Carbohydrate Overload.
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.
Freezing temperatures in spring and fall coincide with outbreaks of laminitis in horses at pasture. While laminitis has never been induced in pasture under controlled conditions, various forms of carbohydrates (fructan and sugar) have been implicated. Under sunny conditions, sugar production in pasture grass and weeds is high. Cold temperatures cause growth to cease so that sugar cannot be utilized as fast as it is produced. This triggers formation of storage carbohydrates in grass. Cool season grasses form fructan, and warm season grasses form starch. Sugars cause increase in insulin levels, which is known to cause laminitis by an unknown mechanism. Fructan, which also is used to induce laminitis in a clinical setting is theorized to cause laminitis by causing an imbalance of the normal bowel flora leading to endotoxin production. These endotoxins may exacerbate insulin resistance, or the damage to the lining of the gut may release other as yet unidentified trigger factors in to the blood stream.
For horses prone to laminitis, restrict or avoid grazing when night temperatures are below 40 °F (5 °C) followed by sunny days. When growth resumes during warmer weather, sugar will be used to form protein and fiber and will not accumulate.
Systemic infections, particularly where caused by bacteria, can cause release of endotoxins into the blood stream. A retained placenta in a mare (see below) is a notorious cause of laminitis and founder.
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.
The inflammatory molecule histamine has also been hypothesized as a causative agent of laminitis. However, contradictory evidence has demonstrated that the role of histamine in laminitis has not been conclusively established.
Commonly known as road founder, this occurs when horses with long toes are worked extensively on hard ground. The long toes and hard ground together contribute to delayed breakover and hence mechanical separation of the laminae at the toe. Historically this was seen in carriage horses. These horses were bred for heavy bodies and long slim legs with relatively small hooves; their hooves were trimmed for long toes (to make them lift their feet higher, enhancing their stylish "action"); and they were worked at speed on hard roads. Road founder is also seen in overweight animals, particularly when hooves are allowed to grow long: classic examples are ponies on pasture board in spring, and pregnant mares.
Poor blood circulation
Normal blood circulation in the lower limbs of a horse depends in part on the horse moving about. Lack of sufficient movement, alone or in combination with other factors, can cause stagnant anoxia, which in turn can cause laminitis.
A horse favoring an injured leg will both severely limit its movement and place greater weight on the other legs. This sometimes leads to static laminitis, particularly if the animal is confined in a stall. A notable example is the 2006 Kentucky Derby winner Barbaro.
Transport laminitis sometimes occurs in horses confined in a trailer or other transportation for long periods of time. Historically, the most extreme instances were of horses shipped overseas on sailing ships. However, there is some evidence that the continual shifting of weight required to balance in a moving vehicle enhances blood circulation. For this reason, some horsemen recommend trailering as an initial step in rehabilitation of a horse after long confinement.
Laminitis has 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.
Pituitary Pars Intermedia Dysfunction (formerly 'Cushing's disease')
Pituitary Pars Intermedia Dysfunction (PPID), or 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.
Early diagnosis is essential to effective treatment. However, early outward signs may be fairly non-specific. Careful physical examination typically is diagnostic, but radiographs are also very useful.
- Increased temperature of the wall, sole and/or coronary band of the foot.
- A pounding pulse in the digital palmar artery. (The pulse is very faint or undetectable in a cold horse, readily evident after hard exercise.)
- Visible trembling
- Increased vital signs and body temperature
- Flared Nostrils
- Walking very tenderly, as if walking on egg shells
- Repeated "easing" of affected feet
- The horse standing in a "founder stance" (the horse will attempt to decrease the load on the affected feet). If it has laminitis in the front hooves, it will bring its hindlegs underneath its body and put its forelegs out in front called "pointing"
- Tendency to lie down, whenever possible or, if extreme, to remain lying down.
A lateral-medial radiograph gives useful information regarding the degree of rotation, the sole thickness, measurement of the dorsal hoof wall thickness, and vertical deviation. It is critical to be consistent in hoof positioning and focal distance in order to make objective comparisons. Digital radiography often provides built-in digital calibration and measurement tools that can be used to provide angle and distance data. Abscesses are sometimes visible as gas pockets. Repeat radiographs can be used to monitor progression of the condition.
The use of venograms can help to add prognostic information, particularly in horses where the degree of pain does not match the radiographic changes. In venography, a contrast agent which is visible on radiographs is injected into a blood vessel in the foot, delineating the vasculature of the foot. Defects in blood filling and length of solar papillae are possible to determine using this technique.
Other imaging tools to show mechanical deviations which have been used in laminitis cases are computed tomography as well as MRI which also provides some physiologic information. Nuclear scintigraphy may also be useful in certain situations. Ultrasonography has been explored as a way to quantify changes in bloodflow to the foot.
The sooner the diagnosis is made the faster the treatment and the recovery process can begin. Rapid diagnosis of laminitis is often difficult since the general problem often starts somewhere else in the horses body. With modern therapies, most laminitics will be able to bear a rider or completely recover, if treated quickly, and 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 often 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. 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. Discovery of laminitis, either active or relatively stabilized, on an equine prepurchase exam typically downgrades the horse's value, as the possibility of recurrence is a significant risk factor for the future performance of the horse.
Several radiographic abnormalities can be judged to correlate with a worsened prognosis:
- Increased degree of rotation of P3 relative to the dorsal hoof wall
- Increased founder distance, the vertical distance from the coronary band (seen with a radiopaque marker) to the dorso-proximal aspect of P3
- Decreased sole depth
- Solar penetration by P3
There is no cure for a laminitic episode and many go undetected. Initial treatment with cryotherapy and anti-inflammatory drugs may prevent mechanical breakdown if instituted immediately, but many cases are only detected after the initial microscopic damage has been done.
Cold exposure in the developmental stages of laminitis 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.
Non-steroidal anti-inflammatory medications (NSAIDS) are the main drug type used for analgesia as well as control of any ongoing inflammation. Phenylbutazone (bute) is commonly used for its strong effect and relatively low cost. Flunixin (Banamine), ketofen, and others are also used. While 'stacking' NSAIDS may provide some analgesic benefit, this considerably increases the risk associated with this type of drug, including gastric ulcers, kidney disease, and colitis. Newer non-specific NSAIDS such as suxibuzone may be somewhat safer than bute. Cox-2 specific drugs are now labeled for use in horses, such as firocoxib and diclofenac, which are much safer than non-selective NSAIDS. Pentoxifylline and isoxsuprine both have anti-inflammatory effects, and may help improve circulation by improving deformability of red blood cells
Other analgesics currently in less widespread use, but with good potential benefit include opioids, gabapentin, and many others.
Vasodilators are often used with the goal of improving laminar blood flow. However, during the develomental phases of laminitis, vasodilation is contraindicated, either through hot water or vasodilatory drugs. Systemic acepromazine as a vasodilator with the fringe benefit of mild sedation which reduces the horse/pony's movements and thus reduces concussion on the hooves, may be beneficial after lamellar damage has occurred, although no effects on laminar blood flow with this medication have been shown. Nitroglycerine has also been applied topically in an attempt to increase blood flow, but this treatment does not appear to be an effective way to increase bloodflow in the equine digit.
Mechanical approaches to hoofcare
Besides pain management and control of any predisposing factors, mechanical stabilization is a primary treatment goal once the initial inflammatory/metabolic issues have resolved. No approach has been shown to be effective in all situations, and there is ongoing debate over the merits and faults of the numerous techniques.
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 deep digital flexor tendon on the coffin bone.
The barefoot movement
Since the beginning of this millennium the barefoot methodology has been proven as a suitable treatment for laminitic and foundered horses. Many case studies and anecdotal successes are described on the internet on the recovery of horses through barefoot methods, although no peer-reviewed journal articles have been published. In the past many farriers have dabbled with the barefoot approach when all else failed, with some rare but good success. Now rather than being a last ditch effort, barefoot trimming properly employed is a front line tool for healing horses. Pete Ramey and others have studied the natural hoof, providing a better understanding of 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. With immediate treatment of a properly trimmed barefoot horse diagnosed with Obel Grade 4 laminitis, where the only treatments are phenylbutazone (bute) and cold water therapy, the horse can be sound again within as little as 7 days and being ridden on the roads within 14 days. This is seen even in high risk horses with a compromised endocrine system (Cushings or Insulin Resistance). An interesting factor is that in these cases, the hoof wall shows no ring that is usually connected to founder, so bad laminitis if managed correctly does not always lead to founder.
Barefoot advocates claim that barefoot trimming will gain the fastest recovery to a normal healthy horse after a medical diagnosis of disruption of the hoof capsule (founder). This is often complicated when horses have previously been shod or trimmed badly, as weak walls, thin soles and hoof contraction contribute to pain as well as difficulty in stabilization of P3. Clip on hoof boots (Old Mac, Epic) are now available 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 believed to occur much faster and with better strength 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. A parallel is seen in fracture repair, where initial stabilization occurs within the cast, but only after removal of the cast in 4–6 weeks does the strength of bone structure develop. Dr. Teskey found that 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.
An advantage that the properly trimmed unshod foot has over a shod or glued-on approach is that the hoof can be trimmed frequently to facilitate healing and minimise pressures within the wall, with the goal of reversing any rotation and allowing the new hoof capsule to grow in tightly to the bone. With barefoot trimming there can be a distinct change in the angulations of the hoof wall growing down from the coronet within 4 weeks. Barefoot trimmers claim that nail-on shoes or screw-on plates, unless removed on a weekly basis, tend to cause the hoof wall to stretch forward and delay healing.
Studies on hoof health by Dr. Hiltrud Strasser (Germany) and Jaime Jackson (U.S.) suggest an alternative, optimistic view on laminitis, which is supported by proponents of the barefoot horse movement. This is a holistic approach to the disease, mainly based on pulling shoes, proper hoof care and trimming, proper diet and movement. However, definitive studies as to the benefits in laminitic equines are still lacking.
The application of external devices to the foot in a horse with non-displaced laminitis and once displacement has occurred is widespread. Most approaches attempt to shift weight away from the laminae and onto secondary weight-bearing structures, while sparing the sole
3M support foam
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Other interventional approaches
Dorsal hoof wall resection
A dorsal hoof wall resection may help in certain conditions after consultation with an experienced veterinarian and farrier team. If decreased bloodflow distal to the coronary plexus is seen on a venogram, or when a laminar wedge forms between P3 and the hoof wall, preventing the proper re-attachment (interdigitation) of the laminae, this procedure may be beneficial. 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, as well as a mass of disorganized tissue called a laminar (or lamellar) wedge.
Deep Digital flexor tenotomy
Because the rotation of P3 is exacerbated by continued pull on the deep digital flexor tendon, one approach to therapy has been to cut this tendon, either in the cannon region or in the pastern region. While this technique has been criticized as being unsuccessful and invasive, its advocates claim that it is too often used in cases which are too far advanced. Advocates claim that by cutting the tendon at the right time, mechanical de-rotation of P3 is possible, which can allow time for the new laminar attachments to form.
Botulinum Toxin infusion
As an alternative to the deep digital flexor tenotomy, Botulinum type A toxin has been infused into the body of the deep digital flexor muscle. This theoretically allows for the same de-rotation as the tenotomy procedure, but without the potential for scarring or contracture associated with that procedure. A recent study used this technique in seven laminitic horses. There was significant improvement in six of the horses, and moderate improvement in the seventh.
- ↑ Pollitt (1995). Color Atlas of the Horse's Foot. Mosby. ISBN 0723417652.
- ↑ 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.
- ↑ http://www.safergrass.org/pdf/CTEPforagelaminitis.pdf
- ↑ Nilsson, S. A. 1963. "Clinical, morphological and experimental studies of laminitis in cattle". Acta Vet. Scand. 4(Suppl. 1):188–222.
- ↑ Takahashi, K., and B. A. Young. 1981. "Effects of grain overfeeding and histamine injection on physiological responses related to acute bovine laminitis". Jpn. J. Vet. Sci. 43:375–385.
- ↑ Thoefner, M.B., C.C. Pollitt, A.W. van Eps, G.J. Milinovich, D.J. Trott, O. Wattle and P.H. Andersen. 2004. "Acute bovine laminitis: A new induction model using alimentary oligofructose overload". J. Dairy Sci. 87:2932–2940.
- ↑ 7.0 7.1 7.2 Nonclassical laminitis, James Rooney, DVM
- ↑ "Transcript of Press Conference on the condition of Barbaro" (PDF). University of Pennsylvania School of Veterinary Medicine. 13 July 2006. http://www.vet.upenn.edu/newsandevents/news/Barbaro_Transcript7-13.pdf.
- ↑ Wongaumnuaykul, Santi; et al. (March 2006). "Doppler Sonograpohic Evaluation of the Digital Blood Flow in Horses with Laminitis or Septic Pododermatitis" (abstract). Veterinary Radiology & Ultrasound 47 (2): pp. 199–205. doi:10.1111/j.1740-8261.2006.00128.x. http://www.blackwell-synergy.com/doi/abs/10.1111/j.1740-8261.2006.00128.x. Retrieved 2008-04-19.
- ↑ Colahan, Patrick; Alfred Merritt, James Moore, I Mayhew (December 1998). Equine Medicine and Surgery (Fifth Edition ed.). Mosby. pp. 408. ISBN 9780815117438. http://www.elsevier.com/wps/find/bookdescription.cws_home/694822/description#description.
- ↑ Pollitt, Christopher (November 2003). "Equine Laminitis" (PDF). Proceedings of the AAEP 49. http://www.ivis.org/proceedings/AAEP/2003/pollitt/IVIS.pdf. Retrieved 2008-04-19.
- ↑ Sabaté, David; et al. (2005) (PDF). Suxibuzone as a Therapeutical Alternative to Phenylbutazone in the Treatment of Lameness in Horses. XIV. http://www.ivis.org/proceedings/SIVE/2005/free_com/Sabate.pdf. Retrieved 2008-04-19.
- ↑ Pollitt, Christopher C. (2003). "Medical Therapy of Laminitis". in Ross MW, Dyson SJ. Diagnosis and Management of Lameness in the Horse. St. Louis, MO: Saunders. p. 330. ISBN 0-7216-8342-8.
- ↑ Adair, HS; Schmidhammer JL, Goble DO, et al. (1997). "Effects of acepromazine maleate, isoxsuprine hydrochloride and prazosin hydrochloride on laminar blood flow in healthy horses". Journal of Equine Veterinary Science 17: 599. doi:10.1016/S0737-0806(97)80186-4.
- ↑ Belknap, JK; Black SJ (2005). "Review of the Pathophysiology of the Developmental Stages of Equine Laminitis". Proceedings American Association of Equine Practitioners 51. doi:P2669.1205 (inactive 2010-03-16).
- ↑ Physiological trimming for a healthy equine foot Michigan State University, College of Veterinary Medicine
- ↑ Eustace (1996). Explaining Laminitis and its Prevention. E.F.S.. pp. 29–31. ISBN 0-9518974-0-3.
- ↑ Eastman, TG; et al. (1998). [http://www.ivis.org/proceedings/AAEP/1998/Eastman.pdf "Deep Digital Flexor Tenotomy as a Treatment for Chronic Laminitis in Horses: 37 Cases"] (PDF). Proceedings of the American Association of Equine Practitioners 44. http://www.ivis.org/proceedings/AAEP/1998/Eastman.pdf. Retrieved 2008-04-19.
- ↑ Carter, D; Renfroe (2009). "A Novel Approach to the Treatment and Prevention of Laminitis: Botulinum Toxin Type A for the Treatment of Laminitis". Journal of Equine Veterinary Science 29.
- Adams Lameness in Horses Ted S. Stashak, D.V.M.
- The Lame Horse James R. Rooney, D.V.M.
- 25 Most Frequently Asked Questions & Answers about Laminitis and Founder Burney Chapman, C.J.F., Bill Moyers, D.V.M, et al.
- The Illustrated Veterinary Encyclopedia for Horsemen Equine Research Inc.
- Veterinary Medications and Treatments for Horsemen Equine Research Inc.
- Horse Owner's Veterinary Handbook James M. Giffin, M.D. and Tom Gore, D.V.M.
- Founder: Prevention & Cure the Natural Way, Jaime Jackson, Star Ridge Company
- Who's Afraid of Founder. Laminitis Demystified: Causes, Prevention and Holistic Rehabilitation, Hiltrud Strasser, The Naked Hoof
- Corrective Farriery, a textbook of remedial horseshoeing Simon Curtis
- The Principles of Horseshoeing II and The Principles of Horseshoeing III Dr. Doug Butler
- Illustrated Atlas of Clinical Equine Anatomy and Common Disorders of the Horse, Vol. One, Ronald J. Riegel, Susan E. Hakola
- Understanding Laminitis, Dr. R.F. Redden
- Laminitis, C.C. Pollitt
- Founder: Prevention & Cure the Natural Way" Jaime Jackson, Star Ridge Publishing, 2001, ISBN 0-9658007-3-3
- Photographic Record of Founder Episode: http://picasaweb.google.com/jandrinkwater/LucyFounder