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Radiograph of a horse hoof showing rotation of the coffin bone and evidence of sinking, a condition often associated with laminitis. The annotation P2 stands for the middle phalanx, or pastern bone, and P3 denotes the distal phalanx, or coffin bone. The yellow lines mark the distance between the top and bottom part of the coffin bone relative to the hoof wall, showing the distal (bottom) of the coffin bone is rotated away from the hoof wall.

Laminitis is a disease that affects the feet of hooved animals (ungulates)and it is best known in horses and cattle. Clinical signs include foot tenderness progressing to inability to walk, inflammation, and increased temperature in the hooves. Laminitis is characterized by pain of the digital laminae of the hoof, and severe cases with outwardly visible clinical signs are known by the colloquial term founder.


The bones of the hoof are suspended within the axial hooves of ungulates by layers (laminae) of modified skin cells which are tightly interwoven and glued together by a matrix of collagens and proteins, and together they act as shock absorbers during locomotion. In horses 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 (a.k.a. PIII, P3, the third phalanx, pedal bone, or distal phalanx).[1]


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.[2]

Laminitis is characterized by a "compromise in the interaction" of the laminae between the hoof wall and the coffin bone, the mechanism of which remains unclear and is the subject of much research.

Laminitis can be either mechanical or systemic.

Mechanical laminitis[edit]

Mechanical laminitis starts when the hoof wall is pulled away from the bone or lost, as a result of external influences. Mechanical laminitis can occur when a horse habitually paws, is ridden or driven on hard surfaces (or loses laminar function, owing to an injury or pathologies affecting the hoof wall).

Systemic laminitis[edit]

Systemic laminitis is usually bilateral (on two feet) and although it can affect any number of feet, it is most common in the front feet.

There are a number of hypotheses for the mechanism that results in laminar failure.

  1. Classical inflammation, which includes infiltration of potentially destructive white blood cells.[3] [4]
  2. 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.[5]
  3. Metabolic derangements that lead to impaired cell function and proteolytic enzyme activation.[6] [7]

Systemic laminitis can lead to rotation or sinking and this in turn may lead to abscesses, within the hoof capsule, that can be severe and very painful.

Hoof specimen, sagittal section. Severe hoof capsule rotation and P3 penetration into the sole
Hoof sheet plastinate showing severe laminitis

Rotation, sinking, and founder[edit]

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.

Normally, the front of the third phalanx is parallel to the hoof wall and its lower surface should be roughly parallel to the ground surface. A single severe laminitic episode or repeated less severe episodes can, depending upon the degree of separation of dermal and epidermal laminae, lead to either rotation or sinking of the pedal bone, both of which result in anatomical changes in the position of the coffin bone with visible separation of the laminae colloquially known as founder.

Rotation occurs when the damage to the laminae is less severe and it will show up mainly in the toe area of the foot. 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. A combination of forces (e.g. the tension of the deep digital flexor tendon and the weight of the horse) result in the deep digital flexor tendon, literally pulling the dorsal face of the coffin bone away from the inside of the hoofwall, which allows the coffin bone to rotate. 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). If rotation of the third phalanx continues, its tip can eventually penetrate the sole of the foot.

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. 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. In extreme cases this event allows the tip to eventually penetrate the sole of the foot. Penetration of the sole is not inherently 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. 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.

Hoof sagittal section with massive inflammation and rotation of third phalanx.


Laminitis has multiple causes, some of which commonly co-occur. These causes can be grouped into broad categories.


Vasoactive amines[edit]

The inflammatory molecule histamine has also been hypothesized as a causative agent of laminitis.[9][10] However, contradictory evidence has demonstrated that the role of histamine in laminitis has not been conclusively established.[11]

Mechanical separation[edit]

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.[12]

Poor blood circulation[edit]

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.[12]

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.[12] A notable example is the 2006 Kentucky Derby winner Barbaro.[13]

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.[citation needed] For this reason, some horsemen recommend trailering as an initial step in rehabilitation of a horse after long confinement.[citation needed]

Laminitis has been observed following an equine standing in extreme conditions of cold, especially if there is a depth of snow.[citation needed] Laminitis has also followed prolonged heating such as may be experienced from prolonged contact with extremely hot soil or from incorrectly applied hot-shoeing.[citation needed]

Complex causes[edit]


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.



A lateral-medial (anatomy)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.[14]

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. The venogram can assess the severity and location of tissue compromise and monitor effectiveness of the current therapy.[14]

Other diagnostics[edit]

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.[citation needed] Nuclear scintigraphy may also be useful in certain situations. Ultrasonography has been explored as a way to quantify changes in bloodflow to the foot.[15]


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 horse's 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 episodes, 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.[16] 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:


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.

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.[citation needed]

Medical therapies[edit]


Cooling of the hoof in the developmental stages of laminitis has been shown to have a protective effect when horses are experimentally exposed to carbohydrate overload. Feet placed in ice slurries were less likely to experience laminitis than "un-iced" feet.[17]

Pain management

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.[citation needed] Newer non-specific NSAIDS such as suxibuzone may be somewhat safer than bute.[18] [19] Cox-2 specific drugs are now labeled for use in horses, such as firocoxib and diclofenac, which are much safer than non-selective NSAIDS. .[20] Pentoxifylline and isoxsuprine both have anti-inflammatory effects, and may help improve circulation by improving deformability of red blood cells.[citation needed]

Other analgesics currently in less widespread use, but with good potential benefit include opioids, gabapentin, and many others.[citation needed]


Vasodilators are often used with the goal of improving laminar blood flow. However, during the developmental phases of laminitis, vasodilation is contraindicated, either through hot water or vasodilatory drugs.[21] 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.[22] 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.[23]

Mechanical treatments[edit]

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. However, this attempt at re-orientation is not always completely effective.

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 application of external orthotic 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

Medical approaches[edit]

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.[24]

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.[25]

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.[26]

Informal use of the word founder[edit]

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.

See also[edit]


  1. ^ Pollitt (1995). Color Atlas of the Horse's Foot. Mosby. ISBN 0-7234-1765-2. 
  2. ^ 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. 
  3. ^ Nourian, AR; Asplin KE, McGowan CM, Sillence MN, Pollitt CC (2009). "Equine laminitis: ultrastructural lesions detected in ponies following hyperinsulinaemia". Equine Vet J. 41 (7): 671–677. PMID 19927586. 
  4. ^ Black, SJ; Lunn DP, Yin C, Hwang M, Lenz SD, Belknap JK. (2006). "Leukocyte emigration in the early stages of laminitis.". Vet Immunol Immunopatho 109 (1-2): 161–166. doi:10.1016/j.vetimm.2005.08.017. PMID 16169600. 
  5. ^ Hood, DM; Grosenbaugh DA, Mostafa MB, Morgan SJ, Thomas BC (1993). "The role of vascular mechanisms in the development of acute equine laminitis". J Vet Intern Med 7 (4): 228–234. PMID 8246212. 
  6. ^ . PMID 15635906.  Missing or empty |title= (help)
  7. ^ . PMID 15635908.  Missing or empty |title= (help)
  8. ^
  9. ^ Nilsson, S. A. 1963. "Clinical, morphological and experimental studies of laminitis in cattle". Acta Vet. Scand. 4(Suppl. 1):188–222.
  10. ^ 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.
  11. ^ 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.
  12. ^ a b c Nonclassical laminitis, James Rooney, DVM
  13. ^ "Transcript of Press Conference on the condition of Barbaro" (PDF). University of Pennsylvania School of Veterinary Medicine. 13 July 2006. 
  14. ^ a b Ramey, Taylor (2011). Care and Rehabilitation of the Equine Foot. Hoof Rehabilitation Publisher. pp. 234–253. ISBN 978-0-615-52453-5. 
  15. ^ 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. Retrieved 2008-04-19. 
  16. ^ Colahan, Patrick; Alfred Merritt, James Moore, I Mayhew (December 1998). Equine Medicine and Surgery (Fifth Edition ed.). Mosby. p. 408. ISBN 978-0-8151-1743-8. 
  17. ^ Pollitt, Christopher (November 2003). "Equine Laminitis" (PDF). Proceedings of the AAEP 49. Retrieved 2008-04-19. 
  18. ^ McAllister, Charles G.; et al. (1993). "Comparison of Adverse Effects of Phenylbutazone, flunixin megalumine, and ketoprofen in horses,". JAVMA. 202(1). 
  19. ^ Sabaté, David; et al. (2005). Suxibuzone as a Therapeutical Alternative to Phenylbutazone in the Treatment of Lameness in Horses (PDF) XIV. Retrieved 2008-04-19. 
  20. ^ Doucet, Michele; et al. (2008). Comparison of efficacy and safety of paste formulations of firocoxib and phenylbutazone in horses with naturally occurring osteoarthritis, JAVMA, Vol 232(1). 
  21. ^ 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. 
  22. ^ 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. 
  23. ^ Belknap, JK; Black SJ (2005). "Review of the Pathophysiology of the Developmental Stages of Equine Laminitis". Proceedings American Association of Equine Practitioners 51. 
  24. ^ Eustace (1996). Explaining Laminitis and its Prevention. E.F.S. pp. 29–31. ISBN 0-9518974-0-3. 
  25. ^ Eastman, TG; et al. (1998). "Deep Digital Flexor Tenotomy as a Treatment for Chronic Laminitis in Horses: 37 Cases" (PDF). Proceedings of the American Association of Equine Practitioners 44. Retrieved 2008-04-19. 
  26. ^ 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. 

Further reading[edit]

External links[edit]