Laminitis

Last updated
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 radiograph with annotation.jpg
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 ungulates and is found mostly in horses and cattle. Clinical signs include foot tenderness progressing to inability to walk, increased digital pulses, and increased temperature in the hooves. Severe cases with outwardly visible clinical signs are known by the colloquial term founder , and progression of the disease will lead to perforation of the coffin bone through the sole of the hoof or being unable to stand up requiring euthanasia.

Horse Domesticated four-footed mammal from the equine family

The horse is one of two extant subspecies of Equus ferus. It is an odd-toed ungulate mammal belonging to the taxonomic family Equidae. The horse has evolved over the past 45 to 55 million years from a small multi-toed creature, Eohippus, into the large, single-toed animal of today. Humans began domesticating horses around 4000 BC, and their domestication is believed to have been widespread by 3000 BC. Horses in the subspecies caballus are domesticated, although some domesticated populations live in the wild as feral horses. These feral populations are not true wild horses, as this term is used to describe horses that have never been domesticated, such as the endangered Przewalski's horse, a separate subspecies, and the only remaining true wild horse. There is an extensive, specialized vocabulary used to describe equine-related concepts, covering everything from anatomy to life stages, size, colors, markings, breeds, locomotion, and behavior.

Cattle domesticated form of Aurochs

Cattle—colloquially cows—are the most common type of large domesticated ungulates. They are a prominent modern member of the subfamily Bovinae, are the most widespread species of the genus Bos, and are most commonly classified collectively as Bos taurus.

Animal euthanasia is the act of putting an animal to death or allowing it to die by withholding extreme medical measures. Reasons for euthanasia include incurable conditions or diseases, lack of resources to continue supporting the animal, or laboratory test procedures. Euthanasia methods are designed to cause minimal pain and distress. Euthanasia is distinct from animal slaughter and pest control although in some cases the procedure is the same.

Contents

Laminae

The bones of the hoof are suspended within the axial hooves of ungulates by layers of modified skin cells, known as laminae or lamellae, which act as shock absorbers during locomotion. In horses, there are about 550–600 pairs of primary epidermal laminae, each with 150–200 secondary laminae projection from their surface. [1] These interdigitate with equivalent structures on the surface of the coffin bone (PIII, P3, the third phalanx, pedal bone, or distal phalanx), known as dermal laminae. [2] The secondary laminae contain basal cells which attach via hemidesmosomes to the basement membrane. The basement membrane is then attached to the coffin bone via the connective tissue of the dermis. [1]

In zoology, the epidermis is an epithelium that covers the body of a eumetazoan. Eumetazoa have a cavity lined with a similar epithelium, the gastrodermis, which forms a boundary with the epidermis at the mouth.

Coffin bone bone

The coffin bone, also known as the pedal bone (U.S.), is the bottommost bone in the front and rear legs of horses, cattle, pigs and other ruminants. In horses it is encased by the hoof capsule. Also known as the distal phalanx, third phalanx, or "P3". The coffin bone meets the short pastern bone or second phalanx at the coffin joint. The coffin bone is connected to the inner wall of the horse hoof by a structure called the laminar layer. The insensitive laminae coming in from the hoof wall connects to the sensitive laminae layer, containing the blood supply and nerves, which is attached to the coffin bone. The lamina is a critical structure for hoof health, therefore any injury to the hoof or its support system can in turn affect the coffin bone.

Hemidesmosome cell-substrate junction (attachment structure) found in epithelial cells that links intermediate filaments to extracellular matrices via transmembrane complexes

Hemidesmosomes are very small stud-like structures found in keratinocytes of the epidermis of skin that attach to the extracellular matrix. They are similar in form to desmosomes when visualized by electron microscopy, however, desmosomes attach to adjacent cells. Hemidesmosomes are also comparable to focal adhesions, as they both attach cells to the extracellular matrix. Instead of desmogleins and desmocollins in the extracellular space, hemidesmosomes utilize integrins. Hemidesmosomes are found in epithelial cells connecting the basal epithelial cells to the lamina lucida, which is part of the basal lamina. Hemidesmosomes are also involved in signaling pathways, such as keratinocyte migration or carcinoma cell intrusion.

Pathophysiology

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. [3] A severe inflammatory event is thought to damage the basal epithelial cells, resulting in dysfunction of the hemidesmosomes and subsequent reduction in adherence between the epithelial cells and the basement membrane. [4] Normal forces placed on the hoof are then strong enough to tear the remaining laminae, resulting in a failure of the interdigitation of the epidermal and dermal laminae between the hoof wall and the coffin bone. When severe enough, this results in displacement of the coffin bone within the hoof capsule. [4] Most cases of laminitis occur in both front feet, but laminitis may be seen in all four feet, both hind feet, or in cases of support limb laminitis, in a single foot. [4]

Basement membrane A thin layer of dense material found in various animal tissues interposed between the cells and the adjacent connective tissue. It consists of the basal lamina plus an associated layer of reticulin fibers.

The basement membrane is a thin, fibrous, extracellular matrix of tissue that separates the lining of an internal or external body surface from underlying connective tissue in metazoans. This surface may be epithelium, mesothelium and endothelium

Mechanism

The mechanism remains unclear and is the subject of much research. Three conditions are thought to cause secondary laminitis:

Sepsis life-threatening organ dysfunction triggered by infection

Sepsis is a life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs. Common signs and symptoms include fever, increased heart rate, increased breathing rate, and confusion. There may also be symptoms related to a specific infection, such as a cough with pneumonia, or painful urination with a kidney infection. In the very young, old, and people with a weakened immune system, there may be no symptoms of a specific infection and the body temperature may be low or normal, rather than high. Severe sepsis is sepsis causing poor organ function or insufficient blood flow. Insufficient blood flow may be evident by low blood pressure, high blood lactate, or low urine output. Septic shock is low blood pressure due to sepsis that does not improve after fluid replacement.

Inflammation

Inflammatory events that are associated with laminitis include sepsis, endotoxemia, retained placenta, carbohydrate overload (excessive grain or pasture), enterocolitis, pleuropneumonia, and contact with black walnut shavings. [5] In these cases, there is an increase in blood flow to the hoof, bringing in damaging substances and inflammatory cells into the hoof.

Placenta organ that connects the developing foetus to the uterine wall

The placenta is a temporary organ that connects the developing fetus via the umbilical cord to the uterine wall to allow nutrient uptake, thermo-regulation, waste elimination, and gas exchange via the mother's blood supply; to fight against internal infection; and to produce hormones which support pregnancy. Placentas are a defining characteristic of placental mammals, but are also found in marsupials and some non-mammals with varying levels of development.

Carbohydrate organic compound that consists only of carbon, hydrogen, and oxygen

A carbohydrate is a biomolecule consisting of carbon (C), hydrogen (H) and oxygen (O) atoms, usually with a hydrogen–oxygen atom ratio of 2:1 (as in water) and thus with the empirical formula Cm(H2O)n (where m may be different from n). This formula holds true for monosaccharides. Some exceptions exist; for example, deoxyribose, a sugar component of DNA, has the empirical formula C5H10O4. The carbohydrates are technically hydrates of carbon; structurally it is more accurate to view them as aldoses and ketoses.

Enterocolitis or coloenteritis is an inflammation of the digestive tract, involving enteritis of the small intestine and colitis of the colon. It may be caused by various infections, with bacteria, viruses, fungi, parasites, or other causes. Common clinical manifestations of enterocolitis are frequent diarrheal defecations, with or without nausea, vomiting, abdominal pain, fever, chills, alteration of general condition. General manifestations are given by the dissemination of the infectious agent or its toxins throughout the body, or – most frequently – by significant losses of water and minerals, the consequence of diarrhea and vomiting.

Endocrinopathy

Endocrinopathy is usually the result of improper insulin regulation, and is most commonly seen with pituitary pars intermedia dysfunction (also called equine Cushing's syndrome) and equine metabolic syndrome (EMS), [4] as well as obesity and glucocorticoid administration. [5] In cases of EMS, most episodes occur in the spring when the grass is lush. [4]

Insulin Hormone in vertebrates

Insulin is a peptide hormone produced by beta cells of the pancreatic islets; it is considered to be the main anabolic hormone of the body. It regulates the metabolism of carbohydrates, fats and protein by promoting the absorption of carbohydrates, especially glucose from the blood into liver, fat and skeletal muscle cells. In these tissues the absorbed glucose is converted into either glycogen via glycogenesis or fats (triglycerides) via lipogenesis, or, in the case of the liver, into both. Glucose production and secretion by the liver is strongly inhibited by high concentrations of insulin in the blood. Circulating insulin also affects the synthesis of proteins in a wide variety of tissues. It is therefore an anabolic hormone, promoting the conversion of small molecules in the blood into large molecules inside the cells. Low insulin levels in the blood have the opposite effect by promoting widespread catabolism, especially of reserve body fat.

Pituitary pars intermedia dysfunction

Pituitary pars intermedia dysfunction (PPID), or equine Cushing's disease, is an endocrine disease affecting the pituitary gland of horses. It is most commonly seen in older animals, and is classically associated with the formation of a long, wavy coat (hirsutism) and chronic laminitis.

Equine metabolic syndrome

Equine metabolic syndrome (EMS), is an endocrinopathy affecting horses and ponies. It is of primary concern due to its link to obesity, insulin resistance, and subsequent laminitis. There are some similarities in clinical signs between EMS and pituitary pars intermedia dysfunction, also known as PPID or Cushing's disease, and some equines may develop both, but they are not the same condition, having different causes and different treatment.

Trauma

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 ("road founder"), or in cases of excessive weight-bearing due to compensation for the opposing limb, a process called support limb laminitis. Support limb laminitis is most common in horses suffering from severe injury to one limb, such as fracture, resulting in a non-weight bearing state that forces them to take excessive load on the opposing limb. This causes decreased blood flow to the cells, decreasing oxygen and nutrient delivery, and thus altering their metabolism which results in laminitis. [1]

Theories of pathophysiology

Matrix metalloproteinases

One of the newest theories for the molecular basis of laminitis involves matrix metalloproteinases (MMPs). Metalloproteinases are enzymes that can degrade collagen, growth factors, and cytokines to remodel the extracellular matrix of tissues. To prevent tissue damage, they are regulated by tissue inhibitors of metalloproteinases (TIMPs). In cases of laminitis, an underlying cause is thought to cause an imbalance of MMPs and TIMPs, favoring MMPs, so that they may cleave substances within the extracellular matrix and therefore break down the basement membrane. [6] Since the basement membrane is the main link between the hoof wall and the connective tissue of P3, it is thought that its destruction results in their separation. [5] MMP-2 and MMP-9 are the primary enzymes thought to be linked to laminitis. [5]

Theories for development

There are multiple theories as to how laminitis develops. These include:

Rotation, sinking, and founder

Hoof sagittal section with massive inflammation and rotation of third phalanx. Laminitis embedding hc biovision.jpg
Hoof sagittal section with massive inflammation and rotation of third phalanx.

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 and distal displacement may occur in the same horse. [4] Both forms of displacement may lead to the coffin bone penetrating the sole. 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.

Rotation is the most common form of displacement, and, in this case, the tip of the coffin bone rotates downward. [4] The degree of rotation may be influenced by the severity of the initial attack and the time of initiation and aggressiveness of treatment. 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 hoof wall, which allows the coffin bone to rotate. Also, ligaments attaching the collateral cartilages to the digit, primarily in the palmar portion of the foot, possibly contribute to a difference in support from front to back. The body weight of the animal probably 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 a significant failure of the interdigitation between the sensitive and insensitive laminae around a significant portion of the hoof occurs. The destruction of the sensitive laminae results in the hoof wall becoming separated from the rest of the hoof, so that it drops within the hoof capsule. Sinking may be symmetrical, i.e., the entire bone moves distally, or asymmetric, where the lateral or medial aspect of the bone displaces distally. [4] 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. A severe "sinker" usually warrants the gravest prognosis and may, depending upon many factors, including the quality of aftercare, age of the horse, diet and nutrition, skill, and knowledge and ability of the attending veterinarian and farrier(s), lead to euthanasia of the patient.

Phases of laminitis

Treatment and prognosis depend on the phase of the disease, with horses treated in earlier stages often having a better prognosis.

Developmental phase

The developmental phase is defined as the time between the initial exposure to the causative agent or incident, until the onset of clinical signs. It generally lasts 24–60 hours, and is the best time to treat a laminitis episode. Clinical laminitis may be prevented if cryotherapy (icing) is initiated during the developmental phase. [1]

Acute phase

The acute phase is the first 72 hours following the initiation of clinical signs. Treatment response during this time determines if the horse will go into the subacute phase or chronic phase. Clinical signs at this time include bounding digital pulses, lameness, heat, and possibly response to hoof testing. [1]

Subacute phase

The subacute phase occurs if there is minimal damage to the lamellae. Clinical signs seen in the acute phase resolve, and the horse becomes sound. The horse never shows radiographic changes, and there is no injury to the coffin bone. [1]

Chronic phase
Hoof specimen, sagittal section. Severe P3 rotation and penetration into the sole. A lamellar wedge is evident. Founder severe rotation.JPG
Hoof specimen, sagittal section. Severe P3 rotation and penetration into the sole. A lamellar wedge is evident.

The chronic phase occurs if damage to the lamellae is not controlled early in the process, so that the coffin bone displaces. Changes that may occur include separation of the dermal and epidermal lamellae, lengthening of the dermal lamellae, and compression of the coronary and solar dermis. If laminitis is allowed to continue, long-term changes such as remodeling of the apex and distal border of the coffin bone (so that a "lip" develops) and osteolysis of the coffin bone can occur. [1]

The chronic phase may be compensated or uncompensated. Compensated cases will have altered hoof structure, including founder rings, wide white lines, and decreased concavity to the sole. Horses will be relatively sound. On radiographs, remodeling of the coffin bone and in cases of rotational displacement, the distal hoof wall will be thicker than that proximally. Venograms will have relatively normal contrast distribution, including to the apex and distal border of the coffin bone, and the coronary band, but "feathering" may be present at the lamellar "scar." [1]

Uncompensated cases will develop a lamellar wedge (pathologic horn), leading to a poor bridge between P3 and the hoof capsule. This will lead to irregular horn growth and chronic lameness, and horses will suffer from laminitis "flares." Inappropriate hoof growth will occur: the dorsal horn will have a tendency to grow outward rather than down, the heels will grow faster than the toe, and the white line will widen, leading to a potential space for packing of debris. The solar dermis is often compressed enough to inhibit growth, leading to a soft, thin sole (<10 mm) that may develop seromas. In severe cases where collapse of the suspensory apparatus of P3 has occurred, the solar dermis or the tip of P3 may penetrate the sole. The horse will also be prone to recurrent abscessation within the hoof capsule. Venogram will show "feathering" into the vascular bed beneath the lamellae, and there will be decreased or absent contrast material in the area distal to the apex of the coffin bone. [1]

Causes

The front feet of this horse exhibit the rings and overgrowth typical of foundered horses 2015-09-07. Arkhipo-Osipovka 026.jpg
The front feet of this horse exhibit the rings and overgrowth typical of foundered horses

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

Endotoxins

Vasoactive amines

The inflammatory molecule histamine has also been hypothesized as a causative agent of laminitis. [8] [9] However, contradictory evidence indicates the role of histamine in laminitis has not been conclusively established. [10]

Mechanical separation

Commonly known as road founder, mechanical separation occurs when horses with long toes are worked extensively on hard ground. The long toes and hard ground together contribute to delayed breakover, hence mechanical separation of the laminae at the toe. Historically, this was seen in carriage horses 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. [11]

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. [11]

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

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, the continual shifting of weight required to balance in a moving vehicle may enhance blood circulation, so 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 in deep 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

Risk factors

Whilst diet has long been known to be linked to laminitis, there is emerging evidence that breed and body condition also play a role. [15] Levels of hormones, particularly adiponectin, and serum insulin are also implicated, opening up new possibilities for developing early prognostic tests and risk assessments. [16]

Diagnosis

Early diagnosis is essential to effective treatment. However, early outward signs may be fairly nonspecific. Careful physical examination typically is diagnostic, but radiographs are also very useful.

Clinical signs

Cross-section of horse with severe laminitis, showing a dished dorsal hoof wall that grows in a more horizontal manner, and a sole that is convex due to pressure from the tip of P3 secondary to rotation. Laminitis plastinate hc biovision.jpg
Cross-section of horse with severe laminitis, showing a dished dorsal hoof wall that grows in a more horizontal manner, and a sole that is convex due to pressure from the tip of P3 secondary to rotation.

Lameness evaluation

Hoof testing

Laminitic horses are generally sore to pressure from hoof testers applied over the toe area. However, there is risk of a false negative if the horse naturally has a thick sole, or if the hoof capsule is about to slough. [1]

Obel grading system

The severity of lameness is qualified using the Obel grading system: [17]

Nerve blocks

Horses suffering from the disease usually require an abaxial sesamoid block to relieve them of pain, since the majority of pain comes from the hoof wall. However, chronic cases may respond to a palmar digital block since they usually have primarily sole pain. [4] Severe cases may not respond fully to nerve blocks. [1]

Radiographs

Radiographs are an important part of evaluating the laminitic horse. They not only allow the practitioner to determine the severity of the episode, which does not always correlate with degree of pain, [1] but also to gauge improvement and response to treatment. Several measurements are made to predict severity. Additionally, radiographs also allow the visualization and evaluation of the hoof capsule, and can help detect the presence of a lamellar wedge or seromas. [1] The lateral view provides the majority of the information regarding degree of rotation, sole depth, dorsal hoof wall thickness, and vertical deviation. [1] [18] A 65-degree dorsopalmar view is useful in the case of chronic laminitis to evaluate the rim of the coffin bone for pathology. [1]

Radiographic measurements
Radiographic measurements, including coronary extensor distance (CE), horn:lamellar distance (HL), sole depth (SD), digital breakover (DB), and palmar angle (PA) LaminiticRadiographicMeasurements.jpg
Radiographic measurements, including coronary extensor distance (CE), horn:lamellar distance (HL), sole depth (SD), digital breakover (DB), and palmar angle (PA)

Several radiographic measurements, made on the lateral view, allow for objective evaluation of the episode.

  1. Coronary extensor distance (CE): the vertical distance from the level of the proximal coronary band to the extensor process of P3. It is often used to compare progression of the disease over time, rather than as a stand-alone value. A rapidly increasing CE value can indicate distal displacement (sinking) of the coffin bone, while a more gradual increase in CE can occur with foot collapse. Normal values range from 0–30 mm, with most horses >12–15 mm. [1]
  2. Sole depth (SD): the distance from the tip of P3 to the ground.
  3. Digital breakover (DB): distance from the tip of P3 to the breakover of the hoof (dorsal toe). [1]
  4. Palmar angle (PA): the angle between a line perpendicular to the ground, and a line at the angle of the palmar surface of P3.
  5. Horn:lamellar distance (HL): the measurement from the most superficial aspect of the dorsal hoof wall to the face of P3. 2 distances are compared: a proximal measurement made just distal to the extensor process of P3, and a distal measurement made toward the tip of P3. These two values should be similar. In cases of rotation, the distal measurement will be higher than the proximal. In cases of distal displacement, both values will increase, but may remain equal. Therefore, it is ideal to have baseline radiographs for horses, especially for those at high-risk for laminitis, to compare to should laminitis ever be suspected. Normal HL values vary by breed and age: [1]
Venograms

Venograms can help determine the prognosis for the animal, particularly in horses where the degree of pain does not match the radiographic changes. In venography, a contrast agent, visible on radiographs, is injected into the palmar digital vein to delineate the vasculature of the foot. [1] The venogram can assess the severity and location of tissue compromise and monitor effectiveness of the current therapy. [18] Compression of veins within the hoof will be seen as sections that do not contain contrast material. Poor or improper blood flow to different regions of the hoof help determine the severity of the laminitic episode. Venography is especially useful for early detection of support limb laminitis, as changes will be seen on venograph (and MRI) within 1–2 weeks, whereas clinical signs and radiographic changes do not manifest until 4–6 weeks. [1]

Horses undergoing venography have plain radiographs taken beforehand to allow for comparison. The feet are blocked to allow the sedated horse to stand comfortably during the procedure. Prior to injection, a tourniquet is placed around the fetlock to help keep the contrast material within the foot during radiography. Diffusion of contrast may make some areas appear hypoperfused, falsely increasing the apparent severity of the laminitic episode. After injection of the contrast material, films are taken within 45 seconds to avoid artifact caused by diffusion. Evaluation of blood supply to several areas of the foot allows the practitioner to distinguish mild, moderate, and severe compromise of the hoof, chronic laminitis, and sinking. [1]

Other diagnostics

Other imaging tools have been used to show mechanical deviations in laminitis cases include 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. [19]

Prognosis

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. Some countermeasures can be adopted for pasture based animals. [20] [21] 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:

Treatment

In laminitis cases, a clear distinction must be made between the acute 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 ] In cases of sepsis or endotoxemia, the underlying cause should be addressed concurrently with laminitis treatment. [4] There are various methods for treating laminitis, and opinions vary on which are most useful. Additionally, the each horse and affected hoof should be evaluated individually to determine the best treatment plan, which may change with time. [1] Ideally, affected hooves are re-evaluated on a regular basis once treatment commences to track progress. [1]

Management

Initial management usually includes stall rest to minimize movement, and deeply bedding the stall with shavings, straw, or sand. Exercise is slowly increased once the horse has improved, ideally in an area with good (soft) footing, beginning with hand-walking, then turn-out, and finally riding under saddle. [1] This process may take months to complete. [1]

Cryotherapy

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 "uniced" feet. [22] Cryotherapy reduces inflammatory events in the lamellae. Ideally, limbs should be placed in an ice bath up to the level of the knee or hock. Hooves need to be maintained at a temperature less than 10 degrees Celsius at the hoof wall, for 24–72 hours. [1]

In the case of a full-blown case of laminitis, use of a cold water spa proved effective in the treatment of Bal a Bali. For the first three days, Bal a Bali was kept in the spa for eight hours at a time. Once his condition stabilized, he continued to be put in the spa twice a day over the next few months. [23]

Drug therapies

Anti-inflammatories and analgesics

Anti-inflammatories are always used when treating acute case of laminitis, and include Nonsteroidal anti-inflammatory medications (NSAIDS), DMSO, pentoxpfylline, and cryotherapy. [4] For analgesia, NSAIDs are often the first line of defense. Phenylbutazone is commonly used for its strong effect and relatively low cost. Flunixin (Banamine), ketofen, and others are also used. Nonspecific NSAIDs such as suxibuzone, or COX-2-specific drugs, such as firocoxib and diclofenac, may be somewhat safer than phenylbutazone in preventing NSAID toxicity such as right dorsal colitis, gastric ulcers, and kidney damage. [24] [25] [26] However, firocoxib provides less pain relief than phenylbutazone or flunixin. [1] Care must be taken that pain is not totally eliminated, since this will encourage the horse to stand and move around, which increases mechanical separation of the laminae. [1]

Pentafusion, or the administration of ketamine, lidocaine, morphine, detomidine, and acepromazine at a constant rate of infusion, may be of particular benefit to horses suffering from laminitis. [4] Epidurals may also be used in hind-limb laminitis. [4]

Vasodilators

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. [27] 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. [28] 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 blood flow in the equine digit. [29]

Trimming and shoeing

Besides pain management and control of any predisposing factors, mechanical stabilization is a primary treatment goal once the initial inflammatory and metabolic issues have resolved. No approach has been shown to be effective in all situations, and debate is ongoing the merits and faults of the numerous techniques. Once the distal phalanx rotates, it is essential to derotate and re-establish its proper spatial orientation 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 reorientation. However, this is not always completely effective.

Trimming

Successful treatment for any type of founder must necessarily involve stabilization of the bony column by some means. Correct trimming can help improve stabilization. This usually includes bringing the "break over" back to decrease the fulcrum-effect that stresses the laminae. Trimming the heels helps to ensure frog pressure and increases surface area for weight-bearing on the back half of the hoof. [1] While horses may stabilize if left barefooted, some veterinarians believe the most successful methods of treating founder involve positive stabilisation of the distal phalanx, by mechanical means, e.g., shoes, pads, polymeric support, etc. Pour-in pads or putty is sometimes placed on the sole to increase surface area for weight-bearing, so that the sole in the area of the quarters, and the bars, will take some of the weight. [1]

Altering the palmar angle

The deep digital flexor tendon places a constant pull on the back of the coffin bone. This is sometimes counteracted by decreasing the palmar angle of the hoof by raising the heels, often with the use of special shoes which have a wedge in the heel of approximately 20 degrees. Shoes are usually glued or cast onto the foot so painful nailing does not have to take place. The position of P3 within the hoof is monitored with radiographs. Once the horse has improved, the wedge of the shoe must be slowly reduced back to normal. [1]

Use of orthotics

The application of external orthotic devices to the foot in a horse with undisplaced 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.

Corrective hoof trimming

Corrective hoof trimming will restore proper hoof form and function. Corrective trimming will allow the hooves to be healthy again.

Realigning trimming

Realigning trimming trims back the toe so that it is in line with the coffin bone. Realigning trimming pushes the coffin bone back into the correct position. The process of a new hoof capsule totally growing out to replace the old one takes up to a year.

Aggressive therapies

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 reattachment (interdigitation) of the laminae, this procedure may be beneficial. When the coffin bone is pulled away from the hoof wall, 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. [30]

Coronary grooving

Coronary grooving involves removing a groove of hoof wall just distal to the coronary band. It is thought to encourage dorsal hoof wall growth and improve alignment of the wall. [4]

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 (mid-metacarpus) [4] or in the pastern region. Over a time period of 6 weeks, tenotomy is thought to allow P3 to realign with the ground surface. [4] Critics claim that this technique is unsuccessful and invasive, with advocates making counter-arguments that it is often used in cases which are too far advanced for treatment to help. [31] Tenotomy does risk subluxation of the distal interphalangeal joint (coffin joint), [4] which may be avoided with the use of heel extensions on the shoe. [1] Horses may return to work after the surgery. [1] This treatment is often recommended for severe cases of laminitis, and requires proper trimming and shoeing to be successful. [1]

Botulinum toxin infusion

As an alternative to the deep digital flexor tenotomy, Clostridium botulinum type A toxin has been infused into the body of the deep digital flexor muscle. This theoretically allows for the same derotation as a tenotomy, but without the potential for scarring or contracture associated with that procedure. A recent study used this technique in seven laminitic horses. Significant improvement was seen in six of the horses, with moderate improvement in the seventh. [32]

Complications

Complications to laminitis include recurrent hoof abscesses, which are sometimes secondary to pedal osteitis, [1] seromas, and fractures to the solar margin of the coffin bone. [4]

Informal use of the word "founder"

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 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

Related Research Articles

Hoof horn structure which surrounds the distal phalange in odd-toed ungulates (horses, donkeys and zebras)

A hoof, plural hooves or hoofs, is the tip of a toe of an ungulate mammal, strengthened by a thick, horny, keratin covering.

Navicular bone bone of the ankle

The navicular bone is a small bone found in the feet of most mammals.

Navicular syndrome, often called navicular disease, is a syndrome of lameness problems in horses. It most commonly describes an inflammation or degeneration of the navicular bone and its surrounding tissues, usually on the front feet. It can lead to significant and even disabling lameness.

Ringbone is exostosis in the pastern or coffin joint of a horse. In severe cases, the growth can encircle the bones, giving ringbone its name. It has been suggested by some authors that such a colloquial term, whilst commonly used, might be misleading and that it would be better to refer to this condition as osteoarthritis of the inter-phalangeal joints in ungulates.

Sidebone is a common condition of horses, characterized by the ossification of the collateral cartilages of the coffin bone. These are found on either side of the foot protruding above the level of the coronary band. The lateral cartilages support the hoof wall and provide an important role in the support and cushioning provided to the heel. The front feet are most commonly affected.

There are many aspects to horse care. Horses, ponies, mules, donkeys and other domesticated equids require attention from humans for optimal health and long life.

Frog (horse anatomy)

The frog is a part of a horse's hoof, located on the underside, which should touch the ground if the horse is standing on soft footing. The frog is triangular in shape, and extends mid way from the heels toward the toe, covering around 25% of the bottom of the hoof.

Barbaro (horse)

Barbaro was an American Thoroughbred racehorse who decisively won the 2006 Kentucky Derby, but shattered his leg two weeks later in the 2006 Preakness Stakes, which ended his racing career and eventually led to his death.

Horse hoof structure surrounding distal phalanx in limbs of horses

A horse hoof is a structure surrounding the distal phalanx of the 3rd digit of each of the four limbs of Equus species, which is covered by complex soft tissue and keratinised (cornified) structures. Since a single digit must bear the full proportion of the animal's weight that is borne by that limb, the hoof is of vital importance to the horse. The phrase "no hoof, no horse" underlines how much the health and the strength of the hoof is crucial for horse soundness.

Hoof boot device made primarily of polyurethane and is designed to cover the hooves of a horse as an alternative to, and occasionally in addition to, horseshoes

A hoof boot is a device made primarily of polyurethane and is designed to cover the hooves of a horse as an alternative to, and occasionally in addition to, horseshoes. Hoof boots can also be used as a protective device when the animal has a hoof injury that requires protection of the sole of the hoof, or to aid in the application of medication. There are many different designs, but all have the goal of protecting the hoof wall and sole of the horse's hoof from hard surfaces, rocks and other difficult terrain.

Equine podiatry is the study and management of the equine foot based on its anatomy and function.

Lameness is an abnormal gait or stance of an animal that is the result of dysfunction of the locomotor system. In the horse, it is most commonly caused by pain, but can be due to neurologic or mechanical dysfunction. Lameness is a common veterinary problem in racehorses, sport horses, and pleasure horses. It is one of the most costly health problems for the equine industry, both monetarily for the cost of diagnosis and treatment, and for the cost of time off resulting in loss-of-use.

Nail prick

Nail prick or quicking occurs in a horse if the sensitive hoof structures are penetrated by a horseshoe nail being driven through the hoof wall while shoeing. The nail creates a wound on the inside of the hoof wall.

Quittor is an infection of the lower leg of equines, sometimes known as graveling. A condition once common in draft horses, it is characterized by inflammation of the cartilage of the lower leg. There are two forms, subcutaneous and cartilaginous. Quittor usually results from an injury to the leg, such as an abscess on the coronary band above the hoof, that allows foreign matter to get into the leg and then collect beneath the hoof, leading to an infection. In some cases, removing this matter requires cutting away parts of the hoof. Abscesses may also form inside the hoof capsule itself from improper shoeing and trimming of the hoof, from laminitis, or from injury to the sole of the hoof, but the horse will be significantly lame for a longer period of time if the infection migrates up to the coronary band rather than down. Treatment of hoof and coronary band abscesses today usually incorporates use of antibiotics, sometimes combined with poulticing.

Natural hoof care

Natural hoof care is the practice of keeping horses so that their hooves are worn down naturally and so do not suffer overgrowth, splitting and other disorders. Horseshoes are not used, but domesticated horses may still require trimming, exercise and other measures to maintain a natural shape and degree of wear.

Limbs of the horse

The limbs of the horse are structures made of dozens of bones, joints, muscles, tendons and ligaments that support the weight of the equine body. They include two apparatuses: the suspensory apparatus, which carries much of the weight, prevents overextension of the joint and absorbs shock, and the stay apparatus, which locks major joints in the limbs, allowing horses to remain standing while relaxed or asleep. The limbs play a major part in the movement of the horse, with the legs performing the functions of absorbing impact, bearing weight, and providing thrust. In general, the majority of the weight is borne by the front legs, while the rear legs provide propulsion. The hooves are also important structures, providing support, traction and shock absorption, and containing structures which provide blood flow through the lower leg. As the horse developed as a cursorial animal, with a primary defense mechanism of running over hard ground, its legs evolved to the long, sturdy, light-weight, one-toed form seen today.

The treatment of equine lameness is a complex subject. Lameness in horses has a variety of causes, and treatment must be tailored to the type and degree of injury, as well as the financial capabilities of the owner. Treatment may be applied locally, systemically, or intralesionally, and the strategy for treatment may change as healing progresses. The end goal is to reduce the pain and inflammation associated with injury, to encourage the injured tissue to heal with normal structure and function, and to ultimately return the horse to the highest level of performance possible following recovery.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 Orsini J, Divers T (2014). Equine Emergencies (4th ed.). St. Louis, MO: Elsevier. pp. 697–712. ISBN   978-1-4557-0892-5.
  2. Pollitt CC (1995). Color Atlas of the Horse's Foot. Mosby. ISBN   978-0-7234-1765-1.
  3. Loftus JP, Black SJ, Pettigrew A, Abrahamsen EJ, Belknap JK (November 2007). "Early laminar events involving endothelial activation in horses with black walnut- induced laminitis". American Journal of Veterinary Research. 68 (11): 1205–11. doi:10.2460/ajvr.68.11.1205. PMID   17975975.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 Baxter G (2011). Manual of Equine Lameness (1st ed.). Ames, Iowa: Wiley-Blackwell. pp. 257–262. ISBN   978-0-8138-1546-6.
  5. 1 2 3 4 5 6 7 8 Huntington P, Pollitt C, McGowan C (September 2009). "Recent research into laminitis" (PDF). Advances in Equine Nutrition. IV: 293. Archived from the original (PDF) on 23 March 2013. Retrieved 28 July 2014.
  6. de Laat MA, Kyaw-Tanner MT, Nourian AR, McGowan CM, Sillence MN, Pollitt CC (April 2011). "The developmental and acute phases of insulin-induced laminitis involve minimal metalloproteinase activity". Veterinary Immunology and Immunopathology. 140 (3–4): 275–81. doi:10.1016/j.vetimm.2011.01.013. PMID   21333362.
  7. Watts KA (March 2004). "Forage and Pasture Management for Laminitic Horses" (PDF). Clinical Techniques in Equine Practice. 3 (1): 88–95. Archived (PDF) from the original on 2010-12-31. Retrieved 2010-04-22.
  8. Nilsson SA (1963). "Clinical, morphological and experimental studies of laminitis in cattle". Acta Veterinaria Scandinavica. 4 (Suppl. 1): 188–222. OCLC   13816616.
  9. Takahashi K, Young BA (June 1981). "Effects of grain overfeeding and histamine injection on physiological responses related to acute bovine laminitis". Nihon Juigaku Zasshi. The Japanese Journal of Veterinary Science. 43 (3): 375–85. doi:10.1292/jvms1939.43.375. PMID   7321364.
  10. Thoefner MB, Pollitt CC, Van Eps AW, Milinovich GJ, Trott DJ, Wattle O, Andersen PH (September 2004). "Acute bovine laminitis: a new induction model using alimentary oligofructose overload". Journal of Dairy Science. 87 (9): 2932–40. doi:10.3168/jds.s0022-0302(04)73424-4. PMID   15375054.
  11. 1 2 3 Rooney J. "Nonclassical laminitis". Archived from the original on 2008-01-24.
  12. "Transcript of Press Conference on the condition of Barbaro" (PDF). University of Pennsylvania School of Veterinary Medicine. 13 July 2006. Archived from the original (PDF) on 4 February 2007.
  13. "Clinical use of triamcinolone acetonide in the horse (205 cases) and the incidence of glucocorticoid‐induced laminitis associated with its use".
  14. "No Evidence That Therapeutic Systemic Corticosteroid Administration is Associated With Laminitis in Adult Horses Without Underlying Endocrine or Severe Systemic Disease".
  15. Luthersson N, Mannfalk M, Parkin TD, Harris P (2017). "Laminitis: Risk Factors and Outcome in a Group of Danish Horses". Journal of Equine Veterinary Science. 53: 68–73. doi:10.1016/j.jevs.2016.03.006.
  16. Menzies-Gow NJ, Harris PA, Elliott J (May 2017). "Prospective cohort study evaluating risk factors for the development of pasture-associated laminitis in the United Kingdom". Equine Veterinary Journal. 49 (3): 300–306. doi:10.1111/evj.12606. PMID   27363591.
  17. Anderson M. "The Obel Grading System for Describing Laminitis". www.thehorse.com. The Horse. Archived from the original on 15 August 2014. Retrieved 30 July 2014.
  18. 1 2 Ramey P, Bowker RM (2011). Care and Rehabilitation of the Equine Foot. Hoof Rehabilitation Publisher. pp. 234–253. ISBN   978-0-615-52453-5.
  19. Wongaumnuaykul S, Siedler C, Schobesberger H, Stanek C (2006). "Doppler sonographic evaluation of the digital blood flow in horses with laminitis or septic pododermatitis". Veterinary Radiology & Ultrasound. 47 (2): 199–205. doi:10.1111/j.1740-8261.2006.00128.x. PMID   16553154.
  20. Harris P, Bailey SR, Elliott J, Longland A (July 2006). "Countermeasures for pasture-associated laminitis in ponies and horses". The Journal of Nutrition. 136 (7 Suppl): 2114S–2121S. doi:10.1093/jn/136.7.2114S. PMID   16772514.
  21. Colahan P, Merritt A, Moore J, Mayhew I (December 1998). Equine Medicine and Surgery (Fifth ed.). Mosby. p. 408. ISBN   978-0-8151-1743-8.
  22. Pollitt C (November 2003). "Equine Laminitis" (PDF). Proceedings of the AAEP. 49. Archived (PDF) from the original on 2008-03-08. Retrieved 2008-04-19.
  23. Shulman L. "Making of a Miracle" (PDF). vet.osu.edu (reprint from The Blood-Horse). Archived (PDF) from the original on 17 December 2016. Retrieved 20 March 2017.
  24. MacAllister CG, Morgan SJ, Borne AT, Pollet RA (January 1993). "Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses". Journal of the American Veterinary Medical Association. 202 (1): 71–7. PMID   8420909.
  25. Sabaté D, Homedes J, Mayós I, Calonge R, et al. (January 2005). Suxibuzone as a Therapeutical Alternative to Phenylbutazone in the Treatment of Lameness in Horses (PDF). 11th SIVE Congress. Pisa. Archived (PDF) from the original on 2005-05-29. Retrieved 2008-04-19.
  26. Doucet MY, Bertone AL, Hendrickson D, Hughes F, Macallister C, McClure S, et al. (January 2008). "Comparison of efficacy and safety of paste formulations of firocoxib and phenylbutazone in horses with naturally occurring osteoarthritis". Journal of the American Veterinary Medical Association. 232 (1): 91–7. doi:10.2460/javma.232.1.91. PMID   18167116.
  27. Pollitt CC (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.
  28. 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: 599–603. doi:10.1016/S0737-0806(97)80186-4.
  29. Belknap JK, Black SJ (2005). "Review of the Pathophysiology of the Developmental Stages of Equine Laminitis". Proceedings American Association of Equine Practitioners. 51.
  30. Eustace RA (1996). Explaining Laminitis and its Prevention. Cherokee, Ala.: Life Data Labs. pp. 29–31. ISBN   978-0-9518974-0-9.
  31. Eastman TG, Honnas CM, Hague BA, Moyer W, von der Rosen HD (February 1999). "Deep digital flexor tenotomy as a treatment for chronic laminitis in horses: 35 cases (1988-1997)" (PDF). Journal of the American Veterinary Medical Association. 214 (4): 517–9. PMID   10029854.
  32. Carter DW, Renfroe JB (July 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 (7): 595–600.

Further reading