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Equine Laminitis John Kurt Iowa State University Volume 37 | Issue 2 Article 5 1975 Equine Laminitis John Kurt Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Large or Food Animal and Equine Medicine Commons, and the Veterinary Pathology and Pathobiology Commons Recommended Citation Kurt, John (1975) "Equine Laminitis," Iowa State University Veterinarian: Vol. 37 : Iss. 2 , Article 5. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol37/iss2/5 This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Equine Laminitis by John Kurt* Larry L. Jackson, D.V.M.t Laminitis is defined as the inflamm:a­ horse is accustomed. All types of grain tion of the lami11ae of the foot. This dis­ and animal feeds ,can cause this type of ease, commonly known as founder, has founder although oats !and bran are prob­ been known for centuries, however the ably the least offensive. The consumption pathogenesis is still under discussion. leads to a gastroenteritis which, accord­ Both cardiovascular as well 'as metabolic in,g to different authors, initiates hista­ changes are known to be involved in the m'ine release, leads to a bacterial entero­ disease.! Capillary perfusion to the lam­ toxemia and/or even an immune response inar corium is decreased in many ways. to the protein of the bacteria itself. This Histamine released from hypoxic mast type of founder is believed by some to de­ cells causes ,capillary dilation. Bacterial pend upon :the presence of certain bac­ endotoxin released during both alimentary teria and can be transmitted to another and post-parturient laminitis causes cir­ horse with the transfer of ingesta.4 culatory ,changes of constriction of ar­ 2. Water Founder.-Water founder is terioles and venules resulting in capillary oaused by the consum,ption of large congestion and edema. Resultant arterio­ amounts of cold water while the horse is venous shunts compounded by RBC's still overheated. The exact mechanism of sludging 'and ,platelet emboli lead to di­ this phenomenon is still not fully under­ version of blood flow from the laminar stood. corium.2 This deprived blood flow leads 3. Road Founder.-Road founder is to the synthesis of structurally incompe­ common in unconditioned horses after tent keratin and to a loss of the mechan­ strenuous work on a hard surface. ical integrity of the disulfide bonds be­ 4. Grass Founder.-Grass founder is tween the sensitive and ins~nsitive lan1­ usually seen in overweigl1t horses that inae.3 consume more lush forage than they are Since the step-limiting substrates in accustomed to. Clover and alfalfa pastures keratin produ,ction are methionine, cyst­ are most commonly at fault. However, eine, and cystine,l a shortage of these lush grass pastures have also been known amino acids has :also been implicated. to cause this type of founder. Wintering These detailed sequences of events with­ overweight horses on legume hays has oc­ in the hoof and especially within the lam­ casionally also been incriminated. inae are still obscure. In view of the di­ 5. Postparturient Founder.-This type verse conditions associated with laminitjs, of founder is a result of a retained pla­ these changes witpin the lamina may not centa or even a uterine infection without always even be the same. retention of any of the fetal membranes. Other systemic infections such as pneu­ Causes monia or viral respiratory diseases have also been thought to cause this severe 1. Grain Founder.-Grain founder is type of founder. caused by the consumption of quantities 6. Miscellaneous Causes.-Laminitis of grain greater than those to which the has been known to follow such things as if< Mr. Kurt is a fourth year student in the College of Veterinary Medicine, Iowa State University. worming, anaphylactoid reactions to some t Dr. Jackson is an Assistant Professor of Veterinary Clin· kal Sciences at Iowa State University. drugs, and large doses of phenylbutuzone 50 Iowa State University Vet,erinarian or steroids. 'l'he exact mechanisms of Dormai, the toe of the hoof will become these and other types of founder are 'Dot long and with tinle will curl up to form understood completely.5 the "sleigh footn appearance. Heavy ring formations will become evident on the Clinical Signs-Acute Stage hoof wall as a result of uneven horn growth because of the inflammation at the If all four feet are affected, the horse is coronary band. These rings are usually reluctant to stand. When standing the present ''for the life of the horse. horse will have his rear feet well under Separation of the sensitive alld insensi­ him anteriorly and his front feet carried tive laminae often predispose the animal posteriorly to have a very narrow based to a condition known as 'Seedy Toe', an in­ stance. Most commonly, only the two fection penetrating the white line alld front feet are affected. In this case, the spreading up the sensitive laminae. Ex­ hind feet are carried well up under the amination of the foot will reveal the sole animal and the front feet are placed for­ to be almost flat rather than concaved as ward with the horse carrying the weight it is normally. The white line will become upon the heels of the feet and showing a noticeably thicker than normal. The sole great reluctance to move. The sale, wall, will be flaky but yet it will be easy to in­ and coronary band will be very warm and duce hemorrhage because of the increased an increased digital pulse can be palpated vascularity. This tendency toward easy on the digital vessels over the fetlock joint. hemorrhage will remain for many months. Many horses show anxiety, trembling, in­ Diagnosis.-Diagnosis of laminitis is jected mucous membranes, sweating, in­ based upon the clinical signs mentioned creased respiratory and heart rates, and above. The typical gate and attitude of may have an increased temperature de­ the animal, the increased heat and tender­ pending upon the etiology. The walk of a ness of the hoof wall, and the almost foundered horse is said to be "peggyn as bounding digital pulse should lead to a he will shuffle his feet and often stumble relatively easy diagnosis. However, a because of the difficulty to lift one leg as volar nerve block may have to be per­ he throws more weight on the other af­ formed occasionally to rule out other fected foot. Hoof testers reveal a unifornl source of the lameness. The radiographic tenderness over the entire sale. Blood evidence of the rotation of P:~ can also be eosinophil counts and histamine levels used for the diagnosis of chronic laminitis, may raise but are often within the normal ranges. Death resulting from acute lami­ Treatment nitis is very uncommon however the whole hoof may slough as a result of a separa­ 1. Acute Laminitis-Regardless of the tion of the sensitive and insenitive lami­ specific cause of the acute laminitis, the nae. therapy for each case should be devised Chronic Stage.-In chronic laminitis, using these basic principles: remove the the pull of the deep flexor tendon causes underlying cause, relieve th~ pain, in­ the third phalanx (Pa) to rotate in such a crease the capillary flow to the laminae, way that the anterior face of P:~ is pulled improve keratin synthesis, and prevent away from the anterior insensitive lami­ secondary infection.1 nae of the hoof wall. This can be seen Since the exact mechanisms of drug­ radiographically.4 The rotation often is to reaction laminitis and other miscellaneous such an extent as to cause the anterior causes are not understood, it has been pro­ point of P:~ to be pushed t11rough the sole posed that all cases of acute laminitis (ex­ when the horse bears weight on the foot. cept postparturient laminitis) be treated Horses affected with chronic laminitis as though their underlying cause is in the have a tendency to walk on their heels. gastrointestinal tract. For this reason all Because of this and because the inflam­ horses with acute laminitis (except post­ mation causes the hoof to grow faster than parturient laminitis) should be purged 52 Iowa State Univ'ersity Vet,erinariarn with mineral oil every 6 hours until all tored. daily until the patient is recovering of the grain, etc. is removed from the gas­ well. This is important since secondary trointestinal tract. If dehydration occurs, sepsis of the laminae is probably the most this should be treated with intravenous conlmon cause of failure of the therapy. fluids. Horses affected with postparturient Immediate treatment of an infection is in­ laminitis should be treated for metritis. dicated. Infection is usually treated with Uterine irrigations, uterine infusion with systemic antibiotics, opening of the wound antibiotics, parenteral antibiotics and per­ to enhance drainage, tetanus antitoxin, haps estrogens have all been recom­ and dressing the foot with tar and oakum. mended. Autogenous blood therapy has long been Phenylbutazone is the .drug of choice used although its mode of action is not for the relief of the pain involved. Occa­ known. This is done by withdrawing 50­ sionally a posterior digital nerve block 200 cc of blood from the jugular vein and may have to be performed to ease the pain administering this intramuscularly in sev­ enough to enable the horse to move about. eral divided doses. This mode of treatment The ambulation of the patient is impor­ was derived from the treatment of shing­ tant to improve the circulation to the foot.
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