Volume 37 | Issue 2 Article 5

1975 Equine Laminitis John Kurt Iowa State University

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Recommended Citation Kurt, John (1975) "Equine Laminitis," Iowa State University : 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 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 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 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 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 . 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, 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 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. les in man. However, the patient's movements should The treatment of acute equine lan1initis not be excessive and limited to soft sur­ is largely empierical and requires more faces so as to prevent further rotation of study and improvement. However, one

P3 • Antihistamines at recommended doses fact is for certain: acute laminitis should are used to increase blood flow to the always be handled as an emergency. This laminae because histamines cause capil­ principle is based on the many experi­ lary pooling by constriction of arterioles mentally induced models that have been and venuoles and dilation of capillaries. studied.7 may increase capillary flow 2. Chronic Laminitis.-Chronic lami­ by vasodilatation, however, their inhibition nitis is very common in overweight horses of local defense mechanisms and keratin and especially . These obese horses synthesis make at least their repeated use often show high cholesterol and serum contraindicated. However, certain authors glutamic oxaloacetic transaminase (SGOT) have proposed the use of intra-arterials ter­ levels. Horses with SGOT levels above oid injections into the digital artery over 400 RF units are often given dextrose, the abaxial surface of the sesamoid bone.6 protein hydrolysate, and vitamin B com­ A tourniquet is applied immediately fol­ plex intravenously, ACTH intramuscular­ lowing the injection leading to supposedly ly and placed on a reducing diet when ne­ better steroid action at the area involved. cessary. The recommended dosages of The feet should be soaked in warm water, these are: 50 ml. of 50% dextrose per possibly containing epsom salts and dis­ 100 lbs., SOD ml. of 5% protein hydroly­ infectant, to improve circulation. The pal­ sate, 10 ml. B complex, 400 units ACTH mar nerve block, if performed, will also on day one, and 200 units on days 2, 3, 4 decrease peripheral resistance, via dilation & 5. A high protein diet with approxi­ of arterioles and vepuoles. mately 50% of the previous caloric intake To enhance keratinization, methionine, has been recommended.~·9 cysteine, and cystine, the step-limiting All horses affected with chronic lami­ substrates of keratin, may have to be nitis should also have the affected feet added to the ration. Ten gm. daily for correctively trimmed so as to bring P R back three days followed by five gm. daily for to its normal angle. When this is ac­ ten days has been proposed as an adequate complished the base of Pa should be as an10unt of methionine for a 1,000 lb. close to parallel to the sole of the foot as horse. With normal liver function methio­ possible. This can be accomplished in nine is converted to cysteine and cystine. many ways. The severity of the rotation To prevent secondary infections of the as determined radiographically should be corium, body temperature should be moni- the deciding factor as to which procedure

Issue No.2, 1975 53 is chosen. on either sIde ot the medIan line of the If the rotation is not very severe, Sin1­ toe wall almost to the depth of the lami­ ply lowering the heel and stubbing off the nae. These grooves can be cut with a excess toe with hoof nippers and a rasp hoof knife or bistoury although this is very may be sufficient. The hoof should then time consuming and arduous. Several au­ be shod with perhaps a bolt-on steel plated thors have suggested the use of. small, shoe to protect the sole. The area between high-speed hand drills which can be fitted the sole and plate is packed with pine tar with a variety of heads and make the job and oakum to help prevent infection. much easier and safer. After th'is is ac­ This dressing is changed weekly and care­ complished the heels are lowered and the ful attention should be paid to developing toe is rolled to complete the job. absceses. The principles of the treatment of

When the distal end of P3 has rotated chronic laminitis are to return P3 to its more than one cm. (as suggested by one normal position, prevent secondary infec­ author)8 radical acrylic repair is recom­ tion and to prevent the recurrence of mended. This is accomplished by again the diseas~. This can be accomplished in trimming the heel as much as possible and many ways, but the most logipal and sim­ undercutting as much of the abnormally ple approach should be used. The owner shaped toe wall as is needed. This may should also be advised that horses recov­ be a small gap or the entire toe wall as ered from laminitis are thought to be more far as up to one cm. from the coronet. The susceptible to its recurrence. toe wall is then replaced with an acrylic, plastic or fiberglass mixture and reshaped Discussion to form a more normal looking hoof wal1. 10 The exact procedure has been des­ Often the exact etiology of laminitis is cribed in detail numerous times in litera­ unknown and corrective hoof trimming is ture and by manufacturers. This new hoof all that can be done. With time many of wall nlaterial protects the laminae, pro­ these horses can be returned to reasonable vides a more normal angle of resistance soundness but few horses regain complete for the hoof wall to grow against and can soundness. allow more radical improvement to the angle of P3' Sometimes some of this plas­ References tic, mixed to a softer texture, is placed I. Coffman, J. R. and Garner, H. E.: Acute latninitis. .JAVMA, 161, December I, 1972. under the sole to protect it. The foot is 2. Ackerman, Norman et al: Angiographic appearance then shod using a shoe with high toe and of the normal equine foot and alterations in chronic laminitis. jAVMA, Vol. 166, january 1, 1975. quarter clips to give good support without 3. Coffman, J. R. et al: Hoof circulation in equine lami­ nitis. jAVMA, 156, January 1, 1970. using many nails. ~ll of these different 4. Adams, O. R.: Lameness in Horses. 2nd ed., Lea & Febiger, Philadelphia, 1973. types of shoes should be reset every four 5. Blood, D. C, and H('nderson, J. A,: Veterinary Medi­ to six weeks. Radiographs should be taken cine. 4th ed. Williams and Wilkins. Baltimore, 1974. 6. Roberts, W. D.: Treatment of laminitis by intra-ar­ periodically to determine the progress terial infusion of steroids. In I)roceeding 10th Ann. Cony. AAEP, 1964. being made. 7. Garner, H. E. et al: Equine laminitis and associated hypertension: a review. JAV~1A 166, January 1, 1975. In cases not subjected to correction of 8. Coffman, J. R. et al: Management of chronic lamin­ itis in the horse. JAVMA 155, July 1, 1969. :pedal rotation, vertical grooves lnay be cut 9. Johnson, J. H.: Equine Medicine and Surgery. 2nd into the hoof wall to allow more expan­ ed. Am. Vet. Publication Inc., "'Theaton, 1972. 1O. .Jenny, Jacqu~s. et al: Hoof repair with pla.,tics. sion of the wall which eases congestion JAVMA 147, December 15, 1965. 1I. Lathom, Robert L.: Use of high speed tools in treat­ and pain'!! Two grooves are cut % inch ing chronic laminitis. Norden News, Winter, 1971.

54 Iowa State Univ,ersity Veterinarian