Difference between revisions of "Gastric Ulceration - Horse"
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− | == | + | {| cellpadding="10" cellspacing="0" border="1" |
+ | | Also known as: | ||
+ | |'''Gastroduodenal ulceration<br> | ||
+ | '''Gastrointestinal ulceration<br> | ||
+ | '''Equine Gastric Ulcer Syndrome<br> | ||
+ | '''Peptic ulcer disease<br> | ||
+ | '''Equine Gastric Ulcer''' | ||
+ | |} | ||
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+ | {| cellpadding="10" cellspacing="0" border="1" | ||
+ | | See also: | ||
+ | |'''[[Gastric Ulceration - all species]]''' | ||
+ | |} | ||
+ | |||
+ | |||
+ | ==Description== | ||
The term ''''Equine gastric ulcer syndrome (EGUS)'''' encompasses a number of disease complexes<ref name="Merritt">Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric | The term ''''Equine gastric ulcer syndrome (EGUS)'''' encompasses a number of disease complexes<ref name="Merritt">Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric | ||
− | ulcer syndrome. ''Equine Vet J'', 41(7):616.</ref> associated with ulceration of the oesophageal, gastric or duodenal mucosa<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> in horses. When such damage is caused by acidic gastric juice, the defect is described as a ''''peptic ulcer''''.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> | + | ulcer syndrome. ''Equine Vet J'', 41(7):616.</ref> associated with ulceration of the oesophageal, gastric or duodenal mucosa<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> in horses. When such damage is caused by acidic gastric juice, the defect is described as a ''''peptic ulcer''''.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> Ulceration of either or both<ref>Andrews, F.M, Bernard, W.V, Byars, T.D ''et al.'' (1999) Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 1:122-134. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> regions of the gastric mucosa is one of the most important problems of the equine stomach as it may limit performance<ref name="Bell">Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review. ''N Z Vet J'', 55(1):1-12).</ref> and compromise welfare.<ref name="Martineau">Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. ''Equine Vet J'', 41(7):638-644.</ref> The non-glandular (proximal or orad) region of the equine stomach is lined by stratified squamous mucosa and a glandular mucosa lines the distal (aborad) portion. The two regions meet abruptly at the '''''margo plicatus'''''<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>, adjacent to where most ulcers occur.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> Damage to these regions occurs via differing pathophysiological routes and varies in severity from inflammation, to cellular death and sloughing causing disruption of the superficial mucosa ('''erosion'''), penetration of the submucosa down to the level of the ''lamina propria''<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref>('''ulceration'''), full thickness ulceration ('''perforation''')<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> and potentially duodenal stricture.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> The occult nature of the disease typically precludes the observation of clinical signs until severe ulceration has developed.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> |
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==Prevalence== | ==Prevalence== | ||
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*Nonracing performance horses (17% pre-competition, 56% post-competition)<ref>Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. ''J Equine Vet Sci'', 23:560-561. In:Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> | *Nonracing performance horses (17% pre-competition, 56% post-competition)<ref>Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. ''J Equine Vet Sci'', 23:560-561. In:Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> | ||
*Pleasure horses in full work ~ 60%<ref name="Bell">Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review. ''N Z Vet J'', 55(1):1-12).</ref> | *Pleasure horses in full work ~ 60%<ref name="Bell">Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review. ''N Z Vet J'', 55(1):1-12).</ref> | ||
− | *Foals ~25-57%<ref>Wilson, J.H (1986) Gastric and duodenal ulcers in foals: a retrospective study. ''Proc Equine Colic Res Symp 2nd:126-128.</ref><ref>Murray, M.J, Grodinsky, C, Cowles, R.R, ''et al.''(1990) Endoscopic evaluation of changes in gastric lesions of Thoroughbred foals. ''J Am Vet Med Assoc'', 196:1623-1627.</ref><ref>Murray, M.J (1989) Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). ''J Am Vet Med Assoc'', 195:1135-1141.</ref> | + | *Pleasure, riding lessons, showing 37%<ref name="Murray 1989">Murray, M.J, Grodinsky, C, Anderson, C.W, Radue, P.F, Schmidt, G.R (1989) Gastric ulcers in horses: a comparison of endoscopic findings in horses with and without clinical signs. ''Equine Vet J Suppl'', 7:68-72.</ref> |
+ | *Foals ~25-57%<ref>Wilson, J.H (1986) Gastric and duodenal ulcers in foals: a retrospective study. ''Proc Equine Colic Res Symp 2nd:126-128.</ref><ref>Murray, M.J, Grodinsky, C, Cowles, R.R, ''et al.''(1990) Endoscopic evaluation of changes in gastric lesions of Thoroughbred foals. ''J Am Vet Med Assoc'', 196:1623-1627.</ref><ref>Murray, M.J (1989) Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). ''J Am Vet Med Assoc'', 195:1135-1141.</ref>, the incidence increases dramatically in foals with clinical signs, especially gastrointestinal signs.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> | ||
− | The prevalence and severity of ulcers increases with work intensity<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> and duration<ref>Orsini, J.A, Pipers, F.S (1997) Endoscopic evaluation of the relationship between training, racing, and gastric ulcers. ''Vet Surg'', 26:424. In: Orsini, J (2000) ''Tutorial Article'' Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref><ref>Murray, M.J (1994) Gastric ulcers in adult horses. ''Comp Cont Educ Pract Vet'', 16:792-794. In:Orsini, J (2000) ''Tutorial Article'' Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>, thus racehorses in active training are more often affected<ref name="Hammond">Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. ''Equine Vet J'', 18(4):284-287.</ref> and in half of these, the lesions are moderate to severe.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> In one study, all horses developed gastric ulcers within 2 weeks of entering simulated race training.<ref name="Vatistas 2">Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> Lesions are thought to be chronically progressive during race training, but to regress during retirement.<ref name="Hammond">Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. ''Equine Vet J'', 18(4):284-287.</ref> Horses with signs of gastrointestinal distress also demonstrate an increased frequency and severity of ulcerative lesions.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref>EGUS prevalence is high in horses with bowel, liver and oesophageal lesions<ref name="Sandin">Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) ''Postmortem'' findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). ''Equine Vet J'', 32(1):36-42 | + | The prevalence and severity of ulcers increases with work intensity<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> and duration<ref>Orsini, J.A, Pipers, F.S (1997) Endoscopic evaluation of the relationship between training, racing, and gastric ulcers. ''Vet Surg'', 26:424. In: Orsini, J (2000) ''Tutorial Article'' Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref><ref>Murray, M.J (1994) Gastric ulcers in adult horses. ''Comp Cont Educ Pract Vet'', 16:792-794. In:Orsini, J (2000) ''Tutorial Article'' Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>, thus racehorses in active training are more often affected<ref name="Hammond">Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. ''Equine Vet J'', 18(4):284-287.</ref> and in half of these, the lesions are moderate to severe.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> In one study, all horses developed gastric ulcers within 2 weeks of entering simulated race training.<ref name="Vatistas 2">Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> Lesions are thought to be chronically progressive during race training, but to regress during retirement.<ref name="Hammond">Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. ''Equine Vet J'', 18(4):284-287.</ref> Horses with signs of gastrointestinal distress also demonstrate an increased frequency and severity of ulcerative lesions.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref>EGUS prevalence is high in horses with bowel, liver and oesophageal lesions.<ref name="Sandin">Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) ''Postmortem'' findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). ''Equine Vet J'', 32(1):36-42.</ref> Among show horses, 82% of those with signs of abdominal discomfort had gastric ulcers<ref>Murray, M. (1992) Gastric ulceration in horses: 91 cases (1987-1990). ''J Am Vet Med Assoc'', 201:117-120. In: Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. ''Equine Vet J'', 41(7):638-644.</ref> Around 30% of adult horses and about 50% of foals have mild gastric erosions which heal without treatment or clinical signs.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> In 201 clinically normal horses in Denmark, 53% had EGUS with severity score >2 and older horses were more likely to have lesions in both regions of the stomach<ref>Luthersson, N, Nielsen, K.H, Harris, P, Parkin, T.D (2009) The prevalence and anatomical distribution of equine gastric ulcer syndrome (EGUS) in 201 horses in Denmark. ''Equine Vet J'', 41(7):619-24.</ref> |
==Signalment== | ==Signalment== | ||
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==Pathophysiology== | ==Pathophysiology== | ||
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− | + | ==Risk Factors== | |
+ | ===Exercise=== | ||
+ | There appears to be a high prevalence of gastric ulcers in horses performing in most disciplines including racing, endurance, show jumping, dressage and western performance.<ref>Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. ''J Equine Vet Sci'', 23:560-561. In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> Although this may be related to exercise, other confounding factors associated with these disciplines such as travel, diet, feeding regime, NSAIDs and stress may be significant. However, Vatistas and co-workers (1999) were able to induce and maintain EGUS in racehorses in fast work without the use of NSAIDs or fasting before exercise.<ref name="Vatistas 2">Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> There is also evidence that training for just 8 days is suffcient to induce gastric ulcers.<ref>White, G, McClure, S.R, Siifferman, R, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration. ''J Am Vet Med Assoc'', 230(11):1680-2.</ref> Furthermore, the higher prevalence of gastric ulcers at post mortem in racehorses in training compared to those in retirement adds weight to the hypothesis that exercise is an important risk factor for EGUS.<ref name="Hammond">Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. ''Equine Vet J'', 18(4):284-287.</ref> Strenuous exercise is known to stimulate gastrin release which has effects on HCl secretion, gastric emptying and gastric blood flow. It is also thought that exposure of the squamous mucosa to acid is increased as the stomach is compressed by the abdominal viscera and diaphragm during excercise.<ref>Lorenzo-Figueras, M, Merritt, A.M (2002) Effects of exercise on gastric volume and pH in the proximal portion of the stomach of horses. ''Am J Vet Res'', 63:1481-1487.</ref> | ||
− | === | + | ===Housing and Transport=== |
− | + | Housing in '''stables''' has been proposed as a risk factor for gastric ulcers, with more lesions being found in confined horses compared to those out at grass.<ref>Murray, M.J, Eichorn, E.S (1996) Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall | |
− | + | confinement with ''ad libitum'' access to hay on gastric ulceration in horses. ''Am J Vet Res'', 57:1599-1603.</ref> However, when comparing solitary stable confinement with stabling next to a companion, and finally turn out in a paddock, Husted and colleagues (2008) found that the environmental situation had no effect on mucosal acid exposure in the equine stomach.<ref>Husted, L, Sanchex, L.C, Olsen, S.N, Baptiste, K.E, Merritt, A.M (2008) Effect of paddock vs. stall housing on 24 hour gastric pH within the proximal and ventral equine stomach. ''Equine Vet J'', 40(4):337-41.</ref> '''Transport''' has also been shown to induce squamous mucosal ulceration in horses.<ref>McClure, S.R, Carithers, D.S, Gross, S.J, Murray, M.J (2005) Gastric ulcer development in horses in a simulated show or training environment. ''J Am Vet Med Assoc'', 227:775-777.</ref> | |
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− | ===== | + | ===Diet=== |
− | The squamous mucosa | + | '''Feed deprivation''' encourages gastric ulceration in two ways: (1) it precludes the buffering capacity of protein leading to a reduced gastric pH<ref>Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. ''Equine Vet J'', 25:417-421. In: Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) ''Postmortem'' findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). ''Equine Vet J'', 32(1):36-42.</ref> and (2) it empties the stomach and exposes the squamous mucosa to the more mobile gastric juice.<ref name="Sandin">Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) ''Postmortem'' findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). ''Equine Vet J'', 32(1):36-42.</ref> It is unsurprising, therefore, that an alternating feed-fast protocol would produce a consistent model of ulcer induction in the equine squamous mucosa.<ref>Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. ''Equine Vet J'', 25:417-421. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref><ref>Murray, M.J (1994) Equine model of inducing ulceration in alimentary squamous epithelial mucosa. ''Dig Dis Sci'', 39:2530-2535. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Despite this, feed deprivation is not a prerequisite for gastric ulceration in the horse.<ref name="Vatistas thesis">Vatistas, N.J (1998) Gastric Ulceration in the Racing Thoroughbred. ''PhD Thesis''. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> Diets that are plentiful in roughage prolong the mastication process and the production of salivary bicarbonate that protects the gastric mucosa. A diet of '''high grain and low roughage''' thus predisposes to EGUS.<ref name="Nadeau"> In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> This sort of diet is commonly fed to racehorses but dietary components have also been shown to influence EGUS risk in nonracehorses.<ref>Luthersson, N, Nielson, K.H, Harris, P, Parkin, T.D (2009) Risk factors associated with equine gastric ulceration syndrome (EGUS) in 201 horses in Denmark. ''Equine Vet J'', 41(7):625-30.</ref> Ponies fed a '''concentrate diet''' had a greater prevalence of gastric ulcers than ponies fed hay alone.<ref name="Vatistas 2">Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> and this may be because grain and pelleted feeds are asssociated with increased serum gastrin.<ref>Smyth, G.B, Young, D.W, Hammond, L.S (1988) Effects of diet and feeding on post-prandial serum gastrin and insulin concentrations in adult horses. ''Equine Vet J Suppl'' 7:56-59.</ref> '''High starch meals''' are also a risk because they are fermented to volatile fatty acids (VFAs) and lactic acid and are emptied from the stomach relatively slowly.<ref>Mètayer, N, Lhôte, M, Bahr, A, Cohen, N.D, Kim, I, Rousell, A.J, Julliand, V (2004) Meal size and starch content affect gastric emptying in horses. ''Equine Vet J'', 36:434-440. In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref><ref>Taharaguchi, S, Okai, K, Orita, Y, Kuwano, M, Ueno, T, Taniyama, H (2004) Relation between amounts of concentrated feed given mares and gastric ulcers in foals. ''J Japan Vet Med Ass'', 57:366-370. In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref><ref>Boswinkel, A.M, Ellis, A.D, Sloet van Oldruitenborgh-Oosterbaan, M.M (2007) The influence of low versus high fibre haylage diets in combination with training or pasture rest on equine gastric ulceration syndrome (EGUS). ''Pferdeheilkunde'', 23:123-130. In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> |
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− | + | ===Other ailments=== | |
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+ | Conditions that produce abdominal pain and/or inappetance are likely to reduce food intake and predipose to gastric ulcers.<ref name="Sandin">Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) ''Postmortem'' findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). ''Equine Vet J'', 32(1):36-42.</ref> This may be the reason that '''colic''' and other gastrointestinal disorders have been associated with EGUS.<ref>Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists. ''Equine Vet J Suppl'', 7:77-79.</ref> Alternatively, EGUS may be part of a more general gastrointestinal disease complex.<ref name="Vatistas 2">Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> '''Stress''' induced by other clinical disorders has been reported to increase the prevalence of EGUS in neonatal foals<ref name="Furr">Furr, M.O, Murray, M.J, Ferguson, D.C (1992) The effects of stress on gastric ulceration, T3, T4, reverse T3 and cortisol in neonatal foals. ''Equine Vet J'', 24:37-40.</ref> and a similar mechanism may exist for adult animals.<ref name="Vatistas 2">Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> | ||
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− | + | As in [[Gastric Ulceration - all species|other species]], nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to cause gastric ulcers in horses. Typicaly this is associated with high doses or frequent administration of phenylbutazone or flunixin meglumine. However, although there is evidence to the contrary,<ref>Andrews, F.M, Reinemeyer, C.R, Longhofer, S.L (2009) Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. ''Vet Ther'', 10(3):113-20.</ref>therapeutic doses of NSAIDs may be sufficient to induce EGUS. Other studies have suggested that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally<ref>Monreal, L, Sabatè, D, Segura, D, Mayós, I, Homedes, J (2004) Lower gastric ulcerogenic effect of suxibuzone compared to phenylbutazone when administered orally to horses. ''Res Vet Sci'', 76:145-149. In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref>and that combination treatment with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone.<ref>Reed, S.K, Messer, N.T, Tessman, R.K, Keegan, K.G (2006) Effects of phenylbutazone alone or in combination with flunixin meglumine on blood protein concentrations in horses. ''Am J Vet Res'', 67:398-402. In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa<ref>MacAllister, C.G, Morgan, S.J, Borne, A.T, Pollet, R.A, (1993) Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses. ''J Am Vet Med Ass'', 202:71-77. In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. ''Equine Vet J'', 38(3):209-213.</ref><ref>Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists. ''Equine Vet J Suppl'', 7:77-79. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref><ref>Kumaran, D, Bhuvanakumar, C.K (1994) Gastro duodenal ulceration in foals - a discussion. ''Cenfaur Mylapore'', 10:83-86. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref>, they may look different endoscopically from ulcers that occur naturally,<ref name="Jonsson">Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. ''Equine Vet J'', 38(3):209-213.</ref> and they appear to heal spontaneously.<ref>Jones, W.E (1983) Gastrointestinal ulcers [foal]. ''Equine Vet Data'', 4:305-308. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref><ref>MacAllister, C.G, Sangiah, S (1993) Effect of ranitidine (in healing of experimentally induced gastric ulcers in ponies. ''Am J Vet Res'', 54:1103-1107. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.<ref>Vatistas N.J, Snyder, J.R, Carlson, G.P, Johnson, B, Arther, R.M, Thurmiind, M, Lloyd, K.C.K (1994) Epidemiology study of gastric ulcerarion in the Thoroughbred race horse: 202 horses. ''Proc Am Ass Equine Pract'', 39:125-126. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref><ref>Murray, M.J, Schusser, G.F, Pipers, F.S, Gro:ss, S.J (1996) Factors associated with gastric lesions in Thoroughbred racehorses. ''Equine Vet J'', 28:368-374. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref><ref name="Vatistas thesis">Vatistas, N.J (1998) Gastric Ulceration in the Racing Thoroughbred. ''PhD Thesis''. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> | |
− | + | ===Temperament=== | |
− | + | A nervous disposition has been linked with gastric ulcers<ref>McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses. ''J Am Vet Med Ass 215:1130-1133. In: In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. ''Equine Vet J'', 38(3):209-213.</ref>but the same association was not seen in another study.<ref>Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthur, R.M, Thurmond, M, Zhou, H, Lloyd, L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses. ''Equine Vet J Suppl'', 29:34-39. In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. ''Equine Vet J'', 38(3):209-213.</ref> The physiological and psychological stresses of training, housing, boredom, travel, mixing, hospitalisation and entering new environments<ref name="Vatistas 2">Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. ''Equine Vet J Suppl'', 29:40-44</ref> may increase the risk of developing EGUS. In foals hypoxia may also be a risk factor. | |
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==Clinical syndrome== | ==Clinical syndrome== | ||
− | The clinical signs associated with gastric ulcers are often very non-sepcific, difficult to document and at times only subjective.<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> In addition, there appears to be a poor correlation between the severity of endoscopic lesions and the clinical presentation.<ref name="Murray 1989">Murray, M.J, Grodinsky, C, Anderson, C.W, Radue, P.F, Schmidt, G.R (1989) Gastric ulcers in horses: a comparison of endoscopic findings in horses with and without clinical signs. ''Equine Vet J Suppl'', 7:68-72.</ref> The significance of gastric ulceration in horses thus remains questionable. However, there have been instances where ulcer treatment has preceded an improvement in clinical status and/or racing perfomance, suggesting that in some horses, ulcers are a considerable burden.<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> Cases | + | The clinical signs associated with gastric ulcers are often very non-sepcific, difficult to document and at times only subjective.<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> In addition, there appears to be a poor correlation between the severity of endoscopic lesions and the clinical presentation.<ref name="Murray 1989">Murray, M.J, Grodinsky, C, Anderson, C.W, Radue, P.F, Schmidt, G.R (1989) Gastric ulcers in horses: a comparison of endoscopic findings in horses with and without clinical signs. ''Equine Vet J Suppl'', 7:68-72.</ref> The significance of gastric ulceration in horses thus remains questionable. However, there have been instances where ulcer treatment has preceded an improvement in clinical status and/or racing perfomance, suggesting that in some horses, ulcers are a considerable burden.<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> Cases gastric ulceration are often asymptomatic, but signs that have been attributed to these lesions in '''mature horses''' include: |
*Poor appetite (particularly decreased consumption of concentrates)<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> | *Poor appetite (particularly decreased consumption of concentrates)<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> | ||
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*Excessive recumbency<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> | *Excessive recumbency<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> | ||
*Mild to severe colic | *Mild to severe colic | ||
− | **Mild, recurrent | + | **Mild, recurrent colic signs post-prandially<ref>Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome. ''Vet Clin North Am Equine Pract'', 25(2):283-301.</ref> |
**In one study, 49% of horses that presented for colic had gastric ulceration and those with duodenitis-proximal jejunitis had a trend towards a higher prevalence of gastric ulceration compared to those with other GI lesions.<ref>Dukti, S.A, Perkins, S, Murphy, J, Barr, B, Boston, R, Southwood, L.L, Bernard, W (2006) Prevalence of gastric squamous ulceration in horses with abdominal pain. ''Equine Vet J'', 38:347-349.</ref> | **In one study, 49% of horses that presented for colic had gastric ulceration and those with duodenitis-proximal jejunitis had a trend towards a higher prevalence of gastric ulceration compared to those with other GI lesions.<ref>Dukti, S.A, Perkins, S, Murphy, J, Barr, B, Boston, R, Southwood, L.L, Bernard, W (2006) Prevalence of gastric squamous ulceration in horses with abdominal pain. ''Equine Vet J'', 38:347-349.</ref> | ||
*Changes in attitude (dullness or depression)<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> | *Changes in attitude (dullness or depression)<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> | ||
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'''Clinical signs in foals vary depending on age and severity:''' | '''Clinical signs in foals vary depending on age and severity:''' | ||
− | *'''Neonatal foals''': many ulcers are silent, some foals only exhibit signs when ulceration has become severe. Glandular ulcers are considered the most significant<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> | + | *'''Neonatal foals''': many ulcers are silent, some foals only exhibit signs when ulceration has become severe. Glandular ulcers are considered the most significant<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> |
**Poor appetite | **Poor appetite | ||
**Diarrhoea | **Diarrhoea | ||
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**Diarrhoea | **Diarrhoea | ||
− | In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> | + | In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> GDUD is the primary differential for ptyalism in foals, other possible diagnoses include oesophageal obstruction and ''Candida'' infection.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> |
==Diagnosis== | ==Diagnosis== | ||
− | A presumptive diagnosis can be based on clinical signs and response to therapy,<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> however, a definitive diagnosis requires visualisation of the stomach. This can be achieved in the live horse using endsocopy or, alternatively, at | + | A presumptive diagnosis can be based on clinical signs and response to therapy,<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> however, a definitive diagnosis requires visualisation of the stomach. This can be achieved in the live horse using endsocopy or, alternatively, at post-mortem.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> |
''EGUS was recently discussed at the 2010 Annual meeting between the Equine Insurers Forum (EIF) and the British Equine Veterinary Association (BEVA). The EIF maintained that in order to support claims for the long term costs associated with treatment of EGUS, there would be a requirement for veterinary surgeons to make a definitive diagnosis prior to prescribing omeprazole.'' | ''EGUS was recently discussed at the 2010 Annual meeting between the Equine Insurers Forum (EIF) and the British Equine Veterinary Association (BEVA). The EIF maintained that in order to support claims for the long term costs associated with treatment of EGUS, there would be a requirement for veterinary surgeons to make a definitive diagnosis prior to prescribing omeprazole.'' | ||
− | + | ===Endoscopy=== | |
− | Oesophagogastroscopy or duodenoscopy can be performed under mild sedation (e.g. 0.6-0.8mg/kg xylazine<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>) in the standing horse. Of these, duodenoscopy is the more specific but more technically demanding method.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Endoscopic examination requires preparatory starving of the patient for 6-8hours,<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> eliciting a certain degree of stress. As such, it is preferable not to carry out this technique in foals. | + | Oesophagogastroscopy or duodenoscopy can be performed under mild sedation (e.g. 0.6-0.8mg/kg xylazine<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>) in the standing horse. Of these, duodenoscopy is the more specific but more technically demanding method.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Endoscopic examination requires preparatory starving of the patient for 6-8hours,<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> eliciting a certain degree of stress. As such, it is preferable not to carry out this technique in foals. In adult horses, a minimum endoscope length of two metres is essential to visualize the gastric body and fundus.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> A 2.8-3.0 metre endoscope is needed to observe the gastric antrum, pylorus and proximal dudoenum.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> In either case, fibreoptic or videoendoscopic equipment can be used.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> |
− | ulcer syndrome. ''Equine Vet J'', 41(7):616.</ref> At the time of writing however, the EGUC system appears to be | + | |
+ | Based on a consensus, the Equine Gastric Ulcer Council (EGUC) published an EGUS Lesion Scoring System which they claimed to be simple and applicable to both regions of the equine gastric mucosa.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> This last point has been debated, since most of the acquired data on gastric lesions refers only to the squamous mucosa.<ref name="Merritt">Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric | ||
+ | ulcer syndrome. ''Equine Vet J'', 41(7):616.</ref> At the time of writing however, the EGUC system appears to be the most well established and useful in practice: | ||
{|cellpadding="10" cellspacing="0" border="1" | {|cellpadding="10" cellspacing="0" border="1" | ||
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|- | |- | ||
|Grade 2 | |Grade 2 | ||
− | |Small single | + | |Small single of multifocal lesions |
|- | |- | ||
|Grade 3 | |Grade 3 | ||
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|} | |} | ||
− | Diffuse inflammation may be the only lesion observed in foals with early GDUD.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> In contrast to other scoring systems,<ref>MacAllister, C.G, Andrews F.M, Deegan E, Ruoff, W, Olovson, S.G (1997) A scoring system for gastric ulcers in horses. ''Equine Vet J'', 29:430-433.</ref> the EGUC approach does not include bleeding when assigning lesion grades. The justification is that the 'snapshot' provided by endoscopy may by chance identify bleeding of superficial erosions whilst missing the intermittent haemorrhage of more severe lesions.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> | + | Diffuse inflammation may be the only lesion observed in foals with early GDUD.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> In contrast to other scoring systems,<ref>MacAllister, C.G, Andrews F.M, Deegan E, Ruoff, W, Olovson, S.G (1997) A scoring system for gastric ulcers in horses. ''Equine Vet J'', 29:430-433.</ref> the EGUC approach does not include bleeding when assigning lesion grades. The justification is that the 'snapshot' provided by endoscopy may by chance identify bleeding of superficial erosions whilst missing the intermittent haemorrhage of more severe lesions. <ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> Endoscopy may assist in understanding the severity of the disease and assessing the therapeutic response, but it is not without disadvantages. Ulcer severity may be underestimated, particularly in the squamous region and glandular ulcers may be missed altogether.<ref>Andrews, F.M, Reinmeyers, C.R, McCracken, M.D, Blackford, J.T, Nadeau, J.A, Saabye, L, Sotell, M, Saxton, A (2002) Comparison of endoscopic, necropsy and histology scoring of equine gastric ulcers. ''Equine Vet J'',34(5):475-478.</ref> Lesions that appear grossly similar may have different grades on histopathology.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> This is important as varying lesions may have different causes, requiring a range of treatment approaches. |
− | === | + | ===Radiography=== |
− | In older foals with GDUD, detection of gastric outflow obstruction via abdominal radiography is essential to treatment and prognosis.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Liquid barium will demonstrate very delayed or no outflow depending on the degree of obstruction. Without contrast medium, a large, gas filled stomach will be obvious.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> The need to perform contrast radiography must be weighed against the stress it would place upon the foal. | + | In older foals with GDUD, detection of gastric outflow obstruction via abdominal radiography is essential to treatment and prognosis.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Liquid barium will demonstrate very delayed or no outflow depending on the degree of obstruction. Without contrast medium, a large, gas filled stomach will be obvious.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>. The need to perform contrast radiography must be weighed against the stress it would place upon the foal. |
− | + | ===Biopsy=== | |
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− | + | A transendoscopic gastric biopsy technique was recently validated for obtaining samples from the gastric glandular mucosa in the live horse.<ref>Rodrigues, N.L, Dore, M, Doucet, M.Y (2009) Validation of a transendoscopic glandular and nonglandular gastric biopsy technique in horses. ''Equine Vet J'', 41(7):631-5.</ref>Unfortunately this technique failed to produce samples of squamous mucosa that would be suitable for histopathological analysis. | |
+ | |||
+ | ===Laboratory tests=== | ||
Currently, useful and reliable markers for EGUS are lacking.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> The SUCCEED® Equine Fecal Blood Test™ uses specific equine monoclonal antibodies to albumin and haemoglobin to detect occult blood in faeces.<ref>Carter, S, Pellegrini, F.A (2006) The use of novel antibody tools to detect the presence of blood in equine feces. ''Company Bulletin Freedom Health LLC'' 1-3. In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref><ref>Pellegrini, F.L, Carter, S.D (2007) An equine necroscopic study to determine the | Currently, useful and reliable markers for EGUS are lacking.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). ''Equine Vet Educ'', 11(5):262-272.</ref> The SUCCEED® Equine Fecal Blood Test™ uses specific equine monoclonal antibodies to albumin and haemoglobin to detect occult blood in faeces.<ref>Carter, S, Pellegrini, F.A (2006) The use of novel antibody tools to detect the presence of blood in equine feces. ''Company Bulletin Freedom Health LLC'' 1-3. In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref><ref>Pellegrini, F.L, Carter, S.D (2007) An equine necroscopic study to determine the | ||
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*Serum alpha1-antitrypsin may be released from damaged gastric tissue<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> and has been detected more frequently in foals with gastric ulceration<ref>Taharaguchi, S, Nagano, A, Okai, K, ''et al.'' (2007) Detection of an isoform of alpha(1)-antitrypsin in serum samples from foals with gastric ulcers. ''Vet Rec'', 161:338-342. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> | *Serum alpha1-antitrypsin may be released from damaged gastric tissue<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> and has been detected more frequently in foals with gastric ulceration<ref>Taharaguchi, S, Nagano, A, Okai, K, ''et al.'' (2007) Detection of an isoform of alpha(1)-antitrypsin in serum samples from foals with gastric ulcers. ''Vet Rec'', 161:338-342. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> | ||
− | + | ===Pathology=== | |
− | Martineau and co-workers (2009) demonstrated that in a mixed population of horses, a wide range of lesions associated with EGUS could be found at | + | Martineau and co-workers (2009) demonstrated that in a mixed population of horses, a wide range of lesions associated with EGUS could be found at post-mortem.<ref name="Martineau">Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: range of lesions present in 21 mature individuals. ''Equine Vet J'',41(7):638-44.</ref> These included hyperkeratosis, punctate scars, diffuse erosions or ulcerations and ''margo injuria'' in the squamous region and hyperaemia, focal erosions and ulcerations in the glandular region. A novel finding was glandular metaplasia.<ref name="Martineau">Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: range of lesions present in 21 mature individuals. ''Equine Vet J'',41(7):638-44.</ref> |
− | + | Equine Vet J. 2009 Sep;41(7):646-51. | |
+ | Pathology of gastritis and gastric ulceration in the horse. Part 2: a scoring system. | ||
+ | Martineau H, Thompson H, Taylor D. | ||
− | |||
− | |||
− | |||
− | + | Lesions in the squamous region are most usefully compared to those of the pig: animals with similar gastric anatomy and a high incidence of gastric disease. Similarities include not only the most frequent lesion location (squamous glandular junction) but also the histological appearance such as parakeratosis, acanthosis, lengthening of rete pegs, balloon keratinocytes, inflammatory cell infiltration, vessel congestion and oedema (Muggenburg et al. 1964; Bivin et al. 1974; Embaye et al. | |
+ | 1990; Doster 2002).(Martinaeu 2009) | ||
− | |||
− | The | + | A proposed pathogenesis for lesion formation in the squamous region is now possible. The stratified squamous epithelium reacts to excessive acidic exposure by thickening and becoming para/hyperkeratotic (Fig 2). Sloughing of superficial layers then predisposes to secondary infection with opportunistic bacteria (Fig3) and inflammatory cells migrate to the area. The lesion deepens and progresses from an erosion to ulceration, exposing unprotected tissue to acid contents. Subsequent healing may or may not occur depending on factors influencing acidity and healing capabilities of the individual animal. Existing experiments in vitro act to confirm this theory (Nadeau et al. 2003a,b; Andrews et al. 2006). |
+ | The 2 animals that displayed diffuse erosions and ulcerations showed little reactivity in the way of hyperkeratosis, acanthosis and rete peg lengthening. The pathogenesis of these lesions is probably due to scalding from acidic gastric contents and bile acids as both horses were suffering from diseases causing gastric reflux (Berschnieder et al. 1999). | ||
+ | Glandular metaplasia was observed in 2 specific sites. The first showed formation of PAS positive mucous glands within the mid lamina propria, away from the margo plicatus underlying erosions and ulcerations (Fig 5). The vulnerability of the squamous region to damage is partly blamed on lack of mucus production, and it is probable that this tissue metaplasia is occurring as a protective mechanism. The second was not always associated with erosion/ ulceration and occurred at the margo plicatus as an extension of glandular tissue, in islet form, towards and within the nonglandular region (Fig 6). This could be a natural progressive development that occurs throughout the life of the horse due to continual exposure of the squamous epithelium to gastric contents adjacent to the margo plicatus (Husted et al. 2008). | ||
+ | It is more difficult to assign a precise pathogenesis to lesions within the glandular region, particularly as the history of NSAIDs was unknown. | ||
+ | The novel histopathological finding was glandular metaplasia, of which there are no existing reports in the horse, pig or composite stomached animal. In the horse, oesophageal glands are said to be present at the level of the trachea within the submucosa but do not extend towards the thoracic inlet. There is one report that details the presence of surface mucus over the nonglandular region, with a suggestion that it might be nasal, salivary or respiratory mucin or come from the glandular region (Bullimore et al. 2001). | ||
+ | It may be that these glands have gone unnoticed and glandular metaplasia is a potential origin for the mucus in this case. In pigs, there is one report (Curtin et al. 1963) where healing of an erosion at the squamous glandular junction was seen to occur by spread of glandular tissue towards the cardia, without formation of scar tissue. However, histological evidence of this phenomena was not given. A similar feature occurs in man at the glandular squamous junction of the distal oesophagus and glandular cardia region of the stomach. This is named the Z line due to the interdigitation of these 2 types of epithelium. It is said to be a normal occurrence if glandular metaplasia is present in the distal 2 cm of the oesophagus (Dixon et al. 1996). However, intestinal metaplasia of the stratified squamous epithelium is a common sequel (Barretts oesophagus) and it is this condition in man which is preneoplastic (Shaheen and Richter 2009). There is no evidence of an increase incidence of intestinal metaplasia or gastric neoplasia of this region in the horse. | ||
+ | This study illustrated the wide variety of gastric lesions present in a mixed population of horses at post mortem. In the squamous region there were examples of hyperkeratosis, punctate scars, diffuse erosions and glandular metaplasia. Glandular lesions ranged in severity from areas of localised hyperaemia, to large erosions with active haemorrhage.(Martineu 2009) | ||
− | ==== | + | ==Treatment== |
+ | Proton pump inhibitors: only omeprazole (Gastroguard) is licensed for horses. Given PO once daily (4mg/kg) for 3-4 wks, most effective drug at controlling HCl secretion (decreases basal and stimulated release). Expensive and not absorbed in foas with diarrhoea | ||
+ | Histamine H2 receptor antagonists: | ||
+ | *ranitidine 7mg/kg TID for 3-4wks | ||
+ | *cimetidine 25mg/kg QID for 3-4wks (cheaper but less effective so must be given more frequently) | ||
+ | Gastric protectants: sucralfate 10-20mg/kg TID for 2-4wks | ||
+ | Antacids: magnesium and aluminium hydroxides (NOT recommended as have massive rebound effect) | ||
− | + | Foals: | |
+ | Omeprazole 4mg/kg PO SID (preferred) | ||
+ | Ranitidine (Zantac, Zeneca, UK) 6mg/kg TID PO, 1-2mg/kg IV BID (second choice) | ||
+ | Sucralfate (Antepsin, Wyeth Labs, Maidenhead, UK)(intestinal mucosal protective), 2-4g total dose or 50kg per foal QID PO (in theory best effect of this compound is in acid medium so should not be given at the same time or after H2 blockers btu latest research shows it appears to work just as well if given at the same time and this reduces stress of handling), NB nto a good prophylactic | ||
+ | Antacids not good - rebound effect | ||
+ | Metocloprmade, gastrci decompression (foals with severe gastor0duodenal stenosis), analgesia (butorphenol or pethidine or morphine NOT NSAIDs) | ||
+ | Supportive nursing by reducing stressors, milk and saliva have preventative effects so good feeding habits should be encouraged | ||
+ | Corn oil (50ml q6h) reportedly anti-ulcerogenic (increases PG production) | ||
+ | PG analogues (Misoprostenol) 5microgram/kg PO q8h | ||
− | ==== | + | ==Prognosis== |
− | + | Complications: | |
− | + | *Recurrence if management not altered | |
+ | *Perforation and peritonitis (rare - foals) | ||
+ | *Pyloric stenosis (rare - foals) | ||
− | + | Complications related to gastric ulcers are most frequent and severe in foals and include perforation, delayed gastric emptying, gastroesophageal reflux and oesophagitis, and megaoesophagus secondary to chronic gastroesophageal reflux. Sudden gastric perforation without prior signs occurs sporadically in foals.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>Ulcers in the proximal duodenum or at the pylorus can cause fibrosis and stricture. The latter complication is seen in both foals and adult horses. In rare cases, severe gastric ulceration causes fibrosis and contracture of the stomach.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> | |
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− | |||
− | |||
− | |||
− | |||
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==Prevention== | ==Prevention== | ||
− | + | Gastroguard at lower dose (1-2mg/kg) daily for 3-4wks (100, 107-109 in Sanchez) | |
+ | Prophylaxis in foals controversial as gastric acidity may be protective against bacterial translocation (Sanchez). It may be beneficial in foals receiving substantial doses of NSAIDs for orthopaedic pain (Sanchez) | ||
+ | Management: diet, training, exercise, stress (company, toys) | ||
+ | Pasture turnout and continuous access to high quality forage especially alfalfa (Sanchez) | ||
+ | Furthermore, recent information suggests that feeding a diet that contains 0.5 kg of grain per 100 kg bwt no more frequently than 6 h apart can reduce the risk of EGUS (Andrews et al. 2006). | ||
+ | It has been suggested that a high-grain, low-hay diet would increase the incidence of ulcers (Hammond et al. 1986). | ||
+ | In another study, alfalfa hay was shown to protect horses against EGUS, by increasing stomach pH. Gastric juice pH and ulcer scores were lower in horses fed a diet containing alfalfa hay compared to the same horses fed dietary brome or costal Bermuda hay (Nadeau et al. 2000; Lybbert et al. 2007). The authors concluded that alfalfa hay may be useful in addition to antiulcer treatment for prevention and treatment of squamous gastric ulcers.(Nadeau 2009) | ||
− | + | ==References== | |
− | + | <references/> | |
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− | * | + | |
− | * | + | * Due to '''parasites''' - [[Gasterophilus spp.|''Gasterophilus'' (Bots)]]. |
− | * | + | * Bots are not as common as they once were. |
+ | * Look like big pink maggots. | ||
+ | * Killed by Ivermectin. | ||
+ | * ''Gasterophilus'' leave large ulcers in glandular regions of the [[Forestomach - Anatomy & Physiology|stomach]]. | ||
+ | ** Ulcers / erosions are quite deep. | ||
+ | * The parasites are believed to be non-pathogenic, but in large numbers they probably produce some discomfort and poor growth. | ||
+ | * Carcinoma can also produce ulceration in the [[Forestomach - Anatomy & Physiology|stomach]] of the horse as, in other species. | ||
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[[Category:Gastric_Ulceration]] | [[Category:Gastric_Ulceration]] | ||
− | + | [[Category:To_Do_-_Nina]] | |
− | [[Category: | + | [[Category:Alimentary_Disorders_-_Horse]] |
− | [[Category: | + | [[Category:Alimentary_Disorders_-_Horse]][[Category:Gastric_Ulceration]] |
− | [[Category: |
Revision as of 22:46, 29 July 2010
This article is still under construction. |
Also known as: | Gastroduodenal ulceration Gastrointestinal ulceration |
See also: | Gastric Ulceration - all species |
Description
The term 'Equine gastric ulcer syndrome (EGUS)' encompasses a number of disease complexes[1] associated with ulceration of the oesophageal, gastric or duodenal mucosa[2] in horses. When such damage is caused by acidic gastric juice, the defect is described as a 'peptic ulcer'.[2] Ulceration of either or both[3] regions of the gastric mucosa is one of the most important problems of the equine stomach as it may limit performance[4] and compromise welfare.[5] The non-glandular (proximal or orad) region of the equine stomach is lined by stratified squamous mucosa and a glandular mucosa lines the distal (aborad) portion. The two regions meet abruptly at the margo plicatus[6], adjacent to where most ulcers occur.[2] Damage to these regions occurs via differing pathophysiological routes and varies in severity from inflammation, to cellular death and sloughing causing disruption of the superficial mucosa (erosion), penetration of the submucosa down to the level of the lamina propria[2](ulceration), full thickness ulceration (perforation)[6] and potentially duodenal stricture.[7] The occult nature of the disease typically precludes the observation of clinical signs until severe ulceration has developed.[2]
Prevalence
The prevalence of equine gastric ulceration has increased over the last century.[8] In a retrospective study of 3715 Swedish horses, ulcers were most often found in the squamous mucosa along the margo plicatus, then the glandular body, proximal squamous mucosa and antrum.[8] For the squamous region, reported prevalences are:
- Racehorses 66-93%[9][10][11]
- Racehorses in active race training 80-93% (incidence 100%)[12][13]
- Show horses 58%[14]
- Ponies 78%[15]
- Endurance horses 67%[16]
- Western performance horses 40%[17]
- Thoroughbred broodmares (67-77%)[18]
- Nonracing performance horses (17% pre-competition, 56% post-competition)[19]
- Pleasure horses in full work ~ 60%[4]
- Pleasure, riding lessons, showing 37%[20]
- Foals ~25-57%[21][22][23], the incidence increases dramatically in foals with clinical signs, especially gastrointestinal signs.[2]
The prevalence and severity of ulcers increases with work intensity[7] and duration[24][25], thus racehorses in active training are more often affected[9] and in half of these, the lesions are moderate to severe.[7] In one study, all horses developed gastric ulcers within 2 weeks of entering simulated race training.[12] Lesions are thought to be chronically progressive during race training, but to regress during retirement.[9] Horses with signs of gastrointestinal distress also demonstrate an increased frequency and severity of ulcerative lesions.[2]EGUS prevalence is high in horses with bowel, liver and oesophageal lesions.[8] Among show horses, 82% of those with signs of abdominal discomfort had gastric ulcers[26] Around 30% of adult horses and about 50% of foals have mild gastric erosions which heal without treatment or clinical signs.[7] In 201 clinically normal horses in Denmark, 53% had EGUS with severity score >2 and older horses were more likely to have lesions in both regions of the stomach[27]
Signalment
EGUS develops in horses of all ages[6] but is most common in young horses in training and foals. Gastric ulceration is considered to be rare in horses at pasture.[28]
Pathophysiology
Risk Factors
Exercise
There appears to be a high prevalence of gastric ulcers in horses performing in most disciplines including racing, endurance, show jumping, dressage and western performance.[29] Although this may be related to exercise, other confounding factors associated with these disciplines such as travel, diet, feeding regime, NSAIDs and stress may be significant. However, Vatistas and co-workers (1999) were able to induce and maintain EGUS in racehorses in fast work without the use of NSAIDs or fasting before exercise.[12] There is also evidence that training for just 8 days is suffcient to induce gastric ulcers.[30] Furthermore, the higher prevalence of gastric ulcers at post mortem in racehorses in training compared to those in retirement adds weight to the hypothesis that exercise is an important risk factor for EGUS.[9] Strenuous exercise is known to stimulate gastrin release which has effects on HCl secretion, gastric emptying and gastric blood flow. It is also thought that exposure of the squamous mucosa to acid is increased as the stomach is compressed by the abdominal viscera and diaphragm during excercise.[31]
Housing and Transport
Housing in stables has been proposed as a risk factor for gastric ulcers, with more lesions being found in confined horses compared to those out at grass.[32] However, when comparing solitary stable confinement with stabling next to a companion, and finally turn out in a paddock, Husted and colleagues (2008) found that the environmental situation had no effect on mucosal acid exposure in the equine stomach.[33] Transport has also been shown to induce squamous mucosal ulceration in horses.[34]
Diet
Feed deprivation encourages gastric ulceration in two ways: (1) it precludes the buffering capacity of protein leading to a reduced gastric pH[35] and (2) it empties the stomach and exposes the squamous mucosa to the more mobile gastric juice.[8] It is unsurprising, therefore, that an alternating feed-fast protocol would produce a consistent model of ulcer induction in the equine squamous mucosa.[36][37] Despite this, feed deprivation is not a prerequisite for gastric ulceration in the horse.[38] Diets that are plentiful in roughage prolong the mastication process and the production of salivary bicarbonate that protects the gastric mucosa. A diet of high grain and low roughage thus predisposes to EGUS.[39] This sort of diet is commonly fed to racehorses but dietary components have also been shown to influence EGUS risk in nonracehorses.[40] Ponies fed a concentrate diet had a greater prevalence of gastric ulcers than ponies fed hay alone.[12] and this may be because grain and pelleted feeds are asssociated with increased serum gastrin.[41] High starch meals are also a risk because they are fermented to volatile fatty acids (VFAs) and lactic acid and are emptied from the stomach relatively slowly.[42][43][44]
Other ailments
Conditions that produce abdominal pain and/or inappetance are likely to reduce food intake and predipose to gastric ulcers.[8] This may be the reason that colic and other gastrointestinal disorders have been associated with EGUS.[45] Alternatively, EGUS may be part of a more general gastrointestinal disease complex.[12] Stress induced by other clinical disorders has been reported to increase the prevalence of EGUS in neonatal foals[46] and a similar mechanism may exist for adult animals.[12]
NSAIDs
As in other species, nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to cause gastric ulcers in horses. Typicaly this is associated with high doses or frequent administration of phenylbutazone or flunixin meglumine. However, although there is evidence to the contrary,[47]therapeutic doses of NSAIDs may be sufficient to induce EGUS. Other studies have suggested that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally[48]and that combination treatment with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone.[49] The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa[50][51][52], they may look different endoscopically from ulcers that occur naturally,[53] and they appear to heal spontaneously.[54][55] Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.[56][57][38]
Temperament
A nervous disposition has been linked with gastric ulcers[58]but the same association was not seen in another study.[59] The physiological and psychological stresses of training, housing, boredom, travel, mixing, hospitalisation and entering new environments[12] may increase the risk of developing EGUS. In foals hypoxia may also be a risk factor.
Clinical syndrome
The clinical signs associated with gastric ulcers are often very non-sepcific, difficult to document and at times only subjective.[60] In addition, there appears to be a poor correlation between the severity of endoscopic lesions and the clinical presentation.[20] The significance of gastric ulceration in horses thus remains questionable. However, there have been instances where ulcer treatment has preceded an improvement in clinical status and/or racing perfomance, suggesting that in some horses, ulcers are a considerable burden.[60] Cases gastric ulceration are often asymptomatic, but signs that have been attributed to these lesions in mature horses include:
- Poor appetite (particularly decreased consumption of concentrates)[6]
- Poor condition
- Rough hair coat
- Weight loss
- Excessive recumbency[2]
- Mild to severe colic
- Changes in attitude (dullness or depression)[60]
- Poor racing performance and reluctance to train
Clinical signs in foals vary depending on age and severity:
- Neonatal foals: many ulcers are silent, some foals only exhibit signs when ulceration has become severe. Glandular ulcers are considered the most significant[6]
- Poor appetite
- Diarrhoea
- Intermittent colic
- Frequent dorsal recumbency
- Sucklings and weanlings:[6]
- Diarrhoea
- Poor appetite (off suck or partially off suck)
- Poor growth, failure to thrive
- Poor body condition
- Rough hair coat
- Potbelly appearance
- Bruxism (almost pathognomonic)
- Colic after feeding or tubing
- Chewing straw
- Dorsal recumbency
- Signs of gastroduodenal ulcer disease (GDUD):[6]
- Bruxism
- Colic
- Gastrooesophageal reflux after suckling
- Ptyalism (secondary to gastric outflow obstruction and gastroesophageal reflux)[7]
- Diarrhoea
In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.[6] GDUD is the primary differential for ptyalism in foals, other possible diagnoses include oesophageal obstruction and Candida infection.[7]
Diagnosis
A presumptive diagnosis can be based on clinical signs and response to therapy,[6] however, a definitive diagnosis requires visualisation of the stomach. This can be achieved in the live horse using endsocopy or, alternatively, at post-mortem.[39]
EGUS was recently discussed at the 2010 Annual meeting between the Equine Insurers Forum (EIF) and the British Equine Veterinary Association (BEVA). The EIF maintained that in order to support claims for the long term costs associated with treatment of EGUS, there would be a requirement for veterinary surgeons to make a definitive diagnosis prior to prescribing omeprazole.
Endoscopy
Oesophagogastroscopy or duodenoscopy can be performed under mild sedation (e.g. 0.6-0.8mg/kg xylazine[60]) in the standing horse. Of these, duodenoscopy is the more specific but more technically demanding method.[6] Endoscopic examination requires preparatory starving of the patient for 6-8hours,[60] eliciting a certain degree of stress. As such, it is preferable not to carry out this technique in foals. In adult horses, a minimum endoscope length of two metres is essential to visualize the gastric body and fundus.[6] A 2.8-3.0 metre endoscope is needed to observe the gastric antrum, pylorus and proximal dudoenum.[6] In either case, fibreoptic or videoendoscopic equipment can be used.[2]
Based on a consensus, the Equine Gastric Ulcer Council (EGUC) published an EGUS Lesion Scoring System which they claimed to be simple and applicable to both regions of the equine gastric mucosa.[2] This last point has been debated, since most of the acquired data on gastric lesions refers only to the squamous mucosa.[1] At the time of writing however, the EGUC system appears to be the most well established and useful in practice:
Lesion Grade | Description |
Grade 0 | Intact epithelium with no appearance of hyperaemia (reddening) or hyperkeratosis (yellowing of the squamous mucosa) |
Grade 1 | Intact mucosa with areas of reddening or hyperkeratosis (squamous) |
Grade 2 | Small single of multifocal lesions |
Grade 3 | Large single or multifocal lesions or extensive superficial lesions |
Grade 4 | Extensive lesions with areas of deep ulceration |
Diffuse inflammation may be the only lesion observed in foals with early GDUD.[6] In contrast to other scoring systems,[65] the EGUC approach does not include bleeding when assigning lesion grades. The justification is that the 'snapshot' provided by endoscopy may by chance identify bleeding of superficial erosions whilst missing the intermittent haemorrhage of more severe lesions. [2] Endoscopy may assist in understanding the severity of the disease and assessing the therapeutic response, but it is not without disadvantages. Ulcer severity may be underestimated, particularly in the squamous region and glandular ulcers may be missed altogether.[66] Lesions that appear grossly similar may have different grades on histopathology.[39] This is important as varying lesions may have different causes, requiring a range of treatment approaches.
Radiography
In older foals with GDUD, detection of gastric outflow obstruction via abdominal radiography is essential to treatment and prognosis.[6] Liquid barium will demonstrate very delayed or no outflow depending on the degree of obstruction. Without contrast medium, a large, gas filled stomach will be obvious.[6]. The need to perform contrast radiography must be weighed against the stress it would place upon the foal.
Biopsy
A transendoscopic gastric biopsy technique was recently validated for obtaining samples from the gastric glandular mucosa in the live horse.[67]Unfortunately this technique failed to produce samples of squamous mucosa that would be suitable for histopathological analysis.
Laboratory tests
Currently, useful and reliable markers for EGUS are lacking.[2] The SUCCEED® Equine Fecal Blood Test™ uses specific equine monoclonal antibodies to albumin and haemoglobin to detect occult blood in faeces.[68][69]The test has a positive predictive value of 77% and a negative predictive value of 72% and thus cannot be relied upon alone to diagnose EGUS.[39] False positive results may arise from rectal trauma (e.g. recent biopsy or rectal examination) or protein losing enteropathy.[39] Other tests that require further analysis for sensitivity and specificity[6] include:
- Urine[70] and blood[71] sucrose absorption as an assay of gastric mucosal permeability
- Serum alpha1-antitrypsin may be released from damaged gastric tissue[39] and has been detected more frequently in foals with gastric ulceration[72]
Pathology
Martineau and co-workers (2009) demonstrated that in a mixed population of horses, a wide range of lesions associated with EGUS could be found at post-mortem.[5] These included hyperkeratosis, punctate scars, diffuse erosions or ulcerations and margo injuria in the squamous region and hyperaemia, focal erosions and ulcerations in the glandular region. A novel finding was glandular metaplasia.[5]
Equine Vet J. 2009 Sep;41(7):646-51. Pathology of gastritis and gastric ulceration in the horse. Part 2: a scoring system. Martineau H, Thompson H, Taylor D.
Lesions in the squamous region are most usefully compared to those of the pig: animals with similar gastric anatomy and a high incidence of gastric disease. Similarities include not only the most frequent lesion location (squamous glandular junction) but also the histological appearance such as parakeratosis, acanthosis, lengthening of rete pegs, balloon keratinocytes, inflammatory cell infiltration, vessel congestion and oedema (Muggenburg et al. 1964; Bivin et al. 1974; Embaye et al.
1990; Doster 2002).(Martinaeu 2009)
A proposed pathogenesis for lesion formation in the squamous region is now possible. The stratified squamous epithelium reacts to excessive acidic exposure by thickening and becoming para/hyperkeratotic (Fig 2). Sloughing of superficial layers then predisposes to secondary infection with opportunistic bacteria (Fig3) and inflammatory cells migrate to the area. The lesion deepens and progresses from an erosion to ulceration, exposing unprotected tissue to acid contents. Subsequent healing may or may not occur depending on factors influencing acidity and healing capabilities of the individual animal. Existing experiments in vitro act to confirm this theory (Nadeau et al. 2003a,b; Andrews et al. 2006).
The 2 animals that displayed diffuse erosions and ulcerations showed little reactivity in the way of hyperkeratosis, acanthosis and rete peg lengthening. The pathogenesis of these lesions is probably due to scalding from acidic gastric contents and bile acids as both horses were suffering from diseases causing gastric reflux (Berschnieder et al. 1999).
Glandular metaplasia was observed in 2 specific sites. The first showed formation of PAS positive mucous glands within the mid lamina propria, away from the margo plicatus underlying erosions and ulcerations (Fig 5). The vulnerability of the squamous region to damage is partly blamed on lack of mucus production, and it is probable that this tissue metaplasia is occurring as a protective mechanism. The second was not always associated with erosion/ ulceration and occurred at the margo plicatus as an extension of glandular tissue, in islet form, towards and within the nonglandular region (Fig 6). This could be a natural progressive development that occurs throughout the life of the horse due to continual exposure of the squamous epithelium to gastric contents adjacent to the margo plicatus (Husted et al. 2008).
It is more difficult to assign a precise pathogenesis to lesions within the glandular region, particularly as the history of NSAIDs was unknown.
The novel histopathological finding was glandular metaplasia, of which there are no existing reports in the horse, pig or composite stomached animal. In the horse, oesophageal glands are said to be present at the level of the trachea within the submucosa but do not extend towards the thoracic inlet. There is one report that details the presence of surface mucus over the nonglandular region, with a suggestion that it might be nasal, salivary or respiratory mucin or come from the glandular region (Bullimore et al. 2001).
It may be that these glands have gone unnoticed and glandular metaplasia is a potential origin for the mucus in this case. In pigs, there is one report (Curtin et al. 1963) where healing of an erosion at the squamous glandular junction was seen to occur by spread of glandular tissue towards the cardia, without formation of scar tissue. However, histological evidence of this phenomena was not given. A similar feature occurs in man at the glandular squamous junction of the distal oesophagus and glandular cardia region of the stomach. This is named the Z line due to the interdigitation of these 2 types of epithelium. It is said to be a normal occurrence if glandular metaplasia is present in the distal 2 cm of the oesophagus (Dixon et al. 1996). However, intestinal metaplasia of the stratified squamous epithelium is a common sequel (Barretts oesophagus) and it is this condition in man which is preneoplastic (Shaheen and Richter 2009). There is no evidence of an increase incidence of intestinal metaplasia or gastric neoplasia of this region in the horse.
This study illustrated the wide variety of gastric lesions present in a mixed population of horses at post mortem. In the squamous region there were examples of hyperkeratosis, punctate scars, diffuse erosions and glandular metaplasia. Glandular lesions ranged in severity from areas of localised hyperaemia, to large erosions with active haemorrhage.(Martineu 2009)
Treatment
Proton pump inhibitors: only omeprazole (Gastroguard) is licensed for horses. Given PO once daily (4mg/kg) for 3-4 wks, most effective drug at controlling HCl secretion (decreases basal and stimulated release). Expensive and not absorbed in foas with diarrhoea Histamine H2 receptor antagonists:
- ranitidine 7mg/kg TID for 3-4wks
- cimetidine 25mg/kg QID for 3-4wks (cheaper but less effective so must be given more frequently)
Gastric protectants: sucralfate 10-20mg/kg TID for 2-4wks Antacids: magnesium and aluminium hydroxides (NOT recommended as have massive rebound effect)
Foals: Omeprazole 4mg/kg PO SID (preferred) Ranitidine (Zantac, Zeneca, UK) 6mg/kg TID PO, 1-2mg/kg IV BID (second choice) Sucralfate (Antepsin, Wyeth Labs, Maidenhead, UK)(intestinal mucosal protective), 2-4g total dose or 50kg per foal QID PO (in theory best effect of this compound is in acid medium so should not be given at the same time or after H2 blockers btu latest research shows it appears to work just as well if given at the same time and this reduces stress of handling), NB nto a good prophylactic Antacids not good - rebound effect Metocloprmade, gastrci decompression (foals with severe gastor0duodenal stenosis), analgesia (butorphenol or pethidine or morphine NOT NSAIDs) Supportive nursing by reducing stressors, milk and saliva have preventative effects so good feeding habits should be encouraged Corn oil (50ml q6h) reportedly anti-ulcerogenic (increases PG production) PG analogues (Misoprostenol) 5microgram/kg PO q8h
Prognosis
Complications:
- Recurrence if management not altered
- Perforation and peritonitis (rare - foals)
- Pyloric stenosis (rare - foals)
Complications related to gastric ulcers are most frequent and severe in foals and include perforation, delayed gastric emptying, gastroesophageal reflux and oesophagitis, and megaoesophagus secondary to chronic gastroesophageal reflux. Sudden gastric perforation without prior signs occurs sporadically in foals.[7]Ulcers in the proximal duodenum or at the pylorus can cause fibrosis and stricture. The latter complication is seen in both foals and adult horses. In rare cases, severe gastric ulceration causes fibrosis and contracture of the stomach.[7]
Prevention
Gastroguard at lower dose (1-2mg/kg) daily for 3-4wks (100, 107-109 in Sanchez) Prophylaxis in foals controversial as gastric acidity may be protective against bacterial translocation (Sanchez). It may be beneficial in foals receiving substantial doses of NSAIDs for orthopaedic pain (Sanchez) Management: diet, training, exercise, stress (company, toys) Pasture turnout and continuous access to high quality forage especially alfalfa (Sanchez) Furthermore, recent information suggests that feeding a diet that contains 0.5 kg of grain per 100 kg bwt no more frequently than 6 h apart can reduce the risk of EGUS (Andrews et al. 2006). It has been suggested that a high-grain, low-hay diet would increase the incidence of ulcers (Hammond et al. 1986). In another study, alfalfa hay was shown to protect horses against EGUS, by increasing stomach pH. Gastric juice pH and ulcer scores were lower in horses fed a diet containing alfalfa hay compared to the same horses fed dietary brome or costal Bermuda hay (Nadeau et al. 2000; Lybbert et al. 2007). The authors concluded that alfalfa hay may be useful in addition to antiulcer treatment for prevention and treatment of squamous gastric ulcers.(Nadeau 2009)
References
- ↑ 1.0 1.1 Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric ulcer syndrome. Equine Vet J, 41(7):616.
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet Educ, 11(5):262-272.
- ↑ Andrews, F.M, Bernard, W.V, Byars, T.D et al. (1999) Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet Educ, 1:122-134. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- ↑ 4.0 4.1 Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review. N Z Vet J, 55(1):1-12).
- ↑ 5.0 5.1 5.2 Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644. Cite error: Invalid
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tag; name "Martineau" defined multiple times with different content - ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 6.13 6.14 6.15 Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial
- ↑ 8.0 8.1 8.2 8.3 8.4 Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.
- ↑ 9.0 9.1 9.2 9.3 Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. Equine Vet J, 18(4):284-287.
- ↑ Vatistas, N.J, Snyder, J.R, Carlson, G, et al (1994) Epidemiological study of gastric ulceration in the thoroughbred racehorse:202 horses 1992-1993. Proc Am Assoc Equine Pract, 40:125-126
- ↑ Murray, M.J, Schusser, G.F, Pipers, F.S, Gross, S.J (1996) Factors associated with gastric lesions in thoroughbred racehorses. Equine Vet J, 28:368-374.
- ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
- ↑ Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthruy, R.M, Thurmond, M, Zhou, H, Lloyd, K.L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses. Equine Vet J, Suppl 29:34-39.
- ↑ McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses. J Am Vet Med Assoc, 215:1130-1133.
- ↑ MacAllister, C.G, Sangiah, S, Mauromoustakos, A (1992) Effect of a histamine H, type receptor antagonist (WY 45, 727) on the healing of gastric ulcers in ponies. J Vet Int Med, 6:271-275.
- ↑ Nieto, J.E, Snyder, J.R, Beldomenico, P et al. (2004) Prevalence of gastric ulcers in endurance horses: a preliminary report. Vet J, 167:33-37.
- ↑ Bertone, J (2000) Prevalence of gastric ulcers in elite, heavy use western performance horses. Proc Am Assoc Equine Pract, 46:256-259.
- ↑ LeJeune, S.S, Nieto, J.E, Dechant, J.E, Snyder, J.R (2009) Prevalence of gastric ulcers in Thoroughbred broodmares in pasture: a preliminary report. Vet J, 181(3):251-5.
- ↑ Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. J Equine Vet Sci, 23:560-561. In:Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- ↑ 20.0 20.1 Murray, M.J, Grodinsky, C, Anderson, C.W, Radue, P.F, Schmidt, G.R (1989) Gastric ulcers in horses: a comparison of endoscopic findings in horses with and without clinical signs. Equine Vet J Suppl, 7:68-72.
- ↑ Wilson, J.H (1986) Gastric and duodenal ulcers in foals: a retrospective study. Proc Equine Colic Res Symp 2nd:126-128.
- ↑ Murray, M.J, Grodinsky, C, Cowles, R.R, et al.(1990) Endoscopic evaluation of changes in gastric lesions of Thoroughbred foals. J Am Vet Med Assoc, 196:1623-1627.
- ↑ Murray, M.J (1989) Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). J Am Vet Med Assoc, 195:1135-1141.
- ↑ Orsini, J.A, Pipers, F.S (1997) Endoscopic evaluation of the relationship between training, racing, and gastric ulcers. Vet Surg, 26:424. In: Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
- ↑ Murray, M.J (1994) Gastric ulcers in adult horses. Comp Cont Educ Pract Vet, 16:792-794. In:Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
- ↑ Murray, M. (1992) Gastric ulceration in horses: 91 cases (1987-1990). J Am Vet Med Assoc, 201:117-120. In: Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644.
- ↑ Luthersson, N, Nielsen, K.H, Harris, P, Parkin, T.D (2009) The prevalence and anatomical distribution of equine gastric ulcer syndrome (EGUS) in 201 horses in Denmark. Equine Vet J, 41(7):619-24.
- ↑ Murray, M.J (1994) Characteristics of gastric ulcer pathophysiology. Proc Am Coll Vet Intern Med, 12:610-612. In: Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.
- ↑ Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. J Equine Vet Sci, 23:560-561. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
- ↑ White, G, McClure, S.R, Siifferman, R, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration. J Am Vet Med Assoc, 230(11):1680-2.
- ↑ Lorenzo-Figueras, M, Merritt, A.M (2002) Effects of exercise on gastric volume and pH in the proximal portion of the stomach of horses. Am J Vet Res, 63:1481-1487.
- ↑ Murray, M.J, Eichorn, E.S (1996) Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall confinement with ad libitum access to hay on gastric ulceration in horses. Am J Vet Res, 57:1599-1603.
- ↑ Husted, L, Sanchex, L.C, Olsen, S.N, Baptiste, K.E, Merritt, A.M (2008) Effect of paddock vs. stall housing on 24 hour gastric pH within the proximal and ventral equine stomach. Equine Vet J, 40(4):337-41.
- ↑ McClure, S.R, Carithers, D.S, Gross, S.J, Murray, M.J (2005) Gastric ulcer development in horses in a simulated show or training environment. J Am Vet Med Assoc, 227:775-777.
- ↑ Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. Equine Vet J, 25:417-421. In: Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.
- ↑ Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. Equine Vet J, 25:417-421. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- ↑ Murray, M.J (1994) Equine model of inducing ulceration in alimentary squamous epithelial mucosa. Dig Dis Sci, 39:2530-2535. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- ↑ 38.0 38.1 Vatistas, N.J (1998) Gastric Ulceration in the Racing Thoroughbred. PhD Thesis. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
- ↑ 39.0 39.1 39.2 39.3 39.4 39.5 In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615. Cite error: Invalid
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tag; name "Nadeau" defined multiple times with different content - ↑ Luthersson, N, Nielson, K.H, Harris, P, Parkin, T.D (2009) Risk factors associated with equine gastric ulceration syndrome (EGUS) in 201 horses in Denmark. Equine Vet J, 41(7):625-30.
- ↑ Smyth, G.B, Young, D.W, Hammond, L.S (1988) Effects of diet and feeding on post-prandial serum gastrin and insulin concentrations in adult horses. Equine Vet J Suppl 7:56-59.
- ↑ Mètayer, N, Lhôte, M, Bahr, A, Cohen, N.D, Kim, I, Rousell, A.J, Julliand, V (2004) Meal size and starch content affect gastric emptying in horses. Equine Vet J, 36:434-440. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
- ↑ Taharaguchi, S, Okai, K, Orita, Y, Kuwano, M, Ueno, T, Taniyama, H (2004) Relation between amounts of concentrated feed given mares and gastric ulcers in foals. J Japan Vet Med Ass, 57:366-370. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
- ↑ Boswinkel, A.M, Ellis, A.D, Sloet van Oldruitenborgh-Oosterbaan, M.M (2007) The influence of low versus high fibre haylage diets in combination with training or pasture rest on equine gastric ulceration syndrome (EGUS). Pferdeheilkunde, 23:123-130. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
- ↑ Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists. Equine Vet J Suppl, 7:77-79.
- ↑ Furr, M.O, Murray, M.J, Ferguson, D.C (1992) The effects of stress on gastric ulceration, T3, T4, reverse T3 and cortisol in neonatal foals. Equine Vet J, 24:37-40.
- ↑ Andrews, F.M, Reinemeyer, C.R, Longhofer, S.L (2009) Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. Vet Ther, 10(3):113-20.
- ↑ Monreal, L, Sabatè, D, Segura, D, Mayós, I, Homedes, J (2004) Lower gastric ulcerogenic effect of suxibuzone compared to phenylbutazone when administered orally to horses. Res Vet Sci, 76:145-149. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
- ↑ Reed, S.K, Messer, N.T, Tessman, R.K, Keegan, K.G (2006) Effects of phenylbutazone alone or in combination with flunixin meglumine on blood protein concentrations in horses. Am J Vet Res, 67:398-402. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
- ↑ MacAllister, C.G, Morgan, S.J, Borne, A.T, Pollet, R.A, (1993) Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses. J Am Vet Med Ass, 202:71-77. In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
- ↑ Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists. Equine Vet J Suppl, 7:77-79. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
- ↑ Kumaran, D, Bhuvanakumar, C.K (1994) Gastro duodenal ulceration in foals - a discussion. Cenfaur Mylapore, 10:83-86. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
- ↑ Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
- ↑ Jones, W.E (1983) Gastrointestinal ulcers [foal]. Equine Vet Data, 4:305-308. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
- ↑ MacAllister, C.G, Sangiah, S (1993) Effect of ranitidine (in healing of experimentally induced gastric ulcers in ponies. Am J Vet Res, 54:1103-1107. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
- ↑ Vatistas N.J, Snyder, J.R, Carlson, G.P, Johnson, B, Arther, R.M, Thurmiind, M, Lloyd, K.C.K (1994) Epidemiology study of gastric ulcerarion in the Thoroughbred race horse: 202 horses. Proc Am Ass Equine Pract, 39:125-126. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
- ↑ Murray, M.J, Schusser, G.F, Pipers, F.S, Gro:ss, S.J (1996) Factors associated with gastric lesions in Thoroughbred racehorses. Equine Vet J, 28:368-374. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
- ↑ McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses. J Am Vet Med Ass 215:1130-1133. In: In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
- ↑ Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthur, R.M, Thurmond, M, Zhou, H, Lloyd, L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses. Equine Vet J Suppl, 29:34-39. In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
- ↑ 60.0 60.1 60.2 60.3 60.4 Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
- ↑ Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome. Vet Clin North Am Equine Pract, 25(2):283-301.
- ↑ Dukti, S.A, Perkins, S, Murphy, J, Barr, B, Boston, R, Southwood, L.L, Bernard, W (2006) Prevalence of gastric squamous ulceration in horses with abdominal pain. Equine Vet J, 38:347-349.
- ↑ Franklin, S.H, Brazil, T.J, Allen, K.J (2008) Poor performance associated with equine gastric ulceration syndrome in four Thoroughbred racehorses. Equine Vet Educ, 20:119-124. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
- ↑ Nieto, J.E, Snyder, J.R, Vatistas, N.J, Jones, J.H (2009) Effect of gastric ulceration on physiologic responses to exercise in horses. Am J Vet Res, 70(6):787-95.
- ↑ MacAllister, C.G, Andrews F.M, Deegan E, Ruoff, W, Olovson, S.G (1997) A scoring system for gastric ulcers in horses. Equine Vet J, 29:430-433.
- ↑ Andrews, F.M, Reinmeyers, C.R, McCracken, M.D, Blackford, J.T, Nadeau, J.A, Saabye, L, Sotell, M, Saxton, A (2002) Comparison of endoscopic, necropsy and histology scoring of equine gastric ulcers. Equine Vet J,34(5):475-478.
- ↑ Rodrigues, N.L, Dore, M, Doucet, M.Y (2009) Validation of a transendoscopic glandular and nonglandular gastric biopsy technique in horses. Equine Vet J, 41(7):631-5.
- ↑ Carter, S, Pellegrini, F.A (2006) The use of novel antibody tools to detect the presence of blood in equine feces. Company Bulletin Freedom Health LLC 1-3. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
- ↑ Pellegrini, F.L, Carter, S.D (2007) An equine necroscopic study to determine the sensitivity and specificity of a dual antibody test. Company Bulletin Freedom Health LLC 1-2. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
- ↑ O'Connor, M.S, Steiner, J.M, Roussel, A.J, et al. (2004) Evaluation of urine sucrose concentration for detection of gastric ucleration in horses. Am J Vet Res, 65:31-39. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- ↑ Hewetson, M, Cohen, N.D, Love, S, et al. (2006) Sucrose concentration in bood: a new method for assessment of gastric permeability in horses with gastric ulceration. J Vet Intern Med, 20:388-394. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- ↑ Taharaguchi, S, Nagano, A, Okai, K, et al. (2007) Detection of an isoform of alpha(1)-antitrypsin in serum samples from foals with gastric ulcers. Vet Rec, 161:338-342. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- Due to parasites - Gasterophilus (Bots).
- Bots are not as common as they once were.
- Look like big pink maggots.
- Killed by Ivermectin.
- Gasterophilus leave large ulcers in glandular regions of the stomach.
- Ulcers / erosions are quite deep.
- The parasites are believed to be non-pathogenic, but in large numbers they probably produce some discomfort and poor growth.
- Carcinoma can also produce ulceration in the stomach of the horse as, in other species.