Gastric Dilation and Rupture - Horse
Also known as: Gastric Rupture
Gastric dilation in the horse may be primary, secondary or idiopathic.
See also: Gastric causes of colic
Gastric impaction, food engorgement, excessive water intake after exercise, aerophagia, Gasterophilus infestation and habrenomiasis. Excessive consumption of fermentable feeds (grains, lush grass, and beet pulp) causes a large increase in the production of volatile fatty acids which is thought to delay gastric emptying.
Primary intestinal ileus or small or large intestinal obstruction. Dilation resulting from small intestinal obstruction is the most common cause. Fluid from the obstructed small intestine accumulates in the stomach, causing nasogastric reflux. Gastric dilation may also occur with certain colonic displacements, especially right dorsal displacement of the colon around the caecum. It is hypothesised that the displaced colon obstructs duodenal outflow. Gastric fluid accumulation is also characteristic of proximal enteritis-jejunitis.
Untreated, gastric dilation can rapidly lead to gastric rupture whereby the stomach usually tears along its greater curvature. It has been proposed that the seromuscularis weakens and tears before the gastric mucosa. Most cases of rupture occur secondary to mechanical obstruction, ileus, and trauma. The rest are due to overload or idiopathic causes. Rupture can occur secondary to gastric ulceration, in which case full-thickness tearing usually occurs in all layers of the gastric wall. Certain risk factors have been identified for gastric rupture including:
- Feeding grass hay
- Not feeding grain
- Non-automatic water sources
Gastric dilation usually produces:
- Acute, severe colic
- Pale mucous membranes
- Ingesta at the nares in severe cases (rare)
- Gastric reflux
NB: the time to development of reflux is proportional to the distance to the intestinal segment involved, (e.g. 4 hours with duodenal obstruction). Furthermore, nasogastric intubation does not preclude the possibility of gastric rupture.
Gastric rupture typically results in:
The inevitable peritonitis and endotoxic shock will lead to:
- Reluctance to move
- Muscle fasciculations
- Blue or purple mucous membranes
NB: rupture of a stomach containing dry, fibrous material may produce a more insidious onset of clinical signs of peritonitis than rupture of a fluid distended viscus. This is probably because it takes longer for the dry gastric contents to disperse around the peritoneum.
Primary gastric dilation should be suspected if there are copious amounts of gastric reflux in the absence of small intestinal distension on rectal examination and the absence of endotoxaemia. A retrospective diagnosis of primary gastric dilation can be made if colic signs cease following decompression, and other clinical parameters return to normal. Primary gastric dilation does not cause any significant change in peritoneal fluid parameters until rupture occurs.
Secondary gastric dilation should be considered if there is persistent colic, repeated retrieval of nasogastric reflux, intestinal distension on rectal examination and clinical signs of endotoxaemia. These are all indications for exploratory laparotomy to look for an intestinal obstruction.
NB: excessive fluid within the stomach is not always detected by nasogastric intubation, despite repeated attempts with frequent repositioning of the tube. Furthermore, gastric impaction with solid food material may be too firm to be retrieved by this method.
- Foetid, turbid sample containing particulate matter
- White cell count >40 x 109/l
- Protein content >30g/l.
- A 'gritty feeling' on the serosal surfaces of intestine due to adherent food material
- An impression of 'space' in the abdomen due to gas in the peritoneal cavity.
If anatomical obstructions have been ruled out, prokinetic agents such as metoclopramide or bethanecol may prove useful to restore gastric motility, especially in the presence of post-operative ileus. Unfortunately, metaclopramide causes neurological side effects and bethanecol produces dose-related gastrointestinal problems including colic, diarrhoea and salivation. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as flunixin meglumine and phenylbutazone may also be beneficial in post operative ileus to help combat the effects of endotoxin. It is crucial that gastric decompression is maintained in cases of delayed gastric emptying. This can be achieved with an indwelling nasogastric tube, (although prolonged intubation carries its own risk) or by repeated intubation. IV fluid therapy should be given to ensure adequate hydration.
The surgical options for managing gastric disease are limited since the equine stomach is difficult to access surgically. Extending the midline laparotomy incision cranially may improve access slightly but also increases the risk of post operative wound problems. Gastrotomy and removal of impacted food material has been reported but carries a high risk of gross peritoneal contamination. For gastric rupture, surgical success has been reported for repairing partial thickness tears and also in one case of a full thickness rupture.
The prognosis for survival may be excellent in most cases of gastric dilation but gastric rupture is usually fatal because of widespread contamination of the peritoneal cavity, septic peritonitis, and septic shock. Food engorgement also carries the risk of secondary laminitis.
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|Gastric Dilatation or Rupture in horses publications|
- Sanchez, L.C (2010) Other Disorders of the Stomach in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- Campbell-Thompson, M.L, Merritt, A.M (1999) Alimentary system: diseases of the stomach. In Colahan, P.T, Mayhew, I.G, Merritt, A.M, Moore, J.N Equine medicine and surgery, St Louis, Mosby, pp 699-715. In: Sanchez, L.C (2010) Other Disorders of the Stomach in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- Todhunter, R.J, Erb, H.N, Roth, L (1986) Gastric rupture in horses: a review of 54 cases. Equine Vet J, 30:344-348.
- Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
- Kiper, M.L, Traub-Dargatz, J, Curtis, C.R (1990) Gastric rupture in horses: 50 cases (1979-1987), J Am Vet Med Assoc, 196:333-336. In: Sanchez, L.C (2010) Other Disorders of the Stomach in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- Puotunen-Reinert, A, Huskamp, B (1986) Experimental duodenal obstruction in the horse. Vet Surg, 15:420-428. In: Sanchez, L.C (2010) Other Disorders of the Stomach in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- Proudman, C.J, Baker, S.J (1994) Satellite Article: Gastric disease in the adult horse: a clinical perspective. Equine Vet Educ, 6(4):178-184.
- Murray, M.J (1990) Gastric ulceration. In: Smith, B.P, Large Animal Internal Medicine, CV Mosby Publishing Company, USA, pp 648-652. In: Proudman, C.J, Baker, S.J (1994) Satellite Article: Gastric disease in the adult horse: a clinical perspective. Equine Vet Educ, 6(4):178-184.
- Clayton-Jones, D.G, Greatorex, J.C, Stockman, M.J.R, Harris, C.P.J (1972) Gastric impaction in a pony: Relief via laparotomy. Equine Vet J, 4:98-99. In: Proudman, C.J, Baker, S.J (1994) Satellite Article: Gastric disease in the adult horse: a clinical perspective. Equine Vet Educ, 6(4):178-184.
- Steenhaut, M, Vlaminck, K, Gasthuys, F (1986) Surgical repair of a partial gastric rupture in a horse. Equine Vet J, 18:331-332. In: Sanchez, L.C (2010) Other Disorders of the Stomach in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
- Hogan, P.M, Bramlage, L.R, Pierce, S.W (1995) Repair of a full-thickness gastric rupture in a horse. J Am Vet Med Assoc, 207:338-340. In: Sanchez, L.C (2010) Other Disorders of the Stomach in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
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