Difference between revisions of "Gastric Dilation and Rupture - Horse"

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*Ingesta appears at the nares in severe cases
 
*Ingesta appears at the nares in severe cases
 
*Gastric reflux  
 
*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(147)).  Furthermore, '''''nasogastric intubation does not preclude the possibility of gastric rupture.<ref name="Todhunter">Todhunter, R.J, Erb, H.N, Roth, L (1986) Gastric rupture in horses: a review of 54 cases. ''Equine Vet J'', 30:344-348.</ref>'''''
+
NB: the time to development of reflux is proportional to the distance to the intestinal segment involved, (e.g. 4 hours with duodenal obstruction<ref>Puotunen-Reinert, A, Huskamp, B (1986) Experimental duodenal obstruction in the horse.  ''Vet Surg'', 15:420-428.  In: </ref>).  Furthermore, '''''nasogastric intubation does not preclude the possibility of gastric rupture.<ref name="Todhunter">Todhunter, R.J, Erb, H.N, Roth, L (1986) Gastric rupture in horses: a review of 54 cases. ''Equine Vet J'', 30:344-348.</ref>'''''
  
 
'''Gastric rupture''' typically results in:
 
'''Gastric rupture''' typically results in:

Revision as of 15:09, 11 August 2010


 This article is still under construction.


Also known as: Gastric Rupture
See also: Colic, Gastric Causes

Description

Gastric dilation in the horse may be primary, secondary or idiopathic.[1]

Aetiology

  • Primary causes: gastric impaction, food engorgement, excessive water intake after exercise, aerophagia, Gasterophilus infestation and habrenomiasis.[2][3] 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.[4]
  • Secondary causes: 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 naso-gastric 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.[4]

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.[3][5] Most cases of rupture occur secondary to mechanical obstruction, ileus, and trauma. The rest are due to overload or idiopathic causes.[4] Rupture can occur secondary to gastric ulceration, in which case full-thickness tearing usually occurs in all layers of the gastric wall.[1] Certain risk factors have been identified for gastric rupture[3][5] including:

  • Feeding grass hay
  • Not feeding grain
  • Gelding
  • Non-automatic water sources

Clinical signs

Gastric dilation usually produces:

  • Acute, severe colic
  • Tachycardia
  • Pale mucous membranes
  • Retching[4]
  • Ingesta appears at the nares in severe cases
  • 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[6]). Furthermore, nasogastric intubation does not preclude the possibility of gastric rupture.[3]

Gastric rupture typically results in:

  • Relief
  • Depression

The inevitable peritonitis and shock will lead to:

  • Tachypnoea
  • Tachycardia
  • Sweating
  • Muscle fasciculations
  • Signs of endotoxaemia

Diagnosis

Laboratory findings:(141)

  • Haemoconcentration
  • Hypokalaemia
  • Hypochloraemia

Treatment

Surgical repair has been reported for partial thickness tears(149) and one case of a full thickness repair(150).

Prognosis

The prognosis for survival may be excellent in most cases of gastric dilation[4] 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.

References

  1. ↑ 1.0 1.1 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.
  2. ↑ 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.
  3. ↑ 3.0 3.1 3.2 3.3 Todhunter, R.J, Erb, H.N, Roth, L (1986) Gastric rupture in horses: a review of 54 cases. Equine Vet J, 30:344-348.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
  5. ↑ 5.0 5.1 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.
  6. ↑ Puotunen-Reinert, A, Huskamp, B (1986) Experimental duodenal obstruction in the horse. Vet Surg, 15:420-428. In:
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