Difference between revisions of "Gastric Dilation and Rupture - Horse"
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==Description== | ==Description== | ||
| − | Gastric dilation in the horse may be primary, secondary or idiopathic.( | + | Gastric dilation in the horse may be primary, secondary or idiopathic.<ref name="Sanchez">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.</ref> |
==Aetiology== | ==Aetiology== | ||
Revision as of 14:21, 11 August 2010
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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 and parasitism(141,146). 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.[2]
- 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.[2]
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(146,148). Most cases of rupture occur secondary to mechanical obstruction, ileus, and trauma. The rest are due to overload or idiopathic causes.[2] Rupture can occur secondary to gastric ulceration, in which case full-thickness tearing usually occurs in all layers of the gastric wall.(Sanchez) Certain risk factors have been identified for gastric rupture(146, 148) 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[2]
- 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(147)). Furthermore, nasogastric intubation does not preclude the possibility of gastric rupture(146).
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[2] 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.