Gastric Dilation and Rupture - Horse

Also known as:

Gastric Rupture

See also:

Colic, Gastric Causes

Description

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

Aetiology

• Primary causes: 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.
• 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 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
• Gelding
• Non-automatic water sources

Clinical signs

Gastric dilation usually produces:

• Acute, severe colic
• Tachycardia
• Pale mucous membranes
• Retching
• Ingesta appears 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:

• Relief
• Depression

The inevitable peritonitis and endotoxic shock will lead to:

• Reluctance to move
• Tachypnoea
• Tachycardia
• Sweating
• 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 probably relates to the speed at which gastric contents are able to disperse around the peritoneum.

Diagnosis

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.

Gastric rupture results in septic peritonitis which will be reflected in the nature of fluid collected by abdominocentesis:

• Foetid, turbid sample containing particulate matter
• White cell count >40 x 10⁹/l
• Protein content >30g/l.

Findings on rectal examination may include:

• 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.

Laboratory findings may include:

• Haemoconcentration
• Hypokalaemia
• Hypochloraemia

Treatment

• Medical treatment: 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.

• Surgical treatment: the surgical options for managing gastric disease are limited since the equine stomach is diffcult 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 reportedbut carries a high risk of gross peritoneal contamination. Other approaches for gastric impaction are described elsewhere. For gastric rupture, surgical success has been reported for repairing partial thickness tears and also in one case of a full thickness rupture.

Prognosis

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.