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 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.

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(Proudman)
• Tachypnoea
• Tachycardia
• Sweating
• Muscle fasciculations
• Blue or purple mucous membranes (Proudman)

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.(Proudman)

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 retrospectvie 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.(Proudman)

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.

Failure to detect excessive gastric contents by stomach tube aspiration does not entirely preclude their presence. Repeated attempts at obtaining reflux with frequent repositioning of the stomach tube are necessary. For reasons unknown, there are occasions when even the most diligent attempts at gastric decompression are unsuccessful in spite of large volumes of fluid being present. It should also be emphasised that gastric impaction with solid food material is probably too firm to be siphoned by stomach tube.

Septic peritonitis as a result of gastric rupture is reflected in a foetid, turbid peritoneal fluid sample containing particulate matter, a white cell count often in excess of 40 x 10% and a protein content of >30g/l. The diagnosis of gastric rupture may be supported by characteristic findings on rectal examination, namely: a gritty feeling on the serosal surfaces of intestine due to adherent food material, and the impression of 'space' in the abdomen due to gas in the peritoneal cavity.(Proudman)

Laboratory findings:

• Haemoconcentration
• Hypokalaemia
• Hypochloraemia

Treatment

Prokinetic agents Impaired gastric motility has been treated with several drugs, especially in the context of treatment for postoperative ileus. Metoclopramide (0.10-0.25 mg/kg bwt 3-4 times daily) has been used, but the frequent occurrence of neurological side effects limits its utility. Cisapride, a 5-HT4 agonist, has received some attention. It has been given per 0s and i.v. but commercially only an oral formulation is available. A suggested dose is 0.1 mg/kg bwt q. 8 h (Gerring et a/. 1991). However, its therapeutic benefits have been found to be equivocal. Bethanecol. a muscarinic agonist, has also been used to promote gastric emptying (0.00250.03 mg/kg bwt sub cut. q. 4 h then 0.3-0.75 mg/kg bwt per 0s 3-4 times daily), but it produces doserelated gastrointestinal side effects including colic, diarrhoea and salivation (Murray 1990). These prokinetic agents should be used only when anatomical obstructions have been ruled out. Nonsteroidal anti-inflammatory drugs appear to be beneficial in equine post operative ileus, possiblyby inhibiting the release of prostaglandin synthesis induced by endotoxin. Both flunixin meglumine and phenylbutazone have been used and there is some evidence to suggest that phenylbutazone may be more efficacious (King and Gerring 1989). Supportive therapy Because of the uncertain benefits of drug treatment for equine gastric diseases, considerable care must taken with non-specific supportive measures. In particular, in cases of delayed gastric emptying, gastric decompression must be maintained either by an indwelling nasogastric tube, with the attendant risks of prolonged intubation, or by repeated intubation. Hydration should be effectively maintained by parenteral fluid therapy.(Proudman)

Surgical The stomach of the adult horse, by virtue of its anatomical location in the cranial abdomen, partially enclosed by C. J. Proudman and S. J. Baker 183 diaphragm and thoracic body wall, is difficult to access surgically. Extension of a midline laparotomy incision cranially improves access marginally but also increases the probability of post operative wound problems. With such difficult access and without the possibility of mobilising the stomach to bring it closer to the incision surgical options for treating gastric disease are very limited. Gastrotomy and evacuation of impacted food material has been reported (Clayton-Jones et a/. 1972) but is extremely difficult to achieve without causing gross peritoneal contamination. Softening of gastric impactions can be successfully achieved during surgery by instillation of fluid into the stomach by stomach tube, or by transmural injection from the peritoneal side; and by manual mixing of the fluid and impacted food material by the surgeon massaging the stomach wall. The latter technique is often used because of the difficulty of passing a nasogastric tube in the anaesthetised horse in dorsal recumbency.(Proudman)

Surgical repair has been reported for partial thickness tears and one case of a full thickness repair

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.