Gastric Dilation and Rupture - Horse

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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, 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 (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[6]). Furthermore, nasogastric intubation does not preclude the possibility of gastric rupture.[3]

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

The identification of copious amounts of gastric reflux in the absence of small intestinal distension on rectal examination and the absence of endotoxaemia, increase the possibility of primary gastric dilation.Should the signs of pain abate following decompression, and other clinical parameters return to normal, then a retrospective diagnosis of primary gastric dilation may be made. Frequently, the situation is more complex and gastric dilation is secondary to some other gastrointestinal disorder.Persistent abdominal pain, repeated retrieval of gastric reflux, intestinal distension on rectal examination and clinical signs of endotoxaemia are all indications that exploratory laparotomy is necessary to determine whether there is 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. Primary gastric dilation does not cause any significant change in peritoneal fluid parameters until rupture occurs. 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[2]:

  • Haemoconcentration
  • Hypokalaemia
  • Hypochloraemia

Treatment

Surgical repair has been reported for partial thickness tears[7] and one case of a full thickness repair[8]

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. ↑ 2.0 2.1 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: 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.
  7. ↑ 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.
  8. ↑ 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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