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[7]
  • Tachypnoea
  • Tachycardia
  • Sweating
  • Muscle fasciculations
  • Blue or purple mucous membranes[7]

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.[7]

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.[7] 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.[7]

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.[7] 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.[7]

Gastric rupture results in septic peritonitis which will be reflected in the nature of fluid collected by abdominocentesis[7]:

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

Findings on rectal examination may include[7]:

  • 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[2] may include:

  • Haemoconcentration
  • Hypokalaemia
  • Hypochloraemia

Treatment

  • Medical treatment: if anatomical obstructions have been ruled out, prokinetic agents may prove useful to restore gastric motility, especially in the presence of post-operative ileus. Metoclopramide (0.10-0.25 mg/kg TID or QID) has neurological side effects. Cisapride is currently unavailable. Bethanecol (at 0.0025 to 0.03mg/kg SC every 4 hours then 0.3-0.75 mg/kg PO TID or QID) has been used to promote gastric emptying but it produces dose-related gastrointestinal side effects including colic, diarrhoea and salivation.[8] 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, possibly by 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). 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 treatment: The stomach of the adult horse, by virtue of its anatomical location in the cranial abdomen, partially enclosed by 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[9] and one case of a full thickness repair[10]

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. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 Proudman, C.J, Baker, S.J (1994) Satellite Article: Gastric disease in the adult horse: a clinical perspective. Equine Vet Educ, 6(4):178-184.
  8. ↑ Murray, M.J (1990) Gastric ulceration. In: Smith, B.P, Large Animal Internal Medicine, CV Mosby Publishing Company, USA, pp 648-652. In:
  9. ↑ 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.
  10. ↑ 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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