Gastric dilation and torsion

By | November 12, 2015

This condition preferentially affects the large deep-chested breeds of dog such as Bassett Hounds, German Shepherd dogs, St. Bernard, Irish Setters, Great Danes and Dobermans but Dachshunds may also be affected. There may be a predilection for young male dogs, but torsion has been observed in dogs from 2 to 10 years of age.

The cause is not known but predisposing factors include; breed, use of dry cereal-based diets, overeating or drinking, stress, exercise and aerophagia (Table Predisposing causes for gastric torsion). Cereal-based diets fed as one large meal per day result in larger and heavier stomachs than those found in dogs fed tinned meat and biscuit. This predisposes the dog to gastric dilation and torsion (). It is also possible that disordered gastric motility may be involved. Torsions most often occur to the left or clockwise effectively sealing off the oesophagus and pylorus (). In our experience the mortality rate can exceed 68%.

Table Predisposing causes for gastric torsion

Breed
Diet
Overeating
Stress, excitement
Gastric stasis
Aerophagia
Motility disorder
Lax gastric ligaments

Normally the pylorus is held in position on the right of the abdomen by the hepatoduodenal ligament, bile duct and lesser omentum. It can be forced to the left but returns to its original position when released. In dogs predisposed to dilation/torsion this does not occur, because there is a greater mobility of the stomach. A study of dogs with gastric dilation has shown that the stomach position may vary from the normally accepted position to that observed in gastric torsion. In some cases the stomach had rotated about 180 degrees, and returned to its normal position again. Instability of the stomach may be very important in the pathogenesis of torsion (). Therefore to create torsion there must be a gastric dilation present and increased gastric mobility. If the latter is absent then dilation is more likely to occur without torsion. Displacement of the stomach can occur if there is gastric retention and delayed gastric emptying. Traction on the ligament attachments of the stomach in deep-chested dogs causes the stomach to become pendulous and so predisposed to torsion.

Aerophagia may also occur in the dog and again may lead to gastric dilation and predisposition to torsion. Gas analysis has been carried out in clinical cases and revealed the presence of a gas mixture similar to air with no evidence of methane thus ruling out possibilities of fermentation ().

Pathophysiology. When the stomach becomes dilated gastric ischaemia and circulatory shock, occur. Distention of the stomach causes pressure occlusion of the vena cava and portal vein. Gastric ischaemia occurs when distention of the stomach wall is great enough to occlude the intramural artcrioles. Necrosis and sloughing of the mucosa occur as a result of such ischaemia exacerbated by the action of gastric acid. If torsion has been present for some time then the muscle layer becomes necrotic and perforation is likely leading to peritonitis. Shock is frequendy the cause of death, so this condition requires urgent treatment in order to save life (Table Pathophysiology of gastric torsion).

Table Pathophysiology of gastric torsion

Dilation of the stomach Compresses blood vessels
Compresses vena cava/portal vein
Ischaemia of tissues
Displaced stomach Occludes arterial supply to organ
Prolonged ischaemia Necrosis of tissue (= perforation)
Renin Angiotensin activation and vasoconstriction
Capillary damage Vascular sludging
Reversible shock Rapidly develops into irreversible shock

Baroreccptors respond to shock and hypotension by increasing sympathetic drive leading to tachycardia, vasoconstriction and splenic contraction. Right atrial receptors detect poor filling and respond by increasing amidiuretic hormone (ADH) output, a potent vasoconstrictor. Renin from underperfused kidneys stimulates angiotensin which again leads to vasoconstriction. As shock continues multiple organ failure together with disseminated intravascular coagulation occurs, leading to death.

Clinical diagnosis

The history and symptoms are usually classical and cannot be readily confused with other conditions. There is a sudden dramatic abdominal enlargement with tympany. Initially there may be attempts at vomiting with salivation and marked restlessness. However the dog will rapidly become shocked and collapse. Occasionally there is no such history but a sudden tympany and collapse.

Diagnosis is based on the history and the presenting signs which are pathognomonic of this condition. It is however necessary to determine if dilation or torsion is present. Further diagnostic information can be obtained from radiography of the abdomen. However the dog is often critically ill and such procedures should be reduced to the minimum necessary in order to obtain a diagnosis. To this end the right lateral recumbent view will reveal a gas-filled pylorus dorsal to a gas-filled fundus in gastric torsion but not in gastric dilation (). Evidence of haemorrhage in the gastric lavage may indicate gastric wall necrosis and risk of imminent rupture.

Treatment

It is essential that treatment is carried out promptly as these cases constitute true veterinary emergencies. There are three steps in the treatment which are carried out in the following chronological order; decompression, treatment of shock and finally surgery.

Decompression. This is the first and most important part of therapy as it improves the circulation and reduces shock and ischaemia. Passage of a stomach tube is the easiest method of decompression and can usually be carried out without sedation. If a small enough stomach tube is used, even when torsion is present, it should pass into the stomach. If the tube will not enter the stomach then gastrocentesis is an essential alternative. Prepare a site behind the costal arch and insert a large bore needle through the abdominal wall and into the stomach. Having partially decompressed the stomach, a stomach tube should be passed to allow air and fluid to be removed. Solids should be removed using a warm water lavage. If after gastrocentesis a stomach tube cannot be passed then exploratory laparotomy must be carried out immediately.

Shock. Intravenous lactated ringer solution should be administered immediately at 90ml/kg/30min, then the rate adjusted according to the animal’s requirements (). If the PCV falls to less than 20% whole blood may be needed. Prednisolone at 10mg/kg or dexamethasone at 4mg/kg should be administered in conjunction with broad spectrum antibiotics such as ampicillin and gentamycin, trimethoprin and sulphonamides, or intravenous penicillins. Intravenous bicarbonate will be needed but the requirement is difficult to assess unless blood gas analysis is available.

Surgery. Surgery should be performed as soon as possible after decompression. Barbiturates should not be used for induction; gaseous anaesthesia should be induced using a face mask. The stomach and spleen should be repositioned by standing on the right and pulling up the pylorus and moving it over to the right while pushing the fundus down and to the left. Resection may be required if tissue is not viable. The best site to evaluate the condition of the stomach is the greater-curvature. Once the spleen is repositioned it should contract down, a splenectomy should only be performed if blood vessels are damaged.

If the tissues are viable then the stomach should be stabilized. Gastropexy is carried out by exposing the serosa and muscle layer at the antrum and suturing this at the twelfth rib on the right costal arch ().

 

Selections from the book: “Digestive Disease in the Dog and Cat” (1991)