Gastric Dilatation and Volvulus

Description

Gastric Dilatation and Volvulus (GDV) is an acute, life-threatening emergency affecting large and giant breed dogs. The condition is characterized by accumulation of gas in the stomach and malpositioning of the stomach with obstruction of eructation and pyloric outflow. Commonly affected breeds include German Shepherds, Great Danes, Irish Wolfhounds, St Bernards and Doberman Pinschers. GDV has also been reported to occur in cats, primates and rarely small breed dogs such as Dachshunds and Miniature Poodles.

Pathogenesis

An obstruction to gastric emptying due to fluid or gas leads to gastric distention and a rapid increase in intra-gastric pressure. As the stomach dilates, the pylorus shifts in a clockwise direction through an angle of between 180 and 360^o from its normal position to a dorsal, cranial and leftward location. The most immediate effect is impairment of the gastric blood supply, leading to severe congestion of the gastric wall and infarction and ulceration of the gastric mucosa. Venous return to heart is reduced due to mechanical compression of the caudal vena cava by the distended stomach, leading to decreased cardiac output and hypovolaemic shock. Gastric distension also causes a mechanical impediment to movement of the diaphragm resulting in reduced tidal volume, hypoxia and hypercapnia.

In addition to the above systemic effects, diplacement of the stomach may lead to avulsion of the gastric branches of the splenic artery. Significant haemorrhage may occur as a result and this may lead to the development of ischaemia-induced gastric necrosis.

Risk factors

Studies have shown that dogs with a reduced thoracic width to depth ratio are at an in increased risk of developing GDV. Other risk factors include obesity, stress, exercise following feeding and feeding of a dry food diet. Female dogs are also more likely to develop GDV than males. Dogs with an aggressive temperament are also more prone to developing GDV.

History and Clinical signs

The clinical signs of GDV are usually acute in onset and may follow a periood of exercise and/or feeding of a large meal. Affected dogs typically display non-productive vomiting and abdominal distension. On physical examination, the dog may be collapsed or reluctant to stand. Signs of cardiovascular shock may be present including tachycardia, pale mucous membranes, prolonged capillary refill time and poor peripheral pulses. Abdominal tympany is often displayed and the animal may be painful.

Diagnosis

Diagnosis is usually based on the patient's history of unproductive vomiting and abdominal distension and signalment (i.e. a large breed dog). Abdominal radiography may be beneficial in confirming a diagnosis of GDV and distinguishing between GDV and gastric dilatation. Radiography should not be carried out until gastric decompression has been performed and intravenous fluids have been started. A radiograph performed in right lateral recumbency shows a dorsally and cranially positioned pylorus to the left of the midline. The stomach will appear compartmentalised with a soft tissue strip separating the two compartments. The oesophagus may appear dilated with air or fluid. Evidence of air in the abdomen indicates that perforation has occurred and requires an exploratory surgical procedure. Loss of contrast in the abdomen may indicate peritonitis or haemoabdomen.

Haematology

• Increased haematocrit
• DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)

Biochemistry

Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

Treatment

Initial treatment should be aimed at managing the dog's hypovolaemic shock. Large bore (16 or 18 gauge) catheters should be placed into the cephalic or jugular veins and a proportion of the shock dose of Compound Sodium Lactate (90ml/kg/h) should be administered intravenously based on the severity of the dog's clinical signs. Hypertonic saline or colloid fluids may be indicated in very large dogs or those who have not responded to a bolus dose of crystalloid fluids. Following a period of aggressive fluid therapy, gastric decompression should be performed. A lubricated large-bore stomach tube is premeasured (from nostril to last rib)and marked. It is then introduced into the oesophagus and should not be advanced beyond the marked point. It is important to mimimise stress when this procedure is carried out. Sedation is not usually required but suitable drugs for this include Butorphanol, Fentanyl or Diazepam. It the animal is resistant to orogastric intubation or becomes stressed, trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. This may allow susequent completion of orogastric intubation for further decompression.

Analgesia in the form of a pure opioid should be provided (e.g.)

Other treatment may include broad spectrum antibiotics e.g. Cephalosporin and a Fluoroquinolone. Thses should also be given at surgical induction through to the postoperative period. For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting acid-base, electrolyte and haemostatic disturbances. The treatment is lidocaine by bolus or continuous rate infusion or procainamide if they persist.

• For analgesia: Pure opioid of morphine, methadone or fentanyl.
• General: Oxygen supplementation if possible

Anaesthesia

Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included fentanyl and diazepam bolus or titrated propofol. Maintenance can be achieved with the use of isoflurane and sevoflurane in oxygen however nitrous oxide should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, central venous pressure, PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial blood pressure.

Surgery

Surgical aims include:

• Gastric decompression and repositioning
• Assessing the organ viability
• Removing necrotic tissue
• Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

Post-operative complications

These are wide and varied and include:

• Hypoperfusion
• Hypotension
• Cardiac arrythmias
• Aspiration pneumonia
• Abnormal gastric motility
• Gastric necrosis
• DIC
• Systemic Inflammatory Response Syndrome (SIRS)

Prognosis

Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necrosis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis.

References

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition) BSAVA

King, L. and Hammond, R. (1999) BSAVA Manual of Canine and Feline Emergency and Critical Care BSAVA

Tivers, M. and Brockman, D. (2009) [dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation] 31(2):66 In Practice

Tivers, M. and Brockman, D. (2009) [dilation–volvulus syndromein dogs 2. Surgical and postoperative management] 31(3):114 In Practice

Also known as:

GDV