Gastric Dilatation and Volvulus

Description

Gastric Dilatation and Volvulus (GDV) is an acute, life-threatening emergency condition affecting large and giant breed dogs. 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.

Risk factors

Studies have shown that dogs with a reduced thoracic width to depth ratio are at a 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.

History and Clinical signs

The owner will often report a history of non-productive vomiting (retching) an an acute onset of abdominal distension. There may be a history of rapid consumption of food followed shortly by exercise.

On physical examination , the dog may be collapsed or reluctant to stand. Abdominal distension and tympany are often

• Non-productive retching
• Weakness
• Collapse
• Salivation
• Abdominal tympany
• Tachycardia
• Pallor
• Hypothermia

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 without volvulus. Radiography should not be performed 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 positioned 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.

(GDV x-ray from WikiCommons[[1]]) The contrast of the abdomen may be lost indicating peritonitis or haemoabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

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

The most important first line treatments are fluid therapy and gastric decompression.

Fluid therapy

Should be individualised to the patient due to the varying nature of the acid-base disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

Gastric decompression

Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include butorphanol, fentanyl or oxymorphone and diazepam.

Other treatment

• For shock: Prednisolone sodium succinate or dexamethasone sodium phosphate.
• For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. cephalosporin and a fluoroquinolone) 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 necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

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

From pathology section

• Is a consequence of gastric dilation.
  • Gastric dilation occurs in dogs, cats, horses, rabbits and primates.
  • Cause unclear but may be associated with overeating.
  • Gastric dilation is most studied in dog, since it can lead to displacement of the stomach within the abdomen.

Clinical

• Mainly affects large, deep-chested dogs - Great Dane, St. Bernard's and occasionally German Shepherd dogs.
  • A similar condition also occurs in the pig.
• Animal collapses suddenly and must be operated on rapidly.

Pathogenesis

• Usually occurs around 30 minutes after a meal, or following aerophagia.
  • Stomach is distended (gastric dilation).
  • Animal excercises, and the stomach twists 180 degrees clockwise on its mesentery.
• Torsion impairs the blood supply- the arterial supply is maintained BUT venous drainage is blocked.
  • Stomach wall becomes severely congested and infarction of gastric mucosa may occur.
• Stomach blows up with gas and fluid.
  • Block venous return to heart.
  • Compresses diaphragm and interferes with respiration.

• The actual cause of the problem and the reason for accumulation of gas is unclear.
  • It is better to feed big dogs small amounts more frequently.

Pathology

Gross

• Following the pathogenesis above the stomach contents appear dark red/black and bloody, and the organ may rupture.
• The spleen is also affected by venous occlusion.
  • Becomes very congested and moves from left to right side of abdomen.

Histological

• Venous obstruction gives rise to congestion, oedema and necrosis of gastric mucosa.

Also known as:

GDV