Gastric Dilatation and Volvulus

Signalment

• Large deep chested breeds including:

• 

  Akitas

• 

  Bloodhounds

• 

  Collies

• 

  Great Danes

• 

  Irish Setters

• 

  Wolfhounds

• 

  Newfoundlands

• 

  Rottweilers

• 

  Saint Bernards

• 

  Standard Poodles

• 

  Weirmaraners

Description

Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis with both conditions leading to compression of the caudal vena cava. GDV can lead to hypovolaemic shock, splenic torsion, gastric wall ischaemia, abdominal viscera congestion, endotoxic shock and disseminated intravascular coagulation (DIC). Risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

Diagnosis

History and Clinical signs

• Abdominal distension
• Non-productive retching
• Weakness
• Collapse
• Salivation
• Abdominal tympany
• Tachycardia
• Pallor
• Hypothermia
• Cardiac arrythmias (present in 40% of patients) (ventricular premature beats, ventricular tachycardia)

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.

Diagnostic imaging

Best performed after fluid therapy and gastric decompression. It allows distinction between GD and GDV:

• Gastric dilatation: gas distension, on right lateral shows air in the fundus.
• Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.

A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or haemabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

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 catheters should be placed into cephalic or jugular 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 stomach tube or by trocharizing the most tympanic area around the stomach with a 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include butorphanol 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)
• For cardiac arrythmias: indicated if weakness, sycope, 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.

Surgery

Surgery is aimed to reposition the stomach and spleen whilst preventing recurrence by performing a gastropexy. If gastric necrosis is present then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

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%)