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options; euthanasia and conservative management. Conservative management is not an appealing option. If decompression successfully repositions the stomach, gastric necrosis and perforation, and repeat GDV can occur within the next 24 hours, causing the patient to suffer. For those dogs that survive the initial GDV, most studies support that repeat GDV will occur in nearly all dogs within a year and, most, sooner.(5, 6)
Food engorgement
Food engorgement, or food bloat, can present with similar history and clinical signs to that of GDV.(2) On physical examination, there may be tachycardia, a distended painful abdomen that can be tympanic and hypersalivation. It is prudent to approach these patients in a similar fashion to a GDV case. Opioid analgesia should be given promptly and if the tachycardia
does not resolve in response to analgesia, then a
small crystalloid fluid bolus should be given. Gastric distension due to food engorgement can be marked on radiographs, however, if there is no gaseous distension and the stomach is correctly positioned, then there
is no indication for surgery. Some clinicians induce emesis, which can be productive and reduce stomach size, however this may also increase abdominal pain due to stomach cramping and places the dog at risk of aspiration.
Fluid therapy, analgesia and time are usually all that is required. It is important to monitor electrolyte and acid- base status, as food engorgement can cause a mild free water deficit (hypernatraemia), and metabolic alkalosis due to third spacing of gastric fluid into the food mass. Close monitoring for any development of signs of GDV also is important. Most dogs improve after 12 hours of hospitalisation, with a decrease in abdominal distension, and can go home with instructions for rest and small meals. Mild diarrhoea or soft stool in the 3 days after engorgement is common.
Fluid distension
Acute fluid distension of the stomach is usually either due to gastric stasis or pyloric outflow obstruction. The degree of gastric distension does not usually cause obvious abdominal distension. Gastric stasis is usually associated with moderate fluid distension whereas pyloric outflow obstruction usually only causes distension if there is a component of decreased gastric motility. Gastric stasis is common in critically ill patients, especially in those suffering from Systemic Inflammatory Response Syndrome or recovering from abdominal surgery. Regional peritonitis, for example, due to pancreatitis,
is also a common cause. Gastric stasis should be suspected in any critically ill patients that continue to vomit or regurgitate despite antiemetic and prokinetic drugs. Abdominal ultrasonography is useful to confirm suspicions, whereby a large fluid filled hypomotile
stomach can be identified.
Fluid distension of the stomach can contribute to dehydration and electrolyte abnormalities via loss through vomiting or regurgitation. The nature of this loss will depend on whether there is duodenal reflux into
the stomach and administration of antacid therapy. If there is no pyloric outflow obstruction, often the vomitus has a neutral to mildly acidic pH, as it is a mixture of stomach and duodenal fluid. If there is either a functional or mechanical pyloric outflow obstruction, or gastric hypersecretory disorder, then the majority of the loss will be hydrochloric acid, promoting a metabolic alkalosis
in the patient. Potassium will also be lost in vomiting
and regurgitation. As the effects on acid-base and electrolytes varies with the type of loss, it is important to monitor these parameters.
Gastric distension secondary to gastric stasis can be uncomfortable for the patient, and promote vomiting
or regurgitation. If there is no response to prokinetic therapy, such as metoclopramide or erythromycin, it may be useful to place an NGT and remove the majority of fluid from the stomach. This helps to relieve some of
the discomfort and often helps to control the vomiting or regurgitation. It also allows for gastric pH monitoring in order to assess efficacy of any antacids administered and allows the administration of enteral nutrition. Small- volume microenteral nutrition stimulates gastric motility, can improve lower esophageal sphincter tone and supplies essential amino acids to the gut, helping it to repair.
Acute fluid distension may also be due to ingestion
of large volumes of water, such as in near-drowning cases. This usually causes vomiting and reduction in stomach size prior to presentation. However, if a patient presents with gastric distension due to water ingestion and requires a general anesthetic, it would be best to decompress the stomach via OGI soon after induction, while keeping the patient in sternal recumbency. This may avoid regurgitation and aspiration while providing mechanical ventilation.
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