Acute gastric distension is a common cause of abdominal pain in emergency medicine, though it can sometimes be difficult to appreciate on physical examination. Findings on abdominal radiographs may also, at times, be ambiguous. This talk will cover the approach to common causes of acute gastric distension, including gaseous gastric dilation (GD), gastric dilation and volvulus (GDV), food engorgement and fluid distension.

Gaseous Distension

Gas dilation of the stomach typically falls into two different categories: gaseous dilation related to the syndrome of GDV and gas distension secondary to aerophagia. Aerophagia, secondary to respiratory distress, usually only causes mild distension. However, sometimes the gaseous distension can impede caudal displacement of the diaphragm and reduce tidal volume, contributing to respiratory distress. In these patients, decompressing the stomach may relieve some of the respiratory distress. Often these patients have such severe respiratory distress that sedation and intubation are imminent. If the patient is already anaesthetized, then it is prudent to decompress the stomach via orogastric intubation (OGI) if distension is evident. If the patient is conscious, then careful nasogastric intubation (NGI) can be attempted; however, the procedure must be aborted if it starts to compromise the patient. Gastric trocarisation is not usually indicated in these patients as the distension is not typically severe or compromising perfusion, and it carries the risk of trauma to abdominal organs.

Gaseous gastric dilation, or dilatation, in a large-breed, deep-chested dog is a problem that is inevitably situated on the continuum to GDV. Typical history is similar to GDV and includes acute retching, hypersalivation, a distended abdomen and agitation. These signs often occur in the early morning or evening, related to meal times. Physical examination findings are often similar to those of a GDV in the early stages, which are predominantly tachycardia, abdominal pain and tympanic abdominal distension. Some dogs do not have obvious tympanic abdominal distension due to their stomach being mostly under the rib cage. Any signs of vasoconstrictive shock (pale mucous membranes, decreased pulse amplitude, delayed capillary refill time, cool extremities) usually indicate that volvulus is present, but can still occur with severe gaseous dilation. Some dogs with early GD or GDV can present with signs of vasodilation (injected or red mucous membranes, fast capillary refill time). Regardless, any compromise to perfusion prompts swift intervention.

The four essential steps for a dog with GD or GDV are opioid analgesia, blood volume expansion, abdominal radiographs and gastric decompression. Pre-treatment electrolyte and blood gas analysis are also useful. Acid-base abnormalities usually parallel a lactic acidosis; however, some dogs display high lactate with a standardised base excess that does not reflect the degree of lactic acidosis.^1,2 This may be due to pyloric outflow obstruction soon before the GDV occurred, causing preceding metabolic alkalosis, and some dogs are known to have either overeating or a gastric foreign body as a feature of their GDV presentation.

Electrocardiographic monitoring is advised if a pulse irregularity is detected; presurgical ventricular arrhythmias have been associated with a higher incidence of gastric necrosis and a higher mortality rate.^3,4 However, these arrhythmias usually involve isolated ventricular premature complexes and usually do not require treatment. An intravenous catheter should be placed promptly and any signs of shock treated with fluid therapy. Gastric dilation, with or without volvulus, causes obstructive shock by compressing the major veins in the cranial abdomen, and reducing venous return to the heart. Expanding blood volume increases perfusion pressure, and therefore venous return. This helps to address hypoperfusion quickly while giving more time to address the cause of obstruction. Crystalloid fluid therapy, such as lactated Ringer’s solution, is often the most appropriate choice as these dogs can have some degree of dehydration. The use of synthetic colloid fluids in the presurgical patient or a patient at risk of systemic inflammatory response syndrome, without a strong indication, is controversial due to possible adverse effects and should not be routinely administered.

Blood volume expansion and radiography can sometimes be done concurrently if the treatment area is alongside diagnostic imaging facilities. It is ideal to perform radiographs before decompression in order to make the diagnosis clear. However, if the dog is in moderate-to-severe shock, decompression should be performed before taking radiographs. Decompression may result in resolution of the volvulus,^5,6 or make it more difficult to appreciate volvulus on radiographs, but should confirm that it was indeed gaseous gastric dilation causing the problem, even if somewhat deflated. Some would debate that if there were no evidence of volvulus on radiographs, then emergency surgery is not indicated. However, if a dog presents with signs of shock on physical examination, then chances are that there was some degree of volvulus present. Delaying surgery puts the dog at risk of complications from gastric necrosis or gastric rupture, ongoing hemorrhage from any ruptured blood vessels or repeat volvulus soon thereafter.^5,7

One of the more difficult decisions is surgical planning for large-breed dogs that have simple gastric gaseous dilation on radiographs and no evidence of shock. It is still advisable to perform a gastropexy in this patient to prevent future GDV; however, it may not be urgently required. Sometimes these dogs can wait until the next day to either have a laparotomy or laparoscopy performed. The decision to delay surgery needs to be weighed up carefully in terms of how closely the dog can be monitored until the procedure is performed and whether or not the dog shows any signs of repeat gastric dilation, after the initial decompression, or abdominal pain.

There are two main methods for stomach decompression for gas: gastric trocarisation and orogastric intubation. There are positives and negatives to each procedure and no one method has been shown to be superior over the other.⁸ Orogastric intubation (OGI) should be attempted first as it is less traumatic to the stomach. However, if it is difficult to decompress the stomach by OGI or the patient requires general anaesthesia to perform OGI due to non-compliance or the distension is severe accompanied by severe shock, then trocarisation is preferred. Sometimes all it takes is a little decompression via trocarisation to facilitate moving the OGI tube through the fundus. Trocarisation is a procedure that should be done carefully, with appreciation for the location of the spleen and being sure not to leave the stylette in place while the gas is being evacuated. Laceration of the spleen or liver is possible with this procedure.

As emergency laparotomy is usually a large expense, and these dogs typically require a high level of care postoperatively, many owners wish to know the presurgical risk of their dog dying before committing to the investment. Researchers have attempted to aid this process by assessing the ability of many presurgical factors to predict outcome. Clinical signs for >5–6 hours, hypothermia at admission and the presence of gastric necrosis combined with the need for splenectomy have been associated with an increased mortality. Presurgical factors that have shown some association with gastric necrosis or a higher rate of complications include high lactate on admission,^1,9 high lactate post-fluids,¹⁰ and ventricular arrhythmias^3,4. However, care must be taken in applying results of these studies to individual dogs; the published mortality rates are often from small studies and some are older studies not reflecting today’s standard of care. Also, each individual is unique for its own risk, which can’t be well predicted. Overall, for dogs that are taken to surgery, the discharge rate is usually above 90% if appropriate supportive postoperative care is given.

If owners decline surgery, then there are only two 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 those 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 vary 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 relieve some of the discomfort and often helps 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.

References

1.  Santoro Beer KS, Syring RS, Drobatz KJ. Evaluation of plasma lactate concentration and base excess at the time of hospital admission as predictors of gastric necrosis and outcome and correlation between those variables in dogs with gastric dilatation-volvulus: 78 cases (2004–2009). Journal of the American Veterinary Medical Association. 2013;242(1):54–8.

2.  Smart L, Reese S, Hosgood G. Food engorgement in 35 dogs (2009–2013) compared with 36 dogs with gastric dilation and volvulus. The Veterinary Record. 2017;181(21):563.

3.  Brourman JD, Schertel ER, Allen DA, Birchard SJ, DeHoff WD. Factors associated with perioperative mortality in dogs with surgically managed gastric dilatation-volvulus: 137 cases (1988–1993). Journal of the American Veterinary Medical Association. 1996;208(11):1855–8.

4.  MacKenzie G, Barnhart M, Kennedy S, DeHoff W, Schertel E. A retrospective study of factors influencing survival following surgery for gastric dilatation-volvulus syndrome in 306 dogs. Journal of the American Animal Hospital Association. 2010;46(2):97–102.

5.  Meyer-Lindenberg A, Harder A, Fehr M, Luerssen D, Brunnberg L. Treatment of gastric dilatation-volvulus and a rapid method for prevention of relapse in dogs: 134 cases (1988–1991). Journal of the American Veterinary Medical Association. 1993;203(9):1303–7.

6.  Eggertsdóttir AV, Moe L. A retrospective study of conservative treatment of gastric dilatation-volvulus in the dog. Acta Veterinaria Scandinavica. 1995;36(2):175–84.

7.  Funkquist B. Gastric torsion in the dog: non-surgical reposition. Journal of Small Animal Practice. 1969;10:507–11.

8.  Goodrich ZP, Powell LL, Hulting, KJ. Assessment of two methods of gastric decompression for the initial management of gastric dilatation-volvulus. Journal of Small Animal Practice. 2013;54:75–9.

9.  de Papp ED, Drobatz KJ, Hughes D. Plasma lactate concentration as a predictor of gastric necrosis and survival among dogs with gastric dilatation-volvulus: 102 cases (1995–1998). Journal of the American Veterinary Medical Association. 1999;215(1):49–52.

10.  Zachar LB, Berg J, Shaw S, Kudej RK. Association between outcome and changes in plasma lactate concentration during pre-surgical treatment in dogs with gastric dilatation-volvulus: 64 cases (2002–2008). Journal of the American Veterinary Medical Association. 2010;236(8):892–7.