GDV is an acute life-threatening condition characterized by malposition of the stomach,
rapid accumulation of air in the stomach, increased intragastric pressure, and shock. Although some progress has been made in determining risk factors, understanding the pathophysiology, and in developing new treatments, the cause is still speculative.2 Overall mortality rate for GDV is 33%.3 Early diagnosis and treatment have improved survival rate significantly, although mortality remains high at 15% even with current treatments.4-6 Risk factors for GDV include purebred status, large- or giantbreed conformation (especially breeds with a deep and narrow thorax such as the Great Dane, Weimaraner, St. Bernard, Gordon Setter, and Irish Setter), middle to older age (mean age approximately 7 years), and a first-degree relative that had GDV (see Chapter 62).3,7-9 Controlled epidemiologic studies show that eating fewer meals per day and a rapid rate of eating increased susceptibility to GDV; dogs characterized by their owners as happy or easygoing were at lower risk than nervous or fearful dogs.7,10 Dogs fed a larger volume of food per meal were at significantly increased risk of GDV, regardless of the number of meals fed daily.11 The risk of GDV was highest for dogs fed a larger volume of food once daily.11 Rapid eating and a raised feeding bowl were also associated with an increased risk of GDV.12 The only breed-specific characteristic significantly associated with a decreased incidence of GDV was an owner-perceived personality trait of happiness.13 Despite popular opinion, epidemiologic studies have not supported a causal relationship between feeding soy-based or cereal-based dry dog food and GDV.14 There is no clinical evidence that fermentation is the cause of gastric gas production. In fact, dry foods containing fats or oils among the first four label ingredients predispose high-risk dogs to GDV, but soy- and cereal-based ingredients do not.14 Scientific studies do not overwhelmingly support the role of previously proposed causes, including hypergastrinemia, exercise after ingestion of large meals of highly processed foods or water, and inflammatory bowel disease.2,3,7,15-18 A seasonal increase in GDV incidence was noted in one population of military working dogs.19 It is well known by veterinarians that dogs can experience GDV when no food is in the stomach. Pathologists have performed necropsies on dogs with GDV that had only a small amount of fluid in the stomach, or had empty stomachs. Anesthesia, surgery, trauma, and parturition have all been observed to be associated with GDV.20 Certain anatomic considerations are important for the development of GDV. In healthy awake dogs, gastric distention with nitrogen consistently decreases lower esophageal sphincter pressure and is followed by eructation.21 The same is true in GDV dogs.21 The gastroesophageal sphincter pressure was not significantly increased compared with normal dogs in dogs tested more than 9 months after treatment for and recovery from GDV.16 Thus, it is unlikely that elevated gastroesophageal sphincter pressure inhibits orad movement and relief of gastric distention in GDV dogs. The gastroesophageal sphincter is physiologically unable to retain gas within the stomach unless volvulus is present. During abdominal surgery, the stomach in normal dogs can be forcibly rotated into a volvulus position, but it immediately returns to a normal position when released because the pylorus is tightly fixed to the right side of the abdomen by the hepatoduodenal and hepatogastric ligaments. The stomach of a dog that has experienced GDV, however, can easily be placed in the volvulus position and remains in an abnormal position once released. With volvulus and twisting of the gastroesophageal sphincter, swallowed air cannot be easily eructated and gastric dilation persists. Therefore, volvulus must precede dilation for gastric distention from aerophagia to occur, which is contrary to the alternative premise that dilation precedes a volvulus. It is well known that chronic gastric volvulus exists, and malpositioning of the stomach may be constant or intermittent. It is also known that adaptive relaxation allows the proximal stomach to stretch and accommodate some degree of gastric distention without an increase in intraluminal pressure (see receptive relaxation and accommodation in Chapter 1). Gastric emptying of liquids can even be normal in dogs with chronic gastric volvulus.22 Initially food, air, and saliva can enter the stomach in the presence of volvulus. At some point, however, perhaps related to the degree of rotation, volvulus prevents further air from entering or leaving the stomach. Up until that point, gas accumulation occurs. Rotation of the stomach is likely the factor that initiates aerophagia. Swallowing of air is accompanied by swallowing of saliva. A considerable amount of gas accumulates because the volvulus prevents belching of air (and vomiting of ingesta) and inhibits pyloric emptying into the duodenum. Delayed gastric emptying of solid particles fed with a meal has been documented in dogs with GDV following surgical treatment and recovery,23,24 whereas the liquid phase of gastric emptying is not similarly affected.22,25 Using radiopaque particles mixed with food, gastric emptying was assessed in healthy dogs not subjected to surgery, in healthy dogs 9 to 35 days after circumcostal gastropexy, and in dogs 1 to 54 months after surgical treatment and recovery from GDV. Circumcostal gastropexy surgery did not alter the 90% gastric emptying time for radiopaque particles in healthy dogs. However, 90% gastric emptying time was significantly increased after circumcostal gastropexy in dogs with GDV, compared with healthy dogs after the same surgical procedure and recovery period. These results suggest that dogs with GDV have delayed gastric emptying of solid particles, although it is still not clear whether delayed gastric emptying of markers in affected dogs after surgical treatment and recovery is the result or the cause of GDV. Other studies indicate that delayed gastric emptying in the GDV syndrome is associated with increased gastric slow wave propagation velocity in the fed state.26 Atypical fasting state phase III activity suggests that gastric emptying may be impaired in the fasting state as well.26 Recordings were not altered in healthy dogs after short-term experimental gastric dilation suggesting that altered electrical and contractile activities in GDV dogs are not likely to be secondary to the process of acute gastric dilation.27 These results imply that electrophysiologic abnormalities in gastric smooth muscle cells may be associated with delayed gastric emptying. Because delayed gastric emptying predisposes to chronic gastric distention, which could stretch the gastrohepatic ligament and permit increased stomach mobility, it has been hypothesized that a primary disorder of gastric motility might precede and predispose the dog to GDV.28 The length of hepatogastric ligaments in GDV-affected dogs is significantly longer than those of control dogs.28 Others have also speculated that gastric dysrhythmias may predispose to GDV.29,30 Two dogs were reported to develop GDV 2 and 17 months after splenectomy for treatment of splenic torsion. Splenic displacement and torsion may stretch the gastric ligaments, allowing increased mobility of the stomach. After splenectomy, an anatomic void may be created in the cranioventral part of the abdomen, contributing to the mobility of the stomach.31 Acute GDV has been reported rarely in cats. Two of five cats reported on in one case series and three cats in another had concomitant diaphragmatic hernia.32,33 Clinical signs and therapeutic management are similar in cats and dogs. Pathophysiology Gastric dilation refers to distention of the stomach, caused most often by swallowed air, fluid, and/or food. Gastric dilation implies an innocuous condition that can easily be corrected by passing a stomach tube to relieve the distention. GDV is different, however, from simple engorgement because of overeating (a syndrome that occurs most commonly in young animals) or gastric distention as a consequence of aerophagia. In GDV, the air-filled stomach becomes tympanic because of the large volume of air present.34 Dogs experiencing gastric dilation almost invariably have gastric volvulus.35 A fundamental abnormality associated with GDV is laxity of the hepatoduodenal and hepatogastric ligaments, leading to a high degree of mobility of the stomach within the abdomen.35 This allows the stomach to twist on its longitudinal axis at the esophageal cardia and the pylorus. In normal dogs, the pylorus is tightly fixed to the cranial right quadrant of the abdomen by the hepatoduodenal ligament, lesser omentum, and common bile duct. Even though the pylorus in normal dogs can be forced to the left and placed in a volvulus position, it immediately returns to its normal position once released. The stomach of a dog that has experienced GDV, however, can easily be placed in the volvulus position and remains in the abnormal position once released. Thus, a predisposition for gastric volvulus must be present to produce the GDV syndrome. Generally, the stomach rotates in a clockwise direction when viewed from the surgeon’s perspective (with the dog on its back and the clinician standing at the dog’s side, facing cranially). The rotation may be 90 to 360 degrees, but is usually 220 to 270 degrees.36 When the stomach twists, the pylorus and duodenum move ventrally, passing under the stomach and to the left of midline, finally coming to rest dorsally above the cardia on the dog’s left side. Because the spleen is attached to the greater curvature of the stomach via the gastrosplenic ligament, twisting of the stomach usually displaces the spleen to the right ventral side of the abdomen and causes congestion and splenomegaly. GDV results in occlusion of the cardia and obstruction of the pylorus. This prevents belching of air or vomiting of ingesta, and inhibits pyloric emptying into the duodenum. It is postulated that after volvulus develops, swallowed air can pass the twisted gastroesophageal junction but cannot escape the stomach. Analysis of gastric gas supports aerophagia as the cause of gastric distention, with dilation explained by an inability to eructate or empty air into the intestines.34 The bicarbonate in swallowed saliva reacts with hydrochloric acid in the stomach to produce carbon dioxide. This may be the reason why carbon dioxide concentrations in gastric gas of GDV dogs are higher than atmospheric carbon dioxide concentrations. Swallowed air is the only explanation for the presence of nitrogen and oxygen in relatively high concentrations in gastric gas of GDV dogs. Caywood’s study34 showed that neither hydrogen nor methane were present in sufficient quantities in the gastric gas samples from dogs with GDV to support fermentation as the source of gastric gas. Gastric dilation results in increased gastric wall tension, decreased blood flow, local ischemic injury, and gastric wall necrosis. Normal gastric secretion and transudation of fluids into the gastric lumen secondary to venous congestion contribute to fluid accumulation. The most commonly infarcted area is along the greater curvature in the area served by the short gastric vessels.37 GDV also causes splenic engorgement and compression of major abdominal vessels returning blood to the heart.38 Occlusion of the portal vein and posterior vena cava reduces venous return to the heart, which in turn dramatically decreases cardiac output and mean arterial pressure, leading to hypovolemic shock. Inadequate tissue perfusion affects multiple organs, including the heart (myocardial ischemia), kidney (acute renal failure), pancreas (myocardial depressant factor is an arrhythmia-inducing compound produced by the ischemic pancreas),39,40 liver (depressed reticuloendothelial cell function prevents removal of endotoxin),41 and small intestine (local acidosis, subepithelial hemorrhage and edema, followed by hemorrhagic enteritis). In addition, occlusion of the portal vein and caudal vena cava cause marked passive chronic congestion of the abdominal viscera. The organs suffer from ischemia as well as accumulation of endotoxin (from the GI tract), which, in turn, activates many inflammatory mediators (e.g., histamine, prostaglandins, leukotrienes, and cytokines). Endotoxemia and endothelial damage lead to coagulation cascade activation, and disseminated intravascular coagulation may result. The enlarged stomach also encroaches on the thoracic diaphragm, which decreases tidal volume of the lungs and further impairs ventilation-perfusion matching. Ultimately, shock reaches a point of irreversibility (likely caused by endotoxemia), wherein death ensues regardless of therapy.35 Clinical Examination Dogs with GDV may present with a history of an acute, progressively distending abdomen, nonproductive retching, hypersalivation, restlessness, depression, weakness, and abdominal pain.1 Physical examination usually reveals abdominal distention with tympany, although it may be difficult to detect gastric distention in heavily muscled large-breed or very obese dogs. There is also evidence of poor tissue perfusion and/or shock, such as weak peripheral pulses, tachycardia, prolonged capillary refill time, pale mucous membranes, or dyspnea. Eventually, depression and a moribund state may occur.42 Cardiac arrhythmias, such as ventricular premature beats or ventricular tachycardia, may be detected on initial examination or may develop up to 72 hours after presentation.43 Clinicopathologic findings often show an increased hematocrit, and a variety of acid–base and electrolyte abnormalities.43 Metabolic acidosis and hypokalemia are the most common finding in about 25% of dogs. Metabolic acidosis is likely the result of tissue hypoperfusion, anaerobic metabolism, and lactic acid accumulation. However, metabolic alkalosis also may occur as a result of sequestration of gastric acid and vomiting. Acid–base abnormalities predispose to cardiac arrhythmias and muscle weakness. Coagulation abnormalities are most consistent with disseminated intravascular coagulation (DIC). Diagnosis Usually GDV is diagnosed in the examination room based on signalment, history, and physical examination findings, and therapy is begun immediately. It is impossible to differentiate between gastric dilation and GDV on the basis of ability or inability to pass an orogastric tube. If unsure, radiographic evaluation may be necessary, although caution should be exercised because positioning these dogs for radiographs may further impair cardiopulmonary function. Affected animals should be decompressed and rehydrated before radiographs are taken. Right lateral and dorsoventral radiographic views are preferred.44 In a right lateral view of a dog with GDV the smaller, gas-filled pylorus lies dorsal and cranial to the larger, ventrally positioned fundus. The dorsally positioned pylorus is separated from the rest of the stomach below by a soft-tissue fold (antral wall folding back). On the dorsoventral view, the pylorus appears as a gas-filled structure to the left of midline. Free abdominal air suggests gastric rupture. Blood should be collected for a complete blood cell count, serum biochemistry profile, and blood gas analysis prior to treatment. Treatment Shock One or more large-bore intravenous catheters are placed in jugular or cephalic veins. High- volume isotonic fluids (60 to 90 mL/kg/h), low-volume hypertonic saline (7% NaCl solution in 6% dextran, 4 to 5 mL/kg over 5 to 15 minutes), hetastarch (5 to 10 mL/kg over 10 to 15 minutes), or a mixture of 7.5% saline and hetastarch (dilute 23.4% saline with 6% hetastarch until a 7.5% solution is achieved; administer at 4 mL/kg over 5 minutes) are administered.45,46 If hypertonic saline or hetastarch is given, the rate of subsequent crystalloid fluid administration must be adjusted accordingly. The animal should be monitored closely and fluid administration rate decreased if clinical improvement occurs. If clinical signs of shock persist, then fluid administration should continue at a high rate until a response is noted. The packed cell volume (PCV) and total protein should be monitored regularly during fluid therapy for shock. Whole blood or plasma should be administered if the PCV falls below 20% or total protein falls below 3.5 g/dL, respectively.35 Although controversial, corticosteroids (dexamethasone sodium phosphate, 4 mg/ kg, or prednisone sodium succinate, 20 mg/kg IV) may be administered for endotoxemia and to stabilize lysosomal membranes. Administration of systemic antibiotics is reasonable as mesenteric congestion caused by the enlarged stomach predisposes to infection and endotoxemia.42 Bactericidal antibiotics should be administered intravenously (e.g., cefazolin or ampicillin plus enrofloxacin). Flunixin meglumine is sometimes recommended (0.5 to 1.1 mg/kg IV once) to decrease prostaglandin synthesis and attenuate the effects of endotoxemia, although it may place the patient at risk for severe GI ulceration.47 Sodium bicarbonate is administered if indicated based on the blood gas analysis.48 Sequestration of hydrogen ions in the gastric lumen can offset the lactic acidosis, causing the blood pH to be normal. Therefore, bicarbonate therapy should not be routinely administered. Gastric Decompression Gastric decompression should be performed at the same time as the other components of shock therapy.49 Gastric decompression improves cardiac output and arterial blood pressure by relieving caudal vena cava and portal vein occlusion. An orogastric tube is premeasured from the point of the nose to the last rib, and a tape mark is made on the tube so that when it is passed it is not advanced too far. Placing the animal in different positions (sitting, on a tilttable, or with front legs elevated on a table) may help to advance the tube by shifting the weight of the abdominal viscera. A welllubricated tube is advanced with firm pressure and in a twisting motion. If an orogastric tube will not pass, then intragastric pressure should be reduced by gastrocentesis. Gastrocentesis is performed in an aseptically prepared area caudal to the costal arch on the right flank with several 16-gauge hypodermic needles. The region should be percussed to determine the location of the spleen. Relief of intragastric pressure by gastrocentesis will usually allow passage of an orogastric tube. Once positioned, the tube is used to remove as much gastric liquid and gas as possible. Gastric lavage using warm water may help to remove ingesta. One should note whether there is evidence of blood in the gastric contents.1 To facilitate intubation, the animal may be lightly sedated with diazepam (0.1 mg/kg IV) plus either butorphanol (0.5 mg/kg IV) or oxymorphone (0.1 mg/kg IV).43 If the stomach tube still cannot be passed after gastrocentesis, temporary decompression may be achieved by performing a temporary gastrostomy. However, this procedure carries a high risk for peritoneal contamination and must be closed before the permanent gastropexy is performed. Surgery Several studies show no association between the time from admission to a clinic to the time of surgery and outcome.4,5 The presence of gastric necrosis at surgery is, however, associated with a much higher risk of dying.4-6 If there is no blood present in the gastric contents, it may be advantageous to stabilize the patient’s condition for a few hours, or even overnight, before performing corrective surgery and gastropexy.1 If the stomach is twisted, it will continue to have impaired mucosal perfusion even with de-rotation50; therefore, surgery should only be delayed as long as is necessary to make the patient the best anesthetic risk possible. The benefits of delaying surgery are that surgery can be performed at a convenient time, the dog can be safely transported to a referral center, and a full preoperative diagnostic evaluation can be performed.49 A pharyngostomy tube may be used to maintain gastric decompression. For example, if immediate surgery is not possible and the stomach dilates rapidly again after decompression, the stomach tube can be exteriorized through a pharyngostomy approach. The disadvantages of delaying surgery include failure to detect necrosis or leakage of gastric contents, emergence of more serious cardiac arrhythmias, and continued damage to the gastric mucosa. An electrocardiogram should be monitored to detect cardiac arrhythmias. If blood is found in the gastric contents, surgery should be performed as soon as the patient is capable of withstanding anesthesia because of the danger of gastric wall devitalization and perforation because of devitalization. The stomach is repositioned and if necessary devitalized gastric wall tissue is resected, or preferably to prevent perforation and abdominal contamination, a partial gastric invagination technique may be performed.51 If there is splenic necrosis or significant splenic infarction, partial or complete splenectomy should be performed. A permanent gastropexy is performed to prevent recurrence of GDV. Many surgical procedures have been developed to permanently attach the stomach to the body wall and prevent recurrence of GDV.52,53 These include tube gastropexy,54,55 circumcostal gastropexy,56-60 muscular flap gastropexy,61 belt- loop gastropexy,62 and incisional gastropexy.63,64 Randomized controlled trials comparing different types of gastropexy have not been conducted. The choice of a particular technique often depends on individual preference. Probably the most critical factors in success rate are the surgeon’s familiarity with a technique and ability to perform it proficiently and in a timely manner.2 Failure rates are in the range of 3% to 8%. Right-sided percutaneous gastrostomy is not recommended as a means of prophylactic gastropexy despite the use of that procedure for nutritional management in other situations.65 Corrective pyloric surgery is no longer recommended.52,66 Intermittent gastric dilation may occur after gastropexy.64,67 Ischemia–Reperfusion Injury Restoration of tissue perfusion and oxygenation can initiate deleterious biochemical reactions that contribute to further tissue damage. This phenomenon is called ischemia–reperfusion injury.68,69 During ischemia, conditions develop that predispose to the production of oxygen free radicals upon reperfusion. First, adenosine triphosphate undergoes degradation resulting in accumulation of hypoxanthine. Second, intracellular calcium increases and activates calpain, a protease which converts xanthine dehydrogenase to xanthine oxidase. Xanthine oxidase catalyzes the conversion of hypoxanthine into superoxide radicals in the presence of oxygen. Superoxide radicals are converted into hydrogen peroxide by superoxide dismutase. Superoxide radicals and hydrogen peroxide react, forming hydroxyl radicals. During reperfusion an overabundance of free radicals are generated, which overwhelms the normal antioxidant defense mechanisms (superoxide dismutase, catalase, glutathione peroxidase, α-tocopherol, ascorbate, beta-carotene). The hydroxyl radical is a potent oxidizing agent, which initiates cell membrane lipid peroxidation. This results in increased cell membrane permeability, increased microvascular permeability, tissue edema, inflammatory cell influx, hemorrhage, and mucosal necrosis. Neutrophils play a major role in the pathophysiology of reperfusion injury. Neutrophil activation and degranulation leads to synthesis and release of numerous enzymes (proteases) and oxygen- free radicals. Inhibition of neutrophil adhesion or neutrophil depletion has been shown to reduce or prevent GI tract injury. Intestinal mucosal injury can be attenuated by both protease inhibitors and scavengers of oxygen free radicals. Lipid peroxidation activity in the duodenum, jejunum, colon, liver, and pancreas was significantly less during reperfusion in dogs with experimentally induced GDV treated with a lipid peroxidation inhibitor.70,71 Free radical scavengers such as deferoxamine and allopurinol may also protect abdominal organs against reperfusion injury. These results suggest that use of drugs that prevent lipid peroxidation (e.g., lazaroids such as U74389G) may be useful for reducing the mortality associated with GDV. These agents work best if given before reperfusion occurs, that is, prior to untwisting a volvulus. Cardiac Arrhythmias Arrhythmias are a common sequela of GDV and usually begin 12 to 36 hours postoperatively.72,73 Electrocardiographic monitoring should be performed in all GDV patients throughout hospitalization. Ventricular tachyarrhythmias (premature ventricular contractions, paroxysmal ventricular tachycardia, and multifocal ventricular tachycardia) are most frequently described.72-74 They are generally self-limiting and resolve after 2 to 4 days.35 The mechanisms that initiate and maintain these arrhythmias are varied and include acid– base abnormalities, electrolyte abnormalities, autonomic imbalances, myocardial depressant factors, and myocardial ischemia.72 Cardiac damage is common as evidenced by increased serum concentrations of troponin.75 They should be treated if they are severe enough to decrease cardiac output, that is, the origin is multifocal, ventricular rate exceeds 160 beats/min, pulses are weak, shock is present, or subsequent premature beats are inscribed on the wave of the previous complex (R on T phenomenon).35,36 Intravenous lidocaine is the preferred antiarrhythmic drug. Lidocaine is administered in boluses of 2 mg/kg up to a total dose of 8 mg/kg IV; if this is successful then an IV drip at 50 to 75 μg/kg/min is used as a constant rate infusion. If lidocaine is ineffective, procainamide may be administered slowly IV as a bolus at 10 to 15 mg/kg or as a continuous IV infusion at 25 to 60 μg/kg/min. Contributing factors (to the arrhythmias) should be corrected. Hypokalemia, acidosis, and hypoxia promote arrhythmogenesis and the patient becomes resistant to antiarrhythmic therapy and, therefore, must be resolved with treatment.1 The presence of cardiac arrhythmias may not be associated with an unfavorable outcome.4,5 In contrast, others have reported mortality rates as high as 38% in dogs with preoperative cardiac arrhythmias.6 Postoperative Care Fluid, electrolyte, and acid–base status should be monitored postoperatively. Fluid therapy is based on clinical findings. Shock that persists into the postoperative period must be treated vigorously with crystalloid fluids. Whole blood and plasma must be administered to maintain the PCV and total protein above critical levels. Intravenous fluid therapy is continued until hydration can be maintained by oral fluid intake. Hypokalemia is common and requires potassium supplementation. Sepsis and DIC are also potential complications. 76 Gastritis secondary to mucosal ischemia is also common and may result in gastric hemorrhage or vomiting. Antiemetic agents and histamine H2-receptor blockers (e.g., cimetidine, ranitidine, or famotidine) may be beneficial to control vomiting and to decrease gastric acidity. Ranitidine may also promote gastric emptying. 77 Metoclopramide may be useful as an antiemetic agent, but would be unlikely to promote increased gastric emptying.78 Cisapride is recommended as a prokinetic agent to improve gastric emptying in dogs with GDV but is available only through compounding pharmacies. 79,80 If mosapride and pruclaopride are available in regional practices, they are now considered superior to cisapride. Prognosis The prognosis for GDV in general is guarded, and dependent upon how quickly the condition is diagnosed and treated. Mortality rate for dogs receiving current treatment recommendations for GDV is approximately 15%.43 Early therapy improves the prognosis, whereas a delay lasting more than 5 hours between onset of signs and presentation to the veterinarian’s office worsens the prognosis. Hypothermia at admission, preoperative cardiac arrhythmias, increased preoperative blood lactate concentrations, gastric wall necrosis, severe DIC, partial gastrectomy, splenectomy, and postoperative development of acute renal failure seem to worsen the prognosis.42 The presence of gastric necrosis can be predicted by measuring plasma lactate concentration, with a value greater than 6 mmol/L having a specificity of 88% and a sensitivity of 61% for necrosis.81 Several studies have been conducted to examine survival and recurrence data following acute GDV. Dogs depressed or comatose upon admission were three and 36 times, respectively, more likely to die than alert cases, whereas cases with gastric necrosis were 11 times more likely to die.4 Recurrence rate ranges from 54.5% to 75.8% for those cases that do not have gastropexy and from 4.3% to 6.6% for those that do.4,64,82,83 Thus, a gastropexy should be performed even when conservative management successfully alleviates the gastric malpositioning. In another prospective study, the recurrence rate of GDV was 9% after circumcostal gastropexy and 20% after gastrocolopexy (not significantly different between treatments).84 In dogs at high risk for GDV, it is prudent to consider gastropexy as an elective surgery to prevent GDV. Circumcostal gastropexy has not been shown to delay gastric emptying nor to alter gastric myoelectric activity.23,85 Gastropexy would be effective in preventing a first episode of GDV in a genetically predisposed dog. Owners of high-risk breeds, for example, Bloodhounds and Great Danes, should be advised to consider prophylactic gastropexy at the time of elective surgical neutering.