Etiology

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.