Definition

• A disease in dogs in which the stomach dilates and subsequently rotates around its short axis.
• Also known by the acronym GDV.

Pathophysiology

• The exact mechanism involved in the development of GDV is poorly understood.
• The volvulus can occur in any direction, but the vast majority occurs in a clockwise rotation when the animal is in dorsal recumbency and the surgeon is viewing the patient from the caudal aspect.
• Factors thought to contribute include ingestion of a large amount of food or water, delayed gastric emptying, and excessive post-prandial activity. However, these factors do not occur with all cases of GDV.
• Subsequent to the gastric rotation, gas and fluid continue to become entrapped within the gastric lumen. Progressive distention of the stomach occurs.
• As the stomach becomes progressively distended, intra-abdominal pressure increases. This leads to compression of the compliant blood vessels of the abdomen including the caudal vena cava and portal vein. The reduction in blood flow through these major vessels leads to decreased cardiac return and hypovolemic shock.
• Decreased perfusion can lead to systemic effects including organ death, local and systemic inflammatory cascades, and disseminated intravascular coagulation.

Systems Affected

• Gastrointestinal-decreased perfusion can lead to ischemic necrosis of the stomach. Due to the higher metabolic demand, the mucosa is predisposed to the effects of ischemia.
• Cardiovascular-significant decrease in the venous return to the heart results in a hypovolemic state. This leads to decreased cardiac output, which can lead to organ hypoxia and tissue damage/tissue death. Decreased myocardial perfusion, as well as the generation of inflammatory mediators, can lead to cardiac arrhythmias, particularly premature ventricular contractions.
• Hemic/Lymphatic/Immune-splenic insult is common, via avulsion of the short gastric vessels, splenic torsion, or splenic infarction.

Genetics

No direct genetic predisposition confirmed; however, dogs with a first-order relative with a history of GDV are at an increased risk for development of GDV.

Incidence/Prevalence

An incidence rate for large- and giant-breed dogs has been reported to be around 6%.

Signalment

Signs

Causes

• Unknown.
• Likely a multifactorial origin that includes anatomic, genetic, and environmental factors.

Risk Factors

• Classically has been linked to activity following a meal.
• Anatomic predisposition in deep-chested dogs, particularly large and giant breeds.
• It was also thought that a lowered food bowl encouraged aerophagia, which could lead to GDV. Recently eating from a RAISED food bowl has been identified as a risk factor for development of GDV.
• Having a first-degree relative with GDV and faster speed of eating have also been identified as being risk factors associated with the development of GDV.
• Possibly having gastrointestinal neoplasia, as it can cause motility disturbances as well as gastric retention of food and/or air.

Differential Diagnosis

• Other diseases that cause acute abdominal distention and potentially circulatory attenuation include septic peritonitis, hemoabdomen, intestinal volvulus, or acute gastroenteritis.
• “Food bloat” is the common name for gastric dilation without concurrent volvulus. This commonly occurs in dogs that engorge themselves with food.

CBC/Biochemistry/Urinalysis

• CBC-stress leukogram, hemoconcentration, thrombocytopenia possibly.
• Biochemistry-electrolyte abnormalities are commonly encountered. May see azotemia due to hypovolemia (prerenal).
• Urinalysis-may see increased specific gravity with dehydration.

Other Laboratory Tests

Plasma lactate concentration has been found to be useful in predicting underlying gastric necrosis as well as prognosis. Median plasma lactate levels in dogs with gastric necrosis were significantly higher (6.6 mmol/L) than in dogs without gastric necrosis (3.3 mmol/L). Survival of dogs with plasma lactate levels <6.0 mmol/L was 99%, compared with the 58% survival experienced by dogs with lactate levels >6.0 mmol/L.

Imaging

• Adequate stabilization is often necessary before obtaining radiographs.
• Abdominal radiography-a right lateral abdominal radiograph is the imaging modality of choice. Classically reveals compartmentalization of the stomach, which is considered to be pathognomonic.
• Dorsoventral view-may be helpful in confirming the disease.

Diagnostic Procedures

• Very rarely, uncertainty may persist subsequent to obtaining survey radiographs.
• A positive-contrast upper GI can be attempted with CAUTION, as these patients are at an increased risk for aspiration&excl

Pathologic Findings

• Splenic torsion may also be a concurrent finding.
• The stomach itself becomes edematous and undergoes vascular congestion and infarction, which can lead to necrosis.

Appropriate Health Care

• This disease syndrome represents an emergency&excl
• Patients should be hospitalized, thoroughly assessed, and aggressively treated for cardiovascular insufficiency.
• A myriad of fluid therapy approaches are employed predicated on patient situation and personal preference. Crystalloid therapy, colloid therapy, or a combination can be used. If crystalloid therapy is chosen a dose of 90 ml/kg of an isotonic solution is administered over 30–60 minutes. Administered through cephalic or jugular venous access sites.
• Subsequent to cardiovascular stabilization, gastric decompression should be performed.
• Orogastric intubation is the preferred method of obtaining gastric decompression. Cardiovascular-sparing medications may be administered to patients in an effort to facilitate orogastric intubation. Commonly, considerable resistance is encountered upon reaching the esophageal hiatus. The lubricated tube can be twisted or repositioned to facilitate passage. Differing patient positions (sitting, standing, etc.) can also be attempted to facilitate passage.
• In cases where orogastric intubation is unsuccessful, percutaneous gastrocentesis can be attempted. A point of maximal tympany is located that typically corresponds to an area of the stomach that is gas-filled. A large diameter needle or catheter is passed into the stomach at this area. Gas typically will elicit an audible noise when escaping. Considerable time is necessary to achieve gastric decompression using this technique.
• Upon patient stabilization and gastric decompression, surgical intervention is indicated. In rare cases in which patient is unresponsive to stabilization attempts, immediate surgical intervention may be taken.

Activity

Restriction of activity for approximately 2 weeks postoperative is recommended.

Diet

• Oral intake of food is recommended as soon as adequate recovery has been achieved.
• The role of food bowl height in the occurrence and recurrence of this disease is unclear at this time.
• Consider fat-restricted diets to enhance gastric emptying.

Client Education

Owners of large- and giant-breed dogs who are not aware of the clinical signs of gastric dilation and volvulus should be educated.

Surgical Considerations

• Surgical intervention should be performed as soon as possible in a stable patient or in a patient in which diligent stabilization efforts have proved ineffective.
• Surgical intervention has three main goals: (1) anatomical reposition of the stomach (and spleen if applicable); (2) assessment of organ viability; (3) prevention of recurrence.
• Once repositioned, the stomach and spleen should be assessed. If non-vital areas are present, removal should be performed via partial gastrectomy and/or splenectomy.
• Prevention of recurrence is achieved through a permanent gastropexy. Multiple techniques for performing gastropexy have been described and choice of technique is largely based on surgeon preference.

Drug(s) Of Choice

• Perioperative antibiotics are indicated. The surgery itself, depending on severity and progression of disease, may be a clean, clean-contaminated, contaminated, or dirty surgery. It is often next to impossible to ascertain this information before the surgery is performed.
• Antibiotic selection should be predicated upon potential pathogens that the patient may be exposed to. Moderate-to-severe disease may expose the host to enteric pathogens due to visceral perforation or loss of normal mucosal barriers to hematogenous bacterial translocation from the gastrointestinal tract. For these patients cefoxitin sodium (30 mg/kg IV q6–8h) may be an appropriate choice. For patients in which no entry into the gastrointestinal tract has occurred, cefazolin sodium (22 mg/kg IV q2h intraoperatively) is sufficient.
• Gastric protectants may be implemented to minimize or prevent gastrointestinal ulcerations.

Contraindications

• The use of some synthetic colloids (e.g., hydroxyethyl starch) has been linked to disruption in the formation of the primary clot and may not be appropriate to use in certain patients with GDV, such as those with an underlying coagulopathy like concurrent DIC.
• Drugs that significantly depress cardiovascular function should be avoided if possible (e.g., acetylpromazine).

Precautions

Patients may acutely decompensate at any time, particularly under anesthetic intervention.

Alternative Drug(s)

Efficacy of the administration of corticosteroids in patients affected with GDV is currently lacking.

Patient Monitoring

• Nursing care-some patients may require recumbent care for several days before eventual recovery.
• Adequate pain control.
• Premature ventricular contractions commonly occur postoperatively. These result from myocardial hypoperfusion and resultant ischemic damage, or due to splenic insult or removal. The monitoring of heart rhythm is recommended.
• Monitor urine production and renal function postoperatively.

Prevention/Avoidance

• Elevation of food bowl is argued.
• Avoid exercise after eating or drinking.
• Possibly slowing the rate of consumption of meals.
• Some soak dry food in water before feeding or feed multiple, smaller meals.

Possible Complications

• Gastric dilation may recur, even after a gastropexy is performed. Recurrence of volvulus with an appropriately performed gastropexy is exceedingly rare.
• Failure to remove necrotic gastric tissue may result in eventual stomach perforation and septic peritonitis.
• Cardiac arrhythmias (particularly premature ventricular complexes), DIC, and gastric ulceration may also occur.

Expected Course and Prognosis

• A heightened awareness by dog owners combined with an increased understanding of the complex pathophysiologic events associated with GDV have significantly reduced the mortality rate associated with this disease over the past 30 years.
• Prognosis in dogs treated appropriately that do not have gastric necrosis is excellent, with a reported survival rate of 98%. Dogs with gastric necrosis have a more guarded prognosis, with a reported survival rate of 66%.
• One article reported an overall short-term survival rate of 83.8%. Negative prognostic indicators included hypotension, DIC, peritonitis, and the need to perform both a splenectomy as well as a partial gastrectomy.

Age-Related Factors

A higher rate of GDV is typically seen in middle-aged to older dogs.

Synonyms

• Bloat
• Gastric torsion

See Also

• Sepsis and Bacteremia
• Shock chapters

Abbreviations

• DIC = disseminated intravascular coagulation
• GDV = gastric dilation and volvulus syndrome
• GI = gastrointestinal

Client Education Handout Available Online