Gastric dilation and volvulus (GDV) is an acute, life-threatening condition that primarily affects large- and giant-breed dogs. Immediate medical and surgical intervention is required to optimize survival.
Etiology and Pathophysiology
The etiology of GDV is unknown, but several phenotypic and environmental risk factors have been identified for developing GDV. Breeds known to be at risk include the Great Dane, German Shepherd, Irish Setter, Gordon Setter, Weimaraner, Saint Bernard, Standard Poodle, and Basset Hound. No sex predisposition exists, and risk appears to increase with age. Other reported predisposing factors include lean body condition, deep/narrow thoracic conformation, a first-degree relative with a history of GDV, stress, aggressive or fearful behavior, once daily feeding, a dry-food diet, rapid consumption of food, previous splenic disease, and increased gastric ligament laxity.
It is unclear if dilation or volvulus occurs first during the development of GDV, although it is postulated that volvulus occurs first. Dilation of the stomach results from accumulation of gas and/or fluid, and volvulus prevents the normal release of these contents. During volvulus, the pylorus and duodenum first migrate ventrally and cranially. Viewed from a caudal to cranial direction, the stomach may rotate 90–360° in a clockwise fashion about the distal esophagus. This rotation displaces the pylorus to the left of midline, entrapping the duodenum between the distal esophagus and the stomach. Depending on the degree of volvulus, the spleen may vary in position from the left caudodorsal to the right craniodorsal abdomen. A volvulus of >180° causes occlusion of the distal esophagus.
After volvulus of the stomach, gas is trapped and increases intragastric pressure. The duodenum may be compressed by the distending stomach against the body wall, resulting in gastric outflow obstruction. Splenic entrapment often accompanies GDV. The progressively distending stomach compromises venous return by compression of the caudal vena cava. Sequestration of blood in the dilated splanchnic, renal, and posterior muscular capillary beds results in portal hypotension, GI tract ischemia, hypovolemia, and systemic hypotension. These factors combine with the loss of fluid in the obstructed stomach and a lack of water intake to produce hypovolemic shock. Dogs are at risk of endotoxemia, hypoxemia, metabolic acidosis, and disseminated intravascular coagulation.
Dogs may present with a history of nonproductive retching, hypersalivation, and restlessness. Acute or progressive abdominal distention may be noted, or the dog may be found recumbent and depressed with an enlarged abdomen.
Physical examination findings include an enlarged or tympanic abdomen, abdominal pain, and/or splenomegaly. Progression from gastric dilation to volvulus predisposes to hypovolemic shock. Signs of shock are common and can include weak peripheral pulses, tachycardia, prolonged capillary refill time, pale mucous membranes, and dyspnea. An irregular heart rate and pulse deficits are common findings and indicate the presence of a cardiac arrhythmias. Additionally, the expanding stomach may compress the thoracic cavity and inhibit diaphragmatic movement, leading to respiratory distress.
History, signalment, and clinical signs can lead to a high suspicion of GDV. Radiographs are valuable in distinguishing simple gastric dilation from GDV. The preferred radiographic views for identification of GDV are right lateral and dorsoventral recumbency. Ventrodorsal positioning should be avoided because of the potential for aspiration of gastric contents and further compression of the caudal vena cava.
The right lateral radiograph usually reveals a large, distended, gas filled gastric shadow with the pylorus located dorsal and slightly cranial to the fundus. The gastric shadow is frequently compartmentalized or divided by a soft tissue “shelf” between the pylorus and fundus. This “shelf,” or “reverse C” sign, is created by the folding of the pyloric antral wall onto the fundic wall. Splenic enlargement or malposition may be noted. Gas within the gastric wall is suggestive of tissue compromise, while free gas within the abdomen indicates gastric rupture.
PCV, total solids, electrolytes, blood glucose, and serum lactate levels should be evaluated, followed by a CBC, serum biochemical profile, and coagulation assays. Continuous ECG and blood pressure monitoring is recommended.
Prerenal azotemia is a common finding and is secondary to systemic hypotension. Elevated CK levels may be present due to striated muscle damage, and serum potassium levels may increase subsequent to cell membrane damage. Serum ALT and AST levels may increase secondary to hypoxic damage. Elevated lactate is a common finding and is secondary to systemic hypotension and inflammation. Hyperlactatemia (>6.0 mmol/L) is associated with an increased likelihood of gastric necrosis and the need for partial gastric resection.
Immediate goals of treatment include restoring circulating blood volume and gastric decompression. Rapid surgical correction of the volvulus follows initial stabilization. Because duration of clinical signs is one of the risk factors of GDV-associated death, immediate recognition and correction is imperative.
Correction of hypovolemia by rapid fluid replacement with one or more large bore (16- to 18-gauge) IV catheters placed in the jugular or cephalic veins is the first treatment priority. Fluid therapy at rates appropriate for shock (90 mL/kg/hr) with crystalloids should commence immediately. In severe shock, fluid therapy with combinations of crystalloids, colloids (eg, hetastarch or pentastarch bolus at a rate of 5 mL/kg, IV, can be repeated up to 20 mL/kg), or hypertonic saline (eg, 7% hypertonic saline solution with dextran 70 at a rate of 5 mL/kg over 15 min) can be considered; the rate of crystalloid fluid infusion can be reduced by as much as 40% if these products are used. Flow-by oxygen should be provided during stabilization. Electrolyte and acid-base disturbances are usually corrected by adequate fluid therapy and gastric decompression. Because of the potential risk of endotoxemia and GI translocation of bacteria, antibiotics (eg, ampicillin at 22 mg/kg, qid, and continued for 2–3 days after surgery) are usually given.
Gastric decompression occurs concurrently with fluid resuscitation. Initial decompression attempts should be made with an orogastric tube, which can be performed after sedation with fentanyl (2–5 μg/kg, IV) or hydromorphone (0.05–0.1 mg/kg, IV), with or without diazepam (0.25–0.5 mg/kg, IV). Agents that cause vasodilation (eg, phenothiazines) should be avoided. A stomach tube is measured from the incisors to the last rib and marked. The tube must not be passed beyond this marking. The lubricated tube is introduced into the mouth (often held open with a mouth gag, roll of tape, or bandage material) while the dog is in a sitting position or sternal recumbency. Some resistance is typically encountered at the esophagealgastric sphincter. Gentle manipulation and counterclockwise rotation of the tube may be necessary to allow passage of the tube into the stomach. Caution must be exercised to avoid perforation of the esophagus with the tube. Once the tube enters the stomach, gastric gas rapidly escapes. Successful passage of a stomach tube does not rule out the presence of volvulus. After gas and stomach contents are released from the stomach via the tube, the stomach should be lavaged with warm water to decrease the rate of redilation with gas and to remove pooling gastric acid and endotoxins.
If an orogastric tube cannot be readily passed, percutaneous gastrocentesis may be performed to release excess gastric gas. An area (10 cm × 10 cm) over the right abdominal wall caudal to the last rib and ventral to the transverse vertebral process should be shaved and aseptically prepared. Percussion of the area should reveal tympany; this helps avoid accidental puncture of an overlying spleen. If a tympanic structure is not identified, the left paracostal region should be assessed. A large-bore needle or over-the-needle catheter (14- to 16-gauge) should be introduced through the skin and body wall into the stomach at the site of greatest tympany. Decompression usually allows for subsequent passage of an orogastric tube and lavage of the stomach.
Surgical correction of GDV should rapidly follow initial stabilization. Aseptic preparation of the abdomen is performed before surgery (cranioventral midline approach). Before the gastric torsion is corrected, decompression of the stomach should be achieved by an assistant placing an orogastric tube or via gastrocentesis intraoperatively. The stomach is then returned to its normal position, and the stomach and spleen are evaluated for ischemia. Any areas of ischemic gastric wall are resected, and a splenectomy is performed if splenic vascular compromise is present. Extensive gastric necrosis and necrosis of the gastric cardia as well as splenic infarction are considered poor prognostic indicators. The stomach is emptied of contents, and a gastropexy performed to decrease risk of recurrence. Several gastropexy techniques have been described and include incisional, belt loop, circumcostal, and tube gastropexies.
Monitoring before, during, and after surgery should include continuous ECG, intermittent blood pressure measurement, and frequent assessment of vital parameters, PCV, total solids, electrolytes, blood glucose, and serum lactate.
Postoperative management includes IV fluid therapy and analgesia. Food should be withheld for 12–24 hr after surgery. Antiemetic agents (metoclopramide 0.2–0.5 mg/kg, SC, or 1–2 mg/kg/day, constant-rate IV infusion; maropitant at 1 mg/kg, SC, sid) may be administered in cases of continued vomiting. Cardiac arrhythmias before, during, and after surgery are common and are most often ventricular in origin. Treatment of arrhythmias is usually not indicated, but should be instituted if one or more of the following criteria is met: persistent tachycardia (>140 bpm), hypotension (systolic blood pressure <90 mm Hg), hypoperfusion (prolonged capillary refill time, weak pulses), “R on T wave” pattern (a phenomenon that predisposes to ventricular fibrillation), or multifocal ventricular premature contractions. A bolus of 2% lidocaine (2–4 mg/kg, slowly IV) can be administered and repeated twice in a 30-min period if necessary. A continuous lidocaine IV infusion (30–80 μg/kg/min) may be indicated to control arrhythmias. Cardiac arrhythmias associated with GDV are often difficult to control. If the arrhythmia is poorly responsive to this therapy, procainamide (6–10 mg/kg, IV over 15 min) should be given. Life-threatening arrhythmias may respond to 20% magnesium sulfate (0.15–0.3 mEq/kg, or 12.5–35 mg/kg, IV over 15–60 min). Oral sotolol (1–2 mg/kg, PO, bid) has also been used to control supraventricular and ventricular tachycardias.
Less common postoperative complications can include life-threatening conditions such as sepsis, peritonitis, and disseminated intravascular coagulation.
The overall mortality rate associated with GDV is ∼25–30%. Risk factors associated with short-term death from GDV include presence of clinical signs >6 hr before examination, performing splenectomy and a partial gastrectomy, hypotension at any time during hospitalization, peritonitis, sepsis, and disseminated intravascular coagulation.
Prophylactic gastropexy is not known to prevent development of GDV if performed at the time of neuter, but it has been shown to help prevent recurrence if performed at the time of the first GDV correction. Owners of breeds at high risk of GDV should be educated about the risk factors for and signs of GDV, and advised to seek immediate veterinary care if clinical signs are seen. Additional precautions include avoiding stress, feeding multiple rather than single daily meals, avoiding exercise immediately after feeding, and not using elevated food dishes.
Last full review/revision March 2012 by Shauna L. Blois, DVM, DVSc, DACVIM; Thomas W. G. Gibson, BSc, BEd, DVM, DACVS