The stomach moves in a clockwise rotation. Displacement of the pylorus occurs from the right side toward the ventral midline.
It passes over the fundus and body to the left abdominal wall close to the lower esophageal sphincter. At the same time, the
fundus goes in a ventral direction toward the right abdominal wall. The pyloric antrum ends up in a dorsal position on the
left side. Because of the attachment of the omentum to the greater curvature of the stomach, the omentum covers the stomach
The displacement of the spleen may be related to the degree of volvulus. The spleen is usually engorged or can undergo torsion
on its own pedicle. Thrombosis of the splenic artery can also occur. Usually, 180 degrees of stomach rotation is seen, but
360-degree rotation is possible. Counterclockwise rotation is not really possible, or it is limited to 90 degrees since the
pylorus cannot move dorsally in the abdominal cavity.
Gastric dilatation causes compression of the caudal vena cava and portal vein.10-13 Sequestration of blood in the spleen, kidneys, and gastrointestinal tract occurs. Compression of the caudal vena cava and
portal vein induces a decreased venous return, resulting in hypovolemic shock. Hypotension and venous stasis result in cellular
hypoxia and anaerobic metabolism. Elevated portal pressure compromises microcirculation in the viscera and reduces oxygen
delivery to the gastrointestinal tract. The pancreas in the presence of ischemia produces myocardial depressant factor.12 Ischemia, acidosis, liberation of the myocardial depressant factor by the pancreas, and the production of free oxygen radicals
induce myocardial ischemia and reduce cardiac contractility.12-14 Subendocardial ischemia and necrosis combined with tachycardia and acid-base imbalance induce arrhythmias. Vascular stasis,
hypoxia, and acidosis can induce disseminated intravascular coagulopathy (DIC).
Mechanical limitation of diaphragmatic movement by a dilated stomach and decreased pulmonary compliance results in respiratory
dysfunction. Tissue hypoxia results from decreased cardiac output and respiratory impairment. Increased gastric intraluminal
pressure, portal hypertension, and venous stasis with thrombosis cause gastric mucosa stasis, hypoxia, and edema. Gastric
wall necrosis can then develop in the fundus along the greater curvature. Because of distention of the stomach, vascular wall
disruption causes mucosal hemorrhage. Avulsion of branches from the short gastric arteries during rotation of the stomach
contributes to blood loss, hypovolemia, and restriction of blood flow to the stomach.
Dogs with GDV are usually presented for evaluation of unproductive vomiting, retching, hypersalivation, and a distended abdomen.
They have progressively distending and tympanic cranial abdomens, and they may be restless. As the severity of the distention
increases, the dog can become weak, laterally recumbent, and tachypneic.
Dogs with GDV often present with weak peripheral pulses, pale mucous membranes, prolonged capillary refill times, tachycardia,
and tachypnea. Abdominal pain is rarely present on palpation.
Dogs with mesenteric volvulus also present with severe abdominal distention. Usually, these dogs are in a lot of pain and
deteriorate rapidly in severe septic shock.
Persistence of the clinical signs of GDV for more than five hours has been associated with a poor prognosis.15 The severity of the clinical signs on presentation has been found to be an indicator of patient survival.16 In general, dogs that are bright and alert when presented have better prognoses than do dogs that are laterally recumbent.
It has been shown that recumbent patients have 4.4 times greater probability of dying than do dogs that are ambulatory. If
a patient is comatose, it has 36 times greater probability of dying. Dogs that appear depressed on presentation have a three
times greater probability of dying.16