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Gastric dilatation-volvulus (GDV) is a life-threatening emergency. Successful management depends on prompt diagnosis and appropriate medical and surgical treatment.

Etiology and Pathophysiology:

GDV tends to primarily affect large, deep-chested dogs. Stress may precipitate an acute episode of GDV. There is no apparent sex or age predisposition, but incidence increases with age, being most common in dogs 7-10 yr old. A familial tendency has been reported but not substantiated. Doberman Pinschers, German Shepherds, Standard Poodles, Great Danes, Saint Bernards, Irish Setters, and Gordon Setters are affected most commonly. An association between GDV and inflammatory bowel disease has been suggested, but the relationship is unclear.

Dilatation likely precedes volvulus. Dilatation develops secondary to the accumulation of gas or fluid (or both) within the stomach, the outflow from which is obstructed. Obstruction may be caused by neoplasia, pyloric stenosis, foreign body, or compression of the duodenum against the body wall by the expanding stomach. Prolonged gastric emptying, chronic dilatation secondary to pyloric dysfunction, and hypotonic gastric and pyloric musculature associated with the ingestion of large meals at protracted intervals have been incriminated in the pathogenesis of GDV. However, there is a lack of evidence for gastric emptying disorders in dogs that develop GDV. Distention of the stomach by gas may be associated with aerophagia, diffusion from the bloodstream, release of carbon dioxide after the reaction of hydrochloric acid and bicarbonate, or bacterial fermentation.

Viewed from a caudal to cranial direction, the stomach rotates 90-360° in a clockwise fashion about the distal esophagus. The pylorus is displaced to the left of the midline, the duodenum becomes entrapped between the distal esophagus and the stomach, and the spleen may vary in position from left posterodorsal to right anterodorsal (depending on the extent of volvulus). If the volvulus is >180°, the distal esophagus becomes occluded.

Clinical Findings:

Clinical signs may include an acute onset of restlessness, apparent discomfort, abdominal pain, repeated unproductive retching, excessive salivation, and abdominal distention. Progression to volvulus predisposes to hypovolemic shock. Abnormalities on physical examination include tachypnea or dyspnea, rapid and weak arterial pulses, pale mucous membranes, and prolonged capillary refill time indicative of hypovolemic shock. An irregular heart rate and associated pulse deficits indicate cardiac arrhythmias. Decrease in venous return, cardiac output, and arterial blood pressure, as well as hypovolemic shock, are caused by compression of the caudal vena cava; sequestration of blood in dilated splanchnic, renal, and posterior muscular capillary beds; loss of fluid into the obstructed stomach; and a lack of water intake. Endotoxemia, hypoxemia, metabolic acidosis, and hypotension predispose to disseminated intravascular coagulation.

Diagnosis:

A history of ingestion of a large meal followed by exercise and repeated attempts to vomit is common. Dogs not in a state of shock may appear anxious. Hypersalivation and abdominal distention with gas are noted on physical examination.

Abdominal radiographs taken in right lateral recumbency are preferred for the diagnosis of volvulus. The gas-filled pylorus is located dorsal and slightly cranial to the gas-filled gastric fundus. A compartmentalization line between the pylorus and fundus that represents folding of the pyloric antral wall back onto the fundic wall is frequently seen.

Systemic hypotension predisposes to prerenal azotemia with increases in serum urea and creatinine concentrations. Serum phosphorus increases similarly. After decompression and the “wash out” of sequestered blood, serum levels of ALT and AST increase. CK levels also increase due to striated muscle damage, and serum potassium levels increase subsequent to cell membrane injury.

Treatment and Control:

The principal goals of initial treatment are to stabilize the animal and decompress the stomach.

Initial management for shock should include the administration of IV fluids (eg, 0.45% saline in 2.5% dextrose or balanced electrolyte solutions) at an initial rate of 90 mL/kg over the first hour. The rate is adjusted thereafter based on clinical response and the need to maintain adequate blood pressure and cardiac output. The rate of administration can be reduced as much as 40% if pentastarch, hetastarch, or dextran 70 (20 mL/kg over 15-30 min) is administered. Dogs in severe shock may benefit from the use of 5% or 7.5% hypertonic saline (4 mL/kg over 5-10 min), followed by isotonic fluids as indicated above, until clinical signs of shock have dissipated. Glucocorticoids (hydrocortisone sodium succinate, 10 mg/kg, IV bolus, followed by dexamethasone, 2-4 mg/kg, every 6 hr) may be used as part of the regimen for shock, but efficacy remains controversial. Because endotoxemia may complicate the disease process, antibiotics (eg, ampicillin at 22 mg/kg, qid, and continued for 2-3 days after surgery) are often given.

Metabolic acidosis frequently accompanies GDV. Adequate fluid therapy and gastric decompression generally correct this problem. Electrolyte abnormalities should be addressed if present.

Gastric decompression should be accomplished as soon as possible. Initially, an attempt should be made to pass a well-lubricated orogastric (stomach) tube. The distance from the incisors to the xiphoid or costal arch should be measured and marked by a piece of tape on the stomach tube. This distance indicates the maximum length of tube that can be safely passed; marking this length decreases the likelihood of passing the stomach tube through a devitalized stomach wall. The dog is positioned in sternal or lateral recumbency. A 2-in. roll of tape or an oral speculum is placed in the dog’s mouth, and the muzzle taped closed around it. The tube can then be readily passed through the center of the roll of tape or the speculum. Some resistance is usually felt as the tube passes through the esophageal-gastric juncture. If resistance is met, the tube should be gently rotated while attempting to advance it. Undue force may tear the esophagus. Successful passage of a tube does not rule out concurrent gastric volvulus. Once the tube enters the stomach, gastric gas readily escapes. Excess fluid and ingesta are removed via gravity and suction. After the stomach has been decompressed, it should be lavaged with warm water or saline to remove any remaining debris.

If a tube cannot be readily passed into the stomach, excess gas may be relieved by inserting a large-bore (16-18 gauge) “over the needle” catheter into the stomach percutaneously. An area (10 cm × 10 cm) on the right abdominal wall caudal to the last rib and ventral to the transverse vertebral process should be shaved and prepared in an aseptic fashion. Before the needle is inserted, the area should be percussed to avoid accidental puncture of an overlying spleen. Gastric decompression generally facilitates the passage of a stomach tube and lavage of the stomach.

If sedation is required, oxymorphone hydrochloride (0.05-0.10 mg/kg, 3 mg maximum) or, alternatively, butorphanol (0.2-0.4 mg/kg, IM or SC) may be used.

Temporary gastrotomy may be useful to decompress the stomach and evacuate its contents while avoiding the need for general anesthesia. This procedure is useful in dogs too critical for immediate general anesthesia and can be used to delay exploratory laparotomy until the animal is stabilized. An area caudal to the right costal arch should be shaved and prepared as indicated above. Local anesthesia is provided by the injection of 2% lidocaine hydrochloride administered in an inverted “L” block pattern. A 5-cm skin incision is made ~2 cm caudal and parallel to the costal arch. Abdominal muscles are separated, and the stomach is exposed. A stay suture is used to anchor the stomach to each end of the skin incision. The skin is sutured to the stomach in a continuous pattern. The stomach thus exposed can be decompressed, its contents evacuated, and the body lavaged. A potential disadvantage of this procedure is that an exploratory laparotomy, including inspection of the stomach and restoring it to its customary position, is delayed. Immediate inspection of the stomach permits evaluation of the extent of injury and the possible need for resection. Gastric wall necrosis, rupture, peritonitis, and sepsis are the most common causes of death in these dogs. Delayed exploratory laparotomy may also predispose to cardiac arrhythmias, which develop in ~40-50% of dogs with GDV.

The goals of surgical management are to assess the integrity of the stomach and spleen, to reposition the stomach to its normal location, and to fix the stomach to the abdominal body wall in an attempt to decrease the likelihood of recurrence of volvulus. A midline celiotomy provides access to the stomach and visualization of the spleen and adjacent abdominal structures. Most often, the stomach and pylorus have shifted to the left (clockwise when viewed caudally to cranially), and the gastric fundus has shifted from its normal position in the left dorsal abdomen to the right ventral sector of the abdomen. Splenic congestion generally resolves after the stomach has been repositioned. Gastric wall resection or splenectomy is reserved for cases in which tissue viability has been compromised.

Several surgical techniques have been used to prevent recurrence of volvulus, and recurrence rates are similar (5-11%) for all. Techniques include simple incisional gastropexy, tube gastrotomy, and circumcostal gastropexy. A recent prospective study indicated that the median survival times for dogs that underwent gastropexy was 547 days compared with 188 days for those that did not. The value of pyloromyotomy and pyloroplasty in an effort to promote gastric emptying has not been substantiated. Medical management alone results in a 75% recurrence rate within a 12-mo period.

Food should be withheld for 24-48 hr after surgery. If vomiting continues, metoclopramide (0.2-0.5 mg/kg, SC, or 1-2 mg/kg/day, constant rate IV infusion) can be administered.

Of dogs that die of GDV, 24% do so within the first 7 days after surgery. Many dogs develop ventricular arrhythmias, the cause of which may include myocardial ischemia, autonomic imbalance, acid-base and electrolyte imbalance, catecholamine release, and the release of myocardial depressant factor. Arrhythmias that warrant medical therapy include those that significantly impair cardiac output, multifocal premature ventricular contractions, a ventricular rate persistently >140 bpm, and the “R on T wave” pattern (a phenomenon that predisposes to ventricular fibrillation). If predisposing factors have been addressed and persistent ventricular arrhythmias warrant therapy, 2% lidocaine hydrochloride without epinephrine (2-4 mg/kg, slowly IV) is given and repeated twice during a 30-min period if necessary. Continuous 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).

Dogs with a tendency to develop dilatation and volvulus should be fed smaller meals more frequently over the course of the day. Excessive exercise should be avoided to decrease the likelihood of volvulus, and consumption of large volumes of water after exercise should be avoided to limit gastric distention. END;