Gastric dilation-volvulus

Acute gastric dilation / volvulus (GDV) is a sudden and often fatal GI disorder that particularly affects large, deep-chested breeds (e.g., Great Danes, German Shepherd dogs, Standard Poodles, large mixed-breed dogs).⁴² It has been estimated that there are as many as 60,000 cases of GDV in the United States each year, with an overall mortality of about 15% to 20% de­pending on the time from the onset of clinical signs to treat­ment.

A single causative agent for the pathogenesis of acute GDV has not yet been identified. Several intrinsic physical risk factors (i.e., body size and thoracoabdominal dimension) and envi­ronmental risk factors (i.e., diet, accumulation of gastric gas, anesthesia, stress, being asleep) have been identified, and many more intrinsic anatomic (i.e., gastric ligament laxity, gastric volume and position, gastric hormones such as gastrin) and pathological (i.e., gastric rhythm, motility, and emptying) risk factors are suspected.^43-45 However, in one study feeding and exercise patterns did not alter the incidence of GDV in a large population of military dogs.

Clinical signs

The onset of clinical signs is usually acute or peracute. Ab­dominal distension is associated with progressive restlessness, unproductive retching, salivation, dyspnea, and gastric tym­pany, leading to severe pain and shock.

Rapid gastric distension adversely affects the function of the lower esophageal sphincter and appears to impair gastric mo­tility and emptying. It has been postulated that distension oc­cludes the gastroesophageal junction, precluding emptying by either eructation or emesis. Distension decreases gastric motil­ity by impairing normal contraction and by reflex nervous inhibition. Following dilation, the gastric mucosa and later the gastric smooth muscle undergoes potentially irreversible ischemic necrosis. There is also an accumulation and seques­tration of gastric secretions. The distended stomach occludes venous return from the rear limbs and caudal abdomen, thereby precipitating hypovolemic and cardiogenic shock. Lactic acid and other metabolic by-products accumulate in the poorly perfused hind limbs and viscera to cause severe metabolic acidosis, especially after relief of the gastric dila­tion. During ischemia the pancreas produces a “myocardial depressant factor”, which, together with the acid-base and electrolyte disturbances may lead to a reduced cardiac contrac- tility.⁴⁶ Signs of reperfusion injury, endotoxemia, DIC, and fatal cardiac arrhythmias often occur. Splenic torsion with infarc­tion and necrosis is also a common sequel.⁴⁴ Due to the re­duced perfusion, animals often go into prerenal oliguria and renal failure, which, together with the lactic acidosis and en­dotoxemia will result in multiple organ failure and finally death of the patient.

Diagnosis

Diagnosis is made from history, signalment, and physical ex­amination findings. In dogs that are presented with unproduc­tive vomiting, retching and hypersalivation, a distended abdo­men is often clearly seen. In more severe cases, animals are laterally recumbent and show clinical signs of tachypnea and shock. With progression of the disease, animals will eventually decompensate, and bradycardia, hypothermia, white mucous membranes and cold extremities are coupled with a poor prognosis.

Treatment

Management of hypovolemia (to prevent or treat shock) is the primary goal of emergency treatment of patients with GDV. Fluid therapy should be started at a rate of 90 ml/kg/hour intravenously through large-bore catheters with crystalloid fluid solutions (e.g., lactated Ringer’s solution) until the ani­mal is stabilized. This fluid bolus is followed by high-volume administration of crystalloid fluids (e.g., 20 ml/kg/hour) for the following time period. A combination of colloids (e.g., hetastarch) combined with crystalloids can also be used; the former may prolong the effects of crystalloid fluids by increas­ing the oncotic pressure. Gastric decompression is attempted only after the correction of hypovolemia is well under way.

Gastric decompression can usually be achieved by orogastric intubation in unsedated patients using an equine nasogastric tube with large end and side holes. If orogastric intubation is unsuccessful, aseptic right- or left-sided gastrocentesis with a large-bore catheter or needle should be performed. Radiogra­phy is not necessary to diagnose gastric dilation but is invaluable in diagnosing gastric volvulus (Figure 4.15). Radiographs should only be taken after the patient has been stabilized. Radiographs in right-lateral recumbency are required to show the typical double-bubble image (i.e., air in both the pylorus and fundus), since the pylorus is displaced to the left-hand side of the ab­

dominal cavity in a dorsocranial position with respect to the fundus.

When its vital signs are stable, the patient should be taken to surgery as quickly as possible for decompression and reversal of the volvulus. Small amounts of induction agents (e.g., thiopen­tal, propofol) are given to effect, and anesthesia should be main­tained with isoflurane or sevoflurane in oxygen. Nitrous oxide, if part of the anesthetic protocol, is not given until complete gastric decompression has been achieved. After the stomach has been decompressed, the torsion is reversed, the viability of the stomach and spleen are evaluated, a partial gastrectomy or splenectomy is performed as needed, and the stomach is pexied to prevent reoccurrence. Both, an incisional or belt-loop gas- tropexy have been described - if a gastropexy is not performed, recurrence rates of up to 80% have been reported.^49,50

Cardiac arrhythmias, such as premature ventricular contrac­tions or ventricular tachycardia, occur frequently in GDV pa­tients. They can be seen up to 3 days after surgical correction, and require treatment if there is evidence of poor cardiac per­formance. Electrolyte and acid-base disturbances must be identified and corrected if present. Follow-up management includes feeding of a meat-based, canned, highly digestible diet at least three times daily. It is important to note that py­loroplasty does not influence the rate of recurrence.⁴⁴ Prophy­lactic gastropexy might be indicated in some dogs that are considered to be at increased risk for GDV and can be achieved by minimally-invasive laparoscopy.⁵¹

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