Emergency stabilization of gastric dilatation and volvulus (Proceedings)

Gastric dilatation and volvulus (GDV) is an acute, life-threatening condition which requires immediate medical and surgical intervention. It occurs in susceptible dogs when the stomach becomes distended with air, and then while dilated, twists on itself.

Signalment, risk factors and prognosis

It most commonly occurs in adult, large to giant breed dogs with a deep chest conformation. Overrepresented breeds include the Great Dane, St. Bernard, Weimeraner, Standard Poodle, Bassett Hound, and various setter breeds. Additional risk factors include having a first degree relative with GDV and increasing age. Mortality rates for dogs with GDV are quite variable and range from 10-90%. Risk factors associated with increased mortality include duration of clinical signs prior to treatment; the presence of gastric necrosis, cardiac arrhythmia, or increased serum lactate concentration; and the need for splenectomy.

Pathophysiology

Gastric distention and volvulus occurs when a distended stomach twists on its long axis and occludes the esophageal hiatus and pylorus, thereby trapping stomach contents. Clockwise rotation is most common (as viewed from caudal to cranial with the dog in dorsal recumbency). Gastric distention results in decreased venous return to the heart, congestion of the splanchnic vessels, and increased gastric wall pressure. Decreased venous return leads to obstructive shock. Splanchnic congestion results in breakdown of the gut mucosal barrier and consequential bacterial translocation, activation of systemic inflammatory mediators (SIRS), and disseminated intravascular coagulation (DIC). Increased gastric wall pressure leads to gastric mucosal ischemia, infarction, ulceration, perforation and peritonitis. The spleen, attached to the stomach via the gastrosplenic ligaments and the short gastric blood vessels, commonly rotates with the stomach to the right ventral abdomen. This may lead to congestion, splenomegaly, infarction and thrombosis, torsion, and significant hemoperitoneum when the gastric branches of the splenic arteries are avulsed.

Clinical signs

The classic presentation is that of a large, deep chest dog with an acute history of agitation and non-productive retching that has a distended, tympanic abdomen, ptyalism, and shock. However, it is important to remember that GDV can occur in atypical breeds and species and that the stomach can be hidden under ribs. Additionally, these patients can present with varying degrees of shock, from well compensated to terminal.

Diagnosis and therapy

An emergency database should include the quick assessment tests of packed cell volume, total solids, blood glucose and azotemia estimate (QATs); a venous blood gas; serum or plasma lactate; and coagulation profile. QATs establish baseline values and aid in monitoring individual patient trends. A venous blood gas provides acid base status which is important as decreased venous return results in vascular stasis, lactic acid accumulation, and ultimately metabolic acidosis. Additionally, compression of the respiratory tract may result in a respiratory acidosis. Correction of acid base or electrolyte abnormalities is important prior to induction of general anesthesia. Lactate is used to evaluate the adequacy of perfusion. It is produced when anaerobic metabolism occurs and is considered an early indicator of tissue hypoxia. It should be interpreted in conjunction with clinical perfusion parameters such as pulse quality, mucus membrane color, capillary refill time, and rectal temperature. Lactate has been evaluated in dogs with GDV [Plasma lactate concentration as a predictor of gastric necrosis and survival among dogs with GDV: 102 cases (1995-1998). JAVMA, 215 (1), 1999]. In this retrospective study a low serum lactate was a better predictor of survival than high lactate was a predictor of death. For this reason a single lactate may have minimal value whereas serial lactate measurements are far most useful. Various coagulation parameters including platelet count, prothrombin and activated partial thromboplastin times, fibrinogen, antithrombin, and fibrin degradation products have also been evaluated in GDV patients [Abnormal hemostatic profiles and gastric necrosis in canine GDV. Vet Surgery. 1993, 22(2):93-7]. In this prospective study, none of the 10 dogs with fewer than 2 abnormal hemostatic test results had evidence of gastric necrosis at surgery or necropsy.

Patients with GDV will present in varying degrees of shock and all should be treated immediately and aggressively before diagnostic tests or decompression is attempted. Once a suspect GDV is identified, two large bore, short length intravenous catheters are placed in two veins (cephalic or jugular) and fluids administered. Isotonic crystalloid fluids [lactated Ringer's solution, Plasmalyte-A, Normosol-R] are administered [30-45 ml/kg bolus and repeat as necessary] until the patient's cardiovascular status, perfusion, and mentation are improved. Additionally, administration of hypertonic saline [4 ml/kg of 7% HTS] or hetastarch (5-10 ml/kg) may reduce the time and volume of crystalloid required to achieve adequate resuscitation.

Once the patient is stabilized abdominal radiographs are indicated to confirm the presence of GDV. When possible, the diagnosis of GDV should be confirmed radiographically prior to gastric decompression. The views of choice are the right lateral and the dorsoventral (DV) or ventrodorsal (VD). With simple gastric distension the stomach is distended with air and may occupy nearly the entire abdominal cavity. With GDV the right lateral view frequently reveals a "double bubble" gas pattern with compartmentalization of gas. A soft tissue fold can be seen separating the displaced pylorus from the distended fundus with volvulus. On the orthogonal view the pylorus will typically be displaced dorsally and to the left of midline. Other radiographic findings of importance include the presence of free air within the abdominal cavity or gastric pneumotosis. Free air is most readily seen between the liver and the diaphragm and most likely indicates gastric necrosis and or stomach rupture. Gastric pneumotosis or gas dissection of the gastric mucosa may also represent gastric necrosis. In a retrospective study [Pneumotosis in canine GDV syndrome. Vet Rad & US. 2004, 45(3):205-209] the author's found that 41% of dogs with radiographic gastric pneumotosis required gastric resection as compared to 25% of dogs without gastric pneumotosis. In aged pets it may be prudent to obtain 3 view thoracic radiographs as evidence of incidental intrathoracic disease such as metastatic neoplasia may change how the owner proceeds.

Gastric decompression

Gastric decompression should not be attempted until after fluid therapy is initiated. Decompression can be accomplished via passage of an orogastric tube or gastrocentesis. There is no evidence in the veterinary literature to suggest that one method is superior to another. While it is the author's experience that orogastric decompression is more effective than gastrocentesis, various circumstances may make one option preferable over the other.

To pass an orogastric tube the patient is generally sedated (opiate combined with benzodiazepine) or may be put under general anesthesia and intubated. An appropriately sized smooth tube is measured from the tip of the nose to the patient's last rib and marked with tape. The tube is generously lubricated, introduced into the mouth and advanced into the esophagus. Palpation of two firm tubes, the trachea and the tube within the esophagus can be used to ensure proper placement. Once entry into the esophagus has been confirmed, the tube is gently rotated and advanced into the stomach. If significant resistance is met, one might perform a gastrocentesis to relieve some of the pressure and then reattempt passing of the orogastric tube. Using excessive force may result in esophageal perforation, a relatively uncommon but potentially devastating complication of the procedure. Once the tube enters the stomach there is generally a rush of sour smelling gastric gas and evidence of gastric reflux within the tube. Multiple warm water gastric lavage infusions can then be administered to further evacuate the stomach.

Gastrocentesis is performed in the area of greatest tympany "ping" located caudal to the last rib. The area should be clipped and aseptically prepared. A 16-18g needle or catheter works well for this purpose.

Emergency laparotomy should be performed as soon as the patient is deemed hemodynamically stable as prompt intervention may minimize gastric necrosis and or splenic congestion or thrombosis. Goals of surgery include correction of gastric malposition, gastropexy, and when necessary resection of necrotic stomach and or splenectomy. In addition, a complete exploration of the abdomen is strongly recommended.

Post-operative monitoring and treatment

Post-operatively the patient's vital signs and blood pressure should be monitored every 1-4 hours. Quick assessment tests, electrolytes and acid-base status should be evaluated 1-4 times daily until the patient is stable. Blood urea nitrogen, creatinine, platelet count and other coagulation parameters are monitored as necessary to permit early detection of complications such as sepsis, oliguria (usually due to inadequate fluid therapy), or disseminated intravascular coagulation. Broad spectrum antibiotics are indicated if sepsis is suspected or if the gut mucosal barrier is compromised. Multi-modal analgesics are beneficial to increase patient comfort while minimizing side-effects of any one drug class. Food and water are reintroduced 12-24 hours post-operatively.