Chapter 3: Gastric Dilation-Volvulus

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Gastric Dilation-Volvulus

A complex medical and surgical emergency, gastric dilation-volvulus (GDV) most commonly occurs in large and giant breeds of dog. However, it potentially can affect any size or breed of dog, as well as cats. In smaller breeds of dog the dachshund is overrepresented. Deep-chested conformation may increase the susceptibility to GDV. The prevalence of GDV increases with increasing age, with the greatest occurrence between 7 and 10 years of age. The frequency of occurrence has been reported at 2.4 to 7.6 per 1000 canine hospital admissions (Glickman et al, 1994). Although the cause of GDV has not been fully explained, potential contributing causes include delayed gastric emptying, pyloric obstruction, aerophagia, and gastric engorgement that contribute to gastric dilation (GD). Volvulus possibly occurs secondarily to the dilation. To further complicate matters, gastric volvulus can occur without prior dilation, for example, with exercise after consumption of a large meal. Splenic torsion has also been causally implicated because malposition of the spleen frequently occurs with GDV; however, GDV also can occur in splenectomized dogs, possibly from increased space within the peritoneal cavity. Inhibition of gastric motility by pharmacologic agents, blunt abdominal trauma, spinal cord injuries, prolonged surgical procedures, or prolonged recumbency can also predispose dogs to GD. Cereal diets have been suggested as a cause for GD; however, studies have not been able to confirm this finding. In predisposed dogs that consumed dry dog foods there was a 2.4-fold increased risk of GDV when an oil or fat was among the first four ingredients (Raghavan, Glickman, and Glickman, 2006).

This chapter focuses on the initial and postoperative treatment of the animal with GDV. A detailed description of the pathophysiology of GD and GDV is covered elsewhere in the literature (Leib, 1987) and is only briefly outlined here as a basis for treatment rationale. The various techniques used for surgical correction of GDV can be obtained from standard surgical texts.


Various studies of dogs with GDV and surgical intervention report overall mortality rates of 10% (Mackenzie et al, 2010), 16.7% (Beck et al, 2006), and 23% (Zacher et al, 2010). The prognosis for recovery may be associated with severity of systemic effects; however, prompt and optimal therapy can result in recovery in a high percentage of dogs that present with GDV. Development of GDV leads to both local and systemic consequences of varying degrees. Gastric ischemia results in gastritis that can progress to necrosis, with possible perforation and peritonitis. Compression of the caudal vena cava and portal vein results in decreased venous return to the heart, with subsequent reductions in cardiac output and systemic arterial blood pressure, and decreased perfusion of the myocardium and gastrointestinal tract. With gastrointestinal mucosal injury and subsequent translocation of bacteria and endotoxins, the patient is predisposed to bacteremia, sepsis, and septic shock. Avulsion of the short gastric and right gastroepiploic vessels may occur and cause intraabdominal hemorrhage. The splenic veins may become thrombosed. The outcomes of these events are hypotension, hypovolemia (from blood loss, plasma loss, and increased production and sequestration of gastric secretions), hypoxemia, acid-base and electrolyte abnormalities, sepsis, myocardial dysfunction, and disseminated intravascular coagulation (DIC).

According to several published studies, certain physical examination and surgical findings, as well as laboratory test results, offer guidance regarding mortality outcomes in dogs with GDV. Because plasma/blood lactate measurements are a valuable indicator of systemic and gastric perfusion in the patient with GDV, this parameter has been used as a potential guide for identifying gastric necrosis. An earlier report indicated that a plasma/blood lactate measurement greater than 6 mmol/L was associated with a 39% incidence of gastric necrosis. This translated to a 28% to 38% postoperative mortality when gastric resection was needed, and a 32% to 38% mortality when splenectomy was performed (De Papp et al, 1999). A more recent retrospective study determined an initial lactate concentration of more than 9 mmol/L as a cut-off value for survivors versus nonsurvivors with GDV (Zacher et al, 2010). In this study there was no significant difference between initial plasma lactate concentrations for survivors (mean ± standard deviation [SD] of 10.6 ± 2.3 mmol/L) and nonsurvivors (mean ± SD of 11.2 ± 2.3 mmol/L). However, after resuscitative treatment and prior to surgery, the plasma lactate concentration was significantly lower (≤ 6.4 mmol/L), while the absolute and percentage changes in lactate concentration from baseline were significantly greater (changes of > 4.0 mmol/L and > 42.5%, respectively) in survivors compared with nonsurvivors. This study also reported that 26 of 64 dogs (41%) had gastric necrosis at the time of surgery; of these 26 dogs, 14 that underwent gastric resection were discharged from the hospital while 12 were euthanized or died during or immediately after surgery. Four dogs in this study were euthanized during the postoperative period because of deteriorating clinical status; three of these had no signs of gastric necrosis at the time of surgery (Zacher et al, 2010).

Prognosis also may be associated with splenic injury. A history of GDV signs for more than 6 hours before presentation has been associated with increased risk of gastric necrosis and requirement for splenectomy (Beck et al, 2006). The requirement for splenectomy can result in mortality rates greater than for partial gastrectomy; however, the combination of partial gastrectomy and splenectomy produced the highest mortality in two studies (Mackenzie et al, 2010; Beck et al, 2006).

The patient’s response to resuscitative therapy, as shown previously, appears to be of more value than initial lactate values in determining prognosis. The author has observed a lactate as high as 17 mmol/L in a patient with GDV, hemorrhage, and shock that within 3 hours of resuscitation returned to 3 mmol/L. This dog presented with a packed cell volume (PCV) of 35%, but with fluid resuscitation serious hemorrhage was revealed with a PCV of 15%. Whole blood was administered. Surgical exploration revealed avulsion of short gastric vessels and hemorrhage. The high lactate in this case was due to reduced oxygen delivery, not gastric necrosis. This case also highlights the importance of frequent monitoring of PCV during resuscitation. Thus, while lactate may be an indicator of prognosis in study populations, caution is required when interpreting this information to clients for a single patient. Importantly, most dogs recover from GDV with optimal preoperative, surgical, and postoperative management.

A recent prospective study investigated whether myoglobin may be a useful prognostic indicator for mortality outcome in dogs with GDV (Adamik, 2009). The cut-off value for myoglobin was 168 ng/ml, with 89% of dogs with less than this value surviving to discharge, whereas only 50% with more than this value surviving. Although these results are interesting, more prospective data are needed to determine the overall prognostic value of this test.


Clinical signs vary with the extent of GD or GDV and may not parallel the degree of gastric or splenic injury. Owners aware of the clinical signs associated with GDV may seek veterinary assistance at the onset of GD, whereas dogs left alone for several hours may present moribund. Typically dogs with GD or GDV have varying degrees of cranial abdominal distention with hypersalivation and unproductive retching. These animals are restless, dyspneic, or tachypneic and may or may not be depressed or moribund. In the early stages of GD, physical examination may reveal increased heart rate with strong pulses, normal or rapid capillary refill time, and normal mucous membrane color. In dogs with advanced GDV, weak, rapid pulses and pulse deficits can be present; mucous membranes may be pale pink to pale gray, with prolonged capillary refill time and the presence of petechiae; and the cranial abdomen may be tympanic with splenomegaly or free abdominal fluid.


The diagnosis of GDV is often obvious from the patient’s signalment and presenting clinical signs. Radiographic examination is necessary and useful if the diagnosis is equivocal or, if after decompression, surgical management may not be an option for the client (as differentiation of dilation alone from GDV will direct further management). The ability to pass an orogastric tube does not rule out the presence of volvulus.

When necessary, abdominal radiographs with the dog in right lateral recumbency are usually diagnostic, unless a 360-degree torsion is present. Evaluation of this single radiographic view initially may minimize the stress to the patient associated with obtaining multiple planes. When volvulus is present, the pylorus is visualized on a right lateral survey radiograph as a gas-filled structure dorsal and cranial to the gastric fundus. A compartmentalization line is frequently observed between the pylorus and fundus. This line represents the pyloric antral wall folding back and contacting the fundic wall. The pylorus cannot be clearly identified in a left lateral projection. Pneumoperitoneum (free air within the abdomen) may indicate gastric rupture or air leakage after gastrocentesis.

Electrocardiographic monitoring is essential in the patient with GDV because cardiac arrhythmias that require treatment (see section on Circulatory Resuscitation later) occur in many patients. Ventricular arrhythmias are the most common (Muir, 1982; Beck et al, 2006; Mackenzie et al, 2010). In addition, sinus tachycardia is almost always present in animals that present with GDV and is frequently associated with hypovolemia, pain, and anxiety.

The minimal database recommended for assessment of the patient with GDV and for diagnosing complications associated with the GDV syndrome includes evaluation of systemic arterial blood pressure; packed cell volume (PCV), total plasma solids (TS), activated clotting time (ACT) or activated partial thromboplastin time (aPTT), platelet count, white blood cell count and differential; blood urea nitrogen, glucose and lactate concentrations; serum electrolytes; and venous blood gases or total serum carbon dioxide. This information is essential to manage the patient appropriately and to optimize outcome. Early on in GD, hypochloremic alkalosis secondary to gastric sequestration may be recognized. As a result of poor systemic perfusion (with or without hemorrhage), a primary lactic acidosis also occurs, resulting in two mixed acid-base disturbances that may produce a normal pH. However, the dog eventually becomes acidemic as the syndrome advances and perfusion is jeopardized further. A complete serum biochemical profile should be submitted to identify other organ dysfunction. Although coagulation status should be assessed, serum concentration of fibrin degradation products (FDPs), PT, aPTT, and platelet count were not found to be significantly associated with development of DIC in one study (Beck et al, 2006; Bateman et al, 1999a). However, the ACT and estimated platelet count from a blood smear provided the best accuracy for point-of-care tests in diagnosing DIC in general (Bateman et al, 1999b). Because the process of DIC is dynamic, it is recommended to perform serial evaluations of ACT* every 8 hours if the results are equivocal and the patient is not improving clinically. Point-of-care testing is not very costly and greatly helps in both the diagnosis and treatment of suspected DIC (Cheng et al, 2011).

Initial Treatment

Initial treatment should be considered in light of the presenting clinical signs and the consequences of the known pathophysiologic events. The primary objectives are to (1) prevent or reverse circulatory collapse (fluid +/– colloid resuscitation), (2) prevent or reduce the local and systemic events associated with GD or GDV by removing the inciting cause (gastric decompression and lavage), (3) treat associated complications (electrolyte and acid-base abnormalities, pain, cardiac arrhythmias, and sepsis), and (4) prepare the animal for surgical treatment. For the rare patient that presents with dilation alone without evidence of circulatory compromise, orogastric decompression is the initial treatment. For the typical patient with GD/GDV, circulatory compromise or collapse is present, and reversal of the shock state should be addressed before gastric decompression. In seriously compromised patients it may be necessary to partially decompress the stomach immediately to circumvent cardiorespiratory arrest. Gastrocentesis (see section on Gastric Decompression) is recommended in these situations to avoid the stress of orogastric intubation. In these patients complete decompression should be avoided until rapid fluid resuscitation is well under way.

All patients with GDV require surgical intervention as soon as possible. Rarely, decompression may correct gastric malposition; however, surgical correction should be performed because medical management alone without surgical gastropexy results in a 75% recurrence rate.

Circulatory Resuscitation

A 14- or 16-gauge 2- to 4-inch catheter is placed into the jugular or peripheral veins. A buffered (lactate or acetate) isotonic, balanced electrolyte solution is administered at an appropriate rate based on clinical presentation. An acidifying solution such as 0.9% saline solution is chosen if the patient is alkalemic. It is essential that rate and volume be administered based on the requirements of the individual patient. Fluid overload based on a preconceived rate can result in edema and be as deleterious as administration of inadequate volumes. A recommended rate for a balanced electrolyte solution is 1.5 to 2 ml/kg/min for dogs and 0.75 to 1 ml/kg/min for cats initially if the patient is hypotensive, if the patient is normotensive but with tachycardia, or when other evidence of hypovolemia is present. The clinician should continuously monitor the patient and make adjustments to the rate and volume of fluid administration on a moment-to-moment basis based on the individual patient’s needs and response to therapy (see Chapter 1). It is important to keep in mind that tachycardia may also be due to pain; therefore in this instance fluid overload must be avoided and appropriate analgesia administered. If large fluid volumes are anticipated for resuscitation, the crystalloid volume can be reduced by up to 40% if pentastarch (Pentaspan), hetastarch (Hespan), or VetStarch (Hospira) is administered at 10 to 20 ml/kg over 15 to 30 minutes (see Chapter 2). If shock is severe, 4 ml/kg of 5% or 7.5% hypertonic saline is administered over 5 to 10 minutes, followed by the aforementioned infusions of isotonic crystalloid or synthetic colloid solution until clinical signs of shock are reversed (Web Table 3-1). The TS and PCV should be measured every 30 minutes because acute hemorrhage may not be apparent at the time of initial presentation but is unmasked during fluid resuscitation. If the PCV decreases to less than 25% or the TS decreases to less than 4.5 g/dl, whole blood, packed red blood cell, or plasma transfusion should be considered. Blood or plasma can be administered at a rate of 20 ml/kg over 1 to 2 hours, or more rapidly depending on the needs of the patient.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Chapter 3: Gastric Dilation-Volvulus

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