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Successful stabilization of the patient with gastric dilatation-volvulus (Proceedings)


Gastric dilatation and volvulus syndrome (GDV) is a life-threatening condition primarily affecting large breed dogs.

Background information, risk factors, and pathophysiology

Gastric dilatation and volvulus syndrome (GDV) is a life-threatening condition primarily affecting large breed dogs. Distension and rotation of the stomach leads to compromised gastric perfusion and obstruction of the caudal vena cava. Sequestration of blood in the splanchic and skeletal muscle beds as well as hemorrhage from torn gastric vessels leads to a state of hypovolemic shock. Without aggressive medical and surgical intervention, the condition is generally fatal. GDV is a very common condition affecting approximately 60,000 dogs per year in the US with mortality rates ranging from 10-60% (overall mortality is much closer to the 10% range).1 Much research interest has focused on identification of risk factors for GDV such that prophylactic measures may be instituted to try to prevent the occurrence of the problem. Presently, the following factors have been identified:

  • Age: Older dogs are more likely to develop GDV than younger dogs.

  • Pure-Breed status: Dogs of pure breeding are 4.4 times more likely to develop GDV than mongrel dogs.

  • Size / Conformation: An increased thoracic depth to width ratio has been associated with an increased risk of developing GDV. This parallels clinical observations that GDV occurs with greater frequency in large, deep chested dogs.

  • First-degree relative with a history of GDV

  • Faster speed of eating

  • Stress

Overall, risk of developing GDV is likely a result of a complex interplay between age, genetic, conformational, environmental, and behavioral factors.

Initial stabilization

Initial stabilization of the dog presenting with suspected GDV should focus on the treatment of hypovolemic shock (decreased oxygen delivery to the tissues due to inadequate circulating volume). Oxygen therapy should be administered initially by mask or flow-by techniques while venous access (14-18g) is acquired via the cephalic veins. Hind-limb catheters should be avoided due to the decreased venous return from the caudal vena cava seen in dogs with GDV. From the catheter, a PCV / TS / Blood Glucose / Venous Blood Gas (Emergency Database) should be collected. If possible, an entire CBC and Serum Biochemical Profile should be drawn prior to fluid therapy. Baseline physiologic data in addition to those gained through major body systems assessment should be collected. These include blood pressure, ECG, and pulse oximetry reading (SpO2).

Assuming that there is no contraindication to aggressive fluid support, (such as history of cardiomyopathy) volume resuscitation should commence with isotonic crystalloid solutions (LRS, Normosol-R, Saline). A shock rate of fluids (90 ml/kg/hr) should be calculated and then administered to effect. The authors prefer administer shock rates of fluids in increments of approximately ¼ of the calculated dose, reassessing major body systems after each bolus. It is important to remember that the endpoint of fluid therapy should be the normalization of vital signs, not the administration of some arbitrary volume. Some dogs may not need the entire 90ml/Kg, while others will need significantly more.

When rapid or small-volume resuscitation is needed, colloids and/or hypertonic saline may be considered. Colloids have the advantage of being retained in the vascular space for longer than crystalloids, allowing for smaller administered volumes. Hetastarch, a synthetic colloid, may be administered for this purpose at a dose of 10-20 ml/kg. Alternately, the following technique may be utilized. In a 60ml syringe, draw up 43ml of synthetic colloid and 17ml of 23% hypertonic saline. Administer at a dose of 5ml/Kg no faster than 1ml/Kg/min. This resuscitation option has the main advantage of speed. The osmotic effect of the hypertonic saline and the oncotic effect of the synthetic colloid will restore intravascular volume extremely rapidly. Additional crystalloid fluids may then be continued as needed.

Gastric decompression should be considered once volume resuscitation is underway. The authors prefer a combination of trocharization and orogastric intubation. Trocharization is performed using an 18g needle or 16-18g over-the-needle intravenous catheter placed transabdominally into the stomach. Anatomically in GDV, the fundus will most often be located on the right side. Palpation for gas distention, will help identify the optimal location for trochar placement. It is important to avoid the often-distended spleen while placing the trochar catheter. Trocharization has the advantage of being quick and easy to perform with minimal risks. It is not stressful and does not require sedation. Disadvantages of trocharization are the risk of puncturing another abdominal structure of importance (spleen), and inability to evacuate liquid and food material from the stomach.

Orogastric intubation is indicated once the patient is more stable. Orogastric intubation has the advantages of being able to completely decompress the stomach and to lavage out any food material within. The primary disadvantages of this technique are the high degree of stress associated with orogastric intubation (often requiring sedation) and the risk of esophageal or gastric injury. During lavage, aspiration pneumonia is a significant risk. Orogastric intubation should be performed using a tube appropriate for the size of the patient, well-lubricated, and measured from the mouth to the last rib. A piece of tape as a marker will ensure that the tube is not advanced too far into the patient. A mouth gag is required (2-3inch PVC tubing works well) to prevent trauma to your orogastric tube. Once the stomach is entered and the gas decompressed, lavage of the stomach with warm water is indicated. For patient safety, the authors prefer to endotracheally intubate the patient if gastric lavage is to be performed. This makes sense logistically as well, since the patient will be proceeding directly to surgery following decompression.

A dose of broad spectrum antibiotics is indicated early in the course of therapy and should be continues through surgical intervention and beyond if specific indications exist.


Abdominal radiography is indicated for the definitive diagnosis and differentiation of gastric dilatation (GD) from GDV. Ideally, radiographs should precede decompression to maximize chances of obtaining an accurate diagnosis. However, if stability has not been achieved with fluid therapy, gastric decompression should be performed first to ensure patient survival.

Right lateral abdominal radiographs should be performed. The radiographic sign most consistent with GDV is compartmentalization of the stomach and displacement of the pyloric antrum dorsally. Other radiographic signs of note are gas within the stomach wall (indicating gastric necrosis), free peritoneal gas (most likely indicating gastric perforation), loss of abdominal detail (from peritonitis or bleeding from the short gastric arteries) and splenomegally (indicating splenic torsion or possibly splenic venous thrombosis). Most dogs with GD and GDV will not tolerate VD views well and such projections could compromise patient stability. In dogs that are older than 7 years of age, opposite lateral radiographic views of the thorax should be obtained to identify concurrent illnesses such as heart disease or neoplasia.

Anesthesia for dogs with GDV

Anesthetic protocols for dogs with GDV should involve the utilization of drugs that are sparing of the cardiovascular system. Pre-oxygenation prior to induction is indicated in any critically ill patient undergoing an anesthetic procedure. Placement of an ECG, pulse oximeter, and oscillometric blood pressure monitor will facilitate monitoring during induction. Two appropriate induction protocols are as follows:

Hydromorphone (.1 – .2mg/Kg)/ Midazolam (.2mg/Kg)/ Lidocainei (1-2mg/Kg)


Ketamine (100mg/ml)/ Valium (5mg/ml) Give 1cc/20lbs body weight of a 50:50 volume mixture. Example: A 100lb Great Dane would receive a total of 5cc (or 2.5ml of Ketamine and 2.5ml of valium). The addition of an analgesic agent (narcotic) is indicated if this protocol is chosen.

Some patients will require less than the aforementioned doses and some will require more. Ongoing monitoring of oxygen saturation, ECG, and blood pressure are indicated throughout surgery. Even if the patient is breathing spontaneously, ventilation may not be effective and intermittent positive pressure breaths should be administered. Fluid therapy should be considered at approximately 10-20ml/Kg/hr or as needed to maintain intravascular volume and blood pressure.

Surgical management

Surgical goals in dogs with GDV should include replacement of the stomach into its normal anatomic location, control of hemorrhage, resection of areas of necrosis or suspected necrosis, splenectomy if indicated, and finally gastropexy. It is crucial to perform a complete abdominal exploratory in dogs with GDV and the abdominal incision should extend from xyphoid all the way to the pubis. Understanding the anatomy of GDV is crucial to restoring the stomach to its normal position. The most common direction of rotation is clockwise. When viewed from a caudal to cranial direction with the patient in ventro-dorsal recumbency, the pylorus has moved from the right side of the abdomen to the left side of the abdomen while tracking along the ventral abdominal wall. Clockwise rotation will result in the omentum being pulled over the stomach. Upon opening the abdomen, identification of the omentum over the stomach is an indication of a clockwise rotation. Complete gastric decompression will facilitate relocation of the stomach.

Hemorrhage commonly originates from torn short gastric arteries and gastric necrosis is most commonly identified along the greater curvature and up along the cardia of the stomach. Be sure to examine all sides of the stomach as necrosis is commonly found on the underside of the stomach as it is viewed from the surgical incision. Gastric resection should be performed using a two-layer technique (the outermost layer being inverting). If a surgical stapling device is used for gastric resection, the staple line should be oversewn with an inverting pattern. Splenic torsion or thrombosis is an indication for resection. If the spleen is torsed, it should NOT be de-rotated prior to removal.

Numerous methods for gastropexy (pyloric antrum to right abdominal wall) have been evaluated and despite differences in tensile strength evaluated in-vitro, incidence of recurrence has not been found to be significantly different between the various methods. Unacceptable methods for gastropexy include suturing the stomach into the abdominal closure line, and methods that do not involve an incision in the seromuscular layer of the stomach (simply scarifying the stomach and the right abdominal wall and suturing the two together). The authors prefer the incisional gastropexy in which an incision in the seromuscular layer of the stomach is sewn to an incision in the right body wall due to its ease and the speed with which it can be performed. A tube gastropexy has the advantage of allowing postoperative feeding and gastric decompression.

Postoperative management and complications

Of greatest importance to the postoperative management of the dog with GDV, is the maintenance of appropriate delivery of oxygen to the tissues. Oxygen support in the immediate postoperative period will minimize the chance of bouts of arterial oxygen desaturation. If the patient is not saturating > 94% on oxygen support, or if there is increased respiratory rate and effort or abnormal lung sounds on auscultation of the thorax, thoracic radiographs are indicated to help identify the complicating process (pneumonia).

Volume support should be directed to replace deficits, provide for maintenance, and to balance out ongoing losses. It is not uncommon for patients to return from the surgical theater and require a bolus of fluids due to increased losses during surgery. Synthetic colloids (hetastarch) are indicated at 20ml/Kg/24hrs in cases in which ongoing intravascular volume support is necessary, or peripheral edema is developing.

Pain control is critical in the postoperative GDV patient. Pure opioid agonists such as fentanyl (CRI: 3-5 ug/kg/hr), hydromorphone (0.1-0.2 mg/kg IV q4h, or CRI: 0.025 mg/kg/hr), or morphine (0.5-1 mg/kg SQ q4h) for patients with moderate to severe pain. Ketamine can be useful for the relief of somatic pain, and may be used in conjunction with narcotics at a constant rate infusion of 0.15-0.6 mg/kg/hr. Lidocaine may provide adjunctive analgesia in addition to free radical scavenging properties, and may also be added at a rate of 1.5-3 mg/kg/hr. If using constant rate infusions, a loading dose equal to the hourly rate should initially be administered.

Ventricular arrhythmias are common after GDV. Irritable ventricular foci likely develop due to decreased delivery of oxygen to the heart during shock, ongoing decreased oxygen delivery to the heart postoperatively, ischemia reperfusion injury, and electrolyte and acid-base disorders. Numerous recommendations exist as to when to institute treatment for these arrhythmias. Guidelines to consider prior to pharmacologic intervention are as follows:

1. Correct hypoxemia. SpO2 should read greater than 95%

2. Restore euvolemia and blood pressure to normal

3. Correct acid-base and electrolyte abnormalities

4. Provide appropriate analgesia

If arrhythmias persist at an overall heart rate of greater than 140-160bpm, pharmacologic intervention in the form of lidocaine (2mg/Kg IV repeated once if necessary and followed by 50-80μg/Kg/min CRI ) will likely solve the problem.

Many dogs with GDV are predisposed to developing dilutional coagulopathy and consumptive coagulopathy. Assessment of a coagulation profile or, at minimum, an activated clotting time (ACT) will direct the need for clotting factor support in the form of fresh frozen plasma. Vitamin K1 will NOT be useful in the coagulopathy seen in dogs with GDV because GDV is not a process that antagonizes Vitamin K1 recycling or absorption from the gastrointestinal system.

If an area of gastric necrosis was missed at the time of surgery or a resection site breaks down, signs of peritonitis may develop approximately 48-72 hrs (up to 7 days) postoperatively. Twice daily, patients should have abdominal palpation performed by the same individual to evaluate for abdominal pain. Abdominal pain, fever, or failure to thrive postoperatively is an indication for abdominocentesis and cytologic evaluation.

The final common postoperative complication of GDV is decreased gastric motility. The authors find this to be most common in the most critically ill of patients (generally those that had evidence of gastric necrosis). Placement of a nasogastric tube at the time of surgery, or using a tube gastropexy allows for gastric decompression and will minimize the likelihood of regurgitation, vomiting, and subsequent aspiration pneumonia. In addition, early "trickle" feeding can be instituted to begin nutrient delivery to the stomach and small intestine. Use of motility agents like metoclopramide can be used to help combat this complication.


Over the years, numerous studies have tried to identify prognostic factors for dogs with GDV. To date, the most substantiated of these are the presence or absence of gastric necrosis, and the blood lactate concentration prior to fluid therapy (often gleaned from the venous blood gas). In one study, 98% of dogs without gastric necrosis survived and only 66% of those with gastric necrosis survived.These were the highest survival statistics reported to date. Gastric necrosis does not necessarily cause mortality, but more likely, it is a marker for more severe compromise to the major body systems, and a more critically ill patient. In the same study, 99% of dogs with a blood lactate <6.0mmol/L prior to fluid therapy survived and only 58% of those with a blood lactate >6.0mmol/L prior to fluid therapy survived.Lactate is a marker of anaerobic glycolysis (as occurs when decreased oxygen is delivered to the tissues) and has been found to be prognostic for numerous human medical and surgical problems.


1. Aronson LR, Brockman DJ, Crown DC. Gastrointestinal Emergencies. Vet Clin N Amer Sm Anim Pract 2000;30:558-569

2. Burrows CF, Ignaszewski LA. Canine gastric dilatation-volvulus. J Small Anim Pract 1990;31: 495.

3. Schaible RH, Ziech J, Glickman NW et al. Predisposition to gastric dilatation-volvulus in relation to genetics of thoracic conformation in Irish setters. J Am Anim Hosp Assoc 1997;33: 379.

4. Glickman LT, Glickman NW, Schellenberg DB et al. Non-dietary risk factors for gastric dilatation-volvulus in large and giant breed dogs. J Am Vet Med Assoc 2000;10: 1492-1499

5. Glickman-LT; Glickman-NW; Schellenberg-DB et al. Multiple risk factors for the gastric dilatation-volvulus syndrome in dogs: a practitioner/owner case-control study. J Am Anim Hosp Assoc 1997;33: 197-204.

6. dePapp E, Drobatz KJ Hughes D. Plasma lactate concentration as a predictor of gastric necrosis and survival among dogs with gastric dilatation-volvulus: 102 cases (1995-1998). J Am Vet Med Assoc 1999;215: 49-52.

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