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Vol. 22, No.

11 November 2000

CE

Refereed Peer Review

FOCAL POINT # Improved knowledge about
the pathophysiology of acute gastric dilatation–volvulus (GDV) and recent advances in critical care services have led to more successful treatment of this condition in dogs.

Management Protocol for Acute Gastric Dilatation–Volvulus Syndrome in Dogs
University of Pennsylvania

KEY FACTS
I Restoration of intravascular volume deficits, gastric decompression, and confirmation of the diagnosis are the goals of initial emergency GDV therapy. I Because a dilated stomach can remain within the rib cage in giant-breed dogs, abdominal distention may not be seen. I Sedative and anesthetic protocols that have minimal deleterious effects on cardiovascular and respiratory system functions should be used in patients with GDV. I Persistent hypotension, hypovolemia, and hypoxia secondary to the systemic inflammatory response syndrome are the most severe complications of GDV and often result in death.

Daniel J. Brockman, BVSc David E. Holt, BVSc
ABSTRACT: Canine acute gastric dilatation–volvulus (GDV) is a potentially catastrophic condition in which emergency medical and surgical therapy and intensive postoperative care are needed to optimize the chance of a successful outcome. The events that precede an episode of GDV vary. Clinical features of the disease include restlessness; retching; and abdominal distention, discomfort, and tympany. Initial patient evaluation and treatment should be aimed at determining the degree of cardiovascular compromise and restoration of intravascular deficits by intravenous fluid administration. Dogs with GDV should receive prompt surgical attention to permit gastric decompression, removal of any devitalized tissue (e.g., stomach, spleen), and gastropexy. Intensive postoperative care is essential for dogs recovering from surgery for GDV. The majority of animals will recover without complications. Some animals, however, will develop potentially life-threatening complications. Although GDV is a challenge to treat, a good survival rate can be achieved.

G

astric dilation and gastric volvulus can occur independently,1,2 but together they represent a potentially catastrophic disease that is referred to as the gastric dilatation–volvulus syndrome (GDV). GDV is most likely a polygenic disease with strong phenotypic and environmental influences.3,4 Most episodes of GDV result from a single overwhelming factor or several combined risk factors.5 Simultaneous gastric dilation and volvulus result in pathophysiologic changes that create a medical and surgical emergency.6,7 Dogs with GDV develop local and systemic consequences that result in hypovolemia, placing them at risk for gastric and splenic vascular compromise, focal and generalized bacterial infections, initiation and propagation of local and systemic inflammation, disseminated intravascular coagulation, shock, and death.6–9 The overall incidence of GDV in dogs is low.5,8 This condition remains an important syndrome, however, because successful management requires intensive emergency, surgical, and postoperative care. Despite what some consider optimal medical management, the mortality rate for this syndrome can be as high as

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15% to 20%.8,9 Consequently, many treatment regimens have been recommended and management of GDV remains controversial. This article discusses a practical and clinically proven protocol8 for the management of this condition. A companion article will explore the pathogenesis of GDV, including an examination of recent scientific and clinical literature.

HISTORY AND CLINICAL FEATURES Gastric dilatation–volvulus syndrome occurs most commonly in large or giant, deep-chested breeds3,4 of dogs but has also been reported in small breeds.10 The onset of clinical signs is typically peracute or acute. Initial signs include restlessness, hypersalivation, and retching. These signs are usually followed by further discomfort and gradual abdominal distention. Eventually, pain becomes evident, along with weakness and abdominal tympany. Physical examination findings reflect gastric dilation and circulatory and respiratory compromise. Therefore, a distended abdomen, tachycardia, poor peripheral pulse quality, prolonged capillary refill time (CRT), pale and dry mucous membranes, tachypnea, and dyspnea may occur depending on the duration and severity of the episode. Because a dilated stomach can remain within the rib cage in giant-breed dogs, classical abdominal distention may not be seen in these breeds. MANAGEMENT OF GASTRIC DILATATION–VOLVULUS The therapeutic goals in cases of suspected acute GDV are to restore and support the circulation, decompress the stomach, establish whether GDV or simple dilation is present, perform rapid surgical correction if volvulus has occurred, and determine environmental influences that may have triggered the condition. Emergency Care Management of hypovolemia—to prevent or treat shock—is the primary goal of emergency treatment of GDV. Two large-bore catheters (ideally 16 or 18 gauge) should be placed in the cephalic or jugular veins. If a facility for rapid results is available, a blood sample should be taken for packed cell volume (PCV), serum total protein (TP) estimation, and serum electrolyte levels. Sufficient blood should also be drawn for subsequent performance of full serum chemistry, hematologic evaluation, and evaluation of coagulation parameters. Fluid therapy should be started at a rate of 90 ml/kg/ hour using a balanced electrolyte solution. In giantbreed dogs, a hypertonic saline–dextran combination (7% sodium chloride in 6% dextran-70) administered at 5 ml/kg over 5 minutes may provide more rapid ini-

tial circulatory resuscitation.11 Both the high-volume crystalloid and low-volume hypertonic saline–dextran fluid resuscitation protocols should be followed by high-volume crystalloid administration (20 ml/kg/ hour) for maintenance of resuscitation. The decision to introduce blood products or a synthetic colloid to provide further circulatory support and help improve oxygen delivery to the tissue should be influenced by subsequent PCV, TP, and circulatory stability estimations. If available, a continuous electrocardiogram (ECG) should be started or a baseline recording made. Gastric decompression should only be attempted after correction of the intravascular volume deficit is well under way. Close patient monitoring is essential. Further delay of decompression could influence gastric wall integrity and the amount of inflammatory mediators that are released from the splanchnic circulation. Gastric decompression can usually be achieved by orogastric intubation of the conscious or sedated animal. For sedation, a combination of fentanyl (2 to 4 µg/kg intravenously [IV]) or oxymorphone (0.1 mg/kg IV) followed by diazepam (0.25 to 0.5 mg/kg IV) can be used. A selection of smooth-surfaced equine nasogastric tubes with large end and side holes can be used. The tube selected should be measured from the external nares to the caudal edge of the last rib and marked. The tube should not be inserted beyond this mark. A bandage roll placed between the dog’s teeth can aid passage of the lubricated tube. If tube passage is not possible, the dog should be placed in a sitting position and the tube gently rotated in a counterclockwise direction. If orogastric intubation is still impossible, gastrocentesis—using a large-bore needle in the right or left paracostal space at the site of greatest tympany—will usually facilitate orogastric intubation and avoid inadvertent splenic damage. Routine aseptic technique should be used. The patient should be assessed frequently by collection and analysis of subjective and objective clinical data (i.e., peripheral pulse pressure and quality, heart rate, mucous membrane color, CRT, PCV and TP concentration, degree of abdominal distention, ECG). To optimize tissue perfusion and oxygen delivery, IV fluid type and composition should be tailored to the patient’s needs.

Radiography Radiography is not necessary to diagnose gastric dilation but is an invaluable aid in diagnosing volvulus.12,13 When considering the need for radiography, it is important to remember that the easy passage of an orogastric tube does not rule out volvulus. A lateral view of the cranial abdomen taken with the animal in right lateral re-

HYPOVOLEMIA I FLUID THERAPY I DECOMPRESSION I OROGASTRIC INTUBATION

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cumbency is the initial examimonitoring should be done nation of choice. 12,13 If the during anesthesia. Intraoperadiagnosis remains uncertain, tive fluids should remain at a additional radiographs (e.g., high rate (10 to 20 ml/kg/hour) ventrodorsal, left lateral) should to offset further deterioration be obtained. The radiographic in hemodynamics during features of GDV include a surgery. A catheter should be large, dilated, gas-filled gastric placed in the urinary bladder shadow, which may be divided and connected to a closed into two compartments by the urine collection system. PCV soft tissue of the lesser curvaand TP should be evaluated ture and the proximal duodeintraoperatively at 30- to 60num, which courses caudally minute intervals. Again, IV from the abnormally posifluid type and composition tioned pylorus in the cranshould be tailored to the paFigure 1—Right lateral radiograph of a dog with gastric diliodorsal quadrant of the abtient’s needs in an attempt to atation–volvulus. The gastric shadow is dilated with gas domen (Figure 1). If stomach and divided into dorsal (malpositioned pylorus) and ven- ensure adequate tissue perfurotation is not severe, the ab- tral (fundus and corpus) compartments by soft tissue of sion and oxygen delivery by normal position of the pylorus the folded lesser curvature of the stomach wall. There is maintaining a mean arterial (dorsal and to the left of the generalized intestinal dilation, suggesting ileus. The metal- blood pressure above 65 mm fundus) is diagnostically help- dense objects seen on this radiograph are the surgical sta- Hg and a hematocrit at or ful, although the pylorus may ples that remain in the peritoneal cavity following splenec- above 25% to 30%. not be visible on left lateral ra- tomy, performed 6 months before this episode. Surgical Therapy diographs. Splenic enlargeThe immediate aim of surment and malposition may be gery is to return the stomach to its normal position and evident. Gas within the gastric wall may indicate gastric evaluate it and the spleen for signs of irreversible vascuwall compromise; if gastric rupture has occurred, free gas lar compromise. Any necrotic portions of stomach and will be present in the abdominal cavity. spleen should be removed and the stomach emptied comAnesthesia pletely. Finally, a gastropexy should be performed in an In practice situations, the choice of anesthetic agents attempt to prevent recurrence of the volvulus. may be limited. If the previously mentioned sedative Following routine aseptic preparation, a cranioventral combination has been used preoperatively, endotracheal midline laparotomy should be performed. The stomach intubation may be achieved after another IV infusion is usually immediately visible and covered by greater of the same cocktail. The inclusion of IV lidocaine (2 omentum when a clockwise volvulus of 180˚ to 270˚ mg/kg) into the induction protocol will help desensitize has occurred. At this stage, gastric decompression will the larynx and facilitate endotracheal intubation as well help subsequent manipulation and relocation of the as enhance the overall state of anesthesia. In addition, if stomach. This can be achieved intraoperatively by neea different induction agent is to be used, the quantity dle gastrocentesis if the stomach is still tightly distendrequired will be reduced because of residual effects of ed. Alternatively, for a less distended stomach, an assisthe sedative. Circulatory compromise will influence the tant (with the intraoperative guidance of the surgeon) speed and efficiency of drug distribution. Because IV can gently place an orogastric tube. After decompresaccess should already be established, small amounts of sion, the pylorus should be identified and grasped geninduction agent should be given to effect. Maintenance tly with the hand. If the gastric rotation is in a clockshould be with halothane or isoflurane and oxygen. Niwise direction, downward pressure on the right side of trous oxide should not be introduced until permanent the visible portion of the stomach along with gentle gastric decompression is achieved. traction on the pylorus will aid counterclockwise rotaThe placement of additional IV and intraarterial tion. The spleen should follow passively. Systematic catheters in the pelvic limbs following the induction of evaluation of the abdomen should then be performed. anesthesia will facilitate intraoperative blood pressure Hemoperitoneum often results from avulsion of the monitoring and the addition of blood products (e.g., to short gastric branches of the splenic arteries. Active sites the intraoperative fluid therapy regimen). Continuous of hemorrhage should be identified and ligated. Careful ECG and continuous or intermittent blood pressure inspection of the stomach and spleen should be perPROXIMAL DUODENUM I SPLEEN I GASTROPEXY I LAPAROTOMY

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formed. If all organs look The cardia or the abdominal grossly normal, an assistant esophagus will occasionally should lavage the stomach usbecome necrotic secondary to ing clean, warm water via the longstanding or severe twistorogastric tube. ing; therefore, this area should The junction between the be examined carefully. Resecfundus and body along the tion of the abdominal esophagreater curvature of the stomgus and gastric cardia can be ach is the most common site technically demanding, and of gastric necrosis following the outcome following such a GDV.14 Evaluation of tissue resection, even in healthy aniblood flow remains subjecmals, is unknown. Because tive; however, gentle palpanecrosis at this site is usually Figure 2—Partial gastric resection using stapling equiption for pulsation in the gasseen in animals that are already ment. The stomach has undergone spontaneous perfortric and splenic vessels can be ation. The demarcation between viable and nonviable severely compromised, the helpful. If the serosal surface tissue (blackened area being removed) is clear. Despite prognosis for recovery is poor. is either torn, gray–green, or successful partial gastric resection, this patient subseThe spleen can sustain vasblack 10 minutes after ana- quently died of systemic inflammatory disease. cular damage or occlusion tomic reduction of the stomfollowing GDV. The spleen ach, ischemia should be susand associated vasculature pected and subsequent tissue should, therefore, be carefully necrosis anticipated (Figure evaluated for the presence of 2). In these situations, resecthrombi and irreversible vastion of the affected portion of cular compromise. Any devithe stomach should be pertalized portion of splenic tisformed. It may be difficult to sue should be resected either determine how much of the by hand or using a surgical stomach to remove. A fullstapling device (Figure 3). If thickness gastric wall resecthe spleen has undergone tortion is carried out until the sion around its pedicle, splecut edges are actively bleeding nectomy should be performed to ensure healing without furbefore reducing the twist to Figure 3—Partial splenic infarction in a patient with gastric lessen the risk of releasing toxther necrosis. Closure of the stomach fol- dilatation–volvulus. The demarcation between viable and ins, myocardial active sublowing partial resection should nonviable splenic tissue is indicated by a color change. The stances, and thromboemboli be in two or three layers. A vascular pedicle at the ventral extremity of the spleen is into the systemic circulation. simple continuous suture pat- torn and partially avulsed from the hilus. Partial splenectoA gastropexy should be pertern in the submucosa should my was performed, and the dog recovered. formed.16–20 Tube gastropexy is easy to perform, creates strong be followed by a simple interadhesions, and has the additional advantage of providrupted pattern in the muscularis and serosa. Oversewing ing enteral access.20 A large (24 or 26 gauge) Foley or the suture line with a continuous or interrupted invertPezzer’s urologic catheter is placed through a stab inciing pattern (e.g., Cushing, Lembert) can reinforce this sion in the body wall approximately 2 cm lateral to the closure. Polydioxanone, polyglactin 910, polyglycolic ventral midline and 2 cm caudal to the last rib on the acid and polyglyconate are all suitable suture materials. right side. The catheter is then passed through a loop of Alternatively, surgical stapling devices can be used to peromentum and into the stomach via a purse-string suture form partial gastric resection. The use of a GI anastomothrough a small incision in the pyloric antrum. The balsis instrument (GIA-50, US Surgical, Norwalk, CT) has loon on the Foley catheter is then inflated but kept away been described for this purpose15; however, we prefer to use a thoracoabdominal stapler (TA-90, US Surgical) from the stomach wall to avoid inadvertent puncture with a 4.8-mm (green) staple cartridge. Again, this clowhile pexy sutures of polypropylene are preplaced sure should be reinforced using a continuous or interaround the abdominal and gastric wall incisions in an rupted Cushing or Lembert inverting pattern to oversew overlapping mattress pattern. The sutures are then tied the staple line. and the balloon or mushroom tip drawn up to the
NECROSIS I PARTIAL GASTRIC RESECTION I FOLEY CATHETER

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be kept clean and protected by a bandage. After removal of the tube, the gastrostomy is left to heal by second intention. Clients should be informed of the signs of recurrence and encouraged to seek veterinary attention as soon as possible if these signs occur.
Figure 4—Electrocardiogram (top) and direct arterial pressure trace (bottom) from a 5-year-old spayed Great Dane recovering from gastric dilatation– volvulus, 1 day after surgery. During the early (rapid) phase of this multiform ventricular tachycardia, there is disparity between the ventricular depolarization and ejection rates. The pulses formed, however, are strong and adequate. This arrhythmia does not require treatment if all other aspects of patient care are appropriately managed.

stomach wall and the tube is secured with either a Chinese finger trap suture or tape tabs sutured to the skin. Alternatively, an incisional gastropexy is simple and effective.21 With this technique, a 5-cm seromuscular incision is made in the pyloric antrum, and a matching incision is made in the parietal peritoneum and transverse abdominal muscle, just caudal to the 13th rib on the right body wall. The edges of the gastric wall incision are sutured to the edges of the body wall incision using either polydioxanone or polypropylene. Care must be taken not to penetrate the gastric lumen. Closure of the abdominal incision is routine. A bandage is placed around the abdomen to protect a gastropexy tube.

Postoperative Care Fluid therapy should be maintained at a rate of 8 to 10 ml/kg/hour using a balanced electrolyte solution for the first 24 hours. Systemic administration of opioid analgesics (e.g., intramuscular morphine at 0.5 mg/kg every 4 to 6 hours) will reduce postoperative discomfort and facilitate recovery. During this period, it is useful to monitor PCV and TP intermittently; peripheral pulse quality, mucous membrane color, and urine output should also be monitored. Again, continuous ECG should be used if available or intermittent records made. The stomach tube, if present, should be vented as needed. Nothing should be given by mouth. If complications do not occur, water can be offered the second day after surgery and the IV fluid rate reduced to 4 ml/kg/hour. Patient comfort level should be assessed and additional analgesia provided as needed. Small amounts of food can be offered by the end of the second postoperative day. Animals that have undergone partial gastrectomy may take longer to regain normal gastric motility. IV metoclopramide (1 to 2 mg/kg/day) or low-dose oral erythromycin (0.5 to 1.0 mg/kg every 8 hours oral) might be beneficial.22,23 The gastropexy tube should remain in place for 7 to 10 days. It should

POSTOPERATIVE COMPLICATIONS Persistent hypotension may be suspected if peripheral pulse quality is poor, tachycardia and poor CRT are evident, and urine output is low. This hypotension is usually caused by hypovolemia secondary to inadequate fluid therapy following surgery. Hypotension may also develop if the IV crystalloid fluid therapy is failing because of inadequate primary surgical hemostasis, subsequent whole blood deficits, reduced colloid osmotic pressure, or abnormal body fluid distribution. Occasionally, hypotension in post-GDV surgery patients is caused by poor cardiac function. If PCV and TP levels reveal hemoconcentration, a return to high-volume, rapid crystalloid infusion may be necessary for a short time (i.e., 1 hour at 90 ml/kg) followed by a return to 10 to 15 ml/kg/hour. If PCV or TP is low, blood products or synthetic colloid should be administered to correct the deficit(s). The patient should be reevaluated frequently following any change in fluid therapy. Cardiac arrhythmias are common following an acute episode of GDV.8,9,24 They are usually ventricular in origin and range from intermittent ventricular premature conductions to sustained ventricular tachycardia. Supraventricular abnormalities (e.g., atrial fibrillation) are occasionally seen.9,25 Cardiac arrhythmias may need to be treated if they are associated with primary heart disease (e.g., dilated cardiomyopathy) or if there is evidence of poor cardiac performance. If continuous ECG and simultaneous blood pressure monitoring are available, a decision about cardiac function with regard to arrhythmia is relatively easy (Figure 4). An attempt to abolish a cardiac arrhythmia that is associated with hypotension using antiarrhythmic drugs is considered only if acid– base and electrolyte imbalances have been corrected and intravascular volume replenishment is adequate. The most common complications of tube gastropexy are local cellulitis caused by leakage of gastric contents around the tube or premature tube dislodgment.18 Occasionally, the balloon of a Foley catheter can be eroded by the acidic gastric fluid, causing early loosening of the tube. Usually this occurs after 5 to 7 days, as the animal becomes more active, and will spontaneously resolve. If it occurs in the first 48 hours, the risk of peritonitis secondary to leakage of gastric contents mandates tube replacement with the patient under general anesthesia.

HYPOTENSION I CRYSTALLOID INFUSION I CARDIAC ARRHYTHMIAS

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Preoperative retching and vomiting, and postoperative esophagitis and regurgitation put these animals at risk for aspiration pneumonia.8 Alterations in breathing rate and pattern coupled with crackles and wheezes on thoracic auscultation are suggestive of pneumonia. Thoracic radiography, arterial blood gas evaluation, and tracheal/bronchoalveolar wash fluid cytology and culture will help confirm this diagnosis. Treatment with the appropriate antibiotic(s), local fluid therapy (nebulization), thoracic coupage, supplemental oxygen, and frequent short periods of exercise should aid recovery. Gastric necrosis and perforation can occur up to 5 days after surgery, especially if resection was performed and despite careful intraoperative assessment of gastric wall viability.14,15 Although this complication may be difficult to confirm without surgical exploration of the abdomen, it may be suspected on the basis of clinical progression of disease, radiographic and ultrasonographic findings, and cytologic evaluation of peritoneal fluid. Treatment is by debridement and repair of the gastric wall defect followed by continued intensive supportive care. If gastric necrosis and perforation occur, the prognosis is grave. Persistent ongoing hypotension, despite appropriate fluid therapy, is a serious concern. Serum electrolyte concentrations (i.e., sodium, potassium, chloride, magnesium, calcium) should be measured, coagulation parameters assessed, acid–base status evaluated, and blood gas levels determined before further altering therapy. Electrolyte abnormalities should be corrected. An abnormal hemostatic profile or a clinical bleeding tendency should be interpreted as evidence of disseminated intravascular coagulation. Replacement of consumed coagulation factors using fresh-frozen plasma should be considered in addition to continued therapy for the underlying cause of shock. Hypoxemia may occur secondary to pneumonia or pulmonary edema. Pulmonary edema may develop secondary to overzealous IV fluid administration, primary cardiac dysfunction, or reduced colloid osmotic pressure or following acute lung injury as a component of the systemic inflammatory response syndrome. In turn, the systemic inflammatory response syndrome can be triggered by several factors, including endotoxemia, organ reperfusion injury, and local inflammatory conditions (e.g., peritonitis, pneumonia, pancreatitis). Thoracic and abdominal radiography, cardiac and abdominal ultrasonography, abdominocentesis, tracheal/ bronchoalveolar wash sample cytology and culture, and further hematologic and serum chemistry evaluation should be considered to assist future therapeutic decision making. Persistent hypovolemia despite aggressive fluid therapy and the development of pulmonary comTHORACIC RADIOGRAPHY I GASTRIC WALL

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plications in which systemic inflammation is suspected are poor prognostic signs. Therapy for such patients may include oxygen supplementation and ventilator-assisted breathing as well as continued intensive circulatory support. The prognosis for animals with these complications is poor.

REFERENCES
1. Andrews AH: A study of ten cases of gastric torsion in the bloodhound. Vet Rec 86:689–693, 1970. 2. Betts CW, Wingfield WE, Green RW: A retrospective study of gastric dilatation–torsion in the dog. J Small Anim Pract 15:727–734, 1974. 3. Glickman LT, Glickman NW, Pérez CM, et al: Analysis of risk factors for gastric dilatation and dilatation–volvulus in dogs. JAVMA 204(9):1465–1471, 1994. 4. Glickman LT, Glickman NW, Schellenberg MS, et al: Multiple risk factors for the gastric dilatation–volvulus syndrome in dogs: A practitioner/owner case-control study. JAAHA 33: 197–204, 1997. 5. Strombeck DR: Small Animal Gastroenterology, Davis, CA, Stonegate, 1990, pp 228–243. 6. Orton EC, Muir WM: Hemodynamics during experimental gastric dilatation–volvulus in dogs. Am J Vet Res 44(8):1512– 1515, 1983. 7. Horne WA, Gilmore DR, Dietze AE, et al. Effects of gastric distention–volvulus on coronary blood flow and myocardial oxygen consumption in the dog. Am J Vet Res 46, 1:98–104, 1985. 8. Brockman DJ, Washabau RJ, Drobatz KJ: Canine gastric dilatation–volvulus syndrome in a veterinary critical care unit: 295 cases (1986–1992). JAVMA 207:460–464, 1995. 9. Brourman JD, Schertel ER, Allen DA, et al: Factors associated with perioperative mortality in dogs with surgically managed gastric dilatation–volvulus: 137 cases (1988–1993). JAVMA 208(11):1855–1858, 1996. 10. Thomas RE: Gastric dilatation and torsion in small or miniature breeds of dogs—Three case reports. J Small Anim Pract 23:271–277, 1982. 11. Schertel ER, Allen DA, Muir WW, et al: Evaluation of a hypertonic saline-dextran solution for treatment of dogs with shock induced by gastric dilatation–volvulus. JAVMA 210: 226–230, 1997. 12. Hathcock JT: Radiographic view of choice for the diagnosis of gastric volvulus: The right lateral recumbent view. JAAHA 20:967–969, 1984. 13. Kneller SK: Radiographic interpretation of the gastric dilatation–volvulus complex in the dog. JAAHA 12:154–157, 1976.

14. Matthiesen DT: Partial gastrectomy as treatment of gastric volvulus: Results in 30 dogs. Vet Surg 14(3):185–193, 1985. 15. Clark GN, Pavletic MM: Partial gastrectomy with an automatic stapling instrument for treatment of gastric necrosis secondary to gastric dilatation–volvulus. Vet Surg 20:61–68, 1991. 16. Whitney WO, Scavelli TD, Matthiesen DT, Burk RL: Belt loop gastropexy: Technique and surgical results in 20 dogs. JAAHA 25:75–83, 1989. 17. Schulman AJ, Lusk R, Lippincott CC, Ettinger SJ: Muscular flap gastropexy: A new surgical technique to prevent recurrences of gastric dilatation–volvulus syndrome. JAAHA 22: 339–346, 1986. 18. Parks JL, Green RW: Tube gastrostomy for the treatment of gastric volvulus. JAAHA 12:168–172, 1976. 19. Frendin J, Funquist B: Fundic gastropexy for the prevention of gastric volvulus. J Small Anim Pract 31:78–82, 1990. 20. Fallah AM, Lumb WV, Nelson AW, et al: Circumcostal gastropexy in the dog—A preliminary study. Vet Surg 11:9–12, 1982. 21. MaCoy DM, Sykes GP, Hoffer RE, Harvey HJ: A gastropexy technique for permanent fixation of the pyloric antrum. JAAHA 18:763–768, 1982. 22. Peeters T, Matthijs G, Depoortere I, et al: Erythromycin is a motilin receptor agonist. Am J Physiol 20:G470–G474, 1989. 23. Mangel AW, Stavorski JR, Pendleton RG: Effects of bethanecol, metaclopromide, and dromperidone on antral contractions in cats and dogs. Digestion 28:205–209, 1983. 24. Muir WW, Lipowitz AJ: Cardiac dysrhythmias associated with gastric dilatation–volvulus in the dog. JAVMA 172:683– 689, 1978. 25. Muir WW, Bonagura JD: Treatment of cardiac arrhythmias in dogs with gastric distension–volvulus. JAVMA 11:1366– 1371, 1984.

About the Authors
When this article was submitted for publication, Drs. Brockman and Holt were affiliated with the Department of Clinical Sciences and the Center for Veterinary Critical Care, School of Veterinary Medicine, University of Pennsylvania, Philadelphia. Dr. Brockman is now affiliated with the Department of Small Animal Medicine and Surgery, The Royal Veterinary College, University of London. Both are Diplomates of the American College of Veterinary Surgeons. Dr. Brockman is also a Diplomate of the European College of Veterinary Surgeons.