Canine-pathogenesis Of Acute Canine Gastric Dilatation-volvulus Syndrom

Vol. 22, No. 12 December 2000

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Refereed Peer Review

FOCAL POINT ★The pathogenesis of canine gastric dilatation-volvulus (GDV) remains a complex multifactorial event that probably differs from patient to patient, but two discrete pathogenetic mechanisms are likely to give rise to this syndrome.

KEY FACTS ■ The pathogenesis of GDV remains complex and poorly understood. ■ Although the precise mechanism of gastric volvulus remains unclear, several intrinsic and extrinsic risk factors have been identified. ■ Failure of the normal eructation and pyloric outflow mechanisms is a fundamental prerequisite for the development of gastric dilation. ■ Whether gastric volvulus consistently precedes or follows gastric dilation is unclear, but both scenarios seem plausible and likely.

Pathogenesis of Acute Canine Gastric Dilatation–Volvulus Syndrome: Is There a Unifying Hypothesis?* University of Pennsylvania

Daniel J. Brockman, BVSc David E. Holt, BVSc. Robert J Washabau, VMD, PhD ABSTRACT: A single etiologic agent in the pathogenesis of acute canine gastric dilatationvolvulus (GDV) has not yet been identified. Several extrinsic physical and environmental risk factors have been identified, and many more intrinsic anatomic or pathologic risk factors are suspected. Many of the proposed intrinsic factors currently lack scientific evidence, and it may be impossible to substantiate these factors. Normal eructation, vomiting, or pyloric outflow mechanisms appear to fail when gastric dilation occurs. Whether volvulus consistently precedes or follows dilation is unclear. This paper explores the known risk factors for GDV and proposes a hypothesis to explain its pathogenesis.

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uch has been learned about the pathophysiology and clinical management of canine acute gastric dilatation–volvulus (GDV), but a unifying hypothesis for the pathogenesis of this syndrome has not yet been elucidated. Several theories have been proposed, but most do not readily explain all clinical findings. A unifying hypothesis must be capable of answering or addressing several important questions: Why are large- and giant-breed dogs at greater risk than are small breeds? If body size and thoracoabdominal dimensions are important factors, why is GDV not more common in relevant breeds? If volvulus is believed to be the initiating event, why are some animals observed with dilation alone? If volvulus induces obstruction and dilation, why do some animals occasionally *A companion article entitled “Management Protocol for Acute Gastric Dilatation– Volvulus Syndrome in Dogs” appeared in the November 2000 (Vol. 22 No. 11) issue of Compendium.

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present with chronic volvulus but without dilation? Why are certain breeds more affected than are others? Are there genetic influences, or do differences in feeding practices or other environmental factors play a role in this syndrome? This paper reviews the relevant intrinsic and extrinsic factors that have been proposed to determine whether a single unifying hypothesis can explain the pathogenesis of GDV.

INTRINSIC FACTORS Body Size Acute canine GDV is predominantly a disease of large body conformation.1 Small dogs appear only sporadically in the large case studies and single case reports describing this condition2–4; therefore, anatomic and genetic features are assumed to predispose large- and giant-breed dogs to this condition. Thoracoabdominal Dimensions Risk factor analysis supports the notion that thoracic conformation is an important factor in the development of GDV. Studies have shown that increased thoracic depth:width ratios are associated with increased risk of development of this syndrome within certain breeds.5,6 Those studies caused further speculation that selective breeding against deep-chest conformation would decrease the prevalence of GDV within breeds.5,6 Despite the apparent association, it is unclear how thoracic and abdominal dimensions influence the development of GDV. Accentuated thoracic and abdominal dimensions have been suggested to play a permissive or active role in the initiation of GDV by virtue of altered position of the gastric cardia.7 Although a relationship between thoracoabdominal conformation and GDV has been identified, the mechanism of its influence is unclear. Gastric Ligament Laxity The canine stomach has evolved to accommodate varying meal size and frequency and, therefore, varying degrees of distention. Gastric ligaments (i.e., lesser omental, greater omental, mesoduodenal) hold the stomach loosely in position to accommodate changes in gastric volume and muscular activity. Despite this anatomic configuration, gastric ligaments do not prevent clockwise rotation of the stomach in canine cadavers or in experimental animals.8,9 Thus laxity of gastric ligaments appears to be sufficient to permit gastric rotation even in healthy dogs. In addition, dogs with GDV may have reduced ability to resolve gastric rotation10 based on the observation that the stomachs of dogs that have had GDV maintain the same clockwise-rotated position. In contrast, the

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stomachs of dogs that have not had GDV return to a normal position after such a rotation.10 More recently, the hepatogastric ligaments of dogs with GDV were shown to be longer than were non-GDV size- and weight-matched controls.11 Abnormalities (e.g., length, elasticity) may contribute to episodes of GDV, but this has not yet been shown in the pre-GDV state.

Gastric Volume Once-daily feedings were found to be a predisposing risk factor for the development of gastric dilation (GD) in Irish setters.12 Once-daily feedings may induce increases in intragastric volume in this breed when compared with three-times-daily feeding.13 Whether or how gastric volume influences the occurrence of GDV is unknown. A consistent feeding pattern is not apparent among the majority of GDV patients reported in the literature. Once-daily feeding may increase risk of GD and GDV in Irish setters, but it is unclear whether once-daily feedings pose a risk for other breeds. Hormonal Influences Mild hypergastrinemia was documented in a group of dogs with acute GDV that were in a fasting state following recovery from surgery.14 Results from this study suggest that preexisting hypergastrinemia may contribute to an increased incidence of GDV because of pharmacologic effects of gastrin on increasing lower gastroesophageal sphincter (GES) tone, promoting gastric mucosal hyperplasia and muscular hypertrophy, and inhibiting gastric emptying. Subsequent studies15 have failed to reveal consistent hypergastrinemia in post-GDV dogs. Further, gastric distention in clinically normal dogs does not induce significant increases in plasma gastrin immunoreactivity or lower GES pressure. Thus there is insufficient evidence to support a role for the gastrointestinal (GI) hormone gastrin in the pathogenesis of canine GDV complex. The roles of other GI hormones, particularly those involved in the regulation of GI motility (e.g., motilin, cholecystokinin), have not yet been investigated. Gastric Position Thoracoabdominal dimensions may influence the resting position of the stomach and, therefore, the gastric cardia and abdominal esophagus.7 It has been suggested that altered conformation may interfere with the normal mechanism of eructation and vomiting.7 Although conjectural, this theory may explain why some animals have chronic GD after acute GDV therapy. The effects of gastric position on gastric distention and GDV development is complex. Based on their study of canine cadavers, Blackburn and Mac-

DEEP-CHEST CONFORMATION ■ GASTRIC ROTATION ■ HYPERGASTRINEMIA

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Farlane8 concluded that GD only resulted in GDV if the stomach was already malpositioned. This observation has led many investigators to consider other factors such as the influence of the spleen, exercise, and concurrent inflammatory GI disease as well as meal size and frequency. The fact that GDV can occur in splenectomized dogs16 suggests that it is not essential in the pathogenesis of GDV in all dogs. Similarly, meal type and feeding frequency are not consistent among GDV patients, ruling out diet as a common etiologic factor. Some dogs clearly tolerate gastric volvulus (without dilation) for extended periods.17,18 Consequently, if the stomach is rotated, its malposition could influence both eructation and pyloric function and thereby lead to dilation. Incomplete GES and pyloric dysfunction in some volvulus patients may permit gas to escape through eructation, gastric emptying, or absorption. Eructation The initiation of eructation and the vomiting reflex occurs at intragastric pressures lower than those recorded from spontaneous cases of GDV.19–21 Factors that can independently influence the eructation mechanism include sleep, certain anesthetic drugs, and damage or infiltration of the vagus nerve or gastric cardia.19,20,22,23 Transient relaxation of the GES following gastric fundus distention is an important mechanism for eructation in dogs.23 Presumably, gastric volvulus mechanically interferes with eructation. If gastric volvulus always preceded GDV, disordered eructation could be easily explained. In situations in which GD precedes GDV, the question of what prevents gastric decompression— either eructation of gas or vomiting of solids—remains. When dogs were gorge-fed in an attempt to create GDV, gastric decompression was achieved rapidly by opening the pyloric canal, vomiting, or both.24 Even if the eructation mechanisms were defective, given that gastric decompression can also be achieved by opening the pyloric canal, failure to eructate or vomit alone should not necessarily initiate GD. Acute failure of the eructation and vomiting mechanism must occur in GDV-affected dogs, perhaps with simultaneous pyloric dysfunction; therefore, disorders of eructation and vomiting most likely contribute to the initiation of GDV. Gastric Rhythm, Motility, and Emptying Funkquist and Garmer25 demonstrated that the gastric emptying of a liquid barium meal was delayed in animals recovering from GDV. This study was prompted by the observation that several of the animals that presented with GDV had historical evidence of chronic

vomiting.25 Together with the fact that some dogs had recurrent episodes of GD following otherwise successful therapy for GDV,26 this evidence suggested the presence of a primary gastric emptying disorder. In addition, spontaneous gastric decompression normally occurs at intragastric pressures far lower than those reported for naturally occurring GDV.19,20,27 Gastric dysrhythmias, eructation disorders, and abnormal pyloric function were suspected to be initiating factors. These factors could influence gastric contents, degree of fill, and gastric position, thereby leading to GDV. Funkquist and Garmer25 demonstrated delayed gastric emptying of a liquid barium sulfate suspension in dogs recovering from GDV, suggesting that delayed gastric emptying played a role in the pathogenesis of this syndrome. A subsequent study that measured gastric emptying (using a radiolabeled test meal administered after recovery from GDV and tube gastropexy) failed to show a difference compared with nondiseased controls.28 Yet another study29 using radiopaque markers determined abnormalities of gastric emptying among dogs that had recovered from GDV and circumcostal gastropexy. These experiments used different methods to evaluate gastric emptying; the timing of the evaluation relative to the acute episode of GDV varied. Typically, dogs with longstanding delayed gastric emptying are presented because of chronic vomiting, as was seen by Funkquist and Garmer.25 Data from owners of dogs with GDV, however, have rarely indicated a clinical syndrome associated with chronic delayed gastric emptying before the acute GDV episode. In addition, results of a clinical trial by Greenfield and colleagues30 suggested that pyloric modification, in an attempt to enhance pyloric outflow, caused increased morbidity without demonstrable enhancement of gastric emptying and could not be justified. These observations suggest that the delayed gastric emptying that is seen experimentally may be the result—rather than the initiator—of GDV and its treatment. Evidence for chronic gastric outflow obstruction in all GDV patients is lacking, and pyloric modification cannot be recommended as routine. Acute pyloric dysfunction, however, is influential in GDV. The pyloric canal normally opens to allow aboral passage of gastric contents at intragastric pressures of 8 to 14 mm Hg,27 far lower than intragastric pressure recorded from clinical cases of GDV.21 Stress, electrolyte disturbances, and certain anesthetic agents can influence pyloric function and delay gastric emptying. In a recent study,12 stress associated with car rides or placement in boarding kennels was calculated as a risk factor for GDV. Obversely, gastric malposition could mechanically interfere with pyloric outflow. Therefore,

PYLORIC CANAL ■ GASTRIC EMPTYING ■ CHRONIC VOMITING

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it is likely that acute pyloric dysfunction exists. Logically, pyloric dysfunction could be either the cause of GDV or the result of gastric malposition. Therefore, its role in this disease may vary from dog to dog. Disorders of gastric myoelectrical and mechanical activity can influence gastric emptying and could conceivably initiate an episode of GDV. Evidence for such myoelectrical disorders in dogs recovering from GDV exists.31,32 Unfortunately, further investigation of the relationship between gastric dysrhythmias and the onset of GDV has been hampered by the lack of practical noninvasive techniques to make such measurements, and the lack of resources needed to screen the large at-risk population.

Age Although GDV may occur at any age, there is a greater risk of occurrence in older dogs.1 Increasing age, however, has not been linked with higher mortality.2,3 Sleep In humans, transient lower GES relaxations induced by gastric fundic distention are apparently abolished during stable sleep.33 Although not yet studied in dogs, this scenario is most likely true in sleeping dogs as well because fundic distention–induced GES relaxations are under the same physiologic regulation as in humans. Fundic distention–induced transient GES relaxations are important in mediating eructation in both dogs and humans. 19,20,23 This theory may explain why some episodes of GDV have been anecdotally associated with sleep34 and anesthetic events. EXTRINSIC FACTORS A synthesis of the events leading up to an episode of GDV and the observations by clinicians caring for animals with this disease have led to a myriad of putative initiators of GDV.28 The identification of risk factors should enable veterinarians to advise clients on how to avoid these risks. Diet The increased incidence of GDV coincided with the use of plant protein (especially soybean meal) by the pet food industry.24 Some reports have also associated a sudden change in diet with precipitation of GDV.35 Others have reported a decrease in the prevalence of GDV associated with altered feeding habits among hospitalized animals.7 More recently, once-daily feeding and feeding a single food type were calculated to be risk factors for GD among Irish setters in the United Kingdom.12 Interest, therefore, has focused on the influence of diet composition and feeding frequency on the development of GDV.13,31

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Postprandial Gastric Dilation Abnormally large meals and/or the consumption of a large amount of water have been associated with the onset of clinical signs of GDV.3,12 Some researchers have hypothesized that dogs with acute GD that consume a large quantity of food and fluids could mediate GDV by altering the position of the gastric cardia, thereby interfering with eructation and vomiting.7 Others have speculated that the weight of a large meal in the stomach, especially when coupled with physical exertion, could mediate gastric rotation by acting like a pendulum.8 Again, the feeding patterns reported for dogs with GDV are varied, and GD initiated predominantly by food or liquid consumption is rare. Food type and composition were not found to have an effect on gastric emptying time and postprandial gastric motility patterns when fed isocalorically to dogs.31 Attempts to induce GDV by engorging dogs with food failed in one study.24 Alterations in feeding and exercise patterns also failed to alter the incidence of GDV in a large population of military dogs reported by the same researchers.24 The relationship between meal volume, postprandial GD, and GDV remains unclear. Diet composition and feeding frequency seem to be insignificant factors for most dogs. Accumulation of Gastric Gas In most dogs with GDV, the stomach is distended predominantly by gas. The origin of this gas has been the subject of several studies.36,37 The suggestion that certain diets contained fermentable substrates36 and favored the formation of intragastric gas gained temporary acceptance. These feeds, therefore, predisposed dogs to GDV by virtue of gas production that exceeded normal mechanisms for gastric gas dispersal. Evidence for intragastric fermentation of food was found by analyzing gas from the stomachs of dogs that died of GDV. The gas composition included the presence of volatile fatty acids, further suggesting intragastric fermentation.36 Normally, the acidity within the gastric lumen precludes the presence of most bacteria, with Clostridium perfringens being the only organism consistently cultured from gastric juice.38 The possibility exists that the process of GDV causes a rapid alteration in intragastric pH, permitting bacteria from the oral cavity to initiate fermentation of food, but scientific proof of this mechanism is lacking. In addition, another study that analyzed the gastric gas of dogs with GDV37 suggested that the source of the gas was predominantly aerophagia in which additional carbon dioxide resulted from the action of gastric acid on salivary bicarbonate. Aerophagia was recently calculated to be a risk factor for GDV among Irish setters in the United Kingdom.12 In addition, van Sluijs26 reported several aerophagic dogs that suffered repeated episodes of

PLANT PROTEIN ■ FEEDING PATTERNS ■ INTRAGASTRIC FERMENTATION

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Normal stomach Anesthesia

Anatomic predisposition (ligaments, thoracic depth:width ratio, gastric volume)

Trauma

Vagus nerve disruption

Anatomic effects

Stress Nutritional effects

Motility disorder?

Sleep

Pyloric obstruction (neoplasia, foreign body)

Gastroesophageal Pyloric dysfunction sphincter dysfunction and (delayed or impaired (failure of eructation) gastric emptying)

Motility disorders?

Transient gastric rotation

Anxiety/excitement Gastric fermentation?

Dyspnea

Aerophagia

Gastric volvulus

Rapid eating

Anxiety/excitement Aerophagia

Gastric dilation

Motility disorder

Dyspnea Splenic influence

Rapid eating Postprandial exercise Gastric fermentation

Gastric dilatation–volvulus Figure 1—Algorithm depicting a unifying hypothesis for the development of gastric dilatation–volvulus syndrome.

GD. Aerophagia, therefore, most likely plays a role in some dogs, either as an initiating or as an exacerbating factor for GDV.

PROPOSED HYPOTHESIS FOR THE PATHOGENESIS OF GASTRIC DILATATION–VOLVULUS The pathogenesis of GDV is influenced by environ-

mental, anatomic, physiologic, and pathologic risk factors. The role of each risk factor has been limited by the inability of researchers to obtain noninvasive data from the at-risk population. The prevalence of this disease is estimated to be 0.8%3 to 2.8%7 of veterinary emergency room and hospital populations, respectively. With such a low disease prevalence, the statistical pow-

AEROPHAGIA ■ MOTILITY DISORDER ■ AT-RISK POPULATION

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er of measurements and observations made from the atrisk population will be low. Additional epidemiologic surveys will be needed to facilitate a better understanding of the pathogenesis of this disease. We have proposed a unifying hypothesis for the pathogenesis of GDV syndrome (Figure 1). In this model, failure of the normal eructation and pyloric outflow mechanisms is a fundamental prerequisite for the development of GD. Whether gastric volvulus consistently precedes or follows these events is unclear. We believe the veterinary literature supports the likelihood and clinical relevance of both scenarios: Normal stomach → Gastric volvulus → GES and pyloric dysfunction → GD/GDV Normal stomach → GES and pyloric dysfunction → GD → Volvulus/GDV We believe this model helps to explain why some animals are occasionally observed with chronic volvulus but without dilation (e.g., incomplete GES and pyloric dysfunction in some volvulus patients would permit gas to escape through eructation, gastric emptying, or absorption). The model would also explain why many dogs are observed with acute GD but without volvulus (e.g., gas

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may accumulate too quickly to permit rotation of the stomach). Finally, the model may explain why some GDV episodes are associated with sleep or anesthesia. Sleep and anesthesia interfere with the fundic distention–induced transient relaxations of the GES.

REFERENCES 1. 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. 2. Thomas RE: Gastric dilatation and torsion in small or miniature breeds of dogs—Three case reports. J Small Anim Pract 17:271–277, 1982. 3. 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. 4. 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. 5. Glickman LT, Emerick, T, Glickman N, et al: Radiological assessment of the relationship between thoracic conformation and the risk of gastric dilatation–volvulus in dogs. Vet Radiol Ultrasound 37(3):174–180, 1996. 6. Schaible RH, Zeich J, Glickman N, et al: Predisposition to gastric dilatation–volvulus in relation to genetics of thoracic conformation in Irish setters. JAAHA 33:379–383, 1997. 7. Strombeck DR: Acute gastric dilation–volvulus, in Strombeck DR (ed): Small Animal Gastroenterology, Davis, CA, Stonegate, 1990, pp 228–183.

DID REACHING A DIAGNOSIS PUZZLE YOU? PUZZLE US WITH IT, TOO! We are looking for submissions for the column, “WHAT’S YOUR DIAGNOSIS?” Any intriguing case in veterinary medicine is welcome. The diagnosis may have turned out to be quite an O. Henry twist in the story, or it may have simply been a stumper. If you have one, send it in. Articles should be 500 words long, with most of the evidence presented; the diagnosis itself should be summed up in one to two sentences at the end. Relevant x-rays, ultrasonograms, photos of the patient’s condition, electrocardiograms, or other pictorial clinical evidence is also welcome. Honorarium is provided upon publication.

CONTACT: Editor Veterinary Forum 275 Phillips Boulevard Trenton NJ 08618 (609) 671-2031 FAX (609) 882-6357 Email: [email protected]

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8. Blackburn PJ, McFarlane D: Acute fatal dilation of the stomach in the dog. J Comp Pathol Therap 54:189–199, 1944. 9. Lantz GC, Bottoms GD, Carlton WW, et al: The effect of 360° gastric volvulus on the blood supply of the nondistended normal dog stomach. Vet Surg 13:189–196, 1984. 10. Orton CE: Gastric dilatation–volvulus, in Kirk RW (ed): Current Veterinary Therapy IX. Philadelphia, WB Saunders Co, 1986, pp 856–862. 11. Hall JA, Willer RL, Seim III HB, Powers BE: Gross and histologic evaluation of hepatogastric ligaments in clinically normal dogs and dogs with gastric dilatation–volvulus. Am J Vet Res 56(12):1611–1614, 1995. 12. Elwood CM: Risk factors for gastric dilatation in Irish setter dogs. J Small Anim Pract 39:185–190, 1998. 13. Van Kruiningen HJ, Wojan LD, Stake PE, Lord PF: The influence of diet and feeding frequency on gastric function in the dog. JAAHA 17:145–153, 1987. 14. Leib MS, Wingfield WE, Twedt DC, Bottoms GD: Plasma gastrin immunoreactivity in dogs with acute gastric dilatation–volvulus. JAVMA 185, 2:205–208, 1984. 15. Hall JA, Twedt DC, Curtis CR: Relationship of plasma gastrin immunoreactivity and gastroesophageal sphincter pressure in clinically normal dogs and in dogs with previous gastric dilatation–volvulus. Am J Vet Res 50(8):1228–1172, 1989. 16. DeHoff WD, Green RW: Gastric dilatation and the gastric torsion complex. Vet Clin North Am Small Anim Pract 2:141–153, 1972. 17. Funkquist B: Gastric torsion in the dog—I. Radiological picture during nonsurgical treatment related to the pathological anatomy and to the further clinical course. J Small Anim Pract 20:73–91, 1979. 18. Leib MS, Monroe WE, Martin RA: Suspected chronic gastric volvulus in a dog with normal gastric emptying of liquids. JAVMA 6:699–700, 1987. 19. Strombeck DR, Harrold D, Ferrier W: Eructation of gas through the gastroesophageal sphincter before and after truncal vagotomy in dogs. Am J Vet Res 48:207–240, 1987. 20. Strombeck DR, Ferrier W, Harrold D: Eructation of gas through the gastroesophageal sphincter before and after gastric fundectomy in dogs. Am J Vet Res 49:87–89, 1988. 21. Orton EC, Muir WW: Hemodynamics during experimental gastric dilatation–volvulus in dogs. Am J Vet Res 44(8): 1512–1515, 1983. 22. Martin CJ, Patrikios J, Dent J: Abolition of gas reflux and transient lower esophageal sphincter relaxation by vagal blockade in the dog. Gastroenterology 91:890–896, 1986. 23. Patrikios J, Martin CJ, Dent J. Relationship of tranisent lower esophageal sphincter relaxation to postprandial gastroesphageal reflux and belching in dogs. Gastroenterology 90:545–551, 1986. 24. van Kruiningen HJ, Gregoire K, Meuten DJ: Acute gastric dilatation: A review of comparative aspects by species and a study in dogs and monkeys. JAAHA 10:294–318, 1974. 25. Funkquist B, Garmer L: Pathogenetic and therapeutic aspects of torsion of the canine stomach. J Small Anim Pract 8:517–532, 1967.

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26. van Sluijs FJ: PhD Thesis, University of Utrecht, Netherlands, 1985. 27. Burrows CF, Ignaszewski LA: Canine gastric dilatation– volvulus. J Small Anim Pract 31:495–501, 1990. 28. van Sluijs FJ, Van Den Brom WE: Gastric emptying of a radionuclide-labelled test meal after surgical correction of gastric dilatation–volvulus in dogs. Am J Vet Res 50:433–435, 1988. 29. Hall JA, Willer R, Seim III HB, et al: Gastric emptying of nondigestible radiopaque markers after circumcostal gastropexy in clinically normal dogs and dogs with gastric dilatation–volvulus. Am J Vet Res 53(10):1961–1965, 1992. 30. Greenfield CL, Walshaw R, Thomas MW: Significance of the Heinekie-Mikulicz pyloroplasty in the treatment of gastric dilation–volvulus syndrome: A prospective clinical study. Vet Surg 18, 1:22–26, 1989. 31. Burrows CF, Bright RM, Spencer CF: Influence of dietary composition on gastric emptying and motility in dogs: Potential involvement in acute gastric dilatation. Am J Vet Res 46:2609–2612, 1985. 32. Hall JA, Solie TN, Seim III HB: Gastric myoelectric and motor activity in dogs with gastric dilatation–volvulus. Am J Physiol 265:G646–G653, 1992. 33. Dent J, Dodds WJ, Friedman RH, et al: Mechanism of gastroesophageal reflux in recumbent human subjects. J Clin Invest 65:256–267, 1980. 34. Washabau RJ, Brockman DJ: Unpublished data, University of Pennsylvania, Philadelphia. 35. Andrews AH: A study of ten cases of gastric torsion in the bloodhound. Vet Rec 86:689–693, 1970. 36. Rogolosky B, Van Kruiningen HJ: Short chain fatty acids and bacterial fermentation in the normal canine stomach and in acute gastric dilatation. JAAHA 14:504–515, 1978. 37. Caywood D, Teague HD, Jackson DA, et al: Gastric gas analysis in the canine gastric dilatation–volvulus syndrome. JAAHA 13:459–462, 1977. 38. Warner NS, Van Kruiningen HJ: The incidence of clostridia in the canine stomach and their relationship to acute gastric dilatation. JAAHA 14:618–623, 1978.

About the Authors When this article was submitted for publication, Drs. Brockman, Holt, and Washabau were affiliated with the Department of Clinical Sciences and the Center for Veterinary Clinical 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. Drs. Brockman and Holt are Diplomates of the American College of Veterinary Surgeons. Dr. Washabau is a Diplomate of the American College of Veterinary Internal Medicine. Dr. Brockman is also a Diplomate of the European College of Veterinary Surgeons.