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CANINE-PAthogenesis of Acute Canine Gastric Dilatation-Volvulus Syndrom

CANINE-PAthogenesis of Acute Canine Gastric Dilatation-Volvulus Syndrom

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Vol. 22, No. 12December 2000
Refereed Peer Review
The pathogenesis of caninegastric dilatation-volvulus (GDV)remains a complex multifactorialevent that probably differsfrom patient to patient, buttwo discrete pathogeneticmechanisms are likely togive rise to this syndrome.
Pathogenesis of AcuteCanine GastricDilatation–VolvulusSyndrome: Is There aUnifying Hypothesis?
University of Pennsylvania
Daniel J. Brockman, BVScDavid E. Holt, BVSc.Robert J Washabau, VMD, PhD
A single etiologic agent in the pathogenesis of acute canine gastric dilatation-volvulus (GDV) has not yet been identified. Several extrinsic physical and environmental riskfactors have been identified, and many more intrinsic anatomic or pathologic risk factors aresuspected. Many of the proposed intrinsic factors currently lack scientific evidence, and it maybe impossible to substantiate these factors. Normal eructation, vomiting, or pyloric outflowmechanisms appear to fail when gastric dilation occurs. Whether volvulus consistently pre-cedes or follows dilation is unclear. This paper explores the known risk factors for GDV andproposes a hypothesis to explain its pathogenesis.
uch has been learned about the pathophysiology and clinical manage-ment of canine acute gastric dilatation
volvulus (GDV), but a unify-ing hypothesis for the pathogenesis of this syndrome has not yet beenelucidated. Several theories have been proposed, but most do not readily explainall clinical findings. A unifying hypothesis must be capable of answering or addressing several im-portant questions: Why are large- and giant-breed dogs at greater risk than aresmall breeds? If body size and thoracoabdominal dimensions are important fac-tors, why is GDV not more common in relevant breeds? If volvulus is believedto 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 
The pathogenesis of GDVremains complex and poorlyunderstood.
Although the precise mechanismof gastric volvulus remainsunclear, several intrinsic andextrinsic risk factors have beenidentified.
Failure of the normal eructationand pyloric outflow mechanismsis a fundamental prerequisite forthe development of gastricdilation.
Whether gastric volvulusconsistently precedes or followsgastric dilation is unclear, butboth scenarios seem plausibleand likely.
present with chronic volvulus but without dilation? Why are certain breeds more affected than are others? Are there genetic influences, or do differences in feed-ing practices or other environmental factors play a rolein this syndrome? This paper reviews the relevant in-trinsic and extrinsic factors that have been proposed todetermine whether a single unifying hypothesis can ex-plain the pathogenesis of GDV.
 Acute canine GDV is predominantly a disease of large body conformation.
Small dogs appear only spo-radically in the large case studies and single case reportsdescribing this condition
; therefore, anatomic andgenetic features are assumed to predispose large- and gi-ant-breed dogs to this condition.
Thoracoabdominal Dimensions
Risk factor analysis supports the notion that thoracicconformation is an important factor in the develop-ment of GDV. Studies have shown that increased tho-racic depth:width ratios are associated with increasedrisk of development of this syndrome within certainbreeds.
Those studies caused further speculation thatselective breeding against deep-chest conformation would decrease the prevalence of GDV within breeds.
Despite the apparent association, it is unclear how tho-racic and abdominal dimensions influence the develop-ment of GDV. Accentuated thoracic and abdominal di-mensions have been suggested to play a permissive oractive role in the initiation of GDV by virtue of alteredposition of the gastric cardia.
 Although a relationshipbetween thoracoabdominal conformation and GDV has been identified, the mechanism of its influence isunclear.
Gastric Ligament Laxity
The canine stomach has evolved to accommodatevarying meal size and frequency and, therefore, varyingdegrees of distention. Gastric ligaments (i.e., lesseromental, greater omental, mesoduodenal) hold thestomach loosely in position to accommodate changes ingastric volume and muscular activity. Despite thisanatomic configuration, gastric ligaments do not pre-vent clockwise rotation of the stomach in canine cadav-ers or in experimental animals.
Thus laxity of gastricligaments appears to be sufficient to permit gastric rota-tion even in healthy dogs.In addition, dogs with GDV may have reduced abili-ty to resolve gastric rotation
based on the observationthat the stomachs of dogs that have had GDV maintainthe same clockwise-rotated position. In contrast, thestomachs of dogs that have not had GDV return to anormal position after such a rotation.
More recently,the hepatogastric ligaments of dogs with GDV wereshown to be longer than were non-GDV size- and weight-matched controls.
 Abnormalities (e.g., length,elasticity) may contribute to episodes of GDV, but thishas not yet been shown in the pre-GDV state.
Gastric Volume
Once-daily feedings were found to be a predisposingrisk factor for the development of gastric dilation (GD)in Irish setters.
Once-daily feedings may induce in-creases in intragastric volume in this breed when com-pared with three-times-daily feeding.
 Whether or howgastric volume influences the occurrence of GDV is un-known. A consistent feeding pattern is not apparentamong the majority of GDV patients reported in theliterature. Once-daily feeding may increase risk of GDand GDV in Irish setters, but it is unclear whetheronce-daily feedings pose a risk for other breeds.
Hormonal Influences
Mild hypergastrinemia was documented in a groupof dogs with acute GDV that were in a fasting state fol-lowing recovery from surgery.
Results from this study suggest that preexisting hypergastrinemia may con-tribute to an increased incidence of GDV because of pharmacologic effects of gastrin on increasing lowergastroesophageal sphincter (GES) tone, promoting gas-tric mucosal hyperplasia and muscular hypertrophy,and inhibiting gastric emptying. Subsequent studies
have failed to reveal consistent hypergastrinemia inpost-GDV dogs. Further, gastric distention in clinically normal dogs does not induce significant increases inplasma gastrin immunoreactivity or lower GES pres-sure. Thus there is insufficient evidence to support arole for the gastrointestinal (GI) hormone gastrin in thepathogenesis of canine GDV complex. The roles of other GI hormones, particularly those involved in theregulation of GI motility (e.g., motilin, cholecystoki-nin), have not yet been investigated.
Gastric Position
Thoracoabdominal dimensions may influence theresting position of the stomach and, therefore, thegastric cardia and abdominal esophagus.
It has beensuggested that alteredconformation may interfere with the normal mechanism of eructation and vomit-ing.
 Although conjectural, this theory may explain why some animals have chronic GD after acute GDV therapy. The effects of gastric position on gastric dis-tention and GDV development is complex. Based ontheir study of canine cadavers, Blackburn and Mac-
December 2000Small Animal/Exotics
concluded that GD only resulted in GDV if the stomach was already malpositioned. This obser-vation has led many investigators to consider otherfactors such as the influence of the spleen, exercise,and concurrent inflammatory GI disease as well asmeal size and frequency. The fact that GDV can oc-cur in splenectomized dogs
suggests that it is not es-sential in the pathogenesis of GDV in all dogs.Similarly, meal type and feeding frequency are notconsistent among GDV patients, ruling out diet as acommon etiologic factor. Some dogs clearly tolerategastric volvulus (without dilation) for extended peri-ods.
Consequently, if the stomach is rotated, itsmalposition could influence both eructation and py-loric function and thereby lead to dilation. I
ncom-plete GES and pyloric dysfunction in some volvuluspatients may permit gas to escape through eructation,gastric emptying, or absorption.
The initiation of eructation and the vomiting reflexoccurs at intragastric pressures lower than those record-ed from spontaneous cases of GDV.
Factors that canindependently influence the eructation mechanism in-clude sleep, certain anesthetic drugs, and damage or in-filtration of the vagus nerve or gastric cardia.
Transient relaxation of the GES following gastric fun-dus distention is an important mechanism for eructa-tion in dogs.
Presumably, gastric volvulus mechanical-ly interferes with eructation. If gastric volvulus alwayspreceded 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 createGDV, gastric decompression was achieved rapidly by opening the pyloric canal, vomiting, or both.
Even if the eructation mechanisms were defective, given thatgastric decompression can also be achieved by openingthe pyloric canal, failure to eructate or vomit aloneshould not necessarily initiate GD. Acute failure of theeructation and vomiting mechanism must occur inGDV-affected dogs, perhaps with simultaneous pyloricdysfunction; therefore, disorders of eructation andvomiting most likely contribute to the initiation of GDV.
Gastric Rhythm, Motility, and Emptying
Funkquist and Garmer
demonstrated that the gas-tric emptying of a liquid barium meal was delayed inanimals recovering from GDV. This study was prompt-ed by the observation that several of the animals thatpresented with GDV had historical evidence of chronicvomiting.
Together with the fact that some dogs hadrecurrent episodes of GD following otherwise success-ful therapy for GDV,
this evidence suggested the pres-ence of a primary gastric emptying disorder. In addi-tion,spontaneous gastric decompression normally occursat intragastric pressures far lower than those reportedfor naturally occurring GDV.
Gastric dysrhyth-mias, eructation disorders, and abnormal pyloric func-tion were suspected to be initiating factors. These fac-tors could influence gastric contents, degree of fill, andgastric position, thereby leading to GDV.Funkquist and Garmer
demonstrated delayed gas-tric emptying of a liquid barium sulfate suspension indogs recovering from GDV, suggesting that delayedgastric emptying played a role in the pathogenesis of this syndrome. A subsequent study that measured gas-tric emptying (using a radiolabeled test meal adminis-tered after recovery from GDV and tube gastropexy)failed to show a difference compared with nondiseasedcontrols.
 Yet another study 
using radiopaque mark-ers determined abnormalities of gastric emptyingamong dogs that had recovered from GDV and cir-cumcostal gastropexy. These experiments used differentmethods to evaluate gastric emptying; the timing of theevaluation relative to the acute episode of GDV varied.Typically, dogs with longstanding delayed gastricemptying are presented because of chronic vomiting, as was seen by Funkquist and Garmer.
Data from own-ers of dogs with GDV, however, have rarely indicated aclinical syndrome associated with chronic delayed gas-tric emptying before the acute GDV episode. In addi-tion, results of a clinical trial by Greenfield and col-leagues
suggested that pyloric modification, in anattempt to enhance pyloric outflow, caused increasedmorbidity without demonstrable enhancement of gas-tric emptying and could not be justified. These obser-vations suggest that the delayed gastric emptying that isseen experimentally may be the result
rather than theinitiator
of GDV and its treatment. Evidence forchronic gastric outflow obstruction in all GDV patientsis lacking, and pyloric modification cannot be recom-mended as routine. Acute pyloric dysfunction, however, is influential inGDV. The pyloric canal normally opens to allow aboralpassage of gastric contents at intragastric pressures of 8to 14 mm Hg,
far lower than intragastric pressurerecorded from clinical cases of GDV.
Stress, elec-trolyte disturbances, and certain anesthetic agents caninfluence pyloric function and delay gastric emptying.In a recent study,
stress associated with car rides orplacement in boarding kennels was calculated as a risk factor for GDV. Obversely, gastric malposition couldmechanically interfere with pyloric outflow. Therefore,
Small Animal/Exotics
December 2000

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