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Acute Gastric Dilatation-Volvulus in Dogs

Introduction: Canine acute gastric dilatation-volvulus (GDV) is a medical and surgical emergency that is seen most commonly in large and giant breed dogs.  The syndrome is characterized by accumulation of gas in the stomach and malpositioning of the stomach with obstruction of eructation and pyloric outflow.  Subsequent systemic effects of GDV including hypovolemic shock, endotoxemic shock, respiratory compromise, concurrent metabolic acidosis and alkalosis, and reperfusion injury are all implicated in the resultant death of affected dogs.  Though this disease has been studied for years, the exact etiology and pathogenesis is still not clear.  However, several risk factors for development of the disease have been found, as well as preventative measures for dogs at increased risk.


Signalment and risk factors: Most dogs with GDV are large and giant breed dogs.  Dogs with narrow, deep chests are at an increased risk for GDV, as are those dogs with history of GDV in a first degree relative.  Eating meals from raised bowls, large meals fed once daily, and high speed of eating are found to be risk factors as well.  Temperament plays a role also, since aggressive dogs are at a higher risk than dogs who are submissive to people and other dogs.  It is also possible that stressful events such as boarding, trips to the veterinarian, and rides in the car can precede an episode of GDV.

Pathophysiology:  It is uncertain whether dilatation or volvulus occurs first in the pathogenesis of the disease.  It is generally accepted that since the majority of the gas in the stomach during an episode of GDV from aerophagia that dilatation happens first, followed by volvulus.  However, it is also possible that volvulus occurs first which causes an inability to eructate and an impairment of gastric outflow.  This pathogenesis is also supported by the prevention of GDV in dogs that have undergone gastropexy.  The pathophysiology of GDV has grievous systemic effects that ultimately end in death of the dog.  Cardiovascular effects include decreased venous return to the heart via mechanical compression of intra-abdominal veins by the grossly distended stomach, decreased cardiac output due to metabolic acidosis and cardiodepressant factors released by the pancreas, all resulting in hypovolemic shock,  Gastric distention also causes a mechanical impediment to movement of the diaphragm, ultimately resulting in hypoxia and hypercapnia.  Decreased respiratory function and increased anaerobic metabolism cause respiratory and metabolic alkalosis.  Translocation of bacteria and endotoxins from the gastrointestinal tract as a result of ischemia can result in endotoxemia.  A more recently recognized factor in the pathophysiology of GDV is reperfusion injury as a result of circulation of oxygen free radicals released from ischemic tissues.

Clinical signs and diagnosis:  Diagnosis of GDV in dogs is most often made on the basis of signalment, history, and clinical signs.  Radiographs can aid in determining the nature of the volvulus but are often not necessary to diagnose GDV.  Clinical signs of the disease include a distended, tympanic abdomen, retching, unproductive vomiting and hypersalivation.  Affected dogs will present with signs of tachypnea, dyspnea, tachycardia, pale, dry, or muddy mucous membranes, lethargy and possibly coma. 

Treatment and Prognosis:  GDV should be considered as a disease requiring emergency management.  Resolution of hypovolemia is the primary concern followed by decompression of the stomach, surgical correction of volvulus, and adequate postoperative care.  Fluid therapy should consist of crystalloid and colloid administration in order to restore circulatory function.  Once fluid support has been initiated, gastric decompression can be attempted via passage of an orogastric tube.  If passage of a tube is impossible or ineffective 14 gauge needles can be used to trocharize the stomach and relieve pressure.  Once the dog has been adequately stabilized, the volvulus should be surgically reduced via cranioventral midline laparotomy.  Care must be taken to evaluate the stomach, intestines, and spleen for ischemic damage and necrosis, and appropriate measures performed if this is found.  Gastropexy should be performed at this time to prevent recurrence of volvulus.  Postoperative care consists of fluid therapy, arrhythmia management, administration of antioxidants to prevent reperfusion injury and opioid pain control.

  The mortality rates for GDV are reported to be as high as 15-25%.  Prognostic indicators such as recumbency, depression or coma on presentation, gastric necrosis, and arrhythmia all increase mortality; thus, the most effective means of reducing mortality is expedient treatment of GDV.

Prevention:  The most effective prevention of GDV in at-risk dogs is thorough understanding of risk factors and subsequent management of those factors.  Several small meals fed throughout the day, coupled with feeding from a bowl at the dog's feet, will help minimize occurrence of GDV as well as minimizing stressful situations that could precipitate an episode.  Avoid breeding affected animals and those animals that have a first degree relative with a history of GDV.  Finally, prophylactic gastropexy is very useful in preventing GDV in high-risk breeds.

-by David Lee, Class of 2005

-edited by Dr. Leon Thacker, ADDL Director

References:

  1. Brockman DJ, Holt DE: 2000. Management Protocol for Acute Gastric Dilatation-Volvulus Syndrome in Dogs. Compendium 22: 1025-1034.

  2. Brockman DJ, Holt DE, Washabau RJ: 2000.  Pathogenesis of Acute Canine Gastric Dilatation-Volvulus Syndrome:  Is There a Unifying Hypothesis:  Compendium 22: 1108-1114.

  3. Broome CJ, Walsh VP: 2003.  Gastric Dilatation-Volvulus in Dogs.  NZ Vet J 51(6): 275-283.

  4. Glickman LT, Glickman NW, Schellenberg DB et al: 2000.  Non-dietary risk factors for gastric dilatation-volvulus in large and giant breed dogs.  JACMA 217(10): 1492-1499.

  5. Monnet E: 2003.  Gastric dilatation-volvulus syndrome in dogs.  Vet Clin Small Anim 33: 987-1005.

 

 

 

 

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