INTRODUCTION AND RISK FACTORS

Gastric dilatation-volvulus (GDV) is most commonly seen in large and giant breed dogs and occasionally in cats. There are some GDV risk factors in dogs that have been identified recently. The temperament of an animal and the tendency to develop GDV seem to be directly related to the incidence of GDV. Animals with a fearful or "unhappy" personality are approximately 2.5 times greater risk of getting GDV. Stress factors and a hyperactive personality also play a role in precipitating GDV.

A thin or lean body condition is a risk factor in giant breeds, but not in large breeds. Having a deep and narrow thorax in some breeds is described as a host-risk factor. A high abdominal depth-to-width ratio in large and giant breeds is a morphometric risk factor as well for GDV.

Rapid rate of eating, eating from a raised bowl, being fed one large meal daily, and restricting water intake before and after eating are considered by some as valid GDV risk factors.

The breeds that seem to be at greatest risk for GDV are Great Danes, Saint Bernards, Weimaraners, golden retrievers, German shepherd dogs, wolfhounds and bloodhounds. Large and giant-breed dogs older than 5 years of age have a greater risk for GDV than younger dogs and the giant breeds tend to have GDV earlier than the large breeds. The incidence of GDV increases in both large and giant breeds as they grow older. The breed with the highest incidence of GDV was the Great Dane (42%). In 11 breeds studied by Glickman et al, the gender distribution was essentially equal.

PATHOPHYSIOLOGY

The cause of GDV appears to be multifactorial. Gastric distention probably results in some degree of functional or mechanical obstruction. Aerophagia causes most of the gas accumulation. Fluid sources include ingesta, gastric secretions, and eventually transudate from venous obstruction. The ability to relieve distention through eructation or passage of gastric contents aborally through the pylorus is impaired. The stomach usually rotates in a clockwise direction when viewing the animal from behind. The short gastric vessels may become twisted with resultant thrombosis or avulsion. The latter may contribute to the hemoabdomen within hours of GDV initiation. Over time, increased intragastric pressure eventually results in decreased blood flow to the stomach wall, which can lead to necrosis. Gastric distention eventually becomes so great that occlusion of the caudal vena cava and portal vein occurs. This results in decreased venous return from the abdomen to the heart leading to decreased cardiac output, myocardial hypoxia, hypovolemic shock, and hypotension. The cardiac related problems may lead to arrhythmias and hypotension and decreased portal blood flow can lead to an increased rate of endotoxin release by gram-negative bacteria. These bacteria and their associated enteric toxins move across the mucosal barrier and enter the circulation via the intestinal or diaphragmatic lymphatics or peritoneal surfaces. Concurrent portal vein occlusion decreases the ability of the reticuloendothelial system to handle toxins and absorbed (translocated) bacteria. Hypoventilation may result from decreased movement of the diaphragm.

The spleen can become congested and thrombosed, and necrosis and splenic torsion can occur. One report describes GDV occurring after splenic torsion in 2 dogs.

It appears that reperfusion injury may be associated with GDV secondary to significant tissue damage.

HISTORY AND CLINICAL SIGNS

The signs of GDV include recent episodes of self-limited mild to moderate gastric distention, anorexia, or occasional vomiting. Restlessness, retching, and excessive eructation or flatulence may be reported. The owner may also report environmental stress factors, such as transportation to and from dog shows, introduction of a new pet or person into the household, boarding, recent surgery, or hospitalization. Hyperpnea and dyspnea may also be seen.

On physical examination, various degrees of depression can be seen. Severe depression often progresses rapidly to a comatose state. A painful abdomen is usually noted and is associated with the abdominal distention. Pulse deficits will be noted in some dogs due to cardiac arrhythmias.

Most laboratory findings are nonspecific for GDV. Hemoconcentration is commonly seen. Hypokalemia usually occurs but is often delayed until after the initial fluid resuscitation efforts. Plasma lactate concentration has been reported as a predictor of gastric necrosis and survival among dogs with GDV.

TREATMENT CONSIDERATIONS

Treatment initially consists of rapid decompression of the stomach with an orogastric tube. If this is unsuccessful, then trocarization of the stomach may be necessary. Trocarization is usually done on the left side with an 18 gauge hypodermic needle; however, the left side should not be used if a "ping" is not heard at the site of penetration. This may indicate the presence of the spleen. Following trocarization and some degree of decompression, another attempt at orogastric decompression should be done. Two large-bore intravenous catheters are placed in the front legs concurrent with decompression. Rapid administration of a balanced electrolyte solution (100 mls/kg the first hour) or hypertonic saline alone or with colloids can be substituted. Broad-spectrum antibiotics are indicated and oxygen therapy is routinely given during the initial treatment period.

With a recurrence rate of 75-80% following medical management, definitive treatment with a gastropexy is highly recommended. Because of the risk for concurrent megaesophagus and subsequent aspiration pneumonia, I recommend perioperative administration of injectable metoclopramide (0.3 mg/kg SQ) and an injectable antacid (famotidine, 0.5-1.0 mg/kg IV). The metoclopramide is discontinued usually after 24 hours. I continue some type of oral antacid (H2-blocker) for at least 7-10 days after surgery to protect against gastric ulceration and possible perforation.

An exploratory laparotomy is recommended and anatomical repositioning of the stomach and spleen is initially done. A right-sided gastropexy is done and the author prefers an incisional gastropexy due to its simplicity, speed, and predictable results. If the spleen or stomach is devitalized, splenectomy and/or partial gastrectomy respectively, is/are done.

Pain management is achieved by using a continuous rate of infusion(CRI) combining a narcotic combined with ketamine. A fentanyl transdermal patch can also be considered. Non-steroidal drugs are usually avoided in GDV patients postoperatively because of their increased risk for gastric ulceration / perforation.

The electrocardiogram is evaluated continuously for 24 hours after surgery. After that, intermittent ECGs are performed.

PROPHYLACTIC GASTROPEXY

The risk factors mentioned above have resulted in a number of surgeons to begin to offer a "prophylactic" gastropexy in those animals considered to be at a significant risk for GDV. The signalment, temperament, and in particular, the identification of a first-degree relative with at least one episode of GDV, all contribute to the decision to perform a prophylactic gastropexy. Although this can be done by standard "open" laparotomy techniques, laparoscopic or laparoscopic assisted techniques are now being used successfully. These minimally invasive techniques allow a gastropexy to be a one-day hospitalization technique. We also recommend a prophylactic gastropexy in dogs that have been diagnosed with a chronic or partial torsion form of GDV as well.

References

1.  Glickman, LT; Glickman, NW et al. Incidence of and breed-related risk factors for gastric dilatation-volvulus in dogs. J Amer Vet Med Assoc. 2000: 216: 40-45

2.  Millis, DL; Nemzek, J et al: Gastric dilatation-volvulus after splenic torsion in two dogs. J Amer Vet Med Assoc. 1995; 207: 314-318

3.  Glickman, LT; Glickman NW et al. Multiple risk factors for the gastric dilatation-volvulus syndrome in dogs: A practitioner/owner case-control study. J Amer Anim Hosp Assoc. 1997; 33: 197-202

4.  Brockman, DJ; Washabau, RJ et al. Canine gastric dilatation/volvulus syndrome in a veterinary critical care unit: 295 cases (1986-1992). J Amer Vet Med Assoc. 1995; 207: 460-464

5.  de Papp E; Drobatz KJ et al. Plasma lactate concentration as a predictor of gastric necrosis and survival among dogs with gastric dilatation-volvulus: 102 cases (1995-1998). J Amer Vet Med Assoc. 1999; 215: 49-52

6.  MacCoy, DM; Sykes, GP et al. A gastropexy technique for permanent fixation of the pyloric antrum. J Amer Anim Hosp Assoc. 1982; 18: 763-767

7.  Wagner, AE; Walton, JA et al. Use of low doses of ketamine administered by constant rate infusion as an adjunct for postoperative analgesia in dogs. J Amer Vet Med Assoc. 2002; 221: 72-75

8.  Hardie, RJ; Flanders, JA et al. Biomechanical and histological evaluation of a laparoscopic stapled gastropexy technique in dogs. Vet Surg. 1996; 25: 127-132

9.  Wilson, ER; Henderson, RA et al. A comparison of laparoscopic and belt-loop gastropexy in dogs. Vet Surg 1996; 25: 221-224

10. Rawlings, CR; Foutz,TL et al. A rapid and strong laparoscopic-assisted gastropexy in dogs. Amer J Vet Res 2000; 62: 871-875

11. Glickman, LT; Glickman, NW et al. Non-dietary risk factors for gastric dilatation-volvulus in large and giant breed dogs. J Amer Vet Med Assoc. 2000; 217: 1492-1497