Gastric Dilatation-Volvulus and Bloat

Chapter 134 Gastric Dilatation-Volvulus and Bloat



Susan W. Volk, VMD, PhD, DACVS



KEY POINTS



• Gastric dilatation-volvulus (GDV) is a life-threatening condition that requires aggressive emergency medical stabilization, surgical intervention, and intensive postoperative care to optimize management.

• The pathogenesis of GDV is complex, with both genetic and environmental influences.

• Distention and displacement of the stomach cause cardio-respiratory dysfunction and gastrointestinal compromise. A cascade of pathophysiologic events further impairs these systems as well as the metabolic, hemolymphatic, renal, and central nervous systems.

• Potential life-threatening postoperative complications include cardiac arrhythmias, persistent hypotension, disseminated intravascular coagulation, peritonitis, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome.

• Client education is key and promotes early intervention and decreased incidence of this condition through breeding and home treatment practices.

• Despite often challenging case management, the overall survival rate for patients treated appropriately for GDV approaches 85%.


INTRODUCTION


Acute gastric dilatation with or without volvulus is a life-threatening condition that is classically described in large or giant breed dogs with deep chests, and appears to occur more frequently in older animals. Although there has been much debate whether dilatation or volvulus occurs first in the gastric dilatation-volvulus (GDV) syndrome, it is plausible that either may occur primarily as isolated cases of both conditions occur. Regardless of the sequence of events, once gastric distention and malpositioning occur, the compression of low-pressure (venous) intraabdominal vasculature leads to cardiovascular, respiratory, and gastrointestinal (GI) compromise. Impaired perfusion causes secondary compromise of multiple organs, the hemolymphatic system, and the metabolic system. Elements of individual treatment regimens remain controversial; however, treatment strategies shown to yield the most successful outcomes combine aggressive emergency medical diagnostics and therapeutics with early surgical intervention and intensive postoperative critical care management. It is clear that an understanding of the etiology, pathophysiology, and clinical features of this syndrome contribute to improved survival rates.



PATHOGENESIS


When considering etiology, it is important to realize that several subpopulations of dogs have gastric dilatation. As previously stated, this may occur in the presence or absence of volvulus and, less commonly, volvulus may occur without significant dilatation. Rapid, significant gastric distention with gas and the ensuing cardiorespiratory dysfunction lead to the typical acute clinical picture, although some dogs may have chronic, subtle GI dysfunction. Multiple contributing factors have been identified and influence incidence within a genetically susceptible population.


Although small dogs and cats can develop GDV, it is predominantly a syndrome of the large and giant breed dogs. Certain breeds, including the Great Dane, Weimaraner, Saint Bernard, Gordon Setter, Irish Setter, and Standard Poodle, are at significantly increased risk.1 Furthermore, having a first-degree relative with a history of GDV was found to be a significant risk factor.2 It has been hypothesized that genetic predisposition to GDV may occur through inheritance of conformation, personality, or temperament that predisposes to the condition. Anatomic studies have shown a correlation between increased thoracic depth-to-width ratio and incidence of GDV within certain breeds.3,4 It has been speculated that this conformation may inhibit eructation. Failure of normal eructation and pyloric outflow mechanisms may be a prerequisite for gastric dilatation.5 Stretching of gastric ligaments, as may occur with previous dilatation, large intraabdominal masses, or splenic torsion may facilitate development of the condition.6,7


Overeating, postprandial exercise, and food type have all been incriminated as causes of GDV, but there remains a lack of evidence to support these assumptions. Based on the results by Glickman and colleagues2 examining nondietary risk factors for GDV in 1637 large and giant breed dogs, feeding fewer meals per day or several small meals per day, moistening dry food before feeding, and restricting exercise or water intake immediately before or after eating were not associated with a decreased risk of GDV on multivariate analysis. In this large, prospective study, factors significantly associated with increased risk were increasing age, having a first-degree relative with a history of GDV, eating faster (for large but not giant breeds of dogs), and having a raised feeding bowl.


A separate study documented that an episode of stress (e.g., boarding, traveling, a veterinary visit) occurred more frequently during the period immediately before development of a GDV than in a comparable disease-free population.8 The propensity to be influenced by a stressful event may be related to the personality of a given individual. In a prospective cohort study of 1914 dogs, the only breed-specific characteristic significantly associated with GDV was a negative correlation between owner-perceived happiness and incidence of GDV.9 However, other studies have suggested that fearful or aggressive dogs may be at increased risk for developing GDV.2,8 The findings in these studies and others may help decrease the incidence of GDV by providing owners and breeders with guidelines for breeding and treatment practices.



PATHOPHYSIOLOGY


Gastric distention and displacement directly affect the cardiovascular, respiratory, and GI systems. Secondary effects on these and other systems (i.e., metabolic, hemolymphatic, renal, and central nervous systems) ensue. Shock is the life-threatening abnormality in dogs with GDV, and an understanding of the cause of this state allows rational treatment. Severe gastric distention results in compression of the intraabdominal veins (caudal vena cava, portal vein, and splanchnic vasculature). This venous occlusion results in decreased venous return and increased venous pressure (splanchnic pooling and portal hypertension). The combination diminishes cardiac output and systemic blood pressure. The collateral circulation is unable to handle the venous return, leading to interstitial edema and loss of intravascular volume, which further contribute to poor perfusion of major organs.


In addition, gastric distention prevents caudal displacement of the diaphragm and therefore impedes normal respiratory excursion. To compensate, respiratory rate and effort may increase. These efforts may become inadequate and eventually respiratory acidosis, due to impaired carbon dioxide clearance, might contribute further to the metabolic acidosis that exists secondary to poor tissue perfusion (lactic acidosis). Aspiration pneumonia may further exacerbate this respiratory compromise.


The increased intraluminal gastric pressures impair flow through the gastric wall vasculature and this, combined with poor cardiac output, may lead to gastric necrosis. Avulsion, thrombosis, and stretching of the short gastric arteries are common and may further contribute to diminished perfusion of the stomach. Mucosal hemorrhage and necrosis are common. Susceptibility of the mucosa to damage by hypoperfusion may be exacerbated by the acidic environment of the gastric lumen and high metabolic demands. Decreased gastric perfusion results in serosal hemorrhage and edema of the stomach wall, which begins in the fundus and spreads to the body of the stomach. Bacterial translocation from the stomach or other portions of the poorly perfused intestinal tract may lead to septicemia. Severe compromise to the gastric wall results in necrosis and perforation, with resultant peritonitis.


Cardiac arrhythmias, mainly ventricular in origin, occur in approximately 40% of patients with GDV.10,11 Several factors have been implicated in the cause of cardiac arrhythmias. Coronary blood flow in experimentally induced GDV is decreased by 50%.12 Histologic lesions compatible with myocardial ischemia are seen in both experimental and spontaneous GDV and may establish ectopic foci of electrical activity. Circulating cardiostimulatory substances such as epinephrine and cardioinhibitory substances such as myocardial depressant factor have also been implicated in the generation of arrhythmias.


Acid-base and electrolyte imbalances are not seen consistently in dogs with GDV. Cellular hypoxia caused by systemic hypoperfusion may result in an increased production of lactic acid by anaerobic energy production, resulting in a metabolic acidosis. Blood pH may be normalized by a concurrent metabolic alkalosis caused by sequestration of hydrogen and chloride ions in the stomach lumen (causing a mixed acid-base disorder). Several pathophysiologic events may promote the development of hypokalemia, including the administration of a large volume of low-potassium fluids, sequestration of potassium within the stomach or loss through vomiting or lavage, hyperchloremic metabolic alkalosis with transcellular shifting, activation of renin-angiotensin-aldosterone system, and catecholamine-induced shifting of potassium into cells. Blood glucose levels may also fall in the later stages of shock as energy demands cannot be met by the inefficient production of adenosine triphosphate through anaerobic metabolism.


Infarction of splenic arteries and thrombosis of splenic veins may occur, resulting in splenic necrosis. Disseminated intravascular coagulation (DIC) is seen frequently in dogs with GDV.13 Contributing factors include pooling of blood in the caudal vena cava, portal vein, or splanchnic circulation, tissue hypoxia, acidosis, endotoxemia, and sepsis.

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  4. Allergic Airway Disease in Dogs and Cats and Feline Bronchopulmonary Disease

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Gastric Dilatation-Volvulus and Bloat

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