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. The highest incidence appears to occur in the Great Dane, Bloodhound, Irish Wolfhound, Akita, Standard Poodle, Weimaraner, Saint Bernard, Gordon Setter, and Irish Setter. 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 mal-positioning occurs, the compression of low-pressure (venous) intra-abdominal vasculature leads to cardiovascular, respiratory, and gastrointestinal compromise. Impaired perfusion causes secondary compromise of multiple organs. Elements of individual treatment regimes 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.
While rapid, significant gastric distention with gas and the ensuing cardio-respiratory dysfunction lead to the typical acute clinical picture, some dogs may have chronic, subtle gastrointestinal 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. Furthermore, having a first-degree relative with a history of GDV has been found to be a significant risk factor. It has been hypothesized that genetic predisposition to GDV may occur through inheritance of conformation, personality, or temperament that predisposes to the condition. An association between GDV and inflammatory bowel disease has been suggested, but the relationship is unclear. Anatomic studies have shown a correlation between increased thoracic depth-to-width ratio and incidence of GDV within certain breeds. 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. Stretching of gastric ligaments, as may occur with previous dilatation, the presence of an intra-abdominal mass or splenic torsion may facilitate development of the condition.
While still a matter of debate, dilatation likely precedes volvulus. Dilatation develops secondary to the accumulation of gas or fluid within the stomach, the outflow from which is obstructed. Obstruction may be caused by neoplasia, pyloric stenosis, the presence of a foreign body, or compression of the duodenum against the body wall by the rapidly expanding stomach. Prolonged gastric emptying, chronic dilatation secondary to pyloric dysfunction, and hypotonic gastric and pyloric musculature associated with the ingestion of large meals at protracted intervals have been incriminated in the pathogenesis of GDV, however, there is a lack of evidence for gastric emptying disorders in dogs that develop GDV. 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. One study documented that an episode of stress occurred more frequently during the period immediately before development of a GDV than in a comparable disease-free population. The propensity to be influenced by a stressful event may be related to the personality of a given individual.
Distention of the stomach by gas may be associated with aerophagia, diffusion from the bloodstream, release of carbon dioxide after the reaction of hydrochloric acid and bicarbonate, or bacterial fermentation. Viewed from a caudal to cranial direction, the stomach rotates 90-360° in a clockwise fashion about the distal esophagus. The pylorus is displaced to the left of the midline, the duodenum becomes entrapped between the distal esophagus and the stomach, and the spleen may vary in position from left posterodorsal to right anterodorsal (depending on the extent of volvulus). If the volvulus is >180°, the distal esophagus becomes occluded. Gastric distention and displacement directly affect the cardiovascular, respiratory, and gastrointestinal systems. Secondary effects on these and other systems (i.e., metabolic, hemolymphatic, renal, and central nervous systems) ensue. Hypovolemic and endotoxic shock are the life threatening abnormalities 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 hypo-perfusion 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 40-75% of patients with GDV. Several factors have been implicated in the cause of cardiac arrhythmias. Coronary blood flow in experimentally induced GDV is decreased by 50%. 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 tri-phosphate 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. Contributing factors include pooling of blood in the caudal vena cava, portal vein, or splanchnic circulation, tissue hypoxia, acidosis, endotoxemia, and sepsis.
Clinical signs may include an acute onset of restlessness, apparent discomfort, abdominal pain, repeated unproductive retching, excessive salivation, and abdominal distention. The abnormalities present on physical examination are manifestations of the circulatory and respiratory compromise that results from acute gastric distention and displacement. Dogs often present in cardiovascular and hypovolemic shock with depressed mentation, rapid and weak arterial pulses, cool extremities, pale mucous membranes, and prolonged capillary refill time. Tachypnea or dyspnea, or both, may reflect both discomfort and a reduction in tidal volume due to gastric distention. The abdomen can vary from unremarkable on palpation, to distended and firm, to tympanic. An irregular heart rate and associated pulse deficits may indicate the presence of cardiac arrhythmias. Decrease in venous return, cardiac output, and arterial blood pressure, as well as hypovolemic shock, are caused by compression of the caudal vena cava; sequestration of blood in dilated splanchnic, renal, and posterior muscular capillary beds; loss of fluid into the obstructed stomach; and a lack of water intake. Endotoxemia, hypoxemia, metabolic acidosis, and hypotension predispose to disseminated intravascular coagulation.
Diagnostic abdominal radiography is used to differentiate simple gastric dilatation from dilatation with volvulus and to rule out other medical conditions. The right lateral recumbent view is the view of choice. If possible, a dorsoventral view may also be taken to help delineate gastric position. Ventrodorsal positioning may lead to further cardiovascular compromise and may predispose to aspiration pneumonia should the patient regurgitate or vomit. The pylorus in a dog with GDV moves cranial to and is separated by soft-tissue opacity from the body of the stomach in the lateral projection and to the left of midline on the dorsoventral view. In comparison, the pylorus lies ventral to the fundus and to the right of midline in a dog without volvulus. Chest radiographs are also be indicated to rule out the presence of coexisting disease and/or aspiration.
The most important goal of treatment is the immediate correction of the circulatory, endotoxic and hypovolemic shock. Aggressive preoperative correction of cardiovascular collapse before surgery has dramatically improved patient survival to an overall rate of approximately 90%. Fluid administration is initiated after placement of one or two large-bore (14 to 18 gauge) catheters in the cephalic or jugular veins. Complete hematologic and biochemical blood testing including a coagulation profile should be performed. Shock doses of crystalloid fluids (90 ml/kg) or a combination of isotonic crystalloids (20 to 40 ml/kg) and synthetic colloids (hydroxyethyl starch 10 to 20 ml/kg; or 7% hypertonic saline in 6% dextran-70 5 ml/kg IV over 5 to 15 minutes) should be administered to effect. After appropriate volume resuscitation, vasopressor therapy may be necessary to further alleviate hypotension. During the initial examination and initiation of fluid administration, supplemental oxygen should be administered, if possible, to optimize oxygen saturation of hemoglobin. Broad-spectrum antibiotic therapy should be utilized because affected animals are at high risk for bacterial translocation from the gastrointestinal tract to the bloodstream with resultant endotoxemia. Continuous electrocardiographic (ECG) monitoring should be performed and arrhythmias (typically ventricular) treated if they interfere with cardiac function and output; the arrhythmias that warrant medical therapy include but are not limited to multifocal premature ventricular contractions, a ventricular rate persistently >140 bpm, and the “R on T wave” pattern (a phenomenon that predisposes to ventricular fibrillation). If predisposing factors have been addressed and persistent ventricular arrhythmias warrant therapy, 2% lidocaine hydrochloride without epinephrine (1-8 mg/kg, slowly IV) is given and repeated if necessary. Continuous rate infusion (CRI) of lidocaine (30-80 µg/kg/min) may be indicated to control arrhythmias. Cardiac arrhythmias associated with GDV are often difficult to control. The lidocaine infusion was continued until arrhythmias improved, then it was slowly decreased over a 12-hour period by cutting the CRI in half every 6 hours. If the arrhythmia is poorly responsive to this therapy, procainamide (6-10 mg/kg, IV over 15 min) should be given.
Following initial stabilization, treatment goals include decompression of the stomach, repositioning and permanent gastropexy, and continued monitoring and treatment of medical complications.
Gastric decompression should be attempted simultaneously with or immediately after cardiovascular stabililization has commenced. Decompression will further improve cardiorespiratory function, however additional cardiovascular insult may occur because of the rapid release of endotoxins and ischemic by products into the circulation (reperfusion injury) as a side effect of appropriate and successful decompression. Gastric decompression usually can be accomplished with the passage of a well-lubricated orogastric (stomach) tube. The distance from the incisors to the xiphoid or costal arch should be measured and marked by a piece of tape on the stomach tube. This distance indicates the maximum length of tube that can be safely passed. Marking this length decreases the likelihood of passing the stomach tube through a devitalized stomach wall. The dog is positioned in sternal or lateral recumbency. A 2-in. roll of tape or an oral speculum is placed in the dog’s mouth, and the muzzle is closed around it. The tube can then be readily passed through the center of the roll of tape or the speculum. Some resistance is usually felt as the tube passes through the esophageal-gastric juncture. If resistance is met, the tube should be gently rotated while attempting to advance it. Undue force may tear the esophagus. Successful passage of a tube does not rule out concurrent gastric volvulus. Once the tube enters the stomach, gastric gas readily escapes. Excess fluid and ingesta are removed via gravity and suction. After the stomach has been decompressed, it should be lavaged with warm water or saline to remove any remaining debris.
In the event that the orogastric tube cannot be passed easily, many surgeons will recommend trocar insertion using a large-gauge, short needle or over-the-needle catheter in a region of the left cranial, dorsolateral abdomen. This should be performed in an area that exhibits the greatest tympany and that has been clipped and aseptically prepared. The main disadvantages associated with this procedure are increased surgical time and increased risk of abdominal contamination at the time of definitive surgical correction. My personal preference is to proceed to surgery immediately and to decompress the distended stomach after performing a ventral midline celiotomy using a blood collection set. In order to minimize the period of time between the initiation of anesthesia and surgical intervention, the patient is clipped and prepped prior to the administration of anesthesia while initial stabilization is being performed; a final sterile preparation is applied as the patient is transferred to the surgery room and as the surgeon is gowning. After utilization of the blood collection set to reduce the tympany present, the surgeon can more easily reposition the stomach into its normal anatomic position and help guide an orogastric tube into the stomach non-traumatically to completely decompress the stomach and remove any remaining fluid and/or ingesta.
While dogs with gastric dilatation in the absence of volvulus typically do not require immediate surgical intervention, gastropexy is recommended for these patients to help prevent the development of GDV in the future. Conservative treatment in these patients is tailored to the individual patient and should consist of the same aggressive medical stabilization upon initial presentation as described above and orogastric intubation as needed throughout the initial hospitalization. It is this surgeon’s opinion that upon stabilization a gastropexy procedure should be performed immediately in light of the extraordinary high recurrence rate and potential for the development of GDV and its more serious consequences. Continued periodic assessment of physical parameters (heart rate, EKG, peripheral pulse pressure and quality, mucous membrane color, capillary refill time, and gastric distention) as well as laboratory data (packed cell volume, total solids, acid-base status, and electrolyte values) should be performed to ensure treatment remains tailored to the individual patient’s response to therapy.
The goals of surgical management are to assess the integrity of the stomach and spleen, to reposition the stomach to its normal location, and to fix the stomach to the abdominal body wall in an attempt to decrease the likelihood of recurrence of volvulus. A midline celiotomy provides access to the stomach and visualization of the spleen and adjacent abdominal structures. Most often, the stomach and pylorus have shifted to the left (clockwise when viewed caudally to cranially), and the gastric fundus has shifted from its normal position in the left dorsal abdomen to the right ventral sector of the abdomen. With this type of rotation, the greater omentum is found draped over the cranial abdominal organs.
The stomach is decompressed by orogastric intubation (by the anesthetist with guidance by the surgeon) or via gastrocentesis as previously described and is rotated back into its normal position. The pylorus can be located by tracing the duodenum (identifiable by the attached pancreas) forward from the duodenocolic ligament. By gently bringing the pylorus back to the right of midline using one hand and using the other hand to push the body of the stomach dorsally, the stomach is derotated. The orogastric tube may then be used to completely decompress the stomach and empty ingesta.
Next, the stomach and the spleen should be assessed for viability and gastric resection or splenectomy performed as needed. Splenectomy is indicated only in those cases demonstrating vessel avulsion, thrombosis, infarction, or all three. Although the spleen is generally involved in cases of GDV, its removal will not prevent recurrences. Partial gastrectomy is required when gastric necrosis has occurred, usually along the greater curvature. Gastric viability is assessed by examination of serosal color, palpation of gastric wall thickness, and preservation of arterial bleeding if incised. Gray or black coloration and palpable thinning of the stomach are signs of necrosis. Serosal discoloration within areas of viable tissue may improve dramatically within minutes of decompression and repositioning. Gastric resection may be accomplished by preplacing stay sutures to minimize or prevent additional abdominal contamination, followed by resection to bleeding tissue and closure. Whether hand-sewing or stapling (typically TA-90 or GIA-50) is used for closure, a second inverting suture line is recommended. Invagination of necrotic tissue has also been used to treat gastric necrosis. Because this technique does not require opening of the gastric lumen, it is technically less demanding and is theoretically less likely to result in peritoneal contamination through gross spillage during partial gastrectomy or due to suture dehiscence; however, it should be noted that invaginated tissue may be prone to ulcer formation. Although there are risks associated with gastric resection and invagination, the devastating sequelae of perforation and peritonitis resulting from necrotic tissue that is not excised make it advisable to remove or invaginate any gastric tissue of questionable viability. Gastric necrosis has been associated with the development of several life-threatening complications including peritonitis, disseminated intravascular coagulation, sepsis, and arrhythmias.
Currently, the most widely used gastropexy techniques are incisional gastropexy (muscular flap), belt-loop gastropexy, circumcostal gastropexy and laparoscopically assisted gastropexy. The ideal gastropexy technique is simple to perform, permanently and predictably attaches the stomach to the abdominal wall in a correct anatomic position to prevent volvulus, does not interfere with gastric function, is associated with minimal intraoperative and postoperative complications, and requires minimal postoperative management of the treated dog. Each of the previously mentioned techniques has been assessed, and each has been found to be an acceptable method of performing a gastropexy. Tube gastrotomy, a once a popular technique, is associated with several problems. In this procedure the gastric lumen is penetrated which can predispose the patient to a peritonitis postoperatively necessitating a second surgical procedure. Refractory peritonitis is a complication which can lean to the demise of the patient. The tube must remain in place for up to 10 days to allow time for formation of adhesions and thus, a potentially permanent attachment site. In addition, subcutaneous cellulitis and persistent stoma drainage are further supplementary complications. The aftercare requires additional hospitalization and adequate nursing care to prevent the tube from being removed prematurely either by the patient or subsequent to balloon rupture from contact with gastric juices. Finally, when compared with other techniques, tube gastropexy breaking strength is relatively low, and therefore recurrence of GDV is approximately 5 to 11% of dogs that undergo this type of surgery.
The circumcostal gastropexy has resolved most of the potential problems inherent with the tube gastropexy procedure. This technique provides a strong adhesion on the basis of findings in breaking-strength studies and results in a low GDV recurrence rate. The technique does not require penetration of the gastric lumen thus reducing the risk of iatrogenic peritonitis. However, there is potential for pneumothorax secondary to penetration of the diaphragm or excess tension on the rib attachment causing the diaphragm to tear or for the rib to fracture.
Advantages of the incisional gastropexy techniques (muscular flap, belt-loop) are that the stomach lumen is not entered (reducing the risk of iatrogenic peritonitis), pneumothorax and/or rib fracture are no longer a concern and fibrous connective tissue cojoins the rectus abdominis muscle and stomach wall to form a strong, mature adhesion with extremely low recurrence rates for GDV. The risks associated with the incisional gastropexy methods are more related to skill and technique; poor positioning or choice of attachment site can cause pyloric outflow obstruction or entrapment of adjacent abdominal viscera. My personal preference is to perform the muscular flap gastropexy as it is even less invasive than the belt-loop procedure as the seromuscular layer of a potentially devitalized stomach wall is not invaded to any extent. Having pioneered this gastropexy procedure over 20 years ago and having successfully employed it in hundreds of GDV cases with virtually no recurrence, I can personally attest to the outstanding success it has achieved in managing the GDV patient.
The goal in the immediate postoperative management period is to maintain tissue perfusion. Because of substantial fluid loss into the peritoneal cavity and GI tract, reasonably high fluid rates often are required for the first 48 to 72 hours. Mucous membrane color, capillary refill time, packed cell volume, total solid values, urine output, ECG, blood pressure, and acid-base balance should be monitored closely postoperatively. Dogs recovering well from surgery can be offered water first, and then a small amount of food if water is tolerated on the first or second day after surgery. These dogs can be weaned gradually off their intravenous fluids over 2 days. Because of the high incidence of gastric mucosal compromise, nonsteroidal antiinflammatory drugs are avoided, and histamine-2 receptor antagonists (ranitidine, cimetidine, famotidine) and coating agents (sucralfate) should be considered. All dogs should receive proper pain management consisting of but not limited to appropriate doses of hydromorphone, tramadol, fentanyl, and buprenorphine as necessary to alleviate pain.
In the past, mortality rates for dogs with GDV were approximately 50%. In a recent study, however, the overall mortality rate was 10%, and the postoperative mortality rate was 6.1%. The factor that was associated with a significant increase in overall mortality was the presence of preoperative cardiac arrhythmias. Additional factors that were associated with a significant increase in postoperative mortality were postoperative cardiac arrhythmias, splenectomy, or splenectomy with partial gastric resection. The factor that was most associated with a significant decrease in the overall mortality rate was time from presentation to surgery. Dogs that had gastropexy alone had a postoperative mortality rate of 3%. Dogs in which splenectomy was the only additional surgical procedure performed had a significantly higher postoperative mortality rate (15%) than dogs that did not require splenectomy. The postoperative mortality rate (9%) for dogs in which partial gastrectomy was the only additional surgical procedure performed was not significantly higher than the rate for dogs that did not have a partial gastrectomy. Dogs that had both splenectomy and partial gastrectomy had a significantly higher postoperative mortality rate of 20% compared to dogs that did not have both splenectomy and partial gastrectomy. This study documents that certain factors continue to affect the overall and postoperative mortality rates associated with GDV, but these mortality rates have decreased compared to previously reported rates. The fact that anesthesia and surgery time were less than half of those previously reported suggests that anesthesia and surgery times play a role in improved survival.
Many veterinarians have recently begun to advocate prophylactic gastropexy for higher- risk patients. Prophylactic gastropexy is performed to prevent the occurrence of GDV in predisposed dogs. The lifetime risk of certain dogs predisposed to develop GDV has been estimated to be between 4% and 37%. In contrast, the lifetime risk of development of GDV if a prophylactic gastropexy is performed in these dogs is 0.3%. These dogs include, but are not limited to, large- to giant-breed dogs (especially Great Danes), dogs with a first-degree relative that has had GDV, excessively anxious dogs, and inappropriately rapid eaters. Other indications include a history of splenic volvulus and a chest shape that has a deep chest-to-width ratio Depending on the breed of dog, prophylactic gastropexy results in a 92% reduction in risk for development of GDV and a 2- to 30-fold reduction in lifetime mortality rates. On the basis of these findings, prophylactic gastropexy can be suggested for dogs of predisposed breeds because it decreases GDV-associated mortality rates.
Currently, prophylactic gastropexies can be performed via any of the previously described techniques (incisional or circumcostal). Each of these techniques requires a ventral midline incision and is considered an “open” major surgical procedure. Many owners and veterinarians consider such a procedure excessively invasive for a young healthy dog with an uncertain probability of developing GDV later in life. Issues associated with performing prophylactic gastropexy include invasiveness of the procedure, lifetime risk of an episode of GDV, and actual necessity of prophylactic surgery. More recently, minimally invasive alternatives have been described and are gaining interest among veterinary surgeons in an effort to decrease pain and potential morbidity associated with the more invasive open surgical approach. These include laparoscopic-assisted gastropexy, grid-approach gastropexy, and total laparoscopic gastropexy. The major drawback to these procedures is the need for expensive instruments for the laparoscopic technique, duration of the procedure, and possible increase in the risk of damaging other organs. Although potentially challenging, these procedures are advantageous in that they are associated with a decrease in incision size, decrease in the duration of hospitalization, decrease in morbidity, decrease in incisional complications, and improved cosmetic appearance, compared with results for conventional surgery.
In summary, while the gastric dilatation-volvulus disease complex is a true medical and surgical emergency, prompt and aggressive administration of appropriate medical and surgical intervention leads to successful case management the overwhelming majority of the time.
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