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Following presentation, dogs should be provided with oxygen supplementation and intravenous access obtained via the cephalic vein. In very large dogs, catheters (two large‐bore 14–18 gauge) should be placed bilaterally, which will aid in rapid administration of fluid. The jugular veins can also be used. An emergency database to include packed cell volume (PCV), total protein, glucose, urea and lactate, if available, should be taken. Blood should also be collected for a complete blood count and a biochemistry profile, which will allow evaluation of red and white blood cell parameters, as well as assessment for organ dysfunction. A coagulation panel can also be run, when possible, to evaluate for the presence of DIC. The presence of three or more abnormal hemostatic parameters, including thrombocytopenia, prolongation of prothrombin time or activated partial thromboplastin time, increases in fibrin degradation products or D‐dimers, hypofibrinogenemia, and depletion of antithrombin has been associated with gastric necrosis [27]. Analgesia should be provided, as most dogs with GDV are uncomfortable or painful. A pure mu opioid agonist (methadone, morphine, oxymorphone or fentanyl) is preferred.

Figure 8.1 Standard poodle collapsed with abdominal distension due to gastric dilatation and volvulus.

Evaluation of lactate may be useful as a prognostic marker, although lactate should not be relied upon as an absolute predictor of outcome. The data examining lactate in GDV are conflicting. Initial work showed an association between preoperative lactate concentration and outcome, with most dogs surviving if their lactate concentration was lower than 6 mmol/l [28]. This study also showed an association between lactate concentration greater than 6 mmol/l with gastric necrosis and death. In more recent studies, lower lactate concentrations were found to be associated with survival, but there was significant overlap in lactate concentration ranges between survivors and non‐survivors [29, 30]. Other studies have not repeated these findings [6, 7, 31]. The most useful finding from these later studies is an association between a decrease in lactate following treatment and outcome, with dogs more likely to survive in the following situations [6, 7]:

 A lactate decrease of at least 42.5% from presenting lactate following fluid therapy and decompression.

 A final lactate less than 6.4 mmol/l.

 An absolute change in lactate greater than 4 mmol/l following fluid therapy and decompression.

 Lactate reduction of 50% or more within 12 hours of presentation.

Continuous electrocardiography is useful for detection and diagnosis of arrhythmias. Therapy for ventricular arrhythmias is suggested in the following circumstances:

 Arrhythmias that are associated with cardiovascular compromise (i.e., hypotension or hypoperfusion; pulse deficits; poor pulse quality).

 There is evidence of R‐on‐T phenomenon.

 Sustained ventricular tachycardia (heart rate above 150 beats/minute).

 Multiform ventricular premature contractions.

First‐line pharmacological therapy for ventricular arrhythmias is lidocaine. A bolus of 2 mg/kg is given intravenously over one to two minutes. Too rapid administration is associated with vomiting. A positive response is seen as a reduction in ventricular rate, associated with an improvement in perfusion, or a conversion to sinus rhythm. The dose may be repeated up to four times [32]. If the bolus is effective, it is recommended that a constant rate infusion be initiated at 50–70 μg/kg/minute. Adverse effects of lidocaine include nausea and seizures. If either is seen, the dog should be managed appropriately for the effect and the drug stopped. It can be restarted at a lower dose once the dog has recovered, as lidocaine has a very short duration of action.

Stabilization of dogs with GDV should be rapid and performed prior to anesthesia and surgery. There are two key steps to stabilization in dogs with GDV:

1 Fluid therapy to restore intravascular volume.

2 Gastric decompression to reduce the influence of the dilated stomach on venous return.

Management of hypoperfusion is a priority in dogs with GDV. As the cause of hypoperfusion is likely multifactorial, fluid therapy alone may not provide complete stabilization. At the authors' facility, shock doses of isotonic crystalloid fluids (up to 90 ml/kg administered in boluses) or a combination of isotonic crystalloids at a lower dose (20–40 ml/kg) in conjunction with 7% hypertonic saline (2–4 ml/kg) is administered and the dog is then reassessed and fluid therapy is adjusted accordingly. Alternative approaches include the use of a synthetic colloid such as hydroxyethyl starch (hetastarch; 10–20 ml/kg) or 7% hypertonic saline in 6% dextran‐70 (5 ml/kg IV over 5–15 minutes).

The use of hypertonic saline–dextran and hemoglobin solutions (Hb‐200) has been associated with lower doses of fluid administration and shorter time to stabilization compared with lactated Ringer's solution or hetastarch [33, 34]. However, these studies were not significantly powered to show differences in outcome. The use of a synthetic colloids such as hetastarch or 7% hypertonic saline has also been associated with a decreased risk of hypotension [23, 34]. As hypotension has been associated with an increased risk of complications in a number of clinical situations [9, 35], a strategy that would limit the risk of developing hypotension is recommended. In the current market, a number of these fluids (including hetastarch, Hb‐200 solutions and dextran combinations) are no longer readily available. There is evidence in human clinical practice that synthetic colloids are associated with an increased risk of morbidity and mortality [36–38], although this finding has not been identified in dogs [39]. Because of the low mortality rate associated with GDV, identifying whether a type of intravenous fluid therapy is associated with improved survival can be challenging.

Experimental data support rapid transition to surgery following presentation, to minimize the duration of ischemia [26, 40]. However, retrospective analysis has identified increased survival rates with longer periods between presentation and surgery [7]. The authors of this study comment that dogs presenting bright and alert are likely being managed more slowly than those presenting as critically ill, and the authors also found that surgical and anesthesia times were significantly shorter in this study compared with previous studies. Further work is warranted to investigate the relationship between time from presentation to surgery on outcome of dogs with GDV. The time of presentation has recently been shown to be associated with outcome, with dogs presenting between 3 a.m. and 9 a.m. being more likely to die than those presenting between 9 a.m. and 9 p.m. [12].

Prior to gastric decompression, it is useful to obtain abdominal radiographs for a definitive diagnosis. A right lateral abdominal radiograph should be taken initially. Thoracic radiographs should be considered in dogs with dyspnea, to evaluate for the presence of aspiration pneumonia, or in older dogs to identify concurrent disease. Abdominal ultrasonography is not considered useful as it does not aid the diagnosis and will not alter the ultimate plan. Radiographic signs consistent with GDV include a gas‐ and fluid‐filled dilated stomach with displacement of the pylorus and pyloric antrum dorsally. On the right lateral projection, there is a prominent shelf of tissue at the cranial aspect of the stomach giving the classic “reverse C” or “Popeye arm” appearance (Figure 8.2). The presence of intramural gas (pneumatosis) and pneumoperitoneum identified on imaging are specific, but not sensitive findings for gastric necrosis (Figure 8.3) [41]. If these findings are present, then the impact of previous procedures (e.g., trocharization or orogastric intubation) should be taken into consideration, since these procedures may increase the number of false positive results.

Figure 8.2 Right lateral abdominal radiograph showing gastric dilatation and volvulus. Note the “Popeye arm” appearance caused by dorsal displacement of the pylorus.

Figure 8.3 Right lateral abdominal radiograph showing gastric dilatation and volvulus with gastric pneumatosis. This is indicative of gastric necrosis.

Once GDV has been confirmed radiographically, gastric decompression should be attempted. Two methods commonly used are orogastric intubation and gastric trocharization. Orogastric intubation is the more common technique allowing for the removal of gas and fluid but can be more challenging to perform. Trocharization is a simple and rapid technique but allows relief of gaseous distension only. One study reported good success rates for both orogastric intubation (75.5% of dogs) and trocharization (86% of dogs), with no serious complications associated with either technique [42]. The techniques can be used concurrently and may be complimentary. The authors prefer to use trocharization.

To perform trocharization, an area is clipped and surgically prepared dorsally over the abdominal wall in an area of palpable gaseous distension. An area of tympany is identified and a 14‐ or 16‐gauge over‐the‐needle catheter is placed percutaneously into the stomach (Figure 8.4a). The bung is removed, and the stylet can be left in place or removed, allowing gas to escape (Figure 8.4b). If the stylet is left in place, there is less susceptibility to the catheter obstructing due to occlusion, but there is a slightly higher risk of trauma. Once the flow of gas has stopped, the catheter/trochar is removed. Following trocharization, the dog should be taken promptly to surgery and the corresponding gastric wall examined for signs of continuing leakage or necrosis. If an area of concern exists, it should be resected.

A modified technique of ultrasound‐guided percutaneous gastropexy and placement of a gastrostomy catheter has been described to allow continuing gastric decompression prior to surgery [43]. This has been recommended for managing dogs where a delay in surgical treatment is anticipated, for example prior to referral or transfer to another clinic as it allows repeat decompression. The study showed that it was reasonably safe and effective. However, it was similarly effective to repeat trocharization [43].

Figure 8.4 (a) Once an area of tympany is identified, a 14‐ or 16‐gauge over‐the‐needle catheter is placed percutaneously into the stomach. (b) An extension set has been placed into water to evaluate for bubbles to determine when the flow of gas has stopped.

For orogastric intubation, a large‐bore stomach tube with an end hole is lubricated, measured from nostril to last rib (Figure 8.5) and then the length is marked. The dog is placed in sternal recumbency and a roll of bandage with a large enough hole to pass the tube through is placed in the mouth and the mouth held closed around the bandage (Figure 8.6). In alert dogs, sedation or anesthesia may be necessary. Sedation can be accomplished using oxymorphone (0.1 mg/kg IV) or fentanyl (2–5 μg/kg) in combination with diazepam (0.2–0.25 mg/kg IV). In compromised dogs, this combination may be adequate to induce anesthesia. Endotracheal intubation is recommended in anesthetized dogs to protect the airway from aspiration of gastric contents. The orogastric tube is advanced slowly into the pharynx and the dog is allowed to swallow so that it enters the esophagus. The tube is advanced to the stomach carefully and upon entering, gas should be released. Once the stomach has been decompressed, the tube should be removed. Some authors recommend lavaging the stomach at this point [42]. If the tube cannot be advanced into the stomach, trocharization should be attempted. The tube should not be forced into the stomach as there is a risk of perforation. If perforation does occur, this is probably an indicator of preexisting gastric or esophageal necrosis. In some cases, gastric decompression may not be possible until the dog has been anesthetized for surgery.

Figure 8.5 Measuring stomach tube prior to orogastric intubation. The end of the stomach tube is measured to the last rib and a tape marker is placed to identify how far it should be inserted.

Figure 8.6 Bandage roll placed in dog's mouth as a gag and to facilitate passage of stomach tube, which is inserted through the hole in the center of the bandage.

Some authors have suggested a role for management of ischemia–reperfusion injury to prevent subsequent complications [10, 25, 26]. Suggested interventions have included desferoxamine, dimethyl sulphoxide and allopurinol. All have been evaluated in experimental GDV, although none have been evaluated clinically [24, 26]. Lidocaine, however, has been evaluated retrospectively and prospectively as part of the management of GDV in dogs [10, 25]. Retrospective evaluation failed to show a survival benefit associated with lidocaine, but use was uncontrolled, and it is likely that lidocaine use was biased toward more seriously affected dogs [10]. In a prospective study, GDV dogs were treated with lidocaine and a historical population of dogs with GDV was used as a retrospective control [25]. Dogs received an intravenous bolus of lidocaine (2 mg/kg) immediately on presentation, followed by a lidocaine constant rate infusion (50 μg/kg/min) given over 24 hours. A reduced rate of arrhythmias and acute kidney injury, and shorter hospitalization time were reported with lidocaine therapy. Although it is unclear if other factors played a role in the decreased complication rate, the administration of lidocaine may be warranted in the management of GDV.

While surgical intervention is considered mandatory for management of GDV, medical management of the condition, consisting of orogastric intubation, trocarization if necessary and treatment for shock, has been evaluated [44, 45]. A high mortality (66%) [44] and recurrence rate of 71–76% has been reported [44, 45]. The authors do not recommend medical management alone for the treatment of GDV.