Small Animal Surgical Emergencies. Группа авторов
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is often contradictory, making firm conclusions difficult. It is likely that GDV is a multifactorial process and therefore the role of single risk factors is unclear. There are certain repeatable findings in many studies, however, that are associated with an increased risk of GDV. Only one finding has been associated with a decreased risk of GDV and this is being of a “happy” temperament [15]. Risk factors that have been proposed as increasing the risk of GDV include breed, with German Shepherds, Great Danes, Standard Poodles and Irish Setters being over‐represented; increasing age; thin body condition; being of anxious temperament and having a first‐degree relative with GDV [2,15–19]. The role of diet has been extensively investigated, although the precise role remains unclear [15, 16, 19, 20]. Being fed large quantities of food, being fed from a raised bowl, dry kibble, being fed one meal a day, and eating quickly are all reported to be associated with an increased risk of GDV [16,19–22].
Pathophysiology
Dogs with GDV have rotation of the stomach, typically clockwise and between 180 and 360 degrees. Once rotation has occurred, a number of local and systemic effects result.
Local Effects
Gastric distension will decrease intramural blood flow and result in stasis, thrombosis, and hypoperfusion to the stomach wall. Gastric rotation will decrease this further; the greater the degree of rotation, the more severe the reduction in gastric blood flow. At its most severe, there will be cessation in blood flow to areas of the stomach that may result in necrosis and possible gastric perforation. Rotation of the stomach can cause stretching and possible rupture of the short gastric arteries, resulting in hemorrhage. In up to 38% of dogs, there will be compromise to the spleen, including torsion and damage to arterial supply, requiring splenectomy [23].
Systemic Effects
Many dogs with GDV are hypoperfused, resulting in generalized tissue ischemia. The hypoperfusion is multifactorial in origin, with the most important cause being obstruction to venous return as a result of occlusion of the caudal vena cava secondary to gastric tympany. Decreased right atrial filling results in decreased cardiac output. Some dogs will also have some degree of hypovolaemia as a result of hemorrhage or third spacing of fluid in the stomach. Cardiogenic shock may also occur as a result of arrhythmias and/or myocardial depression.
It is thought that the majority of postoperative systemic effects occur as a result of ischemia–reperfusion injury [24]. These include systemic inflammatory response syndrome (SIRS), hypotension, cardiac arrhythmias, disseminated intravascular coagulation (DIC), and acute kidney injury [25]. The presence of severe systemic effects is associated with a poorer prognosis [25].
Cardiac arrhythmias can occur in dogs with GDV. Most often these are ventricular in origin and are seen postoperatively (50–77% of dogs) but are also observed preoperatively in a lower proportion of dogs [7, 9]. The exact pathogenesis of these arrhythmias is unclear although alterations in coronary blood flow, circulating epinephrine and myocardial depressant factor have all been implicated [26].
Clinical Presentation
Dogs are often presented acutely. Many have a history of trying to vomit unproductively and some will be presented collapsed. Owners may have noted abdominal distension. Concerned owners should be asked to present their pets as soon as possible. Common findings on physical examination include hypoperfusion (including pale mucous membranes, prolonged capillary refill time, weak pulses, and tachycardia), arrhythmias, obtundation, abdominal pain and distension, gastric tympany, distress, and weakness (Figure 8.1). If the abdominal distension is profound, there may be a degree of dyspnea or tachypnea. Dyspnea can also occur secondary to aspiration of gastric contents.
Stabilization and Diagnostic Evaluation
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.