Small Animal Surgical Emergencies. Группа авторов
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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. 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