Introduction

Gastric dilation and gastric volvulus can occur independently, but together they represent a potentially catastrophic disease that is referred to as the gastric dilation-volvulus syndrome (GDV). Gastric dilation-volvulus is most likely a polygenic disease with strong phenotypic and environmental influences. The precipitation of a GDV episode, in most instances, is probably the result of either a single overwhelming factor or the summation of several risk factors. Simultaneous gastric dilation and volvulus result in pathophysiological changes that create a medical and surgical emergency. Dogs suffering this disease develop local (gastric and splenic) and systemic consequences of GDV resulting in hypovolemia, and placing them at risk for gastric and splenic vascular compromise, focal and generalized bacterial infections, initiation and propagation of local and systemic inflammation, disseminated intravascular coagulation, shock and death. The overall incidence of this condition in the canine population is low. It remains an important syndrome, however, because successful management requires intensive emergency, surgical, and post-operative care. Despite what some would consider optimal management, the fatality rate for this syndrome can still be as high as 15 to 20%. Consequently, many treatment regimes have been recommended and management of GDV remains the subject of controversy. This is the first of a two article series on the topic of GDV. In the first article the authors aim to present a rational, practical and clinically proven protocol for the management of this condition. In the second article, the authors will explore the recent scientific and clinical literature about the pathogenesis of GDV and examine how these data aid the formulation of a unifying hypothesis for the pathogenesis of GDV.

History and Clinical Features

Gastric dilation-volvulus syndrome most commonly occurs in large or giant, deep-chested breeds but has also been reported in small breeds of dog.

The onset of clinical signs is typically peracute or acute. Initial clinical signs include restlessness, hypersalivation and non-productive attempts to vomit. This is usually followed by further discomfort and gradual abdominal distension. Eventually, pain becomes evident, along with weakness and abdominal tympany.

Physical examination findings reflect gastric dilation, circulatory compromise, and respiratory compromise. Therefore, a distended abdomen, tachycardia, poor peripheral pulse quality, a prolonged capillary refill time, pale and dry mucus membranes, tachypnea, and dyspnea are expected, according to duration and severity of the episode. It is important to realize that a dilated stomach in a giant-breed dog can remain within the rib cage and, therefore, in these breeds, classical abdominal distension may not be seen.

Management of Suspected Acute GDV

Therapeutic goals:

1.  Restore and support the circulation

2.  Decompress the stomach

3.  Establish whether GDV or simple dilation is present

4.  Rapid surgical correction if volvulus has occurred

5.  Prophylaxis:

a.  Surgical

b.  Environmental

Emergency Care

Management of hypovolemia, to prevent or treat shock, is the primary goal of emergency treatment. Two large bore catheters (ideally 16g or 18g) should be placed in cranial veins (cephalic or jugular). If the facility for rapid results is available, a blood sample should be taken for packed cell volume (PCV), serum total protein estimation (TP) and serum electrolyte levels. Sufficient blood should also be drawn for subsequent performance of full serum chemistry, hematological evaluation and evaluation of coagulation parameters. Fluid therapy should be started at a rate of 90 ml/kg/hr using a balanced electrolyte solution. In giant breeds, an hypertonic saline-dextran (HSD) combination (7% NaCl in 6% dextran 70), administered at 5ml/kg over a five minute period, may provide more rapid initial circulatory resuscitation. Both the high volume crystalloid and low volume HSD fluid resuscitation protocols should be followed by high volume crystalloid administration (20 ml/kg/hr) for maintenance of resuscitation. The decision to introduce blood products or a synthetic colloid to provide further circulatory support and improve oxygen delivery to tissues should be influenced by subsequent PCV, TP and circulatory stability estimations. If available, continuous ECG should be started or a baseline recording made.

Gastric decompression should only be attempted once correction of the intravascular volume deficit is well underway. Close patient monitoring is essential at this time. Delaying decompression beyond this time could have an important influence on gastric wall integrity and the ultimate systemic levels of inflammatory mediators released from the splanchnic circulation. In most instances, gastric decompression can be achieved by orogastric intubation of the conscious or sedated animal. For sedation, a combination of fentanyl (2-4 micrograms/kg) or oxymorphone (0.1 mg/kg IV) followed by diazepam (0.25-0.5 mg/kg IV) can be used. A selection of smooth surfaced equine nasogastric tubes with large end and side holes, is helpful. The tube selected should be measured from the external nares to the caudal edge of the last rib and marked. The tube should not be inserted beyond this mark. A bandage roll placed between the teeth can aid passage of the lubricated tube. If tube passage is not possible, it may help to place the dog in a sitting position and gently rotate the tube in a counterclockwise direction. If orogastric intubation is still impossible, gastrocentesis using a large bore needle in the right or left paracostal space at the site of greatest tympany will usually facilitate orogastric intubation and avoid inadvertent splenic damage. Routine aseptic technique should be used. The patient should be frequently re-assessed by collection and analysis of subjective and objective clinical data, such as: peripheral pulse pressure and quality, heart rate, mucous membrane color, capillary refill time (CRT), PCV and TP concentration, degree of abdominal distension, and ECG. Intravenous fluid type and composition should be tailored to each individual patient's needs, to optimize tissue perfusion and oxygen delivery.

Radiography

Radiography is not necessary to diagnose gastric dilation but is an invaluable aid to diagnosing volvulus. When considering the need for radiography it is important to remember that the easy passage of an orogastric tube does not rule volvulus out. A right lateral recumbent view of the cranial abdomen is the initial examination of choice. This view should be supplemented by further views if the diagnosis is still uncertain. The radiographic features of GDV include a large dilated gas-filled gastric shadow which may be divided into two compartments by the soft tissue of the lesser curvature and proximal duodenum coursing from their abnormal position in the craniodorsal quadrant of the abdomen caudally (Figure 1). If rotation of the stomach is not severe, the abnormal position of the pylorus, dorsal and to the left of the fundus is diagnostically helpful. This may not be visible on left lateral radiographs. Splenic enlargement and malposition may be evident. Gas within the gastric wall may indicate gastric wall compromise; if gastric rupture has occurred, free gas will be present in the abdominal cavity.

Anaesthesia

In practice situations, the choice of anesthetic agents may be limited. If the previously mentioned sedative combination has been used preoperatively, endotracheal intubation may be achieved after a further intravenous infusion of the same cocktail. The inclusion of lidocaine into the induction protocol (2 mg/kg IV) will help desensitize the larynx and facilitate endotracheal intubation in addition to enhancing the overall state of anesthesia. In addition, if a different induction agent is to be used, the quantity required will be reduced because of residual effects of the sedative. It is also important to realize that circulatory compromise will influence the speed and efficiency of drug distribution. Since intravenous access should already be established, small amounts of induction agent should be given to effect. Maintenance should be with halothane or isoflurane and oxygen. Nitrous oxide should not be introduced until permanent gastric decompression is achieved.

The placement of additional intravenous and intraarterial catheters in the pelvic limbs, following the induction of anesthesia, will facilitate intraoperative blood pressure monitoring and the addition of blood products, for example, to the intraoperative fluid therapy regime. Continuous electrocardiography and continuous or intermittent blood pressure monitoring should be done during anesthesia. Intraoperative fluids should remain at a high rate (10-20 ml/kg/hr) to offset any further deterioration in hemodynamics during surgery. A catheter should be placed in the urinary bladder and connected to a closed urine collection system. Evaluation of PCV and TP should be performed intraoperatively at 30 to 60 minute intervals. Again, intravenous fluid type and composition should be tailored to each individual patient's needs, in an attempt to ensure adequate tissue perfusion and oxygen delivery by maintaining a mean arterial blood pressure above 65mmHg, and a hematocrit at or above 25-30%.