Daniel J. Brockman, BVSc, CVR, CSAO, DACVS, DECVS, FHEA, MRCVS
Gastric dilatation and gastric volvulus can occur independently, but together they represent a potentially catastrophic disease that is referred to as the gastric dilatation-volvulus syndrome (GDV). Gastric dilatation-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 dilatation 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 postoperative 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 regimens have been recommended, and management of GDV remains the subject of controversy. The aim of this lecture is to present a rational, practical and clinically proven protocol for the management of this condition.
History and Clinical Features
Gastric dilatation-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 nonproductive 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 dilatation, circulatory compromise, and respiratory compromise. Therefore, a distended abdomen, tachycardia, poor peripheral pulse quality, a prolonged capillary refill time, pale and dry mucous 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
1. Restore and support the circulation
2. Decompress the stomach
3. Establish whether GDV or simple dilatation is present
4. Rapid surgical correction if volvulus has occurred
Management of hypovolemia to prevent or treat shock is the primary goal of emergency treatment. Two large bore catheters (ideally 16 g or 18 g) 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, a hypertonic saline-dextran (HSD) combination (7% NaCl in 6% dextran 70) administered at 5 ml/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 reassessed 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 is not necessary to diagnose gastric dilatation but it is an invaluable aid in 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.
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 regimen. 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 65 mm Hg and a hematocrit at or above 25–30%.
The immediate aim of surgery is to return the stomach to its normal position and evaluate it and the spleen for signs of irreversible vascular compromise. If present, necrotic portions of stomach and spleen should be removed. The stomach should be emptied completely. Finally, a gastropexy should be performed in an attempt to prevent recurrence of the volvulus.
Following routine aseptic preparation, a cranial ventral midline laparotomy is performed. The stomach is usually immediately visible and covered by greater omentum when a clockwise volvulus of 180°–270° has occurred. Gastric decompression at this stage will help subsequent manipulation and relocation of the stomach. This can be achieved intraoperatively by needle gastrocentesis, if the stomach is still tightly distended. Alternatively, for a less distended stomach, a nonsterile assistant, with the intraoperative guidance of the surgeon, can gently place an orogastric tube. After decompression, the pylorus should be identified and grasped gently with the hand. If the gastric rotation is in a clockwise direction, downward pressure on the right side of the visible portion of the stomach along with gentle traction on the pylorus will aid counterclockwise rotation. The spleen should follow passively. A systematic evaluation of the abdomen should then be performed. Hemoperitoneum often results from avulsion of the short gastric branches of the splenic arteries. Active sites of hemorrhage should be identified and ligated. Careful inspection of the stomach and spleen should be carried out. If all organs look grossly normal, an assistant should lavage the stomach using clean, warm water via the orogastric tube.
The junction between the fundus and body and the greater curvature are the most common sites of gastric necrosis following GDV. Evaluation of tissue blood flow remains subjective; however, gentle palpation for pulsation in the gastric and splenic vessels is helpful. If the serosal surface is either torn, grey/green or black ten minutes after anatomical reduction of the stomach, ischemia is suspected and subsequent tissue necrosis is anticipated (Figure 2). In these situations, resection of the affected portion of the stomach should be performed. It may be difficult to determine how much of the stomach to remove. A full-thickness gastric wall resection is carried out until the cut edges are actively bleeding to ensure healing without further necrosis. Closure of the stomach following partial resection should be in two or three layers. A simple continuous suture pattern in the submucosa is followed by a simple interrupted pattern in the muscularis and serosa. Oversewing the suture line with a continuous or interrupted inverting pattern such as a Cushing or Lembert can reinforce this closure. Polydioxanone (PDS-Ethicon), polyglactin 910 (Vicryl-Ethicon), polyglycolic acid (Dexon-Davis and Geck) and polyglyconate (Maxon-Davis and Geck) are all suitable suture materials. Alternatively, surgical stapling devices can be used to perform partial gastric resection. The use of gastrointestinal anastomosis instrument (GIA-50, US Surgical) has been described for this purpose; however, the author prefers to use a thoracoabdominal stapler (TA-90, US Surgical) with a 4.8-mm (green) staple cartridge. Again, this closure should be reinforced using a continuous or interrupted Cushing or Lembert inverting pattern to oversew the staple line.
Occasionally the cardia or the abdominal esophagus will become necrotic secondary to longstanding or severe twisting. This area should be examined carefully. Resection of the abdominal esophagus and gastric cardia is technically demanding, and the outcome following such a resection - even in healthy animals - is unknown. Since necrosis at this site is usually seen in animals that are already severely compromised, the prognosis for recovery is poor.
Part or all of the spleen can sustain vascular damage or vascular occlusion following GDV. The spleen and associated vasculature should, therefore, be carefully evaluated for the presence of thrombi and irreversible vascular compromise. Any devitalized portion of splenic tissue should be resected either by hand or using a surgical stapling device (Figure 3). If the spleen has undergone torsion around its pedicle, splenectomy should be performed before reducing the twist to lessen the risk of releasing toxins, myocardial active substances, and thromboemboli into the systemic circulation.
A gastropexy should be performed. Many techniques have been described. Tube gastropexy is easy to perform, creates strong adhesions and has the additional advantage of providing enteral access. A large (24 or 26 g) Foley or Pezzer urologic catheter is placed through a stab incision in the body wall approximately 2 cm lateral to the ventral midline and 2 cm caudal to the last rib on the right side. It is then passed through a loop of omentum and into the stomach through a pursestring suture via a small incision in the pyloric antrum. The balloon on the Foley catheter is then inflated but kept away from the stomach wall to avoid inadvertent puncture while pexy sutures of polypropylene (Prolene-Ethicon) are preplaced around the abdominal and gastric wall incisions. The sutures are then tied and the balloon or mushroom tip is drawn up to the stomach wall, and the tube is secured either with a Chinese finger trap suture or tape tabs sutured to the skin.
Closure of the abdominal incision is routine. A bandage is placed around the abdomen to protect a gastropexy tube.
Fluid therapy is maintained at a rate of 8–10 ml/kg/hr using a balanced electrolyte solution for the first 24 hrs. Systemic administration of opioid analgesics (e.g., morphine at 0.5 mg/kg IM every 4–6 hrs) will reduce postoperative discomfort and facilitate recovery. During this period, it is useful to monitor PCV and TP intermittently along with peripheral pulse quality, mucous membrane color and urine output. Again, if continuous ECG is available, it should be used or intermittent records made. If present, the stomach tube should be vented as needed. Nothing should be given by mouth.
If complications do not occur, water can be offered the second day after surgery and the intravenous fluid rate reduced (4 ml/kg/hr). Patient comfort level and the need for further analgesia should be assessed and analgesia provided on an as-needed basis. Small amounts of food can be offered by the end of the second day. Animals that have undergone partial gastrectomy may take longer to regain normal gastric motility. Metoclopramide or very low-dose erythromycin might be beneficial in this situation. The gastropexy tube should remain in place for 7–10 days. During this time, it is kept clean and protected by a bandage. After removal of the tube, the gastrostomy is left to heal by secondary intention.
The clients should be informed of the signs of recurrence and encouraged to seek veterinary attention as soon as possible if they are encountered.
Persistent hypotension may be suspected if peripheral pulse quality is poor, if tachycardia and poor capillary refill time are evident, and urine output is low. Most commonly, this hypotension is caused by hypovolemia secondary to inadequate fluid therapy in the post-surgical period. Hypotension may also develop if the intravenous crystalloid fluid therapy is failing because of inadequate primary surgical hemostasis and subsequent whole blood deficits, reduced colloid osmotic pressure, or abnormal body fluid distribution. Occasionally, hypotension in post GDV surgery patients is due to poor cardiac function. If PCV & TP levels reveal hemoconcentration and a return to high volume, rapid infusion of crystalloid may be necessary for a short time (i.e., 1 hr at 90 ml/kg) followed by a return to 10–15 ml/kg/hr. If the PCV and/or TP are low, blood products or synthetic colloid should be administered to correct the deficit(s). The patient should be reevaluated frequently following any change in fluid therapy.
Cardiac arrhythmias are common following an acute episode of GDV. They are usually ventricular in origin and range from intermittent ventricular premature conductions to sustained ventricular tachycardia. Occasionally supraventricular abnormalities (e.g., atrial fibrillation) are seen. It may be necessary to treat cardiac arrhythmias if they are associated with primary heart disease (e.g., dilated cardiomyopathy) or if there is evidence of poor cardiac performance. If continuous electrocardiogram (ECG) and simultaneous blood pressure monitoring are available, a decision about cardiac function in the face of an arrhythmia is relatively easy (Figure 4). An attempt to abolish a cardiac arrhythmia that is associated with hypotension, using antiarrhythmic drugs, is considered only if acid/base and electrolyte imbalances have been corrected and intravascular volume replenishment is adequate.
The most common complications of tube gastropexy are local cellulitis due to leakage of gastric contents around the tube or following premature tube dislodgement. Occasionally the balloon of a Foley catheter can be eroded by the acidic gastric fluid, causing early loosening of the tube. Usually this occurs after 5–7 days, as the animal becomes more active, and will spontaneously resolve. If this happens in the first 48 hours, the risk of peritonitis secondary to leakage of gastric contents mandates tube replacement under general anesthesia.
Preoperative retching, vomiting, and postoperative esophagitis and regurgitation place these animals at risk for the development of aspiration pneumonia. Alterations in breathing rate and pattern coupled with crackles and wheezes on thoracic auscultation are suggestive of pneumonia. Thoracic radiographs, arterial blood gas evaluation, and tracheal/bronchioalveolar wash fluid cytology and culture will help confirm a clinical diagnosis of pneumonia. Treatment with the appropriate antibiotic(s), local fluid therapy (nebulization), thoracic coupage, supplemental oxygen, and frequent small amounts of exercise should aid recovery.
Gastric necrosis and perforation can occur up to five days postoperatively, especially if resection was performed, and in spite of careful intraoperative assessment of gastric wall viability. This complication may be suspected on the basis of clinical progression of disease, radiographic and ultrasonographic findings, and cytological evaluation of peritoneal fluid. It may be difficult to confirm without surgical exploration of the abdomen. Treatment is by debridement and repair of the gastric wall defect, followed by continued intensive supportive care. If gastric necrosis and perforation occur, the prognosis is grave.
Persistent, ongoing hypotension, despite appropriate fluid therapy, is a serious concern. Serum electrolyte concentrations (sodium, potassium, chloride, magnesium, and calcium) should be measured, coagulation parameters assessed, acid/base status evaluated, and blood gas levels determined before making further alterations to therapy. Electrolyte abnormalities should be carefully corrected. An abnormal hemostatic profile or a clinical bleeding tendency should be interpreted as evidence of DIC. Replacement of consumed coagulation factors using fresh-frozen plasma should be considered in addition to continued therapy for the underlying cause of shock. Hypoxemia in these patients may be secondary to pneumonia or pulmonary edema. Pulmonary edema may develop secondary to overzealous intravenous fluid administration, primary cardiac dysfunction, reduced colloid osmotic pressure, or following acute lung injury as a component of the systemic inflammatory response syndrome. Systemic inflammatory response syndrome, in turn, can be triggered by many factors including endotoxemia, organ reperfusion injury, and local inflammatory conditions such as peritonitis, pneumonia, and pancreatitis. Thoracic and abdominal radiographs, cardiac ultrasound, abdominal ultrasound, abdominocentesis, tracheal/bronchoalveolar wash, sample cytology and culture, and further hematological and serum chemistry evaluation should be considered to assist further therapeutic decision-making. Persistent hypovolemia despite aggressive fluid therapy and the development of pulmonary complications, where systemic inflammation is suspected, are poor prognostic signs. Therapy for such patients may include oxygen supplementation and ventilator-assisted breathing in addition to continued intensive circulatory support, as previously described. The prognosis for animals with these complications is very poor.
VIN editor: Figures were not available at time of publication.
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