D.J. Brockman, BVSc, CVR, CSAO, DACVS, DECVS, FHEA, MRCVS
Department of Small Animal Medicine & Surgery, Royal Veterinary College, North Mymms, Hatfield, UK
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 non-sterile 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 anticipated. 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 (Dexon-Davis and Geck) acid 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 a gastrointestinal anastomosis instrument (GIA-50, US Surgical) has been described for this purpose, however, the authors prefer to use a thoracoabdominal stapler (TA-90, US Surgical) with a 4.8mm (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 oesophagus 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. 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 26g) Foley or Pezzer urologic catheter is placed through a stab incision in the body wall approximately 2cm lateral to the ventral midline and 2cm caudal to the last rib on the right side. It is then passed through a loop of omentum and into the stomach through a purse-string 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 pre-placed around the abdominal and gastric wall incisions in an overlapping mattress pattern. 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. Alternatively, an incisional gastropexy is simple and effective. With this technique, a 5cm seromuscular incision is made in the pyloric antrum, a matching incision is made in the parietal peritoneum and transverse abdominal muscle, just caudal to the thirteenth rib on the right body wall. The edges of the gastric wall incision are sutured to the edges of the body wall incision using either polydioxanone (PDS-Ethicon) or polypropylene (Prolene-Ethicon). Care must be taken not to penetrate the gastric lumen.
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 24hrs. 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 (1-2 mg/kg/day IV) or very low dose erythromycin (0.5-1.0mg/kg every 8 hours) 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.
Post operative complications
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 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 re-evaluated 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. An attempt to abolish a cardiac arrhythmia that is associated 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 occurs, the prognosis is grave.
Persistent ongoing hypotension, despite appropriate fluid therapy, is a serious concern. Serum electrolyte concentrations (sodium, potassium, chloride, magnesium, calcium) should be measured, coagulation parameters assessed, acid/base status evaluated and blood gas levels should be 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/bronchioalveolar wash sample cytology and culture, 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.