Surgery Of The Stomach
The stomach is a C-shaped musculoglandular organ. It has the largest dilatation of the alimentary canal. The stomach lies mainly in a transverse position, Predominantly to the left of the median plane. When it is empty, the stomach lies cranial to the last rib and between the ninth thoracic and first lumbar vertebra.
The stomach is divided into four parts: cardia, pylorus, fundus and body. Four tunics compose the wall of the stomach. These are the mucous, submucosa, muscularis and serosa. The mucosa is lined with columnar epithelium, which can regenerate 48 hours after moderate damage. The submucosa provides most of the holding power. The muscularis is composed of three layers: inner oblique layer, middle circular layer (which forms the pyloric sphincter. and the outer longitudinal layer).
The blood supply to the stomach is from the celiac artery. The stomach receives it's nerve supply from the vagus (extrinsic parasympathetic supply) and thesplanchnic (extrinsic sympathetic supply). The indications for stomach surgery arepyloric stenosis, foreign bodies, certain gastric ulcers, neoplasms, acute dilation and torsion, and pylorospasms.
The pathophysiology of certain conditions of the stomach include gastric dilation-torsion complex. Gastric dilation precedes gastric torsion, The etiology of gastric dilation is vomition, parturition, spinal injuries, trauma, neoplasms, overeating, general anesthesia, abdominal surgery, pica, duodenal obstruction, electrolyte disturbance, and aerophagia. Production of fluid and/or gas plus the presence of anobstruction preventing relief of distention. As intragastric pressure increases, portal hypertension occurs.
General circulatory hypotension occurs due to three factors. One such factor is when there is neurogenic decrease in blood flow with the afferent pathway beingearned via splanchnic nerves. It is also found when there is mechanical occlusion of the caudal vena cava, and mechanical interference with portal venous blood.
Gastic dilation causes the blood to become sequestered in the pancreas, spleen and nearly all of the digestive tract. Splenomegaly occurs and leads to splenic displacement and causes traction on the stomach. Also, sequestered blood has a lowvelocity of flow. Hence, blood tends to increase in viscosity. As viscosity increases, the ability to perfuse tissues at a normal rate decreases and this eventually results in a state of shock.
With decreased perfusion, one finds cellular hypoxia and probably anaerobic metabolism and metabolic acidosis. Eventually there is an increase in cellular catabolism. With increased catabolism, enzymes and histamine-like substances are released from lysosomes with resulting dilation of vasculature and increased permeability with loss of fluid from capillaries into tissue spaces. With fluid loss, higher viscosity of blood and further reduction of blood flow rate occurs.
High viscosity of blood cause the platelets to clump and the micro-vasculature to collapse. Disseminated Intravascular Coagulation (DIC) is likely to occur. The presence of enzymes and histamine-like substances may also explain the hemorrhagic gastritis which is often seen in this disease. Hypoxia will lead to necrosis of interstitial villi and absorption of exogenous endotoxin will be promoted. With obstruction of portal venous blood, the ability of the liver to detoxify endotoxin is impaired. As shock progresses, the liver deteriorates and any actually accelerate the shock.
With altered hemodynamic and metabolic factors, platelets begin to aggregate and fibrin is deposited. If elements of hemostasis are severely depleted, DIC will result from a deficiency of these elements consumed in widespread thrombosis.
Also involved with hypotension and circulatory shock is the release of the myocardial depressant factor (MDF), which is released from the pancreas through damaged cell membranes into the extracellular fluid. MDF is carried by systemic capillaries and lymphatics into venous circulation. MDF has a direct cardiodepressant effect, a vasoconstrictor effect on splanchnic blood vessels, and a depressant effect on phagocytic properties of the RE system.
Volvulus occurs when the pylorus moves from right to ventral to left to dorsal. The greater curvature lies ventrally. These displacements cause the spleen to move with the fundus because of splenic and vascular attachments to the stomach. Vascular tiangles range from fundic hyperemia to necrosis and perforation. Vascular lesion are always found in the area of the grater curvature.
Indications for surgical intervention are noted when the confirmation of gastric dilation-volvulus syndrome (GDV) necessitates surgical intervention. Clinical signs include large breed deep-chested dogs that retch with an inability to vomit. Hyperpnea with increased respiratory efforts are frequently seen. Abdominal asymmetry to the right side is often present.
Shock is a common and rapid sequella to the GDV complex. Physical examination reveals splenomegaly, weak pulse, tachycardia, and increased CRT. Definitive diagnosis may be made on the basis of radiographs (compartmentalization of air in the stomach). Following decompression, the stomach may return to normal position, or remain malpositioned without functional disturbance.
The surgical technique for gastric dilation torsion complex involves
preoperative care that should include the immediate treatment of the shock
state along with decompression. Survival is often closely related to intravenous
volume replacement therapy. Corticosteroids are important, but must always
be preceded by fluid therapy. Corticosteroids stabilize lysosomal membranes,
produce vasodilation, improve perfusion and protect against DIC. Important
in GDV Complex is the corticosteroid inhibition of endotoxin activation:
The administration of bacteriocidal class antibiotics is necessary. Gastric decompression is accomplished via a well lubricated stomach tube followed by warm saline lavage. Should decompression by this means fail, trocarization with a 12-16 gauge needle into the right paracostal area may be successful. Baseline laboratory parameters should be run.
GDV surgery begins with a midventral abdominal incision from the xiphoid cartilage to the umbilicus. The stomach and spleen should be realigned and the stomach wall should be assessed for necrotic areas. Excision of the necrotic areas is followed by routine closure for gastrotomy. Splenectomy is sometimes performed especially with torsion and/or thrombi of the splenic vessels.
Pyloroimyotomy or pyloroplasty is used to relieve gastric retention or obstruction, and decreases gastric emptying time. Commonly utilized techniques to relieve and prevent reocurance of GDV complex include gastropexy, tube gastrostomy, circumcostal gastropexy and others. Tube gastrostomy and circumcostal gastropexy are currently favored.
The procedure for tube gastrostomy is relatively simple for the general practitioner to perform. After a cranial midline abdominal incision has been made, and the stomach derotated, carmalt forceps are passed through the abdominal wall in the right paracostal area near the tip of the thirteenth rib. Insure that the exit hole in the skin is slightly smaller than the tube thus creating a tight fit. A 22-26 French Foley catheter is used. Retrieve the catheter through the paracostal incision. Place a full thickness purse string suture using 2-0 PDS in the pyloric antrum 2/3 of the distance toward the pylorus from the fundus. An incision is made within the purse string suture and the Foley inserted into the stomach. The balloon on the catheter is inflated using saline, and the purse string suture is tightened. The tube is used to pull the stomach into position adjacent to the peritoneal wall. Gastropexy using size 0 PDS suture material is performed between the abdominal wall and stomach around the tube. Sutures must incorporate the submucosal layer of the stomach wall and the Muscle fascia of the Transversus abdominis lying just under the peritoneum.
Post-operative care includes bandaging the abdomen to prevent the animal from damaging the tube. Complications are often associated with shock, cardiac arrythmia and vomiting due to the presence of the tube in the stomach. Leaking of gastric contents around the tube is possible and thus a 'lift and store' dressing should be placed around the tube as it exits the abdominal wall. Fluid therapy, along with careful monitoring is important. The tube should be left for 5-7 days, then deflate the balloon, remove the skin purse string and retract the catheter. The skin wound is not sutured, but dressed with another dressing.
Circumcostal Gastropexy is an alternate procedure that has the advantage of not having to manage a gastrostomy tube for 5-7 days and creates a very secure adhesion of the pylorus to the right abdominal wall; however, it does require an assistant and a slightly longer operating time. The stomach is approached and exteriorized as described above. The pyloric antrum is isolated and an H incision is made in the exterior wall down through the submucosa. The two H flaps are dissected free and retained with two stay sutures on each flap. The cartilaginous portion of the 11th rib is isolated and one flap is passes around behind the rib. The two flaps are sutured together with 2-0 PDS suture material and the sutured incision is pulled back behind the rib and the rest of the H incision is closed with the same suture. The post-op considerations are similar to those described above except for the tube management.
Pyloric disease of the dog can be one of three types: congenital pyloric stenosis, acquired pyloric stenosis or pylorospasm. Congenital pyloric stenosis is a hypertrophy of muscle of the pyloric sphincter. It may be a fibrosis of the muscle layers and degeneration of myenteric plexuses. It is most frequent in brachycephalic breeds. Acquired pyloric stenosis usually is the result of chronic gastritis, gastric ulcers, neoplasms, or chronic pylorospasm. Pylorospasm can occur at any age in dogs that are usually nervous and excitable. Toy and miniature breeds are most commonly affected. Pylorospasm is a failure of relaxation of the pyloric sphincter in the absence or diminution of arterial propulsive waves. It is probably a neurogenic dysfiniction mediated either centrally or locally.
The surgical technique of a gastrotomy is via a ventral mid line approach. The incision is extended from the xiphoid caudally to a point long enough to permit adequate exposure of the cranial abdomen. The stomach is exteriorized through the abdominal incision. With a suspected foreign body, palpate the stomach and locate the foreign body. Pack off the stomach from the rest of the abdominal viscera with laparotomy pads moistened in warm saline. The proposed gastrotomy incision should be located in a relative avascular area, approximately midway between the lesser and greater curvature and equidistant from the pylorus and cardia. Place a stay suture at each end of the proposed incision site. Make a stab incision with a #10 Bard-Parker scalpel blade - 1/2 cm. from either stay suture. The incision penetrates all layers of the stomach wall and is extended toward the opposite stay suture with scissors or scalpel blade. Stay sutures serve to elevate the incision and prevent spillage of gastric contents into the peritoneal cavity. Bleeding vessels may be ligated with fine synthetic absorbable sutures.
The gastrotomy incision is closed with two layers of 2-0 or 3-0 synthetic absorbable suture material. The first layer inverts the wound edges through the use of a continuous Cushing suture pattern. The second layer is then closed with continuous Lembert suture pattern. The stomach is returned to normal position and the omentum is placed over the incision site. If the abdomen has been contaminated with gastric spillage, thorough lavage of the peritoneal cavity with warm saline or lactated Ringer's solution is advised. Antibiotics (i.e. aqueous Penn) may be placed into the peritoneal cavity before closing. Close the abdominal incision in the routine manner.
Post-operatively, the patient should be administered antibiotics for 7-10 days. Continuous IV fluid and electrolyte support is given for 24 hours. Animals can be given oral fluids 12 hours post-operatively. If oral fluids are retained, small frequent feedings may be initiated. The pyloromyotomy (Fredet-Ramstedt) procedure is performed when indications include pyloric dysfunction (i.e., pyloric stenosis) and the gastric dilatation-torsion complex. The same approach is used as that for gastrotomy. It is often useful to transect the gastrohepatic ligament to increase pyloric mobility. The pylorus is grasped and stabilized between the thumb and the index finger. A #15 scalpel is used to make a longitudinal incision on the relative avascular ventral pyloric canal, pylorus and proximal duodenum. The incision should extend 1-2 cm on either side of the pylorus. Care should be taken to only cut serosal and muscle layers of the pylorus. The mucosa must be left intact. As circular muscle is cut until the mucosa bulges into the incision. It is imperative that all constricting bands of the circular muscle layer are cut to assure adequate enlargement of the pyloric lumen. Hemorrhage is usually minimal. Should perforation of the mucosa occur, one or two interrupted PDS (3-0) sutures must be used to close this area, or a pyloroplasty may be performed.
Postoperatively, antibiotics should not be necessary. IV fluids may be discontinued if fluid and electrolyte balances have been corrected. Small, frequent feedings can be initiated on the first post-op day. The patient can go to a normal diet in 5-7 days.
The pyloroplasty (Heineke-Mikulicz) procedure provides a more permanent means for decreasing gastric emptying time. This procedure results in a shorter but wider canal. The procedure begins as a pyloromyotomy with the pylortis incised longitudinally through the circular muscle fibers. At this point a retention suture is placed on either side of the incised pyloric musculature at the center of the incision. The mucosa of the pylorus is incised and the pyloric incision is pulled in opposite directions with the retention suture. The longitudinal incision is thus covered to a transverse incision. The incision can be closed in a single crushing layer method using simple interrupted sutures of 3-0 synthetic absorbable material. No attempt is made to unfold the projections usually resulting at each end of the closure. The first suture should oppose the ends of the original longitudinal incision; this assures equal alignment of wound edges. By closing the incision in an opposite direction, the sphincter mechanism of the pylorus is destroyed.
Post-operatively antibiotics are indicated. IV fluids are continued for 24 hours after the surgery. The animal may be offered small volumes of water 12 hours post-op. if oral fluids are retained, small, frequent feedings may be initiated.