Surgery of the stomach (Proceedings)
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.
Geneial 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.