Peptic ulcer is a mucosal lesion of the stomach or duodenum. The term peptic ulcer is used to describe both gastric and duodenal ulcers. PUD results when gastric mucosal defenses become impaired and no longer protect the epithelium from the effects of acid and pepsin.
When a break in the mucosal barrier occurs, hydrochloric acid injures the epithelium. Gastric ulcers may then develop. With a gastric ulcer the pain occurs 1-2 hours after meals and does not usually wake the patient from sleep. Food worsens the pain. There is an increased risk for malignancy and these ulcers are deep and penetrating and usually occur on the lesser curvature of the stomach.
Most duodenal ulcers occur in the first portion of the duodenum. With this type of ulcer the pain occurs 2-4 hours after meals, pain wakes up the patient, the pain is relieved with the administration of food and there is very little risk for malignancy.
Hemorrhage : With massive bleeding the patient vomits bright red or coffee ground blood. Minimal bleeding from ulcers is manifested by occult blood in a tarry stool (melena). Perforation : Gastric and duodenal ulcers can perforate or bleed. Perforation occurs when the ulcer becomes so deep that the entire thickness of the stomach or duodenum is worn away. The gastroduodenal contents may then empty into the peritoneal cavity. Symptoms of perforation are sudden, sharp pain, the abdomen is tender, rigid, and boardlike. The patient assumes the fetal position, knees to chest. Client can become acutely ill within hours. Peforation is considered a surgical emergency and can be life threatening. If this occurs the physician needs to be notified immediatley.
A barium examination of the GI tract can be used to establish a duodenal ulcer. If perforation is suspected the health care provider usually requests an upright abdomen series to demonstrate free air in the peritoneum. Do not use barium where free air is a possibility.
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Hyposecretory drugs produce a reduction in gastric acid secretions. Your proton pump inhibitors have emerged as the drug class of choice for treating clients with acid-related disorders. These drugs suppress acid production. They include Prilosec and Previcid. Your H2 receptor antagonists block histamine stimulated gastric secretions. Antacids neutralizes acid and prevents formation of pepsin. The prostoglandin analogs reduce gastric acid and enhance mucosal resistance to injury. The drug Carafate acts as a mucosal barrier by forming a protective coating. These drugs are all listed in Chart 59-3 pages 1286-1287.
A simple gastroenterostomy permits neutralization of gastric acid by regurgitation of alkaline duodenal contents into the stomach. The surgeon creates a passage between the body of the stomach and the small bowel. Drainage of the gastric contents diverts acid from the ulcerated area and facilitates healing.
A vagotomy eliminates the acid-secreting stimulus to gastric cells and decreases the responsiveness of parietal cells.
In this procedure the surgeon enlarges the pyloric stricture by incising the pylorus longitudinally and sutures the incision transversely.
The postoperative plan of care is similar for all of the gastric operative procedures. These patients will have NG tubes in place and attached to low wall suction. Ensure the patency of these tubes. Irrigation or repositioning of the NG tube is not done after gastric surgery unless specifically ordered by the doctor.
Observe for any bleeding, monitor vital signs and post surgery hemoglobin and hematocrit. If gastric retention occurs once ng tube is removed, it will have to be put back in.
Dumping Syndrome : is a term that refers to a constellation of vasomotor symptoms after eating, especially following a Billiroth II procedure. This syndrome is believed to be caused because of the rapid emptying of the stomach contents into the small intestine, which shifts fluid into the gut, causing abdominal distention. Early manifestations occur within 30 minutes of eating. Symptoms include vertigo, tachycardia, syncope, pallor, sweating and palpatations. Late dumping syndrome occurs 90 minutes to 3 hours after eating, and is caused by a release of an excessive amount of insulin. The insulin release follows a rapid rise in the blood glucose level that results from the rapid entry of high carbohydrate food into the jejunum. Symptoms include dizziness, light-headedness, palpatations, diaphoresis, and confusion. Dumping syndrome is managed by dietary measures that include decreasing the amount of food taken at one time and eliminating liquids with meals.
