While melena and hematemesis alone may be caused by any lesion in the upper gastrointestinal tract, the appearance of coffee-ground vomitus or gastric aspirate indicates that blood has been in contact with acidic gastric contents. Erosive gastroduodenitis is suspected when a patient with upper gastrointestinal bleeding gives a history of having recently ingested non-steroidal anti-inflammatory drugs or significant amounts of alcohol. These patients may also give a history of upper abdominal discomfort, occurring irregularly for days or weeks prior to the bleeding episode, and may have noted that liquid antacids provided them with temporary relief. The alcoholic patient with erosive gastritis may be either a chronic or a binge drinker; bleeding from such lesions may occur at any age. Stress ulceration is a process similar to erosive gastritis, but occurs primarily in patients confined to intensive care units, suffering from severe injuries, infections, or cardiovascular problems, and not exposed to non-steroidal anti-inflammatory drugs. Their lesions appear to result from transient mucosal ischemia.
Lesions of erosive gastroduodenitis or stress ulcers are most often multiple and tend to occur mainly in the gastric antrum. On microscopic examination, the acute ulcerations demonstrate loss of epithelium and inflammatory cells in the mucosa. The erosions themselves do not usually penetrate into the submucosa and are not surrounded by fibrous tissue.
Hemorrhages from erosive gastroduodenitis or stress ulcers vary greatly in intensity, depending on the extent of the disease process. Upper gastrointestinal endoscopy is necessary to confirm the diagnosis and to estimate the rate of bleeding. Coagulation of the acute ulcers with the Bicap or the heater probe is effective therapy; the disorder is unlikely to recur once the causative agents are discontinued and the patient is removed from life-support systems.
Hemorrhage from stress ulcerations has become a large enough problem during intensive care that most units now advise some sort of prophylaxis in patients at risk. Antacids, H2-blocking agents, and sucralfate have been used to prevent bleeding, and all have been beneficial. However, pneumonia has been a significant complication in ventilated patients on agents that raise gastric pH levels. Because of better protection from bleeding and lower levels of pneumonia, sucralfate presently appears to be the drug of choice in preventing stress ulcers (Iry.ba.1991). With regard to non-steroidal anti-inflammatory drugs and upper gastrointestinal hemorrhage, risk increases with age and with dosage, and the danger lasts for about a month after the medication is discontinued ( M..a.c,D.o,n..aid e.t al 1995).
Misoprostol (400-800 mg daily) reduces both the risk of hemorrhage from non-steroidal anti-inflammatory drugs and the histological gastritis that they cause.
Peptic ulcers may occur in the esophagus as a complication of reflux esophagitis, the stomach, or the duodenum. They may also be found in the jejunum in patients who have previously undergone a partial gastrectomy with gastrojejunostomy (Billroth 2 anastomosis), and are occasionally multiple (mainly duodenal and jejunal) in patients with the Zollinger-Ellison (hypergastrinemia) syndrome. Hemorrhage is a common complication of peptic ulcer at any site, and occurs in about 20 per cent of patients with untreated lesions. Most patients with peptic ulcer have been symptomatic prior to bleeding. Many report a previous diagnosis of ulcer and may have been treated in the past with sucralfate, H2-blocking agents, or gastric acid pump inhibitors. Untreated patients often relate a history of epigastric pain relieved for several hours by meals or antacids, and occurring between meals and while asleep. Loss of weight and vomiting are uncommon symptoms, suggestive rather of obstruction of the gastric outlet. Patients with the Zollinger-Ellison syndrome frequently complain of diarrhea suggesting malabsorption (fatty foul-smelling stools) and loss of weight, and occasionally report lack of success of conventional therapy for peptic ulcer disease. The diarrhea in these patients is believed to result from inactivation of lipases in the highly acidic upper intestinal lumen, and may also be caused by excesses of vasoactive intestinal polypeptide from an associated neuroendocrine tumor.
Once cardiovascular stability has been achieved, ulcer-bleeding suspects should be treated with an intravenous H 2-blocking agent (e.g. ranitidine, 6.25 mg/h) and immediate endoscopy. This procedure will identify the site, depth, and size of the ulcer(s), and whether the ulcer is single or multiple and actively bleeding. A pumping artery in the ulcer base may be difficult to coagulate endoscopically, but surprisingly good results have been obtained using a combination of electrocoagulation of the ulcer base and multiple injections of about 1 ml of epinephrine (adrenaline) (0.005 per cent) in hypertonic (3.6-7.1 per cent) saline around the circumference of the ulcer. Caputi Iambrenghi et al. (1995) found that 25 of 86 patients (29 per cent) with recent ulcer hemorrhage re-bled on 'conservative' treatment, while only three of 34 patients (8.8 per cent) re-bled after receiving periulcer injections of epinephrine and a sclerosing agent.
In instances where the ulcer is not bleeding at the time of endoscopy but instead contains a large clot, electrocoagulation of the clot itself often prevents further bleeding. There is still disagreement among endoscopists as to whether the clot should be removed in these cases before attempting coagulation. Where a visible vessel is seen in the base of the ulcer, there is a slightly lower success rate with electrocoagulation; multiple treatments and, occasionally, surgery are indicated. One study (Grosso. etal 1995) has shown that re-bleeding from ulcers containing a visible vessel (19 per cent) is essentially the same if patients are treated with either perendoscopic injection of sclerosants or with intravenous omeprazole (40 mg twice daily). If multiple ulcers are seen in the lower stomach or duodenum, serum gastrin levels should be measured for the possible presence of a gastrinoma.
The symptoms of gastric and duodenal ulcers are indistinguishable. Upper gastrointestinal endoscopy and barium-contrast radiography are the only techniques available for a precise diagnosis. This distinction should be made as early as possible because of the possibility of dysplastic or malignant changes in gastric lesions. About 2 to 5 per cent of gastric ulcers appear in malignant tissue. Since changes of carcinoma are not always readily apparent on gross endoscopic examination, multiple biopsies should be taken from the circumference and base of gastric ulcers. In lesions that are actively bleeding, or have recently bled, it is probably best to wait several days before obtaining biopsies. The treatment of bleeding peptic ulcers should include the use of intravenous H 2-blocking agents for the first week or so, and a bismuth-antibiotic program if Helicobacter pylori is detected.
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