A Daily Beer Drinker With Agonizing Gas and Back Pain

Erik D. Schraga, MD


February 09, 2021

Uncomplicated peptic ulcer disease is highly prevalent in the United States. When combined with duodenal ulcers, the incidence is 1.8%, or approximately 500,000 new cases annually.[2] In addition, about 4 million recurrences are noted annually.

Approximately 90% of duodenal ulcers and 75% of gastric ulcers are associated with Helicobacter pylori infection.[3] H pylori appears to cause injury to the mucosal lining of the stomach and duodenum through three potential mechanisms: production of toxins that cause local tissue injury, induction of a mucosal immune response, and an increase in gastrin levels with an increase in acid secretion.

After H pylori infection, NSAIDs are the most common cause of peptic ulcer disease. The risk for disease and complications (such as hemorrhage or perforation) are proportional to the daily dose taken. Advanced age and concurrent use of anticoagulants or steroids also increase the risk for complications. Other factors that may predispose a patient to gastric ulceration include chronic alcohol intake, smoking, and infection.[3]

Perforation of a peptic or duodenal ulcer into the peritoneal cavity has the potential for significant morbidity and mortality. Most cases occur in elderly persons and in persons using NSAIDs. In cases of perforated peptic ulcer, low-dose aspirin may be the only NSAID taken. Remarkably, smoking appears to be a stronger risk factor than use of NSAIDs in patients younger than 75 years.

Although most patients give a history of chronic epigastric pain before perforation, caused by the presence of the uncomplicated ulcer itself, 10%-25% of patients have no symptoms leading up to the perforation.[1] In approximately 10% of patients, the perforation is accompanied by hemorrhage.

Perforated peptic ulcers are most often located at the lesser curvature of the stomach. Most perforated duodenal ulcers involve the anterior wall of the duodenal bulb.[1,4,5]

Three classic clinical stages typically occur in patients with perforated ulcers. The first stage, caused by the rapid release of gastric juice into the peritoneal cavity, is characterized by an abrupt onset of intense abdominal pain. The duration and intensity of this stage vary based on the size of the perforation and the extent to which gastric juice leaks into the peritoneal cavity.

During the second stage, which often does not occur, spontaneous improvement in symptoms is observed. This is probably the result of fluid pouring out of the injured intraperitoneal tissues, which causes a buffering of the acidic gastric juice. The clinician should not feel overly reassured if this occurs in a patient with an otherwise concerning presentation. In addition, findings of peritonitis are typically still present despite improvement in the patient's symptoms.

The final stage of frank peritonitis is characterized by increased pain and signs of a systemic inflammatory response. If appropriate therapy is not initiated, death soon follows.


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