6. Dyspepsia / W.G. Thompson  

Indigestion. 

Dyspepsia is an imprecise term. It is best described as a chronic (over three months), recurrent, often meal-related epigastric discomfort, pain or fullness. The location of the pain and the relationship to meals resemble the classic description of peptic ulcer disease, so the physician must consider the possibility that a dyspeptic patient has a peptic ulcer. Dyspepsia is usually a daily experience, yet is seldom disabling. 

The mechanism of dyspepsia is uncertain. Even in those dyspeptic patients who have a peptic ulcer, the cause of the pain is uncertain. It is disputed whether the discomfort is related to (l) impaired gastric emptying, (2) a disorder of the basic electrical rhythm of the stomach or (3) pyloroduodenal dysmotility. None are proven. 

Although many patients believe that specific foods are responsible for dyspepsia, only fat appears to be a consistent offender. Fat may induce dyspepsia by slowing gastric emptying or by releasing cholecystokinin, which is known to affect the smooth muscle of the upper gastrointestinal tract. 

Other upper gastrointestinal symptoms relate to dyspepsia. These include nausea, vomiting (rarely), belching and a feeling of gaseous distention. Terms such as gallbladder dyspepsia, pancreatic dyspepsia, appendiceal dyspepsia and gaseous dyspepsia are misleading and serve no useful purpose. There should be no confusion between the episodic nature and severity of pain due to biliary colic or pancreatic disease and the more predictable and regular occurrence of dyspepsia. Indeed, dyspeptic symptoms are equally common in those who have and in those who do not have gallstones. 

It is important as well to distinguish dyspepsia from the recumbency-aggravated retrosternal burning that we call "heartburn." Heartburn results from gastroesophageal reflux and has different diagnostic and therapeutic approaches than dyspepsia. 

In an individual case it is almost impossible to distinguish ulcer from nonulcer dyspepsia. Large studies have shown that, statistically, epigastric pain occurring at night and relieved with antacids is more likely to be associated with peptic ulcer disease. The pain of dyspepsia is not incapacitating. Of course, evidence of complications such as bleeding, weight loss or vomiting would not be expected in nonulcer dyspepsia. The pain or discomfort of the irritable bowel syndrome may occur in the epigastrium. This is generally distinguished from discomfort originating in the upper gastrointestinal tract by its association with defecation and a coexistent alteration in bowel habit. 

On physical examination epigastric tenderness will not distinguish between ulcer and nonulcer dyspepsia. In the latter there should be no complications suggestive of peptic ulcer disease, such as peritoneal signs, a succussion splash or the presence of an epigastric mass. 

Dyspepsia occurs in about 10% of the population, many of whom do not seek medical help. Of those who do, approximately one-third will not have a peptic ulcer. There is little evidence that those who have nonulcer dyspepsia will eventually develop an ulcer. Yet the symptoms usually persist for long periods in the patient’s life. 

Thus, investigation and management will depend upon the establishment of a clear diagnosis at the outset, the cost of investigation and the cost of treatment. Since anti-ulcer medication is very effective and seemingly safe, one attitude would be to treat all such individuals without investigation. In the United States, where x-ray and endoscopy are very expensive and the cost must be borne by the individual, indiscriminate therapy has achieved some currency. In such countries as Canada, where drug costs are similar but procedural costs are much less and are not borne by the individual, it seems more efficacious to establish the diagnosis at the outset before committing the patient to drug therapy. Now that we know that most non-NSAID-induced ulcers are due to the presence of Helicobacter pylori and are cured once these gastric bacteria are killed, other approaches are proposed. The current recommendation is that those who have both an ulcer and H. pylori should be given appropriate antibiotics. Those without an ulcer will not benefit from eradication of the organism. New strategies suggest testing dyspeptics for H. pylori and endoscoping only those who test positive. Others would treat indiscriminately. Cost and outcome analysis has not established which is the best approach. More details on this fast-evolving issue are found in Chapter 6, "The Stomach and Duodenum."  

Although a carefully conducted upper gastrointestinal series will discover most ulcers, endoscopy is more accurate and will detect mucosal lesions as well. The advantage of early diagnosis is that if no ulcer is found then the futile use of expensive, systemic drugs can be avoided in those with nonulcer dyspepsia. Further, the uncertainty factor in failing to establish a diagnosis compounds inappropriate therapy and aggravates patient unease.