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Indigestion is a nonspecific term that encompasses a variety of upper abdominal complaints including heartburn, regurgitation, and dyspepsia (upper abdominal discomfort or pain). These symptoms are overwhelmingly due to gastroesophageal reflux disease (GERD).

Pathophysiology !!navigator!!

GERD occurs as a consequence of acid reflux into the esophagus from the stomach, gastric motor dysfunction, or visceral afferent hypersensitivity. A wide variety of situations promote GERD: increased gastric contents (from a large meal, gastric stasis, or acid hypersecretion), physical factors (lying down, bending over), increased pressure on the stomach (tight clothes, obesity, ascites, pregnancy), and loss (usually intermittent) of lower esophageal sphincter tone (diseases such as scleroderma, smoking, anticholinergics, calcium antagonists). Hiatal hernia also promotes acid flow into the esophagus.

Natural History !!navigator!!

Heartburn is reported once monthly by 40% of Americans and daily by 7%. Functional dyspepsia is defined as >3 months of dyspepsia without an organic cause. Functional dyspepsia is the cause of symptoms in 60% of pts with dyspeptic symptoms. However, peptic ulcer disease from either Helicobacter pylori infection or ingestion of NSAIDs is present in 15% of cases.

In most cases, the esophagus is not damaged, but 5% of pts develop esophageal ulcers and some form strictures; 8-20% develop glandular epithelial cell metaplasia, termed Barrett's esophagus, which can progress to adenocarcinoma.

Extraesophageal manifestations include asthma, laryngitis, chronic cough, aspiration pneumonitis, chronic bronchitis, sleep apnea, dental caries, halitosis, and hiccups.

Evaluation !!navigator!!

The presence of “alarm” signals, shown in Table 40-2 Alarm Symptoms in Gastroesophageal Reflux Disease, demands directed radiographic, endoscopic, and surgical evaluation. Pts without alarm features are generally treated empirically. Individuals >45 years can be tested for the presence of H. pylori. Pts positive for the infection are treated to eradicate the organism. Pts who fail to respond to H. pylori treatment, those >45 years old, and those with alarm factors generally undergo upper GI endoscopy.

TREATMENT

Indigestion

Weight reduction; elevation of the head of the bed; and avoidance of large meals, smoking, caffeine, alcohol, chocolate, fatty food, citrus juices, and NSAIDs may prevent GERD. Antacids are widely used. Clinical trials suggest that proton pump inhibitors (omeprazole) are more effective than histamine receptor blockers (ranitidine) in pts with or without esophageal erosions. H. pylori eradication regimens are discussed in Chap. 150 Peptic Ulcer and Related Disorders. Motor stimulants like metoclopramide and erythromycin may be useful in a subset of pts with postprandial distress.

Surgical techniques (Nissen fundoplication, Belsey procedure) work best in young individuals whose symptoms have improved on proton pump inhibitors and who otherwise may require lifelong therapy. They can be used in the rare pts who are refractory to medical management. Clinical trials have not documented the superiority of one over another.

Dietary exclusion of gas-producing foods (i.e., low FODMAP [fermentable oligosaccharide, disaccharide, monosaccharide, and polyol] diets), and therapies to modify gut flora can reduce symptoms.

Outline

Section 3. Common Patient Presentations