History and Physical Examination ++ Managing indigestion requires a thorough interview. GERD classically produces heartburn, a substernal warmth that moves toward the neck. Heartburn often is exacerbated by meals and may awaken the patient. Associated symptoms include regurgitation of acid or nonacidic fluid and water brash, the reflex release of salty saliva into the mouth. Atypical symptoms include pharyngitis, asthma, cough, bronchitis, hoarseness, and chest pain that mimics angina. Some patients with acid reflux on esophageal pH testing note abdominal pain instead of heartburn. ++ Dyspeptic patients report symptoms referable to the upper abdomen that may be meal-related (postprandial distress syndrome) or independent of food ingestion (epigastric pain syndrome). The history in functional dyspepsia may also report symptoms of GERD, IBS, or idiopathic gastroparesis. ++ The physical exam with GERD and functional dyspepsia usually is normal. In atypical GERD, pharyngeal erythema and wheezing may be noted. Recurrent regurgitation may cause poor dentition. Dyspeptics may exhibit epigastric tenderness or distention. ++ Discriminating functional from organic causes of indigestion mandates excluding certain historic and exam features. Odynophagia suggests esophageal infection. Dysphagia is concerning for a benign or malignant esophageal blockage. Other alarm features include unexplained weight loss, recurrent vomiting, dysphagia, occult or gross bleeding, nocturnal symptoms, jaundice, palpable mass or adenopathy, and a family history of gastrointestinal neoplasm. Patients with an abdominal wall source of upper abdominal pain may exhibit a positive Carnett’s sign of increased tenderness with tensing of abdominal muscles upon lifting the head from the exam table. +++ Diagnostic Testing ++ Because indigestion is prevalent and most cases result from GERD or functional dyspepsia, it is generally recommended to perform no more than limited and directed diagnostic testing in most individuals. ++ After excluding alarm factors (Table 45-3), patients with typical GERD do not need further evaluation and are treated empirically. Upper endoscopy is indicated only in cases with atypical symptoms or these alarm factors. For heartburn >5 years in duration, especially in patients >50 years old, endoscopy is advocated to screen for Barrett’s metaplasia. Endoscopy is not needed in low-risk patients who respond to acid suppressants. Ambulatory esophageal pH testing using a catheter method or a wireless capsule endoscopically attached to the esophageal wall is considered for drug-refractory symptoms and atypical symptoms like unexplained chest pain. High-resolution esophageal manometry is ordered when surgical treatment of GERD is considered. A low LES pressure predicts failure of drug therapy and provides a rationale to proceed to surgery. Poor esophageal body peristalsis raises concern about postoperative dysphagia and directs the choice of surgical technique. Nonacidic reflux may be detected by combined esophageal impedance-pH testing in medication-unresponsive patients.

History

Physiologically, the UES consists of the cricopharyngeus muscle, the adjacent inferior pharyngeal constrictor, and the proximal portion of the cervical esophagus. UES innervation is derived from the vagus nerve, whereas the innervation to the musculature acting on the UES to facilitate its opening during swallowing comes from the fifth, seventh, and twelfth cranial nerves. The UES remains closed at rest owing to both its inherent elastic properties and neurogenically mediated contraction of the cricopharyngeus muscle. UES opening during swallowing involves both cessation of vagal excitation to the cricopharyngeus and simultaneous contraction of the suprahyoid and geniohyoid muscles that pull open the UES in conjunction with the upward and forward displacement of the larynx. ++ The neuromuscular apparatus for peristalsis is distinct in proximal and distal parts of the esophagus. The cervical esophagus, like the pharyngeal musculature, consists of striated muscle and is directly innervated by lower motor neurons of the vagus nerve. Peristalsis in the proximal esophagus is governed by the sequential activation of the vagal motor neurons in the nucleus ambiguus. In contrast, the distal esophagus and LES are composed of smooth muscle and are controlled by excitatory and inhibitory neurons within the esophageal myenteric plexus. Medullary preganglionic neurons from the dorsal motor nucleus of the vagus trigger peristalsis via these ganglionic neurons during primary peristalsis. Neurotransmitters of the excitatory ganglionic neurons are acetylcholine and substance P; those of the inhibitory neurons are vasoactive intestinal peptide and nitric oxide. Peristalsis results from the patterned activation of inhibitory followed by excitatory ganglionic neurons, with progressive dominance of the inhibitory neurons distally. Similarly, LES relaxation occurs with the onset of deglutitive inhibition and persists until the peristaltic sequence is complete. At rest, the LES is contracted because of excitatory ganglionic stimulation and its intrinsic myogenic tone, a property that distinguishes it from the adjacent esophagus. The function of the LES is supplemented by the surrounding muscle of the right diaphragmatic crus, which acts as an external sphincter during inspiration, cough, or abdominal straining.

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