The cricopharyngeus muscle forms the beginning of the normal esophagus, which is a tubular structure until it culminates at the diaphragmatic hiatus. At endoscopy, the esophageal mucosa is smooth and whitish pink (Fig. 134-2). The esophageal lumen is 1.5 to 2.0 cm in diameter. Normally, the aorta gives an extrinsic compression at about 25 cm in the esophagus. Sometimes the left mainstem bronchus can also indent the esophagus below the aorta. The transformation from whitish to reddish mucosa identifies the squamocolumnar junction or Z line. Usually, the Z line is closely related to the diaphragmatic hiatus and is 40 cm from the incisors. The anatomic gastroesophageal junction is clinically defined at the proximal margin of the gastric folds. There is mild angulation of the distal esophagus close to the diaphragmatic hiatus.

The final maneuver to evaluate the esophagus is endoscopic retroflexion in the stomach to identify the presence of a hiatal hernia. A sliding hiatal hernia is identified by a displacement >2 cm between the Z line and the diaphragmatic hiatus, as described by Boyce.⁸ During the retroflexion in the stomach, if a space between the endoscope and the gastric wall at the cardia is noted, one can also identify a hiatal hernia.

Various disease processes can be identified in patients with dysphagia. Mucosal abnormalities such as gastroesophageal reflux disease (GERD), Barrett’s esophagus, Mallory–Weiss tears, infections as noted by Ollyo and associates,²⁸ pill-induced esophagitis, and malignancy can be diagnosed by esophagoscopy. Structural abnormalities such as diverticula, webs, and rings are identified easily by endoscopy and described in detail by Boyce and Boyce.⁶ Endoscopy is an important step in the evaluation of strictures in that biopsies differentiate benign from malignant strictures.

Endoscopy is very important in detecting and stratifying the extent of suspected GERD. However, the absence of endoscopic features is common and occurs in at least 50% of patients with GERD. Endoscopy therefore should probably be reserved for patients failing to respond to antisecretory therapy, for patients with atypical or alarm symptoms, or for identifying Barrett’s esophagus in those with long-standing symptoms. Endoscopic interobserver variability and the need for consistency in judging treatment response in GERD has led to the development of multiple endoscopic classification schemes. Two of the more popular grading systems (Savary–Miller and Los Angeles) are noted in Tables 134-1 and 134-2. Figure 134-3 demonstrates the appearance of esophagitis and the corresponding classification. Biopsy can be done at the time of endoscopy. Strictures can be dilated, and surveillance for Barrett’s epithelium can be performed.

Recognition of Barrett’s esophagus is on the rise in the United States, as is the incidence of esophageal adenocarcinoma. Barrett’s esophagus is believed to be the major risk factor for esophageal adenocarcinoma.⁴¹ Dysplasia grade determines

not only the appropriate surveillance interval but also the modalities of therapy. The American College of Gastroenterology in 2008 published their guidelines for surveillance and therapeutic measures (Table 134-3). These guidelines do not go into depth on high-grade dysplasia beyond the use of endoscopic resection. The Society of Thoracic Surgeons is preparing a statement on this subject. In anticipation of publication of these additional guidelines, an algorithm for rational management of the patient with dysplasia is included here (Fig. 134-4).

Esophageal varices are best recognized by endoscopy. In patients with portal hypertension and esophageal varices, endoscopy is used for diagnosis and therapy (Fig. 134-5). After initial resuscitation, including the establishment of airway, breathing, and circulation, initial treatment includes early use of vasoactive drug therapy (terlipressin, somatostatin, octreotide).¹ When the patient is stabilized, endoscopic band ligation added to somatostatin is associated with improved mortality and less adverse events over sclerotherapy.⁴⁰

Absorptive or vital stains can be sprayed on the esophageal mucosa to increase detection of Barrett’s esophagus or tumor. Lugol’s 1% or 2% solution binds to glycogen in nonkeratinized squamous epithelium. Glycogen-depleted areas—including ectopic mucosa, ulcers, cancers, and severe dysplasia—will not take up the stain.⁴² Canto¹⁰ demonstrated that methylene blue spraying at the time of endoscopy will reliably stain Barrett’s mucosa and improve the yield of diagnosing high-grade dysplasia. Since classification of mucosal staining is not standardized as well as being subject to observer variability, chromoendoscopy is not sufficiently validated for routine endoscopic practice.⁴²

Narrow-band imaging exploits the phenomenon that the depth of light penetration into tissues depends on wavelength. The combination of blue light absorption by hemoglobin and the utilization of optical filters yields enhanced mucosal architecture while revealing mucosal vascular patterns.²⁰ However, an additive benefit to chromoendoscopy or NBI over high-resolution magnification endoscopy in the detection of early Barrett’s neoplasia could not be demonstrated.¹¹ In 2008, an international multicenter feasibility study of endoscopic trimodal imaging (high-resolution endoscopy, NBI, autofluorescence) revealed an increase in the number of patients and lesions detected when autofluorescence was combined with high-resolution endoscopy. AFI, however, was associated with an 81% false-positive rate, which “was reduced after detailed inspection with NBI.”¹² Further investigation is necessary to elucidate the impact of chromoendoscopy, NBI, as well as AFI on the detection of early Barrett’s neoplasia. Advanced imaging systems including NBI, AFI, as well as confocal microscopy remain promising modalities to evaluate Barrett’s esophagus, but at present there are insufficient data to recommend their routine utilization.⁴¹