Figure 2.1  UPPER ESOPHAGEAL SPHINCTER

The cricopharyngeus muscle is contracting. The proximal esophagus is in the distance.

Figure 2.2  MIDESOPHAGUS

The esophageal mucosa has a whitish appearance with a delicate vascular pattern (A) highlighted by narrow band imaging (B).

Figure 2.3  VASCULAR PATTERN AT THE GASTROESOPHAGEAL JUNCTION

Multiple linearly arranged blood vessels are present proximal to the gastroesophageal junction.

Figure 2.4  GASTROESOPHAGEAL JUNCTION

A, The squamous mucosa and blood vessels end abruptly with a well-demarcated margin. The orange mucosa of the stomach is opposite the esophageal mucosa. B, Note the crisp distinction between the squamous mucosa and the orange appearance of the gastric mucosa. In this case, a paucity of blood vessels appears in the distal esophageal mucosa. C1, C2, The gastroesophageal junction is well delineated by narrow band imaging.

Figure 2.5  GASTROESOPHAGEAL JUNCTION WITH OPENING OF THE LOWER ESOPHAGEAL SPHINCTER

The normal demarcation between the white squamous mucosa and pinkish orange gastric mucosa.

Figure 2.6  RETROFLEX VIEW OF THE GASTROESOPHAGEAL JUNCTION

Retroflexion demonstrates demarcation of the gastroesophageal junction, where squamous mucosa can be seen encircling the endoscope.

Figure 2.7  BARIUM ESOPHAGRAM

A, Barium esophagram shows normal esophageal contour and luminal diameter. The esophageal mucosa is proximal to the barium column. The esophageal walls are smooth and symmetric. Air bubbles are present at the proximal column of barium. The esophagus can be seen entering the stomach at the gastric air bubble. B, With the esophagus collapsed, the esophageal folds are delicate and smooth.

Figure 2.8  NORMAL STRATIFIED SQUAMOUS EPITHELIUM

Vascular channels are seen in the epithelium. Portions of the basal epithelium are present.

Figure 2.9  TRACHEAL IMPRESSION

Tracheal impression on the proximal esophagus.

Figure 2.10  AORTIC IMPRESSION

A, Indentation on the midesophagus from an ectatic aorta. The indentation is smooth and unilateral. B, The normal diameter of the esophageal mucosa is diminished by extrinsic compression; the overlying mucosa is normal. C, With systole, the esophageal lumen is further compressed. D1, Extrinsic compression in the proximal midesophagus. D2, Chest x-ray film demonstrates splaying of the trachea with an enlarged aortic arch. L indicates the left side.

Figure 2.10  AORTIC IMPRESSION

D3, Barium swallow shows slight extrinsic compression related to the aortic arch.

Figure 2.11  AORTIC IMPRESSION

A, Extrinsic compression posteriorly in the midesophagus. Erosions are present on the lesion. B, The contrast-filled esophagus is compressed posteriorly by an ectatic aorta.

Figure 2.12  TERTIARY ESOPHAGEAL CONTRACTIONS

A, Multiple tertiary contractions observed in a patient with dysphagia.

B, Tertiary contractions occur during endoscopy as well. C, Simultaneous contractions on esophageal manometry.

Figure 2.13  CORKSCREW ESOPHAGUS

A, Endoscopic images show circular folds resembling a corkscrew. B, Corresponding barium esophagram.

Figure 2.14  FELINE ESOPHAGUS

Multiple simultaneous smooth muscle contractions result in this ringlike appearance.

Figure 2.15  GASTROESOPHAGEAL REFLUX DISEASE (GERD)

A1, Typical appearance of erosive esophagitis, with linear erythematous streaks and central ulceration emanating from the gastroesophageal junction. Between the lesions, the squamous epithelium is normal. A2, With the lumen collapsed, the ulcerations reside primarily on the surface of the normal esophageal folds. B1, B2, Typical linear ulcerations emanating from the gastroesophageal junction. C, Multiple linear ulcerations in the typical pattern.

Figure 2.16  GASTROESOPHAGEAL REFLUX DISEASE

A, Single linear erosion in the distal esophagus. B, Erythematous erosions at the GE junction. Note the patulous sphincter. C, Streaks of exudate in the distal esophagus. D1, Exudate at the GE junction, which is almost confluent. D2, More proximally, the exudate takes on a linear migration typical for GERD. E1, Circumferential ulceration at the GE junction above a patulous sphincter. E2, More proximally, the mucosa takes on the appearance of multiple, well-circumscribed, squamous “islands” caused by edema with intervening mucosal erosion. F, Circumferential ulcer with fresh bleeding and luminal narrowing above a patulous GE junction. G, Patulous GE junction above a hiatal hernia associated with multiple scars from prior disease. Note the linear erosions.

Figure 2.16  GASTROESOPHAGEAL REFLUX DISEASE

H, Note that some of the exudate has a plaquelike appearance in this patient with a patulous GE junction and hiatal hernia. I, The exudate and ulceration have coalesced. The mucosa has a nodular appearance. J, Note the circumferential ulceration ends abruptly at the GE junction.

Figure 2.18  SEVERE GASTROESOPHAGEAL REFLUX DISEASE

A, Narrowing in the distal esophagus associated with circumferential ulceration. B, More proximally the ulceration is hemicircumferential. C, In the midesophagus, the ulceration takes on the typical linear ulceration. D, Near the upper esophageal sphincter, no exudate is present, but erythema and evidence of scarring exist.

E1, E2, Esophageal wall thickening on CT scan.

Figure 2.19  SEVERE ESOPHAGITIS ASSOCIATED WITH GASTRIC OUTLET OBSTRUCTION

A1, Gastric bile stained fluid present in the distal esophagus. A2, After aspiration, the diffuse nodularity and ulceration are evident.

B1, Bilious fluid is present in the distal esophagus associated with erosions. B2, The stomach is full of bilious fluid because of pyloric obstruction. B3, After aspiration of the fluid, severe erosive esophagitis is evident.

Figure 2.20  BLEEDING GASTROESOPHAGEAL REFLUX DISEASE

A, Arterial bleeding in the distal esophagus. B, Thermal probe applied to the area of bleeding. Note the circumferential erosive esophagitis. C, Hemostasis achieved with a coagulation “footprint” remaining.

Figure 2.21  IRREGULAR Z LINE

A, Irregular squamocolumnar junction associated with a hiatal hernia. B, Irregular squamocolumnar junction associated with a hiatal hernia. C, Mild narrowing at the GE junction suggestive of a ring above a hiatal hernia. Note the patches of gastric mucosa above the ringlike structure. This may suggest patches of Barrett’s mucosa. D, Biopsy confirms gastric cardia mucosa without specialized intestinal epithelium.

Figure 2.22  BARRETT’S ESOPHAGUS

A, Typical-appearing Barrett’s mucosa emanating from the GE junction. B, Tongue of Barrett’s mucosa with a small squamous island. C, Two tongues of Barrett’s mucosa extending from the GE junction. D, Normal squamous mucosa (left) with gastric epithelium. Goblet cells are present in the gastric epithelium, indicating intestinal metaplasia. E, The goblet cells are highlighted with Alcian blue staining. The large vacuoles are purple blue.

Figure 2.23  BARRETT’S MUCOSA

A1-A5, Typical tongues of Barrett’s mucosa of variable lengths emanating from the gastroesophageal junction. B1-B5, The Barrett’s mucosa is well delineated by narrow band imaging. C, Biopsy of the squamocolumnar junction shows squamous tissue, as well as columnar-lined intestinal mucosa with plentiful goblet cells.

Figure 2.24  BARRETT’S MUCOSA WITH SQUAMOUS ISLAND

A, Long-segment Barrett’s mucosa with island of squamous mucosa. B, Barrett’s segment between squamous mucosa. The Barrett’s mucosa shows dysplasia.

C1, C2, Postoperative specimen shows the long-segment Barrett’s mucosa.

D1, D2, Several areas of squamous mucosa are identified in the Barrett’s mucosa.

Figure 2.25  LONG-SEGMENT BARRETT’S ESOPHAGUS

A, Long segment of Barrett’s esophagus extending from the GE junction. B, Note the mucosa has a pale appearance with visible blood vessels.

Figure 2.26  SHORT-SEGMENT BARRETT’S ESOPHAGUS

A, Short tongue of Barrett’s mucosa at the GE junction. B, Short-segment Barrett’s mucosa extending just proximal to the GE junction. Note the two associated small Barrett’s patches. C, Small patch of Barrett’s mucosa that appears distinct from the GE junction.

D, Circumferential short-segment Barrett’s mucosa with an additional associated patch. E, Areas of short-segment Barrett’s mucosa above a hiatal hernia. F, Short-segment Barrett’s mucosa as seen by high-definition endoscopy. G, Narrow band imaging also shows a short segment of Barrett’s mucosa. H, Several areas of Barrett’s mucosa above a hiatal hernia proximal to the most proximal portion of the gastric folds.

Figure 2.27  BARRETT’S ULCER

A, Ulceration with heaped-up margins in the distal esophagus. B, The ulceration becomes circumferential distally and has a black base, indicating necrosis. The gastroesophageal junction appears in the distance. C1, Occasional goblet cells indicate Barrett’s metaplasia of the intestinal type. C2, Ulcerative esophagitis with granulation tissue and gastric epithelium.

Figure 2.28  BARRETT’S ULCER

A, Proximal extent of long-segment Barrett’s mucosa to the midesophagus. B, Long midesophageal ulcer on a background of Barrett’s mucosa. C, The ulcer extends to but does not involve the GE junction. Note the surrounding Barrett’s mucosa.

Figure 2.29  CONFOCAL ENDOMICROSCOPY OF NORMAL AND ABNORMAL ESOPHAGEAL LESIONS

A, Normal squamous tissue. B, Intestinal metaplasia. Note the presence of goblet cells. C, High-grade dysplasia. D, Adenocarcinoma (note the disruption of the normal architecture). (D courtesy Don’t Biopsy Study.)

Figure 2.30  BARRETT’S MUCOSA WITH DYSPLASIA

A, Flat hyperemic area in the midesophagus. B, The biopsy specimen shows high-grade dysplasia.

C1, C2, Narrow band imaging shows the abnormal tissue with a distinct demarcation. Note the intraepithelial papillary capillary loops. D, Mucosal resection was performed. (C courtesy Dr. Cristian Gheorghe.)

Figure 2.31  BARRETT’S MUCOSA WITH HIGH-GRADE DYSPLASIA: ENDOSCOPIC MUCOSAL RESECTION

A, Nodular well-circumscribed area in the distal esophagus. B, Dilute saline and epinephrine are injected underneath the lesion. C, The cap device is placed on the endoscope and positioned over the lesion for resection. D, After endoscopic mucosal resection (EMR), a mucosal defect is produced. E, The argon laser is used to ablate any suspicious surrounding mucosa that was not removed with the resection specimen. F, High-grade dysplasia in Barrett’s mucosa.

Figure 2.32  NODULAR LESION IN BARRETT’S ESOPHAGUS: HIGH-GRADE DYSPLASIA

A, Well-circumscribed nodule in the distal esophagus. B, A cap device is used for resection. C, Mucosal defect after resection.

Figure 2.33  BARRETT’S MUCOSA UNDERGOING RADIOFREQUENCY ABLATION

A, Typical Barrett’s esophagus. This patient had high-grade dysplasia on biopsy. B, After therapy, superficial ulceration is seen. C, Use of the halo device to ablate additional areas of Barrett’s esophagus.

Figure 2.34  BARRETT’S ESOPHAGUS WITH ENDOMICROSCOPY

A, Typical Barrett’s esophagus as seen on narrow band imaging. Numbers represent the area where endomicroscopy was performed. B, Esophageal glands with normal architecture and the presence of goblet cells. No dysplasia is present. (Courtesy F. Alberca, MD, Murcia, Spain.)

Figure 2.35  GASTROESOPHAGEAL REFLUX DISEASE-ASSOCIATED STRICTURE

A, Tight stricture of the distal esophagus associated with proximal ulceration. Note the collection of pills proximal to the stricture. B, C, Severe esophagitis with circumferential exudate and an associated tight stricture.

D, The stricture was dilated and endoscopy performed. Note the luminal caliber is improved and there is underlying ulceration of the dilated area. E, After dilation, a large tear is proximal to the stricture.

Figure 2.36  HEALED SEVERE GASTROESOPHAGEAL REFLUX DISEASE

A, The esophageal mucosa appears thickened, with loss of vascular pattern from fibrosis. A portion of normal mucosa is still present.

B, Retroflex view in the hiatal hernia shows evidence of prior ulcers, with four well-circumscribed, reepithelialized depressions.

Figure 2.37  MILD CANDIDA ESOPHAGITIS

A, Small white plaques throughout the midesophagus and distal esophagus. B, Multiple white plaques stud the distal esophagus. C, Linear confluent plaques in the midesophagus. The surrounding mucosa is normal.

Figure 2.38  CANDIDA ESOPHAGITIS

A, Diffuse irregularity of the wall, with multiple filling defects. These abnormalities result from barium intercalating between the confluent candidal plaques. In most cases, these irregularities do not represent ulceration. B, Typical-appearing raised, confluent yellow plaques. The yellow plaque assumes a linear pattern in some areas, with normal intervening mucosa. C, Severe Candida esophagitis, with confluent circumferential yellow plaque and encroachment on the esophageal lumen. D, If the candidal plaque is vigorously removed, the underlying mucosa appears relatively intact. Denudation of the surface epithelium is seen in a few areas, with associated hemorrhage resulting from the endoscopic trauma. No frank ulceration is present. E, Thick yellow exudate coats the esophagus and results in mild luminal narrowing. F, A portion of the exudate is removed showing inflamed underlying mucosa.

G, Full-thickness squamous epithelium with overlying candidal plaque. The plaque is adherent to the surface epithelium. The plaque is composed of mature squamous epithelial cells, fungal pseudohyphae, and yeast. The Candida does not extend into the deep layers of the epithelium. H, Gomori methenamine silver (GMS) stain of the candidal plaque demonstrates branching fungal mycelia, including pseudohyphae and true hyphae, characteristic of C. albicans.

Figure 2.39  HERPES SIMPLEX VIRUS ESOPHAGITIS

A, Herpes simplex virus esophagitis manifested by multiple whitish plaques. Diffuse erythema surrounds the plaque, representing shallow ulceration. Islands of normal-appearing esophageal mucosa are still present. B, Diffuse shallow ulceration of the entire esophagus, with two areas of normal-appearing squamous tissue present. C, Confluent exudate in the distal esophagus. D, Vesicular lesions in the midesophagus. E, Volcano-like lesions in the midesophagus.

F1, Large, plaquelike, exudative lesions that become confluent more distally (F2). G, Ulceration with narrowing at the GE junction. The ulcer has thick exudate resembling GE reflux disease.

Figure 2.39  HERPES SIMPLEX VIRUS ESOPHAGITIS

H, Herpes simplex virus infection of the esophagus, producing characteristic multinucleated inclusions in squamous epithelial cells. I, Confirmation of herpes simplex virus by in situ DNA hybridization. The intranuclear viral inclusions are stained brown.

Figure 2.41  CYTOMEGALOVIRUS ESOPHAGITIS

A, Three esophageal ulcerations. Two of the lesions are on opposite walls. There is no extravasation of barium to contiguous structures or to the mediastinum. The surrounding mucosa is normal, giving the ulcerations a well-circumscribed appearance.

B, Multiple large ulcerations. The ulcer on the left represents the deep ulcer on the esophagrams. The distal ulcer is not visible at this level. The ulcers are well-circumscribed, having a “punched-out” appearance. The intervening esophageal mucosa is normal. C, Multiple viral inclusions in endothelial cells and stromal cells in the ulcer base. Cytomegalovirus inclusions typically consist of enlarged cells with characteristic “owl eye” intranuclear inclusions and granular eosinophilic cytoplasmic inclusions. In the gastrointestinal tract, atypical viral inclusions (some shown here) are often present. Cells with atypical inclusions may appear smudged or can be similar in appearance to ganglion cells.

D, Immunostain confirms the viral cytopathic effect to be cytomegalovirus.

Figure 2.42  CYTOMEGALOVIRUS ESOPHAGITIS

A, Long, linear ulcer. B, Multiple large, well-circumscribed ulcerations in the midesophagus. C, Shallow ulceration in the distal esophagus.

D1, Diffuse exudate in the midesophagus with areas of depression. D2, Markedly thickened distal esophagus. E, Circumferential ulceration involving the distal esophagus.

F, Deep ulceration extending outward from the lumen in the distal esophagus. G1, Midesophageal ulcer with mild luminal narrowing. G2, After therapy, a stricture has resulted.

G3, Balloon dilation performed. G4, The stricture has torn appropriately, now exposing the submucosa. No perforation resulted.

Figure 2.43  CYTOMEGALOVIRUS ESOPHAGITIS WITH STRICTURE

A, Large, irregular ulceration at the gastroesophageal junction. There appears to be a mass effect just proximal to the gastroesophageal junction.

B, The distal esophagus is markedly thickened.

C, Circumferential ulceration in the distal esophagus, extending into the stomach anteriorly and forming a shelf. The gastric tissue is edematous. D, After therapy, the patient reported dysphagia. A circumferential stricture is now present, with persistent active ulceration.

Figure 2.44  HEALED ULCER SCAR

Large scar in the midesophagus representing healing of a large ulcer. Note the characteristic whitish color.

Figure 2.45  TUBERCULOUS ESOPHAGITIS WITH FISTULA

Ulcer in the midesophagus representing a fistula to the mediastinum (A), well shown on barium esophagram (B).

Figure 2.46  ASCARIS LUMBRICOIDES

Large ascarid in the midesophagus. (Courtesy F. Vida, MD, and A. Tomas, MD, Manresa, Spain.)

Figure 2.47  EOSINOPHILIC ESOPHAGITIS

A, Multiple mild ringlike lesions of the midesophagus are characteristic.

B, Biopsies show numerous eosinophils in the squamous epithelium.

Figure 2.48  EOSINOPHILIC ESOPHAGITIS

A, Multiple ringlike structures in the distal esophagus above a mild narrowing. B, More proximally, the mucosa has a feline appearance. C1-C3, After biopsy, the blood essentially performs chromoendoscopy, and multiple fissures are also now very evident.

Figure 2.49  DILATION OF EOSINOPHILIC ESOPHAGITIS

A, Typical-appearing rings. B, Long tear after dilation. C, Biopsy shows marked eosinophilia. D, Dense fibrosis is also present in the submucosa.

Figure 2.50  ACUTE NECROTIZING ESOPHAGITIS

Diffuse black exudates coat the esophagus (A, B). C, Note the abnormalities stop at the GE junction.

Figure 2.51  PEMPHIGUS

A, Submucosal hemorrhage in the midesophagus. B, The biopsy forceps are used to grasp the overlying mucosa showing that it can be “peeled away.”

C, D, More extensive esophageal involvement with sloughing of a large portion of the mucosa. The thin film of detached mucosa is visible.

Figure 2.52  PARANEOPLASTIC PEMPHIGUS

Diffuse edema and subepithelial hemorrhage.

Figure 2.53  EARLY SQUAMOUS CELL CARCINOMA

A, Focal area of nodularity. Air bubbles can also be seen on the barium-coated esophagus.

B1, B2, Verrucous-appearing lesion in the center of a well-demarcated area of erythema. B3, After washing of the lesion, it is found not to be fixed to the wall. B4, A distal border of erythema is present. Biopsy of the erythematous mucosa demonstrated carcinoma.

Figure 2.54  SQUAMOUS CELL CANCER OF THE ESOPHAGUS WITH RECENT BLEEDING

Raised ulcerative lesion of the midesophagus with overlying blood clot indicating recent bleeding (A, B).

A, Anteroposterior view shows a long segmental lesion, with nodular mucosa and luminal narrowing.

Figure 2.55  SQUAMOUS CELL CARCINOMA

B, A soft-tissue mass anteriorly causes a mass effect, with posterior effacement of the trachea.