Overview of Pathological Findings in the Esophagus

Table 3.1 Diseases of the esophagus (Figs. 3.1–3.8)

Diseases of the gastroesophageal junction Infections and other forms of esophagitis Diverticula Motility disorders Varices Tumors Foreign bodies and rare findings Postoperative conditions

Fig. 3.1 Diseases of the gastroesophageal junction

Fig. 3.2 Infections and other forms of esophagitis

Fig. 3.3 Diverticula

Fig. 3.4 Motility disorders

Fig. 3.5 Varices

Fig. 3.6 Tumors

Fig. 3.7 Foreign bodies and rare findings

Fig. 3.8 Postoperative conditions

Cardial Incompetence

Additional Study

Esophageal manometry

Comments

Since the endoscopic interpretation is highly subjective, you should be careful when making a diagnosis of cardial incompetence.

Fig. 3.9 Gastroesophageal junction a–c Observation of the gastroesophageal junction for approximately 30 seconds. Notice the absence of sphincter closure

Fig. 3.10 Cardial incompetence. Retroflexed view. Note the failure of the cardia to close snugly around the endoscope (cf. p. 47)

Hiatal Hernia: Axial Sliding Hernia

An axial sliding hernia is among the most common endoscopic findings, noted in up to 25% of upper gastrointestinal examinations (Fig. 3.11). In 80% of cases it is an incidental finding that is classified as a normal variant. The significance of a sliding hernia in the pathogenesis of reflux disease is uncertain. While more than 80% of cases are asymptomatic and endoscopy shows no signs of reflux esophagitis, a sliding hernia is commonly found in cases where esophagitis is already present.

Diagnosis

Additional Study

Oral contrast examination with a head-down tilt (only half of radiographically detectable sliding hernias are visible endoscopically)

Comments

Axial sliding hernia is a common finding and is frequently asymptomatic. With symptomatic reflux, initial treatment consists of supportive measures and proton pump inhibitors (PPI). If medical therapy is unsuccessful or if gastric contents are regurgitated, fundoplication should be performed.

Fig. 3.11 Axial sliding hernia

Hiatal Hernia: Paraesophageal Hernia

Paraesophageal hernia is rare, accounting for less than 5 % of all hernias (Fig. 3.13). In this condition, portions of the gastric fundus are herniated into the mediastinum. This usually occurs on the greater curvature side, owing to the relatively firm attachment of the lesser curvature to the cardia. Because the lower esophageal sphincter and cardia are normally positioned, this type of hernia can be seen only with a retroflexed endoscope.

Diagnosis

Additional Study

Radiographic contrast examination

Comments

As there is a potential for incarceration, surgical correction is recommended even for asymptomatic cases (gastropexy, fundoplication for combined hernias).

Fig. 3.12 Paraesophageal hernias

Fig. 3.13 Types of hernia

Hiatal Hernia: Upside-Down Stomach

Upside-down stomach is an extreme form of paraesophageal hernia in which the entire stomach has herniated and rotated upward through the diaphragm into the mediastinum (Fig. 3.14).

Diagnosis

Additional Studies

Plain chest radiograph (Fig. 3.16)

Radiographic contrast examination

Comments

The diagnosis is established by contrast radiographs. Surgical correction is advised for patients who are well enough to tolerate surgery.

Fig. 3.14 Schematic diagram of upside-down stomach. Complete herniation of the stomach into the chest

Fig. 3.15 Upside-down stomachs

Fig. 3.16 Radiographic findings

Gastroesophageal Prolapse

Usually there is coexisting cardial incompetence, and an axial sliding hernia is often present (Fig. 3.17). Clinical complaints may include retrosternal pain, usually after a rise in intraabdominal pressure (coughing), as well as bleeding and transient incarceration.

Diagnosis

Additional Studies

None

Comments

The clinical significance of gastroesophageal prolapse is uncertain. Complaints may occur during coughing and other acts that raise the intraabdominal pressure.

Fig. 3.17 Difference between gastroesophageal prolapse and sliding hernia

Fig. 3.18 a–d Gastroesophageal prolapse

Mallory-Weiss Lesion and Boerhaave Syndrome

Additional Studies

Oral contrast examination with a water-soluble medium (endoscopy is contraindicated in patients with a suspected perforation or if contrast extravasation occurs)

Chest radiograph (pneumomediastinum is common in Boerhaave syndrome) (Fig. 3.21)

Comments

Treatment for a Mallory-Weiss lesion is described on page 155. Gastroscopy should be repeated after 24 hours. Boerhaave syndrome warrants early, aggressive surgical treatment.

Fig. 3.19 Mallory–Weiss lesion

Fig. 3.20 Mallory–Weiss lesions

Fig. 3.21 Pneumomediastinum. Chest radiograph shows definite separation of the mediastinal pleura from the left cardiac border (from: Lange S, Radiologische Diagnostik der Thoraxerkrankung. Stuttgart: Thieme 1996).

Gastroesophageal Reflux and Reflux Esophagitis: Clinical Aspects

Gastroesophageal reflux is a common endoscopic finding (Fig. 3.22). It is seen even in healthy individuals and usually causes no complaints. As a result, endoscopic detection does not necessarily indicate a pathological condition.

Pathophysiology. Because gastric juice contains substances that are corrosive to the esophageal mucosa, there are physiological mechanisms designed to protect the esophagus. Gastroesophageal reflux causes clinical complaints when these antireflux mechanisms fail. They include the sphincter mechanisms, the regenerative capacity of the esophageal epithelium, and the clearance function of esophageal motility, which curtails exposure to the corrosive gastric juice. Factors that predispose to gastroesophageal reflux are listed in Table 3.2.

Complaints. A wide variety of complaints is possible, ranging from mild postprandial discomfort, which the patient may not even consider abnormal, to severe complaints like those seen in reflux esophagitis (Table 3.3).

Reflux Esophagitis

Reflux esophagitis refers to the gross or histological inflammatory changes that occur in the esophageal mucosa in response to reflux. The clinical picture is characterized by retrosternal or epigastric pain, heartburn, and dysphagia that periodically recur. Periods of remission with very mild clinical symptoms are followed by acute exacerbations. In many cases the complaints progress over time, eventually leading to complications such as chronic ulcers, scarring, strictures, columnar metaplasia, and adenocarcinoma.

3.22 Gastroesophageal reflux

Reflux Esophagitis: Diagnosis and Treatment

Additional Studies

24-hour pH monitoring

Esophageal manometry

Radiographic contrast examination to detect or exclude a possible hernia not detectable by endoscopy

Comments

The diagnosis of reflux disease is based on the clinical presentation, endoscopic findings, histological examination, and 24-hour pH monitoring. It should be emphasized that the correlation between clinical complaints and endoscopic findings is poor. Also, there is not always a close correlation between endoscopy and histology, especially in forms with an essentially normal-appearing mucosa.

Treatment

PPI therapy

If unsuccessful: fundoplication

Treatment of complications (see p. 157, 172)

Fig. 3.23 Types of lesion that can occur in reflux esophagitis

Fig. 3.24 Polyps in reflux esophagitis

Reflux Esophagitis: Grading

The inflammatory lesions of reflux esophagitis are currently graded according to the Savary-Miller classification, which is summarized in Table 3.4.

Grades I-III. Grades I-III (Fig. 3.25) reflect a more or less pronounced acute attack. These grades may be complicated by superficial bleeding, but some cases initially resolve without sequelae.

Grade IV. Grade IV (Fig. 3.26) represents the chronic, complicated stage of reflux esophagitis, which is subject to its own dynamic. The most serious complications are obstructive strictures and adenocarcinoma secondary to columnar metaplasia of the esophageal epithelium.

Fig. 3.25 Grading of reflux esophagitis

Fig. 3.26 Grade IV reflux esophagitis

Complications of Reflux Esophagitis: Barrett Esophagus

In simple terms, Barrett esophagus is present when the squamocolumnar junction has migrated proximally into the esophagus by at least 3 cm (Fig. 3.27). This migration occurs when esophageal squamous epithelium that has been damaged by chronic reflux is replaced by metaplastic columnar epithelium.

This condition is found in up to 10% of patients with reflux esophagitis.The importance of the finding—and thus the necessity of identifying it, confirming it by biopsy, and monitoring its progression—lies in the approximately 10% risk of adenocarcinoma formation in the columnar-lined esophagus.

Diagnosis

Additional Studies

See Management

Comment

Barrett epithelium is frequently missed at endoscopy. Adenocarcinoma, which develops in up to 10% of patients with Barrett esophagus, is also frequently missed on gross inspection. Dysplasia can be diagnosed only by histological examination.

Fig. 3.28 Barrett epithelium

Complications of Reflux Esophagitis: Management of Barrett Esophagus

Fig. 3.27 Barrett esophagus and brachyesophagus

Diagnosis

Extended Testing

Endosonography

Treatment and Follow-Up

Barrett epithelium without dysplasia:

– Yearly endoscopic follow-up with specimen collection

Barrett epithelium with low-grade dysplasia:

– 18-month follow-up

Barrett epithelium with high-grade dysplasia:

– Histological surveillance, then esophageal resection

Alternatives:

– Endoscopic treatment: thermal, photodynamic, mechanical

Fig. 3.29 Methylene blue staining

Complications of Reflux Esophagitis: Peptic Stricture

Additional Studies

Biopsy

Cytology

Comments

A peptic stricture often requires endoscope treatment (see Dilation, p. 172).

Fig. 3.30 Peptic stricture of the esophagus

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