Esophageal Disease

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[edit] Esophageal Disease

Robert Burakoff

Scott David Lippe

Reflux esophagitis refers to pathology resulting from frequent contact between the esophageal mucosa and gastric acid. This is the most common disease affecting the esophagus. The resting lower esophageal sphincter (LES) pressure is mainly responsible for preventing reflux of the gastric acid and esophageal mucosal contact. When resting LES pressure decreases, reflux of acid occurs. Whether the decrease of LES pressure precedes or results from reflux is still unknown. Factors contributing to reflux include transient LES relaxations, low or hypotensive LES, and anatomic disruption of the sphincter associated with hiatus (hiatal) hernia. All three mechanisms do not occur in all patients. Also, patients with reflux clear acid more slowly than normal individuals.

[edit] REFLUX ESOPHAGITIS

[edit] Clinical Presentation

The most common reflux symptom is heartburn, a burning sensation in the chest usually after meals, when lying down, or bending over. Specific foods can provoke heartburn, and certain foods (e.g., chocolate, caffeine) can decrease LES pressure, promoting reflux (Box 101-1). When heartburn is severe, the patient may experience a bitter or sour taste in the mouth or a mouthful of fluid (water brash). Relief with antacids helps confirm the presence of heartburn.

Odynophagia, or chest pain on swallowing, is usually seen only in severe and usually longstanding reflux, particularly in patients with severe esophagitis or ulceration of the esophagus. Dysphagia is a transient sensation of food sticking in the esophagus and may result from esophagitis. Organic strictures produce a persistent dysphagia despite repeated swallowing. Night sweats have been associated with esophageal reflux in many patients. The sweating is usually mild, and patients usually do not mention it spontaneously. A history of night sweats suggests gastroesophageal reflux, which may also be causing chest pain, asthma, or chronic cough while not necessarily causing heartburn.

[edit] Diagnosis

Although the symptoms of gastroesophageal reflux disease (GERD) can be characteristic, patients with features of angina pectoris should undergo an electrocardiogram (ECG) and exercise stress testing before evaluation for GERD. No single test provides the diagnosis of GERD in all patients. If a patient presents with isolated heartburn without dysphagia, the best approach is to avoid testing and start a therapeutic trial (Fig. 101-1). If symptoms do not improve with acid-suppressing medication and dietary changes, testing is appropriate.^[1]

Figure 101-1 Algorithm for treatment of patient with heartburn and possible gastroesophageal reflux disease (GERD). H₂RA, H₂ receptor antagonist. (Modified from Sampliner RE: Heartburn. In Greene HL, Johnston WP, Maricic MJ, editors:Decision making in medicine, St Louis, 1992, Mosby.)

If reflux is present, the simplest, least sensitive, and most common test is a barium swallow. This test can determine if a stricture is present but only demonstrates reflux in 25% of patients and usually the most severe cases. The most sensitive test for reflux is the use of a pH probe during esophageal manometry. Reflux can be determined by a decrease in pH, as seen in 85% of GERD patients. Concurrently, resting LES pressure can be determined with an esophageal manometry catheter; it is usually at least 10 mm Hg greater than gastric pressure in normal controls. About 85% of reflux patients also have decreased LES pressure.

Once reflux has been demonstrated, it is necessary to determine the condition of the esophageal mucosa, ideally using endoscopy and biopsy. The physician then determines whether the patient's symptoms are caused by the acid reflux. A positive esophageal acid infusion (Bernstein) test confirms the diagnosis of reflux. If this test is negative and biopsies are inconclusive, a 24-hour ambulatory pH recording is indicated to determine whether the patient has prolonged acid reflux or if the symptoms are temporally related to acid reflux (Fig. 101-2).

Figure 101-2 Approach to patient with reflux esophagitis. LESP, Lower esophageal sphincter pressure.

[edit] Complications

Esophageal stricture occurs with severe reflux esophagitis and results from an extension of the inflammatory process into the submucosa. The stricture usually occurs at the distal esophagus and is smooth, contrasting with the irregular stricture of carcinoma. The presenting symptom of dysphagia is most often progressive. Patients initially complain of dysphagia with solids, not liquids, but with an increasingly tight stricture, dysphagia for liquids can develop. A barium swallow with a bread bolus or barium tablet can determine the stricture's diameter (Fig. 101-3). When a stricture is demonstrated, endoscopy and biopsy are mandatory to help rule out esophageal carcinoma.^[2] The medical treatment of esophageal strictures, in addition to an antireflux regimen (see next section), involves dilation with mercury-filled rubber bougies or dilators to a diameter of 15 mm. This allows patients to swallow a typical well-chewed meal. Esophageal dilation is successful in most patients and therefore avoids the need for surgery. Patients whose strictures are long or tortuous usually require esophageal stent placement or surgery.

Figure 101-3 Barium swallow demonstrating esophagitis with hiatal hernia, stricture, and ulceration.

Esophageal ulceration and hemorrhage from esophagitis are uncommon, but if they do not respond promptly to medical therapy, surgery is indicated. An esophageal ulcer is usually diagnosed with a barium swallow and often presents with worsening of reflux symptoms, from episodic heartburn to a more continuous pain pattern. The diagnosis of hemorrhage from esophagitis can be confirmed only by endoscopy.^[3] Another uncommon but significant complication of chronic reflux esophagitis is Barrett's esophagus, or columnar dysplasia of the esophagus. A portion of the squamous epithelium is replaced with columnar epithelium. Esophageal adenocarcinoma may develop in up to 10% of patients with Barrett's esophagus. Patients should have endoscopy with biopsy every 2 years or yearly if low-grade dysplasia is present.^[4] GERD also should be considered in the differential diagnosis of adult-onset asthma. Some patients show improvement in pulmonary function tests and symptoms after treatment of GERD.

[edit] Treatment

The primary goal of medical therapy is to keep gastric acid from contacting the squamous epithelium of the esophagus (Box 101-2 and Table 101-1). Treatment involves three goals. First, to prevent reflux, the head of the bed is elevated at bedtime, and lying down after meals is avoided. Eating is also avoided for 3 hours before sleep to prevent the acid load produced by a meal. Second, an attempt is made to neutralize gastric acidity with antacids, histamine receptor antagonists (H₂ blockers), or proton pump inhibitors (PPIs). Patients should avoid calcium-containing antacids because calcium stimulates acid production through gastrin; they should take other antacids whenever symptoms occur. If antacids are ingested several times each day or diarrhea results, an H₂ blocker is taken twice daily to reduce gastric acid secretion for more than 6 hours. For patients who do not experience relief with H₂ blockers or who have moderate to severe esophagitis on endoscopy, the use of PPIs is indicated. Omeprazole (Prilosec) or lansoprazole (Prevacid) provides much greater acid suppression than H₂ blockers. Omeprazole is superior to H₂ blockers in treating severe esophagitis and heals almost 90% of patients over 12 weeks. PPIs have now been approved for long-term use.

Table 101-1 Medical Therapy for Gastroesophageal Reflux Disease✢

✢Patients with erosive esophagitis may require up to 12 weeks of treatment.

†Patient with erosive esophagitis may require higher doses.

The third goal in treating reflux is to increase the LES pressure when the patient still has nocturnal reflux while taking an H₂ blocker or a PPI. Metoclopramide, approved in the United States for diabetic gastroparesis, is a potent dopamine inhibitor that increases LES pressure for 2 hours and increases gastric emptying. Metoclopramide, 10 mgbefore meals and at bedtime, is usually given as adjunctive therapy with H₂ blockers or PPIs, although 25% to 50% of patients experience restlessness, tremors, parkinsonism, and tardive dyskinesia. The typical patient should avoid foods and drinks that affect LES pressure (see Box 101-1). Most patients respond to the simple three-pronged regimen of elevating the head of the bed, controlled diet, and postprandial antacids.^[5]

[edit] ACHALASIA

Achalasia is a diffuse motor disorder of the esophagus characterized by incomplete relaxation of the LES and loss of peristaltic activity in the esophageal body. These abnormalities result in a functional obstruction of the lower esophagus. The etiology is unknown, but a consistent pathologic finding is a significant decrease in or absence of ganglion cells in Auerbach's plexus of the esophagus.

[edit] Clinical Presentation

This relatively rare disease has a prevalence of approximately 1 in 100,000 per year. Achalasia rarely appears in members of the same family, and onset of symptoms often occurs between ages 20 and 40, although the disease can affect any age group, including infants. The typical patient presents with dysphagia for solids and liquids, which is often of several years' duration. The patient often regurgitates retained material from the esophagus after lying down or with exercise. Heartburn is rarely a complaint. Further questioning may reveal that the dysphagia worsens with stress or rapid eating. Some patients learn to avoid these symptoms by regurgitating before meals to empty the esophagus. As the disease progresses and the esophagus dilates further, episodes of aspiration pneumonia occur. Odynophagia is seen at the beginning of the illness but abates as the esophagus dilates. Persistent chest pain may indicate a variant called vigorous achalasia.

[edit] Diagnosis

The physical examination is rarely helpful in diagnosing achalasia, except for the findings of halitosis and weight loss. In longstanding achalasia a presumptive diagnosis can be made from a chest radiograph showing retained material in the esophagus (sometimes misdiagnosed as a mediastinal mass on the right side) and absence of air in the stomach. The simplest method for diagnosis is a barium swallow (Fig. 101-4). This test is performed in the supine position to demonstrate loss of peristalsis, which always involves the lower two thirds of the esophagus. The esophagus is usually quite dilated, and an air-fluid level may be secondary to retained secretions. The classic finding is a gradual tapering at the end of the esophagus, similar to a bird's beak, a result of the incomplete relaxation of the often hypertonic sphincter. The differential diagnosis of these radiologic findings includes a stricture from reflux esophagitis and secondary achalasia from carcinoma involving the fundus of the stomach or distal esophagus. Possible tumors include adenocarcinomas of the stomach, pancreas, and lung. Secondary achalasia typically occurs in patients over age 60 with symptoms for less than 1 year.

Figure 101-4 Barium swallow demonstrating classic findings in achalasia, with dilated esophagus (left) terminating at gastroesophageal junction in beaklike narrowing (right).

A radiologic clue in the diagnosis of secondary achalasia is asymmetric narrowing in the distal esophagus. Endoscopy can rule out a stricture or tumor, since the endoscope can be passed into the stomach in the presence of achalasia but not with a peptic stricture or cancer. Also, in reflux esophagitis the esophagus appears erythematous and friable. Biopsies of the stomach fundus are done to rule out adenocarcinoma. Confirmation of the presumptive diagnosis of primary achalasia requires esophageal manometry, which characteristically shows an elevated LES pressure. The barium swallow shows that the sphincter pressure does not relax to gastric baseline. Esophageal body contractions are usually simultaneous or nonperistaltic. Secondary achalasia, however, can give the same manometric tracings.

[edit] Treatment

No medical or surgical therapy for achalasia can restore normal esophageal function. Therefore the goal of therapy is to weaken the LES to allow solids and liquids to empty by gravity. Medical therapy involves pneumatic (balloon) dilation of the LES. Under fluoroscopic guidance a firm balloon is inflated to a predetermined diameter, thus tearing some of the muscle fibers in the LES. Success is obtained in approximately 75% of patients in one or two sessions and is determined by more rapid emptying of barium on radiography and cessation of dysphagia. The major complication of balloon dilation is a mediastinal tear. This occurs in less than 5% of patients and can usually be treated nonsurgically with nasogastric suction and antibiotics.

Calcium channel blockers are potent smooth muscle relaxants and may help in treatment of achalasia. Botulinum toxin is a new therapeutic modality in which the toxin is injected endoscopically into the LES muscle fibers to paralyze the muscle. This therapy seems more effective in elderly patients, in whom effects can last longer than 6 months. Unfortunately, many patients develop antibodies to this treatment, and the efficacy decreases with repeated treatments.^[6] Balloon dilation therapy is still the definitive medical therapy, but botulinum toxin should be considered in all patients.

If medical therapy is unsuccessful, a myotomy (Heller's procedure) can be performed, which involves an incision through the circular muscle down to the mucosa over the entire length of the LES. At least 80% of patients have acceptable results. The major problem after myotomy is severe reflux esophagitis, which occurs in 5% to 25% of patients, depending on the surgeon's experience.

[edit] SMOOTH MUSCLE SPASTIC DISORDERS

[edit] Diffuse Esophageal Spasm

Although diffuse esophageal spasm has never been clearly defined, these criteria provide a working definition: (1) chest pain and dysphagia, (2) spontaneous nonperistaltic contractions (“tertiary contractions”) on barium swallow, and (3) repetitive simultaneous contractions on manometry in 50% or more of the esophagus. With these strict criteria, esophageal spasm is much less prevalent than achalasia. The etiology is unknown, and consistent pathologic findings have not been documented. The diagnosis is usually considered after a complete cardiac evaluation, often including coronary angiography. Diffuse esophageal spasm should be considered before cardiac disease if the patient complains of sharp retrosternal chest pain when eating solids or liquids. This pain can awaken the patient from sleep. Patients may complain of dysphagia for solids and liquids, but unlike achalasia, the symptoms are intermittent and not progressive. The barium swallow may show spontaneous random contractions, also called “corkscrew esophagus,” most often in the lower two thirds of the esophagus. Normal individuals also may show spontaneous or tertiary contractions on barium swallow. Esophageal manometry reveals an LES with normal relaxation after a swallow, although resting pressure may be higher than normal, with spontaneous, high-amplitude, and often repetitive contractions.

[edit] Nutcracker Esophagus

Another motor abnormality of the smooth muscle, nutcracker esophagus, is characterized by chest pain and dysphagia and occurs more often in women (mean age, 40). This disorder is more common than diffuse esophageal spasm and involves high-amplitude peristaltic contractions in the lower two thirds of the esophagus.

[edit] Diagnosis

Since some patients with noncardiac chest pain secondary to an esophageal smooth muscle spastic disorder have normal asymptomatic resting manometry, provocative testing is recommended to increase diagnostic yield. Intravenous edrophonium (Tensilon) can provoke the patient's typical chest pain but does not affect the coronary arteries. Esophageal balloon distention can also provoke a positive response. For those patients with continued noncardiac chest pain with normal manometry and negative provocative testing, 24-hour ambulatory motility manometry is available.

[edit] Treatment

No definitive medical therapy exists for diffuse esophageal spasm or nutcracker esophagus. The goal of therapy is to relieve pain and dysphagia, especially during meals. Nitrates (e.g., sublingual nitroglycerin) or longer-acting preparations (e.g., isosorbide dinitrate) are variable and unpredictable. Calcium channel blockers (e.g., nifedipine, diltiazem) have yielded symptomatic improvement and a decrease in amplitude contractions. Antidepressant therapy (e.g., trazodone) has been used successfully in these conditions, with the rationale of treating an “irritable esophagus” syndrome.

[edit] NONCARDIAC CHEST PAIN

More than 50,000 new cases of noncardiac chest pain occur annually, based on the percentage of normal coronary angiographies done in the United States. In patients with atypical chest pain and normal cardiac evaluation, an esophageal cause for the pain must be considered. The typical patients with noncardiac chest pain are females between ages 30 and 60. The etiology of the pain is most often acid reflux or less often an esophageal motility disorder (Fig. 101-5). Acid reflux should prompt an aggressive antireflux regimen using PPIs (e.g., omeprazole) once or twice daily. If a motility disorder is revealed, other agents are considered (Table 101-2).

Figure 101-5 Diagnosis of noncardiac chest pain.

Table 101-2 Treatment for Noncardiac Chest Pain

[edit] ESOPHAGEAL CANCER

The most common tumors of the esophagus are malignant. Squamous cell carcinoma is decreasing in frequency, whereas adenocarcinoma is becoming more common. Adenocarcinoma usually arises from an extension of the stomach mucosa or can result from malignant degeneration of Barrett's esophagus. Benign tumors are usually an incidental finding without clinical importance.

[edit] Squamous Cell Carcinoma

Squamous cell carcinoma is relatively rare, occurring in two to four white individuals per 100,000 and as many as 15 black males per 100,000. The highest incidence is found in northern China, with 130 cases per 100,000. Certain etiologic factors have been associated with squamous cell esophageal cancer, such as tobacco and alcohol use, as well as long-term stasis, as occurs in achalasia. Lye ingestion and radiation exposure also increase the risk. Patients present with progressive dysphagia for solids, then liquids. Most have unresectable disease by the time of presentation. As such, any patient over age 40 who has progressive dysphagia of less than 6 months' duration is presumed to have esophageal cancer until proved otherwise. Many patients also have anorexia and weight loss by the time they see their physician. The physical examination is not usually helpful unless supraclavicular lymph node enlargement or hepatomegaly is found, indicating metastatic disease. Less common presenting symptoms include hoarseness secondary to involvement of the recurrent laryngeal nerve; coughing secondary to aspiration or a tracheoesophageal fistula; and rarely hematemesis.

The presumptive diagnosis can be made by a barium swallow showing mucosal irregularity and tumor encroaching on the lumen (Fig. 101-6). Difficulty in diagnosis arises when the tumor causes a smooth narrowing, mimicking a benign stricture. Definitive diagnosis is made by esophagoscopy with biopsy and brush cytology in 95% of patients. Endoscopic ultrasound is the most reliable diagnostic technique in staging local cancer. Computed tomography (CT) scan of the chest continues to be useful for determining metastatic disease.

Figure 101-6 Barium swallow demonstrating classic findings in cancer of distal third of esophagus.

Regardless of the type of therapy, the 5-year survival of all patients with esophageal cancer is approximately 5% to 15%. Surgery is the treatment of choice for cancer of the lower third of the esophagus, whereas irradiation is used for involvement of the upper two thirds. The extent of the disease should be determined before surgery. In patients with metastatic disease, surgery is reserved for palliation. Endoscopic techniques for palliation include esophageal dilation or the placement of stents.^[7]

[edit] Adenocarcinoma

Adenocarcinoma arising from the mucous glands of the esophagus is extremely rare, but adenocarcinoma arising in columnar epithelium (Barrett's esophagus) is becoming more common. Barrett's esophagus, as noted earlier, results from reflux esophagitis. Approximately 10% of patients with biopsy-proven Barrett's esophagus develop adenocarcinoma. Patients give a history of heartburn progressing to dysphagia. Diagnosis is made by endoscopic biopsy and brush cytology. Surgery is the treatment of choice, but 5-year survival is only about 5%. As a result, surveillance of Barrett's esophagus with endoscopy is recommended.

[edit] ESOPHAGEAL RINGS

The lower esophageal ring, also called Schatzki's ring or the B ring, marks the junction of the esophageal and gastric mucosa (Fig. 101-7). It is composed of squamous epithelium superiorly and gastric epithelium inferiorly and is frequently associated with hiatal hernias. It is the most common clinical entity among esophageal rings and webs, often resulting in clinical symptoms. A patient without heartburn who reports that solid food, invariably meat or bread, intermittently becomes lodged in the lower end of the chest probably has a lower esophageal ring. It is not known whether lower esophageal rings are congenital or acquired. Patients may develop the condition in their 20s or present initially in the fifth to seventh decades.

Figure 101-7 The esophagus in relation to the trachea and aorta. (From Spechler S, Burakoff R: The esophagus. In Wilkins R, Levinsky N, editors:Medicine: essentials of clinical practice, ed 3, Boston, 1983, Little, Brown.)

The diagnosis is made by barium swallow if care is taken to distend and adequately fill the lower end of the esophagus (Fig. 101-8). A bolus is also swallowed during this test, which demonstrates a holdup at the gastroesophageal junction. The ring appears as a symmetric indentation at the junction and is usually less than 5 mm thick. If the ring is thicker, an esophageal stricture must be considered. Endoscopy is done to rule out carcinoma or stricture. For treatment, passage of mercury-filled bougies relieves symptoms.^[8]

Figure 101-8 Barium swallow demonstrating lower esophageal ring (B ring) at gastroesophageal junction.

[edit] ESOPHAGEAL DIVERTICULA

Esophageal diverticula represent outpouchings of one or more layers of the esophagus. Zenker's diverticulum occurs above the upper esophageal sphincter (cricopharyngeus) and may be associated with incoordination of the pharynx and cricopharyngeus during swallowing (Fig. 101-9, A). The patient presents with intermittent dysphagia. As the pouch enlarges, symptoms progress to aspiration of liquids and regurgitation of food into the mouth. Diagnosis is by barium swallow. Zenker's diverticulum usually requires no therapy, but surgery is available for problematic cases.

Figure 101-9 Barium swallow demonstrating Zenker's diverticulum (A) and large epiphrenic diverticulum of distal esophagus (B).

Epiphrenic diverticulum occurs just above the LES and is associated with failure of the LES to relax and with increased amplitude of esophageal contractions. Patients present with dysphagia and may regurgitate large amounts of accumulated fluid when recumbent. Diagnosis is by barium swallow (Fig. 101-9, B). Esophageal manometry is then performed to rule out an associated motility disorder. Surgery is indicated only if clinical symptoms are significant.

[edit] SYSTEMIC DISEASE WITH ESOPHAGEAL INVOLVEMENT

Several diseases can secondarily involve the esophagus (e.g., diabetes, alcoholism with neuropathy, amyloidosis), but none demonstrates a consistent characteristic abnormality. Collagen vascular disease can also involve the esophagus, resulting in varying degrees of aperistalsis. Invariably, these abnormalities are associated with Raynaud's phenomenon, which is seen with esophageal aperistalsis. Except for scleroderma, these diseases rarely result in significant functional impairment.

Scleroderma causes clinical problems resulting from aperistalsis of the lower two thirds of the esophagus and incompetence of the LES. The combination of these defects produces severe reflux esophagitis. The abnormalities result from atrophy of the smooth esophageal muscle and an abnormality of LES innervation. Patients have symptoms of heartburn and dysphagia for solids. Physical examination reveals evidence of Raynaud's phenomenon. Over time, heartburn may lessen while the dysphagia worsens from stricture development. A presumptive diagnosis is made based on the history and examination. A barium swallow demonstrates aperistalsis from the aortic arch to the LES and barium reflux. A stricture may be seen with longstanding disease. The diagnosis is confirmed with esophageal manometry, demonstrating aperistalsis of the distal two thirds of the esophagus and decreased LES pressure. All patients should undergo esophagoscopy at some point in their illness to evaluate the severity of the esophagitis and to determine if Barrett's esophagus is present.

No specific treatment exists for scleroderma involving the esophagus except aggressive reflux control. This includes the lifestyle modifications noted earlier and either H₂ blockers or PPIs, which decrease the reflux symptoms and the severity of esophagitis seen endoscopically. If a stricture develops, dilation with bougies is usually successful. Surgery is avoided because of the poor peristalsis in the distal esophagus. If the reflux esophagitis cannot be treated medically, surgical fundoplications may be of some benefit.

[edit] DISEASES OF THE HYPOPHARYNX AND PROXIMAL ESOPHAGUS

Systemic diseases can involve the smooth portion of the esophagus. Several diseases, primarily neurologic, can affect the hypopharynx, upper esophageal sphincter, and striated portions of the esophagus. Diseases involving the upper esophagus in patients with dysphagia for solids and liquids include amyloidosis, dermatomyositis, polymyositis, myasthenia gravis, myotonic dystrophy, myxedema, oculopharyngeal muscular dystrophy, and thyrotoxicosis. Patients with difficulty initiating swallowing may have had cerebrovascular accidents (CVAs), strokes, amyotrophic lateral sclerosis, multiple sclerosis, poliomyelitis, or tetanus. Those recovering from CVAs may benefit from speech therapy, with swallowing exercises to improve deglutition. Involvement of the striated muscle is diagnosed by barium swallow and cineradiology and confirmed by demonstrating aperistalsis in the upper third of the esophagus by manometry. The dysphagia may be alleviated by treating the systemic disorder.

[edit] ESOPHAGEAL INFECTIONS

The incidence of infectious diseases of the esophagus has increased primarily because of acquired immunodeficiency syndrome (AIDS). These patients may have candidiasis, herpes simplex virus type 1 (HSV-1), and cytomegalovirus (CMV). Candidiasis is seen with increased frequency in patients with neoplastic diseases, diabetes mellitus, chronic renal failure, and other conditions with immune incompetence. Patients develop severe odynophagia, dysphagia, and if severe, hematemesis. Oral candidiasis (thrush) may be present on physical examination. Barium swallow may reveal ulceration of the esophageal mucosa, but the diagnosis is best confirmed by endoscopy (Fig. 101-10). Brushings show yeast forms, and biopsy of the ulcerations demonstrates the fungus. Treatment of the immunocompetent patient is usually successful with nystatin oral suspension, 250,000 U every 2 hours for 1 week. A total dose of up to 12 million U a day may be required. In the immunocompromised patient, excellent results have been achieved with fluconazole (Diflucan), 50 to 200 mg once daily.^[9]

Figure 101-10 Barium swallow demonstrating mucosal ulcerations of candidal esophagitis.

Patients with HSV-1 and CMV usually complain of odynophagia. Diagnosis is by endoscopy and biopsy of the esophageal mucosal lesion with staining and cultures. Successful treatment includes acyclovir (Zovirax) for HSV-1 and ganciclovir (Cytovene) for CMV.

[edit] MISCELLANEOUS DISORDERS

[edit] Mallory-Weiss Syndrome

Mallory-Weiss syndrome consists of a mucosal tear at the gastroesophageal junction as a result of retching or emesis. It is found in 15% of patients with hematemesis. The classic description is forceful retching followed by hematemesis. As many as 25% of patients vomit blood with the initial emesis. Diagnosis is made by endoscopy, and the tear is usually evident on the gastric side of the gastroesophageal junction. Treatment consists of observation, since nearly all episodes stop spontaneously. Somatostatin can be used if bleeding continues, as can electrocautery. Surgery is rarely required.

[edit] Foreign Bodies

Most often, foreign bodies are the result of poorly chewed, hastily swallowed food, especially bread or meats. Food impaction usually occurs in edentulous elderly or very young patients. Animal bones and other objects, including pins or coins, pass through the gastrointestinal tract more than 90% of the time. Patients describe ingestion of the food or object followed by acute chest pain and salivation. A plain radiograph of the chest or neck frequently visualizes the object. A patient who cannot swallow secretions should undergo prompt endoscopic removal of the object. A nonobstructing foreign body that has not caused a perforation within 24 hours usually passes into the stomach. If the object is impacted or fails to pass, it is removed with a snare by flexible upper endoscopy. Often a lower esophageal ring is found when food impaction occurs. After removal of the object, the ring can be dilated with a bougie.

[edit] REFERENCES