Esophagus, Stomach, and Duodenum

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Chapter 89

Esophagus, Stomach, and Duodenum

Esophageal Obstruction


Patients with ingestion of foreign objects and esophageal food boluses commonly are seen in the emergency department (ED). Although most objects pass spontaneously, approximately 10 to 20% require a nonoperative intervention, and fewer than 1% require surgical removal. Death as a result of foreign body ingestion or impaction is rare. Patients with esophageal foreign bodies can be classified into four major categories: (1) pediatric patients, (2) psychiatric patients and prisoners, (3) patients with underlying esophageal disease, and (4) edentulous adults. Pediatric patients account for more than 75% of ingestions, with the peak incidence between the ages of 18 and 48 months.1 Coins account for the majority of pediatric ingestions, whereas most adult impactions involve pieces of food, particularly meat and bones.2 Patients with structural abnormalities of the esophagus, such as strictures, rings, webs, diverticuli, or malignancies, are at greater risk for foreign body impaction. Edentulous adults are also at increased risk because of impaired oral sensation and have a risk of accidental ingestion of their dental prosthesis.3

Principles of Disease

The adult esophagus is approximately 25 to 30 cm in length. Superiorly, it begins in the hypopharynx as a transverse slit posterior to the larynx and approximately at the level of the cricoid cartilage. On either side of this cephalad slit are the piriform recesses, which are blind pouches that may occasionally harbor a foreign body. The esophagus is distensible; an adult can usually pass an object up to 20 mm in size without difficulty. Throughout its course, the esophagus has four natural areas of narrowing where the majority of foreign bodies become entrapped: at the cricopharyngeus muscle (the upper esophageal sphincter [UES]), the aortic arch, the left mainstem bronchus, and the lower esophageal sphincter (LES) at the diaphragmatic hiatus. Pediatric entrapment occurs primarily at the level of the cricopharyngeus, whereas adult entrapment occurs mainly at the UES. Large, proximal impactions can impinge on the trachea, leading to airway compromise that manifests as choking, stridor, or cough.

The esophagus comprises two main bands of muscle: an inner circular layer and an outer longitudinal layer. The resting tone of these muscles causes the inner epithelium to fold in on itself, effectively obliterating the lumen. Elastic fibers enable the esophageal lumen to expand and allow passage of a food bolus. The upper third of the esophagus, including the cricopharyngeus muscle, contains striated muscle to allow the voluntary initiation of swallowing. The middle portion of the esophagus is a mixture of skeletal and smooth muscle, and the distal third is composed only of smooth muscle.

Although it is relatively fixed at its origin, the esophagus becomes mobile as it traverses the mediastinum. Thus it can be easily displaced by adjacent structures such as an enlarged left atrium or ventricle, a goiter, or a mediastinal tumor. Displacement of the esophagus may alter its shape enough to impede the passage of a food bolus or foreign body.

Clinical Features

Patients with an esophageal obstruction have a wide range of symptoms. Most adults are able to describe the precipitating event and commonly complain of dysphagia (difficulty swallowing), odynophagia (painful swallowing), and neck or chest pain. Entrapment at the UES can generally be localized by the patient because of somatic nerve endings in the upper esophagus. In contrast, entrapment in the lower esophagus causes more visceral-type chest and epigastric discomfort.1 The obstruction may be partial or complete. The patient with complete obstruction is unable to swallow oral secretions and may be violently retching in an attempt to regurgitate the obstructing bolus. Patients should be evaluated for the presence of stridor or signs of perforation or peritonitis.

Pediatric patients are often brought to the ED after a witnessed ingestion. A high degree of suspicion is needed to diagnose foreign body ingestion when the event was unwitnessed, because 7 to 35% of children with proven esophageal foreign body impactions are asymptomatic at the time of presentation. Symptoms that should prompt consideration of unwitnessed foreign body ingestion include fever, wheezing, stridor, rhonchi, or poor feeding.4

A proximal obstruction may arise as a “café coronary,” characterized by sudden cyanosis and collapse caused by food (usually an unchewed piece of meat) lodging in the upper esophagus or oropharynx leading to airway obstruction. Similarly, “steakhouse syndrome” results when a large piece of food, usually improperly chewed, is swallowed and causes esophageal obstruction in the distal esophagus. The obstruction may be transient with spontaneous passage of the bolus and may be complete or partial. Intense discomfort develops shortly after swallowing a large piece of meat, and the patient is usually unable to swallow anything else. Ingestion of alcohol and absence of teeth are predisposing factors. Although obstruction may occur in a patient with a normal esophagus, preexisting structural abnormalities such as carcinoma, peptic stricture, or Schatzki’s ring are identified in almost 90% of patients with an esophageal obstruction. Schatzki’s ring is a fibrous, diaphragm-like stricture near the gastroesophageal junction present in up to 15% of the population.

Aside from naturally occurring areas of anatomic narrowing, there are other pathologic causes of esophageal stenosis that may lead to symptoms of obstruction. Intrinsic causes of luminal narrowing include carcinoma and webs. An esophageal web is a thin structure composed of mucosa and submucosa most commonly found in the middle or proximal esophagus. Although webs can occur in isolation, they are also seen in the Plummer-Vinson syndrome, which is characterized by anterior webs, dysphagia, iron deficiency anemia, cheilosis, spooning of the nails, glossitis, and thin friable mucosa in the mouth, pharynx, and upper esophagus. Most patients with this syndrome are women 30 to 50 years of age. Patients usually report dysphagia that is initially intermittent and worse with solids. If untreated, it may progress and become constant. Surgical changes after a gastric bypass can also predispose a patient to esophageal obstruction.5

Extrinsic compression of the esophagus can occur in a variety of conditions. In the neck, thyroid enlargement from goiter or carcinoma may cause dysphagia. Symptoms may also be seen with a pharyngoesophageal or Zenker’s diverticulum, a progressive outpouching of the pharyngeal mucosa as a result of increased pressure generated by failure of proper relaxation of the cricopharyngeus muscle. Noisy deglutition, dysphagia, halitosis, and a palpable compressible mass in the neck may be present. Laryngotracheal aspiration when the patient is supine results from the emptying of contents from the diverticulum.

Diagnostic Strategies

Anteroposterior (AP) and lateral radiographs of the neck, chest, and/or abdomen can be obtained based on symptoms. Flat objects in the esophagus such as coins or button batteries orient in the coronal plane and appear as a circular object on an AP projection. Button batteries can be differentiated from coins by a characteristic radiographic “double-density” appearance. Small bones or radiopaque objects may occasionally be visualized. Air in the tissues may be present if perforation has occurred. However, failure to demonstrate a foreign body on radiographs does not rule out its presence. Contrast studies with barium or Gastrografin are rarely performed in this setting because they present a significant risk for aspiration and can obscure visualization if subsequent endoscopy is necessary.3 Computed tomography (CT) can be used in equivocal cases to identify and localize foreign bodies before endoscopy. CT is more sensitive than radiography at identifying foreign bodies including chicken or fish bones and other nonorganic objects. CT scans have the additional value of visualizing changes in the surrounding tissues associated with perforation.6

Hand-held metal detectors have been reported to be useful screening devices for locating metallic foreign bodies in children without exposing them to radiation. They may also be of use in finding radiolucent metallic foreign bodies such as aluminum pull tabs. They do not, however, pinpoint the location of the object.7 Caution should be used in interpreting negative metal detector tests in obese children because esophageal coins have been missed in this scenario.8

Persistent or concerning symptoms in a patient without evidence of a radiographic foreign body can be further evaluated by endoscopy.


Both flexible and rigid endoscopy are effective in removing esophageal foreign bodies. Flexible endoscopy is recommended in most cases as the first line in managing esophageal foreign bodies because it is better tolerated by patients and can usually be completed with use of procedural sedation.9 In contrast, rigid endoscopy requires general anesthesia, has a higher complication rate, and more commonly results in postinterventional dysphagia.

Upper Esophagus

Oropharyngeal foreign bodies can usually be removed with a Kelly clamp or Magill forceps under direct visualization. Smooth upper esophageal foreign bodies can often be removed with a Foley catheter. This procedure requires an experienced clinician, a cooperative patient, and fluoroscopic guidance. The patient is placed in a prone position, and the catheter is passed into the esophagus past the point of the foreign body impaction. The balloon is then inflated and the catheter withdrawn, pulling the foreign body with it. In a large study of children undergoing Foley balloon extraction with fluoroscopic guidance, 80% of foreign bodies were successfully removed, and an additional 8% were advanced into the stomach. Failure rates were highest with infants younger than 1 year of age. Controversy exists regarding the safety of this technique because there is no direct control of the foreign body. However, several large studies have shown complication rates to be less than 1% when patients are carefully chosen.10–12 This technique should not be used for a foreign body that has been impacted for more than 1 week, for objects that are not smooth, for patients with radiographic evidence of esophageal perforation, or for patients with any underlying structural esophageal abnormalities. This technique has a significant economic advantage when compared with the costs of general anesthesia in an operating room for performance of rigid endoscopy.10 Another technique is bougienage, which has been shown to be both safe and effective in coin removal.11 In this technique, an esophageal dilator is passed through the mouth into the esophagus to advance the coin into the stomach; the dilator is then quickly removed. In a large study, this procedure took less than 5 seconds to perform and was successful in 95% of cases with no serious complications.12 When these maneuvers fail to dislodge the esophageal foreign body, consultation with a qualified endoscopist is indicated.

Lower Esophagus

Lower esophageal obstruction is usually the result of an impacted food bolus. Anecdotally, administration of 1 mg of glucagon intravenously (IV) (up to a total of 2 mg) can cause enough relaxation of the esophageal smooth muscle to allow passage of a food bolus in the lower esophagus. However, no randomized controlled trials have shown a statistically significant benefit of using glucagon compared with placebo. In a small double-blind placebo-controlled study in children with esophageal coin impaction, glucagon was shown to be ineffective.13 In addition to lack of demonstrated efficacy, glucagon has multiple side effects such as vomiting, which can increase the risk of aspiration or esophageal perforation.14

Effervescent agents are sometimes effective in accelerating the passage of an obstructing food bolus. Although the mechanism of action is unclear, it is hypothesized that the carbon dioxide released from bubbles escaping the fluid acts to disrupt the impacted food bolus and to distend the distal esophagus. There are case reports and case series in which administration of carbonated beverages (including soft drinks) has resulted in the passage of the obstructing food bolus in 60 to 80% of patients treated. However, there is only low-level evidence to support this practice, and the studies showing this benefit had multiple confounding factors.15 It has been recommended that effervescent agents be avoided in cases of complete obstruction and in cases in which an obstruction has been present for over 24 hours because of the theoretic potential of inducing perforation of a possibly ischemic distal esophagus. The use of meat tenderizer (papain) to soften a food bolus is not recommended. Although intact mucosa is resistant to papain’s effects, an inflamed mucosa becomes much more inflamed when exposed to this proteolytic enzyme, and esophageal digestion or perforation may occur.16

Endoscopy should be performed immediately for patients experiencing significant distress and for children with impaction of an alkaline button battery. Button batteries lodged in the esophagus can cause severe tissue damage in just 2 hours. Damage is primarily related to localized corrosive effects and occurs by three main mechanisms: leakage of an alkaline electrolyte, pressure necrosis, and generation of an external current that causes electrolysis of tissue fluids and generates hydroxide at the battery’s negative pole. Larger batteries carry a greater risk of impaction and leakage. Delayed complications include esophageal perforation, tracheoesophageal fistula, exsanguination after development of a fistula with a major blood vessel, and esophageal strictures. In a review of over 8000 battery ingestions that were reported to the National Battery Ingestion Hotline, outcomes have significantly worsened over the past decade. This is primarily attributable to newer 20 mm–diameter lithium cell batteries that now account for 92% of fatal ingestions.17 Batteries that pass into the stomach should be followed radiographically and clinically to ensure passage. Assistance with the management of a patient with button battery ingestion can be obtained through the National Button Battery Ingestion Hotline at 1-202-625-3333 or at

Urgent intervention is also indicated for sharp objects, coins in the proximal esophagus, and impactions that impair the handling of secretions. It is unclear whether patients with mild to moderate symptoms of esophageal obstruction from a suspected food bolus require immediate endoscopy. In such cases, some experts believe that emergent intervention is unnecessary if the patient is still able to handle secretions because the bolus often passes on its own. Others believe that the softened bolus makes endoscopic removal more difficult and predisposes to complications such as ulcers, lacerations, erosions, and perforations. In a recent retrospective review, factors associated with a risk of complications included a longer duration of impaction, bone foreign bodies, and larger-size foreign bodies.19 Although it may be acceptable to delay endoscopy in stable patients without high-grade obstruction to allow possible spontaneous passage, a foreign body or food bolus impaction should not be allowed to remain in the esophagus for longer than 24 hours. Any object remaining in the esophagus for more than 24 hours carries a higher risk of complications, including perforation, aortoenteric fistula, tracheoesophageal fistula, or abscess. These complications may occur up to years after the ingestion. Many experts advocate follow-up endoscopic evaluation after an esophageal obstruction to rule out underlying pathologic conditions.


Conservative outpatient management is appropriate for the vast majority of foreign bodies that have entered the stomach. However, certain foreign bodies that pass into the stomach still require endoscopic retrieval. Objects longer than 5 cm or wider than 2.5 cm in diameter (e.g., toothbrushes, spoons) rarely pass the duodenum. All sharp and pointed foreign bodies (e.g., toothpicks, bones) should be removed before they pass into the stomach because up to 35% may cause intestinal perforation. Smaller objects that pass into the stomach can be followed with stool inspections and with serial radiographs if necessary to confirm passage. Surgical removal should be considered for objects that remain in the stomach for more than 3 to 4 weeks or that remain in the same intestinal location for more than 1 week.3

Esophageal Perforation


Esophageal perforation is a potentially life-threatening condition that is critical to identify and treat early to minimize morbidity and mortality. Boerhaave’s syndrome was first described in the early 1700s as a result of a rapid increase in intraesophageal pressure related to forceful vomiting. It can also result from any Valsalva-like maneuver, including childbirth, coughing, or heavy lifting.20,21 Iatrogenic esophageal perforation has become increasingly common in the past two decades, with endoscopy being the most common cause. Perforation has also been reported as a complication of both nasogastric tube placement and endotracheal intubation. Other causes of perforation include foreign body ingestion, caustic substance ingestion, severe esophagitis, carcinoma, and direct injury related to blunt or penetrating trauma.

Principles of Disease

Spontaneous rupture occurs because of a rapid increase in intraluminal esophageal pressure through a patent LES. The cricopharyngeal muscle fails to relax, leading to transmural rupture of the esophagus. More than 90% of spontaneous esophageal ruptures occur in the distal esophagus. In contrast, rupture resulting from blunt trauma to the neck or thorax usually occurs in the proximal and middle third of the esophagus. Most iatrogenic injuries occur at the pharyngoesophageal junction because the wall in this area is thin and there is no serosal layer to reinforce it, and force is frequently used to pass the tube beyond the level of the cricopharyngeus. Another site of frequent iatrogenic injury is the esophagogastric junction. In this area the esophagus curves anteriorly and to the left as it enters the abdomen, and an endoscope has a greater likelihood of perforating the posterior wall. This usually occurs during therapeutic dilation for strictures or achalasia. Other factors predisposing to iatrogenic perforation include anterior cervical osteophytes, Zenker’s diverticulum, esophageal strictures, and malignancy.

Perforation has been reported as a complication of most endoscopic procedures, including transesophageal echocardiography, sclerotherapy, and inflation of the gastric balloon of a Sengstaken- Blakemore tube to control bleeding esophageal varices. When a perforation occurs, saliva and gastric contents can enter the mediastinum. Rapid spread of an infectious or inflammatory response to the surrounding tissues and organs occurs because of the thinness of the esophageal wall. Changes in intrathoracic pressure during respiration draw contaminants deeper into the mediastinum. The presence of gastric enzymes and other foreign material in the mediastinum induces an intense inflammatory response that may result in enough fluid buildup to displace adjacent structures.

Clinical Features

Clinical presentations vary and can depend on the cause, location, size, degree of contamination, and site of injury. Patients with an upper esophageal perforation usually have neck or chest pain, dysphagia, respiratory distress, and fever. Odynophagia, nausea, vomiting, hoarseness, or aphonia may also result. Mackler’s triad of subcutaneous emphysema, chest pain, and vomiting is considered pathognomonic for spontaneous esophageal rupture. However, the complete triad is seen in less than half of cases.22 Patients with perforation of the lower esophagus may have abdominal pain, pneumothorax, hydropneumothorax, and pneumomediastinum. The pain often radiates into the back, to the left side of the chest, and to the left or both shoulders. Early physical examination findings include epigastric or generalized abdominal tenderness, often with involuntary guarding and rigidity. Up to 30% of patients develop mediastinal or cervical emphysema, which may be noted by crepitus on palpation or by the pathognomonic Hamman’s sign with a “crunching” sound heard during auscultation. Patients with severe mediastinitis may be in fulminant shock.

Pain, fever, dyspnea, or crepitus after esophageal instrumentation should be considered an indication of perforation until proven otherwise. Symptoms related to iatrogenic perforation may not appear until several hours after the procedure.

Diagnostic Strategies

Radiographic studies are used to establish the diagnosis of an esophageal perforation. A chest and an upright abdominal radiograph are usually obtained first. Soft tissue lateral neck radiographs should be considered if a proximal perforation is suspected and may reveal air in the prevertebral fascial planes. Radiographic abnormalities may be detected in up to 90% of patients with esophageal perforation. Patients with upper esophageal injuries commonly have chest radiographs that show pneumomediastinum alone or a right-sided pleural effusion, whereas patients with distal esophageal perforations typically have a left-sided effusion. Other radiographic abnormalities include subcutaneous emphysema, mediastinal widening, or pulmonary infiltrates. These classic radiographic changes are often not present in the first few hours after perforation, so a normal radiograph should not be used early to exclude the possibility of esophageal perforation.23

Patients with possible perforation should undergo contrast radiographic studies. Controversy exists regarding the contrast agent of choice. Barium sulfate is superior in identifying small perforations; however, it may incite an inflammatory response in tissues. For this reason, some experts advocate the use of water-soluble agents (e.g., Gastrografin). However, the water-soluble agents are less dense and may not demonstrate the abnormality. In addition, pneumonitis may result if these agents are aspirated because of their hypertonicity. A prudent approach would be to attempt the study with a water-soluble agent first in patients who are not at risk for aspiration. If a clinically suggested perforation is not identified, the examination should be repeated with barium.

CT of the chest may be considered if a contrast study does not demonstrate a clinically suggested perforation. It can also be used in patients who are intubated or cannot complete an esophagram. Findings such as mediastinal air, extraluminal contrast material, or fluid collections or abscesses adjacent to the esophagus confirm a perforation. CT also allows evaluation of other adjacent areas that may suggest an alternative diagnosis.6 Flexible esophageal endoscopy may be useful to directly visualize the perforation, especially in cases of penetrating external trauma, where this has a sensitivity of 100% and a specificity of 83%.24 This technique is not recommended for other situations because insufflation could potentially enlarge a minimal transmural opening.23 Laboratory studies are not usually helpful soon after a perforation, although leukocytosis may be noted.


Clinically unstable patients with esophageal perforation require rapid resuscitation and treatment. Broad-spectrum intravenous antibiotics should be initiated early. Patients should receive nothing by mouth (NPO), and a nasogastric tube should be considered to eliminate oral and gastric secretions. Early surgical consultation is warranted. A recent study compared survival of patients with esophageal perforation who were treated within 24 hours of perforation and those treated after 24 hours. This study found that aggressive treatment within the first 24 hours resulted in a 97% survival versus 89% survival in those treated after 24 hours.25

There is growing evidence that some iatrogenic perforations in certain patients at low risk can be managed conservatively. These include clinically stable patients with minimal symptoms or fever, those whose perforation is contained, and those who are seen long after their procedure and have demonstrated no ill effects. In a recent retrospective study, patients who had a contained leak without respiratory compromise had worse outcomes when managed operatively compared with nonoperative management. Patients should be kept NPO and treated with broad-spectrum antibiotics and parenteral nutrition. These patients require diligent observation and assessment for failure of nonoperative therapy. In addition to true “nonoperative” management with close observation and intravenous antibiotics, other “palliative interventions,” including endoscopy, stent placement, drainage gastrostomy, feeding jejunostomy, and tube thoracostomy, have become more common.26


Principles of Disease

Infectious Esophagitis

Esophageal infections primarily occur in immunocompromised hosts. When they occur in healthy patients, there is usually an underlying esophageal abnormality or local area of immune compromise, as might occur with the use of inhaled steroids. Iatrogenic alterations in host defenses through the use of immunosuppressive agents, potent chemotherapeutic agents, and broad-spectrum antibiotics can predispose an individual to the development of an esophageal infection. Human immunodeficiency virus (HIV) is a significant risk factor for infectious esophagitis, but rates have decreased since the advent of highly active antiretroviral therapy (HAART). Esophageal candidiasis is one of the most common acquired immunodeficiency syndrome (AIDS)–defining illnesses, but the incidence decreased by over 90% from 1994 to 2004.27 Patients with acute HIV seroconversion syndrome that occurs 2 to 3 weeks after primary exposure to HIV can develop esophageal ulcerations and severe odynophagia.28

In addition to iatrogenic immunosuppression, diseases that weaken immunologic defenses in otherwise normal hosts can predispose the esophagus to infections. These conditions include diabetes mellitus, alcoholism, underlying malignancy, use of corticosteroids, and advanced age. Changes that occur in the mucosal barrier of the esophagus as a result of these conditions lead to an increased susceptibility to infection. The Candida species (primarily Candida albicans) are the most common esophageal pathogens.

As empirical antifungal prophylaxis in immunosuppressive states has become more common, viral esophagitis has become more prominent. Herpes simplex virus 1 (HSV) and cytomegalovirus (CMV) are the most common viral pathogens. Human papillomavirus has been implicated as well. Bacteria, mycobacteria, other fungi, and parasitic organisms such as Trypanosoma cruzi, Cryptosporidium, and Pneumocystis are uncommon causes of infectious esophagitis and are usually diagnosed by culture or biopsy.

Pill Esophagitis

More than 1000 cases of pill-induced esophageal injury have been reported in the literature from nearly 100 different types of pills. The exact incidence of pill esophagitis is unknown because most cases are unrecognized and therefore unreported. The condition results when a pill or capsule fails to pass into the stomach and remains in contact with the esophageal mucosa for a prolonged period. This results in inflammation and injury of the esophageal mucosa. Pill esophagitis has been reported in all age groups. Predisposing factors include advanced age, decreased esophageal motility, and extrinsic compression. Large pills are more likely to be retained, as are those coated with gelatin. Pills can stick to a normal esophagus, especially when taken without water or by a patient in the supine position. Any area of the esophagus can be affected, although sites of natural compression may be more susceptible. Sustained-release compounds may be more damaging than standard preparations. Injury can range from minor irritation to frank ulceration, hemorrhage, and ultimately stricture formation. Some of the more common offending medications include antibiotics (especially the tetracycline family) and antivirals, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), potassium chloride, quinidine, ferrous sulfate, alendronate, and pamidronate.29

Eosinophilic Esophagitis

Eosinophilic esophagitis was first described in 1978 and is defined by the presence of eosinophils within the esophageal mucosa or deeper tissues. Initially thought to be a disease of children, it is being diagnosed in adults with increasing frequency. Although diagnostic guidelines vary, recent reports have suggested use of the following criteria: clinical symptoms of esophageal dysfunction, more than 15 eosinophils in one high-power field on esophageal biopsy, and lack of responsiveness to high-dose proton pump inhibitors (PPIs) or normal pH monitoring of the distal esophagus.30 The cause is unknown, although there is an association with food allergens, especially in the younger age group.31 More than 50% of patients have associated atopic disorders, such as asthma or eczema.32

Caustic and Radiation-Induced Esophagitis

Esophagitis from caustic substance ingestion occurs most commonly in children, although adults may intentionally ingest a large amount of a caustic substance in a suicide attempt. The most corrosive agents are strongly acidic with a pH less than 2 or alkaline with a pH greater than 12. The degree of injury depends on the concentration of the substance, the volume ingested, and the duration of mucosal contact. Strong acids produce coagulation necrosis, which results in eschar formation that usually limits the damage. In contrast, alkalis produce liquefaction necrosis, which continues to cause injury as long as the substance or its active breakdown products are in contact with tissue.29

Patients undergoing radiation treatment for underlying malignancy may develop esophagitis. The degree of injury is related to the total dose of radiation received. The mucosa becomes inflamed and friable. Agents used during sclerotherapy can also cause esophagitis.

Clinical Features

Esophagitis, regardless of cause, most commonly manifests with dysphagia or odynophagia. Chest pain is frequently present, and esophageal bleeding ranging from localized oozing as a result of inflammation to frank hemorrhage can occur. Ulceration and perforation can result in mediastinitis.


Infectious Esophagitis

For infectious esophagitis, therapy should be directed at the causative organism. Patients with normal immune systems and mild cases of oropharyngeal candidiasis can be treated with clotrimazole troches (10 mg dissolved in the mouth five times a day for 1 week) or nystatin (400,000-600,000 million units orally [PO] four to five times per day for 2 weeks). Patients with true esophageal candidiasis should be treated with fluconazole (400 mg as a loading dose and then 100-400 mg daily for 14 to 21 days). In patients unable to tolerate taking oral medication, fluconazole can be given IV.34

Herpes esophagitis is generally a self-limited process that resolves over about 7 days. Immunocompromised patients should be treated with antivirals, such as acyclovir (400 mg PO five times per day for 7-14 days or 5-10 mg/kg IV every 8 hours for 7-14 days), famciclovir (500 mg PO three times a day for 7-14 days), or valacyclovir (1 g three times a day for 7-14 days).35 For CMV, initial treatment can begin with ganciclovir (5 mg/kg IV every 12 hours for 2-3 weeks) or foscarnet (60 mg/kg IV every 8 hours or 90 mg/kg IV every 12 hours for 2-3 weeks).

If the causative organism cannot be adequately identified or if the patient is severely debilitated, admission to the hospital may be required. Patients discharged from the ED should receive appropriate follow-up with the relevant specialist (e.g., gastroenterology, infectious disease). In addition to therapy directed at the infecting organism, treatment with antacids, topical anesthetics, or sucralfate may provide symptomatic relief.

Caustic and Radiation-Induced Esophagitis

Management of caustic injuries includes evaluation and treatment of possible airway injury, followed by assessment of the extent of esophageal involvement. Although the use of mild diluents like water or milk to limit the extent of chemical injury has been advocated by some authorities, others warn against the possibility of inducing emesis, which reexposes the esophagus to the caustic substance. In general, it is probably best to avoid having patients ingest anything by mouth while undergoing evaluation. Likewise, gastric lavage and the administration of charcoal are not indicated. Symptomatic patients should be admitted to a monitored setting for observation, further evaluation with endoscopy, and treatment of potential complications, such as perforation. There is a high morbidity associated with caustic ingestions, with stricture formation in 26 to 55% of patients and possible later malignant transformation.37 As a result, multiple other treatments have been tried in an effort to improve long-term outcomes. This includes the use of intravenous corticosteroids and antibiotics, although the data on these have been mixed and they are not currently recommended.38 Asymptomatic patients who give a reliable history of a low-volume, accidental ingestion of a low concentration of an acidic or alkaline substance can be discharged after a period of observation and followed as outpatients.

Treatment of radiation esophagitis is supportive. Patients who cannot eat or drink because of radiation injury to the esophagus should be admitted for intravenous fluid therapy.