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
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
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
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
Management
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 www.poison.org/prevent/battery.asp.18
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.
Stomach
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.
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.
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
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.
Management
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
Esophagitis
Principles of Disease
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
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
Clinical Features
Eosinophilic Esophagitis
Patients usually have dysphagia, nausea and vomiting, food impaction, or heartburn. This diagnosis should be considered in patients who have severe GERD symptoms despite the use of acid suppression medications and in patients with chronic unexplained dysphagia or recurrent esophageal food impaction. The diagnosis is confirmed by biopsy during endoscopy.33
Management
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).
Eosinophilic Esophagitis
These patients usually are seen after standard antireflux measures have failed or after they have developed a food impaction. The treating physician should consider the possibility of food impaction, ensure that appropriate antacid therapy is used, and refer the patient to a gastroenterologist for further treatment. Untreated eosinophilic esophagitis can lead to esophageal remodeling and stricture formation in up to 40% of adult patients. Although consensus has not yet been reached regarding an optimal treatment regimen, success has been reported with the use of topical (e.g., swallowed) corticosteroids. Recent pediatric studies have also shown efficacy with oral viscous budesonide.36
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.
