Esophagus, Stomach, and Duodenum

Key Concepts

Dysphagia

Dysphagia can be caused by obstructive lesions (e.g., esophageal neoplasm), motility disorders (e.g., achalasia), or neuromuscular disorders that can be vascular (e.g., cerebral vascular accident), immunologic (e.g., myasthenia gravis, multiple sclerosis [MS]), infectious (e.g., botulism), or metabolic in nature.
The incidence of achalasia increases with age, presenting insidiously with equal frequency for solids or liquids.
Dysphasia can be the initial presentation of myasthenia gravis.
Treatment of dysphagia is directed toward the underlying cause (e.g., myasthenia gravis, MS).
An outpatient barium swallow or upper gastrointestinal endoscopy is indicated for most patients with dysphagia.

Upper Gastrointestinal Foreign Bodies

Structural abnormalities of the esophagus are a major risk factor for foreign body obstruction; thus patients who obtain relief of foreign body sensation symptoms should be referred to a gastroenterologist for follow-up evaluation.
Immediate intervention is indicated for button batteries, food boluses causing high-grade obstruction, or patients in significant distress (e.g., vomiting, gagging, choking, stridor, or inability to tolerate oral intake).
Urgent (<24 h, and ideally <12 h) intervention is indicated for low-grade obstructions caused by sharp objects, coins lodged in the proximal esophagus, or food boluses.
Urgent intervention is also recommended for gastric foreign bodies wider than 2.5 cm or longer than 5 cm.
Flexible endoscopy with procedural sedation is the preferred therapeutic intervention to remove most proximal foreign bodies that can be reached by the scope.

Esophageal Perforation

Iatrogenic causes, such as a complication of endoscopy, remain the most common cause of esophageal perforation.
Water-soluble contrast should be used for initial diagnostic imaging studies when esophageal perforation is suspected.
Admission with broad-spectrum antibiotics (e.g., intravenous vancomycin 15 mg/kg plus piperacillin 3.375 g) and early surgical consultation should occur in the majority of cases of esophageal perforation.
Select stable patients with small, contained esophageal perforation may be managed conservatively by keeping the patient nothing per os (NPO), by administering broad-spectrum antibiotics and parenteral nutrition, and with a surgeon readily available.

Esophagitis

Gastroesophageal reflux disease (GERD) is a diagnosis of exclusion in patients who present with chest pain. It is critical to first rule out other diagnoses, such as acute coronary syndrome (ACS).
Empirical treatment of GERD with lifestyle modifications, H2 antihistamines, or proton pump inhibitors (PPIs) is appropriate, but if there is no improvement with these measures, patients should be referred for further evaluation.
Sucralfate (1 g qid) can be safely used in pregnant patients with GERD.
Eosinophilic esophagitis commonly presents as solid food dysphagia. Once food impaction is ruled out, a PPI should be initiated and the patient referred to a gastroenterologist.
Infectious esophagitis primarily occurs in immunocompromised patients, and endoscopy may be helpful in differentiating among causal agents.
Patients with pill esophagitis typically present with sudden onset retrosternal pain and odynophagia in the setting of taking medications without water; the diagnosis can often be made on the history alone.
Medications associated with pill esophagitis include doxycycline, aspirin, nonsteroidal antiinflammatory drugs (NSAIDs), and potassium chloride.

Gastritis and Peptic Ulcer Disease

Although gastritis cannot be definitively diagnosed based on clinical features alone, a clinical history such as recent NSAID use or alcohol ingestion in the setting of classic symptoms supports a presumptive clinical diagnosis of gastritis.
The most common cause of gastritis is Helicobacter pylori infection.
First-line treatment of H. pylori infection is a PPI (e.g., omeprazole 20 mg bid), amoxicillin (1 g bid), and clarithromycin (500 mg bid) for 14 days.
The most serious complications of peptic ulcer disease (PUD) include hemorrhage, perforation, penetration, and gastric outlet obstruction.

Gastric Volvulus

Acute gastric volvulus often presents with the combination of severe epigastric pain, distention, and vomiting, followed by violent nonproductive retching.
Volvulus has a very high morbidity and mortality. Nasogastric tube reduction can be attempted in the emergency department, but ultimately these patients need emergent surgical intervention.

Dysphagia

Foundations

Anatomy and Pathophysiology

Swallowing (also known as deglutition) is a complex phenomenon requiring voluntary and involuntary skeletal muscle activity coordinated by the swallowing center in the medulla. The cranial nerves provide afferent sensory inputs as well as efferent motor activity.

Swallowing is divided into oral, pharyngeal, and esophageal phases. Precise motor control of the act of swallowing is necessary to ensure that food is successfully transferred from the mouth through the esophagus into the stomach. Failure at any one of these levels results in dysphagia , which literally means “difficulty swallowing.”

Although dysphagia at any age is abnormal, it is particularly common in elders, with up to 60% of assisted living and nursing home patients having reported difficulty feeding. Dysphagia is classified as two types, oropharyngeal and esophageal. Oropharyngeal dysphagia, also termed transfer dysphagia , involves difficulty transferring a food bolus from the oropharynx to proximal esophagus. Esophageal dysphagia involves difficulty in transporting material down the esophagus.

Oropharyngeal Dysphagia

Neuromuscular Disorders

Neuromuscular disease causes approximately 80% of cases of oropharyngeal dysphagia, with most remaining causes being localized structural lesions. Most neuromuscular causes of dysphagia result in misdirection of the bolus, sticking, and the need for repeated swallowing attempts. Liquids, especially at extreme temperatures, cause dysphagia more commonly than solids, and symptoms are often intermittent. Strokes resulting in pharyngeal weakness with failure of the cricopharyngeus muscle to relax are the most common cause of neuromuscular dysphagia. Weakness of the tongue may occur, resulting in poor transfer of the bolus, or weakness of the buccal muscles may produce drooling and difficulty prompting the swallowing process.

The second most common cause of neuromuscular dysphagia is inflammatory myopathy, such as polymyositis or dermatomyositis. These disorders are characterized by inflammatory and degenerative changes in striated muscle that can produce dysphagia from weakness of the palate, pharynx, and upper esophagus. Dysphagia may be a presenting symptom of patients with these disorders.

Myasthenia gravis is an important cause of oropharyngeal dysphagia. At least 40% of patients with myasthenia gravis have dysphagia, and it is the presenting symptom in up to 15% of patients. The dysphagia becomes progressively worse with repeated swallowing attempts and is temporarily reversible with edrophonium.

Structural Disorders

Congenital anomalies of the aortic arch may cause dysphagia in children and adults. In children, respiratory symptoms are usually present and commonly predominate. In adults, an anomalous right subclavian artery is the most common vascular cause for dysphagia, often termed dysphagia lusoria. Patients often do not become symptomatic until the fourth decade of life, and the most common symptoms are dyspnea on exertion and dysphagia. Vascular compression of the esophagus causing dysphagia may also occur with aneurysms of the aortic arch and great vessels. Bronchogenic carcinoma can cause dysphagia by direct involvement of the esophagus or by compression from enlarged lymph nodes.

Esophageal Dysphagia

Mechanical Disorders

Esophageal dysphagia is caused by mechanical lesions or a motility disorder. Mechanical lesions may be intrinsic or extrinsic to the esophagus. Intrinsic lesions include strictures, webs, rings, tumors, esophagitis, postsurgical changes, and esophageal foreign bodies. Pressure from extrinsic lesions such as osteophytes, mediastinal masses, or aortic aneurysms can also cause dysphagia.

An esophageal web is a thin structure composed of mucosa and submucosa usually found in the middle or proximal esophagus. Although webs can occur in isolation, they are also seen in 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 Plummer-Vinson syndrome are women between 30 and 50 years of age. Patients usually report dysphagia that is initially intermittent and worse with solids. If untreated, it may progress and become constant. Rarely, motility disorders and surgical changes after a gastric bypass can also cause an esophageal obstruction.

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 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.

Motor Disorders

Patients with esophageal dysphagia who have no readily identifiable mechanical cause may have a motor disorder. Intrinsic motor disorders of the esophagus include achalasia , diffuse esophageal spasm, nutcracker esophagus, and hypertensive lower esophageal sphincter (LES). Systemic connective tissue diseases, such as scleroderma or CREST ( c alcinosis, R aynaud phenomenon, e sophageal dysmotility, s clerodactyly, and t elangiectasia) syndrome, Chagas disease, or a paraneoplastic syndrome may cause secondary motor disorders.

Achalasia is a disorder of unknown etiology in which the resting pressure of the LES is markedly increased, and peristalsis is absent in the body of the esophagus. The incidence increases with age.

Diffuse esophageal spasm is another type of intrinsic motor disorder. When it is severe and prolonged, with associated high-intensity peristaltic waves, it is termed nutcracker esophagus . Nonspecific motor disorders include repetitive esophageal contractions, nontransmitted esophageal contractions, and low-amplitude esophageal contractions.

Clinical Features

A careful history helps to differentiate oropharyngeal from esophageal dysphagia in up to 85% of patients ( Box 75.1 ). The history focuses on determining the anatomic level involved (oropharyngeal vs. esophageal), types of food leading to symptoms (liquids, solids, or both), and whether the symptoms are intermittent or progressive. Associated pain, prior gastrointestinal (GI) history, and family history are also helpful in determining the cause.

BOX 75.1

Causes of Dysphagia

Neuromuscular

Vascular

Cerebrovascular accident

Immunologic

Dermatomyositis
Multiple sclerosis
Myasthenia gravis
Polymyositis
Scleroderma

Infectious

Botulism
Diphtheria
Poliomyelitis
Rabies
Sydenham chorea
Tetanus

Metabolic

Lead poisoning
Magnesium deficiency

Other

Alzheimer disease
Amyotrophic lateral sclerosis
Brain tumor
Depression
Diabetic neuropathy
Familial dysautonomia
Metabolic myopathies (e.g., thyrotoxicosis)
Muscular dystrophies
Parkinson disease

Obstructive

Aortic aneurysm
Esophageal motility disorder (e.g., achalasia, diffuse esophageal spasm, nutcracker esophagus)
Esophageal rings
Esophageal stricture
Esophageal webs
Esophagitis
Foreign bodies
Hypertrophic cervical spurs
Inflammatory lesions
Left atrial enlargement
Mediastinal mass
Neoplasm
Thyroid enlargement
Vascular anomalies (e.g., enlarged aorta, aberrant subclavian artery)
Zenker diverticulum

Other

Alcoholism
Decreased saliva production (Sjögren syndrome, postirradiation)
Diabetes
Functional
Gastroesophageal reflux disease
Postoperative

The examination should include a thorough evaluation of the head and neck and a detailed neurologic examination. The patient should be observed while swallowing. It is helpful to note difficulty in initiating the swallow, misdirection of the bolus with regurgitation or aspiration, or unusual posturing of the patient when swallowing. Many patients with neuromuscular disorders depend on gravity to swallow, and having the patient swallow in the prone position may be helpful in rendering a diagnosis.

Oropharyngeal Dysphagia

Oropharyngeal dysphagia is characterized as an inability or excessive delay in initiation of swallowing, aspiration of the ingestate, nasopharyngeal regurgitation, or residual ingestate within the pharyngeal cavity following a swallowing event. This may be caused by misdirection of the food bolus, pain, or sticking and worsened with multiple swallowing attempts. Symptoms may include discomfort or pain in the cervical region, coughing, choking, drooling, or nasal regurgitation.

Tongue weakness can result in oral regurgitation. Inability to seal the nasopharynx because of obstruction or muscular weakness can cause nasal regurgitation. Inefficient laryngeal elevation from muscular weakness or a fixed larynx can result in laryngotracheal aspiration. Delayed aspiration can occur with pharyngeal weakness and with pooling of food in the piriform recesses or in a diverticulum. Inability to contract the pharyngeal muscles is often compounded by failure of the cricopharyngeus muscle to relax, which causes misdirection of the food bolus or necessitates repeated swallowing attempts. Inflammatory lesions of the tongue or oropharynx can result in odynophagia, which may impede swallowing.

Esophageal Dysphagia

Dysphagia from upper esophageal lesions is usually perceived 2 to 4 seconds after the initiation of swallowing. Dysphagia that the patient localizes to the substernal or retrosternal area may be anatomically accurate, but localization to the neck may be referred from anywhere in the esophagus.

Dysphagia is the most common presenting symptom of achalasia and usually begins insidiously, with equal frequency for solids and liquids. Patients may report that maneuvers that increase esophageal pressure (e.g., raising arms above the head, standing erect with back straight) help pass the food. Odynophagia from esophageal spasm may also be seen early in the course of achalasia. The symptoms are often worse with rapid eating and during periods of stress. The patient may also report chest pain as a symptom. As dilation occurs above the sphincter, retention of undigested food in the esophagus occurs, and the patient may be aware of gurgling while eating. Regurgitation of the undigested material can occur after a meal, prompting consideration of the diagnosis of an eating disorder, or with changes in position or vigorous exercise. The regurgitated food usually has no acid taste unless bacterial contamination causes fermentation of the undigested food. Laryngotracheal aspiration may occur, especially at night, and may cause nocturnal coughing. The physical examination is usually unremarkable, except for weight loss. Radiographically, a dilated esophagus is seen proximal to a narrowed gastroesophageal junction that has a “beaklike” appearance.

Esophageal spasm may be precipitated by swallowing very hot or cold liquids. Symptoms include chest pain, dysphagia, or both. Manometrically, simultaneous prolonged strong esophageal contractions are noted to be interspersed over normal peristaltic waves.

If a barium swallow is performed during a spasm, findings such as corkscrewing, or curling, of the esophagus may be noted.

Differential Diagnoses

The differential diagnosis of esophageal dysphagia includes acute coronary syndrome (ACS). Substernal chest pain is the main symptom in 80% to 90% of patients with esophageal motility disorders. The chest pain can be similar to angina, described as crushing or squeezing, with patterns of radiation similar to those of cardiac chest pain. Nitroglycerin may also relieve the pain of spasm, making the distinction between the two entities even more difficult.

Symptoms that suggest an esophageal cause of chest pain include pain that is prolonged and nonexertional, pain that interrupts sleep, pain related to meals, relief with antacids, and presence of other symptoms of esophageal disease, such as heartburn, dysphagia, or regurgitation. Given the considerable overlap in symptoms, a cardiac diagnosis should be excluded before attributing chest pain to an esophageal cause.

Diagnostic Testing

The history and physical examination direct the need for testing. Nasopharyngoscopy may be used to assess for upper structural abnormalities. The decision and timing of swallowing studies (e.g., video esophagography), barium swallows, manometry, and impedance monitoring are best coordinated with consultants. These studies are rarely indicated in the emergency department (ED).

Management

Achalasia is the only motility disorder for which reasonably reliable studies support specific treatment. Previously, pharmacologic therapies such as nitrates and calcium channel blockers have been used with the goal of decreasing tone of the LES. More recently, surgical interventions such as peroral endoscopic myotomy (POEM) have been used as first-line therapy in patients with achalasia who are able to tolerate surgical intervention. Pharmacologic therapy remains available as a bridge to more definitive intervention or in patients who are unable to tolerate an invasive procedure. Endoscopic botulinum toxin injection remains available as an acceptable treatment option in patients, although as with other medical therapies is commonly reserved for patients unable to tolerate more invasive procedures.

Medical therapy for esophageal motility disorders is limited, and clinical impacts are typically minimal. Anticholinergic drugs such as hyoscyamine sulfate or dicyclomine have been used because they decrease the amplitude of esophageal peristalsis and LES pressure. However, because these drugs delay gastric emptying and decrease esophageal peristalsis, they may exacerbate reflux symptoms. Other therapies include the use of calcium channel blockers, which decrease LES pressure and the amplitude of esophageal contractions.

Disposition

Patients at risk of aspiration or who are unable to maintain hydration may require hospitalization for expedited work-up and management. Otherwise, prompt outpatient evaluation by a gastroenterologist is indicated.

Foreign Bodies

Foundations

Background

Patients with esophageal foreign bodies are generally classified into four major groups: (1) pediatric patients; (2) psychiatric patients or prisoners (typically intentional ingestion); (3) patients with underlying esophageal disease; and (4) edentulous adults. Pediatric patients account for more than 75% of cases, with the peak incidence occurring in those between the ages of 18 and 48 months. Swallowing coins accounts for most cases of pediatric ingestion, whereas most adult impactions involve food, particularly meat or bones. Patients with underlying structural abnormalities of the esophagus are at greater risk for foreign body impaction. Edentulous adults are also at increased risk because of impaired oral sensation, which may contribute to their risk of accidental ingestion of a dental prosthesis.

Anatomy and Physiology

The esophagus begins in the hypopharynx, 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. There are four natural areas of narrowing where most foreign bodies become entrapped: The cricopharyngeus muscle (which is a component of the upper esophageal sphincter [UES]), aortic arch, left mainstem bronchus, and LES at the diaphragmatic hiatus. Pediatric entrapment occurs most commonly at the level of the cricopharyngeus muscle in the UES given the anatomic features present in young children, whereas adult entrapment occurs most commonly at the LES ( Fig. 75.1 ).

Fig. 75.1, Anatomic Differences Between Infant and Adult Airways.

The esophagus comprises two main bands of muscle, an inner circular layer and 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 for 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 and can be easily displaced by adjacent structures. An enlarged left atrium or ventricle, goiter, or mediastinal tumor may cause enough displacement of the esophagus to impede the passage of a food bolus or foreign body.

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