1. 1
    Current Diagnosis

    • The evaluation of dysphagia begins with a careful history, though additional diagnostic testing is often required.

    • Oropharyngeal dysphagia is best initially evaluated with a video fluoroscopoic examination, whereas esophageal dysphagia is best evaluated with endoscopy.

    • Esophageal dysphagia with negative endoscopy and biopsy should be evaluated next with esophageal manometry.

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  2. 2
    Current Therapy

    • Underlying neuromuscular conditions such as amyotrophic lateral sclerosis, myasthenia gravis, or Guillain-Barré syndrome should be treated accordingly.

    • Endoscopic therapy with dilation (often multiple) is the mainstay of treating fibrotic esophageal strictures regardless of etiology.

    • Achalasia can be treated surgically or with dilation, which are equally effective. Minimally invasive endoscopic therapy for achalasia is promising and may provide a competing approach.

    Dysphagia is a symptom generated by the perceived sensation of difficulty or inability to swallow. It ranges in severity from mild difficulty with no associated clinical sequelae, to a complete inability to swallow with aspiration and severe malnutrition. Dysphagia can coexist with and must be distinguished from odynophagia, which is pain when swallowing, with associated swallowing aversion. The etiology of dysphagia is protean and includes two main categories, mechanical obstruction and motor dysfunction.

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  3. 3

    Dysphagia is a common condition. A recent investigation surveyed 790 ambulatory patients who were awaiting their annual primary care visit; 22.6% of patients reported dysphagia at least several times per month. Only half of these patients had discussed their symptoms with their physician. Elderly patients and women were more likely to note symptoms of dysphagia.


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  4. 4

    Effective swallowing and transfer of food bolus into the stomach requires multiple steps. These steps can be broadly placed into two phases: the oropharyngeal phase and the esophageal phase. The oropharyngeal phase of swallowing ultimately transforms the hypopharynx from a respiratory organ to a digestive organ. It requires five main coordinated steps to occur: (1) elevation of the soft palate and closure of the nasopharynx, (2) relaxation of the upper esophageal sphincter (UES), (3) traction opening of the UES, (4) closure of the laryngeal vestibule and hence airway protection, and (5) propulsion of the food bolus by the tongue and pharyngeal constrictors. This process is a carefully coordinated neuromuscular phenomenon with both autonomic and volitional components.

    The esophageal phase of swallowing begins when a food bolus passes through the UES. During swallowing, the rapidity of bolus transit into the stomach is accomplished primarily by gravity.

    Esophageal peristalsis is a secondary contributor that functions to strip the bolus and clear the esophagus. Primary peristalsis is associated with oropharyngeal swallowing and propagates down through the predominantly striated muscle esophagus via a sequential activation pattern originating from the brainstem. This continues into the smooth muscle esophagus where it also engages the intrinsic enteric nervous system to promote peristalsis through a similar but distinct mechanism. Secondary peristalsis is stimulated by distention of the proximal esophagus and will generate a propagating peristaltic contraction similar to primary peristalsis without a swallow-induced trigger. The strength, propagation velocity, and order of peristaltic contractions can be altered and this may lead to motor abnormalities associated with dysphagia.

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  5. 5

    Dysphagia is never a normal symptom and always requires additional investigation. The first step in the diagnostic evaluation of dysphagia begins with a careful history to distinguish true dysphagia from other associated conditions such as odynophagia and globus sensation.

    Odynophagia can coexist with dysphagia; however, the predominant symptom is pain during swallowing. Globus is a sensation of a lump in the throat. It is likely a pharyngeal hypersensitivity that may coexist with other esophageal diseases or occur alone as a functional disorder. Unlike dysphagia, the symptoms in globus persist between swallows and may actually improve during the swallow.

    After the above conditions have been ruled out, the next step focuses on distinguishing oropharyngeal dysphagia from esophageal dysphagia. Unfortunately, patients have a difficult time communicating their symptoms because localization of the point of perceived obstruction is hampered by poor discriminant capacity and may be masked by compensatory mechanisms. Localization of dysphagia to the throat or sternal notch is unreliable because the point of obstruction may be further down in the body. However, localization in the midchest or below is more reliable that the obstruction is esophageal in origin.

    As a result, the most useful and underused test for distinguishing oropharyngeal and esophageal dysphagia focuses on observing the patient swallow sips of water in the office. Often this allows the distinction between oropharyngeal and esophageal dysphagia to become apparent. Patients with oropharyngeal dysphagia will have difficulty almost immediately after initiating a swallow, such as coughing, choking, and nasal regurgitation. Patients who can initiate a swallow without difficulty, but note symptoms soon after the swallow, are likely to have esophageal dysphagia. Furthermore, this exercise may be able to elicit associated odynophagia or regurgitation.

    Physical examination plays a minor role in evaluating dysphagia outside of assessing the patient’s baseline status to rule out malnutrition and dehydration because this will determine whether an expedited evaluation is required. A careful assessment of the oropharynx and a careful neck examination may unmask a mass lesion, and a neurologic examination should be performed if oropharyngeal dysphagia is suspected. Additionally, a skin examination and assessment of the oropharyngeal mucosa may be helpful in assessing for potential dermatologic diseases that are associated with esophageal dysphagia. Regardless of findings, most patients will ultimately be referred for diagnostic testing, and this is dependent on the anatomic zone of interest—oropharyngeal versus esophageal (Figure 1).

    FIGURE 1    The workup of dysphagia and esophageal obstruction.  The first step in the workup of dysphagia focuses on distinguishing oropharyngeal from esophageal dysphagia, which can be done with a history and careful assessment of swallowing during liquid  swallows.

    The workup once this distinction is made is very  different.

    Oropharyngeal dysphagia is typically evaluated by speech pathology and otolaryngology (ENT) based on the results of a video fluoroscopic swallow evaluation. Esophageal dysphagia is evaluated primarily with endoscopy because biopsies and interventions are often required. The primary indication for manometry is to rule out a major motor  disorder in patients with a negative endoscopy. If manometry does not identify a major motor abnormality, a diagnosis of functional dysphagia should be considered; however, underlying GERD must also be  addressed.

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  6. 6
    Diagnostic Testing

    Oropharyngeal Dysphagia

    Once a distinction is made that the patient is experiencing oropharyngeal dysphagia, the next step in the evaluation should be referral for a video fluoroscopic swallowing examination, also known as a modified barium study. Standard upper endoscopy is of limited value given the general inability to evaluate lesions in the hypopharynx and the upper esophageal sphincter. Video fluoroscopic swallow examinations have the added benefit of providing functional information in addition to anatomic information. They differ from a standard fluoroscopic examination (i.e., esophogram) by offering the patient various radiopaque food items of different consistency and are often performed by a speech pathologist. They can evaluate delay in initiation of pharyngeal swallowing, aspiration of solids and liquids, retrograde flow of ingested bolus, and residual pharyngeal contents.

    If there is a suspicion for a malignancy or mechanical obstruction, a referral to otolaryngology is required. Direct laryngoscopy is used to evaluate for anatomic lesions in the nasopharynx and hypopharynx. In addition to anatomic abnormalities, function can be assessed by having the patient drink liquids with the nasal endoscope positioned in the hypopharynx. Oropharyngeal pooling of liquid indicates ineffective hypopharyngeal clearance and can suggest a high aspiration risk. Cross-sectional imaging is often an adjunct to the functional assessment of videoscopic imaging or direct laryngoscopy when an obstruction is noted without a clear lesion noted on direct examination.

    Esophageal Dysphagia

    If oropharyngeal dysphagia is excluded on history, the evaluation of dysphagia should proceed to upper endoscopy to rule out a mechanical obstruction. Although an esophogram can be used to assess for obstruction, most patients will eventually require endoscopy to obtain biopsies to rule out malignancy or eosinophilic esophagitis. Additionally, endoscopy has the added benefit of being therapeutic in some circumstances, and thus it is more cost-effective to begin the evaluation with endoscopy. If the endoscopy is negative, the next step is to perform esophageal manometry to rule out an esophageal motor disorder. If this is negative, a careful evaluation for the presence of gastroesophageal reflux disease (GERD) should be performed and if suspected, the patient may benefit from ambulatory reflux testing or an empiric trial of proton pump inhibitors. Patients with no evidence of obstruction, abnormal esophageal motor function, or evidence of GERD may be classified as having functional dysphagia if the symptoms fulfill the Rome III consensus (onset greater than 6 months before presentation with 3 months of symptoms).

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  7. 7
    Oropharyngeal Dysphagia

    Differential Diagnosis

    The etiology of oropharyngeal dysphagia can be broadly separated based on neuromuscular causes and anatomic causes (Table 1). The most common neurologic cause is cerebrovascular accident (CVA), with an incidence reported between 20% and 80%. CVAs involving the cerebrum, cerebellum, and brainstem can each lead to swallow dysfunction. Cerebral CVA can lead to impairment in mastication and the oral phase of swallowing and can interrupt normal pharyngeal peristalsis. CVA involving the brainstem can lead to disruption of the sensory afferents in the pharynx that help trigger pharyngeal swallow, and can also lead to motor dysfunction of laryngeal elevation, glottic closure, and cricopharyngeal relaxation/opening. Tumors in these areas can also produce similar effects.

    Table 1

    Oropharyngeal Dysphagia


    • Medicadon sicie effects (chemotherapy, neuroleptics, etc.)

    • Postsurgical nxiscular or neurogeiiic

    • Corrosive (pill injury, irdentional)

    •Di  ±eda


    • Ly      disease

    • Syphilis

    • Mucosibs (herpes, cytomegalovirus, car×1ida, etc.) Metabolic

    • Arryloidosis

    • Ct:shrug’s syrxlrorre

    • Thyrotoxicosis

    • Wilson’s disease

    ×y  e’ו

    • Connective tissm disease (overlap syndrorre)

    • Myasthenia gravis

    • Myotonic clystrophy

    • Oculopharyngeal clystrophy

    • Poly rryosibs

    • Sarcoicbsis

    • Paraneoplaséc syndromes Neurologic

    • Brainstem turrc›rs

    • Head traurre

    • Stroke

    • Cerebral palsy

    • Cuillain-Barré syrxirorre

    • Huntington’s disease

    • Muldple sclerosis

    • Polio

    • PostJxilio syndro

    • Tardive dyskinesia

    • Metabolic ercephalopathies

    • Amyotrophic lateral sclerosis

    • Parkinson’s disease


    • Cricopharyngeal bar

    • Zenker’s diverbculum

    • Cervical webs

    • Oropharyngeal tumors

    • Osteophytes and skeletal abrcirrmlities

    • Congenital ahnormalihes (cleft palate, diverticula, pomhes, etc.

    A variety of neuromuscular disease can lead to bulbar symptoms, which manifest as dysphagia. This includes myasthenia gravis, amyotrophic lateral sclerosis (ALS), and Guillain-Barré syndrome (GBS). Clinicians need to be able to identify systemic manifestations of these conditions because dysphagia can often be the first manifestation of neuromuscular disorders.

    The most common structural abnormalities of the hypopharynx associated with dysphagia are hypopharyngeal diverticula and cricopharyngeal bars. Acquired hypopharyngeal diverticula are most common in men after age 60 and typically present with symptoms of dysphagia, halitosis, post-swallow regurgitation, or even aspiration of material from the pharyngeal pouch. Hypopharyngeal diverticula are the result of a restrictive myopathy associated with diminished compliance of the cricopharyngeus muscle. The treatment of hypopharyngeal diverticula is cricopharyngeal myotomy with or without a diverticulectomy. Good or excellent results can be expected in 80% to 100% of Zenker’s patients treated by transcervical myotomy combined with diverticulectomy or diverticulopexy. Small diverticula may spontaneously disappear following myotomy.

    Other anatomic causes associated with oropharyngeal dysphagia that should be considered are cervical osteophytes and head and neck cancers. Cervical osteophytes are associated with cervical spine arthritis and may be confused with a cricopharygeal bar because the dysphagia is structural and localized to the area of the upper esophageal sphincter. It is easily differentiated on contrast studies because the cervical osteophyte can be seen impinging on the upper sphincter. Additionally, head and neck lesions of the larynx, tonsil, tongue, oral cavity, vocal cord, and nasopharynx may also impair bolus transit into the esophagus. Rapid weight loss in a patient with oropharyngeal dysphagia warrants further evaluation for malignancy; however, it is often difficult to distinguish weight loss resulting from malignancy from weight loss secondary to dysphagia. Constitutional symptoms (night sweats, fever, etc.) associated with oropharyngeal dysphagia should raise the suspicion for lymphoma.

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    The management of oropharyngeal dysphagia is dependent on the underlying cause. Neuromuscular conditions such as stroke may respond to speech therapy and rehabilitation. Systemic neuromuscular dysfunction from conditions such as myasthenia gravis, GBS, or ALS will require treatment of the underlying condition. Patients who cannot safely take oral nutrition may need a temporary enteral feeding tube until swallow function is intact.

    Management of dysphagia in patients with head and neck cancers requires a multidisciplinary approach and treatment of the underlying malignancy. Some patients are able to take adequate nutrition with dietary modification (soft or full liquid diet) while undergoing therapy. Patients who are losing weight, are dehydrated, or are unable to meet nutritional requirement by dietary modification alone may require enteral nutrition in the form of a gastrostomy tube. Although endoscopic gastrostomy tube placement is typically safe, and routinely performed in patients with head and neck cancer, there are reports of seeding the gastrostomy tube tract with malignant cells from the pharynx. In such circumstances, a direct gastrostomy tube placed by a radiologist may be preferable.

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  9. 9
    Esophageal Dysphagia

    Esophageal dysphagia can be easily separated into mechanical causes and motor abnormalities after upper endoscopy is performed.

    Mechanical causes can be further separated into malignant and benign causes of dysphagia, and motor disorders can be conceptualized as primary motor abnormalities versus borderline motor abnormalities.

    Patients who have symptoms in the context of a normal endoscopy (negative biopsies for eosinophilic esophagitis) and no evidence of a primary motor disorder may also have underlying GERD or functional dysphagia (see Figure 1).

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  10. 10
    Differential Diagnosis: Mechanical Obstruction (Table 2)


    Fibrotic esophageal strictures are common and can be caused by erosive esophagitis (peptic stricture), radiation therapy, surgical anastomosis, eosinophilic esophagitis, and desquamating lesions (pemphigus, lichen planus, etc.). Peptic strictures are common and are the result of long-standing erosive esophagitis. They typically occur in the distal esophagus. Such patients often have underlying physiologic derangements that favor aggressive reflux (weak lower esophageal sphincter, hiatal hernia, poor esophageal clearance). Postsurgical anastomotic strictures are an unfortunate consequence of surgical therapy for esophageal disease, but these lesions are often amenable to endoscopic therapy.

    Table 2

    Esophageal Dysphagia (Mechanical)

    Eosinophilic Esophagitis

    Eosinophilic esophagitis (EoE) requires some focused discussion because its prevalence in patients presenting with dysphagia is increasing. EoE is a condition characterized by marked eosinophilic infiltrate within the esophageal epithelium. This infiltrate results in characteristic endoscopic findings of esophageal rings, furrows, exudate, and eventually stricture formation. The most common symptom in patients with EoE is dysphagia, which often leads to food bolus impaction. Patients are typically young Caucasians and there is a clear male predominance. Atopic conditions are more prevalent in patients with EoE. Patients should initially be treated with proton pump inhibitor (PPI) therapy because there is an overlap between GERD and EoE. Patients with persistent eosinophilia on PPI therapy can be treated by swallowing inhaled formulations of steroids (fluticasone [Flovent],1 budesonide [Pulmicort]1) or a food elimination diet (avoid: soy, nuts, wheat, eggs, dairy, seafood) to reduce the inflammatory component of the disease. Additional therapy with dilation will be required in many patients because histologic improvement does not always result in regression of fibrotic strictures. The esophageal body is more prone to fracture in EoE, and deep mucosal tears are often associated with dilation therapy; thus these lesions may require a more gradual and careful dilation protocol.


    Esophageal webs can exist along the length of the esophagus and lead to dysphagia. The classic triad of proximal esophageal web, iron deficiency anemia, and dysphagia is Plummer-Vinson syndrome. The etiology of this condition is not entirely known; however, it is thought that iron deficiency leads to a decrease in iron-dependent oxidative enzymes, which results in degradation of esophageal tissue, resulting in web formation. Interestingly, iron supplementation alone may result in resolution of symptoms. Whereas Plummer-Vinson syndrome is a rare condition, esophageal webs are relatively common and should prompt an evaluation for caustic pill injury if localized to the transition zone along the aortic impression or distal esophagus.

    Medications that can be associated with pill esophagitis include NSAIDs, tetracycline, iron, bisphosphonates, potassium, and quinidine.


    Dysphagia is often the presenting symptom in a patient with esophageal cancer. There are two subtypes of mucosal cancer in the esophagus, squamous cell and adenocarcinoma. In general, esophageal cancer has a male predominance and is slightly more prevalent among African Americans. The racial disparity is largely due to squamous cell carcinoma, which has noted a sharp decline since the 1960s. Adenocarcinoma tends to be a disease of white men (SEER database). Squamous cell carcinoma typically occurs in the mid esophagus, whereas adenocarcinoma is localized to the distal esophagus where it is associated with intestinal metaplasia (Barrett’s esophagus).

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    Management for Esophageal Obstruction

    Endoscopic dilation therapy is the most common therapeutic intervention for patients with nonmalignant mechanical dysphagia. This can be done with a single, large-diameter dilating balloon or semirigid bougie over a guide wire. There has not been any convincing data to demonstrate superiority of balloon dilators over bougie dilators. In cases of membranous webs or Schatzki rings, the goal of endoscopic therapy is to tear the lesion with a single, large- diameter dilation. In the case of a Schatzki ring, postdilation PPI therapy is associated with decreased recurrence rates.

    When treating fibrotic strictures (peptic, anastomotic, radiation, EoE), the goal should be gradual stretching of the stricture. The choice of initial dilation size is based on an estimate of the diameter of the stricture. The extent to which a stricture can be dilated is expressed by the endoscopic axiom of the “rule of threes.” This refers to the approach whereby the diameter of the stricture is approximated, and no more than three subsequent dilations are performed at 1-mm intervals once resistance is noted. Though there is no controlled trial for support, this approach is used to minimize the most serious risks of dilation therapy, perforation and bleeding.

    In patients with refractory strictures despite dilation therapy, several therapies have been attempted with variable efficacy.

    Temporary self-expanding stents have been placed to maintain lumen patency. When placed across a stricture, stents serve two purposes.

    First, they relieve symptoms of dysphagia by maintaining a patent lumen. In addition, the self-expanding nature of the stent provides ongoing radial force, which gradually stretches the lumen. The main disadvantage of stents is their tendency to migrate. Plastic and biodegradable stents are currently not available, but may be promising in the future.

    An alternative endoscopic approach is incisional therapy with an electrocautery knife. This is used to make incisions in the mucosa and fibrotic submucosa. This approach has been best studied in the setting of refractory anastomotic strictures; however, no head-to-head comparisons have been made between incisional therapy and other modalities.

    Treatment of malignant etiologies for dysphagia will ultimately depend on the tumor type and extent of disease. Benign tumors and early-stage lesions can be treated with endoscopic resection or surgery. Endoscopic therapy using stents is also an important component of the treatment of malignancy and may be used during the treatment phase of malignant disorders or as a palliative technique for later-stage disease.

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  12. 12
    Differential Diagnosis: Motility Disorders (Table 3)

    Esophageal motor disorders are defined based on patterns of contractile vigor, propagation, and the presence of deglutitive relaxation. Multiple classifications have been proposed; however, a new technique using a more advanced high-resolution manometric system that provides greater detail and accuracy has become available. This classification scheme is based on previous conventional schemes with modifications based on refining disorders into clinically relevant phenotypes.

    Table 3

    Esophageal Dysphagia (Abnormal Motor Function)


    The diagnosis of achalasia is made by esophageal manometry and requires two main manometric criteria: (1) inability of the lower esophageal sphincter to relax and (2) absence of peristalsis. Recently achalasia has been subdivided into three different phenotypes using high-resolution manometry, which are associated with varying clinical outcomes. Patients typically describe both solid and liquid dysphagia. Other common symptoms are regurgitation (especially nocturnal), chest pain, and aspiration. Weight loss and malnutrition may be dominant symptoms as the disease progresses. Given that there is no treatment to reverse absent peristalsis, the treatment is focused on improving esophagogastric junction (EGJ) opening by disrupting the poorly relaxing lower esophageal sphincter. This can be accomplished using pneumatic dilation with rigid balloons ranging in size from 3 to 4 cm or surgical myotomy. It appears that the two treatment approaches are associated with good outcomes with surgery having a more durable single intervention success rate and pneumatic dilation typically requiring multiple sessions. Botulinum toxin type A (Botox)1 injected into the lower esophageal sphincter has been shown to reduce EGJ pressure and improve symptoms; however, this treatment only provides temporary relief and should only be reserved for poor surgical candidates or patients unwilling to undergo surgery or dilation. Occasionally, esophageal dilatation may progress to a point where treatment with pneumatic dilation and myotomy are not adequate and esophagectomy must be performed to prevent severe complications, such as aspiration and severe malnutrition.

    Esophagogastric Junction Outflow Obstruction

    This pattern of motor disturbance is associated with preserved peristalsis and evidence of high pressures through the EGJ during swallowing. This may be an achalasia variant or could be associated with a subtle obstruction at the distal esophagus not evident on endoscopy. Thus, recognition of this pattern should prompt an evaluation for an infiltrating tumor or other potential etiology of obstruction. Treatment is focused on the underlying cause of the obstruction.

    Absent Peristalsis

    Absent peristalsis is defined as complete absence of contractile activity on all swallows in the context of a normal or low EGJ relaxation pressure. This pattern was previously categorized as scleroderma esophagus if it was found in the context of a hypotensive lower esophageal sphincter; however, this has been abandoned because this pattern may be found in patients with severe GERD without scleroderma. Treatment is focused on aggressive antireflux therapy and lifestyle modifications to reduce dysphagia and caustic injury to the esophagus.

    Distal Esophageal Spasm

    Distal esophageal spasm is a rare primary motor disorder that may present with dysphagia and chest pain. It is associated with impaired deglutitive inhibition of the esophageal body and results in unopposed activation of the cholinergic intrinsic neurons resulting in premature contractions associated with a rapid contractile velocity.

    The premature contraction is the most important aspect of this disorder and this has replaced an emphasis on peristaltic velocity because high-resolution manometry has shown that rapid contractions are usually associated with weak contractions. Treatment for this disorder is extremely difficult and focuses on medical management with smooth muscle relaxants, such as calcium channel blockers,1 nitrates,1 and 5-phosphodiesterase inhibitors.1


    Jackhammer esophagus is an extreme form of nutcracker esophagus associated with contractile vigor not encountered in asymptomatic controls or under normal conditions. Previous definitions for hypertensive esophagus had a significant overlap with data from cohorts of asymptomatic controls, and thus the clinical significance of these disorders was unclear. This pattern is associated with dysphagia and chest pain and is typically treated similar to distal esophageal spasm. This motor pattern can also be seen with distal esophageal obstruction, and this should be considered in the differential diagnosis because it would alter management to focus on the obstruction.

    Borderline Motor Abnormalities

    Borderline motor abnormalities are those associated with ineffective esophageal motility and mild abnormalities of peristaltic propagation (rapid contraction) or hypertensive contraction. These disorders are not considered to be primary motor disorders, and secondary cause for symptoms, such as GERD and visceral sensitivity, should be considered and treated.

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    Patients with dysphagia or esophageal obstruction should be monitored for three important complications:

    •   Evidence of aspiration and nocturnal regurgitation because these can be associated with severe complications, such as chemical pneumonitis and aspiration pneumonia.

    •   Malnutrition and dehydration because this may prompt more aggressive therapy or consideration of non-oral feeding methods.

    •   Progressive symptoms because this could lead to progression of the disease and early therapy may avoid the above complications.

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  14. 14

    This work was supported by R01 DK079902 (JEP) from the U.S. National Institutes of Health.

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    Bredenoord A.J., Fox M., Kahrilas P.J., et al. Chicago classification criteria of esophageal motility disorders defined in high resolution esophageal pressure topography.

    Neurogastroenterol Motil. 2012;24(Suppl. 1):57–65.

    Cook I.J., Kahrilas P.J. AGA technical review on management of oropharyngeal dysphagia. Gastroenterology. 1999;116:455–478.

    Drossman D.A. The functional gastrointestinal disorders and the Rome III process. Gastroenterology. 2006;130:1377–1390.

    Egan J.V., Baron T.H., Adler D.G., et al. Esophageal dilation.

    Gastrointest Endosc. 2006;63:755–760.

    Francis D.L., Katzka D.A. Achalasia: update on the disease and its treatment. Gastroenterology. 2010;139:369–374.

    Liacouras C.A., Furuta G.T., Hirano I., et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011;128:3–20 e26; quiz 21– 2.

    Pandolfino J.E., Kahrilas P.J. AGA technical review on the clinical use of esophageal manometry. Gastroenterology. 2005;128:209–224.

    Pandolfino J.E., Kwiatek M.A., Nealis T., et al. Achalasia: a new clinically relevant classification by high-resolution manometry. Gastroenterology. 2008;135:1526–1533.

    Spechler S.J. AGA technical review on treatment of patients with dysphagia caused by benign disorders of the distal esophagus. Gastroenterology. 1999;117:233–254.

    Wilkins T., Gillies R.A., Thomas A.M., et al. The prevalence of dysphagia in primary care patients: a HamesNet Research Network study. J Am Board Fam Med. 2007;20:144–150.

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