Grand Rounds: Man, 29, With Apparent Throat Obstruction

A 29-year-old man presented to the emergency department (ED) with a chief complaint of food stuck in his throat. He reported that he had swallowed a piece of chicken and felt it get stuck. Drinking water to help it go down was unsuccessful.

The patient’s history was positive for childhood asthma and nine years of solid food dysphagia. There was no history of a caustic chemical ingestion or of drug-induced esophagitis. He denied having dyspepsia, heartburn, or chest pain. He was not taking any medications and had no allergies.

When his dysphagia symptoms began nine years ago, he was diagnosed with acid reflux disease, confirmed by an upper gastrointestinal (GI) tract x-ray. Since that time, he reported having to swallow liquid after every bite of food and said he suffered from severe anxiety over fear of choking.

Evaluation in the ED consisted of endoscopic examination by a gastroenterologist. In addition to dislodging a food bolus, the endoscope revealed a narrowed, ringed esophagus with mucosal changes throughout the length of the esophagus (see Figures 1 through 3). Esophageal biopsies were taken, and the esophagus was dilated successfully with a 40-Fr Maloney dilator. The endoscopist detected too much resistance to pass a larger dilator.

Biopsy results revealed eosinophilic esophagitis. The patient was given oral fluticasone propionate. At one-month follow-up, he reported feeling much better. Upper endoscopy revealed some improvement, and the gastroenterologist was able to pass both a 46- and a 48-Fr Maloney dilator with only mild resistance. (The largest Maloney dilator, a 60-Fr dilator, should easily pass through a normal esophagus, according to T. L. Sack, MD, oral communication, June 2009.)

Discussion
Eosinophilic esophagitis (EE) involves the infiltration of the esophageal mucosa with eosinophils, causing edema, inflammation, and eventually, thickening and stenotic changes of the esophageal mucosa.¹

The normal esophageal mucosa contains lymphocytes, mast cells, and dendritic cells, which protect the esophagus from invading toxins and microorganisms. Eosinophils are not usually present, but when they are, they can have toxic effects on the esophageal mucosa.² EE is associated with solid food dysphagia, a direct result of damage to the esophageal mucosa, and other causes that are not clearly understood.

Research findings suggest that symptoms of dysphagia may be caused by degranulating eosinophils and mast cells, which have an antagonistic effect on the muscarinic receptors and cause smooth muscle to contract.^3,4 The proposed triggering mechanism of EE is an immunoglobulin E (IgE) immune–mediated response to an allergen.² Based on results from IgE radioallergosorbent testing (RAST), aeroallergens are more likely than food to act as triggers.⁵

EE in the Adult Patient
Traditionally, EE has been a condition seen in the pediatric population, with symptoms of nausea, vomiting, and failure to thrive; however, it is becoming increasingly recognized among adults. The typical patient is a man in his 20s or 30s (although cases of EE have been reported among women and older adults) with acute and recurrent solid food dysphagia, with or without food impaction.⁴

Often the patient reports a history of environmental or food allergies, asthma, rhinitis, or eczema.^2,4-6 Researchers have reported the presence of allergic symptoms in at least 50% of patients diagnosed with EE,² and many patients experience exacerbations associated with seasonal changes.⁷

GERD may coexist with EE; however, no relationship has been identified between the two.⁸ EE should be considered in patients with gastrointestinal symptoms that persist despite at least four weeks’ treatment with a proton pump inhibitor (PPI).²

Dysphagia: Differential Diagnosis
Adult patients with esophageal dysphagia usually report the feeling of food getting stuck when they try to swallow.⁹ Dysphagia may result from a mechanical obstruction or a neuromuscular/motility condition. Patients with mechanical obstructions usually have difficulty swallowing solids, while those with motility disorders tend to have difficulty with both liquids and solids.^1,9

Mechanical obstructions may include carcinomas (intrinsic and extrinsic), strictures, or Schatzki rings (small thin mucosal rings of unknown etiology located at the gastroesophageal junction).^1,9 Progressive dysphagia to solids over a short period of time is often indicative of esophageal carcinoma. GERD, pill-induced trauma, previous ingestion of a caustic chemical, and radiation are common causes of esophageal stricture formation. For a list of medications that are particularly caustic to the esophageal mucosa, see the table.^9,10

Neuromuscular manifestations of dysphagia include achalasia, diffuse esophageal spasm, nutcracker esophagus, and scleroderma.¹ These are usually associated with progressive difficulty in swallowing.⁹

Evaluating the Patient
A thorough patient history can often reveal potential causes of dysphagia and eliminate others. This should include current medications, chronic medical conditions and details regarding their onset and duration, and symptoms associated with dysphagia.⁹

Physical examination should include palpation of the thyroid because of the potential for a thyroid mass to cause extrinsic compression of the esophagus, palpation of the abdomen for masses or organomegaly, and a complete neurologic evaluation.⁹

Laboratory tests should be ordered based on the information obtained from the history and physical. Testing may include thyroid studies to eliminate hypothyroid or hyperthyroid causes of dysphagia, and complete blood count (CBC) with differential to rule out inflammatory or infectious processes.⁹ While eosinophilia may be present in the differential, it is not a universally accepted marker for establishing the diagnosis of EE.^2,5 Stools should be checked for occult blood, because a positive finding may suggest esophageal carcinoma.⁹

Diagnosis
In the primary care setting, a barium esophagram may be used during the initial workup to evaluate the anatomic structures of the esophagus and to differentiate between a mechanical obstruction and a neuromuscular disorder.^1,9 This noninvasive test requires the patient to swallow a radiopaque liquid as x-rays are taken.

The gold standard for diagnosing EE, however, is upper endoscopy with biopsy of the esophageal mucosa.⁶ Endoscopic findings that indicate EE are atypical of GERD; they may include a narrowed, small-caliber esophagus, concentric mucosal rings, proximal stenosis, linear ulcerations, atrophic changes, and white papules associated with eosinophilic microabscesses.⁶

Although there is no consensus regarding the number of eosinophils that should be present for an accurate diagnosis of EE, microscopic interpretation of the biopsy from both the proximal and the distal esophageal epithelia⁵ usually shows 15 or more eosinophils per high-power field.^2,11 It has been suggested that mucosal biopsies be taken along the entire length of the esophagus, as eosinophilic infiltration may extend from the proximal to the distal esophagus.²

GERD and trauma induced by medication use may also be associated with esophageal eosinophilic infiltration5; however, eosinophils are usually present only in the distal esophageal mucosa³ and are not as abundant as in EE.⁷ If endoscopy reveals persistent eosinophilia despite four to eight weeks’ treatment with a PPI, the diagnosis of EE is confirmed.²

Treatment
Treatment for EE is still under investigation. Research has examined the association between EE and food allergies or aeroallergens.⁴ Evaluation by an allergist using skin prick tests or RAST is recommended in the adult patient to help determine the source of the underlying inflammation.^5,7 Eliminating any identified allergen should help alleviate symptoms.⁴

For patients in whom no source of inflammation can be identified, treatment with 1.0 to 2.0 mg/kg/d of oral prednisone for acute exacerbations has been shown to significantly improve symptoms and histology¹²; however, because of the associated risk for adverse systemic effects, long-term use is not recommended.

In many patients, the inhaled corticosteroid fluticasone has also proved successful in reducing EE—associated inflammation.⁶ Current evidence supports adult dosing between 880 and 1,760 mcg per day for six to eight weeks, administered with a metered-dose inhaler and no spacer. Fluticasone should be sprayed directly into the mouth and swallowed, after which the patient should take nothing by mouth for 30 minutes.¹³ Prolonged fluticasone use has been associated with esophageal candidiasis.² There are currently no recommendations regarding its use as maintenance therapy.

Montelukast, a leukotriene receptor antagonist, has also been shown in some studies to reduce the inflammatory process¹¹; however, one study team recently found it to have no therapeutic effect.¹³

PPIs may be effective for improving EE symptoms even in the absence of GERD because of the reduced gastric acid production,⁷ but they do not usually improve EE’s histologic features.³

Use of esophageal dilation in patients with EE is controversial because of an associated risk for perforation.¹⁴ If this intervention is to be performed, the patient should be treated in advance with oral corticosteroids to reduce esophageal inflammation.^15,16 In addition, the endoscopist should start with small-sized dilators and carefully proceed to larger sizes.¹¹ Critics of esophageal dilation argue that the procedure is only a temporary solution and does nothing for the underlying condition.^4,8

Regarding endoscopic surveillance, an interval of at least four weeks between interventions is recommended.¹³

Role of the Primary Care Clinician
Undiagnosed EE can cause the patient discomfort, frustration, and anxiety, as seen in the case study. Many patients with undiagnosed EE have been exposed to unnecessary medical therapy and antireflux surgery.³ Without proper diagnosis and treatment, EE may worsen, causing complications associated with chronic inflammation (ie, esophageal fibrosis and strictures).^2,6

The long-term prognosis of EE is unknown at this time.⁸ The disease is usually chronic, with periods of remission and exacerbation. With an understanding of EE and appropriate therapies, the primary care practitioner can team with the gastroenterologist to provide effective disease management through endoscopic surveillance and intervention for acute exacerbations. Guidelines recommend that patients be closely followed with regular office visits to reassess symptoms, compliance with therapy, and adverse effects, with the goal of preventing complications associated with EE.¹³

Conclusion
To effectively evaluate the patient who presents with dysphagia, the primary care provider should have a working knowledge of EE, as well as an understanding of the key elements in the history and physical examination to help ensure an accurate diagnosis. This will facilitate timely referral to a gastroenterologist for endoscopic evaluation, when indicated.         

A 29-year-old man presented to the emergency department (ED) with a chief complaint of food stuck in his throat. He reported that he had swallowed a piece of chicken and felt it get stuck. Drinking water to help it go down was unsuccessful.

The patient’s history was positive for childhood asthma and nine years of solid food dysphagia. There was no history of a caustic chemical ingestion or of drug-induced esophagitis. He denied having dyspepsia, heartburn, or chest pain. He was not taking any medications and had no allergies.

When his dysphagia symptoms began nine years ago, he was diagnosed with acid reflux disease, confirmed by an upper gastrointestinal (GI) tract x-ray. Since that time, he reported having to swallow liquid after every bite of food and said he suffered from severe anxiety over fear of choking.

Evaluation in the ED consisted of endoscopic examination by a gastroenterologist. In addition to dislodging a food bolus, the endoscope revealed a narrowed, ringed esophagus with mucosal changes throughout the length of the esophagus (see Figures 1 through 3). Esophageal biopsies were taken, and the esophagus was dilated successfully with a 40-Fr Maloney dilator. The endoscopist detected too much resistance to pass a larger dilator.

Biopsy results revealed eosinophilic esophagitis. The patient was given oral fluticasone propionate. At one-month follow-up, he reported feeling much better. Upper endoscopy revealed some improvement, and the gastroenterologist was able to pass both a 46- and a 48-Fr Maloney dilator with only mild resistance. (The largest Maloney dilator, a 60-Fr dilator, should easily pass through a normal esophagus, according to T. L. Sack, MD, oral communication, June 2009.)

Discussion
Eosinophilic esophagitis (EE) involves the infiltration of the esophageal mucosa with eosinophils, causing edema, inflammation, and eventually, thickening and stenotic changes of the esophageal mucosa.¹

The normal esophageal mucosa contains lymphocytes, mast cells, and dendritic cells, which protect the esophagus from invading toxins and microorganisms. Eosinophils are not usually present, but when they are, they can have toxic effects on the esophageal mucosa.² EE is associated with solid food dysphagia, a direct result of damage to the esophageal mucosa, and other causes that are not clearly understood.

Research findings suggest that symptoms of dysphagia may be caused by degranulating eosinophils and mast cells, which have an antagonistic effect on the muscarinic receptors and cause smooth muscle to contract.^3,4 The proposed triggering mechanism of EE is an immunoglobulin E (IgE) immune–mediated response to an allergen.² Based on results from IgE radioallergosorbent testing (RAST), aeroallergens are more likely than food to act as triggers.⁵

EE in the Adult Patient
Traditionally, EE has been a condition seen in the pediatric population, with symptoms of nausea, vomiting, and failure to thrive; however, it is becoming increasingly recognized among adults. The typical patient is a man in his 20s or 30s (although cases of EE have been reported among women and older adults) with acute and recurrent solid food dysphagia, with or without food impaction.⁴

Often the patient reports a history of environmental or food allergies, asthma, rhinitis, or eczema.^2,4-6 Researchers have reported the presence of allergic symptoms in at least 50% of patients diagnosed with EE,² and many patients experience exacerbations associated with seasonal changes.⁷

GERD may coexist with EE; however, no relationship has been identified between the two.⁸ EE should be considered in patients with gastrointestinal symptoms that persist despite at least four weeks’ treatment with a proton pump inhibitor (PPI).²

Dysphagia: Differential Diagnosis
Adult patients with esophageal dysphagia usually report the feeling of food getting stuck when they try to swallow.⁹ Dysphagia may result from a mechanical obstruction or a neuromuscular/motility condition. Patients with mechanical obstructions usually have difficulty swallowing solids, while those with motility disorders tend to have difficulty with both liquids and solids.^1,9

Mechanical obstructions may include carcinomas (intrinsic and extrinsic), strictures, or Schatzki rings (small thin mucosal rings of unknown etiology located at the gastroesophageal junction).^1,9 Progressive dysphagia to solids over a short period of time is often indicative of esophageal carcinoma. GERD, pill-induced trauma, previous ingestion of a caustic chemical, and radiation are common causes of esophageal stricture formation. For a list of medications that are particularly caustic to the esophageal mucosa, see the table.^9,10

Neuromuscular manifestations of dysphagia include achalasia, diffuse esophageal spasm, nutcracker esophagus, and scleroderma.¹ These are usually associated with progressive difficulty in swallowing.⁹

Evaluating the Patient
A thorough patient history can often reveal potential causes of dysphagia and eliminate others. This should include current medications, chronic medical conditions and details regarding their onset and duration, and symptoms associated with dysphagia.⁹

Physical examination should include palpation of the thyroid because of the potential for a thyroid mass to cause extrinsic compression of the esophagus, palpation of the abdomen for masses or organomegaly, and a complete neurologic evaluation.⁹

Laboratory tests should be ordered based on the information obtained from the history and physical. Testing may include thyroid studies to eliminate hypothyroid or hyperthyroid causes of dysphagia, and complete blood count (CBC) with differential to rule out inflammatory or infectious processes.⁹ While eosinophilia may be present in the differential, it is not a universally accepted marker for establishing the diagnosis of EE.^2,5 Stools should be checked for occult blood, because a positive finding may suggest esophageal carcinoma.⁹

Diagnosis
In the primary care setting, a barium esophagram may be used during the initial workup to evaluate the anatomic structures of the esophagus and to differentiate between a mechanical obstruction and a neuromuscular disorder.^1,9 This noninvasive test requires the patient to swallow a radiopaque liquid as x-rays are taken.

The gold standard for diagnosing EE, however, is upper endoscopy with biopsy of the esophageal mucosa.⁶ Endoscopic findings that indicate EE are atypical of GERD; they may include a narrowed, small-caliber esophagus, concentric mucosal rings, proximal stenosis, linear ulcerations, atrophic changes, and white papules associated with eosinophilic microabscesses.⁶

Although there is no consensus regarding the number of eosinophils that should be present for an accurate diagnosis of EE, microscopic interpretation of the biopsy from both the proximal and the distal esophageal epithelia⁵ usually shows 15 or more eosinophils per high-power field.^2,11 It has been suggested that mucosal biopsies be taken along the entire length of the esophagus, as eosinophilic infiltration may extend from the proximal to the distal esophagus.²

GERD and trauma induced by medication use may also be associated with esophageal eosinophilic infiltration5; however, eosinophils are usually present only in the distal esophageal mucosa³ and are not as abundant as in EE.⁷ If endoscopy reveals persistent eosinophilia despite four to eight weeks’ treatment with a PPI, the diagnosis of EE is confirmed.²

Treatment
Treatment for EE is still under investigation. Research has examined the association between EE and food allergies or aeroallergens.⁴ Evaluation by an allergist using skin prick tests or RAST is recommended in the adult patient to help determine the source of the underlying inflammation.^5,7 Eliminating any identified allergen should help alleviate symptoms.⁴

For patients in whom no source of inflammation can be identified, treatment with 1.0 to 2.0 mg/kg/d of oral prednisone for acute exacerbations has been shown to significantly improve symptoms and histology¹²; however, because of the associated risk for adverse systemic effects, long-term use is not recommended.

In many patients, the inhaled corticosteroid fluticasone has also proved successful in reducing EE—associated inflammation.⁶ Current evidence supports adult dosing between 880 and 1,760 mcg per day for six to eight weeks, administered with a metered-dose inhaler and no spacer. Fluticasone should be sprayed directly into the mouth and swallowed, after which the patient should take nothing by mouth for 30 minutes.¹³ Prolonged fluticasone use has been associated with esophageal candidiasis.² There are currently no recommendations regarding its use as maintenance therapy.

Montelukast, a leukotriene receptor antagonist, has also been shown in some studies to reduce the inflammatory process¹¹; however, one study team recently found it to have no therapeutic effect.¹³

PPIs may be effective for improving EE symptoms even in the absence of GERD because of the reduced gastric acid production,⁷ but they do not usually improve EE’s histologic features.³

Use of esophageal dilation in patients with EE is controversial because of an associated risk for perforation.¹⁴ If this intervention is to be performed, the patient should be treated in advance with oral corticosteroids to reduce esophageal inflammation.^15,16 In addition, the endoscopist should start with small-sized dilators and carefully proceed to larger sizes.¹¹ Critics of esophageal dilation argue that the procedure is only a temporary solution and does nothing for the underlying condition.^4,8

Regarding endoscopic surveillance, an interval of at least four weeks between interventions is recommended.¹³

Role of the Primary Care Clinician
Undiagnosed EE can cause the patient discomfort, frustration, and anxiety, as seen in the case study. Many patients with undiagnosed EE have been exposed to unnecessary medical therapy and antireflux surgery.³ Without proper diagnosis and treatment, EE may worsen, causing complications associated with chronic inflammation (ie, esophageal fibrosis and strictures).^2,6

The long-term prognosis of EE is unknown at this time.⁸ The disease is usually chronic, with periods of remission and exacerbation. With an understanding of EE and appropriate therapies, the primary care practitioner can team with the gastroenterologist to provide effective disease management through endoscopic surveillance and intervention for acute exacerbations. Guidelines recommend that patients be closely followed with regular office visits to reassess symptoms, compliance with therapy, and adverse effects, with the goal of preventing complications associated with EE.¹³

Conclusion
To effectively evaluate the patient who presents with dysphagia, the primary care provider should have a working knowledge of EE, as well as an understanding of the key elements in the history and physical examination to help ensure an accurate diagnosis. This will facilitate timely referral to a gastroenterologist for endoscopic evaluation, when indicated.         

A 29-year-old man presented to the emergency department (ED) with a chief complaint of food stuck in his throat. He reported that he had swallowed a piece of chicken and felt it get stuck. Drinking water to help it go down was unsuccessful.

The patient’s history was positive for childhood asthma and nine years of solid food dysphagia. There was no history of a caustic chemical ingestion or of drug-induced esophagitis. He denied having dyspepsia, heartburn, or chest pain. He was not taking any medications and had no allergies.

When his dysphagia symptoms began nine years ago, he was diagnosed with acid reflux disease, confirmed by an upper gastrointestinal (GI) tract x-ray. Since that time, he reported having to swallow liquid after every bite of food and said he suffered from severe anxiety over fear of choking.

Evaluation in the ED consisted of endoscopic examination by a gastroenterologist. In addition to dislodging a food bolus, the endoscope revealed a narrowed, ringed esophagus with mucosal changes throughout the length of the esophagus (see Figures 1 through 3). Esophageal biopsies were taken, and the esophagus was dilated successfully with a 40-Fr Maloney dilator. The endoscopist detected too much resistance to pass a larger dilator.

Biopsy results revealed eosinophilic esophagitis. The patient was given oral fluticasone propionate. At one-month follow-up, he reported feeling much better. Upper endoscopy revealed some improvement, and the gastroenterologist was able to pass both a 46- and a 48-Fr Maloney dilator with only mild resistance. (The largest Maloney dilator, a 60-Fr dilator, should easily pass through a normal esophagus, according to T. L. Sack, MD, oral communication, June 2009.)

Discussion
Eosinophilic esophagitis (EE) involves the infiltration of the esophageal mucosa with eosinophils, causing edema, inflammation, and eventually, thickening and stenotic changes of the esophageal mucosa.¹

The normal esophageal mucosa contains lymphocytes, mast cells, and dendritic cells, which protect the esophagus from invading toxins and microorganisms. Eosinophils are not usually present, but when they are, they can have toxic effects on the esophageal mucosa.² EE is associated with solid food dysphagia, a direct result of damage to the esophageal mucosa, and other causes that are not clearly understood.

Research findings suggest that symptoms of dysphagia may be caused by degranulating eosinophils and mast cells, which have an antagonistic effect on the muscarinic receptors and cause smooth muscle to contract.^3,4 The proposed triggering mechanism of EE is an immunoglobulin E (IgE) immune–mediated response to an allergen.² Based on results from IgE radioallergosorbent testing (RAST), aeroallergens are more likely than food to act as triggers.⁵

EE in the Adult Patient
Traditionally, EE has been a condition seen in the pediatric population, with symptoms of nausea, vomiting, and failure to thrive; however, it is becoming increasingly recognized among adults. The typical patient is a man in his 20s or 30s (although cases of EE have been reported among women and older adults) with acute and recurrent solid food dysphagia, with or without food impaction.⁴

Often the patient reports a history of environmental or food allergies, asthma, rhinitis, or eczema.^2,4-6 Researchers have reported the presence of allergic symptoms in at least 50% of patients diagnosed with EE,² and many patients experience exacerbations associated with seasonal changes.⁷

GERD may coexist with EE; however, no relationship has been identified between the two.⁸ EE should be considered in patients with gastrointestinal symptoms that persist despite at least four weeks’ treatment with a proton pump inhibitor (PPI).²

Dysphagia: Differential Diagnosis
Adult patients with esophageal dysphagia usually report the feeling of food getting stuck when they try to swallow.⁹ Dysphagia may result from a mechanical obstruction or a neuromuscular/motility condition. Patients with mechanical obstructions usually have difficulty swallowing solids, while those with motility disorders tend to have difficulty with both liquids and solids.^1,9

Mechanical obstructions may include carcinomas (intrinsic and extrinsic), strictures, or Schatzki rings (small thin mucosal rings of unknown etiology located at the gastroesophageal junction).^1,9 Progressive dysphagia to solids over a short period of time is often indicative of esophageal carcinoma. GERD, pill-induced trauma, previous ingestion of a caustic chemical, and radiation are common causes of esophageal stricture formation. For a list of medications that are particularly caustic to the esophageal mucosa, see the table.^9,10

Neuromuscular manifestations of dysphagia include achalasia, diffuse esophageal spasm, nutcracker esophagus, and scleroderma.¹ These are usually associated with progressive difficulty in swallowing.⁹

Evaluating the Patient
A thorough patient history can often reveal potential causes of dysphagia and eliminate others. This should include current medications, chronic medical conditions and details regarding their onset and duration, and symptoms associated with dysphagia.⁹

Physical examination should include palpation of the thyroid because of the potential for a thyroid mass to cause extrinsic compression of the esophagus, palpation of the abdomen for masses or organomegaly, and a complete neurologic evaluation.⁹

Laboratory tests should be ordered based on the information obtained from the history and physical. Testing may include thyroid studies to eliminate hypothyroid or hyperthyroid causes of dysphagia, and complete blood count (CBC) with differential to rule out inflammatory or infectious processes.⁹ While eosinophilia may be present in the differential, it is not a universally accepted marker for establishing the diagnosis of EE.^2,5 Stools should be checked for occult blood, because a positive finding may suggest esophageal carcinoma.⁹

Diagnosis
In the primary care setting, a barium esophagram may be used during the initial workup to evaluate the anatomic structures of the esophagus and to differentiate between a mechanical obstruction and a neuromuscular disorder.^1,9 This noninvasive test requires the patient to swallow a radiopaque liquid as x-rays are taken.

The gold standard for diagnosing EE, however, is upper endoscopy with biopsy of the esophageal mucosa.⁶ Endoscopic findings that indicate EE are atypical of GERD; they may include a narrowed, small-caliber esophagus, concentric mucosal rings, proximal stenosis, linear ulcerations, atrophic changes, and white papules associated with eosinophilic microabscesses.⁶

Although there is no consensus regarding the number of eosinophils that should be present for an accurate diagnosis of EE, microscopic interpretation of the biopsy from both the proximal and the distal esophageal epithelia⁵ usually shows 15 or more eosinophils per high-power field.^2,11 It has been suggested that mucosal biopsies be taken along the entire length of the esophagus, as eosinophilic infiltration may extend from the proximal to the distal esophagus.²

GERD and trauma induced by medication use may also be associated with esophageal eosinophilic infiltration5; however, eosinophils are usually present only in the distal esophageal mucosa³ and are not as abundant as in EE.⁷ If endoscopy reveals persistent eosinophilia despite four to eight weeks’ treatment with a PPI, the diagnosis of EE is confirmed.²

Treatment
Treatment for EE is still under investigation. Research has examined the association between EE and food allergies or aeroallergens.⁴ Evaluation by an allergist using skin prick tests or RAST is recommended in the adult patient to help determine the source of the underlying inflammation.^5,7 Eliminating any identified allergen should help alleviate symptoms.⁴

For patients in whom no source of inflammation can be identified, treatment with 1.0 to 2.0 mg/kg/d of oral prednisone for acute exacerbations has been shown to significantly improve symptoms and histology¹²; however, because of the associated risk for adverse systemic effects, long-term use is not recommended.

In many patients, the inhaled corticosteroid fluticasone has also proved successful in reducing EE—associated inflammation.⁶ Current evidence supports adult dosing between 880 and 1,760 mcg per day for six to eight weeks, administered with a metered-dose inhaler and no spacer. Fluticasone should be sprayed directly into the mouth and swallowed, after which the patient should take nothing by mouth for 30 minutes.¹³ Prolonged fluticasone use has been associated with esophageal candidiasis.² There are currently no recommendations regarding its use as maintenance therapy.

Montelukast, a leukotriene receptor antagonist, has also been shown in some studies to reduce the inflammatory process¹¹; however, one study team recently found it to have no therapeutic effect.¹³

PPIs may be effective for improving EE symptoms even in the absence of GERD because of the reduced gastric acid production,⁷ but they do not usually improve EE’s histologic features.³

Use of esophageal dilation in patients with EE is controversial because of an associated risk for perforation.¹⁴ If this intervention is to be performed, the patient should be treated in advance with oral corticosteroids to reduce esophageal inflammation.^15,16 In addition, the endoscopist should start with small-sized dilators and carefully proceed to larger sizes.¹¹ Critics of esophageal dilation argue that the procedure is only a temporary solution and does nothing for the underlying condition.^4,8

Regarding endoscopic surveillance, an interval of at least four weeks between interventions is recommended.¹³

Role of the Primary Care Clinician
Undiagnosed EE can cause the patient discomfort, frustration, and anxiety, as seen in the case study. Many patients with undiagnosed EE have been exposed to unnecessary medical therapy and antireflux surgery.³ Without proper diagnosis and treatment, EE may worsen, causing complications associated with chronic inflammation (ie, esophageal fibrosis and strictures).^2,6

The long-term prognosis of EE is unknown at this time.⁸ The disease is usually chronic, with periods of remission and exacerbation. With an understanding of EE and appropriate therapies, the primary care practitioner can team with the gastroenterologist to provide effective disease management through endoscopic surveillance and intervention for acute exacerbations. Guidelines recommend that patients be closely followed with regular office visits to reassess symptoms, compliance with therapy, and adverse effects, with the goal of preventing complications associated with EE.¹³

Conclusion
To effectively evaluate the patient who presents with dysphagia, the primary care provider should have a working knowledge of EE, as well as an understanding of the key elements in the history and physical examination to help ensure an accurate diagnosis. This will facilitate timely referral to a gastroenterologist for endoscopic evaluation, when indicated.