Esophagitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]] ; Aditya Ganti M.B.B.S. [3]

The esophagus is a part of the gastrointestinal tract which is responsible of moving the food from the mouth to the rectum. Esophagitis is a general term for any inflammation, irritation, or swelling of the esophagus. The inflammation can be due to a variety of causes such as gastroesophageal reflux disease, viruses, or chemical injuries. Basing on the etiology and severity of disease, esophagitis into 4 types ( eosinophilic esophagitis, infectious esophagitis, pill induced esophagitis, and reflux esophagitis) and 4 grades (grade 1, grade 2, grade 3, and grade4) respectively. When ever esophagus gets irritated whether due to acid reflux or any other disease process inflammation sets in. If left untreated, chronic inflammation can lead to metaplasia of lower esophagus and ultimately leading to carcinoma of esopahgus. The most common symptoms of the esophagitis include halitosis, epigastric chest pain, often radiating to the back, dysphagia, odynophagia, hoarseness, oral ulcers and must be differentiated from other diseases such as peptic ulcer disease, acute coronary syndrome, angina pectoris, cholecystitis, biliary colic, pulmonary embolism and esophageal perforation. Prognosis of esophagitis is generally good with appropriate treatment. Diagnosis of esophagitis is mostly clinical. The mainstay of therapy for reflux esophagitis is acid suppression therapy. Patients with infectious esophagitis are treated with antimicrobial therapy, whereas patients with eosinophilic esophagitis are treated with corticosteroids.

GERD is believed to be first described and treated by the ancient Egyptians according to the papyrus which was discovered by Edwin Smith at Thebes. The esophagus itself was named by the ancient Greeks. Friedenwald, and Feldman described the symptoms of GERD in 1925. Robbins and Jankelson used the radiological procedures to observe GERD in 1926. In 1981, Picus and Frank reported a case of a 16-year-old boy with progressive dysphagia for 1.5 years, endoscopic findings were suggestive of multiple 1-mm nodular filling defects in the esophagus in an area of stricture with dilatation above. The radiology showed a luminal narrowing, wall rigidity, and high circulating eosinophil count assumed to be a variant of eosinophilic gastroenteritis.

Esophagitis may be classified according to the Los Angeles Classification into 4 grades.

The esophagus is a part of the gastrointestinal tract which is responsible of moving the food from the mouth to the rectum. Esophagitis is defined as inflammation of mucosal layer of esophagus. Based on the etiology of inflammation esophagitis can be classified into reflux esophagitis and eosinophilic esophagitis. Any condition that lead to the reflux of the gastric acidic contents into the esophagus results in reflux esophagitis. Eosinophilic esophagitis is an immunoallergic disorder resulting from the interaction between genetics and environmental triggers such as repeated exposure to food and aeroallergens. TH2 inflammatory cell response play a major role in the production of eosinophils. Activated TH2 response leads to the recruitment and activation of eosinophils and mast cells. Characteristic gross pathology findings of esophagitis include fixed esophageal ring, white exudates, longitudinal furrows/ fibrosis, mucosal pallor, Diffuse esophageal narrowing. Characteristic microscopic findings of esophagitis include edema and basal hyperplasia (non-specific inflammatory changes), lymphocytic infiltration, neutrophilic infiltration, eosinophilic infiltration, goblet cell intestinal metaplasia or Barrett’s esophagus and elongation of the papillae.

Common causes of esophagitis include gastroesophageal reflux disease, Barrett’s esophagus, caustic burns, and chemical injury by either alkaline or acid solutions. Among immuncompromised patients, the most common causes of esophagitis are Candidiasis, Cytomegalovirus, and Herpes simplex virus

Esophagitis must be differentiated from gastritis, peptic ulcer disease, gastroesophageal reflux disease, acute coronary syndrome, angina pectoris, cholecystitis, biliary colic, pulmonary embolism and esophageal perforation, rupture and tears.

In the USA and Europe, the prevalence of GERD ranges from low of 10,000 per 100,000 persons to high of 20,000 per 100,000 people. In Asia, the prevalence of GERD is 5,000 per 100,000 people. The prevalence of EoE is approximately 50-100 per 100,000 individuals worldwide. In the USA, the incidence of GERD is 5,400 per 100,000 persons. In Europe, the incidence of GERD is 840 per 100,000 persons. The incidence of EoE is approximately 10 per 100,000 individuals worldwide. The prevalence of GERD increases with age. GERD affects all age groups but it affects more the people older than 40 years. Patients of all age groups may develop EoE. Men and women are affected equally by GERD. Males are more commonly affected by EoE than females. There is no racial predilection for GERD. EoE usually affects individuals of the white race.

Common risk factors in the development of esophagitis are immunosuppression, alcohol use, smoking, excessive vomiting, certain medications, and surgery or radiation to the chest.

There is insufficient evidence to recommend routine screening for Esophagitis.

If left untreated, 20% of patients with esophagitis may progress to develop esophageal stricture due to excessive acid in the lower esophagus. Common complications of esophagitis include esophageal ulcer, and esophageal adenocarcinoma. Prognosis of esophagitis is generally good with appropriate treatment.

The most common symptoms of the esophagitis include halitosis, epigastric chest pain, often radiating to the back, dysphagia, odynophagia, hoarseness, oral ulcers.

The physical examination usually is not helpful in confirming the diagnosis of uncomplicated esophagitis. However, the examination may reveal other potential sources of chest or abdominal pain.

A complete blood count (CBC) is performed in patients with neutropenia or who are immunosuppressed. A CD4 count and HIV test are performed in patients with risk factors for HIV. A collagen workup (eg, antinuclear antibody [ANA], anti-dsDNA) may be performed based on the underlying disease.

There are no specific electrocardiogram findings associated with esophagitis.

Barium studies cannot diagnose esophagitis but are helpful in identifying any underlying anatomical abnormalities such as strictures or rings.

There are no echocardiography/ultrasound findings associated with esophagitis.

There are no CT scan findings associated with esophagitis. However, a CT scan may be helpful in the diagnosis of complications of esophagitis such as tears, perforation, strictures, etc.

There are no MRI findings associated with esophagitis. however, MRI may be helpful in the diagnosis of complications of esophagitis such as tears, perforation, strictures, etc.

There are no other imaging findings associated with esophagitis.

The endoscope has been before one of the diagnostic tools for esophagitis. However, endoscopy is not recommended now for the diagnosis of esophagitis with the typical symptoms, however, it is used in screening for the esophagitis complications such as esophageal strictures, and barrett’s esophagus. 

The mainstay of therapy for reflux esophagitis is acid suppression therapy. Patients with infectious esophagitis are treated with antimicrobial therapy, whereas patients with eosinophilic esophagitis are treated with corticosteroids. Supportive therapy for esophagitis includes proton pump inhibitors, topical pain medications (gargled or swallowed), smoking and alcohol cessation, and endoscopy to remove any lodged pill fragments.

Surgical intervention is not recommended for the management of esophagitis. However, esophageal dilation can be employed in cases of severe dysphagianot responding to medial therapy.

Effective primary preventive measures for esophagitis include weight loss, having head elevated while sleeping, and avoidance of certain foods that can trigger inflammation of esophagus.

There are no established measures for the secondary prevention of esophagitis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

Esophagitis is believed to be first described and treated by the ancient Egyptians according to the papyrus which was discovered by Edwin Smith at Thebes. The esophagus was first named by the ancient Greeks as “oisophagos” at which “oiso” means carry and “phagema” means food. Friedenwald, and Feldman was the first to give a detailed description of the constellation of symptoms for GERD in 1925. Robbins and Jankelson used the radiological procedures to observe GERD in 1926. In 1981, Picus and Frank reported a case of a 16-year-old boy with progressive dysphagia for 1.5 years, endoscopic findings were suggestive of multiple 1-mm nodular filling defects in the esophagus in an area of stricture with dilatation above. The radiology showed a luminal narrowing, wall rigidity, and high circulating eosinophil count assumed to be a variant of eosinophilic gastroenteritis.

The historical perspective of the esophagitis is as the follows:^{[1][2][3][4][5][6][7][8][9][10]}

• The esophagus was first named by the ancient Greeks as “oisophagos” at which “oiso” means carry and “phagema” means food.^[11]
• In 1541, Gyudon was the first to give a detailed description of the esophagus and its function.
• In 1704, Anton Maria Valsalva published an article where he described the lower esophageal sphincter (LES). The LES was first named as cardiac sphincter as it is very near to the heart.
• In 1862, the American Egyptologist Edwin Smith discovered a papyrus at Thebes. This papyrus, which was named after him, contain 48 cases of different illnesses and their treatment.
• In 1930, the Edwin Smith papyrus was translated by Henry Breasted. Among the 48 cases, the case number 28 was titled with “Instructions concerning a wound in his throat” which was most probably a case of GERD.
• In 1925, Friedenwald and Feldman described the presenting symptoms of GERD. They described the association between the symptoms of GERD and the presence of hiatus hernia.
• In 1926, Robbins and Jankelson was the first to use radiological procedures to diagnose esophagitis.

• In 1978, Landres et al reported an isolated case of vigorous achalasia and concluded that this was a variant of eosinophilic gastroenteritis in a patient with marked hypertrophy and eosinophilic infiltration of esophagus.
• In 1981, Picus and Frank reported a case of a 16-year-old boy with progressive dysphagia for 1.5 years, endoscopic findings were suggestive of multiple 1-mm nodular filling defects in the esophagus in an area of stricture with dilatation above.
• The radiology showed a luminal narrowing, wall rigidity, and high circulating eosinophil count assumed to be a variant of eosinophilic gastroenteritis.
• In 1982, Münch et al and in 1983, Matzinger and Daneman both described isolated cases of esophageal eosinophilia with dysphagia in patients with assumed eosinophilic gastroenteritis.
• In 1985, Feczko et al reported 3 cases of eosinophilic infiltration of esophagus, with 2 of the patients showing eosinophilic gastroenteritis. Two out of the three patients developed esophageal stricture secondary to submucosal fibrosis.
• In 1985, eosinophilic infiltration was reported in esophageal mucosal biopsy of 11 patients with average age of 14.6 years. These patients had reflux symptoms and their eosinophil density was low. In retrospect, these were probably patients with gastroesophageal reflux disease (GERD).
• In 1989, Attwood et al described esophageal asthma, an episodic dysphagia with eosinophilic infiltrates.
• These investigators compared a group of 15 adults who presented with dysphagia without esophageal obstruction and normal pH monitoring to a group of 100 adults with GERD as defined by increased acid exposure in the distal esophagus.
• The characteristics in pediatric EoE appeared to reflect greater amounts of regurgitation and failure to thrive, while the typical presentation in adults with EoE was dysphagia and food impaction.

• In 2003 the chronic nature of the natural history of EoE was described by Straumann et after the follow-up of 30 adults with EoE.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ajay Gade MD[2]] ; Aditya Ganti M.B.B.S. [3]

According to the Los Angeles Classification of esophagitis, esophagitis may be classified based on severity and etiology into 4 grades and 4 types

According to the Los Angeles Classification of esophagitis, esophagitis may be classified based on severity into 4 grades.^[1][2]

Grade A	One or more mucosal breaks < 5 mm in maximal length
Grade B	One or more mucosal breaks > 5mm, but without continuity across mucosal folds
Grade C	Mucosal breaks continuous between > 2 mucosal folds, but involving less than 75% of the esophageal circumference
Grade D	Mucosal breaks involving more than 75% of esophageal circumference

Type of esophagitis	Etiology
Eosinophilic esophagitis	Milk Soy Eggs Wheat Peanuts Shellfish
Reflux esophagitis	Caffeinated drinks Spicy foods
Drug-induced esophagitis	Analgesics Antibiotics Potassium chloride Bisphosphonates
Infectious esophagitis	History of weakened immune system increases the risk of infections with Bacteria Viruses Fungi Parasites

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ajay Gade MD[2]] ; Aditya Ganti M.B.B.S. [3]

The esophagus is a part of the gastrointestinal tract which is responsible of moving the food from the mouth to the rectum. Esophagitis is defined as inflammation of mucosal layer of esophagus. Based on the etiology of inflammation esophagitis can be classified into reflux esophagitis and eosinophilic esophagitis. Any condition that lead to the reflux of the gastric acidic contents into the esophagus results in reflux esophagitis. Eosinophilic esophagitis is an immunoallergic disorder resulting from the interaction between genetics and environmental triggers such as repeated exposure to food and aeroallergens. TH2 inflammatory cell response play a major role in the production of eosinophils. Activated TH2 response leads to the recruitment and activation of eosinophils and mast cells. Characteristic gross pathology findings of esophagitis include fixed esophageal ring, white exudates, longitudinal furrows/ fibrosis, mucosal pallor, Diffuse esophageal narrowing. Characteristic microscopic findings of esophagitis include edema and basal hyperplasia (non-specific inflammatory changes), lymphocytic infiltration, neutrophilic infiltration, eosinophilic infiltration, goblet cell intestinal metaplasia or Barrett’s esophagus and elongation of the papillae.

• The esophagus is a part of the gastrointestinal tract which is responsible of moving the food from the mouth to the rectum.^[1]
• The esophagus has anti-reflux barrier which prevents the return of the acidic contentof the stomach back to the esophagus. The anti-reflux barrier consists of the lower esophageal sphincter (LES) and the related part of the diaphragm.
• The lower esophageal sphincter is contracting smooth muscle at the end of the esophagus responsible for the food passage to the stomach. LES has high pressure tone which helps keeping it a strong barrier between the esophagus and the stomach.

Esophagitis is defined as inflammation of mucosal layer of esophagus. Based on the etiology of inflammation esophagitis can be discussed under two categories

• Reflux esophagitis
• Eosinophilic esophagitis

Pathogenesis of reflux esophagitis depends on various mechanisms that lead to the reflux of the gastric acidic contents into the esophagus. Several mechanisms impair the anti-reflux barrier and cause esophageal dysmotility. These mechanisms include the following:^[2][3]

• Transient lower esophageal sphincter relaxations ^[4][5]
• Hypotensive lower esophageal sphincter
• Hiatus hernia.^[6]
• Impaired esophageal acid clearance
• Delayed gastric emptying

Eosinophilic esophagitis is an immunoallergic disorder resulting from the interaction between genetics and environmental triggers such as repeated exposure to food and aeroallergens. The pathophysiology of the EoE is as follows:^{[7][8][9][10][11][12][13][14][15][16]}

• The eosinophils are absent in an otherwise normal esophagus, the presence of the eosinophils in the esophagus suggests GERD or EoE.
• They tend to be present in all layers of the esophagus in EoE, but predominate in the lamina propria and submucosal regions.

• TH2 inflammatory cell response play a major role in the production of eosinophils.
• Activated TH2 response leads to the recruitment and activation of eosinophils and mast cells.
• T cells (Th2) cell response also stimulates production of IL-5 and IL-13.
• IL-13 stimulates the epithelial cells of the esophagus to induce a gene called eotaxin-3, which in turn recruits eosinophils from the peripheral blood into the tissue.
• IL-5 prolongs the survival of the eosinophils.

Granule proteins of the eosinophils
ECP	Eosinophil Cationic Protein
MBP	Major Basic Protein
EPO	Eosinophil Peroxidase
EDN	Eosinophil Derived Neurotoxin

Eosinophils cause inflammation in the EoE patients by the following mechanisms

• Upon the stimulation and the degranulation, the eosinophils release the granule proteins into the tissues.
• Granule proteins from eosinophils recruits the inflammatory cells and increase the vascularity.
• Increased vascularity stimulates fibrogenic mediators such as TGF-β1 and matrix metalloproteinase 9 (MMP)-9.
• TGF-β and eosinophilic granule proteins MBP and EPO are the key eosinophil effector proteins.
• MBP and MMP-9 disrupt the integrity of the epithelial cells of the esophagus through their involvement in the smooth muscles, fibroblasts, and cell-adhesion molecules.
• Eventually resulting in tissue remodeling and esophageal dysfunction.

• Endoscopic abnormalities in patients with esophagitis are as follows:^{[17][18][19][20][21]}
  • Fixed esophageal ring
  • White exudates
  • Longitudinal furrows/ fibrosis
  • Mucosal pallor
  • Diffuse esophageal narrowing
  • Mucosal fragility leading to esophageal lacerations during the endoscopy
• However, because these endoscopic features have been described in other esophageal disorders, none can be considered pathognomonic for esophagitis.

On histopathological analysis, based on the type of esophagitis microscopic findings include:^[22]

• Eosinophilic esophagitis
  • > 20 eosinophils/0.24 mm2.
  • Papillae are elongated
  • Papillae reach into the top 1/3 of the epithelial layer
  • Basal cell hyperplasia; > 3 cells thick or >15% of epithelial thickness

• Reflux esophagitis
  • Edema and basal hyperplasia (non-specific inflammatory changes)
  • Lymphocytic infiltration (non-specific)
  • Neutrophilic infiltration
  • Eosinophilic infiltration
  • Goblet cell intestinal metaplasia or Barrett’s esophagus.
  • Elongation of the papillae
  • Thinning of the squamous cell layer
  • Dysplasia or pre-cancer.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

Common causes of esophagitis include gastroesophageal reflux disease, Barrett’s esophagus, caustic burns, and chemical injury by either alkaline or acid solutions. Among immunocompromised patients, the most common causes of esophagitis are Candidiasis, Cytomegalovirus, and Herpes simplex virus

Common causes of esophagitis include:^{[1][2][3][4][5][6][7][8]}

• Barrett’s esophagus
• Candidiasis in immunocompromised patients
• Caustic burn
• Chemical injury by alkaline or acid solutions
• Cytomegalovirus in immunocompromised patients
• Gastroesophageal reflux disease
• Herpes simplex virus in immunocompromised patients
• Radiation therapy

Cardiovascular	No underlying causes
Chemical/Poisoning	Caustic burn, Chemical esophagitis, Chemical injury, Formaldehyde, Toxins
Dental	No underlying causes
Dermatologic	Lichen planus, Scleroderma
Drug Side Effect	Alendronate, Alprenolol, Amlodipine and Benazepril, Ascorbic acid, Bisphosphonate, Caffeine, Cidofovir, Clindamycin, Dactinomycin, Doxorubicin Hydrochloride, Doxycycline, Emepronium, Etidronate, ethanolamine oleate, Felbamate, Ferrous sulfate, ibandronate, iron compounds, Ixabepilone, Leflunomide, Mycophenolic acid, Pergolide, Oxaprozin, Oxcarbazepine, Oxytetracycline, Pinaverium , Potassium chloride, Pramipexole, Quinidine, Rauwolfia, Risedronate, Sertraline, Tetracycline
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	Barrett’s esophagus, Candidiasis, Chemical esophagitis, Crohn’s Disease, Dyspepsia, Eosinophilic esophagitis, Eosinophilic gastroenteritis, Esophageal achalasia, Esophageal food bolus obstruction, Esophageal stricture, Esophageal varices, Gastroesophageal reflux disease, Gastroscopy, Hernias, Hiatus hernia, Impaired esophageal motility, inflammatory bowel disease, Nasogastric tube, Reflux esophagitis, Rumination disorder, Upper gastrointestinal bleeding
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	Gastric tube, Gastroscopy, Nasogastric tube, Radiation therapy
Infectious Disease	Acquired Immune Deficiency Syndrome, Candidiasis, Cytomegalovirus, Fungal infection, Herpes simplex, HSV-1, Varicella zoster virus
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Tumor
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	Acquired Immune Deficiency Syndrome, Behcet disease, Candidiasis, Crohn’s Disease, Cytomegalovirus, Eosinophilic esophagitis, Eosinophilic gastroenteritis, Food allergy, Graft versus host disease, inflammatory bowel disease, Lichen planus, Scleroderma
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	Esophageal achalasia, Esophageal food bolus obstruction, Esophageal stricture, Esophageal varices, Food allergy, Foreign bodies, Gastric tube, Impaired esophageal motility, Lichen planus, Physical injury, Rumination disorder

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

Esophagitis must be differentiated from gastritis, peptic ulcer disease, gastroesophageal reflux disease, acute coronary syndrome, angina pectoris, cholecystitis, biliary colic, pulmonary embolism and esophageal perforation, rupture and tears.

• Acute Coronary Syndrome
• Angina Pectoris
• Cholecystitis and Biliary Colic
• Esophageal Perforation, Rupture, and Tears
• Foreign Bodies, Gastrointestinal
• Gastritis and Peptic Ulcer Disease
• Gastroesophageal Reflux Disease
• Myocardial Infarction
• Peptic Ulcer Disease
• Pulmonary Embolism
• Candida esophagitis

Dysphagia

Oropharyngeal dysphagia

Esophageal dysphagia

Solids only

Solids and Liquids

Solids only

Solids and Liquids

•Zenker’s diverticulum •Neoplasm •Webs

Neurogenic

Myogenic

Pain

•Achalasia •Scleroderma •DES

•Myasthenia gravis •Connective tissue disorder •Myotonic dystrophy

No

Yes

Heart burn

Barium swallow

Mental status

•Pill esophagitis •Caustic injury •Chemotherapy

Yes

No

Impaired

Normal

Non progressive

Progressive

Sac

Webs

Mass

Scleroderma

•Achalasia •DES

Stroke

•ALS •Parkinsonism

•Rings •Webs

•Strictures •Cancer

Zenker’s diverticulum

Plummer-Vinson syndrome

Carcinoma

Chest pain and manometry

Barium swallow

Weight loss

Increase LES pressure

Rings

Webs

Yes

No

Rapid

Slow

Achalasia

DES

Cancer

Strictures/GERD

Eosinophilic esophagitis must be differentiated from other diseases that cause dysphagia such as reflux esophagitis, esophageal carcinoma, and systemic sclerosis.^{[1][2][3][4][5][6][7][8][9][10][11]}

Disease	Signs and Symptoms								Barium esophagogram	Endoscopy	Other imaging and laboratory findings	Gold Standard
	Onset	Dysphagia			Weight loss	Heartburn	Other findings	Mental status
		Solids	Liquids	Type
Plummer-Vinson syndrome	Gradual	+	–	Non progressive	+/-	–	Glossitis Koilonychia	Normal	Thin projections on the anterior esophageal wall Multiple upper esophageal constrictions	Direct visualization of esophageal webs Superior to esophagogram	Videofluoroscopy shows mucosal and submucosal foldings	Triad of Iron deficiency anemia Esophageal webs Glossitis
Esophageal stricture	Gradual Sudden onset	+	–	Progressive	+/-	+/-	Odynophagia Cough Chest pain	Normal	Sacculations Fixed transverse folds Esophageal intramural pseudodiverticula	Mucosal edema Circumferential thickening in GERD Pale mucosa with white exudate in lymphocytic esophagitis Swelling and hemorrhagic congestion in caustic ingestion	Manometry may show dysmotility CT scan for staging malignant strictures	Barium esophagogram
Diffuse esophageal spasm	Sudden	+	+	Non progressive	+	+	Chest pain	Normal	Nonperistaltic and nonpropulsive contractions Corkscrew or rosary bead esophagus	Inconclusive	Manometry shows high-amplitude esophageal contractions CT scan may show hypertrophy of esophageal muscles	Manometry
Achalasia	Gradual	+	+	Non progressive	+/-	–	Regurgitation of undigested food Chest pain	Normal	“Bird’s beak” or “rat tail” appearance Dilated esophageal body Air fluid level (absent peristalsis) Absence of an intragastric air bubble	Dilated esophagus Residual food fragments Normal mucosa	Residual pressure of LES > 10 mmHg Incomplete relaxation of the LES Increased resting tone of LES Aperistalsis	History of dysphagia with positive endoscopy and manometry
Systemic sclerosis	Gradual	+	+	Progressive	+/-	+	Muscle and joint pain Raynaud’s phenomenon Skin changes	Normal	Dysmotility Patulous esophagus	Mucosal damage Peptic stricture (advanced cases)	Positive serology for Antinuclear antibodies Rheumatoid factor Creatine kinase ESR	Skin biopsy
Zenker’s diverticulum	Gradual	+	–		+/-	–	Food regurgitation Halitosis Cough Hoarseness	Normal	Thin projections on esophageal wall over Killian’s triangle	Outpouching of posterior pharyngeal wall Exclude the presence of SCC	CT & MRI shows out-pouching over the posterior esophagus in the Killian’s triangle	Barium esophagography
Esophageal carcinoma	Gradual	+	+	Progressive	+	+/-	Lymphadenopathy Cachexia	Normal	Irregular stricture Pre-stricture dilatation	Esophageal obstruction Staging of disease	CT and PET scan is an optional test for staging of the disease	Biopsy
Stroke (Cerebral hemorrhage)	Sudden	+	+	Progressive	+	+/-	Dysarthria Limb weakness Fatigue	Impaired	Pooling of contrast in the pharynx Aspiration of barium contrast into the airway	Reduced opening of upper esophageal sphincter Reduced larynx elevation	CT without contrast shows acute hemorrhage as a hyperattenuating clot	CT without contrast
Motor disorders (Myasthenia gravis)	Gradual	+	+	Progressive	+/-		Ptosis Diplopia Fatigue	Normal	Stasis in pharynx and pooling in pharyngeal recesses	Velopharyngeal insufficiency Delayed swallowing function	CT may show anterior mediastinal mass (thymoma) Positive tensilon test	Anti–acetylcholine receptor antibody test
GERD	Gradual Sudden onset	+	–	Progressive	+/-	+	Cough Hoarseness	Normal	Free acid reflux Esophagitis with scarring Strictures Barrett’s oesophagus	Erythema, erosions and ulceration Barrett’s esophagus	Esophageal manometry may show decreased tone of LES	24 hour esophageal pH monitoring
Esophageal web	Gradual	+	+/-	Progressive	–	+/-	Findings of the underlying cause such as iron deficiency anemia or bullous pemphigoid	Normal	Symmetrical narrowing of the esophagus	Smooth membrane not encircling the whole lumen	Videofluoroscopy shows mucosal and submucosal foldings	Barium esophagogram
Eosinophilic esophagitis	Gradual	+		Progressive	+/-	+/-	Chest pain Food impaction Cough	Normal	Multiple rings in the esophagus	Concentric rings of the esophagus- Trachealization of the esophagus	Increased serum IgE levels	Esophageal biopsy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

In the USA and Europe, the prevalence of esophagitis ranges from low of 10,000 per 100,000 persons to high of 20,000 per 100,000 people. In Asia, the prevalence of esophagitis is 5,000 per 100,000 people. In the USA, the incidence of esophagitis is 5,400 per 100,000 persons. In Europe, the incidence of esophagitis is 840 per 100,000 persons.The prevalence of esophagitis increases with age. Men and women are affected equally by esophagitis. There is no racial predilection for esophagitis.

• In the USA and Europe, the prevalence of esophagitis ranges from low of 10,000 per 100,000 persons to high of 20,000 per 100,000 people.^{[1][2][3][4][5][6][7]}
• In Asia, the prevalence of esophagitis is 5,000 per 100,000 people.
• The prevalence of EoE is approximately 50-100 per 100,000 individuals worldwide.

• In the USA, the incidence of esophagitis is 5,400 per 100,000 persons.
• In Europe, the incidence of esophagitis is 840 per 100,000 persons.
• The incidence of EoE is approximately 10 per 100,000 individuals worldwide.

• The prevalence of esophagitis increases with age.
• Esophagitis affects all age groups but it affects more the people older than 40 years.
• Patients of all age groups may develop EoE.

• Men and women are affected equally by esophagitis.
• Males are more commonly affected by EoE than females.

• There is no racial predilection for esophagitis.
• EoE usually affects individuals of the white race.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

Common risk factors in the development of esophagitis are immunosuppression, alcohol use, smoking, excessive vomiting, certain medications, and surgery or radiation to the chest.

Common risk factors in the development of EoE include:^{[1][2][3][4][5][6]}

• Age- EoE has a bimodal age distribution common in both children and adults.
• Sex- Males are more prone to EoE than the females.
• Weather- Cold and dry climate trigger EoE.
• Location- EoE is common in people with a history of European ancestry.
• Season- Summer and fall, this is because people stay outdoors during this time and the higher levels of the pollen and the other allergens during these seasons.
• Family history- EoE runs in the family and it is more common in people with a positive family history of the EoE.
• History of allergies- EoE is very common in patient with a history of allergies such as asthma, industrial exposures, environmental allergies, chronic respiratory disease, food allergies and atopic dermatitis.

Common risk factors in the development of reflux esophagitis include:

• Smoking
• Obesity
• Pregnancy
• Hiatal hernia
• Scleroderma
• Alcohol consumption
• Consuming drinks that contain caffeine

• Medications:

• Anticholinergics (e.g. for seasickness)
• Beta blockers for high blood pressure or heart disease
• Bronchodilators for asthma
• Calcium channel blockers for high blood pressure
• Dopamine-active drugs for Parkinson’s disease
• Progestin for abnormal menstrual bleeding or birth control
• Sedatives for insomnia or anxiety
• Tricyclic antidepressants

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

There is insufficient evidence to recommend routine screening for Esophagitis.

There is insufficient evidence to recommend routine screening for Esophagitis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

If left untreated, 20% of patients with esophagitis may progress to develop esophageal stricture due to excessive acid in the lower esophagus. Common complications of esophagitis include esophageal ulcer, and esophageal adenocarcinoma. Prognosis of esophagitis is generally good with appropriate treatment.

• If left untreated, 20% of patients with esophagitis may progress to develop esophageal stricture due to excessive acid in the lower esophagus..^[1]
• Symptoms often persist for years in eosinophilic esophagitis raising suspicion of a underlying chronic inflammatory disease process.
• The inflammatory activity is proportional to the density of the eosinophilic infiltration in the esophageal tissue.
• Similar to asthma, EoE has chronic persistent eosinophilic inflammation and can eventually lead to irreversible structural changes of the esophagus which is called re-modeling of the esophagus.
• The esophageal mucosa in patients with a longstanding EoE is characterized by a loss of elasticity.

Common complications of esophagitis include:^[2]

• Esophageal ulcer
• Esophageal adenocarcinoma
• Esophageal scarring / stenois resulting in progressive dysphagia
• Tears of perforation during endoscopy or retching leading to boerhaave syndrome

• Prognosis of esophagitis is generally excellent with appropriate treatment.
• The majority of people respond to non-surgical measures, with lifestyle changes and medications. However, many patients need to take medications to control their symptoms.

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