Esophageal stricture

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

Esophageal stricture is the result of increased pressure of lower esophageal sphincter. It is associated with disorders such as gastroesophageal reflux disease, esophageal motor disorders, inflammation and fibrosis in neoplasia. Common causes of esophageal stricture include gastroesophageal reflux disease and caustic ingestions. Overall incidence of esophageal stricture is approximately 11 per 100,000 individuals and the prevalence of esophageal stricture is approximately 70-120 per 100,000 individuals in united states.The most potent risk factor in the development of esophageal stricture is frequent acid reflux. Esophageal stricture is diagnosed based on history of dysphagia and diagnostic studies such as barium esophagography, esophagogastroduodenoscopy, endoscopic ultrasound, and manometry. Pharmacologic medical therapy for esophageal stricture secondary to gastroesophageal reflux disease includes proton pump inhibitors or H2 antagonists. The mainstay of treatment for esophageal stricture is dilation. Self-expandable plastic or metal stents placement is indicated for patients with refractory esophageal stricture. Surgery is usually reserved for patients with either inability to dilate the stricture, frequent recurrence of dysphagia, extraesophageal manifestations and long term side effects of medical therapy.

The first intervention for esophageal stricture was done in the 17th century by Whalebone. The first bougienage was performed in 1801. In 1868, esophagoscope was developed for the first time. In 1877, first surgical resection for esophageal carcinoma was performed by Vincenz Czerny. The first stent was introduced in 1990.

There is no established system for the classification of esophageal stricture, but it may be classified into benign and malignant according to causes.

Esophageal stricture is the result of lower pressure of esophageal sphincter in gastroesophageal reflux disease, esophageal motor disorder, inflammation and fibrosis in neoplasia. The most characteristic finding in gross pathology is thickening of the lower esophageal wall in gastroesophageal reflux disease, a pale mucosa in lymphocytic esophagitis and hemorrhagic congestion in caustic ingestion. Microscopic histopathological characteristic findings of esophageal stricture is intraepithelial lymphocytosis, basal cell hyperplasia in gastroesophageal reflux disease, T lymphocytes infiltration in squamous mucosa in lymphocytic esophagitis and eosinophilic necrosis in caustic ingestion

Common causes of esophageal stricture include gastroesophageal reflux disease and caustic ingestions.

Esophageal stricture must be differentiated from Plummer-Vinson syndrome, achalasia, diffuse esophageal spasm, systemic sclerosis, zenker’s diverticulum, esophageal carcinoma, stroke, motor disorders such as Myasthenia Gravis, GERD, esophageal web.

Most of the esophageal strictures are related to gastroesophageal reflux disease. The overall incidence of esophageal stricture is approximately 11 per 100,000 individuals and the prevalence of esophageal stricture is approximately 70-120 per 100,000 individuals in united states. The incidence of esophageal stricture increases with age. There is no racial predilection to esophageal stricture. The risk of esophageal stricture is higher in men under 60 years but there is similar incidence in men and women after age 60.

The most potent risk factor in the development of esophageal stricture is frequent acid reflux. Other risk factors include hiatal hernia, obesity, smoking, esophageal dysmotility, increased gastric acidity, and heavy alcohol use.

There is insufficient evidence to recommend routine screening for esophageal stricture.

If left untreated, patients with esophageal stricture may progress to develop pulmonary aspiration, weight loss, and dehydration. Common complications of esophageal stricture include perforation, bleeding, pneumonia and bacteremia. Prognosis is generally good but recurrence of symptoms after dilation are prevalent and usually recurrent dilation is necessary.

Esophageal stricture is diagnosed based on history of dysphagia and diagnostic studies such as barium esophagography, esophagogastroduodenoscopy, endoscopic ultrasound and manometry.

The hallmark of esophageal stricture is dysphagia . A positive history of heartburn is suggestive of esophageal stricture. The most common symptoms of esophageal stricture include dysphagia, odynophagia, and heartburn. Less common symptoms of esophageal stricture include chronic cough and wheezing.

Patients with esophageal stricture can usually appear normal. Cachexia and pallor are notable in patients with esophageal stricture due to neoplastic causes.

Laboratory findings are usually normal among patients with esophageal stricture although anemia may be seen with neoplastic causes of esophageal stricture. Other possible laboratory tests are high serum gastrin level in zollinger ellison syndrome and peripheral eosinophilia in eosinophilic esophagitis as causes of esophageal stricture.

There are no ECG findings associated with esophageal stricture.

A chest x-ray may be helpful in the diagnosis of tumors as a cause of esophageal stricture.

Chest CT scan may be helpful in the diagnosis of malignant causes of esophageal stricture.

In general MRI has not been routinely recommended for esophageal stricture.

There are no echocardiography findings associated with esophageal stricture. Endoscopic ultrasound may be helpful in the diagnosis of malignant causes of esophageal stricture.

Barium esophagography is helpful in the diagnosis of esophageal stricture. Findings on a barium esophagogram suggestive of benign esophageal stricture include concentric narrowing and smooth tapering. Eccentric narrowing, abrupt and asymmetric narrowing are suggestive of malignant causes.

Other diagnostic studies for esophageal stricture include esophagogastroduodenoscopy (EGD) for detection malignant causes. Manometry is used in cases of esophageal stricture due to dysmotility.

Pharmacologic medical therapy for esophageal stricture secondary to gastroesophageal reflux disease includes proton pump inhibitors or H2 antagonists. Patients are advised to consider life style modification for gastroesophageal reflux disease.

The mainstay of treatment for esophageal stricture is dilation. Self-expandable plastic or metal stents placement is indicated for patients with refractory esophageal stricture.

Surgery is usually reserved for patients with either inability to dilate the stricture, frequent recurrence of dysphagia, extraesophageal manifestations and long term side effects of medical therapy

Effective measures for the primary prevention of esophageal stricture include treatment and life style modification for gastroesophageal reflux disease, taking pills with a full glass of water and storing all corrosive chemicals.

Effective measures for the secondary prevention of esophageal stricture include lifestyle modification, proton pump inhibitors or H2 antagonists.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

The first intervention for esophageal stricture was done in the 17th century by halebone. The first bougienage was performed in 1801. In 1868, esophagoscope was developed for the first time. In 1877, first surgical resection for esophageal carcinoma was performed by Vincenz Czerny. The first stent was introduced in 1990.

There have been no outbreaks of esophageal stricture.

• Esophageal dialtion was first done in the 17 century by a curved whalebone.^[1]
• In 1801, the first bougienage was performed by Alexis Boyer.^[1]

• In 1868, esophagoscope was developed by Adolf Kussmaul to diagnose esophageal cancer as a one of the most causes of esophageal stricture.^[2]
• In 1877, first resection of the cervical esophagus for carcinoma was performed by Vincenz Czerny.^[2]
• In 1913, the first subtotal thoracic esophagectomy was performed by Franz Torek.^[2]
• In 1913, the first esophagectomy with an intrathoracic esophagogastric anastomosis was performed by Tohru Ohsawa.^[2]
• In 1966, steroid injection added to endoscopic dilation to prevent stricture recurrence.^[3]
• In 1990, the first self expandable metal stent was introduced.^[4]

• The following are a few famous cases of esophageal stricture due to esophageal carcinoma:
  • Humphrey DeForest Bogart
  • Christopher Eric Hitchens
  • Ron Silver
  • Richard Dawson
  • Jean Hagen
  • Sylvia Maria Kristel 

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

There is no established system for the classification of esophageal stricture, but it may be classified into benign and malignant according to causes.

There is no established system for the classification of esophageal stricture, however it may be classified according to etiologic causes into benign and malignant. ^{[1][2][3][4][5]}

^{[6][7][8][9][10]}

Esophageal stricture

Benign

Malignant

GERD

Chemical induced

Iatrogenic

Esophagitis

Dyskeratosis congenita (DC)

Esophageal cancer

Malignant transformation due to DC

Extrinsic compression due to malignant tumors

Idiopathic

Drug induced

Infections

Congenital

Eosinophilic

Lymphocytic

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

Esophageal stricture is the result of lower pressure of esophageal sphincter in gastroesophageal reflux disease, esophageal motor disorder, and inflammation and fibrosis in neoplasia. The characteristic findings on gross pathology are thickening of the lower esophageal wall in gastroesophageal reflux disease, pale mucosa in lymphocytic esophagitis, and hemorrhagic congestion in caustic ingestion. Characteristic histopathological findings of esophageal stricture are intraepithelial lymphocytosis and basal cell hyperplasia in gastroesophageal reflux disease; T lymphocyte infiltration in squamous mucosa in lymphocytic esophagitis and eosinophilic necrosis in caustic ingestion.

The normal esophageal diameter is up to 30 mm. An esophageal stricture is a narrowing of the esophagus usually 13 mm or less in diameter that causes dysphagia. Peptic strictures occur usually at the squamocolumnar junction.^[2]

Esophageal stricture is the result of:^[3][4]

• Lower pressure of esophageal sphincter in gastroesophageal reflux disease
• Esophageal motor disorders
• Inflammation and fibrosis due to intrinsic diseases of esophagus, such as neoplasia
• Surgical esophageal anastomosis
• Esophageal compression by other organs

• Most peptic strictures are result of chronic reflux esophagitis and the process of esophageal stricture is due to mucosal edema and infiltration of inflammatory cells in lamina propria and finally collagen deposits, fibrosis and scar of esophagus.^[2]
  • Lower esophageal sphincter (LES) tone is usually less than 8 mmHg in esophageal stricture due to reflux esophagitis.
• Radiation therapy for thoracic or head and neck tumors is one of the less common cause of proximal esophageal stricture by inducing chronic ischemia and fibrosis.^[5]

• Liquefactive necrosis is the mechanism of esophageal stricture in alkali ingestion and superficial coagulation necrosis is the mechanism of esophageal stricture in acid ingestion.^[6][7]
  • A grading system for esophageal injury due to caustic ingestion:

Grade	pathophysiological injury
0	Normal
1	Mucosal edema and hyperemia
2A	Superficial ulcers, bleeding, exudates
2B	Deep focal or circumferential ulcers
3A	Focal necrosis
3B	Extensive necrosis

Genes involved in the pathogenesis of esophageal stricture due to Dyskeratosis Congenita include:^[8]

• ACD
• CTC1
• DKC1 
• NHP2
• NOP10
• PARN
• RTEL1
• TERC
• TERT
• TINF2
• WRAP53 

• The most important diseases associated with esophageal stricture include:
  • Gastroesophageal reflux disease
  • Caustic ingestion

• On gross pathology, circumferential thickening of the lower esophageal wall are characteristic finding of esophageal stricture due to gastroesophageal reflux disease.^[9]
• Pale mucosa with white exudate in lymphocytic esophagitis^[10]
• Swelling and hemorrhagic congestion in caustic ingestion^[11]
• Multiple yellow plaques in infectious esophagitis due to Candida^[12]
• Ulceration of the esophagus in viral esophagitis

• On microscopic histopathological analysis, characteristic findings of esophageal stricture due to gastroesophageal reflux disease are:^[15]
  • Intraepithelial lymphocytosis
  • Basal cell hyperplasia
  • Ulceration ^[9]

• Microscopic histopathological characteristic findings of esophageal stricture due to lymphocytic esophagitis are:^[10]
  • Infiltration of many CD3+ /CD4+ / CD8+ T lymphocytes in squamous mucosa in the peripapaillary region without any granulocytes

• Eosinophilic necrosis in esophageal stricture due to caustic ingestion^[11]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

Common causes of esophageal stricture include gastroesophageal reflux disease and caustic ingestions.

• Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of esophageal stricture, however complications resulting from untreated esophageal stricture is common.

Esophageal stricture may be caused by:^[1]

• Gastroesophageal reflux disease^[2]
• Caustic ingestions^[3]
• Radiation therapy for thoracic or head and neck tumors^[4]
• Esophageal cancer
• Congenital causes such as rings and webs^[5]
• Nasogastric intubation^[6]

Less common causes of esophageal stricture include:

• Esophageal sclerotherapy^[7]
• Eosinophilic esophagitis^[8]
• Lymphocytic esophagitis

• Dyskeratosis congenita (DC)^[9]
• Rare dermatologic diseases (eg, epidermolysis bullosa dystrophica)^[10]
• Mediastinal fibrosis due to tuberculosis or idiopathic fibrosing mediastinitis^[11]
• Drug-induced stricture:^[12]
  • Aspirin and anti-inflammatory medications^[13]
  • Tetracycline
  • Doxycycline
  • Clindamycin
  • Bisphosphonates
  • Potassium chloride
  • Quinidine preparations
  • Iron compounds
  • Emepronium
  • Alprenolol
  • Pinaverium 

• Infectious esophagitis^[14]

• Candida
• Herpes simplex virus (HSV)
• Cytomegalovirus (CMV)
• Human immunodeficiency virus (HIV)

• Tracheoesophageal fistula repair and esophageal stricture at the anastomosis^[15]
• Esophageal diverticula^[16]
• Increased level of gastric acid exposure to esophageal tissue, for example:
  • Systemic sclerosis^[17]
  • Zollinger-Ellison syndrome^[18]
  • Nasogastric tube placement^[18]
  • Heller myotomy for achalasia^[19]

Cardiovascular	No underlying causes
Chemical/Poisoning	Caustic ingestion
Dental	No underlying causes
Dermatologic	Dyskeratosis congenita (DC), epidermolysis bullosa dystrophica
Drug Side Effect	Drug-induced stricture:[12] Aspirin and anti-inflammatory medications[13] Tetracycline Doxycycline Clindamycin Bisphosphonates Potassium chloride Quinidine preparations Iron compounds Emepronium Alprenolol Pinaverium
Ear Nose Throat	No underlying causes
Endocrine	Zollinger-Ellison syndrome,
Environmental	No underlying causes
Gastroenterologic	Gastroesophageal reflux disease, Eosinophilic esophagitis, Esophageal diverticula, Zollinger-Ellison syndrome, Systemic sclerosis
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	Previous surgery on the esophagus, Radiation therapy for thoracic or head and neck tumors, Esophageal sclerotherapy,Tracheoesophageal fistula repair, Nasogastric tube placement, Heller myotomy for achalasia
Infectious Disease	Infectious esophagitis Candida  Herpes simplex virus (HSV) Cytomegalovirus (CMV) Human immunodeficiency virus (HIV)
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	Mediastinal fibrosis due to tuberculosis or idiopathic fibrosing mediastinitis
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	Systemic sclerosis
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	No underlying causes

List the causes of the disease in alphabetical order.

• Caustic ingestions

• Drug-induced stricture
• Dyskeratosis congenita (DC)
• Eosinophilic esophagitis
• Esophageal diverticula
• Esophageal sclerotherapy
• Gastroesophageal reflux disease
• Increased level of gastric acid exposure to esophageal tissue
• Infectious esophagitis
• Mediastinal fibrosis due to tuberculosis or idiopathic fibrosing mediastinitis
• Nasogastric intubation
• Radiation therapy for thoracic or head and neck tumors
• Rare dermatologic diseases (eg, epidermolysis bullosa dystrophica)
• Tracheoesophageal fistula repair and esophageal stricture at the anastomosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

Esophageal stricture must be differentiated from Plummer-Vinson syndrome, achalasia, diffuse esophageal spasm, systemic sclerosis, zenker’s diverticulum, esophageal carcinoma, stroke, motor disorders, GERD, esophageal web.

• Esophageal stricture must be differentiated from other diseases that cause dysphagia such as Plummer-Vinson syndrome, achalasia , diffuse esophageal spasm, systemic sclerosis, zenker’s diverticulum, esophageal carcinoma, stroke(cerebral hemorrhage), motor disorders (Myasthenia Gravis), GERD, esophageal web.

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

Preferred Table

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 {{#ev:youtube|HFfsTgsB6Pg}}	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 {{#ev:youtube|-vax5E-jMnQ}}	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 {{#ev:youtube|2ipA34iMA3c}}	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 {{#ev:youtube|ydLcskQzEjM}}	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 {{#ev:youtube|FdEruFsNdVA}}	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 {{#ev:youtube|5ucSlgqGAno}}	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

	Manifestations	Diagnostic tools
Achalasia	Dyspnea[1] Dysphagia for solids and liquids is the most common feature, being seen in 91 % and 85% of patients respectively[2] Regurgitation of undigested food occurs in 76-91% of patients[2] Cough mainly when lying down in 30%[2]	Esophagogastroduodenoscopy findings include a dilated esophagus with residual food fragments, normal mucosa and occasionally candidiasis (due to the prolonged stasis). Barium swallow shows the characteristic bird’s beak appearance.
GERD	Retrosternal burning chest pain. Cough and hoarseness of voice. May present with complications such as strictures and dysphagia.[3]	Upper GI endoscopy shows the complications such as esophagitis and barret esophagus. Esophageal manometry may show decreased tone of the lower esophageal sphincter. 24-hour esophageal pH monitoring may be done to confirm the diagnosis.
Esophageal carcinoma	Dysphagia Odynophagia– fluids and soft foods are usually tolerated, while hard or bulky substances (such as bread or meat) cause much more difficulty[4] Weight loss Pain, often of a burning nature, may be severe and worsened by swallowing, and can be spasmodic in character Nausea and vomiting[4]	Upper GI endoscopy and esophageal biopsy the gold standard for the diagnosis of esophageal
Corckscrew esophagus	Retrosternal chest pain that presents with or without food intake.[5] The condition is not progressive and not causing complications.[6]	Barium swallow shows the characteristic corckscrew appearance of the esophagus.
Esophageal stricture	Patient may present with the symptoms of the underlying GERD. Dysphagia and odynophagia.[7]	Barium esophagography provides information about the site and the diameter of the stricture before the endoscopic intervention.[8]
Plummer-Vinson syndrome	Common symptoms of Plummer-Vinson syndrome include:[9][10][11] Difficulty swallowing (more for solids) Weakness Pain Burning sensation in mouth Dry tongue Painful cracks in the angles of a dry mouth Pale color of the skin Less common symptoms Cold intolerance Reduced resistance to infection Altered behavior Craving for for unusual items (such as ice or cold vegetables)	Lab tests are consistent with the diagnosis of iron deficiency anemia. Findings on an x-ray (barium esophagogram) suggestive of esophageal web/strictures associated with Plummer-Vinson syndrome appear as either: Thin projections on the anterior esophageal wall. Multiple upper (cervical) esophageal constrictions consistent with esophageal webs.

References

1. ↑ Ferri, Fred (2015). Ferri’s clinical advisor 2015 : 5 books in 1. Philadelphia, PA: Elsevier/Mosby. ISBN 978-0323083751.
2. ↑ ^{2.0 2.1 2.2} Boeckxstaens GE, Zaninotto G, Richter JE (2013). “Achalasia”. Lancet. doi:10.1016/S0140-6736(13)60651-0. PMID 23871090.CS1 maint: Multiple names: authors list (link)
3. ↑ Badillo R, Francis D (2014). “Diagnosis and treatment of gastroesophageal reflux disease”. World J Gastrointest Pharmacol Ther. 5 (3): 105–12. doi:10.4292/wjgpt.v5.i3.105. PMC 4133436. PMID 25133039.
4. ↑ ^{4.0 4.1} Napier KJ, Scheerer M, Misra S (2014). “Esophageal cancer: A Review of epidemiology, pathogenesis, staging workup and treatment modalities”. World J Gastrointest Oncol. 6 (5): 112–20. doi:10.4251/wjgo.v6.i5.112. PMC 4021327. PMID 24834141.
5. ↑ Matsuura H (2017). “Diffuse Esophageal Spasm: Corkscrew Esophagus”. Am. J. Med. doi:10.1016/j.amjmed.2017.08.041. PMID 28943381.
6. ↑ Lassen JF, Jensen TM (1992). “[Corkscrew esophagus]”. Ugeskr. Laeg. (in Danish). 154 (5): 277–80. PMID 1736462.CS1 maint: Unrecognized language (link)
7. ↑ Ruigómez A, García Rodríguez LA, Wallander MA, Johansson S, Eklund S (2006). “Esophageal stricture: incidence, treatment patterns, and recurrence rate”. Am. J. Gastroenterol. 101 (12): 2685–92. doi:10.1111/j.1572-0241.2006.00828.x. PMID 17227515.
8. ↑ Shami VM (2014). “Endoscopic management of esophageal strictures”. Gastroenterol Hepatol (N Y). 10 (6): 389–91. PMC 4080876. PMID 25013392.
9. ↑ López Rodríguez MJ, Robledo Andrés P, Amarilla Jiménez A, Roncero Maíllo M, López Lafuente A, Arroyo Carrera I (2002). “Sideropenic dysphagia in an adolescent”. J. Pediatr. Gastroenterol. Nutr. 34 (1): 87–90. PMID 11753173.
10. ↑ Chisholm M (1974). “The association between webs, iron and post-cricoid carcinoma”. Postgrad Med J. 50 (582): 215–9. PMC 2495558. PMID 4449772.
11. ↑ Larsson LG, Sandström A, Westling P (1975). “Relationship of Plummer-Vinson disease to cancer of the upper alimentary tract in Sweden”. Cancer Res. 35 (11 Pt. 2): 3308–16. PMID 1192404.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

Most of the esophageal strictures are related to gastroesophageal reflux disease. The overall incidence of esophageal stricture is approximately 11 per 100,000 individuals and the prevalence of esophageal stricture is approximately 70-120 per 100,000 individuals in united states. The incidence of esophageal stricture increases with age. There is no racial predilection to esophageal stricture. The risk of esophageal stricture is higher in men under 60 years but there is similar incidence in men and women after age 60.

• In one study the overall incidence of esophageal stricture is approximately 11 per 100,000 individuals. The incidence of benign esophageal stricture was 8 per 100,000 individuals and malignant stricture was 3 per 100,000 individuals.^[1]
• 60–70% of benign strictures of the esophagus are related to gastroesophageal reflux disease.^[2]
• Incidence of benign esophageal stricture decreased in recent years because of using proton pump inhibitor (PPI) for treatment of gastroesophageal reflux disease.

• The prevalence of esophageal stricture is approximately 70-120 per 100,000 individuals in united states. ^[3]
• In Hong kong, the prevalence of benign esophageal stricture was estimated to be 80 cases per 100,000 individuals.^[4]

• Mortality rate of esophageal stricture due to benign causes is not increased compare to normal population, but malignant causes and complications after procedures such as dilation of esophageal stricture can increase mortality.^[1]

• The incidence of esophageal stricture increases with age in both of benign and malignant strictures.^[1]

• There is no racial predilection to esophageal stricture. Frequency of esophageal stricture was similar in African Americans and non-Hispanic whites.^[5]

• The risk of esophageal stricture due to gastroesophageal reflux disease is higher in men in age group under 60 yr but similar incidence of esophageal stricture in men and women beyond age 60. ^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

The most potent risk factor in the development of esophageal stricture is frequent acid reflux. Other risk factors include hiatal hernia, obesity, smoking, esophageal dysmotility, increased gastric acidity, and heavy alcohol use.

• Common risk factors in the development of esophageal stricture include:
  • Frequent acid reflux^[1] 
  • Hital hernia^[2]

• Less common risk factors in the development of esophageal stricture include:
  • Obesity^[3]
  • Smoking^[3]
  • Esophageal dysmotility in scleroderma and systemic sclerosis^[4]
  • Increased gastric acidity in zollinger-Ellison syndrome^[5]
  • Heavy alcohol use^[6]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

If left untreated, patients with esophageal stricture may progress to develop pulmonary aspiration, weight loss, and dehydration. Common complications of esophageal stricture include perforation, bleeding, pneumonia, bacteremia. Prognosis is generally good but recurrence of symptoms after dilation are prevalent and usually recurrent dilation is necessary.

• The natural history of benign esophageal strictures starts with gradual dysphagia to solid food and heartburn.^[1]
• In some cases of esophageal stricture, symptoms of heartburn disappear when fibrosis is established.^[2]
• If left untreated, patients with esophageal stricture may progress to develop:^[3]
  • Pulmonary aspiration
  • Weight loss
  • Dehydration

• Common complications of esophageal stricture include:^[4][5]
  • Perforation
  • Bleeding
  • Pneumonia
  • Bacteremia

• Prognosis is generally good and depends on the cause of esophageal stricture. More than 80-90% of esophageal strictures respond well to endoscopic dilation but one third of patients have recurrent symptoms after one year.^[4][6]
• Weight loss is associated with poor prognosis among patients with esophageal stricture.^[7]
• Progressive gastroesophageal reflux may lead to extended esophageal stricture which prevent gastric acid to flow back in the esophagus. Loss of previous heartburn is related to more esophageal stricture.^[2]

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