Dysphagia
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2], Hamid Qazi, MD, BSc [3]
Synonyms and keywords: Difficulty swallowing
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2], Hamid Qazi, MD, BSc [3]
Overview
Dysphagia derives from the Greek root dys meaning difficulty or disordered, and phagia meaning “to eat”. Dysphagia is a medical term defined as “difficulty swallowing.” It is a sensation that suggests difficulty in the passage of solids or liquids from the mouth to the stomach. According to the International Classification of Diseases (ICD-10) which is endorsed by the WHO, dysphagia is a symptom rather than a disease. Dysphagia can result from propulsive failure, motility disorders, structural disorders, intrinsic or extrinsic compression of the oropharynx or esophagus. Dysphagia is distinguished from similar symptoms including odynophagia, which is defined as painful swallowing, and globus, which is the sensation of a lump in the throat. The endoscopy for esophageal dysphagia should be performed when the patient presented with symptoms of difficulty swallowing, painful swallowing, and aspiration. This is the standard test performed when patient has risk of developing pneumonia and diagnosing swallowing difficuties. Video fluoroscopic swallowing study is performed for oropharyngeal dysphagia. It provides information about delay in initiation of pharyngeal swallowing, nasopharyngeal regurgitation, residue of ingestate within the pharyngeal cavity after swallowing, and aspiration of ingestate. The cornerstone of any dysphagia evaluation is a detailed history, and a thorough review of symptoms that can differentiate esophageal from oropharyngeal dysphagia and help predict the specific etiology of dysphagia with an accuracy of approximately 80% confirmed by specific testing. How a patient describes his or her difficulty and its timing, associated symptoms, and other characterizations may specifically denote the anatomic level of swallowing dysfunction.
Historical Perspective
In 1800, Dr. Patrick Paterson reported a case of gangrenous stomach with dysphagia from lightening. In 1811, Dr. TJ Armiger reported a case of aortic aneurysm causing dysphagia. 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. 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 1989, Attwood et al described esophageal asthma, an episodic dysphagia with eosinophilic infiltrates. In 1993, Attwood et al reported 12 adults with dysphagia, normal pH monitoring, and dense esophageal eosinophilia. Seven patients had food hypersensitivity, and all required advanced intervention (dilatation and/or steroids in 1 case) for resolution of symptoms. In 1994, Straumann et al described a series of 10 patients with acute recurrent dysphagia seen over a 4-year period.
Classification
Dysphagia is classified according to location into two groups: oropharyngeal dysphagia or esophageal dysphagia. It may be classified into further six subclasses based on etiology: infectious, metabolic, myopathic, neurological, structural, and iatrogenic.
Pathophysiology
Dysphagia can result from propulsive failure, motility disorders, structural disorders, intrinsic or extrinsic compression of the oropharynx or esophagus. Propulsive failure can result from dysfunction of the central nervous system control mechanisms, intrinsic musculature, or peripheral nerves. Structural abnormalities may result from surgery, neoplasm, caustic injury, or congenital anomalies.
Causes
Dysphagia has a couple of categories of causes which can be classified on the basis of location and the organ system involved.
Differentiating dysphagia from Other Diseases
Dysphagia is distinguished from similar symptoms including odynophagia, which is defined as painful swallowing, and globus, which is the sensation of a lump in the throat. A psychogenic dysphagia is known as phagophobia.
Epidemiology and Demographics
Dysphagia is a common symptom seen in the elderly poplulation owing to senile physiological changes in the muscles involved in deglutition. It is also seen in other age groups, subsequent to other diseases such as esophageal webs, esophageal cancer, structural damage to the esophagus.
Risk Factors
The risk factors for dysphagia are smoking, obesity, pregnancy, hiatal hernia, scleroderma, alcohol consumption, consuming drinks that contain caffeine, and medications. Medications include anticholinergics, beta blockers, bronchodilators, calcium channel blockers, dopamine-active drugs for Parkinson’s disease, progestin for abnormal menstrual bleeding or birth control, sedatives for insomnia or anxiety, and tricyclic antidepressants.
Screening
There is insufficient evidence to recommend routine screening for dysphagia.
Natural History, Complications, and Prognosis
If left untreated, dysphagia can potentially cause aspiration pneumonia, malnutrition, or dehydration, all of which can be symptoms of dysphagia as well. Prognosis is dependent on the underlying disease. However, prognosis is generally regarded as good.
Diagnosis
Diagnostic Criteria
The endoscopy for esophageal dysphagia should be performed when the patient presented with symptoms of difficulty swallowing, painful swallowing, and aspiration. This is the standard test performed when patient has risk of developing pneumonia and diagnosing swallowing difficuties. Video fluoroscopic swallowing study is performed for oropharyngeal dysphagia. It provides information about delay in initiation of pharyngeal swallowing, nasopharyngeal regurgitation, residue of ingestate within the pharyngeal cavity after swallowing, and aspiration of ingestate.
History and Symptoms
The most important factor in the evaluation of any dysphagia is a detailed history, and a thorough review of symptoms that can differentiate esophageal from oropharyngeal dysphagia and help predict the specific etiology. How a patient describes the symptoms and their timing, associated historical features, and other characterizations may specifically denote the anatomic level of swallowing dysfunction.
Physical Examination
A speech language pathologist is most often the first person called upon to evaluate a patient with suspected dysphagia. During this informal examination, medical history is obtained, the mini-mental state examination is administered, and oral and facial sensorimotor function, speech, and swallowing are evaluated non-instrumentally.
Laboratory Findings
There are no diagnostic laboratory findings associated with dysphagia per se. However, in certain diseases leading to dysphagia, laboratory evaluation is done to look for the underlying disease.
Electrocardiogram
There are no ECG findings associated with dysphagia.
X-ray
An x-ray may be helpful in the diagnosis of the underlying cause of dysphagia. Findings on an x-ray suggestive of of dysphagia include structural abnormalities, masses, and to rule out causes.
Ultrasound
Ultrasound may be helpful in the diagnosis of dysphagia. Findings on an ultrasound suggestive of dysphagia muscular function, and hypertrophy of the muscular layer.
CT scan
CT scan may be helpful in the diagnosis of the underlying cause of dysphagia. Findings on CT scan suggestive of dysphagia include structural abnormalities and central nervous system (CNS) abnormalities.
MRI
MRI may be helpful in the diagnosis of the underlying cause of dysphagia. Findings on MRI suggestive of dysphagia include structural abnormalities and central nervous system abnormalities.
Other Imaging Findings
There are no other imaging findings associated with the diagnosis of dysphagia.
Other Diagnostic Studies
Other diagnostic studies for dysphagia include video fluoroscopic swallowing study and esophageal manometry. Video fluoroscopic swallowing study, also known as modified barium swallow, is used as the initial study for the evaluation of oropharyngeal dysphagia.
Treatment
Medical Therapy
The main objective of treating dysphagia is to avoid aspiration of the food and bolus impaction, reduce the morbidity associated with ongoing symptoms. Effective medical management begins with early identification of the underlying cause with a detailed history, physical examination and, judicious use of investigations.
Surgery
Surgery is not the first-line treatment option for patients with dysphagia. Surgery is usually reserved for patients with either dysphagia leading to life-threatening aspiration and airway protection.
Primary Prevention
There are no established measures for the primary prevention of dysphagia.
Secondary Prevention
Effective measures for the secondary prevention of dysphagia include chewing your food thoroughly and eating slowly
References
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2], Ajay Gade MD[3]], Hamid Qazi, MD, BSc [4]
Overview
Dysphagia derives from the Greek root dys meaning difficulty or disordered, and phagia meaning “to eat”. In 1800, Dr. Patrick Paterson reported a case of gangrenous stomach with dysphagia from lightening. In 1811, Dr. TJ Armiger reported a case of aortic aneurysm causing dysphagia. 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. 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 1989, Attwood et al described esophageal asthma, an episodic dysphagia with eosinophilic infiltrates. In 1993, Attwood et al reported 12 adults with dysphagia, normal pH monitoring, and dense esophageal eosinophilia. Seven patients had food hypersensitivity, and all required advanced intervention (dilatation and/or steroids in 1 case) for resolution of symptoms. In 1994, Straumann et al described a series of 10 patients with acute recurrent dysphagia seen over a 4-year period.
Dysphagia historical perspective
The historical perspective of dysphagia is as follows:[1][2][3][4][5][6][7][8][9]
- In 1800, Dr. Patrick Paterson reported a case of gangrenous stomach with dysphagia from lightening.
- In 1811, Dr. TJ Armiger reported a case of aortic aneurysm causing dysphagia.
- In 1911, Dr. Walter Howarth reported a case of laryngeal Tuberculosis leading to dysphagia.
- 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.
- 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 1989, Attwood et al described esophageal asthma, an episodic dysphagia with eosinophilic infiltrates.
- In 1993, Attwood et al reported 12 adults with dysphagia, normal pH monitoring, and dense esophageal eosinophilia. Seven patients had food hypersensitivity, and all required advanced intervention (dilatation and/or steroids in 1 case) for resolution of symptoms.
- In 1994, Straumann et al described a series of 10 patients with acute recurrent dysphagia seen over a 4-year period. These patients showed discrete endoscopic changes, and high concentrations of epithelial esophageal eosinophils. They improved following systemic steroid and antihistamine treatment.
Landmark Events in the Development of Treatment Strategies
- In 1988, Fibreoptic endoscopic evaluation of swallowing (FEES) evolved as a valid, low-cost, and quick bedside technique for the evaluation of dysphagia among different hospital settings and all age groups.[10][11]
References
- ↑ Landres RT, Kuster GG, Strum WB (1978). “Eosinophilic esophagitis in a patient with vigorous achalasia”. Gastroenterology. 74 (6): 1298–1301. PMID 648822.
- ↑ Picus D, Frank PH (1981). “Eosinophilic esophagitis”. AJR Am J Roentgenol. 136 (5): 1001–3. doi:10.2214/ajr.136.5.1001. PMID 6784497.
- ↑ Matzinger MA, Daneman A (1983). “Esophageal involvement in eosinophilic gastroenteritis”. Pediatr Radiol. 13 (1): 35–8. PMID 6844053.
- ↑ Attwood SE, Smyrk TC, Demeester TR, Jones JB (1993). “Esophageal eosinophilia with dysphagia. A distinct clinicopathologic syndrome”. Dig. Dis. Sci. 38 (1): 109–16. PMID 8420741.
- ↑ Straumann A, Spichtin HP, Bernoulli R, Loosli J, Vögtlin J (1994). “[Idiopathic eosinophilic esophagitis: a frequently overlooked disease with typical clinical aspects and discrete endoscopic findings]”. Schweiz Med Wochenschr (in German). 124 (33): 1419–29. PMID 7939509.
- ↑ Kelly KJ, Lazenby AJ, Rowe PC, Yardley JH, Perman JA, Sampson HA (1995). “Eosinophilic esophagitis attributed to gastroesophageal reflux: improvement with an amino acid-based formula”. Gastroenterology. 109 (5): 1503–12. PMID 7557132.
- ↑ Straumann A, Spichtin HP, Grize L, Bucher KA, Beglinger C, Simon HU (2003). “Natural history of primary eosinophilic esophagitis: a follow-up of 30 adult patients for up to 11.5 years”. Gastroenterology. 125 (6): 1660–9. PMID 14724818.
- ↑ Paterson P (1800). “Case of Gangrenous Stomach, with Dysphagia, from Lightning: Communicated in a Letter to Dr. Simmons”. Med Facts Obs. 8: 111–121. PMC 5111436. PMID 29106246.
- ↑ Howarth W (1910). “Tuberculosis of the Larynx, with considerable Dysphagia, treated and relieved by Congestion Hyperaemia”. Proc R Soc Med. 3 (Laryngol Sect): 164–5. PMC 1961421. PMID 19974394.
- ↑ Crespin OM, Liu LWC, Parmar A, Jackson TD, Hamid J, Shlomovitz E; et al. (2017). “Safety and efficacy of POEM for treatment of achalasia: a systematic review of the literature”. Surg Endosc. 31 (5): 2187–2201. doi:10.1007/s00464-016-5217-y. PMID 27633440.
- ↑ El Khoury R, Teitelbaum EN, Sternbach JM, Soper NJ, Harmath CB, Pandolfino JE; et al. (2016). “Evaluation of the need for routine esophagram after peroral endoscopic myotomy (POEM)”. Surg Endosc. 30 (7): 2969–74. doi:10.1007/s00464-015-4585-z. PMID 26487213.
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Feham Tariq, MD [2]
Overview
Dysphagia may be classified based on the location into oropharyngeal dysphagia or esophageal dysphagia. Dysphagia may also be classified based on etiology into further six subclasses which include infectious, metabolic, myopathic, neurological, structural and, iatrogenic.
Classification of Dysphagia
Dysphagia may be classified based on the location into two major types:[1][2][3]
- Oropharyngeal dysphagia
- Esophageal dysphagia
Dysphagia can also be classified based on the etiology into six sub classes:
- Infectious
- Metabolic
- Myopathic
- Neurological
- Structural
- Iatrogenic
Oropharyngeal Dysphagia
- Arises from abnormalities of the upper esophagus, pharynx, and oral cavity.
Esophageal Dysphagia
- Arises from the body of the esophagus, lower esophageal sphincter, or cardia of the stomach.
- Most commonly esophageal dysphagia is either due to mechanical obstruction of esophageal lumen or motility problems.
Functional dysphagia
- Dysphagia due to no organic cause.
- Diagnosis of exclusion.
| Classification of Dysphagia | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Based on etiology | Based on location | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Metabolic | Infectious | Myopathic | Neurological | Structural | Iatrogenic | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| •Amyloidosis •Cushings syndrome •Thyrotoxicosis •Wilsons disease | • Mucositis •Diphtheria •Botulism •Lymes disease •Syphilis | •Connective tissue disease •Dermatomyositis •Myasthenia gravis •Myotonic dystrophy • Polymyositis •Sarcoidosis •Paraneoplastic syndromes | •Brainstem tumors •Head trauma • Stroke • Cerebral palsy • Gullian barre syndrome • Huntington disease • Multiple sclerosis • Postpolio syndrome • Tardive dyskinesia • Metabolic encephalopathies • Amyotrophic lateral sclerosis • Parkinson’s disease • Dementia | • Cricopharyngeal bar • Zenkers diverticulum • Cervical webs • Oropharyngeal tumors • Osteophytes and skeletal abnormalities •Congenital(cleft palate,diverticula,pouches) | •Medication side effects(neuroleptics) • Radiation •Corrosive(pill injury,intentional) •Postsurgical muscular or neurogenic | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Esophageal dysphagia | Oropharyngeal dysphagia | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
References
- ↑ Wilcox CM, Alexander LN, Clark WS (1995). “Localization of an obstructing esophageal lesion. Is the patient accurate?”. Dig Dis Sci. 40 (10): 2192–6. PMID 7587788.
- ↑ Kruger D (2014). “Assessing esophageal dysphagia”. JAAPA. 27 (5): 23–30. doi:10.1097/01.JAA.0000446227.85554.fb. PMID 24691181.
- ↑ Scheurer U (1991). “[Dysphagia]”. Ther Umsch. 48 (3): 150–61. PMID 2042117.
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Feham Tariq, MD [2]
Overview
Dysphagia can result from propulsive failure, motility disorders, structural disorders, intrinsic or extrinsic compression of the oropharynx or esophagus. Propulsive failure can result from dysfunction of the central nervous system control mechanisms, intrinsic musculature, or peripheral nerves. Structural abnormalities may result from surgery, neoplasm, caustic injury, or congenital anomalies.
Pathophysiology
Physiology of normal swallowing
Normal physiology of swallowing can be discussed under three phases:[1][2][3][4]
Oral phase
- Preparatory phase:
- Preparatory phase involves mastication and formation of a bolus in the oral cavity.
- Voluntary phase:
- Voluntary phase is characterized by propelling the bolus into the pharyngeal phase.
- Voluntary phase is controlled by
- Corticobulbar tracts
- Cranial nerves V, VII, and XII.
Pharyngeal phase:
Esophageal phase:
- Once the bolus reaches esophageal phase, esophagus is responsible for moving the bolus along the upper gastrointestinal tract to initiate the process of digestion by delivering it to stomach.[5]
- The esophagus has anti-reflux barrier which prevents the return of the acidic contents of the stomach back to the esophagus.
- The anti-reflux barrier is formed by the lower esophageal sphincter (LES) and a part of the diaphragm.
- The lower esophageal sphincter is contracting smooth muscle located at the end of the esophagus.
- Due to it’s high pressure tone LES, acts as a strong barrier between the esophagus and the stomach contents.

Pathogenesis of physiological dysphagia
Physiological dysphagia occurs as a result of normal aging. Normal aging results in certain changes that affect the swallowing mechanism which include:[6][7][8][9][10]
- Reduced lingual movement.
- Delayed onset of the pharyngeal swallow.
- Delayed upper esophageal sphincter relaxation during swallowing.
- Diminished pharyngo–laryngeal response.
- Decreased nerve function.
- Decline in muscle mass.
Pathogenesis of pathological dysphagia
Pathological dysphagia can occur as a result of the following mechanisms.
1. Luminal Stenosis
2. Non-obstructing gastro-esophageal disease
- Majority of the patients that present with dysphagia will have normal investigation findings.
- Normal findings suggests a somato-sensory dysfunction rather than neuro-muscular cause of dysphagia.[15]
- Non-obstructive causes of dysphagia include:
- Motility disorders of esophagus
- Rheumatological conditions
- Medication induced dysphagia
- Neurological disorders
Motility disorders of esophagus
- Motility disorder of esophagus occurs when there is an imbalance between inhibitory and excitatory neurons of the myenteric plexus at the distal esophageal sphincter.[16][17][18][19]
- This imbalance results in a decrement of inhibitory innervation leading to aperistalsis.[20]
- Reduced inhibitory innervation also leads to failure of relaxation of the lower esophageal sphincter resulting in difficulty in swallowing (dysphagia).[21]
Rheumatological conditions
- The smooth muscle of the mid and lower esophagus is replaced by fibrous tissue secondary to the underlying autoimmune pathology leading to incompetence of the lower esophageal sphincter (LES) and subsequently to GERD and dysphagia.[22][23]
- Most common rheumatological conditions associated with dysphagia include:
Medication induced
- Medications can contribute to dysphagia by making peristalsis difficult either by:[26][27][28][29]
- Decreasing the strength of lower esophageal sphincter relaxation.
- Reducing the lubrication of esophageal lumen by decreasing the salivary secretions.
- Some medications also have a local or systemic immunosuppressant effect can predispose to infective oesophagitis.
Neurological disorders
- Neurological disorders predominanlty affect the oropharyngeal phase. However, pharyngeal phase of swallowing can also be involved in cases of stroke affecting the basal ganglia and the cortex, as it affects the ability to initiate the swallow and decrement in bolus transit between pharynx and esophagus.[31][32][33]
- Neurological deficits can cause weakness of the oral musculature and tongue movements resulting in failure to form a intact food bolus and decreased sensitivity of the pharyngeal receptors, subsequent to neurological compromise leading to dysphagia.
- The central, autonomic or peripheral nervous system is affected by several neurological diseases such as:
Genetics
The following genes can be involved in the development of dysphagia subsequent to different pathologies:
- CTC1
- DKC1
- NHP2
- NOP10
- RTEL1
- TERC
- WRAP53
Mutations in the following genes can cause esophageal cancer:
- Chromosomal losses (4q, 5q, 9p, and 18q)
- Chromosomal gains (8q, 17q, and 20q)
- Gene amplifications (7, 8, and 17q)
- PT53 genes and P16 genes
- Variants in ADH and/or ALDH2 genes
- HLA class II molecules
- Vasoactive intestinal peptide
- KIT
- Interleukin 23 receptor
Associated Conditions
Common conditions associated with dysphagia include:
- Peptic stricture
- Esophageal rings and webs
- Esophageal cancer
- Achalasia
- Spastic motility disorders
- Diffuse esophageal spasm
- Nutcracker esophagus
- Hypertensive lower esophageal sphincter
- Nonspecific spastic esophageal motility disorders
Gross Morphology
The gross morphology of dysphagia depends on the underlying pathologic condition. Following are the gross morphologic features of some important causes of dysphagia:
Zenkers diverticulum:
- Diverticulum or a sac is seen in the esophagus
Esophageal stricture:
- Pale mucosa with white exudate in lymphocytic esophagitis
- Swelling and hemorrhagic congestion in caustic ingestion
- Multiple yellow plaques in infectious esophagitis due to Candida
- Ulceration of the esophagus in viral esophagitis
Esophageal cancer:
Squamous cell carcinoma or adenocarcinoma of the esophagus may appear as:
- Flat and irregular plaque
- Polypoid lesion
- Ulcerating, fungating mass.
- Location:
- Squamous cell carcinoma is usually found in the mid-third of the esophagus.
- Adenocarcinomais usually found in the lower third of the esophagus near the gastric opening.
Achalasia:
- There is defect in the nerves that control the motility of the esophagus (the myenteric plexus).
- The esophagus is dilated and hypertrophied.
Diffuse esophageal spasm(DES):
Gross thickening of muscularis propria layer and lower esophageal sphincter (LES) due to hyperplasia are characteristic findings of DES.
Microscopic Pathology
Esophagitis

Esophageal stricture


References
- ↑ Cook, Ian J.; Kahrilas, Peter J. (1999). “AGA technical review on management of oropharyngeal dysphagia”. Gastroenterology. 116 (2): 455–478. doi:10.1016/S0016-5085(99)70144-7. ISSN 0016-5085.
- ↑ Aslam M, Vaezi MF (2013). “Dysphagia in the elderly”. Gastroenterol Hepatol (N Y). 9 (12): 784–95. PMC 3999993. PMID 24772045.
- ↑ Cassiani RA, Santos CM, Parreira LC, Dantas RO (2011). “The relationship between the oral and pharyngeal phases of swallowing”. Clinics (Sao Paulo). 66 (8): 1385–8. PMC 3161216. PMID 21915488.
- ↑ Dantas RO, Kern MK, Massey BT, Dodds WJ, Kahrilas PJ, Brasseur JG; et al. (1990). “Effect of swallowed bolus variables on oral and pharyngeal phases of swallowing”. Am J Physiol. 258 (5 Pt 1): G675–81. doi:10.1152/ajpgi.1990.258.5.G675. PMID 2333995.
- ↑ Stein HJ, DeMeester TR (1992). “Outpatient physiologic testing and surgical management of foregut motility disorders”. Curr Probl Surg. 29 (7): 413–555. PMID 1606845.
- ↑ Masoro EJ (1987). “Biology of aging. Current state of knowledge”. Arch Intern Med. 147 (1): 166–9. PMID 3541821.
- ↑ Carucci LR, Turner MA (2015). “Dysphagia revisited: common and unusual causes”. Radiographics. 35 (1): 105–22. doi:10.1148/rg.351130150. PMID 25590391.
- ↑ Cook IJ, Weltman MD, Wallace K, Shaw DW, McKay E, Smart RC; et al. (1994). “Influence of aging on oral-pharyngeal bolus transit and clearance during swallowing: scintigraphic study”. Am J Physiol. 266 (6 Pt 1): G972–7. doi:10.1152/ajpgi.1994.266.6.G972. PMID 8023945.
- ↑ Shaw DW, Cook IJ, Gabb M, Holloway RH, Simula ME, Panagopoulos V; et al. (1995). “Influence of normal aging on oral-pharyngeal and upper esophageal sphincter function during swallowing”. Am J Physiol. 268 (3 Pt 1): G389–96. doi:10.1152/ajpgi.1995.268.3.G389. PMID 7900799.
- ↑ Easterling, Caryn S.; Robbins, Elizabeth (2008). “Dementia and Dysphagia”. Geriatric Nursing. 29 (4): 275–285. doi:10.1016/j.gerinurse.2007.10.015. ISSN 0197-4572.
- ↑ Starmer HM, Riley LH, Hillel AT, Akst LM, Best SR, Gourin CG (2014). “Dysphagia, short-term outcomes, and cost of care after anterior cervical disc surgery”. Dysphagia. 29 (1): 68–77. doi:10.1007/s00455-013-9482-9. PMID 23943072.
- ↑ Inayat F, Hussain Q, Shafique K (2017). “Dysphagia Caused by Extrinsic Esophageal Compression From Mediastinal Lymphadenopathy in Patients With Sarcoidosis”. Clin Gastroenterol Hepatol. 15 (7): e119–e120. doi:10.1016/j.cgh.2016.11.010. PMID 27840183.
- ↑ Oda K, Iwakiri R, Hara M, Watanabe K, Danjo A, Shimoda R; et al. (2005). “Dysphagia associated with gastroesophageal reflux disease is improved by proton pump inhibitor”. Dig Dis Sci. 50 (10): 1921–6. doi:10.1007/s10620-005-2962-5. PMID 16187198.
- ↑ Roman S, Kahrilas PJ (2014). “The diagnosis and management of hiatus hernia”. BMJ. 349: g6154. doi:10.1136/bmj.g6154. PMID 25341679.
- ↑ Philpott H, Nandurkar S, Royce SG, Thien F, Gibson PR (2014). “Risk factors for eosinophilic esophagitis”. Clin Exp Allergy. 44 (8): 1012–9. doi:10.1111/cea.12363. PMID 24990069.
- ↑ Xiao Y, Kahrilas PJ, Nicodème F, Lin Z, Roman S, Pandolfino JE (2014). “Lack of correlation between HRM metrics and symptoms during the manometric protocol”. Am J Gastroenterol. 109 (4): 521–6. doi:10.1038/ajg.2014.13. PMC 4120962. PMID 24513804.
- ↑ Enestvedt BK, Williams JL, Sonnenberg A (2011). “Epidemiology and practice patterns of achalasia in a large multi-centre database”. Aliment Pharmacol Ther. 33 (11): 1209–14. doi:10.1111/j.1365-2036.2011.04655.x. PMC 3857989. PMID 21480936.
- ↑ Howard PJ, Maher L, Pryde A, Cameron EW, Heading RC (1992). “Five year prospective study of the incidence, clinical features, and diagnosis of achalasia in Edinburgh”. Gut. 33 (8): 1011–5. PMC 1379432. PMID 1398223.
- ↑ Pandolfino JE, Gawron AJ (2015). “Achalasia: a systematic review”. JAMA. 313 (18): 1841–52. doi:10.1001/jama.2015.2996. PMID 25965233.
- ↑ Gockel I, Lord RV, Bremner CG, Crookes PF, Hamrah P, DeMeester TR (2003). “The hypertensive lower esophageal sphincter: a motility disorder with manometric features of outflow obstruction”. J Gastrointest Surg. 7 (5): 692–700. PMID 12850684.
- ↑ Vaezi MF, Pandolfino JE, Vela MF (2013). “ACG clinical guideline: diagnosis and management of achalasia”. Am J Gastroenterol. 108 (8): 1238–49, quiz 1250. doi:10.1038/ajg.2013.196. PMID 23877351.
- ↑ Bredenoord AJ (2015). “Minor Disorders of Esophageal Peristalsis: Highly Prevalent, Minimally Relevant?”. Clin Gastroenterol Hepatol. 13 (8): 1424–5. doi:10.1016/j.cgh.2015.03.013. PMID 25796576.
- ↑ Anselmino M, Zaninotto G, Costantini M, Ostuni P, Ianniello A, Boccú C; et al. (1997). “Esophageal motor function in primary Sjögren’s syndrome: correlation with dysphagia and xerostomia”. Dig Dis Sci. 42 (1): 113–8. PMID 9009125.
- ↑ Carlson DA, Hinchcliff M, Pandolfino JE (2015). “Advances in the evaluation and management of esophageal disease of systemic sclerosis”. Curr Rheumatol Rep. 17 (1): 475. doi:10.1007/s11926-014-0475-y. PMC 4343525. PMID 25475597.
- ↑ Tang DM, Pathikonda M, Harrison M, Fisher RS, Friedenberg FK, Parkman HP (2013). “Symptoms and esophageal motility based on phenotypic findings of scleroderma”. Dis Esophagus. 26 (2): 197–203. doi:10.1111/j.1442-2050.2012.01349.x. PMID 22590983.
- ↑ Bonavina L, DeMeester TR, McChesney L, Schwizer W, Albertucci M, Bailey RT (1987). “Drug-induced esophageal strictures”. Ann Surg. 206 (2): 173–83. PMC 1493104. PMID 3606243.
- ↑ Philpott-Howard JN, Wade JJ, Mufti GJ, Brammer KW, Ehninger G (1993). “Randomized comparison of oral fluconazole versus oral polyenes for the prevention of fungal infection in patients at risk of neutropenia. Multicentre Study Group”. J Antimicrob Chemother. 31 (6): 973–84. PMID 8360134.
- ↑ Sagar R, Varghese ST, Balhara YP (2005). “Dysphagia due to olanzepine, an antipsychotic medication”. Indian J Gastroenterol. 24 (1): 37–8. PMID 15778537.
- ↑ McCord GS, Clouse RE (1990). “Pill-induced esophageal strictures: clinical features and risk factors for development”. Am J Med. 88 (5): 512–8. PMID 2186626.
- ↑ Kohen I, Lester P (2009). “Quetiapine-associated dysphagia”. World J Biol Psychiatry. 10 (4 Pt 2): 623–5. doi:10.1080/15622970802176495. PMID 18615368.
- ↑ Takizawa C, Gemmell E, Kenworthy J, Speyer R (2016). “A Systematic Review of the Prevalence of Oropharyngeal Dysphagia in Stroke, Parkinson’s Disease, Alzheimer’s Disease, Head Injury, and Pneumonia”. Dysphagia. 31 (3): 434–41. doi:10.1007/s00455-016-9695-9. PMID 26970760.
- ↑ Martino R, Foley N, Bhogal S, Diamant N, Speechley M, Teasell R (2005). “Dysphagia after stroke: incidence, diagnosis, and pulmonary complications”. Stroke. 36 (12): 2756–63. doi:10.1161/01.STR.0000190056.76543.eb. PMID 16269630.
- ↑ Martino R, Pron G, Diamant N (2000). “Screening for oropharyngeal dysphagia in stroke: insufficient evidence for guidelines”. Dysphagia. 15 (1): 19–30. doi:10.1007/s004559910006. PMID 10594255.
- ↑ From en.wikipedia.org, Public Domain, <“https://commons.wikimedia.org/w/index.php?curid=1931423“>
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2]Kiran Singh, M.D. [3]
Overview
Dysphagia can be caused by many diseases such as neurological disorders, structural disorders of esophagus, tumors and motor disorders.
Causes
Depending upon the type of dysphagia, causes can be categorized into two subsections.[1][2][3][4]
Common Causes of Oropharyngeal Dysphagia
| Common causes of oropharyngeal dysphagia | ||
|---|---|---|
| Neurological | Medication side effects | Others |
|
| |
Common causes of Esophageal Dysphagia
The common causes of esophageal dysphagia can be divided into four categories.[5][6][7][8][9]
| Structural (Mechanical) disorders | Motor disorders | Esophageal tumors | Systemic diseases | Miscellaneous | ||||
|---|---|---|---|---|---|---|---|---|
| Intrinsic compression | Extrinsic Compression | Primary | Secondary | |||||
Mucosal rings and webs
|
Strictures: | Vascular compression:
|
|
|
|
|
|
|
Less Common Causes
Less common causes of dysphagia include:
- Scleredema adultorum[10][11]
- Post chemotherapy and radiation therapy[12]
- Descending thoracic aorta aneurysm[13]
- Hypertrophy of cricopharyngeal muscles[14]
Causes by Organ System
The causes of dysphagia based on the organ system are as follows:[15][16]
References
- ↑ Starmer HM, Riley LH, Hillel AT, Akst LM, Best SR, Gourin CG (2014). “Dysphagia, short-term outcomes, and cost of care after anterior cervical disc surgery”. Dysphagia. 29 (1): 68–77. doi:10.1007/s00455-013-9482-9. PMID 23943072.
- ↑ Inayat F, Hussain Q, Shafique K (2017). “Dysphagia Caused by Extrinsic Esophageal Compression From Mediastinal Lymphadenopathy in Patients With Sarcoidosis”. Clin Gastroenterol Hepatol. 15 (7): e119–e120. doi:10.1016/j.cgh.2016.11.010. PMID 27840183.
- ↑ Oda K, Iwakiri R, Hara M, Watanabe K, Danjo A, Shimoda R; et al. (2005). “Dysphagia associated with gastroesophageal reflux disease is improved by proton pump inhibitor”. Dig Dis Sci. 50 (10): 1921–6. doi:10.1007/s10620-005-2962-5. PMID 16187198.
- ↑ Roman S, Kahrilas PJ (2014). “The diagnosis and management of hiatus hernia”. BMJ. 349: g6154. doi:10.1136/bmj.g6154. PMID 25341679.
- ↑ Xiao Y, Kahrilas PJ, Nicodème F, Lin Z, Roman S, Pandolfino JE (2014). “Lack of correlation between HRM metrics and symptoms during the manometric protocol”. Am J Gastroenterol. 109 (4): 521–6. doi:10.1038/ajg.2014.13. PMC 4120962. PMID 24513804.
- ↑ Enestvedt BK, Williams JL, Sonnenberg A (2011). “Epidemiology and practice patterns of achalasia in a large multi-centre database”. Aliment Pharmacol Ther. 33 (11): 1209–14. doi:10.1111/j.1365-2036.2011.04655.x. PMC 3857989. PMID 21480936.
- ↑ Howard PJ, Maher L, Pryde A, Cameron EW, Heading RC (1992). “Five year prospective study of the incidence, clinical features, and diagnosis of achalasia in Edinburgh”. Gut. 33 (8): 1011–5. PMC 1379432. PMID 1398223.
- ↑ Pandolfino JE, Gawron AJ (2015). “Achalasia: a systematic review”. JAMA. 313 (18): 1841–52. doi:10.1001/jama.2015.2996. PMID 25965233.
- ↑ Gockel I, Lord RV, Bremner CG, Crookes PF, Hamrah P, DeMeester TR (2003). “The hypertensive lower esophageal sphincter: a motility disorder with manometric features of outflow obstruction”. J Gastrointest Surg. 7 (5): 692–700. PMID 12850684.
- ↑ Chatterjee S, Hedman BJ, Kirby DF (2017). “An Unusual Cause of Dysphagia”. J Clin Rheumatol. doi:10.1097/RHU.0000000000000666. PMID 29280826.
- ↑ Wright RA, Bernie H (1982). “Scleredema adultorum of Buschke with upper esophageal involvement”. Am J Gastroenterol. 77 (1): 9–11. PMID 7064968.
- ↑ Nguyen NP, Sallah S, Karlsson U, Antoine JE (2002). “Combined chemotherapy and radiation therapy for head and neck malignancies: quality of life issues”. Cancer. 94 (4): 1131–41. PMID 11920484.
- ↑ Conte, Blagio A. (1966). “Dysphagia Caused by an Aneurysm of the Descending Thoracic Aorta”. New England Journal of Medicine. 274 (17): 956–957. doi:10.1056/NEJM196604282741710. ISSN 0028-4793.
- ↑ Benedict, Edward B.; Sweet, Richard H. (1955). “Dysphagia Due to Hypertrophy of the Cricopharyngeus Muscle or Hypopharyngeal Bar”. New England Journal of Medicine. 253 (26): 1161–1162. doi:10.1056/NEJM195512292532607. ISSN 0028-4793.
- ↑ Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016
- ↑ Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X
Differentiating Dysphagia from other Conditions

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2]
Overview
Several diseases such as reflux esophagitis, esophageal carcinoma, systemic sclerosis, esophageal spasm, pseudoachalasia, stroke, esophageal candidiasis and Chagas disease can present with dysphagia, and hence must be differentiated from one another.
Dysphagia Differential Diagnosis
To review the differential diagnosis of dysphagia click here.
To review the differential diagnosis of dysphagia and weight loss click here.
To review the differential diagnosis of dysphagia and heartburn click here.
To review the differential diagnosis of dysphagia, weight loss and heartburn click here.
Dysphagia
| 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 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Several diseases such as reflux esophagitis, esophageal carcinoma, systemic sclerosis, esophageal spasm, pseudoachalasia, stroke, esophageal candidiasis and Chagas disease can present with dysphagia, and hence must be differentiated from one another.[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 | +/- | – | Normal |
|
|
|
Triad of | |
| Esophageal stricture | Gradual or sudden | + | – | Progressive | +/- | +/- | Normal |
|
|
|
||
| Diffuse esophageal spasm | Sudden | + | + | Non progressive | + | + | Normal |
|
|
|
||
| Achalasia | Gradual | + | + | Non progressive | +/- | – |
|
Normal |
|
|||
| Systemic sclerosis | Gradual | + | + | Progressive | +/- | + |
|
Normal |
|
|
Positive serology for | |
| Zenker’s diverticulum | Gradual | + | – | +/- | – |
|
Normal |
|
|
| ||
| Esophageal carcinoma | Gradual | + | + | Progressive | + | +/- | Normal |
|
|
|||
| Stroke | Sudden | + | + | Progressive | + | +/- |
|
Impaired |
|
|
||
| Motor disorders | Gradual | + | + | Progressive | +/- | Normal |
|
|
|
| ||
| GERD | Gradual or
sudden onset |
+ | – | Progressive | +/- | + | Normal |
|
|
| ||
| Esophageal web | Gradual | + | +/- | Progressive | – | +/- |
|
Normal |
|
|
|
|
- For the differential diagnosis based on dysphagia and weight loss click here.
- For the differential diagnosis based on dysphagia and heartburn click here.
References
- ↑ Ferri, Fred (2015). Ferri’s clinical advisor 2015 : 5 books in 1. Philadelphia, PA: Elsevier/Mosby. ISBN 978-0323083751.
- ↑ Boeckxstaens GE, Zaninotto G, Richter JE (2013). “Achalasia”. Lancet. doi:10.1016/S0140-6736(13)60651-0. PMID 23871090.
- ↑ 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.
- ↑ 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.
- ↑ Matsuura H (2017). “Diffuse Esophageal Spasm: Corkscrew Esophagus”. Am. J. Med. doi:10.1016/j.amjmed.2017.08.041. PMID 28943381.
- ↑ Lassen JF, Jensen TM (1992). “[Corkscrew esophagus]”. Ugeskr. Laeg. (in Danish). 154 (5): 277–80. PMID 1736462.
- ↑ 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.
- ↑ Shami VM (2014). “Endoscopic management of esophageal strictures”. Gastroenterol Hepatol (N Y). 10 (6): 389–91. PMC 4080876. PMID 25013392.
- ↑ 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.
- ↑ Chisholm M (1974). “The association between webs, iron and post-cricoid carcinoma”. Postgrad Med J. 50 (582): 215–9. PMC 2495558. PMID 4449772.
- ↑ 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.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2], Hamid Qazi, MD, BSc [3]
Overview
Dysphagia is a common symptom seen in the elderly poplulation owing to senile physiological changes in the muscles involved in deglutition. The prevalance of dysphagia in the elderly population is 7% to 22% per 100,000 individuals. Patients of all age groups may develop dysphagia and the incidence of dysphagia increases with age.
Epidemiology and Demographics
The epidemiology and demographics of dysphagia are as follows:[1][2][3][4][5][6][7][8][9][10][11][12][13]
Incidence
- The annual incidence of esophageal food impaction is 25 per 100,000 persons per year.
- There are a number of causes of different types of dysphagia across the world of which the most common is stroke among the elderly.
- In Asia, esophageal squamous cell cancer is a common cause of dysphagia while in Africa, Chagas disease is a prevailing etiology.[14]
- The incidence progressively increases with age, reaching the peak around seventh decade of life.
- The incidence is higher in males as compared to females.
Prevalance
- The prevalance of dysphagia in the elderly population is 7% to 22% per 100,000 individuals.
- It increases to 40% to 50% per 100,000 individuals among geriatric population residing in long-term care facility.
- Increased prevalance of dysphagia is found in post-stroke patients, acute care settings and nursing care facilities.
Age
- Patients of all age groups may develop dysphagia, resulting either from structural damage, congenital abnormalities and medical conditions.
- The incidence of dysphagia increases with age.
References
- ↑ Gretarsdottir HM, Jonasson JG, Björnsson ES (2015). “Etiology and management of esophageal food impaction: a population based study”. Scand J Gastroenterol. 50 (5): 513–8. doi:10.3109/00365521.2014.983159. PMID 25704642.
- ↑ Sperry SL, Crockett SD, Miller CB, Shaheen NJ, Dellon ES (2011). “Esophageal foreign-body impactions: epidemiology, time trends, and the impact of the increasing prevalence of eosinophilic esophagitis”. Gastrointest Endosc. 74 (5): 985–91. doi:10.1016/j.gie.2011.06.029. PMC 3951006. PMID 21889135.
- ↑ Siebens H, Trupe E, Siebens A, Cook F, Anshen S, Hanauer R; et al. (1986). “Correlates and consequences of eating dependency in institutionalized elderly”. J Am Geriatr Soc. 34 (3): 192–8. PMID 3950287.
- ↑ Easterling CS, Robbins E (2008). “Dementia and dysphagia”. Geriatr Nurs. 29 (4): 275–85. doi:10.1016/j.gerinurse.2007.10.015. PMID 18694703.
- ↑ Schweizer V (2010). “[Swallowing disorders in the elderly]”. Rev Med Suisse. 6 (265): 1859–62. PMID 21053492.
- ↑ Lindgren S, Janzon L (1991). “Prevalence of swallowing complaints and clinical findings among 50-79-year-old men and women in an urban population”. Dysphagia. 6 (4): 187–92. PMID 1778094.
- ↑ Martino R, Foley N, Bhogal S, Diamant N, Speechley M, Teasell R (2005). “Dysphagia after stroke: incidence, diagnosis, and pulmonary complications”. Stroke. 36 (12): 2756–63. doi:10.1161/01.STR.0000190056.76543.eb. PMID 16269630.
- ↑ Rösler, Alexander; Pfeil, Silke; Lessmann, Hendrik; Höder, Jürgen; Befahr, Alina; von Renteln-Kruse, Wolfgang (2015). “Dysphagia in Dementia: Influence of Dementia Severity and Food Texture on the Prevalence of Aspiration and Latency to Swallow in Hospitalized Geriatric Patients”. Journal of the American Medical Directors Association. 16 (8): 697–701. doi:10.1016/j.jamda.2015.03.020. ISSN 1525-8610.
- ↑ Wilkins T, Gillies RA, Thomas AM, Wagner PJ (2007). “The prevalence of dysphagia in primary care patients: a HamesNet Research Network study”. J Am Board Fam Med. 20 (2): 144–50. doi:10.3122/jabfm.2007.02.060045. PMID 17341750.
- ↑ Logemann, Jeri A. (1998). Evaluation and treatment of swallowing disorders. Austin, Tex: Pro-Ed. ISBN 0-89079-728-5.
- ↑ Shamburek RD; Farrar JT. Disorders of the digestive system in the elderly. N Engl J Med 1990 Feb 15;322(7):438-43.
- ↑ Allepaerts S, Delcourt S, Petermans J (2014). “[Swallowing disorders in elderly patients: a multidisciplinary approach]”. Rev Med Liege. 69 (5–6): 349–56. PMID 25065244.
- ↑ Carucci LR, Turner MA (2015). “Dysphagia revisited: common and unusual causes”. Radiographics. 35 (1): 105–22. doi:10.1148/rg.351130150. PMID 25590391.
- ↑ Malagelada JR, Bazzoli F, Boeckxstaens G, De Looze D, Fried M, Kahrilas P; et al. (2015). “World gastroenterology organisation global guidelines: dysphagia–global guidelines and cascades update September 2014”. J Clin Gastroenterol. 49 (5): 370–8. doi:10.1097/MCG.0000000000000307. PMID 25853874.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2], Hamid Qazi, MD, BSc [3]
Overview
Common risk factors in the development of dysphagia include smoking, obesity, pregnancy, hiatal hernia, scleroderma, alcohol consumption, consuming drinks that contain caffeine, and medications. Medications include anticholinergics, beta blockers, bronchodilators, calcium channel blockers, dopamine-active drugs for Parkinson’s disease, progestin for abnormal menstrual bleeding or birth control, sedatives for insomnia or anxiety, and tricyclic antidepressants.
Dysphagia risk factors
Common risk factors in the development of dysphagia include:[1][2][3][4][5][6]
- Aging
- Dementia
- Stroke
- 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
References
- ↑ “Genetic dissection of eosinophilic esophagitis provides insight into disease pathogenesis and treatment strategies. – PubMed – NCBI”.
- ↑ “www.ncbi.nlm.nih.gov” (PDF).
- ↑ “Genetics of Eosinophilic Esophagitis – FullText – Digestive Diseases 2014, Vol. 32, No. 1-2 – Karger Publishers”.
- ↑ Furuta GT, Katzka DA (2015). “Eosinophilic Esophagitis”. N. Engl. J. Med. 373 (17): 1640–8. doi:10.1056/NEJMra1502863. PMC 4905697. PMID 26488694.
- ↑ Kocsis D, Tulassay Z, Juhász M (2015). “[Dietary and pharmacological aspects of eosinophilic esophagitis]”. Orv Hetil (in Hungarian). 156 (23): 927–32. doi:10.1556/650.2015.30164. PMID 26027600.
- ↑ Jarosz M, Taraszewska A (2014). “Risk factors for gastroesophageal reflux disease: the role of diet”. Prz Gastroenterol. 9 (5): 297–301. doi:10.5114/pg.2014.46166. PMC 4223119. PMID 25396005.
Screening
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2], Hamid Qazi, MD, BSc [3]
Overview
There is insufficient evidence to recommend routine screening for dysphagia.
Screening
There is insufficient evidence to recommend routine screening for dysphagia.
References
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2], Hamid Qazi, MD, BSc [3]
Overview
If left untreated, dysphagia can potentially cause aspiration pneumonia, malnutrition, or dehydration. Common complications of dysphagia include aspiration pneumonia, malnutrition, dehydration. Prognosis of dysphagia is dependent on the underlying disease. However, prognosis is generally regarded as good.
Natural History, Complications, and Prognosis
Natural History
- The symptoms of dysphagia usually develop in any decade of life, and start with symptoms such as difficulty eating solids or drinking fluids. If left untreated, dysphagia can potentially cause aspiration pneumonia, malnutrition, or dehydration.[1][2]
Complications
- Common complications of dysphagia include:
Prognosis
- Depending on the extent of the disease causing dysphagia at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good.
References
- ↑ Philpott, Hamish; Garg, Mayur; Tomic, Dunya; Balasubramanian, Smrithya; Sweis, Rami (2017). “Dysphagia: Thinking outside the box”. World Journal of Gastroenterology. 23 (38): 6942–6951. doi:10.3748/wjg.v23.i38.6942. ISSN 1007-9327.
- ↑ Cho, S. Y.; Choung, R. S.; Saito, Y. A.; Schleck, C. D.; Zinsmeister, A. R.; Locke, G. R.; Talley, N. J. (2015). “Prevalence and risk factors for dysphagia: a USA community study”. Neurogastroenterology & Motility. 27 (2): 212–219. doi:10.1111/nmo.12467. ISSN 1350-1925.
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Chest X Ray | X Ray | Barium Swallow | Endoscopy | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
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