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Dysphagia

Dr. Ravi Gadani


MS, FMAS
Introduction
• Dysphagia—difficulty with swallowing—is a common condition
• Reported by 7-10% of the general population aged over 50 years,
• 16% of the elderly
• Up to 25% of hospitalized patients
• Oropharyngeal dysphagia, is even more common in the chronic-care
setting; up to 60% of nursing-home occupants have feeding difficulties
that include dysphagia.
Swallowing
• Involves the actions of 26 muscles and 5 cranial nerves.
• A normal adult swallows unconsciously 600 times a day
Swallowing
Cranial Function
Nerve
V Both sensory and motor fibres; important in chewing
VII Both sensory and motor fibres; important for sensation of
oropharynx & taste to anterior 2/3 of tongue
IX Both sensory and motor fibres; important for taste to posterior
tongue, sensory and motor functions of the pharynx
X Both sensory and motor fibres; important for taste to oropharynx,
and sensation and motor function to larynx and laryngopharynx;
important for airway protection
XII Motor fibres that primarily innervate the tongue
Anatomy
Esophageal Anatomy
• Upper one-third is composed of skeletal muscle
• Distal two-thirds is smooth muscle
• NO SEROSA
• Outer longitudinal, inner circular muscle layer
• Myenteric plexus of Auerbach, parasympathetic ganglion cells,
interspersed among the muscle layers
• Submucosa – blood vessels/lymphatics, myenteric plexus of Meissner
(parasympathetic ganglion cells)
• Mucosa – stratified squamous epithelium
Phases

Oropharyngea
Oral Esophageal
l
Food enters oral Mastication &
cavity bolus formation

Tongue elevates
and propels
bolus to pharynx
Tongue elevates and
Food enters oral Mastication & bolus Soft palate elevates
propels bolus to
cavity formation to seal nasopharynx
pharynx

Larynx & hyoid bone Epiglottis moves


move anterior and posteriorly & Respiration stops Pharynx shortens
upwards downwards to close

Upper esophageal Bolus passes to


sphincter relaxes esophagus
Tongue elevates and
Food enters oral Mastication & bolus Soft palate elevates
propels bolus to
cavity formation to seal nasopharynx
pharynx

Larynx & hyoid bone Epiglottis moves


move anterior and posteriorly & Respiration stops Pharynx shortens
upwards downwards to close

Upper esophageal Bolus passes to Esophagus contracts Lower esophageal


sphincter relaxes esophagus serially sphincter relaxes

Bolus reaches
stomach
HISTORY
• Taking a careful history is vital for the evaluation of dysphagia.
• The history will yield the likely underlying -pathophysiologic process
-anatomic site of the problem in most patients - 80%
• Crucial for determining whether subsequently detected radiographic
or endoscopic 'anomalies' are relevant or incidental.
HISTORY
• First, establish whether or not dysphagia is actually present
• Globus sensation (in b/w meals),
• Xerostomia-lose the lubrication properties and stimulus
• Odynophagia- pain w/swallowing, transient than dysphagia, and
persists only during the 15–30s that a bolus takes to traverse the
esophagus.
• Second, determine whether the site of the problem is esophageal or
oropharyngeal.
• Third , distinguish a structural abnormality from a motor disorder.
Where is the site of bolus hold-up?
• Retrosternal bolus hold-up indicates that the disorder lies within the
esophagus.
Symptoms that suggest
oropharyngeal cause
• 4 symptoms have high specificity for oropharyngeal dysfunction:
• delayed or absent oropharyngeal swallow initiation
• deglutitive postnasal regurgitation or egress of fluid through the nose during
swallowing
• deglutitive cough indicative of aspiration
• the need to swallow repetitively to achieve satisfactory clearance of
swallowed material from the hypopharynx.
Dysphagia for solids or liquids
• Patients who have a motor disorder will describe dysphagia for BOTH
liquids and solids.
• Patients who have structural disorders will describe dysphagia for
solids only.
• Once a solid bolus becomes impacted, the patient will report
dysphagia for liquids and solids.
Dysphagia intermittent or
progressive
• Slowly progressive, long-standing dysphagia, particularly against a
background of reflux, is suggestive of a peptic stricture.
• A short history of dysphagia—particularly with rapid progression
(weeks or months) and associated weight loss—is highly suggestive of
esophageal cancer.
• Long-standing, intermittent, non-progressive dysphagia purely for
solids is indicative of a fixed structural lesion such as a distal
esophageal ring or proximal esophageal mucosal web.
Associated Symptoms and Possible
Etiologies of Dysphagia
• Progressive dysphagia -> Neuromuscular dysphagia
• Sudden dysphagia -> Obstructive dysphagia, esophagitis
• Difficulty initiating swallow -> Oropharyngeal dysphagia
• Food "sticks" after swallow -> Esophageal dysphagia
• Cough Early in swallow -> Neuromuscular dysphagia
Associated Symptoms and Possible
Etiologies of Dysphagia
• Cough Late in swallow -> Obstructive dysphagia
• Weight loss In the elderly -> Carcinoma
• Weight loss with regurgitation -> Achalasia
• Progressive symptoms Heartburn -> Peptic stricture, scleroderma
• Intermittent symptoms -> Rings and webs, diffuse esophageal spasm,
nutcracker esophagus
Associated Symptoms and Possible
Etiologies of Dysphagia
• Pain with dysphagia -> Esophagitis, Infectious (HSV, monilia), Pill-
induced
• Pain made worse by: Solids only -> Obstructive dysphagia
• Pain made worse by: Solids and liquids -> Neuromuscular dysphagias
• Regurgitation of old food -> Zenker's diverticulum
Associated Symptoms and Possible
Etiologies of Dysphagia
• Weakness and dysphagia -> Cerebrovascular accidents, muscular
dystrophies, myasthenia gravis, multiple sclerosis
• Halitosis -> diverticulum
• Dysphagia relieved with repeated swallows -> Achalasia
• Dysphagia made worse with cold foods -> Neuromuscular motility
disorders
Etiology of Oropharyngeal
Dysphagia 
• Structural/Obstructive
• Head or neck tumors
• Postsurgical/Radiation stenosis
• Cervical spondylosis
• Zenker's diverticulum
• Cricopharyngeal web
• Infectious (tonsilar hypertrophy/abscess)
• Extrinsic compression (goiter)
Etiology of Oropharyngeal
Dysphagia 
• Neuromuscular • Myasthenia Gravis
• CVA • Botulism
• Eaton-Lambert Syndrome
• Alzheimer’s, Parkinson's disease
• Myopathies
• Brain stem tumors • Polymyositis
• Degenerative/Demylenating diseases • Dermatomyositis
• ALS, MS, Huntington's • Muscular dystrophy (myotonic
• Acute transverse myelitis, ADEM, and dystrophy, oculopharyngeal dystrophy)
acute hemorrhagic leukoencephalitis • Thyroid myopathy
• Sjogren’s • Amyloidosis
• Postinfectious • Cricopharyngeal (upper esophageal
• Poliomyelitis, Syphilis sphincter)
• Peripheral nervous system • Sarcoidosis
• Peripheral neuropathy • Paraneoplastic Syndromes
• Motor end-plate dysfunction
Causes of Esophageal Dysphagia
• Structural disorders • Pemphigus and pemphigoid conditions
• Inflammatory and/or fibrotic • Lichen planus
strictures • Scleroderma (multifactorial)
• Peptic • Intramural lesions
• Caustic • Leiomyoma
• Pill-induced • Granular cell tumor
• Radiation-induced • Sarcoidosis
• Mucosal rings and webs • Extramural lesions
• Schatzki's ring • Aberrant right subclavian artery
(dysphagia lusoria)
• Multiringed esophagus (eosinophilic • Mediastinal masses (thyroidomegaly)
esophagitis)
• Bronchial carcinoma
• Foreign body
• Anatomical abnormalities
• Carcinoma • Hiatal hernia
• Primary (squamous, adenocarcinoma)
• Esophageal diverticulum
• Secondary (e.g. breast, melanoma)
• Disorders related to Systemic Diseases
Causes of Esophageal Dysphagia
• Neuromuscular/Motility • Hypertensive lower esophageal
sphincter
disorders • Nutcracker esophagus
• Achalasia (idiopathic or secondary) • Diabetes
• Spastic motor disorders • Amyloidosis
• Diffuse esophageal spasm
Physical Exam
• If oropharyngeal dysphagia is suspected, evaluation for
neuromuscular disorders is important.
• Thorough neurological, head and neck exam
• Skin should be examined for features of connective tissue disorders,
particularly scleroderma and CREST syndrome.
Physical Exam
• Muscle weakness or wasting might be evident if myositis is present,
and myositis can overlap with other connective tissue disorders that
affect the esophagus.
• Look for tremors, rigidity, fasciculations
• Signs of malnutrition, weight loss and pulmonary complications from
aspiration should be looked for.
Laboratory and Imaging
• CBC to screen for infectious or inflammatory conditions
• TFT’s may detect hypo- or hyperthyroid-associated causes of
dysphagia ( Grave's disease or thyroid carcinoma),
• Anti-acetylcholine antibodies to diagnose myasthenia gravis
• Muscular enzymes to diagnose myositis
• Autoimmune studies (ANA, RF, Anti-SSA, Anti-SSB, Anti-Scl-70, anti-
centromere)
• CT/MRI to evaluate for CVA, MS, tumors
Investigations
• Video Fluoroscopic Swallowing Study (VFSS)
• “Modified barium swallow", is the "gold standard" for diagnosing
oropharyngeal dysphagia.
• Dynamic test in which the patient is asked to swallow a variety of food items
of different consistencies covered with barium.
• A video fluoroscopic recording is made in both A/P and lateral views.
• Allows for observation of bolus progress throughout the different stages of
the swallowing process.
Investigations
• Video Endoscopic Swallowing Study (VESS)
• Direct visualization of the oropharynx in action with and without swallowing,
using a fiberoptic scope inserted nasally.
• This test is valuable when VFSS can not be performed and is usually done by
an otolaryngologist
• Barium swallow studies
• Initial recommended test if esophageal dysphagia is suspected
• Suspected obstructive lesion (e.g., Schatzki's ring, tumor)
• Suspected esophageal motility disorder
Investigations
• EGD
• Suspected acute obstructive lesion (impacted food bolus)
• Evaluation of the esophageal mucosa
• Confirmation of a positive barium study with biopsies or cytology
• Manometry
• Abnormality not identified on barium study or by endoscopy
NO DYSPHAGIA
INTERMITTENT DYSPHAGIA FOR
SOLIDS
DYSPHAGIA WITH LONG HX OF
GERD
DYSPHAGIA FOR SOLIDS AND
LIQUIDS WITH WT LOSS
Management of Oropharyngeal
Dysphagia
• Treat underlying cause
• Determine whether patient can obtain adequate nutrition orally and
risk of aspiration
• Feeding tube should be considered, although no evidence that it
reduces risk of aspiration, so tracheostomy may also be needed.
Management of Oropharyngeal
Dysphagia
• Dietary modifications
• Thickened liquids when tongue function is disordered or laryngeal closure is
impaired.
• Thin liquids are used for weak pharyngeal contraction and reduced
cricopharyngeal opening.
• Facilitatory techniques, such as strengthening exercises, biofeedback,
thermal and gustatory stimulation.
Management Options for
Esophageal Dysphagia
Condition Conservative treatment Invasive treatment
Diffuse esophageal Serial dilations or longitudinal
Nitrate, calcium channel blockers
spasms myotomy
Soft food, anticholinergics, Dilation, botulinium toxin
Achalasia
calcium channel blockers injections, Hellers myotomy
Anti-reflux, systemic medical
Scleroderma None
management of scleroderma
Anti-reflux drugs (H2 blockers,
GERD PPIs) and prokinetic agents Fundoplication
(Reglan)
Infectious esophagitis Antibiotics (nystatin, acyclovir) None
Endoscopic or external repair in
Zenker’sdiverticulum None addition to cricopharyngeal
myotomy
Schatzki_s ring Soft food Dilation

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