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Lianne Beck, MD

Assistant Professor
Emory Family Medicine
 Define dysphagia
 Know the 2 main types and how to
differentiate them
 Learn the major causes of dysphagia
 Understand how to work up a patient with
dysphagia
 Become familiar with the treatment options
 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.
 Involves the actions of 26 muscles and 5 cranial nerves
 CN V -- both sensory and motor fibers; important in chewing

 CN VII -- both sensory and motor fibers; important for sensation of


oropharynx & taste to anterior 2/3 of tongue

 CN IX -- both sensory and motor fibers; important for taste to


posterior tongue, sensory and motor functions of the pharynx

 CN X -- both sensory and motor fibers; important for taste to


oropharynx, and sensation and motor function to larynx and
laryngopharynx; important for airway protection

 CN XII -- motor fibers that primarily innervate the tongue

 A normal adult swallows unconsciously 600 times a day


 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
 The outermost collection, lying between
the inner circular and outer longitudinal
smooth-muscle layers of the gut, is called
the myenteric (or Auerbach's) plexus.
 Neurons of this plexus regulate the
peristaltic waves, consisting of polarized
muscular activity, that move digestive
products from oral to anal openings.
 In addition, myenteric neurons control
local muscular contractions that are
responsible for stationary mixing and
churning.
 The innermost group of neurons is called
the submucosal (or Meissner's) plexus.
This group regulates the configuration of
the luminal surface, controls glandular
secretions, alters electrolyte and water
transport, and regulates local blood flow
 Oral
 Food ingested, prepared
(mastication) and modified
(lubrication)
 Voluntary control
 Frequently results from
weakness – lips, tongue,
cheeks
 Unable to organize food into
well formed bolus and move
posteriorly
 Xerostomia – difficulty
breaking down solids
 Pharyngeal
 Prevented from entering
nasopharynx, larynx rises,
retroflexion of epiglottis and vocal
fold closure, synchronized
contraction of middle and inferior
constrictors, and synchronized
relaxation of the cricopharyngeal
muscle -Involuntary
 Timing – neurologic – epiglottis
doesn’t protect larynx - leads to
cough/aspiration
 Weakness – neurologic injury/cancer
– residual food after swallow – can
lead to aspiration
 Esophageal
 Begins with crico-
pharyngeal relaxation
 Involuntary
 Most common
 Sensation of food
sticking at base of
throat/chest
 Peristalsis, tumor,
stricture
 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.
 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.
 The history will also dictate whether the next diagnostic
procedure should be endoscopy or barium swallow.
 Retrosternal bolus hold-up indicates that the disorder
lies within the esophagus.
 However, the patient's perception of an apparent
bolus hold-up in the neck has low diagnostic
specificity, and cervical localization per se does not
help the clinician to distinguish pharyngeal from
esophageal causes of dysphagia.
 Owing to viscerosomatic referral, in 30% of cases the
perceived site of hold-up is above the suprasternal
notch when the actual hold-up is within the
esophageal.
 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.
 If one or more of these four symptoms are present then the cause
of dysphagia is probably oropharyngeal, either structural or
neuromyogenic
 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
 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
 Pain with dysphagia -> Esophagitis: Postradiation, 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
 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
 Oropharyngeal function
 Xerostomia
 Sedation, pharyngeal
▪ Anticholinergics
weakness, dystonia
▪ Antihypertensives
▪ Benzodiazepines
▪ Antihistamines
▪ Neuroleptics
▪ Antipsychotics
▪ Anticonvulsants
▪ Narcotics
• Myopathy
▪ Anticonvulsants
• Corticosteroids
▪ Antiparkinsonian agents
▪ Lipid-lowering drugs
▪ Antineoplastics
• Inflammation/swelling
▪ Antidepressants
▪ Antibiotics
▪ Anxiolytics
▪ Muscle relaxants
▪ Diuretics
 Esophageal function
 Inflammation (resulting from irritation by pill)
▪ Tetracycline, Doxycycline (Vibramycin)
▪ Iron preparations
▪ Quinidine
▪ Nonsteroidal anti-inflammatory drugs
▪ Potassium
 Impaired motility or exacerbated gastroesophageal reflux
▪ Anticholinergics
▪ Calcium channel blockers
▪ Theophylline
▪ Nitrates
 Esophagitis (related to immunosuppression)
▪ Corticosteroids
 Structural/Obstructive
 Head or neck tumors
 Postsurgical/Radiation stenosis
 Cervical spondylosis
 Zenker's diverticulum
 Cricopharyngeal web
 Infectious (tonsilar hypertrophy/abscess)
 Extrinsic compression (goiter)
 Neuromuscular  Motor end-plate dysfunction
 CVA ▪ Myasthenia Gravis
 Alzheimer’s, Parkinson's disease ▪ Botulism
 Brain stem tumors ▪ Eaton-Lambert Syndrome
 Myopathies
 Degenerative/Demylenating  Polymyositis
diseases  Dermatomyositis
▪ ALS, MS, Huntington's  Muscular dystrophy (myotonic
▪ Acute transverse myelitis, ADEM, dystrophy, oculopharyngeal
and acute hemorrhagic dystrophy)
leukoencephalitis  Thyroid myopathy
▪ Sjogren’s  Amyloidosis
 Cricopharyngeal (upper
 Postinfectious
esophageal sphincter)
▪ Poliomyelitis, Syphilis  Sarcoidosis
 Peripheral nervous system  Paraneoplastic Syndromes
▪ Peripheral neuropathy
 Structural disorders  Disorders related to Systemic Diseases
 Inflammatory and/or fibrotic ▪ Pemphigus and pemphigoid conditions
strictures
▪ Lichen planus
▪ Peptic
▪ Scleroderma (multifactorial)
▪ Caustic
▪ Intramural lesions
▪ Pill-induced
▪ Leiomyoma
▪ Radiation-induced
▪ Granular cell tumor
▪ Sarcoidosis
 Mucosal rings and webs
▪ Schatzki's ring  Extramural lesions
▪ Multiringed esophagus ▪ Aberrant right subclavian artery
(eosinophilic esophagitis) (dysphagia lusoria)
▪ Mediastinal masses (thyroidomegaly)
 Foreign body ▪ Bronchial carcinoma

 Carcinoma  Anatomical abnormalities


▪ Primary (squamous, ▪ Hiatal hernia
adenocarcinoma) ▪ Esophageal diverticulum
▪ Secondary (e.g. breast, melanoma)
 Neuromuscular/Motility disorders
 Achalasia (idiopathic or secondary)
 Spastic motor disorders
▪ Diffuse esophageal spasm
▪ Hypertensive lower esophageal sphincter
▪ Nutcracker esophagus
 Diabetes
 Amyloidosis
 Is it a structural vs motility disorder?
 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.
 Three cardinal features of dysmotility
 dysphagia (for solids and liquids)
 chest pain and
 regurgitation

 Regurgitation during meals, as well as spontaneous


regurgitation between meals or at night, is highly
suggestive of dysmotility.
 Unlike regurgitation that is related to GERD, the
regurgitated fluid in patients with esophageal
dysmotility is generally not noxious to taste.
 In addition, spasm or achalasia typically cause
chest pain. Although this chest pain is frequently
described as 'heavy' or 'crushing', it can be
indistinguishable from the typical 'heartburn' of
reflux.
 The pain frequently occurs during meals, but it
can be quite unpredictable and sporadic or
nocturnal.
 Sipping antacids or even water can relieve the
pain related to dysmotility, which further
confuses its distinction from reflux-related pain.
 Slowly progressive, long-standing dysphagia, particularly
against a background of reflux, is suggestive of a peptic
stricture.
 Caveat - severity of heartburn correlates poorly with
esophageal mucosal damage.
 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.
 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.
 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.
 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
 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. The presence of pooling, delayed
transit and laryngeal aspiration can be detected.
 The dynamic nature of this study provides an opportunity to evaluate
the response to certain correctional techniques (e.g., chin tucking)
during the study.
 This technique requires the cooperation of an alert patient, which is the
most limiting factor to performing VFSS.
 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
 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
 Numerous nonpropulsive contractions
 “corkscrew/ rosary bead” esophagus
 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.
 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.
 Swallowing maneuvers
 Postural adjustments
 Facilitatory techniques, such as strengthening exercises, biofeedback,
thermal and gustatory stimulation.
Condition Conservative treatment Invasive treatment
Diffuse esophageal Serial dilations or longitudinal
Nitrate, calcium channel blockers
spasms myotomy

Soft food, anticholinergics, calcium Dilation, botulinium toxin


Achalasia
channel blockers injections, Hellers myotomy

Anti-reflux, systemic medical


Scleroderma None
management of scleroderma

Anti-reflux drugs (H2 blockers, PPIs) and


GERD Fundoplication
prokinetic agents (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
 Omran L. Dyphagia. http://www.cyberounds.com/cmecontent/art76.html
 Speiker M. Evaluating Dysphagia. American Family Physician. June 15,
2000.
 Palmer J, Drennan J, Baba M. Evaluation and Treatment of Swallowing
Impairments. American Family Physician. April 15, 2000.
 www.medicine.nevada.edu/residency/lasvegas/.../DYSPHAGIA.ppt

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