2. BACKGROUND
The term dysphagia, a Greek word that means disordered
eating, typically refers to difficulty in eating as a result of
disruption in the swallowing process.
Dysphagia can be a serious health threat because of the
risk of aspiration pneumonia,malnutrition, dehydration,
weight loss, and airway obstruction, and it exerts a large
influence on the outcome of rehabilitation (eg, length of
hospital stay, mortality/morbidity).
3. As typically defined, dysphagia is a condition in
which disruption of the swallowing process
interferes with a patient’s ability to eat. It can
result in aspiration pneumonia, malnutrition,
dehydration, weight loss, and airway
obstruction.
4. EPIDEMIOLOGY
The incidence of poststroke dysphagia is higher in Asians.
Stroke is the leading cause of neurologic dysphagia, with the
condition occurring in approximately 51-73% of patients with
stroke.
Delay functional recovery in patients with stroke and is also
the most significant risk factor for the development of
pneumonia.
5. ANATOMY
Deglutition is the act of swallowing, which
allows a food or liquid bolus to be transported
from the mouth to the pharynx and
esophagus, through which it enters the
stomach.
Normal deglutition is a smooth, coordinated
process that involves a complex series of
voluntary and involuntary neuromuscular
contractions and typically is divided into
distinct phases: oral, pharyngeal, and
esophageal.
6. The process of swallowing is organized with sensory
input from receptors in the base of the tongue, as well
as in the soft palate, faucial arches, tonsils, and
posterior pharyngeal wall; this input is transmitted to
the swallowing center, located within the pontine
reticular system, through the facial (VII),
glossopharyngeal (IX), and vagus (X) cranial nerves.
Information from the swallowing center then is
conveyed back to the muscles that help in swallowing
through trigeminal (V), facial (VII), glossopharyngeal
(IX), vagus (X), and hypoglossal (XII) cranial nerves,
with the trigeminal, hypoglossal, and nucleus
ambiguus constituting the efferent levels.
7. The act of swallowing usually interrupts the expiratory
phase of ventilation, while the completion of expiration
occurs when swallowing ends. In situations in which
the swallowing is initiated during the inspiratory phase
of ventilation, a brief expiration ensues after the
completion of swallowing.
The medulla controls this involuntary swallowing reflex,
although voluntary swallowing may be initiated by the
cerebral cortex
8. THE ORAL PHASE OF SWALLOWING IS DIVIDED INTO THE FOLLOWING 2 PARTS:
ORAL PREPARATORY PHASE: THE PROCESSING OF THE BOLUS TO RENDER IT
SWALLOWABLE
ORAL PROPULSIVE (OR TRANSIT) PHASE: THE PROPELLING OF FOOD FROM THE ORAL
CAVITY INTO THE OROPHARYNX
9. THE PHARYNGEAL PHASE OF SWALLOWING IS
INVOLUNTARY AND TOTALLY REFLEXIVE, SO NO
PHARYNGEAL ACTIVITY OCCURS UNTIL THE
SWALLOWING REFLEX IS TRIGGERED
11. PATHOPHYSIOLOGY
Aspiration is a term referring to the passive
entry of any food item into the trachea (eg, during
inhalation), although the word often is used to
denote any entry of a bolus into the trachea in any
manner
Penetration refers to the active entry of any
food item into the trachea (eg, during swallowing),
although the term often is used to denote the entry
of any bolus into the laryngeal vestibule
12. A lesion in the cerebral cortex or the brainstem can cause
swallowing disorders as a result of the following:
Decrease in range of motion (ROM) of muscles of mastication
and bolus propulsion, especially those responsible for buccal,
labial, and lingual strength and the cricopharyngeus
Decreased sensation
Delayed or absent pharyngeal swallowing and reductions in
pharyngeal peristalsis[6]
Delayed or absent laryngeal adduction and elevation
The locations of specific lesions, however, do not show
correlation with findings on computed tomography (CT) or
magnetic resonance imaging (MRI) scans.
13. ORAL-PHASE DISORDERS
Pocketing of food in the mouth, circumoral leakage, and
early pharyngeal spill can occur with weakness and poor
coordination of the lips, cheeks, and tongue. Weak
posterior tongue can lead to abnormal tongue thrusting.
Aspiration of food or drink, especially during inhalation, can
occur before pharyngeal swallowing due to premature
pharyngeal spillage.
Changes in mental status with cognitive deficits also may
affect the initiation of swallowing, increasing the tendency
to pocket food in the lateral sulci and leading to possible
aspiration.
14. PHARYNGEAL-PHASE DISORDERS
If pharyngeal clearance is severely impaired, a patient may be
unable to ingest sufficient amounts of food and drink to sustain
life. In people without dysphasia, small amounts of food
commonly are retained in the valleculae or pyriform sinus after
swallowing. If there is weakness in or a lack of coordination of
the pharyngeal muscles or if there is a poor opening of the
upper esophageal sphincter, patients may retain excessive
amounts of food in the pharynx and experience overflow
aspiration after swallowing.
Dysfunction or abnormalities of the soft palate and superior
pharynx (eg, cleft palate) can lead to nasopharyngeal reflux
following uvulectomy
17. Neuropathic disorders
Dysphagia can result from sensory neuropathies affecting the
laryngeal nerves.[12, 13]
Endocrine disorders
Dysphagia can result from the following:
Secondary myopathies in Cushing syndrome, hyperthyroidism,
and hypothyroidism
Vitamin B-12 deficiency: Leading to pseudobulbar palsy
secondary to corticobulbar tract dysfunction
19. ACQUIRED: TRAUMATIC
Accidental and iatrogenic
Blunt trauma, penetrating injuries and compression
effects
Direct damage and injury to cranial nerves
Head injury
21. ACQUIRED: INFLAMMATORY
GERD with or without stricture formation
Patterson Brown-Kelly syndrome
Autoimmune disorders like scleroderma, Sjogrens
disease, rheumatoid arthritis
22. ACQUIRED: NEOPLASTIC
Benign and malignant tumors of oral
cavity, pharynx and oesophagus
Nasopharyngeal Carcinoma
Skull base tumors
Leukemia and lymphomas
Enlarged mediastinal lymph nodes
23. PHARMACOLOGIC CAUSES
Various medications, including the following, can
produce dysphagia by causing a decrease in
cognition or giving rise to drug-induced myopathies:
CNS depressants
Antipsychotics
Corticosteroids
Lipid-lowering agents
Colchicine
Aminoglycosides
Anticholinergic drugs
24. Mucosal injury may be caused by the following drugs:
Potassium chloride tablets
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Antibiotics (eg, doxycycline, tetracycline, clindamycin,
trimethoprim-sulfamethoxazole)
Xerostomia may be caused by the following agents:
Anticholinergics
Alpha-adrenergic blockers
Angiotensin-converting enzyme (ACE) inhibitors
Antihistamines
25. SURGICAL CAUSES
Surgeries that can lead to dysphagia include the
following:
Laryngectomy
Pharyngectomy, esophagectomy reconstructed by
gastric pull-up
Head and neck surgery (oral cavity cancer)[14]
Surgery involving the pharyngeal plexus during
cervical fusion or carotid endarterectomy
26. TRACHEOSTOMY
The frequency of aspiration in patients with a tracheostomy is
50-83%. The tracheostomy tube affects airway protection and
swallowing in many ways. It impairs the glottic closure reflex,
reduces subglottic pressure and laryngeal elevation, impairs
hypopharyngeal and laryngeal sensation, and leads to disuse
muscle atrophy.
The tracheostomy desensitizes laryngeal and hypopharyngeal
receptors, delaying onset of the laryngeal adductor reflex
response and leading to aspiration.
27. ENDOTRACHEAL INTUBATION
Directly- Supraglottic and glottic edema reduces the patient's
ability to sense the presence of secretions in the larynx or
hypopharynx, which in turn can inhibit the timely triggering of the
pharyngeal swallow response, causing aspiration.
Indirect effects on continuous, positive airway pressure delays
the latency of the swallow response and reduces the number of
swallows, because it alters the peripheral sensory receptors that
assist with the triggering of a pharyngeal swallow.
28. PSYCHOGENIC DYSPHAGIA
This diagnosis is one of exclusion. The condition is
characterized by oral apraxia with intact speech
and pharyngoesophageal and neurologic function.
Associated psychiatric conditions include anxiety,
depression, somatoform disorders,
hypochondriasis, conversion disorders, and eating
disorders. Psychiatric evaluation and treatment
often are needed.
Instances of swallowed foreign bodies do occur
(bezoars), especially in patients with developmental
disabilities, and this possibility also should be
considered.
29. MOTILITY DISORDERS
Motility disorders that can produce dysphagia
include the following:
Diffuse esophageal spasms (DES)
Achalasia (megaesophagus)
Scleroderma
Presbyesophagus
Cricopharyngeal dysfunction
30. ESOPHAGITIS
Gastroesophageal reflux disease (GERD)
Infectious esophagitis (eg, as in human
immunodeficiency virus [HIV], herpes, candidiasis)
Radiation esophagitis: Especially after radiation
treatments of 4500 to 6000 rad over 6-8 weeks
Medication-induced esophagitis: May develop from
enteric-coated nonsteroidal anti-inflammatory drugs
(NSAIDs); substances such as quinidine,
potassium, vitamins, and FeSO4 also may produce
esophageal injury
31. STRUCTURAL DISORDERS
Zenker diverticulum at the upper esophagus or epiphrenic
diverticula at the midesophagus or distal esophagus
Esophageal strictures, webs, or rings
Tracheoesophageal fistula
Schatzki rings
Plummer-Vinson or Paterson-Kelly syndromes and
hypopharyngeal webs with iron deficiency anemia
Cervical spondylosis
32. ADDITIONAL IATROGENIC CAUSES OF
DYSPHAGIA
These include the following:
Use of a cervical brace
Ventilator dependency
33. THE HISTORY
The history can also be used to help
differentiate structural from functional (i.e.,
motility disorders) causes of dysphagia.
Dysphagia that is episodic and occurs with
both liquids and solids from the outset (Equal
dysphagia) suggests a motor disorder,
whereas when the dysphagia is initially for
solids, and then progresses with time to
semisolids and liquids, one should suspect a
structural cause (e.g., stricture).
If such a progression is rapid and associated
with significant weight loss, a malignant
stricture is suspected
34. HISTORY AND EXAMINATION
Patients complain that foods or liquids
are no longer being swallowed easily
and there is a sensation of food
sticking.
Clinician must try to distinguish
oropharyngeal from oesophageal
dysphagia
35. OROPHARYNGEAL VS.OESOPHAGEAL DYSPHAGIA
In Oropharyngeal dysphagia, there is difficulty in
preparing and transporting the food bolus through the
oral cavity as well as initiating the swallow. This may be
associated with aspiration or nasopharyngeal
regurgitation.
In Oesophageal dysphagia, patients complain of food
sticking in their lower throat, neck, retro-sternal
discomfort or epigastrium.
36. AGE: POSSIBLE CAUSES
Children : Foreign body or congenital malformation
Middle aged patients: Reflux oesophagitis, hiatus
hernia, anaemia, achlasia, globus syndrome.
Elderly patients: Malignancy, stricture formation from
longstanding reflux, pharyngeal pouch, motility disorders
associated with aging and neurological disorders.
39. SYMPTOM ONSET AND PROGRESSION
Sudden onset of symptoms may result from a stroke
(OPD) or food impaction (OD).
Intermittent non progressive or slowly progressive
dysphagia suggests a benign cause, such as a motility
disorder or a stable peptic esophageal stricture.
A history of prolonged heartburn may suggest peptic
esophageal stricture, neoplasm, or esophageal ring.
40. EXACERBATING AND RELIEVING FACTORS
Greater difficulty swallowing liquids than solids (OPD)
Precipitation or worsening of dysphagia with
consumption of very cold liquids or ice cream (ED)
Dysphagia that progresses from solid to semisolid
food or liquid in a brief period of time suggests
esophageal stricture related to tumor.
41. PHARYNGEAL DYSPHAGIA INCLUDE
THE FOLLOWING:
Coughing or choking with swallowing
Difficulty initiating swallowing
Food sticking in the throat
Sialorrhea
Unexplained weight loss
Change in dietary habits
Recurrent pneumonia
Change in voice or speech (wet voice)
Nasal regurgitation
42. ESOPHAGEAL DYSPHAGIA INCLUDE
THE FOLLOWING:
Sensation of food sticking in the chest or throat
Change in dietary habits
Recurrent pneumonia [1]
Symptoms of gastroesophageal reflux disease
(GERD), including heartburn, belching, sour
regurgitation, and water brash
Other associated factors/symptoms of dysphagia
include the following:
General weakness
Mental status changes
43. INCLUDES OCCURRENCE OF THE
FOLLOWING:
Recent stroke [19, 1, 2, 6]
Neuromuscular disease
Hypertension
Diabetes mellitus (DM)
Thyroid disease
Cancer
Nephropathic cystinosis
Dementia
Recent injection of botulinum toxin [27]
Traumatic brain injury (TBI) [
44. KEY POINTS
Age suggests most likely cause of dysphagia
Globus pharyngeus rarely associated with any serious
disease
Dysphagia of short duration in elderly patient who smoke
or drink and which progress from solids to liquids is a
classic case of malignancy
Referred otalgia with dysphagia is a sinister symptom
and poor prognostic sign
45. KEY POINTS (2)
Neurological causes of dysphagia mostly affect orpharyngeal
phase
Ingested foreign bodies tend to lodge at sites of constriction
Barium study is contraindicated in patients with suspected
perforation of oesophagus
46. CLINICAL EXAMINATION
Complete Head and neck examination
Inspection of oral cavity
Dentition
Oropharynx
IDL
Nasolaryngoscopy
Cranial nerve examination ( tongue, gag and
cough reflex, hoarseness, vocal cord mobility)
Neck for lymph nodes, neck masses, thyroid
enlargement, loss of laryngeal crepitus and
integrity of laryngeal cartilages.
47. PHYSICAL EXAMINATION
General factors such as body habitus, drooling,
and mental status should be noted.
Voice quality (e.g. a wet sounding voice
suggesting pooling of secretions), Wheezing or
labored breathing, and any cranial nerve
weakness should be noted.
Gurgling noise in the neck or crepitus in the
neck may indicate the presence of Zenker’s
diverticulum.
Inspection or palpation of the tongue and
tongue strength may unmask fibrillation or
fasciculation of one or both sides.
48. The oropharynx should be inspected for
palatal elevation and posterior
pharyngeal wall motion on phonation
Laryngeal examination is important but
can be made difficult by the presence of
pooled secretions
49. DIAGNOSTIC CONSIDERATIONS
Cerebrovascular accident
Brainstem tumors
Degenerative diseases, such as ALS, multiple sclerosis (MS), and
Huntington disease
Peripheral neuropathy
Muscular dystrophy (myotonic dystrophy, oculopharyngeal dystrophy)
Cricopharyngeal achalasia
Obstructive lesions, such as tumors, inflammatory masses, Zenker
diverticulum, esophageal webs, extrinsic structural lesions, anterior
mediastinal masses, and cervical spondylosis
Spastic motor disorders, such as diffuse esophageal spasm, hypertensive
lower esophageal sphincter, and nutcracker esophagus
Scleroderma
Obstructive lesions (eg, tumors, strictures, lower esophageal rings [Schatzki
rings], esophageal webs, foreign bodies, vascular compression, mediastinal
masses)
51. APPROACH CONSIDERATIONS
Transnasal esophagoscopy: Especially useful in cases of
esophageal diverticula or tumor [30]
Cervical auscultation: to assess pharyngeal swallow by listening to
stereotypical sounds through a stethoscope; cervical auscultation may
be a useful bedside tool, especially in the absence of other diagnostic
tools
Blood tests: Including thyroid-stimulating hormone, vitamin B-12, and
creatine kinase; may be useful, especially in neurogenic dysphagia
Imaging studies: May include videofluoroscopy, CT scanning, MRI,
chest radiography
Endoscopic examination
Esophageal pH monitoring: The criterion standard for diagnosing
reflux disease; a nasogastric probe is inserted into the patient's
esophagus to record pH levels, and these are compared with the
patient's record of symptoms over 24 hours to determine whether acid
reflux contributes to the patient’s symptoms
Pulmonary function tests
54. Investigations for Dysphagia:
Plain Films
Inflammatory (epiglottitis, Retro-Pharyngeal
abscess), radio-opaque foreign bodies.
Barium
Esophagram
Indicated in patients in whom structural disorders
are suspected (e.g. dysphagia to solid foods)
Manometry Rarely used except in cases where elevated
intraluminal pressures must be followed (e.g.
achalasia).
Bolus
Scintigraphy
Indicated to follow improvement in a patient with
h/O aspiration or to follow esophageal emptying
in achalasia.
Video
fluoroscopic
examination or
modified
barium
swallow
"Gold standard", study the anatomy and
physiology of the oral, pharyngeal, and
esophageal stages of deglutition.
55. Lateral projection of the videoprint of a videographic swallowing
study shows the epiglottis (E), pyriform sinuses (P), tongue (Tg),
trachea (Tr), and vallecula (V).
56. Lateral projection of the videoprint of a videographic swallowing
study shows residues on the vallecula (Vr) and pyriform sinuses
(Pr) and a small amount of aspirated liquid barium in the trachea
(As).
57. Anterior projection of the videoprint of a videographic
swallowing study shows residues on the vallecula (Vr)
and pyriform sinuses (Pr).
58. Scintigraphy
This test is useful in quantitative and qualitative evaluation of
subglottic aspiration, esophageal motility disorders, and
gastroesophageal reflux.[33]
Endoscopy
• To evaluate any structural abnormalities in the
nasopharynx, laryngopharynx, and hypopharynx.
•It is a sensitive technique for detecting premature
bolus loss, laryngeal penetration, tracheal aspiration,
and pharyngeal residue.
60. DYSPHAGIA TREATMENT & MANAGEMENT
The goals of dysphagia treatment are to maintain adequate
nutritional intake for the patient and to maximize airway
protection.
Disorders of oral and pharyngeal swallowing are usually
amenable to rehabilitation, including dietary modification and
training in swallowing techniques and maneuvers.
In adults
Direct techniques include modifications of food consistency;
indirect techniques include stimulation of the oropharyngeal
structures and the adoption of behavioral techniques,
61. PHARMACOLOGIC TREATMENT
Botulinum toxin type A (BoNT-A): Injected endoscopically
into the gastroesophageal sphincter and upper esophagus to
decrease tone; this can be very useful in cricopharyngeal
spasms causing dysphagia [39]
Diltiazem: Can aid in esophageal contractions and motility,
especially in the disorder known as the nutcracker esophagus
Glucagon: Used in disimpacting esophageal bodies; diazepam
also is sometimes used; no major study has proved the
effectiveness of either drug
Cystine-depleting therapy with cysteamine: Treatment of
choice for patients with dysphagia due to pretransplantation or
posttransplantation cystinosis [40]
Nitrates: Including isosorbide dinitrate, which can especially
be recommended in achalasia
62. DIETARY MODIFICATION
Diet classifications
The dysphagia diet can be classified according to viscosity,
as follows:
level I: Pudding, crushed potato, and ground meat
level II: Curd-type yogurt, orange juice (mixed with 3%
thickener), cream soup, and thin soup with starch
level III: Tomato juice, fluid-type yogurt, and thick, fluid rice
level IV: Water and orange juice
63. DIETS FOR PATIENTS WITH DYSPHAGIA
INCLUDE THE FOLLOWING:
Dysphagia diet 1: Thin liquids (eg, fruit juice, coffee, tea)
Dysphagia diet 2: Nectar-thick liquids (eg, cream soup,
tomato juice)
Dysphagia diet 3: Honey-thick liquids (ie, liquids that are
thickened to a honey consistency)
Dysphagia diet 4: Pudding-thick liquids/foods (eg, mashed
bananas, cooked cereals, purees)
Dysphagia diet 5: Mechanical soft foods (eg, meat loaf,
baked beans, casseroles)
Dysphagia diet 6: Chewy foods (eg, pizza, cheese, bagels)
Dysphagia diet 7: Foods that fall apart (eg, bread, rice,
muffins)
Dysphagia diet 8: Mixed textures
64. NUTRITIONAL EVALUATION AND SUPPORT
As the patient's ability to swallow becomes
impaired, adequate dietary intake becomes a
challenge, and vice versa.
Therefore, early detection and management of
dysphagia are critical to halting malnutrition.
Nutritional needs are determined by means of
thorough body composition analysis, clinical
examination, and biochemical assessment. Energy,
protein, and fluid requirements must also be
assessed.
65. Hydration
Oral Hygiene and Dental Care
Lips
Exercise
Head lift
Facilitation Techniques
Deep pharyngeal neuromuscular stimulation (DPNS)
Tactile-thermal stimulation (TTS)
66. COMPENSATORY TECHNIQUES
Chin-tuck position
Rotation of the head to the affected side
Tilting of the head to the strong side
Lying on one's side or back during swallowing
Supraglottic swallow
Bolus-clearing maneuvers The effortful swallow is designed
to improve posterior tongue-base movement, in that way
improving clearance of the bolus from the valleculae. Patients
are instructed to swallow hard.
67. ENTERAL FEEDING
Nasogastric tube feeding
Oroesophageal tube feeding
Percutaneous endoscopic gastrostomy
These include reduced procedure time, cost, and
recovery time, as well as the fact that PEG requires
no general anesthesia.
PEG was found to be safer and more effective than
NGT use.
69. SURGERY FOR CHRONIC
ASPIRATION
Medialization: This helps to restore glottic closure and
subglottic pressure during the swallow
Laryngeal suspension: The larynx is in a relatively protected
position under the tongue base
Laryngeal closure: This may be performed to close the glottis
off, in this way protecting the airway at the expense of phonation
Laryngotracheal separation-diversion: This procedure may
be done to separate the airway from the alimentary tract
71. MOTILITY DISORDERS
These conditions include:
Achlasia
Scleroderma
Diffuse Esophageal Spasm
Nutcracker Esophagus
Up to 30% pts with diagnosis of MI will be
found to have an esophageal cause of pain
and motility disorders account for over
50% of these patients.
Mainstay of investigation is manometry ,
endoscopy, barium studies
72. ACHLASIA-TREATMENT
Sequential dilatation of Lower
Oesophageal Sphincter with intraluminal
balloons under fluoroscopic control
Balloon myotomy is safe, effective in 3/4th
cases and can be repeated
Surgical myotomy (Open/laparoscopic)
reserved for failed balloon failures
Failed myotomy can be treated with
balloon dilatation
73. DES & NUTCRACKER ESOPHAGUS
Characterized by severe chest pain and dysphagia
Primarily involvement of lower 1/3, muscle hypertrophy
and high pressure contractions
Symptoms intermittent so ambulatory manometry is
required
Treat with calcium channel blockers or balloon dilatation
Results disappointing
74. ESOPHAGEAL CARCINOMA
EC is increasing in faster in incidence than any
other malignancy in developed world with a ten
fold rise in the last 20 years
This increase is not squamous cell carcinoma
but in the incidence of adenocarcinoma
Classification of AC
Type 1: Lower 1/3 of esophagus
Type 2: At oesophago-gastric junction
Type 3: In gastric cardia with 5cm of GE Junction
Related to damaging effects of GE Reflux.
H pylori eradication distal vs. proximal disease
77. BARRETT'S ESOPHAGUS
A well-recognized pre malignant condition for the
development of adenocarcinoma and results
from chronic gastroesophageal reflux.
It is characterized by a metaplastic
transformation of the typically squamous
epithelium native of the esophagus, to a
columnar type highlighted by the presence of
goblet cells appreciated on histologic evaluation.
The condition entails a 30- to 50-fold greater risk
of developing adenocarcinoma.
78. TREATMENT
Early esophageal cancers, those confined to the
mucosa or upper submucosa of the esophagus,
are termed T1, N0, M0. The traditional approach
for these early cancers is surgical resection.
Primary surgical therapy for cancers limited to
the esophagus, stage I or IIa disease, has had
good results without the need for or morbidity of
chemotherapy
More than 50% of those with this cancer present
with stage III or IV disease. The prognosis
remains dismal, with an overall 5-year survival of
approximately 20%
More promising have been the results of studies
combining neo adjuvant chemotherapy with
radiation therapy.
79. PALLIATIVE MEASURES
Despite advances in diagnosis and treatment, up to 50%
of patients have incurable disease at presentation,
therefore necessitating palliative measure
A variety of therapies have been employed to palliate
dysphagia in patients with oesophageal carcinoma
including oesophageal dilation, radiation therapy,
Nd:YAG laser, thermal electrocoagulation, and
sclerotherapy of the tumor.
