brief presentation of swallowing physiology and dysphagia for ENT

1. Dr Kaushik Sarangi
PG / 1ST Year
Dept of ENT
Scbmch
PHYSIOLOGY OF
SWALLOWING AND
DYSPHAGIA

2. SWALLOWING PHYSIOLOGY
 INTRO
 SEQUENCE OF EVENTS IN NORMAL SWALLOW
 ORAL PHASE
 PHARYNGEAL PHASE
 ESOPHAGEAL PHASE
 NEURAL CONTROL
 RESPIRATION AND SWALLOWING

3. PHYSIOLOGY OF SWALLOWING-
INTRODUCTION
 Swallowing involves coordinated activity of muscles of
oral cavity, pharynx, and esophagus.
 The whole process is partly under voluntary control &
partly reflexive in nature
 Swallowing by definition involves passage of bolus of
food (solid / liquid) from the oral cavity to stomach via
the pharynx and esophagus, passing over the entrance
to laryngeal vestibule.
 Basic musculature of Swallowing controls the jaw,
tongue, degree of constriction and length of pharynx
and closure of laryngeal inlet.

4. Components of Deglutition
1. Passage of bolus from oral cavity to stomach
2. Protection of airway
These two mechanisms also serve to inhibit air entry into
the stomach.

5. Deglutition - phases
Three stages have been traditionally described by
Magendie for the sake of convenience. They help in
the better understanding of the physiological process
involved.
 Oral
 Pharyngeal
 Esophageal

6. Oral phase
 In this phase food is
prepared for swallowing
 Tongue plays a vital role
in this process.
 This phase is under
voluntary control.
 This phase is divided into
 oral preparatory phase and
 oral phase proper

7. Oral preparatory phase
 This phase involves breaking down of food in the
oral cavity
 During this phase the food is chewed and mixed with
saliva making it into a bolus which can be swallowed
 The elevators of lower jaw play an important role in
bolus preparation.
 Tongue
 Intrinsic muscles which alters its shape.
 Extrinsic muscles changes its position within the oral cavity

8. Oral preparatory phase (contd..)
 Occlusal of the lips help in creating an effective seal
preventing the bolus from dribbling out of the oral
cavity
 The action of buccinator muscle helps in pushing the
bolus out of the vestibule into the oral cavity proper
 Salivary Glands produce saliva which contains
mucin.
 Mucin binds the food together and helps in bolus
formation.

9. Bolus formation
 This is the most important function of preparatory
phase
 This involves repeated transfer of food from oral
cavity to oropharyngeal surface of tongue.
 Bolus accumulates on the oropharyngeal surface
of tongue due to repeated cycles of upward &
downward movement of the tongue.

10. Oral phase proper
 During this phase the bolus is moved
towards the back of the tongue.
 The contraction of soft palate prevents
nasal regurgitation, also prevents
premature movement of bolus into the
oropharynx.
 Once the bolus is of suitable
consistency the transit from mouth to
oropharynx just takes one to two
seconds.
 Tongue plays a vital role during this
phase also.
 Its intrinsic muscles contracts and
reduces its size,
 while genioglossus muscle elevates
the tongue towards the palate

11. Oral phase proper (contd..)

12. Pharyngeal phase
 This phase of deglutition is reflexive in nature (as the
bolus passes the palatoglossal & palatopharyngeal
folds the act of swallowing becomes reflexive)
 Airway protective mechanisms are activated in advance
of passing the bolus.
 As bolus reaches back of tongue a sequence of events
initiated-
1. Contraction of diaphragm is inhibited making simultaneous
breathing & swallowing impossible
2. Soft palate is elevated in order to seal off the nasopharynx (T.
palatini & L.palatini )
3. Vocal cords starts to adduct protecting the airway (aryepiglottic
ms.).

13. Pharyngeal phase..contd

14. Pharyngeal
phase..contd

15.  At this stage pharynx
constricts behind the
bolus as the superior
constrictor contracts.
 Bolus carried down the
pharynx by a
coordinated peristaltic
wave of three
constrictors in
appropriate sequence.

16.  Laryngeal inlet (formed by
sup margin of
quadrangular membrane)
itself is never actually fully
closed.
 If food enters laryngeal
vestibule the true and
false cord guard the
airway
 Then cough reflex
initiated to remove the
object.

17. Pharyngeal phase ( contd..)
 During this phase Ventilatory and alimentary streams
cross each other.
 Dynamic separation of these streams is possible due
to the co-ordination of reflex phase that occurs.
 It just takes a second for the bolus to traverse the
pharynx and reach the cricopharyngeal area.

19. Functions of Trigger Points
 Stimulation of trigger points
present in the oropharynx
starts off the pharyngeal
reflexive stage of swallowing.
 Present at the faucial arches
& mucosa of the posterior
pharyngeal wall.
 Innervated by
glossopharyngeal nerve (CN
IX).

20. Functions of Trigger Points…
Stimulation of these trigger points causes
1. Dilatation of pharynx due to relaxation of the
constrictors, and
2. Elevation of pharynx & larynx due to contraction of
longitudinal muscles(palatopharyngeus &
stylopharyngeus)
3. The pharynx constricts behind the bolus thereby
propelling it.
4. Contraction of the inferior constrictor moves the bolus
towards the esophagus.

21. Importance of laryngeal elevation during
pharyngeal stage
 It narrows the laryngeal
inlet
 It ensures better sealing of
the laryngeal inlet by the
downturned epiglottis
 The laryngeal inlet is
closed due to the actions
of interarytenoid,
aryepiglottic and
thyroepiglottic muscles

22. Role of epiglottis in the pharyngeal phase
 The movement of epiglottis
occurs in two stages (by
thyroepiglotticus ms.)
 The epiglottis moves from
vertical – horizontal
position
 The upper third of
epiglottis moves below the
horizontal to a slightly
lower level to cover the
narrowed laryngeal inlet

23. Esophageal stage
 This is purely reflexive
 In this phase
cricopharyngeus relaxes
and the anterior superior
movement of the
laryngohyoid complex acts
to open the upper
oesophageal
sphincter(UES).
 The bolus passes through
the sphincter and moves
along the esophagus by
peristalsis.

24. Contd..
 The levator and tensor veli palatini relax lowering the
soft palate
 The laryngeal vestibule opens, the hyoid drops and
the vocal cords open
This opening of the glottis at the very end of
oropharyngeal swallow sequence is part of the
airway protection mechanism

25. Neural control of swallowing
 Two areas of brain are involved
1. Cerebral Cortex – for initiation
2. Brain Stem – for regulation

26. Neural control (Initiation)
 Initiation of swallow is voluntary.
 Bilateral prefrontal, frontal and parietal cortices are
involved.
 Swallowing is initiated when food comes into contact
with certain trigger areas like fauces / mucosa of
posterior pharyngeal wall.
 Afferent nerve is the glossopharyngeal nerve (CN
IX) 

27. Neural control (initiation)..contd.
Medulla -Nucleus tractus solitarius &
spinal nucleus of trigeminal nerve
play a vital role in receiving
touch & pressure sensation
from trigger zones.
Efferents involve several cranial
nerve nuclei which include
 NUCLEUS AMBIGUUS (muscles of
palate, pharynx and larynx) – by CN
X
 HYPOGLOSSAL NUCLEUS supplying
the muscles of the tongue, by CN XII
 MOTOR NUCLEI OF TRIGEMINAL AND
FACIAL NERVES supplying the
muscles of face, jaws and lips by CN
V & VII

28. Cortical asymmetry
 In most people swallowing control is asymmetrical
with one hemisphere dominating.
 This explains prevalence of swallowing problems and
recovery following stroke over a period of weeks. 
 Damage to hemisphere with greater projection accounts for
initial difficulty.
 Recovery occurs as the intact projection from undamaged
hemisphere is reorganized.

29. Role of medulla
 Cortical areas are not imp for coordinated swallow,
which can occur in significant brain damage.
 Between the afferent and efferent system there are
two groups of neurons in the medulla which are
necessary for coordination & regulation of
swallowing.
 Lateral medullary swallowing centers.  converge
sensory input – lie in the dorsal medulla above the
nucleus of the solitary tract(NTS) -
 Medial medullary swallowing centers  distributes
output – The second group lie in the ventral medulla
around nucleus ambiguus(NA)-

30. Neural Control

31. Role of central pattern generator
 Important for correct sequencing of events.
 Since the process of swallowing and breathing are
interlinked there is a certain degree of central co-
ordination taking place
 Concept of central pattern generation is that afferent
activity is not necessary to evoke rhythmic activity ..
Thus these neurons act like a cardiac pacemaker.
 Thus Swallowing, Ventillation and Masticatory
movements are all interconnected.

32. Phase of respiration & swallowing
 Swallowing occurs during expiratory phase of
respiration
 This helps in clearing food material left in the
vestibule. Thus it should be considered to be a
protective phenomenon.

33. C A U S E S
A P P R O A C H
I N V E S T I G A T I O N
DYSPHAGIA

34. CAUSES OF DYSPHAGIA
CONGENITAL
• TRAUMATIC
• INFECTIONS
• INFLAMMATORY
• ESOPHAGEAL MOTILITY DISORDERS
• NEOPLASTIC
• NEUROLOGICAL
• DRUG INDUCED
• AGEING
• MISCELLANEOUS
AQUIRED

35. CONGENITAL CAUSES OF DYSPHAGIA
Choanal Atresia
 Neonate is an obligate nasal breather
 When partial presents withFeeding difficulty at birth, unable to suckle
adequately
 When complete – respiratory distress
 Diagnosis –
 Lack of air pasage at nostril
 Failure to pass nasopharyngeal catheter
 Axial CT after nasal decongestion
Cleft Lip And Palate
 Inefficient Suckling due to inadequate lip and nasopharynx seal
Laryngomalacia
 MC cause of stridor in 1st year of life
 Diagnosis bt nasolaryngoscopy

36. Congenital causes of dysphagia..contd
Unilateral & Bilateral Vocal Cord Paralysis
 u/l – swallowing difficulty, hoarseness, aspiration
 b/l - stridor
Laryngeal cleft
 Asso with dysphagia
 There is an asso between these and TEF
 Diagnosis – by endoscopy under GA
Tracheoesophageal fistula and esophageal atresia
Vascular rings
 Due to anomaly of great vessels,
 subclavian(dysphagia lusoria) – may present with dysphagia in adulthood
 double aortic arch,
 anomalous left pulmonary artery
 Diagnosis – endoscopy, barium swallow, CT, MRI

37. AQUIRED CAUSES OF DYSPHAGIA
CONGENITAL
• TRAUMATIC
• INFECTIONS
• INFLAMMATORY
• ESOPHAGEAL MOTILITY DISORDERS
• NEOPLASTIC
• NEUROLOGICAL
• DRUG INDUCED
• AGEING
• MISCELLANEOUS
AQUIRED

38. Traumatic causes
 Accidental and iatrogenic
 Blunt trauma, penetrating injuries and compression
effects
 Direct injuries and cranial n. damage
 Head injuries – imp bcoz may not become apparent
until pt resumes consciousness, starts feeding again
and aspirates.

39. INFECTIONS causing Dysphagia
1.Acute pharyngitis,tonsilitis, quinsy
 MC cause
 Despite appropriate antibiotic therapy tonsilitis can progress to peritonsillar
abscess
2.Glandular fever
 by EBV
 Painful dysphagia with marked cervical lymphadenopathy
3.Acute supraglottitis - Now rare due to Hib immunisation
 Epiglottitis – sd be suspected if child becomes rapidly unwel with fever,
stridor, painful dysphagia and drooling.
4.Herpetic, fungal, or CMV mucosal infection
 Usually seen in immunocompromised pts( on chemotherapy or head & neck
RT, Diabetes
 Candidal infections are common in pts on broad spectrum antibiotics and
steroids

40. INFECTIONS causing Dysphagia
5.Candidiasis
 Oral – diagnosed clinically
 Hypopharynx - endoscopy
 Esophagus –
 barium swallow (shaggy mucosal appearance)
 Esophagoscopy
6.Tubercuosis
 Mucosal lesion – endoscopic biopsy
 Compression by LN – axial CT chest
7.Abscesses
 In head & neck can cause severe painful
dysphagia with drooling, fever, torticolis
 MC is peritonsillar abscess follwed by
submandibular & parapharyngeal abscess

41. Inflammatory causes of Dysphagia
GERD
 One of the MC causes
 Complaints are - tightness in lower neck, constant throat
clearing, retrosternal discomfort & hoarseness
 Clinical exam – erythema & edema of posterior larynx and
lower pharynx
 Invetigation - Flexible esophagoscopy, 24hr ambulatory
esophageal pH monitoring(most accurte)
 Barrett esophagus (BE) is a potentially serious complication of
long-standing GERD.

42. Inflammatory causes of Dysphagia..contd
Patterson Brown-Kelly or Plummer-
Vincent syndrome
 Dysphagia mostly affects middle-aged or
elderly women
 triad that consists of
 proximal esophageal webs,
 iron deficiency anemia, and
 dysphagia.
 Dysphagia is due to hyperkeratinisation with
web formation in the post cricoid region
 Web can be seen on Barium swallow, but may
be missed on rigid endoscopy.
 Iron supplement treats hyperkeratinisation
and dysphagia, but the web needs dilatation.
 Associated with post cricoid carcinoma in
small percentage.

43. Inflammatory causes of Dysphagia..contd
Systemic autoimmune disorders
 Most of them are associated with dysphagia
 diagnosis is by clinical picture & auto-antibody profile(ANA,
RF)
 t/t with steroid and immuno supressives does not improve
dysphagia
Scleroderma and CREST( Calcinosis, Raynaud’s,
Esophageal involvement, Sclerodactyly, Telengiectasia)
 May include atrophy and fibrosis of smooth muscles
 Often affect lower esophagus resulting in poor peristalsis,
severe GE reflux with stricture formation & Barrett’s.

44. Inflammatory causes of Dysphagia..contd
SLE
 Mainly affects skin, joints, internal organs.
 Dysphagia is mild
Dermatomyositis
 Mainly affects skin, skeletal muscles
 High percentage of pts are asso with malignancy
 Dysphagia is due to hypopharyngeal and upper esophagus
involvement
Mixed connective tissue disorder

45. Inflammatory causes of Dysphagia..contd
Benign Pemphigoid and Epidermolysis Bullosa
 Subepidermal and submucosal blisters respectively
 Leads to scarring and obstruction of pharynx and esophagus
 Good response to steroids and dilatation
Primary and secondary Sjogren’s Syndrome
 Xerostomia causes dysphagia
Rheumatoid arthritis
 May involve cricoarytenoids causing hoarseness & dysphagia
Crohn’s
Sarcoid
 Compression of esophagus by lymph nodes

46. Esophagial Motility Disorders
1. Achalasia
2. Diffuse Esophagial Spasm
3. Nutcraker Esophagus

47. Esophagial Motility Disorders..contd
 Achalasia(cardiospasm)
 Failure of relaxation of lower esophageal sphincter
with progressive dilation and hypertrophy of
esophageal wall above.
 Due to degeneration or absence of ganglion cells of
auerbach’s myenteric plexus in esophageal wall.
 Pt c/o progressive dysphagia to fluids and then
solids. and eventually regurgitation of undigested
food
 Diagnosis –
 Barium swallow
 Initially  smooth “Bird’s beak” tapering of
esophagogastrc junction
 Later  associated with dilated esophagus
 Manometry
 Early diagnosis can be made before barium
appearance.
 Shows failure of relaxation of LES, absence of
esophageal peristalsis and a raised resting
pressure of esophagus.

48. Esophagial Motility Disorders..contd
 Diffuse Esophagial Spasm
 Causes angina like chest pain in the
presence of normal coronal arteries
and dysphagia
 Diagnosis
 Barium swallow
 Nonpropulsive peristaltic wave
(cocksrew appaearance)
 Manometry
 Repititive nonperistaltic multipeaked
contractions of high amplitude of
body of esophagus
 With intermittent normal peristalsis

49. Esophagial Motility Disorders..contd
 Nutcraker Esophagus
 Noncardiac chest pain with dysphagia
 Diagnosis
 Manometry – shows normal peristatic waves of high amplitude in
the distal esophagus

50. Neoplastic causes of Dysphagia
 Both benign and malignant tumors – by mechanical
obstruction and also by neuromuscular invasion.
 IN ORAL CAVITY
 Most are malignant- 95% of these are SCC.
 Presentation - Lump or ulcer causing odynophagia.
 Dysphagia is caused by tongue fixation.
 In OROPHARYNX
 Most are malignant and of SCC type
 Usually ulcerative (lymphoma may present as smooth lump)
and visible clinically.
 Presentation – sore throat, referred otalgia or dysphagia

51. Neoplastic causes of Dysphagia.. contd
 In HYPOPHARYNX
 Rare benign tumors ( leimyoma, lipoma, fibrolipoma)
 Most are malignant of SCC type – 60% occuring in Pyriform
fosa.
 Presentation – may only c/o feeling ‘something in the throat’,
crumb being stuck or an episode of food sticking
 Diagnosis –
 Clinical exam ( Barium swallow may be normal)
 If symptoms persist – direct pharyngoscopy or esophagoscopy is
needed; - especially when asso with arytenoid edema or pooling of
saliva.

52. Neoplastic causes of Dysphagia.. contd
 In ESOPHAGUS
 Majority are SCC, though benign leiomyoma found occasionally.
 Adenocarcinoma seen in lower end of esophagus arises
 Either in gastric metaplasia (as in Barrette’s) or invasion of tumor from
cardiac end of stomach
 Presentation – classical is “ dysphagia of short duration in an elderly
male who smokes and drinks and which progresses from solid to
liqquid”.
 O/E – In advanced diseases –
 wt loss,
 anemia,
 cervical lymphadenopathy, and
 hoarseness with bovine cough.
 Diagnosis is made by Barium swallow
In all pharyngeal and esophageal malignancy
 Biopsy under GA – confirms the diagnosis,and staging tumor.
 CT scan of neck, chest, upper abdomen – for staging, local
spread, and secondary deposits.

53. Neoplastic causes of Dysphagia.. contd
 Nasopharyngeal CA
 Cranial N palsy from skull base invasion
 presents with speech & swallowng problems and hoarseness.
 Diagnosis – by nasopharyngoscopy & CT.
 Skull base tumors( craniopharyngeomas & chordomas)
 By compression of parapharyngeal space or invasion of cranial
nerves
 Leukemias & Lymphomas
 By esophageal wall infiltration
 Enlarged mediastinal LN( due to lymphoma, LN
metastasis, bronchial CA, thyroid malignancy)
 By external compression
 Diagnosis – barium swallow & CT chest

54. Neurological causes of Dysphagia
 CVA or Stroke
 MC neurological disorder causing dysphagia by affecting
 Cortex or
 Corticobulbar tracts ( pseudobulbar palsy ) or
 bulbar nerve nuclei ( bulbar palsy )
 Recovery takes place in first week in majority of pts.
 Dysphagia is due to
 Delayed triggering of swallowing reflex.
 Cricopharyngeal dysfunction
 Reduced tongue control and pharyngeal contraction and cough
 Cause ASPIRATION – aspiration pneumonia being
commonest cause of death after a stroke.

55. Neurological causes of Dysphagia
 Isolated recurrent nerve palsy
 Cause dyphagia & aspiration by
 Decresed pharyngeal gradient pressure
 Decreased glottic clossure pressure
 Inf. Constrictor and cricopharyngeal ms. Dysfunction
 Parkinson’s disease
 Oral & pharyngeal phase are affected
 Oral – rigidity of tongue musculature
 Pharyngeal – delayed contraction of pharyngeal muscles
 Due changes in striated muscle under dopaminergic control and
smooth muscle under autonomic control.
 Multiple sclerosis
 Myasthenia gravis
 Motor Neuron Disease( amyotrophic lateral sclerosis)

56. Drug Induced Dysphagia
 Mechanisms
1. Directly causing esophagitis
2. As a part of pharmacological action
3. Normal side effects
Directly Causing Esophagitis
 Tablets with insufficient water
 Taking tablet just before going to bed bcoz esophageal transit time is
longer during sleep
 MC injured area Esophagus at the level of Aortic Arch
 Due to lack of neutralization of saliva
 And contact by acid producing drugs with pH<3
• Tetracycline, Doxyycycline, Vitamin C, Ferrous Sulphate
 Secondary viral and fungal infection by
• Broad spectrum antibiotics
• Chemotherapeutic drugs
 Antibiotics  steven-johnson’s syndrome with acute erosive pharyngitis and
esophagitis causing dysphagia and delayed esophageal strictures

57. Drug Induced Dysphagia.. contd
As a part of pharmacological action causing Xerostomia
 Anti hypertensives
 ACE inhibitors
 Anticholinergics
 Antiemetics
 Antihistaminics
 Opiates

58. Drug Induced Dysphagia.. contd
Normal side effects
Inhibitory By decreasing
 Esophageal peristalsis
 Tone of LES
 Anticholinergics
 TCA
 Calcium channel blockers
 Excitatory
 Cause rapid esophageal motility and GE Reflux
 Cholinergic agonist, cisapride, metoclopramide

59. Presbydysphagia
 Affects all stages of swallowing by
 Despite these changes barium swallow abnormality
is found in 1/3rd pts only and few complain
dysphagia
Oral phase Pharyngeal phase Esophageal phase
•Loss of teeth & tongue
connective tissue
•Reduced strength of
mastication
•Wakness of reflexes
•Decreased elevation of
larynx
•Prolongation of
pharyngeal transit time
•Prolongation of UES
relaxation time
•Increased esophageal
transit time

60. MISCELLANEOUS CAUSES
Foreign body in pharynx
 Fish bone or spicules of meat bones
 Sites – tonsils, base of tongue, vallecula or pyriform fossa –
MC is tonsils.
 Clinical ( inspection, palpation, IL ) and endoscopes help
locate the site.
 Radiograph is useful if bone is ossified.
Foreign body in esophagus
 MC is coin. Others are like large piece of meat w/wo bone.
 MC sites – constrictions at
 Cricopharyngeous,
 Level of aortic arch,
 Cardia

61. MISCELLANEOUS CAUSES.. contd
Caustic stricture
 Acids or alkali( caustic soda, ammonia)
 Usually accidental, but may be an suicidal attampt
 Effect –
 Edema – of laryngopharynx causing respiratory difficulty
 Superficial burns – heal completely
 Deep burns – repair by fibrosis with stricture formation and
dysphagia.
 Intervention –
 In acute phase Flexible Esophagoscopy is mandatory to assess the
extent of damage prior to placing feeding gastrostomy
 Barium swallow & esophagoscopy – done to diagnose stricture
formation

62. MISCELLANEOUS CAUSES.. contd
Pharyngeal pouch
 Mucosal dehiscence between thyro &
cricopharyngeous (parts of IC)
 called Killian’s dehiscence in posterior
pharynx
 Pt c/o
 Lump – initially when pouch is small
 Dysphagia – later when pouch enlarges with food
filled pouch compressing esophagus.
 Others like regurgitation of undigested food into
pharynx, and overflow into larynx causing
aspiration with bouts of coughing and then
pnumonia
 Diagnosis – confirmed by Barium Swallow

63. MISCELLANEOUS CAUSES.. contd
Globus pharyngeous
 Pt c/o – “constant feeling of lump in throat” which is
worse on swallowing saliva, but does not interfere
with swallowing of either fluid or food.”
 Asso with GERD w/ wo esophagitis in significant
number of pts.

64. MISCELLANEOUS CAUSES.. contd
Pts having Tracheostomy
 Can cause dysphagia by
 interfering with laryngeal elevation during swallowing
 direct pressure on esophagus if cuff is overinflated
Thyroid Disease
 Due to compression of upper esophagus
 Diagnosis
 Barium swallow
 Axial CT scan of neck and chest
 Thyroid function & antibody test , FNAC, USG, thyroid
scanning

65. APPROACH..
HISTORY TAKING AND EVALUATION
 Taking a careful history is vital for evaluation of
dysphagia
 The history will yield
 Pathophysiologic process
 Anatomic site of problem in most pts – 80%
 Crucial for determining whether subsequently detected
radiographic or endoscopic anomalies are relevant or
incidental

66. HISTORY TAKING AND EVALUATION
Three fundamental aims of history taking
1. To distinguish true dysphagia from
i. Globus sensation(in between meals )
ii. Xerostomia – loss of lubrication and stimulus
iii. Odynophagia – transient than dysphagia
2. To distigealnguish site of problem- esophageal or
pharygeal
3. To distinguish structural from motor disorder
History will also dictate the proper next diagnostic
procedure.

67. HISTORY TAKING AND EVALUATION
Symptoms indicating oropharyngel dysfunction
 There are four symptoms that have high specificity
for oropharyngel dysfunction
1. Delayed or absent oropharyngeal swallow initiation
2. Deglutitive postnasal regurgitation or egress of fluid
through the nose during swallowing
3. Deglutitive cough indicative of aspiration
4. The need to swallow repititively to achieve
satisfactory clearance of swallowed material from
the hypopharynx
If one or more of these symptoms are present then cause
of dysphagia is probably Oropharyngeal, eithr structural
or neuromyogenic.

68. Oropharyngeal vs. Esophageal Dysphagia
Difficulty swallowing
Food sticks
during meals
Lump in throat
between meals
Globus
Neck Retrosternum
Pharynx OR Esophagus ?
Cardinal
Oropharyngeal Symptoms
Pharyngeal Esophageal
“How does it feel like ?”
“Where does it stick ?”
“Initiation?”
“Postnasal regurgitation?”
“Deglutitive cough?”
“Repetitive swallows?”
Yes No

69. Algorithm for Dysphagia

70. Physical examination for dysphagia
 Level of alertness and cognitive status, vitals
 Examination of CN V and VII – XII
 Complete exam of neck & chest including cervical LN
status
 Assessment of Voice
 Direct observation of lip & jaw closure, chewing and
mastication, tongue mobility & strength, palatal &
laryngeal elevation and salivation with oral sensitivity
 Inspection of oral cavity and pharynx

71. Physical examination for dysphagia
 Evaluation of laryngeal elevation by placing 2 fingers on
larynx and assessing movement during volitional
swallow
 Gag reflex
 Direct observation of the act of swallow, at least a few
ounces of water. After swallow, observe for 1 minute or
more for delayed cough response if present.
 Skin for scleroderma and CREST syndrome
 Signs of malnutrition, wt loss, pulmonary c/c

72. Blood investigations
To screen for
 Infection or inflammatory conditions
 Nutritional status
 Fluid electrolyte imbalance
 Thyroid function

73. Radiography
 Chest x-ray - Mediastinum, cardiac and pulmonary
status, aspiration pneumonia, also to rule out
secondaries.
 Lateral x-ray soft tissue neck – to detect any soft
tissue lesion of post cricoid or retropharyngeal space,
prevertebral widening, osteophytes, FB etc
 Barium swallow
 CT scan – to evaluate mass lesion in neck
 MRI –
 useful when neurologic disorders are suspected
 Delineate mass lesion in brain
 Degenerative processes inn brain & spinal cord

74. Endoscopies
 Laryngeal endoscopy
 Direct laryngoscopy
 Flexible nasopharyngoscopy
 Brochoscopy
 Esophagoscopy
Advantage – permits biopsy

75. Special Tests
Videofluroscopic swallowing study (or Videofluroscopy)
 aka modified barium swallow
 Definitive study for evaluation of swallowing mechanism
 Superior to FEES for evaluating Oral phase and aspiration
FEES – fibreoptic endoscopic evaluation of swallowing
 Using a transnasal laryngoscope
 Advantages –
 for detection of premature bolus loss, laryngeal penetration, trachaeal
aspiration and pharyngeal residue
 Helpful when VFS not feasible (critically ill, ICU pt)
 Disadv – don’t demonstrate motion of food pathway str

77. Special Tests
 Esophageal manometry
 Toassess motor function of esophagus
 Esophageal pH monitoring
 Standard criteria for diagnosing reflux disease
 Swallowing and Laryngeal Electromyography
 Scintigraphy

78. To summarize
 Swallowing is NOT a stepwise progression, it is a
cyclical and irregular process.
 Neural control is divided between the cortex and
brainstem.
 Cortical control of swallowing is bilateral,
although one hemisphere is usually dominating.
 Airway protection is activated in advance of
pharyngeal phase of swallowing.
 Impaired respiration pattern will affect
swallowing and vice versa.

79.  Age of patient suggests most likely cause of
dysphagia.
 Globus pharyngeous is common in middle aged women
and rarely asso with serious disease.
 Neurological causes of dysphagia mostly affect
oropharyngeal phase of swallowing.
 Ingested FB tend to lodge at sites of constriction at
cricopharyngeous, aortic arch, and cardia.
 A contrast swallow for suspected perforation
and/or aspiration should be with low MW, non-ionic,
water soluble contrast medium. Barium is
contraindicated.

80.  Esophageal manometry can be helpful in atypical
chest pain and unexplained dysphagia.
 24 hr ambulatory esophageal pH monitoring is
most accurate method of diagnosing GER.
 A barium videofluoroscopy swallowing is gold
standard for evaluating swallowing mechanism,
particularly oral & pharyngeal phase.

82. REFERENCE
1. Scott-Brown’s Otorhinolaryngology & HNS
2. Cummin otolaryngology.
3. Internet.