PHARYNX

• Clinical anatomy
• The upper aerodigestive section between
the choanae and the criccopharyngeal
muscles
• Divided into three parts
• a) nasopharynx – from the choanae to the
lower edge of the soft palate
• b) oropharynx - from the edge of the soft
palate to the level of the tip of the epiglottis
• c) hypopharynx – from the tip of the
epiglottis to the entrance of the esophagus
• All the three areas above have a continuous
carpet of mucous membrane of common
epithelial cells
• The continuous mucous membrane is important
in spread of inflammation from one area to
another
• The walls of the pharynx consist of layers of
muscles that regulate the passage of feeds and
air – swallowing and breathing
• Specialized nerve supply makes this intricate
control of swallowing and breathing possible
• The pharynx is separated from the oral cavity by
the anterior faucet – ant palatoglossal pillar
• The pharynx contain a specific arrangement of
lymphoid tissues referred to as the Waldeyer’s
Ring
• The ring comprise of
- Adenoid – pharyngeal tonsil
- palatal tonsils – left + right
- lingual tonsil at the base of the tongue
• The tissues play an important role in monitoring
the substances that pass through the pharynx
and the development of immunity
OESOPHAGUS
• From criccopharyngeal sphincter to the gastro-
esophageal junction
• The narrowest portion of the GIT
• Has three even narrower parts in its course
• Upper sphincter is always closed
• Lower sphincter is physiological
• 1st oesophageal sphincter is 15 cm from the
incisors
• 2nd is as it crosses the left main bronchus and is
23 cm from incisors
• 3rd is at diaphragm level and is 40 cm from
incisors
• Function of the oesophagus is normaly for
swallowing
i.e. the relocation of feeds from the oral cavity to
the stomach and has three phases
1. oral phase – is voluntary

2. pharyngeal phase during which feeds are

channeled into the oesophagus and the other 5
pharyngeal openings are closed and protected
- velopharyngeal closure prevents reflux into
the nose and eustachian tubes
- there is pharyngeal peristalsis
- faucal pillars and the tongue blocks the
food bolus from reentering the oral cavity
- there is pharyngeal peristalsis that
conveys feeds towards the gullet
- air way is protected by the epiglottis
- criccopharyngeal opening allows
food bolus into the oesophagus
3. oesophageal phase
• Stage 1 is the only voluntary one and the rest
are involuntary
 NORMAL SWALLOWING
• relocation of feeds from oral cavity to
stomach
• Three intricately controlled phases
- oral phase
- pharyngeal phase
- oesophageal phase
• Ensures protection of the adjacent
openings to the food passage
Oral Preparatory Phase
Break down food
Mix with saliva
Prevent premature escape into pharynx

Oral Phase
Tongue elevates ant to post
Tongue forms central groove
Labial and buccal seal
Begins when tongue moves bolus
posteriorly,
and ends when bolus passes anterior pillar
of fauces

Voluntary control - ( XII )

Pharyngeal Phase
Begins when bolus passes anterior pillar or faucets
Ends when bolus passes through upper oesophageal sphincter into
oesophagus
Velum elevates and contracts, closing nasal passage, bolus
propelled through pharynx, larynx closed and elevated, respiration
inhibited, upper oesophageal sphincter relaxes

Involuntary control – ( IX, X, XII )

Oesophageal Phase
Begins when bolus enters oesophagus
Ends when bolus passes through lower
oesophageal sphincter into stomach 8-20 seconds
later
Sequential peristaltic wave propels bolus
Relaxation of lower oesophageal sphincter
 Dysphagia
• Esophageal dysphagia
• Oropharyngeal dysphagia
• True Dysphagia or feeling of a lump?
• Dysphagia for what?
• Regurgitation or Aspiration?
• Gastro-oesophageal reflux current or
past?
• Change of Diet or weight loss?
• Odynophagia
 Dysphagia
• must be distinguished from globus
sensation
• Globus is a sensation of a lump in
the throat in which food transport is
not limited
• globus is not related to swallowing
and, in fact, may improve with
swallowing
 Dysphagia
• Esophageal dysphagia
• Oropharyngeal dysphagia
 CONSULTATION
• True Dysphagia or feeling of a lump?
• Dysphagia for what?
• Regurgitation or Aspiration?
• Gastro-oesophageal reflux current or
past?
• Change of Diet or weight loss?
• Odynophagia
 ACUTE DYSPHAGIA
• History: FB. Previous problems.
• Examination: Drooling. Pain. Pyrexia.
Odynophagia
• Treatment:
• Food bolus: Buscopan, fizzy drink, refer at
1 hour
• FB: Refer
 Oropharyngeal dysphagia Esophageal dysphagia

Neuromuscular dysfunction •Achalasia

•Nonachalasia Motility
Disorders
•Cerebrovascular accidents •Strictures
•Amyotrophic Lateral •Rings/Webs
Sclerosis (AML) •GERD
•Parkinson's disease •Extraesophageal GERD
•Myasthenia gravis
•Tardive dyskinesia. •Neoplasia
•Esophageal Diverticula
•Foreign Bodies
•Pill-Induced Injury
•Infectious Esophagitis
•Caustic Injury
 Oropharyngeal dysphagia
• abnormality related to the movement
of a food bolus from the hypopharynx
to the esophagus
• arises from disease of the upper
esophagus, pharynx, or UES.
 Esophageal
dysphagia
↙ ↘
Solids only Solids & liquids
▼ ▼
Mechanical obstruction Motility disorder
↙ ↘ ↙ ↘
Intermittent progressive Intermittent progressive
▼ ▼ ▼ ▼

•Rings/Webs •Strictures •Esophageal •Achalasia

•Malignancy spasm •Scleroderma
 Oropharyngeal dysphagia
• typically present with difficulty
initiating a swallow and
immediately experience coughing,
choking, gagging, or nasal
regurgitation when attempting to
swallow
• most common caused by disruptions
in swallowing secondary to
neuromuscular dysfunction
• this setting, the symptoms may be
more severe when swallowing liquids
• The history and physical
examination should focus on
neurologic signs and symptoms
Neuromuscular dysfunction

• Cerebrovascular accidents
• Amyotrophic Lateral Sclerosis
(AML)
• Parkinson's dis­ease
• Myasthenia gravis
• Tardive dyskinesia.
• Rarely, structural abnormalities
caused such as
♥ cervical osteophytes
♥ hypopharyngeal diverticulum
(Zenker's diverticulum)
♥ tumors
♥ postcricoid webs
• typically note difficulty with a solid
food bolus leaving the mouth
• Oropharyngeal swallow is best
assessed by videofluoroscopy, also
known as the modified barium
swallow
• Videofluoroscopy not only serves
to confirm the presence of
oropharyngeal dysfunction
• It can also assess the degree of
aspiration
Esophageal Disease States
• Achalasia
• Nonachalasia Motility Disorders
• Strictures
• Rings/Webs
• Gastroesophageal Reflux Disease
• Extraesophageal GERD
• Neoplasia
• Esophageal Diverticula
• Foreign Bodies
• Pill-Induced Injury
• Infectious Esophagitis
• Caustic Injury
1. Achalasia
 Achalasia
• a primary esophageal motility
problem of unknown cause
• characterized by insufficient LES
relaxation and loss of esophageal
peristalsis
• hereditary, degenerative,
autoimmune, and infectious factors
as possible causes
• Pathologic changes occur in the
myenteric plexus
• consist of a patchy inflammatory
infiltrate of T lymphocytes,
eosinophils, and mast cells
• loss of ganglion cells and myenteric
neural fibrosis
• selective loss of post-ganglionic
inhibitory neurons, nitric oxide and
vasoactive intestinal polypeptide
• The postganglionic cholinergic
neurons are spared, leading to
unopposed cholinergic stimulation.
• This produces high basal LES
pressures, and the loss of inhibitory
input
• results in insufficient LES relaxation
• Aperistalsis along the esophageal
body—a process mediated by nitric
oxide.
• m/c symptoms of achalasia include
♥ dysphagia for solid & liquid

♥ regurgitation
♥ chest pain
• Patients with achalasia localize
their dysphagia to the cervical or
xiphoid areas.
• Initially, the dysphagia may be for
solids only
• most patients have dysphagia for
solids and liquids at time of
presentation
• Regurgitation occurs in 75% of
achalasia and becomes a greater
problem as the esophagus dilates
with progression of disease
• Choking and Coughing may
awaken the patient from sleep
• Chest pain 40%
• Weight loss 60% (minimal loss)
• barium esophagram with
fluoroscopy is the best initial
diagnostic study
• This test will reveal a loss of
primary peristalsis in the distal two
thirds of the esophagus
• In the upright position, there will be
poor emptying
• with retained food and saliva
producing a heterogeneous air-fluid
level at the top of the barium
column.
Achalasia
• The esophagus may be dilated (Figure
80-18).
esophagus is
dilated with a
"bird's beak"
tapering of the
distal
esophagus
Retained
secretions form
the heteroge-
nous air-fluid
level seen at
the top of the
barium column.
• chronic disease be massive with
sigmoid-like tortuosity

sigmoid-
like
tortuosity
with
large
amount of
retained
debris.

late-stage achalasia
• smooth tapering of the lower
esophagus leading to closed LES,
resembling a bird's beak
• presence of epiphrenie diverticulum
may suggest achalasia
Bird’s beak deformity at LES
• Esophageal manometry can be
used to diagnosis
• In the body of the esophagus,
aperistalsis is always present
• all swallows are typically with low
contraction amplitudes.
 Manometry

• Elevated resting
LES pressure
(>35 mmHg )
• Incomplete LES
relaxation
• Absence of
peristalsis
Manometry
Manometric findings in
achalasia
The aperistalsis is
manifested by isobaric
contractions without
propagation
The LES pressure,
which is elevated, shows
minimal relaxation with
swallowing.
Manometry
Manometric findings in
achalasia
The aperistalsis is
manifested by isobaric
contractions without
propagation
The LES pressure,
which is elevated, shows
minimal relaxation with
swallowing.
• Abnormal LES relaxation in all ach
alasia
• 70% - 80% of patients absent/ inco
mplete LES relaxation with swallow
s
• baseline LES pressure is usually el
evated but may be normal in up to
45% of patients
Esophagus is dilated with
retained fiuid and debris.
 • Non-relaxation of LES

• Asynchronous contraction and Non-peristaltic

• Fibrotic and atrophic

• Retention and stagnation of chronic food

• Retention esophagitis
• All should undergo upper GIT
endoseopy to exclude
Pseudoaehalasia arising from a tumor
at the GEJ
• Pseudoaehalasia may mimic with
classic achalasia both clinically and
manometrically
• suspected in older age with short
duration of symptoms and more
significant weight loss
 Therapy
• 1.Medical therapy
• 2.Pneumatic dilation of the LES
• 3.Surgical myotomy
• 4.Botulinum toxin injection
• The two most effective treatments
- graded pneumatic dilation
- surgical myotomy
• 1.Medical therapy
– Nitrates, calcium channel block
ers (nifedipine)
– Cause smooth muscle relaxatio
n but with limited success
• 2.Pneumatic dilation of the LES
-good short-term results
-2% to 5% risk of perforation
- performed endoscopy uses air
pressure to dilate and disrupt the

circular muscle fibers of the LES

• Balloon dilators,: three diameters
• (3, 3.5, and 4 cm) are positioned ov
er a guidewire
• After pneumatic dilation
 gastrograffin study
by barium swallow to
exclude esophageal
perforation
• relief of symptoms in 50% to 93%
Pneumatic dilation of the LES
• 3.Surgical myotomy
-fail repeated pneumatic dilations
-an anterior myotomy across the LE
S

(Heller's myotomy) usually associ

ated with an antire-flux procedure
-laparoscopy
• good-to-excellent
response rate of 8
0% to 94%
• A potential compli
cation of myotom
y

is GERD, which o
ccurs in 10% to 2
0%
• 4.Botulinum toxin injection
-Inhibits release of excitatory
acetylcholine from nerve endings
(thus causing lower LES
pressures)
-Good short-term results, but long
term efficacy unknow
-Effective in about; 85% of
patients
• However, symptoms recur in more
than 50% of patients after 6 months
• do not improve LES relaxation or i
mprove peristalsis
• do not provide complete symptom r
elief
• The clinical response is short acting
• efficacy decreases with time.
2.Non-achalasia M
otility Disorders
Non-achalasia Motility Diso
rders
• Other described primary motility dis
orders of the esophagus
• Defined based on the presence of s
pecific manomctrie criteria
• Most often noted on manometry in
patients with chest pain or dysphagia
2.1 Diffuse esophageal spasm (DES)
2.2 Scleroderma or
progressive systemic sclerosis (PSS)
2.3 Other systemic conditions
 Diffuse Esophageal Spasm
• Repetitive, high amplitude contractions
of smooth muscle portion of the
esophagus
• The striated portion and LES
relaxation normally.
• Histopathology : muscular hypertrophy
with lymphocytic infiltration of
Auerbach’plexus
• S&S: dysphagia and chest pain
(substernal) or esophageal colic
which may occur with or without
swallowing.
• Triggered by emotional stress, hot
or cold liquids and GE reflux
• DES may present with:
a) chest pain if the contraction
amplitudes are high
b) dysphagia if the contraction
amplitudes are low.
• Investigations: CXR, cardiac
evaluation, barium study and
manometry
• LES relaxation is also normal in DES
• The classic finding on esophagogram
is the "corkscrew" esophagus
 Radiographic
– Classic
“corkscrew”
– Beak-like
taper
– Increase in
esophageal
wall thickness
• Manometrie :simultaneous and
repetitive contractions in the
esophageal body
• but in contrast to achalasia, some
normal peristalsis is maintained
• Typical : corkscrew
pattern
• Manometry :
prolong, high
amplitude
nonperistalsis
• Both UES and LES
normal, but elevate
LES pressure may
be found.
• "Nutcracker" esophagus is another
common manometrie diagnosis in n
oncardiac chest pain
• defined by high-amplitude peristalsi
s
• distal esophageal contraction ampli
tude less than 30 mmHg in 30% or
more of wet swallows
• a food bolus may not be effectively
transported, resulting in dysphagia
 Treatment
• 1.Reassuring the disease is not heart
disease.
• 2.Medication : nitroglycerine, calcium
blocker, anticholinergic, PPI (Rx for
GERD) (not completely effective)
• 3.Surgery :
– 3.1 Dilation: help only in LES
dysfunction, improve dysphagia
temporarily
– 3.2 Surgical myotomy
 Scleroderma
• progressive systemic sclerosis (PSS
)
• Secondary motility disorders are co
mmonly a result of systemic conditio
ns
• The most common condition affectin
g esophageal motility
• Esophageal motor disturbances
occur in several of the collagen
vascular diseases
– Dermatomyositis
– Polymyositis
– Lupus erythematosus
– Scleroderma (extremely common)
• Characterized by :
• Smooth muscle atrophy and collagen
deposition in the submucosa

• Decrease peristalsis and LES resting

pressure

• Refulx esophagitis, ulceration,

bleeding
 Radiography
• Dilate
esophagus with
decreased
motility (unlike
achalasia,
persistent patent
GE junction and
no air fluid level)
Scleroderma
• Endoscopy:
• Reflux
esophagitis
 Other systemic conditions
• results in esophageal hypomotility
– hypothyroidism
– diabetes mellitus
– amy-loidosis
 Investigation
• Esophageal manometry and
intraesophageal pH readings are the
most sensitive means of detection
• Diminished contractions in LES and
distal two thirds of the esophagus
 Treatment
• Standard antireflux medicine
• In patients with intractable symptoms
gastroesophageal reflux surgery
should be considered
 3.Strictures

• .
 Strictures
• defined as any loss of lumen area
within the esophagus
• The normal esophagus measures 2
0 mm in diameter
• The predominant clinical symptom
of strictures is dysphagia, which is
usually when the lumenal diameter
is less than 15 mm.
• Even less severe strictures can cau
se intermittent dysphagia to large fo
od piece ; meat and bread
• There are multiple intrinsic and extri
nsic causes for esophageal strictur
es
 Etiology of Esophageal Strictures
• Intrinsic strictures
– Acid (peptic)
– Pill-induced
– Chemical/lye
– Post-nasogastric tube
– Infectious esophagitis
– Sclerotherapy
– Radiation-induced
– Esophageal/gastric malignancies
– Surgical anastomotic
– Congenital
– Systemic inflammatory disease
• Extrinsic strictures
– Pulmonary/mediastinal malignancies
– Anomalous vessels and aneurysms
– Metastatic submucosal infiltration (bre
ast cancer, mesothelioma, adenoeare
inoma of gastric eardia)
• Intrinsic strictures are most commo
n, with acid/ peptic cause accountin
g for the majority of cases (60%-70
%)
Strictures / Caustic Ingestion
 Treatment
• esophageal dilation.
• There are several different types: of dilat
ors, including:
(1) mercury-filled, rubber Maloney dilator
s;
(2) wire-guided rigid Savary-Gilliard di
lators;
(3) balloon dilators that can either be thr
ough-the-scope (TT8) or wire guided
• Maloney bougies are used in unco
mplicated, short, straight strictures
• The wire-guided Savary-Gilliard an
d TTS balloons are both best suited
for long, tight, or tortuous strictures.
• Complications of esophageal dilation
– perforation (0.5%)
– bleeding (0.3%)
– bacteremia (20%-50% )
• Those with radiation-induced or mali
gnant strictures are at higher risk of
perforation.
• To minimize the risk of perforation, th
e "rule of. threes" applies.
• That is, no more than three sequen­t
ial dilators should be performed per
session.
• The goal of esophageal dilation is t
o obtain an objective diame­ter of gr
eater than 15 mm
• Approximately 90% of; patients dila
ted to 15 mm have no recurrence at
; 24 months
• Refractory esophageal strictures are d
efined by lack of response to two or m
ore dilations.
• The causes, for refractory strictures ca
n include
• ongoing insults from pills or nonsteroid
a] antiinfkunmatory drugs(NSAlDs)
• uncontrolled acid reflux
• inadequate lumen diameter with
dilations
• PPIs are superior to H-2 blockers in
preventing the recurrence of acid-re
lated strictures
• The treatment of refractory stricture
s includes the elimination of the off
ending agents (pills and acid) and g
entle dilation to 15 mm.
• Intralesional steroids injected befor
e dilation are safe and probably eff
ective for refractory strictures
• Surgery may be considered in thos
e who fail to respond to aggressive
medical therapy and dilation.
4.Rings/Webs
 Rings/Webs
• common findings on upper endosc
opy,
• many are asymptomatic
• Symptoms can include intermittent
solid food dysphagia, aspira­tion, an
d regurgitation.
• Rings are circumferential, can consi
st of mucosa or muscle, and most c
ommonly occur in the distal esopha
gus
• Esophageal webs occupy only part
of the esophageal lumen, are alway
s mucosal, and are usually located i
n the proximal esophagus.
• Esophageal webs can be found as
5% of asymptomatic individuals
• When symptomatic, usually
dysphagia
• iron deficiency was noted by gas-
troenterologists
• Plummer and Vinson in the United
States, as well as otolaryngologists
Paterson and Kelly in the United
Kingdom.
• Plummer-Vinson or Paterson-Kclly
syndrome to the triad of proximal e
sophageal webs, iron deficiency an
emia, and dysphagia
• Barium radiography is the most sen
sitive test to diagnose esophageal
webs
• endoscopic visualization, web will a
ppear as a thin, eccentric lesion wit
h normal-appuaring mucosa
• Some webs are located so proximal
ly that routine passage of the endos
cope through the UES with fracture
the web
• Treatment of symptomatic esophag
eal webs consists of mechanical dis
rup­tion
• This can be accomplished with bou
gie or balloon dilators.
• Schatzki's ring (B ring) occurs at th
e GEJ at the distal margin of the LE
S
• most common cause of intermittent
solid food dysphagia and food impa
ction
• The presence of symptoms depend
s on the luminal diameter
• If the ring diameter is less than 13
mm, the patient will have symptoms
• If greater than 20 mm the patient will
almost never have symptoms
• Between 13 and 20 mm, which
accounts for the majority of
Sehatzki's rings, symptoms are
variable
• The pathogenesis of esophageal
rings is controversial
• Recurrent symptoms requiring repe
at dilation is not uncommon, and so
me authors recommend maintainin
g the patient on acid suppression gi
ven the possible association with G
ERD
• The second type of esophageal ring is
the A ring",
• which is a muscular ring most common
ly detected on barium swallow
• This lower esophageal muscular ring
is rarely symptomatic and occurs at
the proximal margin of the LES
approximately 2 cm proximal to SGM.
• "Ringed" esophagus is a rare condi
tion that occurs in young men
• The syndrome consists of endosco
pie findings of multiple esophageal
rings in patients with dysphagia
• The cause is unclear
• GERD. congenital abnormality, and
possible allergic conditions have be
en implicated
Esophageal Webs and Rings
 Treatment
• Treatment consists of dilation with b
ougienage and possibly acid suppre
ssion
• Many of these patients require more
than one treatment session to obtain
a desired esophageal lumen of 15 m
m
• They are also at higher risk of painfu
l deep mucosal tears
 5.
Gastroesophageal
Reflux Disease
 Gastroesophageal Reflux
Disease
• chronic symptoms or mucosal dam
age caused by the abnormal reflux
of gastric contents into the esophag
us.
• Reflux esophagitis refers to a sub
group of GERD that involves histop
athologically characteristic change
s in the esophageal mucosa
• Nonerosive reflux disease (NERD)
refers to endoseopy-negative patie
nts with typical GERD symptoms
• NERD accounts for approximately
50% of patients
• Reflux esophagitis for 30% to 40%
• Barrett's esophagus in the remainin
g 10% to 20%
Barrett’s esophagus
Barrett’s esophagus with
ulceration
Barrett’s esophagus
 Pathophysiology
• Transient relaxation of the GE
sphincter
• Esophageal motility disorders
• Delayed gastric emptying
• Hiatal hernia
• Acidic gastric contents
• Bile acids (more severe eophagitis )
• normal antireflux barrier between th
e stomach and the esophagus is im
paired transient / permanently
• defects in the esophagogastric barri
er such as LES incompetence, TLE
SR, and hiatal hernia in the devel
opment of GERD
• TLESRs are short relaxations of the
LES that do not occur in response
to swallow
• TLESRs are the primary
mechanism for gastroesophageal
reflux in healthy persons and in
those with mild GERD
• severe GERD and related
complications have a permanent
structural alteration
– low LES pressure
– a large hiatal hernia
• Symptoms develop when the offens
ive factors in the gastroduodenal co
ntents overcome several lines of es
ophageal defense
• As more components of esophagea
l defense break down, the severity
of reflux increases
• Classic symptoms of GERD are he
artburn
• defined as a retrosternal burning di
scomfort, and acid regurgitation
• Symptoms often occur after meals
• Other in typical reflux are dysphagi
a, odynophagia, and belching
• Atypical GERD symptoms include a
sthma, chest pain, cough, laryngitis
, and dental erosions.
• There is no diagnostic gold .standar
d for detecting GERD
• Classic symptoms of acid regurgitat
ion and heartburn are specific but n
ot sensitive for the diagnosis of GE
RD
• as determined by abnormal 24-hour
pH monitoring.
• initial empiric trial of antisecretory t
herapy in a patient with classic GE
RD symptoms
• Further diagnostic should be done
– if there is a failure to respond to a
n empiric course
– if alarm signs such as dysphagia,
odynophagia, weight loss, chest
pain, or choking are present.
 Atypical symptoms
• Atypical chest pain • Globus sensation
• Hoarseness • Onset after age 45
• Nausea • Recurrent laryngitis
• Cough • Recurrent sore
• Odynophagia throat
• Asthma • Subglottic stenosis
• Dental enamel loss
• Endoscopy is the technique of choice t
o evaluate GERD
• Reflux esophagitis is present when er
osions or ulcerations are present at S
CM
• There are many grading systems to ch
aracterize the severity of esophagitis,
• the most common of which is the
Los Angeles classification
• Results are normal in 25% of patien
ts with erosive esophagitis and 33
% of patients with nonerosive reflux
disease
 Radiologic Finding
• Only 1/3 of patients have radiologic
findings
– Erosions
– Ulcerations
– Strictures
– Hiatal hernia
– Thickening of mucosal folds
• Not the test of choice for diagnosis
Esophagogram

Extensive linear
superficial
ulcerations and
erosions involving
the distal 1/3 of
the esophagus.
 Endoscopy
• Useful for diagnosing complications
of GERD
– Barrett’s
– Esophagitis
– Strictures
• Not sensitive for GERD itself
• Only 50% of patients manifest
evidence on endoscopy
Gastroesophageal Reflux Disease
Esophagoscopy
 Ambulatory pH Mornitoring
• Diagnostic gold standard
• pH monitor placed in esophagus
above sphincter
• Patient symptom log
• Correlate symptoms with low pH
 TREATMENT
• Lifestyle modifications
• Antacids
• Histamine H2 receptor antagonists
• Prokinetic Agents
• Proton Pump inhibitors
• Anti-reflux surgery
• Newer endoscopic treatments
 LIFESTYLE MODIFICATION
• Head of bed elevated six inches
• Decreased fat intake
• Smoking cessation
• Weight loss
• Avoidance of recumbency for 3 hours post-
prandially
• Avoidance of large meals and trigger foods
• Avoidance of exacerbating medications
• The goals of treatment in GERD are to
– relieve symptoms
– heal esophagitis
– prevent recurrence of symtoms
– prevent complications
• A variety of lifestyle modifications are r
ecommended in the treatment off GER
D.
• These include
– avoidance of precipitating foods(f
atty foods, alcohol, caffeine)
– avoidance of recumbency for 3 h
ours postprandially
– elevation of the head of the bed
– smoking cessation
– weight loss
• Histamine receptor antagonists
(H2RAs) in standard doses
achieve complete symptom relief
in 60% of patients and heal
esophagitis in bout 50%
• PPIs are superior to H2RAs in both
healing rosive esophagitis and
symptoms relief, with healing 90%
• GERD is a chronic relapsing
disease with almost universal
recurence of symptoms after
treatment withdrawal
• requires maintenance therapy in
many patients
• longterm therapy with PPIs is
again superior to H2RAs, with
remission maintained in 80% and
50% of patients, respectively
• "step-down" therapy is recommend
ed
• Antireflux surgery, now
laparoscopic approach, remains an
option for carefully selected patient
s with well documented GERD
 Surgical Treatment
• Nissen fundoplication
– Total or partial
• Their aim is to:
– Restore normal anatomy (intra-
abdominal segment of esophagus)
– Re-creating an appropriate high-
pressure sound at the
esophagogastric junction
– Maintaining this repair in the normal
anatomic position
6.Extraesophageal
GERD
 Extraesophageal GERD
• Patients with GERD may present wi
th symptoms other heartburn and r
egurgitation
• This includes asthma, chest pain, c
hronic cough, laryngitis, and dental
erosions
• lack of the classic heartburn and re
gurgitation symptoms
• Esophagitis/Barrett's esophagus is
usually not present
• an empiric trial of bid PPIs is indicat
ed as initial treatment because ther
e is no definitive diagnostic gold sta
ndard for GERD.
• If treatment fails
– full investigation
– ambulatory pH testing
• Confirm diagnosis of GERD when
– symptoms relieve by specific antireflu
x therapy
Extraesophageal GERD
• Laryngitis
• Asthma
• Chest pain
• Chronic cough
• Dental erosions
7.Neoplasia
 Neoplasia

• uncommon
• when present is typically malignant.
• The two main culprits are
– esophageal squamous cell carcin
oma
– esophageal adenocarcinoma.
Benign Esophageal Tumors and
Cysts

• Benign tumors are rare (< 1 %)

• Classified in two groups
– Mucosal
– Extramucosal (intramural)
• More useful classification:
– 60% of benign neoplasms are
leiomyomas
– 20% are cysts
– 5% are polyps
– Others (< 2 percent)
 Leiomyomas
• Most common benign tumor of the
esophagus
• Intramural
• Occur between 20-50 years of age
with no gender preponderance
• 80% occur in the middle and lower
third of the esophagus, rare in the
cervical region
• Obstruction and regurgitation may
occur in large lesions
• Bleeding is a more common
symptom of the malignant form of
the tumor: leiomyosarcoma
Cancer
Malignant Tumors of the
Esophagus
• Usually are in advanced stages at
the time of diagnosis (involving the
muscular wall and extending into
adjacent tissues)
• Alcohol consumption and cigarette
smoking seem to be the most
consistent risk factors
• Esophageal squamous cell
carcinoma
– Esophageal squamous cell
carcinoma (95% of all esophageal
cancers) is a disease of men (5:
1)
– most often in the upper and
midthoracic segments
– least frequently in the cervical
esophagus
• Adenocarcinoma
– approximate 8% of primary
esophageal cancers
– Most often occur in the distal third of
the esophagus in the 6th decade of
life.
– Male to female ratio is 3:1
– Patients with Barretts metaplasia are
40 times more likely to develop
adenocarcinoma
 Clinical Presentation
• Dysphagia is the presenting
complaint in 80-90% of patients with
esophageal carcinoma
• Early symptoms are sometimes
nonspecific retrosternal discomfort or
indigestion
• As the tumor enlarges, dysphagia
becomes more progressive.
• Later symptoms include weight
loss, odynophagia, chest pain and
hematemesis
 Diagnosis
• Barium swallow
• Esophagoscopy
• Esophageal biopsy
• Brushings for cytologic evaluation
Barium
Barium
Cancer: apple core appearance
Current AJCC 2002 staging
 Treatment
• Surgical resection is the standard
treatment for early esophageal
cancer in Stages I, II and most cases
of III
• During the past decade, outcomes
with surgery have improved resulting
in a better 5 year survival due to:
– Better staging techniques
– Increased rate of curative resection
– A decreased rate of postoperative
death
– Palliative endoscopic measures
• Palliative endoscopic measures inclu
de
– repeated dilation,
– laser/photo dynamic therapy ablati
on
– esophageal stent placement
– percutaneous gastrostomy tube pla
cement
 Neoadjuvant /adjuvant
therapy
• Neo-adjuvant Chemotherapy
• Neo-adjuvant Radiation
• Neo-adjuvant Chemo-Radiation
• Adjuvant Chemotherapy
• Adjuvant Radiation
• Adjuvant chemoradiation
8.Esophageal Dive
rticula
 Esophageal Diverticula
• is a sac that protrudes from the esoph
ageal wall
• As in the rest of the Gl tract
• a true diverticulum is one that contain
s all layers of the wall.
• Esophageal diverticula are most pr
actically classified, based on anato
my, into four categories:
– Zenker's diverticula
– midesophageal diverticula
– epiphrenic diverticula
– intramural pseudodiverticulosis.
• Zenker's divertieulum referred to as
an esophageal diverticulum
• its location is proximal to the
esophagus, above the UES, and it
should be considered a
hypopharyngeal diverticulum.
• believed to form as a result of an
area of weakness
• Killian's triangle, which exists
between the cricopharyngeal
sphincter and the inferior
pharyngeal constrictor muscle
Zenker’s diverticulum
• Occurs in Killian’s
area.
• Associated with failure
of cricopharyngeal
dilatation.
• Symptoms:
regurgitation,
dysphagia, weight loss.
• Symptoms include
– oropharyngeal dysphagia
– regurgitation
– halitosis
– cough
– aspiration pneumonia
• Barium swallow is an excellent test
• Many small diverticula are asympto
matic
• patients with large diverticula shoul
d be offered treatment
• The classic treatment
– open surgical resection of the divertic
ulum with division of the cricopharyng
cus muscles
• Another option for extremely large
diverticula
– diverticulopexy
– suspension of the diverticulum in a cr
anial direction.
• Midesophageal diverticula are most
commonly asymptomatic, occur in th
e midesophagus
• Traction diverticuli form as a result o
f external pulling of the esophageal
wall
from neighboring inflammatory or

fibrotic tissue, such as adjacent tube

rculous mediastinitis
• Traction diverticuli are located in th
e middle third of the esophagus.
• Midesophageal traction diverticula
are the only true diverticula in the e
sophagus
• Epiphrenic diverticula, located near
the diaphragmatic hiatus, occur in t
he distal esophagus near the LES
• These diverticula are often the resu
lt of a motility disorder such as ach
alasia or DES
• manometric studies in patients with
epiphrenic diverticulum to rule out a
n associated motility disorder
• Most diverticula are asymptomatic,
but occasionally chest pain or regur
gitation can be prominent symptom
s
Midesophageal Diverticula
Epiphrenic Diverticula
 Treatment
• Treatment consists of
• managing the underlying motilit
y disorder
• diverticulotomy with/without my
otomy for symptomatic diverticu
la
9.Foreign Bodies
Foreign Bodies
 Foreign Bodies
• The esophagus is one of the locations
where intervention is often required
• Underlying alterations in the lumen of
the esophagus play an important role
in the risk of a swallowed object beco
ming lodged
• The esophagus has several areas
of physiologic narrowing
– the upper esophageal sphincter
– the level of the aortic arch
– the diaphragmatic hiatus/LES wh
ere a foreign body can become i
mpacted.
• The key to the management of forei
gn bodies is understanding that diff
erent foreign bodies require differe
nt interventions
• It is important to distinguish a true f
oreign body from a food impaction.
• A trial of pharmacologic therapy
with .1 to 2 mg of glucagon given
intravenously, which relaxes the LES,
can be given but is rarely successful
in relieving a food' impaction.
10.Pill-Induced Injur
y
 Pill-Induced Injury
• Pill-induced injury to the esophagus
is an underappreciated entity.
• over 70 drugs are capable of produ
cing injury to the esophagus
• Drugs commonly associated with pi
ll-induced injury include potassium
chloride tablets, doxycycline, quuud
ine, NSAIDs. iron, and alendronate
• Pills can damage the esophagus by
various mechanisms such as acidit
y, size, and contact time with esoph
ageal mucosa
• There is a wide spectrum of injury

from acute self-limited esophagitis t

o refractory strictures
• The typical sites of pill-induced injur
y are at the level of the aortic arch
and the distal esophagus, where th
ere is anatomic narrowing.
11.Infectious Esop
hagitis
 Infectious Esophagitis
• Infectious esophagitis is common, e
specially in immunosuppressed hos
ts such as patients with human imm
unodeficiency virus (HIV), transplan
t patients, and chemotherapy patie
nts.
• The cardinal symptom of infectious
esophagitis is
– odynophagia
– pain
– swallowing
• immunodeficient patients can prese
nt with a variety of symptoms includ
ing heartburn, nausea, fever, or ble
eding.
• The three most common causes of
infectious esophagitis are
– Candida albicans
– cytomegalo virus (CMV)
– herpes simplex virus (HSV)
• Treatment consists of antifungal the
rapy, most commonly with fluconaz
ole100 to 200 mg/day for10 to 14 d
ays
• In patients with only mild immunolo
gic deficiencies, the topical antifung
al agents clotrimazole and nystatm
are reasonable alternatives
12.Caustic Injury
 Caustic Ingestion
• Esophagus, pharynx, larynx
• Bases ( most severe injuries )
– Drain cleaners
– Electric dishwasher soap
– Hair relaxant
• Acids
• Bleaches
 Mechanism of injury
• Alkalis – pH > 7
– Liquefaction necrosis
• Acids – pH < 7
– Coagulation necrosis
• Bleaches – pH = 7
– Irritants
 Severity of burn
• Type
• Amount
• Concentration
• Time of contact
• Stricture formation
 Signs and symptoms
• Pharyngeal or • Esophageal
laryngeal – Dysphagia
– Odynophagia – Odynophagia
– Mucosal – Chest or back
erythema, pain
ulceration • Gastric
– Drooling
– Epigastric pain or
– Tongue edema tenderness
– Stridor – Vomiting
– Hoarseness – Hematemesis
 Radiography
• Radiologic exam
– Chest & neck
radiographs
• Barium swallow
– Will not reveal 1st
and 2nd degree
injuries
 Esophagoscopy
• Esophagoscopy in virtually all patients at
24-48 hours post-ingestion
• < 24 hours – underestimation of injury
• > 48-72 hours with risk of iatrogenic
perforation – barium swallow
• Rigid vs. flexible debatable
• Endoscopy to upper limit of severe burn
 Management

• 1. Stable airway
• dexamethasone (adult 20 to 30
mg intravenous bolus, pediatric
0.5 to 1 mg/kg) can help
prevent further deterioration
• 2. Acute airway obstruction
• Blind nasotracheal intubation
should be avoided
• If direct visualization of the
larynx for intubation is not
possible because of edema
and exudate, emergent
cricothyrotomy or tracheotomy
is a safer choice
 Therapy
• Choice of therapy depends on the
degree of injury.
• 1. First-degree burns of the
esophageal mucosa require no
further therapy
• 2. Second- and localized third-
degree injuries without transmural
necrosis:
• pharmacologic reduction or
prevention of stricture formation
and to maintain a conduit from
the hypopharynx to the stomach
by esophageal dilation,
stenting, or reconstruction
• 3. Fourth-degree and even selected
extensive third-degree esophageal
burns:
• thoracotomy for direct
examination of the esophageal
wall esophagectomy
Foreign bodies
 Strictures and narrowing
• Malignant/benign
• Cricopharyngeal bar
• C-spine osteophytes
• Kyphosis
• Post cricoid web
Cricopharyngeal bar
Osteophytes
 Neurogenic
• CVA
• Motor neurone disease
• Multiple Sclerosis
• Parkinson’s disease
• Myaesthena gravis
 GLOBUS PHARYGEUS
• Previously Globus Hystericus
• Worse when NOT eating or drinking
• Actually improves on swallowing
• No true dysphagia solids/liquids
• No odynophagia
• No regurgitation/aspiration
• Variable history? exclude reflux…..
 Laryngopharyngeal Reflux
(LPR)
• Reflux of gastric acid to larynx/pharynx
• May be “silent”
• Symptoms include feeling of a lump,
odynophagia/chronic sore throat, chronic
cough (especially nightime), hoarse voice
and “mucous in throat”.
 LPR Investigations
• Nasopharyngoscopy, red post cricoid
region.
• ? Barium swallow?
• Oesophageal pH manometry
 LPR treatment
• 6 weeks PPI + Gaviscon initially
• At review further 6 weeks treatment if
improving
• General laryngeal hygiene measures
• If no better, rigid pharyngo-
oesophagoscopy
• pH manometry ?fundoplication
 Pharyngeal pouches
• HISTORY
• Long Hx dysphagia
• Regurgitation esp at night
• “gurgling” swallow
• Aspiration (recurrent pneumonia)
• Weight loss and change in Diet.
 Pharyngeal Pouches
• EXAMINATION
• Nasopharyngoscopy might show pooling
• Unlikely to feel anything in neck
• Barium swallow
 Pharyngeal pouches
• TREATMENT
• Surgical if fit for GA
• (External approach)
• Endoscopic stapling, low morbidity and
high success rate.
 Pouches

BARIUM SWALLOW.jpg
Pouches

BARIUM SWALLOW.jpg
 Summary :Fast track patients
• Young male patient
• Short history
• Odynophagia
• Smoking and Alcohol
• Weight loss
• Aspiration and reguritation
 Summary: Globus patients
• Variable history
• No true dysphagia
• Young female
• No weight loss
• Associated anxiety
 Summary: Pouch patients
• Older male/female
• REGURGITATION
• Gurgling swallow
• Recurrent chest infections
• Weight loss
Diseases of the pharynx

• May be a generalized disease of the whole

pharyngeal structure
• May affect the specific pharyngeal structures
A. Acute pharyngitis
- due to allergic reaction
- effect of toxic fumes
- bacterial infection e.g. Streptococcal spp
Symptoms
- odynophagia, fever, lymph adenopathy
Mgt. – systemic ABC
B. Chronic pharyngitis
• is a long standing or protracted
pharyngeal infection
• Has low grade complaints
• Symptoms are also milder than those of
the acute form
• Mgt. is usually by ABC and/or removal of
the causative organisms
• Other specific infections of the pharynx include
fungal infection, diphtheria, TB, retropharyngeal
and parapharyngeal abscesses
• Diseases of the specific structures of the
pharynx include
- structures of the Waldeyer’s ring
a) Adenoiditis
nasal obstruction, d/c, mouth breathing, otitis
media, CSOM, OME
Diagnosis is from history and clin exam
Mgt. adenoidectomy
b) Tonsillitis
- may be bacterial or viral
- may exhibit odynophagia, pus exudates, crypt
debris, cervical gland enlargement, fever,
otalgia, TMJ pain syndrome
- may give a complication of peritonsillar abscess
(Quincy)
- ABC
- symptomatic for viral infections
- tonsillectomy for recurrent bact infections –
done 4 – 6 weeks post healing
c) chronic tonsillitis
- result from repeated acute attacks or from
incomplete resolution
d) peritonsillar abscess
- infection passes into peritonsillar tissues
causing cellulitis
- symptoms include
odynophagia, drooling, otalgia, trismus, soft
palate swelling, jugulodigastric lymph node
swellings
- Mgt I & D then 4 – 6 weeks later, tonsillectomy
Obstructive Sleep Apnea Syndrome
• Symptoms of snoring, mouth breathing,
behavioral changes, poor growth,
hypersomnolence
-due to physical hypertrophy of adenoid and
tonsils
-due to congenital malformations such as Down
Syndrome

Mgt. in case of adenotonsillar hypertrophy is

adenotonsillectomy
Indications for tonsillectomy
- Recurrent infection
- Peritonsillar abscess
- Sleep apnea
- Unilateral hypertrophy
- Rheumatoid disease

Complications of tonsillectomy
- Reactionary bleeding within 24 hrs
- Secondary bleeding due to sloughing