Transcript Dysphagia disease

Dysphagia
Dr.Krisana Thaitong
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
Oropharyngeal dysphagia
Esophageal dysphagia
Dysphagia
Dysphagia
↙
Oropharyngeal dysphagia
▼
Neuromuscular
dysfunction
▼
•Cerebrovascular accidents
•Amyotrophic Lateral
Sclerosis (AML)
•Parkinson's disease
•Myasthenia gravis
•Tardive dyskinesia.
↘
Esophageal dysphagia
▼
•Achalasia
•Nonachalasia Motility
Disorders
•Strictures
•Rings/Webs
•GERD
•Extraesophageal GERD
•Neoplasia
•Esophageal Diverticula
•Foreign Bodies
•Pill-Induced Injury
•Infectious Esophagitis
•Caustic Injury
Esophageal dysphagia
↙
Solids only
↘
Solids & liquids
▼
▼
Mechanical obstruction
↙
Intermittent
▼
Motility disorder
↘
progressive
▼
•Rings/Webs •Strictures
•Malignancy
↙
Intermittent
▼
•Esophageal
spasm
↘
progressive
▼
•Achalasia
•Scleroderma
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.
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 dysphagia
 the difficulty in propagating food down the
esophagus
 arises within the body of the esophagus
either due to a mechanical or a motility
disturbance.
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 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 heterogenous air-fluid
level seen at
the top of the
barium column.
 chronic disease be massive with
sigmoid-like tortuosity
sigmoidlike
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.
 Abnormal LES relaxation in all
achalasia
 70% - 80% of patients absent/
incomplete LES relaxation with
swallows
 baseline LES pressure is usually
elevated but may be normal in up to
45% of patients
Esophagus is dilated with
retained fiuid and debris.
 Nonrelaxation of LES
 Asynchronous contraction and Nonperistaltic
 Fibrotic and atrophic
 Retention and stagnation of chronic food
 Retention esophagitis
 All should upper 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 and surgical
myotomy
 1.Medical therapy
– Nitrates, calcium channel blockers
(nifedipine)
– Cause smooth muscle relaxation
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 over 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 LES
(Heller's myotomy) usually
associated with an antire-flux
procedure
-laparoscopy
 good-to-excellent
response rate of
80% to 94%
 A potential
complication of
myotomy
is GERD, which
occurs in 10% to
20%
 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
improve peristalsis
 do not provide complete symptom
relief
 The clinical response is short acting
 efficacy decreases with time.
2.Nonachalasia
Motility Disorders
Nonachalasia Motility
Disorders
 Other described primary motility
disorders of the esophagus
 Defined based on the presence of
specific 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 with
may occur with or without swallowing.
 Trigger by emotional stress, hot or cold
liquids and GE reflux
 DES may present with chest pain if the
contraction amplitudes are high
 dysphagia if the contraction amplitudes
are low.
 Investigate: 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”
– Beaklike 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
nonperistaltic
 Both UES and LES
normal,but elevate
LES pressure may be
found.
 "Nutcracker" esophagus is another
common manometrie diagnosis in
noncardiac chest pain
 defined by high-amplitude peristalsis
 distal esophageal contraction
amplitude 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
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 arc
commonly a result of systemic
conditions
 The most common condition affecting
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 20
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 cause
intermittent dysphagia to large food
piece ; meat and bread
 There are multiple intrinsic and
extrinsic causes for esophageal
strictures
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
Epidermolysis bullosa
 Extrinsic strictures
– Pulmonary/mediastinai malignancies
– Anomalous vessels and aneurysms
– Metastatic submucosal infiltration (breast
cancer, mesothelioma, adenoeareinoma of
gastric eardia)
 Intrinsic strictures are most common,
with acid/ peptic cause accounting for
the majority of cases (60%-70%)
Strictures / Caustic Ingestion
Treatment
 esophageal dilation.
 There are several different types: of
dilators, including:
(1) mercury-filled, rubber Maloney dilators;
(2) wire-guided rigid Savary-Gilliard
dilators; (3) balloon dilators that can either
be through-the-scope (TT8) or wire guided
 Maloney bougies are used in
uncomplicated, short, straight strictures
 The wire-guided Savary-Gilliard and
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
malignant strictures are at higher risk
of perforation.
 To minimize the risk of perforation, the
"rule of. threes" applies.
 That is, no more than three sequential
dilators should be performed per
session.
 The goal of esophageal dilation is to
obtain an objective diameter of greater
than 15 mm
 Approximately 90% of; patients dilated
to 15 mm have no recurrence at; 24
months
 Refractory esophageal strictures are
defined by lack of response to two or
more dilations.
 The causes, for refractory strictures can
include
 ongoing insults from pills or
nonsteroida] antiinfkunmatory
drugs(NSAlDs)
 uncontrolled acid reflux
 inadequate lumen diameter with
dilations
 PPIs are superior to H-2 blockers in
preventing the recurrence of acidrelated strictures
 The treatment of refractory strictures
includes the elimination of the
offending agents (pills and acid) and
gentle dilation to 15 mm.
 Intralesional steroids injected before
dilation are safe and probably effective
for refractory strictures
 Surgery may be considered in those
who fail to respond to aggressive
medical therapy and dilation.
4.Rings/Webs
Rings/Webs
 common findings on upper endoscopy,
 many are asymptomatic
 Symptoms can include intermittent
solid
food dysphagia, aspiration, and
regurgitation.
 Rings are circumferential, can consist
of mucosa or muscle, and most
commonly occur in the distal
esophagus
 Esophageal webs occupy only part of
the esophageal lumen, are always
mucosal, and are usually located in the
proximal esophagus.
 Esophageal webs can be found as 5%
of asymptomatic individuals
 When symptomatic, usually
dysphagia
 iron deficiency was noted by gastroenterologists
 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
esophageal webs, iron deficiency
anemia, and dysphagia
 Barium radiography is the most
sensitive test to diagnose esophageal
webs
 endoscopic visualization, web will
appear as a thin, eccentric lesion with
normal-appuaring mucosa
 Some webs are located so proximally
that routine passage of the endoscope
through the UES with fracture the web
 Treatment of symptomatic esophageal
webs consists of mechanical disruption
 This can be accomplished with bougie
or balloon dilators.
 Schatzki's ring (B ring) occurs at the
GEJ at the distal margin of the LES
 most common cause of intermittent
solid food dysphagia and food
impaction
 The presence of symptoms depends 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 repeat
dilation is not uncommon, and some
authors recommend maintaining the
patient on acid suppression given the
possible association with GERD
 The second type of esophageal ring is
the A ring",
 which is a muscular ring most
commonly detected on barium swallow
 This lower esophageal muscular ring
 rarely symptomatic and occurs at the
proximal margin of the LES
approximately 2 cm proximal to SGM.
 "Ringed" esophagus is a rare condition
that occurs in young men
 The syndrome consists of endoscopie
findings of multiple esophageal rings
in patients with dysphagia
 The cause is unclear
 GERD. congenital abnormality, and
possible allergic conditions have been
implicated
Esophageal Webs and Rings
Treatment
 Treatment consists of dilation with
bougienage and possibly acid
suppression
 Many of these patients require more
than one treatment session to obtain a
desired esophageal lumen of 15 mm
 They are also at higher risk of painful
deep mucosal tears
5. Gastroesophageal
Reflux Disease
Gastroesophageal Reflux
Disease
 chronic symptoms or mucosal damage
caused by the abnormal reflux of
gastric contents into the esophagus.
 Reflux esophagitis refers to a subgroup
of GERD that involves
histopathologically characteristic
changes in the esophageal mucosa
 Nonerosive reflux disease (NERD)
refers to endoseopy-negative patients
with typical GERD symptoms
 NERD accounts for approximately
50% of patients
 Reflux esophagitis for 30% to 40%
 Barrett's esophagus in the remaining
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 the
stomach and the esophagus is impaired
transient / permanently
 defects in the esophagogastric barrier
such as LES incompetence, TLESR,
and hiatal hernia in the development
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 offensive
factors in the gastroduodenal contents
overcome several lines of esophageal
defense
 As more components of esophageal
defense break down, the severity of
reflux increases
 Classic symptoms of GERD are
heartburn
 defined as a retrosternal burning
discomfort, and acid regurgitation
 Symptoms often occur after meals
 Other in typical reflux are dysphagia,
odynophagia, and belching
 Atypical GERD symptoms include
asthma, chest pain, cough, laryngitis,
and dental erosions.
 There is no diagnostic gold .standard
for detecting GERD
 Classic symptoms of acid regurgitation
and heartburn are specific but not
sensitive for the diagnosis of GERD
 as determined by abnormal 24-hour pH
monitoring.
 initial empiric trial of antisecretory
therapy in a patient with classic GERD
symptoms
 Further diagnostic should be done
– if there is a failure to respond to an
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
 Subglottic stenosis
 Dental enamel loss
 Asthma
 Endoscopy is the technique of choice
to evaluate GERD
 Reflux esophagitis is present when
erosions or ulcerations are present at
SCM
 There are many grading systems to
characterize the severity of esophagitis,
 the most common of which is the
Los Angeles classification
 The presence of esophagitis and the
finding of Barrett's esophagus are
diagnostic of GERD
 24-hour pH monitoring has long been
thought to be the gold standard for the
diagnosis of GERD
 limitations that remain
underappreciated.
 Results are normal in 25% of patients
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
recommended in the treatment off
GERD.
 These include
– avoidance of precipitating
foods(fatty foods, alcohol, caffeine)
– avoidance of recumbency for 3 hours
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 recommended
 Antireflux surgery, now laparoscopie
approach, remains an option for
carefully selected patients 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 with
symptoms other heartburn and
regurgitation
 This includes asthma, chest pain,
chronic cough, laryngitis, and dental
erosions
 lack of the classic heartburn and
regurgitation symptoms
 Esophagitis/Barrett's esophagus is
usually not present
 an empiric trial of bid PPIs is indicated
as initial treatment because there is no
definitive diagnostic gold standard for
GERD.
 If treatment fails
– full investigation
– ambulatory pH testing
 Confirm diagnosis of GERD when
– symptoms relieve by specific antireflux
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 carcinoma
– 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 include
– repeated dilation,
– laser/photo dynamic therapy ablation
– esophageal stent placement
– percutaneous gastrostomy tube
placement
Neoadjuvant /adjuvant therapy
 Neo-adjuvant Chemotherapy
 Neo-adjuvant Radiation
 Neo-adjuvant Chemo-Radiation
 Adjuvant Chemotherapy
 Adjuvant Radiation
 Adjuvant chemoradiation
8.Esophageal
Diverticula
Esophageal Diverticula
 is a sac that protrudes from the
esophageal wall
 As in the rest of the Gl tract
 a true diverticulum is one that contains
all layers of the wall.
 Esophageal diverticula are most
practically classified, based on
anatomy, 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
asymptomatic
 patients with large diverticula should
be offered treatment
 The classic treatment
– open surgical resection of the
diverticulum with division of the
cricopharyngcus muscles
 Another option for extremely large
diverticula
– diverticulopexy
– suspension of the diverticulum in a
cranial direction.
 Midesophageal diverticula are most
commonly asymptomatic, occur in the
midesophagus
 Traction diverticuli form as a result of
external pulling of the esophageal wall
from neighboring inflammatory or
fibrotic tissue, such as adjacent
tuberculous mediastinitis
 Traction diverticuli are located in the
middle third of the esophagus.
 Midesophageal traction diverticula are
the only true diverticula in the
esophagus
 Epiphrenic diverticula, located near the
diaphragmatic hiatus, occur in the
distal esophagus near the LES
 These diverticula are often the result of
a motility disorder such as achalasia or
DES
 manometric studies in patients with
epiphrenic diverticulum to rule out an
associated motility disorder
 Most diverticula are asymptomatic, but
occasionally chest pain or regurgitation
can be prominent symptoms
Midesophageal Diverticula
Epiphrenic Diverticula
Treatment
 Treatment consists of
• managing the underlying motility
disorder
• diverticulotomy with/without
myotomy for symptomatic
diverticula
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
becoming lodged
 The esophagus has several areas of
physiologic narrowing
– the upper esophageal sphincter
– the level of the aortic arch
– the diaphragmatic hiatus/LES where
a foreign body can become
impacted.
 The key to the management of foreign
bodies is understanding that different
foreign bodies require different
interventions
 It is important to distinguish a true
foreign 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 Injury
Pill-Induced Injury
 Pill-induced injury to the esophagus is
an underappreciated entity.
 over 70 drugs are capable of producing
injury to the esophagus
 Drugs commonly associated with pill-
induced injury include potassium
chloride tablets, doxycycline,
quuudine, NSAIDs. iron, and
alendronate
 Pills can damage the esophagus by
various mechanisms such as acidity,
size, and contact time with esophageal
mucosa
 There is a wide spectrum of injury
from acute self-limited esophagitis to
refractory strictures
 The typical sites of pill-induced injury
are at the level of the aortic arch and
the distal esophagus, where there is
anatomic narrowing.
11.Infectious
Esophagitis
Infectious Esophagitis
 Infectious esophagitis is common,
especially in immunosuppressed hosts
such as patients with human
immunodeficiency virus (HIV),
transplant patients, and chemotherapy
patients.
 The cardinal symptom of infectious
esophagitis is
– odynophagia
– pain
– swallowing
 immunodeficient patients can present
with a variety of symptoms including
heartburn, nausea, fever, or bleeding.
 The three most common causes of
infectious esophagitis are
– Candida albicans
– cytomegalo virus (CMV)
– herpes simplex virus (HSV)
 Treatment consists of antifungal
therapy, most commonly with
fluconazole100 to 200 mg/day for10 to
14 days
 In patients with only mild
immunologic deficiencies, the topical
antifungal 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
laryngeal
– Odynophagia
– Mucosal erythema,
ulceration
– Drooling
– Tongue edema
– Stridor
– Hoarseness
 Esophageal
– Dysphagia
– Odynophagia
– Chest or back pain
 Gastric
– Epigastric pain or
tenderness
– Vomiting
– 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
Thank You