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Pathology of the
esoPhagus
Presented by:
Dr Barkam Nagaraju
MD(General Medicine)
Outline of Content
•
•
•
•
•
•
•
•

Normal anatomy and histology
Congenital and acquired malformations
Lesions associated with motor dysfunction
Esophagitis
Barrett esophagus
Esophageal varices
Benign neoplasms and tumor-like lesions
Malignant neoplasms and staging
Normal
anatomy/physiology
Muscular tube from pharynx (C6) to
esophageal-gastric junction, about 25 cm long
• Endoscopy: defined as 15-40 cm from incisor
teeth
• Two areas of increased intraluminal pressure
that normally remain contracted at rest:
•

Upper esophageal sphincter: 3 cm segment at
cricopharyngeus muscle
• Lower esophageal sphincter (LES): 3-5 cm segment
of thickened smooth muscle around diaphragmatic
esophageal hiatus, just proximal to histologic EG
junction
•
Normal Histology and Pathologic Correlations
•
•

•
•
•

•

•

Mucosa: nonkeratinized squamous;
basal zone is 10-15% of thickness
Lymphocytes: CD8 T cells in
epithelium; CD4 T cells and B cells
in lamina propria
Muscularis mucosa: smooth muscle
between mucosa and submucosa
Submucosal mucous glands:
mainly proximal & distal esophagus
Muscularis propria: skel. muscle
upper 1/3 (voluntary swallow); sm.
muscle lower 1/3; middle 1/3
mixed
Myenteric nerve plexus: between
circular inner and longitudinal
outer layers of muscularis propria
Serosa: mostly absent, facilitating
spread of invasive tumors or
infections into mediastinum
Esophageal-gastric junction
Normal smooth gray-white
squamous mucosa of esophagus

3 parts of mucosa?
1)
mucosa

submucosa

2)

muscularis propria

3)
Congenital & Acquired Malformations

Ectopias
Atresias
Stenoses
Duplications
Webs and Rings
Congenital Malformations


Ectopias; About 4% of persons by endoscopic exam



“inlet patch” of gastric-type epithelium replaces
squamous, just below upper esophageal sphincter

•

Atresias; atresia = segment reduced to thin cord, no
lumen

•

• 1/1000 live births

•

• usually near tracheal bifurcation, usually with
associated tracheal-esophageal fistula

•

• mechanism: failed septation of foregut

•

• symptoms: regurgitation, paroxysmal choking,
aspiration of liquid into lungs
Ectopic gastric mucosa

Endoscopy: red patch within
otherwise gray mucosa

Biopsy: normal appearing
gastric-type mucosa
Atresia and tracheoesophageal fistula:
5 types
Which two cause
paroxysms of
coughing upon
baby’s first feeding?

B

A

________
Which one is the most
common type, and
causes immediate
regurgitation upon
baby’s first feeding?
_________

C

D

E

All need immediate
surgical correction
Congenital & Acquired
Malformations
 Stenoses:(narrowing of a duct or passage)Usually

acquired due to chronic gastro-esophageal reflux,
radiation, or ingested caustic substances; result in
progressive dysphagia


Duplications: • congenital duplication cysts of

60% occur in lower

esophagus


• Lined by epithelium (squamous, gastric, or respiratory
type) with smooth muscle wall



• Imaging studies: differential diagnosis includes other
thoracic cysts (bronchogenic, thymic, thyroidal)
Acquired Malformations
•

Webs: • usually women > 40 years old
• web: a mucosal fold (2-4 mm thick)

•

which protrudes into the lumen, causing dysphagia with
solid foods

•

Plummer-Vinson syndrome

• dysphagia due to upper esophageal web + Fe deficiency
anemia + glossitis
•

• mucosal abnormalities: glossitis and angular stomatitis
(mouth) secondary to mucosal atrophy associated with Fe
lack
• in P-V
syndrome, chronic iron-deficiency anemia precedes
development of web, but how or whether Fe deficiency
causes the web to form is controversial
• associated with increased risk for
squamous carcinoma in oral cavity, hypopharynx, and
esophagu
WEB

Glossitis with angular stomatitis
Plummer-Vinson syndrome:
potential sequela
upper esophageal web

Endoscopic view of
esophagus: ulcerated and
nodular mass
What is the most likely
What is the most likely
diagnosis for this mass
diagnosis for this mass
lesion?
lesion?

Courtesy www.gastrointestinalatlas.com
Schatzki’s Ring
Circumferential ring in lower esophagus near EG junction; thicker than
webs (may contain hyperplastic muscularis propria)  dysphagia

barium swallow esophagram

endoscopic view
Lesions affecting motor function
Achalasia

Zenker
diverticulum

Sliding
hiatal
hernia

Epiphrenic
diverticulum

Rolling
hiatal
hernia

MalloryWeiss
tear
Diverticula
Definition: outpouching comprised of
all visceral layers (mucosa, submucosa,
muscularis)
• Sites: hypopharynx, thoracic,
epiphrenic
• Pathogenesis
•

Congenital: embryologic defect
• Traction: fibrous scarring of soft tissue
adherent to serosa, pulling wall of
esophagus outward
• Pulsion: unclear mechanism; potentially
weak area at junction of pharyngeal
constrictors (Killian’s triangle) allowing
diverticulum to develop in response to
increased intraluminal pressure.
•
Zenker’s Diverticulum
•
•
•

•
•

•

27 cases described in 1877 by Zenker &
Ziemssen
Most common esophageal diverticulum
Pathogenesis: pulsion explanation favored
(increased pressure in lumen forces tissue
through weak spot in muscle layer)
Location: hypopharynx of older persons
(superior to upper esophageal sphincter)
May become large and sequester food,
with regurgitation or mass effect in the
neck
Treatment: surgical resection of larger
lesions
Zenker’s Diverticulum (pulsion)

Barium swallow esophagram

Resection of upper esophagus
Less common diverticula
•

•

Traction
• Usually small, mid-esophagus
• Few symptoms
• Pathogenesis: uncertain; motor disorder or postinflammatory fibrosis
Epiphrenic
• Just above LES, may be wide-mouthed; 1-10 cm.
diameter
• Pathogenesis: majority of patients have motility
disorder (achalasia or diffuse esophageal spasm)
• Symptoms: nocturnal regurgitation of large volumes
of fluid
• Treatment: resection large ones; address motor
disorder
Epiphrenic diverticulum
Achalasia
•

Swallowing disorder defined by 3 major problems
•

Aperistalsis

•

Incomplete relaxation LES with swallowing

•

Increased resting tone of LES (impaired relaxation)

•

Pathogenesis: normally, distal inhibitory neurons and interruption of
cholinergic signals allow relaxation of LES. Degenerative failure of
inhibitory neurons  impaired relaxation. Usually primary (idiopathic),
but also secondary to malignancy, amyloidosis, sarcoidosis, Chagas disease

•

Symptoms:
•

progressive dysphagia; nocturnal regurgitation of food

•

Treatment: surgical myotomy with balloon dilation of LES

•

Sequelae:
•

5% develop squamous carcinoma

•

epiphrenic diverticulum, aspiration pneumonitis
Achalasia

Pathology: progressive
dilation of esophagus,
proximal to an abnormal
segment which is
functionally denervated
Hiatal Hernia
•
•
•

•

•

Definition: pouch of proximal stomach extending >2cm
above diaphragmatic hiatus into thorax
Incidence: VERY COMMON, 15-50% adults (depending on
strictness of definition); incidence increases with age
Types
• Sliding: 95%; stomach and esophagus bulge through hiatus
together
• Paraesophageal: 5%; stomach alone herniates adjacent to
esophagus
Complications
• Reflux esophagitis (to be discussed)
• Incarceration: more likely in paraesophageal;
uncommon in sliding
Treatment: surgery for paraesophageal HH; degree of
morbidity determines medical vs. surgical therapy for sliding
Hiatal Hernia, sliding
type
Anatomy: widened space
between muscular crura of
diaphragm and wall of
esophagus
Pathogenesis: unknown;
possible congenital
weakness (some children
have HH) combined with
acquired defect
Symptoms: Only 10-20% of
adults with anatomically
demonstrable sliding HH have
“heartburn” (substernal pain
caused by regurgitation of
gastric juices into esophagus)
Lacerations (Mallory-Weiss
syndrome)
•

Def: linear lacerations in mucosa near EG junction

•

Pathogenesis: presumably mechanical trauma due to
prolonged retching; failure of E-G muscular relaxation

•

Risk factors: EtOH binges; prolonged vomiting

•

Pathology: mucosal defect of variable depth

•

Complications: mild to massive hemorrhage, ulceration or
perforation, mediastinitis, rarely rupture of esophagus
(Boerhaave syndrome)

•

Therapy: usually supportive because bleeding often stops
spontaneously. May need endoscopic coagulation, balloon
tamponade, or rarely surgery.
Mallory-Weiss laceration

Endoscopy: laceration straddling
the squamo-columnar junction

Surgical resection of distal esophagus
and proximal stomach for uncontrolled
hemorrhage caused by Mallory-Weiss
laceration
Esophagitis
Reflux Esophagitis
Infectious Esophagitis
Chemical/Physical Esophagitis
Eosinophilic Esophagitis
Eosinophilic Esophagitis
Reflux esophagitis
•

•
•
•
•
•

Def: mucosal injury secondary to reflux of acidic gastric
contents into lower esophagus; clinical term is GERD
(gastroesophageal reflux disease)
Incidence: 5% U.S. adults (millions of people!)
Clinical features: “heartburn”, chest pain mimicking MI,
regurgitation, dysphagia
Complications: ulceration, stricture, Barrett’s metaplasia
Pathogenesis: decreased LES tone or increased abdominal
pressure
Risk factors
• sliding hiatal hernia
• delayed gastric emptying ⇒ increased gastric volume
• obesity
• CNS depressant drugs; EtOH abuse, smoking
Histopathology of Reflux Esophagitis
Evidence of mild acute injury:
• Reactive squamous
hyperplasia • Scattered
eosinophils or neutrophils within
mucosa

PBD 8th ed, Elsevier 2010

More severe acute reflux injury:
mucosal ulceration

Evidence chronic reflux injury:
• basal zone hyperplasia (early)
• Barrett intestinal metaplasia
(later)
Chronic Reflux: hyperplastic basal
layer comprises > 20% of mucosal
thickness (normal basal layer is
< 20% of mucosal thickness)
• most commonly seen in immunocompromised patients
• three organisms comprise >90% esophageal infections
1) Candida:
Endoscopy shows
white patches
Silver stain:
pseudohyphae in
squamous mucosa
2) Herpes simplex, ground glass nuclei, intranuclear
inclusions in squamous cells, multinucleated cells

3) CMV, large intranuclear basophilic
inclusions in endothelial or stromal cells;
dot-like cytoplasmic inclusions
Infectious Esophagitis
•

most commonly seen in
immunocompromised patients

• three organisms comprise >90% esophageal
infections
1) Candida: Endoscopy shows white patches


Silver stain: pseudohyphae in squamous
mucosa


2) Herpes simplex, ground glass nuclei,
intranuclear inclusions in squamous cells,
multinucleated cells


3) CMV, large intranuclear basophilic inclusions in
endothelial or stromal cells; dot-like cytoplasmic
inclusions
Chemical/Physical Esophagitis
Causes:
Ethanol abuse,
heavy smoking
Acid or alkali
(accidental or
suicide attempt)
Very hot tea
Chronic uremia
Chemotherapy
Post-radiation
therapy for tumors
Post-arsenic ingestion

Post-radiation Therapy (stricture)
Eosinophilic Esophagitis


Path: abundant intraepithelial
eosinophils



Symptoms: dysphagia
(adults); reflux-like (children)



Associations: hypersensitivity
(atopic dermatitis, allergic
rhinitis, asthma)



Peripheral blood eosinophilia



Must prove absence of reflux
to make this diagnosis

Fig. 17-5B, PBD 8thth,2010
Fig. 17-5B, PBD 8 , 2010
Barrett esophagus (BE)
•

Definition (2 criteria):
•
•

•

(1) endoscopic evidence of abnormal mucosa above EG junction
(clinical criterion)
(2) intestinal metaplasia of squamous mucosa in biopsies of
esophagus (pathologic criterion)

Pathogenesis
•

Precise molecular mechanisms unclear

•

Acid reflux ⇒ inflammation⇒ chronic mucosal injury ⇒
metaplasia into more acid-resistant epithelium

•

Clinical: BE develops in 10-20% those with symptomatic chronic
reflux esophagitis; usually presents ages 40-60 after years of chronic
GERD.

•

MAJOR CONCERN: a minority of patients with BE develop epithelial
dysplasia which may progress into adenocarcinoma. Life-long risk
of adenocarcinoma is 10-15% in patients with BE, but this risk is
40x that of general population!
Barrett gross pathology: red granular mucosa

Metaplasia = gray hatched areas
Long segment (>3cm)

Short segment
(< 3cm, near EG jct)

Long segment
Natural History of Barrett Esophagus
Not completely predictable, but well-studied
• Four histopathologic categories predict risk for future
development of adenocarcinoma
• Negative for dysplasia (intestinal metaplasia only)
• Indefinite for dysplasia (unclear: inflammation or dysplasia)
• Low-grade dysplasia
• High-grade dysplasia
• Some things are known
• Low-grade dysplasia progresses to high-grade within 5 years in
10-30% patients. **
• Many low-grade dysplasias are not present on subsequent
endoscopic biopsies (regression or sampling error?) *
• High-grade dysplasia progresses to invasive adenocarcinoma in
30-60% patients within 5 years. **
•

* Sharma, Barrett’s Esophagus, NEJM 361:2548, 2009
** Spechler, Barrett’s Esophagus, NEJM
Barrett esophagus: histopathology 1

Diagnosis: intestinal
metaplasia, negative for
dysplasia

Diagnosis: intestinal metaplasia,
indefinite for dysplasia (reactive
inflammatory changes vs. lowgrade dysplasia
Barrett’s: histopathology 2

Diagnosis: intestinal
metaplasia with low grade
dysplasia

Diagnosis: intestinal
metaplasia with high grade
dysplasia
Proposed Treatment
Algorithm for Patients
with Barrett's
Esophagus

Sharma P. N Engl J Med
2009;361:2548-2556
Esophageal Varices
•

Definition: permanently dilated submucosal veins

•

Pathogenesis
•

Normal venous circulation: GI tract to liver to inferior vena cava

•

Chronic portal venous hypertension ⇒ development of collateral
bypass channels (portal venous blood diverted into esophageal plexus,
then azygos veins, then superior vena cava)

•

Clinical setting: cirrhosis with portal venous hypertension

•

Clinical presentation
•
•

40% die during first bleeding episode

•

If survive first episode, 50% re-bleed in one year

•
•

No symptoms until varices rupture!!

Cause of death: hypovolemic shock ⇒ multi-organ failure

Rx: replace intravascular volume, give packed RBCs, stop bleeding
Esophageal varices: pathology
Dilated blue
varices
beneath intact
squamous
mucosa

Hemorrhage
secondary to
ruptured
varices
(KMC autopsy)

EG junction
Benign neoplasms & tumorlike lesions
•

Esophageal benign neoplasms are mostly of mesenchymal
origin (non-epithelial): leiomyomas, lipomas,
hemangiomas, neurofibromas.

•

Two distinctive lesions:
•

Fibrovascular polyp

•

Squamous papilloma
Esophageal Carcinoma


•Squamouscell

carcinomas
•Adenocarcinomas •Worldwide,
squamouscell carcinomas constitute 90% of
esophageal cancers, but in the United
States there has been a very large increase
(three-to fivefold in the last 40 years) in
the incidence of adenocarcinomas
associated with Barrett esophagus.
SquamousCell Carcinoma


•Mucosal epithelial dysplasia •Carcinoma
in situ •Invasive cancer
•Polypoidexophyticmasses that protrude
into the lumen; •Necrotizing cancerous
ulcerations that extend deeply and
sometimes erode into the respiratory tree,
aorta, or elsewhere; •Diffuse infiltrative
neoplasms


A,Large ulcerated squamous cell carcinoma of the
esophagus. B,Low power view of cancer invasion of the
submucosa.

A

B
Adenocarcinoma





•Barrett esophagus is the only recognized
precursor of esophageal adenocarcinoma. •Large
nodular masses •Deeply ulcerative •Diffusely
infiltrative features •Mucin-producing glandular
tumors
Clinical Features
•Esophageal carcinoma is insidious in onset and
produces dysphagiaand obstruction gradually and
late. •Weight loss, anorexia, fatigue, and weakness
appear, followed by pain, usually related to
swallowing. •Diagnosis is usually made by imaging
techniques and endoscopic biopsy. •Surgical
excision is rarely curative. •Esophageal cancer
confined to the mucosa or submucosais amenable
to surgical treatment.
Fibrovascular polyp

Presentation: dysphagia; lesion usually in upper 1/3 esophagus

Histopathology:
abundant
vascularized
connective tissue
covered by
squamous mucosa

Is this a
neoplasm or
exuberant
hyperplasia?
Squamous papilloma

Low magnification: fronds of
thickened squamous epithelium
supported by connective tissue cores

Some have HPV-related cytologic
changes or evidence of HPV DNA
by in-situ hybridization methods

If squamous papilloma identified, respiratory tract should be
examined for HPV-related papillomatosis (especially children)
Malignant neoplasms of
esophagus: overview
Malignant tumors of esophagus comprise 6% of
all gastrointestinal cancers, but account for
10% GI cancer mortality
• Problem: often asymptomatic until late, when
they are deeply invasive or already metastatic
• Worldwide: 90% squamous / 10%
adenocarcinoma
• U.S.: 50% squamous / 50% adenocarcinoma;
incidence of adenocarcinoma rising
steadily since 1970, almost always arising in
Barrett esophagus
•
Squamous Carcinoma

Descriptor

Adenocarcinoma

M:F = 4:1; high incidence Iran,
China, Puerto Rico
(environmental initiators)

Epidemiology M:F = 7:1; >95% from

Initiators: environmental
carcinogens; promoters:
nutritional deficiencies
(vitamins A, B1, B2, B6, trace
metals)

Pathogenesis Barrett dysplasia:

Ethanol, tobacco, achalasia,
chronic esophagitis, PlummerVinson syndrome

Clinical Risk
Factors

chronic reflux
esophagitis
tobacco, obesity

20% upper third
50% middle third
30% lower third

Anatomic
Distribution

>95% lower third

5 yr. survival: 5-10%
--75% 5 yr. survival if T1 lesion
--25% 5 yr. survival for all
cases subjected to surgery

Prognosis

5 yr. survival: 25%
>80% 5 yr. survival with
esophagectomy for T1
lesion

Barrett metaplasia; <5%
from submucosal glands
early mutation or
overexpression of p53;
amplfication cERB-B2,
cyclin D, cyclin E
Staging esophageal carcinoma
Squamous carcinoma: putative carcinogenesis

Fig. 1.21, Tumors of Digestive System, IARC Press, 2000.
Squamous CA: gross pathology

Exophytic polypoid (obstructing lesion)

Ulcerated stricture (dysphagia)

Early, superficial T1
lesion, good prognosis
Adenocarcinoma: gross pathology

Barrett associated
adenocarcinoma:
circumferential
papillary lesion
(left)
ulcerated polypoid
lesion (right)
Adenocarcinoma: early invasive lesions
developing in setting of high grade dysplasia

High-grade dysplasia with
single dysplastic cell invading
lamina propria (intramucosal
adenocarcinoma = T1)

Adenocarcinoma invading submucosa,
T1 lesion (circled), arising in Barrett
intestinal metaplasia with high-grade
dysplasia (right half)

left photo courtesy University of Washington department pathology;
right photo courtesy University of Pittsburgh
Invasive Adenocarcinoma arising in Barrett esophagus
Intestinal metaplasia
with dysplasia (red)

Malignant glands invading into
submucosa (black)

Fig. 17-11B, Pathologic Basis of Disease, 7th ed, Elsevier 2005
Pathology of the Esophagus

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Pathology of the Esophagus

  • 1. Pathology of the esoPhagus Presented by: Dr Barkam Nagaraju MD(General Medicine)
  • 2. Outline of Content • • • • • • • • Normal anatomy and histology Congenital and acquired malformations Lesions associated with motor dysfunction Esophagitis Barrett esophagus Esophageal varices Benign neoplasms and tumor-like lesions Malignant neoplasms and staging
  • 3. Normal anatomy/physiology Muscular tube from pharynx (C6) to esophageal-gastric junction, about 25 cm long • Endoscopy: defined as 15-40 cm from incisor teeth • Two areas of increased intraluminal pressure that normally remain contracted at rest: • Upper esophageal sphincter: 3 cm segment at cricopharyngeus muscle • Lower esophageal sphincter (LES): 3-5 cm segment of thickened smooth muscle around diaphragmatic esophageal hiatus, just proximal to histologic EG junction •
  • 4. Normal Histology and Pathologic Correlations • • • • • • • Mucosa: nonkeratinized squamous; basal zone is 10-15% of thickness Lymphocytes: CD8 T cells in epithelium; CD4 T cells and B cells in lamina propria Muscularis mucosa: smooth muscle between mucosa and submucosa Submucosal mucous glands: mainly proximal & distal esophagus Muscularis propria: skel. muscle upper 1/3 (voluntary swallow); sm. muscle lower 1/3; middle 1/3 mixed Myenteric nerve plexus: between circular inner and longitudinal outer layers of muscularis propria Serosa: mostly absent, facilitating spread of invasive tumors or infections into mediastinum
  • 5. Esophageal-gastric junction Normal smooth gray-white squamous mucosa of esophagus 3 parts of mucosa? 1) mucosa submucosa 2) muscularis propria 3)
  • 6. Congenital & Acquired Malformations Ectopias Atresias Stenoses Duplications Webs and Rings
  • 7. Congenital Malformations  Ectopias; About 4% of persons by endoscopic exam  “inlet patch” of gastric-type epithelium replaces squamous, just below upper esophageal sphincter • Atresias; atresia = segment reduced to thin cord, no lumen • • 1/1000 live births • • usually near tracheal bifurcation, usually with associated tracheal-esophageal fistula • • mechanism: failed septation of foregut • • symptoms: regurgitation, paroxysmal choking, aspiration of liquid into lungs
  • 8. Ectopic gastric mucosa Endoscopy: red patch within otherwise gray mucosa Biopsy: normal appearing gastric-type mucosa
  • 9. Atresia and tracheoesophageal fistula: 5 types Which two cause paroxysms of coughing upon baby’s first feeding? B A ________ Which one is the most common type, and causes immediate regurgitation upon baby’s first feeding? _________ C D E All need immediate surgical correction
  • 10. Congenital & Acquired Malformations  Stenoses:(narrowing of a duct or passage)Usually acquired due to chronic gastro-esophageal reflux, radiation, or ingested caustic substances; result in progressive dysphagia  Duplications: • congenital duplication cysts of 60% occur in lower esophagus  • Lined by epithelium (squamous, gastric, or respiratory type) with smooth muscle wall  • Imaging studies: differential diagnosis includes other thoracic cysts (bronchogenic, thymic, thyroidal)
  • 11. Acquired Malformations • Webs: • usually women > 40 years old • web: a mucosal fold (2-4 mm thick) • which protrudes into the lumen, causing dysphagia with solid foods • Plummer-Vinson syndrome • dysphagia due to upper esophageal web + Fe deficiency anemia + glossitis • • mucosal abnormalities: glossitis and angular stomatitis (mouth) secondary to mucosal atrophy associated with Fe lack • in P-V syndrome, chronic iron-deficiency anemia precedes development of web, but how or whether Fe deficiency causes the web to form is controversial • associated with increased risk for squamous carcinoma in oral cavity, hypopharynx, and esophagu
  • 13. Plummer-Vinson syndrome: potential sequela upper esophageal web Endoscopic view of esophagus: ulcerated and nodular mass What is the most likely What is the most likely diagnosis for this mass diagnosis for this mass lesion? lesion? Courtesy www.gastrointestinalatlas.com
  • 14. Schatzki’s Ring Circumferential ring in lower esophagus near EG junction; thicker than webs (may contain hyperplastic muscularis propria)  dysphagia barium swallow esophagram endoscopic view
  • 15. Lesions affecting motor function Achalasia Zenker diverticulum Sliding hiatal hernia Epiphrenic diverticulum Rolling hiatal hernia MalloryWeiss tear
  • 16. Diverticula Definition: outpouching comprised of all visceral layers (mucosa, submucosa, muscularis) • Sites: hypopharynx, thoracic, epiphrenic • Pathogenesis • Congenital: embryologic defect • Traction: fibrous scarring of soft tissue adherent to serosa, pulling wall of esophagus outward • Pulsion: unclear mechanism; potentially weak area at junction of pharyngeal constrictors (Killian’s triangle) allowing diverticulum to develop in response to increased intraluminal pressure. •
  • 17. Zenker’s Diverticulum • • • • • • 27 cases described in 1877 by Zenker & Ziemssen Most common esophageal diverticulum Pathogenesis: pulsion explanation favored (increased pressure in lumen forces tissue through weak spot in muscle layer) Location: hypopharynx of older persons (superior to upper esophageal sphincter) May become large and sequester food, with regurgitation or mass effect in the neck Treatment: surgical resection of larger lesions
  • 18. Zenker’s Diverticulum (pulsion) Barium swallow esophagram Resection of upper esophagus
  • 19. Less common diverticula • • Traction • Usually small, mid-esophagus • Few symptoms • Pathogenesis: uncertain; motor disorder or postinflammatory fibrosis Epiphrenic • Just above LES, may be wide-mouthed; 1-10 cm. diameter • Pathogenesis: majority of patients have motility disorder (achalasia or diffuse esophageal spasm) • Symptoms: nocturnal regurgitation of large volumes of fluid • Treatment: resection large ones; address motor disorder
  • 21. Achalasia • Swallowing disorder defined by 3 major problems • Aperistalsis • Incomplete relaxation LES with swallowing • Increased resting tone of LES (impaired relaxation) • Pathogenesis: normally, distal inhibitory neurons and interruption of cholinergic signals allow relaxation of LES. Degenerative failure of inhibitory neurons  impaired relaxation. Usually primary (idiopathic), but also secondary to malignancy, amyloidosis, sarcoidosis, Chagas disease • Symptoms: • progressive dysphagia; nocturnal regurgitation of food • Treatment: surgical myotomy with balloon dilation of LES • Sequelae: • 5% develop squamous carcinoma • epiphrenic diverticulum, aspiration pneumonitis
  • 22. Achalasia Pathology: progressive dilation of esophagus, proximal to an abnormal segment which is functionally denervated
  • 23. Hiatal Hernia • • • • • Definition: pouch of proximal stomach extending >2cm above diaphragmatic hiatus into thorax Incidence: VERY COMMON, 15-50% adults (depending on strictness of definition); incidence increases with age Types • Sliding: 95%; stomach and esophagus bulge through hiatus together • Paraesophageal: 5%; stomach alone herniates adjacent to esophagus Complications • Reflux esophagitis (to be discussed) • Incarceration: more likely in paraesophageal; uncommon in sliding Treatment: surgery for paraesophageal HH; degree of morbidity determines medical vs. surgical therapy for sliding
  • 24. Hiatal Hernia, sliding type Anatomy: widened space between muscular crura of diaphragm and wall of esophagus Pathogenesis: unknown; possible congenital weakness (some children have HH) combined with acquired defect Symptoms: Only 10-20% of adults with anatomically demonstrable sliding HH have “heartburn” (substernal pain caused by regurgitation of gastric juices into esophagus)
  • 25. Lacerations (Mallory-Weiss syndrome) • Def: linear lacerations in mucosa near EG junction • Pathogenesis: presumably mechanical trauma due to prolonged retching; failure of E-G muscular relaxation • Risk factors: EtOH binges; prolonged vomiting • Pathology: mucosal defect of variable depth • Complications: mild to massive hemorrhage, ulceration or perforation, mediastinitis, rarely rupture of esophagus (Boerhaave syndrome) • Therapy: usually supportive because bleeding often stops spontaneously. May need endoscopic coagulation, balloon tamponade, or rarely surgery.
  • 26. Mallory-Weiss laceration Endoscopy: laceration straddling the squamo-columnar junction Surgical resection of distal esophagus and proximal stomach for uncontrolled hemorrhage caused by Mallory-Weiss laceration
  • 27. Esophagitis Reflux Esophagitis Infectious Esophagitis Chemical/Physical Esophagitis Eosinophilic Esophagitis Eosinophilic Esophagitis
  • 28. Reflux esophagitis • • • • • • Def: mucosal injury secondary to reflux of acidic gastric contents into lower esophagus; clinical term is GERD (gastroesophageal reflux disease) Incidence: 5% U.S. adults (millions of people!) Clinical features: “heartburn”, chest pain mimicking MI, regurgitation, dysphagia Complications: ulceration, stricture, Barrett’s metaplasia Pathogenesis: decreased LES tone or increased abdominal pressure Risk factors • sliding hiatal hernia • delayed gastric emptying ⇒ increased gastric volume • obesity • CNS depressant drugs; EtOH abuse, smoking
  • 29. Histopathology of Reflux Esophagitis Evidence of mild acute injury: • Reactive squamous hyperplasia • Scattered eosinophils or neutrophils within mucosa PBD 8th ed, Elsevier 2010 More severe acute reflux injury: mucosal ulceration Evidence chronic reflux injury: • basal zone hyperplasia (early) • Barrett intestinal metaplasia (later) Chronic Reflux: hyperplastic basal layer comprises > 20% of mucosal thickness (normal basal layer is < 20% of mucosal thickness)
  • 30. • most commonly seen in immunocompromised patients • three organisms comprise >90% esophageal infections 1) Candida: Endoscopy shows white patches Silver stain: pseudohyphae in squamous mucosa 2) Herpes simplex, ground glass nuclei, intranuclear inclusions in squamous cells, multinucleated cells 3) CMV, large intranuclear basophilic inclusions in endothelial or stromal cells; dot-like cytoplasmic inclusions
  • 31. Infectious Esophagitis • most commonly seen in immunocompromised patients • three organisms comprise >90% esophageal infections 1) Candida: Endoscopy shows white patches  Silver stain: pseudohyphae in squamous mucosa
  • 32.  2) Herpes simplex, ground glass nuclei, intranuclear inclusions in squamous cells, multinucleated cells
  • 33.  3) CMV, large intranuclear basophilic inclusions in endothelial or stromal cells; dot-like cytoplasmic inclusions
  • 34. Chemical/Physical Esophagitis Causes: Ethanol abuse, heavy smoking Acid or alkali (accidental or suicide attempt) Very hot tea Chronic uremia Chemotherapy Post-radiation therapy for tumors Post-arsenic ingestion Post-radiation Therapy (stricture)
  • 35. Eosinophilic Esophagitis  Path: abundant intraepithelial eosinophils  Symptoms: dysphagia (adults); reflux-like (children)  Associations: hypersensitivity (atopic dermatitis, allergic rhinitis, asthma)  Peripheral blood eosinophilia  Must prove absence of reflux to make this diagnosis Fig. 17-5B, PBD 8thth,2010 Fig. 17-5B, PBD 8 , 2010
  • 36. Barrett esophagus (BE) • Definition (2 criteria): • • • (1) endoscopic evidence of abnormal mucosa above EG junction (clinical criterion) (2) intestinal metaplasia of squamous mucosa in biopsies of esophagus (pathologic criterion) Pathogenesis • Precise molecular mechanisms unclear • Acid reflux ⇒ inflammation⇒ chronic mucosal injury ⇒ metaplasia into more acid-resistant epithelium • Clinical: BE develops in 10-20% those with symptomatic chronic reflux esophagitis; usually presents ages 40-60 after years of chronic GERD. • MAJOR CONCERN: a minority of patients with BE develop epithelial dysplasia which may progress into adenocarcinoma. Life-long risk of adenocarcinoma is 10-15% in patients with BE, but this risk is 40x that of general population!
  • 37. Barrett gross pathology: red granular mucosa Metaplasia = gray hatched areas Long segment (>3cm) Short segment (< 3cm, near EG jct) Long segment
  • 38. Natural History of Barrett Esophagus Not completely predictable, but well-studied • Four histopathologic categories predict risk for future development of adenocarcinoma • Negative for dysplasia (intestinal metaplasia only) • Indefinite for dysplasia (unclear: inflammation or dysplasia) • Low-grade dysplasia • High-grade dysplasia • Some things are known • Low-grade dysplasia progresses to high-grade within 5 years in 10-30% patients. ** • Many low-grade dysplasias are not present on subsequent endoscopic biopsies (regression or sampling error?) * • High-grade dysplasia progresses to invasive adenocarcinoma in 30-60% patients within 5 years. ** • * Sharma, Barrett’s Esophagus, NEJM 361:2548, 2009 ** Spechler, Barrett’s Esophagus, NEJM
  • 39. Barrett esophagus: histopathology 1 Diagnosis: intestinal metaplasia, negative for dysplasia Diagnosis: intestinal metaplasia, indefinite for dysplasia (reactive inflammatory changes vs. lowgrade dysplasia
  • 40. Barrett’s: histopathology 2 Diagnosis: intestinal metaplasia with low grade dysplasia Diagnosis: intestinal metaplasia with high grade dysplasia
  • 41. Proposed Treatment Algorithm for Patients with Barrett's Esophagus Sharma P. N Engl J Med 2009;361:2548-2556
  • 42. Esophageal Varices • Definition: permanently dilated submucosal veins • Pathogenesis • Normal venous circulation: GI tract to liver to inferior vena cava • Chronic portal venous hypertension ⇒ development of collateral bypass channels (portal venous blood diverted into esophageal plexus, then azygos veins, then superior vena cava) • Clinical setting: cirrhosis with portal venous hypertension • Clinical presentation • • 40% die during first bleeding episode • If survive first episode, 50% re-bleed in one year • • No symptoms until varices rupture!! Cause of death: hypovolemic shock ⇒ multi-organ failure Rx: replace intravascular volume, give packed RBCs, stop bleeding
  • 43. Esophageal varices: pathology Dilated blue varices beneath intact squamous mucosa Hemorrhage secondary to ruptured varices (KMC autopsy) EG junction
  • 44. Benign neoplasms & tumorlike lesions • Esophageal benign neoplasms are mostly of mesenchymal origin (non-epithelial): leiomyomas, lipomas, hemangiomas, neurofibromas. • Two distinctive lesions: • Fibrovascular polyp • Squamous papilloma
  • 45. Esophageal Carcinoma  •Squamouscell carcinomas •Adenocarcinomas •Worldwide, squamouscell carcinomas constitute 90% of esophageal cancers, but in the United States there has been a very large increase (three-to fivefold in the last 40 years) in the incidence of adenocarcinomas associated with Barrett esophagus.
  • 46. SquamousCell Carcinoma  •Mucosal epithelial dysplasia •Carcinoma in situ •Invasive cancer •Polypoidexophyticmasses that protrude into the lumen; •Necrotizing cancerous ulcerations that extend deeply and sometimes erode into the respiratory tree, aorta, or elsewhere; •Diffuse infiltrative neoplasms
  • 47.  A,Large ulcerated squamous cell carcinoma of the esophagus. B,Low power view of cancer invasion of the submucosa. A B
  • 48. Adenocarcinoma    •Barrett esophagus is the only recognized precursor of esophageal adenocarcinoma. •Large nodular masses •Deeply ulcerative •Diffusely infiltrative features •Mucin-producing glandular tumors Clinical Features •Esophageal carcinoma is insidious in onset and produces dysphagiaand obstruction gradually and late. •Weight loss, anorexia, fatigue, and weakness appear, followed by pain, usually related to swallowing. •Diagnosis is usually made by imaging techniques and endoscopic biopsy. •Surgical excision is rarely curative. •Esophageal cancer confined to the mucosa or submucosais amenable to surgical treatment.
  • 49. Fibrovascular polyp Presentation: dysphagia; lesion usually in upper 1/3 esophagus Histopathology: abundant vascularized connective tissue covered by squamous mucosa Is this a neoplasm or exuberant hyperplasia?
  • 50. Squamous papilloma Low magnification: fronds of thickened squamous epithelium supported by connective tissue cores Some have HPV-related cytologic changes or evidence of HPV DNA by in-situ hybridization methods If squamous papilloma identified, respiratory tract should be examined for HPV-related papillomatosis (especially children)
  • 51. Malignant neoplasms of esophagus: overview Malignant tumors of esophagus comprise 6% of all gastrointestinal cancers, but account for 10% GI cancer mortality • Problem: often asymptomatic until late, when they are deeply invasive or already metastatic • Worldwide: 90% squamous / 10% adenocarcinoma • U.S.: 50% squamous / 50% adenocarcinoma; incidence of adenocarcinoma rising steadily since 1970, almost always arising in Barrett esophagus •
  • 52. Squamous Carcinoma Descriptor Adenocarcinoma M:F = 4:1; high incidence Iran, China, Puerto Rico (environmental initiators) Epidemiology M:F = 7:1; >95% from Initiators: environmental carcinogens; promoters: nutritional deficiencies (vitamins A, B1, B2, B6, trace metals) Pathogenesis Barrett dysplasia: Ethanol, tobacco, achalasia, chronic esophagitis, PlummerVinson syndrome Clinical Risk Factors chronic reflux esophagitis tobacco, obesity 20% upper third 50% middle third 30% lower third Anatomic Distribution >95% lower third 5 yr. survival: 5-10% --75% 5 yr. survival if T1 lesion --25% 5 yr. survival for all cases subjected to surgery Prognosis 5 yr. survival: 25% >80% 5 yr. survival with esophagectomy for T1 lesion Barrett metaplasia; <5% from submucosal glands early mutation or overexpression of p53; amplfication cERB-B2, cyclin D, cyclin E
  • 54. Squamous carcinoma: putative carcinogenesis Fig. 1.21, Tumors of Digestive System, IARC Press, 2000.
  • 55. Squamous CA: gross pathology Exophytic polypoid (obstructing lesion) Ulcerated stricture (dysphagia) Early, superficial T1 lesion, good prognosis
  • 56. Adenocarcinoma: gross pathology Barrett associated adenocarcinoma: circumferential papillary lesion (left) ulcerated polypoid lesion (right)
  • 57. Adenocarcinoma: early invasive lesions developing in setting of high grade dysplasia High-grade dysplasia with single dysplastic cell invading lamina propria (intramucosal adenocarcinoma = T1) Adenocarcinoma invading submucosa, T1 lesion (circled), arising in Barrett intestinal metaplasia with high-grade dysplasia (right half) left photo courtesy University of Washington department pathology; right photo courtesy University of Pittsburgh
  • 58. Invasive Adenocarcinoma arising in Barrett esophagus Intestinal metaplasia with dysplasia (red) Malignant glands invading into submucosa (black) Fig. 17-11B, Pathologic Basis of Disease, 7th ed, Elsevier 2005

Editor's Notes

  1. Figure 3. Proposed Treatment Algorithm for Patients with Barrett&apos;s Esophagus.