Transcript ESOFAGUL - UMF IASI 2015

ESOPHAGUS
MOTILITY DISORDERS

SES

Peristaltic waves



LES
Primary – deglutition
Secundary – GERD
Tertiary – autonomic muscle
control independent of
deglutition
MOTILITY DISORDERS

Primary motility disorders
Achalasia: cricopharingian, cardia
 Diffuse esophageal spasm
 LES and SES hypertonia


Secondary motility disorders
sclerodermia
 diabetes
 Parkinson
 amiloidosis
 colagenosis
 miastenia gravis

ACHALASIA

Definition

Lack of LES relaxation + loss of capacity to transmit
peristaltic waves, replaced by incoordinated
ocntractions
ACHALASIA - pathogeny





Unknown
Degeneration of ganglia cells in Auerbach plexus
and vagal motor nuclei.
 increased basal pressure in LES and lack of
relaxation during deglutition, esophageal pressure
and progressive loss of peristalsis
Functional obstruction  progressive distension of
the esophagus
In time alterations visible on X-Ray exam:
E. dilated, beak-like ending
 Level of water = pressure in LES
 Long standing = dilated, tortuous

ACHALASIA - pathology

Macroscopic
dilated “botle”, “socket”, initially distal end, followed by
all esophagus
 Thick wall
 Esophagitis due to stasis and fermentation  uleration and
bleeding


Microscopy

Low or absence of ganglia cells in the nervous plexus of
Auerbach
ACHALASIA clinical presentation



20 – 40y subtle onset
May be asymptomatic
THE ESOPHAGEAL SYNDROME:
Disphagia (intermitent, sometimes very acute,
paradoxical!!)
 Pain (epigastric, thoracic) - radiates precordial,
cervical, ear
 Regurgitation (time after eating – depending on
dilation of esophagus) – may produce aspiration

ACHALASIA clinical presentation


Periodic development with moment sof
“complete” remission
In the stage with competent muscles: fight


predominent pain, disphagia, regurgitation
End stage
Regurgitation
 Respiratory: compression, aspiration
 Denutrition


Clinical examination: objective findings: nothing
ACHALASIA imagistic
Radiology

funcţional

initial
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

advansed

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
Organic
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
Upper 1/3 peristalsis
Cabnormal, disorganised
contraction that fail to relax cardia
End stage


Peristalsis OK
Slow relaxation of cardia
No peristalsis
 diameter of E
length increased, bent, sinuos
Lower extremity narrow: “beak”
or “candle”
 Endoscopy



Narrow passage
Does not open, BUT
easy passage
cancer
 Manometry



No harmonious peristalsis, tertiary waves
High pressure LES
Incomplete relaxation of LES
ACHALASIA – differential dg
 Cancer
of lower esophagus
 Benign peptic stenosis
 Difuse esophageal spasmul
 Ischemic heart diseases
 Respiratory problems
 Chagas disease (Trypanosoma cruzi) – damage
to myenteric plexus same clinical presentation
ACHALASIA progress

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Long, unpredictable over 2030 years
3 stages
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Complications
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denutrition  cachexia
regional
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Dysphagia and regurgitation
Latent clinical stage
Megaesophagus
Progressive loss of weight :
malnutrition
general
Mediastinal compression
Aspiration: pulmonary
complications
TB decreased immune
reaction: reactivation
local




Esofagitis
UGI bleeding, ulcer
Cancer
Perforation + mediastinitis
ACHALASIA treatment

Conservative

avoid
Very cold food, very hot food
 Rapid eating with large bulky swallows

Decrease LES tonus: nitrates, calcium chanle blockers
 Mucosa protection – Sucralfat


Little benefit in time

Forcefull dilation – endoscopic

Good initial approach
2 dilations  NU  surgery
RISK: perforation
CIND: - long standing disease, tortuous esophagus, association with GERD
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Injection of Botulinum toxine
ACHALASIA - surgery
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Indications
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Per primam
Failure after dilation
Extramucosal Heller myotomy
8-10 cm incision of the muscular wall over the esogastric junction
Abdominal/thoracic approach
Fundoplication n(antireflux procedure)
ESOPHAGEAL DIVERTICULA

Classification:

- pharingo-esophageal – Zenker junction between
pharinx and esophagus;
- midd-esophageal close to trachea and bronchi;
- epiphrenic (supradiaphragmatic) last 10 cm of
esophagus


Histology

Structure of the wall:

- true diverticula – all strata of the esophageal wall;
- false (pulsion) – only mucosa and submucosa
are present
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PATHOGENY
 TYPE


- pulsion diverticula due to high pressure in
the lumen + motility disorder
- traction diverticula – inflammatory processes
in the vicinity with traction on the wall during
scaring.
ZENKER diverticula
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
fals diverticula
Pulsion type
Weak area: posterior aspect
of the pharynx between the
inferior constrictir and
transversal situatated
cricopharingeal = triangle
of triunghiul Killian (only mucosa
and some fibrotic tissue)
ZENKER
diverticula
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CLINICAL ASPECT
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Initial
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Burning sensation, non-productive cough, sensation
of foreign body in the neck
Late – big diverticula
Disphagia
 Regurgitation
 Bead smell
 Compression

DIVERTICULUL
ZENKER
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

IMAGISTIC
X-Ray
Endoscopy
ZENKER DIVERTICULA

Complications

Hemorhage
Perforation
Carcinoma
Chronic pulmonary infections
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ZENKER DIVERTICULA

TREATMENT

Small


Nothing much
Big, symptomatic, complications
Resection of the diverticula ± miotomy of SES
 Endoscopic treatment
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MIDDLE ESOPHAGEAL
DIVERTICULA

Traction type
Middle thoracic
Adjacent inflammatory pathology

ETHIOLOGY

infections


Mediastinal TB (lymph nodes)
 Pleural infections
 Pericarditis


congenital
PATHOLOGY
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Traction type
True diverticula
Lateral wall of the
esophagus in the lateral wall
Large mouth to
communicate with the
esophageal lumen = no
retention
Can also be pulsion type
(not usual)
IMAGISTIC
DIAGNOSTIC

Clinical


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Complications
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asymptomatic
disphagia
Hemorrhage
Perforation
Cancer
Imagistic


X-Ray
Endoscopy
TREATMENT
Conservative (no clinical signs)
 Surgery

 Excision
 Open
or thoracoscopic
EPIPHRENIC
DIVERTICULA


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Inferior esophagus
PATHOGENY
Associated with motility
disorders – achalasia,
difuse esophageal spasm
Combines: high pressure
+ lack of relaxation
EPIPHRENIC DIVERTICULA

DIAGNOSTIC
Similar to thoracic type
 +manometry for motility disorder

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TREATMENT
Rezection + myotomy
 +tratament of associated disease
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GERD
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Physiologic reflux
Normal in some instances, but quickly cleared
 More often standing and while awake

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LES tonus influenced by different factors:


α stimulators, β blockers
α blockers, β stimulators
gastrine, motiline
colecistochinine,
estrogen,
progesteron, glucagon, somatostatin,
secretine
antiacide
PGF2
medication,
domperidol, anticholinergics, barbiturics, calcium
chanel blockers, cafeine, dopamine,
teophiline, PGE1-2, diazepam
Pepermint, chiocolate, coffee, alchool,
fatty food
GERD

Diagnostic:
Presence of symptoms
 Endoscopic demonstration of esophagitis
  LES

GERD

PATHOGENY

A. Mechanic failure of LES – valve effect





Inadequate  LES pressure
Inadequate length of LES
Abnormal position of cardia
Brahiesophagus
B. Inefficient clearance – 4 factors:




Gravity
Normal peristaltic movements of the esophagus
Salivary gland production
Positioning of distal esophagus in abdomen
GERD PATHOGENY

C. Gastric reservoir

Gastric distention:
Decreases the length of LES
 Causes: chewing gum, low saliva production (Sjogren), motility
disorders.


High Gastric pressure
Outlet syndrome – pyloric stenosis, vagotomy
 Diabetic gastroparesis


Prolonged gastric stasis
Miogenic causes (diabetes, neuromuscular problesm,
anticholinergic medication, etc)
 Non-miogenic causes (vagotomy, antropyloric disfunctin,
duodenal motility disorders, duodeno-gastric reflux)


Gastric hypersecretion – exposure to low pH
GERD: E mucosa aggression

Gastric juice:
Low pH – long term exposure
 Pepsine – proteolytic at pH<2

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Duodenal reflux:

Billiary salts – E not used to deal with high pH
 Pancreatic enzymes
Differences
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HCl, billiary acids   mucosal permeability
pepsine, tripsine  mucosal erosions
Very little correlation between symptoms and endoscopic
appearance of lesions.
GERD complications

ESOPHAGUS: prolonged exposure
esofagitis
 strictures
 Barrett



RESPIRATORY: repeated aspiration  pneumonia,
pulmonary fibrosis
Pathological seen lesion correlate with
1. LES pressure (sphincter volume)
 2. Acid + bile is more aggressive toward mucosa

GERD symptoms
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Digestive
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Respiratory symptoms

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Retrosternal burning pain pirozisul
Regurgitations (according to body
position)
Dysphagia (edema, stenosis, damaged
peristalsis)
Chronic cogh
Senzation of lack of air
Horse voice (chronic laryngitis)
Wheezing
Unusual symptoms



Nausea, vomiting
Full stomach
Atypical thoracic pain
GERD imagistic

Barium mealesophagus, stomach and
duodenum
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Reflux of barium
Hiatus hernia
Strictures
Associated lesions
GERD endoscopy
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Every patient with dysphagia - compulsory
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Esophagitis
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
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gr I – congestion of mucosa, no ulcerations
gr II – linear ulcerations bordered by granulation tissue that bleeds on touch
gr III – confluent ulcerations with isles of normal mucosa
gr IV - stenosis
GERD – Barrett esophagus

Epitelial metapasis:


Normal squamos cell epithelium – into gastric columnar
epithelium
Biopsy: metaplasia, displasia, adenocarcinoma
GERD and hiatus hernia

HH often associated with GERD (main symptom)


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Sliding
Rolling – not often associated with reflux (cardia normal)
Combined
GERD - manometry

Stationary
manometry
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Evaluation of LES


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
pressure<6mmHg
Total length in abdomen < 1cm
Total LES <2cm
Sphincter area volume
Primary motility disorders
(achalasia, difuse spasm)
GERD induced motility
disorders RGEafect SEI/
peristaltica E/ amplitudinea
contracţiilor
GERD manometry

24 hours ambulatory manometry
Better diagnostic of motor dysfunctin
 In non-obstructive dysphagia: non coordinated muscle
function


Scintigrapic evaluation of esophageal transit
10 ml water with Tc99
 Non specific
 Quantification of esophageal transit time
 Prolonged time in achalasia, sclerodermia, difuse spasm,
nutcracker syndrome
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GERD pH monitoring

Quantification time
with pH<4

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Total time of pH<4
exposure
Frequency of exposure
Duration of epsiodes >5
minutes
Longest period of reflux
Association with events
Acid relfux: pH<4
Alkaline reflux pH>7
Pletismography:
quantification of billiary
reflux
GERD differential diagnstic

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Achalasia –dysphagia + lack of esophageal empting
(Rx + endoscopy)
Esophageal cancer: dysphagia (endoscopy)
Hiatus hernia: may be clinical silent
Esophageal diverticula motility disorders,
regurgitation (Rx, endoscopy)
UGI pathology
Ischemic heart disease
Pneumonia and other respiratory problems
GERD treatment

Medical – first step (no evaluation)

Minor changes in habits
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Raised position in bed
Avoid very tight clothing
Small frequent meals
Dine before 6pm and small quantity
Loose weight
Avoid alcohol, smoking, coffeee, tea, pepermint, chocolate, fat
Protective tratement for mucosa (alginat – creates a barrier) +
antacides (may relieve symptoms but rebound)
Promotilic medication
REFLUXUL GASTROESOFAGIAN
 Step II persistent symptoms)
Endoscopy +/- Rx studies for complications; manometry
 PPI – decrease gastric acid output (high recurrence when
stop) – continuous medication with periods without. Long
term: increases risk of hyperplastic gastric polyps



Persistent symptoms: aggressive exploration
TREATMENT: aggressive
Medical
 Surgical

GERD surgery

Indications
Persistence of endoscopic lesions in spite of
aggressive medication
 Young patients – long term treatment
 No response to treatment


FUNDOPLICATION
 LOGIC
LES

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
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
– rebuild competence of
1. Restore LES pressure 2x over gastric pressure over
>3cm: fundoplication
2. Restore the length of intraabdominal esophagus
(positive pressure) – 2 cm
3. Allow for a normal swallow: gastric fundus used in
wrap arround LES + avoid vagus nerve injury + loose
wrap
4. Degree of fundoplication: according to diameter
and degree of motility disorder
5. Intraabdomina position of the fundoplication :
Collis gastroplasty
BARRETT esophagus



Acquired problem in 10% of GERD patients – end stage
GERD mucosa destruction  replaced with columnar
epithelium more resistant to acid aggression
It implies



Major deficiency in LES function
Major deficiens in esophageal clearance
Long term exposure to acid

BARRETT
COMPLICATIONS
 Ulcer
formation (very similar with gastric
ulcer) – same complications
 Stricture formation
 Displasia – metaplasia - cancer
BARRETT - diagnostic

Rx - indirect



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Brachiesopagus
Ulcer
Stricture
EndoscopY - BIOPSY

Presence and degree of metaplasia
BARRETT - treatment

Medical



No metaplasia: treatment of GERD – surveilance
Dysplasia: destruction: radiofrequency ablation,
photodynamic ablation
Surgical

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Antireflux surgery
High risk dysplasia: esophagectomy
Esophageal peptic stricture



Stenosis developing as a result of long standing reflux
Dg: need to exclude a malingnant stenosis
Essential in deciding upon therapy




1.  response to dilatation
2.  length of staneosis and length of esophagus
3.  nromal vs abnormal motility
Treatament

Dilatation + treatment of GERD
HIATUS HERNIA

Definition: herniation of the stomach through the
esophageal hiatus
HIATUS HERNIA classification

Tip I - sliding


90-95%
Cardia positioned in the thorax
HIATUS HERNIA classification

Tip II - paraesophageal or rolling


5-10%
Cardia within abdominal cavity
HIATUS HERNIA classification

Tip III - combined


brachyesophagus - 1-2%
Congenital or aquired due to GERD
HIATUS HERNIA pathogeny

Mechanism - failure of the mechansim that fix the
eso-cardial complex
HIATUS HERNIA - causes





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
1. age: changes in strcutures with age
2. obesity: infiltration with fat lowers resistance
3. high abdominal pressure (pregnancy, constipation,
chronic cough, prostatic problems, chronic effort, etc)
4. anomalies of the rachis (scoliosis, cifosis) change in the
diaphragmatic pillars
5. trauma
6. iatrogenic – dissection in area for other pathologies
8. asociated problems – billiary stones and diverticula of
colon
(sdr Saint ) = muscular hipertonicity (colics) + increased in
abdominal pressure
9. Gastric problems

Peptic ulcer disease: pyloric spasm → ↑ gastric pressure
HIATUS HERNIA pathogeny


GERD with all symptoms associated wioth reflux
Mechanic effects of gastric herniation
Gastric wall lesions (compression, acidity in the puch)
 Ulcerations, edema – UGI bleeding
 Strangulation – gangrene and paerforation


Respiratory and cardiac problems
Dispnoea and irritative cough
 Tachycardia, abnormal heart beats, mimics angina
 Develop after eating or aggravated, in decubitus and may
dissapear in ortostatism

HIATUS HERNIA symptoms
 A.
GERD symptoms
Epigastric pain  50%
 Anterior thoraci burning pain  67%
 Regurgitations - 40%

After meal and bending down
 Nocturnal  tracheal aspiration, pneumonia


Dysphagia
intermitent - spasm
 permanent – stenosis

HIATUS HERNIA symptoms

B. Volume of hernia

Respiratory problems




Dispnoea, coughing
After large meals + positions
Cardiac problems - palpitation, extrasistolic heart
beats, angina-like
Hickups
HIATUS HERNIA symptoms

C. Complications





UGI bleeding versus occult bleeding and anemia
Gastric puch discomfort: meteorism, belching, lack of air
stenoza esofagiană sau/ şi cancerul esofagian
Strangulation + perforation
Stenosis (+/- malignancy)
HIATUS HERNIA imagistic

Radiology




All positions: orto-,
clinostatism, lateral,
Trendelemburg
Presence of the gastric
puch with mucosal folds
Position of cardia
E - long and curved or
straight and short
(brachyesophagus)
HIATUS HERNIA imagistic

ENDOSCOPY





See the hernia
Free reflux (bulk)
Associated esophagitis
Essential for stenosis
and ulcer
Biopsy
HIATUS HERNIA evaluation

Functional tests:

manometry



Evaluation of LES
Motility disorders
24 hours pH monitoring

Time with pH<4
HIATUS HERNIA treatment

Medical – any HH with GERD symptoms medical
treatment for a minimum of 6 months


Change in posture after meal and during sleep
Changes in eating habits




Decrease abdominal pressure



Loose weight (obese patients)
Avoid constipation and major efforts
Indications:



Small meals, more frequent
No large meals in the evening
Avoid alcohol, spices, carbonated drinks
gr. I – II esophagitis: avoid and operation
Gr. III-IV esophagitis: prepare for an operation
CIND: old people, comorbidities +/- laparoscopy
HIATUS HERNIA treatment

Medication




Lower acid secretion PPI, H2 blockers
Sedatives?
Promotilics
Endoscopic



Induce sclerosis: cautery applications
Dilation in cases of stenosis
Endoluminal mucosal plicature – antireflux
procedure
HIATUS HERNIA treatment

Surgical

Indications:

No response to medical treatment
Large HH with respiratory, cardiac symptoms or UGI
bleeding risk
Complications






gr. III-IV esophagitis
UGI bleeding, stenosis, brachyesophagus
Rolling type hernia- risk of strangulation
HH in new born children
HIATUS HERNIA treatment

Principles
Reposition the stomach in abdomen and fix it there
 Calibration of the hiatus
 Closure of the angle of Hiss
 Reconstruct gastro-phrenic ligament
 Prevent reflux (wrap formation)

HIATUS
HERNIA
 Tehnics:


gastropexy
Fundoplication (270-360
degree wrap)
ESOPHAGUS - CANCER





7% of all digestive cancer; 2% of all
M>F
60-70y
Asia (China, Iran, Japonia), South
Afrika, USA
6th cause of detah related to cancer
RISK FACTORS
Risk Factor
Squamous-Cell Carcinoma
Tobacco use
Alcohol use
Barrett’s esophagus
Weekly reflux symptoms
Obesity
Poverty
Achalasia
Caustic injury to the esophagus
Nonepidermolytic palmoplantar keratoderma
(tylosis)
Plummer–Vinson syndrome
History of head and neck cancer
History of breast cancer treated with radiotherapy
Frequent consumption of extremely hot beverages
Prior use of beta-blockers, anticholinergic agents,
or aminophor aminophyllines
Adenocarcinoma
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PATHOLOGY

SQUAMOS CELL CARCINOMA





Most frequent
Frequent multicentric
Upper part of esophagus
Narrow anatomy: rapid invasion in bronchi and trachea, aorta, pleura,
left recurrent nerve.
Adenocarcinoma


Cardia and distal esophagus
Origin:





Submucosal glands of esophagus
Cylindric epithelium of distal esophagus
Cylindric epithelium of Barrett
Frequent extension (submucosal proximal and subserosal distal)
Larger mediastinum – late invasion in adjacent structures
ESOPHAGUS - CANCER

Macroscopy: squamos
cell carcinoma
CANCERUL ESOFAGIAN

MACROSCOPY: adenocarcinoma
Microscopy
 Most
typical
form =
squamas cell
carcinoma
 Often
MTS
 Radiosensibile
Microscopy

Adenocarcinoma


Esophageal or gastric
origin?
Not responding well
to radiotherapy
CANCER - invasion

Local invasion
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
Adjacent organs
Lymphatics – regional LN
1/3 inf – mediastinum – abdomen (celiac trunk)
 1/3 middle – trachea bifurcation - mediastinum
 1/3 sup – recurrent – supraclavicular – cervical


Blood born metastasis
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Liver, lungs, scheleton, etc
STAGING
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T:
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N:

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T1 – lamina
propria/submucosa
T2 – muscularis propria
T3 – adventicia
T4 – neighbor organs

Stages:

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N0 – no LN
N1 – invasion in regional
LN
M:


M0 – no MTS
M1 – distant MTS
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I: T1N0M0
IIa: T2N0M0 or T3N0M0
IIb: T1N1M0 or
T2N1M0
III: T3N1M0 or T4N01M0
IV: any T any N M1
SYMPTOMS

Always with malnutrition
Late – very late presentation

DYSPHAGIA
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PAIN
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First and dominant symptom in 90 % of cases (esophageal lumen
diminised with ≈ 90 %)
progressive
Sometimes sudden onset (large piece of food impacted)
Retrosternal and back irradiation – not very often and can have
significance in diagnostic
MASSIVE WEIGHT LOSS


Major symptom
Not able to eat; late cachexia due to advanced neoplasia
SYMPTOMS
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

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Regurgitation – late
symptom
Hypersalivation
Non-specific UGI
symptoms
Low grade fever
UGI bleeding – usually
occult



Changes in voice quality
Cough and respiratory
symtoms
Signs of aero-digetsive
fistula
CLINICAL EVALUATION

General


Loss of weight (massive), dehydration
Abdominal
Epigastrum → low development of tumor may be
palpable
 Liver→ MTS

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
Cervical – LN
Respiratory

fistula
IMAGISTIC

Barium meal
IMAGISTIC
CT - MRI
ENDOSCOPIC ULTRASOUND
EVALUATION

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Brush cytology – early lesions
Laringoscopy + Bronchoscopy

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Laparoscopy
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Liver MTS
Abdominal LN evaluation
Respiratory evaluation

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Invasion in bronchi or trachea
Compression
Fistula formation
VEMS < 1 = CIND for operations
Lab

Non specific
TREATMENT

Pathologic type
Squamocelular – RXT + surgery
 Adenocarcinoma - surgery


Stage
Rezectable?
 Curative versus paliative


General status: can he survive an operation?
PROGNOSTIC

Curative intent

In countries without screening ≈ 10-20 %
CHT-RXT versus CHT-RXT + Surgery
Goal: resect the T with negative margins + ALL
regional LN


10 cm away from macroscopic margin
 Often total esophagectomy
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Mucosal resection
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Treat dysphagia

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Stoma for artifical feeding
Restore the lumen of the esophagus
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Laser
Alcohol sclerotherapy
Photodynamic therapy
Brahytherapy
Stents
PALIATIVE
TREATMENT
COROSIVE ESOPHAGITIS AND
STENOSIS OF THE ESOPHAGUS
PATHOGENY


AGENT  acute injury
+ chronic sequels
Matters: type,
concentration, quantity,
time of contact
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3 Stages of development:

Mouth to pylorus
Natural narrow places
Alcaline: little effect on
stomach
Acute necrosis: 1-4 days
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Protein coagulation = necrosis
Inflammation fallows
Ulceration and granulation 1012 days

ACID: dry necrosis
ALCALINE: necrosis and
liquefaction
Location of maximum
injury


Necrotic membrane is
eliminated
Large ulcerated raw surface
filled by granulation tissue
Esophageal wall very friable
Scar formation



From 3rd week
Fibrosis leads to stenosis
Treatment tries to prevent
fibrosis
DIAGNOSTIC

Symptoms
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Clinical evaluation  lesions of the lips and mouth 
Early endoscopy

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3 stages
Early presentation: shock, acidosis, renal failure
Respiratory: laryngeal spasm, edema of larynx, pulmonary edema
1. mucosal edema
2. bleeding, exudat, ulcerations and pseudomembranes
3. ulcers, massive bleeding, obstructions (edema) and perforations
 X-Ray –strictures



farinx
Esophagus
Stomach
TREATMENT

A. Immediate (on site)

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NO attempt to neutralize the substance

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There is no antidote
Favors diffusion of toxic
Burns due to antidote
NO - do not induce vomiting
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Find the bottle
Check airways freedom
Venous access
Promotes burns in the respiratory tract
Inhales toxic
NO - nasogastric tube

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Induces reflux
Vomiting
Perforation
TREATMENT
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TRANSPORTATION: hospital + care
ICU
Endoscopy +/- bronchoscopy
Specialized surgery
Toxicology determinations
In hospital treatment

A. – Treat respiratory failures



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O2
Cortisone
Intubation +/- tracheostomy
Treat soc and acidosis

B. Endoscopy  grade lesions

C. Bronchoscopy – respiratory lesions
TREATMENT PROTOCOL



gr. III burns
Surgery immediate
Endoscopic aspect essential:
Difuse necrosis eophagus and stomach: high chances
of mediastinitis and perforation
 Early operation
 Esogastrectomy: stripping + jejunostomy
 Late reconstruction
 Difuse necrosis only esophagus: esophagectomy
(stripping) + reconstruction later
 Difuse gastric necrosis: total gastrectomy and
reconstruction

TREATMENT PROTOCOL

gr. II medical treatment
Nothing per mouth ~20 days
 +/- jejunostomy/gastrostomy


Prognostic
No complications no sequele
 Complications: bleeding, perforation, stenosis


STENOSIS:
Dilatation (risk of perforation)
 Construction of a neo-esophagus (stomach, colon,
jejunum)

TREATMENT PROTOCOL

gr. I moderate lesions
Healing without sequels
 Short surveilance (3 days)

BENIGN TUMORS

<1% of all E tumors

Leiomioma
 Develops
inside the wall
 Can be visible within the lumen
 Treatment
 Endoscopic
removal if pediculated
 Surgical rezectin + reconstruction of neo-esophagus
 Enucleation
OTHER BENIGN TUMORS


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Fibroma
Schwannom
Branchial development cysts
Hemangioama
Adenomatous polyp


Papiloma


Originates in submucosal gland or ectopic mucosa
Squamos cell epithelium
Mixoma
BENIGN TUMORS
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CAUSE



unknown
Inflammatory strictures may be a cause that favors
Diagnostic

clinical



imagistic


Esophageal syndrome or nothing
Complications: bleeding, compression
Barium swallow, endoscopy, CR, MRI, endoscopic US
Tratament




conservativ
Dilatation +/Surgical removal
RXT for hemangioma