Mohd Azam Haseen Associate Professor DO Cardiothoracic surgery JNMedical CollegeAMUAligarh Introduction Anatomyphysiology Causes Individual entities Questions Anatomy ID: 912294
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Slide1
Esophageal stricture
Dr.
Mohd
Azam
Haseen
Associate Professor
D/O
Cardiothoracic surgery
J.N.Medical
College,AMU,Aligarh
Slide2Introduction
Anatomy/physiology
Causes
Individual entities
Questions
Slide3Anatomy
Muscular tube
25cm
Cricopharyngeus
to LES
Mainly posterior
mediastinum
Outer longitudinal & inner circular muscles
Upper 1/3 striated , lower half smooth muscle
Two sphincters; UES-
cricopharyngeus
muscle, LES lower 1-2 cm of esophagus
Slide4Lies in midline, with a deviation to the LEFT in the lower portion of neck and upper portion of thorax
Returns to midline in midportion of thorax near bifurcation of the trachea
Surgical Approach: Cervical
Left, Upper Thoracic Right, Lower Thoracic Left
Slide5Three anatomic constrictions:
-
Cricopharyneus
-Aortic arch/left
mainstem
bronchus
-
Gastroesophageal
junction
Slide6Anatomy
Blood supply:
inferior thyroid artery
branches from thoracic aorta, bronchial A.
branches from left gastric and inferior
phrenic
arteries
Slide7Anatomy/Physiology
Venous; submucosal plexus drains into plexus outside of esophagus
Outer plexus to :
Inferior thyroid
Azygos
Coronary
Gastric venous system
Slide8Defination
A
ny loss of lumen area within the esophagus
The normal esophagus measures 20 mm in diameter
P
redominant symptom of strictures is dysphagia, which is usually when the lum
i
nal diameter is less than 15 mm
.
Slide9Etiology
Intrinsic strictures
Acid peptic
disorder (GERD)
Foreign body induced
Chemical/lye
ingestion
Iatrogenic -
Post-nasogastric tube
,post endoscopy ,
Sclerotherapy
Infectious esophagitis
Radiation-induced
Esophageal/gastric malignancie
s
Slide10Etiology
Extrinsic strictures
Pulmonary/mediastina
l
malignancies
Anomalous vessels and aneurysms
Metastatic submucosal infiltration (breast cancer, m
e
sothelioma, adenoeareinoma of gastric eardia)
Diverticula
Intrinsic strictures are most common, with acid/ peptic cause accounting for the majority of cases (60%-70%)
Slide12Clinical picture of Esophageal
stricture
Heartburn
D
ysphagia
O
dynophagia
F
ood impaction
W
eight loss
C
hest pain.
Slide13Diagnostic work up in Esophageal
stricture
Barium swallow
ENDOSCOPY
Esophagoscopy
–rigid/flexible
Biopsy
CECT
Slide14Slide15Slide16Slide17Endoscopy
Slide18Slide19Slide20Rigid
esophagoscopy
Slide21Esophageal stricture treatment
Dilation. The esophagus is stretched by passing a dilator or air-filled balloon is passed through a endoscope.
Ballooon dilatation
Slide23Slide24Esophageal stricture treatment
Surgery
is
needed
if
repeated dilations do not keep these strictures from returning.
Slide25Slide26Esophageal bypass grafting
(Esophagoplasty)
Total colonoesophagoplasty
Total gastroesophagoplasty
Total jejunoesophagoplasty
Slide27Slide28Slide29Swallowed FB
Peds 80% of all cases
Prisoners, psych, edentulous adults
Adults=meat and bones
Peds = coins, toys, crayons, pen caps
Psych and prisoners = unlikely objects, spoons, razors
Slide30Slide31Swallowed FB
Most pass spontaneously
10-20% require some intervention
1% surgical
Most are at “anatomic
narrowings
”
Cricopharyngeal
(C6) most commonthoracic inlet(T1
)
aortic
arch(T4
)
tracheal
bifurcation(T6
)
hiatal
narrowing(T10-11)
Slide32Pathophysiology
Once object passes pylorus, usually passes out with stool.
Irregular or sharp edges may lodge anywhere though
.
Neglected Foreign bodies can lead to stricture formation
Slide33Esophagitis
Inflammatory: can progress to ulceration, scarring,
stricture
Med induced-NSAIDs, KCL, doxy,
clindamycin
,
tetracycline,iron,alendronate
Infectious:
immunosuppression; AIDSCandida, HSV, CMV,
aphthous
ulceration
Fungal,
varicella
, EBV.
Slide34Caustic Injury
Caustic ingestion can result in severe injury to the esophagus and stomach.
Most ingestions occur accidentally in the pediatric population and the remainder in suicidal, psychotic, and alcoholic adults
Slide35Caustic Ingestion
Esophagus, pharynx, larynx
Bases ( most severe injuries )
Drain cleaners
Dishwasher soap
Acids
Bleaches
Slide36Mechanism of injury
Alkalis – pH > 7
Liquefaction necrosis
Acids – pH < 7
Coagulation necrosis
Bleaches – pH = 7
Irritants
Slide37Severity of burn
Type
Amount
Concentration
Time of
contact
Slide38Signs 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
Slide39Esophagoscopy
Esophagoscopy
in virtually all patients at 24-48 hours
post-ingestion
Signs and symptoms are not entirely predictive of esophageal injury
48-72 hrs – structural weakness in esophageal
wall
< 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
Slide40Slide41Radiography
Radiologic exam
Chest & neck
radiographs - WNL
Barium swallow
Will not reveal 1
st
and 2
nd
degree injuries
Slide42Immediate Treatment
Lye or other alkali
neutralized with half-strength vinegar, lemon juice, or orange juice
Acid
neutralized with milk, egg white, or antacids
sodium bicarbonate is not used because it generates CO2, which might increase the danger of perforation
Emetics are contraindicated
vomiting renews the contact of the caustic substance with the esophagus
Slide43Management of caustic injury
No evidence of burns at endoscopy
Keep under observation
Oral nutrition resumed when patient can painlessly swallow saliva.
First degree burn
Observation for 24-48 hrs.
Oral nutrition resumed when patient can painlessly swallow saliva.
Barium swallow at 24 hrs.
Repeat endoscopy & barium swallow at 1,2 and 8 months.
Slide44Management of caustic injury
Second & third degree burns
Resuscitation is aggressively pursued
NPO, IV fluid, PPI, Antibiotics, steroids.
Conservative management if no perforation.
Perforation/full thickness necrosis – exploratory
thoracotomy
/
laparotomy.
Slide45Management of Chronic phase
Aimed at managing strictures & fistulas.
Stent placement
during acute phase to prevent stricture formation. Stent removed at 3 weeks &
bougie
dilatation continued to achieve adequate lumen (40 French).
Reconstructive surgery
at 6 month to 1 year.
Esophagectomy with gastric pullup
Esophagectomy
with
jejunal
interposition
Esophagectomy
with
colonal
interposition
Slide46Surgical Intervention
complete
stenosis
in which all attempts have failed to establish a lumen
marked irregularity and pocketing on barium swallow
development of a severe
periesophageal
reaction or
mediastinitis
with dilatation
fistula
inability to dilate or maintain the lumen above a 40F
bougie
a patient who is unwilling or unable to undergo prolonged periods of dilation
Slide47Surgery
Esophageal Substitute
Colon
Stomach
Jejunum: free/transfer grafts based on the superior thyroid artery or internal mammary artery
Slide48Schatzki ring:
most common cause of intermittent
dysphagia
with solids
Fibrous stricture near GE junction in 15 % of population
Pts frequently present with food impacted after poorly chewed meat
Slide49SCHATZKI
’
S RING
Slide50Slide51Tt:
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
Slide52Esophageal webs
Thin strictures of mucosa and
submucosa
Often mid or proximal esophagus
Congenital or acquired
Plummer-Vinson syndrome, with iron deficiency anemia
Tx
is dilatation
Slide53External compression -
Diverticula
can be found throughout
esaphagus
Zenker
; progressive
outpouching
of pharyngeal mucosa above UES. d/t increased pressure when swallowing.
Usually seen after age 50HalitosisFeeling of a neck masscommonly associated with motor dysfunction
Slide54Zenker’s
itself can either be
resected
or suspended
Slide55Traction Diverticulum
a “true diverticulum”
usually lies
lateral
, and is in
midesophagus
due to inflammation, granulomatous disease, or tumor
Rx: excision and primary closure, may need palliative therapy if due to invasive Ca
Slide56Hiatus hernia
Important cause of reflux and
esophagitis
Types –true
paraesophageal
hernia(rolling hernia)
--mixed type is most common
C/F –
dysphagia,chest pain -- strangulation,gastric perforation
Slide57Slide58EOSINOPHILIC ESOPHAGITIS
Also known as
“
allergic
esophagitis
”
.
Predominant symptom is
dysphagia
.
Increasing incidence over past two decades.
Occurs in both children and adults with majority being males. In adults, majority are in their 20
’
s and 30
’
s.
High percentage have allergic issues including asthma, food allergies, hives, hay fever.
Slide59EOSINOPHILIC ESPHAGITIS (CONT)
Findings can include multiple rings, narrowed esophagus, whitish nodules, furrows, & strictures in upper esophagus.
Some cases have involved several family members.
Etiology may relate to food allergies, additives, pollen, reflux?
Slide60Slide61Slide62Slide63FURROWS
Slide64Slide65Slide66TREATMENT
Trial of anti-reflux medication-PPI.
Allergy testing and diet changes. Elemental diet
Avoidance of six most frequent allergenic foods (eggs, soy, wheat, cow-milk protein, peanuts, and seafood). SFED
Steroid inhaler- swallowing rather than inhaling the medication.
Fluticasone
propionate.
Oral Prednisone- higher incidence of side effects.
Dilatation-
risks of perforation.
Slide67Slide68Slide69ACHALASIA
Achalasia
is well recognized as a cause of swallowing difficulty.
Distal esophageal sphincter does not relax with a swallow and the muscle of the lower esophagus does not propel the food or liquid downwards i.e. abnormal peristalsis.
Result is
dysphagia
, occasionally chest pain and regurgitation, and weight loss
X-rays can reveal a dilated esophagus.
Slide70ACHALASIA (CONT.)
On endoscopy often see retained food and secretions in esophagus even though patient has been NPO.
Characteristic “yield” of LES to the scope being advanced.
“
Pseudo-achalasia
”
Slide71X-RAYS OF ACHALASIA
Slide72ACHALASIA TREATMENT
Three common treatment options
Pneumatic forceful balloon
dilitation
with
Rigiflex
balloon. May not work; uncomfortable for patient; 3-5% risk of perforation.
Botox injection. Not always successful. Tends to lose effect in 6-12 months requiring reinjection. Good option for poor surgical candidates.
Surgery-laparoscopic
myotomy
. Cut the sphincter and add partial fundoplication.
Rarely, Calcium Channel blockers or Nitrates.
Slide73Esophageal Varices
All patients with cirrhosis should have EGD screening for varices.
No varices- rescope in couple years.
Small varices- consider NSBB in these patients
Large varices- low risk group probably use NSBB. High risk group (red wale signs, advanced liver disease) can choose between NSBB and EVL. Add PPI after EVL (ulceration)
Sclerotherapy not warranted for primary prevention of bleeding.
Slide74Esophageal Varices
Slide75Esophageal Varices
Slide76Slide77CA Esophagus
common cause of both types.
95 %
squamous
cell
Male : female , 3:1
Fast progression from solids to liquid
dysphagia
Pts >40 yo with dysphagia assume neoplasm. Need expedient work up to rule out malignancy
Slide78A 74 year old male presents with dysphagia, gurgling sounds in his neck, and regurgitation of undigested food. What is the most likely diagnosis?
Slide79Case Presentation
18 y/o female in excellent general health awakens in the morning with rather severe substernal chest pain when she swallows anything even saliva. Has never had similar problems in the past.
Her only medication is doxycycline which she has taken for acne for 2 years.
WHAT IS YOUR DIFFERENTIAL DIAGNOSIS?
Slide80Slide81Treatment of Pill Ulcers
No evidence that any medication speeds healing. Typically resolves in a few days.
Pain meds.
May need parenteral support in rare cases.
Can try suspension of sucralfate (Carafate) or topical anesthetic (xylocaine).