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ESOPHAGUS

Surgical anatomy Esophagus

 Key points
 Anatomy & histology
 Physiology
 Esophageal symptoms
assessment
 Esophageal testing

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Anatomy
 The esophagusis a muscular tube
connecting the pharynx to the stomach
 23-25 cm in lengthcombo of both
 • Contains two sphincters
 • Lined by squamous
 epithelium
 • < 3 cm below diaphragm

 The structure and function are much

more complex.
 A thorough understanding of the anatomy
and physiology is essential to
understanding esophageal disease
states.

Anatomy Sites of external

compression

 The Aorta.
 Left main stem bronchus.
 Diaphragm.
 **Clinical application in
foreign body impaction.

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Histology

 Mucosa.
 Stratified squamous
epithelium
 Lamina propria,
 Muscularismucosa.
 Submucosa.
 Muscularispropria.
 Skeletal muscle. Upper 1/3
 Smooth muscle. Lower 2/3
 Adventitia.
 No serosa, ( unique ).

Anatomy innervation
 Vagus nerve Smooth muscle
 Myentericplexus. ( peristalsis)
 Meissner's plexus.
 Neurotransmitters:
 ACH ( excitatory) , proximal
 NO ( inhibitory ) , distal

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Anatomy blood supply

 Segmental orientation .
 Blood supply to other viscera.

Physiology

 Primary Peristalsis:
 Food bolus, contracts
proximally to distally
 Secondary Peristalsis:
 Esophageal distention
(residual food bolus) and
reflux
 Tertiary Contractions:
 Nonperistalticpropel bolus in
a retrograde direction to
proximal esophagus

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Physiology
Upper esophageal sphincter Lower esophageal sphincter
UES LES

 Composed of the  10–40 mm Hg

cricopharyngeus muscle  Below Diaphragm
 Rest : Tonic contracture  Physiological sphincter (not a
 Pharyngeal phase: Relaxation true anatomic sphincter)

Esophageal testing

 Barium swallow
 Endoscopy
 Manometry.
 24-hours PH monitoring

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Endoscopy
 Evaluation
 Mucosa
 Structural abnormalities.
 Rigid or flexible
 Diagnostic and/or therapeutic.

Indications
 Weight loss
 Upper gastrointestinal bleeding,
 Dysphagia, odynophagia and chest pain,
 Partial or no response to empiric therapy,
 Evaluation for Barrett's esophagus
 Foreign body

Manometry

 Measures
 Intraluminal pressures .
 Coordination of the pressure
activities of LES, esophageal body,
and UES.
 Assessment of patients with
symptoms suggestive of
esophageal motor dysfunction (
achalasia , Scleroderma)

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Esophageal Symptom
Assessment
 Heartburn.
 Dysphagia: sensation of food being delayed in its normal passage
from mouth to stomach. Patients often complain of a sensation of
food “sticking.”
 Odynophagia.
 Regurgitation.
 Aspiration.

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Atypical Symptoms
Dyspepsia(epigastric burning and fullness)
Nausea and Vomiting
Hematemesis
Globus
Coughing
Throat clearing
Throat pain
Hoarseness
Wheezing/stridor
Dyspnea
Apnea
Halitosis

FOREIGN BODIES IN THE

OESOPHAGUS

 The most common is a food

bolus, which usually signifies
underlying disease
 It is usually possible to
remove foreign bodies by
flexible or rigid endoscopy
 Beware of button batteries in
the esophagus

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PERFORATION
 Perforation of the oesophagus is
usually iatrogenic (at therapeutic
endoscopy) or due to ‘barotrauma’
(spontaneous perforation).
 Surgical emphysema is virtually
pathognomonic
 Many instrumental perforations
can be managed conservatively,
but spontaneous perforation is
often a life-threatening condition
that regularly requires surgical
intervention

Barotrauma (spontaneous
perforation,
Boerhaave syndrome)
 This occurs classically when a
person vomits against a closed
glottis. The pressure in the
oesophagus increases rapidly,
and the oesophagus bursts at
its weakest point in the lower
third, sending a stream of
material into the mediastinum
and often the pleural cavity as
well
 Boerhaave syndrome is the
most serious type of
perforation . WHY????.
 This causes rapid chemical
irritation in the mediastinum
and pleura followed by
infection if untreated.
Barotrauma has also been
described in relation to other
pressure events when the
patient strains against a
closed glottis (e.g.
defaecation, labour, weight-
lifting).

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Diagnosis of spontaneous
perforation
 The clinical history is usually of
severe pain in the chest or upper
abdomen following a meal or a
bout of drinking. Associated
shortness of breath is common.
Many cases are misdiagnosed
as myocardial infarction,
perforated peptic ulcer or
pancreatitis if the pain is
confined to the upper abdomen.
 There may be a surprising
amount of rigidity on
examination of the upper
abdomen, even in the absence
of any peritoneal contamination.

Other types of perforation

 Penetrating injury
 Perforation by knives and bullets is
uncommon, even in war, as the
oesophagus is a relatively small target
surrounded by other vital organs.
Pathological perforation  Foreign bodies
 The oesophagus may be perforated during
 Rare. Erosion into an removal of a foreign body but,
occasionally, an object that has been left in
adjacent structure with fistula
the oesophagus for several days will erode
formation is more common. through the wall.
Aerodigestive fistula is most
 Instrumental perforation
common and usually
 Instrumentation is by far the most common
encountered in primary
cause of perforation. Modern
malignant disease of the instrumentation is remarkably safe, but
oesophagus or bronchus perforation remains a risk that should
never be forgotten.
 The risk is considerably higher in patients
with malignancy.

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Treatment of oesophageal
perforations
 What factor(s) enhances
spread of gastro-intestinal
fluid to mediastinum????
The aim of treatment is to limit
mediastinal contamination and
prevent or deal with infection.
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 The decision between operative
and non-operative management
rests on four factors. These are:
 1 the site of the perforation
(cervical versus
thoracoabdominal oesophagus);
 2 the event causing the
perforation (spontaneous versus
instrumental);
 3 underlying pathology (benign or
malignant);
 4 the status of the oesophagus
before the perforation (fasted and
empty versus obstructed with a
stagnant residue).
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Lacerations (Mallory-Weiss
Syndrome)
 Longitudinal tears in the
esophagus at the
esophagogastric junction.
 The presumed pathogenesis
is inadequate relaxation of
the musculature of the lower
esophageal sphincter during
vomiting, with stretching and
tearing of the
esophagogastric junction at
the moment of propulsive
expulsion of gastric contents.

MALLORY–WEISS SYNDROME

 Forceful vomiting may produce a mucosal tear at the

cardia rather than a full perforation.
 vigorous vomiting produces a vertical split in the gastric
mucosa, immediately below the squamocolumnar
junction at the cardia in 90 per cent of cases.
 The condition presents with haematemesis. Usually, the
bleeding is not severe, but endoscopic injection therapy
may be required for the occasional, severe case.
Surgery is rarely required

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CORROSIVE INJURY
 Corrosives such as sodium hydroxide (lye, caustic soda) or sulphuric
acid may be taken in attempted suicide. Accidental ingestion occurs
in children and when corrosives are stored in bottles labeled as
beverages.
 All can cause severe damage to the mouth, pharynx, larynx,
esophagus and stomach. The type of agent, its concentration and
the volume ingested largely determine the extent of damage. In
general, alkalis are relatively odorless and tasteless, making them
more likely to be ingested in large volume.
 Alkalis cause liquefaction, saponification of fats, dehydration and
thrombosis of blood vessels.
 Acids cause coagulative necrosis with eschar formation, and this
coagulant may limit penetration to deeper layers of the oesophageal
wall. Acids also cause more gastric damage than alkalis because of
the induction of intense pylorospasm with pooling in the antrum

 The key to management is early endoscopy by an

experienced endoscopist to inspect the whole of the
oesophagus and stomach.
 Minor injuries with only oedema of the mucosa resolve
rapidly with no late sequelae.
 With more severe injuries, a feeding jejunostomy may be
appropriate until the patient can swallow saliva
satisfactorily.
 The widespread use of broadspectrum antibiotics and
steroids is controversial

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Management
Regular endoscopic examinations
are the best way to assess
stricture development.
 Significant stricture formation
occurs in about 50 per cent of
patients with extensive mucosal
damage
 emergency surgery for bleeding
or perforation, elective
oesophageal resection should
be deferred for at least three
months until the fibrotic phase
is established.
 Oesophageal replacement (
colon) is usually required for
very long or multiple strictures

Gastro esophageal Reflux

Disease
 American College of
Gastroenterology (ACG)
 Symptoms OR mucosal damage
produced by the abnormal reflux of
gastric contents into the esophagus
 Often chronic and relapsing
 May see complications of GERD in
patients who lack typical symptoms

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Physiologic vs Pathologic

 Physiologic GERD  Pathologic GERD

 Postprandial  Symptoms
 Short lived  Mucosal injury
 Asymptomatic  Nocturnal sx
 No nocturnal sx

Pathophysiology
 Primary barrier to
gastroesophageal reflux is
the lower esophageal
sphincter LES normally
works in conjunction with
the diaphragm
 If barrier disrupted, acid
goes from stomach to
esophagus

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Gastroesophageal Reflux Disease (GERD)

2.Pathophysiology
 a. Gastroesophageal reflux results from transient
relaxation or incompetence of lower esophageal
sphincter, sphincter, or increased pressure within
stomach.

 b. Factors contributing to Gastroesophageal reflux

1.Increased gastric volume (post meals)
2.Position pushing gastric contents close to
Gastroesophageal juncture (such as bending or lying
down)
3.Increased gastric pressure (obesity or tight clothing)
4.Hiatal hernia 31

Gastroesophageal Reflux Disease

(GERD)
Manifestations
1. Heartburn after meals, while bending over, or
recumbent
2. Dyspepsia or indigestion
3. May have regurgitation of sour materials in
mouth, pain with swallowing
4. Atypical chest pain
5. Extraesophageal manifestations: Asthma,
laryngitis, chronic cough , Sore throat with
hoarseness

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Alarms

Alarm Signs/Symptoms 
Dysphagia 
Early satiety 
GI bleeding 
Odynophagia 
Vomiting 
Weight loss 
Iron deficiency anemia 

Complications

 Erosive esophagitis
 Stricture
 Barrett’s esophagus

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Complications
 Erosive esophagitis
 Responsible for 40-60%
of GERD symptoms
 Severity of symptoms
often fail to match severity
of erosive esophagitis

Complications
 Esophageal stricture
 Result of healing of
erosive esophagitis
 May need dilation

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Complications

 Barrett’s Esophagus
 Columnar metaplasia of the
esophagus
 Associated with the
development of
adenocarcinoma

Complications
 Barrett’s Esophagus
 Acid damages lining of
esophagus and causes
chronic esophagitis
 Damaged area heals in a
metaplastic process and
abnormal columnar cells
replace squamous cells
 This specialized intestinal
metaplasia can progress to
dysplasia and
adenocarcinoma

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Gastroesophageal Reflux Disease (GERD)

Diagnostic Tests
 a. Barium swallow (evaluation of esophagus, stomach,
small intestine)
 b. Upper endoscopy: direct visualization; biopsies may
be done
 c. 24-hour ambulatory pH monitoring

Husni Rousan 39

Management
1)Dietary and Lifestyle Management
 a. Elimination of acid foods (tomatoes, spicy,
citrus foods, coffee)
 b. Avoiding food which relax esophageal
sphincter or delay gastric emptying (fatty foods,
chocolate, alcohol)
 c. Maintain ideal body weight
 d. Eat small meals and stay upright 2 hours post
eating; no eating 3 hours prior to going to bed
 e. Elevate head of bed on 6 – 8 blocks to
decrease reflux
 f. No smoking
 g. Avoiding bending and wear loose fitting
clothing

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2.Medications
 a. Antacids for mild to moderate symptoms, e.g. Maalox,
Gaviscon
 b. H2-receptor blockers: decrease acid production; given BID
or more often, e.g. cimetidine, ranitidine, famotidine, nizatidine
 c. Proton-pump inhibitors: reduce gastric secretions, promote
healing of esophageal erosion and relieve symptoms, e.g.
omeprazole ; lansoprazole
 d. Promotility agent( prokinetic ): enhances esophageal
clearance and gastric emptying e.g domperidone

Husni Rousan 41

3. Surgery indicated for persons not improved

by diet and life style changes:
Failed medical treatment
Severe Oesophagitis
Young patients with ongoing regurgitation
Respiratory symptoms
Barretts Oesophagus.
 a. Laparoscopic or open procedures to
tighten lower esophageal sphincter . E.g
Nissen fundoplication

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Nissen Fundoplication

 Most commonly preferred surgery

 360 degree fundus wrap

 Effective

Complications

 Inability to vomit

 Gas bloat syndrome

 Dysphagia
Paul

Paul

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Recent Techniques for GERD

1. Transoral Endoscopic Suturing – to plicate the GE junction

2. Endoscopic Application of Radiofrequency Energy (Stretta

Procedure)

Two novel endoluminal therapies approved by the Food and Drug

Administration FDA, USA. Paul

Complications

 Barrett’s Esophagus
 Manage in same manner as GERD
 EGD every 3 years in patient’s without dysplasia
 In patients with dysplasia annual to shorter interval
surveillance

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Complications

 Patient’s with GERD who need regular EGD

 Alarm symptoms
 Poor therapeutic response
 Long symptom duration
 “Once in a lifetime” EGD for patient’s with chronic
GERD becoming accepted practice
 Many patients with Barrett’s are asymptomatic

Classification of Hiatus of hernia

Definition
Part of stomach protrudes through the esophageal hiatus of the
diaphragm into thoracic cavity. The classification of hiatus hernia is
based upon the position of the gastro esophageal junction.

• Sliding Hernia
Type I

• Rolling Hernia
Type II

• Combined I + II
Type III

Type IV
• Stomach + Viscera
Paul

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Type I (Sliding hernia)

 Due to the laxity of the Phrenoesophageal
membrane

 Cephalad displacement of the

GE junction through the hiatus
into the mediastinum

 the commonest type

 Asymptomatic

 5% associated with GERD

Paul

Type IIII(Rolling
TYPE hernia)
(ROLLING)

 Due to a focal defect in the

phrenoesophageal membrane

 Superior migration of the fundus of the

stomach alongside the GE junction and
oesophagus into the mediastinum

 GE junction in this type remains in its normal

intra-abdominal location

Paul

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Type III (Hiatus

TYPE III hernia)
It is the Combination of Type I and Type II

Paul

Type IV (Hiatus hernia)

TYPE IV
It is the hernia containing other abdominal viscera like
transverse colon and omentum

Paul

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Complications

• Gastric volvulus

• Obstruction

• Infarction

• Ischemia – Cameron Ulcer

• GERD – Barretts Oesophagus

Paul

Treatment

Type 1: Like GERD

Type II , III , IV :

Surgical Treatment

Hernia Repair

 Reduction of hernia
 Resection of sac
 Closure of hiatal defect

Paul

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