Download Esophagus I

Surgery of the Esophagus – I
For undergraduate
Staff Members of Cardio-thoracic
Surgery Departments
Egypt
DYSPHAGIA
Dysphagia is difficulty in swallowing (functional
or organic).
Odynophagia is painful dysphagia.
Psychogenic dysphagia
• Globus hystericus → sensation of a lump in
the throat.
• Phagophobia → fear of swallowing.
Esophageal peristaltic waves: Primary peristaltic waves: from the upper to
lower esophagus.
Secondary peristaltic waves: from the site of
a solid bolus in a segment of the esophagus
downward.
Tertiary peristaltic waves: pathological, nonpropulsive and non-peristaltic.
Etiology:
• Oropharyngeal dysphagia: Functional & Organic
• Esophageal dysphagia:
Functional
Motility disorders
Organic
1. In the lumine: FB
2. In the wall (Mural):
A-Congenital: Stenosis, atresia, short esophagus,
duplication cysts and congenital webs + dysphagia
lusoria (vascular ring).
B-Acquired: Strictures (peptic, corrosive, anastomotic),
tumours (B or M) or diverticulae.
3. Pressure from outside:
Etiology:
I-Oropharyngeal dysphagia:
Disorders in the mouth, tongue and pharynx.
A- Functional:
• Loss of tongue function (myasthenia gravis).
• Pharyngeal dysfunction (myasthenia gravis, vascular
brainstem disease (pseudo-bulbar syndrome),
hyperthyroidism, poliomyelitis, scleroderma,
amyloidosis).
B- Organic:
• Mechanical obstruction (Zenker’s diverticulum,
tumours as oral carcinoma, inflammatory stricture,
postcricoid carcinoma, retropharyngeal abscess).
II-Esophageal dysphagia:
Functional (esophageal motility disorders)
• Achalasia.
• Scleroderma.
• Diffuse esophageal spasm.
• Nutcracker esophagus
• Diabetic neuropathy.
• Amyloidosis.
• Parasitic infection (Chagas’ disease).
• Emotional (globus hystericus).
• Plummer-Vinson's syndrome.
• Contractile lower esophageal ring (Schatzki ring).
• Lower esophageal sphincter spasm (hypertensive
sphincter).
Organic:
A. Congenital
• Atresia with or without tracheooesphageal fistula
• Stenosis
• Short esophagus
• Dysphagia lusoria (vascular ring)
• Foregut duplication.
Organic:
B. Acquired
Intraluminal obstruction:
• Foreign body.
Lesions in the wall:
• Esophageal webs.
• Esophageal tumors.
• Inflammatory stricture (peptic stricture).
• Anastomotic stricture, post-injection sclerotherapy, postSangestaken tube, post traumatic strictures.
• Caustic stricture.
• Esophageal diverticulae.
Extraluminal obstruction.
• Compression by tumors, enlarged lymph nodes, retrosternal goiter.
• Vascular abnormalities (aortic aneurysm) and enlarged left atrium.
• Spurs from anterior cervical spine.
• Rolling hiatal hernia, tight hiatal hernia repair, perioesphagitis after
vagotomy.
Clinical presentation
• Grades:
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Grade I: dysphagia for solids
Grade II: dysphagia for semisolids
Grade III: dysphagia for liquids
Grade IV: dysphagia for own saliva
Site:
The patient can point to the site of obstruction.
Duration: Long: Benign (stricture, achalasia)
Short: Cancer
Sudden: foreign body
Since birth: Congenital
Timing:
Within 15 minutes from swallowing
Nature:
Organic: First to solids then to fluids
Achalasia: First to fluids then to solids
Course:
Intermittent (benign), progressive (malignant)
Associated: Heart burn → GER (gastroesophageal reflux)
Skin changes → Scleroderma
Cervical lymph nodes → Neoplasm, T.B
Iron deficiency → Plummer-Vinson’s syndrome
Emotional → Globus hystericus.
Investigations:
1. Esophagogram.
2. Esophagoscopy.
3. Esophageal function studies.
Investigations
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Laboratory
Increase tumor markers for mediastinal tumours.
Iron deficiency anemia in Plummer-Vinson’s syndrome.
Radiological
Barium swallow, oesophagogram (most important),
Fluoroscopy (for motility disturbances),
Barium meal in Trendelenburg position (for hiatal hernia and GER),
Chest X-ray (plain),
CT scan (for masses),
MRI,
Angiography (dysphagia lusoria).
Instrumental & Biopsy
Esophagoscopy and biopsy
Esophageal function studies.
Manometric study (for motility disturbances)
24-hours pH recording (GER).
Esophagoscopy
Types:
• Rigid: done under general anesthesia (Fig.67)
• Flexible, fiberoptic: done under conscious sedation
Indications:
 Diagnostic
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Cancer eosophagus: locate site, taking biopsy (bite , brush biopsy)
Hiatal hernia: to access degree of reflux
Achalasia:
Identify cause of dysphagia and hematemesis
 Therapeutic
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Removal of foreign body
Insertion of Stent in cancer esophagus
Sclerotherapy in haematemesis
Dilatation of esophageal stricture
Laser therapy
Rigid Esophagoscopy
Esophageal function studies:
Esophageal manometry. is used to evaluate motility of esophageal
body, UES and LES. Examples:
• Achalasia
• Diffuse esophageal spasm
Ambulatory 24-hour pH monitoring .
Indications:
• To detect and quantitate exposure of lower esophagus to gastric
acid.
• To test the relationship between symptoms and esophageal
exposure to acid refluxate.
Ambulatory 24-hour bile reflux monitoring.
The reflux of bile &/or acid predisposes to esophageal injury
(esophagitis) and Barrett’s esophagus and malignancy.
Provocative test: Acid perfusion (Berstein test).
Determines whether symptoms are reproduced by the infusion of acid
into the esophagus. A positive test reproduces the patient’s
symptoms only during acid perfusion.
Treatment:
1. Medical:
• Neuromuscular: Calcium channel blockers.
• Emotional: Assurance, Sedatives.
• GER: Antacids, H2 blockers, Proton Pump Inhibitors.
• Radio-chemotherapy for inoperable tumours.
2. Instrumental:
• Esophageal dilatation (Guidewire directed bougies,
Balloon).
• Esophagoscopic F.B extraction.
• Intubation in inoperable carcinoma (pulsion or
traction; simple or expandable prosthesis).
• Endoscopic laser for benign or malignant strictures.
• Hydrostatic dilatation of achalasia
3- Surgical:
I-Removal of extrinsic compression: (thyroidectomy,
diverticulectomy, hiatal hernia repair, removal of
mediastinal masses…)
II-Esophageal resection and substitution using:
• Stomach: Esphagogastrectomy with
esophagogastrostomy.
• Colon interposition.
• Jejunal conduit (loop, pedicle, free)
• Skin flaps in pharyngeal and upper oesophageal
neoplasms.
III-Esophagocardiomyotomy for achalasia (Heller’
operation).
Motility disorders
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Achalasia.
Diffuse esophageal spasm.
Scleroderma: Skin disease and dysphagia.
Nutcracker esophagus; contractions in a normal
sequence but at an excessive amplitude or
duration. Chest pain mimics angina + Dysphagia.
• Diabetic neuropathy.
• Amyloidosis.
• Parasitic infection (Chagas’ disease).
Diffuse esophageal spasm
(DES) is a condition in which
uncoordinated contractions of the
esophagus occur.
Ba Swallow →Corkscrew
appearance of the esophagus (or
"rosary bead esophagus" )
ACHALASIA
Definition:
Failure of relaxation of the lower esophageal
sphincter in response to swallowing.
Achalasia is a motility disorder of the esophagus.
Etiology:
It represents a degenerative nerve process with loss
of ganglion cells in the myenteric plexus and a
reduction in vagal nerve fibers within the wall of
the esophagus.
There is hypertrophy of the circular muscle layer of
the esophagus, while the longitudinal layer
retains its normal thickness.
• The combination of achalasia, adrenal
insufficiency, and alacrima (lack of tear
production) in children is known as the triple A
(Allgrove) syndrome.
• In most cases the cause is unknown (idiopathic).
• In some regions of the world, achalasia can also
be caused by Chagas disease due to infection by
Trypanosoma cruzi.
Clinical Picture :
• Progressive dysphagia to liquids and solids over
several years (first for fluids).
• Regurgitation of undigested food especially in
recumbent position.
• Weight loss.
• Coughing or wheezing secondary to aspiration.
Investigations:
Radiology:
 CXR is normal, or shows widened mediastinum with an air-fluid level
within the dilated esophagus. Absence of gastric air bubble.
Pulmonary infiltrates of aspiration .
 Barium swallow demonstrates smooth tapering of the distal
esophagus (bird’s beak, or pencil end) and a dilated or sigmoid
esophagus and absence of gastric air bubble.
Endoscopy:
• Dilated esophageal body containing food residue (despite fasting).
• Easy passage of the rigid oesophagoscope through the
esophagogastric junction but failure of esophagogastric junction to
open spontaneously with repeated air insufflation using the fiberoptic
esophagoscope.
Esophageal function studies:
 Esophageal manometry demonstrates incomplete relaxation of the
LES with swallowing and ineffective peristalsis of the body of the
esophagus.
Esophagogram in
achalasia: smooth
central narrowing,
Bird’s peak- Parrot’s
peak – Pencil end,
dilated esophagus,
narrowing present
below cupola of
diaphragm & absence
of gastric air babble.
Complications
• Mucosal ulcerations by irritation of retained
food.
• Aspiration which leads to pneumonitis.
• Malignancy in 2-3% (squamous cell carcinoma
usually at dilated site).
Management
Medical treatment:
• Oral medications as nitrates, calcium channel
blockers and sildenafil (taken 20 min before
meal).
Pneumonetic dilatation:
Balloon pneumatic dilatation produces a
forceful disruption of the lower esophageal
sphincter.
Botulinum toxin: It is endoscopically injected
into the lower sphincter to weaken it.
Pneumatic dilatation of the lower
esophagus
Surgical Treatment:
– Esophagocardiomyotomy (modified Heller):
Surgical longitudinal section of the outer
longitudinal and inner circular smooth muscle
without damaging the submucosa and mucosa.
Myotomy achieved using an abdominal or thoracic
approach. Incision extends for about 7-10 cm
including lower end of the esophagus and
oesophago-gastric junction.
– Laparoscopic or thoracoscopic myotomy (VATS).
– Esophageal resection and reconstruction is
considered in patients who have failed esophageal
myotomy (or re-myotomy), or who have an endstage megaesophagus.
Modified Heller’s myotomy
VATS
CORROSIVE ESOPHAGEAL INJURY
From accidental (children) or suicidal (adults)
ingestion of strong alkali or acid.
Liquefaction necrosis from alkali, coagulation
necrosis from acid.
In Egypt → commercial caustic potash. This is a
mixture of potassium hydroxide, potassium
carbonate and sodium carbonate. It is used
primarily for washing clothes, cleaning floors
and in some homes for making soap.
Classification of corrosive esophageal burns
• First degree (superficial) burn: Superficial
mucosal hyperemia, mucosal edema with or
without superficial sloughing.
• Second degree (medium, transmucosal) burn:
The submucosal and muscular layers are
involved, being left exposed after desquamation
of the mucosa.
• Third degree (deep, full-thickness burn): Necrosis
through the entire wall of the esophagus, causing
periesophagitis and possibly perforation with
mediastinitis, pericarditis or broncho-esophageal
fistula.
Clinical Picture:
I. Acute Phase:
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Pain and inability to swallow.
Excessive salivation.
Respiratory distress.
Dehydration.
In severe cases, there might be laryngitis and stridor.
II. Chronic Phase:
This started 4-6 weeks from the incidence of potash
ingestion
• Dysphagia
• Dehydration
• Weight loss
PPOS
Barium Swallow
Treatment:
I- Initial management of acute
corrosive esophagitis:
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Antibiotics.
Parenteral or oral fluids.
Corticosteroids.
Tracheostomy with stridor.
Neither instrumentation (Gastric lavage) nor
dilatation should be performed at this stage to
avoid esophageal perforation.
• Esophagoscopy and radiography:
Done at any time after corrosive ingestion provided the
condition of the patient allows.
• If no burn is found in the esophagus, antibiotics are
discontinued. Oral feedings are started as soon as the
patient comes out of anesthesia following
esophagoscopy.
• In the presence of first degree burn, antibiotics are
continued for ten days. Oral feedings are started
progressing from clear liquid diet to a full diet over a
period of three days.
• In the presence of second and/or third degree burn, a
siliconized catheter splint is applied through
transcervical pharyngostomy or oesophagostomy. If
the patient refuses splinting, he is followed and
managed as in the chronic stage.
II- Patients who present in the chronic stage of
corrosive esophagitis are examined by
esophagoscopy and esophagography and managed
as follow:
• Esophageal dilatation:
If there is short smooth segment (less than twovertebrae), patients are dilated antegradely, using
Savary dilators.
If there is Long segment or irregular strictures (more
than two-vertebrae); patients are dilated
retrogradely, using Tucker’s dilators. Gastrostomy
feeding is required.
Esophageal perforation following dilatation is treated
conservatively: Stop oral intake, give massive
antibiotics, drain any collection (mediastinal abscess,
empyema), and institute gastrostomy feeding.
II- Patients who present in the chronic
stage of corrosive (Cont.):
• Retrosternal colon interposition is indicated
if dilatation failed. A segment of transverse
colon interposed between the proximal
esophagus and the stomach.
ESOPHAGEAL CANCER
Premalignant lesions:
• Achalasia,
• Barrett’s esophagus,
• Reflux stricture,
• Post-corrosive stricture,
• Plummer-Vinson syndrome.
Clinical Picture:
• Primary tumour: Dysphagia, regurgitation,
vomiting, odynophagia, pain (epigastric, back,
neck) arising from local tumour infiltration,
esophagitis, and metastasis to intraabdominal lymph nodes or bone, respiratory
symptoms (cough after swallowing) suggesting
aspiration or an esophagotracheal or
bronchial fistula. General symptoms of weight
loss and cachexia are present in 50% of
patients.
Clinical Picture: Cont.
• Distant metastases: lung, liver, bone, adrenal,
kidney, abdominal lymph nodes, ….
• Physical examination: Enlarged cervical or
supraclavicular lymph nodes, signs of
aspiration (rales, rhonchi, consolidation),
upper abdominal mass, hepatomegaly,
generalized wasting.
Investigations:
• Laboratory: Anemia, hypoproteinemia, abnormal
liver function tests, hypercalcemia.
• CXR: Pulmonary metastases, infiltrates or
pneumonia, soft-tissue mass or air-fluid level in the
mediastinum.
• Barium esophagogram: Defines level and extent of
oesophageal obstruction → fixed irregular filling
defect, rate tail appearance and shouldering.
• Esophagogastroscopy: flexible or rigid
esophagoscope. It defines the site and extent of
the tumor. Multiple biopsies are taken to obtain a
histologic diagnosis. Obstructing tumors may be
dilated or stented during esophagoscopy.
Investigations: Cont.
• CT: to assess extent of local disease and
enlarged nodes. Scanning of the brain, lung,
and liver for the possibility of metastases.
• Endoscopic ultrasound: To assess the depth of
tumor penetration and peri-esophageal lymph
node metastasis.
• Bronchoscopy: if a malignant fistula is
suspected.
• MRI: Has little advantage over CT.
Barium swallow
in cancer
esophagus:
Filling defect, rat
tail appearance,
shouldering,
irregular
eccentric
stricture.
Esophagogram:
Upper, middle and lower 1/3
Endoscopic image of patient
with esophageal cancer
TNM subsets
T descriptor
• Tis
Carcinoma in situ.
• T1
Tumor invades lamina propria, muscularis mucosa or submucosa.
• T2:
Tumor invades muscularis propria.
• T3
Tumor extends into periesophageal tissue.
• T4
Tumor invades adjacent structures.
N descriptor
• N0
No regional lymph node metastasis.
• N1
Regional lymph node metastasis .
M descriptor
• M0
No distant metastases
• M1
Distant metastases.
Stage
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Tis N0 M0
I
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T1 N0 M0
IIA
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T2 N0 M0
T3 N0 M0
IIB
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T1 N1 M0
T2 N1 M0
III
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T3 N1 M0
T4 Any N M0
IV
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Any T Any N
M1
Pathology of esophageal cancer
Squamous cell carcinoma :
• 80% of all primary esophageal cancers.
• Mid-third (50%), lower-third (25%), upper-third
(15%).
• Macroscopic types: Fungating, ulcerating,
infiltrating, polypoid.
• Histologically: Well-differentiated or poorlydifferentiated.
• Submucosal proximal tumor spread is frequent.
• Metastasis to regional lymph nodes > 50%.
• Metastasis to lung 50% and liver 50%.
Pathology of esophageal cancer Cont.
Adenocarcinoma :
• 20 - 40% of primary esophageal cancer.
• Should be distinguished from adenocarcinoma of
gastric origin. Criteria in favor of esophageal
origin include:
Associated Barrett’s epithelium.
Greater than 75% of tumor mass involving
the body of esophagus.
Direct invasion of periesophageal tissues.
Minimal gastric involvement.
Clinical symptoms of esophageal
obstruction.
Treatment:
• Early stage tumors (Tis, Stage I): Surgical resection.
• Locally advanced (T4) & metastatic (M1) tumors : Are
excluded from surgery.
I - Surgery:
Procedure: esophagectomy with gastric pull up and
esophagogastric anastomosis.
Idea of procedure :
Resection of the esophageal tumour with proximal extension
of resected esophagus of 10 cm & distal extension of
resection at least 5 cm from tumor.
Esophageal reconstruction: this achieved by gastric pull up
with the stomach positioned in the posterior mediastinum.
The healthy proximal portion of the esophagus is then
anastomosed to the stomach (esophagogastric
anastomosis). A pyloromyotomy or pyloroplasty is done to
improve gastric drainage.
Approach :
• Right thoracotomy & laparotomy
• Left thoracotomy or Thoracoabdominal
• Transhiatal (non-thoracotomy, Blind
esophagectomy)
• Video assisted thoracoscopic surgery (VATS)
Esophagectomy for Cancer esophagus
Circular Stapler - Product nomenclature
Detachable head
assembly
Tying
notch
Locking spring
Adjusting knob
Gap setting scale
Anvil Shaft
Safety
Trocar
Orange Tying
area
Staple
Housing
Firing
handle
56
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II- Radiotherapy:
– Preoperative: Improves resection and reduces local
recurrence.
– Postoperative: Not recommended as a routine after
surgical resection.
III- Chemotherapy:
• Single agent (cisplatin, 5-fluro-uracil, mytomycin,
bleomycin).
• Combination (cisplatin + 5-fluro-uracil).
• Preoperative: Eliminates micro-metastases and
improve respectability.
• Postoperative: Cannot be recommended for
routine clinical use.
Palliation:
Causes of irresectability (Inoperable Cancer
esophagus)
• General: Cachectic patients unfit for surgery,
deteriorated cardiac, renal, hepatic and
pulmonary functions.
• Local:
– Tumour more than 10 cm.
– Spread to tracheobronchial tree, Aorta.
– Peritoneal seedlings.
– Celiac and hepatic lymph node affection.
• Distant metastesis e.g liver, lung.
Types of Palliation
• Esophageal dilatation.
• Esophageal stents:
– Covered self-expandable metallic stents, inserted
through endoscopy.
– Mousseau Barbin intubation, inserted through
laparotomy .
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Radiochemotherapy.
Endoluminal brachytherapy.
Laser therapy.
Surgery:
– Feeding gastrostomy
– Retrosternal Colon interposition or
esophagogastrectomy. Those 2 aggressive surgeries
are rarely used as palliation.
Esophageal stenting
Diaphragmatic Herniae
I- Congenital:
Morgagni’s hernia
Bochdalek hernia
II- Acquired:
Hiatal Hernia
Traumatic (Accidental, Iatrogenic)
Congenital
diaphragmatic hernia
Morgagni’s hernia
Congenital diaphragmatic hernia
Bochdalek hernia
Barrett’s esophagus
Definition:
Lining of the lower esophagus with columnar
epithelium instead of squamous epithelium
(columnar metaplesia).
Pathology:
Finding of specialized columnar epithelium,
characterized by intestinal metaplasia.
Endoscopic appearance in Barrett’s
esophagus
Etiology
Barrett’s esophagus results from chronic GERD.
Chronic reflux esophagitis lead to loss of esophageal
mucosa and replacement of columnar epithelium with
squamous epithelium.
Clinical importance of Barrett’s
esophagus:
Barrett’s esophagus predisposes to esophageal cancer i.e.
precancerous, particularly adenocarcinoma.
Clinical Picture:
Symptoms related to GERD.
Investigations:
• Radiology (Ba Swallow): Reflux-related
findings (mucosal ulceration, strictures).
• Endoscopy and biopsy:
Barrett’s columnar mucosa is deeper pink
compared with the pale squamous mucosa
and > 3 cm from the EGJ.
Multiple biopsies at 2-cm intervals are taken.
Endoscopic application of vital stains (Lugol’s
iodine, toluidine blue) improves recognition of
columnar mucosa.
Treatment:
• Control of GERD by medical and
surgical anti-reflux therapy.
• Endoscopic surveillance to detect
early stage adenocarcinoma &
surgical resection in high-grade
dysplasia.