? By the end of this lecture the student should be able to
? Describe the anatomy of the esophagus: extent, length,
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parts, strictures, relations, blood supply, innervationand lymphatics.
2
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ESOPHAGUS
? Tubular structure about 25
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cm long.
Cervical
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? Begins at the level of C6.? Pierces the diaphragm atT10.
? It is divided into 3 parts:
? 1- Cervical.
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? 2- Thoracic.
? 3- Abdominal.
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? Proximal and distal- oncosurgerythoracic
Abdominal
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3
RELATIONS
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CERVICAL PART? Posteriorly
? Post: Vertebral column.
? Lateral y:
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? Lat: Lobes of thethyroid gland.
? Anteriorly:
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? Ant: Trachea and therecurrent laryngeal
nerves.
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4
THORACIC PART
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? In the thorax, it passes
downward and to the left
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through superior then toposterior mediastinum
? At the level of the sternal angle,
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the aortic arch pushes the
esophagus again to the midline.
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5Thoracic part
ANTERIOR
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RELATIONS
? Trachea
? Left recurrent
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laryngeal nerve
? Left principal
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bronchus? Pericardium
? Left atrium
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6POSTERIOR RELATIONS ? Thoracic duct
? Bodies of the thoracic vertebrae
? Thoracic duct
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? Azygos vein? Right posterior intercostal arteries
? Descending thoracic aorta (at the
lower end)
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7
LATERAL RELATION
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? On the Right side:? Right mediastinal pleura
? Terminal part of the azygos vein.
? On the Left side:
? Left mediastinal pleura
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? Left subclavian artery? Aortic arch
? Thoracic duct
8
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ESOPHAGUS AND LEFT ATRIUM
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? close relationship
? What is the clinical
application?
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? A barium swallow will
help the physician to
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assess the size of theleft atrium (dilation).
RELATIONS IN THE ABDOMEN
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? In the Abdomen, the esophagus
? Fibers from the right crus of the
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descends for 1.3 cm and joins thediaphragm form a sling around the
stomach.
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esophagus.
? At the opening of the diaphragm, the
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? Anteriorly, left lobe of the liver.esophagus is accompanied by:
? Posteriorly, left crus of the
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? The two vagi
? Branches of the left gastric vessels
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10diaphragm.
? Lymphatic vessels.
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ESOPHAGEAL
CONSTRICTIONS
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? The esophagus has 3 anatomic
constrictions.
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? The first is at the junction with thepharynx(pharyngeoesophageal
junction).
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? The second is at the crossing with
the aortic arch and the left main
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bronchus.? The third is at the junction with the
stomach.
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? They have a considerable clinical
importance.
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? Why?1. They may cause difficulties in
passing an endoscope.
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2. In case of swallowing of caustic
liquids (mostly in children), this
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is where the burning is theworst and strictures develop.
3. The esophageal strictures are a
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common sites of the
development of esophageal
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carcinoma.4. In this picture what is the
importance of the scale?
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ARTERIAL SUPPLY
? Upper third by the
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inferior thyroid
artery.
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? The middle third bythe thoracic aorta.
? The lower third by the
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left gastric artery.
13
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VENOUSDRAINAGE
? The upper third drains
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in into the inferior
thyroid veins.
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? The middle third intothe azygos veins.
? The lower third into
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the left gastric vein,
which is a tributary of
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the portal vein.? NB. Esophageal varices.
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LYMPH DRAINAGE? The upper third is drained into the
deep cervical nodes.
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? The middle third is drained into the
superior and inferior mediastinal
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nodes.? The lower third is drained in the celiac
lymph nodes in the abdomen.
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15
NERVE SUPPLY
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? It is supplied by sympathetic fibers from thesympathetic trunks.
? The parasympathetic supply comes form the
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vagus nerves.
? Inferior to the roots of the lungs, the vagus
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nerves join the sympathetic nerves to formthe esophageal plexus.
? The left vagus lies anterior to the esophagus.
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? The right vagus lies posterior to it.16
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CARDIAC ORIFICE? It is the site of the gastro-
esophageal sphincter.
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? It is a physiological rather
than an anatomical,
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sphincter.? Consists of a circular layer of
smooth muscle (under vagal
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and hormonal control).
? Function:
? Prevents (GER)
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regurgitation (reflux)
? NB. Notice the abrupt
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mucosal transition fromesophagus to stomach (Z-
line)
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17
Microscopic anatomy
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? 2 layers of muscles- longitudinal and circular.? Lined by non keratinizing stratified squamous epithelium.
? Squamocolumnar jn.
Recap
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? Length ?? Parts?
? Arterial supply?
? Venous drainage?
? Constrictions ?
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? Relation with lt atrium?? Barett's esophagus?
Stricture
? Causes can be grouped into:
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? Intrinsic ? due to inflammation, fibrosis or neoplasia
? Extrinsic ? due to external compression
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? Disruption of peristalsisProximal and mid esophagus
? Caustic ingestion (acid or alkali)
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? Malignancy
? Radiation therapy
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? Infectious esophagitis - Candida, herpes simplex virus (HSV),cytomegalovirus (CMV), human immunodeficiency virus (HIV)
? AIDS and immunosuppressed patients
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? Diseases of the skin - Pemphigus vulgaris, benign mucous membrane
(cicatricial) pemphigoid, epidermolysis bullosa dystrophica
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? Idiopathic eosinophilic esophagitis? Extrinsic compression
? Squamous cel carcinoma
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Distal esophagus? Peptic stricture
? Adenocarcinoma
? Collagen vascular disease - Scleroderma, systemic lupus
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erythematosus (SLE), rheumatoid arthritis
? Extrinsic compression
? Alkaline reflux following gastric resection
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? Sclerotherapy and prolonged nasogastric intubation? Heartburn
? Dysphagia, odynophagia
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? Food impaction
? Weight loss
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? Chest pain? Poor nutritional status
? Patients with collagen vascular diseases -- joint abnormalities,
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calcinosis, telangiectasias, sclerodactyly, or rashes
? Virchow node
Corrosive injury
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? Accidental or suicidal.
? The type of agent, its concentration and the volume ingested
determine the extent of damage.
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? Pathophysiology:
? Alkalis cause liquefaction that leads to fibrous scarring.
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? Acids cause coagulative necrosis with eschar formation, and this coagulumlimit penetration to deeper layers.
? Acids cause more gastric damage because of intense pylorospasm with
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pooling in the antrum.
Treatment
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? Supportive? Feeding jejunostomy until patient starts swallowing saliva.
? Repeated endoscopy and dilation.
? Esophageal replacement for very long or multiple strictures. Why not
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resection?Corrosive injury- Key points
Skil ed early endoscopy is mandatory
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Esophageal perforation? Usually iatrogenic or due to `barotrauma'.
? Spontaneous perforation is a life-threatening condition.
? Iatrogenic perforation can be managed conservatively.
? Can be pathological
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? Due to penetrating injury or foreign bodyBarotrauma (spontaneous perforation,
Boerhaave syndrome)
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? 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. The condition was first reported by
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? Boerhaave, who reported the case of a grand admiral of the? Dutch fleet who was a glutton and practised autoemesis.
? Boerhaave syndrome is the most serious type of perforation
Pathophysiology
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VomittingPressure in
Perforates at
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against
esophagus
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its weakestMediastinitis
closed glottis
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increases
point
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Clinical presentation? Severe pain in the chest or upper abdomen following a meal or a bout
of drinking
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? SOB
? Sometimes misdiagnosed as MI, perforated peptic ulcer or
pancreatitis
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? Rigidity of the upper abdomen
? Dec. breath sounds
? Dullness on percussion, subcutaneous emphysema
? In late cases sepsis is present
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Investigations? CXR - air in the mediastinum, pleura or peritoneum.
? Pleural effusion
? A barium swallow
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? CECTIatrogenic injury
? Most common cause of esophageal perforation.
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? Most common site is the cricopharyngeus.? Factors associated with increased risk are including large anterior
cervical osteophytes, the presence of a pharyngeal pouch and
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mechanical causes of obstruction? It may follow biopsy
? Patients undergoing therapeutic endoscopy have a 10 times greater
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perforation risk than those undergoing diagnostic endoscopy.Treatment
? Aim is to limit mediastinal contamination and infection
? The decision between operative and non-operative management
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rests on four factors:
1 the site of the perforation (cervical vs. thoracoabdominal oesophagus)
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2 the event causing the perforation (spontaneous vs. instrumental)3 underlying pathology (benign or malignant)
4 the status of the oesophagus before the perforation (fasted and empty vs.
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obstructed with a stagnant residue).
? Indications for non-operative management include:
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? pain that is readily controlled with opiates;? absence of crepitus, diffuse mediastinal gas, hydropneumothorax or
pneumoperitoneum;
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? no evidence of widespread extravasation of contrast material;
? no evidence of on-going luminal obstruction or a retained foreign body.
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? patients who have remained clinically stable despite diagnostic delay.? The principles of non-operative management are hyperalimentation,
nasogastric suction and broad-spectrum intravenous antibiotics.
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? Surgical management is indicated when:? Patients are unstable with sepsis or shock
? Have evidence of a heavily contaminated mediastinum, pleural space
or peritoneum.
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? Surgery can be a primary repair, creation of an external fistula or
resection.
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Key points? Most perforations are iatrogenic.
? Surgical emphysema is pathognomonic.
? Complications are mediastinitis and sepsis.
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? Treatment is both conservative or surgical but requires specialisedcare.