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Transcript
Morning Meeting
Department of Thoracic
cardiovascular
PERFORATION OF THE
ESOPHAGUS
ETIOLOGY
 Iatrogenic
Perforations
 Spontaneous Perforations
 Trauma to the Esophagus
 Esophageal Disease
Iatrogenic Perforations
 Endoscopy
and of endoscopic
manipulation are the most cause of
esophageal perforations about 0.4-1%
Pharyngoesophageal junction  C6-7
 Stricture dilatation is 2nd most cause
 Others : Neck surgery and procedures
Spontaneous Perforations
 Boerhaave's
syndrome
esophageal rupture induced by
vomiting, Childbirth, defecation, lifting
heavy objects,
any acute rise in intra-abdominal
pressure against a closed glottis
 Left lateral wall, Lower third above the
diaphragm
Trauma to the Esophagus
 Penetrating
or blunt trauma
 Foreign bodies
 Self-induced esophageal lesions by
alkali or acid may cause extensive
necrosis and esophageal destruction.
Esophageal Disease
 Gastroesophageal
reflux disease
 Candidal, herpetic, and human
immunodeficiency infections also cause
pathologic perforations.
 Invasion and destruction of the
esophageal wall by carcinoma
 Mallory-Weiss syndrome but rare
CLINICAL PRESENTATION
Symptoms
Signs
Vomiting
Pain
Hematemesis
Dysphagia
Dyspnea
Tachycardia
Fever
Subcutaneous emphysema
Chest hypersonarity/dullness
Cardiac crunch
TREATMENT
 Derbes
and Mitchell 13 and Blichert-Toft
10 show a 60% to 100% mortality when
conservative management or no
treatment is offered
 Surgical treatment remains the
mainstay of management in esophageal
perforation.
 An
early operative repair provides the
best chances of survival. Sepsis, shock,
pneumothorax, pneumoperitoneum,
mediastinal emphysema, and
respiratory failure are all absolute
indications to intervene rapidly
Non-operative management
 NPO,
broad antibiotics, NG tube
decompression, Fluid supply
 The criteria set by Cameron and
colleagues :
a well-contained leak in a stable patient
without evidence of sepsis and without
communication with the pleural or
peritoneal cavity suggests a patient who
has already defended himself against
the perforation.
Perforation with Early Diagnosis
 Primary
repair of the perforation is the
first choice of therapy
 The goals of the operation include
extensive debridement of all nonviable
tissue in the mediastinum and around
the esophagus.
 Edema and necrotic tissue may be
extensive even if the esophageal
damage is recent.
Perforation with Late Diagnosis
 Esophageal
exclusion, T-tube drainage,
and esophageal resection.
 Resection must be considered with
cervical esophagostomy, jejunostomy,
and gastric decompression
CORROSIVE STRICTURES
OF THE ESOPHAGUS
ETIOLOGY
Alkaline caustics, acid or acidlike
corrosives, and household bleaches.
Hydrochloric, sulfuric, nitric, and
phosphoric acids are contained in
automobile battery acids.
Age
 75%
of injuries involving children
younger than 5 years and a much lower,
secondary peak occurring in 20-30
The severity of esophageal and
gastric damage resulting from a
caustic ingestion depends on
 Corrosive properties
 Concentration of the agent
 Quantity swallowed
Pathophysiology
Alkalis: bite the esophagus and lick the
stomach
Acids: Lick the esophagus and bite the
stomach
Alkali
 Liquefactive
Necrosis
 Vascular thrombosis
 Cell membrances are destroyed as their
lipids are saponified and cellular
proteins are denatured
 Destroy the protein, may persist for 7
days
Acid
 Coagulation
Necrosis
 Clumping and opacification of the
cellular cytoplasm
The goals of emergency
management
 Limit
and treat the immediately lifethreatening consequences
 Control subsequent stricture formation
Emergency management
 Keep
airway
 The epiglottis or vocal cords are
edematous
 endothracheal intubation is
contraindication
 Trachostomy
Contraindication
 The
use of emetics
 Not OG or NG
 Neutralization
Alkali may try Milk
Acid not try anything
 Surgery
is warranted if evidence
Perforation of the esophagus or stomach,
Mediastinitis
Peritonitis exists.
Corrosive stricture
 Esophagus
is stricture formation, which
usually develops between 3 and 8
weeks after the initial injury but
sometimes requires a much longer
period for evolution
Treatment
 Corticosteroids
to modify the
inflammatory response to the burn injury
 Antibiotics to control secondary
bacterial infection
 Esophagoscopy within 12-24 hrs
 On NG tube when severe burn
 CXR, endoscopy, Barium swallow



1.
2.
Bougienage
Esophageal stents
Colon interposition
Forearm tube
Free jejunal flap
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