Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Surgery 16 Corrosive Strictures PPT-Powerpoint Presentations and lecture notes
Esophagus: Anatomy, Physiology,
Corrosive stricture
&
Perforation of Esophagus
Anatomy
The primitive foregut forms during the fourth week of
gestation by a longitudinal folding and incorporation of the
dorsal part of the yolk sac into the embryo.
34th day: The distal esophagus elongates first, followed by
the proximal.
6th week: Mesenchymal circular muscle coat develops
Three to nine weeks later, longitudinal musculature
appears.
Seventh to eighth week: Esophageal lumen is almost
filled with cells from the proliferated esophageal epithelium.
During the 4th month, the muscularis mucosa appears
narrowest tube of the gastrointestinal tract
Midline structure anterior to the spine and posterior
to the trachea
Length: ranges from 21 cm-34 cm (27 cm average).
Classical anatomy divides the esophagus into three
parts:
Cervical
Thoracic
Abdominal
Function divides the esophagus according to its differing
forms of motility into the following three zones :
Upper esophageal sphincter (UES)
Esophageal body
Lower esophageal sphincter (LES)
Arterial Supply
Venous Supply
Innervation
Lymphatic drainage
Histology
It lacks a serosal coating
The four layers are:
mucosa
Submucosa
muscularis
tunica adventitia
Corrosive stricture
Stricture formation, which usually develops between 3
and 8 weeks after the initial injury but sometimes
requires a much longer period for evolution
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
Type of caustic related to injury
Acid
Alkaline
? Generally less severe
? Liquefactive necrosis
injury
? Sodium hydroxide
? Coagulative necrosis
? Very hazardous
? Coagulum lessen tissue
? 30% causes full
penetration
thickness necrosis
The severity of esophageal and gastric damage resulting
from a caustic ingestion depends on
Corrosive properties
Concentration of the agent
Quantity swallowed
Pathogenesis
Corrosive enter to stomach > reflex pyloric spasm
Limit passage of corrosive to duodenum
Regurgitation of corrosive against a closed cricopharyngeus
> damage to esophagus and Stomach
35 mins > gastric atonia > opening of pylorus
Goal of emergency management
Limit and treat the immediately life-threatening
consequences
Control subsequent stricture formation
Endoscopic findings
Zargar et al GIE 1991; Orringer 1993
Early management
Resuscitation
Upper airway
? Assessment of severity of damage
? Secure the airway
Fiberoptic intubation
Tracheostomy
Contraindication
Emetics
OG or NG
Neutralization
Alkali ---try Milk
Acid---- do not try anything
Surgery is warranted if evidence of
Perforation of the esophagus or stomach
Mediastinitis
Peritonitis exists
Treatment
Corticosteroids to modify the inflammatory response
to the burn injury
Antibiotics to control secondary bacterial infection
Esophagoscopy within 12-24 hrs
Bougienage
Esophageal stents
Colon interposition
Forearm tube
Free jejunal flap
Perforation of Esophagus
Introduction
Grand Admiral of Holland died of spontaneous
rupture of the esophagus in 1724
J. R. Meyer of Berlin was the first to recognize this
disease prior to death
Barrett made the first early diagnosis and performed
the first surgical repair in 1946
Anatomy
Esophagus lacks serosa
More likely to rupture
Site of rupture:
More commonly on left side
Due to instrumentation: distal esophagus
Spontaneous: posterolateral esophagus
Tears are usually longitudinal
Etiology
Iatrogenic
Instrumentation (MC cause)
most common site of perforation during endoscopy is at
the cricopharyngeus
Surgical injury
Boerhaave Syndrome (barogenic perforation,
postemetic perforation,spontaneous esophageal rupture)
Always occurs on the left side of the distal third of esophagus
Most tears occur along the longitudinal axis (0.6 to 8.9 cm) long
The mucosal tear is often longer than the muscle tear, which is
important to repair the esophageal wall completely
Trauma (8% to 15.3%)
The MC cause is chest injury by a steering wheel in a traffic
accident
The incidence of esophageal perforation by penetrating injuries
is 11% to 17%
Perforation is more common in the cervical than thoracic
esophagus
The overall mortality rate remains high (15% to 40%).
Tumor
Foreign Body ( 7-14%)
Caustic Injury
Drug Induced eg. tetracycline, KCL,quinidine, NSAID's
Infection
Other Causes eg.Barrett ulcer and ulcerative esophagitis
with Zollinger-Ellison syndrome
Pathophysiology
Air, Saliva, and Gastric contents released
mediastinitis
pneumomediastinum
empyema
can progress to sepsis, shock, resp failure
Diagnosis
Chest X ray
Chest radiographs appear normal in the early phase
Emphysema becomes manifestated by 1 hour after the
perforation
Pleural effusion is detected several hours after the
perforation
Pneumomediastinum is present in 60% of cases.
Perforation of the mid-thoracic esophagus is associated with right-sided pleural
effusion and perforation of the distal thoracic esophagus is associated with left-
sided pleural effusion
Esophagography
The detection rate is 60% for cervical perforation and 90%
for surgically confirmed perforations.
Computerized tomography (CT)
Endoscopy
Diagnostic thoracentesis
Treatment
The goal of treatment is to:
Prevent further contamination
Eliminate infection produced by contamination
Restore the integrity and continuity of the GIT
Restore and maintain adequate nutrition
There are two major types of treatment
Surgical
Nonsurgical
Surgical treatment
Primary closure
Reinforced closure
Resection
Drainage alone
T-tube drainage
Exclusion and diversion
Intraluminal stents
Primary repair of Esophagus
The principles of surgical treatment are :
Debridement of all infected and necrotic tissue
Secure closure of the perforation
Correction or elimination of distal obstruction
Drainage of contaminated and infected areas
An enteral nutrition route, such as a jejunostomy, should be
added for nutritional support to any surgical method
Choice of Treatment
Surgical
Non Surgical
Patient selection according to strict criteria is necessary to
make such comparisons
Indications for nonsurgical treatment are limited.
Survival depends on rapid diagnosis and surgery
Within 24 hours of rupture: 70-75% survival
Within 25-48 hours: 35-50% survival
Beyond 48 hours: 10% survival
Conclusion
Diagnosis & treatment of esophageal perforation remains a
challenge to surgeons
Early diagnosis and treatment are important to prevent
morbidity and mortality
Optimal treatment consists of complete repair with tissue
reinforcement and elimination of distal obstruction
Esophagectomy should be performed in patients with cancer
or extensive necrosis of the esophagus
Nonsurgical treatment may be used in carefully selected
patients
Thank you
This post was last modified on 08 April 2022