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Download MBBS Surgery Presentations 16 Corrosive Strictures Lecture Notes

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This post was last modified on 08 April 2022

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&

Perforation of Esophagus

Anatomy

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The primitive foregut forms during the fourth week of

gestation by a longitudinal folding and incorporation of the

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dorsal part of the yolk sac into the embryo.

34th day: The distal esophagus elongates first, followed by

the proximal.

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6th week: Mesenchymal circular muscle coat develops

Three to nine weeks later, longitudinal musculature

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appears.


Seventh to eighth week: Esophageal lumen is almost
filled with cells from the proliferated esophageal epithelium.

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During the 4th month, the muscularis mucosa appears


narrowest tube of the gastrointestinal tract

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Midline structure anterior to the spine and posterior

to the trachea

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Length: ranges from 21 cm-34 cm (27 cm average).

Classical anatomy divides the esophagus into three

parts:

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Cervical
Thoracic
Abdominal

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Function divides the esophagus according to its differing

forms of motility into the following three zones :

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Upper esophageal sphincter (UES)

Esophageal body

Lower esophageal sphincter (LES)

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Arterial Supply


Venous Supply

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Innervation


Lymphatic drainage

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Histology

It lacks a serosal coating

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The four layers are:

mucosa
Submucosa
muscularis

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tunica adventitia


Corrosive stricture

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Stricture formation, which usually develops between 3

and 8 weeks after the initial injury but sometimes

requires a much longer period for evolution

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Etiology

Alkaline caustics, acid or acidlike corrosives, and

household bleaches. Hydrochloric, sulfuric, nitric, and

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phosphoric acids are contained in automobile battery

acids.

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Age

75% of injuries involving children younger than 5

years and a much lower, secondary peak occurring in

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20-30
Type of caustic related to injury

Acid

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Alkaline

? Generally less severe

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? Liquefactive necrosis

injury

? Sodium hydroxide

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? Coagulative necrosis

? Very hazardous

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? Coagulum lessen tissue

? 30% causes full

penetration

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thickness necrosis

The severity of esophageal and gastric damage resulting
from a caustic ingestion depends on

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Corrosive properties

Concentration of the agent

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Quantity swallowed
Pathogenesis

Corrosive enter to stomach > reflex pyloric spasm

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Limit passage of corrosive to duodenum

Regurgitation of corrosive against a closed cricopharyngeus
> damage to esophagus and Stomach

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35 mins > gastric atonia > opening of pylorus

Goal of emergency management

Limit and treat the immediately life-threatening

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consequences

Control subsequent stricture formation
Endoscopic findings

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Zargar et al GIE 1991; Orringer 1993


Early management

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Resuscitation

Upper airway

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? Assessment of severity of damage
? Secure the airway

Fiberoptic intubation

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Tracheostomy

Contraindication

Emetics

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OG or NG

Neutralization

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Alkali ---try Milk
Acid---- do not try anything


Surgery is warranted if evidence of

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Perforation of the esophagus or stomach

Mediastinitis

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Peritonitis exists

Treatment

Corticosteroids to modify the inflammatory response

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to the burn injury


Antibiotics to control secondary bacterial infection

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Esophagoscopy within 12-24 hrs


Bougienage

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Esophageal stents

Colon interposition

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Forearm tube
Free jejunal flap


Perforation of Esophagus

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Introduction

Grand Admiral of Holland died of spontaneous

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rupture of the esophagus in 1724

J. R. Meyer of Berlin was the first to recognize this

disease prior to death

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Barrett made the first early diagnosis and performed

the first surgical repair in 1946
Anatomy

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Esophagus lacks serosa

More likely to rupture

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Site of rupture:

More commonly on left side
Due to instrumentation: distal esophagus
Spontaneous: posterolateral esophagus

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Tears are usually longitudinal

Etiology

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Iatrogenic

Instrumentation (MC cause)
most common site of perforation during endoscopy is at

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the cricopharyngeus

Surgical injury


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Boerhaave Syndrome (barogenic perforation,

postemetic perforation,spontaneous esophageal rupture)

Always occurs on the left side of the distal third of esophagus

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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

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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

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accident

The incidence of esophageal perforation by penetrating injuries

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is 11% to 17%


Perforation is more common in the cervical than thoracic

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esophagus

The overall mortality rate remains high (15% to 40%).


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Tumor

Foreign Body ( 7-14%)

Caustic Injury

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Drug Induced eg. tetracycline, KCL,quinidine, NSAID's

Infection

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Other Causes eg.Barrett ulcer and ulcerative esophagitis

with Zollinger-Ellison syndrome

Pathophysiology

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Air, Saliva, and Gastric contents released


mediastinitis

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pneumomediastinum

empyema

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can progress to sepsis, shock, resp failure
Diagnosis

Chest X ray

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Chest radiographs appear normal in the early phase


Emphysema becomes manifestated by 1 hour after the

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perforation

Pleural effusion is detected several hours after the

perforation

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Pneumomediastinum is present in 60% of cases.

Perforation of the mid-thoracic esophagus is associated with right-sided pleural

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effusion and perforation of the distal thoracic esophagus is associated with left-

sided pleural effusion


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Esophagography

The detection rate is 60% for cervical perforation and 90%

for surgically confirmed perforations.

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Computerized tomography (CT)

Endoscopy

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Diagnostic thoracentesis


Treatment

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The goal of treatment is to:

Prevent further contamination

Eliminate infection produced by contamination

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Restore the integrity and continuity of the GIT

Restore and maintain adequate nutrition

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There are two major types of treatment

Surgical

Nonsurgical

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Surgical treatment

Primary closure

Reinforced closure

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Resection

Drainage alone

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T-tube drainage

Exclusion and diversion

Intraluminal stents

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Primary repair of Esophagus


The principles of surgical treatment are :

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Debridement of all infected and necrotic tissue

Secure closure of the perforation

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Correction or elimination of distal obstruction

Drainage of contaminated and infected areas

An enteral nutrition route, such as a jejunostomy, should be

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added for nutritional support to any surgical method

Choice of Treatment

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Surgical

Non Surgical

Patient selection according to strict criteria is necessary to

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make such comparisons

Indications for nonsurgical treatment are limited.

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Survival depends on rapid diagnosis and surgery

Within 24 hours of rupture: 70-75% survival

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Within 25-48 hours: 35-50% survival

Beyond 48 hours: 10% survival

Conclusion

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Diagnosis & treatment of esophageal perforation remains a

challenge to surgeons

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Early diagnosis and treatment are important to prevent

morbidity and mortality

Optimal treatment consists of complete repair with tissue

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reinforcement and elimination of distal obstruction

Esophagectomy should be performed in patients with cancer

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or extensive necrosis of the esophagus

Nonsurgical treatment may be used in carefully selected

patients

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Thank you