Download MBBS Surgery Presentations 16 Corrosive Strictures Lecture Notes

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