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Esophagus: Anatomy Physiology Corrosive stricture and Perforation of Esophagus PowerPoint Presentation

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Description : Check out this medical presentation on Esophageal Cancer, which is titled "Esophagus: Anatomy, Physiology, Corrosive stricture & Perforation of Esophagus", to know about esophagus, a muscular tube connecting the throat (pharynx) with the stomach, and Anatomy, Physiology, Corrosive stricture & Perforation of Esophagus.

Tags : Esophageal Cancer, Esophagus, Anatomy, Physiology, Corrosive stricture, Perforation of Esophagus

Published on : May 13, 2021 | Views : 3040 | Downloads : 8

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Slide 1-

Esophagus: Anatomy, Physiology, Corrosive stricture & Perforation of Esophagus Dr Amit Gupta Associate Professor Dept. of Surgery
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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. Anatomy
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Seventh to eighth week: Esophageal lumen is almost filled with cells from the proliferated esophageal epithelium. During the 4th month, the muscularis mucosa appears
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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).
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Classical anatomy divides the esophagus into three parts: Cervical Thoracic Abdominal
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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)
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Arterial Supply
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Venous Supply
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Innervation
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Lymphatic drainage
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It lacks a serosal coating The four layers are: mucosa Submucosa muscularis tunica adventitia Histology
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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 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 20-30
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Acid – Generally less severe injury – Coagulative necrosis – Coagulum lessen tissue penetration Type of caustic related to injury Alkaline Liquefactive necrosis Sodium hydroxide Very hazardous 30% causes full thickness necrosis
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The severity of esophageal and gastric damage resulting from a caustic ingestion depends on Corrosive properties Concentration of the agent Quantity swallowed
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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 3‐5 mins ‐> gastric atonia ‐> opening of pylorus Pathogenesis
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Goal of emergency management Limit and treat the immediately life-threatening consequences Control subsequent stricture formation
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Endoscopic findings Zargar et al GIE 1991; Orringer 1993
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Resuscitation Upper airway – Assessment of severity of damage – Secure the airway Fiberoptic intubation Tracheostomy Early management
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Contraindication Emetics OG or NG Neutralization Alkali ---try Milk Acid---- do not try anything
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Surgery is warranted if evidence of Perforation of the esophagus or stomach Mediastinitis Peritonitis exists
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Treatment Corticosteroids to modify the inflammatory response to the burn injury Antibiotics to control secondary bacterial infection Esophagoscopy within 12-24 hrs
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Bougienage Esophageal stents Colon interposition Forearm tube Free jejunal flap
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Perforation of Esophagus
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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 Introduction
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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
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Iatrogenic Instrumentation (MC cause) most common site of perforation during endoscopy is at the cricopharyngeus Surgical injury Etiology
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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 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
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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%).
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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
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Pathophysiology Air, Saliva, and Gastric contents released mediastinitis pneumomediastinum empyema can progress to sepsis, shock, resp failure
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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 Diagnosis
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Esophagography The detection rate is 60% for cervical perforation and 90% for surgically confirmed perforations. Computerized tomography (CT) Endoscopy Diagnostic thoracentesis
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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 Treatment
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There are two major types of treatment Surgical Nonsurgical
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Primary closure Reinforced closure Resection Drainage alone T-tube drainage Exclusion and diversion Intraluminal stents Surgical treatment
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Primary repair of Esophagus
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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 The principles of surgical treatment are :
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Choice of Treatment Surgical Non Surgical Patient selection according to strict criteria is necessary to 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 Within 25-48 hours: 35-50% survival Beyond 48 hours: 10% survival
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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 Conclusion
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Thank you