Corrosive esophagitisPresented by

Tapendra Koirala2nd Batch

Senior Clerkship

22nd April 2016

Introduction

•Antirust compounds•Battery fluid•Toilet bowl or swimming pool cleaners

•Drain cleaners•Disc batteries•Household cleaning products

Corrosive injuries Ingestion can be accidental or suicidal Most ingestion occurs in children and the remainder

in psychotic, suicidal, and alcoholic subjects Cause severe damage to the mouth, pharynx,

larynx, esophagus and stomach The type of agent, its concentration, volume

ingested and the duration of mucosal contact largely determine the extent of damage

Alkali vs Acid injuriesACID

• Acids are potent dessicants • Cause coagulative necrosis

with eschar formation• Eschar may limit penetration

to deeper layers of the oesophageal wall• Induce intense pylorospasm

with pooling in the antrum• More gastric damage than

alkalis

AKALI

• Alkalis cause liquefaction necrosis, saponification of fats, dehydration and thrombosis of blood vessels• No eschar formation, hence

deeper injuries• Usually leads to fibrous scarring

• More esophageal damage than stomach and duodenum• Do not induce pylorospasm

Pathology Phases of tissue injury in corrosive ingestion

Phase 1: Acute necrosis— 1-4 days Phase 2: Ulceration— granulation— 4-12 days Phase 3: Cicatrisation and scarring— 3 weeks-6 months

Degrees of burns 1st degree: [Mucosal] Mucosal hyperaemia and oedema 2nd degree: [Mucosal & Submucosal] Small bleeding,

exudates, ulcers, pseudomembrane 3rd degree: [Transmural] Mucosal slough, deep ulcers,

massive bleed, complete obstruction, charring, perforation

Clinical features

Symptoms and signs unreliable in predicting the severity of injury

Common presentation• Oropharyngeal, retrosternal or

epigastric pain• Dysphagia/odynophagia• Hypersalivation• Vomiting• Hematemesis Burns of the epiglottis &

larynxHoarseness, stridor, aphonia and respiratory difficulties

Perforation /with peritonitisPersistent, localized abdominal tenderness, rebound, and rigidity

General Management Asymptomatic pt. who gives a reliable history of a low

volume, accidental ingestion of low concentration; endoscopy may not be necessary Discharged and F/U in OPD

Cases of suspected significant ingestion generally be treated in a surgical or medical ICUs

NPO, Hemodynamic stability, PPIs, Adequate analgesia Assess signs of perforation, mediastinitis or peritonitis–

need Em. Surgery Assess need for ET intubation or tracheostomy

Management

General Management Use of emetics, neutralizing agents, or nasogastric

intubation to remove remaining corrosive material is contraindicated

In most patients, gastrointestinal endoscopy should be performed during the first 24 hours Contraindication: hemodynamic instability, evidence

of perforation, severe respiratory distress, or severe oropharyngeal or glottic edema and necrosis

In 1st degree burns: 48 hours observation; oral feeds are started once patient swallows saliva painlessly. Regular follow-up endoscopy at 1st, 2nd and 8th months. Stricture if formed can be identified by this time.

2nd and 3rd degree burns: They are treated with fluid therapy, antibiotics, nutrition, PPIs, aerosolised steroidsFiberoptic guided airway intubation if needed tracheostomy; Endoscopic oesophageal stenting, feeding jejunostomy, laparoscopy for evaluation

Management

Careful early gentle repeated endoscopy is mandatory

Regular oesophageal dilatation is done for stricture Stricture is dilated endoscopically using guidewire Dilators are solid type with gradual increase in diameters Often radiologic C-ARM guidance is needed to pass the

guide wire into the stomach Dilatation should be done up to minimum 16 mm

diameter. Earlier, blind dilatation using oesophageal bougies of increased diameters was the practice, which is followed even now in many

places, but chances of perforation is more.

Pneumatic or balloon dilatation, Gum elastic dilators, mercury weighted dilators, Eder-Puestow dilators, Savary-Gilliard dilators,

balloon dilators are other dilators used

Other than emergency surgery for bleeding or perforation, elective oesophageal resection

should be deferred for at least three months until the fibrotic phase is established

Oesophageal resection in corrosive strictures is technically difficult and may be hazardous

Oesophageal bypass is better and easier, and following later by regular endoscopic surveillance for malignant transformation (5%)

Colon is used as replacing conduit as stomach itself may be diseased in corrosive pathology

In multiple strictures oesophageal resection and colonic transposition may be advocated if risk of malignancy is considered

Where is the controversy? Use of broad spectrum antibiotics and

steroids [Benefits not supported by evidence]

Regarding risk of developing carcinoma in the damaged oesophagus and stomach and how this might influence management

Summary Severity and extent of damage depend upon:

Corrosive properties; amount, concentration, and physical form of the agent; and the duration of contact with the mucosa

Absence of oropharyngeal burns does not preclude the presence of esophageal or gastric injury

Use of emetics, neutralizing agents, or nasogastric intubation to remove remaining corrosive material is contraindicated

In most patients, gastrointestinal endoscopy should be performed during the first 24 hours

Contraindication: hemodynamic instability, evidence of perforation, severe respiratory distress, or severe oropharyngeal or glottic edema and necrosis

Patients with moderate to severe injury require management in an intensive care unit to monitor for potential life-threatening complications

Clinical signs of perforation, mediastinitis or peritonitis are indications for emergency surgery

Thank You