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Epidemiology
Incidence: 5000-15000 / Yr in US Etiology:
Infant and toddler: Accidental Adolescent and Adult: Suicide attempts
Ronald Amedee,2009
Alkali ingestion
Liquefaction necrosis early disintegration of the mucosa deep penetration into tissues Direct contact with cell membranes leads to their disruption secondary to saponification and proteinate formation as the alkali reacts with membrane components More oral and upper esophageal involvement
Acid ingestion
Coagulation necrosis
Causes a coagulum to form on the mucosa Eschar formation Limiting deeper absorption
Acid Ingestion
Esophageal damage is less
Protection by the slightly alkaline pH of the esophagus Resistance of squamous epithelium to acids
Bleaches
Neutral pH Esophageal irritants No significant morbidity & mortality
Disk Batteries
Leakage of contents: NaOH, KOH, Hg
Mucosal damage: 1hr Erosion: 2-4 hrs Perforation: 8-12 hrs
Direct caustic injury Absorption of toxic substances Pressure necrosis Electrical discharge
Severity of injury
Amount and type of agent ingested Presence of other food in the stomach GI transit time Presence of gastroesophageal reflux
Acute Injury
Immediate changes to mucosa which progress during the next 3 days
Latent periode
Stricture formation may occur The process may proceed as rapidly as 1 month or during a period of years
Stricture Formation
Mild Nonulcerative Esophagitis Mild Ulcerative Esophagitis Moderate to Severe Ulcerative Esophagitis Severe Ulcerative, Uncomplicated esophagitis Severe Ulcerative Esophagitis with Complications
Laryngeal injury
Hoarseness, stridor, dyspnea
Severe injury
Odynophagia, drooling, refusal of food
Perforation
Chest pain, abdominal pain, rigidity
Diagnosis
History PE Examination of lips, chin, hands, chest, clothing Examination at the oropharyng Examination at the Larynx/Hypopharynx Laryngeal mirror Flexible nasopharyngoscope Obtain Container
Ancillary Procedure
Chest & Neck Radiography Foreign body ingestion (disc battery) Esophagoscopy at 24-48 hours post-ingestion < 24 hours underestimation of injury > 48-72 hours with risk of iatrogenic Ba swallow Not for acute management 30-90% false (-) rates for moderate esophageal involvement Verify perforation Evaluate progressive dysphagia due to stricture formation
Remember
Oral injuries (lip or buccal burns) cannot predict the presence or absence of more distal involvement 20% without oral burns have esophageal burns 70% with oral burns dont have esophageal burns
Management 1
Diluting agents such as water or milk to remove the agent from the esophagus Fluid intake should be no more than 15 mL/kg of weight No Gastric lavage No induced vomiting with emetics (ipecac)
Management 2
Steroid administration in the transmucosal (grade 2) injuries Prednison 1 to 2 mg/kg/day (max 60 mg) This dosage is continued for a 21-day period on a tapered regimen Steroids are contraindicated in grade 3 injuries Protection from gastric acid
Sucralfate Antacids, H2 Blocker, PPI
Management 3
Antibiotics
Do not prevent from stricture formation Signs or symptoms of a secondary infection
Lathyrogenic agents
Aminopropionitrile, Acetylcysteine, and Penicillamine Reduce collagen cross-bonding
Management 4
Esophageal dilatation for stricture formation Prograde Retrograde Balloon catheters
Complications
Stricture formation Esophageal perforation Tracheoesophageal fistula Gastric perforation Mediastinitis Peritonitis Pneumonia Sepsis, Hiatal hernia Reflux esophagitis Esophageal Ca