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DISORDER OF ESOPHAGUS GASTROESOPHGEAL REFLUX (GER) CORROSIVE STRICTURE
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Learning Objectives Definition. Incidence. Pathogenesis. Clinical Presentation. Diagnosis. Treatment. Corrosive Stricture.
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Definition It is a digestive disorder that affect lower esophagus sphincter (LES). The ring of muscle between esophagus and stomach. So, Return of the stomach contents back up into esophagus and irritate the esophageal mucosa esophagitis.
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Incidence 85 % of affected infants (1 st week of life). An additional 10 % have symptoms by 6 weeks. Symptoms abate without treat in 60 % by age of 2 years. The remainder continue to have symptoms until 4 years of age. The incidence increases in Down Syndrome and C.P, Preterm, Obesity, H.H, Repaired Cong. Diaphragmatic Hernia and Repaired Cong. Esophageal Atresia.
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Pathogenesis
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Different Between GER & GERD The difference between GER and GERD is matter of severity and associated consequences to the patient. So, 2-8% of children 3-12 years have GERD which is more serious.
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Clinical Presentation Recurrent Vomiting. Persistent Cough or wheezing. Refusal to eat or difficult feeding or chocking. Abd. pain. Or frequent crying associating with feeding (Dysphagia). Poor growth 60% of Pt. Recurrent Pneumonia 30% of Pt.
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Continue Esophagitis. Hematemesis. 5% of untreated develop stricture. Sandifer Syndrome: opisthontons, abnormal head position. Laryngospasm, Apnea, Brady cardia.
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Diagnosis CBC Hb. S. Iron level. Stool Occult blood. PH Probe to confirm.
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Continue Ba meal to detect any abnormality or erosion of esophagus. Endoscopy.
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Treatment Feeding changes. Thickening milk by rice cereal or AR milk. Semi setting position. Brup after feeding. Avoid overfeeding. Trial of Hydrolyzed milk for 4 weeks if suspect sensitivity to milk protein. Drugs to reduce stomach acidity. Histamine – 2 blockers. PPI. Surgery if not responding to medication (Nissan Fundoplication).
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CORRESIVE STRICTURE 1. Alkalis: ◦ Most cases of caustic injury in western countries ◦ Cleaning agents (NaOH), drain openers, bleaches, toilet bowel cleaners, and detergents… 2. Acids ◦ Less frequently in western countries; more common in countries like India (glacial acetic acid) ◦ Toilet bowel cleaners ( sulfuric, hydrochloric ), anti rust compounds ( hydrochloric, oxalic, hydrofluoric ), swimming pool cleaners ( hydrofluoric )
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Alkalis V.S Acid Alkalis PH > 7 Tasteless, odorless → larger amounts liquefaction necrosis => direct extension, deeper injuries Solid form : limited quantities, oropharyngal and supraglottic injuries Liquid form: significant quantities, esophageal injury, extensive, circumferential burns Acid PH < 7 Pungent odor and noxious taste coagulation necrosis => formation of a coagulum layer : limit the depth of injury Less esophageal injury More gastric injury
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Pathologic severity of injury
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Clinical presentation 1. Vary widely ◦ Hoarseness, stridor, dyspnea => Airway evaluation ◦ Perforation: (During first 2 weeks) Retro-sternal or back pain Localized abdominal tenderness, rebound, rigidity. Massive hematemesis ◦ Dysphagia, odynophagia, drooling, nausea, vomiting 2. Early signs and symptoms may not correlate with the severity and extent of tissue injury 3. Oropharyngeal burns (-):10-30% esophageal burns(+) Oropharyngeal burns (+): 70% esophageal burns(-)
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Diagnosis and staging 1. Upper gastrointestinal endoscopy 2. Endoscopic grading system ◦ Grade 0: Normal ◦ Grade 1: Mucosal edema and hyperemia ◦ Grade 2A: Superficial ulcers, bleeding, exudates => Excellent prognosis ◦ Grade 2B: Deep focal or circumferential ulcers ◦ Grade 3A: Focal necrosis => Develop strictures: 70-100% ◦ Grade 3B: Extensive necrosis => Early mortality rate: 65%
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Late sequelae 1. Stricture formation ◦ Primarily in those with grade 2B or 3 injury ◦ Peak incidence: two months ◦ Occur as early as two weeks or as late as years after ingestion ◦ 2. Gastric outlet obstruction ◦ Early satiety, weight loss ◦ Less frequently ◦ 5-6 weeks ~ several years ◦ Usually acid ingestion
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Management Identify the swallowed toxic agents. Avoid: emetics and gastric lavage. NPO. CXR and abd. XR to R/O perforation. Endoscopy up to 48 hr. Grade 1: Liquid diet. Grade 2: NG feeding. TPN may be used in some patient. Dilatation may be needed later.
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