Presentation is loading. Please wait.

Presentation is loading. Please wait.

Corrosive injury 報告人: R3 張淳翔.

Similar presentations

Presentation on theme: "Corrosive injury 報告人: R3 張淳翔."— Presentation transcript:

1 Corrosive injury 報告人: R3 張淳翔

2 Introduction Two groups: Pediatric: <5 y/o, accidental ingestion
In Taiwan: alkaline oil Adult: Suicidal attempts, intentional More serious corrosive properties In Taiwan: 無煙鹽酸及通樂(Alkalis)、魔術靈、漂白水… Outcome: Caustic properties Amount, concentration, and physical form Duration of contact Treatment modalities

3 Substances Alkalis: Most cases of caustic injury in western countries
Cleaning agents (NaOH), drain openers, bleaches, toilet bowel cleaners, and detergents… 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 )

4 Alkalis V.S Acid Alkalis Acid 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

5 Pathophysiology Alkali-induced injury: Acid-induced injury:
Liquefactive necrosis 1-2 days: Thrombosis of small vessels 2-4 days : Newly forming blood vessels , fibroblasts migration 4-7 days: Mucosal sloughing, bacterial invasion, inflammatory response, and development of granulation tissue > 2 weeks: Collagen deposition > 3 weeks: Scar retraction => may continue for several months Acid-induced injury: Superficial coagulation necrosis Thromboses the underlying mucosal blood vessels and consolidates the connective tissue => Protective eschar

6 Pathologic severity of injury
First-degree: Superficial mucosal damage Focal or diffuse erythema, edema, hemorrhage Without scar formation Second-degree Mucosal and sub-mucosal damage Ulcerations, exudates, vesicle formation, granulation, fibroblastic reaction Scar formation Third-degree Trans-mural Deep ulcers and black discoloration and perforation of the wall

7 Pathologic severity of injury

8 Clinical presentation
Vary widely Hoarseness, stridor, dyspnea => Airway evaluation Perforation: (During first 2 weeks) Retro-sternal or back pain Localized abdominal tenderness, rebound, rigidity, Psoas sign, obturator sign Massive hematemesis Dysphagia, odynophagia, drooling, nausea, vomiting Early signs and symptoms may not correlate with the severity and extent of tissue injury Oropharyngeal burns (-):10-30% esophageal burns(+)  Oropharyngeal burns (+): 70% esophageal burns(-)

9 Diagnosis and staging Upper gastrointestinal endoscopy
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: % Grade 3B: Extensive necrosis => Early mortality rate: 65%

10 Late sequelae Stricture formation Gastric outlet obstruction
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 Gastric outlet obstruction Early satiety , weight loss Less frequently 5-6 weeks ~ several years Usually acid ingestion

11 Late sequelae Esophageal carcinoma Gastric carcinoma rare occurrence
Incidence: 1000 to 3000-fold increase 3% have history of caustic ingestion Mean latency: 41 years (13-71years) Scar carcinoma: Less distensible => dysphagia presents earlier Lymphatic spread and direct extension Surveillance Begin years after ingestion The time interval : No more than every 1-3 years Gastric carcinoma rare occurrence

12 Management – General management
First aid Identify the swallowed toxic agents Avoid: The use of emetics: re-exposes Neutralizing agents: thermal injury Gastric lavage: lead to perforation Transfer to hospital immediately Keep NPO Insert NG tube ? R/O perforation Plain films of chest and abdomen Esophagogram: Water-soluble agent For ENT doctor Airway evaluation Oropharyngeal burns

13 Management - Endoscopy
Timing: No later than 48 hours Usually avoided from 5-15 days Purpose: Grading, manage appropriately Risk of perforation: Low, under adequate sedation Extent: Advance until a circumferential second-degree or third degree burn is seen To first part of duodenum

14 Management - Oral intake
NPO before PES Grade 1 or 2A injury: A liquid diet may be initiated Advance to a regular diet in hours Grade 2B or 3 injury: Controversial NG feeding, initiated after 24 hours => oral liquids are allowed after the first 48 hours if the patient is able to swallow saliva TPN use with delayed oral feeding (7 days) => Avoid food irritation

15 Management - Prevention of strictures
Steroids In animal studies: incidence of stricture formation In human studies: Inconclusive so far NEJM. 1990: Prospective study over an 18-year period No benefit Related only to the severity of the corrosive injury Toxicol Rev. 2005: in the English, German, French, Spanish

16 Management - Prevention of strictures
Antibiotics Decreased bacterial counts, reduction in inflammation Mask the sign of more severe infection A prophylactic antibiotic, in the absence of steroid therapy, is not advocated Nasogastric tube Feeding and stenting Contribute to the development of long strictures Routine use is not warranted

17 Management - Prevention of strictures
Total parental nutrition: No human randomized study NPO allowing the re-epithelialization Intraluminal stent: Controversial Prevents opposite raw surfaces contact and decreases stricture formation (Gastrointest Endosc. 2004)

18 Management - Prevention of strictures
Early dilataion: Less than one week Controversial, most study: not recommended Start during the 1st week => The stricture can resolve more easily (Pediatr Surg Int ) Anti-reflux treatment and Sucralfate: Empirically use ; PPI, H2 blockers Prevention of injured esophageal mucosa from gastric acid reflux

19 Management – Treatment of strictures
Endoscopic dilatation The goal: dilate the esophageal lumen to 15 mm Perforation rate: 0.5% Special consideration: Long, eccentric strictures: risk of perforation increased Thick-walled strictures: recur rapidly Multiple sessions: elective esophageal resection Intraluminal stent Temporary placement of a self-expanding plastic stent Successful in case reports Surgery Esophagectomy with colonic interposition Gastric transposition: high leak rate Perform 6 months later

20 Proposal for management

21 Conclusion Signs and symptoms alone are an unreliable guide to injury
Early endoscopy has a crucial role Grading, manage appropriately

22 Reference Ramasamy K, Gumaste VV. Corrosive ingestion in adults. J Clin Gastroenterol. 2003;37: Huang YC, Ni YH, Lai HS, Chang MH. Corrosive esophagitis in children. Pediatr Surg Int. 2004;20: Pelclova D, Navratil T. Do corticosteroids prevent oesophageal stricture after corrosive ingestion? Toxicol Rev. 2005;24:125-9. Baskin D, Urganci N, Abbasoglu L, et al. A standardised protocol for the acute management of corrosive ingestion in children. Pediatr Surg Int. 2004;20:824-8. Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med. 1990;323: Poley JW, Steyerberg EW, Kuipers EJ, et al. Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy. Gastrointest Endosc. 2004;60:372-7. Tiryaki T, Livanelioglu Z, Atayurt H. Early bougienage for relief of stricture formation following caustic esophageal burns. Pediatr Surg Int. 2005;21:78-80. Evrard S, Le Moine O, Lazaraki G, et al. Self-expanding plastic stents for benign esophageal lesions. Gastrointest Endosc. 2004;60:

23 Thanks for your attention

Download ppt "Corrosive injury 報告人: R3 張淳翔."

Similar presentations

Ads by Google