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