Corrosive injury
報告人: R3 張淳翔
Introduction
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2.
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Two groups:
Pediatric:
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<5 y/o, accidental ingestion
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In Taiwan: alkaline oil
Adult:
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Suicidal attempts, intentional
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More serious corrosive properties
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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
Substances
1.
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2.
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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 )
Alkalis V.S Acid
Alkalis
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Acid
PH > 7
Tasteless, odorless →larger
amounts
liquefaction necrosis => direct
extension, deeper injuries
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Solid form : limited quantities,
oropharyngal and supraglottic
injuries
Liquid form: significant
quantities, esophageal injury,
extensive, circumferential
burns
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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
Pathophysiology
Alkali-induced injury:
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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:
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Superficial coagulation necrosis
Thromboses the underlying mucosal blood vessels and consolidates
the connective tissue => Protective eschar
Pathologic severity of injury
1.
First-degree:
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2.
Second-degree
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3.
Superficial mucosal damage
Focal or diffuse erythema, edema, hemorrhage
Without scar formation
Mucosal and sub-mucosal damage
Ulcerations, exudates, vesicle formation, granulation, fibroblastic
reaction
Scar formation
Third-degree
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Trans-mural
Deep ulcers and black discoloration and perforation of the wall
Pathologic severity of injury
Clinical presentation
Vary widely
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2.
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Hoarseness, stridor, dyspnea => Airway evaluation
Perforation: (During first 2 weeks)
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Retro-sternal or back pain
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Localized abdominal tenderness, rebound, rigidity,
Psoas sign, obturator sign
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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(-)
Diagnosis and staging
Upper gastrointestinal endoscopy
Endoscopic grading system
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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%
Late sequelae
Stricture formation
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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
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Gastric outlet obstruction
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Early satiety , weight loss
Less frequently
5-6 weeks ~ several years
Usually acid ingestion
Late sequelae
Esophageal carcinoma
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Incidence: 1000 to 3000-fold increase
3% have history of caustic ingestion
Mean latency: 41 years (13-71years)
Scar carcinoma:
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Less distensible => dysphagia presents earlier
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Lymphatic spread and direct extension
Surveillance
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Begin 15-20 years after ingestion
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The time interval : No more than every 1-3 years
Gastric carcinoma
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rare occurrence
Management – General management
First aid
1.
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Identify the swallowed toxic agents
Avoid:
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The use of emetics: re-exposes
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Neutralizing agents: thermal injury
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Gastric lavage: lead to perforation
Transfer to hospital immediately
2.
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Keep NPO
Insert NG tube ?
R/O perforation
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Plain films of chest and abdomen
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Esophagogram: Water-soluble agent
For ENT doctor
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Airway evaluation
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Oropharyngeal burns
Management - Endoscopy
Timing:
1.
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No later than 48 hours
Usually avoided from 5-15 days
Purpose:
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Grading, manage appropriately
Risk of perforation:
3.
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Low, under adequate sedation
Extent:
4.
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Advance until a circumferential second-degree or third degree burn is
seen
To first part of duodenum
Management - Oral intake
NPO before PES
Grade 1 or 2A injury:
1.
2.
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A liquid diet may be initiated
Advance to a regular diet in 24 - 48 hours
Grade 2B or 3 injury:
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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
Management - Prevention of strictures
Steroids
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In animal studies: incidence of stricture formation
In human studies: Inconclusive so far
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NEJM. 1990:
 Prospective study over an 18-year period
 No benefit
 Related only to the severity of the corrosive injury
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Toxicol Rev. 2005:
 1991-2004 in the English, German, French, Spanish
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No benefit
Management - Prevention of strictures
Antibiotics
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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
3.
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Feeding and stenting
Contribute to the development of long strictures
Routine use is not warranted
Management - Prevention of strictures
Total parental nutrition:
4.
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No human randomized study
NPO allowing the re-epithelialization
Intraluminal stent:
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Controversial
Prevents opposite raw surfaces contact and decreases stricture
formation (Gastrointest Endosc. 2004)
Management - Prevention of strictures
Early dilataion:
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Less than one week
Controversial, most study: not recommended
Start during the 1st week => The stricture can resolve more easily
(Pediatr Surg Int. 2005 )
Anti-reflux treatment and Sucralfate:
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Empirically use ; PPI, H2 blockers
Prevention of injured esophageal mucosa from gastric acid reflux
Management – Treatment of strictures
Endoscopic dilatation
1.
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The goal: dilate the esophageal lumen to 15 mm
Perforation rate: 0.5%
Special consideration:
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Long, eccentric strictures: risk of perforation increased
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Thick-walled strictures: recur rapidly
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Multiple sessions: elective esophageal resection
Intraluminal stent
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Temporary placement of a self-expanding plastic stent
Successful in case reports
Surgery
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Esophagectomy with colonic interposition
Gastric transposition: high leak rate
Perform 6 months later
Proposal for management
Conclusion
1.
Signs and symptoms alone are an unreliable
guide to injury
2.
Early endoscopy has a crucial role
3.
Grading, manage appropriately
Reference
1.
Ramasamy K, Gumaste VV. Corrosive ingestion in adults. J Clin Gastroenterol. 2003;37:119-24.
2.
Huang YC, Ni YH, Lai HS, Chang MH. Corrosive esophagitis in children.
Pediatr Surg Int. 2004;20:207-10.
3.
Pelclova D, Navratil T. Do corticosteroids prevent oesophageal stricture after corrosive ingestion? Toxicol Rev.
2005;24:125-9.
4.
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.
5.
Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the
esophagus. N Engl J Med. 1990;323:637-40.
6.
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.
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.
8.
Evrard S, Le Moine O, Lazaraki G, et al. Self-expanding plastic stents for benign esophageal lesions.
Gastrointest Endosc. 2004;60:894-900.
Thanks for your attention