Corrosive injury

報告人 : R3 張淳翔

Introduction

1. 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…

2. Outcome: Caustic properties Amount, concentration, and physical form Duration of contact Treatment modalities

Substances

1. Alkalis: Most cases of caustic injury in western countries Cleaning agents (NaOH), drain openers, bleaches, toilet bowel cleaner

s, and detergents…

2. Acids Less frequently in western countries; more common in countries like In

dia (glacial acetic acid) Toilet bowel cleaners ( sulfuric, hydrochloric ), anti rust compounds ( hy

drochloric, oxalic, hydrofluoric ), swimming pool cleaners ( hydrofluoric )

Alkalis V.S Acid

Alkalis PH > 7 Tasteless, odorless →larger a

mounts 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

Pathophysiology1. Alkali-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 respons

e, and development of granulation tissue > 2 weeks: Collagen deposition > 3 weeks: Scar retraction => may continue for several months

2. Acid-induced injury: Superficial coagulation necrosis Thromboses the underlying mucosal blood vessels and consolidates th

e connective tissue => Protective eschar

Pathologic severity of injury

1. First-degree: Superficial mucosal damage Focal or diffuse erythema, edema, hemorrhage Without scar formation

2. Second-degree Mucosal and sub-mucosal damage Ulcerations, exudates, vesicle formation, granulation, fibroblastic rea

ction Scar formation

3. Third-degree Trans-mural Deep ulcers and black discoloration and perforation of the wall

Pathologic severity of injury

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,

Psoas sign, obturator sign 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(-)

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%

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

Late sequelae

3. Esophageal carcinoma 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 15-20 years after ingestion The time interval : No more than every 1-3 years

4. Gastric carcinoma rare occurrence

Management – General management

1. First aid Identify the swallowed toxic agents Avoid:

The use of emetics: re-exposes Neutralizing agents: thermal injury Gastric lavage: lead to perforation

2. 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

Management - Endoscopy

1. Timing: No later than 48 hours Usually avoided from 5-15 days

2. Purpose: Grading, manage appropriately

3. Risk of perforation: Low, under adequate sedation

4. Extent: Advance until a circumferential second-degree or third degree burn is

seen To first part of duodenum

Management - Oral intake

1. NPO before PES

2. Grade 1 or 2A injury: A liquid diet may be initiated Advance to a regular diet in 24 - 48 hours

3. 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

Management - Prevention of strictures

1. 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: 1991-2004 in the English, German, French, Spanish No benefit

Management - Prevention of strictures

2. 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 advoc

ated

3. Nasogastric tube Feeding and stenting Contribute to the development of long strictures Routine use is not warranted

Management - Prevention of strictures

4. Total parental nutrition: No human randomized study NPO allowing the re-epithelialization

5. Intraluminal stent: Controversial Prevents opposite raw surfaces contact and decreases stricture formation (Gastrointest Endosc. 2004)

Management - Prevention of strictures

6. Early dilataion: Less than one week Controversial, most study: not recommended Start during the 1st week => The stricture can resolve more easily (Pe

diatr Surg Int. 2005 )

7. Anti-reflux treatment and Sucralfate: Empirically use ; PPI, H2 blockers Prevention of injured esophageal mucosa from gastric acid reflux

Management – Treatment of strictures

1. 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

2. Intraluminal stent Temporary placement of a self-expanding plastic stent Successful in case reports

3. Surgery 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

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Thanks for your attention