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Junior Surgery Lecture
CAUSTIC INGESTIONS

Ronald W. Deskin, M.D., FAAP

 

See SLIDES 47-50, and 58 (PediOto.pps)

I. Incidence in past ten years --

  1. Why?
    -Public awareness
    -Legislative action to lower concentrations of corrosives in household products
    -Improved medical/surgical management
  2. Still important to make early diagnosis and proper management.

II. Histopathology

A. Acids - coagulation necrosis forms barrier to penetration.

B. Alkali - liquefaction necrosis causes disintegration of mucosa and early penetration of muscular layer.  Lip, pharynx, esophageal burns frequent.

C. Bleaches - mild esophageal irritants and cause mild esophagitis and no actual tissue necrosis.  Long-term following not necessary.

D. Three stages evolve --

1) Acute phase - time of ingestion to 4-5 days
- Vascular thrombosis and inflammation
- bacterial invasion and intramural abscess.

2) Latent phase - day 5-15
- actual cell death, necrotic tissue
- sloughs, ulcerated base of granulation,
- new blood vessel formation and fibro-blast production
- esophageal wall fragile now

3) Chronic phase - connective tissue forms in ulcerations
- fibrous tissue replaces damaged tissue
- stricture formation occurs and causes slow
partial or complete obstruction

III. Complications

IV. Clinical presentation

  1. History Vital
  2. Symptoms/signs may be unreliable Dysphagia, drooling, N&V, abdominal pain Presence/Absence of above not good Predictor of damage.
    8-20% with no lip or oral burns have esophageal damage CBC, ESR, temperature not reliable
  3. More reliable signs/symptoms are retrosternal pain, progressive respiratory distress, symptoms of vascular collapse.

V. Acute Management

  1. Airway management, volume replacement
  2. Chemical epiglottitis with hoarseness and stridor require artificial airway.
  3. Type and cross if severe tissue damage
  4. NO EMETICS -- avoid vomiting
  5. Neutralizing agents (baking soda for acids and vinegar for alkali) cause exothermic reaction and more damage. Water O.K. initially.

  6. NG tube? --
    Safer to use I.V. fluid and even gastrostomy feedings

  7. Early Esophagoscopy
    -Determine extent of damage
    -Allow patients with no damage to forego unnecessary testing
    -Must be done in first forty-eight hours before period of weakest wall
    -Pass scope only to first level of burn
  8. Burn description

    1) Depth
        - Superficial
        - Transmucosal
        - Transmural

2) Area
    - Localized
    - Linear
    - Circumferential

    I.  Steroid use -- ?

Antifibroblastic effect
    -Delayed epithelization
    -Must be used in first twenty-four hours to have these effects

Superficial - risk of stricture and perforation low Steroids not necessary

Transmucosal - steroids seem to decrease stricture formation

< age 2 -- 20 mg. Solu-Medrol every 8 hours
> age 2 -- 40 mg. Solu-Medrol every 8 hours
Change to P.O. when able and treat three weeks.
(2mg per kg per day)

Transmural - involves all three layers of esophagus and high risk for perforation and steroids may prolong weakness of wall and mask complications

J. Antibiotics -- ?
    May help if used at first sign of infection

VI. Early and late management

A. Barium swallow one month post ingestion.

Earlier esophagogram helpful in patient who presents day two or more and esophagoscopy is dangerous

B. Stricture formation

-Dysphagia, malnutrition, anemia and chronic debilitation.
-Dilatation main treatment - if not able to maintain lumen Colon interposition may be necessary.

VII. Summary --  Incidence has decreased but significant morbidity and mortality mandates familiarity of the physician with newest concepts or acute management.

Last Updated: 11/19/98, 12:30
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