CORROSIVE LESSION OF

ESOPHAGUS

WAYAN SUCIPTA
 INTRODUCTION
CORROSIVE INGESTION

Clinical manifestations :

very mild fatal outcome

esophageal stricture

Optimal treatment :
• remains controversial
• differ ~ patient’s condition
~ policy of the center
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 MODE OF INJURY
• Children :
▪ accidental

• Adult :
▪ accidental
▪ suicide
 worse prognosis :
* quantity >
* longer interval before receive medical attention

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 CORROSIVE AGENTS

 COMMONLY AVAILABLE :
home, laboratory, office

 AVAILABLE IN PUBLIC :
sold at supermarket / grocery store

 UNSAFELY PACKAGE :
no label ~ its potential danger

 Form : granular, paste or liquid

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 Corrosive agents ...

 drain / oven cleaner

(sodium/potassium hydroxide)
 ALKALI : pH >  dishwashing / clothing detergent
7 (silicate/sodium carbonate)
 denture cleaner
(sodium/potassium hydroxide)
 disc battery
(sodium/potassium hydroxide, mercury oxide)

 toilet bowl or drain cleaner

(sulfuric, hydrochloric)
 ACID : pH < 7  rust remover
(hydrofluoric, sulfuric or phosphoric)
 battery fluid
(sulfuric)

 NEUTRAL : pH ± 7  bleach
(sodium and calcium hypochlorite)

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 PATHOPHYSIOLOGY
Agent ingested :
o alkali or acid
o solid or liquid
o concentration

Quantity ingested
SEVERITY OF INJURY
Residual food in the stomach

Duration of tissue contact

Reflux

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 Pathophysiology..

ALKALI ACID
liquefaction necrosis coagulation necrosis
denaturation of protein
saponification of fat denaturation of protein
disintegration of the tissue form coagulum
deep penetration protect some of the underlying tissue
damage of the muscle layers

more severely injures the stomach

more severely injures the esophagus

Strong solutions of either alkali or acids

 will injure the esophagus, stomach, small intestine

Bleaching agent :
mucosal irritant  close observation  acute laryngeal edema 13
 SITE OF INJURY
 Area of alimentary stagnation :
o glossoepiglottic vallecula
o vestibule of the larynx
o arytenoid cartilage
o pyriform sinus
o retrocricoid region

 Esophagus  at anatomically narrowing areas :

o cricopharyngeus
o crossing of the aorta & left main bronchus
o cardia

(Zwischenberger, 2001; Chung, 2002; Saeti,2003) 14

 PHASES OF CORROSIVE INJURY
1st – 3rd day
ACUTE o intense inflammatory reaction
o coagulation of cellular protein
o destruction of cells with necrosis

2-6 weeks
LATENT = SUBACUTE o necrotic tissue sloughs away
leaving a denuded ulcerated surface
o granulation appear
as fibroblasts & new vessels develop
o esophagus is weakest
o edema subsides
CHRONIC o swallowing begins to return to normal

1-3 years
o inflammatory reaction <<
o connective tissue contractures begin
o submucosa and muscularis are replaced by dense fibrous tissue
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 SYMPTOMS AND SIGNS
o coughing, crying and vomiting
ACUTE o refusal to drink, drooling and mark of salivation
o dysphagia / odinophagia 20-40%

Burns on the lips, chin, hands, chest  manipulation of the agent / regurgitation

Edema & erythema of lips, tongue & palate

The presence or absence of oral injuries cannot accurately predict

the presence or absence of more distal involvement

Pain : retrosternal, in the back & abdominal mediastinal or peritoneal extension

 laryngeal edema
Hoarseness, stridor and dyspnea
 epiglottic and laryngeal destruction

CHRONIC gradual swallowing difficulty

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 MANAGEMENT
Acute phases
Stabilizing the airway
Maintaining the circulatory system
Complete head and neck examination
Corrosive agent : alkali / acid ?
Patient should be maintained NPO until :
 can swallow their own secretion
 after esophagoscopy, barium swallow
 adequate esophageal mucosal
Resting the esophagus  NGT
Or resting the whole of the GIT
 total parenteral nutrition
Emetic and gastric lavage are not indicated
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 Neutralization

o Must be done within the 1st hour

o Alkali with : dilute vinegar, lemon / orange juice
o Acid with : egg, antacid
o Use diluting agents : water, milk
 to remove the agent from the esophagus

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 Radiologic studies
o Chest and Abdominal X-ray
▪ view the mediastinum and subdiaphragmatic region
 free air : perforation
▪ aspiration pneumonia

o Barium study
▪ most useful : to verify perforation
: to detect esophageal stricture
(± 3 weeks after injury)
▪ acute phase : not adequate
: interfere endoscopy
o CT Scan
▪ visualizing paraesophageal abscess
▪ evaluating perforation 19
 Esophagoscopy
o Under general anesthesia
o Rigid or flexible esophagoscope
o Should be performed between 24-48 hours after ingestion
 injury grading
 insert NGT (?)
o > 48 hours after ingestion
 barium swallow
o Repeated esophagogram
 3 , 6 weeks; 3, 6 months and 1 year
 especially grade II and III
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 Endoscopic appearance
of esophageal burns
GRADE I Superficial mucosal injury

 mild mucosal erythema & edema

GRADE II Ulceration / transmucosal

 whitish exudate
 erythema
 ulceration may extend  muscularis
GRADE III Massive edema / transmural

 with or without full thickness necrosis

 mucosa appears very dusky / black
 involve transmural tissue
 deep ulceration  periesophageal tissue 21
 lumen may be completely obliterated
Videopharyngolaryngoscopy with 70 telescope
shows grade 1 to 2 lesion

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Fibrin adhesion release of right pyriform sinus
with suction tube (grade 3 lesion)
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Tissue sloughing and white exudates
in the middle of the esophagus
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 Medication
o Antibiotic
 to overcome the infection
o Analgetic
 to overcome the pain
o Antacida & H2 receptor blocker
 to reduce stomach acidity

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 Steroid

o Still controversial
o To : reduce inflammation response
: decrease stricture formation
o Howell et al (2003)  361 px
- stricture rate : steroid + : 19%
steroid - : 41%
o Within the first 24 hours
o Most effective : transmucosal injury (grade 2)

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 BOUGINASE

• Latent or chronic phases

• Once a week, 2 weeks
• after 1 month every 3 month….
• 3x not improvement : end to end

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 COMPLICATION

 Airway obstruction
 Neurogenic shock
 Esophageal perforation
 Pneumonia
 Mediastinitis
 Pharyngeal stenosis
 Esophageal stricture
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