By: Dr. Mahwish Khan
 Corrosive Ingestion is a disease of industrial
age.
 A major health hazard in children.
 In rural areas, and in developing countries,
caustic soda is used in home industry for
soap making, fruit drying and container
cleaning on farms.
 Most Ingestions occur in children younger
than 3-years ---- entirely preventable.
 Boys are frequently involved.
 In children more than 5-years is suspect.
 Ingestion in adolescents (where girls
predominate) is usually intentional
 Mortality is rare, morbidity is devastating,
and can be associated with life long
consequences.
 20% ingestions of caustic substances result in
some degree of esophageal injury.
 Physical form of substance ingested and its
pH, play a substantial role in the site and type
of post ingestion esophageal injury.
 pH > 12 or < 1.5 being associated with
severe corrosive injuries.
 Crystalline drain cleaners e:g. sodium
hydroxide adhere to oropharynx or become
lodged in the upper esophagus, where injury
is more severe.
 With alkali ingestion
◦ Tissue penetration + liquefactive necrosis.
◦ Destruction of Epithelium and sub mucosa which may
extend to the muscle layer.
◦ Ischemia and thrombosis are dominant early processes.
◦ Friable eschar develops.
◦ Tissue destruction continues until alkali is neutralized.
 With Acid Ingestion
 Coagulation Necrosis of mucosa
 Hard eschar formation
 Limitation of acid penetration through
mucosa occurs.
 Cricopharyngeal area
 Mid esophagus, where it is crossed by aortic
arch and left bronchus.
 Above the GE Junction
 Immediate spasm and disorganized motility
occur
 Resulting in delayed emptying and even
gastic regurgitation.
 Hemorrhage, thrombosis and marked
inflammation with edema seen in first 24-
hours
 After 48-hours thrombosis of submucosal
vessels occurs, leading to local necrosis and
gangrene.
 Bacterial contamination leading to
development of small intramural abscesses
occur.
 After several days, necrotic tissue is
sloughed, edema decreases and
neovascularization begins.
 Scar formation begins in 3rd week.
 During 3rd to 6th week adhesions forms,
narrowing or obliterating the esophageal
lumen.
 In transmural injury, necrosis extends to
surrounding mediastinum, leading to
mediastinitis or tracheo-esophageal or even
aorta-esophageal fistulas.
 Mitomycin C has been reported to be efficient
at a dose of 1mg/ml, applied locally with a
soaked swab for 4-minutes immediately
after dilatation.
 Few symptoms and signs – One quarter
 Pain oropharyngeal burns
 Esophageal injuries unlikely if only the tongue
or soft palate involved.
 Acid Ingestion is associated with rapid transit
through the esophagus. Leading to
pylorospasm.
 Inflammatory edema of oropharynx.
 Agitation and tachycardia
 Drooling and inability to swallow indicate
severe posterior pharyngeal or upper
esophageal injury.
 Acute obstruction of upper airway resulting
from pharyngeal and laryngeal edema.
 Maintain Adequate Airway and oxygenation.
 CVS stability.
 Few patients require immediate intervention
for airway maintenance.
 History regarding noxious agent, its
composition and concentration and
circumstances of ingestion.
 Inducing vomiting
 Incurring ingestion of any liquid,
 Passing NG tube.
 All are contraindicated,
 Why?
 Fiberoptic endoscopy is both accurate and
safe, especially done within 24-48 Hrs, after
ingestion.
 TC labeled sucralfate radio-isotope scanning
of esophagus is a screening device
 Lack of sucralfate adherence indicating the
absence of significant injury.
 In the presence of pharyngeal burns with
stridor, early esophagoscopy is
contraindicated because of risk of
aggravating airway obstruction.
 IDL is useful to access upper airway.
 Fever systemic sepsis and upper abdominal
signs are indicative of perforation.
 Water soluble contrast esophagogram may be
useful to detect perforation.
 For patients with First degree burns (grade 1
injury) – No Specific treatment is necessary.
 Liquid Oral is started and extended to solids.
 If solids are tolerated, child can be discharged.
 Follow up at 2-3 weeks.
 Contrast Examination is done if symptoms of
Dysphagia are noted.
 Patient with moderate or severe injuries
require further treatment, aimed at
prevention of stricture formation, Up to 50%
developed strictures.
 Most patients with grade 2A Injuries recover
completely, close follow up, endoscopy and
dilatation are required.
 Grade 3B Injuries are rare in peads
 These require immediate and aggressive
surgery, if extensive necrosis and perforation
are present, especially if stomach is involved.
 In clinical trials using a variety of dosing
regimens, no statistical difference in
prevention of stricture formation was evident.
 Steroids are not useful for stricture formation
 More recently, the use of high-dose steroids
(dexamethasone1mg/kg/day) has been
advocated.
 For patients with severe injuries, NG tube may be
passed for early feeding purposes.
 Oral feeding commences as soon as patient can
swallow saliva.
 If dysphagia occurs, esophagogram can identify
extent of involvement.
 Use of anti-fungal agents, antacids and H2
blockers or proton pump inhibitors is
widespread, but no proved efficacy.
Stricture formation
If structure demonstrated on contrast radiography, done
10-14 days, after injury, a program of dilatation is
commensed.
Dilators used are
1. Mercury filled bougies.
2. Flexible graded bougie dilatation
3.guide wire directed metal olives
4. Various balloon dilators
Dilatation should be attempted with great care
Initial dilatation is done under G.A with flexible
guide wire introduced.
Dilatation should be done once a week.
Started with catheters that are one or two french
sizes smaller than estimated dm of stricture.
If dilatation fails and a dense stricture develops it requires
Rx
Localized strictures may be resected with end to end
anastomosis
Local injection of steroids(1% triamcenolone acetate) and
mitomycin into short strictures is also effective
Esophageal stenting by means of indwelling NG tube is
also advocated
Stents used are silicone and PTFE .
Should remain in place for 6 wks until healing
occurs.
Stents also used in management of esophageal
fistulas resulting from caustic injury or dilatation
therapy
 There is still a great need
◦ For adult education
◦ For legislation
◦ To ensure correct labeling and safe packaging and
to restrict the strength and availability of caustic
agents.

Caustic strictures of the esophagus

  • 1.
  • 2.
     Corrosive Ingestionis a disease of industrial age.  A major health hazard in children.  In rural areas, and in developing countries, caustic soda is used in home industry for soap making, fruit drying and container cleaning on farms.
  • 3.
     Most Ingestionsoccur in children younger than 3-years ---- entirely preventable.  Boys are frequently involved.  In children more than 5-years is suspect.  Ingestion in adolescents (where girls predominate) is usually intentional
  • 4.
     Mortality israre, morbidity is devastating, and can be associated with life long consequences.  20% ingestions of caustic substances result in some degree of esophageal injury.
  • 5.
     Physical formof substance ingested and its pH, play a substantial role in the site and type of post ingestion esophageal injury.  pH > 12 or < 1.5 being associated with severe corrosive injuries.
  • 7.
     Crystalline draincleaners e:g. sodium hydroxide adhere to oropharynx or become lodged in the upper esophagus, where injury is more severe.
  • 8.
     With alkaliingestion ◦ Tissue penetration + liquefactive necrosis. ◦ Destruction of Epithelium and sub mucosa which may extend to the muscle layer. ◦ Ischemia and thrombosis are dominant early processes. ◦ Friable eschar develops. ◦ Tissue destruction continues until alkali is neutralized.
  • 9.
     With AcidIngestion  Coagulation Necrosis of mucosa  Hard eschar formation  Limitation of acid penetration through mucosa occurs.
  • 10.
     Cricopharyngeal area Mid esophagus, where it is crossed by aortic arch and left bronchus.  Above the GE Junction
  • 11.
     Immediate spasmand disorganized motility occur  Resulting in delayed emptying and even gastic regurgitation.  Hemorrhage, thrombosis and marked inflammation with edema seen in first 24- hours
  • 12.
     After 48-hoursthrombosis of submucosal vessels occurs, leading to local necrosis and gangrene.  Bacterial contamination leading to development of small intramural abscesses occur.  After several days, necrotic tissue is sloughed, edema decreases and neovascularization begins.
  • 13.
     Scar formationbegins in 3rd week.  During 3rd to 6th week adhesions forms, narrowing or obliterating the esophageal lumen.  In transmural injury, necrosis extends to surrounding mediastinum, leading to mediastinitis or tracheo-esophageal or even aorta-esophageal fistulas.
  • 14.
     Mitomycin Chas been reported to be efficient at a dose of 1mg/ml, applied locally with a soaked swab for 4-minutes immediately after dilatation.
  • 15.
     Few symptomsand signs – One quarter  Pain oropharyngeal burns  Esophageal injuries unlikely if only the tongue or soft palate involved.  Acid Ingestion is associated with rapid transit through the esophagus. Leading to pylorospasm.
  • 16.
     Inflammatory edemaof oropharynx.  Agitation and tachycardia  Drooling and inability to swallow indicate severe posterior pharyngeal or upper esophageal injury.  Acute obstruction of upper airway resulting from pharyngeal and laryngeal edema.
  • 17.
     Maintain AdequateAirway and oxygenation.  CVS stability.  Few patients require immediate intervention for airway maintenance.  History regarding noxious agent, its composition and concentration and circumstances of ingestion.
  • 18.
     Inducing vomiting Incurring ingestion of any liquid,  Passing NG tube.  All are contraindicated,  Why?
  • 19.
     Fiberoptic endoscopyis both accurate and safe, especially done within 24-48 Hrs, after ingestion.  TC labeled sucralfate radio-isotope scanning of esophagus is a screening device  Lack of sucralfate adherence indicating the absence of significant injury.
  • 20.
     In thepresence of pharyngeal burns with stridor, early esophagoscopy is contraindicated because of risk of aggravating airway obstruction.  IDL is useful to access upper airway.  Fever systemic sepsis and upper abdominal signs are indicative of perforation.
  • 21.
     Water solublecontrast esophagogram may be useful to detect perforation.
  • 24.
     For patientswith First degree burns (grade 1 injury) – No Specific treatment is necessary.  Liquid Oral is started and extended to solids.  If solids are tolerated, child can be discharged.  Follow up at 2-3 weeks.  Contrast Examination is done if symptoms of Dysphagia are noted.
  • 25.
     Patient withmoderate or severe injuries require further treatment, aimed at prevention of stricture formation, Up to 50% developed strictures.  Most patients with grade 2A Injuries recover completely, close follow up, endoscopy and dilatation are required.
  • 26.
     Grade 3BInjuries are rare in peads  These require immediate and aggressive surgery, if extensive necrosis and perforation are present, especially if stomach is involved.
  • 27.
     In clinicaltrials using a variety of dosing regimens, no statistical difference in prevention of stricture formation was evident.  Steroids are not useful for stricture formation  More recently, the use of high-dose steroids (dexamethasone1mg/kg/day) has been advocated.
  • 28.
     For patientswith severe injuries, NG tube may be passed for early feeding purposes.  Oral feeding commences as soon as patient can swallow saliva.  If dysphagia occurs, esophagogram can identify extent of involvement.  Use of anti-fungal agents, antacids and H2 blockers or proton pump inhibitors is widespread, but no proved efficacy.
  • 29.
    Stricture formation If structuredemonstrated on contrast radiography, done 10-14 days, after injury, a program of dilatation is commensed. Dilators used are 1. Mercury filled bougies. 2. Flexible graded bougie dilatation 3.guide wire directed metal olives 4. Various balloon dilators Dilatation should be attempted with great care
  • 31.
    Initial dilatation isdone under G.A with flexible guide wire introduced. Dilatation should be done once a week. Started with catheters that are one or two french sizes smaller than estimated dm of stricture.
  • 32.
    If dilatation failsand a dense stricture develops it requires Rx Localized strictures may be resected with end to end anastomosis Local injection of steroids(1% triamcenolone acetate) and mitomycin into short strictures is also effective Esophageal stenting by means of indwelling NG tube is also advocated
  • 33.
    Stents used aresilicone and PTFE . Should remain in place for 6 wks until healing occurs. Stents also used in management of esophageal fistulas resulting from caustic injury or dilatation therapy
  • 34.
     There isstill a great need ◦ For adult education ◦ For legislation ◦ To ensure correct labeling and safe packaging and to restrict the strength and availability of caustic agents.