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Presented by
Tapendra Koirala
2nd Batch
Senior Clerkship
22nd April 2016
Introduction
• Antirust compounds
• Battery fluid
• Toilet bowl or
swimming pool
• Drain cleaners
• Disc batteries
• Household
cleaning products
Corrosive injuries
 Ingestion can be accidental or suicidal
 Most ingestion occurs in children and the remainder in
psychotic, suicidal, and alcoholic subjects
 Cause severe damage to the mouth, pharynx, larynx,
esophagus and stomach
 The type of agent, its concentration, volume ingested and
the duration of mucosal contact largely determine the
extent of damage
Alkali vs Acid injuries
ACID
• Acids are potent dessicants
• Cause coagulative necrosis with
eschar formation
• Eschar may limit penetration to
deeper layers of the oesophageal
wall
• Induce intense pylorospasm with
pooling in the antrum
• More gastric damage than alkalis
AKALI
• Alkalis cause liquefaction necrosis,
saponification of fats, dehydration
and thrombosis of blood vessels
• No eschar formation, hence
deeper injuries
• Usually leads to fibrous scarring
• More esophageal damage than
stomach and duodenum
• Do not induce pylorospasm
Pathology
 Phases of tissue injury in corrosive ingestion
 Phase 1: Acute necrosis— 1-4 days
 Phase 2: Ulceration— granulation— 4-12 days
 Phase 3: Cicatrisation and scarring— 3 weeks-6 months
 Degrees of burns
 1st degree: [Mucosal] Mucosal hyperaemia and oedema
 2nd degree: [Mucosal & Submucosal] Small bleeding, exudates,
ulcers, pseudomembrane
 3rd degree: [Transmural] Mucosal slough, deep ulcers, massive
bleed, complete obstruction, charring, perforation
Clinical features
 Symptoms and signs unreliable in predicting the severity
of injury
Common presentation
• Oropharyngeal, retrosternal or
epigastric pain
• Dysphagia/odynophagia
• Hypersalivation
• Vomiting
• Hematemesis
Burns of the epiglottis & larynx
Hoarseness, stridor, aphonia and
respiratory difficulties
Perforation /with
peritonitis
Persistent, localized
abdominal tenderness,
rebound, and rigidity
General Management
 Asymptomatic pt. who gives a reliable history of a low volume,
accidental ingestion of low concentration; endoscopy may not be
necessary Discharged and F/U in OPD
 Cases of suspected significant ingestion generally be treated in a
surgical or medical ICUs
 NPO, Hemodynamic stability, PPIs, Adequate analgesia
 Assess signs of perforation, mediastinitis or peritonitis– need Em.
Surgery
 Assess need for ET intubation or tracheostomy
Management
General Management
 Use of emetics, neutralizing agents, or nasogastric intubation to
remove remaining corrosive material is contraindicated
 In most patients, gastrointestinal endoscopy should be
performed during the first 24 hours
 Contraindication: hemodynamic instability, evidence of
perforation, severe respiratory distress, or severe
oropharyngeal or glottic edema and necrosis
 In 1st degree burns:
48 hours observation; oral feeds are started once patient swallows saliva
painlessly.
Regular follow-up endoscopy at 1st, 2nd and 8th months. Stricture if
formed can be identified by this time.
 2nd and 3rd degree burns:
They are treated with fluid therapy, antibiotics, nutrition, PPIs, aerosolised
steroids
Fiberoptic guided airway intubation if needed tracheostomy;
Endoscopic oesophageal stenting, feeding jejunostomy, laparoscopy for
evaluation
Management
 Careful early gentle repeated endoscopy is mandatory
 Regular oesophageal dilatation is done for stricture
 Stricture is dilated endoscopically using guidewire
 Dilators are solid type with gradual increase in diameters
 Often radiologic C-ARM guidance is needed to pass the guide
wire into the stomach
 Dilatation should be done up to minimum 16 mm diameter.
Earlier, blind dilatation using oesophageal bougies of increased diameters
was the practice, which is followed even now in many places, but chances
of perforation is more.
Pneumatic or balloon dilatation, Gum elastic dilators, mercury weighted
dilators, Eder-Puestow dilators, Savary-Gilliard dilators, balloon dilators are
other dilators used
Other than emergency surgery for bleeding or
perforation, elective oesophageal resection should be
deferred for at least three months until the fibrotic
phase is established
 Oesophageal resection in corrosive strictures is technically
difficult and may be hazardous
 Oesophageal bypass is better and easier, and following
later by regular endoscopic surveillance for malignant
transformation (5%)
 Colon is used as replacing conduit as stomach itself may be
diseased in corrosive pathology
 In multiple strictures oesophageal resection and colonic
transposition may be advocated if risk of malignancy is
considered
Where is the controversy?
 Use of broad spectrum antibiotics and steroids
[Benefits not supported by evidence]
 Regarding risk of developing carcinoma in the
damaged oesophagus and stomach and how
this might influence management
Summary
 Severity and extent of damage depend upon:
 Corrosive properties; amount, concentration, and physical form of the agent; and the
duration of contact with the mucosa
 Absence of oropharyngeal burns does not preclude the presence of
esophageal or gastric injury
 Use of emetics, neutralizing agents, or nasogastric intubation to remove
remaining corrosive material is contraindicated
 In most patients, gastrointestinal endoscopy should be performed during the
first 24 hours
 Contraindication: hemodynamic instability, evidence of perforation, severe respiratory
distress, or severe oropharyngeal or glottic edema and necrosis
 Patients with moderate to severe injury require management in an intensive
care unit to monitor for potential life-threatening complications
 Clinical signs of perforation, mediastinitis or peritonitis are indications for
emergency surgery
Thank You

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Corrosive Ingestion Management

  • 1. Presented by Tapendra Koirala 2nd Batch Senior Clerkship 22nd April 2016
  • 2. Introduction • Antirust compounds • Battery fluid • Toilet bowl or swimming pool • Drain cleaners • Disc batteries • Household cleaning products
  • 3. Corrosive injuries  Ingestion can be accidental or suicidal  Most ingestion occurs in children and the remainder in psychotic, suicidal, and alcoholic subjects  Cause severe damage to the mouth, pharynx, larynx, esophagus and stomach  The type of agent, its concentration, volume ingested and the duration of mucosal contact largely determine the extent of damage
  • 4. Alkali vs Acid injuries ACID • Acids are potent dessicants • Cause coagulative necrosis with eschar formation • Eschar may limit penetration to deeper layers of the oesophageal wall • Induce intense pylorospasm with pooling in the antrum • More gastric damage than alkalis AKALI • Alkalis cause liquefaction necrosis, saponification of fats, dehydration and thrombosis of blood vessels • No eschar formation, hence deeper injuries • Usually leads to fibrous scarring • More esophageal damage than stomach and duodenum • Do not induce pylorospasm
  • 5. Pathology  Phases of tissue injury in corrosive ingestion  Phase 1: Acute necrosis— 1-4 days  Phase 2: Ulceration— granulation— 4-12 days  Phase 3: Cicatrisation and scarring— 3 weeks-6 months  Degrees of burns  1st degree: [Mucosal] Mucosal hyperaemia and oedema  2nd degree: [Mucosal & Submucosal] Small bleeding, exudates, ulcers, pseudomembrane  3rd degree: [Transmural] Mucosal slough, deep ulcers, massive bleed, complete obstruction, charring, perforation
  • 6. Clinical features  Symptoms and signs unreliable in predicting the severity of injury Common presentation • Oropharyngeal, retrosternal or epigastric pain • Dysphagia/odynophagia • Hypersalivation • Vomiting • Hematemesis Burns of the epiglottis & larynx Hoarseness, stridor, aphonia and respiratory difficulties Perforation /with peritonitis Persistent, localized abdominal tenderness, rebound, and rigidity
  • 7. General Management  Asymptomatic pt. who gives a reliable history of a low volume, accidental ingestion of low concentration; endoscopy may not be necessary Discharged and F/U in OPD  Cases of suspected significant ingestion generally be treated in a surgical or medical ICUs  NPO, Hemodynamic stability, PPIs, Adequate analgesia  Assess signs of perforation, mediastinitis or peritonitis– need Em. Surgery  Assess need for ET intubation or tracheostomy Management
  • 8. General Management  Use of emetics, neutralizing agents, or nasogastric intubation to remove remaining corrosive material is contraindicated  In most patients, gastrointestinal endoscopy should be performed during the first 24 hours  Contraindication: hemodynamic instability, evidence of perforation, severe respiratory distress, or severe oropharyngeal or glottic edema and necrosis
  • 9.  In 1st degree burns: 48 hours observation; oral feeds are started once patient swallows saliva painlessly. Regular follow-up endoscopy at 1st, 2nd and 8th months. Stricture if formed can be identified by this time.  2nd and 3rd degree burns: They are treated with fluid therapy, antibiotics, nutrition, PPIs, aerosolised steroids Fiberoptic guided airway intubation if needed tracheostomy; Endoscopic oesophageal stenting, feeding jejunostomy, laparoscopy for evaluation Management
  • 10.  Careful early gentle repeated endoscopy is mandatory  Regular oesophageal dilatation is done for stricture  Stricture is dilated endoscopically using guidewire  Dilators are solid type with gradual increase in diameters  Often radiologic C-ARM guidance is needed to pass the guide wire into the stomach  Dilatation should be done up to minimum 16 mm diameter. Earlier, blind dilatation using oesophageal bougies of increased diameters was the practice, which is followed even now in many places, but chances of perforation is more. Pneumatic or balloon dilatation, Gum elastic dilators, mercury weighted dilators, Eder-Puestow dilators, Savary-Gilliard dilators, balloon dilators are other dilators used Other than emergency surgery for bleeding or perforation, elective oesophageal resection should be deferred for at least three months until the fibrotic phase is established
  • 11.  Oesophageal resection in corrosive strictures is technically difficult and may be hazardous  Oesophageal bypass is better and easier, and following later by regular endoscopic surveillance for malignant transformation (5%)  Colon is used as replacing conduit as stomach itself may be diseased in corrosive pathology  In multiple strictures oesophageal resection and colonic transposition may be advocated if risk of malignancy is considered
  • 12. Where is the controversy?  Use of broad spectrum antibiotics and steroids [Benefits not supported by evidence]  Regarding risk of developing carcinoma in the damaged oesophagus and stomach and how this might influence management
  • 13. Summary  Severity and extent of damage depend upon:  Corrosive properties; amount, concentration, and physical form of the agent; and the duration of contact with the mucosa  Absence of oropharyngeal burns does not preclude the presence of esophageal or gastric injury  Use of emetics, neutralizing agents, or nasogastric intubation to remove remaining corrosive material is contraindicated  In most patients, gastrointestinal endoscopy should be performed during the first 24 hours  Contraindication: hemodynamic instability, evidence of perforation, severe respiratory distress, or severe oropharyngeal or glottic edema and necrosis  Patients with moderate to severe injury require management in an intensive care unit to monitor for potential life-threatening complications  Clinical signs of perforation, mediastinitis or peritonitis are indications for emergency surgery

Editor's Notes

  1. ICU? in order to manage the acute, life-threatening complications of injury (mediastinitis, peritonitis, respiratory distress, shock)
  2. squamous cell ca