Corrosive Caustic injury of gastrointestinal tract

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Corrosive (Caustic) injury of gastrointestinal
tract

• Classified by cause of ingestion
• Accidental
• More popular in developed countries
• Almost all child ingestion accounts to this
  reason
• Approximately 80 of caustic ingestions occur in
  children younger than 5 years
• Intentional (suicide)
• Most intentional ingestions occur in adults

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• Classified by ingested caustic material
• Alkaline material
• liquefactive necrosis (saponification of fats and
  solubilization of proteins)
• Most common in developed contries
• The most severely injured tissues are the
  squamous epithelial cells of the oropharynx,
  hypopharynx, and esophagus (the most commonly
  involved organ)
• The stomach is involved in only 20 of all
  alkaline ingestions
• Acid material
• coagulation necrosis (desiccation or denaturation
  of superficial tissue proteins)
• More common in developing countries
• The squamous epithelium of the pharynx and
  esophagus are relatively resistant to this type
  of injury. The esophagus is involved in 6-20 of
  acid ingestions.
• The stomach is the most commonly involved organ
  in an acid ingestion

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Evaluation of patient of acute corrosive injury

• Attempt to identify the specific product,
  concentration of active ingredients, and
  estimated volume and amount ingested
• Physical examination
• Monitor peritoneal signs
• Complete blood count (CBC), electrolyte levels,
  BUN levels, creatinine level, and ABG levels
• pH testing of product
• A pH less than 2.0 or greater than 12 indicates
  the potential for severe tissue damage
• Chest X-ray
• Be cautious of peritoneal free air
• Upper digestive endoscopy
• Performed within 24 hours is safe
• Gold standard
• Esophagoscopy should not be performed in patients
  with evidence of gastrointestinal perforation,
  significant airway edema, or necrosis and in
  those who are hemodynamically unstable.
• Bronchoscopy
• EUS (endoscopic ultra-sound)

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Classification of endoscopic finding of
corrosive injury
Prediction of bleeding and stricture formation
after corrosive ingestion by EUS concurrent with
upper endoscopy. Gastrointest Endosc. 2004
Nov60(5)827-33
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Figure 1. A, Endoscopic view of esophagus,
showing grade 2a corrosive injury. B, Endoscopic
view of stomach, showing grade 2b corrosive
injury. C, Endoscopic view of stomach, showing
grade 3a corrosive injury. D, Endoscopic view of
stomach, showing grade 3b corrosive injury.
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Ingestion of acid and alkaline agents outcome
and prognostic value of early upper endoscopy.
Gastrointest Endosc. 2004 Sep60(3)372-7.
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Laryngoscope 116 August 2006
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(No Transcript)
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Classification of EUS findings
Prediction of bleeding and stricture formation
after corrosive ingestion by EUS concurrent with
upper endoscopy. Gastrointest Endosc. 2004
Nov60(5)827-33
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Figure 2. A, EUS image of stomach, showing grade
M corrosive injury. B, EUS image of esophagus,
showing grade SM corrosive injury. C, EUS image
of esophagus, showing grade MP injury. D, EUS
image of stomach, showing grade SS corrosive
injury with adjacent ascitic fluid.
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Prediction of bleeding and stricture formation
after corrosive ingestion by EUS concurrent with
upper endoscopy. Gastrointest Endosc. 2004
Nov60(5)827-33
12
Prediction of bleeding and stricture formation
after corrosive ingestion by EUS concurrent with
upper endoscopy. Gastrointest Endosc. 2004
Nov60(5)827-33
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Emergency Department Care

• Airway control
• Equipment for endotracheal intubation and
  cricothyrotomy should be readily available.
• Gastric emptying and decontamination
• Do not administer emetics
• Gastric lavage by traditional methods using large
  bore orogastric Ewald tubes are contraindicated
• Large-volume liquid acid ingestions may benefit
  from nasogastric tube (NGT) suction.
• Activated charcoal is relatively contraindicated
• Dilution
• Dilution may be beneficial for ingestion of solid
  or granular alkaline material if performed within
  30 minutes postingestion.
• Neutralization
• Do not administer a weak acid in alkaline
  ingestions or a weak base in acid ingestions.

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Treatment of acute corrosive injury

• Because controlled, randomized trials with
  adequate numbers of patients are lacking,
  treatment in many respects remains controversial
• Principle
• Admit all small children, symptomatic patients,
  and those with altered mental status
• Ensure that all patients take nothing per mouth
  (NPO) until extent of injury has been determined
• PPN (partial parenteral nutrition)
• Administer parenteral analgesics as needed for
  pain
• Antacid agent
• Monitor respiratory pattern and prevent pneumonia
• Early exploratory laparotomy if acute abdomen is
  suspected
• Obtain a psychiatric evaluation for all patients
  with intentional ingestion.

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Alternative treatments

• Early discharge, oral intake and out patient
  follow up in patients minor than grade 2a injury
• Prediction of bleeding and stricture formation
  after corrosive ingestion by EUS concurrent with
  upper endoscopy. Gastrointest Endosc. 2004
  Nov60(5)827-33
• Ingestion of Caustic Substances by Adults,
  American Journal of Therapeutics 11, 258261
  (2004)
• Methyl prednisolone, 1mg/kg intravenously
• Ingestion of Caustic Substances by Adults,
  American Journal of Therapeutics 11, 258261
  (2004)
• Short-term intravenous antibiotics
• Ingestion of Caustic Substances by Adults,
  American Journal of Therapeutics 11, 258261
  (2004)
• Neutralization by weak acid or alkali
  administration
• Successful in canine models
• Thermal characteristics of neutralization therapy
  and water dilution for strong acid ingestion an
  in-vivo canine model. Acad Emerg Med 1998 5286
  292.
• Modified Intraluminal Stenting
• Management of corrosive esophageal burns in 149
  cases. The Journal of Thoracic and Cardiovascular
  Surgery. Volume 130, Number 2 449.e1

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The physiopathological characteristics of the
caustic lesions

• During the first hours
• there is eosinophilic necrosis with edema and
  intense hemorrhagic congestion (caustic
  esophagitis).
• During the first days
• Perforation will occur if ulceration exceeds the
  muscle plane.
• Mucosal sloughing occurs 47 days after the
  initial injury
• Repair occurs during the first weeks, especially
  after the 10th day.
• the tensile strength of healing tissue is low
  during first 3 weeks
• Fibrosis occurs in layers whose depth depends on
  the severity of the caustic injury (caustic
  stenosis).
• During the first month
• epithelialization of the mucosal ulcerations
  occurs with difficulty due to the vascular
  lesions.
• For the rest of their lives
• these patients may present new ulcerations
  followed by re-epithelialization due to small
  traumas provoked by food. These traumas increase
  the scars, reducing even more the lumen of the
  organ.

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Complications of corrosive injury

• Complications
• Bleeding
• Perforation
• Acid regurgitation
• Stricture formation
• Pyloric stenosis
• Respiratory failure
• Pneumonia
• Tracheoesophageal fistula
• The major early complication
• Bleeding within 1 month
• The major late complication
• Stricture
• Use of endoscopic grade 3a as a cutoff point
  accurately predict the occurrence of bleeding or
  stricture

Prediction of bleeding and stricture formation
after corrosive ingestion by EUS concurrent with
upper endoscopy. Gastrointest Endosc. 2004
Nov60(5)827-33
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• Airway edema or obstruction
• Immediately or up to 48 hours following an
  alkaline exposure
• Upper gastrointestinal hemorrhage
• May occur acutely in caustic exposures
• Gastroesophageal perforation
• Secondary complications include mediastinitis,
  pericarditis, pleuritis, tracheoesophageal
  fistula formation, esophageal-aortic fistula
  formation, and peritonitis.
• Delayed perforation may occur as many as 4 days
  after an acid exposure
• Delayed upper GI bleeding
• May occur in acid burns 3-4 days after exposure
  as the eschar sloughs
• Esophageal stricture
• Deep circumferential or deep focal burns
• Develop 2-4 weeks postingestion
• Gastric outlet obstruction
• May develop 3-4 weeks after an acid exposure
• Long-term risks include squamous cell carcinoma,
  which occurs in 1-4 of all significant exposures
  and may occur as many as 40 years after exposure.

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Medical/Legal Pitfalls

• Failure to evaluate and aggressively manage the
  airway in patients with respiratory distress or
  significant laryngeal involvement
• Attempting to neutralize the ingested caustic
  agent with a weak acid or alkaline agent
• Inducing emesis
• Assuming that the absence of oropharyngeal burns
  precludes the presence of significant distal
  injuries
• Failing to consult a gastroenterologist or
  surgeon for evaluation of all symptomatic patients

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References

• Prediction of bleeding and stricture formation
  after corrosive ingestion by EUS concurrent with
  upper endoscopy. Gastrointest Endosc. 2004
  Nov60(5)827-33.
• Ingestion of caustic substances a 15-year
  experience. Laryngoscope. 2006 Aug116(8)1422-6.
  
• Ingestion of caustic substances by adults.Am J
  Ther. 2004 Jul-Aug11(4)258-61.
• Ingestion of acid and alkaline agents outcome
  and prognostic value of early upper endoscopy.
  Gastrointest Endosc. 2004 Sep60(3)372-7.
• Ingestion of caustic substances and its
  complications.Sao Paulo Med J. 2001 Jan
  4119(1)10-5.
• A,B,Cs of caustic ingestions in suicidal
  adults.Ann Emerg Med. 2007 Feb49(2)246-7. No
  abstract available.
• Management of corrosive esophageal burns in 149
  cases.J Thorac Cardiovasc Surg. 2005
  Aug130(2)449-55.
• Toxicity, Caustic Ingestions. http//www.emedicine
  .com/emerg/topic86.htm

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Thanks for your attention!