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  • Acids—cause immediate coagulative necrosis. Usually self-limiting injury
  • Alkalis—cause liquefactive necrosis resulting in deeper penetration and more extensive injury. Neutralization by the tissues themselves will terminate reaction
    • NB: Alkalis are typically odorless and tasteless, which can lead to consumption of larger volumes than acids
    • Alkalis also cause blood vessel thrombosis, which can worsen necrosis

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Common Caustic Substances Ingested
Found in
Alkali
Sodium hydroxideIndustrial chemicals, drain openers, oven cleaners
Potassium hydroxideDrain openers, batteries
Calcium hydroxideCement, hair relaxers, and perm products
Ammonium hydroxideHair relaxers and perm products, dermal peeling/exfoliation, toilet bowl cleaners, glass cleaners, fertilizers
Lithium hydroxidePhotographic developer, batteries
Sodium tripolyphosphateDetergents
Sodium hypochloriteBleach
Acid
Sulfuric acidCar batteries, drain openers, explosives, fertilizer
Acetic acidPrinting and photography, disinfectants, hair perm neutralizer
Hydrochloric acidCleaning agents, metal cleaning, chemical production, swimming pool products
Hydrofluoric acidRust remover, glass and microchip etching, jewelry cleaners
Formic acidModel glue, leather and textile manufacturing, tissue preservation
Chromic acidMetal plating, photography
Nitric acidFertilizer, engraving, electroplating
Phosphoric acidRustproofing, metal cleaners, disinfectants
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  • Oropharynx/nasopharynx
  • Esophagus
  • Larynx
  • Trachea

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  • Amount of caustic fluid ingested
  • Type of caustic (pH)
  • Concentration
  • Duration of contact with mucosa—if vomiting, duration of contact will be lengthened

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  • The main issues to decide are:
    • Should the patient be intubated?
    • Is there an indication for immediate surgical intervention?
    • Is there an indication for early (before 6 hours) esophagoscopy?
  • History—type and amount of caustic ingested. ±Vomiting? If pediatric ingestion, parents should bring container of caustic ingested for correct identification
  • Symptoms:
    • Hoarseness, stridor, dyspnea → indicate airway injury
    • Odynophagia, drooling, refusal of food → indicate orophayngeal/nasophayngeal and esophageal injury
    • Abdominal pain and peritoneal signs: immediate CXR and abdominal x-ray to r/o intraperitoneal or mediastinal air
    • Substernal chest pain, abdominal pain, rigidity → indicate profound injury or perforation of esophagus/stomach
    • Signs of perforated viscus, peritonitis, mediastinitis, or hemodynamic instability: immediate surgical evaluation
    • Criteria for emergent surgery:
      • Presence of shock
      • Disseminated intravascular coagulation
      • Need for hemodialysis
      • Acidosis (arterial pH <7.22 or base excess <−12)
      • Grade 3 esophageal injury (see below) seen on endoscopy (controversial)
  • Physical exam—injury to lips, chin, hand, clothing, mouth, and pharynx
    • Note: Absence of injury to mouth/pharynx is not predictive of esophageal or laryngeal injury
    • If airway stable—examine pharynx and hypopharynx with flexible fiber-optic scope

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Patients with caustic ingestions should always be considered “difficult airways”.

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  • Respiratory distress and stridor indicate pharyngeal or laryngotracheal injuries
  • Place oral/nasal airway early in management prior to rapid worsening of airway edema
  • Consider administration of dexamethasone (10 mg IV) to counteract upper airway edema
  • Intubate if symptomatic, or if massive ingestion, even without symptoms
  • Awake oral intubation using flexible fiber-optic scope is preferred
    • Surgical backup should always be available for emergent cricothyroidotomy/tracheotomy as tissue friability, bleeding, and edema may make intubation impossible
    • Avoid long-acting paralytics as airway edema and muscle relaxation may make mask ventilation impossible
    • Contraindicated: blind ...

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