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Caustic ingestion
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				Contents
Background
Caustics
- Substances that cause damage on contact with body surfaces
 - Degree of injury determined by pH, concentration, volume, duration of contact
 - Acidic agents cause coagulative necrosis
 - Alkaline agents cause liquefactive necrosis (considered more damaging to most tissues)
 - Corrosive agents have reducing, oxidising, denaturing or defatting potential
 
Alkalis
- Accepts protons → free hydroxide ion, which easily penetrates tissue → cellular destruction
- Liquefactive necrosis and protein disruption may allow for deep penetration into surrounding tissues
 
 - Examples
- Sodium hydroxide (NaOH), potassium hydroxide (KOH), ammonia (NH3)
 - Found in: bleach, drain openers, oven cleaners, toilet cleaner, hair relaxers
 
 
Acids
- Proton donor → free hydrogen ion → cell death and eschar formation, which limits deeper involvement
- However, due to pylorospasm and pooling of acid, high-grade gastric injuries are common
- Mortality rate is higher compared to strong alkali ingestions
 
 
 - However, due to pylorospasm and pooling of acid, high-grade gastric injuries are common
 - Can be systemically absorbed and → metabolic acidosis, hemolysis, AKI
 - Examples
- Hydrochloric acid (HCl), hydrofluoric acid (HF), Sulfuric acid (H2SO4)
 - Found in: auto batteries, drain openers, metal cleaners, swimming pool products, rust remover, nail primer
 
 
Clinical Features
- Signs and symptoms are inadequate to predict presence or severity of injury after caustic ingestion [1]
 - Exam eyes and skin (splash and dribble injuries may easily be missed)
 - GI tract injury
- Dysphagia, odynophagia, epigastric pain, vomiting
 
 - Laryngotracheal injury
- Dysphonia, stridor, respiratory distress
 - Occurs via aspiration of caustic or vomitus or inhalation of acidic fumes
 
 
Differential Diagnosis
Caustic Burns
- Caustic ingestion
 - Caustic eye exposure (Caustic keratoconjunctivitis)
 - Caustic dermal burn
 - Airbag-related burns
 - Hydrofluoric acid
 - Tar burn
 - Cement burn
 
Evaluation
Labs
Only necessary in patients with significant injury or volume of ingestion
- CBC
 - Chemistry
 - Lactic Acid
 - ECG
 - Calcium level (if Hydrofluoric Acid exposure)
 - Acetaminophen and Salicylate levels (in patients with concern for intentional ingestion)
 
Imaging
- 3-View CXR CXR
- Look for free air under the diaphragm or signs of mediastinal air[2]
 
 - CT
- Consider when perforated viscus is suspected but CXR is negative
 
 - Button battery XR - two rings, will likely need to remove it no matter where it is, whether post-pyloric or pre-pyloric
 
Management
- Prevent provider and continued patient exposure to the caustic agent by removing all clothing and decontaminating the patient
 
Airway Management
- Monitor closely for stridor, airway edema, hoarseness, or other signs of airway injury
 - Intubate early if signs of airway injury exist, before airway becomes more difficult to manage.
 - Consider awake fiberoptic or video laryngoscopy if concern for difficult airway
 - Blind nasotracheal intubation is contraindicated due to the potential for perforations and false passages
 
Endoscopy
Should be performed within 12-24 hours of ingestion (too early can underestimate extent of injury, too late increases risk of wound softening and perforation).
- Indications
 
- Intentional ingestion (higher likelihood of high volume ingestion)
 - Unintentional ingestion with signs of:
 
Esophageal Stricture Mitigation[3]
- Discuss with GI or medical toxicologist
 - For grade IIb or higher esophageal burns:
- Methylprednisolone (1 g/1.73 m2 per day for 3 days)
 - Ranitidine
 - Ceftriaxone
 - Total parenteral nutrition
 
 
Surgical Intervention
- Indicated for:
- Perforation
 - Peritoneal signs
 
 
Caustic Specific Treatment
-  Can include chelation, dialysis, or specific antidotes
- Especially in caustics that cause systemic toxicity
 
 
Controversial or Contraindicated
- Antibiotics
- No evidence to support or reject the use of prophylactic antibiotics
 - Only indicated if also giving steriods (see stricture mitigation above)
 
 - Activated charcoal
- May infiltrate damaged mucosa & interfere with EGD
 - Only consider when coingestants pose a risk for severe systemic toxicity
 
 - Gastric lavage
- Contraindicated due to potential to cause reflux of caustic agent into esophagus, creating more damage
 
 - Dilution with water or milk causes vomiting, elevating risk for perforation
- Possible benefit only for solid alkali ingestions
 
 - Neutralization generates excess heat
- Milk or magnesium citrate only for hydrofluoric acid ingestion
 
 
Disposition
- All patients with symptoms from a caustic ingestion should be admitted
 - All patients with intentional ingestion should be evaluated by psych prior to discharge
 
Prognosis
- Depending on severity may have full return of mobility and function or can progress to perforation followed by stricture formation
 - Days 2-14 post-injury are associated with highest tissue friability / risk of perforation
 - High-grade caustic burns associated with 1000x increase in esophageal SCC
 
See Also
References
- ↑ Gaudreault, P. et al. Predictability of esophageal injury from signs and symptoms: a study of caustic ingestion in 378 children. Pediatrics. 1983;71(5):767-770.
 - ↑ Muhletaler C. et al. Acid corrosive esophagitis: radiographic findings. AJR Am J Roentgenol. 1980. Jun;134(6):1137-40. PMID: 6770621
 - ↑ High Doses of Methylprednisolone in the Management of Caustic Esophageal Burns. Pediatrics 2014;133:e1518–e1524
 
