Caustic ingestion
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)
- Lye present in drain cleaners, hair relaxers, grease remover
- Bleach (sodium hypochlorite) and Ammonia (NH3)
- Sodium hydroxide (NaOH), potassium hydroxide (KOH)
Acids
- Proton donor → free hydrogen ion → cell death via denatured protein → coagulation necrosis 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), Phosphoric acid, Oxalic Acid, Acetic acid
- Found in: auto batteries, drain openers, toilet bowl, metal cleaners, swimming pool cleaners, rust remover, nail primer
- Hydrochloric acid (HCl), hydrofluoric acid (HF), Sulfuric acid (H2SO4), Phosphoric acid, Oxalic Acid, Acetic acid
Clinical Features
- All pts w/ serious esophageal injuries have some initial sign or symptom
- E.g. stridor, drooling, vomiting
- 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
Diagnosis
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 pts with concern for intentional ingestion)
Imaging
- 3-View CXR CXR
- Look for free air under the diaphragm or signs of mediastinal air[3]
- 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
Treatment
- 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[4]
- 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
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
- 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 symptomats from a caustic ingestion should be admitted
- All patients with intentional ingestion should be evaluated by psych prior to discharge
Prognosis
- depending 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
- ↑ Wasserman RL, Ginsburg CM. Caustic substance injuries. J Pediatr. 1985;107(2):169-174. doi:10.1016/s0022-3476(85)80119-0
- ↑ Harley EH, Collins MD. Liquid household bleach ingestion in children: a retrospective review. Laryngoscope. 1997;107(1):122-125. doi:10.1097/00005537-199701000-00023
- ↑ 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
