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
Diagnosis
- 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
Work-Up
Labs
Only necessary in patients with significant injury or volume of ingestion
Consider:
- CBC
- Chemistry
- Lactic Acid
- Lactate
- Calcium level (if Hydrofluoric Acid exposure)
- ECG
- May show QT-prolongation if hypocalcemic secondary to HF acid
- Screens for tylenol levels in suicidal patients at risk for congestions
Imaging
- Upright CXR
- Look for free air under the diaphragm indicating a perforation or mediastinal air[3]
- CT
- Consider when perforated viscus is suspected based on severity of ingestion or peritoneal signs on exam
Treatment
- First prevent personal exposure to the caustic agent by removing all clothing and decontaminating the patient
Airway Management
- First-line is awake oral intubation with direct visualization
- Should be considered as a difficult airway
- Blind nasotracheal intubation is contraindicated due to the potential for perforations and false passages
- LMAs, combitubes, bougies are probably may be safe depending on the type of caustic ingestion
- Consider surgical back-up
Endoscopy
Should be performed <12hr after ingestion and no later than >24hr after ingestion
- Indications
- Intentional ingestion
- Unintentional ingestion with signs of:
- Stridor
- Significant oropharyngeal burns
- Vomiting
- Drooling
- Food refusal
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:
- Perforations
- Peritoneal signs
- Free intraperitoneal or mediastinal air
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
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
Source
- Riffat F, Cheng A. Pediatric caustic ingestion: 50 consecutive cases and a review of the literature. Dis Esophagus. 2009;22(1):89-94. 2008 Oct 1. PMID: 18847446
- Zargar S et al. Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history. The American Journal of Gastroenterology. 1992 87 (3), 337-41 PMID: 1539568
- ↑ 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