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Caustic Ingestion, Emergency Medicine

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Caustic Ingestion, Emergency Medicine

Basics

Description

Psychiatric referral for intentional ingestion á

  • Alkalis:Dissociate in the presence of H2O to produce hydroxy (OH-) ions, which leads to liquefaction necrosisPostingestion-mainly damages the esophagus:Gastric damage can occur (see "Acids"Ł).Esophageal damage (in the order of increasing damage) consists of:Superficial hyperemiaMucosal edemaSuperficial blistersExudative ulcerationsFull-thickness necrosisPerforationFibrosis with resulting esophageal stricturesDo not directly produce systemic complications.
  • Acids:Dissociate in the presence of H2O to produce hydrogen (H+) ions, which leads to a coagulation necrosis with eschar formationPostingestion-damages the stomach because of rapid transit time through esophagus:Esophageal damage can occur (see "Alkalis"Ł).Gastric damage (in the order of increasing damage) consists of:EdemaInflammationImmediate or delayed hemorrhageFull-thickness necrosisPerforationFibrosis with resulting gastric outlet obstructionWell-absorbed and can cause hemolysis of RBCs and a systemic metabolic acidosis
  • Dissociate in the presence of H2O to produce hydroxy (OH-) ions, which leads to liquefaction necrosis
  • Postingestion-mainly damages the esophagus:Gastric damage can occur (see "Acids"Ł).
  • Esophageal damage (in the order of increasing damage) consists of:Superficial hyperemiaMucosal edemaSuperficial blistersExudative ulcerationsFull-thickness necrosisPerforationFibrosis with resulting esophageal strictures
  • Do not directly produce systemic complications.
  • Gastric damage can occur (see "Acids"Ł).
  • Superficial hyperemia
  • Mucosal edema
  • Superficial blisters
  • Exudative ulcerations
  • Full-thickness necrosis
  • Perforation
  • Fibrosis with resulting esophageal strictures
  • Dissociate in the presence of H2O to produce hydrogen (H+) ions, which leads to a coagulation necrosis with eschar formation
  • Postingestion-damages the stomach because of rapid transit time through esophagus:Esophageal damage can occur (see "Alkalis"Ł).
  • Gastric damage (in the order of increasing damage) consists of:EdemaInflammationImmediate or delayed hemorrhageFull-thickness necrosisPerforationFibrosis with resulting gastric outlet obstruction
  • Well-absorbed and can cause hemolysis of RBCs and a systemic metabolic acidosis
  • Esophageal damage can occur (see "Alkalis"Ł).
  • Edema
  • Inflammation
  • Immediate or delayed hemorrhage
  • Full-thickness necrosis
  • Perforation
  • Fibrosis with resulting gastric outlet obstruction

Etiology

  • Direct chemical injuries
  • Injuries occur secondary to acid and alkali exposures.
  • Many caustic agents (acids and alkalis) are found in common household and industrial products.
  • Caustic substances:Ammonia hydroxide
  • Glass cleaners:Formaldehyde:Embalming agentHydrochloric acid:Toilet bowel cleanersHydrofluoric acid:Glass etching industryMicrochip industryRust removersIodine:AntisepticsPhenol:AntisepticsSodium hydroxide:Drain cleanersDrain openersOven cleanersSodium borates, carbonates, phosphates, and silicates:DetergentsDishwasher preparationsSodium hypochloriteBleachesSulfuric acid:Car batteriesButton batteries
  • Ammonia hydroxide
  • Formaldehyde:Embalming agent
  • Hydrochloric acid:Toilet bowel cleaners
  • Hydrofluoric acid:Glass etching industryMicrochip industryRust removers
  • Iodine:Antiseptics
  • Phenol:Antiseptics
  • Sodium hydroxide:Drain cleanersDrain openersOven cleaners
  • Sodium borates, carbonates, phosphates, and silicates:DetergentsDishwasher preparationsSodium hypochloriteBleaches
  • Sulfuric acid:Car batteriesButton batteries
  • Embalming agent
  • Toilet bowel cleaners
  • Glass etching industry
  • Microchip industry
  • Rust removers
  • Antiseptics
  • Antiseptics
  • Drain cleaners
  • Drain openers
  • Oven cleaners
  • Detergents
  • Dishwasher preparations
  • Sodium hypochlorite
  • Bleaches
  • Car batteries
  • Button batteries

Diagnosis

Signs and Symptoms

  • Oropharyngeal:PainErythemaBurnsErosionsUlcersDroolingHoarsenessStridorAphoniaAbsence of visible lesions in the oropharynx does not exclude visceral injuries.
  • Pulmonary:TachypneaCoughPneumonitis if aspirated
  • GI:PainEmesis or hematemesisMelena, dysphagiaOdynophagiaEsophageal or gastric perforationPeritonitis owing to perforation
  • Cardiovascular:TachycardiaHypotensionOrthostatic changes
  • Hematologic:Acid ingestion can cause RBC hemolysis.
  • Dermatologic:PainErythema1st-, 2nd-, or 3rd-degree burns
  • Ocular:PainErythemaInjectionCorneal burnsFull-thickness corneal damage
  • Metabolic:Metabolic acidosis
  • Pain
  • Erythema
  • Burns
  • Erosions
  • Ulcers
  • Drooling
  • Hoarseness
  • Stridor
  • Aphonia
  • Absence of visible lesions in the oropharynx does not exclude visceral injuries.
  • Tachypnea
  • Cough
  • Pneumonitis if aspirated
  • Pain
  • Emesis or hematemesis
  • Melena, dysphagia
  • Odynophagia
  • Esophageal or gastric perforation
  • Peritonitis owing to perforation
  • Tachycardia
  • Hypotension
  • Orthostatic changes
  • Acid ingestion can cause RBC hemolysis.
  • Pain
  • Erythema
  • 1st-, 2nd-, or 3rd-degree burns
  • Pain
  • Erythema
  • Injection
  • Corneal burns
  • Full-thickness corneal damage
  • Metabolic acidosis

Essential Workup

  • History of or signs and symptoms of an exposure
  • Absence of oropharyngeal lesions does not exclude visceral injury.

Diagnosis Tests & Interpretation

  • CBC
  • Electrolytes, BUN, creatinine, glucose
  • Arterial blood gas
  • Blood cultures:If mediastinitis or peritonitis suspected
  • Type and cross-match
  • If mediastinitis or peritonitis suspected
  • Esophageal or gastric perforation
  • Esophageal and gastric endoscopy:For symptomatic patients to determine the extent of injuryPerform within the 1st 12-24 hr after ingestion.Not recommended in the presence of respiratory distress without proper airway managementNot recommended in the presence of severe pharyngeal damage
  • Radiographic oral contrast imaging not recommended acutely:May be used in follow-up for assessment for strictures
  • For symptomatic patients to determine the extent of injury
  • Perform within the 1st 12-24 hr after ingestion.
  • Not recommended in the presence of respiratory distress without proper airway management
  • Not recommended in the presence of severe pharyngeal damage
  • May be used in follow-up for assessment for strictures

Differential Diagnosis

  • Chemical injuries from corrosives, acids, alkalis, desiccants, vesicants, and oxidizing and reducing agents
  • Foreign body ingestion
  • Upper airway infection or angioedema

Treatment

Pre-Hospital

  • For oral burns or symptoms: Rinse mouth liberally with water or milk.
  • Water or milk can be given to following patients:Able to drinkNot complaining of significant abdominal painDo not have airway compromise or vomiting
  • Copious irrigation for ocular or dermal exposure
  • Able to drink
  • Not complaining of significant abdominal pain
  • Do not have airway compromise or vomiting

Initial Stabilization/Therapy

  • ABCs:Prophylactic intubation if there is any evidence of respiratory compromiseBlind nasotracheal intubation contraindicated
  • Treat hypotension with 0.9% NS IV fluid resuscitation.
  • Prophylactic intubation if there is any evidence of respiratory compromise
  • Blind nasotracheal intubation contraindicated

Ed Treatment/Procedures

  • Decontamination:Dermal or ocular exposure:Immediate and thorough irrigation with water or 0.9% NS until physiologic pH attainedAlkalis typically require more irrigation than acids.Ipecac, activated charcoal, gastroesophageal lavage (large-bore or an NG tube), and a neutralizing acid or base are all contraindicated with caustic ingestions.
  • Dilution:Water or milk in the 1st 30 min of ingestion:Especially useful for solid caustic alkali ingestionsExcessive intake may induce vomiting and worsen esophageal damage.If respiratory distress, intubate before dilution.Contraindicated if esophageal or gastric perforation suspected
  • Keep patient NPO if oral exposure.
  • Broad-spectrum antibiotics if mediastinitis or peritonitis suspected
  • Antiemetics for nausea and vomiting
  • Treat dermal exposures according to standard burn recommendations.
  • Detailed exam for ocular exposures
  • IV proton pump inhibitors or H2 blockers for symptomatic relief
  • Gastroenterology and surgical consultation
  • Benefit of corticosteroids following esophageal damage is controversial:May prevent the formation of esophageal strictureMay promote bacterial invasion, immune suppression, and tissue softeningThe decision to initiate corticosteroids requires input from entire team caring for patient.Initiate broad-spectrum antibiotics if corticosteroids are given.
  • Laparoscopy or laparotomy for perforation and full-thickness necrosis
  • Topical hydrofluoric acid exposure (options depend on severity and location):IM injection of 5% calcium gluconate (0.5 mL/cm2 of skin with 30G needle)Intra-arterial infusion of 10 mL of 10% calcium gluconate in 40 mL D5W over 4 hr
  • Dermal or ocular exposure:Immediate and thorough irrigation with water or 0.9% NS until physiologic pH attainedAlkalis typically require more irrigation than acids.
  • Ipecac, activated charcoal, gastroesophageal lavage (large-bore or an NG tube), and a neutralizing acid or base are all contraindicated with caustic ingestions.
  • Immediate and thorough irrigation with water or 0.9% NS until physiologic pH attained
  • Alkalis typically require more irrigation than acids.
  • Water or milk in the 1st 30 min of ingestion:Especially useful for solid caustic alkali ingestionsExcessive intake may induce vomiting and worsen esophageal damage.
  • If respiratory distress, intubate before dilution.
  • Contraindicated if esophageal or gastric perforation suspected
  • Especially useful for solid caustic alkali ingestions
  • Excessive intake may induce vomiting and worsen esophageal damage.
  • May prevent the formation of esophageal stricture
  • May promote bacterial invasion, immune suppression, and tissue softening
  • The decision to initiate corticosteroids requires input from entire team caring for patient.
  • Initiate broad-spectrum antibiotics if corticosteroids are given.
  • IM injection of 5% calcium gluconate (0.5 mL/cm2 of skin with 30G needle)
  • Intra-arterial infusion of 10 mL of 10% calcium gluconate in 40 mL D5W over 4 hr

Medication

  • Methylprednisolone: 40 mg q8h IV (peds: 2 mg/kg/d IV); the course of therapy is 14-21 days followed by a corticosteroid taper.
  • Ondansetron: 4 mg (peds: 0.1-0.15 mg/kg) IV
  • Pantoprazole: 40 mg IV
  • Prochlorperazine (Compazine): 5-10 mg IV (peds: 0.13 mg/kg per dose IM)
  • Ranitidine (Zantac): 50 mg IV q6-8h

Follow-Up

Disposition

  • All symptomatic patients
  • Nonaccidental ingestion
  • Asymptomatic patients who accidentally ingested and are able to swallow without difficulty
  • Minimal oropharyngeal pain with a corresponding visible lesion; no drooling; no respiratory compromise; no deep throat, chest, or abdominal pain; and able to swallow without difficulty

Followup Recommendations

Pearls and Pitfalls

  • Dilute with milk or water at home or in the ED within the 1st 30 min.
  • Perform copious irrigation of ocular or dermal exposure:Alkalis require more irrigation than acids.
  • Alkalis require more irrigation than acids.

Additional Reading

  • Lupa áM, Magne áJ, Guarisco áL, et al. Update on the diagnosis and treatment of caustic ingestions. Ochsner J. 2009;9:54-59.
  • Riffat áF, Cheng áA. Pediatric caustic ingestion: 50 consecutive cases and a review of the literature. Dis Esophagus. 2009;22:89-94.
  • Salzman áM, O'Malley áRN. Updates on the evaluation and management of caustic exposures. Emerg Med Clin North Am. 2007;25(2):459-476.

Codes

ICD9

  • 947.0 Burn of mouth and pharynx
  • 947.2 Burn of esophagus
  • 947.3 Burn of gastrointestinal tract
  • 947.1 Burn of larynx, trachea, and lung
  • 947.8 Burn of other specified sites of internal organs
  • 947.9 Burn of internal organs, unspecified site

ICD10

  • T28.5XXA Corrosion of mouth and pharynx, initial encounter
  • T28.6XXA Corrosion of esophagus, initial encounter
  • T28.7XXA Corrosion of other parts of alimentary tract, init encntr
  • T27.5XXA Corrosion involving larynx and trachea w lung, init encntr
  • T28.90XA Corrosions of unspecified internal organs, initial encounter
  • T28.99XA Corrosions of other internal organs, initial encounter

SNOMED

  • 23509002 Caustic esophageal injury (disorder)
  • 37693008 Caustic injury gastritis (disorder)
  • 235021001 Chemical burn of oral mucosa (disorder)
  • 212039008 Corrosion involving larynx and trachea with lung (disorder)
  • 219171000 Suicide and selfinflicted injury by caustic substances, excluding poisoning (navigational concept)
  • 219362003 Injury undetermined whether accidentally or purposely inflicted, by caustic substances, excluding poisoning (disorder)
  • 269737002 Injury of unknown intent by local effect of caustic substance (disorder)
  • 418409002 Poisoning of undetermined intent by corrosive, acid or caustic alkali (disorder)