Caustic burn

Background

• Substances that cause damage on contact with body surfaces
• Degree of injury determined by pH, concentration, volume, duration of contact
• Etiologies for shock include GI bleeding, perforation, volume depletion
  • Intentional ingestion a/w higher grade injuries
• Esophageal injuries
  • Mild injuries - normal function is restored
  • Severe injuries - strictures
• Days 2-14 post-injury are a/w highest tissue friability / risk of perforation
• High-grade caustic burns a/w 1000x increase in esophageal SCC

Alkalis

• Hydroxide ion easily penetrates tissue causing immediate cellular destruction
  • May cause deep penetration into surrounding tissues (e.g. abd/mediastinal necrosis)
• Examples
  • Bleach, drain openers, oven cleaners, toilet cleaner, hair relaxers
  • Household bleach rarely causes significant injury

Acids

• Hydrogen ion leads to cell death and eschar formation, which limits deeper involvement
  • However, due to pylorospasm and pooling high-grade gastric injuries are common
    • Mortality rate is higher compared to strong alkali ingestions
• Ingestion may be complicated by systemic absorption (met acidosis, hemolysis, ARF)
• Examples
  • Auto batteries, drain openers, metal cleaners, swimming pool products, rust remover

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

Work-Up

Labs

Only necessary in pts w/ significant injury

• • CBC
  • Chemistry
  • VBG
    • Anion gap acidosis due to lactate production (tissue injury) or from the acid itself
      • May also have non-anion gap acidosis (e.g. HCl)
  • Lactate
  • LFTs
  • Coags
  • Type and screen
  • Calcium level
    • If HF acid exposure
  • ECG
  • Screens for coingestants in suicidal pts
  • May show QT-prolongation if hypocalcemic 2/2 HF acid

Imaging

• Upright CXR
  • Detect peritoneal and mediastinal air
• Left-side down CXR
  • Indicated if unable to tolerate upright CXR
• CT
  • Consider when perforated viscus is suspected or after intentional ingestion

Treatment

1. Prevent personal exposure to the caustic agent
2. Airway
   1. Should be considered as a difficult airway
   2. Blind nasotracheal intubation is contraindicated
   3. First-line is awake oral intubation w/ direct visualization
   4. LMAs, combitubes, bougies are probably unsafe; should be used as last resort
   5. Surgical back-up is recommended
3. Steroids
   1. Some toxicologists recommend single dose of dexamethasone 10mg IV (06mg/kg in peds)
4. Decontaminate in usual manner
5. Activated charcoal
   1. Only consider when coingestants pose a risk for severe systemic toxicity
6. Endoscopy
   1. Should be performed <12hr after ingestion and no later than >24hr after ingestion
   2. Indications:
      1. Intentional ingestion
      2. Unintentional ingestion with signs of:
         1. Stridor
         2. Significant oropharyngeal burns
         3. Vomiting
         4. Drooling
         5. Food refusal
7. Surgery
   1. Indicated for peritoneal signs, free intraperitoneal or mediastinal air
8. No evidence to support prophylactic abx

Disposition

• All pts w/ symptomatic caustic ingestions should be admitted

Special Situations

Ocular Exposure

• Alkali injuries are more severe than acidic injuries
• Treatment
  • Copious irrigation in 15min intervals followed by pH check
  • LR, NS, or 3% saline works best
  • Treat until pH is 7.5-8.0
  • Severe exposures may require anterior chamber irrigation
  • Avoid testing pH of the irrigation fluid (wait few min before checking ocular fluid)
• After irrigation perform complete eye exam
  • Prognosis determined by extent of injury at limbus and area/depth of injury to cornea
• Disposition
  • Admit all pts w/ corneal haziness or opacity or limbal ischemia (paleness at limbus)
  • Discharge w/ 24hr f/u if pt only has corneal epithelial injury (fluorescein uptake)

Dermal Exposure

• Acidic injuries (except HF acid)
  • Respond well to copious saline or water irrigation
• Alkali injuries
  • May appear superficial but often are deeper w/ ongoing burn
  • Treat w/ copious irrigation and local wound debridement to remove residual compound
• Disposition
  • Admit the following:
    • Injuries that cross flexor or extensor surfaces
    • Facial injuries
    • Perineum injuries
    • Partial-thickness injuries >10-15% of BSA
    • All full-thickness burns

Hydrofluoric Acid

Background

• Uses
  • Glass etching, metal cleaning, petroleum processing
  • Found in chrome wheel cleaner, rust remover
• Kills via calcium chelation/cardiac arrest, not via burn
• Oral ingestion has very high mortality rate

Diagnosis

• Onset of symptoms (pain, erythema) correlated w/ concentration
  • Dilute solutions (<20%) may have delayed onset up to 24hr post-exposure
  • Moderate solutions (20-50%) develop symptoms w/in 1-8hr
  • Concentrated solutions (>50%) develop symptoms immediately
    • These pts are at risk for systemic toxicity/death
    • Pain immediately (even if wound appears minor) implies severe injury
• Trend calcium and potassium levels
  • HF acid chelates calcium and poisons the Na+/K+ pump

Treatment

• Minor injuries (<50 cm2 from dilute solutions <20%)

1. Copious irrigation
2. Application of gel paste of Ca gluconate or benzalkonium Cl
   1. Rub into affected area for 10-15min w/ pain relief being used as end-point of tx
   2. Calcium gel is commercially available (found in industrial first-aid kits)
   3. Calcium gel can be made:
      1. Mix calcium gluconate powder 3.5gm w/ 150mL water-soluble lubricant OR
      2. Mix 25mL 10% calcium gluconate solution w/ 75mL water-soluble lubricant
   4. Benzalkonium Cl is commercially available
   5. If calcium gluconate is not available calcium chloride can be used

• Severe injuries

1. Treat w/ intradermal injections of 5% calcium gluconate
   1. Prepare by diluting conventional 10% Ca gluconate w/ sterile NS in 1:1 ratio
   2. Inject in and around the burned area in amount not to exceed 0.5mL per cm2

• Refractory injuries

1. Treat w/ intra-arterial infusion of calcium gluconate
   1. Deliver via arterial line placed proximal to injury in the same limb
   2. Infuse 10mL of 10% Ca gluconate dilued in 40mL of NS or D5water over 4 hr

• Ingestion

1. If <1hr of ingestion place NG tube, suction, gastric lavage
   1. Follow lavage by 300mL 10% Ca gluconate down NGT
   2. Provide aggressive IV supplementation if ECG signs of hypoCa or hyperK

Airbag-Related Burns

• Deployment releases small amount of alkali
  • Skin burns are usually minor
  • Ocular burns require irrigation, pH testing and ophto f/u
    • Long-term sequelae is rare

Source

Tintinalli