Chemical burns

Intro

  • Make up only 10% of burns centre admissions but 30% of deaths
  • Acids cause coagulative necrosis with protein precipitation and a tough leathery eschar that can limit deeper penetration of the agent
  • Alkalis cause liquefactive necrosis with deeper, ongoing burns
  • Early death is usually due to hypotension, acute renal failure and shock, however, systemic absorption of the chemical can lead to acidosis, hypotension, hyperkalaemia and dysrhythmias

General approach

  • Remove patient from further exposure with universal precautions
  • Aggressive irrigation with water is the cornerstone for almost all cases
    • Dry chemical particles e.g. lime should be brushed away before irrigation
    • Sodium metal and related compounds should be brushed away or covered with mineral oil or excised prior to irrigation as water induces a severe exothermic reaction
    • Dilution of phenol (carbolic acid) with water may enhance penetration
  • Almost universally, early irrigation means a better prognosis
  • Time to irrigation
    • If done at 3 minutes, twofold greater chance of full thickness burn than if done at 1 minute
  • Irrigation should continue until pH neutral
  • Then treat as for thermal burn

Factors influencing tissue damage

  • Type of chemical
  • Concentration of agent
  • Quantity of agent
  • Duration of exposure
  • Mechanism of action
  • Extent of penetration

Factors influencing percutaneous absorption

  • Body site – Thin skin, large surface area, age
  • Integrity of skin
  • Nature of the chemical – Lipid solubility, pH, concentration
  • Duration of contact – Inadequate irrigation, chemical-soaked clothing, occlusive garments

Classification of agents

  • Acids – Coagulative necrosis via proton donation
  • Alkali – Liquefactive necrosis via proton acceptance
  • Organic solvents – Disruption of cellular membranes
  • Inorganic solvents – Scavenge ions and salt production within tissues

Acid burns

  • Factors that increase severity
    • pH
    • Concentration
    • Molarity
    • Complexing affinity for hydroxyl ions
    • Type e.g. hydrofluoric acid does not cause coagulation necrosis
  • Contact time with skin is the most important feature that healthcare workers can alter

Acid burns

  • Acetic acid
    • Dilute (<40%) acetic acid in chemical hair straightener is the most common chemical burn to the scalp in females
    • Prolonged contact, especially with damaged scalp skin, can cause a partial thickness burn that heals slowly and is prone to infection
    • Copious wound irrigation and oral antibiotics if open scalp wound

Acid burns

  • Carbolic acid (phenol)
    • Corrosive organic acid causes relatively painless white or brown coagulum
    • Dilute phenol penetrates tissues more readily than concentrated
    • Systemic absorption can lead to dysrhythmias or seizures
    • 1-2% concentrations can cause burns if contact period is long enough
    • Cresol, creosote and cresylic acid are chemically related compounds
    • Coagulation necrosis is common with phenol trapped under eschar
      • Water lavage alone may not reach this
      • Thus can use undiluted PEG (MW 200-4oo) or gentle wash with isopropyl alcohol (equally effective)
      • Reduce cutaneous corrosion and decreases systemic toxicity

Acid burns

  • Chromic acid
    • Powerful oxidisers
    • Chromate ion produces chronic penetrating ulceration
    • Also get conjunctivitis, lacrimation and ulceration of the nasal septum
    • Systemic chromium toxicity can cause liver or renal failure, GI bleeding, coagulopathy and CNS disturbances
    • 1-2% BSA can cause significant symptoms
    • 10% BSA cutaneous burn can be fatal due to systemic toxicity
    • Copious water irrigation and observation for systemic features
    • Aggressive excision of coagulum prevents absorption of chromium from burn site

Acid burns

  • Formic acid
    • Coagulative necrosis
    • Reduced ventilation, HAGMA and haemolysis can all occur
    • Immediate decontamination and irrigation with water
    • IV bicarb may be required or exchange transfusions for severe haemolysis

Acid burns

  • Hydrochloric and sulfuric acid
    • Burn skin dark brown or black
    • Treat as for formic acid burns
    • Copious irrigation is usually sufficient to prevent severe skin burns

Acid burns

  • Hydrofluoric acid
    • Penetrates deeply unlike other acids
    • Products burns by:
      • 1) Hydro ions cause direct cellular damage
      • 2) Free fluoride ions scavenge intracellular cations, such as calcium and magnesium, disrupt cellular membranes and inhibit Na/K ATPase
    • Leads to systemic hypocalcaemia/hypomagnesaemia and hyperkalaemia
    • Free fluoride ions cause spontaneous depolarisation of nerve tissue and severe pain
    • Pain persists until all free fluoride ions neutralised
    • Initial dermal effects are minimal and are related to concentration rather than duration of exposure
      • >50% cause immediate pain and tisue damage
      • <20% no signs and symptoms until 12-24 hours later with blue-grey skin and surrounding erythema

Acid burns

  • Hydrofluoric acid
    • Treatment
      • Phase 1
        • Copious water irrigation for 30 minutes
        • If <20% concentration, brief exposure and decontamination initiated rapidly this may be enough
        • Severe, persistent pain denotes more severe injury and second phase required
      • Phase 2
        • Calcium gluconate topically (25mL of 10% calcium gluconate in 75mL of water-soluble lubricant) generously applied to affected skin to replace calcium ions and detoxify the enzyme-poisoning fluoride ions
          • Limited to mild, superficial burns as will not penetrate deeper burns
        • Severe burns require intradermal and intra-arterial injections
          • 0.5mL/cm2 of 10% calcium gluconate via 27G needle intradermal injection
          • Elimination of pain can be used as a guide to therapy

Acid burns

  • Hydrofluoric acid
    • Issues with intradermal injection
      • Limited delivery of calcium
      • Free calcium ions cause more pain initially
      • Vascular compromise if inject large volumes
      • Rapid penetration of hydrofluoric acid beneath nail bed requires nail removal and injection directly into nail bed
    • Contamination of hands, feet, digits or nails requires toxicology and plastics consult
    • Intra-arterial injection
      • Arterial line proximal to site involved
      • 50mL syringe with 10mL 10% calcium gluconate and 40mL 5% dextrose infused over 4 hours
      • Art line trace confirms siting in vessel as extravasation can be catastrophic
      • Can repeat if still painful at 4 hours

Acid burns

  • Hydrofluoric acid
    • Inhalational injury
      • Can cause immediate or delayed pulmonary injury
      • Admit all for observation
      • Nebulised calcium gluconate 1.5mL of 10% calcium gluconate into 4.5mL of sterile water for nebulisation
    • Ocular injury
      • Water irrigation for at least 30 minutes and urgent ophthal review
      • Calcium-containing irrigating solutions may be harmful and are not recommended
      • Systemic absorption is also possible
    • Systemic toxicity
      • VF due to systemic acidosis, hyperkalaemia, hypomagnesaemia and/or hypocalcaemia
      • Administer IV calcium and magnesium in major HFl acid burns before lab results back
      • Once hypoCa or hypoMg have developed, it is very hard to remedy the situation so need to be proactive

Acid burns

  • Methacrylic acid
    • Copious water irrigation
  • Nitric acid
    • Oxidation with yellow skin discolouration
    • Copious water irrigation
  • Oxalic acid
    • Binds calcium and prevents muscle contraction
    • Irrigate and IV calcium may be required

Alkali burns

  • Penetrate deeper and greater risk of systemic toxicity
  • May initially appear superficial but develop full-thickness over 2-3 days
  • Combine with proteins and lipids to form soluble protein complexes and soaps that permit hydroxyl ions to penetrate tissues
  • Soft, gelatinous, brownish eschars develop
  • Strong alkalis have pH >12

Alkali burns

  • Lyes
    • Strong, corrosive alkalis including ammonium, barium, calcium, lithium, potassium (caustic potash) and sodium (caustic soda) hydroxides
    • Immediate, voluminous and persistent irrigation is key
    • Extremely corrosive and penetrating requiring copious irrigation for long periods of time
    • Early surgical intervention and airway intervention for ingestion is key

Alkali burns

  • Lime
    • Calcium oxide
    • Converted by water to alkali calcium hydroxide
    • Upon skin contact, draws water out of skin
    • All dry lime particles therefore need to be brushed off prior to irrigation
    • Even small amount of water can cause exothermic reaction and burns
    • Brisk irrigation can then lessen burn and dissipate heat

Metal burns

  • When exposed to air, some elemental metal spontaneously ignite
  • Water is generally contraindicated for extinguishing burning metal fragments embedded in skin due to risk of ignition, exothermic reaction and further tissue injury
  • Can use class D fire extinguisher, smother with sand or cover with mineral oil
  • Wound debridement should include metal FB excision and placement in mineral oil to prevent further ignition

Hydrocarbons

  • Gasoline
    • Fat-dissolving corrosive injury (defatting dermatitis)
    • Resembles thermal scald
    • Can cause neurological, pulmonary, cardiovascular, GI and hepatic injuries
    • Treat by decontamination with soap and water and then as for a thermal burn
  • Hot tar
    • Usually more thermal than chemical burns (260 degrees)
    • If hot, the tar should be cooled to prevent continued thermal injury
    • Polysorbate (in many topical antimicrobials), baby oil and industrial removal agents (De-Solv-It) can all help to remove solidifed tar

Vesicants

  • Dimethyl sulfoxide (non-prescription topical agent for minor sprains/burns), cantharides (Spanish fly aphrodisiac) and mustard gas (chemical warfare)
  • Drying agents
  • Get ischaemia and anoxic necrosis at site of exposure
  • Immediate copious irrigation
  • Decontaminate with adsorbent agents e.g. flour, talcum powder and fuller’s earth if supply of water is limited
    • The wipe away with moist towel
  • Povidone iodine may be very helpful for sulfur mustard decontamination

Potassium permanganate

  • Concentrated solutions of this oxidising agents can produce dermal burns with thick, purple eschar of coagulated protein
  • Copiously irrigate

Alkyl mercury compounds

  • Reducing agents used in disinfectants and fungicides
  • Erythematous with blistering
  • Blister fluid is high in mercury content and continues the burning process
  • Need blister debridement, drainage and copious irrigation

Tear gas

  • Skin and mucosal irritation within 20-60 seconds of exposure
  • Can cause contact dermatitis
  • Inhalational and eye injuries can be severe
  • Need rapid removal and copious irrigation
  • Ocular irrigation is required with subsequent slit lamp exam
  • Arrange ophthal follow-up within 24 hours
  • Inhalational injuries require bronchodilators and oxygen therapy. No role for steroids

White phosphorous

  • Used in fireworks, firearms, insecticides, rodenticides and fertiliser
  • Ignites when exposed to air
  • Flaming droplets may embed beneath the skin and continue to oxidise
  • Copiously irrigate and immerse in water until completely debrided
  • Wood’s lamp examination aids debridement as it fluoresces
  • Copper sulfate solution can detoxify phosphorous but causes haemolysis and increased mortality (DO NOT USE)
  • Systemic absorption can cause hypocalcaemia, hyperkalaemia, hepatic and renal injury
  • Avoid direct contact with any secretions/body fluids and agent itself
  • Admit all and consider transfer to burns centre

Airbag burns

  • Sodium azide and cupric oxide solid propellants result in exothermic reaction and rapid inflation
  • Corrosives such as sodium hydroxide, nitric oxide, ammonia and multiple hydrocarbons can result from detonation leading to friction, thermal and chemical burns
  • Sodium hydroxide can cause chemical keratitis
  • Need slit-lamp examination and treat any burns as for alkali burns with copious prolonged irrigation with water or saline

Ocular burns

  • 30 minutes minimum water/saline irrigation
  • For severe alkali burns, up to 24 hours of irrigation may be required
  • Conjunctival sac pH to return to 7.4 is helpful for continuing irrigation decisions
    • However, if strong alkaline or hydrofluoric acid burns with obvious examination abnormality, should continue for at least 2-3 hours despite normal pH to ensure anterior chamber neutralisation
  • Can sweep fornices with a wet cotton applicator to remove any particular matter, particularly if irrigation is not neutralising pH effectively
  • IV narcotic analgesia may be required
  • Emergent ophthalmology is required

Last Updated on October 9, 2020 by Andrew Crofton