Chemical burns - pathophysiology and treatment - handout


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Chemical burns - pathophysiology and treatment - handout

  1. 1. Adapted from Palao et al, Chemical burns: Pathophysiology and treatment, Burns, 36 (2010) 295 – 304 Chemical burns: Pathophysiology and treatment Chemicals that can cause burns are numerous and common in industry, agriculture, and households and increasingly in domestic violence and warfare. Harm potential is often underestimated. Chemical burns are rare (3%) but carry significant morbidity and mortality (55% require surgery, 30% of burn deaths). See original article for images. Pathophysiology All burns cause protein denaturation, however chemical burns tend to be:  Associate with longer duration of exposure  Ongoing in the ED  Caused by more complex mechanisms than protein cross-linking and coagulation (e.g. hydrolysis) Severity depends on: (a) Concentration (b) Quantity of burning agent (c) Duration of skin contact (d) Penetration (e) Mechanism of action. 6 Mechanisms of action (1) Oxidation: The protein denaturation is caused by inserting an oxygen, sulphur, or halogen atom to viable body proteins. E.g. sodium hypochlorite, potassium permanganate, and chromic acid. (2) Reduction: Reducing agents act by binding free electrons in tissue proteins. Heat from exothermic reaction may cause a mixed picture. E.g. hydrochloric acid, nitric acid and alkyl mercuric compounds. (3) Corrosion: Corrosive agents cause protein denaturation on contact. Produce a soft eschar, which may progress to shallow ulceration. E.g. phenols, sodium hypochlorite, and white phosphorous. (4) Protoplasmic poisons: Produce their effects by causing the formation of esters with proteins or by binding or inhibiting calcium or other organic ions necessary for tissue viability and function. E.g. ester formers: formic and acetic acids, inhibitors: oxalic and hydrofluoric acids. (5) Vesicants: produce ischemia with anoxic necrosis at the site of contact. Characterized to produce cutaneous blisters. E.g. mustard gas, dimethyl sulfoxide (DMSO), and Lewisite. (6) Desiccants: cause damage by dehydration of tissues. Often exacerbated by heat production due to exothermic reactions. E.g. sulphuric and muriatic (concentrated hydrochloric) acids. Classification by type of chemical 1. Acids: Proton donors. Release H+ ions and ↓pH from 7 down to values as low as 0. Acids with a pH < 2 can produce coagulation necrosis on contact with the skin. A better predictor than pH alone is the amount of alkali needed to raise the pH of an acid to neutrality. This may reflect the strength of the acid involved. 2. Bases: Proton acceptors. Strip H+ ions from protonated amine groups and carboxylic groups. Alkalis with a pH > 11.5 produce severe tissue injury through liquefaction necrosis, which loosens tissue planes and allows deeper penetration of the agent. For this reason, alkali burns tend to be more severe than acid burns. 3. Organic solutions act dissolving the lipid membrane of cells and disrupting the cellular protein structure. 4. Inorganic solutions damage the skin by direct binding and salt formation. It should be noted that all of these reactions may be accompanied by exothermy, which contributes to tissue injury. Farooq Khan MDCM PGY3 FRCP-EM McGill University November 14 th 2011
  2. 2. Adapted from Palao et al, Chemical burns: Pathophysiology and treatment, Burns, 36 (2010) 295 – 304 Management General principles In addition to standard ATLS and Burn care, stabilisation, consultation with Poison Control, and transfer to Burn Units: Material Safety Data Sheets are mandated to be available for all chemicals present in the workplace, which can be valuable resources for potential systemic toxicity and side-effects of an agent. Decontamination  Remember to remove clothing  Early and copious water irrigation (0.5 – 2h) has been shown to reduce the severity of burn and hospital LOS  Monitoring of the lavage solution pH will give a good indication of lavage effectiveness and completion  Maintain 28-30° temperature for copious lavage to avoid hypothermia  Note exceptions to lavage above: o sulphuric and muriatic acids cause severe exothermic reaction with water o dry lime creates calcium oxide, potent alkali, in combination with water Neutralizing agents  Controversial theoretical benefits  Ideal agent would be sterile polyvalent (actively binds multiple substances), amphoteric, hypertonic, chelating molecule with active binding sites for acids, bases, oxidizing agents, reducing agent, vesicant, lachrymators, irritants, solvents, etc. E.g. Diphoterine being used in Europe  Risks include: o Agents own toxicity (may need toxic dose of antidote to neutralize amount of chemical) o Potential for exothermic reaction o Delay of hydrotherapy
  3. 3. Adapted from Palao et al, Chemical burns: Pathophysiology and treatment, Burns, 36 (2010) 295 – 304 Estimation of burns and local care  ABCs and resuscitation following thermal burn formulas  Assessment of depth and extent is challenging due to tanning and anaesthetic properties of some chemicals, i.e. deep burns can appear deceptively superficial  Lavage and excision of blisters  Chemotherapeutic agents, creams, dressings  Early excision and grafting of non-viable tissue  Ocular injury mandates Ophthalmology consultation, early copious irrigation is standard but new evidence to suggest it may have some harm, research ongoing into neutralizing agents (e.g. Diphoterine) Systemic toxicity and inhalational injury  Monitor end organ perfusion  Check pH and extended electrolytes  Examples of systemic toxicity o HF – hypocalcemia and V-fib o Formic acid – intravascular hemolysis, renal failure, pancreatitis  Aerosolize chemical exposures should be treated like smoke inhalation injuries, with O2, early intubation and mechanical ventilation using ARDS-like strategies 6 Specific agents Cement  Mechanisms of injury (1) Allergic dermatitis: caused by the reaction to its hexavalent chromate ions. Irritation from the sand and gravel within cement can similarly cause dermatitis. (2) Abrasions: The gritty nature of the coarse and fine aggregate in the cement is responsible for these lesions. (3) Chemical Burns: Most significant injuries. 65% calcium oxide (CaO) which is an alkali and dessicant. On contact with water becomes calcium hydroxide (Ca(OH)2), also alkali that can cause liquefaction necrosis.  Patients unaware of risks and insidious onset of symptoms (hours)  Commonly deep injuries to lower extremities  Remove clothing, clean with sterile water, apply topical antibiotic cream  Evaluate periodically for need for surgical excision and skin grafting  Special care of ocular and aerosolized exposures Hydrochloric/muriatic acid  Denatures proteins into chloride salts  Needs quick and continuous irrigation  Can produce upper airway edema and ARDS if fumes inhaled Hydrofluoric acid  Easily available and present in the community. Used in frosting, etching and polishing glass and ceramics, removal of metal castings, cleaning stone and marble, and in the treatment of textiles  Stored as a colourless liquid  Causes severe burns and systemic effects, despite minimally apparent cutaneous damage o H+ ions cause superficial burns
  4. 4. Adapted from Palao et al, Chemical burns: Pathophysiology and treatment, Burns, 36 (2010) 295 – 304 o Fl- penetrates down to the deeper soft tissue  interferes with cellular metabolism causing cell death and liquefactive necrosis  binds Ca++ and Mg++ causing systemic hypocalcemia and hypomagnesemia  inhibits Na+ -K+ ATPase causing efflux of K+ and E+ shifts at nerve endings causing extreme pain  Clinical presentation depends on: o route of exposure  Wide variety of systemic cardiac, respiratory, GI and neurological effects o concentration of acid  >50% - immediate tissue destruction and pain  20-50% - burns become apparent within hours  <20% - may take up to 24h to appear o duration of contact o penetrability or resistance of the tissue exposed  Most frequently in digits, subungual area. Can be other skin, ocular, inhalational or digestive  Symptoms typical of ↓Ca++ and ↓Mg++ generally absent o Serum calcium levels and electrocardiogram (↑QT) are important monitors o Fl- may be direct myocardial irritant and can be removed by HD  Treatment includes four phases: o Hydrotherapy – immediate and prolonged o Topical treatment – Controversial. Try to inactive Fl- and create insoluble fluoride salt.  Mg compounds: generally ineffective and anecdotal  Quaternary ammonium compounds (e.g Hyamine) Multiple proposed mechanisms, but may be too toxic in doses required to neutralize 1 cc of 20% HF solution.  Ca++ gel: easily applied, but poorly permeable and stains skin o Infiltration – Ca++ gluconate 10% 0.5ml SC/cm2 of burned tissue until painless. Consider nail removal o Intra-arterial infusion – CaCl2 in severe digital burns with large amount of Fl- ions to be neutralized. Controversial as exposure may be fatal despite treatment Phosphorus  Most frequently used in military where  White phosphorus ignites in the presence of air and burns until the entire agent is oxidized or the oxygen source is removed  Irrigation with water is the most important point of treatment  Removal of macroscopic clusters of phosphorus in contact with patient. Application of a 0.5% copper sulphate solution impedes oxidation and turns the particles black, making identification and removal easier.  Alteration of calcium, phosphorus or cardiac changes can occur Strong Alkali  Lime(CaO + Ca(OH)2), NaOH, and KOH present in many household cleaners  Mechanisms 1. Saponification of fat is an exothermic reaction severe tissue damage through heat. Destruction of fat allows increased water penetration of the alkali into the burn eschar, destroying the natural water barrier of lipids. 2. Extraction of considerable water from cells causes damage due to the hygroscopic nature of alkalis, causing extensive cell death and damage to tissues. 3. Alkalis dissolve proteins of the tissues to form alkaline proteinates, which are soluble and contain OH- ions that cause further chemical reaction initiating deeper tissue injury (liquefaction necrosis).
  5. 5. Adapted from Palao et al, Chemical burns: Pathophysiology and treatment, Burns, 36 (2010) 295 – 304  All clothes should be removed and the dry residues of alkali (e.g. lime) should be brushed away  Washing induces : - dilution and elimination of a chemical substance - attenuation of the chemical and exothermic reaction - suppression of any raised tissue metabolism - anti-inflammatory action - suppression of the hygroscopic action - return skin pH levels to normal  Irrigate 2h with 4h rest, maintain body temp. and use appropriate tanks with drains (esp. for large BSA)  Once stable, tangential excision of deep burned tissue with skin grafting Sulphuric acid  Non-occupational exposures can be related to violence and often involve drain cleaner  Along with precursor sulphur trioxide cause dehydration and excessive heat in tissues leading to tissue coagulation and microvascular thrombi.  Remove clothing and irrigate with soda lime/soap wash before copious lavage with water  Nitric oxide burns similar but may look deceptively superficial Vesicant chemical warfare agents  Lewisite (L) and Sulphur Mustard (SM) gases  Affects all epithelia with initial symptoms of burning eyes/throat and suffocation  Delayed (24h) partial thickness injury with large bullae and delayed healing (months) due to damaged dermis  Severity of lesion dependent upon the dose of the agent, ambient temperature and moisture level in the skin  Blister aspiration and/or deroofing, epidermal removal, physical debridement, irrigation, topical antibiotics and sterile dressings to treat cutaneous SM burns