Chemical Burns

Introduction

Chemical burns represent a small percentage of burn injuries yet up to one third of burn-related deaths. Many common household and industrial compounds have the potential to induce severe chemical burns. The American Association of Poison Control Centers' National Poison Data System 2014 annual report demonstrated 199,291 cases of exposure to cosmetic or personal care products; 198,018 household cleaning substances; 83,005 pesticides; 31,903 hydrocarbons; and 38,975 unspecified chemicals. Exposure to specific chemicals, including acids, alkalines, peroxides, bleaches, and phenols, in 2014 totaled 38,594, which was up from the 38,552 cases of exposures in 2013. The unfortunate reality concerning the ease of access to toxic products is evident in the presence of a rising number of pediatric exposures to chemical injuries. Most chemical burns involving children are secondary to common household products. Domestic chemical burn injuries are often due to poor labeling and storage, as well as secondary to intentional assault and suicide attempts. The most commonly affected areas of the body are the face, eyes, and arms and legs. As a result, the length of hospital stay and duration of healing tend to be greater with chemical burns. The majority of these deaths are related to the ingestion of chemical substances. This chapter provides general principles for the treatment of chemical injuries.

Pathophysiology

All burn wounds, whether caused by chemical or thermal sources, have in common the denaturation of key structural and functional proteins. The structure of biological proteins involves not only a specific amino acid sequence but also a three-dimensional structure depending on weak forces, such as hydrogen bonding or van der Waals' forces. These three-dimensional structures impart biological activity to the proteins and are easily disrupted by outside influences, specifically chemical and thermal energy sources. Weak bonds are impaired by heat energy sources degrading and denaturing proteins. Moreover, any variations in pH or dissolution of surrounding lipids may neutralize a protein and disrupt its function. Direct chemical effects on a reactive group in a protein will similarly render it inactive.

The severity of a chemical burn injury is determined by several factors:

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  Concentration of chemical in contact or ingested

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  Quantity of chemical agent

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  Manner and duration of contact (skin or ingestion)

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  Extent of penetration

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  Mechanism of action of the chemical

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  Physical state of agent (liquid, solid, gas).

There are six mechanisms of action for chemical agents in biological systems, classified by how they denature and damage proteins:

• 1.

  Reduction : Reducing agents act by binding free electrons in tissue proteins, causing denaturation. In general, they do so by reducing the amide link. Examples include hydrochloric acid, nitric acid, alkyl mercuric compounds, ferrous iron, and sulfite compounds.

• 2.

  Oxidation : Oxidizing agents are oxidized on contact with tissue proteins. These agents cause destruction by inserting oxygen, sulfur, or halogen atoms to structural and functional proteins. Byproducts are often toxic and continue to react with the surrounding tissue. Examples of oxidizing agents are sodium hypochlorite, potassium permanganate, chromic acid, and peroxide.

• 3.

  Corrosive agents : Corrosive substances denature tissue proteins on contact and form eschar and a shallow ulcer. Examples of corrosive agents include phenols, cresols, white phosphorus, dichromate salts, sodium metals, lyes, sulfuric acid, and hydrochloric acid.

• 4.

  Protoplasmic poisons : These agents produce their effects by binding or inhibiting calcium or other organic ions necessary for tissue viability and function. These agents form esters with proteins and/or chelate calcium or other ions. Examples of protoplasmic poisons include “alkaloidal” acids; acetic acid; formic acid; and metabolic competitors and inhibitors such as oxalic acid, hydrofluoric acid, and hydrazoic acid.

• 5.

  Vesicants : Vesicant agents produce ischemia with necrosis at the site of contact. There is associated tissue cytokine release and blister formation. Examples include cantharides, dimethyl sulfoxide (DMSO), mustard gas (sulfur and nitrogen), and Lewisite.

• 6.

  Desiccants : These substances cause damage by dehydrating tissues and exothermic reactions, causing the release of heat into the tissue. Examples include sulfuric acid, muriatic acid, calcium sulfate, and silica gel.

Chemical burns are often described as acidic or alkali. Acids act as proton donors in the biological system, and strong acids have a pH less than 2. Alkali, or basic, materials capable of producing injury typically have a pH greater than 11.5. In general, alkaline materials cause more injury than acidic compounds. Whereas acids cause coagulation necrosis with precipitation of protein, the reaction to alkali is “liquefaction” necrosis, allowing the alkali to penetrate deeper into the injured tissue. The presence of hydroxyl ions within these tissues increases their solubility, allowing alkaline proteinases to form when the alkalis dissolve the proteins of the tissues. Organic solutions tend to dissolve the lipid membrane of cell walls and cause disruption of cellular architecture as their mechanism of action. Inorganic solutions tend more to remain on the exterior of cells but may act as transporters to carry the above-mentioned agents that denature proteins or form salts with proteins themselves.

General Principles of Management

The most important aspects of first aid for patients with chemical burns involve removal of the offending agent from contact with the patient—stop the burn. This requires removal of all potentially contaminated clothing and copious irrigation. Irrigation of chemical burns requires protection of healthcare providers to prevent additional injuries and additional patients. In addition, the wounds should not be irrigated by placing the patient into a tub, thereby containing the chemical and spreading the injurious material. Irrigation should be a large-volume shower or decontamination station and drained out of an appropriate drain. Immediate copious irrigation has been shown to reduce the extent and depth of injury, especially to eyes. No measure of adequacy of lavage has been developed, but monitoring the pH from the effluent can provide quantifiable information as to adequacy of lavage. Thirty minutes to 2 hours of lavage is often necessary.

Safety data sheets (SDS) are mandated to be available for all chemicals present in the workplace. These can be valuable resources for potential systemic toxicity and adverse effects of an agent. Further assistance is available from regional poison control centers for household chemicals or unidentified agents.

The use of neutralizing agents is generally contraindicated. Neutralizing agents cause exothermic reactions, producing a thermal component along with a chemical injury. When the chemical agent is known and an appropriate antidote to support the physiologic changes incited by the original agent is known, some benefit to its use has been documented but has not been found to be superior to water for irrigation. An example is calcium gluconate for hydrofluoric acid burns (discussed later in the chapter).

Treatment paradigms remain unchanged for burn and trauma patients with strict adherence to Advanced Trauma Life Support (ATLS)and Advanced Burn Life Support (ABLS)guidelines. After airway patency is assured, adequate air movement and hemodynamics should be maintained. Conventional thermal burn formulas are used for resuscitation at maintaining end-organ perfusion. Monitoring of urine output remains paramount to assessment of adequacy of end-organ perfusion and hence resuscitation. Systemic disturbances of pH are potential complications and must be monitored until acid–base disorder and electrolyte abnormalities are corrected.

The typical large-volume lavage required to adequately dilute chemical exposures puts the patient at potential risk for hypothermia, both from evaporative cooling losses and from the use of unwarmed lavage fluid. Principles of wound care for chemical burns are typically the same as for thermal burns. Early excision and grafting of obviously nonviable tissue is advocated, particularly in light of the observation that chemical burns tend to be deeper than they initially appear. As a result, they tend to heal more slowly.

Specific Agents