Introduction

Many compounds have the potential to induce chemical burns. Individuals are exposed in both occupational and personal environments. The American Association of Poison Control Centers’ (AAPCC) National Poison Data System (NPDS) 2008 annual report demonstrated 224 884 cases of exposure to cosmetic/personal care products, 213 595 household cleaning substances, 93 998 pesticides, 46 418 hydrocarbons, and 44 736 unspecified chemicals.¹ In 2007, 137 055 cases of exposure were specific to acids, alkalines, peroxide, bleach, and phenol products alone.² The 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 extremities. Chemical burn injuries compose only 3% of all burns, yet they are the etiology behind approximately 30% of burn deaths. As a result, 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.³ This chapter will provide general principles for the treatment of chemical injuries.

Pathophysiology

All burn wounds, whether due to chemical or thermal sources, have in common the denaturation of proteins. The structure of biological proteins involves not only a specific amino acid sequence, but also a three-dimensional structure dependent 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. Heat energy breaks these weak bonds to unfold and denature proteins. In addition, changes in pH or dissolution of surrounding lipids may stabilize a protein and disrupt its function. Direct chemical effects on a reactive group in a protein will similarly render it ineffective.

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

• concentration

• quantity of chemical agent

• manner and duration of skin contact

• extent of penetration

• mechanism of action

• phase of agent (liquid, solid, gas).

There are six mechanisms of action for chemical agents in biological systems:⁴

1 Reduction: Reducing agents act by binding free electrons in tissue proteins, causing denaturation. Examples include hydrochloric acid, nitric acid, alkyl mercuric compounds, ferrous iron, and sulphite compounds.⁵

2 Oxidation: Oxidizing agents are oxidized on contact with tissue 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, sulphuric 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. Examples of protoplasmic poisons include ‘alkaloidal’ acids, acetic acid, formic acid, and metabolic competitors/inhibitors such as oxalic, hydrofluoric, 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 (sulphur 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 sulphate, and silica gel.

Within these groups there are different categories of compound. Chemical burns are often described as acidic or alkalinic.⁶ Acids act as proton donors in the biological system, and strong acids have a pH < 2. Alkali, or basic material, capable of producing injury typically have a pH > 11.5.⁷ In general, alkaline materials cause more injury than acidic compounds. Acids cause coagulation necrosis with precipitation of protein, whereas the reaction to alkali is ‘liquefaction’ necrosis allowing the alkali to penetrate deeper into the injured tissue.⁸ The presence of hydroxyl ions within these tissues increases their solubility, allowing alkaline proteinates to form when the alkalis dissolve the proteins of the tissues.⁹ 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 vehicles 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 chemical burns involve removal of the offending agent from contact with the patient. This requires removal of all potentially contaminated clothing and copious irrigation. Irrigation of chemical burns requires protection of healthcare providers to prevent additional injuries. Further, 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 large volume and drained ‘to the floor,’ or out of an appropriate drain. Immediate copious irrigation has been shown to reduce the extent and depth of injury, especially to eyes.¹⁰ 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 may be necessary.

Material Safety Data Sheets (MSDS) are mandated to be available for all chemicals present in the workplace. These can be valuable resources for potential systemic toxicity and side 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 discouraged. The practical problems encountered with their use are exothermic reactions causing further thermal damage. When the burning agent is known and an appropriate antidote is known, some benefit to its use has been demonstrated.¹¹ Despite this, no agent has been found to be more effective than plain water for irrigation.¹²

Burn and trauma patients should be managed with the same principles in mind. After airway patency is assured, adequate air movement and hemodynamics should be maintained. Conventional thermal burn formulas are used for resuscitation. 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 non-viable 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

Acids

Acetic acid

Acetic acid, also known as ethanoic acid, ethylic acid, and methane carboxylic acid, is a mild chelating agent. Solutions diluted to <40% concentrations, such as table vinegar and hair-wave neutralizing products, are usually harmless, but if used inappropriately may cause injuries such as partial-thickness burns. In such cases, initial treatment involves irrigation.^13,¹⁴

Carbolic acid (phenol)

Carbolic acid is a hydrocarbon derived from coal tar, which acts to cause damage secondary to its ability to induce denaturation and necrosis.^15,¹⁶ The most common adverse effects are dermatitis, abnormal pigmentation, and burns to the skin.¹⁷ Concentrated amounts of phenol are caustic; therefore, prolonged skin contact causes partial- or full-thickness burns. These burns tend to become extensive prior to detection, secondary to the local anesthetic properties of phenol. Ingestion of as little as 1 g may cause death. Systemic effects include ventricular arrhythmias,¹⁸ pulmonary edema, stridor, and tachypnea. Locally, conjunctivitis, corneal edema/necrosis, and skin necrosis result.¹⁵

Acute poisonings are potentially fatal, hence prompt action is necessary with copious irrigation.¹⁹ Polyethylene glycol (PEG molecular weight 300 or 400 Da) has been shown to be of potential benefit,^20,²¹ but large-volume lavage should not be delayed while PEG application is begun. Reports in the literature indicate that intravenous sodium bicarbonate may be of use to prevent some of the systemic effects of phenol.²²

Chromic acid

This acid causes non-painful but corrosive ulcers upon contact with the skin.^23,²⁴ Ulceration of the nasal septum and bronchospasm can also occur with inhalation. This agent will cause protein coagulation. Peak blood levels are thought to be achieved within 5 hours of exposure. Symptoms may occur with just 1% total body surface area (TBSA) burn, but a 10% burn or greater is often fatal owing to its systemic effects. Irrigation is the primary treatment for exposure, but in an industrial setting, washing with a dilute solution of sodium hyposulfite or water, followed by rinsing in a buffered phosphate solution, may be a more specific antidote. Dimercaprol may be used at 4 mg/kg IM every 4 hours for 2 days, followed by 2–4 mg/kg/day for 7 days in total to treat the systemic effects. Dialysis in the first 24 hours is a reasonable means to remove circulating chromium and to address existing electrolyte imbalances. Exchange transfusion may be necessary. Various ointments containing products such as 10% calcium EDTA or ascorbic acid are available for small superficial burns.^14,²⁵ There have been case reports supporting the early excision of chromic acid burn to assist in preventing systemic toxicity.^26,²⁷

Epichlorohydrin acid

Epichlorohydrin is a rare, corrosive carcinogen that is colorless and exudes a garlic-like odor. It is used in the production of glues, plastic, glycerols and resins, as well as in paper reinforcement and water purification.²⁸ It can also be converted into a binder used in the production of explosives.²⁹ At our burn center in Galveston, Texas, four patients were exposed to epichlorohydrin after an industrial accident. The TBSA burned ranged from 10% to 60%, with the largest burn showing rapid progression to a full-thickness wound within hours. Management of these patients was commenced with copious irrigation and hemodynamic monitoring (Fig. 41.1).

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