Chemical Burns

Published on 14/03/2015 by admin

Filed under Emergency Medicine

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1253 times

190 Chemical Burns

Epidemiology

Chemical burns are an unusual type of burn because the tissue injury is caused by the chemical reaction rather than by thermal damage. Chemical burns are common at work, at home, or in association with hobbies. One study found 22% of all pediatric burns to be a result of chemical burns,1 whereas other studies have estimated the percentage of admitted burned patients with chemical burns to be between 10% and 14%.2,3 With the recent concerns over terrorism, chemical agents have been emphasized as a possible method of attack, so knowledge of chemical burns is critical in the education of today’s emergency physicians. In addition, failure to recognize chemical burns or to treat them appropriately can have a detrimental impact not only on patients but also on care providers.

Pathophysiology

Different chemical burns affect tissue by different mechanisms. Table 190.1 provides different categories of chemical agents and their mechanism of tissue damage. Most chemical burns involve skin; accordingly, knowledge of skin anatomy is key to understanding the pathophysiology of various chemical burns because of the link to treatment. A direct injury results when the epidermis is penetrated. Systemic absorption is possible once the injury extends through the dermis.

Table 190.1 Chemical Agents and Their Mechanisms of Tissue Damage

TYPE OF CHEMICAL AGENT MECHANISM OF TISSUE DAMAGE EXAMPLE OF AGENT
Acids Coagulative necrosis Sulfuric acid
Alkali agents Saponification and liquefactive necrosis Calcium hydroxide
Desiccants and vesicants Dehydration of cells through exothermic reactions, release of amines within cells Nitrogen mustards
Oxidizing and reducing agents Denaturing of proteins and direct cytotoxic effects Bleach
Protoplasmic poisons Formation of salts with cellular proteins Picric acid

Differential Diagnosis and Medical Decision Making

With chemical agents, the initial complaint may be a red, burning rash; because some agents cause a delayed onset of symptoms, chemical burns should be considered in the differential diagnosis of all rashes. However, there is usually a direct cause-and-effect relationship that makes the diagnosis easy. Treatment, however, varies with the agent, identification of which may be more difficult. The most important task is to identify the offending agent. Various resources can be used, but the best source of information is usually patients themselves. The job site may provide clues, but the employer should also have the material safety data sheet available. Paramedics or others can bring in bottles of the agent, which may have a list of ingredients. The presence of systemic symptoms may also suggest specific agents.

Although the specific agent may be difficult to identify without other information, further testing can assist in the diagnosis. pH paper can be used on the wound to determine the presence of acid or base. A chemistry panel may suggest acidosis, whereas hypocalcemia may suggest exposure to hydrofluoric acid.

The gowns and gloves readily available in the hospital are not sufficient for many substances. Most chemicals penetrate these materials immediately. Relatively inexpensive, chemical-resistant, multilayer suits are available. Furthermore, respiratory precautions may be indicated for some agents. For these reasons, both hospital and community resources may be required for safe and expedient decontamination.

Treatment

The first step in caring for patients with chemical burns is removal of the offending agent. This involves copious irrigation with several liters of either water or normal saline solution. All contaminated clothing should be removed, with care taken to ensure that health care providers are not exposed.

Directed Therapies

Specific agents are known to cause specific toxicities. If the substance is known, therapy should be directed against that toxicity (Table 190.2).

Table 190.2 Specific Therapies for Chemical Burns

AGENT SPECIFIC TOXICITY ADDITIONAL TREATMENT
Hydrofluoric acid Severe hypocalcemia and continued liquefactive necrosis Superficial wounds: calcium gluconate 2.5% gel
Deep wounds: local infiltration (10% solution) or intraarterial injection (5% solution) of calcium gluconate
Formic acid Severe acidosis Bicarbonate administration, possible exchange transfusions or hemodialysis for high serum levels and persistent acidosis
Cement (alkali burn) Persistent burns when exposed to water if not irrigated away completely Thorough irrigation
Phenol Systemic absorption causing central nervous system depression, coma, and death Because a more dilute solution is absorbed more rapidly, deep, continuous irrigation is performed until undiluted polyethylene glycol solution is available for topical application; all other treatment is supportive for systemic symptoms
White phosphorus Continued thermal burning resulting from burns on exposure to oxygen; systemic absorption causing acidosis and electrocardiographic abnormalities, possibly sudden death Removal of as much phosphorus as possible through irrigation with cool water, then placement of a solution of 5% sodium bicarbonate and 3% copper sulfate in 1% hydroxyethyl cellulose
Elemental metals (sodium, potassium) Exothermic reaction when exposed to water Wiping away of material and contacting a poison control center for disposal instructions
Nitrates Methemoglobinemia Administration of methylene blue
Monochloroacetic acid Systemic lactic acidosis Administration of dichloroacetate and possible hemodialysis
Nitrogen mustards Vesicle formation Steroid and antibiotic dressings after copious irrigation

Hydrofluoric Acid

Hydrofluoric acid is used in glass etching, automotive and industrial wheel cleaning, brick cleaning, semiconductor manufacturing, metal purification, and other industries. Immediate irrigation is indicated, as with other chemical injuries, but hydrofluoric acid can cause progressive tissue damage. Extensive exposure of an uncovered arm or leg can be fatal. Pain may be delayed but can subsequently continue for hours or days. The hydrofluoric acid ion does not dissociate but rather penetrates tissues deeply and reacts with calcium and magnesium. Hypocalcemia can result.

Patients with mild, limited superficial exposure can be treated with topical calcium gluconate, which must usually be mixed in the emergency department by combining calcium gluconate powder with commonly available lubricant jelly. Affected fingers and hands can be placed in a medical glove that contains the solution.7

Subcutaneous infiltration of 10% calcium gluconate may help relieve the pain, but it also irritates the tissue. Slow infiltration with the smallest available needle, preferably 30 gauge, or dilution of the solution may minimize tissue damage. Intraarterial administration of 10 mL of calcium gluconate mixed in 50 mL of 5% dextrose in water through the radial or ulnar artery via an arterial line over a 4-hour period may be beneficial for severe exposures to the hand.

Cardiac dysrhythmias may result from systemic hypocalcemia and hypomagnesemia. The electrocardiogram should be monitored for QT prolongation. Calcium and magnesium should be administered as needed.