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Chemical Injuries
Key Concepts
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For chemical injury, the degree of skin destruction is determined mainly by the properties of the toxic agent, its concentration, and the duration of its contact.
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Chemical injuries are commonly encountered after exposures to acids and alkalis.
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Hazardous materials (HazMat) are substances that can cause physical injury and damage the environment if improperly handled.
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In dealing with HazMat incidents, two distinct goals need to be achieved: (1) Containing the HazMat, extinguishing the fire and explosions, and eventually cleaning the site, and (2) evacuating victims exposed to the HazMat from the scene, decontaminating, and rapidly evaluating for treatment.
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Decontamination consists of removing contaminated clothing and hydrotherapy (i.e., washing of the skin) for the majority of exposures. For lithium, potassium, and sodium exposure, hydrotherapy is contraindicated because of the exothermic reaction upon contact with water.
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Alkali burns tend to penetrate deeper into tissue layers than acidic burns; and as a result, are associated with greater morbidity.
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Hydrofluoric acid burns can be associated with significant systemic hypocalcemia.
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Exposure to various toxic gases can occur from common industrial settings, and knowledge of these agents is necessary for proper treatment by the emergency clinician.
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Unconventional chemical weapons may be categorized into four major classifications: nerve agents, vesicants, choking agents, and cyanide agents.
General Approach to a Hazmat Event
Foundations
Background and Importance
During the past century, there has been a dramatic increase in the number of chemicals produced. Worldwide, there are more than 5 million known chemicals, with thousands of new chemicals developed annually. The chemical industry is a critical component to the US economy, producing more than 600,000 jobs. Large chemical incidents, such as the 1974 cyclohexane vapor leak and subsequent explosion in Flixborough, UK, and the 1984 methyl isocyanate release from a pesticide plant in Bhopal, India, have drawn large-scale media attention, and many smaller chemical spills occur daily.
It is estimated that 25,000 to 35,000 chemical incidents occur annually in the United States alone, with the majority resulting from either equipment failure or human error. Many individuals suffer injuries or deaths annually due to these chemical spills. While these chemical incidents can occur in rural or urban environments, they are more common in rural areas. Individuals living close to an industrial complex may be exposed to a chemical following inadvertent release from the industrial site. However, other individuals living far from any stored chemicals may be exposed due to accidents during transport.
It is estimated that half of all pesticide or agricultural chemical spills occur during transportation. The transport of hazardous materials occurs throughout the United States; it is estimated more than 1 million hazardous substances are shipped throughout the United States daily. These chemicals, which include acids, alkalis, and other highly reactive substances, not only are found throughout industry but also are ingredients in many household products. Exposure to these substances can result in multi-system injuries.
A hazardous material (HazMat) is defined as a substance, including gases, solids, or liquids, that has the potential to cause harm to people or the environment. Historically, the Hazardous Substances Emergency Events Surveillance (HSEES) system collected information on chemical exposures, but this program concluded in 2009. The following year, the National Toxic Substances Incidents Program (NTSIP) was established, which compiles data from multiple sources to perform chemical surveillance. The most commonly released hazardous substances are volatile organic compounds, herbicides, acids, and ammonia. Various other products, such as cement, drain cleaners, and gasoline, are also hazardous, and exposure can result in severe disability or death.
Community Preparedness and HazMat Response
HazMats are found throughout society, including rural and urban settings. Furthermore, because these substances are often transported on highways and railroads, a HazMat exposure could potentially occur in any community. While industrial settings account for the largest percentage of chemical incidents, exposures in rural residential settings and agricultural settings occur. First responders, paramedics, and members of the HazMat response team must work together to identify toxic chemicals and assess hazardous environments. Placards, shipping papers, United Nations chemical identification numbers, and markings on shipping containers help identify the offending agent. The Chemical Transportation Emergency Center (CHEMTREC) in Arlington, Virginia, maintains a 24-hour telephone hotline ( Box 55.1 ) to assist in the rapid identification and management of hazards caused by chemical agents. Standardized placards have also been developed by the National Fire Protection Association (NFPA). These placards use four diamonds to identify specific hazards associated with this project. In addition, regional poison control centers (see Box 55.1 ) provide specific health information regarding individual chemicals.
Box 55.1
Important Phone Numbers to Assist in the Identification and Management of Chemicals and Chemical Injuries
CHEMTREC: 1-800-424-9300
Poison Control: 1-800-222-1222
Although placards can identify chemicals in the case of a known industrial exposure, it is not always clear an exposure has occurred. The challenges in identifying a HazMat scene are highlighted in Japan, where there has been an epidemic of chemical suicides with hydrogen sulfide gas inside locked cars. Following widespread internet awareness of this situation, there were a series of similar “copy-cat” incidents in the United States. Such exposures put first responders at particularly high risk of chemical injury, because they might have been unaware of any history of potential chemical exposure.
Contingency Plan
The contingency plan for HazMat management is comprised of two distinct parts: initiation of the site plan, and evacuation. Initiation of the site plan begins after the specific offending agent has been identified and the surrounding environment has been assessed. It is only after the substance has been identified that the risks to the public and the environment can be accurately identified. First responders should be trained to recognize the potential for a HazMat incident and establish a perimeter. During the evacuation phase, the HazMat technicians are specifically trained in the use of personal protective equipment (PPE), establishing entry into a HazMat scene, victim rescue, and determining the type and extent of a HazMat emergency. A central command post should be established in an area far enough from the incident to avoid direct contamination. Local geographic and environmental factors (e.g., wind direction and speed) may need to be considered when choosing a location for the command post, depending on the specific chemicals involved. The command post should coordinate the activities of the HazMat team with those of the emergency medical services personnel, firefighters, police officers, and other relevant personnel.
Anatomy, Physiology, and Pathophysiology
Most chemical agents cause skin damage by producing a chemical reaction rather than a hyperthermic injury. However, certain chemicals can generate significant heat production via an exothermic reaction after exposure to moisture. Nonetheless, the majority of dermal injuries result from direct damage to the skin rather than from a hyperthermic injury. The type of chemical reaction produced depends on the properties of the individual agent. In general, the degree of damage correlates directly with the toxic agent’s concentration and duration of exposure. Several other factors contribute to the degree of injury—for example, areas of the body where the skin is particularly thin (e.g., face, scrotum) are more at risk than areas of the body where the skin is thicker (e.g., palms of hands and soles of feet). Skin that is thin or broken is at risk for more severe injury.
Clinical Features and Differential Diagnoses
Exposure to acidic compounds can produce protein denaturation and subsequent coagulative necrosis . In theory, the eschar limits the depth by which an acid can penetrate. Various acids produce eschars with characteristic colors. For example, nitric acid burns result in a yellow eschar, whereas sulfuric acid burns result in a black or brown eschar. Hydrochloric acid and phenol burns produce a white to gray-brown eschar. Despite the eschar formation, profound chemical burns can occur following exposure to an acid. Alkali agents, in contrast, produce a saponification and reactive liquefactive necrosis . Because there is no eschar to limit penetration, alkali burns tend to penetrate deeper into the tissues, which results in significant tissue damage.
Other infections (e.g., cutaneous anthrax), injury (e.g., full-thickness burn), or envenomation (e.g., Brown recluse spider bites or Loxosceles sp.) that result in eschar formation can be confused with chemical injury. However, history and physical findings differ, allowing for distinction from chemical injury. For example, a splash pattern may be seen following exposure to liquid chemicals. Ocular injection may be seen following exposure to chemical fumes that affect mucosal membranes. Wheezing may be heard following various inhalational injuries.
Diagnostic Testing
Patients with significant burns or systemic toxicity are required to do a complete blood count, metabolic profile, including serum electrolytes, with hepatic and renal function tests. Monitor the urine output and check for infection or sepsis; an arterial or venous blood gas and serum lactic acid level is recommended. A chest radiograph is obtained following inhalational injuries.
Management
In dealing with a HazMat incident, two distinct processes occur simultaneously. First, the scene should be secured; this involves containing the substance, extinguishing fires, and controlling other environmental hazards. The second process involves treatment, which begins with decontamination. The exact decontamination depends on the specific agent and route of exposure. In general, all decontamination should be performed before arrival in the emergency department (ED). Individuals who are not exposed to the hazardous material are kept safely away from the scene to prevent subsequent exposure.
At the outset of any contamination event, the offending agent may not be known. Therefore, first responders and those having direct contact with exposed patients must wear appropriate PPE. Once the first responder is dressed appropriately, decontamination begins by removing the patient’s contaminated clothes. It is critical that dry (anhydrous) chemicals can be brushed off the patient’s skin, to the extent feasible, followed by copious irrigation with water delivered under low pressure. Ideally, the contaminated water will be contained on the scene for appropriate disposal. Liquid chemicals can be copiously irrigated directly. Decontaminate the patient before entering the ED if it was indicated but not performed on scene. The primary and secondary survey can occur simultaneously with decontamination.
Although the exact requirements for PPE among hospital personnel are somewhat controversial, at a minimum all personnel involved with decontamination should wear chemical-resistant clothing with a hood, boots, eyewear, at least two layers of gloves, and some form of respiratory protection.
The initial management of the chemically burned patient involves removing the individual from the hazardous environment. Because various chemicals will continue to destroy tissues until they are removed from the skin, the clothing should be removed, and prompt decontamination measures should be initiated at first chance.
Hydrotherapy involves the gentile irrigation of a large volume of water under low pressure for a prolonged time. Such therapy dilutes the toxic agent and washes it out of the skin. High-pressure irrigation should not be used, because it can drive the chemical deeper into the tissues, as well as produce splattering of the chemical into the eyes of the patient or rescuer.
Water should be used for irrigation after acid or alkali burns. Chemical neutralization may be more deleterious to victims with chemical burns. Additionally, it has been hypothesized that neutralizing agents produced additional heat, thereby augmenting the burn. Although the same effect may occur when certain chemicals come in contact with water, large volumes of water tend to limit the exothermic reaction. More recently, scientists began to question the belief that neutralization of an alkaline burn of the skin with an acid increases tissue damage because of the exothermic nature of acid-base reactions. Nonetheless, at present, we recommend irrigation with water alone as the best method for decontamination. Not all agents are best decontaminated with irrigation or hydrotherapy. Dry chemical agents, such as lye or elemental metals (e.g., sodium), should be brushed away prior to instituting hydrotherapy. Elemental metals (e.g., sodium or potassium) may produce exothermic reactions when combined with water. To minimize the exothermic reaction from such compounds, mineral oil may be applied to the skin before water. However, copious irrigation should not be delayed while waiting for mineral oil. In addition to lye and elemental metals, some argue that phenol (carbolic acid) should not be irrigated with water owing to concern for enhanced skin penetration after exposure to water. The use of a substance that has both hydrophobic and hydrophilic properties for irrigation (i.e., polyethylene glycol [PEG]) has not been proven to exhibit clear benefit over water alone; therefore, hydrotherapy should not be delayed while waiting for PEG. If PEG solution is used for decontamination, a low-molecular-weight PEG solution (200 to 400 Da) is preferred. This solution is different than the PEG solution typically used for gastrointestinal procedures.
Disposition
Treat patients in a similar manner as those with thermal burns, and criteria for transfer to a burn center are identical (see Chapter 54 ). Those with minor symptoms, in whom pain is controlled, and who lack systemic symptoms can be referred home. Admit patients with systemic toxicity, significant opioid analgesic requirements, and those requiring systemic administration of an antidote (e.g., intra-arterial calcium for hydrofluoric acid).
Ocular Injuries
Foundations
Background and Importance
Chemical burns to the eye require emergent management due to the potential for irreversible vision loss. Common causes include inadvertent handling of chemicals with resultant splash injury, exploding batteries, airbag deployment, and intentional assaults.
Anatomy, Physiology, and Pathophysiology
Alkali burns can initially appear trivial, but because of an interaction with lipids in the corneal epithelial cells, a liquefaction necrosis results, and deep penetration through the corneal stroma can ensue. The injury can occur rapidly; for example, anhydrous ammonia can penetrate the anterior chamber in less than 1 minute, resulting in complete blindness.
There are numerous grading systems that have been developed to describe ocular burns, including the Roper-Hall classification, which divides the injury into four grades based on the amount of corneal haze and perilimbal ischemia; and the Dua classification, which has six grades, and is based on the amount of limbal involvement ( Table 55.1 ). Exact classification systems are not particularly relevant for the emergency physician.
Table 55.1
Dua Classification
| Grade | Prognosis | Clinical Findings | Conjunctival Involvement |
|---|---|---|---|
| I | Very good | 0 clock hours of limbal involvement | 0 |
| II | Good | <3 clock hours of limbal involvement | <30% |
| III | Good | 3 to 6 clock hours of limbal involvement | 30%–50% |
| IV | Good to guarded | 6 to 9 clock hours of limbal involvement | 50%–75% |
| V | Guarded to poor | 9 to 12 clock hours of limbal involvement | 75%–100% |
| VI | Very poor | Complete limbal involvement | 100% |
Clinical Features
Ocular chemical exposures can present with conjunctival injection, chemosis, cutaneous eyelid burns, subconjunctival hemorrhage and various degrees of vision impairment.
Differential Diagnoses
The differential diagnosis for a red eye or vision loss is broad and is more fully discussed in Chapter 18 . In the setting of trauma, the differential diagnosis includes subconjunctival hemorrhage, perforation, foreign body, and corneal abrasions. In the absence of trauma, the differential diagnosis includes benign etiologies (such as, subconjunctival hemorrhage or conjunctivitis) to more concerning etiologies (such as, iritis, uveitis, episcleritis, glaucoma, optic neuropathy, central retinal artery occlusion, or central retinal vein occlusion).
Diagnostic Testing
Perform a visual acuity test in all patients with ocular complaints. Check the ocular pH with litmus paper, ideally before and after irrigation. If the patient can tolerate the procedure, a comprehensive slit-lamp examination is preferred.
Management
The management of acute chemical burns to the eye involves several stages including removal of the offending substance, and administration of medications to decrease inflammation, avoid further tissue injury, and ultimately foster re-epithealization. When a chemical injury to the eye is suspected, start copious irrigation immediately. In the pre-hospital setting, tap water irrigation is generally readily available and the ideal choice for irrigation. At the scene, it is recommended that the victim submerge the eyes in running tap water and continuously open and close the eyes with the head turned such that the affected eye is lower than the unaffected eye to minimize any contamination into the unaffected eye. In the ED, tap water irrigation can be continued in preparation for a more definitive irrigation system. However, because there is some concern for possible promotion of corneal edema, based on the hypotonicity of tap water, some advocate for use of other readily available solutions for ocular irrigation. Such solutions include either lactated Ringers, a balanced salt solution (BSS), or amphoteric solutions such as Diphoterine®. The repeated application of topical anesthetics (such as, proparacaine) can decrease pain and facilitate irrigation. Hydrotherapy can also be accomplished by connecting intravenous tubing to a bag containing normal saline or lactated Ringers solution. The initial therapy consists of continual irrigation of the eye with 2 L of lactated Ringers during the first 30 minutes. A Morgan lens can be used for irrigation, although there is a theoretic risk of trapping the chemical between the conjunctiva and the Morgan lens, thereby increasing the burn. If a Morgan lens is used, we recommend replacing the lens between each liter. After 2 L has been infused, as described earlier, litmus paper is inserted into the conjunctiva to determine the pH; irrigation is continued until the pH is at a near-physiologic level (pH of 7.4). Alkali burns are likely to require more irrigation than acidic burns. In either case, depending on the chemical’s pH and amount of exposure, additional liters may be required to restore a near-neutral pH. Following irrigation, it is important that the emergency physician evert the upper eyelid and visually inspect the area for any lodged or hidden particulate matter. A slit-lamp examination with fluorescence staining is recommended to assess for any corneal abrasion. Although of undetermined benefit, ocular antibiotics are commonly used after appropriate decontamination if a corneal abrasion is present.
The use of topical or subconjunctival corticosteroids following alkali burns has been associated with reduced corneal opacity, vascularization, and inflammation. Topical corticosteroids, such as fluorometholone 1% or prednisolone 0.5% can reduce inflammation and should be continued for approximately 1 week. We recommend consulting an ophthalmologist prior to implementing corticosteroids.
Disposition
Emergent ophthalmologic consultation and close follow-up are indicated for all significant exposures. Most ocular burns, other than the mildest burns, are treated with a long-acting cycloplegic and a mydriatic. In addition, after consulting an ophthalmologist, a carbonic anhydrase inhibitor may be used for 2 weeks (or until the ocular pain subsides). These medications decrease the potential for pupillary constriction, increased intraocular pressure, and early glaucoma. Procedures such as amniotic membrane patching, anterior chamber paracentesis, and corneal transplant have been used for chemical injuries to the eye but should only be performed by an ophthalmologist.
Patients with lower grade ocular injuries can be managed as outpatients, but patients with higher-grade injuries should be admitted to the hospital for more intensive treatment.
Specific Toxins
Hydrofluoric Acid
Foundations
Background and importance
Hydrofluoric acid is an acidic aqueous solution made from fluorine. It has a variety of industrial indications, including glass etching, the production of semiconductors, rust removal products, insecticides, tile-cleaning agents, and automobile wheel cleaning products. It is available in many over-the-counter products in concentrations ranging from 6% to 12% but can be used in the industrial setting in concentrations exceeding 70%.
Anatomy, physiology, and pathophysiology
Absorption of hydrofluoric acid can occur upon exposure to the lung, skin, and eyes. In a 20-year review of all hydrofluoric acid deaths reported to the Taiwan Poison Control Center, dermal exposure accounted for 84% of all exposures, and the majority occurred in an occupational setting. Of these 324 subjects, the majority of subjects had mild toxicity. However, approximately 40% of subjects had moderate toxicity and 1% had severe toxicity. Two subjects died strictly from hydrofluoric acid-related dysrhythmias and shock. The timing of onset of pain after a hydrofluoric acid burn is inversely related to the concentration. For example, burns from a 20% hydrofluoric acid solution can have pain delayed for up to a day, whereas burns from a 50% hydrofluoric acid concentration will likely result in immediate pain. , Hydrofluoric acid is unique in its mechanism of action. Despite being an acid, it is capable of causing a liquefactive necrosis with subsequent deep tissue burn, similar to alkalis. The free fluoride ion is responsible for most of the damage associated with hydrofluoric acid exposure. However, both the hydrogen ions as well as the fluoride ions cause tissue damage. In the setting of high concentrations of hydrofluoric acid (>50%), the hydrogen ion itself can cause damage to the skin, eyes, and mucosal membranes. Later, the fluoride ion causes both local and systemic toxicity, regardless of the concentration of hydrofluoric acid. The free fluoride ion scavenges cations, such as calcium and magnesium, thereby resulting in systemic hypocalcemia and hypomagnesemia. In addition, free fluoride ions can inhibit sodium, potassium–ATPase (Na + , K + -ATPase), and the Krebs cycle. The combination of cellular destruction and inhibition of Na + , K + -ATPase can also result in hyperkalemia as a preterminal finding. As a result of the numerous electrolyte disturbances, QT prolongation, hypotension, and ventricular arrhythmias can occur. The severity of injury depends on the concentration of the substance and the duration of exposure.
Clinical Features
Inhalational Exposure
Inhalation of hydrofluoric acid is rare, and it almost always occurs in the industrial setting. Patient outcomes vary considerably depending on the concentration and duration of exposure to hydrofluoric acid. Inhalation and skin exposure to 70% hydrofluoric acid can result in pulmonary edema and death within hours. However, delayed pneumonitis and adult respiratory distress syndrome can occur, and the symptoms can be present for months. Pneumonitis can be severe and require ventilatory support.
Gastrointestinal Exposure
Gastrointestinal exposures are rare, except for cases of intentional ingestions. When such an exposure does occur, symptoms can include nausea, vomiting, and abdominal pain. Life-threatening fluoride toxicity can occur with large oral ingestions.
Ocular Exposure
Even though hydrofluoric acid is an acid, exposure of the eye to hydrofluoric acid can result in a severe burn with penetration and necrosis of the structures throughout the anterior chamber. As with other ocular injuries, immediate and copious irrigation of the eye is indicated. Systemic absorption is possible.
Dermal Exposure
Dermal exposure is the most common route of hydrofluoric acid injury. During handling of containers in which hydrofluoric acid is stored, contamination of inadequately protected fingers and hands often results in a chemical burn injury. The hydrofluoric acid skin burn has a distinct characteristic: the exposure causes progressive tissue destruction. Intense pain can occur; the onset of the pain is inversely related to the concentration of the hydrofluoric acid, such that the lower the concentration of hydrofluoric acid, the longer the time until symptoms may manifest. The pain may seem out of proportion the examination. With larger exposures, the involved skin may develop a tough, coagulated appearance. If untreated, the burn can progress to an indurated, whitish appearance with vesicle formation. Within the digits, hydrofluoric acid has a predilection for subungual tissue. Severe untreated burns can progress to full thickness burns and can even result in loss of digits.
Differential Diagnoses
Because pain may seem out of proportion to the examination findings, shingles, neuropathy, and other chemical injuries are within the differential diagnosis. Numerous other gases causing respiratory compromise should also be included. In the presence of apparent burns, the differential diagnosis includes blistering disorders, toxic epidermal necrolysis, and infectious etiologies.
Diagnostic Testing
Test serum potassium, magnesium and ionized calcium levels in patients with hydrofluoric acid burns. With electrolyte abnormalities, an electrocardiogram (ECG) will assess for dysrhythmias or changes in the QTc or QRS intervals. Obtain a chest radiograph in individuals with inhalant or pulmonary symptoms. Finally, perform a detailed eye examination, including a slit-lamp examination, fluorescein staining, and visual acuities on individuals with ocular exposure.
Management
The initial treatment of hydrofluoric acid skin exposure is immediate irrigation with copious amounts of water for at least 15 to 30 minutes. Most exposures to dilute solutions of hydrofluoric acid respond favorably to immediate irrigation. Severe pain or any pain that persists after irrigation indicates a more severe burn that requires detoxification of the fluoride ion. Detoxification is accomplished when an insoluble calcium salt is formed. In the case of digital exposure, in which the fingertip is exposed, the fingernail should be removed.
In contrast to thermal burns, blisters are burst because necrotic tissue may harbor fluoride ions. The fluoride ions can then be detoxified through topical treatment, local infiltrative therapy, or intra-arterial infusion of calcium. Calcium gluconate (2.5%) gel can be administered topically. Calcium chloride should not be used topically, as it is irritating to the dermis. Calcium gluconate gel is often not available in hospital pharmacies, but it can be made by mixing 3.5 g of calcium gluconate powder in 150 mL of a water-soluble lubricant (e.g., glycerin-hydroxyethyl cellulose lubricant [K-Y Jelly]). This gel is secured by an occlusive cover (e.g., powder-free latex glove). Because the skin is impermeable to calcium, topical treatment is effective only for mild, superficial burns.
Infiltration Therapy
Subcutaneous
Infiltrative therapy is necessary for treatment of deep, painful hydrofluoric acid burns. Calcium gluconate is the agent of choice and can be administered by either direct infiltration or intra-arterial injection. A common technique involves injecting 0.5 mL/cm 2 of 10% calcium gluconate subcutaneously through a 27- or 30-gauge needle. The use of an equal volume mixture of 5% calcium gluconate and 0.9% normal saline has been shown to reduce irritation of tissues and decrease subsequent scarring.
Despite its wide acceptance, the infiltration technique has disadvantages, especially in treating digits. A regional nerve block is recommended because the injections may be very painful. Removal of the nail to expose the nail bed is required if subungual tissue is involved. Vascular compromise can occur if excessive fluid is injected into the skin exposure sites, and unbound calcium ions have a direct toxic effect on tissue. Because of these disadvantages with subcutaneous infiltration in the hand, we recommend intra-arterial infusion in most instances.
Intravenous and intra-arterial
Patients with pain refractory to local or subcutaneous calcium administration may benefit from regional anesthesia, either intravenously (e.g., Bier block) or intra-arterially. Various dilute solutions of calcium have been used. Perhaps the simplest method involves the administration of a mixture of 10 mL of solution of 10% calcium gluconate in 40 to 50 mL of normal saline infused over 4 hours. Because of ease of administration, we recommend starting with this approach, although other approaches can be used in conjunction with this approach if pain persists. If more than 6 hours has elapsed since the time of hydrofluoric acid exposure, tissue necrosis cannot be prevented, even though pain relief can be achieved up to 24 hours after exposure. There is a direct correlation between the speed by which arterial infusion of calcium administration occurred and both the time of wound healing and the need for surgical intervention.
The intra-arterial infusion technique has potential disadvantages. Arterial spasm or thrombosis may result in significant skin loss. The intra-arterial procedure is more expensive, largely because it requires hospitalization for the use of the infusion pump and the monitoring of serum calcium concentrations if repeated infusions are used. Recently, the use of epidermal growth factor was found to be superior to saline, calcium gluconate, or magnesium sulfate.
Respiratory Exposures
In the case of an inhalational exposure to hydrofluoric acid, prompt airway management is paramount, with endotracheal intubation occurring for the usual indications. Calcium gluconate can be nebulized as a 2.5% to 5% solution. Racemic epinephrine or albuterol can be used for bronchospasm. Bronchoscopy can be performed to assess the degree of injury.
Ocular Exposures
The ocular use of calcium gluconate is somewhat controversial, because it has the potential to cause further damage to the eye. The use of ocular calcium gluconate is not routinely recommended. In the occupational setting, use of hexafluorine may be considered after copious irrigation of the eye with tap water or normal saline.
Systemic Toxicity
Hydrofluoric acid binds calcium and magnesium ions with strong affinity. Systemic manifestations of fluoride toxicity are related to hypocalcemia and include abdominal pain, muscle fasciculations, nausea, seizures, ventricular dysrhythmias, and cardiovascular collapse. Burns as small as 2.5% of the total body surface area caused by concentrated hydrofluoric acid are fatal. Hypocalcemia can occur after significant exposure to hydrofluoric acid and is corrected with an intravenous 10% calcium gluconate infusion. Calcium chloride can be used, but its administration requires central venous access. In addition, fluoride ion toxicity has cardiac and neurotoxic effects.
Disposition
Patients treated with calcium therapy with continued refractory pain should be hospitalized for observation and should undergo a toxicological consultation. Patients with significant hydrofluoric acid exposure with systemic toxicity require hospitalization to monitor for cardiac dysrhythmias for 24 to 48 hours.
Formic Acid
Foundations
Background and importance
Formic acid is a caustic organic acid used in rubber, paper, tanning, agricultural, and electroplating industries. It has also been used to manufacture disinfectants and in various cosmetics.
Anatomy, physiology, and pathophysiology
Formic acid causes cutaneous injury by inducing a coagulative necrosis.
Clinical Features
Systemic toxicity occurs after absorption and is manifested by metabolic acidosis, gastrointestinal bleeding, bowel perforation, and aspiration. Because of its ability to induce oxidant stress, hemolysis may occur.
Differential Diagnoses
Similar to hydrofluoric acid, the differential diagnosis includes various other chemical burns, infectious etiologies, toxic epidermal necrolysis, and blistering disorders.
Diagnostic Testing
No specific diagnostic testing is indicated. If the patient shows any signs of systemic toxicity, obtain a complete blood count, serum electrolytes, and either an arterial or venous blood gas.
Management
Begin copious irrigation immediately. Acidosis (pH < 7.30) should be treated with sodium bicarbonate. Mannitol may be used to expand plasma volume and promote osmotic diuresis in patients with hemolysis. Folinic acid, which enhances the conversion of formic acid to carbon dioxide and water can be administered for severe toxicity. Hemodialysis may be required for patients with systemic toxicity, renal failure, and metabolic acidosis. Exchange transfusion may be indicated for those patients that are refractory to standard medical management, including hemodialysis.
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