Introduction

Ethanol and recreational drugs are by far the most common chemical exposures associated with trauma. This chapter, however, covers other possibly associated exposures: toxic industrial chemicals (TIC), chemical weapons (CW), and radiation.

Limited exposures occur commonly in the industrial setting. The Bhopal disaster of 1984; mustard use during the Iran–Iraq War; the recent use of chlorine and sarin in Syria; the recent use of VX and Novichok in targeted assasinations; and the 2011 Fukushima earthquake, tsunami, and nuclear disaster are examples of combined trauma/toxic exposure. Indeed, chemical weapons of World War I are common industrial chemicals such as phosgene, chlorine, and cyanide, which are still used in vast quantities.

Combined trauma-exposure management begins with advanced trauma life support (ATLS) guidelines, balanced by the need for caregiver personal protective equipment (PPE) and rapid decontamination. After resuscitation, toxidrome treatment and advanced management commence. No specific antidotes exist for most chemical exposures; supportive care through emergency, operative, and critical care phases is key.

Common toxic injury patterns include inhalational injury, chemical burns, and metabolic poisoning. Frequently, two or more types are present. When combined with conventional trauma, they synergistically increase morbidity and mortality. In a mass casualty disaster setting, exposure to toxic chemicals or radiation add a further layer of complication that endangers responders as well.

Resources for Agent Identification and Management

The US Department of Health and Human Services’ Chemical Hazards Emergency Medical Management (CHEMM) website () allows “first responders, first receivers, other healthcare providers, and planners to plan for, respond to, recover from, and mitigate the effects of mass-casualty incidents involving chemicals.” The site has tools for rapid toxidrome (i.e. clinical syndromes) identification, patient management, and planning. Similarly, the Radiation Emergency Medical Management (REMM) website (www.remm.nlm.gov/index.html) focuses on radiation events. Additional resources include Wireless Information System for Emergency Responders (WISER, ) and CHEMTREC® (www.chemtrec.com/), a commercial service focused on industrial and transportation accidents involving chemicals. WISER is available for download to mobile devices. Finally, a chemical-induced illness pocket card (“Chem card”) can be downloaded at www.healthquality.va.gov/biochem/bio_poc_chem.pdf (Figure 15.1).

Figure 15.1 Chemical-induced illness pocket card.

Decontamination and Personal Protective Equipment (PPE)

Decontamination begins as soon as possible, preferably pre-hospital. Simply removing clothing can dramatically reduce both patient and caregiver exposure. Large volumes of water (with or without detergent) remove more persistent agents. Water should be avoided when flammable metals (e.g. lithium, sodium, potassium) are suspected; in such cases, mineral oil is used until debridement is possible. Adsorbants (e.g. sand, cat litter) are also effective. Topical decontamination of military agents can be accomplished using reactive decontamination skin lotion (RDSL, www.rsdecon.com/). First responders should wear PPE Level C or higher when treating contaminated patients (www.remm.nlm.gov/osha_epa_ppe.htm). Level A or B is indicated for unknown agents or high concentrations. Additional decontamination at the hospital is indicated for persistent agents or when field decontamination was incomplete.

Lifesaving medical treatment takes precedence over decontamination. The “ABCs” should be managed throughout the decontamination process. Level C PPE respiratory protection includes hooded NIOSH-certified powered air-purifying respirators (PAPR) with assigned protection factors (APF) of ≥1000 and appropriate chemical/radiological filters. These respirators should be used by hospital personnel receiving contaminated victims. OR procedures can be performed wearing PAPR when needed. Double gloving with at least one nitrile glove is recommended when dealing with chemical exposure victims.

Several studies demonstrate the difficulty of performing manual medical procedures (intubation, venipuncture) while wearing PPE. Maneuvers requiring less fine motor skill (e.g. laryngeal mask airway or intraosseous needle placement) should be considered, especially in mass casualties.

Inhalational Injuries

Acute inhalation injuries are frequently a consequence of industrial or household accidents. Agents released into confined spaces result in relatively high concentrations. Larger releases may result from bulk stored agents at industrial sites or during transportation accidents.

Several mechanisms of toxicity exist. Acute asphyxiants (e.g. carbon dioxide, argon, methane, nitrogen) simply displace oxygen and prevent its uptake, resulting in hypoxemia, anerobic metabolism, and metabolic acidosis. Water-soluble agents (e.g. chlorine, ammonia) at low concentrations cause upper airway mucosal injury, while higher concentrations penetrate deeper into the airway and may induce bronchospasm and mucosal sloughing. Less-soluble agents cause injury to lung parenchyma, resulting in necrosis or pulmonary edema. Pulmonary edema is also common with nitrogen oxides, isocyanate, and phosgene. Different inhalational injury mechanisms are commonly superimposed. Survivors often develop chronic obstructive pulmonary disease.

Mainstays of acute asphyxiant therapy are supportive oxygenation, ventilation, and bronchodilators. Positive end-expiratory pressure (PEEP) helps reduce pulmonary edema, while diuretics are of limited value, and steroids have been shown to be ineffective. Serial chest X-rays, arterial blood gases, and pulmonary function tests allow clinicians to follow the disease course closely. Once the acute phase subsides, therapy follows conventional critical care management guidelines.

Chemical Burns

Chemical injuries cause 3% of burn admissions but 30% of burn deaths. Degree of injury frequently parallels exposure time. Decontamination should occur as soon as possible at the scene and emergency department to limit the extent of injury; the incidence of full thickness burns increases fivefold when irrigation is not initiated within 10 minutes. General decontamination procedures includes clothing removal and flushing with water or adsorbents; however, water is contraindicated in case of reactive metals or phenol injury. Tissue destruction occurs due to saponification of fats by alkali, coagulative necrosis by acids, and protein denaturation by organic materials and reactive metals. Chemical warfare agents produce both local and systemic toxicity. The extent of chemical injury is frequently under-estimated.

Management includes ATLS followed by burn center admission, if available. The “ABCs” should generally not be delayed due to the presence of chemicals. However, caregivers should wear PPE. The advanced life support for acute toxic injury (TOXALS) protocol, introduced by Baker in 1996, is one method for managing acute chemical injury.

Identification of the chemical agent allows for more specific treatment and prognostication. Material safety data sheets (MSDS) and chemical placards on transport vehicles should be noted. Firefighters are often excellent sources of chemical information in the pre-hospital setting. Poison control centers, CHEMM, WISER, and CHEMTREC are also useful. Consultation with or transfer to a burn center should be considered if possible.

Hydrogen fluoride binds calcium, penetrating deeply into tissues and bone. Patients with skin involvement should receive topical calcium gluconate and monitoring for hypocalcemia. Hand injuries are treated with fasciotomy and intra-arterial calcium gluconate infusions. Injury is often more extensive than initially thought. Burn center and surgical consultation is always indicated.

Mustard (bis-(2-chloroethyl) sulfide) binds to DNA, interrupting rapidly dividing cells such as epithelium and resulting in inflammation, pain, and blistering. Moist areas (e.g. eyes, genitals) are easily affected, while pulmonary and systemic effects are also possible. After decontamination, treatment is largely supportive. Irrigation, topical antibiotics, and systemic analgesics reduce symptoms and scarring. Small skin blisters can be left intact, while large bullae should be unroofed, irrigated, and treated with a topical antibiotic in the same manner as a thermal burn. Fluid loss into blisters may be significant, necessitating volume resuscitation. Pulmonary mucosal injury is managed supportively. Large mustard exposures depress bone marrow within 3–5 days; resuscitative surgery should occur before immune compromise occurs or after the white count rebounds. Gut sterilization can be considered if leukopenia develops.

Lewisite (2-chlorovinyl dichloroarsine) is similar to mustard, but immediate pain is the prominent symptom. There are no immunologic effects. Treatment includes early dimercaprol application and supportive care.

Metabolic Poisons

Hydrogen cyanide (HCN), hydrogen sulfide (H₂S), and carbon monoxide (CO) are classic inhaled metabolic poisons. They act at the cellular level, inhibiting oxygen binding or utilization. Supplemental or hyperbaric oxygen are therapeutic mainstays for CO. Sodium nitrite and sodium thiosulfate are indicated for HCN toxicity, while only sodium nitrite treats H₂S.

Heavy metals like lead (Pb) respond to chelation therapy. Calcium disodium ethylenediaminetetraacetic acid (EDTA) and dimercaptosuccinic acid (DMSA) are effective.

Nerve agents (NA), such as tabun (GA), sarin (GB), soman (GD), and VX, are another metabolic toxin class. Organophosphate toxidromes may also occur from pesticide exposures. Both types of agents bind and inhibit cholinesterase, resulting in excess acetylcholine and over-stimulation of nicotinic and muscarinic receptors resulting in miosis, lacrimation, salivation, bronchospasm, dyspnea, vomiting, incontinence, seizures, central apnea, and respiratory paralysis. Patients require respiratory support and treatment with atropine and an oxime (pralidoxime, obidoxime, HI-6). Seizures are treated with benzodiazepines or propofol. Benactyzine, aprophen, azaprophen, trihexyphenidyl, procyclidine, biperiden, and scopolamine have been demonstrated to terminate soman-induced seizures at lower concentrations than diazepam. There is recent literature supporting the use of magnesium sulfate and ketamine, as well. Heavy exposures require substantial critical care resources. Caregivers should wear Level C PPE until patients are fully decontaminated to avoid exposure.

Delayed onset of succinylcholine and vecuronium action has been reported in NA-exposed swine. Prolongation of muscle-relaxant effect may also occur. All NA-exposed patients should be considered to have a “full stomach.” Etomidate and ketamine are appropriate induction hypnotics in these patients. While propofol and thiopental are also acceptable, they may result in profound cardiac depression, bradycardia, and vasodilation. Opioids may be used, however morphine may exacerbate bronchospasm. Fentanyl and morphine may also induce bradycardia, while remifentanyl action may be prolonged by NA inhibition of non-specific tissue esterases.

The use of Novichok agents in the UK in 2018 has introduced a new class of neurotoxins to the world. They are thought to be more potent than the classic nerve agents and harder to treat. To date, all treatment protocols remain highly classified, but three patients ultimately survived a severe exposure. It is presumed that the treatment followed roughly that of standard nerve agent protocols, with additions.

Severe opioid intoxication is another recent development, especially with potent synthetic fentanyl derivatives. These may require very high doses of naloxone.

Multiple other toxins exist. Some biologic agents (e.g. botulinum, anthrax toxin) are treated with early administration of antitoxin. Others, such as ricin, are treated supportively (an antiricin monoclonal antibody has been licensed but is not yet in production). The CHEMM website can guide casualty care.