Remember that the Unthinkable is Possible—Follow These Principles in the Evaluation and Treatment of Patients Suffering from Nerve Agent Poisoning
Daniel J. Bochicchio MD, FCCP
It’s rush hour on a warm June afternoon. While walking past a television in the operating room (OR) lounge, a news flash breaks into today’s soap opera. A reporter at the baseball stadium approximately 7 miles away from your hospital is describing a plane crash. A small crop-dusting aircraft flew low over the grandstands and crashed into the press box. Apparently, some form of toxic chemical was being released by the aircraft at the time of the crash. The scene on television is chaotic. The news camera pans toward the stadium exits, where there are numerous dead bodies. Several individuals are staggering about. Several collapse onto the sidewalk. One victim vomits, collapses, and begins seizing. The chemical is tentatively identified as a “nerve agent.” Absolute chaos is an appropriate description for the scene at the trauma center closest to the disaster. The press is estimating as many as 1,000 causalities, with >100 dead at the scene. You hear over the public address system that the hospital is implementing its mass casualty disaster plan. You have just been informed that your hospital can expect >100 casualties. Among the casualties are numerous police, fire, and emergency medical personnel. In an effort to evacuate the site rapidly, some victims may not have received adequate decontamination.
Thirty minutes later you receive your first victim from the scene. A 28-year-old woman, while attempting to flee, fell and was trampled by the crowd. She now presents with multiple contusions and abrasions for a laparotomy and possible splenectomy. She is awake and alert but appears very anxious, tremulous and tearful. Her blood pressure is 119/74 mm Hg, pulse 118 beats/min, respirations 32/min with mild dyspnea. While the staff in the emergency department is performing a brief focused physical exam, she vomits and voids on the stretcher. The patient’s respiratory condition begins to deteriorate. She is promptly brought to the OR. You are informed that the agent has been identified as Sarin. You consider that the luckiest moment in your life is when the anesthesiologist who is covering the intensive care unit (ICU) this week comes over to help you start your case. He is a colonel in the Army Reserves with a specialty in chemical warfare.
He induces general endotracheal anesthesia. You notice that the airway pressure at 7-mL/kg tidal volume is 52 cm H2O. There are copious secretions noted in the no. 8 endotracheal tube. The surgeons are asking to begin. The patient’s blood pressure is 134/67, pulse is 110 beats/min, SaO2 is 92% by pulse oximetry on 100% inspired oxygen. Approximately 30 minutes after induction, your anesthesia technician begins to complain of blurry vision and rhinorrhea.
The surgical procedure, an exploratory laparotomy and splenectomy, requires 1 hour to complete. It is without significant surgical complication. The patient is brought to the postanesthesia care unit (PACU). In the PACU there are again copious secretions noted in the endotracheal tube. Your ICU colleague says he will give more antidote (in the chaos, you were not completely clear that “antidote” had been given in the first place) and asks you to resuction the airway. After a few more minutes the spontaneous respirations appear much less labored and the secretions are improving. Your senior colleague decides not to extubate at this time and leaves you to care for the patient while he goes downstairs to help there. The nurse in pre-op holding calls you to come quickly; your next patient is apneic and seizing. She also confirms that there are hundreds of patients downstairs who need care.
How do you approach this mass casualty situation? What is meant by decontamination? What is meant by “the antidote?” How will you do the anesthesia for the next patient? Can you keep yourself safe?
DISCUSSION
Chemical warfare agents are chemicals that have direct toxic effects on mammalian tissue. The modern era of chemical warfare began on the French battlefields of World War I. On April 22, 1915, the German Army attacked the Allied positions with chlorine gas. The bombardment caused 15,000 Allied casualties, with 5,000 dead. In 1936, Dr. Gerhard Schrader discovered the highly toxic effects of the pesticide Tabun on mammalian tissue. This was quickly followed by the discovery of several more nerve agents. Although these highly toxic compounds have been in existence for 70 years, the vast majority of civilian health professionals have received little if any education or training on the medical management of victims of nerve agent poisoning.
Accordingly, most physicians and other health care providers caring for chemical casualties in recent conflicts lacked any formal training in this area. There are case reports of casualties contaminated with mustard agent in the Iraq-Iran war having been evacuated as far as hospitals in France without adequate decontamination. Lack of adequate knowledge to deal with the problem under the stress of a mass casualty situation will have a serious negative effect on survivability. There is nothing unique about the pathophysiology of chemical injury that is beyond the understanding of properly
trained clinicians. The principles of rapid, thorough decontamination, self-protection, and an understanding of the actions of antidotes are the keys to effective chemical casualty care.
trained clinicians. The principles of rapid, thorough decontamination, self-protection, and an understanding of the actions of antidotes are the keys to effective chemical casualty care.
Nerve agents are the most toxic chemical weapons known. They exert their biologic effect by inhibiting the enzyme acetylcholinesterase (AChE), thereby precipitating a cholinergic crisis. There are two major classes, the carbamates and the organophosphates (OPs). Among the former are neostigmine, physostigmine, pyridostigmine, and several commercially available insecticides. The OPs include the “military” nerve agents and several insecticides. Five OP AChE inhibitors are recognized as military nerve agents (NAs). They are commonly known as Tabun (North Atlantic Treaty Organization [NATO] designation: GA), Sarin (NATO: GB), Soman (GD), GF, and VX. The agents GF and VX do not have common names. The “G” agents were developed in Nazi Germany by Gerhard Schrader and his associates while researching insecticides for the conglomerate IG Farben between 1936 and 1944. VX was developed by the British in 1954 while searching for a replacement for the insecticide DDT. A nerve agent, given adequate time, will irreversibly bind all three forms of AChE.
The binding of NAs to AChE prevents the degradation of acetylcholine (ACh). The toxic effects of NAs are a result of massive excess of ACh. The symptoms are related to both the dose and the route of exposure. Inhalation of vapor causes immediate symptoms. If the vapor concentration (mg/m3) and exposure time are significantly high, then the onset will be immediate and death may occur in minutes. Nerve agents are readily absorbed through intact skin and will penetrate clothing. The onset of symptoms after skin exposure to liquid agent can be delayed. Onset of systems depends on the amount of exposure, the promptness of decontamination, and temperature, moisture, and location on the body. Time of onset can range from several minutes up to 12 to 18 hours (Sidel et al., 1997).
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