S35 Simple and Chemical Asphyxiants Asphyxiants: Simple and Chemical Ken-Hing Tan, MD; Tzong-Luen Wang, MD, PhD Abstract Asphyxiants are gases that cause tissue hypoxia. They are classified as either simple or chemical on the basis of the mechanism of toxicity. Simple asphyxiants decrease FiO2 by displacing oxygen in inspired air, results in hypoxemia. Chemical asphyxiants interfere with oxygen transport system and cellular respiration and thereby cause tissue hypoxia. Mild symptoms of asphyxia include headache, dizziness, nausea, and vomiting. More severe symptoms range from dyspnea, altered sensorium, cardiac dysrhythmia, ischemia, syncope, seizure, and even death. Clinical diagnosis of asphyxiant exposure is limited. A consistent history, myriad spectrum of complaints, group victims, and rapid resolution on away from exposure are generally sufficient. Occupational exposures and fires are the most common sources of inhalation injuries. Working in confined spaces are harzardous to workers. Rapid removal, supportive care and preventing hypoxemia are the mainstay of treatment. Emer- gency planning should be applicable to both accidental and deliberate chemical disasters. (Ann Disaster Med. 2005;4 Suppl 1:S35-S40) Key words: Asphyxiants; Asphyxiation; Toxic Inhalation; Carbon Monoxide; Cyanide; Hydro- gen Sulfide Introduction hypoxemia, secondary to gases inhalation.4 Asphyxiants are gases that deprive body tissues Occupational exposures and fires are the most of oxygen. They are generally divided into two common sources of the numerous agents ac- categories, simple and chemical.1 Simple countable for accidental inhalation injuries. When asphyxiants merely displace oxygen from ambi- obvious historical evidence or a heightened sus- ent air whereas chemical asphyxiants react in the picion for an acute inhalation exposure does not human body to interrupt either the delivery or exist, misdiagnosis and maltreatment are likely utilization of oxygen.2 When the concentration to occur. of any gases increase, the fraction of inspired Clinical diagnosis of simple asphyxiant ex- oxygen (FiO2) tends to decrease, rendering to posure is limited. A consistent history, myriad hypoxemia. spectrum of complaints, group of victims, and Working in confined spaces are hazard- rapid resolution on away from exposure are ous to workers.3 The death is usually due to generally sufficient. Identification of particular From Department of Emergency Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan; Medical College, Taipei Medical University, Taipei, Taiwan Address for reprints: Dr. Tzong-Luen Wang, Department of Emergency Medicine, Shin-Kong Wu Ho-Su Memorial Hospital, 95 Wen Chang Road, Taipei, Taiwan Received: Sep 5 2005. Revised: Sep 13 2005. Accepted: Sep 20 2005. TEL: 886-2-28389425 FAX: 886-2-28353547 E-mail: [email protected] Ann Disaster Med Vol 4 Suppl 1 2005 Simple and Chemical Asphyxiants S36 gases is not necessary except for government Many cases of CO poisoning, even re- health politics. cover well without any complication with hy- Supportive care and preventing hypoxemia perbaric or high oxygen therapy, revisit hospi- is central to the treatment of all pulmonary and tal with delayed neuropsychiatry sequelae, such systemic inhalation injuries.5 Patients at risk for as cognitive and personality changes, hypoxia should be observed for the delayed incontinence, dementia, and psychosis.8 development or progression of post hypoxic neurological sequelae. Clinical Features Decrease FiO2 from ambient, (i.e., 21%) to Classification 15% brings acute effects of hypoxia within min- Simple asphyxiants, such as carbon dioxide utes after exposure to simple asphyxiant. It re- (CO2), Nitrogen (N2), and Propane (C3H8), sults in autonomic stimulation (e.g., tachycardia, when present in high concentrations in air, es- tachypnea, and dyspnea) and cerebral hypoxia pecially within a confined space, act by limiting (e.g., ataxia, dizziness, incoordination, and the utilization of the oxygen, without producing confusion). Life probably cannot be sustained significant toxic effects on the body per se. at a FiO2 level below 6%.9 Clinical reports on unintentional mass ex- posure to extreme concentrations of carbon Carbon Dioxide dioxide occurs in Israel, caused by a leakage Carbon dioxide (CO2) is a colorless, odorless, of container of liquid carbon dioxide in an en- nonirritating gas that is widely used as a fire closed working environment. Twenty-five ca- extinguisher, in ice-making factories and oc- sualties developed symptoms included dyspnea, cupational or recreational (diving) settings. The cough, dizziness, chest pain, and headache. It potential severity of toxicity from carbon diox- resulted in significant but transient cardiopulmo- ide was tragically exemplified by the disaster in nary morbidity with no mortality when victims Cameroon in 1986, when many people were were promptly evacuated and given supportive killed by the expulsion of carbon dioxide from therapy.6 a volcano.11 Most diving injuries are related not only CO2 closely resembles simple asphyxiants to barotraumas, decompression illness, pulmo- from a toxicological standpoint. CO2 in high nary edema, but also nitrogen narcosis at el- concentration, however, has direct toxic evated levels. 7 effects, mainly those of sympathetic Another categories of asphyxiants, i.e., stimulation, including increased heart rates, chemical such as carbon monoxide (CO), cya- cardiac output, mean pulmonary artery nide (CN-), and hydrogen sulfide (H2S), bind pressure, and pulmonary vascular resistance, and to and inhibit the ultimate step in electron trans- therefore impose excess load on the port chain system of the mitochondria, the Fe3+ myocardium. The most important action in CO2 containing cytochrome a-a3 in complex IV, intoxication is to remove the victims from the therefore, rendering tissue hypoxia and the de- exposed environment and to provide cardio- velopment of lactic acidosis. respiratory support until spontaneous recov- Ann Disaster Med Vol 4 Suppl 1 2005 S37 Simple and Chemical Asphyxiants ery occurs.6 discharges. The key to the pathogenicity of CO is its Nitrogen propensity to attach itself to the ferrous (Fe3+) Nitrogen gas (N2) is a colorless, odorless, in the heme prosthetic group of hemoproteins, tasteless, and constitutes about 80% of air in which includes hemoglobin, myoglobin, and atmosphere. The incident rate of nitrogen nar- some intracellular enzymes (cytochromes, P- cosis (12%) is the most frequent, followed by 450). Contributing to tissue hypoxia is the fail- barotraumas of the ear (11%) and paranasal si- ure of carboxyhemoglobin to dissociate in the nus (5.6%) during scuba diving. 11 The major tissues.15 toxic effect is simple asphyxiation. N2 is thought Mild CO poisoning occurs frequently, to act by interacting directly with neuronal ion- leading to headache, nausea, vomiting, dizziness, channel receptors i.e., [gamma] - aminobutyric myalgia or confusion. However, in severe CO acid (GABA) receptor antagonists.12 intoxication, patients suffered from neuropsy- chiatry abnormality or cardiovascular instability Propane (e.g. alter sensorium, seizure, coma, syncope, Propane (C3H8), which is both colorless and ischemia, infarction, or dysrthymia). It would odorless in its gaseous state, has highly flam- depress myocardium contractility and lead to mable and explosive characteristics. It displaces acute rhabdomyosis. oxygen, consequently causing hypoxia and eventually anoxia. The depletion of oxygen in Hydrogen Cyanide the air, and the build up of propane and carbon Cyanides (CN-) are utilized in mining operations, dioxide, lead to unconsciousness and eventual photographic materials, the production of death. Death results not from the toxic nature plastics, pigments, and dyes, and often used as of the gas but simply from the displacement of fumigant pesticides. During fires, victims can also atmospheric oxygen.13 inhale significant carbon monoxide and cyanide Inhalation of gaseous propane can cause gases, which may cause synergistic toxicity in dizziness, nausea, vomiting, confusion, humans. hallucinations, and a feeling of euphoria. At high CN- is described as a cellular toxin be- concentrations, it has a narcotic effect and can cause it inhibits aerobic metabolism. It revers- bring about cardiac arrest resulting from sup- ibly binds to cytochrome oxidase and inhibits pression of central nervous system activity.14 the last step of mitochondrial oxidative phosphorylation. This inhibition halts carbohy- Carbon monoxide drate metabolism from the citric acid cycle, and Carbon monoxide (CO) is, after carbon intracellular concentrations of adenosine triph- dioxide, the most abundant atmospheric osphate are rapidly depleted. 16 pollutant. It originates partly from natural sources With the inhalation of high concentration such as forest fires and volcanic eruptions, but hydrogen cyanide (300 mg/m3), the victim’s skin mostly from human activity, in particular from is a flushed reddish pink, and tachypnea, the internal combustion engine and industrial tachycardia, and nonspecific central nervous Ann Disaster Med Vol 4 Suppl 1 2005 Simple and Chemical Asphyxiants S38 symptoms appear. Stupor, coma, and seizure presentations. The circumstances and locations immediately precede respiratory arrest and car- of the exposure, presence of combustion or diovascular collapse. Death shortly occurs. odors, and number and condition of victims as- sist in diagnosis. Hydrogen Sulfide In case of chemical