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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 . They are classified as either simple or chemical on the basis of the mechanism of toxicity. Simple asphyxiants decrease FiO2 by displacing in inspired air, results in . Chemical asphyxiants interfere with oxygen transport system and cellular and thereby cause tissue hypoxia. Mild symptoms of include headache, dizziness, , and . More severe symptoms range from dyspnea, altered sensorium, cardiac dysrhythmia, ischemia, syncope, , 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 . 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 to interrupt either the delivery or exist, misdiagnosis and maltreatment are likely utilization of oxygen.2 When the 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 - 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 with hy- Supportive care and preventing hypoxemia perbaric or high , 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 utes after exposure to simple asphyxiant. It re-

(CO2), (N2), and Propane (C3H8), sults in autonomic stimulation (e.g., tachycardia, when present in high in air, es- , and dyspnea) and 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 , dizziness, chest , 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, illness, pulmo- from a toxicological standpoint. CO2 in high nary edema, but also 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 sulfide (H2S), bind , 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 , 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 . 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, , 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 the air, and the build up of propane and carbon Cyanides (CN-) are utilized in 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. , and a feeling of . At high CN- is described as a cellular toxin be- concentrations, it has a effect and can cause it inhibits aerobic . It revers- bring about cardiac arrest resulting from sup- ibly binds to cytochrome oxidase and inhibits pression of central 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 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 asphyxiant, there are

Hydrogen sulfide (H2S) is a colorless, flammable certain kinds of laboratory test (CO-oximeter, gas. H2S has a pungent odorreminiscent of rot- pulse oxymetry, arterial blood gas, MetHb level, ten eggs. There is the potential for widespread lactate) can be used to aid in confirm diagnosis. occupational exposure to H2S, including in the oil and watertreatment industries. H2S selec- Treatment tively binds to the enzymes involved in cellular Rapid removal, away from the asphyxiant, and respiration thereby causing a shift towards supportive treatment with oxygen supplement anaerobic respiration. are the mainstay of treatment. Neurological in- At higher concentrations, death is caused jury and cardiorespiratory instablability should by of respiratory center in the ; be managed with standard resuscitation at lower concentrations, death is caused by protocols. and congestion. Survivors Patients with asymptomatic or mild poi- wtih periods of unconsciousness may suffer soning who recover after removal from the ex- permanent neurological sequelae such as posure can be observed briefly and referred to memory loss. High exposures to near lethal con- outpatient for follow up of possible delayed centrations in animals have shown destruction neurological sequalae. Patients who are at risk to nasal epithelium. During vigorous exercise, of hypoxia, such as cardiopulmonary co- low level exposures (5–10 ppm) cause a shift morbidity, advanced age, or exacerbating medi- to anaerobic respiration, leading to increased cal conditions, should admitted for further man- lactic acid formation. Eye irritation, so-called agement and observation. “gas eye, only occurs at high exposure In cases of carbon monoxide, cyanide or concentrations.17 hydrogen sulfide, administer 100% oxygen. Oxygen reverses hypoxemia and accelerates the Diagnostic Strategies elimination of asphyxiants. 19 HBO has been Clinical diagnosis of simple asphyxiant exposure shown to be the standard treatment for severe is limited. A consistent history, myriad spectrum CO poisoning. It reverses hypoxia, competes of complaints, group of victims, and rapid reso- with CO for hemoglobin binding, and promotes lution on away from exposure alert the suspi- carboxyhemoglobin dissociation. It shortens cion of asphyxic agent. The diagnosis always carboxyhemoglobin half-life from 4–6 h to <30 required scene investigation by a trained and min.20 outfitted team. CN- poisoning is treated with amyl nitrites, Since the presenting complaints are non- sodium nitrite and thiosulfate, all of which are in specific and protean, alertness should be kept the Antidote Kit. Nitrite induces the formation for those who visit ED with unusual of methemoglobin, which is bound by CN-,

Ann Disaster Med Vol 4 Suppl 1 2005 S39 Simple and Chemical Asphyxiants yielding cyanomethemoglobin. Thiosulfate acts acute inhalation exposure does not exist, mis- synergistically to accelerate the detoxification diagnosis and maltreatment are likely to occur. of CN- to thiocyanate.21, 22 Supportive care and preventing hypoxemia is For CN- poisoning due to smoke central to the treatment of inhalation injuries. inhalation, most authorities recommend the use Antidotes and hyperbaric therapy aid in treat- of thiosulfate, oxygen, and supportive measures. ment of specific chemical asphyxiant. Patients Nitrite-induced methemoglobinemia aggravates at risk for hypoxia should be observed for the the decrease in oxygen-carrying capacity that is delayed development or progression of post due to carboxyhemoglobinemia. 23 hypoxic neurological sequelae. Alertness should

The treatment of victims of H2S poisoning be paid on group of victims who visit ED with is similar to that used for hydrogen cyanide unusual presentations of illnesses. poisoning. It involves parenteral administration of a methemoglobin inducing agent such as so- References dium nitrite. Methemoglobin binds with HS- ions Pamela J. Spotlight on Asphyxiants. www. to form sulfamethemoglobin, and thus restores eh.doe.gov/chem safety. assessed on Aug the activity of the sulfide inhibited cytochrome 21, 2005 oxidase enzyme.17 Bioterrorism. Toxic Gases. www.acponline. org/bioterro/toxic_gas.htm. 2005. assessed General Precautions on Aug 21, 2005 In all cases of exposure to chemical asphyxiants, Shields PG, McCunney RJ, Chase KH. a successful outcome emphases on the extrica- Confined space : combined expo- tion of casualties, immediate provision of basic sure to styrene, fiberglass, and silica. J Oc- life resuscitation, and follow-up with good sup- cupation Environ Med 1995;37:185-8. portive care. Community alertness for 4. Winek CL, Wahba WW, Rozin L. Acci- nonpredictable toxic chemical releases requires dental death by inhalation. well-organized emergency-medical-response Forensic Sci Internation 1995;73:139-41. systems, as well as emergency physicians and 5. Rorison DG, McPherson SJ. Acute toxic hospitals trained for readiness. Emergency plan- inhalations. Emerg Med Clin North ning should be applicable to both accidental and America 1992;10:409-35. deliberate chemical disasters.19 6. Halpern P, Raskin Y, Sorkine P, Oganezov A. Exposure to extremely high concentra- Conclusion tions of carbon dioxide: a clinical descrip- Asphyxiants are gases that deprive body tissues tion of a mass casualty incident. Ann Emerg of oxygen. The fraction of inspired oxygen Med 2004;43:196-9. (FiO2) tends to decrease with the present of 7. DeGorordo A, Vallejo-Manzur F, Chanin high concentration of certain asphyxiant, espe- K, Varon J. Diving emergencies. Resusci- cially in a confined space, accountable for acci- tation 2003;59:171-80. dental inhalation injuries. When obvious histori- 8. Kwon OY, Chung SP, Ha YR, Yoo IS, cal evidence or a heightened suspicion for an Kim SW. Delayed postanoxic encephal-

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Ann Disaster Med Vol 4 Suppl 1 2005