Systemic asphyxiants are a type of chemical-warfare agent and include (1)
Cyanide compounds
Hydrogen sulfide
Systemic asphyxiants have also been called blood agents because they are systemically distributed via the blood. However, their site of action is not the blood but rather at the cellular level throughout the body.
Cyanide salts have been used to murder via ingestion, but mass casualties could also result from inhalation of hydrogen cyanide or cyanogen chloride, which are highly volatile liquids or gases at ambient temperatures. Cyanides are also products of combustion of numerous household and industrial contents, and patients with smoke inhalation may also have cyanide poisoning. Cyanide has a characteristic bitter-almond odor, but ability to detect this odor is conferred by a single gene that is absent in half the population.
Hydrogen sulfide is always a gas at ambient temperatures. Exposure is thus usually by inhalation. Hydrogen sulfide can be produced by mixing sulfur-containing household chemicals with acids; this combination has been used for suicide (termed detergent suicide), and residual gas can affect rescuers, causing multiple casualties. Hydrogen sulfide is also produced when manure decomposes. Large farm manure pits often contain lethal quantities of the gas, which may cause multiple casualties as would-be rescuers without proper protective gear succumb. Hydrogen sulfide has a characteristic rotten egg odor, but high concentrations damage olfactory fibers so that this odor will not be perceived in the most lethal environments.
(See also Overview of Chemical-Warfare Agents.)
Pearls & Pitfalls
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General reference
1. Borron SW, Bebarta VS. Asphyxiants. Emerg Med Clin North Am. 2015;33(1):89-115. doi:10.1016/j.emc.2014.09.014
Pathophysiology of Systemic Asphyxiant Chemical Injuries
Symptoms and Signs of Systemic Asphyxiant Chemical Injuries
Cyanide initially causes gasping, tachycardia, and hypertension. Loss of consciousness and convulsions may occur in as little as 30 seconds. Tetanus-like signs, including trismus (lockjaw), risus sardonicus (grimacing), and opisthotonus (neck arching), may occur. The skin may be flushed, but about half of casualties are cyanotic. Apnea usually precedes bradycardia and hypotension, and decorticate posturing may be noted prior to death.
Hydrogen sulfide in high doses also causes abrupt loss of consciousness with convulsions. Direct damage to myocardium may be prominent. Continued exposure to initially sublethal concentrations may induce eye irritation with conjunctivitis and corneal abrasions and ulcerations (gas eye), irritation of nasal and pharyngeal mucous membranes, headache, weakness, ataxia, nausea, vomiting, chest tightness, and hyperventilation. Some of these manifestations appear to be a reaction to the offensive odor of the compound. A green discoloration or darkening of coins carried by the patient should lead to a heightened suspicion of hydrogen-sulfide poisoning.
Diagnosis of Systemic Asphyxiant Chemical Injuries
Clinical evaluation
Severely affected patients must be treated before testing is available, so diagnosis is mainly clinical. Laboratory findings include a decreased arteriovenous oxygen difference (due to higher-than-usual venous oxygen content) and high-anion-gap acidemia with increased lactate.
Triage
All unconscious patients with a pulse are potentially salvageable and should be triaged for immediate medical treatment. Because patients with inhalational exposure usually do not get worse after removal from the contaminated environment, conscious patients who are reporting decreasing symptoms may be triaged as delayed (ie, able to tolerate a short delay while immediate casualties are being treated).
Treatment of Systemic Asphyxiant Chemical Injuries
Airway support and 100% oxygen
For cyanide, specific antidotes
Attention should be given to airway, breathing, and circulation. Water with or without soap suffices for skin decontamination; patients exposed only to vapor or gas usually do not require decontamination.
Cyanide casualties
Cyanide casualties resulting from smoke inhalation may also have carbon monoxide poisoning. In such cases, hydroxycobalamin has been recommended over nitrates by some authorities because hydroxycobalamin does not decrease oxygen-carrying capacity as nitrites do (1, 2). However, concerns about administering nitrites in this situation are probably overstated. Hyperbaric oxygen has not been proven to improve outcomes in patients poisoned with cyanide.
Hydrogen-sulfide3, 4).
Treatment references
1. Anseeuw K, Delvau N, Burillo-Putze G, et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med. 2013;20(1):2-9. doi:10.1097/MEJ.0b013e328357170b
2. Kirk MA, Gerace R, Kulig KW. Cyanide and methemoglobin kinetics in smoke inhalation victims treated with the cyanide antidote kit. Ann Emerg Med. 1993;22(9):1413-1418. doi:10.1016/s0196-0644(05)81988-2
3. Guidotti TL: Hydrogen sulfide: Advances in understanding human toxicity. Int J Toxicol, 29(6):569-581, 2010. doi: 10.1177/1091581810384882
4. Ng PC, Hendry-Hofer TB, Witeof AE, et al. Hydrogen Sulfide Toxicity: Mechanism of Action, Clinical Presentation, and Countermeasure Development. J Med Toxicol. 2019;15(4):287-294. doi:10.1007/s13181-019-00710-5
