eMedicine Specialties > Emergency Medicine > Warfare - Chemical, Biological, Radiological, Nuclear and Explosives

CBRNE - Cyanides, Hydrogen

Author: Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Coauthor(s): Andre Pennardt, MD, FACEP, FAAEM, Adjunct Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences; Consulting Staff, Department of Emergency Medicine, Aviation Medicine and Dive Medicine, Womack Army Medical Center
Contributor Information and Disclosures

Updated: Mar 11, 2008

Introduction

Background

Hydrogen cyanide (HCN; North Atlantic Treaty Organization [NATO] designation AC) is 1 of 2 cyanide chemical warfare agents. The other is cyanogen chloride (NATO designation CK). Cyanide was first used as a chemical weapon in the form of gaseous HCN in World War I. The French used approximately 4000 tons without notable military success starting in 1915. This was most likely because of the high volatility of cyanide and the fact that the 1- to 2-lb munitions used could not deliver the amounts of chemical required for biological effects. The introduction of cyanogen chloride by the French in 1916 presented a more toxic compound with less volatility, improving its effectiveness as a chemical agent. Other alleged military uses of cyanide include Japanese attacks on China before and during World War II and Iraqi attacks on Kurds in the 1980s.

Cyanide is a rapidly lethal agent when used in enclosed spaces where high concentrations can be achieved easily. In addition, because of the extensive use of cyanide in industry in the United States, this agent presents a credible threat for terrorist use. Emergency physicians may also encounter cyanide casualties resulting from industrial accidents. Specific industrial processes involving cyanide include metal cleaning, reclaiming, and/or hardening, fumigation, electroplating, and photoprocessing. Other potential sources of cyanide are fires involving plastics and/or synthetics, acrylic nail removers containing acetonitrile or propionitrile, or nitroprusside infusions. Numerous plants such as apricots, apples, and bitter almonds contain within their seeds and pits amygdalin, which can be hydrolyzed to AC following the ingestion of large quantities.

For related information, see Medscape's Disaster Preparedness and Aftermath Resource Center.

Pathophysiology

While liquid cyanide can be absorbed through the skin or eyes, the primary route of exposure is by inhalation or ingestion. Following absorption, cyanide is distributed rapidly to all organs and tissues in the body. Cyanide combines with ferric iron in cytochrome a3 (the last component of the cytochrome oxidase electron transport chain in mitochondria) and inhibits this enzyme. This prevents intracellular oxygen use and the generation of cellular ATP, ceasing aerobic energy production. Anaerobic production of ATP continues as pyruvate is converted to lactate. Metabolic acidosis ensues rapidly not due to lactic acidosis, but rather as a result of cells continuing to produce hydrogen ions through use of ATP without the balance of consumption by oxidative phosphorylation.

Frequency

United States

Emergency physicians are unlikely to encounter casualties from hydrogen cyanide used as a weapon except in the setting of a terrorist attack. Typical cyanide exposures are the result of liberation of the chemical during house and/or industrial fires or accidents.

Mortality/Morbidity

The LCt50 (concentration-time product capable of killing 50% of exposed group) for AC is 2500-5000 mg·min/m³. The lethal oral dose of AC and cyanide salts is estimated to be 50 mg and 100-200 mg, respectively. The LD50 (dose capable of killing 50% of exposed group) for skin exposures is estimated at 100 mg/kg. Vapor exposures in high concentrations (at or above the LCt50) typically can cause death in 6-8 minutes.

Clinical

History

Key historic features for suspected hydrogen cyanide casualties include onset, severity, and time course of symptoms, time and nature of exposure, route of exposure, presence of smoke, odors and colors of gas, effects on surroundings (dead animals, other human casualties), and evidence of exposure to other chemicals or co-ingestants. As many as 50% of patients exposed to cyanide may describe an odor of bitter almonds.

• Symptoms after high vapor exposure
  • Transient hyperpnea and hypertension 15 seconds after inhalation
  • Convulsions in 30-45 seconds
  • Loss of consciousness in 30 seconds
  • Respiratory arrest in 3-5 minutes
  • Bradycardia, hypotension, and cardiac arrest within 5-8 minutes of exposure
• Symptoms after exposure to lower vapor concentrations or after ingestion and/or liquid exposure
  • May be several minutes before onset
  • Feelings of apprehension or anxiety
  • Vertigo
  • Feeling of weakness
  • Nausea with or without vomiting
  • Muscular trembling
  • Progression of symptoms to unconsciousness
  • Headache
  • Dyspnea
• Patients exposed to cyanogen chloride experience severe eye and mucous membrane irritation.
  • Low-dose exposure results in rhinorrhea, bronchorrhea, and lacrimation.
  • Inhalational exposure results in dyspnea, cough, and chest discomfort.
• Exposure to nitriles (acetonitrile and/or propionitrile) may be associated with a significant delay in onset of symptoms.

Physical

Physical findings are nonspecific and are similar to those of severe hypoxemia.

• Altered mental status
• Convulsions
• Hypotension
• Transient hyperpnea
• Bradypnea followed by apnea
• Cardiac dysrhythmias followed by cardiac arrest
• Severe respiratory distress in an acyanotic patient suggests possible cyanide toxicity.
• When observed, cherry-red skin suggests concomitant carbon monoxide poisoning or high venous oxygen content from failure of tissues to extract oxygen. Arterialization of the venous blood may also be noted during phlebotomy or examination of the retinal veins.
• Bright red skin and absence of cyanosis seldom are described in patients with cyanide poisoning, most likely because of concomitant cardiovascular collapse. Patients may also present cyanotic after prolonged respiratory failure and shock.
• Patients may demonstrate diaphoresis with normal or dilated pupils.
• Initial hypertension and compensatory bradycardia are followed by hypotension and tachycardia.
• Terminal hypotension is accompanied by bradyarrhythmias prior to asystole.

Causes

Causes of cyanide casualties include deliberate use as a chemical warfare agent, industrial exposures, and toxic byproducts of fires.

• Search for CME/CE on This Topic »

• CBRNE - Cyanides, Cyanogen Chloride (Emergency Medicine)
• Toxicity, Hydrogen Sulfide (Emergency Medicine)
• Metabolic Acidosis (Nephrology)
• Acidosis, Metabolic (Pediatrics: Cardiac Disease and Critical Care Medicine)

• Bioterrorism and Warfare Center
• Chemical Warfare
• Personal Protective Equipment
• Poisoning Center
• Carbon Monoxide Poisoning Overview

• Hydrogen Sulfide: Potential Help for ED

• T670X KIT Mutations in Gastrointestinal Stromal Tumors: Making Sense of Missense
• Review Article: Lactose Intolerance in Clinical Practice – Myths and Realities
• Targeting Cancer With Small Molecule Kinase Inhibitors