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Hydrogen Cyanide- A deadly toxicant

Hydrogen Cyanide
Hydrogen cyanide(HCN), whose lethal dose is approximately 25 times smaller than that of carbon monoxide, is a very rapidly acting toxicant. The action of toxicant is due to the cyanide ion, which is formed by hydrolysis in the blood. Unlike CO, which remains primarily in the blood, cyanide ions are distributed throughout the body water and make contact with the cells of tissues and organs. If the concentration of cyanide ion is not sufficiently great to cause death. 

In contrast to CO, cyanide ions do not decrease the availability of oxygen but rather prevent the utilization of oxygen by cells. The heart and brain are particularly susceptible to this inhibition of cellular respiration, with bradycardia(abnormally slow heart action.), cardiac arrhythmia ( the heart can beat too fast, too slow or irregular rhythm.), and EEG brain wave activity (The electroencephalogram (EEG) is the depiction of the electrical activity occurring at the surface of the brain.), indicative of Central nervous system depression, having been reported in studies using monkeys. Although cardiac irregularities are often noted in HCN intoxication, the heart tends carry on respiration, and death is usually due to respiratory arrest of Central nervous system. 
HCN is produced when materials that cohtain nitrogen in their structure, e.g., nylon, wool, polyurethane, urea- formaldehyde and ABS (Acrylonitrile-Butadiene-Styrene) are involved in fire. Hydrogen Cyanide and other cyanogen compounds (Cyanogen is a colourless flammable highly poisonous gas made by oxidizing hydrogen cyanide) arrest the activity of all forms of living matter. They exert an obstructing action on the use of oxygen by the living cells of the body tissues. The physiological response to various concentrations of hydrogen cyanide is presented in below table. 

HCN is a by-product of the combustion of materials such as green wood, tobacco, cotton, paper, wool and silk. When burned, these materials release nitrogen gas into air. Hot fires in enclosed spaces can convert the nitrogen gas to small amounts of cyanide and this cyanide affects the cell and accumulates the lactic acid and intracellular ph drops. 
The immediate danger to life and health toxicity for cyanide is much lower (50ppm) when compared to CO(1200ppm), so firefighters should be extremely cautious about working in a smoket environment unless wearing self-contained breathing apparatus (SCBA). 
CLICK HERE👉 Discussion about Hydrogen Cyanide

Symptoms:-

  • TIME COURSE: Effects can be seen very rapidly following exposure to hydrogen cyanide (AC). After inhalation exposure, symptoms begin within seconds to minutes; death may occur within minutes. After skin exposure, onset of symptoms may be immediate or delayed for 30 to 60 minutes. Ingestion of hydrogen cyanide (AC) solutions or cyanide salts can be extremely fatal. The time of onset of effects depends on the concentration and duration of exposure.
  • ACUTE EFFECT(LESS THAN 8-HOURS):- Early symptoms of cyanide poisoning include lightheadedness, giddiness, rapid breathing, nausea, vomiting, feeling of neck constriction and suffocation, confusion, restlessness, and anxiety. Accumulation of fluid in the lungs (pulmonary edema) may complicate severe intoxications. Rapid breathing is soon followed by respiratory arrest (cessation of breathing). Severe cyanide poisonings progress to stupor, coma, muscle spasms (in which head, neck, and spine are arched backwards), convulsions (seizures), fixed and dilated pupils, and death. The CNS is the most sensitive target organ of cyanide poisoning. Cardiovascular effects require higher cyanide doses than those necessary for CNS effects. In serious poisonings, the skin is cold, clammy, and diaphoretic. Blue discoloration of the skin may be a late finding. Severe signs of oxygen deprivation in the absence of blue discoloration of the skin suggest cyanide poisoning.   
  • EYE IRRITATION
    • Irritation.
    • Contact with only the eyes does not normally result in whole-body (systemic) toxicity.
    • Contact with the eyes can contribute to whole-body (systemic) toxicity. •INGESTION EXPOSURE:
    • Burning sensation in mouth and throat, nausea, vomiting, and abdominal pain
    • Whole-body (systemic) toxicity can occur.
    • •INHALATION EXPOSURE:
    • Mild to moderate: CNS effects: headache, confusion, anxiety, dizziness, weakness (malaise), and loss of consciousness. Cardiovascular effects: palpitations. Respiratory effects: respiratory tract irritation, difficulty breathing or shortness of breath (dyspnea), and transient increase in the rate and depth of breathing (hyperpnea). GI effects: nausea and vomiting (emes
    • Severe: CNS effects: coma, seizures, and dilated pupils (mydriasis). Cardiovascular effects: shock, abnormal or disordered heart rhythms (dysrhythmias), critically low blood pressure, and cardiac arrest. Respiratory effects: abnormally rapid, followed by abnormally slow respirations; accumulation of fluid in the lungs (pulmonary edema); and respiratory arrest. Eye effects: dilated pupils, inflammation of the surface of the eye, and temporary blindness.
    • •SKIN EXPOSURE:
    • Irritation.
    • Absorption through the skin is rapid and can contribute to whole-body (systemic) toxicity. See Inhalation Exposure.
    • Absorption through the skin occurs more readily when ambient temperature and relative humidity are high.
TREATMENT OF EXPOSURE:-

Hydroxocobalamin
  • A dose of 70 mg/kg (not to exceed 5 grams initially) administered over 15 minutes is recommended. This dose can be given IV push in situations of cyanide induced cardiac arrest.
  • Based upon the severity of the poisoning and the clinical response, a second dose of 70 mg/kg (not to exceed 5 g) may be administered by intravenous infusion for a total dose of 10 g. The rate of infusion for the second dose may range from 15 minutes (for patients in extremis) to two hours, as clinically indicated
  • Many patients with cyanide poisoning will be hypotensive; however, elevations in blood pressure have also been observed in known or suspected cyanide poisoning victims. Elevations in blood pressure (≥180 mmHg systolic or ≥110 mmHg diastolic) were observed in approximately 18% of healthy subjects (not exposed to cyanide) receiving hydroxocobalamin 5 g and 28% of subjects receiving 10 g. Increases in blood pressure were noted shortly after the infusions were started; the maximal increase in blood pressure was observed toward the end of the infusion. These elevations were generally transient and returned to baseline levels within 4 hours of dosing.
  • While a safe drug, animal and anecdotal human studies have demonstrated limited or no additional therapeutic benefit by administering sodium thiosulfate in addition to treatment with hydroxocobalamin.
  • Physical incompatibility (particle formation) and chemical incompatibility were observed with the mixture of hydroxocobalamin in solution with selected drugs that are frequently used in resuscitation efforts. Hydroxocobalamin is chemically incompatible with sodium thiosulfate or sodium nitrite. Therefore, these and other drugs should not be administered simultaneously through the same intravenous line as hydroxocobalamin. If a second line is unavailable thoroughly flush the single line prior to administering sodium thiosulfate or sodium nitrite.
  • Simultaneous administration of hydroxocobalamin and blood products (whole blood, packed red cells, platelet concentrate and/or fresh frozen plasma) through the same intravenous line is also not recommended. However, blood products and hydroxocobalamin can be administered simultaneously using separate intravenous lines (preferably on contralateral extremities, if peripheral lines are being used).
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