What Are the Symptoms of Cyanide Poisoning?

Cyanide is a compound containing cyano (CN). It is a commonly used chemical raw material. It is divided into two types: inorganic cyanide (cyanide) and organic cyanide (nitrile). The former mainly includes hydrocyanic acid and cyanate (cyanide). Potassium cyanide, sodium cyanide, amine hydride, potassium ferrocyanide, etc.), and halogen cyanide (cyanide chloride, cyanogen bromide, cyanide iodide), etc., the latter are mainly propionitrile, acrylonitrile, acetonitrile, etc. In professional activities, exposure to cyanide can cause acute cyanide poisoning; while in non-professional activities, exposure to cyanide or eating plant fruits and roots containing cyanogenic glycosides (such as bitter almonds, barley kernels, peach kernels, cassava, ginkgo, etc. all contain Cyanide) can also cause acute cyanide poisoning. The oral lethal amount of hydrocyanic acid is 0.06g, and the cyanate is 0.1-0.3g.

Basic Information

English name

cyanide poisoning

Visiting department

Emergency Department

Common causes

Caused by respiratory inhalation and skin absorption

Common symptoms

Exhaled breath and vomiting contain bitter almond odor, or skin irritation, erythema, and ulceration.

Mechanism of cyanide poisoning

Occupational cyanide poisoning is caused by inhalation of the respiratory tract and skin absorption. Oral poisoning is mainly oral, and the oral mucosa and gastrointestinal tract can be fully absorbed. The toxicity of cyanide is mainly caused by CN dissociated in the body ^- causing symptoms of multisystem poisoning, mainly the central nervous system and cardiovascular system. CN ^- Binding to Fe ³⁺ in the terminal enzyme of the respiratory chain (cytochrome oxidase aa3) makes the enzyme inactive, leading to interruption of intracellular breathing, blocking electron transfer and oxidative phosphorylation, and fundamentally inhibiting the adenosine triphosphate Synthesis, thereby inhibiting the utilization of intracellular oxygen; although mitochondrial oxygen supply is sufficient, aerobic metabolism is disturbed, anaerobic metabolism is enhanced, glycolysis occurs, and ultimately lactic acid production is increased due to obstacles to oxygen uptake and utilization Metabolic acidosis. Isocyanates and thiocyanates do not release CN ^- in the body, but they can directly inhibit the central and strong respiratory tract irritation and sensitization.

Clinical manifestations of cyanide poisoning

The incubation period after acute cyanide poisoning is directly related to the concentration and time of exposure to cyanide. Inhalation of high concentrations of cyanide (> 300mg / m) or lethal dose of sodium cyanide (potassium) can cause a few seconds to 5 minutes after exposure. Symptoms occur within a few hours after exposure to low concentrations of hydrogen cyanide (<40mg / m). Patients with this type of exhaled breath and oral poisoning may have bitter almond odor. Skin contact can cause skin irritation, erythema, and ulcers.

General acute cyanide poisoning can be divided into four phases: prodromal phase: inhalers have eye and upper respiratory tract irritation symptoms, blurred vision; oral poisoning have nausea, vomiting, diarrhea and other gastrointestinal symptoms. Dyspnea: chest tightness, dyspnea, headache, palpitations, increased heart rate, cherry red skin and mucous membranes. Convulsive phase: Ankylosing or paroxysmal spasms occur immediately, and even the arch of the angle is reversed, and the incontinence is caused. Paralysis period: If not rescued in time, the patient's whole body muscles relax, the reflection disappears, coma, sudden drop in blood pressure, shallow and irregular breathing, and soon death before breathing stops.

Cyanide poisoning test

The determination of CN-concentration in whole blood has specific diagnostic value. Generally, the CN ^- concentration in whole blood is <20g / dL (7.69mol / L). The CN ^- concentration in the blood of cyanide poisoning is significantly increased, and it is best to detect it within 8 hours after the poisoning.

The arterial and venous blood gas analysis was performed at the same time in the early stage of poisoning, showing the specific manifestation of venous blood arterialization, that is, the arterial blood oxygen partial pressure is normal, while the venous blood oxygen partial pressure is significantly increased, and the difference between the arterial and venous oxygen partial pressure is reduced to 1% Normally 4% to 5%).

Diagnosis of cyanide poisoning

It is not difficult to diagnose cyanide poisoning based on professional history and clinical manifestations and auxiliary examinations. The patient's lips, skin, and venous blood were bright red, and the exhaled breath had a bitter almond smell, which also helped clinical diagnosis.

Cyanide poisoning treatment

Cyanide ions are easily combined with ferric iron in the body, and then combined with sulfur to form thiocyanate with low toxicity, which is excreted from the urine. The combined application of methemoglobin generator and sulfur supply agent can achieve the purpose of detoxification.

Treatment in acute poisoning:

1. Quickly remove the patient from the poisoning site and remove contaminated clothing. For oral poisoning, immediately wash the stomach with an oxidant solution (5% sodium thiosulfate or 0.02% potassium permanganate), and use a large amount of water when the skin or eyes are contaminated rinse. If breathing is slow or stopped, immediately give breathing stimulants or artificial respiration.

2. Immediately put isoamyl nitrite in a handkerchief and crush it to the patient for inhalation until intravenous sodium nitrite is injected.

3. Immediately inject glucose with sodium nitrite (6 ~ 12mg / kg) slowly into the glucose solution, not less than 10 minutes, pay attention to blood pressure, and once the blood pressure drops, the drug should be discontinued.

4. Immediately inject 50% sodium thiosulfate at the same rate, and if necessary, repeat the injection in half or full amount after 1 hour. Mild poisoning can be used alone.

5.4-Dimethylaminophenol (4-DMAP) and p-aminophenylacetone (PAPP) are methemoglobin generators. Moderate amounts of 4-DMAP and PAPP were taken orally for mild poisoning, and 4-DMAP was immediately intramuscularly injected for moderate-to-severe poisoning, and repeated half an hour later if necessary. Those who use this product are strictly prohibited from re-using nitrous acid drugs to prevent excessive production of methemoglobin (cyanosis).

6. Cobalt compounds: Cobalt has strong affinity with CN ^- and can form stable and low toxicity cyano-cobalt compounds to be eliminated from the urine. Commonly used 1.5% dicobalate edetate (prepared in glucose solution) 20ml intravenously or 40% hydroxycobalamin 10ml slowly intravenously (0.5ml / min).

7. Symptomatic supportive treatment.