[Clinical analysis of 10 cases of acute occupational poisoning caused by acetonitrile].

Objective: To investigate the first aid diagnosis and treatment of acute inhalation acetonitrile poisoning and to improve the ability of clinicians to diagnose and treat the disease. Methods: Retrospective analysis was performed on the diagnosis and treatment of 10 cases of acute occupational poisoning caused by acetonitrile gas, and clinical experience was summarized. Results: All the poisoned patients were cured and discharged after rescue and cooperation from various specialties. Conclusion: Acetonitrile poisoning treatment early to take the right first aid measures is the key, while safety education, training and enterprise supervision can not be ignored.

Suicide attempt with acetonitrile ingestion in a nursing mother.

CONTEXT: Acetonitrile (ACN) is a solvent rapidly absorbed through lungs and intestinal tract, and is slowly metabolized to cyanide (CN) by enzymatic processes mediated by CYP2E1. OBJECTIVE: To describe the clinical and laboratory evolution, ACN elimination half-life, and its presence in breast milk in a nursing mother who attempted suicide. CASE DETAILS: A 25-year-old 2-month nursing mother ingested an estimated dose of 2.1 g/kg of ACN. Blood and urine samples were collected 24 h later for ACN, CN and thiocyanate analysis, and 12.5 g sodium thiosulfate i.v. in 1-h infusion was started and repeated every 24 h for 4 days. ACN results showed 200 mg/L in blood and 235 mg/L in urine. ACN analysis in the breast milk at Day 6 showed level of 21 mg/L compared to 27 mg/L in blood collected at the same time, suggesting a possible relationship of 1.3:1.0 ratio. An elimination half-life of 40.4 h was calculated, compared to 32 and 36 h showed in other studies. DISCUSSION: The clinical management must involve the use of CN antidotes for more than 24 h depending on the symptoms and blood levels of ACN. Furthermore, our data showed the possible existence of a close relationship between plasma and breast milk levels.

Disulfiram inhibition of cyanide formation after acetonitrile poisoning.

CONTEXT: Cyanide poisoning may be caused by acetonitrile, a common industrial organic solvent and laboratory agent. OBJECTIVE: To describe the potential use of disulfiram in treating acetonitrile poisoning in a human clinical case and to further study its effect in human liver microsomes in vitro. CASE DETAILS: A 30-year-old man initially presented with a cholinergic toxic syndrome following ingestion of aldicarb. Toxicological analysis revealed coingestion of ethanol. He subsequently developed severe metabolic acidosis caused by the cyanogenic compound acetonitrile which was erroneously interpreted as acetone in the chromatogram. After three treatments with hydroxocobalamin (5 g i.v.) and sodium thiosulfate (12.5 g i.v.) on days 2, 3, and 5, he had transient improvement but recurrent lactic acidosis. Treatment with disulfiram was associated on day 7 with resolution of metabolic acidosis and slowing of the decrease in acetonitrile concentration. He recovered from acetonitrile toxicity completely. The time course of acetonitrile, thiocyanate, and cyanide concentrations suggested that disulfiram inhibited cyanide formation. RESULTS: In vitro experiments with human liver microsomes showed the cyanide concentration was significantly lower after incubation with acetonitrile and disulfiram than acetonitrile alone (a mean 60% reduction in cyanide level). DISCUSSION: Although disulfiram was given late in the course of the poisoning it is possible that it contributed to the recovery.

[Measurement of acetonitrile in blood and urine by head-space gas chromatography].

OBJECTIVE: To establish the method for measurement of acetonitrile in blood and urine by head-space gas chromatography. METHODS: DB-ALC1 (30 m x 320 microm x 1.8 microm) and DB-ALC2 (30 m x 320 microm x 1.2 microm) capillary column were used to measure the acetonitrile in blood and urine with the isopropanol as internal standard reference. RESULTS: The limits of detection of acetonitrile in both blood and urine were 0.5 microg/mL, with a linear range of 5-1000 microg/mL (r = 0.999).The accuracy of this method was 93.2%-98.0%. The RSD for the intra-day and inter-day were less than 3.7%. CONCLUSION: The method is capable for measurement analysis of acetonitrile in blood and urine.

[Cyanide poisoning]. / Cyanidforgiftning.

Cyanide is a toxic compound which inhibits the cellular utilization of oxygen. A number of substances can give rise to cyanide intoxication, which in some cases may have a delayed onset. The symptoms are non-specific and reflect cellular hypoxia. Several strategies may be employed in the treatment. Hydroxycobalamine is an effective and non-toxic antidote. On the basis of a case story, the toxicology, symptoms and treatment of cyanide poisoning are discussed.

Massive rhabdomyolysis and acute renal failure after acetonitrile exposure.

A case of systemic rhabomyolysis after acetonitrile exposure is reported. A 35-year-old previously healthy man suffered from vomiting, convulsion and consciousness loss 15 hours after exposure to acetonitrile. Since acetonitrile is known to be metabolized into cyanide, antidote therapy against cyanide poisoning was given. On admission, pain and all-over muscle swelling were marked. Although the initial therapy was effective, rhabdomyolysis and then acute renal failure developed. Renal function improved very slowly after six weeks of hemodialysis, but atrophy of the muscles remained. The rhabdomyolysis may have been caused by toxicity of the cyanide itself in combination with hypoxia and convulsion.

[Forensic chemical testing of cadaveric material for acetonitrile]. / Sudebno-khimicheskoe issledovanie trupnogo materiala na atsetonitril.

Gas chromatographic conditions for qualitative and quantitative evaluation of acetonitrile in biological material were determined, including those for reactive gas chromatography. Absolute and relative time of acetonitrile and concomitant substances retention in three columns of different polarity was determined. Study of the time of acetonitrile retention in biological material showed that acetonitrile concentration in the blood virtually did not change in cadaveric material stored in a hermetically closed flask for 2 weeks at 20 +/- 3 degrees C, while its concentration in the stomach decreased by 10-15%. Distribution of acetonitrile in human viscera in lethal poisoning was studied; the agent was evenly distributed in the gastric wall, intestine, liver, and kidney, while its concentrations in the lung and brain were 2-3 times higher. Forensic chemical expert analyses of the blood, urine, and viscera from corpses of humans dead from lethal acetonitrile poisoning showed that lethal concentration in the blood was 28.3-57.0 mg and in the urine 23.2-40.6 mg/100 ml.

[The effect of thymogen on the postintoxication immunodeficiency state induced by acute acetonitrile poisoning]. / Vliianie timogena na postintoksikatsionnoe immunodefitsitnoe sostoianie, vyzvannoe ostrym otravleniem atsetonitrilom.

It was demonstrated in experiments on Wistar rats that acute acetonitrile (AN) intoxication (0.8L D50) causes decrease of antibody-forming cells in the spleen, mainly those related to the T-dependent antigen, functioning of the natural cell-killers, antibody-dependent cytotoxicity, the ability of macrophages to induce the humoral immune responses and the delayed hypersensitivity reaction. Thymogen restored most of the humoral and cell immune reactions which were reduced by AN.

Delayed cyanide poisoning following acetonitrile ingestion.

Acetonitrile (methyl cyanide) is a common industrial organic solvent but is a rare cause of poisoning. We report the first recorded UK case. Acetonitrile is slowly converted to cyanide, resulting in delayed toxicity. We describe a case of deliberate self-poisoning by a 39-year-old woman resulting in cyanide poisoning 11 hours later which was successfully treated by repeated boluses of sodium nitrite and thiosulphate. The half-life of conversion of acetonitrile was 40 hours and harmful blood cyanide levels persisted for over 24 hours after ingestion. Departments treating or advising in cases of poisoning need to be aware of the delayed toxicity of acetonitrile. Monitoring in an intensive care unit of cases of acetonitrile poisoning should continue for 24-48 hours.

An acetonitrile-related death.

A 39-year-old female who lived alone was discovered dead in her home. An autopsy produced no cause of death. The blood sedative screen was negative and only diphenhydramine was found by the urine organic base analysis. Examination of the blood and urine for volatiles produced an unexpected peak by GC analysis, which was then identified as acetonitrile by GC/MS. Acetonitrile concentrations were 31 and 56 mg/dL in two separate blood samples and 44 mg/dL in the urine. The blood cyanide concentration was 4.4 micrograms/mL. The cause of death was determined to be acetonitrile poisoning although the source of the acetonitrile was not discovered.

Diagnosis and misdiagnosis of poisoning with the cyanide precursor acetonitrile: nail polish remover or nail glue remover?

Accurate diagnosis of acetonitrile ingestion is critical to management. Often this involves differentiating nail polish remover (acetone) from nail glue remover (acetonitrile). Initial symptoms of acetonitrile ingestion are indistinguishable from those of acetone and common alcohols. However, acetonitrile is metabolized to cyanide, producing severe delayed toxicity. Acetonitrile produced increased serum osmolality and osmolal gap, but these findings are non-specific and normal values cannot rule out potentially fatal exposure. Acetone, but not acetonitrile, was detectable in urine or serum with Acetest tablets; both were unreactive with a ketone dipstick. Acetone and acetonitrile could be detected with routine gas chromatography methods for alcohols. Both substances had identical retention times on the widely used stationary phase, 5% Carbowax 20M on graphitized carbon, and with GasChrom 254. Three other systems afforded unique retention times, but acetonitrile was easily mistaken for ethanol in two. Physicians and laboratories must take care to avoid misdiagnosis of acetonitrile ingestion as exposure to acetone, ethanol or another alcohol.

Two fatalities from ingestion of acetonitrile: limited specificity of analysis by headspace gas chromatography.

A married couple was found dead in bed at their home, and the police investigation indicated that they might have ingested methanol and/or ethanol the previous evening. Postmortem examinations were performed and samples of femoral vein blood, urine, and stomach contents were submitted for toxicological analysis. Headspace gas chromatography (HSGC) using two different column packings (Carbopak B and Carbopak C) was used for qualitative and quantitative analysis of organic volatile substances. The apparent concentrations of ethanol in blood and urine were 0.20 and 0.27 g% w/v, respectively. On reanalysis of body fluids by another HSGC method and gas chromatography/mass spectrometry (GC/MS), the presence of ethanol was not confirmed. Instead, acetonitrile was identified at concentrations of 0.8 g/L in blood, 1.0 g/L in urine, and 1.3 g/L in stomach contents. Inorganic cyanide, the toxic metabolite of acetonitrile, was identified in blood from both victims at concentrations of 2.4 micrograms/g (female) and 4.5 micrograms/g (male). Despite the use of two different column packing materials for HSGC, acetonitrile was mistakenly identified as ethanol.

[Toxicology of acetonitrile].

Acetonitrile is a high-polarity organic solvent widely used in various chemical industries and laboratories. It was once used in consumer goods such as cosmetics. Acetonitrile is readily absorbed through the skin, by inhalation and by ingestion, and acute poisoning and even fatal effects are possible via these routes. The oral LD50 of acetonitrile in mice, which are one of the most susceptible animals to acetonitrile, is 170-520 mg/kg, and LC50 is about 2,700 ppm after one hour of inhalation. The toxic effects of acetonitrile are attributable to the metabolic release of cyanide, but the symptoms of poisoning may be delayed a few hours or more due to slow hepatic metabolism. No information is available yet about the toxicity of intact molecules of acetonitrile or formaldehyde which may be formed together with cyanide in the body. In subacute toxicity experiments in animals, slight changes in hemograms, histopathologic changes in the lung, increase in thyroid function, and other changes have been reported. No information is available about the accumulation of acetonitrile or its metabolites in tissues following repeated administrations, although formaldehyde is known to have high reactivity with macromolecules. No study has yet been done on the chronic toxicity or carcinogenicity of acetonitrile after prolonged administration. Acetonitrile is not mutagenic in the standard test using Salmonella typhimurium. Inhalation of acetonitrile by pregnant animals may produce malformations in the offspring such as axial skeletal disorders at maternally toxic levels. Education and information about the toxicity and regulations on the marketing of acetonitrile are of great importance for the safe use of this material. Further studies and information are needed on the chronic effects of acetonitrile, especially its carcinogenic potency, to human beings.

Severe cyanide poisoning from the ingestion of an acetonitrile-containing cosmetic.

A 39-year-old woman ingested 59 mL of Super Nail Nail Off (American International Industries, Hollywood, CA) (containing 99% acetonitrile) in a suicide attempt. Following a latent period of approximately 12 hours, the patient developed cyanide poisoning with severe metabolic acidosis, seizures, and shallow respirations. She responded to the administration of sodium nitrite and sodium thiosulfate, although the administration of nitrite produced bradycardia and hypotension. She developed several relapses over the course of her hospitalization and each time responded to sodium thiosulfate administration. The patient developed hypernatremia from the sodium load given to her; hemodialysis and charcoal hemoperfusion were initiated to correct the hypernatremia and to attempt to remove cyanide, thiocyanate, and acetonitrile. On the fifth hospital day, the patient was fully recovered and was discharged.

Cyanide toxicity from acetonitrile-containing false nail remover.

A patient presented without symptoms 30 minutes after ingesting acetonitrile, also known as methylacyanide. He had prompt gastric lavage and activated charcoal administration. Hours later, the onset of clinical toxicity was heralded by mental status abnormalities and vomiting prior to a generalized seizure. Following administration of sodium thiosulfate, the patient made an uneventful recovery. A blood cyanide level drawn shortly after presentation, but reported after the patient had been discharged, documented significant exposure. During hospitalization, cyanide toxicity was inferred from the history of ingestion of acetonitrile, plus a significant absence of venous blood hemoglobin desaturation. Because even small amounts can be harmful and toxicity is delayed, all acetonitrile ingestions should be presumed dangerous. Patients should be observed and repeatedly evaluated for at least 24 hours. In the absence of cyanide level determinations, lethargy, vomiting, seizures, and the lack of normal venous blood hemoglobin desaturation are clues to cyanide toxicity.