The Fatal Toxic Manifestations of the Thiocyanates

Garvin, Curtis F.

doi:10.1001/jama.1939.02800120011003

Cited by 25 publications

(4 citation statements)

References 5 publications

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“…Differentiating the relative contribution of the cyanide and thiocyanate to the toxicity described in these reports is difficult. Older reports [1,[8][9][10][11]] of thiocyanate toxicity from over 60 years ago when it was used as an antihypertensive agent are very similar to our patient suggesting that thiocyanate was the predominate substance involved in the toxicity seen in our patient.…”

Section: Discussionsupporting

confidence: 75%

Severe Toxicity with Guanidine Thiocyanate Ingestion

Page¹,

Krüger²,

Dimeski³

et al. 2016

J Clinic Toxicol

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Objective: To describe the toxicity of deliberate guanidine thiocyanate ingestion and it's treatment including dialysis.Case report: A 52-year-old male presented to hospital with abdominal pain after giving a history of ingesting bottled water. His initial vital signs and examination were normal. Soon after the patient became confused and agitated, necessitating intubation and ventilation for presumed encephalitis. His chloride was unmeasurable and the ionised calcium was low at 0.59 mmol/L (reference range [RR] 1.15-1.32 mmol/L). His pH and osmolar gap were normal. Analysis of the ingested water on two chemistry analysers gave discrepant chloride readings (129 mmol/L and 49 mmol/L) suggesting interference from a cross reacting analyte, which subsequently was proven to be thiocyanate with a concentration of 1485mg/L and 538mg/L in the bottled water and admission serum respectively (RR 0.1-4 mg/L). Dialysis in the form of continuous veno-venous haemodiafiltration (CVVHDF) was instituted based on this high level. Serial thiocyanate levels demonstrated zero order elimination kinetics pre dialysis and first order kinetics with a half-life of 5.4 h during dialysis. The patient made a full recovery and admitted to the addition of guanidine thiocyanate to the bottled water.Discussion: Guanidine thiocyanate appears to cause an encephalopathic type presentation with discordant and/or error chloride readings and ionised hypocalcaemia. Dialysis could be considered in the management of its toxicity.

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Section: Discussionsupporting

confidence: 75%

Severe Toxicity with Guanidine Thiocyanate Ingestion

Page¹,

Krüger²,

Dimeski³

et al. 2016

J Clinic Toxicol

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“…Different moisture regimens and soil characteristics could have significant effects on the disappearance of SCN − from soil amended with Brassicaceae seed meals, and it is possible that heavy rainfall immediately after amendment could facilitate more extensive leaching of this anion. However, soil concentrations of SCN − that have been measured after amendment with seed meals of S. alba , B. juncea , and B. napus are orders of magnitude lower than concentrations considered to be harmful to humans and wildlife , . Current results and past evidence of rapid microbial degradation indicate that the use of Brassicaceae meals as agricultural soil amendments does not appear to pose environmental hazards when applied at rates of 2 t ha −1 or less.…”

Section: Resultsmentioning

confidence: 91%

Ionic Thiocyanate (SCN⁻) Production, Fate, and Phytotoxicity in Soil Amended with Brassicaceae Seed Meals

Hansson

Morra

Borek

et al. 2008

J. Agric. Food Chem.

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Brassicaceae seed meals produce ionic thiocyanate (SCN (-)), a bioherbicidal compound. This study determined the fate of SCN (-) in a field soil amended with seed meals of Sinapis alba, Brassica juncea, and Brassica napus and quantified crop phytotoxicity by monitoring carrot ( Daucus carota) emergence. Meals were applied at 1 or 2 t ha (-1), and soils were sampled to 35 cm for SCN (-). Maximum SCN (-) (211 micromol kg (-1) of soil) was measured at 5 days in 0-5 cm samples from plots amended with S. alba meal at 2 t ha (-1). Less than 30 micromol of SCN (-) kg (-1) of soil was measured at soil depths below 15 cm. At 44 days, SCN (-) was <15 micromol kg (-1) of soil in all treatments. Emergence inhibition of carrots seeded 15-36 days after meal amendment was found only in S. alba treatments. The rapid decrease of SCN (-) concentrations in Brassicaceae meal-amended soil indicates limited potential for off-site environmental impacts.

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“…Although SCN is generally considered to be nontoxic, it was shown early to have a weak hypotensive action (Pauli, 1903;Barker, 1936) and, until the late 1950s, patients with refractory hypertension were prescribed large doses of sodium or potassium thiocyanate to be taken by mouth over long periods, sometimes for many years. Toxic effects, such as anaemia, psychosis, coma and death, occurred at plasma SCN concentrations greater than 2 0 m g d r 1 or 3450 (xmol litre" 1 (Garvin, 1939;Barker, Lindberg and Wald, 1941;Barnett, Jackson and Spaulding, 1951;Frohman and Klocke, 1963). Barker (1936), therefore, introduced the monitoring of plasma SCN concentrations during thiocyanate therapy and suggested that concentrations between 6 and 10 mg dl" 1 (1035-1725 [imol litre" 1 ) decrease arterial pressure, while significant toxicity occurred only above 15-20 m g d l " 1 (2590-3450 nmol litre" 1 ).…”

Section: Thiocyanate Accumulation Related To Snp Dosementioning

confidence: 99%

Blood Cyanide and Thiocyanate Concentrations Produced by Long-Term Therapy With Sodium Nitroprusside

Vesey

Cole

1985

British Journal of Anaesthesia

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Blood cyanide (HCN) or plasma thiocyanate (SCN) concentrations, or both, were measured in 30 patients (ages 11 months-72 yr) receiving sodium nitroprusside (SNP) for 12-314 h. Sequential measurements in three of these patients (infused 5, 12 and 13 days) showed that HCN concentrations varied with dose rate, while SCN concentrations increased linearly with increasing SNP dose. The accumulated data confirmed that the rate of administration (0.3-6.5 micrograms kg-1 min-1) determined the plasma HCN concentrations (0-3.8 mumol litre-1; y = 0.267 X -0.0733; r = 0.64; n = 51; P less than 0.001). Thus, if prolonged exposure to plasma HCN concentrations greater than 1 mumol litre-1 is to be avoided, the maximum safe sustained dose rate of SNP will lie near to 4 micrograms kg-1 min-1. Likewise, the SCN results (30--880 mumol litre-1) confirmed the close relationship between plasma concentrations and the total SNP dose (0.44-32.9 mg kg-1; y = 24.6x + 74.9; r = 0.95, n = 51, P less than 0.001). Therefore, we suggest that, to avoid SCN toxicity (plasma SCN greater than 1.75 mumol litre-1), in the absence of SCN monitoring, the total SNP dose should be less than 70 mg kg-1 in patients with normal renal function.

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The Fatal Toxic Manifestations of the Thiocyanates

Cited by 25 publications

References 5 publications

Severe Toxicity with Guanidine Thiocyanate Ingestion

Severe Toxicity with Guanidine Thiocyanate Ingestion

Ionic Thiocyanate (SCN⁻) Production, Fate, and Phytotoxicity in Soil Amended with Brassicaceae Seed Meals

Blood Cyanide and Thiocyanate Concentrations Produced by Long-Term Therapy With Sodium Nitroprusside

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The Fatal Toxic Manifestations of the Thiocyanates

Cited by 25 publications

References 5 publications

Severe Toxicity with Guanidine Thiocyanate Ingestion

Severe Toxicity with Guanidine Thiocyanate Ingestion

Ionic Thiocyanate (SCN−) Production, Fate, and Phytotoxicity in Soil Amended with Brassicaceae Seed Meals

Blood Cyanide and Thiocyanate Concentrations Produced by Long-Term Therapy With Sodium Nitroprusside

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Ionic Thiocyanate (SCN⁻) Production, Fate, and Phytotoxicity in Soil Amended with Brassicaceae Seed Meals