scholarly journals Sodium Nitrite and Sodium Thiosulfate Are Effective Against Acute Cyanide Poisoning When Administered by Intramuscular Injection

2017 ◽  
Vol 69 (6) ◽  
pp. 718-725.e4 ◽  
Author(s):  
Vikhyat S. Bebarta ◽  
Matthew Brittain ◽  
Adriano Chan ◽  
Norma Garrett ◽  
David Yoon ◽  
...  
1992 ◽  
Vol 32 (4) ◽  
pp. 368-375 ◽  
Author(s):  
Steven I. Baskin ◽  
Arthur M. Horowitz ◽  
Eric W. Nealley

2019 ◽  
Vol 19 (4A) ◽  
pp. 139-150
Author(s):  
Le Ho Khanh Hy ◽  
Pham Xuan Ky ◽  
Dao Viet Ha ◽  
Nguyen Phuong Anh ◽  
Phan Bao Vy ◽  
...  

The Oceanographic Museum offers interesting exhibits of several marine lives for tourist sightseeing and entertainment. These sea water ornamental fish are all caught in the wild. However, its health can be affected by cyanide poisoning during human fishing. Depending on the level of cyanide poisoning, fish can die after one and two weeks that caused economic damages for the museum. The present study is concerned with results of cyanide detoxification by using direct injection into cinnamon clownfish or soak of hydroxocobalamin, sodium nitrite and sodium thiosulfate with the aim of improving the health, survival and life time for fish, contributing to increasing economic efficiency for the Oceanographic Museum.


PEDIATRICS ◽  
1971 ◽  
Vol 47 (6) ◽  
pp. 1093-1093
Author(s):  
Howard C. Mofenson ◽  
Joseph Greensher ◽  
Ray Horowitz ◽  
Cheston M. Berlin

Dr. Berlin's schedule of treating cyanide poisoning by sodium nitrite and sodium thiosulfate should be in every emergency room and poison control center.1 It should also be included in Lilly's Cyanide Antidote Kit which contains these materials. (I have written the Eli Lilly Company concerning this.) Since cyanide is a spectacular poison and evokes such a frightening response and vigorous treatment, it is important to emphasize that ferrocyanide and ferricyanide as found in Turndall's Blue and Prussian Blue are of low toxicity (potential single adult fatal dose 50 gm).


2015 ◽  
Vol 12 (3) ◽  
Author(s):  
Craig B Barraclough

IntroductionCyanide, due to its toxicity and prevalence in a variety of industries, is a suitable agent for terrorists or disaffected persons to use as a weapon of terror. New Zealand’s National Poisons Centre lists five cyanide antidotes. This review aimed to identify whether there is an ideal pre-hospital drug treatment for acute cyanide poisoning.MethodsLiterature less than 10 years old was selected after a keyword search. The articles were reviewed for specific positive and negative properties of each antidote.ResultsThirty-nine articles were reviewed of which four were excluded. Results varied, with hydroxocobalamin scoring highly on effectiveness, with limited negative effects. It also demonstrated positive haemodynamic effects, suitability in cases involving trauma, carbon monoxide (CO), smoke inhalation casualties and was safe for pre-hospital use. Sodium nitrite, followed by dicobalt edetate had the next highest scores for efficacy. However, both scored negatively for their effects on blood, causing hypotension and toxicity, and they are unsuitable for trauma, CO or smoke inhalation casualties. Sodium thiosulphate, with a moderate level of efficiency, remained most effective when co-administered with other antidotes. 4-dimethylaminophenol and amyl nitrite rated the lowest, with negative effects similar to sodium nitrite. Adrenaline was tested as an antidote in one study where two novel antidotes both demonstrated promising results.ConclusionHydroxocobalamin had the highest success rate and its safety profile make it the most suitable pre-hospital drug treatment for acute cyanide poisoning.


2013 ◽  
Vol 26 (5) ◽  
pp. 828-836 ◽  
Author(s):  
Leah K. Cambal ◽  
Andrew C. Weitz ◽  
Hui-Hua Li ◽  
Yang Zhang ◽  
Xi Zheng ◽  
...  

1996 ◽  
Vol 85 (3) ◽  
pp. 558-564. ◽  
Author(s):  
Peter H. Breen ◽  
Schlomo A. Isserles ◽  
Eric Tabac ◽  
Michael F. Roizen ◽  
Uri Z. Taitelman

Background During fire exposure, cyanide toxicity can block aerobic metabolism. Oxygen and sodium thiosulfate are accepted therapy. However, nitrite-induced methemoglobinemia, which avidly binds cyanide, decreases oxygen-carrying capacity that is already reduced by the presence of carboxyhemoglobin (inhalation of carbon monoxide in smoke). This study tested whether exogenous stroma-free methemoglobin (SFmetHb) can prevent depression of hemodynamics and metabolism during canine cyanide poisoning. Methods In 10 dogs (weighing 18.8 +/- 3.5 kg) anesthetized with chloralose-urethane and mechanically ventilated with air, baseline hemodynamic and metabolic measurements were made. Then, 137 +/- 31 ml of 12 g% SFmetHb was infused into five dogs (SFmetHb group). Finally, the SFmetHb group and the control group (n = 5, no SFmetHb) received an intravenous potassium cyanide infusion (0.072 mg.kg-1.min-1) for 20 min. Oxygen consumption (VO2) was measured with a Datex Deltatrac (Datex Instruments, Helsinki, Finland) metabolic monitor and cardiac output (QT) was measured by pulmonary artery thermodilution. Results From baseline to cyanide infusion in the control group, QT decreased significantly (p < 0.05) from 2.9 +/- 0.8 to 1.5 +/- 0.4 l/min, mixed venous PCO2 (PvCO2) tended to decrease from 35 +/- 4 to 23 +/- 2 mmHg, PvO2 increased from 43 +/- 4 to 62 +/- 8 mmHg, VO2 decreased from 93 +/- 8 to 64 +/- 19 ml/min, and lactate increased from 2.3 +/- 0.5 to 7.1 +/- 0.7 mM. In the SFmetHb group, cyanide infusion did not significantly change these variables. From baseline to infused cyanide, the increases in blood cyanide (4.8 +/- 1.0 to 452 +/- 97 microM) and plasma thiocyanate cyanide (18 +/- 5 to 65 +/- 22 microM) in the SFmetHb group were significantly greater than those increases in the control group. SFmetHb itself caused no physiologic changes, except small decreases in heart rate and PvO2. Peak SFmetHb reached 7.7 +/- 1.0% of total hemoglobin. Conclusions Prophylactic intravenous SFmetHb preserved cardiovascular and metabolic function in dogs exposed to significant intravenous cyanide. Blood concentrations of cyanide, and its metabolite, thiocyanate, revealed that SFmetHb trapped significant cyanide in blood before tissue penetration.


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