ini ada artilkel mengenai sianida.

ini lah alasan kenapa si J memesan 2 cocktail dengan alcohol yang tinggi

We present a patient with a lethal blood concentration of cyanide. Additionally, he was found to have an alcohol blood level of 270 mg.dl−1, but made a complete recovery following administration of the antidotes dimethylaminophenol and thiosulphate. It is postulated that the patient may have been able to detoxify himself as a result of metabolism of cyanide to the non-toxic form, thiocyanate.

Cyanide is one of the earliest organic molecules ever detected in space and is an essential precursor in the synthesis of amino acids, purines and pyrimidines [1]. In healthy individuals, cyanide appears in the blood under normal conditions as a result of vitamin B metabolism and environmental factors such as food or smoking [2]. It is well known to the public for its use in concentration camps in the World War II, homicidal disasters or the cyanide Tylenol deaths which occurred in the United States in 1982 [3].

Cyanide is a potent oral poison producing symptoms in minutes and death in minutes to hours. The lethal oral dose of cyanide salts is 200–300 mg [2]. Whole blood cyanide levels in excess of 2.5 mg.l−1 are associated with coma and are potentially lethal [2]. We report the successful treatment of a patient with a whole blood cyanide level of 6.9 mg.l−1. His blood alcohol level was 270 mg.dl−1.

case historinya :

A 29-year-old man, weight 85 kg, height 180 cm, was seen by emergency staff 8 min after being alerted by the patient's father. He was noted to be unconscious with a respiratory rate of 35–45 breath.min −1. His Glasgow Coma Scale was 3 at initial assessment. His pupils were dilated but reacted to light. The emergency team noted that his breath smelled of alcohol and found cyanide powder along with 12 empty bottles of beer next to the patient. His breath did not smell of bitter almond, but the absence of cyanosis despite obvious respiratory failure suggested a diagnosis of cyanide toxicity.

A blood pressure of 80/60 mmHg was measured and his heart rate was 95 beat.min−1. Following insertion of an intravenous cannula, the patient was intubated after administration of thiopental. He was moderately hyperventilated on 100% oxygen. A crystalloid infusion was commenced and he received an initial bolus of 1000 ml of 0.9% saline. Ten minutes after the arrival of the emergency staff, the patient received 250 mg of dimethylaminophenol, and thiosulphate was started during transportation to hospital. The patient was transferred directly to the Intensive Care Unit (ICU) where he received further thiosulphate (9 g in total). Blood samples were sent for analysis of cyanide and alcohol levels. The patient was sedated with a propofol infusion (250 mg.h−1) and received IPPV on 100% oxygen, with a positive end-expiratory pressure of 10 mmHg and moderately hyperventilated to an arterial partial pressure of 30 mmHg carbon dioxide. The first measured oxygen saturation with pulse oximetry was 82%, corresponding with an arterial partial pressure of 420 mmHg of oxygen.

Chest radiography was normal and an electrocardiogram showed no ischaemia or arrhythmias. The methaemoglobin level was 8.8% and this peaked 2 h later at 9.9%. Five hours after administration of thiosulphate, this level declined to 2.5%, reaching 0.9% after 9 h of treatment. A pH of 7.30 was treated with 100 ml of sodium bicarbonate 8.4%. This increased the arterial pH to 7.5. Gastric and bowel lavage, activated charcoal and laxatives were used after administration of the antidotes. Diuresis was promoted by infusing furosemide at 20 mg.h−1. Sixteen hours after admission, a gastroscopy excluded ulceration of the upper gastrointestinal system and a bronchoscopy was performed which was completely normal. The patient was extubated 18 h after arriving on the ICU. He made a completely uneventful recovery and was discharged from the ICU to a psychiatric ward on the second day.

The patient had a 2-week history of a depressive illness and worked in a metal processing factory from where he had stolen the cyanide (K[Au(CN)2] 100 g, Wieland Edelmetalle GmBH, Pforzheim, Germany). He admitted the ingestion of approximately 50 g of cyanide (half of the total amount of cyanide powder) dissolved in some beer with the intention of committing suicide. The patient left hospital 7 days after his overdose and was included in an outpatient rehabilitation programme.

The forensic department examined the white powder found at the scene and the blood level of the patient for cyanide content using the pyridine–barbituric acid reaction. The powder was identified as cyanide 25 mg.g−1. This led to the conclusion that he had ingested approximately 1250 mg, which is a five-fold lethal dose of cyanide salt. The patient's cyanide blood level was 6.9 mg.l−1.

kesimpulannya :

A review of the literature of the past few years shows that little attention has been given to cyanide toxicity, except for in vitro and in vivo comparisons of antidotes [4–7]. The case reports fail to specify the exact cyanide blood levels [8, 9].

This patient survived after having ingested an extremely high dose of cyanide salt. The presence of alcohol may have limited the uptake of the cyanide by the stomach. Hydrochloric acid in the stomach causes the release of liquid hydrogen cyanide (HCN) which is rapidly adsorbed as the cyanide ion (CN−). The alcohol may have neutralised the acid and therefore limited the uptake of cyanide. However, a lethal cyanide blood level was reached. We postulate that despite the administration of antidotes and supportive therapy, our patient may have been able to detoxify himself.

Cyanide is metabolised by at least four pathways. The enzyme rhodanese converts 80% of cyanide in the presence of thiosulphate to thiocyanate which is then excreted by the kidneys. The rate-limiting step is the amount of thiosulphate. Rhodanese is present in high concentrations in the liver and kidneys, but the supply of thiosulphate is limited. Alternative pathways include the conversion of hydroxycobalamin (vitamin B12a) in the presence of HCN to the non-toxic form, cyanocobalamin (vitamin B12). Small amounts of cyanide are excreted in the lungs and sweat, where they produce a bitter almond odour [1].

Liebowitz et al. [10] reported a case of uneventful recovery in a patient with a blood level of 7.7 mmol.l−1 who did not receive any specific or supportive therapy. Hardy et al. described variations in individual ability to metabolise and therefore to detoxify cyanide by conversion to thiocyanate [11].

A patient with Leber's optic atrophy will be unable to detoxify cyanide by conversion to thiocyanate, since this condition results from a congenital metabolic defect in cyanide metabolism [1].

Cyanide is known to be one of the most rapidly acting lethal poisons. Although a variety of agents are effective antidotes in the experimental animal [4–7], dimethylaminophenol and thiosulphate are recommended in Germany because of fast onset and reduced adverse effects.

In conclusion, we report a mixed poisoning of cyanide and alcohol with an extremely high blood cyanide level. The patient made a complete uneventful recovery because of the immediate administration of appropriate antidotes, and he might have been able to detoxify himself by metabolising the cyanide by conversion to the non-toxic form, thiocyanate.

We thank Dr Caren Cranfield, Consultant Anaesthetist of the Aberdeen Royal Infirmary, Scotland, for her critical reading of the manuscript.


jadi: Jika saat kejadian M meminta J untuk mencoba kopi Vietnamnya,
tubuh J sudah ready untuk menerima sianida (pasti sedikit saja di seruput), karena di lambung sudah ada alcohol 1 gelas. kemudian J bisa menambah konsentrasi alkohol dalam tubuhnya dengan 1 gelas cocktail lg..

mungkin J juga akan pingsan atau keracunan, tetapi tidak menyebabkan kematian seperti yang dialami oleh M.

apa pendapat saudara? #truthbehindcoffee