Intoxicación por cianuro como método suicida: reporte de caso / Cyanide poisoning as a suicide method: case report

Resumen Las intoxicaciones derivan de la presencia en el organismo de un tóxico o veneno, la muerte por intoxicación es una muerte violenta y por tanto requiere de la realización de una autopsia medico legal, la misma puede darse en el contexto de una exposición accidental ya sea en el hogar o laboral o sucitada por un intento de autoeliminación. La intoxicación por cianuro puede ser intencional (suicidio u homicidio) o accidental, los hallazgos en la autopsia medico legal son inespecíficos por lo que son importantes los datos aportados en el informe sobre muerte en investigación, el informe del escenario de muerte en caso de que un médico forense se hiciera presente al mismo y el resultado de los análisis toxicológicos, los cuales actualmente no se realizan en la sección de toxicología del poder judicial. Se realizó una revisión bibliográfica en diferentes bases de datos, de los artículos publicados referentes al tema de los últimos cinco años, con el objetivo de revisar las caracteristicas del químico, el metabolismo y la intoxicación como tal, tanto por sus secuelas como por sus implicaciones letales. Se concluye que para mejorar la pericia médico legal ante casos de intoxicacion por cianuro es fundamental conocer el mecanismo de acción y los posibles hallazgos presentes tanto al examen externo como interno, así como implementar que dicho escrutinio se incluya dentro del listado de sustancias a analizar.

Abstract Poisoning derives from the presence of a toxic substance or poison in the body, death by poisoning is a violent death and requires a legal medical autopsy, it may occur in the context of an accidental exposure at home or work, or caused by an attempt of self-elimination. Cyanide poisoning can be intentional (suicide / homicide) or accidental, the findings in the autopsy are unspecific, so data provided in the report of death in investigation, the report of the death scene (in case a forensic doctor was present) and the result of the toxicological analyzes, which are not currently performed in the toxicology section of the judiciary, are important. A bibliographic review was carried out in different databases of articles published in the last five years on the subject, with the objective of reviewing the chemical characteristics, the metabolism and the intoxication, as well, including their sequels and lethal implications. It is concluded that to improve the medical legal expertise in cases of cyanide poisoning, it is essential to know the mechanism of action and the possible findings in the external and internal examination; and to implement such scrutiny in the list of substances to be analyzed.

Postmortem examination cases of cyanide poisoning A biological hazard.

Hydrocyanic acid and various cyanides are relatively common poisons both in suicide, accident and occasionally homicide. Acute poisoning with cyanide is most often self administered as the swift and sure action is generally known. Accidental poisoning from inhalation of vapours due to fires in buildings or by the free gas liberated from some commercial processes is also known to occur. The preparations are rarely used with homicidal intent. Whatever be the manner of poisoning, in medical settings the persons involved in postmortem examination of cases of death of cyanide poisoning are exposed to significant degree of cyanide remaining in the body cavities and tissues of the deceased. This risk is not only for the persons attending postmortem examination but also for the first respondents like police, rescue persons and also persons extending emergency care both outside and within hospital. Hydrocyanic acid is rapidly absorbed from all mucous surfaces and even from unabraded skin .Hence attending a case of cyanide poisoning involves a hazard of inhalation of cyanide gas from the victim The hazards involved in such situations are briefly reviewed.

Revisión de la toxicocinética y la toxicodinamia del ácido cianhídrico y los cianuros / Review of toxicokinetics and toxicodynamics of cyanides and hydrogen cyanide

El cianuro es uno de los tóxicos más peligrosos por su rápida y potente acción, muchas veces letal. Los diferentes tratamientos de la intoxicación tienen su base o explicación en el conocimiento de la toxicocinética y la toxicodinamia. La revisión de la toxicocinética del cianuro muestra que, si bien la vía de la tiosulfato-cianuro sulfotransferasa (rodanasa) es la principal vía metabólica, el complejo con albúmina sérica sería el primer proceso de detoxificación del cianuro en el metabolismo normal. El efecto protector de formadores de cianhidrinas en casos de intoxicación sigue siendo evaluado a nivel experimental. Los estudios actuales sobre la toxicodinamia del cianuro se enfocan en la afinidad de la unión del cianuro al centro binuclear hemo a3-CuB de la citocromo oxidasa en sus diferentes estados redox y enel mecanismo de inhibición de enzimas antioxidantes. Un mayor y mejor entendimiento de la detoxificación del cianuro así como de los mecanismos de acción tóxica podrían llevar al desarrollo de potenciales antídotos.

Cyanide is one of the most dangerous poisons because of its rapid and potent toxicity, most times with lethal outcomes. Different poisoning treatments are based on knowledge of cyanide’s toxicokinetic and toxicodynamic. The review of cyanide’s toxicokinetics shows that, although thiosulfate-cyanide sulfotransferase (rhodanese) is the major metabolic pathway, binding serum albumin would be the first process of detoxification of cyanide in normal metabolism. The protective effect of cyanohydrin formers in cases of poisoning remains experimentally evaluated. Cyanide’s binding affinity to the binuclear center heme a3-CuB of cytochrome oxidase within their different redox states and cyanide’s mechanism of inhibition of antioxidant enzymes are currently still being investigated. More and better understanding of cyanide’s detoxification pathways and/or mechanisms of toxic action could lead to the development of new potential antidotes.

Cyanide poisoning, 2 cases report and treatment review.

Two patients, a 4-year-old girl and her brother 1 1/2 year-old, with cyanide poisoning are reported. They vomited and became comatose 9 hours after ingestion of boiled cassava. At a community hospital, they were intubated and given ventilatory support. The girl was transferred to Ramathibodi Intensive Care Unit. At 19 hours after ingestion, sodium nitrite and sodium thiosulfate were given as well as other supportive treatment. She recovered with normal breathing on the next day. The boy was referred to Ramathibodi 4 hours later. On arrival, he appeared normal except for the bitter almond breathe. Only supportive treatment was given. Their blood cyanide levels on arrival were 0.56 and 0.32 microgram/ml (normal value < 0.3 microgram/ml) respectively confirming the diagnosis of cyanide poisoning. Other abnormal laboratory findings included metabolic acidosis and lactic acidemia. The pathogenesis and management of cyanide poisoning are reviewed.

Effect of naloxone hydrochloride on acute toxicity of sodium cyanide in mice

Cyanide intoxication in mice can be antagonized by the opiate antagonist, naloxone hydrochloride alone or in combination with sodium thiosulfate. Potency ratios, derived from acute lethality values, arterial blood gases analysis and electrocardiogram tracting, were compared in groups of mice treated with sodium thiosulfate [i.p. 1 g/kg] and naloxone HCl [s.c. 3.33 mg/kg], either alone or in combination with sodium cyanide. These results indicated that naloxone HCl provided a significant protection against the lethal effects of sodium cyanide. The protective effect of sodium thiosulfate was enhanced with naloxone HCl. Naloxone HCl also provided a significant protection against the effects of sodium cyanide on arterial blood gases and on electrocardiagram, and the protective effect of sodium thiosulfate was enhanced with naloxone HCl

Epidemiological evidence from Zaire for a dietary etiology of konzo, an upper motor neuron disease

A clear association between seasonal outbreaks of a paralytic disease called konzo and toxic effects from consumption of insufficiently processed bitter cassava roots has been demonstrated in Bandundu region, Zaire. A community-based survey of 6764 inhabitants identified 110 live and 24 dead konzo-affected persons with a history of isolated non-progressive spastic paraparesis of abrupt onset. The start of these annual outbreaks of konzo in 1974 coincided with the completion of a new tarmac road to the capital, which facilitated the transport of cassava and made it the main cash crop. The extensive cassava sales encouraged the consumption by the peasant families of roots that had not been adequately processed; frequent acute cyanide intoxications resulted when the naturally occurring cyanogens in the roots were eaten. The disease mainly appeared in the dry season when there was high consumption of insufficiently processed cassava and the diet lacked supplementary foods with sulfur-containing amino acids which promote cyanide detoxification. These results, which confirm the earlier findings in East Africa, show that, owing to the high cyanide and low sulfur dietary intake, there is an increased risk of konzo outbreaks in cassava-growing areas during periods of adverse agro-economic changes

Serum rhodanese in goitre and calcific pancreatitis of tropics.

Rhodanese is one of the enzymes concerned in the detoxification of cyanide. Cassava intake and consequent cyanide toxicity are incriminated in the pathogenesis of goitre and calcific pancreatitis of tropics. So we studied the activity of rhodanese in these patients. 14 controls, 13 patients with pancreatitis and 12 with goitre were studied. The median (and range) of rhodanese in these groups were 82 (50-144), 110 (64-180) and 71 (22-160) units respectively. The serum rhodanese was significantly higher (P less than 0.05) in patients with pancreatitis when compared to the other groups. There was no significant difference between the serum rhodanese in patients with goitre and the controls. The presence of adequate amounts of rhodanese indicates that goitre and chronic pancreatitis are not produced by impaired cyanide detoxification.

Plasma thiocyanate and free radicals in jaaraparesis

Tropical Spastic Paraparesis (TSP) in West African contries is countries is caused by combination of excess cyanide from the ingestion of Cassava and a deficiency of the sulphur-containing amino-acids required to detosify the cyanide. Free radical damage to long axons has also been reported to results in damage similar to that seen in Jamaican TSP. To investigate the possibility that these mechanisms may be responsible for Jamican TSP, venous blood from non-smoking blood donors and 22 patients with TSP were analysed for thiocyanate, superoxide dismutase and glutahione. Serum thiocyanate is an index of cyanide exposure. Superoxide dismutase protects against free radical damage, and glutathione in addition to rotecting against free radical damage is ana important sulphur-containing peptiae. Levels of thiocyanate in the patients with TSP were similar to those in control patients. Glutathione was elevated in all the patients, and superoxide dimutase activity was normal. The low levels of thiocyanate suggest that cyanide toxicity is not the primary cause of Jamaican TSP and, in any event, sufficient amounts of sulphur-containing amino-acids are present to detoxify cyanide. Free radical mechanisms ara also unlikely to be responsible for damage to the neurons in thes patients