Fatal methemoglobinemia in three suicidal sodium nitrite poisonings.

Nitrites are chemicals that are abundant in the environment, widely used as preservatives for meat, and in pharmaceuticals. Volatile products containing nitrites have been used recreationally for the euphoric effect associated with mild hypoxia. Dietary exposure to small amounts is considered harmless. Deaths by ingestion of nitrite salts are not common, but accidental exposure and as suicidal and homicidal agents have been noted. Death is a consequence of oxidation of hemoglobin ferrous (Fe+2 ) iron (Hb) to the ferric (Fe+3 ) form (methemoglobin, MetHb), causing a reduction in the oxygen-carrying capacity of the blood. We report three cases of ingestion of sodium nitrite in two college students (one mildly decomposed) and one adult in early middle age. All of the decedents in these cases developed fatal methemoglobinemia. Sodium nitrite in chemical form was found near the bodies. MetHb was detected in the postmortem blood of each decedent. The MetHb concentrations in the two decedents with a short postmortem interval were less than MetHb concentrations reported in the current literature. The MetHb concentrations reported in the mildly decomposed person were greater than for the other two, but still less than the concentration previously considered lethal. The data from these cases indicate that levels of MetHb can vary widely in fatal cases, and should not be used as the sole criterion for determination of a death caused by sodium nitrite. Following a discussion of the cases, there is a review of the pathophysiology of MetHb production and a current literature review.

A fatal case by a suicide kit containing sodium nitrite ordered on the internet.

Fatal sodium nitrite poisonings are rare in the forensic context. The present work describes a first fatal case of sodium nitrite contained in a suicide kit that the victim acquired over the internet. The results of the autopsy showed general signs of asphyxia, such as intense cyanosis of the extremities, brown-gray-blue-red livor mortis, and some Tardieu petechiae in addition to intense visceral congestion. It is clear that forensic experts must be aware of the proliferation of this market and the risks of improper selling of these substances through suicide support networks available on the internet. The lack of knowledge of this reality may become unidentifiable, when toxicological analysis contemplates only the most classical and frequent substances involved in poisoning and reinforce the importance of a careful analysis of the death scene.

[Autointoxication with 'suicide powder']. / Auto-intoxicatie met 'zelfmoordpoeder'.

We present two patients who were treated for an intentional overdose of sodium nitrite. When ingested sodium nitrite leads to severe methaemoglobinaemia, resulting in severe hypoxia (as methaemoglobin does not transport oxygen), vasodilation and hypotension. Symptoms include cyanosis, headache, nausea, convulsions, coma and death. When measured by pulse oximetry, patients with a sodium nitrite intoxication and severe methaemoglobinaemia generally have an oxygen saturation of around 85%. This value is unreliable as the oxygen content of the blood is often extremely low - this can be confirmed by arterial blood gas analysis. Treatment of sodium nitrite intoxication consists of intravenous administration of methylthioninium chloride 1-2 mg/kg. Methylthioninium chloride converts the methaemoglobin back to haemoglobin. Due to the pharmacokinetics of methylthioninium chloride and sodium nitrite, a rebound effect is not to be expected. The only contra-indication for methylthioninium chloride is glucose-6-phosphate dehydrogenase deficiency, which is extremely rare in the Netherlands.

Sodium nitrite food poisoning in one family.

Sodium nitrite is used as a coloring agent or preservative in food, as well as an antimicrobial agent in meat and fish and some cheeses. In high amounts it can be toxic for humans, causing methemoglobinemia. This is an unusual and potentially fatal condition in which hemoglobin is oxidized to methemoglobin (MHb), reducing the amount of oxygen that is released from hemoglobin, similar to carbon monoxide poisoning. MHb levels of 70% are generally lethal, but the existence of underlying anemia, acidosis, respiratory compromise, and cardiac disease may exacerbate the toxicity of MHb. We present a case of poisoning with sodium nitrite in three family members after eating homemade sausages given to them by their neighbor who was a butcher. According to the findings of the veterinary inspectorate in charge of food control in this case, the concentration of sodium nitrite in the homemade sausages was about 3.5 g per 1 kg of meat, almost 30 times higher than allowed according to legislation. In this case report, a 70-year-old man died about 7 h after consuming the meal, while two women, 53 and 67 years of age, respectively, were admitted to a toxicology clinic the following day due to food poisoning, with the maximum concentration of MHb in blood of 33.7 and 20.4%, respectively. They were discharged 3 days later. The autopsy of the deceased man showed sodium nitrite poisoning with a relatively low concentration of MHb in his blood - 9.87%. Death was attributed to the exacerbation of hypertensive and ischemic heart disease, resulting from accidental sodium nitrite poisoning. The presented cases illustrate the necessity of close cooperation between the authorities, medical staff, veterinary inspectorate, and forensic pathologists in determining the source of poisoning, the cause of death of the victim, and preventing the outbreak of poisoning among a greater number of consumers.

[Sodium azide poisoning--a rare reason of hospitalization in toxicological units--case report]. / Zatrucie azydkiem sodu--rzadka przyczyna hospitalizacji w osrodkach toksykologicznych--opis przypadku.

Sodium azide poisonings are a rare reason for hospitalization in toxicological units. They are observed as rarely as once within a number of years per hospital. Consequently, an algorithm for the optimum procedure of treating such intoxications does not exist and, as a result, there is a need to describe every single clinical case. A female, aged 55, was directed to the toxicological unit from a county hospital after swallowing four tablets of sodium azide, 150 mg each, in the form of preservative for fresh milk samples. Two hours after the incident a gastric lavage was performed and the tableting blend was retrieved. In the clinical examination higher concentration of lactic acid, ALAT and TSH were observed. In the ECG record unspecific aberrations in the ST segment were noticed. Due to the patient's general good condition and the fact that the tableting blend had been retrieved from the gastric rinse, further use of the antidote indicated in the therapy of cyanide intoxications was abandoned. Symptomatic treatment was used along with the patient's eight-day observation. In the described case the early decontamination prevented the development of acute poisoning.

[Myocardial electrogenesis in laboratory rats under conditions of acute nitrite intoxication].

In anesthetized male rats the arterial blood pressure in femoral artery and electrocardiogram in standard leads were recorded uninterruptedly for 1-1.5 h under conditions of acute nitrite intoxication produced by a subcutaneous injection of water solution of sodium nitrite (donor of nitric oxide) at concentrations of 10, 30, and 50 mg/kg body mass. Results of the study have shown dose-dependent changes of arterial pressure as well as of time and amplitude characteristics of electrocardiogram under effect of NaNO2. At the threshold hypoxic dose, an increase of amplitude of R and S waves was observed by the 30-45th min, while at the maximal NaNO2 dose, amplitude of all waves rose by the 15th min of intoxication. High nitric doses often caused an increase of the ST segment above the isoelectric line and a rise of the amplitude of the T wave, on which a notch appeared in some cases. The change of the ECG time parameters was expressed in the dose-dependent development of bradycardia for the first 4-7 min; its level correlated with the progressively decreasing arterial pressure in the beginning (the 2-4th min) of nitrite intoxication. Variation analysis of heart rate spectral characteristics by Baevskii has revealed a rise of the total spectral power of pulse oscillations. Under effect of nitrite, in the spectrum of cardiointervals, quent recovery of the normal ECG spectrum in the end of the experimental period. The maximal nitrite dose produced more pronounced shifts of the heart rate spectrum towards the LF and VLF diapasons that were not restored for 1 h of experiment. Transitory processes of readjustment of the cardiac rhythm had discrete character. The nitrite dose of 50 mg/kg body mass increased the RR-interval after 4-7 min with amplitude steps of 3-5 imp/s and the time constant of 20-40 s. The revealed ECG changes had the reflex (enhancement of parasympathetic tonus) and metabolic (the hypoxic and histotoxic damage of myocardium) nature.

Methemoglobinemia misdiagnosed as ruptured ectopic pregnancy.

A 22-year-old woman with an initial diagnosis of 'ruptured ectopic pregnancy' and 'hemorrhagic shock' was sent to the operation room for surgical treatment. The mucocutaneous color was deeply cyanosed and the pulse oximeter oxygen saturation (SpO2) was only 86% after tracheal intubation (100% O2). 'Chocolate-brown' blood was observed and methemoglobinemia was considered. Then the arterial blood gas (ABG) sample was obtained, an intravenous infusion of methylene blue and vitamin C followed. The patient recovered quickly, and later two other patients with similar symptoms were treated in the same way. The success was due to a correct diagnosis accompanied with prompt treatment and quick recognition of the etiology.

Methemoglobinemia following unintentional ingestion of sodium nitrite--New York, 2002.

Methemoglobinemia is an unusual and potentially fatal condition in which hemoglobin is oxidized to methemoglobin and loses its ability to bind and transport oxygen. The most common cause of methemoglobinemia is the ingestion or inhalation of oxidizing agents such as nitrates or nitrites (e.g., sodium nitrite, which is used commonly as a preservative in curing meats and fish). This report summarizes the investigation of an incident of methemoglobinemia in five members of a household in New York who became ill after eating a meal seasoned with a white crystalline substance from a plastic bag labeled "Refined Iodized Table Salt" (Figure). The findings underscore the need for proper storage of hazardous materials to avoid unintentional ingestion and the importance of collaboration by multiple agencies to address a potential public health emergency.

Faulty sausage production causing methaemoglobinaemia.

A family outbreak of methaemoglobinaemia following ingestion of sausages made using 'saltpetre' is reported. Saltpetre is a generic term for several potassium and sodium based compounds. On this occasion imprecise ordering led to the use of sodium nitrite rather than the usual potassium nitrate, with extremely serious consequences.