[Clinical analysis of 4 cases of acute nitrite food poisoning].

Nitrite has high toxicity and is commonly found in food poisoning. Poisoned patients may experience cyanosis of the skin and lips, nausea, vomiting, and difficulty breathing or coma may occur in severe cases. Four cases of nitrite poisoning patients who were transferred from primary hospitals to the Third Affiliated Hospital of Gansu University of Chinese Medicine, the First People's Hospital of Baiyin were reported. After symptomatic supportive treatment with special antidote methylene blue, oxygen inhalation, blood purification, etc., the patients recovered and were discharged after 4 days of treatment.

[One case of acute severe nitrite poisoning with massive pulmonary thromboembolism].

This paper reported a case of acute severe nitrite poisoning with massive pulmonary thromboembolism (PTE), discussed the pathogenesis and summarized the treatment experience. Common symptoms of nitrite poisoning include headache, abdominal pain, shortness of breath, cyanosis, etc., which can be followed by encephalopathy, neurological dysfunction, hemolysis, etc. However, the cases of PTE are rare in clinical practice and are prone to missed diagnosis. Nitrite and methemoglobin may lead to vascular endothelial damage and promote thrombosis. In the diagnosis and treatment of acute severe nitrite poisoning patients, the targeted preventive measures should be taken.

[Methemoglobinemia as a result of acute accidental "poppres" poisoning ­ a case report].

Recently we observe an increase in the number of intoxications due to xenobiotics that may induce acute methemoglobinemia. Our study showed a case of acute methemoglobinemia (MetHb 55..2%) in 25 ­ year old man. Clinical symptoms were caused by ingestion of "poppers" which was used by patient as "aphrodisiac". Summary: Conclusions: 1. Oral intake of alkyl nitrites, including isobutyl nitrite, is burdened with the risk of life-threatening methemoglobinemia . 2. In the case of poisonings running with normal pO2, reduced level of oxygen saturation, clinical signs of cyanosis does not react to oxygen therapy, and "chocolate" tinge of blood methemoglobinemia should be suspected. 3. In every case of MetHb the use of antidote, which is methylene blue, should be considered. 4. The severity of cyanosis correlates with the level of methemoglobin.

[Poppers-associated maculopathy]. / Poppers-Makulopathie.

BACKGROUND: Poppers are a common drug belonging to the alkyl nitrite group and in use for several decades. They can be legally purchased for air freshening, but are illegal to buy for inhalation. Abuse is associated with maculopathy and visual loss as a rare side effect. METHOD: A case series of 27 male, homosexual patients with poppers abuse presenting to a single eye clinic in Berlin, Germany, is described. Four patients with visual impairment and maculopathy associated with the inhalation of poppers were found. RESULTS: Four patients experienced subacute visual loss over 2-6 months, one patient can no longer read without a magnifying glass. The median age is 40.25 years (28-45 years). Three patients are HIV-positive (known since 10-22 years, HAART), a patient is also hepatitis C-positive. No other ocular and systemic diseases are known. Poppers have been inhaled for about 1.5, 12, 15 and 25 years (3-4 ×/week); all patients have a mixed use with the brands Jungle Juice, Rush and Amsterdam. Three patients noticed a simultaneous change in colour and shade. Clinical signs on fundoscopy ranged from normal foveal appearance to yellowish, dull macula. Optical coherence tomography (HD-OCT) showed varying degrees of disruption of the presumed inner segment/outer segment (IS/OS) junction; 3 cases bilaterally symmetrical. DISCUSSION: Although poppers have been in use for several decades, in 2007 in England, the popper composition was changed by law from isobutyl nitrite to isopropyl nitrite. It is hard to distinguish whether a specific nitrite group triggers the maculopathy or whether it is the dose level, thus suggesting the existence of a cumulative dose-response relationship. We postulate that a major factor of the manifestation of maculopathy is the individual limit of vulnerability. Despite decades of use, the majority of our series does not present any pathology. Limits of our patient population represents the HIV disease: three maculopathies of our series are HIV-associated and controlled by antiretroviral therapy, so that a clear distinction to the disease is absent. Poppers were earlier regarded to cause an AIDS-defining disease of viral aetiology: Kaposi sarcoma. We are well aware of that association and postulate that the observed maculopathies are not causally related to HIV disease and antiretroviral therapy. Considering the cultural background of our patients (multiple partners, frequent sex) and the disinhibiting effect of poppers, an increased risk of HIV disease is found. Since this disease is a rare disorder, patients should be asked specifically about poppers abuse. Further study of the effect of poppers on maculopathy is needed.

Fatal Methemoglobinemia Due to Acute Inhalation of Methyl Nitrite in an Industrial Accident.

Methyl nitrite is suggested to cause methemoglobinemia by generating methemoglobin, which may be lethal when the methemoglobin concentration exceeds 70%. However, intoxication with methyl nitrite is seldom reported compared with that with other nitrites. Here, we present an industrial accident involving methyl nitrite inhalation during its synthesis process that resulted in three fatalities and one survivor. The autopsy revealed conspicuous blue-gray discoloration in various parts of the body, including the skin, airway mucosa, vessels, brain, heart, and among other areas. The toxicological tests on the deceased showed methemoglobin concentrations in the blood over the lethal level and increased nitrite ion levels in the blood, gastric contents, liver, and lung tissue compared with those in control samples. The cause of death was determined to be methemoglobinemia-induced hypoxia due to methyl nitrite inhalation. This report provides evidence that in methyl nitrite intoxication, exposure duration has a significant influence on the postmortem changes and likelihood of a fatal outcome may be related to the age of the victim. More attention is required regarding the industrial hazards of this substance.

Alpaca plant poisonings: nitrate-nitrite and possible cyanide.

Nitrate-nitrite poisoning killed four adult alpacas and induced the abortion of a full-term fetus after access to oaten hay (Avena sativa) containing 3.2% KNO(3) equivalent in dry matter. Necropsy findings were cyanosis, dark-coloured blood, and pulmonary congestion and oedema. Aqueous humour from two adults contained 25 mg NO(3)/L and that from the fetus contained 10 mg NO(3)/L. Cyanide poisoning possibly killed two adult wether alpacas that ate a garden-cultivated variety of Osteospermum ecklonis (South African daisy, bietou) with a cyanide potential of 6800 mg HCN/kg dry matter.

Nitrite-induced acute kidney injury with secondary hyperparathyroidism: Case report and literature review.

RATIONALE: Acute kidney injury (AKI) with hyperparathyroidism caused by nitrite was rare, and renal function and parathyroid hormone (PTH) decreased to normal range after therapy. PATIENT CONCERNS: Acute kidney injury was diagnosed in a 40-year-old male with hyperparathyroidism and cyanosis of his hands and both forearms. DIAGNOSES: The patient ate some recently pickled vegetables, and he experienced nausea, vomiting and diarrhoea without oliguria or anuria; Additionally, his hands and both forearms had a typical blue ash appearance. After admission, the laboratory findings indicated theincreasing serum creatinine (Scr) and parathyroid hormone (PTH). He was diagnosed as acute kidney injury with hyperparathyroidism caused by nitrite. INTERVENTIONS: The patient stopped eating the pickled vegetables and was given rehydration, added calories and other supportive therapy without any glucocorticoids. OUTCOMES: According to his clinical manifestations, laboratory findings and imaging results, the patient was diagnosed with acute kidney injury with secondary hyperparathyroidism. He was given symptomatic supportive care therapy. After one week, the serum creatinine, parathyroid hormone (PTH), hypercalcemia, hyperphosphatemia, proteinuria, and urine red blood cell values decreased to normal range. LESSONS: Nitrite-induced acute kidney injury with secondary hyperparathyroidism was relatively rare. After therapy, the function of the kidney and parathyroid returned to normal. This case suggests that detailed collection of medical history, physical examination and correct symptomatic treatment is very important.

Cyanide poisoning in cattle from Dysphania glomulifera (red crumbweed): using the internet for rapid plant identification and diagnostic advice.

A 300-strong Angus-Brahman cattle herd near Springsure, central Queensland, was being fed Acacia shirleyi (lancewood) browse during drought and crossed a 5-hectare, previously burnt area with an almost pure growth of Dysphania glomulifera subspecies glomulifera (red crumbweed) on their way to drinking water. Forty cows died of cyanide poisoning over 2 days before further access to the plant was prevented. A digital image of a plant specimen made on a flat-bed scanner and transmitted by email was used to identify D glomulifera. Specific advice on the plant's poisonous properties and management of the case was then provided by email within 2 hours of an initial telephone call by the field veterinarian to the laboratory some 600 km away. The conventional method using physical transport of a pressed dried plant specimen to confirm the identification took 5 days. D glomulifera was identified in the rumen of one of two cows necropsied. The cyanogenic potential of D glomulifera measured 4 days after collection from the site of cattle deaths was 18,600 mg HCN/kg in dry matter. The lethal dose of D glomulifera for a 420 kg cow was estimated as 150 to 190 g wet weight. The plant also contained 4.8% KNO3 equivalent in dry matter, but nitrate-nitrite poisoning was not involved in the deaths.

Clinical and toxicological findings in nitrate and nitrite poisoning in cattle in Northeastern Brazil / Achados clínicos e toxicológicos na intoxicação por nitrato e nitrito em bovinos no Nordeste do Brasil

We report two outbreaks of nitrate and nitrite poisoning in Paraíba, Northeast Brazil. The first, due to Pennisetum purpureum (elephant grass), and the second, due to P. purpureum and Brachiaria spp. (brachiaria grass), both occurred during a prolonged drought. In the first outbreak, the irrigation of the pastures with wastewater and sewage contributed to nitrate accumulation. The second outbreak occurred in pastures cultivated in the border of a dam, that had been submerged for long time accumulating large amounts of organic matter in the soil. Other probably risk factors for nitrate accumulation included the use of chemical fertilizers and herbicides and burning of the vegetation. In the first outbreak, four calves out of a total of 42 cattle died, and in the second outbreak 49 out of 243 cattle, including adults, yearlings, and a 2-day-old calf died. The clinical signs included dyspnea, cyanosis, ataxia, and falls, leading to death. The presence of nitrates was detected in both outbreaks using the diphenylamine test. Quantitative tests were performed in the second outbreak using a portable nitrate meter, and high nitrate concentrations were found. The characteristic macroscopic findings and absence of microscopic lesions and response to treatment with methylene blue were key to the diagnosis of poisoning by nitrates and nitrites. We conclude that poisoning by nitrates and nitrites in ruminants in the semiarid region of Northeastern Brazil is frequent due to the cultivation of grasses in the border of dams that had been covered by water for long periods or in areas irrigated by wastewater and/or sewage. In addition, the use of a portable measuring device is an effective alternative for the quantification of nitrates in pastures.(AU)

Relatamos dois surtos de intoxicação por nitrato e nitrito na Paraíba, Nordeste do Brasil. O primeiro por Pennisetum purpureum (capim-elefante), e o segundo por P. purpureum e Brachiaria spp. (capim braquiária); ambos ocorreram durante uma estiagem prolongada. No primeiro surto, a irrigação das pastagens com água poluída e esgoto contribuiu para o acúmulo de nitrato. O segundo surto ocorreu em pastagens cultivadas na borda de uma barragem, que há muito tempo ficavam submersas, acumulando grande quantidade de matéria orgânica no solo. Outros prováveis fatores de risco para o acúmulo de nitrato incluíram o uso de fertilizantes químicos e herbicidas e a queima da vegetação. No primeiro surto, quatro bezerros de um total de 42 bovinos morreram, e no segundo surto 49 de 243 bovinos, incluindo adultos, jovens de um ano e um bezerro de 2 dias de idade morreram. Os sinais clínicos incluíram dispneia, cianose, ataxia e quedas, levando à morte. A presença de nitratos foi detectada em ambos os surtos pelo teste de difenilamina. Testes quantitativos foram realizados no segundo surto usando um medidor portátil de nitrato, e altas concentrações de nitrato foram encontradas. Os achados macroscópicos característicos e a ausência de lesões microscópicas e a resposta ao tratamento com azul de metileno foram fundamentais para o diagnóstico de intoxicação por nitratos e nitritos. Concluímos que a intoxicação por nitratos e nitritos em ruminantes na região semiárida do Nordeste do Brasil é frequente devido ao cultivo de gramíneas nas bordas de barragens que estiveram cobertas por água por longos períodos ou em áreas irrigadas por água poluída e/ou esgoto. Além disso, o uso de medidor portátil é uma alternativa eficaz para a quantificação de nitratos em pastagens.(AU)

Clinical and toxicological findings in nitrate and nitrite poisoning in cattle in Northeastern Brazil / Achados clínicos e toxicológicos na intoxicação por nitrato e nitrito em bovinos no Nordeste do Brasil

We report two outbreaks of nitrate and nitrite poisoning in Paraíba, Northeast Brazil. The first, due to Pennisetum purpureum (elephant grass), and the second, due to P. purpureum and Brachiaria spp. (brachiaria grass), both occurred during a prolonged drought. In the first outbreak, the irrigation of the pastures with wastewater and sewage contributed to nitrate accumulation. The second outbreak occurred in pastures cultivated in the border of a dam, that had been submerged for long time accumulating large amounts of organic matter in the soil. Other probably risk factors for nitrate accumulation included the use of chemical fertilizers and herbicides and burning of the vegetation. In the first outbreak, four calves out of a total of 42 cattle died, and in the second outbreak 49 out of 243 cattle, including adults, yearlings, and a 2-day-old calf died. The clinical signs included dyspnea, cyanosis, ataxia, and falls, leading to death. The presence of nitrates was detected in both outbreaks using the diphenylamine test. Quantitative tests were performed in the second outbreak using a portable nitrate meter, and high nitrate concentrations were found. The characteristic macroscopic findings and absence of microscopic lesions and response to treatment with methylene blue were key to the diagnosis of poisoning by nitrates and nitrites. We conclude that poisoning by nitrates and nitrites in ruminants in the semiarid region of Northeastern Brazil is frequent due to the cultivation of grasses in the border of dams that had been covered by water for long periods or in areas irrigated by wastewater and/or sewage. In addition, the use of a portable measuring device is an effective alternative for the quantification of nitrates in pastures.

Relatamos dois surtos de intoxicação por nitrato e nitrito na Paraíba, Nordeste do Brasil. O primeiro por Pennisetum purpureum (capim-elefante), e o segundo por P. purpureum e Brachiaria spp. (capim braquiária); ambos ocorreram durante uma estiagem prolongada. No primeiro surto, a irrigação das pastagens com água poluída e esgoto contribuiu para o acúmulo de nitrato. O segundo surto ocorreu em pastagens cultivadas na borda de uma barragem, que há muito tempo ficavam submersas, acumulando grande quantidade de matéria orgânica no solo. Outros prováveis fatores de risco para o acúmulo de nitrato incluíram o uso de fertilizantes químicos e herbicidas e a queima da vegetação. No primeiro surto, quatro bezerros de um total de 42 bovinos morreram, e no segundo surto 49 de 243 bovinos, incluindo adultos, jovens de um ano e um bezerro de 2 dias de idade morreram. Os sinais clínicos incluíram dispneia, cianose, ataxia e quedas, levando à morte. A presença de nitratos foi detectada em ambos os surtos pelo teste de difenilamina. Testes quantitativos foram realizados no segundo surto usando um medidor portátil de nitrato, e altas concentrações de nitrato foram encontradas. Os achados macroscópicos característicos e a ausência de lesões microscópicas e a resposta ao tratamento com azul de metileno foram fundamentais para o diagnóstico de intoxicação por nitratos e nitritos. Concluímos que a intoxicação por nitratos e nitritos em ruminantes na região semiárida do Nordeste do Brasil é frequente devido ao cultivo de gramíneas nas bordas de barragens que estiveram cobertas por água por longos períodos ou em áreas irrigadas por água poluída e/ou esgoto. Além disso, o uso de medidor portátil é uma alternativa eficaz para a quantificação de nitratos em pastagens.

[Protective effects of the regulators of energy metabolism and essentiale in case of nitrite intoxication].

The objective of this investigation was to assess immuno-, hepato- and actoprotective activity of mildronate and the impact of riboxin, elcar and essentiale on this drug in Wistar rats receiving the injections of sodium nitrite. The parameters characterizing non-specific resistance, immunological reactivity, the membranes state, detoxicating hepatic activity and physical performance. Mildronate administration increased functional activity of immune cells, hepatocytes and myocytes (but not up to normal limit) that had been reduced by sodium nitrite. The combination of mildronate and riboxine normalized phagocytic and metabolic activity of polymorphonuclear leucocytes, induced humoral immune response and delayed-onset hyperresponsiveness and normalized the ability of the intoxicated rats to perform submaximal physical activity. The combined administration of mildronate and essentiale normalized immune reactions, hepatic metabolism and physical performance of the rats poisoned by sodium nitrite. The combination of mildronate and riboxin or essentiale decreased the severity of damaged oxidation potential of the red blood cells of the intoxicated rats and prevented the development of erythrocytic immunosuppressive properties.

[Methaemoglobinaemia induced by ingestion of alkyl nitrite, "poppers"].

We present a case report of an 18-year-old male who was referred to the emergency department with evidence of methaemoglobinaemia. He presented with classic symptoms with peripheral cyanosis and hypoxia. Arterial blood gas showed a methaemoglobin level of 36%. This was caused by ingestion of alkyl nitrate, a widespread party drug called "poppers". When inhaled it causes euphoria, reduced pain and relaxation of the anal sphincter, but oral use may induce life-threatening methaemoglobinaemia. The treatment of choice is the antidote methylene blue. After treatment the patient regained full recovery and was discharged on the following day. We discuss classic symptoms, diagnosis and treatment of intoxication with methylene blue.

Determination of Nitrite in Whole Blood by High-Performance Liquid Chromatography with Electrochemical Detection and a Case of Nitrite Poisoning.

Although nitrite is widely used in meat processing, it is a major toxicity hazard to children and is responsible for the blue-baby syndrome. A simple and effective method to determine nitrite in whole blood has been devised using ion chromatography with suppressed conductivity detection. The blood sample was deproteinized by adding acetonitrile and purified with mini-cartridges to remove hydrophobic compounds, chloride ions, and metal ions. An aliquot of the filtrate was injected onto the ion chromatography. The retention time for nitrite was 13.8 min and the detection limit of nitrite in whole blood was 0.4 µmol/L. The calibration curve was linear (r(2) = 0.9999) over the concentration working range. The blood nitrite concentration of a victim who attempted suicide by ingesting sodium nitrite powder was determined using the present method. The basal levels for nitrite in human blood was determined with 7.1 ± 0.9 µmol/L (n = 12).

[Forensic medical diagnostics of nitrate and nitrite intoxication].

Nitrates and nitrites, accumulating in toxic concentrations in soil, plants, water and foodstuffs, can cause lethal intoxication. The method of isolation, identification and quantitation has been elaborated for their diagnosis. It is based on the isolation of water and subsequent chromogenic test plus photoelectrocolorimetry.

Severe methaemoglobinaemia treated with adjunctive hyperbaric oxygenation.

Methaemoglobinaemia results from exposure to oxidizing substances such as nitrates or nitrites. Iron within haemoglobin is oxidized from the ferrous to the ferric state, which blocks the transport of oxygen and carbon dioxide, with subsequent inhibition of the respiratory chain. We describe the case of a 23-year-old male suffering from severe methaemoglobinaemia of 68% after consumption of nitrites ('poppers') in association with considerable ethanol consumption. Toluidine-blue was administered as first-line antidotal therapy immediately followed by hyperbaric oxygenation (HBOT). HBOT resulted in enhanced reduction of methaemoglobin, and rapid tissue re-oxygenation by the oxygen dissolved in plasma was provided, independent of the degree of methaemoglobinaemia. The patient recovered uneventfully and was discharged three days later. This case illustrates the potential of supportive HBOT as a time-saving therapeutic tool in this unusual situation, enabling a quick and sustained reduction in methaemoglobinaemia.

Boilerbaisse: an outbreak of methemoglobinemia in New Jersey in 1992.

BACKGROUND: On October 20, 1992, > 40 children from one elementary school visited the school nurse due to the acute onset of blue lips and hands, vomiting, and headache during and after the school lunch periods. Forty-nine children were seen by physicians that day and 14 were hospitalized. Laboratory analysis revealed methemoglobinemia in many of the children. All recovered in 36 hours. OBJECTIVE: A case-control study was supplemented by environmental and laboratory investigations to determine the outbreak source. METHODS: Cases were selected based on the laboratory diagnosis of methemoglobinemia (methemoglobin level > 2%). Children whose methemoglobin levels were missing or < 2% were excluded from analysis. Controls were obtained by selecting every third name from a school roster. The parents of 29 students who met the case definition and 52 controls were interviewed. RESULTS: All 29 cases and 33% (17/52) of the controls ate soup during the school lunch (odds ratio undefined, lower 95% confidence limit 16.1). Two pots of soup were prepared from ready-to-serve cans, which were diluted with water and enriched with a commercially prepared flavor enhancer. The school's boiler, dormant during the previous 5 months, was restarted on the morning of the outbreak. The boiler also served as a tankless hot water heater. Laboratory analysis of the soup identified abnormally high quantities of nitrite (459 ppm) and sodium metaborate, major components of the boiler water treatment solution. Undiluted soup from the same lot had 2.0 ppm nitrites; the flavor enhancer had 2.2 ppm nitrites. Nitrites were present in the hot potable water system (4 to 10 ppm) and absent in the cold potable water system. CONCLUSIONS: This outbreak of methemoglobinemia due to nitrite poisoning was traced to soup contaminated by nitrites in a boiler additive. Nitrites are ubiquitous and potentially hazardous inorganic ions. Extreme caution should be used when the possibility for toxic human exposure to nitrites exists.