sodium-nitrite and Poisoning

Sodium azide is a highly toxic chemical. Its production has increased dramatically over the last 30 years due to its widespread use in vehicular airbags, and it is available for purchase online. Thus, accidental exposure to azide or use as a homicidal or suicidal agent could be on the rise, and secondary exposure to medical personnel can occur. No antidote exists for azide poisoning. We conducted a systematic review of azide poisoning to assess recent poisoning reports, exposure scenarios, clinical presentations, and treatment strategies.. We searched both medical and newspaper databases to review the literature between 01/01/2000 and 12/31/2020, pairing the controlled vocabulary and keyword terms "sodium azide" or "hydrazoic acid" with terms relating to exposures and outcomes, such as "ingestion," "inhalation," "exposure," "poisoning," and "death." We included all peer-reviewed papers and news articles describing human azide poisoning cases from English and non-English publications that could be identified using English keywords. Data abstracted included the number, age, and gender of cases, mode of exposure, exposure setting, azide dose and route of exposure, symptoms, outcome, and treatment modalities.. We identified 663 peer-reviewed papers and 303 newspaper articles. After removing duplicated and non-qualifying sources, 54 publications were reviewed describing 156 cases, yielding an average of 7.8 reported azide poisoning cases per year. This rate is three times higher than in a previous review covering the period of 1927 to 1999. Poisoning occurred most commonly in laboratory workers, during secondary exposure of medical personnel, or from a ripped airbag. Hypotension occurred commonly, in some cases requiring vasopressors and one patient received an intra-aortic ballon pump. Gastric lavage and/or activated charcoal were used for oral azide ingestion, and sodium nitrite, sodium thiosulfate, and/or hydroxocobalamin were used in severely poisoned patients.. Recent increases in azide poisoning reports may stem from greater commercial use and availability. Treatment of systemic poisoning may require aggressive hemodynamic support due to profound hypotension. Based on mechanistic considerations, hydroxocobalamin is a rational choice for treating azide poisoning.

Topics: Adult; Aged; Antidotes; Female; Humans; Hypotension; Male; Middle Aged; Occupational Exposure; Poisoning; Sodium Azide; Sodium Nitrite; Suicide, Attempted; Thiosulfates

The importance of cyanide toxicity as a component of inhalational injury in patients with burns is increasingly being recognised, and its prompt recognition and management is vital for optimising burns survival. The evidence base for the use of cyanide antidotes is limited by a lack of randomised controlled trials in humans, and in addition consideration must be given to the concomitant pathophysiological processes in patients with burns when interpreting the literature. We present a literature review of the evidence base for cyanide antidotes with interpretation in the context of patients with burns. We conclude that hydroxycobalamin should be utilised as the first-line antidote of choice in patients with burns with inhalational injury where features consistent with cyanide toxicity are present.

Topics: Adenosine; Amyl Nitrite; Burns; Chelating Agents; Cyanides; Edetic Acid; Humans; Hydroxocobalamin; Hyperbaric Oxygenation; Oxygen Inhalation Therapy; Poisoning; Pteridines; Smoke Inhalation Injury; Sodium Nitrite; Thiosulfates

Topics: Adult; Antidotes; Female; Humans; Hydrogen Sulfide; Hyperbaric Oxygenation; Magnetic Resonance Imaging; Male; Monitoring, Physiologic; Poisoning; Prognosis; Sodium Nitrite; Young Adult

Topics: Acute Disease; Adult; Aftercare; Amyl Nitrite; Antidotes; Cyanides; Decontamination; Emergency Medical Services; Emergency Nursing; Emergency Treatment; Humans; Hydroxocobalamin; Life Support Care; Male; Nurse's Role; Parkinsonian Disorders; Poisoning; Sodium Nitrite; Suicide, Attempted; Thiosulfates; Triage

The United States is under the constant threat of a mass casualty cyanide disaster from industrial accidents, hazardous material transportation incidents, and deliberate terrorist attacks. The current readiness for cyanide disaster by the emergency medical system in the United States is abysmal. We, as a nation, are simply not prepared for a significant cyanide-related event. The standard of care for cyanide intoxication is the cyanide antidote kit, which is based on the use of nitrites to induce methemoglobinemia. This kit is both expensive and ill suited for out-of-hospital use. It also has its own inherent toxicity that prevents rapid administration. Furthermore, our hospitals frequently fail to stock this life-saving antidote or decline to stock more than one. Hydroxocobalamin is well recognized as an efficacious, safe, and easily administered cyanide antidote. Because of its extremely low adverse effect profile, it is ideal for out-of-hospital use in suspected cyanide intoxication. To effectively prepare for a cyanide disaster, the United States must investigate, adopt, manufacture, and stockpile hydroxocobalamin to prevent needless morbidity and mortality.

Topics: Accidents, Occupational; Amyl Nitrite; Antidotes; Chemical Warfare; Cyanides; Disaster Planning; Emergency Medical Services; Emergency Treatment; Hazardous Substances; Humans; Hydroxocobalamin; Needs Assessment; Poisoning; Public Health Practice; Sodium Nitrite; Terrorism; Thiosulfates; Transportation; United States

In 2 separate incidents, 6 patients were poisoned with hydrogen sulfide (H2S) in sewer gas. In the first incident, mixing acid- and sodium hydroxide-based drain cleaners in a confined space resulted in 4 poisonings and 2 deaths. Three would-be rescuers were seriously poisoned and 1 died. Two survivors had neurological sequelae. Sodium nitrite appeared to have some clinical efficacy in 1 case. The second incident involved 2 patients working on a pump in a sewage pond. A patient lying on a raft close to the pond surface was seriously poisoned; sodium nitrite was clinically efficacious and this patient survived without developing neurological sequelae. Sodium nitrite deserves further clinical study as a potential H2S antidote.

Topics: Adolescent; Adult; Animals; Antidotes; Fatal Outcome; Humans; Hydrogen Sulfide; Male; Middle Aged; Poisoning; Sodium Nitrite

The combination of sodium thiosulfate and sodium nitrite has been used in the United States since the 1930s as the primary antidote for cyanide intoxication. Although this combination was shown to exhibit much greater efficacy than either ingredient alone, the two compounds could not be used prophylactically because each exhibits a number of side effects. This review discusses the pharmacodynamics, pharmacokinetics, and toxicology of the individual agents, and their combination.

Topics: Animals; Antidotes; Biological Availability; Cyanides; Drug Therapy, Combination; Humans; Poisoning; Sodium Nitrite; Thiosulfates

Cyanide is a potent and rapidly-acting asphyxiant which prevents tissue utilization of oxygen by inhibition of the cellular respiratory enzyme, cytochrome oxidase. Inhalation or ingestion of cyanide produces reactions within a few seconds and death within minutes. Cyanide toxicity of dietary origin has been implicated in acute animal deaths and as major etiologic factors in toxic ataxic neuropathy in man and as a cause of vision failure in humans suffering from tobacco amblyopia and leber's hereditary optic atrophy. Diagnosis of cyanide toxicity may be confirmed by a variety of laboratory procedures, but accurate assay is essential for proper conclusions from analysis of animal tissues several hours after death or from human samples in instances of chronic dietary exposure. Biological detoxification of cyanide is available through several routes, and the application of sodium nitrite with sodium thiosulfate or administration of methylene blue are effective treatment procedure. The environmental availability of cyanide in its various forms necessitates an understanding of its pathophysiology and responsible management of hazardous situations.

Topics: Absorption; Animal Husbandry; Animals; Chelating Agents; Chemical Phenomena; Chemistry; Cyanides; Electron Transport Complex IV; Environmental Pollutants; Humans; Hydroxocobalamin; Hypoxia; Inactivation, Metabolic; Poisoning; Postmortem Changes; Sodium Nitrite; Thiosulfates

Topics: Eating; Humans; Methemoglobinemia; Poisoning; Sodium Nitrite; Suicide

Toxic baiting of wild pigs (Sus scrofa) is a potential new tool for population control and damage reduction in the US. Field trials testing a prototype toxic bait (HOGGONE 2 containing 5% sodium nitrite [SN]), though, revealed that wild pigs spilled small particles of toxic bait outside of bait stations which subsequently created hazards for non-target species that consumed those particles, primarily passerine birds. To deter non-target birds from consuming particles of spilled bait, we tested four deterrents at mock bait sites (i.e., baited with bird seed) in north-central Colorado, USA during April-May 2020. We found a programable, inflatable deterrent device (scare dancer) reduced bird visitation by an average of 96%. Then, we evaluated the deterrent devices at SN-toxic bait sites in north-central Texas, USA during July 2020, where the devices were activated the morning following deployment of SN-toxic bait. Overall, we found 139 dead wild pigs at 10 bait sites following one night of toxic baiting, which represented an average of 91% reduction in wild pigs visiting bait sites. We found that deterrent devices were 100% effective at deterring birds from toxic bait sites. We found two dead non-target mice at bait sites without deterrent devices. We noted that deploying toxic bait in mid-summer rather than late-winter/early-spring reduced hazards to migrating birds because they were not present in our study area during July. We recommend using deterrent devices (i.e., novel, programmable, battery operated, continuous and erratic movement, and snapping sounds) to reduce hazards to non-target birds at SN-toxic bait sites. We further recommend deploying SN-toxic bait during seasons when migrating birds are not as abundant until further research demonstrates minimal risks to migrating birds.

Topics: Animals; Animals, Wild; Birds; Colorado; Pest Control; Poisoning; Sodium Nitrite; Sus scrofa; Texas

Sodium nitrite is an oxidizing agent capable of producing profound methemoglobinemia. Large quantities of sodium nitrite can be purchased online, and recent literature has identified several cases of intentional self-poisoning, including multiple cases of mortality. This has raised concern that intentional sodium nitrite poisoning and resultant severe methemoglobinemia may be increasing in incidence and could represent a substantial public health threat.. This study used data obtained from the National Poison Data System (NPDS) to evaluate the incidence and mortality rate of intentional sodium nitrite poisoning of suicidal intent reported to US poison centers over a five-year period. Patient demographics, exposure characteristics, treatments administered, and patient outcomes were analyzed. Temporal patterns in exposure were also investigated.. Forty-seven cases were identified in the NPDS database, of which three were excluded due to lack of outcome data. Median patient age was 23 years, 52% of patients were female and 86% of exposures occurred at the patient's residence. Serious outcomes were observed in 84% of cases, 77% of patients included were treated with methylene blue and 30% of patients died. No intentional sodium nitrite exposures were reported in the first two years studied, but we observed an increase in the incidence of exposures reported through the remainder of the investigation period.. The incidence of intentional self-poisoning with sodium nitrite has been increasing since 2017. Many of these exposures result in toxicity requiring antidotal therapy, and a high mortality rate was observed. Recent literature indicates that this trend may be the result of ready access to this poison through online vendors combined with recommendations shared in online communities that sodium nitrite be used as an effective method of suicide. Further study is needed to better characterize this phenomenon and develop public health interventions to prevent future morbidity and mortality.

Topics: Adult; Antidotes; Female; Humans; Incidence; Poison Control Centers; Poisoning; Poisons; Sodium Nitrite; United States; Young Adult

In recent years, a significant increase of reports about suicidal cases due to intentional sodium nitrite intake has been described. In the forensic pathology context, the strategy to approach intoxication cases by sodium nitrite, without any preliminary information or hint, is not straightforward. Indeed, in a number of cases the lack of crime scene data and/or specific pathological signs makes difficult the identification of nitrite poisoning. Moreover, the analytical determination of nitrite in blood is challenging, due to its rapid oxidization to nitrate by hemoglobin. Although several methods have been proposed for the clinical analysis of nitrate and/or nitrite in biological samples, none of these is specifically focused on the determination of these ions in cadaveric samples. Consequently, the diagnosis of nitrite fatal intoxication is still based on methemoglobin analysis. The present paper reports the optimization and validation of an analytical method of capillary ion analysis (CIA) with UV detection, for the determination of nitrite and nitrate in biological fluids and its application to two authentic cases of death by nitrite intake. The analyses were carried out in a bare fused-silica capillary (75 µm inner diameter) using 100 mM sodium tetraborate (pH 9.24) as background electrolyte and applying a voltage of - 15 kV between the capillary ends. The detection was obtained by direct UV absorption recorded at 214 nm wavelength. Bromide was used as the internal standard. Linearity was established in the range of 0.25-5 mmol/L). Reproducibility (intraday and day-to-day) was characterized by relative standard deviations (RSDs) 14.7% for peak areas. The method was applied to the determination of nitrite and nitrate in two real forensic cases, where high concentrations of nitrate were found in cadaveric blood samples (6.5 and 4.4 mmol/L, respectively). Nitrite was found only in trace amounts, due to the instability of this ion in cadaveric blood where it is oxidized to nitrate. The present method represents a new tool for the direct and rapid determination of nitrite and nitrate in cases of forensic interest, and thus offers a diagnostic tool more sensitive and precise than the need methemoglobin analysis.

Topics: Adult; Electrophoresis, Capillary; Forensic Toxicology; Humans; Male; Nitrates; Poisoning; Reproducibility of Results; Sodium Nitrite; Ultraviolet Rays

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.

Topics: Adult; Drug Overdose; Enzyme Inhibitors; Food Preservatives; Humans; Hypoxia; Male; Methemoglobinemia; Methylene Blue; Oxygen; Poisoning; Sodium Nitrite; Suicide, Attempted

An acute and orally delivered toxic bait containing micro-encapsulated sodium nitrite (MESN), is under development to provide a novel and humane technology to help curtail damage caused by invasive wild pigs (Sus scrofa). We evaluated potential secondary risks for non-target species by: testing whether four different types of micro-encapsulation coatings could reduce vomiting by invasive wild pigs, testing the levels of residual sodium nitrite (SN) in tissues of invasive wild pigs, testing the environmental persistence of SN in vomitus, and conducting a risk assessment for scavengers.. Micro-encapsulation coatings did not affect the frequency of vomiting. We identified no risk of secondary poisoning for non-target scavengers that consume muscle, eyes, and livers of invasive wild pig carcasses because residual SN from the toxic bait was not detected in those tissues. The risk of secondary poisoning from consuming vomitus appeared low because ∼90% of the SN was metabolized or broken down prior to vomiting, and continued to degrade after being exposed to the environment. Secondary poisoning could occur for common scavengers that consume approximately ≥15% of their daily dietary requirements of digestive tract tissues or undigested bait from carcasses of invasive wild pigs in a rapid, single-feeding event. The likelihood of this occurring in a natural setting is unknown. The digestive tracts of poisoned invasive wild pigs contained an average of ∼4.35 mg/g of residual SN.. Data from this study suggest no risks of secondary poisoning for non-target species (including humans) that consume muscle, liver, or eyes of invasive wild pigs poisoned with a MESN toxic bait. More species-specific testing for scavengers that consume digestive tract tissues and undigested bait is needed to reduce uncertainty about these potential risks. © 2017 Society of Chemical Industry.

Topics: Animals; Animals, Wild; Female; Male; Pest Control; Poisoning; Sodium Nitrite; Sus scrofa; Vomiting

Acquired methemoglobinemia is a potentially fatal condition that leads to tissue hypoxia. Although the clinical features of methemoglobinemia depend on the methemoglobin levels, the clinical course would differ depending on the causative agents.. We attempted to clarify this issue by comparing the clinical course of methemoglobinemia caused by dapsone and that caused by other toxic agents.. A retrospective case-control study was performed. All patients with methemoglobinemia and who were admitted to the emergency department (ED) of our hospital from 1 January 2002 to 31 December 2014 were included.. Of the 34 patients with methemoglobinemia, 15 ingested dapsone (14 with acute overdose and one with chronic therapeutic use) and 19 had been exposed to other toxic agents, such as sodium nitrites, indoxacarb, primaquine, and lidocaine. The clinical characteristics and the course of dapsone-induced and other toxic-agent-induced methemoglobinemia were compared. There was no significant difference in clinical presentation and methemoglobin level (38.5% vs. 35.0%, p = 0.456) upon their ED arrival between the two groups. However, the methemoglobin level after use of methylene blue and the total dose of methylene blue were higher in patients with dapsone-induced methemoglobinemia than in those with other agent-induced methemoglobinemia (11.9% vs. 1.7%, p = 0.001, 455 mg vs. 144 mg, p = 0.006). The majority of dapsone-induced methemoglobinemia (93.3%) required more than 72 h for normalization of the methemoglobin level, despite the use of methylene blue. Five of the study patients died due to multiorgan failure, and all of whom were inpatients with dapsone-induced methemoglobinemia.. The clinical course of dapsone-induced methemoglobinemia was worse than that of other toxic-agent-induced methemoglobinemia despite no significant difference in their initial clinical presentation. Continuous treatment with serial monitoring of the serum methemoglobin is necessary for patients with dapsone-induced methemoglobinemia.

Topics: Adult; Aged; Aged, 80 and over; Case-Control Studies; Dapsone; Dose-Response Relationship, Drug; Drug Overdose; Emergency Service, Hospital; Female; Humans; Lidocaine; Male; Methemoglobin; Methemoglobinemia; Methylene Blue; Middle Aged; Oxazines; Poisoning; Primaquine; Retrospective Studies; Sodium Nitrite; Treatment Outcome; Young Adult

More effective, rapidly delivered, safer antidotes are needed for cyanide poisoning. Previous study has demonstrated a beneficial effect of isosorbide dinitrate on the survival of cyanide-poisoned mice.. To evaluate the effectiveness of isosorbide dinitrate compared with that of sodium nitrite in cyanide poisoning.. A comparative animal study was performed using 18 rabbits, randomized into 3 study groups. Animals were poisoned intravenously with potassium cyanide (1 mg/kg). The first group was not given any further treatment. The second and third groups were treated intravenously 1 min after poisoning with sodium nitrite (6 mg/kg) and isosorbide dinitrate (50 μg/kg), respectively. The primary outcome was short-term survival of up to 30 min. Secondary outcomes included time to death, a clinical score, mean blood pressure, pulse, blood pH, and lactate and methemoglobin levels.. Rabbits treated with isosorbide dinitrate or sodium nitrite survived while only one untreated rabbit survived. Median time to death of the 5 poisoned and untreated animals was 10 min. All the animals collapsed soon after poisoning, exhibiting rapidly disturbed vital signs and developed lactic metabolic acidosis; average peak blood lactate levels were 15.5-19.1 mmol/L at 10 min after poisoning. The treated animals improved gradually with practically full recovery of the clinical scores, vital signs, and blood gas levels. Sodium nitrite administration raised methemoglobin to an average peak of 7.9%, while isosorbide dinitrate did not change methemoglobin levels.. Early administration of isosorbide dinitrate improved the short-term survival of cyanide-poisoned rabbits. Isosorbide dinitrate shows potential as an antidote for cyanide poisoning and may exert its effect using a nitric-oxide-dependent mechanism.

Topics: Acidosis; Administration, Intravenous; Animals; Isosorbide Dinitrate; Male; Methemoglobin; Poisoning; Potassium Cyanide; Rabbits; Sodium Nitrite

Investigation of hydroxylamine sulfate toxicity mechanism in vivo and estimation of α-tocopherol acetate and methylene blue efficiency in poisoning treatments.. In vivo experiments were conducted on 102 Wistar Han rats. The experiments investigated the hematotoxic and oxidative stress effects of hydroxylamine sulfate in acute and subacute toxicity treatment of animals. Electron Spin Resonance was used for quantitative determination of blood and liver tissue parameters alterations after intoxication. The osmotic fragility of erythrocytes, lipid peroxidation intensity and level of SH-groups in liver of rats were determined by established biochemical assays.. Hydroxylamine sulfate cause an acute hematotoxicity and oxidative stress in vivo as demonstrated by the appearance of free oxidized iron in blood, reduced glutathione content and increased lipid peroxidation in liver. The experimental studies showed the formation of Hb-NO, MetHb in erythrocytes and as well of stable complex of reduced iron (Fe(2+)) with hydroxylamine sulfate. Methylene blue treatment does not reduce the Hb-NO or MetHb levels in intoxicated animals while administration of α-tocopherol acetate reduces substantially lipid peroxidation.. Oxidative stress is a key mechanism of acute hematotoxicity caused by hydroxylamine sulfate. Methylene blue is not suitable antidote in case of hydroxylamine intoxication.

Topics: alpha-Tocopherol; Animals; Electron Spin Resonance Spectroscopy; Erythrocytes; Hydroxylamines; Lipid Peroxidation; Liver; Methylene Blue; Oxidative Stress; Poisoning; Rats; Rats, Wistar; Sodium Nitrite; Toxicity Tests, Acute; Toxicity Tests, Subacute

Most fire-related deaths are attributable to smoke inhalation rather than burns. The inhalation of fire smoke, which contains not only carbon monoxide but also a complex mixture of gases, seems to be the major cause of morbidity and mortality in fire victims, mainly in enclosed spaces. Cyanide gas exposure is quite common during smoke inhalation, and cyanide is present in the blood of fire victims in most cases and may play an important role in death by smoke inhalation. Cyanide poisoning may, however, be difficult to diagnose and treat. In these children, hydrogen cyanide seems to be a major source of concern, and the rapid administration of the antidote, hydroxocobalamin, may be critical for these children.European experts recently met to formulate an algorithm for prehospital and hospital management of adult patients with acute cyanide poisoning. Subsequently, a group of European pediatric experts met to evaluate and adopt that algorithm for use in the pediatric population.

Topics: 4-Aminopyridine; Age Factors; Algorithms; Antidotes; Child; Child, Preschool; Cyanides; Disease Management; Disease Susceptibility; Emergencies; Emergency Medical Services; Europe; Fires; Humans; Hydroxocobalamin; Infant; Methemoglobinemia; Poisoning; Smoke; Smoke Inhalation Injury; Sodium Nitrite; Thiosulfates

A case of poisoning with a Cotoneaster sp. is described in a llama (Lama glama). The clinical signs were dyspnea, with congested mucous membranes, chewing, recumbency, and opisthotonos. Several hours after ingestion of the plant, the llama died, despite treatment with sodium thiosulfate and nitrite. Necropsy revealed approximately 676 g of leaves and fruit of Cotoneaster in the first compartment of the stomach. The blood was light red and did not clot. Because Cotoneaster sp. contains low concentrations of cyanogenic glycosides, toxicosis occurs only following massive ingestion of plant material.

Topics: Animals; Antidotes; Camelids, New World; Dyspnea; Fatal Outcome; Poisoning; Rosaceae; Sodium Nitrite; Thiosulfates

Currently, no reliable noninvasive methods exist for monitoring the severity of in vivo cyanide (CN) toxicity, treatment, and resulting physiological changes. We developed a broadband diffuse optical spectroscopy (DOS) system to measure bulk tissue absorption and scattering. DOS was used to optically monitor CN toxicity and treatment with sodium nitrite (NaNO2). To perform experiments, the DOS probe was placed on the hind leg of rabbits. A sodium CN solution was infused intravenously. DOS and concurrent physiologic measurements were obtained. After completion of CN infusion, NaNO2 was infused to induce methemoglobinemia (MetHb). During infusion of CN, blood gas measurements showed an increase in venous partial pressure of oxygen (pO2), and following reversal, venous pO2 values decreased. DOS measurements demonstrated corresponding changes in hemoglobin oxygenation states and redox states of cytochrome-c oxidase (CcO) during CN infusion and NaNO2 treatment. Therefore, DOS enables detection and monitoring of CN toxicity and treatment with NaNO2.

Topics: Animals; Blood Gas Analysis; Electron Transport Complex IV; Feasibility Studies; Hematinics; Hemoglobins; Hydroxocobalamin; Indicators and Reagents; Male; Methemoglobin; Models, Animal; Oximetry; Oxyhemoglobins; Poisoning; Potassium Cyanide; Rabbits; Sodium Nitrite; Spectrophotometry, Infrared; Spectrum Analysis; Statistics as Topic; Toxicity Tests, Acute

Sodium azide poisonings occur very rarely. The mechanism of sodium azide toxic effect has not yet been fully explained. Despite the lack of an explicit procedure for the cases of sodium azide poisonings, in vitro tests and rare case reports suggest that treatment with antidotes for cyanide poisoning victims can be effective. This study describes two cases of suicidal sodium azide ingestion. Case 1. 30-year-old male ingested ca. 180 mg of sodium azide. On admission to hospital, within 4 hours from poisoning, the man complained of dizziness and anxiety. Physical examination revealed horizontal nystagmus, flapping tremor, HR 135/min. In laboratory tests, higher blood concentration of lactates (3 mmol/l) was detected, as well as lower potassium concentration (3.4 mmol/L) and increased transaminase activity (ALT 74 U/l, AST 90 U/l). Electrocardiographic tests showed a negative T wave in limb lead III. Other results were within normal. As the patient ingested a toxic dose of sodium azide, he was treated according to the therapy prescription for cyanide poisoning (amyl nitrite inhalation followed by intravenous administration of sodium nitrite and sodium thiosulphate). ECG record of the last day of hospitalization (7th day of treatment) showed negative T waves in lead III, V4-V6. He was discharged from hospital in good condition. Case 2.23-year-old male ingested 10 g of sodium azide 1.5 hours prior to admission to hospital. At the beginning, the patient's condition was good, but it changed to critical state within the first hours of hospitalization. He developed a deep coma, respiratory and circulatory insufficiency, metabolic acidosis, cardiac dysrrhythmias and anuria. Cardiac activity monitoring showed alternating tachycardia (140 beats per minute) and bradycardia (48 beats per minute), numerous additional supraventricular and ventricular extrasystoles and sinus dysrrhythmia. Cardiac arrest (asystolia) occurred twice, the second incident with fatal outcome. The patient received supportive therapy, he was also treated according to the therapy prescription for cyanide poisoning. Circulatory disturbances observed in both cases have been described in literature as symptoms of sodium azide poisoning. However, available literature data are scarce and lack systematization, most of them coming from several decades ago. The lack of patient's consent for detailed examination of circulatory system and liver made it impossible to gather further knowledge on the subject. T

Topics: Adult; Antidotes; Arrhythmias, Cardiac; Bradycardia; Clinical Protocols; Dose-Response Relationship, Drug; Electrocardiography; Fatal Outcome; Heart Arrest; Humans; Hydroxocobalamin; Hypokalemia; Lactates; Male; Monitoring, Physiologic; Nitrates; Pentanols; Poisoning; Sodium Azide; Sodium Nitrite; Suicide, Attempted; Thiosulfates; Transaminases; Treatment Outcome

Natrium nitrosum intoxication is usually associated with a subsequent methemoglobinemia. Beside it, nitrates can cause also some other pathological states. Treatment with the toluidine blue may have various adverse side effects. Newborn intoxication by natrium nitrosum developing after the intoxication of the bearing mother before the parturition has not been described yet. Our own observation is referred.

Topics: Adult; Cesarean Section; Female; Humans; Infant, Newborn; Medication Errors; Poisoning; Pregnancy; Sodium Nitrite

Topics: Amyl Nitrite; Antidotes; Cyanides; Decontamination; Emergency Medical Services; Humans; Poisoning; Protective Clothing; Sodium Nitrite; Thiosulfates; Triage; United States; Violence

Topics: Antidotes; Carbon Monoxide Poisoning; Cyanides; Drug Therapy, Combination; Humans; Hydroxocobalamin; Poisoning; Sodium Nitrite

A 41-year-old woman ingested apricot kernels purchased at a health food store and became weak and dyspneic within 20 minutes. The patient was comatose and hypothermic on presentation but responded promptly to antidotal therapy for cyanide poisoning. She was later treated with a continuous thiosulfate infusion for persistent metabolic acidosis. This is the first reported case of cyanide toxicity from apricot kernel ingestion in the United States since 1979.

Topics: Acidosis; Acute Disease; Adult; Antidotes; Emergency Treatment; Female; Food, Organic; Fruit; Humans; Hydrogen Cyanide; Poisoning; Poisons; Seeds; Sodium Nitrite; Thiosulfates

Acetonitrile (methyl cyanide) is a common industrial organic solvent but is a rare cause of poisoning. We report the first recorded UK case. Acetonitrile is slowly converted to cyanide, resulting in delayed toxicity. We describe a case of deliberate self-poisoning by a 39-year-old woman resulting in cyanide poisoning 11 hours later which was successfully treated by repeated boluses of sodium nitrite and thiosulphate. The half-life of conversion of acetonitrile was 40 hours and harmful blood cyanide levels persisted for over 24 hours after ingestion. Departments treating or advising in cases of poisoning need to be aware of the delayed toxicity of acetonitrile. Monitoring in an intensive care unit of cases of acetonitrile poisoning should continue for 24-48 hours.

Topics: Acetonitriles; Adult; Antidotes; Cyanides; Female; Humans; Poisoning; Sodium Nitrite; Suicide, Attempted; Thiosulfates; Time Factors

Thirty-seven employees were exposed to cyanide between 1956 and 1985. One was found dead. Thirty-six employees were treated; most were given nitrite and oxygen. Some received oxygen alone. All recovered completely. One-third of these employees were unconscious. One was convulsing. Most were discharged home at 6 h post-exposure. Some employees remained at the plant to work an additional shift. Amyl nitrite and/or oxygen were the only agents used with 33 employees. Forced oxygen was administered to the unconscious, apneic employees. Three employees were given sodium nitrite and sodium thiosulfate iv. Treatment generally began within 3 min. In 5 to 20 min all of the unconscious employees reacted positively to the use of forced oxygen and forced amyl nitrite or sodium nitrite. There were no residual effects except headache and transient loss of appetite. Amyl nitrite and oxygen have been effective tools in the treatment of cyanide intoxication at this plant site. There have been no intercurrent or residual drug effects that outweigh the life-saving capacity of these agents. Sodium nitrite should be employed if the use of oxygen and amyl nitrite fail to improve the cardiovascular status/level of consciousness in 5-10 min.

Topics: Amyl Nitrite; Antidotes; Cohort Studies; Cyanides; Hemoglobins; Humans; Methemoglobin; Occupational Exposure; Occupational Health; Oxygen Inhalation Therapy; Poisoning; Sodium Nitrite; Thiosulfates

The authors reviewed the clinical manifestations, complications, and the prognosis affected by Lilly Cyanide Antidote in 21 victims of acute cyanide poisoning over a 10-year period. The clinical signs and symptoms in cyanide poisoning are variable. Among 21 cases, loss of consciousness (15), metabolic acidosis (14), and cardiopulmonary failure (9) were the three leading manifestations of cyanide intoxication. Anoxic encephalopathy (6) was not uncommon in the severely intoxicated victims. Diabetes insipidus (1) or clinical signs and symptoms mimicking diabetes insipidus (3) may be an ominous sign to encephalopathy victims. The major cause of fatal cyanide poisoning is the intentional ingestion of cyanide compounds as part of a suicide attempt. Decrease of arteriovenous difference of O2 partial pressure may be a clue for the suspicion of cyanide intoxication. Although the authors cannot show a statistically significant difference (P = .47) for the Lilly cyanide antidote kit in terms of improving the survival rate for victims of cyanide poisoning, the antidote kit was always mandatory in our study in the cases of severely intoxicated victims who survived. Early diagnosis, prompt, intensive therapy with antidote, and supportive care are still the golden rules for the treatment of acute cyanide poisoning, whether in the ED or on the scene.

Topics: Acute Disease; Adult; Amyl Nitrite; Antidotes; Cyanides; Drug Combinations; Emergencies; Female; Humans; Male; Middle Aged; Poison Control Centers; Poisoning; Prognosis; Retrospective Studies; Severity of Illness Index; Sex Factors; Sodium Nitrite; Survival Rate; Taiwan; Thiosulfates

Topics: 4-Aminopyridine; Antidotes; Humans; Hyperbaric Oxygenation; Nitriles; Occupational Exposure; Poisoning; Sodium Nitrite; Thiosulfates

Topics: Carbon Monoxide Poisoning; Carboxyhemoglobin; Cyanides; Humans; Poisoning; Sodium Nitrite

1. The protectiveness of combined treatment with sodium nitrite (SN) and hydroxylamine (HA) in cyanide intoxication was investigated in male rats. 2. Pretreatment with equimolar dose of SN or HA produced a significant protection against cyanide poisoning as shown by the protection index (LD50 of cyanide in protected rats/LD50 of cyanide in saline-treated rats). 3. The co-administration of SN and HA as a split dose produced an optimal and sustained methaemoglobinaemia. 4. Pretreatment with combined SN and HA administration at different time intervals offered sustained protection against cyanide and resultant cytochrome oxidase inhibition. 5. Adjunction of sodium thiosulphate (STS) in the SN+HA regimen further augmented the protection against cyanide poisoning. 6. The results suggest that pretreatment with SN+HA co-administration could significantly reduce the toxic manifestation of cyanide.

Topics: Animals; Antidotes; Drug Therapy, Combination; Humans; Hydroxylamine; Hydroxylamines; Male; Methemoglobin; Poisoning; Potassium Cyanide; Rats; Rats, Wistar; Sodium Nitrite

To evaluate serial cyanide, methemoglobin, and carbon monoxide levels in smoke inhalation patients.. Regional poison center and regional toxicology treatment center.. Seven critically ill smoke inhalation patients referred to the regional poison center.. Peak level and half-life were determined by obtaining serial carboxyhemoglobin, cyanide, and methemoglobin levels.. The mean observed half-life of cyanide was 3.0 +/- 0.6 hours. Methemoglobinemia was evaluated in four patients after sodium nitrite administration. The peak measured methemoglobin levels (mean, 10.5% +/- 2%; range, 7.9% to 13.4%) did not occur until a mean of 50 minutes (range, 35 to 70 minutes) following administration of sodium nitrite. The total oxygen-carrying capacity reduced by the combination of carboxyhemoglobin and methemoglobin was never more than 21% (range, 10% to 21%) in this series.. The administration of sodium nitrite to smoke inhalation patients in the presence of concomitant carbon monoxide poisoning may be relatively safe.

Topics: Adult; Antidotes; Carbon Monoxide Poisoning; Carboxyhemoglobin; Combined Modality Therapy; Cyanides; Drug Evaluation; Drug Therapy, Combination; Female; Humans; Hyperbaric Oxygenation; Infusions, Intravenous; Male; Methemoglobin; Methemoglobinemia; Middle Aged; Poison Control Centers; Poisoning; Prospective Studies; Smoke Inhalation Injury; Sodium Nitrite; Thiosulfates; Time Factors

Topics: Administration, Inhalation; Amyl Nitrite; Cyanides; Humans; Infusions, Intravenous; Nitroprusside; Poisoning; Sodium Nitrite

Topics: Administration, Inhalation; Amyl Nitrite; Antidotes; Cyanides; Humans; Infusions, Intravenous; Nitroprusside; Poisoning; Sodium Nitrite; Thiosulfates

Cyanide poisoning is a life threatening condition. But specific antidotes exist and can be easily prepared from available substances in hospital. Administration of antidotes will produce methemoglobin, which itself causes hypoxia. Nitrite induced methemoglobin can be extremely dangerous and even lethal. Before administering the antidotes, the diagnosis should be confirmed. Nitrite should not be given if the poisoning is mild or diagnosis is uncertain, to avoid excessive methemoglobin, dosage of sodium nitrite must be adjusted according to hemoglobin level (Table 1). Usage of sodium nitrite and sodium thiosulfate in the recommended doses are safe and effective for cyanide poisoning.

Topics: Acute Disease; Adult; Antidotes; Humans; Male; Methemoglobinemia; Poisoning; Potassium Cyanide; Sodium Nitrite; Thiosulfates

The anti-anoxic experiments have indicated that the petroleum ether extract of Rhizoma Zingiberis can prolong the survival time in mice poisoned by KCN or under the condition of normobaric hypoxia, as well as decapitation-induced gasping duration in mice, but can not prolong the survival time in mice poisoned by NaNO4. The anti-anoxic action might be related to the reduction rate of O2 consumption of the body. The aqueous extract of Rhizoma Zingiberis does not possess the above-mentioned anti-anoxic action. Both extracts do not affect the survival time in cooled mice.

Topics: Animals; Cold Temperature; Drugs, Chinese Herbal; Female; Hypoxia; Male; Mice; Oxygen Consumption; Poisoning; Potassium Cyanide; Sodium Nitrite

Management of the acutely poisoned patient should start with decontamination of the skin and irrigation of the eyes, if necessary, and assessment of cardiorespiratory status, neurologic status, and pupils and eye movement. If a definable toxic syndrome is present, the specific "antidote" should be given. If no such syndrome is apparent and the patient is comatose, 50 ml of 50% glucose and 0.4 mg of naloxone (Narcan) intravenously should be tried. General measures, applicable in either situation, include induction of emesis or lavage and administration of charcoal and cathartics.

Topics: Acute Disease; Antidotes; Carbon Monoxide Poisoning; Consciousness; Cyanides; Depression, Chemical; Humans; Naloxone; Nitrates; Nitrites; Organophosphate Poisoning; Oxygen; Parasympatholytics; Poisoning; Pupil; Sodium Nitrite; Thiosulfates

Topics: Adult; Autopsy; Humans; Male; Nitrites; Poisoning; Sodium Nitrite; Tissue Distribution

Prophylactic protection against cyanide intoxication in mice can be enhanced by the administration of oxygen, especially when it is used in combination with the conventional cyanide antidotes, sodium nitrite and sodium thiosulfate. The LD(50) values were compared in groups of mice premedicated with sodium thiosulfate or sodium nitrite, or both, in air and in oxygen. These results indicate that oxygen alone provides only minimal protection. Although oxygen enhances the protective effect of sodium thiosulfate to a minor degree, it does not enhance the protection of sodium nitrite at all; and yet, it potentiates the effectiveness of a combination of these two antagonists against cyanide intoxication.

Topics: Animals; Drug Synergism; Lethal Dose 50; Male; Mice; Oxygen; Poisoning; Potassium Cyanide; Random Allocation; Sodium Nitrite; Thiosulfates

Topics: Animals; Cats; Cattle; Cytoplasm; Electron Spin Resonance Spectroscopy; Guinea Pigs; Hemoglobins; Horses; Lagomorpha; Methemoglobin; Methemoglobinemia; Nitrites; Nitroso Compounds; Oxidation-Reduction; Pharmacology; Poisoning; Rabbits; Rats; Research; Sodium Nitrite; Species Specificity; Swine; Toxicology

Topics: Blood Transfusion; Child; Humans; Infant; Nitrites; Poisoning; Sodium; Sodium Nitrite; Sodium, Dietary

Topics: Humans; Nitrites; Poisoning; Sodium; Sodium Nitrite; Sodium, Dietary

Topics: Humans; Nitrites; Poisoning; Sodium Nitrite