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Sample records for acute cyanide poisoning

  1. Antidotes for acute cyanide poisoning.

    PubMed

    Borron, Stephen W; Baud, Frederic J

    2012-08-01

    Cyanide poisoning can present in multiple ways, given its widespread industrial use, presence in combustion products, multiple physical forms, and chemical structures. The primary target of toxicity is mitochondrial cytochrome oxidase. The onset and severity of poisoning depend on the route, dose, physicochemical structure and other variables. Common poisoning features include dyspnea, altered respiratory patterns, abnormal vital signs, altered mental status, seizures, and lactic acidosis. Our present knowledge supports cyanide poisoning treatment based on excellent supportive care with adjunctive antidotal therapy. Multiple antidotes exist and vary in regional availability. All currently marketed antidotes appear to be effective. Antidotal mechanisms include chelation, formation of stable, less toxic complexes, methemoglobin induction, and sulfane sulfur supplementation for detoxification by endogenous rhodanese. Each antidote has advantages and disadvantages. For example, hydroxocobalamin is safer than the methemoglobin inducers in patients with smoke inhalation. Research for new, safer and more effective cyanide antidotes continues.

  2. The clinical experience of acute cyanide poisoning.

    PubMed

    Yen, D; Tsai, J; Wang, L M; Kao, W F; Hu, S C; Lee, C H; Deng, J F

    1995-09-01

    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.

  3. Acute cyanide poisoning: clinical spectrum, diagnosis, and treatment.

    PubMed

    Borron, S W; Baud, F J

    1996-09-01

    Cyanide poisoning presents in many forms. Industrial intoxications occur due to extensive use of cyanide compounds as reaction products. Smoke inhalation, a polyintoxication, is most often responsible for domestic cyanide poisonings. Suicidal poisonings are rare. Cyanogenic compounds may produce acute or subacute toxicity. Signs of cyanide poisoning include headache, vertigo, agitation, confusion, coma, convulsions and death. Definitive laboratory confirmation is generally delayed. Elevated plasma lactate, associated with cardiovascular collapse, should suggest cyanide intoxication. Immediate treatment includes 100% oxygen, assisted ventilation, decontamination, correction of acidosis and blood pressure support. Antidotes include oxygen, hydroxocobalamin, di-cobalt EDTA and methaemoglobin-inducers. Hydroxocobalamin is an attractive antidote due to its rapid cyanide binding and its lack of serious side-effects, even in the absence of cyanide intoxication. Sodium thiosulphate acts more slowly than other antidotes and is indicated in subacute cyanogen poisoning and as an adjunct to acute cyanide poisoning. Initial evaluation of antidotal efficacy is based on correction of hypotension and lactic acidosis; the final analysis rests on the degree of permanent central nervous system injury.

  4. Acute cyanide poisoning among jewelry and textile industry workers.

    PubMed

    Coentrão, Luís; Moura, Daniel

    2011-01-01

    Limited work has focused on occupational exposures that may increase the risk of cyanide poisoning by ingestion. A retrospective chart review of all admissions for acute cyanide poisoning by ingestion for the years 1988 to 2008 was conducted in a tertiary university hospital serving the largest population in the country working in jewelry and textile facilities. Of the 9 patients admitted to the hospital during the study period, 8 (7 males, 1 female; age 36 ± 11 years, mean ± SD) attempted suicide by ingestion of potassium cyanide used in their profession as goldsmiths or textile industry workers. Five patients had severe neurologic impairment and severe metabolic acidosis (pH 7.02 ± 0.08, mean ± SD) with high anion gap (23 ± 4 mmol/L, mean ± SD). Of the 5 severely intoxicated patients, 3 received antidote therapy (sodium thiosulfate or hydroxocobalamin) and resumed full consciousness in less than 8 hours. All patients survived without major sequelae. Cyanide intoxication by ingestion in our patients was mainly suicidal and occurred in specific jobs where potassium cyanide is used. Metabolic acidosis with high anion is a good surrogated marker of severe cyanide poisoning. Sodium thiosulfate and hydroxocobalamin are both safe and effective antidotes.

  5. [Cyanide poisoning].

    PubMed

    Møller, Søren; Hemmingsen, Claus

    2003-06-16

    Cyanide is a toxic compound which inhibits the cellular utilization of oxygen. A number of substances can give rise to cyanide intoxication, which in some cases may have a delayed onset. The symptoms are non-specific and reflect cellular hypoxia. Several strategies may be employed in the treatment. Hydroxycobalamine is an effective and non-toxic antidote. On the basis of a case story, the toxicology, symptoms and treatment of cyanide poisoning are discussed.

  6. Occupational cyanide poisoning

    PubMed Central

    Amizet, Loic; Pruvot, Gauthier; Remy, Sophie; Kfoury, Michel

    2011-01-01

    Cyanide poisoning has existed for centuries. In most cases, cyanide is combined with other toxic substances; for example with carbon monoxide in fire smoke. Cases of pure cyanide poisoning are rare, and usually due to accidental exposure. Their treatment is based on oxygenation and the infusion of hydroxocobalamin. The seriousness of this type of poisoning calls for a rapid and specific response, which demonstrates the usefulness of non-hospital based medical treatment. The authors report here the case of a man who was the victim of occupational poisoning with sodium cyanide and who was treated at the workplace by fire-fighters and the Service Mobile d’Urgence et Reanimation emergency ambulance service. PMID:22674698

  7. The treatment of cyanide poisoning.

    PubMed

    Cummings, T F

    2004-03-01

    Cyanide has gained historical notoriety as a poison used with intent to cause fatality. Its occurrence in industry is confined to a small number of uses in a relatively narrow range of industries, including the manufacture of Perspex and nylon and in electroplating. With proper controls in these settings, episodes of poisoning are extremely rare. However, because of the potential for a fatal outcome, procedures for the treatment of acute poisoning are essential. Antidotes include methaemoglobin generators, direct binding agents and sulphur donors, but there is a lack of international consensus about the treatment of choice. This article reviews the mechanisms and treatment of cyanide intoxication and emphasizes the importance of having agreed local procedures for the emergency treatment of poisoning.

  8. Antidotes for Cyanide Poisoning

    DTIC Science & Technology

    2013-01-01

    challenging position as professor ordinarius at the Depart- ment of Anaesthesiology . I pioneered from scratch in this position until 2009. My academic... experience in the Paris Fire Brigade. Clin Toxicol (Phila) 2006; 44 (Suppl 1):37 44. Antidotes for cyanide poisoning Kurt Anseeuwa*, Nicolas Delvaub...hydro- xocobalamin higher than 150 mg/kg. Given the theoretically synergistic action and given the experience in the treatment of the toxicity of

  9. Antidotal treatment of cyanide poisoning.

    PubMed

    Mégarbane, Bruno; Delahaye, Arnaud; Goldgran-Tolédano, Dany; Baud, Frédéric J

    2003-04-01

    Cyanide poisoning may result from different exposures: residential fires, industrial accidents, drug and plant intoxication. Clinical features include coma, respiratory arrest and cardiovascular collapse. The biological hallmark is lactic acidosis. A plasma lactate concentration > or = 10 mmol/L in fire victims without severe burns and > or = 8 mmol/L in pure cyanide poisoned patients is a sensitive and specific indicator of cyanide intoxication. Many antidotes are available and efficient. However, therapeutic strategies are still debated. Our objective was to compare conventional treatments to hydroxocobalamin. This article reviews the literature on cyanide poisoning treatment. Conventional treatment of cyanide poisoning includes decontamination, supportive and specific treatment. Decontamination should be adapted to the route of poisoning and never postpone supportive treatment. Basic life support includes immediate administration of high flow of oxygen, airway protection and cardiopulmonary resuscitation. Advanced life support includes mechanical ventilation, catecholamine and sodium bicarbonate infusion. Supportive treatment is efficient but does not modify the time course or the body burden of cyanide. Numerous antidotes are available. Oxygen counteracts efficiently cyanide action at the mitochondrial level. Sodium thiosulfate, methemoglobin forming agents and cobalt compounds act efficiently by complexing or transforming cyanide into non-toxic stable derivatives. However, regarding the main clinical condition of cyanide poisoning, i.e. smoke inhalation, we should take into account not only the efficiency of antidotes but also their safety. Sodium thiosulfate is both efficient and safe, but acts with delay. Methemoglobin-forming agents are potent, but due to the transformation of hemoglobin into methemoglobin, they impair tissue delivery of oxygen. Experimental data showed increased mortality in carbon monoxide- and cyanide-poisoned rats treated with these

  10. Combined administration of hyperbaric oxygen and hydroxocobalamin improves cerebral metabolism after acute cyanide poisoning in rats.

    PubMed

    Hansen, M B; Olsen, N V; Hyldegaard, O

    2013-11-01

    Hyperbaric oxygen therapy (HBOT) or intravenous hydroxocobalamin (OHCob) both abolish cyanide (CN)-induced surges in interstitial brain lactate and glucose concentrations. HBOT has been shown to induce a delayed increase in whole blood CN concentrations, whereas OHCob may act as an intravascular CN scavenger. Additionally, HBOT may prevent respiratory distress and restore blood pressure during CN intoxication, an effect not seen with OHCob administration. In this report, we evaluated the combined effects of HBOT and OHCob on interstitial lactate, glucose, and glycerol concentrations as well as lactate-to-pyruvate ratio in rat brain by means of microdialysis during acute CN poisoning. Anesthetized rats were allocated to three groups: 1) vehicle (1.2 ml isotonic NaCl intra-arterially); 2) potassium CN (5.4 mg/kg intra-arterially); 3) potassium CN, OHCob (100 mg/kg intra-arterially) and subsequent HBOT (284 kPa in 90 min). OHCob and HBOT significantly attenuated the acute surges in interstitial cerebral lactate, glucose, and glycerol concentrations compared with the intoxicated rats given no treatment. Furthermore, the combined treatment resulted in consistent low lactate, glucose, and glycerol concentrations, as well as in low lactate-to-pyruvate ratios compared with CN intoxicated controls. In rats receiving OHCob and HBOT, respiration improved and cyanosis disappeared, with subsequent stabilization of mean arterial blood pressure. The present findings indicate that a combined administration of OHCob and HBOT has a beneficial and persistent effect on the cerebral metabolism during CN intoxication.

  11. Citrus peel extract attenuates acute cyanide poisoning-induced seizures and oxidative stress in rats.

    PubMed

    Abdel Moneim, Ahmed E

    2014-01-01

    The primary aimed of this study was to investigate the potential protective effects of methanolic extract of citrus peel (MECP) on acute cyanide (KCN) poisoning-induced seizures and oxidative stress in rats. The intraperitoneal LD50 value of KCN (6.3 mg/Kg bwt), based on 24 hrs mortality, was significantly increased by 9, 52 or 113% by oral administration of MECP (500 mg/Kg bwt) pre-administered for 1, 2 and 3 days, respectively, in rats in a time-dependent manner. Intraperitoneal injection of the sublethal dose of KCN (3 mg/Kg bwt) into rats increased, 24 hrs later, lipid peroxidation (LPO), nitric oxide (NO), glutamate levels and acetylcholinesterase (AChE) activity in hippocampus, striatum and cerebral cortex. KCN also decreased brain glutathione (GSH) level and superoxide dismutase (SOD) and catalase (CAT) activities in these animals. Pre-treatment of rats with MECP inhibited KCN-induced increases in LPO, NO, and glutamate levels and AChE activity as well as decreases in brain GSH level and SOD and CAT activities. In addition, KCN significantly decreased norepinephrine, dopamine and serotonin levels in different brain regions which were resolved by MECP. From the present results, it can be concluded that the neuroprotective effects of MECP against KCN-induced seizures and oxidative stress may be due to the inhibition of oxidative stress overproduction and maintenance of antioxidant defense mechanisms.

  12. Study of Potential Prophylactic and Antidotal Use of Scavenging Agents in Treatment of Cyanide Poisoning

    DTIC Science & Technology

    1984-11-15

    oxaloacetic cyanohydrins. Biochem. J. 31, 617-618, 1937. 9 13. Cittadini, A., Caprino , L. and Terronova, T. Effect of pyruvate on the acute cyanide...Boston, Mass. p. 173, 1973. 3. Cittadini, A., Caprino , L. and Ternanova, T. Effect of pyruvate on the acute cyanide poisoning in mice. Experientia

  13. Physiology and pathophysiology of respiratory arrest by cyanide poisoning

    SciTech Connect

    Klimmek, R.

    1993-05-13

    Respiratory arrest, preceded by hyperventilation, is the primary cause of death in acute cyanide poisoning. Hyperventilation followed by apnea is also observed without intoxication. Hyperventilation and apnea in untoxicated subjects and animals are analyzed for the underlying physiological and biochemical changes and compared with those found during cyanide poisoning. The study reveals that the respiratory autoregulation appears to be the same under both conditions. Respiratory arrest is controlled by cerebral PCO2 and can occur without hypoxia or inhibition of cytochrome oxidase. It is postulated that respiratory arrest is a 'desperate act' thrust on the respiratory neurons by a critical exhaustion of their energy store (ATP) due to the rapid firing in the period of hyperventilation. The point of no return may be reached when anoxia and/or partial inhibition of cytochrome oxidase prevent the neurons from replenishing the ATP store. The formation of Fe3+ cyanide complexes. exemplified by the metHb producer DMAP, appears to give the best results with regard to the restoration of spontaneous respiration. The study of respiratory autoregulation may also be helpful in developing and understanding other therapeutic approaches.

  14. Effect of acute and delayed hyperbaric oxygen therapy on cyanide whole blood levels during acute cyanide intoxication.

    PubMed

    Lawson-Smith, P; Jansen, E C; Hilsted, L; Johnsen, A H; Hyldegaard, O

    2011-01-01

    Cyanide and carbon monoxide, which are often found in fire victims, are toxic gases emitted from fires. Cyanide and carbon monoxide have similar molecular structure. Cyanide binds to the enzyme cytochrome oxidase a, a3 similar to carbon monoxide, thus blocking the mitochondrial respiration chain causing depletion of adenosine triphosphate. Hyperbaric oxygen (HBO2) is recommended for treating carbon monoxide poisoning. The therapeutic effect is due to a high oxygen pressure removing carbon monoxide from the cells. We hypothesise that HBO2 induces changes in whole-blood-cyanide by a competitive mechanism forcing cyanide out of cellular tissues. A rat model was developed to study this effect. Female Sprague Dawley rats were anesthetized with a fentanyl + fluanizone combination and midazolam given subcutaneously (s.c.). Rats were poisoned with 5.4 mg/kg KCN injected intra-peritoneally in Group 1 and intra-arterially in Group 2. Blood samples were taken immediately after poisoning, and at one and a half, three and five hours. Blood was drawn from a jugular vein in Group 1 and from a femoral artery in Group 2. Group 1 rats were divided into a control group of 12 rats without HBO2, 10 rats had acute HBO2 immediately after poisoning and a group of 10 rats had HBO2 one and a half hours after poisoning. Group 2 rats were divided into a control group and an acute HBO2 group, with 10 rats in both groups. Whole-blood-cyanide concentrations were measured using the Conway method based on diffusion and the subsequent formation of cyanocobalamin measured by a spectrophotometer. Results showed that whole-blood-cyanide concentration in Group 1 controls and acute HBO2 initially rose and then fell towards zero. In rats treated with delayed HBO2, the reduction in whole-blood-cyanide concentration was significantly less as compared to controls and acute HBO2-treated rats. Group 2 controls whole-blood-cyanide concentration decreased towards zero throughout the observation period. However

  15. Cyanide poisoning by fire smoke inhalation: a European expert consensus.

    PubMed

    Anseeuw, Kurt; Delvau, Nicolas; Burillo-Putze, Guillermo; De Iaco, Fabio; Geldner, Götz; Holmström, Peter; Lambert, Yves; Sabbe, Marc

    2013-02-01

    Smoke inhalation is a common cause of cyanide poisoning during fires, resulting in injury and even death. In many cases of smoke inhalation, cyanide has increasingly been recognized as a significant toxicant. The diagnosis of cyanide poisoning remains very difficult, and failure to recognize it may result in inadequate or inappropriate treatment. Findings suggesting cyanide toxicity include the following: (a) a history of enclosed-space fire; (b) any alteration in the level of consciousness; (c) any cardiovascular changes (particularly inexplicable hypotension); and (d) elevated plasma lactate. The feasibility and safety of empiric treatment with hydroxocobalamin for fire smoke victims have been reported in the literature. On the basis of a literature review and a panel discussion, a group of European experts has proposed emergency management protocols for cyanide toxicity in fire smoke victims.

  16. Cyanide poisoning, 2 cases report and treatment review.

    PubMed

    Ruangkanchanasetr, S; Wananukul, V; Suwanjutha, S

    1999-11-01

    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.

  17. Antagonism of cyanide poisoning by dihydroxyacetone.

    PubMed

    Niknahad, Hossein; Ghelichkhani, Esmaeel

    2002-06-14

    Dihydroxyacetone (DHA) effectively antagonized the lethal effect of cyanide in mice and rabbits, particularly if administered in combination with thiosulfate. Oral DHA (2 and 4 g/kg) given to mice 10 min before injection (i.p.) of cyanide increased the LD50 values of cyanide from 5.7 mg/kg to 12 and 17.6 mg/kg, respectively. DHA prevented cyanide-induced lethality most effectively, if given orally 10-15 min before injection of cyanide. A combination of pretreatment with oral DHA (4 g/kg) and post-treatment with sodium thiosulfate (1 g/kg) increased the LD50 of cyanide by a factor of 9.9. Furthermore, DHA given intravenously to rabbits 5 min after subcutaneous injection of cyanide increased the LD50 of cyanide from 6 mg/kg to more than 11 mg/kg, while thiosulfate (1 g/kg) given intravenously 5 min after cyanide injection increased the LD50 of cyanide only to 8.5 mg/kg. DHA also prevented the convulsions that occurred after cyanide intoxication.

  18. MR changes after acute cyanide intoxication.

    PubMed

    Rachinger, Johanna; Fellner, Franz A; Stieglbauer, Karl; Trenkler, Johannes

    2002-09-01

    We describe MR changes that occurred 3 and 6 weeks after a suicide attempt with cyanide. The toxicity of cyanide causes damage, primarily to the basal ganglia, and those changes were visible as altered signal intensity on the first MR images. Extensive areas of hemorrhagic necrosis were seen 6 weeks later. Our case shows pseudolaminar necrosis along the central cerebral cortex 3 weeks after cyanide poisoning, showing that the sensorimotor cortex is also a site for toxic necrosis because of its high oxygen dependency.

  19. Acute oral toxicity of sodium cyanide in birds

    USGS Publications Warehouse

    Wiemeyer, Stanley N.; Hill, E.F.; Carpenter, J.W.; Krynitsky, A.J.

    1986-01-01

    Sensitivities of six avian species, black vulture (Coragyps atratus), American kestrel (Falco sparverius), Japanese quail (Coturnix japonica), domestic chicken (Gallus domesticus), eastern screech-owl (Otus asio), and European starling (Sturnus vulgaris), to acute poisoning by sodium cyanide (NaCN) were compared by single dose LD50's. Three species, domestic chickens, black vultures, and turkey vultures (Cathartes aura), were dosed with NaCN to determine cyanide residues in those that died and also in survivors, in addition to postmortem fate. Three flesh-eating species (black vulture, American kestrel, and eastern screech-owl; LD50's 4.0-8.6 mg/kg) were more sensitive to NaCN than three species (Japanese quail, domestic chicken, and European starling; LD50's 9.4-21 mg/kg) that fed predominantly on plant material. Elevated concentrations of cyanide were found in the blood of birds that died of cyanide poisoning; however, concentrations in birds that died overlapped those in survivors. Blood was superior to liver as the tissue of choice for detecting cyanide exposure. No gross pathological changes related to dosing were observed at necropsy.

  20. Treatment of acute cyanide intoxication with hemodialysis.

    PubMed

    Wesson, D E; Foley, R; Sabatini, S; Wharton, J; Kapusnik, J; Kurtzman, N A

    1985-01-01

    A dramatic response was noted in a patient at our hospital who received hemodialysis therapy for severe acidosis secondary to an unknown toxin, subsequently identified as cyanide. We were unable to find any information concerning the hemodialysis clearance and extraction ratio of cyanide; thus, we studied the effect of hemodialysis in dogs receiving a constant infusion of cyanide with and without a simultaneous infusion of thiosulfate. The hemodialysis clearance of cyanide in the presence of thiosulfate was 38.3 +/- 5.4 ml/min with an extraction ratio of 0.43 +/- 0.06 (n = 4). Hemodialysis was found to increase the lethal dose of cyanide without thiosulfate infusion, and a further increase was noted with the thiosulfate infusion. Thiosulfate promotes mitochondrial metabolism of cyanide to thiocyanate. The end product, thiocyanate, is quickly removed by hemodialysis. We believe that the demonstrated effectiveness of hemodialysis in the treatment of acute cyanide intoxication is related not only to the hemodialysis clearance of cyanide, but also to the removal of its metabolic end product, thiocyanate. Based on our observations, we feel that hemodialysis is an effective adjunct in the treatment of acute cyanide intoxication.

  1. Analysis of hydrogen cyanide in air in a case of attempted cyanide poisoning.

    PubMed

    Magnusson, R; Nyholm, S; Åstot, C

    2012-10-10

    A 32-year-old man attempted to poison his ex-girlfriend with hydrogen cyanide by hiding the pesticide Uragan D2 in her car. During the police investigation, chemical analysis of the air inside the car was performed. Hydrogen cyanide was detected through on-site air analysis using a portable Fourier transform infrared (FTIR) spectroscopy gas analyzer and colorimetric gas detection tubes. Furthermore, impinger air-sampling was performed for off-site sample preparation and analysis by gas chromatography-mass spectrometry (GC-MS). All three independent techniques demonstrated the presence of hydrogen cyanide, at concentrations of 14-20 ppm. Owing to the high volatility of hydrogen cyanide, the temperature and the time since exposure have a substantial effect on the likelihood of detecting hydrogen cyanide at a crime scene. The prevailing conditions (closed space, low temperature) must have supported the preservation of HCN in the car thus enabling the identification even though the analysis was performed several days after the hydrogen cyanide source was removed. This paper demonstrates the applicability of combining on-site FTIR measurements and off-site GC-MS analysis of a crime scene in order to ensure fast detection as well as unambiguous identification for forensic purposes of hydrogen cyanide in air.

  2. Acute organophosphorus poisoning.

    PubMed

    Chowdhary, Sheemona; Bhattacharyya, Rajasri; Banerjee, Dibyajyoti

    2014-04-20

    Acute organophosphorus poisoning continues to be a detrimental problem and a potential cause of mortality especially in developing countries. Inhibition of acetylcholinesterase enzyme is the main mechanism of toxicity of such pesticides and measurement of acetylcholinesterase activity is the commonly used laboratory diagnosis approved for the purpose. It is now proved beyond any doubt that early intervention is beneficial for cases of acute organophosphorus poisoning and, therefore, considerable current interest has been generated for development of point of care testing tool for screening of the same. However, to the best of our knowledge so far the matter is not reviewed from the view of point of care testing tool development. In this paper, this subject is reviewed highlighting the methodological aspects and point of care testing tool development in the context of organophosphorus poisoning.

  3. Acute cyanide intoxication and central transmitter systems.

    PubMed

    Persson, S A; Cassel, G; Sellström, A

    1985-12-01

    In rats treated with sodium cyanide (5-20 mg/kg, ip) dopamine was dose dependently decreased in the striatum within 60 sec. One of the main metabolites of dopamine in the central nervous system, 3-methoxy-4-hydroxyphenylacetic acid (HVA), was decreased in striatum, olfactory tubercle, and hippocampus. However, the oxidatively deaminated metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), was not significantly altered in any of the brain regions studied. Naturally occurring levels of 3,4-dihydroxy-L-phenylalanine (L-dopa), as well as L-dopa accumulated after inhibition of the neuronal L-aromatic amino acid decarboxylase, increased in cyanide-treated rats. The dopamine receptor antagonist spiperone (0.05 mg/kg, ip) slightly increased the survival in acute cyanide intoxication. Sodium cyanide increased the levels of glutamine in frontal cortex and striatum at all doses studied. Glutamic acid was increased in the cerebellum, striatum, and hippocampus after sodium cyanide (5-10 mg/kg, ip). Higher doses decreased glutamic acid in the cerebellum, the frontal cortex, and the striatum. gamma-Aminobutyric acid (GABA) concentrations were diminished at high doses in all regions studied. Cyanide increased the levels of cyclic GMP in the cerebellum. In the striatum cyclic GMP was decreased after sodium cyanide (10 and 20 mg/kg). No significant alterations in the concentrations of acetylcholine or choline were seen in the striatum of cyanide-treated rats. The acetylcholinesterase inhibitor physostigmine and the muscarinic receptor antagonist atropine decreased the survival of mice given sodium cyanide. Acute cyanide intoxication thus produces rapid and fairly specific changes in central dopaminergic and GABA-ergic pathways.

  4. Calcium antagonists. A role in the management of cyanide poisoning

    SciTech Connect

    Maduh, E.U.; Porter, D.W.; Baskin, S.I.

    1993-12-31

    The physiological role of calcium was demonstrated by Ringer (1883) when he linked the omission of calcium (Ca++) from the bathing medium to the induction of cardiac arrest in the isolated frog heart. This observation established that Ca++ controlled muscle contraction but it was not until the autumn of 1963 that the specific pharmacological significance of this contribution was realised by Fleckenstein (1964), leading to the development of Ca++ antagonism as a concept in drug action (Fleckenstein 1977). Identifying the precise role of Ca++ ions in toxic cell injury and tissue death attributable to drug and chemical intoxication has lagged behind developments in Ca++ physiology and pharmacology and to date, much remains to be learned, although studies aimed at characterising the role of Ca++ in cytotoxic cell injury are receiving intense attention (Bondy Komulainen 1988; Maduh et al. l988a, l99Oa,b; Orrenius et al. 1989; Trump et al. 1989). On the other hand, the importance of cyanide as a poison has been known from antiquity (for references to earlier literature see Baskin Fricke 1992; Solomonson 1981). In experimental cyanide poisoning, recent studies have examined alterations in cell Ca++ and the influence of Ca++ antagonists in the management of this chemical toxicological emergency. These efforts have principally focused on the cellular Ca++ homeostasis system, its interrelationship with cellular components, and its susceptibility to cyanide action.

  5. High Anion Gap Metabolic Acidosis after a Suicide Attempt with Cyanide: The Rebirth of Cyanide Poisoning.

    PubMed

    Hsiao, Po-Jen; Chang, Che-Fu; Chiu, Chih-Chien; Chan, Jenq-Shyong; Chiang, Wen-Fang; Wu, Chia-Chao; Lin, Shih-Hua; Chen, Jin-Shuen

    2015-01-01

    A 33-year-old woman was admitted to our emergency department in a state of unconsciousness after attempting suicide with unknown substances. Severe metabolic acidosis (pH: 6.81), with a high anion gap (36.2) and high lactate level (20.2 mmol/L), was observed. After four hours of intensive medical treatment, the patient regained consciousness, with a return of the arterial pH to 7.42. Finally, cyanide intoxication was diagnosed based on the detection of a serum cyanide level of 3.5 mg/L. The presence of a high anion gap associated with severe lactic acidosis is a clue for making a rapid differential diagnosis of acute cyanide intoxication. Providing intensive and immediate supportive management is also crucial, even in cases without obtainable specific antidotes.

  6. Acute, sublethal cyanide poisoning in mice is ameliorated by nitrite alone: complications arising from concomitant administration of nitrite and thiosulfate as an antidotal combination.

    PubMed

    Cambal, Leah K; Swanson, Megan R; Yuan, Quan; Weitz, Andrew C; Li, Hui-Hua; Pitt, Bruce R; Pearce, Linda L; Peterson, Jim

    2011-07-18

    Sodium nitrite alone is shown to ameliorate sublethal cyanide toxicity in mice when given from ∼1 h before until 20 min after the toxic dose as demonstrated by the recovery of righting ability. An optimum dose (12 mg/kg) was determined to significantly relieve cyanide toxicity (5.0 mg/kg) when administered to mice intraperitoneally. Nitrite so administered was shown to rapidly produce NO in the bloodsteam as judged by the dose-dependent appearance of EPR signals attributable to nitrosylhemoglobin and methemoglobin. It is argued that antagonism of cyanide inhibition of cytochrome c oxidase by NO is the crucial antidotal activity rather than the methemoglobin-forming action of nitrite. Concomitant addition of sodium thiosulfate to nitrite-treated blood resulted in the detection of sulfidomethemoblobin by EPR spectroscopy. Sulfide is a product of thiosulfate hydrolysis and, like cyanide, is known to be a potent inhibitor of cytochrome c oxidase, the effects of the two inhibitors being essentially additive under standard assay conditions rather than dominated by either one. The findings afford a plausible explanation for an observed detrimental effect in mice associated with the use of the standard nitrite-thiosulfate combination therapy at sublethal levels of cyanide intoxication.

  7. [Acute zincteral oral poisoning].

    PubMed

    Kamenczak, A; Pokorska, M; Wołek, E; Kobyłecka, K

    Zinc vapour poisoning by inhalation in the form of zinc fever is more frequent than oral zinc product poisoning, the product used in therapy. The main aim of the study was the evaluation of clinical manifestation present after Zincteral ingestion as well as attempt to find the relationship between the presence and aggravation of the clinical manifestation and zinc level in the blood. The course of acute clinical suicidal poisoning by ingestion of Zincteral 50 tablets (10.0 g) and 100 tablets (20.0 g) is presented. The clinical picture revealed the following symptoms and signs: tachycardia, changes of arterial BP, vascular shock; dyspeptic nausea, vomiting cramps in abdominal region, diarrhoea. Damage of the parenchymatous organs, mainly liver was evident. In pregnant woman (9-week-pregnancy) on the 12-th day of her stay in the Clinic complete miscarriage took place accompanied by haemorrhage from reproductive organs. The kind and exacerbation of the clinical manifestations in relation to the zinc level in body fluid were analysed.

  8. Effect of alpha-ketoglutarate on neurobehavioral, neurochemical and oxidative changes caused by sub-chronic cyanide poisoning in rats.

    PubMed

    Mathangi, D C; Shyamala, R; Vijayashree, R; Rao, K R; Ruckmani, A; Vijayaraghavan, R; Bhattacharya, R

    2011-03-01

    Recent studies revealed that alpha-ketoglutarate (A-KG) alone or with sodium thiosulfate (STS) provide significant protection against acute and sub-acute cyanide poisoning in rodents. This study addresses the protective effect of A-KG and/or STS in sub-chronic (90 days) cyanide poisoning. Wistar rats were divided into seven groups (n = 10): Control animals, potassium cyanide (KCN) A-KG, STS, KCN + A-KG, KCN + STS and KCN + A-KG + STS. Spontaneous motor activity and motor coordination were recorded every 15th day. Lipid peroxidation (LPO), reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) in blood, brain, liver and kidney, and glutamate, aspartate and dopamine in discrete regions of brain were measured following 90 days exposure. Cyanide significantly decreased motor coordination, accompanied by increase in LPO (blood, brain and liver) and dopamine (corpus striatum and cerebral cortex) levels, and depletion in GSH (blood, brain and liver), GPx (brain and liver), SOD (brain and liver), and CAT (blood and brain) levels. Although treatment of A-KG and STS alone significantly blunted the toxicity of KCN, concomitant use of both afforded the maximum protection. This study shows a promising role of A-KG and STS as treatment regime for long term cyanide exposure.

  9. Pediatric cyanide poisoning by fire smoke inhalation: a European expert consensus. Toxicology Surveillance System of the Intoxications Working Group of the Spanish Society of Paediatric Emergencies.

    PubMed

    Mintegi, Santiago; Clerigue, Nuria; Tipo, Vincenzo; Ponticiello, Eduardo; Lonati, Davide; Burillo-Putze, Guillermo; Delvau, Nicolas; Anseeuw, Kurt

    2013-11-01

    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.

  10. Accidental choke-cherry poisoning: early symptoms and neurological sequelae of an unusual case of cyanide intoxication.

    PubMed

    Pentore, R; Venneri, A; Nichelli, P

    1996-06-01

    We report the case of a 56-year-old woman who was accidentally poisoned when she ingested choke cherries whose pulp contained cyanide, and describe the acute clinical picture, the neurological sequelae and the neuroradiological findings. After recovery from coma, the patient showed signs of a parkinsonian syndrome, retrobulbar neuritis and sensory-motor neuropathy. MRI showed abnormal signal intensities involving the basal ganglia. Since no memory deficits were observed, we argue that the parkinsonian syndrome was caused by cyanide intoxication rather than by subcortical damage due to hypoxia.

  11. A field-deployable device for the rapid detection of cyanide poisoning in whole blood

    NASA Astrophysics Data System (ADS)

    Boehringer, Hans; Tong, Winnie; Chung, Roy; Boss, Gerry; O'Farrell, Brendan

    2012-06-01

    Feasibility of a field-deployable device for the rapid and early diagnosis of cyanide poisoning in whole blood using the spectral shift of the vitamin B12 precursor cobinamide upon binding with cyanide as an indicator is being assessed. Cyanide is an extremely potent and rapid acting poison with as little as 50 mg fatal to humans. Cyanide poisoning has been recognized as a threat from smoke inhalation and potentially through weapons of mass destruction. Currently, no portable rapid tests for the detection of cyanide in whole blood are available. Cobinamide has an extremely high affinity for cyanide and captures hemoglobin associated cyanide from red blood cells. Upon binding of cyanide, cobinamide undergoes a spectral shift that can be measured with a spectrophotometer. We have combined the unique cyanide-binding properties of cobinamide with blood separation technology, sample transport and a detection system, and are developing a rapid, field deployable, disposable device which will deliver an intuitive result to a first responder, allowing for rapid response to exposure events. Feasibility of the cobinamide-Cyanide chemistry in a rapid test using a whole blood sample from a finger-stick has been demonstrated with an assay time from sample collection to a valid result of under 5 minutes. Data showing the efficacy of the diagnostic method and initial device design concepts will be shown.

  12. [Acute carbon monoxide poisoning].

    PubMed

    Raphaël, Jean-Claude

    2008-04-30

    Carbon monoxide (CO) poisoning is still complicated by a high mortality and morbidity rate. Diagnosis can be obvious but is most of time difficult and sometimes remained unknown. It is usually based on clinical signs and must be confirmed by assessment of CO level in room air or in patient's expired breathing or blood and detection of a source. Mild neurological sequelae are very common. Normobaric oxygen is the first line treatment. Comatose and pregnant patients must undergo hyperbaric oxygen. All CO poisoning has to be declared to sanitary authority, which will in turn conduct a technical inspection to remove the source. The patient must be informed that he is at risk of new poisoning and of neurological complications. Progress in prevention and research in therapeutics are needed in order to reduce CO related morbidity.

  13. [Acute phostoxin poisoning].

    PubMed

    Idali, B; Miguil, M; Moutawakkil, S; Bouaggad, A; Guartit, A; Abassi, O; Ben Aguida, M

    1995-04-01

    Phostoxin is a mixture of aluminium phosphide and ammonium carbonate. When exposed to water, it releases phosphorus hydrogen (PH3), a highly-poisonous gas. In Morocco, death rate from suicide due to self-administration of phostoxin pills is high. Clinical signs include abrupt digestive and nervous disorders. Pulmonary oedema or cardiogenic shock dominate early prognosis. Liver and renal damage is secondary. Prevention requires both legal constraints and regulation of sales.

  14. Reversal of cyanide inhibition of cytochrome c oxidase by the auxiliary substrate nitric oxide: an endogenous antidote to cyanide poisoning?

    PubMed

    Pearce, Linda L; Bominaar, Emile L; Hill, Bruce C; Peterson, Jim

    2003-12-26

    Nitric oxide (NO) is shown to overcome the cyanide inhibition of cytochrome c oxidase in the presence of excess ferrocytochrome c and oxygen. Addition of NO to the partially reduced cyanide-inhibited form of the bovine enzyme is shown by electron paramagnetic resonance spectroscopy to result in substitution of cyanide at ferriheme a3 by NO with reduction of the heme. The resulting nitrosylferroheme a3 is a 5-coordinate structure, the proximal bond to histidine having been broken. NO does not simply act as a reversibly bound competitive inhibitor but is an auxiliary substrate consumed in a catalytic cycle along with ferrocytochrome c and oxygen. The implications of this observation with regard to estimates of steady-state NO levels in vivo is discussed. Given the multiple sources of NO available to mitochondria, the present results appear to explain in part some of the curious biomedical observations reported by other laboratories; for example, the kidneys of cyanide poisoning victims surprisingly exhibit no significant irreversible damage, and lethal doses of potassium cyanide are able to inhibit cytochrome c oxidase activity by only approximately 50% in brain mitochondria.

  15. Antidote treatment for cyanide poisoning with hydroxocobalamin causes bright pink discolouration and chemical-analytical interferences.

    PubMed

    Brunel, C; Widmer, C; Augsburger, M; Dussy, F; Fracasso, T

    2012-11-30

    Here we report the case of a 70-year-old woman who committed suicide by cyanide poisoning. During resuscitation cares, she underwent an antidote treatment by hydroxocobalamin. Postmortem investigations showed marked bright pink discolouration of organs and fluids, and a lethal cyanide blood concentration of 43 mg/L was detected by toxicological investigation. Discolouration of hypostasis and organs has widely been studied in forensic literature. In our case, we interpreted the unusual pink coloration as the result of the presence of hydroxocobalamin. This substance is a known antidote against cyanide poisoning, indicated because of its efficiency and poor adverse effects. However, its main drawback is to interfere with measurements of many routine biochemical parameters. We have tested the potential influence of this molecule in some routine postmortem investigations. The results are discussed.

  16. [Resuscitation in acute poisonings based on 2005 and 2010 Resuscitation Guideline].

    PubMed

    Macheta, Alicja; Pach, Janusz; Andres, Janusz

    2011-01-01

    Acute poisonings in USA are a leading cause of cardiac arrest, especially in youngsters. Primary survey and cardiopulmonary resuscitation for poisoning is based on ABCDE procedure. One of the most common manifestation of acute poisoning is coma. An open airway should be ensured. Endotracheal intubation should be performed by an experienced person. The mouth-to mouth method of artificial respiration can be applied ultimately. In case of cyanide, hydrogen sulfide, organophosphates and corrosives poisonings a special caution is needed and pocket mask or self-inflating bag with a face mask should be rather used. A quick poison identification and a contact with regional poison information centre regarding patient management are crucial. Different procedures include prolonged cardiopulmonary resuscitation.

  17. Cyanide and the human brain: perspectives from a model of food (cassava) poisoning.

    PubMed

    Tshala-Katumbay, Desire D; Ngombe, Nadege N; Okitundu, Daniel; David, Larry; Westaway, Shawn K; Boivin, Michael J; Mumba, Ngoyi D; Banea, Jean-Pierre

    2016-08-01

    Threats by fundamentalist leaders to use chemical weapons have resulted in renewed interest in cyanide toxicity. Relevant insights may be gained from studies on cyanide mass intoxication in populations relying on cyanogenic cassava as the main source of food. In these populations, sublethal concentrations (up to 80 μmol/l) of cyanide in the blood are commonplace and lead to signs of acute toxicity. Long-term toxicity signs include a distinct and irreversible spastic paralysis, known as konzo, and cognition deficits, mainly in sequential processing (visual-spatial analysis) domains. Toxic culprits include cyanide (mitochondrial toxicant), thiocyanate (AMPA-receptor chaotropic cyanide metabolite), cyanate (protein-carbamoylating cyanide metabolite), and 2-iminothiazolidine-4-carboxylic acid (seizure inducer). Factors of susceptibility include younger age, female gender, protein-deficient diet, and, possibly, the gut functional metagenome. The existence of uniquely exposed and neurologically affected populations offers invaluable research opportunities to develop a comprehensive understanding of cyanide toxicity and test or validate point-of-care diagnostic tools and treatment options to be included in preparedness kits in response to cyanide-related threats.

  18. Catalytic Antibodies for Prophylaxis/Treatment of Cyanide Poisoning

    DTIC Science & Technology

    1993-05-28

    resulting methe- moglobin binding cyanide, and * Administration of drugs that augment endogenous enzymatic detoxification. An extension of the last method...0.025 M1 h -1 for the reaction In buffer containing a small amount of acetonitrile. Compi ter simulation studies indicated that an overall rate...fragments given intravenously to rats over a 1 h peiod *ithout apparent toxicity (Pentel et al., 1988). Several enone/TSA combinations were

  19. Cyanide poisoning of a Cooper’s hawk (Accipiter cooperii)

    USGS Publications Warehouse

    Franson, J Christian

    2017-01-01

    A Cooper’s hawk (Accipiter cooperii) was found dead in a ditch leading from a heap leach pad at a gold mine in Nevada. Observations at autopsy included an absence of external lesions, traces of subcutaneous and coronary fat, no food in the upper gastrointestinal tract, and no lesions in the viscera. Cyanide concentrations (µg/g ww) were 5.04 in blood, 3.88 in liver, and 1.79 in brain. No bacteria or viruses were isolated from tissues, and brain cholinesterase activity was within the normal range for a Cooper’s hawk.

  20. QCM Real-Time Sensor for monitoring of Poisonous Cyanide from Drinking Water and Environmental

    NASA Astrophysics Data System (ADS)

    Cimpoca, Gh. V.; Radulescu, C.; Popescu, I. V.; Dulama, I. D.; Bancuta, I.; Gheboianu, A. I.; Cimpoca, M.; Cernica, I.; Staicu, L.

    2010-01-01

    The paper present Quartz Crystal Microbalance (QCM) used for monitoring of poisonous cyanide in real-time at both drinking water standard and environmental regulatory concentrations. Through the use of a flow cell, aqueous samples containing cyanide react with a gold electrode of a piezoelectric quartz crystal and extract the gold from electrode in solution. The dissolution of metallic gold depends by cyanide concentration, pH of solution, the flow debit and the time. The sensor is an AT-cut quartz crystal with CrAu or TiAu electrode metallization, 1.27 cm2 active areas and 5 MHz resonance frequency. We use QCM with the static liquid from 0.2 to 1 ml solution and dynamic liquid with flow debit from 0.2 to 1 mL/minute. The detection limits at pH 12 are about 5 ppb for analysis times of 10 min, and 2 ppb for analysis times of 20 minutes. The calibrations show excellent linearity over a variety of cyanide concentrations ranging from 50 ppb to hundreds of ppm. The ability to provide real-time monitoring of cyanide contaminants in water samples can be used for a variety of applications: on-line monitoring of contaminants in process, recycle, and waste water; groundwater quality monitoring; detection of contaminants in streams, lakes and water supplies; monitoring dumping in off-shore waterways.

  1. Effect of sub-acute oral cyanide administration in rats: protective efficacy of alpha-ketoglutarate and sodium thiosulfate.

    PubMed

    Tulsawani, R K; Debnath, M; Pant, S C; Kumar, Om; Prakash, A O; Vijayaraghavan, R; Bhattacharya, R

    2005-09-10

    Chronic toxicity of cyanide in humans and animals has been previously described. Alpha-ketoglutarate (alpha-KG) and sodium thiosulfate (STS) are known to confer remarkable protection against acute cyanide poisoning in rodents. Their efficacy against sub-acute or chronic cyanide exposure is not known. The objective of the present study was to assess the sub-acute toxicity of potassium cyanide (KCN) in female rats following oral administration of 7.0 mg/kg (0.5 LD50) for 14 d. The effect of alpha-KG (oral; 1.0 g/kg) and/or STS (intraperitoneal, 1.0 g/kg) on cyanide toxicity was also evaluated. Various hematological and biochemical indices were determined after 7 d of treatment and additional parameters like organ-body weight index (OBI) and histology of brain, heart, lung, liver, kidney and spleen were performed after 14 and 21 d (recovery group) of cyanide exposure. Sub-acute exposure of KCN did not produce any significant change in body weight of the animals, OBI, hematology and the levels of blood urea, creatinine, aspartate aminotransferase, triiodothyronine (T3) and tetraiodothyronine (T4). The levels of temporal glutathione disulfide (GSSG) and hepatic malondialdehyde (MDA), reduced glutathione (GSH) and GSSG were unaffected. However, in KCN treated animals elevated levels of blood glucose and reduced levels of alanine aminotransferase were observed. Activities of cytochrome c oxidase in the brain and rhodanese in the liver were diminished. Reduced levels of GSH and enhanced levels of MDA in brain were observed. Increased levels of blood thiocyanate were observed in all the treatments of KCN. Additionally, KCN also produced various histological changes in the brain, heart, liver and kidney. Although, treatment of alpha-KG and STS alone significantly blunted the toxicity of KCN, concomitant use of both interventions afforded to maximum protection. This study indicates a promising role of alpha-KG and STS for the treatment of prolonged cyanide exposures.

  2. Laboratory interferences with the newer cyanide antidote: hydroxocobalamin.

    PubMed

    Beckerman, Nathan; Leikin, Scott M; Aitchinson, Robert; Yen, May; Wills, Brandon K

    2009-02-01

    Cyanide poisoning occurs in many smoke inhalation victims. The newest FDA-approved treatment for acute cyanide intoxication is hydroxocobalamin (Cyanokit). However, hydroxocobalamin exhibits chemical properties that can disrupt several clinical laboratory tests. Knowledge of these effects on laboratory tests can be useful in assisting laboratory technicians and clinicians in managing these patients. This article briefly discusses acute cyanide poisoning and treatment, and summarizes laboratory interferences that have been reported with the use of hydroxocobalamin.

  3. Acute cyanide Intoxication: A rare case of survival.

    PubMed

    Jethava, Durga; Gupta, Priyamvada; Kothari, Sandeep; Rijhwani, Puneet; Kumar, Ankit

    2014-05-01

    A 30-year-old male jewellery factory worker accidentally ingested silver potassium cyanide and was brought to the emergency department in a state of shock and profound metabolic acidosis. This patient was managed hypothetically with use of injection thiopentone sodium intravenously until the antidote was received. Cyanide is a highly cytotoxic poison and it rapidly reacts with the trivalent iron of cytochrome oxidase thus paralysing the aerobic respiration. The result is severe lactic acidosis, profound shock, and its fatal outcome. The patient dies of cardio-respiratory arrest secondary to dysfunction of the medullary centres. It is rapidly absorbed, symptoms begin few seconds after exposure and death usually occurs in <30 min. The average lethal dose for potassium cyanide is about 250 mg. We used repeated doses of thiopentone sodium till the antidote kit was finally in our hands, hypothesising that it contains thiol group similar to the antidote thiosulphate. Moreover, it is an anticonvulsant. We were successful in our attempts and the patient survived though the specific antidotes could be administered after about an hour.

  4. Acute Electrocardiographic ST Segment Elevation May Predict Hypotension in a Swine Model of Severe Cyanide Toxicity

    DTIC Science & Technology

    2012-04-21

    induced shock, 30 swine were anesthetized and monitored and then intoxicated with a continuous cyanide infusion until severe hypotension (50 % of...TOXICOLOGY INVESTIGATION Acute Electrocardiographic ST Segment ElevationMay Predict Hypotension in a Swine Model of Severe Cyanide Toxicity Tylan A...Toxicology 2012 Abstract Cyanide causes severe cardiac toxicity resulting in tachycardia, hypotension, and cardiac arrest; however, the clinical diagnosis can

  5. Zebrafish Models for Human Acute Organophosphorus Poisoning.

    PubMed

    Faria, Melissa; Garcia-Reyero, Natàlia; Padrós, Francesc; Babin, Patrick J; Sebastián, David; Cachot, Jérôme; Prats, Eva; Arick Ii, Mark; Rial, Eduardo; Knoll-Gellida, Anja; Mathieu, Guilaine; Le Bihanic, Florane; Escalon, B Lynn; Zorzano, Antonio; Soares, Amadeu M V M; Raldúa, Demetrio

    2015-10-22

    Terrorist use of organophosphorus-based nerve agents and toxic industrial chemicals against civilian populations constitutes a real threat, as demonstrated by the terrorist attacks in Japan in the 1990 s or, even more recently, in the Syrian civil war. Thus, development of more effective countermeasures against acute organophosphorus poisoning is urgently needed. Here, we have generated and validated zebrafish models for mild, moderate and severe acute organophosphorus poisoning by exposing zebrafish larvae to different concentrations of the prototypic organophosphorus compound chlorpyrifos-oxon. Our results show that zebrafish models mimic most of the pathophysiological mechanisms behind this toxidrome in humans, including acetylcholinesterase inhibition, N-methyl-D-aspartate receptor activation, and calcium dysregulation as well as inflammatory and immune responses. The suitability of the zebrafish larvae to in vivo high-throughput screenings of small molecule libraries makes these models a valuable tool for identifying new drugs for multifunctional drug therapy against acute organophosphorus poisoning.

  6. Zebrafish Models for Human Acute Organophosphorus Poisoning

    PubMed Central

    Faria, Melissa; Garcia-Reyero, Natàlia; Padrós, Francesc; Babin, Patrick J.; Sebastián, David; Cachot, Jérôme; Prats, Eva; Arick II, Mark; Rial, Eduardo; Knoll-Gellida, Anja; Mathieu, Guilaine; Le Bihanic, Florane; Escalon, B. Lynn; Zorzano, Antonio; Soares, Amadeu M.V.M; Raldúa, Demetrio

    2015-01-01

    Terrorist use of organophosphorus-based nerve agents and toxic industrial chemicals against civilian populations constitutes a real threat, as demonstrated by the terrorist attacks in Japan in the 1990 s or, even more recently, in the Syrian civil war. Thus, development of more effective countermeasures against acute organophosphorus poisoning is urgently needed. Here, we have generated and validated zebrafish models for mild, moderate and severe acute organophosphorus poisoning by exposing zebrafish larvae to different concentrations of the prototypic organophosphorus compound chlorpyrifos-oxon. Our results show that zebrafish models mimic most of the pathophysiological mechanisms behind this toxidrome in humans, including acetylcholinesterase inhibition, N-methyl-D-aspartate receptor activation, and calcium dysregulation as well as inflammatory and immune responses. The suitability of the zebrafish larvae to in vivo high-throughput screenings of small molecule libraries makes these models a valuable tool for identifying new drugs for multifunctional drug therapy against acute organophosphorus poisoning. PMID:26489395

  7. Pancreatic pseudocyst after acute organophosphate poisoning.

    PubMed

    Kawabe, Ken; Ito, Tetsuhide; Arita, Yoshiyuki; Sadamoto, Yojiro; Harada, Naohiko; Yamaguchi, Koji; Tanaka, Masao; Nakano, Itsuro; Nawata, Hajime; Takayanagi, Ryoichi

    2006-04-01

    Acute organophosphate poisoning (OP) shows several severe clinical symptoms due to its strong blocking effect on cholinesterase. Acute pancreatitis is one of the complications associated with acute OP, but this association still may not be widely recognized. We report here the case of a 73-year-old man who had repeated abdominal pain during and after the treatment of acute OP. Hyperamylasemia and a 7-cm pseudocyst in the pancreatic tail were noted on investigations. We diagnosed pancreatic pseudocyst that likely was secondary to an episode of acute pancreatitis following acute OP. He was initially treated with a long-term intravenous hyperalimentation, protease inhibitors and octerotide, but eventually required surgical intervention, a cystgastrostomy. Acute pancreatitis and hyperamylasemia are known to be possible complications of acute OP. It is necessary to examine and assess pancreatic damage in patients with acute OP.

  8. Rapid multicomponent analysis of hemoglobin derivatives for controlled antidotal use of methemoglobin-forming agents in cyanide poisoning.

    PubMed

    Zijlstra, W G; Buursma, A

    1993-08-01

    When cyanide poisoning is treated with a methemoglobin-forming agent, oxidative metabolism is protected at the expense of the oxygen capacity of the blood. The affinity of methemoglobin for CN- is high enough to compete with cytochrome oxidase, which protects the latter from becoming blocked, but all hemoglobin used for this purpose is lost for the transport of oxygen. Therefore, the fractions of the various hemoglobin derivatives present in the blood should be carefully monitored during this kind of treatment. After we had developed a multiwavelength spectrophotometric method for this purpose, we studied the feasibility of using a modified commercial six-wavelength hemoglobin photometer (Radiometer OSM3) for easy and rapid analysis of methemoglobin and methemoglobin cyanide in small samples of blood. All conditions appeared to be fulfilled for the construction of a practical multiwavelength photometer for reliably monitoring methemoglobin therapy in patients with cyanide poisoning, even in the presence of carboxyhemoglobin, as often occurs in fire victims.

  9. Acute Poisoning in Children in Bahia, Brazil

    PubMed Central

    Rodrigues Mendonça, Dilton; Menezes, Marta Silva; Matos, Marcos Antônio Almeida; Rebouças, Daniel Santos; Filho, Jucelino Nery da Conceição; de Assis, Reginara Souza; Carneiro, Leila

    2016-01-01

    Acute poisoning is a frequent accident in childhood, particularly in children under 4 years of age. This was a descriptive study with data collected from standardized forms of the Poison Control Center and patient record charts. All the cases of acute poisoning in children aged 0 to 14 years during the period 2008 to 2012 were selected. The variables studied comprised characteristics of the events and toxic agents, clinical development, and outcome. A total of 657 cases of acute poisoning, with higher frequency in the age-group from 1 to 4 years (48.7%) and male sex (53.4%), were recorded. The occurrences were accidental in 92% of the cases, and 5.8% were due to suicide attempts. Among the toxic agents, medications (28.5%), venomous animals (19.3%), nonvenomous animals (10%), household cleaning products (9.0%), and raticide agents (8.7%) predominated. The majority of cases were characterized as light (73.5%) and around 18% required hospitalization, and there was low lethality (0.5%). PMID:27335994

  10. Acute cyanide intoxication treated with a combination of hydroxycobalamin, sodium nitrite, and sodium thiosulfate.

    PubMed

    Mannaioni, Guido; Vannacci, Alfredo; Marzocca, Cosimo; Zorn, Anna Monica; Peruzzi, Sandro; Moroni, Flavio

    2002-01-01

    An 80-year-old diabetic patient was admitted to the hospital because of sudden unconsciousness and severe metabolic acidosis. His son reported the possibility of cyanide poisoning. Clinical data and the detection of cyanide in blood and gastric material confirmed this possibility. Supportive therapy and the following antidotes--sodium nitrite two doses 300 mg i.v., sodium thiosulfate 3 g i.v., and hydroxocobalamin 4 g in 24 hours--were administered immediately and the patient completely recovered in 48 hours. Our observations suggest that timely and appropriate use of antidotes for cyanide intoxication may prevent death, even in aged diabetic patients.

  11. Acute poisoning: understanding 90% of cases in a nutshell

    PubMed Central

    Greene, S; Dargan, P; Jones, A

    2005-01-01

    The acutely poisoned patient remains a common problem facing doctors working in acute medicine in the United Kingdom and worldwide. This review examines the initial management of the acutely poisoned patient. Aspects of general management are reviewed including immediate interventions, investigations, gastrointestinal decontamination techniques, use of antidotes, methods to increase poison elimination, and psychological assessment. More common and serious poisonings caused by paracetamol, salicylates, opioids, tricyclic antidepressants, selective serotonin reuptake inhibitors, benzodiazepines, non-steroidal anti-inflammatory drugs, and cocaine are discussed in detail. Specific aspects of common paediatric poisonings are reviewed. PMID:15811881

  12. Central respiratory failure during acute organophosphate poisoning.

    PubMed

    Carey, Jennifer L; Dunn, Courtney; Gaspari, Romolo J

    2013-11-01

    Organophosphate (OP) pesticide poisoning is a global health problem with over 250,000 deaths per year. OPs affect neuronal signaling through acetylcholine (Ach) neurotransmission via inhibition of acetylcholinesterase (AChE), leading to accumulation of Ach at the synaptic cleft and excessive stimulation at post-synaptic receptors. Mortality due to OP agents is attributed to respiratory dysfunction, including central apnea. Cholinergic circuits are integral to many aspects of the central control of respiration, however it is unclear which mechanisms predominate during acute OP intoxication. A more complete understanding of the cholinergic aspects of both respiratory control as well as neural modification of pulmonary function is needed to better understand OP-induced respiratory dysfunction. In this article, we review the physiologic mechanisms of acute OP exposure in the context of the known cholinergic contributions to the central control of respiration. We also discuss the potential central cholinergic contributions to the known peripheral physiologic effects of OP intoxication.

  13. ECG manifestations in acute organophosphorus poisoning.

    PubMed

    Paul, Uttam Kumar; Bhattacharyya, Anup Kumar

    2012-02-01

    A cross-sectional study was conducted to evaluate the electrocardiographic changes in 107 patients of acute organophosphorus poisoning admitted at casuality ward of MGM Medical College, Kisanganj from June 2007 to June 2010. Electrocardiographic changes were recorded before the administration of atropine. Prolonged Q-Tc interval was the commonest ECG abnormality, found in 67 patients (62.6%), followed by sinus tachycardia in 36 patients (33.6%). Sinus bradycardia was found in 33 patients (30.8%). Elevation of ST segment was seen in 27 patients (25.2%). T wave inversion was seen in 21 patients (19.6%). First-degree heart block (P-R interval >0.20 seconds) occurred in 9 cases (8.4%). Atrial fibrillation was seen in 5 patients (4.6%). Ventricular tachycardia was seen in 6 cases (5.6%) and ventricular premature complexes in 3 patients (2.8%). Of these 6 cases of ventricular tachycardia 1 responded to intravenous lignocaine, and the other 5 developed ventricular fibrillation leading to death despite other resuscitative measures. All the electrocardiographical abnormalities returned to normal before the patients were discharged. Seventeen patients died. The cause of death was ventricular fibrillation in 5 patients and non-cardiogenic pulmonary oedema in others. In conclusion it can be said that ECG should be carefully recorded and analysed in all patients of acute organophosphorus poisoning, and depending upon these changes and other clinical and biochemical parameters, the patients should immediately be shifted to well equipped ICU for better care which will reduce the mortality rate caused by these highly lethal poisons.

  14. Glyphosate Poisoning with Acute Pulmonary Edema

    PubMed Central

    Thakur, Darshana Sudip; Khot, Rajashree; Joshi, P. P.; Pandharipande, Madhuri; Nagpure, Keshav

    2014-01-01

    GlySH-surfactant herbicide (GlySH), one of the most commonly used herbicides worldwide, has been considered as minimally toxic to humans. However, clinical toxicologists occasionally encounter cases of severe systemic toxicity. The US Environmental Protection Agency (EPA) states that ‘GlySH’ is of relatively low oral and acute dermal toxicity. It does not have anticholinesterase effect and no organophosphate-like central nervous system (CNS) effects. The clinical features range from skin and throat irritation to hypotension and death. Severe GlySH-surfactant poisoning is manifested by gastroenteritis, respiratory disturbances, altered mental status, hypotension refractory to the treatment, renal failure, and shock.[1] GlySH intoxication has a case fatality rate 3.2–29.3%. Pulmonary toxicity and renal toxicity seem to be responsible for mortality. Metabolic acidosis, abnormal chest X-ray, arrhythmias, and elevated serum creatinine levels are useful prognostic factors for predicting GlySH mortality.[2] There is no antidote and the mainstay of treatment for systemic toxicity is decontamination and aggressive supportive therapy. We report a case of acute pulmonary edema, which is a rare but severe manifestation of oral GlySH poisoning, where patient survived with aggressive supportive therapy. PMID:25948977

  15. Acute Pancreatitis Caused By Mushroom Poisoning

    PubMed Central

    Karahan, Samet; Erden, Abdulsamet; Cetinkaya, Ali; Avci, Deniz; Ortakoyluoglu, Adile Irfan; Karagoz, Hatice; Bulut, Kadir; Basak, Mustafa

    2016-01-01

    Of the more than 5000 species of mushrooms known, 100 types are toxic and approximately 10% of these toxic types can cause fatal toxicity. A type of mushroom called Amanita phalloides is responsible for 95% of toxic mushroom poisonings. In this article, we report 2 cases of mushroom poisonings caused by Lactarius volemus, known as Tirmit by the local people. The patient and his wife were admitted to the emergency room with abdominal pain, nausea, and vomiting 20 hours after consuming Lactarius volemus, an edible type of mushroom. The patients reported that they had been collecting this mushroom from the mountains and eating them for several years but had never developed any clinicopathology to date. Further examination of the patients revealed a very rare case of acute pancreatitis due to mushroom intoxication. The male patient was admitted to the intensive care unit while his wife was followed in the internal medicine service, because of her relative mild clinical symptoms. Both patients recovered without sequelae and were discharged. In this article, we aimed to emphasize that gastrointestinal symptoms are often observed in mushroom intoxications and can be confused with acute pancreatitis, thus leading to misdiagnosis of patients. Early diagnosis and appropriate treatment can improve patients’ prognosis and prevent the development of complications. PMID:26835473

  16. Analysis of hemoglobin derivatives by capillary isoelectric focusing and its application in the antidotal research of cyanide poisoning

    SciTech Connect

    Shih, M.L.; Korte, W.D.

    1996-07-01

    Cyanide toxicity can be reduced by the use of methemoglobin (MetHb) formers, and antidotal dosage is based on the extent of MetHb formation. Hemoglobin and ferrihemoglobin (MetHb, hemimethemoglobins {alpha}{sup 3+}{beta}{sup 2+} and {alpha}{sup 2-}{beta}{sup 3-}, tetracyanmethemoglobin, and dicyanmethemoglobin) concentrations in human, pig, and mouse blood were determined after separation by isoelectric focusing with an octyl-bonded capillary. The predominant species formed in blood when MetHb formers, such as potassium ferricyanide, hydroxylamine, sodium nitrite, and 4-dimethylaminophenol (DMAP), added at molar ratios ranging from 1:10 to 1:1 to hemoglobin, are the valency hybrid intermediates {alpha}{sup 3+}{beta}{sup 2+} and {alpha}{sup 2+}{beta}{sup 3+}. In the detoxication of cyanide with methemoglobin, an intermediate dicyanhemimethemoglobin was demonstrated to be the predominant species in the formation of tetracyanmethemoglobin. Complex mixtures of hemoglobin derivatives were observed with DMAP at 1:1 or greater molar ratio to hemoglobin. Comparison of the MetHb values obtained with a hemoxometer indicated that the valency hybrids were measured as MetHb and the values of oxidized hemoglobin were overestimated. In cyanide poisoning, incorrect dosages of MetHb formers could be calculated, and misinterpretation of MetHb data would results from methods that fail to discriminate among the various species of MetHb. 24 refs., 4 figs., 2 tabs.

  17. Serum Metabolomics in Rats after Acute Paraquat Poisoning.

    PubMed

    Wang, Zhiyi; Ma, Jianshe; Zhang, Meiling; Wen, Congcong; Huang, Xueli; Sun, Fa; Wang, Shuanghu; Hu, Lufeng; Lin, Guanyang; Wang, Xianqin

    2015-01-01

    Paraquat is one of the most widely used herbicides in the world and is highly toxic to humans and animals. In this study, we developed a serum metabolomic method based on GC/MS to evaluate the effects of acute paraquat poisoning on rats. Pattern recognition analysis, including both principal component analysis and partial least squares-discriminate analysis revealed that acute paraquat poisoning induced metabolic perturbations. Compared with the control group, the level of octadecanoic acid, L-serine, L-threonine, L-valine, and glycerol in the acute paraquat poisoning group (36 mg/kg) increased, while the levels of hexadecanoic acid, D-galactose, and decanoic acid decreased. These findings provide an overview of systematic responses to paraquat exposure and metabolomic insight into the toxicological mechanism of paraquat. Our results indicate that metabolomic methods based on GC/MS may be useful to elucidate the mechanism of acute paraquat poisoning through the exploration of biomarkers.

  18. Poisoning

    MedlinePlus

    ... as poison ivy and poison oakvenom from certain snakes and insects. How is poisoning diagnosed? The doctor ... poison, poison control, poison symptoms, poison treatments, poisoning, snake bite, syrup of ipecac First Aid and Injury ...

  19. Toxicokinetic profiles of α-ketoglutarate cyanohydrin, a cyanide detoxification product, following exposure to potassium cyanide.

    PubMed

    Mitchell, Brendan L; Bhandari, Raj K; Bebarta, Vikhyat S; Rockwood, Gary A; Boss, Gerry R; Logue, Brian A

    2013-09-12

    Poisoning by cyanide can be verified by analysis of the cyanide detoxification product, α-ketoglutarate cyanohydrin (α-KgCN), which is produced from the reaction of cyanide and endogenous α-ketoglutarate. Although α-KgCN can potentially be used to verify cyanide exposure, limited toxicokinetic data in cyanide-poisoned animals are available. We, therefore, studied the toxicokinetics of α-KgCN and compared its behavior to other cyanide metabolites, thiocyanate and 2-amino-2-thiazoline-4-carboxylic acid (ATCA), in the plasma of 31 Yorkshire pigs that received KCN (4mg/mL) intravenously (IV) (0.17 mg/kg/min). α-KgCN concentrations rose rapidly during KCN administration until the onset of apnea, and then decreased over time in all groups with a half-life of 15 min. The maximum concentrations of α-KgCN and cyanide were 2.35 and 30.18 μM, respectively, suggesting that only a small fraction of the administered cyanide is converted to α-KgCN. Although this is the case, the α-KgCN concentration increased >100-fold over endogenous concentrations compared to only a three-fold increase for cyanide and ATCA. The plasma profile of α-KgCN was similar to that of cyanide, ATCA, and thiocyanate. The results of this study suggest that the use of α-KgCN as a biomarker for cyanide exposure is best suited immediately following exposure for instances of acute, high-dose cyanide poisoning.

  20. Antidotal action of sodium nitrite and sodium thiosulfate against cyanide poisoning. (Reannouncement with new availability information)

    SciTech Connect

    Baskin, S.I.; Horowitz, A.M.; Nealley, E.W.

    1992-04-01

    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....Cyanide, Blood agent, Chemical warfare agents, Antidotes, Sodium nitrite, Sodium thiosulfate.

  1. Acute abdominal pain and constipation due to lead poisoning.

    PubMed

    Mongolu, S; Sharp, P

    2013-01-01

    Although uncommon, lead poisoning should be considered as a differential diagnosis in cases of unexplained acute abdominal pain in both adults and children. We present the case of a 35-year-old Asian male who presented with abdominal pain and constipation secondary to lead poisoning. Initially, the source of lead exposure was not apparent; this was later found to be due to ingestion of an Ayurvedic herbal medicine for the treatment of infertility. Lead poisoning due to the ingestion of Ayurvedic remedies is well described. We discuss the diagnosis, pathophysiology and treatment of lead poisoning. This case illustrates one of the rarer medical causes of acute abdominal pain and emphasizes the need to take a thorough history (including specific questioning regarding the use of over-the-counter and traditional/ herbal remedies) in cases of suspected poisoning or drug toxicity.

  2. Acute diquat poisoning with intracerebral bleeding

    PubMed Central

    Saeed, S; Wilks, M; Coupe, M

    2001-01-01

    A case of severe diquat poisoning complicated by the development of aggressive behaviour, oliguric renal failure, and intracerebral bleeding is described. The patient was successfully managed and made a complete recovery. In this paper special attention has been given to the major clinical differences between diquat and paraquat intoxication.


Keywords: poisoning; diquat; paraquat PMID:11320278

  3. Sodium Thiosulfate Versus Hydroxocobalamin in the Treatment of Acute, Severe Cyanide Induced Cardiotoxicity in a Swine (Sus Scrofa) Model

    DTIC Science & Technology

    2011-09-22

    intoxicated by cyanide develop cardiac-ar.rest or severely low blood pressure. Currently several antidotes exist, but many have severe adverse effects...machine. They were intoxicated with cyanide (infused through the vein) until the blood pressure was low. The animals were assigned to-one of three...IUIVIJ:lt:M Sodium thiosulfate versus hydroxocoba~amin in the treatment of acute, severe cyanide induced cardiotoxicity in a swine (Sus Scrofa)model on

  4. Acute nicotine poisoning associated with a traditional remedy for eczema

    PubMed Central

    Davies, P; Levy, S; Pahari, A; Martinez, D

    2001-01-01

    We present a case of severe acute nicotine poisoning in an 8 year old boy with moderate eczema after topical application of a traditional remedy from a book published in Bangladesh. Symptoms consistent with nicotine poisoning developed within 30 minutes of application of the remedy. The child subsequently improved with supportive care and was discharged after five days with no neurological sequelae. Diagnosis of nicotine poisoning was not initially made due to difficulty in obtaining an accurate history via an interpreter from the parents who did not speak English. Samples taken 12 hours after application of the remedy showed a serum nicotine of 89 µg/l, serum cotinine of 1430 µg/l, urine nicotine of 1120 µg/l, and a urine cotinine of 6960 µg/l confirming acute nicotine poisoning.

 PMID:11719343

  5. Recognition and management of acute pesticide poisoning.

    PubMed

    Simpson, William M; Schuman, Stanley H

    2002-04-15

    Most poisonings from pesticides do not have a specific antidote, making decontamination the most important intervention. For maximal benefit to the patient, skin, eye, and gastric decontamination should be undertaken while specifics of the poisoning are being determined. As in most illnesses and injuries, the history of the poisoning is of great importance and will determine specific needs for decontamination and therapy, if any exist. Protection of health care workers during the decontamination process is important and frequently overlooked. Skin decontamination is primarily accomplished with large volumes of water, soap, and shampoo. Gastric decontamination by lavage is indicated if ingestion of the poisoning has occurred within 60 minutes of patient presentation. Activated charcoal, combined with a cathartic, is also indicated in most poisonings presenting within 60 minutes of ingestion. With large volume ingestion poisonings, activated charcoal may be used after 60 minutes, but little data exist to support this practice. Syrup of ipecac is no longer recommended for routine use. The cholinergic syndrome "all faucets on" characterizes poisoning by organophosphates and carbamates. Organochlorine insecticides (lindane and other treatments for scabies and lice) can produce seizures with excessive use or use on large areas of nonintact skin. Non-dipyridyl herbicides, biocides (including pyrethrins, pyrethroids, and Bacillus thuringiensis) rarely produce anything other than mild skin, eye, and/or gastrointestinal irritation on topical exposure or ingestion.

  6. Comparison of the treatment of cyanide poisoning in the cynomolgus monkey with sodium nitrite of 4-dimethylaminophenol (4-dmap), with and without sodium thiosulfate. Technical report, April 1979-September 1981

    SciTech Connect

    Stemler, F.W.; Groff, W.A.; Kaminskis, A.; Johnson, R.P.; Froehlich, H.L.

    1994-02-01

    Two methemoglobin generating compounds, sodium nitrite (iv) or 4-dimethylaminophenol (4-DMAP) (im), with and without sodium thiosulfate (iv), were compared as post-treatment therapy in anesthetized monkeys poisoning with cyanide. Arterial blood samples were taken before and after an injection of sodium cyanide (8.4 mg/kg) and treatment for analyses of blood cyanide, plasma cyanide, thiocyanate and methemoglobin content. Physiologic parameters were monitored in these treated cyanide-poisoned animals. The time course of methemoglobin formation and physiologic parameters were also monitored in animals receiving only 4-DMAP or sodium nitrite. A maximal methemoglobin level was observed at 30 minutes following injection of 4-DMAP, and 60 minutes post injection with sodium nitrite. Volumes of distribution (Vd) of cyanide were calculated from the concentrations of cyanide in blood samples and doses of cyanide injected. Although 4-DMAP forms methemoglobin more rapidly than sodium nitrite, both compounds form methemoglobin quickly enough to provide protection against cyanide poisoning. The protection offered by either compound against the lethal effects of cyanide was potentiated when used in combination with sodium thiosulfate.

  7. Memory deficits associated with sublethal cyanide poisoning relative to cyanate toxicity in rodents.

    PubMed

    Kimani, S; Sinei, K; Bukachi, F; Tshala-Katumbay, D; Maitai, C

    2014-03-01

    Food (cassava) linamarin is metabolized into neurotoxicants cyanide and cyanate, metabolites of which we sought to elucidate the differential toxicity effects on memory. Young 6-8 weeks old male rats were treated intraperitoneally with either 2.5 mg/kg body weight (bw) cyanide (NaCN), or 50 mg/kg bw cyanate (NaOCN), or 1 μl/g bw saline, daily for 6 weeks. Short-term and long-term memories were assessed using a radial arm maze (RAM) testing paradigm. Toxic exposures had an influence on short-term working memory with fewer correct arm entries (F(2, 19) = 4.57 p < 0.05), higher working memory errors (WME) (F(2, 19) = 5.09, p < 0.05) and longer RAM navigation time (F(2, 19) = 3.91, p < 0.05) for NaOCN relative to NaCN and saline treatments. The long-term working memory was significantly impaired by cyanide with fewer correct arm entries (F(2, 19) = 7.45, p < 0.01) and increased working memory errors (F(2, 19) = 9.35 p < 0.05) in NaCN relative to NaOCN or vehicle treated animals. Reference memory was not affected by either cyanide or cyanate. Our study findings provide an experimental evidence for the biological plausibility that cassava cyanogens may induce cognition deficits. Differential patterns of memory deficits may reflect the differences in toxicity mechanisms of NaOCN relative to NaCN. Cognition deficits associated with cassava cyanogenesis may reflect a dual toxicity effect of cyanide and cyanate.

  8. A gene horizontally transferred from bacteria protects arthropods from host plant cyanide poisoning

    PubMed Central

    Wybouw, Nicky; Dermauw, Wannes; Tirry, Luc; Stevens, Christian; Grbić, Miodrag; Feyereisen, René; Van Leeuwen, Thomas

    2014-01-01

    Cyanogenic glucosides are among the most widespread defense chemicals of plants. Upon plant tissue disruption, these glucosides are hydrolyzed to a reactive hydroxynitrile that releases toxic hydrogen cyanide (HCN). Yet many mite and lepidopteran species can thrive on plants defended by cyanogenic glucosides. The nature of the enzyme known to detoxify HCN to β-cyanoalanine in arthropods has remained enigmatic. Here we identify this enzyme by transcriptome analysis and functional expression. Phylogenetic analysis showed that the gene is a member of the cysteine synthase family horizontally transferred from bacteria to phytophagous mites and Lepidoptera. The recombinant mite enzyme had both β-cyanoalanine synthase and cysteine synthase activity but enzyme kinetics showed that cyanide detoxification activity was strongly favored. Our results therefore suggest that an ancient horizontal transfer of a gene originally involved in sulfur amino acid biosynthesis in bacteria was co-opted by herbivorous arthropods to detoxify plant produced cyanide. DOI: http://dx.doi.org/10.7554/eLife.02365.001 PMID:24843024

  9. Mass cyanide intoxication in sheep.

    PubMed

    Aslani, M R; Mohri, M; Maleki, M; Sharifi, K; Mohammadi, G R; Chamsaz, M

    2004-08-01

    An outbreak of cyanide poisoning that killed 56 ewes and 2 goats is reported. Fluid released into a ditch contained 1 g cyanide/L and produced toxicity in 3 ewes experimentally dosed with the liquid waste.

  10. Gastrointestinal decontamination in the acutely poisoned patient

    PubMed Central

    2011-01-01

    Objective To define the role of gastrointestinal (GI) decontamination of the poisoned patient. Data Sources A computer-based PubMed/MEDLINE search of the literature on GI decontamination in the poisoned patient with cross referencing of sources. Study Selection and Data Extraction Clinical, animal and in vitro studies were reviewed for clinical relevance to GI decontamination of the poisoned patient. Data Synthesis The literature suggests that previously, widely used, aggressive approaches including the use of ipecac syrup, gastric lavage, and cathartics are now rarely recommended. Whole bowel irrigation is still often recommended for slow-release drugs, metals, and patients who "pack" or "stuff" foreign bodies filled with drugs of abuse, but with little quality data to support it. Activated charcoal (AC), single or multiple doses, was also a previous mainstay of GI decontamination, but the utility of AC is now recognized to be limited and more time dependent than previously practiced. These recommendations have resulted in several treatment guidelines that are mostly based on retrospective analysis, animal studies or small case series, and rarely based on randomized clinical trials. Conclusions The current literature supports limited use of GI decontamination of the poisoned patient. PMID:21992527

  11. Intravenous Cobinamide, a Novel Cyanide Antidote, versus Hydroxocobalamin in the Treatment of Acute Cyanide Toxicity and Apnea in a Swine (Sus scrofa) Model

    DTIC Science & Technology

    2013-02-12

    cobinamide, a novel cyanide antidote , versus hydroxocobalamin in the treatment of acute cyanide toxicity and apnea in a swine (Sus Scrofa) model...60min. Results:Weight, time to apnea, & CN dose similar (p>0.10). At treatment, blood CN, lactate levels, & decrease in MAP similar (p>0.10). 2/11 swine...in NS group survived(pɘ.001), compared to 10/11 in HOC & 10/11 in COB group. Time to breaths post treatment similar(HOC 1:48min, COB 1:49min). Blood

  12. Development of a complicated pain syndrome following cyanide poisoning in a U.S. soldier.

    PubMed

    Lenart, Mark; Buckenmaier, Chester C; Kim, Moon J; Plunkett, Anthony R

    2010-04-01

    A majority of modern war wounds are caused by blasts and high-energy ballistics. Extremity injuries predominate since modern body armor does not protect these areas due to mobility limitations. A less known and more insidious mechanism of enemy attack among our soldiers involves treachery by the local populace posing as noncombatants. One such recent event involved the contamination of tobacco with cyanide (CN). We describe a case of a soldier with CN intoxication due to ingestion of tobacco purchased from a local merchant. The soldier developed a complex neuropathic pain syndrome and was successfully treated with an inpatient high-dose intravenous ketamine infusion in combination with continuous peripheral nerve blockade.

  13. Respiratory Complications from Acute Corrosive Poisonings in Adults

    PubMed Central

    Chibishev, Andon A.; Simonovska, Natasa; Bozinovska, Cvetanka; Pereska, Zanina; Smokovski, Ivica; Glasnovic, Marija

    2014-01-01

    Introduction: Acute corrosive poisonings are caused by ingestion of corrosive chemicals which are most commonly used as household agents. Intoxications with these kind of agents produce numerous and severe post-corrosive complications of the upper gastrointestinal tract. On the other hand, our experience showed that corrosive agents may also cause injuries of the respiratory system, which makes the treatment very hard and additionally complicates the severe clinical condition of the patient. Objective: The aim of the study is to show the incidence of respiratory complications in acute corrosive poisonings, the need of various clinical investigations and also the treatment and final outcome of these kind of poisoning. Methods: We retrospectively analyzed clinical records of 415 patients hospitalized and treated at the University clinic for toxicology and urgent internal medicine, in Skopje, Republic of Macedonia, in the period between 2007 and 2011. The protocol consisted of methods for analyzing the systemic complications, with an accent on the post-corrosive respiratory complications. Results: From the total number of patients even 98 (23.61%) exhibited systemic complications, from which 51 (52.04%) are respiratory complications. The majority of patients are female (n=40, 78.43%) and the most common complication is pneumonia (n=47). The youngest patient in this study was 14 and the oldest was 87 years old. Conclusion: Besides the gastrointestinal complications in the acute corrosive poisonings respiratory complications are also very often. They complicate the clinical state of patient and very often lead to fatal endings. PMID:24944527

  14. Development of sulfanegen for mass cyanide casualties.

    PubMed

    Patterson, Steven E; Moeller, Bryant; Nagasawa, Herbert T; Vince, Robert; Crankshaw, Daune L; Briggs, Jacquie; Stutelberg, Michael W; Vinnakota, Chakravarthy V; Logue, Brian A

    2016-06-01

    Cyanide is a metabolic poison that inhibits the utilization of oxygen to form ATP. The consequences of acute cyanide exposure are severe; exposure results in loss of consciousness, cardiac and respiratory failure, hypoxic brain injury, and dose-dependent death within minutes to hours. In a mass-casualty scenario, such as an industrial accident or terrorist attack, currently available cyanide antidotes would leave many victims untreated in the short time available for successful administration of a medical countermeasure. This restricted therapeutic window reflects the rate-limiting step of intravenous administration, which requires both time and trained medical personnel. Therefore, there is a need for rapidly acting antidotes that can be quickly administered to large numbers of people. To meet this need, our laboratory is developing sulfanegen, a potential antidote for cyanide poisoning with a novel mechanism based on 3-mercaptopyruvate sulfurtransferase (3-MST) for the detoxification of cyanide. Additionally, sulfanegen can be rapidly administered by intramuscular injection and has shown efficacy in many species of animal models. This article summarizes the journey from concept to clinical leads for this promising cyanide antidote.

  15. Transient and reversible parkinsonism after acute organophosphate poisoning.

    PubMed

    Arima, Hajime; Sobue, Kazuya; So, MinHye; Morishima, Tetsuro; Ando, Hirkoshi; Katsuya, Hirotada

    2003-01-01

    Parkinsonism is a rare complication in patients with organophosphate poisoning. To date there have been two cases of transient parkinsonism after acute and severe cholinergic crisis, both of which were successfully treated using amantadine, an anti-parkinsonism drug. We report on an 81-year-old woman who was admitted for the treatment of acute severe organophosphate poisoning. Although acute cholinergic crisis was treated successfully with large doses of atropine and 2-pyridine aldoxime methiodide (PAM), extrapyramidal manifestations were noticed on hospital day 6. The neurological symptoms worsened, and the diagnosis of parkinsonism was made by a neurologist on hospital day 9. Immediately, biperiden (5mg), an anti-parkinsonism drug, was administered intravenously, and her symptoms markedly improved. From the following day, biperiden (5 mg/day) was given intramuscularly for eight days. Subsequently, neurological symptoms did not relapse, and no drugs were required. Our patient is the third case of parkinsonism developing after an acute severe cholinergic crisis and the first case successfully treated with biperiden. Patients should be carefully observed for the presence of neurological signs in this kind of poisoning. If present, an anti-parkinsonism drug should be considered.

  16. Acute Poisoning During Pregnancy: Observations from the Toxicology Investigators Consortium.

    PubMed

    Zelner, Irene; Matlow, Jeremy; Hutson, Janine R; Wax, Paul; Koren, Gideon; Brent, Jeffrey; Finkelstein, Yaron

    2015-09-01

    Acute poisonings during pregnancy pose a particular challenge to health care providers because of the potential for an immediate life threat or possible life-long implications for both the mother and fetus, including teratogenicity of the poison or its antidote. We describe recent consequential exposures among pregnant women in the USA. We identified all poisoning cases involving pregnant women that were catalogued by the medical toxicology services across the 37 sites of the Toxicology Investigators Consortium (ToxIC) Registry of the American College of Medical Toxicology between January 2010 and December 2012. Of 17,529 exposure cases reported in the ToxIC Registry, 103 (0.6 %) involved pregnant women, 80 % of whom were symptomatic and about a quarter displayed a specific toxidrome. The majority of cases (n = 53; 51.5 %) involved intentional exposures, most commonly to pharmaceutical agents, followed by unintentional pharmaceutical exposures (10 %) and withdrawal syndromes (9 %). Non-opioid analgesics were the most common class of agents encountered (31 %), followed by sedative-hypnotics/muscle relaxants (18 %), opioids (17 %), anti-convulsants (10 %), and anti-depressants (10 %). Over a third of cases involved exposure to multiple substances, and 32 % involved exposure to more than one drug class. The most commonly administered antidotes were N-acetylcysteine (23 %), sodium bicarbonate (10 %), flumazenil (4 %), and physostigmine (4 %). About half of acute poisoning cases among pregnant women presenting for emergency care involved intentional exposures, mostly with over-the-counter analgesics and psychoactive medications. Clinicians should be cognizant of the unique circumstances, maternal and fetal risks, and management principles of the acutely poisoned pregnant woman.

  17. Poisoning severity score, Glasgow coma scale, corrected QT interval in acute organophosphate poisoning.

    PubMed

    Akdur, Okhan; Durukan, Polat; Ozkan, Seda; Avsarogullari, Levent; Vardar, Alper; Kavalci, Cemil; Ikizceli, Ibrahim

    2010-05-01

    The aim of this study was to investigate effectiveness of the poisoning severity score (PSS), Glasgow coma scale (GCS), and corrected QT (QTc) interval in predicting outcomes in acute organophosphates (OP) poisoning. Over a period of 2 years, 62 patients with OP poisoning were admitted to emergency department (ED) of Erciyes University Medical School Hospital. The age, sex, cause of contact, compound involved, time elapsed between exposure and admission to the ED, duration of hospital stay, and cardiac manifestations at the time of presentation were recorded. GCS and poisoning severity score (PSS) was calculated for each patient. Electrocardiogram (ECG) analysis included the rate, rhythm, ST-T abnormalities, conduction defects, and measurement of PR and QT intervals. Sixty-two patients with OP poisoning presented to our ED from January 2007 to December 2008 from which 54 patients were included in the study. The mean age was 34.1 +/- 14.8 years. Of the cases, 53.7% were female. Twenty-six patients had a prolonged QTc interval. Mean PSS of men and women was 1.8 +/- 1.0. No statistically significant correlation was found between the PSS and QTc intervals of the cases. A significant correlation was determined between the GCS and PSS of grade 3 and grade 4 cases. GCS is a parameter that helps clinician to identify advanced grade OP poisoning patients in the initial assessment in the ED. However, ECG findings, such as prolonged QTc interval, are not effective in determination of short-term prognosis and show no relationship with PSS.

  18. An unusual presentation of mad honey poisoning: acute myocardial infarction.

    PubMed

    Akinci, Sinan; Arslan, Uğur; Karakurt, Kamber; Cengel, Atiye

    2008-09-26

    An unusual type of food poisoning is commonly seen in the Black Sea coast of Turkey due to grayanotoxin containing toxic honey so called "mad honey" ingestion. In cases of toxication bradycardia and rhythm disturbances are commonly observed. Herein, we present a case of a patient who was admitted to the hospital because of acute myocardial infarction with normal coronary arteries after "mad honey" ingestion.

  19. [An atypical case of acute zinc poisoning].

    PubMed

    Andrzejak, R; Antonowicz, J; Andreasik, Z

    1992-01-01

    The paper discussed a case of acute zinc intoxication in a 48-year old welder, after four days of cutting zinc-plated pipes with an oxy-acetylene torch, in poorly ventilated places. The zinc fever has been diagnosed on the basis of the symptoms and confirmed by laboratory findings: high zinc blood and erythrocyte concentration and increased urinary excretion of zinc. One year the intoxication the manifestations of the psycho-organic syndrome with predilection to pseudoneurotic reactions were still present. The non-standard factor in this case is the very short time of exposure to zinc oxide and the occurrence of chronic encephalopathy is also singular.

  20. Electrocardiographic findings and cardiac manifestations in acute aluminum phosphide poisoning.

    PubMed

    Soltaninejad, Kambiz; Beyranvand, Mohammad-Reza; Momenzadeh, Seyed-Akbar; Shadnia, Shahin

    2012-07-01

    Aluminium phosphide (AlP) poisoning has a high mortality due to cardiovascular involvement. In this study, we evaluated the frequency of cardiac manifestations and electrocardiographic (ECG) findings in 20 patients with acute AlP poisoning, who were admitted to the intensive care unit (ICU) in Tehran, Iran, over a period of 6 months (between October 2008 and April 2009). The sex, age, cause and manner of ingestion, number of ingested AlP tablets, cardiac and ECG manifestations, creatine phosphokinase (CPK), CPK-myocardial band (CPK-mb) and troponin-T (TnT) were extracted from the patients' files. All data were analysed with Statistical Package for the Social Sciences (SPSS) software. The majority (60%) of patients were male. The mean age was 27 ± 8.7 years. The mortality rate was 40%. In all of the patients, the cause of poisoning was intentional suicide and ingestion was the route of exposure. The mean number of ingested AlP tablets per patient was 2.2 ± 1.1. The average time interval between admission and cardiovascular manifestations or ECG findings was 168.8 ± 116.2 min. The range of systolic (SBP) and diastolic blood pressure was 60-130 mmHg and 40-70 mmHg, respectively. Dysrhythmia was observed in nine (45%) cases. Elevation of the ST segment was seen in nine cases (45%). Seven patients (35%) had prolonged QTc intervals. Bundle branch block (BBB) was observed in four (20%) patients. In nine (45%) patients, the serum cardiac TnT qualitative assay was positive. There were no significant differences between normal and abnormal ECG groups according to sex, age, number and manner of ingested AlP tablets and SBP. There was a significant correlation between cardiac manifestations and ECG findings and TnT-positive results with mortality in acute AlP poisoning.

  1. Acute lead poisoning in two users of illicit methamphetamine

    SciTech Connect

    Allcott, J.V. III; Barnhart, R.A.; Mooney, L.A.

    1987-07-31

    Acute lead poisoning can present a difficult diagnostic dilemma, with symptoms that mimic those of hepatitis, nephritis, and encephalopathy. The authors report two cases in intravenous methamphetamine users who presented with abnormal liver function values, low hematocrit values, basophilic stippling of red blood cells, and elevated blood lead levels. Both patients excreted large amounts of lead in their urine after treatment with edetic acid, followed by resolution of their symptoms. Lead contamination was proved in one drug sample. Basophilic stippling of the red blood cells was the one key laboratory result that led to the definitive diagnosis in both cases.

  2. [Follow-up and therapy of acute colchicine poisoning].

    PubMed

    Stern, N; Kupferschmidt, H; Meier-Abt, P J

    1997-05-28

    Colchicine poisoning is a rare event. Its outcome is, compared to other drug intoxications, often serious or even fatal. Intaxications with colchicine may occur by ingestion of tablets as well as by consumption of meadow saffron leaves (Colchicum autumnale) that are often mistakenly collected instead of the leaves of ramson herb (Allium ursinum). Colchicine poisoning typically shows three phases: initially gastrointestinal symptoms predominate, in the second phase multiorgan failure may occur possibly leading to death. In case the patient survives, the third phase of recovery follows during which the patients often present with hair loss. The fatal dose of acute colchicine poisoning is estimated at about 0.9 mg/kg. Since hemodialysis and hemoperfusion are not effective measures because of the high volume of distribution, an aggressive primary decontamination with gastric lavage and activated charcoal is required as early as possible. A promising new aspect in the treatment of heavy colchicine overdose is the immunotherapy with colchicine-specific fab-fragments. At present this treatment is still in an experimental stage and has been applied so far to one patient with beneficial effects. Unfortunately colchicine-specific antibodies are not yet commercially available.

  3. Prediction of patient survival in cases of acute paraquat poisoning.

    PubMed

    Hong, Sae-Yong; Lee, Ji-Sung; Sun, In O; Lee, Kwang-Young; Gil, Hyo-Wook

    2014-01-01

    Paraquat concentration-time data have been used to predict the clinical outcome following ingestion. However, these studies have included only small populations, although paraquat poisoning has a very high mortality rate. The purpose of this study was to develop a simple and reliable model to predict survival according to the time interval post-ingestion in patients with acute paraquat poisoning. Data were retrospectively collected for patients who were admitted with paraquat poisoning to Soonchunhyang University Choenan Hospital between January 2005 and December 2012. Plasma paraquat levels were measured using high-performance liquid chromatography. To validate the model we developed, we used external data from 788 subjects admitted to the Presbyterian Medical Center, Jeonju, Korea, between January 2007 and December 2012. Two thousand one hundred thirty six patients were included in this study. The overall survival rate was 44% (939/2136). The probability of survival for any specified time and concentration could be predicted as (exp(logit))/(1+exp(logit)), where logit = 1.3544+[-3.4688 × log10(plasma paraquat μg/M[Formula: see text])]+[-2.3169 × log10(hours since ingestion)]. The external validation study showed that our model was highly accurate for the prediction of survival (C statics 0.964; 95% CI [0.952-0.975]). We have developed a model that is effective for predicting survival after paraquat intoxication.

  4. Which cyanide antidote?

    PubMed

    Hall, Alan H; Saiers, Jane; Baud, Frédéric

    2009-01-01

    Cyanide has several antidotes, with differing mechanisms of action and diverse toxicological, clinical, and risk-benefit profiles. The international medical community lacks consensus about the antidote or antidotes with the best risk-benefit ratio. Critical assessment of cyanide antidotes is needed to aid in therapeutic and administrative decisions that will improve care for victims of cyanide poisoning (particularly poisoning from enclosed-space fire-smoke inhalation), and enhance readiness for cyanide toxic terrorism and other mass-casualty incidents. This paper reviews preclinical and clinical data on available cyanide antidotes and considers the profiles of these antidotes relative to properties of a hypothetical ideal cyanide antidote. Each of the antidotes shows evidence of efficacy in animal studies and clinical experience. The data available to date do not suggest obvious differences in efficacy among antidotes, with the exception of a slower onset of action of sodium thiosulfate (administered alone) than of the other antidotes. The potential for serious toxicity limits or prevents the use of the Cyanide Antidote Kit, dicobalt edetate, and 4-dimethylaminophenol in prehospital empiric treatment of suspected cyanide poisoning. Hydroxocobalamin differs from these antidotes in that it has not been associated with clinically significant toxicity in antidotal doses. Hydroxocobalamin is an antidote that seems to have many of the characteristics of the ideal cyanide antidote: rapid onset of action, neutralizes cyanide without interfering with cellular oxygen use, tolerability and safety profiles conducive to prehospital use, safe for use with smoke-inhalation victims, not harmful when administered to non-poisoned patients, easy to administer.

  5. Severe but reversible acute kidney injury resulting from Amanita punctata poisoning

    PubMed Central

    Kang, Eunjung; Cheong, Ka-Young; Lee, Min-Jeong; Kim, Seirhan; Shin, Gyu-Tae; Kim, Heungsoo; Park, In-Whee

    2015-01-01

    Mushroom-related poisoning can cause acute kidney injury. Here we report a case of acute kidney injury after ingestion of Amanita punctata, which is considered an edible mushroom. Gastrointestinal symptoms occurred within 24 hours from the mushroom intake and were followed by an asymptomatic period, acute kidney injury, and elevation of liver and pancreatic enzymes. Kidney function recovered with supportive care. Nephrotoxic mushroom poisoning should be considered as a cause of acute kidney injury. PMID:26779427

  6. Muscular strength and vibration thresholds during two years after acute poisoning with organophosphate insecticides

    PubMed Central

    Miranda, J; McConnell, R; Wesseling, C; Cuadra, R; Delgado, E; Torres, E; Keifer, M; Lundberg, I

    2004-01-01

    Methods: This study concerns the third of a series of three examinations of hand strength and vibration thresholds in a two year period after acute OP poisoning among 48 Nicaraguan men. The first two examinations were performed at hospital discharge and seven weeks after poisoning, and the present examination two years later. Twenty eight cattle ranchers and fishermen who had never experienced pesticide poisoning were examined as controls, also three times over the two year period. The poisonings were categorised as caused by "non-neuropathic" OPs and "neuropathic" OPs, each subdivided in moderate and severe poisonings. Results: Men poisoned with OP insecticides had persistent reduced hand strength. We previously reported weakness at hospital discharge for OP poisoned in all categories that worsened seven weeks later for those severely poisoned with neuropathic OPs. Strength improved over time, but the poisoned were still weaker than controls two years after the poisoning, most noticeably among the subjects most severely poisoned with neuropathic OPs. Also, index finger and toe vibration thresholds were slightly increased at the end of the two year period, among men with OP poisonings in all categories, but patterns of onset and evolvement of impairment of vibration sensitivity were less clear than with grip and pinch strength. Conclusions: Persistent, mainly motor, impairment of the peripheral nervous system was found in men two years after OP poisoning, in particular in severe occupational and intentional poisonings with neuropathic OPs. This finding is possibly due to remaining organophosphate induced delayed polyneuropathy. PMID:14691285

  7. Development of a Fluorescence-Based Sensor for Rapid Diagnosis of Cyanide Exposure

    PubMed Central

    2015-01-01

    Although commonly known as a highly toxic chemical, cyanide is also an essential reagent for many industrial processes in areas such as mining, electroplating, and synthetic fiber production. The “heavy” use of cyanide in these industries, along with its necessary transportation, increases the possibility of human exposure. Because the onset of cyanide toxicity is fast, a rapid, sensitive, and accurate method for the diagnosis of cyanide exposure is necessary. Therefore, a field sensor for the diagnosis of cyanide exposure was developed based on the reaction of naphthalene dialdehyde, taurine, and cyanide, yielding a fluorescent β-isoindole. An integrated cyanide capture “apparatus”, consisting of sample and cyanide capture chambers, allowed rapid separation of cyanide from blood samples. Rabbit whole blood was added to the sample chamber, acidified, and the HCN gas evolved was actively transferred through a stainless steel channel to the capture chamber containing a basic solution of naphthalene dialdehyde (NDA) and taurine. The overall analysis time (including the addition of the sample) was <3 min, the linear range was 3.13–200 μM, and the limit of detection was 0.78 μM. None of the potential interferents investigated (NaHS, NH4OH, NaSCN, and human serum albumin) produced a signal that could be interpreted as a false positive or a false negative for cyanide exposure. Most importantly, the sensor was 100% accurate in diagnosing cyanide poisoning for acutely exposed rabbits. PMID:24383576

  8. Development of a fluorescence-based sensor for rapid diagnosis of cyanide exposure.

    PubMed

    Jackson, Randy; Oda, Robert P; Bhandari, Raj K; Mahon, Sari B; Brenner, Matthew; Rockwood, Gary A; Logue, Brian A

    2014-02-04

    Although commonly known as a highly toxic chemical, cyanide is also an essential reagent for many industrial processes in areas such as mining, electroplating, and synthetic fiber production. The "heavy" use of cyanide in these industries, along with its necessary transportation, increases the possibility of human exposure. Because the onset of cyanide toxicity is fast, a rapid, sensitive, and accurate method for the diagnosis of cyanide exposure is necessary. Therefore, a field sensor for the diagnosis of cyanide exposure was developed based on the reaction of naphthalene dialdehyde, taurine, and cyanide, yielding a fluorescent β-isoindole. An integrated cyanide capture "apparatus", consisting of sample and cyanide capture chambers, allowed rapid separation of cyanide from blood samples. Rabbit whole blood was added to the sample chamber, acidified, and the HCN gas evolved was actively transferred through a stainless steel channel to the capture chamber containing a basic solution of naphthalene dialdehyde (NDA) and taurine. The overall analysis time (including the addition of the sample) was <3 min, the linear range was 3.13-200 μM, and the limit of detection was 0.78 μM. None of the potential interferents investigated (NaHS, NH4OH, NaSCN, and human serum albumin) produced a signal that could be interpreted as a false positive or a false negative for cyanide exposure. Most importantly, the sensor was 100% accurate in diagnosing cyanide poisoning for acutely exposed rabbits.

  9. Patterns of Acute Poisoning in Childhood in Zagazig, Egypt: An Epidemiological Study

    PubMed Central

    Hassan, Basheir A.; Siam, Mohamed G.

    2014-01-01

    Background. Acute poisoning represents one of the most common medical emergencies in childhood. In view of paucity of literature on accidental poisoning among children in Egypt, this study was designed to describe the pattern of childhood poisoning in Zagazig University Hospitals. Patients and Methods. This retrospective study included 300 children up to 12 years with acute poisoning admitted to the Pediatric Department and Poisoning Treatment Unit, Zagazig University Hospitals, from January 2011 to August 2012. Complete epidemiological and clinical data were recorded and analyzed. Results. Three hundred of poisoned children were enrolled in this study. Children from 1 to 6 years were more liable to poisoning (81%). More boys than girls were poisoned at all age groups. The majority of all cases (99%) were due to accidental poisoning. Overall, 32% of the poisoned cases were living in Zagazig city while 68% were living in the rural areas. The presenting symptoms were classic in 60% of the cases. Pesticides, therapeutic drugs, and cleaning and disinfectant agents were the most frequent poisoning agents (28.7%, 22.7%, and 17.0%, resp.). In 86.0% of cases, observation with or without supportive measures together with decontamination and specific antidote therapy whenever needed was sufficient. Conclusion. Most of the poisonings were due to accidental ingestions by infants and young children. Pesticides and medications were the most commonly involved agents. PMID:27351009

  10. Cortical venous infarcts and acute limb ischaemia in acute carbon monoxide poisoning: A rare case report.

    PubMed

    Hanif, Muhammad Farooq; Iqbal, Beenish; Gilani, Nooman

    2016-06-01

    A case of carbon monoxide poisoning is presented with unusual complications; some of which have not been reported previously. A 48-years-old Asian male presented to the emergency department with dyspnoea, altered state of consciousness and pale discolouration of skin after being locked inside a factory room with burning coal. Patient was in acute respiratory distress. Arterial blood gas analysis showed respiratory acidosis with hypoxaemia. On 3rd day, patient developed dark coloured urine and right upper limb ischaemia. Acute renal failure was diagnosed. A doppler ultrasound showed stenosis of radial and ulnar arteries. 0n 8th day, patient regained consciousness and complained of loss of vision. An MRI of the brain revealed bilateral occipital venous infarcts. Cortical venous infarcts and arterial stenosis are rare complications of acute carbon monoxide poisoning.

  11. Acute dapsone poisoning in a 3-year-old child: Case report with review of literature

    PubMed Central

    Sunilkumar, Menon Narayanankutty; Ajith, Thekkuttuparambil Ananthanarayanan; Parvathy, Vadakut Krishnan

    2015-01-01

    Dapsone (DDS-diamino diphenyl sulphone) is a sulfone antibiotic being used for a variety of clinical conditions. Poisoning in children by DDS is rarely reported. Poisoning in acute cases will be frequently unrecognized due to relative lack of severe signs and symptoms. Methemoglobinemia is the major life-threatening situation associated with poisoning of DDS. Hence, any delay for medical attention can lead to increased rate of mortality. In this case, we describe acute DDS poisoning in a 3-year-old child and the successful management using intravenous methylene blue. PMID:26488029

  12. [Decontamination and antidotes in acute cases of poisoning].

    PubMed

    Kupferschmidt, Hugo; Züst, Ariane; Rauber-Lüthy, Christine

    2009-05-01

    In acute poisoning the maintenance or reconstitution of vital functions is the first and most critical action. All subsequent therapies and the prognosis depend on the identification of the causative agent and on information about substance-specific toxicity. Despite incomplete evidence the concept of harm reduction by decreased absorption of the toxicants and by shortening the course of illness is consistent with toxicokinetic-dynamic principles and is therefore still used by clinical toxicologists. All these treatment options have to be seen within the context of the prognosis and the time course of an individual case of poisoning. Treatment options of gastrointestinal decontamination are (in decreasing order of importance) single-dose activated charcoal, whole bowel irritation, and gastric lavage. Induced emesis by ipecac syrup is not practiced anymore. Enhanced elimination techniques are multiple-dose activated charcoal, urine alkalinization, and extracorporeal techniques such as hemodialysis and hemoperfusion. Enhanced elimination is only beneficial in toxicants with long half-life. Antidotes are directed against specific agents and therefore may be used only in a limited number of cases. The procurement of specific antidotes, often hardly available and not approved, is facilitated if the supply is organized in a transparent and standardized manner.

  13. [Acute poisoning with anticholinesterase carbamate pesticides: methomyl-lannate®].

    PubMed

    Chaouali, Nadia; Amira, Dorra; Zitouni, Eya; Gana, Ines; Nouioui, Anouer; Khelifi, Fathia; Belwaer, Ines; Masri, Wafa; Ghorbal, Hayet; Hedhili, Abderazzek

    2014-01-01

    The methomyl is increasingly involved in suicidal and autolytic attempts. Intoxication with carbamate (CM) compounds is still a frequent cause for admission in the Emergency department of the medical assistance center (MAC) in Tunis, Tunisia. The aim of this study was to describe the demographics, clinical features and hospital course of patients presenting with CM intoxication to the ED of MAC in Tunis, Tunisia. This was a retrospective study about 52 cases of acute poisoning by methomyl, compiled in the MAC from 1st January, 2009 to December 31, 2012. Intoxications were all oral, mostly intentional (33 cases: 65%) and in young patients (29 years old). Females outnumbered males by almost 2:1. The most frequent symptom was hypotension (41 cases: 80%), followed by miosis (39 cases: 75%), rhabdomyolysis (29 cases: 55%), vomiting (18 cases: 43%), bronchorrhea (14 cases: 27%), diarrhea (11 cases: 21%) and fasciculations (8 cases: 17%). Treatments included gastric lavage in 16 patients (32%), assisted ventilation in 8 cases (17%) and atropine in 44 patients (85%). Seven patients died during hospitalization. Pesticide poisoning is a significant public health problem and some preventive measures must be strictly enforced to limit this kind of intoxication.

  14. Acute lung injury in fulminant hepatic failure following paracetamol poisoning.

    PubMed Central

    Baudouin, S. V.; Howdle, P.; O'Grady, J. G.; Webster, N. R.

    1995-01-01

    BACKGROUND--There is little information on the incidence of acute lung injury or changes in the pulmonary circulation in acute liver failure. The aim of this study was to record the incidence of acute lung injury in fulminant hepatic failure caused by paracetamol poisoning, to document the associated pulmonary circulatory changes, and to assess the impact of lung injury on patient outcome. METHODS--The degree of lung injury was retrospectively assessed by a standard scoring system (modified from Murray) in all patients with fulminant hepatic failure caused by paracetamol poisoning, admitted to the intensive care unit over a one year period. The severity of liver failure and illness, other organ system failure, and patient outcome were also analysed. RESULTS--Twenty four patients with paracetamol-induced liver failure were admitted and nine developed lung injury of whom eight (33%) had severe injury (Murray score > 2.5). In two patients hypoxaemia contributed to death. Patients with lung injury had higher median encephalopathy grades (4 v 2 in the non-injured group) and APACHE II scores (29 v 16). Circulatory failure, requiring vasoconstrictor support, occurred in all patients with lung injury but in only 40% of those without. Cerebral oedema, as detected by abnormal rises in intracranial pressure, also occurred in all patients with lung injury but in only 27% of the non-injured patients. The incidence of renal failure requiring renal replacement therapy was similar in both groups (67% and 47%). Pulmonary artery occlusion pressures were normal in the lung injury group. Cardiac output was high (median 11.2 1/min), systemic vascular resistance low (median 503 dynes/s/cm-5), and pulmonary vascular resistance low (median 70 dynes/s/cm-5), but not significantly different from the group without lung injury. Mortality was much higher in the lung injury group than in the non-injured group (89% v 13%). CONCLUSIONS--Acute lung injury was common in patients with paracetamol

  15. Use of continuous renal replacement therapy in acute aluminum phosphide poisoning: a novel therapy.

    PubMed

    Nasa, Prashant; Gupta, Ankur; Mangal, Kishore; Nagrani, S K; Raina, Sanjay; Yadav, Rohit

    2013-09-01

    Aluminum phosphide is most common cause of poisoning in northern India. There is no specific antidote available and management of such cases is mainly supportive with high mortality. We present two cases of severe acute aluminium phosphide poisoning where continuous renal replacement therapy (CRRT) was started early along with other resuscitative measures and both the patients survived.

  16. Non-muscarinic therapeutic targets for acute organophosphorus poisoning.

    PubMed

    Rosenbaum, Christopher; Bird, Steven B

    2010-12-01

    Organophosphorus (OP) pesticides are a broad class of acetylcholinesterase inhibitors that are responsible for tremendous morbidity and mortality worldwide, contributing to an estimated 300,000 deaths annually. Current pharmacotherapy for acute OP poisoning includes the use of atropine, an oxime, and benzodiazepines. However, even with such therapy, the mortality from these agents is as high as 40%. It is increasingly recognized that not all OPs are the same. Significant differences exist in their toxicity, lipophilicity, and response to oxime therapy. Other non-muscarinic effects of OP pesticides exist, such as acute and chronic neuromuscular junction failure and central respiratory failure. In part because most of the mortality from these chemicals takes place in the developing world, little National Institutes of Health (NIH) research has been directed towards these agents. However, the similar mechanism of action of OP pesticides and the military nerve agents, along with increasing concerns about chemical terrorism has lead to the formation of the NIH Countermeasures Against Chemical Threats (CounterACT) Program. As part of the CounterACT Program, the NIH has recently designated six OP pesticides as "threat agents". This concept paper describes some of the knowledge gaps related to non-muscarinic effects of OP pesticides and highlights needed areas of further research. Leveraging the current NIH interest in these chemicals to medical necessities in the developing world offers the possibility of delivering new therapeutics where they are needed on a daily basis.

  17. Acute poisoning types and prevalence in Shanghai, China, from January 2010 to August 2011.

    PubMed

    Zhang, Jingshuo; Xiang, Ping; Zhuo, Xianyi; Shen, Min

    2014-03-01

    In recent years, the number of cases of acute poisoning has increased in China, yet; currently, there is no detailed report published that addresses acute poisoning in the mainland of China. We collected biological samples from 466 cases of suspected acute poisoning at the hospitals in Shanghai, China, and examined them using spectroscopy, chromatography and chromatography/mass spectrometry. Of the 466 cases, 230 cases (100 men and 130 women) were positively confirmed as acute poisonings. There were 80 types of compounds identified in this study. Medications were the most frequent substances identified, and the other substances included pesticides, multiple compounds, volatile compounds, natural toxins, and others. The results of this study indicate a need for strengthening the education about and management of the rational and safe use of drugs in Shanghai.

  18. Acute Poisoning in Children; a Population Study in Isfahan, Iran, 2008-2010

    PubMed Central

    Gheshlaghi, Farzad; Piri-Ardakani, Mohammad-Reza; Yaraghi, Mansooreh; Shafiei, Faranak; Behjati, Mohaddaseh

    2013-01-01

    Objective Acute accidental poisoning in children is still an important public health problem. The epidemiological investigation specific for each country is necessary to determine the extent and characteristics of the problem. The aim of our study was to elucidate the current pattern of acute poisoning among children. Methods The present retrospective study describes the epidemiology of acute accidental poisoning in children (less than 10 years old) admitted to the Emergency Department of two teaching hospitals during a period of two years. Findings Three hundred and forty four children under 10 years old were admitted to emergency department of two teaching hospitals due to acute accidental poisoning. Drugs were the most common agents causing the poisoning (58.1%), followed by Hydrocarbons (13.1%), and opioids (9.3%). Common signs were neurological (42.6%) with lethargy being the most common (39.1%). 50.6% of cases were discharged from hospital within 6-12 hours, 91.6% of them without any complication. Conclusion Accidental poisonings are still a significant cause of morbidity among children in developing countries. Regarding the high prevalence of pharmaceutical drug poisoning and because lethargic was the most frequent neurological sign, comprehensive toxicology screen tests should be included as part of the routine evaluation of children presenting to an ED with an apparent life-threatening event. PMID:23724181

  19. Edaravone attenuates brain damage in rats after acute CO poisoning through inhibiting apoptosis and oxidative stress.

    PubMed

    Li, Qin; Bi, Ming Jun; Bi, Wei Kang; Kang, Hai; Yan, Le Jing; Guo, Yun-Liang

    2016-03-01

    Acute carbon monoxide (CO) poisoning is the most common cause of death from poisoning all over the world and may result in neuropathologic and neurophysiologic changes. Acute brain damage and delayed encephalopathy are the most serious complication, yet their pathogenesis is poorly understood. The present study aimed to evaluate the neuroprotective effects of Edaravone against apoptosis and oxidative stress after acute CO poisoning. The rat model of CO poisoning was established in a hyperbaric oxygen chamber by exposed to CO. Ultrastructure changes were observed by transmission electron microscopy (TEM). TUNEL stain was used to assess apoptosis. Immunohistochemistry and immunofluorescence double stain were used to evaluate the expression levels of heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf-2) protein and their relationship. By dynamically monitored the carboxyhemoglobin (HbCO) level in blood, we successfully established rat model of severe CO poisoning. Ultrastructure changes, including chromatin condensation, cytoplasm dissolution, vacuoles formation, nucleus membrane and cell organelles decomposition, could be observed after CO poisoning. Edaravone could improve the ultrastructure damage. CO poisoning could induce apoptosis. Apoptotic cells were widely distributed in cortex, striatum and hippocampus. Edaravone treatment attenuated neuronal apoptosis as compared with the poisoning group (P < 0.01). Basal expressions of HO-1 and Nrf-2 proteins were found in normal brain tissue. CO poisoning could activate HO-1/Nrf-2 pathway, start oxidative stress response. After the administration of Edaravone, the expression of HO-1 and Nrf-2 significantly increased (P < 0.01). These findings suggest that Edaravone may inhibit apoptosis, activate the Keapl-Nrf/ARE pathway, and thus improve the ultrastructure damage and neurophysiologic changes following acute CO poisoning.

  20. Metabolic changes in rat urine after acute paraquat poisoning and discriminated by support vector machine.

    PubMed

    Wen, Congcong; Wang, Zhiyi; Zhang, Meiling; Wang, Shuanghu; Geng, Peiwu; Sun, Fa; Chen, Mengchun; Lin, Guanyang; Hu, Lufeng; Ma, Jianshe; Wang, Xianqin

    2016-01-01

    Paraquat is quick-acting and non-selective, killing green plant tissue on contact; it is also toxic to human beings and animals. In this study, we developed a urine metabonomic method by gas chromatography-mass spectrometry to evaluate the effect of acute paraquat poisoning on rats. Pattern recognition analysis, including both partial least squares discriminate analysis and principal component analysis revealed that acute paraquat poisoning induced metabolic perturbations. Compared with the control group, the levels of benzeneacetic acid and hexadecanoic acid of the acute paraquat poisoning group (intragastric administration 36 mg/kg) increased, while the levels of butanedioic acid, pentanedioic acid, altronic acid decreased. Based on these urinary metabolomics data, support vector machine was applied to discriminate the metabolomic change of paraquat groups from the control group, which achieved 100% classification accuracy. In conclusion, metabonomic method combined with support vector machine can be used as a useful diagnostic tool in paraquat-poisoned rats.

  1. [Poison cases and types of poisons based on data obtained of patients hospitalized from 1995-2009 with acute poisoning in the second internal ward in a multi-profile provincial hospital in Tarnow].

    PubMed

    Lata, Stanisław; Janiszewski, Jacek

    2010-01-01

    The thesis presents a short history and organization of an acute poisoning centre in the1995 functioning within the internal diseases department in a multi-profile provincial hospital. The data show the number of patients treated beetween 1995-2009 an the types of toxic substances that caused poisoning. The conclusions presented refer to the role of the centre to help people suffering from acute poisoning within the city of Tarnow.

  2. A case report of massive acute boric acid poisoning.

    PubMed

    Corradi, Francesco; Brusasco, Claudia; Palermo, Salvatore; Belvederi, Giulio

    2010-02-01

    Boric acid comes as colourless, odourless white powder and, if ingested, has potential fatal effects including metabolic acidosis, acute renal failure and shock. An 82-year-old male was brought to the emergency room 3 h after unintentional ingestion of a large amount of boric acid. Clinical course was monitored by collecting data at admittance, 12 h after admission, every 24 h for 5 days and again 1 week after admission. During the first 132 h, serum and urinary concentrations of boric acid were measured. Serum boric acid levels decreased from 1800 to 530 microg/ml after haemodialysis and from 530 to 30 microg/ml during the forced diuresis period. During dialysis, boric acid clearance averaged 235 ml/min with an extraction ratio of 70%. The overall patient's condition steadily improved over 84 h after admission. In conclusion, early treatment with forced diuresis and haemodialysis may be considered for boric acid poisoning, even if signs of renal dysfunction are not apparent, to prevent severe renal damage and its complications.

  3. Poisoning

    MedlinePlus

    ... been swallowed, DO NOT give the person activated charcoal. DO NOT give children ipecac syrup. DO NOT ... poison from being absorbed, you may receive: Activated charcoal A tube through the nose into the stomach ...

  4. Characteristics of Children with Acute Carbon Monoxide Poisoning in Ankara: A Single Centre Experience.

    PubMed

    Unsal Sac, Rukiye; Taşar, Medine Ayşin; Bostancı, İlknur; Şimşek, Yurda; Bilge Dallar, Yıldız

    2015-12-01

    The purpose of the study was to define characteristics of children with acute carbon monoxide poisoning. Eighty children hospitalized with acute carbon monoxide poisoning were recruited prospectively over a period of 12 months. Sociodemographic features, complaints and laboratory data were recorded. When the patient was discharged, necessary preventive measures to be taken were explained to parents. One month later, the parents were questioned during a control examination regarding the precautions that they took. The ages of the cases were between one month and 16 yr. Education levels were low in 86.2% of mothers and 52.6% of fathers. All families had low income and 48.8% did not have formal housing. The source of the acute carbon monoxide poisoning was stoves in 71.2% of cases and hot-water heaters in 28.8% of cases. Three or more people were poisoned at home in 85.1% of the cases. The most frequent symptoms of poisoning were headache and vertigo (58.8%). Median carboxyhemoglobin levels at admission to the hospital and discharge were measured as 19.5% and 1.1% (P < 0.001). When families were called for re-evaluation, it was determined that most of them had taken the necessary precautions after the poisoning incident (86.3%). This study determined that children with acute childhood carbon monoxide poisoning are usually from families with low socioeconomic and education levels. Education about prevention should be provided to all people who are at risk of carbon monoxide poisoning before a poisoning incident occurs.

  5. Characteristics of Children with Acute Carbon Monoxide Poisoning in Ankara: A Single Centre Experience

    PubMed Central

    Unsal Sac, Rukiye; Bostancı, İlknur; Şimşek, Yurda; Bilge Dallar, Yıldız

    2015-01-01

    The purpose of the study was to define characteristics of children with acute carbon monoxide poisoning. Eighty children hospitalized with acute carbon monoxide poisoning were recruited prospectively over a period of 12 months. Sociodemographic features, complaints and laboratory data were recorded. When the patient was discharged, necessary preventive measures to be taken were explained to parents. One month later, the parents were questioned during a control examination regarding the precautions that they took. The ages of the cases were between one month and 16 yr. Education levels were low in 86.2% of mothers and 52.6% of fathers. All families had low income and 48.8% did not have formal housing. The source of the acute carbon monoxide poisoning was stoves in 71.2% of cases and hot-water heaters in 28.8% of cases. Three or more people were poisoned at home in 85.1% of the cases. The most frequent symptoms of poisoning were headache and vertigo (58.8%). Median carboxyhemoglobin levels at admission to the hospital and discharge were measured as 19.5% and 1.1% (P < 0.001). When families were called for re-evaluation, it was determined that most of them had taken the necessary precautions after the poisoning incident (86.3%). This study determined that children with acute childhood carbon monoxide poisoning are usually from families with low socioeconomic and education levels. Education about prevention should be provided to all people who are at risk of carbon monoxide poisoning before a poisoning incident occurs. PMID:26713060

  6. Organophosphate Poisoning and Subsequent Acute Kidney Injury Risk: A Nationwide Population-Based Cohort Study.

    PubMed

    Lee, Feng-You; Chen, Wei-Kung; Lin, Cheng-Li; Lai, Ching-Yuan; Wu, Yung-Shun; Lin, I-Ching; Kao, Chia-Hung

    2015-11-01

    Small numbers of the papers have studied the association between organophosphate (OP) poisoning and the subsequent acute kidney injury (AKI). Therefore, we used the National Health Insurance Research Database (NHIRD) to study whether patients with OP poisoning are associated with a higher risk to have subsequent AKI.The retrospective cohort study comprised patients aged ≥20 years with OP poisoning and hospitalized diagnosis during 2000-2011 (N = 8924). Each OP poisoning patient was frequency-matched to 4 control patients based on age, sex, index year, and comorbidities of diabetes, hypertension, hyperlipidemia, chronic obstructive pulmonary disease, coronary artery disease, and stroke (N = 35,696). We conducted Cox proportional hazard regression analysis to estimate the effects of OP poisoning on AKI risk.The overall incidence of AKI was higher in the patients with OP poisoning than in the controls (4.85 vs 3.47/1000 person-years). After adjustment for age, sex, comorbidity, and interaction terms, patients with OP poisoning were associated with a 6.17-fold higher risk of AKI compared with the comparison cohort. Patients with highly severe OP poisoning were associated with a substantially increased risk of AKI.The study found OP poisoning is associated with increased risk of subsequent AKI. Future studies are encouraged to evaluate whether long-term effects exist and the best guideline to prevent the continuously impaired renal function.

  7. Hospital Performance Indicators and Their Associated Factors in Acute Child Poisoning at a Single Poison Center, Central Saudi Arabia

    PubMed Central

    Alanazi, Menyfah Q.; Al-Jeriasy, Majed I.; Al-Assiri, Mohammed H.; Afesh, Lara Y.; Alhammad, Fahad; Salam, Mahmoud

    2015-01-01

    Abstract Admission rate and length of stay (LOS) are two hospital performance indicators that affect the quality of care, patients’ satisfaction, bed turnover, and health cost expenditures. The aim of the study was to identify factors associated with higher admission rates and extended average LOS among acutely poisoned children at a single poison center, central Saudi Arabia. This is a cross-sectional, poison and medical chart review between 2009 and 2011. Exposures were child characteristics, that is, gender, age, body mass index (BMI), health history, and Canadian 5-level triage scale. Poison incident characteristics were, that is, type, exposure route, amount, form, home remedy, and arrival time to center. Admission status and LOS were obtained from records. Chronic poisoning, plant allergies, and venomous bites were excluded. Bivariate and regression analyses were applied. Significance at P < 0.05. Of the 315 eligible cases, (72%) were toddlers with equal gender distribution, (58%) had normal BMI, and (77%) were previously healthy. Poison substances were pharmaceutical drugs (63%) versus chemical products (37%). Main exposure route was oral (98%). Home remedy was observed in (21.9%), which were fluids, solutes, and/or gag-induced vomiting. Almost (52%) arrived to center >1 h. Triage levels: non-urgent cases (58%), less urgent (11%), urgent (18%), emergency (12%), resuscitative (1%). Admission rate was (20.6%) whereas av. LOS was 13 ± 22 h. After adjusting and controlling for confounders, older children (adj.OR = 1.19) and more critical triage levels (adj.OR = 1.35) were significantly associated with higher admission rates compared to younger children and less critical triage levels (adj.P = 0.006) and (adj.P = 0.042) respectively. Home remedy prior arrival was significantly associated with higher av. LOS (Beta = 9.48, t = 2.99), compared to those who directly visited the center, adj.P = 0.003. Hospital administrators

  8. Metalloporphyrin Co(III)TMPyP ameliorates acute, sublethal cyanide toxicity in mice.

    PubMed

    Benz, Oscar S; Yuan, Quan; Amoscato, Andrew A; Pearce, Linda L; Peterson, Jim

    2012-12-17

    The formation of Co(III)TMPyP(CN)(2) at pH 7.4 has been shown to be completely cooperative (α(H) = 2) with an association constant of 2.1 (±0.2) × 10(11). The kinetics were investigated by stopped-flow spectrophotometry and revealed a complicated net reaction exhibiting 4 phases at pH 7.4 under conditions where cyanide was in excess. The data suggest molecular HCN (rather than CN(-)) to be the attacking nucleophile around neutrality. The two slower phases do not seem to be present when cyanide is not in excess, and the other two phases have rates comparable to that observed for cobalamin, a known effective cyanide scavenger. Addition of bovine serum albumin (BSA) did not affect the cooperativity of cyanide binding to Co(III)TMPyP, only lowered the equilibrium constant slightly to 1.2 (±0.2) × 10(11) and had an insignificant effect on the observed rate. A sublethal mouse model was used to assess the effectiveness of Co(III)TMPyP as a potential cyanide antidote. The administration of Co(III)TMPyP to sodium cyanide intoxicated mice resulted in the time required for the surviving mice to right themselves from a supine position being significantly decreased (9 ± 2 min) compared to that of the controls (33 ± 2 min). All observations were consistent with the demonstrated antidotal activity of Co(III)TMPyP operating through a cyanide-binding (i.e., scavenging) mechanism.

  9. Is there a relationship between admission blood glucose level following acute poisoning and clinical outcome?

    PubMed Central

    Sabzghabaee, Ali Mohammad; Eizadi-Mood, Nastaran; Gheshlaghi, Farzad; Adib, Nooshin; Safaeian, Leila

    2011-01-01

    Introduction The aim of this study was to investigate the relationship between the admission blood glucose level following acute poisoning, severity of acute poisoning and clinical outcome. Material and methods This prospective study was conducted on 345 deliberate self-poisoning patients. Standard demographic and clinical information; admission blood glucose level; poisoning severity score and outcome were recorded. Patients with a history of diabetes mellitus, receipt of pre-sampling intravenous dextrose solution or glucocorticoids, and poisoning with toxic agents which produce hyper- or hypoglycaemia were excluded. Results Mean age of the patients was 27.5 ±8.6 years. Females outnumbered males (57.9%). Oral ingestion of more than one drug (46.7%) and opiates (14.2%) were the main causes of poisoning. Blood glucose values ranged from 50 mg/dl to 396 mg/dl. Hyper- and hypoglycaemia were observed in 23.8% and 13.91% respectively. A total of 24.41% and 22.92% of the patients in hyper- and hypoglycaemic groups had grade 3 and 4 severity score in comparison with 4.18% in the normoglycaemic group. Development of complications and death were 14.64% and 10.42% in patients with hyper- and hypoglycaemia versus 3.73% in patients with normoglycaemia. A significant difference between normoglycaemic and hyperglycaemic patients in the severity of poisoning and clinical outcome was observed (P < 0.001). Conclusions Admission blood glucose levels may have a relationship with the severity of poisoning and clinical outcome following acute poisoning. PMID:22291737

  10. Acute Datura Stramonium poisoning in East of Iran - a case series

    PubMed Central

    Amini, Mahnaz; Khosrojerdi, Hamid; Afshari, Reza

    2012-01-01

    Objectives: Datura Stramonium (DS) is a common weed along roadsides, in cornfields and pastures and in waste areas. It belongs to the family Solanaceae and its toxic components are tropane belladonna alkaloids. It has been used voluntarily by teenagers for its hallucinogenic effect. The plant is named in Iran as Tatoore. Symptoms and signs of acute D. Stramonium poisoning usually are similar to anticholinergic syndrome. This study is done in order to clarify the status of this poisoning in our region. Materials and Methods: This study is a case series on all patients admitted to Imam Reza Hospital, Mashhad, Iran, with acute D. Stramonium poisoning between 2008 and 2011. We observed their symptoms, signs, routine laboratory test results and treatment used to control their symptoms. Results: There were 19 patients included in our study. Children were poisoned more commonly than teenagers and poisoning in adults was rare. All of the children ingested the plant accidentally. The most presenting symptom was irritability and the most common sign was sinus tachycardia. There was not any presentation of seizure or coma. Most of the symptoms were controlled by parenteral benzodiazepines and there were no need to use of cholinergic agents such as physostigmine. Conclusion: Our study showed most of D. Stramonium poisoned population in our region are children. We suggest decreasing accessibility to the plant in order to decrease the incidence of its poisoning. PMID:25050235

  11. A Study of Acute Poisoning Cases Admitted to the University Hospital Emergency Department in Tabriz, Iran.

    PubMed

    Oraie, Mehdi; Hosseini, Mir-Jamal; Islambulchilar, Mina; Hosseini, Seyed-Hasan; Ahadi-Barzoki, Mehdi; Sadr, Habib; Yaghoubi, Hashem

    2017-03-01

    Chemical substances have an important threat due to extensive use in medicine, agriculture, industry and environment. In this retrospective study, etiological and demographic characteristics of acute poisoning cases admitted to a hospital in Iran were investigated. We compared these data with those reported from other parts of the country and the international experiences to evaluate any difference if exists. 7 052 poisoned cases admitted to the hospital from April 2006 to March 2013, by data collected from the medical record in poison center section. According to our results there is a predominance of male patients and the majority of the poisoned patients were between 20-30 years old. Drug poisoning was the most common cause of poisonings. The most frequently involved drugs were benzodiazepines and antidepressants. The seasonal distribution of our study showed a peak in summer. To prevent acute poisonings, the social education about the risk assessment of central nervous system-acting drugs and reduction of the exposure period of people to pesticides are recommended. This study suggested a proper educational program for the public and primary care units. Our results provide useful information for preventive strategies.

  12. Epidemiology of acute drug poisoning in a tertiary center from Iasi County, Romania.

    PubMed

    Sorodoc, Victorita; Jaba, Irina M; Lionte, Catalina; Mungiu, Ostin C; Sorodoc, Laurentiu

    2011-12-01

    The aim of this retrospective epidemiological study was to investigate the demographical, etiological and clinical characteristics of acute drug poisonings in Iasi County, Romania. All patients were referred and admitted in the Toxicology Clinic of "Sf. Ioan" Emergency Clinic Hospital Iasi, Romania. Between 2003 and 2009, 811 cases of acute drug poisonings were recorded, counting for 28.43% from the total number of poisonings. The majority of these poisonings resulted in mild (51.94%) and medium (28.35%) clinical forms, while 19.71% were coma situations. In all, 63.51% of patients originated from urban areas, 39.94% were unemployed and the patients were predominantly women (66.46%). A high percentage (97.27%) were suicide attempts, using only one type of drug (65.88%) and the 21-30 years group (29.8%) records the highest incidence, for both women and men. The most frequently involved drugs were benzodiazepines 13.69%, anticonvulsive drugs 8.63%, barbiturates 8.51% and cardiovascular drugs 5.92%. Drugs combinations were recorded in 32.92% of cases and 1.2% were combinations between drugs and other substances. Mortality was the outcome in 0.3% of the total registered number of acute drug poisonings. This study underlines that in order to provide a proper management of these situations, a Regional Poison Information Center is absolutely necessary.

  13. An interesting cause of pulmonary emboli: Acute carbon monoxide poisoning

    SciTech Connect

    Sevinc, A.; Savli, H.; Atmaca, H.

    2005-07-01

    Carbon monoxide poisoning, a public health problem of considerable significance, is a relatively frequent event today, resulting in thousands of hospitalizations annually. A 70-year-old lady was seen in the emergency department with a provisional diagnosis of carbon monoxide poisoning. The previous night, she slept in a tightly closed room heated with coal ember. She was found unconscious in the morning with poor ventilation. She had a rare presentation of popliteal vein thrombosis, pulmonary emboli, and possible tissue necrosis with carbon monoxide poisoning. Oxygen treatment with low-molecular-weight heparin (nadroparine) and warfarin therapy resulted in an improvement in both popliteal and pulmonary circulations. In conclusion, the presence of pulmonary emboli should be sought in patients with carbon monoxide poisoning.

  14. An unusual case of reversible acute kidney injury due to chlorine dioxide poisoning.

    PubMed

    Bathina, Gangadhar; Yadla, Manjusha; Burri, Srikanth; Enganti, Rama; Prasad Ch, Rajendra; Deshpande, Pradeep; Ch, Ramesh; Prayaga, Aruna; Uppin, Megha

    2013-09-01

    Chlorine dioxide is a commonly used water disinfectant. Toxicity of chlorine dioxide and its metabolites is rare. In experimental studies, it was shown that acute and chronic toxicity were associated with insignificant hematological changes. Acute kidney injury due to chlorine dioxide was not reported. Two cases of renal toxicity due to its metabolites, chlorate and chlorite were reported. Herein, we report a case of chlorine dioxide poisoning presenting with acute kidney injury.

  15. Medical treatment of acute poisoning with organophosphorus and carbamate pesticides.

    PubMed

    Jokanović, Milan

    2009-10-28

    Organophosphorus compounds (OPs) are used as pesticides and developed as warfare nerve agents such as tabun, soman, sarin, VX and others. Exposure to even small amounts of an OP can be fatal and death is usually caused by respiratory failure. The mechanism of OP poisoning involves inhibition of acetylcholinesterase (AChE) leading to inactivation of the enzyme which has an important role in neurotransmission. AChE inhibition results in the accumulation of acetylcholine at cholinergic receptor sites, producing continuous stimulation of cholinergic fibers throughout the nervous systems. During more than five decades, pyridinium oximes have been developed as therapeutic agents used in the medical treatment of poisoning with OP. They act by reactivation of AChE inhibited by OP. However, they differ in their activity in poisoning with pesticides and warfare nerve agents and there is still no universal broad-spectrum oxime capable of protecting against all known OP. In spite of enormous efforts devoted to development of new pyridinium oximes as potential antidotes against poisoning with OP only four compounds so far have found its application in human medicine. Presently, a combination of an antimuscarinic agent, e.g. atropine, AChE reactivator such as one of the recommended pyridinium oximes (pralidoxime, trimedoxime, obidoxime and HI-6) and diazepam are used for the treatment of OP poisoning in humans. In this article the available data related to medical treatment of poisoning with OP pesticides are reviewed and the current recommendations are presented.

  16. Successful Treatment of Severe Metabolic Acidosis Due to Acute Aluminum Phosphide Poisoning With Peritoneal Dialysis: a Report of 2 Cases.

    PubMed

    Bashardoust, Bahman; Farzaneh, Esmaeil; Habibzadeh, Afshin; Seyyed Sadeghi, Mir Salim

    2017-03-01

    Aluminum phosphide poisoning is common in our region. It can cause severe metabolic acidosis and persistent hypotension, which lead to cardiogenic shock and subsequently mortality. Oliguric or anuric acute kidney injury is seen in almost all patients with aluminum phosphide poisoning. Renal replacement therapies are recommended in these patients to improve metabolic acidosis and increase the rate of survival. We report 2 cases of severe acute aluminum phosphide poisoning treated successfully with peritoneal dialysis.

  17. Effectiveness of intramuscularly administered cyanide antidotes on methemoglobin formation and survival.

    PubMed

    Vick, J A; Von Bredow, J D

    1996-01-01

    Successful first aid therapy for cyanide intoxication is dependent upon immediate administration of antidotes which directly or indirectly interact with the cyanide ion to remove it from circulation. Owing to the severe respiratory, cardiovascular and convulsive episodes following acute cyanide intoxication, the most practical approach is to administer antidotes by intramuscular injection. Exceptionally rapid methemoglobin formers-hydroxylamine hydrochloride (HH) and dimethylaminophenol (DMAP)-are usually able to prevent the lethal effect of cyanide following intramuscular injections in doses sufficient to induce 20% methemoglobin (HH = 20 mg kg-1 and DMAP = 2 mg kg-1). Sodium nitrite, the methemoglobin inducer approved for military use, must be administered by intravenous infusion because it is not an effective cyanide antidote by the intramuscular route. In the normal unintoxicated animal an intramuscular injection of 20 mg kg-1 sodium nitrite will form 20% methemoglobin; however, in acute cyanide intoxication the associated severe bradycardia appears to limit the rate of absorption and thus the rapid formation of methemoglobin. If the bradycardia is prevented or reversed by atropine, the rate of absorption of sodium nitrite and the formation of methemoglobin is able to reverse the otherwise lethal effects of cyanide. Thus, an intramuscularly administered combination of 20 mg kg-1 sodium nitrite and 1 mg kg-1 atropine sulfate, rapidly absorbed from the intramuscular site, appears to achieve the same degree of effectiveness against acute cyanide intoxication as intramuscularly administered HH or DMAP. It would appear from these studies that HH, DMAP and sodium nitrite with atropine are all potentially effective intramuscular antidotes for acute cyanide poisoning.

  18. Acute kidney injury and disseminated intravascular coagulation due to mercuric chloride poisoning

    PubMed Central

    Dhanapriya, J.; Gopalakrishnan, N.; Arun, V.; Dineshkumar, T.; Sakthirajan, R.; Balasubramaniyan, T.; Haris, M.

    2016-01-01

    Mercury is a toxic heavy metal and occurs in organic and inorganic forms. Inorganic mercury includes elemental mercury and mercury salts. Mercury salts are usually white powder or crystals, and widely used in indigenous medicines and folk remedies in Asia. Inorganic mercury poisoning causes acute kidney injury (AKI) and gastrointestinal manifestations and can be life-threatening. We describe a case with unknown substance poisoning who developed AKI and disseminated intravascular coagulation (DIC). Renal biopsy showed acute tubular necrosis. Later, the consumed substance was proven to be mercuric chloride. His renal failure improved over time, and his creatinine normalized after 2 months. PMID:27194836

  19. Toxicokinetic Profiles of Alpha-ketoglutarate Cyanohydrin, a Cyanide Detoxification Product, following Exposure to Potassium Cyanide

    DTIC Science & Technology

    2013-07-15

    tox le t Toxicokinetic profiles of -ketoglutarate cyanohydrin, a cyanide detoxification product, following exposure to potassium cyanide ...KgCN in swine was investigated. • Measuring plasma -KgCN provides definitive confirmation of cyanide exposure. • Treatment of... cyanide poisoning with cobinamide renders -KgCN an ineffective diagnostic marker. a r t i c l e i n f o Article history: Received 6 May

  20. Comparative analysis of acute toxic poisoning in 2003 and 2011: analysis of 3 academic hospitals.

    PubMed

    Jang, Hak-Soo; Kim, Jung-Youn; Choi, Sung-Hyuk; Yoon, Young-Hoon; Moon, Sung-Woo; Hong, Yun-Sik; Lee, Sung-Woo

    2013-10-01

    Social factors may affect the available sources of toxic substances and causes of poisoning; and these factors may change over time. Additionally, understanding the characteristics of patients with acute toxic poisoning is important for treating such patients. Therefore, this study investigated the characteristics of patients with toxic poisoning. Patients visiting one of 3 hospitals in 2003 and 2011 were included in this study. Data on all patients who were admitted to the emergency departments with acute toxic poisoning were retrospectively obtained from medical records. Total 939 patients were analyzed. The average age of patients was 40.0 ± 20 yr, and 335 (36.9%) patients were men. Among the elements that did not change over time were the facts that suicide was the most common cause, that alcohol consumption was involved in roughly 1 of 4 cases, and that there were more women than men. Furthermore, acetaminophen and doxylamine remained the most common poisoning agents. In conclusion, the average patient age and psychotic drug poisoning has increased over time, and the use of lavage treatment has decreased.

  1. A Case of Mushroom Poisoning with Russula subnigricans: Development of Rhabdomyolysis, Acute Kidney Injury, Cardiogenic Shock, and Death

    PubMed Central

    2016-01-01

    Mushroom exposures are increasing worldwide. The incidence and fatality of mushroom poisoning are reported to be increasing. Several new syndromes in mushroom poisoning have been described. Rhabdomyolytic mushroom poisoning is one of new syndromes. Russula subnigricans mushroom can cause delayed-onset rhabdomyolysis with acute kidney injury in the severely poisoned patient. There are few reports on the toxicity of R. subnigricans. This report represents the first record of R. subnigricans poisoning with rhabdomyolysis in Korea, describing a 51-year-old man who suffered from rhabdomyolysis, acute kidney injury, severe hypocalcemia, respiratory failure, ventricular tachycardia, cardiogenic shock, and death. Mushroom poisoning should be considered in the evaluation of rhabdomyolysis of unknown cause. Furthermore, R. subnigricans should be considered in the mushroom poisoning with rhabdomyolysis. PMID:27366018

  2. Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning

    SciTech Connect

    Van Hoesen, K.B.; Camporesi, E.M.; Moon, R.E.; Hage, M.L.; Piantadosi, C.A. )

    1989-02-17

    Carbon monoxide (CO) is the leading cause of death due to poisoning. Although uncommon, CO poisoning does occur during pregnancy and can result in fetal mortality and neurological malformations in fetuses who survive to term. Uncertainty arises regarding the use of hyperbaric oxygen (HBO) as a treatment for the pregnant patient because of possible adverse effects on the fetus that could be induced by oxygen at high partial pressures. While the dangers of hyperoxia to the fetus have been demonstrated in animal models, careful review of animal studies and human clinical experience indicates that the short duration of hyperoxic exposure attained during HBO therapy for CO poisoning can be tolerated by the fetus in all stages of pregnancy and reduces the risk of death or deformity to the mother and fetus. A case is presented of acute CO poisoning during pregnancy that was successfully treated with HBO. Recommendations are suggested for the use of HBO during pregnancy.

  3. Epidemiology of acute poisoning in children presenting to the poisoning treatment center at Ain Shams University in Cairo, Egypt, 2009–2013

    PubMed Central

    Azab, Sonya M. S.; Hirshon, Jon Mark; Hayes, Bryan D.; El-Setouhy, Maged; Smith, Gordon S.; Sakr, Mahmoud Lotfy; Tawfik, Hany; Klein-Schwartz, Wendy

    2016-01-01

    Introduction Pediatric poisonings represent a major and preventable cause of morbidity and mortality throughout the world. Epidemiologic information about poisoning among children in many lower- and middle-income countries is scarce. This study describes the epidemiology of acute poisonings in children presenting to Ain Shams University's Poisoning Treatment Center (ASU-PTC) in Cairo and determines the causative agents and characteristics of acute poisoning in several pediatric age groups. Methods This retrospective study involved acutely poisoned patients, 0 to 18 years of age, who presented to the ASU-PTC between 1/1/2009 and 12/31/2013. Data were extracted from electronic records maintained by the ASU-PTC. Collected data included demographics, substance of exposure, circumstances of the poisoning, patient disposition, and outcome. Results During the 5-year study period, 38,470 patients meeting our criteria were treated by the ASU-PTC; 19,987 (52%) were younger than 6 years of age; 4,196 (11%) were 6 to 12 years; and 14,287 (37%) were >12 years. Unintentional poisoning accounted for 68.5% of the ingestions, though among adolescents 84.1% of ingestions were with self-harm intent. In all age groups, the most frequent causative drugs were non-opioid analgesics, antipyretics, and antirheumatics. The most common nonpharmaceutical agents were corrosives in preschool children and pesticides in adolescents. Most patients had no/minor effects (29,174 [75.8%]); hospitalization rates were highest among adolescents. There were 119 deaths (case fatality rate of 0.3), primarily from pesticide ingestion. Conclusion Poisoning in preschool children is mainly unintentional and commonly due to nonpharmaceutical agents while poisoning in adolescents is mainly intentional (self-harm). Pesticides, mainly organophosphorous compounds and carbamates, were the most frequent agent leading to morbidity and mortality. PMID:26653953

  4. The profile evolution of acute severe poisoning in Spain.

    PubMed

    Nogué, S; Marruecos, L; Nolla, J; Monteís, J; Ferrer, A; Civeira, E

    1992-12-01

    About 5% of the patients admitted to emergency departments with poisonings are seriously ill and need admission to intensive care units (ICUs). This paper presents the result of three multicentric studies carried out in Spain during the last ten years. A study was made of 6 ICUs in 1980, 41 in 1987 and 15 in 1990 with a total of 596 patients. The average age (36) remained stable throughout, but the number of female cases decreased each time. The most frequent cause (79%) was attempted suicide. The products used most frequently were therapeutic drugs (82, 71 and 58%) followed by drugs of abuse, and then agricultural, household and industrial products. We observed a progressive decrease in barbiturates (54, 15 and 2%) and an increase in benzodiazepines and cyclic antidepressants. Therapeutic methods used were mostly gastric lavage (64%), activated charcoal (35%), forced diuresis (43%), extracorporeal therapy (11%) and antidotes. The mortality rate fluctuated between 6.4 and 9.1%, being significantly higher with poisoning by non-therapeutic drugs. In conclusion, the most common poisoning admitted to our ICUs was by psychoactive drugs in suicide attempts. We observed the under-use of activated charcoal and an excessive usage of kidney and extracorporeal methods. The prognosis was worse for poisonings with non-therapeutic drugs.

  5. Acute toxicity of some synthetic cyanogens in rats: time-dependent cyanide generation and cytochrome oxidase inhibition in soft tissues after sub-lethal oral intoxication.

    PubMed

    Rao, Pooja; Singh, Poonam; Yadav, Shiv Kumar; Gujar, Niranjan L; Bhattacharya, Rahul

    2013-09-01

    Cyanogens include complex nitrile-containing compounds that can generate free cyanide of toxicological significance. Acute toxicity, time-dependent cyanide generation and cytochrome oxidase (CYTOX) inhibition in soft tissues, and urinary thiocyanate levels were measured after acute cyanogen intoxication in rats. Order of cyanogens in terms of LD₅₀ was: malononitrile (MCN)>propionitrile (PCN)≈sodium nitroprusside (SNP)>acrylonitrile (ACN)>succinonitrile (SCN)>acetonitrile (ATCN) for oral, and SNP>MCN>ACN>PCN>SCN>ATCN for intraperitoneal and subcutaneous routes. MCN was most toxic by oral (LD₅₀=66.4 mg/kg) and SNP by intraperitoneal (LD₅₀=16.7 mg/kg) and subcutaneous (LD₅₀=11.9 mg/kg) routes. Minimum survival time (25 min) was recorded after 4.0 LD₅₀ ATCN. Order of cyanogens (0.75 LD₅₀; oral) on the basis of maximum blood cyanide and time of peak cyanide generation were: ATCN>SNP>SCN>PCN>MCN>ACN, and MCN (30 min)cyanide generation correlated with corresponding CYTOX inhibition and urinary thiocyanate levels. With the understanding of time-dependent toxicity of different cyanogens, suitable therapeutic windows can be designed for their management.

  6. [The significance of ethanolemia for the diagnosis of death from acute ethanol poisoning].

    PubMed

    Kapustin, A V; Panfilenko, O A; Serebriakova, V G

    2002-01-01

    Foci of myolysis of cardiac muscle fibers are suggested to be used for evaluation of thanatogenetic significance of ethanol concentration in cadaveric blood. This sign of acute ethanol poisoning is absent in case of other cause of death in a state of ethanol intoxication, even in the presence of high ethanolemia. Therefore, foci of myolysis are a sign of ethanol tolerance.

  7. The effects of acute hydrogen sulfide poisoning on cytochrome P450 isoforms activity in rats.

    PubMed

    Wang, Xianqin; Chen, Mengchun; Chen, Xinxin; Ma, Jianshe; Wen, Congcong; Pan, Jianchun; Hu, Lufeng; Lin, Guanyang

    2014-01-01

    Hydrogen sulfide (H2S) is the second leading cause of toxin related death (after carbon monoxide) in the workplace. H2S is absorbed by the upper respiratory tract mucosa, and it causes histotoxic hypoxemia and respiratory depression. Cocktail method was used to evaluate the influences of acute H2S poisoning on the activities of cytochrome P450 isoforms CYP2B6, CYP2D6, CYP3A4, CYP1A2, CYP2C19, and CYP2C9, which were reflected by the changes of pharmacokinetic parameters of six specific probe drugs, bupropion, metoprolol, midazolam, phenacetin, omeprazole, and tolbutamide, respectively. The experimental rats were randomly divided into two groups, control group and acute H2S poisoning group (inhaling 300 ppm for 2 h). The mixture of six probes was given to rats by oral administration and the blood samples were obtained at a series of time points through the caudal vein. The concentrations of probe drugs in rat plasma were measured by LC-MS. The results for acute H2S poisoning and control groups were as follows: there was a statistically significant difference in the AUC and C max for bupropion, metoprolol, phenacetin, and tolbutamide, while there was no statistical pharmacokinetic difference for midazolam and omeprazole. Acute H2S poisoning could inhibit the activity of CYP2B6, CYP2D6, CYP1A2, and CYP2C9 in rats.

  8. Toxicological and clinical aspects of cyanide metabolism.

    PubMed

    Baumeister, R G; Schievelbein, H; Zickgraf-Rüdel, G

    1975-07-01

    This contribution deals with the occurrence of cyanide and its biological pathways in the body. Especially possibilities of detoxification are pointed out. Intoxications are caused by acute and chronical cyanide uptake. Tobacco amblyopia, retrobulbar neuritis in pernicious anaemia, Leber's optic atrophy, Nigerian nutritional neuropathy, and sterility in female heavy smokers are attributed to cyanide intoxication. Various methods for treating acute and chronic cyanide intoxication are discussed.

  9. An epidemiological study of acute carbon monoxide poisoning in the West Midlands

    PubMed Central

    Wilson, R. C.; Saunders, P. J.; Smith, G.

    1998-01-01

    OBJECTIVES: To describe the epidemiology of carbon monoxide (CO) poisoning in a defined population, identifying those at greatest risk from acute poisoning resulting in admission to hospital or death. METHODS: A retrospective study with routinely collected information, set in the former West Midlands Regional Health Authority; population of 5.2 million. The data comprised 939 deaths and 701 hospital admissions due to CO poisoning between January 1988 to December 1994. The main outcome measures were age and sex standardised incidence rates (SIRs) for non-intentional, suicidal, and undetermined poisonings for health authorities and the linear relation with socioeconomic deprivation. RESULTS: Overall rate of non-intentional poisonings over the 7 year period was 7.6/100,000, an annual rate of 1.1/100,000. The 7 year rates were highest in people > or = 85; men 24.0/100,000 and women 19.7/100,000. For suicides the 7 year rate was 19.6/100,000, an annual rate of 2.8/100,000. The 7 year rates were highest for men of 35-39, 64.1/100,000, and for women aged 45-49, 15.3/100,000. None of the causes of poisoning were related to deprivation. Non-intentional poisonings showed a strong seasonal variation with the highest rates being recorded in the months October to March. Increased rates of poisoning were found in the rural districts of the West Midlands. There seems to have been a decline in suicides coinciding with the introduction of three way catalytic converters on cars. CONCLUSIONS: Elderly people and the very young are at the greatest risk from non- intentional CO poisoning and rates are highest in the winter months. Although deaths from non-intentional CO poisoning are declining nationally, in the West Midlands they have remained stable and hospital admissions are increasing. It is not solely an urban phenomenon with rates for non-intentional CO poisoning and suicides higher in the rural districts. Health authorities need to consider all populations in any prevention

  10. Respiratory failure induced by acute organophosphate poisoning in rats: effects of vagotomy.

    PubMed

    Gaspari, Romolo J; Paydarfar, David

    2009-03-01

    Acute organophosphate (OP) poisoning causes respiratory failure through two mechanisms: central apnea and pulmonary dysfunction. The vagus nerve is involved in both the central control of respiratory rhythm as well as the control of pulmonary vasculature, airways and secretions. We used a rat model of acute OP poisoning with and without a surgical vagotomy to explore the role of the vagus in OP-induced respiratory failure. Dichlorvos (2,2-dichlorovinyl dimethyl phosphate) injection (100mg/kg subcutaneously, 3 x LD50) resulted in progressive hypoventilation and apnea in all animals, irrespective of whether or not the vagi were intact. However, vagotomized animals exhibited a more rapidly progressive decline in ventilation and oxygenation. Artificial mechanical ventilation initiated at onset of apnea resulted in improvement in oxygenation and arterial pressure in poisoned animals with no difference between vagus intact or vagotomized animals. Our observations suggest that vagal mechanisms have a beneficial effect during the poisoning process. We speculate that vagally mediated feedback signals from the lung to the brainstem serve as a modest protective mechanism against central respiratory depressive effects of the poison and that bulbar-generated efferent vagal signals do not cause sufficient pulmonary dysfunction to impair pulmonary gas exchange.

  11. Acute pesticide poisoning and pesticide registration in Central America

    SciTech Connect

    Wesseling, Catharina . E-mail: cwesseli@una.ac.cr; Corriols, Marianela; Bravo, Viria

    2005-09-01

    The International Code of Conduct on the Distribution and Use of Pesticides of the Food and Agriculture Organization (FAO) of the United Nations has been for 20 years the most acknowledged international initiative for reducing negative impact from pesticide use in developing countries. We analyzed pesticide use and poisoning in Central America, particularly in Costa Rica and Nicaragua, and evaluated whether registration decisions are based on such data, in accordance with the FAO Code. Extensive use of very hazardous pesticides continues in Central America and so do poisonings with organophosphates, carbamates, endosulfan and paraquat as the main causative agents. Central American governments do not carry out or commission scientific risk assessments. Instead, guidelines from international agencies are followed for risk management through the registration process. Documentation of pesticide poisonings during several decades never induced any decision to ban or restrict a pesticide. However, based on the official surveillance systems, in 2000, the ministers of health of the seven Central American countries agreed to ban or restrict twelve of these pesticides. Now, almost 4 years later, restrictions have been implemented in El Salvador and in Nicaragua public debate is ongoing. Chemical and agricultural industries do not withdraw problematic pesticides voluntarily. In conclusion, the registration processes in Central America do not comply satisfactorily with the FAO Code. However, international regulatory guidelines are important in developing countries, and international agencies should strongly extend its scope and influence, limiting industry involvement. Profound changes in international and national agricultural policies, steering towards sustainable agriculture based on non-chemical pest management, are the only way to reduce poisonings.

  12. Follow-up after acute poisoning by substances of abuse: a prospective observational cohort study

    PubMed Central

    Vallersnes, Odd Martin; Jacobsen, Dag; Ekeberg, Øivind; Brekke, Mette

    2016-01-01

    Objective To chart follow-up of patients after acute poisoning by substances of abuse, register whether patients referred to specialist health services attended, and whether patients contacted a general practitioner (GP) after the poisoning episode. Design Observational cohort study. Setting A primary care emergency outpatient clinic in Oslo, Norway. Subjects Patients ≥12 years treated for acute poisoning by substances of abuse were included consecutively from October 2011 to September 2012. Main outcome measures Follow-up initiated at discharge, proportion of cases in which referred patients attended within three months, and proportion of cases in which the patient consulted a GP the first month following discharge. Results There were 2343 episodes of acute poisoning by substances of abuse. In 391 (17%) cases the patient was hospitalised, including 49 (2%) in psychiatric wards. In 235 (10%) cases the patient was referred to specialist health services, in 91 (4%) advised to see their GP, in 82 (3%) to contact social services, in 74 (3%) allotted place in a homeless shelter, and in 93 (4%) other follow-up was initiated. In 1096 (47%) cases, the patient was discharged without follow-up, and in a further 324 (14%), the patient self-discharged. When referred to specialist health services, in 200/235 (85%) cases the patient attended within three months. Among all discharges, in 527/1952 (27%) cases the patient consulted a GP within one month. When advised to see their GP, in 45/91 (49%) cases the patient did. Conclusion Attendance was high for follow-up initiated after acute poisoning by substances of abuse. Key Points Despite poor long-term prognosis, patients treated for acute poisoning by substances of abuse are frequently not referred to follow-up.Nearly all patients referred to specialist health services attended, indicating the acute poisoning as an opportune moment for intervention.Advising patients to contact their GP was significantly associated with

  13. N-acetylcysteine in Acute Organophosphorus Pesticide Poisoning: A Randomized, Clinical Trial.

    PubMed

    El-Ebiary, Ahmad A; Elsharkawy, Rasha E; Soliman, Nema A; Soliman, Mohammed A; Hashem, Ahmed A

    2016-08-01

    Organophosphorus poisoning is a major global health problem with hundreds of thousands of deaths each year. Research interest in N-acetylcysteine has grown among increasing evidence of the role of oxidative stress in organophosphorus poisoning. We aimed to assess the safety and efficacy of N-acetylcysteine as an adjuvant treatment in patients with acute organophosphorus poisoning. This was a randomized, controlled, parallel-group trial on 30 patients suffering from acute organophosphorus poisoning, who were admitted to the Poison Control Center of Tanta University Emergency Hospital, Tanta, Egypt, between April and September 2014. Interventions included oral N-acetylcysteine (600 mg three times daily for 3 days) as an added treatment to the conventional measures versus only the conventional treatment. Outcome measures included mortality, total dose of atropine administered, duration of hospitalization and the need for ICU admission and/or mechanical ventilation. A total of 46 patients were screened and 30 were randomized. No significant difference was found between both groups regarding demographic characteristics and the nature or severity of baseline clinical manifestations. No major adverse effects to N-acetylcysteine therapy were reported. Malondialdehyde significantly decreased and reduced glutathione significantly increased only in the NAC-treated patients. The patients on NAC therapy required less atropine doses than those who received only the conventional treatment; however, the length of hospital stay showed no significant difference between both groups. The study concluded that the use of N-acetylcysteine as an added treatment was apparently safe, and it reduced atropine requirements in patients with acute organophosphorus pesticide poisoning.

  14. Work-related risk factors by severity for acute pesticide poisoning among male farmers in South Korea.

    PubMed

    Kim, Ji-Hyun; Kim, Jaeyoung; Cha, Eun Shil; Ko, Yousun; Kim, Doo Hwan; Lee, Won Jin

    2013-03-14

    The objective of this study was to explore work-related risk factors of acute occupational pesticide poisoning among male farmers according to the severity of the poisoning. A nationwide sampling survey of male farmers was conducted in South Korea in 2011. A total of 1,958 male farmers were interviewed. Severity of occupational pesticide poisoning in 2010 was evaluated according to symptoms, types of treatment, and number of pesticide poisoning incidents per individual. A multinomial logistic regression model was used to estimate the odds ratio with 95% confidence intervals for risk factors of acute occupational pesticide poisoning. We found that the risk of acute occupational pesticide poisoning increased with lifetime days of pesticide application (OR = 1.74; 95% CI = 1.32-2.29), working a farm of three or more acres in size (OR = 1.49), not wearing personal protective equipment such as gloves (OR = 1.29) or masks (OR = 1.39). Those who engaged in inappropriate work behaviors such as not following pesticide label instructions (OR = 1.61), applying the pesticide in full sun (OR = 1.48), and applying the pesticide upwind (OR = 1.54) had a significantly increased risk of pesticide poisoning. There was no significant risk difference by type of farming. In addition, the magnitude of these risk factors did not differ significantly by severity of acute pesticide poisoning. In fact, our findings suggest that work-related risk factors contributed to the development of acute occupational pesticide poisoning without relation to its severity. Therefore, prevention strategies for reducing occupational pesticide poisoning, regardless of severity, should be recommended to all types of farming and the level of poisoning severity.

  15. [Acute carbon monoxide poisoning after water pipe tobacco smoking].

    PubMed

    Paulsen, Jakob Felbo; Villads, Kasper von Rosen; Sonne, Morten Egede

    2016-12-05

    Carbon monoxide poisoning is potentially lethal, and early recognition and treatment is essential. An 18-year-old man was admitted due to syncope and a carboxyhaemoglobin level of 17% after water pipe tobacco smoking. He received normo- and hyperbaric oxygen as treatment and was discharged after two days without neurological sequelae. This case is the first in Denmark, but recently seven similar cases have been reported. The number of young people smoking water pipe tobacco is increasing, and we fear that more cases like this will occur in the future.

  16. Acute ammonium dichromate poisoning in a 2 year-old child.

    PubMed

    Sunilkumar, Menon Narayanankutty; Ajith, Thekkuttuparambil Ananthanarayanan; Parvathy, Vadakut Krishnan

    2014-11-01

    Hexavalent chromium compounds are most commonly used in printing, dyeing, plastics and rayon manufacturing. Poisoning in children by ammonium dichromate, an odorless and bright orange-red crystal, are rarely reported. Acute poisoning will result in death due to multi-organ failure. The target organs that are affected by this poison are the respiratory system, kidneys, liver, eyes and skin. On ingestion, initially there is a relative lack of severe symptoms and signs. Hence, the delay in seeking medical attention could lead to the increased rate of mortality. In this case study, we report the ingestion of ammonium dichromate by a child. Despite appropriate management, such as hepatic supportive measures and plasma transfusion, the toxicity progressed to multi-organ failure and death.

  17. Acute liver failure caused by mushroom poisoning: a case report and review of the literature.

    PubMed

    Erden, Abdulsamet; Esmeray, Kübra; Karagöz, Hatice; Karahan, Samet; Gümüşçü, Hasan Hüseyin; Başak, Mustafa; Cetinkaya, Ali; Avcı, Deniz; Poyrazoğlu, Orhan Kürşat

    2013-01-01

    It is estimated that there are over 5,000 species of mushrooms worldwide. Some of them are edible and some are poisonous due to containing significant toxins. In more than 95% of mushroom toxicity cases, poisoning occurs as a result of misidentification of the mushroom by an amateur mushroom hunter. The severity of mushroom poisoning may vary, depending on the geographic location where the mushroom is grown, growth conditions, the amount of toxin delivered, and the genetic characteristics of the mushroom. Amanita phalloides is the most common and fatal cause of mushroom poisoning. This mushroom contains amanitins, which are powerful hepatotoxins that inhibit RNA polymerase II in liver. Mushroom poisoning is a relatively rare cause of acute liver failure. A 63-year-old male patient was admitted to the emergency room with weakness, nausea, vomiting, and diarrhea. He reported ingesting several wild mushrooms about 36 hours earlier. In this article we report a case of lethal Amanita phalloides intoxication from stored mushrooms.

  18. Profile of adult acute cholinesterase inhibitors substances poisoning – a 30 years analysis

    PubMed Central

    Gazzi, Eugen N.; Jaba, Irina M.; Lionte, Catalina; Bologa, Cristina; Lupusoru, Catalina E.; Lupusoru, Raoul; Sorodoc, Laurentiu; Petris, Ovidiu

    2015-01-01

    Objectives The objective of this study was to assess the pattern and outcome of acute cholinesterase inhibitors substances (CIS) poisoning cases, in a cohort from a regional tertiary care hospital. Methods cases admitted in the Toxicology Clinic of “Sf. Spiridon” Emergency Clinic Hospital Iasi, Romania between 1983 and 2013 were studied. Results a total number of 606 patients were included. The reason for exposures was intentional in 70% of cases and the commonest route of poisoning was oral in 92.2%. The highest percent of cases was females (56.4), the age group 20–29 (25.4%) and the majority (66.7%) coming from rural areas, 28.2% being agricultural workers. 36.6% of cases were severe clinical forms. Overall mortality rates were 3.8%, more than half of the death patients (65.2%) had concomitant alcohol intake. It was a significant statistical association between decrease level of serum cholinesterase on admittance and severe forms (p 0.000) and between survival and deaths groups (p 0.000). The pattern of poisoning described by our retrospective study suggests that CIS poisoning are mainly preventable. The main effective goals for prevention are restriction in free accessibility to toxic pesticides, together with sustained efforts in education concerning the life-threatening danger of pesticide poisoning. PMID:28352706

  19. Acute lead poisoning in western Canadian cattle - A 16-year retrospective study of diagnostic case records.

    PubMed

    Cowan, Vanessa; Blakley, Barry

    2016-04-01

    This study describes the epidemiology of acute lead poisoning in western Canadian cattle over the 16-year period of 1998 to 2013 and reports background bovine tissue lead concentrations. Case records from Prairie Diagnostic Services, Western College of Veterinary Medicine, identified 525 cases of acute lead toxicity over the investigational period. Poisonings were influenced by year (P < 0.0001) and month (P < 0.0001). Submissions were highest in 2009 (15.6%), 2001 (11.2%), and 2006 (9.9%). Most cases were observed during May, June, and July (62.3%). Cattle 6 months of age and younger were frequently poisoned (53.5%; P < 0.0001). Beef breeds were predominantly poisoned. Mean toxic lead concentrations (mg/kg wet weight) in the blood, liver, and kidney were 1.30 ± 1.70 (n = 301), 33.5 ± 80.5 (n = 172), and 56.3 ± 39.7 (n = 61). Mean normal lead concentrations in the blood, liver, and kidney were 0.036 ± 0.003 mg/kg (n= 1081), 0.16 ± 0.63 mg/kg (n = 382), and 0.41 ± 0.62 mg/kg (n = 64).

  20. Is there a role for progesterone in the management of acute organophosphate poisoning during pregnancy?

    PubMed

    Jafarzadeh, Mostafa; Nasrabadi, Zeynab Nasri; Sheikhazadi, Ardeshir; Abbaspour, Abdollah; Vasigh, Shayesteh; Yousefinejad, Vahid; Marashi, Sayed Mahdi

    2013-06-01

    Organophosphates are commonly used pesticides and cause about one million unintentional and 2 million suicidal exposures with up to 300,000 fatalities every year around the world. Toxicity of organophosphates is due to inhibition cholinesterase activity and prolonging the effects of acetylcholine in the receptor site. Clinical features of organophosphate poisoning are defecation, urination, miosis, bronchorrhea, emesis, lacrimation and salivation. Spontaneous abortion reported some when in pregnant patients. Intravenous administration of benzodiazepines, atropine and pralidoxime is the formal treatment of this toxicity. Atropine and pralidoxime have been assigned to pregnancy class C by the FDA and should be recommended for use in pregnant women clinically suffer organophosphate poisoning. Benzodiazepines have been assigned to pregnancy class D and should be avoided during pregnancy. Clinical experiments suggest transplacental transfer of organophosphates is possible, and fetal sensitivity is probable, but a single acute overdose most likely don't make any physical deformities, therefore termination of pregnancy is not imperative. Nonetheless, no definite strategy focused on maintaining pregnancy. Here we propose an idea that in any female case of acute organophosphate poisoning in childbearing range of age, maternal serum Beta-HCG should be tested for pregnancy and prophylactic progesterone should be used in pregnant cases of organophosphate poisoning.

  1. In vitro and in vivo comparison of sulfur donors as antidotes to acute cyanide intoxication.

    PubMed

    Baskin, S I; Porter, D W; Rockwood, G A; Romano, J A; Patel, H C; Kiser, R C; Cook, C M; Ternay, A L

    1999-01-01

    Antidotes for cyanide (CN) intoxication include the use of sulfane sulfur donors (SSDs), such as thiosulfate, which increase the conversion of CN to thiocyanate by the enzyme rhodanese. To develop pretreatments that might be useful against CN, SSDs with greater lipophilicity than thiosulfate were synthesized and assessed. The ability of SSDs to protect mice against 2LD50 of sodium cyanide (NaCN) administered either 15 or 60 min following administration of an SSD was assessed. To study the mechanism of action of the SSD, the candidate compounds were examined in vitro for their effect on rhodanese and 3-mercaptopyruvate sulfurtransferase (MST) activity under increasing SSD concentrations. Tests were conducted on nine candidate SSDs: ICD1021 (3-hydroxypyridin-2-yl N-[(N-methyl-3-aminopropyl)]-2-aminoethyl disulfide dihydrochloride), ICD1022, (3-hydroxypyridin-2-yl N-[(N-methyl-3-aminopropyl)]-2-aminoethyl disulfide trihydrochloride), ICD1584 (diethyl tetrasulfide), ICD1585 (diallyl tetrasulfide), ICD1587 (diisopropyl tetrasulfide); ICD1738 (N-(3-aminopropyl)-2-aminoethyl 2-oxopropyl disulfide dihydrochloride), ICD1816 (3,3'-tetrathiobis-N-acctyl-L-alanine), ICD2214 (2-aminoethyl 4-methoxyphenyl disulfide hydrochloride) and ICD2467 (bis(4-methoxyphenyl) disulfide). These tests demonstrated that altering the chemical substituent of the longer chain sulfide modified the ability of the candidate SSD to protect against CN toxicity. At least two of the SSDs at selected doses provided 100% protection against 2LD50 of NaCN, normally an LD99. All compounds were evaluated using locomotor activity as a measure of potential adverse behavioral effects. Positive hypoactivity relationships were found with several disulfides but none was found with ICD1584, a tetrasulfide. Separate studies suggest that the chemical reaction of potassium cyanide (KCN) and cystine forms the toxic metabolite 2-iminothiazolidine-4-carboxylic acid. An alternative detoxification pathway, one not primarily

  2. Pseudolaminar necrosis in cyanide intoxication: a neuropathology case report.

    PubMed

    Riudavets, Miguel Angel; Aronica-Pollak, Patricia; Troncoso, Juan C

    2005-06-01

    We describe the gross and microscopic neuropathological changes in the brain of a 17-year-old male who died 4 days after being poisoned with cyanide. Previous reports indicate that following cyanide intoxication, the brain develops diffuse hypoxic/ischemic changes, predominantly of the basal ganglia. The case we describe here had similar features but in addition showed striking laminar necrosis of the cerebral cortex. This finding in cyanide poisoning has been previously demonstrated by neuroimaging, but not pathologically.

  3. Anticholinesterase poisoning of birds: Field monitoring and diagnosis of acute poisoning

    USGS Publications Warehouse

    Hill, E.F.; Fleming, W.J.

    1982-01-01

    Organophosphorus and carbamate pesticides are cholinesterase (ChE) inhibiting chemicals that have been responsible for avian die-offs. Identification of chemicals implicated in these die-offs is difficult and sometimes conclusions are solely circumstantial. However, when marked depression (inhibition) of brain ChE activity accompanies organophosphorus or carbamate residues in body tissues or ingesta, cause-effect diagnosis is enhanced. To achieve this end, normal brain ChE activity is estimated for controls of the affected species and then die-off specimens are individually evaluated for evidence of ChE inhibition. This approach to evaluation of antiChE poisoning may also be used to monitor exposure of vertebrates to field application of organophosphorus or carbamate pesticides. Problems associated with this kind of evaluation, and the main topic of this report, include variability of brain ChE activity among species, postmortem influences of ambient conditions (storage or field) on ChE activity, and differential patterns of ChE activity when inhibited by organophosphorus or carbamate compounds. Other topics discussed are the ChE assay procedure, example case reports and interpretation, and research needed for improving the diagnostic utility of ChE activity in a field situation.

  4. Evaluation of brain function in acute carbon monoxide poisoning with multimodality evoked potentials

    SciTech Connect

    He, Fengsheng; Liu, Xibao; Yang, Shi; Zhang, Shoulin ); Xu, Guanghua; Fang, Guangchai; Pan, Xiaowen )

    1993-02-01

    The median nerve somatosensory evoked potentials (SEP), pattern reversal visual evoked potentials (VEP), and brain stem auditory evoked potentials (BAEP) were studied in 109 healthy adults and in 88 patients with acute carbon monoxide (CO) poisoning. The upper limits for normal values of peak and interpeak latencies of multimodalities of evoked potentials in the reference group were established by a stepwise multiple regression analysis. SEP changes selectively affecting N32 and N60 were found in 78.8% of patients. There was prolonged PI00 latency of VEP in 58.2% of the cases examined. The prevalence of BAEP abnormalities in comatose patients (36%) was significantly higher than that (8.6%) in conscious patients. BAEP abnormalities were most frequently seen in comatose patients who had diminished brain stem reflexes (77.8%). It has been found that a consistent abnormality involving N2O and subsequent peaks in SEP, a remarkable prolongation of PI00 latency in VEP, or a prolongation of Ill-V interpeak latency in BAEP as well as the reoccurrence of evoked potential abnormalities after initial recovery all indicate unfavorable outcomes in patients with acute CO poisoning. The multimodality evoked potentials have proved to be sensitive indicators in the evaluation of brain dysfunction and in the prediction of prognosis of acute CO poisoning and the development of delayed encephalopathy. 16 refs., 4 figs., 6 tabs.

  5. Intraosseous Versus Intravenous Infusion of Hydroxocobalamin for the Treatment Of Acute Severe Cyanide Toxicity in a Swine Model

    DTIC Science & Technology

    2014-11-01

    to smoke inhalation during fires involving many victims. Hydroxocobalamin has proven to be an effective antidote, but cannot be given intramuscularly...car-diac arrest in 50% of cyanide-exposed patients.1,2 In addition, smoke inhalation has produced toxic cyanide levels in over 30% of patients who...died after smoke inhalation .2–4 Hydroxocobalamin is approved by the U.S. Food and Drug Administration for the treatment of cyanide toxic- ity. We have

  6. Ammonium dichromate poisoning: A rare cause of acute kidney injury.

    PubMed

    Radhakrishnan, H; Gopi, M; Arumugam, A

    2014-11-01

    Ammonium dichromate is an inorganic compound frequently used in screen and color printing. Being a strong oxidizing agent, it causes oxygen free radical injury resulting in organ failure. We report a 25-year-old female who presented with acute kidney injury after consumption of ammonium dichromate. She was managed successfully with hemodialysis and supportive measures. This case is reported to highlight the toxicity of ammonium dichromate.

  7. Prediction and validation of hemodialysis duration in acute methanol poisoning.

    PubMed

    Lachance, Philippe; Mac-Way, Fabrice; Desmeules, Simon; De Serres, Sacha A; Julien, Anne-Sophie; Douville, Pierre; Ghannoum, Marc; Agharazii, Mohsen

    2015-11-01

    The duration of hemodialysis (HD) in methanol poisoning (MP) is dependent on the methanol concentration, the operational parameters used during HD, and the presence and severity of metabolic acidosis. However, methanol assays are not easily available, potentially leading to undue extension or premature termination of treatment. Here we provide a prediction model for the duration of high-efficiency HD in MP. In a retrospective cohort study, we identified 71 episodes of MP in 55 individuals who were treated with alcohol dehydrogenase inhibition and HD. Four patients had residual visual abnormality at discharge and only one patient died. In 46 unique episodes of MP with high-efficiency HD the mean methanol elimination half-life (T1/2) during HD was 108 min in women, significantly different from the 129 min in men. In a training set of 28 patients with MP, using the 90th percentile of gender-specific elimination T1/2 (147 min in men and 141 min in women) and a target methanol concentration of 4 mmol/l allowed all cases to reach a safe methanol of under 6 mmol/l. The prediction model was confirmed in a validation set of 18 patients with MP. High-efficiency HD time in hours can be estimated using 3.390 × (Ln (MCi/4)) for women and 3.534 × (Ln (MCi/4)) for men, where MCi is the initial methanol concentration in mmol/l, provided that metabolic acidosis is corrected.

  8. Prevalence of pulmonary edema among the deceased cases with acute Methadone poisoning: A report from Iran

    PubMed Central

    Eizadi-Mood, Nastaran; Naeini, Seyed Amir Hossein Madani; Hedaiaty, Mahrang; Sabzghabaee, Ali Mohammad; Moudi, Maryam

    2016-01-01

    Objective: Methadone poisoning is common in our society, mainly in drug addicts. One of its lethal complications is pulmonary edema. Therefore, we evaluated the prevalence of pulmonary edema in the deceased cases with methadone poisoning and its possible relationship with some medical variables. Methods: In this cross-sectional study which was done in 2014, we have investigated the deceased patients with methadone toxicity who underwent autopsy at Isfahan Forensic Medicine Department (Iran). All variables including age, gender, and autopsy findings were recorded and analyzed. Demographic characteristics and medical complications of the patients were compared between the patients with or without pulmonary edema in the autopsy findings. Findings: There were 64 cases who died with methadone poisoning during the 1-year study period. The average age of cases (±standard deviation) was 32.1 ± 10.29 years, among which 92.2% were male. Based on the autopsy findings, 64.1% were diagnosed with pulmonary edema. There was no statistically significant relationship between pulmonary edema and age, gender, history of addiction, and hepatic or cardiovascular complications. Conclusion: Pulmonary edema is a common finding in deceased methadone poisoning cases and must be considered and ruled out in patients with acute methadone toxicity. PMID:27843967

  9. Acute collective gas poisoning at work in a manure storage tank.

    PubMed

    Żaba, Czesław; Marcinkowski, Jerzy T; Wojtyła, Andrzej; Tężyk, Artur; Tobolski, Jarosław; Zaba, Zbigniew

    2011-01-01

    Cases of deaths in manure or septic tanks are rare in legal-medical practice, more frequently as unfortunate occupational accidents. Poisoning with toxic gases, especially with hydrogen sulfide, is reported as the cause of death, while the exhaustion of oxygen in the air is omitted with the simultaneous excess of carbon dioxide. In such cases, determination of the direct cause of death constitutes a big problem because post-mortem examination does not reveal the specific changes. A case of acute collective poisoning by gases in a manure storage tank is presented of 5 agricultural workers, 2 of whom died. While explaining the cause of poisoning and deaths, toxicological blood tests were performed in the victims of the accident, as well as gases inside the manure storage tank. The post-mortem examinations and toxicological blood tests performed did not allow determination of the direct cause of death. Toxicological tests of gases from inside the manure tank showed a very low concentration of oxygen, with a simultaneous very high concentration of carbon dioxide, and a considerable level of hydrogen sulfide. The cause of fainting of three and deaths of two workers was not the poisoning with hydrogen sulfide, but oxygen deficiency in the air of the tank.

  10. The characteristics of emergency department presentations related to acute herbicide or insecticide poisoning in South Korea between 2011 and 2014.

    PubMed

    Moon, Jeong Mi; Chun, Byeong Jo; Cho, Yong Soo

    2016-01-01

    The aim of this study was to examine epidemiologic data regarding acute herbicide or insecticide poisoning in adults from 2011 to 2014 at the national level in South Korea. Further, the association between governmental regulations involving pesticides and changes in pesticide poisoning occurrences over time was determined. Data were obtained from the emergency department (ED)-based Injury In-depth Surveillance system conducted by the Korea Center for Disease Control and Prevention (KCDC). Governmental regulations on pesticides were downloaded from the homepage of the Korea Rural Development Administration. Pesticides were classified according to guidelines provided by the World Health Organization (WHO) and by the respective Resistance Action Committee (RAC). Trends in the number of ED presentations and case fatality rate (CFR) due to pesticide poisoning were investigated. The overall CFR due to poisoning from herbicides or insecticides in adults in South Korea was 16.8% during 2011-2014. However, CFR significantly decreased over the 4-year period. The ED presentations of paraquat (PQ) poisoning fell significantly, whereas poisoning due to glyphosate, glufosinate, or combined herbicides increased markedly over the 4 years. Between 2011 and 2013, PQ was the most common pesticide poisoning, whereas glyphosate became the most frequent in 2014. PQ produced the highest rate of fatality followed by endosulfan. Although the frequency of PQ poisoning decreased, which may be attributed to governmental regulations, the CFR and incidence of pesticide poisoning in adults remain a public health concern that needs to be addressed.

  11. Fresh frozen plasma as a successful antidotal supplement in acute organophosphate poisoning.

    PubMed

    Vučinić, Slavica; Zlatković, Milica; Antonijević, Biljana; Ćurčić, Marijana; Bošković, Bogdan

    2013-06-01

    Despite improvements to intensive care management and specific pharmacological treatments (atropine, oxime, diazepam), the mortality associated with organophosphate (OP) poisoning has not substantially decreased. The objective of this examination was to describe the role of fresh frozen plasma (FFP) in acute OP poisoning. After a deliberate ingestion of malathion, a 55-year-old male suffering from miosis, somnolence, bradycardia, muscular fasciculations, rales on auscultation, respiratory insufficiency, as well as from an inhibition of red blood cell acetylcholinesterase (AChE) and plasma butyrylcholinesterase (BuChE), was admitted to hospital. Malathion was confirmed in a concentration of 18.01 mg L(-1). Apart from supportive measures (including mechanical ventilation for four days), antidotal treatment with atropine, oxime-pralidoxime methylsulphate (Contrathion(R)), and diazepam was administered, along with FFP. The potentially beneficial effects of FFP therapy included a prompt increase of BuChE activity (from 926 IU L(-1) to 3277 IU L(-1); reference range from 7000 IU L(-1) to 19000 IU L(-1)) and a reduction in the malathion concentration, followed by clinical recovery. Due to BuChE replacement, albumin content, and volume restitution, FFP treatment may be used as an alternative approach in patients with acute OP poisoning, especially when oximes are not available.

  12. Acute mercury poisoning among children in two provinces of Turkey.

    PubMed

    Carman, Kursat Bora; Tutkun, Engin; Yilmaz, Hinc; Dilber, Cengiz; Dalkiran, Tahir; Cakir, Baris; Arslantas, Didem; Cesaretli, Yildirim; Aykanat, Selin Aktaş

    2013-06-01

    Elemental mercury exposure occurs frequently and is potentially a toxic, particularly in children. Children are often attracted to elemental mercury because of its color, density, and tendency to form beads. Clinical manifestations of elemental mercury intoxication vary depending on its form, concentration, route of ingestion, and the duration of exposure. We present data on 179 pediatric cases of elemental mercury poisoning from exposure to mercury in schools in two different provinces of Turkey. Of all patients, 160 children had both touched/played with the mercury and inhaled its vapors, while 26 children had only inhaled the mercury vapor, two children reported having tasted the mercury. The median duration of exposure was 5 min (min 1-max 100), and 11 (6 %) children were exposed to the mercury for more than 24 h at home. More than half of the children (51.9 %) were asymptomatic at admission. Headache was the most common presenting complaint. The results of physical and neurological examinations were normal in 80 (44.6 %) children. Mid-dilated/dilated pupils were the most common neurological abnormality, and this sign was present in 90 (50.2 %) children. Mercury levels were measured in 24-h urine samples daily, and it was shown that the median urinary level of mercury was 29.80 μg/L (min, 2.40 μg/L; max, 4,687 μg/L). A positive correlation was also found between the duration of exposure and urinary mercury levels (r = 0.23, p = 0.001). All patients were followed up for 6 months. On the first follow-up visit performed 1 month after discharge, the neurological examinations of all patients were normal except for those patients with peripheral neuropathy and visual field defects. On the last follow-up visit at the sixth month, only two children still experienced visual field defects. In conclusion, this study is one of the largest case series of mercury intoxication of students in schools. Elemental mercury exposure can be potentially toxic, and its

  13. Acute Self-Induced Poisoning With Sodium Ferrocyanide and Methanol Treated With Plasmapheresis and Continuous Renal Replacement Therapy Successfully

    PubMed Central

    Liu, Zhenning; Sun, Mingli; Zhao, Hongyu; Zhao, Min

    2015-01-01

    Abstract Self-induced poisoning with chemicals is one of the most commonly used suicide methods. Suicide attempts using massive pure sodium ferrocyanide and methanol are rare. This article discusses the management of acute intentional self-poisoning using sodium ferrocyanide and methanol. We present a case of acute self-induced poisoning using sodium ferrocyanide and methanol admitted to our hospital 2 hours after ingestion. He was deeply unconscious and unresponsive to painful stimuli. The laboratory findings showed acute kidney injury and severe metabolic acidosis. We took effective measures including endotracheal intubation and mechanical ventilation to ensure the vital signs were stable. Subsequently, we treated the patient using gastric lavage, bicarbonate, ethanol, plasmapheresis (plasma exchange), and continuous renal replacement therapy (CRRT) successfully. He gradually recovered from poisoning and was discharged without abnormalities on the 6th day. Follow-up for 3 months revealed no sequelae. Blood purification including plasmapheresis and CRRT is an effective method to scavenge toxicants from the body for acute self-poisoning with sodium ferrocyanide and methanol. Treatment strategies in the management of poisoning, multiple factors including the removal efficiency of toxin, the protection of vital organs, and the maintenance of homeostasis must be considered. PMID:26020397

  14. Mania following organophosphate poisoning.

    PubMed

    Mohapatra, Satyakam; Rath, Neelmadhav

    2014-11-01

    Organophosphate poisoning is the most common poisoning in developing countries. Although the acute muscarinic and nicotinic side-effects of organophosphate poisoning are well known and easily recognized, but neuropsychiatric changes are rarely reported. We are reporting a case of a 33-year-old female who developed manic episode following acute organophosphate poisoning.

  15. Hydrogen Cyanide and Cyanide Salts

    Integrated Risk Information System (IRIS)

    EPA / 635 / R - 08 / 016 F www.epa.gov / iris TOXICOLOGICAL REVIEW OF HYDROGEN CYANIDE AND CYANIDE SALTS ( CAS No . various ) In Support of Summary Information on the Integrated Risk Information System ( IRIS ) September 2010 U.S . Environmental Protection Agency Washington , DC DISCLAIMER This docu

  16. [Acute poisoning with methomyl and other pesticides in the province of Ragusa, Sicily].

    PubMed

    Miceli, G; Ravalli, P; Settimi, L; Ballard, T J; Bascherini, S

    2001-01-01

    In 1995-96, the Occupational Medicine Service of the province of Ragusa, Sicily, examined all cases of pesticide poisonings among persons seen in two local emergency departments, identifying 86 cases due to unintentional pesticide exposure. Methomyl, a highly toxic carbamate, was indicated for 51% of all cases. The most frequently reported symptoms included nausea and vomiting (48%), excessive perspiration (33%), and dyspnea (16%). Fifty-nine cases (69%) were hospitalized, 5 in intensive care. The methomyl cases occurred more frequently during summer months while the cases from all other pesticides showed no seasonal patterns. These observations point out the relevance of identifying acute pesticide poisonings in the province of Ragusa and suggest that ongoing registration of these events should be a public health priority.

  17. [Clinical symptoms and circumastances of acute poisonings with fly agaric (Amanita muscaria) and panther cap (Amanita pantherina)].

    PubMed

    Łukasik-Głebocka, Magdalena; Druzdz, Artur; Naskret, Maciej

    2011-01-01

    Mushroom poisonings in Poland are quite common, especially in summer and autumn, but fly agaric (Amanita muscaria) and panther cap (Amanita pantherina) are rather rare cause of these intoxications. Fly agaric is a cause of deliberate poisoning, whereas panther cap poisoning also happens accidentally. The main toxins of these two mushrooms are ibotenic acid (pantherine, agarine), muscimol, muscazone and muscaridine. The other bioactive substances are stizolobic and stizolobinic acids and aminodicarboxyethylthiopropanoic acids. All these compounds are responsible for diverse picture of intoxication. An analysis of patients with Amanita muscaria and Amanita pantherina poisoning hospitalized in the Poznan Departament of Toxicology revealed that symptoms occurred after 30 minutes to 2 hours with vomiting, hallucinations, restlessness, increased psychomotor drive and central nervous system depression. Other antycholinergic symptoms like tachycardia and increased blood pressure, mydriasis, dry and red skin were seen only in a few cases. Acute respiratory failure was the most dangerous symptom observed in the course of poisoning.

  18. Early Clinical Outcome of Acute Poisoning Cases Treated in Intensive Care Unit

    PubMed Central

    Sulaj, Zihni; Prifti, Edvin; Demiraj, Aurel; Strakosha, Arjana

    2015-01-01

    Introduction: A variety of factors have influenced the significant incidence of morbidity and mortality of acute poisoning and the timely recognition and properly management of critically ill poisoned patients is a key component. The aim of this study is to reveal the reasons for ICU admission of acutely poisoned patients, the main factors influencing the course and outcome of patients in relation with clinical approaches applied, available resources and infrastructure of treatment. Materials and Methods: This is a retrospective study based on most reachable variables extracted from patients’ medical records and ED registers of patients admitted at the medical ICU of “Mother Teresa” University Hospital in Tirana over two (2012-2013) years. Demography, time of exposure, etiology and circumstances of poisonings, assessment and treatment, reasons for ICU admission, course and outcome were duly obtained. Results: The number of ICU treated patients was 118, consisting in 47.4% (56) males and 52.5% (62) females which represented 10.2% of poisoned patients admitted during this two-year-period in ED and 9.2% of other etiology ICU admitted patients. Mean was 42.6 years for males, and 38 years for females. About 55.9% were urban residents and 44% rural ones. The elapsed time from toxic exposure to treatment initiation had varied between 2-6 hours, 44% arrived in the hospital <4 hours. The toxic exposures were intentional in 87.2% of cases, with a male:female ratio was 0.8:1. Agrochemicals such as Aluminum phosphide and organophosphates were involved in 77.1% of cases. Cardiovascular collapse and respiratory failure were the main clinical syndromes encountered. Mechanical ventilation was required in 31.4% of patients. The length of ICU stay was 2.73 (0.96) days and the mortality was 54.2%. Conclusion: This study evidenced that highly lethal toxicants used in poisoning acts such as agrochemicals, high rate of suicide, notwithstanding the infrastructure and resources

  19. Toxicokinetics of paraquat in Korean patients with acute poisoning

    PubMed Central

    Kim, Hak-Jae; Kim, Hyung-Ki; Lee, Hwayoung; Bae, Jun-Seok; Kown, Jun-Tack; Gil, Hyo-Wook

    2016-01-01

    To conduct a kinetic study of paraquat (PQ), we investigated 9 patients with acute PQ intoxication. All of them ingested more than 20 ml of undiluted PQ herbicide to commit suicide and arrived at our hospital early, not later than 7 h after PQ ingestion. The urine dithionite test for PQ in all of the nine patients was strongly positive at emergency room. Blood samples were obtained every 30 min for the first 2~3 h and then every 1 or 2 h, as long as the clinical progression was stable among the patients for 30 h after PQ ingestion. The area under the plasma concentration-time curve (AUCinf), which was extrapolated to infinity, was calculated using the trapezoidal rule. Toxicokinetic parameters, such as the terminal elimination half-life, apparent oral clearance, and apparent volume of distribution (Vd/F) were calculated. The maximum PQ concentration (Cmax) and the time to reach maximum PQ concentration (Tmax) were also obtained. Plasma PQ concentrations in nine patients were well described by a bi-exponential curve with a mean terminal elimination half-life of 13.1±6.8 h. Cmax and AUCinf were 20.8±25.7 mg/l and 172.5±160.3 h·mg/l, respectively. Apparent volume of distribution and apparent oral clearance were 50.9±61.3 l/kg and 173.4±111.2 l/h, respectively. There were a significant correlation (r =0.84; p<0.05) between the PQ amount ingested and Cmax. AUCinf also showed a significant correlation (r =0.83; p<0.05) with the PQ amount ingested. These correlations provide evidence that PQ has dose-linear toxicokinetic characteristics. PMID:26807021

  20. Impairment of striatal mitochondrial function by acute paraquat poisoning.

    PubMed

    Czerniczyniec, Analía; Lanza, E M; Karadayian, A G; Bustamante, J; Lores-Arnaiz, S

    2015-10-01

    Mitochondria are essential for survival. Their primary function is to support aerobic respiration and to provide energy for intracellular metabolic pathways. Paraquat is a redox cycling agent capable of generating reactive oxygen species. The aim of the present study was to evaluate changes in cortical and striatal mitochondrial function in an experimental model of acute paraquat toxicity and to compare if the brain areas and the molecular mechanisms involved were similar to those observed after chronic exposure. Sprague-Dawley rats received paraquat (25 mg/Kg i.p.) or saline and were sacrificed after 24 h. Paraquat treatment decreased complex I and IV activity by 37 and 21 % respectively in striatal mitochondria. Paraquat inhibited striatal state 4 and state 3 KCN-sensitive respiration by 80 % and 62 % respectively, indicating a direct effect on respiratory chain. An increase of 2.2 fold in state 4 and 2.3 fold in state 3 in KCN-insensitive respiration was observed in striatal mitochondria from paraquat animals, suggesting that paraquat redox cycling also consumed oxygen. Paraquat treatment increased hydrogen peroxide production (150 %), TBARS production (42 %) and cardiolipin oxidation/depletion (12 %) in striatal mitochondria. Also, changes in mitochondrial polarization was induced after paraquat treatment. However, no changes were observed in any of these parameters in cortical mitochondria from paraquat treated-animals. These results suggest that paraquat treatment induced a clear striatal mitochondrial dysfunction due to both paraquat redox cycling reactions and impairment of the mitochondrial electron transport, causing oxidative damage. As a consequence, mitochondrial dysfunction could probably lead to alterations in cellular bioenergetics.

  1. On the mechanisms underlying poisoning-induced rhabdomyolysis and acute renal failure.

    PubMed

    Talaie, Haleh; Emam-Hadi, Mohammad; Panahandeh, Reyhaneh; Hassanian-Moghaddam, Hosein; Abdollahi, Mohammad

    2008-01-01

    ABSTRACT The clinical syndrome of rhabdomyolysis is caused by injury of skeletal muscles resulting in release of intracellular muscle constituents. Drug poisoning is one of the causes of severe rhabdomyolysis. Severe electrolyte disorders and acute renal failure may occur in rhabdomyolysis, leading to life-threatening situations. Early initiation of renal replacement therapy can help improve outcome. In the present retrospective study, medical records of 181 patients suspected of rhabdomyolysis from Loghman-Hakim Hospital in the period of 2004 to 2005 were reviewed. A creatinine phosphokinase (CPK) value of greater than five times normal (>/=975 IU/L) was the basis for confirmation of a rhabdomyolysis diagnosis. An increased serum creatinine level of more than 30% was the basis for acute renal failure diagnosis. Out of 156 patients, 100 were male with an age range of 13 to 78 years. One hundred and two (92%) patients had CPK >975 U/L, and 36 patients (28.6%) had a 30% or more increase in their creatinine level during their admission days. Mean fluid intake was the same in patients with renal failure and those without renal failure. In 8.3% of the cases, multiple drug poisoning was observed. The most common compound overdose associated with rhabdomyolysis was opium. It is concluded that fluid therapy alone is not adequate in the management of acute renal failure in rhabdomyolysis. Therefore, other etiological factors are involved that remain to be elucidated by further studies.

  2. Increased Risk of Dementia in Patients With Acute Organophosphate and Carbamate Poisoning: A Nationwide Population-Based Cohort Study.

    PubMed

    Lin, Jiun-Nong; Lin, Cheng-Li; Lin, Ming-Chia; Lai, Chung-Hsu; Lin, Hsi-Hsun; Yang, Chih-Hui; Kao, Chia-Hung

    2015-07-01

    Organophosphate (OP) and carbamate (CM) are the most commonly used pesticides against insects. Little is known regarding the relationship between dementia and acute OP and CM poisoning. A nationwide population-based cohort study was conducted from the National Health Insurance Research Database in Taiwan. The incidence and relative risk of dementia were assessed in patients hospitalized for acute OP and CM poisoning from 2000 to 2011. The comparison cohort was matched with the poisoned cohort at a 4:1 ratio based on age, sex, and the year of hospitalization. During the follow-up period, the incidence of dementia was 29.4 per 10,000 person-years in the poisoned group, and represented a 1.98-fold increased risk of dementia compared with the control cohort (95% confidence interval, 1.59-2.47). This study provides evidence on the association between dementia and acute OP and CM poisoning. Regular follow-up of poisoned patients for dementia is suggested.

  3. Hyperglycemia in acute aluminum phosphide poisoning as a potential prognostic factor.

    PubMed

    Mehrpour, O; Alfred, S; Shadnia, S; Keyler, D E; Soltaninejad, K; Chalaki, N; Sedaghat, M

    2008-07-01

    Aluminum phosphide (AlP) is a solid fumigant widely used in Iran as a grain preservative. When reacted with water or acids, AIP produces phosphine gas, a mitochondrial poison that interferes with oxidative phosphorylation and protein synthesis. Poisoning by AIP is one of the most important causes of fatal chemical toxicity in Iran. There are few studies in the medical literature addressing prognostic factors associated with AlP poisoning. In this prospective study conducted across a 14-month period commencing on 21st March 2006, we enrolled all patients admitted to the ICU of Loghman-Hakim Hospital Poison Center (Tehran, Iran) with AIP poisoning, no history of diabetes mellitus diagnosed before hospitalization, and normal body mass index. We recorded patient-specific demographic information, blood glucose level on presentation (before treatment), arterial blood gas (ABG) analysis, time elapsed between ingestion and presentation, ingested dose, duration of intensive care admission, and outcome data related to each presentation. We enrolled the group of patients who survived the intoxication as a control group and compared their blood glucose levels with those who died because of AlP poisoning. Data were analyzed by Statistical Product and Service Solutions (SPSS) software (Version 12; Chicago, Ilinois, USA) using logistic regression, Pearson correlation coefficient and Student's t-test. P values of 0.05 or less were considered as the statistical significant levels. Forty-five patients (21 women and 24 men) with acute AlP poisoning were included in the study. The mean age was 27.3 +/- 11.5 years (range: 14-62 years). Thirteen patients survived (29%) and 32 expired (71%). AlP poisoning followed deliberate ingestion in all patients. The time elapsed between ingestion and arrival at the hospital was 3.2 +/- 0.4 h. There was no significant difference between survived and non-survived groups according to age, gender, and time to treatment. However, the difference between

  4. Evidence for metal poisoning in acute deaths of large red drum (Scianeops ocellata)

    SciTech Connect

    Cardeihac, P.T.; Simpson, C.F.; White, F.H.; Thompson, N.P.; Carr, W.E.

    1981-12-01

    Two of the approximately 100 large, mature, red drum found dead or dying in Florida's Indian River and Mosquito Lagoon were examined. Determinations were made of serum electrolyte concentrations, total proteins, albumins, globulins, creatinine values, and enzyme activity. Concentrations of copper, zinc, arsenic, chromium, cadmium, mercury, lead, and selenium were determined by atomic aborption. The outstanding histological lesions were found in the gills of a moribund specimen. Results indicate that the acute episode was triggered by ingestion of copper, zinc, and arsenic. However, cadmium, mercury and chromium may have been contributory by binding with metallothionein and thus lowering tolerance to metal poisoning. (JMT)

  5. Minamata disease revisited: an update on the acute and chronic manifestations of methyl mercury poisoning.

    PubMed

    Ekino, Shigeo; Susa, Mari; Ninomiya, Tadashi; Imamura, Keiko; Kitamura, Toshinori

    2007-11-15

    The first well-documented outbreak of acute methyl mercury (MeHg) poisoning by consumption of contaminated fish occurred in Minamata, Japan, in 1953. The clinical picture was officially recognized and called Minamata disease (MD) in 1956. However, 50 years later there are still arguments about the definition of MD in terms of clinical symptoms and extent of lesions. We provide a historical review of this epidemic and an update of the problem of MeHg toxicity. Since MeHg dispersed from Minamata to the Shiranui Sea, residents living around the sea were exposed to low-dose MeHg through fish consumption for about 20 years (at least from 1950 to 1968). These patients with chronic MeHg poisoning continue to complain of distal paresthesias of the extremities and the lips even 30 years after cessation of exposure to MeHg. Based on findings in these patients the symptoms and lesions in MeHg poisoning are reappraised. The persisting somatosensory disorders after discontinuation of exposure to MeHg were induced by diffuse damage to the somatosensory cortex, but not by damage to the peripheral nervous system, as previously believed.

  6. Stonefish poisoning.

    PubMed

    Lyon, Richard Mark

    2004-01-01

    Scuba diving is becoming an increasingly popular recreation. Divers are traveling further afield, often to remote dive locations. These locations are often home to poisonous marine creatures such as stonefish. A case of acute stonefish poisoning in a scuba diver is described, including his treatment, the difficulties encountered with his management and evacuation, and his subsequent return to full health. The proper management of stonefish poisoning is reviewed, and the implications for divers traveling to remote locations are given.

  7. Acute Poisonings Admitted to a Tertiary Level Intensive Care Unit in Northern India: Patient Profile and Outcomes

    PubMed Central

    Mathai, Ashu Sara; Pannu, Aman; Arora, Rohit

    2015-01-01

    Background Poisoning is becoming a real health care burden for developing countries like India. An improved knowledge of the patterns of poisonings, as well as the clinical course and outcomes of these cases can help to formulate better preventive and management strategies. Aim To study the demographic and clinical profiles of patients admitted to the ICU with acute poisoning and to study the factors that predict their mortality. Materials and Methods Retrospective two years (September 1, 2010 to August 31, 2012) study of all consecutive patients admitted to the Intensive Care Unit (ICU) with acute poisoning at a tertiary care hospital in Northern India. Results Out of the 67 patients admitted to the ICU during the study period, the majority were young (median age 29 years) males (69%) who had consumed poison intentionally. Pesticides were the most commonly employed poison, notably organophosphorus compounds (22 patients, 32.8%) and aluminium phosphide (14 patients, 20.9%). While the overall mortality from all poisonings was low (18%), aluminium phosphide was highly toxic, with a mortality rate of 35%. The factors at ICU admission that were found to be associated with a significant risk of death were, high APACHE II and SOFA scores (p =0.0001 and p=0.006, respectively), as well as the need for mechanical ventilation and drugs for vasoactive support (p=0.012 and p= 0.0001, respectively). Conclusion Use of pesticides for intentional poisoning continues to be rampant in Northern India, with many patients presenting in a critical condition to tertiary level hospitals. Pesticide regulations laws, educational awareness, counseling and poison information centers will help to curtail this public health problem. PMID:26557594

  8. Neurotoxicity and reactive astrogliosis in the anterior cingulate cortex in acute ciguatera poisoning.

    PubMed

    Zhang, Xu; Cao, Bing; Wang, Jun; Liu, Jin; Tung, Vivian Oi Vian; Lam, Paul Kwan Sing; Chan, Leo Lai; Li, Ying

    2013-06-01

    Ciguatoxins (CTXs) cause long-term disturbance of cerebral functions. The primary mechanism of neurotoxicity is related to their interaction with voltage-gated sodium channels. However, until now, the neurological targets for CTXs in the brain of intact animals have not been described. In our study, 1 day following oral exposure to 0.26 ng/g of Pacific ciguatoxin 1 (P-CTX-1), we performed in vivo electrophysiological recordings in the rat anterior cingulate cortex (ACC) and identified the increase in spontaneous firings and enhanced responses to visceral noxious stimulation. Local field recordings characterized the P-CTX-1-induced synaptic potentiation and blockage of the induction of electrical stimulation-induced long-term potentiation in the medial thalamus (MT)-ACC pathway. Furthermore, intracerebroventricular administration of P-CTX-1 at doses of 1.0, 5.0, and 10 nM produced a dose-dependent increase in ACC neuronal firings and MT-ACC synaptic transmission. Further studies showed upregulated Na(+) channel expression in astrocytes under pathological conditions. We hypothesized that the astrocytes might have been activated in the ciguatera poisoning in vivo. Increases in glial fibrillary acid protein expression were detected in reactive astrocytes in the rat ACC. The activation of astroglia was further indicated by activation of the gap junction protein connexin 43 and upregulation of excitatory amino acid transporter 2 expression suggesting that glutamate was normally rapidly cleared from the synaptic cleft during acute ciguatera poisoning. However, neurotoxicity and reactive astrogliosis were not detected in the ACC after 7 days of P-CTX-1 exposure. The present results are the first characterization of P-CTX-1-invoked brain cortex neuronal excitotoxicity in vivo and supported the theme that neuron and astroglia signals might play roles in acute ciguatera poisoning.

  9. Ophthalmic findings in acute mercury poisoning in adults: A case series study.

    PubMed

    Aslan, Lokman; Aslankurt, Murat; Bozkurt, Selim; Aksoy, Adnan; Ozdemir, Murat; Gizir, Harun; Yasar, Ibrahim

    2015-08-01

    The aim of this study is to report ophthalmic findings of acute mercury poisoning in 48 adults referred to emergency department. Full ophthalmologic examination including the best corrected visual acuity, external eye examination, reaction to light, a slit-lamp examination, funduscopy, intraocular pressure measurements, and visual field (VF) and color vision (CV) tests were performed at the presentation and repeated after 6 months. The parametric values of VF test, the mean deviation (MD), and pattern standard deviation (PSD) were recorded in order to compare patients and the 30 healthy controls. The mean parameter of color confusion index in patients was found to be statistically different than controls (p < 0.01). The MD and PSD in patients were different from controls statistically significant (p < 0.01 and p < 0.01, respectively). There was no correlation between the ocular findings and the urine and blood mercury levels. Methyl mercury, held in the school laboratory for experimental purpose, may be a source of poisoning. In this case series, we showed that acute exposure to mercury had hazardous effect on the visual system, especially CV and VF. We propose that emphasizing the public education on the potential hazards of mercury is crucial for preventive community health.

  10. Abnormal pancreatic enzymes and their prognostic role after acute paraquat poisoning.

    PubMed

    Li, Yi; Wang, Meng; Gao, Yanxia; Yang, Wen; Xu, Qun; Eddleston, Michael; Li, Li; Yu, Xuezhong

    2015-11-25

    Ingestion of paraquat causes multi-organ failure. Prognosis is best estimated through measurement of blood paraquat concentrations but this facility is not available in most hospitals. We studied the prognostic significance of abnormal pancreatic enzymes for survival. Patients with acute paraquat poisoning were recruited. An extensive series of blood tests including serum amylase were serially checked. Patients were sorted according to their serum amylase activity (normal [<220 U/L], mildly elevated [220 to 660 U/L], elevated [>660 U/L]), and survival compared between groups. 177 patients were enrolled to the study, of whom 67 died and 110 survived. 122 (70.62%), 27 (15.25%) and 25 (14.13%) patients were in the normal, mildly elevated and elevated amylase activity groups, respectively. The case fatality in the elevated group was 100% compared to 17% in the normal group (P < 0.001). We found four independent factors for paraquat death prediction: amylase, PaCO2, leukocyte number, and neutrophil percentage. Models using pancreatic enzyme activity showed good prediction power. We have found that abnormal pancreatic enzymes are useful prognostic marker of death after acute paraquat poisoning. Including serum amylase activity into a prognostic model provides a good prognostication.

  11. Utility of the Measurement of Carboxyhemoglobin Level at the Site of Acute Carbon Monoxide Poisoning in Rural Areas.

    PubMed

    Onodera, Makoto; Fujino, Yasuhisa; Kikuchi, Satoshi; Sato, Masayuki; Mori, Kiyofumi; Beppu, Takaaki; Inoue, Yoshihiro

    2016-01-01

    Objective. This study examined the hypothesis that correlations exist between the carbon monoxide exposure time and the carboxyhemoglobin concentration at the site of carbon monoxide poisoning, using a pulse carbon monoxide oximeter in rural areas or the carboxyhemoglobin concentration measured at a given medical institution. Background. In previous studies, no definitive relationships between the arterial blood carboxyhemoglobin level and the severity of carbon monoxide poisoning have been observed. Method. The subjects included patients treated for acute carbon monoxide poisoning in whom a medical emergency team was able to measure the carboxyhemoglobin level at the site of poisoning. We examined the relationship between the carboxyhemoglobin level at the site of poisoning and carbon monoxide exposure time and the relationships between the arterial blood carboxyhemoglobin level and carbon monoxide exposure time. Results. A total of 10 patients met the above criteria. The carboxyhemoglobin levels at the site of poisoning were significantly and positively correlated with the exposure time (rs = 0.710, p = 0.021), but the arterial blood carboxyhemoglobin levels were not correlated with the exposure time. Conclusion. In rural areas, the carboxyhemoglobin level measured at the site of carbon monoxide poisoning correlated with the exposure time.

  12. Utility of the Measurement of Carboxyhemoglobin Level at the Site of Acute Carbon Monoxide Poisoning in Rural Areas

    PubMed Central

    Onodera, Makoto; Fujino, Yasuhisa; Kikuchi, Satoshi; Sato, Masayuki; Mori, Kiyofumi; Beppu, Takaaki; Inoue, Yoshihiro

    2016-01-01

    Objective. This study examined the hypothesis that correlations exist between the carbon monoxide exposure time and the carboxyhemoglobin concentration at the site of carbon monoxide poisoning, using a pulse carbon monoxide oximeter in rural areas or the carboxyhemoglobin concentration measured at a given medical institution. Background. In previous studies, no definitive relationships between the arterial blood carboxyhemoglobin level and the severity of carbon monoxide poisoning have been observed. Method. The subjects included patients treated for acute carbon monoxide poisoning in whom a medical emergency team was able to measure the carboxyhemoglobin level at the site of poisoning. We examined the relationship between the carboxyhemoglobin level at the site of poisoning and carbon monoxide exposure time and the relationships between the arterial blood carboxyhemoglobin level and carbon monoxide exposure time. Results. A total of 10 patients met the above criteria. The carboxyhemoglobin levels at the site of poisoning were significantly and positively correlated with the exposure time (rs = 0.710, p = 0.021), but the arterial blood carboxyhemoglobin levels were not correlated with the exposure time. Conclusion. In rural areas, the carboxyhemoglobin level measured at the site of carbon monoxide poisoning correlated with the exposure time. PMID:27239377

  13. Application of 2-Aminothiazoline-4-carboxylic Acid as a Forensic Marker of Cyanide Exposure.

    PubMed

    Rużycka, Monika; Giebułtowicz, Joanna; Fudalej, Marcin; Krajewski, Paweł; Wroczyński, Piotr

    2017-02-20

    Cyanides are infamous for their highly poisonous properties. Accidental cyanide poisoning occurs frequently, but occasionally, intentional poisonings also occur. Inhalation of fumes generated by fire may also cause cyanide poisoning. There are many limitations in direct analysis of cyanide. 2-Aminothiazoline-4-carboxylic acid (ATCA), a cyanide metabolite, seems to be the only surrogate that is being used in the detection of cyanide because of its stability and its cyanide-dependent quality in a biological matrix. Unfortunately, toxicokinetic studies on diverse animal models suggest significant interspecies differences; therefore, the attempt to extrapolate animal models to human models may be unsuccessful. The aim of the present study was to evaluate the use of ATCA as a forensic marker of cyanide exposure. For this purpose, post-mortem materials (blood and organs) from fire victims (n = 32) and cyanide-poisoned persons (n = 3) were collected. The distribution of ATCA in organs and its thermal stability were evaluated. The variability of cyanides in a putrid sample and in the context of their long-term and higher temperature stability was established. The presence of ATCA was detected by using an LC-MS/MS method and that of cyanide was detected spectrofluorimetrically. This is the first report on the endogenous ATCA concentrations and the determination of ATCA distribution in tissues of fire victims and cyanide-poisoned persons. It was found that blood and heart had the highest ATCA concentrations. ATCA was observed to be thermally stable even at 90 °C. Even though the cyanide concentration was not elevated in putrid samples, it was unstable during long-term storage and at higher temperature, as expected. The relationship between ATCA and cyanides was also observed. Higher ATCA concentrations were related to increased levels of cyanide in blood and organs (less prominent). ATCA seems to be a reliable forensic marker of exposure to lethal doses of cyanide.

  14. An evaluation of acute hydrogen sulfide poisoning in rats through serum metabolomics based on gas chromatography-mass spectrometry.

    PubMed

    Zhang, Meiling; Deng, Mingjie; Ma, Jianshe; Wang, Xianqin

    2014-01-01

    Hydrogen sulfide (H2S) is the second leading cause of toxin-related deaths in the operational site. Its main target organs of toxic effects are the central nervous system and respiratory system. In this study, we developed a serum metabonomic method, based on gas chromatography-mass spectrometry (GC/MS), to evaluate the effect of acute poisoning by hydrogen sulfide on rats. Pattern recognition analysis, including both principal component analysis (PCA) and partial least squares-discriminate analysis (PLS-DA), revealed that acute hydrogen sulfide poisoning induced metabolic perturbations. Compared to the control group, the level of urea, glucose, glyceryl stearate in rat serum of the poisoning group increased after two hours, and the level of glucose, docosahexaenoic acid, glyceryl stearate and arachidonic acid in rat serum of the poisoning group increased after 48 h, while the L-valine, galactose, L-tyrosine levels decreased. Our results indicate that metabonomic methods based on GC/MS may be useful to elucidate acute hydrogen sulfide poisoning through the exploration of biomarkers.

  15. Clinical analysis of penehyclidine hydrochloride combined with hemoperfusion in the treatment of acute severe organophosphorus pesticide poisoning.

    PubMed

    Liang, M J; Zhang, Y

    2015-05-11

    This study aimed to observe the clinical curative effect of penehyclidine hydrochloride (PHC) combined with hemoperfusion in treating acute severe organophosphorus pesticide poisoning. We randomly divided 61 patients with severe organophosphorus pesticide poisoning into an experimental group (N = 31) and a control group (N = 30), and we compared the coma-recovery time, mechanical ventilation time, healing time, hospital expenses, and mortality between the two groups. The coma-recovery time, mechanical ventilation time, and healing time were lower in the experimental group than in the control group (P < 0.05), while the hospitalization expenses were higher in the experimental group than in the control group (P < 0.01); moreover, no significant difference was observed in the mortality rate between the two groups. Thus, PHC combined with hemoperfusion exerts a better therapeutic effect in acute severe organophosphorus pesticide poisoning than PHC alone.

  16. Evaluation of Potential Oxidative Stress in Egyptian Patients with Acute Zinc Phosphide Poisoning and the Role of Vitamin C

    PubMed Central

    Sagah, Ghada A.; Oreby, Merfat M.; El-Gharbawy, Rehab M.; Ahmed Fathy, Amal S.

    2015-01-01

    Objective To evaluate potential oxidative stress in patients with acute phosphide poisoning and the effect of vitamin C. Methods Participants were females and divided into three groups; group I: healthy volunteers group II: healthy volunteers received vitamin C, group III: patients with acute phosphide poisoning received the supportive and symptomatic treatment and group IV: patients with acute phosphide poisoning received the supportive and symptomatic treatment in addition to vitamin C. All the participants were subjected to thorough history, clinical examination, ECG and laboratory investigations were carried on collected blood and gastric lavage samples on admission. Blood samples were divided into two parts, one for measurement of routine investigations and the second part was used for evaluation of malondialdehyde and total thiol levels before and after receiving the treatment regimen. Results Most of the cases in this study were among the age group of 15–25 years, females, single, secondary school education, from rural areas and suicidal. All vital signs were within normal range and the most common complaint was vomiting and abdominal pain. All cases in this study showed normal routine investigations. The mean MDA levels after receiving treatment decreased significantly in groups II and IV. The mean total thiol levels increased significantly after receiving treatment in groups II and IV. Conclusion It can be concluded that vitamin C has a potential benefit due to its antioxidant property on zinc phosphide induced-oxidative stress in acute zinc phosphide poisoned patients. PMID:26715917

  17. Sodium cyanide

    Integrated Risk Information System (IRIS)

    Jump to main content . Integrated Risk Information System Recent Additions | Contact Us Search : All EPA IRIS • You are here : EPA Home • Research • Environmental Assessment • IRIS • IRIS Summaries Redirect Page As of September 28 , 2010 , the assessment summary for sodium cyanide is included in the

  18. Copper cyanide

    Integrated Risk Information System (IRIS)

    Copper cyanide ; CASRN 544 - 92 - 3 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic Ef

  19. Barium cyanide

    Integrated Risk Information System (IRIS)

    Barium cyanide ; CASRN 542 - 62 - 1 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic Ef

  20. Chlorine cyanide

    Integrated Risk Information System (IRIS)

    Chlorine cyanide ; CASRN 506 - 77 - 4 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic

  1. Potassium cyanide

    Integrated Risk Information System (IRIS)

    Jump to main content . Integrated Risk Information System Recent Additions | Contact Us Search : All EPA IRIS • You are here : EPA Home • Research • Environmental Assessment • IRIS • IRIS Summaries Redirect Page As of September 28 , 2010 , the assessment summary for potassium cyanide is included in

  2. Zinc cyanide

    Integrated Risk Information System (IRIS)

    Zinc cyanide ; CASRN 557 - 21 - 1 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic Effe

  3. Calcium cyanide

    Integrated Risk Information System (IRIS)

    Jump to main content . Integrated Risk Information System Recent Additions | Contact Us Search : All EPA IRIS • You are here : EPA Home • Research • Environmental Assessment • IRIS • IRIS Summaries Redirect Page As of September 28 , 2010 , the assessment summary for calcium cyanide is included in th

  4. Silver cyanide

    Integrated Risk Information System (IRIS)

    Silver cyanide ; CASRN 506 - 64 - 9 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic Ef

  5. Cardiac and renal nitrosative-oxidative stress after acute poisoning by a nerve agent Tabun.

    PubMed

    Dimov, Dimo; Hadjiolova, Radka; Kanev, Kamen; Tomova, Radka; Michova, Anna; Todorov, Todor; Murdjev, Rumen; Boneva, Temenujka; Dimova, Ivanka

    2015-01-01

    We hypothesized that Tabun poisoning, as well as other organophosphorous treatment, cause specific organs' oxidative changes that have not previously been substantiated investigated. In this regard, a marker for nitrosative-oxidative stress in the main haemodynamic organs (heart and kidney) could reveal the existence of such changes. In this study, for the first time we studied the nitrosative/oxidative stress in heart and kidney after acute Tabun (Ethyl N,N- Dimethylphosphoramidocyanidate) poisoning measuring by immunohistochemistry the expression of 3-nitrotyrosine--a marker for nitrosative-oxidative stress. We investigated nitrotyrozine expression in three different groups of animals (with at least 3 animals in each group): the first group was treated with 0.5 LD50 Tabun and organs were collected after 24 h; the second group received vehicle for the same period; in the third group a highly specific re-activator was applied immediately after Tabun application. Heart and kidney were collected after 24 h. The levels of nitrotyrozine production significantly increased (more than 3 times) in cardiomyocytes after Tabun. The application of re-activator slightly reduced these levels not reaching the basal heart levels. Nitrotyrozine expression in kidney increased more than 2 times after Tabun and application of re-activator did not change it significantly. In conclusion, our study evidently demonstrated that Tabun trigger oxidative-nitrosative stress in heart and kidney and these cellular effects should be protected by an additional anti-oxidant therapy, since acetylcholinesterase re-activator is not efficient in this manner.

  6. Acute Cadmium Fume Poisoning: Five Cases with one Death from Renal Necrosis

    PubMed Central

    Beton, D. C.; Andrews, G. S.; Davies, H. J.; Howells, Leonard; Smith, G. F.

    1966-01-01

    This paper describes the accidental poisoning of five workers by cadmium fume. The men were dismantling a frame of girders in a confined space by cutting bolts with an oxyacetylene burner. They were unaware at the time that the bolts were cadmium-plated or that this presented a serious industrial hazard. The paper sets out to give an appreciation of acute cadmium poisoning, the characteristics and uses of cadmium, and a review of the literature. The clinical picture of these cases is described, with the pathology of the fatal case which showed severe pulmonary oedema, alveolar metaplasia of the lung, and bilateral cortical necrosis of the kidneys. The lungs contained 0·25 g. cadmium oxide (CdO) per 100 g. wet specimen. An attempted estimation of the fatal dose of CdO fume is made. From the post-mortem findings, using an assumption that 11% of inhaled CdO will be retained in the lungs, approximately 51·7 mg. CdO fume must have been inhaled by the fatal case. As he worked for five hours with a probable ventilatory rate of 20 l./min. the concentration of CdO in the air breathed would be of the order of 8·6 mg./m.3. An estimation of the dose from a study of the working conditions proved unsatisfactory due to certain variables listed in the text. Images PMID:5928153

  7. Chronic Neuropsychological Sequelae of Cholinesterase Inhibitors in the Absence of Structural Brain Damage: Two Cases of Acute Poisoning

    PubMed Central

    Roldán-Tapia, Lola; Leyva, Antonia; Laynez, Francisco; Santed, Fernando Sánchez

    2005-01-01

    Here we describe two cases of carbamate poisoning. Patients AMF and PVM were accidentally poisoned by cholinesterase inhibitors. The medical diagnosis in both cases was overcholinergic syndrome, as demonstrated by exposure to cholinesterase inhibitors. The widespread use of cholinesterase inhibitors, especially as pesticides, produces a great number of human poisoning events annually. The main known neurotoxic effect of these substances is cholinesterase inhibition, which causes cholinergic overstimulation. Once AMF and PVM had recovered from acute intoxication, they were subjected to extensive neuropsychological evaluation 3 and 12 months after the poisoning event. These assessments point to a cognitive deficit in attention, memory, perceptual, and motor domains 3 months after intoxication. One year later these sequelae remained, even though the brain magnetic resonance imaging (MRI) and computed tomography (CT) scans were interpreted as being within normal limits. We present these cases as examples of neuropsychological profiles of long-term sequelae related to acute poisoning by cholinesterase inhibitor pesticides and show the usefulness of neuropsychological assessment in detecting central nervous system dysfunction in the absence of biochemical or structural markers. PMID:15929901

  8. Cyanide Antidotes for Mass Casualties: Comparison of Intramuscular Injector by Autoinjector, Intraosseous Injection, and Inhalational Delivery

    DTIC Science & Technology

    2014-10-01

    AD_________________ Award Number: W81XWH-12-2-0114 TITLE: Cyanide Antidotes for Mass Casualties... Cyanide Antidotes for Mass Casualties: Comparison of Intramuscular Injector by Autoinjector, Intraosseous Injection, and Inhalational Delivery 5a...Release; Distribution Unlimited 13. SUPPLEMENTARY NOTES 14. ABSTRACT Current antidotes for cyanide poisoning must be administered by

  9. [Acute lead poisoning in cows due to feeding of lead contaminated ash residue].

    PubMed

    Schlerka, Gerd; Tataruch, Frieda; Högler, Sandra; Url, Angelika; Krametter, Reinhild; Kössler, Dieter; Schmidt, Peter

    2004-01-01

    In a dairy herd of 21 cows which were on pasture during the day at the end of May 2002, four eight years old cows were suddenly inappetent and showed severe diarrhoea consisting of black discolorate feces. A few days after the onset of the disease, three affected cows exhibited neurological disorders. These cows were admitted to the IInd Medical Clinic of the University for Veterinary Medicine in Vienna. Following clinical signs were observed: circulatory weakness, anorexia, atony of the rumen, diarrhoea and in accordance with acute lead poisoning typical signs of the central nervous system. One cow died and the other two animals were euthanized. Results of blood testing were anaemia, basophil spotting of erythrocytes, increase of liver enzymes and CK, hypocalcaemia, decrease of potassium and phosphate. The cerebrospinal fluid of two cows showed increased CK-, LDH- and AST-values. The lead contents of whole blood samples were between 0.486 and 0.928 mg/kg, of liver samples 13.3 to 114.4 mg/kg, of kidney samples 172.2 to 448 mg/kg and of rumen content 59 mg/kg fresh matter. At necropsy, enteritis, liver fluke disease and severe interstitial and alveolar pulmonary emphysema were found. Pathohistologically typical ischaemic necrosis of neurons predominantly at the tips of the gyri, disseminated petechial hemorrhages and moderate diffuse neovascularisation, but no acid-fast intranucleolar inclusion bodies in the renal tubules were observed. As causative agent of the acute lead poisoning a residue on combustion, taken up by the cows on the pasture, was confirmed. The ash residue was formed by combustion of three tires which contained 450 g heavy weights of 96.5% lead for wheel balance. The lead content of the ash residue was between 2.9 and 28 g/kg dry matter.

  10. Antagonism of Acute Sulfide Poisoning in Mice by Nitrite Anion without Methemoglobinemia.

    PubMed

    Cronican, Andrea A; Frawley, Kristin L; Ahmed, Humza; Pearce, Linda L; Peterson, Jim

    2015-07-20

    There are currently no FDA-approved antidotes for H2S/sulfide intoxication. Sodium nitrite, if given prophylactically to Swiss Webster mice, was shown to be highly protective against the acute toxic effects of sodium hydrosulfide (∼LD40 dose) with both agents administered by intraperitoneal injections. However, sodium nitrite administered after the toxicant dose did not detectably ameliorate sulfide toxicity in this fast-delivery, single-shot experimental paradigm. Nitrite anion was shown to rapidly produce NO in the bloodstream, as judged by the appearance of EPR signals attributable to nitrosylhemoglobin and methemoglobin, together amounting to less than 5% of the total hemoglobin present. Sulfide-intoxicated mice were neither helped by the supplemental administration of 100% oxygen nor were there any detrimental effects. Compared to cyanide-intoxicated mice, animals surviving sulfide intoxication exhibited very short knockdown times (if any) and full recovery was extremely fast (∼15 min) irrespective of whether sodium nitrite was administered. Behavioral experiments testing the ability of mice to maintain balance on a rotating cylinder showed no motor impairment up to 24 h post sulfide exposure. It is argued that antagonism of sulfide inhibition of cytochrome c oxidase by NO is the crucial antidotal activity of nitrite rather than formation of methemoglobin.

  11. Acute severe organophosphate poisoning in a child who was successfully treated with therapeutic plasma exchange, high-volume hemodiafiltration, and lipid infusion.

    PubMed

    Yesilbas, Osman; Kihtir, Hasan S; Altiti, Mohammad; Petmezci, Mey Talip; Balkaya, Seda; Bursal Duramaz, Burcu; Ersoy, Melike; Sevketoglu, Esra

    2016-10-01

    Acute severe organophosphate poisoning is a serious complication seen in developing and agricultural countries. Pralidoxime and high dose atropine are the standard treatments. There is no consensus about acute severe organophosphate poisonings that are unresponsive to pralidoxime, atropine, and supportive therapies. We report a case of acute severe organophosphate poisoning that was unresponsive to standard treatments and successfully treated with high-volume continuous venovenous hemodiafiltration and therapeutic plasma exchange combined with lipid infusion. J. Clin. Apheresis 31:467-469, 2016. © 2015 Wiley Periodicals, Inc.

  12. A Comparison of the Treatment of Cyanide Poisoning in the Cynomolgus Monkey with Sodium Nitrite of 4-Dimethylaminophenol (4-DMAP), with and without Sodium Thiosulfate

    DTIC Science & Technology

    1994-02-01

    140 - pCO 2 120- 120 0 -0 80{-)100 .0 • 100 60 60 7.5 -7.5K .4] 7.4 .-t . * * 7.3 -7.3 140 - 140- 0120 -- 120S.., 0 100 U Blood Pressure 100 o 0 0...200 .O . P O , 160 - 160- v PCOS - so. L. o-. •’r.120- r 120 0 0 80 :V< -& 0 40 40 7.6 7.6 01 7.4 0 7.4 160 - Blood presure v 160 - fBlood pressure V...Mushett, C.W., Kelley, K.L., Boxer, G.E., and Rickards, J.C. (1952). Antidotal efficacy of vitamin b12 (hydroxo-cobalamin) in experimental cyanide

  13. [Pharmacological analysis of the pathogenesis of acute poisoning with the synthetic pyrethroid cypermethrin using the hydrobiont Daphnia magna Straus].

    PubMed

    Podosinovikova, N P; Solov'eva, N E; Mukovskiĭ, L A; Petrov, V V; Matveev, B B; Dolgo-Saburov, V B

    2002-01-01

    The results of pharmacological analysis are presented which provide information on the pathogenesis of acute cypermethrin poisoning that involves disturbances in various systems of the organism. These include changes in the system of excitatory amino acids (EAAs) and violation of the free radical generation processes, Na + channel functioning, cholinergic transmission, etc. The screening of drugs belonging to various pharmacological groups influencing the toxicity of pyrethroids (EAA receptor antagonists, antioxidants, Na + channel blockers, M-cholinoreceptor blockers) revealed promising agents for the treatment of cypermethrin poisoning.

  14. Acute Pancreatitis, Hepatitis and Bone Erosion in Acute Yellow Phosphorous Compound Poisoning – A Rare Complication

    PubMed Central

    Kamarthi, Prabhakar; Gopu, Arun Vardharaju; Prasad, Reddy; Srinivasa, Chandrakala

    2016-01-01

    We report a case of acute pancreatitis and hepatitis following ingestion of yellow phosphorous. The condition of the patient progressed to encephalopathy and bony erosion of the nasal septum. Fungal mass was observed in both the nasal cavities by endoscopy. Microbiological investigation revealed the identity of the fungus as Aspergillus flavus and Candida tropicalis. Patient improved with fluconazole treatment. PMID:27504287

  15. [The morphofunctional features of the heart associated with acute morphine poisoning during the period of chronic drug intoxication].

    PubMed

    Altaeva, A Zh; Galitsky, F A; Zhakupova, T Z; Aidarkulov, A Sh; Selivokhina, N V; Zhunisov, S S

    2016-01-01

    The objective of the present study was to improve forensic medical diagnostics of the cases of death associated with morphine poisoning based on the investigation into the biochemical changes in blood and pericardial fluid as well as morphological changes in the myocardial structures. The studies were carried out with the use of thin-layer chromatography, colorimetric and morphological methods including hematoxylin and eosin, Lee's methylene blue, and van Gieson's picrofuscin staining. These techniques were supplemented by light and polarization microscopy. The study has demonstrated the presence of morphine in 99.16% of the blood and pericardial samples obtained in the cases of poisoning. The comparison of the results of biochemical and pathomorphological studies of the myocardium made it possible to evaluate the functional and morphological conditions of the heart in the case of acute morphine poisoning during the period of chronic drug intoxication.

  16. Hydroxocobalamin Versus Sodium Thiosulfate for the Treatment of Acute Cyanide Toxicity in a Swine (Sus scrofa) Model

    DTIC Science & Technology

    2012-06-01

    effective for smoke inhalation ? searching for guidance in the haze. Ann Emerg Med. 2007;49:814-816. 6. Velez LI, Delaney LS. Cyanide. In: Tintinalli JE, ed...than sodium nitrite. However, it is not clear whether the sodium thiosulfate adds a beneficial effect to hydroxocobalamin alone.3,6,11,12 Experts...This Investigation The primary hypothesis of our study is that sodium thiosulfate is as effective as hydroxocobalamin in reversing the hypotension

  17. Cyanide toxicity and exposure risk. January 1980-March 1992 (Citations from the NTIS Data Base). Rept. for Jan 80-Mar 92

    SciTech Connect

    Not Available

    1992-02-01

    The bibliography contains citations concerning the biological hazards associated with exposure to cyanide. Cyanide poisoning and antidotes, combustion products containing cyanide, clinical toxicology, environmental effects, exposure hazards, occupational safety, and other topics relating to the health hazards of cyanide compounds are discussed. Methods of analysis and monitoring are also considered. (Contains 119 citations with title list and subject index.)

  18. Cyanide toxicity and exposure risk. January 1970-November 1989 (Citations from the NTIS data base). Report for January 1970-November 1989

    SciTech Connect

    Not Available

    1989-12-01

    This bibliography contains citations concerning the biological hazards associated with exposure to cyanide. Cyanide poisoning and antidotes, combustion products containing cyanide, clinical toxicology, environmental effects, exposure hazards, occupational safety, and other topics relating to the health hazards of cyanide compounds are discussed. Methods of analysis and monitoring are also considered. (Contains 126 citations fully indexed and including a title list.)

  19. Severe acute poisoning with homemade Aconitum napellus capsules: toxicokinetic and clinical data.

    PubMed

    Moritz, Fabienne; Compagnon, Patricia; Kaliszczak, Isabelle Guery; Kaliszczak, Yann; Caliskan, Valérie; Girault, Christophe

    2005-01-01

    Aconitum napellus is an extremely dangerous plant that contains various toxic diterpenoid alkaloids, mainly aconitine primarily concentrated in the roots. We report a case of acute intoxication of a 21-year-old man admitted to our Emergency Department after the ingestion, in order to sleep, of three homemade Aconitum napellus capsules. Capsules were measured to contain 237 mg of root and 19 microg of aconitine. The patient experienced the first symptoms on wakening 5 hours later with generalized paresthesia, nausea, diarrhea, vertigo, thoracic pain dyspnea, and dyschromatopsia. At admission, 7 hours after intake electrocardiographic analysis showed a sinusal bradycardia with polymorphic and bigeminal ventricular extrasystolia. Cardiovascular and neurological symptoms disappeared, respectively within 11 and 13 hours of ingestion. The patient was discharged from the ICU on day 2. Plasmatic concentrations at H7, H9, H14 H19, and after ingestion were, respectively, of 1.75, 0.75, 0.35, and 0.02 ng/mL. The calculated half-life of aconitine was 3 hours. To our knowledge, this is the first reported case with an aconitine toxicokinetic-effect relationship. The authors stress that clinicians must be aware of possible occurrence of acute poisoning with Aconitum napellus in European countries and in the United States as herbal medicine is becoming increasingly popular.

  20. Is there a relationship between the blood cholinesterase and QTc interval in the patients with acute organophosphate poisoning?

    PubMed

    Baydin, A; Aygun, D; Yazici, M; Karatas, A; Deniz, T; Yardan, T

    2007-06-01

    Organophosphates cause poisoning as a result of the excessive accumulation of acetylcholine at the cholinergic synapses due to inhibition of acetylcholinesterase (ChE). In the literature, it has been reported that there have been electrocardiographic abnormalities, including QT-interval prolongation in most patients with acute organophosphate poisoning (OPP), and a relation between blood ChE level and clinical severity in acute OPP. The aim of this study is to assess the relationship between blood ChE level and QTc interval in the patients with acute OPP. This retrospective study consists of 20 patients admitted to the emergency intensive care unit. A total of 93 QTc interval and blood ChE measures obtained on the same day from 20 cases were compared for their correlation. There were prolonged QTc intervals in 35.4% of the ECGs. There was a negative correlation between QTc interval and blood ChE measures. In following up the patients with acute OPP, QTc interval may be useful when blood ChE levels are low and may provide complementary information concerning the severity of poisoning. However, further prospective studies, supporting the present results, are needed.

  1. Cyanide toxicity and exposure risk. (Latest citations from the NTIS database). Published Search

    SciTech Connect

    Not Available

    1993-04-01

    The bibliography contains citations concerning the biological hazards associated with exposure to cyanide. Cyanide poisoning and antidotes, combustion products containing cyanide, clinical toxicology, environmental effects, exposure hazards, occupational safety, and other topics relating to the health hazards of cyanide compounds are discussed. Methods of analysis and monitoring are also considered. (Contains a minimum of 188 citations and includes a subject term index and title list.)

  2. Acute lead poisoning in western Canadian cattle — A 16-year retrospective study of diagnostic case records

    PubMed Central

    Cowan, Vanessa; Blakley, Barry

    2016-01-01

    This study describes the epidemiology of acute lead poisoning in western Canadian cattle over the 16-year period of 1998 to 2013 and reports background bovine tissue lead concentrations. Case records from Prairie Diagnostic Services, Western College of Veterinary Medicine, identified 525 cases of acute lead toxicity over the investigational period. Poisonings were influenced by year (P < 0.0001) and month (P < 0.0001). Submissions were highest in 2009 (15.6%), 2001 (11.2%), and 2006 (9.9%). Most cases were observed during May, June, and July (62.3%). Cattle 6 months of age and younger were frequently poisoned (53.5%; P < 0.0001). Beef breeds were predominantly poisoned. Mean toxic lead concentrations (mg/kg wet weight) in the blood, liver, and kidney were 1.30 ± 1.70 (n = 301), 33.5 ± 80.5 (n = 172), and 56.3 ± 39.7 (n = 61). Mean normal lead concentrations in the blood, liver, and kidney were 0.036 ± 0.003 mg/kg (n= 1081), 0.16 ± 0.63 mg/kg (n = 382), and 0.41 ± 0.62 mg/kg (n = 64). PMID:27041761

  3. A hospital base epidemiology and pattern of acute adult poisoning across Iran: a systematic review

    PubMed Central

    Moradi, Malihe; Ghaemi, Kazem; Mehrpour, Omid

    2016-01-01

    Introduction Poisoning is one of the most important health issues in the world. There is no exact statistic regarding the epidemiology of poisoning in Iran. The aim of this systematic review was to study the epidemiology of poisoning of adults in Iran. Methods All the published papers regarding the epidemiology and patterns of adult poisonings in different parts of Iran were reviewed in bibliographical databases, including SID, Iran Medex, Medlib, Magiran and Embase, Scopus, PubMed, and Google Scholar, without time limitation up to March 21, 2016. We searched for the terms poisoning, Iran, and epidemiology. After the final analysis, 38 articles that fulfilled all the required conditions were selected. Result In this article, we show that in most Iranian cities, except Ahvaz, pharmaceutical drugs, especially psychiatric pharmaceutical drugs, are the most common cause of poisoning in adults. In the Southwest region of Iran, poisoning due to envenomation is a very common. Although pesticide and opioid poisonings are less common, they are an important cause of death due to poisoning in Iran. Conclusion Pharmaceutical drugs are the most common cause of poisoning in most Iranian cities and it is recommended not to store pharmaceutical drugs at home and to set special rules regarding proper description of pharmaceutical drugs. More public health instruction is essential in the Southwest cities of Iran in order to reduce animal poisonings. PMID:27790337

  4. [Cyanides--treatment beneath the shade of terror].

    PubMed

    Krivoy, Amir; Finkelstein, Arseny; Rotman, Eran; Layish, Ido; Tashma, Zeev; Hoffman, Azik; Schein, Ophir; Yehezkelli, Yoav; Dushnitsky, Tsvika; Eisenkraft, Arik

    2007-03-01

    Although the use of cyanides as warfare agents has not been documented since the Iran-Iraq war in the 1980s, there are rising fears of cyanide being used by terrorists. An Al-Qaeda terror plot to use cyanide gas in the London Underground was foiled in 2002. The threat of similar events becomes more imminent in light of the terror attacks in our country and worldwide, accompanied by statements and threats by fundamentalist leaders to employ chemical weapons. Therefore, mass-intoxication with cyanides is not merely a hypothetical scenario. The treatment of cyanide poisoning is under constant evaluation and there is no international consensus on the subject. The medical treatment of victims at the scene and in hospitals should be rapid and efficient. Current treatment dictates establishing an intravenous line and a slow rate of administration of antidotes. Both demands are not feasible in this specific mass casualty event. The clinical signs of cyanide poisoning are complex, variable and not necessarily obvious for the medical team. There is great interest in reconsidering the existing treatment protocols for cyanide intoxication in light of current research. This review describes the mechanisms of cyanide toxicity, clinical signs of exposure, and current treatment protocols in use worldwide. On the basis of this evidence we suggest a medical treatment protocol for a mass casualty event caused by cyanide.

  5. Plasma copeptin as a predictor of intoxication severity and delayed neurological sequelae in acute carbon monoxide poisoning.

    PubMed

    Pang, Li; Wang, He-Lei; Wang, Zhi-Hao; Wu, Yang; Dong, Ning; Xu, Da-Hai; Wang, Da-Wei; Xu, Hong; Zhang, Nan

    2014-09-01

    The present study was designed to assess the usefulness of measuring plasma levels of copeptin (a peptide co-released with the hypothalamic stress hormone vasopressin) as a biomarker for the severity of carbon monoxide (CO) poisoning and for predicting delayed neurological sequelae (DNS). Seventy-two patients with CO poisoning and 72 sex and age matched healthy individuals were recruited. Plasma copeptin levels were measured on admission from CO poisoning patients and for healthy individuals at study entry by using a sandwich immunoassay. The CO poisoning patients were divided into two groups according to severity (unconscious and conscious) and occurrence of DNS. The mean plasma copeptin levels (52.5±18.5 pmol/L) in the unconscious group were significantly higher than in the conscious group (26.3±12.7 pmol/L) (P<0.001). Plasma copeptin levels of more than 39.0 pmol/L detected CO poisoning with severe neurological symptoms e.g. unconsciousness (sensitivity 84.6% and specificity 81.4%). The plasma copeptin levels were higher in patients with DNS compared to patients without DNS (52.2±20.6 pmol/L vs. 27.9±14.8 pmol/L, P<0.001). Plasma copeptin levels higher than 40.5 pmol/L predicted the development of DNS (sensitivity 77.8%, specificity 82.1%). Plasma copeptin levels were identified as an independent predictor for intoxication severity [odds ratio (OR) 1.261, 95% confidence interval (CI) 1.112-1.638, P=0.002] and DNS (OR 1.313, 95% CI 1.106-1.859, P=0.001). Thus, plasma copeptin levels independently related to intoxication severity and were identified as a novel biomarker for predicting DNS after acute CO poisoning.

  6. Child labor and acute pesticide poisoning in Nicaragua: failure to comply with children's rights.

    PubMed

    Corriols, Marianela; Aragón, Aurora

    2010-01-01

    Since 1995, Nicaragua has adopted several legal instruments to comply with children's rights, including international conventions and a minimum working age of 14 years. However, records from the Ministry of Health's Pesticide Program show continuing occupational acute pesticide poisonings (APP) among children five to 14-years-old from 1995 to 2006. We reviewed and described all reported APPs and estimated the yearly incidence and underreporting rates. Of 2069 APP cases, 432 were occupational. Annual incidence rates (range: 1-4.7/100,000) have been decreasing since 1997. Six fatal and most non-fatal cases were related to work in tobacco and basic grain crops. Based on underreporting data, we estimate actual incidence during the period studied to be 18,516 (95% CI, 3840-33,204) cases among five- to fourteen-year-olds. With regard to child labor and pesticide exposure, children's rights violations still exist and must be abolished in both formal employment and in the informal economy, including in family-based agricultural activities.

  7. Fatal acute poisoning from massive inhalation of gasoline vapors: case report and comparison with similar cases.

    PubMed

    Papi, Luigi; Chericoni, Silvio; Bresci, Francesco; Giusiani, Mario

    2013-03-01

    We describe a case of an acute lethal poisoning with hydrocarbons resulting from massive accidental inhalation of gasoline vapors. The victim, a 50-year-old man was found unconscious inside a control room for the transport of unleaded fuel. Complete autopsy was performed and showed evidence of congestion and edema of the lungs. Toxicological investigation was therefore fundamental to confirm exposure to fumes of gasoline. Both venous and arterial blood showed high values of volatiles in particular for benzene (39.0 and 30.4 μg/mL, respectively), toluene (23.7 and 20.4 μg/mL), and xylene isomers (29.8 and 19.3 μg/mL). The relatively low values found in the lungs are consistent with the fact that the subject, during the rescue, underwent orotracheal intubation followed by resuscitation techniques, while the low concentrations for all substances found in urine and kidneys could point to a death that occurred in a very short time after first contact with the fumes of gasoline.

  8. Identification of urinary metabolites of human subjects acutely poisoned by p-chloronitrobenzene.

    PubMed

    Yoshida, T; Tabuchi, T; Andoh, K

    1992-12-01

    1. Urinary metabolites from human subjects acutely poisoned with p-chloro-nitrobenzene (p-CNB) were identified by g.l.c.-mass spectrometry. 2. Eight substances, namely, a very large amount of N-acetyl-S-(4-nitrophenyl)-L-cysteine, relatively large quantities of p-chloroaniline, 2-chloro-5-nitrophenol and p-chloroformanilide produced by pyrolysis of a substance originating from p-CNB, small amounts of 2-amino-5-chlorophenol and 2,4-dichloroaniline, and traces of p-chloroacetanilide and 4-chloro-2-hydroxyacetanilide, were detected in urine samples. 3. All of the absorbed p-CNB was metabolized prior to excretion, as the parent compound was not found in urine. 4. N-Acetylated metabolites of p-chloroaniline and 2-amino-5-chlorophenol, resulting from p-CNB by metabolism, were found in only one of eight individuals indicating that this pathway is weak or may be absent in some humans. 5. A scheme for the pattern of metabolic pathways of p-CNB is proposed, and chlorination was considered to be a possible novel metabolic pathway.

  9. Simultaneous determination of two acute poisoning rodenticides tetramine and fluoroacetamide with a coupled column in poisoning cases.

    PubMed

    Xu, Xiaomin; Song, Guoliang; Zhu, Yan; Zhang, Jing; Zhao, Yongxin; Shen, Haitao; Cai, Zengxuan; Han, Jianlong; Ren, Yiping

    2008-12-01

    A coupled column system was developed for the simultaneous determination of both rodenticides fluoroacetamide and tetramine in this paper by gas chromatography/mass spectrometry (GC/MS). A short length of strong polar column (1.5 m of Innowax) was coupled to the top of a 30 m of DB-5 ms with a quartz capillary column connector. Peak width at half height (W(h)) was used to evaluate the band broadening of the coupled column system. The length of the short couple column and oven temperature program were discussed according to W(h). The precisions of the coupled column were analyzed with peak area and retention time. Good linear correlations were found for both rodenticides. Typical samples were discussed for each rodenticide and some poisoning cases were presented.

  10. Rare alleles within the CYP2E1 (MEOS system) could be associated with better short-term health outcome after acute methanol poisoning.

    PubMed

    Hubacek, Jaroslav A; Pelclova, Daniela; Seidl, Zdenek; Vaneckova, Manuela; Klempir, Jiri; Ruzicka, Evzen; Ridzon, Petr; Urban, Pavel; Fenclova, Zdenka; Petrik, Vit; Diblik, Pavel; Kuthan, Pavel; Miovsky, Michal; Janikova, Barbara; Adamkova, Vera; Zakharov, Sergey

    2015-02-01

    Genetic polymorphisms influence the metabolism of ethanol and methanol, but the potential effects of genetic predisposition on the clinical course, outcome and short-term health sequelae of acute methanol poisoning are unknown. To evaluate the role of the MEOS system in methanol poisoning, we analysed the effect of three polymorphisms (RsaI - rs2031920; PstI - rs3813867; insertion/deletion I/D) within the CYP2E1 enzyme (MEOS system) in 50 adult survivors of methanol poisoning and compared their genotype frequencies with 460 controls. The minor allele frequencies of all three polymorphisms were below 5% in both groups. We did not detect significant differences in the genotype frequencies between survivors of methanol poisoning and controls (p = 0.34 for the RsaI variant; p = 0.59 for the PstI variant and p = 0.21 for the I/D polymorphism). The carriers of at least one minor allele in the CYP2E1 gene had less severe clinical symptoms and better short-term outcome after acute poisoning. Variants within the CYP2E1 gene are likely not significant genetic determinants of acute methanol poisoning (if survivors are analysed), but they may influence the severity of methanol poisoning and its visual/central nervous system (CNS) outcome.

  11. A Disposable Blood Cyanide Sensor

    PubMed Central

    Tian, Yong; Dasgupta, Purnendu K.; Mahon, Sari B.; Ma, Jian; Brenner, Matthew; Wang, Jian-Hua; Boss, Gerry R.

    2013-01-01

    Deaths due to smoke inhalation in fires are often due to poisoning by HCN. Rapid administration of antidotes can result in complete resuscitation of the patient but judicious dosing requires the knowledge of the level of cyanide exposure. Rapid sensitive means for blood cyanide quantitation are needed. Hydroxocyanocobinamide (OH(CN)Cbi) reacts with cyanide rapidly; this is accompanied by a large spectral change. The disposable device consists of a pair of nested petri dish bottoms and a single top that fits the outer bottom dish. The top cover has a diametrically strung porous polypropylene membrane tube filled with aqueous OH(CN)Cbi. One end of the tube terminates in an amber (583 nm) light emitting diode; the other end in a photodiode via an acrylic optical fiber. An aliquot of the blood sample is put in the inner dish, the assembly covered and acid is added through a port in the cover. Evolved HCN diffuses into the OH(CN)Cbi solution and the absorbance in the long path porous membrane tube cell is measured within 160s. The LOD was 0.047, 1.0, 0.15, 5.0 and 2.2 μM, respectively, for water (1 mL), bovine blood (100 μL, 1 mL), and rabbit blood (20μL, 50 μL). RSDs were < 10% in all cases and the linear range extended from 0.5 to 200 μM. The method was validated against a microdiffusion approach and applied to the measurement of cyanide in rabbit and human blood. The disposable device permits field measurement of blood cyanide in < 4 min. PMID:23473259

  12. Kind and estimated stocking amount of antidotes for initial treatment for acute poisoning at emergency medical centers in Korea.

    PubMed

    Sohn, Chang Hwan; Ryoo, Seung Mok; Lim, Kyoung Soo; Kim, Won; Lim, Hoon; Oh, Bum Jin

    2014-11-01

    Antidotes for toxicological emergencies can be life-saving. However, there is no nationwide estimation of the antidotes stocking amount in Korea. This study tried to estimate the quantities of stocking antidotes at emergency department (ED). An expert panel of clinical toxicologists made a list of 18 emergency antidotes. The quantity was estimated by comparing the antidote utilization frequency in a multicenter epidemiological study and the nation-wide EDs' data of National Emergency Department Information System (NEDIS). In an epidemiological study of 11 nationwide EDs from January 2009 to December 2010, only 92 (1.9%) patients had been administered emergency antidotes except activated charcoal among 4,870 cases of acute adult poisoning patients. Comparing with NEDIS data, about 1,400,000 patients visited the 124 EDs nationwide due to acute poisoning and about 103,348 adult doses of the 18 emergency antidotes may be required considering poisoning severity score. Of these, 13,224 (1.9%) adult doses of emergency antidotes (575 of atropine, 144 of calcium gluconate or other calcium salts, 2,587 of flumazenil, 3,450 of N-acetylcysteine, 5,893 of pralidoxime, 287 of hydroxocobalamin, 144 of sodium nitrite, and 144 of sodium thiosulfate) would be needed for maintaining the present level of initial treatment with emergency antidotes at EDs in Korea.

  13. Reduced risk of acute poisoning in Australian cattle from used motor oils after introduction of lead-free petrol.

    PubMed

    Burren, B G; Reichmann, K G; McKenzie, R A

    2010-06-01

    Lead (Pb) poisoning of cattle has been relatively common in Australia and sump oil has been identified as an important cause of Pb toxicity for cattle because they seem to have a tendency to drink it. Lead-free petrol has been available in Australia since 1975, so the aim of this study was to assess the current risk to cattle from drinking used automotive oils. Sump or gear box oil was collected from 56 vehicles being serviced. The low levels of Pb found suggest that the removal of leaded petrol from the Australian market as a public health measure has benefited cattle by eliminating the risk of acute poisoning from used engine oil.

  14. Exposure to cyanide following a meal of cassava food.

    PubMed

    Oluwole, O S A; Onabolu, A O; Sowunmi, A

    2002-09-05

    Exposure to cyanide from gari, a popular cassava food in West Africa, is implicated in the causation of ataxic polyneuropathy and amblyopia, but this has been questioned because cyanide was not detected in gari in a study. This study was carried out to determine if gari is a source of exposure to cyanide. Gari (150 g) containing cyanohydrin, from which 128 micromol of cyanide ions could be released, was dissolved in 500 ml of cold water for each of the 12 healthy subjects to drink. Concentrations of cyanide in plasma and erythrocytes were determined at baseline and following the meal at 30 min, 1 h, hourly for 4 h and two hourly for 12 h. The mean concentrations of cyanide in the plasma were 6 micromol/l (95% CI 2-10) at baseline, 12 micromol/l (95% CI 6-17) at peak and 6 micromol/l (95% CI 2-10) on return to baseline. The mean amount of cyanide absorbed into the plasma was 13 micromol (S.D. 12), while the transit time of absorbed cyanide was 7.3 h (S.D. 2.1). This study shows that exposure to cyanide follows consumption of gari, but the amount of cyanide absorbed into the plasma from a single meal is small and unlikely to cause acute intoxication. The long transit time of absorbed cyanide in the plasma suggests that frequent intake of gari could cause cyanide to accumulate in the plasma.

  15. [Methods for the prevention and treatment of toxico-hypoxic encephalopathy in patients with acute severe poisoning].

    PubMed

    2011-01-01

    The study included 147 patients with toxico-hypoxic encephalopathy resulting from acute poisoning. It was shown that intensive therapy with cytoflavin (20 ml in 400 ml of 5% glucose solution twice daily for 7 days) reduced severity of hypoxic brain lesions and suppression of CNS as apparent from the improvement of its bioelectric activity. The recovery of CNS regulatory action on the life-sustaining systems of the body promoted normalization of the respiratory component of oxygen transport. The improvement of the patients' conditions in the acute phase contributed to accelerated recovery of cognitive-amnestic functions and social adaptation. Cytoflavin therapy improved the clinical picture of toxico-hypoxic encephalopathy due to the reduction in the duration of the comatose state from 45.3 +/- 8.2 to 27.7 +/- 6.9 hr and the decrease in the frequency of secondary pulmonary complications from 72.7 to 35.9%.

  16. Expression of mRNA in the frontal cortex and hypothalamus in a rat model of acute carbon dioxide poisoning.

    PubMed

    Sato, Kazuo; Tsuji, Akiko; Usumoto, Yosuke; Kudo, Keiko; Yokoyama, Takeshi; Ikeda, Noriaki

    2016-03-01

    Acute carbon dioxide (CO2) poisoning causes no specific features that are revealed upon autopsy, and the pathophysiological mechanism of this syndrome is unclear. To address this issue, in the present study, we exposed rats to CO2 concentrations ranging from 10% to 60% and determined the effects on mRNA expression. According to the results of Gene Ontology (GO) and cluster analyses of microarrays data, we selected the following genes for further analysis: alkylglycerone phosphate synthase (Agps), hypocretin (Hcrt), tyrosine hydroxylase (Th), heat shock protein beta 2 (Hspb2), and opioid receptor delta 1 (Oprd1) expressed in the frontal cortex and renin (Ren), pancreatic polypeptide (Ppy), corticotropin releasing hormone receptor 2 (Crhr2), carbonic anhydrase 1 (Car1), and hypocretin receptor 1 (Hcrtr1) expressed in the hypothalamus. We found significant differences between the expression levels of Agps and Hspb2 mRNAs in the frontal cortex and that of Ppy, Crhr2 mRNAs in the hypothalamus in the presence of high concentrations of CO2. Further investigation of these genes may clarify the pathophysiology of acute CO2 poisoning and facilitate the development of novel forensic tests that can diagnose the cause of death.

  17. Rapid Field-Usable Cyanide Sensor Development for Blood and Saliva

    DTIC Science & Technology

    2013-12-01

    AD_________________ Award Number: W81XWH-12-2-0123 TITLE: Rapid Field-Usable Cyanide Sensor...ANNUAL REPORT 3. DATES COVERED (From - To) 26 2012 25 2013 4. TITLE AND SUBTITLE Rapid Field-Usable Cyanide Sensor Development for Blood and...Approved for Public Release; Distribution Unlimited 13. SUPPLEMENTARY NOTES 14. ABSTRACT Cyanide is a deadly poison which may be ingested or inhaled

  18. [Acute accidental poisoning in children: aspects of their epidemiology, aetiology, and outcome at the Charles de Gaulle Paediatric Hospital in Ouagadougou (Burkina Faso)].

    PubMed

    Kouéta, Fla; Dao, Lassina; Yé, Diarra; Fayama, Zéinabou; Sawadogo, Alphonse

    2009-01-01

    Accidents are a daily concern in the paediatric ward because of their frequency, diversity and severity. Acute accidental poisoning (AAP) accounts for an important portion of these. To help improvement management of AAP, we conducted a retrospective study covering a period of 2 years from January 2005 to December 2006 at Charles de Gaulle Paediatric University Hospital in Ouagadougou. Of 9390 admissions during the study period, 123 children, or 1.3%, were admitted for poisoning. A cumulative average of 11 were admitted monthly, with a peak of 16 patients in April 2005 and 2006, together. AAP was most common among children aged 1 to 4 years. Their mean age was 3 years and ranged from 6 days to 12 years. Boys outnumbered girls, with a sex ratio of 1.2. Mothers of more than half (61%) of the children poisoned worked in the home. Household products accounted for 44.7% of AAPs, followed by drug (22.7%) and food (22%) poisoning. Kerosene and other petroleum products topped the list of household products, with 54.5%. Tranquilizers (46.4%) and dairy products (37%) dominated the drug and food poisoning categories. Immediate outcome was fatal in 3% of cases, and three quarters of these deaths occurred during drug poisoning of children aged 1 to 4 years. The mean hospital stay was 2 days, and ranged from 0 to 9 days. Health officials, the media, and community outreach must all help to increase awareness about the dangers of poisoning and of preventive measures.

  19. Influence of pesticide regulation on acute poisoning deaths in Sri Lanka.

    PubMed Central

    Roberts, Darren M.; Karunarathna, Ayanthi; Buckley, Nick A.; Manuweera, Gamini; Sheriff, M. H. Rezvi; Eddleston, Michael

    2003-01-01

    OBJECTIVES: To assess in a developing Asian country the impact of pesticide regulation on the number of deaths from poisoning. These regulations, which were implemented in Sri Lanka from the 1970s, aimed to reduce the number of deaths - the majority from self-poisoning - by limiting the availability and use of highly toxic pesticides. METHODS: Information on legislative changes was obtained from the Ministry of Agriculture, national and district hospital admission data were obtained from the Sri Lanka Health Statistics Unit, and individual details of deaths by pesticide poisoning were obtained from a manual review of patients' notes and intensive care unit records in Anuradhapura. FINDINGS: Between 1986 and 2000, the total national number of admissions due to poisoning doubled, and admissions due to pesticide poisoning increased by more than 50%. At the same time, the case fatality proportion (CFP) fell for total poisonings and for poisonings due to pesticides. In 1991_92, 72% of pesticide-induced deaths in Anuradhapura were caused by organophosphorus (OP) and carbamate pesticides - in particular, the WHO class I OPs monocrotophos and methamidophos. From 1991, the import of these pesticides was reduced gradually until they were banned for routine use in January 1995, with a corresponding fall in deaths. Unfortunately, their place in agricultural practice was taken by the WHO class II organochlorine endosulfan, which led to a rise in deaths from status epilepticus - from one in 1994 to 50 in 1998. Endosulfan was banned in 1998, and over the following three years the number of endosulfan deaths fell to three. However, at the end of the decade, the number of deaths from pesticides was at a similar level to that of 1991, with WHO class II OPs causing the most deaths. Although these drugs are less toxic than class I OPs, the management of class II OPs remains difficult because they are, nevertheless, still highly toxic, and their toxicity is exacerbated by the paucity

  20. Acute kidney injury by cantharidin poisoning following a silly bet on an ugly beetle

    PubMed Central

    Cotovio, Patrícia; Silva, Cristina; Guedes Marques, Maria; Ferrer, Francisco; Costa, Fátima; Carreira, Armando; Campos, Mário

    2013-01-01

    Cantharidin is a poisonous substance secreted by blister beetles, including the ‘Spanish fly’. Historically, cantharidin was used as an aphrodisiac, vesicant and abortifacient. Symptoms of poisoning include gastrointestinal and genitourinary mucosal irritation along with renal dysfunction. We present the case of a reckless 23-year-old soldier who accepted the challenge of eating a beetle (Berberomeloe majalis). Six hours later he was admitted to the emergency room with abdominal pain, dysuria, gross haematuria with clots, hypotension, fever and renal insufficiency. With intravenous fluid therapy, he recovered clinically. Laboratory parameters returned to normal within 1 week. PMID:26019851

  1. Reversible cerebral periventricular white matter changes with corpus callosum involvement in acute toluene-poisoning.

    PubMed

    Lin, Chih-Ming; Liu, Chi-Kuang

    2015-01-01

    Substance poisoning, such as toluene intoxication, has seldom been reported in the relevant literature. The documented cerebral neuroimaging has mostly described reversible symmetrical white matter changes in both the cerebral and cerebellar hemispheres. This paper presents 2 patients with toluene poisoning, whose brain magnetic resonance imaging studies showed a similar picture that included extra involvement over the corpus callosum; however, such corpus callosum involvement has never been mentioned and is quite rare in the literature. We discussed the underlying neuropathological pathways in this article. Hopefully, these cases will provide first-line clinicians with some valuable information with regard to toluene intoxication and clinical neuroimaging presentations.

  2. Physiologically available cyanide (PAC) in manufactured gas plant waste and soil samples

    SciTech Connect

    Magee, B.; Taft, A.; Ratliff, W.; Kelley, J.; Sullivan, J.; Pancorbo, O.

    1995-12-31

    Iron-complexed cyanide compounds, such as ferri-ferrocyanide (Prussian Blue), are wastes associated with former manufactured gas plant (MGP) facilities. When tested for total cyanide, these wastes often show a high total cyanide content. Because simple cyanide salts are acutely toxic, cyanide compounds can be the subject of concern. However, Prussian Blue and related species are known to have a low order of human and animal toxicity. Toxicology data on complexed cyanides will be presented. Another issue regarding Prussian Blue and related species is that the total cyanide method does not accurately represent the amount of free cyanide released from these cyanide species. The method involves boiling the sample in an acidic solution under vacuum to force the formation of HCN gas. Thus, Prussian Blue, which is known to be low in toxicity, cannot be properly evaluated with current methods. The Massachusetts Natural Gas Council initiated a program with the Massachusetts Department of Environmental Protection to develop a method that would define the amount of cyanide that is able to be converted into hydrogen cyanide under the pH conditions of the stomach. It is demonstrated that less than 1% of the cyanide present in Prussian Blue samples and soils from MGP sites can be converted to HCN under the conditions of the human stomach. The physiologically available cyanide method has been designed to be executed at a higher temperature for one hour. It is shown that physiologically available cyanide in MGP samples is < 5--15% of total cyanide.

  3. Cyanide intoxication as part of smoke inhalation--a review on diagnosis and treatment from the emergency perspective.

    PubMed

    Lawson-Smith, Pia; Jansen, Erik C; Hyldegaard, Ole

    2011-03-03

    This paper reviews the current literature on smoke inhalation injuries with special attention to the effects of hydrogen cyanide. It is assumed that cyanide poisoning is still an overlooked diagnosis in fire victims. Treatment against cyanide poisoning in the emergency setting should be given based on the clinical diagnosis only. Oxygen in combination with a recommended antidote should be given immediately, the first to reduce cellular hypoxia and the second to eliminate cyanide. A specific antidote is hydroxycobalamin, which can be given iv. and has few side effects.

  4. Cyanide and migratory birds at gold mines in Nevada, USA

    USGS Publications Warehouse

    Henny, C.J.; Hallock, R.J.; Hill, E.F.

    1994-01-01

    Since the mid-1980s, cyanide in heap leach solutions and mill tailings ponds at gold mines in Nevada has killed a large but incompletely documented number of wildlife ( gt 9,500 individuals, primarily migratory birds). This field investigation documents the availability of cyanide at a variety of 'typical' Nevada gold mines during 1990 and 1991, describes wildlife reactions to cyanide solutions, and discusses procedures for eliminating wildlife loss from cyanide poisoning. Substantial progress has been made to reduce wildlife loss. About half of the mill tailings ponds (some up to 150 ha) in Nevada have been chemically treated to reduce cyanide concentrations (the number needing treatment is uncertain) and many of the smaller heap leach solution ponds and channels are now covered with netting to exclude birds and most mammals. The discovery of a cyanide gradient in mill tailings ponds (concentration usually 2-3 times higher at the inflow point than at reclaim point) provides new insight into wildlife responses (mortality) observed in different portions of the ponds. Finding dead birds on the tops of ore heaps and associated with solution puddling is a new problem, but management procedures for eliminating this source of mortality are available. A safe threshold concentration of cyanide to eliminate wildlife loss could not be determined from the field data and initial laboratory studies. New analytical methods may be required to assess further the wildlife hazard of cyanide in mining solutions.

  5. Intravenous Lipid Emulsion as an Antidote for the Treatment of Acute Poisoning: A Bibliometric Analysis of Human and Animal Studies.

    PubMed

    Zyoud, Sa'ed H; Waring, W Stephen; Al-Jabi, Samah W; Sweileh, Waleed M; Rahhal, Belal; Awang, Rahmat

    2016-11-01

    In recent years, there has been increasing interest in the role of intravenous lipid formulations as potential antidotes in patients with severe cardiotoxicity caused by drug toxicity. The aim of this study was to conduct a comprehensive bibliometric analysis of all human and animal studies featuring lipid emulsion as an antidote for the treatment of acute poisoning. The Scopus database search was performed on 5 February 2016 to analyse the research output related to intravenous lipid emulsion as an antidote for the treatment of acute poisoning. Research indicators used for analysis included total number of articles, date (year) of publication, total citations, value of the h-index, document types, countries of publication, journal names, collaboration patterns and institutions. A total of 594 articles were retrieved from Scopus database for the period of 1955-2015. The percentage share of global intravenous lipid emulsion research output showed that research output was 85.86% in 2006-2015 with yearly average growth in this field of 51 articles per year. The USA, United Kingdom (UK), France, Canada, New Zealand, Germany, Australia, China, Turkey and Japan accounted for 449 (75.6%) of all the publications. The total number of citations for all documents was 9,333, with an average of 15.7 citations per document. The h-index of the retrieved documents for lipid emulsion research as antidote for the treatment of acute poisoning was 49. The USA and the UK achieved the highest h-indices, 34 and 14, respectively. New Zealand produced the greatest number of documents with international collaboration (51.9%) followed by Australia (50%) and Canada (41.4%) out of the total number of publications for each country. In summary, we found an increase in the number of publications in the field of lipid emulsion after 2006. The results of this study demonstrate that the majority of publications in the field of lipid emulsion were published by high-income countries. Researchers from

  6. Whole blood cyanide levels in patients with tobacco amblyopia.

    PubMed

    Jestico, J V; O'Brien, M D; Teoh, R; Toseland, P A; Wong, H C

    1984-06-01

    Three patients presented with painless bilateral visual failure due to tobacco amblyopia. The whole blood cyanide levels were raised above those predicted from their high tobacco consumption, approaching lethal levels reported from acute inhalation of cyanide. Each patient had an excessive alcohol intake with biochemical evidence of hepatic dysfunction, the elevated whole blood cyanide levels being attributed to the associated impairment of cyanide detoxification. In each case the improvement in visual acuities following abstinence and hydroxycobalamin therapy was accompanied by a reduction in the whole blood cyanide level to within the normal range. Serial measurements of whole blood cyanide, serum alcohol, and the detection of urinary nicotine provided valuable indices of the patient's subsequent compliance and clinical progress.

  7. Phosphorus poisoning in waterfowl

    USGS Publications Warehouse

    Coburn, D.R.; DeWitt, J.B.; Derby, J.V.; Ediger, E.

    1950-01-01

    Black ducks and mallards were found to be highly susceptible to phosphorus poisoning. 3 mg. of white phosphorus per kg. of body weight given in a single dose resulted in death of a black duck in 6 hours. Pathologic changes in both acute and chronic poisoning were studied. Data are presented showing that diagnosis can be made accurately by chemical analysis of stored tissues in cases of phosphorus poisoning.

  8. Acute cardiogenic pulmonary oedema with multiorgan dysfunction--still to learn more about nitrobenzene poisoning.

    PubMed

    Agrawal, Avinash; Gutch, Manish; Arora, Rahul; Jain, Nirdesh

    2011-12-20

    Nitrobenzene is a nitrite compound often used in polishes or solvents. Its toxic effects are due to its ability to induce methaemoglobinaemia. The clinical presentation of this poisoning varies according to the concentration of methaemoglobin level in blood. The importance of early identification of the compound on the basis of clinical suspicion corroborative with methaemoglobin level with timely intervention is required to prevent fatal outcome. It is also important to take care of the secondary cycling of nitrobenzene from body stores to prevent secondary recurrence of symptoms in patients after heavy exposure. Here author reports a rare case of accidental poisoning with nitrobenzene presented with respiratory distress and cyanosis. On investigation, he was diagnosed to have cardiogenic pulmonary oedema and multiorgan dysfunction. The urgent institution of methylene blue as specific antidote along with haemodynamic and ventilatory support was proved crucial for life saving of the patient.

  9. Acute cardiogenic pulmonary oedema with multiorgan dysfunction – still to learn more about nitrobenzene poisoning

    PubMed Central

    Agrawal, Avinash; Gutch, Manish; Arora, Rahul; Jain, Nirdesh

    2011-01-01

    Nitrobenzene is a nitrite compound often used in polishes or solvents. Its toxic effects are due to its ability to induce methaemoglobinaemia. The clinical presentation of this poisoning varies according to the concentration of methaemoglobin level in blood. The importance of early identification of the compound on the basis of clinical suspicion corroborative with methaemoglobin level with timely intervention is required to prevent fatal outcome. It is also important to take care of the secondary cycling of nitrobenzene from body stores to prevent secondary recurrence of symptoms in patients after heavy exposure. Here author reports a rare case of accidental poisoning with nitrobenzene presented with respiratory distress and cyanosis. On investigation, he was diagnosed to have cardiogenic pulmonary oedema and multiorgan dysfunction. The urgent institution of methylene blue as specific antidote along with haemodynamic and ventilatory support was proved crucial for life saving of the patient. PMID:22669995

  10. Legalon® SIL: the antidote of choice in patients with acute hepatotoxicity from amatoxin poisoning.

    PubMed

    Mengs, Ulrich; Pohl, Ralf-Torsten; Mitchell, Todd

    2012-08-01

    More than 90% of all fatal mushroom poisonings worldwide are due to amatoxin containing species that grow abundantly in Europe, South Asia, and the Indian subcontinent. Many cases have also been reported in North America. Initial symptoms of abdominal cramps, vomiting, and a severe cholera-like diarrhea generally do not manifest until at least six to eight hours following ingestion and can be followed by renal and hepatic failure. Outcomes range from complete recovery to fulminant organ failure and death which can sometimes be averted by liver transplant. There are no controlled clinical studies available due to ethical reasons, but uncontrolled trials and case reports describe successful treatment with intravenous silibinin (Legalon® SIL). In nearly 1,500 documented cases, the overall mortality in patients treated with Legalon® SIL is less than 10% in comparison to more than 20% when using penicillin or a combination of silibinin and penicillin. Silibinin, a proven antioxidative and anti-inflammatory acting flavonolignan isolated from milk thistle extracts, has been shown to interact with specific hepatic transport proteins blocking cellular amatoxin re-uptake and thus interrupting enterohepatic circulation of the toxin. The addition of intravenous silibinin to aggressive intravenous fluid management serves to arrest and allow reversal of the manifestation of fulminant hepatic failure, even in severely poisoned patients. These findings together with the available clinical experience justify the use of silibinin as Legalon® SIL in Amanita poisoning cases.

  11. Cyanides and their toxicity: a literature review.

    PubMed

    Egekeze, J O; Oehme, F W

    1980-04-15

    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.

  12. Food Poisoning

    MedlinePlus

    ... de los dientes Video: Getting an X-ray Food Poisoning KidsHealth > For Kids > Food Poisoning Print A ... find out how to avoid it. What Is Food Poisoning? Food poisoning comes from eating foods that ...

  13. Nitrocobinamide, a new cyanide antidote that can be administered by intramuscular injection.

    PubMed

    Chan, Adriano; Jiang, Jingjing; Fridman, Alla; Guo, Ling T; Shelton, G Diane; Liu, Ming-Tao; Green, Carol; Haushalter, Kristofer J; Patel, Hemal H; Lee, Jangwoen; Yoon, David; Burney, Tanya; Mukai, David; Mahon, Sari B; Brenner, Matthew; Pilz, Renate B; Boss, Gerry R

    2015-02-26

    Currently available cyanide antidotes must be given by intravenous injection over 5-10 min, making them ill-suited for treating many people in the field, as could occur in a major fire, an industrial accident, or a terrorist attack. These scenarios call for a drug that can be given quickly, e.g., by intramuscular injection. We have shown that aquohydroxocobinamide is a potent cyanide antidote in animal models of cyanide poisoning, but it is unstable in solution and poorly absorbed after intramuscular injection. Here we show that adding sodium nitrite to cobinamide yields a stable derivative (referred to as nitrocobinamide) that rescues cyanide-poisoned mice and rabbits when given by intramuscular injection. We also show that the efficacy of nitrocobinamide is markedly enhanced by coadministering sodium thiosulfate (reducing the total injected volume), and we calculate that ∼1.4 mL each of nitrocobinamide and sodium thiosulfate should rescue a human from a lethal cyanide exposure.

  14. Cyanide Suicide After Deep Web Shopping: A Case Report.

    PubMed

    Le Garff, Erwan; Delannoy, Yann; Mesli, Vadim; Allorge, Delphine; Hédouin, Valéry; Tournel, Gilles

    2016-09-01

    Cyanide is a product that is known for its use in industrial or laboratory processes, as well as for intentional intoxication. The toxicity of cyanide is well described in humans with rapid inhibition of cellular aerobic metabolism after ingestion or inhalation, leading to severe clinical effects that are frequently lethal. We report the case of a young white man found dead in a hotel room after self-poisoning with cyanide ordered in the deep Web. This case shows a probable complex suicide kit use including cyanide, as a lethal tool, and dextromethorphan, as a sedative and anxiolytic substance. This case is an original example of the emerging deep Web shopping in illegal drug procurement.

  15. [Analysis of psychotropic drug mixtures using high-pressure liquid chromatography in acute poisoning cases].

    PubMed

    Kazlauskiene, Daiva; Vainauskas, Paulius; Kazlauskas, Saulius

    2002-01-01

    The qualitative and quantitative method of determination of amitryptilin, codeine and fluoxetine in the mixture using high-pressure liquid chromatography is described in this paper. Chromatogram is presented which shows, that preparations are fully separated and do not interfere each others analysis. Tables with chromatographical separation characteristics are also presented. Proposed calibration curves of quantitative analysis and calculated medium relative error of quantitative ascertainment for every preparation of the mixture are shown. Final conclusion: method is applicable for qualitative and quantitative analysis of amitryptiline, fluoxetine and codeine in the mixture in hasty poisoning cases.

  16. Use of β-Blockade and Hemoperfusion for Acute Theophylline Poisoning

    PubMed Central

    Biberstein, Michael P.; Ziegler, Michael G.; Ward, David M.

    1984-01-01

    Five adults were treated successfully for severe theophylline poisoning due to intentional overdosage. Clinical features included nausea, tremor, delirium, hypotension and cardiac arrhythmias, metabolic acidosis, hyperglycemia, hypokalemia and hypophosphatemia. No seizures or deaths occurred despite very high serum theophylline concentrations (between 96 and 194 μg per ml). Extreme elevations of plasma catecholamines were documented and are implicated in the toxicity. β-Blockade with intravenous administration of propranolol hydrochloride was the most effective therapy for theophylline-induced hypotension. All patients were treated with resin hemoperfusion, which resulted in significant clinical improvement and rapid lowering of the serum theophylline level. PMID:6506685

  17. A Direct and Rapid Method to Determine Cyanide in Urine by Capillary Electrophoresis

    PubMed Central

    Zhang, Qiyang; Maddukuri, Naveen; Gong, Maojun

    2015-01-01

    Cyanides are poisonous chemicals that widely exist in nature and industrial processes as well as accidental fires. Rapid and accurate determination of cyanide exposure would facilitate forensic investigation, medical diagnosis, and chronic cyanide monitoring. Here, a rapid and direct method was developed for the determination of cyanide ions in urinary samples. This technique was based on an integrated capillary electrophoresis system coupled with laser-induced fluorescence (LIF) detection. Cyanide ions were derivatized with naphthalene-2,3-dicarboxaldehyde (NDA) and a primary amine (glycine) for LIF detection. Three separate reagents, NDA, glycine, and cyanide sample, were mixed online, which secured uniform conditions between samples for cyanide derivatization and reduced the risk of precipitation formation of mixtures. Conditions were optimized; the derivatization was completed in 2-4 minutes, and the separation was observed in 25 s. The limit of detection (LOD) was 4.0 nM at 3-fold signal-to-noise ratio for standard cyanide in buffer. The cyanide levels in urine samples from smokers and non-smokers were determined by using the method of standard addition, which demonstrated significant difference of cyanide levels in urinary samples from the two groups of people. The developed method was rapid and accurate, and is anticipated to be applicable to cyanide detection in waste water with appropriate modification. PMID:26342870

  18. A direct and rapid method to determine cyanide in urine by capillary electrophoresis.

    PubMed

    Zhang, Qiyang; Maddukuri, Naveen; Gong, Maojun

    2015-10-02

    Cyanides are poisonous chemicals that widely exist in nature and industrial processes as well as accidental fires. Rapid and accurate determination of cyanide exposure would facilitate forensic investigation, medical diagnosis, and chronic cyanide monitoring. Here, a rapid and direct method was developed for the determination of cyanide ions in urinary samples. This technique was based on an integrated capillary electrophoresis system coupled with laser-induced fluorescence (LIF) detection. Cyanide ions were derivatized with naphthalene-2,3-dicarboxaldehyde (NDA) and a primary amine (glycine) for LIF detection. Three separate reagents, NDA, glycine, and cyanide sample, were mixed online, which secured uniform conditions between samples for cyanide derivatization and reduced the risk of precipitation formation of mixtures. Conditions were optimized; the derivatization was completed in 2-4min, and the separation was observed in 25s. The limit of detection (LOD) was 4.0nM at 3-fold signal-to-noise ratio for standard cyanide in buffer. The cyanide levels in urine samples from smokers and non-smokers were determined by using the method of standard addition, which demonstrated significant difference of cyanide levels in urinary samples from the two groups of people. The developed method was rapid and accurate, and is anticipated to be applicable to cyanide detection in waste water with appropriate modification.

  19. Toxicology in the Old Testament. Did the High Priest Alcimus die of acute aconitine poisoning?

    PubMed

    Moog, Ferdinand P; Karenberg, Axel

    2002-01-01

    The Bible contains several interesting contributions to the history of neurology, as is the case of the High Priest Alkimos, who died suddenly in 159 BC. He was regarded as a stereotypical stroke victim for a long time. The reports on his death in the Septauginta and the later 'Jewish Antiquities' of Flavius Josephus present some typical symptoms of stroke (collapse, loss of speech and death within a short time), but they also describe severe pains, which are very unusual among patients with stroke. Similar symptoms can be found in the case of the Roman emperor Claudius, who was poisoned by his spouse Agrippina. It was thought that she used aconitine, an ingredient of the monkshood plant (Aconitum napellus L.), which imitates an apoplectic insult, but also causes vehement pains. It was therefore possible that something similar had happened to Alkimos, as aconitine was a common poison in ancient times and the surroundings of his death may confirm the suspicion. Reigning during a time of great upheaval, Alkimos was able to maintain his high office chiefly because of the help of the Seleucides. He has just begun construction work on the temple of Jerusalem, an order, which was regarded as a sacrilege by his foes. This impression was enhanced by his subsequent illness which could be considered as a divine punishment.

  20. Effects of a selective Rho-kinase inhibitor Y-27632 on oxidative stress parameters in acute dichlorvos poisoning in rats.

    PubMed

    Gunay, N; Kose, B; Demiryurek, S; Ocak, A R; Erel, O; Demiryurek, A T

    2008-10-01

    This study examined the effects of Y-27632, a selective Rho-kinase inhibitor, on organophosphate-induced acute toxicity in rats. Rats were randomly divided into four groups as control (corn oil), dichlorvos (30 mg kg(-1) i.p.), 1 and 10 mg kg(-1) Y-27632 + dichlorvos groups. Cholinergic signs (fatigue, tremor, cyanosis, hyper-secretion, fasciculations) were observed in all the rats in the dichlorvos group and the mortality rate was 50%. No cholinergic findings and deaths were observed in the control and Y-27632 groups. Plasma cholinesterase activities were suppressed with dichlorvos and these reductions were attenuated with Y-27632 pretreatment. There was a marked increase in plasma malondialdehyde level in the dichlorvos group, but Y-27632 pretreatment abolished this elevation. Dichlorvos markedly depressed cardiac paraoxonase activity, but these changes were not markedly modified with Y-27632. Total antioxidant capacities, total oxidant status, oxidative stress index, total free sulfhydryl groups and catalase activities in plasma and cardiac tissues were not markedly different between the groups. No significant changes were observed with cardiac myeloperoxidase activities or plasma arylesterase and ceruloplasmin activities. In conclusion, our results suggest that Rho-kinase pathway is involved in organophosphate intoxication, and a decrease in cardiac paraoxonase activities may play a role in the pathogenesis of acute organophosphate poisoning in rats.

  1. Therapeutic effectiveness of sustained low-efficiency hemodialysis plus hemoperfusion and continuous hemofiltration plus hemoperfusion for acute severe organophosphate poisoning.

    PubMed

    Hu, Shou-liang; Wang, Dan; Jiang, Hong; Lei, Qing-feng; Zhu, Xiao-hua; Cheng, Jun-zhang

    2014-02-01

    There is no report on the effects of sustained low-efficiency dialysis (SLED) plus hemoperfusion (HP) (SLED + HP) in patients with acute severe organophosphate (OP) poisoning (ASOPP). This study was designed to compare the therapeutic effectiveness between SLED + HP and continuous hemofiltration (CHF) plus HP (CHF + HP) in patients with ASOPP. In order to assess the two treatment methods, 56 patients with ASOPP were divided into CHF + HP group and SLED + HP group. The biochemical indicators, in-hospital duration, hemodynamic parameters, Acute Physiology, and Chronic Health Evaluation (APACHE II) score, and survival and mortality rates were compared. In both groups after treatment, the levels of serum creatine kinase isozyme MB, creatine kinase, creatinine, glutamic-oxalacetic transaminease, and glutamate-pyruvate transaminase, and the APACHE II scores on the first, second, and seventh day decreased (P < 0.05), whereas the levels of serum acetylcholinesterase increased. The two groups showed no statistical differences in in-hospital duration, biochemical indicators, APACHE II score, hemodynamic parameters, survival rate, or the mortality rate (P > 0.05). In conclusion, SLED has similar hemodynamic stability to CHF and the two treatment methods have similar effects on ASOPP patients. More importantly, SLED plus HP is relatively economical and convenient for patients with ASOPP in clinical practice.

  2. Acute severe poisoning in Spain: clinical outcome related to the implicated drugs.

    PubMed

    Frati, M E; Marruecos, L; Porta, M; Martín, M L; Laporte, J R

    1983-10-01

    The 91 patients over the age of 10 (57 women and 32 men) with severe self-poisoning admitted to the ICU of a general hospital in Barcelona during the period 1974-1980 have been retrospectively studied. Previous suicidal attempts have been identified among 32 patients; 26 patients presented a history of personality disorders, and 19 had a neurological disease, a chronic physical illness, or a history of alcoholism. Sedative-hypnotic drugs were involved in about half the number of cases, and one fifth of total cases were due to tricyclic antidepressants and phenothiazines. Paracetamol was only involved in 2 cases, and heroin in another 2 cases. Many of the most severe morbidity manifestations were related to overdoses by intermediate-acting barbiturates. Two out of a total of 5 deaths were related to butalbitone overdose. Butalbitone had been ingested as a fixed-dose combination containing butalbitone, propyphenazone, and caffeine, which is freely dispensed as an analgesic in Spain.

  3. Acute and chronic methyl mercury poisoning impairs rat adrenal and testicular function

    SciTech Connect

    Burton, G.V.; Meikle, A.W.

    1980-05-01

    Animals poisoned with methyl mercury (CH/sub 3/Hg) exhibit stress intolerance and decreased sexual activity, which suggest both adrenal and testicular dysfunction. Adrenal and testicular function was studied in male rats after treatment with CH/sub 3/Hg. In animals treated chronically, the adrenal glands were markedly hyperplastic with enlargement of the zona fasciculata. The mean basal serum levels of corticosterone were similar in experimental (17.8 ..mu..g/dl) and control (16.8 ..mu..g/dl) groups. However, with ether stress, experimental animals had a subnormal response, and the mean serum levels of corticosterone increased to only 23.9 ..mu../dl compared to 40.6 ..mu..g/dl in the controls. Exogenous ACTH stimulation produced a mean level of 19.0 ..mu..g/dl in the CH/sub 3/Hg-treated animals and 49.7 ..mu..g/dl in the controls. In vitro studies demonstrated a defect in the conversion of cholesterol to pregnenolone. A profound impairment in swimming was partially reversed with glucocorticoid therapy. In animals treated with CH/sub 3/Hg, serum testosterone was lower than normal in the basal state. Human chorionic gonadotropin stimulation increased the mean serum concentration of testosterone to 23.4 ng/ml in controls, but it was only 4.50 ng/ml in experimental animals. The data indicate that CH/sub 3/Hg poisoning impairs adrenal and testicular steroid hormone secretion, which accounts in part for the diminished stress tolerance and decreased sexual activity observed in CH/sub 3/Hg-intoxicated animals.

  4. Limitations and challenges in treatment of acute chemical warfare agent poisoning.

    PubMed

    Thiermann, Horst; Worek, Franz; Kehe, Kai

    2013-12-05

    Recent news from Syria on a possible use of chemical warfare agents made the headlines. Furthermore, the motivation of terrorists to cause maximal harm shifts these agents into the public focus. For incidents with mass casualties appropriate medical countermeasures must be available. At present, the most important threats arise from nerve agents and sulfur mustard. At first, self-protection and protection of medical units from contamination is of utmost importance. Volatile nerve agent exposure, e.g. sarin, results in fast development of cholinergic crisis. Immediate clinical diagnosis can be confirmed on-site by assessment of acetylcholinesterase activity. Treatment with autoinjectors that are filled with 2mg atropine and an oxime (at present obidoxime, pralidoxime, TMB-4 or HI-6) are not effective against all nerve agents. A more aggressive atropinisation has to be considered and more effective oximes (if possible with a broad spectrum or a combination of different oximes) as well as alternative strategies to cope with high acetylcholine levels at synaptic sites should be developed. A further gap exists for the treatment of patients with sustained cholinergic crisis that has to be expected after exposure to persistent nerve agents, e.g. VX. The requirement for long-lasting artificial ventilation can be reduced with an oxime therapy that is optimized by using the cholinesterase status for guidance or by measures (e.g. scavengers) that are able to reduce the poison load substantially in the patients. For sulfur mustard poisoning no specific antidote is available until now. Symptomatic measures as used for treatment of burns are recommended together with surgical or laser debridement. Thus, huge amounts of resources are expected to be consumed as wound healing is impaired. Possible depots of sulfur mustard in tissues may aggravate the situation. More basic knowledge is necessary to improve substantially therapeutic options. The use of stem cells may provide a new

  5. Electrolyte Imbalances and Nephrocalcinosis in Acute Phosphate Poisoning on Chronic Type 1 Renal Tubular Acidosis due to Sjögren's Syndrome

    PubMed Central

    Cho, Sung-Gun; Han, Sang-Woong; Kim, Ho-Jung

    2013-01-01

    Although renal calcium crystal deposits (nephrocalcinosis) may occur in acute phosphate poisoning as well as type 1 renal tubular acidosis (RTA), hyperphosphatemic hypocalcemia is common in the former while normocalcemic hypokalemia is typical in the latter. Here, as a unique coexistence of these two seperated clinical entities, we report a 30-yr-old woman presenting with carpal spasm related to hypocalcemia (ionized calcium of 1.90 mM/L) due to acute phosphate poisoning after oral sodium phosphate bowel preparation, which resolved rapidly after calcium gluconate intravenously. Subsequently, type 1 RTA due to Sjögren's syndrome was unveiled by sustained hypokalemia (3.3 to 3.4 mEq/L), persistent alkaline urine pH (> 6.0) despite metabolic acidosis, and medullary nephrocalcinosis. Through this case report, the differential points of nephrocalcinosis and electrolyte imbalances between them are discussed, and focused more on diagnostic tests and managements of type 1 RTA. PMID:23400265

  6. Nitryl cyanide, NCNO₂.

    PubMed

    Rahm, Martin; Bélanger-Chabot, Guillaume; Haiges, Ralf; Christe, Karl O

    2014-07-01

    The elusive nitryl cyanide, NCNO2, has been synthesized and characterized. It was prepared in good yield, isolated by fractional condensation, characterized by NMR and vibrational spectroscopy, and studied by theoretical calculations. Nitryl cyanide holds promise as a high energy density material (HEDM) and might also prove useful as a HEDM building block. The simplicity and inherent stability of nitryl cyanide, together with the known multitude of nitriles in interstellar space, suggest that the compound might also be a potential candidate for observations in atmospheric and interstellar chemistry.

  7. Acute pancreatitis: a lesser-known complication of aluminum phosphide poisoning.

    PubMed

    Verma, S K; Ahmad, S; Shirazi, N; Barthwal, S P; Khurana, D; Chugh, M; Gambhir, H S

    2007-12-01

    There have been no case reports on aluminum phosphide-induced pancreatitis in the literature available. In this report, we present the case of a young man who developed acute pancreatitis and probably acute myocarditis following ingestion of aluminum phosphide pellets in the absence of the usual risk factors and after exclusion of other possible causes of pancreatitis. In the absence of re-challenge, we put forth the probable causative association of pancreatitis with aluminum phosphide or phosphine gas, its active pesticidal component.

  8. Inconceivable Hypokalemia: A Case Report of Acute Severe Barium Chloride Poisoning

    PubMed Central

    Man, Yanru; Shi, Xiaoyuan; Zhu, Jun; Pan, Hang; Qin, Qin

    2016-01-01

    Barium is a heavy divalent alkaline earth metal that has been known as a muscle poison. Barium can cause human toxicity, which may lead to significant hypokalemia and have serious consequences. This paper reports a case of unprecedented barium intoxication in which the patient, who suffered from depression, swallowed at least 3.0 g barium chloride to commit suicide. On admission, the patient presented with nausea, vomiting, stomach burning feeling, dizziness, and weakness. Emergency biochemical testing showed that the patient was suffering from severe hypokalemia (K+ 1.7 mmol/L). His electrocardiogram (ECG) prompted atrioventricular blocking, ventricular tachycardia, prolongation of PR interval, ST segment depression with U waves, and T wave inversion. Intravenous potassium supplements were given immediately to correct hypokalemia and regular monitoring of vital signs and fluid balance was arranged. After all-out rescue of our hospital personnel, the condition of the patient is currently stable and he is gradually recovering. This case exemplifies the weaknesses of the management of toxic substances and the lack of mental health education for young people. We hope to get more attention for the supervision of toxic substances and the healthy development of young people. PMID:27840643

  9. [Study of blood concentration analysis for formate in acute methanol poisoning].

    PubMed

    Morikawa, Go; Okazawa, Katsuko; Shimizu, Takahiro; Otagiri, Sayoko; Fuwa, Fumiko; Nakagawa, Saori; Yamato, Susumu

    2015-09-01

    A 53-year-old woman ingested about 300 mL of 95% methanol. After immediate ethanol antagonist therapy and hemodialysis, she recovered completely. Few days later, the plasma concentration of methanol and formate was measured. A gas chromatography was used for the plasma methanol concentration measurement, and a colorimetric method was used for plasma formate concentration measurement (Formate Colorimetric Assay Kit; BioVision, California, USA). Patient's plasma methanol concentration before hemodialysis was 676.9 mg/dL and plasma formate concentration was 16.9 mg/dL. By removing blood methanol and formate using hemodialysis before formate accumulations in the body, the patient was discharged without any sequelae. We were able to obtain correlation between a gas chromatography and colorimetric method without gas chromatography-mass spectrometry, with good correlation coefficients. The sensitivity was sufficient for analyzing blood sample. Monitoring formate concentration is useful in determining the treatment and evaluating the prognosis of methanol poisoning. We suggest that this colorimetric method is useful in a facility with no access to a gas chromatography in order to measure a plasma formate concentration.

  10. Protection from cyanide-induced brain injury by the Nrf2 transcriptional activator carnosic acid.

    PubMed

    Zhang, Dongxian; Lee, Brian; Nutter, Anthony; Song, Paul; Dolatabadi, Nima; Parker, James; Sanz-Blasco, Sara; Newmeyer, Traci; Ambasudhan, Rajesh; McKercher, Scott R; Masliah, Eliezer; Lipton, Stuart A

    2015-06-01

    Cyanide is a life-threatening, bioterrorist agent, preventing cellular respiration by inhibiting cytochrome c oxidase, resulting in cardiopulmonary failure, hypoxic brain injury, and death within minutes. However, even after treatment with various antidotes to protect cytochrome oxidase, cyanide intoxication in humans can induce a delayed-onset neurological syndrome that includes symptoms of Parkinsonism. Additional mechanisms are thought to underlie cyanide-induced neuronal damage, including generation of reactive oxygen species. This may account for the fact that antioxidants prevent some aspects of cyanide-induced neuronal damage. Here, as a potential preemptive countermeasure against a bioterrorist attack with cyanide, we tested the CNS protective effect of carnosic acid (CA), a pro-electrophilic compound found in the herb rosemary. CA crosses the blood-brain barrier to up-regulate endogenous antioxidant enzymes via activation of the Nrf2 transcriptional pathway. We demonstrate that CA exerts neuroprotective effects on cyanide-induced brain damage in cultured rodent and human-induced pluripotent stem cell-derived neurons in vitro, and in vivo in various brain areas of a non-Swiss albino mouse model of cyanide poisoning that simulates damage observed in the human brain. Cyanide, a potential bioterrorist agent, can produce a chronic delayed-onset neurological syndrome that includes symptoms of Parkinsonism. Here, cyanide poisoning treated with the proelectrophillic compound carnosic acid, results in reduced neuronal cell death in both in vitro and in vivo models through activation of the Nrf2/ARE transcriptional pathway. Carnosic acid is therefore a potential treatment for the toxic central nervous system (CNS) effects of cyanide poisoning. ARE, antioxidant responsive element; Nrf2 (NFE2L2, Nuclear factor (erythroid-derived 2)-like 2).

  11. Use of cyanide antidotes in burn patients with suspected inhalation injuries in North America: a cross-sectional survey.

    PubMed

    Dumestre, Danielle; Nickerson, Duncan

    2014-01-01

    This study aimed to assess the use of cyanide antidotes and the determine the opinion on empiric administration of hydroxocobalamin in North American burn patients with suspected smoke inhalation injuries. An online cross-sectional survey was sent to directors of 90 major burn centers in North America, which were listed on the American Burn Association Web site. A multiple-choice format was used to determine the percentage of patients tested for cyanide poisoning on admission, the current administration of a cyanide antidote based solely on clinical suspicion of poisoning, and the antidote used. To ascertain views on immediate administration of hydroxocobalamin before confirmation of cyanide poisoning an option was included to expand the response in written format. Twenty-nine of 90 burn directors (32%) completed the survey. For the population of interest, the majority of burn centers (59%) do not test for cyanide poisoning on admission and do not administer an antidote based solely on clinical suspicion of cyanide poisoning (58%). The most commonly available antidote is hydroxocobalamin (50%), followed by the cyanide antidote kit (29%). The opinion regarding instant administration of hydroxocobalamin when inhalation injury is suspected is mixed: 31% support its empiric use, 17% do not, and the remaining 52% have varying degrees of confidence in its utility. In North America, most patients burnt in closed-space fires with inhalation injuries are neither tested for cyanide poisoning in a timely manner nor empirically treated with a cyanide antidote. Although studies have shown the safety and efficacy of empiric and immediate administration of hydroxocobalamin, most centers are not willing to do so.

  12. Acute liver failure due to zinc phosphide containing rodenticide poisoning: Clinical features and prognostic indicators of need for liver transplantation.

    PubMed

    Saraf, Vivek; Pande, Supriya; Gopalakrishnan, Unnikrishnan; Balakrishnan, Dinesh; Menon, Ramachandran N; Sudheer, O V; Dhar, Puneet; Sudhindran, S

    2015-07-01

    Zinc phosphide (ZnP) containing rodenticide poisoning is a recognized cause of acute liver failure (ALF) in India. When standard conservative measures fail, the sole option is liver transplantation. Records of 41 patients admitted to a single centre with ZnP-induced ALF were reviewed to identify prognostic indicators for requirement of liver transplantation. Patients were analyzed in two groups: group I (n = 22) consisted of patients who either underwent a liver transplant (n = 14) or died without a transplant (n = 8); group II (n = 19) comprised those who survived without liver transplantation. International normalized ratio (INR) in group I was 9 compared to 3 in group II (p < 0.001). Encephalopathy occurred only in group I. Model for End-Stage Liver Disease (MELD) score in group I was 41 compared to 24 in group II (p < 0.001). MELD score of 36 (sensitivity of 86.7 %, specificity of 90 %) or a combination of INR of 6 and encephalopathy (sensitivity of 100 %, specificity of 83 %) were the best indicators of mortality. Such patients should undergo urgent liver transplantation.

  13. Cologne poisoning

    MedlinePlus

    ... the product Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  14. Deodorant poisoning

    MedlinePlus

    ... if known) Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  15. Yew poisoning

    MedlinePlus

    ... if known Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  16. Bee poison

    MedlinePlus

    ... page: //medlineplus.gov/ency/article/002847.htm Bee poison To use the sharing features on this page, ... of insect, if possible Time of the sting Poison Control Your local poison center can be reached ...

  17. Tetrahydrozoline poisoning

    MedlinePlus

    ... help if this information is not immediately available. Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  18. Oleander poisoning

    MedlinePlus

    ... if known Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  19. Foxglove poisoning

    MedlinePlus

    ... if known Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  20. Dieffenbachia poisoning

    MedlinePlus

    ... were eaten, if known Time swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  1. Nicotine poisoning

    MedlinePlus

    ... help if this information is not immediately available. Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  2. Kerosene poisoning

    MedlinePlus

    ... from anywhere in the United States. Poisonous Ingredient Hydrocarbons, substances that contain only hydrogen and carbon. Where ... oil poisoning; Coal oil poisoning References Lee DC. Hydrocarbons. In: Marx JA, Hockberger RS, Walls RM, et ...

  3. Acute arsenic poisoning: absence of polyneuropathy after treatment with 2,3-dimercaptopropanesulphonate (DMPS).

    PubMed Central

    Moore, D F; O'Callaghan, C A; Berlyne, G; Ogg, C S; Davies, H A; House, I M; Henry, J A

    1994-01-01

    Two men aged 19 and 21 years ingested 1 g and 4 g respectively from 3 kg of a white crystalline powder that they thought was a substance of abuse. It was later identified as almost pure arsenic trioxide. Both had nausea and vomiting and one developed acute renal failure. Each was treated with 2,3-dimercaptopropanesulphonate (DMPS), and made a full recovery with no evidence of prolonged renal or neurological impairment. The DMPS-arsenic complex is probably associated with lower penetration into the CNS and as a consequence treatment with DMPS may result in lower acute and chronic neurotoxicity than treatment with the currently standard recommended chelating agent dimercaprol (British Anti-Lewisite; BAL). PMID:8089687

  4. Assessment of Efficacy of Activated Charcoal for Treatment of Acute T-2 Toxin Poisoning,

    DTIC Science & Technology

    1986-11-14

    Command 14 November 15Mi IS. "U"SGIEf, OP Rs) 14. i*OXSIT01GMQ AGENCY MAMIE A A0ONZS.S( 1f Etsr *0 CAMORdlim4 OM.0) IL S*Cu~jTY "ALA (of 00* mae ~-s ~ 14L...Procedures of Statistics, McGraw-Hill, New York, 1960. 14. R. C. Hatch, J. D. Clark , A. V. Jain, and R. Weiss, Induced acute aflatox~cosis in goats

  5. [Variants of the signs of death from acute alcohol poisoning stipulated by different features of thanatogenesis].

    PubMed

    Kapustin, A V; Zombkovskaia, L S; Panfilenko, O A; Serebriakova, V G

    2003-01-01

    Two variants of thanatogenesis were formulated in cases of death of acute alcohol intoxication; according to the above variants, different combinations of macro- and micro signs as well as of biochemical indices of carbohydrates content in the hepatic tissues and blood are revealed during cadaver examinations. The diagnostic value of the mentioned signs demands that the thanatogenesis specific features must be taken into account in each separate case.

  6. [Mercury poisoning].

    PubMed

    Bensefa-Colas, L; Andujar, P; Descatha, A

    2011-07-01

    Mercury is a widespread heavy metal with potential severe impacts on human health. Exposure conditions to mercury and profile of toxicity among humans depend on the chemical forms of the mercury: elemental or metallic mercury, inorganic or organic mercury compounds. This article aims to reviewing and synthesizing the main knowledge of the mercury toxicity and its organic compounds that clinicians should know. Acute inhalation of metallic or inorganic mercury vapours mainly induces pulmonary diseases, whereas chronic inhalation rather induces neurological or renal disorders (encephalopathy and interstitial or glomerular nephritis). Methylmercury poisonings from intoxicated food occurred among some populations resulting in neurological disorders and developmental troubles for children exposed in utero. Treatment using chelating agents is recommended in case of symptomatic acute mercury intoxication; sometimes it improves the clinical effects of chronic mercury poisoning. Although it is currently rare to encounter situations of severe intoxication, efforts remain necessary to decrease the mercury concentration in the environment and to reduce risk on human health due to low level exposure (dental amalgam, fish contamination by organic mercury compounds…). In case of occupational exposure to mercury and its compounds, some disorders could be compensated in France. Clinicians should work with toxicologists for the diagnosis and treatment of mercury intoxication.

  7. Hydroxyethyl Starch Could Save a Patient With Acute Aluminum Phosphide Poisoning.

    PubMed

    Marashi, Sayed Mahdi; Nasri Nasrabadi, Zeynab; Jafarzadeh, Mostafa; Mohammadi, Sogand

    2016-07-01

    A 40-year-old male patient with suicidal ingestion of one tablet of aluminium phosphide was referred to the department of toxicology emergency of Baharloo Hospital, Tehran, Iran. The garlic odor was smelled from the patient and abdominal pain and continuous vomiting as well as agitation and heartburn were the first signs and symptoms. Systolic and diastolic blood pressures at the arrival time were 95 and 67 mmHg, respectively. Gastric lavage with potassium permanganate (1:10,000), and 2 vials of sodium bicarbonate through a nasogastric tube was started for the patient and the management was continued with free intravenous infusion of 1 liter of NaCl 0.9% serum plus NaHCO3, hydrocortisone acetate (200 mg), calcium gluconate (1 g) and magnesium sulfate (1 g). Regarding the large intravenous fluid therapy and vasoconstrictor administering (norepinephrine started by 5 µg/min and continued till 15 µg/min), there were no signs of response and the systolic blood pressure was 49 mmHg. At this time, hydroxyethyl starch (HES) (6% hetastarch 600/0.75 in 0.9% sodium chloride) with a dose of 600 cc in 6 hours was started for the patient. At the end of therapy with HES, the patient was stable with systolic and diastolic blood pressure of 110 and 77 mmHg, respectively. He was discharged on the 6th day after the psychological consultation, with normal clinical and paraclinical examinations. This is the first report of using HES in the management of AlP poisoning and its benefit to survive the patient.

  8. [Pecularities of correction of alcohol affctions of liver in patients with acute ethanol poisoning in the setting of consequence of toxic effect of ethanol].

    PubMed

    Shilov, V V; batotsyrenov, B V; Vasil'ev, S A; Shikalova, I A; Kuznetsov, O A

    2012-06-01

    The aim of this work was to test the usage of infusion of hepatoprotector "remaxol" in intensive therapy of acute ethanol poisoning accompanied with severe alcohol affections of the lever. In the result of the examination and treatment of 130 patients it was established that severe alcohol poisonings registered on alcohol abused patients with toxic hepatopathy, are always accompanied with serious metabolic violations. In the process of a comparative valuation of the using of heptral (ademethionin) and remaxol in the intensive therapy of alcohol poisonings it has been revealed that the using of remaxol led to improvement of the clinic of that poisonings, what had been registered as a decrease of frequency and duration of an alcohol delirium from 33,9% to 10,8%, a decrease of frequency of secondary lung complication from 18,5 to 3,1%, a decrease of a duration of treatment in intensive care unit from 7,3 +/- 0,6 to 5,6 +/- 0,3 and a hospital treatment duration from 11,8 +/- 0,5 to 9,0 +/- 0,3 days. Biochemical investigation has shown that using as heptral, as remaxol led to improvement of lever damages due to alcohol. However remaxol compared with heptral was better in the treatment of metabolic violations.

  9. Sulfanegen sodium treatment in a rabbit model of sub-lethal cyanide toxicity

    SciTech Connect

    Brenner, Matthew; Kim, Jae G.; Lee, Jangwoen; Mahon, Sari B.; Lemor, Daniel; Ahdout, Rebecca; Boss, Gerry R.; Blackledge, William; Jann, Lauren; Nagasawa, Herbert T.; Patterson, Steven E.

    2010-11-01

    The aim of this study is to investigate the ability of intramuscular and intravenous sulfanegen sodium treatment to reverse cyanide effects in a rabbit model as a potential treatment for mass casualty resulting from cyanide exposure. Cyanide poisoning is a serious chemical threat from accidental or intentional exposures. Current cyanide exposure treatments, including direct binding agents, methemoglobin donors, and sulfur donors, have several limitations. Non-rhodanese mediated sulfur transferase pathways, including 3-mercaptopyruvate sulfurtransferase (3-MPST) catalyze the transfer of sulfur from 3-MP to cyanide, forming pyruvate and less toxic thiocyanate. We developed a water-soluble 3-MP prodrug, 3-mercaptopyruvatedithiane (sulfanegen sodium), with the potential to provide a continuous supply of substrate for CN detoxification. In addition to developing a mass casualty cyanide reversal agent, methods are needed to rapidly and reliably diagnose and monitor cyanide poisoning and reversal. We use non-invasive technology, diffuse optical spectroscopy (DOS) and continuous wave near infrared spectroscopy (CWNIRS) to monitor physiologic changes associated with cyanide exposure and reversal. A total of 35 animals were studied. Sulfanegen sodium was shown to reverse the effects of cyanide exposure on oxyhemoglobin and deoxyhemoglobin rapidly, significantly faster than control animals when administered by intravenous or intramuscular routes. RBC cyanide levels also returned to normal faster following both intramuscular and intravenous sulfanegen sodium treatment than controls. These studies demonstrate the clinical potential for the novel approach of supplying substrate for non-rhodanese mediated sulfur transferase pathways for cyanide detoxification. DOS and CWNIRS demonstrated their usefulness in optimizing the dose of sulfanegen sodium treatment.

  10. Prognosis for children with acute liver failure due to Amanita phalloides poisoning

    NASA Astrophysics Data System (ADS)

    Wachulski, Marcin F.; Kamińska-Gocał, Diana; Dądalski, Maciej; Socha, Piotr; Mulawka, Jan J.

    2011-10-01

    The primary objective of this article is to find new effective methods of diagnosis of urgent liver transplantation after Amanita phalloides intoxication amongst pediatric patients. The research was carried out using a medical database of pediatric patients who suffered from acute liver failure after amatoxin consumption. After data preprocessing and attribute selection steps, a two-phase experiment was conducted, which incorporated a wide variety of data mining algorithms. The results deliver two equivalent classification models with simple decision structure and reasonable quality of surgery prediction.

  11. Study of Effect of Magnesium Sulphate in Management of Acute Organophosphorous Pesticide Poisoning

    PubMed Central

    Vijayakumar, H. N.; Kannan, Sudheesh; Tejasvi, C.; Duggappa, Devika Rani; Veeranna Gowda, K. M.; Nethra, S. S.

    2017-01-01

    Background: Organophosphorus compound poisoning (OPCP) is a major public health problem in developing countries like India. Atropine and oximes remain the main-stay of management. Magnesium sulfate (MgSO4) has shown benefit in the management of OPCP. Aims: This study was designed to assess the effect of MgSO4 on outcome in OPCP patients admitted to Intensive Care Unit (ICU). Settings and Design: Double-blind prospective randomized clinical trial in an ICU of tertiary care institution. Methods: One hundred patients (50 in each group) of OPCP, confirmed by history and syndrome of OPCP with low plasma pseudocholinesterase, aged between 18 and 60 years were studied. Magnesium group (Group M) received 4 g of 20% MgSO4 infusion over 30 min at admission to ICU, control group (Group C) received normal saline placebo in the same manner. Patients were assessed for the need for intubation, requirement of atropine, duration of mechanical ventilation, duration of ICU stay, and its effect on mortality. Statistical Analysis: Chi-square test and Fisher's exact test for categorical data, independent sample t-test, and paired t-test for nominal data. Results: Demographics and basal serum magnesium levels were comparable. Atropine requirement was higher in Group C (74.82 ± 22.39 mg) compared to Group M (53.11 ± 45.83 mg) (P < 0.001). A total of 33 patients in Group C and 23 patients in Group M required intubation, respectively (P = 0.043). The mean duration of mechanical ventilation was 4.51 ± 2 days in Group C compared to 4.13 ± 1.6 days in Group M (P = 0.45). ICU stay was 5.36 ± 2.018 days in Group C compared to 4.54 ± 1.581 days in Group M (P = 0.026). There was no significant difference in mortality between the groups. Conclusion: Four grams of MgSO4 given to OPCP patients within 24 h of admission to ICU, decreases atropine requirement, need for intubation, and ICU stay. PMID:28298783

  12. [Electron miscroscopic liver changes in acute carbon tetrachloride poisoning in man)].

    PubMed

    Kendrey, G; László, B

    1975-01-01

    Lesions of the liver revealed by light and electron microscopy at two young men, workers of the chemical industry are described. At one of the patients biopsy was performed twice at the other three times. Patient having jaundice were admitted to hospital because of the suspected acute viral hepatitis. Laboratory findings have shown an acute parenchymal lesion. By light microscopy at one of them mid-zonal, at the other centro-lobular necrosis of hepatic cells further lipoid droplets of the cytoplasma of hepatocytes were revealed. Electronmicroscopically in the first biopsy specimens, and at one of the ptients at the second biopsy as well mostly damage to the mitochondria (enormous osmiophilia of the matrix, presence of osmiophil granules) and enlargement of the tubules of the endoplasmic reticulum could be seen. The controll clinical and morphological findings evidenced the reversible character of the process. Authors stress the differences existing between hepatic lesions caused by CCl4 at different persons on one side, and at rat and human liver on the other.

  13. Use of OpdA, an Organophosphorus (OP) Hydrolase, Prevents Lethality in an African Green Monkey Model of Acute OP Poisoning

    PubMed Central

    Jackson, Colin J; Carville, Angela; Ward, Jeanine; Mansfield, Keith; Ollis, David L.; Khurana, Tejvir; Bird, Steven B.

    2014-01-01

    Organophosphorus (OP) pesticides are a diverse class of acetylcholinesterase (AChE) inhibitors that are responsible for tremendous morbidity and mortality worldwide, killing approximately 300,000 people annually. Enzymatic hydrolysis of OPs is a potential therapy for acute poisoning. OpdA, an OP hydrolase isolated from Agrobacterium radiobacter, has been shown to decrease lethality in rodent models of OP poisoning. This study investigated the effects of OpdA on AChE activity, plasma concentrations of OP, and signs of toxicity after administration of dichlorvos to nonhuman primates. A dose of 75 mg/kg dichlorvos given orally caused apnea within 10 minutes with a progressive decrease in heart rate. Blood AChE activity decreased to zero within ten minutes. Respirations and AChE activity did not recover. The mean dichlorvos concentration rose to a peak of 0.66 μg/ml. Treated monkeys received 1.2 mg/kg OpdA iv immediately after poisoning with dichlorvos. In Opda-treated animals, heart and respiratory rates were unchanged from baseline over a 240-minute observation period. AChE activity slowly declined, but remained above 25% of baseline for the entire duration. Dichlorvos concentrations reached a mean peak of 0.19 μg/ml at 40 minutes after poisoning and decreased to a mean of 0.05 μg/ml at 240 minutes. These results show that OpdA hydrolyzes dichlorvos in an African Green Monkey model of lethal poisoning, delays AChE inhibition, and prevents lethality. PMID:24447378

  14. Acute intentional self-poisoning with a herbicide product containing fenoxaprop-P-ethyl, ethoxysulfuron and isoxadifen ethyl. A prospective observational study

    PubMed Central

    ZAWAHIR, SHUKRY; ROBERTS, DARREN M.; PALANGASINGHE, CHATHURA; MOHAMED, FAHIM; EDDLESTON, MICHAEL; DAWSON, ANDREW H.; BUCKLEY, NICK A.; REN, LINGLING; MEDLEY, GREGORY A.; GAWARAMMANA, INDIKA

    2011-01-01

    BACKGROUND Herbicides are commonly ingested for self-harm; however, relatively little has been published on poisoning with herbicides other than paraquat and glyphosate. We report here a case series of patients with acute exposure to a combination herbicide (brand name Tiller Gold or Whip Super) containing the selective phenoxy herbicide fenoxaprop-P-ethyl, the sulfonylurea herbicide ethoxysulfuron and the safener isoxadifen ethyl. METHOD Clinical data on all patients presenting with Tiller Gold or Whip Super poisoning to two General Hospital in Sri Lanka from 2002-2008 were collected prospectively until discharge. RESULTS Eighty-six patients with a history of Tiller Gold or Whip Super ingestion were included. The median time to presentation was 4 hours post-ingestion (IQR 2 to 10 hrs) and the median volume ingested was 22.5ml (IQR: 20-60; n=64). Most patients demonstrated limited clinical signs of poisoning and none required mechanical ventilation or intensive care treatment. The main clinical features were an epigastric burning sensation and vomiting; however, most of those who vomited had received gastric lavage or forced emesis. Eight patients had a reduced level of consciousness on admission (GCS 9 -14) that resolved without intervention over several hours. Only symptomatic and supportive care was required. The median hospital stay was 1 day (IQR: 1 to 2) and the case fatality was zero (95% CI: zero to 4.2%). This low case fatality compared favorably with the case fatality of other common herbicides in our cohort: paraquat >40%, propanil >10%, 4-chloro-2-methylphenoxyacetic acid (MCPA) > 5% and glyphosate >2%. CONCLUSION This combination herbicide product appears to be safe in patients with acute self-poisoning, particularly in comparison with other herbicides, and causing few clinical features PMID:19663557

  15. Solder poisoning

    MedlinePlus

    ... Ethylene glycol is extremely poisonous. Complete recovery from lead poisoning takes a year or more. It may cause ... Long-term poisoning with antimony and cadmium may lead to lung cancer. Recovery from acid poisoning depends on how much tissue has been damaged.

  16. Novel, orally effective cyanide antidotes.

    PubMed

    Nagasawa, Herbert T; Goon, David J W; Crankshaw, Daune L; Vince, Robert; Patterson, Steven E

    2007-12-27

    A series of prodrugs of 3-mercaptopyruvate (3-MP), the substrate for the enzyme 3-mercaptopyruvate/cyanide sulfurtransferase (3-MPST) that converts cyanide to the nontoxic thiocyanate, which are highly effective cyanide antidotes, have been developed. These prodrugs of 3-MP are unique in being not only orally bioavailable, but may be administered up to an hour prior to cyanide as a prophylactic agent and are both rapid- or slow-acting when given parenterally.

  17. Role of biomarkers of nephrotoxic acute kidney injury in deliberate poisoning and envenomation in less developed countries

    PubMed Central

    Mohamed, Fahim; Endre, Zoltan H; Buckley, Nicholas A

    2015-01-01

    Acute kidney injury (AKI) has diverse causes and is associated with increased mortality and morbidity. In less developed countries (LDC), nephrotoxic AKI (ToxAKI) is common and mainly due to deliberate ingestion of nephrotoxic pesticides, toxic plants or to snake envenomation. ToxAKI shares some pathophysiological pathways with the much more intensively studied ischaemic AKI, but in contrast to ischaemic AKI, most victims are young, previously healthy adults. Diagnosis of AKI is currently based on a rise in serum creatinine. However this may delay diagnosis because of the kinetics of creatinine. Baseline creatinine values are also rarely available in LDC. Novel renal injury biomarkers offer a way forward because they usually increase more rapidly in AKI and are normally regarded as absent or very low in concentration, thereby reducing the need for a baseline estimate. This should increase sensitivity and speed of diagnosis. Specificity should also be increased for urine biomarkers since many originate from the renal tubular epithelium. Earlier diagnosis of ToxAKI should allow earlier initiation of appropriate therapy. However, translation of novel biomarkers of ToxAKI into clinical practice requires better understanding of non-renal factors in poisoning that alter biomarkers and the influence of dose of nephrotoxin on biomarker performance. Further issues are establishing LDC population-based normal ranges and assessing sampling and analytical parameters for low resource settings. The potential role of renal biomarkers in exploring ToxAKI aetiologies for chronic kidney disease of unknown origin (CKDu) is a high research priority in LDC. Therefore, developing more sensitive biomarkers for early diagnosis of nephrotoxicity is a critical step to making progress against AKI and CKDu in the developing world. PMID:26099916

  18. Identification of a crystalline cyanide-containing compound in blast furnace sludge deposits.

    PubMed

    Mansfeldt, T; Dohrmann, R

    2001-01-01

    During blast furnace operation, a cyanide-containing muddy waste referred to as blast furnace sludge is generated in large amounts. In Germany it was and is still common practice to pump this sludge into surface deposits. Depending on species, cyanide has very different toxicity. To this day there is no information about the type of cyanide occurring in blast furnace sludge deposits. In order to identify the type of cyanide we investigated by means of wet chemical and powder X-ray diffraction analyses 37 samples of three blast furnace deposits. Wet chemical results indicate that both the extremely toxic free cyanide (HCN and CN ) and toxic weak metal-cyanide complexes, for example [Zn(CN)4]2-, are not present in the sludge. By powder X-ray diffraction we identified the crystalline cyanide-containing compound potassium zinc hexacyanoferrate(II) nonahydrate, K2Zn3[Fe(CN)6]2 x 9H2O, as the cyanide-bearing compound. Our study is the first that identifies potassium zinc hexacyanoferrate(II) nonahydrate in the environment. As the iron-cyanide complex [Fe(CN)6] is not acutely toxic, any direct hazard comes from cyanide occurring in the investigated wastes. Under the predominant pH milieu of the sludge (pH about 8) the solubility of potassium zinc hexacyanoferrate(II) nonahydrate is low, thus minimizing the mobility of cyanide.

  19. Ciguatera poisoning.

    PubMed

    Achaibar, Kira C; Moore, Simon; Bain, Peter G

    2007-10-01

    Ciguatera is a form of poisoning that occurs after eating tropical and subtropical ciguatoxic fish. The ciguatoxins are a family of heat stable, lipid soluble cyclic polyether compounds that bind to and open voltage-sensitive Na(+) channels at resting membrane potential, resulting in neural hyperexcitability, as well as swelling of the nodes of Ranvier. The authors describe a 45-year-old man who developed acute gastrointestinal symptoms in Antigua soon after eating red snapper and grouper, potentially "ciguatoxic fish". This was followed by neurological symptoms 24-48 hours later, including temperature reversal (paradoxical dysaesthesia), intense pruritus and increased nociception as a result of a small fibre peripheral neuropathy. The patient's symptoms and small fibre neuropathy improved over a period of 10 months.

  20. Electroplating and Cyanide Waste.

    ERIC Educational Resources Information Center

    Torpy, Michael F.; Runke, Henry M.

    1978-01-01

    Presents a literature review of wastes from electroplating industry, covering publications of 1977. This review covers studies such as: (1) ion exchange treatment process; (2) use of reverse osmosis; and (3) cyanide removal and detection. A list of 75 references is also presented. (HM)

  1. Potassium silver cyanide

    Integrated Risk Information System (IRIS)

    Jump to main content . Integrated Risk Information System Recent Additions | Contact Us Search : All EPA IRIS • You are here : EPA Home • Research • Environmental Assessment • IRIS • IRIS Summaries Redirect Page As of September 28 , 2010 , the assessment summary for potassium silver cyanide is inclu

  2. Cyanide Formation by Chromobacterium violaceum

    PubMed Central

    Michaels, Ruth; Corpe, W. A.

    1965-01-01

    Michaels, Ruth (Columbia University, New York, N.Y.), and W. A. Corpe. Cyanide formation by Chromobacterium violaceum. J. Bacteriol. 89:106–112. 1965.—The formation of cyanide by a Chromobacterium violaceum strain was studied with growing cultures and with nonproliferating cells grown in complex and chemically defined media. Most of the cyanide was produced during the log-phase growth of the organism, and accumulated in the culture supernatant fluid. A synergistic effect of glycine and methionine on cyanide formation in a chemically defined medium was observed, and the amount of cyanide formed was found to be dependent on the concentrations of the two substances. Cyanide formation by nonproliferating cells was stimulated by preincubation with glycine and methionine. Cyanide formation by adapted cells in the presence of glycine and methionine was stimulated by succinate, malate, or fumarate, and depressed by azide and 2,4-dinitrophenol. Methionine could be replaced by betaine, dimethylglycine, and choline. PMID:14255648

  3. Toxic leukoencephalopathy due to yam bean seeds poisoning.

    PubMed

    Fu, Pin-Kuei; Wang, Pao-Yu

    2012-07-01

    Toxic leukoencephalopathy is attributed to exposure to a wide variety of agents, including systemic chemotherapy, cranial irradiation, illicit drug abuse, and toxins from the environment. Diagnosis of this disease requires documented exposure to a toxin, neurobehavioral deficits, and typical neuroimaging abnormalities. Intoxication by compounds extracted from yam bean seeds may mimic cyanide poisoning but fail to respond to antidotal therapy. We report a 54-year-old Chinese woman who developed disturbed consciousness after eating 40 pieces of yam bean seeds. Head computed tomography obtained 24 hours after the episode was normal. However, magnetic resonance imaging obtained 20 days after the episode revealed symmetrical faint high signal over the bilateral periventricular white matter on T1-weighted image, which turned into diffuse and symmetrical bright high signal on FLAIR. The diagnosis of this patient was toxic leukoencephalopathy by yam bean seeds intoxication. The changes in brain images after yam bean seeds intoxication have not ever been reported. Physicians in Asia and the Pacific islands should have a high index of suspicion when they care for patients with acute confusion and a high anion gap metabolic acidosis but normal serum cyanide level.

  4. Comparison of two commonly practiced atropinization regimens in acute organophosphorus and carbamate poisoning, doubling doses vs. ad hoc: a prospective observational study.

    PubMed

    Perera, P M S; Shahmy, S; Gawarammana, I; Dawson, A H

    2008-06-01

    There is a wide variation and lack of evidence in current recommendations for atropine dosing schedules leading to subsequent variation in clinical practice. Therefore, we sought to examine the safety and effectiveness of a titrated vs. ad hoc atropine treatment regimen in a cohort of patients with acute cholinesterase inhibitor pesticide poisoning. A prospective cohort study was conducted in three district secondary referral hospitals in Sri Lanka using a structured data collection form that collected details of clinical symptoms and outcomes of cholinesterase inhibitor pesticide poisoning, atropine doses, and signs of atropinization. We compared two hospitals that used a titrated dosing protocol based on a structured monitoring sheet for atropine infusion with another hospital using an ad hoc regime. During the study, 272 symptomatic patients with anticholinesterase poisoning requiring atropine were admitted to the three hospitals. Outcomes of death and ventilation were analyzed for all patients, 226 patients were prospectively assessed for atropine toxicity. At baseline, patients in the titrated dose cohort had clinical signs consistent with greater toxicity. This in part may be due to ingestion of more toxic organophosphates. They received less pralidoxime and atropine, and were less likely to develop features of atropine toxicity, such as delirium (1% vs. 17%), hallucinations (1% vs. 35%), or either (1% vs. 35%) and need for patient restraint (3% vs. 48%) compared with the ad hoc dose regime. After adjusting for the pesticides ingested, there was no difference in mortality and ventilatory rates between protocols. Ad hoc high dose atropine regimens are associated with more frequent atropine toxicity without any obvious improvement in patient outcome compared with doses titrated to clinical effect. Atropine doses should be titrated against response and toxicity. Further education and the use of a structured monitoring sheet may assist in more appropriate

  5. Paraquat Poisoning: A Case Report

    PubMed Central

    Singh, Veer Bahadur; Meena, Babu Lal; Gaur, Subhash; Singla, Rahul

    2016-01-01

    Paraquat is commonly used herbicide by farmers in North West Rajasthan. Despite its easy availability, poisoning of its not common. Fatal dose of paraquat is so small that >10 ml poison can damage lungs permanently. Diagnosis is often difficult without proper history, absence of specific clinical feature and lack of diagnostic test. Inhalation exposures represent one of the most important routes of poisoning. We are reporting a case of inhaled paraquat poisoning with complication of irreversible acute kidney, liver and lung injury. PMID:27042505

  6. Lead Poisoning

    MedlinePlus

    ... from lead poisoning in New Hampshire and in Alabama. Lead poisoning has also been associated with juvenile ... for decades—after it first enters the blood stream. (The same process can occur with the onset ...

  7. Varnish poisoning

    MedlinePlus

    ... is a clear liquid that is used as coating on woodwork and other products. Varnish poisoning occurs ... NOT make the person throw up unless poison control or a health care provider tells you to. ...

  8. Copper poisoning

    MedlinePlus

    ... Poisoning and Drug Overdose . 4th ed. Philadelphia, PA: Elsevier Saunders; 2007:chap 75. Holland MG. Pulmonary toxicology. ... Poisoning and Drug Overdose . 4th ed. Philadelphia, PA: Elsevier Saunders; 2007:chap 9. Jones AL, Dargan PI. ...

  9. Malathion poisoning

    MedlinePlus

    ... poisoning References Cannon RD, Ruha A-M. Insecticides, herbicides, and rodenticides. In: Adams JG. Emergency Medicine . 2nd ... A.M. Editorial team. Related MedlinePlus Health Topics Pesticides Poisoning Browse the Encyclopedia A.D.A.M., ...

  10. Poisonous Plants

    MedlinePlus

    ... Publications and Products Programs Contact NIOSH NIOSH POISONOUS PLANTS Recommend on Facebook Tweet Share Compartir Photo courtesy ... U.S. Department of Agriculture Many native and exotic plants are poisonous to humans when ingested or if ...

  11. Poison Ivy

    MedlinePlus

    ... leaves of the plants. Look Out for Poison Plants These plants can be anywhere — from the woods ... pill or liquid form. Preventing Rashes From Poison Plants The best approach is to avoid getting the ...

  12. Ethanol poisoning

    MedlinePlus

    ... this page: //medlineplus.gov/ency/article/002644.htm Ethanol poisoning To use the sharing features on this page, please enable JavaScript. Ethanol poisoning is caused by drinking too much alcohol. ...

  13. Mistletoe poisoning

    MedlinePlus

    ... page, please enable JavaScript. Mistletoe is an evergreen plant with white berries. Mistletoe poisoning occurs when someone eats any part of this plant. Poisoning can also occur if you drink tea ...

  14. Starch poisoning

    MedlinePlus

    Cooking starch poisoning; Laundry starch poisoning ... Cooking and laundry starch are both made from vegetable products, most commonly: Corn Potatoes Rice Wheat Both are usually considered nonpoisonous (nontoxic), but ...

  15. Poison Prevention

    MedlinePlus

    ... the Word Shop AAP Find a Pediatrician Safety & Prevention Immunizations All Around At Home At Play On ... Listen Español Text Size Email Print Share Poison Prevention Page Content Article Body Post the Poison Help ...

  16. Methylmercury poisoning

    MedlinePlus

    Methylmercury is a type of mercury , a metal that is liquid at room temperature. A nickname for mercury is quicksilver. Most compounds containing mercury are poisonous. Methylmercury is a very poisonous ...

  17. A label-free gold-nanoparticle-based SERS assay for direct cyanide detection at the parts-per-trillion level.

    PubMed

    Senapati, Dulal; Dasary, Samuel S R; Singh, Anant K; Senapati, Tapas; Yu, Hongtao; Ray, Paresh C

    2011-07-18

    Cyanide is an extremely toxic lethal poison known to humankind. Developing rapid, highly sensitive, and selective detection of cyanide from water samples is extremely essential for human life safety. Driven by the need, here we report a gold-nanoparticle-based label-free surface-enhanced Raman spectroscopy (SERS) system for highly toxic cyanide ion recognition in parts-per-trillion level and to examine gold-nanoparticle-cyanide interaction. We have shown that the SERS assay can be used to probe the gold nanoparticle dissociation process in the presence of cyanide ions. Our experimental data indicates that gold-nanoparticle-based SERS can detect cyanide from a water sample at the 110 ppt level with excellent discrimination against other common anions and cations. The results also show that the SERS probe can be used to detect cyanide from environmental samples.

  18. Hydrogen cyanide health effects. Final report

    SciTech Connect

    Carson, B.L.; Baker, L.H.; Herndon, B.L.; Ellis, H.V. III; Horn, E.M.

    1981-09-01

    Health effects literature primarily related to inhalation exposures to hydrogen cyanide was collected, evaluated, tabulated and summarized. Approximately 170 documents were collected from computerized and manual literature searches covering the period 1899-1981. Pharmacologists and an M.D. epidemiologist rated the documents according to their applicability to the study and their methodology. The approximately 20 documents considered useful for deriving a range of concern for human exposure to hydrogen cyanide from automotive emissions were tabulated. The 25 pages of tables detail the results of acute and repeated dose testing of mice, rats, guinea pigs, rabbits, cats, monkeys, dogs, goats, donkeys and humans as well as human occupational studies. Most of the documents evaluated are described in an annotated bibliography.

  19. Overview of Poisoning

    MedlinePlus

    ... Carbon Monoxide Poisoning Caustic Substances Poisoning Hydrocarbon Poisoning Insecticide Poisoning Iron Poisoning Lead Poisoning Overview of Food ... in their original containers. Toxic substances, such as insecticides and cleaning agents, should not be put in ...

  20. Anti-Cyanide Drugs

    DTIC Science & Technology

    1991-06-01

    for Metalloporphyrins and Phthalocyanines 13 N- Methyl -Metalloporphyrins 3nd Cyanide .................................................. 14 Table 3...tetrasulfonated phthalocyanine , TMPyP(4,3) are the tetrakis(N- Methyl -4(or 3)pyridyl)porphyrins, TAP is tetrakis(4.NNN.tnmethylanilinium)porphynn...porphyrins. These species have a central porphyrin proton replaced by an N- methyl group , and this group foi" steric reasons raises the metal ion above

  1. Acute ammonium dichromate poisoning.

    PubMed

    Meert, K L; Ellis, J; Aronow, R; Perrin, E

    1994-10-01

    We report the ingestion of ammonium dichromate by a child that resulted in multiple-organ-system failure and death. Exchange transfusion and hemodialysis were ineffective in removing significant amounts of chromium or causing sustained clinical improvement. We suggest that immediate, large doses of the reducing agent ascorbic acid would allow effective reduction of hexavalent chromium with less cellular toxicity.

  2. Light addressable photoelectrochemical cyanide sensor

    SciTech Connect

    Licht, S.; Myung, N.; Sun, Y.

    1996-03-15

    A sensor is demonstrated that is capable of spatial discrimination of cyanide with use of only a single stationary sensing element. Different spatial regions of the sensing element are light activated to reveal the solution cyanide concentration only at the point of illumination. In this light addressable photoelectrochemical (LAP) sensor the sensing element consists of an n-CdSe electrode immersed in solution, with the open-circuit potential determined under illumination. In alkaline ferro-ferri-cyanide solution, the open-circuit photopotential is highly responsive to cyanide, with a linear response of (120 mV) log [KCN]. LAP detection with a spatial resolution of {+-}1 mm for cyanide detection is demonstrated. The response is almost linear for 0.001-0.100 m cyanide with a resolution of 5 mV. 38 refs., 7 figs., 1 tab.

  3. The toxicokinetics of cyanide and mandelonitrile in the horse and their relevance to the mare reproductive loss syndrome.

    PubMed

    Dirikolu, Levent; Hughes, Charlie; Harkins, Dan; Boyles, Jeff; Bosken, Jeff; Lehner, Fritz; Troppmann, Amy; McDowell, Karen; Tobin, Thomas; Sebastian, Manu M; Harrison, Lenn; Crutchfield, James; Baskin, Steven I; Fitzgerald, Terrence D

    2003-01-01

    ). No clinical signs of cyanide intoxication or distress were observed during these experiments. These data show that during acute exposure to higher doses of cyanide (~600 mg/horse; 2500 ng/mL of cyanide in blood), redistribution of cyanide rapidly terminated the acute toxic responses. Similarly, mandelonitrile rapidly delivered its cyanide content, and acute cyanide intoxications following mandelonitrile administration can also be terminated by redistribution. Rapid termination of cyanide intoxication by redistribution is consistent with and explains many of the clinical and biochemical characteristics of acute, high-dose cyanide toxicity. On the other hand, at lower concentrations (<100 ng/mL in blood), metabolic transformation of cyanide is likely the dominant mechanism of termination of action. This process is slow, with terminal half-lives ranging from 12-16 hours. The large volume of distribution and the long terminal-phase-elimination half-life of cyanide suggest different mechanisms for toxicities and termination of toxicities associated with low-level exposure to cyanide. If environmental exposure to cyanide is a factor in the cause of MRLS, then it is likely in the more subtle effects of low concentrations of cyanide on specific metabolic processes that the associations will be found.

  4. Is the measurement of serum formate concentration useful in the diagnostics of acute methanol poisoning? A prospective study of 38 patients.

    PubMed

    Zakharov, Sergey; Kurcova, Ivana; Navratil, Tomas; Salek, Tomas; Komarc, Martin; Pelclova, Daniela

    2015-05-01

    The aim of this article was to study the role of serum formate (S-formate) in diagnosing methanol poisoning. A prospective study was undertaken of 38 patients from the Czech methanol mass poisoning in 2012 - median age 51 [interquartile range (IQR) 37-62] years with confirmed methanol poisoning. S-formate was measured enzymatically. The receiver operating characteristics (ROC) curve was used to examine the predictive ability of S-formate. Asymptomatic patients had median S-formate of 1.9 (IQR 1.5-2.4) mmol/L. The median S-formate was 15.2 (IQR 13.9-17.6) mmol/L in symptomatic subjects with visual disturbances, 15.4 (12.1-18.0) mmol/L in subjects with dyspnoea and 15.7 (IQR 12.8-18.5) mmol/L in comatose patients. The differences in serum formate concentrations in symptomatic patients depending on clinical features were not significant (all p > 0.05). Patients with long-term visual sequelae of poisoning had median S-formate of 16.1 (IQR 14.3-19.9) mmol/L; with central nervous system (CNS) sequelae, patients had 15.9 (IQR 14.2-19.5) mmol/L. In lethal cases, the median S-formate was 15.2 (IQR 13.8-15.9) mmol/L. The probability of a poor outcome (death or survival with sequelae) was higher than 90% in patients with S-formate ≥17.5 mmol/L, S-lactate ≥7.0 mmol/L and/or pH <6.87. The ROC analysis showed that the corresponding areas under the curve (AUC) were 0.64 (0.44-0.85 CI 95%) for S-formate, 0.75 (0.56-0.93 CI 95%) for 'S-formate+S-lactate' and only 0.54 (0.38-0.69 CI 95%) for serum methanol, which is lower than for S-formate (p < 0.05). The measurement of S-formate is an important tool in the laboratory diagnostics and clinical management of acute methanol poisoning. S-formate ≥3.7 mmol/L can lead to the first clinical signs of visual toxicity, indicating haemodialysis. S-formate ≥11-12 mmol/L is associated with visual/CNS sequelae and a lethal outcome.

  5. Ecotoxicity of cyanide complexes in industrially contaminated soils.

    PubMed

    Manar, Rachid; Bonnard, Marc; Rast, Claudine; Veber, Anne-Marie; Vasseur, Paule

    2011-12-15

    This study deals with acute and chronic ecotoxicity of leachates from industrially contaminated soils. Analyses focused on cyanides (complex and free forms) to study their possible involvement in leachates toxicity. No acute toxicity on the Microtox and 48 h-Daphnia magna tests was found in leachates collected over 18 months, but a high chronic toxicity was recorded on the reproduction of Ceriodaphnia dubia (EC50-7d=0.31±0.07%) and on the algal growth of Pseudokirchneriella subcapitata (EC50-72 h=0.27±0.09%). Ceriodaphnids were as sensitive to free cyanide as to complex forms (EC50-7d as CN(-)=98 μg/L, 194 μg/L and 216 μg/L for KCN, Fe(CN)(6)K(3) and Fe(CN)(6)K(4), respectively). The EC50-72 h of KCN to P. subcapitata (116 μg/L) as CN(-) was also of the same level as the EC50-72 h of potassium ferricyanide (127 μg/L) and ferrocyanide (267 μg/L). Complex cyanides explained a major part of the toxicity of leachates of the soil. On the other hand, cyanide complexes had no effect on survival of the earthworm Eisenia fetida up to 131 mg CN(-)/kg, while potassium cyanide was highly toxic [EC50-14 d as CN(-)=74 μg/kg soil]. Thermodesorption treatment eliminated a majority of cyanides from the soil and generated much less toxic leachates. Complex cyanides must be integrated into environmental studies to assess the impact of multi-contaminated soils.

  6. Cyanide analyses for risk and treatability assessments

    SciTech Connect

    MacFarlane, I.D.; Elseroad, H.J.; Pergrin, D.E.; Logan, C.M.

    1994-12-31

    Cyanide, an EPA priority pollutant and target analyte, is typically measured as total. However, cyanide complexation, information which is not acquired through total cyanide analysis, is often a driver of cyanide toxicity and treatability. A case study of a former manufacture gas plant (MGP) is used to demonstrate the usability of various cyanide analytical methods for risk and treatability assessments. Several analytical methods, including cyanide amenable to chlorination and weak acid dissociable cyanide help test the degree of cyanide complexation. Generally, free or uncomplexed cyanide is more biologically available, toxic, and reactive than complexed cyanide. Extensive site testing has shown that free and weakly dissociable cyanide composes only a small fraction of total cyanide as would be expected from the literature, and that risk assessment will be more realistic considering cyanide form. Likewise, aqueous treatment for cyanide can be properly tested if cyanide form is accounted for. Weak acid dissociable cyanide analyses proved to be the most reliable (and potentially acceptable) cyanide method, as well as represent the most toxic and reactive cyanide forms.

  7. [Antidotal effects of sulfhydryl compounds on acute poisonings by sodium ammonium dimethyl-2-(propane-1,3-dithiosulfate) monohydrate, nereistoxin and cartap].

    PubMed

    Cao, B J; Chen, Z K; Chi, Z Q

    1990-03-01

    Sodium dimercaptopropanesulphonate (DMPS) and sodium dimercaptosuccinate (DMS) were discovered to be effective antidotes for acute poisoning of insecticides SCD [sodium ammonium dimethyl-2-(propane-1,3-dithiosulfate) monohydrate], nereistoxin (4-N,N-dimethylamino-1,2-dithiolane) and cartap (dihydronereistoxin dicarbamate). In mice, DMPS (250 mg/kg) or DMS (1000 mg/kg) ip 20 min before SCD increased LD50 of ig SCD from 97 to 374 or 251 mg/kg, respectively. The prophylactic effect of DMPS was better than that of DMS. Administration of DMPS prior to cartap increased LD50 of ig cartap from 130 to 375 mg/kg. The therapeutic effect of DMPS was also demonstrated in SCD-poisoned conscious rabbits. DMPS 62.5 mg/kg or DMS 500 mg/kg iv completely antagonized the neuromuscular blockade and respiratory depression caused by SCD, nereistoxin and cartap in anesthetized rabbits. The antagonism of SCD-induced neuromuscular blockade by cysteine (400 mg/kg, iv) was less effective and of shorter duration than that by DMPS and DMS. Dimercaprol 50 mg/kg im showed little effect on SCD-induced paralysis. The antagonistic actions of sulfhydryl compounds on neuromuscular blockade induced by these insecticides probably belong to chemical antagonism.

  8. Protection from cyanide-induced brain injury by the Nrf2 transcriptional activator carnosic acid

    PubMed Central

    Zhang, Dongxian; Lee, Brian; Nutter, Anthony; Song, Paul; Dolatabadi, Nima; Parker, James; Sanz-Blasco, Sara; Newmeyer, Traci; Ambasudhan, Rajesh; McKercher, Scott R.; Masliah, Eliezer; Lipton, Stuart A.

    2015-01-01

    Cyanide is a life threatening, bioterrorist agent, preventing cellular respiration by inhibiting cytochrome c oxidase, resulting in cardiopulmonary failure, hypoxic brain injury, and death within minutes. However, even after treatment with various antidotes to protect cytochrome oxidase, cyanide intoxication in humans can induce a delayed-onset neurological syndrome that includes symptoms of Parkinsonism. Additional mechanisms are thought to underlie cyanide-induced neuronal damage, including generation of reactive oxygen species (ROS). This may account for the fact that antioxidants prevent some aspects of cyanide-induced neuronal damage. Here, as a potential preemptive countermeasure against a bioterrorist attack with cyanide, we tested the CNS protective effect of carnosic acid (CA), a pro-electrophilic compound found in the herb rosemary. CA crosses the blood-brain-barrier to upregulate endogenous antioxidant enzymes via activation of the Nrf2 transcriptional pathway. We demonstrate that CA exerts neuroprotective effects on cyanide-induced brain damage in cultured rodent and human induced pluripotent stem cell (hiPSC)-derived neurons in vitro, and in vivo in various brain areas of a non-Swiss albino (NSA) mouse model of cyanide poisoning that simulates damage observed in the human brain. PMID:25692407

  9. [Poisonous plants].

    PubMed

    Hoppu, Kalle; Mustonen, Harriet; Pohjalainen, Tiina

    2011-01-01

    Approximately ten species of dangerously poisonous plants are found in Finland. Severe plant poisonings are very rare. Edible plants eaten raw or wrongly processed may cause severe symptoms. As first aid, activated charcoal should be given to the person who has eaten a plant causing a risk of significant poisoning. In case of exposure to topically irritating plant fluids, the exposed person's eyes must be irrigated and mouth or skin washed with copious amounts of water. In combination with solar UV radiation, light-sensitizing plants cause local burns. The diagnosis of plant poisoning is usually based on incidental information; the plant should be identified in order to make the correct treatment decisions.

  10. Outsmarting Poison Ivy and Other Poisonous Plants

    MedlinePlus

    ... Consumer Updates Outsmarting Poison Ivy and Other Poisonous Plants Share Tweet Linkedin Pin it More sharing options ... hang in loose clusters. back to top Poison Plant Rashes Aren’t Contagious Poison ivy and other ...

  11. Combined application of dexamethasone and hyperbaric oxygen therapy yields better efficacy for patients with delayed encephalopathy after acute carbon monoxide poisoning

    PubMed Central

    Xiang, Wenping; Xue, Hui; Wang, Baojun; Li, Yuechun; Zhang, Jun; Jiang, Changchun; Liang, Furu; Pang, Jiangxia; Yu, Lehua

    2017-01-01

    Background Delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP) commonly occurs after recovering from acute CO poisoning. This study was performed to assess the efficacy of the combined application of dexamethasone and hyperbaric oxygen (HBO) therapy in patients with DEACMP. Patients and methods A total of 120 patients with DEACMP were recruited and randomly assigned into the experimental group (receiving dexamethasone 5 mg/day or 10 mg/day plus HBO therapy) and control group (HBO therapy as monotherapy). Meanwhile, the conventional treatments were provided for all the patients. We used the Mini-Mental State Examination (MMSE) scale to assess the cognitive function, the National Institutes of Health Stroke Scale (NIHSS) to assess the neurological function and the remission rate (RR) to assess the clinical efficacy. Myelin basic protein (MBP) in the cerebrospinal fluid (CSF) was also measured. Results After 4 weeks of treatment, compared to the control group, the experimental group had a significantly higher remission rate (P=0.032), a significantly higher average MMSE score (P=0.037) and a significantly lower average NIHSS score (P=0.002). Meanwhile, there was a trend toward better improvement with dexamethasone 10 mg/day, and the level of MBP in the CSF of patients was significantly lower in the experimental group than in the control group (P<0.0001). The addition of dexamethasone did not significantly increase the incidence of adverse events. Conclusion These results indicate that the combined application of dexamethasone and HBO therapy could yield better efficacy for patients with DEACMP and should be viewed as a potential new therapy. PMID:28260864

  12. Dose and time-dependent effects of cyanide on thiosulfate sulfurtransferase, 3-mercaptopyruvate sulfurtransferase, and cystathionine λ-lyase activities.

    PubMed

    Singh, Poonam; Rao, Pooja; Bhattacharya, Rahul

    2013-12-01

    We assessed the dose-dependent effect of potassium cyanide (KCN) on thiosulfate sulfurtransferase (TST), 3-mercaptopyruvate sulfurtransferase (3-MPST), and cystathionine λ-lyase (CST) activities in mice. The time-dependent effect of 0.5 LD50 KCN on cyanide level and cytochrome c oxidase (CCO), TST, 3-MPST, and CST activities was also examined. Furthermore, TST, 3-MPST, and CST activities were measured in stored mice cadavers. Hepatic and renal TST activity increased by 0.5 LD50 KCN but diminished by ≥2.0 LD50. After 0.5 LD50 KCN, the elevated hepatic cyanide level was accompanied by increased TST, 3-MPST, and CST activities, and CCO inhibition. Elevated renal cyanide level was only accompanied by increased 3-MPST activity. No appreciable change in enzyme activities was observed in mice cadavers. The study concludes that high doses of cyanide exert saturating effects on its detoxification enzymes, indicating their exogenous use during cyanide poisoning. Also, these enzymes are not reliable markers of cyanide poisoning in autopsied samples.

  13. Studies on solvent extraction of copper and cyanide from waste cyanide solution.

    PubMed

    Xie, Feng; Dreisinger, David

    2009-09-30

    The recovery of copper and cyanide from waste cyanide solution with the guanidine extractant (LIX 7950) and the modified amine extractant (LIX 7820) has been investigated. Copper can be effectively extracted from alkaline cyanide solutions by both extractants. The free cyanide remains in the aqueous phase due to the preferential extraction of Cu(CN)(3)(2-) over Cu(CN)(4)(3-) and CN(-) by the extractants. The selectivity of the metals with the extractants under different cyanide levels has been examined. High cyanide levels tend to depress extraction of copper and silver cyanides, but exhibit insignificant effect on extraction of gold, zinc, nickel and iron cyanides. A possible solution to the separation of copper cyanides and free cyanide in cyanide effluents has been suggested, by which copper can be concentrated into a small volume of solution and the barren cyanide solution recycled to the cyanidation process.

  14. Non-lethal, repeated testing, anesthetized canine model for the evaluation of effectiveness of new forms of prophylaxis and therapy for cyanide intoxication

    SciTech Connect

    Von Bredow, J.; Vick, J.; Kaminskis, A.; Brewer, T.

    1993-05-13

    Acute cyanide intoxication has most often been modeled through the bolos intravenous administration of a lethal amount of sodium or potassium cyanide which provides reproducible effects and represents the most severe challenge to any new form of prophylaxis and therapy. Inhalation of cyanide leads to a similar acute onset of toxic signs which is controlled by the rate and depth of respiration. The cyanide induced halt in respiration also halts the continued absorption of cyanide leading to a well defined, consistent end point of the amount of cyanide absorbed. Regardless of the abundance of cyanide in the ambient air, the casualty can only absorb cyanide during respiration. A slow intravenous infusion of cyanide which is continued only until respiratory arrest is achieved should define the same limit of cyanide intoxication. Cyanide intoxication defined by the amount of sodium cyanide infused to induce respiratory arrest (RA) in pentobarbital anesthetized dogs provides the basis for the development of a useful repeated testing animal model. Utilization of the RA yields a surrogate endpoint in the anesthetized dog model and provides a non-traumatic, reproducible procedure to estimate the lethal level of CN in each dog as well defining the protective effect of pretreatments and antidotes.

  15. Hyperbaric oxygen therapy or hydroxycobalamin attenuates surges in brain interstitial lactate and glucose; and hyperbaric oxygen improves respiratory status in cyanide-intoxicated rats.

    PubMed

    Lawson-Smith, P; Olsen, N V; Hyldegaard, O

    2011-01-01

    Cyanide (CN) intoxication inhibits cellular oxidative metabolism and may result in brain damage. Hydroxycobalamin (OHCob) is one among other antidotes that may be used following intoxication with CN. Hyperbaric oxygen (HBO2) is recommended when supportive measures or antidotes fail. However, the effect of hydroxycobalamin or HBO2 on brain lactate and glucose concentrations during CN intoxication is unknown. We used intracerebral microdialysis to study the in vivo effect of hydroxycobalamin or HBO2 treatment on acute CN-induced deterioration in brain metabolism. Anesthetized rats were allocated to four groups receiving potassium CN (KCN) 5.4 mg/kg or vehicle intra-arterially: 1) vehicle-treated control rats; 2) KCN-poisoned rats; 3) KCN-poisoned rats receiving hydroxycobalamin (25 mg); and 4) KCN-poisoned rats treated with HBO2 (284 kPa for 90 minutes). KCN alone caused a prompt increase in interstitial brain lactate and glucose concentrations peaking at 60 minutes. Both hydroxycobalamin and HBO2 abolished KCN-induced increases in brain lactate and glucose concentration. However, whereas HBO2 treatment increased cerebral PtO2 and reduced respiratory distress and cyanosis, OHCob did not have this beneficial effect. In conclusion, CN intoxication in anesthetized rats produces specific uncoupling of cerebral oxidative metabolism resulting in interstitial lactate and glucose surges that may be ameliorated by treatment with either hydroxycobalamin or HBO2.

  16. Failure to elicit conditioned taste aversion by severe poisoning.

    PubMed

    Ionescu, E; Buresová, O

    1977-03-01

    In an attempt to assess the universal validity of the conditioned taste aversion (CTA) paradigm, various types of poisoning (UC) were associated with the gustatory CS. Water deprived rats were habituated for two days to the drinking box, where water was available for 15 min. On Day 3, access to the CS (0.1% saccharin 15 min) was followed after 30 min by a sublethal dose of the poison (0.15 M LiCl, 4% body weight; 0.1 M sodium malonate, 1% body weight; pyrrolopyrimidine drug BW 58-271, 15 mg/kg; sodium cyanide 4 mg/kg; sodium iodoacetate 40 mg/kg; sodium fluoride 30 mg/kg; gallamine triethiodide 40 mg/kg). Rats injected with the last drug were maintained under artificial respiration until muscular paralysis disappeared. After 4 days of recovery, water deprivation schedule was resumed on Days 8 and 9. During the retention test on Day 10 saccharin consumption dropped by 60% in the LiCl poisoned rats, but not CTA developed in animals poisoned by pyrrolopyrimidine, gallamine, malonate and cyanide. CTA of intermediate intensity was evoked by iodoacetate and fluoride. The absence of CTA was not due to the amnesic effect of poisoning, since LiCl administration to NaCN poisoned rats produced CTA of usual intensity. It is concluded that CTA is not related to the overall severity of poisoning but rather to the effect of the poison on specific interoceptors.

  17. Methanol poisoning

    MedlinePlus

    ... with has an exposure, call your local emergency number (such as 911), or your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere in the United States.

  18. Severe hypoglycemia following acute aluminum phosphide (rice tablet) poisoning; a case report and review of the literature.

    PubMed

    Mehrpour, Omid; Aghabiklooei, Abbas; Abdollahi, Mohammad; Singh, Surjit

    2012-01-01

    Aluminum phosphide (AlP) as 3 g tablet is widely used in Iran to protect stored food grains from pests. Hyperglycemia following its ingestion has been already reported in the recent years but severe hypoglycemia is uncommon. Here, we report a 19 year old male who attempted suicide with one tablet of AlP and demonstrated severe hypoglycemia. Despite restoration of blood glucose concentration to normal, he failed to respond to supportive treatment and died. The possible mechanisms leading to severe hypoglycemia are discussed. Though severe hypoglycemia is rare following AlP poisoning, physicians managing such patients should be aware of it.

  19. Cyanide hazards to plants and animals from gold mining and related water issues.

    PubMed

    Eisler, Ronald; Wiemeyer, Stanley N

    2004-01-01

    Cyanide extraction of gold through milling of high-grade ores and heap leaching of low-grade ores requires cycling of millions of liters of alkaline water containing high concentrations of potentially toxic sodium cyanide (NaCN), free cyanide, and metal-cyanide complexes. Some milling operations result in tailings ponds of 150 ha and larger. Heap leach operations that spray or drip cyanide onto the flattened top of the ore heap require solution processing ponds of about 1 ha in surface area. Puddles of various sizes may occur on the top of heaps, where the highest concentrations of NaCN are found. Solution recovery channels are usually constructed at the base of leach heaps, some of which may be exposed. All these cyanide-containing water bodies are hazardous to wildlife, especially migratory waterfowl and bats, if not properly managed. Accidental spills of cyanide solutions into rivers and streams have produced massive kills of fish and other aquatic biota. Freshwater fish are the most cyanide-sensitive group of aquatic organisms tested, with high mortality documented at free cyanide concentrations >20 microg/L and adverse effects on swimming and reproduction at >5 microg/L. Exclusion from cyanide solutions or reductions of cyanide concentrations to nontoxic levels are the only certain methods of protecting terrestrial vertebrate wildlife from cyanide poisoning; a variety of exclusion/cyanide reduction techniques are presented and discussed. Additional research is recommended on (1) effects of low-level, long-term, cyanide intoxication in birds and mammals by oral and inhalation routes in the vicinity of high cyanide concentrations; (2) long-term effects of low concentrations of cyanide on aquatic biota; (3) adaptive resistance to cyanide; and (4) usefulness of various biochemical indicators of cyanide poisoning. To prevent flooding in mine open pits, and to enable earth moving on a large scale, it is often necessary to withdraw groundwater and use it for

  20. Modulating effect of aqueous extract of Telfairia occidentalis on induced cyanide toxicity in rats.

    PubMed

    Bolaji, O M; Olabode, O O

    2011-12-20

    were moderated mildly by Telfairia occidentalis. Group 4, treated with the vegetable alone had none of the observed histopathology in the organs examined. We concluded that lyophilised aqueous extracts of Telfairia occidentalis showed good potential as a safe antidote for cyanide poisoning when administered concomitantly or very shortly after ingestion of sub-lethal dose of cyanide. However, further bioassay guided fractionation and analytical studies are needed to identify the actual chemical compound or molecule in the vegetable responsible for or associated with the observed effects.

  1. Comparison of brain mitochondrial cytochrome c oxidase activity with cyanide LD(50) yields insight into the efficacy of prophylactics.

    PubMed

    Marziaz, Mandy L; Frazier, Kathryn; Guidry, Paul B; Ruiz, Robyn A; Petrikovics, Ilona; Haines, Donovan C

    2013-01-01

    Cyanide inhibits cytochrome c oxidase, the terminal oxidase of the mitochondrial respiratory pathway, therefore inhibiting the cell oxygen utilization and resulting in the condition of histotoxic anoxia. The enzyme rhodanese detoxifies cyanide by utilizing sulfur donors to convert cyanide to thiocyanate, and new and improved sulfur donors are actively sought as researchers seek to improve cyanide prophylactics. We have determined brain cytochrome c oxidase activity as a marker for cyanide exposure for mice pre-treated with various cyanide poisoning prophylactics, including sulfur donors thiosulfate (TS) and thiotaurine (TT3). Brain mitochondria were isolated by differential centrifugation, the outer mitochondrial membrane was disrupted by a maltoside detergent, and the decrease in absorbance at 550 nm as horse heart ferrocytochrome c (generated by the dithiothreitol reduction of ferricytochrome c) was oxidized was monitored. Overall, the TS control prophylactic treatment provided significant protection of the cytochrome c oxidase activity. The TT3-treated mice showed reduced cytochrome c oxidase activity even in the absence of cyanide. In both treatment series, addition of exogenous Rh did not significantly enhance the prevention of cytochrome c oxidase inhibition, but the addition of sodium nitrite did. These findings can lead to a better understanding of the protection mechanism by various cyanide antidotal systems.

  2. Efficacy of N-Butylphthalide and Hyperbaric Oxygen Therapy on Cognitive Dysfunction in Patients with Delayed Encephalopathy After Acute Carbon Monoxide Poisoning

    PubMed Central

    Xiang, Wenping; Xue, Hui; Wang, Baojun; Li, Yuechun; Zhang, Jun; Jiang, Changchun; Pang, Jiangxia

    2017-01-01

    Background Delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP) is one of the most serious complications after CO poisoning. This study was conducted to explore the efficacy of the combined application of N-Butylphthalide and hyperbaric oxygenation therapy (HBO) on cognitive dysfunction in patients with DEACMP. Material/Methods A total of 184 patients with DEACMP were randomly assigned to either receive HBO or N-Butylphthalide and HBO. Meanwhile, all patients received conventional treatment. The total remission rate (RR) was used to assess the clinical efficacy. The Mini-Mental State Examination (MMSE) was used to assess the cognitive function, and the National Institutes of Health Stroke Scale (NIHSS) was used to assess the neurological function. Results Finally, there were 90 and 94 patients in the control and experimental groups, respectively. After eight weeks of treatment, the total RR in the experimental group (47.9%) was significantly higher than that in the control group (33.3%). Compared to the control group, significantly more patients in the experimental group had MMSE scores of 24–30. The lower NIHSS score in the experimental group showed that N-Butylphthalide had the effect of preservation and restoration of neurological function. No obvious drug toxicity or liver and kidney dysfunction was observed, and there was no significant change in the level of blood glucose and blood lipids. Conclusions These results indicated that the combined application of N-Butylphthalide and HBO could significantly improve the cognitive dysfunction of patients with DEACMP and have great clinical efficacy, which should be further studied. PMID:28352069

  3. Development of a site-specific marine water quality standard for cyanide

    SciTech Connect

    Arredondo, L.A.; Brix, K.V.; Cardwell, R.D.; Marsden, A.

    1995-12-31

    A study was conducted to develop a site-specific marine standard for cyanide. The generic cyanide standard of 1 {micro}g/L is ``driven`` by toxicity data for eastern rock crab (Cancer irroratus) zoeae. The reported LC50 for C. irroratus is 4.9 {micro}g/L cyanide and is six times more sensitive that any other marine species tested. In order to develop a site-specific standard for Washington state, cyanide toxicity tests were conducted using the first stage zoeae of Cancer magister and Cancer oregonensis, two Cancer resident to Puget Sound, in accordance with standard ASTM test methods. Testing with C. magister and C. oregonensis resulted in Species Mean Acute Values (SMAVS) of 68 and 131 {micro}g/L cyanide based on measured test concentrations. This is considerably higher than that reported for C. irroratus, is more consistent with cyanide toxicity values for other species tested, and results in a water quality criterion of 9.85 {micro}g/L cyanide with inclusion of these values in the data set. This paper presents the test methods used and the potential effects the test results may have on the marine water quality criterion for cyanide.

  4. [Cyanide with vitamin B12 deficiency as the cause of experimental tobacco amblyopia].

    PubMed

    Oku, H; Fukushima, K; Miyata, M; Wakakura, M; Ishikawa, S

    1991-02-01

    The visual toxicity of tobacco smoke was studied and demyelination change of retrobulbar portion of the rat's optic nerve with an elongation of a peak latency time of visual evoked potentials (VEP) was demonstrated. Cyanide detoxication incapacity and deficiency of vitamin B12 (B12) have been considered as possible causes of tobacco amblyopia. In order to elucidate an influence of cyanide poisoning and B12 deficiency on the visual system, 12 male Wistar rats were subjected to 5 hour's daily inhalation of cyanide gas for 52 weeks, the concentration of which was adjusted to that of tobacco smoke. Six rats of these 12 were fed with a lacking B12 diet. Another 12 male Wistar rats were controls which did not undergo inhalation of cyanide gas, and half of them were fed a diet without B12. In 2 out of 6 rats with cyanide and inhalation and B12 deficiency, demyelination change could be recognized in the central portion of the retrobulbar optic nerve. The histological change was segmental and significant elongation of the peak latency time of VEP was not recognized. Cyanide gas inhalation at a low concentration was proved to be harmful to the optic nerve under the condition of B12 deficiency, but other toxic elements such as nicotine and carbon monoxide may be important factors to cause the more severe changes of the optic nerve with an abnormal VEP response recognized in the experimental tobacco amblyopia.

  5. Shellac poisoning

    MedlinePlus

    ... shellac that can be harmful are: Ethanol Isopropanol Methanol Methyl isobutyl ketone ... Isopropanol and methanol are extremely poisonous. As little as 2 tablespoons (14.8 mL) of methanol can kill a child, while ...

  6. Paraffin poisoning

    MedlinePlus

    ... patient. In: Marx J, ed. Rosen's Emergency Medicine: Concepts and Clinical Practice . 8th ed. Philadelphia, PA: Elsevier Mosby; 2013:chap 147. Shannon MW. Emergency management of poisoning. In: Shannon MW, ed. Haddad and ...

  7. Menthol poisoning

    MedlinePlus

    Menthol is used to add peppermint flavor to candy and other products. It is also used in certain skin lotions and ointments. This article discusses menthol poisoning from swallowing pure menthol. This article is ...

  8. Ammonia poisoning

    MedlinePlus

    ... K. General approach to the poisoned patient. In: Marx J, ed. Rosen's Emergency Medicine: Concepts and Clinical ... 147. Levine MD, Zane R. Chemical injuries. In: Marx J, ed. Rosen's Emergency Medicine: Concepts and Clinical ...

  9. Food Poisoning

    MedlinePlus

    ... comes from eating foods that contain germs like bad bacteria or toxins, which are poisonous substances. Bacteria ... But you can learn how to avoid those bad germs in food. Which Germs Are to Blame? ...

  10. Lacquer poisoning

    MedlinePlus

    Poisoning from lacquers is due to hydrocarbons, which are substances that contain only hydrogen and carbon. ... Lee DC. Hydrocarbons. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice . 8th ed. Philadelphia, ...

  11. Gasoline poisoning

    MedlinePlus

    ... The poisonous ingredients in gasoline are chemicals called hydrocarbons, which are substances that contain only hydrogen and ... dangerous and is not advised. References Lee DC. Hydrocarbons. In: Marx JA, Hockberger RS, Walls RM, et ...

  12. Wax poisoning

    MedlinePlus

    Crayons poisoning ... This ingredient is found in: Crayons Candles Canning wax Note: This list may not be all-inclusive. ... If a child eats a small amount of crayon, the wax will pass through the child's system ...

  13. Diazinon poisoning

    MedlinePlus

    ... poisoning References Cannon RD, Ruha A-M. Insecticides, herbicides, and rodenticides. In: Adams JG. Emergency Medicine . 2nd ... A.M. Editorial team. Related MedlinePlus Health Topics Pesticides Browse the Encyclopedia A.D.A.M., Inc. ...

  14. Lead poisoning

    MedlinePlus

    ... Failure at school Hearing problems Kidney damage Reduced IQ Slowed body growth The symptoms of lead poisoning ... can have a permanent impact on attention and IQ. People with higher lead levels have a greater ...

  15. Detergent poisoning

    MedlinePlus

    ... this page: //medlineplus.gov/ency/article/002777.htm Detergent poisoning To use the sharing features on this page, please enable JavaScript. Detergents are powerful cleaning products that may contain strong ...

  16. Naphthalene poisoning

    MedlinePlus

    ... to the poisoned patient. In: Marx J, ed. Rosen's Emergency Medicine: Concepts and Clinical Practice . 8th ed. ... Zane R. Chemical injuries. In: Marx J, ed. Rosen's Emergency Medicine: Concepts and Clinical Practice . 8th ed. ...

  17. Antifreeze poisoning

    MedlinePlus

    The poisonous ingredients in antifreeze are: Ethylene glycol Methanol Propylene glycol ... For ethylene glycol: Death may occur within the first 24 hours. If the patient survives, there may be little ...

  18. Cyanide enhances hydrogen peroxide toxicity by recruiting endogenous iron to trigger catastrophic chromosomal fragmentation

    PubMed Central

    Mahaseth, Tulip; Kuzminov, Andrei

    2015-01-01

    Hydrogen peroxide (HP) or cyanide (CN) are bacteriostatic at low-millimolar concentrations for growing Escherichia coli, whereas CN+HP mixture is strongly bactericidal. We show that this synergistic toxicity is associated with catastrophic chromosomal fragmentation. Since CN-alone does not kill at any concentration, while HP-alone kills at 20 mM, CN must potentiate HP poisoning. The CN+HP killing is blocked by iron chelators, suggesting Fenton’s reaction. Indeed, we show that CN enhances plasmid DNA relaxation due to Fenton’s reaction in vitro. However, mutants with elevated iron or HP pools are not acutely sensitive to HP-alone treatment, suggesting that, in addition, in vivo CN recruits iron from intracellular depots. We found that part of the CN-recruited iron pool is managed by ferritin and Dps: ferritin releases iron on cue from CN, while Dps sequesters it, quelling Fenton’s reaction. We propose that disrupting intracellular iron trafficking is a common strategy employed by the immune system to kill microbes. PMID:25598241

  19. Acute inhalation toxicity of carbon monoxide and hydrogen cyanide revisited: Comparison of models to disentangle the concentration × time conundrum of lethality and incapacitation.

    PubMed

    Pauluhn, Juergen

    2016-10-01

    Contemporary emergency response planning guidelines are stratified to consider the threshold for serious toxicity and/or impairment of escape, relative to the potentially lethal level above this threshold and the lower level at which individuals should not experience or develop effects more serious than mild irritation. While harmonized testing guidelines and risk assessment paradigms are available for the quantification of thresholds for lethality or establishing no adverse effect levels, the quantification of 'impairment of escape' appears to be a more elusive goal. Approaches were explored in context with CO and HCN in past experimental combustion toxicology studies to estimate the time available for escape. This point of departure (POD) was compared with the non-lethal threshold (LC01) and one third thereof from published recent acute inhalation studies in rats examining the Cxt-matrix of both CO and HCN. The findings from this analysis suggest that the rat delivers the most consistent data. However, it remains challenging yet to bridge the behavioral variables of human behavior typical of escape to any surrogate animal model. For the asphyxiant gases examined, the PODs characterizing 'impairment of escape' were difficult to distinguish from those indicative of impending death. No specific modeled carboxyhemoglobin (COHb) level could be linked to onset of incapacitation. In summary, the higher ventilation of rats (kg body weight adjusted) renders this species even more susceptible than heavy breathing humans. LCt01 × 1/3 values derived from the comprehensive Cxt matrix of rat inhalation studies are considered to be most suitable and robust to estimate the human equivalent threshold (POD) of 'impairment of escape'.

  20. Ultrastructural changes in rat thyroid tissue after acute organophosphate poisoning and effects of antidotal therapy with atropine and pralidoxime: A single-blind, ex vivo study

    PubMed Central

    Satar, Deniz; Satar, Salim; Mete, Ufuk Ozgu; Suchard, Jeffrey R.; Topal, Metin; Karakoc, Emre; Kaya, Mehmet

    2008-01-01

    Background: Organophosphate (OP) insecticides are widely used in both agricultural and landscape pest control, and the potential for human exposure to these compounds is significant. Objectives: The aims of this study were to investigate the effects of acute poisoning with the OP methamidophos and the effects of antidotal therapy with atropine and pralidoxime on rat thyroid tissue ultrastructure. Methods: In this single-blind, ex vivo study, male Wistar albino rats weighing 220 to 230 g were divided into 4 treatment groups. Group 1 received a median lethal dose of methamidophos (30 mg/kg) via oral gavage. Group 2 received saline via oral gavage and served as the control group for group 1. Group 3 received methamidophos (30 mg/kg) via oral gavage, and after 8 minutes atropine 0.05 mg/kg and pralidoxime chloride (2-FAM) (40 mg/kg) were administered intraperitoneally (IP). Atropine was titrated to reverse signs of cholinergic excess. Group 4 received saline via oral gavage followed by IP injections and served as the control for group 3. Rat thyroid tissues were examined using electron microscopy, and the histologic changes were examined by a histopathologist who was blinded to treatment. All rats were euthanized by intracardiac blood collection. The rats in groups 1 and 2 were euthanized 8 minutes after treatment. The rats in groups 3 and 4 were euthanized 96 hours after treatment. Results: Thirty-four male rats (aged 16 weeks) were included in the study. The rats were grouped accordingly: group 1 (n = 10); group 2 (n = 7); group 3 (n = 10); and group 4 (n = 7). The mean (SD) pseudocholinesterase (FCE) activity was significantly lower in the methamidophos-treated rats (group 1) compared with the corresponding control group (group 2) (32.6 [17.0] vs 579.4 [59.0] U/L, respectively; P < 0.001). PCE activity was significantly higher in rats treated with atropine and 2-PAM (group 3) (392.5 [39.4] U/L; P < 0.001) compared with those not receiving antidotal therapy (group 1

  1. Cyanide hydratases and cyanide dihydratases: emerging tools in the biodegradation and biodetection of cyanide.

    PubMed

    Martínková, Ludmila; Veselá, Alicja Barbara; Rinágelová, Anna; Chmátal, Martin

    2015-11-01

    The purpose of this study is to summarize the current knowledge of the enzymes which are involved in the hydrolysis of cyanide, i.e., cyanide hydratases (CHTs; EC 4.2.1.66) and cyanide dihydratases (CynD; EC 3.5.5.1). CHTs are probably exclusively produced by filamentous fungi and widely occur in these organisms; in contrast, CynDs were only found in a few bacterial genera. CHTs differ from CynDs in their reaction products (formamide vs. formic acid and ammonia, respectively). Several CHTs were also found to transform nitriles but with lower relative activities compared to HCN. Mutants of CynDs and CHTs were constructed to study the structure-activity relationships in these enzymes or to improve their catalytic properties. The effect of the C-terminal part of the protein on the enzyme activity was determined by constructing the corresponding deletion mutants. CynDs are less active at alkaline pH than CHTs. To improve its bioremediation potential, CynD from Bacillus pumilus was engineered by directed evolution combined with site-directed mutagenesis, and its operation at pH 10 was thus enabled. Some of the enzymes have been tested for their potential to eliminate cyanide from cyanide-containing wastewaters. CynDs were also used to construct cyanide biosensors.

  2. Poison Ivy Treatment

    MedlinePlus

    ... Treatment Page Content Article Body Poison ivy, poison oak, and poison sumac commonly cause skin rashes in ... swampy areas of the Mississippi River region. Poison oak grows as a shrub, and it is seen ...

  3. Anticoagulant rodenticides poisoning

    MedlinePlus

    Rat killer poisoning; Rodenticide poisoning ... up unless told to do so by poison control or a health care professional. ... a free and confidential service. All local poison control centers in the United States use this national ...

  4. Catalytic Antibodies for Prophylaxis/Treatment of Cyanide Poisoning

    DTIC Science & Technology

    1991-10-09

    dimethylhydrazone ( 1 -2) with dimethylhydrazine . However the hydrazone could not be alkylated under conditions (h) or (i) of Chart I. The next step would be to...Suite t2041, Arffivgton. VA 2220.0,ardt the Office of Management and Audget. Paperworkc Reduction Project (0704-0`18111), Washington. D 00 1 . AGENCY...6l’lDAE _ Acuc~lon For NTIS CRA&I DriC TAB 1 U’larnouncud L-’Judtification_- By......... ... DiAt. Ibutlon I Avallability Codr" I DAV Dis t• I

  5. Mechanism of Chemical Action and Treatment of Cyanide Poisoning

    DTIC Science & Technology

    1986-08-01

    htpodcdaaogu0fetonlierTisuso_ asgvn etxni io f t t hr-emepsrstcynd i h clueswr rvribeb rpain h mdu wt necnai0gn cynd r yadn koncaid nioesdrcl t h ...eiu.Tuadiino L(dmtylmnpenl oal(I hl dsdimnt ts umti lftCo cobntino telsttoanioest hemdumrvrsdKN-nueddpesino heaoyt T i ocetaio-eedetmnnr h rltveefcivns oshs...Hepatocytes H as a Function of KCN Concentration ............................. 5 3 Time Course Changes in Cytotoxicity Indicators in Hepatocyte Monolayer

  6. Hyperbaric programs in the United States: Locations and capabilities of treating decompression sickness, arterial gas embolisms, and acute carbon monoxide poisoning: survey results.

    PubMed

    Chin, Walter; Jacoby, Laura; Simon, Olivia; Talati, Nisha; Wegrzyn, Gracelene; Jacoby, Rachelle; Proano, Jacob; Sprau, Susan E; Markovitz, Gerald; Hsu, Rita; Joo, Ellie

    2016-01-01

    Hyperbaric oxygen therapy is the primary treatment for arterial gas embolism, decompression sickness and acute carbon monoxide poisoning. Though there has been a proliferation of hyperbaric centers throughout the United States, a scarcity of centers equipped to treat emergency indications makes transport of patients necessary. To locate and characterize hyperbaric chambers capable of treating emergency cases, a survey of centers throughout the entire United States was conducted. Using Google, Yahoo, HyperbaricLink and the UHMS directory, a database for United States chambers was created. Four researchers called clinicians from the database to administer the survey. All centers were contacted for response until four calls went unreturned or a center declined to be included. The survey assessed chamber readiness to respond to high-acuity patients, including staff availability, use of medical equipment such as ventilators and intravenous infusion devices, and responding yes to treating hyperbaric emergencies within a 12-month period. Only 43 (11.9%, N = 361) centers had equipment, intravenous infusion pumps and ventilators, and staff necessary to treat high-acuity patients. Considering that a primary purpose of hyperbaric oxygen therapy is the treatment of arterial gas embolism and decompression sickness, more hyperbaric centers nationwide should be able to accommodate these emergency cases quickly and safely.

  7. Bioavailability of cyanide and metal-cyanide mixtures to aquatic life.

    PubMed

    Redman, Aaron; Santore, Robert

    2012-08-01

    Cyanide can be toxic to aquatic organisms, and the U.S. Environmental Protection Agency has developed ambient water-quality criteria to protect aquatic life. Recent work suggests that considering free, rather than total, cyanide provides a more accurate measure of the biological effects of cyanides and provides a basis for water-quality criteria. Aquatic organisms are sensitive to free cyanide, although certain metals can form stable complexes and reduce the amount of free cyanide. As a result, total cyanide is less toxic when complexing metals are present. Cyanide is often present in complex effluents, which requires understanding how other components within these complex effluents can affect cyanide speciation and bioavailability. The authors have developed a model to predict the aqueous speciation of cyanide and have shown that this model can predict the toxicity of metal-cyanide complexes in terms of free cyanide in solutions with varying water chemistry. Toxicity endpoints based on total cyanide ranged over several orders of magnitude for various metal-cyanide mixtures. However, predicted free cyanide concentrations among these same tests described the observed toxicity data to within a factor of 2. Aquatic toxicity can be well-described using free cyanide, and under certain conditions the toxicity was jointly described by free cyanide and elevated levels of bioavailable metals.

  8. Prophylaxis and Treatment of Cyanide Intoxication Cyanide - Mechanism of Prophylaxis.

    DTIC Science & Technology

    1982-07-15

    sodium dihydrogen phosphate were products of Fisher Scientific Company (Fairlawn, NJ). Sodium thiosulfate, sodium hydroxide, sodium cyanide, sodium...acetate buffer , 4 4 pH 5.2, and 0.5 ml of a 0.1 mM solution of SDS was added to the outer well of the diffusion cell, and 2.0 ml of 0.1 N sodium...digital pH meter (Orion Research, Inc.) that contained 10 U1 of a silver potassium cyanide indicator- buffer solution (17.69 g Na2 HPO4 , 5.5 ml 10 M NaOH

  9. CYANIDE HEAP BILOGICAL DETOXIFICATION - PHASE II

    EPA Science Inventory

    Many active mine sites, mines in closure stage and some abandoned mines are and have utilized cyanidation to remove and recover precious metals. Discharges from these sites normally contain significant amounts of metal cyanide complexes and concentrations of thiocyanate, soluble...

  10. Incident, accident, catastrophe: cyanide on the Danube.

    PubMed

    Cunningham, Solveig Argeseanu

    2005-06-01

    It has been described as the worst disaster since Chernobyl. In January 2000, a retaining wall failed at the Aurul gold processing plant in Romania, releasing a wave of cyanide and heavy metals that moved quickly from one river to the next through Romania, Hungary, the Federal Republic of Yugoslavia and Bulgaria, killing tens of thousands of fish and other forms of wildlife and poisoning drinking-water supplies. This paper examines how and why the chemical spill at Baia Mare occurred and how responses to it emerged from circumstances at the global, local and immediate levels. The spill demonstrates the importance of the flow of information in framing and interpreting disasters, suggesting that such an event can go unnoticed or be viewed as catastrophic, depending on the political, historical and personal struggles that lead to its publicity. The paper offers a framework for understanding why the spill was alternately perceived as an incident, an accident and a catastrophe based on changing perceptions of culpability.

  11. Solar-Assisted Oxidation of Toxic Cyanide

    NASA Technical Reports Server (NTRS)

    Byvik, C. E.; Miles, A.

    1985-01-01

    In solar-assisted oxidation technique, oxygen-bearing air bubbled through cyanide solution in which platinized powdered TiO2 is suspended. Light from either artifical source or natural Sunlight irradiates. Experiments demonstrated this technique effective in reducing concentration of cyanide to levels well below those achieved by other methods. Results suggest effective and inexpensive method for oxidizing cyanide in industrial wastewaters.

  12. Association of Blood Lead Level with Neurological Features in 972 Children Affected by an Acute Severe Lead Poisoning Outbreak in Zamfara State, Northern Nigeria

    PubMed Central

    Greig, Jane; Thurtle, Natalie; Cooney, Lauren; Ariti, Cono; Ahmed, Abdulkadir Ola; Ashagre, Teshome; Ayela, Anthony; Chukwumalu, Kingsley; Criado-Perez, Alison; Gómez-Restrepo, Camilo; Meredith, Caitlin; Neri, Antonio; Stellmach, Darryl; Sani-Gwarzo, Nasir; Nasidi, Abdulsalami; Shanks, Leslie; Dargan, Paul I.

    2014-01-01

    Background In 2010, Médecins Sans Frontières (MSF) investigated reports of high mortality in young children in Zamfara State, Nigeria, leading to confirmation of villages with widespread acute severe lead poisoning. In a retrospective analysis, we aimed to determine venous blood lead level (VBLL) thresholds and risk factors for encephalopathy using MSF programmatic data from the first year of the outbreak response. Methods and Findings We included children aged ≤5 years with VBLL ≥45 µg/dL before any chelation and recorded neurological status. Odds ratios (OR) for neurological features were estimated; the final model was adjusted for age and baseline VBLL, using random effects for village of residence. 972 children met inclusion criteria: 885 (91%) had no neurological features; 34 (4%) had severe features; 47 (5%) had reported recent seizures; and six (1%) had other neurological abnormalities. The geometric mean VBLLs for all groups with neurological features were >100 µg/dL vs 65.9 µg/dL for those without neurological features. The adjusted OR for neurological features increased with increasing VBLL: from 2.75, 95%CI 1.27–5.98 (80–99.9 µg/dL) to 22.95, 95%CI 10.54–49.96 (≥120 µg/dL). Neurological features were associated with younger age (OR 4.77 [95% CI 2.50–9.11] for 1–<2 years and 2.69 [95%CI 1.15–6.26] for 2–<3 years, both vs 3–5 years). Severe neurological features were seen at VBLL <105 µg/dL only in those with malaria. Interpretation Increasing VBLL (from ≥80 µg/dL) and age 1–<3 years were strongly associated with neurological features; in those tested for malaria, a positive test was also strongly associated. These factors will help clinicians managing children with lead poisoning in prioritising therapy and developing chelation protocols. PMID:24740291

  13. Scombroid Poisoning

    PubMed Central

    Lerke, Peter A.; Werner, S. Benson; Taylor, Stephen L.; Guthertz, Linda S.

    1978-01-01

    An outbreak of scombroid poisoning occurred in San Francisco in the fall of 1977. The vehicle was sashimi prepared from spoiled tuna fish. Prompt public health measures prevented further consumption of the implicated food. Laboratory studies showed the presence in the tuna of bacterial species capable of producing large amounts of histamine, a substance strongly implicated in scombroid poisoning. Chemical analysis showed that histamine is very unevenly distributed in the flesh of spoiling tuna, therefore accounting for the sometimes random occurrence of disease among people eating the same food at the same table. PMID:569397

  14. Pentachlorophenol poisoning

    SciTech Connect

    Wood, S.; Rom, W.N.; White, G.L. Jr.; Logan, D.C.

    1983-07-01

    Pentachlorophenol (PCP) is a pesticide commonly used as a wood preservative. Although exposure has been well controlled in large chemical manufacturing plants, over-exposures have recently becomes a concern at smaller facilities. Five cases of PCP poisoning, including two fatalities, occurred in two small wood preservative plants. All cases presented with fever, including severe hyperpyrexia in two; an increased anion gap and renal insufficiency were noted in two others. PCP may uncouple oxidative phosphorylation, resulting in a poisoning syndrome characterized by hyperpyrexia, diaphoresis, tachycardia, tachypnea, abdominal pain, nausea, and even death.

  15. Suicide by cyanide: 17 deaths.

    PubMed

    Gill, James R; Marker, Elizabeth; Stajic, Marina

    2004-07-01

    We reviewed 17 intentional ingestions of cyanide that occurred in New York City over a ten-year interval. The toxicologic and postmortem findings were reviewed. Certain occupations and nationalities of the decedents predominated among this group of suicides. Scientists, jewelers. and metal workers were common occupations among the decedents. In addition, 8 of 17 fatalities were West Indian/Caribbean Island and South American decedents, including three decedents from Guyana. Fourteen of the 17 fatalities were male. Pink lividity, a "bitter-almond" smell. and a hemorrhagic gastric mucosa were not prevailing findings in these decedents. A color test was used for screening for cyanide with confirmation and quantitation using gas chromatography.

  16. The Dose Makes the Poison.

    ERIC Educational Resources Information Center

    Ottoboni, Alice

    1992-01-01

    A Toxicologist discusses common misconception that all chemicals are poisonous to people and the environment and how these misconceptions are perpetuated. Describes what makes a chemical toxic. Defines related concepts including dose, acute and chronic toxicity, and natural verses synthetic chemicals. (MCO)

  17. Lead poisoning in children: a case report.

    PubMed

    Jouhadi, Zineb; Bensabbahia, Dalal; Chafiq, Fouad; Oukkache, Bouchra; Guebessi, Nisrine Bennani; Abdellah, El Abidi; Najib, Jilali

    2016-01-01

    Lead colic is a rare cause of abdominal pain. The diagnosis of lead poisoning is most often mentioned in at risk populations (children, psychotic). We report the case of a 2 year old child that was presented for acute abdomen. Abdominal plain radiograph showed multiple intra-colonic metallic particles and suggested lead poisoning diagnosis. Anamnesis found a notion of pica and consumption of peeling paint. Elevated blood lead levels (BLL) confirmed the diagnosis. The lead poisoning is a public health problem especially in children, but its manifestation by a lead colic is rare and could simulate an acute abdomen table.

  18. Lead poisoning in children: a case report

    PubMed Central

    Jouhadi, Zineb; Bensabbahia, Dalal; Chafiq, Fouad; Oukkache, Bouchra; Guebessi, Nisrine Bennani; Abdellah, El Abidi; Najib, Jilali

    2016-01-01

    Lead colic is a rare cause of abdominal pain. The diagnosis of lead poisoning is most often mentioned in at risk populations (children, psychotic). We report the case of a 2 year old child that was presented for acute abdomen. Abdominal plain radiograph showed multiple intra-colonic metallic particles and suggested lead poisoning diagnosis. Anamnesis found a notion of pica and consumption of peeling paint. Elevated blood lead levels (BLL) confirmed the diagnosis. The lead poisoning is a public health problem especially in children, but its manifestation by a lead colic is rare and could simulate an acute abdomen table. PMID:28154671

  19. Cyanide in human disease: a review of clinical and laboratory evidence.

    PubMed

    Wilson, J

    1983-01-01

    Experimental cyanide exposure in animals causes demyelination and circumstantial clinical and laboratory evidence suggest that there are human parallels. In Leber's hereditary optic atrophy there appears to be a defect in the conversion of cyanide to thiocyanate because of deficient rhodanese activity. For transmitters of the disease smoking carries the risk of blindness and in the most severely affected patients, there is diffuse neurological disease. It is possible that other hereditary optic atrophies (dominant and recessive) may also reflect inborn errors of cyanide metabolism. In the retrobulbar neuritis and optic atrophy of vitamin B12 deficiency there may be a conditional abnormality of cyanide metabolism in smokers, and likewise in so-called tobacco-alcohol amblyopia in which there are more complex nutritional deficiencies. Epidemiological evidence (differing sex ratios, excess of smokers) indicates that defective cyanide metabolism may contribute to the development of sub-acute combined degeneration of the cord in vitamin B12 deficiency. In protein-malnourished populations consuming large amounts of cyanide or cyanogens, viz. in tropical Africa where the staple diet includes cassava containing large amounts of linamarin, similar maladies occur as acquired disorders. There may be a similar explanation for lathyrism. The known pathways of human cyanide metabolism are reviewed and evidence supporting the clinical data is presented.

  20. Poison Ivy

    MedlinePlus

    ... poison ivy”. The plant is found around the world, but it usually doesn’t grow in the desert or in high elevations. It usually grows in clusters in the woods, up in trees, and on the ground. Every part of the ...

  1. Lead poisoning

    SciTech Connect

    Rekus, J.F.

    1992-08-01

    Construction workers who weld, cut or blast structural steel coated with lead-based paint are at significant risk of lead poisoning. Although technology to control these exposures may not have existed when the lead standard was promulgated, it is available today. Employers who do not take steps to protect their employees from lead exposure may be cited and fined severely for their failure.

  2. Acute Poisonings from Synthetic Cannabinoids - 50 U.S. Toxicology Investigators Consortium Registry Sites, 2010-2015.

    PubMed

    Riederer, Anne M; Campleman, Sharan L; Carlson, Robert G; Boyer, Edward W; Manini, Alex F; Wax, Paul M; Brent, Jeffrey A

    2016-07-15

    Recent reports suggest that acute intoxications by synthetic cannabinoids are increasing in the United States (1,2). Synthetic cannabinoids, which were research compounds in the 1980s, are now produced overseas; the first shipment recognized to contain synthetic cannabinoids was seized at a U.S. border in 2008 (3). Fifteen synthetic cannabinoids are Schedule I controlled substances (3), but enforcement is hampered by the continual introduction of new chemical compounds (1,3). Studies of synthetic cannabinoids indicate higher cannabinoid receptor binding affinities, effects two to 100 times more potent than Δ(9)-tetrahydrocannabinol (the principal psychoactive constituent of cannabis), noncannabinoid receptor binding, and genotoxicity (4,5). Acute synthetic cannabinoid exposure reportedly causes a range of mild to severe neuropsychiatric, cardiovascular, renal, and other effects (4,6,7); chronic use might lead to psychosis (6,8). During 2010-2015, physicians in the Toxicology Investigators Consortium (ToxIC) treated 456 patients for synthetic cannabinoid intoxications; 277 of the 456 patients reported synthetic cannabinoids as the sole toxicologic agent. Among these 277 patients, the most common clinical signs of intoxication were neurologic (agitation, central nervous system depression/coma, and delirium/toxic psychosis). Relative to all cases logged by 50 different sites in the ToxIC Case Registry, there was a statistically significant association between reporting year and the annual proportion of synthetic cannabinoid cases. In 2015, reported cases of synthetic cannabinoid intoxication increased at several ToxIC sites, corroborating reported upward trends in the numbers of such cases (1,2) and underscoring the need for prevention.

  3. Detection of interstellar ethyl cyanide

    NASA Technical Reports Server (NTRS)

    Johnson, D. R.; Lovas, F. J.; Gottlieb, C. A.; Gottlieb, E. W.; Litvak, M. M.; Thaddeus, P.; Guelin, M.

    1977-01-01

    Twenty-four millimeter-wave emission lines of ethyl cyanide (CH3CH2CN) have been detected in the Orion Nebula (OMC-1) and seven in Sgr B2. To derive precise radial velocities from the astronomical data, a laboratory measurement of the rotational spectrum of ethyl cyanide has been made at frequencies above 41 GHz. In OMC-1, the rotational temperature of ethyl cyanide is 90 K (in good agreement with other molecules), the local-standard-of-rest radial velocity is 4.5 + or - 1.0 km/s (versus 8.5 km/s for most molecules), and the column density is 1.8 by 10 to the 14th power per sq cm (a surprisingly high figure for a complicated molecule). The high abundance of ethyl cyanide in the Orion Nebula suggests that ethane and perhaps larger saturated hydrocarbons may be common constituents of molecular clouds and have escaped detection only because they are nonpolar or only weakly polar.

  4. Glyphosate poisoning.

    PubMed

    Bradberry, Sally M; Proudfoot, Alex T; Vale, J Allister

    2004-01-01

    Glyphosate is used extensively as a non-selective herbicide by both professional applicators and consumers and its use is likely to increase further as it is one of the first herbicides against which crops have been genetically modified to increase their tolerance. Commercial glyphosate-based formulations most commonly range from concentrates containing 41% or more glyphosate to 1% glyphosate formulations marketed for domestic use. They generally consist of an aqueous mixture of the isopropylamine (IPA) salt of glyphosate, a surfactant, and various minor components including anti-foaming and colour agents, biocides and inorganic ions to produce pH adjustment. The mechanisms of toxicity of glyphosate formulations are complicated. Not only is glyphosate used as five different salts but commercial formulations of it contain surfactants, which vary in nature and concentration. As a result, human poisoning with this herbicide is not with the active ingredient alone but with complex and variable mixtures. Therefore, It is difficult to separate the toxicity of glyphosate from that of the formulation as a whole or to determine the contribution of surfactants to overall toxicity. Experimental studies suggest that the toxicity of the surfactant, polyoxyethyleneamine (POEA), is greater than the toxicity of glyphosate alone and commercial formulations alone. There is insufficient evidence to conclude that glyphosate preparations containing POEA are more toxic than those containing alternative surfactants. Although surfactants probably contribute to the acute toxicity of glyphosate formulations, the weight of evidence is against surfactants potentiating the toxicity of glyphosate. Accidental ingestion of glyphosate formulations is generally associated with only mild, transient, gastrointestinal features. Most reported cases have followed the deliberate ingestion of the concentrated formulation of Roundup (The use of trade names is for product identification purposes only and

  5. [Sodium azide poisoning--a rare reason of hospitalization in toxicological units--case report].

    PubMed

    Kostek, Halina; Sawiniec, Jarosław; Lewandowska-Stanek, Hanna; Kujawa, Anna; Majewska, Magdalena; Szponar, Jarosław

    2012-01-01

    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.

  6. The poison oligonucleotide F10 is highly effective against acute lymphoblastic leukemia while sparing normal hematopoietic cells.

    PubMed

    Pardee, Timothy S; Stadelman, Kristin; Jennings-Gee, Jamie; Caudell, David L; Gmeiner, William H

    2014-06-30

    F10 is an oligonucleotide based on the thymidylate synthase (TS) inhibitory 5-fluorouracil (5-FU) metabolite, 5-fluoro-2'-deoxyuridine-5'-O-monophosphate. We sought to determine the activity of F10 against preclinical models of acute lymphoblastic leukemia (ALL). F10 treatment resulted in robust induction of apoptosis that could not be equaled by 100 fold more 5-FU. F10 was more potent than Ara-C and doxorubicin against a panel of murine and human ALL cells with an average IC50 value of 1.48 nM (range 0.07 to 5.4 nM). F10 was more than 1000 times more potent than 5-FU. In vivo, F10 treatment significantly increased survival in 2 separate syngeneic ALL mouse models and 3 separate xenograft models. F10 also protected mice from leukemia-induced weight loss. In ALL cells made resistant to Ara-C, F10 remained highly active in vitro and in vivo. Using labeled F10, uptake by the ALL cell lines DG75 and SUP-B15 was rapid and profoundly temperature-dependent. Both cell lines demonstrated increased uptake compared to normal murine lineage- depleted marrow cells. Consistent with this decreased uptake, F10 treatment did not alter the ability of human hematopoietic stem cells to engraft in immunodeficient mice.

  7. The poison oligonucleotide F10 is highly effective against acute lymphoblastic leukemia while sparing normal hematopoietic cells

    PubMed Central

    Pardee, Timothy S.; Stadelman, Kristin; Jennings-Gee, Jamie; Caudell, David L.; Gmeiner, William H.

    2014-01-01

    F10 is an oligonucleotide based on the thymidylate synthase (TS) inhibitory 5-fluorouracil (5-FU) metabolite, 5-fluoro-2'-deoxyuridine-5'-O-monophosphate. We sought to determine the activity of F10 against preclinical models of acute lymphoblastic leukemia (ALL). F10 treatment resulted in robust induction of apoptosis that could not be equaled by 100 fold more 5-FU. F10 was more potent than Ara-C and doxorubicin against a panel of murine and human ALL cells with an average IC50 value of 1.48 nM (range 0.07 to 5.4 nM). F10 was more than 1000 times more potent than 5-FU. In vivo, F10 treatment significantly increased survival in 2 separate syngeneic ALL mouse models and 3 separate xenograft models. F10 also protected mice from leukemia-induced weight loss. In ALL cells made resistant to Ara-C, F10 remained highly active in vitro and in vivo. Using labeled F10, uptake by the ALL cell lines DG75 and SUP-B15 was rapid and profoundly temperature-dependent. Both cell lines demonstrated increased uptake compared to normal murine lineage- depleted marrow cells. Consistent with this decreased uptake, F10 treatment did not alter the ability of human hematopoietic stem cells to engraft in immunodeficient mice. PMID:24961587

  8. Parathion Poisoning from Flannelette Sheets

    PubMed Central

    Anderson, L. S.; Warner, D. L.; Parker, J. E.; Bluman, N.; Page, B. D.

    1965-01-01

    Two small boys were admitted to the Lions Gate Hospital in coma and acute respiratory distress. They improved and the first boy was sent home; after two nights he was back in hospital in a worsened state. Poisoning with organic phosphate was suspected, and after investigation some flannelette sheets were taken from his home for testing. They proved to have been contaminated with parathion (“nerve gas”) in the hold of a ship sailing from Antwerp to Vancouver; the parathion had been offloaded in California. The remainder of the sheets were traced. The symptomatology and treatment of organic phosphate ester poisoning and the chemical testing of parathion are discussed. PMID:14272498

  9. Accidental poisoning with autumn crocus.

    PubMed

    Gabrscek, Lucija; Lesnicar, Gorazd; Krivec, Bojan; Voga, Gorazd; Sibanc, Branko; Blatnik, Janja; Jagodic, Boris

    2004-01-01

    We describe a case of a 43-yr-old female with severe multiorgan injury after accidental poisoning with Colchicum autumnale, which was mistaken for wild garlic (Allium ursinum). Both plants grow on damp meadows and can be confused in the spring when both plants have leaves but no blossoms. The autumn crocus contains colchicine, which inhibits cellular division. Treatment consisted of supportive care, antibiotic therapy, and granulocyte-directed growth factor. The patient was discharged from the hospital after three weeks. Three years after recovery from the acute poisoning, the patient continued to complain of muscle weakness and intermittent episodes of hair loss.

  10. Sodium fluoroacetate poisoning.

    PubMed

    Proudfoot, Alex T; Bradberry, Sally M; Vale, J Allister

    2006-01-01

    liberated from fluoroacetate, citrate and fluorocitrate are calcium chelators and there are both animal and clinical data to support hypocalcaemia as a mechanism of fluoroacetate toxicity. However, the available evidence suggests the fluoride component does not contribute. Acute poisoning with sodium fluoroacetate is uncommon. Ingestion is the major route by which poisoning occurs. Nausea, vomiting and abdominal pain are common within 1 hour of ingestion. Sweating, apprehension, confusion and agitation follow. Both supraventricular and ventricular arrhythmias have been reported and nonspecific ST- and T-wave changes are common, the QTc may be prolonged and hypotension may develop. Seizures are the main neurological feature. Coma may persist for several days. Although several possible antidotes have been investigated, they are of unproven value in humans. The immediate, and probably only, management of fluoroacetate poisoning is therefore supportive, including the correction of hypocalcaemia.

  11. A drug from poison: how the therapeutic effect of arsenic trioxide on acute promyelocytic leukemia was discovered.

    PubMed

    Rao, Yi; Li, Runhong; Zhang, Daqing

    2013-06-01

    It is surprising that, while arsenic trioxide (ATO) is now considered as "the single most active agent in patients with acute promyelocytic leukemia (APL)", the most important discoverer remains obscure and his original papers have not been cited by a single English paper. The discovery was made during the Cultural Revolution when most Chinese scientists and doctors struggled to survive. Beginning with recipes from a countryside practitioner that were vague in applicable diseases, Zhang TingDong and colleagues proposed in the 1970s that a single chemical in the recipe is most effective and that its target is APL. More than 20 years of work by Zhang and colleagues eliminated the confusions about whether and how ATO can be used effectively. Other researchers, first in China and then in the West, followed his lead. Retrospective analysis of data from his own group proved that APL was indeed the most sensitive target. Removal of a trace amount of mercury chloride from the recipe by another group in his hospital proved that only ATO was required. Publication of Western replication in 1998 made the therapy widely accepted, though neither Western, nor Chinese authors of English papers on ATO cited Zhang's papers in the 1970s. This article focuses on the early papers of Zhang, but also suggests it worth further work to validate Chinese reports of ATO treatment of other cancers, and infers that some findings published in Chinese journals are of considerable value to patients and that doctors from other countries can benefit from the clinical experience of Chinese doctors with the largest population of patients.

  12. [Superwarfarine Poisoning].

    PubMed

    Freixo, Ana; Lopes, Luís; Carvalho, Manuela; Araújo, Fernando

    2015-01-01

    The superwarfarin-type anticoagulant rodenticides are used throughout the world and distinguish themselves from warfarin for its high potency and long acting anticoagulant activity. Easy access to these products enables the accidental or deliberate human poisoning. A case of voluntary rodenticide poisoning (RATIBRONÂ) by a woman who ingested an estimated 27.5 mg of bromadiolone total quantity for two weeks, with minor bleeding episodes, whose reversal of the anticoagulant effect with the correction of the abnormal values of the clotting tests took about one month to reverse is reported here. The correction of the haemostasis defects takes usually a long time and there are no treatment guidelines, but a gradually vitamin K dosage reduction, as out patients, along with the monitoring of the International Normalized Ratio levels, allows a safe evaluation of the therapeutic response.

  13. Oxidative stress mediated cytotoxicity of cyanide in LLC-MK2 cells and its attenuation by alpha-ketoglutarate and N-acetyl cysteine.

    PubMed

    Hariharakrishnan, J; Satpute, R M; Prasad, G B K S; Bhattacharya, R

    2009-03-10

    Cyanide is a rapidly acting mitochondrial poison that inhibits cellular respiration and energy metabolism leading to histotoxic hypoxia followed by cell death. Cyanide is predominantly a neurotoxin but its toxic manifestations in non-neuronal cells are also documented. This study addresses the oxidative stress mediated cytotoxicity of cyanide in Rhesus monkey kidney epithelial cells (LLC-MK2). Cells were treated with various concentrations of potassium cyanide (KCN) for different time intervals and cytotoxicity was evidenced by increased leakage of intracellular lactate dehydrogenase, mitochondrial dysfunction (MTT assay) and depleted energy status of cells (ATP assay). Cytotoxicity was accompanied by lipid peroxidation indicated by elevated levels of malondialdehyde (MDA), reactive oxygen species (ROS) and reactive nitrogen species (RNS) (DCF-DA staining), diminished cellular antioxidant status (reduced glutathione (GSH), glutathione peroxidase, superoxide dismutase and catalase). These cascading events triggered an apoptotic kind of cell death characterized by oligonucleosomal DNA fragmentation and nuclear fragmentation (Hoechst 33342 staining). Apoptosis was further confirmed by increased caspase-3 activity. Cyanide-induced cytotoxicity, oxidative stress, and DNA fragmentation were prevented by alpha-ketoglutarate (A-KG) and N-acetyl cysteine (NAC). A-KG is a potential cyanide antidote that confers protection by interacting with cyanide to form cyanohydrin complex while NAC is a free radical scavenger and enhances the cellular GSH levels. The study reveals cytotoxicity of cyanide in cells of renal origin and the protective efficacy of A-KG and NAC.

  14. Metabolism of cyanide by Chinese vegetation.

    PubMed

    Yu, Xiaozhang; Trapp, Stefan; Zhou, Puhua; Wang, Chang; Zhou, Xishi

    2004-07-01

    Cyanide is a high-volume production chemical and the most commonly used leaching reagent for gold and silver extraction. Its environmental behavior and fate is of significant concern because it is a highly toxic compound. Vascular plants possess an enzyme system that detoxifies cyanide by converting it to the amino acid asparagine. This paper presents an investigation of the potential of Chinese vegetation to degrade cyanide. Detached leaves (1.5 g fresh weight) from 28 species of 23 families were kept in glass vessel with 100 ml of aqueous solution spiked with potassium cyanide at 23.5 degrees C for 28 h. Cyanide concentrations ranged from 0.83 to 1.0 CN mg l(-1). The disappearance of cyanide from the aqueous solution was analyzed spectrophotometrically. The fastest cyanide removal was by Chinese elder, Sambucus chinensis, with a removal capacity of 8.8 mg CN kg(-1) h(-1), followed by upright hedge-parsley (Torilis japonica) with a value of 7.5 mg CN kg(-1) h(-1). The lowest removal capacity had the snow-pine tree (Credrus deodara (Roxb.) Loud). Results from this investigation indicated that a wide range of plant species is able to efficiently metabolize cyanide. Therefore, cyanide elimination with plants seems to be a feasible option for cleaning soils and water contaminated by cyanide from gold and silver mines or from other sources.

  15. Cyanide inactivation of hydrogenase from Azotobacter vinelandii

    SciTech Connect

    Seefeldt, L.C.; Arp, D.J. )

    1989-06-01

    The effects of cyanide on membrane-associated and purified hydrogenase from Azotobacter vinelandii were characterized. Inactivation of hydrogenase by cyanide was dependent on the activity (oxidation) state of the enzyme. Active (reduced) hydrogenase showed no inactivation when treated with cyanide over several hours. Treatment of reversibly inactive (oxidized) states of both membrane-associated and purified hydrogenase, however, resulted in a time-dependent, irreversible loss of hydrogenase activity. The rate of cyanide inactivation was dependent on the cyanide concentration and was an apparent first-order process for purified enzyme (bimolecular rate constant, 23.1 M{sup {minus}1} min{sup {minus}1} for CN{sup {minus}}). The rate of inactivation decreased with decreasing pH. ({sup 14}C)cyanide remained associated with cyanide-inactivated hydrogenase after gel filtration chromatography, with a stoichiometry of 1.7 mol of cyanide bound per mol of inactive enzyme. The presence of saturating concentrations of CO had no effect on the rate or extent of cyanide inactivation of hydrogenases. The results indicate that cyanide can cause a time-dependent, irreversible inactivation of hydrogenase in the oxidized, activatable state but has no effect when hydrogenase is in the reduced, active state.

  16. Cyanide inactivation of hydrogenase from Azotobacter vinelandii.

    PubMed Central

    Seefeldt, L C; Arp, D J

    1989-01-01

    The effects of cyanide on membrane-associated and purified hydrogenase from Azotobacter vinelandii were characterized. Inactivation of hydrogenase by cyanide was dependent on the activity (oxidation) state of the enzyme. Active (reduced) hydrogenase showed no inactivation when treated with cyanide over several hours. Treatment of reversibly inactive (oxidized) states of both membrane-associated and purified hydrogenase, however, resulted in a time-dependent, irreversible loss of hydrogenase activity. The rate of cyanide inactivation was dependent on the cyanide concentration and was an apparent first-order process for purified enzyme (bimolecular rate constant, 23.1 M-1 min-1 for CN-). The rate of inactivation decreased with decreasing pH. [14C]cyanide remained associated with cyanide-inactivated hydrogenase after gel filtration chromatography, with a stoichiometry of 1.7 mol of cyanide bound per mol of inactive enzyme. The presence of saturating concentrations of CO had no effect on the rate or extent of cyanide inactivation of hydrogenases. The results indicate that cyanide can cause a time-dependent, irreversible inactivation of hydrogenase in the oxidized, activatable state but has no effect when hydrogenase is in the reduced, active state. PMID:2656648

  17. In situ treatment of cyanide-contaminated groundwater by iron cyanide precipitation

    SciTech Connect

    Ghosh, R.S.; Dzombak, D.A.; Luthy, R.G.; Smith, J.R.

    1999-10-01

    Groundwater contamination with cyanide is common at many former or active industrial sites. Metal-cyanide complexes typically dominate aqueous speciation of cyanide in groundwater systems, with iron-cyanide complexes often most abundant. Typically, metal-cyanide complexes behave as nonadsorbing solutes in sand-gravel aquifer systems in the neutral pH range, rendering cyanide relatively mobile in groundwater systems. Groundwater pump-and-treat systems have often been used to manage cyanide contamination in groundwater. This study examined the feasibility of using in situ precipitation of iron cyanide in a reactive barrier to attenuate the movement of cyanide in groundwater. Laboratory column experiments were performed in which cyanide solutions were passed through mixtures of sand and elemental iron filings. Removal of dissolved cyanide was evaluated in a variety of cyanide-containing influents under various flow rates and sand-to-iron weight ratios. Long-term column tests performed with various cyanide-containing influents under both oxic and anoxic conditions, at neutral pH and at flow rates typical of sand-gravel porous media, yielded effluent concentrations of total cyanide as low as 0.5 mg/L. Effluent cyanide concentrations achieved were close to the solubilities of Turnbull's blue-hydrous ferric oxide solid solutions, indicating co-precipitation of the two solids. Maximum cyanide removal efficiency was achieved with approximately 10% by weight of iron in the sand-iron mixtures; higher iron contents did not increase removal efficiency significantly. Results obtained indicate that in situ precipitation is a promising passive treatment approach for cyanide in groundwater.

  18. Poison Ivy Rash

    MedlinePlus

    ... to poison ivy, poison oak and poison sumac: Farming Forestry Landscaping Gardening Firefighting Construction Camping Fishing from ... Terms and Conditions Privacy Policy Notice of Privacy Practices Notice of Nondiscrimination Advertising Mayo Clinic is a ...

  19. Cold wave lotion poisoning

    MedlinePlus

    ... if known) Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  20. Rhubarb leaves poisoning

    MedlinePlus

    ... if known Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  1. Face powder poisoning

    MedlinePlus

    ... if known) Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  2. Hair tonic poisoning

    MedlinePlus

    ... if known) Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  3. Cuticle remover poisoning

    MedlinePlus

    ... if known) Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  4. Bubble bath soap poisoning

    MedlinePlus

    ... if known) Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  5. Drain cleaner poisoning

    MedlinePlus

    ... help if this information is not immediately available. Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  6. Shaving cream poisoning

    MedlinePlus

    ... if known) Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  7. Hair bleach poisoning

    MedlinePlus

    ... if known) Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  8. Hand lotion poisoning

    MedlinePlus

    ... if known) Time it was swallowed Amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  9. Lip moisturizer poisoning

    MedlinePlus

    ... The time it was swallowed The amount swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  10. Plastic casting resin poisoning

    MedlinePlus

    Epoxy poisoning; Resin poisoning ... Epoxy and resin can be poisonous if they are swallowed or their fumes are breathed in. ... Plastic casting resins are found in various plastic casting resin products.

  11. Caladium plant poisoning

    MedlinePlus

    ... eaten Amount swallowed The time it was swallowed Poison Control Your local poison center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere ...

  12. Mercuric chloride poisoning

    MedlinePlus

    ... Mercuric chloride is a very poisonous form of mercury. It is a type of mercury salt. There are different types of mercury poisonings . This article discusses poisoning from swallowing mercuric ...

  13. [Sodium azide--clinical course of the poisoning and treatment].

    PubMed

    Łopaciński, Bogdan; Kołacinski, Zbigniew; Winnicka, Renata

    2007-01-01

    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

  14. Protecting Yourself from Poisonous Plants

    MedlinePlus

    ... NIOSH NIOSH Fast Facts: Protecting Yourself from Poisonous Plants Language: English Español (Spanish) Kreyol Haitien (Hatian Creole) ... outdoors is at risk of exposure to poisonous plants, such as poison ivy, poison oak, and poison ...

  15. Assay development status report for total cyanide

    SciTech Connect

    Simpson, B.C.; Jones, T.E.; Pool, K.H.

    1993-02-01

    A validated cyanide assay that is applicable to a variety of tank waste matrices is necessary to resolve certain waste tank safety issues and for purposes of overall waste characterization. The target for this effort is an assay with an applicable range of greater than 1,000 ppM (0.10 wt%) total cyanide and a confidence level greater than 80%. Figure 1 illustrates the operating regime of the proposed cyanide assay method. The Assay Development Status Report for Total Cyanide will summarize the past experience with cyanide analyses on-tank waste matrices and will rate the status of the analytical methods used to assay total cyanide (CN{sup {minus}} ion) in the tank waste matrices as acceptable or unacceptable. This paper will also briefly describe the current efforts for improving analytical resolution of the assays and the attempts at speciation.

  16. Diagnosis and Treatment of Cyanide Toxicity

    DTIC Science & Technology

    2009-02-01

    treat toxic amblyopia and optic neuritises caused by the cyanide present in tobacco smoke.64,65 Hydroxycobalamin therapy is usually well tolerated,44,59...JAN 2009 2. REPORT TYPE N/A 3. DATES COVERED - 4. TITLE AND SUBTITLE Diagnosis and treatment of cyanide toxicity 5a. CONTRACT NUMBER 5b...ABSTRACT unclassified c. THIS PAGE unclassified Standard Form 298 (Rev. 8-98) Prescribed by ANSI Std Z39-18 Diagnosis and Treatment of Cyanide Toxicity

  17. Distribution of cyanide in heart blood, peripheral blood and gastric contents in 21 cyanide related fatalities.

    PubMed

    Rhee, Jongsook; Jung, Jinmi; Yeom, Hyesun; Lee, Hansun; Lee, Sangki; Park, Yoosin; Chung, Heesun

    2011-07-15

    This paper presents 21 cases related to cyanide intoxication by oral ingestion. Cyanide concentrations in biological specimens are especially different from the type of postmortem specimens, and very important in interpreting the cause of death in postmortem forensic toxicology. Besides the detection of cyanide in autopsy specimens, the autopsy findings were unremarkable. Biological samples (0.2mL or equal to less than 10μg of cyanide) were analyzed colorimetrically for cyanide. In a series of 21 cyanide fatalities, the concentration ranges (mean±SD) of cyanide in heart blood, peripheral blood and gastric contents were 0.1-248.6mg/L (38.1±56.6mg/L), 0.3-212.4mg/L (17.1±45.1mg/L) and 2.0-6398.0mg/kg (859.0±1486.2mg/kg), respectively. The ranges of the heart/peripheral blood concentration ratio and gastric contents/peripheral blood concentration ratio were 0.3-10.6 (mean 3.4) and 3.4-402.4 (mean 86.0), respectively. From the difference of cyanide concentration and the concentration ratio of cyanide in different types of postmortem specimens, the possibility of the postmortem redistribution of cyanide and death by oral ingestion of cyanide could be confirmed. We reported cyanide fatal cases along with a review of literature.

  18. Cyanide bioremediation: the potential of engineered nitrilases.

    PubMed

    Park, Jason M; Trevor Sewell, B; Benedik, Michael J

    2017-04-01

    The cyanide-degrading nitrilases are of notable interest for their potential to remediate cyanide contaminated waste streams, especially as generated in the gold mining, pharmaceutical, and electroplating industries. This review provides a brief overview of cyanide remediation in general but with a particular focus on the cyanide-degrading nitrilases. These are of special interest as the hydrolysis reaction does not require secondary substrates or cofactors, making these enzymes particularly good candidates for industrial remediation processes. The genetic approaches that have been used to date for engineering improved enzymes are described; however, recent structural insights provide a promising new approach.

  19. Washout kinetics of inhaled hydrogen cyanide in breath.

    PubMed

    Stamyr, Kristin; Nord, Pierre; Johanson, Gunnar

    2008-06-10

    Hydrogen cyanide (HCN) intoxication causes or contributes significantly to many of the fatalities among fire victims. To enable fast treatment of HCN poisoning, a more rapid diagnostic method than currently available is required. One possibility would be measurement in exhaled air. However, as HCN is highly water soluble, it may be absorbed during inhalation and reabsorbed during exhalation. If this, so-called, washin-washout effect is substantial it may interfere with the diagnosis, as a major part of breath HCN may originate from the respiratory tract, due to recent exposure, and not from systemic exposure. The aim of this study was to estimate the importance of the washin-washout effect of HCN. The time-course of cyanide in exhaled air was measured with an electrochemical detector in 10 volunteers during and after a 1 min x 10 ppm exposure to HCN. The experiment revealed an average half-life of 16s (range 10-24s) in breath. Extrapolating the results to higher exposures suggests that the contribution from washin-washout from the airways will be negligible even at fatal exposures. The results support the use of breath HCN as a potential indicator of systemic intoxication.

  20. Konzo and continuing cyanide intoxication from cassava in Mozambique.

    PubMed

    Cliff, J; Muquingue, H; Nhassico, D; Nzwalo, H; Bradbury, J H

    2011-03-01

    In Mozambique, epidemics of the cassava-associated paralytic disease, konzo, have been reported in association with drought or war: over 1100 cases in 1981, over 600 cases in 1992-1993, and over 100 cases in 2005. Smaller epidemics and sporadic cases have also been reported. Large epidemics have occurred at times of agricultural crisis, during the cassava harvest, when the population has been dependent on a diet of insufficiently processed bitter cassava. Konzo mostly affects women of child-bearing age and children over 2 years of age. When measured, serum or urinary thiocyanate concentrations, indicative of cyanide poisoning, have been high in konzo patients during epidemics and in succeeding years. Monitoring of urinary thiocyanate concentrations in schoolchildren in konzo areas has shown persistently high concentrations at the time of the cassava harvest. Inorganic sulphate concentrations have been low during and soon after epidemics. Programmes to prevent konzo have focused on distributing less toxic varieties of cassava and disseminating new processing methods, such as grating and the flour wetting method. Attention should be given to the wider question of agricultural development and food security in the regions of Africa where dependence on bitter cassava results in chronic cyanide intoxication and persistent and emerging konzo.

  1. House of Poison: Poisons in the Home.

    ERIC Educational Resources Information Center

    Keller, Rosanne

    One of a series of instructional materials produced by the Literacy Council of Alaska, this booklet provides information about common household poisons. Using a simplified vocabulary and shorter sentences, it provides statistics concerning accidental poisonings; a list of the places poisons are usually found in the home; steps to make the home…

  2. Patterns of cyanide antidote use since regulatory approval of hydroxocobalamin in the United States.

    PubMed

    Streitz, Matthew J; Bebarta, Vikhyat S; Borys, Douglas J; Morgan, David L

    2014-01-01

    Sodium nitrite and sodium thiosulfate are common cyanide antidotes. Hydroxocobalamin was approved for use in the United States in 2006. Our objective was to determine the frequency of antidote use as reported to the US poison centers from 2005 to 2009 and describe which antidotes were used in critically ill cyanide toxic patients. We performed a retrospective review over 5 years (2005-2009) from 61 US poison centers. We identified all cyanide-exposed cases that received a cyanide antidote. Variables collected included demographics, gastric decontamination, antidote used, predefined serious clinical effects (hypotension, cardiac arrest, respiratory arrest, and coma), and predefined serious therapies (cardiopulmonary resuscitation, vasopressors, atropine, anticonvulsant, antidysrhythmic, and intubation/ventilation). One trained abstractor abstracted each chart to a standardized electronic form. Another investigator audited 20% of the charts. Kappa values were calculated. One hundred sixty-five exposures were identified. Mean age was 42 years (range, 3-93 years). Seventy-one percent were male. Exposures were 27% ingestion and 53% inhalation. Thirty-two percent of the ingestions were suicide attempts. Twenty percent (32 of 157) of all cases died. Over all years reported, hydroxocobalamin was administered to 29% (45 of 157) of patients, sodium nitrite to 25%, and sodium thiosulfate to 46%. Hydroxocobalamin use increased from 24% to 54% from 2007 to 2009, respectively (P = 0.024). Sodium thiosulfate use decreased from 73% to 31% (P = 0.002) and sodium nitrite use decreased from 26% to 14% (P = 0.39). The proportion of cases with serious clinical effects that received hydroxocobalamin increased each year, and the proportion that received other antidotes decreased. Hydroxocobalamin was also administered more often in cases that required serious therapies and increased each year. Hydroxocobalamin use for cyanide toxicity increased each year as reported to the US poison

  3. Pediatric cyanide intoxication and death from an acetonitrile-containing cosmetic

    SciTech Connect

    Caravati, E.M.; Litovitz, T.L. )

    1988-12-16

    Two cases of pediatric accidental ingestion of an acetonitrile-containing cosmetic are reported. One of the children, a 16-month-old boy, was found dead in bed the morning after ingesting the product. No therapy had been undertaken, as the product was mistakenly assumed to be an acetone-containing nail polish remover. The second child, a 2-year-old boy, experienced signs of severe cyanide poisoning, but survived with vigorous supportive care. Both children had blood cyanide levels in the potentially lethal range. The observed delayed onset of severe toxic reactions supports the proposed mechanism of acetonitrile conversion to inorganic cyanide via hepatic microsomal enzymes. Physicians and poison centers should be alerted to the existence of this highly toxic product, sold for removal of sculptured nails and likely to be confused with the less toxic acetone-containing nail polish removers. The authors urge regulatory agencies to reconsider the wisdom of marketing a cosmetic that poses such an extreme health hazard.

  4. Dimethyl trisulfide: A novel cyanide countermeasure.

    PubMed

    Rockwood, Gary A; Thompson, David E; Petrikovics, Ilona

    2016-12-01

    In the present studies, the in vitro and in vivo efficacies of a novel cyanide countermeasure, dimethyl trisulfide (DMTS), were evaluated. DMTS is a sulfur-based molecule found in garlic, onion, broccoli, and similar plants. DMTS was studied for effectiveness as a sulfur donor-type cyanide countermeasure. The sulfur donor reactivity of DMTS was determined by measuring the rate of the formation of the cyanide metabolite thiocyanate. In experiments carried out in vitro in the presence of the sulfurtransferase rhodanese (Rh) and at the experimental pH of 7.4, DMTS was observed to convert cyanide to thiocyanate with greater than 40 times higher efficacy than does thiosulfate, the sulfur donor component of the US Food and Drug Administration-approved cyanide countermeasure Nithiodote(®) In the absence of Rh, DMTS was observed to be almost 80 times more efficient than sodium thiosulfate in vitro The fact that DMTS converts cyanide to thiocyanate more efficiently than does thiosulfate both with and without Rh makes it a promising sulfur donor-type cyanide antidote (scavenger) with reduced enzyme dependence in vitro The therapeutic cyanide antidotal efficacies for DMTS versus sodium thiosulfate were measured following intramuscular administration in a mouse model and expressed as antidotal potency ratios (APR = LD50 of cyanide with antidote/LD50 of cyanide without antidote). A dose of 100 mg/kg sodium thiosulfate given intramuscularly showed only slight therapeutic protection (APR = 1.1), whereas the antidotal protection from DMTS given intramuscularly at the same dose was substantial (APR = 3.3). Based on these data, DMTS will be studied further as a promising next-generation countermeasure for cyanide intoxication.

  5. New fungal biomasses for cyanide biodegradation.

    PubMed

    Ozel, Yasemin Kevser; Gedikli, Serap; Aytar, Pınar; Unal, Arzu; Yamaç, Mustafa; Cabuk, Ahmet; Kolankaya, Nazif

    2010-10-01

    Cyanide, a hazardous substance, is released into the environment as a result of natural processes of various industrial activities which is a toxic pollutant according to Environmental Protection Agency. In nature, some microorganisms are responsible for the degradation of cyanide, but there is only limited information about the degradation characteristics of Basidiomycetes for cyanide. The aim of the present study is to determine cyanide degradation characteristics in some Basidiomycetes strains including Polyporus arcularius (T 438), Schizophyllum commune (T 701), Clavariadelphus truncatus (T 192), Pleurotus eryngii (M 102), Ganoderma applanatum (M 105), Trametes versicolor (D 22), Cerrena unicolor (D 30), Schizophyllum commune (D 35) and Ganoderma lucidum (D 33). The cyanide degradation activities of P. arcularius S. commune and G. lucidum were found to be more than that of the other fungi examined. The parameters including incubation time, amount of biomass, initial cyanide concentration, temperature, pH and agitation rate were optimized for the selected three potential fungal strains. The maximum cyanide degradation was obtained after 48 h of incubation at 30°C by P. arcularius (T 438). The optimum pH and agitation rate were measured as 10.5 and 150 rev/min, respectively. The amount of biomass was found as 3.0 g for the maximum cyanide biodegradation with an initial cyanide concentration of 100mg/L. In this study, agar was chosen entrapment agent for the immobilization of effective biomass. We suggested that P. arcularius (T 438) could be effective in the treatment of contaminated sites with cyanide due to capability of degrading cyanide.

  6. Prevention of Food Poisoning.

    ERIC Educational Resources Information Center

    Army Quartermaster School, Ft. Lee, VA.

    The programed text provides a single lesson, four-hour, correspondence subcourse on the prevention of food poisoning. It covers the following areas: a definition of food poisoning; chemical food poisoning; biological food poisoning; causes and prevention of trichinosis; six factors controlling bacteria growth; bacterial infection; prevention of…

  7. Effect of alpha-ketoglutarate and N-acetyl cysteine on cyanide-induced oxidative stress mediated cell death in PC12 cells.

    PubMed

    Satpute, R M; Hariharakrishnan, J; Bhattacharya, R

    2010-06-01

    Cyanide is a mitochondrial poison, which is ubiquitously present in the environment. Cyanide-induced oxidative stress is known to play a key role in mediating the neurotoxicity and cell death in rat pheochromocytoma (PC12) cells. PC12 cells are widely used as a model for neurotoxicity assays in vitro. In the present study, we investigated the protective effects of alpha-ketoglutarate (A-KG), a potential cyanide antidote, and N-acetyl cysteine (NAC), an antioxidant against toxicity of cyanide in PC12 cells. Cells were treated with various concentrations (0.625-1.25 mM) of potassium cyanide (KCN) for 4 hours, in the presence or absence of simultaneous treatment of A-KG (0.5 mM) and NAC (0.25 mM). Cyanide caused marked decrease in the levels of cellular antioxidants like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR). Lipid peroxidation indicated by elevated levels of malondialdehyde (MDA) was found to be accompanied by decreased levels of reduced glutathione (GSH) and total antioxidant status (TAS) of the cells. Cyanide-treated cells showed notable increase in caspase-3 activity and induction of apoptotic type of cell death after 24 hours. A-KG and NAC alone were very effective in restoring the levels of GSH and TAS, but together they significantly resolved the effects of cyanide on antioxidant enzymes, MDA levels, and caspase-3 activity. The present study reveals that combination of A-KG and NAC has critical role in abbrogating the oxidative stress-mediated toxicity of cyanide in PC12 cells. The results suggest potential role of A-KG and NAC in cyanide antagonism.

  8. Characterization of a Mouse Model of Oral Potassium Cyanide Intoxication.

    PubMed

    Sabourin, Patrick J; Kobs, Christina L; Gibbs, Seth T; Hong, Peter; Matthews, Claire M; Patton, Kristen M; Sabourin, Carol L; Wakayama, Edgar J

    2016-09-01

    Potassium cyanide (KCN) is an inhibitor of cytochrome C oxidase causing rapid death due to hypoxia. A well-characterized model of oral KCN intoxication is needed to test new therapeutics under the Food and Drug Administration Animal Rule. Clinical signs, plasma pH and lactate concentrations, biomarkers, histopathology, and cyanide and thiocyanate toxicokinetics were used to characterize the pathology of KCN intoxication in adult and juvenile mice. The acute oral LD50s were determined to be 11.8, 11.0, 10.9, and 9.9 mg/kg in water for adult male, adult female, juvenile male, and juvenile female mice, respectively. The time to death was rapid and dose dependent; juvenile mice had a shorter mean time to death. Juvenile mice displayed a more rapid onset and higher incidence of seizures. The time to observance of respiratory signs and prostration was rapid, but mice surviving beyond 2 hours generally recovered fully within 8 hours. At doses up to the LD50, there were no gross necropsy or microscopic findings clearly attributed to administration of KCN in juvenile or adult CD-1 mice from 24 hours to 28 days post-KCN challenge. Toxicokinetic analysis indicated rapid uptake, metabolism, and clearance of plasma cyanide. Potassium cyanide caused a rapid, dose-related decrease in blood pH and increase in serum lactate concentration. An increase in fatty acid-binding protein 3 was observed at 11.5 mg/kg KCN in adult but not in juvenile mice. These studies provide a characterization of KCN intoxication in adult and juvenile mice that can be used to screen or conduct preclinical efficacy studies of potential countermeasures.

  9. Noninvasive monitoring of treatment response in a rabbit cyanide toxicity model reveals differences in brain and muscle metabolism

    NASA Astrophysics Data System (ADS)

    Kim, Jae G.; Lee, Jangwoen; Mahon, Sari B.; Mukai, David; Patterson, Steven E.; Boss, Gerry R.; Tromberg, Bruce J.; Brenner, Matthew

    2012-10-01

    Noninvasive near infrared spectroscopy measurements were performed to monitor cyanide (CN) poisoning and recovery in the brain region and in foreleg muscle simultaneously, and the effects of a novel CN antidote, sulfanegen sodium, on tissue hemoglobin oxygenation changes were compared using a sub-lethal rabbit model. The results demonstrated that the brain region is more susceptible to CN poisoning and slower in endogenous CN detoxification following exposure than peripheral muscles. However, sulfanegen sodium rapidly reversed CN toxicity, with brain region effects reversing more quickly than muscle. In vivo monitoring of multiple organs may provide important clinical information regarding the extent of CN toxicity and subsequent recovery, and facilitate antidote drug development.

  10. Stability Characterization of a Polysorbate 80-Dimethyl Trisulfide Formulation, a Cyanide Antidote Candidate.

    PubMed

    Bartling, Craig M; Andre, Jon C; Howland, Carrie A; Hester, Mark E; Cafmeyer, Jeffrey T; Kerr, Andrew; Petrel, Trevor; Petrikovics, Ilona; Rockwood, Gary A

    2016-03-01

    Novel cyanide countermeasures are needed for cases of a mass-exposure cyanide emergency. A lead candidate compound is dimethyl trisulfide (DMTS), which acts as a sulfur donor for rhodanese, thereby assisting the conversion of cyanide into thiocyanate. DMTS is a safe compound for consumption and, in a 15% polysorbate 80 (DMTS-PS80) formulation, has demonstrated good efficacy against cyanide poisoning in several animal models. We performed a stability study that investigated the effect of temperature, location of formulation preparation, and pH under buffered conditions. We found that while the stability of the DMTS component was fairly independent of which laboratory prepared the formulation, the concentration of DMTS in the formulation was reduced 36-58% over the course of 29 weeks when stored at room temperature. This loss typically increased with increasing temperatures, although we did not find statistical differences between the stability at different storage temperatures in all formulations. Further, we found that addition of a light buffer negatively impacted the stability, whereas the pH of that buffer did not impact stability. We investigated the factors behind the reduction of DMTS over time using various techniques, and we suggest that the instability of the formulation is governed at least partially by precipitation and evaporation, although a combination of factors is likely involved.

  11. Cyanide inhibition and pyruvate-induced recovery of cytochrome c oxidase.

    PubMed

    Nůsková, Hana; Vrbacký, Marek; Drahota, Zdeněk; Houštěk, Josef

    2010-10-01

    The mechanism of cyanide's inhibitory effect on the mitochondrial cytochrome c oxidase (COX) as well as the conditions for its recovery have not yet been fully explained. We investigated three parameters of COX function, namely electron transport (oxygen consumption), proton transport (mitochondrial membrane potential Δψ(m)) and the enzyme affinity to oxygen (p₅₀ value) with regard to the inhibition by KCN and its reversal by pyruvate. 250 μM KCN completely inhibited both the electron and proton transport function of COX. The inhibition was reversible as demonstrated by washing of mitochondria. The addition of 60 mM pyruvate induced the maximal recovery of both parameters to 60-80% of the original values. When using low KCN concentrations of up to 5 μM, we observed a profound, 30-fold decrease of COX affinity for oxygen. Again, this decrease was completely reversed by washing mitochondria while pyruvate induced only a partial, yet significant recovery of oxygen affinity. Our results demonstrate that the inhibition of COX by cyanide is reversible and that the potential of pyruvate as a cyanide poisoning antidote is limited. Importantly, we also showed that the COX affinity for oxygen is the most sensitive indicator of cyanide toxic effects.

  12. CYANIDE HEAP BIOLOGICAL DETOXIFICATION - PHASE II

    EPA Science Inventory

    Many active mine sites, mines in the closure stage and some abandoned mines are and have utilized cyanidation to remove and recover precious metals. Discharges from these sites normally contain significant amounts of metal cyanide complexes and concentrations of thiocyanate, solu...

  13. Non-cyanide silver plating

    SciTech Connect

    Dini, J.W.

    1995-11-07

    Lawrence Livermore National Laboratory (LLNL) and Technic, Inc. have entered into a CRADA (Cooperative Research and Development Agreement) with the goal of providing industry with an environmentally benign alternative to the presently used silver cyanide plating process. This project has been in place for about six months and results are quite promising. The main objective, that of deposition of deposits as thick as 125 um (5 mils), has been met. Property data such as stress and hardness have been obtained and the structure of the deposit has been analyzed via metallography and x-ray diffraction. These results will be presented in this paper, along with plans for future work.

  14. Recent Advances in the Clinical Management of Lead Poisoning.

    PubMed

    Kianoush, Sina; Sadeghi, Mahmood; Balali-Mood, Mahdi

    2015-01-01

    Lead poisoning is a historic universal disease. Acute or chronic lead exposure may cause reversible or even permanent damages in human beings. Environmental lead exposure is a global health concern in children. Occupational lead poisoning is still a health issue, particularly in developing countries. During the last decades, new methods and medications have been advocated for the prevention and treatment of lead poisoning. This review deals mainly with recent developments in the management of lead poisoning. Sources of lead exposure are introduced, and methods for the primary prevention of lead poisoning are discussed. Details for the screening of adults and children are also explained to serve as a practical guideline for the secondary prevention. Standard chelation therapy in different groups and up-to-date less toxic new medications for the treatment of lead poisoning are finally discussed. Our published clinical research on the therapeutic effects of garlic tablets in mild to moderate occupational lead poisoning will also be discussed.

  15. Alpha-ketoglutarate and N-acetyl cysteine protect PC12 cells from cyanide-induced cytotoxicity and altered energy metabolism.

    PubMed

    Satpute, R M; Hariharakrishnan, J; Bhattacharya, R

    2008-01-01

    Cyanide is a rapidly acting neurotoxin that inhibits cellular respiration and energy metabolism leading to histotoxic hypoxia. This results in the dissipation of mitochondrial membrane potential (MMP) accompanied by decreased cellular ATP content which in turn is responsible for increased levels of intracellular calcium ions ([Ca(2+)](i)) and total lactic acid content of the cells. Rat pheochromocytoma (PC12) cells possess much of the biochemical machinery associated with synaptic neurons. In the present study, we evaluated the cytoprotective effects of alpha-ketoglutarate (A-KG) and N-acetylcysteine (NAC) against cyanide-induced cytotoxicity and altered energy metabolism in PC12 cells. Cyanide-antagonism by A-KG is attributed to cyanohydrin formation whereas NAC is known for its antioxidant properties. Data on leakage of intracellular lactate dehydrogenase and mitochondrial function (MTT assay) revealed that simultaneous treatment of A-KG (0.5 mM) and NAC (0.25 mM) significantly prevented the cytotoxicity of cyanide. Also, cellular ATP content was found to improve, followed by restoration of MMP, intracellular calcium [Ca(2+)](i) and lactic acid levels. Treatment with A-KG and NAC also attenuated the levels of peroxides generated by cyanide. The study indicates that combined administration of A-KG and NAC protected the cyanide-challenged PC12 cells by resolving the altered energy metabolism. The results have implications in the development of new treatment regimen for cyanide poisoning.

  16. Time- and temperature-dependent changes in cytochrome c oxidase activity and cyanide concentration in excised mice organs and mice cadavers.

    PubMed

    Singh, Poonam; Rao, Pooja; Yadav, Shiv K; Gujar, Niranjan L; Satpute, Ravindra M; Bhattacharya, Rahul

    2015-01-01

    Postmortem stability of cyanide biomarkers is often disputed. We assessed the time and temperature-dependent changes in cytochrome c oxidase (CCO) activity and cyanide concentration in various organs of mice succumbing to cyanide. Immediately after death, excised mice organs and mice cadavers were stored at room temperature (35°C ± 5°C) or in frozen storage (-20°C ± 2°C). At various times after death, CCO activity and cyanide concentrations were measured in excised mice organs or organs removed from mice cadavers. The study revealed that (i) measuring both the biomarkers in mice cadavers was more reliable compared to excised mice organs, (ii) measuring temporal CCO activity and cyanide concentration in vital organs from mice cadavers (room temperature) was reliable up to 24 h, and (iii) CCO activity in the brain and lungs and cyanide concentration in organs from mice cadavers (frozen) were measurable beyond 21 days. This study will be helpful in postmortem determination of cyanide poisoning.

  17. Fiber optic sensing of cyanides in solutions

    SciTech Connect

    Park, S.S.; Mackenzie, J.D.; Li, C.Y.; Guerreiro, P.; Peyghambarian, N.

    1996-12-31

    A novel sol-gel technique was used to immobilize malachite green ions (MG{sup +}) in stable, optically transparent, porous silica gel films. A simple and sensitive method was developed for the detection of cyanides in solutions using spectrophotometry to measure changes caused by cyanide ions (CN{sup {minus}}) in the absorption spectra of the green-colored silica gel films. After reaction with cyanide ions, the absorption spectra of the films changed with a typical decrease in absorbance at 620 nm. On the basis of the absorption spectra of the films, a portable and easy to use fiber optic cyanide film sensor was fabricated. Decolorization undergone by the green-colored gel films, as they were exposed to cyanide ions, was detected through a fiber. Preliminary results indicate concentrations on the order of a few ppm are detected using the fiber optic sensor.

  18. Determination of cyanide using a microbial sensor

    SciTech Connect

    Nakanishi, Keijiro; Ikebukuro, Kazunori; Karube, Isao

    1996-08-01

    A microbial cyanide sensor was prepared, consisting of immobilized Saccharomyces cerevisiae and an oxygen electrode. When the electrode was inserted into a solution containing glucose, the respiration activity of the microorganisms increased. The change in the respiration activity is monitored with the oxygen electrode. When cyanide is added to the sample solution, the electron transport chain reaction of the respiration system in the mitochondria is inhibited, resulting in a decrease in respiration. The inhibition is caused by cyanide binding with respiration enzymes such as the cytochrome oxidase complex in the mitochondrial inner membrane. Therefore, the cyanide concentration can be measured from the change in the respiration rate. When the sensor was applied to a batch system at pH 8.0 and 30{degrees}C, the cyanide calibration curve showed linearity in the concentration range between 0.3 pM and 150 {mu}m CN{sup -}. 13 refs., 8 figs., 1 tab.

  19. [Arsenic - Poison or medicine?].

    PubMed

    Kulik-Kupka, Karolina; Koszowska, Aneta; Brończyk-Puzoń, Anna; Nowak, Justyna; Gwizdek, Katarzyna; Zubelewicz-Szkodzińska, Barbara

    2016-01-01

    Arsenic (As) is commonly known as a poison. Only a few people know that As has also been widely used in medicine. In the past years As and its compounds were used as a medicine for the treatment of such diseases as diabetes, psoriasis, syphilis, skin ulcers and joint diseases. Nowadays As is also used especially in the treatment of patients with acute promyelocytic leukemia. The International Agency for Research on Cancer (IARC) has recognized arsenic as an element with carcinogenic effect evidenced by epidemiological studies, but as previously mentioned it is also used in the treatment of neoplastic diseases. This underlines the specificity of the arsenic effects. Arsenic occurs widely in the natural environment, for example, it is present in soil and water, which contributes to its migration to food products. Long exposure to this element may lead to liver damages and also to changes in myocardium. Bearing in mind that such serious health problems can occur, monitoring of the As presence in the environmental media plays a very important role. In addition, the occupational risk of As exposure in the workplace should be identified and checked. Also the standards for As presence in food should be established. This paper presents a review of the 2015 publications based on the Medical database like PubMed and Polish Medical Bibliography. It includes the most important information about arsenic in both forms, poison and medicine.

  20. High lethality and minimal variation after acute self-poisoning with carbamate insecticides in Sri Lanka – implications for global suicide prevention

    PubMed Central

    Lamb, Thomas; Selvarajah, Liza R.; Mohamed, Fahim; Jayamanne, Shaluka; Gawarammana, Indika; Mostafa, Ahmed; Buckley, Nicholas A.; Roberts, Michael S.; Eddleston, Michael

    2016-01-01

    Abstract Background: Highly hazardous organophosphorus (OP) insecticides are responsible for most pesticide poisoning deaths. As they are removed from agricultural practice, they are often replaced by carbamate insecticides of perceived lower toxicity. However, relatively little is known about poisoning with these insecticides. Methods: We prospectively studied 1288 patients self-poisoned with carbamate insecticides admitted to six Sri Lankan hospitals. Clinical outcomes were recorded for each patient and plasma carbamate concentration measured in a sample to confirm the carbamate ingested. Findings: Patients had ingested 3% carbofuran powder (719), carbosulfan EC25 liquid (25% w/v, 389), or fenobucarb EC50 liquid (50% w/v, 127) formulations, carbamate insecticides of WHO Toxicity Classes Ib, II, and II, respectively. Intubation and ventilation was required for 183 (14.2%) patients while 71 (5.5%) died. Compared with carbofuran, poisoning with carbosulfan or fenobucarb was associated with significantly higher risk of death [carbofuran 2.2%; carbosulfan 11.1%, OR 5.5 (95% CI 3.0–9.8); fenobucarb 6.3%, OR 3.0 (1.2–7.1)] and intubation [carbofuran 6.1%; carbosulfan 27.0%, OR 5.7 (3.9–8.3); fenobucarb 18.9%, OR 3.6 (2.1–6.1)]. The clinical presentation and cause of death did not differ markedly between carbamates. Median time to death was similar: carbofuran 42.3 h (IQR 5.5–67.3), carbosulfan 21.3 h (11.5–71.3), and fenobucarb 25.3 h (17.3–72.1) (p = 0.99); no patients showed delayed onset of toxicity akin to the intermediate syndrome seen after OP insecticide poisoning. For survivors, median duration of intubation was 67.8 h (IQR 27.5–118.8) with no difference in duration between carbamates. Reduced GCS at presentation was associated with worse outcome although some patients with carbosulfan died after presentation with normal GCS. Conclusions: We did not find carbamate insecticide self-poisoning to vary markedly according to the carbamate

  1. Amatoxin-containing mushroom (Lepiota brunneoincarnata) familial poisoning.

    PubMed

    Varvenne, David; Retornaz, Karine; Metge, Prune; De Haro, Luc; Minodier, Philippe

    2015-04-01

    Serious to fatal toxicity may occur with amanitin-containing mushrooms ingestions. A Lepiota brunneoincarnata familial poisoning with hepatic toxicity is reported. In such poisonings, acute gastroenteritis may be firstly misdiagnosed leading to delay in preventing liver dysfunction by silibinin or penicillin G. Mushroom picking finally requires experience and caution.

  2. 40 CFR 180.130 - Hydrogen Cyanide; tolerances for residues.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 23 2010-07-01 2010-07-01 false Hydrogen Cyanide; tolerances for... § 180.130 Hydrogen Cyanide; tolerances for residues. (a) General. A tolerance for residues of the insecticide hydrogen cyanide from postharvest fumigation as a result of application of sodium cyanide...

  3. 40 CFR 180.130 - Hydrogen Cyanide; tolerances for residues.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 24 2011-07-01 2011-07-01 false Hydrogen Cyanide; tolerances for... § 180.130 Hydrogen Cyanide; tolerances for residues. (a) General. A tolerance for residues of the insecticide hydrogen cyanide from postharvest fumigation as a result of application of sodium cyanide...

  4. 40 CFR 180.130 - Hydrogen Cyanide; tolerances for residues.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 25 2012-07-01 2012-07-01 false Hydrogen Cyanide; tolerances for... § 180.130 Hydrogen Cyanide; tolerances for residues. (a) General. A tolerance for residues of the insecticide hydrogen cyanide from postharvest fumigation as a result of application of sodium cyanide...

  5. 40 CFR 180.130 - Hydrogen Cyanide; tolerances for residues.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 25 2013-07-01 2013-07-01 false Hydrogen Cyanide; tolerances for... § 180.130 Hydrogen Cyanide; tolerances for residues. (a) General. A tolerance for residues of the insecticide hydrogen cyanide from postharvest fumigation as a result of application of sodium cyanide...

  6. 40 CFR 180.130 - Hydrogen Cyanide; tolerances for residues.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 24 2014-07-01 2014-07-01 false Hydrogen Cyanide; tolerances for... § 180.130 Hydrogen Cyanide; tolerances for residues. (a) General. A tolerance for residues of the insecticide hydrogen cyanide from postharvest fumigation as a result of application of sodium cyanide...

  7. Cyanide

    MedlinePlus

    ... CDC.gov . Specific Hazards Bioterrorism A-Z Anthrax (Bacillus anthracis) Arenaviruses Treatment & Infection Control Specimen Submission & Lab Testing Education & Training Related Bioterrorism Resources Bacillus anthracis (Anthrax) Botulism (Clostridium botulinum toxin) Brucella species ( ...

  8. [Mushroom poisoning in Portugal].

    PubMed

    Brandão, José Luís; Pinheiro, J; Pinho, D; Correia da Silva, D; Fernandes, E; Fragoso, G; Costa, M I; Silva, A

    2011-12-01

    The renewed interest in mycology has been reflected in growing use of wild mushrooms in culinary, driven by its nutritional, organoleptic and commercial value. However, the international scientific literature describes several syndromes of poisoning by mushrooms. We live, therefore, a paradigm conducive to an increase of mycetism, whose diagnosis requires a high level of suspicion and knowledge of clinical profiles. In Portugal, the real dimension of this problem is unknown. Although some mycetisms, such as the hepatotoxic syndrome, have high morbidity and mortality, their relative incidences are unknown. Add up to the shortage of international scientific literature, often outdated and inappropriate to clinical practice. In this context, this article provides an updated epidemiological and clinical perspective emphasizing a narrative and descriptive information on the forms of presentation, differential diagnosis and therapeutic approach, with the ultimate goal of the elaboration of a national diagram-oriented approach to decision-making diagnosis. We analyzed all the clinical records of patients admitted into ten hospitals between 1990 and 2008, notified with the code 988.1 of GDH (acute poisoning by mushrooms). There were registered demographic data, way of presentation, time between ingestion and onset of symptoms, the annual distribution, clinical profile, clinical and analytical treatment performed and complications. We identified 93 cases of acute poisoning by mushrooms, with equal gender distribution and inclusion of individuals of all age groups (from 1 to 85 years), but with greater representation from 21 to 50 years. There was a bimodal seasonal pattern, with a higher peak between September and December and a second in the spring. The hepatotoxic profile presentation corresponded to 63.4% and 31.7% of the cases to gastroenteritis syndrome. The mortality in cases of hepatotoxicity was 11.8%. The developmental profile of the rate of prothrombin time (PT

  9. Photochemical destruction of cyanide in landfill leachate

    SciTech Connect

    Kim, B.R.; Podsiadlik, D.H.; Hartlund, J.L.; Gaines, W.A.; Kalis, E.M.

    1998-11-01

    The Allen Park Clay Mine Landfill, owned by Ford, produces a leachate that occasionally contains cyanide at levels marginally below the discharge limit. The form of the cyanide in the leachate was found to be iron-cyanide complexes that resist oxidation by a conventional treatment method, alkaline oxidation. Furthermore, the leachate also was found to contain a relatively large amount of organics which would exert additional demand for oxidizing agents (e.g., chlorine). A study was performed to determine what treatment technology could be employed in the event treatment becomes necessary because of potential changes in the leachate characteristics and/or discharge limits. In this study, among several chemical oxidation methods, ultraviolet (UV) irradiation with or without ozone was investigated as a treatment option. The following are the primary findings: (1) UV irradiation alone was effective for removing the iron-cyanide complex in both the leachate and the clean water; (2) the demand for UV or ozone by chemical oxygen demand was relatively low for this leachate; (3) ozone alone was not effective for removing the iron-cyanide complex; and (4) UV irradiation alone and UV irradiation with ozone resulted in the same removal for total cyanide in clean-water experiments, but the UV irradiation alone left some free cyanide whereas the UV irradiation with ozone did not.

  10. Prolonged N-acetylcysteine therapy in late acetaminophen poisoning associated with acute liver failure--a need to be more cautious?

    PubMed

    Athuraliya, T Nimmi C; Jones, Alison L

    2009-01-01

    Since the 1970s, N-acetylcysteine (NAC) has shown proven efficacy as an antidote for acetaminophen (APAP) poisoning and APAP-induced liver failure for early presenters. The current evidence of benefits of NAC for late presenters is controversial because of the poor understanding of the mechanism of late toxicity. In the previous issue of Critical Care, Yang and colleagues use a mouse model to demonstrate that NAC in doses similar to those used therapeutically to treat APAP poisoning in humans impairs liver regenerative capacity and that the effect is more pronounced when administered for a longer duration. Studies based on cell cultures support this evidence. Cytokine and growth factor signalling pathways are recognised to be involved in the process of liver regeneration and apoptosis. This research paper generates several issues related to the future management of APAP-induced liver failure and research into the mechanism of toxicity, especially of late toxicity.

  11. Disulfides as Cyanide Antidotes: Evidence for a New In Vivo Oxidative Pathway for Cyanide Detoxification

    DTIC Science & Technology

    2009-01-01

    defense against cyanide intoxication . The oxidation of disulfides to the corresponding thiosulfinate or thiosulfonate will result in facilitating their...high probability (1). While antidotes for cyanide intoxication exist (2-4), it has yet to be shown that they can be effectively administered in the...garlic] have been found to be effective as in vivo therapeutic agents for cyanide intoxication (10, 11). It is believed that the efficacy of these

  12. Growth and cyanide degradation of Azotobacter vinelandii in cyanide-containing wastewater system.

    PubMed

    Koksunan, Sarawut; Vichitphan, Sukanda; Laopaiboon, Lakkana; Vichitphan, Kanit; Han, Jaehong

    2013-04-01

    Azotobacter vinelandii, a strict aerobic nitrogen-fixing bacterium, has been extensively studied with regard to the ability of N2-fixation due to its high expression of nitrogenase and fast growth. Because nitrogenase can also reduce cyanide to ammonia and methane, cyanide degradation by A. vinelandii has been studied for the application in the bioremediation of cyanide-contaminated wastewater. Cyanide degradation by A. vinelandii in NFS (nitrogen-free sucrose) medium was examined in terms of cell growth and cyanide reduction, and the results were applied for cyanide-contaminated cassava mill wastewater. From the NFS medium study in the 300 ml flask, it was found that A. vinelandii in the early stationary growth phase could reduce cyanide more rapidly than the cells in the exponential growth phase, and 84.4% of cyanide was degraded in 66 h incubation upon addition of 3.0 mM of NaCN. The resting cells of A. vinelandii could also reduce cyanide concentration by 90.4% with 3.0 mM of NaCN in the large-scale (3 L) fermentation with the same incubation time. Finally, the optimized conditions were applied to the cassava mill wastewater bioremediation, and A. vinelandii was able to reduce the cyanide concentration by 69.7% after 66 h in the cassava mill wastewater containing 4.0 mM of NaCN in the 3 L fermenter. Related to cyanide degradation in the cassava mill wastewater, nitrogenase was the responsible enzyme, which was confirmed by methane production. These findings would be helpful to design a practical bioremediation system for the treatment of cyanide-contaminated wastewater.

  13. Removal of Zn or Cd and cyanide from cyanide electroplating wastes

    DOEpatents

    Moore, Fletcher L.

    1977-05-31

    A method is described for the efficient stripping of stable complexes of a selected quaternary amine and a cyanide of Zn or Cd. An alkali metal hydroxide solution such as NaOH or KOH will quantitatively strip a pregnant extract of the quaternary ammonium complex of its metal and cyanide content and regenerate a quaternary ammonium hydroxide salt which can be used for extracting further metal cyanide values.

  14. Process for the displacement of cyanide ions from metal-cyanide complexes

    DOEpatents

    Smith, Barbara F.; Robinson, Thomas W.

    1997-01-01

    The present invention relates to water-soluble polymers and the use of such water-soluble polymers in a process for the displacement of the cyanide ions from the metal ions within metal-cyanide complexes. The process waste streams can include metal-cyanide containing electroplating waste streams, mining leach waste streams, mineral processing waste streams, and related metal-cyanide containing waste streams. The metal ions of interest are metals that give very strong complexes with cyanide, mostly iron, nickel, and copper. The physical separation of the water-soluble polymer-metal complex from the cyanide ions can be accomplished through the use of ultrafiltration. Once the metal-cyanide complex is disrupted, the freed cyanide ions can be recovered for reuse or destroyed using available oxidative processes rendering the cyanide nonhazardous. The metal ions are released from the polymer, using dilute acid, metal ion oxidation state adjustment, or competing chelating agents, and collected and recovered or disposed of by appropriate waste management techniques. The water-soluble polymer can then be recycled. Preferred water-soluble polymers include polyethyleneimine and polyethyleneimine having a catechol or hydroxamate group.

  15. A novel cyanide ion sensing approach based on Raman scattering for the detection of environmental cyanides.

    PubMed

    Yan, Fei; Gopal Reddy, C V; Zhang, Yan; Vo-Dinh, Tuan

    2010-09-01

    This paper describes a direct optical approach based on Raman scattering for selective and sensitive detection of cyanide ions in aqueous environment without requiring time-consuming sample pretreatment and the formation of hydrogen cyanide. Due to the strong affinity between copper (I) and cyanide ion, evaporated copper (I) iodide (CuI) thin films are shown to be excellent substrates for selective recognition of free cyanide ions in aqueous matrices. The amount of cyanide ion retained by the copper (I) in the CuI thin films reflects its actual concentration in tested samples, and the subsequent Raman measurements of the substrate are shown to be capable of detecting toxic cyanide content at levels under international drinking water standard and environmental regulatory concentrations. Measurements obtained from the same batch of evaporated CuI thin films (approximately 100-nm thickness) show excellent linearity over a variety of cyanide concentrations ranging from 1.5 microM to 0.15 mM. This detection method offers the advantage of selectively detecting cyanides causing a health hazard while avoiding detection of other common interfering anions such as Cl-, Br-, PO4(3-), SO4(2-), NO2-, S2- and SCN-. Coupled with portable Raman systems that are commercially available, our detection approach will provide on-site monitoring capability with little sample preparation or instrument supervision, which will greatly expedite the assessment of potential environmental cyanide risks.

  16. Hair spray poisoning

    MedlinePlus

    ... this page: //medlineplus.gov/ency/article/002705.htm Hair spray poisoning To use the sharing features on this page, please enable JavaScript. Hair spray poisoning occurs when someone breathes in (inhales) ...

  17. Hair straightener poisoning

    MedlinePlus

    ... this page: //medlineplus.gov/ency/article/002706.htm Hair straightener poisoning To use the sharing features on this page, please enable JavaScript. Hair straightener poisoning occurs when someone swallows products that ...

  18. Bracken fern poisoning

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Bracken fern (Pteridium aquilinum) is found throughout the world and enzootic hematuria, bright blindness, and bracken staggers. This chapter reviews the plant, the various poisoning syndrome that it produces, the current strategies to prevent poisoning, and recommended treatments....

  19. Tips to Prevent Poisonings

    MedlinePlus

    ... back programs in your community . Household Chemicals and Carbon Monoxide Always read the label before using a ... American Association of Poison Control Centers, Inc. CDC: Carbon Monoxide Poisoning: Prevention Guidelines U.S. Food and Drug ...

  20. Plant fertilizer poisoning

    MedlinePlus

    Plant fertilizers and household plant foods are used to improve plant growth. Poisoning can occur if someone swallows these products. Plant fertilizers are mildly poisonous if small amounts are swallowed. ...

  1. Oxalic acid poisoning

    MedlinePlus

    ... national toll-free Poison Help hotline (1-800-222-1222) from anywhere in the United States. ... national toll-free Poison Help hotline (1-800-222-1222) from anywhere in the United States. This ...

  2. Nitric acid poisoning

    MedlinePlus

    ... national toll-free Poison Help hotline (1-800-222-1222) from anywhere in the United States. ... national toll-free Poison Help hotline (1-800-222-1222) from anywhere in the United States. This ...

  3. Hydrochloric acid poisoning

    MedlinePlus

    Hydrochloric acid is a clear, poisonous liquid. It is highly corrosive, which means it immediately causes severe damage, such ... poisoning due to swallowing or breathing in hydrochloric acid. This article is for information only. Do NOT ...

  4. Teenagers with Jimson weed (Datura stramonium) poisoning.

    PubMed

    Spina, Sean P; Taddei, Anthony

    2007-11-01

    We report 2 cases of teenagers who were poisoned with Jimson weed (Datura stramonium) and presented to the emergency department with a severe acute anticholinergic toxidrome after ingestion of several hundred seeds. The patients presented with visual hallucinations, disorientation, incomprehensible and nonsensical speech, and dilated sluggish pupils. Both patients required restraints for combativeness until adequate sedation with lorazepam and haloperidol was achieved. Jimson weed is found in southern Canada and the United States and can cause acute anticholinergic poisoning and death in humans and animals. The treatment of choice for anticholinergic poisoning is mainly supportive care and gastrointestinal decontamination with activated charcoal. Jimson weed intoxication should be considered in cases of patients presenting with unexplained peripheral and central anticholinergic symptoms including delirium, agitation and seizures, especially among younger patients and partygoers. It is important that health care professionals recognize that Jimson weed is a toxic, indigenous, "wild" growing plant, subject to misuse and potentially serious intoxication requiring hospitalization.

  5. CAPSULE REPORT - MANAGING CYANIDE IN METAL FINISHING

    EPA Science Inventory

    The purpose of this document is to provide guidance to surface finishing manufacturers, metal finishing decision maker and regulators on management practices and control technologies for managing cyanide in the workplace. This information can benefit key industry stakeholder gro...

  6. Modeling hydrogen-cyanide absorption in fires

    NASA Technical Reports Server (NTRS)

    Cagliostro, D. E.; Islas, A.

    1981-01-01

    A mathematical model is developed for predicting blood concentrations of cyanide as functions of exposure time to constant levels of cyanide in the atmosphere. A toxic gas (which may form as a result of decomposition of combustion materials used in transportation vehicles) is breathed into the alveolar space and transferred from the alveolar space to the blood by a first-order process, dependent on the concentration of the toxicant in the alveolar space. The model predicts that blood cyanide levels are more sensitive to the breathing cycle than to blood circulation. A model estimate of the relative effects of CO and HCN atmospheres, generated in an experimental chamber with an epoxy polymer, shows that toxic effects of cyanide occur long before those of carbon monoxide.

  7. The Kidney in Lead Poisoning

    PubMed Central

    Radošević, Zdenko; Šarić, Marko; Beritić, Tihomil; Knežević, Jelica

    1961-01-01

    Kidney damage due to lead is still an interesting problem of industrial toxicology. In spite of abundant literature data, much still remains to be explained. There are controversial opinions, not only on the type of renal lesions due to lead, but also on whether lead affects the kidney at all. In this paper our clinical observations on the effect of lead upon the kidney in 53 patients suffering from lead poisoning are presented. In 44 patients (40 men and four women) lead poisoning was due to occupation, and in nine (five men and four women) to the use of lead-glazed pottery. The length of exposure varied from two months to 35 years. In all cases the diagnosis of lead poisoning was made clinically and confirmed by laboratory tests. Permanent changes in the form of chronic nephropathy were observed in only two patients. These were the two cases in which exposure to lead was the longest and most intense. Twenty-three patients showed functional renal lesions tending to normalize. In addition to the cases of organic nephropathy, blood pressure was persistently raised in one further patient; in two patients a raised blood pressure was observed only in the acute stage of poisoning. On the basis of these findings we consider that lead intoxication can cause renal lesions. These lesions are for the most part functional and temporary. In cases of long and severe exposure and repeated lead intoxication, organic renal lesions seem possible. The disturbances of renal function observed in this study may be ascribed to disordered intrarenal circulation, due to the spastic effect of lead on intrarenal blood vessels, and to a direct toxic or indirect hypoxic effect of lead on the tubules. When investigating renal function, we have observed that the timing of individual tests is of paramount importance. Some lesions are subject to changes in the natural course of lead poisoning, and unless this is borne in mind, apparently contradictory results may be obtained. PMID:13739013

  8. Lead Poisoning in Childhood.

    ERIC Educational Resources Information Center

    Pueschel, Siegfried M., Ed.; Linakis, James G., Ed.; Anderson, Angela C., Ed.

    The magnitude of childhood lead poisoning has been inexplicably neglected by modern medicine and by legislators. However, since the 1970s, increased attention has been focused on lead poisoning, and advances have been made in several areas, including understanding of the neurodevelopmental and behavioral ramifications of lead poisoning, and…

  9. Lead Poisoning in Children.

    ERIC Educational Resources Information Center

    Drummond, A. H., Jr.

    1981-01-01

    Early symptoms of lead poisoning in children are often overlooked. Lead poisoning has its greatest effects on the brain and nervous system. The obvious long-term solution to the lead poisoning problem is removal of harmful forms of the metal from the environment. (JN)

  10. Lead poisoning: An overview

    NASA Technical Reports Server (NTRS)

    Gendel, Neil

    1993-01-01

    A problem that should be of great concern to all of us is the lead poisoning of children. First, I would like to present a short overview concerning the reasons everyone should care about lead poisoning, then discuss the history of lead poisoning, what is happening today across the country, and the future.

  11. Metal Complexes for Defense against Cyanide Intoxication

    DTIC Science & Technology

    1986-11-01

    cyanide toxicity might be compared with that of other asphyxiants, particularly carbon monoxide. Carbon monoxide forms a complex with hemoglobin... carbon monoxide is present to disrupt the oxygen transport to the tissue. However, cyanide is toxic at much lower concentrations. According to ligand... carbon to an empty d-orbital on the metal, plus a it-bond, which is formed by the back-donation of a filled metal d-orbital to the empty antibonding

  12. Spectroscopic detection of stratospheric hydrogen cyanide

    NASA Technical Reports Server (NTRS)

    Coffey, M. T.; Mankin, W. G.; Cicerone, R. J.

    1981-01-01

    A number of features have been identified as absorption lines of hydrogen cyanide in infrared spectra of stratospheric absorption obtained from a high-altitude aircraft. Column amounts of stratospheric hydrogen cyanide have been derived from spectra recorded on eight flights. The average vertical column amount above 12 kilometers is 7.1 + or - 0.8 x 10 to the 14th molecules per square centimeter, corresponding to an average mixing ratio of 170 parts per trillion by volume.

  13. Epidemiology and toxicology of arsenic poisoning in domestic animals.

    PubMed Central

    Selby, L A; Case, A A; Osweiler, G D; Hayes, H M

    1977-01-01

    Arsenic poisoning is one of the more important causes of heavy metal poisoning in domestic animals. Two species--dogs and cattle--are intoxicated more frequently than other animals; yet sporadic instances of poisoning have been observed in cats, horses, and pigs. Cases observed by veterinary clinicians are either peracute, acute, or chronic intoxications. Frequently the initial and only indication that a severe problem exists with peracute poisoning in a cattle herd is dead animals. Chronic intoxications are also observed in cattle. Acute intoxication is the most common form of arsenic poisoning observed and documented in the dog. Also intoxicated dogs were younger, i.e., 2-6 months of age. Arsenic is a severe alimentary tract irritant in domestic animals, and treatment in most instances consists mainly of symptomatic and supportive treatment. The source of intoxication, when it can be determined, is usually dips, sprays, powders, or vegetation contaminated by pesticides containing arsenic. PMID:908297

  14. Ferrate(VI) oxidation of aqueous cyanide

    SciTech Connect

    Sharma, V.K.; Rivera, W.; Smith, J.O.; O`Brien, B.

    1998-09-01

    The rates of oxidation of cyanide with Fe(VI) were measured as a function of pH and temperature. The reaction was found to be first order for each reactant. The rates decrease with increasing pH. The energy of activation was found to be 38.9 {+-} 1.0 kJ mol{sup {minus}1} at pH 9.0. The removal of cyanide by oxidation with Fe(VI) was studied at pH 7.5, 9.0, and 12.0. Fe(VI) removal efficiency was greater at pH 9.0 than at pH 7.5 and 12.0. At pH 9.0, Fe(VI) molar consumption was nearly equal to that of oxidized cyanide. Cyanate and nitrite ions were identified as the products of the reaction at pH 7.5. The experiments indicated 1:1 stoichiometric conversion of cyanide to nitrite ion at pH 9.0 and 12.0. Experiments were conducted to test the Fe(VI) removal efficiency of cyanide in electroplating rinsewater. The results indicate that Fe(VI) has the potential to serve as a reliable and safe oxidative treatment for removing cyanide in wastewater effluent.

  15. Non-cancer health risk assessment from exposure to cyanide by resident adults from the mining operations of Bogoso Gold Limited in Ghana.

    PubMed

    Obiri, S; Dodoo, D K; Okai-Sam, F; Essumang, D K

    2006-07-01

    Cyanide is a very toxic chemical that is used to extract gold from its ores. Wastewaters from gold mining companies such as Bogoso Gold Limited (BGL) contain cyanide and other potentially toxic chemicals that have adverse effects on human beings and aquatic organisms. This study was conducted to evaluate the human health risk assessment from exposure to free cyanide via oral and dermal contact of surface/underground water by resident adults within the concession of Bogoso Gold Limited. The chronic non-cancer health risk from exposure to cyanide in River Bogo Upstream is 230 and 43 (by Central Tendency Exposure (CTE) parameters respectively). This means that approximately 230 and 43 resident adults are likely to suffer diseases related to cyanide intoxication via oral and dermal contact respectively. For chronic exposure to River Bogo Downstream by resident adults, the non-cancer health risks are: 0.031 and 0.57 via oral and dermal contact for CTE parameters respectively, which also means that, the non-cancer health risks associated with cyanide intoxication is negligible as the hazard index is less than 1.0 via oral and dermal contacts respectively. The results showed that health risk for acute exposure to cyanide by the resident adults is very high. Hence the residents attribute most of the unexplained deaths in the communities to accidental ingestion and dermal contact of cyanide water.

  16. Mercury poisoning: an unusual cause of polyarthritis.

    PubMed

    Karataş, G K; Tosun, A K; Karacehennem, E; Sepici, V

    2002-02-01

    Mercury is a toxic metal that is widely used in everyday life. It has organic and inorganic forms that are both toxic. As acute mercury poisoning is uncommon, diagnosis is difficult if the exposure is not manifest. It has usually a slow onset and non-specific symptoms. In this paper we report a patient who developed polyarthritis after mercury exposure.

  17. Clinical and therapeutic aspects of childhood kerosene poisoning in Djibouti.

    PubMed

    Benois, Alain; Petitjeans, Fabrice; Raynaud, Laurent; Dardare, Eric; Sergent, Hervé

    2009-10-01

    We report a prospective and descriptive study about childhood acute poisoning with kerosene in Djibouti. Acute poisoning is a common and stable occurrence in low socioeconomic groups in Africa, where negligence is the main cause of poisoning. The respiratory system was the main target, with 41% of patients having pneumonia, which may become life-threatening, but with low mortality rate. Asymptomatic patients (35%) can be discharged, while those with pulmonary or neurological signs must be admitted for observation and supportive treatment based on oxygen administration. Our study suggests management and provides a discussion for therapeutic options and emphasizes the importance of prevention.

  18. Heap leach cyanide irrigation and risk to wildlife: Ramifications for the international cyanide management code.

    PubMed

    Donato, D B; Madden-Hallett, D M; Smith, G B; Gursansky, W

    2017-06-01

    Exposed cyanide-bearing solutions associated with gold and silver recovery processes in the mining industry pose a risk to wildlife that interact with these solutions. This has been documented with cyanide-bearing tailings storage facilities, however risks associated with heap leach facilities are poorly documented, monitored and audited. Gold and silver leaching heap leach facilities use cyanide, pH-stabilised, at concentrations deemed toxic to wildlife. Their design and management are known to result in exposed cyanide-bearing solutions that are accessible to and present a risk to wildlife. Monitoring of the presence of exposed solutions, wildlife interaction, interpretation of risks and associated wildlife deaths are poorly documented. This paper provides a list of critical monitoring criteria and attempts to predict wildlife guilds most at risk. Understanding the significance of risks to wildlife from exposed cyanide solutions is complex, involving seasonality, relative position of ponding, temporal nature of ponding, solution palatability, environmental conditions, in situ wildlife species inventory and provision of alternative drinking sources for wildlife. Although a number of heap leach operations are certified as complaint with the International Cyanide Management Code (Cyanide Code), these criteria are not considered by auditors nor has systematic monitoring regime data been published. Without systematic monitoring and further knowledge, wildlife deaths on heap leach facilities are likely to remain largely unrecorded. This has ramifications for those operations certified as compliance with the Cyanide Code.

  19. IRIS Toxicological Review of Hydrogen Cyanide and Cyanide Salts (Final Report)

    EPA Science Inventory

    EPA has finalized the Toxicological Review of Hydrogen Cyanide and Cyanide Salts: in support of the Integrated Risk Information System (IRIS). Now final, this assessment may be used by EPA’s program and regional offices to inform decisions to protect human health.

  20. IRIS Toxicological Review of Hydrogen Cyanide and Cyanide Salts (Interagency Science Discussion Draft)

    EPA Science Inventory

    EPA is releasing the draft report, Toxicological Review of Hydrogen Cyanide (HCN) and Cyanide Salts, that was distributed to Federal agencies and White House Offices for comment during the Science Discussion step of the IRIS As...

  1. MIN-CYANIDE: An expert system for cyanide waste minimization in electroplating plants

    SciTech Connect

    Huang, Y.L.; Sundar, G.; Fan, L.T. )

    1991-05-01

    An expert system, MIN-CYANIDE, has been constructed to assist engineers and technicians in the source reduction of cyanide-waste solutions in an electroplating plant by resorting to these techniques and experience, and to train plant operators in the application of the techniques. MIN-CYANIDE evaluates options, such as drag-out minimization, bath-life extension, rinse-water reduction, replacement with a non-cyanide solution, use of an alternative plating technique, and improvement of the operating procedure; furthermore, it identifies the most effective among them. The knowledge about the cyanide source reduction is acquired from available publications, represented by numerous fuzzy or non-fuzzy heuristic rules, and codified into a commercial export system shell, Personal Consultant Plus, on an IBM PC/AT compatible computer. MIN-CYANIDE provides a user friendly interface; in operating it, the user answers various questions concerning the operational situations of the production and/or current equipment and techniques in the plant. In response, MIN-CYANIDE will present instantaneously a series of options for cyanide minimization and eventually rank them.

  2. C-11 cyanide production system

    DOEpatents

    Kim, Dohyun; Alexoff, David; Kim, Sung Won; Hooker, Jacob; Ferrieri, Richard A

    2015-01-13

    A method for providing .sup.11C-labeled cyanides from .sup.11C labeled oxides in a target gas stream retrieved from an irradiated high pressure gaseous target containing O.sub.2 is provided, wherein .sup.11C labeled oxides are reduced with H.sub.2 in the presence of a nickel catalyst under a pressure and a temperature sufficient to form a product stream comprising at least about 95% .sup.11CH.sup.4 , the .sup.11CH.sub.4 is then combined with an excess of NH.sub.3 in a carrier/reaction stream flowing at an accelerated velocity and the combined .sup.11CH4 carrier/reaction stream is then contacted with a platinum (Pt) catalyst particulate supported on a substantially-chemically-nonreactive heat-stable support at a temperature of at least about 900 .degree. C., whereby a product stream comprising at least about 60%H.sup.11CN is provided in less than 10 minutes from retrieval of the .sup.11C labeled oxide.

  3. Cyanide phytoremediation by water hyacinths (Eichhornia crassipes).

    PubMed

    Ebel, Mathias; Evangelou, Michael W H; Schaeffer, Andreas

    2007-01-01

    Although cyanide is highly toxic, it is economically attractive for extracting gold from ore bodies containing only a few grams per 1000 kg. Most of the cyanide used in industrial mining is handled without observable devastating consequences, but in informal, small-scale mining, the use is poorly regulated and the waste treatment is insufficient. Cyanide in the effluents from the latter mines could possibly be removed by the water hyacinth Eichhornia crassipes because of its high biomass production, wide distribution, and tolerance to cyanide (CN) and metals. We determined the sodium cyanide phytotoxicity and removal capacity of E. crassipes. Toxicity to 5-50 mg CN L(-1) was quantified by measuring the mean relative transpiration over 96 h. At 5 mgCNL(-1), only a slight reduction in transpiration but no morphological changes were observed. The EC(50) value was calculated by probit analysis to be 13 mgCNL(-1). Spectrophotometric analysis indicated that cyanide at 5.8 and 10 mgL(-1) was completely eliminated after 23-32 h. Metabolism of K(14)CN was measured in batch systems with leaf and root cuttings. Leaf cuttings removed about 40% of the radioactivity from solution after 28 h and 10% was converted to (14)CO(2); root cuttings converted 25% into (14)CO(2) after 48 h but only absorbed 12% in their tissues. The calculated K(m) of the leaf cuttings was 12 mgCNL(-1), and the V(max) was 35 mg CN(kg fresh weight)(-1)h(-1). Our results indicate that E. crassipes could be useful in treating cyanide effluents from small-scale gold mines.

  4. Occupational triphenyltin acetate poisoning: a case report.

    PubMed Central

    Colosio, C; Tomasini, M; Cairoli, S; Foà, V; Minoia, C; Marinovich, M; Galli, C L

    1991-01-01

    A case of triphenyltin acetate (TPTA) poisoning is described. The patient, who had been exposed mainly to cutaneous absorption, showed acute stages of an urticarial eruption, signs of hepatic injury, slight glucose intolerance, and electroencephalographic abnormalities. Concomitant with the highest concentrations of tin in plasma and the peak of tin excretion in urine, neutrophils did not show the normal increase in actin polymerisation after stimulation with a chemotactic peptide (100 nM fMLP). The peak of urinary excretion of tin occurred between the fifth and the sixth day after poisoning; subsequently, the rate of excretion became slow, suggesting biphasic kinetics with the possibility of a cumulative trend. Images PMID:1825604

  5. Cowfish (Umisuzume, Lactoria diaphana) poisoning with rhabdomyolysis.

    PubMed

    Shinzato, Takeaki; Furusu, Akira; Nishino, Tomoya; Abe, Katsushige; Kanda, Tetsuro; Maeda, Takahiro; Kohno, Shigeru

    2008-01-01

    A 40-year-old man developed weakness and myalgia of the shoulders and brachia nine hours after eating a cowfish (Umisuzume, Lactoria diaphana). A clinical symptom showed rhabdomyolysis and serum creatine phosphokinase was elevated to 180,000 IU/L on day 3. Cardiopulmonary arrest and acute renal failure developed after 59 hours and hemodiafiltration was performed. Cerebral death was diagnosed on day 9 and the patient died on day 16. The case has the characteristic clinical course of palytoxin poisoning, which has also been reported as blue humphead parrotfish poisoning from other kinds of fish.

  6. The many faces of methylmercury poisoning

    SciTech Connect

    Elhassani, S.B.

    1982-10-01

    Methylmercury (MM) is a very potent neurotoxic agent. Its role in polluting the environment is well documented. A vast amount of study over the past several decades has finally provided insight into many aspects of its effect. Exposure to MM may be through ingestion of poisoned fish or inadvertent misuse of grain treated with the poison as a fungicide. Major epidemics have occurred in Japan (Fetal Minamata disease), Iraq, Pakistan, Guatemala, and Ghana. Sporadic incidences have occurred in the United States and Canada. There is no effective antidote to counteract the effect of MM on the central nervous system, although the information documented should provide hope for more effective therapy in acute cases.

  7. Recent developments in cyanide detection: A review

    PubMed Central

    Ma, Jian; Dasgupta, Purnendu K.

    2010-01-01

    The extreme toxicity of cyanide and environmental concerns from its continued industrial use continue to generate interest in facile and sensitive methods for cyanide detection. In recent years there is also additional recognition of HCN toxicity from smoke inhalation and potential use of cyanide as a weapon of terrorism. This review summarizes the literature since 2005 on cyanide measurement in different matrices ranging from drinking water and wastewater, to cigarette smoke and exhaled breath to biological fluids like blood, urine and saliva. The dramatic increase in the number of publications on cyanide measurement is indicative of the great interest in this field not only from analytical chemists, but also researchers from diverse environmental, medical, forensic and clinical arena. The recent methods cover both established and emerging analytical disciplines and include naked eye visual detection, spectrophotometry/colorimetry, capillary electrophoresis with optical absorbance detection, fluorometry, chemiluminescence, near-infrared cavity ring down spectroscopy, atomic absorption spectrometry, electrochemical methods (potentiometry/amperometry/ion chromatography-pulsed amperometry), mass spectrometry (selected ion flow tube mass spectrometry, electrospray ionization mass spectrometry, gas chromatography-mass spectrometry), gas chromatography (nitrogen phosphorus detector, electron capture detector) and quartz crystal mass monitors. PMID:20599024

  8. Recent developments in cyanide detection: a review.

    PubMed

    Ma, Jian; Dasgupta, Purnendu K

    2010-07-19

    The extreme toxicity of cyanide and environmental concerns from its continued industrial use continue to generate interest in facile and sensitive methods for cyanide detection. In recent years, there is also additional recognition of HCN toxicity from smoke inhalation and potential use of cyanide as a weapon of terrorism. This review summarizes the literature since 2005 on cyanide measurement in different matrices ranging from drinking water and wastewater, to cigarette smoke and exhaled breath to biological fluids like blood, urine and saliva. The dramatic increase in the number of publications on cyanide measurement is indicative of the great interest in this field not only from analytical chemists, but also researchers from diverse environmental, medical, forensic and clinical arena. The recent methods cover both established and emerging analytical disciplines and include naked eye visual detection, spectrophotometry/colorimetry, capillary electrophoresis with optical absorbance detection, fluorometry, chemiluminescence, near-infrared cavity ring down spectroscopy, atomic absorption spectrometry, electrochemical methods (potentiometry/amperometry/ion chromatography-pulsed amperometry), mass spectrometry (selected ion flow tube mass spectrometry, electrospray ionization mass spectrometry, gas chromatography-mass spectrometry), gas chromatography (nitrogen phosphorus detector, electron capture detector) and quartz crystal mass monitors.

  9. Complex samples cyanide detection with immobilized corrinoids.

    PubMed

    Männel-Croisé, Christine; Zelder, Felix

    2012-02-01

    Colorimetric solid phase with spatially separated extraction and detection zones as a rapid, effective and economic method for the optical detection of cyanide in complex samples is described. The system is seven times more sensitive for the optical detection of cyanide than the same class of chemical sensors used under homogeneous conditions. The application of the method in the detection of (i) endogenous cyanide in colored plant samples and of (ii) hydrogen cyanide in tobacco smoke is shown. The optical detection of multiple anions within a single sample has been demonstrated in principle for the detection of both CN(-) and SCN(-). Immobilized aquacyano-corrinoids and immobilized vitamin B12 are applied as chemical sensors, and cyanide is qualitatively identified by the violet color (λ(max) = 583 nm) of the corresponding dicyano-complex. Quantitative determinations with diffuse reflectance spectroscopy (DRUV-vis) are possible in the linear range up to 0.2 mg/L with a LOD of 1 μg/L. Alkyl-modified silica particles are employed for immobilization of the indicator on the surface of the solid phase (detection zone), and for removal of colored hydrophobic interferents (extraction zone).

  10. Food Poisonings by Ingestion of Cyprinid Fish

    PubMed Central

    Asakawa, Manabu; Noguchi, Tamao

    2014-01-01

    Raw or dried gallbladders of cyprinid fish have long been ingested as a traditional medicine in the Asian countries, particularly in China, for ameliorating visual acuity, rheumatism, and general health; however, sporadic poisoning incidences have occurred after their ingestion. The poisoning causes complex symptoms in patients, including acute renal failure, liver dysfunction, paralysis, and convulsions of limbs. The causative substance for the poisoning was isolated, and its basic properties were examined. The purified toxin revealed a minimum lethal dose of 2.6 mg/20 g in mouse, when injected intraperitoneally. The main symptoms were paralysis and convulsions of the hind legs, along with other neurological signs. Liver biopsy of the euthanized mice clearly exhibited hepatocytes necrosis and infiltration of neutrophils and lymphocytes, suggesting the acute dysfunction of the liver. Blood tests disclosed the characteristics of acute renal failure and liver injury. Infrared (IR) spectrometry, fast atom bombardment (FAB) mass spectrometry, and 1H- and 13C-nuclear magnetic resonance (NMR) analysis indicated, a molecular formula of C27H48O8S, containing a sulfate ester group for the toxin. Thus, we concluded that the structure of carp toxin to be 5α-cyprinol sulfate (5α-cholestane-3α, 7α, 12α, 26, 27-pentol 26-sulfate). This indicated that carp toxin is a nephro- and hepato- toxin, which could be the responsible toxin for carp bile poisoning in humans. PMID:24476713

  11. IRIS Toxicological Review of Hydrogen Cyanide (External Review Draft)

    EPA Science Inventory

    EPA is conducting a peer review of the scientific basis supporting the human health hazard and dose-response assessment of hydrogen cyanide and cyanide salts that will appear on the Integrated Risk Information System (IRIS) database.

  12. Beyond toxicity: a regulatory role for mitochondrial cyanide.

    PubMed

    García, Irene; Gotor, Cecilia; Romero, Luis C

    2014-01-01

    In non-cyanogenic plants, cyanide is a co-product of ethylene and camalexin biosynthesis. To maintain cyanide at non-toxic levels, Arabidopsis plants express the mitochondrial β-cyanoalanine synthase CYS-C1. CYS-C1 knockout leads to an increased level of cyanide in the roots and leaves and a severe defect in root hair morphogenesis, suggesting that cyanide acts as a signaling factor in root development. During compatible and incompatible plant-bacteria interactions, cyanide accumulation and CYS-C1 gene expression are negatively correlated. Moreover, CYS-C1 mutation increases both plant tolerance to biotrophic pathogens and their susceptibility to necrotrophic fungi, indicating that cyanide could stimulate the salicylic acid-dependent signaling pathway of the plant immune system. We hypothesize that CYS-C1 is essential for maintaining non-toxic concentrations of cyanide in the mitochondria to facilitate cyanide's role in signaling.

  13. SUBSTITUTION OF CADMIUM CYANIDE ELECTROPLATING WITH ZINC CHLORIDE ELECTROPLATING

    EPA Science Inventory

    The study evaluated the zinc chloride electroplating process as a substitute for cadmium cyanide electroplating in the manufacture of industrial connectors and fittings at Aeroquip Corporation. The process substitution eliminates certain wastes, specifically cadmium and cyanide, ...

  14. Toxicokinetics of cyanide in rats, pigs and goats after oral dosing with potassium cyanide.

    PubMed

    Sousa, Altamir B; Manzano, Helena; Soto-Blanco, Benito; Górniak, Silvana L

    2003-06-01

    The aim of the present study was to determine the effect of the species on the toxicokinetics of cyanide and its main metabolite, thiocyanate. Forty-two rats, six pigs and six goats were dosed orally with 3.0 mg KCN/kg body weight, and cyanide and thiocyanate concentrations in blood were measured within 24 h. After the single oral dose, KCN was rapidly absorbed by rats and goats, with a time of peak concentration ( T(max)) of 15 min. The maximum plasma concentration ( C(max)) of cyanide was observed in goats (93.5 micro mol/l), whereas the C(max) of thiocyanate was higher in rats (58.1 micro mol/l). The elimination half-life ( t(1/2)) and volume of distribution ( Vd(area)) of both cyanide and thiocyanate were higher in goats (1.28 and 13.9 h, and 0.41 and 1.76 l/kg, respectively). Whereas the area under the curve (AUC) of cyanide was significantly higher in goats (234.6 micro mol.l/h), the AUC of thiocyanate was higher in rats (846.5 micro mol.l/h). In conclusion, the results of the present study support the hypothesis that the metabolism of cyanide and its main metabolite, thiocyanate, is species-linked, with the goat being more sensitive to the toxic effects of cyanide/thiocyanate.

  15. Three hydroxy aurone compounds as chemosensors for cyanide anions.

    PubMed

    Chen, Huihui; Sun, Yunhui; Zhou, Chuanjian; Cao, Duxia; Liu, Zhiqiang; Ma, Lin

    2013-12-01

    Three new 4-hydroxy aurone compounds 1-3 with dimethylamino (1), bromine (2) and cyano (3) as terminal group have been synthesized. Their photophysical properties as well as recognition properties for cyanide anions in acetonitrile and aqueous solution have also been examined. These compounds exhibit remarkable response to cyanide anions with obvious color and fluorescence change owing to hydrogen bonding reaction between cyanide anions and the O-H moiety of the sensors, which allows naked eye detection of cyanide anions.

  16. Millimeter wave spectra of carbonyl cyanide

    PubMed Central

    Bteich, S.B.; Tercero, B.; Cernicharo, J.; Motiyenko, R.A.; Margulès, L.; Guillemin, J.-C.

    2016-01-01

    Context More than 30 cyanide derivatives of simple organic molecules have been detected in the interstellar medium, but only one dicarbonitrile has been found and that very recently. There is still a lack of high-resolution spectroscopic data particularly for dinitriles derivatives. The carbonyl cyanide molecule is a new and interesting candidate for astrophysical detection. It could be formed by the reaction of CO and CN radicals, or by substitution of the hydrogen atom by a cyano group in cyanoformaldehyde, HC(=O)CN, that has already been detected in the interstellar medium. Aims The available data on the rotational spectrum of carbonyl cyanide is limited in terms of quantum number values and frequency range, and does not allow accurate extrapolation of the spectrum into the millimeter-wave range. To provide a firm basis for astrophysical detection of carbonyl cyanide we studied its millimeter-wave spectrum. Methods The rotational spectrum of carbonyl cyanide was measured in the frequency range 152 - 308 GHz and analyzed using Watson’s A- and S-reduction Hamiltonians. Results The ground and first excited state of v5 vibrational mode were assigned and analyzed. More than 1100 distinct frequency lines of the ground state were fitted to produce an accurate set of rotational and centrifugal distortion constants up to the eighth order. The frequency predictions based on these constants should be accurate enough for astrophysical searches in the frequency range up to 500 GHz and for transition involving energy levels with J ≤ 100 and Ka ≤ 42. Based on the results we searched for interstellar carbonyl cyanide in available observational data without success. Thus, we derived upper limits to its column density in different sources. PMID:27738349

  17. Cyanide-resistant Respiration in Freshly Cut Potato Slices.

    PubMed

    Rychter, A; Janes, H W; Frenkel, C

    1978-04-01

    Treating intact white potato (Solanum tuberosum L.) tuber with ethylene in air or O(2) made it possible to obtain freshly cut slices which exhibit cyanide-resistant respiration. The cyanide-resistant path requires induction in whole tubers. The data also indicate that high O(2) concentration is necessary for the full development of cyanide-resistant respiration.

  18. Cyanide speciation at four gold leach operations undergoing remediation

    USGS Publications Warehouse

    Johnson, Craig A.; Grimes, David J.; Leinz, Reinhard W.; Rye, Robert O.

    2008-01-01

    Analyses have been made of 81 effluents from four gold leach operations in various stages of remediation to identify the most-persistent cyanide species. Total cyanide and weak acid-dissociable (WAD) cyanide were measured using improved methods, and metals known to form stable cyanocomplexes were also measured. Typically, total cyanide greatly exceeded WAD indicating that cyanide was predominantly in strong cyanometallic complexes. Iron was generally too low to accommodate the strongly complexed cyanide as Fe(CN)63- or Fe(CN)64-, but cobalt was abundant enough to implicate Co(CN)63- or its dissociation products (Co(CN)6-x(H2O)x(3-x)-). Supporting evidence for cobalt-cyanide complexation was found in tight correlations between cobalt and cyanide in some sample suites. Also, abundant free cyanide was produced upon UV illumination. Iron and cobalt cyanocomplexes both photodissociate; however, the iron concentration was insufficient to have carried the liberated cyanide, while the cobalt concentration was sufficient. Cobalt cyanocomplexes have not previously been recognized in cyanidation wastes. Their identification at four separate operations, which had treated ores that were not especially rich in cobalt, suggests that cobalt complexation may be a common source of cyanide persistence. There is a need for more information on the importance and behavior of cobalt cyanocomplexes in ore-processing wastes at gold mines.

  19. Evaluation of Commercially Available Cyanide Test Kits against Various Matrices

    DTIC Science & Technology

    2016-08-01

    EVALUATION OF COMMERCIALLY AVAILABLE CYANIDE TEST KITS AGAINST VARIOUS MATRICES ECBC-TR-1382 Darren W. Hicklin...3. DATES COVERED (From - To) Mar 2015 – Sep 2015 4. TITLE AND SUBTITLE Evaluation of Commercially Available Cyanide Test Kits against Various...available cyanide -detection test kits or strips were selected for evaluation based upon a premarket survey: Quantofix test strips, Cyantesmo test paper

  20. Toxicological criterion of the heroin poisoning.

    PubMed

    Shigeev, S

    2007-01-01

    The paper presents toxicological characteristics of 198 cases of acute parenteral heroin intoxication, analyzes the clinically encountered range of blood and urinary concentrations of its metabolites. The principal causes of death are elucidated in victims of heroin poisoning at the hospital stage. Where there is a relationship of death probability to the detection of morphine in the victims' biological fluids is considered; its blood and urinary concentrations are determined, which undoubtedly suggests the occurrence of poisoning-related death. It has been established that death from poisoning by heroin may occur in the whole range of its detectable concentrations. There is no doubt that the blood morphine concentrations of at least 2.0 microg/ml should be considered to be fatal.

  1. The analysis of protein-bound thiocyanate in plasma of smokers and non-smokers as a marker of cyanide exposure.

    PubMed

    Youso, Stephanie L; Rockwood, Gary A; Logue, Brian A

    2012-05-01

    When cyanide is introduced into the body, it quickly transforms through a variety of chemical reactions, normally involving sulfur donors, to form more stable chemical species. Depending on the nature of the sulfur donor, cyanide may be transformed into free thiocyanate, the major metabolite of cyanide transformation, 2-amino-2-thiazoline-4-carboxylic acid or protein-bound thiocyanate (PB-SCN) adducts. Because protein adducts are generally stable in biological systems, it has been suggested that PB-SCN may have distinct advantages as a marker of cyanide exposure. In this study, plasma was analyzed from 25 smokers (chronic low-level cyanide exposure group) and 25 non-smokers for PB-SCN. The amount of PB-SCN found in the plasma of smokers, 1.35 µM, was significantly elevated (p < 0.0001) when compared to non-smokers, 0.66 µM. Differences in sub-groups of smokers and non-smokers were also evaluated. The results of this study indicate the effectiveness of analyzing PB-SCN in determining instances of chronic cyanide exposure with possible extension to confirmation of acute cyanide exposure.

  2. Biotransformation and metabolic response of cyanide in weeping willows.

    PubMed

    Yu, Xiao-Zhang; Gu, Ji-Dong; Liu, Shuo

    2007-08-25

    Biotransformation and metabolic responses of plants to cyanide were investigated using pre-rooted plants of weeping willows (Salix babylonica L.) grown hydroponically in growth chambers and treated with potassium cyanide. Various physiological parameters of the plants were monitored to determine toxicity from exogenous cyanide exposure. Cyanide doses used in this study showed growth-promoting effects on plants, exhibiting higher measured values of transpiration rates, chlorophyll contents and soluble protein contents compared with the non-treated control plants. Superoxide dismutases (SOD), catalase (CAT) and peroxidase (POD) activities in leaves showed a slight change to cyanide application in most treatments. Of all selected parameters, soluble proteins of plants were the most sensitive indicator to cyanide application. Almost all applied cyanide was removed from the hydroponic solution in the presence of plants in all treatment groups. Small amounts of cyanide were detected in the plant tissues. Recovery of cyanide in different compartments of plants varied significantly, root being the dominant sink for cyanide accumulation. Mass balance studies showed that >97% of the applied cyanide was metabolized during transport through weeping willows and the metabolic rates of cyanide by plants were linearly increased with increasing of cyanide applied in the growth media. Results from this study indicated that neither visible toxic symptom nor metabolic lesion was observed for the plants after 192h of exposure, largely due to the well-established detoxification systems in willows. These findings suggest that cyanide has a beneficial role in plants and phytoremediation is a desirable solution of treating environmental sites contaminated with cyanide.

  3. GC-MS analysis of the designer drug α-pyrrolidinovalerophenone and its metabolites in urine and blood in an acute poisoning case.

    PubMed

    Grapp, Marcel; Sauer, Christoph; Vidal, Christian; Müller, Dieter

    2016-02-01

    α-Pyrrolidinovalerophenone (α-PVP) is a synthetic cathinone belonging to the group of "second generation" pyrrolidinophenones that becomes more and more popular as a designer psychostimulant. Here we provide toxicological analytical support for a severe poisoning with α-PVP. Serum and urine samples that were sent to our laboratory were subjected to a general unknown screening procedure. The procedure includes immunoassay-based screening of drugs of abuse in serum and systematic toxicological analysis of urine and serum after neutral and basic liquid-liquid extraction followed by gas chromatography-mass spectrometry (GC-MS). Whereas the immunoassay delivered negative results, analyzing the urine sample by GC-MS in full scan mode disclosed the presence of α-PVP and its metabolites α-(2″-oxo-pyrrolidino)valerophenone (2″-oxo-α-PVP) and 1-phenyl-2-(pyrrolidin-1-yl)pentan-1-ol (OH-α-PVP). In the acetylated urine sample we found additionally N,N-bis-dealkyl-PVP. In serum, α-PVP could be detected after solid phase extraction and a concentration of 29ng/mL was determined. Other forensic relevant substances were not detected. The presented data can explain the psychotic symptoms and behavioural pattern of the subject after abuse of α-PVP, leading to a clinical condition similar to excited delirium syndrome.

  4. [Poisonous mushrooms, mushroom poisons and mushroom poisoning. A review].

    PubMed

    Holsen, D S; Aarebrot, S

    1997-09-30

    Of 1,500 different types of Norwegian mushrooms, 60-100 are considered poisonous. Fatal intoxications occur very infrequently. Lack of knowledge of picking and preparing mushrooms and accidental or deliberate consumption are recognised causes of mushroom poisoning. Delayed onset of symptoms (> 5-6 hrs) indicates serious poisoning, and these patients must be admitted to hospital. Cytotoxic toxins (e.g. amatoxin, orellanin) cause serious damage to the visceral organs (liver, kidney) and require intensive treatment, including hemoperfusion. Neurotoxic toxins may cause dramatic, but less harmful peripheral or central symptoms affecting the peripheral and central nervous systems, including hallucinations. Some mushrooms cause gastroenteritis of low clinical significance within a few hours after consumption. Interaction between mushrooms and alcohol may lead to a disulfiram-like effect. Induced vomiting and activated charcoal are important initial therapeutic measures. The precise history of the patient and the collecting of mushroom remnants, including vomitus, may help to identify the particular mushroom. In Norway, the National Poison Information Centre may be contacted for further advice.

  5. Bioavailability of cyanide after consumption of a single meal of foods containing high levels of cyanogenic glycosides: a crossover study in humans.

    PubMed

    Abraham, Klaus; Buhrke, Thorsten; Lampen, Alfonso

    2016-03-01

    The acute toxicity of cyanide is determined by its peak levels reached in the body. Compared to the ingestion of free cyanide, lower peak levels may be expected after consumption of foods containing cyanogenic glycosides with the same equivalent dose of cyanide. This is due to possible delayed and/or incomplete release of cyanide from the cyanogenic glycosides depending on many factors. Data on bioavailability of cyanide after consumption of foods containing high levels of cyanogenic glycosides as presented herein were necessary to allow a meaningful risk assessment for these foods. A crossover study was carried out in 12 healthy adults who consumed persipan paste (equivalent total cyanide: 68 mg/kg), linseed (220 mg/kg), bitter apricot kernels (about 3250 mg/kg), and fresh cassava roots (76-150 mg/kg), with each "meal" containing equivalents of 6.8 mg cyanide. Cyanide levels were determined in whole blood using a GC-MS method with K(13)C(15)N as internal standard. Mean levels of cyanide at the different time points were highest after consumption of cassava (15.4 µM, after 37.5 min) and bitter apricot kernels (14.3 µM, after 20 min), followed by linseed (5.7 µM, after 40 min) and 100 g persipan (1.3 µM, after 105 min). The double dose of 13.6 mg cyanide eaten with 200 g persipan paste resulted in a mean peak level of 2.9 µM (after 150 min). An acute reference dose of 0.075 mg/kg body weight was derived being valid for a single application/meal of cyanides or hydrocyanic acid as well as of unprocessed foods with cyanogenic glycosides also containing the accompanying intact β-glucosidase. For some of these foods, this approach may be overly conservative due to delayed release of cyanide, as demonstrated for linseed. In case of missing or inactivated β-glucosidase, the hazard potential is much lower.

  6. Several hemicyanine dyes as fluorescence chemosensors for cyanide anions

    NASA Astrophysics Data System (ADS)

    Liang, Muhan; Wang, Kangnan; Guan, Ruifang; Liu, Zhiqiang; Cao, Duxia; Wu, Qianqian; Shan, Yanyan; Xu, Yongxiao

    2016-05-01

    Four hemicyanine dyes as chemosensors for cyanide anions were synthesized easily. Their photophysical properties and recognition properties for cyanide anions were investigated. The results indicate that all the dyes can recognize cyanide anions with obvious color, absorption and fluorescence change. The recognition mechanism analysis basing on in situ 1H NMR and Job plot data indicates that to the compounds with hydroxyl group, the recognition mechanism is intramolecular hydrogen bonding interaction. However, to the compounds without hydroxyl group, cyanide anion is bonded to carbon-carbon double bond in conjugated bridge and induces N+ CH3 to neutral NCH3. Fluorescence of the compounds is almost quenched upon the addition of cyanide anions.

  7. Cyanide Formation from Oxidation of Glycine by a Pseudomonas Species

    PubMed Central

    Wissing, Frode

    1974-01-01

    With whole cells of a hydrogen cyanide-producing bacterium strain C, of the genus Pseudomonas, it was found that the oxygen necessary for the oxidation of glycine to cyanide could be replaced by various artificial electron acceptors. The order of reactivity was: oxygen > phenazine methosulphate > methylene blue > 2,6-dichlorophenolindophenol > ferricyanide. Cyanide production was inhibited by pyrrolnitrin, a well-known inhibitor of many flavine enzymes. The molar ratio of added glycine to cyanide produced was found to be 1.09. With whole bacteria the apparent Km (glycine) for the cyanide production was found to be 5.0 × 10−4 M. PMID:4813896

  8. Cyanide formation from oxidation of glycine of Pseudomonas species.

    PubMed

    Wissing, F

    1974-03-01

    With whole cells of a hydrogen cyanide-producing bacterium strain C, of the genus Pseudomonas, it was found that the oxygen necessary for the oxidation of glycine to cyanide could be replaced by various artificial electron acceptors. The order of reactivity was: oxygen > phenazine methosulphate > methylene blue > 2,6-dichlorophenolindophenol > ferricyanide. Cyanide production was inhibited by pyrrolnitrin, a well-known inhibitor of many flavine enzymes. The molar ratio of added glycine to cyanide produced was found to be 1.09. With whole bacteria the apparent K(m) (glycine) for the cyanide production was found to be 5.0 x 10(-4) M.

  9. Hypotension in Severe Dimethoate Self-Poisoning

    PubMed Central

    Davies, James; Roberts, Darren; Eyer, Peter; Buckley, Nick; Eddleston, Michael

    2008-01-01

    Introduction Acute self-poisoning with the organophosphorus (OP) pesticide dimethoate has a human case fatality three-fold higher than poisoning with chlorpyrifos despite similar animal toxicity. The typical clinical presentation of severe dimethoate poisoning is quite distinct from that of chlorpyrifos and other OP pesticides: many patients present with hypotension that progresses to shock and death within 12–48 h post-ingestion. The pathophysiology of this syndrome is not clear. Case reports We present here three patients with proven severe dimethoate poisoning. Clinically, all had inappropriate peripheral vasodilatation and profound hypotension on presentation, which progressed despite treatment with atropine, i.v. fluids, pralidoxime chloride, and inotropes. All died 2.5–32 h post-admission. Continuous cardiac monitoring and quantification of troponin T provided little evidence for a primary cardiotoxic effect of dimethoate. Conclusion Severe dimethoate self-poisoning causes a syndrome characterized by marked hypotension with progression to distributive shock and death despite standard treatments. A lack of cardiotoxicity until just before death suggests that the mechanism is of OP-induced low systemic vascular resistance (SVR). Further invasive studies of cardiac function and SVR, and post-mortem histology, are required to better describe this syndrome and to establish the role of vasopressors and high-dose atropine in therapy. PMID:19003596

  10. [Abdominal pain as a presentation by lead poisoning. Case report].

    PubMed

    Mottiera, Daniel M; Cargnel, Elda

    2017-04-01

    Acute lead poisoning is not a common pathology seen in the pediatrician's office. Lead poisoning symptoms can be digestive or neurological, and they can be confused with other pathologies. That is the reason why it should be considered and, in case of doubt, complementary studies to confirm lead poisoning should be requested. This is the case of a nine-year-old child that comes to the office with a strong abdominal pain and vomiting, and after a close physical examination and a detailed anamnesis, a suspicious diagnosis of "acute" lead poisoning is obtained. Therefore, the infant is hospitalized, and after taking a venous sampling to confirm the lead level, a chelation therapy is performed under the toxicology expert's supervision.

  11. Disulfides as cyanide antidotes: evidence for a new in vivo oxidative pathway for cyanide detoxification.

    PubMed

    Zottola, Mark A; Beigel, Keith; Soni, Sunil-Datta; Lawrence, Richard

    2009-12-01

    It is known that cyanide is converted to thiocyanate in the presence of the enzyme rhodanese. The enzyme is activated by sulfur transfer from an appropriate sulfur donor. The activated enzyme then binds cyanide and transfers the sulfur atom to cyanide to form thiocyanate. This project began as an exploration of the ability of disulfides to act as sulfur donors in the rhodanese-mediated detoxification of cyanide. To our surprise, and contrary to expectations based on efficacy studies in vivo, our in vitro results showed that disulfides are rather poor sulfur donors. The transfer of a sulfur atom from a disulfide to the enzyme must occur via cleavage of a carbon-sulfur bond either of the original disulfide or in a mixed disulfide arising from the reaction of rhodanese with the original disulfide. Extending the reaction time and addition of chloride anion (a nucleophile) did not significantly change the results of the experiment. Using ultrasound as a means of accelerating bond cleavage also had a minimal effect. Those results ruled out cleavage of the carbon-sulfur bond in the original disulfide but did not preclude formation of a mixed disulfide. S-Methyl methylthiosulfonate (MTSO) was used to determine whether a mixed disulfide, if formed, would result in transfer of a sulfur atom to rhodanese. While no thiocyanate was formed in the reaction between cyanide and rhodanese exposed to MTSO, NMR analysis revealed that MTSO reacted directly with cyanide anion to form methyl thiocyanate. This result reveals the body's possible use of oxidized disulfides as a first line of defense against cyanide intoxication. The oxidation of disulfides to the corresponding thiosulfinate or thiosulfonate will result in facilitating their reaction with other nucleophiles. The reaction of an oxidized disulfide with a sulfur nucleophile from glutathione could be a plausible origin for the cyanide metabolite 2-aminothiazoline-4-carboxylic acid.

  12. Advanced Optical Technologies for Defense Trauma and Critical Care

    DTIC Science & Technology

    2014-02-04

    during acute smoke inhalation and battlefield relevant combined acute smoke/ cyanide exposures, including: 1. Determined the capability of the...smoke inhalation injury and concomitant cyanide poisoning. The model system was designed to mimic conditions found in battlefield and other smoke...monitor the physiological consequences of cyanide poisoning progression, including oxy- and deoxyhemoglobin and cytochrome c oxidase concentrations

  13. Accidental carbon monoxide poisoning.

    PubMed

    Zeller, W P; Miele, A; Suarez, C; Hannigan, J; Hurley, R M

    1984-12-01

    In this case report of an accidental automobile carbon monoxide poisoning, we identify the following risk factors: freezing temperature, young passenger age, location in the rear of the auto, smaller patient mass, and auto disrepair. The pathogenesis of carbon monoxide poisoning is reviewed. Emergency treatment and suggested criteria for hyperbaric oxygen use in pediatric patients are discussed.

  14. Poisoning - fish and shellfish

    MedlinePlus

    ... contaminated waters. Scombroid poisoning usually occurs from large, dark meat fish such as tuna, mackerel, mahi mahi, and albacore. Because this poison develops after a fish is caught and dies, it does not matter where the fish is caught. The main factor ...

  15. Sweet clover poisoning

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Sweet clover poisoning occurs when spoiled sweet clover (Melilotus officinalis and M. alva) hay or silage that contain dicumarol are consumed by livestock. This updated chapter is a succinct review of the clinical disease and pathologic lesions of poisoning. It also reviews current strategies and ...

  16. Cartap Hydrochloride Poisoning.

    PubMed

    Kalyaniwala, Kimmin; Abhilash, Kpp; Victor, Peter John

    2016-08-01

    Cartap hydrochloride is a moderately hazardous nereistoxin insecticide that is increasingly used for deliberate self-harm in India. It can cause neuromuscular weakness resulting in respiratory failure. We report a patient with 4% Cartap hydrochloride poisoning who required mechanical ventilation for 36-hours. He recovered without any neurological deficits. We also review literature on Cartap hydrochloride poisoning.

  17. Lead Poisoning in Children.

    ERIC Educational Resources Information Center

    Lin-Fu, Jane S.

    This publication is a guide to help social and health workers plan a preventive campaign against lead poisoning, a cause of mental retardation other neurological handicaps, and death among children. The main victims are 1- to 6-year-olds living in areas where deteriorating housing prevails. Among the causes of lead poisoning are: ingestion of…

  18. Ferrate(VI) and ferrate(V) oxidation of cyanide, thiocyanate, and copper(I) cyanide

    NASA Astrophysics Data System (ADS)

    Sharma, Virender K.; Yngard, Ria A.; Cabelli, Diane E.; Clayton Baum, J.

    2008-06-01

    Cyanide (CN -), thiocyanate (SCN -), and copper(I) cyanide (Cu(CN) 43-) are common constituents in the wastes of many industrial processes such as metal finishing and gold mining, and their treatment is required before the safe discharge of effluent. The oxidation of CN -, SCN -, and Cu(CN) 43- by ferrate(VI) (Fe VIO 42-; Fe(VI)) and ferrate(V) (Fe VO 43-; Fe(V)) has been studied using stopped-flow and premix pulse radiolysis techniques. The rate laws for the oxidation of cyanides were found to be first-order with respect to each reactant. The second-order rate constants decreased with increasing pH because the deprotonated species, FeO 42-, is less reactive than the protonated Fe(VI) species, HFeO 4-. Cyanides react 10 3-10 5 times faster with Fe(V) than with Fe(VI). The Fe(V) reaction with CN - proceeds by sequential one-electron reductions from Fe(V) to Fe(IV) to Fe(III). However, a two-electron transfer process from Fe(V) to Fe(III) occurs in the reaction of Fe(V) with SCN - and Cu(CN) 43-. The toxic CN - species of cyanide wastes is converted into relatively non-toxic cyanate (NCO -). Results indicate that Fe(VI) is highly efficient in removing cyanides from electroplating rinse water and gold mill effluent.

  19. Copper recovery and cyanide oxidation by electrowinning from a spent copper-cyanide electroplating electrolyte.

    PubMed

    Dutra, A J B; Rocha, G P; Pombo, F R

    2008-04-01

    Copper-cyanide bleed streams arise from contaminated baths from industrial electroplating processes due to the buildup of impurities during continuous operation. These streams present an elevated concentration of carbonate, cyanide and copper, constituting a heavy hazard, which has to be treated for cyanide destruction and heavy metals removal, according to the local environmental laws. In the Brazilian Mint, bleed streams are treated with sodium hypochlorite, to destroy cyanide and precipitate copper hydroxide, a solid hazardous waste that has to be disposed properly in a landfill or treated for metal recovery. In this paper, a laboratory-scale electrolytic cell was developed to remove the copper from the bleed stream of the electroplating unit of the Brazilian Mint, permitting its reutilization in the plant and decreasing the amount of sludge to waste. Under favorable conditions copper recoveries around 99.9% were achieved, with an energy consumption of about 11 kWh/kg, after a 5-h electrolysis of a bath containing copper and total cyanide concentrations of 26 and 27 g/L, respectively. Additionally, a substantial reduction of the cyanide concentration was also achieved, decreasing the pollution load and final treatment costs.

  20. Nephropathy in Chronic Lead Poisoning

    PubMed Central

    Lilis, Ruth; Gavrilescu, N.; Nestorescu, B.; Dumitriu, C.; Roventa, Ana

    1968-01-01

    may follow in time, accompanied rather frequently by arterial hypertension. A study of some of the cases followed for several years demonstrated this progressive evolution of lead nephropathy. A functional and transitory impairment of renal function is very probably caused by an impairment of intrarenal circulation, resulting from marked vasoconstriction of the renal vessels, forming part of the generalized vasoconstriction of lead poisoning. Prolonged exposure and frequently recurring episodes of acute poisoning may lead to progressive impairment of renal function and to the development of organic lesions. Special attention should be paid to renal function tests in all cases with prolonged exposure to lead in order to prevent the development of severe lead nephropathy. PMID:5663423