Severe chlorate poisoning successfully treated with methylene blue.

BACKGROUND: Chlorate poisoning as a cause of methemoglobinemia is regarded in current literature to be resistant to treatment by methylene blue due to the oxidizing and denaturing properties of the chlorate anion, and often leads to severe renal and hematological complications with a high mortality rate. Recent case studies suggest practitioners have eschewed the use of methylene blue in such situations. OBJECTIVES: This report describes a case of chlorate poisoning presenting as severe methemoglobinemia successfully treated with methylene blue alone, believed to be a first in reported literature. CASE REPORT: A 34-year-old male construction worker presented 4 h after accidental ingestion of an industrial chemical, with giddiness and breathlessness. Physical examination did not reveal any abnormal cardiorespiratory findings, although arterial blood gas analysis and pulse oximetry revealed an "oxygen saturation gap." Methemoglobin levels were found to be severely elevated at 66.8% 6 h after ingestion, and the patient was promptly treated with methylene blue. Clinical examination and laboratory tests suggested the absence of hemolysis at the time of treatment. The patient was discharged after a brief and uneventful hospital stay. Subsequent tests revealed the chemical ingested to be sodium chlorate. CONCLUSION: The successful outcome in our case suggests that a window of opportunity as long as 6 h may exist during which treatment of chlorate poisoning with methylene blue may be of clinical value. We postulate that the absence of significant hemolysis and hematological alterations at the time of antidote administration may be a necessary prerequisite for treatment success.

Suicidal intoxication with potassium chlorate successfully treated with renal replacement therapy and extracorporeal liver support.

We present a case of a 22-year-old male who, in a suicide attempt, ingested approximately 200 g of potassium chlorate. Upon admission to the hospital, he presented in full respiratory failure with cyanosis. Methylene blue antidote was given but found to be ineffective. The patient was intubated and mechanical ventilation was initiated. Because of renal failure with anuria, intermittent haemodialysis (iHD) followed by continuous venovenous hemodiafiltration (CVVHDF) was performed. His hospital stay was also complicated by hemolysis, disseminated intravascular coagulation, and atrial fibrillation. Transfusions of packed red blood cells, platelets, and fresh frozen plasma were necessary to correct the deficits. He also developed liver failure and required two sessions of molecular adsorbent recirculating system (MARS) therapy. On day 14 of his hospitalization, he regained consciousness, as well as full respiratory and circulatory function. There are no controlled studies addressing management of potassium chlorate poisoning. We suggest that early renal replacement therapy should be strongly considered.

A fatal case of severe methemoglobinemia presumably due to chlorate ingestion.

A fatal case due to severe methemoglobinemia is presented. A male in his forties was found unconscious in his house and, despite intensive care, death was confirmed approximately 11 hours later. Toxicological analysis using ion chromatography revealed the presence of chlorate in the stomach contents. However, chlorate was not detected in the blood, and no other drugs or ethanol were detected in the blood either. We concluded that the cause of death was presumably due to chlorate poisoning, based on the results of the autopsy and the toxicological examination.

Chlorate poisoning in beef cattle.

A disease syndrome characterized by hemolysis, methemoglobinemia, methemoglobinuria, and death was observed in a herd of purebred Limousin beef cattle grazing on pasture in November in Alberta. Improper disposal of the nonselective herbicide, sodium chlorate, was identified as the causal agent. Highly variable blood methemoglobin levels reflected differences in herbicide consumption.

Cranial MR imaging findings of potassium chlorate intoxication.

We present the case of a patient who attempted suicide by ingesting matchstick heads (55% potassium chlorate). The patient presented to the emergency room with loss of consciousness, and MR imaging revealed symmetric hyperintense signal within the deep gray matter and medial temporal lobes. The patient improved after undergoing conventional treatment and hyperbaric oxygen.

A fatal case of chlorate poisoning: confirmation by ion chromatography of body fluids.

A 49-year-old male chemical industry worker was admitted to intensive care with a 24-hour history of respiratory failure, vomiting, headache, stupor, arterial hypotension, and cyanosed face and limbs. He had acute haemolysis (3.9 g/L plasma haemoglobin concentration) and 30% methaemoglobinaemia. Whereas the search for alcohol, barbiturates and opiates was negative, benzodiazepines and tricyclic antidepressants were present. The patient was in fact being treated with fluvoxamine, amitryptiline, and alprazolam. As the clinical and biological signs suggested chlorate poisoning, chlorate was looked for by using an aniline color reaction. It was found in gastric content and urine. Treatment consisted in mechanical ventilation, vasoactive amines, methylene blue, plasma exchange, exchange transfusion, and haemodialysis. Despite this, the patient had several cardiac arrests and refractory metabolic acidosis. He died 12 h after his admission. Specific ion chromatography was used afterhand to assay the chlorate in various body fluids. The technique was based on a separation on an ion exchange Dionex AS 12A column coupled with conductivity detection. A quantitative estimation was carried out by using external calibration with a four-point calibration curve which was linear between 1 and 15 mg/L. The measured plasma levels of chlorate were 78 and 29 mg/L respectively before and after exchange transfusion. Gastric-lavage liquid contained 1300 mg/L of chlorate and urine 4300 mg/L. Ion chromatography, which is routinely used in environmental studies helped to confirm a massive oral intake of chlorate by measuring the corresponding blood and urine chlorate concentrations, data which had only rarely been reported previously.

[Anabolic effects of sodium selenite, vitamin E and retabolil in experimental hypotrophy induced by a pesticide]. / Anabolicheskii éffekt selenita natriia, vitamina E, retabolila na fone éksperimental'noi gipotrofii, vyzvannoi pestitsidom.

Forty Chinchilla rabbits of both sexes were examined for changes in some parameters of protein, lipid and trace elements metabolism (total protein, protein fractions, urea, residual nitrogen in blood serum, lipids, total cholesterol, free cholesterol, diglycerides, phospholipids, triglycerides, free fatty acids and the trace elements selenium, iron, zinc and so forth in the liver) during the animals' poisoning with the defoliant magnesium chlorate. A study was made of the effect on these changes of the administration for 3 weeks of sodium selenite (15 micrograms/kg), vitamin E (25 mg/kg) and retabolil (2 mg/kg once a week). It has been established that the combined administration of these agents removes and prevents the changes in protein, lipid and trace elements (hypoproteinemia, dysproteinemia and impairment of the nitrous balance) and lipid metabolism because of the animals' poisoning with magnesium chlorate.

Severe chlorate poisoning: report of a case.

A case of severe sodium chlorate poisoning was observed within 5 h after suicidal ingestion of 150-200 g of the herbicide. Methaemoglobinaemia was the early symptom of the intoxication. Treatment with methylene blue and ascorbic acid could not prevent a massive haemolysis with disseminated intravascular coagulation. Hypercoagulation and hyperfibrinolysis could be treated successfully with exchange transfusions, heparin and fresh plasma. During the first hours, 70 mmol chlorate were excreted before complete renal failure occurred which required haemodialysis for several weeks. Clinical observations and in vitro experiments provide evidence that methylene blue is effective only in the very early stages of chlorate poisoning. Consequently, the following treatment is suggested: gastric lavage, exchange transfusion, bicarbonate infusion, haemodialysis, anticoagulation with heparin and substitution of clotting factors if necessary.