Methemoglobinemia in Hemodialysis Patients due to Acute Chlorine Intoxication: A Case Series Calling Attention on an Old Problem.

INTRODUCTION: Hemodialysis uses municipal water that must be strictly purified and sterilized to be used for that procedure. Large amounts of decontaminants are often used, such as chlorine, and if these compounds are not subsequently removed they can be transferred to the blood of patients causing complications including methemoglobinemia. METHODS: In this case series study, dialysis patients in one unit were evaluated. We reviewed clinical characteristics and laboratory findings obtained on the day when the water supply was disinfected with chlorine, with the aim to quantify methemoglobin concentrations. Our objective was to characterize the clinical presentation and management of patients who presented with methemoglobinemia on a specific index day. We also reviewed reported cases in the literature regarding this underreported complication. RESULTS: Eight patients who presented with chlorine intoxication were evaluated. The methemoglobin concentrations were between 1.3% and 7.9% (reference value 0-1%). We believe this to be caused by water containing 0.78 mg/L of total chlorine. Seven patients presented with cyanosis, 4 with dizziness, 6 with dark brown blood, 4 with dyspnea, and 4 with headache and hemolytic anemia. Subjects were treated with supplemental oxygen, methylene blue, intravenous vitamin C, blood transfusions, and increased doses of erythropoietin. No patient died, and all continued with their usual hemodialysis sessions. CONCLUSION: Acute chlorine intoxication transferred by the water used during hemodialysis sessions can present with methemoglobinemia accompanied by cyanosis, oxygen desaturation, and hemolytic anemia. Chlorine levels should be carefully monitored in the water used for hemodialysis treatment.

Siblings with pediatric sodium chlorite toxicity causing methemoglobinemia, renal failure and hemolytic anemia.

INTRODUCTION: Over the past decade, Miracle Mineral Solution (sodium chlorite) has been promoted as a cure-all for many conditions. CASE REPORT: A 9-year-old boy presented with his brother after they accidentally ingested a small amount of undiluted 22.4% sodium chlorite. Symptoms included nausea, vomiting, diarrhea, and dyspnea. Oxygen saturation remained 71% despite supplemental oxygen (15L/min). The patient was noted to have dark chocolate-appearing blood, minimal urine output, diffuse pallor and cyanosis. He developed methemoglobinemia, renal failure requiring renal replacement therapy and hemolysis requiring blood transfusion. DISCUSSION: These are the 7th and 8th reported cases of sodium chlorite toxicity by ingestion and the second and third in children. Takeaway for Physicians: Miracle Mineral Solution is a commonly purchased potentially lethal compound that can cause methemoglobinemia with respiratory failure, hemolytic anemia requiring transfusion and renal failure requiring dialysis.

[1,4-diaminobenzene and diphenylamine-induced severe methemoglobinaemia treated by hyperbaric oxygen therapy - Case report]. / Zastosowanie tlenoterapii hiperbarycznej w ciezkiej methemoglobinemii wywolanej zatruciem 1,4-diaminobenzenem i difenyloamina ­ opis przypadku.

Methemoglobin is an oxidized form of hemoglobin that is not capable of carrying oxygen. Exposure to exogenous oxidizing agents can cause severe methemoglobinemia and subsequent hypoxia. This article presents the rare case of a 23-year old patient with methemoglobinemia of 54.2% of total hemoglobin, induced by workplace exposure to 1,4-diaminobenzene and diphenylamine. Following the hyperbaric oxygen therapy the patient was discharged in good general condition and referred to a district hospital for observation. Med Pr 2018;69(3):345-350.

A Case of Methemoglobinemia Successfully Treated with Hyperbaric Oxygenation Monotherapy.

BACKGROUND: Methylene blue is the first-line therapy for methemoglobinemia, but it can be intermittently unavailable due to production issues. For this clinical scenario, alternative treatment options need to be explored. Hyperbaric oxygenation (HBO) is conventionally applied as an adjunctive therapy during the systemic administration of methylene blue. Currently, little is known regarding the effects of HBO monotherapy in methemoglobinemia. We report a case of methemoglobinemia that was successfully treated with HBO monotherapy. CASE REPORT: A 41-year-old man presented to the Emergency Department with dyspnea and dizziness subsequent to smoking in a garage filled with motor vehicle exhaust gas. There were no abnormal heart or lung sounds. While administering oxygen flowing at 15 L/min via a mask with a reservoir bag, blood tests revealed high methemoglobin (MetHb) levels at 59.6%. He was treated with HBO monotherapy, and sequential tests showed that the MetHb level decreased significantly to 34.0%, 12.8%, 6.2%, and eventually, 3.5%. He was discharged with stable vital signs the next day. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: HBO monotherapy is an effective alternative treatment for methemoglobinemia when methylene blue is not available.

Severe methaemoglobinaemia treated with adjunctive hyperbaric oxygenation.

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

Severe haemolytic anaemia due to ingestion of naphthalene (mothball) containing coconut oil.

Naphthalene, a widely used industrial and household chemical, has rarely been an agent of poisoning worldwide. Severe haemolysis from naphthalene poisoning is rare and can be a challenge to clinicians. We report a 22-year-old female, who accidentally ingested naphthalene mixed coconut oil and got admitted with recurrent vomiting, headache and passage of dark urine. Severe intravascular haemolysis with hypotension and neutrophilic leukocytosis was detected. She was treated with red blood cell transfusions, intravenous saline infusion and ascorbic acid.

Metahemoglobinemia en una lactante por consumo de puré vegetal / Infant methemoglobinemia after eating mixed vegetable puree

La cianosis es un signo clínico consistente en coloración azulada de piel y mucosas debida a un aumento de la hemoglobina reducida en los capilares, o menos frecuentemente, a la presencia de metahemoglobinemia (forma férrica de la hemoglobina) que puede ser ocasionada por contacto o ingesta de agentes oxidantes exógenos tóxicos como tintes de anilina, nitrobenceno, fármacos o compuestos nitrogenados de diferente procedencia, como son las verduras con alto contenido en nitratos (1 y 2). Presentamos el caso clínico de una lactante de 8 meses que fue traída a urgencias por presentar cianosis labial y de partes acras (manos y pies), sin otro tipo de sintomatología, tras la ingestión de un puré vegetal preparado y conservado a temperatura ambiente. La determinación de metahemoglobina fue del 22,8% mediante determinación por cooximetría. La evolución del lactante fue satisfactoria con tratamiento con oxígeno y observación durante 24 horas (AU)

Cyanosis is a clinical sign due to the presence of bluish coloration of skin and mucosae, caused by an increase in the reduced form of hemoglobin in the capillaries, or, less frequently, to the presence of methemoglobinemia (ferric form of hemoglobin). Its origin can be contact or ingestion of exogenous oxidating toxic agents like aniline dyes, nitrobencene, drugs or nitrogen compounds from different origin or vegetables with high nitrate content (1 and 2). We report a case of a 8-month-old female infant who was brought to the emergency room with no symptoms except cyanosis of the lips and acral areas (hands and feet) after the ingestion of a mixed vegetable puree, prepared and conserved at room temperature. Her methemoglobin level determined by cooximetry was 22.8%. She was treated during 24 hour with oxygen and observation and evolved satisfactorily (AU)

Hyperbaric oxygenation in the treatment of life-threatening isobutyl nitrite-induced methemoglobinemia--a case report.

Methemoglobinemia usually results from exposure to oxidizing substances such as nitrates or nitrites. Iron within hemoglobin is oxidized from the ferrous (Fe2+) state to the ferric (Fe3+) state, resulting in the inability to transport oxygen and carbon dioxide. Clinically, this condition causes functional cyanosis. As methemoglobin levels increase, patients show evidence of cellular hypoxia in all tissues. Death usually occurs when methemoglobin fractions approach 70% of total hemoglobin. We describe the case of a 35-year-old female patient with severe life-threatening isobutyl nitrite-induced methemoglobinemia of 75% of total hemoglobin. Toluidine-blue was administered as first-line antidotal therapy immediately, followed by hyperbaric oxygenation. The patient recovered uneventfully and could be discharged 3 days later.

Toxins.

Exposures to toxins are prevalent, frequently complicate surgical emergencies, and impact critical care. A fundamental understanding of pathophysiologic principles and management strategies is essential for the anesthesiologist frequently responsible for the acute care of patients who have toxicologic exposures. Given their pervasiveness and ability to confound the clinical presentations in the perioperative or intensive care setting, substances of abuse and asphyxiants warrant particular attention and a high degree of vigilance.

Isobutyl-nitrite-induced methemoglobinemia; treatment with an exchange blood transfusion during hyperbaric oxygenation.

A young man was accidentally intoxicated with isobutyl nitrite by a threefold lethal dose. Due to nitrites' ability to change hemoglobine into methemoglobine the patient showed signs of severe hypoxia, which could not be treated by conventional means. Therefore the patient was rapidly transferred to a hyperbaric chamber. The patient was treated with pure oxygen at 283 kPa under which a blood exchange transfusion was performed. The patient fully recovered.

Occupational methaemoglobinaemia. Mechanisms of production, features, diagnosis and management including the use of methylene blue.

Methaemoglobin is formed by oxidation of ferrous (FeII) haem to the ferric (FeIII) state and the mechanisms by which this occurs are complex. Most cases are due to one of three processes. Firstly, direct oxidation of ferrohaemoglobin, which involves the transfer of electrons from ferrous haem to the oxidising compound. This mechanism proceeds most readily in the absence of oxygen. Secondly, indirect oxidation, a process of co-oxidation which requires haemoglobin-bound oxygen and is involved, for example, in nitrite-induced methaemoglobinaemia. Thirdly, biotransformation of a chemical to an active intermediate that initiates methaemoglobin formation by a variety of mechanisms. This is the means by which most aromatic compounds, such as amino- and nitro-derivatives of benzene, produce methaemoglobin. Methaemoglobinaemia is an uncommon occupational occurrence. Aromatic compounds are responsible for most cases, their lipophilic nature and volatility facilitating absorption during dermal and inhalational exposure, the principal routes implicated in the workplace. Methaemoglobinaemia presents clinically with symptoms and signs of tissue hypoxia. Concentrations around 80% are life-threatening. Features of toxicity may develop over hours or even days when exposure, whether by inhalation or repeated skin contact, is to relatively low concentrations of inducing chemical(s). Not all features observed in patients with methaemoglobinaemia are due to methaemoglobin formation. For example, the intravascular haemolysis caused by oxidising chemicals such as chlorates poses more risk to life than the methaemoglobinaemia that such chemicals induce. If an occupational history is taken, the diagnosis of methaemoglobinaemia should be relatively straightforward. In addition, two clinical observations may help: firstly, the victim is often less unwell than one would expect from the severity of 'cyanosis' and, secondly, the 'cyanosis' is unresponsive to oxygen therapy. Pulse oximetry is unreliable in the presence of methaemoglobinaemia. Arterial blood gas analysis is mandatory in severe poisoning and reveals normal partial pressures of oxygen (pO2) and carbon dioxide (pCO2,), a normal 'calculated' haemoglobin oxygen saturation, an increased methaemoglobin concentration and possibly a metabolic acidosis. Following decontamination, high-flow oxygen should be given to maximise oxygen carriage by remaining ferrous haem. No controlled trial of the efficacy of methylene blue has been performed but clinical experience suggests that methylene blue can increase the rate of methaemoglobin conversion to haemoglobin some 6-fold. Patients with features and/or methaemoglobin concentrations of 30-50%, should be administered methylene blue 1-2 mg/kg/bodyweight intravenously (the dose depending on the severity of the features), whereas those with methaemoglobin concentrations exceeding 50% should be given methylene blue 2 mg/kg intravenously. Symptomatic improvement usually occurs within 30 minutes and a second dose of methylene blue will be required in only very severe cases or if there is evidence of ongoing methaemoglobin formation. Methylene blue is less effective or ineffective in the presence of glucose-6-phosphate dehydrogenase deficiency since its antidotal action is dependent on nicotinamide-adenine dinucleotide phosphate (NADP+). In addition, methylene blue is most effective in intact erythrocytes; efficacy is reduced in the presence of haemolysis. Moreover, in the presence of haemolysis, high dose methylene blue (20-30 mg/kg) can itself initiate methaemoglobin formation. Supplemental antioxidants such as ascorbic acid (vitamin C), N-acetylcysteine and tocopherol (vitamin E) have been used as adjuvants or alternatives to methylene blue with no confirmed benefit. Exchange transfusion may have a role in the management of severe haemolysis or in G-6-P-D deficiency associated with life-threatening methaemoglobinaemia where methylene blue is relatively contraindicated.

[Methemoglobinemia in a newborn infant following pudendal anesthesia in labor with prilocaine. A case report]. / Methämoglominämie bei einem Neugeborenen nach Pudendus-Anästhesie der Gebärenden mit Prilocain. Ein Fallbericht.

A genetically intact newborn suffered from methaemoglobinaemia after delivery under pudendum anaesthesia with prilocaine. Complete restitution was promoted by i.v. applied ascorbic acid and thionine. This is of special importance because in this case methaemoglobinaemia was not produced by medication of the patient herself but must be attributed to the local anaesthesia of the mother with prilocaine. The special sensitivity of newborn and infants, as well as the use of possible treatment methods as described in literature, are discussed.