• Journal of Dental Anesthesia and Pain Medicine
• /
• v.21 no.5
• /
• pp.471-474
• /
• 2021

Methemoglobinemia is rare. It is classified into two types: congenital methemoglobinemia and acquired methemoglobinemia. Methemoglobin is incapable of binding oxygen, leading to complications such as cyanosis, dyspnea, headache, and heart failure. In the present case, a 35-year-old man with congenital methemoglobinemia underwent general anesthesia for thyroidectomy. The patient was diagnosed with hemoglobin M at 7 years of age. Ventilation was performed with FiO₂ 1.0. Arterial blood gas analysis showed that the pH was 7.4, PaO₂ 439 mmHg, PaCO₂ 40.5 mmHg, oxyhemoglobin level of 83.2%, and methemoglobin level of 15.5%. The patient had a stable course, although cyanosis was observed during surgery.

• Journal of Medicine and Life Science
• /
• v.18 no.1
• /
• pp.20-23
• /
• 2021

Methemoglobin is generated by the oxidation of ferrous iron to ferric iron within a hemoglobin molecule. Methemoglobin is unable to bind and transport oxygen, resulting in methemoglobinemia, which can lead to fatal tissue hypoxia. The most common cause of methemoglobinemia is poisoning by oxidizing agents such as dapsone, benzocaine, and primaquine. However, methemoglobinemia can also be caused by normal dietary sources. We present two cases of methemoglobinemia that developed after a normal diet in two male patients. In this case report, the patients suddenly developed dyspnea and cyanosis after eating the same meal. They had no history of suspected poisoning, such as the use of drugs, exposure to chemicals, or gas inhalation. Their symptoms did not improve even after a high dose of oxygen was administered; further, an abnormal 'oxygen saturation gap' was observed. Because of CO-oximetry, the methemoglobin levels of the patients were 50.0% and 46.6%, respectively. We administered methylene blue (1 mg/kg), and the patients recovered completely without any complications. Emergency physicians should, therefore, be aware that methemoglobinemia can also be caused by normal dietary sources. In addition, if the source and route of contamination are unclear, an epidemiological investigation should be conducted.

• Journal of The Korean Society of Clinical Toxicology
• /
• v.4 no.2
• /
• pp.158-160
• /
• 2006

Acute methemoglobinemia is induced by various causes, especially ingestion of oxidizing agents such as phenazopyridine, dapsone, and nitrite. Indoxacarb is an oxadiazine insecticide with high insecticidal activity and low mammalian toxicity. It is known to block voltage-gated Na+ channels in insects and mammals, but the mechanism is not yet well understood. We describe a case of a 41-year-old woman with methemoglobinemia that developed following Indoxacarb ingestion, which improved after intravenous injection of methylene blue. This is the first known such case. If signs and symptoms of methemoglobinemia occur after Indoxacarb ingestion, antidotal therapy with methylene blue should be considered as a necessary treatment.

• Korean Journal of Veterinary Research
• /
• v.31 no.1
• /
• pp.41-47
• /
• 1991

The protective of influences of sodium selenitc ($Na_2SeO_3$) against the methemoglobinemia with sodium nitrite were investigated on hemoglobin, methemoglobin, glutathione peroxidase and NADH-methemoglobin reductase activity in rabbits which were given 0,1,3 and 9ppm sodium selenite of drinking water for a week. Dietary selenium did not alter total hemoglobin in the blood of rabbits. Selenium was found to decrease nitrite-induced methemoglobin in a dose-dependent manner. The glutathione peroxidase activity was also increased by selenium in all the experimental groups. However, the NADH-methemoglobin reductase activity by selenite did not show significant differences as concerns the methemoglobinemia. These results showed that selenium could inhibit nitrite-induced methemoglobinemia. Its influence of inhibition is suggested that the effect of the reduction of methemoglobin was greatly stimulated by glutathione peroxidase activity.

• Journal of The Korean Society of Clinical Toxicology
• /
• v.4 no.2
• /
• pp.151-154
• /
• 2006

Acute toxic methemoglobinemia is an infrequent complication of the use of various drugs. Severe methemoglobinemia is very often fatal. Methylene blue is an effective drug in the treatment of methemoglobinemia patients. However, failure to respond to methylene blue has been described in patients with sulfhemoglobinemia, chlorate poisoning, and glucose-6-phosphate dehydrogenase deficiency. It is even possible that hemolysis may occur due to methylene blue treatment itself. We encountered a case of a 71-year-old woman who developed methemoglobinemia caused by alprazolam intoxication. She presented with hemolytic anemia and did not respond to methylene blue. In spite of concerted N-acetylcysteine therapy, the hemolytic anemia became aggravated and the patient died eleven days after intoxication.

• Journal of The Korean Society of Clinical Toxicology
• /
• v.15 no.2
• /
• pp.148-151
• /
• 2017

Methemoglobinemia is a condition in which the iron portion of hemoglobin, which binds to oxygen, is oxidized to produce methemoglobin, which increases blood concentration. There are many causes of methemoglobinemia, the most common being food, drugs, and chemicals. A 75-year-old male patient who had taken an herbicide did not notice any nonspecific symptoms. However, after 4 hours, his methemoglobin levels increased to 17.1%, while after 7 hours it increased to 26.5%, at which time intravenous administration of methylene blue 1 mg/kg (an antidote) was started. After a total of five doses of methylene blue at 1 mg/kg due to reactive methemoglobinemia for about 36 hours, the methemoglobin levels increased to 23.7%. Because no more methylene blue could be administered, 10 g of ascorbic acid (vitamin C) was administered intravenously. After 82 hours, ascorbic acid 10 g was administered six times for repeated reactive methemoglobinemia. No additional reactive methemoglobinemia was observed. The ventilator and endotracheal tube were successfully removed on day 5 after admission.

• Journal of The Korean Society of Clinical Toxicology
• /
• v.6 no.1
• /
• pp.37-41
• /
• 2008

Methemoglobinemia can be caused by dapsone toxicity. We report a case dapsone induced methemoglobinemia unresponsive to methylene blue successfully treated by exchange transfusion. A 52-year-old male ingested a handful of dapsone. He presented with severe peripheral cyanosis in lips and fingertips and his methemoglobin level was found to be 21.9%. After admission, methylene blue (1%) at 1 mg/kg was injected each time peripheral cyanosis and rising serum methemoglobin occurred. Despite methylene blue therapy, the patient‘s methemoglobin level continued to fluctuate. Five days after the injections of methylene blue, many Heinz bodies were visualized in the peripheral blood, suggestive of hemolytic anemia occurrence. By hospital day 6, serum methemoglobine levels were elevated and not measurable (> 50%) and the patient was constantly in a semi-comatose mental state. An exchange transfusion carried out by utilizing 6 units of packed red blood cells and 4 units of fresh frozen plasma was performed. The patient's methemoglobin levels were subsequently kept up below 20% and his peripheral cyanosis receded. Physicians should recognize the important role of exchange transfusion in refractory dapsoneinduced methemoglobinemia.

• Journal of Dental Anesthesia and Pain Medicine
• /
• v.21 no.4
• /
• pp.357-361
• /
• 2021

Methemoglobinemia is a blood disorder in which an abnormal amount of methemoglobin is produced, and prilocaine is one of the drugs that can cause this disorder. The maximum recommended dose of prilocaine is 8 mg/kg. We report a case of methemoglobinemia caused by the administration of 4.2 mg/kg of prilocaine without other methemoglobinemia-inducing drugs during general anesthesia. A 17-year-old girl with hyperthyroidism and anemia was scheduled to undergo maxillary sinus floor elevation and tooth extraction. The patient's peripheral oxygen saturation (SpO₂) decreased from 100% at arrival to 95% after receiving prilocaine with felypressin following induction of general anesthesia. However, the fraction of inspired oxygen was 0.6. Blood gas analysis showed that the methemoglobin level was 3.8% (normal level, 1%-2%), fractional oxygen saturation was 93.9%, partial pressure of oxygen was 327 mmHg, and arterial oxygen saturation was 97.6%. After administration of 1 mg/kg of methylene blue, her SpO₂ improved gradually to 99%, and the methemoglobin value decreased to 1.2%. When using prilocaine as a local anesthetic, it is important to be aware that methemoglobinemia may occur even at doses much lower than the maximum recommended dose.

• Journal of the korean academy of Pediatric Dentistry
• /
• v.45 no.3
• /
• pp.393-399
• /
• 2018

The aim of this review is to introduce about the issue of benzocaine and methemoglobinemia. Through blocking the pain during dental treatment, fear and anxiety of patients will be reduced. Thus, anesthetic agent containing benzocaine is commonly used while controlling the pain of patients during treatment. However, on May 28, 2018, the Ministry of Food and Drug Safety reported a medication safety report about restricting the use of benzocaine-containing agents in infants under 24 months and children. Also, they recommended a cautious use to adolescents and adults to prevent methemoglobinemia (MHb). This report was published due to an advice from Food and Drug Administration (FDA) on May 23, 2018. When using agents containing benzocaine, dentists must consider the probability of MHb and prepare for early diagnosis and appropriate action. Since 1930s, methylene blue is known to cure MHb patients. Therefore, the proper use of methylene blue for emergencies and diagnosis methods for early diagnosis of MHb should be familiar to dentists planning for the use of topical anesthetic agents. Dentists should be trained for emergency situation of MHb caused by the use of benzocaine.

• Journal of Preventive Medicine and Public Health
• /
• v.26 no.2 s.42
• /
• pp.192-201
• /
• 1993

Epidemiologic investigation was conducted on January, 1993 in Seoul to identify the cause of an infant methemoglobinemia. Field investigation of the area of outbreak, survey of household and family members, analysis of ground water, and blood tests of involved family members were performed. Following results were obtained On analyzing the quality of the ground water on patient's household high levels of nitrate was found indicating contamination of water as the cause of a methemoglobinemia outbreak. On analysing the quality of the ground waters on seven other places within the neighborhood five were contaminated by nitrate in concentration that exceeded the permissible limit implying presence nearby source of contamination. Sources of contamination were thought to be originating from human waste in conventional bathroom facilities, chicken manure used in nearby orchards and plant fields or fertilizers. But the results of water analysis with presence of bacteria or E.coli, concentration of potassium, phosphate and the past history of diarrhea among family members, chicken manure suggested the most possible source of contamination. To evaluate the health status of members in the neighborhood past history was reviewed revealing no prior existence of patient with cyanosis and 65 people in the neighborhood had normal levels of methemoglobin concentration in their blood. Conclusively, the ground water on patient's household was contaminated with nitrate and despite provision of adequate water supply, family members of the patient along with their distrust in the water supply system had used ground water as their source of drinking water resulting of methemoglobinemia. Many suburban area of Seoul and country side thought to be having similar problems concerning contaminated ground water supply and dormant outbreak of patients as a result of the drinking of the contaminated water. Epidemiologic investigation and water analysis of ground waters are advised.