High dose vitamin C induced methemoglobinemia and hemolytic anemia in glucose-6-phosphate dehydrogenase deficiency.

Investigational use of intravenous vitamin C has been on the rise, but its side effects may be underreported. A 75-year-old woman presented with acute onset of jaundice, dark urine and shortness of breath after receiving 30 g of vitamin C infusion as an unconventional therapy for her hemifacial spasm. Diagnosis of methemoglobinemia and hemolytic anemia was made clinically and confirmed on laboratory tests. She recovered with supportive treatment and packed cell transfusion. Her previously unrecognised underlying condition of glucose-6-phosphate dehydrogenase (G6PD) deficiency was confirmed months after the initial presentation. This is the first reported case of methemoglobinemia and hemolytic anemia induced by high dose vitamin C in a female patient with G6PD deficiency. The dosage of vitamin C administered was also relatively low compared with previous adult reports. When administered at physiological dose, vitamin C can be used as an alternative to methylene blue in treatment of methemoglobinemia in patients with G6PD deficiency. However at supraphysiological dose vitamin C can paradoxically lead to hemolytic anemia in the same group of patients. Physicians should be alert of these potential complications of high dose vitamin C.

Local Anesthetic-Induced Methemoglobinemia During Pregnancy: A Case Report and Evaluation of Treatment Options.

BACKGROUND: Methemoglobinemia is a well-recognized adverse drug reaction related to the use of certain local anesthetic agents. The mainstay of treatment for methemoglobinemia is i.v. methylene blue, along with provision of supplemental oxygen; however, methylene blue is listed as a category X teratogen. This poses an issue should methemoglobinemia develop during pregnancy. CASE REPORT: A 35-year-old, 20-week and 5-day gravid female was transferred from an outpatient oral surgeon's office for hypoxia. She was undergoing extraction of 28 teeth and was administered an unknown, but "large" quantity of prilocaine during the procedure. Given this exposure, the concern was for methemoglobinemia. This was confirmed with co-oximetry, which showed 34.7% methemoglobin. The initial treatment plan was methylene blue; however, this drug is a category X teratogen. Thus, an interdisciplinary team deliberated and decided on treatment with high-dose ascorbic acid and transfusion of a single unit of packed red blood cells. The patient was managed with noninvasive ventilation strategies and a total of 8 g ascorbic acid. She was discharged on hospital day 3 with no obstetric issues noted. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Intravenous ascorbic acid appears to be a potential alternative to methylene blue in this patient population. The data surrounding teratogenicity of methylene blue are mostly related to intra-amniotic or intra-uterine administration. In life-threatening cases of methemoglobinemia during pregnancy, the benefits of i.v. methylene blue may outweigh the risks.

Methemoglobinemia induced by vegetable intake in infants in northern Spain.

BACKGROUND AND OBJECTIVE: Acquired methemoglobinemia (MHb) induced in infants by intake of vegetables is a condition uncommonly reported in the literature. The purpose of the present study was to study new vegetables involved and other epidemiological risk factors. METHODS: Seventy-eight cases of diet-induced MHb seen in Pamplona from 1987 to 2010 are reported. Infant characteristics were collected, and a case-control study was conducted using as controls 78 age- and sex-matched infants selected at the same geographic area. Bivariate logistic regression analyses were performed to detect factors involved in MHb occurrence. Nitrate levels were tested in natural vegetables used to prepare purées. RESULTS: A clear relation was found between MHb and use of borage (Borago officinalis) (OR 5.2; 95% CI 1.1-24.6) and maybe chard (Beta vulgaris var cicla) (OR 2.0; 95% CI 0.4-8.7), time from preparation to use (OR 17.4, 95% CI 3.5-86.3 if the purée had been prepared 24-48 hours before and OR 24.9, 95% CI 3.3-187.6 if prepared >48 hours before), and breast-feeding (OR 10.4; 95% CI 1.9-57.2). Tests confirmed that vegetables with the highest nitrate levels were borage (n = 15), with mean nitrate levels of 3968 mg/kg, and chard (n = 17), with mean levels of 2811 mg/kg. CONCLUSIONS: The main associated factors were shown to be time from purée preparation to use (>24 hours), use of certain vegetables (borage and chard), and breast-feeding. Nitrate levels in both vegetables implicated as etiological factors in acquired MHb are high.

Intoxicación por puré de acelgas / Poisoning by Swiss chard puree

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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.

Acquired methemoglobinemia: a rare but serious complication.

Topical and local anesthetics are employed during minor invasive procedures to increase patient tolerance and to reduce the need for intravenous sedation. A potentially fatal complication of these anesthetics is methemoglobinemia (Met-Hgb). Met-Hgb should be suspected in patients with cyanosis that does not respond to administration of oxygen and who have a discrepancy in oxygen saturation measured by pulse oximetry compared with the arterial partial pressure of oxygen (PaO2) determined by blood gas analysis. We present a patient who developed life-threatening Met-Hgb from the local anesthesia required during percutaneous endoscopic gastrostomy tube placement.

A nested case-control study of methemoglobinemia risk factors in children of Transylvania, Romania.

In this nested case-control study, we investigated the risk factors for methemoglobinemia (MHG) in 71 children in the Transylvania region of Romania. This study was unique in that the exposures for cases and controls were calculated as continuous values and were reported in milligrams per kilogram per day of nitrate/nitrite based on careful dietary reconstruction and environmental sampling. This procedure allowed us to compare point estimates of nitrate/nitrite exposure with other continuous, categoric, and ranked risk factors such as the presence or absence of diarrheal disease, reported severity of diarrheal disease, the use of vitamin supplements, the presence, absence, and/or duration of breast-feeding, and whether or not first-generation relatives experienced MHG. Analysis of these factors and exposure levels using both univariate and multivariate whole-model tests was performed to understand the relative significance of risk factors at varying levels of exposure to the development of MHG. Univariate and multifactorial analysis of risk factors for MHG underscored that, for this population, MHG is most strongly associated with nitrate/nitrite exposure through the dietary route (p = 0.0318), via feeding of formula and tea made with water containing high levels of nitrates, and that breast-feeding protects infants younger than 6 months of age (p = 0.0244). Our findings also raise questions about the role of diarrheal disease in the development of MHG, as likelihood ratios (likelihood 4.323, p = 0.0376) and multifactorial analysis indicated a significant role for diarrheal disease for some individuals.

Eight blue babies.

Methemoglobinemia is a serious medical condition that affects hundreds of infants in the United States each year. The condition involves the oxidation of red cell hemoglobin to a state that is unable to transport oxygen. Affected infants appear cyanotic and may have altered mental status. The condition is readily reversible if recognized and treated appropriately. The Wisconsin Division of Public Health investigates all cases of infant methemoglobinemia in an attempt to determine their cause. Between January 1990 and September 1999, 8 infants were diagnosed with this condition. Review of their hospitalization records found that 3 of these cases involved infants whose formula was prepared with water from nitrate-contaminated wels. Risk factors identified in the remaining cases included use of folk remedies, misuse of over-the-counter analgesics, and an inherited enzyme deficiency. Causes were not identified for 2 of the cases. All of the affected infants recovered.

Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning.

The optimum therapy for hydrogen sulfide poisoning is unclear. Adjuncts used in the treatment of cyanide poisoning have been advocated because of the shared mechanism of toxicity between hydrogen sulfide and cyanide. Following success in cyanide poisoning, hyperbaric oxygen therapy (HBO) has been suggested for use in treating hydrogen sulfide poisoning. A case of severe hydrogen sulfide poisoning was successfully treated with HBO after standard therapy was apparently ineffective. HBO as a therapeutic adjunct in hydrogen sulfide poisoning and the rationale for its use are discussed.

Citanest Forte--its use in oral surgery.

A clinical evaluation of Citanest Forte (brand of prilocaine HCL) was carried out on 3,000 oral surgery patients to determine the effectiveness and safety of the drug. Citanest Forte has been found to be a useful local anesthetic, and the results of this study would indicate that it can be effectively and safely substituted for other local anesthetic solutions currently in use for all routine oral surgery procedures.