Methemoglobinemia Related to Local Anesthetics: A Summary of 242 Episodes

Guay, Joanne

doi:10.1213/ane.0b013e318187c4b1

Cited by 263 publications

(247 citation statements)

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“…25,26,37 The mechanism of anesthetic-induced methemoglobinemia is thought to occur as a result of direct oxidation of hemoglobin by amine metabolites derived from the amide-anesthetics. 37 Benzocaine use appears to have the highest incidence of methemoglobinemia. 37 However, many other drugs which possess oxidizing capacity can overwhelm the endogenous MetHb reductase and cause methemoglobinemia.…”

Section: Discussionmentioning

confidence: 99%

“…37 Benzocaine use appears to have the highest incidence of methemoglobinemia. 37 However, many other drugs which possess oxidizing capacity can overwhelm the endogenous MetHb reductase and cause methemoglobinemia. 25 In addition, direct exposure to inhaled NO can have significant impact on the systemic circulation and remote tissue perfusion via the action of stable NO metabolites.…”

Section: Discussionmentioning

confidence: 99%

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Plasma methemoglobin as a potential biomarker of anemic stress in humans

Hare

Romaschin

et al. 2012

Can J Anesth/J Can Anesth

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Purpose Transfusion of allogeneic red blood cells (RBCs) is one of the main treatments of acute anemia secondary to blood loss and fluid resuscitation within the operating room. Decisions to transfuse blood are based largely on intermediate biological markers (hemoglobin, arterial oxygen saturation, blood pressure, heart rate) which may not accurately reflect inadequacy of tissue oxygen delivery.Based on experimental studies, we hypothesized that anemia-induced tissue hypoxia activates adaptive mechanisms which promote local vascular nitric oxide (NO) production to improve tissue perfusion and survival during acute anemia. Hemoglobin (Hb) oxidation to methemoglobin (MetHb) may be a byproduct of such local NO production. Therefore, we tested the hypothesis that MetHb is a biomarker of hypoxic-anemic stress during acute hemodilution associated with cardiopulmonary bypass. Methods With institutional ethics approval, routine laboratory arterial blood gas and co-oximetry values were obtained from 295 patients undergoing heart surgery during February 1 to September 30, 2010, and the values were assessed retrospectively. All samples with an arterial oxygen saturation value C90% were included (n = 1,421). The maximal change in Hb associated with hemodilution on cardiopulmonary bypass was determined within 48 hr of surgery (n = 180). A chart review was performed to determine the incidence of RBC transfusion and exogenous nitrate administration. All anonymous data were analyzed by linear regression to determine the relationship between Author contributions Gregory M.T. Hare designed the research, performed the research, contributed novel intellectual input, analyzed the data, and wrote the paper. Alexander Mu performed the research, contributed novel intellectual input, and analyzed the data. Alexander Romaschin designed the research, performed the research, contributed novel intellectual input, and analyzed the data. Nadine Shehata designed the research, performed the research, contributed novel intellectual input, and analyzed the data. W. Scott Beattie designed the research, performed the research, contributed novel intellectual input, analyzed the data, and wrote the paper. C. David Mazer designed the research, performed the research, contributed novel intellectual input, analyzed the data, and wrote the paper. Albert K.Y. Tsui contributed novel intellectual input, analyzed the data, and wrote the paper. RésuméObjectif La transfusion de globules rouges alloge´niques est l'un des principaux traitements de l'ane´mie aigues econdaire a`une perte sanguine et au remplissage liquidien en salle d'ope´ration. La de´cision de transfuser du sang repose essentiellement sur des marqueurs biologiques interme´diaires (he´moglobine, saturation en oxyge`ne du sang arte´riel, pression arte´rielle, fre´quence cardiaque) qui pourraient ne pas refle´ter avec pre´cision l'insuffisance d'apport d'oxyge`ne aux tissus. A`partir d'e´tudes expe´rimentales nous avons fait l'hypothe`se qu'une hypoxie tissulaire induite par l'ane´mie act...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Plasma methemoglobin as a potential biomarker of anemic stress in humans

Hare

Romaschin

et al. 2012

Can J Anesth/J Can Anesth

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“…Regardless of the cause or predisposing condition, the final pathway is similar: oxidation of deoxyhemoglobin, converting the ferrous (Fe 2+ ) ion in heme to the ferric (Fe 3+ ) valence. This oxidized species of hemoglobin is unable to bind to oxygen and instead binds to a molecule of water [1,2]. Normally, when oxygen binds to deoxyhemoglobin, an electron is shared between the iron in heme and the oxygen molecule, thus, the iron is reversibly oxidized.…”

Section: What Is the Pathophysiologic Basis For Methemoglobin Formation?mentioning

confidence: 99%

“…In RBCs, there are both major (95%) and minor (5%) pathways to reduce methemoglobin back to its oxygen-carrying state. Cytochrome-b 5 reductase (also known as NADH methemoglobin reductase) is the primary pathway involved in this reduction [1][2][3][4][5]. An additional enzyme, nicotinamide adenine dinucleotide phosphate (NADPH) methemoglobin reductase, is also capable of reducing methemoglobin; although its activity is quite limited during normal physiologic conditions, it becomes highly significant in the presence of methylene blue (see Fig.…”

Section: What Is the Pathophysiologic Basis For Methemoglobin Formation?mentioning

confidence: 99%

“…Methemoglobinemia occurs when the formation of methemoglobin (via auto-or xenobiotic-induced oxidation of hemoglobin) occurs at a faster rate than cytochrome-b 5 reductase, and other non-enzymatic pathways can reduce it back to deoxyhemoglobin [1,2,7]. Auto-oxidation from O 2 forms a baseline methemoglobin fraction of approximately 0.5% [4].…”

Section: What Is the Pathophysiologic Basis For Methemoglobin Formation?mentioning

confidence: 99%

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Case Files of the Medical Toxicology Fellowship at Banner Good Samaritan Medical Center in Phoenix, AZ: Methemoglobinemia Following Dapsone Exposure

Canning

Levine

2011

J. Med. Toxicol.

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Acquired methemoglobinemia is a common, potentially fatal syndrome that can occur as a result of exposure to numerous xenobiotics. A case report of a 14-month-old female who developed methemoglobinemia following a dapsone ingestion. The child was treated with numerous boluses of methylene blue and ultimately required a continuous infusion of methylene blue. The common causes of methemoglobinemia, as well as the underlying pathophysiology, diagnosis, and treatment strategies are discussed.Keywords Methemoglobinemia . Methemoglobin . Dapsone . Cyanosis . Poisoning . Methylene blue Case PresentationA 14-month-old female infant presented to the emergency department (ED) with a chief complaint of cyanosis. The child had no significant past medical history and appeared normal throughout the prior day, except for some mild rhinorrhea and a single episode of non-bloody, non-bilious emesis the night prior to admission. An additional episode of emesis occurred the morning of admission. There were no other complaints, and the remainder of the review of systems was negative. The patient's mother noted cyanosis around the face and lips, prompting evaluation in the ED. The patient's room air oxygen saturation by pulse oximetry (SpO 2 ) was 87%, and a chest X-ray was negative. She was transferred to a pediatric tertiary care center for further evaluation of suspected congenital heart disease.On arrival to the referral center, the child was noted to be tachycardic, tachypneic, and cyanotic in mild respiratory distress. The pertinent abnormal vital signs were a heart rate of 212 beats per minute and a respiratory rate of 48 breaths per minute. The SpO 2 on 15 L of oxygen administered via a non-rebreather mask was 88%. The remainder of the physical examination was unremarkable. The venous blood gas (VBG) drawn on arrival revealed a pH of 7.42, a pCO 2 of 30 mmHg, a pO 2 of 43 mmHg, HCO 3 of 18.8 mmol/L, and methemoglobin, "high." The initial venous blood drawn for the laboratory testing was noted to have a brownish hue. The hemoglobin concentration was 13.0 g/dL, and the remainder of the baseline complete blood count and comprehensive metabolic profile were normal.Given the elevated methemoglobin fraction and clinical picture consistent with methemoglobinemia, the child received a 2-mg/kg IV bolus of methylene blue. The child's symptoms improved promptly and a repeat examination of the patient approximately 1 h later revealed an asymptomatic, playful child without cyanosis. A repeat VBG at this time revealed a methemoglobin fraction of 13.3%. The child was transferred to the PICU for further observation.

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