Cases reported "Methemoglobinemia"

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1/47. methemoglobinemia after axillary block with bupivacaine and additional injection of lidocaine in the operative field.

    methemoglobinemia may occur after the administration of various drugs, including some local anesthetics. We report a patient with chronic renal failure and ischemic heart disease who developed clinically significant methemoglobinemia after an axillary block with bupivacaine and additional injection of lidocaine in the operative field. Although the two local anesthetics usually do not cause methemoglobinemia, we suspect that the displacement of lidocaine from protein binding by bupivacaine, in combination with metabolic acidosis and treatment with other oxidants, was the reason for the development of methemoglobinemia.
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2/47. methemoglobinemia induced by topical anesthesia: a case report and review.

    Topical anesthetic drugs are widely used by clinicians during hospital and outpatient procedures and are also available to the public in a variety of over-the-counter preparations. Although generally safe, they may cause potentially life-threatening methemoglobinemia. We describe a patient who developed repeated episodes of severe methemoglobinemia after administration of topical Cetacaine spray (a proprietary mixture of benzocaine, tetracaine, and butamben) employed for pharyngeal anesthesia before endotracheal intubation, and briefly review the etiology and pathophysiology of this disorder. Cautious interpretation of oxyhemoglobin saturation values obtained by pulse oximetry or estimated from arterial blood gas analysis is crucial lest the diagnosis of severe methemoglobinemia and the resulting hypoxemia are overlooked. If necessary, the condition is usually readily corrected by intravenous administration of methylene blue.
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3/47. Methaemoglobinemia in nitrobenzene poisoning.

    A young girl with nitrobenzene induced methaemoglobinaemia was saved by the timely use of mechanical ventilator, administration of oral methylene blue and parenteral ascorbic acid. Though parenteral methylene blue is the antidote of choice, due to its non-availability, the laboratory preparation of methylene blue have been utilized orally. The rare occurrence of such cases, and the efficacy of oral methylene blue and other supportive measures in evading death due to Nitrobenzene poisoning have been highlighted.
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4/47. benzocaine-induced methemoglobinemia during an outpatient procedure.

    Outpatient transesophageal echocardiography was performed in a 69-year-old man with a history of aortic valve repair. During the procedure the patient became markedly cyanotic and hypotensive. oxygen saturation measured by pulse oximetry decreased from 97% to the mid-80s. The man's condition continued to deteriorate. On transfer to a critical care unit, blood analysis by co-oximetry showed methemoglobin saturation of 67.8%. The patient's condition improved significantly after intravenous administration of methylene blue 1 mg/kg. With increasing numbers of outpatient procedures performed under topical anesthesia, measures should be in place to deal with a potential life-threatening adverse event such as methemoglobinemia.
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5/47. Unexpected cyanosis in the surgical patient.

    benzocaine is a commonly used topical anesthetic present in many over-the-counter preparations. The development of methemoglobinemia, associated with the use of benzocaine, is potentially fatal. methemoglobinemia remains unresponsive to the administration of oxygen alone and, in fact, results in greater tissue hypoxemia than the usual monitoring techniques indicate. We report two cases of benzocaine-induced methemoglobinemia occurring 3 months apart at the same institution. A brief discussion regarding methemoglobin is presented.
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6/47. Cyanotic child--can it be methaemoglobinemia?

    Methaemoglobinemia is a rare condition and can give surprise in emergency setup. We have encountered one such case in emergency recently that presented with both peripheral and central cyanosis without cardio-respiratory compromise. The patient was confirmed to be suffering from methaemoglobinemia due to antimalarials that he had received before coming to the hospital. cyanosis due to methaemoglobinemia in our patient was precipitated by concomitant glucose 6-phosphate dehydrogenase (G6PD) deficiency. The patient was managed with conservative management and vitamin C administration.
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7/47. Congenital methemoglobinemia: a rare cause of cyanosis in the newborn--a case report.

    cyanosis is a physical finding that can occur at any age but presents the greatest challenge when it occurs in the newborn. The cause is multiple, and it usually represents an ominous sign, especially when it occurs in association with neonatal sepsis, cyanotic congenital heart disease, and airway abnormalities. cyanosis caused by abnormal forms of hemoglobin can also be life-threatening, and early recognition is mandatory to prevent unnecessary investigations and delay in management. Abnormal hemoglobin, such as hemoglobin m, is traditionally discovered by electrophoresis, so the newborn screen, which is mandatory in several states, is a useful tool for the diagnosis. Although acquired methemoglobinemia, caused by environmental oxidizing agents, is common, congenital deficiency of the innate reducing enzyme is so rare that only a few cases are documented in the medical literature around the world. We present a neonate with cyanosis as a result of congenital deficiency of the reduced nicotinamide adenine dinucleotide-cytochrome b5 reductase enzyme. This infant was found to be blue at a routine newborn follow-up visit. sepsis, structural congenital heart disease, prenatal administration, and ingestion of oxidant dyes were excluded as a cause of the cyanosis by history and appropriate tests. Chocolate discoloration of arterial blood provided a clue to the diagnosis. A normal newborn screen and hemoglobin electrophoresis made the diagnosis of hemoglobin m unlikely as the cause of the methemoglobinemia (Hb A 59.4%, A2 1.8%, and F 38.8%). Red blood cell enzyme activity and dna analysis revealed a homozygous form of the cytochrome b5 reductase enzyme deficiency. He responded very well to daily methylene blue and ascorbic acid administration, and he has normal growth and developmental parameters, although he shows an exaggerated increase in his methemoglobin level with minor oxidant stress such as diarrhea.
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8/47. 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.
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9/47. methemoglobinemia secondary to automobile exhaust fumes.

    methemoglobinemia is an uncommon cause of cyanosis. A 28-year-old male presented to the emergency department cyanotic and short of breath after exposure to noxious automobile fumes. He did not improve with the administration of 100% oxygen therapy. The initial arterial blood gas with cooximetry was: pH of 7.38, PaCO2 of 43 mm Hg, PaO2 of 118 mm Hg, measured oxygen saturation of 70%, and a methemoglobin level of 24.8%. methylene blue was given (2 mg/kg intravenously) and the patient's symptoms resolved. On the following day he was discharged home without complication. A comprehensive review of the literature revealed no reported cases of methemoglobinemia secondary to accidental exposure to exhaust fumes.
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10/47. A severe methaemoglobinemia induced by nitrates: a case report.

    Methaemoglobinemia is a disorder in which the haemoglobin molecule is functionally altered and prevented from carrying oxygen. A variety of aetiologies including genetic, dietary, idiopathic and toxicological sources may cause methaemoglobinemia. Symptoms vary from mild headache to coma or death, and may not correlate with measured methaemoglobin concentrations. patients with methaemoglobinemia appear deeply cyanotic, but are unresponsive to standard oxygen therapy. It is essential for the clinician to recognize the problem rapidly in patients without hypoxia by analysing their arterial blood gas. Methaemoglobin interferes with the accuracy of pulse oximetry. The antidote is methylene blue. We report a very unusual and dramatic case of methaemoglobinemia. A 23-year-old girl who arrived in the emergency department in a state of confusion with intense cyanosis. The night before she had drunk water with ice defiled by ammonium nitrate, poured from a broken pack of instant ice. The absence of improvement after the administration of oxygen and the 'chocolate brown' colour of the arterial blood gave us the most important clue in suspecting the diagnosis of methaemoglobinemia.
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