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PubMed2000

A case of methemoglobinemia type II due to NADH-cytochrome b5 reductase deficiency: determination of the molecular basis.

Clinical, biochemical and molecular findings in a patient with methemoglobinemia type II are described. Furthermore, a comparison between methemoglobinemia type I and type II, both caused by a deficiency of NADH-cytochrome b5 reductase (b5R), is made. Although the clinical pictures of type I and II are strikingly different, mutations in the diaphorase (DIA1) gene located on chromosome 22 have been described in both types. In the present patient, two newly identified mutations, both leading to a stop codon in exon 4 (Gln77Ter) and in exon 6 (Arg160Ter), were found. Identification of different mutations at different positions in the DIA1 gene might shed light on the clinical and biochemical differences between methemoglobinemia type I and type II.

Child↗

PubMed1994

Chronic methemoglobinemia: improving hemoglobin saturation monitoring during anesthesia.

Methemoglobin interferes with the accuracy of pulse oximetry data. Methemoglobinemia is caused by many factors, both congenital and acquired. However, the increasing usage of dapsone, which converts hemoglobin to methemoglobin, is increasing the number of patients with methemoglobinemia. We present the case of a patient with dapsone-induced methemoglobinemia who was successfully treated with methylene blue, which converts methemoglobin back to hemoglobin.

Aged↗

PubMed2005

Prophylactic methylene blue in a patient with congenital methemoglobinemia.

PURPOSE: To report the beneficial effect of prophylactic methylene blue administration before induction of anesthesia in a patient with congenital methemoglobinemia. CLINICAL FEATURES: A 26-yr-old male patient known to have congenital methemoglobinemia was scheduled for turbinectomy under general anesthesia. The patient was clinically cyanotic with a pulse oximetry of 91%. Arterial blood gas analysis showed a partial pressure of oxygen (PaO(2)) of 81.3 mmHg associated with a fractional oxyhemoglobin of 80.7%, and a methemoglobin fraction of 0.159. Preoperative iv administration of 1 mg.kg(-1) of methylene blue resulted, within five minutes, in a decrease of methemoglobin fraction down to 0.05 associated with an increase of the fractional oxyhemoglobin saturation up to 94.7%. After two hours, the methemoglobin fraction decreased to 0.01 and the fractional oxyhemoglobin concentration increased to 97.7%. Induction of anesthesia as well as intraoperative and postoperative course were uneventful without any episode of hypoxemia. Postoperatively, the methemoglobin fractions remained low for 24 hr, to be followed by a gradual increase up to 0.02 on the second day to reach 0.094 on the fifth day. CONCLUSION: The prophylactic preoperative methylene blue administration in a patient with congenital methemoglobinemia significantly decreased the methemoglobin level and increased the fractional oxygen saturation with a consequent increase of the safety margin against perioperative hypoxemia.

Adult↗

PubMed2005

Methemoglobinemia induced by automobile exhaust fumes.

Although methemoglobinemia is an uncommon disorder, it should always be considered in the differential diagnosis of cyanosis. Major causes of acquired methemoglobinemia are nitrates, aniline, and analgesics, though rare cases have been reported to have been caused by automobile exhaust fumes. A 24-year-old man had inhaled a large amount of automobile exhaust fumes, intending to commit suicide. He had become unconscious, with dilated pupils and symptoms of cyanosis. Arterial hemoglobin oxygen saturation (Sp(O2)) was 86%, with a methemoglobin level of 44.3% and a carboxyhemoglobin level of 0%, while electrolytes, blood urea nitrogen, creatine, and glucose measurement results were normal. He was treated with methylene blue 250 mg (approximately 4 mg/kg) through a nasogastric tube. Four hours after the treatment, because the methemoglobin level was slightly above normal (2.2%), we added 180 mg of methylene blue. The results of final arterial blood gas analysis were a methemoglobin level of 0.4% and a carboxyhemoglobin level of 0.8%. He recovered uneventfully and returned home by himself the next day. To summarize, we successfully treated, with methylene blue given through a nasogastric tube, a young man who had developed severe methemoglobinemia from inhaling automobile exhaust fumes.

Adult↗

PubMed1984

Benzocaine-induced methemoglobinemia during general anesthesia.

A case is reported in which a patient developed cyanosis under general anesthesia due to methemoglobinemia. The cause of the methemoglobinemia was benzocaine applied topically to the pharynx and trachea. When confronted with cyanosis in the absence of cardiac or pulmonary disease, one must seriously consider the diagnosis of methemoglobinemia. Supplemental oxygen should be administered and methylene blue given intravenously. If possible, determination of arterial blood gases should be made to obtain the methemoglobin concentration. Finally, all medical and dental personnel using benzocaine should be aware of the recommended dose and the possible complications of overdosage.

Adult↗

PubMed1985

An infant with sepsis and methemoglobinemia.

A 3-week-old child arrived at the emergency room with the concurrent onset of sepsis and methemoglobinemia associated with diarrhea. Subsequently, the child had two recurrent episodes of methemoglobinemia with re-exacerbations of his diarrhea. Possible causes and associations of methemoglobinemia are presented: particular emphasis is placed on the early recognition and rapid diagnosis of this life-threatening condition.

Acidosis↗

PubMed1996

[Pulse oximetry and methemoglobinemia].

BACKGROUND: Cyanosis associated to low oxygen saturation may reveal hemoglobin pathology. CASE REPORT: A 3 year-old child had a nephroblastoma with pleural effusion. He suddenly developed persistent cyanosis despite pleural effusion drainage; transcutaneous and measured oxygen saturations were low and PaO2 on arterial blood gases was high. Methemoglobinemia was diagnosed, due to prilocaine-lignocaine cream used for local anesthesia, associated to partial G6PD deficiency. The methemoglobinemia disappeared after methylene blue treatment. CONCLUSION: Cyanosis with low oxygen saturation and high or normal PaO2 should lead to the search of a hemoglobin pathology, especially methemoglobinemia, by appropriate methods.

Anesthetics, Local↗

PubMed2005

Methemoglobinemia revisited: an important complication after transesophageal echocardiography.

Methemoglobinemia induced by the use of benzocaine-containing topical anesthetics is a rare, but potentially lethal complication after transesophageal echocardiography (TEE). We report a patient who developed methemoglobinemia after TEE. A review of the literature was performed and the majority of cases of benzocaine-induced methemoglobinemia reported thus far have occurred in patients undergoing TEE, endotracheal intubation, esophagogastroduodenoscopy, and bronchoscopy. All of these procedures have become more frequent than before, and there is a need to reemphasize the potential problem and to reconsider the need for further use of topical anesthetics.

Aged, 80 and over↗

PubMed2006

Methemoglobinemia and acute hemolysis after tetracaine lozenge use.

Acquired methemoglobinemia is a rare but severe condition associated with oxidizing stressors, most notably medications. Although the symptoms can be life threatening, they usually respond promptly to exposure cessation and methylene blue injection. We describe the first case of methemoglobinemia associated with tetracaine lozenge use. A previously healthy 33-year-old man was admitted with fever, respiratory distress, cyanosis, and acute hemolysis. Physical findings and chest radiograph were normal. Low pulse oximetry readings contrasted with normal partial pressure of oxygen and calculated oxygen saturation. The methemoglobin level was 10.8%. The patient recovered with methylene blue injection and blood transfusions. He reported recent self-medication with tetracaine lozenges for a sore throat during a flu-like illness. No other cause of methemoglobinemia was found.

Acute Disease↗

PubMed2006

The role of methemoglobinemia in early and late complicated pregnancy.

The objective of this review was to direct attention about methemoglobin as a biomarker which has an important role in the detection of adverse effects of the oxidative stress, misbalanced production of ROS, RNS and RSS. According to our hypothesis, a pregnant woman continuously inhaling environmental toxics as fuel burning products, will traverse three, not two from current thought, distinct stages. The main difference among present three-stage hypothesis and other hypotheses is the assertion that, in the pathogenesis of early and late complicated pregnancy, methemoglobin takes on an important role. Secondly, we also observed the utero-placental changes as "locus manifesting minoris resistentiae" in complicated pregnancy are not the causes but a consequence of increased systemic oxidative stress. Methemoglobin and hemolysis both occur as a result of oxidative stress, but the prevalent difference between them is that methemoglobin is a reversible phenomenon (oxidant-antioxidant balance) whereas hemolysis, which occurs as a result of oxidative stress on the erythrocyte membrane, is an irreversible event. Methemoglobinemia can additionally exacerbate an existing anemia, stimulating hypoxia that may be dangerous for both mother and fetus. Own prospective study of methemoglobin in pregnancy, revealed a significant rise in the level of methemoglobin >1.5 g/L (r=0.72, p<0.01) in the exposure period, which can be explained on the basis of an oxidant-antioxidant imbalance, resulting in methemoglobinemia. Methemoglobinemia and stillbirth recorded throughout exposure period are significantly higher than those recorded in the control period (p=0.0205), and the frequencies of reproductive loss were significantly lower in the control than in the exposure period (p<0.05). Results suggest that methemoglobin as individual indicator of oxidative stress is an early marker of the identification of women with a pregnancy risk. It has the advantage of being applicable some time before ultrasonic examination becomes feasible. Further support for this assumption will require further investigations that may lead to the supposition that increasing level of methemoglobin is related to environmental toxicities complicated pregnancy and IUGR, preeclampsia, and a high percentage of perinatal mortality and morbidity.

Biomarkers↗

PubMed1987

Methemoglobinemia from intravenous nitroglycerin: a word of caution.

The dose of intravenously administered nitroglycerin (IV NTG) used to control ischemic chest pain usually is limited by hypotension from decreased preload. Herein we describe 2 patients who tolerated IV NTG without hemodynamic compromise but in whom severe impairment of blood oxygen content developed from methemoglobinemia noted during coronary bypass surgery. Methemoglobinemia must be suspected if chocolate-brown blood is encountered despite a normal arterial oxygen tension and calculated oxygen saturation. Before a methemoglobin level is available, the extent of hypoxemia can be determined by an oximetric oxygen saturation and therapy begun with intravenous administration of methylene blue. These case reports focus attention on the potential deleterious effects of undetected hypoxemia from methemoglobinemia in patients being stabilized with high-dose IV NTG for urgent cardiac surgery.

Aged↗

PubMed2002

Methemoglobinemia following chromopertubation in treated pelvic tuberculosis.

Methylene blue administered through cervix is used to check tubal patency at laparoscopy. Although methylene blue is used to treat methemoglobinemia it can also produce methemoglobinemia in susceptible individuals. A case of methemoglobinemia induced by methylene blue in a patient with treated pelvic tuberculosis is presented.

Adult↗

PubMed1993

Dietary protein intolerance in infants with transient methemoglobinemia and diarrhea.

Of 17 infants requiring hospitalization for primary soy or cow milk protein intolerance, six infants (35%) had transient methemoglobinemia. Reexposure to the offending protein caused diarrhea, metabolic acidosis, and transient methemoglobinemia in all patients. These six patients represented 65% of the total hospitalizations resulting from methemoglobinemia of any cause.

Acidosis↗

PubMed1981

Acute toxic methemoglobinemia following dental analgesia.

This communication reports a case of acute toxic methemoglobinemia associated with hypoxia and general motor seizures following dental anesthesia using nitrous oxide and prilocaine hydrochloride. The dosage of prilocaine hydrochloride used was 5.6% of the recognized toxic dosage associated with clinical methemoglobinemia. The patient had no demonstrable congenital tendency toward methemoglobinemia, suggesting this case may represent a previously unreported and potentially fatal reaction to prilocaine hydrochloride. The etiology of the methemoglobin production, the diagnosis of the syndrome, and the emergency treatment are discussed.

Acute Disease↗

PubMed1988

Methemoglobinemia due to ingestion of N,N-dimethyl-p-toluidine, a component used in the fabrication of artificial fingernails.

An acute cyanotic episode due to methemoglobinemia occurred in a 16-month old girl following the ingestion of N,N-dimethyl-p-toluidine, a commercially available component used in the production of artificial fingernails. The amount of the parent compound ingested was about 6 mg/kg of body weight. Administration of methylene blue was effective in the reversal of the methemoglobinemia. In vitro studies suggest that the activity of the compound was probably due to its biochemical transformation to the toxic metabolite p-methylphenylhydroxylamine. We expand the list of aromatic amino or nitro compounds and their derivatives capable of producing methemoglobinemia and call attention to the hazard of their ingestion.

Accidents, Home↗

PubMed1999

Methemoglobinemia as an uncommon cause of cyanosis.

Cyanosis is usually caused by decreased arterial oxygen saturation due to pulmonary or cardiac diseases. Methemoglobinemia is a rare cause, sometimes with lethal outcome. Two patients are described, both with an unremarkable cardiopulmonary history, presented with severe cyanosis due to aniline-induced methemoglobinemia that developed at work. The symptoms and the treatment of methemoglobinemia are discussed.

Adult↗

PubMed1999

Methemoglobinemia secondary to topical silver nitrate therapy--a case report.

Methemoglobinemia is a rare complication in individuals exposed to nitrates or nitrites. Whereas methemoglobinemia is a recognized potential complication in burn patients treated with topical 0.5% silver nitrate solution, no report of methemoglobinemia in burn patients has been present in the literature for more than 15 years. We raise consciousness about this complication with a case report of a 12-month-old child with necrotizing fasciitis resulting from a cutaneous flank infection. The patient developed cyanosis 20 days after initiation of topical treatment with 0.5% silver nitrate solution. Intravenous injection of methylene blue can restore normal blood oxygenation.

Administration, Topical↗

PubMedDate not supplied

Toxic methemoglobinemia caused by topical anesthetic given before transesophageal echocardiography.

Transesophageal echocardiography was performed on a patient with critical aortic stenosis and severe three-vessel coronary artery disease. Immediately after the procedure the patient experienced marked cyanosis (oxygen saturation of 53%) secondary to methemoglobinemia (methemoglobin saturation of 45%). Toxic methemoglobinemia was thought to be caused by topical anesthetic. He responded dramatically to treatment with intravenous methylene blue. Toxic methemoglobinemia should be suspected in unexplained cyanosis occurring after transesophageal echocardiography and other endoscopic procedures during which potentially causative agents have been used.

Aerosols↗