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At least 73 records · Page 4Linked to original sources

PubMed1992

Methemoglobinemia in a patient undergoing gastrointestinal endoscopy.

OBJECTIVE: To report a case of methemoglobinemia induced by benzocaine in a patient undergoing gastrointestinal endoscopy. CASE SUMMARY: Before undergoing an upper gastrointestinal endoscopy, a 15-year-old girl received 20% benzocaine as a spray, to locally anesthetize the pharyngeal mucosa. Thirty minutes after the endoscopy, the patient suddenly became cyanotic, short of breath, and comatose. She was intubated and transferred to the intensive care unit. Her blood methemoglobin concentration was 54 percent. The patient was treated with intravenous methylene blue. Four hours later she was extubated. She was alert, awake, and asymptomatic. DISCUSSION: This is the fourth reported case of methemoglobinemia induced by benzocaine spray in patients undergoing gastrointestinal endoscopy. Pathways for the formation of methemoglobin in the body are reviewed. Intravenous methylene blue is the drug of choice for this condition, and produces rapid and dramatic reversal of methemoglobinemia. CONCLUSIONS: It is common to use benzocaine spray prior to upper gastrointestinal endoscopy. Benzocaine rarely induces methemoglobinemia in these patients. Prompt diagnosis and treatment with intravenous methylene blue is warranted in such cases.

Adolescent↗

PubMed2004

Drinking-water nitrate, methemoglobinemia, and global burden of disease: a discussion.

On behalf of the World Health Organization (WHO), I have undertaken a series of literature-based investigations examining the global burden of disease related to a number of environmental risk factors associated with drinking water. In this article I outline the investigation of drinking-water nitrate concentration and methemoglobinemia. The exposure assessment was based on levels of nitrate in drinking water greater than the WHO guideline value of 50 mg/L. No exposure-response relationship, however, could be identified that related drinking-water nitrate level to methemoglobinemia. Indeed, although it has previously been accepted that consumption of drinking water high in nitrates causes methemoglobinemia in infants, it appears now that nitrate may be one of a number of co-factors that play a sometimes complex role in causing the disease. I conclude that, given the apparently low incidence of possible water-related methemoglobinemia, the complex nature of the role of nitrates, and that of individual behavior, it is currently inappropriate to attempt to link illness rates with drinking-water nitrate levels.

Adolescent↗

PubMed1999

Infantile methemoglobinemia: reexamining the role of drinking water nitrates.

Ingestion of nitrates in drinking water has long been thought to be a primary cause of acquired infantile methemoglobinemia, often called blue baby syndrome. However, recent research and a review of historical cases offer a more complex picture of the causes of infantile methemoglobinemia. Gastrointestinal infection and inflammation and the ensuing overproduction of nitric oxide may be the cause of many cases of infantile methemoglobinemia previously attributed to drinking water nitrates. If so, current limits on allowable levels of nitrates in drinking water, which are based solely on the health threat of infantile methemoglobinemia, may be unnecessarily strict.

Diarrhea, Infantile↗

PubMed2005

Methemoglobinemia secondary to topical benzocaine use in a lung transplant patient.

OBJECTIVE: To report a case of methemoglobinemia secondary to the administration of topical benzocaine spray in an anemic patient who had previously undergone a lung transplant. CASE SUMMARY: A 40-year-old white man with a past medical history significant for lung transplant acutely decompensated following oropharyngeal administration of topical benzocaine spray. Subsequent blood analysis revealed a methemoglobin concentration of 51.2%. Following the administration of a single dose of methylene blue 2 mg/kg intravenously, the patient's respiratory status dramatically improved and stabilized. DISCUSSION: Methemoglobinemia is a rare but potentially fatal condition that may be either acquired or congenital; however, the disorder is most commonly acquired secondary to exposure to oxidizing chemicals, which are often routinely prescribed medications, including benzocaine. Benzocaine can react with hemoglobin to form methemoglobin at a rate that exceeds reduction capabilities, which may result in oxygenation difficulty and respiratory distress. In severe or symptomatic methemoglobinemia, the treatment of choice is methylene blue. CONCLUSIONS: Application of the Naranjo probability scale established a highly probable relationship between topical benzocaine spray and methemoglobinemia and associated respiratory compromise. The risks of palliative use of topical benzocaine in patients with preexisting disorders that compromise oxygen delivery may outweigh any benefit. In our patient, anemia and lung disease increased his risk for clinically significant adverse respiratory events secondary to deficiencies or interferences in oxygen delivery. Topical benzocaine should be administered with caution and careful monitoring in such patient populations.

Administration, Topical↗

PubMed2005

Hemolysis and methemoglobinemia secondary to rasburicase administration.

OBJECTIVE: To report a case of hemolytic anemia and methemoglobinemia developing after rasburicase administration to a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency. CASE SUMMARY: A 50-year-old African American man was hospitalized with new onset seizure, diabetic ketoacidosis, respiratory failure, and acute renal failure. Serum uric acid concentrations were elevated, and the patient was treated with one dose of intravenous rasburicase 22.5 mg for acute renal failure secondary to hyperuricemia. Routine arterial blood gas analyses performed after rasburicase was administered revealed elevated methemoglobin concentrations, which peaked at 14.7%. Hemolytic anemia developed as evidenced by a fall in blood hemoglobin from 14.8 to 5.3 g/dL. The patient made a full recovery following aggressive fluid therapy, blood transfusions, and respiratory support. G6PD deficiency was subsequently confirmed. The Naranjo probability scale indicated that rasburicase was a probable cause of hemolytic anemia and methemoglobinemia. DISCUSSION: Rasburicase is contraindicated in patients with G6PD deficiency as it may cause hemolytic anemia and methemoglobinemia. As of September 26, 2005, simultaneous occurrence of hemolytic anemia and methemoglobinemia has not been reported in patients receiving rasburicase. CONCLUSIONS: As of September 26, 2005, screening for G6PD deficiency should be performed whenever possible prior to chemotherapy administration in patients at risk of developing tumor lysis syndrome.

Anemia, Hemolytic↗

PubMed2005

Topical benzocaine (Hurricaine) induced methemoglobinemia during endoscopic procedures in gastric bypass patients.

BACKGROUND: Methemoglobinemia results from oxidation of ferrous to ferric iron in hemoglobin. In addition to a functional anemia, methhemoglobinemia causes the O2-binding affinity of the remaining O2 sites in the hemoglobin tetramer to increase; essentially shifting the oxyhemoglobin dissociation curve to the left and decreasing O2 delivery. Patients develop profound cyanosis unresponsive to O2 when methemoglobin (MHb) levels exceed 10%. It can be lethal if levels exceed 70%. Benzocaine 20% (Hurricaine) spray, commonly used in endoscopy (EGD) can cause methemoglobinemia. We report our experience. METHODS: Two patients out of >1,000 EGDs in 4 yrs developed methemoglobinemia. RESULTS: Patient 1: 34 F, BMI 46, open distal gastric bypass. Patient 2: 26 F, BMI 49, laparoscopic proximal gastric bypass. Both had nausea and vomiting from stomal stenosis requiring EGD for which benzocaine 20% spray was used. Severe cyanosis (despite pulse oximetry readings of 86% and 89%), dyspnea and tachycardia, were seen within 13 and 7 minutes. They were unresponsive to O2, despite being awake and conversant after complete reversal of sedatives. MHb levels were 35.6% and 18.8% (normal <1%). Patients dramatically improved after 1% methylene blue at 1-2 mg/kg IV over 5 minutes. MHb levels dropped to 2.3% and 0.8 % within 150 and 110 minutes. Neither patient had any evidence of pulmonary embolism or DVT or G6PD deficiency. CONCLUSION: Topical benzocaine 20% (Hurricaine) spray used in EGDs gets absorbed and can cause methemoglobinemia. Sprays should be limited to 1 second. Prompt treatment with 1% methylene blue IV can be life-saving.

Administration, Topical↗

PubMed2000

Benzocaine-associated methemoglobinemia following bronchoscopy in a healthy research participant.

Benzocaine (ethyl aminobenzoate) is a local anesthetic commonly used to achieve topical anesthesia of the skin and mucous membranes prior to endoscopic procedures. Methemoglobinemia, a condition in which hemoglobin cannot bind and deliver oxygen normally, has been associated with benzocaine use in various patient populations. This is the first report of benzocaine-associated methemoglobinemia occurring in a healthy research participant. The research participant developed a methemoglobin level of 27% and marked cyanosis. No adverse sequelae other than cyanosis were identified. This report extends the population in which benzocaine-associated methemoglobinemia has been described. Additionally, this report supports the observation that methemoglobin levels approaching 30% may be tolerated in otherwise healthy individuals, producing few clinically important effects. Finally, this case also indicates that, in obtaining informed consent for a procedure in which benzocaine will be administered, patients and research participants should be specifically informed of the risk of benzocaine-induced methemoglobinemia. This information is especially important in those settings in which the manufacturer-recommended dose of benzocaine may either intentionally or inadvertently be exceeded.

Administration, Topical↗

PubMed1992

Methemoglobinemia induced by a benzocaine-based topically administered anesthetic in eight sheep.

Benzocaine-based anesthetic sprays are commonly used in sheep to anesthetize the nasal passages and glottis before intubation. Sprays containing benzocaine have been identified as causing methemoglobinemia in dogs, cats, and human beings. Diagnosis of benzocaine-induced methemoglobinemia was made in 8 Dorset-Finn ewes exposed to a 2-second burst of (approx 56 to 112 mg of benzocaine) anesthetic spray. Venous blood samples taken 10 to 20 minutes after intranasal application of the spray revealed methemoglobinemia of 22.6 +/- 1.8% (mean +/- SD) in 9 samples from 8 ewes. Four other ewes intentionally exposed did not have methemoglobinemia. Topical use of benzocaine-containing anesthetics in sheep is not recommended. The high methemoglobin concentration induced by this product may substantially alter the cardiovascular and pulmonary function, blood gas analyses, and exercise capacity, thereby compromising animal health and/or research results. Although it appears that minimal clinical signs are induced in healthy animals, the risks of compromising a subclinically ill animal do not offset the benefits of this product.

Administration, Topical↗

PubMed1997

[Arginine-glutamine replacement at residue 57 of NADH-cytochrome b5 reductase in Chinese hereditary methemoglobinemia].

OBJECTIVE: To elucidate the molecular mechanism of NADH cytochrome b5 reductase (Cytb5R) deficiency in hereditary methemoglobinemia. METHODS: Cytb5R cDNA was cloned from white blood cells from patient with hereditary methemoglobinemia by RT-PCR method, and the genomic DNA from 3 pedigrees with hereditary methemoglobinemia were analyzed by restriction enzyme analysis. RESULTS: On sequencing the cDNA, two missense mutation were found. One is CGG-->CAG at codon 57 of exon 3, caused Arg-Gln replacement. The other is GAG-->GGG at codon 222 of exon 8. The former mutation abolishes the Msp I recognition site which was confirmed in two of three hereditary methemoglobinemia family. The latter mutation generates a recognition site for Bsi Y I. Amplification of exon 8 by PCR followed by digestion with Bsi Y I revealed no mutation in all patients from the three families. CONCLUSION: Arg57-Gln replacement is responsible for Cytb5R deficiency in the two Chinese pedigrees.

Adult↗

PubMed2005

Heterogeneity of the molecular biology of methemoglobinemia: a study of eight consecutive patients.

Congenital methemoglobinemia can be caused by mutations involving five different genes. We studied the etiology and molecular biology of eight consecutive patients with methemoglobinemia. Four had b5R mutations; two were novel. A novel intronic mutation caused markedly reduced mRNA resulting in type II methemoglobinemia. Three patients had acquired methemoglobinemia without any b5R mutations.

Amino Acid Substitution↗

PubMed1992

Fatal methemoglobinemia caused by inadvertent contamination of a laxative solution with sodium nitrite.

We describe two cases of fatal methemoglobinemia resulting from ingestion of laxative solution inadvertently contaminated with sodium nitrite. Postmortem toxicological examination revealed methemoglobin levels in excess of 75% in both patients--a level that is uniformly fatal. The laxative solution was found to contain sodium nitrite instead of sodium sulphate at a concentration of 15 g/l. The pathophysiology of methemoglobinemia and a review of other reported cases of toxic methemoglobinemia are presented. Marked cyanosis in the face of intact cardiorespiratory function should alert the physician to the possibility of toxic methemoglobinemia.

Aged↗

PubMed1983

[Methemoglobinemia in acute diarrhea in infants].

8 cases of methemoglobinemia are observed in infants of 28 days to 138 days of age, who have all acute diarrhea. They are divided in two groups. --4 infants who have eaten for a long time a rich nitrate and nitrite content carrot soup. --4 cases of severe diarrhea with probable endogenous nitrification due to microbial proliferation. The methemoglobinemia level is here not very high and represents more a witness that an alarming symptom. Those infants are compared with 10 infants who have diarrhea without methemoglobinemia. Symptoms and treatment of methemoglobinemia are revisited.

Acute Disease↗

PubMed1981

Methemoglobinemia induced by local anesthetics.

A case of methemoglobinemia secondary to topical local anesthetic agents is reported. A 28-year-old, 80-kg white man was admitted to a hospital for respiratory distress two days after an accident. During intubation, Cetacaine (benzocaine, butamben, and tetracaine) spray and Americaine (benzocaine) ointment were used topically for local anesthesia. Ninety minutes later, the patient was cyanotic despite ventilation, and an arterial blood sample was chocolate-brown and contained 29 d/dl methemoglobin (normal less than 1.7 g/ dl). Methylene blue, 80 mg as a 1% solution in 5% dextrose in water, was infused over 20 minutes, and hte patient's cyanosis disappeared within the next 30 minutes. The following afternoon, the patient was reintubated, using 4% lidocaine and benzocaine as local anesthetics. He again developed cyanosis. Methylene blue again cleared the cyanosis. Abnormal hemoglobin variants and NADH-methemoglobin reductase deficiency were ruled out as sources of methemoglobinemia. A discussion of methemoglobinemia, including biochemistry, pathogenesis, symptomatology, and management, is presented. If cyanosis occurs following application of local anesthetics, methemoglobinemia secondary to these drugs should be considered in the differential diagnosis.

4-Aminobenzoic Acid↗

PubMed1980

Acute methemoglobinemia induced by topical benzocaine and lidocaine.

Acute methemoglobinemia may result from the use of several local anesthetic agents. Benzocaine (Cetacaine) spray has been shown previously to cause methemoglobinemia in two patients when applied topically to the mucous membranes. We describe a patient with respiratory failure following trauma who had two episodes of acute methemoglobinemia, one after the topical application of benzocaine and the second following lidocaine administration for endotracheal intubation. The episodes occurred more than 20 hours apart, and no other drugs known to induce methemoglobinemia were given. On both occasions, intravenous methylene blue was effective in correcting the disorder.

Adult↗

PubMed1994

[Another reason for cyanosis--methemoglobinemia].

Intraoperative cyanosis is an utmost emergency for anesthesiologist. If the patient has adequate control ventilation, and normal cardiac pulmonary physiology, then methemoglobinemia must be considered. Reported here is a normal female with dark color lip on the second day after her second parturition and was undergoing tubal ligation. Twenty minutes after induction of general anesthesia and endotracheal intubation, dark blood at the incision site was noted by the operator. After emergent check up of the anesthesia machine, tubings, breathing sound and arterial blood gas, there was only one suspicion left. Methemoglobinemia was confirmed by the hematological examination. Methemoglobinemia is a product from the oxidation of the iron atom in the heme ring when oxygen dissociates from it. This process exists in nature, but can also be induced by nitrate or nitrite-containing drugs or foods or benzene-like organic compounds. Methemoglobinemia can be differentiated from normal hemoglobin by mass spectrometry. If acute illness develops, patients should be treated with methylene blue. Otherwise ascorbic acid will do. This case is reported to remind all anesthesia personnel about one of the rare but serious hemoglobinopathy.

Adult↗

PubMed1996

The concentrations of nitrates and nitrites in food products and environment and the occurrence of acute toxic methemoglobinemias.

In the study it was intended to evaluate the concentration of nitrates and nitrites in some food products and samples of potable water collected in Kraków region and compile these results with frequency of recognised toxic methemoglobinemia cases. In the years 1991-1993 91 food samples, 288 samples of tap water from the central waterworks of Kraków and 399 samples of well-water from the country side of Kraków region were collected. In the chemical laboratories the nitrates and nitrites concentration has been defined. The clinical material of inpatients from 2 hospitals of Kraków and the data from the Poison Information Centre in Kraków have been analysed. The examined food samples did not present, in general, raised levels of nitrates and nitrites. Also the tap water samples presented a low concentration of these substances. The well-water samples demonstrated in considerable percentage increased levels of nitrates and nitrites and exceed the level permitted by sanitary law. In the Provincial Childrens Hospital during recent 14 years 8 infants with recognised methemoglobinemia were treated. All cases were connected with environmental pollution. At the Department of Toxicology, where only adults are treated, no methemoglobinemia cases resulting from environmental pollution during recent 26 years were hospitalized. The Poison Information Centre during recent 14 years consulted 239 cases of methemoglobinemia; 90% of them concerned children intoxicated because of environmental pollution.

Environmental Monitoring↗

PubMed1996

Food-borne nitrates and nitrites as a cause of methemoglobinemia.

Methemoglobinemia is a potentially fatal condition. Previous reports of toxic methemoglobinemia due to food-borne nitrates and nitrites are reviewed. Contamination of food during manufacture or degradation of nitrates in vegetables appear to be the most important factors. Some food items, such as refrigerated "dim-sum", stuffed pork and Chinese sausages, are very popular among some Asian populations; a stringent control against the excessive use of nitrates and nitrites is required in order to prevent outbreaks of toxic methemoglobinemia. Patients with glucose-6-phosphate dehydrogenase deficiency, a common condition in some Asian populations, may present with methemoglobinemia and intravascular hemolysis following exposure to oxidant drugs or chemicals. Methylene blue is inefficient and may exacerbate hemolysis in these patients; partial exchange transfusion may be required.

Adolescent↗

PubMed1977

Acute methemoglobinemia and hemolytic anemia with phenazopyridine: possible relation to acute renal failure.

An 18-year-old woman with no prior history of renal or hematologic dysfunction developed severe, acute methemoglobinemia after an overdose of phenazopyridine hydrochloride (Pyridium). The methemoglobinemia was reversed acutely with methylene blue, and during the course of ten days, the patient developed a hemolytic anemia with "bite cells" and acute renal failure. The patient recovered fully with conservative management. Several putative pathophysiologic explanations for the development of methemoglobinemia, hemolytic anemia, and renal failure following oxidative stress are considered and include a direct toxic effect on the renal tubules or methemoglobin-caused damage. Renal failure as a complication of phenazopyridine-related methemoglobinemia and hemolytic anemia should be borne in mind in cases of overdosage with this common drug.

Acute Kidney Injury↗