PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “METHEMOGLOBINEMIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources

Acute hemolytic anemia, methemoglobinemia, and heinz body formation associated with ingestion of red maple leaves by horses.

From June 1975 through June 1979, acute hemolytic anemia developed in 11 horses from 7 New York farms. Of the 7 horses that died, 6 had methemoglobinemia. In the 4 horses that recovered, methemoglobinemia was not observed. but Heinz body formation was seen in 3 of the 4. On 2 of the premises involved, frank methemoglobinemia was observed concurrently with Heinz body formation, suggesting a relationship between the pathogenesis of methemoglobinemia and Heinz body formation in the hemolytic process. In addition to the 11 cases described, 22 clinically similar cases were reported to us during the period of this investigation by practicing veterinarians from New York, Pennsylvania, and the New England states. All 33 cases of hemolytic anemia occurred between June and October of each year, and affected horses had access to outside paddocks or fields containing a variety of native grasses, weeds, and trees. On 2 farms, hemolytic anemia developed after the horses were observed browsing fallen branches of red maple trees (Acer rubrum). Red maple leaves and bark were obtained from 1 of these farms, and approximately 1 kg of a leaf and bark mixture was fed to each of 2 ponies. Within 48 hours, both ponies became ill. The syndrome was indistinguishable from that observed in clinical patients and was characterized by methemoglobinemia and intravascular hemolysis. The ponies died 5 and 6 days after which time the packed cell volumes were 6% and 7% respectively. It was concluded that many cases of hemolytic anemia in horses in northeastern states may be related to ingestion of leaves or bark from red maple trees. The studies did not, however, define the factors that predispose to poisoning and did not exclude the possibility that other environmental toxins may have been involved.

Acute Disease↗

Electrophoretic and functional variants of NADH-methemoglobin reductase in hereditary methemoglobinemia.

The electrophoretic mobility and activity of NADH-methemoglobin reductase in erythrocytes of patients with hereditary methemoglobinemia, obligatory heterozygotes, and normal subjects were examined. Six distinct electrophoretic variants were found in studies of erythrocytes from members of ten different families. Five variants (Boston Slow, Duarte, Princeton, Puerto Rico, and California) were associated with significant methemoglobinemia and moderate to marked decreases in enzymic activity. Precise correlations between levels of NADH-methemoglobin reductase activity, electrophoretic mobility, and clinical severity of methemoglobinemia, however, could not be drawn. One variant (Boston Fast) was associated with almost normal activity and very minimal methemoglobinemia. Nine members from three generations of two Italian families were found to have two bands with NADH-methemoglobin reductase activity in their erythrocytes, one with normal mobility and one with a mobility identical with that of Boston Fast. No functional or clinical impairment could be attributed to this abnormality. The observations made in this investigation were consistent with an autosomal recessive mode of inheritance of multiple alleles for NADH-methemoglobin reductase. As has been shown to be true for hemoglobin and glucose-6-phosphate dehydrogenase, multiple aberrations in the NADH-methemoglobin reductase of human erythrocytes apparently exist, some with and some without functional consequences. Two bands with NADPH-methemoglobin reductase activity with electrophoretic mobilities distinct from those of the NADH-methemoglobin reductase were found in human erythrocytes. These bands were normal in hemolysates of erythrocytes from patients with hereditary methemoglobinemia, but were absent from the hemolysate of erythrocytes deficient in NADPH-methemoglobin reductase activity. These latter erythrocytes, however, contained normal concentrations of methemoglobin and had a normal ability to reduce methemoglobin in vitro. These observations were most consistent with the thesis that the NADH-methemoglobin reductase, distinct from any NADPH-methemoglobin reductase, was the major system responsible for the reduction of methemoglobin to hemoglobin in human erythrocytes.

Alleles↗

Infant Methemoglobinemia in the Transylvania Region of Romania.

The incidence of infant methemoglobinemia reported in three counties of Transylvania, Romania, was evaluated from medical records, field visits, and interviews. Well water was the main source of nitrate for induction of acquired infant methemoglobinemia, which occurred post-breast-feeding when the infants consumed nitrate-contaminated water used in mixing formula. The average age of reported infants with methemoglobinemia was 39 days, supporting earlier observations that infants less than 4 months old are the most susceptible segment of the population. Vitamin C, rather than methylene blue, was the main medical intervention in the Transylvania region. The mean incidence rates of methemoglobinemia in the three counties (Saut-Mare, Mures, and Bistrita-Nasaud) ranged from 24 to 363 per 100,000 live births over a five-year period (1990-1994). These rates are below earlier reported incidence rates of up to 13% (13,000 per 100,000 live births). Three selected case reports are presented to describe hospital/clinic data, well-water data, and infant feeding practices. Recommendations for appropriate intervention programs are described. The significances of possible physical and neuropsychological effects on the development of children following methemoglobinemia are discussed and the need for further investigations is outlined.

Journal Article↗

Treatment of high-risk, refractory acquired methemoglobinemia with automated red blood cell exchange.

Ingestion of strong oxidant substances may result in acquired methemoglobinemia, a clinical condition in which the oxidized blood hemoglobin is incapable of delivering oxygen to the tissues, and the patient becomes cyanotic. Traditional first-line therapy consists of infusion of methylene blue, whose action depends on the availability of reduced nicotinamide adenine nucleotide phosphate (NADPH) within the red blood cell (RBC). Some patients, particularly those who are deficient in glucose-6-phosphate dehydrogenase (G6PD), will not benefit from methylene blue. In these patients, and in some patients who have ingested very strong oxidants, methylene blue may also precipitate Heinz body hemolytic anemia. We present a case of severe, acquired methemoglobinemia in a 26-month-old, 9.8-kg boy with G6PD deficiency. He was cyanotic, in respiratory failure, intubated in a pediatric intensive care unit. In typical fashion, he did not respond to methylene blue. Manual exchange of two whole blood volumes, performed over 4 1/2 hr, also failed to resolve his severe methemoglobinemia. An automated RBC exchange (1.3 RBC volume), lowered his methemoglobin content from 31.8% to 7% in a single 40-min procedure. Thereafter his methemoglobin level continued to decrease rapidly and spontaneously. He was discharged home 2 days later, with 0.4% methemoglobin. To our knowledge, this is the first report to demonstrate the (potentially superior) effectiveness of automated RBC exchange for treatment of patients with high-risk acquired methemoglobinemia, that is, those with G6PD deficiency or who have ingested strong oxidants.

Automation↗

Presentation of dapsone-induced methemoglobinemia in a patient status post small bowel transplant.

Methemoglobinemia, an uncommon hemoglobinopathy, affects oxygen transport, causing tissue hypoxia. In the perioperative period, methemoglobinemia is often overlooked as a cause of low oxygen saturation, often mistaken for the more common causes of hypoxia, such as atelectasis, pulmonary edema, or pulmonary embolus, among other causes of respiratory failure. Most cases of methemoglobinemia in the perioperative period are precipitated by local anesthetics, especially benzocaine. Dapsone, a sulfone antibiotic, is used for prophylaxis against Pneumocystis carinii pneumonia in immunosuppressed patients. It is commonly used in organ transplant patients, especially those intolerant to sulfa. With the expansion of organ transplantation and improved long-term survival of these patients, presentation of status post organ transplant patients for surgery will inevitably increase. We report a case of dapsone-induced methemoglobinemia observed in a status post small bowel transplant patient in the postanesthesia care unit.

Adolescent↗

Methemoglobinemia: an unusual cause of postoperative cyanosis.

Methemoglobinemia, although rare, must be considered in surgical patients presenting with acute respiratory distress and cyanosis. We report two cases of methemoglobinemia in patients undergoing aortic reconstruction. The first patient developed methemoglobinemia while on a nitroglycerin infusion, and the second after receiving benzocaine spray before intubation. Both patients were treated with methylene blue and ascorbic acid, with resolution of their hypoxia and cyanosis. The pathophysiology, etiology, diagnosis, and treatment of methemoglobinemia are reviewed.

Aged↗

Methemoglobinemia secondary to cleaning solution ingestion.

Methemoglobinemia is a rare cause of cyanosis in pediatric patients. A 16-month-old male presented to the Emergency Department cyanotic and short of breath after ingestion of a hair-care-equipment cleaning solution. After calling the salon and consulting Poisindex, the substance was found to be Mar-V-cide, containing 20% Hyamine 3500, 50% cationic detergents, 20% isopropyl alcohol, and 1% sodium nitrite, which caused the methemoglobinemia in this case. Initial pulse oximetry on room air was 72% and improved minimally with supplemented oxygen. The patient's methemoglobin level was 63%. Methylene blue was administered (2 mg/kg intravenously), and the patient rapidly improved. Nitrates occur in high concentrations in some food and water. Infants are particularly susceptible to chronic nitrate-induced methemoglobinemia because of their low stomach acid production, large numbers of nitrite-reducing bacteria, and the relatively easy oxidation of fetal hemoglobin. Acute nitrite toxicity results from industrial exposure, accidental ingestion (e.g., abuse of organic nitrites as an aphrodisiac, especially in the male homosexual population), and suicidal ingestion. Methemoglobinemia may occur in a number of drug or chemical ingestions, but a comprehensive review of the literature failed to identify a similar reported case.

Antidotes↗

[Hereditary methemoglobinemias].

The different forms of hereditary methemoglobinemia are described. Dominant hereditary methemoglobinemia (hemoglobin M diseases) is due to punctual mutations on the alpha or beta globin chain leading to its permanent oxidation. Recessive hereditary methemoglobinemia is due to a deficit of the NADH-cytochrome b5 reductase, with two different clinical presentations according to whether the deficit is limited to blood cells (type I) or is generalized (type II); the latter is extremely severe and justifies a prenatal diagnosis. Finally, the only known case of recessive hereditary methemoglobinemia due to a deficit of b5 cytochrome is quoted.

Cytochrome Reductases↗

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.

Acidosis↗

Benzocaine-induced methemoglobinemia: experience from a high-volume transesophageal echocardiography laboratory.

Benzocaine (ethyl aminobenzoate), a topical anesthetic widely used before transesophageal echocardiography, has been reported to cause acquired methemoglobinemia. The incidence of benzocaine-induced methemoglobinemia in clinical practice, however, has been difficult to estimate. After systematic review of our institutional experience for clinically recognized cases of benzocaine-induced methemoglobinemia in patients undergoing transesophageal echocardiography, we report an estimated incidence of 0.115% (95% confidence interval 0.037-0.269). This report also provides the largest analysis of the incidence of methemoglobinemia in readministration cases. Although controversy remains as to whether this is an idiosyncratic versus dose-related response, a description of purported patient risk factors is included.

Adult↗

Methemoglobinemia induced by refrigerated vegetable puree in conjunction with supraventricular tachycardia.

UNLABELLED: We report on a case of methemoglobinemia in conjunction with supraventricular tachycardia. A 6-mo-old infant was admitted to hospital with perioral cyanosis three hours after eating a refrigerated mixed-vegetable puree. The patient developed supraventricular tachycardia (SVT) and had a heart rate of 230 beats/min. The arrhythmia resolved spontaneously. A chemical analysis showed oxygen saturation of 85% and a methemoglobin level of 25%. The infant was treated with oxygen and referred to the Pediatric Intensive Care Unit. The patient had two additional short episodes of SVT, which were resolved spontaneously without treatment. She received oxygen for 8 h until the methemoglobin level dropped to 1%. CONCLUSION: Long-term storage of refrigerated vegetables can cause methemoglobinemia in infants. Methemoglobinemia can appear in conjunction with SVT, but it is also possible that in a child with a tendency to develop SVT, methemoglobinemia involved hypoxemia, which then triggers SVT.

Female↗

Characterization of methemoglobinemia induced by 3,5-xylidine in rats.

The objective of this study was to characterize the dose effect and kinetics of methemoglobinemia in rats following oral or intravenous administration of 3,5-xylidine (XYL). The first set of experiments involved the intravenous administration of 0.06, 0.12, 0.24, 0.48, or 0.60 mmol XYL/kg to groups of 3 rats each and the serial sampling of blood from the tail vein of individual animals for the determination of methemoglobin levels. An additional series of experiments involved the oral administration of 0.24, 0.48, 0.72, 0.96, 1.2, 1.8, 2.4, or 4.8 mmol XYL/kg and the serial sampling of blood for the determination of methemoglobin levels. The results showed a dose-dependent induction of methemoglobinemia by XYL in the rat, for both routes of administration. The maximal percent methemoglobin observed in the treated animals was 28.90 +/- 0.34% and 32.67 +/- 2.14% for the intravenous (0.6 mmol/kg) and oral (4.8 mmol/kg) routes, respectively. The dose levels of 0.06 mmol/kg (iv) and 0.96 mmol/kg (po) were the no-observable-adverse-effect levels with respect to XYL-induced methemoglobinemia in the rat. The dose-effect information on XYL-induced methemoglobinemia obtained in this study may be useful for the characterization of noncarcinogenic risks of acute human exposure to this chemical.

Administration, Oral↗

The need for caution with topical anesthesia during endoscopic procedures, as liberal use may result in methemoglobinemia.

During upper gastrointestinal endoscopy, topical oropharyngeal anesthesia with lidocaine and/or benzocaine is used routinely by many endodscopists. Although such a practice is usually safe, there have been a number of reports of methemoglobinemia induced by topical anesthesia. Early treatment is extremely important as the development of methemoglobinemia is potentially fatal. Methemoglobinemia should be considered when oxygen desaturation occurs without another explanation. In this case series, we report 4 cases of methemoglobinemia that followed the liberal application of Cetacaine for ERCP. All patients recovered after appropriate treatment but these cases serve to highlight the potential problem, the importance of early recognition and treatment, and the most appropriate treatment options.

4-Aminobenzoic Acid↗

Severe methemoglobinemia after transesophageal echocardiography.

Methemoglobinemia, an increased concentration of methemoglobin in the blood, is an altered state of hemoglobin whereby the ferrous form of iron is oxidized to the ferric state, rendering the heme moiety incapable of carrying oxygen. This can cause hypoxia, cyanosis, or even death. Severe methemoglobinemia resulting from oral benzocaine spray before endoscopic procedures has been reported as a rare complication. We report a case of severe acquired methemoglobinemia resulting from topical benzocaine use before transesophageal echocardiography. This case serves to highlight the severity of methemoglobinemia that can result from an otherwise innocuous agent even in small doses and the fact that prompt recognition and treatment of this disorder can be lifesaving.

Aerosols↗

Methemoglobinemia after fiberoptic intubation in a patient with an unstable cervical fracture: a case report.

Methemoglobinemia, a condition associated with cyanosis and diminished pulse oximetry values, has been reported after use of local anesthetics to facilitate fiberoptic intubation. The majority of reports in the literature detail this development during diagnostic procedures such as endoscopy and bronchoscopy. A case of methemoglobinemia in a multiple-injury patient with an unstable compressive-flexion injury of the cervical spine undergoing fiberoptic intubation is presented. A literature review of this entity is also presented. The patient underwent fiberoptic intubation using topical pharyngeal anesthetics before planned cervical corpectomy, strut grafting and instrumentation. He became acutely cyanotic with abruptly diminished pulse oximetry readings. Subsequent blood gas analysis demonstrated methemoglobinemia. Intravenous methylene blue administration led to an uncomplicated resolution of the condition. Surgeons and anesthesiologists who manage such patients should be aware of methemoglobinemia, a rare but potentially fatal complication related to topical airway anesthetics.

4-Aminobenzoic Acid↗

Benzocaine-induced methemoglobinemia: a condition of which all endoscopists should be aware.

Methemoglobinemia is a rare complication that can occur with the use of benzocaine-containing compounds. Two cases of methemoglobinemia are reported, and the pathophysiology and treatment of methemoglobinemia are reviewed. Both patients received topical 20% benzocaine spray before endoscopy. Immediately following the procedure, there was a reduction in O2 saturation assessed by pulse oximetry that was refractory to O2 therapy. Dramatic peripheral and central cyanosis developed. O2 saturation measured by pulse oximetry ranged from 83% to 87% on O2 by nasal prongs and 100% O2 by a nonrebreathing mask. Both patients were mildly confused and one patient complained of a significant headache. The diagnosis of methemoglobinemia was considered and arterial blood gas sampling was performed. In both patients, the arterial blood had a chocolate brown colour. A methemoglobin level of 48% and 18% was noted in patient 1 and patient 2, respectively. Both patients were treated with methylene blue, resulting in a significant improvement with gradual normalization of their O2 saturation within 10 min to 30 min. The use of benzocaine spray may not markedly alter the patient's perception of endoscopy and thus, the routine use of these agents should be questioned. If such agents are used, the physician must be aware of this association to prevent a delay in the diagnosis and management of this rare, but potentially lethal, condition.

Adult↗

Organic nitrate-induced methemoglobinemia.

Metabolism of organic nitrates results in the formation of inorganic nitrites that can oxidize hemoglobin to methemoglobin. Clinical trials have investigated the risk of developing methemoglobinemia during the therapeutic use of organic nitrates. Based on the results of these trials, organic nitrate use does appear to increase methemoglobin content but not to a clinically significant extent. These elevations may be related to dose but study design prevents determination of any dose-response relationship. Despite these results, several case reports of patients experiencing clinically significant methemoglobinemia can be found in the literature. These patients generally received organic nitrates at doses greater than those used in the clinical trials, and several were diagnosed early during coronary surgery. Renal dysfunction and concurrent use of methemoglobin inducers may be contributing factors. Patients receiving organic nitrates should be monitored for symptoms suggestive of methemoglobinemia, especially while receiving large doses. Treatment of nitrate-induced methemoglobinemia consists of discontinuing the medication and, when necessary, administering methylene blue.

Animals↗

Flutamide-induced methemoglobinemia.

The authors report a case of clinical methemoglobinemia occurring one year after a patient began receiving flutamide 750 mg/d for prostate cancer with bone metastasis. The patient presented with severe cyanosis involving his lips and proximal extremities and moderate dyspnea. Methemoglobinemia was 16.2 percent of the total hemoglobin and intravenous ascorbic acid was administered. Clinical examination and laboratory analysis revealed no other cause. There was no biochemical evidence of congenital methemoglobinemia and no other regular drug use or chemical exposure was found. Moreover, clinical improvement and normalization of the methemoglobin level after the drug was discontinued is highly suggestive of flutamide-induced methemoglobinemia. Due to its chemical structure derived from anilide, flutamide may be considered as a potential methemoglobin-inducing agent.

Aged↗