Fatal Methemoglobinemia Due to Well Water Nitrates

R, Bucklin; Myint, Melissa

doi:10.7326/0003-4819-52-3-703

Cited by 22 publications

(3 citation statements)

References 2 publications

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“…Methemoglobinemia can be induced by multiple pharmacological and chemical exposures, including nitrites. Fatalities from recreational usages of amyl nitrite (AN) as well as nitrite contamination of well water have been described (5,6,36,37). Significantly elevated levels of methemoglobin have been reported in patients with sepsis (26,28), infants who develop severe metabolic acidosis (blue baby syndrome), and individuals with rare congenital metabolic anomalies such as glucose phosphate dehydrogenase deficiency (9,41).…”

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confidence: 99%

Noninvasive in vivo monitoring of methemoglobin formation and reduction with broadband diffuse optical spectroscopy

Lee

El-Abaddi²,

Duke³

et al. 2006

Journal of Applied Physiology

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We present noninvasive, quantitative in vivo measurements of methemoglobin formation and reduction in a rabbit model using broadband diffuse optical spectroscopy (DOS). Broadband DOS combines multifrequency frequency-domain photon migration (FDPM) with time-independent near infrared (NIR) spectroscopy to quantitatively measure bulk tissue absorption and scattering spectra between 600 nm and 1,000 nm. Tissue concentrations (denoted by brackets) of methemoglobin ([MetHb]), deoxyhemoglobin ([Hb-R]), and oxyhemoglobin ([HbO2]) were determined from absorption spectra acquired in "real time" during nitrite infusions in nine pathogen-free New Zealand White rabbits. As little as 30 nM [MetHb] changes were detected for levels of [MetHb] that ranged from 0.80 to 5.72 microM, representing 2.2 to 14.9% of the total hemoglobin content (%MetHb). These values agreed well with on-site ex vivo cooximetry data (r2= 0.902, P < 0.0001, n = 4). The reduction of MetHb to functional hemoglobins was also carried out with intravenous injections of methylene blue (MB). As little as 10 nM changes in [MB] were detectable at levels of up to 150 nM in tissue. Our results demonstrate, for the first time, the ability of broadband DOS to noninvasively quantify real-time changes in [MetHb] and four additional chromophore concentrations ([Hb-R], [HbO2], [H2O], and [MB]) despite significant overlapping spectral features. These techniques are expected to be useful in evaluating dynamics of drug delivery and therapeutic efficacy in blood chemistry, human, and preclinical animal models.

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confidence: 99%

Noninvasive in vivo monitoring of methemoglobin formation and reduction with broadband diffuse optical spectroscopy

Lee

El-Abaddi²,

Duke³

et al. 2006

Journal of Applied Physiology

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“…Infants treated with silver nitrate for burns have also developed methaemoglobinaemia, probably due to the conversion of the nitrate to the more potent methaemoglobin-inducer nitrite by bacteria colonising the denuded skin (Cushing & Smith 1969;Strauch et al 1969;Ternberg & Luce 1968). Rural well-water contaminated with agricultural nitrates has frequently been documented as a source of neonatal methaemoglobinaemia (Bucklin & Myint 1960;Ewing & Mayon-White 1951). It is postulated that infants have a different intestinal flora than adults which converts the ingested nitrates to nitrites (Filer et al 1970).…”

Section: Acquired Methaemoglobinaemiamentioning

confidence: 99%

Drug- and Chemical-Induced Methaemoglobinaemia

1986

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Methaemoglobin is haemoglobin with the iron oxidised to the ferric (Fe ) state from the normal (or reduced) ferrous (Fe++) state. Methaemoglobinaemia refers to the presence of greater than the normal physiological concentration of 1 to 2% methaemoglobin in erythrocytes. Methaemoglobin is incapable of transporting oxygen. It has an intense dark blue colour; thus, clinical cyanosis becomes apparent at a concentration of about 15%. The symptoms are manifestations of hypoxaemia with increasing concentrations of methaemoglobin. Concentrations in excess of 70% are rare, but are associated with a high incidence of mortality. Methaemoglobinaemia may be congenital but is most often acquired. Congenital methaemoglobinaemia is of two types. The first is haemoglobin M disease (several variants) which is due to the presence of amino acid substitutions in either the alpha or beta chains. The second type is due to a deficiency of the NADH-dependent methaemoglobin reductase enzyme. This deficiency has an autosomal dominant transmission, and both homozygous and heterozygous forms have been reported. The heterozygous form is not normally associated with clinical cyanosis, but such individuals are more susceptible to form methaemoglobin when exposed to inducing agents. A wide variety of chemicals including several drugs, e.g. the antimalarials chloroquine and primaquine, local anaesthetics such as lignocaine, benzocaine and prilocaine, glyceryl trinitrate, sulphonamides and phenacetin, have been reported to induce methaemoglobinaemia. An intense 'chocolate brown' coloured blood and central cyanosis unresponsive to the administration of 100% oxygen suggests the diagnosis. A simple bedside test using a drop of the patient's blood on filter paper helps to confirm the clinical suspicion. Methaemoglobin can be quantitated rapidly by a spectrophotometric method.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…For example, a relatively common cause of methemoglobinemia in small infants is the ingestion of well water containing high concentrations of nitrate. 54,93,96,100,129,131,132,355,360 This phenomenon appears to be restricted to infants less than 2 to 3 months of age,96, 3GO and adults have been noted not to develop striking methemoglobinemia despite the fact that infants using the same water supply have been severely involved. 96 , 12!…”

Section: Clinical Pharmacology and Therapeuticsmentioning

confidence: 99%