Environmental Medicine Integrating a Missing Element into Medical Education (1995) / Chapter Skim
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Case Study 27: Nitrate/Nitrite Toxicity
Case Study 27: Nitrate/Nitrite Toxicity
Pages 518-537
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From page 518... ...
See page 21 for more information about continuing medical education credits and continuing education units. Guest Contributor: Burton C
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From page 519... ...
, heart rate is 1 40/min, and respiration rate is 40/mint An ambulance is summoned and 100% oxygen by face mask is administered; however, no improvement in the cyanosis is noted on her arrival at the hospital emergency department. The examining emergency physician now notes a grade IINI systolic murmurand central cyanosis, which has not improved despite administration of 100% oxygen for nearly 1 hour.
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From page 520... ...
Other sources of nitrate contamination are organic animal wastes and contamination from septic sewer systems, especially in wells less than 100 feet deep. During spring melt ordrought conditions, both domesticwells and public water systems using surface water may have increased nitrate concentrations.
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From page 521... ...
Sodium nitrite used as an anticorrosive agent in cooling fluids, ammonium nitrate found in cold packs, and nitrous gases used in arc welding are other possible sources of exposure. An ethyl nitrite folk remedy called Sweet spirits of nkreU has caused fatalities.
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From page 522... ...
population that uses drinking water from public water systems may be exposed to nitrates in excess of the EPA-recommended maximum concentration. Infants less than 4 months of age who are fed formula diluted with water from rural domestic wells are especially prone to developing acute acquired methemoglobinemia from nitrate exposure.
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From page 523... ...
Although suppliers of public water sources are required to monitor nitrate concentrations regularly, rural wells often are not routinely tested for nitrates. Nitrate/Nitnte Toxicity Ch~en,g?
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From page 524... ...
Nitrates are rapidly converted in the liberty denitrated metabolites and inorganic nitrites, which are then excreted in urine. Approximately 60% to 70% of an ingested nitrate dose is excreted in urine within the first 24 hours.
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From page 525... ...
Hemoglobin protein may also be oxidized, causing denaturation and erythrocyte hemolysis and resulting in hemolytic anemia. The denatured protein is visible on special peripheral blood stains as Heinz bodies (minute bodies sometimes seen in erythrocytes by the dark illumination method)
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From page 526... ...
Systolic flow murmurs may be heard on auscultation in persons with severe methemoglobinemia, which may develop with too-rapid intravenous administration of sodium nitrite (used as an antidote for cyanide and hydrogen sulfide poisoning) or sodium nitropNsside (used in hypertensive crisis therapy)
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From page 527... ...
· Family history, including recent use of medications by infant and mother · History of recent gastroenteritis with vomiting or diarrhea Physical examination should include special attention to the color of the skin and mucous membranes. If a history of gastroenteritis is present (especially in infants)
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From page 528... ...
The cardiac and pulmonary examinations are usually normal, but systolic flow murrnurs may be detected. Cardiac arrhythmias and hypotension may occur in patients wan severe poisoning, although death from methemoglobinemia alone is uncommon, except in infants.
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From page 529... ...
· Heinz bodies on peripheral blood smear Urinalysis Specialized Tests . Determination of methemoglobin level - Tests for causes of congenital methemoglobinemia: Hemoglobin electrophoresis Activity of NADH-dependent methemoglobin reductase · Tests for causes of failure of methylene blue therapy (see Treatment and Management, page 13~: Activity of glucose-6-phosphate dehydrogenase (G-6-PD)
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From page 530... ...
However, the percent O2 saturation actually measured with a Co-Oximeterwill decreased, resulting in a calculated versus measured arterial percent O2 saturation gap."This firming is not specific for methemoglobinemia, however, since carboxyhemoglobinemia and su~hemogbbinemia produce the same findings. Percent O2 saturation determined with a pulse oximeter may be unreliable in patients with methemoglobinemia, especially after administration of methylene blue (see Treatment and Management, page 13~.
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From page 531... ...
Within 15 minutes of methylene blue administration, cyanosis will usually begin to improve obviously. If no response to the initial injection has occurred within 15 minutes in seriously ill patients, orwithin30to 60 minutes in moderately ill patients, a second methylene blue dose of 0.1 mL/kg body weight may be given.
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From page 532... ...
In the case of infantile acquired methemoglobinemia, well water used in preparing formula is a primary etiologic suspect. Physicians and community health personnel should be aware that high nitrate levels in water supplies may suggest the presence of bacterial contamination or agricultural chemicals, which might have serious consequences, especially for infants and pregnant women (increased methemoglobin sensitivity)
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From page 533... ...
(8J What options are available to treat significant methemoglobinemia in a patient known to have G-6-PD deficiency? Standards and Regu/ations The nitrate limit in drinking water was established as a safeguard against infantile acquired methemoglobinemia.
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From page 534... ...
Methemoglobin levels in young children consuming high nitrate well water in the United States. Int J Epidemiol 1981 ;10(4)
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From page 535... ...
Evaluation of the nitrate drinking water standard with reference to infant methemoglobinemia and potential reproductive toxicity. Regul Toxicol Pharmacol 1987;7~2~:135-48.
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From page 536... ...
(2) Causes of high nitrate concentrations in well water include runoff from the use of nitrogen-containir~ agricultural fertilizers (including anhydrous ammonia)
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From page 537... ...
. If congenital methemoglobinemia is suspected or if the patient responds poorly to treatment with methylene blue, the following tests should be performed: hemoglobin electrophoresis, G-6-PD activity, and the activities of NADH- and NADPH-dependent methemoglobin reductases.
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