sodium-nitrite and Respiratory-Insufficiency

sodium-nitrite has been researched along with Respiratory-Insufficiency* in 3 studies

Other Studies

3 other study(ies) available for sodium-nitrite and Respiratory-Insufficiency

ArticleYear
Methemoglobinemia following unintentional ingestion of sodium nitrite--New York, 2002.
    MMWR. Morbidity and mortality weekly report, 2002, Jul-26, Volume: 51, Issue:29

    Methemoglobinemia is an unusual and potentially fatal condition in which hemoglobin is oxidized to methemoglobin and loses its ability to bind and transport oxygen. The most common cause of methemoglobinemia is the ingestion or inhalation of oxidizing agents such as nitrates or nitrites (e.g., sodium nitrite, which is used commonly as a preservative in curing meats and fish). This report summarizes the investigation of an incident of methemoglobinemia in five members of a household in New York who became ill after eating a meal seasoned with a white crystalline substance from a plastic bag labeled "Refined Iodized Table Salt" (Figure). The findings underscore the need for proper storage of hazardous materials to avoid unintentional ingestion and the importance of collaboration by multiple agencies to address a potential public health emergency.

    Topics: Adult; Cyanosis; Dizziness; Enzyme Inhibitors; Female; Food Labeling; Food Preservatives; Humans; Male; Methemoglobin; Methemoglobinemia; Methylene Blue; Middle Aged; New York; Respiratory Insufficiency; Seizures; Sodium Chloride, Dietary; Sodium Nitrite; Unconsciousness; Vomiting

2002
Successful treatment of life-threatening propionitrile exposure with sodium nitrite/sodium thiosulfate followed by hyperbaric oxygen.
    Journal of occupational medicine. : official publication of the Industrial Medical Association, 1993, Volume: 35, Issue:6

    Propionitrile, a substituted aliphatic nitrile commonly used in the chemical manufacturing industry, is capable of generating cyanide. However, there are few reports of human intoxication involving propionitrile. We report two workers at an organic chemical manufacturing plant who were overcome by fumes while treating a waste slurry into which unreacted propionitrile was discharged by mistake. One victim was comatose, acidotic, and hypotensive; his blood cyanide level was later measured at 5.0 micrograms/ml. He responded to sodium nitrite/sodium thiosulfate therapy by regaining consciousness. Continued symptoms were treated with hyperbaric oxygen at 2 atmospheres for a total of 4 hours. The second victim, who complained only of nausea, dizziness, and headache and who never lost consciousness, was treated with sodium nitrite/sodium thiosulfate. His measured blood cyanide concentration was 3.5 micrograms/ml. The ambient concentration of propionitrile in air samples at the work site shortly after the exposure was 77.5 mg/m3. In occupational situations in which workers exhibit rapidly progressive symptoms of headache, dizziness, collapse, and coma, and where substituted nitriles are known to be on site, acute cyanide poisoning should be strongly considered. Because of continued endogenous generation of cyanide from the metabolism of the parent compound, hyperbaric oxygen may be a valuable adjunctive therapy to consider, in addition to the immediate use of the cyanide antidote kit, in cases of poisoning by propionitrile or other substituted nitrile compounds. We urge the Occupational Safety and Health Administration to adopt workplace standards for the maximum ambient air concentrations for propionitrile.

    Topics: Adult; Antidotes; Coma; Combined Modality Therapy; Humans; Hyperbaric Oxygenation; Male; Neurologic Examination; Nitriles; Occupational Diseases; Respiratory Insufficiency; Sodium Nitrite; Thiosulfates

1993
The effect of hyperbaric oxygen on acute experimental sulfide poisoning in the rat.
    Toxicology and applied pharmacology, 1986, Jun-30, Volume: 84, Issue:2

    In order to evaluate the efficiency of hyperbaric oxygen in experimental acute sulfide poisoning, we studied the effect of 1 ATA (atmosphere absolute) oxygen and sodium nitrite therapy. We then studied the effect of oxygen at 3 ATA alone and in combination with intraperitoneal sodium nitrite injection on rats poisoned by intraperitoneal injection of LD75 sulfide. Electroencephalogram and heart rate were continuously monitored. We also studied the effect of sodium nitrite and hyperbaric oxygen administered before the poisoning (protective effect). In our experimental set, death of untreated poisoned animals occurred within 5 min. There is a parallel between modification of the EEG pattern and apnea. Respiratory arrest always preceded cardiac arrest. Pure oxygen (1 ATA O2) is effective in preventing death in experimental sulfide poisoning. 3 ATA oxygen was significantly more effective in preventing death than 1 ATA oxygen, or sodium nitrite alone. The best therapeutic regimen was a combination of 3 ATA oxygen and sodium nitrite administration.

    Topics: Animals; Apnea; Electrocardiography; Electroencephalography; Heart Rate; Hyperbaric Oxygenation; Injections, Intraperitoneal; Lethal Dose 50; Male; Rats; Respiratory Insufficiency; Sodium Nitrite; Sulfides

1986