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Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
Thiosulfate reversibly combines with cyanide and with the help of rhodanese it get converted into a less toxic thiocyanate which got excreted in urine. The primary concerns in this administration of the cyanide antidote kit are, it's side effects, which include severe hypotension, methemoglobinemia and hypersensitivity reactions. However, the antidote for methemoglobinemia is methylene blue and this agent will counteract excess methemoglobin formation.
Pharmacology of Local Anesthetics
Published in Pamela E. Macintyre, Stephan A. Schug, Acute Pain Management, 2021
Pamela E. Macintyre, Stephan A. Schug
The initial step in the metabolism of prilocaine forms orthotoluidine. The administration of large doses of prilocaine may lead to the accumulation of this metabolite, which, in turn, leads to an increase in the oxidation of hemoglobin to methemoglobin (Becker & Reed, 2012). If the level of methemoglobin becomes excessive, the patient may appear cyanotic. This metabolic toxicity limits the use of prilocaine in anemic patients and leads to the recommendation to avoid repeat injections or infusions, thereby limiting its use in acute pain therapy.
Inhalational Durg Abuse
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Jacob Loke, Richard Rowley, Herbert D. Kleber, Peter Jatlow
Amyl nitrite has been used for the medical treatment of angina pectoris for more than 100 years. It has been abused as an intoxicant and as a sex stimulant (Sigell et al, 1978). The street names for amyl nitrite include snappers, poppers, and pearls. Butyl and isobutyl nitrites used as room odorizers are also inhaled for their “high” effect. The effects of the volatile nitrites are on the central nervous system, the cardiovascular, and hematologic systems (Newell et al., 1985; Haley, 1980). There is hypotension with peripheral vasodilatation and tachycardia. Toxic effects consist of flushing of the face, headache, eye orbital pain, increase in intraocular pressure (Pearlman and Adams, 1970), cyanosis, syncope, and cardiovascular collapse. There is also formation of methemoglobinemia with nitrites, which can be fatal (Shesser et al., 1982). Clues to the diagnosis of significant levels of methemoglobinemia include central and peripheral cyanosis, a dark blue color of the arterial blood gas sample, and the methemoglobin value. Volatile nitrites can be nitrosation reagents, which can lead to formation of N-nitrosamines and N-nitrosamides. These are mutogenic and carcinogenic compounds. The abuse of amyl nitrite among male homosexuals may be related to the current epidemic of the acquired immune deficiency syndrome and to Kaposi’s sarcoma (Newell et al., 1985; Jorgensen and Lawesson, 1982).
Acquired methemoglobinemia in children presenting to Italian pediatric emergency departments: a multicenter report
Published in Clinical Toxicology, 2022
Umberto Raucci, Michela Stanco, Marco Roversi, Eduardo Ponticiello, Mara Pisani, Margherita Rosa, Raffaele Falsaperla, Piero Pavone, Claudia Bondone, Irene Raffaldi, Lucia Calistri, Stefano Masi, Antonino Reale, Alberto Villani, Marco Marano
As cited above, 76% was the highest methemoglobin value recorded in our sample. This belonged to a 6-month-old infant transferred from another hospital to the pediatric ICU of the Bambino Gesù Children's Hospital with a diagnosis of septic shock. On arrival the patient had a Glasgow Coma Scale of 8, was hemodynamically unstable and required mechanical ventilation. After administration of crystalloids and inotropic support, hemodynamic conditions progressively worsened to an asystolic cardiac arrest. Cardiopulmonary resuscitation was successfully performed. After collection, the blood presented the characteristic dark brown discoloration that suggested the diagnosis of MetHb, as confirmed by the blood gas analysis performed on the same blood sample. The laboratory workup showed 35.0 * 103 leukocytes per μl and negative indices of inflammation. The chest X-ray was also negative. Intravenous methylene blue therapy was then administered slowly at a dose of 1 mg/kg and repeated after 1 h, allowing reduction of methemoglobin from 76% to a value of less than 1%.
Fatal Sodium Nitrite Poisoning: Key Considerations for Prehospital Providers
Published in Prehospital Emergency Care, 2021
Matthew R. Neth, Jennifer S. Love, B. Zane Horowitz, Michael D. Shertz, Ritu Sahni, Mohamud R. Daya
During a normal physiologic state, methemoglobin levels are less than 1% (31). This steady state is primarily achieved through the enzymatic action of cytochrome-b5 reductase, which reduces methemoglobin back to functional hemoglobin (31). Methemoglobinemia can develop when the body is exposed to an oxidant stress and reduction though cytochrome-b5 reductase is overwhelmed (31,32). Cyanosis, the blue discoloration of the skin, is ordinarily apparent to an observer when deoxygenated hemoglobin represents 15% of the available hemoglobin. However, in methemoglobinemia, only 5% of the abnormal hemoglobin is needed for the patient to appear cyanotic. At lower concentrations, the patient is generally not truly hypoxic. However, the pulse oximeter will misread the abnormal hemoglobin and give a reading of 85%, which will not change despite supplemental oxygen. As methemoglobin concentrations rise above 30%, other symptoms appear that are related to inadequate oxygen delivery to the central nervous system (headache, lightheadedness, confusion, seizure, coma, death) and the heart (dysrhythmias, hypotension, pulseless electrical activity). These progressively worsen with increasing concentrations (8–10).
Cyanosis, hemolysis, decreased HbA1c and abnormal co-oximetry in a patient with hemoglobin M Saskatoon [HBB:c.190C > T p.His64Tyr]
Published in Hematology, 2021
Eva-Leonne Göttgens, Kristian Baks, Cornelis L. Harteveld, Kristel Goossens, Adriaan J. van Gammeren
Methemoglobinemia may arise as a result of genetic or acquired causes. Acquired methemoglobinemia is most prevalent and commonly caused by oxidative stress, which can have exogenous or endogenous origins. Endogenous forms of oxidative stress include but are not limited to free radicals such as nitric oxide, hydrogen peroxide and hydroxyl radicals. Exogenous substances may also trigger the oxidation of hemoglobin and this occurs most often as a result of medication. Dapsone, topical anesthetics (benzocaine, lidocaine), anti-malarial agents (chloroquine, hydroxychloroquine) and street drugs account for the majority of iatrogenic methemoglobinemia [25,26]. In addition to the formation of methemoglobin in healthy patients, these drugs may seriously exacerbate the condition of patients who are prone to methemoglobinemia due to genetic mutations causing hemoglobinopathies. Genetic defects that result in methemoglobinemia are commonly found in the CYB5R3 gene, which encodes the cytochrome b5 reductase enzyme. This enzyme is responsible for the reduction of the Fe3+ ion in methemoglobin to Fe2+. Mutations in this gene can both affect the enzymatic stability as well as its catalytic activity [27,28]. Most other genetic defects giving rise to (unstable) methemoglobinemia are hemoglobinopathies that result in the formation of HbM variants due to the defects in the alpha, beta, or gamma globins [29].