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M I Herman

Publications and source records attributed to M I Herman.

6 recordsLinked to original sources

Ferrous sulfate adsorption by activated charcoal.

Although activated charcoal is thought to not appreciably adsorb iron salts, previous in vitro work indicates some adsorption of iron. This study characterized the adsorptive capacity of activated charcoal for ferrous sulfate at 3 pH environments. Langmuir adsorption isotherms were determined with a fixed amount of iron in the reaction vessels. Activated charcoal USP (20, 40, 60, 80, 100, or 120 mg) was placed in plastic tubes to which were added 1 of 3 different simulated gastrointestinal fluids (pH = 1.5, 4.5, or 7.5) and 1.49% ferrous sulfate in water. The reaction vessels were agitated and immersed in a water bath at 37 C for 30 min. Each series was performed in triplicate. Following temperature eQuilibration filtration yielded an aliquot that was assayed for iron by atomic absorption spectrophotometry. Adsorptive capacities (mean +/- SD) of activated charcoal for ferrous sulfate (mg elemental iron/g charcoal) at pH 4.5 (102.96+/-4.49) and pH 7.5 (100.94+/-19.02) were higher (P<0.01) than at pH 1.5 (-0.01+/-0.26). At pH 1.5 iron was not appreciably adsorbed by activated charcoal. Activated charcoal adsorbed ferrous sulfate to a greater extent at pH environments where iron is typically absorbed from the gastrointestinal tract. These results indicate that activated charcoal may prove an effective therapy for acute iron poisoning and further investigation is warranted.

Adsorption↗

Utility of acetylcysteine in treating poisonings and adverse drug reactions.

As recognition of the role of free radicals and reactive toxins in the pathogenesis of disease, poisoning, and adverse drug reactions has evolved, interest in the use of acetylcysteine as a modulator of these effects has steadily increased in recent years. Acetylcysteine is commonly thought to serve as a glutathione precursor and consequently can increase or sustain intracellular glutathione which scavenges reactive oxygen species caused by toxins or subsequent tissue injury. At least 10 additional mechanisms of action for acetylcysteine have been demonstrated in various laboratory models, but a unifying framework of its actions is still to be proposed. This paper reviews the current experimental and therapeutic status of acetylcysteine for the treatment of poisonings and adverse drug reactions. Of the 45 potential uses of acetylcysteine that were identified for the treatment of poisonings or adverse drug reactions, 14 of the toxic effects have little support for its use while promising results have been demonstrated for 27 toxicities. Currently, treatment of acute paracetamol (acetaminophen) poisoning is the only widely accepted clinical indication for acetylcysteine as a treatment for poisoning or adverse drug reactions. In many clinical situations acetylcysteine is used empirically utilising modifications of dosage regimens employed for paracetamol poisoning. Often it is difficult to determine the benefit of therapy with acetylcysteine owing to the nature of the toxicity being treated, the use of other therapies, the presence of comorbid conditions, and the small number of patients studied. The diverse and positive nature of the investigations suggest that there is considerable promise in acetylcysteine as a research tool and pharmacological agent.

Acetylcysteine↗

Methylene blue by intraosseous infusion for methemoglobinemia.

Intraosseous administration of methylene blue may be an emergency alternative to intravascular administration. A 6-week-old female infant (3 kg) presented to the emergency department after a 1-week illness and appeared cyanotic and listless. Oxygen saturation by oximetry was 86% while the patient was receiving oxygen. Vital signs were blood pressure, 107/80 mm Hg; pulse, 190; respirations, 47; temperature, 39.0 degreesC. A metabolic acidosis and a methemoglobin level of 29.3% were present. After several unsuccessful attempts to establish intravenous access, an intraosseous needle was placed in the infant's left tibia. Methylene blue, 1 mg/kg, normal saline solution, and sodium bicarbonate were given intraosseously. The patient's oxygen saturation rose to 98% to 100%, and her cyanosis improved. Three hours later, her methemoglobin level was 8.2%. The child recovered uneventfully and was sent home after 3 days. Intraosseous administration of standard intravenous doses of methylene blue rapidly terminated the effects of acquired methemoglobinemia.

Antidotes↗