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Acetaminophen (Tylenol) Poisoning
Published in Charles Theisler, Adjuvant Medical Care, 2023
N-acetylcysteine, a derivative of the amino acid L-cysteine, taken within eight hours of a Tylenol overdose mitigates liver toxicity4 and is effective in reducing the death rate and preventing the permanent harm caused by acetaminophen poisoning. For this use, N-acetylcysteine given by mouth (140 mg/kg, followed by 70 mg/kg every four hours for three days)5 is as effective as when given intravenously.1 N-acetylcysteine remains the preferred antidote for acetaminophen overdose in the U.S., Canada, Scotland, and most of England.6,7 Taking both Tylenol and NAC together can provide a convenient and effective way of preventing toxicity associated with large doses of acetaminophen.8 As a caution, taking N-acetylcysteine at the same time as activated charcoal may decrease the effectiveness of NAC to prevent poisoning.
Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
Combination of hydroxocobalamin as a first-line antidote followed by the continuous administration of sodium thiosulfate can have a positive effect on the survival without long-term neurological and visual sequelae in cases of massive cyanide poisonings.18
Specific Management of PPH
Published in Gowri Dorairajan, Management of Normal and High Risk Labour During Childbirth, 2022
Known use of anticoagulation: The woman may be on anticoagulants due to underlying problems like a prosthetic valve and acquired or inherited thrombophilias. The vitamin antagonists should be changed to unfractionated heparin or enoxaparin at term. At the onset of labour, the subsequent doses should be skipped and resumed 6–12 hours after child birth depending on the mode of delivery. Antidotes like protamine sulfate should be stocked and used if the delivery is impending within 6 hours of the last dose of heparin. Fresh frozen plasma and platelet transfusion might be needed in the wake of excessive bleeding or if the women came in labour before switching over from vitamin antagonists like the coumarin group of drugs.
Life-Threatening Cyanide Intoxication after Ingestion of Amygdalin in Prehospital Care
Published in Prehospital Emergency Care, 2022
Patrik Cmorej, Petr Bruthans, Jaroslav Halamka, Irena Voriskova, David Peran
Upon admission, the patient’s blood pressure was 127/54 mmHg with vasopressor support with norepinephrine 0.9 micrograms per kg per min. Arterial blood gases revealed a metabolic acidosis with pH 7.089, lactate 16.75 mmol/l, pCO2 3.83 kPa, pO2 17.06 kPa, HCO 3 − 8.6 mml/l, Base excess −20.8 mmol/l. Oxygen saturation was 96.6% on FiO2 50%. Increased cardiac parameters, were found with NT -proBNP values of 550.6 ng/l, myoglobin 1018 µg/l and troponin T 38 ng/l. Based on the recommendation of the Toxicological Information Center, the patient was given charcoal via nasogastric tube and sodium bicarbonate intravenously. The antidote hydroxocobalamin (Cyanokit) was recommended but was not available in the hospital, requiring it to be transported from the Toxicology Information Center (100 km). The antidote was administered three hours after the patient’s admission to the hospital in a single infusion of 5 g of hydroxocobalamin (Cyanokit) in 100 ml of normal saline for 15 minutes. Hydroxocobalamin administration was followed by rapid stabilization of vital signs and the arterial blood gasses. Lactic acidosis resolved six hours after antidote administration. A timeline of the first day is presented in Table 1. On the second day, the patient was extubated, and on the third day, the patient left the hospital in a stable condition at his own request. Prior to discharge, the patient was advised of the risks associated with the use of amygdalin
Paracetamol poisoning: a population-based study from Iceland
Published in Scandinavian Journal of Gastroenterology, 2021
Þorbjörg Andrea Friðriksdóttir, Freyja Jónsdóttir, Curtis P. Snook, Helena Líndal, Einar S. Björnsson
Paracetamol poisoning is a relatively common health problem and the most common cause of acute liver failure (ALF) in many European countries and the United States of America [1–3]. Within Europe, a vast difference has been observed between countries in the rate of paracetamol overdose leading to ALF; overall, paracetamol overdose accounted for one-sixth of all-cause ALF leading to registration for transplantation [3]. The wide availability of and easy access to paracetamol has made it one of the most common drugs ingested in overdose [4–6]. Paracetamol is safe and effective when ingested in therapeutic doses; however, hepatotoxicity can occur in an overdose [7]. N-acetylcysteine (NAC) is an effective antidote in treating paracetamol-induced hepatotoxicity [8]. Hepatotoxicity and/or nephrotoxicity are the well-recognized complications of overdose [9]. Paracetamol poisoning is usually related to a single overdose leading to acute poisoning, whereas accidental poisoning involving repeated doses has been associated with worse liver-related outcomes in many studies [8,10–14].
Advances in the treatment of thrombotic thrombocytopenic purpura: repurposed drugs and novel agents
Published in Expert Review of Hematology, 2020
Andrés Gómez-De León, Luis Mario Villela-Martínez, José Miguel Yáñez-Reyes, David Gómez-Almaguer
N-acetylcysteine (NAC), a mucolytic agent and antidote for acetaminophen overdose, is a precursor of the amino acid L-cysteine and glutathione. A possible strategy for its use in TTP is based on its ability at very high doses to reduce disulfide bonds in VWF in vitro, as its thiol portion binds to the disulfide component, thereby decreasing the size of VWF multimers, hence their prothrombotic potential [80]. Tersteeg et al. [81] developed in vitro and preclinical models in mice and baboons to test the concept of NAC use in TTP without PEx. The authors concluded that NAC was effective in reducing the size of VWF multimers in vivo, while it was insufficient to treat TTP as monotherapy. There are some case reports of patients with refractory TTP where high NAC doses similar to those used in acetaminophen intoxication were combined with PEx, observing heterogeneous results [82–85]. Like other therapies, NAC was used together with plasma exchange and thus its true value has not been evaluated in depth. A pilot study using NAC in TTP has been completed, where patients with acute TTP received a bolus injection of NAC (150 mg/kg over 1 hour) followed by an infusion of 150 mg/kg over 17 hours after PEx. Although the study is reported as completed since July 2018, outcomes are yet to be reported (ClinicalTrials.gov NCT01808521).