High-dose insulin euglycemic therapy (HIET) is used for calcium channel blocker (CCB) and β-blocker (BB) overdose.Signs and symptoms of ricin poisoning depend on whether a person inhales or ingests ricin. Enhanced elimination of toxin can be facilitated through urinary alkalization (e.g., salicylates, phenobarbital) and hemadsorption with the use of resin or charcoal (B) Action on the toxin binding site can be achieved by competitive inhibition of the enzyme (e.g., ethanol or fomepizole for methanol and ethylene glycol poisoning) or by competitive blockade of the receptor (e.g., naloxone for opioid overdose and flumazenil for benzodiazepine overdose (C) Decreasing toxic metabolites can be done by binding (e.g., N-acetyl cysteine (NAC) as for paracetamol overdose) and conversion to less toxic metabolites (e.g., sodium thiosulphate for cyanide poisoning) (D) Counteracting the effects: drugs such as atropine counteract the muscarinic effects of OP poisoning. Nonspecific binding occurs with the use of activated charcoal and intralipid therapy (e.g., lipophilic local anesthetics (LA) and non-LA drugs). Specific binding can be achieved by chelation (e.g., heavy metals), immunotherapy (e.g., digoxin), and bioscavenger therapy (e.g., organophosphorus (OP) compounds). Indian J Crit Care Med 2019 23(Suppl 4):S241-S249.Ĭopyright © 2019 Jaypee Brothers Medical Publishers (P) Ltd.Īntidotes act by four predominant mechanisms (A) Direct action on the toxin involves specific and nonspecific binding and enhanced elimination. This review provides an overview of the role of antidotes in poisoning.Ĭhacko B, Peter JV. Vitamins such as vitamin K, folic acid and pyridoxine are used to antagonise the effects of warfarin, methotrexate and INH respectively in the setting of toxicity or overdose. Drugs such as atropine and magnesium are used to counteract the end-organ effects in organophosphorus poisoning. Drugs such as N-acetyl cysteine and sodium thiocyanate reduce the formation of toxic metabolites in paracetamol and cyanide poisoning respectively. naloxone, flumazenil) are other mechanisms by which antidotes act. oximes for organophosphorus poisoning) and competitive receptor blockade (e.g. ethanol for methanol poisoning), enhancement of enzyme function (e.g. In some situations, enhanced elimination can be achieved by urinary alkalization or hemadsorption. Specific binders include chelating agents, bioscavenger therapy and immunotherapy. The most commonly used non-specific binding agent is activated charcoal.
#DEFINE ANTIDOTE FREE#
Reduction in free toxin level can be achieved by specific and non-specific agents that bind to the toxin.
Antidote administration may not only result in the reduction of free or active toxin level, but also in the mitigation of end-organ effects of the toxin by mechanisms that include competitive inhibition, receptor blockade or direct antagonism of the toxin.
Antidotes mediate its effect either by preventing the absorption of the toxin, by binding and neutralizing the poison, antagonizing its end-organ effect, or by inhibition of conversion of the toxin to more toxic metabolites. Antidotes are agents that negate the effect of a poison or toxin.
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