![]() ![]() Methadone is a particularly long acting opioid and has a higher risk of cardiac arrhythmias. methadone.Īn infusion may be needed in these cases - this is typically calculated as ⅔ of the successful reversal dose per hour. The clinical half life of naloxone is 20-60 mins, which can be significantly less that some of the very long acting opioids e.g. In non dependent users, less careful titration is needed In these cases, careful IV titration to effect is important ![]() This can include cardiovascular instability, severe agitation, and vomiting. The important factors for consideration when administering are:įull rapid reversal of opioids in an opioid dependent patient is potentially hazardous because of the effects of the adverse effects of sudden withdrawal. It can be given by IV, IM, IO, intranasal and endotracheal routes. Naloxone is the specific reversal agent - it is a competitive antagonist at the opioid receptors, blocking the effect of the ingested opioid. ‘Aggressive’ airway control is the central component of management, as per ALS management, to provide airway protection and ventilatory support for obtunded patients. The broader picture of the presentation will depend on other factors of the drug such as the route of administration, specific opioid and co-ingestants. The presence of miosis shouldn’t be relied upon because of the potential absence with ingestion of other drugs or severe overdose with hypoxia. The classic triad for opioid toxicity is: The term opiates refers to the naturally occurring opioids - morphine, codeine and papaverine. Opioids are the class of drugs which have action at opioid receptors - these have the classic effects of analgesia, somnolence, respiratory depression, cardiovascular depression and reduced gastric motility. The term narcotic refers to a drug that induces sleep or stupor, and generally refers to the opioid class of drugs. The mainstay of treatment is anticholinergics, primarily in the form of atropine, titrated to effect. sarin gas), but also some medicines (e.g. These chemicals include insecticides, chemical warfare agents (e.g. The classic causes of this are the organophosphates. ![]() Respiratory failure - secondary to diaphragmatic weakness. The acronym SLUDGE is useful for thinking about the muscarinic effects.: The syndrome can be surmised based on this pathophysiology - increased acetylcholine activity at the peripheral muscarinic, nicotinic and central receptors. Treatment described on Toxbase is generally purely supportive though.Īgain, unsurprisingly, this syndrome is characterised by the features of excess acetylcholine activity - primarily parasympathetic nervous system effects. Most patients don’t require it - advised for compromising tacchydysrhythmias, intractable seizures, or severe agitation. The specific antidote is phytostigmine salicylate - it works by inhibiting acetylcholinesterase, allowing more endogenous acetylcholine to compete at the receptors. Management is initially supportive and as per management of general toxic ingestion. As well as the specific anticholinergic drugs, a very wide range of drugs have anticholinergic side effects.Īnticholinergics - atropine, glycopyrolate.Īntihistamines - promethazine, chlorphenarimine,hydroxyzineĪntipsychotics - quetiapine, olanzapine, clozapine, chlorpromazine.Ĭyclic antidepressants - amitriptyline, doxepin, nortriptyline There is a very wide range of drugs which can cause this toxidrome. This represents mydriasis (with subsequent loss of accommodation), altered mental state, flushing, pyrexia, dry skin and mucous membranes, which are the most common manifestations. The well known mnemonic for this toxidrome is:īlind as a bat, mad as a hatter, red as a beet, hot as hell, and dry as a bone. The extent of the central effects is dependent on the ability of the drug to cross the blood brain barrier. The effects result from this blockade in both the central and peripheral nervous systems.Ī wide range of drugs cause this through competition with acetylcholine at the receptor site, and as such has little impact on the other acetylcholine receptors. The toxidrome is, unsurprisingly, a consequence of excessive choline blockade at muscarinic receptors. ![]()
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