![]() In the wisdom of hindsight, it shouldn't be surprising that many of these patients died, since they had extremely severe tricyclic intoxications that weren't treated appropriately.(c) Physostigmine was pushed relatively rapidly (e.g., 2 mg over three minutes).(b) Patients were not treated based on modern standards of care (e.g., they didn't receive hypertonic bicarbonate).(a) Patients had extremely severe tricyclic antidepressant intoxication.These cases generally involved the following elements: A handful of case reports from ~1980 suggested that physostigmine might cause bradyasystolic cardiac arrest.Physostigmine was enormously popular in the 1970s, when it was used with abandon for all sorts of toxicologic abnormalities (including administration in some “coma cocktails” which were broadly administered to comatose patients).Administration of the two agents is similar. The difference between the two agents is that physostigmine penetrates the brain, whereas neostigmine doesn't. Physostigmine is extremely similar to neostigmine, which is commonly used in intensive care units for management of colonic pseudo-obstruction (more on neostigmine here).It inhibits degradation of acetylcholine within the synapse, thereby increasing acetylcholine signaling levels. Physostigmine is an acetylcholinesterase inhibitor.If physostigmine causes a resolution of delirium, this establishes the presence of an anticholinergic toxidrome and removes the need for further neurodiagnostic testing. If anticholinergic intoxication is strongly suspected, then a physostigmine challenge may be used diagnostically (more on this below).Depending on the clinical context, additional studies may be considered (e.g., head CT scan and potentially lumbar puncture).If evidence of sodium channel blockade is found, this has important clinical implications (more on this below).įurther investigation of altered mental status.More on the EKG findings of sodium channel blockers here.This is essential to evaluate, especially for any evidence of sodium channel blocker activity (e.g., QRS widening and tall R-wave in aVR).Serum acetaminophen and salicylate levels.Creatinine kinase level (with a repeat value if concern for the evolution of rhabdomyolysis).Electrolytes, Ca/Mg/Phos, complete blood count.STAT fingerstick glucose, if mental status alteration. ![]() This will vary depending on the context, with common considerations including: It has a broad differential including infection, infarction, stroke, or intoxication (lithium, phenytoin, anticholinergics, organophosphates) ( 8879053) Opsoclonus is rapid involuntary eye movements in all directions. An EKG may be helpful in sorting out a pure anticholinergic syndrome versus the combination of an antiholinergic syndrome plus sodium channel blockade. Anticholinergic toxicity is often one component of tricyclic intoxication.These four elements suggest an anticholinergic toxidrome.□ Dry skin – This is an essential element, which helps separate anticholinergic toxidromes from sympathomimetic toxidromes.Hyperthermia with dry, flushed skin (examination may reveal no sweat in the armpits).Ĭore elements of the anticholinergic toxidrome.Pupillary dilation, causing blurry vision and photophobia.CNS effects may persist after peripheral features have resolved.More severe cases may present with seizure and/or coma. ![]() Most often causes agitated delirium (often with hallucinations, incoherent speech, picking at the air or objects).Mad as a hatter, blind as a bat, red as a beet, hot as a hare, dry as a bone, full as a flask. ![]()
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