Background: Atropine is a competitive acetylcholine antagonist at muscarinic receptors. In overdose it can cause tachycardia and altered mental status (AMS). Physostigmine (physo) is a carbamate that reversibly inhibits acetylcholinesterase. The usual dose is 0.5-2 mg slow intravenous (IV) push, repeated every 15-40 minutes as needed. It is unusual for doses in the emergency department (ED) to exceed 4 mg. We describe a patient with a massive atropine eye drop ingestion treated with 14 mg physo, resulting in improvement of AMS and avoidance of intubation and mechanical ventilation and the potential associated morbidity with these invasive procedures.
Case Report: A 34-year-old man presented to an ED after ingesting 150 mg of eye drop atropine. He had AMS, heart rate (HR) of 150 beats/min, flushed skin, dry mucosa, normal glucose, and temp of 100.3 degrees F. The remainder of his exam was unremarkable. ECG showed sinus rhythm and no interval/segment abnormalities. Sedation and intubation were eminent, and in attempt to avoid the morbidity of this procedure, physo was used. Over the next 75 minutes, physo was given in 1 mg doses to a total of 11 mg. There was minimal change with the initial doses; after the 4th dose each subsequent 1 mg improved the AMS and HR, which would worsen again over the next 10 minutes, necessitating another dose. At completion of ED treatment, HR was 90, and AMS resolved. Lab studies included a negative ethanol, acetaminophen, and urine drug screen, normal Chem 7, and serum atropine level of 240 ng/mL. He was admitted to the ICU for further care, where he required 3 additional 1 mg doses of physo for agitation. Intubation was never needed. The remainder of his hospital stay was uneventful.
Discussion: There is a paucity of documented atropine eye drop ingestions. Atropine toxicity is not predictable by dose. Fatalities have been reported with less than 100 mg; survival with more than 1 g. Following a 1980 report of 2 patients with cardiac arrests after cyclic antidepressant overdose where treatment included physo, its use declined. Recent literature has tempered some concern about its deleterious effects; its use has again become more common. A large total dose of physo was needed in this case, with doses repeated in rapid succession. This was likely due to the massive atropine ingestion, confirmed by the symptoms and serum atropine concentration. This case illustrates the most beneficial aspect of physo use: the ability to control agitation and reverse delirium thereby reducing the need for invasive interventions.
Conclusion: High doses of physostigmine may be considered in severe pure antimuscarinic toxicity to prevent the morbidity associated with the invasive interventions of intubation and mechanical ventilation.
