Case report: Amanita muscaria (fly agaric) poisoning

Mikhail Kochlev/

Mikhail Kochlev/

2 out of 5 stars

Coma in the course of severe poisoning after  consumption of red fly agaric (Amanita muscaria). Mikaszewska-Sokolewicz MA et al. Acta Biochim Pol 2016 Feb 1 [Epub ahead of print]

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Probably the most recognizable mushroom in the world is Amanita muscaria (the “fly agaric”), This striking red-and-white fungus contains several distinct neurotoxins:

    • ibotenic acid this toxin is structurally similar to the excitatory neurotransmitter glutamic acid
    • muscimol: structurally similar to GABAA  this is the main psychoactive component of A muscaria producing sedative and dissociative manifestations
    • muscarine: contrary to the common belief that it is a major contributor to poisoning from A muscaria , this cholinergic toxin is usually present in such small amounts that it rarely contributes to significant clinical toxicity

Because of the variety of toxins present in A muscaria and their different effects, ingestion of the mushroom often does not produce a clear and consistent toxidrome. This case report, from the Medical University of Warsaw, describes a 21-year-old man who was brought to hospital after intentional ingestion of A muscaria. He was unresponsive to pain or voice. Physical examination revealed tachycardia (pulse 127/min) along with mitosis and warm, dry skin. He subsequently developed seizure activity and increased oropharyngeal and respiratory secretions. After intubation, gastric lavage retrieved undigested mushroom fragments that the authors suggest were clearly A muscaria.

The patient was admitted to the ICU and regained consciousness after 11 hours of supportive care. He was discharged on day 3.

Manifestations of A muscaria poisoning include: weakness, altered mental status, dizziness, somnolence, coma, hypersalivation, and hallucinations. Onset is within 30-120 min of ingestion with symptoms typically lasting for 8-12 hours. Deaths are rare.

This paper may be worth looking at, since reports of A muscaria poisoning are so unusual. However, the report contains some unsubstantiated claims that should have been removed if they could not be supported with evidence. The authors state that muscimol is a GABAB-receptor antagonist, a contention that I believe is incorrect. Also, they argue that the gastric lavage the patient received “probably” was responsible for the good outcome and quick recovery. There is absolutely nothing in the case description or in the medical literature that would back up this claim. They key to treating these patients is good supportive care with benzodiazepines as needed for agitation.

Peds in a POD- Why does it keep coming back?

Your Case:

A previously healthy, 8 year-old Hispanic boy presents to the ED with a recurrent rash on his right posterior thigh. The involved area always becomes “infected” whenever the patient develops a fever, and this is the 3rd and most severe episode.

1st episode– 2 years ago, the family was still living in Mexico, and at that time the rash was diagnosed as an insect bite. Mom empirically treated with topical antibiotics. Within a week, the lesion resolved, but the patient was left with a small, dark, discolored area in its place.

2nd episode – 1 year ago, he had an episode of fever and diarrhea with a red, pruritic lesion on right posterior thigh. Again, a topical antibiotic was placed on the area. After resolution of the illness, the redness improved, but he was left with an even larger dark discoloration at the site.

3rd episode– 5 days ago, the patient developed fever and URI symptoms. On Day 2 of illness, a red, pruritic, blistering area started developing on right posterior thigh. He was diagnosed in ED with cellulitis and sent home with trimethoprim/sulfamethoxazole. On Day 3, the fever and URI symptoms began to resolve, but the rash was progressing despite compliance with the antibiotic.

Today, the rash looks like this:


Physical Exam– Well appearing, afebrile. Lesion as shown above, non-tender, negative Nikolsky sign, no fluctuance, no mucous membrane involvement, no other skin lesions.

Labs– CBC/CRP/CMP/LFT- all normal

What is your differential diagnosis?
Fixed drug reactions, Insect bites, Bruises, Focal skin infections, Contact dermatitis, Child abuse, Bullous skin eruption, Burn/child abuse, Bullous erythema multiforme, Bullous pemphigoid, Bullous reaction to insect bites (most commonly fleas), Staphylococcal scalded skin syndrome, Bullous impetigo or cellulitis, Stevens-Johnson syndrome or toxic epidermal necrolysis


What is the most likely diagnosis?

Fixed Drug Reaction


What you need to know

  • The most reliable and characteristic finding of a fixed drug eruption is the recurrence of the lesion at the same site, which can be anywhere on the skin or mucosa.
  • History-taking is key
  • Trimethoprim-sulfamethoxazole and acetaminophen are commonly implicated in fixed drug eruptions.
  • The mainstay of treatment is to prevent recurrence of the eruption by avoiding the offending drug



Cossey, M. et al. Visual Diagnosis:8-Year-Old Boy With Recurrent Rash. Pediatrics in Review 2000;36;4



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Subacute STEMI. Should the patient go for emergent PCI, or can he wait until the next day?

This was sent by a very good medical student, who had a very good question.  He wishes to remain anonymous.

A 56 y/o male presented with Chest Pain radiating to the left jaw, starting at 8pm the previous night (15 hours prior), which was 10/10 at that time.  He decided to wait it out at home, then presented at around 11 AM, pain now reported at 2/10.

Here is the initial ECG (see the patient's previous ECG below for comparison):
There is sinus rhythm and new inferior QS-waves with less than 1 mm of inferior ST elevation, and reciprocal ST depression in aVL, and T-wave inversion.  
Such T-wave inversion is common not only in reperfusion, but in persistent and prolonged occlusion after formation of Q-waves, especially QS-waves.

Here is the patient's previous ECG:
This old ECG confirms that the first ECG shows a new MI

So this patient has a subacute STEMI.   

The initial troponin T returned at 0.47 ng/mL (quite high for Troponin T) and rose from there to 0.81, then 1.96 (typical of a large STEMI).  Whether the troponin continues to rise or not says nothing about ongoing ischemia: it takes time for complete troponin rise and fall even after infarction is completed.  Only the ECG and pain can tell you prospectively whether ischemia is ongoing.

The patient was admitted with "NonSTEMI" and did not undergo emergent angiogram and PCI.  He went the next day.

This is a nearly completed STEMI (a very advanced subacute STEMI). To call it a NonSTEMI is misleading.

Is it too late for emergency cath lab activation?  Should he go now, or with less urgency (tomorrow)?

My answer is this: 

If there is:
1) persistent ST elevation (as there is here) or 
2) persistent pain (as there is here)

Then the patient should go emergently.

But I know of no data to support this.

There are 2 excellent articles addressing whether a patient with completed MI should undergo PCI at all (vs. medical therapy alone), but none addressing this situation.

Schomig et al. published this in JAMA in 2005:  
Data presented shows benefit of PCI (vs. medical therapy alone) for patients who present between 12-48 hours after STEMI if there was persistent STE, or simply new Q-waveseven in the absence of pain.  But they did not assess the urgency of PCI.

Hochman et al. published the Occluded Arteries Trial (in the New England Journal).  
In this article, they assessed arteries occluded for 3 days or more, and found that PCI resulted in worse outcomes than medical therapy.

The question this student posed was slightly different: beyond 12 hours, is emergent PCI better than delayed PCI (both groups getting PCI).

ACC/AHA 2013 STEMI guidelines say this:

Primary PCI is reasonable in patients with STEMI if there is clinical and/or ECG evidence of ongoing ischemia between 12 and 24 hours after symptom onset (94,95). (Level of Evidence: B).  This means if there is chest pain, persistent ST elevation, or especially upright T-waves.

But the ACC/AHA guidelines do NOT address the timing (emergent vs. urgent) and they reference two studies, one of which is the Schomig article above, and the other of which also does not address emergent vs. urgent PCI.  

94. Schömig A, Mehilli J, Antoniucci D, et al. Mechanical reperfusion in patients with acute myocardial infarction presenting more than 12 hours from symptom onset: a randomized controlled trial. JAMA. 2005;293: 2865–72.

95. Gierlotka M, Gasior M, Wilczek K, et al. Reperfusion by primarypercutaneous coronary intervention in patients with ST-segment elevationmyocardial infarction within 12 to 24 hours of the onset ofsymptoms (from a prospective national observational study [PL-ACS]). Am J Cardiol. 2011;107:501–8.

Learning Points
1. I think if there is ongoing pain or ST Elevation, it is wise to go emergently to the cath lab to save any remaining viable myocardium.  Randomized data on this is lacking.  Probably, most researchers would be reluctant to test such management.  Similarly, no one has ever conducted a randomized trial of emergent vs. delayed PCI for NonSTEMI with refractory (continued) symptoms.
2. PCI at some point within the first 12-48 hours of STEMI is definitely indicated.

Dr. Goldsmith of our Cardiology Department added his opinion in an email:

This is a gray zone. Apropos of your general thinking that we should act to make a clinical difference and not just on the basis of guidelines (!) the issue of timing here relates to how much salvage is likely. Points in favor of going now: the relatively low trop on presentation (suggests possible opening/closing of an artery) with pain. If the trop had been 20 I probably would not have gone.....pain and ST elev are problematic guides because both can persist for many hours after there is no chance of successful reperfusion (MI pain in the old days required morphine for 24 hours, usually, as I remember from my residency!). So these are tough, and as you say there is no firm guidance. The low trop with a rise suggest a new event or recurrent event to me, rather than a done deal, so I probably would have argued for earlier study knowing it might or might not help but would not likely hurt. Perfect Pathway B case, by the way!

…New (immuno)therapies….new toxicities…

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