History
In patients with suspected amatoxin poisoning it is important to attempt to collect the following information:
-
Time of mushroom ingestion - Patiens who develop GI symptoms (abdominal cramping, nausea, vomiting, and diarrhea) within 5 hours of the ingestion of the mushroom are unlikely to have ingested an amatoxin containing mushroom. GI symtpoms which manifest more the 6 hours from ingestion should make health care providers suspicious for ingestion of a possible amatoxin containing mushroom.
-
Time of onset of symptoms – Phalloidin causes gastrointestinal (GI) symptoms about 6-12 hours after ingestion; renal and liver toxicity caused by amanitin is evident 24-48 hours after ingestion, though a pattern of delayed-onset renal toxic mushroom ingestion has been seen in western North America [12]
-
Description of the mushrooms ingested – If a mushroom sample is available, place it in a dry paper bag (do not moisten or refrigerate it)
-
Location at which the mushrooms were obtained
-
Other mushrooms or toxins concurrently ingested – GI symptoms occurring earlier than 6-12 hours after ingestion suggest that another mushroom is responsible, but if the patient’s meal included several different mushrooms, earlier onset of symptoms does not rule out concomitant amatoxin ingestion; if the setting is an attempted suicide, every effort should be made to identify any other toxins that may have been ingested
Toxicity from amatoxin and other cyclopeptides occurs over several days and usually develops in the following stages:
-
Stage I – Sudden onset of nausea, vomiting, watery diarrhea, and cramping abdominal pain between 6 and 12 hours after ingestion, potentially resulting in dehydration and hypotension; patients often present during this stage and, if misdiagnosed, may be erroneously discharged without further care. There is some evidence that in the development of early diarrhea (within 8 hours of ingestion) may protend more serious outcomes [13]
-
Stage II – Clinical improvement with supportive care; however, despite the resolution of symptoms, hepatic and renal damage is ongoing, as evidenced by rising laboratory test values
-
Stage III – If discharged, patients may return to the hospital 2-6 days later with severe hepatica injury or failure, severe coagulopathy, renal failure, and encephalopathy
Physical Examination
The examination findings depend on the stage of the poisoning. As a consequence of profuse vomiting and watery diarrhea, the patient may present in hypovolemic shock during the GI phase. Accordingly, assessing the patient’s volume status is an important component of the initial evaluation. With delayed presentations, it is important to look for signs of hepatic dysfunction (eg, jaundice, lethargy, or bruising), renal injury, or central nervous system (CNS) dysfunction.
Examination findings may include the following:
-
Vital signs – Tachycardia, hypotension
-
Skin – Poor turgor, jaundice, bruising (with hepatic failure)
-
Head, ears, eyes, nose, and throat – Epistaxis or scleral icterus that is related to hepatic failure may appear in a patient with delayed presentation
-
Abdomen – The patient can have mild diffuse tenderness, and a rectal examination reveals occult bloody stool. Hepatomegaly results from hepatitis late in the course of the disease.
-
Nervous system – Neurologic effects are related to hepatic failure; depending on the time elapsed since ingestion, the examination findings may range from normal to confusion, agitation, lethargy, somnolence, seizures, or coma.
Complications
Complications of amatoxin poisoning include:
-
Volume depletion and shock from GI distress
-
Hepatotoxicity
-
Hepatic failure
-
Acute kidney injury
-
Encephalopathy
-
Pancreatitis
-
Polyneuropathy
-
Amanita muscaria.
-
Amanita phalloides.
