Welcome to the fourth case in the One Pill Can Kill series. Let’s focus on something a bit different this time: plant poisonings. Ingestion of various plants, including leaves, flowers, seeds, and mushrooms, accounts for more than a quarter of calls to poison control centers and about 5% of hospital admissions. While most are harmless, there are several case reports of children dying after ingesting toxic plants. While many of these plants will cause symptoms quickly, facilitating care for clinicians attuned to the temporal relationship between ingestion and presentation, some plants cause delayed toxicity that may even go undiagnosed.
Generally you can think of plant toxins causing one of four toxidromes.
Anticholinergic plants include jimsonweed (Datura stramonium) and angel’s trumpet (Brugmansia species), which are clinically similar in their effects to atropine and scopolamine and present with the “mad as a hatter, hot as a hare, blind as a bat, red as a beet” syndrome.
The “low and slow” toxidrome, with hypotension and bradycardia, can be caused by digoxin-containing plants such as foxglove (Digitalis species), oleander (Nerium species) and milkweed (Asclepias species), among others. These cardioactive steroids work in the same fashion as digoxin, blocking the sodium/potassium ATPase pump in cardiac cells.
Wormwood (Artemisia absinthium) and the false morel mushroom (Gyromitra esculenta) are known to cause seizures; these can be delayed several hours after ingestion and difficult to control.
Lastly, a gastrointestinal toxidrome can be caused by several plants; in this case, we’ll talk about delayed GI symptoms after ingestion of mushrooms. Interestingly, when GI symptoms occur within six hours of mushroom ingestion, the poison is rarely serious. Yet delayed GI symptoms, after 12 hours, are always a cause of concern. The reason for this is similar to the toxicity seen in acetaminophen overdose: It’s silent at first, but once symptoms of liver toxicity are displayed at around 24 hours, aggressive critical care can often be unsuccessful, leaving liver transplant as the only option.
Let’s jump into a case based on a real-life case report.
You are the second unit responding to rental cottage two hours north of Big City. Two children, aged 9 and 5, are reported to have nausea, vomiting, and confusion.
On arrival you find a girl and her younger brother with their mother and father. Both children look very unwell. The first unit hands you the vital signs: Both children are tachycardic, though they have normal blood pressures for their ages. They are holding their abdomens, vomiting (no bile, no blood), and have nonbloody diarrhea. The parents report no cough or fever.
On physical exam, both look unwell and dehydrated, with dry lips and diminished skin turgor. The boy seems to have a yellowish tinge to his sclera.
Recognizing how strange it is that both children would fall ill together, you immediately suspect poisoning. After ruling out carbon monoxide, you question their diet. The family is renting the cottage to escape the boredom of the Big City lockdown and brought their own groceries for the weekend away. Nothing seems out of the usual. You dig deeper, convinced there must be a common toxin. After some time the mother exclaims, “Oh! Yesterday I cooked the pasta sauce with some puffball mushrooms we picked.”
List five toxic differential diagnoses for children with gastrointestinal upset.
List five nontoxic differential diagnoses for children with gastrointestinal upset.
What is your approach to vomiting in a 3-day-old, 3-month-old, and 3-year-old child?
List three diagnoses specific to vomiting in a 3-day-old, 3-month-old, and 3-year-old child.
What are your next three steps once arriving at the patient’s side?
You recall it can be very difficult to speciate mushrooms; puffball and paddy straw mushrooms, for example, look a lot like the amatoxin-containing Amanita phalloides, or death cap mushroom.
Both children are rapidly transported to the local hospital, where they deteriorate. They are subsequently flown by helicopter to the pediatric hospital in the Big City. The 9-year-old girl receives a liver transplant three days later. Sadly, the 5-year-old boy dies of fulminant liver failure four days after the 9-1-1 call.
Death Cap Mushrooms
Amatoxin causes hepatic toxicity and has correlates to acetaminophen toxicity, though the mechanisms are different. The toxin destroys hepatic cells, leading to hepatic failure. Many organs can be supported during toxic failures; venoarterial extracorporeal membrane oxygenation (ECMO) can support recovering hearts, and dialysis machines can replace failed kidneys. However, there are no external technologies that can support a failed liver.
While some medications, such as high-dose penicillin, silibinin, and n-acetylcysteine, have proposed benefits, there are no antidotes to amatoxin.
After an initial asymptomatic period, GI upset begins 6–24 hours after ingestion. Rapid progression of liver failure occurs, leading to synthetic dysfunction that presents as jaundice, confusion, and abdominal pain. Stigmata of liver failure associated with cirrhosis are often absent because, unlike most cases of cirrhosis, progression is rapid, a matter of days. Still, some features, such as ascites, asterixis, and jaundice, can be seen.
As the liver is responsible for clearing toxins, maintaining coagulation factors, and synthesizing protein, symptoms of liver failure include confusion caused by brain swelling, bruising and bleeding, and extremity edema and ascites.
Once the liver fails, the only option to save the patient’s life is a prompt transplant.
After a decade working as a helicopter paramedic, Blair Bigham, MD, MSc, EMT-P, completed medical school. He is now an attending emergency physician in Ontario and critical care fellow in California. E-mail him at email@example.com; on Twitter follow @BlairBigham.