What kind of herbal tea can kill you? When can a so-called cancer treatment become more lethal than the disease? A holiday brunch turns into a toxicology emergency involving profoundly low blood pressure and cardiac arrest. Follow the clues through dangerous plant toxins, alternative cancer remedies, and a centuries-old connection to Hecate, Shakespeare’s witches, and Celtic graveyards.
Transcript
This is Pick Your Poison. I'm Dr. JP, ER doctor, toxicologist, and unapologetic lover of all things poison. Wanna know what kind of herbal tea can kill you? When the so-called treatment for cancer is more lethal than the disease?
What toxin is associated with Greek goddess Hecate, Shakespeare's witches, and Celtic graveyards? Stay right here to find out.
Before we get started, two quick announcements. First, some exciting news I can't wait to share with you. Pick Your Poison won a Signal Award for Best Science Podcast. It couldn't have happened without you listening and supporting the pod, so thank you so, so much.
Second, I've launched a newsletter called The Poison Archive, featuring strange stories from the darker side of medicine. It's full of fascinating poisons, medical mysteries, and unusual historical cases, things that I can't always fit into the podcast. It's free, and you can subscribe at pickpoison.substack.com.
on to today's episode.
Will our patient live or die? It's up to you and the choices you make. So check your vitals and let's get started.
Today's episode starts at a holiday brunch. Your parents are hosting friends and family for an early holiday celebration.
The house is warm and crowded, filled with conversation and the smell of the quiche and pastries your dad baked that morning
A fire crackles and pops in the background, throwing warmth across the room. Outside, a light dusting of snow covers the street. A friend of your dad's is sitting beside you, repeatedly trying to fill your glass with champagne. You have a shift later this afternoon, so after declining for the third time, you pick up the glass and carry it into the kitchen safely out of his reach.
As you set it on the counter, you hear shouting outside
At first you assume it's the neighborhood kids playing in the snow, but as you turn back towards the dining room, you stop. It doesn't sound like kids playing, it sounds like someone wailing, and it hasn't stopped. You cross to the window and pull back the curtain. Across the street, a man is lying motionless in his driveway, a thin layer of snow around him.
His wife is standing nearby screaming for help. You don't know the neighbors well, but you do recognize them. You once toured their garden with your parents. They're famous in the neighborhood for it, somehow managing to keep flowers and color blooming almost year-round. You run outside. Maybe he slipped on the ice, hit his head.
He's collapsed at the edge of one of the flower beds. His wife is frantic. She tells you he vomited several times, complained of feeling dizzy, and then a moment later, passed out and fell down. Behind you, the front door opens. Your parents have heard the commotion and followed you outside. The man is extremely pale and sweaty.
"Call nine, one, one," you say to your mom. You kneel beside the man and reach for his wrist. You can't find a pulse. Question number one, if you can't find a pulse in his wrist, which of the following are true? A, he's dead, B, his blood pressure is low, C, you need to try another location, or D, all of the above.
The answer is B and C, and this is important, and it's the reason why when you take a CPR class, you're taught to check for the pulse in the neck or the groin. Just because you can't find a pulse in the wrist definitely doesn't mean the person is dead. It could mean that their blood pressure is low and you just can't feel it.
But if you go more centrally, like we said, the neck or the groin, the pulse will be present. The man is clearly alive. His eyes are open and he's awake, so you move your fingers to his neck.
There it is. Now it's beating under your fingertips But it's very slow and very weak. You don't have a blood pressure cuff, but it's a pretty safe bet that his blood pressure is extremely low
The medics arrive, and since this is fiction, of course, you are the doctor. In the emergency department, the nurses brush snow and ice from the patient's hair while getting him undressed and hooking him up to the monitor. The man is fifty-two years old. He has a temperature of ninety-five Fahrenheit or thirty-five Celsius.
This is low, but he was lying outside in the driveway in the cold weather for at least twenty or thirty minutes, so probably we just need to warm him up. His blood pressure is sixty over forty, confirming your suspicion about hypotension, i.e, low blood pressure. His heart rate is also low at fifty beats per minute.
His respiratory rate is twenty, and his oxygen saturation is a hundred percent on room air. On physical exam, he's very lethargic. He does wake up when you ask him questions, but he's only giving very short answers. He says he was well until an hour ago when he became dizzy, then developed nausea and vomiting.
He and his wife were on the way to the grocery store, but when he walked outside to get into the car, he passed out. He hasn't had a fever, no abdominal pain, constipation, or diarrhea. The dizziness is not vertigo, but rather the lightheadedness and the feeling like he's about to pass out.
He's not had a headache, no weakness in his arms or his legs, and he denies other complaints. He says he has diabetes and takes metformin, an antidiabetic agent. Occasionally, he takes ibuprofen, i.e. Motrin for pain, but he denies other medicines. He doesn't have any allergies to medicines. On physical exam, his pupils are equal, round, and reactive to light.
His cranial nerves are intact. His lungs are clear, as is his heart. He doesn't have any abdominal tenderness, and he's moving all of his extremities with good strength.
Essentially, what we have is a patient with hypotension and syncope, i.e., passing out. This is most likely caused by the low blood pressure. Tons of things cause low blood pressure, and one of the big things we worry about in the emergency department is infection and sepsis or septic shock. You order a liter of IV fluid, hoping it brings his blood pressure up.
The nurse checks a finger stick and tells you his glucose is a hundred milligrams per deciliter, which is normal. They also get a device to warm him up. basically a blanket hooked up to a machine that blows in hot air.
We do need to warm him up, but you have to keep a close eye on his blood pressure because warmth causes blood vessels to dilate and cold causes them to constrict, so we have to be careful. Back at your desk, you open his chart, ordering a head CT to rule out an intracranial hemorrhage as either the cause of this problem or the result of the fall.
You also order labs, including lactate and blood cultures, a urinalysis and a urine culture to check for infection, and a chest X-ray to look for pneumonia. Of course, this is a toxicology podcast, not an infectious disease one, so I think you already know this isn't gonna be sepsis. Let's talk about toxins that cause low blood pressure.
At the very top of the list, of course, are blood pressure medicines, common culprits for obvious reasons. He says he doesn't take any blood pressure medicine, and a low blood pressure certainly wouldn't be caused by metformin or ibuprofen. The tech brings you his EKG. You take one look at it and rush back into the room. Why? The EKG shows a wide QRS. The big peak that you see on the EKG is the QRS, and widening is a sign of sodium channel toxicity. What it really means is that he's at risk for a lethal complication. And that's question number two.
Is the lethal complication A, ventricular tachycardia, B, a stroke, or C, myocardial ischemia, i.e. a heart attack?
The answer is A, ventricular tachycardia or V-tach for short. In the heart, sodium channel poisoning means the heart can't conduct properly, leading to life-threatening arrhythmias. Can we treat this?
Yes, we can. So question number three, should you order A, potassium, B, sodium, or C, bicarbonate?
The answer is C. The treatment is bicarbonate, which technically comes as sodium bicarbonate, But it isn't actually the sodium in this case working to reverse the effects of the sodium channel blockade, even though that seems confusing.
It's the bicarb that helps. You start with a bolus of one mil equivalent of bicarb per kilo. He's about eighty kilos, so that'd be two amps of bicarb in the US. Then you start a bicarb drip. You can make it yourself by putting three amps of bicarb into a liter of D5 water. You run it at about one and a half times maintenance.
In his case, probably about a hundred and fifty cc an hour. The nurse gives the bolus, and you're happy to see the QRS narrows on the EKG, meaning the bicarb is working. While mixing the drip, the monitor suddenly starts beeping. A wide complex tachycardia races across the screen. You check for a pulse.
This time, it's really absent. This is pulseless V-tach, so you start CPR and advanced life support, including epinephrine, while the nurse starts the bicarb drip. Fortunately, this patient came to the emergency department relatively early. There are one million things that can cause ventricular tachycardia and ventricular fibrillation, and even more that cause cardiac arrest.
But we were able to get this important clue before it happened, and that was the QRS widening on the EKG, meaning we can narrow this down to a sodium channel blocker. What toxins cause sodium channel blockade? Well, the classic association is tricyclic antidepressants, old-school medicines like nortriptyline and amitriptyline.
We rarely see these in modern times because psychiatry generally prescribes newer and safer antidepressants like SSRIs, for example. Bupropion is a more modern antidepressant, and it does cause it. Diphenhydramine, i.e. Benadryl, which of course is over-the-counter, can cause sodium blockade in overdose. Some anti-dysrhythmic drugs themselves cause it.
Medicines we use to treat arrhythmias like flecainide and procainamide. Cocaine is another cause. We've also talked before about local anesthetic toxicity. Both lidocaine and bupivacaine can cause sodium channel blockade.
The patient's wife has arrived and is at the bedside. She confirms he's not taking any medicines other than what we discussed earlier, ruling out antidepressants and antiarrhythmics. He's not taking Benadryl, and even if he was, he'd have other symptoms of anticholinergic toxicity, like a high heart rate and high blood pressure.
It's unlikely he was injected with local anesthetics right before collapsing. She says he doesn't use illicit drugs. Unfortunately, in the ER, we always have to be skeptical. So that's question number four. Could this be cocaine toxicity? A, yes, or B, no?
The answer is B, no. Cocaine doesn't fit. His heart rate and his blood pressure would both be high rather than low.
So what is going on here? Nothing you can think of seems to fit, and also nothing seems to be helping. You continue CPR, epinephrine, and shocks. You add amiodarone to try to stop the ventricular tachycardia, but he continues to be in pulseless VT. " Could this be the pancreatic cancer?" the wife asks. "What?" you say.
"Cancer? Why didn't anyone mention this sooner?" " They found a mass on his pancreas," she says. "We're waiting for the biopsy results, but they think it's probably pancreatic cancer." Question number five. This cardiac arrest is probably from pancreatic cancer: A, true, B, false
The answer is B, false.
It's useful information, but wouldn't have changed what we were doing. And in and of itself, cancer doesn't cause cardiac arrest directly. Of course, you can have a cardiac arrest when you have cancer, but it usually happens because of infection, electrolyte disturbances, or something else, none of which we have any evidence of so far.
I'm not aware of any cancers that can cause sodium channel blockade directly by themselves. But this information brings us into an area of toxicology that we toxicologists are pretty familiar with, and that's alternative treatments for cancer. It's a pretty depressing part in my opinion, and I use the word treatment here very loosely.
Patients diagnosed with cancer are understandably desperate for help and for treatments to save their lives or to alleviate suffering. Unfortunately, this leaves them susceptible to snake oil salesmen, essentially convincing patients they have answers that traditional medicine doesn't.
The reason I say it's depressing is not because the patients are seeking alternative therapy, but because they sometimes die from the alternative, quote unquote, treatment before they would have died from the disease. One example of this that was particularly popular in the '60s and '70s, but still pops up every so often, is Laetrile.
Laetrile is a brand name for amygdalin. That's a compound found in peach pits and apple seeds. It's a cyanogenic glycoside, meaning it contains cyanide. There was never any evidence that Laetrile worked, but nevertheless, people desperate for help would go to places like Mexico to get injections, and unfortunately, many died of cyanide toxicity before they died of the underlying disease.
What do you think about amygdalin here? Could our patient have gotten it from somewhere? Well, it doesn't fit. Certainly, cyanide toxicity does cause low blood pressure and cardiac arrest, but typically not sodium channel blockade. Another cancer treatment recommended mega doses of vitamins like B6, for example, but in that case, he'd have neuropathy, not sodium channel blockade.
Another one is cesium. Cesium can cause syncope and cardiac arrest and EKG changes, all of which our patient obviously has. However, it causes prolongation in the QTc interval, a different part of the EKG from the QRS, and that prolongation is called by potassium rather than sodium channel blockade in the heart.
So here at the bedside in this moment, I don't think we can a hundred percent rule out cesium, but I don't think it's very likely either
Herbal preparations are popular, things like kava, which we previously talked about, or chaparral, which is a shrub. These can cause hepatic failure, which doesn't fit here. there was a very sad case recently where an influencer died after treating her cancer with coffee enemas.
Those can cause electrolyte disturbances and bowel perforation, sepsis, but again, doesn't quite fit. You're racking your brain for an answer here, trying to remember every case report and internet headline you've seen on alternative cancer treatments. The patient is still in cardiac arrest, and you have no idea what the cause is.
" Is he taking anything? Supplements?" you ask the wife. "Alternative treatments? Chemo?" She says no. You continue CPR, electrical shocks, and you continue to try to come up with something. After a few minutes, she pulls a plastic water bottle out of her bag. It's filled with a yellow liquid. It looks like urine.
" Well, there was this," she says, "but it's all natural from our garden." Uh-oh. People love to think that all-natural things are by definition safe. Cocaine and opium are all natural, so is amygdalin, which we mentioned, just to name a few.
she takes the lid off the bottle and passes it to you. It has a strong smell. It's not urine. It smells like pine trees. All right, it's time to pick your poison. We have two clues here. The toxin is associated with cancer treatment, and it smells like pine trees. Can you guess what it is?
Question number six. Is this A, pinecone toxicity; B, Douglas fir toxicity; C, mistletoe toxicity; or D, yew tree toxicity?
The answer, this is yew tree toxicity, Y-E-W, in case you're confused while listening. pinecones and Douglas firs aren't toxic. It'd be tough to eat a pinecone, but it's basically fiber, and it isn't likely to cause much toxicity,
Douglas firs are not toxic, and people use them to make pine needle tea, for example. Mistletoe is mildly toxic, but it's not enough to cause death, generally just nausea, vomiting, and abdominal pain. Yew trees, however, are extremely toxic. Almost every part of the tree is poisonous, including the leaves and the seeds.
I mentioned the trees are associated with cancer treatment. Why? Because a modern medicine is actually derived from yew trees, and that's question number seven. Is it A, quinine, B, salicylate, or C, taxol?
The answer is C, Taxol, a common chemotherapeutic agent, is actually derived from yew trees. You'll hear arguments made by snake oil salesmen that chemo and modern medicines are toxic too. That's certainly true. But the idea is that chemo is given in regulated doses by oncologists who closely monitor for side effects, whether it's monitoring for symptoms, lab results, et cetera.
And the doses have been studied closely to balance the risks and the benefits, meaning a high enough dose to treat the cancer, but a low enough dose not to kill the patient. Yew trees contain a number of taxane alkaloids. Taxane B is responsible for most of the toxicity. It's a sodium and calcium channel blocker
It causes a number of different disturbances in the heart at the same time. First, calcium channel blockade causes calcium inside the cells to increase, and this slows conduction in the heart. Some patients have actually required pacing as a result of yew toxicity. Second, sodium channel blockade causes QRS resulting in V-tach and V-fib, resulting in ventricular tachycardia and ventricular fibrillation, as with our patient.
And very interestingly, it works similar to some class one antiarrhythmic drugs that we use in medicine, like quinidine and procainamide. All right, so back to our patient. His wife says they grow ornamental yew trees in their yard. The tree has beautiful red berries, which they like for color in their winter garden.
The patient took the leaves. They really look like needles from a pine tree, but since they're softer, I guess they're technically considered leaves. He brewed them into a tea and drank it, hoping the natural ingredients might reduce his risk of having pancreatic cancer
All right. Now we know what it is. What do we do other than standard cardiac arrest protocols? Did I hear somebody ask about GID decontamination? Should we pump his stomach? Well, interestingly, gastric lavage has been done in a number of cases reported in the medical literature.
Also, yew leaves have been found in the stomach on postmortem exam. This would suggest that gastric lavage might help, but I have some concerns. First, and most importantly, our patient drank tea. Liquids are rapidly absorbed from the stomach, usually within thirty minutes. So if we do a lavage, will the liquid still be in the stomach?
Probably not. But what if our patient had ingested the leaves? Is that different? Well, I would think it's much more likely for the leaves to be in the stomach, but the next question you have to ask is will the leaves fit through the lavage holes? The holes are as big as they can be, but the lavage tube is still a tube that has to fit down the back of the throat into the esophagus and the stomach.
The holes are actually smaller than some big extended release pills. So the fact that the leaves are found clumped in the stomach postmortem makes me think they might be too big to be sucked up the hose. I don't think it's gonna help our patient, and I think it's of debatable value in other patients.
Sodium bicarbonate is recommended. We're already doing that. Lipid emulsion therapy, i.e. intralipid, has been suggested. We talked about this in more detail in the episode Desensitized, so listen to that if you wanna hear more. Now, theoretically, lipid might help, though there's very little evidence to prove this.
As I said in almost every episode, we can't poison half the people in a study with life-threatening tea to see how well an antidote works or doesn't work. in this case, I think there's little harm in giving intralipid,
so I'd go ahead with a bolus followed by an infusion Overdrive pacing is reported to help in some cases. This is when you put pacer pads on a patient and artificially increase their heart rate because lethal arrhythmias like V-fib and V-tach are more likely to occur with slow heart rates than fast.
Several cases in the literature suggested a benefit. There's definitely no harm in trying, so between the electrical shocks, you set the pacer pads to a heart rate of 130 beats per minute. But none of these things helps. Another treatment that's reported and is probably the most useful, particularly with our patient, is ECMO, or extracorporeal membrane oxygenation.
Essentially, this is when you take the patient's blood out through a series of tubes and artificially pump to help the heart and oxygenate at the same time. Many reports about survivors of you toxicity were attributed to ECMO. So you call the ECMO team who comes down and hooks him up, hoping that this machine will keep him alive until his body is able to metabolize and eliminate the you.
How long will it take? It's a good question. We'd probably expect to see improvement around 24 hours with symptoms pretty much resolving by 48 hours. So not really that long.
Ingestion of yew is often life-threatening in intentional ingestions, like with our patient, or in cases of foraging where yew leaves were mistakenly
substituted for non-toxic pine needles. And fatality rates after intentional ingestions were as high as 42% in one series.
ingestions in pediatric patients often have good outcomes and minimal symptoms. Why the discrepancy? As I said earlier, almost every part of the plant is toxic, but there is one exception, and this is the fleshy red part of the berry, though the seeds inside the berry are very toxic.
So the thought is that if the kids eat the berry without chewing up the seeds, It'll most likely pass through without significant symptoms. In case cardiac arrest wasn't enough to keep you from eating the berries, the consistency has been described as, quote, "snot-like."
Another interesting fact is that the concentrations of taxines in the tree is actually highest in the winter. All right, so back to our patient. He's transferred up to the ICU on ECMO, where he continues to improve and is taken off 36 hours later. Yew is a pretty fascinating tree. It's extremely old, and it has a huge history in myth, religion, poetry, and medicine.
Just how old are yew trees? Well, old enough to have survived the last Ice Age. They are literally prehistoric. A woolly mammoth skeleton found in England has a spear embedded in it made from a yew tree. The woolly mammoth skeleton was dated to at least 20,000 BCE. Not only are the trees old as a species, but a single tree itself can live for thousands of years.
There's a yew tree in Scotland that's somewhere between 2,000 and 5,000 years old. Why isn't the dating more exact? Because unlike regular trees, they don't have rings you can count. Yew toxicity has been known for a very long time.
in 53 BCE, Julius Caesar recorded that a neighboring king committed suicide using yew juice rather than face capture or old age. How did it come to be used as a medicine? Well, in 1962, the US National Cancer Institute collected plant specimens from all over the country to test them for useful cancer treatment properties.
Two years later, chemists discovered that yew bark killed cells, now brand name Taxol, and started using it for chemotherapy. How does it work? Well, it stops mitosis, i.e. cell division. It binds to microtubules These are structural elements inside the cell, and they're necessary for cell division.
If a cell can't divide, it dies. Historically, the bark was stripped off the yew trees to make paclitaxel. It was estimated that the bark from six trees was needed to treat one cancer patient. it became so sought after, Pacific yews and other species were actually on the endangered species list, and they almost became extinct before alternative methods of production were found.
I thought about doing this episode actually for Halloween. Why? Because yew trees have long been associated with death and cemeteries.
In Celtic lore, yew trees are associated with death and resurrection. Why? Because the trees grow in a very interesting way. Drooping branches of old trees can actually root and form new trunks where they touch the ground, and this is why we can't age the trees simply by counting the number of rings in the trunk Yew trees are very commonly found in cemeteries in the UK, and they're almost always planted on the south and west side of churchyards, because it was thought that decaying bodies released fumes in these directions.
Additionally, it was believed that yew itself was toxic because its roots were in the soil with the decaying flesh, causing the tree in turn to become poisonous Yew was sacred to Hecate, the Greek goddess associated with magic, witchcraft, and necromancy. It was said to purify the dead as they entered Hades, and Shakespeare's witches in Macbeth added yew to their poisonous brew.
Remember Double, double toil and trouble, Fire burn and cauldron bubble. Gall of goat and slips of yew Silvered in the moon's eclipse. Anyway, back to our patient. He makes a full recovery. The day after he's removed from ECMO, the ICU notes green clumping fibrous material in his stool.
He was in fact eating the yew leaves as well as drinking the tea. Unfortunately, though, his biopsy does come back positive for pancreatic cancer. When you next talk to him, he promises to stick to traditional methods of cancer treatment from here on in. This is a fictional case, as are all our cases, to protect the innocent, but it is based on real poisonings.
The last question in today's podcast is also a pop culture consult. In Harry Potter, wands are made from different materials. Whose wand contains wood from a yew tree? Is it A, Harry's wand, B, Hermione's wand, C, Draco's wand, D, Voldemort's wand, or Dumbledore?
Follow the X and Instagram feeds both at pickpoison1 for the answer.
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