Culinary Catastrophe
Want to know what favorite poison of Agatha Christie’s is also used as a performance enhancer? What compound was used as rat poison and also in doping during the Tour de France? Listen to find out!
This is the Pick Your Poison podcast. I’m your host Dr. JP and I’m here to share my passion for poisons in this interactive show. Will our patients survive this podcast? It’s up to you and the choices you make. Our episode today is called the Culinary Catastrophe.
Want to know what favorite poison of Agatha Christie’s is also used as a performance enhancer? What compound was used as rat poison and also in doping during the Tour de France? Listen to find out!
Today’s episode starts in Hong Kong. You’re attending a conference and visiting some colleagues. As you’re touring the emergency department, medics wheel a 27-year-old woman into a room, saying she’s having seizures. An overhead speaker booms with an announcement about a Code Blue upstairs in the hospital. As you watch, the patient convulses in what looks like a seizure, freezing with her back arched and her face stretched into a grimace.
Of course, we don’t have a license to practice in Hong Kong, and normally wouldn’t be involved in her care, but this is fiction, so let’s pretend we’re the attending physicians. Per the medics, she has no prior past medical history including a history of seizures. The nurses are attempting to get vital signs, but as I’ve mentioned before this is difficult. The medics did check them enroute. Her temperature was 99.0 F, (37.2C), heart rate 103 beats per minute, blood pressure normal at 120/80, respiratory rate 18 breaths per minute, also normal and oxygen saturation, 100% on room air. You ask the nurse who’s placing the IV to get blood for a glucose check. It’s normal at 100mg/dL.
There are several different types of seizures, the most common is a generalized tonic clonic seizure, when a person loses consciousness, and has strong jerking movements in the arms and legs. This woman’s arched back, and flexed limbs are bizarre, but it looks like a seizure so we’d better do something.
Question #1. What is the first line treatment for seizures in the emergency department?
A. Naloxone (Narcan)
B. Lorazepam (Ativan)
C. Phenobarbital
D. Nitroglycerin
Answer: B Lorazepam, a benzodiazepine, is the first line treatment in the ER. Barbiturates, like phenobarbital are useful, but we consider them second line because they have more sedating effects, so we reserve them for patients who don’t respond to benzos. Neither naloxone or nitro will help with a seizure. You give 4 mg of lorazepam. Nothing happens. She’s still seizing. You give a second dose. It also doesn’t help.
An isolated seizure by itself isn’t a huge emergency. Most seizures stop by themselves, and unless the person is swimming, driving or something similar, they’ll wake up and return to normal. Patients with epilepsy certainly don’t need to come to the ER every time they have a seizure.
Status epilepticus, on the other hand is a true emergency. We used to define it as seizures lasting for 30 minutes, but the definition was revised to continuous seizures for 5 minutes, or two seizures in a row without returning to baseline, ie waking up, in between. Our patient meets the criteria, as it’s now been ongoing for more than 5 minutes.
What’s the concern about status epilepticus? First, it has a mortality rate somewhere between 10-30%. Not good. In addition, assuming she survives, there’s a risk of brain damage. Not surprisingly, the risk increases with the length of seizures, and this is the reason the time was shortened in the definition as neurological damage can occur before thirty minutes.
Question number 2. Which of the following causes status?
A. Epilepsy
B. Low blood sugar
C. Fever
D. Toxins
E. All of the above
Answer: All of the above. Anyone with epilepsy can develop it. Febrile seizures don’t often result in status epileptics, but it is possible. We always check the blood sugar in seizing patients to rule out, or fix, low blood sugar. We also hook them up to the cardiac monitor, for monitoring of course, but to check the cardiac rhythm and rule out an arrythmia, which can look surprisingly like a seizure, even to experienced eyes. Our patient’s rhythm on the monitor is fine.
This is a toxicology podcast, so let’s get right to it. There are a lot of toxins causing seizures. In fact seizure, coma, death is the endpoint of many, many poisons. However, there aren’t that many toxins causing actual status epileptics. Alcohol withdrawal for example, commonly causes seizures, but almost never status.
The list is relatively short. It includes medicines like bupropion, an antidepressant, theophylline, an old drug for asthma, diphenhydramine, ie Benadryl, and isoniazid, an anti-tuberculosis drug. Anything causing high or low sodium, ecstasy for example. Causes of low blood sugar, like insulin. Camphor, formerly in VicksVaporRub and currently used as rat poison. Carbon monoxide poisoning and lastly, tetramine, a cage convulsant.
The patient’s husband is in the waiting room. You send the intern out for more history, while you give a third dose of lorazepam and decide what to do next, if it doesn’t work. You’re relieved when she does stop seizing. Her limbs relax onto the bed. She’s awake, and alert, but barely moving and still not talking.
The intern, returns, confirming the patient doesn’t take any medicines including over the counter meds, so it’s not bupropion, theophylline, diphenhydramine or isoniazid. Her labs are back with a normal sodium and are otherwise unremarkable. The husband was at home when she became ill, ruling out carbon monoxide. Anyone in the house with her would’ve developed symptoms as well. He says they don’t have rats and don’t use rodenticides, making camphor and tetramine less likely. That said, I wouldn’t exclude tetramine just yet.
Why not? Tetramine causes intractable seizures. It was banned by most of the world in the 1980s, but nevertheless gained notoriety in China in the 2000s. During a ten-year period, there were more than 3,000 tetramine poisonings and 225 deaths. High profile cases included a shop owner poisoning his rival’s customers and university students poisoning other students.
Could it be tetramine? Yes. I’d cross my fingers and hope it’s not the case. The treatment if so? Same as we are doing. Antiepileptics. Just as you’re about to leave the bedside to call the ICU, the overhead speaker blares about another code upstairs. Immediately, the patient’s body stiffens again. She has a strange expression on her face. Her lips are pulled back into a grimace. The arching of her back is now extremely pronounced. It’s no longer touching the bed.
Good news, this isn’t tetramine. Bad news, it’s something equally as toxic. The worst part our patient is completely awake, though all of her muscles are contracted and she’s unable to move. You order another dose of lorazepam.
Question #3. Which of the following toxins could be poisoning our patient?
A. Strychnine
B. Botulism
C. Tetanus
D. Cyanide
Answer: A and C. This could be either strychnine or tetanus. Botulism causes flaccid paralysis, not muscle spasms. Cyanide causes cardiovascular collapse. Patients with cyanide poisoning can have seizures, but they’d also have a low blood pressure and probably cardiac arrest by now.
Strychnine and tetanus both cause muscle spasms. Our patient’s eyebrows are raised because of the contraction of her forehead muscles, her facial muscles are also clenched, pulling her lips back into a terrible facsimile of a smile. This is called risus sardonicus, because of the grizzly resemblance to a sardonic grin. Her arms are on the bed, as is her head. However, her back is completely arched, with only her heels touching the mattres. Like a bridge pose in yoga, but gone horribly wrong. Opisthotonos is the medical word for this, and it’s also caused by both toxins. Charles Bell’s painting titled Opisthotonos is an incredible depiction of the medical condition that also conveys the terror associated with it. It was based on his work as a physician with soldiers dying of tetanus after contamination of battlefield wounds.
How do we tell tetanus and strychnine apart? It’s difficult to do so definitely, but a few things differentiate them. The main thing is time of onset. Tetanus usually develops slowly. Patient may have muscle pain and lockjaw symptoms for weeks to months. Symptoms from strychnine develop about 30 minutes after oral exposure. Also, the muscle exam is different. With tetanus, the muscles stay stiff in between spasms. For example, the lockjaw doesn’t relax.
Our patient’s symptoms started one hour ago at most. So that’s not consistent with tetanus. After the lorazepam, her muscles and her face relaxed. Again, unlike we’d expect from tetanus, especially in her jaw muscles. Strychnine is the best answer here.
What does strychnine do? It works in the spinal cord and interferes with glycine, the main inhibitory neurotransmitter. Inhibiting the inhibitor results in an imbalance, and thus overstimulation. Overstimulation equals uncontrolled muscle contraction. The worst part is the patient is almost always awake during this.
You don’t need me to tell you strychnine is a lethal poison. There are a lot of ways it can kill you. The first, is respiratory failure. Remember the diaphragm is a muscle, if it’s not working, the patient isn’t breathing. Also, ventilation fails if the chest wall is contracted and frozen. Hypoxia, or low oxygen, results in anoxic brain injury. Renal failure occurs secondary to rhabdomyolysis or excessive creatine kinase released during muscle injury. Patients can aspirate. They can get severe acidosis from unrelenting muscle contraction. Hyperthermia occurs, with temperatures as high as 109 F (42.8 C) reported due to heat generated by the extreme muscle activity.
Question three. If we were in an underresourced area, or say this was the 1800s, what might be a critical part of a strychnine poisoned patient’s care?
A. A dark, quiet room
B. Cool compresses
C. Frequent sips of water
D. Warm compresses
Answer: A dark, quiet room was and can still be important. It’s not a coincidence our patient’s spasms occurred with the sound of the overhead speaker. Any stimuli, especially loud noises, but even just turning on a light, can trigger the contractions. In the past, treatment included minimizing stimuli in the hope the toxin wore off before the patient died.
If the patient gets medical care in time, they can survive. How do you treat it? There’s no antidote, treatment is supportive. First, I’d think about GI decontamination. I’d consider orogastric lavage, or pumping the stomach. We rarely do it these days, but it might help. Strychnine is rapidly absorbed so the window of potential benefit from lavage is short. The tube is extremely large and goes down the back of the patient’s throat into their stomach. It’s without question a noxious stimuli, so you’d have to weight the risks against the likelihood of any strychnine remaining in the stomach.
Another option for GI decontamination is activated charcoal. Charcoal is good at binding to strychnine, a fact we know from a very dramatic demonstration at the French Academy of Medicine in 1831. Professor PF Tourey ingested activated charcoal with a lethal dose of strychnine and survived. Again, you must weigh the risks against the benefits, because charcoal, if aspirated, is very toxic to the lungs. We’ve already mentioned the risk of aspiration with poisoning.
I’d have an extremely low threshold for intubating any patient with serious strychnine poisoning. Why? Several reasons. First, you can sedate and paralyze patients greatly alleviating their suffering. With sedation, they won’t know what’s happening and with paralysis, won’t have the tetanic muscle contractions. Second, airway compromise is a definite risk with poisoning given the concerns I mentioned earlier, so you’d be protecting their airway. Third it reduces the risk of aspirating, increasing the safety of gastric lavage, if indicated, and a dose of activated charcoal.
A critical component of treatment is stopping the muscle contractions with antiepileptic, or antiseizure drugs. The third dose of lorazepam hasn’t worked. Our patient’s still twisted into a horrible backbend. It’s time to try another class of drugs. A good second line agent is a barbiturate, like phenobarbital. You could also use new antiepileptics like phosphenytoin or levetiracetam. The choice of drugs is less important than the goal of treating until the seizures are controlled.
Other supportive care includes cooling for hyperthermia and IV fluids to prevent renal failure. After 24 hours, sedatives, paralytics and antiepileptics can be tapered down and hopefully stopped. If you can take good care of the patient, the toxin will be eliminated from the body, and they’ll survive.
Back to our patient. You talk to the husband and agree to intubate her to protect her airway and relieve her symptoms. Question #4. This is a tough one. More of a toxicology board level question. What paralytic must be avoided in patients with strychnine poisoning?
A. Succhyncholine
B. Non-depolarizing neuromuscular blockers
Answer: Succynile choline depolarizes muscle cells, causing contraction and so should be avoided.
You don’t do gastric lavage, since more than an hour has passed at this point, and there’s likely little strychnine in her stomach. You do give a dose of charcoal. Now she needs close monitoring in the ICU and time for the strychnine to be eliminated.
While we wait, let’s talk about where Strychnine comes from. It’s a tree native to Asia, the Strychnos nux-vomica tree. It’d often referred to as the vomiting nut. Medical use is recorded as far back as the 900s AD, in an Arabic medical text. It’s been used as a rodenticide since at least 1540 and it spread to Europe on ships, which usually had a lot of rats. It was commonly available in Europe in the 1700 and 1800s as a rat poison and was responsible for many poisoning deaths.
Disturbingly, it’s been used as a medicine to treat problems ranging from opioid overdoses, heart attacks, digestive problems and even snake bites. It seems to be the one thing we’ve discussed so far not used to treat syphilis or gonorrhea. It was used as a general tonic to combat shock which I thought was strange until I found it seems to coincide with the discovery and use of chloroform as an anesthetic. It was noted chloroform provided some relief of the symptoms of strychnine poisoning. So interestingly, the reverse was postulated. Perhaps strychnine could be used as an antidote for chloroform overdose.
This was then extrapolated to use in shock in general. As usual, I’m glad not to have been a physician in the 17 or 1800s, because it’s hard to believe we haven’t always understood shock. In those days, medicine and pharmacology were advancing, but physiology was still poorly understood. The word shock is probably derived from the French “choc” meaning jolt or blow. Treatment involved basically anything you can think of. Initially, there were no hypodermic needles, so substances were administered via oral, rectal or inhalation routes. Smelling salts are a great example. Alcohol was used both orally and rectally for treatment of shock. Seems like that might burn. Alcohol lowers blood pressure and makes patients less awake, not more.
Once injection became available it seems like they tried everything, including camphor, alcohol, caffeine and digitalis. And you guessed it, strychnine. One physician said, “I prefer twitching to a pulseless patient.” Though the patient’s preferences aren’t recorded. It became controversial as higher doses were used followed by significant toxicity and suffering was noted.
I was surprised to learn strychnine is used as a performance enhancer. Thomas Hicks, a runner in the 1904 marathon was dosed by his assistants with a concoction of strychnine, eggs whites and brandy, without his knowledge. He managed to win the marathon, but collapsed after the finish line. It’s a banned substance by the International Olympic Committee. In 2016 a weight lifter from Kyrgyzstan was stripped of his bronze medal for doping with strychnine. It’s also banned by WADA because it was frequently used by riders in Tour de France in the early 1900s.
Between 1926 and 1928, three Americans per week died from strychnine poisoning. In 1932, it was the most common cause of poisoning deaths in children. Shockingly enough, it could be found in over-the-counter products in the US until the 1980s, in things like digestive aids and cold remedies. Today, fortunately, it’s rare and mostly illegal. In the US, its only legal use is mole and gopher bait formulated in a low concentration. Occasionally, a suicidal patient ingests the mole bait, fortunately ingesting a lethal dose takes alot. It’s been found as an adulterant in drugs of abuse, including cocaine, heroin, and ecstasy.
Strychnine is still present in traditional medicine. In Chinese it’s called Maqianzi and used for limb paralysis, rheumatism, and inflammatory disease. In Cambodian, it’s called slang nut, and used for gastrointestinal problems.
Our patient wakes up and we find out what happened. She’s a Tiktok star, famous for cooking traditional dishes. She bought the dried seeds from a pharmacy to use in a recipe. The recipe was mistaken, causing her to unintentionally use a lethal dose.
A case series from Hong Kong in 2021, documented 12 cases of strychnine poisoning, all survived. Interesting three of the patients were Traditional Chinese Medicine practitioners, .
As a famously lethal poison, it’s been used by serial killers. In the UK, Christiana Edmunds, called the Chocolate Cream Poisoner, poisoned several and killed a 4-year-old child with strychnine laced chocolates. Serial killer Thomas Neill Cream murdered at least 10 people, prostitutes and women seeking abortions. It’s been used in political assignation attempts. It’s found as and adulterant in drugs of abuse, including cocaine, heroin, and ecstasy.
Today’s pop culture consult could be its own podcast. Agatha Christie’s murderers of course loved to use strychnine. Arthur Conan Doyle, William Burroughs, Jack London and HG Wells all wrote about it. In film, In Jaws, a strychnine laced dart was planned to kill the shark. In Psycho Norman Bates kills his mother and her lover with strychnine.
Last Question in today’s podcast. What is the name for strychnine contaminated heroin used in the TV series The Wire.
A. Fireball
B. Hot shot
C. Speedball
D. TNT
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