Sudden Death
Want to know what toxin was used by Nazis and is treated with vitamins? Is potent enough to kill a moose in 20 minutes. A poison where the antidote changes the color of your blood and skin?
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 patient survive this podcast? It’s up to you and the choices you make. Our episode today is called Sudden Death.
Want to know what toxin was used by Nazis and is treated with vitamins? Is potent enough to kill a moose in 20 minutes. A poison where the antidote changes the color of your blood and skin? Listen to find out!
Today's episode starts in the emergency department. You're sitting at your desk, taking advantage of a momentary lull to sign some charts and eat a granola bar, when the charge nurse shouts for help. Not her usual Doctor, room 1 now, but a panicked shout. He;s been an ER nurse for 20 years, he doesn’t panic, not ever. Not for any reason.
You jump up and run over. One of the other nurses collapsed in the nurses’ station. She’s on the floor, unconscious. You check for a pulse, it's weak and thready, but present and help get her into a room, expecting her to be awake by the time you get there. Syncope, the medical word for passing out, is extremely common, often from standing too long, not have enough to eat or dehydration.
The team hooks her up to the monitor to get vital signs. You ask the charge nurse what happened. He says the patient was sitting at her computer and drinking a protein shake while calling report on a patient being admitted. She hung up the phone, said she didn’t feel good, was dizzy and had a headache. He says she was pale, sweaty and looked terrible.
He says, “I told her to take a break and go rest in the back. She was too weak to stand, so I went to get the blood pressure machine. Then she just collapsed to the ground.” According the patient’s chart, she has no medical problems and doesn’t take any medicines.
A nurse reads out the vital signs. Temperature 98.5 F or 37 C, pulse 44 bpm, respiratory rate 8, Oxygen saturation is 90% on room air. And the blood pressure, the nurse hesitates frowning at the monitor. It’s reading 50/30. Probably and error. She hits button on the machine to recycle the cuff to see if it’s a real measurement.
On exam, the patient is unconscious, not even responding to pain. Her pupils are normal size. She is breathing, but with a shallow effort. Her heart is slow, but otherwise normal and her lungs are clear. The nurse calls out the repeat blood pressure 54/29.
Uh oh. This does not look like a simple case. Vasovagal syncope is a common cause of passing out, caused by standing too long, not eating enough or being too hot. Its probably happened to you or someone you know. It’s not life-threatening, unless you’re driving, and resolves on its own. Which is not what’s happening here.
As usual, we start with the ABCs. The nurse puts an oxygen mask with 100% oxygen, improving her saturation to 94%. Airway and breathing are tenuous, but ok for now. C, circulation, is the immediate issue. The nurses are working on IV access. You order 2 liters of normal saline to improve her blood pressure.
It's odd her heart rate is low. An otherwise healthy person with low blood pressure should compensate with a rapid heart rate, in an attempt to increase cardiac output i.e. blood flow. Is this perhaps a primary heart problem causing the low heart rate? It’s not impossible, though very unlikely. Otherwise healthy 30-year-olds don’t suddenly need pacemakers out of the blue. In prior episodes we’ve discussed medicines causing low heart rate and blood pressure, possible, but per the chart at least, she’s not taking any medicine.
There are way more questions here than answers. You force yourself to focus on resuscitation first. The nurses are having trouble with IV access. The resident grabs a central line kit and gowns up. A central line is a very large catheter placed into a vein in the neck, chest or groin. He asks you to hold the ultrasound probe to visualize the vein, pops it in and starts drawing blood. He stops and holds up the first tube saying I think the lines in the wrong place. The tube is filled with bright red blood.
Question #1. What does he mean?
A. He hit a nerve
B. He caused internal bleeding
C. He hit and collapsed the patient’s lung
D. He put the catheter in the artery instead of the vein
Answer: D, He’s questioning if he put the catheter in the artery instead of the vein. Arterial blood and venous blood aren’t the same color. Arterial blood is oxygenated, and therefore bright red. Venus blood is deoxygenated after circulating through the tissues and typically dark red.
It does look arterial. Central lines are supposed to be venous, because arterial lines are too risky, an if so, we need to remove it and try again. He repositions the ultrasound probe, you both look at it from several angles. The catheter is in the vein, where it belongs. You reassure him and use it infuse the fluids as rapidly as possible.
A tech hands you the EKG. It shows a slow heart rate, but nothing else. No heart attack, no abnormal intervals, including the QRS and QTC. The radiology tech shoots a portable chest xray. It’s also normal.
Despite 2 liters of IV fluid, her blood pressure doesn't improve and in fact, her heart rate gets worse. It's now in the 30s. You order norepinephrine, a strong vasopressor, in the hopes it will increase both her heart rate and her blood pressure. The vital signs improve, mildly, her heart rate goes up to the 50s and her systolic blood pressure comes up to the 90s.
You make a risky decision to send her for a CT scan. It’s every EM doctor’s worst nightmare to have a cardiac arrest in radiology, but we have no idea what’s happened to our nurse and we need answers. You send the resident down with her, telling him to scan her head and if she’s stable enough, her chest and abdomen as well.
What are you expecting to find? Anything we can get; this is a Hail Mary. Spontaneous rupture of an aneurysm, with resulting intracranial hemorrhage is possible. She did say she had a headache, though immediate cardiovascular collapse isn’t likely. A ruptured aortic aneurysm or aortic dissection can cause cardiovascular collapse, but in a healthy 30-year-old? Not very likely either. A pulmonary embolus might cause it, but you’d expect her to have shortness of breath or chest pain prior.
Back at your desk, you run your fingers through your hair, hoping not to hear a code call to radiology. What the hell happened to our nurse and what the hell should we do next? It's never a good feeling when you don't know what's happened to the patient dying in front of you. It's worse when the patient was otherwise healthy and one million times worse when it's someone you know.
The images come across from radiology. You scan through them. You're no radiologist, but nothing is catastrophically wrong. Good and bad news at the same time. The resident brings her back, safely.
It's difficult to generate a differential diagnosis when you're in the midst of a life and death struggle trying to resuscitate a patient. But you do have to give some attention to what might've happened to determine what might help.
This is sudden cardiac death, essentially, though we are doing our best to avoid the death part. A lethal arrythmia would be diagnoses 1-10 on my list. Unlike an out of hospital arrest, we had her on the monitor almost immediately and would’ve seen vfib or vtach. We didn’t. A pulmonary embolus, as I mentioned earlier can cause it. The radiologist officially reports all of the scans are normal. Meaning no blood clot. Things like long QT syndrome, either congenital or acquired from drugs. But her EKG was normal and again, no dysrhythmia. Myocarditis, infection in the heart, as well as valvular disease are on the list, but again, she should’ve had preceding symptoms. Certainly, we’ll need an echocardiogram to take a closer look, but this isn't a cardiology podcast. It's a toxicology podcast, so what about toxins causing sudden cardiac death?
We’ve discussed some of these on prior episodes. Many medicines, drugs and toxins cause long QT, but we’ve ruled that out. Same with sodium channel blockers, causing QRS prolongation. Aconitine is great for sudden death, see the toxic tea episode, but it doesn’t fit here.
What about toxins causing a slow heart rate? Yes, beta blockers and calcium channel blockers could fit, but they don’t cause this dramatic collapse. She’d have symptoms over at least and hour, if not hours. Same with imidazolines, we previously talked about eyedrops mistakenly said to cause diarrhea in the movie the Wedding crashers, but really causing altered mental status and low blood pressure and heart rate. Her symptoms fit, but again not this sudden onset.
Sudden sniffing death would fit, but she wasn't sniffing glue in the middle of the emergency department and again no v. tach.
I don’t love this list, we could go on, but the bottom line, she needs an ICU bed. The nurse tells you she’s maxed out the norepi. The initial improvement was transient, the heart rate and blood pressure are coming back down. You order a second pressor.
Minutes later, the patient loses her pulse and codes.
You call CT surgery for ECMO, extracorporeal membrane oxygenation. After several rounds of epi and CPR, she gets a pulse back, though I wouldn’t be optimistic it will stay that way. The CT surgery fellow inserts two huge catheters. One arterial and one venous for the machine to oxygenate and pump her blood. You see him frowning as he discusses arterial vs. venous access with his nurse practionioner.
The patient’s labs result, all normal, except an extremely high lactate at 12. You click past it, you’ve already covered with antibiotics in case of infection. The lactate is common in shock and cardiac arrest. Except she didn’t have a long down time, like out of hospital patients. You click back.
Question number 2. There are two clues here in the history as to what might be poisoning our patient. What are they?
A. Elevated lactate
B. Bright red venous blood
C. Low heart rate
D. Low blood pressure
Answer: A and B. Lactate and bright red blood.
Obviously, the low heart rate and blood pressure are significant and life threatening, but in this case, they're the result of exposure to the toxin rather than real clues. Elevated lactate and bright red blood go along with a certain toxin that can cause cardiovascular collapse.
It's time to Pick Your Poison and that's question number three. What is poisoning our patient?
A. Arsenic
B. Carbon monoxide
C. Cyanide
D. Chloral hydrate
Answer: C. This is very worrisome for cyanide toxicity. Neither the red blood or elevated lactate is diagnostic. However, cyanide poisoning causes sudden cardiovascular collapse.
Carbon monoxide can cause cherry red skin, though it’s rarely seen and mostly postmortem. CO definitely fits, but if she were poisoned, you and the rest of the nurses would be sick or dead. Arsenic is very lethal, but she’d have had some preceding symptoms, like GI complaints. Chloral hydrate, ingredient in a Mickey Finn, causes sedation and rapid onset of symptoms, but not profound bradycardia and hypotension.
Cyanide!?! What do we do now? Is there an antidote? That's question number four.
A. Hydroxocobalamin, Vitamin B12
B. Naloxone, Narcan
C. Prussian blue
D. Vitamin K
Answer: A. Hydroxocobalamin B12. Naloxone is for opioid overdoses, Prussian blue for thallium or radioactive cesium and vitamin K reverses some anticoagulants like warfarin or coumadin.
We actually have several antidotes for cyanide, believe it or not. Currently we use B12. The old cyanide antidote kit, used before B12 was approved, consisted of three parts. Amyl nitrate, in a vial like smelling salts, to use before IV access was obtained. There were always missing, because they themselves can be a drug of abuse, ie poppers. The second step was sodium nitrate and the third step sodium thiosulfate.
Should we treat our patient? Or wait to confirm the diagnosis? The answer: if you're even considering cyanide, treat immediately. For two reasons. First cyanide is rapidly lethal and there's no time to wait. The second is testing will take days, if not longer.
You order the cyanokit with B12, and the nurse starts it immediately. How does it work? Basically, it binds up and essentially inactivates cyanide. Hydroxocobalamin is a large molecule. When it binds cyanide, it becomes cyanocobalamin with the cyanide sequestered inside.
Vitamin B12, as you can imagine is very safe. The antidote has one big side effect. It turns everything bright red. The patient’s skin, secretions and urine are red which isn’t harmful. It also turns their blood red, not harmful either, but interferes with lab testing, much of which is colorimetric. You have to anticipate a lot of spurious lab results.
How does cyanide poison you? It causes complete energy failure by disrupting oxidative phosphorylation, and energy production. It interferes with the electron transport chain, causing hypoxia or a lack of oxygen, at the cellular level. This lack of oxygen, results in failure of normal aerobic metabolism, and in turn the elevated lactate. It’s the reason venous blood is red, cells can’t extract and utilize oxygen. Both our resident and the CT surgery fellow initially suspected mistaken line placement when the venous blood looked arterial.
Cyanide exposure is lethal via many routes, including ingestion and inhalation. As usual, I’m leaving out details in case anyone with nefarious intent is listening. Symptom onset can be as quickly as seconds after exposure to cyanide gas or minutes after ingestion or injection. Patients might complain of headache, anxiety, agitation, they can become confused and lethargic progressing to, you guessed it, seizure, coma and death.
Cyanide is used in many industries including electroplating of jewelry, mining, and plastic manufacture just to name a few. It’s used as a pesticide. In New Zealand it’s used to poison possums which carry tuberculosis and transmit it to cows.
Cyanide occurs naturally as amygdalin in peach and cherry pits, and bitter almonds just to name a few. You can actually buy dried cherry pits in health food stores. Shocking, and people have unintentionally poisoned themselves. Do not eat them. Outside the US, Amygdalin is marketed as Laetrile, an anticancer agent, which not only doesn’t work, but causes cyanide toxicity and has killed patients.
I mentioned pesticides. Animals can also die of naturally occurring cyanide toxicity. Seeds and leaves from chokecherries for example, are toxic in small amounts. Eating less than 1% of their body weight is enough to be lethal. A huge animal like a moose, which can be six feet tall and weight as much as 450kg, or 1,000 lbs, can die in as little as 20 minutes after exposure. Interestingly enough, naturally occurring cyanogenic glycosides are mostly poisonous to animals with rumens because the glycosides are hydrolyzed inside to free hydrogen cyanide.
Gas, hydrogen cyanide, was used in WWI though in the open air it dispersed rather than causing toxicity. It’s been used in murder and suicide. The Nazis used it to kill millions in the gas chambers. They used it to kill themselves. Hitler and Eva Braun both took cyanide. Hitler also shot himself. Himmler and Goring committed suicide with cyanide after they were captured by the Allies. Jim Jones put cyanide in the Kool-Aid at Jonestown, more than 900 people died. There is very dramatic footage of Bosnia Slobodan Praljak ingesting cyanide and committing suicide in the Hague after his conviction for war crimes.
Question #5. Cyanide was used to poison which medicine, killing 7 people in Chicago in 1982?
A. Motrin
B. Tylenol
C. Cough syrup
D. Tums
Answer: B Tylenol. These murders are still unsolved after an unknown person poisoned Tylenol bottles with cyanide. Manufacturers Johnson and Johnson introduced tamperproof packing, which is now standard industry practice.
Back to our patient. Her heart rate and blood pressure improve after 5mg of hydroxycobalamin. She’s now in the ICU. You recommend a second dose, hoping the antidote will be enough to save her life. You send off blood cyanide levels, though the hospital laboratory will have to send it to an outside lab and it's unclear how long the results will take.
Cyanide toxicity, fortunately, isn’t common. There is one exception where we EM physicians are always on the lookout for it. This is in fire victims. Many things that burn give off cyanide. Any fire victim with an elevated lactate above 10, or other concerning symptoms is treated with B12. Of course, they might have smoke inhalation, carbon monoxide toxicity or other problems, but cyanide is always on the list. A nightclub fire in Brazil resulted in the death of 250 people, many of whom died of cyanide toxicity secondary to hydrogen cyanide released from burning of the soundproofing materials.
How did our patient develop cyanide toxicity? While at work in the hospital? That’s a good question. The ICU team call law enforcement to investigate. In typical ER fashion, the protein shake is exactly where she left it, in a water bottle, next to the computer she was using in the nurse’s station. They discover cyanide in the drink, along with searches on her husband’s computer about most lethal poisons, undetectable poisons and how to buy cyanide. She recovers, though slowly including a long period of rehab. Her husband is eventually convicted of attempted murder after trying to kill her when she said she was leaving him.
This is a fictional case, as are all our cases, to protect the innocent. But it is based on real poisonings.
Cyanide, you may remember was a favorite of Agatha Christie’s. It’s classically associated with the smell of bitter almonds. If we’d smelled the protein shake would we’ve made the diagnosis quicker? Maybe, but an interesting fact is that only about 40% of the population has the gene allowing them to discern this smell.
Bitter almonds make me think of one of my all-time favorite books, the opening line in Gabriel Garcia Marquez’s Love in the Time of Cholera. “It was inevitable: the scent of bitter almonds always reminded him of the fate of unrequited love.”
Anyway, it’s time for the last question in the podcast and today’s pop culture consult. In the James Bond movie Skyfall the villain Raoul Silva is disfigured with a misshapen jaw and face, reportedly after taking a cyanide pill in a suicide attempt. This could really happen with a cyanide pill, true or false?
A. True
B. False
Follow the Twitter and Instagram feeds both @pickpoison1 for the answer. Remember, never try anything on this podcast at home or anywhere else.
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While I’m a real doctor this podcast is fictional, meant for entertainment and educational purposes, not medical advice. If you have a medical problem, please see your primary care practitioner. Thank you. Until next time, take care and stay safe.