White Lightning
Want to know what poison causes blindness? Why some prison commissaries don’t stock fruit? What toxins were intentionally used to adulterate alcohol during Prohibition? 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 patient survive this podcast? It’s up to you and the choices you make. Our episode today is called White Lightening.
Want to know what poison causes blindness? Why some prison commissaries don’t stock fruit? What toxins were intentionally used to adulterate alcohol during Prohibition? Then stay tuned!
A 46-year-old woman presents to the emergency department. She’s agitated. The medics say her sister called EMS. They know the patient well, she’s a frequent flyer. More sensitive term – an ER high utilizer. She has an alcohol use disorder and is homeless. The patient interrupts, saying she’s no longer on the streets and is now living with her sister. She is clean and well kempt, in fact she smells so strongly of perfume, your asthmatic nurse starts coughing and leaves the room.
Another nurse manages to hook her up to the monitor, despite the patient attempting to rip off the stickers and shouting she wants to be left alone. You order labs, a urinalysis, some IVF and consider a psych consult when the results are back.
In the meantime, you call the sister. A week ago, she took the patient into her home with the stipulation the patient not drink or use drugs. As far as she knows, the patient had been compliant with the rules, but the sister now suspects otherwise and sounds generally fed up. She confirms a history of bipolar disease with psychosis, but no other medical problems. She doesn’t know if the patient has been taking her psych meds or not.
The patient denies complaints including pain, infectious complaints, and suicidal ideation. She hasn’t been taking her psych meds because in her opinion “That crap doesn’t help me.” She adamantly denies alcohol and drugs.
Her vital signs are as follows: temperature 98.5, heart rate 115 beats per minute, blood pressure 110/81, respiratory rate 18 and pox 100% on room air. Essentially, normal except for a mildly fast heartbeat.
The physical exam shows a woman who appears older than her stated age, but is otherwise unremarkable. When asked, she denies auditory or visual hallucinations, but she’s obviously responding to internal stimuli and occasionally shouting at someone who’s not there to shut up and leave her alone. People often deny hallucinations to cover up the extent of their psychiatric illness.
We know the patient recently stopped drinking. Question #1 This is delirium tremens due to alcohol withdrawal?
A. True
B. False
Answer: B. False. I’d definitely have alcohol withdrawal on my list of concerns in a patient with this history. However, her symptoms don’t fit. Withdrawal is a spectrum of disease beginning with the need for a drink, then mild symptoms like anxiety and difficulty sleeping. It can progress to severe and life-threatening delirium tremens on the opposite side of the spectrum.
The name includes two important symptoms. Delirium, or confusion, often with hallucinations. And tremulousness. Today’s pop culture consult, Question #2. What classic reference to hallucinations due to DTs was popularized in a cartoon?
A. Green snakes
B. Blue mice
C. Tiny figures
D. Pink Elephants
Answer: D pink elephants, shown in the Disney movie Dumbo. Despite her denial, it's clear our patient is hallucinating. But she has a history of psychosis which occurs in severe psychiatric disease. Classically psychiatric disease causes auditory hallucinations, like hearing voices. In contrast, dementia and alcohol withdrawal cause visual hallucinations, though this is far from an absolute distinction. She doesn’t have a tremor or tongue fasciculations which we’d expect to see in withdrawal. Additionally, patients with DTs have rapid heart rates, faster than hers, and elevated blood pressures.
In short, I’d watch for withdrawal, but I’m not convinced this is the right diagnosis. At this point, it’s looking more like a psychiatric problem than a medical illness. A flag pops up in her chart with her lab results. Hmmm, looks like we’re going to have to revise our first impression. She definitely has a medical problem. Specifically, a severe acid-base disturbance. Acid has built up in her blood.
Acid-base disturbances are a fascinating, but complicated topic. When I was a fellow at the poison center, I often felt callers wanted help figuring out their patient’s acid-base problems, without any real belief the patient was poisoned. I love to talk about these and could go on for hours. You might be driving, and I wouldn’t want you to fall asleep, so I’ll keep it brief and boil it down to the basics.
An acid-base disturbance is when the blood is too acidic or too basic ie alkaline. Each has two categories, respiratory and metabolic. Respiratory acidosis is caused by respiratory failure, like asthma or emphysema, resulting in Co2 build up in the blood causing the acidosis. Her Co2 is normal and she’s breathing normally, meaning she has a metabolic acidosis. It’s caused by a huge list of things. Her lab work shows specifically a metabolic acidosis with an elevated anion gap, caused by problems like diabetes or renal failure or by exposure to toxins. The “gap” is caused by an acid or acids not measured by basic blood work. We’ll need some more tests to figure out the cause. It’s a serious disturbance which can be cause by a number of different life-threatening problems. There’s a pneumonic to help medical students remember the causes of anion gaps acidosis. CAT MUDPILES.
C for cyanide and carbon monoxide. A for aminoglycoside antibiotics, not likely since our patient hasn’t been on any medicines. T= toluene. We discussed this in more detail in the Deadly breath=sudden death episode. M=methanol, U=uremia, the acids that build up in kidney failure, D= diabetes. P=paraldehyde, phenformin. I=isoniazid, iron L=lactic acidosis, E= ethanol, ethylene glycol, S=Salicylates, ie aspirin.
This is a toxicology podcast, so let’s get right to it. If her gap acidosis was from cyanide, she’d be deathly ill. Carbon monoxide isn’t likely, as everyone in the house, including her sister would be ill. If she were huffing toluene, I’d expect to see a low potassium and/or renal failure. Paraldehyde is an old sedative, phenformin an old diabetes drug, both no longer made in the US. While this doesn’t completely rule them out, it’s not likely. Isoniazid is a drug used to treat tuberculosis, in overdose it causes seizures, again not the case here. Lactic acid is easy to check, it’s elevated in metabolic disturbances including infection and sepsis and after seizures. Iron, ethanol or alcohol, and aspirin levels are also easy to check. All are negative in the case of our patient.
What are we left with? Methanol and ethylene glycol, two of the toxic alcohols. I’m going to use ethanol, the real word for alcohol for the rest of this podcast to avoid confusion. We don’t consider it a toxic alcohol, though maybe we should. Obviously long-term use is bad, but there’s no end organ toxicity after a few drinks, unlike the toxic alcohols. There are several toxic alcohols, rubbing alcohol or isopropanol is one. It causes intoxication and acid build up in the blood, but rarely causes end organ damage. Diethylene glycol is another, often found as a contaminant in medicines, it causes renal failure and neurologic damage.
Ethylene glycol is commonly found in radiator fluid. People drink it intentionally to commit suicide or accidently, often babies and pets because it tastes sweet and it’s fluorescent. I remember a case with a patient, a mechanic, who said he accidentally took a sip of radiator fluid from a cup. We believed this story until he had a large volume of fluorescent vomit. Ethylene glycol causes kidney failure, and ultimately seizures, coma, death.
Methanol is the toxic alcohol in moonshine and the reason for it’s dangerous reputation. Question #3 What end organ damage does methanol cause?
A. Kidney failure
B. Blindness
C. Heart failure
D. Seizures
Answer: B. blindness. Also, seizures, coma and death.
You go back into the patient’s room. She’s calmer and more cooperative. Between sneezes caused by the smell of the exceedingly floral perfume, you question her again. She adamantly denies drinking moonshine or radiator fluid. What’s going on here?
First things first. We have a strong suspicion she’s been poisoned with a toxic alcohol. You can send blood for ethylene glycol and methanol levels. Let’s do that immediately. In some hospitals you can get the results emergently. I’ve never worked in one of these places, often it’s a send out test that takes days, or involves a complicated courier system that no one knows how to activate to get the specimen to a hospital or lab with the capacity to run it emergently.
So, in real life, I’d risk stratify the patient and determine the treatment from there. Question 4. Potential treatment options for toxic alcohols include:
A. Ethanol
B. Fomepizole (brand name Antizol)
C. Dialysis
D. Gastric lavage or pumping the stomach
E. All of the above
Answer: E all of the above. Yes, you heard me right. Ethanol, ie regular alcohol is one of the potential treatment options for toxic alcohols. More on this fascinating fact in a minute.
Stomach pumping is no longer a popular treatment for overdoses. If you’ve been listening, you might’ve noticed we haven’t pumped anyone’s stomach so far in 14 episodes. Not because our patients weren’t sick, but because gastric lavage has never been proven to be effective. It’s a complicated issue going back to the fact that we often can’t conduct good randomized controlled trials in toxicology. We just aren’t allowed to poison half the patients in a study to see what happens. Even if lavage might help in theory, it has to be done while the toxin is still in the stomach, basically within one hour. Assuming she took something, its anybody’s guess when she did.
In low-risk patients, maybe someone who took a sip of something by accident or a child who maybe drank something but probably didn’t, we could do serial lab testing. Basically watchful waiting, to see if acidosis develops or their renal functions becomes abnormal.
Our patient is already symptomatic, so this option is out. Her kidney function is normal, so she doesn’t need emergent dialysis at this moment. Dialysis is an invasive procedure. If you want to convince the nephrologist to do it, you’re going to need more evidence.
This leaves us with two treatment options, ethanol and fomepizole, which is the antidote for toxic alcohols. They both work the exact same way. Let’s talk about how toxic alcohols cause toxicity, then about how the antidotes work.
First, the toxic alcohols themselves can cause intoxication; patients may be drunk. It’s not usually dangerous, and wears off after a few hours. These compounds are metabolized in the liver, like ethanol. Methanol, becomes formate, which causes ocular toxicity and blindness. Ethylene glycol has several metabolites, but it’s oxalic acid that causes renal failure.
One of the enzymes that metabolizes them is easy to remember, because it’s name is alcohol dehydrogenase. What this enzyme likes to bind to best is ethanol, and that’s the reason ethanol is an antidote. Blocking the metabolism of these toxic alcohols prevents the formation of the toxic metabolites and prevents blindness and renal failure. The body will eventually excrete the alcohol itself without any end organ damage. So it’s pretty cool chemistry.
Some hospital formularies have IV ethanol for this reason. Fun fact, the VA hospitals used to have beer on the formulary, to treat alcohol withdrawal, but could be used for a toxic alcohol as well.
Ethanol works great as an antidote, but it’s extremely difficult to use. The blood alcohol level has to stay above 100, over the legal limit of 80. If it drops, the enzyme might start metabolizing the toxic alcohol. Everyone metabolizes alcohol at different rates depending on gender, ethnicity and chronic use. The patient has to be admitted to the ICU for close monitoring. The nurse will have to draw an alcohol level every hour or two, to make sure the level is high enough.
Generally what you get is a drunk, uncooperative person in the ICU, causing problems for nurses and the other patients. Fortunately, we have another option. Fomepizole, blocks the enzyme, and unlike ethanol is given at a standard dose, no titration required.
Why even bother to mention ethanol? Because fomepizole is expensive and not every hospital has it. I vividly remember a call during my toxicology fellowship from a doctor in a small, remote hospital. He had a poisoned patient and no fomepizole. I told him to give ethanol. He called me from the liquor store to ask what kind of alcohol. I recommended vodka. Also, outbreaks frequently happen in developing countries and places without much medical care. More on that in a bit.
Back to our patient. Fortunately we do have fomepizole, so I’d give her a dose. There are two lab tests that are abnormal in toxic alcohol exposure, the osmolar gap, this is elevated when the alcohol is present, and the anion gap which becomes elevated as the alcohol is metabolized to the metabolites. The high anion gap in our patient suggests the toxin is already being metabolized, so don’t waste any more time.
The perfume smell has permeated the entire emergency department. It gives you an idea. You ask her about her vision, she says its blurry. You ask if she drank perfume. After a few minutes, she admits she drank her sister’s perfume, in order to avoid going back to the street, in an effort to follow the rules. Perfumes can contain methanol.
What next? Now it is time to call nephrology for dialysis. Fomepizole blocks any further conversion of methanol to the toxic metabolite formate, as I said. With some toxic alcohol exposures, this might be treatment enough. However, methanol is eliminated from the body by exhalation. Meaning it has a very long half-life, meaning it will take days or longer to be eliminated. In this case she needs dialysis to remove the methanol and the formate.
Currently her vision is blurry, but she can still see. Hopefully, with aggressive treatment, it won’t get any worse, but only time will tell. Long term data on vision loss and recovery is difficult to interpret as methanol users are often repeat offenders and many are lost to follow up. Certainly blindness may be permanent. A quick aside on an interesting development. Stem cell transplants have given vision back to a few victims of methanol poisoning and seems to be a promising treatment.
This brings us to the topic of nonbeverage alcohols including mouthwatering items like hand sanitizer, mouthwash, aftershave and lotions. One study estimated 7% of working age males in Russia drink nonbeverage alcohols. I couldn’t tell you if that’s an over or underestimation, either way its an astonishing number. Another study suggested 30% of ethanol consumed in Russia was homemade moonshine. Nonbeverage alcohol consumption is even found in Russian literature and opera. For example, Shostakovich’s opera from 1927, The Nose mentions drinking aftershave.
Why drink nonbeverage alcohols? Well like many things we’ve touched on recently, it’s complicated. Cheaper cost and easy access are two main reasons.
Back to our patient. Her methanol level comes back at 250 mg/dL well above the toxic level. The cutoff is debated, some say 50 is a toxic level, others 100. Either way, that perfume had a lot of methanol in it. We continue fomepizole and she gets dialysis.
Methanol is a fascinating toxin, with a long, colorful history. It was used as far back as ancient Egypt in embalming fluid. It has tons of industrial uses. Something I didn’t know – and an overlap with the deadly breath episode. People who huff carburetor fluid, which contains methanol, go blind. In a different route, methanol can be absorbed via the skin. Vision changes have occurred after it’s use in massage and on bandages for wounds.
The most colorful history is methanol’s association with moonshine and the Prohibition Era in the US. What exactly is moonshine? In the US, where the term comes from, it originally referred to corn liquor. It was called moonshine because it was often distilled late at night to avoid detection. The distillation process for moonshine is the same as for any alcohol, homebrewed or not.
After fermenting, corn mash is placed into a still. Methanol is a very volatile compound, therefore it boils off first. Most distillers throw away the first liquid from the still, knowing it will contain methanol. What’s the difference between regular ethanol and moonshine? Nothing except testing, regulation, and taxes. There’s a saying about testing moonshine by burning to determine if it’s safe to drink. Red means dead, yellow risks blindness, blue means pure. However, this is not a guarantee of safety. Legit distillers test for methanol ensuring none is present. Moonshine is also called white lightening because of it’s clear color and it’s potency.
Question 5: What other toxin is associated with moonshine?
A. Mercury
B. Cobalt
C. Lead
D. Morphine
Answer: C. Lead. Sometimes the saying is red means lead. Saturnine gout is associated with moonshine. Car radiators were used as stills. Lead from the radiators leached into the moonshine and caused gout, referred to as saturnine gout.
Bootleggers came to prominence during prohibition in the 1920s, but moonshine was illegal before and after. That’s because the bootleggers don’t pay excise taxes on their products, like legal distillers do.
The history of prohibition is fascinating and another astonishing part is the intentional addition of poisons to ethanol. Of course, ethanol can legally be sold in the US for industrial purposes and taxes and regulation are different for obvious reasons. Often the ethanol is denatured by the addition of another compound. Even today, denatured alcohol can contain methanol. During prohibition, this industrial supply was diverted for drinking.
The bootleggers had chemists who removed the methanol. In response the US government added more and different poisons to deter drinking. They added mercury, chloroform, gasoline, nicotine, ether, formaldehyde, and brucine (like strychnine) just to name a few. Unbelievable considering, they knew people would drink it. Not surprisingly it disproportionately affected the poor who couldn’t afford better moonshine. According to some estimates, >100,000 people were poisoned by the additives and 750 died, were blinded or paralyzed by these actions.
Our patient’s vision clears up and once the level is less than 50, she’s discharged in good health to follow up with psychiatry for help with her alcohol use disorder. This is a fictional case, as are all our cases, to protect the innocent. But it is based on real poisonings that have occurred periodically.
Tragically, methanol outbreaks occur with astonishing frequency. Sometimes due to mistakes in homebrewing, other times careless or malicious behavior. One interesting source of methanol is pruno, or prison wine. Also called toilet wine if you’d like a more vivid description. Typically, fruit is placed into a plastic bag along with sugar and water. Ketchup can be the source of the sugar, apparently. It’s allowed to ferment and then turns into alcohol. It can contain methanol. Also a good way to grow botulism. Patients have suffered both methanol poisoning as well as botulism toxicity. It’s such a problem, some prison commissaries don’t stock fruit and Maryland now has moonshine sniffing dogs.
Methanol poisoning is a huge problem worldwide. MSF or Doctors without Borders has a Methanol Poisoning Initiative. To highlight just a few recent tragedies, 21 teenagers collapsed and died on a dance floor in South Africa due to methanol poisoning. In Iran, 300 people died after taking a so-called COVID remedy containing methanol. Unfortunately, moonshine and nonbeverage alcohol consumption continues to be a widespread problem. If you watch the news, I’m sure you’ll hear of an outbreak before too long.
Last question in this episode. Question 6. What sport started around moonshine production?
A. The NFL
B. The MLB
C. Nascar
D. Powerboat racing
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