LtCol Joseph Maddry is an Air Force emergency physician and toxicologist. Here he shares the unique aspects of deployment toxicology.
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All right, so I'm Joe Maddry. I'm an emergency physician, medical toxicologist, my background graduate from the Air Force Academy in 2001. Went to Minot Air Force Base as a bio environmental engineer there for three years. During that time, got to the mostly tested for toxins and then got to respond to the world's largest anhydrous ammonia spill, which was a cool experience. And then went to use us for medical school residency at SAMMC, BAMC, whatever you want to call it, and then went to Denver health for tox fellowship for two years, and then I've been back at BAMC for I think, almost five years now. Currently, I'm assigned at the Institute for surgical research as the director of the en route Care Research Center. So we do all the CCATT research, and medivac type research things along those lines. Today I'm going to talk to you about the introduction to toxicology, we're going to go through the general approach to the tox patient. First things you want to do what you want to worry about first, then various decontamination techniques when they're indicated when they're not. And then we'll go through the toxic drums, which are very popular on board exams, for those that are concerned about that in the future. And then some specific drugs and therapies for those drugs and then conclude. So your general approach just like anything else, in emergency medicine, it's ABC airway, breathing circulation, the vast majority of deaths from tox patients are airway death. So they take something that causes enough sedation that they quit breathing, and they die from that. The next most common causes cardiac dysrhythmias. Those are the big things you're going to be looking forward trying to treat up front, get your safety net with your IV o to monitor. And then an EKG is definitely one of the tests you want to hurry up and run. And like I said cardiac is a common cause of death. So you want to look for those abnormalities. Chemistry, which you're going to use if you need to, to calculate your inang gap, do not calculate a Nana gap off of a blood gas that is already calculate values on accurate values. So you'll come up with the wrong answer if you use that. And then aspirin and acetaminophen level, there's been multiple studies looking at what testing should you actually do for a tox patient. And really the only thing that's consistently panned out as Yes, you should run this test. And you should run this test on every psych patient who says I want to kill myself, but I didn't take anything about 1% of those patients will have a dangerous level of acetaminophen that you need to treat. So that's the one big test you want to take tests for. And there's no toxic drum to warn you about that, at least not a classic toxic drum where you're going to pick up easily on it. So you want to test for that value. And then so let's late I recommend just because none of no one's really familiar with this late overdose anymore. It's pretty easy to miss kind of findings on physical exam, and it's definitely something that will kill you during my tox fellowship, the majority of cases that died that we could have been able to save if interventions had been done earlier or more appropriately. It was the solice late overdoses and usually there's a delay in diagnosis in those cases. So get us literally level just to make sure.Unknown:
For the acetaminophen level. If it's a psych patient, one level undetectable, you're done. If it's someone who says they overdosed on acetaminophen or something with acetaminophen in it, then you need you can get initial level but you need to get a level ideally four hours from the time that they took it but definitely at least a couple hours because if they took it right before they got in, you could have an undetectable acetaminophen level and then it will spike after that as they start to absorb the acetaminophen. Things to consider based on history and exam are the alcohol serum Osmonds, if you suspect a toxic alcohol, the drugs screen so toxicologists hate the urine drug screen, your doctors hate the urine drug screen, it's more likely to lead you astray and cause you to make an error than it is to help you. It's based off of drugs that were abused in the 1980s is not particularly accurate. I could give you an entire lecture on urine drug screens, but just know just because it's on the urine drug screen doesn't mean much if they test positive for amphetamine. And they're taca Kartik with a fever, and they have hypotension Yeah, it could be the amphetamine that they overdosed on, but it's also a very good chance that the patient who abuses amphetamine became septic because the lifestyle they live so focus on the sepsis before you get stuck too much on the amphetamine and then look for toxic, toxic, Jerome's are going to be how it helps guide you this but toxicology is something where it's physical exam history and physical exam not so much lab tests that are going to guide you on how you caring for these patients. For decontamination. So if it's a liquid they came in contact with or they have iron rotation, those are things you're going to irrigate. You don't need to decontaminate someone that was exposed to methane gas, for example, that's something that evaporates instantaneously. That's not something that needs decontaminated. So, be prudent with your decontamination. When in doubt, call the poison center and we'll let you know whether or not it's something that needs to be decontaminated. Ipecac essentially no Don't ever give it, people will still have it. They can buy it at various stores ordered online, people will have it in their kitchen cabinet and they'll give it to their kid when they overdose on something, the answer's no, don't do it. It takes about 30 minutes to work, which is too long anyways, and a lot of times requires multiple doses. And then if it's something where they're going to become sedated from what they took, now they're taking something's gonna make them vomit while they're sedated, they're at risk for aspiration. Having said that, I'm okay with self decontamination. So a lot of times people overdose on stuff, and that stuff makes them vomit. As long as they're awake and alert enough to protect their airway, I generally tend to just let them vomit and get what they have out. activated charcoal is certainly beneficial. In certain cases, you'll hear the one hour rule which is don't give it unless it's within one hour of the overdose. I generally don't recommend that because that's based on a therapeutic dose. So yes, if you take a therapeutic dose of Tylenol, and I want to keep your Tylenol level lower, I have to give you that activated charcoal within one hour because you absorb your towel pretty rapidly. If you ingest 100 tablets of acetaminophen, that is going to take you longer than an hour to absorb all that it's because it's such a big dose. Now it's even if it's probably a bad example, because we have a perfectly good antidote. So I generally don't recommend activated charcoal for acetaminophen because I can completely treat that. If it's something that's more difficult to treat aspirin, for example, and aspirin is known to respond to multi dose multiple doses of activated charcoal, then those patients I'll give charcoal to so the one key with charcoal is they have to be able to self administer it. So if you are having to help the patient get it down, they are too sedated for them to be getting activated charcoal, because if they aspirate activated charcoal that can be fatal because it binds up the surfactant in the lungs. If you put in a cup, you can mix stuff in it. So with a little kids, you can put chocolate milk or whatever else you want in there that will get them to drink it but they have to be able to drink it on their own. If they can't drink it on their own. They're too sedated. Either they don't get it or you need to intubate and protect their airway before they get it so you decrease that risk of aspiration. gastric lavas is only indicated if ever, which is open for debate if it's a fatal dose of a fatal drug for which there's no good antidote. Most people will never perform gastric lavas if you want to watch a video on it, I actually have one you can you search on YouTube and my video will be the first one that comes up but it kind of goes through it. But just know the risk are pretty substantial with it. And it has to be a fatal dose of a failed drug for which there's no good antidote. Otherwise, the risks certainly outweigh the benefits. Even if it is a fatal dose of a fatal drug for which is no bad. We don't know if it's the right therapy or not. But it might be your only option. Hold out irrigation. Maybe particularly for certain things called the poison center will let you know pH manipulation, especially for salicylates will do pH manipulation. And then haemodialysis is indicated sometimes those are all things where you should be talking about poison center and will help guide you through that. So case number 127 year old male presents the ED with vomiting, drooling lacrimation after being exposed to an unknown vapor at a train station. physical exam reveals meiosis pinpoint pupils and the patient's pants are soiled with urine and diarrhea. What toxin drum is this patient's presentation consistent with? Cholinergic? Yep, good. And hat class of agent was this pat ent most likely exposed to kin of factoring the terror sts sounding kind of inci organophosphate we call it chol nergic but we should really call it muscarinic because it acts on both the nicotinic and the choli ergic receptors and so icotinic receptors when you verdose on nicotine, initially ou develop tachycardia, hypertension, and then you remember the poison hemlock thing we all learned about way back when you sit you become paralyzed as those nicotinic receptors become stimulated to long so there's a muscular neuromuscular component with the nicotinic piece, but then there's the muscarinic or the culinaria component with all the fluids so what happens normally, your presynaptic your body releases acetylcholine and crosses the synaptic cleft, hits postsynaptic Li stimulates causes the electricity to go down the neuron, the nerve, and then the acetylcholine esterase is the little Pac Man guys that chew up the acetylcholine so that stimulation process stops. This is the only mechanism I know of that works this way like nor epi and epi is brought back into the pre synaptic cleft is how it's removed to stop stimulation, the acetylcholine that's what it normally does. What happens is you someone gets an organophosphate that binds up the acetylcholine esterase makes it inactive no longer able to do its job. So the when the acetylcholine is released, it continues to stimulate the nerve and there's nothing to shut that process off common things that cause it so in military especially we think organophosphates carbon mates are similar to organophosphates are all pesticides, organophosphates can be a chemical warfare agent or it can be used as a pesticide, they are very effective pesticides in the United States very difficult to get your hands on unless you have a special permit to have that. So some farmers will have this, the overdoses I've dealt with were farmers who consume their own pesticide. But for the normal civilian not really an issue, you can go buy it at your local hardware store. But when you look at the package, it will show the ingredients and the percentage will be like point 00 1%. So it's just such a low concentration that it's not a significant concern. Then, obviously the chemical warfare agents carbonates, those are very similar except they don't age and they're shorter acting less toxic, but same toxic drum play callers can contain those substances. So some people have heard dumbbells that's often the acronym used to memorize it. I'm not a fan of acronyms in general. But when you do use one for this one, I prefer sludge and sludge in the killer B's so it sounds like a 80s band or something. So the sludge salivation lacrimation, urination, defecation, gi upset with emesis, and then meiosis for the eyes. So essentially, you can memorize this if you want, what I actually recommend is you go on YouTube, and Google videos about the siren attacks in Syria. And once you see a toxic drum, it kind of gets burned into your brain. And when you see it again, you don't go through this, at least for me, I don't go through this acronym in my head, I just looked at the patient and I know that's colon ergic. So they're gonna have fluid coming out of everywhere, foaming at the mouth, lungs filling with fluid seizure is often especially in those videos, you'll see a fair amount of seizure for the Nova Chuck, which is the recent issue in the UK where individuals were poisoned allegedly by Russia, those individuals were poisoned cutaneous Lee, they didn't inhale it. So they actually had very little of the sludge and actually had much more of the altered mental status coma seizure picture. And the theory at least is that that's because they absorb it through their skin, and it can come in contact with their mucous membranes. So that's something to think about too, depending on your route of exposure. So most of the chemical warfare agents are inhaled VX is typically designed to be absorbed through the skin. From a military perspective, VX thinks contact more than inhalation hazard. The killer bees, that's the bradycardia Bronco Ria and the Bridget Nia so everything slows down, the heart slows down initially that attack a cardiac, but they'll move on to bradycardia. And then the lungs fill with fluid and that's typically what kills them as they drown on their own fluid filling up in their lungs. So that's what you want to focus your treatment on. Also seizures. So your treatment is atrophying and that treats the muscarinic receptors, not the nicotinic receptors. So this is going to help dry everybody up so you're trying to dry up all the fluid in their lungs. It does cause tachycardia. That's okay deal with the tech of cardia. There have been cases where people accidentally overdose patients on atrophying trying to dry them up. So be prudent with it. But your end goal is not tachycardia, you don't stop it because it becoming tachycardic you keep giving it those necessary to stop the fluid building up in their lungs when they inhale it a chemical warfare agent as you might imagine, that is a much lower dose than the farmer who drinks a cup of it just the amount that you're exposed to. So in inhalation cases, it generally doesn't require more than three doses of two milligrams of atropine to improve the symptoms unless they're too far gone. pralidoxime is given because so you atropine does not stimulate the nicotinic receptors. So the pralidoxime will reactivate the acetylcholine esterase basically acts like a crowbar comes in here pulls off the organophosphate, there is aging, which is where this bond becomes covalent. And you remember way back from chemistry covalent bonds very strong, very difficult to break. So that once that thing is aged that acetylcholine esterase is done and your body has to produce more of it, which takes months to do so you want to try and give the Prowler doxing. Before it ages depending on the agent, it may never age, or it may age in just a matter of minutes. So depending on what you're exposed to determines how prineas get pralidoxime but either way you want to give it because you want to free up this acetylcholine esterase so that the acetylcholine can re stimulate the nicotinic receptors because atrophy is not treating that. And then if that doesn't work, even if you drive up at the atrophying you may have to intubate them and ventilate them because their muscles are going to be too weak for them to breathe on their own. So that's a big thing to think about in a mass casualty incident because how many ventilators do you have? How many patients can you get on a ventilator before you run out and you start to have problems? Yeah, it's an issue at most even major medical centers. Most of ventilators are being used at any given time, and then benzos the seizures, so you definitely want to treat the seizure with the benzos. Get that under control. Obviously status is bad for the patient. case number 214 year old male presents with agitations slurred speech and appears to be picking at invisible bugs. Fixed exam reveals dry mucous membranes of flesh face and dry armpits. What talks drum is this patient's presentation most consistent month? anti going so basically everything dries up. Causes so atrophy which we just talked about anti histamines. Most cases I've seen are Benadryl or some kind of plant that they were abusing. That's an anticholinergic plant. tcaa is are often listed, although tricyclic antidepressants cause some features of an anticholinergic toxin drum, but not like a true Frank. No kidding. anticholinergic oxygen, like Benadryl one chlorpromazine, and then our antiparkinson man's, there's some long list amazing pause, anticholinergic talks drum. You can memorize this if you want, they're mad as a hatter odd as a hair red as a beet. blind as a bat, they'll get madrasas, that's usually pretty significant when you look at their eyes and then they'll get dry as a bone. So we have what's called the toxicology handshake part of your physical exam, so put a glove on, but then check their armpit. If their armpits dry, like bone dries, think anticholinergic, you know and your altered patient who's typically tacky in the low hypertensive, falls flat so they get urinary retention. tacky, like a pink flamingo that I learned from my mentors, it'll be tacky and then seizing like a squirrel. Again, how helpful that is to you. I don't know for me, it's more helpful just to remember they're going to be the same as sympathomimetic. Everything's going to be kind of amped up tech a Kartik except they're going to be bone dry. And then the big thing for me is their speech. So any eight sympathomimetic toxic drum patient is going to be screaming at you four letter words, you'll know exactly what they're saying. And it's not nice unless the toxic drum is so severe that they've become altered and they can't speak to you anymore. anticholinergic patients will mumble because miming speech is what you'll be hearing from them, you won't be able to tell what they're saying is actually I've heard of a case where they thought the patient was speaking a foreign language and was until he gave him the antidote that they started speaking normally they realized No, it was just a mumbled speech was so bad. The other thing is, you'll, when you shake your hand, you'll walk in the room, introduce yourself, they'll reach up and start picking bugs off of your arm, that they're hallucinating and saying, when they do become agitated, which in my experience is more the exception than the rule. First of all, think about putting in a Foley because a lot of times they're trying to get agitated because their bladder feels like it's about to explode because they have so much urinary retention. The other thing, so it can just be from the toxic drum itself. You can't give them benzos if need be to calm them down. And same as the mathematic but no sweating, and they get that mumbled speech. And the antidote. fizeau stick means so this is pretty controversial. Honestly, about the only people that give this are we toxicologists who, sometimes we do it just to kind of show the cool effect to our residents of Hey, we took this patient who was abnormal, and now they're back to normal after we gave them this, it only lasts for an hour. So it's a pretty short half life and most of drugs they overdose on are longer just expect them to go back into their altered state. The two big reasons we would give it so one, you're not sure what's going on. And before you do a CT LP go down that workout to make sure it's not meningitis or encephalitis. If you give them the antidote, and they suddenly get better, then you've confirmed the diagnosis and you don't need to go chasing after that other stuff. The other reason if there's becoming too agitated to manage, you can give them the Feisal stigma and they'll go back to normal calm down. And in general, when they do become altered again, they're less agitated than they were before and they're more relaxed and so it keeps you from perhaps having to sedate them so much you have to intubate them. You can repeat the dosage just repeating it every hour to give a little cumbersome contra indicated in TCPA overdose. So back in the 80s we emfs used to give a cocktail of drugs Narcan, and then or Naloxone and then they would give Pfizer stick mean and what they noticed with the tcaa overdoses they given the Pfizer stick mean and then they would become altered their QRS with y now they would seize and they would die. And so this got blamed on the Pfizer stick mean and so they stopped giving in the pre hospital setting. And for that reason it's er physicians do not give it in general it's a contraindication it's listed on that package is a contraindication to give it for someone who has TC overdose or signs of tcaa overdose which will be cqrs whining and seizures. So if they have that as contra indicated whether or not that's truly effective, the Pfizer stick mean or that's just the natural course of a tcaa which it is consistent with the natural course of a TC a is kind of up for debate but more for medical legal purposes. And because there may be some risks don't get Pfizer stick mean if you suspect gcaa case number three patient brought into the is a 19 year old male who is agitated hallucinating tachycardic to kidney diaphoretic as a T max of one to 1.4. And he's using a lot of four letter words, what's this guy's talk syndrome some Fatima met with sympathomimetic. Just think too much epinephrine and norepinephrine flowing through your bloodstream. What would happen if you overdose your patient on epi nor epi that's what these patients are going to be doing. The common cause is cocaine generally relatively short acting, so only lasts a few hours depending on the dose they took. So easier to dispo those people amphetamines are much longer acting so those people get more difficult to deal with in the military. This becomes an issue because of the ADHD medications people will either abuse them or they'll be using their buddies, ADHD medication. PCP, although that's relatively uncommon ecstasy, there's a long list of other sympathomimetics they cause amped up. So basically, everything is elevated heart rate tech accardi unless I get super, super sick and then their blood pressure will start to drop as they become near the near the point of death, hypertension, hyperthermia. So Daya freeze, this is supposed to be what helps you differentiate between sympathomimetic and anticholinergic. However, most of my sympathomimetic patients that are brought in by Ms, for example, I had one guy a couple months ago, who is laying down on the interstate in San Antonio somehow did not get hit and killed in the middle of the interstate. high as a kite yelling a lot of four letter words at S. Wooden coporate had to keep trying to hold him down, which is concerning and of itself. He was bone dry, dry mucous membranes, but he told us he was doing meth, everything was consistent with meth. It's just when you do meth for three days and you don't drink any fluid, you tend to be very dehydrated. And so there'll be dry instead of diaphoretic. Just bear that in mind that exception there. That's why on exams, look for dire for recess versus they're dry, in the real world look more at their language and their behavior, and to determine whether which of those whether it's some path of memetic or anticholinergic treatment, benzos, benzos, and more benzo? So a lot of times, I'll get calls from the ER saying, Hey, I gave six milligrams of abdomen and he's still agitated and thrashing around and cussing at us, what do I do, and I say, give more of an or as a Pam, and call me when you've hit 50 milligrams. So at 50 milligrams of Lorazepam, you can start to get some toxicity from the diluent that it's put into, you can switch to the other benzodiazepines, as Lam drips, if you're concerned about that, or the other thing to think about too, is the anti psychotic if they seem to be hallucinating a lot. So if they seem to be agitated, because they're seeing things that aren't there, then there are cases or reports of patients responding well to anti psychotic. So that's something to consider to a lot of emf crews now and especially in the ER when these patients get really combative. So you've heard about these cases where the cops are holding someone down, they're totally thrashing around and then all of a sudden, they go into cardiac arrest. So the theory as to what happens with those patients is they become so acidotic which if you take a healthy person, you have them sprint all out hard as they can, for 100 meters and check their pH immediately at the end of it, they'll be six points, some odd if they're really pushing themselves super hard, and they'll have an elevated lactate. So these guys are like that. But unlike you or I we're at the end of 100 meters all out sprint, our brain tells us that's enough I quit their brains not saying that it's saying keep going because they've got too much adrenaline flowing through their system. So these patients will become super acidotic go into cardiac arrest because it becomes so acidotic and now because they're not breathing because they went into cardiac arrest, their body has no way to correct that acidosis and that's why in general when these patients become pulseless, no one's able to recover them or get them back. What we do to try and deal with that is prevent it. One of the ways we prevent that is by giving them ketamine. So if you give 500 milligrams of Im ketamine in about three to five minutes. An adult patient in general and this are crazy high doses of sympathomimetic will become unresponsive. Now the good thing about ketamine I am especially compared to the other agents like anti-psychotics and benzos, especially as they don't get respiratory depression, you can't get temporary rest or depression and IV, but in iv boluses, that is but with the i m it's slow enough onset they don't typically get I never heard of a case of them getting that what you'll they'll be doing this weird breathing thing where they're hyperventilating, they're basically taking poo small respirations because they're blowing off their co2, even though they're unresponsive when you try and examine them. And so we're doing all that to try and prevent that acidosis especially in the ER when you got like, you know, the security forces or nurses, everybody's trying to hold the patient down. If you hold the patient down. You just gave them something to pull up against just like you can cause you're a lot more exhaustion to your body by doing squats with it, too. 100 pound barbell on your back that with no weight you're doing the same thing by loading them with people holding them down. So you want to do that as little as possible in a hurry up and get them sedated and calm down complications, so rhabdo hyperthermia that can definitely be fatal. EMI and intracranial hemorrhage, or infarct, classic teachings more on intracranial hemorrhage, or they're actually more likely to get a infarct. The EMI can be due to chronic coronary artery disease because of the persistent strain on their body from the chronic use of cocaine or it can be due to vasospasm due to an acute overdose or a mixture of both. Cocaine can cause QRS whitening like DC A's. We'll talk more about that in a bit. But just bear that in mind with it. Two patients found unresponsive in their car they both have a GCS of six pinpoint pupils respiratory rate of six, and they're developing cyanosis what talks drum is this most consistent with opioid This is the biggest killer in the United States by far right now as far as tox cases are concerned. It's pretty straightforward. They develop respiratory depression, altered mental status, they die from hypoxia, and this is why we're starting to get dark and a lot more again in the EMF setting is to deal with these. These patients actually seldom present to the emergency department is are usually found dead when they do present you give Narcan or intubate them if they are intubated, I recommend against giving them Narcan Naloxone because if you give them the lock zone with a tube down their throat, they're going to wake up and they're going to start trying to rip that tube out and they run the risk of aspiration. There's two therapies for opioid overdose one is an endotracheal tube and the other is Naloxone. Just pick one and go with it. You can with fentanyl especially you can require super high doses of Naloxone up to 10 milligrams. If you have no response after 10 milligrams. It's not an opioid talk syndrome. It's something else that has them sedated. The other thing is if they go from unresponsive to wiggling around a little bit, that's not consistent with an opioid toxic drum that's consistent with their own endogenous opioid a runner's high is caused by endogenous opioids and you can take away a runner's high by giving him Naloxone. We all have endogenous opioids. And if you take that away when we're in a coma from what like cyclobenzaprine, or whatever else we overdose on, will start to wake up a little bit, but we won't like wake up and start screaming at you for ruining our heroin. Hi. So that's what you're expecting. Don't give more Naloxone than you need to because you just create a combative patient who's now vomiting and making things difficult. You see all the different morphine, hydrocodone, oxycodone, there's tons of different ones out there talking about that stuff, some old school things to kind of know about, we don't really deal with it propoxyphene got pulled off the market because it causes a sodium channel blockade which causes curious whining and seizures similar to TC A's. And then the paradeen very, I don't I haven't seen it used him forever. I don't know if you guys have but it used to be used much more often used to be one that patients would come into the ER asking for by name that's been generally replaced by dilaudid. And it can cause seizures and the meiosis is less prominent. So mostly relevant for board exams, not seeing that much anymore. opioid withdrawal syndrome. So is he giving too much Narcan or classically they presented the ER with these vague abdominal diarrhea complaints and then after you do a giant workup, the patient finally admits to you Well, yeah, the problem is, is that I ran out of my oxy cotton and I'm withdrawing vomiting, diarrhea, abdominal pain, they can give a dry, assess yawning and then the pilot erection is supposed to be is one of the more classic findings you look for. But in general, when you have nausea, vomiting, diarrhea patient, something just seems a little off. I tend to ask him about Hey, did you run out of your opioid is that the problem and a lot of times are actually pretty honest about it and say what the issue is. It's not life threatening. So there are some fatal withdrawal syndromes. This is not one of them. can't kill them in a week in which they were going to die but it can't kill. treatment. benzos clonidine, and then a lot of places now are starting to give buprenorphine and Naloxone combination under Suboxone by training. There's a lot of clinics opening up for this now to since we have this huge opioid epidemic, there's a lot of people needing treatment. The one thing to know about this is if this is a partial agonist that buprenorphine, so buprenorphine can cause a withdrawal syndrome. When you give it the Naloxone will not because it's given orally and Naloxone is not absorbed to the GI tract. So this is just to prevent people from crushing up the pill and injecting it although some patients have still done that, knowing they're going to feel like horrible for an hour with the Naloxone and then after that their high will kick in. acetaminophen This is by far the most common overdose we see in the emergency department that is potentially dangerous cinnamon if it is metabolized to nappy and that causes a central novar necrosis comes in four different stages in general stage one, nausea and vomiting stage two they feel better they look okay but if you check their lab work, you'll see things are not going well. Their lfts are starting Arise and phase three, they go into a panic failure. And phase four is either recovery from that hepatic failure which if they do recover, they make a full recover with their liver function. So their liver will go back to normal functions you can dose your medications just like you would as if they had never injured their liver to begin with. Or they'll die. Those are two options. For acute overdoses you'll use the rheumatic nomogram and the number if you want to memorize is it at four hours, their level needs to be less than 150 milligrams per liter that's the threshold at four hours. And then for repeat supratherapeutic ingestion so this is grandma has tooth pain and she's been taking six grams of acetaminophen a day for the last week. Man your concerns you might have a chronic overdose you'll check acetaminophen level and lfts. Both of these need to be normal to rule out a chronic overdose. So both those come back normal you're done. They will not go on to develop liver failure. This is a that nomogram basically what happened is they looked in like a people above this point they all died. People below the line they all lived after they overdose on acetaminophen. The initial line was supposed to be at 200. But the FDA wanted a more conservative value. So they dropped it down to 150. treatment is nak acetylcysteine the dose it can give MPO most facilities don't carry po anymore, but if you do have the P o form you can give that it doesn't smell very good. So put in a cup with a straw that'll help patients to take it. You give 140 Meg's per keg and then the 70. Meg's per kid queue for hours times 17 doses, IV is generally what's used now. So I'm 50 milligrams per kilogram IV. And then the important thing when you write your order is do not make the mistake of saying 50 milligrams per kilogram per hour, it's 50 milligrams per kilogram over four hours. Or what we did in my fellowship was we always wrote 12.5 milligrams per kilogram per hour, because this given 50 milligrams per kilogram per hour as an accident is this is a case of a fatal overdose of nack due to that so and then after that 6.25 milligrams per kilogram per hour. Same treatment for pregnant alcoholics extended release tabs, chronic overdose doesn't matter, same treatment for all those patients, and then follow their glucose. If they're really sick. If they're starting to go into liver failure, and they become altered. It's one of two things becoming altered hepatic encephalopathy, which is certainly expected if they got a big enough overdose and they didn't get the knack in time, but do check a glucose because they can become altered because their livers not working anymore. They're not generating enough glucose and their serum for them to use. So check a glucose and see if you need to give them glucose, consider transplant if their pH is less than 7.3. Or they have an IRR of greater than 6.5 and a cranny and grid and 3.4 and grade three or four encephalopathy which is essentially coma or near coma. And then if they have a lactate greater than 3.5. If they meet any of those, then they should be considered for transplant called the poison center. They will let you know whether or not they're a candidate for transplant. What facilities can do a transplant. Yep. So if you can get a level back within eight hours of when they overdose on the acetaminophen, do not give them anything until you have a level and then plot that level. If they cross the line treat them if they don't, don't treat them. If you cannot get a level back within eight hours eight hours of the magic Mark based on a study. If you can't get the level back by then then go ahead and give them the initial dose of knack while you're waiting for the lab work to come back. salicylates. This one gets missed a lot just because we're not used to it anymore. Aspirin oil wintergreen Pepto bismol is less late in it. It's a weak acid. It's a direct respiratory stimulator. So it causes hyperventilation by stimulating the respiratory center in the brain, which is actually protective against the toxicity and then it uncouples oxidative phosphorylation. Early on, they get a respiratory alkalosis so they're hyperventilating because it stimulates that center and then oftentimes they'll complain of tinnitus or hearing loss. Probably about half the Phyllis lay cases I was consulted on I couldn't get a history from because they couldn't hear me talking to them. We had to write stuff down because their tinnitus or hearing loss was going on. Usually with nausea, vomiting, abdominal pain later on, they'll go from this respiratory alkalosis to an anion gap metabolic acidosis. With the combination of those two hyperthermia is a very late finding essentially pre terminal, they're about to die, they get CNS toxicity, so start to become usually more agitated and then they become altered. This is very concerning because solice late in the brain is what kills them. So if they start showing neuro symptoms that's extremely concerning, and then they do constantly get a hypokalemia which you want to know Give them some tasks to them to treat with that. Treatment multi dose activated charcoal actually works with this exact mechanism. Don't worry about it just give them multiple doses of activated charcoal every two to four hours give them another dose of activated charcoal to help keep absorbing it. The antidote, if you will, which is not really a true antidote is sodium bicarb. That increases the urinary excretion. And it also keeps their pH elevated and by keeping their pH elevated, you keep the solicite late in the serum and keep it from crossing the blood brain barrier. When they become more acidotic, more of that salicylate is able to cross the blood brain barrier. So you want to avoid that. Where that's classically a huge issue is If so, most of these patients you don't need to intubate, but they co ingested on something where they're too sedated to hyperventilate. Or if they becoming so sick that they they're starting to lose neurologic function you need to intubate them. If you put them on normal ARDS net protocol settings, you're not giving them near enough hyperventilation to continue to blow off the co2 and keep them from coming acidotic and these patients pH will plummet when you intubate them and put them on normal events setting avoid innovation if you can, but if you need to make sure that you're using larger tidal volumes and hyperventilating them to blow off that co2, check very frequent blood gases and if they do need to be intubated, they need to be also getting to dialysis immediately. indications for dialysis so they have CNS symptoms renal failure because their kidneys aren't going to eliminate if there are any renal failure and organ damage and acute overdose level grade 100 and chronic levels of 60 to 70 depending on which reference you look at for the sodium bicarb. So generally I say three amps of bicarbonate leader a D five w running at 200 an hour and provide them potassium to supplement their potassium. I don't expect you to memorize that when you have this case called the poison center and we'll walk you through it. 30 year old with a history of depression arrives unconscious she is endotracheal intubated and there are no focal neuro findings. She has tagged Kartik and hypotensive EKG shows a QRS of 140 what therapy should you administer to her? This is much more common than 1980s. These drugs have kind of made a comeback but not as much not as high of a dose. Notice. tricyclic antidepressants good. The big thing to watch out for them with the cqrs widens. cqrs knows normally less than 100 greater than 100, you worry about this toxicity greater than 120, you start to worry a lot about this toxicity. So when you block the sodium channels of the brain it causes a seizure when you block the sodium channels of the heart It causes cqrs widening and V TAC. And as you might imagine, so when you block them in the brain the patient sees is that drops their pH dropping the pH increases the affinity for the TCGA for the sodium channel, which further widens out their QRS and leads them to be tagged. Classically, the story is they sees the nurse yells for the doctor because the patient seizing doctor runs in the room patient goes into V TAC and dies when the doctor gets in the room. And this usually is pretty quick. So these patients generally die about three hours after their overdose and I like some of the other ones that are more delayed. So the antidote for these patients is sodium bicarb. The sodium channels blocked you're going to try and overcome that by giving them more sodium and also the bicarb helps increase the pH that helps decrease the affinity for the tcaa mechanism is that it causes a bunch of different symptoms with the one we worried about sodium channel blockade. Like I said they get anticholinergic features, but not true anticholinergic syndrome. They can get hypotension from the alpha blockade seizure from the gabbeh in addition to the sodium and then Long QT, although you don't typically worry about these patients going into Assad's because they become tachycardic. And that's protective against Assad's. Why QRS is really what you're looking for. That's why you get your EKG on your tox patients and his terminal are in a VR in general, people don't pay a lot of attention to AVR. There are actually a few like indications of EMI and stuff that show up that we need to be aware about but most people don't pay too much attention to it. This is what AVR normally looks like whole bunch of cue a little bit of our, if you just memorize that image, burn it in your brain. Every time you look on a you have taught you how to overdose patient, you look at their EKG, you make sure it looks like that if it doesn't look like that worry about something else. This is that terminal R and AVR. Instead of being all q with a tiny R, it's actually some pretty significant our wave there. So that's an indication toxicity also a QRS wider than 100 to 120 kind of depending on your patient's history, it gets complicated. So this looks a lot like a right bundle branch block. So it gets a little confusing and patients who have a history right bundle branch block or you don't know if maybe they do. One way to kind of help you tell is in right bundle branch block. The QRS should still be really narrow, whereas the QRS starts winding out more with especially the component with overdoses. But if you see something like this and it's an overdose case, I would just you can always just give some bicarb. And if it narrows down after you give them bicarb, you confirm that you have sodium channel blockade. So this is a case you can see big wide QRS dysrhythmia going on here, they gave a dose of bicarb. Now we have mostly Q, a little bit of terminal RNA VR, and then they get more bicarb. And now that terminal R and AVR is completely gone. That what you'd expect in response to that, if you can't give them any more bicarb because their sodium has become too high or sorry, their pH has become to ISO pH like 7.5 7.55 then you can give them hypertonic saline to give them more sodium and if that doesn't work, you can give them light again, light again is a sodium channel blocker. And that's why it does cause seizures and cardiac dysrhythmia but it has a it dissociates faster from sodium channels then tch do so essentially what you're doing is you're giving a less toxic poison to compete against the more toxic poison. I have had to use that before for a citalopram overdose who did respond well, IV fluid and pressors if need be, do not give intra lipids. So there's got one of the more modern antidotes, people are trying it for anything and everything. There's animal studies that show they do worse if you give them intralipid. So at least for now, until we have more evidence I recommend against it and then give them seizure for benzos for seizures, and you want to get those seizures under control immediately because that's going to make them at a higher risk for going into the tag of their season. Toxic alcohols. In general, I will say first of all that toxic alcohol is a majority of the time I get consulted and they say hey, we think it might be a toxic alcohol. The vast majority time is not a toxic alcohol. It's actually usually alcoholic ketoacidosis patients will. They're alcoholics they drink every day they get sick with some kind of gastritis or pancreatitis or something so they quit consuming their alcohol. And so their blood alcohol drops down they get sick, they consume a bit more alcohol and alcohol somewhere around 100 give or take a bit and then they check their labs and they've got an acidosis well it's a ketoacidosis it is an air gap metabolic acidosis does not typically a toxic alcohol, I can't guarantee is not so you still need to work them up. But remember that ethanol is the antidote for toxic alcohol so if they have a blood alcohol of greater than 70 and they have an anion gap metabolic acidosis The only way if that to be a toxic alcohol is a to ingest the toxic alcohol, metabolize it so it started developing the acidosis and then go and drink alcohol after that, which has happened but it's not that common think horses before you go chasing down zebras. ethylene glycol, antifreeze, this actually becomes an issue downrange. So military members who are alcoholics will get deployed, they won't be able to get their hands on their toxic, toxic or their normal alcohol so they'll go reaching for something else. It's metabolized by alcohol dehydrogenase is a toxic and aldehyde dehydrogenase to form glycolic acid and oxalate they have these calcium oxalate crystals in the kidney leading to renal failure and then we'll get the metabolic acidosis. So they're toxic drome, they're negated, they'll get the acidosis hypercalcemia and go on to renal failure. And then from there, they can either die more acutely because the acidosis gets so bad or they die from renal failure. Although if you provide dialysis and good supportive care, they'll generally improve their renal function and survive. treatment is the antidote is either ethanol or methanol. And the reason you give these is because the alcohol dehydrogenase has a higher affinity for these and for the toxic alcohol so you're just giving them something else to metabolize instead of the toxic alcohol. You can dialyze it off. In general with ethylene glycol it's metabolized pretty quickly by other means. So most of those patients we put them on from that Rizal or ethanol and you always want from episode if you can, because it's much easier to dose and they don't get drunk off of it. But there is a shortage of episodes so we've had to resort back to ethanol. That becomes problematic because some patients know this and they'll say they overdose on antifreeze so they get their free ethanol drip it's very difficult to manage these because everyone's metabolism so different there's no fixed dose of this it's an infusion you got to adjust based on their blood alcohol. So if at all possible go with from episode that's dose q 12 hours IV Oh, in general, we don't have to dialyze these people unless they're too acidotic or if they have kidney failure. If they have reached those points, then we need to go and dialyze that to correct the kidney failure and to correct the acidosis and you get vitamin A B six to stimulate some of the other mechanisms metabolism. Don't worry about memorizing those methanol, get that windshield washer fluid sterno cans also in moonshine. When it's not produced correctly. That's what they get. You'll hear about outbreaks of like 5060 people suddenly blind and another 20 dead and seems like most cases are in India in North Africa. where people are trying to make moonshine but screwing something up or they know they screwed it up and they just want to make money anyways. And so people are trying and trying to consume alcohol butter accidentally ingesting methanol is metabolized, the formic acid, inhibits cellular respiration again and I got metabolic acidosis. And it concentrates in the vitreous humor and optic nerve is where they get the blindness. Usually, the blindness is described as a snowstorm, or for those of us who are old enough back in the old TVs where if you've turned into a channel where there was no channel, you just got this static screen thing going on. That's kind of what they report as far as what they're seeing. If you're really good at your optimal logic exam, you can pick up the disk hyperemia and papilledema. Treatment again, ethanol from EPA is all when you get them from EPA is all the half life and go up to 50 hours, which is a really long stay in the hospital. So on almost all of these will console nephrology to dialyze them just to hurry up and get the toxic alcohol out you don't have to, but it shortens their hospital stay from a week down to a day or two. And you get fully to isopropanol there was this one lady in Denver when I did my fellowship, who always got called, because she would be found unresponsive on the bathroom floor at the fast food joints across the street from the hospital. And she was drinking the hand sanitizer, which was a superb alcohol. The classic thing is Oh get an Osmo or gap. So all the other toxic alcohol is you consume it you get an Osmo or gap, then you metabolize it and it becomes an anion gap metabolic acidosis as you convert it from an Osmo to a acid. In these cases, it's not metabolized is only metabolized to acetone by by alcohol dehydrogenase. They don't metabolize it any further so they don't get the anti gap metabolic acidosis. They just get usually pretty profound CNS depression, they get drunk and then they get really sedated, they will have an Osmo or gap. One other thing to mention the Osmo gap if you're fat if you're calculating that for some reason like your concern, they said I drink I don't I'm not saying he checked on everyone but if they said I drank ethylene glycol and you calculate I was more gap. Remember that ethanol has to be factored into that equation. So you need to get a blood alcohol to put that into the equation to the equation we all memorize a medical school doesn't have the ethanol in it. And so you need to add that and they had gi bleed is classic error reported how legitimate that is, as far as a true issue of isopropanol alcohol versus that's just what alcoholics tend to get is gi bleeding is unknown but and then supportive care and given them to find meaning since they probably have pretty severe alcoholism, low and slow. In general, if you have a patient who's bradycardic and hypotensive, there's three big causes to think about cardiac so they haven't actual cardiac dysrhythmia or they're having an inferior EMI or something along those lines, but electrolytes, particularly hyperkalemia. So some patients will get the classic t wave changes, but some patients won't and they'll just get a bradycardia or they'll just start skipping beats on their EKG that can be a sign of hyperkalemia. And then besides the EMI of the cardiac and the electrolytes The next thing to think about is talks and when you think talks there's really four big ones to think about beta blockers calcium channel, boxers digitoxin, which is used to be less in favor, but the cardiologists seem to be bringing it back and it's kind of making a comeback. And then clonidine. With beta blockers, you get your cardiovascular you can't get beta to stimulation which is supposed to cause pulmonary issues and inhibit gluconeogenesis. You seen lots of asmat acts who are on beta blockers and I have not ever seen a case that they seem to be having exacerbation due to the beta blocker but that's pot and a lot of the textbooks. Classically they'll come in with bradycardia and hypotension. And then the textbook will say hypoglycemia, although I will say that in adults, we generally don't see that they maintain a normal glucose. I've actually never seen a case of beta blocker overdose that had hypoglycemia in an adult pediatric cases. I've seen it so be more concerned about with pediatric cases but adult I don't typically see it. propranolol is a big one to know about because it causes sodium channel blockade. So like Tch, you get your widen QRS, you get seizure and you get V TAC. This is the most dangerous to over beta blocker to overdose on treatment, there's no perfect antidote, so it's really a laundry list of things we throw at him. In general, the textbook will tell you to go from the top of the list working your way down. I personally tend to jump to the pressors very quickly because it's easy to do. And all these other ones don't work great. They work somewhat but they have tacky flags and so glucagon tacky flexes so the first dose works pretty well. second dose works a little bit third dose doesn't do anything and most facilities buy are completely out of it by then after you've given the third dose. The dose is five to 10 milligrams, so it's a big dose and that causes vomiting. So just be ready for that. You can't give atrophying and calcium don't get too aggressive with a fluid, they have a very poor cardiac output. And so if you keep trying to correct their blood pressure by giving him more and more fluids, they're going to develop congestive heart failure, pulmonary edema, and most of the cases I've had that have died typically die about three days after the admission in florid pulmonary edema and cardiac failure. So give them some fluid, maybe a leader to but don't go crazy with it. Again, the pressors most beta blocker overdoses, you can get them through with a presser. calcium channel blockers are more difficult. You can't do high dose insulin you glycaemic therapy, it's a huge dose of insulin. 70 units of insulin is the loading dose and then one unit per kilogram per hour drip so it's a huge dose way more than you typically give for a DK is 10 times what you would normally get for DK. It sounds ridiculous, you can actually titrate that up another tenfold, just call us the poison center, we'll walk you through it if you have to put them on pressors call your pharmacy and tell them you want this high dose insulin because it's going to take a while to mix this and it takes about an hour from when you start this before it has significant effect. intralipid there are case reports of that working well pacing although remember the issue is that every single cell in their heart is poisoned. So pacing may not overcome that it's worth a shot. I've had one patient respond well to it all the other patients did not respond to the Pacer at all now i'm not saying don't try it just know that don't expect it to be miraculous. ECMO is really the ideal therapy if you can get him on ECMO because this is a perfect ECMO patient because they have a completely reversible condition that will be gone in three days if you can just get them through it by keeping their heart functioning. And the propranolol if they went out there QRS treat him with sodium bicarb. And the other stuff we talked about with TC is calcium channel blockers. Same essentially the difference is is they will get hyperglycaemic. I won't go into details of why but classically they have a glucose in the two to three hundreds. So if you have a bradycardic hydrogens to patient check their D stick if it's in the three hundreds, that's probably a calcium channel blocker. treatment is very similar except minus the glucagon you could still give it if you want, but I don't recommend it because the vomiting issue pressors these are more difficult to treat. they're easier to deal with the high dose insulin you glycaemic therapy because they're already hyperglycaemic and they will stay hyperglycaemic. Despite the fact you gave them this huge dose of insulin. When they start developing hypoglycemia, that's actually a good marker that they've certain metabolize most of the calcium channel blocker off and you can start playing back your therapies. And again, ECMO the ideal ECMO patient to Jackson. I actually saw this plant tear during my visit to Japan, which was cool for me in a dorky toxicologist kind of way. But so Jackson is making a comeback, and then foxglove old yellow oleander, those are kind of some of the plants people can ingest. It blocks the sodium potassium atpase pump and that's kind of the big thing that like to ask for on exams increases vagal tone, they tend to get more bradycardia and less hypotension compared to the other ones. They will eventually get hypotension but bradycardia is more common and the dysrhythmias. On your EKG, you're looking for digit fact blocks slow a fib. That's pretty classic. A lot of times two people will think it's slow a fib but we actually pace out the QRS complexes, you'll realize they're actually in a third degree heart block with a fib. So look for that, too, because that's actually an indication for the antidote. Sometimes they'll complain of halos and blurred vision don't bank on that. A lot of times most of the cases I've seen is the little old lady who feels weak and her heart rates a bit slow and you check her lab work and her digit levels elevated. Classically EKG you see Salvador Dali his mustache, this is a sign of didja effect, not ditch toxicity. So this this just means they're taking ditch doesn't mean you need to give them the antidote based on that finding alone. This bi directional v TAC This is pathognomonic for dej. I've never seen it. I've only seen it in textbooks and on the internet. I don't know any toxicologists who have seen it, I'm sure there are some out there. But usually you get the more like the slowly faded, and the other heart blocks. But if you see this, especially on a board exam, this is ditch lab. So john Johnson level, first of all, it takes about six hours, six to eight hours for your body to distribute the Jacksons. So if they took a dose right before they came in, that level is going to be falsely elevated because it hasn't distributed. Don't treat based on that level alone. Look for the symptoms. If it's an acute overdose, the big thing to look for is not so much the Didge level is this look at this potassium. So when they blocked that sodium atpase pump in an acute overdose, not a chronic in acute overdose, they block all of them including the ones in the skeletal muscle, and that causes your potassium to become elevated. So there's a fascinating old study where all the patients who have potassium less than five survived. All the patients that have potassium greater than 5.5 died. and everyone in between was a 5050 shot. So that's really the lab you want in an acute overdose in chronic overdoses they'll actually have hypokalemia and the hypokalemia is a problem so you may actually need to give them potassium you want to potassium before in a chronic overdose, the treatment is digibyte acute overdose give them 10 miles. Don't worry about reversing the digit effect. You there are other ways for you to treat their congestive heart failure just eliminated from the table and then chronic give them one to two vials maybe three, there are all these different equations you can use called the poison center will help you with the equations but if you just eat when you do the equations, they almost always come out to this is how much you should give. And then don't give calcium for hyperkalemia the whole stone heart effect the idea if you give a date overdose patient calcium, you cause their stone their heart to turn to stone and they suddenly die based off of one study how legitimate that is is very open for debate. But since there's lots of other ways to deal with this, just don't give it for the hyperkalemia isoniazid the big one to know for this and so just know if you have a seizure that they overdose on, they tell you fine, that's great, that's helpful. But if you have seizure status that is not responding to benzos and you suspect overdose think ionize it because they have an inhibition of B six formation which is necessary for gabbeh you don't have enough gabbeh so they'll get these intractable seizures, you still need to give them benzos but you give them benzos plus the pyridoxine so one gram per gram ingested or five grams empirically this becomes an issue I had a case in Kansas that I was called on where we gave five grams they were no nice and I say we get five grams you're still seizing give another five grams. I told him we'll give him five grams more. We used up all the all of it in the hospital. So there was none available. Just know about that if there overdosed on ice and I said you may do you know depending on your travels across the world, you may be in locations where this drug is much more common that is in the United States. cyanide basically it's on the test exam. It's always in a fire or it's a suicidal lab tech. In real life experience. Most of my patients that have overdosed on this have ordered it online. That's how they've gotten their hands on it. It uncouples mitochondrial oxidative phosphorylation, they get hypotension, bradycardia, hyperventilation, ultimate status and seizure. So because you've bought the mitochondria from functioning, now they're functioning entirely off of anaerobic metabolism. So what that means is, their lactate is going to become profoundly elevated. Since that's all you got to work on. Just like when you're running your 100 meter sprint and you don't have enough oxygen anymore, you start to produce lactate. The other thing is their Pulse ox is going to be normal, like 100% Normal. So classically, when I asked, especially medical students about cyanide, they'll be like, well, they're gonna be hypoxic. No, they're not hypoxic, they can't use oxygen. So their oxygens become elevated. There's the old cyanide antidote kit which is amyl nitrate, sodium nitrite and sodium thiosulfate we won't get all the mechanisms almost always how we use hydroxocobalamin just know when you give hydroxocobalamin This is a patient's urine after they got it. All of your colorimetric tests are gonna be screwed up after you get this so just be aware of it and their skin will turn this pink color the bottle when you pull it out the package will be that bright red color EMF may give this pre hospital there's some cities now our TMS has that for like fire victims and stuff. serotonin syndrome so this one is important because you know what famous law that impacted all of us at least all of us younger people. And I know that's very relative and I call myself younger but what law the serotonin syndrome had an impact on I may not law I should say law more. regulation. Yeah, duty our limitations. So this is where the 80 Hour Workweek came from. So Libby's ion was a patient who was admitted she was on phenelzine and she started developing tremors and yeast. I don't know if people still use it but it used to be people use my paradeen for tremors for chills, gave her a paradeen what they didn't realize was clonus as what she was having me do is obviously put you at risk for serotonin syndrome, so does my paradeen combine the two together mostly tears serotonin syndrome cases I've seen are combination of pills. I have seen some where they just overdosed over a single serotonergic agent, but it's usually a combo, at least in my experience. So what do they get? They get altered mental status. This is a trifecta they need altered mental status, autonomic instability, which is usually tachycardia and hypertension, but it can be anything. And then neuro muscular hyperactivity. And the classic finding is I had a patient who on her exams I went examined her she was in a coma unresponsive at that time had been sedated because she'd become combative. her upper extremities you move around her extremities are completely normal. everything's normal about her upper extremities, her lower extremities push up on her foot and it was this clonus that would just not Stop on indefinitely. And so that's classic serotonin syndrome. If they get too sick, they may go on to develop muscle rigidity, but most of the time they'll have this clone is much greater in the lower extremities in the upper extremities. And if you find that you've confirmed your diagnosis, the answer on the test is often cyproheptadine. I don't give cyproheptadine a lot of toxicologists don't because it can only be given to so you either need to mash it up and put it through an mg tube, or the benzos work just fine. You would always give the benzos cyproheptadine. Would it be an adjunct to that? And then most of these cases resolved within about 24 hours. So if you just sedate him with benzos for 24 hours, then you don't need to give the cyproheptadine they've made a recovery if necessary. So when they get hyperthermic, it's because of all the muscle contraction. So if you can't get that are in control of benzos then you paralyze them in that way, you've shut down that neuromuscular process and said I'll fix that. And then environmental cooling if you get that far they're still hyperthermic. So when they die, it's the hyperthermia that you worry about and that's what happened with Libby's ion. I think it was like 107 before she went into cardiac arrest, and Ms or Molina hypothermia and malignant hyperthermia, similar differences NMS is caused by anti psychotics. That's how you tell the difference. Was it a serotonergic agent or an anti psychotic you might not know by history, lead pipe rigidity is more classic for NMS. Same thing benzos, intubated, paralyzed if necessary. dantrolene has been reported. And then environmental cooling malignant hyperthermia, that's due to general anesthesia, or succinylcholine. For those patients, you give dantrolene environmental coin, there's actually a hotline, so call the poison center and they'll give you the national hotline for that and they'll help you walk you through the management. for that one. summary we talked about general approach to tox patient what lads you want to get salicylates and acetaminophen. Those are the two big labs you want to get everything else only get if it's indicated based on the exam. Urine drug screens are probably helpful in pediatric cases because most times they shouldn't be on anything to trigger it. EKG looking for that QRS whining or Qt prolongation, or some of the digitech other things like that. manage the airway. That's the biggest thing. Martin managed our cardiac dysrhythmias decontamination most of things are not indicated. Sometimes activated charcoal is but they need to be awake or they need to be intubated. We went through the toxic drums and then the specific drugs