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Multiprofessional Critical Care Review: Adult 2024 ...
1: Toxicology and Drug Overdoses (Heatherlee Baile ...
1: Toxicology and Drug Overdoses (Heatherlee Bailey, MD, FCCM)
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Hello, I'm Dr. Heatherly Bailey, an emergency medicine intensivist and a past president of SOCIETY, and this talk is on toxicology and drug overdose. Obviously, it's a vast topic to cover, so we will focus in this talk on some common overdoses and key features that will help you identify the overdose and treat these patients. Hopefully, you can obtain a history. That is not always possible, sometimes due to the patient's mental status or the fact that this was an intentional overdose and they are not forthcoming, but these are some key pieces of information, especially if you can obtain the information that this is enteric coated or sustained release product. That will be helpful in how you care for these individuals. Obviously, the entire physical exam is important, but these are key features and we'll go through them individually about what you should focus on in the tox overdose patient. There are some very common patterns that need to be recognized. You learn many in med school and in residency, and this is just a reminder that if you recognize these patterns, you will go a long way to treating your patients. Starting with vital signs, classically, the items on the left drop their core temperature, drop their blood pressure, drop their heart rate, and those on the right have the opposite effect. But the picture is not always cut and dry. It's not uncommon, especially in overdoses from the street, that there are polysubstances involved, and patients may also be on a host of medications that will alter these findings. The important part about neurologic findings is looking at their level of consciousness. Are they agitated? Are they depressed? It goes classically along with these, but as I mentioned before, this polysubstance abuse and drugs obtained from the street are not always pure, and we'll get to that a little bit later. Looking at their pupil size may be helpful, and many different things present with seizures. Then you want to see, is it hot? Is it dry? Is it warm? Is it moist? Are they ruby red, and they look like they've had a carbon monoxide overdose? And also important to look for injury or integrity of potential burns, such as a hydrofluoric acid exposure, and perhaps your patient needs DECON. Starting with GI, everyone growing up, I remember everybody was told to have syrup of epicac in their house in case your child ingested something that they shouldn't. Those on the right, the gastric lavage cathartics, are essentially out. Activated charcoal should be given, provided it's within an hour or two of presentation from ingestion, and your patient is able to maintain their airway and mentate and not aspirate. Whole bowel irrigation is used in some of the more dangerous overdoses, things that are not absorbed by charcoal, that don't readily have treatment or antidotes, such as lithium, iron. Also individuals who may be transporting drugs or have been incarcerated by the police and have ingested packets, those individuals also need whole bowel irrigation for their safety in case those packets were to rupture while they were still in their intestinal tract. There are many different ways to get rid of the toxins. Charcoal we mentioned. Some overdoses require multidose charcoal, can also have forced urine diuresis and alkaline diuresis. Barbiturates, as you see, are common to all of those. Fortunately, barbiturates are prescribed much less frequently than they used to be in the past. Dialysis can treat some of these overdoses. I want to point out that doactobigatran is cleared by dialysis, but there also is now a MAB that can be used in overdose patients. Then there are many different things that have antidotes, I've highlighted a few here that are of the more common, and we will go through some of these. For the practical standpoint, there are a couple things to remember about if you have a known overdose patient and they're having an arrhythmia. Sodium bicarb is your go-to medication. Sodium bicarb has been removed from a lot of our treatment algorithms, but when it comes to tox overdose, unless it is sinus tach, you want to be giving sodium bicarb. If your patient's hypotensive, norepinephrine is your presser of choice. If your patient is seizing, obviously ensure that they are not hypoglycemic first, but give benzos. Those are your treatment of choice in these overdose patients. You can always call for help. Even though you may not have a toxicologist on service, anywhere in the United States, you can call 1-800-222-1222, and that gets you into the poison control system. They respond to more than 2 million calls every year. On average, they're getting an exposure case every 15 seconds, and it serves all 50 states, including some of the territories. There's always someone that you can call for help. Not all of them have a board-certified toxicologist available, though. The data for 2020 isn't out yet, and I would imagine it will probably change, but for the last several years, up until the pandemic started, this has been the relative breakdown of the top five calls to poison control center. Problems with pain relievers, both prescription and non-prescription, followed by cleaning substances. It would be interesting to see what comes out for 2020. Of the calls to poison control center, the majority of them were single-substance exposures, which is not necessarily the reality of what shows up in the emergency department and the ICU. Overdoses we've seen in the last 20 years have dramatically spiked. They have just recently released the 2020 data, where over 93,000 individuals have died in the United States from overdose. The combination of the opiate crisis epidemic and COVID have dramatically decreased life expectancy in the United States, and this is a tragedy that we have yet to get a good handle on. Jumping straight in to Tylenol, acetaminophen, it is very common to be a co-ingestion, and people don't always know what they take. They may come in and say, oh, I took a bunch of aspirin, I took a bunch of Motrin. They don't necessarily know the substance, especially if it was a generic from a large box store, so it's a common co-ingestion. Always check a Tylenol level. Tylenol is asymptomatic until they're far along down the game, and so you want to make sure you know what their Tylenol level is. It may be unintentional, and these patients may present with liver failure. We saw frequently, typically dental pain is one of the most common reasons that people just take Tylenol, Tylenol, Tylenol, acetaminophen, and they don't realize, they think, oh, it's just Tylenol, it doesn't do much, and then they come in a couple days later not even thinking about all those pain pills that they took, feeling a little sick to their stomach, they don't feel right, their family may have said, oh, you look a bit yellow, and they present in florid liver failure because of an unintended Tylenol overdose. There are case reports of patients developing hepatotoxicity in the hospital from IV APAP, so make sure you're appropriately dosing your patients. You need a four-hour level. The initial level is not helpful because of the way the nomogram works, and I'll show you that in a moment, and always, if you're concerned about significant overdose or delay in presentation of the patient, look at your transaminases and your COAGs, and charcoal is effective treatment, so if it's early on, please give activated charcoal, and this is the nomogram that I was talking about, the Rumac Matthew nomogram, and what they've done is they started at four hours, and they have likely safe exposure, you know, the 140 milligram per kilo is your toxic line and your toxic level, and depending on what your level is, how far out you think from exposure tells you is this a potential significant overdose where they may not yet have symptoms or signs on their labs, and acetylcysteine is available. It originally was only approved orally, but now it is approved by IV method. IV is much easier for a variety of reasons. One, if you've ever smelled oral NAC, it has a horrible smell of sulfur rotten egg, so not only does it smell bad, it is very difficult for the patients to ingest, and many of the patients, especially if it was an intentional overdose, are not keen on taking this. There are dosing regimens. Their toxicology experts will tell you that if you get N-acetylcysteine started within the first eight hours of an acute ingestion, it is curative, and it can be given further out, so even if they show up at 24 hours after ingestion, it is still safe to give, and it may make a difference. If you have any evidence of hepatic dysfunction, you need to start the IV NAC regardless of how far out you are, and you follow the levels of the acetaminophen. Aspirin, salicylates, also another very common ingestion, and about 25,000 per year, and in this group, it's typically more unintentional, and part of that is because there's both an acute and a chronic type of overdose, and aspirin salicylate is present in many things, and many individuals that have a lot of arthritis or other issues are using topical medications that have salicylate in it, and perhaps they're also taking pill form and then unintentionally taking oral oil of wintergreen as one of the highest salicylate concentrations, and peptobismal bismuth salicylate has aspirin in it, and so if you take all of these things in combination, it's not uncommon to see these patients present, and again, there's acute or chronic, and aspirin is one of those interesting drugs that can actually form a b-zor, so you have to be very concerned if there's a constant leak of aspirin level that you've got a b-zor in the stomach, they may need a GI endoscopy to take a look and retrieve and break up the b-zor. Chronic toxicity is more common and typically delayed in being diagnosed. In our elderly patients, you may have polypharmacy because of all their different medical conditions, also very common from nursing homes. These individuals, again, may be on both oral and topical aspirin. Food actually does have some salicylate in it. If they consume a lot of ginger or mint tea, those are both high in salicylates, and the chronic toxicity, less classic symptoms, so these patients may just come in with acute delirium, and there's a lot of different mimics. They could appear to be septic or other issues or just worsening dementia, so here's your first pattern to recognize. In your patient that has tachypnea, who has an acid-base imbalance, who has an acid-base disorder, predominantly respiratory alkalosis, a non-focal neuro exam you need to think about, is this a chronic aspirin toxicity, especially in the older patients who may be on, you know, that full-dose aspirin using some topical for arthritis and have decreased gut motility or other processes going on. Salicylate toxicity has a distinct acid-base disorder, and there are two parts of it. It is not compensatory. There is actually respiratory alkalosis, which starts first, and that's from direct CNS effect, causes increased respiratory rate, gives you the respiratory alkalosis, and then your metabolic acidosis, because there is direct effect on the mitochondria, you have decreased aerobic ATP production, leads to uncoupled oxidative phosphorylation and anaerobic production, leading to gap metabolic acidosis, primarily lactate, so it is two distinct acid-base disorders, and that may be a question on an exam. If it's acute, give activated charcoal. If it is enteric-coated, this is one of those times where multi-dose charcoal may be of benefit. Patients typically need volume resuscitation. Alkalinization of the urine will help both with acute and chronic, so the D5 normal bicarb, remember how you mix that and give that, your pharmacist can be of help with that, but it increases your renal clearance of the salicylate, and dialysis is the main therapy for this. If your patient has severe signs and symptoms, the recommendation by our tox experts is that if your level is over 90 mg per deciliter, regardless of what the patient's symptoms are, and if it's at 80, if there's impaired renal function, or they're starting to have symptoms, and be aware of making sure you evaluate for recurrent hypokalemia and hypoglycemia, because they are associated with this. Salicylates is part of that mud piles that we all learned in medical school, and there are many other drugs that can create a metabolic, a gap metabolic acidosis, so just refresh that in your mind. Toxic alcohols, the main three, ethylene glycol, methanol, and isopropyl alcohol are some of those. Now the isopropyl alcohol is a little bit different, that's your rubbing alcohol, causes actually a non-gap metabolic acidosis, but it does create an osm gap, and these things are found around the house, in your garage, in your bathroom, your perfumes, and don't forget about the home still, and those who make their own moonshine, or their own alcohol, sometimes these entities, both methanol and ethylene glycol, depending on the components that you're using to make your still, can get in into that as well. So the metabolism is interesting, both ethylene glycol and methanol, and alcohol that we drink, are metabolized using through alcohol dehydrogenase. The good news for this part of toxicity, is that ethanol has a much higher affinity for alcohol dehydrogenase, over the ethylene glycol, or the methanol. Ethylene glycol is broken down to oxalic acid, and methanol to formic acid, and what you get is changes in your osm gap, and your anion gap, and as you can see here on this chart, you've got the osm gap on the left, time frame on the x-axis, the osm gap in blue, the anion gap in red, and the osm gap in these toxic alcohols starts out high, because of the unionized alcohol, and then over time, as you get the ionized metabolites, the osm gap will drop, versus the anion gap starts out normal, and then increases over time, because of the reverse, as you increase your ionized metabolites. The dashed line that you see here, is if the patient has also ingested ethanol, because as we mentioned before, the ethanol has a higher affinity for the alcohol dehydrogenase, so that is processed first, so these findings will be delayed, and depending on what time frame your patient shows up, they may have a high osm gap, and a low, and a normal anion gap, or vice versa, and it can be altered, depending on how much alcohol the patient has on board. CNS effects can range anywhere from being a little bit altered, to frank coma, we already talked about the anion and the osm gaps, classically, if it's methanol that's been injected, patients come in complaining of blindness, or perhaps looking through a snowstorm, speckled white lights, the ethylene glycol is, breaks down into oxalic acid, it's important to check for hypocalcemia, and QT prolongation with this, and it also forms oxalate crystals, leads to direct renal toxicity, and these are the patients who you can fluoresce their urine, and depending on what phase you catch them in, if you get the oxalate acid in the urine, it actually will fluoresce with the wood's lamp, all of these toxic alcohols, after ingestion, if the patient survives, you can have delayed parkinsonism, and neuropathy, so good to be counseling your patients, so here's another pattern, elevated anion gap, low bicarb, and an osm gap, think toxic alcohol, and just a reminder, when you calculate out your osm gap, you must measure your ethanol, because that is a significant piece of the osm gap, and specific to these toxic alcohols, so you know what you're dealing with. Treatment is, first you need to inhibit the metabolism, that is used by alcohol, before formipazole, which is the antidote, was developed, we gave infusions of alcohol, which sometimes patients had as much issue with the alcohol, and I know several patients who did not do well with IV infusions of alcohol, but that was to inhibit the breakdown of the toxic alcohols into their metabolites, and then you must remove both the alcohol and the metabolites, regardless if you're using alcohol or formipazole, these patients need to be dialyzed, and once they've been dialyzed, you probably will need to re-dose her formipazole, formipazole directly inhibits the alcohol dehydrogenase, so that the toxic alcohols will not be broken down, it's impacted by dialysis, and like many of our antidotes, you give a bolus load, and then a q24 hour for 48 hours, and you treat them until the toxic level is below 20. Now this can be challenging, because many hospitals, even some of our bigger quaternary centers, don't directly measure toxic alcohol as a send-out, so a lot of times it's also following the gaps, making sure everything else normalizes. There's some additional therapy that's been recommended with the toxic alcohols, you can normalize your pH with sodium bicarb, I know that we mentioned before using sodium bicarb and sodium bicarb drips, we still use it a lot in toxicology, and it's important because if you're acidonic, and you give the sodium bicarb, it's going to prevent additional conversion of those toxic metabolites, because it may take you some time to actually get that formipazole. It also limits the diffusion across the CNS of the toxic metabolites, so you won't maybe get some of that long-term delayed Parkinsonism. You can always use also use leucovorin and folic acid, and thiamine and pyridoxine as adjuncts in care for these individuals. So first question, the 25-year-old woman who presents after ingesting unknown pills, she's lethargic, has a pulse of 62, blood pressure of 86 over 40, which of the following is the best initial intervention? Transthoracic pacing, lipid emulsion, glucagon and calcium, or dopamine? And I'll let you think on that for a moment of what your answer would be. There are many things that cause bradycardia in toxicology, some are medications that patients may be on already, some are potential exposures from chemicals. So beta blocker and calcium channel blocker, very common, very common source of unintentional overdose, especially in children who get into their parents or their grandparents medication, and this is in the topic of one pill can kill a child, these medications can do that if the child is young enough. They lead to hypotension, bradycardia, altered mental status, more so with the beta blockers, hyperglycemia with the calcium channel blocker. So the answer in that patient who was bradycardic, lethargic, altered mental status, and hypotensive is to give calcium and glucagon, which are antidotes for these treatments. And as I mentioned here, you've got the beta blocker and the calcium channel blocker, you can use norepinephrine or epi if they are hypotensive, can give that high dose insulin for either, works better with calcium channel blockers, and you can also try atropine, but atropine typically doesn't work very well in significant overdose. If that fails, you go up to high dose insulin, pacing, and the use of lipid emulsion. But initially, early on, remember to give calcium if you think it's a calcium channel blocker and glucagon for either one of them. You can also use some of these adjunct therapies, the milrinone balloon pumps and ECMO in patients who are not responding, and there's case reports on all of these. So something to consider in these patients who are persistently hypoperfused. Lipid emulsion has been tried as an antidote in many different things. As you can see, here's a partial list, more commonly in the calcium and beta blocker, organophosphates, and lidocaine toxicity. And there are many different adverse effects that you need to be aware of. And again, this is another therapy of bolus then infusion. Moving on to cholinergic syndrome. Classically, this has been a problem with agriculture, over 3 million cases worldwide, organophosphate and carbamate. This is actually decreasing in the United States because of EPA regulations and more of the household toxins that have been used in the past have been banned. But one of the problems is that these are all, you get cholinergic syndrome from nerve gas. And unfortunately, in the world in which we live, this is a significant concern. For those of you who are movie buffs, The Rock, VX was the gas that was featured and VX is the most potent of all of these. There are antidotes and this is a key board question. They really like cholinergic syndrome and how you treat it. And it's atropine and pralidoxine. And you also want to avoid succinylcholine because that persists in the depolarization with the acetylcholine and worsens the cholinergic crisis. It's important to note that these can be absorbed, the organophosphates, through a variety of ways. Can be direct through skin, can be ingested in the GI, can be inhaled in the lungs and decontamination of these patients is key because you don't want your staff to become infected. If you recall years ago with the sarin gas in the Japan subway, many initial healthcare providers on scene and in the hospital became ill and some of them didn't die because they weren't properly protected. So decontamination of this is absolutely essential to protect your staff. So the mechanism is you have acetylcholinesterase and it is bound and becomes non-functional. You metabolize acetylcholinesterase, it's metabolized to choline and acetic acid. What happens is you then get acetylcholine excess and increased activity. And this is where the term aging, you may have heard that term aging comes in and that is when the acetylcholinesterase is rendered non-functional permanently. It is irreversibly resistant to reactivation. Organophosphates bind irreversibly, carbamates are reversible. So that is if you have to have exposure to one, the carbamate is better because you can reverse this irreversible bond. But the aging process is variable. Sometimes it's seconds to minutes, sometimes it's hours. So that's why as soon as you've identified the fact that you have an organophosphate or nerve gas agent, you wanna get the treatment started because the sooner you stop the aging process, the important that it is. So the sludge, cholinergic excess, you probably remember from medical school and pharmacy. So salivation, lacrimation, urination, defecation, gastric emptying, and then the three Bs, the bronchorrhea, bradycardia, bronchospasm. If you see someone who is having these symptoms, this should go off in your head. This is cholinergic excess. You need to do something about this. You have to be worried about organophosphate or some other type of exposure. And then the nicotinic effects are more of the neurologic, the fasciculations, the seizure, the coma, and the paralysis. And it gives similar to what you have with depolarization from succinylcholine. There's cardiac effects as well. And it can really be anything from blocks to leading to cardiac ischemia to a prolonged QT syndrome. So expect anything. Absolutely need to get an EKG and follow these patients on the monitor. And respiratory effects. There are four main. You have respiratory failure. You get physical neuromuscular weakness where they cannot actually breathe. Their diaphragm is weak. Excess secretions and bronchoconstriction. And excess secretions is one of the early hallmarks that these will just be drooling copiously. And that, and we'll get to the treatment in a moment. And then there's this delayed neurologic syndrome. One is relatively acute. And then one is in this one to three weeks, the organophosphate-induced delayed neuropathy. And they appear to be, the early one looks like Guillain-Barre. The delayed one, excuse me, the delayed one looks like Guillain-Barre. You get flaccid paralysis that's extending lower extremity to upper. And it's important to note that it is not dose-related. Even a small exposure, for whatever reason, certain individuals seem to be more prone and they can develop this even if it is not a significant overdose. Other areas are affected as well. We already talked about the Parkinson's. Kidney injury is very common in many overdose cases, as is pancreatitis. So they recommend surveilling for pancreatitis in these individuals. Now we get to the treatment, the cholinergic toxic rescue. This is also a typical key question if they're gonna ask it is, it's atropine treats those muscarinic effects and you give atropine until you clear the secretions. And that's very important when you first realize that you may have an organophosphate overdose that you're gonna need atropine and pralidoxine. Someone needs to call your pharmacist if you don't have a PharmD in your ICU and give them a heads up because A, they're probably gonna need to look for that pralidoxine. They may or may not have it readily if you're a smaller hospital. And they're gonna need to pull all of the atropine which is not uncommon in a significant overdose that you can empty an entire pharmacy of your atropine trying to control these individual secretions. So it's atropine first and you use it to secretion clearance and then your pralidoxine is given both as a bolus and then an effusion over typically 48 hours. It's important to make sure the infusion runs slowly because there have been case reports where giving a bolus too quickly can lead to cardiac arrest in these patients. Mentioned already about scene safety, healthcare worker exposure, the patients need to be deconed, your staff may need to be deconed, clothing needs to go. You have to make sure that there is a good ventilation and you must have a decontamination plan readily available for these types of patients. Next topic is benzos. It's commonly a co-ingestion, not typically on their own. It's really supportive care for our anesthesiologists that are listening. I know you use a lot of flumazenil in moderate sedation and in the OR. This is not the time to use that. You don't know what else they have on board. And if they start to seize, you are unable then to control their seizure. So we recommend against not giving flumazenil in overdose cases because you don't know what other co-ingestions there are. Antidepressants, especially the tricyclics need to monitor their airway, cardiac monitoring, charcoal. This is where we still might consider lavage because if it's a tricyclic antidepressant is high risk of morbidity and mortality. When tricyclics were very common before the SSRIs came out, every week we had significant overdoses that we would deal with in the emergency department. And every month a couple of people would unfortunately die from their overdose. Again, that's sodium bicarb, you want to alkalinize their blood. And if they're refractory, should consider getting hypertonic saline and lipid emulsion. The SSRIs have much higher safety profile than the prior tricyclics. And typically they're relatively safe in overdose. So you can get some depression, some individuals may have seizures, some may have arrhythmia, but they're relatively safe. But one of the issues is the serotonin syndrome. For those who are not familiar with serotonin syndrome, it's actually not necessarily an overdose, it's more of an interaction with other medications that they're on. And serotonin syndrome is actually why there is an 80 hour rule in place because it was a individual who was given a bunch of medications and had some substances on board that led to an unidentified serotonin syndrome and died. And that led to the Belt Commission investigation and a change in the way we practice and learn medicine. So on exam, these patients are going to be altered, they're going to have autonomic dysfunction, will have neuromuscular abnormality. One of the interesting findings that you can have in these patients that you don't really see anything else is teeth chattering. They'll come in and they'll be having their teeth chatter and not because they're cold, but it is some type of autonomic dysfunction, neuromuscular process. You want to stop the offending agent in the ICU, can be from having other opiates on board, antiemetics, linazolid is a common cause. You need to cool the individuals and give them benzos or propofol to help get them through the process. And giving them an agonist, antagonist, is not recommended at this time. For the hypoglycemic agents, obviously giving D50 is important. One of the things to remember is that if you need to put these individuals on a D5 or more likely a D10 drip to maintain their glucose, don't forget to give them thiamine. I've seen some Wernicke's encephalopathy syndrome presented by this unintended persistent D10 drip and not giving thiamine. Also important to keep in mind octreotide, sulfonylureas are not used as much anymore with new medications that have come out, but they still are out there. And if the patient has had an overdose of sulfonylurea, you need to break the cycle by giving the octreotide and it can be given either sub-Q or IV every eight hours and it inhibits the insulin release, which is being driven by the sulfonylurea. Looking at the overdoses, we mentioned already that, and we saw the original trend of the overdoses have been dramatically increasing in the last 20 years. There was a suggestion in 2018 that there may be a little bit of a downtrend, but we know that that really didn't occur. And one of the reasons for that is the release of the fentanyls and the synthetics that have made it out into the population. And this has dramatically increased the number of overdoses and the number of deaths because they're so much more potent. I don't think anyone is surprised that as we were shut down for COVID, that overdoses and drug use spiked. And you can see here as the shutdown occurred, the dramatic spike, and this is looking at all deaths, opioid deaths, and then in the red is the synthetic, everything increased. Naloxone, Narcan is your antidote. It can be given through essentially any route, IV, IM, sub-Q, ET, intranasal, there's even case reports of giving rectal, and it works. What's important to remember is that in these synthetic overdoses, this is another time to alert your pharmacist. You may need to use all of the Narcan that you have in the hospital. And for patients, once they respond, you need to put them on a Narcan drip if it takes more than one dose of 0.4, and that's two thirds bolus dose per hour. A frequent challenge with these individuals is that once they're up and aware, they wanna leave AMA. And most of the overdose substances have a much longer half-life than does the Narcan, which is only about 30 minutes in reality, even though the half-life is listed as 45 to 70. With the synthetics, again, you probably are going to need more than two doses of Narcan. They have a much higher potency, estimated to be about 100 times that of fentanyl, and we don't see them on routine drug screen. These are a send-out lab. Also need to evaluate these individuals for injury. These are the ones who have the needle still in their arm and may not have even completely injected everything because it hits them that quick, it's that potent, and they just go down. Some of the thought of the deaths of these individuals is possibly due to the chest wall rigidity. If you've ever seen fentanyl on occasion given quickly or in large doses, you can get that chest wall, stone chest, and it's almost impossible to bag them through. You need to give these individuals a neuromuscular blockade typically to add Narcan to get them through that. So perhaps some of the death is related to this rapid chest wall rigidity that occurs. And as I said before, these synthetics are exceedingly potent. There's more than 20,000 deaths from these synthetics every year, and 20% of those deaths didn't even inject an IV. They snorted it, they smoked it, they ingested it. It went through their skin, and that has important ramifications for our healthcare workers. When you're dealing potentially with a synthetic overdose, they recommend not using the alcohol-based hand sanitizer because that can actually increase the absorption through the skin. Same with the nitrile gloves because the latex apparently allows for that synthetic opioid to get through. And because they're so potent, even if you have a mass spec or something else, you just may not be able to detect the levels. Police and EMS need to be educated, looking for syncope, weakness, numbness, nausea, vomiting, and treated appropriately. And NIOSH has yet to declare any type of official level or data on fentanyl. And don't forget about the police dogs. They are also at risk, and the treatment is also the same. They get Narcan, IM or IV. Nobody's, I've not found anything about intranasal for the dogs. Cocaine. Cocaine is king in certain areas of the country, and it is prone to causing cardiovascular toxicity. And it can cause a wide range of problems from dysrhythmia to hypertensive crisis, aortic dissection, and early-onset ACS. So the 30-year-old who comes in may be having an MI, and it may very well be from cocaine. This also does bad things to your brain. Increased risk of intracranial bleeding, probably a combination of the thrombotic state that it can cause and the hypertensive crisis. It can affect other organ systems as well. It's important to evaluate these patients who have abdominal pain because they may have developed intestinal ischemia. Hyperthermia is common as is rhabdo. Amphetamines and methamphetamines, multiple different routes to do them. And typically what you see with others, the rhabdo, arrhythmias, myocardial ischemia, bleeds in the head. Not surprising. Next question. 24-year-old patient is admitted to the ICU for seizures, hyperthermia, tachycardia, and agitation. Drug use is suspected, but the urine tox screen is negative for PCP, cocaine, and amphetamines. Which of the following is the most likely toxin? Ketamine, LSD, methadone, or gamma-hydroxybutyrate? Well, there could be a variety of things, but of those choices would probably be bath salts, the methadone. It's a stimulant and hallucinogen, can be snorted, injected, inhaled, has sympathetic, sympathomimetic effects. Paranoia and aggressive behavior are very common. And these are the people who come in and rip the emergency department apart. And typically, you know, rhabdo, the renal failure, the stroke, things that go along with overdose. Benzos and supportive care are the treatments. The synthetic cannabinoids give similar presentations. They're actually opposite for the plant-based marijuana. It does the other. It makes them paranoid, hallucinate, gives them very severe anxiety. Seizures are also a big problem. Supportive care is the treatment. And this was in a small case series of synthetic cannabinoids. And the patients that came in were evenly broke down in about a third had seizures, a third were in a coma, and a third were agitated. And of this small cohort was a little less than 20 patients. 60% had respiratory failure, 70% required an ET tube, some because of needing airway protection and some for respiratory failure. Half of them had a co-ingestion. Half of them left AMA before they was really well enough to do so. And only 25% had rhabdo. So it seemed to be a much higher respiratory component problem with this group. And these are sympathomimetic effects. They're paranoid, aggressive. These also, individuals are likely to rip apart your emergency department or your ICU. Sedation with benzos and supportive care. Last question, 30-year-old woman with a history of depression presents with altered mental status and EKG shown below. Which of the following interventions is indicated for the arrhythmia? Amiodarone, cardioversion, magnesium sulfate, or sodium bicarb? Well, as you've heard me say several times, sodium bicarb is your treatment of choice initially in that case. Energy drinks are very popular. There have been cases of caffeine intoxication and cardiac arrest from a caffeine overdose. E-cigarettes prior to pandemic, vaping and vaping associated lung injury was the biggest crisis that we were facing in some of our young individuals. It still is out there. We just have other things that we're now focused on. So nicotine poisoning is also a problem. Just because your patient's in the hospital doesn't mean they can't have a problem. And some of the medication that we give can lead to overdose such as gabapentin, especially if they have renal dysfunction, narcotics, hand sanitizers. We've had patients who try and drink the hand sanitizers to try and get the alcohol. Methemoglobinemia developed from topical anesthetics, propylene glycol. Remember when we used to give a lot of Lorazepam drips before we had better medication, propylene glycol is the diluent that it's mixed in and you would develop a problem with that. And then propofol infusion syndrome. Anybody who's on propofol is technically at risk, more so if they have head injury, if they're septic, if they are on prolonged higher doses of propofol. So you really wanna be following their lactate. And if their lactate starts to trend and they're developing a metabolic acidosis, should be very concerned for the propofol. More common in doses greater than four mgs per kg per hour. More common the longer that they are on it. You also have to be aware for arrhythmias if they're on for more than 48 hours and rhabdo and hyperlipidemia with high doses and longer than 96 hours. One other thing to mention, I've mentioned it along the way is polysubstances, but not as much contaminants. Especially with people buying drugs on the street, even if you know your dealer and you go to the same guy every time, sometimes they don't get the same product. And this will present in your emergency department and in your ICU, you may suddenly have individuals who come in with overdose and having all these strange symptoms. This was in 2018. There was a rat poison, super warfarin that was mixed in with a synthetic cannabinoid. And they had many cases of patients coming in and just bleeding everywhere. And then good public health measures to track that down. This is just a list of common toxins and antidotes. There are many more. This is really just for your information. If you have any patients who present with this, there are potential antidotes that you can give. So in conclusion, I know there's a lot of information, a lot of topics that we covered, typically in tox overdose, the patients are going to either be dead immediately, get watched in the emergency department for four to six hours, that magic four to six hours, or they're coming to the ICU. Sometimes patients that come to the ICU have an overdose or an exposure that wasn't recognized in the emergency department and may present itself in the ICU. So you must remain vigilant. When you see those classic syndromes, they should ring a bell and you need to act. And if something's not making sense, these patients have a persistent acidosis, they're agitated and you really can't figure out why, you need to try and search for context of what happened to them to bring them into the ICU. Thank you very much for your time.
Video Summary
In this video, Dr. Heatherly Bailey discusses toxicology and drug overdose, focusing on common overdoses and key features for identification and treatment. She emphasizes the importance of obtaining a patient history and highlights key information such as the type of drug ingested (e.g., enteric-coated or sustained release). Dr. Bailey discusses vital signs, neurologic findings, GI symptoms, and specific treatments for various overdose scenarios. She mentions the use of activated charcoal, whole bowel irrigation, dialysis, and specific antidotes for different toxic substances. Dr. Bailey also covers the opioid crisis, synthetic opioids, and the use of naloxone as an antidote. She discusses specific overdose scenarios including acetaminophen, salicylates, toxic alcohols, cholinergic syndrome, benzodiazepines, antidepressants, cocaine, and synthetic cannabinoids. Dr. Bailey highlights the importance of proper decontamination and personal protective measures, and urges healthcare providers to be prepared for various overdose presentations. The video provides important information for identifying and treating drug overdoses in an emergency medicine and critical care setting.
Keywords
toxicology
drug overdose
identification
treatment
patient history
vital signs
activated charcoal
naloxone
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