Hello, I'm Dr. Heather Lee Bailey, an emergency medicine intensivist and a past president of the Society. This talk is on toxicology and drug overdose. This is a huge topic, so we're going to focus on some of the common overdoses and key features that can help you identify the overdose patient and treat them. It's very important to take a thorough history and complete a physical exam, as this will be helpful in identifying potentially what the individual has ingested. If the individual is able to tell you, ideally you want to know the substance, the quantity, the timing, is it a sustained release type of medication, but in general, it's typically an unknown overdose, and many times patients don't even know that they've had an overdose or they present and they're not forthcoming with what has gone on. The physical exam, there are several areas that you need to focus on, obviously vital signs just like any other critical patient, airway, neurologic findings, and skin findings. Pattern recognition is important. There are several classic pathognomonic patterns that you should be able to recognize to help you in the care of these patients. In the vital signs, elevated temperature, heart rate, blood pressure is typically the sympathomimetics, amphetamines, anticholinergics, while the opposite, decreased hypothermia, hypotension, bradycardia, typically narcotics, sedative hypnotics, antihypertensives. Unfortunately, many overdoses are co-ingestions, so this is just a guideline, not 100%. The neurologic findings, it may be all over the place. It could have mild agitation. They may be in a coma. Pupil size is important. Do they have wide eyes, midriasis, looking for sympathomimetics or anticholinergics, or meiosis, small pupils, typical of the narcotics and the cholinergics, and seizures are very common regardless of the type of substance that is ingested, and also from withdrawal, but that's a different topic. And the skin, what's the temperature? What's the color? Are they cherry red? Could this be a carbon monoxide poisoning? Are they hot and dry? Are they moist? And is the skin intact? And do they have the potential of absorption of one of these substances through the skin? That leads us to decontamination. In the past, everyone was recommended to have a bottle of Ipecac at home. That has been removed from the formulary as that is not a good plan of causing individuals who have the potential to lose their airway and have decreased altered consciousness making them vomit. Same with activated charcoal. Everyone used to get activated charcoal, but now they recommend only if they are in the first hour or two of the ingestion and they must be awake. For those of you who have cared for charcoal pneumonitis, it can cause significant morbidity and mortality. And certain medications and certain substances may benefit from whole bowel irrigation, some of the more toxic ones such as iron overdose ingestion or individuals who have ingested packets of drug either because they're in a custody situation or they are transporting substances across the border. These individuals may need whole bowel irrigation as well. There are multiple ways to eliminate toxin. Mentioned about charcoal, which can be effective for several different medications. Forced diuresis, which can typically be in lithium or the barbiturates, alkalinizing the urine in salicylates and barbiturates, hemodialysis may be helpful, and then there are some that have specific antidotes and a handful of them are listed here including acetaminophen and organophosphates. And we will touch on those briefly. There are several therapeutic adjuncts to keep in mind. And these can be pertinent to almost any type of overdose. First is where do you go to get assistance? Now if you're at a high level academic center, you may be fortunate enough to have a toxicologic center and toxicologists on staff. The majority of places unfortunately do not have an available toxicologist in their facility. However, there are the poison control centers. There is a network across both the United States and the world that have direct access to people that have this good information. Only about less than half of the World Health Organization members have a poison center, but in the United States we're very fortunate. There's more than 2 million cases per year that are reported to the poison centers and cleaning solutions, I'm sure you're not surprised with cleaning solutions and rubbing alcohol, the hand sanitizers now make up more than 10% of all reported overdose cases to poison control centers since the beginning of the pandemic. If you're a patient, you're concerned about an overdose and they have an arrhythmia, sodium bicarb by push dosing and potentially a drip is your go-to choice. In critical care, we have gotten away from using sodium bicarb for many things, however in poisonings, sodium bicarb is very important to help improve perfusion and improve the arrhythmia. If your patient is hypotensive, your drugs of choice are phenylephrine for push dosing or norepinephrine infusion for hemodynamic support and there is literature to support improved outcomes using these two medications over other possible vasoactive pressors. With seizures, once you've determined that the patient is not hypoglycemic, benzodiazepines are your first line of choice for seizure treatment. I'm going to look at several specific overdose agents. Sedamine is very common both as a primary and as a co-ingestion and a lot of times individuals don't know what they've taken, they say oh it's Tylenol, oh it's Motrin, oh it's Aspirin but in general they're very unclear and unsure of what they have taken so it's helpful if they've brought the bottle but that's not usually the case. It's common to be an unintentional overdose, especially in people who are trying to self-medicate at home, commonly after a dental or other type of procedure, they think oh it's an over-the-counter medicine and they take a significant amount of acetaminophen. So it's always important to ask when people come in and their symptoms don't make sense, quantify how much that they have taken. Charcoal, just as we mentioned before, is effective early on but you want to make sure these individuals are protecting their airway. There have been case reports of hepatotoxicity in individuals in the hospital who've received IV acetaminophen. There is a nomogram known the Rumac-Matthew nomogram and this is very important to help determine what level of toxicity this patient may have been exposed to and you want to have a four-hour level. The nomogram will take the time out but the first time on the nomogram starts at four hours so it is helpful to follow the levels but the four-hour level is where you decide is this person going to beneficial from N-acetylcysteine. You should also, in patients who you're concerned about acetaminophen overdose, be looking at liver functions and the coagulation profile. N-acetylcysteine can be given either orally or IV. If you have the option, I strongly recommend IV orally. Not only does it have a terrible odor, it is also very, because of the odor, very difficult for the individuals to ingest. There is a dosing regimen, they're given a bolus and then typically treated for 48 hours after that. If the individual receives their first dose of N-acetylcysteine within the first eight hours of overdose, it's almost 100% curative and preventing hepatic failure. Depending on when the patient presents, especially in an unintentional overdose, maybe 24 or 48 hours after the fact, most toxicologists recommend that if you have a Tylenol level or if there's concern for acetaminophen overdose and they're symptomatic, even if it's a prolonged time frame, you should start the N-acetylcysteine because you may save their hepatic function, you may keep them from dying or requiring a liver transplant, and it's very important to follow the acetaminophen level. Salicylates are also a very common overdose. Typically they're a bit more unintentional, is more common than intentional, and one of the reasons is it's found in so many different formulations. Medications for upset stomach and topical arthritis medications, so our patients tend to self-medicate. Oh, they take a pill, they apply something topically, so it is very, very common. Oil of wintergreen actually has one of the highest concentrations of salicylates and people don't really use it, and so along with the other over-the-counter medications such as the bismuth in some of the GI preparations. There are both acute and chronic salicylate toxicity. In the acute salicylate overdose, you have a mixed acid-base process. You have a primary respiratory alkalosis that is from direct stimulation of the central nervous system leads to increased respiratory rate, and you also have a primary metabolic acidosis with direct effect on the mitochondria, you have decreased aerobic production of ATP, leading to increase in lactate and keto acids. And especially the enteric-coated aspirin can lead to besore formation, and another reason why it's important to follow the levels. If you're treating the patient and you're dialyzing the patient, but they have a persistent aspirin level, you have to be concerned that there's a besore, so it may require endoscopic evaluation to remove the besore. Chronic toxicity is a little bit different. These are also associated with polypharmacy from the combination of the oral and the topical medication that can be found in some foods, such as ginger tea. It's really a less classic symptoms and they tend to have more neurologic non-focal findings and they can mimic things such as sepsis or other types of infection or worsening dementia. So a pattern to recognize for chronic aspirin's toxicity is tachypnea with an acid-based disorder, typically the respiratory alkalosis and just non-specific neurologic findings. They're a little bit altered. They may not be quite acting right. You shouldn't be concerned for chronic aspirin toxicity. The important thing is that the salicylate level is not necessarily elevated in these individuals so you must really be vigilant about this. Treatment in the acute setting is activated charcoal and as I mentioned already, if it's enteric-coated, they can not only form a bezoar but these individuals may require multi-dose activated charcoal because of the delayed breakdown of the medication. Regardless if it's acute or chronic, you should alkalinize the patient so that the urine becomes alkalinized and this increases the renal clearance of the drug and hemodialysis is the mainstay of treatment. Any individual who's having severe signs or symptoms, if the level is greater than 90, toxicologists in the literature recommend dialysis regardless of what the patient's symptom level are and then if the patient has real impairment and the level is 80 or greater, those patients should also have hemodialysis. It's important to remember that hypokalemia and evaluate for hypokalemia and hypoglycemia and in a patient who has salicylate toxicity, they may not have a peripheral lab value that's hypoglycemic so if you have someone who you're worried has salicylate toxicity and they're altered, the CNS can have hypoglycemia with the aspirin so it's important to try giving a dose of D50 to see if that improves the patient's mental status. Salicylates are part of the MUDPILES acronym that we all learned in basic chemistry and biology and it's just one of the many substances and this is just a slide for a reminder of the many different things that cause a metabolic acidosis. One of those is toxic alcohols. There are three primary toxic alcohols that you may encounter, ethylene glycol, methanol and isopropyl alcohol. The ethylene glycol and the methanol will both cause an anion gap and an osmum gap metabolic acidosis while isopropyl alcohol which is typically found in rubbing alcohol and hand sanitizers, we've seen an increase in this type of overdose with the pandemic, will cause an osmum gap but it does not give a gap metabolic acidosis, it's a non-gap metabolic acidosis. So it can be a little bit confusing. The central nervous system effects, patients can just be a little bit altered to be in profound coma, look for the anion gap, check the osmum gap. Methanol is broken down to formaldehyde and formic acid and leads to patients complaining of change in vision, they may complain of seeing a snowstorm. Ethylene glycol will break down to oxalic acid and that can cause hypocalcemia and QTC prolongation. If the calcium oxalates will precipitate out in the renal tubules and could lead to renal toxicity, if in the Foley bag you can fluoresce the urine but this is a transient effect, so just because you take the Woods lamp and fluoresce the urine, if it doesn't turn purple, you should not eliminate ethylene glycol because you just may have missed it. Now, alcohol is broken down, these are all broken down by alcohol dehydrogenase. Fortunately, ethanol has a higher affinity for alcohol dehydrogenase, so if there's a co-ingestion, patients may have a delayed presentation. So one of the treatments before we had specific antidote was giving alcohol to try and prevent the breakdown. And this is another pattern to recognize. If you have an anion gap metabolic acidosis, a low bicarb, an osm gap, you should be concerned for toxic alcohol. And it's important to remember that when you calculate the osmolar gap, you must check the ethanol level and include that in the calculation. So the first step is you have to inhibit the metabolism of alcohol. To do that, we used to use alcohol, IV, but then there is about 25, 30 years ago, famipazole, which inhibits alcohol dehydrogenase, which then prevents the breakdown of the toxic alcohols. So you have to give something to inhibit the metabolism first. Then you then have to remove the alcohol and the toxic metabolites, and that is done by dialysis. It's important to remember that you will most likely, at least early on in the course, need to re-dose your famipazole. As I mentioned, it inhibits alcohol dehydrogenase, which prevents the toxic alcohols from being degraded. It's given as a load, and then followed by bolus dosing, also for 48 hours. And it is affected by the hemodialysis. Most institutions are unable to directly measure the toxic alcohol level. It is a send-out. So to follow these patients, you follow their mental status, you follow their anion and their osm-gap, and you follow their hemodynamics. And that is one of the ways that you'll be able to determine when you've given your final dose of famipazole. Keep in mind, it is relatively expensive, but it is life-saving, and the cost, not the charge, the cost is still about $1,000 a vial. There are other some useful adjunct therapies that can be used for the toxic alcohols. We talked briefly about sodium bicarb already, but it can be useful to normalize the pH in these individuals, because it also helps prevent the conversion to toxic metabolites. And it eliminates the CNS diffusion of the toxic metabolites into the brain. Leucovorin and folic acid can help process formic acid, the breakdown from methanol. And thymine and pyridoxine can help with the breakdown of ethylene glycol that causes the glyco, that leads to oxalic acid. Here's the first question. 25-year-old woman presents after ingesting an unknown pills. She is lethargic, and her pulse is 62 beats per minute. Her blood pressure is 86 over 40. Which of the following is the best initial intervention? Transthoracic pacing, lipid emulsion, glucagon and calcium, or dopamine? And the answer is glucagon and calcium. So there are many agents that can cause bradycardia and toxicology. Some of them may be medications that the patient is already taking, such as beta blockers or calcium channel blockers. They're very common, they're very common in overdoses, especially in children who get into either their parents or their grandparents' medication. And both beta blockers and calcium channel blockers are in the context of one pill can kill a child. So it's very important to keep those medications locked up. It can lead to hypotension, bradycardia, more likely to get altered mental status with a beta blocker overdose, more likely to get hyperglycemic with calcium channel blocker overdose, but it can occur in either. So give glucagon initially, and calcium if the concern is either one of these two, nor epinephrine and epinephrine kit to help support the hemodynamics. If the glucagon and the calcium do not help improve heart rate and hemodynamics, start with high-dose insulin. More likely to work with the calcium channel blockers, but you can use it for either. Of course, with severe bradycardia, atropine is very handy in our code cards. You can utilize that as well. However, it typically does not work. If high insulin does not work, your patient may require transcutaneous or transvenous pacing or the use of lipid emulsion. There are some other adjunctive therapies that may be useful in overdose patients as well. Methylene blue, placing them on a milrinone or a balloon pump, or using extracorporeal membrane support. Now, lipid emulsion has been used for many different substance overdoses as an antidote. This is just a partial list. It's very common with severe calcium channel blocker and beta blocker overdoses, can also be used in lidocaine toxicity. There are some adverse effects, which I'm sure that you are familiar. Just remember to evaluate and monitor for pancreatitis, liver injury. It can also be challenging if the patient requires dialysis. Cholinergic syndrome is a major overdose and exposure problem across the world. Still used in agriculture in many areas of the world and more than three million cases occur worldwide. There's organophosphates and carbamates are the two main types of exposure. Unfortunately, it's also used in nerve gas such as sarin and VX, which is the most toxic substance. It can be absorbed through several different modalities, directly through the skin, through GI absorption or inhaled through the lungs. And the antidotes are both atropine and pralidoxine. And we'll go through that a little bit more in a moment. And you should avoid disoxynilcholine as this can worsen the outcome. The mechanism is that acetylcholinesterase causes binding and it becomes non-functional. So you have excess acetylcholine. Needs to increase activity. And the term aging is important. This is where the acetylcholineesterase is totally bound and cannot then be broken down. It's resistant to reactivation. So the aging of a medication or exposure is key. Some of them are very rapid. Some of them can take days. The ones that take longer to have irreversible binding, you have much more likelihood to treat the individual and get them through this course. So another well-known acronym, SLUDGE, for cholinergic excess, salivation, lacrimation, urination, defecation, and gastric emptying. The patient will have fluids coming from mold The patient will have fluids coming from multiple and probably all orifices. And then they also will have significant pulmonary findings and cardiovascular findings. Classically, they are bradycardic. work. These patients will spend a prolonged amount of time in the critical care setting and there are two neurologic syndromes to be aware of. There is one that is relatively acute in the first few days after exposure. They have weakness of flexion, decreased reflexes, their alter, their cranial nerve have abnormalities, they can have respiratory compromise. Then there's the delayed which is several weeks out which are which is known as organophosphate-induced delayed neuropathy and that is a stocking glove type pain, polymotor neuropathy. They have flaccid lower extremities similar to a Guillain-Barre kind of picture and what's interesting is that the risk of developing this is not aligned with the severity of the overdose so even a mild overdose or an exposure can have this significant sequelae so it's important if the patient is leaving the intensive care unit that you relay this information to the team that will be taking further care of the individual. They can have permanent Parkinsonian syndromes, memory can be affected, they develop acute kidney injury, may require dialysis, pancreatitis is very common cause or development from these overdoses and exposures so you should monitor for that. Now the treatment for the cholinergic rescue is twofold as atropine for the muscarinic effects and you should and must give the atropine first and the atropine is bolus dosing and it is until secretion clearance not based on heart rate. These individuals be drowning in secretions and fluid. You can also give some bronchospasm release because you're drying up the secretions. This is a time that you need to notify your pharmacist, your PharmD that you have a potential cholinergic exposure and you may in many hospitals use the entire amount of atropine in the hospital. A hospital depending on the size may or may not have the antidote the pralodoxine so your pharmacist may need to be calling around to other facilities to get the pralodoxine. This is going to treat the nicotinic effects, it's an oxime therapy and just like many of the other antidotes you give a bolus dose first and then an infusion. It's important that it's bolus is given slowly because it can cause cardiovascular collapse. Organophosphate and cholinergic toxicity is important they have seen safety especially if the individual came in and had it on their body or on their clothes so health care workers have been known to become symptomatic and sometimes have fatal outcomes with both nerve gases and environmental agricultural exposure. Clothing should be bundled and discarded, skin should be irrigated, there needs to be good ventilation and you should have a decontamination plan that you can refer to. Benzodiazepines are very common co-ingestant and typically it's really just supportive care. Many of us for moderate sedation will use the antidote flumazenil and but this is a totally different entity. You know what the patient has been given in the moderate sedation so flumazenil in the appropriate setting is very safe but in an unknown overdose even if you think it's only just benzodiazepines if you give the flumazenil you will have blocked the receptors and so if the individual starts to seize you will have no recourse to control the epileptic event. Antidepressants especially the cyclic antidepressants the older antidepressants high likelihood of morbidity and mortality. These are individuals not only to give charcoal you want to consider lavage because of the level of toxicity they were in benefit from blood alkalinization and refractory cyclic antidepressants might benefit from hypertonic saline and lipid emulsion. Fortunately for the last 20 so years or so selective SSRIs have been available and they have a much higher safety profile. In general in overdose these patients are going to do well but a select individual with a large volume of overdose can have central nervous system effects. They can also have what's known as a serotonin syndrome which has altered mental status, autonomic dysfunction, and neuromuscular abnormality and rigidity. The treatment is supportive care giving benzodiazepines putting the place in them on propofol, cooling them if they are hyperthermic and stopping any potential offending agents. Hypoglycemic agents treatment obviously is giving d50 and then placing the individual on a d5 or d10 drip to maintain their glucose. Initially if in the field of it or an IV is not accessible you can give glucagon by IM or subcutaneous manner. It's important to remember that if you're giving large doses of glucose that you should also be supplementing with thiamine so that you do not precipitate Warnecke's syndrome. Now sulfonylureas were very common they're less common now but if the patient has a potential of a sulfonylurea overdose you can use octreotide and this can be given subcu or IV every eight hours and it inhibits insulin release because what happens with the sulfonylurea you give the d50 it will drive insulin release and precipitate worsening hypoglycemia so if a sulfonylurea is involved you should give octreotide. Everywhere in the world unfortunately is having an opiate and specifically a synthetic opiate crisis especially in the United States with thousands of individuals unfortunately dying every year. There is an excellent antidote if you have it available naloxone can be given by essentially any route. The half-life unfortunately is relatively short somewhere between 30 to 70 minutes and it typically lasts less time than the substance that's been ingested. For synthetic agents you may need large volume of naloxone this is another time to notify your pharmacist that you are concerned about a synthetic opioid overdose and that you may need and use all of the naloxone that you have available in your hospital. Once you've resuscitated the patient this is another medication that you're going to place a drip. You're going to give two-thirds the bolus dose that improve the patient's hemodynamics and their respiratory status per hour and unfortunately it's not uncommon that once patients become awake and aware they want to leave against medical advice. Specifically for the synthetics most of them are going to require at least two doses sometimes of high dose naloxone. They have much higher potency and some of the synthetics are more than a hundred times more potent than fentanyl. They're also not seen on a routine drug screen so that would have to get sent out for a selected drug screen which is not going to be helpful in the acute phase and these individuals you need to evaluate them closely for injury. These drugs are so potent that not only are the many times the pre-hospital personnel and the police finding the individuals with IVs in the arm they just drop because it is so potent so you evaluate them for trauma. Same thing for neurologic evaluation they need a thorough neuro exam. It's important to note that it's not just IV ingestion and exposure that can cause severe overdose. These can get inhaled they can get ingested they can get absorbed so it's not just IV and about one in five deaths from synthetic opioids are due to a non IV route of ingestion. The phenomenon of fentanyl induced chest wall rigidity is thought to perhaps be one of the causes of the rapid respiratory depression. Get rigid chest you treat with naloxone and short-acting neuromuscular blockade. Just like the organophosphates you must be mindful of a potential occupational exposure. A few important points is if you're worried about synthetic opioids you should not be using alcohol-based hand sanitizer this can actually help metabolize its absorption into the skin so soap and water. Nitrile gloves should be used not latex now most places don't have latex gloves anymore and also gloves that do not have powder because all of those things the latex the synthetic opioid has been shown to be able to get through and it can attach to the powder. These levels that cause almost instantaneous death are so low they may not be able to be detected even if you send this to a specialized lab and be mindful of police or other EMS individuals who come in having symptoms of respiratory depression or weakness numbness nausea vomiting syncope on scene especially if there's a concern for substances on site. There is no occupational level that's been deemed to be safe by NIOSH and don't forget about the working dogs. The drug dogs are also at risk and they can be given naloxone as well similar doses to humans. Cocaine causes multiple different toxicities specifically aimed at cardiovascular and central nervous system arrhythmias, dissection, they can have acute coronary syndrome, intracranial hemorrhage, seizure, coma. They can also have vasoconstriction leading to thrombosis. There are other also associated effects such as rhabdomyolysis and hyperthermia. Many of the substances also have co-contaminants so it may not appear to be a straight sympathomimetic overdose. Amphetamines and methamphetamines, multiple different routes of ingestion, similar complications to cocaine and other sympathomimetics. Next question, 24 year old patient is admitted to the ICU for seizures, hyperthermia, he's tachycardic and he's agitated. 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, mephedrone or gamma hydroxybutyrate? And the answer is mephedrone which is also a type of bath salts. Bath salts are derived from the cot plant, it's a stimulant and it's hallucinogenic. Multiple methods of ingestion, snorted, injected, it can be inhaled, gives sympathomimetic effects. Patient becomes very aggressive, very paranoid, this is the strength of ten men. Sedation with benzos and good supportive care. Same for the synthetic cannabinoids, also they're not detected on the urine drug screen. They tend to have some GI side effect but similarly will present with paranoia, hallucinations, anxiety and violent behavior. It's important with any of these entities that restraint can be challenging both from a safety standpoint for the patient and for the staff but once they you have them sedated they can have sudden death from arrhythmia and asphyxiation so you must be very careful caring for these patients especially if they need to be physically and chemically controlled. Chemical control is key because physical control can lead to a bad outcome. There's a small case series on synthetic cannabinoids that looked at presentation and it was essentially equal. A third presented with seizures, a third were agitated and a third presented with coma so it seems to be depending on individual on how they're going to present and it's just unclear. You cannot hang your hat on any one specific presentation. About two-thirds of them developed respiratory failure, almost three-quarters of them required airway support and intubation, half of them had a co-ingestion and once they recovered about half of them also signed out against medical advice and a quarter of them developed rhabdomyolysis. heart rate. Energy drinks are very popular as is caffeine intoxication. In fact there's recently been some difficulty with a chain restaurant that had a caffeinated drink that was very caffeinated that may or may not have been appropriately notification to individuals and several individuals unfortunately have consumed this drink and suffered cardiac arrest who had known underlying cardiac disease. E-cigarettes also can lead to nicotine poisoning, can cause a cholinergic toxidrome, seizure, cardiac arrest and of nicotine have increased every year for the last 15 years. Sometimes the overdoses and toxicities don't occur before they come to the hospital they can occur in the hospital and it can be iatrogenic and these are some of the more common ones. Hand sanitizers have increased in toxicity as individuals have been searching for sources of ethanol. Methemoglobinemia can come from topical anesthetics. Propylene glycol is a diluent in many different medications including lorazepam and phenytoin and there's of course the propofol infusion syndrome. Individuals who have head injury, have sepsis, are having prolonged dosing of the medication are at high risk for developing this. They develop a lactic acidosis, can have arrhythmias, hyperkalemia, rhabdomyolysis, renal failure. Much more likely the higher the dose, much more likely the length of time that they're on it. So it's important to be mindful. And then here's just a list of some common toxins and their antidotes for your review and here I did add under organophosphates they just had listed atropine but atropine helps for the muscarinic effects to dry up those secretions it's the pralidoxine that will bind to the organophosphate that will help prevent further aging of that individual so the pralidoxine must be given atropine is only an adjunct. So just a reminder not all overdoses or toxidromes are immediately recognized especially if the individual is either unable to relay the information they come in altered or it was an unintentional overdose and they were using polypharmacy and didn't think to notify the clinician who is taking the history so you must remain vigilant if it's not if any just like any other patient if it's not making sense you must go further good history and physical exam can answer a lot of these questions remember to make sure that you and your staff are safe for follow good decontamination processes and it's important to recognize and act on classic syndromes. Thank you for your attention.

toxicology

drug overdoses

identification

treatment strategies

decontamination

antidotes

poison control

patient assessment