Thank you very much, Dr. Hughes. So for those of you that don't know me, my name is Walid. I'm one of our chief medicine residents. And I have the good fortune of introducing our grand round speaker. 

So it's an honor for us today to welcome our great round speaker today, Dr. Heather Borek, from our very own emergency room. Dr. Borek completed her medical degree up at the University of Connecticut before coming down here to UVA for her emergency medicine residency and fellowship in medical toxicology. She then served as an attending over at the Martha Jefferson for a while, as well as the Einstein Medical Center up in Philadelphia before kind of we had the good fortune of recruiting her back here to UVA. 

She serves in multiple roles here at the University of Virginia, including assistant professor of medicine for emergency medicine and toxicology, fellowship director for the medical toxicology fellowship, as well as director of the Blue Ridge Poison Center. And over the years, she has become an expert in trauma assessment and the complex management of toxicology-- complex toxicology patients, teaching and publishing widely in kind of both of those areas. So we're certainly very, very fortunate to have her with us here to speak to us today and maybe give us all a little bit of insight on the intricacies of managing the critically ill toxicology patients. So without further ado, you can please join me in welcoming Dr. Borek. 

[APPLAUSE] 

Well, thank you everybody for having me here today. I know many of you through working with you and our collaboration through emergency medicine and the admission process, as well as consultations. So I really appreciate you having me. 

I'd like to today just kind of go over an overview of some complications that we commonly see in our more critically ill tox patients that get admitted, whether it's to the floor or to the ICU setting. So I have no financial disclosures, no conflicts of interest. 

We'll go over kind of some case-based discussions, talk about these common complications review, kind of recognition and management of these complications. There are some differences in how I manage my tox patients versus how I manage some other medical conditions that may come in with similar vital signs or similar mental status changes. And so kind to talk about how those might get manageable, but differently for the toxicological population. 

And then drug screens always come up. There's lots of limitations with them. And so just kind of briefly touching on some of the limitations that you'll see as we go through some of these cases. 

So the first case is a 51-year-old female, who's found down outside of a methadone clinic. She presents unresponsive. She's got hypoxic respiratory failure. And so she gets intubated for airway protection and goes to the McCue. 

She has an uncomplicated extubation the next day. When she wakes up, she starts complaining of her arm hurting. And when you look at her arm, it's very red. It's swollen, fairly well demarcated. And so the team-- this was not here. The team started her on some antibiotics for cellulitis. Seems reasonable. 

However, the next day, when you reassess her, she's not really improving. She's continuing to have pretty severe pain and continues to have kind of this red and swollen arm. So what sorts of things would you be thinking about this person? 

Necrotizing fasciitis? We don't know if she's an IV drug abuser-- so an embolic event, thrombotic event. This actually ended up being compartment syndrome. And unfortunately, it was an unrecognized compartment syndrome. 

What had happened was she was found down. And she was laying on her arm. And so she had compression of her arm. 

And we tried to point out that we had concerns from a tox point of view of compartment syndrome. Unfortunately, our concerns fell by the wayside until she got transferred to a different team, a few days later. And then went for fasciotomy. Unfortunately, it was a delay in getting the proper testing. So just recognizing that that can be a complication. 

And so why do patients get compartment syndrome? Well, it may be from wearing skinny jeans. There actually is a case report out there of skinny jeans causing compartment syndrome. But that's probably not the case for our patient. 

So the found-down patient, if you're able to get the information on knowing their positioning-- sometimes we don't have that available in the emergency department. We have the benefit of having the team that found her a lot of times, bring them in. And so we can specifically ask that question. Sometimes you can look at their documentation, the run sheets. 

A lot of times we're not necessarily going to know that. So then you have to kind of look for physical exam findings that might suggest their positioning. And so when you get kind of occlusal services, this is between the knees. 

That's kind of cool-- between the knees. The skin is touching. And you get some skin breakdown. That may suggest knees were touching, common at the ankles as well. 

This was a case I had of a young woman that overdosed on heroin, as well as many other drugs, who is in a position like this. And so she actually had these skin changes along her neck. Did get started on some antibiotics as well. Again, can look similar to a cellulitis. But keep in mind in the tox patient this might not be an infectious cause. It may just be a compressive cause. She ended up doing OK. 

So a lot of these people, if they're using drugs, end up in a unresponsive or semiunresponsive state. If you are injecting drugs while you're sitting in a chair or while in a seated position and you kind of pass out, you end up being on your gluteal area for a long period of time. And there are cases of gluteal compartment syndrome after overdoses. And so you do have to be aware. 

Compartment syndrome, not kind of in the classical locations. But you think of it like a leg or an arm or something. 

So along the lines of compartment syndrome, rhabdomyolysis, who else gets rhabdo besides the found down patient. And that's the agitated patient, right. You kind of get your unresponsive tox patient. You get your very agitated tox patient as well. 

And so this is just a sample case of this, that was here in 2010. This was a 25-year-old male, that was brought in by EMS and police. He had injected bath salts and was running around the neighborhood, combative, foaming at the mouth. 

Takes nine police and security to hold him down. You can kind of imagine-- get a picture of this. But the manpower that was needed to even get him to the hospital. 

So his initial vital signs. He was a little bit hypertensive, but nothing too impressive. But quite tachycardic, temperature of 41.3. His pupils were dilated. 

He had some eye deviation. His skin was very hot. He ended up getting intubated. His head CT was unremarkable. 

And this was his initial set of labs. So white blood cell count was elevated. He already had signs of kidney injury. He had signs of liver injury. 

His glucose was low. His troponin was elevated. And his CK was 2,000. And so already having signs of multiorgan system effects, minutes to hours after the ingestion. 

Unfortunately, it only got worse from there. He got admitted to the intensive care unit. He ended up requiring dialysis. And over the next two days, went into fulminant renal failure, hepatic failure, DIC, cardiac ischemia, rhabdo. He had started out at Augusta and ended up getting transferred to us at the day two mark. 

And these were his labs upon transfer to us. So at this point, you could see the creatinine. This is after multiple rounds of dialysis. 

That CPK, 235,000. So he had peaked at 239,000 or something. That was starting to come down at that point. But to this day, it's still the highest CPK elevation I've ever had. Component of 29. INR above the detection limit. Again, [INAUDIBLE] and DIC for this gentleman. 

And so he got further hemodialysis here. He got an echo here, that showed globally reduced LV function, and EF of 30%. 

He ended up getting extubated on day 9. His mental status did improve by day 13. He was discharged on day 18. Continued dialysis for about a month afterwards. And was eventually able to come off of dialysis. 

This was his drug screen. Completely negative, all the things that we test for on our drug screen at the time. Did this guy do drugs? Absolutely. 

Did he do amphetamines? Not methamphetamine, which is why the amphetamine screen is negative. We did a synthetic amphetamine, with these fat cells. And so with the newer synthetic drugs, they're not reliably picked up on these drug screens. But that doesn't mean they didn't do drugs. 

So what we ended up doing-- this was right at the start of the bath salts craze, before there was really any literature on this. We had a sense because the trends kind of started in Europe. We had a sense of what might be in this. 

So we sent it for some very extensive drug testing. And it came back MDPV. And we ended up publishing a case on it. Again, one of the earliest clinical cases OF the effects of bath salts. And again, this NDPV is just a synthetic amphetamine-like compound stimulant. 

So moving on. So we've kind of talked about the found down patient, the agitated patient. There's some kind of notable mentions of specific agents. So certain drugs themselves are mild toxic. 

We've kind of talked about this with the stimulants, these amphetamines, cocaine. It can cause some direct tissue injury. Diphenhydramine actually can be directly mild toxic. And barbiturates can cause skin changes, that kind of look like skin breakdown. But they're actually from the drug themselves. 

So this was actually described in the 1960s. They found about 6.5% of patients had these kind of bolus lesions or what we call barbiturate burns. And so just kind of these skin changes. Boli tend to be more on the lower extremities. 

Some barbiturates themselves. We don't have too many patients on barbiturates these days. But every few months we'll get one, that'll come in. So looking for those skin changes would be important. 

And so how are we not going to miss this on the next person that comes in? So doing a good physical exam. Doing a good skin assessment. Looking for signs of skin breakdown. Looking for clues as to how they might be positioned, kind of feeling their compartments. 

Trending the CPKs. And so the bath salts gentleman that came in, his was 2,000. That's high, certainly. But none of us are getting all that excited about that. 235,000, yeah, I think we're all getting pretty excited about that. 

So if there's a reason to suspect that that's CPK might rise? This person who comes in agitated, having 10 people holding them down, you're going to need to trend that. 

And then if you are trending it, and the patient seems to be getting better, but that's CPK just isn't coming down, at that point make sure you're checking for compartments. And make sure you're rolling them, checking their gluteal area, checking all their muscle compartments to make sure they're nice and soft. 

So next case is a 21-year-old female that was found unresponsive by family, with a suicide note next to empty bottles of methadone and alprazolam. EMS arrives to find vomit in the bed. She's got normal blood pressure. Heart rate stats are low. 90% on rheum-ar. 

Her pupils are 4 millimeters. She moans to sternal rub, but really doesn't do much more than that. She's generally decreased tone, no clonus, normal bowel sounds. And her lung sounds are fairly coarse. 

So which of the following would you do next? Would you give her NARCAN, 0.4, start her on BiPAP, intubate her, or give her some flumazenil? We'll go through some scenarios here. 

So I would intubate. And we'll talk about kind of what might happen if you go through some of these other scenarios. Flumazenil, it's a benzo reversal agent. We generally are not using it for intentional overdose. And that's for a few reasons. 

So if we give it and we precipitate benzo withdrawal-- so this person is chronically on Xanax. And so now we're precipitating benzo withdrawal. That can be life threatening. It can cause seizures. 

We now have what the benzo receptor. And so when we go to treat seizures, we can't use benzos to treat seizures. So now we have to reach for barbiturates and other things that may not be in our kind of routine management for seizures. So we don't want to precipitate withdrawal for this person. 

This patient population, also pretty unreliable. And so even if it was somebody else's med, we don't know what they're doing on a daily basis. They often will get things from friends or use family members' prescriptions on a regular basis. And so even if it's not technically their medicine, it's still risky to try and reverse it. 

So what about BiPAP So I love BiPAP for non-tox patients. I had a flush pulmonary edema that came in the other day, that was tripoding. And we got him turned around in an hour with bypass. That was great. 

But in tox patients, the issue is airway protection most of the time. And so when you ask what's the status of their airway, it's not really important what their stats are at the time. It's more, are they an aspiration risk? 

So a lot of patients that come in, they're sleepy. They're just sleepy. But they wake up and talk to you. They're fine to let ride. You probably don't have to intervene. 

When you start to get, they only moan to sternal rub and you're not sure if they're about to vomit, if you start them on BiPAP, their mental status is not going to allow for that positive pressure. It's going to inflate their stomach. That's going to increase their aspiration risk. 

And so a lot of these folks, if they need to be intubated, if they get intubated, they metabolize by the next day. They're off the vent the next day. It's a pretty uncomplicated admission. 

If you kind of let them sit, don't protect their airway, they vomit, they aspirate, now they're 2, 3, 4 days on the vent. You're talking about more ICU delirium risk and other kind of complications of hospitalization. And it's just more of a prolonged course for them. 

And then the use of narcan. So narcan's very popular. Police are using it, first responders. It's kind of more widely available in the community. And so there are some intricacies to it, some nuances to it. 

So in this case, we had both an opioid and a benzodiazepine overdose. And so the narcan will reverse the methadone, but it's not really going to do anything for the benzo. And so opioid withdrawal can precipitate nausea, vomiting, diarrhea. So now you've got a vomiting patient who's still sedate from their benzo. You might actually increase their aspiration risk with the narcan. 

The other thing to keep in mind, so everyone has endogenous opioids. And so if you have the little old lady in the nursing home who comes in altered and you give a trial of narcan as a diagnostic tool, they may have some non-specific awakening. It's not as profound as the person who's blue and not breathing to awake and talking and saying, hey, let me out of here. But you can get some nonspecific response just from that reversal. 

And this person had no signs on exam of opioid toxidrome. If you remember the scenario, their pupils were kind of mid-range. They had good respiratory effort. 

So if you are going to use narcan, you want to look for the opioid toxidrome. Classically, we talk about CNS depression, respiratory depression, and small pupils. They're also going to have decreased bowel sounds. And there's lots of agents. I'm guilty of just casually saying opiate and opioid interchangeably. But there is technically a difference. So opiates are those derived from the plant. They're kind of the natural opiates, if you will. Opioids, they're anything that act on the opioid receptor to exert a similar effect. So these are more of the synthetics, your methadone, your fentanyl, other ones, as opposed to the natural ones, like morphine, codeine, opium. 

And so what if you have someone that did an upper and a downer, if they did a speedball, they did some cocaine and heroin together? If you reverse the heroin aspect of that, now you kind of have this pure stimulant effect. And so they may get more agitated. They may be more difficult to manage, hypertensive, tachycardic. You may end up giving them some sort of sedative to try and calm them down. 

So I'm not saying don't do it. There still is a role for narcan. If you're going to do it, though, look for signs of opioid toxidrome. Look for the small pupils, the poor respiratory effort. If they're just kind of sleepy and hanging out and protecting their airway, let them be sleepy. 

If you are going to use it, don't give a big slug of it. So we'll generally mix a 0.4 milligram vial in a 10cc syringe and then give a cc at a time. You know, wait 30 seconds, give another cc. You want them to wake up somewhat. We want them certainly breathing at a good rate. We don't necessarily need them up and screaming and vomiting at us. 

And then just a note. So once they're intubated, there's really not much of a role for narcan. So people die from opioid-related deaths because of respiratory issues, they either stop breathing, or other secondary complications of that. So once you've taken control of that, there's little role to giving narcan. So I would avoid it in your already intubated patients. 

All right. So next case was a 16-year-old that was found unresponsive by friends at a friend's house. He was given narcan 2 milligrams intramuscularly from EMS. And he woke up, was talking, was confused, and sats were hanging out around 70%. And so he gets intubated, and they really couldn't get his sats up. They're remaining kind of 40% to 83% on positive pressure. 

So he gets transferred to our PICU, en route becomes hypotensive and is started on pressers. And this is his initial chest X-ray at the outside hospital. Kind of this diffuse picture, diffuse infiltrates, if you will. 

They continue to have difficulty oxygenating him here. He gets very high PEEP. They ended up having to paralyze him, kept him on high FiO2 requirements, and repeated a chest X-ray 12 hours into his stay here. This is what we see now. 

So you can see, all the air in the sub Q tissues here. You can see air around the heart. So he's got pneumomediastinum. And this was all probably related to the positive pressure. 

The next X-ray that we have, you will still notice all the air in the sub Q tissues. You'll also notice the echo cannula that he has. So he ended up on ECMO. 

And so this is a case of opioid-induced pulmonary edema. Hard to say what the exact incidence of this is. What we do know is a lot of these cases show up in the MEs office with this dried edema around their nose and mouth. And the MEs pretty much know from the get go that that's an opioid-related death. But hard to say what the kind of denominator is, estimated maybe about 2% in some studies for heroin. But the ranges are really kind of all over the place. 

And there's lots of different proposed mechanisms for that. Some people think it's related to narcan. But again, we know that it's not exclusively related to narcan. We know there are certainly other mechanisms, because there are these people that never get narcan that end up dying related to this. So it's the thought maybe the negative intrathoracic pressure from inhaling against a closed glottis, is it disruption of the alveolar barrier due to direct effect of the drug. Is it just the hypoxemia and respiratory depression that develops? 

And this can sometimes be a delayed finding. So one of the reasons we watch people after narcan is to see if they re-sedate, but also to see if they develop this. It can take a few hours to develop in some folks. 

So the next case-- so switching gears to a little bit of a different population-- this was a 78-year-old female on sotalol who accidentally takes a double dose of the medicine. She's feeling dizzy, calls the poison center. We recommend that she go in for evaluation. She was a little bradycardic en route, and then suddenly becomes unresponsive. And when you look at what her rhythm did during this unresponsive period, you've got this episode of torsades. 

And disrhythmias are common in our tox patient population. A lot of drugs exert effects on multiple channels. The main ones we focus on are kind of the QRS and the QTc. This is by no means an extensive list of medicines in either of these categories. You open up any book and you've got pages and pages of drugs that affect each of them. But keep in mind, QRS prolongation due to sodium channel blockade, QTc prolongation due to potassium efflux blockade. 

And so why do these happen? So if you remember your action potential here, phase zero is a rush of sodium into the cell, phase one is your small potassium channels, phase two your plateau phases, your calcium channels, phase three is your large potassium efflux channels, and then phase four is your resting sodium potassium ATPase. And so that corresponds to what your EKG looks like down here. And so if you've got a sodium channel blocker onboard, it's going to take longer for that sodium to rush into the cell. It's going to prolong that phase zero, and therefore prolong that QRS and cause the widening. Similarly, if you've got a potassium efflux channel, same thing is going to happen with phase three, and then you're going to get your QTc prolongation. 

And so what happened with sotalol? So sotalol is a beta blocker, but it's also a potassium efflux blocker. Most medicines that are potassium efflux blockers, you will have tachycardia from, as well, which is actually protective. So if you take a tricyclic, it has some potassium efflux blockade, but it's also anticholinergic and so you're tachycardic. And so that's usually a little bit protective, if you think of the treatments for torsades, magnesium overdrive pacing is one of them. And so you kind of self overdrive pace if you're tachycardic. But you combine a beta blocker with a QT prolonger, sotalol, very high risk for torsade. So unfortunately, a double dose of this could put you at risk for torsades. Those folks are going in for overnight observation, most of the time. 

So an honorary mention, as we're in the midst of the opioid epidemic. So people are abusing Imodium, either to try and get themselves off of opioids or to get kind of a legal high, if you will. So normal dose is about 4 milligrams. People will be taking 200, 400 milligrams a day. High doses can also have cardiac interval abnormalities and lead to cardiac arrest. And we've had a few cases of that over the past year or two. 

So if you remember nothing else from this lecture, I ask that you try and remember this slide. Over the years, I've had a number of very smart people who get these two things mixed up. So remember, sodium channel blockade, QRS prolongation. We're going to treat that with sodium bicarb. Potassium efflux blockade can cause QTc prolongation. That's going to predispose to torsades and you're going to stabilize that with magnesium. 

Why do I say that? A lot of people get confused, and they're like, oh, they've got QT prolongation, we'll give them some bicarb. So not only does that not really help, but you can actually potentially hurt. The bicarb, remember, can shift your potassium into cells. You can now get a little hypokalemic. Hypokalemia can worsen QT prolongation. And so just try and keep them straight. 

So next case is a 65-year-old gentleman I had. He was discharged from the hospital two days prior for acute kidney injury and some prostate issues. During his hospitalization, they switched his calcium channel blocker from one extended release to a different one. And so he accidentally took both the morning of presentation. 

They called his PCP. His PCP referred him to the emergency department. By the time all that happened, it ended up it was about four hours after this medication mix up. He had normal vital signs. He got observed in the emergency department. And about eight hours after ingestion, his numbers just started to tank. He ended up profoundly hypotensive and bradycardic. He ended up getting the kitchen sink thrown at him. So fluids, calcium, multiple pressers, high dose insulin-euglycemia therapy, which is something that we'll do for calcium channel blockers and beta blockers, which is another lecture in and of itself. Gave him intralipids. He had this refractory hypotension. Fortunately, we were able to support him through it and he ended up doing OK, and numbers kind of came around as he metabolized. 

So sustained release products are something that are good in the primary care setting, right, because then you don't have to take something twice a day. You can just take something once a day. So compliance is generally better. But in the toxicologic setting, we really worry about these. They might look good on initial evaluation. The effects might not manifest for a number of hours out. And then once they do, they may last for a lot longer. 

And so just some samples here. So a six-year-old that ingested a sulfonylurea. It wasn't discovered till 45 hours after ingestion, when she was unresponsive at school. Bupropion, so extended release greater than 600 milligrams, you've got about a 30-plus percent seizure risk. And so all these folks get admitted for 24 hours for observation. 

So one thing to keep in my mind, the most common questions we get is, well, how long do I have to watch this person? Or, well, when are they going to get better? How long until they clear? So, hard to predict. So the numbers you look up, when you look up half lives and say, oh, the half life of this drug is four hours, they should be better in 8, 12 hours. That's different. That's tested in someone who is generally healthy, who does not have other drugs on board, who's taking a therapeutic dose in a controlled setting. This is someone who may have taken multiple things, took above the therapeutic dose, and so you can't really predict. 

The other thing is kinetics sometimes change in folks. So you may go from first order to zero order. You may have a clump of something sitting in your stomach that's altering your kinetics. 

So aspirin is known to be very erratic. There is a case of someone who reportedly ingested 25 tablets of non-enteric coated. Their initial salicylate level was undetectable. Their repeat was just barely detectable but nothing to get excited about. And so they ended up getting cleared for psychiatry, got admitted off-site to a psychiatric hospital. And eight hours later started having vomiting, tinnitus. Because they were off-site, it took a while to get back to a medical facility. And so 22 hours later, their level was 41.5, which is a treatable level. And so it probably got even higher than that between the 8 and 22 hour mark. And so there's just certain medicines that are very erratic, aspirin being one of them. The anti-epileptics also very erratic. 

Just to go through one more case here. A 40-year-old female was found by her family unresponsive. There are empty bottles of baclofen and an NSAID, diphenhydramine, and alprazolam. She gets intubated, had a GCS of 3, was hypothermic, had fixed, dilated pupils with absent corneal and ocular reflexes. 

Her labs were unremarkable. Her head CT was normal. Her QTc was a little bit prolonged. She got admitted to the ICU, got rewarmed, was mildly hypotensive, was kind of transiently on pressers. Then on hospital day 2, had some seizure-like activity that was able to be controlled with propofol. 

Hospital day 3, she had no further seizure-like activity. They were able to discontinue the propofol. She still had a GCS of 3, at that point. And so brought neuro in to do brain death testing, found she was choose unresponsive to all stimuli with fixed pupils, absent reflexes. And when they did apnea testing, she didn't quite meet the criteria for apnea testing. She had weak inspiratory effort. But it was felt by the team that her prognosis was very poor. And so discussion was had for organ procurement, and family agreed to that. 

So hospital day 5, she proceeds to organ procurement. And in the pre-op area, she starts opening her eyes and moving her extremities. So fortunately, they aborted that procurement. And so she actually came out of this neurologically intact. She was discharged to a psychiatric facility on hospital day 15 and had admitted to a large baclofen overdose, which the hypothermia, the seizures would all fit, and the unresponsiveness, with a baclofen overdose. 

And so the question comes up, how do you declare brain death in a poisoning patient? This is certainly very challenging. If you try and pull data on this, the poison center, and the National Poison Data System that we use, we don't really distinguish a brain death from cardiac death. So when there's a death reported, we kind of lump them all together. So kind of hard to sort out how many cases there actually are. 

There are lots of drugs that can mimic brain death. And so if you look at the checklist for determining brain death, there's lots of things on here. But I want to direct your attention to the fact that you're not allowed to have a CNS depressant drug effect on board when you're doing all of this testing, and also not having paralytics onboard. 

And so hard to prognosticate. If you had a patient with that clinical exam who had some end stage cancer or some huge trauma, yeah, probably a very poor prognosis and the right thing to do is to go to organ procurement or comfort care or something. But that's not necessarily the case with these tox patients. These drugs kind of put them in a suspended animated state where they don't have as high energy needs, they don't have as high metabolic needs. And so that can come out of these kind of concerning exams fairly neurologically intact. 

And so if you look, there's, again, lots of drugs that can do this. And it can cause kind of these flat lines on EEG, as well. You can have some drugs that cause more of the clinical exam, but not necessarily EEG findings. Paralytics, I think we all recognize. You can't base your physical exam when there's paralytics onboard. But barbiturates, benzos, the sleep aids, TCAs, baclofen kind of the big offenders that we think of. 

And so how do we manage this? So, hard to say. Again, no great data on this. Do we routinely drug test? So no, we don't necessarily send levels on TCAs if someone comes in after a TCA overdose. But if you're to the point where you're thinking brain death and they don't have a structural abnormality, they don't have cerebral edema in their brain or something, you might want to send a TCA level. It's going to take a couple of days to come back. That will give you a few more days to see if the clinical exam improves. And then once that send out comes back, you can kind of base your decision making on that. So in these cases, where we're thinking moving towards brain death, sometimes we will request some of these send out labs that we don't routinely otherwise perform. 

The other thing to keep in mind, if people co-ingest things or have delayed absorption. Again, this just goes along with your kinetics are going to be different. And so if they've got multi-organ system injuries, these drugs may stick around. Their metabolites may stick around longer than you would think, based on half lives. 

And so my thoughts on how to do this. If you have someone who's a big heroin overdose, who is found with sats of 40 and they were last seen normal 12 hours ago and they've got signs of hypoxic injury throughout their body and you scan their head and they've got loss of gray-white junction and cerebral edema and you've got an exam consistent with brain death, I think you've got some structural findings. I think that's fine to continue brain death, or a discussion with family at that point. But if you don't have those things, if you've got normal neuro imaging, if it's only the exam, the EEG only helps if it shows activity, but if it's kind of flat, that still could just be drug effect onboard. So if you're thinking in that person, I would give them a little more time or start thinking send out labs, or do some sort of repeat imaging or MRI, for example. 

So in summary, just a review, what we've been talking about today. So the toxicology patient population, either the ones that are found down or the ones that are agitated are at risk for rhabdo. Aspiration risk is high, especially for sedating medicine. So think about early intubation, avoiding BiPAP, and avoiding narcan once they are intubated. 

Opioid overdoses. Think about pulmonary edema. And again, this can be delayed a number of hours. And then dysrhythmias being common. Again, QRS prolongation, we're going to treat with bicarb. QTc prolongation, treat with magnesium. And then just use caution in declaring brain death in tox patients if they don't have structural abnormality on their imaging. 

This is the number for the poison center. We're available 24/7 for consults. You guys give us some of the most interesting consults, and we love putting our heads together and trying to solve unexplained acidosis. Or maybe this is a serotonin syndrome. So thanks for the interesting consults, and we're available for you. You should call the poison center. 

Any questions at all? Yes. 

I was wondering, can you-- with the increased availability of narcan and just having it over the counter, have you seen any differences [INAUDIBLE]? 

You know, we're trying to figure out how to study that question. And we've had a few people that have come in that have gotten community access narcan, and or family member-- they were prescribed narcan because they were a higher risk patient. So family member give them narcan. It's really hard to study whether that made a difference. We're still seeing a lot of opioid overdoses. Yes. 

Does a narcan drip [INAUDIBLE]? It almost seems like [INAUDIBLE]. 

Yeah. So there's different practice styles. I have done a narcan drip. It depends. If they're a pure opioid and you give them, say they took a long acting opioid, methadone or something, you give them narcan, they wake up, then they re-sedate an hour or two later, you give them narcan, they wake up, they re-sedate. That's someone who there may be a role for a narcan drip. You may be able to save the intubation. So I think there is a role. And some of it's practice style, as well. So I think there probably is some role for it still. 

Other questions? Yes. 

[INAUDIBLE]. Are there new diagnostics coming out? 

Yeah. The question was for the synthetic drugs that aren't picked up on routine drug screens, are there diagnostics? 

Yes, we work-- so we have a kind of PhD toxicologist that works in the lab. She's looking to bring in-house some more things for some of the synthetic cannabinoids and synthetic marijuanas, and possibly some of the synthetic amphetamines, as well. We also work with this lab, NMS Lab, that does a lot of testing that was that panel that we sent off on the bath salts case, that they do have some extensive testing. Part of the problem with the new synthetics is you change one site, you throw in a another carbon or another OH group or something, and it takes months to develop the actual test for that standard, if you will, for the GC mass spec. 

And so that was part of the problem when the bath salts came out. As soon as they would catch one, there were no laws on the books at the time, so they would just change one site, throw another carbon on, throw another iodide on, throw whatever on some different site. There is now some laws saying, well, chemically similar drugs, like the whole class of chemically similar drugs are illegal. But people are smart. These chemists in the drug field are very smart. But yes, there are ways to test for most things. 

So please, I also ask you, if there's cases, certainly we're available to consult. But if you have cases that you manage that you don't necessarily have questions, just so we can kind of trend what the trends are doing in our area. If you have a straightforward heroin or benzo or something overdose that you just kind of watch overnight and discharge, just call the poison center to let us know about that, so we can kind of see what the trends are in the area. 

Thank you very much. 

Thank you. 

[APPLAUSE]