Alcohol Withdrawal Syndrome

If you, like me, have been reflecting on what a decadent Christmas period you've had, too much chocolate, far too much cake, and much too much alcohol, you might have tried dry January last month. Now, hopefully this isn't leading to alcohol withdrawal symptoms for any of you, but we thought, as this time of year is one where many people consider their relationship with alcohol, this would be a good opportunity to reflect and learn about a population group that many CPD forums don't cover. Alcohol dependency is, well, so it was to me when I was a student, a surprisingly common epidemic within the population. It's believed that around 11% of the UK population have what's termed high risk-drinking behaviour, with around 1% believed to be alcohol dependent, and this figure being highest among lower income individuals. So alcohol withdrawal syndrome is definitely a condition that you would have seen, and one where mortality can be as high as 5.5% in the most severe conditions, often presenting in a vulnerable population group with low trust and low engagement with health services. That's why this month we're taking a look at alcohol withdrawal syndrome. So if you're not sure when a patient requires their withdrawal symptoms, medicating, if you could use a refresher on your GABA glutamate neuroscience, or you're not sure whether there's any treatment that we can offer pre-hospitalia, be sure to keep listening and see what we cover. So, hello and welcome to General Broadcast, my name is Josh, and I'm George. And this month we're discussing alcohol withdrawal syndrome, something which is often encountered, but probably not covered in great depth in our formal education. But before we get into it, we need to thank Giky Mereksu support this podcast, helping to make it free and open access. 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Okay, so alcohol withdrawal, and particularly fits from alcohol withdrawal, is something that's been known about for some time. It used to be called the Rum Fits, and there's a phenomena that's been noted in medicine and literature throughout the ages, fitting as a direct result of alcohol withdrawal however, was debated until an experiment in the 1960s that definitively proved that link. So this study that could be described somewhat ethically questionable, looked at taking 10 former morphine addicts who'd been incarcerated in a detox center. So these were people that had spent months kicking their opiate addiction, and they were then given large quantities of alcohol over about three months and moved onto alcohol addiction, which isn't much better. And after three months of heavy alcohol consumption, they were then put into a abrupt withdrawal, they were completely cut off, and their symptoms were measured. So all of the participants in this study developed symptoms of alcohol withdrawal syndrome that we're going to go on to talk about, and then several had large tonic, clonic fits. And whilst clearly this study was very unethical, it couldn't be repeated today, it's one that has helped to definitively prove that link between alcohol consumption and withdrawal syndrome, as well as demonstrate a correlation between the intensity of symptoms and the amount of alcohol that was consumed. So refreshing to see a study from the 60s that used morphine addicts rather than suggestible, vulnerable medical students. Well, we still use medical students today, don't we? So clearly that is the ethically correct choice. Anything to pay the rent? And to be honest, you would struggle to find, you'd have a lot of confounders, wouldn't you? I would struggle to find a medical student that already didn't have a high alcohol consumption. Yes, yeah, the trick is a medical student is to never actually withdraw from alcohol. Is that what's got you through? So what does the picture look like today? Well, as I discussed in the intro, around 11% of the UK population are believed to have what's termed a high-risk alcohol intake, and around 1% of the population are dependent on alcohol. Some data suggests that as many as half of people who use alcohol heavily may suffer withdrawal symptoms in the early stages of abstinence, which is probably why as much as 16% of all hospital admissions involve or are complicated by an element of alcohol withdrawal. So clearly this is a condition that has the potential to affect a large degree of patients that we encounter. So let's move on to consider what's happening in patients that withdraw from alcohol. As with any pathophysiology, if you're going to understand what happens when something's gone wrong, you first need to understand how it works normally. So as a quick reminder, why don't we take a moment to recap on the function of the central nervous system? The central nervous system, which is the nerves within the brain and the spinal cord, run on a balance. As you will remember, neurons communicate with each other using chemicals called neurotransmitters. In simplistic terms, these neurotransmitters either speed the communication up or slow it down. They do this by affecting the amount of ions that flow into the post-anaptic neuron, determining whether it will fire or not. The main slowing or inhibitory neurotransmitter is gabar amino butyric acid, which is known to as friends as gabar. You can think of gabar as the brain's brake pedal. Its inhibitory effects reduce neuronal firing and keep the signaling controlled. In contrast to this, the main speeding up or excitatory neurotransmitter is glutamate. Glutamate is the accelerator. It increases neuronal firing and promotes central nervous system activity. These are not the only two neurotransmitters involved in inhibition and excitation within the central nervous system. But they are the two most pertinent to talk about today whilst we're discussing alcohol withdrawal. In a healthy brain, there's a careful balance between these inhibitory and excitatory systems. So what happens when we drink alcohol? Alcohol is a central nervous system depressant. It does this in two main ways. Firstly, alcohol increases the effect of the inhibitory neurotransmitter gabar. It does this by binding to gabar receptors on post-anaptic neurons, reducing their ability to fire. To compound these effects, the other major effect of alcohol is it blocks the effects of glutamate, the excitatory neurotransmitter, also reducing the ability of the post-anaptic neuron to fire. So in combination, both of these effects lead to the depressant effects of alcohol. Initially, these effects are calming, before leading to impaired judgement, slurred speech, slowed reaction times, impaired coordination, and eventually amnesia, drowsiness and unconsciousness. Sounds like a good time, right? Well apart from being expensive, the occasional exposure to this neurotoxin causes minimal long-term effects. However, repeated exposure to alcohol over a prolonged period of time will cause the brain to take action. To counteract the depressant effects, it undergoes changes at the neuronal level, to ensure a normal balance of inhibition and excitation is restored. Over time, the brain starts to down-regulate its gabar receptors. This reduces the ability of alcohol to exert its inhibitory effect. In simple terms, think of it as the removal of some of the brake pads. At the same time, the brain begins to up-regulate its glutamate receptors. In addition to this, it will also up-regulate the number of calcium channels in the post-anaptic neuron, which will increase the likelihood of neuronal firing. This makes post-anaptic neurons more electrically excitable. You can think of this. as the accelerator becoming more powerful, so to keep things simple, we now have a brain with weak brakes and a very strong accelerator. As long as the central nervous system depressant like alcohol is still present, these changes are balanced out. The alcohol is still pushing on the brakes. The problem starts when that depressant is suddenly removed. The result is widespread, uncontrolled neuronal firing. Clinically, this will show up with all the classic features of alcohol withdrawal. Tremor, anxiety, agitation, sweating, tachycardia, hypertension, and in more severe cases, this excessive excitation can trigger seizures and delirium tremens. So really, in alcohol withdrawal, we shouldn't think of the clinical problem being the absence of alcohol, but rather unopposed excitation of the central nervous system. George, one of the things that you'll read about when you're looking at the pathophysiology of alcohol withdrawal is something called the kindling effect. And so can you just speak to exactly what that is and how that can impact our perception of histories and risk-ratifying patients because it's quite an interesting phenomena, isn't it? Yeah, absolutely. So the kindling effect was described first, sort of towards the end of the late 1970s, and it came from clinical manifestations that were seen in epilepsy and other seizure-like disorders. So with repeated cycles of chronic alcohol use and abstinence, leading to episodes of withdrawal, the brain is repeatedly exposed to periods of excessive excitation. Such withdrawal episode involves increasing glutamate activity and increased calcium impacts into the neurons, so this further stresses and sensitises those neural circuits. Over time, this causes lasting changes in the brain. Neurons become more excitable and easier to trigger, even when the amount of alcohol consumed is relatively small. So how does that translate? Well the practical result is that each withdrawal episode will tend to present earlier, progress more quickly and with clinical effects that are of increasing significance. These patients are therefore at higher risk of seizures and delirium trebens, even if their current drinking doesn't seem extreme. Some people describe the kindling effect, like repeatedly striking a match, and each with withdrawal primes the brain to ignite more easily the next time. I don't really understand that analogy because you can only light a match once. I really prefer to think of it as like an ankle that's been sprained multiple times. Each injury weakens that ankle and eventually it takes less and less force to cause serious damage. So let's summarize the pathophysiology of alcohol with withdrawal syndrome. Chronic alcohol use causes the brain to take regulatory steps to counteract the effects of prolonged exposure to the central nervous system depressant. It weakens its response to inhibition and it increases its response to excitation. When the depressant effect of alcohol is taken away, the brain is left in a dangerous state of overexitation. Additionally, repeated episodes of withdrawal from alcohol lower the threshold for serious clinical manifestations of symptoms known as the kindling effect. Let's move on to assessment then. When we're considering alcohol withdrawal syndrome or AWS, it's really important we see this as a spectrum because patients require really holistic assessment to determine where they fall on that spectrum. And something that was new to me the first time that I looked into this was a lot of my focus was around fitting because I don't know about you, George, in your ED experience, but the vast, vast majority of how these patients present to me or so presented to me when I was working on the road is following an alcohol withdrawal fit. Is that generally the kind of cases that you've seen? Yeah, absolutely. If someone's presenting because of alcohol withdrawal, it's generally because they've had a seizure. Although that said, that might just be because we don't necessarily pick up so well on the people that are a bit tacky and a bit sweaty and a little bit agitated. And they themselves probably, as I said at the start, often this patient group is one that isn't particularly keen to get involved with the health system either because of mistrust or previous experiences or whatever. So it may be that they're not picking up on those symptoms either. Yeah, absolutely. The thing that I particularly looked into was around fitting because that's quite a dramatic presentation and it seems really sinister and serious. And obviously it is, but what's important to bear in mind when we're assessing these patients is that fitting in isolation is not indicative of serious alcohol withdrawal syndrome or the fact that this patient's in the DTs. So whilst we should monitor and assess these patients because they can progress to develop further symptoms, it's important that we bear in mind for our own risk stratification that a single fit in isolation can present without other symptoms of withdrawal. Okay, so how do we assess these patients? Well, as always, you're going to get the standard line from us, which is we should begin with an A to E assessment and address life-threatening symptoms first. That's pretty obvious. But in my experience, these patients typically present with a seizure. That seizure is generally self-limiting. And often by the time that we arrive, these patients are conscious and breathing, talkative and amenable to a standard sort of more lengthy workup. So we've got two jobs when we're assessing these patients. One, it's to assess the severity of AWS and risk stratify them. And then two, is to not anchor on the fact that they're an alcoholic and that is the principal issue because it's really, really easy to assume that everything in this patient group is alcohol-related. And what we need to bear in mind is that they're a vulnerable patient group and they are at higher risk of lots and lots of other comorbidities and issues. You know, by virtue of the fact that they have a high alcohol intake, they are at high risk for infection. They're at higher risk for bleeding because they are often coagulopathic to an extent. They're at higher risk for electrolyte disturbance. So we need to ensure that we don't forget to consider all of these differentials. So I'm going to come on to talk about later and only anchor to AWS. Does that fit with your sort of perception of how you work these patients up, George? Yeah, absolutely. I think probably most clinicians know of some sort of horror story where something's been blamed on alcohol when really there was something else going on, whether it was drowsiness from intoxication that was actually a subjoral or a high lactate on a blood gas that was put down to somebody being drunk and actually it was some sort of ischemia. We really have to be careful that we don't blame the alcohol. Yeah, 100%. And I think we cannot stress this enough because it takes a real cognitive force, I think, to undo that bias that we get and to undo or reduce the risk of anchoring. Now I remember once going to a patient who was found in the street who had not too much of a concerning head injury, it didn't look visually impressive. The patient was a known alcohol, heavy alcohol user to the crew and it was like a Saturday night that they were found. I don't know, 100 meters down the road from the local pub and all that kind of stuff. It's a smell of alcohol, sounded intoxicated, lowering speech and all that kind of stuff. And this patient looked like they were intoxicated with a head injury and we were trying to decide which destination to go to but their GCS was reduced. And we had a really, really long discussion about, "Oh, do we really want to fly this patient to a major trauma center?" Blah, blah, blah, blah, blah. And in the end, we removed, tried to remove obias, especially we could remove the presence of alcohol and then the known judgments that you'd make about this person because of their life choices and fluid into a major trauma center. And I remember being so surprised when on their scan they had a huge subdueral hematoma and went up to neurosurgery because there was not really physical signs that would have suggested that that was going on. And that was a real teachable moment for me and actually one that I was like, "Oh, God, I'm glad that I'm glad that we ended our bias on that one." But my reflection from that is it requires real cognitive force to push back against those biases and we really need to keep that in our mind. Okay, so let's move on to our history taking because, as I said, the majority of these patients are amenable to a more lengthy workup by the time that we get to them. And in combination with our standard history taking questions, some focus questions that we'd probably want to ask are about their drinking behavior. So we want to know what their pattern to drinking is. Do they drink daily? Do they drink large amounts of alcohol daily? Or do they drink more of a sort of a binge fashion? And how long have they drank heavily for? Because this does influence to an extent our risk stratification of them. like there's reasonable evidence. suggests abuse daily for over three months would put somebody at risk of withdrawal, but equally a large binge for over a week, so they may not be regular drinkers, they may not be what we class as an alcohol-dependent patient or a high-risk alcohol user, but large binges for over a week also put somebody at risk of withdrawal. So we need to ask about that patterning. We need to ask about the timing of their last drink. Again, that's really important and useful when it comes to examining our differential diagnoses because symptoms can start to present as early as a few hours from the patient's last drink with more severe symptoms, so things like fits and the more severe elements of DTs beginning to peak around the eight to 12 hour mark after the patient's last drink. So that's really useful for symptom examination. And is there anything else in your history, take George any focused areas that you might think you pertinent to look for? Yeah, I'm always interested in the reason for the cessation of alcohol intake. Was this intentional? Have they decided that actually I don't want to drink alcohol anymore? This is having a big impact on my life. Or is this more a different reason, for example, run out of money, not able to buy the alcohol, perhaps not feeling very well, had diarrhea and vomiting, which has impacted on their ability to absorb it. Is this social reasons? Have they not no longer got access to alcohol? So I think that's really important to address because sometimes the withdrawal from alcohol is a symptom of a different clinical problem. That's all worth worth investigating. Yeah, that's a really good point and going back to your point about kindling phenomena as well. If patients haven't, if this is an accidental cessation from alcohol drinking, you know, that they're not trying to do it, there's no psychological gumption, so to speak, to continue with the detox program. Then a medical detox may not be in their best interests because they're not going to apply with the treatment if they're going to, for one, to the better world fall back off the wagon, then their withdrawal next time is going to be that much worse. Yeah, absolutely. And we'll talk a bit more in management about how we decide when that's, when someone's right for medical detox from alcohol. Okay. And then finally, we should, on that point, examine their history of withdrawal when it comes to alcohol cessation. So has this happened before? How have their symptoms been? Have they had severe symptoms? Have they previously had fits? Have they previously had the DTs? Because as George has already explained, past history of severe symptoms can predict future severe withdrawal. So this is particularly useful to know and to document when it comes to examining this patient holistically. ECGs aren't my strong point. If I had a pound for every time I heard this, maybe it's your mentor, your colleague, or even you. Interpreting and understanding ECGs is a core part of paramedic practice. And they can be complex to get your head around, particularly when you're just starting out. Well, geeky medics can help you out with their ECG case collection. Learn to interpret ECGs using a systematic approach with their collection of over 85 clinical cases written by experienced clinicians. Their online and easy-to-access collection means you can learn to diagnose arrhythmias, conduction abnormalities, and electrolyte disorders with clear and detailed explanations to help you master the ECG. Thanks again to geeky medics for supporting this podcast. So as we've talked about, alcohol withdrawal syndrome is a spectrum of disease. And patients can fall anywhere on that spectrum, and they can move up and down it, dependent on how they're withdrawal progresses, and their time from previous drinks. So what we're doing is part of our history is screening for these symptoms, and then trying to restratify them of where they sit along that spectrum. The next thing that we're going to do is part of our history taken and physical assessment of these patients, is to screen them for these symptoms of withdrawal syndrome, and come to a conclusion about where they sit on this spectrum of withdrawal. Have they got more minor symptoms and their less of a concern? Or do they have really significant high risk, highly concerning, highly autonomic signs of withdrawal syndrome, and they are in the territory or firmly in the location of delirium trimmins, and we can talk about what that difference is. And perhaps one of the easiest ways to frame this discussion, George, is by talking about the CWR score. So do you just want to touch on what that is, and when it's used, and then I'll break it down specifically for those that don't know what it is? Yeah, so the CWR score is an objective way of measuring the signs and symptoms of alcohol withdrawal to give a value on whether that how severe the withdrawal from alcohol seems for that patient. Depends on the setting that you're working in, but it has been designed and validated to be used in a number of settings. So it can be used in primary care, we do use it in the emergency department and in hospital. So it does have use pre-hospitalia as well. And so we do use the CWR score, scoring system for hospital in patients. We certainly use it in the emergency department, and when we're admitting people to hospital. I would say it's probably more useful for assessing whether you need to treat someone's symptoms of withdrawal at that moment in time, and it's not really useful for guiding sustained reducing regime of detox. So most hospitals will have a sort of inpatient guideline regime on alcohol withdrawal based on the number of units that they drink every day. And so the CWR score usually is used to help the nurses with whether that patient might need some PRN, Claude-Azzy-Poxide on top. Does that make sense? So we use that to recognize whether the reducing regime that we're using is not covering their symptoms. Okay, fine. So you're using it as a monitoring tool rather than your assessment framework, kind of? In my experience, yes. Yeah. Okay. Yeah. And I think that, like you say, is very much how it's designed to be used. I typically do my history take in my assessment of these patients, and then will work out a CWR score. Almost as a little addendum at the end of that assessment, I think it's so it's fairly comprehensive and let's go through it. And I think one of my not issues with it, because who am I to, you know, talk down and internationally recognise the power data tool. But one of my, I guess, concerns with it is that it is fairly detailed in each segment. And I suppose the, the, the, the, inter-rater reliability in our setting could potentially be poor if we're not doing it properly. So the inter-rater reliability of it when it's used in alcohol withdrawal, that sort of detox settings is pretty good. But that's because it's, it, those studies have been done on people that are looking and talking about detox all the time and quite often minute. They've had a lot of training on it. My experience with this score is that the score that I've come up with and then the score that the triage nurse may, may do when we work through it together based on my history can, can fluctuate slightly. So what do I mean by that? Well, the CWR score looks at 10 different types of signs and symptoms that are associated with, with withdrawal. And many of these are reported by the patient. And I think about three of them are physical signs that we can assess for. And then it grades each of these on the severity. And the combination of this score results in a, a final total. And the, the suggestion is patients who have a score of around or, or under eight, typically would, it would be suggested don't require medication for, for withdrawal. Is it, is that your understanding of the bottom figure, George? Yeah, absolutely. So yeah, exactly. So the first section is nausea and vomiting. And what you'll, what you'll recognize in each of these sections is it's, it's examining for these autonomic signs that we associate with the hypersitilation of those glutamate receptors. So as George was saying in the start, these patients normally have their foot on the brake with their resting level of alcohol. And they've upregulated their accelerator. We've now removed that brake. So what this score is doing and what our assessment is doing is looking. for those foot-on-the-accelerated signs, those autonomic sympathetic signs. So, nausea and vomiting is the first thing. We ask the patient, "Do you feel sick to your stomach? Have you vomited?" And then it grades out in a school between zero and seven, based on no nausea and vomiting, all the way up to constant nausea, frequent diet, dry heaves, lots of vomiting. And we then move on to examining the tremor. So tremor is something that most people will be familiar with assessing for these patients. Again, it's scored between zero and seven. No tremor at all, not visible tremor, but can be felt at the fingertips, all the way through to a moderate tremor with arms extended, and severe tremor, even at rest with the arms. We examine the patient for paroxysmal sweats, so are they, you know, what do they feel like? Are they dry, barely perceptible, sweating just in their palms, or are they completely diaphetic? We then ask the patient about anxiety, so do they feel nervous? Do they have a background level of anxiety? And quite often, again, this will be the principal component, or certainly again, in my experience. This is one of the predominant symptoms, is this background feeling of anxiety and nervousness. And part of that might be the fact that they've just had a fit, and this is very disconcerting. But a lot of this is the autonomic sympathetic drive that's ongoing. They have their fight or flight reflex activated, so it's examining for this. So asking the patient, do you feel nervous and grading that? Looking for objective signs of agitation. And again, this is a useful objective sign, one that we can grade patients on. So do they have a little bit of fidgeting, more activity than normal? Are they restless, or are they completely delirious? Are they pacing back and forth? Are they uncooperative with assessment? So we then move on to assessing these patients for tactile disturbances and auditory disturbances. So a really classic symptom is something called formication, which is the feeling of stuff crawling on your skin. So bugs crawling up your backs and on your arms can be really classic. But this can just be a pirator. So itching, you might have mild parasesia pins and needles or a burning numbness in your limbs. And likewise with auditory hallucinations, the classic thing is like a pink elephant, isn't it? And is pink elephants knit for DTs? Yeah. Yeah. And that's crazy, isn't it? That there's this common visual hallucination of pink elephants. And I've seen like pink snakes and stuff in some of the right ups. I wonder why it's pink. I'm sure. I wonder if there's a reasoning for that. Yeah, I've found that with. There's something about snakes, spiders and elephants. They seem to be the three things that are classically reported almost every time. Yeah. And I wonder if that's. It comes back to that innate fight or flight response. You know, the. They think a racconophobia comes down to just an innate fear, an innate warning sign to just stay away from that thing because it kills people. So I wonder if it's that lizard brain just part acting up. I wonder if that's where that comes from. But yeah, so we assess for auditory disturbances, visual disturbances, and again, grade all of that. And then finally, the last two, we assess patients for a presence of a headache, whether it's a slight fullness in their head or extreme severe, and whether or not there's any disorientation or clouding of their mental state. And this might just be an inability to do a simple thinking, simple tasks, small additions and simple calculations, or it might be complete disorientation to time, person and place. And by grading each segment on that score, we come up with a bottom figure, and the higher the figure, the more severe this patient's alcohol draws in drone. The more aggressive that we require our management to be. Now, even just explaining all of that, George, has been fairly detailed and fairly in depth. And this sort of comes back to one of my points about the CWAR score is that it's really in depth, but it's also really ambiguous about what some of the scores mean. Like loads of them, you've got not present, or very, very mild, only perceptible for whatever the thing is. And then at the top end, you've got really definable, continuous hallucinations, completely delirious. But a lot of the things in between just say, more severe symptoms, more severe symptoms. And I guess when 50% almost of an individual scoring component is ambiguous stuff like more severe symptoms, to me, it just means that there's a risk there that interrated reliability might be a bit poor. And you could potentially just by individual clinician perception of what most severe symptoms mean, radically change somebody's score. But that doesn't seem to be what the evidence shows in hospital. There is some suggestion that in the emergency setting, the interrated reliability is worse, and I guess that would make sense because of time pressures and lack of specialisation. But yeah, is that something that you find when you've done the scores in your setting? And speaking entirely anecdotally from my own experience here, I think in the emergency department, its use is varied. I think in admission areas, like the acute medical unit, and in the gastroenterology ward, I think this is used much better. But outside of those settings, I think it's used extremely variably. And I actually think it leans towards under-treating people. Oh, that's interesting. I think more often I'll review a CY chart that suggests someone isn't withdrawing from alcohol, but then when I go and see them, I might find them in a state where I would lean more towards giving them a higher score than the person who's assistant before me. Yeah, exactly. And again, it comes back to that point of bias, doesn't it, when you have such ambiguous scoring points, the risk of under-playing or over-playing based on your own perspective of the situation. Exactly. So I spent a minute looking to see whether there was anything else, whether there was anything better potentially. One thing that was suggested was the RACS sedation scale, which is something that you definitely will be familiar with George. It's something that we use at work relatively often to assess and measure patient's response to anaesthetics and chemical station that we're doing. So that might be useful. It's very simple. It's very objective, and it's quite easy to grade. And then another thing that one of the literature suggested was something called the Bores scale, brief alcohol withdrawal scale. And again, it's really simple and it's far more objective. Looking at many of the same features that we've talked about, so it looks at tremor, diaphoresis, the RACS agitation scale, confusion and hallucinations. And again, within itself makes some comparisons and draws across to the CYR score. So that to me looks really simple and easy to use. And so it might be something that aids our clinical decision making or certain needs, other assessments. The main issue with that is if you go and tell people that you've got a Bores score of eight, people are going to go, what the hell is that? Because I'd never heard of the Bores score until just now. I don't know if you've ever seen the brief alcohol withdrawal scale, George. No, I've never heard of it, to leave just mentioned it there. And even the RAS scoring system, even in people that were sedating every day, I don't even think we're very good at using that on intensive care every day. Oh, really? Okay. Well, there you go. And the other problem is that the highest score you can get on the Bores score is eight, which would be severe DTs, whereas on the CYR score, eight is the cutoff for whether or not you do treatment at all. So there's a risk there of miscommunication. So I don't know that that's particularly necessarily helpful or gives anybody any any clear answers, because another one of the benefits of the CYR score is a bit like the news score. It's a useful tool, isn't it, between professionals at Hanover for saying this person is big sick, medium sick, severe sick, and you know CYR followed by big numbers, immediately gets people's attention. So maybe in the emergency and pre hospital setting, that is where the benefit comes from. But we'll link to all of those scores in the article. One of the things that consistently comes out when they're talking about interrater reliability for CYR is that clinicians should have some training on that. So we'll link to some videos and some useful resources there, because a lot of that comes down to the pre-mer classification and what we'd class as something that's severe versus something that is less so. Okay, so I think we've talked there a little bit about assessment and the things that we're going to look for. One thing that we did talk about George, wasn't it, is a differential diagnosis and how we don't want to get anchored to alcohol being the predominant issue here. Yeah. Do you maybe just, I'll talk about a few more differentials in a second, but delirium is something that can be quite obvious and easily picked up in these patients. Do you want to maybe talk a little bit about some of the other causes of delirium that we might want to think about and how patients with a high alcohol intake can be at risk of these? Yeah, absolutely. No problem. So, delirium, just to recap, that's an acute, confusional state that can be fluctuant, can be hyperactive or hyperactive. And I think the best way for remembering the causes of delirium is pinch me. I'm sure you've heard of pinch me as well, Josh. So just to go through those pain, infection, nutrition, constipation, hydration, medications, and medications, electrolyte disturbance and environment, how a number of those factors can affect someone who is a chronic user of alcohol, particularly things like electrolyte disturbance, hydration, constipation and nutrition. Definitely things that we need to think about. Other things that might be on our radar could be benzo, diasopene with gruel, so again, it's exactly the same mechanism as alcohol that you've described, but patients that are heavy benzoan users, I know Xanax is becoming a popular or is a popular street drug, particularly in the UK now. So it could be benzo, diasopene with gruel compounding things, so we need to examine for that. Reeling off a fair few now, so thyroid toxicosis, often these patients, as we've said, have poor medical follow-up, so they may have undiagnosed thyroid diseases and heavy alcohol use can particularly mask early symptoms of thyroid issues, so they may not present until we've become particularly severe. We shouldn't forget about hypoglycemia, so these patients may have sugar control issues, even if they aren't obviously a diabetic or a known diabetic. They might have concomonate diabetes, so they could be presenting in diabetic ketoacidosis, there could be other stimulant abuse, so this could be something like a serotonin syndrome, so we want to see whether or not they might have taken concomonate stimulant use. Often, the treatment is quite similar, as we're going to come on to talk about, so it's all about getting something on that brake pedal, but it's important to know, you know, what we're treating and know the difference there. The patient could be presenting in status epilepticus, so is what we're seeing just a patient being post-ictal? How long has it been since the last fit? They could be presenting with a CNS infection, again, alcoholics, a bit like frequent drug users, have big impacts on their immune system, so they may not mount an immune response in typically the way that we might expect them to, so could this be a CNS infection screen for that as we would ordinarily signs of photophobia, as they neutralize your giddity, as they're on rashes? Could this be an intranial hemorrhage? So as we've talked about, these patients often have deranged guagulopathy, so could this be an intranial hemorrhage? Could it be a CVE? Scan them for head injuries? We want to be reporting pertinent negatives there. This is their first fit. Typically, these patients will get a scan of their head in the ED department just because of the risk of bleeding there. Could it be a mental health crisis? So could this just be another cause of psychosis connected to mental health problems? And then one of the other points that I just wanted to touch on, because particularly in this group, it's something that could be a reasonably large risk, and that's herpatic encephalopathy. So just a few points on that then. This is what is it? It's a reversible neuropsychiatrics syndrome, which is linked to liver failure. So we know these patients are going to have liver issues. If they've got liver cirrhosis, then that results in high hepatic portal vein pressure. That results in backflow and results in our blood, the blood from our gut bypassing the liver and draining into the systemic circulation. So they don't get that sort of first pass metabolism that we would ordinarily expect in normal physiology. This results in a build up of toxins that are normally neutralised by the liver. Now, there's a lot of them. The main one that we need to be aware of is ammonia, which is normally converted by the liver into urea and excreted by the kidneys, as most people will know. Acrosis, the blood brain barrier really well. So this results in swelling, cerebral edema and altered urine function. So that could be a result of some of the deranged neurology and delirium that we're seeing. It can be quite tricky to determine the difference between these. If the patients quite sick, then ultimately either way, they're going into hospital and it doesn't matter massively from our perspective, whether we differentiate the two. But when it comes to thinking about treating these patients, it is a distinction that we need to make. So if you're a practitioner that can offer sedation and can offer benzoes in the way that George is going to talk about in a second, it's important that we make this distinction. Because if we give benzoes and sedation to a patient with hepatic endocophylopathy, that can make the situation worse, they will become more the lethargic, they may need airway, management issues. And I guess this is probably something that you could maybe speak to George why we don't want to give these patient's benzoes. Yeah. So I would think of these patients into very different channels. The patients who were trying from alcohol tend to have that over excitatory state. The patients with hepatic endocophylopathy tend to go the other way and tend to be very drowsy. And just like you say, if you were to give those patients benzoes, they're going to become even more unconscious and we are going to then need to control their airway and so on. Yeah, exactly. And that is one of our key determinants for what we're looking for here. So if your patient is really stimulated, they are fight or flight. They've got lots of these autonomic signs, tachycardia, sweating, hypertension and their accelerator is being pressed. And we can probably swing more towards the alcohol withdrawal syndrome side of this balancing act. Whereas if your patient is very lethargic, they've got altered neurology, but it's not always fitting this accelerator pedal being pressed. They've got other symptoms of altered neuron function that doesn't fit this fight or flight to process. And particularly if they're presenting with an asteriscus, which can be mistaken for a tremor, that can be another useful determinant. So an asteriscus is a voluntary lapse in muscle tone from the impaired cortical motor control because of the the edema and the high levels of ammonia in the neurons. So that is very different to a tremor, which presents in AWS asteriscus is very much a hand-flapping motion. And again, we'll link some videos of the difference there on the article. Any more comments from you, George, on that point before we do our management? Great. No, great point. The tremor should not be mistaken for an asteriscus and vice versa. I think the only other really common overlap between hypatocaine, kevlobsy and acute alcohol withdrawal would be that altered sensorium. So we talked about altered sensorium when we were talking about seawater, both these patients can have disordered cognitive thinking thought processes. They might be speaking abnormally, behaving abnormally. That can be hard to differentiate, but the rest is is more down to their physiological excitation as you've touched on. OK, then. So shall we talk about management? So we've already really alluded to the management, the main pharmacological management of this multiple times throughout this talk. Haven't we Josh? The key principle for the management of alcohol withdrawal relates to the pathophysiology that we've discussed earlier. Alcohol withdrawal is this state of dangerous over excitation. So we just need to dampen that down. That helps prevent the complications and we need to support the patient through that whilst their brain rebalances. So in the UK, multiple guidelines, including nice, the first treatment for alcohol withdrawal is going to be replaced that central nervous system to present with another one. And universally we achieve that with benzoes, benzodiazepines. So benzoes just like alcohol work by enhancing GABA activity, they don't just sedate patients. They act as that break that we've talked about. That's why they're effective for tremor, agitation, autonomic instability and critically for preventing the withdrawal seizures and delirium tremors. In clinical practice, we talked about an assessment. The management depends on the amount of alcohol that the patients consume per day. So in my history, taking, I'll ask a patient if they drink any alcohol at all. And if they do, I'll ask them how much they drink in a day. If I'm admitting them to hospital, I will prescribe a weaning regime of a benzo, depending on how much they drink in a the CWR scoring system used much more for PRN alongside for any symptoms of withdrawal that are breaking through that. So, just on that point, George, because I think it's probably an interesting point for those of us that don't work in hospital and don't necessarily see this side of management of these patients. Are you saying that you'll provide a prophylactic benzoyrigium for patients based on their alcohol history, regardless of whether or not they're actively in AWS, so they might have a CWR score of zero? Yeah, absolutely. So we will take a history at the point of admission to hospital and one of those, if you've done your history taking correctly, you should be able to identify not only how many units of alcohol a patient drinks in a week, but also how much they drink in a day. And it's surprising how many patients drink enough alcohol to warrant a prophylactic weaning regime of benzoes coming into hospital. And it's not just the people that you classically associate as being some working class alcoholic who spends all their money on some sort of white lightning or Lamborghini. There is a huge number of patients who've been wrong with whitelining, mate. I've got me through uni. It did, yeah. To be honest, I find that whitelining helps make you tolerable to be around. So big shout out to the whitelining who's kindly sponsored this podcast. Who sponsored our friendship. So yes, it's surprising how many patients on admission to hospital may need a prophylactic weaning regime of a benzoyrigium to prevent them developing alcohol withdrawal. But most acute trusts will have their own guideline on this. And it's usually based on how much alcohol so usually it's something around zero to 15 units a day. A PR and dose of a benzo 15 to 29 units a day will be us of the small reducing regime and over 30 units a day would be the higher regime. And I think whilst we're talking about admitting patient to hospital and talking about weaning regimes, it's probably just worth mentioning that NHS hospital facilities are not the inpatient treatment facility for alcohol withdrawal in elective situations. So if somebody is looking to reduce their alcohol intake and is looking for a medical way to do that, and NHS hospital is not the place for that, we would not admit someone's hospital for an elective withdrawal from alcohol. What I'm talking about here are patients who have needed admission to hospital either because they have already withdrawn from alcohol and are at risk if they go home or patients who are being admitted to hospital for another reason, such as having pneumonia, fractured leg or diarrhea and vomiting and we have to ensure that they withdraw from alcohol safely. So for the patients who chronically use alcohol and they're wishing to electively stop, they need to see their primary care doctor or professional to arrange for safe withdrawal from alcohol and they'll use a similar system, they'll work out how many units of alcohol that person drinks in a day and decide whether this can be done safely in the community or whether they need admission to a different inpatient facility. We've talked a little bit about benzo's then but thus far fairly generically. I think most people will be familiar with the benzo used which is Liberia or Chloridae as a Poxys. Could you just speak to a little bit about why we use that and benzo choice because I have only ever heard of Chloridae as a Poxys being used in the context of alcohol withdrawal. It seems like there's a lot of other benzos out there so why are we still using that? Yeah, great question. So historically we use diazepam for a long time for alcohol withdrawal and then Chloridae as a Poxys started being used which is known as Librium as you mentioned. We use Librium over diazepam because it has a slower onset, it lasts for longer and it's effects are more predictable. So it's a safer drug to use than diazepam really. With that said, the patients that can't tolerate Chloridae as a Poxys we can still use diazepam. Other benzos are a bit too fast acting like Chloridae as a Pym on the dazeland they're on sets too quick and they will be sedating. It's important to touch on that actually because one of the real caveats with Chloridae as a Poxys and diazepam is that neither of them can be used in patients with acute hepatic failure or liver cirrhosis which is obviously going to be a reasonable number of patients in this category. Both of those drugs are hepastically metabolised and so you get this risk of accumulation. So it's more for a long term treatment plan rather than simple start doses? Yeah, exactly. So a one off stat might just have a prolonged effect but if you admit someone to hospital who is in liver failure and withdrawing from alcohol we actually wouldn't use Chloridae as a Poxys or diazepam because they will start to accumulate that drug. So instead we actually we use Chloridae in that circumstance accepting and acknowledging the fact that it is more rapid onset and the risk of sedation is higher. Okay, so we've talked about those sort of I guess those middleing CWR school patients jaw so we've talked about prophylactic management we've talked about a reducing regime and how we would manage patients with Chloridae as a Poxys or Diolular as a Pym if they are actively symptomatic. But what about those patients that are at a higher end of this withdrawal spectrum that we've described? So patients that have had seizures actively, intimately having seizures they've got some of those high autonomic signs or even patients that are verging on or in the DTs. How does treatment differ for them? So it's probably important to mention that Chloridae's epoxide doesn't have a parental root. So you're talking about a drug that can only be given orally and takes a long time to work and although it lasts for a long time you sometimes don't have time to wait around particularly if the patient's just been having seizures or is at risk of having a seizure any moment. So in that circumstance we're going to go for something parental aren't we we're going to start talking about IV medication. Chlorasopam again going back to it is probably the one that's most predictable most you know quick acting and one that we can titrate more easily. But there is also still a role for IV diazepam and also moduslam. So in critical care we may use moduslam diffusion depending on the circumstance. Probably still more likely just to give aliquots of IV Chlorasopam here and there to manage things. I know prehospically outside of critical care environment that you work in Josh the range of available benzos is probably just diazepam isn't it? Well it used to be so diazepam was the benzo that was typically carried on UK ambulances because that is a exemption in law so that's where paramedics get their exemption to give it. Yeah. Certainly my experience we've seen more and more services move towards the moduslam option. So there may be a blended carriage of both buckle moduslam and IV diazepam. But I think a lot of services have buckle modus and IV modus now both of which when it this is relevant when we come on to talk about I guess prehospital options both of which are given under PGD not under legal exemption. So there is no flex or clinical decision for how we would use those outside of the PGD whereas a legal exemption is just for emergency situations. So there they would potentially be some flex there but we can talk about that when we talk about prehospital management. Yes so that's probably probably in those more emergent situations we're going to use the IV route realistically going to be using IV diazepam. I probably just want to touch on seizures and other pharmacological treatments as well. So if you've got a patient who's having a seizure and the underlying cause is alcohol with Jorrel there is absolutely no role for other anti epileptic drugs like phenotone because the problem here is not focal seizure disorder it's global gathered efficiency so we're still going to use the benzos. So sorry because that's an interesting point so do you not end up with hang on let me think how I'm going to phrase this question. So if your seizures are secondary to an alcohol with Jorrel syndrome. Yeah does that mean you'll not have seizures that are a factory to benzos. So will benzos always sort the seizures out and if they aren't should we be considering other mechanisms for that fit. That's a very good question. If the cause of the seizure is going to be alcohol with Jorrel then you're going to need something that something that will improve that GABA deficiency situation, which is why the benzo is a sureffective. And in those circumstances, giving something like levatoracetam or pheneto and other anti-apelaptic is unlikely to be effective. We're probably going to end up putting that person off to sleep and using something like probefol or phenobarbotone. But it's a good point. And if they're having a seizure, that's not responding to benzo. There's probably no harm in giving them anti-apelaptic medication. - Okay. - I don't know. It's a good question. If you're not going to harm them by giving them some Keppro. - Yeah, okay. Because I'm trying to think of the mechanism of Keppro because I thought it still acted on GABA, but from a bit like how we don't class a probefol as a benzo because it doesn't act on GABA in the same way, but it's still act on GABA, doesn't it? - Yeah, that's right, yeah. - So if we've given them lots of benzos, I mean, like we talked about at the start, these are normally self-limiting seizures. They might be frequent, but they're normally self-limiting. So as soon as you've got a decent dose of benzos on board, I can't imagine why they would continue. - Yeah. - But it would probably, I guess in a very rare instance where they are, personally, I would just follow a normal seizure guidelines and move on to a second's mind-anti-applylaptic, but. - Yeah, you make a really good point. I think if you've given benzos and it hasn't terminated, it's probably not an alcohol with choral seizure. And so yes, you probably do need to follow the, the state's sepulapsicose policy. - Okay. Sorry, I interrupted you with all my awkward questions, George. Do you wanna come around talking about. - No, it's interesting, it's nuanced, and I'm no neurologist, so. - Well, I certainly am not either. Do you wanna come around talking about how you would manage these patients? And what you sort of end up giving then if you do need something past benzos? - So alongside the benzo-dazapines that we've talked about, there are a few other key principles for managing these patients. When we treat them in hospital, we use thiamine. So thiamine is a, is a, a b-vitamin, which is significantly impaired in those who chronically use alcohol that both the absorption and storage is impaired. And the absence of this b-vitamin can lead to vernicus and kephlopthi. So we replace that, or see, these patients are in hospital. Additionally, we touched on this earlier when we were talking about delirium, but patients who chronically use alcohol are vulnerable and have many other physiological problems, such as dehydration, electrolyte abnormalities, and they're even at risk of refeeding syndrome. So we really closely monitor their electrolytes and their hydration status, whilst they're in hospital. - Yeah, can you just talk a little bit about what refeeding syndrome is? - Yeah, of course. So refeeding syndrome is a state of star, when someone is in a state of starvation, where they've not eaten properly for a prolonged period of time, they're at risk of severe electrolyte derangement as their body suddenly absorbs food with electrolytes in. And it's extremely dangerous. It causes rapid shifts, and can cause phosphatemia, hypokalemia, and it can be fatal. So have you encountered that much drosh, or are you? - No. - No, the only, I haven't had the term. Is it similar? I guess it's not unique to alcoholics, right? It's anybody with really poor nutrition. - Yeah, exactly. It's not unique to alcoholics at all. - Okay. - If anyone who's had a period of starvation, strictly speaking, even five days of not eating, puts you at risk of refeeding syndrome. - So I've probably talked a lot there about how we manage these patients in hospital, and actually, we'll probably be useful if we touch on the pre-hospital side of things too, Josh, which I think will be better explained by you. - Cool, we take them to the hospital. - Great, thank you for that. - Because we're really overcrowded. (laughing) - Yeah, so slightly tongue in cheek. As you've already said, George, the primary goal of withdrawal management is the prevention of further withdrawal syndromes or treating them if they're present. And when it comes to deciding who does need to go to hospital, because of the nature of the way these patients present to the 9-0-9 system, I guess nearly all of them are going to end up going to hospital. So, nice guidance is that patients that present with or over close at risk of the disease should go into hospital and be admitted, patients with or at risk of seizure should go into hospital and be admitted, and patients that are frail, vulnerable, all have significant comorbidities, or they should probably be admitted for medical observation. And so, I don't think I've ever been to a patient who has alcohol withdrawal syndrome that doesn't fit one of these sections. They are nearly always an extent of symptomatic. And I don't think I've seen somebody who has a CWASCOR underrate. So, they all probably meet features for treatment, and then additionally, warming through and excluding any of the other sinister differential diagnoses without in hospital tests. So, without at least something like blood tests, like I say, a large majority of these patients may have their heads scanned because of the risk of bleeding and the nature of a lot of the lives they lead and the risk of falls. I think it's very difficult to manage these patients in any other way than taking the hospital. Inveriably, as much as Simon and I like to discuss discharging community management, invariably, ED is the right place for these patients to be seen. When it comes to management of symptoms, then, that's where some of the limitations can be. So, if patients are fitting, that's easy. We're gonna give them some benzodiazepines. If patients are in stasis epilepticus, then that's easy because we're indicated to give them some benzodiazepines. The difficulty comes when they are, either in this middling ground, where they would potentially receive some a PRN or a stat dose of a benzone ED. All these patients that are full on DT, they're delirious, they're shaking, they are not with it and they're agitated and all of that, but they are at the point sub seizure or they're not actively fitting. That's where the difficulty comes because looking at the gyrocalc guidelines, they don't really offer anything to these patients. They're talked about briefly under the ABD guidance, so the alcohol withdrawal may be a symptom of ABD. I think there's some nuance there that we could discuss, but we probably don't have a lot of time for, whether or not that really counts as ABD, probably not. So, the only other place that is talked about is in that section of the guideline. And again, paramedics that aren't critical care specialists, currently in UK guidance to my knowledge, there isn't a route to offer benzos to them. That would be the per view of an enhanced care team, critical care team to come out and give something, which can always be called upon. And if you've got a patient that is really difficult to manage, at real life threatening risk of the DTs, then we should absolutely be calling them. As I alluded to beforehand, there's certain drugs that there is absolutely no flex there. So, if you're giving medazo am under a PGD, legally there is no flex there. There's no framework for you to give medazo am. So, it would be breaking the law to do so. Diazepam, if you have that, if you have IV diazepam, and that's available to you, that's under a legal exemption. And the legal framework for giving that is in emergency conditions. So, if you're trained in sedation and comfortable with giving benzos in that way, then there may be some remit and decision making available to you to do that. So, I think I would definitely justify giving benzos, giving diazepam in a patient that's massively symptomatic in that cohort. And again, prescribers, so because I'm a prescriber, I could also give medazo am if I had that available. So, that's probably what I would look to do is give some medazo am IV or I am, but that isn't something that is available to the vast majority of paramedics on ambulances. And it would be a case of just managing ABCDs, getting this patient to hospital and staying in urgent benzos. That would be done either by a critical care team or in their research room. And I guess given we have the benefit of you working in a different health care system at the moment, is that the same in Canada or do you have different options available to you and your other? Yeah, so it is different over here and this is very much where. the Canadian EMS system is, I would say, overtaking the UK system in the treatment. In these patients, so we've got a number of options available to us. The standard would be l'Harrasapam. We carry a number of doses of l'Harrasapam for a variety of reasons. Here, the difficulty prehospitalia isn't it, is you don't have a big pharmacy attached to your ambulance, so you sometimes have to use a medicine that works versus a medicine that is the absolute best-in-gold standard. So we'd be indicated to give doses of l'Harrasapam to these patients symptomatic and we're empowered to give a dose that's appropriate to the symptomatology that the patients are presenting. So last week, I had a guy that had a middling seabass score who was quite anxious, a little bit sweaty, a little bit tremulous. So managed him quite nicely with just one milligram of l'Harrasapam and that eased his symptoms and give up to four. And then if patients are way more symptomatic and requiring more management past that, then we could manage them under our behavioral sedation guidelines. So that would start with something like maybe an IM dose of medazalam, maybe five milligrams or something like that. And then we've also got the ability to mix caliperadol into the mix there. So either a combination of the both or just a decent dose of medazalam to get on top of symptoms, depending on what's appropriate. So yeah, a lot more flex to offer treatments to these patients in this system, which is something that would be nice to see the UK catching up with because it is particularly useful and rewarding to be able to even just with a little bit of P.O. l'Harrasapam just give these patients something to just get on top of their symptoms rather than sitting for a reasonable time to hospital and a reasonable time in a queue or less any bit rubbish. That's so interesting. And nice to have that option. I don't know what your experience is, Josh, as well, but these patients who've got such down-regulated GABA receptors, they actually can chew through these drugs and really high doses with limited effect. Yeah, absolutely. I was really surprised. So the guy I was just describing before, he was a sort of a big guy, heavy alcohol intake. I was surprised that the one milligram of l'Harrasapam was sort of going to be just pissing in the wind kind of thing, but he responded really well to that. And I think potentially, I don't know if this is the reason, but he was more of a binger than a chronic everyday user. So I don't know if that has anything to do with the up and down regulation, but yeah, you're right, they can absolutely chew through benzo's and end up needing doses. Sometimes scare really high. Yeah, I can recall a chap. This is a few years ago. I can recall a chap in ED who was withdrawing from alcohol and he'd had something like 20 milligrams of IV diasapam inside half an hour with absolutely no effect. Wow. His wife, his wife went down to the local corner shop, bought him a bottle of vodka, came back, he drank it and they left. Well, there you go. And he was the charge. He was a registrar in charge. Came back in for his shift a little bit later later. Right. That sort of brings us on nicely to talk about refusals because a lot of these patients don't want to go to hospital. And in the, like we talk about these middling, middling severity patients, they might know exactly what's going on. The fit was accidental, but this has happened before and they've got the ability to acquire alcohol or they've even got alcohol, but they're refusing and they don't want to go to hospital. And obviously if they're capacitance and they're able to make those decisions, then they're entitled to do that. So we would have that discussion with them. We would obviously advise that they go to hospital if they're indicated to do so. But one of the points I just wanted to touch on is that it's actually our common nice guidance that patients that are being discharged. And in this case, we can read refusing to go to hospital are never advised to suddenly stop or reduce their their alcohol intake because this could obviously go on to precipitate severe symptoms. And then nice would go on to recommend that they be signed post to outpatient services. So I just want to touch on that because it's very rare that we've got two national guidelines that are like, or you must advocate that this patient continues drinking their alcohol as normal. That seems like an odd thing to document and an odd thing to advise to the patient, but it's really important that we do that. And from our perspective is when it comes to safety netting and recording appropriate safety netting advice, there's some more information on our safety netting podcasts, which I'll link in the notes to this. That's an important thing to put in that we've advised the patient if they're refusing to go to hospital that they continue drinking their normal out of alcohol and don't suddenly stop. Okay, so let's summarize. We've discussed the epidemiology of alcohol draws in-drome, noting that around 11% of the UK population may be a severe risk of withdrawal following alcohol cessation. We discussed the pathology of alcohol withdrawal syndrome looking at the GABA glutamate effects. The cessation of alcohol removes the foot that's normally applied to the brake pedal. That, combined with the up-regulation in glutamate, means that patients that suddenly withdraw from alcohol are at risk of autonomic excitability, from unopposed CNS excitation. Alcohol withdrawal presents on a spectrum and talked about the assessment of these patients, what symptoms we're going to look for, what differentials we need to consider, and exclude, and how the CWAR school may help our judgments of how severe the symptoms are. First line treatment is benzo diazopines, and this is to increase GABA agonism and get on top of that CNS excitation. This might take the form of oral benzos with a reducing treatment regime in hospital. Or for severe or fitting cases may require IV drugs. Finally, we talked about these patients need for admission and typically, unless presenting with very mild symptoms, will probably need conveyance to ED for further workup. However, patients that are remaining on scene or who are refusing our care need to be advised about the risks of abrupt alcohol cessation, and if at risk of withdrawal, shouldn't ever stop drinking cold turkey. But that's all for this month, thank you very much for joining us, a huge thank you to Giki Merex, who sponsor the podcast, and to you are fantastic supporters on coffee.com, and if you would like to buy us a coffee, you can find out how to do that in the show notes attached to this episode. That's all for this month, make sure to join us next time.