I would like to welcome everyone to TCA's webinar, Pharmacology and the Elderly Trauma Patient. Thank you so much for joining us today, and thank you, Dr. Jason Young, for being our presenter. All right. Thanks, Christine. Good morning, everybody, or good afternoon, depending on what time zone you're in. Thanks for having me and joining us today for our discussion on Pharmacology and the Elderly Trauma Patient. Feel free throughout. I know we'll have discussion at the end and time for questions, but throughout the discussion, feel free to stop me at any time if you guys have questions, and I'll stop periodically too when we're switching sections and gears to see if anybody has questions and to generate any discussion. All right. So, I have no disclosures. Objectives for today's discussion is trauma in the elderly patient, generic background information before we get started. Then we'll get into pharmacokinetic differences in the elderly patients compared to younger patients. We will then get into the meat of the talk with describing current medications and how they can alter the management of elderly patients with acute traumatic injuries. And then we'll discuss a quick blurb on multimodal medication regimens for the elderly patient specifically, and we see this in our rib fracture population and multimodal analgesic regimens. And then at the end, we can discuss strategies for improving outcomes in elderly trauma. So, our older patients, as defined now by greater than 65 years of age, and that's debatable, but the most consistent age that we see in the literature is defining older patients or our elderly patients greater than 65 years of age, comprise the fastest-growing segment of our population. In 2014, there were 40 million elderly Americans, comprising about 14.5% of our population in the U.S. Projections by 2030, there'll be about 72 million elderly Americans, and by 2060, nearly 100 million elderly in the United States. We're seeing that our elderly population is living longer. Part of that is due to access to higher quality of healthcare. And because, in part, that our elderly population is living longer, we're seeing increasing mobility and active lifestyles. However, that is good, but that subsequently increases the risk for injury. That's part of what we're going to be talking about today. So, according to the CDC, currently, the last set of data I've seen is 2019. I'll show you a graph in our next slide. Injury, and when I say injury, I specifically mean unintentional injury, is the seventh-leading cause of death in the elderly population. This mortality is seen with similar severity of injury in the elderly when compared to our younger trauma population, in part due to pre-existing disease states, comorbidities, which we'll get into. We'll talk about some of those, and that is obviously an exhaustive list. Also due to senescence or aging of the organ systems and the physiologic response to injury in elderly patients. And also, too, I briefly mentioned frailty here. This is actually a huge, I don't want to say emerging topic. This has been going on for a few years now. There's a large body and growing body of literature specifically devoted to frailty. Our partners and colleagues in Arizona and at Vanderbilt have done extensive work on this, and we can give a one- to two-hour talk on this specifically, but I just mentioned frailty briefly as a part of increasing mortality and morbidity in our elderly trauma population. So just briefly, as highlighted here, pre-existing medical conditions with the addition of declining functional reserve in our elderly patients will lead to poor outcomes after trauma. And ways to mitigate these poor outcomes, I mean, there's multiple ways, and we will discuss this more towards the end of our talk. One of those ways is early ICU admission and aggressive management. That's one type of an approach. From a financial standpoint, elderly trauma encompasses about 33% of the healthcare expenditures in the United States, and that's equated to about $9 billion annually. So this is not insignificant. Looking at our National Trauma Data Bank 2016 numbers, about 43% of the registry is comprised of patients that are greater than or equal to 55 years of age with a mortality of 58, almost up to 60%. So again, this is not insignificant. This, as I mentioned previously, this is a graph, or in graph form, graph data from the CDC. I'm looking at the tingly and causes of death by age group. This is actually a pretty good graph to look at. This changes with time, and specifically what we're talking about, unintentional injuries in the elderly population. So you're looking down this column and then this row. So you see unintentional injury in patients 65 years of age or older. This is a 2015 slide, but if you look at the 2019 slide, I just didn't put that on there. We are still the same at number seven. I've seen these numbers from unintentional injury up to five and down to nine, but we're currently about the seventh leading cause of death because of unintentional injury in this patient population. Continuing on with just some background information. So understanding the elderly patient anatomy and physiology is key to appropriate care, especially in the acutely injured patient. As a provider, having that awareness of the polypharmacy, which comes along with the elderly population and knowing that that may and how it directly affects treatment, some specific examples with beta blockers, anticoagulants, et cetera, and how they can blunt response to hypovolemia, how they can worsen bleeding and traumatic brain injury or other types of hemorrhage. Appropriate triage and its impact on mortality is very important. We see in the literature that oftentimes our elderly patients are under triaged when they come in as trauma activations or if they are coming into a trauma center. One of those reasons, there's multiple reasons, but specifically honing in on, let's look at our trauma criteria, our triage criteria for blood pressure and how that will triage our patients into whatever type of category that we use for our activations. We typically use the cutoff of 90 millimeters of a mercury of systolic blood pressure rate to define hypotension. This is actually significantly lower of a number when we're looking at our elderly patients as they tend to have a higher baseline blood pressure on a day-to-day basis, and we can talk about that once we get to organ-specific situations. But that number of 90 is pretty low, so what we've seen in the literature is that that number has increased for triage criteria for elderly patients up to 110 millimeters of mercury for systolic blood pressure. So anything less than that in the elderly patient or a patient greater than 65 years of age would constitute hypotension and therefore a specific type of trauma activation. So I guess the takeaway from that is 110 is the new 90 as far as systolic blood pressure goes in the elderly patients. Also with regards to injuries, so minor external injuries when we're evaluating patients may actually signify major internal injuries. One example here is because of atrophy in elderly patients' organs, specifically in the brain, you can see atrophy in the brain, but the cranium does not change that structure, therefore you can have more shear injuries, et cetera, when you have acceleration-deceleration injuries. So those minor abrasions or scrapes or whatnot above the neck can actually signify major internal injury. Outcomes are also influenced by, so as previously mentioned, pre-existing comorbidities. Up to 80% of geriatric trauma patients have at least one or more chronic disease states, and there's an increased susceptibility to stress of injury and a decreased physiologic reserve in these patients. Some, again, of many listed would be less fever response, less oxygen consumption, more hyperglycemia, more renal failure or insufficiency, you can see that by azotemia, decreased creatinine clearance, et cetera, and then attenuated immune function and impaired cytokine response. This is just a very, very short list of pre-existing conditions. The actual list is very long, but just some to mention here. So patients with cardiac issues, pacemakers, defibrillators, valves, stents, and then those medications that come along with that, with stents and valves, et cetera, obesity, diabetes, hypertension, renal and hepatic impairment or insufficiency, delayed gastric emptying, and how that plays into aspiration risks, which I know we're all aware of, that is very prevalent in our patient population, especially the elderly. More prone to hypothermia, the pre-injury skin breakdown and those issues and how that can lead to significant issues later in wound care and pressure ulcer development. Impaired cognitive function, a lot of elderly patients may have pre-injury history of stroke or dementia and how that plays into their care, especially in the ICU with delirium, which we can talk about in a bit. Decreased vision and hearing, slower reflexes and worsening balance. Decreased joint flexibility and bone density, and then that can play into increased risk of fractures. Obviously, we can talk about all the organ systems at length, but I've just chosen two briefly to touch on for this talk, so heart and renal, cardiac and renal. So from a cardiac standpoint, cardiac function declines by about 50% between ages 20 and 80 years, which is significant. What we see is a conductive system in the myocytes. They're replaced by fatty and fibrous tissue, which leads to less resilience or basically a stiffer heart, which is more prone to dysfunction and dysrhythmias. We also see valvular anatomy changes from tissue thickening. We see increased afterload. Patients have hypertension. They have atherosclerosis, and that can subsequently lead to hypertrophy of the ventricle and then subsequent heart failure. We also see decreased sensitivity to catecholamines, secondary to decreased baroreceptor reflexes, and this can be further complicated by medications such as beta blockers. We see decreased response to hypovolemia, in part by that decreased sensitivity to catecholamines and in conjunction with the addition of beta blockers that patients are taking. Also an increased risk for cardiac ischemia. As previously mentioned, we see those atherosclerotic changes in the arteries, and you can increase afterload and therefore hypertrophy and heart failure. And then a little bit more specific on that, hypovolemia. So basically the patients are unable to compensate with tachycardia that we typically see in hypovolemia or in the trauma world that equates to hemorrhage, that they can't compensate with that tachycardia that we see that accompanies that hypotension, and then therefore also an increased cardiac output because we see a fixed cardiac output. So that could be problematic. The response by the aged heart is what we see with an increased, or excuse me, an increase in systemic vascular resistance. So this leads to what I previously mentioned, that baseline elevated blood pressure. So despite the quote unquote normal blood pressure, let's say somebody comes in with a systolic of 109, right, how we maybe lulled in that false sense of security, oh, this patient's fine, but they can actually have ongoing or evidence of tissue hypoperfusion if we look a little bit more closely. So again, something to look at for when we're triaging these patients. With regards to kidney function, so we see a loss of renal mass, there's decreased GFR, which actually may be difficult to detect by routine renal function testing, and what is that? You know, what's creatinine clearance, and looking at that and based off of our commonly used formulas, Cockroft-Galt equation is what I put in here, but these patients are essentially at increased risk for acute kidney insufficiency, and what does that mean for renal dosing of drugs and drugs that are renally cleared, and we'll talk about that a little bit later. Also there's an abnormal response of the kidney to ADH and aldosterone, which leads to decreased ability to concentrate urine, and because of that inability or decreased ability to concentrate urine, we can see that output can be maintained as quote unquote adequate, even in the setting of hypovolemia, so again, that can throw us into a false sense of security. So using output, urine output specifically, as a sole marker for volume status and resuscitation, I would just say use caution with that as a surrogate for renal perfusion. There's an impaired thirst response to dehydration, especially in the underlying neurologic disease, so that can further compound hypovolemia, especially in states of hemorrhage and shock. Also to mention, with adverse effects with aggressive volume resuscitation, as many of us know, on the surgical side, surgeons, we're pretty aggressive with volume resuscitation, so with these patients, we have to be very judicious with that, especially in a setting of heart failure, as we can quickly tip these patients over into volume overload, decompensated heart failure, and then I mentioned hyperchloramic metabolic acidosis. With the more crystalloid, specifically normal saline, as I like to mention abnormal saline, you can lead to, when you're giving 5, 6, 7, 8, 9, 10 liters of this stuff, you can, we can, as providers, iatrogenically cause a hyperchloramic metabolic acidosis, so that's something to keep an eye out. And then again, as previously mentioned, carefully monitoring renally excreted drugs and dosing them appropriately is important. Before we get into pharmacokinetics, I'll just open it up, does anybody have any questions? Let's see, we've got something in the chat. I believe, so will this video be available after, I believe it will, and that it's being recorded, and then also, too, I believe a copy of this PowerPoint should be sent out to everybody. Yeah, if anybody has any questions right now. All right, we'll move on. So pharmacokinetics and aging, I'll just break it down by the differences in pharmacokinetics. So first, we talk about absorption of the drug, whether it's given intravenously or by mouth, enteral. The absorption portion of pharmacokinetics is essentially unchanged, caveats to that are an increase in gastric pH that we see, whether that's due to age itself, age-related issues, or patients that are on PPIs, H2 blockers, et cetera. So with that specifically, we can see decrease in absorption of medications with calcium, such as calcium gluconate, calcium citrate actually may be a better alternative, a better salt for that absorption in this type of patient. And also, too, early release, because of that increase in gastric pH, early release of enteric dosage forms, such as aspirin, basically, is what we're used to seeing from an enteric dosage form, or enteric coded form, excuse me, erythromycin also is another example, and what we can see is increased GI side effects. From a distribution standpoint, we see increased body fat and decreased total body water. So when I say distribution, we usually hear volume of distribution, that's what I mean by that. So increased volume of distribution for specifically highly lipophilic drugs, some examples are the benzodiazepines, diazepam, Librium, and you see an increase in the half-life, therefore these drugs stay around longer, therefore they're more likely to increase their concentration and lead to more toxicity, especially with those narrow therapeutic index drugs. We also, too, see serum albumin decreases. So from a nutrition standpoint, if patients have protein calorie malnutrition, which we see more often in our elderly patients, that becomes important from a standpoint of pharmacology and pharmacokinetics and drugs that are specifically highly protein-bound and rely on albumin for transport. So we can see increased concentrations, then, of the unbound or free drug, drugs such as phenytoin or coumadin, which are highly protein-bound, and then, therefore, that unbound drug is freely circulating and we can increase toxicity with that, we can see that. Dr. Young? Yeah. We have a couple of questions. Okay. What about MI types in elderly based on hypoxemia, how do you say that? Mm-hmm. Yeah, based on how, so yeah, good question. So what about MI types, myocardial infarction types? You know, typically, we see that demand ischemia, non-ST elevation type two demand ischemia, if you will, which eventually can lead to failure, especially in the elderly population. You know, in the younger population, we can see that type of demand tolerated for quite some time. However, in the elderly population, that can be detrimental earlier on. The other questions? Is there any difference in medication absorption with the fit elderly runners or skiers or swimmers versus inactive couch potato elderly patients? Good question. We can still see those increases in gastric pH. I haven't seen any studies. I'm sure there's some good physiologic bench studies, basic science studies, really looking at that if we needed to be. I don't have any great data on that, but I would say there still are, even with the fit elderly, some pH changes that we're going to see. And even so, if those patients are taking PPIs. What labs would most indicate nutritional status to enhance ability to absorb drugs? So, you know, our basic nutrition labs, you can look at albumin, the protein generation, the liver function tests, but those numbers can be skewed or inaccurate, if you will, in states of acute inflammation or injury or trauma. Still, it's a good market to trend, if you will. Other drugs and that albumin itself has a longer half-life. It's better to look at markers that have a shorter half-life, such as prealbumin rather than albumin. You can look at other transparent, other vitamin markers, CRP, et cetera, so you can look at all of those and trend those, basically. So if you have a patient coming in with an albumin of 1.5 or 2, I look at that as relevant and that this patient is coming in malnourished, and you can even just by assessing the patient visually, are they catechetic, are they underweight, that there's going to be protein, calorie malnutrition there. That being said, though, even in our morbidly obese patients, oftentimes we see these patients, whether elderly or not, that they also have a component of protein, calorie malnutrition. All right, so moving on. So now let's get into the metabolism of the drugs. So there's different metabolism areas of the body or organs, specifically hepatic and renal, and there's some non-hepatic and non-renal metabolic reactions, but these are the basic ones that we see. So hepatic metabolism usually break this down into either phase one or phase two reactions, if you all are familiar with. So phase one are basically the oxidation and reduction hydrolysis reactions, the cytochrome P450 system that specifically deals with oxidation metabolism in phase one. These types of reactions are decreased with age. So drugs that undergo phase one metabolism, you'll see decreases in that ability to metabolize these drugs, therefore clearance decreases. Therefore you will see these drug levels start to go up and increase in the serum concentration and therefore increase the risk for toxicity. So dose adjustments may be warranted in these patients. On the contrary, phase two reactions, these are the conjugation reactions, glucuronidation, et cetera. These are relatively unchanged with patient age. So drugs that undergo phase two reactions may not necessarily need to be dose adjusted. We talk about first pass metabolism. This is specifically talking about internal administration of drugs or that PO routes. You'll see first pass metabolism decreased by 1% per year after the age of 40. Therefore you're going to see increased serum concentrations of orally administered drugs. Therefore dose adjustments may be warranted. Other factors that can affect metabolism of drugs with any age, whether it's due to induction of metabolism or enzymes or inhibition of metabolism or enzymes specifically with the cytochrome P450 system, or which I didn't mention the P-glycoprotein, the transport system across the membranes, smoking can play an effect in that. So can heart failure because you see decreased blood flow, right, and therefore decreased flow to the kidneys, decreased flow to the liver, which I put here, hepatic flow. Therefore you can have decreased clearance and increased drug levels. With renal elimination or kidney elimination, we see that creatinine clearance decreases with age after 40 years. Age-related decreases varies from person to person, however, so do take that with a grain of salt. Serum, also too, this is important, serum creatinine may remain within normal limits despite a decrease in glomerular filtration rate, and this may be secondary to decreased muscle mass. So that ratio plays an effect. So actually what some centers do, I know our ICU pharmacists look at another renally cleared marker, Cystatin C. This is another market that actually is a more precise marker for renal function. It's less dependent on age, on gender, on ethnicity, diet, muscle mass. So if there's especially drugs that are renally excreted or metabolized and that have high or excuse me, low therapeutic indices and high risk for toxicity, vancomycin, aminoglycosides, digoxin, et cetera, we may want to look at Cystatin C for clearance and really pinpoint how that patient's kidney function is before we start dosing these and then subsequently monitoring them. Renal elimination of drugs, many drugs are decreased as already mentioned. So toxicity of these drugs, once they increase their serum concentrations, what are they dependent upon? Well, that are renally cleared, I should say. It's dependent upon the extent of how much renal elimination contributes to the total systemic elimination of the drug. And then again, how I mentioned the therapeutic index, what is that specifically? It's a ratio. It's the maximum tolerated dose of the drug and the minimum effective dose. So maximum tolerated meaning, well, if I get to this next concentration, I'm going to start seeing toxicity and adverse drug reactions or effects. So if that window is high, then that's better from a toxicity standpoint. So let's get into, well, before I guess we get into now the specific drugs, are there any other questions right now that we can discuss? And yeah, feel free to type those in the chat and stop me whenever, Christine, I'll just keep continuing on. So let's get into the medications. I put them in different categories and then we can go from there. So we can start with alphabetically basically is what I'm doing. So medications, so we'll start with anticholinergics and there's different drug groups that have the overall categorized anticholinergic effect. So let's talk about first-generation antihistamines. We're talking about Benadryl, Hydroxyzine, Promethazine, Meclizine, et cetera. So these drugs are highly, so yeah, they work on the histamine receptor, right? But they also have significant anticholinergic effects, which can be manifested by dry mouth, blurry vision, constipation, drowsiness, hallucinations, memory problems, confusion, delirium, difficulty urinating. And delirium is a big thing here, right? And we see that a lot, especially in our critically ill patients, that ICU delirium. Delirium is an ongoing topic in the literature and it's a hot topic in the literature. And we're always looking at this because we know from the literature that patients that do experience delirium, ICU delirium, can have these effects that last for months after hospitalization. And not only that, from a morbidity standpoint, there's actually a significantly increased mortality difference in these patients that do develop delirium. So trying to mitigate delirium, especially in the elderly population, is paramount. So looking at these drugs that are prone to increased delirium is an important issue in trying to mitigate that and decrease the administration of those drugs. So clearance of these are reduced with advanced age, the antihistamines. There's a tolerance that develops when they are used specifically as hypnotics. So we see that, you know, I need to use this to go to sleep at night. And then months later, you know, that same effective dose is really not helping me get to sleep. However, that increased dose that I'm trying to take to get to sleep is, you know, those drug levels are increasing, but you're still seeing those other adverse effects and other pharmacologic mechanisms, again, such as anticholinergic effects, risk of confusion, dry mouth constipation as already mentioned, and specifically with Benadryl. So if you're using Benadryl or diphenhydramine in the use or for the use of an acute, you know, for the use of acute treatment and severe allergic reaction, the anaphylactic reactions, that still may be appropriate. So, you know, when I mention all these drugs and say don't give them or recommend not to, you know, take that with a grain of salt, and obviously every patient's different, and the reason why you're using that, the indication for the administration of that drug is very important. So it's, at the end of the day, it's all risk benefit, right? And it's the specific patient that you're treating and what you're treating them for and what you're treating them with. Moving on to the anti-Parkinson drugs, so benztropine, trihexyphenidyl. So again, these are anticholinergics that are used for Parkinson's disease. There are more effective agents available, specifically the dopaminergic medications, levodopa, carbidopa, Sinemet specifically, the brand name for that combination drug. So those are more effective and they don't have these anticholinergic effects, right? And also too, these aren't recommended for the prevention of the EPS or extrapyramidal symptoms that we see sometimes as adverse reactions or side effects of antipsychotic medications that we use. Moving on, so antispasmodics, atropine, belladonna, chlorinated epoxide, dicyclamine, etc., scopolamine that we can use, you know, scopolamine that we'll use for nausea as well. These are also highly anticholinergic and therefore have all of these side effects that were previously mentioned. And then you can argue, you know, their effectiveness specifically, especially in elderly patients. And again, there are likely better agents available that we can be using. So let's move on to antithrombotics. We'll start with diprotamol or persantine. This is the short acting form, not the extended release combination that we see with aspirin. So what this can cause significant orthostatic hypotension, especially in that hypovolemic patient and worsen that hypotension and therefore its adverse effects. Again, there's more effective alternatives available. I can say that with a lot of these drugs that we're talking about today. The IV form is acceptable for the use in cardiac stress testing, that persantine stress test that we hear about or that we see our patients have, you know, pre-op or before they come to the hospital that have a history of that. Again, just like Benadryl, if you're using it for a specific reason and there's a risk benefit that's recognized and discussed, then so be it. Moving on with the antithrombotics, these next set of medications I'll spend a little bit more time on because, you know, these are the big players that we see, especially the antithrombotics now, and we see more of these being used and there's more drugs coming out to the market. So, you know, I'll give a little more detail on what some of these, so, you know, warfarin is an old historical drug that originally was used as rat poison, came out of Wisconsin, but then the effects of anticoagulation were seen and therefore we turned that into a pharmacologic therapeutic agent in humans. Brand name is Coumadin. Essentially, it's a vitamin K antagonist in that pathway, basically. So what we see with the literature, we see increased adverse outcomes after traumatic injury in patients that have pre-injury administration of warfarin for various reasons, DVTs, PEs, AFib, etc. We see increased risk of intracranial hemorrhage after trauma in patients that are taking warfarin, which, I mean, that makes sense. What we also do see in the literature significantly is increased mortality after injury in patients that are taking warfarin, specifically and particularly with intracranial hemorrhage, so subdurals, epidurals, subarachnoid hemorrhage, etc. Age increases the risk of the anticoagulant bleeding effects, so that's something to take into account. Therefore, you know, dose adjustments is important and it's key, so starting at a lower dose and, again, monitoring those levels of warfarin is a drug that should be monitored as it has a neurotherapeutic index, and we do have monitoring capability of that, which we'll talk about here in a second. There's the fall risk in the elderly, right? Elderly have increased risk of falls, especially patients that have baseline dementia or motor deficits after strokes, so increasing risks of falls are going to increase your trauma burden and especially bleeding in patients that are on warfarin. There's an increased mortality from major bleeding events in patients that are on warfarin when compared to some of the DOACs or the NOACs, the novel oral anticoagulants, which we'll talk about, the Xarelto's, the Eliquis, the Pradaxa, etc. The half-life of warfarin, it depends on which clotting factor we're looking at. We're basically looking at the extrinsic clotting cascade factors 2, 7, 9, and 10, but depending on what factor you're looking at, the half-life is anywhere from 36 to 42 hours, so basically this drug sticks around longer, right? So it takes a while for the body to eliminate that, and in the setting of decreased clearance or metabolism, these effects can be longer-lasting. So it's metabolized in the liver, it's a cytochrome P450 enzyme that metabolizes it, so again, it undergoes, as we previously mentioned, phase 1 metabolisms. There's a significant amount of drug-drug interactions that we see when drugs are metabolized by the cytochrome P450 system, so especially with warfarin, when we're monitoring that drug because of its neurotherapeutic index, when we're looking at that international normalized ratio or INR, you know, we're trying to get that sweet spot therapeutically of 2 to 3 for that INR. One week it could be higher, one week it could be lower based off of, oh, I just started, you know, Diflucan, fluconazole for a fungal infection, or I'm eating more, you know, spinach or green leafy vegetables, or you're not, or you're looking at an inducing agent that will increase the metabolism and decrease the concentrations, and therefore, you're now subtherapeutic and you're at risk for more clotting, and your INR is 1.2 on your next week's check. Decreased dose in renal and hepatic insufficiency as it's hepatically metabolized, renally excreted. Antidotes too, which I'll talk about, which are important, you know, what are available, what do we have to use, vitamin K, as this is a vitamin K antagonist, that's historically one of the antidotes. Does it work immediately? No. It works over a few days. I mean, that depends on if it's IV, IM, PO, and there's different adverse reaction profiles with vitamin K itself, depending on what route you give it. What also is used, FFP, fresh frozen plasma, we use that, and that is more quickly acting, more immediately acting. However, do use this in caution in patients that are elderly, and especially elderly patients with heart failure, as FFP is volume, right? It's liquid, it's volume that we have to give, and we can put these patients into heart failure. What we have seen now more recently on the market over the previous years is PCC, prothrombin complex concentrate, if you guys are familiar with that, this comes in many different flavors. There's three-factor, there's four-factor, there's activated, there's inactivated. Typically what we see is nowadays a four-factor PCC, and whether it's inactivated, that's case centra, or it's activated, that's FEBA, F-E-I-B-A. Those are typically used, those are immediately acting, however they are, and it's an IV push type of medication, right? So it's not a huge volume like FFP, it acts even quicker, however there are adverse reactions with PCC that you have to take into effect, like potentially increased risk for thrombotic complications. So now let's get into the direct thrombin inhibitors. So the main drug on the market is Pradax or Dabigatran. This is a more predictable anticoagulant with its effect, and that's when I compare it to Warfarin. It can be given in fixed doses without routine coagulation monitoring, so that's good, there's no monitoring, there's one dose. The half-life is less, about 15 hours, so it will be cleared quicker, and there's insignificant, I should say, hepatic metabolism, so there's no dose adjustment with that in patients with liver insufficiency or decreased phase one metabolic reactions. The P-glycoprotein, however that's a transporter, it is a substrate for that, so the classic drug reaction with drinking grapefruit juice and it knocking out the P-glycoprotein substrate, that can have an effect. This drug, this is, I guess, one of the important pearls of Pradaxa, it is dialyzable, so as far as an antidote, quote-unquote, if this drug is on board and you're seeing significant toxicity or bleeding, especially in that traumatic hemorrhagic shock patient or TBI patient, and you need to get this drug off board quickly, you know, there's other drugs which we'll talk about now, but it is a dialyzable agent, unlike the other, well, I guess, once we get into the fact, antitinnate inhibitors. Bleeding is an issue, obviously, with all of these antithrombotics, anticoagulants. What you may see on your anticoagulation profiles is a prolonged PTT with a minimal effect on INR. That's hard to interpret. Some of these drugs are going to elevate or alter those profiles, however, you still do not need to routinely monitor this. There's some GI events that have been reported, dyspepsia, abdominal pain and ulcers, hypersensitivity reactions. What we have seen in a few papers and studies is that there's some increased risks of MI and strokes in these patients, especially when being used for mechanical heart valves, so be cognizant of the indications that we're using these for and their risks. Now talking about antidotes, so Praxibind, that's available in some centers. That's a monoclonal antibody that can be used to quickly get and deactivate this drug. There obviously is a cost with that, just as PCC. Activated charcoal can be used for many different drugs, however, you know, take that with a grain of salt in the fact that you have to use that in the right timing and that the drug was just recently ingested and has not cleared the stomach and moved on into the systemic circulation. And then again, to mention just to hit home is that Praxibind is a dialyzable drug, so hemodialysis is a useful therapeutic tool for an antidote or for metabolism. Now getting on to the factor Xa inhibitors, so the two that we see mostly in the United States are Apixaban and Ribaroxaban, just as Praxibind in comparison to the vitamin K antagonist Warfarin specifically, it's a more predictable anticoagulant and it also can be given in fixed doses without routine coagulation monitoring. So Ribaroxaban, or the brand name Xarelto, it has an even shorter half-life than the two drugs mentioned, so up to 10 hours. It does undergo hepatic metabolism, so you gotta watch out for those. The cytochrome P450 oxidates inducers and inhibitors, and in patients with just intrinsic hepatic dysfunction, it's excreted in the urine, so renal failure comes into play with these drugs as well. It's also a PGP substrate, and how I mentioned with renal insufficiency, it is contraindicated in severe renal impairment, chronic kidney disease, four or five stages. This drug is not dialyzable. Also, apixaban is the same way. Monitoring, none needed, so that's good. But again, if you check a coagulation profile, which we routinely do, especially in these trauma patients upon admission as they come in through the trauma vein in the emergency department, you may see an altered or an abnormal PT, INR, PTT, and it's highly variable amongst patients. So that's difficult at times to, well, what do I do with that? Well, if we know, which we'll talk about later, knowing what these polypharmacy regimens are in these patients, that's important. Well, they're on a factor 10A inhibitor, so okay, I can put two and two together there, and that's why we're seeing those effects. The other factor 10A inhibitor that we're used to seeing is Eloquus or apixaban, little longer half-life than Xarelto, but still not significantly close to warfarin. Again, undergoes hepatic metabolism and renally excreted and not dialyzable, so essentially equivalent to Xarelto. However, it does have a minimal PGP interaction, so a little better profile there than Xarelto from that standpoint specifically. Dose adjustment for age, renal function, liver function, also weight as well. And again, monitoring, we do not need to monitor these medications. Antidotes for these, for the factor 10A inhibitors, and dexanet is a drug on the market. So that is a binder of the 10A inhibitors and knocks them out. So that is a potential medication that we can use in these patients that come in, let's say with significant traumatic brain injury from an intracranial hemorrhage standpoint, which is blossoming or expanding on subsequent CT head images, and they're having neurologic effects, and we need to get these drugs off board quickly. Also, we can use PCC. I know I put activated charcoal on there, but that's really not gonna work immediately. And again, that has to be used if the drug was just administered. PCC is our, at our institution, our drug of choice to reverse this medication. And we typically use Kcentra, and again, that's a four-factor inactivated form of prothrombin complex concentrate. FFP you can use as well. PCC, I would say, is the best agent though for these right now. If you do not have indexamide available. Antiplatelets, the non-aspirin antiplatelets, so the ADP drugs, so clopidogrel, Plavix. We also have Effiant and Brolenta. These are the antiplatelet drugs. They do increase bleeding risk, just like the anticoagulants, the antiplatelets do as well. Use these drugs in caution with dose adjustments. No dose adjustments, however, in renal insufficiency. There's a five, so this is an interesting, I guess, finding in the literature. There's a five-fold increase in progression of intracranial hemorrhage in patients taking Plavix. So Plavix is significant. When we knock out those platelets and its specific mechanism of action, and then you see that in conjunction with a patient with acute traumatic injury, specifically TBI from intracranial hemorrhage, that's significant. These head bleeds can quickly and rapidly progress, so we need to be aware of these patients that are on Plavix and how to deal with that. So management of the TBI in these patients on pre-injury antiplatelets. So there's a lot of debate in the literature on, well, what do we do with that? Especially knowing the increase in progression of the bleeding. So do we, well, I don't wanna say prophylactically. I mean, it'd be therapeutically, right? Because we already know we've knocked out the platelets with pre-injury Plavix. Do we give them platelet transfusions? There's mixed feelings on that in the data, and it's inconclusive, essentially, is I guess what I'll say. Some centers do give platelets based off of the actual platelet number. Some wanna see the platelet number, the absolute number be 100,000 or 150,000. If they are less than that, then we will give impaired transfusions of platelets. Also, too, to look at what I like using, it comes with a cost, and it's not an immediately available turnaround time laboratory value. Our specific platelet function analysis laboratory values that we can look at to really see, just as with our TEGS and Rotems, what the exact coagulation profile looks like moment to moment and which specific factors are contributing to that or deficient and how we can affect those. We do have a couple of questions. Logan, I'd like you to wait. Oh, yeah, yeah, sorry. That's okay. When the patient goes to surgery for evacuation of bleed, is there a limit of time related to use of Andexa? I would say give that as soon as possible. If you have it and if that's available and you know the patient is on or are on these types of medications and you need to reverse that and you don't have any other reversal agents or you're waiting for your FFP to thaw and you have it, I would give it. Again, knowing that there's risk benefit, right? So giving this, it's, well, this is a lifesaving procedure. I need to go take this patient to the operating room for craniotomy for evacuation of a bleed. However, so I'm gonna give this medication to reverse this anticoagulant, antiplatelet, whatever we're talking about, whatever drug, warfarin, et cetera. However, by reversing that, we can increase thrombotic events in that patient with a mechanical heart valve and then therefore create strokes, et cetera. Thereafter, again, at the end of the day, it's risk benefit. What is the most important thing right now? You know, this patient is at risk of dying from this head bleed, so I have to give this medication. A follow-up question to that, does Andexa interfere with anesthesia meds? We were told there was. Is it, it is limited to use by neurosurgery? Yeah, so the neurosurgeon's obviously gonna be using this. I would think, you know, there can be interactions with the anesthetic medications. That also is, you know, it's good to bring up. That sparks the conversation of having that conversation in between all providers involved. So, you know, pharmacy, who's actually releasing these medications. Some institutions actually have protocols in place where hematology has to be involved to release these drugs. And I know that's just one more cog in the wheel, right? One more person we have to talk to, especially when time is of the essence. But having that conversation with your anesthetic provider, with the trauma provider, with the neurosurgeon, with the pharmacist, plus minus the hematologist, what are the indications, why we're giving this? What are the risks? What are the benefits? And if this is something that's, you know, life or death right now that we have to use, and then we can, you know, talk about the adverse reactions thereafter. So, you know, it's a good question. Obviously, all these drugs have interactions and there's adverse reactions that we have to deal with. Another question. Most patients I see are on Plavix and ASAY. So that's the DAPT, if you will, dual antiplatelet therapy. That's the acronym that you'll always see our cardiologists write in the chart. These are the patients that usually, typically what we see, they've just had fresh stents put in, drug eluting stents in their coronary vasculature for ischemia, for heart attacks, et cetera. These stents are highly thrombogenic and therefore increase risk for instant re-stenosis. Therefore, we've seen with literature, you know, instead of aspirin alone, or instead of Plavix alone, that dual antiplatelet therapy is more beneficial to prevent those re-stenosis and thrombosis. They typically are only given for a set amount of time, six months, 12 months, et cetera. And then they can be, the regimen can be downgraded, if you will. And which brings up a whole nother conversation, you know, another tangent I can get into is medication reconciliation, right? And how we can use that to benefit our patients and their outcomes, where we see somebody that comes in and they've been on Coumadin and we're trying to chart dig and chart biopsy and we can't understand why they're on that because they had one unprovoked clot in their left leg 20 years ago, right? And there's no true indication for them to be on that. It's interesting that we see certain, you know, us as providers, we'll put a patient on a medication, but then they're lost to follow up or we're not following them specifically for that medication. And then that patient somehow continues these medications on for months to years to come. And, you know, which in a situation that they could have had those medications discontinued. And I specifically mentioned the antithrombotics or the anticoagulants because those have significant effects in our world, right? And in the trauma world, specifically with bleeding. One last question, Dr. Young, what are your thoughts on TBI patients who are planned for surgery and are transfused platelets, but surgery is canceled? Okay, sorry. My phone was kind of cutting out there. That's okay. Let me read this here. What are your thoughts on TBI patients who are planned for surgery and are transfused platelets? Okay. So, I mean, that happens, unfortunately, where we have procedures canceled or delayed for whatever reason, and we're giving therapeutic medications or we're, you know, to increase platelets, the platelet transfusion, or we're holding the anticoagulants, we're holding that heparin drip and therefore increasing thrombotic risk in these patients before they go to surgery. Or after, right? Because we need to restart these medications, but we don't want them to bleed during surgery. You know, that is a significant issue. Or I've just given this patient a platelet transfusion and they can't be, you know, we're not going to surgery for whatever reason. Now we're talking about resource utilization, right? You know, now I'm exhausting my blood bank of this, you know, precious resource. You know, if you give that, that's fine. I'm there, you know, and you're getting that platelet level up to a number. That is now deemed reasonable to operate on for whatever operation you're doing, whatever bleeding risk there is with that. However, if that procedure is delayed, I would just obviously repeat your labs and see where your platelet count is now, you know, the next day before you go operate on that patient because they actually may need another platelet transfusion. Again, that's, you know, that argument and that, you know, philosophical argument of resource utilization. So yeah, good questions. Low molecular weight heparins. We'll move on to lovanox, tinzaparin, anoxaparin, fondoparanox, et cetera. So there's increased risk of bleeding in the setting of renal dysfunction. So specifically with creatinine clearance less than 30. So significant renal dysfunction. These drug levels are significantly elevated in the patient's serum concentrations, and therefore there's significant increased risk of bleeding and that's why unfractionated heparin is actually perverted in these patients. Now I say that with a grain of salt because looking at a whole, in general, the trauma patient, we know that the trauma patient in and of themselves, regardless of age, I'm talking about adults, you know, younger adults versus older adults, they are themselves thrombogenic and, you know, hyper-inflammatory, if you will. So we know that low molecular weight heparins are better at preventing DVTPE than heparin. However, in the setting of renal failure, you got to take that with a grain of salt and that's a caveat that you may need to use unfractionated heparin. If you're not and you're still going to use low molecular weight heparin, I would recommend, highly recommend monitoring. We do have monitoring capabilities now for low molecular weights and that's specifically anti-10A levels. So definitely be monitoring those or just use heparin, subcutaneous heparin, I should say, because this is prophylactic from what I'm talking about. And if you're, you know, going down the therapeutic realm, we can talk about that as well from, you know, therapeutic heparin drips and other medications. Moving on, sorry, I know we're kind of getting late on time. Other medications I'll get into. So anti-infectives, nitrofurantoin, there's a lot of toxicity with that and avoid in patients with renal failure. Peripheral neuropathies, pulmonary toxicity, hepatotoxicity, basically they're safer alternatives for nitrofurantoin and these are usually used for the UTIs, right? Fluoroquinolones, we see prolonged QTC intervals so that can cause arrhythmias, torsades, et cetera. Seizure threshold is lowered in fluoroquinolones and also in that elderly population, also in the early, you know, pediatric population, we see that tendon rupture risk with those. Macromycin and aminoglycosides are very important medications. However, in patients with AKI, their metabolism is altered and they themselves, in and of themselves, can cause AKI as well. So these drugs need to be heavily monitored, their drug level's monitored. So with the help of our clinical pharmacists. Bactrim, you can see hyperkalemia in patients with decreased renal function. So be monitoring those electrolytes if patients are on Bactrim. Moving on, cardiovascular. So the peripheral to alpha-1 blockers, doxazosin, parazitin, tarazosin, these show high risk and have high risk for orthostatic hypertension. Again, especially in that hypovolemic elderly patients. So do use these with caution. Not recommended, you know, per our guidelines for hypertension treatment. They're not first line specifically for hypertension. So do use those with caution. And again, there's alternative agents. The central alpha actors are the agonists, clonidine specifically. These have high risk for adverse CNS effects, bradycardia, orthostatic hypertension. Again, not recommended as first line. That being said, there's a little blurb at the end of this with the ACSTQIP guidelines. You know, some of the questions that you guys may have out there are, well, what about these medications that these people are on that actually have significant withdrawal effects, right? Once we stop them, clonidine being one of them. Again, patient-specific management, right? If these patients are on these drugs, then, you know, we can't abruptly stop them and continue to hold them. If we stop them for 24 hours, that's fine. But these are, you know, some of these medications we have to get back on board, knowing that they do have risks. Disopiramide, so that's, you know, an antiarrhythmic. It has strong anti-cholinergic effects. That's what I'll say about, you know, using this drug in the elderly. Other antiarrhythmic drugs are preferred. Nifedipine, so that's a calcium channel blocker. You can see significant hypotension and precipitating myocardial ischemia in these patients. Beta blockers, so this is, you know, the big drug that we always see, you know, and how I've already mentioned, you can blunt that response of tachycardia in the patient who's hypovolemic and hypotensive, who you should see that reflex tachycardia to help you assess these patients who are in shock and who are in hypovolemia. About 20% of elderly patients are on these medications for the indication coronary artery disease, and 10% are on them for the indication of hypertension. So baseline decreased sensitivity to catecholamines in the elderly population that I mentioned previously is also complicated and compounded by that patient who's on the beta blockers. I mean, again, because of that hypovolemia. So knowing that these patients are on these drugs early and soon is very important. You know, and again, to not put us in that, lull us into that false sense of security, well, oh, their blood pressure is 110 and their heart rate's normal. So these patients are fine and they just got into a high-speed motor vehicle collision because they, you know, again, that external minimal injury, they can still have significant internal injuries and they're not gonna manifest it physiologically, right? Digoxin, old historic drug for compensated AFib maintenance, or excuse me, heart failure, and then also too for AFib for rate control. This is excreted unchanged in the urine majorly. So decreased renal clearance in AKI and therefore you can see those increased toxic effects. It is not dialyzable. And also, so dose reductions are very important with this drug. I mean, it has a very narrow therapeutic Windex, a large volume of distribution, a long half-life, up to two days, and then that's extended up to five days in that aneuric patient, in that chronic kidney, you know, stage five patient. And again, this drug is not dialyzable. So really use this drug in caution. And again, there's more safer alternatives out there. Ambioderone, we see this all the time in the acute, more so nowadays in the acute setting rather than the long-term maintenance chronic medication. You know, that patient who's fluid overloaded post-op or after a significant resuscitation and trauma, we're gonna flip them into AFib usually at that post-hospital day two or three, right? We see that acute AFib, and then we're throwing ambioderone on these patients. It's the class three antiarrhythmic. There are a ton of drug reactions, drug-drug reaction with ambioderone. There are multiple side effects, hepatotoxicity, skin toxicity, SID, ADH, all the pulmonary toxicity events that we see, thyroid toxicity, et cetera. Large volume of distribution, huge half-life, up to 100 days. So I mean, you take a few, and that's more for chronic dosing of this medication. This drug will stay on board forever and cause a significant amount of toxicity. So again, if you have to use this, and this is your only drug that, you know, next to cardioversion, basically, in a patient with acute AFib, if you have to use that, then that's fine. But again, just know that it has significant consequences potentially. And again, this, or not again, but this drug, just to mention, is not dialyzable. Central nervous system drugs, the antidepressants. These are tricyclics. Some of the SSRIs, again, highly anticholinergic. All that drowsiness and delirium that comes with that. So be very cautious with that. Orthostatic hypotension more so with the tricyclics rather than the SSRIs. So be cognizant of that. The antipsychotics, so the first generations, the typicals, the antidopamine, you know, Haldol's are the second generation that work on serotonin. The Seroquel's, the Geodon's, Zeprex's. You know, we typically try and avoid these. Again, except in patients who have clear indications for them, schizophrenia, bipolar, who are coming in pre-hospital, pre-injury with these. They can increase risk of stroke. They can increase the rate of cognitive decline and mortality. We've seen data with this in the setting of dementia that antipsychotics can increase mortality. And then with, I guess, a blurb on delirium, you know, we see all these delirium bundles nowadays, again, because delirium is such a hot topic and a significant topic because of that mortality increase. You know, part of those bundles, you know, the first steps down that progression in that bundle is, you know, trying to attempt non-pharmacological behavioral interventions first. And then if you have to go to those, you know, second, third progressions of now starting to use pharmacologic medications. Barbiturates, phenobarb, pentobarb, high rates of physical dependence. Really not used much anymore. Really don't see those out chronically. Those are used more for specific indications acutely in the hospital. Greater risk of overdose at lower dosages. Kind of like the antihistamines, there is a tolerance that builds up to these sleep benefits. So there's better drugs out there. Hepatic metabolism, you can see, and clearance decreases with age also too. So in that half-life for these, some of these benzo, or excuse me, barbiturates is significantly high, up to a hundred hours. Benzos now, let's start talking about these. This is another drug class of the withdrawal agents. You know, patient X has been on Ativan for years, but we know that these drugs can increase delirium, right? And cognitive impairment and link to falls and fractures and MVCs. So we shudder when we see these patients and let's get them off of these. However, there is a withdrawal effect. So you do have to take that into account. And they may be, again, that specific patient population and that patient with seizures, status, benzo withdrawal, alcohol withdrawal. These drugs are actually useful and beneficial. So knowing what you're using and why you're using it, that's very important. But if we're just willy-nilly throwing benzos at the elderly population for agitation or whatnot, there could be serious consequences. And the same thing for the non-benzodiazepines, and this is kind of a mouthful. The non-benzodiazepine, benzodiazepine receptor agonist, these are the Z drugs, right? The zolpidem, valoplanet, et cetera. So same thing, delirium, increased risk, falls, fractures. They're actually linked to increased numbers of ED visits as well in hospitalizations. And there's, you know, minimum proven when we're using these meds. So there's other alternatives. Dr. Young, I know we're at the one hour mark. We're gonna run over a little, but in case anyone has to jump off, do we wanna stop right here and ask for any questions? Sure, yeah, please. So if anybody has any questions and needs to leave now, we'll probably be running over. Please submit any questions in the Q&A box. See if Dr. Young can answer those before you have to jump off. I guess you can keep going, and if I see anything, I'll stop you. Okay, sounds good, thank you. Dilantin and Keppra, I'll just say, you know, briefly, Dilantin, a lot of, you know, neurotherapeutic index, a lot of drug interactions. So, and it requires drug level monitoring. Be cautious in using this medication in the elderly. Keppra is a more forgiving medication. We're seeing this used more and more nowadays for seizures, especially for that seizure prophylaxis for the first seven days after traumatic brain injury. So this is actually a better drug. There are some side effects, however, that we see. So do use that in caution. Lower half-life, it should be cleared fairly quickly. Neurontin and Lyrica for pain. We're seeing that used more often in that multimodal regimen. I think Lyrica is being used a little bit more now than Neurontin, as Neurontin has some more side effects as far as its ADR profile. So more vasodilation, which you can see with, you know, manifested by hypotension, and also more somnolence in patients that are on Neurontin. So if you're gonna use this, especially in patients with renal dysfunction, start at lower doses. That's, I guess, what I would say about these two drugs. Endocrine, so insulin, giving that, giving fast-acting, short-acting insulin doses in the elderly, we can see higher risks for hypoglycemia without that improvement of, or hypoglycemia, I should say. So use that in caution. Usually these patients should be on more longer-acting kind of basal rate medications for their diabetes. Oral drugs, sulfonylureas. You can see prolonged hypoglycemia, basically, with those. And then with the old, the thiazolidine diomes, the Actos and Avandia drugs, these actually can worsen heart failure. That's what's mentioned on these. The GI drugs, Reglan, metoclopramide. Avoid this. You know, these are for the nausea, anti-nausea patients. Avoid these for gastroparesis if you're gonna use these for a prolonged period of time. Again, there's other better medications. And then they also do have UPS side effects. So that's important. The antiemetics, prochlorperazine, promethazine, they can worsen Parkinson's symptoms. And some of these also, too, have anticholinergic effects. Then I mentioned earlier with the PPIs, with the pH changes and how that can affect drug absorption. Also, too, just the PPIs in and of themselves, they can increase risk for C. diff, bone loss, osteoporosis, therefore fractures. We see that they can increase pneumonia. We could have nutrients and electrolyte deficits as well. And there's a lot of drug-drug interactions with PPIs. So I would say, you know, some people say, well, let's use H2 blockers instead, which is fine. But again, you know, those drugs themselves have some side effects. So use these specifically for indications that warrant them and for a transient period of time. Going into the opioids, Demerol, I'll just say that's out of favor. There's a lot of toxicity with that, especially with its metabolite normoperidine. It's a neurotoxin, causes seizures, basically. Ultram, that's more forgiving. However, it does lower the seizure profile. And in conjunction with SSRIs, we can increase risk of serotonin syndrome. Those are the two main things to say about that. It has been linked to increased ED visits. However, if it's being managed appropriately and we're trying to use multimodal regimens, it potentially is a good alternative. Morphine and Dilaudid, we're seeing that, especially in renal dysfunction, the metabolites are increased and less cleared. So we see more side effects with morphine and Dilaudid. I think fentanyl is a safer drug to use in this patient population, especially in those with renal and hepatic insufficiency. There's no active metabolites and it has a very short half-life. Methadone, that's a whole nother kind of beast in and of its own. And more for chronic medications, I'll just say use that with caution in patients with hepatic insufficiency. But the take-home for this slide is, I think fentanyl is a way to go if you need an opioid or an IV route opioid in the elderly population. And then the NSAIDs, we know, in anybody, there's increased risk for peptic ulcer disease, GI bleeding, acute kidney injury, some hypertension, of all of them used in the medicine has the most adverse effects. And then with skeletal muscle relaxants, Soma, cyclobenzaprine, Flexeril, et cetera, these have also anticholinergic effects, so that delirium, drowsiness, sedation, those are significant in these patients. Genital urinary, basically the diuretics, there's electrolyte abnormalities, there is hypovolemia, obviously. I mean, if we have to use these in patients with heart failure, we have to, that's fine. But just be careful when we're dosing these, especially in the acute setting. There's volume shift, there's electrolyte abnormalities, and we could put these patients into AKI with that. Now, just gonna mention, with the multimodal regimens, with the rib fractures, we're seeing a lot now that early initiation of the multimodal analgesic therapies and bundles, the NSAIDs, the muscle relaxants, the lidocaine patches, Toradol, and plus minus opioids. Epidurals, paravertebral blocks, those are seeing, when we bundle that, we're decreasing the use of opioids, and we're seeing better outcomes, decreased length of stay in the ICU and hospital overall, less pneumonia, less mortality. And these multimodal regimens, especially the epidurals, are definitely prompted by the EAST societies and the trauma anesthesiology societies. We do have a quick question. Yeah. In the morbidity obese trauma patient, would albumin still be an indication of a malnutrition state, or is there another lab value that would be useful? This is in the chat, the question. Yeah, you can use albumin. We can use that in the obese trauma patient, that's fine. If you're really wanting to pinpoint down the nutrition status, you can look at those other markers as well, usually order basically a prealbumin and look at that, is that a single digit number? Is it in the low teens? And I'm looking for 15, 20 or higher on that prealbumin. But yeah, somebody who's coming in off the bat with an albumin of two, I can tell whether or not they're cachectic or morbidly obese, that they have some protein calorie malnutrition. Yes. I guess just, these are kind of the last few slides. If you guys wanna go for another five minutes, if not, I'm happy to stop and you can have all these slides obviously sent to you guys. I say, yeah, why don't you just continue on. Okay, sound good. I'll just briefly mention some of these. So strategies for now, what do we do about this, right? How do we improve the outcomes in these patients and the elderly patients? There, so I've already mentioned, medication reconciliation is huge, right? That is extremely important. However, it's time consuming and it's expensive and there's different ways we can do this. It's actually now a requirement by the joint commission that we do med recs. I can't say enough about our clinical pharmacists. I mean, these folks are amazing that we work with, especially now in the days of the multidisciplinary approach. They put a lot of time and effort into this and are extremely helpful. And they're, you know, they're really, extremely helpful and they're the most well-studied as far as pharmacist-based interventions for medication reconciliation. And again, it's time consuming and it's costly. It costs up to about $60 per patient and it can take up to about three days on average to complete these. So that being said, the caveat is trying to know what this patient is on immediately as they're coming through the door can still be a challenge, right? And which I'll mention briefly, one of my actual new partners is working on ways to mitigate that. But what we're seeing is we're seeing reduction in errors, complications and readmissions with reconciliation of medications. And then again, just to add to this, you know, what do the elderly patients bring to the table? Right on top of their multiple comorbidities, they bring, you know, their polypharmacy and also too, they can be poor historians at times. You look at some of the literature and they compare what does the patient tell you they're on versus what does their chart tell you they're on? And I'm not saying the chart is always 100% perfect, right? But usually it's underreported the number of medications per the patient as, you know, the average of nine in this particular study I was looking at versus the EMR says they're on 14 medications. So getting that med rec down and correct is very important. And just to mention, one of my partners, Dr. Jayaraman, she's joining us from VCU in Richmond, which their group is looking actually at a novel diagnostic assay using liquid chromatography and mass spec to be able to rapidly detect critical medications, anticoagulants, et cetera, as a point of care test once they hit the door and we're getting those first set of labs in the trauma bay. So this assay is currently being developed and the results are pending. So I'm actually really excited to see what this looks like in the future. Now, I guess the last few things to say, this is a major thing I'll mention. I don't know if you guys have heard of or are familiar with the BEERS criteria. This is after Dr. Mark Beers. He was a geriatrician at UCLA and basically developed this tool to improve medication safety in older adults and reduce exposure to PIMS. What's PIMS? P-I-M, it's a potentially inappropriate medication and basically it catalogs medications that cause side effects in the elderly due to physiologic changes of aging. And it's one of many components that we can use for our comprehensive approach to medication use in the elderly. So I highly recommend to all of you just essentially do a Google search on BEERS criteria. The most up-to-date is 2019. He started this in 2008, or excuse me, 1991, I'm sorry. And the most updated version is 2019. If you just Google in BEERS criteria and then you can find little pocket guides for him. You can print off a couple page report and it shows you a list of all these medications that we talked about today. And the most recent iterations are now basically via the Delphi approach. There's panels now that look at these. So there's good evidence, there's good quality of evidence and strength of evidence on these medications. And then in conjunction with that, I don't know if you all have heard of the STOP-START criteria. This is just another addition. This is, as you can see by the names of the colleagues that have written these papers, O'Mahoney, O'Sullivan, O'Connor, these are our colleagues from Ireland that have put this tool together. There's two screening tools, basically. And it looks at inappropriate prescribing, potentially inappropriate medications and potential prescribing omissions. So these two things, basically the BEERS criteria and the STOP-START criteria are good to look at. So I would, again, recommend downloading these basically pocket guides, which is nice. They've done studies on these, actually, using the STOP-START criteria. The Senator trial looked at this, basically from computer-generated forms of STOP-START and how this can help prompt us as providers that, whoa, wait, this medication may be harmful in this elderly patient. What some prelim data show that it wasn't helpful. I mean, it didn't worsen outcomes, but it didn't improve them. However, I think the reason for that was we saw there was poor implementation, basically. The prescribing advice points by the providers for implementation of this was only 15%. So that prompted us looking at not only computer reminders, but actually having physical conversations between all the providers involved, the pharmacists and the physicians. And I think that would definitely help improve these. And then there's the OPERAM trial that's looking at this as well, but this is an ongoing trial that we'll see results in the future. And then also, I just wanna briefly mention who else can help us? Basically the geriatric specialists, right? We don't have protocols in our institution right now, but I think this is something that definitely would be worth looking at. Getting our geriatricians involved, right? And forming that geriatric trauma team that they can be looking at pain management, rehab, delirium, advanced care planning. And what we see in the literature is that patients evaluated by our geriatric colleagues show that there are lower mortality rates. So I think this is something to jump onto. And some of our trauma centers have created these geriatric trauma consultive services comprised of our geriatricians, our APNs, and they provide these comprehensive assessments and they help with a multitude of issues with our patients and help improve outcomes. And then lastly is the, these are my last two slides, the ACST clip, there's best practice guidelines that have been published by our ACST clip folks. Basically any trauma patient, primary survey, obviously that's the same as for any injured patient. And then once we've got that patient stabilized, now to really start looking at determining and doing that med rec and what are these meds that are affecting their initial evaluation of care? So the anti-platelets, the anti-coagulants, the beta blockers, et cetera. They also recognize and subsequently recommend looking at the BEERS criteria, following the BEERS criteria, discontinuing non-essential medications. This is that slide where I said, this kind of mentions those medications are at risk for withdrawal when we do discontinue these meds with these patients that come in. So the SSRIs, the tricyclics, the benzos, antipsychotics, the beta blockers, steroids, clonidine, those actually do have significant withdrawal. So if the patient's already on these, then we should restart them when appropriate, right? So that's important. And then again, dose adjust medications based off of renal function and hepatic function. And recommended pain medication strategies, use elderly appropriate doses. Again, with those IV opioids, fentanyl, over Dilaudid and morphine. Avoid the benzos unless you're using it for a specific indication, status, withdrawal, et cetera. Monitor the use of narcotics. Use those multimodal analgesic regimens. Use the epidural, use the prevertebral block. And also when we're getting these patients ready for discharge, having a good document for them to go home with, talking to their caregivers, their family, they themselves, clear instructions on their medications, why they're taking them. If these are only gonna be used for a few months, then a clear plan on when to discontinue them. And then I think what's really important is to establish that close follow-up appointment with their PCP within a week or two after discharge so they can get another exam, another evaluation, another step in medication reconciliation.

pharmacology

elderly trauma patients

pharmacokinetic differences

antihistamines

antithrombotic medications

medication management

medication reconciliation

Beers criteria

STOP-START criteria

geriatric specialists

improving outcomes