Transcript: HelixTalk #199 - Axe the Anaerobes, Drop the Docuste, Free the Fluids Episode ID: 233 Generated: 2026-09-24 13:58:15 ------------------------------------------------------------ [00:00] (Music) Announcer: Welcome to HelixTalk, an educational podcast for healthcare students and providers covering real-life clinical pearls, professional pharmacy topics, and drug therapy discussions. This podcast is provided by pharmacists and faculty members at Rosalind Franklin University College of Pharmacy. This podcast contains general information for educational purposes only. This is not professional advice and should not be used in lieu of obtaining advice from a qualified healthcare provider. And now, on to the show. (Music) Dr. Sean Kane: Welcome to HelixTalk episode 199. I'm your co-host, Dr. Kane. Dr. Khyati Patel: And I'm Dr. Patel. Dr. Sean Kane: And the title of today's episode is Axe the Anaerobes, Drop the Docusate, Free the Fluids. We're going to go through some medical myths today. Dr. Khyati Patel: Oh, okay. I am just loving the title and I can't wait to jump into it. Dr. Sean Kane: Yeah, so the vision of today's episode, Dr. Patel, was inspired by an article series in the Journal of Hospital Medicine. And the article series is called Things We Do for No Reason. It's literally a trademarked thing of Things We Do for No Reason. And these are basically articles that cover practices or beliefs that are common, mostly in hospital medicine because it's from the Journal of Hospital Medicine, but these practices are either not supported by any literature or evidence, or there's evidence that shows that there's a better alternative that we should be moving towards instead. Dr. Khyati Patel: Yeah, I thought that this was one of those Gen Z, you know, TWDFNR. I literally had to Google it and find out that there is this section in the Journal of Hospital Medicine. So that's pretty neat. And I agree with you, old medicine is maybe or may not be evidence-based, so we need to move on to evidence-based practice. Dr. Sean Kane: So these are basically like medical myths or mythbusters. And I really like these articles because they're pretty short, like probably two-page articles, and they do a great job of summarizing why we do what we do, what evidence there is to do that, and then what are better alternatives instead. And usually, again, these are inpatient topics, but not always, and you'll see that today. Dr. Khyati Patel: Yeah, some of the practices may apply to chronic management of these conditions on an outpatient basis as well. Dr. Sean Kane: So if you want to look like a superstar on rounds or with your clinical team, I would highly suggest you take a look at some of these Things We Do for No Reason articles. There's at least a hundred of them published, and if you go to our show notes, there's a link to PubMed that will show you just this article series called Things We Do for No Reason. So it's part of a PubMed query and you can just see them all and order them by date or whatever you want. And the citations for the articles we're talking about today will also be in the show notes as well. Dr. Khyati Patel: So Dr. Kane, which one's your favorite one you want to start with? Dr. Sean Kane: I'm going to start with aspiration pneumonia and the need or lack of need for anaerobic coverage. And this is so common on the inpatient side in terms of patient comes in and we are worried about aspiration pneumonia and it comes up very frequently of, do we need to cover anaerobes because of their aspiration event? Dr. Khyati Patel: And where are the anaerobes coming from? Dr. Sean Kane: Yeah, so basically of anaerobes in your mouth. And aspiration pneumonia means that you vomit or have contents from your mouth that go into your lung. So it could be that you vomit with an unprotected airway. It could be that you have a choking event, or even someone, probably most commonly would be someone who has dysphagia or difficulty swallowing. And because they can't swallow effectively, sometimes either spit or food or other contents end up in the lung when they obviously shouldn't, and that's called an aspiration event. Dr. Khyati Patel: And I guess that this is more common in older patients, patients who are perhaps deconditioned, so those who reside in long-term care, nursing home facility, or those who have, you know, alcohol use disorder, like intoxication can do that too. Dr. Sean Kane: Yeah, and what makes this a little bit tricky is that most of the time it's not an observed event. Meaning it's not like you see a patient vomit and then they get pneumonia after that and you know that that vomit went into their lung. More commonly it's presumed. Meaning you have a patient with pneumonia and they're deconditioned nursing home patient like you mentioned, and there are certain signs or symptoms that are more consistent with aspiration pneumonia, but it's not 100% definitive to diagnose it one way or the other. So the only time you know for sure that someone aspirated is literally you see them vomit and they have an unprotected airway and it goes in their lung. Dr. Khyati Patel: So it's kind of hard to differentiate whether it's the, I should say not hospital-acquired or institution-acquired pneumonia versus a truly an aspiration pneumonia. Dr. Sean Kane: Yeah, there isn't like a specific test that you can do to say, yes, it's aspiration versus CAP or HAP. It's also really not possible to differentiate between aspiration pneumonia, where you have a bacterial infection caused by the pathogens in your mouth or stomach, versus aspiration pneumonitis, which is the stomach acid itself causing irritation in the lung lining. And you don't have bacteria that is causing problems, but you have similar hypoxia, things like that, shortness of breath caused by the lung tissue being damaged by stomach acid, not by a bacterial infection. [05:11] Dr. Khyati Patel: And the treatment obviously would be different, you know, you're not going to subject them to antibiotic if they just have the pneumonitis we are talking about. Dr. Sean Kane: Exactly. Dr. Khyati Patel: So where, where does this myth to cover for anaerobes come from then? Dr. Sean Kane: So we're going to have to get in our time machine, more than 50 years. We're not joking here. 1970s, there were a couple articles that identified anaerobes as common pathogens for aspiration pneumonia patients. The trick though is that most of these patients had what was called an empyema, which means basically an abscess around the lung in the pleural space or the pleural cavity. And the pathogens that were identified in that empyema type patient with aspiration pneumonia were Bacteroides, Fusobacterium, and Peptostreptococcus. All of these are common anaerobes that you would generally find in the mouth or GI tract. And that's where that myth came from is that everyone who aspirates must have these anaerobic pathogens that we have to cover for based on that a couple articles. Dr. Khyati Patel: But then not everybody will have the abscess, right? So the new evidence kind of tells you, like data from 1999 and onward, that the bacteriology, the presence of bacteria, it's not anaerobic in nature. They are similar to what we find in community-acquired pneumonia or hospital-acquired pneumonia. Dr. Sean Kane: Exactly. And just for clarity, if a patient has an empyema, that's a very different picture than someone who just has pneumonia. Like those patients commonly need chest tubes to get the pus drained out of their pleural space. They might need decortication where they do a surgical procedure to like literally get the abscess out of the pleural space. Very different than just having bacteria that happens to be sitting in the, you know, distal airways of the lung. Dr. Khyati Patel: Right. And so to remind the audience about what are those common CAP or HAP pathogens, we are looking at the Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, MSSA, which is the methicillin-sensitive Streptococcus aureus, or our atypicals like the Legionella, Chlamydia, and Mycoplasma. Dr. Sean Kane: And then if it's more of a hospital-acquired picture in terms of patients with nosocomial risk factors, we can still see the community pathogens, but we're also going to see things like MRSA, so methicillin-resistant Staph aureus, Pseudomonas, a bunch of other gram-negatives that like to be resistant to a lot of stuff, so like Citrobacter, Enterobacter. And then we can also see kind of your more basic gram-negatives like E. coli and Klebsiella, but they can also develop resistance patterns and become things like multi-drug resistant, like carbapenemase-resistant Enterobacteriaceae or ESBL-producing bacteria that degrade some of our more common antibiotics and we need to use broader spectrum gram-negative coverage for those patients. Dr. Khyati Patel: So with us understanding the bacteriology a little bit better, what are some of the guideline recommendations of how we should go about treating it? Dr. Sean Kane: So it was kind of nice in the 2019 community-acquired pneumonia guidelines from the IDSA, the Infectious Diseases Society of America, they said that they suggest not routinely adding anaerobic coverage for aspiration pneumonia unless an abscess or an empyema is suspected. And that was conditional recommendation, very low quality of evidence. So that kind of gets at what we're talking about here. We don't have much data, and of the data we do have for anaerobic coverage, it's mostly with abscesses and empyemas, which is a very uncommon thing compared to aspiration pneumonia events. And that's where the data was in the 1970s anyway. Dr. Khyati Patel: And then the 2016 IDSA hospital-acquired pneumonia guidelines really does not discuss this in detail. Dr. Sean Kane: And I'm just going to call it out, Dr. Patel, we are now 10 years removed from the last IDSA update. So in true IDSA fashion, I would say that these are pretty outdated and it's probably time for them to come up with a new guideline update. Dr. Khyati Patel: Yeah, as I said 2016, I'm like, holy cow, that's 10 years old. Dr. Sean Kane: So then you have to ask yourself, okay, what's the harm, right? Like if I add anaerobic coverage just in case, like is that a bad thing? Like what's the worst that would happen? Dr. Khyati Patel: I can imagine if you're adding anaerobe coverage, then you're expanding the spectrum of the antibiotic and that means your gut is not happy. Dr. Sean Kane: Yeah, so anaerobes are all over your GI flora. So we call this gut dysbiosis, which just means that we're changing the normal flora of your GI tract, which is actually not a good thing. There's a ton of data about antibiotic exposure, how it changes your microbiome, and that that can have negative consequences for patients. Obviously also exposing patients to antibiotics that they don't need means that we have an increased risk of resistance for the bacteria that the patient could be exposed to in the future. And then also C. diff risk. Depending on which anti-anaerobic coverage you're using, you could potentially increase the risk of C. diff for that patient as well. [10:00] Dr. Khyati Patel: So I think where we are heading, the direction on what we should do in such cases is kind of clear, right? We only should add anaerobic coverage if we are having patient with necrotizing pneumonia, empyema, or that diagnosed abscess. Dr. Sean Kane: Exactly. So if you have that patient, which is not common, where they have clear like degradation of their lung tissue caused by likely an abscess or an empyema, you need to give them anaerobic coverage. So we're thinking clindamycin, because clindamycin is going to have superior coverage for the kinds of anaerobes that we're worried about in the mouth versus like metronidazole. You could also choose a beta-lactam/beta-lactamase inhibitor. A common example would be Zosyn, piperacillin-tazobactam. If it was an outpatient, you could use Augmentin, amoxicillin-clavulanate. But that beta-lactamase inhibitor is going to convey that anaerobic coverage that you might be looking for. Dr. Khyati Patel: And I noticed, Dr. Kane, you did not mention metronidazole. Dr. Sean Kane: Yeah. So common misconception, metronidazole is great for those lower GI anaerobes, but it's not great for what is sometimes referred to as like above the diaphragm anaerobes, so things in your mouth primarily. So clindamycin is better than metronidazole if you wanted to cover for anaerobes in the mouth or in the lung. In general, I would say it's more common to use the beta-lactamase inhibitor though, because clindamycin comes with a lot of problems on its own, like diarrhea and C. diff and things like that. Dr. Khyati Patel: Right. And so in patients who don't have necrotizing pneumonia, empyema, or lung abscess, we are going to treat them just as a CAP or a HAP patients that we normally would. Dr. Sean Kane: Exactly. So common inpatient community-acquired pneumonia regimen would be Rocephin, which is ceftriaxone, and then either azithromycin or doxycycline for your atypical coverage. And that's kind of it. Dr. Khyati Patel: Yeah. And then for hospital-acquired pneumonia, we are going to go with the Zosyn, piperacillin-tazobactam, which is your beta-lactam/beta-lactamase inhibitor, or cefepime with or without that vancomycin if you have MRSA possibility. Dr. Sean Kane: And it just so happens that Zosyn would have the anaerobic coverage, but it doesn't mean that it's like a better choice versus cefepime, which doesn't have anaerobic coverage. We're not intentionally giving anti-anaerobes, but it comes along with the Zosyn, which is going to cover some of those more multi-drug resistant gram-negative pathogens. Dr. Khyati Patel: Well, that was a really good review for how we should axe the anaerobes. What's next, Dr. Kane? Dr. Sean Kane: So Dr. Patel, our next stop is going to be docusate for constipation. And I know people are familiar with docusate because it is very commonly used as an outpatient laxative. It's also relatively commonly used on the inpatient side too as a laxative as well. So this is a very commonly prescribed medication. Dr. Khyati Patel: It's out there. I teach this in self-care as well as pharmacotherapy, and so yes, we go after this one for sure. Brand name is Colace. It's a stool softener because it has that surfactant-like property where it helps to mix the fatty content of the stool with the water that's available in the gut. And the idea is that by better incorporation of the water with the stool material, it will soften the stool. These come in a couple different salt forms, sodium as well as calcium. Dr. Sean Kane: And some students may be familiar with the kind of joking phrase, but not joking, of all mush, no push. Dr. Patel, can you kind of elucidate what that means? Dr. Khyati Patel: Yeah, so with that surfactant and stool softening property, it helps to soften the stool, but it doesn't necessarily augment the propulsion of the stool along the gut. And so it doesn't produce a bowel movement, but it makes it easier to go when patient has the urge to go. Dr. Sean Kane: So really you're drawing the distinction between stimulant laxatives that are stimulating peristalsis versus this one doesn't give you like cramping, for example, because it's not moving the smooth muscle along faster. It's just making it so there's more water content in the stool. Dr. Khyati Patel: Right. And I think this is kind of goes along with the line of how what's the deal with constipation, right? Untreated constipation can result into things such as hemorrhoids, fissures, and that's because patient sitting on the toilet straining, right, because the stool is really hard to void. And that's where this idea of let's soften the stool so that patient doesn't have hemorrhoids or fissures thereafter. Dr. Sean Kane: So Dr. Patel, I know it's common. Why is it so common? Dr. Khyati Patel: Well, I guess, you know, we have to again go back into the time machine, Dr. Kane. Go back to the 50s and 60s. Those studies are obviously old, and we know that that those studies were also not very good quality studies. But another reason why it's so common, it's because it's cheap. Very easy to add as an inpatient regimen, but also very easy to pick up at your local pharmacy. [15:04] Dr. Sean Kane: And also like patients don't complain about this laxative versus others where you might get cramping, bloating, depending on what you're taking. For the most part, the side effect profile of this is pretty minimal. Because it isn't a stimulant or it, you know, isn't terribly effective, you're not going to get diarrhea, for example, versus other therapies, you can actually go the wrong direction and go from constipation to diarrhea if you overdo it, right? So because it's not super effective and doesn't have a lot of side effects, patients don't commonly complain about it. Dr. Khyati Patel: Right. So I think you kind of mentioned it that it's not super effective. And so I'm kind of going along the lines of the new evidence or summarization of the evidence that's available. Does it really work? Dr. Sean Kane: It does not. So we have now multiple randomized control trials, not done in the 50s and 60s, but more recent, that compared it to placebo, and there was no difference in stool weight, frequency, water content, stool consistency, things like that. There was a 2021 systematic review of all over-the-counter laxatives, and it basically concluded that Miralax, PEG 3350, has the best data by far because it was a prescription product before it went OTC. And docusate was found to be no more effective than placebo and inferior to psyllium. Psyllium is like Metamucil. And the quote from the article is that docusate lacks well-controlled trials demonstrating its efficacy and has poor evidence to support its use in clinical practice. Dr. Khyati Patel: And this includes, as you mentioned earlier, no difference in the water content of the stool. So the whole notion about it makes your stool softer, that's totally not true. Dr. Sean Kane: Not true. Dr. Khyati Patel: All right. Well, that defeats the purpose of it used as a stool softener. I didn't ever think that this was a laxative. I always thought of this was like a, a friend of a laxative. Dr. Sean Kane: Yeah. And then you might be asking yourself, Dr. Patel, okay, we have an FDA, right? One role of the FDA is to ensure that all drugs on the market are safe and effective. And historically, we, pre-1937, we didn't have that period. And then in the 1930s, we decided all drugs need to be safe. And then in the 1960s, we decided all drugs need to be effective. How is it that we have a drug on the market that's widely used, not a safety issue, but definitely an efficacy problem? Dr. Khyati Patel: I'm afraid to ask. Dr. Sean Kane: So docusate came out in 1957, and at that time it was under the must be safe, no need to demonstrate effectiveness. But then in 1962, it was called the Kefauver-Harris Amendment, and this was the amendment that made it so that all new drugs needed to be approved for both safety and efficacy. And then in that same decade, in the 1960s, the FDA kicked off a program called DESI drugs. So DESI stands for Drug Efficacy Study Implementation. And basically they took all drugs from 1937, 1938 all the way to 1962, and they re-reviewed them for effectiveness, not just for safety. Dr. Khyati Patel: And then comes the twist. Dr. Sean Kane: In 1970, the FDA decided to approve this entire class, the drug class of laxatives OTC, instead of kind of reviewing each drug that was on the market. And I guess that intuitively makes sense that if there's like 10, 15 laxatives on the market, if you could bulk approve them all at in one go, maybe that makes sense. But in like true government fashion, Dr. Patel, this started in the 1970s, and then it wasn't until 1993 that it was tentatively approved in terms of its efficacy. And it wasn't actually approved based on efficacy, it was classified as GRASE. So G-R-A-S-E, generally recognized as safe and effective. And that's kind of a euphemism for, we got a bunch of experts together and they all agreed docusate seems to be effective and safe, but there was no requirement for data showing that it was actually efficacious. Dr. Khyati Patel: So you're saying that the final monograph for docusate was not done until 1993? Dr. Sean Kane: So that would be the optimist viewpoint. But no, it actually wasn't until 2023. 2023, docusate was finally recognized under the OTC monograph for laxatives, and it was final, final by the FDA. This process started in 1970. So from 1970 all the way to 2023, that's how long it took us to decide that all of the OTC laxatives on the market were generally recognized as safe and effective. Dr. Khyati Patel: So, but the bottom line is if you're practicing evidence-based medicine, the evidence says that this doesn't really work. Dr. Sean Kane: Yeah, I mean, it's like a vitamin. So if you want to take it to make yourself feel better, fine, it might not be effective. It's definitely safe. Like as far as we know, there's no reason that you couldn't take it. But from an efficacy standpoint, there's just no data. And if a patient swears by it, they can continue taking it, but I would never recommend it because we have no data that it actually works. [19:56] Dr. Khyati Patel: An interesting thing is like maybe the placebo comparison was water, just drink water and the placebo, right? But then drinking water is actually a lifestyle change that we recommend for patients with constipation. So just drink water. Dr. Sean Kane: Who knows, maybe. And at the end of the day, you know, again, a thing I like about the Things We Do for No Reason articles is that they always end with like, what should you do or what would be a better alternative. So Dr. Patel, what is a common laxative that you think patients and providers should be thinking about for run-of-the-mill normal constipation? Dr. Khyati Patel: And that's where the Miralax kind of comes to mind. That one has good data for multiple different types of constipation. If we recall, that purple cap bottle was a prescription only and then eventually became OTC. So there are store versions of Miralax powder available as well. Dr. Sean Kane: And then there are other options too, for whatever reason if someone doesn't want to do that, what are some other ones to consider? Dr. Khyati Patel: Fiber, right? So those we kind of call in the category of bulk-forming laxatives. These are good way to intake fiber if dietary fiber alone is not sufficient to relieve constipation. This is not for all patients. So if you have opioid-induced constipation, adding more fiber can add more bulk and kind of jam the pipes, per se. So it can aggravate that constipation. But generally pretty safe for all our specific patient populations as well. Dr. Sean Kane: And there are some other ones like senna, bisacodyl, even like enemas, suppositories. There's a lot of different options. I think the key take-home point is for almost everyone, Miralax tends to be the most evidence-based laxative for constipation. Dr. Khyati Patel: Right. And if you're interested in learning more about how you can use over-the-counter medications and self-care of constipation, we can direct you back to our HelixTalk episode of 46, Self-Care of Constipation. Dr. Sean Kane: Perfect. So Dr. Patel, our last stop for the day is heart failure, specifically heart failure exacerbation or acute decompensated heart failure. And the notion that patients should fluid restrict themselves to treat or prevent them from going into heart failure. Dr. Khyati Patel: And so this is where we are discussing free the fluids. And are we then talking about fluid restrictions in patients who are in the hospital, meaning acutely decompensated, or even those who are managed outpatient, meaning they have heart failure but they're not hospitalized? Dr. Sean Kane: It's really both. For the most part, most of the data comes from heart failure exacerbations in the hospital setting, but even on the outpatient side, the theme of not restricting fluid in patients is going to hold true in both settings. Dr. Khyati Patel: Right. So fluid overloaded patients, we are talking about decompensated heart failure patients, may present with symptoms such as peripheral edema, and then pulmonary edema. And that's where the symptomatic issues come in, such as shortness of breath, kind of hearing rales and crackles on the physical exam. Dr. Sean Kane: And intuitively it makes sense. If you have too much fluid in your lungs, maybe you shouldn't drink so much fluid. But it's actually way more complicated of a pathophysiology than that. The reason is that the fluid is not staying in your body because you drank too much. The fluid is staying in your body because in patients with heart failure, they have what is called a neurohormonal compensatory mechanisms. Things like the renin-angiotensin-aldosterone system gets hyperactivated and it causes salt and water retention by the kidney, in addition to other effects as well. So when that RAAS system is activated, whether you drink a lot or a little, you're still going to hold on to a bunch of salt and water in your body. Dr. Khyati Patel: And they always say, Dr. Kane, it's not the fluid problem, it's the sodium problem, right? Dr. Sean Kane: It's true, yeah. And in terms of talking to patients about this, one, it's important that they recognize that just because they drank more doesn't mean that that's why they have pulmonary edema. But then two, if you were to fluid restrict, this is kind of a mean thing to do to patients, to be honest with you. Like it's hard to fluid restrict a patient effectively. Dr. Khyati Patel: Right. And you think that fluid is just, you know, water or juices they're drinking, but any form of food that melts, so we are talking ice cream or other form where we don't think that this is fluid, like milk, also counts. So imagine if they have to count every one of these items they're eating. [24:21] Dr. Sean Kane: And even think about like fruit, right? Like watermelon. It's in the name, right? Yeah. So with that in mind though, there are some patients where fluid restriction is a completely reasonable and effective therapy for patients. The main thing is going to be in hyponatremic patients, so sodium level less than 135. So Dr. Patel, even though it's a sodium problem for hyponatremic patients, intuitively you'd say like, oh, just give them more salt if they're hyponatremic. The actual treatment though is to reduce their intake of water. So it ends up being a water problem, not a sodium problem. It's actually fairly uncommon and not very effective if you have a low serum sodium to make people ingest more sodium, that's actually not very effective. Dr. Khyati Patel: So we're going to restrict the water in these patients, but not in heart failure patients. These are patients who have severely low sodium levels. Dr. Sean Kane: Exactly. And there is a subset of heart failure patients that end up being hyponatremic because of how their kidney is handling water versus sodium. So there is a patient population where that is true, where you can have a heart failure exacerbation and be hyponatremic. And there's actually a whole drug class that was approved basically for that subset of patients called vaptans. Dr. Khyati Patel: And this is again, if the water restriction did not work, the vaptans, which are vasopressin receptor antagonists, can be given. And basically these drugs work by blocking vasopressin receptors in the kidney. And by stopping the action of vasopressin in the kidney, it will kind of cause more that free water excretion from the kidney, so kidney won't retain the water. Dr. Sean Kane: Exactly. So like conivaptan IV or tolvaptan oral, those are two vaptan antagonists. These are not commonly used at all on the market. They do tend to be really effective, but it's a pretty small subset of patients where you'd ever need to get to that point. Fluid restriction is way more common. Dr. Khyati Patel: So then what's going to be the best trial that we can look at for the evidence whether the fluid restriction worked or did not work? Dr. Sean Kane: So I love the trial name. It's called the FRESH-UP trial. This was actually fairly new, 2025. We have it linked in our show notes. And this was about 500 patients with outpatient heart failure, meaning they were class II and III, so New York Heart Association class II and III patients, that were not on the inpatient side, but on the outpatient side who had heart failure. Dr. Khyati Patel: And they were restricted to a fluid restriction of less than 1500 mLs, so less than 1.5 liter, or no restriction at all, drink whatever you want. And really the actual difference between these two subset of population was those who were drinking liberal drank about 1700 mL versus those who were restricted drank about 1400 mL. So you're talking seven cups versus six cups, run rough estimates. Dr. Sean Kane: Which is really not that much, right? And Dr. Patel, I love that you commented on this because it's very common in clinical trials where you have patients that are asked to achieve a goal, goal blood pressure, goal A1C, whatever. It's really important that you don't just look at what were the goals, but like what did they actually do. And in this case, like liberal fluid intake was not that different than a more conservative intake. We're talking 300 mLs. Dr. Khyati Patel: And what was the primary outcome they assessed, Dr. Kane, then? Dr. Sean Kane: So it was a quality of life measure called the Kansas City Cardiomyopathy Questionnaire, or KCCQ. This is a very common quality of life survey instrument used in heart failure patients. And it was not different between the restrict your fluid intake group versus the drink however much you want group. Dr. Khyati Patel: And did you say there was a numerical advantage favoring those who didn't have the restriction? Dr. Sean Kane: Yeah, so if anything, the quality of life measure of the KCCQ was a little bit better, but not statistically significant, in those that could drink however much they wanted to. And this probably came from not having to calculate how much they're drinking throughout the day, but also from probably a thirst distress scale as well. Dr. Sean Kane: Yeah, so they had a thirst distress scale where they asked the patient like, how thirsty are you? Which is kind of mean if you're like, oh yeah, you can't drink and then we're going to see how thirsty you get, right? And it was obviously better in those that could drink as much as they wanted, they weren't as thirsty. But if you think about it, like if a patient is asked to stay less than 1500 mLs indefinitely, they're probably going to get thirsty if they're actually adhering to this fluid restriction ask. Dr. Khyati Patel: Right. And then their lives can revolve around that fact that their mouth is constantly dry and that they have to limit themselves from drinking more water. So how do you resolve that dry mouth, you know? Dr. Sean Kane: Yeah. And again, like why are we doing it? Of the data we have, there is no reason to do it, right? It's not like there's a potential benefit or an upside to making yourself thirsty. There was no quality of life benefit in this 500-patient trial, and all of the data that we have historically doesn't really support a fluid restriction anyway. So we just shouldn't do it. Dr. Khyati Patel: So based on this evidence, I guess the trial that we talked about is fairly new. I'm assuming the guidelines don't have that incorporated yet? Dr. Sean Kane: They didn't incorporate the FRESH-UP trial because it happened three years later, but in the 2022 heart failure guidelines, they do say for patients with advanced heart failure and hyponatremia, and that's the key here, hyponatremia, the benefit of fluid restriction to reduce heart failure symptoms is uncertain. So even among that patient population where they're hyponatremic, we know it can help with their serum sodium, but even in those people, there's no data that says that their outcomes for heart failure are any different or better. Dr. Khyati Patel: And then furthermore, the fluid restriction has not been shown to improve clinical outcomes or the use of diuretics. [30:02] Dr. Sean Kane: Exactly. So we shouldn't do it for heart failure. If you want to do it for hyponatremia, great, but not for heart failure. Dr. Khyati Patel: So then what should we do instead? Allow patients to drink? Dr. Sean Kane: Yeah, just be normal humans, right? Like if they want to drink, drink. If they're thirsty, they should drink some water. It's not going to help or hurt their heart failure symptoms if they choose to drink a normal amount of fluid whenever they feel thirsty. Dr. Khyati Patel: And if they are fluid overloaded, I guess then we could focus on using those loop diuretics to get rid of the extra volume. Dr. Sean Kane: Exactly. So loop diuretics are going to be our mainstay of therapy to get rid of pulmonary edema, peripheral edema. And then of course, optimizing the GDMT, the guideline-directed medical therapy, in terms of their ACE, ARB, or ARNI, their beta blocker, their MRA, their SGLT2 inhibitor if they have reduced EF heart failure. Optimizing those things because that will eventually help their heart failure over time. But if they are on a loop diuretic, they're probably going to get thirsty. And if they're thirsty, they should be allowed to drink water. It's not like they're going backwards if they drink, you know, 500 mLs of water after urinating 500 mLs of water. That's not a net even because when they pee, they're peeing out salt water. Like salt is lost in their urine and that will help with their pulmonary edema even if they intake a similar amount of fluid. Dr. Khyati Patel: And as we talked about, the underlying etiology for why this dysregulation happens is more so that neurohormonal dysregulation. And our GDMT therapies do target that. So really optimizing that should also help with the fluid concerns in these patients. Dr. Sean Kane: Exactly. Yeah. So for the listeners, we do have show notes. So if you want to read the Things We Do for No Reason article, it's at our website, helixtalk.com. Again, this is episode 199. Couple take-home points. So Dr. Patel, what is something that you wanted to remind the audience about? Dr. Khyati Patel: Well, reminder that in aspiration pneumonia, addition of anaerobic coverage is not needed unless patient has necrotizing pneumonia, empyema, or lung abscess that's been diagnosed. So our antibiotic selection should be along the lines of CAP or HAP guidelines, even if the aspiration is suspected or observed, because commonly those will be the pathogens that we would like to cover. Dr. Sean Kane: And then our second item was drop the docusate. So docusate probably is really safe, but not shown to be effective. So current data says we shouldn't really be using docusate if you want an effective therapy. Instead, things like polyethylene glycol 3350, also called Miralax or PEG 3350, psyllium, any of our stimulant laxatives, there's a bunch of other options, but PEG 3350 tends to have the best data in terms of undifferentiated constipation treatment. Dr. Khyati Patel: And then patients with heart failure should not be fluid restricted unless they have that, you know, hyponatremia. The extra fluid overload can be treated with the diuretics, and then we should definitely target the GDMT optimization in these patients. Dr. Sean Kane: So for the listeners, if you want to get an email when new episodes come out, you can sign up for our mailing list at helixtalk.com. We're also on Apple Podcasts and any other podcast app, and we love the five-star reviews there. And then again, show notes are at our website, helixtalk.com, episode 199. So with that, I'm Dr. Kane. Dr. Khyati Patel: And I'm Dr. Patel. And as always, study hard. (Music) Announcer: If you enjoyed the show, please help us climb the iTunes rankings for medical podcasts by giving us a five-star review in the iTunes store. Search for HelixTalk and place your review there. To suggest an episode or contact us, we're online at helixtalk.com. Thank you for listening to this episode of HelixTalk. This is an educational production, copyright Rosalind Franklin University of Medicine and Science.