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Acute Pancreatitis
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Acute Pancreatitis
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Segment:0 .
[Dr. Smith] Welcome back to Run the List, a medical education podcast in partnership with McGraw Hill Medical. Our hosts are Dr. Navin Kumar, Dr. Walker Redd, Dr. Emily Gutowski, Dr. Joyce Zhou, and myself, Blake Smith. As a quick disclaimer, this podcast is meant for informational and educational purposes only, and should not be understood as medical advice under any circumstances.
[upbeat music] [upbeat music] [upbeat music] Welcome back to Run the List. As we mentioned in our previous two-part series on medical education, we're really excited to officially launch our second season in partnership with McGraw Hill Medical, and our goal for the second season is to continue to cover core topics in internal medicine, where we're going to be aiming for biweekly episode releases, so make sure to check back every other week wherever you get your podcasts.
In this second season, we're going to be doing a deep dive on some of our very first episodes, and today, we're going to be starting with gastroenterology. We're going to be re-recording with some brand new content and enhanced audio, and we're going to be having new guests this season, so stay tuned for our new episodes. So to keep the momentum going, we're going to continue with a guest we recently have had, which is our very own Dr. Navin Kumar, who's an attending gastroenterologist at Brigham and Women's Hospital and the associate medicine clerkship director also at the Brigham, and at Harvard Medical School.
So, Navin, we're going to talk to you today about pancreatitis, do you want to Run the List? [Dr. Kumar] Thanks so much for having me, Blake, very excited to come back as the expert and do this episode with you again. [Dr. Smith] Awesome. So let me introduce the case of a 39-year-old male who has no significant documented past medical history, who presented with intractable epigastric abdominal pain that he notes radiated to his back, and he also presented with nausea and vomiting.
So he has been pretty unwell with these symptoms. His vitals are a heart rate of 94, blood pressure of 130/76, he's satting 99% of room air, and he's breathing 18 times a minute. He notes that he doesn't take any prescription meds at home, and there's no notes in the electronic medical record. The emergency medicine resident said the patient was very tender on exam, and that he's been on a bit of an alcohol bender recently, and he's intentionally avoided seeing doctors in recent years, as they've typically advised him to decrease his alcohol intake.
The resident also mentioned that his lipase was extremely elevated, at 1,200. I could go into the labs if you want, but maybe I'll pause there. [Dr. Kumar] Yeah, Blake, thanks for that initial intro. So, given the patient's risk factor of alcohol usage, and it looks like he recently increased that alcohol intake, and with his pain localized to his epigastrium, radiating to his back, with associated nausea and vomiting, it's always important to keep a very broad differential, but I think it's also important to put your nickel down on what you think is most likely going on, especially when you're in the emergency room.
And so I think, very much so, for this clinical presentation my number one diagnosis is acute pancreatitis, but you'll provide some labs that's going to help rule in or rule out that diagnosis, and we'll keep moving through this case together. [Dr. Smith] Definitely. So some other labs came in. He had a BUN that was elevated at 28, he had a normal creatinine of 0.8, CBC with mild leukocytosis of 11,000, hemoglobin of 17, hematocrit of 51, and liver enzymes with an AST of 82, ALT of 40, and otherwise normal alk phos and total bilirubin.
And again, his lipase was returned elevated at 1,200. So, beyond those labs, Navin, do you need any additional testing at this point to further cinch your diagnosis of acute pancreatitis? [Dr. Kumar] Yeah. It's a really important question. Do we have the diagnosis already? And so when I think about acute pancreatitis, I think about the three criteria for making that diagnosis and the need to have at least two of those criteria to confirm that this is acute pancreatitis.
So the first criterion is clinical, and by that I mean, does a patient have the typical clinical presentation of acute pancreatitis, with acute onset epigastric pain, often with radiation to the back, with associated nausea and vomiting? He surely has that. So he has the clinical, he meets the clinical criterion. The next criterion is laboratory evidence, and so that means that the patient has a serum lipase or amylase that's greater than or equal to three times the upper limit of normal.
This patient has a lipase of 1,200. And this brings up a good teaching point, which is that various hospitals have different reference ranges for their pancreatic enzymes, so it's really important to go back and look at the actual lab value to see what the normal range is. Blake, do you have the normal range for this patient's lipase? [Dr. Smith] Yeah, the upper limit of normal in our hospital is 60.
[Dr. Kumar] Perfect, so as long as the lipase is above or equal to 180, that would be consistent with acute pancreatitis, and sure enough, if his lipase was 1,200, we meet that criterion. So we already have two out of the three criteria, we have the clinical and laboratory criteria met. So he meets criteria for acute pancreatitis. Now, the third criterion is imaging, and typically, this is looking for findings consistent with acute pancreatitis on a contrast-enhanced CT, but also MRI or ultrasound could potentially pick up on that diagnosis as well.
In this scenario, we don't need radiographic imaging, because we already met the first two criteria, and I would also be very cautious about ordering a contrast-enhanced CT of this patient, given the lab findings that you already mentioned. The BUN of 28 with a creatinine of 0.8 suggests that he already has some intravascular volume depletion that's leading to prerenal azotemia, and then you also mentioned his hemoglobin of 17 and hematocrit of 51, that's very high and so I'm suspecting that he has some degree of hemoconcentration in the setting of intravascular volume depletion due to the acute pancreatitis.
So if this patient is already intravascularly depleted, giving him additional IV contrast would really put him at risk for contrast-induced nephropathy, and so I would be very, very careful about ordering a CT ab and pelvis, it's not going to change my management, I have the diagnosis. And if you're looking for complications in a patient with acute pancreatitis, they don't appear this early, they usually appear about 72 hours later.
So there's really no reason to order a CT ab and pelvis in this patient. [Dr. Smith] Wow, so many teaching points all in one about pancreatitis there. So what are the very first steps in management and stabilizing this patient, now that we've kind of cinched a diagnosis of acute pancreatitis, and how do we think about the severity of this acute pancreatitis?
[Dr. Kumar] Yeah, so the first thing after I made a diagnosis of acute pancreatitis is I want to get a sense of, how severe is this patient's presentation? So I first just kind of glance at the labs, as we already kind of did together, I look at the BUN, the creatinine, the hemoglobin. In this patient, the BUN is elevated, the hemoglobin is elevated, fortunately, the creatinine is still normal, so at least this patient hasn't developed any renal insufficiency, but the fact that the BUN and hemoglobin are up, that's suggesting that this patient, like I said, is intravascularly volume depleted, and that's generally how these patients develop complications, is that they have decreased perfusion, end organ perfusion in the setting of all the third spacing due to the inflammatory reaction set off by the pancreatitis.
And so, I'm already a bit worried about this patient, because I'm seeing those signs early on. Then you can get a little bit more specific, and so, looking to see if the patient meets criteria for SIRS, or systemic inflammatory response syndrome, is helpful because patients who meet criteria for SIRS and acute pancreatitis have a higher risk of mortality. And we don't need to go through the specific criteria of SIRS, but in general, it has to do with the temperature being elevated or low, the heart rate being elevated, the white blood cell count being high, low, or having a lot of bands, and then having a high respiratory rate.
If you have two of those four criteria, you meet criteria for SIRS, and again, seeing that in a patient with acute pancreatitis, that increases the risk for mortality. The specific score for pancreatitis that I like to use is called the BISAP score, and it's an acronym, so each of these letters stands for one of the criteria. "B" is BUN above 25, "I" is impaired mental status, "S" is SIRS, "A" is age greater than 60, and then "P" is the presence of a pleural effusion on chest X-ray.
And so you get a point for each of those, and if you have three or more of those criteria met, that patient's considered to have severe acute pancreatitis, and they have a much higher mortality rate than someone who has a BISAP score of 0 or 1. So I really like to use that score, because it's an objective way of getting a sense of where's my patient going, what's their risk for actually having some really bad complications.
And if they have a very high BISAP score, I'm more inclined to triage them to the ICU for a higher level of care. So that's job number one, is risk stratification, and I like to use an evidence-based score like the BISAP score to do that. And then the pillars of treatment are bowel rest, because you want to rest the pancreas, you don't want to stimulate the pancreas anymore, so NPO status upfront.
And then fluid resuscitation is really important, and we've been talking a lot with this patient about how their volume status is low. And so you need to fluid resuscitate them, and you have to do it aggressively. So the types of fluids that you should be using in a patient with acute pancreatitis should be isotonic crystalloids, and those are either normal saline or lactated Ringer's.
Lactated Ringer's is actually preferred, it's been shown to decrease the risk of SIRS, and so that is the IV fluid of choice in my practice. And then it's important to think about the rates. So usually when you think about maintenance fluid rates in a patient who's hospitalized, you think about rates about 75 cc's an hour to 125 cc's an hour. You are aiming for much higher rates in acute pancreatitis, generally between 250 and 500 cc's of fluid per hour.
generally between 250 and 500 cc's of fluid per hour. So it's a lot of fluid, and if they're severely volume depleted, which you may note by some additional exam maneuvers, like checking orthostatics on exam, you actually bolus them with a pretty significant fluid bolus, 20 cc's per kg over the first half an hour to 60 minutes, and then you start the continuous drip at 3 cc's per kg per hour.
So if a patient weighs, let's say, 100 kilos, that means you're giving them a 2 liter bolus over 30 to 60 minutes, and then starting a rate of 300 cc's an hour, so these are really high rates of fluid. And I think in general, on internal medicine, we often under-resuscitate because we're so nervous about the complications of fluid overload, but this is really the only way to prevent acute pancreatitis complications, is restoring that intravascular volume to prevent the end organ malperfusion.
And fortunately, it's not something you do for a very long time. The evidence shows it's most beneficial within the first 24 to 48 hours, and particularly the first 12 to 24. So you really only do this upfront, after that, the benefits are outweighed by the cons, and so this is something that you're doing upfront with very careful monitoring of the patient to see if they're developing signs of fluid overload, but also recognizing that after day one, and especially day two, you really need to come back down on the fluids, because it's not going to actually benefit the patient.
The last piece, we talked about risk stratification, bowel rest, and IV fluids, is pain management. These patients are in a significant amount of pain. They almost always need opioid therapy to actually deliver adequate pain control, and most of the GI physicians, we prefer, and I think also hospitalist medicine as well, prefer when a PCA can be administered. Blake, have you heard of a PCA before?
[Dr. Smith] A little bit, but why don't you expand upon it for the listeners? [Dr. Kumar] Yeah, for sure. It's called patient-controlled analgesia, and so how it works is that a patient will have a set rate of continuous IV infusion of a narcotic, a set rate of continuous IV infusion of a narcotic, but then on top of that, they can actually bolus themselves up to a certain threshold as needed.
And this provides them with much better pain control, because as you can imagine, the time it takes for a patient to reach out to a nurse to say they're in pain, for that nurse to then page the respondent clinician to put in an order for additional pain medication, and then that pain medication to actually get to the patient takes time. So this allows them to control their pain much more acutely, but then also realize that since they're getting IV narcotics with a basal infusion as well, you have to think about side effects.
So obviously, with IV narcotics, you have to worry about CNS or respiratory depression. If the opiate dose is far too much, you can actually start to see vital sign changes like hypotension. And then, something that we see often in acute pancreatitis is decreased gut motility or ileus, which can be due to the inflammation, but more oftentimes is due to the opiates that the patients are requiring for pain control as well.
[Dr. Smith] Thanks for that super comprehensive answer. And with any pancreatitis case, there's always a lot going on with the patient, a lot to consider, and a lot to do. So just to summarize real quick, Navin mentioned risk stratification using the BISAP score, making sure they have bowel rest and they're NPO, aggressive volume resuscitation using IV fluids, that will depend on the level of volume depletion, and pain management as the mainstay of early treatment within the first 24 to 48 hours.
So once we've made sure those first steps have been taken, how do you then think about the possible causes of the acute pancreatitis? [Dr. Kumar] Yeah, it's a great question, Blake, because oftentimes I feel like we make the diagnosis and then we just started management, and we don't really think about why a certain diagnosis occurred. So I think in acute pancreatitis, it's really important to think about all the different causes, especially when a patient's coming in with their first episode and you don't have a clear etiology yet.
So I always think about the top two causes, those being gallstones and alcohol, when evaluating a patient who's presenting with acute pancreatitis. And then I like to, honestly, I lean on a mnemonic that I learned as a med student, the I GET SMASHED mnemonic. Blake, is that still something that's taught today, or- [Dr. Smith] I was totally taught it as well. [both chuckle] [Dr. Kumar] Yeah. So we don't necessarily need to go through every single aspect of the mnemonic, but obviously, gallstones and ethanol are on there.
Triglycerides are something I think about, when the triglycerides are above 1,000, that can cause acute pancreatitis. Obviously, anyone post ERCP is going to be at risk for pancreatitis because the pancreatic duct is often intervened upon during those ERCPs. And then drugs is a really big one, looking through the list of medications that your patients are on to see if they are on any medication that may increase the risk of acute pancreatitis.
So I think the main take-home point here is remember the top two, gallstones and alcohol, but also be systematic about thinking about the other potential causes using a mnemonic like I GET SMASHED. [Dr. Smith] Yeah, and that mnemonic, embedded in it is one of the top two causes of alcohol use. And as we've already seen in the history of this patient, our 39-year-old male has been on kind of a recent alcohol bender.
So, with this case, and others more broadly, Navin, how do you go about finding a possible cause within that mnemonic? [Dr. Kumar] That's great. So I always go through the order of things in the way that I'm obtaining the information from the patient. So you start with the history, you assess for risk factors, and then you look at their medications and see if there are any typically offending medications for acute pancreatitis, and then the labs are helpful.
If you look at the liver enzymes, you may see potentially a cholestatic pattern with an elevated alkaline phosphatase, potentially an elevated T-bili that would point towards this potentially being a biliary cause. Just a quick note, depending on the timing of when you are catching those labs, you can see hepatocellular types of injury in biliary obstruction if you're catching it early, so don't be alarmed if you see AST, ALT in the high hundreds, even thousands, in the setting of biliary obstruction.
It's all about when that blood is drawn, compared to when the initial obstructive event occurred. But obviously, if the liver enzymes are off, I'm thinking that there could be a gallstone etiology. And then I'll confirm that I think all patients who come in with acute pancreatitis with no clear cause should first have an ultrasound looking for gallstones or even common bile duct dilation that would suggest a gallstone embedded in the common bile duct.
And then, we talked about this earlier, but really, you're only using a CT scan or MRI, this cross-sectional imaging, if your diagnosis is in question or later in the course if the patient's may be developing a complication like fever. Otherwise, you really should not be ordering a CT scan upfront on these patients. We mentioned triglycerides, if they're above 1,000, they can cause acute pancreatitis, so you should get a fasting lipid panel.
You look at the serum calcium, hypercalcemia's part of that mnemonic, and so you'll look at that with your basic labs upfront. And then, if a patient's having recurrent episodes of unclear etiology, you should be considering an autoimmune pancreatitis, and the IgG4 level is actually helpful in that scenario. So if recurrent episodes, I would think about studying that lab as well.
[Dr. Smith] Yeah, awesome. And so, for our patient, we did a right upper quadrant ultrasound, which was negative, and given the history and their AST/ALT ratio, we were thinking it's most likely alcohol-related pancreatitis. So the patient does remain hemodynamically stable. Their pain is improving with our initial pain management on a PCA.
And Navin, what are the most important aspects now of therapy and treatment after that initial wave of treatments we've provided? [Dr. Kumar] Yeah, so you want to think about what is the cause, and is there anything you can do to reverse that cause so that another episode doesn't occur. So in this case, it would be really, really useful to provide resources for this patient to hopefully achieve alcohol cessation.
In someone who's coming with an episode of gallstone pancreatitis, a key teaching point is that the gallbladder should be removed, ideally on that same admission, if the patient's coming in with a mild case of acute pancreatitis, this is, again, a BISAP score of 0 or 1, because if you leave that gallbladder in, within three months, there's a 30% chance they come back with another episode of gallstone pancreatitis, and it might be that next time is more severe.
So that's a good teaching point on gallstone pancreatitis. Take the gallbladder out on the same admission, if mild, if it's severe, they have to come back in six or eight weeks for surgery, because they need time for the inflammation to heal. And then, other causes, again, looking at the medication list, if they're on anything that could be contributing, you have to consider stopping those medications.
And then the more unique situations of hypercalcemia or hypertriglyceridemia, you will address those while they're inpatient. Then you want to, again, think about the fluid management, and as we discussed earlier, aggressive fluid resuscitation early is a key part of treatment, but remember, after day one, day two, those aggressive fluid resuscitation efforts are no longer helpful, and so, make sure to come back down on your fluids after that period of time.
And then I think the question of when to feed your patients always comes up, and so you have to think about where your patient is in their presentation. If their pain is improving and they're moving their bowels, so there's no evidence of ileus, no nausea or vomiting, then it may be time to try some PO diet. then it may be time to try some PO diet. And so there's good evidence, actually, RCT-based evidence, that you can go straight to a low fat solid diet when the patient is ready in cases of mild acute pancreatitis.
We used to do this ramp-up, clear liquids, full liquids, soft solids, but now we've learned that you can go straight to a low fat solid diet for those cases. And then those who have a severe acute pancreatitis, again, this is randomized controlled trial data informing this decision that you can actually wait 72 hours for them to be NPO. So on day three of this trial, they then challenged their patients to eat, and those who failed then had an NG tube, a nasoenteric tube, placed the following day.
And they compared that strategy to having a nasoenteric feeding tube placed on the initial day of admission. So half those patients had a full 72 hours to recover before they got fed, the other half got the nasoenteric feeding tube placed upfront. And what they found was there's no difference in the clinical outcomes between those two groups, which heavily favors the wait-and-watch approach, because having a nasoenteric feeding tube placed is very painful and is not without risk, and so, if you can wait three days and have the same outcomes- Interestingly enough, those patients who were given a chance to feed on day three, over two-thirds of them actually could, and so they avoided that whole placement of a nasoenteric feeding tube.
So now we know for severe cases, we can wait three days, challenge them, if they fail, then do a nasoenteric feeding tube. And we always want to use the gut if we can. So let's say you start with a nasogastric tube, it doesn't work, you then can use a nasojejunal tube, with the idea being that you're depositing the tube feeds distal to the pancreas, so you won't activate the pancreas.
That is a little bit more complicated to schedule, either interventional radiology or GI has to do that. You can't just do at the bedside. So it's always good to start with an NG tube because it's more readily available, but if they still are failing nasojejunal feeding, then, last resort, we'll opt for TPN. We really want to use the gut when we can, so TPN is really a last resort.
And then the last, last point I just want to make is that antibiotics should not be given prophylactically. They actually preselect for fungal infections when used in that manner. So you only use antibiotics if you are convinced there's an infection brewing. [Dr. Smith] Thanks for that, Navin. And just as a student, this is what I love about pancreatitis as a clinical topic, because there's so many evidence-based treatments that are provided, as with any other condition, but it's very stepwise and it's all within a very acute, early time, phased treatments that make sense and are very logical.
And I actually forgot about the enteral feeding point that I had learned, so thank you for the reminder there. You know, because pancreatitis is systemic in some ways and could lead to things like ARDS, when should we call a consultant in these cases? [Dr. Kumar] You know, if you've listened to this episode, I feel like you will know the pillars of management for acute pancreatitis and you really only call a consultant when either you feel uncomfortable with the patient or the patient's not doing well.
So I think that's true for any case, but specifically for acute pancreatitis, if someone's having recurrent episodes of acute pancreatitis of unclear etiology, I think that's a good time to call GI to help investigate for more rare causes, and then, certainly, if they have biliary obstruction, that may warrant a GI consult because if it's just gallstone pancreatitis and there's no concern of a retained stone, that can generally be managed by a medical team, but if there is concern that there's a stone stuck in the common bile duct, that patient may need an ERCP.
And a key teaching point here is that you don't do an ERCP for a patient with gallstone pancreatitis and concern for a CBD stone upfront, because that would be very damaging to the pancreas to intervene on that area with an ERCP, you have to wait at least, generally, 72 hours, and maybe even more, for the inflammation to improve before you do an ERCP to remove the stone, except, there's one caveat, and that's if the patient has fevers and you're concerned for cholangitis.
If they're cholangitic, yes, you have to move forward with an ERCP acutely, while they're still inflamed, because that is a life-threatening issue, but if they're not cholangitic, you wait, and hopefully the stone passes on its own and they just need to have a cholecystectomy, but if there's still evidence of biliary obstruction, even after day three, then GI will most likely go in with an ERCP.
[Dr. Smith] Yeah, and we went easy on the listeners in this case by not having cholangitis, choledocholithiasis, and pancreatitis all at once- [chuckles] But thank you, thank you for that GI trivia there. So as we near the end of this patient's case, what are some of the complications we need to watch out for, especially as we fluid resuscitate these patients? [Dr. Kumar] So upfront, we talked about looking for SIRS, and so you'll do that as part of your risk stratification, but you also should acutely- The things can happen, like a splenic vein thrombosis, the splenic vein courses right behind the pancreas, so that inflammation can extend into the splenic vein and lead to thrombosis in that area.
When that happens, the splenic vein can't drain into the portal vein, so all that blood gets backed up, it goes to the spleen, and then in some instances, collaterals form between the spleen and the stomach, and you actually can get a gastric variceal bleed from backup from a splenic vein thrombosis. And so, especially if you have a patient with acute pancreatitis who all of a sudden has hematemesis, you have to think, could they have a splenic vein thrombosis leading to a gastric varix?
And then you want to address the thrombosis, ideally, but if you can't, if you take the spleen out, you actually prevent that backflow to the stomach, and so a splenectomy is considered definitive therapy for gastric variceal bleed due to an SVT. You mentioned ARDS, so, ARDS, definitely need to be monitoring for that, and those patients obviously need to be in the ICU. And then, once you're out of the acute period and more in the subacute period, you can have issues with fluid collections, necrosis can happen.
This is more in the matter of days, as opposed to weeks. And so if a patient develops fever or worsening pain, that's when you want to actually get a CT ab and pelvis and look for necrosis. And on longer term, after four weeks, sometimes that fluid collection doesn't just resorb, it gets reorganized into a pseudocyst, and that can cause obstructive symptoms, depending on what the cyst is pushing on.
Oftentimes, it pushes on the duodenum or the stomach, so patients feel nausea, vomiting, early satiety, and so that can benefit from drainage. Usually now we're doing endoscopic drainage, as opposed to IR. And then you can also develop abscesses, the necrosis can get infected, the necrosis can get walled off, and we, again, can endoscopically treat those complications.
And then lastly, long, long term, if a significant amount of the pancreas was involved in the initial episode of acute pancreatitis, some patients actually develop chronic pancreatitis, so you kind of have to think about the timeline from acute all the way to even years after when you're thinking about what complications can occur. [Dr. Smith] Yeah. That was great. Thanks for taking us on that timeline from acute to subacute, and even on the year time scale.
So just returning to the case and to wrap up, we have a 39-year-old male who had no significant documented past medical history who presented with intractable epigastric abdominal pain that radiated to his back with nausea and vomiting. He really ended up doing well in this case, and workup was otherwise unrevealing. His ultrasound was negative of the right upper quadrant. So this was kind of understood to be likely alcohol-induced acute pancreatitis.
We gave him early and aggressive IV fluids with lactated Ringer's, and this volume resuscitation alongside IV pain meds and remaining NPO, resulted in him doing well. We initiated enteral feeding with a low fat diet on hospital day three, and he was able to ultimately advance diet over the next day or two. And throughout, he remained hemodynamically stable, and he was given resources to help with his alcohol use disorder, and we scheduled close follow-up with his PCP.
So, Navin, if you want to just take us through your three clinical pearls as takeaways, because even though it was kind of an easier case of pancreatitis, there's so much to consider with each and every patient. So without further ado- [Dr. Kumar chuckles] Thanks, Blake. Yeah, so my first pearl is, think about what's common in terms of causes, so causes of acute pancreatitis, the leading two are gallstones and alcohol.
So have those upfront when you're assessing what could be the etiology of the acute pancreatitis. In terms of management, for my second pearl, it's four things, right? So you have to risk stratify, aggressive IV fluids, bowel rest, but then remember to initiate a PO or enteral diet when those patients are ready, and then lastly, manage their pain well with generally IV narcotics, but PCAs can give you a better balance of pain administration.
And then the last pearl is that there are many complications that can occur in acute pancreatitis, so think about the timeline of where your patient is in their presentation in terms of what complications could occur. And then, if they have any features that are concerning, or have a high risk assessment on your initial risk stratification, have a low threshold to elevate them to an ICU level of care because these patients, especially those who have severe acute pancreatitis, can have really bad outcomes unless they're addressed early.
And so, Blake, I know you're going to wrap up, I just want to thank you for this episode. I think what our listeners are going to see, we spent a little bit more time today, and so that's what we're going to do for the remainder of the season, like Blake said, we're going to do a deeper dive and really try to flesh out these topics so that our listeners will have even more to take home and deliver high level care to their patients as we move through these various blocks.
[Dr. Smith] Couldn't have said it better. Thank you, Navin, for joining us as our guest on this episode of Run the List, and listeners, we hope you enjoyed this first episode in our second season with McGraw Hill. And to the new interns, good luck as you hit the wards. This will be released on July 1st, so we wish you well as you listen to Run the List and help your patients.
And join us again in two weeks for our next episode. [outro music] [outro music]